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Chancroid

Disease Name : Chancroid, Treatment : medication : Ceftriaxone , Azithromycin , Ciprofloxacin , Erythromycin , Prompt antibiotic treatment is essential to reduce the risk of ,complications as well as the risk of acquisition and onward ,transmission of HIV. Partner notification should be undertaken.,Single-dose treatment with either ciprofloxacin or azithromycin ,or ceftriaxone are associated with cure rates in excess of 90%. ,Single-dose regimens have the advantage of ensuring compliance.,First line,•\tAzithromycin 1 g orally in a single dose,Or,•\t Ceftriaxone 250 mg IM in a single dose,Second line,•\t Ciprofloxacin 500 mg orally twice a day for 3 days,Or,•\tErythromycin base 500 mg orally four times a day for ,7 days, Pathophysiology : It has been experimentally demonstrated that inoculation with one colony-forming unit of Haemophilus ducreyi results in papule formation in 50% of individuals. This increases to papule formation in 90% of individuals after inoculation with 100 CFU.  Gene clusters have been noted in H. ducreyi,  which encode for a cytolethal distending toxin similar to those found in invasive enteric bacteria such as Campylobacter, Shigella, and Escherichia coli. This toxin causes irreversible cell cycle death of epithelial cells and may lead to the development of skin breakdown and subsequent ulcer development ., Epidemiology : highest prevalence among women in the United States, global incidence of chancroid to be approximately 6 million cases per year, Left untreated, patients may develop complications, There some things you can do to reduce your risk of developing chancroid, including : ,,Abstaining from sex completely.,Having sex with only one uninfected partner.,Having safe sex by using condoms for oral, vaginal and anal sex. The condoms must cover any infected area.,Making sure pus from any infected area doesn’t touch you. If you have a soft chancre, make sure you don’t transfer any pus to another place on your body or to another person., Complications : PHIMOSIS, ulceration, DEFORMITY, Diagnostics : Bacteria Culture Test, PCR, Differential diagnosis : HERPES SIMPLEX, HIV infection and AIDS, Syphilis, disease description : Chancroid is a bacterial condition that causes open sores on or around the genitals . It is an exceedingly rare sexually transmitted infection, both in the United States and globally. Understanding its true prevalence is made difficult by the lack of readily available diagnostic testing and similar presentation to other more common causes of genital ulcer diseases.

Chediak Higashi Syndrome

Disease Name : Chediak Higashi Syndrome, Treatment : The only cure is an allogeneic hematopoietic stem cell transplantation (HSCT). Therefore, HSCT should be done as soon as the diagnosis is established., Ocular symptoms,,Visual acuity might be improved by correcting refractive errors.,Sunglasses should be worn for protecting sensitive eyes against UV rays.,(c) Hypopigmentation : Individuals must wear sunscreen to prevent skin cancers and sun damage. The degree of protection depends on the severity of hypopigmentation.,,(d) Neurological manifestation : since the symptoms are progressive in nature, rehabilitation should be started for older patients as early as possible during the course of the disease., Pathophysiology : The mutation of the lysosomal trafficking regulator  (LYST) gene or Chediak-Higashi syndrome  (CHS1) gene disrupts the protein synthesis and affects the storage and secretory functions of lysosomal granules of leukocytes, fibroblasts, dense bodies of platelets, azurophilic granules of neutrophils, and melanosomes of melanocytes. The defects result in enlarged vesicles and non-functional lysosomes .On cytology, large, fused, azurophilic granules can be seen mainly in the granulocytes and monocytes but also can be noted in the fibroblasts, Schwann cells,   astrocytes, melanocytes, and hematopoietic cells. These granules are made up of an abnormal fusion between the primary granules (azurophilic) and the secondary granules (specific).  Lymphocytes containing these large granules function poorly in the antibody-dependent, cell-mediated cytolysis. Patients also exhibit alterations in the neutrophils, leading to neutropenia, impaired chemotaxis, and delayed phagolysosomal fusion which, in turn, leads to an impaired bactericidal activity. It also was seen that the functions of the natural killer cells also were reduced ., Epidemiology : The exact prevalence is unknown., ABOUT 200 cases of the condition have been reported worldwide, POOR, Education of the child and caregivers regarding effective hygiene, Complications : Bruising, Bleeding disorders, Diagnostics : BONE MARROW ASPIRATION, Peripheral Blood Smear, GENETIC TESTING, CYTOLOGY, Differential diagnosis : Cutaneous T-cell lymphoma, Oculocutaneous albinism (OCA), pancytopenia, pyoderma gangrenosum, disease description : Chediak Higashi syndrome (CHS) is a rare autosomal recessive condition that was initially described by Beguez-Cesar in1943. Chediak in 1952 and Higashi in 1954 then discovered the maldistribution of myeloperoxidases in the granules of the neutrophils in affected patients. It is characterized by oculocutaneous albinism, easy bruising, abnormal functions of the natural killer cells, and recurrent pyogenic infections and is a result of a mutation in the lysosomal trafficking regulator (LYST) gene. The presence of abnormally large intracytoplasmic granules, especially in white blood cells and bone marrow, is diagnostic. 

Cheilitis

Disease Name : Cheilitis, Treatment : . Topical corticosteroids or pimecrolimus will often ,give symptomatic relief but the offending substance should be ,identifi ed and avoided., Pathophysiology : nan, Epidemiology : To Do : .you can lower your risk of becoming infected with RBF and other rodent diseases by avoiding direct contact with rodents, places with rodent infestations, or other areas where rodents may be present.,.Wear protective gear, such as gloves.,.Avoid touching your mouth and face after handling rodents..,.Wash your hands with soap and warm water for at least 20 seconds after handling rodents, their cages, bedding, urine, or droppings.,.If you are bitten or scratched, immediately clean the wound with soap and warm water.,.wash hands and face after contact and any scratches should be cleaned, and antiseptics applied., Complications : hyperpigmentation, Diagnostics : Patch Test, Differential diagnosis : nan, disease description : Cheilitis may arise as a primary disorder of the vermilion zone or the inflammation may extend from nearby skin or, less often, from the oral mucosa. Contact cheilitis Contact cheilitis is an inflammatory reaction provoked by the irritant or sensitizing action of chemicals. Most cases are caused by the deliberate application of lipsticks or lipsalves but many substances have been incriminated, sometimes from accidental contact with an offending substance. Causes of cheilitis • Chapping due to cold and wind • Eczematous cheilitis • Contact cheilitis • Drug-induced cheilitis (retinoids, voriconazole) • Infective cheilitis • Angular cheilitis • Ultraviolet irradiation • Actinic cheilitis • Actinic prurigo of the lip • Glandular cheilitis • Granulomatous cheilitis • Exfoliative (factitious) cheilitis • Plasma cell cheilitis • Nutritional cheilitis • Dermatoses • Trauma

Chemical Injuries To Eye

Disease Name : Chemical Injuries To Eye, Treatment : medication : Acetazolamide, Timolol , Doxycycline , Vitamin C/Ascorbic Acid, Moxifloxacin , Sodium Citrate (Trisodium Citrate), 1. Prevent further damage by following measures : ,• Immediate and thorough irrigation with the,available clean water or saline delivered through,an IV tubing. Deliver minimum of 2 L of water in,20–30 minutes or until pH is restored.,2. Maintenance of favourable conditions for rapid and,uncomplicated healing by following measures : ,• Topical antibiotic drops, e.g., moxifloxacin 4–6,times a day to prevent infection.,• Steroid eye drops to reduce inflammation, ,neutrophil infiltration, and address anterior uveitis.,• Cycloplegics, e.g., atropine, may improve the,comfort.,• Ascorbic acid, in the form of 10% sodium ascorbate,eyedrops (4–5 times), along with systemic use (1–2 gm orally/day) improves wound healing and,promotes synthesis of the mature collagen by,corneal fibroblasts, • Lubricant eyedrops, • Autologous serum, instilled as eyedrops, provides,growth factors, collagenase inhibitors, retinoic acid, ,fibrinogen activator and promotes epithelial healing, • Sodium citrate, used as 10% topical eyedrops,stabilizes neutrophils and reduces collagenase,release, • Doxycycline, 100 mg BD, chelates zinc which is,necessary for collagenase., Pathophysiology : These usually occur due to external contact with chemicals under following circumstances : 1. Domestic accidents, e.g., with ammonia, solvents, detergents and cosmetics. 2. Agricultural accidents, e.g., due to fertilizers, insecticides, toxins of vegetable and animal origin. 3. Chemical laboratory accidents, with acids and alkalies. 4. Deliberate chemical attacks, especially with acids to disfigure the face. 5. Chemical warfare injuries. 6. Self-inflicted chemical injuries are seen in malingerers and psychopaths. Types of chemical injuries In general, the serious chemical burns mainly comprise alkali and acid burns. A. Alkali burns Alkali burns are among the most severe chemical injuries known to the ophthalmologists. Common alkalies responsible for burns are : lime, caustic potash or caustic soda and liquid ammonia (most harmful). Mechanisms of damage produced by alkalies includes : 1. Alkalies dissociate and saponify fatty acids of the cell membrane and, therefore, destroy the structure of cell membrane of the tissues. 2. Being hygroscopic, they extract water from the cells, a factor which contributes to the total necrosis. 3. They combine with lipids of cells to form soluble compounds, which produce a condition of softening and gelatinisation. The above effects result in an increased deep penetration of the alkalies into the tissues. Alkali burns, therefore, spread widely, their action continues for some days and their effects are difficult to circumscribe. Hence, prognosis in such cases must always be guarded. B. Acid burns Acid burns are less serious than alkali burns. Common acids responsible for burns are : sulphuric acid, hydrochloric acid and nitric acid. Chemical effects. Strong acids cause instant coagulation of all the proteins which then act as a barrier and prevent deeper penetration of the acids into the tissues. Thus, the lesions become sharply demarcated. Ocular lesions include : 1. Conjunctiva. There occurs immediate necrosis followed by sloughing. Later on, symblepharon is formed due to fibrosis. 2. Cornea. It is also necrosed and sloughed out. The extent of damage depends upon the concentration of acid and the duration of contact. • In mild to moderate degree of corneal burns end result is corneal opacification of varying degree. • In severe cases, the whole cornea may slough out followed by staphyloma formation., Epidemiology : between 11.5%-22.1% of ocular traumas, POOR, Always wear appropriate safety goggles or a face shield when handling liquid or powder chemicals.,. For splashes of non-toxic liquids, such as soaps or shampoos, flushing the eye with fresh water is usually all the treatment you need ., Complications : cataract, Glaucoma, corneal ulceration, Symblepharon, Diagnostics : VISUAL ACUITY TEST, ophthalmoscopy, Differential diagnosis : corneal abrasions, CORNEAL LACERATION, Intraocular foreign body, RUPTURED GLOBE, uveitis, disease description : Chemical injuries are by no means uncommon. These vary in severity from a trivial and transient irritation of little significance to complete and sudden loss of vision. These usually occur due to external contact with chemicals under following circumstances : 1. Domestic accidents, e.g., with ammonia, solvents, detergents and cosmetics. 2. Agricultural accidents, e.g., due to fertilizers, insecticides, toxins of vegetable and animal origin. 3. Chemical laboratory accidents, with acids and alkalies. 4. Deliberate chemical attacks, especially with acids to disfigure the face. 5. Chemical warfare injuries. 6. Self-inflicted chemical injuries are seen in malingerers and psychopaths.

Cherry Angiomas

Disease Name : Cherry Angiomas, Treatment : cryosurgery, electrosurgery, or curettage have been employed in the treatment of cherry hemangioma, more recently, pulsed dye laser or intense pulsed light has been used with success. Krypton and 532 nm diode lasers work very well in eradicating these lesions., pulsed dye laser and intense pulsed,light, Treatment for smaller lesions includes local anesthesia with 1% lidocaine, followed by electrocauterization. Larger lesions are often treated with shave excision, with electrocauterization of the base. In addition, cryotherapy may be employed. Superficial lesions may also be treated with CO2 laser therapy., Pathophysiology : Cherry angiomas mostly appear with age. Although they are found to have an association with some malignancies, they are mostly developed in healthy individuals. These lesions begin as bright red, flat macules and grow to become 1 to 5 mm red papules. They are usually asymptomatic but can bleed with trauma. They can appear on both sun-exposed and unexposed skin but usually spare mucous membranes. These lesions are present in the dermal papillae, and they consist of tortuous and spherical dilatations of capillary loops.It has been noted that the color of the cherry angiomas changes with hypoxia; they become blue rather than red. The small spots are noted to turn blue sooner than the larger ones. Once the patient is restored to cardiovascular stability, the lesions revert to their ruddy red color., Epidemiology : 50% of adults have cherry angiomas on their skin after age 30, increases with age in both sexes and all races, prognosis for most patients is excellent, Since the direct cause of cherry angiomas is unknown, there isn’t a prevention tip that’s 100% successful. It’s recommended that you avoid specific chemicals or treatments, including topical nitrogen mustard, bromides and butoxyethanol, which are known to cause cherry angiomas., Complications : bleeding, Scarring, Diagnostics : skin lesion biopsy, Differential diagnosis : angiokeratomas, BACILLARY ANGIOMATOSIS, Blue rubber bleb naevus syndrome, infantile haemangiomas, Pyogenic granulomas, disease description : Cherry hemangiomas are common benign cutaneous vascular proliferations. They are also known as cherry angiomas, adult hemangiomas, or senile angiomas as their number tends to increase with age .Cherry angiomas are made of small blood vessels, which gives them a reddish or purplish appearance. They most commonlyTrusted Source occur in older adults, but for some people, they may appear in their 20s or earlier. Around 5% of adolescents develop them. 

Chest Wall Hamartoma

Disease Name : Chest Wall Hamartoma, Treatment : En bloc resection is curative, but the large residual chest wall defect can frequently result in scoliosis, Its early and complete excision is the adequate therapy to avoid lethal respiratory complications and more aggressive treatments, although there is recommendation for conservative management in asymptomatic cases., Pathophysiology : Typically, these lesions arise from the central portions of one or several ribs, and can range in size from several centimeters to very large expansile lesions involving most of the thoracic cage. Radiological findings on chest x-ray, CT, and MRI are usually quite typical.Histologically, the lesion is composed of cartilage, smooth muscle, and respiratory epithelium forming a disorderly mass. The stroma consists of oval or spindle mesenchymal cells with no atypia or abnormal mitotic activity. Osteoclast-like giant cells in the vicinity of blood-filled cysts resemble aneurysmal bone cysts.Furthermore, glucose transporter-1 protein (Glut-1) is the major glucose transporter protein in tumor cells. Fluorodexyglucose is now widely used to evaluate regional glucose metabolism in a variety of tumors, and high correlations were found between FDG uptake and Glut-1 expression in most malignant tumors. Uptake of FDG includes many complicated factors, and it would be difficult to make a differential diagnosis in mesenchymal tumors using FDG uptake alone. Zhao et al23 reported that the benign tumor patients who had high FDG uptake had negative scores in Glut-1. Even in our case, Glut-1 might be useful for preoperative diagnosis., Epidemiology : 0.25% in general population., It has an incidence of about 0.03% among the primary bone tumors., variable, patients should avoid excessive heat after the surgery., Complications : airway obstruction, Diagnostics : MRI, USG, Differential diagnosis : Hemothorax, PNEUMOTHORAX, disease description : Mesenchymal hamartoma of the chest wall is a rare benign tumor that usually presents as a visible chest wall mass or respiratory problems secondary to compression of the lung in early infancy. It is often reported that malignant transformation is extraordinarily rare. 

Chickenpox

Disease Name : Chickenpox, Treatment : medication : Aciclovir , Management is symptomatic and includes antipyretics, ,antipruritic agents and good hygiene. Aspirin is contra-indicated due to risk of Reye syndrome. The child should,not attend school until new lesions stop appearing and all,lesions have crusted. Administration of oral acyclovir (20,mg/kg/ dose four times a day for 5 days) within 24 hr of,onset of rash in healthy children reduces the duration of,rash by one day and lesions by 25%. IV acyclovir (10 mg/,kg every 8 hr for 7 days) is given to patients with complicated,varicella and for illness in high risk patients (neonates, ,immunocompromised children, pregnant women)., Pathophysiology : Chickenpox is caused by the varicella zoster virus (VZV), a DNA virus of the herpes virus family. The virus is present in respiratory secretions and skin lesions of affected children and is transmitted by air-borne spread or direct contact. The portal of entry is the respiratory tract. During the incubation period of 10-21 days, the virus replicates in the respiratory mucosa followed by viremic dissemination to skin and various organs. The host immune responses limit infection and promote recovery. In immunocompromised children, unchecked replication and dissemination of virus leads to complications. During the latter part of the incubation period, the virus is transported to the respiratory mucosa and leads to infectivity even prior to appearance of the rash. The period of infectivity lasts from 24 to 48 hr before the rash until all the vesicles are crusted (the scabs are not infective, unlike small-pox). The disease is highly contagious with secondary attack rates of 80% among household contacts. VZV establishes lifelong latent infection in the sensory ganglia. Reactivation, especially during periods of depressed immunity, leads to the dermatomal rash of herpes zoster. Chickenpox is rarely subclinical; however, in some children only a few lesions may be present. The peak age of disease is 5-10 yr. The prodromal period is short with mild to moderate fever, malaise, headache and anorexia. The rash appears 24--48 hr after the prodromal symptoms as intensely pruritic erythematous macules, seen first on the trunk. The rash rapidly spreads to the face and extremities while it evolves into papules, clear fluid-filled vesicles, clouded vesicles and then crusted vesicles. Several crops of lesions appear and simultaneous presence of skin lesions in varying stages of evolution is characteristic of varicella. The median number of lesions is around 300 but may vary from 10 to 1500. Systemic symptoms persist for 2-4 days after appearance of the rash. The rash lasts 3-7 days and leaves behind hypopigmented or hyperpigmented macules that persist for days to weeks. Scarring is unusual unless lesions are secondarily infected., Epidemiology : highest prevalence is in the 4 to 10 years old age group, Annual incidence is estimated at 80-90 million cases, GOOD, Yes, there’s a vaccine for chickenpox. It’s recommended, so ask your healthcare provider about the vaccine., Complications : hepatitis, stroke, thrombocytopenic purpura, toxic shock syndrome, neurological problem, Bacterial infection, airway obstruction, Diagnostics : SERUM IgM ANTIBODY, Tzanck smear, Differential diagnosis : animal bites, Bullous pemphigoid, Dermatitis herpetiformis, erythema multiforme, h/o Drug intake, HAND FOOT MOUTH DISEASE, HERPES SIMPLEX, insect bites, disease description : Chickenpox is a mild exanthematous illness in most healthy children but can be a serious disease in neonates, immunocompromised, pregnant women and even healthy adults. Chickenpox is caused by the varicella zoster virus (VZV), a DNA virus of the herpes virus family. The virus is present in respiratory secretions and skin lesions of affected children and is transmitted by air-borne spread or direct contact. The portal of entry is the respiratory tract. During the incubation period of 10-21 days, the virus replicates in the respiratory mucosa followed by viremic dissemination to skin and various organs.

Chikungunya

Disease Name : Chikungunya, Treatment : no specific treatment for chikungunya is available. Supportive care is recommended, and symptomatic treatment of fever and joint swelling, "Acetaminophen will help with pain and fever, but you shouldnt take any of the following medicines until you rule out similar infections (like dengue) : ,,Aspirin,Ibuprofen,Naproxen sodium,Drink plenty of liquids and get a lot of rest.", Pathophysiology : CHIKV is known to transmit in 2 cycles : urban and sylvatic. Urban transmission is from human to mosquito to human and is the main source of the current Western Hemisphere epidemic. Sylvatic transmission can be found in Africa and is based on animal to mosquito to human. As mentioned previously, CHIKV was initially transmitted through the vector Ae. aegypti, but incorporation of Ae. albopictus through a mutation in the E1 envelope protein not only increased the fitness of the virus in this species but improved transmissibility to vertebrates.The route of infection used by CHIKV starts after inoculation and infection of human epithelial and endothelial cells, primary fibroblasts, and monocyte-derived macrophages. After an initial immune response and sheltering in the lymph nodes, CHIKV travels through the lymphatic and circulatory system causing significant viremia.Transportation into target organs (muscles, joints, liver, and brain) has been found to be caused by infected monocyte-derived macrophages. Inflammatory reaction mediated by CD8+ (acute), CD4+ T lymphocytes, and pro-inflammatory cytokines are thought to be responsible for the acute symptoms, while a persistent reservoir of infected monocytes in the joints may be responsible for chronic joint disease., Epidemiology : Prevalence of Chikungunya was 22.3%, predominantly affecting the age group of 15-44 years and females., GOOD, "Use an insect repellent that has DEET or picaridin. Check that its registered by the Environmental Protection Agency.,Wear long sleeves and pants.,Remove standing water when possible.,Protect yourself indoors with screens, air conditioning and mosquito netting.,If youre pregnant, especially late in your pregnancy, dont travel anywhere with a chikungunya outbreak.", Complications : conjunctivitis, retinitis, uveitis, Iridocyclitis, Diagnostics : LYMPHOCYTES - ABSOLUTE COUNT, RT PCR, PCR tests, Differential diagnosis : Dengue without warning signs, Ebola virus disease (EVD), Hantavirus pulmonary syndrome, infectious mononucleosis, Influenza, Leptospirosis, Malaria, parvovirus infection, rubella, yellow fever, disease description : Chikungunya is an infection caused by the Chikungunya virus (CHIKV) Symptoms include fever and joint pains . These typically occur two to twelve days after exposure Other symptoms may include headache, muscle pain, joint swelling, and a rash.  Symptoms usually improve within a week; however, occasionally the joint pain may last for months or years The risk of death is around 1 in 1, 000 .Chikungunya is spread through bites from Aedes mosquitoes, and the species A. aegypti was identified as the most common vector, though the virus has recently been associated with many other species, including A. albopictus.

Childhood Absence Epilepsy

Disease Name : Childhood Absence Epilepsy, Treatment : medication : Valproic acid(sodium valproate)/ Divalproex Sodium, Ethosuximide , Lamotrigine , Pathophysiology : Although some of the pathways involved in the development of absence seizures have been described, their pathophysiological mechanisms are yet to be fully understood. The cortico-thalamic-cortical circuit is considered to play a significant role in the pathophysiology of absence seizures.Some of the neurons involved in the cortico-thalamic-cortical system include :   Cortical glutamatergic neurons originating on cortical layer VI and projecting to the nucleus reticularis of the thalamusThalamic relay neurons with excitatory projections to cortical pyramidal neuronsNeurons from the thalamic nucleus reticularis containing inhibitory GABA-ergic projections that connect with other neurons from the same nucleus and with thalamic relay neurons; these neurons do not connect directly with the cortex ., Epidemiology : five to 50 per 100, 000 persons in the general population., 2 to 8 in 100, 000 children under age 15 each year., variable, Get plenty of sleep each night. · ,Find ways to manage your stress. · ,Eat a healthy diet. ·, Exercise regularly., Complications : social isolation, Diagnostics : EEG, Differential diagnosis : automatism, focal seizures, sudden behavioral arrest or motionless stare, disease description : Childhood absence epilepsy (CAE) is an epilepsy syndrome with absence seizures  that begin in young children .During an absence seizure, the child stares blankly and is not aware or responsive. The childs eyes may roll up briefly or the eyes may blink. Some children have repetitive movements like mouth chewing  .Each seizure lasts about 10 to 20 seconds and ends abruptly. The child resumes normal activity right after the seizure and often doesn’t know that a seizure happened.  Typically children have multiple absence seizures in a day before medication is started.

Chlamydial Infections

Disease Name : Chlamydial Infections, Treatment : medication : Azithromycin , Doxycycline , Erythromycin , Levofloxacin , Ofloxacin , Tetracycline , Pathophysiology : Chlamydia is unique among bacteria, having an infectious cycle and two developmental forms. These include the infectious form called the elementary body (EB) and the reticulate body (RB). The EB is metabolically inactive and is taken up by host cells. Within the host cell, the EB will differentiate into the metabolically active RB. The RB will then use host energy sources and amino acids to replicate and form new EB, which can then infect additional cells. C. trachomatis targets the squamocolumnar epithelial cells of the endocervix and upper genital tract in women, and the conjunctiva, urethra, and rectum in both men and women. The bacterium is transmitted through direct contact with infected tissue, including vaginal, anal, or oral sex, and can even be passed from an infected mother to the newborn during childbirth., Epidemiology : higher prevalence in women 15-24 years of age, higher incidence in men between 20-24 years of age., good, The only way to avoid getting chlamydia is to abstain from having vaginal, anal or oral sex with someone who has a chlamydia infection. And be sure that sex toys that carry the bacteria don’t come in contact with your genitals.,,With prevention in mind, it’s a good idea to make safer sex practices a regular part of your sex life : ,,Use condoms during intercourse, anal sex and oral sex.,Use dental dams during oral sex or vagina-to-vagina contact.,Don’t share sex toys, but if you do, wash them after each use and cover toys used for penetration with a condom.,Have sex with only one partner, who only has sex with you., Complications : inflammation, Pelvic Inflamatory Disease, Scarring, Diagnostics : Bacteria Culture Test, ELISA, NAAT TEST, Bacteria CELL CULTURE, MICROIMMUNOFLUORESCENCE, Differential diagnosis : bacterial vaginosis, cholecystitis, GENITAL HERPES, gonorrhea infection, mycoplasma infection, Syphilis, Trichomonas vaginalis infection, Urinary Tract Infection, vaginal candidiasis, disease description : Chlamydia is a sexually transmitted infectious disease caused by the bacterium Chlamydia trachomatis. In the United States, it is the most commonly reported bacterial infection. Globally, it is the most common sexually transmitted infection. It causes an ocular infection called "trachoma, " which is the leading infectious cause of blindness worldwide.In females, the cervix is the anatomic site that is most commonly infected. This can manifest as cervicitis, urethritis, pelvic inflammatory disease, perihepatitis, or proctitis. Chlamydial infections in women, especially if untreated, increase the risk of infertility and ectopic pregnancy, leading to high medical cost .

Chlamydophila Pneumoniae Infection (taiwan Acute Respiratory Agent Or Twar )

Disease Name : Chlamydophila Pneumoniae Infection (taiwan Acute Respiratory Agent Or Twar ), Treatment : medication : Erythromycin , Other than the antibiotics, antipyretics, fluids, personal hygiene, and rest is advised to the patient to enhance recovery, Empirical Therapy, Pathophysiology : The human respiratory tract is susceptible to microbial proliferation whenever the pathogens overcome the host defense mechanisms (mechanical barrier by hair and mucus, chemical opsonization by the secreted proteins, and immune action by alveolar macrophages).The extracellular infectious form of Chlamydiae, the elementary body (EB), which is metabolically inactive, enters the respiratory tract via inhalation and then attaches to the mucosal surface. The EB enters the cells via receptor-mediated endocytosis differentiating into a reticulate body (RB) in the inclusion. RBs are metabolically active, capable of modifying host cell pathways, and replicating within 24 hours post-infection.After about 48 to 72 hours, the RBs are finally released as EBs outside the cells by cell lysis and infect the neighboring cells, thus continuing the infection. The organism can escape the endocytic-lysosomal pathway of host cells to remain persistent within tissues under stressful conditions and reactivate when favorable condition resumes. This attributes to the chronic inflammatory state in the host that is often present in C. pneumonia infections.Patients reinfected with C. pneumonia are reported to have less severe illness than those with evidence of primary infection ., Epidemiology : It has a 50% antibody prevalence by 20 years of age and 80% by the age of 60 to 70 years, the age group of 5 to 15 years has the highest rate of new infections., poor, Put your used tissue in the waste basket.,Cough or sneeze into your upper sleeve or elbow, not your hands, if you don’t have a tissue.,Wash your hands often with soap and water for at least 20 seconds.,Use a hand sanitizer that contains at least 60% alcohol if soap and water are not available. Cover all surfaces of your hands and rub them together until they feel dry.,Avoid touching your eyes, nose, and mouth with unwashed hands., Complications : Asthma, ENCEPHALITIS, myocarditis, Diagnostics : Complete Blood Count CBC, SPUTUM CULTURE, Nasal Swab, Differential diagnosis : Bacterial pneumonia, Influenza, TUBERCULOSIS, disease description : Pneumonia is an infection of lung parenchyma caused by a variety of pathogens such as bacteria, viruses, fungi, and parasites. One type of bacteria includes Chlamydia species. These species consist of C. pneumoniae, C. psittaci,  and C. trachomatis,  which are obligate intracellular bacterial pathogens. They frequently infect the respiratory tract in humans.

Choanal Atresia

Disease Name : Choanal Atresia, Treatment : Emergency management may be required in bilateral,choanal atresia to provide an airway. A feeding nipple,with a large hole provides a good oral airway (McGovern’s,technique) and obviates the need for tracheostomy., correction of atresia by,transnasal or transpalatal approach. The latter is usually,done at one and a half years. Choanal atresia can be corrected,by using nasal endoscopes and drill. Removal of,a part of posterior nasal septum transnasally is another,option to treat such cases., Pathophysiology : Current knowledge of the pathophysiology of the respiration of the neonate led to the conclusion that the infant, except when crying, is an obligate nasal breather. This is due to the elevated laryngeal position in the newborn as compared to the adult. When neonate swallows, the larynx touches the nasopharynx and locks between the soft palate and side of the nasopharynx. During inspiration, the neonate sucks the tongue, and a vacuum is created in the oropharynx, which helps to move soft tissue of the floor of the mouth up and back towards the soft palate. During expiration, the pressure in the airway causes the soft palate to push forward against the soft tissue and the tongue in the mouth, also obstructing the oral airway. As a result, the infant with bilateral choanal atresia experiences episodes of asphyxia and severe distress in quiet respiration when its mouth is closed, especially during periods of sleep or during feeding. The infant will become cyanotic, which is relieved by crying or gasping when the child opens the mouth widely, releasing the air obstruction., Epidemiology : occurs more frequently in females than in males (ratio 2 : 1), incidence of this malformation is between 1 : 5000 and 1 : 8000 live births., POOR, The risk factors of choanal atresia cannot really be avoided, as we still do not have a clear understanding about the causes of the condition. We can do little about genetic factors, which may contribute to the problem. Certain environmental allergens or triggers have also been identified as being possible risk factors in the recent past, and in light of these findings, it would be a good idea to avoid or reduce exposure to the following during pregnancy : ,,Atrazine, a chemical compound present in certain herbicides.,Cigarette smoke, including second hand smoke.,Excessive coffee consumption.,Zinc and B-12 supplements.,Some anti-infective urinary tract medications., Complications : Respiratory arrest, Aspiration, Diagnostics : CT, plain radiograph, Nasal endoscopy, NASAL EXAMINATION, Differential diagnosis : ANTROCHOANAL POLYP, Chordoma, deviated nasal septum, hematomas, NASAL DERMOID, TURBINATE HYPERTROPHY, disease description : Choanal atresia is a congenital disorder in which the nasal choanae, (i.e., paired openings that connect the nasal cavity with the nasopharynx), are occluded by soft tissue (membranous), bone, or a combination of both, due to failed recanalization of the nasal fossae during fetal development. If unilateral, it presents with unilateral mucopurulent discharge. If bilateral, the neonate is unable to breathe. Since newborns are obligate nasal breathers, establishing an airway is an acute otolaryngologic emergency .

Cholangiocarcinoma

Disease Name : Cholangiocarcinoma, Treatment : Chemotherapy-5 FU ; Gemcitabine, cis platin. ,Chemotherapy, with external beam radiotherapy (ERST)., "When operable, portal region clearance with hemihepatectomy can be done. lntrahepatic type is treated with hemihepatectomy. Perihilar type is treated with hemihepatectomy ,or extensive bile duct resection, nodal clearance, caudate ,lobe removal, cholecystectomy. Distal tumour is treated with ,Whipples pancreaticoduodenectomy", Pathophysiology : Cholangiocarcinoma is a tumor that arises from the malignant transformation of the epithelial cells of the intrahepatic or extrahepatic bile ducts. This type of liver cancer has very poor prognosis and is extremely aggressive with symptoms unobservable until there is a blockage of the bile duct by the tumor. Liver solid lesions can commonly be divided into two categories, as benign and malignant liver lesion. Common benign liver lesions include, hepatic hemangioma, focal nodular hyperplasia, and hepatic adenoma. On the other hand, the common malignant hepatic lesions include hepatocellular carcinoma (HCC), cholangiocarcinoma (CCA), and other metastatic diseases.. , Epidemiology : About 8, 000 people in the United States are diagnosed with it each year., 0.3-6 per 100, 000 inhabitants per year., POOR, "To reduce your risk of cholangiocarcinoma, you can : ,,Stop smoking. Smoking is linked to an increased risk of cholangiocarcinoma. If you smoke, stop. If you have tried quitting in the past and havent been successful, talk with your doctor about strategies to help you quit.,Reduce your risk of liver disease. Chronic liver disease is associated with an increased risk of cholangiocarcinoma. Some causes of liver disease cant be prevented, but others can. Do what you can to take care of your liver.,,For instance, to reduce your risk of liver inflammation (cirrhosis), drink alcohol in moderation, if you choose to drink. For healthy adults, that means up to one drink a day for women and up to two drinks a day for men. Maintain a healthy weight. When working with chemicals, follow the safety instructions.", Complications : cholangitis, CIRRHOSIS, liver failure, Diagnostics : GGT (gamma-glutamyl transpeptidase), Serum Alkaline Phosphatase ALP, Serum Bilirubin (Total ), MRCP, MRI Abdomen, USG ABDOMEN(W/A), MRI, PERCUTANEOUS TRANSHEPATIC CHOLANGIOGRAPHY(PTC), CT SCAN, SERUM CA 19-9 LEVEL, MDR CT, Differential diagnosis : CARCINOMA OF THE PANCREAS, CARCINOMA GALL BLADDER, cholangitis, cholecystitis, hepatocellular carcinoma, Pancreatic Cancer, PRIMARY BILIARY CIRRHOSIS, PRIMARY SCLEROSING CHOLANGITIS, disease description : A rare cancer that forms in the bile ducts. A bile duct is a tube that carries bile (fluid made by the liver) between the liver and gallbladder and the small intestine. Intrahepatic cholangiocarcinoma is found inside the liver. Extrahepatic cholangiocarcinoma is found outside the liver. Also called bile duct cancer.

