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Acute Pelvic Pain | Disease Name : Acute Pelvic Pain, Treatment : "Pain relievers. Over-the-counter pain remedies, such as aspirin, ibuprofen (Advil, Motrin IB, others) or acetaminophen (Tylenol, others), may provide partial relief from your pelvic pain. Sometimes a prescription pain reliever may be necessary. Pain medication alone, however, rarely solves the problem of chronic pain.,Hormone treatments. Some women find that the days when they have pelvic pain may coincide with a particular phase of their menstrual cycle and the hormonal changes that control ovulation and menstruation. When this is the case, birth control pills or other hormonal medications may help relieve pelvic pain.,Antibiotics. If an infection is the source of your pain, your doctor may prescribe antibiotics.,Antidepressants. Some types of antidepressants can be helpful for chronic pain. Tricyclic antidepressants, such as amitriptyline, nortriptyline (Pamelor) and others, seem to have pain-relieving as well as antidepressant effects. They may help improve chronic pelvic pain even in women who dont have depression.", Laparoscopic surgery. If you have endometriosis, the adhesions or endometrial tissue using laparoscopic surgery. During laparoscopic surgery, your surgeon inserts a slender viewing instrument (laparoscope) through a small incision near your navel and inserts instruments to remove endometrial tissue through one or more additional small incisions.,Hysterectomy. In rare complicated cases, removal of your uterus (hysterectomy), fallopian tubes (salpingectomy) or ovaries (oophorectomy). There are important health consequences to having this procedure, Pathophysiology : Pelvic pain may have multiple causes, including : Inflammation or direct irritation of nerves caused by injury, fibrosis, pressure, or intraperitoneal inflammationContractions or cramps of both smooth and skeletal musclesSome of the more common sources of acute pelvic pain, or pain that happens very suddenly, may include : Ectopic pregnancy (a pregnancy that happens outside the uterus)Pelvic inflammatory disease (also called PID, an infection of the reproductive organs)Twisted or ruptured ovarian cystMiscarriage or threatened miscarriageUrinary tract infectionAppendicitisRuptured fallopian tubeSome of the conditions that can lead to chronic pelvic pain may include : Menstrual crampsEndometriosisUterine fibroids (abnormal growths on or in the uterine wall)Scar tissue between the internal organs in the pelvic cavityEndometrial polypsCancers of the reproductive tractOther causes may be related to problems in the digestive, urinary, or nervous systems., Epidemiology : 1 in 7 women., GOOD, To Do : MAINTAIN HYGIENE -,PERINEAL HYGIENE IS MUST, Complications : infertility, TUBO OVARIAN ABSCESS, CHRONIC PELVIC PAIN, Diagnostics : USG ABDOMEN(W/A), MRI, CT SCAN, HISTORY TAKING, Differential diagnosis : abdominal tuberculosis, Abortion, dermoid cyst / mature cystic teratoma, Endometriosis, Ovarian Cyst, Ovarian Tumours, placenta abruptio, Red degeneration of Fibroid, disease description : Pelvic pain is not an uncommon complaint in women, and
its diagnosis and management can be taxing at times.
Acute pelvic pain is an emergency and requires prompt
and selective investigations to deal with the condition.
Treatment is either medical or surgical. |
Acute Pericarditis | Disease Name : Acute Pericarditis, Treatment : medication : Ibuprofen , Indomethacin , Colchicine , Aspirin/Acetylsalicylic acid, Treatment for acute pericarditis may include medication for pain and inflammation, such as ibuprofen or high-dose aspirin. Depending on the cause of your pericarditis, you may need an antibiotic or antifungal medication.,,If you have severe symptoms that last longer than two weeks, or they clear up and then return, your healthcare provider may also prescribe an anti-inflammatory drug called colchicine (Colcrys® or Gloperba®). Colchicine can help control the inflammation and prevent pericarditis from returning weeks or even months later. Your provider may also prescribe a steroid medicine called prednisone, especially if you have kidney disease that makes it difficult for you to take ibuprofen and colchicine.,,If you need to take large doses of ibuprofen, your provider may prescribe medications to ease gastrointestinal (stomach and digestive) symptoms. If you take large doses of nonsteroidal anti-inflammatory drugs (NSAIDs), you’ll need frequent follow-up appointments to look for changes in your kidney and liver function.,,If you have chronic or recurrent pericarditis, you may need to take NSAIDs or colchicine for several years, even if you feel well. A diuretic (“water pill”) usually helps get rid of the extra fluid constrictive pericarditis causes. If you develop a heart rhythm problem, your provider will talk to you about treatment.,,Your provider may also talk to you about treatment with steroids or other medications, such as azathioprine (Azasan® or Imuran®), IV human immunoglobulins or anakinra or rilonacept.,If your pericarditis is caused by an infection, your provider will prescribe specific medicines to treat that infection. If your pericarditis is caused by cancer, the most effective treatment is to treat the cancer., If you have constrictive pericarditis, you may need to have some of your pericardium removed. This surgery is called a pericardiectomy. Surgeons perform this on people who develop scar tissue in their pericardium. It’s not normally for people who have active inflammation and chest pain from pericarditis., Pathophysiology : Under normal circumstances, the pericardium has enough room inside it for your heart to expand and fill up with blood between heartbeats. Inflammation of the pericardium is usually not dangerous on its own, but it can lead to dangerous complications. These happen when fluid buildup inside the pericardium — a pericardial effusion — compresses your heart.Swelling and fluid buildup inside the pericardium can fill that space and crowd out your heart. When this happens slowly, sometimes the pericardium can stretch to allow for the extra fluid and your heart to beat properly. But when it happens quickly, the fluid pushes on your heart. So the heart doesnt have room to expand and can’t fill up with blood as it should. This reduces how much blood your heart can pump and causes a condition known as cardiac tamponade, which is a life-threatening medical emergency. Tamponade can stop your heart, which is deadly within minutes., Epidemiology : 27.7 per 100, 000 individuals annually, good, Because acute pericarditis happens unpredictably, it isn’t a preventable condition. The only thing you can do is reduce your risk of developing it by avoiding situations or circumstances that can cause it.,,The only way to avoid developing pericarditis is to avoid circumstances that can cause it. The ways you can do this include : ,,Get bacterial infections treated,Avoid injuries, Complications : cardiac tamponade, PERICARDIAL EFFUSION, constrictive pericarditis, Diagnostics : Amylase, Lipase, 2-D Echo, ECG, Endoscopic USG, X RAY CHEST, CARDIAC MRI, Differential diagnosis : hyperkalemia, Myocardial infarction, myocarditis, Pleurisy, PNEUMONIA, PNEUMOTHORAX, disease description : Acute pericarditis is painful inflammation of the pericardium, the fluid-filled pouch surrounding your heart. The pain usually gets worse when you’re lying down or when you breathe in. Depending on the cause, it’s almost always treatable, and most people with this condition will recover with few or no complications. |
Acute Pericoronitis | Disease Name : Acute Pericoronitis, Treatment : Your dentist may recommend using a prescription mouthwash that contains chlorhexidine, a topical antiseptic. It helps destroy harmful bacteria in your mouth.,,People who use chlorhexidine rinses may develop temporary side effects, such as a change in taste or dental staining. These side effects are typically short-lived. Be sure to follow the instructions provided by your dentist., Oral antibiotics can help clear up a pericoronitis infection. Be sure to take any medications exactly as directed by your healthcare provider., Your dentist irrigates the affected area to flush out any food particles, bacteria or other debris. They may also prescribe medications, such as antibiotics or an antibacterial mouthwash., If your wisdom tooth continues to cause pericoronitis and other problems, wisdom tooth removal may be necessary. An oral surgeon or periodontist can perform this procedure with or without sedation., In many cases, your dentist may recommend removing the gum flap (operculum). This requires a short oral surgery procedure. Sedation is available, but often unnecessary. Typically, your provider can complete this procedure with local anesthesia in less than one hour., Pathophysiology : The previously sterile space formed between the crown of a tooth and the dental follicle is exposed to intraoral microflora as the tooth erupts into the oral cavity. This small pocket that is surrounded by the soft tissue overlying the erupting tooth is difficult to clean. This forms an excellent environment for obligatory and facultative anaerobic bacteria to dwell. In addition, food can easily get impacted into this space, promoting bacterial growth and causing infection of the surrounding soft tissue, so-called pericoronitis. The microflora of pericoronitis is diverse and differs from pathogens that cause periodontitis. In a study of microbiota of pericoronitis, Actinomyces oris, Eikenella corrodens, Eubacterium nodatum, Fusobacterium nucleatum, Treponema denticola, and Eubacterium saburreum were present in high levels. In short, pericoronitis results from bacterial overgrowth in a confined space that is exacerbated by poor cleansability.A factor that can exacerbate pericoronitis is mechanical trauma from the opposing dentition. As maxillary third molars erupt, they can occlude onto the operculum overlaying the erupting mandibular third molars. Such repeated trauma can cause ulcerations and worsen the symptoms., Epidemiology : 4.92% prevalence among patients who are between 20 and 25 years old., good, You can’t prevent pericoronitis altogether. Sometimes, it can occur even if you have excellent oral hygiene. But there are ways to reduce your risk : ,,Brush your teeth two to three times a day.,Floss between your teeth once a day.,Use an antibacterial mouthwash twice daily.,Visit your dentist regularly for exams and cleanings.,Follow your dentist’s treatment recommendations., Complications : sepsis, "ludwigs angina", lockjaw, Diagnostics : X RAY, PHYSICAL EXAMINATION, Differential diagnosis : Acute Periodontitis, Dental Caries, Periapical Abscess, Pyogenic granulomas, disease description : Pericoronitis is swelling of the gum tissue around your wisdom teeth. Sometimes called third molars, your wisdom teeth are the last set of adult teeth to erupt (grow in) — usually in your late teens or early 20s. Pericoronitis may develop around one or more wisdom teeth.Pericoronitis may develop around one or more wisdom teeth. |
Acute Periodontitis | Disease Name : Acute Periodontitis, Treatment : Oral hygiene practices,Brush your teeth twice a day with a fluoride toothpaste.,Consider using an electric toothbrush, which may be more effective.,Floss at least once a day to remove plaque.,Visit your dentist at least twice a year for a professional cleaning.,Don’t smoke or chew tobacco., Professional cleanings,During a professional cleaning, your dentist will remove plaque buildup and tartar from your teeth and their roots, and then polish your teeth and treat them with fluoride. Any periodontal pockets that have formed could require deep cleaning to enable healing. A deep-cleaning method called scaling and root planing will help scrape off tartar and also remove any rough spots on the tooth root where bacteria tend to gather., Antibiotics,In some cases, your dentist will prescribe antibiotics to help with persistent gum infections that haven’t responded to cleanings. The antibiotic might be in the form of a mouthwash, gel, or an oral tablet or capsule., If inflammation persists in sites that are inaccessible to brushing and flossing, your dentist may recommend a surgical procedure called flap surgery to clean deposits under your gums. Under anesthesia, your gums are lifted away and the roots of your teeth cleaned. Your gums are then sutured (stitched) back into place.,,If you’ve had any bone loss, a procedure known as bone grafting may be done at the same time as flap surgery to regenerate the lost bone., Pathophysiology : The main cause of periodontitis is poor oral hygiene. Bacteria cling to plaque and tartar on your teeth surfaces. If you don’t clean your teeth as well or as often as you should, bacteria travel down beneath your gum line, where your toothbrush and floss can’t reach. These harmful bacteria erode the tissues that support your teeth, leading to infection, bone loss and tooth loss.Other factors can increase your risk of developing periodontitis, including : Smoking, the most significant factor, weakens your body’s ability to fight infection.People with diabetes have a higher risk of developing infections, including periodontitis.Your genetics and family history can put you at higher risk for gum disease.Hormonal changes in women and people assigned female at birth, such as pregnancy or using birth control pills, can increase your chances of developing periodontitis.Health conditions that cause inflammation in your body — such as arthritis, COVID-19 and cardiovascular disease — are linked to periodontitis.
, Epidemiology : The prevalence of periodontitis is high, with approximately 10% of the global population affected by severe periodontitis, 47.2% of adults aged 30 years and older have some form of periodontal disease. Periodontal disease increases with age, 70.1% of adults 65 years and older have periodontal disease., good, The best way to prevent periodontitis is to follow a program of good oral hygiene, one that you begin early and practice consistently throughout life.,,Good oral hygiene. That means brushing your teeth for two minutes at least twice daily — in the morning and before going to bed — and flossing at least once a day. Flossing before you brush allows you to clean away the loosened food particles and bacteria. Good oral hygiene prevents the development of an environment around your teeth that is favorable to specific bacteria that cause periodontal disease.,Regular dental visits. See your dentist or dental hygienist regularly for cleanings, usually every six to 12 months. If you have risk factors that increase your chance of developing periodontitis — such as having dry mouth, taking certain medications or smoking — you may need professional cleaning more often., Complications : rheumatoid arthritis, Diagnostics : X RAY, X RAY, PHYSICAL EXAMINATION, Differential diagnosis : Acute necrotizing (ulcerative) gingivitis and noma, gingivitis, periodontal abscess, disease description : Periodontitis (per-e-o-don-TIE-tis), also called gum disease, is a serious gum infection that damages the soft tissue and without treatment, can destroy the bone that supports your teeth. Periodontitis can cause teeth to loosen or lead to tooth loss. |
Acute Peritonitis | Disease Name : Acute Peritonitis, Treatment : medication : Ceftriaxone , Cefotaxime , "Antibiotics. Youll likely take antibiotic medicine through a needle in a vein. This clears out the infection and keeps it from spreading. The type of antibiotic youll need and how long youll have to take it will vary. It depends on how serious your condition is and the kind of peritonitis you have.,Depending on your symptoms, your treatment while in the hospital will likely include : ,Pain medications.,Fluids given through a tube, called intravenous fluids.,Oxygen.,In some cases, a blood transfusion.", Successful treatment depends on correcting any electrolyte abnormalities, restoration of fluid volume and stabilization of the cardiovascular ,system, appropriate antibiotic therapy., surgical correction of any ,underlying abnormalities., Pathophysiology : Intra-abdominal sepsis from a perforated viscus (ie, secondary peritonitis or suppurative peritonitis) results from direct spillage of luminal contents into the peritoneum (eg, perforated peptic ulcer, diverticulitis, appendicitis, iatrogenic perforation). With the spillage of the contents, gram-negative and anaerobic bacteria, including common gut flora, such as Escherichia coli and Klebsiella pneumoniae, enter the peritoneal cavity. Endotoxins produced by gram-negative bacteria lead to the release of cytokines that induce cellular and humoral cascades, resulting in cellular damage, septic shock, and multiple organ dysfunction syndrome (MODS).A host of factors contributes to the formation of peritoneal inflammation and bacterial growth in the ascitic fluid. A key predisposing factor may be the intestinal bacterial overgrowth found in people with cirrhosis, mainly attributed to decreased intestinal transit time. Intestinal bacterial overgrowth, along with impaired phagocytic function, low serum and ascites complement levels, and decreased activity of the reticuloendothelial system, contributes to an increased number of microorganisms and decreased capacity to clear them from the bloodstream, resulting in their migration into and eventual proliferation within ascites fluid., Epidemiology : 0.74 episodes per patient per year, GOOD, "Peritonitis thats linked with peritoneal dialysis is often caused by germs around the catheter. If you use peritoneal dialysis, take these steps to prevent peritonitis : ,,Wash your hands before you touch the catheter. Scrub under your fingernails and between your fingers.,Clean the skin around the catheter with an antiseptic every day.,Store your supplies in a clean place.,Wear a surgical mask during your dialysis fluid exchanges.,Talk with your dialysis care team about the correct care for your peritoneal dialysis catheter.,Your health care provider may prescribe antibiotics to prevent peritonitis, especially if youve had peritonitis before. Antibiotics also might be prescribed if you have a buildup of peritoneal fluid due to a medical condition such as liver cirrhosis. If you take medicine called a proton pump inhibitor, you may be asked to stop taking it.", Complications : paralytic ileus, Dehydration and hypotension, organ failure, septicemia, Burst abdomen, Diagnostics : Anti HBc Antibody ELISA, Hb, Total Leucocyte Count (TLC), CT Abdomen, USG ABDOMEN(W/A), X RAY ABDOMEN, Differential diagnosis : Cystitis, EMPYMA, hematomas, Pyelonephritis, rectus hematoma, URINARY TRACT OBSTRUCTION, disease description : Acute peritonitis, or inflammation of the visceral and parietal peritoneum, is most often but not always infectious in origin, resulting from perforation of a hollow viscus. This is called secondary peritonitis, as opposed to primary or spontaneous peritonitis, when a specific intraabdominal source cannot be identified. In either instance, the inflammation
can be localized or diffuse. |
Acute Pharyngitis | Disease Name : Acute Pharyngitis, Treatment : medication : Amoxicillin and Clavulanic acid , Erythromycin , PENICILLIN G, Penicillin V (Penoxymethyl penicillin) : \t1.2 M I.U./oral/12 h\t8–10 days.,,Amoxicillin : 500 mg/12 h\t8–10 days.,, Clindamycin : 300 mg/8 h\t10 days, Pathophysiology : Bacteria and viruses can cause direct invasion of the pharyngeal mucosa. Certain viruses like rhinovirus can cause irritation secondary to nasal secretions. In almost all cases, there is a local invasion of the pharyngeal mucosa which also results in excess secretion and edema., Epidemiology : In 2010, there were 1.814 million emergency department visits for pharyngitis, of which 692, 000 were for patients under the age of 15. Most cases of pharyngitis occur in children under the age of 5., GOOD, Viral infections like colds and flu often cause sore throats. You can reduce your sore throat by protecting yourself against colds and flu. Some ways to do that include : ,,Washing your hands often, using soap and water or alcohol-based hand sanitizers.,Avoid people who are sneezing and coughing.,If you do spend time with people who are sneezing and coughing, avoid sharing food, drink or utensils.,Be vaccinated against flu., Complications : ACUTE RHEUMATIC FEVER, otitis media, sinusitis, Epiglottitis, Diagnostics : THROAT SWAB CULTURE, Differential diagnosis : airway obstruction, allergic rhinitis, diphtheria, Epiglottitis, Gastroesophageal reflux disease (GERD), HSV 1 infection, infectious mononucleosis, Peritonsillar abscess, disease description : Acute pharyngitis is characterized by the rapid onset of sore throat and pharyngeal inflammation (with or without exudate). Absence of cough, nasal congestion, and nasal discharge suggests a bacterial, rather than viral, etiology. |
Acute Pid | Disease Name : Acute Pid, Treatment : medication : Cefoxitin , Doxycycline , Erythromycin , Gentamicin , Clindamycin , Tetracycline , Partner should be investigated and treated. There is no need to remove IUCD if the woman responds to antibiotics. Failed response calls for its removal. Barrier contraceptives should be recommended thereafter., Rest.,-Intravenous fluids ,Analgesics, Antibiotics, Medical treatment, antimicrobial,- Minimal invasive surgery,- Major surgery, Pathophysiology : Most cases of PID are presumed to occur in 2 stages. The first stage is acquisition of a vaginal or cervical infection. This infection is often sexually transmitted and may be asymptomatic. The second stage is direct ascent of microorganisms from the vagina or cervix to the upper genital tract, with infection and inflammation of these structures.The mechanism (or mechanisms) by which microorganisms ascend from the lower genital tract is unclear. Studies suggest that multiple factors may be involved. Although cervical mucus provides a functional barrier against upward spread, the efficacy of this barrier may be decreased by vaginal inflammation and by hormonal changes that occur during ovulation and menstruation.In the upper genital tract, a number of microbial and host factors appear to influence the degree of inflammation that occurs and, thus, the amount of subsequent scarring that develops. Infection of the fallopian tubes initially affects the mucosa, but inflammation may rapidly become transmural. This inflammation, which appears to be mediated by complement, may increase in intensity with subsequent infections.Inflammation may extend to uninfected parametrial structures, including the bowel. Infection may extend via spillage of purulent materials from the fallopian tubes or via lymphatic spread beyond the pelvis to produce acute peritonitis and acute perihepatitis (Fitz-Hugh-Curtis syndrome)., Epidemiology : more than 1 million women experience an episode of PID every year., GOOD, - Avoiding douching may lower the risk.,,- Most of the time, though, PID happens because of unprotected sex. Take steps to practice safe sex. Ways to protect yourself from sexually transmitted infections (STIs) that can cause PID include : ,,Limiting sexual partners,Choosing barrier methods of birth control,Seeking treatment if you notice symptoms,Getting regular checkups, Complications : Haemorrhage, infections, infertility, Ectopic pregnency, Diagnostics : VAGINAL SWAB CULTURE, USG ABDOMEN(W/A), MRI, CT SCAN, SPECULUM EXAMINATION, ENDOMETRIAL BIOPSY, Differential diagnosis : appendicitis, Cystitis, DIVERTICULITIS, Ectopic pregnency, Endometriosis, Microcystic adnexal carcinoma, Ovarian Cyst, Pyelonephritis, Torsion or rupture of ovarian cyst, disease description : Pelvic inflammatory disease (PID) implies inflammation of the
upper genital tract involving the fallopian tubes as well as the
ovaries. Because most of the PIDs are due to ascending or
blood-borne infection, the lesion is often bilateral, though one
tube may be more affected than the other. The ovaries are so
closely linked to the fallopian tubes anatomically that they are
coincidentally involved in infection, and it is therefore customary
to consider inflammations of the two organs together. |
Acute Primary Angle-closure Glaucoma | Disease Name : Acute Primary Angle-closure Glaucoma, Treatment : medication : Acetazolamide, Timolol , Latanoprost , Brimonidine , Pilocarpine , Mannitol , A. Immediate medical therapy to lower IOP,1. Systemic hyperosmotic agents are required initially,if IOP is more than 40 mm Hg.,• Intravenous mannitol (1 gm/kg body weight),should be preferred in the presence of nausea and,vomiting.,• Oral hyperosmotics, e.g., glycerol 1 gm/kg body,weight of 50% solution in lemon juice may be,given if well tolerated and not contraindicated (as,in diabetes mellitus).,2. Systemic carbonic anhydrase inhibitors, e.g., ,acetazolamide 500 mg IV stat followed by 250 mg,tablet 3 times a day.,3. Topical antiglaucoma drugs to be instilled,immediately include : ,• Beta-blocker, e.g., 0.5% timolol or 0.5% betaxolol,• Alpha adrenergic agonists, e.g., brimonidine,0.1–0.2%.,• Prostaglandin analogue, e.g., latanoprost 0.005%.,Role of miotic therapy : ,• Pilocarpine 2% QID should be started after 1 hour of,the commencement of the treatment, i.e., when IOP,is lowered, as at higher IOP sphincter is ischaemic,and unresponsive to pilocarpine., 1. Laser peripheral iridotomy (LPI), 2. Filtration surgery, i.e., trabeculectomy, 3. Clear lens extraction, Pathophysiology : An acute attack of angle-closure glaucoma is precipitated by pupillary dilatation, leading to increasing iris and lens contact increasing the pupillary block. The increasing pupillary block leads to bulging of the iris, acutely closing the angle between the iris and cornea, thus obstructing the aqueous humor outflow tract. The intraocular pressure rises acutely, leading to symptomology., Epidemiology : 0.6%, 12.2 per 100 000 per year, good, Early detection of glaucoma through routine eye exams is the best way to protect eye health and prevent vision loss. Glaucoma testing should occur every : ,,One to three years after age 35 for people at high risk.,Two to four years before age 40.,One to three years between ages 40 and 54.,One to two years between ages 55 to 64.,Six months to 12 months after age 65., Complications : blindness, Spontaneous angle reopening, Ciliary body shut down, Vogt’s triad (Glaukomflecken, Patches of iris atrophy and • Slightly dilated nonreacting pupil), Diagnostics : FUNDOSCOPY, GONIOSCOPY, TONOMETRY TEST, slit-lamp biomicroscopic examination, Differential diagnosis : acute angle-closure glaucoma, central retinal artery occlusion, corneal abrasion, CRVO, EPISCLERITIS, Fuchs Endothelial Corneal Dystrophy, neovascular glaucoma, optic neuritis, SCLERITIS, disease description : An attack of acute rise in IOP in patients with primary
angle closure (PAC) may occur due to pupillary block
causing sudden closure of the angle. It usually does
not terminate of its own and thus if not treated lasts
for many days. It is a sight threatening emergency |
Acute Prostatitis | Disease Name : Acute Prostatitis, Treatment : medication : Sulfamethoxazole and Trimethoprim (Co-trimoxazole), Ciprofloxacin , Doxycycline , avoid bicycling or wear padded shorts to decrease pressure on your prostate,avoid alcohol, caffeine, and foods that are spicy and acidic,sit on a pillow or donut cushion,take warm baths, Your doctor will likely prescribe antibiotics for four to six weeks to treat acute bacterial prostatitis. Your treatment may last longer if you have recurrent episodes. The specific type of antibiotic will depend on the bacteria causing your condition.,,Your doctor may also prescribe alpha-blockers to help relieve symptoms. These drugs relax your bladder muscles. They can help decrease urinary discomfort. Examples include doxazosin, terazosin, and tamsulosin. Your doctor may also recommend over-the-counter pain relievers, such as acetaminophen and ibuprofen., Pathophysiology : Theories regarding the pathogenesis of acute bacterial prostatitis include the following : Intraprostatic urinary refluxAscending urethral infectionDirect invasion or lymphogenous spread from the rectumDirect hematogenous infectionon, Epidemiology : Prostatitis is a common condition, with about 50 percent of all men likely to experience it in their lifetimes. Acute prostatitis, on the other hand, is quite rare., Compared to men 20–39 years old, the risk of prostatitis was 1.7 times greater for men 40–49 years old, and 3.1 times greater for men 50–59 years old., good, Prompt treatment for UTIs may keep the infection from spreading to the prostate. If you have pain in your perineum when sitting, see a provider. You can take steps to address this problem before it leads to chronic pelvic pain syndrome., Complications : epididymitis, prostatic abscess, Diagnostics : Erythrocyte Sedimentation Rate (ESR), HISTOPATHLOGY, URINE CULTURE, URINE R/M, CT Abdomen, USG KUB, BLOOD CULTURE, TRANSRECTAL USG, CYSTOSCOPY, Differential diagnosis : adenofibroma, BENIGN PROSTATIC HYPERPLASIA, Bladder cancer, Bladder infection, prostatic abscess, Urethritis, URINARY TRACT OBSTRUCTION, disease description : Prostatitis is a group of conditions that includes acute and chronic bacterial prostatitis and chronic pelvic pain syndrome (CPPS). It can cause infection, inflammation and pain in the prostate gland. Men with asymptomatic inflammatory prostatitis don’t have symptoms. Acute (sudden) prostatitis is a medical emergency. |
Acute Pulpitis | Disease Name : Acute Pulpitis, Treatment : For reversible pulpitis, your dentist will try to remove the cause. Often, this involves the removal of the decay and sealing the tooth with a normal filling., Irreversible pulpitis requires more intensive treatment to remove the pulp tissue. Treatment options include : ,,Root canal : You usually go to an endodontist (a dentist who specializes in treating pulp infections) for a root canal. They remove the infected pulp and clean out the root. Next, they fill the empty root canal and seal the tooth. You’ll return to your dentist a few weeks later for a crown to cap your tooth.,Tooth removal : Some people opt for tooth extraction. Your dentist will discuss your options for replacing the tooth, including a dental implant or dental bridge., Antibiotics aren’t a treatment for pulpitis, but they may help prevent the problem from progressing into an infection if there’s a delay in your treatment., Pathophysiology : This center part of your tooth is made of connective tissue, nerves, and blood vessels. It can become inflamed because of cavities or other dental health reasons. ?There are 2 types of pulpitis.
Reversible pulpitis. This type of pulpitis is the early stages of inflammation. It has limited inflammation and can be fixed by treating the tooth.
Irreversible pulpitis. This is when the inflammation has completely damaged the pulp, which can’t be saved.Reversible pulpitis. This type of pulpitis is the early stages of inflammation. It has limited inflammation and can be fixed by treating the tooth. Irreversible pulpitis. This is when the inflammation has completely damaged the pulp, which can’t be saved. , Epidemiology : prevalence of irreversible pulpitis in males is 53%, and in females, it is 39%, The prevalence of irreversible pulpitis was 60.7%, 68.2% and 43.8% in molars, premolars and anterior teeth, respectively., good, Good oral hygiene is the best way to prevent pulpitis. This consists of : ,,Brushing your teeth two times a day.,Flossing every day.,Seeing your dentist for routine cleanings and checkups.,Wearing a night guard if you grind your teeth at night.,Also, make sure to let your dentist know right away if you’re having any tooth pain or sensitivity., Complications : abscess, fever, osteomyelitis, Diagnostics : HISTOPATHLOGY, X RAY, X RAY, PHYSICAL EXAMINATION, Differential diagnosis : Dental abscesses, Dental Caries, dental trauma, sinusitis, disease description : Pulp is the soft inner tissue of your teeth. It contains nerves, blood vessels and connective tissue. The pulp supplies blood and nutrients to the hard, outer layers of your teeth to keep them healthy.Pulpitis is an inflammation of the pulp. It usually happens when there’s an irritation inside a tooth due to things such as grinding or a cavity. |
Acute Pyelonephritis | Disease Name : Acute Pyelonephritis, Treatment : medication : Ceftriaxone , Amikacin , levofloxacin, ,ciprofloxacin, ,co-trimoxazole, ,ampicillin, The mainstay of treatment of acute pyelonephritis is antibiotics, analgesics, and antipyretics. Nonsteroidal anti-inflammatory drugs (NSAIDs) work well to treat both pain and fever associated with acute pyelonephritis. ,f IV antibiotics include piperacillin-tazobactam, fluoroquinolones, meropenem, and cefepime. For patients who have allergies to penicillin, vancomycin can be used. Follow up for non-admitted patients for resolution of symptoms should be in 1 to 2 days. Follow up urine culture results should be obtained only in patients who had a complicated course and are usually not needed in healthy, non-pregnant women, Recurrent kidney infections may result from an underlying medical problem. In those cases, surgery may be required to remove any obstructions or to correct any structural problems in the kidneys. Surgery may also be necessary to drain an abscess that doesn’t respond to antibiotics.,,In cases of severe infection, a nephrectomy may be necessary. In this procedure, a surgeon removes part of the kidney., Pathophysiology : E. coli is the most common bacteria causing acute pyelonephritis due to its unique ability to adhere to and colonize the urinary tract and kidneys. E.coli has adhesive molecules called P-fimbriae, which interact with receptors on the surface of uroepithelial cells. Kidneys infected with E. coli can lead to an acute inflammatory response which can cause scarring of the renal parenchyma. Though the mechanism in which renal scarring occurs is still poorly understood, it has been hypothesized that the adhesion of bacteria to the renal cells disrupts the protective barriers, which leads to localized infection, hypoxia, ischemia, and clotting in an attempt to contain the infection. Inflammatory cytokines, bacterial toxins, and other reactive processes further lead to complete pyelonephritis and, in many cases, systemic symptoms of sepsis and shock., Epidemiology : A population-based study of acute pyelonephritis in the United States found overall annual rates of 15-17 cases per 10, 000 females and 3-4 cases per 10, 000 males., good, Kidney infections often start as infections in your bladder. Preventing these lower urinary tract infections is the first step in preventing kidney infections. Some ways to prevent infections in all parts of your urinary tract include : ,,Drink plenty of fluids. Talk to your healthcare provider about the amount of water and other fluids they recommend for you each day.,Empty your bladder completely. Holding in your pee can help bacteria grow.,Pee before and after having sex. This helps remove any bacteria that’s in your urinary tract.,Practice good hygiene. Things like showering regularly and changing out of wet or sweaty underwear can help prevent bacteria from getting into your body. After you poop, wipe from front to back. This helps push bacteria in your poop away from openings in your body., Complications : Acute Renal Failure, sepsis, Renal Vein Thrombosis, papillary necrosis in kidney, Emphysematous pyelonephritis, Diagnostics : random blood sugar RBS, HISTOPATHLOGY, PUS CULTURE, URINE CULTURE, URINE CULTURE, Urine Protein, USG KUB, BLOOD CULTURE, CT SCAN, Differential diagnosis : Abdominal Abscess, appendicitis, cholecystitis, Ectopic pregnency, nephrolithiasis, Pancreatitis, PID, URINARY TRACT OBSTRUCTION, disease description : Acute pyelonephritis is a bacterial infection causing inflammation of the kidneys and is one of the most common diseases of the kidney. Pyelonephritis occurs as a complication of an ascending urinary tract infection (UTI) which spreads from the bladder to the kidneys and their collecting systems. |
Acute Renal Failure | Disease Name : Acute Renal Failure, Treatment : Acidosis : ,Reversing acidosis through administration of an alkaline solution—sodium bicarbonate—would seem to be sensible, but there is very little evidence to show that it provides benefit., Hyperkalemia treatment : ,,Calcium gluconate/carbonate\t,Insulin (+/- dextrose)\t,Salbutamol (nebulised/intravenous),Ion exchange resin\t,Haemodialysis, If hyperkalemia develops, it needs to be managed in a robust manner because, in AKI patients, it can be catastrophic. Approaches to lower potassium in the body include : ,,Dietary restriction,Insulin, IV dextrose and beta-agonists,potassium-binding resins,Calcium gluconate to stabilize cardiac membrane,Dialysis for nonresponsive hyperkalemia,Some AKI patients tend to develop volume overload, which should be corrected as early as possible to avoid pulmonary and cardiac complications. Euvolemic state can be achieved with the help of furosemide, which is a cornerstone in managing such patients. Usually, high doses of IV furosemide are needed to correct volume overload in AKI patients; however, it plays no role in converting oliguric AKI to non-oliguric AKI., Pulmonary oedema,The oligo-anuric patient with pulmonary oedema resulting from fluid overload (with/without underlying cardiac disease) represents a clinical challenge. As previously mentioned, if significant ventilatory failure is present, this must be dealt with first, through supplementary oxygen, non-invasive ventilation, or intubation and ventilation, depending on the state of the patient. While these measures are being undertaken, pharmacological treatment to offload the decompensated heart can be started—intravenous opioids (diamorphine 2.5–5 mg, with care taken depending on the degree of respiratory distress) and an intravenous infusion of nitrate (for example, glyceryl trinitrate 50 mg in 50 ml 0.9% saline, at a rate of 2–20 ml/h keeping the systolic blood pressure >95 mm Hg)—and attempts made to provoke a diuresis, Pathophysiology : The pathogenesis of AKI is etiology-driven. The common endpoint in all types of acute tubular necrosis is a cellular insult either secondary to ischemia or direct toxins, which results in effacement of the brush border and eventually cell death, thus shutting down the function of tubular cells. Intratubular obstruction by pigments such as myoglobin or crystals such as uric acid in tumor lysis syndrome or immunoglobulin light chains, as seen in monoclonal gammopathy, may also lead to the same result. On the other hand, the mechanism of injury in glomerulonephritis may be due to direct immune-mediated injury of the vessels or immune complex deposition leading to an immune response and damage to the glomeruli., Epidemiology : eight per 1000 admissions., In the United States, 1% of all hospital admissions have AKI on admission, good, Though kidney failure and CKD aren’t reversible, you can take steps to help preserve your kidney function. Healthy habits and routines may slow down how quickly your kidneys lose their ability to function.,,If you have CKD or kidney failure, it’s a good idea to : ,,Monitor your kidney function.,Keep your blood sugar levels in normal range if you have diabetes.,Keep your blood pressure levels in a normal range.,Avoid using tobacco products.,Avoid foods high in protein and sodium.,Go to every regularly scheduled appointment with your healthcare provider., Complications : hyperkalemia, Hyperphosphataemia, metabolic acidosis, Diagnostics : HISTOPATHLOGY, Blood Urea, CT SCAN, CYSTOSCOPY, kidney biopsy, Urine analysis, Renal ultrasonography, Differential diagnosis : Chronic renal failure, Diabetic Ketoacidosis, gastrointestinal bleeding, heart failure, RENAL CALCULI, Severe dehydration, sickle cell anemia, Urinary Tract Infection, URINARY TRACT OBSTRUCTION, disease description : Acute kidney injury (AKI), also known as acute renal failure (ARF), is a sudden episode of kidney failure or kidney damage that happens within a few hours or a few days. AKI causes a build-up of waste products in your blood and makes it hard for your kidneys to keep the right balance of fluid in your body. |
Acute Respiratory Distress Syndrome | Disease Name : Acute Respiratory Distress Syndrome, Treatment : Oxygen therapy is a treatment that delivers oxygen for you to breathe. You can receive oxygen therapy from tubes resting in your nose, a face mask, or a tube placed in your trachea (windpipe). You may need oxygen therapy if you have a condition that causes your blood oxygen levels to be too low.,,Noninvasive ventilation, such as use of bilevel positive airway pressure (BiPAP) or continuous positive airway pressure (CPAP) machines, which are electronic breathing devices that help keep your airways open by blowing air through a face mask.,A ventilator may help restore your blood oxygen levels. Some people transition from a ventilator to portable oxygen therapy. Risks from being on a ventilator include pneumonia and pneumothorax (collapsed lung).,,MEDICINES : ,Acid-reducing medicines prevent stress ulcers, which can cause bleeding in the intestines.,Antibiotics treat or prevent infections. If you are on a ventilator, your healthcare team may do tests, such as lung fluid lab tests or CT scans, to look for signs of new infection.,Blood thinners stop blood clots from forming or growing larger. Heparin is a common blood thinner for adults.,Muscle relaxants help prevent coughing or gagging while on a ventilator or reduce the amount of oxygen your body needs.,Sedatives help relieve anxiety, make it easier to breathe on a ventilator, or lower your body’s oxygen needs. Sometimes your doctor may pair a sedative with another medicine to make delivering the oxygen easier. Complications vary depending on the sedative used, the dose, and how long it is used. They can include depression, post-traumatic stress disorder (PTSD), problems with thinking or memory, or a delay in removing the ventilator.,,OTHER TREATMENT : ,A feeding tube can ensure you get enough of the right nutrients while you are on a ventilator.,Blood transfusions treat low hemoglobin levels. Hemoglobin carries oxygen in the blood, so a transfusion can improve the delivery of oxygen to the body’s organs.,Extracorporeal membrane oxygenation (ECMO) or a similar device helps when ventilation alone cannot deliver enough oxygen or while a patient waits for a lung transplant. ECMO works like an artificial lung, removing carbon dioxide and pumping oxygen-rich blood back into the body.,Fluid management through an intravenous (IV) line helps restore fluid levels if needed. Low fluid levels in your blood vessels can prevent oxygen from getting to your organs. If you have too much fluid in the lungs, your doctor may give you medicines that help your body get rid of the extra fluid.,Lying facedown helps get more oxygen to your lungs.,Physical therapy maintains muscle strength and prevent sores from forming. Movement may help shorten the time you are on a ventilator and improve recovery after you leave the hospital., Pathophysiology : Respiratory failure can be classified into hypoxic respiratory failure (failure of
oxygenation) and hypercarbic respiratory failure (failure of ventilation).
Systemic venous (pulmonary arterial) blood is arterialized after equilibration
with alveolar gas in the pulmonary capillaries and is carried back to the heart by
pulmonary veins. The ABG is influenced by the composition of inspired gas,
effectiveness of alveolar ventilation, pulmonary capillary perfusion, and
diffusion capacity of the alveolar capillary membrane. Abnormality in any of
these steps can result in respiratory failure. Hypoxic respiratory failure results
from intrapulmonary shunting and venous admixture or insufficient diffusion of
oxygen from alveoli into pulmonary capillaries. This physiology can be caused
by small airways obstruction, increased barriers to diffusion (e.g., interstitial edema, fibrosis), and conditions in which alveoli are collapsed or filled with
fluid (e.g., ARDS, pneumonia, atelectasis, pulmonary edema). In most cases,
hypoxic respiratory failure is associated with decreased functional residual
capacity and can be managed by lung volume recruitment with positive pressure
ventilation. Hypercarbic respiratory failure is caused by decreased minute
ventilation (i.e., tidal volume multiplied by respiratory rate). This physiology can
result from centrally mediated disorders of respiratory drive, increased dead
space ventilation, or obstructive airways disease. Hypoxic and hypercarbic
respiratory failure may coexist as a combined failure of oxygenation and
ventilation., Epidemiology : 64.2 to 78.9 cases/100, 000 person-years., BAD, There’s no way to prevent ARDS completely. However, you may be able to lower your risk of ARDS by doing the following : ,,Seek prompt medical assistance for any trauma, infection, or illness.,If you smoke, consider stopping smoking cigarettes.,Try to stay away from secondhand smoke.,Avoid alcohol. Chronic alcohol use may increase your mortality risk and prevent proper lung function.,Get your flu vaccine annually and pneumonia vaccine every 5 years. This decreases your risk of lung infections., Complications : delirium, muscle weakness, PNEUMONIA, respiratory failure, anxiety, Diagnostics : ABG, HISTOPATHLOGY, X RAY CHEST, CT CHEST, Differential diagnosis : Asthma, Congestive heart failure, diffuse alveolar hemorrhage., Interstitial pneumonia, PNEUMONIA, disease description : It is defined as pulmonary edema not originating from
the heart. Most common cause is severe pneumonia
followed by sepsis.Other predisposing factors include shock, tissue injury, aspiration, toxins, microthrombi,
intravascular coagulation, uremia and increased intracranial
pressure. |
Acute Respiratory Failure | Disease Name : Acute Respiratory Failure, Treatment : Oxygen therapy, through a nasal cannula (two small plastic tubes that go in your nostrils) or through a mask that fits over your nose and mouth, Medicines for discomfort,Treatments for the cause of the respiratory failure. These treatments may include medicines and procedures.,If you have respiratory failure, see your health care provider for ongoing medical care. Your provider may suggest pulmonary rehabilitation., Other breathing treatments, such as noninvasive positive pressure ventilation (NPPV), which uses mild air pressure to keep your airways open while you sleep. Another treatment is a special bed that rocks back and forth, to help you breathe in and out.,Fluids, often through an intravenous (IV), to improve blood flow throughout your body. They also provide nutrition., Tracheostomy, a surgically-made hole that goes through the front of your neck and into your windpipe. A breathing tube, also called a tracheostomy, or trach tube, is placed in the hole to help you breathe.,Ventilator, a breathing machine that blows air into your lungs. It also carries carbon dioxide out of your lungs., Pathophysiology : Hypoxemic respiratory failureIn this type of the condition, there is not enough oxygen in a person’s blood. This is due to a failure in oxygen exchange in the lungs, which can result from swelling of the lungs or fluid buildup.A person experiencing this will still have stable CO2 levels in their blood.Hypercapnic respiratory failureA person with hypercapnic respiratory failure will have higher levels of CO2 in their blood. Their blood oxygen levels may remain steady or be lower than usual.Hypercapnic respiratory failure occurs when the lungs’ alveoli, or air sacs, cannot adequately excrete CO2 that the body produces.Acute vs. chronicRespiratory failure can be acute or chronic. Acute respiratory failure will occur suddenly and require immediate medical attention. This may be due to direct injury or rapid changes in lung function., Epidemiology : 64.2 to 78.9 cases/100, 000 person-years., 10-80/100, 000/y, poor, You can’t always prevent respiratory failure. You can lower your risk of chronic respiratory failure by managing ongoing heart, lung and neurological conditions. Talk to your healthcare provider about ways to reduce your risk if you have a condition that can cause respiratory failure., Complications : kidney damage, Pulmonary Embolism, thrombocytopenia, neurological problem, Fibrosis, Diagnostics : Arterial Blood Gas Analysis(ABG), CHEST X RAY, X RAY, Differential diagnosis : acute respiratory distress syndrome, aspiration pneumonia, Asthma, bronchitis, congestive heart failure (CHF), PNEUMONIA, PNEUMOTHORAX, pulmonary edema, Pulmonary Embolism, disease description : Acute respiratory failure occurs when fluid builds up in the air sacs in your lungs. When that happens, your lungs can’t release oxygen into your blood. In turn, your organs can’t get enough oxygen-rich blood to function. You can also develop acute respiratory failure if your lungs can’t remove carbon dioxide from your blood.
Respiratory failure happens when the capillaries, or tiny blood vessels, surrounding your air sacs can’t properly exchange carbon dioxide for oxygen. |
Acute Retinal Necrosis | Disease Name : Acute Retinal Necrosis, Treatment : Acyclovir should be started at 10-13 mg/kg every 8 hours or 1500mg/m2/day intravenously (IV) for 5-10 days. This should be followed by acyclovir 800 mg five times daily orally for 6 weeks to 3 months. ,,Valacyclovir can be given 1000-2000 mg orally every 8 hours. This has good bioavailability and avoids the need for intravenous access. ,,Famciclovir should be given at 500 mg orally every 8 hours.,,Valganciclovir started at 900 mg twice daily orally for 3 weeks induction, followed by 900mg once daily orally for maintenance. Valganciclovir has been successfully used for CMV retinitis. It has activity against HSV, VZV, and CMV., • Barrier laser photocoagulation for retinal breaks.,• Vitrectomy with silicon oil injection for associated,retinal detachment., Pathophysiology : Viral particles in the retina and vitreous provoke an intense inflammatory response. Retinal opacification corresponds with infiltration of the retina with viral particles and mononuclear cells. Lymphocytes and plasma cells, which produce antibodies to the provocative viral agent, likewise permeate the vitreous. Additionally, characteristic inflammation of the retinal arterioles occurs, resulting in vaso-occlusion and rapid necrosis of dependent, downstream retinal tissue.
Contractile membranes may form in the vitreous and on the surface of the thinned, necrotic retina. Approximately 50 - 75% of patients will develop retinal detachments in the affected eye after ARN; the majority of retinal detachments occur within 3 months of the onset of ARN., Epidemiology : 6.3 per 100, 000 individuals, good, The use of systemic or intravitreal antiviral agents reduces the duration of the active phase of ARN and may thereby potentially minimize the duration and extent of retinal necrosis. Chronic use of antivirals (for 6 weeks to 3 months) after resolution of the active phase of ARN in one eye has also been shown to reduce the incidence of ARN in the fellow eye.,,Prevention of the late visual sequelae of acute retinal necrosis, namely that of retinal detachment, may be partially reduced through prophylactic laser photocoagulation of the retina surrounding areas of prior retinitis or atrophy. However, retinal detachment may still occur/progress even after laser. Laser may be difficult in view of painful red eye, severe media haze due to vitritis, posterior synechia, and cataract. Also, laser over the necrotic, swollen white retina may cause iatrogenic breaks., Complications : cystoid macular edema, epiretinal membrane, Glaucoma, optic neuropathy, RETINAL DETACHMENT, Diagnostics : Complete Blood Count CBC, Optical coherence tomography (OCT), Slit lamp examination, PCR, ophthalmoscopy, Differential diagnosis : "Behcets syndrome/disease", CMV disease, endophthalmitis, Intraocular lymphoma, Syphilis, Toxoplasmosis, disease description : Acute retinal necrosis (ARN) is a devastating syndrome characterized by panuveitis, retinal necrosis, and a high rate of retinal detachment that may result in poor visual outcomes if not promptly diagnosed and treated. ARN is most commonly caused by viruses within the herpesvirus family.Acute retinal necrosis is a clinical diagnosis and treatment should not be delayed in a typical case. The classical triad of ARN consists of (1) arteritis and phlebitis of the retinal and choroidal vasculature, (2) a confluent, necrotizing retinitis that preferentially affects the peripheral retina, and (3) a moderate to severe vitritis. |
Acute Retropharyngeal Abcess | Disease Name : Acute Retropharyngeal Abcess, Treatment : All patients must have careful airway monitoring when undergoing treatment of retropharyngeal abscess, especially during the first 24 to 48 hours of therapy.,,Initial antibiotic therapy should include either ampicillin-sulbactam (50 mg/kg every 6 hours) or clindamycin (15 mg/kg every 8 hours). If patients appear septic or do not respond to initial antibiotic therapy, vancomycin or linezolid also should be administered. Parenteral antibiotics should be continued until patients are clinically improved and afebrile for 24 hours. After patients demonstrate clinical improvement and remain afebrile, they may be transitioned to oral antibiotics. Amoxicillin-clavulanate (45 mg/kg every 12 hours) or clindamycin (13 mg/kg every 8 hours) are acceptable oral regimens. Oral antibiotics should be prescribed for 14 days, and the patient may be discharged home with strict return precautions., Incision and Drainage of Abscess, Pathophysiology : It is commonly seen in children below 3 years. It is the result
of suppuration of retropharyngeal lymph nodes secondary
to infection in the adenoids, nasopharynx, posterior
nasal sinuses or nasal cavity. In adults, it may result
from penetrating injury of posterior pharyngeal wall or
cervical oesophagus. Rarely, pus from acute mastoiditis
tracks along the undersurface of petrous bone to present
as retropharyngeal abscess. Dysphagia and difficulty in breathing are prominent
symptoms as the abscess obstructs the air and food
passages. Stridor and croupy cough may be present. Torticollis. The neck becomes stiff and the head is kept
extended. Bulge in posterior pharyngeal wall. Usually seen on one
side of the midline., Epidemiology : 2.64 per 100, 000 people., GOOD, Don’t delay seeking treatment if your child is sick, especially if they have an upper respiratory infection.,,You can prevent complications from a retropharyngeal abscess by taking symptoms seriously. If you’re noticing signs of a retropharyngeal abscess — in either yourself or your child — see your healthcare provider immediately., Complications : acute respiratory distress syndrome, sepsis, airway obstruction, cranial nerve palsies, PERFORATION OF ESOPHAGUS, Diagnostics : HISTOPATHLOGY, CECT, X RAY, plain radiograph cervical, Differential diagnosis : branchial cleft cyst, Epiglottitis, lymphadenitis, Peritonsillar abscess, pharyngitis, PNEUMONIA, disease description : A retropharyngeal abscess is a collection of pus in the back of the throat. A retropharyngeal abscess is caused by a bacterial infection. Symptoms include difficulty and pain when swallowing, a fever, stiff neck, and noisy breathing. This disease is most common in children under the age of five but also occurs in adults. Typically patients under the age of five have an antecedent upper respiratory tract infection leading to suppurative cervical lymphadenitis and eventually retropharyngeal abscess. Primary infections of the tonsils and of the dentition can also evolve into retropharyngeal abscesses, though more commonly into peritonsillar (Quinsy) or parapharyngeal abscesses, respectively. |
Acute Rheumatic Fever | Disease Name : Acute Rheumatic Fever, Treatment : medication : Furosemide , Digoxin , Carbamazepine, Benzathine benzylpenicillin , Erythromycin , Prednisolone, Human normal immunoglobulin , Diazepam , Aspirin/Acetylsalicylic acid, A single injection of,benzathine penicillin can be administered when the,diagnosis of rheumatic fever is made. Penicillin V (250 mg,four times a day for 10 days) is another alternative;,erythromycin (250 mg qid for 10 days) can be administered,for those with penicillin allergy. Aspirin or steroids are given as,suppressive therapy. Since untreated rheumatic fever,subsides in 12 weeks in 80% of the patients, either of the two,suppressive agents is given for 12 weeks. Aspirin is given at a dose,of 90-120 mg/kg/ day (in 4 divided doses) for 10 weeks, ,and then tapered in the next two weeks. Alternatively, ,prednisolone (2 mg/kg daily; maximum dose 60 mg) is,given for three weeks and then tapered gradually in next,9 weeks., Surgical replacement of the mitral and/or aortic valve,is indicated if the patient is deteriorating despite,aggressive decongestive measures., Pathophysiology : A strong
association with beta hemolytic streptococci of group A
is indicated by a number of observations :
i. History of preceding sore throat is available in less than
50% patients
ii. Epidemics of streptococcal infection are followed by
higher incidence of rheumatic fever
iii. The seasonal variation of rheumatic fever and
streptococcal infection are identical
iv. In patients with established RHD streptococcal
infection is followed by recurrence of acute rheumatic
fever
v. Penicillin prophylaxis for streptococcal infection
prevents recurrences of rheumatic fever in those
patients who have had it earlier
vi. More than 85% of the patients with acute rheumatic
fever show elevated levels of anti-streptococcal
antibody titer
Streptococci have never been isolated from rheumatic
lesions in joints, heart or the blood stream. Considerable
evidence suggests that rheumatic fever is an antigenantibody
reaction. Following streptococcal sore throat,
there is a latent period of 10 days to several weeks before
the onset of rheumatic fever. This latent period is similar
to other antigen-antibody diseases like serum sickness.
Streptococcal cell wall proteins as well as carbohydrates
have the capacity to produce antibodies capable of reacting
with human connective tissue, resulting in rheumatic
fever. Rheumatic fever appears to be the result of the hosts
unusual response at both the cellular and humoral level
to Streptococcus. There is no marker that identifies genetic
susceptibility to rheumatic fever.
Only heart valves are permanently damaged during an
episode of rheumatic fever. All other affected tissues
typically heal without residua : pericarditis, chorea and
arthritis resolve completely without constriction, longterm
neurologic consequences or joint disability, respectively., Epidemiology : 5.3/1000, GOOD, Treating strep throat and scarlet fever early is essential. It can prevent rheumatic fever. Strep throat and scarlet fever symptoms aren’t always obvious or easy to spot. Call your healthcare provider for guidance if your child has a sore throat for more than three days or has other symptoms that concern you.,,If your child has strep throat or scarlet fever, make sure you follow your provider’s instructions carefully. Your child needs to finish the full course of antibiotics, even if they feel better. Otherwise, the infection may not go away and make you more prone to rheumatic fever., Complications : aortic regurgitation, mitral regurgitation, PERICARDIAL EFFUSION, polyarthritis, carditis, Diagnostics : ANTI NUCLEAR ANTI BODY(ANA), CRP, Erythrocyte Sedimentation Rate (ESR), HISTOPATHLOGY, Rheumatoid Factor Quantitative, 2-D Echo, ANTISTREPTOLYSIN O (ASO) TITRE, ECG, THROAT SWAB CULTURE, CT SCAN, NEUTROPHILS - ABSOLUTE COUNT, Differential diagnosis : arthritis, Gout, Infective endocarditis, juvenile idiopathic arthritis, leukemia, "lymes disease", rheumatoid arthritis, Sarcoidosis, Septic arthritis, SYSTEMIC LUPUS ERYTHEMATOSUS, disease description : Rheumatic fever is an immunological disorder initiated
by group A beta hemolytic streptococci. Antibodies produced against selected streptococcal cell wall proteins
and sugars react with the connective tissues of the body
as well as the heart and result in rheumatic fever. There is
no single test for the confirmation of diagnosis. There is a
strong relationship with streptococcal infection and it is
possible to prevent rheumatic fever by prompt treatment
of streptococcal infections with penicillin. |
Acute Rhinitis | Disease Name : Acute Rhinitis, Treatment : Antihistamines : ,fexofenadine (Allegra),diphenhydramine (Benadryl),desloratadine (Clarinex),loratadine (Claritin),,Decongestants : ,oxymetazoline (Afrin nasal spray),pseudoephedrine (Sudafed),phenylephrine (Sudafed PE),,Eye drops and nasal sprays can help relieve itchiness and other allergy-related symptoms for a short time., Symptoms can be ,easily controlled with antihistaminics and nasal deconges\x02tants. Analgesics are useful to relieve headache, fever and ,myalgia. Nonaspirin containing analgesics are preferable ,as aspirin causes increased shedding of virus. Antibiotics ,are required when secondary infection supervenes., Pathophysiology : VIRAL RHINITIS
It is caused by a virus. The infection is usually
contracted through airborne droplets. Several viruses
(adenovirus, picornavirus and its subgroups such as rhinovirus, coxsackie virus and enteric cytopathic human
orphan virus) are responsible. Incubation period is
1–4 days and illness lasts for 2–3 weeks.
BACTERIAL RHINITISNonspecific infections. It may be primary or secondary.
Primary bacterial rhinitis is seen in children and is usually
the result of infection with pneumococcus, streptococcus or
staphylococcus. A greyish white tenacious membrane may form in the nose, which with attempted removal causes
bleeding.
Secondary bacterial rhinitis is the result of bacterial infection supervening acute viral rhinitis., Epidemiology : Estimates of the prevalence of allergic rhinitis range from as low as 9% to as high as 42%., 20-30% of the Indian population, GOOD, Preventive measures for avoiding allergic rhinitis include : ,,Avoiding areas where there is heavy dust, mites, or molds,,Avoiding pets,,Avoiding what you know you are allergic to,,Controls in your environment, such as air conditioning during pollen season,,Avoid touching your face and rubbing your eyes or nose.,,Close windows in your home and car during the spring, summer and early fall when pollen counts are higher.,,Enclose pillows, mattresses and box springs in dust mite covers.,,Keep pets off couches and beds, and close doors to bedrooms you don’t want them to enter.,,Use filters in your vacuum cleaner and air conditioner to reduce the amount of allergens in the air.,,Wash your hands often, especially after playing with pets.,,Wear a hat and sunglasses to protect your eyes from pollen when you’re outside. ,,Change your clothes as soon as you come indoors., Complications : bronchitis, otitis media, pharyngitis, PNEUMONIA, sinusitis, tonsillitis, Diagnostics : serum IgE level, serum IgE level, Skin test, Nasal endoscopy, HISTORY TAKING, Differential diagnosis : allergic rhinitis, atrophic rhinitis, Influenza, nasal polyps, sinusitis, vasomotor rhinitis, disease description : Acute rhinitis is associated with environmental allergies or respiratory viral infections. Viral microbes with numerous types and subtypes can infect the respiratory epithelium of the nasal cavity in a repetitive fashion throughout the year, or during a specific period of time such as winter or fall.Allergic rhinitis (AR) is a common inflammatory process that manifests as nasal itchiness and congestion, postnasal drip, sore throat, cough, itchy swollen eyes and sometimes airway hyper-reactivity (AHR) if asthma coexists. |
Acute Rhinosinusitis | Disease Name : Acute Rhinosinusitis, Treatment : amoxicillin with or without clavulanate in adults as first-line therapy for a period of 5 to 10 days in most adults.,,patients allergic to penicillin, a third-generation cephalosporin plus clindamycin (for adequate coverage of non-susceptible S. pneumoniae) or doxycycline could be therapeutic possibilities. Third-generation cephalosporins alone have variable efficacy rates against S. pneumonia., Topical nasal decongestants, such as ephedrine,nasal drops, will often encourage the sinus to drain and topical,corticosteroids are used to reduce inflammation. Saline,douches can also be beneficial.Antral lavage under local or general anaesthesia was previously,used to confirm the diagnosis and provided the opportunity,to obtain samples for bacteriology, Endoscopic sinus,surgery allows a more functional approach to diseases of the,paranasal sinuses and enables the drainage pathways of the,paranasal sinuses to be opened., Pathophysiology : Rhinosinusitis is inflammation of the sinonasal mucosa and is
defined as the presence of nasal congestion or nasal discharge
and at least one of facial pain or hyposmia with endoscopic
and/or CT changes to confirm the diagnosis. It can be divided
into acute rhinosinusitis (ARS) and chronic rhinosinusitis
(CRS) depending on the timing of symptoms. Symptoms
are present for less than 12 weeks in ARS and more than
12 weeks in CRS.ARS is thought to result from bacterial superinfection of
virally damaged mucosa. The commonest bacteria involved
are Streptococcus pneumoniae, Haemophilus influenzae and
Moraxella catarrhalis. Upper dental sepsis may also predispose
to acute maxillary sinusitis. Patients with maxillary sinusitis
have a mucopurulent discharge, facial pain and nasal obstruction.
Irritation of the superior alveolar nerve may give rise
to referred upper toothache. In ARS nasendoscopy reveals
inflammed and swollen nasal mucosa with mucopurulent
secretions in the middle meatus. Dental sepsis from anaerobic
organisms causes around 10% of cases of maxillary sinusitis.
The resultant mucopurulent nasal secretion has a foul taste
and smell., Epidemiology : 16% of adults are diagnosed with ABRS annually.6% to 7% of children with respiratory symptoms have acute rhinosinusitis., good, Do not smoke. Smoking is not good for you or for people around you, since this can cause mucous to become clogged in the nose/sinuses. Avoid being around second-hand smoke, as well as other triggers like animal dander, dust, mold and pollen. Take pains to prevent sinus and other infections by : ,,Washing your hands well before and after eating and after using the bathroom.,Staying away from sick people.,Treating your allergies, possibly with nasal steroid therapy or immunotherapy (primarily known as allergy shots).,Keeping your body and your immune system in good shape by eating well (lots of vegetables and fruits) and staying hydrated.,Using a humidifier if your house is dry or an air purifier. Make sure to clean your equipment regularly.,Irrigating your nose when necessary with a saline rinse., Complications : abscess, CAVERNOUS SINUS THROMBOSIS, ocular pain, ptosis, Orbital abscess, Diagnostics : CT SCAN, Nasal endoscopy, allergy skin test, Differential diagnosis : allergic rhinitis, dental problem, migraine, nasal foreign bodies, nasal polyps, STATUS MIGRAINOUS, Tension-Type Headaches, upper respiratory tract infection, disease description : ARS is thought to result from bacterial superinfection of
virally damaged mucosa. The commonest bacteria involved
are Streptococcus pneumoniae, Haemophilus influenzae and
Moraxella catarrhalis. Upper dental sepsis may also predispose
to acute maxillary sinusitis. Patients with maxillary sinusitis
have a mucopurulent discharge, facial pain and nasal obstruction.
Irritation of the superior alveolar nerve may give rise
to referred upper toothache |
Acute Severe Asthma | Disease Name : Acute Severe Asthma, Treatment : medication : Magnesium/Magnesium Sulphate, Ipratropium bromide , Aminophylline , Theophylline , oxygen should be titrated to achieve oxygen saturation of at least 92%.,,Rapid-acting inhaled ß2-adrenergic bronchodilators are first-line therapy for acute asthma. Because the optimal doses necessary to achieve maximal bronchodilation have not been defined, dosing is empiric and should be titrated using an objective measure of airflow obstruction, such as FEV1 or peak expiratory flow and clinical response.,,A dose of systemic corticosteroids should be administered within the first hour of treatment for acute asthma for all but patients with the mildest form of the disease.This therapy is particularly important for patients with severe asthma and those already receiving systemic corticosteroids, as recently confirmed by a large prospective study of asthma care that clearly demonstrated an inverse relation between need for hospital admission for acute asthma and time to administration of systemic corticosteroids., Pathophysiology : At a physiological level, premature airway closure during exhalation causes an increase in functional residual capacity and air trapping. Heterogeneous distribution of air trapping results in ventilation-perfusion mismatch and hypoxemia- triggering anaerobic metabolism and lactic acidosis. It is offset initially by respiratory alkalosis and is compounded once respiratory fatigue and respiratory acidosis ensue.Physiologically, acute asthma is divided into two phases. An early bronchospastic phase is observed within minutes after exposure to the allergen with mast cell degranulation and release of inflammatory mediators like histamine, prostaglandin D2, and leukotriene C4. A later inflammatory phase causing airway swelling and edema due to eosinophils released eosinophilic cationic proteins (ECP) and major basic protein (MBP)., Epidemiology : Asthma affected an estimated 262 million people in 2019 and caused 455 000 deaths., POOR, If your healthcare provider says you have asthma, you’ll need to figure out what triggers an attack. Avoiding the triggers can help you avoid an attack. You can’t prevent yourself from getting asthma, though., Complications : Cardiac arrest, hypoxaemia, respiratory failure, Diagnostics : PET SCAN, ABG PO2, ABG PCO2, CHEST X RAY, PULMONARY FUNCTION TEST(PFT), CT SCAN, Differential diagnosis : Anaphylaxis, Anaphylaxis, BRONCHIOLITIS, Chronic Obstructive Pulmonary Disease, Congestive heart failure, PNEUMONIA, Pulmonary Embolism, disease description : Acute severe asthma, formerly known as status asthmaticus, is defined as severe asthma unresponsive to repeated courses of beta-agonist therapy such as inhaled albuterol, levalbuterol, or subcutaneous epinephrine. It is a medical emergency that requires immediate recognition and treatment. |
Acute Sphenoid Sinusitis | Disease Name : Acute Sphenoid Sinusitis, Treatment : medication : Ephedrine , Phenylephrine , A nebulizer can treat many sphenoid sinusitis symptoms like postnasal drip or nasal congestion. They moisturize and provide relief from pain and irritation. Systemic or topical decongestants, hot fermentation, steam inhalation, and steroid nasal sprays can also help the situation., Endoscopic transnasal sphenoidotomy is one of the most reliable surgical procedures and is considered the gold standard for treating chronic sphenoid sinusitis. The endoscopic method aids better visualization and has faster healing and a higher success rate. Microscopic sphenoidotomy and balloon-assisted endoscopic sphenoidotomy are other methods to treat sphenoid sinusitis surgically. A sphenoidotomy aims to improve sinus drainage and reduce pressure on your optic nerve (which could cause vision problems). It can be done by removing bone or tissue, blocking the sinus openings, or widening them., Pathophysiology : Sinuses function to filter out pollutants, microorganisms, dust, and other antigens. Sinuses drain into the intranasal meatus via small channels called ostia. The maxillary, frontal, and anterior ethmoid sinuses drain into the middle meatus, creating a congested area called the osteomeatal complex. The posterior ethmoid and sphenoid sinuses drain into the superior meatus. Tiny hairs called "cilia" line the mucous membranes of the nasal cavity and nasopharynx, and work in an integrated and coordinated fashion to carry out this function of circulating mucus and filtered debris, ultimately leading them to the nasopharynx and oropharynx, where they are swallowed. Rhinosinusitis occurs when the sinuses and nasal passages cannot effectively clear out these antigens, leading to an inflammatory state. This condition usually results from three key factors : obstruction of the sinus ostia (i.e., anatomic causes such as a tumor or septal deviation), dysfunction of the cilia (i.e., Kartagener syndrome), or thickening of sinus secretions (cystic fibrosis). The most common cause of temporary obstruction of these outflow regions is local edema due to upper respiratory tract infections (URI) or nasal allergy, both of which predispose to rhinosinusitis. When this occurs, bacteria can remain in, gain access to, and proliferate within the usually sterile paranasal sinuses. Severe complications can occur when the sinus infection spreads to surrounding structures, such as the brain and orbit, via the valve-less diploic veins. These are veins located within the inner cancellous bone layer of the skull. This is thankfully a rare phenomenon, but important to remember.Adults have four developed and paired sinus cavities. The ethmoid, sphenoid, frontal, and maxillary sinuses. In children, only the ethmoid and maxillary sinuses are present at birth. The ethmoid sinus separates from the orbit by only a thin layer of bone (the lamina papyrecia). Thus, orbital infections typically arise from the ethmoid sinus, which occurs more often in younger children. The frontal sinuses do not appear to develop until 5 to 6 years of age and do not reach full development until after puberty. Intracranial complications typically arise from the frontal sinuses and thus occur more often in older children or adults. The sphenoid sinus starts to pneumatize at 5 years of age but does not fully develop until 20 to 30 years of age. , Epidemiology : approximately 3% of all cases of acute sinusitis., 2.7% of all sinus infections., good, Take pains to prevent sinus and other infections by : ,,Washing your hands well before and after eating and after using the bathroom.,Staying away from sick people.,Treating your allergies, possibly with nasal steroid therapy or immunotherapy (primarily known as allergy shots).,Keeping your body and your immune system in good shape by eating well (lots of vegetables and fruits) and staying hydrated.,Using a humidifier if your house is dry or an air purifier. Make sure to clean your equipment regularly.,Irrigating your nose when necessary with a saline rinse., Complications : CAVERNOUS SINUS THROMBOSIS, orbital cellulitis, PRESEPTAL CELLULITIS, Orbital abscess, Subperiosteal abscess, Diagnostics : X RAY PNS(OF/OM), CT SCAN, Differential diagnosis : cluster headache, migraine, Mucocele of the sphenoid sinus, Nasal foreign body, neoplasms of the sphenoid sinus, optic neuritis, temporal arteritis, TRIGEMINAL NEURALGIA, upper respiratory tract infection, disease description : Acute sphenoid sinusitis is an inflammation of the sinuses. Sphenoid sinusitis is typically described as an acute inflammation of—either one or both—of the sphenoid sinuses (the two large cavities located directly behind the nose and set between the eyes). The condition is sometimes limited to the sphenoid cavities, which is typically referred to as isolated sphenoid sinusitis. |
Acute Suppurative Arthritis | Disease Name : Acute Suppurative Arthritis, Treatment : medication : Flucloxacillin, 1-DRAINAGE,2-ANTIBIOTICS,3-SPLINTAGE,4-AFTERCARE, Treatment of septic arthritis comprises antimicrobial therapy and joint fluid drainage (arthrotomy, arthroscopy, or daily needle aspiration). Empiric intravenous antimicrobial therapy should be initiated promptly after joint aspiration is complete and cultures obtained. Empiric antibiotic coverage includes antistaphylococcal coverage (nafcillin, oxacillin, or vancomycin) for all age and risk categories. Empiric antibiotics for nongonococcal septic arthritis usually involves the use of intravenous vancomycin directed against gram-positive organisms especially if there is a suspicion of MRSA based on community and institutional data. If the patient is immunocompromised, abuses intravenous drugs or the gram stain is negative, then a third-generation cephalosporin like ceftriaxone, ceftazidime or cefotaxime should be added for the additional gram-negative coverage. Age, risk factors, and gram stain result should direct additional antibiotics (e.g., a third-generation cephalosporin for suspected Salmonella or N. gonorrhea). Blood and synovial fluid cultures and sensitivities should direct prolonged antimicrobial treatment. Early involvement by an orthopedic surgeon is essential. The procedure used to drain joint fluid depends on multiple factors and is determined by the orthopedic surgeon.,,Nongonococcal septic arthritis is usually treated with intravenous antibiotics for 2 weeks followed by another 1 to 2 weeks of oral antibiotic therapy for a total duration of three to four weeks. Longer antibiotic therapy for 4 to 6 weeks may be reasonable in cases of Pseudomonas aeruginosa. Gonococcal arthritis responds well to intravenous ceftriaxone which is continued for 24 to 48 hours after clinical improvement then transitioned to oral therapy for the remainder of the treatment, Pathophysiology : The highly vascularized joint synovium lacks a limiting basement membrane so is prone to infection via hematogenous seeding from systemic infection. Septic arthritis may also result from direct injury, puncture wounds, and intra-articular injections. Contiguous spread from adjacent osteomyelitis may occur. The hip and shoulder are vulnerable to contiguous spread. Septic arthritis occurs when there is a bacterial invasion of the synovium and joint space followed by an inflammatory process. Inflammatory cytokines and proteases mediate joint destruction. Other factors which play a role in joint damage are bacterial toxins (based on animal models) and microbial surface components like staphylococcal adhesins which promote the binding of the bacteria to intra-articular proteins.Prosthetic joint infections are classified into : Early within 3 months of implantationDelayed within 3-24 months of surgeryLate : occurring after 24 monthsMost early prosthetic joint infections are caused by staphylococcus, whereas delayed cases are due to gram negatives and coagulase-negative staphylococcus. Late cases are usually secondary to hematogenous spread from various foci., Epidemiology : (7.8 cases per 100, 000 person-years), NOT SPECIFIC, While not all cases of septic arthritis are preventable, there are a few things you can do to try to prevent getting it, including : ,,Make sure cuts and wounds don’t get infected : If you have a cut or wound on your skin, keep it clean to prevent infection. If you are experiencing signs of an infection — such as redness, warmth and/or pus in or around your wound — contact your healthcare provider immediately.,Try to manage your chronic health condition(s) well : If you have a chronic health condition such as diabetes or AIDS (acquired immunodeficiency syndrome), try to manage your condition as well as you can in order to stay healthy.,Practice safe sex : Always follow safe sex practices, such as always using a condom or dental dam and talking with your sexual partner about past partners and STI (sexually transmitted infection) history.,Don’t abuse drugs : Injection drug use can cause infections. Only take medications as prescribed by your healthcare provider., Complications : death, Osteonecrosis, sepsis, osteomyelitis, CHRONIC PAIN, Diagnostics : CRP, Erythrocyte Sedimentation Rate (ESR), Radionuclide Imaging technique, fluid culture, White Blood Cell count WBC, BLOOD CULTURE, MRI, X RAY, USG, Differential diagnosis : Acute bursitis, Acute lymphadenitis, bacterial endocarditis, Gout, Hemarthrosis, "lymes disease", Osteoarthritis, disease description : Acute Septic arthritis ( also know as acute suppurative arthritis) is joint inflammation secondary to an infectious etiology, usually bacterial, but occasionally fungal, mycobacterial, viral, or other uncommon pathogens. Septic arthritis is usually monoarticular involving one large joint such as the hip or knee; however, polyarticular septic arthritis involving multiple or smaller joints may also occur. Though uncommon, septic arthritis is an orthopedic emergency that can cause significant joint damage leading to increased morbidity and mortality. |
Acute Suppurative Otitis Media | Disease Name : Acute Suppurative Otitis Media, Treatment : medication : Ephedrine , Oxymetazoline , Noscapine , Amoxicillin and Clavulanic acid , Ampicillin , Cefuroxime/Cefuroxime axetil, Pseudoephedrine, Ear toilet and Dry local heat helps to relieve pain., 1. Antibacterial therapy, 2. Decongestant nasal drops, 3. Oral nasal decongestants, 4. Analgesics and antipyretics., Myringotomy, Pathophysiology : Otitis media begins as an inflammatory process following a viral upper respiratory tract infection involving the mucosa of the nose, nasopharynx, middle ear mucosa, and Eustachian tubes. Due to the constricted anatomical space of the middle ear, the edema caused by the inflammatory process obstructs the narrowest part of the Eustachian tube leading to a decrease in ventilation. This leads to a cascade of events resulting in an increase in negative pressure in the middle ear, increasing exudate from the inflamed mucosa, and buildup of mucosal secretions, which allows for the colonization of bacterial and viral organisms in the middle ear. The growth of these microbes in the middle ear then leads to suppuration and eventually frank purulence in the middle ear space. This is demonstrated clinically by a bulging or erythematous tympanic membrane and purulent middle ear fluid. This must be differentiated from chronic serous otitis media (CSOM), which presents with thick, amber-colored fluid in the middle ear space and a retracted tympanic membrane on otoscopic examination. Both will yield decreased TM mobility on tympanometry or pneumatic otoscopy.Several risk factors can predispose children to develop acute otitis media. The most common risk factor is a preceding upper respiratory tract infection. Other risk factors include male gender, adenoid hypertrophy (obstructing), allergy, daycare attendance, environmental smoke exposure, pacifier use, immunodeficiency, gastroesophageal reflux, parental history of recurrent childhood OM, and other genetic predispositions ., Epidemiology : The peak incidence of otitis media occurs between six and twelve months of life and declines after age five. Approximately 80% of all children will experience a case of otitis media during their lifetime, and between 80% and 90% of all children will experience otitis media with an effusion before school age., GOOD, "Here are some ways to reduce risk of ear infections in you or your child : ,,Don’t smoke. Studies have shown that second-hand smoking increases the likelihood of ear infections. Be sure no one smokes in the house or car — especially when children are present — or at your day care facility.,Control allergies. Inflammation and mucus caused by allergic reactions can block the eustachian tube and make ear infections more likely.,Prevent colds. Reduce your childs exposure to colds during the first year of life. Don’t share toys, foods, drinking cups or utensils. Wash your hands frequently. Most ear infections start with a cold. If possible, try to delay the use of large day care centers during the first year.,Breastfeed your baby. Breastfeed your baby during the first 6 to 12 months of life. Antibodies in breast milk reduce the rate of ear infections.,Bottle feed baby in upright angle. If you bottle feed, hold your baby in an upright angle (head higher than stomach). Feeding in the horizontal position can cause formula and other fluids to flow back into the eustachian tubes. Allowing an infant to hold his or her own bottle also can cause milk to drain into the middle ear. Weaning your baby from a bottle between nine and 12 months of age will help stop this problem.,Watch for mouth breathing or snoring. Constant snoring or breathing through the mouth may be caused by large adenoids. These may contribute to ear infections. An exam by an otolaryngologist, and even surgery to remove the adenoids (adenoidectomy), may be necessary.,Get vaccinations. Make sure your child’s immunizations are up to date, including yearly influenza vaccine (flu shot) for those 6 months and older. Ask your doctor about the pneumococcal, meningitis and other vaccines too. Preventing viral infections and other infections help prevent ear infections.", Complications : abscess, acute labyrinthitis, Brain Abscess, petrositis, acute mastoiditis, FACIAL PARALYSIS, Diagnostics : Otoscopy, X Ray skull, Tuning Fork Tests, Differential diagnosis : allergic rhinitis, CHOLESTEATOMA, hearing impairment, Human Parainfluenza virus infection, lungs disease, NASOPHARYNGEAL CANCER, OTITIS EXTERNA, disease description : Acute otitis media is defined as an infection of the middle ear space. It is a spectrum of diseases that include acute otitis media (AOM), chronic suppurative otitis media (CSOM), and otitis media with effusion (OME). Acute otitis media is the second most common pediatric diagnosis in the emergency department following upper respiratory infections. |
Acute Suppurative Parotitis | Disease Name : Acute Suppurative Parotitis, Treatment : Appropriate antibiotics, preferably administered through i.v. route, adequate hydration, measures ,to promote salivary flow and attention to oral hygiene., Treatment of acute bacterial parotitis should include intravenous (IV) hydration, analgesics, and 7 to 10 days of IV antibiotics. In community-acquired parotitis, the first-line treatment is with antistaphylococcal penicillin (nafcillin, oxacillin), first-generation cephalosporin (cefazolin), vancomycin, or clindamycin for suspected methicillin-resistant S. aureus (MRSA). For healthcare-associated parotitis, use cefoxitin, ertapenem, or ampicillin/sulbactam, with levofloxacin, clindamycin, or piperacillin-tazobactam as alternatives. For patients at high risk of MRSA, start with vancomycin or use linezolid or daptomycin as alternatives. In case of dental infection, parotitis should prompt the use of clindamycin or metronidazole (anaerobic coverage) and ceftriaxone or piperacillin-tazobactam as an alternative., incision and drainage for cases of acute parotitis refractory to conservative measures of hydration and antibiotics. Specialists might consider saline irrigation of the duct system to remove inspissated mucus or pus.,,Treatment of HIV parotitis may include antiviral therapy, low-dose radiation, or partial parotidectomy to reduce glandular size.,,Superficial parotidectomy is usually the last resort for chronic parotitis and may involve ligation of the duct or the instillation of methylene violet. Surgery may be necessary for disfiguring swelling, chronic autoimmune parotitis at risk for neoplastic lymphoma, or adjacent inflammation resulting in facial nerve paralysis., Pathophysiology : A ductal valve creates a unidirectional flow of saliva out of the gland, preventing bacteria from entering. However, this valve may sometimes become incompetent and result in ascending bacterial infection. Dehydration or drying medications, such as atropine, antihistamines, and psychotropic agents, which decrease salivary production and flow, can increase the risk of parotitis from either infectious or inflammatory causes. Sialolithiasis is a common condition where calculi formed from inorganic crystals can obstruct the gland duct, although less common in the parotid than submandibular glands due to serous rather than mucoid saliva. Bacteria trapped behind a high-grade obstruction can proliferate and result in acute suppurative parotitis. In the hospital setting, methicillin-resistant Staphylococcus aureus (MRSA) and atypical infections, such as candida, should be considered.