Cholecystitis

Disease Name : Cholecystitis, Treatment : medication : Pethidine/Meperidine , Imipenem , Piperacillin and tazobactum , Levofloxacin , Metronidazole , Ketorolac trometamol, Oral intake is ,eliminated, nasogastric suction may be indicated, and extracellular ,volume depletion and electrolyte abnormalities are repaired. Meperidine or nonsteroidal anti-inflammatory drugs (NSAIDs) such as ,ketoralac or opioids, that is, morphine and hydromorphone, are usually employed for analgesia. Intravenous antibiotic therapy is usually indicated in patients with severe acute cholecystitis, even though ,bacterial superinfection of bile may not have occurred in the early ,stages of the inflammatory process. Antibiotic therapy is guided by ,the most common gram-negative organisms and anaerobes likely to ,be present, which are E. coli, Klebsiella spp., and Streptococcus spp. ,Effective antibiotics include piperacillin plus tazobactam, ceftriaxone ,plus metronidazole, levofloxacin plus metronidazole. Anaerobic coverage by a drug such as metronidazole should be added if gangrenous or emphysematous cholecystitis is suspected., Urgent (emergency) cholecystectomy or ,cholecystostomy is probably appropriate in most patients in whom ,a complication of acute cholecystitis such as empyema, emphysematous cholecystitis, or perforation is suspected or confirmed. Patients ,with uncomplicated acute cholecystitis should undergo early elective laparoscopic cholecystectomy, ideally within 48–72 h after diagnosis., Pathophysiology : Occlusion of the cystic duct or malfunction of the mechanics of gallbladder emptying is the pathophysiology of this disease. Cases of acute untreated cholecystitis could lead to perforation of the gallbladder, sepsis, and death. Gallstones form from various materials such as bilirubinate or cholesterol. These materials increase the likelihood of cholecystitis and cholelithiasis in conditions such as sickle cell disease where red blood cells are broken down forming excess bilirubin and forming pigmented stones. Patients with excessive calcium such as in hyperparathyroidism can form calcium stones. Patients with excessive cholesterol can form cholesterol stones. Occlusion of the common bile duct such as in neoplasms or strictures can also lead to stasis of the bile flow causing gallstone formation., Epidemiology : 0.2% to 0.4% of all critically ill patients, usually in patients aged 50 years or older, and is at least 3 times more common in men than women., incidence rate of 0.12% in the entire population, GOOD, You can reduce your risk of developing cholecystitis by : ,,Eating a healthy diet : Choose to eat a healthy diet – one high in fruits, vegetables whole grains and healthy fats – such as the Mediterranean diet. Stay away from foods high in fat and cholesterol.,Exercising : Exercise reduces cholesterol, and the lower the cholesterol level the lower the chance of getting gallstones.,Losing weight slowly : If you are making efforts to lose weight, don’t lose more than one to two pounds a week. Rapid weight loss increases your risk for developing gallstones., Complications : CHOLELITHIASIS, EMPYEMA OF GALL BLADDER, gangrene, infection, perforation, hepatic injury, Diagnostics : Complete Blood Count CBC, MRCP, USG ABDOMEN(W/A), LIVER FUNCTION TEST LFT, CT, Differential diagnosis : Acute Pancreatitis, AMOEBIC LIVER ABSCESS, appendicitis, ASCENDING CHOLANGITIS, LIVER ABSCESS, Myocardial infarction, perforated peptic ulcer, PNEUMONIA, disease description : Cholecystitis is an inflammation of the gallbladder.   Cholecystitis usually develops when the bile gets trapped in your gallbladder, and becomes infected with bacteria .The main symptom of acute cholecystitis is a sudden sharp pain in the upper right side of your abdomen that spreads towards your right shoulder.

Choledochal Cyst

Disease Name : Choledochal Cyst, Treatment : Resection of extrahepatic biliary tree with removal of chole\x02dochal cyst along with cholecystectomy and Roux-en-Y ,hepaticojejunostomy is the ideal treatment for choledochal ,cyst especially types I, 11 and IVb. ,In type I-excision of cyst with its mucosa and reconstruction ,by Roux-en-Y hepaticojejunostomy. ,In type II-excision of the diverticulum and suturing of the ,CBD wall, can be done. ,In type Ill-endoscopic sphincterotomy is done. Excision is ,also often needed., Pathophysiology : There are multiple classifications for choledochal cysts : Type IType I cysts represent 50% to 80% of CCs and are characterized by cystic dilation of the common bile duct. It is further divided into three subgroups. Type IA involves cystic dilation of the whole extrahepatic biliary tree, with APBJ. Type IB involves segmental dilation of the extrahepatic biliary tree, without APBJ .Type II Type II cysts represent 2% of CCs. It involves diverticular dilation anywhere along the extrahepatic duct.Type IIIType III cysts, also known as choledochocele, represent 1.4% to 4.5% of CCs. It involves Intraduodenal cystic dilation of the distal common bile duct.Type IVType IV cysts represent 15% to 35% of CCs and are multiple. It is further divided into 2 subgroups. Type IVA involves multiple dilations affecting both the intrahepatic and extrahepatic biliary tree. Type IVB involves multiple dilations confined to the extrahepatic biliary tree Type VType V cysts, also known as Caroli’s disease, represent 20% of CCs. It involves multiple dilations confined to the intrahepatic biliary tree. Caroli syndrome refers to the presence of type V CC as well as congenital hepatic fibrosis. , Epidemiology : more commonly in females and have a female to male ratio of 4 : 1 or 3 : 1, incidence of 1 in 1000 live births, with a 5-year survival rate of around 5%, There is no known way to prevent choledochal cyst., Complications : Acute Pancreatitis, ASCENDING CHOLANGITIS, CHOLELITHIASIS, Fibrosis, Diagnostics : Serum Bilirubin (Total ), CT Abdomen, MRCP, MRI Abdomen, USG ABDOMEN(W/A), USG, Differential diagnosis : CHOLANGIOCARCINOMA, Mesenteric cyst, recurrent ovarian cysts, disease description : A choledochal cyst (CC) has traditionally been considered as a cystic dilation of the extrahepatic bile duct. Choledochal cysts are now termed biliary cysts to include intrahepatic cysts also. Biliary cysts are defined as cystic dilations involving the biliary tree at single or multiple segments of both the extrahepatic as well as intrahepatic bile ducts.

Cholelithiasis

Disease Name : Cholelithiasis, Treatment : CHOLECYSTECTOMY-,prophylactic cholecystectomy may be considered for diabetic,patients, those with congenital haemolytic anaemia and,those patients who are undergoing bariatric surgery for morbid,obesity, Pathophysiology : Cholesterol gallstones are formed mainly due to over secretion of cholesterol by liver cells and hypomotility or impaired emptying of the gallbladder. In pigmented gallstones, conditions with high heme turnover, bilirubin may be present in bile at higher than normal concentrations. Bilirubin may then crystallize and eventually form stones.Symptoms and complications of cholelithiasis result when stones obstruct the cystic duct, bile ducts or both. Temporary obstruction of the cystic duct (as when a stone lodges in cystic duct before the duct dilates and the stone returns to gallbladder) results in biliary pain but is usually short-lived. This is known as cholelithiasis. More persistent obstruction of cystic duct (as when a large stone gets permanently lodged in the neck of the gallbladder) can lead to acute cholecystitis. Sometimes a gallstone may get pass through the cystic duct and get lodged and impacted the common bile duct, and causes obstruction and jaundice. This complication is known as choledocholithiasis., Epidemiology : prevalence of cholelithiasis is 10–15% in the general population., 6.12% (men 3.07% and women 9.6%), good, You can reduce your risk of cholesterol gallstones, which are the most common type, by reducing cholesterol in your diet. Here are some quick tips : ,,Limit fried and fast foods. These foods are usually fried in saturated fats, which promote LDL cholesterol (the “bad” type). If you cook with oil, choose plant oils instead of animal fats.,Replace red meat with fish. Red meat is high in saturated fats, while fish is high in omega-3 fatty acids, which promote HDL cholesterol (the “good” type). The good type helps balance the bad type.,Eat more plants. High-fiber fruits, vegetables and whole grains help to clear out excess cholesterol from your body. Eating more plants can also help you keep your overall weight down.,Lose weight gradually. Dieting to lose weight can help reduce the cholesterol content in your blood. But it’s better to lose weight at a slow, steady pace of one to two pounds a week. Rapid weight loss can encourage gallstones., Complications : cholecystitis, Gallbladder Cancer, Blockage of the common bile duct, Blockage of the pancreatic duct, Diagnostics : Total Leucocyte Count (TLC), CT Abdomen, Radionuclide Imaging technique, USG ABDOMEN(W/A), LIVER FUNCTION TEST LFT, X RAY, Differential diagnosis : Acute Pancreatitis, appendicitis, cholecystitis, hepatitis, PEPTIC ULCER DISEASE, disease description : Cholelithiasis or gallstones are hardened deposits of digestive fluid that can form in your gallbladder. The gallbladder is a small organ located just beneath the liver. The gallbladder holds a digestive fluid known as bile that is released into your small intestine. In patients with asymptomatic gallstones discovered incidentally, the likelihood of developing symptoms or complications is 1% to 2% per year. Asymptomatic gallbladder stones found in a normal gallbladder and normal biliary tree do not need treatment unless they develop symptoms.

Cholera

Disease Name : Cholera, Treatment : medication : Doxycycline , Tetracycline , Oral or intravenous hydration is the primary treatment for cholera.,In conjunction with hydration, treatment with antibiotics is recommended for severely ill patients. It is also recommended for patients who have severe or some dehydration and continue to pass a large volume of stool during rehydration treatment. Antibiotic treatment is also recommended for all pregnant women and patients with comorbidities (e.g., severe acute malnutrition, HIV infection).,Antibiotics are given as soon as the patient can tolerate oral medication. The choice of antibiotic should be informed by local antibiotic susceptibility patterns. In most countries, doxycycline is recommended as first-line treatment for adults (including pregnant women) and children. If resistance to doxycycline is documented, azithromycin and ciprofloxacin are alternative options., During an epidemic or outbreak, antibiotic susceptibility should be monitored through regular testing of sample isolates from various geographic areas.,None of the guidelines recommend antibiotics as prophylaxis for cholera prevention, and all emphasize that antibiotics should be used in conjunction with aggressive hydration.,Education of healthcare workers, assurance of adequate supplies, and monitoring of practices are all important for appropriate dispensation of antibiotics., other electrolyte solutions, zinc supplements, Pathophysiology : Ingestion of V. cholerae can lead to colonization of the small intestine. Its flagella allow the organism to swim through mucus and arrive at the intestinal wall. There, toxigenic V. cholerae produces toxin-coregulated pilus that attaches to gangliosides receptors in the mucosal wall. Cholera toxin is produced, which ADP-ribosylates the Gs subunit of the G protein complex in the gut epithelium. This leads to constitutive action of adenylate cyclase, thereby increasing cAMP intracellularly. As a result, increased secretion of chloride, bicarbonate, sodium, and potassium is observed. The secretion of these electrolytes pulls water out of the intestinal cells osmotically, thereby causing diarrhea.Host susceptibility is affected by previous exposure to the organism which can result in immunity, although this is dependent on the biotype and serotype of the previous organism encountered. Since it is a labile acid organism, a large inoculation dose is required to cause infection in a healthy adult. This can explain why lowered gastric acidity (as seen in cases of achlorhydria) can lower the threshold needed for the bacteria to cause infection. Interestingly, blood type O has also been associated with an increased likelihood of infection. The mechanism of this increased susceptibility to disease is not yet clear ., Epidemiology : 1.3 to 4 million people around the world get cholera each year, approximately 3–5 million cholera cases occur, good, A multifaceted approach is key to control cholera, and to reduce deaths. A combination of surveillance, water, sanitation and hygiene, social mobilisation, treatment, and oral cholera vaccines are used.,,1. Surveillance,Cholera surveillance should be part of an integrated disease surveillance system that includes feedback at the local level and information-sharing at the global level.,,2. Water and sanitation interventions,The long-term solution for cholera control lies in economic development and universal access to safe drinking water and adequate sanitation. ,,3. Treatment,Cholera is an easily treatable disease. The majority of people can be treated successfully through prompt administration of oral rehydration solution (ORS). ,,4. Community Engagement,Community Engagement means that people and communities are part of the process of developing and implementing programmes. Local culture practices and beliefs are central to promoting actions such as the adoption of protective hygiene measures such as handwashing with soap, safe preparation and storage of food and safe disposal of the faeces of children.funeral practices for individuals who die from cholera to prevent infection among attendees.,,5. Oral cholera vaccines,Currently there are three WHO pre-qualified oral cholera vaccines (OCV) : Dukoral®, Shanchol™, and Euvichol-Plus®. All three vaccines require two doses for full protection., Complications : death, renal failure, Severe hypotension, Dehydration, Diagnostics : STOOL CULTURE, RAPID VIRAL TEST, Differential diagnosis : Amebiasis, Escherichia coli, Food poisoning, giardiasis, Rota virus, salmonellosis, TYPHOID FEVER, disease description : Cholera is an acute secretory diarrheal illness caused by the bacteria Vibrio cholerae. High-volume fluid loss with electrolyte derangements that can progress to hypovolemic shock and ultimately death characterizes this gastrointestinal disease. The infection is transmitted via the fecal-oral route and can vary in severity. The key is replacing the fluid and electrolytes lost as soon as possible.

Cholestasis Of Pregnancy

Disease Name : Cholestasis Of Pregnancy, Treatment : medication : Diphenhydramine , Cholestyramine/Colestyramine, Neomycin , Ursodeoxycholic Acid, Cholestyramine ,is effective for itching. All women with OC should be given vit K to reduce postpartum hemorrhage and ,neonatal bleeding. The neonate should be given vit K as a routine. Combined oral contraceptives should ,be avoided in women with history of obstetric cholestasis. Prothrombin time should be monitored. ,Ursodeoxycholic acid (UDCA) is found helpful. It increases bile acid excretion. It improves pruritus, Pathophysiology : Genetic susceptibility and reproductive hormones, especially estrogen, are found to be the principal contributing factors to the development of intrahepatic cholestasis of pregnancy (ICP). Estrogen reduces the expression of nuclear hepatic bile acid receptors and hepatic biliary canalicular transport proteins in genetically susceptible women causing impairment of hepatic bile acid homeostasis and subsequent increased level of bile acids. Downregulation of placental expression of bile acid transporters organic anion transporting polypeptides OATP1A2 and OATP1B3 in ICP placenta in one report also indicates a role in pathophysiology., Epidemiology : ranging from <1 to 27.6 percent, , 1–4 per 1, 000 deliveries, GOOD, There is no known way to prevent cholestasis of pregnancy., Complications : low birth weight, Meconium Aspiration Syndrome, post partum hemorrhage , preterm labour, Fetal distress, Diagnostics : Serum Bilirubin Direct, Serum Bilirubin (Total ), Serum Bilirubin Indirect, USG ABDOMEN(W/A), LIVER FUNCTION TEST LFT, PHYSICAL EXAMINATION, Differential diagnosis : allergic reaction, Atopic dermatitis, HELLP SYNDROME, pemphigoid gestations, PRIMARY BILIARY CIRRHOSIS, viral hepatitis, disease description : Cholestasis of pregnancy is a liver condition that causes severe itching late in pregnancy. It’s also known as intrahepatic cholestasis of pregnancy (ICP) or obstetric cholestasis.  ICP temporarily lowers liver function in some pregnant people. This causes bile to build up in your liver and bloodstream. Bile is a substance produced by your liver and stored in your gall bladder . Every time you eat, bile breaks down fats so you can digest them properly. When levels of bile in your blood reach a certain level, you may begin to itch.

Cholestatic Liver Disease

Disease Name : Cholestatic Liver Disease, Treatment : The underlying cause of cholestasis must be treated., Treatment may include : ,,Nutrition. Dietary changes and supplements can help compensate for malabsorption and vitamin deficiencies.,Ursodeoxycholic acid. This medication, which is usually used to dissolve gallstones, can sometimes help cholestasis by increasing bile production and mediating the effects of extra bile salts in your blood.,Naltrexone. This opioid antagonist is sometimes prescribed to treat severe pruritus. It works by blocking the pathways to the nerves that are irritated by bile acids in your blood. Pruritus isn’t a histamine-related itch, so typical itching relief medications (antihistamines) don’t help.,Cholestyramine. This cholesterol medication can help bind cholesterol to bile salts in your intestines so that more comes out in your poop and less is reabsorbed into your blood. It may help with hyperlipidemia and with pruritus., Pathophysiology : Cholestasis can occur either in a hepatocellular pattern where there is an impairment in bile synthesis. Bile is a highly complex,  water-soluble medium. Bile formation included multiple different mechanisms of conjugation with multilevel regulation. The content of bile is transported in canaliculus via transported protein which creates a chemical and osmotic gradient through which water enters the canaliculi. Identification of abnormalities within some of these transporter proteins has led to an understanding mechanism of certain diseases better such as benign recurrent intrahepatic cholestasis (F1C1 locus gene) and progressive familial intrahepatic cholestasis (F1C2 locus gene). Failure to transport this bile salts lead to its accumulation within the liver. The strong detergent-like effect of the bile salts causes membrane injury and impairment of membrane function. Another mechanism of cholestasis is the physical obstruction to bile flow at the level of extrahepatic biliary ducts. Retained bile similarly causes hepatotoxicity., Epidemiology : 0.3-0.5% among the general population with up to 15% incidence in Latin American countries., VARIABLE, Get vaccinated for hepatitis A and B if you are at risk. Do not use intravenous drugs and share needles., Complications : Bone fragility, diarrhea, organ failure, Diagnostics : PLATELET COUNT, ERCP, MRI Abdomen, CT, CT SCAN, Bilirubin Blood Test, Differential diagnosis : Acute Hepatitis, acute liver failure, Acute Pancreatitis, amyloidosis, AUTOIMMUNE HEPATITIS, biliary obstruction, disease description : Cholestasis is the slowing or stalling of bile flow through your biliary system. It can be a problem in your liver or in your bile ducts. Bile that can’t flow leaks into your bloodstream and backs up into your organs, causing inflammation. Bile that can’t reach your intestines can also cause problems in your digestive system.

Cholesteatoma

Disease Name : Cholesteatoma, Treatment : The definitive treatment for cholesteatoma is surgical removal of the disease to provide a safe and dry ear. Patients often present with debilitating pain and hearing loss, and it is very important to explain that the goal of surgery is cholesteatoma removal and this may not restore the patient’s hearing to normal. In fact, the patient’s hearing could decline after surgery, and it is important to discuss this possibility with the patient. Audiograms should be obtained before and after surgery. The type of surgery performed depends largely on the type and location of the cholesteatoma, but tympanomastoidectomy is commonly performed to ensure the removal of all cholesteatoma. There are two major types of mastoidectomies performed for this surgery : canal wall up (CWU) and canal wall down (CWD). Each has advantages and disadvantages, but the canal wall down procedures result in lower rates of recurrence but require lifelong mastoid cleaning for the patient., Pathophysiology : The accumulation of skin in the middle ear can cause many problems and damage nearby structures. One of the most common problems is hearing loss due to the erosion of the middle ear bones. The cholesteatoma causes an inflammatory reaction that releases lytic enzymes, growth factors, and cytokines which can recruit osteoclasts to initiate destruction of bone. Cholesteatoma, if left untreated, can also erode the bony confines of the middle ear and extend to adjacent areas such as the face,  brain, and the neck. When cholesteatomas become infected, they can grow faster and cause more bony erosion. They can also cause a chronically draining ear, which is often foul smelling ., Epidemiology : 4.2 cases per 100, 000 inhabitants/year, GOOD, It’s not possible to prevent some cholesteatomas, especially if they are congenital. Timely ear care is key to avoiding primary or secondary acquired cholesteatoma. This includes getting an evaluation when there are concerns with simple infections or drainage that is not going away., Complications : Meningitis, Bone fragility, CONDUCTIVE HEARING LOSS, Diagnostics : Otoscopy, CT SCAN, Differential diagnosis : ACUTE SUPPURATIVE OTITIS MEDIA, middle ear tumours, disease description : A cholesteatoma is an abnormal, noncancerous growth that forms behind the eardrum or from the eardrum. It’s like a cyst that contains skin cells and connective tissue. Without treatment, the mass continues growing. Some cholesteatomas become large. In rare cases, they cause permanent hearing loss and other serious complications.

Cholesterol Embolus

Disease Name : Cholesterol Embolus, Treatment : Statins, iloprost (prostacyclin analogue), pentoxifylline (oxpentifylline) and steroid, Treatment in acute settings is mostly supportive. Long term treatment includes identifying the source of the emboli and preventing its further spread and risk modifications. Patients who have clots formed in heart structures are anticoagulated. Patients with atherosclerosis of the larger arteries are usually treated with antiplatelet agents and statins (HMG-CoA reductase inhibitors) to stabilize the plaques., Pathophysiology : The presence of plaque in large-caliber arteries like aorta and its branches leads to spontaneous, traumatic, or iatrogenic plaque rupture. Plaque debris, including cholesterol crystals, fibrins, platelets, calcified debris embolize, and lodge into small to medium arteries causing mechanical occlusion. The combined effect of mechanical occlusion and resultant inflammation from the foreign body, leukocyte infiltration, and complement activation, leads to end-organ damage ., Epidemiology : much more common in patients 60 years or older who have atherosclerotic heart disease, incidence of only 0.31 to 2.4 percent, poor, Doing whatever you can to slow the progression of atherosclerosis can help lower your risk of cholesterol emboli. Steps you can take include : ,,Avoid all tobacco products. If you currently smoke or use tobacco products, ask your provider for resources to help you quit.,Eat a heart-healthy diet, like the Mediterranean diet.,Exercise regularly, according to your provider’s guidance.,Take your medications as your provider prescribes them.,Visit your provider for a yearly check-up and keep all of your follow-up appointments., Complications : cholecystitis, death, hypertension, Pancreatitis, SPLENIC INFARCTION, MULTIORGAN FAILURE, renal insufficiency, Diagnostics : COMPLEMENT 3(C3) LEVEL, CRP, Differential Leucocyte Count DLC, Erythrocyte Sedimentation Rate (ESR), PLATELET COUNT, Total Leucocyte Count (TLC), Blood Urea, STOOL EXAMINATION, CT SCAN, plasma creatinine, Urine analysis, Urine analysis, Urine analysis, Differential diagnosis : acute cholecystitis, acute respiratory distress syndrome, ANTIPHOSPHOLIPID SYNDROME, Biliary colic, cardiogenic shock, CELLULITIS, deep venous thrombosis, delirium, Diabetic Foot Ulcers, HENOCH-SCHONLEIN PURURA, hypertensive encephalopathy, Infective endocarditis, Myocardial infarction, PHEOCHROMOCYTOMA, Polyarteritis Nodosa, Raynaud phenomenon, Upper gastrointestinal bleeding, disease description : Cholesterol embolism or atheroembolism is a phenomenon where cholesterol crystals and atheroma debris such as cholesterol, platelets, and fibrins embolizes from proximal large arteries such as the aorta and its major branches to distal small arteries. Cholesterol embolism frequently occurs after the intraarterial procedures, but it can also occur spontaneously. Cholesterol embolism is an uncommon multisystemic disease where multiple organs are involved, including the brain, muscles, skin, eyes, kidneys, and gastrointestinal (GI) tract .

Chondroblastoma

Disease Name : Chondroblastoma, Treatment : The treatment of choice of chondroblastoma is surgical. It consists of complete surgical curettage with or without bone grafting, en bloc resection, or rarely, amputation. Surgical resection alleviates pain, avoids propagation into the joint and adjacent soft tissues, diminishes the likelihood of recurrence, and accurately establishes the diagnosis of chondroblastomas. Surgical management depends on : ,,The extent of bone and/or joint involvement,Anatomic location of the lesion,Staging,Stage 1 (latent) or stage 2 (active) may be an indication for intralesional excision.,,Stage 3 (aggressive) is an indication of marginal or wide resection.,,Adjunctive therapy includes chemical cauterization with phenol or cryosurgery. Bone grafting and cryotherapy after surgical curettage decrease the risk of recurrence.Some authors suggest that radiofrequency should be an option as an alternative treatment method in managing chondroblastomas., Pathophysiology : The histogenesis of chondroblastomas remains controversial. Possible proposed cells of origin include cartilage germ cells or epiphyseal cartilage cells. A possible multipotent mesenchymal cell or tendon sheath synovial cell origin is another proposed etiological site .Genetics : Flow cytometric studies reveal that most chondroblastomas are diploid with low proliferation fractions. There are reports of clonal abnormalities in 14 chondroblastomas. Heterogeneous rearrangements of chromosomes 5 and 8, both balanced and unbalanced, appear to be the most common. IDH1 and IDH2 mutations are absent .Recently, research has shown that chondroblastomas have distinctive driver mutations in the genes that encode histone H3.3. Chondroblastomas harbor mutations in the H3F3B gene far more commonly than the H3F3A gene. Research has found an antibody directed against the H3F3 K36M mutation to be specific for chondroblastoma, Epidemiology : second to third decade of life (mean age, 19 to 23 years) with a male predominance (2 to 1), less than 1% of all primary bone tumors., NOT SPECIFIC, Since the cause of chondroblastoma is unknown, there is no way to reduce your risk of developing chondroblastoma. Chondroblastoma symptoms go away with treatment to remove the tumor., Complications : death, pathological fracture, Diagnostics : LESION TISSUE HISTOLOGY, MRI, X RAY, X RAY, Differential diagnosis : Aneurysmal bone cyst, Clear cell chondrosarcoma, Geode or intraosseous ganglion, Giant cell tumor of bone, Osteoblastoma, Osteoid osteoma, osteomyelitis, osteosarcoma, disease description : Chondroblastoma is a benign, chondroid-producing neoplasm composed of chondroblasts. It accounts for less than 1% of all bone tumors and usually arises in the epiphyses or apophysis of skeletally immature patients. . These neoplasms usually occur in the long bones and are important, considering both benign and malignant etiologies in the differential diagnosis. The proximal humerus is the most common site of involvement, followed by the distal femur and proximal femur. Chondroblastomas require surgical treatment. In general, chondroblastoma has a good prognosis, and patients often experience full resolution after surgical treatment

Chondroid Lipoma

Disease Name : Chondroid Lipoma, Treatment : Complete simple surgical resection is curative.,Does not recur or metastasize., Pathophysiology : Chondroid lipomas are well circumscribed tumours consisting of mature adipocytes in common lipoma like areas and of a chondroid component in which vacuolated lipoblast like cells are surrounded by myxohyaline matrix. Both components are connected and mutually transient. The vacuoles can be shown to contain lipids using Oil red O stain and glycogen using Periodic Acid-Schiff stain. Presence of stromal mucins support chondroid differentiation ., Epidemiology : M : F = 1 : 4, 2 out of every 100 people. Lipomas typically occur in adults between 40 and 60 years of age, good, Complications : nan, Diagnostics : Cytogenetics, PET SCAN, MRI, MRI, CT SCAN, ELECTRON MICROSCOPY, Immunostaining, Immunostaining, Differential diagnosis : Extraskeletal myxoid chondrosarcoma ("chordoid" ty, Liposarcoma, Myxoid liposarcoma, Soft tissue chondroma, disease description : chondroid lipomas are rare benign soft tissue tumors that contain a varied ratio of both fat and cartilage. These lesions can be diagnostically confusing as they may mimic other fat-containing neoplasms, including more aggressive lesions such as myxoid liposarcoma and extraskeletal myxoid chondrosarcoma .

Chondromyxoid Fibroma

Disease Name : Chondromyxoid Fibroma, Treatment : intralesional curettage, Intraoperative adjuvants — such as cryotherapy (liquid nitrogen), phenol (a chemical) or cauterization (burning the tumor bed) — which are used to remove microscopic tumor cells.,,Bone grafting : a surgical procedure to replace missing bone with artificial graft material or cadaver bone., Pathophysiology : Exact pathogenesis is unknown but upregulation of glutamate receptor gene GRM1 coding region of chromosome 6 through recombination with several partner genes in up to 90% of cases., Epidemiology : 0.5% of all bone tumors, about 2% of all benign neoplasms) and prefers male sex by 1.5 : 1., less than 1% of all bone tumors., NOT SPECIFIED, As far as researchers know, there’s no way to prevent benign bone tumors from forming., Complications : Malignant transformation, recurrence, Diagnostics : LESION TISSUE HISTOLOGY, X RAY, X RAY, Differential diagnosis : Aneurysmal bone cyst, Central chondrosarcoma, Chondroblastoma, Giant cell tumour, NON-OSSIFYING FIBROMA, Osteochondromyxoma, disease description : Chondromyxoid fibroma, or CMF, is a tumor of the cartilage found between your bones. Cartilage is a rubber-like tissue that cushions and protects the ends of your bones, sits in between the disks in your spine, and makes up the ear and nose. CMF tumors are benign, which means they are not cancer.

Chordoma

Disease Name : Chordoma, Treatment : medication : Nilotinib , Cisplatin , Methotrexate, Vincristine, Fludarabine, Doxorubicin (Liposomal), radiation alone in poor surgical candidates, Usually surgery followed by radiation, Pathophysiology : Chordomas present with slow-growing, locally invasive tumors with distant metastases are rarely occurring and only late in the disease. Although they are considered indolent tumors, there is a significant risk for multiple recurrences locally., Epidemiology : Male predominance (~2 : 1) in sacrococcygeal and vertebral body cases; no sex difference in tumors involving the skull base, incidence of 1 : 1, 000, 000, Median survival is 7 years 5 year overall and dise, There’s nothing you can do to prevent developing chordoma. Most cases happen randomly. ,,If you have a family history of chordoma or tuberous sclerosis, be sure to see your healthcare team regularly so they can monitor you for signs of chordoma. The earlier they can catch it, the better., Complications : Metastasis, Normal pressure hydrocephalus, Diagnostics : BONE SCAN, MRI, X RAY, CT SCAN, immunohistochemistry, Histopathological examination, Differential diagnosis : Chondrosarcoma : Central, primary, and secondary, P, Giant cell tumor of bone, Meningioma, metastatic carcinoma, Myoepithelial tumours, plasmacytoma, disease description : Chordoma is a rare type of bone cancer that happens most often in the bones of the spine or the skull. It most often forms where the skull sits atop the spine (skull base) or at the bottom of the spine (sacrum).Chordoma begins in cells that once made up a collection of cells in the developing embryo that go on to become the disks of the spine. Most of these cells go away by the time youre born or soon after. But sometimes a few of these cells remain and, rarely, they can become cancerous.

Choreoathetosis

Disease Name : Choreoathetosis, Treatment : nan, Pathophysiology : nan, Epidemiology : nan, Complications : nan, Diagnostics : nan, Differential diagnosis : nan, disease description : nan

Choriocarcinoma

Disease Name : Choriocarcinoma, Treatment : Chemotherapy ,Choice of chemotherapy is based on the FIGO / WHO prognostic score,Low risk : single agent, including methotrexate and actinomycin D,High risk : multi agent, including etoposide, methotrexate, actinomycin, cyclophosphamide, vincristine (EMA-CO); etoposide, cisplatin - etoposide, methotrexate, actinomycin (EP-EMA); paclitaxel, etoposide - paclitaxel, cisplatin (TE / TP), Surgery only performed in selected cases (older age, chemoresistance, uterine rupture by tumor, life threatening hemorrhage), Pathophysiology : The exact pathogenesis of choriocarcinoma has not been fully explained or understood, but studies have shown cytotrophoblastic cells function as stem cells and undergo malignant transformation. The neoplastic cytotrophoblast further differentiates into intermediate trophoblasts and syncytiotrophoblast. The mixture of cells mimics the normal development of a previllous blastocyst, a feature seen in other gestational trophoblastic neoplasms.Overexpression of p53 and MDM2 have been demonstrated in choriocarcinoma, with no evidence of somatic mutation. Other genes implicated with either overexpression or down-regulation via hyper-methylation include NECC1, epidermal growth factor receptor, DOC-2/hDab2, Ras GTPase-activating protein, E-cadherin, HIC-1, p16, and TIMP3. HLA-G is demonstrated at very high levels in choriocarcinoma and functions to change the tumor microenvironment through the inactivation of the local immune system., Epidemiology : 1 in 24 000–40 000 pregnancies., 2 to 7 per 100, 000 pregnancies, The hCG levels should be monitored frequently in the first year following chemotherapy since the risk of relapse is ~3%. Women should avoid getting pregnant during this period.,,Following choriocarcinoma, fertility is not affected. The chances of developing congenital abnormalities in future babies are not increased., Complications : diarrhea, hair loss, infections, nausea, vomiting, fever, Secondary malignancies, Diagnostics : HCG, MRI, CHEST X RAY, CT SCAN, USG, Immunostaining, Immunostaining, Differential diagnosis : Embryonal carcinoma, Mixed germ cell tumour, Placental site trophoblastic tumour, SEMINOMA, disease description : Choriocarcinoma, a subtype of gestational trophoblastic disease,  is a rare and aggressive neoplasm. The 2 significant choriocarcinoma subtypes, namely : gestational and non-gestational, have very different biological activity and prognoses. Choriocarcinoma predominately occurs in women but can also occur in men, usually as part of a mixed germ cell tumor.

Choroid Glioma Of The Third Ventricle (who Grade 2

Disease Name : Choroid Glioma Of The Third Ventricle (who Grade 2, Treatment : Resection; rarely radiotherapy, occasionally recurs due to incomplete excision (16%)., Pathophysiology : Chordoid gliomas are considered circumscribed astrocytic gliomas under the WHO classification of CNS tumor. They are believed to originate from the ependymal cells of the lamina terminalis and are thus of glial origin, specifically of tanycytes, a type of ependymal cells. It is considered a WHO grade 2 tumor., Epidemiology : 5%, almost exclusively in the adult population with a female predilection (F : M 2 : 1), poor, Complications : Hydrocephalus, Mental Disorder, memory deficits, Diagnostics : CT SCAN, ELECTRON MICROSCOPY, Immunostaining, Immunostaining, Differential diagnosis : ANEURYSM, central neurocytoma (who grade 2), Chordoma, Craniopharyngioma, ependymoma (who grade 2), GERM CELL TUMOR, subependymal giant cell astrocytoma (who grade 1), disease description : Rare, discrete, slow growing glial tumor of third ventricle of adults, characterized by chordoid architecture and myxoid background.Cells may resemble ependyma of subcommissural organ, present in dorsocaudal third ventricle during embryonic life, which regresses after birth.

Choroid Plexus Carcinoma (who Grade 3)

Disease Name : Choroid Plexus Carcinoma (who Grade 3), Treatment : The use of neoadjuvant chemotherapy to reduce tumor vascularity prior to surgery has been reported., Gross total resection allows for the best chance of survival and improves the overall prognosis., Pathophysiology : Choroid plexus carcinoma is a WHO grade III tumor which is distinguished histologically from CPP based on increased nuclear to cytoplasmic ratios, increased mitotic figures, nuclear pleomorphism, the presence of necrosis, and distortion or blurring of the papillary structure of CPP by sheets of cells in the malignant ., Epidemiology : 6%,Although reported in adults, 80% of CPCs occur in the pediatric population, and 20% to 40% of all choroid plexus tumors in children are CPCs.1, Within the pediatric population, however, these neoplasms are more common, representing approximately 1% to 4% of all childhood brain tumors, with 10% to 20% occurring during the first year of life., poor, . reduce your risk of developing a brain tumor by avoiding environmental hazards, Complications : bleeding, Metastatic malignancy, Diagnostics : MRI, MRI, Immunostaining, Differential diagnosis : central neurocytoma (who grade 2), choroid plexus papilloma (who grade 1), disease description : A choroid plexus carcinoma is a rare cancerous (malignant) brain tumor that occurs mainly in children .A choroid plexus carcinoma begins near the brain tissue that secretes cerebrospinal fluid. choroid plexus carcinoma are malignant (cancerous). This means they are fast-growing tumors that tend to invade nearby tissue.

Choroid Plexus Papilloma (who Grade 1)

Disease Name : Choroid Plexus Papilloma (who Grade 1), Treatment : Adjuvant radiotherapy or chemotherapy, based on the clinical need, In symptomatic patients, gross total resection (GTR) is the treatment of choice as these tumors are benign. Recent advances in imaging, surgical approaches, and quality of intensive care have improved surgical outcomes with the chances of a cure reaching almost 100%. In the pediatric population, there is significant (12%) perioperative mortality, mainly from catastrophic blood loss. Preoperative embolization can minimize this risk, along with optimization of the ability to resect the tumor completely, Surgery to achieve gross total resection., Pathophysiology : According to the World Health Organization classification (2016),  choroid plexus tumors are classified as papillomas (grade I), atypical tumors (grade II), and carcinomas (grade III). CPPs have less than two mitotic figures per 10 high power fields, atypical ones have two to five per 10 high power fields, and carcinomas have greater than five mitotic figures per 10 high power fields. Grossly, the tumors are soft, globular, friable pink masses with irregular projections and high vascularity., Epidemiology : Predominantly occurs in children.,Accounts for 2 - 5% of all pediatric brain tumors ,M : F = 1.2 : 1, Approximately 85% of all choroid plexus papillomas occur in children under the age of 5 years, good, Any child presenting with altered sensorium has to be evaluated for an intraventricular tumor, Complications : bleeding, Optic Atrophy, papilledema, raised intracranial pressure, seizures, CSF RHINORRHOEA, visual loss, Diagnostics : Cytogenetics, MRI, T2 WEIGHTED CONTRAST MRI, CT SCAN, Immunostaining, Immunostaining, Differential diagnosis : central neurocytoma (who grade 2), GERM CELL TUMOR, medulloblastoma, Meningioma, Metastasis, metastatic adenocarcinoma, rosette forming glioneuronal tumour of the fourth , subependymoma (who grade 1), disease description : Choroid plexus papillomas (CPPs) are rare central nervous system tumors. They may be seen at any age, but are more common in infants. Their site of occurrence varies according to age. They usually present with the increasing head circumference or altered mental status in children; whereas in adults they present with signs of increased intracranial tension. Imaging shows intraventricular enhancing masses .

Chromhidrosis

Disease Name : Chromhidrosis, Treatment : First line,•\tTopical capsaicin,Second line,•\tIntralesional botulinum toxin,•\tTopical capsaicin has satisfactorily reduced facial and nipple chromhidrosis ,•\tBotulinum toxin has been used to successfully suppress ,facial chromhidrosis, Pathophysiology : Apocrine chromhidrosis is considered an intrinsic process. The greater the extent of lipofuscin oxidation, the darker the lipofuscin color, which can range from yellow, green, blue, black, or brown. Apocrine glands are provoked by hot showers and baths, rubbing of the skin, and emotional stimuli such as pain, sexual arousal, or anxiety, which leads to the secretion of colored sweat in the case of apocrine chromhidrosis. Substance P may also play a role in the pathogenesis, which is why capsaicin has shown to be an effective treatment in some patients.Eccrine chromhidrosis is most often caused exogenously by the coloring of clear sweat with the ingestion of water-soluble dyes such as tartrazine, heavy metals such as copper, coloring and flavoring substances in food products, and drugs such as quinines, levodopa, tartrazine-coated bisacodyl, and rifampin. It is caused endogenously secondarily to hyperbilirubinemia in which patients may present with a greenish hue in a palmoplantar distribution with or without pompholyx-like lesions. , Epidemiology : poor, Some skin diseases are not preventable. For example, there is no way to change your genetics or prevent an autoimmune disorder.,,You can take steps to avoid contagious or infectious skin diseases. You may prevent contagious skin diseases or reduce their symptoms if you : ,,Avoid sharing utensils, personal items or cosmetics.,Disinfect objects you use in public spaces, such as gym equipment.,Drink plenty of water and eat a nutritious diet.,Limit contact with irritants or harsh chemicals.,Sleep seven to eight hours per night.,Use sun protection to prevent sunburn and other sun damage.,Wash your hands regularly with soap and water., Complications : Psychiatric disturbances, anxiety, DEPRESSION, Diagnostics : biopsy, Fluorescence with Wood’s light, Differential diagnosis : "Addisons Disease", ALKAPTONURIA, bleeding diathesis, Dermatitis simulata, Hemochromatosis, hyperbilirubinemia, Poisoning, Pseudomonas infection, disease description : Chromhidrosis is a rare condition with a characteristic presentation of the secretion of colored sweat and was first reported by Yonge in 1709. Chromhidrosis can subdivide into three categories : Apocrine chromhidrosis, eccrine chromhidrosis, and pseudochromhidrosis (pseudo-eccrine chromhidrosis). Apocrine chromhidrosis occurs in the areas where apocrine glands are present and are mostly limited to the anogenital and axillary areas, eyelids, ears, scalp, trunk, and areola. Normally, apocrine glands secrete scant amounts of odorless, oily fluid into the hair canal that, upon reaching the skin surface, is degraded by bacteria producing a pheromonal body odor .

Chromoblastomycosis

Disease Name : Chromoblastomycosis, Treatment : Surgery, cryoablation and targeted systemic chemotherapy for metastatic disease with antiangiogenic, TK and mTOR inhibitors., Treatment options include oral itraconazole (as monotherapy or with oral 5-flucytosine 5-FC), locally applied heat therapy, cryosurgery, photodynamic therapy (PDT) using 5-aminolevulinic acid (ALA) irradiation, and combination therapy., Pathophysiology : The fungi enter the skin following trauma, evoking a granulomatous response. The epidermis shows pseudoepitheliomatous hyperplasia. In the dermis, a granuloma composed of epithelioid cells and Langhans giant cells is visible. The fungal elements ae visible as sclerotic bodies, which are brown septate cells. The sclerotic bodies (medlar bodies/ muriform bodies/copper pennies) are extruded transepidermally, and they appear as black dots on the surface of the lesion; this is characteristic of chromoblastomycosis., Epidemiology : Third most common renal cell carcinoma (RCC) subtype; 7% of adult renal epithelial tumors, poor, Prevention is difficult, but it is useful to advise people not to walk barefoot in areas where infection has been detected.,,Chromoblastomycosis is considered an occupational disease, occurring among farm labourers, babassu coconut harvesters, lumberjacks, or vendors of farm products. ,Lack of protective shoes, gloves or garments and poor nutrition and hygienic habits are risk factors associated with chromoblastomycosis., Complications : hypercalcemia, hypertension, renal failure, Diagnostics : Cytogenetics, CT SCAN, HISTOLOGIC EXAMINATION, "SABORAUDS MEDIUM", Immunostaining, Immunostaining, Immunostaining, Differential diagnosis : Blastomycosis dermatology, Clear cell renal cell carcinoma, Leishmaniasis, Oncocytoma, Verrucas : Verruca vulgaris, Verruca plantaris, Ver, disease description : Chromoblastomycosis is a chronic granulomatous infection of the skin and subcutaneous tissue caused by several different dematiaceous fungi (brown pigment-producing), resulting in the formation of slow-growing, warty plaques, cauliflower-like lesions which may ulcerate.

Chromophobe Renal Cell Carcinoma

Disease Name : Chromophobe Renal Cell Carcinoma, Treatment : Surgery, cryoablation and targeted systemic chemotherapy for metastatic disease with antiangiogenic, TK and mTOR inhibitors., Pathophysiology : ChRCC arises from the intercalated cells of the collecting duct. (Störkel et al., 1989) Grossly, chRCC is a well-circumscribed unencapsulated mass with solid, homogeneous, and pale tan to dark brown cut surfaces. Gross hemorrhage, necrosis, cystic changes, and a central scar may be seen (Moch et al., 2016; Cheng et al., 2020)., Epidemiology : Third most common renal cell carcinoma (RCC) subtype; 7% of adult renal epithelial tumors, poor, Renal cell carcinoma isn’t always preventable, but you can reduce your risk. For example, choosing not to smoke (and quitting if you do) is one of the best things you can do to reduce your cancer risk., Complications : hypercalcemia, hypertension, renal failure, Diagnostics : Cytogenetics, MRI, CT SCAN, Immunostaining, Immunostaining, Immunostaining, Differential diagnosis : Clear cell renal cell carcinoma, Oncocytoma, disease description : Solid tumor composed of granular pale cells with prominent cell borders, finely reticular cytoplasm, perinuclear halos and wrinkled hyperchromatic nuclei.

Chronic Active Epstein–barr Virus Infection

Disease Name : Chronic Active Epstein–barr Virus Infection, Treatment : medication : Cyclosporine/Ciclosporine, Rituximab, Human normal immunoglobulin , Pathophysiology : Pathogenesis involves high levels of EBV DNA in the blood with circulating antibodies against VCA and EA-restricted proteins. As well as the features as above, there may be leukocytoclastic vasculitis with cutaneous features similar to Henoch–Schoenlein purpura. Hydroa vacciniforme developing in children or adults as a UV-associated eruption is linked with high EBV viral loads. Pruritic necrotic plaques as a presenting feature of lymphocytic variant hypereosinophilic syndrome have been ascribed to chronic active EBV infection. Hypersensitivity to mosquito bites This may indicate a primary persistent EBV infection, usually occurring in childhood. Intense inflammation, often with purpura, bullae and necrosis, develops at the sites of mosquito bites . There is usually regional lymphadenopathy and there may be systemic features such as pyrexia and hepatitis. Most cases are reported from east Asia. These patients should be monitored for the possible development of NK/T-cell lymphoma., Epidemiology : EBV infects 95% of the human population and usually is asymptomatic, or in the case of adolescents and young adults, over 90% of the population worldwide has been infected., poor, There is no vaccine to protect against EBV infection. You can help protect yourself by not kissing or sharing drinks, food, or personal items, like toothbrushes, with people who have EBV infection.,,There is no specific treatment for EBV. However, some things can be done to help relieve symptoms, including,,drinking fluids to stay hydrated,getting plenty of rest,taking over-the-counter medications for pain and fever, Complications : myocarditis, sepsis, lymphoma, MULTIORGAN FAILURE, Ruptured spleen, Diagnostics : PLATELET COUNT, hemoglobin HB, PCR, MRI, Differential diagnosis : autoimmune disease, cervical lymphadenopathy, Chronic fatigue syndrome, Cyto megalovirus infection, infectious mononucleosis, pharyngitis, disease description : Chronic active Epstein-Barr virus infection (CAEBV) is a very rare complication of an Epstein Barr virus (EBV) infection. Symptoms of CAEBV may include fever, swollen lymph nodes, and an enlarged liver and/or spleen. More serious complications may include anemia, nerve damage, liver failure, and/or interstitial pneumonia. Symptoms may be constant or come and go, and tend to get worse over time. CAEBV occurs when the virus remains active and the symptoms of an EBV infection do not go away. It is diagnosed based on the symptoms, clinical exam, and blood tests that show EBV DNA remaining at high levels for at least 3 months

Chronic And Recurrent Meningitis

Disease Name : Chronic And Recurrent Meningitis, Treatment : Recurrent bacterial meningitis is treated with antibiotics and dexamethasone (a corticosteroid)., Pathophysiology : Chronic meningitis is defined as the persistence of clinical symptoms and signs of meningitis, with or without abnormal cerebrospinal fluid, for more than four weeks. In as many as one third of cases, no cause is found. In the remainder, infective, neoplastic and so-called aseptic disorders may be identified. Important infective causes include partially treated bacterial (pyogenic), tuberculous, syphilitic, Lyme and fungal meningitis. Sarcoidosis, Behçet’s disease, vasculitis and drugs are major non-infective, non-malignant causes. The definitive diagnosis of the cause of chronic meningitis may be made only after extensive investigation. This review describes the clinical features and causes of chronic and recurrent meningitis, and provides an algorithm for investigation and treatment., Epidemiology : 0.12 cases per 100, 000 adults., VARIABLE, Complications : nan, Diagnostics : Protein, CT SCAN, Differential diagnosis : BACTERIAL MENINGITIS, "Behcets syndrome/disease", Connective tissue disorders, MALIGNANCY, Sarcoidosis, disease description : Chronic meningitis is defined as the persistence of clinical symptoms and signs of meningitis, with or without abnormal cerebrospinal fluid, for more than four weeks. In as many as one third of cases, no cause is found. In the remainder, infective, neoplastic and so-called aseptic disorders may be identified. Important infective causes include partially treated bacterial (pyogenic), tuberculous, syphilitic, Lyme and fungal meningitis. Sarcoidosis, Behçets disease, vasculitis and drugs are major non-infective, non-malignant causes. 

Chronic Ankle Sprain

Disease Name : Chronic Ankle Sprain, Treatment : Arthroscopy, Nonsteroidal anti-inflammatory drugs (NSAID), used topically or taken orally, can be utilized in addition to PRICE therapy for short term symptomatic pain control, Pathophysiology : After an index ankle sprain, the microscopic tears due to the overstressing of the ankle ligaments can lead to attenuation. As a result, functional and mechanical instability may ensue, which increases the likelihood of recurrent ankle sprain when proper treatment is not applied. As previously mentioned, the ATFL is the most commonly injured ankle ligament, followed by the calcaneofibular ligament (CFL), and then posterior talofibular ligament (PTFL).Mechanical instability entails excessive motion in the ankle joint that can be assessed clinically by performing an anterior drawer sign or radiographically stressing the ankle joint.  , Epidemiology : 2.15 per 1000 persons, overall males had an incidence rate of 2.20, and females had an incidence rate of 2.10, ankle sprains per 1000 person annually, GOOD, Maintain a healthy weight and well-balanced diet to keep muscles strong.,Wear shoes that fit properly and be sure any sports equipment is also fitting well.,Practice safety measures to prevent falls., Complications : CHRONIC PAIN, Diagnostics : MRI, MRI, Arthrography, Differential diagnosis : ankle injury, "FRACTURE OF THE BASE OF 5TH METATARSAL (Jones fra", FRACTURE OF THE CALCANEUM, NEUROMUSCULAR DISORDER, disease description : Chronic recurrent sprain ankle is a disabling condition. If a course of physiotherapy and modification in shoe has not helped, a detailed evaluation with MRI and arthroscopy may be necessary. Pain in a number of these so-called chronic ankle sprains is in fact due to impingement of the scarred capsule or chondromalacia of the talus. Arthroscopy is a good technique for diagnosis and treatment of such cases.

Chronic Bacterial Conjunctivitis

Disease Name : Chronic Bacterial Conjunctivitis, Treatment : medication : Chloramphenicol , Gentamicin , Tobramycin sulfate , medication : Chloramphenicol , Gentamicin , Tobramycin sulfate , For Neisseria gonorrhoeae and Chlamydia trachomatis, systemic antibiotics are necessary as follows : ,,Chlamydia : ,Macrolides : Azithromycin (1gm single dose) or Erythromycin,Tetracyclines : Doxycycline or Tetracycline (Avoid in pregnant, nursing mothers),Children less than or equal to 45 kg : Erythromycin 50 mg/kg/day PO divided into four doses daily for 14 days,Neisseria gonorrhoeae : ,Ceftriaxone 250mg Intramuscular injection once + Azithromycin 1 gram PO once.,Doxycyline 100mg PO BID for 7 days,For cephalosporin allergy, Azithromycin 2g PO once,For Children < 18 years old : Ceftriaxone 125mg IM once OR Spectinomycin 40mg/kg IM once (max dose 2grams), Pathophysiology : Direct transmission of pathogens onto the conjunctiva leads to infectious conjunctivitis. Conjunctivitis can occur when the epithelial layer of the eye is compromised, or there is disruption in overall defense mechanisms. An immunocompromised state may also predispose to bacteri?al conjunctivitis., Epidemiology : highest incidence is in sexually active women aged 15 to 24, GOOD, If you or your child has bacterial or viral pink eye, your healthcare provider may recommend staying home from work, school or daycare until you’re no longer contagious. Check with your healthcare provider to find out how long that may be. You’re usually less likely to spread the infection if you’ve been on antibiotics for 24 hours or no longer have symptoms.,,Following good general hygiene and eye care practices can also help prevent the spread of pink eye.,,Don’t touch or rub the infected eye(s).,Wash your hands often with soap and water.,Wash any discharge from your eyes twice a day using a fresh cotton ball. Throw away the cotton ball and wash your hands with soap and warm water afterward.,Wash your hands after applying eye drops or ointment to your eye or someone else’s eye.,Don’t share personal items such as makeup, contact lenses, towels or cups., To Do : MAINTAIN HYGIENE,BALANCED DIET,. use condoms consistently and correctly each time you have sex. Condoms are very effective against the spread of STIs, such as gonorrhea and chlamydia, which can lead to cervicitis., Complications : PID, HIV, blindness, Corneal perforation, corneal ulceration, Diagnostics : Complete Blood Count CBC, Gram Staining, MRI, HISTORY TAKING, PHYSICAL EXAMINATION, conjunctival swab, Differential diagnosis : acute angle-closure glaucoma, Acute Pyelonephritis, allergic conjunctivitis, bacterial vaginosis, candidiasis, Chemical burns, dry eyes, EPISCLERITIS, Lichen Planus, vaginitis, disease description : Chronic cervicitis is commonly encountered in practice. It affects almost 80% women. It commonly follows genital tract trauma sustained during childbirth, the tissue trauma may follow instrumentation (D&C), or be a sequel of a sexually transmitted disease (STD) infection. chronic having mostly non-infectious sources .

Chronic Cervicitis

Disease Name : Chronic Cervicitis, Treatment : Chlamydia : Azithromycin 1 g orally once or doxycycline 100 mg orally twice a day for 7 days,Gonorrhea : Ceftriaxone 500 mg IM once for patients weighing < 150 kg or 1g IM once for patients weighing = 150 kg plus azithromycin 1 g orally once (due to emerging resistance of N. gonorrhoeae to cephalosporins).,If cervicitis persists despite treatment, reinfection with chlamydiae and N. gonorrhoeae should be ruled out, and empiric treatment with moxifloxacin 400 mg orally once a day for 7 to 14 days (eg, for 10 days) should be started to cover possible M. genitalium infection., DIATHERMY CAUTERIZATION, CRYOSURGERY, LASER THERAPY, CONIZATION, Policresulen : nan, Pathophysiology : In chronic cervicitis, pus and mucus are discharged from the cervical canal and bathe the cervix. The discharge is alkaline and tends to cause maceration of the squamous epithelium so that after a time the cells desquamate and leave a raw red area denuded of epithelium around the external os. In the process of healing, columnar epithelium from the cervical canal grows over and covers the denuded area so that macroscopically the red area is covered by smooth glistening translucent epithelium. The affected area around the external os is a simple flat erosion. After a variable interval, the squamous epithelium of the vaginal portion of cervix replaces the columnar epithelium of the erosion, the squamous epithelium growing under the columnar epithelium and gradually pushing it away, until finally the squamous epithelium has completely grown over the eroded area. Unless chronic cervicitis has been cured in the meantime, chronic cervicitis leads to recurrent erosions of the cervix. Sometimes, the columnar epithelial cells of endocervix undergo squamous change. This squamous downgrowth is known as epidermization. Its importance lies in the fact that, to the untutored eye, it looks like an epidermoid carcinoma which has invaded the glands. The condition is neither malignant nor premalignant. Follicular cystic erosion is produced by the squamous epithelium occluding the mouths of these glands, as it replaces the columnar epithelium of the erosion during the stage of healing. The blocked glands become distended with secretion and form small cysts which can be seen with the naked eye, the so-called nabothian follicles Hormonal or Papillary Erosion Hyperplasia of endocervical epithelium has been postulated to cause the papillary type of cervical erosion. One cause of this columnar epithelial hyperplasia is hormonal overactivity. These papillary erosions are therefore commonly seen in pregnancy and they tend to regress spontaneously in the puerperium. During pregnancy, oestrogen is mainly responsible for causing erosion. Women who take hormonal contraceptives also show hyperplasia of the endocervical epithelium and papillary erosion on the cervix. These regress after the drug is discontinued. These erosions can become infected by microorganisms from the vagina, when chronic cervicitis coexists with erosion., Epidemiology : 7.3% M genitalium urogenital infection in high-risk populations and 2.0% in low-risk populations., highest incidence is in sexually active women aged 15 to 24, GOOD, Though you can’t always prevent cervicitis, you can reduce your risk by practicing safe sex. Using condoms every time you have intercourse will drastically reduce your risk of sexually transmitted infections., Complications : abscess, infection, PID, HIV, CHRONIC PAIN, Ectopic pregnency, Diagnostics : Complete Blood Count CBC, PAP SMEAR, Total Leucocyte Count (TLC), USG ABDOMEN(W/A), biopsy, CERVICAL SWAB CULTURE, BIMANUAL EXAMINATION, HISTORY TAKING, Differential diagnosis : Acute Pyelonephritis, allergic reaction, candidiasis, Cytomegalovirus (CMV), Lichen Planus, Trauma, vaginitis, disease description : Chronic cervicitis is commonly encountered in practice. It affects almost 80% women. It commonly follows genital tract trauma sustained during childbirth, the tissue trauma may follow instrumentation (D&C), or be a sequel of a sexually transmitted disease (STD) infection .chronic having mostly non-infectious sources.

Chronic Constrictive Pericarditis

Disease Name : Chronic Constrictive Pericarditis, Treatment : medication : Furosemide , Spironolactone , Diuretics are useful during preoperative preparation., Pericardial resection is the only definitive treatment of constrictive,pericarditis and should be as complete as possible.. Coronary arteriography should be carried out preoperatively,in patients aged >50 years to exclude unsuspected accompanying,coronary artery disease. The benefits derived from cardiac decortication are usually progressive over a period of months., Pathophysiology : The basic physiologic abnormality in patients with chronic constrictive pericarditis is the inability of the ventricles to fill because of the limitations imposed by the rigid, thickened pericardium. Ventricular filling is unimpeded during early diastole but is reduced abruptly when the elastic limit of the pericardium is reached, whereas in cardiac tamponade, ventricular filling is impeded throughout diastole. In both conditions, ventricular end-diastolic and stroke volumes are reduced and the end-diastolic pressures in both ventricles and the mean pressures in the atria, pulmonary veins, and systemic veins are all elevated to similar levels (i.e., within 5 mmHg of one another). Despite these hemodynamic changes, systolic function may be normal or only slightly impaired at rest. However, in advanced cases, the fibrotic process may extend into the myocardium and cause myocardial scarring and atrophy, and venous congestion may then be due to the combined effects of the pericardial and myocardial lesions. In constrictive pericarditis, the right and left atrial pressure pulses display an M-shaped contour, with prominent x and y descents. The y descent, which is absent or diminished in cardiac tamponade, is the most prominent deflection in constrictive pericarditis; it reflects rapid early filling of the ventricles. The y descent is interrupted by a rapid rise in atrial pressure during early diastole, when ventricular filling is impeded by the constricting pericardium. These characteristic changes are transmitted to the jugular veins, where they may be recognized by inspection. In constrictive pericarditis, the ventricular pressure pulses in both ventricles exhibit characteristic “square root” signs during diastole. These hemodynamic changes, although characteristic, are not pathognomonic of constrictive pericarditis and may also be observed in restrictive cardiomyopathies., Epidemiology : There is a 3 : 1 male predominance., about 9% of people with acute pericarditis, NOT SPECIFIED, Constrictive pericarditis happens unpredictably, so it’s not possible to prevent it. The only thing you can do to reduce your risk of developing this condition is to avoid situations that might lead to developing it. One example is getting bacterial infections treated quickly rather than delaying care. Another is for medical personnel to limit radiation damage to your pericardium if you receive radiation therapy., Complications : death, Hypoxia, metabolic acidosis, pulmonary hypertension, renal failure, HEPATOMEGALY, Diagnostics : CT Thorax, ECG, X RAY CHEST, doppler echocardiography, MRI, X RAY, Differential diagnosis : Acute Pericarditis, amyloidosis, ATRIAL MYXOMA, cardiac temponade, Hemochromatosis, HIV infection and AIDS, nephrotic syndrome, OVARIAN CANCER, PERICARDIAL EFFUSION, Sarcoidosis, tricuspid regurgitation, disease description : Constrictive pericarditis is a condition in which granulation tissue formation in the pericardium results in loss of pericardial elasticity leading to restriction in the ventricular filling. It is usually a chronic condition .

Chronic Dacryocystitis

Disease Name : Chronic Dacryocystitis, Treatment : medication : Oxymetazoline , Moxifloxacin , 1. Balloon catheter dilation, 2.Dacryocystorhinostomy (DCR), 3.Dacryocystectomy (DCT), 4.Conjunctivodacryocystorhinostomy (CDCR), Pathophysiology : Dacryocystitis, regardless of etiology, is almost always caused by an obstruction in the nasolacrimal system with the resultant stagnation of tears. There can be obstructions at any level of the nasolacrimal system. Stagnation of tears will provide a favorable environment for infectious organisms to propagate and proteinaceous debris to form. The lacrimal sac will then inflame causing the characteristic swelling in the inferomedial portion of the orbit . Chronic dacryocystitis is commonly attributed to the effects of stricture of the nasal duct arising from chronic inflammation, usually of nasal origin. Obstruction to the lower end of the nasal duct may also be caused by the pressure of nasal polypi, a hypertrophied inferior turbinate bone or extreme deviation of the septum. This accumulation of secretions and tears within the lacrimal sac is easily infected. Ethmoidal infections are frequently associated with dacryocystitis., Epidemiology : The prevalence rate of dacryocystitis was 19.5 cases per 10, 000 patients, and the incidence rate was 15 cases per 10, 000 patients., occurs in roughly 1 in 3884 live births., GOOD, You can prevent future infections by having surgery called dacryocystorhinostomy to widen the blocked duct.,,If you or your child often gets tear duct infections, one way to prevent them is to drain the tear sac. Wash your hands, then hold a warm, wet washcloth over the tear sac. Carefully place your finger in the corner of your eye near your nose and apply pressure to the tear sac. Fluid or pus should release from the sac. Afterward, hold the warm compress to your eye again., Complications : chronic dacryocystitis, conjunctivitis, endophthalmitis, Loss of vision, ECTROPION, corneal ulceration, Diagnostics : CT SCAN, Regurgitation test, Dacryocystography, Differential diagnosis : ACUTE ETHMOID SINUSITIS, ACUTE FRONTAL SINUSITIS, Dacryoadenitis, maxillary sinusitis, orbital cellulitis, periorbital cellulitis, PRESEPTAL CELLULITIS, Sebaceous cyst, disease description : Dacryocystitis is characterized as an inflammatory state of the nasolacrimal sac. It is typically caused by an obstruction within the nasolacrimal duct and subsequent stagnation of tears in the lacrimal sac. When the lacrimal sac inflames and swells at the inferomedial canthus, dacryocystitis can be appreciated clinically  .Chronic dacryocystitis is a result of chronic obstruction due to systemic disease, repeated infection, dacryoliths, and chronic inflammatory debris of the nasolacrimal system. Chronic dacryocystitis is more common than the acute dacryocystitis.

Chronic Diarrhea

Disease Name : Chronic Diarrhea, Treatment : medication : Sulfamethoxazole and Trimethoprim (Co-trimoxazole), Albendazole , Ceftriaxone , Azithromycin , Ciprofloxacin , Nitazoxanide , Vancomycin , Metronidazole , Zinc/Zinc Sulphate, Sulfamethoxazole + Trimethoprim Co-trimoxazole , Treatment,includes general supportive measures, nutritional rehabilitation, elimination diet, ,and medications.,In moderate to severe malnutrition, caloric intake,should be carefully advanced to avoid the development of refeeding syndrome,and may be progressively increased to 50% or more above the recommended,dietary allowances. The intestinal absorptive capacity should be monitored by,digestive function tests. In children with steatorrhea, medium-chain triglycerides,may be the main source of lipids.,A lactose-free diet should be started in all,children with chronic diarrhea and is recommended by the World Health,Organization. Lactose is generally replaced by maltodextrin or a combination of,complex carbohydrates.,Micronutrient and vitamin supplementation are part of nutritional,rehabilitation, especially in malnourished children in developing countries. Zinc,supplementation is important in both prevention and therapy of chronic diarrhea, ,since it promotes ion absorption, restores epithelial proliferation, and stimulates,immune response.,Pharmacologic therapy includes, based on the etiology, anti-infectious drugs, ,immune suppression, and drugs that may inhibit fluid loss and promote cell,growth. If a bacterial agent is detected, specific antibiotics should be prescribed., Pathophysiology : The mechanisms of diarrhea are generally divided into secretory and osmotic , but often diarrhea is a combination of both mechanisms . In addition, inflammation and motility disorders may contribute to diarrhea. Secretory diarrhea is usually associated with large volumes of watery stools and persists when oral feeding is withdrawn. Osmotic diarrhea is dependent on oral feeding, and stool volumes are usually not as massive as in secretory diarrhea. Secretory diarrhea is characterized by active electrolyte and water fluxes toward the intestinal lumen, resulting from either the inhibition of neutral NaCl absorption in villous enterocytes or an increase in electrogenic chloride secretion in secretory crypt cells as a result of the opening of the cystic fibrosis transmembrane regulator (CFTR) chloride channel or both. The result is more secretion from the crypts than absorption in the villous that persists during fasting. The other components of the enterocyte ion secretory machinery are (1) the Na-K 2Cl cotransporter for the electroneutral chloride entrance into the enterocyte; (2) the Na-K pump, which decreases the intracellular Na+ concentration, determining the driving gradient for further Na+ influx; and (3) the K+ selective channel, that enables K+ , once it has entered the cell together with Na+ , to return to the extracellular fluid. Electrogenic secretion is induced by an increase of intracellular concentration of cyclic adenosine monophosphate, cyclic guanosine monophosphate, or calcium in response to microbial enterotoxins, or to endogenous endocrine or nonendocrine molecules, including inflammatory cytokines. Another mechanism of secretory diarrhea is the inhibition of the electroneutral NaCl-coupled pathway that involves the Na+ /H+ and the Cl- /HCO3 - exchangers. Defects in the genes of the Na+ /H+ and the Cl- /HCO3 - exchangers are responsible for congenital Na+ and Cl- diarrhea, respectively. Osmotic diarrhea is caused by nonabsorbed nutrients in the intestinal lumen as a result of one or more of the following mechanisms : (1) intestinal damage (e.g., enteric infection); (2) reduced absorptive surface area (e.g., active celiac disease); (3) defective digestive enzyme or nutrient carrier (e.g., lactase deficiency); (4) decreased intestinal transit time (e.g., functional diarrhea); and (5) nutrient overload, exceeding the digestive capacity (e.g., overfeeding, sorbitol in fruit juice). Whatever the mechanism, the osmotic force generated by nonabsorbed solutes drives water into the intestinal lumen. A very common example of osmotic diarrhea is lactose intolerance. Lactose, if not absorbed in the small intestine, reaches the colon, where it is fermented to short-chain organic acids, releasing hydrogen that is detected in the lactose breath test, and generating an osmotic overload. Another risk for chronic osmotic diarrhea often noted in patients with diarrhea-associated irritable bowel syndrome are foods containing FODMAPs (fermentable oligo-di-monosaccharides and polyols). In many children chronic diarrhea may be caused by the combination of multiple mechanisms., Epidemiology : 3–15% of the population suffers from chronic diarrhea., 300-500 per 100, 000 persons., DEPENDS ON SEVERITY OF SYMPTOMS, Chronic diarrhea caused by an underlying medical condition isn’t always preventable. But you can prevent chronic diarrhea due to infection by taking steps to keep your food and water supply clean. For example : ,,Drink from a clean water source or filter your water.,Thoroughly clean meat before cooking.,Cook meat thoroughly.,Wash your hands after handling food.,Clean kitchen surfaces to prevent contamination.,Wash fruits and vegetables before consuming them.,Wash your hands after using the bathroom, changing a diaper, or attending to a sick person., Complications : Disturbances of electrolyte balance, failure to thrive, Dehydration, Diagnostics : Complete Blood Count CBC, Erythrocyte Sedimentation Rate (ESR), STOOL CULTURE, Thyroid Stimulating Hormone TSH, Differential diagnosis : Bile Acid Malabsorption, CELIAC DISEASE, Cholestasis, colon cancer, Crohn disease, CYSTIC FIBROSIS, Digestion and Absorption of food, DIVERTICULITIS, hyperthyroidism, impaired gastric motility, INFLAMMATORY BOWEL DISEASES, Irritable Bowel Syndrome, lymphoma, Mesenteric ischemia, Pancreatitis, Ulcerative Colitis, disease description : Diarrhea is a common term used to describe loose/watery stools which occur three or more times within 24 hours.  For diarrhea to be considered chronic, symptoms must be ongoing for four or more weeks .Virtually all patients will experience diarrhea at some point in time, and the definition of diarrhea will vary from patient to patient. It is essential for the physician to obtain specific information as to the precise nature of the patient’s symptoms to establish a definite diagnosis of diarrhea.  Most patients will use the term diarrhea to describe loose or watery stools, regardless of the frequency.