In autoimmune parotitis (such as Sjögren or rheumatoid arthritis), an antigen-antibody complex is endocytosed into epithelial cells, processed into a human leukocyte antigen expressed on the cell surface, and recognized by specific CD4 T-lymphocytes, which release cytokines and chemotactic factors augmenting more CD4 activation. B-lymphocytes enter the acini and produce antibodies presenting antigens to CD4 T-cells, with resultant oligoclonal expansion and acinar destruction that can increase the risk of neoplastic transformation. These autoimmune causes result in chronic parotitis, often termed chronic punctate parotitis. Chronic parotitis eventually results in scar tissue, stricture, and sialectasis.
Human immunodeficiency virus (HIV) can result in asymptomatic, firm parotid swelling, more pronounced in children than adults, due to CD8+ lymphocytes responding to HIV or other viruses, such as Epstein-Barr, hepatitis C, cytomegalovirus, or adenovirus, infiltrating and ultimately depositing in the gland.
Sarcoidosis can lead to parotid gland inflammation but is less commonly seen than the involvement of lungs, lymph nodes, and skin. Noncaseating granulomas are present in both parotid glands causing swelling but minimal symptoms or inflammation. Rarely, sarcoid involvement can be severe and result in the Heerfordt-Waldenström syndrome characterized by fever, anterior uveitis, parotid enlargement, and facial nerve paralysis.Staphylococcus aureus (MRSA) and atypical infections, such as candida, should be considered.In autoimmune parotitis (such as Sjögren or rheumatoid arthritis), an antigen-antibody complex is endocytosed into epithelial cells, processed into a human leukocyte antigen expressed on the cell surface, and recognized by specific CD4 T-lymphocytes, which release cytokines and chemotactic factors augmenting more CD4 activation. B-lymphocytes enter the acini and produce antibodies presenting antigens to CD4 T-cells, with resultant oligoclonal expansion and acinar destruction that can increase the risk of neoplastic transformation. These autoimmune causes result in chronic parotitis, often termed chronic punctate parotitis. Chronic parotitis eventually results in scar tissue, stricture, and sialectasis.Human immunodeficiency virus (HIV) can result in asymptomatic, firm parotid swelling, more pronounced in children than adults, due to CD8+ lymphocytes responding to HIV or other viruses, such as Epstein-Barr, hepatitis C, cytomegalovirus, or adenovirus, infiltrating and ultimately depositing in the gland.Sarcoidosis can lead to parotid gland inflammation but is less commonly seen than the involvement of lungs, lymph nodes, and skin. Noncaseating granulomas are present in both parotid glands causing swelling but minimal symptoms or inflammation. Rarely, sarcoid involvement can be severe and result in the Heerfordt-Waldenström syndrome characterized by fever, anterior uveitis, parotid enlargement, and facial nerve paralysis., Epidemiology : 3.8–14/10 000 in early infancy, GOOD, The best way to prevent acute parotitis is to get the MMR vaccine. To reduce your risk of other types of parotitis : ,,Stay hydrated.,Wash your hands frequently.,Get adequate nutrition.,Practice good oral hygiene.,Don’t smoke.,Avoid alcohol.,Practice safe sex., Complications : Mumps, Xerostomia, FACIAL PARALYSIS, eagle syndrome, Diagnostics : BLOOD CULTURE test, White Blood Cell count WBC, CT SCAN, Differential diagnosis : Dacryoadenitis, Obstructive parotitis, Pneumoparotitis, SIALOLETHIASES, Sjogren syndrome, VIRAL PAROTITIS, disease description : Acute suppurative Parotitis is inflammation of the parotid glands and is the most common inflammation of the major salivary glands. Parotitis can present as a local process or a manifestation of systemic illness.Acute suppurative parotitis (ASP) is an uncommon infection, and the sudden onset of fever and swelling of the face or neck are typical clinical features. |
Acute Suppurative Tenosynovitis | Disease Name : Acute Suppurative Tenosynovitis, Treatment : Early recognition and treatment is critical,Consult hand surgery urgently (within 72 hours),Hand surgery indications : No improvement in 24 hours of antibiotics,Minimal incision with catheter irrigation of tendon sheath (preferred) OR,Wide Incision and Drainage,May be indicated in High Pressure Injection Wound,Extremity elevation and Splinting,Remove rings from fingers, Initial parenteral antibiotics,First-line parenteral coverage for MRSA,Vancomycin,Daptomycin,Linezolid,Televancin,Clindamycin (depending on local sensitivities to MRSA),Injection drug use (polymicrobial coverage as well as MRSA),Vancomycin AND,Piperacillin/Tazobactam (Zosyn),Disseminated Neisseria gonorrhoeae suspected,Ceftriaxone (Rocephin),Older antibiotic regimens that may be considered in more mild, borderline cases (Streptococcus, Staphylococcus),Cefazolin (Ancef) or,Ampicillin-sulbactam (Unasyn), Pathophysiology : The flexor tendons of the hand
are covered with fibrous and synovial flexor
sheaths . The fibrous sheaths exist only
up to the bases of the digits. A synovial sheath
lines the fibrous sheaths. In the thumb and little
finger, the synovial lining extends proximally
through the palm and ends 2–3 cms above the
wrist. The synovial sheaths of the index, middle and ring fingers end proximally at the level of the
transverse palmar skin crease. The proximal part
of the sheath of the flexor tendon of the thumb is
known as the radial bursa. The sheath of the little
finger tendons open proximally into the ulnar
bursa, which encloses the grouped tendons of the flexor digitorum superficialis and flexor digitorum
profundus.
It should be noted that there is normal but great
anatomical variation in the arrangement of the
synovial tendon sheaths. The ulnar and radial
bursae may communicate. The tendon sheaths
of the index, middle and ring fingers may
communicate with the ulnar bursa..The bacteria enter the tendon sheath
with the point of a needle or other sharp objects
penetrating the tendon sheath. Exceptionally, the
sheath is infected by extension from the terminal
pulp space infection.
The finger is swollen throughout its length, and
is acutely tender over the flexor tendon sheath.
It is held semi-flexed, and active or passive
extension at the inter-phalangeal joint is very
painful. In tenosynovitis of the little finger, the
ulnar bursa also becomes involved, giving rise
to swelling of the palm and sometimes fullness
immediately above the flexor retinaculum. The
area of maximum tenderness in an ulnar bursa
infection can be elicited over that part of the bursa
lying between the transverse palmar creases.
This is Kanavels sign. In infections of
the radial bursa, there is more swelling over the
thenar eminence and thumb. The other findings
are similar to other tendon sheath infections., Epidemiology : GOOD, The best way to reduce your risk of tenosynovitis is to avoid overusing your tendons. Give your body time to recover after workouts, sports, jobs or other activities that require you to perform the same movements repeatedly.,,You can prevent strain on your body (including your tendons) by wearing proper safety equipment and working out safely., Complications : necrosis, tendon rupture, Pus accumulation, Diagnostics : USG, PHYSICAL EXAMINATION, Differential diagnosis : BURSITIS, CELLULITIS, Deep space abscess, Herpetic whitlow, Necrotizing fasciitis, osteomyelitis, rheumatoid arthritis, Septic arthritis, Tendonitis, disease description : Pyogenic flexor tenosynovitis (PFT), also known as septic or suppurative flexor tenosynovitis, is a closed-space infection of the flexor tendon sheath of the hand and remains a challenging problem within the realm of hand surgery. PFT remains a common problem and has been shown to make up 2.5 to 9.4% of all hand infections. |
Acute Tonsillitis | Disease Name : Acute Tonsillitis, Treatment : medication : Amoxicillin and Clavulanic acid , Benzylpenicillin/ penicillin-G, Azithromycin , Clarithromycin , Clindamycin , Because copathogens such as,staphylococci or anaerobes can produce ß-lactamase that can inactivate,penicillin, the use of cephalosporins or clindamycin may be more efficacious in,the treatment of chronic throat infections. Tonsillolith or debris may be,expressed manually with either a cotton-tipped applicator or a water jet.,Chronically infected tonsillar crypts can be cauterized using silver nitrate., Tonsillectomy alone is most commonly performed for recurrent or chronic,pharyngotonsillitis., Pathophysiology : Acute Infection
Most episodes of acute pharyngotonsillitis are caused by viruses. Group A ß-hemolytic streptococcus (GABHS) is the most common cause
of bacterial infection in the pharynx.
Chronic Infection
The tonsils and adenoids can be chronically infected by multiple microbes,
which can include a high incidence of ß-lactamase–producing organisms. Both
aerobic species, such as streptococci and Haemophilus influenzae, and anaerobic
species, such as Peptostreptococcus, Prevotella, and Fusobacterium, contribute.
The tonsillar crypts can accumulate desquamated epithelial cells, lymphocytes,
bacteria, and other debris, causing cryptic tonsillitis. With time, these cryptic
plugs can calcify into tonsillar concretions or tonsillolith. Biofilms appear to
play a role in chronic inflammation of the tonsils., Epidemiology : is a common disease and makes up approximately 1.3% of outpatient visits., GOOD, While you can’t totally prevent tonsillitis, there are things you can do to reduce your risk. For example : ,,Wash your hands often, especially before touching your nose or mouth.,Avoid sharing food, drink, or utensils with someone who’s sick.,Replace your toothbrush regularly., Complications : ACUTE RHEUMATIC FEVER, chronic tonsillitis, infection, Poststreptococcal Glomerulonephritis, Diagnostics : THROAT SWAB CULTURE, MRI, CHEST X RAY, CT SCAN, Differential diagnosis : acute pharyngitis, candidiasis, diphtheria, Epstein-Barr Virus, infectious mononucleosis, Laryngeal Diphtheria, leukemia, Peritonsillar abscess, scarlet fever, tonsillar malignancy, disease description : Acute tonsillitis is an inflammatory process of the tonsillar tissues and is usually infectious in nature. Acute infections of the palatine tonsils predominantly occur in school-aged children, but patients of any age may be affected. Tonsillitis of viral origin is usually treated with supportive care. |
Acute Tubulointerstitial Nephritis | Disease Name : Acute Tubulointerstitial Nephritis, Treatment : medication : Mycophenolate mofetil/ Mycophenolate sodium, Prednisolone, Current recommendations favor the use of oral prednisone in children,whose kidney function fails to improve after stopping the suspected agent.,Intravenous methylprednisolone is used in severe cases. Mycophenolate mofetil,has been found to be beneficial in steroid-unresponsive cases., Pathophysiology : The hallmarks of acute TIN are an extensive lymphocytic infiltration of the
tubulointerstitium, interstitial edema, and varying degrees of tubular necrosis
and regeneration. Eosinophils may be present, particularly in drug-induced TIN;
occasionally, interstitial granulomas with giant cells occur. Glomeruli are usually
normal in primary TIN. The pathogenesis is not fully understood, but a T-cell–
mediated immune mechanism has been postulated. Drugs are the most
common cause of acute TIN in children. A large number of medications,
especially antimicrobials, anticonvulsants, and analgesics, have been implicated
as etiologic agents. Nonsteroidal antiinflammatory agents
(NSAIDs), penicillins, and sulfonamides account for most cases. Drug-induced
TIN is an idiosyncratic reaction that occurs in only a very small subset of
patients who ingest the medication, typically with repeated exposure. Drugs of
abuse (including synthetic cannabinoids, bath salts, ecstasy, anabolic steroids,
inhaled solvents, heroin, and cocaine) are an increasingly common problem in
certain populations. Other causes of acute TIN include infections, primaryglomerular diseases, and systemic diseases such as systemic lupus
erythematosus., Epidemiology : GOOD, "Often, the disorder cant be prevented. Avoiding or reducing your use of medicines that can cause this condition can help reduce your risk. If needed, your provider will tell you which medicines to stop or reduce.", Complications : Acute Renal Failure, hyperkalemia, CHRONIC TUBULOINTERSTITIAL NEPHRITIS, Diagnostics : SERUM Creatinine, USG KUB, CT SCAN, EOSINOPHILS, Urine analysis, Differential diagnosis : autoimmune disease, Epstein-Barr Virus, Glomerulonephritis, polyangitis, Renal tubular necrosis, systemic lupus erythematosus (SLE), URINARY TRACT OBSTRUCTION, disease description : Tubulointerstitial nephritis (TIN, also called interstitial nephritis) is the term
applied to conditions characterized by tubulointerstitial inflammation and
damage with relative sparing of glomeruli and vessels. Both acute and chronic
primary forms exist. Acute TIN is characterized by an acute extensive
lymphocytic inflammatory response and a rapid decline in renal function.
Chronic TIN usually displays a protracted onset and also a chronic patchy
lymphocytic infiltrate, interstitial fibrosis, and a slow deterioration in renal
function. Secondary forms of interstitial nephritis can be associated with primary
glomerular diseases, as well as systemic diseases affecting the kidney. |
Acute Viral Hepatitis | Disease Name : Acute Viral Hepatitis, Treatment : medication : Ribavirin , Adefovir dipivoxil , Lamivudine, Interferon Alpha, Entecavir,Telbivudine ,Tenofovir alafenamide ,Tenofovir disoproxil fumarate (,Interferon alfa-2b ,Peginterferon alfa-2a,Simeprevir,Daclatasvir ,Sofosbuvir ,Ombitasvir/paritaprevir/ritonavir,Elbasivir/grazoprevir,Glecaprevir/pibrentasvir, These new drugs are sometimes given with older drugs like ribavirin and peginterferon alfa-2a and peginterferon-2b. You might have to take these medicines for some time, even as long as six months.,,If you have chronic hepatitis D, your doctor may prescribe drugs with interferons and might also add medicines for hepatitis B. Hepatitis E treatments include peginterferon alfa-2a and ribavirin., Pathophysiology : The histopathology of acute hepatitis is determined by the underlying etiology causing the hepatocellular injury. Acute hepatitis secondary to acetaminophen overdose demonstrates characteristic histological features such as central to central bridging necrosis and minimal inflammatory cell infiltrates. The histopathology features of acute hepatitis secondary to viral infections usually show intranuclear viral inclusions and surrounding neutrophils. Classical historical features of autoimmune hepatitis demonstrate portal inflammation and interface hepatitis formally known as piecemeal necrosis which is essentially the presence of portal inflammatory cells between the portal and liver parenchyma. Diffuse microvesicular steatosis, Mallory bodies, fibrosis, or cirrhosis of the typical findings seen in alcohol-related liver injury.Iron accumulation with hepatocellular hemosiderin pigment and increase hepatic copper concentrations and liver biopsy samples are the classical histopathological findings in patients with hereditary hemochromatosis and Wilsons disease respectively. The microscopic changes in PSC and PBC are not pathognomonic for the condition. PBC is characterized by classical findings of florid duct lesion which is essentially granulomatous and lymphocytic portal inflammation centered around the interlobular bile ducts. The presence of concentric rings of fibrosis known as onion skin fibrosis is the hallmark historical features of PSC., Epidemiology : 385 million carriers of hepatitis B virus and 170 million carriers of hepatitis C virus. More than 1 million deaths each year are attributable to hepatitis B., good, "There are many ways you can reduce your chances of getting hepatitis : ,,Get the vaccines for hepatitis A and hepatitis B.,Use a condom during sex.,Dont share needles to take drugs.,Practice good personal hygiene such as thorough hand-washing with soap and water.,Dont use an infected persons personal items.,Take precautions when getting any tattoos or body piercings.,Take precaution when traveling to areas of the world with poor sanitation. (Make sure to get your vaccines.),Drink bottled water when traveling.,It is very important that you take these preventive measures if you participate in risky behaviors. Take preventive steps, too, if you work in places like a nursing homes, dormitories, daycare centers, or restaurants where there you have extended contact with other people and a risk of coming into contact with the disease.", Complications : HEPATIC ENCEPHALOPATHY, hyperbilirubinemia, liver failure, Coagulopathy, Diagnostics : HBeAg, HBsAg, USG ABDOMEN(W/A), LIVER FUNCTION TEST LFT, SERUM GLOBULIN, MRI, CT SCAN, Differential diagnosis : acute cholecystitis, AUTOIMMUNE HEPATITIS, congestive heart failure (CHF), Cytomegalovirus (CMV), Hepatic artery thrombosis, sepsis, Varicella zoster, Wilson disease, disease description : Acute Viral Hepatitis Is A Systemic Infection Affecting The Liver Predominantly. Almost All Cases Of Acute Viral Hepatitis Are Caused By One Of Five Viral Agents : Hepatitis A Virus (HAV), Hepatitis B Virus (HBV), Hepatitis C Virus (HCV), The HBV-Associated Delta Agent Or Hepatitis D Virus (HDV), And Hepatitis E Virus (HEV). All These Human Hepatitis Viruses Are RNA Viruses, Except For Hepatitis B, Which Is A DNA Virus But Replicates Like A Retrovirus. |
Adamantinoma | Disease Name : Adamantinoma, Treatment : If the lesion extends to the endosteal surface, a full segment of bone must be excised; the gap is filled with a vascularized graft or a suitable endoprosthesis, or managed by distraction osteogenesis. If there has been more than one recurrence, or if the tumour extends into the surrounding soft tissues, radical resection or amputation is advisable., Pathophysiology : A recurrent pattern of numerical abnormalities featuring extra copies of chromosomes 7, 8, 12, 19, and 21 have been detected in classic as well as osteofibrous dysplasia-like forms of adamantinoma ., Epidemiology : It is a rare neoplasm., There is a slight male predominance with a sex ratio of 5 : 4., Adamantinomas are rare, Adamantinomas frequently occur in young to middle-aged adults between the ages of 20 to 40., bad, Patients with signs and symptoms of bone pain, soft tissue swelling, or any subjective palpable mass should seek early intervention., Complications : Metastasis, Diagnostics : MRI, MRI, plain radiograph, ELECTRON MICROSCOPY, Histopathological examination, Differential diagnosis : Adamantinoma-like Ewing sarcoma, fibrous dysplasia, metastatic carcinoma, Osteofibrous dysplasia, disease description : Adamantinoma is a rare low-grade malignant bone tumor of uncertain histogenesis, which occurs commonly in the diaphyses and metaphyses of the tibia. The term adamantinoma has been given to this tumor due to its histological resemblance to ameloblastoma of the mandible. Its histopathology shows biphasic patterns of epithelial cells and osteofibrous components. |
Addisons Disease | Disease Name : Addisons Disease, Treatment : If you’re taking fludrocortisone, your provider might tell you to increase your salt intake, especially in hot and humid weather and after vigorous exercise., "Medicines are used to treat Addisons disease. Hormone replacement therapy corrects the levels of steroid hormones the body isnt making enough of. Some treatments include oral corticosteroids such as : ,,Hydrocortisone (Cortef), prednisone (Rayos) or methylprednisolone (Medrol) to replace cortisol. These hormones are given on a schedule to act like the changes in cortisol levels the body goes through over 24 hours.,Fludrocortisone acetate to replace aldosterone.", Some people take dehydroepiandrosterone (DHEA) to improve their stamina or libido (sex drive)., Pathophysiology : Adrenal failure in Addison disease results in decreased cortisol production initially followed by that of aldosterone, both of which will eventually result in an elevation of adrenocorticotropic (ACTH) and melanocyte-stimulating hormone (MSH) hormones due to the loss of negative feedback inhibition., Epidemiology : 40 and 60 people per million of the general population., Addison disease is rare. The incidence is 0.6 per 100, 000 of the population per year. The total number of people affected by this condition at a given time ranges from 4 to 11 per 100, 000 of the population. In adults, the common age of presentation is 30 to 50 years. It is more common in women., good, Unfortunately, there’s nothing you can do to prevent Addison’s disease., Complications : death, hypertension, Hypoglycaemia, infection, acute cardiovascular decompensation, Diagnostics : Complete Blood Count CBC, HISTOPATHLOGY, Insulin in Blood test, ACTH Stimulation Test (Cosyntropin), MRI, CT SCAN, Differential diagnosis : Chronic fatigue syndrome, Hypothyroidism, infectious mononucleosis, Pituitary apoplexy, sepsis, shock, disease description : Addison disease is an acquired primary adrenal insufficiency. A primary adrenal insufficiency is termed Addison disease when an autoimmune process causes the condition. It is a rare but potentially life-threatening emergency condition. It results from bilateral adrenal cortex destruction leading to decreased adrenocortical hormones, which may include cortisol, aldosterone, and androgens. |
Addisonian Crisis | Disease Name : Addisonian Crisis, Treatment : medication : Hydrocortisone , Pathophysiology : nan, Epidemiology : nan, Complications : diarrhea, vomiting, Abdominal Pain, Dehydration, Confusion, Diagnostics : CECT Abdomen, USG ABDOMEN(W/A), Differential diagnosis : Congenital adrenal hyperplasia (CAH), disease description : An addisonian crisis is a life-threatening situation that results in low blood pressure, low blood levels of sugar and high blood levels of potassium. You will need immediate medical care. People with Addisons disease commonly have associated autoimmune diseases. |
Adenocarcinofibroma (malignant Adenofibroma) | Disease Name : Adenocarcinofibroma (malignant Adenofibroma), Treatment : Adenocarcinomas are diverse and can involve any part of the body. The management and treatment of adenocarcinoma differ depending on the primary site of disease as well as the stage of cancer. Prior to the initiation of any treatment, it is very important to first characterize the site and type of adenocarcinoma. Multidisciplinary care is of utmost importance with the involvement of pathology, radiology, surgical oncology, radiation oncology, and medical oncology along with the other allied health professionals. The earlier stages of cancer, where surgical resection is feasible, surgery offers the best opportunity for long term survival. Depending on the location, type, stage, as well as the performance status of the patient, different types of treatments, are proposed.,,Curative intent treatments usually include surgery, neoadjuvant or adjuvant systemic chemotherapy, radiation therapy, or a combination of concurrent radiation and chemotherapy, hormonal therapy in breast and prostate cancer. Management also involves close follow up of these patients with repeat blood work, surveillance scans, and long term symptom and survivorship care. The palliative treatment is proposed in the incurable setting and usually involves systemic chemotherapy, immunotherapy, targeted therapies to prolong the survival of the patient. There is a role for palliative radiation and surgery for symptom control, Pathophysiology : Adenocarcinomas are easily diagnosed and distinguished from other cancer histologies by a light microscopy examination. The diagnosis is usually based on the identification of glandular structures under the light microscopy. As these features are shared by all types of adenocarcinomas, it is impossible to diagnose the primary site of origin of these tumors, especially in a metastatic setting. Also, with poorly differentiated adenocarcinomas, where the minimal glandular formation is seen on light microscopy or no glandular formation but stain for mucin, immunohistochemistry (IHC) is an important tool to help further diagnose the type of adenocarcinoma.Positive staining for CK-7 along with TTF-1 (+/- napsin), which is a pneumocyte marker expressor, is highly suggestive of adenocarcinoma of the lung. Adenocarcinoma of the lung also tend to have mutations in the epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), and c-ROS oncogene 1(ROS-1), which are important to diagnose, as targeted therapies are available for treatment. PD-L1 IHC assays are also performed in advanced lung cancers to help with treatment selection with immunotherapy. The College of American Pathologists recommends obtaining the above testing on all patients with advanced adenocarcinoma of the lungPositive staining for CK-7, GATA -3 ( GATA-binding protein 3), and gross cystic fluid protein 15 is suggestive of breast adenocarcinoma. Positive staining for prostate-specific antigen (PSA) is specific for adenocarcinoma of the prostate. P63 a nuclear basal protein helps to differentiate from normal prostatic tissue and adenocarcinoma of the prostate. Positive CDX-2 or cytokeratin-20 (CK-20) positive with CK-7 negative is suggestive of colorectal adenocarcinoma.Positive staining for CK-7, PAX 8, and WT-1 is suggestive of ovarian adenocarcinoma.Positive staining for thyroglobulin and thyroid transcription factor-1 is suggestive of adenocarcinoma of thyroid., Epidemiology : variable, NA, Complications : Metastasis, Diagnostics : CA 125, MRI, Differential diagnosis : intestinal adenocarcinoma, Metastatic tumours, Ovarian Tumours, prostate cancer, disease description : A malignant neoplasm of the ovary with an invasive epithelial component and a fibrotic stroma. Histologic variants include clear cell, serous, and mucinous adenocarcinofibroma.Ovarian cystadenofibroma is a relatively rare benign ovarian tumor that contains both epithelial and fibrous stromal components. The appearance of cystadenofibroma on imaging is often complex; cystic- to solid-appearing masses may be visualized and it often resembles a malignant tumor. |
Adenocarcinoma Of Cervix | Disease Name : Adenocarcinoma Of Cervix, Treatment : Chemotherapy is a type of treatment in which a healthcare professional delivers cancer-killing medication into a vein using a needle or intravenous (IV) drip. Some people may take chemotherapy drugs orally.,,This treatment destroys cancer cells but may also kill some healthy cells. Many people going through chemotherapy become sick, lose their hair, feel fatigued, or experience other adverse effects., Immunotherapy uses medications that support the immune system to kill cancer., Radiation uses high energy waves to target and kill cancer cells.,,External radiation delivers these waves from a machine outside the body. Internal radiation involves implanting a needle, seed, or another device near the tumor to release radiation over time., Surgery is the removal of the tumor and some surrounding healthy tissue during an operation. For cancer that has not spread beyond the cervix, these procedures are often used : ,,Conization. The use of the same procedure as a cone biopsy (see Diagnosis) to remove all of the abnormal tissue. It can be used to remove cervical cancer that can only be seen with a microscope, called microinvasive cancer.,,Loop electrosurgical excision procedure (LEEP). The use of an electrical current passed through a thin wire hook. The hook removes the tissue. It can be used to remove microinvasive cervical cancer.,,Hysterectomy. The removal of the uterus and cervix. A hysterectomy can be either simple or radical. A simple hysterectomy is the removal of the uterus and cervix. A radical hysterectomy is the removal of the uterus, cervix, upper vagina, and the tissue around the cervix. A radical hysterectomy also includes an extensive pelvic lymph node dissection, which means lymph nodes are removed. This procedure can be done using a large cut in the abdomen, called laparotomy, or using smaller cuts, called laparoscopy.,,Bilateral salpingo-oophorectomy. If needed, this surgery is the removal of both fallopian tubes and both ovaries. It is done at the same time as a hysterectomy.,,Radical trachelectomy. A surgical procedure in which the cervix is removed, but the uterus is left intact. It includes pelvic lymph node dissection (see above). This surgery may be used for young patients who want to preserve their fertility. This procedure has become an acceptable alternative to a hysterectomy for some patients.,,Exenteration. The removal of the uterus, vagina, lower colon, rectum, or bladder if cervical cancer has spread to these organs after radiation therapy (see below). Exenteration is rarely recommended. It is most often used when cancer has come back after radiation therapy., Pathophysiology : Adenocarcinoma is a cancer that starts in the gland cells that produce mucus. The cervix has glandular cells scattered along the inside of the passage that runs from the cervix to the womb (the endocervical canal).Adenocarcinoma is less common than squamous cell cancer, but has become more common in recent years., Epidemiology : In 2012, there were an estimated 192, 446 women li, Ovarian cancer accounts for 3% of all cancers in f, variable, Cervical cancer can be prevented by doing the following : ,,Get the HPV vaccine. The vaccine prevents most types of HPV infection that cause cervical cancer. Your provider can tell you if the vaccine is right for you.,Practice safer sex. Using condoms during sex reduces the risk for HPV and other sexually transmitted infections (STIs).,Limit the number of sexual partners you have. Avoid partners who are active in high-risk sexual behaviors.,Get Pap smears as often as your provider recommends. Pap smears can help detect early changes, which can be treated before they turn into cervical cancer.,Get the HPV test if recommended by your provider. It can be used along with the Pap test to screen for cervical cancer in women 30 years and older.,If you smoke, quit. Smoking increases your chance of getting cervical cancer., Complications : bleeding, neuropathy, pancytopenia, skin rash, tumors, Diagnostics : Biopsy Large, Complete Blood Count CBC, MRI, USG, Differential diagnosis : cervical intraepithelial neoplasia., Cervicitis, Endometrial cancer, PID, squamous cell carcinoma., disease description : Adenocarcinoma is a malignant neoplasm arising from epithelial cells of the glands or glandular like structures. Adenocarcinoma can arise in multiple sites of the body. Some of the common sites that develop adenocarcinoma are the breast, lung, prostate, gastrointestinal tract like the colon, rectum, pancreas, stomach, esophagus. Adenocarcinomas also make 70 percent of cancer of unknown origin . |
Adenocarcinoma Of Lung | Disease Name : Adenocarcinoma Of Lung, Treatment : medication : Cisplatin , Gefitinib, Chemotherapy treats adenocarcinoma with drugs that destroy cancer cells either at the site of the cancer or throughout the entire body. These drugs work by stopping cancer cells from growing and spreading. Chemotherapy is often given in combination with other forms of lung cancer treatments, like surgery or radiation., This type of therapy is often given in combination with surgery or chemotherapy. Radiation therapy sends beams of radiation to kill cancerous cells, which can shrink your tumor. The two types of radiation therapy doctors use are called external radiation and internal radiation. Sometimes, both internal and external radiation therapies are used at the same time to treat adenocarcinoma., Surgery may be the right treatment for your adenocarcinoma. If you have surgery for lung cancer, your doctor will remove the cancerous tissue in your lung as well as some of the healthy tissue around it. ,,There are three types of surgery commonly used to treat lung cancer. These include : ,,Segmentectomy or wedge resection (removing a small part of the lung),Lobectomy (removing one or two lobes of the lung),Pneumonectomy (removing one entire lung), Pathophysiology : Lung adenocarcinoma is classified into 4 types : adenocarcinoma in situ (AIS), minimally invasive adenocarcinoma (MIA), invasive adenocarcinoma, and variants of adenocarcinoma. Of these AIS and MIA have better outcomes when resected early. Local spread may involve spread directly to the pleura, diaphragm, pericardium, or bronchi with advanced disease spreading to the mediastinum, great vessels, trachea, esophagus, vertebral column, or adjacent lobe. Lymph node metastasis occurs in peribronchial lymph nodes before moving to mediastinal or subcarinal nodes and then the contralateral lung. Distant metastasis includes extension to a contralateral lobe, pleural nodules, malignant pleural or pericardial effusion, or any distant site such as the brain, bones, or liver. There is a subset of NSCLC that have mutations in epidermal growth factor receptor (EGFR), which sensitizes them to tyrosine kinase inhibitors, as well as anaplastic lymphoma kinase (ALK) fusion oncogene rearrangements, Epidemiology : 225, 000 individuals will be diagnosed with lung ca, poor, Since we don’t know what causes most cancers for sure, the only preventative measures are focused on reducing your risk. Some ways to reduce your risk include : ,,Don’t smoke or quit smoking if you do. Your risk of lung cancer starts coming down within five years of quitting.,Avoid second hand smoke and other substances that can harm your lungs.,Eat a healthy diet and maintain a weight that’s healthy for you. Some studies suggest that eating fruits and vegetables (two to six-and-a-half cups per day) can help reduce your risk of cancer.,Get screened for lung cancer if you’re at high risk., Complications : PLEURAL EFFUSION, Metastasis, Breathing difficulty, "Horners syndrome", Diagnostics : HISTOPATHLOGY, PET SCAN, TISSUE BIOPSY, X RAY CHEST, CT SCAN, Differential diagnosis : Benign lung lesions, granulomas, Hamartoma, Metastatic lesion, PNEUMONIA, disease description : Lung adenocarcinoma is the most common primary lung cancer seen in the United States. It falls under the umbrella of non-small cell lung cancer (NSCLC) and has a strong association with previous smoking. While incidence and mortality have declined, it remains the leading cause of cancer death in the United States. Adenocarcinoma of the lung usually evolves from the mucosal glands and represents about 40% of all lung cancers. |