Chronic Eosinophilic Pneumonia

Disease Name : Chronic Eosinophilic Pneumonia, Treatment : medication : Prednisolone, Treatment is similar to most eosinophilic lung syndromes where,corticosteroids (oral) are the mainstay of treatment. The minimum dose of,steroid needed to induce remission is not known, but most clinicians recommend,prednisone (or equivalent) at 0.5 mg/kg/day for 2 wk. The dose is reduced to half,(0.025 mg/kg/day) for an additional 2 wk if symptoms have abated. The,remaining dose of steroid may need to be weaned over 6 mo. Symptoms and,pulmonary infiltrates rapidly disappear after initiation of this treatment but,frequently recur with tapering of the steroid., Pathophysiology : Eosinophils are multifunctional leukocytes implicated in innate and adaptive immunity. They mature in the bone marrow under stimulation from cytokines. In particular they are influenced by IL-5, IL-3, granulocyte-macrophage colony-stimulating factor, and transcription factors including delta-dbl-GATA-1, before circulating into the blood and subsequently into tissues. Eosinophils have intracytoplasmic granules containing proteins, toxins, chemokines, and proinflammatory degranulation of eosinophils releases these toxic substances into the tissues, which contributes to the pathophysiology of eosinophilic disorders. Eosinophils interact with multiple cellular pathways, including T helper lymphocytes, mast cells and basophils, macrophages, and multiple ILs, but recruitment of the eosinophil to the lung is likely mostly directed by IL-5 and the eotaxin subfamily of chemokines. In addition, recent work by Katoh et al suggests that IL-25 may perpetuate chronic eosinophilic inflammation of the lung. Histopathological lesions are related to the toxicity of granule release of eosinophils and are largely reversible with treatment, although tissue damage and remodeling can be seen. Osteopontin levels have been found to be elevated in bronchoalveolar lavage (BAL) fluid of patients with eosinophilic pneumonia including drug-induced eosinophilic pneumonia. They may play a role in the eosinophilic inflammation., Epidemiology : 0.54 cases per 100, 000 population per year., good, "Your ability to reduce your risk of developing eosinophilic pneumonia depends on what caused the condition. Allergies are the most common cause of high eosinophil levels and may be passed down in families (inherited). Medication can help prevent or control your immune systems allergic reactions.,,A healthy lifestyle, which includes reducing or quitting smoking, can also help reduce your overall risk of disease. Your healthcare provider can discuss options to help you reduce your risk of developing eosinophilic pneumonia.", Complications : Asthma, Churg-Strauss Syndrome, respiratory failure, Diagnostics : HRCT Thorax, CHEST X RAY, PULMONARY FUNCTION TEST(PFT), X RAY, EOSINOPHILS, BRONCHOALVEOLAR LAVAGE, Differential diagnosis : BRONCHIAL ASTHMA, Churg-Strauss Syndrome, Interstitial Lung Disease, MALIGNANCY, Pneumocystis jirovecii, Superficial Aspergillus infections, disease description : Chronic eosinophilic pneumonia (CEP) is a rare disorder characterized by the massive accumulation of eosinophils in the lungs (pulmonary eosinophilia). Eosinophils are a type of white blood cell and are part of the immune system. They are usually produced in response to allergens, inflammation or infection .

Chronic Fatigue Syndrome

Disease Name : Chronic Fatigue Syndrome, Treatment : CBT and graded exercise therapy (GET) have been found to be the,only beneficial interventions in CFS.,The intervention, ,typically consisting of 12–14 sessions over 6 months performed by,an experienced cognitive behavior therapist, helps CFS patients gain,control over their symptoms.GET targets deconditioning and exercise intolerance and usually,involves a home exercise program that continues for 3–5 months.,Walking or cycling is systematically increased, with set goals for,maximal heart rates., "Pain. If medicines such as ibuprofen (Advil, Motrin IB, others) and naproxen sodium (Aleve) dont help enough, prescription drugs sometimes used to treat fibromyalgia might be options for you. These include pregabalin (Lyrica), duloxetine (Cymbalta), amitriptyline or gabapentin (Neurontin).,Orthostatic intolerance. Some people with this condition, particularly adolescents, feel faint or nauseated when they stand or sit upright. Medications to regulate blood pressure or heart rhythms may be helpful.,Depression. Many people with long-term health problems, such as ME/CFS, are also depressed. Treating your depression can make it easier for you to cope with the problems associated with having a chronic disease. Low doses of some antidepressants also can help improve sleep and relieve pain.", Predictors of poor outcome are,insufficient motivation for the treatment, medical (including psychiatric) comorbidities, current disability claims, and severe pain., Pathophysiology : The pathophysiological mechanisms leading to chronic fatigue syndrome are not entirely understood. It is proposed that an alteration in the nervous system occurs secondary to the body’s unintended responses to commonly encountered antigens leading to changes in the cell-mediated immunity, activation of oxidative pathways, and alteration in the neuroendocrinal and autoimmune responses against neurons. Multiple studies have shown alterations in the functioning of the natural killer (NK) cells, interleukins profile, and the decreased response of T cells to specific antigens .Some studies report chronic fatigue syndrome patients to have significantly increased oxidative stress, which plays a vital role in the etiopathogenesis of the disease. There is an increase in oxidative stress biomarkers like oxidized LDL and certain prostaglandins and, at the same time, a decrease in the amounts of the antioxidants like glutathione.The association between the onset of CFS with a viral infection has always been speculated. One of the interferon-activated antiviral pathways involves activating the 2’-5’-oligoadenylate (2-5A) synthetase/RNase L system., Epidemiology : CFS is seen worldwide, with adult prevalence rates, 0.2 and 0.4%., median annual recovery rate is 5% (range, 0–31%), Currently, there is no known way to prevent ME/CFS., Complications : muscle pain, muscle weakness, Irritability, Diagnostics : Blood Glucose test, Complete Blood Count CBC, CRP, SERUM IRON, SERUM Creatinine, Thyroid Stimulating Hormone TSH, SERUM CALCIUM LEVEL, Differential diagnosis : Adrenal Insufficiency, anemia, CELIAC DISEASE, DEPRESSION, HIV infection and AIDS, Hypothyroidism, "lymes disease", Multiple Sclerosis, obstructive sleep apnea, Orthostatic hypotension, Restless legs syndrome, disease description : Chronic fatigue syndrome, also called myalgic encephalomyelitis, is a complex multisystem disease commonly characterized by severe fatigue, cognitive dysfunction, sleep problems, autonomic dysfunction, and post-exertional malaise severely impairing activities of daily living. Outcomes become worse due to the condition remaining undiagnosed for years, secondary to inadequate medical teaching on the subject, provider bias,  and confusion regarding diagnosis and treatment of the disease. CFS does not only present with fatigue but also cognitive dysfunction and impairment of routine functioning that persists for six months or more. CFS is a biological condition, not a psychological disorder.

Chronic Graft-versus-host Disease

Disease Name : Chronic Graft-versus-host Disease, Treatment : medication : Mycophenolate mofetil/ Mycophenolate sodium, Hydroxychloroquine , Cyclophosphamide , Rituximab, Methotrexate, Imatinib, Azathioprine , Prednisolone, Thalidomide, Sirolimus / Rapamycin, Alemtuzumab, Moderate or severe cGvHD,First line,• Corticosteroids, e.g. prednisolone 1 mg/kg oral or IV – ,no standardized tapering regimens,• Oral calcineurin inhibitors – ciclosporin as a steroid sparer ,Second line,• Extracorporeal photopheresis,• Imatinib,• Sirolimus,• Pentostatin,• Rituximab ,Third line,• Mycophenolate mofetil,• Pulsed high-dose corticosteroids,• Methotrexate,Others,• Hydroxychloroquine, clofazemine, cyclophosphamide, ,alemtuzumab, anti-TNF antibodies, thalidomide, ,alefacept, retinoids, azathioprine, mesenchymal stem cells, Pathophysiology : Chronic GvHD was historically defi ned as occurring more than 100 days post-HSCT. However, classical cGvHD can present before 100 days. The skin is the most common site involved, followed by mucosa, but virtually any organ can be affected. Patients can report the insidious onset of dry, tight or itchy skin. It is important to ask about ocular discomfort and dryness as well as oral discomfort, often noted after eating spicy foods or using toothpaste. Patients may be hesitant to report genital symptoms such as vulvovaginal dryness, itch and discomfort without direct questioning. GI symptoms of nausea, diarrhoea and vomiting, respiratory symptoms of shortness of breath (where infection has been excluded) and musculoskeletal symptoms, including muscle weakness and limited range of movement, are important in this multisystem disease. The pathogenesis of cGvHD is not clearly understood. As yet, the complexity of cGvHD has not been reproducible in mouse models. Two theories of pathogenesis have been proposed as follows. ‘Autoimmune’ model of cGvHD pathogenesis. Clinical similarities with autoimmune diseases led to an autoimmune model of GvHD. GvHD patients have a high incidence of detectable autoantigens (such as antinuclear, double-stranded DNA, smooth muscle autoantibodies) and disease-related gene polymorphisms also found in patients with autoimmune disease. In the autoimmune model of cGvHD, decreased immune tolerance is postulated to allow the activation and proliferation of donor T cells directed at ‘self’-antigens shared between host and donor. Murine models suggest that donor T cells maturing in the host’s damaged thymus (due to conditioning regimens, age of recipient or aGvHD) escape from negative selection and then escape peripheral tolerance mechanisms, mediated by regulatory T cells (Tregs). Hence, analogous to autoimmunity, an imbalance between alloreactive T cells and Tregs may contribute. to GvHD developing. In support, alloreactive T-cell clones have been found in cGvHD animal models. These pathogenic T cells escape thymic tolerance mechanisms. Further work is needed to determine the relevance of these observations in humans. Chronic donor T-cell activation. A second model postulates that the presence of numerous disparate antigens may simply cause chronic stimulation of donor T cells, causing tissue damage and GvHD. This theory suggests that whilst non-polymorphic autoantigens are implicated in patients with autoimmunity, disparate histocompatibility antigens are targeted in GvHD patients. In support of this, the GvHD patient autoantibodies found do not correlate with organ-specifi c manifestations of GvHD., Epidemiology : The occurrence is typically higher in unmatched donors, incidence of chronic GVHD ranges from 6% to 80%, VARIABLE, Tissue typing labs are continually developing and using more precise DNA level tests to enable your care team to select the best HLA-matched donor for you. Closer matches can help prevent GvHD.,,Your healthcare provider will prescribe immunosuppressants after your transplant to prevent GvHD., Complications : bronchitis, Interstitial Lung Disease, Psychotic symptoms, limitations in range of motion, Diagnostics : Biopsy Large, skin biopsy with immunohistochemistry, Differential diagnosis : ADENOVIRUS INFECTION, Clostridium difficile infection, drug-induced liver injury, MALIGNANCY, Mycobacterium avium complex, Radiation recall dermatitis, thrombotic microangiopathy, Viral exanthem, viral hepatitis, disease description : Graft-versus-host disease (GvHD) is a systemic disorder that occurs when the grafts immune cells recognize the host as foreign and attack the recipient’s body cells. “Graft” refers to transplanted, or donated tissue, and “host” refers to the tissues of the recipient. Classic chronic GVHD : Presents after 100 days of transplant with classic clinical features of chronic GvHD.

Chronic Granulomatous Disease

Disease Name : Chronic Granulomatous Disease, Treatment : HSCT is the only known cure for CGD, although gene therapy has been,transiently successful in a few patients and is the topic of active research. HSCT,transplant for all patients with CGD is strongly recommended if a suitable,sibling or unrelated donor can be identified, Patients with CGD should be given daily oral TMP/SMX because it reduces,the number of bacterial infections. A placebo-controlled study found that,interferon 50 µg/m2 3 times/wk significantly reduces the number of,hospitalizations and serious infections, although the mechanism of action is,unclear. Itraconazole (200 mg/day for patients weighing >50 kg and 100 mg/day,for patients <50 kg and =5 yr old) administered prophylactically reduces the,frequency of fungal infections., Pathophysiology : CGD is due to a failure of the patient’s phagocytic leucocytes to kill various pathogens due to defective NADPH oxidase. This ultimately leads to poor ROS formation, which is a key molecule in the destruction of microbes. Most commonly, patients with CGD present with pneumonia typically due to catalase-positive organisms. Catalase is an enzyme that can inactivate the hydrogen peroxide that is produced by some bacteria and fungi. It is believed that patients with CGD can use hydrogen peroxide produced by catalase-negative microbes to form reactive oxidants and, consequentially, bypass the intrinsic CGD defect. However, catalase-positive organisms have a greater propensity to infect patients with CGD since phagocytes cannot hijack microbial hydrogen peroxide production., Epidemiology : occurs in 1 in every 200, 000 live births in the United States, On average, CGD patients survive at least 40 years, "When chronic granulomatous disease is caused by mutations in the CYBB gene, the condition is inherited in an X-linked recessive pattern and therefore it cant be prevented. ,,You cannot prevent CGD.,People with a family history of the disease who want to have children should seek genetic counseling to learn about the risk of having a child with the disorder.", Complications : infection, PNEUMONIA, lung damage, swollen lymphnodes, Diagnostics : Erythrocyte Sedimentation Rate (ESR) test, CT SCAN, NEUTROPHILS, Differential diagnosis : Acne conglobata, Acneiform eruptions, Aphthous stomatitis, Chronic mucocutaneous candidosis, Cutaneous candidiasis, Eosinophilic pustular folliculitis, folliculitis, Impetigo, iron deficiency anemia, seborrheic dermatitis, disease description : Chronic granulomatous  disease (CGD) is an inherited disorder that occurs when a type of white blood cell (phagocyte) that usually helps your body fight infections doesnt work properly. As a result, the phagocytes cant protect your body from bacterial and fungal infections.

Chronic Hepatitis B

Disease Name : Chronic Hepatitis B, Treatment : medication : Tenofovir/Tenofovir disoproxil fumarate, Entecavir , Lamivudine, Treatment of acute HBV infection is largely supportive. Close monitoring for,liver failure and extrahepatic morbidities is key. Treatment of chronic HBV,infection is in evolution; no 1 drug currently achieves consistent, complete,eradication of the virus.,The goal of treatment is to reduce viral replication defined by having,undetectable HBV DNA in the serum and development of anti-HBe, termed,seroconversion. The development of anti-HBe transforms the disease into an,inactive form, thereby decreasing infectivity, active liver injury and,inflammation, fibrosis progression, and the risk of HCC.,Interferon-a2b (IFN-a2b) has immunomodulatory and antiviral effects. It has been used in children, with long-term viral response rates similar,to the 25% rate reported in adults. Interferon (IFN) use is limited by its,subcutaneous administration, treatment duration of 24 wk, and side effects (flulike,symptoms, marrow suppression, depression, retinal changes, autoimmune,disorders). IFN is further contraindicated in decompensated cirrhosis. One,advantage of IFN, compared to other treatments, is that viral resistance does not,develop with its use., Pathophysiology : The acute response of the liver to hepatotropic viruses involves a direct cytopathic and/or an immune-mediated injury. The entire liver is involved. Necrosis is usually most marked in the centrilobular areas. An acute mixed inflammatory infiltrate predominates in the portal areas but also affects the lobules. The lobular architecture remains intact, although balloon degeneration and necrosis of single or groups of parenchymal cells commonly occur. Fatty change is rare except with HCV infection. Bile duct proliferation, but not bile duct damage, is common. Diffuse Kupffer cell hyperplasia is noticeable in the sinusoids. Neonates often respond to hepatic injury by forming giant cells . In fulminant hepatitis, parenchymal collapse occurs on the described background. With recovery, the liver morphology returns to normal within 3 mo of the acute infection. If chronic hepatitis develops, the inflammatory infiltrate settles in the periportal areas and often leads to progressive scarring. Both of these hallmarks of chronic hepatitis are seen in cases of HBV and HCV. HBV, a member of the Hepadnaviridae family, has a circular, partially doublestranded DNA genome composed of approximately 3, 200 nucleotides. Four constitutive genes have been identified : the S (surface), C (core), X, and P (polymer) genes. The surface of the virus includes particles, designated as the hepatitis B surface antigen (HBsAg), which consist of 22 nm diameter spherical particles and 22 nm wide tubular particles with a variable length of up to 200 nm. The inner portion of the virion contains the hepatitis B core antigen (HBcAg), the nucleocapsid that encodes the viral DNA, and a nonstructural antigen called the hepatitis B e antigen (HBeAg), a nonparticulate soluble antigen derived from HBcAg by proteolytic self-cleavage. HBeAg serves as a marker of active viral replication and usually correlates with the HBV DNA levels. Replication of HBV occurs predominantly in the liver but also occurs in the lymphocytes, spleen, kidney, and pancreas. The acute response of the liver to HBV is similar to that of other viruses. Persistence of histologic changes in patients with hepatitis B indicates development of chronic liver disease. HBV, unlike the other hepatotropic viruses, is a predominantly noncytopathogenic virus that causes injury mostly by immune-mediated processes. The severity of hepatocyte injury reflects the degree of the immune response, with the most complete immune response being associated with the greatest likelihood of viral clearance but also the most severe injury to hepatocytes. The first step in the process of acute hepatitis is infection of hepatocytes by HBV, resulting in expression of viral antigens on the cell surface. The most important of these viral antigens may be the nucleocapsid antigens—HBcAg and HBeAg. These antigens, in combination with class I major histocompatibility proteins, make the cell a target for cytotoxic T-cell lysis. The mechanism for development of chronic hepatitis B is less well understood. To permit hepatocytes to continue to be infected, the core protein or major histocompatibility class I protein might not be recognized, the cytotoxic lymphocytes might not be activated, or some other, yet unknown mechanism might interfere with destruction of hepatocytes., Epidemiology : WHO estimates that 296 million people were living with chronic hepatitis B infection in 2019, with 1.5 million new infections each year., 5.0 cases per 100, 000 people., GOOD, The best way to prevent infection is vaccination. If you’re vaccinated against the virus, you won’t have to worry about accidental exposure in your day-to-day life. However, it does take about six months to complete the three doses of the hepatitis B vaccine.,,In the short-term, you can reduce your risk by : ,,Practicing safe sex. If you don’t know whether your partner is infected, use a latex or polyurethane condom.,Not sharing personal items that might be exposed to blood, such as toothbrushes, razors, medical equipment or needles.,Planning ahead for travel abroad. If you plan to travel to regions where the rate of infection is relatively high, schedule your vaccinations for before you go.,Prophylactic treatment. If you think you may have recently been exposed, you can reduce your risk of infection by receiving a dose of vaccine and hepatitis B immune globulin within 24 hours., Complications : acute liver failure, Cerebral oedema, encephalopathy, Glomerulonephritis, Hepatic cirrhosis, hepatocellular carcinoma, Coagulopathy, Diagnostics : Anti HBc Antibody ELISA, Anti HBs Antibody ELISA, HBsAg, HBV DNA, HBV DNA, AST (SGOT), ALT blood test, Differential diagnosis : CHOLEDOCHAL CYST, CHOLELITHIASIS, CYSTIC FIBROSIS, EXTRAHEPATIC BILIARY ATRESIA, Hepatitis A, Hepatitis C, Hepatitis D, Hepatitis E, JUVENILE IDIOPATHIC ARTHITIS, Leptospirosis, Malaria, PRIMARY SCLEROSING CHOLANGITIS, WILSONS DISEASE, disease description : Hepatitis B is a viral infection that attacks the liver and can cause both acute and chronic disease.The virus is most commonly transmitted from mother to child during birth and delivery, as well as through contact with blood or other body fluids during sex with an infected partner, unsafe injections or exposures to sharp instruments. Less than 5% of otherwise healthy adults who are infected will develop chronic infection. About 15-25% of adults who become chronically infected during childhood die from hepatitis B related liver cancer or cirrhosis

Chronic Hypertrophic Laryngitis

Disease Name : Chronic Hypertrophic Laryngitis, Treatment : Voice rest and speech therapy. Voice rest has to be,prolonged for weeks or months. Patient should receive,training in proper use of voice., Eliminate infection of upper or lower respiratory,tract. Infection in the sinuses, tonsils, teeth or chronic,chest infection (bronchitis, bronchiectasis, tuberculosis, ,etc.) should be treated, Avoidance of irritating factors. E.g. smoking, alcohol,or polluted environment, dust and fumes, , STEAM INHALATIONS & EXPECTORANTS, AVOIDANCE OF IRRITANTS, Stripping of vocal cords, removing the hyperplastic,and oedematous mucosa, may be done in selected,cases., Pathophysiology : Pathological changes start in the glottic region and later may extend to ventricular bands, base of epiglottis and even subglottis. Mucosa, submucosa, mucous glands and in later stages intrinsic laryngeal muscles and joints may be affected. Initially, there is hyperaemia, oedema and cellular infiltration in the submucosa. The pseudostratified ciliated epithelium of respiratory mucosa changes to squamous type, and squamous epithelium of the vocal cords to hyperplasia and keratinization. The mucous glands suffer hypertrophy at first but later undergo atrophy with diminished secretion and dryness of larynx., Epidemiology : incidence was 3.47 per 1, 000 people. Up to 21% of the population may develop CL in their lifetime, GOOD, The best way to prevent infection is vaccination. If you’re vaccinated against the virus, you won’t have to worry about accidental exposure in your day-to-day life. However, it does take about six months to complete the three doses of the hepatitis B vaccine.,,In the short-term, you can reduce your risk by : ,,Practicing safe sex. If you don’t know whether your partner is infected, use a latex or polyurethane condom.,Not sharing personal items that might be exposed to blood, such as toothbrushes, razors, medical equipment or needles.,Planning ahead for travel abroad. If you plan to travel to regions where the rate of infection is relatively high, schedule your vaccinations for before you go.,Prophylactic treatment. If you think you may have recently been exposed, you can reduce your risk of infection by receiving a dose of vaccine and hepatitis B immune globulin within 24 hours., Complications : Breathing difficulty, loss of voice, Diagnostics : X RAY, PHYSICAL EXAMINATION, Differential diagnosis : allergic rhinitis, Laryngeal Carcinoma, laryngeal stenosis, upper respiratory tract infection, Vocal cord cysts, Vocal Nodule, Vocal Polyp, disease description : Chronic hypertrophic laryngitis occurs often as a result of abuse or misuse of the larynx. Constant trauma, especially in the presence of infection, produces permanent changes in the tissues. The result of this process may take the form of a localized area of inflammation or involvement of the entire membranous cord.It may be either a diffuse and symmetrical process or a localized one, the latter appearing like a tumour of the larynx. Localized variety presents as dysphonia plica ventricularis , vocal nodules, vocal polyp, Reinke’s oedema and contact ulcer.

Chronic Iridocyclitis

Disease Name : Chronic Iridocyclitis, Treatment : medication : Dexamethasone , Prednisolone, Moxifloxacin , Atropine/ Atropine methonitrate, Aspirin/Acetylsalicylic acid, Pathophysiology : Here is a general overview of the pathophysiological processes involved : Immune dysregulation : Chronic iridocyclitis is typically characterized by an abnormal immune response. It may result from an autoimmune disorder, such as ankylosing spondylitis, rheumatoid arthritis, or juvenile idiopathic arthritis. In these conditions, the immune system mistakenly targets the tissues of the eye, leading to chronic inflammation.Antigen presentation : Antigen-presenting cells (APCs), such as dendritic cells, encounter antigens within the eye or surrounding tissues. These antigens can be self-antigens or microbial antigens. The activated APCs process and present these antigens to T cells.T cell activation : The presented antigens interact with T cells, leading to their activation. In chronic iridocyclitis, there is an increased presence of activated T cells within the affected eye. These T cells produce various cytokines, particularly pro-inflammatory ones such as tumor necrosis factor-alpha (TNF-a), interleukin-1 (IL-1), and interleukin-6 (IL-6).Inflammatory cascade : The cytokines released by activated T cells recruit and activate other immune cells, such as macrophages and neutrophils, into the eye. This results in the release of additional inflammatory mediators, including prostaglandins, leukotrienes, and chemokines, which perpetuate the inflammatory response.Damage to ocular tissues : The chronic inflammation and influx of immune cells can lead to damage and destruction of ocular tissues, primarily affecting the iris and ciliary body. This damage can cause symptoms like eye pain, photophobia (sensitivity to light), blurred vision, and redness.Fibrosis and complications : Prolonged inflammation can lead to fibrosis and scarring within the eye, causing structural changes and potentially leading to complications such as posterior synechiae (adhesion of the iris to the lens), cataracts, glaucoma, or even vision loss., Epidemiology : approximately 5% of these patients, variable, There is not much you can do to prevent iritis. If you have an autoimmune condition, taking your medicines as prescribed may help prevent, Complications : blindness, endophthalmitis, RETINAL DETACHMENT, festooned pupil, Diagnostics : Differential Leucocyte Count DLC, Hb, PUS CULTURE, RBC Count, STOOL CULTURE, Total Leucocyte Count (TLC), URINE CULTURE, Urine Protein, X-RAY Abdomen, X RAY CHEST, Differential diagnosis : conjunctivitis, CORNEAL ULCER, EPISCLERITIS, SCLERITIS, Subconjunctival hemorrhages, ulcerative keratitis, WIDESPREAD INFLAMMATION OF THE SCLERA, disease description : Iridocyclitis is a type of anterior uveitis that involves the iris and ciliary body. It is a leading cause of visual impairment in many people. Persistent inflammation of the iris and ciliary body. The condition lasts more than 3 months, then recurs within 3 months of finishing treatment.

Chronic Iron Overload

Disease Name : Chronic Iron Overload, Treatment : medication : deferoxamine / desferrioxamine, The treatment for iron overload is reduction therapy. This is most commonly achieved through therapeutic phlebotomy. In patients with an acceptable hemoglobin level, phlebotomy can initially be prescribed every 1 to 2 weeks until serum ferritin is brought within acceptable levels. Then a schedule of periodic phlebotomy can be maintained, generally every 2 to 3 months, according to achieved serum ferritin levels, Pathophysiology : Primary iron overload is often inherited. Hereditary hemochromatosis is the leading case of iron overload disease. In 1996, 2 gene mutations (C282Y and H63D) of the HFE gene were discovered and linked to primary iron overload. The most common is C282Y. The introduction of excess iron into the body causes secondary iron overload. This occurs most commonly through blood transfusion but also can be due to hemolysis or excessive parenteral and/or dietary consumption, Epidemiology : 1 in 300 to 500 individuals., It is estimated that one in every 200 US white patients is positive for iron overload, and 10% to 14% are genetic mutation carriers., VARIABLE, You can’t prevent hemochromatosis, but you can get help controlling your iron levels. By identifying and treating hemochromatosis early, healthcare providers can help you avoid complications., Complications : Hypothyroidism, liver damage, hypogonadism in males, Diagnostics : LIVER FUNCTION TEST LFT, GENETIC TESTING, CHEST X RAY, SERUM FERRITIN LEVEL, Differential diagnosis : ALCOHOLIC LIVER DISEASE, Hemolytic anemia, Iron deficiency anemia, Porphyria Cutanea Tarda, disease description : Iron overload is defined as excess stores of iron in the body. Excess iron is deposited in organs throughout the body. The most notable organs with iron deposition are the liver, heart, and endocrine glands. The resulting symptoms and disease are related to specific organ damage.

Chronic Kidney Disease

Disease Name : Chronic Kidney Disease, Treatment : Eliminate infection of upper or lower respiratory tract. Infection in the sinuses, tonsils, teeth or chronic chest infection should be treated. Avoidance of irritating factors, e.g. smoking, alcohol or polluted environment. Voice rest and speech therapy. Voice rest has to be prolonged for weeks or months. Steam inhalations. They help to loosen secretions and give relief. Expectorants. They help to loosen viscid secretions and give relief from hawking., Pathophysiology : The pathophysiology of CKD involves two broad sets of mechanisms of damage : (1) initiating mechanisms specific to the underlying etiology (e.g., abnormalities in kidney development or integrity, immune complex deposition and inflammation in certain types of glomerulonephritis, or toxin exposure in certain diseases of the renal tubules and interstitium ) and (2) hyperfiltration and hypertrophy of the remaining viable nephrons, that are a common consequence following long-term reduction of renal mass, irrespective of underlying etiology and lead to further decline in kidney function . The responses to reduction in nephron number are mediated by vasoactive hormones, cytokines, and growth factors. Eventually, these short-term adaptations of hyperfiltration and hypertrophy to maintain GFR become maladaptive as the increased pressure and flow within the nephron predisposes to distortion of glomerular architecture, abnormal podocyte function, and disruption of the filtration barrier leading to sclerosis and dropout of the remaining nephrons .Increased intrarenal activity of the renin-angiotensin system (RAS) appears to contribute both to the initial compensatory hyperfiltration and to the subsequent maladaptive hypertrophy and sclerosis. This process explains why a reduction in renal mass from an isolated insult may lead to a progressive decline in renal function over many years ., Epidemiology : prevalence of CKD is around 10% to 14% in the general population, poor, "To Do : vaccination of pneumococcal vaccine, influenza vaccine, hepatitis b vaccine. Not To Do : salt and water restriction,stop nephrotoxic drugs. ,Follow instructions on over-the-counter medications. ,Dont smoke", Complications : fluid retention, Hyperparathyroidism, kidney damage, pericarditis, renal failure, Changes in blood sugar concentration, kidney dysfunction, heart disease, Diagnostics : ABG, SERUM Creatinine, Parathyroid Hormone (PTH), serum potassium K+, serum calcium Ca++, hemoglobin HB, SERUM PHOSPHATE TEST, USG, Differential diagnosis : acute kidney injury, Alport Syndrome, Diabetic Nephropathy, Glomerulonephritis, multiple myeloma, nephrolithiasis, Rapidly Progressive (Crescentic) Glomerulonephriti, RENAL ARTERY STENOSIS, disease description : Chronic kidney disease, also called chronic kidney failure, involves a gradual loss of kidney function. Your kidneys filter wastes and excess fluids from your blood, which are then removed in your urine. Advanced chronic kidney disease can cause dangerous levels of fluid, electrolytes and wastes to build up in your body. The risk of CKD progression is closely linked to both the GFR and the amount of albuminuria.

Chronic Laryngitis Without Hyperplasia

Disease Name : Chronic Laryngitis Without Hyperplasia, Treatment : Avoidance of irritating factors. E.g. smoking, alcohol,or polluted environment, dust and fumes.,3. Voice rest and speech therapy. Voice rest has to be,prolonged for weeks or months. Patient should receive,training in proper use of voice., Steam inhalations. They help to loosen secretions,and give relief.,5. Expectorants. They help to loosen viscid secretions,and give relief from hawking.,Eliminate infection of upper or lower respiratory,tract. Infection in the sinuses, tonsils, teeth or chronic,chest infection (bronchitis, bronchiectasis, tuberculosis, ,etc.) should be treated., Pathophysiology : Pathogenesis covers-1. It may follow incompletely resolved acute simple laryngitis or its recurrent attacks. 2. Presence of chronic infection in paranasal sinuses, teeth and tonsils and the chest are important contributory causes. 3. Occupational factors, e.g. exposure to dust and fumes such as in miners, strokers, gold or iron smiths and workers in chemical industries. 4. Smoking and alcohol. 5. Persistent trauma of cough as in chronic lung diseases. 6. Vocal abuse., Epidemiology : incidence of 3.5 /1000 in the general population, GOOD, Seeing your healthcare provider on a regular basis throughout your life is a good start for preventing kidney disease. About 1 in every 3 people in the United States is at risk for kidney disease. People at high risk may have regular tests to check for CKD so it’s detected as early as possible. Some other things you can do to prevent CKD are : ,,Manage your high blood pressure.,Manage your blood sugar if you have diabetes.,Eat a well-balanced diet.,Don’t smoke or use tobacco.,Be active for 30 minutes at least five days a week.,Maintain a healthy weight.,Take nonprescription pain relievers only as directed. Taking more than directed can damage your kidneys.,Limit alcohol-containing beverages., Complications : hoarseness of voice, loss of voice, Diagnostics : Direct Laryngoscopy, Differential diagnosis : Acute Epiglottits, chronic infection, Gastroesophageal reflux disease (GERD), granulomas, MALIGNANCY, smoking, disease description : It is a diffuse inflammatory condition symmetrically involving the whole larynx, i.e. true cords, ventricular bands, interarytenoid region and root of the epiglottis. Chronic laryngitis develops more slowly, with symptoms lasting over 3 weeks .Chronic laryngitis is a more severe condition than acute laryngitis as it can cause longer-lasting and more uncomfortable symptoms. It may also be a sign of a more serious underlying condition, such as an autoimmune disorder .

Chronic Liver Disease

Disease Name : Chronic Liver Disease, Treatment : medication : Lactulose , Rifaximin is a new,drug with a better safety profile. Nonabsorbable,disaccharides like lactulose and lactitol reach the colon,intact and then are metabolized by bacteria into variety,of small molecular weight organic acids. It acts by,acidifying fecal contents and trapping the diffusible,ammonia as ammonium ion in the fecal stream along with,alteration in colonic flora (loss of ammonia producing,bacteria). In infants and children, protein intake should,not be restricted to the point of causing growth failure or,compromising overall nutritional status and a target range,of 1-2 g/kg/day is often recommended, Pathophysiology : Chronic liver disease represents a continuous and progressive process of hepatic fibrosis, liver tissue architectural distortion, and regeneration nodule formation. While fibrosis is usually irreversible, but it can be reversible in the initial stage of development. The transition time point of reversible fibrosis to irreversible fibrosis is still not completely understood. In chronic liver disease, if not treated, the endpoint is usually irreversible fibrosis, regeneration nodule formation, and development of cirrhosis liver. The development rate of fibrosis is dependent on the underlying etiologies, environmental, and host factors. The evolution of liver fibrosis was studied in 4852 patients with different underlying etiology in one study. The author observed significant differences in the rate of development of fibrosis and its progression. The rate was most rapid in patients with coinfection with HIV- HCV, while primary biliary cirrhosis was the slowest. Fibrosis progression rate was higher with increasing age, and females demonstrated a more gradual progression of liver fibrosis in all but alcoholic liver disease .Similarly, in another study, genetic polymorphism was attributed as an underlying factor for the difference in fibrosis rate progressions and the development of more severe disease in some individuals compared to others with the same underlying etiology. Hepatic fibrosis is the deposition of extracellular matrix (ECM) in response to chronic liver injury by any etiology. The common pathway is initiated by hepatic stellate cells (HSC), which usually are vitamin A storing dormant cells found in space between sinusoids and hepatocytes., Epidemiology : 1, 395 cases per 100, 000 population, approximately 4.5 million adults had chronic liver, DEPENDS ON SEVERITY OF SYMPTOMS, You can take steps to prevent some types of liver disease — especially those affected by your diet and lifestyle. If you are at risk for liver disease, your provider may recommend lifestyle changes including : ,,Avoiding or limiting alcohol.,Avoiding foods and drinks that contain trans fats or high-fructose corn syrup.,Carefully managing your intake of prescription and over-the-counter medications to avoid liver damage, as medications like acetaminophen (Tylenol®) are a common cause of liver injury.,Getting regular exercise.,Limiting consumption of red meat.,You can minimize the likelihood of contracting viral hepatitis by practicing safe sex and not sharing needles., Complications : ascites, Hepatic cirrhosis, HEPATIC ENCEPHALOPATHY, hepatocellular carcinoma, PORTAL HYPERTENSION, hepatorenal syndrome, Diagnostics : Prothrombin Time Test and INR (PT/INR), USG ABDOMEN(W/A), serum albumin, CT SCAN, ALANINE TRANSAMINASE (SGPT), Bilirubin Conjugated, Differential diagnosis : CHOLEDOCHAL CYST, Chronic Hepatitis B, congestive heart failure (CHF), constrictive pericarditis, DILATED CARDIOMYOPATHY, EXTRAHEPATIC BILIARY ATRESIA, Galactosemia, Hepatitis C, Sarcoidosis, disease description : Chronic liver disease (CLD) is a progressive deterioration of liver functions for more than six months, which includes synthesis of clotting factors, other proteins, detoxification of harmful products of metabolism, and excretion of bile. CLD is a continuous process of inflammation, destruction, and regeneration of liver parenchyma, which leads to fibrosis and cirrhosis. The spectrum of etiologies is broad for chronic liver disease, which includes toxins, alcohol abuse for a prolonged time, infection, autoimmune diseases, genetic and metabolic disorders. Cirrhosis is a final stage of chronic liver disease that results in disruption of liver architecture, the formation of widespread nodules, vascular reorganization, neo-angiogenesis, and deposition of an extracellular matrix.

Chronic Lymphocytic(autoimmune) Thyroiditis

Disease Name : Chronic Lymphocytic(autoimmune) Thyroiditis, Treatment : medication : Levothyroxine/Tetra idothyronine, Amoxicillin and Clavulanic acid , The drug of choice is titrated levothyroxine sodium administered orally. It has a half-life of 7 days and can be given daily. It should not be given with iron or calcium supplements, aluminum hydroxide, and proton pump inhibitors to avoid suboptimal absorption. It is best taken early in the morning on an empty stomach for optimum absorption.,,The standard dose is 1.6 - 1.8 mcg/kg per day, but it can vary from one patient to another. Patients less than 50 years old should be commenced on a standard full dose; however, lower doses should be used in patients with cardiovascular diseases and the elderly. In patients older than 50 years, the recommended starting dose is 25 mcg/day with reevaluation in six to eight weeks., Pathophysiology : The pathophysiology of chronic lymphocytic thyroiditis involves various immune-mediated processes that result in the destruction of thyroid tissue. Here is a summary of the pathophysiological mechanisms involved : Autoantibody production : In chronic lymphocytic thyroiditis, the immune system mistakenly recognizes components of the thyroid gland as foreign. This leads to the production of autoantibodies, specifically anti-thyroid peroxidase (anti-TPO) and anti-thyroglobulin (anti-TG) antibodies. These antibodies target the thyroid gland and initiate an immune response.Infiltration of immune cells : The autoantibodies produced in the initial phase of the disease activate immune cells, particularly T lymphocytes. These immune cells infiltrate the thyroid gland, leading to the formation of lymphocytic infiltrates. These infiltrates consist of various immune cells, including T cells, B cells, macrophages, and natural killer cells.Cytokine release : The immune cells present in the thyroid gland release pro-inflammatory cytokines, such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-a). These cytokines further stimulate the immune response and contribute to the inflammation and destruction of thyroid tissue.Destruction of thyroid follicles : The immune response, along with the presence of autoantibodies, causes damage to the thyroid gland. The thyroid follicles, which are responsible for the production and release of thyroid hormones, undergo destruction. As a result, the thyroid glands ability to produce and secrete hormones is impaired.Hormonal imbalances : The destruction of thyroid follicles leads to a decrease in the production of thyroid hormones, primarily thyroxine (T4) and triiodothyronine (T3). This disruption in hormone production can result in a condition known as hypothyroidism, where the thyroid gland is underactive.Progression of the disease : Over time, chronic lymphocytic thyroiditis can lead to the formation of fibrous tissue within the thyroid gland, resulting in its shrinkage and a decrease in overall thyroid function. This fibrosis can further contribute to the development of hypothyroidism., Epidemiology : female-to-male ratio is at least 10 : 1., The incidence is estimated to be 0.8 per 1000 per year in men and 3.5 per 1000 per year in women, POOR, "There is no known way to prevent Hashimotos thyroiditis (or inflammation of the thyroid gland). But on the bright side, this disorder is very treatable. The sooner you get diagnosed, the sooner you can start receiving treatment.,,Hashimotos thyroiditis is an autoimmune disorder.", Complications : Goiter, Myxedema, Diagnostics : Anti TPO Antibodies, HISTOPATHLOGY, PROLACTIN, USG Thyroid, PLASMA CREATINE KINASE, THYROID PROFILE, Differential diagnosis : Goiter, "Graves disease", Hypopituitarism, Thyroid cancer, disease description : Hashimoto thyroiditis is an autoimmune disease that destroys thyroid cells by cell and antibody-mediated immune processes. It is the most common cause of hypothyroidism in developed countries. In contrast, worldwide, the most common cause of hypothyroidism is an inadequate dietary intake of iodine. This disease is also known as chronic autoimmune thyroiditis and chronic lymphocytic thyroiditis. The pathology of the disease involves the formation of antithyroid antibodies that attack the thyroid tissue, causing progressive fibrosis. The diagnosis is often challenging and may take time until later in the disease process. 

Chronic Lymphoid Leukemia (cll)

Disease Name : Chronic Lymphoid Leukemia (cll), Treatment : medication : Cyclophosphamide , Rituximab, Fludarabine, "Immunotherapy,Immunotherapy is a treatment that uses the patients immune system to fight cancer. Substances made by the body or made in a laboratory are used to boost, direct, or restore the bodys natural defenses against cancer. ,,Immunomodulating agent : Lenalidomide stimulates T cells to kill leukemia cells. It may be used alone or with rituximab in patients with symptomatic or progressive, recurrent, or refractory CLL.,CAR T-cell therapy : This treatment changes the patients T cells (a type of immune system cell) so they will attack certain proteins on the surface of cancer cells.", Targeted therapy,Targeted therapy is a type of treatment that uses drugs or other substances to identify and attack specific cancer cells.,,Tyrosine kinase inhibitor (TKI) therapy : This treatment blocks the enzyme, tyrosine kinase, that causes stem cells to develop into more white blood cells than the body needs. Ibrutinib, acalabrutinib, idelalisib, and duvelisib .,,BCL2 inhibitor therapy : This treatment blocks a protein called BCL2 which is found on some leukemia cells. This may kill leukemia cells and make them more sensitive to other anticancer drugs.,Monoclonal antibody therapy : Monoclonal antibodies are immune system proteins made in the laboratory to treat many diseases, including cancer. As a cancer treatment, these antibodies can attach to a specific target on cancer cells or other cells that may help cancer cells grow., Pathophysiology : The pathogenesis of CLL/SLL is a two-step process that leads to the clonal replication of malignant B lymphocytes. The first step is the development of MBL cells secondary to multiple factors such as antigenic stimulation, genetic mutations, and cytogenetic abnormalities. The second step is the progression of MBL to CLL/SLL by the further insult to the B-cell clone, either due to additional genetic abnormalities or changes in the bone marrow microenvironment. B-cell antigen receptor (BCR) expression induces antigen-independent cell-autonomous signaling, which is an important step in the pathogenesis of CLL., Epidemiology : 4.5/100000 IN US, POOR, There’s no known way to prevent CLL., Complications : autoimmune haemolytic anaemia, CARCINOMA OF BREAST, Glomerulonephritis, granulocytopenia, infections, neuropathy, PNEUMONIA, prostate cancer, vasculitis, Immune thrombocytopenia, Skin cancer lesions, Diagnostics : Flowcytometry CLL Panel, Peripheral Blood Smear, Peripheral Blood Smear, LYMPHOCYTES - ABSOLUTE COUNT, B CELL MARKER CD19, T CELL MARKER CD5, skin lesion biopsy, Differential diagnosis : Acute lymphoblastic leukemia, Acute promyelocytic leukemia, autoimmune haemolytic anaemia, Diffuse large B-cell lymphoma, hairy cell leukemia, mantle cell lymphoma, "non-hodgkins lymphoma", disease description : Chronic lymphocytic leukemia (CLL) is a monoclonal proliferation of mature B lymphocytes defined by an absolute number of malignant cells in the blood (5 × 109/mL). The presence of malignant B cells under this count in the blood without nodal, spleen, or liver involvement and absent cytopenias is a precursor of this disease called monoclonal B-cell lymphocytosis (MBL) with ~1–2% chance per year of progressing to overt CLL. CLL is a heterogeneous disease in terms of natural history, with some pat

Chronic Mucocutaneous Candidosis

Disease Name : Chronic Mucocutaneous Candidosis, Treatment : medication : Fluconazole , Itraconazole , Voriconazole , Systemic anti-,Candida therapy with fluconazole, itraconazole or voriconazole ,is usually necessary, and treatment may have to be prolonged ,and repeated., Therapy for cutaneous candidiasis is dominated by topical antifungal agents. Azole antifungal cream (e.g., bifonazole, ketoconazole, neticonazole hydrochloride, lanoconazole and luliconazole) is most effective. Terbinafine hydrochloride and amorolfine hydrochloride are also useful., Pathophysiology : Overall, the pathophysiology of CMC involves a complex interplay of innate and adaptive immune responses. Defects in epithelial barrier function, phagocyte function, T-cell function, regulatory T-cell function, and the development of autoantibodies can all contribute to the susceptibility to chronic and recurrent Candida infections seen in individuals with CMC.Chronic mucocutaneous candidiasis (CMC) is a rare immune disorder characterized by recurrent or persistent infections caused by Candida species, particularly Candida albicans. The pathophysiology of CMC involves both innate and adaptive immune responses., Epidemiology : occurring in about 1 : 100, 000 individuals, most common in babies younger than 6 months old and in older adults., poor, the infections of chronic mucocutaneous candidiasis can be controlled with a topical antifungal ., Complications : death, sepsis, mycotic infection, Diagnostics : FUNGAL CULTURE, PHYSICAL EXAMINATION, Differential diagnosis : anaemia, Cutaneous candidiasis, Denture-related stomatitis, Diabetes mellitus type 1, DiGeorge syndrome, erythema migrans, Erythroplakia, mucositis, disease description : chronic mucocutaneous candidiasis (CMCC) is a heterogeneous group of syndromes with the common features of chronic noninvasive Candida infections of the skin, nails, and mucous membranes that are usually resistant to topic treatment and absence of invasive fungal infections. The classic forms have associated autoimmune manifestations (most commonly endocrinopathies), and patients may have other microbial infections. Milder forms have oral candidiasis with or without associated staphylococcal skin infections. CMCC is caused by genetic defects in the immune system .

Chronic Myeloid Leukemia

Disease Name : Chronic Myeloid Leukemia, Treatment : medication : Hydroxycarbamide (Hydroxyurea), Imatinib, Interferon Beta, bosutinib, Adult Variety of CML : The aim of treatment during chronic phase is to control,the increasing white cell counts. This can usually be,achieved by single agent chemotherapy with either,busulfan or hydroxyurea. However, these agents are being,replaced with P-interferon and tyrosine kinase inhibitor, ,imatinib mesylate. The blood counts return to normal or near,normal in almost all patients within 6-8 weeks. Spleen,size also decreases. Allogeneic stem cell,transplantation is now used for patients who do not,respond to tyrosine kinase inhibitors. Juvenile Chronic Myeloid Leukemia : Management,involves supportive care including packed red cell,and platelet transfusions, treatment of infections and,allogeneic stem cell transplant if a matched sibling donor,is present. Even with transplant, there is 30-50% eventfree,survival rate at 3 yr. Cis-retinoic acid has been tried,with some benefit., Pathophysiology : The pathophysiology of CML involves a genetic abnormality known as the Philadelphia chromosome and dysregulated signaling pathways.Philadelphia Chromosome : The majority of CML cases (about 95%) are associated with a specific genetic abnormality called the Philadelphia chromosome. This chromosome results from a reciprocal translocation between chromosomes 9 and 22. It leads to the fusion of two genes : the Abelson (ABL) gene from chromosome 9 and the breakpoint cluster region (BCR) gene from chromosome 22. The resulting fusion gene is called BCR-ABL.BCR-ABL Oncogene : The BCR-ABL fusion gene produces a protein with constitutive tyrosine kinase activity. This abnormal protein, known as BCR-ABL oncoprotein, is the key driver of CML pathogenesis. It leads to dysregulated signaling pathways involved in cell proliferation, survival, and differentiation.Dysregulated Signaling Pathways : The BCR-ABL oncoprotein activates several signaling pathways, including the Ras/MAPK, JAK/STAT, and PI3K/AKT pathways. These pathways are involved in cell growth, survival, and differentiation. The constitutive activation of these pathways in CML disrupts normal cellular processes and promotes uncontrolled proliferation of myeloid cells.Increased Myeloid Cell Production : The dysregulated signaling pathways caused by the BCR-ABL oncoprotein lead to an overproduction of myeloid cells in the bone marrow. These abnormal myeloid cells, including granulocytes, monocytes, and platelets, accumulate and interfere with the normal production of healthy blood cells.Altered Apoptosis : The BCR-ABL oncoprotein inhibits programmed cell death, or apoptosis, which normally eliminates damaged or abnormal cells. This leads to the survival and accumulation of malignant myeloid cells in the bone marrow and peripheral blood.Progression to Blast Crisis : Without appropriate treatment, CML can progress from the chronic phase to an accelerated phase and eventually to a blast crisis. In the blast crisis phase, the disease becomes more aggressive, and immature blast cells resembling those found in acute leukemia proliferate rapidly.Understanding the pathophysiology of CML has led to the development of targeted therapies known as tyrosine kinase inhibitors (TKIs), which specifically inhibit the activity of the BCR-ABL oncoprotein. TKIs have revolutionized the treatment of CML, allowing for effective disease control and prolonged survival for many patients., Epidemiology : rare in children accounting for 3-5% cases, 1-2 per 100, 000 population per year, POOR, No, it can’t. Medical researchers know CML happens when a specific gene mutates, but they haven’t discovered why that mutation happens., Complications : bone pain, hepatosplenomegaly, thrombocytopenia, Recurrent infection, Diagnostics : BONE MARROW ASPIRATION, BONE MARROW ASPIRATION, Hb, PLATELET COUNT, White Blood Cell count WBC, RT PCR AMPLIFICATION, Differential diagnosis : Acute Myeloid Leukemia, Essential Thrombocytosis, Idiopathic Thrombocytopenic Purpura, myelodysplastic syndrome (MDS), myelofibrosis, Polycythemia vera, disease description : Chronic myeloid or myelogenous leukemia (CML) is a myeloproliferative disorder. CML is primarily a disease of middle age; the peak incidence is in the fourth and fifth decade. However, it may occur at any age including infants and young children. Chronic myeloid leukemia is a slow-growing cancer of the blood-forming tissue (bone marrow). Normal bone marrow produces red blood cells (erythrocytes) that carry oxygen, white blood cells (leukocytes) that protect the body from infection, and platelets (thrombocytes) that are involved in blood clotting.In chronic myeloid leukemia, the bone marrow produces too many white blood cells.

Chronic Nasopharyngitis

Disease Name : Chronic Nasopharyngitis, Treatment : Chronic infections of the nose, paranasal sinuses and oropharynx,should be attended to. Excessive smoking and,drinking should be corrected. Preventive measures should,be taken to avoid dust and fumes. Alkaline nasal douche,helps to remove crusts and mucopus, Initial medical management consisted of regular saline irrigation plus a 14-day course of doxycycline 100 mg daily, combined with rifampicin 200 mg twice daily. When this proved unsuccessful, patients subsequently received a four-week course of omeprazole 40 mg daily., Pathophysiology : It is often associated with chronic infections of nose, paranasal sinuses and pharynx. It is commonly seen in heavy smokers, drinkers and those exposed to dust and fumes. Postnasal discharge and crusting with irritation at the back of nose is the most common complaint. Patient has a constant desire to clear the throat by hawking or inspiratory snorting (forcefully drawing nasal secretions back into the throat). Examination of nasopharynx reveals congested mucosa and mucopus or dry crusts. In children, adenoids are often enlarged and infected (chronic adenoiditis)., Epidemiology : nan, adults have two to four colds per year, and children may have between six and 10 colds per year., 500 out of every 1, 000 family physician, GOOD, The best way to treat a cold is to prevent one from happening in the first place. Here are some tips for preventing a cold : ,,Wash your hands often with soap, especially when around others with colds.,Wash or disinfect commonly used items, like toys, doorknobs, phones, and faucet handles.,Use a hand sanitizer when you don’t have access to soap and water.,Use your own pen to sign receipts in stores.,Sneeze into a tissue or your sleeve, and cover your mouth when you cough to stop the spread of the virus.,Get a flu shot.,Some evidence also suggests that taking a garlic supplement with 180 milligrams of allicin for 3 months, or taking 0.25 grams of vitamin C daily, may help prevent colds., Complications : bronchitis, PNEUMONIA, Diagnostics : PHYSICAL EXAMINATION, Differential diagnosis : allergic reaction, chronic tonsillitis, Influenza, Nasopharyngeal carcinoma, PNEUMONIA, vasomotor rhinitis, disease description : Nasopharyngitis is another name for the common cold. It is a mild infection of the nose and throat that can produce symptoms such as a runny nose, sneezing, and coughing.Nasopharyngitis develops due to viruses.Nasopharyngitis is the inflammation of the nasal passages and the pharynx, or throat. 

Chronic Obstructive Pulmonary Disease

Disease Name : Chronic Obstructive Pulmonary Disease, Treatment : medication : Ipratropium bromide , Formoterol Fumarate , Azithromycin , Prednisolone, Bronchodilators, Anticholinergic Muscarinic Antagonists, Beta Agonists, Combinations of Beta Agonist — Muscarinic Antagonist, Inhaled Corticosteroids, Oral Glucocorticoids, Theophylline, PDE4 Inhibitors, Antibiotics, Oxygen are used., Pathophysiology : COPD is an inflammatory condition involving the airways, lung parenchyma, and pulmonary vasculature. The process is thought to involve oxidative stress and protease-antiprotease imbalances. Emphysema describes one of the structural changes seen in COPD where there is destruction of the alveolar air sacs (gas-exchanging surfaces of the lungs) leading to obstructive physiology. In emphysema, an irritant (e.g., smoking) causes an inflammatory response. Neutrophils and macrophages are recruited and release multiple inflammatory mediators. Oxidants and excess proteases leading to the destruction of the air sacs. The protease-mediated destruction of elastin leads to a loss of elastic recoil and results in airway collapse during exhalation. Alpha-1 antitrypsin deficiency is a rare cause of emphysema which involves a lack of antiproteases and the imbalance leaves the lung parenchyma at risk for protease-mediated damage. AATD is caused by misfolding of the mutated protein which can accumulate in the liver. AATD should be suspected in COPD patients who present with liver damage. As opposed to smoking-related emphysema, AATD primarily involves the lower lobes.  The inflammatory response and obstruction of the airways cause a decrease in the forced expiratory volume (FEV1) and tissue destruction leads to airflow limitation and impaired gas exchange. Hyperinflation of the lungs is often seen on imaging studies and occurs due to air trapping from airway collapse during exhalation. The inability to fully exhale also causes elevations in carbon dioxide (CO2) levels. As the disease progresses, impairment of gas exchange is often seen. The reduction in ventilation or increase in physiologic dead space leads to CO2 retention. Pulmonary hypertension may occur due to diffuse vasoconstriction from hypoxemia ., Epidemiology : prevalence of COPD was 174 million and there were approximately 3.2 million deaths due to COPD worldwide, >10 million persons in the United States, POOR, Not smoking is the best thing you can do to avoid developing COPD. If you’d like to quit, smoking cessation programs can help you. Also, avoid any environment that has poor air quality — air that has particles like dust, smoke, gases and fumes.,,,,People with COPD have difficulty clearing their lungs of bacteria, dusts and other pollutants in the air. This makes them at risk for lung infections that may cause further damage to the lungs.,,Therefore, it is important to watch for signs of infection and follow these tips to help prevent infections. You probably won’t be able to avoid infections entirely, but these tips will help you prevent infections as much as possible., Complications : Flu-like illness, Lung cancer, PNEUMONIA, heart problem, DEPRESSION, Diagnostics : X RAY CHEST, PULMONARY FUNCTION TEST(PFT), CT SCAN, spirometry, Differential diagnosis : Asthma, BRONCHIECTASIS, BRONCHIOLITIS, bronchitis, BRONCHOGENIC CARCINOMA, chronic cough, Congestive heart failure, emphysema, heart failure, Pulmonary Embolism, TUBERCULOSIS, disease description : Chronic obstructive pulmonary disease (COPD) is a common lung disease causing restricted airflow and breathing problems. It is sometimes called emphysema or chronic bronchitis.In people with COPD, the lungs can get damaged or clogged with phlegm. Symptoms include cough, sometimes with phlegm, difficulty breathing, wheezing and tiredness.Smoking and air pollution are the most common causes of COPD. People with COPD are at higher risk of other health problems.COPD is not curable but symptoms can improve if one avoids smoking and exposure to air pollution and gets vaccines to prevent infections. It can also be treated with medicines, oxygen and pulmonary rehabilitation.

Chronic Osteomyelitis

Disease Name : Chronic Osteomyelitis, Treatment : medication : Clindamycin , Vancomycin , Fusidic acid /Sodium Fusidate, Teicoplanin, cephalosporins, LOCAL TREATMENT,A sinus may be painless and need dressing simply to,protect the clothing. Colostomy paste can be used,to stop excoriation of the skin. An acute abscess may,need urgent incision and drainage, but this is only a,temporary measure., 1- Debridement,2- Dealing with the ‘dead space,3- Soft-tissue cover,4- Aftercare, Pathophysiology : Bone is destroyed or devitalized, either in a discrete area around the focus of infection or more diffusely along the surface of an implant. Cavities containing pus and pieces of dead bone (sequestra) are surrounded by vascular tissue, and beyond that by areas of sclerosis – the result of chronic reactive new bone formation – which may take the form of a distinct bony sheath (involucrum). In the worst cases a sizeable length of the diaphysis may be devitalized and encased in a thick involucrum. Sequestra act as substrates for bacterial adhesion in much the same way as foreign implants, ensuring the persistence of infection until they are removed or discharged through perforations in the involucrum and sinuses that drain to the skin. A sinus may seal off for weeks or even months, giving the appearance of healing, only to reopen (or appear somewhere else) when the tissue tension rises. Bone destruction, and the increasingly brittle sclerosis, sometimes results in a pathological fracture. The histological picture is one of chronic inflammatory cell infiltration around areas of acellular bone or microscopic sequestra., Epidemiology : Osteomyelitis affects about 2 to 5 out of every 10, 000 people, 1 case per 5, 000 children., variable, It’s important to clean and treat wounds to keep out bacteria and prevent infections. If you’ve had a recent bone break or surgery, or have an artificial joint, contact your healthcare provider at the first sign of any infection. But in many instances, there isn’t anything you can do to prevent osteomyelitis., Complications : amyloidosis, squamous cell carcinoma., Septic arthritis, BONE DEFORMITY, Diagnostics : Erythrocyte Sedimentation Rate (ESR), PUS CULTURE, BONE SCAN, SINGLE-PHOTON EMISSION COMPUTED TOMOGRAPHY (SPECT), PCR OF TISSUE/PUS, White Blood Cell count WBC, BLOOD CULTURE, MRI, X RAY, CT SCAN, Differential diagnosis : avascular necrosis of bone, BURSITIS, "Ewings sarcoma", fracture, Gout, osteomyelitis, Soft tissue infection, disease description : Osteomyelitis is a bone infection caused by bacteria or fungi. It causes painful swelling of bone marrow, the soft tissue inside your bones. Without treatment, swelling from this bone infection can cut off blood supply to your bone, causing bone to die. Osteomyelitis affects people of all ages and genders. Children younger than 3, the elderly and people with serious medical conditions are more prone to the condition.In children, the infection is more likely to affect long bones, such as those found in the legs and arms. In adults, bone infections more often target the spine.

Chronic Pancreatitis

Disease Name : Chronic Pancreatitis, Treatment : medication : Tramadol , Puestow Procedure (Longitudinal Pancreaticojejunostomy).,Whipple Procedure (Pancreaticoduodenectomy).,Total Pancreatectomy and Auto Islet Transplantation.,Distal Pancreatectomy.,Endoscopic Pancreatic Sphincterotomy., Pathophysiology : Chronic pancreatitis is a disease process characterized by irreversible damage to the pancreas as distinct from the reversible changes noted in acute pancreatitis. The events that initiate and then perpetuate the inflammatory process in the pancreas, are becoming more clearly understood. Irrespective of the mechanism of injury, it is becoming apparent that stellate cell activation that results in cytokine expression and production of extracellular matrix proteins cause acute and chronic inflammation and collagen deposition in the pancreas. Thus, the condition is defined by the presence of histologic abnormalities, including chronic inflammation, fibrosis, and the progressive destruction of both exocrine and eventually endocrine tissue (atrophy). A number of etiologies have been associated with chronic pancreatitis resulting in the cardinal manifestations of the disease such as abdominal pain, steatorrhea, weight loss, and diabetes mellitus Although alcohol has been believed to be the primary cause of chronic pancreatitis, other factors contribute to the disease because not all heavy consumers of alcohol develop the pancreatic disease. There is also a strong association between smoking and chronic pancreatitis. Cigarette smoke leads to an increased susceptibility to pancreatic autodigestion and predisposes to dysregulation of duct cell CFTR function. Smoking is an independent, dose-dependent risk factor for chronic pancreatitis and recurrent acute pancreatitis. Both continued alcohol and smoking exposure are associated with pancreatic fibrosis, calcifications, and progression of disease. Recent characterization of pancreatic stellate cells (PSCs) has added insight into the underlying cellular responses behind development of chronic pancreatitis. Specifically, PSCs are believed to play a role in maintaining normal pancreatic architecture that can shift toward fibrogenesis in the case of chronic pancreatitis. The sentinel acute pancreatitis event (SAPE) hypothesis uniformly describes the events in the pathogenesis of chronic pancreatitis. It is believed that alcohol or additional stimuli lead to matrix metalloproteinase–mediated destruction of normal collagen in pancreatic parenchyma, which later allows for pancreatic remodeling. Proinflammatory cytokines, tumor necrosis factor a (TNF-a), interleukin 1 (IL-1), and interleukin 6 (IL-6), as well as oxidant complexes, are able to induce PSC activity with subsequent new collagen synthesis. In addition to being stimulated by cytokines, oxidants, or growth factors, PSCs also possess transforming growth factor ß (TGF-ß)–mediated self-activating autocrine pathways that may explain disease progression in chronic pancreatitis even after removal of noxious stimuli., Epidemiology : a prevalence of around 13 cases per 100 000, although there are suspicions that the prevalence is actually higher, 2 to 10 new cases per 100 000 population per year, , POOR, Not all causes are preventable, but you can reduce your risk by moderating your alcohol consumption. You can reduce your risk of gallstones, the other leading cause, by reducing cholesterol. If you’ve had acute pancreatitis, you can help prevent it from happening again by quitting alcohol and smoking. If you’ve had gallstone pancreatitis, removing your gallbladder can prevent it from recurring., Complications : CARCINOMA OF THE PANCREAS, Diabetic state, Diagnostics : Endoscopic USG, ERCP, MRCP, USG ABDOMEN(W/A), SERUM AMYLASE, SERUM LIPASE, MRI, STOOL EXAMINATION, CT SCAN, Differential diagnosis : ACALCULOUS CHOLECYSTITIS, Acute Pancreatitis, ANNULAR PANCREAS, Biliary colic, biliary obstruction, CHOLELITHIASIS, EXTERNAL INJURY TO PANCREAS, pancreatic pseudocyst, PEPTIC ULCER DISEASE, disease description : Chronic pancreatitis is a progressive inflammatory disorder that leads to irreversible destruction of exocrine and endocrine pancreatic parenchyma caused by atrophy and/ or replacement with fibrotic tissue.  Pancreatic insufficiency results when greater than 90% of the organ is damagedFunctional consequences include severe abdominal pain, diabetes mellitus, and malabsorption. 

Chronic Pelvic Pain

Disease Name : Chronic Pelvic Pain, Treatment : medication : Medroxy Progesterone Acetate , Progesterone , MIRENA IUCD, Psychotherapy alone or combined with drugs will be,useful in pelvic pain syndrome and irritable bowel,syndrome.,Acupuncture and short-wave diathermy are adjuvants, ,and are effective in some women, Medroxyprogesterone acetate (MDPA) up to 30 mg daily (Provera) given for ,9–12 months relieves pelvic pain, Pathophysiology : The pathogenesis of chronic pelvic pain is diverse. They involve gynaecological and nongynaecological such as gastrointestinal tract, renal tract, skeletomuscular and peritoneal. 1. Gynaecological causes are often organic but can be functional. The well-recognized organic lesions are :   Pelvic endometriosis, chocolate cyst of the ovary (30–35%)  Ovaries—ovarian adhesions, polycystic ovarian disease, residual ovarian syndrome, ovarian tumours (benign and malignant)  Tubal—chronic PID, tubal adhesions, postoperative adhesions, parametritis due to infection or malignancy (24%)  Pelvic tuberculosis and adhesions  Uterine—uterine fibroids and adenomyosis, pyometra in menopausal women, fixed retroverted uterus 2. Functional causes include :   Congestive dysmenorrhoea, Mittelschmerz and postcoital pain, CPPS, pelvic varicose or dilated veins (30%) 3. Nongynaecological causes are :   Intestinal tuberculosis, diverticulitis, colitis, appendicitis, irritable bowel syndrome which account for 20% cases. Carcinoma rectum. Chronic intestinal obstruction.  Renal—ureteric colic, bladder stone, urinary tract infection, cystitis, chronic retention of urine.  Skeletomuscular—joint pains (referred pain).  Chronic pelvic pain is common in reproductive years. The onset, type, duration and location of pain will provide guidance to the probable cause of the pain. Radiation of pain and its relation to menstruation is important. Obstetric and sexual history are significant. History of intrauterine contraceptive device suggests pelvic infection. Associated urinary and bowel symptoms should be inquired into. Some women with chronic pelvic pain also complain of dysmenorrhoea and dyspareunia. Past history of tuberculosis and psychiatric problem will help. Vaginal discharge is seen in PID. Bimanual pelvic examination is necessary to rule out organic pelvic lesion. A full bladder is felt anterior to the uterus and is tender on palpation. Rectal examination may reveal a mass or stricture. Pain and restriction of joint movements suggest referred pain to the pelvis. Tenderness in the pelvis is caused by endometriosis, adenomyosis, pelvic adhesion, PID diverticulitis and urinary infection., Epidemiology : approximately between four to sixteen percent of women, 15% of women, GOOD, Pelvic pain can’t always be prevented. However, incorporating these recommendations into your daily life can help reduce your risk : ,,Don’t overuse. Limit activities that require you to stand or walk for long periods of time.,Eat more fiber. This is particularly helpful if your pelvic pain is due to diverticulitis.,Exercise regularly. Staying physically active helps keep your joints and muscles in good condition.,Stretch your muscles. Warm up before exercising to help reduce the risk of pelvic pain.,Visit your healthcare provider regularly. Routine examinations can help your medical team detect issues early on before they worsen., Complications : bleeding, infection, DEPRESSION, Diagnostics : Sigmoidoscopy, USG ABDOMEN(W/A), MRI, STOOL EXAMINATION, CT SCAN, CYSTOSCOPY, LAPROSCOPIC USG, DOPPLER USG, COTTON SWAB STICK TEST, Urine analysis, Differential diagnosis : adenomyosis, Bladder cancer, CELIAC DISEASE, Endometriosis, Fibromyalgia, Hernia, HYDROSALPINX, INFLAMMATORY BOWEL DISEASES, INTERSTITIAL CYSTITIS, Interstitial cystitis or bladder pain syndrome, Irritable Bowel Syndrome, leiomyoma, Pelvic Inflamatory Disease, Peripheral neuropathy, recurrent ovarian cysts, disease description : Chronic pelvic pain can be a disabling, chronic, persistent pain, within the pelvis in women. Relatively common, chronic pelvic pain is associated with comorbidities such as irritable bowel syndrome, major depressive disorder, or pelvic inflammatory syndrome.chronic pelvic pain has a strong association with previous physical or emotional trauma. 