Adenoid Basal Carcinoma | Disease Name : Adenoid Basal Carcinoma, Treatment : Chemotherapy : this injected drug floods the body and works to destroy cancerous cells found within. ,Radiotherapy : this treatment uses a machine to direct radiotherapy at a tumorous area to break it up and ultimately destroy it. This is a surgery-free method with minimal side effects., Mohs surgery : with this procedure, a surgeon uses a scalpel to cut the cancerous lesion out of the skin, removing the unhealthy tissue., Pathophysiology : Most of the proliferations referred to as adenoid basal carcinoma have a clinically benign course--leading some to suggest the term "adenoid basal epithelioma." However, rarely, these may be associated with invasive carcinomas. These tumors have been etiologically linked with high-risk human papillomavirus (HR-HPV) infection. Here, we investigate the use of p16 immunohistochemistry and HR-HPV RNA in situ hybridization (ISH) in the classification of adenoid basal tumors of the cervix. Seventeen cases of adenoid basal tumors of the cervix were included. The patients age ranged from 19 to 79 yr (average, 59 yr). p16 immunostain was performed on all cases and RNA ISH was performed in 4 cases with available formalin-fixed paraffin-embedded tissue. There were 11 low-grade tumors, 5 frankly invasive carcinomas, and 1 with histologic features that were intermediate between the former 2 categories. p16 immunostain was negative or showed patchy cytoplasmic staining in the low-grade tumors and was strongly and diffusely positive in the invasive carcinomas. HR-HPV RNA ISH was negative in the 3 low-grade tumors and was positive in 1 case of invasive carcinoma including the adenoid basal component. Distinct p16 immunostaining and HR-HPV RNA ISH patterns exist between low-grade adenoid basal tumors and invasive adenoid basal carcinomas. Our study indicates that p16 immunostaining and HR-HPV RNA ISH can be employed as useful ancillary tools in differentiating between noninvasive and invasive adenoid basal tumors along with careful histopathologic evaluation., Epidemiology : It is mostly seen in women over 50 years old,Generally, all racial and ethnic groups are at risk and the cancer is observed worldwide ., ABCs have a favorable prognosis, Some steps for the prevention of Adenoid Basal Carcinoma of Uterine Cervix include : ,,Use of measures to prevent sexually-transmitted infections, such as usage of condoms, avoiding multiple sexual partners, and circumcision in men,Avoidance of smoking,Regular screening to detect pre-cancers, Complications : bleeding, infection, skin rash, Metastasis, Diagnostics : Immunostaining, Immunostaining, Differential diagnosis : Adenoid basal hyperplasia, adenoid cystic carcinoma, Basal cell carcinoma, Invasive squamous cell carcinoma, Merkel Cell Carcinoma, Metastatic tumours, Sebaceous carcinoma, Trichoepithelioma, disease description : Adenoid basal carcinoma (ABC) is a rare cervical carcinoma of postmenopausal women composed of small basal-type (basaloid) cells with focal endocervical ("adenoid") differentiation. ABCs are associated with high-grade squamous intraepithelial lesions (HSIL) and contain integrated human papillomavirus type 16 DNA. |
Adenoid Cystic Carcinoma | Disease Name : Adenoid Cystic Carcinoma, Treatment : Agents commonly given as monotherapy for treating ACC are cisplatin, mitoxantrone, epirubicin, vinorelbine, paclitaxel, and gemcitabine, Radiation therapy, or radiotherapy (a cancer treatment that uses high doses of radiation to kill cancer cells and shrink tumors), Surgical removal of the tumor, Pathophysiology : The pathophysiology of ACC is an understudied area because of the rarity of the condition. A few studies looking at the molecular pathogenesis have provided vital information regarding the genes associated with dysregulation of cellular proliferation leading to this cancer. Nonrandom loss or gain of specific chromosomal segments has been seen in the tumor cells, particularly the most frequently encountered deletion of chromosome 1p35-36, which might be an ACC-specific chromosomal trait. Another ACC-specific chromosomal abnormality is the translocation between chromosomes 6q and 9p, which is found in greater than 85% of these tumors. This translocation creates the MYB : NFIB gene fusion, which leads to the overexpression of the MYB oncoprotein, which in turn promotes tumorigenesis. This is suggestive that the dysregulated MYB plays a key role in the pathogenesis and proliferation of ACC. Interestingly, important oncogenes and tumor suppressor genes that are frequently mutated in other cancers like the p53 tumor suppressor, RAS, and phosphatidylinositol-3-kinase (PI3K) growth factor signaling proteins are rarely altered in these tumors. Much remains to be understood regarding the specific mutations associated with ACC as they would pave the way for novel targeted immunotherapy, particularly in patients with advanced disease., Epidemiology : . Each year, an estimated 1, 300 people in the United States are diagnosed with AdCC. Worldwide, an estimated 200, 000 people have this disease., Five-year survival is up to 96%, Because there are no identifiable risk factors for adenoid cystic carcinoma, there is currently no known way to reduce your risk of the disease. There is also no known way to prevent ACC from coming back., Complications : facial pain, paralysis, recurrence of the malignancy, Diagnostics : HISTOPATHLOGY, PET SCAN, biopsy, MRI, CT SCAN, Differential diagnosis : basaloid carcinoma, BENIGN TUMORS, malignant tumors, MUCOEPIDERMOID CARCINOMA, Pleomorphic adenoma, disease description : Adenoid cystic carcinoma (ACC) is a rare malignancy arising from the secretory glands, most commonly seen involving the salivary glands. It accounts for approximately 1% of all malignancies of the head and neck region. However, it is the most common tumor of the minor salivary glands and the second most common tumor of the major salivary glands. Overall, it accounts for 10% of all salivary gland tumors. The tumor is typically slow-growing compared to other carcinomas and has a tendency for perineural invasion as well as hematogenous spread to distant organs and is most commonly seen in the elderly. |
Adenoid Hypertrophy | Disease Name : Adenoid Hypertrophy, Treatment : medication : Mometasone, In acute and chronic infectious adenoid hypertrophy, medical management with antibiotics is the appropriate first step. Amoxicillin can be used for uncomplicated acute adenoiditis, however, a beta-lactamase inhibitor such as clavulanic acid should be included for chronic or recurrent infections. Clindamycin or azithromycin are considered as alternatives in patients with penicillin allergies. Nasal steroids have been suggested as an additional option for medical treatment with some short-term success noted, Adenoidectomy is the surgical treatment option of choice for adenoid hypertrophy. Adenoidectomy is considered for patients with recurrent or persistent obstructive or infectious symptoms related to adenoid hypertrophy.Adenoidectomy is performed under general anesthesia with the patient in the supine position with the neck extended slightly and the surgeon seated at the head of the operating table. Adequate exposure of the posterior pharynx is achieved by use of a self-retaining oral retractor, such as a Crowe-Davis mouth gag, and the adenoids are visualized using an angled mirror or a nasal endoscope. Many techniques have been described for performing an adenoidectomy. Sharp instruments such as the adenoid curette or adenotome can be used to sharply dissect the adenoid tissue from the posterior pharyngeal wall, followed by packing of the pharynx or use of suction electrocautery for hemostasis. Suction electrocautery, co-ablation, plasma, laser, and microdebrider instruments have all been described in the literature as tools used for the removal of excessive adenoid tissue during adenoidectomy.Regardless of the tools employed, the goal of adenoidectomy is the surgical reduction of adenoid tissue mass and/or to eliminate bacterial biofilm from the surface of the adenoid tissue., Pathophysiology : Adenoid hypertrophy can occur because of infectious and non-infectious etiologies. Infectious causes of adenoid hypertrophy include both viral and bacterial pathogens. Viral pathogens associated with adenoid hypertrophy include adenovirus, coronavirus, coxsackievirus, cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpes simplex virus, parainfluenza virus, and rhinovirus. Many aerobic bacterial species have been implicated in contributing to infectious adenoid hypertrophy including alpha-, beta-, and gamma-hemolytic Streptococcus species, Haemophilus influenzae, Moraxella catarrhalis, Staphylococcus aureus, Neisseria gonorrhoeae, Corynebacterium diphtheriae, Chlamydophila pneumoniae, and Mycoplasma pneumoniae. Fusobacterium, Peptostreptococcus, and Prevotella species have also been identified as anaerobic organisms involved in infectious adenoid hypertrophy. Multiple non-infectious causes of adenoid hypertrophy have also been suggested including gastroesophageal reflux, allergies, and exposure to cigarette smoke. In adults, adenoid hypertrophy can also be a sign of a more serious condition such as HIV infection, lymphoma, or sino-nasal malignancy., Epidemiology : Adenoid hypertrophy is more common in children than in adults, as the adenoids naturally atrophy and regress during adolescence. A recent meta-analysis showed the prevalence of adenoid hypertrophy among a randomized representative sample of children and adolescents was 34.46%, A recent meta-analysis showed the prevalence of adenoid hypertrophy among a randomized representative sample of children and adolescents was 34.46%, good, Adenoid enlargement is caused due to infection and allergies. You can prevent development of such condition in your child by giving them a healthy lifestyle that helps fight infections and allergies., Complications : ear infection, nasal congestion, obstructive sleep apnea, SNORING, Diagnostics : HISTOPATHLOGY, Diagnostic nasal Examination(DNE), CT SCAN, rigid nasopharyngoscope, Flexible Nasopharyngoscopy, Soft Tissue Radiograph, PHYSICAL EXAMINATION, Differential diagnosis : Acute Otitis Media, adenoid hypertrophy, allergic rhinitis, choanal atresia, CHOLESTEATOMA, chronic rhinosinusitis, Chronic Sinusitis, encephalocele, HIV, NASAL DERMOID, NASAL DERMOID, nasal lymphoma, pyrifrom aperture stenosis, disease description : Adenoid hypertrophy is an obstructive condition related to an increased size of the adenoids. The condition can occur with or without an acute or chronic infection of the adenoids. The adenoids are a collection of lymphoepithelial tissue in the superior aspect of the nasopharynx medial to the Eustachian tube orifices. |
Adenoids | Disease Name : Adenoids, Treatment : symptoms are not marked, breathing exercises, ,decongestant nasal drops and antihistaminics for any,co-existent nasal allergy can cure the condition without,resort to surgery, ADENOIDECTOMY, Pathophysiology : Adenoids are subject to physiological enlargement in childhood.
Certain children have a tendency to generalized
lymphoid hyperplasia in which adenoids also take part.
Recurrent attacks of rhinitis, sinusitis or chronic tonsillitis
may cause chronic adenoid infection and hyperplasia.
Allergy of the upper respiratory tract may also contribute
to the enlargement of adenoids.
CLINICAL FEATURES
Symptoms and signs depend not merely on the absolute
size of the adenoid mass but are relative to the available
space in the nasopharynx.
Enlarged and infected adenoids may cause nasal, aural
or general symptoms., Epidemiology : GOOD, NA, Complications : nasal congestion, Nasal discomfort, sinus infections, Diagnostics : HISTOPATHLOGY, rigid nasopharyngoscope, Flexible Nasopharyngoscopy, Soft Tissue Radiograph, PHYSICAL EXAMINATION, Differential diagnosis : allergic rhinitis, choanal atresia, Chronic Sinusitis, nasal polyps, disease description : The nasopharyngeal tonsil, commonly called “adenoids”,
is situated at the junction of the roof and posterior wall of
the nasopharynx. It is composed of vertical ridges of lymphoid
tissue separated by deep clefts. Covering
epithelium is of three types : ciliated pseudostratified
columnar, stratified squamous and transitional. Unlike
palatine tonsils, adenoids have no crypts and no capsule.
Adenoid tissue is present at birth, shows physiological
enlargement up to the age of 6 years, and then tends to
atrophy at puberty and almost completely disappears by
the age of 20.
In relation to Sella turcica, three types of pneumatization
of sphenoid is seen : presellar, sellar and postsellar.
This has a bearing on transnasal surgery of the
pitutary.
Blood supply. |
Adenomyoepithelial Adenosis | Disease Name : Adenomyoepithelial Adenosis, Treatment : Excision recommended due to possibility of recurrence and association with malignancy,Best predictors of recurrence are initial incomplete excision and close margins., Pathophysiology : Unknown, Epidemiology : Wide age range but most frequent in third to fourth decades, NA, Complications : nan, Diagnostics : Immunostaining, Differential diagnosis : Adenomyoepithelioma, disease description : Adenomyoepithelial adenosis is an uncommon variant of adenosis with proliferation of epithelial and myoepithelial cells. |
Adenomyoepithelioma | Disease Name : Adenomyoepithelioma, Treatment : Complete wide excision with negative margins is standard treatment to prevent local recurrence,Mastectomy with or without axillary node dissection - only needed if malignant transformation., Pathophysiology : Adenomyoepithelioma of the breast is an uncommon tumor characterized by dual differentiation into luminal cells and myoepithelial cells. A spectrum of histologic patterns is observed among these tumors and even in different areas of individual tumors., Epidemiology : F > M, Uncommon tumor, NA, Complications : post-surgical complications, Diagnostics : mammography, MRI, CT SCAN, ELECTRON MICROSCOPY, Immunostaining, Immunostaining, Differential diagnosis : Adenomas : Tubular adenoma, Lactating adenoma, Apoc, Fibroadenoma, Nipple adenoma, PHYLLOIDES TUMOUR, Pleomorphic adenoma, Tubular carcinoma, disease description : It is a biphasic tumor composed of variable number of myoepithelial cells surrounding epithelial lined spaces
Usually expanded and prominent myoepithelial component. |
Adenomyoma | Disease Name : Adenomyoma, Treatment : Anti-inflammatory drugs. Your doctor might recommend anti-inflammatory medications, such as ibuprofen (Advil, Motrin IB, others), to control the pain. By starting an anti-inflammatory medicine one to two days before your period begins and taking it during your period, you can reduce menstrual blood flow and help relieve pain.,Hormone medications. Combined estrogen-progestin birth control pills or hormone-containing patches or vaginal rings might lessen heavy bleeding and pain associated with adenomyosis. Progestin-only contraception, such as an intrauterine device, or continuous-use birth control pills often cause amenorrhea — the absence of your menstrual periods — which might provide some relief., total hysterectomy, subtotal hysterectomy , polypectomy or tumor removal, and curettage., Pathophysiology : The adenomyomas were firm in consistency and, on cut section, show a gray-white surface. On microscopic examination, the tumors are well demarcated from the surrounding structures. The endometrial glands are mostly tubular and showed relatively regular spacing from each other without any back-to-back arrangement. The glands were lined by benign proliferative pseudostratified columnar epithelium. An occasional typical mitotic figure is noted in these glands in a few cases. The glands are surrounded by endometrial stroma which was compact and spindly. This stroma was, in turn, bordered by leiomyomatous smooth muscle. Thick-walled blood vessels were commonly observed. One to two typical mitotic figures per 10 hpf are noted in the endometrial stroma in few cases., Epidemiology : 16% to 62%, Incidence of adenomyosis is still under discussion, good, As the cause of adenomyosis isn’t well understood, healthcare providers don’t know of anything you can do to prevent it., Complications : Dysmenorrhoea, pelvic pain, DYSPAREUNIA, heavy menstrual bleeding, Diagnostics : HISTOPATHLOGY, USG Pelvis, MRI PELVIS, Differential diagnosis : adenomyosis, Endometrial cancer, ENDOMETRIAL HYPERPLASIA, Endometrial polyp, Endometriosis, leiomyoma, PID, Uterine fibroids, disease description : Adenomyoma of the uterus is a circumscribed nodular aggregate of benign endometrial glands surrounded by endometrial stroma with leiomyomatous smooth muscle bordering the endometrial stromal component. It may be located within the myometrium, or it may involve or originate in the endometrium and grow as a polyp. |
Adenomyosis | Disease Name : Adenomyosis, Treatment : medication : Danazol, MIRENA IUCD, Hormone treatment,The first-line therapy for managing the symptoms of adenomyosis is usually hormonal contraceptives. These include birth control pills or progesterone-releasing intrauterine devices (IUDs.,,Tranexamic acid,Tranexamic acid is a nonhormonal medication that helps reduce heavy bleeding during periods. It is a pill you take while you menstruate. This treatment may help women who cannot or choose not to have hormonal treatments., Hysterectomy,The only way to fully stop adenomyosis is with a hysterectomy (surgery to remove the uterus). “Since adenomyosis causes diffuse, often fingerlike projections of tissue to invade the uterine wall, we can’t just go in and remove the abnormal tissue like we might be able to do with fibroids, ” explains Chernofsky.,,The hysterectomy may remove only the uterus or the uterus and the cervix, depending on the patient’s preference and the surgeon’s recommendation. The ovaries and fallopian tubes can stay in place.,,Hysterectomies can be performed a few different ways : ,,Abdominally : An open hysterectomy involves a large incision (cut) in your abdomen.,Laparoscopically : A surgeon makes a few small cuts in your abdomen to remove the uterus. They view the procedure with a special telescope that contains a video camera (laparoscope).,Vaginally : Sometimes surgeons can remove the uterus through the vagina, but this procedure is not an option if your vagina is narrow or if your uterus is very enlarged., MRI-guided and ultrasound-guided high-intensity ultrasound thermal ablation can be done to target focal disease.Uterine artery embolization reduces blood flow to the uterus as a whole, thereby inducing necrosis leading to an overall reduction in uterine size., Pathophysiology : Grossly, the uterus appears symmetrically enlarged to not more than 14 weeks size. The cut section may show only a localized nodular enlargement. Most of the time, the
affected area reveals a peculiar, diffuse, striated and noncapsulated
involvement of the myometrium, mostly the posterior wall, with tiny dark haemorrhagic areas interspersed in between Laparoscopy reveals a uniformly enlarged uterus
Histological examination reveals islands of endometrial
glands surrounded by stroma, in the midst of myometrial
tissue at least two low-power fields beyond the endomyometrial
junction, more than 2.5 mm beneath
the basal endometrium.
These women are usually parous, around the age of
40 years. Some are asymptomatic, others present with menorrhagia and progressively increasing dysmenorrhoea.
Pelvic discomfort, backache and dyspareunia are the other
symptoms of adenomyosis. Clinical examination reveals a
symmetrical enlargement of the uterus if the adenomyosis
is diffuse and the uterus is tender. The uterine enlargement
rarely exceeds that of a 3-month pregnancy and is often
mistaken for a myoma. If a patient gives a history of menorrhagia
with accompanying dysmenorrhoea, one should
always consider the possibility of adenomyosis. If the adenomyosis
is localized, the enlargement is asymmetrical
and the resemblance to a myoma is more close. A myoma
of this size is rarely painful. Therefore, a painful, symmetrical
enlargement of the uterus should suggest the correct
diagnosis. MRI is superior to ultrasound showing hypo- or
anechoic area in the uterine wall. Ultrasound shows illdefined
hypoechoic areas, heterogeneous echoes in the
myometrium, asymmetrical uterine enlargement and subendometrial
halo thickening. It also shows
endometrial infiltration into the myometrium...., Epidemiology : Estimates range from 5% to 70% with more recent data suggesting a prevalence of 20% to 35%, GOOD, As the cause of adenomyosis isn’t well understood, healthcare providers don’t know of anything you can do to prevent it., Complications : infertility, painful intercourse, heavy menstrual bleeding, Diagnostics : HISTOPATHLOGY, MRI, MRI, CT SCAN, USG, HYSTEROSCOPY, LAPAROSCOPY, HISTOLOGIC EXAMINATION, Differential diagnosis : adenomyosis, Endometriosis, endometrium carcinoma, FIBROID UTERUS, PID, Polyps, disease description : Adenomyosis, also labelled uterine endometriosis, is a relatively
common condition in which islands of endometrium
are found in the wall of the uterus. It is observed frequently
in elderly women. More than one-third of the hysterectomy
specimens from women aged 40 years and above reveal the
presence of adenomyosis, irrespective of the indications
for hysterectomy. The disease often coexists with uterine
fibromyomas, pelvic endometriosis (15%) and endometrial
carcinoma. |
Adenopathy | Disease Name : Adenopathy, Treatment : medication : Ibuprofen , paracetamol, Usually, the lymph nodes will not be treated directly. Instead, the underlying condition causing adenopathy will be treated.,Home treatments, such as warm compresses or ice pads, may help soothe any discomfort in the area., Pathophysiology : The most common cause of swollen lymph nodes is a viral infection like the common cold or flu. Another common cause is a bacterial infection like strep throat. More rarely, lymph nodes can swell because of injury, other diseases, or cancer. The following are common causes of swollen lymph nodes, but there are many other potential causes that your doctor can identify.Swollen lymph nodes can occasionally be caused by cancer — but lymphadenopathy is much more likely to be caused by an infection.In rare instances, swollen lymph nodes may be a sign of : Lymphoma : This is a type of cancer that starts in the lymph system or in a lymph node.Leukemia : This is a cancer of your blood and bone marrow, which can also affect your lymph system., Epidemiology : NA, Complications : lymphoma, Diagnostics : Complete Blood Count CBC, LYMPH NODE BIOPSY, X RAY CHEST, Antibody Serology Tests, MRI, CT, X RAY, Differential diagnosis : HIV, "Hodgkins lymphoma", infectious mononucleosis, leukemia, Syphilis, TYPHOID FEVER, disease description : Adenopathy is a word used for swelling of the glands, which release chemicals like sweat, tears, and hormones. Adenopathy typically refers to swollen lymph nodes (lymphadenopathy). Lymph nodes arent technically glands, because they dont produce and release chemicals. |
Adenosine Deaminase Deficiency | Disease Name : Adenosine Deaminase Deficiency, Treatment : Gene therapy, bone marrow transplant, hematopoietic stem cell transplantation,(HSCT ) , gene therapy and, polyethylene glycol–modified bovine ADA (PEG-ADA )PEGADA., Pathophysiology : ADA deficiency is due to a lack of the enzyme adenosine deaminase. This deficiency results in an accumulation of deoxyadenosine, which, in turn, leads to : a buildup of dATP in all cells, which inhibits ribonucleotide reductase and prevents DNA synthesis, so cells are unable to divide. Since developing T cells and B cells are some of the most mitotically active cells, they are highly susceptible to this condition.an increase in S-adenosylhomocysteine since the enzyme adenosine deaminase is important in the purine salvage pathway; both substances are toxic to immature lymphocytes, which thus fail to mature.Because T cells undergo proliferation and development in the thymus, affected individuals typically have a small, underdeveloped thymus. As a result, the immune system is severely compromised or completely lacking., Epidemiology : fewer than one in 100, 000 live births worldwide., Poor, "Cant be prevented since its a genetic disorder. Consult your doctor when planning pregnancy.", Complications : Malnutrition, Diagnostics : GENETIC TESTING, LYMPHOCYTES - ABSOLUTE COUNT, Differential diagnosis : DiGeorge syndrome, hyper IgM syndrome, Purine nucleoside phosphorylase deficiency, severe combined immunodeficiency (SCID), WISKOTT-ALDRICH SYNDROME, disease description : Adenosine deaminase (ADA) deficiency is an inherited disorder that damages the immune system and causes severe combined immunodeficiency (SCID). People with SCID lack virtually all immune protection from bacteria, viruses, and fungi. |
Adenosis Including Variants | Disease Name : Adenosis Including Variants : Sclerosing Adenosis, , Treatment : Presence of sclerosing adenosis alone in a core biopsy does not require surgical excision.,Coexisting atypia will typically prompt surgical consultation., Pathophysiology : Adenosis is a benign (non-cancerous) breast condition in which the lobules (milk-producing glands) are enlarged, and there are more glands than usual. Adenosis is often found in biopsy samples of women who have fibrocystic changes in their breasts., Epidemiology : Found in 12 - 28% of all benign and 5 - 7% of malignant biopsies, NA, Complications : breast cancer., Diagnostics : mammography, MRI, USG, Immunostaining, Differential diagnosis : Adenomas : Tubular adenoma, Lactating adenoma, Apoc, disease description : Adenosis or lobulocentric processes with increase in glandular elements of terminal duct lobular unit (TDLU) with stromal fibrosis / sclerosis that distorts and compresses glands with preserved 2 cell layer (inner epithelial and outer myoepithelial cells). |
Adenoviral Conjunctivitis | Disease Name : Adenoviral Conjunctivitis, Treatment : 1. Supportive treatment for amelioration of symptoms,is the only treatment required and includes : ,• Cold compresses, and sun glasses to decrease glare, ,• Decongestant and lubricant tear drops to decrease,discomfort. 2. Topical antibiotics help to prevent superadded,bacterial infections. Weak steroids,such as fluorometholone or loteprednol (0.5%) are,indicated in patients with subepithelial infiltrates, ,and in those with membrane formation., "Povidone-iodine (PVI) is a broad-spectrum microbicide solution, which exists in multiple forms that are easily accessible, and a cost-effective disinfectant agent.,,Ganciclovir (GCV), a synthetic nucleoside analog of 2-deoxyguanosine, has been proven effective in the inhibition of the herpes family of viruses, specifically herpes simplex types 1 and 2, varicella-zoster virus, cytomegalovirus, and Epstein-Barr. ,Valganciclovir, Ribavirin and cidofovir have also been shown to exhibit antiviral activity against HAdV .,,Immunoglobulin (Ig) may offer the same effect on ocular tissue and prevent transmission and replication of the virus.,,Topical cyclosporine (both 1% and 2% concentrations) is an alternative option which, if used in the acute phase of adenoviral keratoconjunctivitis, is successful in both reducing the risk of developing corneal findings as well as the chronic treatment of persistent SEIs, with most cases resolving over a course of 3–4 weeks.", Pathophysiology : Epidemic Keratoconjunctivitis (EKC)
It is a type of acute follicular conjunctivitis mostly
associated with superficial punctate keratitis
and usually occurs in epidemics, hence the name
EKC. EKC is mostly caused by adenoviruses type 8 and 19.
The condition is markedly contagious and spreads
through contact with contaminated fingers, solutions
and tonometers. Incubation period after infection is about 8 days and
virus is shed from the inflamed eye for 2–3 weeks., Epidemiology : 15%–70%, good, You can reduce your risk of getting sick with an adenovirus infection by protecting yourself and your family. Ways to prevent infections include : ,,Wash your hands with soap and water often. Wash for at least 20 seconds.,Avoid touching your mouth, nose or eyes if you haven’t washed your hands.,Try to stay away from people who are sick.,Clean and disinfect your child’s toys often.,Clean counters, sinks and other hard surfaces with a bleach and water mixture.,If you’re already sick with adenovirus infection, take steps to prevent the spread. You can protect others by : ,,Staying home if you’re sick.,Sneezing and coughing into your elbow or a tissue. Don’t cough or sneeze into your hand.,Not sharing utensils, cups, towels and pillows with others.,Keeping your distance from other people. Avoid hugging and kissing.,Washing your hands frequently., Complications : superficial punctate keratitis, Symblepharon, subconjunctival haemorrhage, Corneal scarring, Diagnostics : PCR, GIEMSA STAINED CONJUNCTIVAL SMEAR, Point-of-care immunochromatography test, Viral cultures, Differential diagnosis : allergic conjunctivitis, bacterial conjunctivitis, dry eye syndrome, GIANT PAPILLARY CONJUNCTIVITIS, HERPES SIMPLEX, disease description : In the eye, adenovirus most commonly manifests as a follicular conjunctivitis. Though symptoms may range in severity, a common constellation of signs and symptoms is frequently manifest. Red and irritated conjunctiva is typical of the infection. |
Adenylate Kinase (ak) Deficiency | Disease Name : Adenylate Kinase (ak) Deficiency, Treatment : a diterpene lactone neoandrographolide from extracts of the traditional medicinal herb Andrographis paniculata has been suggested to inhibit AK2 and has strong anticancer properties. Further studies that involve all AK isoforms have the potential to bring new understanding and novel therapeutic strategies targeting the AK isoform network to suppress growth and metastasis of cancer cells., Pathophysiology : Demonstration of low enzyme activity in red blood cells and detection of mutations in AK1 gene. To investigate the molecular bases of the AK deficiency, we characterized five variants of AK1 isoenzyme-bearing mutations (118G>A, 190G>A, 382C>T, 418-420del, and 491A>G) found in AK-deficient patients with chronic hemolytic anemia., Epidemiology : variable, Complications : Hemolytic anemia, psychomotor impairment, mental retardation, Diagnostics : nan, Differential diagnosis : Carnitine palmitoyltransferase 2 deficiency, mitochondrial disorders, MYASTHENIA GRAVIS, myopathies, disease description : Adenylate kinase (RED CELL) deficiency is a rare hereditary erythroenzymopathy associated with moderate to severe nonspherocytic hemolytic anemia and, in some cases, with mental retardation and psychomotor impairment. |
Adenylosuccinate Lyase Deficiency | Disease Name : Adenylosuccinate Lyase Deficiency, Treatment : Additionally the following options include : ,1. D-ribose and uridine administration,2. Ketogenic diet,3. S-adenosyl-l-methionine, Treatment of adenylosuccinate lyase deficiency can be done via epilepsy management with anticonvulsive drugs., Treatment with anticonvulsive drugs (e.g., valproic acid, phenobarbital, carbamazepine, topiramate, levetiracetam, phenitoin, clobazam) depends on the type of seizures. Patients with ADSL deficiency often require polypharmacy with the use of two or more anticonvulsants, Pathophysiology : Adenylosuccinate lyase deficiency (ASLD) is a rare, inherited metabolic disorder caused by a genetic change which lowers the effectiveness of the enzyme adenylosuccinate lyase (ASL). The disorder causes the buildup of two chemicals in body fluids (such as cerebrospinal fluid, plasma, and urine) that aren’t normally seen in healthy individuals. These two chemicals are succinylaminoimidazole carboxamide riboside (SAICA riboside) and succinyladenosine.Adenylosuccinate lyase deficiency is categorized as a purine biosynthesis disorder. Purines are nucleotides that play vital roles in the cells, particularly in the process of building up or breaking down complex chemicals (intermediary metabolism) and in providing energy for cellular activity (energy-transforming reactions). Purines also serve as building blocks of nucleic acids and thus participate in molecular mechanisms by which genetic information is stored. Biosynthesis is how an organism makes different molecules and is often used to describe the synthesis of molecules that are particularly important for the organism to survive. ASLD changes the body’s ability to make these important purines. Researchers are still debating how these genetic and molecular mechanisms cause the symptoms seen in people with ASLD., Epidemiology : incidence of the disease remains unknown., Childhood - Stable outcome. Neonates - Fatal., "Cant be prevented since its a genetic disorder. Since ASLD is an autosomal recessive genetic disorder, therefore consult your doctor while planning pregnancy.", Complications : seizures, Psychomotor delay, lethal encephalopathy, Diagnostics : CSF EXAMINATION, URINE R/M, GENETIC TESTING, CT/MRI, Differential diagnosis : Autism spectrum disorder, developmental delay, encephalopathy, intellectual disability, mitochondrial disorders, seizures, disease description : Adenylosuccinate lyase deficiency is a neurological disorder that causes brain dysfunction (encephalopathy) leading to delayed development of mental and movement abilities (psychomotor delay), autistic behaviors that affect communication and social interaction, and seizures. |
Adrenal Cancer | Disease Name : Adrenal Cancer, Treatment : nan, Pathophysiology : nan, Epidemiology : nan, Complications : nan, Diagnostics : CT SCAN, Differential diagnosis : nan, disease description : nan |
Adrenal Insufficiency | Disease Name : Adrenal Insufficiency, Treatment : medication : Fludrocortisone , Hydrocortisone , The initial management of salt wasting crisis includes,correction of shock by fluid boluses. Longterm management of adrenal insufficiency requires,lifelong replacement of glucocorticoids and mineralocorticoids. ,Patients,with secondary adrenal insufficiency require lower dose,of glucocorticoids (6-10 mg/m2/day); mineralocorticoid,replacement is not necessary, Pathophysiology : Adrenal insufficiency may be related to adrenal defects
(primary adrenal insufficiency; autoimmune destruction,
infection, steroidogenic defect, hemorrhage), decreased
ACTH production (secondary adrenal insufficiency) or
ACTH resistance. Autoimmune adrenal dysfunction is the commonest
cause of primary adrenal failure (Addison disease) beyond
infancy. Autoimmune adrenal failure is often associated
with autoimmune polyendocrinopathy type 1 and 2.