Chronic Periodontitis

Disease Name : Chronic Periodontitis, Treatment : Scaling., Flap surgery (pocket reduction surgery), Soft tissue grafts., Pathophysiology : To understand the pathophysiology of periodontal disease, it is essential to know about the complex dental biofilm as well as the Immune response associated with the disease.Dental plaque is a complex biofilm, which is the colonization of bacteria enclosed by a protective matrix. This matrix is composed of extracellular polysaccharide and glycoproteins providing a protective environment for microbes in the dental biofilm. This component of the dental biofilm makes it 1000 to 1500 times more resistant to antimicrobial agents. The various circulatory channels present in the biofilm aid in the distribution of many nutrients and excretion of the generated metabolic wastes. "Quorum sensing" is a mode of communication between the microcolonies of bacteria within the dental biofilm. "Autoinducers" are molecules secreted by microbes; the concentration of these molecules helps in regulating bacterial gene expression. The biofilm, by different pH concentrations and metabolites, has various microenvironments within the biofilm. These microenvironments make the ecosystem suitable for a variety of microbes inhabiting in the same dental plaque. The initial layer deposited on the surface of teeth in the formation of dental plaque is "acquired pellicle." This layer is formed within seconds of the exposure of tooth surfaces, followed by the initial attachment of the early colonizers of the biofilm. Streptococcus and Actinomyces species are the primary colonizers which are gram-positive, facultative bacteria. The "adhesin receptors" present on the surface of primary colonizers bind with the proline-rich proteins of the pellicle. This binding leads to revealing of receptor sites known as "cryptitope" which further leads to coaggregation. Gradually there is a layer by layer deposition of dental plaque leading to a deficiency of oxygen in the environment eventually leading to colonization of anaerobic bacteria.  The bridging microbe between primary and secondary colonizers is Fusobacterium species .The gradual shift of these aerobic conditions to anaerobic condition marks the progression of gingivitis to periodontitis. Socransky et al. in a study divided the microbes into microbial complexes based on colors. Red and orange complexes bacteria present in the subgingival area are intricately associated with periodontal disease., Epidemiology : Periodontal disease increases with age, 70.1% of adults 65 years and older have periodontal disease., 47.2% of adults aged 30 years and older have some form of periodontal disease., GOOD, The best way to prevent periodontitis is to have regular dental cleanings and practice good oral hygiene at home between visits. People who are prone to periodontitis may require more frequent cleanings than people without gum disease. Ask your dentist how often you should have your teeth cleaned to maintain optimal oral health., Complications : rheumatoid arthritis, Diabetes mellitus type 2, heart disease, tooth anomalies, Diagnostics : PPD, PHYSICAL EXAMINATION, Differential diagnosis : Acute necrotizing (ulcerative) gingivitis and noma, gingival bleeding, periodontal abscess, disease description : Periodontitis is one of the most common ailments affecting the teeth, leading to the destruction of the supporting and surrounding tooth structure. Periodontitis is originally a disease originating from the gingival tissue which if left untreated results in penetration of inflammation to the deeper tissues, altering the bone homeostasis causing tooth loss. Periodontal disease has a multifactorial origin.  The main culprit identified in periodontitis is the bacterial biofilm growing on the tooth surfaces

Chronic Pharyngitis

Disease Name : Chronic Pharyngitis, Treatment : medication : Pantoprazole , Amoxicillin and Clavulanic acid , Penicillin/Penicillin V/Phenoxymethylpenicillin, acetaminophen, Warm saline gargles, especially in the morning, are ,soothing and relieve discomfort.Mandl’s paint may be applied to pharyngeal mucosa., Treatment options for Group A beta-hemolytic streptococcal pharyngitis include oral treatment with penicillin V or oral amoxicillin. Cephalosporins, macrolides, and clindamycin may also be used. Intramuscular penicillin is also a treatment option. Resistance may develop during treatment with azithromycin and clarithromycin, and it is not considered a first-line antibiotic for this indication. In patients with a mild penicillin allergy, cephalosporins can be used. In patients with a history of anaphylaxis to penicillin, azithromycin or clindamycin can be used. The disease is no longer infectious after 24 hours of antibiotics, Cautery of lymphoid granules is suggested. Throat ,is sprayed with local anaesthetic and granules are ,touched with 10–25% silver nitrate. Electrocautery or ,diathermy of nodules may require general anaesthesia., 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 . A large number of factors are responsible : 1. Persistent infection in the neighbourhood. In chronic rhinitis and sinusitis, purulent discharge constantly trickles down the pharynx and provides a constant source of infection. This causes hypertrophy of the lateral pharyngeal bands. 2. Mouth breathing. Breathing through the mouth exposes the pharynx to air which has not been filtered, humidified and adjusted to body temperature thus making it more susceptible to infections. Mouth breathing is due to : (a) Obstruction in the nose, e.g. nasal polypi, allergic or vasomotor rhinitis, turbinal hypertrophy, deviated septum or tumours. (b) Obstruction in the nasopharynx, e.g. adenoids and tumours. (c) Protruding teeth which prevent apposition of lips. (d) Habitual, without any organic cause. 3. Chronic irritants. Excessive smoking, chewing of tobacco and pan, heavy drinking or highly spiced food can all lead to chronic pharyngitis. 4. Environmental pollution. Smoky or dusty environment or irritant industrial fumes may also be responsible for chronic pharyngitis. 5. Faulty voice production. Less often realized but an important cause of chronic pharyngitis is the faulty voice production. Excessive use of voice or faulty voice production seen in certain professionals or in “pharyngeal neurosis” where person resorts to constant throat clearing, hawking or snorting, and that may cause chronic pharyngitis, especially of hypertrophic variety., Epidemiology : 16% of adults and 41% of children reported an illness with sore throat over a 1-year, good, To Do : VOICE REST ,Hawking, clearing, ,throat frequently or any other such habit should be,stopped.,Warm saline gargles, especially in the morning, are,soothing and relieve discomfort., Complications : ACUTE RHEUMATIC FEVER, otitis media, sinusitis, toxic shock syndrome, Epiglottitis, Diagnostics : White Blood Cell count WBC, THROAT SWAB CULTURE, X RAY, RAPID ANTIGEN DETECTION, CT SCAN, Differential diagnosis : airway obstruction, allergic rhinitis, diphtheria, Epiglottitis, Gastroesophageal reflux disease (GERD), infectious mononucleosis, Peritonsillar abscess, disease description : Pharyngitis is the inflammation of the mucous membranes of the oropharynx. In most cases, the cause is an infection, either bacterial or viral. Other less common causes of pharyngitis include allergies, trauma, cancer, reflux, and certain toxins. Other less common causes of pharyngitis include allergies, trauma, cancer, reflux, and certain toxins.

Chronic Pid

Disease Name : Chronic Pid, Treatment : medication : Cefazolin , Doxycycline , Metronidazole , *Tetracycline 500 mg qid 3 10 days., *Erythromycin 500 mg 3 7 days., *Doxycycline 100 mg bd 3 10 days.,* Clindamycin 450 mg qid 3 10 days.,* Gentamycin 80 mg 8 hourly 3 5 days., Tuboplasty.,*Hysteroscopic falloposcopy or laparoscopic salpingoscopy ,*,Hysteroscopic balloon plasty or cannulation, Pathophysiology : Normally several natural barriers to the ascent of pathogenic organisms from the vagina to the fallopian tubes exist. Intact hymen prevents ascending infection. When a virgin girl presents with PID, it is usually tubercular in nature. The acidity of the vaginal secretion inhibits the growth of bacteria; the cervical canal has a relatively small lumen and is normally filled with a plug of alkaline mucus. The ciliary movement of endometrial lining in the uterus and the cervical canal is directed downwards and discourages the upward spread of nonmotile organisms to the cavity of the uterus. This natural protective mechanism is impaired during menstruation, after abortion and delivery, because the cervical canal becomes dilated, the protecting epithelium of the endometrium is shed, and raw surfaces are present in the cavity of the uterus. The vaginal pH is increased, rendering the genital tract more vulnerable to infection. In addition to these factors, intrauterine manipulations such as curettage for evacuation in abortion and manual removal of placenta favour entry and spread of pathogenic organisms. Intrauterine contraceptive device (IUCD) is also a source of infection, particularly when it is not introduced under aseptic conditions, or introduced in the presence of vaginal infection. The most common cause of PID is sexually transmitted diseases (STD), the incidence of which has risen in the past 20 years. Gonococcal and chlamydial infections are most common, the incidence of the two varying in different communities. Sixty to seventy-five per cent of PIDs are caused by STD, of which gonorrhoea accounts for about 30% in the developed countries. The importance and high incidence of chlamydial infection has been recognized with availability of culture facilities and enzyme-linked immunosorbent assay (ELISA) kits. . The organisms probably ride up the tract along with the motile sperms in a piggy-back fashion. Sperms also help in transportation of trichomonas similarly. Other organisms directly ascend along the lining of the genital tract. This partly explains the absence of gonococcal inflammatory disease in a woman whose husband is azoospermic. The cervix and the urethra are the common sites where chlamydia lodge and ascend upwards. The incidence of this infection is not easy to obtain in many countries because of the lack of culture facilities. The development of immunological tests has now made it possible to detect the antibodies in the sera of infected patients. Gonococci and chlamydia create an environment for secondary invasion by other organisms normally residing in the lower genital tract. Other organisms which cause PID include : (i) mycoplasma (M. hominis and M. ureolyticus), (ii) tubercle bacillus, (iii) viruses, and (iv) E. coli (30%) Mycoplasma hominis is isolated in 50% sexually active women, but detected in only 7% in PID. Mycoplasma genitalium is now the new organism that is seen to cause PID. Bacterial vaginosis can also cause upper genital tract infection. These organisms reach the tube via the lymphatics bypassing the endometrium. The polymicrobial nature of this infection has been observed and some 40 organisms, both aerobes and anaerobes, have been implicated in PID : Aerobes. Both Gram-positive and Gram-negative. Anaerobes. Bacteroides fragilis (20%), fusobacteria, Bacteroides melaninogenicus, anaerobic cocci such as peptococci and peptostreptococci, clostridia, facultative anaerobes, Actinomyces (Gram-positive) and E. coli (30–40%). The infection by anaerobic organisms is greatly favoured by blood loss, anaemia and tissue damage such as which occurs in septic haemorrhage. A polymicrobial infection in PID mandates the administration of more than one antibiotic. n In India, as in other developing countries, many deliveries are conducted at home by dais (untrained midwives). Criminal abortions continue to take place despite Government of India’s liberal policy on induced abortions. Postabortal and puerperal sepsis are therefore common occurrences. It is estimated that about 40–50% of all PID cases in developing countries are caused in this manner and the rest by STDs. n Minor operative procedures such as D&C and hysterosalpingogram can cause ascending infection. Manual removal of placenta and evacuation of products of conception are other important sources of infection in the upper genital tract. n The introduction of IUCDs has increased the incidence of PID threefold.. The PID is a disease of young women, who are sexually and reproductively active. The increased promiscuity and frequent change of sex partners are mainly responsible for PID in developed countries, and amongst sex workers. Septic abortions and puerperal sepsis are the important aetiological factors in developing countries . Seventy-five per cent PID are STDs in developed countries. Sterilization operation prevents PID by blockage of the tubes. Apart from barrier contraceptives, progestogencontaining pills produce a thick plug of mucus in the cervical canal and prevent ascent of organisms Westrom (1975) reported that women with one previous attack of PID are predisposed to another attack in 12% of the cases two attacks of PID increase the risk to 35% and three attacks to as much as 75%. Golden (2003) reported 8% recurrence in a woman with previous PID versus 1% occurrence with no PID previously., Epidemiology : was 4.4% in sexually experienced women of reproductive age (18–44 years)., GOOD, Sometimes, PID isn’t due to a sexually transmitted infection. It can come from normal vaginal bacteria traveling to your reproductive organs. 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 : Your risk increases if you have multiple partners.,Choosing barrier methods of birth control : These types of birth control include condoms and diaphragms. Combine a barrier method with spermicide, even if you take birth control pills.,Seeking treatment if you notice symptoms : If you notice signs of PID or other STIs, get treatment right away. Symptoms include unusual vaginal discharge, pelvic pain or bleeding between periods.,Getting regular checkups : Have regular gynecological exams and screenings. Often, providers can identify and treat cervical infections before they spread to reproductive organs., Complications : infection, infertility, CHRONIC PAIN, Diagnostics : LAPAROSCOPY, BLOOD IN URINE TEST, ENDOMETRIAL BIOPSY, PHYSICAL EXAMINATION, Differential diagnosis : appendicitis, DIVERTICULITIS, ectopic pregnancy, Endometriosis, increased risk of ectopic pregnancy, Ovarian Cyst, Pyelonephritis, disease description : Pelvic inflammatory disease (PID) is defined as an inflammation of the upper genital tract due to an infection in women. The disease affects the uterus, fallopian tubes, and/or ovaries. It is typically an ascending infection, spreading from the lower genital tract. The majority of cases of PID are related to a sexually transmitted infection. The diagnosis of PID is primarily clinical and should be suspected in female patients with lower abdominal or pelvic pain and genital tract tenderness.Sometimes PID can lead to long-term (chronic) pain around your pelvis and lower abdomen, which can be difficult to live with and lead to further problems, such as depression and difficulty sleeping (insomnia).

Chronic Pulpitis

Disease Name : Chronic Pulpitis, Treatment : Root canal, Tooth removal : options for replacing the tooth, including a dental implant or dental bridge., Pathophysiology : The hard enamel of your tooth protects the pulp. If the enamel becomes damaged, it could lead to pulpitis. Tooth damage can occur from : Cavities : Bacteria in your mouth produce acid that can eat away at your enamel and create holes.Cracks : Small cracks can happen if you chew on hard foods or injure your tooth.Dental procedures : Treatment of a tooth alone can cause pulpitis. If a tooth isn’t sealed correctly during a dental procedure, it can allow the filling to leak and cause pulpitis, too.Worn enamel : Grinding your teeth or brushing aggressively can wear down your enamel and make the nerve more susceptible to inflammation., Epidemiology : 1 in 4 adults between the ages of 20 and 64 ., variable, 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, infection, osteomyelitis, swollen lymphnodes, Diagnostics : nan, Differential diagnosis : Dental abscesses, Dental Caries, neuritis, oral infection, Oral ulcers, sinusitis, TRIGEMINAL NEURALGIA, disease description : Pulpitis is an inflammation of the pulp, the soft inner tissue of your teeth. Pulpitis is reversible if you identify it early.Pulpitis can cause severe tooth pain and dental emergencies. It is caused by inflammation inside your tooth.

Chronic Pyelonephritis

Disease Name : Chronic Pyelonephritis, Treatment : medication : Levofloxacin , "After starting antibiotics, pus is immediately drained ,from the kidney through a loin incision and nephro\x02stomytube (Cabots nephrostomy) (Malecots catheter) ,is placed. ,, , . If kidney is totally destroyed, subcapsular nephrectomy ,is done. This also prevents other kidney from getting ,infected through perirenal lymphatic connections. ,, , . In bilateral pyonephrosis, bilateral nephrostomy is the ,only choice. J stenting is done often to keep the ureters ,patent.", 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 lead 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 : About 1 in every 30 cases of UTI leads to a kidney infection., 12–13 cases annually per 10, 000 population in women, 2–3 cases per 10, 000 In men., variable, 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 : kidney damage, sepsis, Diagnostics : Renal Biopsy, CT SCAN, CYSTOSCOPY, IVU, Differential diagnosis : Acute Pyelonephritis, Azotaemia, chronic kidney disease, Cystitis, hypertension, nephrolithiasis, PERINEPHRIC ABSCESS, PYONEPHROSIS, Uremia, disease description : Chronic pyelonephritis is characterized by renal inflammation and scarring induced by recurrent or persistent renal infection, vesicoureteral reflux, or other causes of urinary tract obstruction. It occurs almost exclusively in patients with major anatomic anomalies . The chronic form is rare, but it happens more often in children or people with urinary obstructions.

Chronic Recurrent Sialdenitis

Disease Name : Chronic Recurrent Sialdenitis, Treatment : medication : Pilocarpine , bethanechol , Medical management is with hydration, oral hygiene, pain relief, sialogogues. In cases of infection, broad-spectrum antibiotics are added., In the case of sialolithiasis, salivary gland stone removal should take place, using interventional sialendoscopy or direct surgical removal. EWSL under ultrasonic guidance is used for intraglandular duct stone removal.Recurrent sialadenitis (>3 episodes/year) or in chronic sclerosing sialadenitis : excision of the salivary gland is the recommendation., Pathophysiology : This usually involves parotid gland which shows recurrent bacterial infection. During acute exacerbation, parotid is enlarged and tender, and pus can be expressed from its duct. Between the acute episodes, gland is firm and slightly enlarged. Culture of pus from the duct reveals staphylococci or streptococci. Sialography shows normal duct system. Treatment of acute episode is similar to that of acute bacterial sialadenitis. Between the attacks, patient is instructed to keep good oral hygiene, avoid drugs which dry oral mucosa and use sialogogues to promote salivation., Epidemiology : about 10% of all cases of sialadenitis., Prognosis is dependent on the etiology., You may not be able to prevent sialadenitis completely. But there are a few things you can do to reduce your risk : ,,Drink plenty of water.,Practice good oral hygiene.,Eat a diet that’s healthy for you.,Avoid smoking and using other tobacco products., Complications : abscess, Recurrent infection, dental infections, Diagnostics : Complete Blood Count CBC, FNAC, HISTOPATHLOGY, PUS CULTURE, USG, USG, SIALOGRAPHY, Differential diagnosis : Bacterial infection, Pleomorphic adenoma, Sarcoidosis, Sjogren’s Syndrome, disease description : Sialadenitis is inflammation of the salivary gland. Sialadenitis of the submandibular gland is less common than that of the parotid gland. Acute sialadenitis is usually due to bacterial or viral infections and usually presents with rapid onset pain and swelling.Chronic sialadenitis is characterized by recurrent or persistent of the salivary gland. Chronic sialadenitis is usually due to obstruction, e.g., calculi, stricture, and usually presents with swelling without erythema.

Chronic Renal Failure

Disease Name : Chronic Renal Failure, Treatment : Depending on the cause of your kidney disease, a healthcare provider may prescribe one or more of the following medications : ,,Angiotensin-converting enzyme (ACE) inhibitor or angiotensin II receptor blocker (ARB). These medications help lower your blood pressure.,Diuretics. These help remove extra fluid from your body.,Statins. These help lower your cholesterol levels.,Erythropoietin-stimulating agents. These help build red blood cells if you have anemia.,Vitamin D and calcitriol. These help prevent bone loss.,Phosphate binders. These help remove extra phosphorus in your blood., Dialysis,Dialysis helps your body filter blood. There are two types of dialysis : ,,Hemodialysis. In hemodialysis, a machine regularly cleans your blood for you. Most people get hemodialysis three to four days a week at a hospital or dialysis clinic.,Peritoneal dialysis. In peritoneal dialysis, a provider attaches a bag with a dialysis solution to a catheter in your abdominal lining. The solution flows from the bag into your abdominal lining, absorbs waste products and extra fluids and drains back into the bag. Sometimes people can receive peritoneal dialysis at home., Kidney transplant,A surgeon places a healthy kidney in your body during a kidney transplant to take over for your damaged kidney. The healthy kidney (donor organ) may come from a deceased donor or a living donor. You can live well with one healthy kidney., Pathophysiology : Unlike acute kidney injury (AKI), where the healing process is complete with complete functional kidney recovery, chronic and sustained insults from chronic and progressive nephropathies evolve to progressive kidney fibrosis and destruction of the normal architecture of the kidney. This affects all the 3 compartments of the kidney, namely glomeruli, the tubules, the interstitium, and the vessels. It manifests histologically as glomerulosclerosis, tubulointerstitial fibrosis, and vascular sclerosis.The sequence of events which lead to scarring and fibrosis are complex, overlapping, and are multistage phenomena.Infiltration of damaged kidneys with extrinsic inflammatory cellsActivation, proliferation, and loss of intrinsic renal cells (through apoptosis, necrosis, mesangiolysis, and podocytopenia)Activation and proliferation of extracellular matrix (ECM) producing cells including myofibroblasts and fibroblastsDeposition of ECM replacing the normal architectureMechanisms of Accelerated Progression of CKDSystemic and intraglomerular hypertensionGlomerular hypertrophyIntrarenal precipitation of calcium phosphateAltered prostanoid metabolism All these mechanisms lead to a histological entity called focal segmental glomerulosclerosis.Clinical risk factors for accelerated progression of CKD are proteinuria, hypertension, black race, and hyperglycemia. Also, environmental exposures such as lead, smoking, metabolic syndrome, possibly some analgesic agents, and obesity have also been linked to accelerated progression of CKD  , Epidemiology : 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, pericarditis, heart disease, anemia, Diagnostics : Complete Blood Count CBC, MRI, Differential diagnosis : acute kidney injury, Alport Syndrome, Diabetic Nephropathy, multiple myeloma, necrotizing glomerulonephritis, disease description : Chronic kidney disease (CKD) is defined as the presence of kidney damage or an estimated glomerular filtration rate (eGFR) less than 60 ml/min per 1.73 square meters, persisting for 3 months or more. It is a state of progressive loss of kidney function ultimately resulting in the need for renal replacement therapy (dialysis or transplantation). This activity reviews the etiology, evaluation, and management of chronic kidney disease and emphasizes the roles of the interprofessional team in caring for patients with chronic kidney disease.

Chronic Retropharyngeal Abscess

Disease Name : Chronic Retropharyngeal Abscess, Treatment : medication : Amoxicillin and Clavulanic acid , Ampicillin , Linezolid , Clindamycin , Vancomycin , In patients not presenting with severe respiratory distress or airway compromise, management typically begins with a 24 to 48 hour trial of intravenous antibiotic therapy. After 24 to 48 hours of antibiotic therapy, the need for surgical incision and drainage will be reevaluated by a trained otolaryngologist. Factors that have been associated with an increased need for surgical incision and drainage include an abscess with a cross-sectional area greater than 2 cm2 and symptoms for greater than two days., INCISION & DRAINAGE, Pathophysiology : In children younger than five years old, the retropharyngeal space contains chains of lymph nodes that drain the nasopharynx, adenoids, posterior paranasal sinuses, and middle ear. An antecedent upper respiratory tract infection can result in suppurative adenitis of these retropharyngeal lymph nodes and eventual abscess formation. As these retropharyngeal lymph nodes atrophy and involute during normal development, antecedent upper respiratory tract infection resulting in retropharyngeal abscess becomes less likely. In older children and adults, trauma to the posterior pharynx resulting in retropharyngeal infection is the more likely mechanism through which retropharyngeal abscess originates.After suppurative adenitis or trauma results in the seeding of the retropharyngeal space, cellulitis results and eventually leads to phlegmon and abscess formation in the retropharyngeal space. Retropharyngeal abscesses are often polymicrobial infections. Bacteria that commonly contribute to these infections include Group A Streptococcus pyogenes,  Staphylococcus aureus,  Fusobacterium,  Haemophilus species, and other respiratory anaerobic organisms.As the retropharyngeal abscess grows in size, it results in gradual upper airway obstruction and eventually asphyxiation if left untreated. Although mortality from sepsis does occur in these patients, the number one cause of death in patients with retropharyngeal abscess remains upper airway occlusion, Epidemiology : occurs in children between the ages of two and four years but can occur at any age., 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 : esophageal damage, sepsis, airway obstruction, cranial nerve palsies, Diagnostics : X RAY, CT SCAN, plain radiograph, Soft Tissue Lateral View Neck Radiographs, Differential diagnosis : angioedema, Bacterial pneumonia, diphtheria, Epiglottitis, esophagitis, Kawasaki Disease, mediastinitis, Meningitis, neonatal sepsis, parapharyngeal abscess, Peritonsillar abscess, pharyngitis, PNEUMONIA, Sialadenitis, disease description : Retropharyngeal abscesses are uncommon but potentially life-threatening diagnoses. They can occur at any age, although are most commonly found in children under the age of five. older children and adults, a retropharyngeal abscess can be caused by trauma to the posterior pharynx, which leads to inoculation of the retropharyngeal space and results in abscess formation. 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. Direct expansion from spinal discitis or osteomyelitis is a rare cause of a retropharyngeal abscess as well. As a retropharyngeal abscess grows in size, it can lead to upper airway obstruction and asphyxiation.

Chronic Rhinitis

Disease Name : Chronic Rhinitis, Treatment : Nasal irrigations with alkaline solution, Nasal decongestants and Antibiotics., In Hypertrophic rhinitis-Lasers have also been used to reduce the size of ,turbinates.,In Atrophic Rhinitis-Young’s operation and Modified Young’s operation.,In Rhinitis Caseosa-removal of debris and granulation ,tissue and free drainage of the affected sinus., Pathophysiology : Simple chronic rhinitis is an early stage of hypertrophic rhinitis. There is hyperaemia and oedema of mucous membrane with hypertrophy of seromucinous glands and increase in goblet cells. Blood sinusoids particularly those over the turbinates are distended. 1. Nasal obstruction. Usually worse on lying and affects the dependent side of nose. 2. Nasal discharge. It may be mucoid or mucopurulent, thick and viscid and often trickles into the throat as postnasal drip. Patient has a constant desire to blow the nose or clear the throat. 3. Headache. It is due to swollen turbinates impinging on the nasal septum. 4. Swollen turbinates. Nasal mucosa is dull red in colour. Turbinates are swollen; they pit on pressure and shrink with application of vasoconstrictor drops (this differentiates the condition from hypertrophic rhinitis). Middle turbinate may also be swollen and impinge on the septum. 5. Postnasal discharge. Mucoid or mucopurulent discharge is seen on the posterior pharyngeal wall., Epidemiology : The prevalence of allergic rhinitis has been reported to be as high as 40% in children, subsequently decreasing with age, affects 5% to 12% of the general population., GOOD, 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 : nasal polyps, persistent cough, Diagnostics : rhinoscopy, Differential diagnosis : nasal polyps, Sarcoidosis, sickle cell anemia, vasomotor rhinitis, disease description : Chronic rhinitis is usually an extension of rhinitis caused by inflammation or a viral infection. However, it also may rarely occur with diseases.  Chronic nasal inflammation lasts over a long period of time, typically longer than12 weeks . It’s different from acute rhinitis, which lasts a few days or up to 4 weeks before going away.

Chronic Rhinosinusitis

Disease Name : Chronic Rhinosinusitis, Treatment : Medical systemic steroids, Steroid nasal sprays, Nasal irrigations and Antibiotics., Medical treatment often fails in massive nasal polyposis and requires endoscopic surgery.Endoscopic sinus surgery popularly ,called FESS (functional endoscopic sinus surgery) is preffered now a days., Pathophysiology : There are several proposed mechanisms for the pathophysiology of chronic rhinosinusitis .Fungus : Proteins of the fungus trigger T cell response, causing cytokine storm which in turn leads to recruitment of the eosinophils to mucus. Degranulated eosinophils target the fungi causing collateral tissue damage.Bacteria, mostly contribute to the pathogenesis of chronic rhinosinusitis without nasal polyps and are composed of three hypotheses : Super antigen : Staphylococcus aureus superantigenic exotoxins bind T cells outside their antigen binding site, bypassing the antigen recognition pathway, thus provoking polyclonal T cell response which in turn leads to cytokine storm.Biofilm : Biofilms are composed of bacteria embedded in an extracellular matrix, protecting them from antibiotics.Microbiome : It is suggested that external factors could change the normal microbiome of the nasal and sinus mucosa facilitating the growth of pathogens that were normally suppressed by the commensals., Epidemiology : Chronic rhinosinusitis (CRS) is a significant health problem and affects 5% to 12% of the general population., Chronic rhinosinusitis (CRS) affects 1 in 8 people in India; about 5-15% of urban population., fair, "Take these steps to reduce your risk of getting chronic sinusitis : ,,Avoid upper respiratory infections. Avoid contact with people who have colds or who are sick with other infections. Wash your hands frequently with soap and water, especially before meals.,Manage your allergies. Work with your doctor to keep symptoms under control. Avoid exposure to things youre allergic to whenever possible.,Avoid cigarette smoke and polluted air. Tobacco smoke and air contaminants can irritate and inflame your lungs and nasal passages.,Use a humidifier. If the air in your home is dry, such as it is if you have forced hot air heat, adding moisture to the air may help prevent sinusitis. Be sure to keep the humidifier clean and free of mold with regular, thorough cleaning.", Complications : Asthma, PNEUMONIA, Diagnostics : MRI CHEST CONTRAST, CT SCAN, rhinoscopy, Differential diagnosis : acute rhinosinusitis, allergic rhinitis, deviated nasal septum, nasal lymphoma, nasal polyps, primary ciliary dyskinesia, rhabdomyosarcoma, "wegeners granulomatosis", disease description : Chronic rhinosinusitis refers to a condition that lasts at least 12 weeks . Chronic rhinosinusitis is different from the more common form of rhinosinusitis (called acute rhinosinusitis), which is a temporary infection of the sinuses that often occurs following coldsIt is a chronic inflammatory disease of nasal and paranasal sinus mucosa where symptomatology has continued beyond 12 weeks. Sometimes there are acute exacerbations superimposed on chronic rhinosinusitis (CRS), where symptoms worsen but return to baseline of CRS after treatment.

Chronic Sarcoidosis

Disease Name : Chronic Sarcoidosis, Treatment : For patients with pulmonary sarcoidosis causing worsening symptoms, stage II to III radiographic findings should be considered for oral glucocorticoids at 0.3 to 0.6 mg/kg for 4 to 6 weeks. If there is no improvement in symptoms, radiographic abnormalities, and pulmonary function tests, steroids may be continued for an additional four to six weeks. Maintainance steroids are not needed; steroid tapering to a dose of 0.25 to 0.5mg/kg (usually 10 to 20 mg) per day should be considered over a period of at least six to eight months. Methotrexate, azathioprine, infliximab, leflunomide, and antimalarial agents may be considered as steroid-sparing agents in patients who are unable to tolerate steroids, Pathophysiology : Doctors dont know the exact cause of sarcoidosis. Some people appear to have a genetic predisposition to develop the disease, which may be triggered by bacteria, viruses, dust or chemicals.This triggers an overreaction of your immune system, and immune cells begin to collect in a pattern of inflammation called granulomas. As granulomas build up in an organ, the function of that organ can be affected., Epidemiology : here are fewer than 200, 000 cases per year in the United States, The annual incidence of sarcoidosis varies between 1 and 15 per 100, 000 depending on the region., variable, Since we don’t know for sure what causes sarcoidosis, there’s no way to prevent it or reduce your risk of getting it. Taking medications as prescribed by your healthcare provider will reduce your risk of organ damage that granulomas can cause., Complications : pulmonary hypertension, end stage lung diseases, Diagnostics : ECG, PULMONARY FUNCTION TEST(PFT), Nuclear Imaging (including 18F-fluorodeoxyglucose positron emission tomography FDG-PET), Differential diagnosis : Cat scratch disease, fungal infections, LEPROSY, Lung cancer, lymphoma, "non-hodgkins lymphoma", SMALL CELL CARCINOMA OF LUNG, TUBERCULOSIS, disease description : Sarcoidosis is a disease characterized by the growth of tiny collections of inflammatory cells (granulomas) in any part of your body — most commonly the lungs and lymph nodes. But it can also affect the eyes, skin, heart and other organs. The cause of sarcoidosis is unknown, but experts think it results from the bodys immune system responding to an unknown substance. Some research suggests that infectious agents, chemicals, dust and a potential abnormal reaction to the bodys own proteins (self-proteins) could be responsible for the formation of granulomas in people who are genetically predisposed.

Chronic Sinusitis

Disease Name : Chronic Sinusitis, Treatment : Nasal steroids should be used with or without nasal saline irrigation. The treatment should last at least eight to 12 weeks with proper usage.,Nasal saline irrigation is inferior to nasal steroids. However, nasal saline irrigation can serve as a useful adjunct. High volume nasal saline irrigation was found to be more effective than low-volume nasal spray techniques.,Antihistamines should only be used if an allergic component is suspected.,Decongestants can be used for symptomatic relief, but evidence for supporting their use in chronic sinusitis is lacking.,Antibiotics can be given for an extended period of three weeks. However, there is no consensus on their routine use in chronic sinusitis, nor is their consensus on antibiotic selection.,Anti-fungal empiric therapy should not be given.,Oral steroids can be used, endoscopic sinus surgery, Pathophysiology : There are four paired sinus cavities : the ethmoid, sphenoid, frontal, and maxillary sinus cavities. These paired cavities allow air to be filtered during inhalation. For the antigens to be filtered and expelled, sinuses need to drain. Chronic inflammation can cause obstruction to the nasal passage, hinder drainage, and lead to lower oxygen tension. This creates foci for bacteria to build up. Ciliary dysfunction or structural abnormalities can further exacerbate this processAcute infection destroys normal ciliated epithelium impairing drainage from the sinus. Pooling and stagnation of secretions in the sinus invites infection. Persistence of infection causes mucosal changes, such as loss of cilia, oedema and polyp formation, thus continuing the vicious cycle. In chronic infections, process of destruction and attempts at healing proceed simultaneously. Sinus mucosa becomes thick and polypoidal (hypertrophic sinusitis) or undergoes atrophy (atrophic sinusitis). Surface epithelium may show desquamation, regeneration or metaplasia. Submucosa is infiltrated with lymphocytes and plasma cells and may show microabscesses, granulations, fibrosis or polyp formation., Epidemiology : 146 per 1000 population., You may be able to prevent infections and chronic sinusitis if you : ,,Treat the underlying conditions behind chronic sinusitis, like asthma and allergies.,Avoid allergens such as animal dander, dust, pollen, smoke and mold that trigger swelling in the sinuses.,Quit smoking if you do smoke and avoid any secondhand smoke.,Wash your hands thoroughly with soap and water.,Rinse your nasal passages with saline solution, either purchased or with a neti pot. (This is a small item that is filled with sterile water and salt. You pour, or gently squeeze, the water into one side of your nose and it comes out the other.),Eat healthy foods, stay hydrated and exercise regularly to stay healthy overall.,Use a humidifier to keep nasal tissues moist., Complications : CAVERNOUS SINUS THROMBOSIS, laryngitis, Mucocele, orbital cellulitis, mucous retention cyst, osteomyelitis, SUBDURAL ABSCESS, Diagnostics : CT PNS, CT SCAN, Flexible Nasopharyngoscopy, allergy skin test, X-ray PNS, Differential diagnosis : allergic rhinitis, Asthma, Gastroesophageal reflux disease (GERD), oral infection, disease description : Sinusitis is inflammation of the sinus or nasal passage. Chronic sinusitis is chronic inflammation of the sinus or nasal passages occurring for more than 12 weeks at a time. Recurrent sinusitis is defined as greater than four episodes of sinusitis within a one-year period. The evaluation and management of acute and chronic sinusitis are similar. Chronic sinusitis may present as (1) chronic sinusitis without nasal polyps, (2) chronic sinusitis with nasal polyps, and (3) allergic fungal rhinosinusitis.

Chronic Superficial Scaly Dermatitis

Disease Name : Chronic Superficial Scaly Dermatitis, Treatment : First line ,• Emollient,, Second line ,• Mild topical corticosteroids, Third line ,• Phototherapy (narrow-band UVB/PUVA, Pathophysiology : The pathophysiology of the condition is unknown. The histology is not characteristic. It usually shows the changes of a very mild eczematous eruption, consisting of patchy parakeratosis, mild spongiosis and a slight, mainly perivascular, infiltrate in the dermis, chiefly composed of lymphocytes., Epidemiology : Approximately 7.5% to 14%, variable, There is no known way of preventing CSSD., Complications : hyperpigmentation of the skin, skin atrophy, Diagnostics : biopsy, PCR, immunohistochemistry, Differential diagnosis : eczematides, Mycosis fungoides, nummular dermatitis, poikiloderma, disease description : This is a chronic condition characterized by the presence of round or oval erythematous, slightly scaly patches on the limbs and trunk, which histologically show mild eczematous changes with little or no dermal infiltrate. Abortive T-cell lymphoma is still a T-cell lymphoma, so this condition is a clinical presentation of mycosis fungoides.

Chronic Suppurative Otitis Media(attico Antral)

Disease Name : Chronic Suppurative Otitis Media(attico Antral), Treatment : medication : Ciprofloxacin , The mainstay of treatment of this disease is surgery, preferably of canal down method. Primary aim in ,surgical treatment is to remove the disease and render the ,ear safe, and second in priority is to preserve or reconstruct ,hearing but never at the cost of the primary aim., Pathophysiology : Atticoantral diseases are associated with the following pathophysiological processes : 1. Cholesteatoma 2. Osteitis and Granulation Tissue. Osteitis involves outer attic wall and posterosuperior margin of the tympanic ring. A mass of granulation tissue surrounds the area of osteitis and may even fill the attic, antrum, posterior tympanum and mastoid. A fleshy red polypus may be seen filling the meatus. 3. Ossicular Necrosis. It is common in atticoantral disease. Destruction may be limited to the long process of incus or may also involve stapes superstructure, handle of malleus or the entire ossicular chain. Therefore, hearing loss is always greater than in disease of tubotympanic type. Occasionally, the cholesteatoma bridges the gap caused by the destroyed ossicles and hearing loss is not apparent (cholesteatoma hearer). 4. Cholesterol Granuloma. It is a mass of granulation tissue with foreign body giant cells surrounding the cholesterol crystals. It is a reaction to long-standing retention of secretions or haemorrhage, and may or may not coexist with cholesteatoma. When present in the mesotympanum, behind an intact drum, the latter appears blue. 1. Ear discharge. Usually scanty, but always foul-smelling due to bone destruction. Discharge may be so scanty that the patient may not even be aware of it. Total cessation of discharge from an ear which has been active till recently should be viewed seriously, as perforation in these cases might be sealed by crusted discharge, inflammatory mucosa or a polyp, obstructing the free flow of discharge. Pus, in these cases, may find its way internally and cause complications. 2. Hearing loss. Hearing is normal when ossicular chain is intact or when cholesteatoma, having destroyed the ossicles, bridges the gap caused by destroyed ossicles (cholesteatoma hearer). Hearing loss is mostly conductive but sensorineural element may be added. 3. Bleeding. It may occur from granulations or the polyp when cleaning the ear.  4. Perforation. It is either attic or posterosuperior marginal type. A small attic perforation may be missed due to presence of a small amount of crusted discharge. Sometimes, the area of perforation is masked by a small granuloma. 5. Retraction pocket. An invagination of tympanic membrane is seen in the attic or posterosuperior area of pars tensa. Degree of retraction and invagination varies. In early stages, pocket is shallow and self-cleansing but later when pocket is deep, it accumulates keratin mass and gets infected. Stages of retraction pockets. There are four stages of tympanic membrane retraction. (a) Stage I. Tympanic membrane is retracted but does not contact the incus. It is a mild form of retraction. (b) Stage II. Tympanic membrane is retracted deep and contacts the incus; middle ear mucosa is not affected. (c) Stage III. Also called middle ear atelectasis. Tympanic membrane comes to lie on the promontory and ossicles. Middle ear space is totally or partially obliterated but middle ear mucosa is intact. Tympanic membrane can be lifted from the promontory with suction tip. It also balloons up when N2O is used during anaesthesia. Tympanic membrane is thin because its collagenous middle layer has been absorbed due to prolonged retraction. In these cases long process of incus and stapes superstructure are absorbed. Placement of a ventilation tube helps to restore the position of tympanic membrane. (d) Stage IV. Also called adhesive otitis media. Tympanic membrane is very thin and wraps the promontory and ossicles. There is no middle ear space, mucosal lining of the middle ear is absent and tympanic membrane gets adherent to the promontory. Retraction pockets are formed which may collect keratin plugs and form cholesteatoma. Erosion of the long process of incus and stapes superstructure is common in such cases. 6. Cholesteatoma. Pearly-white flakes of cholesteatoma can be sucked from the retraction pockets. Suction clearance and examination under operating microscope forms an important part of the clinical examination and assessment of any type of CSOM., Epidemiology : 29 (80.5%) of them had mucosal disease and 7 (19.4%) of them had atticoantral disease which means there is a higher prevalence of safe disease, 39 cases per 100, 000 persons in children and adolescents aged 15 years and younger., GOOD, Here are some ways to reduce your or your child’s risk of ear infections : ,,Prevent colds and other respiratory illnesses. Be proactive in preventing colds, especially during your child’s first year. Teach them about frequent handwashing and coughing or sneezing into their elbow. Don’t allow them to share food, cups or utensils. If it’s an option, avoid large daycare centers until they’re older.,Avoid secondhand smoke. Avoid exposure to secondhand smoke, and don’t allow others to smoke around your child.,Breastfeed (chestfeed) your baby. If possible, breastfeed your baby during the first six to 12 months. Antibodies in breast milk (chest milk) fight viruses and bacteria that cause infections.,Bottle-feed your baby in an upright position. If you bottle-feed, hold your baby upright so their head is higher than their stomach. This position can prevent formula or other fluids from flowing backward and collecting in their eustachian tubes.,Stay up to date on vaccinations. Ensure your child’s immunizations are current, including yearly flu shots for children 6 months and older. Ask your child’s pediatrician about vaccines for pneumococcal disease and meningitis., Complications : Brain Abscess, petrositis, acute mastoiditis, FACIAL PARALYSIS, Diagnostics : PUS CULTURE, Otoscopy, CT SCAN, Audiogram, HISTORY TAKING, Differential diagnosis : Acute Otitis Media, CHOLESTEATOMA, foreign body, granulation tissue in the external ear canal at its cartilaginous–bony junction, Langerhans cell histiocytosis (LCH), Meningitis., petrositis, tympanosclerosis, disease description : Chronic suppurative otitis media,  also known as chronic otitis media, is a stage of ear disease in which there is an on-going chronic infection of the middle ear without an intact tympanic membrane. This disease is a chronic inflammation of the middle ear and mastoid cavity. The characteristic presentation is chronic or persistent otorrhoea over 2 to 6 weeks through a perforated tympanic membrane. The Eustachian tube plays an important role in this disease, and dysfunction of this tube is found in 70% of patients undergoing middle ear surgery. When dysfunction of the Eustachian tube occurs, the pressure equilibration in the middle ear is impaired, and the middle ear aeration is perturbed, resulting in the classic symptoms of chronic suppurative otitis media

Chronic Thyroiditis(riedels)

Disease Name : Chronic Thyroiditis(riedels), Treatment : medication : Tamoxifen citrate , Glucocorticoids are the mainstay of medical treatment. The anti-inflammatory effects of glucocorticoids are most effective when used early in the disease process. There is no dosing guideline available; however, prednisone 15 mg to 100 mg daily has been shown to be effective .,Tamoxifen is a selective estrogen receptor modulator (SERM) used in the treatment of Riedel thyroiditis and other systemic fibrosing disorders. It induces tumor growth factor-beta (TGF-ß), which is a potent growth inhibitor. A dose of 10-20 mg, given alone or in combination with prednisone, has been successful in decreasing the mass size.Mycophenolate mofetil is an immunosuppressive agent with anti-fibrotic properties which has therapeutic use in systemic fibrosis. It converts to mycophenolic acid, which inhibits the antibody production from T and B lymphocytes., Surgery with subtotal or partial thyroidectomy is indicated only to relieve compressive symptoms., Pathophysiology : The hallmark of Riedel thyroiditis is the replacement of thyroid tissue with dense fibrotic tissue. Fibrosis involves extra-thyroidal structures, including the trachea, parathyroid glands, neck musculature, laryngeal nerves, and blood vessels. This causes the thyroid to become immobile and fixed and is described as stone-hard or woody on palpation, Epidemiology : Adult females from 30 to 50 years of age., incidence is suggested to be 1.06 cases per 100, 000 people., GOOD, Unfortunately, most cases of thyroiditis can’t be prevented.,,If you have a condition that requires treatment using radioactive iodine or radiation therapy, talk to your healthcare provider about your risk of thyroiditis. You may be able to start with other treatments to avoid developing thyroiditis.,,If you take prescription drugs that can cause thyroiditis, talk to your provider about your risk and if you can stop taking them. You still may not be able to avoid thyroiditis., Complications : respiratory failure, stridor, dyspnea, Diagnostics : FNAC, PET SCAN, USG Thyroid, CT SCAN, Differential diagnosis : ANAPLASTIC CARCINOMA OF THYROID, Goiter, hashimotos disease, Thyroid cancer, THYROID NODULE, thyroiditis, disease description : Riedel thyroiditis (also known as Riedel struma, chronic invasive fibrous thyroiditis, or ligneous struma) is a rare fibrotic condition that involves the thyroid gland and often invades the surrounding structures. It most commonly presents with obstructive symptoms such as dyspnea, dysphagia, and hoarseness as the structures surrounding the thyroid are involved. It can also present with hypoparathyroidism, hypothyroidism, or Horner syndrome.

Chronic Tonsillitis

Disease Name : Chronic Tonsillitis, Treatment : Conservative treatment consists of attention to general health, diet, treatment of coexistent infection of ,teeth, nose and sinuses., Tonsillectomy is indicated when tonsils interfere with,speech, deglutition and respiration or cause recurrent,attacks, Pathophysiology : 1. Chronic Follicular Tonsillitis. Here tonsillar crypts are full of infected cheesy material which shows on the surface as yellowish spots. 2. Chronic Parenchymatous Tonsillitis. There is hyperplasia of lymphoid tissue. Tonsils are very much enlarged and may interfere with speech, deglutition and respiration. Attacks of sleep apnoea may occur. Long-standing cases develop features of cor pulmonale. 3. Chronic Fibroid Tonsillitis. Tonsils are small but infected, with history of repeated sore throats. 4. Recurrent attacks of sore throat or acute tonsillitis. 5. Chronic irritation in throat with cough.6. Bad taste in mouth and foul breath (halitosis) due to pus in crypts. 7. Thick speech, difficulty in swallowing and choking spells at night (when tonsils are large and obstructive)., Epidemiology : 5% to 15% of adults with pharyngitis and 15% to 30% of patients between the ages of five and fifteen, Tonsillitis is most commonly caused by a viral infection and about 5% to 40% of cases are caused by a bacterial infection., 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 : parapharyngeal abscess, Peritonsillar abscess, cyst, Tonsilloliths (calculus of the tonsil), Diagnostics : Complete Blood Count CBC, THROAT SWAB, CT SCAN, Oral cavity examination, Differential diagnosis : coxsackie virus infection, Kawasaki Disease, oral candidiasis, retropharyngeal abscess, disease description : Tonsillitis can be caused by infections such as viruses (cytomegalovirus, herpes simplex, Epstein-Barr) or bacteria such as those that cause strep throat.Tonsillitis occurs more commonly in children than in adults, but it does not usually affect children under the age of 2.Chronic tonsillitis is an infection of the tonsils. Chronic tonsillitis can cause swelling and inflammation of the tonsils, as well as accompanying symptoms like sore throat, bad breath, and enlarged lymph nodes. 

Chronic Tubulointerstitial Nephritis

Disease Name : Chronic Tubulointerstitial Nephritis, Treatment : Therapy is directed at maintaining the fluid and electrolyte balance and avoiding,further exposure to nephrotoxic agents. Patients with obstructive uropathies can,require salt supplementation and treatment with potassium-binding resin,(Kayexalate). Prevention of infection by antibiotic prophylaxis can slow the,progression of renal damage in appropriate patients., Pathophysiology : The pathophysiology of chronic TIN is undefined, but data suggest that, in addition to abnormal cilia structure and function in JN and MCKD, it is immune mediated. Cells making up the interstitial infiltrate appear to be a combination of native interstitial cells, inflammatory cells recruited from the circulation, and resident tubular cells that undergo epithelial-mesenchymal transformation. Grossly, kidneys can appear pale and small for age. Microscopically, tubular atrophy and “dropout” with interstitial fibrosis and a patchy lymphocytic interstitial inflammation are seen. Patients with JN often have characteristic small cysts in the corticomedullary region. In primary chronic TIN, glomeruli are relatively spared until late in the disease course. Patients with chronic TIN secondary to a primary glomerular disease have histologic evidence of the primary disease. Chronic TIN due to cyclosporine or tacrolimus use is characterized by tubular atrophy, “stripe” interstitial fibrosis, and vascular sclerosis. In children, chronic TIN most commonly occurs in the context of (1) an underlying congenital urologic renal disease, such as obstructive uropathy or vesicoureteral reflux, or (2) an underlying metabolic disorder affecting the kidneys. Some commonly used drugs such as cyclosporine and tacrolimus also cause chronic TIN. Chronic TIN can occur as an idiopathic disease, although this is more common in adults. The juvenile nephronophthisis (JN)–medullary cystic kidney disease complex (MCKD) is a group of inherited, genetically determined cystic renal diseases that share the common histologic finding of chronic TIN. TIN with uveitis (TINU syndrome) is a rare autoimmune syndrome of chronic TIN with bilateral anterior uveitis and bone marrow granulomas that occurs primarily in adolescent girls. Clinical manifestations include photophobia, ocular pain and redness, and visual impairment. Chronic TIN is seen in all forms of progressive renal disease, regardless of the underlying cause, and the severity of interstitial disease is the single most important factor predicting progression to ESRD., Epidemiology : prevalence of 0.13%, TIN increased to 15-27%, DEPENDS UPON UNDERLYING ETIOLOGY, In most cases, there’s nothing you can do to prevent interstitial nephritis. You can reduce your risk of getting it by avoiding medicines that can cause the condition., Complications : Chronic renal failure, hepatic fibrosis, Diagnostics : Complete Blood Count CBC, USG KUB, USG, HISTOLOGIC EXAMINATION, kidney biopsy, URINE ANALYSIS (Volume), vesicocystourethrogram, Differential diagnosis : ACUTE GLOMERULONEPHRITIS, acute kidney injury, Glomerulonephritis, Pyelonephritis, 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 Venous Disease

Disease Name : Chronic Venous Disease, Treatment : External compression with elastic stockings or stretch bandages ,provides a counterbalance to the hydrostatic pressure in the veins., Topical steroids may be used for a short period of time ,to treat inflammation associated with stasis dermatitis. Several herbal ,supplements, such as horse chestnut seed extract (aescin); flavonoids ,including diosmin, hesperidin, or the two combined as micronized ,purified flavonoid fraction; and French maritime pine bark extract, ,are touted to have venoconstrictive and anti-inflammatory properties., Endovenous thermal ablation procedures of the saphenous veins ,include endovenous laser therapy and radiofrequency ablation. Sclerotherapy involves the injection of a chemical into a vein to ,cause fibrosis and obstruction. Surgical therapy usually involves ligation and stripping of the ,great and small saphenous veins., Pathophysiology : Varicose veinsare dilated, bulging, tortuous superficial veins, measuring at least 3 mm in diameter. The smaller and less tortuous reticular veins are dilated intradermal veins, which appear blue-green, measure 1–3 mm in diameter, and do not protrude from the skin surface. Telangiectasias, or spider veins, are small, dilated veins, <1 mm in diameter, located near the skin surface, and form blue, purple, or red linear, branching, or spider-web patterns. Varicose veins can be categorized as primary or secondary. Primary varicose veins originate in the superficial system and result from defective structure and function of the valves of the saphenous veins, intrinsic weakness of the vein wall, and high intraluminal pressure. Approximately one-half of these patients have a family history of varicose veins. Other factors associated with primary varicose veins include aging, pregnancy, hormonal therapy, obesity, and prolonged standing. Secondary varicose veins result from venous hypertension, associated with deep-venous insufficiency or deep-venous obstruction, and incompetent perforating veins that cause enlargement of superficial veins. Arteriovenous fistulas also cause varicose veins in the affected limb. Chronic venous insufficiency is a consequence of incompetent veins in which there is venous hypertension and extravasation of fluid and blood elements into the tissue of the limb. It may occur in patients with varicose veins but usually is caused by disease in the deep veins. It also is categorized as primary or secondary. Primary deep-venous insufficiency is a consequence of an intrinsic structural or functional abnormality in the vein wall or venous valves leading to valvular reflux. Secondary deep-venous insufficiency is caused by obstruction and/or valvular incompetence from previous deep-vein thrombosis Deep-venous insufficiency occurs following deep-vein thrombosis, as the delicate valve leaflets become thickened and contracted and can no longer prevent retrograde flow of blood and the vein itself becomes rigid and thick walled. Although most veins recanalize after an episode of thrombosis, the large proximal veins may remain occluded. Secondary incompetence develops in distal valves because high pressures distend the vein and separate the leaflets. Other causes of secondary deep-venous insufficiency include May-Thurner syndrome, where the left iliac vein is occluded or stenosed by extrinsic compression from the overlapping right common iliac artery; arteriovenous fistulas resulting in increased venous pressure; congenital deep-vein agenesis or hypoplasia; and venous malformations as may occur in Klippel-Trénaunay and Parkes-Weber syndromes.., Epidemiology : ~15% in men and 30% in women, 2% among those <50 years of age to 10% of those 70, POOR, Sometimes, CVI can’t be prevented. But you can lower your risk of CVI and other vein problems by making some lifestyle changes. These include : ,,Avoid smoking and tobacco use.,Avoid wearing restrictive clothing like tight girdles or belts.,Don’t sit or stand for too long at a time. Get up and move around as often as you can.,Eat a heart-healthy diet. This includes reducing your sodium (salt) intake.,Exercise regularly.,Keep a healthy weight.,If you’ve had DVT, your provider may recommend anticoagulants., Complications : venous leg ulcers, Diagnostics : Color Doppler, MRI, DUPLEX ULTRASONOGRAPHY, X RAY, USG, PHYSICAL EXAMINATION, Differential diagnosis : CELLULITIS, CIRRHOSIS, deep venous thrombosis, Endocrine disorders, heart failure, lymphedema, renal failure, disease description : Chronic venous diseases range from telangiectasias and reticular veins, to varicose veins, to chronic venous insufficiency with edema, skin changes, and ulceration.Chronic venous insufficiency (CVI) is a form of venous disease that occurs when veins in your legs are damaged. As a result, these veins can’t manage blood flow as well as they should, and it’s harder for blood in your legs to return to your heart. CVI causes blood to pool in your leg veins, leading to high pressure in those veins.

Chronic Venous Insufficiency

Disease Name : Chronic Venous Insufficiency, Treatment : Compression therapy, Microincision/ambulatory phlebectomy, Subfascial Endoscopic Perforator Surgery (SEPS) : nan, Valvuloplasty, Vein bypass, Pathophysiology : Chronic venous insufficiency pathophysiology is either due to reflux (backward flow) or obstruction of venous blood flow. Chronic venous insufficiency can develop from the protracted valvular incompetence of superficial veins, deep veins or perforating veins that connect them. In all cases, the result is venous hypertension of the lower extremities.Superficial incompetence is usually due to weakened or abnormally shaped valves or widened venous diameter which prevents normal valve congruence. The leaky valve in most cases is located near the termination of the greater saphenous vein into the common femoral vein. While in some cases the valve dysfunction may be congenital, it can also be a result of trauma, prolonged standing, hormonal changes or thrombosis.Deep vein dysfunction is usually owing to the previous DVT which results in inflammation, valve scarring and adhesion, and luminal narrowing. Perforating vein valvular failure allows higher pressure to enter the superficial venous system. The subsequent dilation prevents the proper closure of the valve cusps in the superficial veins. Most patients will also have the disease in the superficial veins. The resting venous pressure is a summation of the outflow obstruction, capillary inflow, valve function, and muscle pump function., Epidemiology : 1% to 17% of men and 1% to 40% of women may experience chronic venous insufficiency., POOR, Avoid smoking and tobacco use.,Avoid wearing restrictive clothing like tight girdles or belts.,Don’t sit or stand for too long at a time. Get up and move around as often as you can.,Eat a heart-healthy diet. This includes reducing your sodium (salt) intake.,Exercise regularly.,Keep a healthy weight., Complications : infection, NERVE INJURY, Scarring, Diagnostics : MRI, X RAY, Differential diagnosis : CELLULITIS, lymphedema, stasis dermatitis, VARICOSE VEINS, disease description : Chronic venous insufficiency (CVI) is a form of VENOUS DISEASE that occurs when veins in your legs are damaged. As a result, these veins can’t manage blood flow as well as they should, and it’s harder for blood in your legs to return to your heart. CVI causes blood to pool in your leg veins, leading to high pressure in those veins.CVI can happen due to damage in any of your leg veins.

Chronic Viral Hepatitis

Disease Name : Chronic Viral Hepatitis, Treatment : medication : Ribavirin , Adefovir dipivoxil , Lamivudine, Interferon Alpha, chronic hepatitis B can be cured with a drug called pegylated interferon-alpha, which is taken as a weekly injection for six months. The alternative is suppression of the virus with oral medications, such as lamivudine and adefovir.,most effective therapy for hepatitis C is a drug combination consisting of pegylated interferon and ribavirin. Pegylated interferon is taken weekly as an injection and ribavirin is a twice daily tablet. The treatment is a form of chemotherapy and the ability to tolerate it varies widely for each person., Liver transplant may be an option for people whose hepatitis progresses to liver failure and who fail to respond to treatment or cannot tolerate treatment., Pathophysiology : Whether a virus gains entry via the blood or the enteric system, it eventually travels to the liver where it enters hepatocytes, replicates, and sheds virions. Replication occurs via either direct translation of viral RNA or via reverse transcription of viral DNA. Hepatocyte injury can be acute and self-limited or insidious and chronic. The mechanism of hepatocyte injury is mediated by the host immune response to viral antigens that are expressed by infected hepatocytes and not so much by cytopathic effects of the viruses themselves. The progression to chronic infection observed with HBV and HCV is associated with attenuation of virus-specific T-cells. Studies have shown that exhaustion of these virus-specific T-cells leads to an inability to clear the viruses, therefore allowing the viruses to dwell chronically in host hepatocyte ., Epidemiology : An estimated 354 million people worldwide live with hepatitis B or C, highest incidence is among those aged 20 to 39 years of age. About 100 million people have a chronic HBV infection, POOR, "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 : CIRRHOSIS, liver failure, Diagnostics : ANA, Anti HBe Antibody ELISA, Anti HBs Antibody ELISA, Anti HCV Antibody ELISA, HBeAg, HBsAg, HBV DNA, PT/PC/INR, LIVER FUNCTION TEST LFT, IgG anti HBc, HDV RNA, Anti LKM 1, SERUM GLOBULIN, CT SCAN, Differential diagnosis : ASCENDING CHOLANGITIS, ASCENDING CHOLANGITIS, AUTOIMMUNE HEPATITIS, biliary obstruction, disease description : Viral hepatitis is an infection that causes liver inflammation and damage. Inflammation is swelling that occurs when tissues of the body become injured or infected. Inflammation can damage organs. Researchers have discovered several different viruses NIH external link that cause hepatitis, including hepatitis A, B, C, D, and E. Hepatitis A and hepatitis E typically spread through contact with food or water that has been contaminated by an infected person’s stool. People may also get hepatitis E by eating undercooked pork, deer, or shellfish. Hepatitis B, hepatitis C, and hepatitis D spread through contact with an infected person’s blood. Hepatitis B and D may also spread through contact with other body fluids. This contact can occur in many ways, including sharing drug needles or having unprotected sex.Chronic hepatitis occurs when your body isnt able to fight off the hepatitis virus and the virus does not go away. Chronic hepatitis can lead to complications such as cirrhosis, liver failure, and liver cancer.

Churg-strauss Syndrome

Disease Name : Churg-strauss Syndrome, Treatment : medication : Cyclophosphamide , Methyl prednisolone , Oral prednisone : 1 mg/kg daily for 3 weeks, then tapering 5 mg every 10 days to 0.5 mg/kg. Then taper 2.5 mg every 10 days to the minimal effective dosage, or until definite withdrawal.,Intravenous methylprednisolone pulse (15 mg/kg) followed by oral prednisone as above., Pathophysiology : The pathogenesis and clinical phenotype follow a dichotomy of either eosinophil-mediated damage or ANCA-induced endothelial injury.An initial TH2-mediated immune response provokes the margination of eosinophils. Eosinophilic presence in active disease is likely a consequence of increased synthesis, enhanced extravasation, and prolonged survival in target tissues. IL-3 and IL-5, produced by TH-2 lymphocytes, are the key regulators in the maturation and release of eosinophils, as well as their survival in blood. Serum levels of IL-5 correlate consistently with disease activity and go down with the initiation of immunosuppressive therapy.When activated by Th-2 type cytokines, Epithelial and endothelial cells also secrete eosinophil-specific chemokines like eotaxin 3(CCL26), CCL17, and CCL22. They act on CCR4 receptors to facilitate the recruitment of eosinophils and effector Th2 cells to the end organs–thus amplifying the immune response .   Eosinophils, in turn,  release the cationic proteins like eosinophil cationic protein (ECP), eosinophil peroxidases, eosinophil-derived neurotoxins, and eosinophil granule major basic protein which is directly involved in mediating tissue damage.Eosinophils also secrete cytokines like IL- 1, IL-3, IL-5, TGF- beta, and vascular endothelial growth factor. IL-5, in turn,  plays an active role in the maturation, differentiation, and survival of eosinophils.Histological findings in EGPA are characterized by eosinophilic infiltrates in walls of small and medium-sized blood vessels and extravascular tissue spaces. In EGPA with acute pulmonary exacerbations, Bronchoalveolar lavage fluid is also rich in eosinophils, similar to acute or chronic eosinophilic pneumonia. Extravascular eosinophilic granulomas are also observed, particularly in the gastrointestinal tract ., Epidemiology : 10.7 to 14 per million adults worldwide., 5-year survival of 90%, At this time there are no known ways to prevent this disease., Complications : myopathy, Osteoporosis, heart disease, diabetes mellitus, Diagnostics : EOSINOPHILS - ABSOLUTE COUNT, Erythrocyte Sedimentation Rate (ESR), PLASMA FIBRINOGEN, ANCA, biopsy, ALFA2 GLOBULIN, ANTI MYELOPEROXIDASE, CT SCAN, Differential diagnosis : Acute Eosinophilic Pneumonia, Aspergillosis, Chronic Eosinophilic Pneumonia, Granulomatosis with polyangiitis, Microscopic polyangiitis, Polyarteritis Nodosa, disease description : Churg Straus syndrome – renamed as eosinophilic granulomatosis with polyangiitis (EGPA) – is a specific variant of the group of diseases characterized by necrotizing vasculitis of small and medium-sized systemic blood vessels. Other subtypes within the broad group include granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA), and polyarteritis nodosa. It is distinctive from the other diseases in the category of the coexistence of asthma, rhinosinusitis, and the presence of peripheral eosinophilia 

Chylothorax

Disease Name : Chylothorax, Treatment : medication : Octreotide , Therapy,includes enteral feedings with a low-fat or medium-chain triglyceride, highprotein,diet, and total parenteral nutrition. Somatostatin,and octreotide have been used to manage chylothorax. Various octreotide,dosages have been described in the literature including 1-4 µg/kg/hr,intravenously and 10 µg/kg/day subcutaneously; however, the optimal dose is,not known and further study is needed. Etilefrine, a sympathomimetic agent with both a- and ß-,adrenergic activity, has been successfully used in a few patients. Constriction of,the thoracic duct by this drug may reduce pleural chyle accumulation., Thoracentesis is repeated as needed to,relieve pressure symptoms; tube thoracostomy is often performed., Pathophysiology : Chylothorax in children occurs most frequently because of thoracic duct injury as a complication of cardiothoracic surgery (post Fontan surgery) . Other cases are associated with chest injury, extracorporeal membrane oxygenation, or with primary or metastatic intrathoracic malignancy, particularly lymphoma. In newborns, rapidly increased venous pressure during delivery may lead to thoracic duct rupture. Chylothorax has also been associated with Down syndrome, Noonan syndrome, and Turner syndrome. Less common causes include lymphangiomatosis; restrictive pulmonary diseases; thrombosis of the duct, superior vena cava, or subclavian vein; tuberculosis or histoplasmosis; and congenital anomalies of the lymphatic system. Refractory chylothorax in the fetus has been associated with a missense mutation in integrin a9 ß1 gene. Chylothorax can occur in trauma and child abuse . It is important to establish the etiology because treatment varies with the cause. In some patients no specific cause is identified., Epidemiology : prevalence after various cardiothoracic surgeries is 0.2% to 1%., 0.4–4% in esophageal procedures to 2.5–4.7% in congenital cardiac procedures., DEPENDS ON UNDERLYING ETIOLOGY, Complications : death, infection, respiratory difficulties, Malnutrition, Diagnostics : ultrasound, X RAY CHEST, CT CHEST, LIPID PROFILE, MRI, Differential diagnosis : CHRONIC PLEURAL EFFUSIONS, Congestive heart failure, Hemothorax, HIV infection and AIDS, PLEURAL EFFUSION, disease description : Chylothorax is the accumulation of chyle in the pleural cavity.Chylothorax is a rare but serious condition in which lymph formed in the digestive system (chyle) accumulates in your chest cavity. Lymph is a fluid containing white blood cells and proteins that moves through your lymphatic system and drains into your bloodstream.

Chytridiomycosis

Disease Name : Chytridiomycosis, Treatment : Cycloplegic agents, including tropicamide, cyclopentolate, and topical atropine.,Topical phenylephrine is used to tighten the zonules by stimulating the longitudinal muscle of the ciliary body.,Topical beta-blockers, alpha-adrenergic agonists, and topical and oral carbonic anhydrase inhibitors.,Osmotic agents used to decrease vitreous volume include oral glycerol or isosorbide, or intravenous mannitol.,Bimatoprost, travoprost, tafluprost, and latanoprost are effective new medications for lowering intraocular pressure in patients with glaucoma and ocular hypertension, Pathophysiology : Once the host is infected with Bd, chytridiomycosis may or may not develop. The disease is transmitted through contact with zoospores in the environment, and possibly through direct contact with diseased amphibians, though this has not yet been confirmed. Research has shown that Bd grows best in water that is between 17-25°C (62-77°F) and that in the wild, most disease outbreaks occur at higher elevations during cooler months., Epidemiology : nan, Complications : uveitis, CORNEAL EDEMA, Diagnostics : Protein, Differential diagnosis : nan, disease description : Chytridiomycosis is an infectious disease of amphibians caused by the fungus Batrachochytrium dendrobatidis (Bd). It an emerging disease that is significantly impacting amphibian populations across the globe. The disease has caused the decline or complete extinction of over 200 species of frogs and other amphibians. (THIS DISEASE IS NOT KNOW TO AFFECT HUMANS )

Ciliary Block Glaucoma

Disease Name : Ciliary Block Glaucoma, Treatment : medication : Acetazolamide, Timolol , Atropine/ Atropine methonitrate, Mannitol , Medical therapy consists of 1% atropine drops or,ointment to dilate ciliary ring and break the ciliolenticular,or cilio-vitreal contact, acetazolamide,250 mg QID and 0.5% timolol maleate eyedrops,to decrease aqueous production, and intravenous,mannitol to cause deturgescence of the vitreous gel., YAG laser hyaloidotomy can be undertaken in aphakic,and pseudophakic patients.,Surgical therapy in the form of pars plana vitrectomy,with or without lensectomy (as the case may be) is,required when the above measures fail., Pathophysiology : It is believed that, rarely following intraocular operation, the tips of ciliary processes rotate forward and press against the equator of the lens in phakic eyes (cilio-lenticular block) or against the intraocular lens in pseudophakic eyes (cilio-IOL block) or against the anterior hyaloid phase of vitreous in aphakic eyes (cilio-vitreal block) and thus block the forward flow of aqueous humour, which is diverted posteriorly and collects as aqueous pockets in the vitreous. As a consequence of this the iris lens diaphragm is pushed forward, IOP is raised and anterior chamber becomes flat. Patient develops severe pain and blurring of vision following any intraocular operation (usually after peripheral iridectomy, filtering surgery or trabeculectomy in patients with primary anglemclosure glaucoma). The main features of the ciliary block glaucoma noted are : • Persistent flat anterior chamber following any intraocular operation, • Markedly raised IOP in early postoperative period, • Negative Seidel’s test and • Unresponsiveness or even aggravation by miotics. • Malignant glaucoma may be phakic, aphakic or pseudophakic. Note. It is important to note that the fellow eye is also prone to meet the same fate., Epidemiology : 2.54 million., An estimated 57.5 million people worldwide are affected by POAG with a global prevalence of 2.2%, variable, Complications : nan, Diagnostics : GONIOSCOPY, Slit lamp examination, Seidel’s test, Differential diagnosis : JUVENILE IDIOPATHIC ARTHITIS, Posner-Schlossman syndrome (PSS), Sarcoidosis, Vogt-Koyanagi-Harada (VKH) Syndrome, disease description : Ciliary block glaucoma (originally termed as malignant glaucoma) is a rare condition which may occur as a complication of any intraocular operation. It classically occurs in patients with primary angle closure glaucoma operated for peripheral iridectomy or filtration (e.g., trabeculectomy) surgery. It is characterised by a markedly raised IOP associated with shallow or absent anterior chamber.