Infections like tuberculosis and HIV can result in primary
adrenal failure. Adrenal hemorrhage in the setting of
meningococcal and other bacterial infections (WaterhouseFriderichsen
syndrome) is an important cause o f
insufficiency. Congenital adrenal hyperplasia (CAH) due
to deficiency of 21-hydroxylase or 3-P hydroxysteroid
dehydrogenase and deficient steroidogenesis due to
defective steroidogenic acute regulatory protein (StAR;
causing lipoid CAH) are the commonest causes in the
neonatal period. Secondary adrenal insufficiency is caused by congenital
malformations (holoprosencephaly, midline defects),
genetic defects or acquired insults (neurosurgery, tumor,
radiation). This is usually associated with other anterior
pituitary hormone deficiencies as well. In secondary
adrenal insufficiency, mineralocorticoid function is
preserved as aldosterone is not regulated by ACTH. Thus,
salt wasting is not observed. Prolonged steroid treatment
is associated with suppression of the hypothalamicpituitary
axis resulting in adrenal insufficiency after
discontinuation of medications. Again, mineralocorticoid
activity is preserved in these patients., Epidemiology : GOOD, Complications : hyperkalemia, hyponatremia, shock, Diagnostics : random blood sugar RBS, ACTH Stimulation Test (Cosyntropin), CT Abdomen, Plasma Renin, SERUM CORTISOL LEVEL, Differential diagnosis : eosinophilia, Histoplasmosis, hyperkalemia, Sarcoidosis, TUBERCULOSIS, disease description : Adrenal insufficiency may be related to adrenal defects
(primary adrenal insufficiency; autoimmune destruction,
infection, steroidogenic defect, hemorrhage), decreased
ACTH production (secondary adrenal insufficiency) or
ACTH resistance. |
Adrenoleukodystrophy | Disease Name : Adrenoleukodystrophy, Treatment : Adrenal dysfunction may be treated with steroids (such as cortisol) if the adrenal gland is not producing enough hormones.,,A specific treatment for X-linked adrenoleukodystrophy is not available. A bone marrow transplant may stop worsening of the condition.,,Supportive care and careful monitoring of impaired adrenal gland function may help in improving comfort and quality of life., Currently, there are no good treatments for X-ALD, The only effective treatment option for cerebral ALD is a stem cell transplant, a procedure in which the patient receives blood stem cells from a genetically matched donor. The purpose is to provide healthy stem cells that produce the protein lacking in boys with ALD., Pathophysiology : The most common form of ALD is an X-linked disorder with various
presentations. The most common clinical picture is of a degenerative neurologic
disorder appearing in childhood or adolescence and progressing to severe
dementia and deterioration of vision, hearing, speech, and gait, with death
occurring within a few years. Neurologic symptoms may be subtle at onset,
sometimes consisting only of behavioral changes or deteriorating academic
performance. Generalized but incomplete alopecia, resembling that of
chemotherapy, is a characteristic but inconsistent finding. A milder form of Xlinked ALD is adrenomyeloneuropathy, which begins in later adolescence or
early adulthood. Patients may have evidence of adrenal insufficiency before, at
the time of, or after neurologic symptoms develop, often with years separating
their presentation. X-linked ALD is caused by mutations in the ABCD1 gene
located on Xq28. The gene encodes a transmembrane transporter involved in the
importation of very-long-chain fatty acids into peroxisomes . More than 400
mutations have been described in patients with X-linked ALD. Clinical
phenotypes can vary even within families, perhaps owing to modifier genes or
other unknown factors. There is no correlation between the degree of neurologic
impairment and severity of adrenal insufficiency. Prenatal diagnosis by DNA
analysis and family screening by very-long-chain fatty acid assays and mutation
analysis are available. Women who are heterozygous carriers of the X-linked
ALD gene can develop symptoms in midlife or later; adrenal insufficiency is
rare.
Neonatal ALD is a rare autosomal recessive disorder. Infants have neurologic
deterioration and have or acquire evidence of adrenocortical dysfunction. Most
patients have severe, progressive cognitive impairment and die before 5 yr of
age. This disorder is a subset of Zellweger (cerebrohepatorenal) syndrome , in
which peroxisomes do not develop at all owing to mutations in any of several
genes (PEX5, PEX1, PEX10, PEX13, and PEX26 ) controlling the development
of this organelle., Epidemiology : The prevalence of X-linked adrenoleukodystrophy is 1 in 15, 000 individuals worldwide., bad, Genetic counseling is recommended for couples with a family history of X-linked adrenoleukodystrophy. Mothers of affected sons have an 85% chance of being a carrier for this condition.,,Prenatal diagnosis of X-linked adrenoleukodystrophy is also available. It is done by testing cells from chorionic villus sampling or amniocentesis. These tests look for either a known genetic change in the family or for very long chain fatty acid levels., Complications : Adrenal crisis, Vegetative state, Diagnostics : Complete Blood Count CBC, MRI Head, GENETIC TESTING, skin lesion biopsy, Differential diagnosis : Infantile Refsum disease, Leigh syndrome, Metachromatic Leucodystrophy, Multiple Sclerosis, Neonatal adrenoleukodystrophy, Niemann-Pick disease (NPD) typeA and B, Zellweger Syndrome, disease description : Adrenoleukodystrophy (ALD) is a genetic condition that damages the membrane (myelin sheath) that covers nerve cells in the brain and spinal cord. Myelin acts as insulation around the nerve fibers. When this insolating layer is damaged, nerve signals from the brain cannot communicate across the body properly, causing impaired bodily functions or paralysis. |
Adult Growth Hormone Deficiency | Disease Name : Adult Growth Hormone Deficiency, Treatment : medication : Somatropin , Treatment involves growth hormone shots (injections) given at home. The shots are most often given once a day. Older children can often learn how to give themselves the shot.,,Treatment with growth hormone is long-term, often lasting for several years. During this time, the child needs to be seen regularly by the pediatrician to ensure the treatment is working. If needed, the health care provider will change the dosage of the medicine., GH dose requirements are lower in older patients. For patients aged 30–60 years, a starting dose of 300 µg/day is reasonable and is usually not associated with any side effects. Daily dosing should be increased by 100–200 µg every 1–2 months titrated to the IGF-1, which should generally be kept in the upper half of the reference range, Pathophysiology : Adult growth hormone deficiency (AGHD) is being recognized increasingly and has been thought to be associated with premature mortality. Pituitary tumors are the commonest cause for AGHD. Growth hormone deficiency (GHD) has been associated with neuropsychiatric-cognitive, cardiovascular, neuromuscular, metabolic, and skeletal abnormalities. Most of these can be reversed with growth hormone therapy. The insulin tolerance test still remains the gold standard dynamic test to diagnose AGHD. Growth hormone is administered subcutaneously once a day, titrated to clinical symptoms, signs and IGF-1 (insulin like growth factor-1). It is generally well tolerated at the low-doses used in adults. Pegylated human growth hormone therapy is on the horizon, with a convenient once a week dosing., Epidemiology : 1 in 100, 000 people annually, good, Unfortunately, most cases of growth hormone deficiency (GHD) aren’t preventable. Certain risk factors can increase you or your child’s likelihood of developing acquired GHD, including : ,,Cancer treatment before reaching adult height.,Radiation to your head or brain.,Total body irradiation.,Surgery to your brain, especially the central region of your brain where your pituitary gland is located.,If any of these risk factors apply to you or your child, it’s important to talk to your healthcare provider about the signs and symptoms of GHD to look out for., Complications : Cardiovascular Disease, Metabolic disorders, skeletal abnormalities, Diagnostics : LDL - Cholesterol, MRI Brain, Serum GH, Serum IGF-1, IGF Binding Protein-3 (IGFBP-3), Differential diagnosis : Achondroplasia, Aging, Chronic fatigue syndrome, familial short stature, Hypothyroidism, Noonan syndrome, obesity, Panhypopituitarism, sleep disorders, disease description : Growth hormone deficiency means the pituitary gland does not make enough growth hormone.Adult onset growth hormone deficiency (AGHD) may represent two distinct clinical situations : Children with growth hormone (GH) deficiency transitioning to adulthood orGH deficiency acquired during adulthood (structural/trauma or idiopathic). |
Adult Inclusion Conjunctivitis | Disease Name : Adult Inclusion Conjunctivitis, Treatment : medication : Azithromycin , Azithromycin 1 g orally once only or either doxycycline 100 mg orally twice a day or erythromycin 500 mg orally 4 times a day for 1 week cures the conjunctivitis and concomitant genital infection. Sex partners also require treatment., Pathophysiology : Adult inclusion conjunctivitis or Paratrachoma results due to infection by obligate intracellular bacterium, Chlamydia trachomatis (serotypes D to K), which causes chronic follicular conjunctivitis (follicular conjunctivitis lasting for more than 16- 28 days). These organisms infect the epithelium of mucoid surfaces and were once identified as the trachoma-inclusion conjunctivitis agents (TRIC agents). These organisms can also infect a neonate during birth and may lead to neonatal conjunctivitis.Chlamydia trachomatis also includes the agents of classic trachoma (serotypes A, B, Ba and C). Lymphogranuloma venereum, a sexually transmitted infection, is caused by Chlamydia trachomatis (serotypes L1 to L3) which infect tissues deeper to the epithelium.Adult inclusion conjunctivitis is transmitted sexually (oro-genital activities) or from hand-to-eye contact. Gonorrhoea is the most common co-infection associated with adult inclusion conjunctivitis. Rarely, adult inclusion conjunctivitis is transmitted through eye-to-eye contact (e.g. by sharing mascara)., Epidemiology : makes up 1.8 to 5.6% of all cases of acute conjunctivitis, 1.8 to 5.6% of all cases of acute conjunctivitis, , good, Adult inclusion conjunctivitis is usually self-limiting.,,To prevent re-infection, all sexual partners should be treated simultaneously. All sexual partners should also be examined for other sexually transmitted diseases such as gonorrhoea, syphilis and Human immunodeficiency virus (HIV)., Complications : Pelvic Inflamatory Disease, MUCOPURULENT CERVICAL DISCHARGE, URETHERITIS, Diagnostics : ANTIGEN DETECTION ELISA, PCR, GIEMSA STAINED CONJUNCTIVAL SMEAR, Differential diagnosis : allergic conjunctivitis, bacterial conjunctivitis, dry eye syndrome, GIANT PAPILLARY CONJUNCTIVITIS, VIRAL CONJUNCTIVITIS, disease description : Adult inclusion conjunctivitis is known as chlamydial conjunctivitis. It is a sexually transmitted disease that occurs most commonly in sexually active young adults. The disease is usually transmitted through the hand-to-eye spread of infected genital secretions |
Adult- Onset Still Disease (aosd) | Disease Name : Adult- Onset Still Disease (aosd), Treatment : The goal of treatment for adult Still disease is to control the symptoms of arthritis. Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, are most often used first.,,Prednisone may be used for more severe cases.,,If the disease is severe or persists for a long time (becomes chronic), medicines that suppress the immune system might be needed. Such medicines include : ,,Methotrexate,Anakinra (interleukin-1 receptor agonist),Tocilizumab (interleukin 6 inhibitor),Tumor necrosis factor (TNF) antagonists such as etanercept (Enbrel), Pathophysiology : There are two immune dysregulations described in the pathogenesis of AOSD. Innate immunity with neutrophil and macrophage activation under the effect of pro-inflammatory cytokine IL-18 is one pathway. A study has shown the upregulation of CD64 in active ASD which is a marker of neutrophil activation . Secondly, CD4+ T helper (Th) cells may also play a role in the pathogenesis of AOSD with the predominance of the Th1 subset over Th2 as seen in a study that showed significantly higher expression of interferon-gamma mRNA expression than interleukin-4 in tissue biopsies . Moreover, the role of Th-17 responses is emerging in the pathogenesis of AOSD, and levels of Th-17 related cytokines, interleukins-1, 6, 17, 18, 21, and 23 are elevated., Epidemiology : Adult-onset Still disease is a very uncommon disease. Its annual incidence has been estimated to be 0.1 to 0.4 cases per 100, 000 people in Europe. Females are affected slightly more than males., variable, There is no known prevention., Complications : thrombotic thrombocytopenic purpura, amyloidosis, PULMONARY ARTERIAL HYPERTENSION, macrophage activation syndrome, diffuse alveolar hemorrhage., Diagnostics : HISTOPATHLOGY, HISTOPATHLOGY, Protein, Differential diagnosis : Familial Mediterranean Fever+++, hepatitis, HIV, MALIGNANCY, MEASLES, PARVOVIRUS B19, rheumatoid arthritis, rheumatologic disorders, Sarcoidosis, systemic lupus erythematosus (SLE), TUBERCULOSIS, viral hepatitis, disease description : Adult onset Still disease (AOSD) is a rare systemic inflammatory disorder characterized by daily fever, inflammatory polyarthritis, and a transient salmon-pink maculopapular rash. AOSD is alternatively known as systemic onset juvenile idiopathic arthritis. Even though there is no specific diagnostic test, a serum ferritin level of more than 1000ng/ml is common in AOSD. |
Adynamic Ileus | Disease Name : Adynamic Ileus, Treatment : Bowel rest, through restriction of food consumption, and intravenous (IV) fluid therapy is often suggested for individuals with ileus. If the individual is unable to eat food or drink liquids for over 7 days, total parenteral nutrition (TPN), which is a feeding method that bypasses the gastrointestinal tract, may be necessary. Severe or prolonged ileus with continuous vomiting often requires insertion of a tube extending from the nose to the stomach (i.e., nasogastric tube) in order to remove gastrointestinal contents and thus relieve pressure., Pathophysiology : Paralytic ileus (or adynamic ileus) is a condition in which there is a functional motor paralysis of the digestive tract secondary to neuromuscular failure involving the myenteric (Auerbach’s) and submucous (Meissner’s) plexus. The intestine fails to transmit peristaltic waves, resulting in a functional obstruction, and allowing fluid and gas to collect in the intestine. It is the small intestine that is predominantly affected, but the colon and stomach could also be involved. The resultant stasis leads to accumulation of fluid and gas within the bowel with associated distension, vomiting, decrease of bowel sounds, and absolute constipation. Paralytic ileus is a neurogenic condition, in which the normal electrical slow wave is present in the smooth muscle, but does not excite any action potentials. The mechanism is thought to be adrenergic stimulation, possibly involving dopamine release, but adrenoceptor blockade or dopamine inhibition have not been shown to be therapeutically effective., Epidemiology : 1, 400 per 100, 000 cases worldwide., variable, If ileus occurs as a natural side effect of surgery, your healthcare team will already have a treatment plan in place. Treatment includes : ,,Bowel rest. You’ll avoid eating by mouth until your bowel function has returned.,Parenteral nutrition. You may need to have your fluids, electrolytes, and nutrients replaced through an IV.,Prokinetics. Medications to promote peristalsis may help reboot your bowel function if it doesn’t recover soon enough on its own.,Nasogastric tube. In severe cases, a thin tube may be passed into your stomach through your nose to drain air and fluid., Complications : nausea, vomiting, prolonged hospital stay, Diagnostics : SERUM ELECTROLYTE, X RAY ABDOMEN, CT SCAN, USG, Differential diagnosis : Electrolyte imbalance, infections, intestinal obstruction , Metabolic disorders, Multiple Sclerosis, Parkinson’s Disease, peritonitis, disease description : Paralytic ileus (or adynamic ileus) is a condition in which there is a functional motor paralysis of the digestive tract secondary to neuromuscular failure involving the myenteric (Auerbachs) and submucous (Meissners) plexus |
Aero-otitis Media (otitic Barotrauma) | Disease Name : Aero-otitis Media (otitic Barotrauma), Treatment : restore middle ear aeration. This is done by,catheterization or politzerization. In mild cases, decongestant,nasal drops or oral nasal decongestant with antihistaminics,are helpful. In the presence of fluid or failure,of the above methods, myringotomy may be performed,to “unlock” the tube and aspirate the fluid, Treatment of MEBT varies along a spectrum, from trigger management and enhanced equalization education to medical and/or surgical interventions. Most commonly, MEBT is managed by the hyperbaric team, emergency physician, or general practitioner. ,If MEBT occurs during pressurization, then further pressurization should be stopped in order to allow the ET and middle ear space to clear. Decompressing a few feet and reinforced equalization techniques may be beneficial to allow for equalization. In the event of underlying ETD, physician-prescribed medical therapy such as oral decongestants may be beneficial., Pathophysiology : Eustachian tube allows easy and passive egress of air from
middle ear to the pharynx if middle ear pressure is high.
In the reverse situation, where nasopharyngeal air pressure
is high, air cannot enter the middle ear unless tube is
actively opened by the contraction of muscles as in swallowing,
yawning or Valsalva manoeuvre. When atmospheric
pressure is higher than that of middle ear by critical
level of 90 mm Hg, eustachian tube gets “locked, ” i.e.
soft tissues of pharyngeal end of the tube are forced into
its lumen. In the presence of eustachian tube oedema,
even smaller pressure differentials cause “locking” of the
tube. Sudden negative pressure in the middle ear causes
retraction of tympanic membrane, hyperaemia and engorgement
of vessels, transudation and haemorrhages.
Sometimes, though rarely, there is rupture of labyrinthine
membranes with vertigo and sensorineural hearing
loss., Epidemiology : 2%–17%, GOOD, To Do : Avoid air travel in the presence of upper respiratory,infection or allergy.,2. Swallow repeatedly during descent. Sucking sweets or chewing gum is useful.,3. Do not permit sleep during descent as number of swallows normally decrease during sleep,Autoinflation of the tube by Valsalva should be performed intermittently during descent.,5. Use vasoconstrictor nasal spray and a tablet of antihistaminic and systemic decongestant, half an hour before descent in persons with previous history of this episode.,6. In recurrent barotrauma, attention should be paid to nasal polyps, septal deviation, nasal allergy and chronic sinus infections..., Complications : Hearing loss, vertigo, serous effusion, Diagnostics : Otoscopy, Audiometry, Differential diagnosis : acoustic neuroma, eustachian tube dysfunction, Foreign Bodies of Ear, "menieres disease", OTITIS EXTERNA, otitis media, disease description : It is a nonsuppurative condition resulting from failure of
eustachian tube to maintain middle ear pressure at ambient
atmospheric level. The usual cause is rapid descent
during air flight, underwater diving or compression in
pressure chamber |
Aerophagia | Disease Name : Aerophagia, Treatment : medication : Pantoprazole , Try to eat or drink slowly so that you swallow less air.,Thoroughly chew your food before swallowing.,Try to eat your food with your mouth closed.,Avoid drinking carbonated drinks, such as cold drinks, soda, or beer.,Do not drink your beverages through a straw.,You should become conscious of air swallowing, and when you notice the habit, immediately stop gulping and practice slow breathing to calm yourself.,Stress and anxiety increase aerophagia. You should practice relaxing techniques or professional help to stay calm, such as meditation, yoga, muscle relaxation therapy, aromatherapy, or awareness about the disease.,Avoid smoking, as while you inhale smoke, you also swallow air. ,Don’t chew bubble gum or suck on hard candy.,Use masks or tubes with proper fits if you are breathing with the help of a CPAP machine.,Check the fit of your denture if you wear them. The ill-fitting dentures can cause you to gulp more air while you drink or eat. Therefore, readjust them if you feel they are misfits, Pathophysiology : Aerophagia occurs when a person swallows too much air and experiences bloating and belching. The disorder is very common, but despite frequent gulping and other telltale signs, people may not realize that air swallowing is the cause of their discomfort. One survey found that although 23% of people surveyed had symptoms of aerophagia, only 13% had sought treatment.Although researchers have long suspected that the symptoms of aerophagia were due to people swallowing excessive air, the first clinical trial to scientifically demonstrate this mechanism was performed in 2009.If you use continuous positive airway pressure (CPAP) therapy for obstructive sleep apnea, you may have noticed symptoms of aerophagia. It is important to know that there are many ways to reduce discomfort from swallowed air. Understanding what causes aerophagia and when to visit a doctor are the first steps toward attaining relief from your symptoms.Aerophagia is characterized by excessive air swallowing. The air enters the gastrointestinal tract and causes a range of symptoms. The word aerophagia means “ air eating ” in Greek.Though some of the symptoms are similar, aerophagia is considered a different disorder than excessive belching, irritable bowel syndrome, constipation, or functional dyspepsia, which is indigestion with no known cause. Aerophagia is not caused by a blockage in the intestines. That being said, it is not uncommon for people with aerophagia to have another gastrointestinal disorder as well., Epidemiology : 3.66%, good, Doctors may try several methods to improve your aerophagia symptoms while using CPAP therapy.,,Adjust CPAP Pressure,Reducing the total amount of air entering the body is one way to protect against aerophagia, but it can be counterproductive if the low air pressure causes a rebound in apnea symptoms. To work around this problem, some researchers have proposed switching to an automatic positive airway pressure (APAP) device, which adjusts air pressure throughout the night as needed. Initial research suggests this switch can relieve symptoms of bloating, flatulence, belching, and abdominal pain, without negatively affecting OSA treatment.,Change Mask,Some researchers believe that full face CPAP masks may cause more aerophagia symptoms than nasal masks. Using a mask that covers both the nose and the mouth may leave you more susceptible to leaks, and the larger mask may require higher pressure. Your doctor can help you find a mask that seals properly and allows you to receive the air you need, according to whether you primarily breathe through your mouth or nose.,,If adjusting pressure on your CPAP device or switching you to a nasal mask does not ease your aerophagia, talk to your doctor about alternate options to treat your obstructive sleep apnea. They may suggest a bi-level positive airway pressure (BiPAP) device instead, as this type of device offers lower pressure during exhalation., Complications : Abdominal Pain, Diagnostics : ECG, X RAY ABDOMEN, CT SCAN, Differential diagnosis : anxiety, dyspepsia, Gastroesophageal reflux disease (GERD), gastroparesis, inflammatory bowel disorders, Irritable Bowel Syndrome, disease description : Aerophagia, which is “a repetitive pattern of swallowing or ingesting air and belching. Air swallowing, whether inadvertent or purposeful, is not an uncommon symptom of psychopathology.Symptoms resulting from aerophagia include bloating, belching, decreased appetite, diarrhea, flatulence, and stomach noise. |
Age Related Macular Degeneration | Disease Name : Age Related Macular Degeneration, Treatment : medication : Ranibizumab , Bevacizumab , Vitamin C/Ascorbic Acid, Vitamin E / Tocopherol, Treatment of non-exudative ARMD. Currently, there is,no effective treatment that stop progression of dry,AMD. Measures to be tried include : ,• Dietary supplements and antioxidants. The agerelated,eye disease study (AREDS) has suggested,that use of certain specific antioxidants, vitamins,and minerals vitamin C (500 mg) and vitamin E,(400 IU), beta carotene (15 mg), zinc oxide (80 mg),and cupric oxide (2 mg) could possibly prevent or,delay the progression of ARMD. Treatment modalities available for exudative (neovascular),ARMD : ,Intravitreal anti-VEGF therapy has become the,treatment of first choice for all CNV lesions. Anti-,VEGFs are injected intravitreally. These include : ,• Bevacizumab (Avastin), dose : 1.25 mg, or,• Ranibizumab (Lucentis), dose : 0.5 mg/0.05 ml, or,• Pegaptanib (Macugen), dose : 0.3 mg in 90 ml, Photodynamic therapy (PDT) is the treatment of,choice after anti-VEGF injections for subfoveal,and juxtafoveal classic CNVM. Transpupillary thermotherapy (TTT) with a diode laser,(810 nm) may be considered for subfoveal occult,CNVM. PDT is definitely better than TTT but is very,expensive.,Double frequency and YAG 532 nm photocoagulation,may be used for extrafoveal choroidal neovascular,membrane (CNVM)., Submacular surgery to remove,CNVM and macular translocation surgery are being,evaluated., Pathophysiology : 1. Non-exudative or atrophic ARMD
It is also called dry or geographic ARMD and is
responsible for 90% cases.
Symptoms. It typically causes mild to moderate,
gradual loss of vision. Patients may complain of
distorted vision and difficulty in reading due to
central shadowing.
Signs. Ophthalmoscopically, lesions of non exudative
ARMD can be described into three stages :
Early stage cases are characterized by occurrence
of macular drusens, focal hyperpigmentation and
pale area of retinal pigment atrophy (RPE atrophy).
Macular drusens are well defined, yellowish white,
slightly-elevated spots. In early cases less than 20
small to medium sized (60–125 mm) drusens are
seen.
Intermediate stage cases show sharply circumscribed
circular areas of RPE atrophy with variable loss of
choriocapillaries along with drusens 1 large drusen
>125 mm and/or >20 medium drusens (60–125 mm).
Large drusens are soft drusens with less sharply
defined edges, tend to enlarge or coalesce.
Advanced stage cases show enlargement of atrophic
areas within which the larger choroidal vessels may
become visible and pre-existing drusen disappear
(Geographical atrophy).
2. Exudative ARMD
It is also called wet or neovascular ARMD. It is
responsible for only 10% cases of ARMD but is
associated with comparatively rapidly progressive
marked loss of vision.
Typical lesions of exudative ARMD seen in chro-
nological
order are as below :
• Drusens with retinal pigment epithelial detachment
(PED) seen as sharply circumscribed domeshaped
elevation.
• Choroidal neovascularization (CNV) proliferating
in sub-RPE space (type 1) is seen as greyish green
or pinkish yellow raised lesion. The
CNV proliferating in sub-retinal space (type 2) is
seen as sub-retinal halo or pigment plaque.
• Haemorrhagic pigment epithelial detachment
(PED). It appears as dark elevated mount.
• Haemorrhagic detachment of neurosensory retina
which assumes diffuse outline and a lighter red
colour around and adjacent to the PED.
• Disciform sub-retinal scarring in the macular
region may result from gradual organization of
blood with further fibrovascular ingrowth., Epidemiology : one in eight people 60 years of age, bad, To Do : Smoking cessation may slow down the progress, Complications : Visual impairment, Diagnostics : Optical coherence tomography (OCT), ophthalmoscopy, slit-lamp biomicroscopic examination, indocyanine green angiography, Fundus fluorescein angiography (FFA), Differential diagnosis : CENTRAL SEROUS CHORIORETINOPATHY, Diabetic Retinopathy, macular drusens, macular hole, pathological myopia, RETINAL DETACHMENT, Retinal vein occlusion, STARGARDT DISEASE, disease description : Age-related macular degeneration (ARMD), also
called senile macular degeneration, is a bilateral
disease of persons over 50 years of age. It is a
leading cause of blindness in developed countries,
in population above the age of 65 years. It is of two
types non-exudative and exudative.
Etiopathogenesis
ARMD is an age-related disease of worldwide
prevalence. Certain risk factors which may affect the
age of onset and/or progression include heredity,
nutrition, smoking, hypertension, exposure to sun light,
hyperopia, blue eyes and cataract particularly nuclear
opacity. The disease is most prevalent in Caucasians. |
Age-related(senile) Cataract | Disease Name : Age-related(senile) Cataract, Treatment : • Prescription of glasses refractive status, which,often changes with considerable rapidity in patients with cataract, should be corrected at,frequent intervals.,• Arrangement of illumination. Patients with,peripheral opacities (pupillary area still free), may,be instructed to use brilliant illumination.,• Conversely, in the presence of central opacities, ,a dull light placed beside and slightly behind the,patient’s head will give the best result.,• Use of dark goggles in patients with central,opacities is of great value and comfort when worn,outdoors.,• Mydriatics. Patients with a small axial cataract, ,frequently may benefit from papillary dilatation.,This allows the clear paraxial lens to participate in,light transmission, image formation and focussing.,Mydriatics such as 5% phenylephrine or 1%,tropicamide; 1 drop b.i.d. in the affected eye may,clarify vision., • Adequate control of diabetes mellitus, when,discovered.,• Removal of cataractog enic dr ugs such as,corticosteroids, phenothiazenes and strong,miotics, may delay or prevent cataractogenesis.,• Removal of irradiation (infrared or X-rays) may,also delay or prevent cataract formation.,• Early and adequate treatment of ocular diseases,like uveitis may prevent occurrence of complicated,cataract. • Topical preparations containing iodide salts of,calcium and potassium are being prescribed in,abundance in early stages of cataract (especially,in senile cataract) in a bid to delay its progression.,• However, till date no conclusive results about their,role are available.,• Role of vitamin E and aspirin in delaying the,process of cataractogenesis is also mentioned., I. Intracapsular cataract extraction (ICCE), II. Extracapsular cataract extraction techniques., Pathophysiology : A. Risk factors
Risk factors affecting age of onset, type and
maturation of senile cataract are as below :
1. Age. Age is the most important risk factor, i.e., why
it is called age related cataract. As mentioned above
it usually occurs after the age of 50 years. When it
occur before 45 years of age, the term pre-senile
cataract is used. By the age of 70 years, over 90% of
the individuals develop senile cataract.
2. Sex. Without any doubt, the senile cataract affects
both males as well as females. However, in many
studies it is reported that prevalence of cataract is
greater in females than males at all ages.
3. Heredity. It plays a considerable role in the
incidence, age of onset and maturation of senile
cataract in different families.
4. Ultraviolet irradiations. More exposure to UV
irradiation from sunlight have been implicated for
early onset and maturation of senile cataract in many
epidemiological studies.
5. Dietary factors. Diet deficient in certain proteins,
amino acids, vitamins (riboflavin, vitamin E, vitamin
C), and essential elements have also been blamed for
early onset and maturation of senile cataract.
6. Dehydrational crisis. An association with prior
episode of severe dehydrational crisis (due to
diarrhoea, cholera, etc.) and age of onset and
maturation of cataract is also suggested.
7. Smoking has also been reported to have some effect
on the age of onset of senile cataract. In numerous
studies worldwide smoking has consistently been
associated with an increase in the frequency of
nuclear cataract. Smoking causes accumulation
of pigmented molecules—3-hydroxykynurenine
and chromophores, which lead to yellowing.
Cyanates in smoke causes carbamylation and protein
denaturation.
B. Etiopathogenesis of pre-senile cataract
The term pre-senile cataract is used when the
cataractous changes similar to senile cataract occur
before 50 years of age. Its common causes are :
1. Heredity. As mentioned above because of
influence of heredity, the cataractous changes may
occur at an earlier age in successive generations.
2. Diabetes mellitus. Age-related cataract occurs
earlier in diabetics. Nuclear cataract is more
common and tends to progress rapidly.
3. Myotonic dystrophy is associated with posterior
subcapsular type of pre-senile cataract. Christmas
tree cataract is typically seen in this condition.
4. Atopic dermatitis may be associated with
pre-senile cataract (atopic cataract) in 10% of the
cases.
C. Concept of syn- and co-cataractogenic factors
It has been conceptualised that cataract is the result of
multiple subthreshold cataractogenic stresses acting
in a concert. Age has been implicated as one of these
cataractogenic stresses and that superimposition of
other toxic stresses on the ageing lens may accelerate
the rate of cataract formation. Conversely, the
elimination of one or more cataractogenic stresses
may delay the cataract formation.
D. Mechanism of loss of transparency
It is basically different in nuclear and cortical senile
cataracts.
1. Cortical senile cataract. Its main biochemical
features are decreased levels in the crystalline lens of
total proteins, amino acids and potassium associated
with increased concentration of sodium and marked
hydration of the lens, followed by coagulation of lens
proteins.
2. Nuclear senile cataract. In this the usual
degenerative changes are intensification of the
age-related nuclear sclerosis associated with
dehydration and compaction of the nucleus resulting
in a hard cataract. It is accompanied by a significant
increase in water insoluble proteins. However, the
total protein content and distribution of cations
remain normal. There may or may not be associated
deposition of pigment urochrome and/or melanin
derived from amino acids in the lens.
Stages of Maturation
A. Maturation of the cortical type of senile cataract
1. Stage of lamellar separation. The earliest senile
change is demarcation of cortical fibres owing to
their separation by fluid. This phenomenon of
lamellar separation can be demonstrated by slit-lamp
examination only. These changes are reversible.
2. Stage of incipient cataract. In this stage, early
detectable opacities with clear areas between
them are seen. Two distinct types of senile cortical
cataracts can be recognised at this stage :
a. Cuneiform senile cortical cataract. It is characterised
by wedge-shaped opacities with clear areas in
between. These extend from equator towards centre
and in early stages can only be demonstrated after
dilatation of the pupil. They are first seen in the lower
nasal quadrant. These opacities are present both in
anterior and posterior cortex and their apices slowly
progress towards the pupil. On oblique illumination
these present a typical radial spoke-like pattern of
greyish white opacities. On distant direct
ophthalmoscopy, these opacities appear as dark lines
against the red fundal glow.
Since the cuneiform cataract starts at periphery
and extends centrally, the visual disturbances are
noted at a comparatively late stage.
b. Cupuliform senile cortical cataract. Here a
saucer-shaped opacity develops just below the
capsule usually in the central part of posterior
cortex (posterior subcapsular cataract), which
gradually extends outwards. There is usually a
definite demarcation between the cataract and the
surrounding clear cortex. Cupuliform cataract lies
right in the pathway of the axial rays and thus causes
an early loss of visual acuity.
3. Immature senile cataract (ISC). In this stage,
opacification progresses further. The cuneiform or cupuliform patterns can be recognised till the
advanced stage of ISC when opacification becomes
more diffuse and irregular. The lens appears greyish
white but clear cortex is still present and
so iris shadow is visible.
In some patients, at this stage, lens may become
swollen due to continued hydration. This condition
is called ‘intumescent cataract’. Intumescence may
persist even in the next stage of maturation. Due to
swollen lens anterior chamber becomes shallow.
4. Mature senile cataract (MSC). In this stage,
opacification becomes complete, i.e., whole of
the cortex is involved. Lens becomes pearly white
in colour. Such a cataract is also labelled as ‘ripe
cataract’.
5. Hypermature senile cataract (HMSC). When
the mature cataract is left in situ, the stage of
hypermaturity sets in. The hypermature cataract may
occur in any of the two forms :
a. Morgagnian hypermature cataract. In some
patients, after maturity the whole cortex liquefies
and the lens is converted into a bag of milky fluid.
The small brownish nucleus settles at the bottom,
altering its position with change in the position
of the head. Such a cataract is called Morgagnian
cataract. Sometimes in this stage,
calcium deposits may also be seen on the lens
capsule.
b. Sclerotic type hypermature cataract. Sometimes
after the stage of maturity, the cortex becomes
disintegrated and the lens becomes shrunken
due to leakage of water. The anterior capsule
is wrinkled and thickened due to proliferation
of anterior cells and a dense white capsular
cataract may be formed in the pupillary area.
Due to shrinkage of lens, anterior chamber
becomes deep and iris becomes tremulous
(iridodonesis).
Maturation of nuclear senile cataract
Progressive nuclear sclerotic process renders the
lens inelastic and hard, decreases its ability to
accommodate and obstructs the light rays. These
changes begin centrally and spread
slowly peripherally almost up to the capsule when it
becomes mature; however, a very thin layer of clear
cortex may remain unaffected.
The nucleus may become diffusely cloudy
(greyish) or tinted (yellow to black) due to deposition
of pigments. In practice, the commonly observed
pigmented nuclear cataracts are either amber, brown
(cataracta brunescens) or black (cataracta nigra) and
rarely reddish (cataracta rubra) in colour., Epidemiology : Many studies in 2010 reveal that cataracts are most common in the White American race, where prevalence ranges from 17 to 18% per 100 people., GOOD, FDA approved and scientifically proven measures for the prevention of senile cataracts do not exist as of yet. Study and research is being conducted regarding this matter.,,Avoiding any and all factors that increase the risk of cataracts still does not provide guaranteed protection from this disorder.,,Since the exact pathophysiology of this disorder is still being studied by the medical community, there aren’t much alternatives for its treatment other than surgery. The only alternate option worth mentioning is homeopathic treatment, but its effectiveness is debatable. Herbal treatment and nutrition therapy are also considered by some people, but both these methods focus on the prevention of cataracts in healthy individuals and not on the cure or treatment of those already diagnosed with this condition. Thus, these methods serve as preventive measures, and not treatment. Both herbal treatment and nutritional therapy are not scientifically approved measures. So surgery, specifically phacoemulsification, remains the most effective treatment for senile cataracts., Complications : Phacoanaphylactic uveitis, Lens-induced glaucoma, Subluxation or dislocation of lens, Diagnostics : Slit lamp examination, VISUAL ACUITY TEST, Oblique illumination examination, Distant direct ophthalmoscopic examination, Test for iris shadow, Differential diagnosis : age related macular degeneration, Diabetic Retinopathy, dry eye syndrome, Glaucoma, REFRACTIVE ERROR, RETINAL DETACHMENT, disease description : In acquired cataract,
opacification occurs due to degeneration of the
already formed normal fibres. A few common
varieties of acquired cataract are described here.
‘Age-related cataract’ also called as senile cataract is
the commonest type of acquired cataract affecting
equally persons of either sex usually above the age of
50 years. The condition is usually bilateral, but almost
always one eye is affected earlier than the other.
Morphologically, the senile cataract occurs in two
forms, the cortical (soft cataract) and the nuclear
(hard cataract). The cortical senile cataract may start
as cuneiform (more commonly) or cupuliform—
posterior subcapsular (PSC) cataract. |
Aggravation Of Hyperparathyroidism | Disease Name : Aggravation Of Hyperparathyroidism, Treatment : nan, Pathophysiology : nan, Epidemiology : one to seven cases per 1000 adults, Complications : Cardiovascular Disease, Osteoporosis, kidney stone, Diagnostics : Parathyroid Hormone (PTH), serum calcium Ca++, Differential diagnosis : nan, disease description : Hyperparathyroidism is when your parathyroid glands create high amounts of parathyroid hormone in the bloodstream. |
Aica-ribosiduria | Disease Name : Aica-ribosiduria, Treatment : Genetic counseling : nan,The pattern of inheritance is autosomal recessive. For the parents of an affected child, the risk of recurrence for each future pregnancy is 25%. Genetic counseling is highly recommended for affected families., Neurodevelopment should be supported through an early intervention program. Growth retardation is not usually subject to specific measures., Management is multidisciplinary. There is no preventive, curative, or specific treatment to date. Epilepsy should be sought, and when present should be treated by an experienced neuropediatrician according to the standard protocols. It may become pharmacoresistant., The patient should be referred to an experienced ophthalmologist. Hypermetropia can be treated according to standard procedures; however, chorio-retinal atrophy has no specific treatment., Pathophysiology : The pathogenesis seems to involve a cytotoxic effect of abnormally accumulated substrates of ATIC enzyme : AICAR and AICA-riboside. No genotype-phenotype relationship has been identified., Epidemiology : To date only 4 affected individuals from 3 independent families have been reported worldwide., Require extensive support. Life expectancy is unkn, "Cant be prevented since its a genetic disorder. Consult your doctor while planning pregnancy.", Complications : COARCTATION OF AORTA, nephrocalcinosis, Diagnostics : PRNP GENE SEQUENCE, High-performance liquid chromatography (HPLC), Differential diagnosis : Aromatic L-amino acid decarboxylase (AADC) deficiency, developmental delay, Glycogen Storage Diseases, Lesch-Nyhan syndrome, mitochondrial disorders, movement disorders, disease description : A rare and severe inborn metabolic disease characterized clinically by the association of severe-to-profound neurodevelopmental impairment, severe visual impairment, ante-postnatal growth impairment, severe scoliosis and, frequently, early-onset epilepsy. |
Alagille Syndrome | Disease Name : Alagille Syndrome, Treatment : Alagille syndrome prognosis and mortality risk vary with the difference of organ involvement and the severity. Severe cardiac or hepatic disease cause early mortality, in contrast to vascular accidents, which result in later mortality. Management needs a multidisciplinary approach, depending on the findings of each affected individual. With liver disease, the treatment is mainly supportive, trying to ameliorate severe pruritus and xanthomas with agents that help with the cholestasis (ursodeoxycholic acid, naltrexone, rifampin, colesevelam, and cholestyramine). Surgical partial internal biliary diversion and ileal exclusion also have been used for this purpose, without preventing the progression of liver disease. Even though the Kasai procedure (portoenterostomy) is used in a patient with biliary atresia, this procedure does not benefit children with Alagille syndrome and may worsen the outcome. Liver transplantation for end-stage liver disease has an 80% five-year survival rate, improving liver function and catch-up growth.,,Cardiac, renal, and vascular involvement are managed according to the existing symptoms. No neurovascular screening guidelines exist for Alagille syndrome, and manifestations are treated in a standard manner.,Ophthalmological and vertebral anomalies usually do not need intervention.,Malnutrition should be managed proactively with supplements and fat-soluble vitamin supplementation; optimization maximizes growth and development.,To prevent secondary complications, contact sports should be avoided; this is especially true for those patients with splenomegaly, chronic liver disease, and vascular involvement. Regular monitoring by specialists in the fields of cardiology, gastroenterology, ophthalmology, nephrology, and nutrition should be performed., Pathophysiology : Alagille syndrome is related to the JAG1 gene mutation. It may be passed from parent to child. If you have one parent with Alagille syndrome, you have a 50% chance of developing the condition. It appears in one out of 70, 000 babies and occurs in both sexes. However, about half the time, the mutation is new and not from a parent., Epidemiology : 1 in 70, 000 newborns, 1 : 30, 000 to 1 : 100, 000., good, "This condition is inherited in an autosomal dominant pattern and thus, it cant be prevented. ,Although Genetic Counselling is advisable.", Complications : chronic liver disease, splenomegaly, Diagnostics : HISTOPATHLOGY, LIVER BIOPSY, USG ABDOMEN(W/A), kidney function test KFT, GENETIC TESTING, X RAY, Differential diagnosis : CYSTIC FIBROSIS, Hypopituitarism, mitochondrial disorders, PRIMARY SCLEROSING CHOLANGITIS, Syphilis, Zellweger Syndrome, disease description : Alagille syndrome (arteriohepatic dysplasia) is the most common syndrome
with intrahepatic bile duct paucity. Bile duct paucity (often erroneously called
intrahepatic biliary atresia ) designates an absence or marked reduction in the
number of interlobular bile ducts in the portal triads, with normal-size branches
of portal vein and hepatic arteriole. |
Albinism | Disease Name : Albinism, Treatment : Nitisinone triggers tyrosine accumulation in blood and mouse models have suggested that it could improve pigmentation in OCA1B subjects, but a clinical trial is currently underway. Aminoglycosides are a potential and unconfirmed therapy. Despite anecdotal reports, L-DOPA did not result in any improvement in visual acuity in a study of 45 patients. Adeno-associated viruses (AAV) vectors is a potential gene therapy introducing a functional copy of the tyrosinase gene in OCA1 and OA1 patients., Pathophysiology : The first (and rate-limiting) step in eumelanin synthesis involves the oxidation of L-tyrosine to DOPA by tyrosinase. Mutations in the tyrosinase gene, as seen in OCA1A, leads to complete loss of the ability to produce eumelanin. The loss-of-function mutations in any type of OCA, however, impair eumelanin synthesis directly or affect melanosome maturation but may leave pheomelanin levels unaffected. Most of the non-OCA1A pigmentation that accounts for the varied phenotypes is pheomelanin, which imbues the skin, hair, and iris with color. Syndromic albinism does not always affect melanin synthesis so much as it does the production or distribution of melanosomes through the basal layer into keratinocytes from melanocytes.The two significant results of hypomelanosis can be divided into dermatological and ophthalmologic consequences. Since eumelanin is photo-protective, albinism leads to increased risk of sun-damage (solar lentigines, actinic keratoses, solar erythema) and UV-associated malignancies (especially squamous cell carcinomas). Melanin acts as an inducer and organizer of formation of the fovea, optic nerves, optic tracts, and visual cortex, in utero. In albinism, the fovea fails to develop as robustly as normal and is hypoplastic or even absent. Melanin in utero cues the migration of developing optic nerve fibers. Some crossover of nerve fibers from each eye at the optic chiasm to the contralateral occipital lobe is necessary for binocular vision. In albinism, however, some axons that originate in the retinal ganglion cells project mistakenly to the contralateral hemisphere dorsal lateral geniculate nucleus. This means an increase in optic fiber crossover. Nerve fibers misrouted from the organ or reception (the eye) to the organ of perception (the brain) further contributes to binocular vision deficits, manifesting as strabismus. The occipital lobe in albinism also shows decreased gyrification (theorized to be due to a dearth of foveal input), and localized increases in cortical thickness. The latter finding has also been found in congenitally blind subjects, Epidemiology : ratio is one in every 3, 000 people, good, Albinism is an inherited condition. People with a family history of albinism should consider genetic counseling., Complications : Eye disorder, social isolation, astigmatism., Diagnostics : DNA analysis for mutation, PHYSICAL EXAMINATION, Differential diagnosis : amblyopia, ANIRIDIA, astigmatism., athetosis, chediak higashi syndrome, Night blindness, nystagmus, OCULAR ALBINISM, optic nerve atrophy, disease description : Albinism is a rare genetic condition caused by mutations of certain genes that affect the amount of melanin your body produces. Melanin controls the pigmentation (color) of your skin, eyes and hair. People with albinism have extremely pale skin, eyes and hair. They are at an increased risk of vision, skin and social issues. |
Albuminuria | Disease Name : Albuminuria, Treatment : nan, Pathophysiology : nan, Epidemiology : nan, Complications : nan, Diagnostics : nan, Differential diagnosis : nan, disease description : Albuminuria is a sign of kidney disease and means that you have too much albumin in your urine. Albumin is a protein found in the blood. A healthy kidney doesn’t let albumin pass from the blood into the urine. A damaged kidney lets some albumin pass into the urine. The less albumin in your urine, the better. |
Alcoholic Liver Disease | Disease Name : Alcoholic Liver Disease, Treatment : medication : Pentoxifylline/Oxpentifylline, Prednisolone, "Malnutrition is common in people with ARLD, so its important to eat a balanced diet to make sure you get all the nutrients you need.,,Avoiding salty foods and not adding salt to foods you eat can reduce your risk of developing swelling in your legs, feet and tummy caused by a build-up of fluid.", medicine to help you abstain from alcohol, such as : nan,,acamprosate,disulfiram,naltrexone, LIVER TRANSPLANTATION, Pathophysiology : The liver has a limited repertoire in response to injury. Fatty liver is the
initial and most common histologic response to hepatotoxic stimuli,
including excessive alcohol ingestion. The accumulation of fat within the
perivenular hepatocytes coincides with the location of alcohol dehydrogenase,
the major enzyme responsible for alcohol metabolism. Continuing
alcohol ingestion results in fat accumulation throughout the entire hepatic
lobule. Despite extensive fatty change and distortion of the hepatocytes
with macrovesicular fat, the cessation of drinking results in normalization
of hepatic architecture and fat content. Alcoholic fatty liver has traditionally
been regarded as entirely benign, but similar to the spectrum of nonalcoholic
fatty liver disease, the appearance of steatohepatitis and certain pathologic features such as giant mitochondria, perivenular fibrosis, and
macrovesicular fat may be associated with progressive liver injury.
The transition between fatty liver and the development of alcoholic
hepatitis is blurred. The hallmark of alcoholic hepatitis is hepatocyte
injury characterized by ballooning degeneration, spotty necrosis, polymorphonuclear
infiltrate, and fibrosis in the perivenular and perisinusoidal
space of Disse. Mallory-Denk bodies are often present in florid cases
but are neither specific nor necessary to establish the diagnosis. Alcoholic
hepatitis is thought to be a precursor to the development of cirrhosis.
However, like fatty liver, it is potentially reversible with cessation of
drinking. Cirrhosis is present in up to 50% of patients with biopsy-proven
alcoholic hepatitis, and its regression is uncertain, even with abstention., Epidemiology : 3.5 million deaths, POOR, Talk openly to your provider about your alcohol intake. The provider can counsel you about how much alcohol is safe for you., Complications : ascites, CIRRHOSIS, gall stones formation, PORTAL HYPERTENSION, Diagnostics : PT/PC/INR, Serum Bilirubin Direct, SERUM Creatinine, CT Abdomen, LIVER BIOPSY, MRI Abdomen, USG ABDOMEN(W/A), LIVER FUNCTION TEST LFT, CT SCAN, Differential diagnosis : ACUTE VIRAL HEPATITIS, ASCENDING CHOLANGITIS, autoimmune liver disease, CHRONIC VIRAL HEPATITIS, drug-induced liver injury, emphysema, nonalcoholic steatohepatitis, pyogenic hepatic abscess, REYE SYNDROME, WILSONS DISEASE, disease description : Alcoholic liver disease is common, but can be prevented. There are 3 types. Many heavy drinkers progress through these 3 types over time : Fatty liver. Fatty liver is the build-up of fat inside the liver cells. It leads to an enlarged liver. It’s the most common alcohol-induced liver problem.
Alcoholic hepatitis. Alcoholic hepatitis is an acute inflammation of the liver. There is death of liver cells, often followed by permanent scarring.
Alcoholic cirrhosis. Alcoholic cirrhosis is the destruction of normal liver tissue. It leaves scar tissue in place of the working liver tissue.Fatty liver. Fatty liver is the build-up of fat inside the liver cells. It leads to an enlarged liver. It’s the most common alcohol-induced liver problem.Alcoholic hepatitis. Alcoholic hepatitis is an acute inflammation of the liver. There is death of liver cells, often followed by permanent scarring.Alcoholic cirrhosis. Alcoholic cirrhosis is the destruction of normal liver tissue. It leaves scar tissue in place of the working liver tissue. |
Aldosterone Biosynthesis Defects | Disease Name : Aldosterone Biosynthesis Defects, Treatment : Drugs that promote hyperkalemia, such as ß-adrenergic antagonists, cyclooxygenase inhibitors, angiotensin-converting enzyme inhibitors, heparin, and potassium-sparing diuretics, should be avoided. Dietary potassium intake should be reduced, if possible. Diuretics are the initial treatment for patients who have disorders associated with sodium retention, such as hypertension and congestive heart failure. Mineralocorticoid replacement with fludrocortisone is reserved for patients with severe hyperkalemia without hypertension and congestive heart failure., MINERALOCORTICOID REPLACEMENT THERAPY, Pathophysiology : Aldosterones main actions are to regulate intravascular volume and serum electrolytes by controlling sodium absorbtion and potassium excretion in the distal nephron. Inherited defects in aldosterone biosynthesis thus cause hypovolemia, hyponatremia and hyperkalemia. Defective aldosterone biosynthesis may be caused by congenital adrenal hyperplasia due to 21-hydroxylase (CYP21) deficiency, in which case cortisol biosynthesis is also affected, or as an isolated defect termed aldosterone synthase (corticosterone methyloxidase, CYP11B2) deficiency. Many mutations have been documented in each of these genes; in general enzymatic activity must be reduced to <1% of normal for aldosterone biosynthesis to be impaired. An additional form of familial hyperreninemic hypoaldosteronism has been described that is not due to mutations in CYP11B2, but its etiology remains to be elucidated., Epidemiology : nan, Complications : Arrhythmias, heart attacks, kidney faliure, Diagnostics : nan, Differential diagnosis : Apparent mineralocorticoid excess syndrome, "conns syndrome", Glucocorticoid-remediable aldosteronism (GRA), "Liddles syndrome", disease description : Aldosterones main actions are to regulate intravascular volume and serum electrolytes by controlling sodium absorbtion and potassium excretion in the distal nephron. Inherited defects in aldosterone biosynthesis thus cause hypovolemia, hyponatremia and hyperkalemia. Defective aldosterone biosynthesis may be caused by congenital adrenal hyperplasia due to 21-hydroxylase (CYP21) deficiency, in which case cortisol biosynthesis is also affected, or as an isolated defect termed aldosterone synthase (corticosterone methyloxidase, CYP11B2) deficiency. Many mutations have been documented in each of these genes; in general enzymatic activity must be reduced to <1% of normal for aldosterone biosynthesis to be impaired. An additional form of familial hyperreninemic hypoaldosteronism has been described that is not due to mutations in CYP11B2, but its etiology remains to be elucidated. |
Aldosterone Synthase Deficiency | Disease Name : Aldosterone Synthase Deficiency, Treatment : medication : Fludrocortisone , Sodium chloride , Pathophysiology : This is an autosomal recessive disorder in which conversion of corticosterone to
aldosterone is impaired, mutations in the CYP11B2
gene coding for aldosterone synthase, Epidemiology : Fair, "Aldosterone synthase deficiency is inherited as an autosomal recessive trait and cant be prevented. Although its advisable to consult your doctor while planning pregnancy.", Complications : coma, hyperkalemia, hyponatremia, metabolic acidosis, seizures, Diagnostics : SERUM Sodium Na+, 11-deoxy corticosterone, Plasma Aldosterone, Plasma Renin, serum potassium K+, Differential diagnosis : Adrenal hypoplasia congenita, primary adrenal insufficiency, disease description : Corticosterone methyloxidase deficiency, also known as aldosterone synthase deficiency, is a disorder characterized by excessive amounts of sodium released in the urine (salt wasting), along with insufficient release of potassium in the urine, usually beginning in the first few weeks of life. |
Alexander Disease | Disease Name : Alexander Disease, Treatment : medication : Copper/copper sulfate, There is no cure for Alexander disease, nor is there a standard course of treatment. Treatment of Alexander disease is symptomatic and supportive., Pathophysiology : This is a rare disorder that causes progressive macrocephaly and leukodystrophy.
Alexander disease is caused by dominant mutations in the glial fibrillary acidic
protein (GFAP) gene, on chromosome 17q21, and cases are usually sporadic in
families. Pathologic examination of the brain discloses deposition of
eosinophilic hyaline bodies called Rosenthal fibers in astrocyte processes. These
accumulate in a perivascular distribution throughout the brain. In the classic
infantile form of Alexander disease, degeneration of white matter is most
prominent frontally., Epidemiology : 550 cases have been described, gerally poor, "This condition is inherited in an autosomal dominant pattern and thus, it cant be prevented. ,Although Genetic Counselling is advisable.", Complications : seizures, Speech disorders, Swallowing defect, Diagnostics : HISTOPATHLOGY, MRI, Differential diagnosis : Adrenoleukodystrophy, Canavan Disease, Metachromatic leukodystrophy (MLD), disease description : Alexander disease is one of a group of neurological conditions known as the leukodystrophies. Leukodystrophies are disorders that result from abnormalities in myelin, the “white matter” that protects nerve fibers in the brain. |
Alkalosis | Disease Name : Alkalosis, Treatment : The appropriate management of alkalosis rests on prompt identification followed by management of the primary etiology of the alkalosis and the type of the alkalosis (metabolic, respiratory, or mixed). Specific etiologies like pyloric stenosis need surgical correction, while excessive ingestion of alkali will respond to restriction of excess intake. Alkalosis associated with conditions of excess aldosterone may need hormonal correction or replacement along with the treatment of associated hypertension. Correction of chloride responsive alkalosis caused by volume depletion is possible by replenishment of extracellular volume. Electrolyte disturbances associated with alkalosis such as hypokalemia and hypocalcemia are the chief causes of clinical deterioration in the patient and must undergo correction before the onset of life-threatening complications. Slow acid administration or dialysis with low bicarbonate baths may be necessary for emergent situations, Pathophysiology : The body has a robust buffering system that acts to minimize pH change in the initial stages of acid-base derangements. When these buffering systems are overwhelmed, alkalosis may result.
The kidney attempts to maintain normal acid-base balance by the dual mechanisms of bicarbonate reabsorption, mainly in the proximal tubule, and bicarbonate production in the distal nephron. Reabsorption of bicarbonate is mediated by a Na-H (sodium-hydrogen) antiporter and also by the H (+)-ATPase (adenosine triphosphate-ase). Influences on bicarbonate reabsorption include effective arterial blood volume, glomerular filtration rate, chloride, and potassium concentrations in the serum. In conditions resulting in respiratory alkalosis, the kidney acts to both decrease bicarbonate reabsorption and bicarbonate production as a compensatory mechanism. This process helps maintain the pH of the extracellular compartment to neutralize the effect of the low pCO2 that is the primary derangement of respiratory alkalosis. However, the kidneys complex buffering mechanisms may take several days to achieve full effect, with an eventual expected fall of bicarbonate by 4 to 5 mmol/L for every 10 mmHg fall in pCO2.
On the other hand, respiratory depression resulting in increased PaCO2 occurs promptly and predictably to buffer the alkalemia resulting from metabolic conditions (while this is variable, expectations are that there will be a 0.5 mmHg increase in PaCO2 per 1 mmol/L increase in HCO). Alkalemia also causes a shift in the oxyhemoglobin dissociation curve towards the left, thus increasing hemoglobins affinity for oxygen and decreasing oxygen release to the tissues., Epidemiology : around 29%, Among the various acid-base disorders, metabolic alkalosis is the most frequently occurring derangement in hospitalized patients, with an incidence of 51% in this group. Respiratory alkalosis is also commonly seen in the hospitalized patient population., good, Reduce your risk for developing alkalosis by maintaining good health, eating a healthy diet, and staying hydrated. Choosing foods high in nutrients and potassium can help combat electrolyte deficiencies. Nutrients and potassium are primarily found in fruits and vegetables, as well as some other foods, such as : ,,carrots,bananas,milk,beans,spinach,bran,Steps you can take to prevent dehydration include : ,,drinking 8 to 10 glasses of water per day,drinking water before, during, and after exercise,using electrolyte-replacement drinks for high-intensity exercises,avoiding sodas or juices, which have a high sugar content and can make dehydration worse,limiting caffeine, which is found in soda, tea, and coffee,It’s important to remember that you’re already dehydrated if you feel thirsty.,,Dehydration can also occur rapidly if you lose a lot of electrolytes. This can happen when you’re vomiting from the flu. If you cannot keep potassium-rich foods in your stomach, make sure you still drink adequate fluids, such as water, sports drinks, and broth-based soups., Complications : Arrhythmias, Hypocalcemia, hypokalemia, muscle weakness, ALTERED MENTAL STATUS, carpopedal spasms, Diagnostics : ABG pH, Urine analysis, Differential diagnosis : Hypocalcemia, hypochloremia, hypokalemia, disease description : Alkalosis is an abnormal pathophysiological condition characterized by the buildup of excess base or alkali in the body.Alkalosis is an abnormal pathophysiological condition characterized by the buildup of excess base or alkali in the body. It results in an abnormally high serum pH (arterial pH greater than 7.45), which is termed alkalemia and forms one end of the spectrum of acid-base disorders. |
Alkaptonuria | Disease Name : Alkaptonuria, Treatment : medication : Nitisinone , nitisinone (2-2-nitro-4-trifluoromethylbenzoyl-1, 3-cyclohexanedione), a drug used in tyrosinemia type I, ,reduces urinary excretion of homogentisic acid., Pathophysiology : Mutations in the HGD gene cause alkaptonuria. The HGD gene provides instructions for making an enzyme called homogentisate oxidase. This enzyme helps break down the amino acids phenylalanine and tyrosine, which are important building blocks of proteins. Mutations in the HGD gene impair the enzymes role in this process. As a result, a substance called homogentisic acid, which is produced as phenylalanine and tyrosine are broken down, accumulates in the body. Excess homogentisic acid and related compounds are deposited in connective tissues, which causes cartilage and skin to darken. Over time, a buildup of this substance in the joints leads to arthritis. Homogentisic acid is also excreted in urine, making the urine turn dark when exposed to air., Epidemiology : (approximately 1 in 250, 000 live births), GOOD, Genetic counseling is recommended for people with a family history of alkaptonuria who are considering having children.,,A blood test can be done to see if you carry the gene for alkaptonuria.,,Prenatal tests (amniocentesis or chorionic villus sampling) can be done to screen a developing baby for this condition if the genetic change has been identified., Complications : VALVULAR HEART DISEASE, Osteoarthritis, Diagnostics : HISTOPATHLOGY, URINE ANALYSIS (Color), URINE pH Level, X RAY, urinary homogentisic acid, Differential diagnosis : Ankylosing spondylitis, Ochronosis, Osteoarthritis, rheumatoid arthritis, VALVULAR HEART DISEASE, disease description : Alkaptonuria is a rare autosomal
recessive disorder caused by a deficiency of homogentisate 1, 2-
dioxigenase.Large amounts of homogentisic acid are formed
which are excreted in urine or deposited in tissues. |
Allergic Contact Dermatitis | Disease Name : Allergic Contact Dermatitis, Treatment : The mainstay of treatment of allergic contact dermatitis is avoidance of the causative factor(s), although topical corticosteroids will ,be required in most instances to control the disorder.e. Alternatively, zinc and salicylic acid paste BPC twice ,daily may be helpful, and cyanoacrylates (superglues) have been ,used with benefit.c therapy such as alitretinoin, azathioprine and ciclosporin., Phototherapy, both PUVA and UVB, is helpful in some subjects, including Compositae-allergic individuals ,with photosensitivity, Pathophysiology : nan, Epidemiology : Following interview and examination, a lifetime pr, Contact dermatitis accounts for 4–7% of all dermat, The prognosis is generally relatively poor for tho, To Do : Examples of specifi c avoidance ,measures include plastic instead of rubber gloves, cosmetics and ,medicaments free of an identifi ed allergen, and clothing free of ,nickel-containing studs, zips, etc.,Cotton-lined gloves should be worn when the hands ,are in contact with irritants, including food, cleaning agents and ,polishes. Plastic gloves are less allergenic than rubber but are less ,pliable and malleable., Complications : ECZEMA, Diagnostics : Patch Test, Doppler ultrasound, Differential diagnosis : angioedema, Atopic eczema, basal cell carcinoma(RODENT ULCER), CELLULITIS, Lichen Planus, Porphyria Cutanea Tarda, psoriasis, Seborrhoeic eczema, disease description : Allergic contact dermatitis is an eczematous reaction that occurs as
an immunological response following exposure to a substance to
which the immune system has previously been sensitized.
The diagnosis of allergic contact dermatitis can only be confi rmed by patch testing and should always be used to exclude
contact allergy as a complicating factor in stubborn cases of eczematous diseases, as well as cases where allergic contact dermatitis
is suspected from the pattern or distribution of the eczema. It is
particularly important in chronic cases of dermatitis that are unresponsive to traditional treatment.
Children
are sensitized as easily as adults, and both infants and elderly
people can be sensitized to poison ivy ( Toxicodendron spp.). Toxicodendron dermatitis is very common in american children.
Sex
Women have stronger cell-mediated immune responses than men and yet, at least experimentally, women do not appear to
be more susceptible to sensitization |
Allergic Dermatitis | Disease Name : Allergic Dermatitis, Treatment : The only definitive treatment of ACD is the identification and removal of the offending agent, and all patients with suspected or confirmed ACD should be advised of this. First-line medical therapy includes topical steroids when ACD is confined to less than 20% of the body, and oral corticosteroids when greater than 20% of the body is involved. If ACD involves a delicate area such as skin folds or eyelids, topical calcineurin inhibitors or PDE4 inhibitors may also be effective. Upon identification of the allergen, strict avoidance is necessary to prevent a recurrence.Symptomatic management includes oral antihistamines, topical hydrocortisone, and cool water soaks. Vesicles should not be ruptured as there is a risk of infection. The use of moisturizers is a recommended adjunct.,,For severe cases, topical immunomodulators like tacrolimus may be beneficial. Some patients may benefit from phototherapy using UV A plus psoralen. Rarely in severe cases, one may require immunosuppressive agents like mycophenolate., Pathophysiology : The pathophysiology of allergic contact dermatitis starts with the contact of the allergen to the skin. This allergen penetrates that stratum corneum of the skin and is taken up by Langerhans cells.The antigens subsequently undergo processing by these cells and get displayed on their surface. Langerhans cells then migrate towards regional lymph nodes. The antigens taken up by these cells come in contact with the adjacent T-lymphocytes. Due to the process of clonal expansion as well as cytokine-induced proliferation, antigen-specific T lymphocytes get created. These lymphocytes may then travel through the blood and into the epidermis. This process collectively is known as the sensitization phase of allergic contact dermatitis. The elicitation phase is what occurs after reexposure to the antigen takes place. The Langerhans cells containing the antigen interacts with the antigen-specific T-lymphocytes for that antigen, which triggers a cytokine-induced proliferation process. This proliferation, in turn, creates a localized inflammatory response., Epidemiology : 0.9% in adults., good, "You can take the following steps to help prevent contact dermatitis : ,,Avoid irritants and allergens. Try to identify and avoid the cause of your rash. For ear and body piercings, use jewelry made of hypoallergenic material, such as surgical steel or gold.,Wash your skin. For poison ivy, poison oak or poison sumac, you might be able to remove most of the rash-causing substance if you wash your skin right away after coming into contact with it. Use a mild, fragrance-free soap and warm water. Rinse completely. Also wash any clothing or other items that may have come into contact with a plant allergen, such as poison ivy.,Wear protective clothing or gloves. Face masks, goggles, gloves and other protective items can shield you from irritating substances, including household cleansers.,Apply an iron-on patch to cover metal fasteners next to your skin. This can help you avoid a reaction to jean snaps, for example.,Apply a barrier cream or gel. These products can provide a protective layer for your skin. For example, a nonprescription skin cream containing bentoquatam (Ivy Block) may prevent or lessen your skins reaction to poison ivy.,Use moisturizer. Regularly applying moisturizing lotions can help restore your skins outermost layer and keep your skin supple.,Take care around pets. Allergens from plants, such as poison ivy, can cling to pets and then be spread to people. Bathe your pet if you think it got into poison ivy or something similar.", Complications : infections, Sleep disturbances, Diagnostics : HISTOPATHLOGY, Patch Test, PHYSICAL EXAMINATION, Differential diagnosis : Atopic dermatitis, Contact dermatitis, infections, Irritant contact dermatitis, nummular dermatitis, psoriasis, scabies, seborrhoeic dermatitis, Urticaria, disease description : Allergic contact dermatitis (ACD) is a type 4 or delayed-type hypersensitivity response (DTH) by an individual’s immune system to a small molecule (less than 500 daltons), or hapten, that contacts a sensitized individual’s skin. ACD accounts for 20% of contact dermatoses, and allergens differ greatly based upon geography, personal habits, and hobbies, and often, the types of preservatives that are legally permissible |
Allergic Hypersensitivity Reactions | Disease Name : Allergic Hypersensitivity Reactions, Treatment : The treatment of immediate hypersensitivity reactions includes the management of anaphylaxis with intramuscular adrenaline (epinephrine), oxygen, intravenous (IV) antihistamines, support blood pressure with IV fluids, avoid latex gloves and equipment in patients who are allergic, and surgical procedures such as tracheotomy if there is severe laryngeal edema. Allergic bronchial asthma can be treated with any of the following : inhaled short- and long-acting bronchodilators (anticholinergics) along with inhaled corticosteroids, leukotriene antagonists, use of disodium cromoglycate, and environmental controls. Experimentally, a low dose of methotrexate or cyclosporin and omalizumab (a monoclonal anti-IgE antibody) has been used. Treatment of autoimmune disorders (e.g., SLE) includes one or a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) and hydroxychloroquine, azathioprine, methotrexate, mycophenolate, cyclophosphamide, low dose IL-2, intravenous immunoglobulins, and belimumab. Omalizumab is a monoclonal antibody that interacts with the binding site of the high-affinity IgE receptor on mast cells. It is an engineered, humanized recombinant immunoglobulin. Moderate to severe allergic bronchial asthma can improve with omalizumab, Pathophysiology : In type I hypersensitivity reactions after a previous sensitization, the immunoglobulin (Ig) E is produced and binds to Fc receptors on mast cells and basophils. On encountering the allergen, it triggers cross-linking of mast-cell cytophilic IgE, causing the activation of mast cells and their degranulation of mediators that cause an allergic reaction. The mediators that participate in this type of hypersensitivity reaction include histamine and lipid mediators such as PAF, LTC4, and PGD2 that cause vascular leak, bronchoconstriction, inflammation, and intestinal hypermotility. Enzymes (e.g., tryptase causes tissue damage) and tumor necrosis factor (TNF) causes inflammation. Eosinophils release cationic granule proteins, e.g., major basic protein (causes death of host cells and parasites) and enzymes (e.g., eosinophil peroxidase, which participates in tissue remodeling).