Circumscribed Labyrinthitis

Disease Name : Circumscribed Labyrinthitis, Treatment : Systemic antibiotic therapy should be instituted before and after operation to prevent spread of infection into the labyrinth.,If bacterial meningitis is queried, then treat immediately with intravenous antibiotics. A concurrent otogenic source should still be ruled out, and topical and IV antibiotics can be given simultaneously if appropriate.,The initial management of autoimmune labyrinthitis is corticosteroids. If patients are refractory to corticosteroid therapy, other immunomodulators may be considered, such as azathioprine, etanercept, or cyclophosphamide. These agents are often used in chronic conditions due to their reduced side effect profile compared to corticosteroids, mastoid exploration is often required to,eliminate the cause., Pathophysiology : The pathophysiology of circumscribed labyrinthitis involves an inflammatory process that affects the vestibular nerve and associated structures. Here is an overview of the pathophysiological mechanisms involved : Viral infection : The most common cause of circumscribed labyrinthitis is believed to be a viral infection. It is thought that a viral pathogen, such as the herpes simplex virus (HSV), varicella-zoster virus (VZV), or Epstein-Barr virus (EBV), infects the vestibular nerve or the adjacent structures in the inner ear. The exact mechanism by which the virus enters the inner ear is not fully understood.Inflammatory response : The viral infection triggers an immune response in the affected area. Immune cells, particularly lymphocytes, infiltrate the vestibular nerve and surrounding tissues. This immune response leads to the release of pro-inflammatory molecules, including cytokines and chemokines.Nerve damage : The inflammatory response causes damage to the vestibular nerve, leading to its dysfunction. The inflammation may result in edema (swelling) and disruption of the nerve fibers, interfering with the transmission of sensory signals from the inner ear to the brain.Disruption of balance and spatial orientation : The dysfunction of the vestibular nerve affects the normal functioning of the balance and spatial orientation systems. The brain relies on the signals from the vestibular nerve to maintain balance and coordinate movements. When the vestibular nerve is inflamed and damaged, it results in vertigo (a spinning sensation), dizziness, and problems with balance and coordination.Resolution and recovery : In most cases, the inflammation subsides over time, and the bodys immune system clears the viral infection. The damaged vestibular nerve undergoes a process of healing and repair. However, the recovery can vary from person to person, and some individuals may experience residual symptoms or long-term vestibular dysfunction., Epidemiology : 3.5 cases per 100, 000 people), GOOD, Complications : nan, Diagnostics : MRI, Audiogram, FISTULA TEST, Differential diagnosis : acoustic neuroma, "menieres disease", Multiple Sclerosis, vestibular neuronitis, disease description : Labyrinthitis is an inner ear infection characterized by inflammation of the labyrinth. The labyrinth is the inner ear system responsible for your hearing and sense of balance. When your labyrinth or one of the nerves inside your labyrinth is inflamed or irritated, hearing and balance can be affected.While labyrinthitis can affect people of all ages, the condition is most common in adults between the ages of 30 and 60. 

Cirrhosis

Disease Name : Cirrhosis, Treatment : diuretics, which are used in combination with a low-salt diet to reduce the amount of fluid in your body, which helps with swelling (oedema),medicine to help with high blood pressure in the main vein that takes blood to the liver (portal hypertension), Liver transplant surgery, Pathophysiology : Multiple cells play a role in liver cirrhosis, including hepatocytes and sinusoidal lining cells such as hepatic stellate cells (HSCs), sinusoidal endothelial cells (SECs), and Kupffer cells (KCs). HSCs form a part of the wall of the liver sinusoids, and their function is to store vitamin A. When these cells are exposed to inflammatory cytokines, they get activated, transform into myofibroblasts, and start depositing collagen, which results in fibrosis. SECs form the endothelial lining and are characterized by the fenestrations they make in the wall that allow the exchange of fluid and nutrients between the sinusoids and the hepatocytes. Defenestration of the sinusoidal wall can happen secondary to chronic alcohol use and promote perisinusoidal fibrosis. KCs are satellite macrophages that line the wall of the sinusoids as well. Studies mainly from animal models have shown that they play a role in liver fibrosis by releasing harmful mediators when exposed to injurious agents and acting as antigen-presenting cells for viruses. Hepatocytes are also involved in cirrhosiss pathogenesis, as damaged hepatocytes release reactive oxygen species and inflammatory mediators that can promote activating HSCs and liver fibrosis.The major cause of morbidity and mortality in cirrhotic patients is the development of portal hypertension and hyperdynamic circulation. Portal hypertension develops secondary to fibrosis and vasoregulatory changes, both intrahepatically and systematically, leading to collateral circulation formation and hyperdynamic circulation ., Epidemiology : 1, 395 cases per 100, 000 population, poor, You might be able to prevent liver disease from progressing to cirrhosis by intervening earlier in the process. This depends on whether you’re aware of it and whether there are steps you can take to prevent it. Many people don’t have symptoms in the early stages, but a routine health checkup could help bring it to light. This could give you the chance to make important changes or begin treatment., Complications : bleeding, infection, jaundice, splenomegaly, Malnutrition, swelling in abdomen, Diagnostics : BONE MARROW BIOPSY, Prothrombin Time Test and INR (PT/INR), Complete Blood Count CBC, alanine transaminase (ALT), CT SCAN, Differential diagnosis : Alcoholic Fatty Liver, Ebola virus disease (EVD), Galactosemia, HELLP SYNDROME, disease description : Cirrhosis is a late stage of scarring (fibrosis) of the liver caused by many forms of liver diseases and conditions, such as hepatitis and chronic alcoholism.  Each time  liver is injured — whether by disease, excessive alcohol consumption or another cause — it tries to repair itself. In the process, scar tissue forms. As cirrhosis progresses, more and more scar tissue forms, making it difficult for the liver to function (decompensated cirrhosis). Advanced cirrhosis is life-threatening.

Cirrhotic Cardiomyopathy

Disease Name : Cirrhotic Cardiomyopathy, Treatment : As CCM develops due to cirrhosis, liver transplantation is the cornerstone of treatment. Transplantation has been shown to significantly improve systolic and diastolic dysfunction and reverse QT prolongation in 50% of patients. Cardiac benefits are observed within 3 to 12 months following surgery., Medical therapy will generally include angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), loop and thiazide diuretics, aldosterone receptor antagonists, and beta-blockers., Transjugular intrahepatic portosystemic shunt (TIPS) placement is used to reduce portal hypertension in patients with cirrhosis, but this procedure is not expected to improve cardiomyopathy., Pathophysiology : Cirrhotic cardiomyopathy is characterized by an impaired cardiac response to stress, which results from a combination of autonomic dysfunction, alterations in cell membrane composition, ion channel defects, and an overproduction of cardio depressant factors. Patients with cirrhosis have effective central hypovolemia, despite an absolute volume overload, due to splanchnic vasodilation caused by the production of nitric oxide, carbon monoxide, and endocannabinoids. (This splanchnic vasodilation results in a decrease in systemic vascular resistance, initially compensating for cardiac dysfunction and producing an asymptomatic clinical picture at rest.) The state of functional hypovolemia activates the renin-angiotensin-aldosterone system and the sympathetic nervous system, which chronically leads to the downregulation of beta-adrenergic receptors in the plasma membrane with resultant autonomic dysfunction., Epidemiology : As many as 50% of cirrhotic patients undergoing liver transplantation show signs of cardiac dysfunction, and 7% to 21% of deaths after orthotopic liver transplantation result from overt heart failure. I, As many as 1 of 500 adults, unfavourable, Cirrhotic cardiomyopathy is an under-recognized condition that carries a poor prognosis. As this disease develops due to cirrhosis, early recognition and management of conditions predispose to liver disease is key. This requires the efforts of an interprofessional healthcare team. Primary care physicians and mid-level providers should monitor patients for alcohol use disorder, screen for hepatitis, and encourage lifestyle modifications in patients at risk for non-alcoholic fatty liver disease (NAFLD)., Complications : Arrhythmias, pulmonary hypertension, sudden cardiac death, hepatorenal syndrome, Congestive heart failure, Diagnostics : NT- Pro- BNP, Protein, SERUM TROPONIN- I(TROP I), 2-D Echo, X RAY CHEST, X RAY, Electrocardiography (EKG), Differential diagnosis : HYPERTROPHIC CARDIOMYOPATHY, ischaemic heart disease, restrictive cardiomyopathy, VALVULAR HEART DISEASE, disease description : Cirrhotic cardiomyopathy is a cardiac condition observed in patients with cirrhotic regardless of the etiologies. It is characterized by the impaired systolic response to physical stress, diastolic dysfunction, and electrophysiological abnormalities, especially QT interval prolongation.  The impairment of ß-adrenergic receptor, the increase in endogenous cannabinoids, the presence of cardiosuppressants such as nitric oxide and inflammatory cytokines are the proposed mechanisms of systolic dysfunction. The activation of cardiac renin-angiotensin system and salt retention play the role in the development of cardiac hypertrophy and impaired diastolic function. QT interval prolongation, which is observed in 40-50 % of cirrhotic patients, occurs as a result of the derangement in membrane fluidity and ion channel defect

Citrullinemia Type I (ctln1)

Disease Name : Citrullinemia Type I (ctln1), Treatment : Infants are placed a low protein, high calorie diet supplemented by essential amino acids,Treatment of an individual with CTLN1 requires the coordinated efforts of a team of specialists. Biochemical geneticists, pediatricians, neurologists, and dieticians, are needed to work together to ensure a comprehensive approach to treatment. Management involves prompt diagnosis, control of hyperammonemia and control of intracranial pressure., Pathophysiology : CTLN1 is caused by mutations in the ASS1 gene that is responsible for production of the argininosuccinate synthetase (ASS) enzyme. The symptoms of CTLN1 develop due to deficiency of this enzyme, which is needed to detoxify ammonia in the body. Failure to properly remove ammonia via synthesis of urea leads to the abnormal accumulation of ammonia in the blood (hyperammonemia).CTLN1 is inherited as an autosomal recessive genetic condition. Recessive genetic disorders occur when an individual inherits two copies of an abnormal gene for the same trait, one from each parent. If an individual receives one normal gene and one gene for the disease, the person will be a carrier for the disease but usually will not show symptoms., Epidemiology : 1 : 250, 000 live births, CTLN1 occurs in approximately 1/57, 000 births., variable, Not To Do : Dietary restrictions are aimed at limiting the amount of protein intake to avoid the development of excess ammonia., Complications : liver failure, Diagnostics : MRI, molecular genetic testing, Differential diagnosis : Argininosuccinic aciduria (Argininosuccinate lyase deficiency), Carbamoyl Phosphate Synthetase Deficiency, disease description : Citrullinemia type I (CTLN1) is a rare autosomal recessive genetic disorder that includes a neonatal acute (classic) form, a milder late-onset form, a form that begins during or after pregnancy, and an asymptomatic form.CTLN1 is caused by deficiency or absence of the enzyme argininosuccinate synthetase (ASS). ASS is one of six enzymes that play a role in the removal of nitrogen from the body, a process known as the urea cycle. The lack of this enzyme results in excessive accumulation of nitrogen, in the form of ammonia (hyperammonemia), in the blood and all body fluids.

Ck Syndrome (cks)

Disease Name : Ck Syndrome (cks), Treatment : nan, Pathophysiology : In affected members of a 3-generation family with X-linked mental retardation, Tarpey et al. (2009) identified a 1-bp duplication in the NSDHL gene (300275.0007). In affected members of the original family with CK syndrome reported by du Souich et al. (2009), McLarren et al. (2010) identified a hemizygous truncating mutation in the NSDHL gene (300275.0008). In vitro functional expression studies showed that both mutations acted as temperature-sensitive hypomorphic alleles, resulting in a less severe phenotype than that observed with mutations associated with CHILD syndrome. Cells and cerebrospinal fluid from an affected individual showed increased methylsterol levels. McLarren et al. (2010) suggested that the phenotype resulted mainly from the accumulation of toxic methylsterols, not necessarily from cholesterol deficiency. , Epidemiology : <1/1000000 (Worldwide, variable, Complications : nan, Diagnostics : nan, Differential diagnosis : chondrodysplasia punctata 2, x-linked dominant, congenital hemidysplasia with ichthyosiform erythroderma and limb defects, kaposi sarcoma, sarcoma, disease description : CK syndrome (CKS) is an X-linked recessive disorder characterized by mild to severe cognitive impairment, seizures, microcephaly, cerebral cortical malformations, dysmorphic facial features, and thin body habitus.  it is an allelic disorder with a different phenotype .

Clavicle Fracture

Disease Name : Clavicle Fracture, Treatment : 1-triangular sling,2-8 bandage,3-Open reduction and internal fixation,is required, either when the fracture is associated,with neurovascular deficit, or in some severely,displaced fractures, where it may be more of a,cosmetic concern., Pathophysiology : The junction of the middle and outer-third of the clavicle is the commonest site; the other common site being the outer-third of the clavicle. This fracture is usually displaced. The outer fragment displaces medially and downwards because of the gravity and pull by the pectoralis major muscle attached to it. The inner fragment displaces upwards because of the pull by the sterno-cleidomastoid muscle attached to it. The clavicle is an S-shaped bone and is the only osseous link between the upper extremity and the trunk. The clavicle articulates distally with the acromion at the acromioclavicular joint and articulates proximally with the sternum at the sternoclavicular joint. Due to its superficial subcutaneous location and the numerous ligamentous and muscular forces applied to it, the clavicle is easily fractured. Because the midshaft of the clavicle is the thinnest segment and does not contain ligamentous attachments, it is the most easily fractured location.Fractures of the clavicle are typically described using the Allman classification system, dividing the clavicle into 3 groups based on location. Fractures of the middle third or midshaft fractures are in Group I (the most common), fractures of the distal or lateral third are in Group II,  and fractures of the proximal or medial third are in Group III, Epidemiology : 1 in 1000 people per year., GOOD, Clavicle fractures happen suddenly and are difficult to prevent. But certain things can help keep your bones safer : ,,Drive safely and wear a seatbelt when riding in a vehicle.,Eat a well-balanced diet with plenty of calcium to keep your bones strong.,Use good technique and body positioning for any sports you play or activities you do (such as bike riding).,Wear protective gear when playing sports or participating in hobbies., Complications : arthritis, Diagnostics : X RAY, CT SCAN, Differential diagnosis : Brachial plexus block, PNEUMOTHORAX, rib fracture, scapula fracture, Shoulder dislocation, disease description : This is a common fracture at all age groups. It usually results from a fall on the shoulder or sometimes on an out stretched hand. Fractures of the clavicle are quite common, accounting for up to 10% of all fractures. It is the most common fracture of childhood. A fall onto the lateral shoulder most frequently causes a clavicle fracture. Radiographs confirm the diagnosis and aid in further evaluation and treatment. While most clavicle fractures are treated conservatively, severely displaced or comminuted fractures may require surgical fixation.

Clear Cell Adenocarcinoma

Disease Name : Clear Cell Adenocarcinoma, Treatment : medication : Cisplatin , Etoposide, Irinotecan, The treatment of clear cell carcinoma is similar to that of cervical cancer. Radical hysterectomy and pelvic lymphadenectomy constitute a standard surgical treatment for patients with early-stage cervical carcinoma FIGO stage IB or IIA, which results in permanent infertility in the patient. External beam radiotherapy is the standard of care for stage IIB and IIIB., Pathophysiology : Consequently, its pathogenesis remains largely unknown, with no cell lines established from primary tumors Researchers investigated genetic instability in these tumors as manifested by somatic mutation of microsatellite repeats. Evidence of microsatellite instability was present in 50% of clear cell carcinomas of the uterine cervix not associated with DES exposure and in all DES-associated tumors examined. No evidence of mutations in HRAS proto-oncogenes or the KRAS or, the Wilms tumor (WT1) tumor suppressor gene or the estrogen receptor gene was present in clear cell carcinoma of the uterine cervix., Epidemiology : Very rare. No prevalence study, Rare disease accounting for only 4% of all adenoca, POOR, Quitting smoking · Lowering blood pressure · ,Maintaining a healthy body weight · ,Eating a diet high in fruits and vegetables and low in fat., Complications : hypercalcemia, hypertension, Diagnostics : MRI, CT SCAN, FDG-PET, Differential diagnosis : Adenosis, medullary carcinoma, neuroendocrine carcinoma, disease description : Clear cell renal cell carcinoma, or ccRCC, is a type of kidney cancer. The kidneys are located on either side of the spine towards the lower back. The kidneys work by cleaning out waste products in the blood. Clear cell renal cell carcinoma is also called conventional renal cell carcinoma. ccRCC is the most common type of kidney cancer, and makes up about 80% of all renal cell carcinoma cases. ccRCC is more common in adults than children. Renal cell carcinoma makes up 2-6% of childhood and young adult kidney cancer cases.

Clear Cell Renal Cell Carcinoma

Disease Name : Clear Cell Renal Cell Carcinoma, Treatment : medication : Sorafenib, Sunitinib, Everolimus, "Stages 1 to 3 are characterized as localized, and stage 4 is advanced disease. The treatment for localized disease is surgery with curative intent. Radical nephrectomy or partial nephrectomy is preferred depending upon the extent of the disease, patients comorbidities, and underlying renal function. Cryotherapy and radiofrequency ablation are reserved for unresectable or nonsurgical candidates presenting with a small renal mass. Tyrosine kinase inhibitors (sunitinib and pazopanib) are used in metastatic ccRCC as they act by inhibiting VEGFR. The mammalian target of rapamycin (mTOR inhibitors) everolimus and temsirolimus have been approved for metastatic ccRCC. mTOR inhibitor, along with lenvatinib (VEGFR inhibitor), is used as a second-line agent in metastatic ccRCC. The use of selective HIF2 blockers is under investigation.", Pathophysiology : Mutations in the VHL gene can be transmitted in an autosomal dominant fashion or in a sporadic way. More than 50% of the patients with ccRCC sporadically have VHL gene abnormalities. Double hit theory is that some patients are born with one copy of defective VHL gene, and the second hit is due to the somatic mutation. Normally, VHL is a tumor suppressor gene that regulates the levels of intracellular proteins and hypoxia-inducible factor 1 alpha and 2 alpha (HIF1A and HIF2A).A defective VHL gene results in the interaction among intracellular proteins resulting in the upregulation of messenger RNA (mRNA) encoding for growth factors such as platelet-derived growth factor-beta (PDGFB), vascular endothelial cell growth factor (VEGF), and transforming growth factor-alpha (TGFA). All these growth factors promote the development of these vascular tumors. Under normal oxygen conditions, HIF1A and HIF2A undergo hydroxylation and binds to a protein called pVHL and are degraded. In hypoxemic conditions or the absence of pVHL, HIFA accumulates, leading to the upregulation of mRNA and increased production of the growth factors., Epidemiology : Renal cell carcinoma is more prevalent in North America and the Czech Republic., Globally, the incidence of renal cell carcinoma about 64, 000, and the mortality is as high as 14, 000, poor, Quitting smoking.,Lowering blood pressure.,Maintaining a healthy body weight.,Eating a diet high in fruits and vegetables and low in fat., Complications : hepatic dysfunction, hypercalcemia, amyloidosis, Diagnostics : CT SCAN, Differential diagnosis : ANGIOMYOLIPOMA, metastatic disease, Simple cyst, disease description : Clear cell renal cell carcinoma (ccRCC) is a subtype of renal cell carcinoma, a kidney cancer. Its name comes from the cancer cells.ccRCC cancer cells rapidly multiply, forming one or more tumors. This cancer typically only affects one kidney but can affect both. Clear cell carcinoma is also frequently associated with endometriosis, clear cell adenofibromas, and clear cell atypical proliferative (borderline) tumors,

Clear Cell Sarcoma Of Soft Tissue

Disease Name : Clear Cell Sarcoma Of Soft Tissue, Treatment : When surgery is not possible or when the cancer has spread, chemotherapy can be used to treat CCS. But it does not seem to be an effective way to treat CCS., Radiation therapy can be used before or after surgery if doctors think that surgery alone will not remove all the tumor cells. Even so, we don’t know if radiation therapy will help you live longer., Surgery to remove the tumor and some healthy tissue around it is the best treatment for CCS. In some cases, an entire arm or leg may need to be amputated. If some cancer cells are left behind, there is a greater chance of the cancer coming back in the same spot. Or, it may spread to a different part of the body., Pathophysiology : Clear-cell sarcoma of soft tissue appears as a macroscopically tan-gray firm mass. With a size that may range from 0.4 to 14.5 cm, it commonly shows infiltration along with the tendons and aponeuroses. Immunohistochemical studies commonly show neoplastic cells positive with HMB-45, S100 protein, and Melan-A. Most cases exhibit a t(12;22)(q13;q12) translocation causing an EWSR1/ATF1 gene fusion, a finding that helps differentiate these lesions from MM., Epidemiology : Sarcomas are rare cancers and CCS is a rare type of sarcoma, making up 1% of sarcoma cases., most often found in teens and young adults in their 20s., 5-year survival rate of CCS is between 30% and 67%, avoid exposure to risk factors whenever possible. Still, most sarcomas develop in people with no known risk factor, Complications : Pain, Tenderness, Diagnostics : MRI, X RAY, PHYSICAL EXAMINATION, Differential diagnosis : Malignant melanoma, rhabdomyosarcoma, Synovial sarcoma, disease description : Clear cell sarcoma of soft tissue (CCSST) is an exceedingly rare tumor that originates from neural crest cells and is histologically characterized by clear cells representing intracellular glycogen accumulation. These tumors share histological and immunohistochemical characteristics with malignant melanoma (MM). They commonly arise from tendinous sheaths and aponeuroses, with the majority described in the lower limbs, particularly around the ankles. Tumors arising in the upper extremities are rare, and very few cases of primary CCSST have been described as arising in the chest wall and scapular soft tissues . CCS has also been found in the genitals and head. Clear cell sarcoma gets its name from the fact that the cells of the tumor look clear under a microscope.

Cleft Lip With Cleft Palale

Disease Name : Cleft Lip With Cleft Palale, Treatment : Surgical closure of a cleft lip is usually performed by 3 mo of age, when the,infant has shown satisfactory weight gain and is free of any oral, respiratory, or,systemic infection. Modification of the Millard rotation–advancement technique,is the most commonly used technique; a staggered suture line minimizes,notching of the lip from retraction of scar tissue. The initial repair may be,revised at 4 or 5 yr of age. Corrective surgery on the nose may be delayed until,adolescence. Nasal surgery can also be performed at the time of the lip repair.,Cosmetic results depend on the extent of the original deformity, healing potential,of the individual patient, absence of infection, and the skill of the surgeon., Pathophysiology : Clefts of the lip and palate are distinct entities which are closely related embryologically, functionally, and genetically. It is thought that cleft of the lip appears because of hypoplasia of the mesenchymal layer, resulting in a failure of the medial nasal and maxillary processes to join. Cleft of the palate results from failure of palatal shelves to approximate or fuse. Possible causes include maternal drug exposure, a syndrome-malformation complex, or genetic factors. Although clefts of lips and palates appear to occur sporadically, the presence of susceptible genes appears important. There are approximately 400 syndromes associated with cleft lip and palates. There are families in which a cleft lip or palate, or both, is inherited in a dominant fashion (van der Woude syndrome ), and careful examination of parents is important to distinguish this type from others, because the recurrence risk is 50%., Epidemiology : incidence is highest among Asians (~1 in 500) and , GOOD, Complications : Atelectasis, Hearing loss, otitis media, PNEUMONIA, Speech disorders, Diagnostics : ultrasound, Differential diagnosis : APHTHOUS ULCER, Lichen Planus, oral aphthous ulcers, pemphigoid gestations, Pemphigus, disease description : Clefts of the lip and palate are distinct entities which are closely related embryologically, functionally, and genetically. It is thought that cleft of the lip appears because of hypoplasia of the mesenchymal layer, resulting in a failure of the medial nasal and maxillary processes to join. Cleft of the palate results from failure of palatal shelves to approximate or fuse.

Cleft Lip

Disease Name : Cleft Lip, Treatment : retained nasopharyngeal intubation, Cleft lip reconstruction surgery, Cleft lip repair. To close the separation in the lip, the surgeon makes incisions on both sides of the cleft and creates flaps of tissue. The flaps are then stitched together, including the lip muscles. ,Cleft lip repair — within the first 3 to 6 months of age, Pathophysiology : Patients with cleft lips have altered anatomy, including a short philtrum with one or both of the philtral columns affected as well as an abnormal orbicularis oris which is inserted into the cleft margin and alar wing. In addition, the children will have a predictable pattern of nasal deformities including a caudally dislocated nasal septum separated from a displaced anterior nasal spine of the maxilla, a shortened columella, attenuated flattened lower lateral nasal cartilage on the cleft side with the flared alar base, and an inferiorly rotated upper later nasal cartilage. Also, patients with cleft lips inherently will have some degree of the alveolar cleft with potential for collapse of the maxillary arch and class III malocclusion (the maxillary teeth sit posterior to the mandibular teeth). These hard and soft tissue anatomic changes translate to the various changes in appearance, speech, and swallowing/feeding seen in cleft lip patients.Cleft lip usually develops at the junction between the lateral and central segments of the upper lip. The cleft usually affects the upper lip and may extend into the maxilla and palate., Epidemiology : nan, with 2 out of 1000 babies born with cleft lip versus 1 out of 1000 in Caucasians and 0.5 out of 1000 in African Americans., 1 : 600 live births and of isolated cleft palate is , GOOD, Having a baby born with congenital anomalies like cleft lip is unpreventable. However, you can do things to reduce your risk, like avoiding using cigarettes, alcohol, and certain medications. Talk to your healthcare provider if you are concerned about cleft lip or cleft palate., Complications : DENASAL SSPEECH, ear infection, Hearing loss, Speech Difficulties, dental problem, regurgitation, Hypertrophic scars, Diagnostics : ultrasound, GENETIC TESTING, Differential diagnosis : nan, disease description : Cleft lip deformity is one of the most common congenital deformities, and management requires an interprofessional approach to address the physical cleft deformity along with resulting issues in speech and swallowing. A microform or occult cleft occurs when the patient has incomplete separation of the lip with distortion but not separation of the white roll/vermillion border. A complete cleft lip has complete separation of lip and nasal sill. Patients also can have either unilateral or bilateral cleft lips .

Cleft Palate

Disease Name : Cleft Palate, Treatment : CLEFT LIP & PALATE REPAIR, "Cleft palate repair. Various procedures may be used to close the separation and rebuild the roof of the mouth (hard and soft palate), depending on your childs situation. The surgeon makes incisions on both sides of the cleft and repositions the tissue and muscles. The repair is then stitched closed.,Ear tube surgery. For children with cleft palate, ear tubes may be placed to reduce the risk of chronic ear fluid, which can lead to hearing loss.", Pathophysiology : Cleft palate arises from a failure of development during gestation. The primordial mouth, or stomodeum, begins to form around week four. The five facial prominences arise around the mouth : frontonasal prominence in the median, bilateral maxillary prominences, and bilateral mandibular prominences. The frontonasal prominence develops into medial and lateral nasal prominences. Over the next week, the two maxillary prominences grow toward the nasal prominences, meeting the lateral nasal prominences to develop into the nasolabial region and the medial nasal prominences to create the lip. The failure to merge around the end of week five yields a unilateral or bilateral cleft lip.At this time, the development of the palate begins and is complete around week twelve. The medial nasal prominences fuse at the midline to form the median palatine process or the primary palate. The medial portions of the maxillary processes rotate from a vertical to a lateral position around week seven to form the lateral palatine processes, which fuse at the midline from anterior to posterior to form the secondary palate. Failure of midline fusion results in cleft palate.CP are found in over 200 different congenital syndromes. The most commonly discussed are CHARGE (coloboma, heart defects, atresia choanae, growth retardation, genital abnormalities, and ear abnormalities) syndrome and velocardiofacial or DiGeorge syndrome (22q11.2 deletion). Cleft palate alone is more commonly associated with other congenital anomalies, about 50%, than CL/P, about 15%. The most commonly discussed anomalies associated with CPO is the Pierre Robin sequence of micro/retrognathia, glossoptosis, and cleft palate. , Epidemiology : the prevalence was 3.28 per 10, 000. Of these, 77% were isolated, 16% had other malformations, , 1 : 600 live births and of isolated cleft palate is , GOOD, Having a baby born with congenital anomalies like cleft palate is unpreventable. However, you can do things to reduce your risk, like avoiding using cigarettes, alcohol, and certain medications. Talk to your healthcare provider if you are concerned about cleft lip or cleft palate., Complications : Speech Difficulties, regurgitation, Diagnostics : CT SCAN, USG, AMNIOTIC FLUID EXAMINATION, Differential diagnosis : CHARGE Syndrome, disease description : Cleft palate results in failure of fusion of the two palatine shelves. This failure may be confined to the soft palate alone or involve both hard and soft palate. When the cleft of the hard palate remains attached to the nasal septum and vomer, the cleft is termed incomplete. When the nasal septum and vomer are completely separated from the palatine processes, the cleft palate is termed complete. Cleft palate arises from a failure of development during gestation .

Cleidocranial Dysplasia

Disease Name : Cleidocranial Dysplasia, Treatment : Wearing headgear or a helmet until the skull bones close.,Speech therapy.,Ear tubes.,Wearing hearing aids.,Calcium and vitamin D supplementation.,Surgery for upper airway obstruction (sleep apnea), Dental maintenance, orthodontic care or dental surgery.,Surgery to correct any bone growth symptoms.,Craniofacial surgery to repair any symptoms of the bones in the skull and face., Pathophysiology : Cleidocranial dysplasia is a skeletal dysplasia which affects bones formed by intramembranous ossification. It is inherited in an autosomal dominant pattern and is due to a mutation in the RUNX2 gene causing an abnormality in the transcription factor regulating differentiation of osteoblasts., Epidemiology : approximately 1 per million individuals worldwide., POOR, "theres no way to prevent it., If you plan on becoming pregnant and want to understand the risks of having a child with a genetic condition, talk with your healthcare provider about genetic testing.", Complications : ear infection, Hearing loss, upper respiratory tract irritation, Diagnostics : X RAY, Differential diagnosis : Hypophosphatasia, mandibuloacral dysplasia, disease description : Cleidocranial dysplasia is a genetic condition caused by abnormal growth and development of certain parts of the skeletal system, including the skull, bones and teeth. People diagnosed with cleidocranial dysplasia may have distinct physical characteristics like underdeveloped collarbones, short stature, unique facial characteristics and delayed tooth development.

Clonorchiasis

Disease Name : Clonorchiasis, Treatment : Choledochotomy and T-tube drainage and, in some ,cases, choledochoduodenostomy are required, Pathophysiology : C. sinensis is one of the most common parasitic infections in the world. In 2009,  C. sinensis was classified as a carcinogen by the international agency for cancer research. It is estimated that 25 to 35 per 100.000 cholangiocarcinomas are attributable to clonorchiasis in endemic areas. The exact events leading to cholangiocarcinoma are unknown; several different mechanisms are believed to play a role. One mechanism includes mechanical injury related to damage to the bile duct mucosa related to the feeding activities of the parasite. Secondly, local accumulation of worms results in bile stasis favoring bacterial growth, inflammation, and subsequently, recurrent cholangitis. Thirdly, toxic effects of excretory-secretory products (ESPs) released by the parasite also result in inflammation., Epidemiology : Endemic areas are in East Asia (including Korea, China, Taiwan, and northern Vietnam) and into far eastern Russia. Cases of clonorchiasis have been reported in non-endemic areas, including the United States, typically in Asian immigrants, or following ingestion of infected undercooked/pickled freshwater fish imported from endemic areas., About 15–20 million people are infected and more than 200 million people are at risk of infection, variable, can be prevented by avoiding raw or undercooked freshwater fish., Lightly salted, smoked, or pickled fish can contain infectious parasites., Complications : cholangitis, CIRRHOSIS, LIVER ABSCESS, Pancreatitis, Malnutrition, anemia, Diagnostics : ERCP, USG ABDOMEN(W/A), stool microscopy, X RAY, CT SCAN, CHOLANGIOGRAPHY, Differential diagnosis : Acute Hepatitis, Ascariasis, Ascariasis, CHOLANGIOCARCINOMA, cholecystitis, fascioliasis, PRIMARY SCLEROSING CHOLANGITIS, schistosomiasis, disease description : Clonorchis sinensis is a trematode also known as the Chinese or Oriental liver fluke. This parasitic infection is most commonly found in Eastern Asia, including Korea, China, and Vietnam, but it can be endemic in far eastern regions of Russia. These liver flukes are common parasites of fish-eating mammals. Cats and dogs of endemic areas are the most common hosts,   but C. sinensis can be transmitted to humans who eat infected fish.

Clostridium Difficile Colitis

Disease Name : Clostridium Difficile Colitis, Treatment : medication : Clindamycin , Penicillin, Metronidazole : Mild CDI : 500 mg 3 times daily for 10 days (PO or IV).,Vancomycin : Mild to severe cases : 125 mg 4 times daily for 10-14 days PO.,Fidaxomicin\t : All forms of CDI : 200 mg PO twice daily for 10 days, Pathophysiology : The pathogenesis of C difficile infection can be considered in 3 clinical phases : microbial suppression, collateral damage, and a window of vulnerability. The first phase involves suppression of the normal protective intestinal microbiota. This can occur as a result of antibiotics such as clindamycin, ciprofloxacin, cephalosporin, and fluoroquinolones. Subsequent ingestion of C difficile, which is ubiquitous, leads to germination of C difficile spores and growth of toxin-producing cells that change the gastrointestinal epithelium and invoke an immune response, leading to CDAD symptoms—the collateral damage.Recent evidence suggests that not only groups of bacteria but also specific bacteria can play a role in C difficile pathogenesis. In one study, a single bacteria was associated with cachexia in severely ill patients., Epidemiology : 369.8 cases per 10 000 hospitalizations for inflammatory bowel disease., as many as 500, 000 people in the United States annually, poor, Avoid unnecessary use of antibiotics.,Hand-washing.,Contact precautions. ,Wash your hands with soap and water after you use the bathroom and before you eat.,If you have diarrhea, clean the bathroom that you used before anyone else uses it. Use bleach mixed with water or another disinfectant to clean the toilet seat, handle, and lid., Complications : kidney damage, Toxic megacolon, bowel perforation, Dehydration, Diagnostics : STOOL CULTURE, STOOL EXAMINATION, CT SCAN, flexible sigmoidoscopy, Differential diagnosis : appendicitis, Crohn disease, DIVERTICULITIS, Irritable Bowel Syndrome, MALABSORPTION, MALIGNANCY, peritonitis, Salmonella Infection (Salmonellosis), Shigellosis, Ulcerative Colitis, viral gastroenteritis, disease description : Clostridioides difficile  is a bacterium that causes an infection of the large intestine (colon). Symptoms can range from diarrhea to life-threatening damage to the colon. The bacterium is often referred to as C. difficile or C. diff.