In type II hypersensitivity reactions, antibodies against basement membranes produce nephritis in Goodpastures syndrome. Myasthenia gravis and Lambert-Eaton syndrome are caused by antibodies that reduce the amount of acetylcholine at motor endplates, and autoantibodies to an intercellular adhesion molecule causes pemphigus. In type III hypersensitivity reactions, immune-complex deposition (ICD) causes autoimmune diseases, which are often a complication. As the disease progresses, further accumulation of immune complexes occurs, and when the body becomes overloaded, the complexes are deposited in the tissues and cause inflammation as the mononuclear phagocytes, erythrocytes, and complement system fail to remove immune complexes from the blood., Epidemiology : Hypersensitivity reactions are very common. Fifteen percent of the world population will be affected by a type of allergic reaction during their lives, 10–20% of hospitalized patients and more than 7% of the general population., good, You can also take antihistamines or other medications daily to help control your symptoms and reduce your allergic reaction.,,If you have animal allergies, avoid petting, hugging or kissing animals. Don’t allow them in your bedroom or on your furniture.,,Regularly vacuuming rugs, carpets and other surfaces helps remove dust, animal dander, pollen and other allergens.,,High-efficiency particulate (HEPA) air filters can also help. These air purifiers remove airborne allergens from your environment., Complications : Anaphylactoid reactions, Serum sickness, post transfusion reaction, Diagnostics : Differential Leucocyte Count DLC, Total Leucocyte Count (TLC), Differential diagnosis : Anaphylaxis, angioedema, ECZEMA, insect bites, Mastocytosis, Steven-Johnson syndrome, systemic lupus erythematosus (SLE), Urticaria, Viral exanthem, disease description : Hypersensitivity reactions are exaggerated or inappropriate immunologic responses occurring in response to an antigen or allergen. Type I, II and III hypersensitivity reactions are known as immediate hypersensitivity reactions because they occur within 24 hours of exposure to the antigen or allergen. |
Allergic Pneumonitis | Disease Name : Allergic Pneumonitis, Treatment : medication : Mycophenolate mofetil/ Mycophenolate sodium, Cyclophosphamide , Glucocorticoid treatment has not shown any benefit for long-term outcomes. Inhaled steroids have not shown to be effective as a replacement for systemic glucocorticoids. Patients are usually started on 0.5 to 1 mg/kg per day (up to a maximum of 60 mg per day). Usually treated with a high dose for 1 to 2 weeks and then tapered over 2 to 4 weeks with the goal of using the lowest dose and shortest duration of glucocorticoids, Lung transplantation has been shown to have excellent medium-term survival in patients with advanced lung disease due to HP when compared to patients with UIP/IPF., Pathophysiology : Hypersensitivity pneumonitis can happen when you repeatedly breathe in bacteria, mold, or chemicals in your environment that cause inflammation in your lungs.These harmful substances may be found in : Air conditioners, humidifiers, and ventilation systemsBird droppings, feathers, and animal fursContaminated foods or factory productsContaminated fluids from metal workHardwood dustsHay or grain for feeding animalsHot tubs, Epidemiology : 1.67 to 2.71 per 100, 000 persons and increased with age up to 11.2 per 100, 000 among those age 65 years and older., variable, The damage chronic HP causes isn’t reversible. The best way to prevent hypersensitivity pneumonitis is by avoiding exposure to allergens that cause lung inflammation. If you have to be around potential allergens, ways you may be able to reduce your risk include : ,,If you have a job that puts you at risk (like working with metal, birds or other animals, lumber, paper, grain and more), wear personal protective equipment (PPE) while working. This includes wearing a mask that filters small particles.,Keep humidifiers, hot tubs and heating and cooling systems clean and in good condition.,Avoid feather-filled bedding.,Keep your pets’ living spaces (especially bird cages) clean. Wear a mask when you clean them., Complications : pulmonary fibrosis, Diagnostics : CRP, Erythrocyte Sedimentation Rate (ESR), HRCT LUNG, PULMONARY FUNCTION TEST(PFT), CT SCAN, BRONCHOSCOPY, Differential diagnosis : Asthma, Bronchiolitis obliterans, chronic bronchitis, Chronic Obstructive Pulmonary Disease, Eosinophilic pneumonia, pulmonary fibrosis, disease description : Allergic pneumonitis is a pulmonary disease that occurs due to inhalational exposure to a variety of antigens leading to an inflammatory response of the alveoli and small airways. Systemic manifestations such as fever and fatigue can accompany respiratory symptoms. Although sensitization to an inhaled antigen as manifested by specific circulating IgG antibodies is necessary for the development of HP, sensitization alone is not sufficient as a defining characteristic, because many sensitized ind |
Allergic Rhinitis | Disease Name : Allergic Rhinitis, Treatment : medication : Chlorpheniramine/ Pheniramine Maleate / Dexchlorpheniramine Maleate, Montelukast , Cetirizine, Levocetirizine, Desloratadine, Sublingual immunotherapy (SLIT) and Allergy immunotherapy (AIT) is an effective treatment for AR and allergic,conjunctivitis., Second-generation,antihistamines are preferred because they cause less sedation . Preparations,containing pseudoephedrine , typically in combination with other agents, are,used for relief of nasal and sinus congestion and pressure and other symptoms,such as rhinorrhea, sneezing, lacrimation, itching eyes, oronasopharyngeal,itching, and cough. Pseudoephedrine is available without prescription (generally,in fixed combination with other agents such as first-generation antihistamines : ,brompheniramine, chlorpheniramine, triprolidine; second-generation,antihistamines : desloratadine, fexofenadine, loratadine; antipyretics : ,acetaminophen, ibuprofen; antitussives : guaifenesin, dextromethorphan;,anticholinergic : methscopolamine)., Pathophysiology : The exposure of an atopic host to an allergen leads to the production of sIgE, which is strongly associated with eczema throughout childhood and with asthma and rhinitis after age 4 yr. The clinical reactions on reexposure to the allergen have been designated as early-phase and late-phase allergic responses. Bridging of the IgE molecules on the surface of mast cells by allergen initiates the earlyphase allergic response, characterized by degranulation of mast cells and release of preformed and newly generated inflammatory mediators, including histamine, prostaglandin 2, and the cysteinyl leukotrienes. The late-phase allergic response appears 4-8 hr following allergen exposure. Inflammatory cells, including
basophils, eosinophils, neutrophils, mast cells, and mononuclear cells, infiltrate, the nasal mucosa. Eosinophils release proinflammatory mediators, including cysteinyl leukotrienes, cationic proteins, eosinophil peroxidase, and major basic protein, and serve as a source of interleukin-3 (IL-3), IL-5, granulocytemacrophage colony-stimulating factor, and IL-13. Repeated intranasal introduction of allergens causes “priming”—a more brisk response even with a lesser provocation. Over the course of an allergy season, a multifold increase in submucosal mast cells takes place. These cells, once thought to have a role exclusively in the early-phase allergic response, have an important function in sustaining chronic allergic disease., Epidemiology : GOOD, There is no way to prevent hay fever, but lifestyle changes can help you live with allergies. You can relieve hay fever symptoms by avoiding irritants as much as possible. To reduce symptoms, you should : ,,Avoid touching your face and rubbing your eyes or nose.,Close windows in your home and car during the spring, summer and early fall when pollen counts are higher.,Enclose pillows, mattresses and box springs in dust mite covers.,Keep pets off couches and beds, and close doors to bedrooms you don’t want them to enter.,Use filters in your vacuum cleaner and air conditioner to reduce the amount of allergens in the air.,Wash your hands often, especially after playing with pets.,Wear a hat and sunglasses to protect your eyes from pollen when you’re outside. Change your clothes as soon as you come indoors., Complications : adenoid hypertrophy, aggravation of existing asthma, allergic conjunctivitis, enlarged tonsils, sinusitis, Sleep disturbances, Diagnostics : Complete Blood Count CBC, EOSINOPHILS - ABSOLUTE COUNT, serum IgE level, Nasal Smear, allergy skin test, Differential diagnosis : atrophic rhinitis, deviated nasal septum, nasal foreign bodies, Primary Ciliary Dyskinesia(Immotile Cilia Syndrome, rhinitis medicamentosa, Sarcoidosis, sickle cell anemia, vasomotor rhinitis, disease description : Allergic rhinitis is inflammation of the inside of the nose caused by an allergen, such as pollen, dust, mould, or flakes of skin from certain animals. |
Alopecia Areata | Disease Name : Alopecia Areata, Treatment : Triamcinolone acetonide 5-10 mg per milliliter given every 2 – 6 weeks.Patients with extensive disease, often defined as greater than 50% scalp hair loss, may be treated with topical immunotherapy. This approach avoids the large number of injections that would be otherwise required when using intralesional corticosteroids. Moreover, one retrospective study reported superior efficacy of topical immunotherapy over intralesional corticosteroids for patients with patches of hair loss exceeding 50 cm2 in size, Pathophysiology : There is abundant evidence, albeit circumstantial, that alopecia areata is an autoimmune disease :
• There is an increased frequency of other autoimmune diseases in patients with alopecia areata.
• There is an increased frequency of organ-specific autoantibodies in patients with alopecia areata. Serum antibodies to hair follicle tissue also occur with increased frequency in alopecia areata although these antibodies appear not to bind to hair follicles in
vivo and their pathogenetic significance is not known.
• The pathology is characterized by infiltration of hair bulbs by activated T-lymphocytes.
• In animal models of alopecia areata, the depletion of CD4 and CD8 T cells results in hair regrowth.
• Alopecia areata shares genetic associations with several autoimmune diseases, particularly with genes of the major histocompatibility complex., Epidemiology : 0.6% to 2.0% of new cases in dermatology clinics in the UK and US. Similarly, hospital-based studies worldwide have estimated the incidence risk of AA to be between 0.57% to 3.8%., good, Eat a healthy diet that includes enough calories, protein and iron.,Find ways to cope with stress.,Manage thyroid disease or other medical conditions that could result in hair loss.,Avoid hairstyles that pull hair tightly.,During chemotherapy treatment, try a cooling cap., Complications : anxiety, insulin Resistance, DEPRESSION, Diagnostics : HISTOPATHLOGY, FUNGAL CULTURE, Antibody Serology Tests, Antibody Serology Tests, Differential diagnosis : lupus erythematosus, seborrhoeic dermatitis, TINEA CAPITIS, TRICHOTILLOMANIA, disease description : Alopecia areata is a common, chronic, inflammatory disease that causes non-scarring hair loss. The severity ranges from small patches of hair loss, which usually recover spontaneously, to complete alopecia where the prognosis for hair regrowth is poor. The nails may also be affected. Current evidence indicates that alopecia areata is caused by a T-cell-mediated autoimmune mechanism occurring in genetically predisposed individuals. |
Alpha-aminoadipic Aciduria | Disease Name : Alpha-aminoadipic Aciduria, Treatment : treatment with vigabatrin (VGB). A significant increase in alpha-aminoadipic acid (AAA) occurred in plasma and urine of VGB-treated children, thus mimicking a known rare metabolic disease, alpha-aminoadipic aciduria (AAAuria)., Pathophysiology : Alpha-aminoadipic and alpha-ketoadipic aciduria is an autosomal recessive metabolic disorder characterized by an increased urinary excretion of alpha-ketoadipic acid and alpha-aminoadipic acid. It is caused by mutations in DHTKD1, which encodes the E1 subunit of the oxoglutarate dehydrogenase complex (alpha-ketoglutarate dehydrogenase complex)., Epidemiology : <1/1000000 (Worldwide), "It is an autosomal recessive metabolic disorder and therefore cant be prevented. Although consult your doctor while planning pregnancy.", Complications : developmental delay, Muscular hypotonia, mental retardation, Diagnostics : Urine analysis, Differential diagnosis : mitochondrial disorders, Pyridoxine-dependent epilepsy, disease description : Alpha-aminoadipic and alpha-ketoadipic aciduria is an autosomal recessive inborn error of lysine, hydroxylysine, and tryptophan degradation. To date, DHTKD1 mutations have been reported in two alpha-aminoadipic and alpha-ketoadipic aciduria patients. We have now sequenced DHTKD1 in nine patients diagnosed with alpha-aminoadipic and alpha-ketoadipic aciduria as well as one patient with isolated alpha-aminoadipic aciduria, and identified causal mutations in eight. |
Alport Syndrome | Disease Name : Alport Syndrome, Treatment : medication : Telmisartan , The goal is to treat the symptoms and help slow the progression of kidney disease. This may include : ,,ACE inhibitor or ARB medicines (medications to control high blood pressure),Diuretics (water pills),Limit sodium (salt) in your diet, Patients with ESRD(end stage renal disease) are treated with dialysis,and kidney transplantation., Pathophysiology : Approximately 85% of patients have X-linked inheritance caused by a mutation
in the COL4A5 gene encoding the a5 chain of type IV collagen. Patients with a
subtype of X-linked AS and diffuse leiomyomatosis demonstrate a contiguous
mutation within the COL4A5 and COL4A6 genes that encodes the a5 and a6
chains, respectively, of type IV collagen. Autosomal recessive forms of AS in
approximately 15% of patients are caused by mutations in the COL4A3 and
COL4A4 genes on chromosome 2 encoding the a3 and a4 chains, respectively,
of type IV collagen. An autosomal dominant form of AS linked to the COL4A3-
COL4A4 gene locus occurs in 5% of cases.
Fechtner syndrome (AS with macrothrombocytopenia) is an autosomal
dominant disorder due to mutations in MYH9 . Hereditary angiopathy with
nephropathy-aneurysms-muscle cramps (HANAC) may initially resemble AS.
HANAC is due to mutations in the COL4A1 gene.
Kidney biopsy specimens during the first decade of life will show only a few
changes on light microscopy. Later, the glomeruli may develop mesangial
proliferation and capillary wall thickening, leading to progressive glomerular
sclerosis. Tubular atrophy, interstitial inflammation and fibrosis, and lipidcontaining
tubular or interstitial cells, called foam cells, develop as the disease
progresses. Immunopathologic studies are usually nondiagnostic.
In most patients, electron microscopy reveals diffuse thickening, thinning,
splitting, and layering of the glomerular and tubular basement membranes ., Epidemiology : 1 in 5, 000-10, 000 people in the general population in the United States, which means that approximately 30, 000-60, 000 people in the United States have the disorder., POOR, You can’t prevent Alport syndrome, but being aware of your family history can help you detect it early. Awareness can also help prevent you from passing it on to your biological child.,,Diagnosing Alport syndrome early and starting therapy with ACE inhibitors/ARBs and SGLT-2 inhibitors is the best way to delay kidney failure.,,If a provider diagnoses blood in your pee, it’s a good idea to get additional testing for Alport syndrome, especially if you have any hearing issues or decreased kidney function.,,If you have a family history of hematuria, a provider should test your pee for blood and order blood tests to check your kidney function., Complications : Chronic renal failure, hypertension, mental retardation, Electrolyte disturbances, Diagnostics : HISTOPATHLOGY, Renal Biopsy, Slit lamp examination, URINARY PROTEIN, URINE MICROSCOPY, USG, Audiogram, Differential diagnosis : Glomerulonephritis, Polycystic Kidney Disease, disease description : Alport syndrome (AS), or hereditary nephritis, is a genetically heterogeneous
disease caused by mutations in the genes coding for type IV collagen, a major
component of basement membranes. These genetic alterations are associated
with marked variability in the clinical presentation, natural history, and
histologic abnormalities. |
Alzheimers Disease | Disease Name : Alzheimers Disease, Treatment : Cholinesterase inhibitors.,NMDA antagonists.,Cholinesterase inhibitors,The following cholinesterase inhibitors can help treat the symptoms of mild to moderate Alzheimer’s disease : ,,Donepezil (Aricept®). This is also FDA-approved to treat moderate to severe AD.,Rivastigmine (Exelon®).,Galantamine (Razadyne®).,NMDA antagonists,Memantine (Namenda®) is FDA-approved for treating moderate to severe Alzheimer’s disease. It helps keep certain brain cells healthier., The slow and ongoing death of the nerve cells results in the symptoms of Alzheimer’s disease. Nerve cell death starts in one area of your brain (usually in the area of your brain that controls memory — the hippocampus) and then spreads to other areas.,,Despite ongoing research, scientists still don’t know what exactly causes these proteins to build up. So far, they believe that a genetic mutation may cause early-onset Alzheimer’s. They think that late-onset Alzheimer’s happens due to a complex series of brain changes that may occur over decades. A combination of genetic, environmental and lifestyle factors likely contribute to the cause., Pathophysiology : An abnormal build-up of proteins in your brain causes Alzheimer’s disease. The build-up of these proteins — amyloid protein and tau protein — causes brain cells to die.The human brain contains over 100 billion nerve cells and other cells. The nerve cells work together to fulfill all the communications needed to perform functions such as thinking, learning, remembering and planning.The slow and ongoing death of the nerve cells results in the symptoms of Alzheimer’s disease. Nerve cell death starts in one area of your brain (usually in the area of your brain that controls memory — the hippocampus) and then spreads to other areas.Despite ongoing research, scientists still don’t know what exactly causes these proteins to build up. So far, they believe that a genetic mutation may cause early-onset Alzheimer’s. They think that late-onset Alzheimer’s happens due to a complex series of brain changes that may occur over decades. A combination of genetic, environmental and lifestyle factors likely contribute to the cause., Epidemiology : It affects approximately 24 million people across the world., One in 10 people older than 65 and nearly a third of people older than 85 have the condition., variable, Research shows that having a healthy lifestyle helps protect your brain from cognitive decline. The following strategies may help decrease your risk of developing Alzheimer’s disease : ,,Stay mentally active : Play board games, read, do crossword puzzles, play a musical instrument or do other hobbies that require “brain power.”,Get physically active : Exercise increases blood flow and oxygen to your brain, which may affect brain cell health. Wear protective headgear if you’re participating in activities that increase your risk of a head injury.,Stay socially active : Regularly talk with friends and family and join in on group activities, such as religious services, exercise classes, book clubs or community volunteer work.,Eat healthily : Follow the Mediterranean or DASH diet or another healthy diet that includes antioxidants. Consume alcoholic beverages in moderation., Complications : infections, Restlessness, Aspiration, Malnutrition and cachexia, Diagnostics : HISTOPATHLOGY, MRI Brain, PET SCAN, CT SCAN, PHYSICAL EXAMINATION, Differential diagnosis : Dementia, Dementia with Lewy Bodies, FRONTOTEMPORAL DEMENTIA, disease description : Alzheimer disease (AD) is a neurodegenerative disorder marked by cognitive and behavioral impairment that significantly interferes with social and occupational functioning.Alzheimer’s disease causes a decline in memory, thinking, learning and organizing skills over time. It’s the most common cause of dementia and usually affects people over the age of 65. There’s no cure for Alzheimer’s, but certain medications and therapies can help manage symptoms temporarily. |
Amblyopia | Disease Name : Amblyopia, Treatment : Eye patches for kids : Your child may wear a patch over the better eye for at least a few hours per day. This effective treatment can last months or even years. The patch forces the brain to use the images from the weaker eye, eventually making that eye stronger.,Glasses : Eyeglasses are also a common lazy eye treatment. They can help amblyopia by improving nearsightedness, farsightedness and eye crossing.,Eye drops : For mild cases, your provider may recommend eye drops (atropine) to temporarily blur vision in the better eye. The goal is the same as a patch : to force the brain to use the weaker eye., An operation for amblyopia is rare. Your healthcare provider may suggest surgery to fix certain causes of amblyopia, such as cataracts., Pathophysiology : Amblyopia occurs when there is a major difference between the two eyes in their ability to focus. The most common cause of amblyopia is other vision problems. It’s important to treat these other conditions, or the brain starts relying on the eye with better vision, leading to amblyopia., Epidemiology : Up to 3 out of 100 children have it., early treatment works well and usually prevents lo, You can’t prevent amblyopia or the other vision problems that may cause it. But you can stop it from getting worse or causing permanent problems. The best way to prevent vision loss from amblyopia is to get regular eye exams. Make sure your child has a thorough eye exam by the age of 6 months and then again by 3 years., Complications : Visual acuity is markedly reduced, poor stereovision, Diagnostics : VISUAL ACUITY TEST, Differential diagnosis : Accommodative Esotropia, Acquired Esotropia, cataract, REFRACTIVE ERROR, RETINOBLASTOMA, Strabismus, disease description : Amblyopia, or lazy eye, occurs when one eye becomes weaker than the other during infancy or childhood. The brain favors the better eye, allowing the weaker eye to get worse over time. Early screening is important because treatment is more effective when started early. Treatments include an eye patch or glasses. |
Amebiasis | Disease Name : Amebiasis, Treatment : medication : Tinidazole , Diloxanide , Metronidazole , Paromomycin , Therapeutic aspiration guided by CT in the,treatment of uncomplicated amebic liver abscess is,controversial. Large amebic liver abscesses (>300 ml) may,benefit from aspiration with decrease in duration of,hospital stay and faster clinical improvement recovery,when compared to those managed medically alone., Metronidazole is the drug of choice for treating amebic,colitis. Alternatives include tinidazole, ,orindazole and secnidazole. Since metronidazole does not,destroy the cysts, a luminal agent (paro momycin, ,iodoquinol, or diloxanide furoate) should be used to,eradicate colonization., Pathophysiology : An ingested cyst divides in the small intestine to form
8 trophozoites that colonize the mucosa of the large
intestine. Trophozoites cause tissue invasion and
destruction with little or no local inflammation, resulting
in characteristic flask shaped ulcers in cecum, transverse
colon and sigmoid colon. Extraintestinal complications
occur when trophozoites invade the bloodstream and
migrate through the portal circulation to lodge, most
commonly, in the liver. Amebic liver abscess is usually single
(95%) and more frequently involves the posterosuperior
part of right lobe of the liver. The abscess may regress,
rupture or disseminate; transdiaphragmatic rupture may
cause amebic empyema and pulmonary amebiasis. Rare
complications include amebic involvement of peritoneum,
pericardium, pleura, lungs, brain, genitourinary system
and skin., Epidemiology : "infect 10% of the worlds population", GOOD, You can reduce your risk of amebiasis infection by being careful about what you eat and drink when traveling to areas with poor sanitation. You should : ,,Avoid eating raw fruits and vegetables. Peel and wash produce before cooking.,Avoid drinks with ice cubes.,Drink only sealed bottled water (or boil water before you drink it if bottled water is unavailable).,Wash your hands frequently with soap and water after using the toilet or changing a baby’s diaper.,Use condoms and safe sex practices to reduce your exposure to feces during sexual activity.,If you do experience symptoms, see your provider right away. Waiting too long for treatment can lead to complications and severe illness., Complications : Amebiasis, LIVER ABSCESS, Toxic megacolon, bowel perforation, secondary bacterial infections, Diagnostics : Complete Blood Count CBC, HISTOPATHLOGY, Entamoeba Histolytica Antibody TEST, USG ABDOMEN(W/A), stool microscopy, IgM ELISA, MRI, CT SCAN, USG, Differential diagnosis : cholecystitis, colitis, DIVERTICULITIS, Hepatitis A, pericarditis, salmonellosis, Shigellosis, disease description : Amebiasis is a disease caused by the parasite Entamoeba histolytica. It can affect anyone, although it is more common in people who live in tropical areas with poor sanitary conditions. Diagnosis can be difficult because other parasites can look very similar to E. histolytica when seen under a microscope. |
Aminoacylase 1 Deficiency | Disease Name : Aminoacylase 1 Deficiency, Treatment : Management is symptomatic only., Pathophysiology : This condition is inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.
Mutations in the ACY1 gene lead to an aminoacylase 1 enzyme with little or no function. Without this enzymes function, acetyl groups are not efficiently removed from a subset of amino acids during the breakdown of proteins. The excess N-acetylated amino acids are released from the body in urine. It is not known how a reduction of aminoacylase 1 function leads to neurological problems in people with aminoacylase 1 deficiency., Epidemiology : Neurological Conditions Associated with Aminoacylase 1 Deficiency : <1/1000000 (Worldwide), variable, "Cant be prevented since its a genetic inborn disorder. Although if you are planning a pregnancy, check in with your Doctor.", Complications : developmental delay, Psychomotor delay, Diagnostics : GENETIC TESTING, Differential diagnosis : nan, disease description : Aminoacylase 1 deficiency is an inherited disorder that can cause neurological problems; the pattern and severity of signs and symptoms vary widely among affected individuals. Individuals with this condition typically have delayed development of mental and motor skills (psychomotor delay). They can have movement problems, reduced muscle tone (hypotonia), mild intellectual disability, and seizures. However, some people with aminoacylase 1 deficiency have no health problems related to the condition. A key feature common to all people with aminoacylase 1 deficiency is high levels of modified protein building blocks (amino acids), called N-acetylated amino acids, in the urine. |
Amoebic Liver Abscess | Disease Name : Amoebic Liver Abscess, Treatment : medication : Piperacillin and tazobactum , Vancomycin , Metronidazole , Ultrasound guided percutaneous,needle aspiration and/ or catheter drainage is,required for abscesses that fail to improve after 3--4 days of,antibiotic therapy, large abscesses in left lobe and impending,rupture (narrow rim <1 cm)., Patients with pyogenic liver abscesses are,treated with broad spectrum antibiotics (against grampositive, ,gram-negative aerobic and anerobic bacteria) for,4-6 weeks. Metronidazole is used for 10-14 days in patients,with amebic liver abscess., Surgery is required for,abscesses complicated by frank intraperitoneal rupture or,multiseptate abscesses not responding to percutaneous,catheter drainage and antibiotics., Pathophysiology : The life cycle of Entameba Histolytica was first explained by Clifford Dobell in 1928. The organism has 2 stages of life, the cystic stage which is the infective stage and the trophozoite stage which ends up causing invasive disease. Upon ingestion of contaminated food and water; the infection starts with ingestion of the quadrinucleate cyst of E. histolytica. Excystation in the small intestinal lumen is followed by production of motile, potentially invasive trophozoites. In most infections, the trophozoites form new cysts and are limited to the intestinal mucin layer. In other cases, the trophozoites adhere to and lyse the colonic epithelium with subsequent invasion of the colon. Neutrophils respond, resulting in further cellular damage at the invasion site. Once the trophozoites invade the colonic epithelium, subsequent spread to extraintestinal sites such as the liver (by hematogenous spread through the portal circulation) and peritoneum can occur. The organism causes hepatic inflammation followed by necrosis which results in an abscess formation.Adherence of E. histolytica to colonic epithelial cells is thought to be through the galactose/N-acetylgalactosamine-specific lectin. E. histolytica carries cytolytic capabilities and also kills mammalian cells through programmed apoptosis. Once E. histolytica trophozoites reach the liver, they create abscesses comprising well-circumscribed areas of cellular debris, dead hepatocytes, and liquefied cells. The lesion is surrounded by a rim of connective tissue with some inflammatory cells and amebic trophozoites. In humans, the small number of organisms compared to the actual dimensions of the abscess supports the concept that E. histolytica can destroy hepatocytes without contact with the cells., Epidemiology : An estimated 10% of the population is infected with Entamoeba, 2.3 cases per 100, 000 people, good, When traveling in tropical countries with poor sanitation, drink purified water and do not eat uncooked vegetables or unpeeled fruit., Complications : abscess, peritonitis, sepsis, intraperitonial rupture, Diagnostics : Erythrocyte Sedimentation Rate (ESR), CT Abdomen, USG ABDOMEN(W/A), LIVER FUNCTION TEST LFT, White Blood Cell count WBC, ANTIGEN DETECTION ELISA, ANTIGEN DETECTION ELISA, BLOOD CULTURE, MRI, CHEST X RAY, CT SCAN, TOTAL SERUM PROTEIN LEVEL, Differential diagnosis : ACALCULOUS CHOLECYSTITIS, candidial infection, CHOLELITHIASIS, hepatocellular carcinoma, Hydatid cysts, PRIMARY BILIARY CIRRHOSIS, PYOGENIC LIVER ABSCESSS, TUBERCULOSIS, viral hepatitis, disease description : Amebic liver abscess is the most common extra-intestinal manifestation of the protozoan, Entamoeba histolytica. The life cycle involves consumption of fecally contaminated food and water, that reaches and penetrates the small intestine to enter the mesenteric vessels and finally the liver. |
Amyloid Degeneration Of Conjunctiva | Disease Name : Amyloid Degeneration Of Conjunctiva, Treatment : Lubricating drops for mild symptoms., Excision., Pathophysiology : nan, Epidemiology : nan, Complications : corneal abrasions, Diagnostics : nan, Differential diagnosis : nan, disease description : Conjunctival amyloid, though rare, is reported to
occur in two forms :
• Primary conjunctival amyloid is associated with
deposition of light-chain immunoglobulin by the
monoclonal B cells and plasma cells.
• Secondary conjunctival amyloid may occur
secondary to systemic diseases or secondary to
chronic conjunctival inflammations. |
Amyloidosis | Disease Name : Amyloidosis, Treatment : medication : Riluzole , Edaravone, High-dose chemotherapy with stem cell transplant can help remove the substance that leads to amyloid formation in some people with primary AL amyloidosis. Chemotherapy medicines alone may be used to treat other patients with primary AL amyloidosis.,Secondary (AA) amyloidosis is treated by controlling the underlying disorder and with powerful anti-inflammatory medicines called steroids, which fight inflammation.,A liver transplant may treat the disease if you have certain types of hereditary amyloidosis.,New therapies can slow the production of the abnormal protein TTR.,Your doctor might also recommend a kidney transplant., Pathophysiology : In all forms of amyloidosis, the cell secretes the precursor protein in a soluble form that becomes insoluble at some tissue site, compromising organ function. All the amyloid precursor proteins are relatively small (ie, molecular weights 4000-25, 000) and do not share any amino acid sequence homology. The secondary protein structures of most soluble precursor proteins (except for SAA and chromosomal prion protein Prpc) have substantial beta-pleated sheet structure, while extensive beta-sheet structure occurs in all of the deposited fibrils.In some cases, hereditary abnormalities (primarily point mutations or polymorphisms) in the precursor proteins are present (eg, lysozyme, fibrinogen, cystatin C, gelsolin). In other cases, fibrils form from normal-sequence molecules (eg, AL, ß2 M). In other cases, normal-sequence proteins can form amyloid, but mutations underlying inflammatory milieu accelerate the process (eg, TTR, beta protein precursor or CAPS)., Epidemiology : It is estimated that about 4, 000 people in the United States develop amyloid and light chain (AL) amyloidosis each year. The disease is typically diagnosed between the ages of 50 and 65., varible, No, you can’t prevent amyloidosis. Researchers have identified several risk factors. But you can’t control those factors and prevent amyloidosis.,,People often develop some form of amyloidosis because they have an underlying condition. In some cases, they inherit a form of amyloidosis. You may be able to control how much amyloidosis affects your quality of life by understanding your risk for developing amyloidosis so you and your healthcare provider can monitor your well-being so they can diagnose and treat amyloidosis while the disease is in its early stages., Complications : heart failure, Malnutrition, kidney faliure, Diagnostics : HISTOPATHLOGY, Protein, Differential diagnosis : Mastocytosis, Pseudoxanthoma elasticum, Renal Vein Thrombosis, disease description : Amyloidosis is the name for a group of rare, serious conditions caused by a build-up of an abnormal protein called amyloid in organs and tissues throughout the body. The build-up of amyloid proteins (deposits) can make it difficult for the organs and tissues to work properly. |
Amyotrophic Lateral Sclerosis | Disease Name : Amyotrophic Lateral Sclerosis, Treatment : medication : Riluzole , Edaravone, Physical therapy to help you stay mobile. It can ease discomfort from stiff muscles, cramps and fluid retention.,Nutritional counseling ensures you eat a healthy, balanced diet. A nutritionist can also recommend other food options when swallowing becomes difficult.,Speech therapy provides strategies for safer swallowing and communication training help you maintain verbal communication for as long as possible. You may also learn nonverbal communication techniques.,Assistive devices, including splints, braces, grab bars and reach devices, help you stay independent. You use these devices to get dressed, eat, use the toilet and bathe.,Special equipment such as wheelchairs and electric beds to help you function independently., Medications to relieve muscle cramps, extra saliva and other symptoms., Pathophysiology : About 20–40%Trusted Source of familial ALS cases, and a small number of sporadic cases, stem from a difference in the C9ORF72 gene. This gene makes a protein in nerve cells in the brain and spinal cord.And 12–20%Trusted Source of familial cases result from mutations in the SOD1 gene, which is key to the functioning of motor neurons and other cells.A 2021 studyTrusted Source, meanwhile, linked mutations in the SPTLC1 gene with a rare form of genetic ALS that affects children as young as 4 years.People with ALS might consider genetic testing. If the test identifies a disease-causing variant, family members might also get tested.Other possible causes of ALS include : Disorganized immune response : The immune system may attack some of the body’s cells, possibly killing nerve cells.Chemical imbalance : People with ALS often have higher levels of glutamate, a chemical messenger in the brain, near the motor neurons. Glutamate in high quantities can be toxic to nerve cells.Mishandling of proteins : If nerve cells do not process proteins correctly, the resulting atypical proteins might accumulate and cause the nerve cells to die., Epidemiology : 3–5 per 100, 000, VERY POOR, There’s no proven way to prevent ALS. If you have ALS, you can take part in clinical trials and the National ALS Registry. Doing so can help further understanding of the disease. As researchers gain more knowledge about ALS, they can learn more about causes and risk factors. This information may lead to prevention methods and better treatments., Complications : aspiration pneumonia, BEDSORES, lung damage, weight loss, Diagnostics : Complete Blood Count CBC, CSF EXAMINATION, HISTOPATHLOGY, URINE R/M, ELECTROMYOGRAPHY, MRI Spine, NERVE CONDUCTION VELOCITY(NCV), Differential diagnosis : Hexosaminidase A deficiency, Motor neuropathies, MYASTHENIA GRAVIS, myopathies, poliomyelitis, Spinal Muscular Atrophies, THYROTOXICOSIS, disease description : Amyotrophic lateral sclerosis, or ALS, is a type of motor neuron disease. It’s also known as Lou Gehrig’s disease. ALS affects motor neurons — nerves that control your voluntary muscles. Voluntary muscles are the ones you use for actions like chewing, talking and moving your arms and legs. ALS is progressive, meaning that the symptoms get worse over time. If you have ALS, your muscles begin to atrophy or waste away. Your muscles get weaker over time, making it difficult to walk, talk, swallow and eventually breathe. Most people with ALS die of respiratory failure when their lungs can’t get enough oxygen to the blood. |
Anaemic Retinopathy | Disease Name : Anaemic Retinopathy, Treatment : • Treatment of anemia, which leads to reversal of,retinopathy in most cases.,• Intervention for a large subhyaloid haemorrhage, ,which does not resolve spontaneously, in the form,of intravitreal tissue plasminogen activator (tPA)., YAG posterior hyaloidotomy, or pars plana,vitrectomy, may be required., Pathophysiology : In anaemia, retinal changes are liable to occur when
haemoglobin level falls by 50% and are consistently
present when it is below 35% (5 gm%). Duration and
type of anaemia do not influence the occurrence of
retinopathy.
Pathogenesis involves factors like anoxia, venous
stasis, angiospasm, increased capillary permeability,
and thrombocytopenia.
Characteristc features of anaemic retinopathy are as
below :
• Fundus background becomes pale
• Retinal arterioles are also pale
• Retinal veins are tortuous and dilated
• Retinal haemorrhages, superficial flame shaped
and preretinal (subhyaloid) may be seen in the
posterior half of fundus
• Roth spots, i.e., haemorrhages with white center
and platelet-fibrin emboli constitute the white
centre
• Cotton wool spots may also be seen especially
in patients with coexisting thrombocytopenia in
aplastic anaemia.Anemia causes retinopathy in 28% of patients, especially when there is coexisting thrombocytopenia (38%). As the severity of anemia increases, the risk of retinopathy increases, particularly when the hemoglobin (Hb) level is below 6 gm/dL.3A variety of pathologic changes occurring due to and associated with anemia are implicated in the clinical features of anemic retinopathy. Anemia causes retinal hypoxia, which leads to infarction of the nerve fiber layer and clinically manifests as cotton wool spots. Retinal hypoxia also leads to vascular dilatation; increased transmural pressure owing to hypoproteinemia; and microtraumas to the vessel walls, which cause retinal edema and hemorrhages. In many clinical situations, thrombocytopenia is associated with anemia, and that leads to defective coagulation and hemorrhages.Other factors implicated in the pathology are venous stasis, angiospasm, increased blood viscosity (myeloproliferative disorders), hypotension (following hemorrhage), etc. Hypotension may lead to optic neuropathy.Rarely, loss of vision can be a presenting complaint, because most cases are asymptomatic. At the macula, hemorrhages, edema, or hard exudates can cause impairment of vision. Alternatively, vision loss may occur due to disc edema or optic neuropathy., Epidemiology : 28.3%, good, Correction of the underlying deficiencies ..., Complications : RETINAL EDEMA AND SOFT EXUDATES, retinal haemorrhage, Diagnostics : FUNDOSCOPY, RETINOSCOPY, Slit lamp examination, Differential diagnosis : Diabetic Retinopathy, HYPERTENSIVE RETINOPATHY, RETINAL ARTERY OCCLUSIONS, Retinal vein occlusion, Sickle-cell Retinopathy, disease description : In anaemia, retinal changes are liable to occur when
haemoglobin level falls by 50% and are consistently
present when it is below 35% (5 gm%). Duration and
type of anaemia do not influence the occurrence of
retinopathy.Anemic retinopathy is usually asymptomatic with findings ranging from retinal hemorrhage, cotton wool spots, venous tortuosity, and occasionally white-centered hemorrhages called Roth spots. |
Anal And Perianal Malignancy | Disease Name : Anal And Perianal Malignancy, Treatment : The aim of treatment is to achieve cure with preservation ,of faecal continence. Chemoradiotherapy using a combination of 5-fl uorouracil and mitomycin C have been established ,as fi rst line treatment for invasive anal canal disease 10 . Small, ,well-differentiated anal margin tumours without nodal involvement can be treated with wide local excision if anal sphincter function can be preserved, Surgical resection with wide local excision for small tumors or abdominoperineal resection (APR) for larger, invasive tumors has been the traditional method of treatment., The main role for surgery in anal cancer is for residual or recurrent disease after failure of chemoradiotherapy and is referred to ,as salvage surgery. Abdomino-perineal resection with perineal ,reconstruction is the most frequently performed operation. This ,operation involves resection of the anus and rectum, end colostomy formation and reconstruction of the perineum, Pathophysiology : Predisposing factors
Factors that increase the risk of ano-genital HPV infection or modulate the host immune response to HPV are associated with anal SCC.
These include anoreceptive sex, lifetime number of sexual partners,
immunosuppression (including organ transplant recipients) and
smoking. Anal SCC is also increased in autoimmune disease including psoriasis and granulomatosis with polyangiitis. The highest
risk group is HIV-positive MSM. HIV control as measured by the
per cent of time with undetectable HIV viral load has been reported
to decrease the risk of anal SCC. Optimizing antiretroviral therapy and control of HIV viral load may decrease the risk of anal SCC.
Perianal SCC can also develop on a background of chronic dermatoses including lichen planus, lichen sclerosus and hidradenitis
suppurativa. Anal intraepithelial neoplasia is thought to be the precursor
of invasive SCC . Histological features of anal SCC include hyperkeratosis, acanthosis, ectopic keratinization,
nuclear pleomorphism and mitoses. Cells can vary from large,
pale eosinophilic cells to small, basaloid or spindle-shaped cells.
Tongues of atypical keratinocytes invade the dermis. The invasive margin can vary from well circumscribed to irregular. A
lymphocytic infiltrate of varying degrees may be present. No significant association between histological subtype and prognosis
has been established.
Causative organisms
Anal SCC is associated with high-risk HPV infection, including
HPV-16, in more than 96% of cases.
Clinical variants
Buschke–Löwenstein tumour (also called giant condyloma
acuminatum or verrucous carcinoma) is a rare, slow-growing,
cauliflower-like exophytic tumour of the ano-genital region
caused by HPV and characterized by invasive growth. HPV-6 and -11 are the most common HPV genotypes
identified. HPV-16 and -18 can also be detected, especially in
cases with foci of invasive SCC. The histological features are
similar to those of condyloma acuminatum. The Buschke–
Löwenstein tumour is thought to exhibit intermediate biological behaviour towards malignancy. Wide local excision or
abdomino-perineal resection are considered the treatment of
choice. Adjuvant chemoradiotherapy may be necessary if there
is an invasive component. Malignant transformation to SCC can
occur in 40–60% of cases, Epidemiology : The incidence is estimated between 0.2 to 1.4/100, 000, variable, Preventive measures include : ,,- Avoid unprotected anal intercourse.,- Quit smoking. Quitting smoking or chewing tobacco can decrease the risk of developing cancer.,- Use condoms to prevent HIV or HPV infection., Complications : Metastasis, Diagnostics : HISTOPATHLOGY, CT SCAN, HISTOLOGIC EXAMINATION, Differential diagnosis : ANAL FISSURE, Crohns Disease, HAEMORRHOIDS, Lichen Planus, lichen sclerosus, Perianal abscess, disease description : Tumors of the anus and perianal skin are rare. Their presentation can vary and often mimics common benign anal pathology, thereby delaying diagnosis and appropriate and timely treatment. The anatomy of this region is complex because it represents the progressive transition from the digestive system to the skin with many different co-existing types of cells and tissues. Squamous cell carcinoma of the anal canal is the most frequent tumor found in the anal and perianal region. Less-frequent lesions include Bowens and Pagets disease, basal cell carcinoma, melanoma, and adenocarcinoma. |
Anal Fissure, . Acute fi ssures are usually superfi cial with well-delineated mucosal edges and granulation tissue at the base., constipation, bleeding, itching, anal pain, DISCHARGE, PROBLEM IN DEFECATION, Treatment | Disease Name : Anal Fissure, . Acute fi ssures are usually superfi cial with well-delineated mucosal edges and granulation tissue at the base., constipation, bleeding, itching, anal pain, DISCHARGE, PROBLEM IN DEFECATION, Treatment : The use of topical nitrate (e.g. glyceryl trinitrate 0.4% ointment) may ,be considered. Topical calcium channel blockers (e.g. diltiazem 2% ,gel) can be tried in patients unresponsive to topical nitrates., Surgery is the mainstay of treatment for chronic anal fi ssures unresponsive to first line measures. Lateral internal sphincterotomy ,results in cure rates of up to 98% but may compromise anal continence in up to 30%.,Fissurectomy and endoanal advancement fl ap are surgical options, Pathophysiology : The aetiology is poorly understood. Trauma causing pressure or
necrosis by the passage of hard stools is thought to be an initiating
factor. Pregnancy-associated anal fissures are thought to arise due
to shearing forces during labour. Histology in idiopathic cases is of non-specific ulceration. In secondary anal fissures, specific pathology such as anal carcinoma or
Crohn disease will be identified.
Associated diseases
Atypical fissures (large, irregular, multiple and non-midline) are
associated with underlying disease such as Crohn disease, HIV
infection, syphilis, tuberculosis and malignancy., Epidemiology : The incidence of anal fissure is approximately 1100 (700-1700) per 100, 000 individuals in US which is about 7.8% lifetime risk., More than 50% of acute fissures heal spontaneously, If you have a chronic condition that affects your anus, whether it’s a disease, trouble with pooping or unexplained pain, see a healthcare provider about it. Treating these conditions sooner can prevent complications like anal fissures from developing or returning., Complications : constipation, Perianal conditions, Diagnostics : HISTOPATHLOGY, PROCTOSCOPY, Differential diagnosis : Anal cancer, Crohns Disease, ECZEMA, Fistula, Hemorrhoids, HIV, INFLAMMATORY BOWEL DISEASES, PROCTITIS, psoriasis, SEXUALLY TRANSMITTED DISEASE, syphilis, disease description : An anal fissure is a longitudinal ulcer occurring in the squamous
epithelium of the anal canal located distal to the dentate line. Primary anal fissures are idiopathic and usually affect the posterior midline. Secondary anal fissures usually occur in the lateral
aspect of the anal canal and are associated with underling diseases
such as Crohn disease.
Anal fi ssures are commonly encountered in young adults but may
affect extremes of age.
Sex
There is an equal prevalence in males and females. |
Anal Warts | Disease Name : Anal Warts, Treatment : Anal warts that are small and located only on the skin around your anus can usually be treated with topical ointments. These treatments include : ,,Imiquimod (Zyclara® or Aldara®).,Podofilox (Condylox®).,Podophyllin (Podocon-25®),Sinecatechins (Veregen®).,There are also topical treatments that "freeze" or "burn" warts. These treatments cause minor side effects like discomfort or swelling : ,,Liquid nitrogen (cryotherapy) : When liquid nitrogen is applied, it freezes the skin, causing the warts to fall off.,Trichloroacetic acid : Acid is applied to the warts, destroying and breaking down the warts., electrocautery excision, Pathophysiology : HPV causes anal warts, and there are many strains of the virus.According to the CDC, an estimated 90%Trusted Source of anal warts occur due to HPV types 6 or 11. These strains can also cause warts on other areas, including the nose, eyes, and mouth.The CDC also note that scientists associate the HPV strains 16, 18, 31, 33, and 35 with lesions that may become cancerous.In most cases, people develop anal warts as a result of having receptive anal intercourse with someone who has HPV.The virus can also transmit and cause anal warts through hand-to-anal contact or the anal area being exposed to someone’s bodily fluids that contain the virus., Epidemiology : prevalence is as high as 10% to 20%., Warts are common worldwide and affect approximately 10% of the population. In school-aged children, variable, Use a condom every time you have sex.,Not having sex with someone who has anal or genital warts.,Refraining from sex if you have anal or genital warts.,Get checked for HPV and STIs regularly (as recommended by your healthcare provider) and encourage your sexual partners to do the same.,Get the HPV vaccine if you are eligible. Your provider can tell you if you’re a candidate for this vaccine., Complications : Skin cancer lesions, Fistula, painful defecation, Diagnostics : HISTOPATHLOGY, Bacteria Culture Test, PROCTOSCOPY, Differential diagnosis : Anal cancer, ANAL FISSURE, CARCINOMA ANAL CANAL, GENITAL HERPES, HAEMORRHOIDS, Molluscum Contagiosum, POST ANAL DERMOID, psoriasis, Syphilis, disease description : Anal warts (condyloma) are warts in and around your anus. They’re caused by human papilloma virus (HPV), which is spread through sexual or skin-to-skin contact. Symptoms include itching, bleeding or feeling a lump in your anus. Most anal warts need treatment with topical medication or surgery.Anal warts (also known as condyloma) are warts that grow in or around your anus (the opening to your rectum). They’re caused by human papillomavirus (HPV), a sexually transmitted infection (STI) that spreads through sexual or skin-to-skin contact with an infected person. Warts caused by HPV can show up on different areas of your body — in this case, the virus shows up as warts in your anal area. |
Anaphylactic Reactions | Disease Name : Anaphylactic Reactions, Treatment : Airway-Airway management is paramount. Thoroughly examine the patient for airway patency or any indications of an impending loss of airway. Perioral edema, stridor, and angioedema are very high risk, and obtaining a definitive airway is imperative.,,,Epinephrine is given through intramuscular injection and at a dose of 0.3 to 0.5 mL of 1 : 1, 000 concentration of epinephrine. Pediatric dosing is 0.01 mg/kg or 0.15 mg intramuscularly (IM) (epinephrine injection for pediatric dosage). Intramuscular delivery has proven to provide more rapid delivery and produce better outcomes than subcutaneous or intravascular. Note if intravenous (IV) epinephrine is to be given, the concentration required is 1 : 10, 000, see the next paragraph. The thigh is preferred to the deltoid when possible. Repeat studies have shown that providers often wait too long before giving epinephrine, it is the treatment of choice and the rapid benefit much outweighs the risks of withholding treatment. While most patients require only a single dose, repeat doses may be given every 5 to 10 minutes as needed until symptoms improve.,,Anaphylaxis induces a distributive shock that typically is responsive to fluid resuscitation and the above epinephrine. One to 2 L or 10 to 20 mL/kg isotonic crystalloid bolus should be given for observed hypotension. Albumin or hypertonic solutions are not indicated.,Corticosteroids are given for the reduction of length or biphasic response of anaphylaxis., Pathophysiology : Anaphylaxis is typically an IgE-mediated (type 1) hypersensitivity reaction that involves the release of numerous chemical mediators from the degranulation of basophils and mast cells after re-exposure to a specific antigen. IgE crosslinking and resultant aggregation of high-affinity receptors induce the rapid release of stored chemical mediators. These chemical mediators include histamine, tryptase, carboxypeptidase A, and proteoglycans. Via activation of phospholipase A, cyclooxygenases, and lipoxygenases they then form arachidonic acid metabolites including leukotrienes, prostaglandins, and platelet-activating factors. The inflammatory response is then mediated by TNF-alpha (tumor necrosis factor), both as a preformed and late-phase reactant. The detailed physiology of these chemical mediators is as follows : Histamine increases vascular permeability and vasodilation leading to hypoperfusion of tissues. The body responds to these changes by increasing heart rate and cardiac contraction.Prostaglandin D functions as a bronchoconstrictor, with simultaneous cardiac and pulmonary vascular constriction. It also potentiates peripheral vasodilation thus contributing to the hypo-perfusion of vital organs.Leukotrienes add to bronchoconstriction, vascular permeability, and induce airway remodeling.The platelet activation factor also acts as a bronchoconstrictor and increases vascular permeability.TNF-alpha activates neutrophils (as part of stress response leukocytosis) and increases chemokine synthesis., Epidemiology : 0.05-2 % in the USA and ~3 % in Europe, 40–500 per million person-years, variable, If you have severe allergies, make sure you carry an epinephrine injection wherever you go.,,Take steps to avoid your triggers : ,,Food : Read food labels carefully. Ask restaurants what ingredients are in their dishes and how they prepare them. (Sometimes, restaurants may prepare an allergen-free dish in the same pot or pan as an ingredient you’re allergic to.),Medications : Tell all healthcare providers if you’re allergic to any medications and if you’ve had allergic reactions in the past. They can make sure to prescribe a safe alternative for you and avoid anything you may be allergic to.,Insect stings : Don’t walk barefoot in the grass. It’s also smart not to drink from open cans since insects can lurk around the opening. Try to avoid wearing bright, flowery clothing or perfumes, hairsprays and lotions that could attract insects., Complications : death, stridor, Hypotension, Diagnostics : SERUM HISTAMINE LEVEL, SERUM SPECIFIC IgE TESTING, SERUM TRYPTASE, Differential diagnosis : acute myocardial infarction, angioedema, anxiety, Arrhythmias, Asthma, Epiglottitis, foreign body, panic attacks, disease description : Anaphylaxis is a severe, potentially life-threatening allergic reaction. It can occur within seconds or minutes of exposure to something youre allergic to, such as peanuts or bee stings. |
Anaphylactoid Reactions | Disease Name : Anaphylactoid Reactions, Treatment : Airway-Airway management is paramount. Thoroughly examine the patient for airway patency or any indications of an impending loss of airway. Perioral edema, stridor, and angioedema are very high risk, and obtaining a definitive airway is imperative.,,,Epinephrine is given through intramuscular injection and at a dose of 0.3 to 0.5 mL of 1 : 1, 000 concentration of epinephrine. Pediatric dosing is 0.01 mg/kg or 0.15 mg intramuscularly (IM) (epinephrine injection for pediatric dosage). Intramuscular delivery has proven to provide more rapid delivery and produce better outcomes than subcutaneous or intravascular. Note if intravenous (IV) epinephrine is to be given, the concentration required is 1 : 10, 000, see the next paragraph. The thigh is preferred to the deltoid when possible. Repeat studies have shown that providers often wait too long before giving epinephrine, it is the treatment of choice and the rapid benefit much outweighs the risks of withholding treatment. While most patients require only a single dose, repeat doses may be given every 5 to 10 minutes as needed until symptoms improve.,,Anaphylaxis induces a distributive shock that typically is responsive to fluid resuscitation and the above epinephrine. One to 2 L or 10 to 20 mL/kg isotonic crystalloid bolus should be given for observed hypotension. Albumin or hypertonic solutions are not indicated.,Corticosteroids are given for the reduction of length or biphasic response of anaphylaxis., Pathophysiology : Anaphylactoid reactions are derived from the activation of the complement and/or bradykinin cascade and the direct activation of mast cells and/or basophils. The clinical symptoms of these reactions are similar and indistinguishable from anaphylaxis, and sometimes severe, leading to cardiovascular collapse and death., Epidemiology : lifetime prevalence of 0.05–2%, 3–50 per 100, 000, variable, Complications : death, Hypotension, Diagnostics : Skin test, SERUM TRYPTASE, Differential diagnosis : Arrhythmias, infection, Mastocytosis, Metabolic disorders, Myocardial infarction, disease description : Anaphylaxis is a severe, potentially life-threatening, generalized, or systemic hypersensitivity reaction that results from the sudden release of mediators derived from mast cells and basophils via degranulation . Drugs are the most common anaphylaxis triggers in adults representing up to 10% of overall causes in outpatient studies , whereas for emergency department and hospitalized patients the proportion ranges from 27–60% |
Anaphylaxis | Disease Name : Anaphylaxis, Treatment : medication : Adrenaline (Epinephrine), TOLERANCE INDUCTION & DESENSITIZATION, oxygen supply alone can be helpful, Pathophysiology : Many of the important early mediators of anaphylaxis are derived from
mast cells, basophils, and eosinophils. Mast cells and basophils contain
preformed granules comprised of histamine, proteases (tryptase,
chymase), proteoglycans (heparin, chondroitin sulfate), and TNF-a,
which are rapidly released into surrounding tissue upon cell activation,
a process known as degranulation. Mast cells, basophils, and eosinophils
are also sources of arachidonic acid-derived products which
include cysteinyl leukotrienes, prostaglandins, and platelet activating
factor (PAF). Histamine release results in flushing, urticaria, pruritus,
and, in high concentrations, hypotension and tachycardia. Cysteinyl
leukotrienes and prostaglandin D2 cause bronchoconstriction and
increased microvascular permeability. Prostaglandin D2 causes cutaneous
flushing, and attracts eosinophils and basophils to the site of mast
cell activation. Serum PAF levels correlate with anaphylaxis severity
and are inversely proportional to the constitutive level of PAF acetylhydrolase,
which is necessary for PAF inactivation. Tryptase and chymase
can activate complement and coagulation pathways. Activation of these
pathways results in production of the anaphylotoxins, C3a and C5a, and
activation of the kallikrein-kinin system which regulates blood pressure
and vascular permeability. The actions of these anaphylactic mediators
are likely additive or synergistic at the target tissues.
Non-IgE-mediated reactions to certain drugs (which may occur upon
the first exposure) can mimic the pathophysiology of IgE-dependent anaphylaxis
due to a similar profile of mediators. For example, paclitaxel is a chemotherapy agent derived from yew tree bark and needles that 2507
requires polyethoxylated castor oil (Cremophor) to be solubilized into
aqueous solution. Cremophor directly activates the complement cascade,
resulting in complement-dependent induced histamine release
from mast cells and basophils. A version of paclitaxel that is solubilized
by being bound to albumin nanoparticles, Abraxane, has a far lower
rate of hypersensitivity, especially for patients who have had infusion
reactions to Cremophor-solubilized paclitaxel. Reactions to radiocontrast
and vancomycin are other examples of non-IgE-mediated
hypersensitivity. Opiates and NSAIDs are other drug categories that
can have similar adverse reactions., Epidemiology : GOODD, To Do : trigger is an occupational exposure, hymenoptera sting, ,a common food (i.e., peanut), or a drug representing the sole or best,therapeutic option for the patient, Complications : bronchospasm, laryngospasm, respiratory difficulties, Diagnostics : Complete Blood Count CBC, EOSINOPHILS - ABSOLUTE COUNT, serum IgE level, SERUM TRYPTASE, Differential diagnosis : acute anxiety, acute asthma, hereditary or idiopathic angioedema, panic attacks, syncope, Urticaria, disease description : Anaphylaxis is a potentially life-threatening systemic allergic reaction
involving one or more organ systems that typically occurs within
seconds to minutes of exposure to the anaphylactic trigger, most often
a drug, food, or hymenoptera sting. Other triggers of anaphylaxis
include radiocontrast administration or latex exposure. The term
“anaphylaxis” was first described in 1902 by Charles Richet and Paul
Portier who attempted to immunize dogs against sea anemone toxin
in the same way Pasteur was able to vaccinate individuals against the
smallpox virus. To their surprise, repeated administration of small,
sub-lethal doses of sea anemone toxin reliably induced acute-onset
death when re-administered 2–3 weeks after initial “vaccination” to
the toxin. The phenomenon was termed ana (anti)-phylaxis (“protection
or guarding”) because vaccination with anemone toxin resulted in
the opposite intended immune effect. Charles Richet was awarded the
Nobel Prize in Physiology or Medicine in 1913 for this work which led
to further insights into hypersensitivity and mast cell biology. |
Anaplasmosis | Disease Name : Anaplasmosis, Treatment : Doxycycline is the first-line treatment for anaplasmosis in adult and pediatric cases. A 14-day to the 21-day course is recommended or continuation of antibiotics for a minimum of 3 days after defervescence. For patients co-infected with Lyme disease (known or suspected), therapy should be continued for 10 days.,,To prevent tooth discoloration, pediatric patients younger than 8 years of age co-infected with Borrelia burgdorferi should remain on doxycycline until they have been afebrile for 3 days. They should then switch to an active agent against the pathogen, for example, amoxicillin or cefuroxime, for the remainder of the 14-day course., Pathophysiology : Anaplasma phagocytophilum is an obligate intracellular bacteria that survives and propagates within the host cell and can evade neutrophil antimicrobial functions. A. phagocytophilum infection is acquired through a tick bite and disseminates to the bone marrow and spleen. A. phagocytophilum can selectively survive and multiply within cytoplasmic vacuoles of polymorphonuclear cells. It affects the progenitors of myeloid and monocytic lineages, and it is seen in neutrophils in peripheral blood and tissue. The presence of Anaplasma in neutrophils induces proinflammatory responses leading to neutrophil deactivation, and the release of cytokines promotes neutrophil degranulation. Interleukin-10, IL12, and IFN-gamma are among the cytokines released which contribute to continuous tissue injury. IFN-gamma is primarily produced by innate immune NK and NKT cells as well as CD8 T lymphocytes. The development of tissue injury prevents neutrophils from exerting effective antimicrobial response. These cytokine-driven mechanisms as a response to infection explain the clinical manifestations associated with human granulocytic anaplasmosis. Clinical cases may present with fever, pancytopenia, liver dysfunction or more severe manifestations such as shock or organ failure.In animal models, A. phagocytophilum infection-induced IFN-gamma production which also activates macrophages and increases inflammatory tissue injury. Further, Anaplasma also can inhibit the fusion of lysosomes with the cytoplasmic vacuoles and inhibiting signaling pathways responsible for respiratory burst. Other effects of Anaplasma include downregulation of phagocyte oxidase activity, delay in apoptosis, ineffective binding to and transmigration of activated endothelium, and inhibition of phagocytosis., Epidemiology : In the 10 year period between 2000 through 2010, cases increased from 346 to 1761 with estimates of 1.4 to 6.1 cases per million., variable, Prevent illness by preventing tick bites, preventing ticks on your pets, and preventing ticks in your yard. Ticks live in grassy, brushy, or wooded areas, or even on animals, so spending time outside camping, gardening, or hunting will bring you in close contact with ticks., Complications : inflammation, tissue damage, Diagnostics : Peripheral Blood Smear, LIVER FUNCTION TEST LFT, SEROLOGIC TEST, CT SCAN, Differential diagnosis : Babesiosis, Colorado tick fever, "lymes disease", relapsing fever, Rocky Mountain spotted fever, tularemia, disease description : Anaplasma phagocytophilum is a gram-negative intracellular bacteria that causes an acute febrile illness known as anaplasmosis or human granulocytic anaplasmosis (HGA). Anaplasmosis generally presents with nonspecific symptoms such as fever, chills, malaise, headache, and myalgia. On rare occasions, a rash may be present. Patients may also report nonspecific gastrointestinal or respiratory symptoms. A minority of patients will develop life-threatening complications. |
Anaplastic Astrocytoma | Disease Name : Anaplastic Astrocytoma, Treatment : Grade III (anaplastic astrocytoma or oligoastrocytoma),,Standard of care : surgical resection followed by EBRT (60 Gy in 30 to 35 fractions) and adjuvant temozolomide, 75 mg/m^2/day orally on days 1 to 42, usually 1 to 1.5 hours before radiation,Post–radiation therapy : Continue temozolomide at higher doses of 150 to 200 mg/m^2/day PO on days 1 to 5 every 28 days or,PCV (procarbazine, lomustine, vincristine) : lomustine (CCNU) 90 to 130 mg/m^2 PO on day 1 plus procarbazine 60 to 75 mg/m^2 PO on days 8 to 21 plus vincristine 1.4 mg/m^2 IV (not to exceed 2 mg/dose) on days 8 and 29; administer every 6 weeks for up to 4 cycles with deferred radiotherapy, Total microsurgical excision, Pathophysiology : The local effects of astrocytoma are a result of multiple mechanisms. These include direct invasion and competition for oxygen, leading to hypoxic injury to normal brain parenchyma. Apart from this, free radicals, neurotransmitters, and inflammatory mediators are also responsible for disturbing the homeostasis. The mass effect due to the tumor is also responsible for the various clinical signs and symptoms., Epidemiology : 34%, variable, Unlike some other cancers, however, most gliomas happen without previous warning and, as of now, there are no known prevention methods., Complications : seizures, VISION DEFICITS, Glioblastoma multiforme, Diagnostics : MRI Brain, CT SCAN, Differential diagnosis : Brain Abscess, ENCEPHALITIS, Glioblastoma multiforme, Multiple Sclerosis, oligodendroglioma (who grade 2), Toxoplasmosis, disease description : Astrocytoma originates in astrocytes, which are a kind of glial cells in the cerebrum which are star-shaped. It is the most common glioma, usually affecting the brain and sometimes the spinal cord. |
Anaplastic Carcinoma Of Thyroid | Disease Name : Anaplastic Carcinoma Of Thyroid, Treatment : Adriamycin as chemotherapy., External-beam irradiation is effective in improving local control. For patients with locally advanced unresectable disease, definitive radiation therapy and chemotherapy are the recommendations. Adjuvant radiation therapy should be performed in all cases, including completely resected small-size incidental anaplastic thyroid carcinoma and anaplastic thyroid carcinoma with a differentiated component.,,Anaplastic thyroid carcinoma is usually not responsive to I131 therapy. Radioiodine is only a recommendation upon identification of a differentiated iodine-positive component. New insights into biological behavior and the genetic and molecular pathogenesis of anaplastic thyroid carcinoma might offer novel targeted therapies., Surgery,,Debulking surgery is the most common procedure in anaplastic thyroid carcinoma. It consists of removing any gross tumor that is potentially threatening the airway with the aim of preserving the larynx. However, a tracheostomy may be necessary in cases of airway compromise. While complete excision is often impossible due to the local extension of the disease, the quality of resection is a significant prognostic factor for surviva, Pathophysiology : Approximately 20 percent of patients with ATC have a history of differentiated thyroid cancer. Up to 30 percent of ATC may have associated synchronous differentiated cancer. The majority of the synchronous thyroid tumors are papillary cancer, but follicular types have also been reported. The transformation from differentiated to anaplastic cancer has also been described. Tp53 gene inactivation may play an important role in the progression from differentiated to undifferentiated carcinoma. Thyroid-specific rearrangements RET/PTC and PAX8/PPAR? are rarely found in poorly differentiated or undifferentiated thyroid cancer, suggesting that these genetic alterations do not predispose cells to dedifferentiationCytogeneticsThe cytogenetics are often complex and show progressive accumulation of chromosomal alterations (numerical and structural aberrations). The following gene mutation is commonly reported in ATC : p53 (most common), RAS, BRAF, ß-catenin, PIK3CA, Axin, APC, and PTEN., Epidemiology : incidence is about 0.6 per million of the population, poor, Unfortunately, in most cases, anaplastic thyroid cancer (ATC) can’t be prevented.,,If you’ve been diagnosed with goiter or a benign (noncancerous) thyroid nodule, it’s important to see your healthcare provider regularly to monitor the health of your thyroid. ATC can sometimes develop from other types of thyroid cancer and/or goiter., Complications : METASTASES AT DIFFERENT SITES, Diagnostics : FNAC, HISTOPATHLOGY, Thyroid Stimulating Hormone TSH, TISSUE BIOPSY, USG Thyroid, THYROID SCAN, RADIO IODINE UPTAKE SCAN, CECT NECK, CECT THORAX, CT SCAN, Differential diagnosis : CHRONIC LYMPHOCYTIC(AUTOIMMUNE) THYROIDITIS, medullary carcinoma, PARATHYROID CARCINOMA, THYROID NODULE, disease description : The vast majority of primary malignancies are carcinomas derived from the follicular cells. Such tumors were thought of as differentiated (papillary, follicular and Hürthle cell) and undifferentiated (anaplastic). However, now an intermediate class of ‘poorly differentiated carcinoma’
is recognised, which is likely to represent a state of dedifferentiated,
between classic differentiated and undifferentiated diseases. The parafollicular C cells can undergo malignant transformation into medullary carcinoma, and thyroid lymphoma is another primary thyroid malignancy. In addition, the thyroid can be involved by direct spread from surrounding structures (larynx and oesophagus) or metastases (most
commonly from renal cell carcinoma). Lymph node and blood-borne metastases of thyroid cancer occur primarily to bone and lung and may be the mode of presentation |
Anaplastic Ependymoma (who Grade 3) | Disease Name : Anaplastic Ependymoma (who Grade 3), Treatment : "Chemotherapy uses drugs to kill cancer cells. Chemotherapy isnt very effective for most cases of ependymoma", During radiation therapy, your child lies on a table while a machine moves around him or her, directing beams to precise points in the brain, Radiosurgery is sometimes used when an ependymoma recurs after surgery and radiation., The goal is to remove the entire tumor, but sometimes the ependymoma is located near sensitive brain or spinal tissue that makes that too risky., Pathophysiology : Based on genetic mutations and variations, ependymomas are classified as follows : Posterior fossa (PF) : PF-EPN-SE (subependymoma)PF-EPN-B (group B)PF-EPN-A (group A)Supratentorial (ST) : ST-EPN-SE (subependymoma)ST-EPN-YAP1 (YAP1 fusions)ST-EPN-RELA (RELA fusions)Spinal ependymomas : SP-EPN-MPE (myxopapillary)SP-EPN-SE (subependymoma)SP-EPN, Epidemiology : 2%, Approximately 1, 100 adults are diagnosed with ependymoma per year., e 5-year survival rate for ependymoma is 83.9%, There is no way to prevent ependymoma, Complications : fatigue, Numbness, Sleep disturbances, Pain, SENSORINEURAL HEARING LOSS, Diagnostics : HISTOPATHLOGY, MRI, MRI, Differential diagnosis : anaplastic astrocytoma, choroid plexus carcinoma (who grade 3), choroid plexus papilloma (who grade 1), ependymoma, Glioblastoma multiforme, medulloblastoma, Metastatic tumours, disease description : Grade III Often cerebrum or cerebellum of children / young adults but all ages and locations.Infiltrates leptomeninges, spreads along CSF pathways like medulloblastoma. Grade III ependymomas are malignant (cancerous). This means they are fast-growing tumors. The subtypes include anaplastic ependymomas. These most often occur in the brain, but can also occur in the spine. |
Anaplastic Ependymoma | Disease Name : Anaplastic Ependymoma, Treatment : Surgery is the crucial initial treatment in both children and adults. In pediatric patients with intracranial ependymomas of WHO grades II or III, surgery is followed by local radiotherapy regardless of residual tumor volume., Pathophysiology : Single cell sequencing across all major molecular ependymoma groups revealed hierarchical cellular populations, including undifferentiated neural stem cells, radial glia cells and more differentiated cells towards ependymal, astrocytic and neuronal lineagesProportion of undifferentiated or less differentiated cells correlates with poor prognosis and increased recurrenceAuthors suggest that aberrant radial glia-like cells are potential cells of origin for supratentorial ependymoma, with C11orf95-RELA fusions and neural stem cell-like cells the origin of posterior fossa ependymoma, Epidemiology : (0.43 cases per 100 000, The relative 5-year survival rate for ependymoma i, Because experts don’t know what causes ependymomas, there’s no way to prevent them. See your healthcare provider right away if you develop any symptoms that could point to an ependymoma. Treating a tumor is often easier when it’s in the early stages of development., Complications : fatigue, neurological deficit, Numbness, SENSORINEURAL HEARING LOSS, growth abnormality, Diagnostics : MRI, CT SCAN, Differential diagnosis : choroid plexus carcinoma (who grade 3), Embryonal carcinoma, medulloblastoma, disease description : Anaplastic ependymoma is a type of ependymoma, which is a tumor that forms when cells in the central nervous system (including the brain and spinal cord) begin to multiply rapidly. An ependymoma is anaplastic if the cells grow very quickly and are significantly unusual in shape. Ependymomas can occur at any age. When ependymomas occur in children, they are more frequently located in the brain (intracranial). Ependymomas are more often found in the spinal cord of affected adults. |
Anaplastic Ganglioglioma | Disease Name : Anaplastic Ganglioglioma, Treatment : chemotherapy with temozolomide, Subtotal surgical resection with chemoradiotherapy, Pathophysiology : Pathologically, these tumors are graded by the degree of malignancy in their glial portion and radiologic diagnosis is difficult due to the wide variation in its degree of solid and cystic components, contrast uptake, and calcification patterns, Epidemiology : < 2% of all brain tumors, Three- and 5-year tumor recurrence ., Unfortunately, you can’t prevent a brain tumor. You can reduce your risk of developing a brain tumor by avoiding environmental hazards such as smoking and excessive radiation exposure.,,If you have a first-degree biological relative (sibling or parent) who has been diagnosed with a brain tumor, it’s important to tell your healthcare provider. They may recommend genetic counseling to see if you have an inherited genetic syndrome that’s associated with brain tumors., Complications : Metastasis, local recurrence, Diagnostics : NEUROIMAGING, CT SCAN, ELECTRON MICROSCOPY, Immunostaining, Differential diagnosis : desmoplastic infantile astrocytoma and ganglioglio, gangliocytoma, Hypothalamic hamartoma, oligodendroglioma (who grade 2), pleomorphic xanthoastrocytoma (who grade 2), disease description : Gangliogliomas are rare tumors of the central nervous system that are thought to arise from a glioneuronal precursor and consist of both neuronal and glial elements. Grade III, or anaplastic ganglioglioma (AGG), most commonly affects children and young adults, generally arises in a supratentorial location, is highly epileptogenic, and often results in diffuse local and distant failure within the craniospinal axis.Well differentiated neuroepithelial tumors composed of neoplastic ganglion cells (gangliocytoma) or combination of neoplastic ganglion cells and neoplastic glial component (ganglioglioma). |
Anaplastic Meningioma | Disease Name : Anaplastic Meningioma, Treatment : . After surgery, radiation is often recommended to delay the return of grade II and III meningiomas., the goal of surgery is to obtain tissue to determine the tumor type and to remove as much tumor as possible without causing more symptoms for the person., Pathophysiology : Originates from arachnoid border cells or dural based cells The driver genetic event in most cases is NF2 inactivation by mutation or chromosome 22q lossProgression from lower grade meningioma follows pTERT mutation, CDKN2A / CDKN2B homozygous deletion, loss of chromosomes 9p, 1p, 6q, 10, 14q, 18q, gains of chromosomes 1q, 9q, 12q, 15q, 17q, 20, Epidemiology : 2.3–8.3 in 100, 000, he 5-year survival rate for malignant meningioma i, There is no known way to prevent meningiomas., Complications : seizures, weakness, Personality change, Language difficulties and learning disabilities., Difficulty concentrating, Diagnostics : HISTOPATHLOGY, MRI, Differential diagnosis : Glioblastoma multiforme, lymphoma, recurrent or progressive malignant gliomas, disease description : A meningioma with overtly malignant cytomorphology that can resemble a carcinoma, melanoma or high grade sarcoma .A meningioma is a primary cns tumor. This means it begins in the brain or spinal cord. Overall, meningiomas are the most common type of primary brain tumor. However, higher grade meningiomas are very rare. |