Persius/hicric huggingface dataset:
Ampicillin adverse reactions

# Adverse Reactions
As with other penicillins, it may be expected that untoward reactions will be essentially limited to sensitivity phenomena. They are more likely to occur in individuals who have previously demonstrated hypersensitivity to penicillins and in those with a history of allergy, asthma, hay fever, or urticaria.
The following adverse reactions have been reported as associated with the use of ampicillin:

### Gastrointestinal
Glossitis, stomatitis, black "hairy" tongue, nausea, vomiting, enterocolitis, pseudomembranous colitis, and diarrhea. (These reactions are usually associated with oral dosage forms.)

### Hypersensitivity Reactions
Skin rashes and urticaria have been reported frequently. A few cases of exfoliative dermatitis and erythema multiforme have been reported. Anaphylaxis is the most serious reaction experienced and has usually been associated with the parenteral dosage form.
Note: Urticaria, other skin rashes, and serum sickness-like reactions may be controlled with antihistamines and, if necessary, systemic corticosteroids. Whenever such reactions occur, ampicillin should be discontinued, unless, in the opinion of the physician, the condition being treated is life-threatening and amenable only to ampicillin therapy. Serious anaphylactic reactions require the immediate use of epinephrine, oxygen, and intravenous steroids.
Liver A moderate rise in serum glutamic oxaloacetic transaminase (SGOT) has been noted, particularly in infants, but the significance of this finding is unknown. Mild transitory SGOT elevations have been observed in individuals receiving larger (two to four times) than usual and oft-repeated intramuscular injections. Evidence indicates that glutamic oxaloacetic transaminase (GOT) is released at the site of intramuscular injection of ampicillin sodium and that the presence of increased amounts of this enzyme in the blood does not necessarily indicate liver involvement.
Hemic and Lymphatic Systems Anemia, thrombocytopenia, thrombocytopenic purpura, eosinophilia, leukopenia, and agranulocytosis have been reported during therapy with the penicillins. These reactions are usually reversible on discontinuation of therapy and are believed to be hypersensitivity phenomena.
Anoxic brain injury overview

# Overview
Anoxic brain injury or post-cardiac arrest is defined as absence of pulses requiring chest compressions, regardless of location or presenting rhythm. Post-cardiac arrest syndrome is characterized by resumption of spontaneous systemic circulation after prolonged ischemia of whole body. Anoxic or hypoxic brain injury is often seen after cardiac arrest as part of the post-cardiac arrest syndrome. Major efforts are underway to improve "The Chain of Survival" based upon early access to medical care, early defibrillation, early CPR and early hospital care. Therapeutic hypothermia may improve outcomes. Steroids, mannitol, diuresis and hyperventilation have not been documented to meaningfully improve clinical outcomes.

# Pathophysiology
There are a variety of factors that contribute to anoxic brain injury. The primary mechanism for injury is a result of a lack of oxygen to the brain, therefore any condition which causes this, such as cardiac arrest or airway obstruction, can cause anoxic brain injury.

# Natural History, Complications and Prognosis
Persons with anoxic brain injury are at a high risk of death due to factors such as cardiac arrest, congestive heart failure, pneumonia, and sepsis. There are predictors of survival that have been studied. For example, persons with in-hospital cardiac arrest have a better chance of survival than out-of-hospital arrest, rapid defibrillation improves survival, and VT and VF have a better prognosis than asystole or PEA.

# Diagnosis

## Physical Examination
Physical examination involves a thorough neurologic evaluation, with a focus on the extent of involvement of the brainstem.

## Laboratory Findings
A number of laboratory tests are obtained in order to evaluate the underlying cause of the anoxic brain injury. Common laboratory tests include complete blood count, ABG, electrolytes, cardiac enzymes and serum lactate.

## CT
In the early hours and days after anoxic brain injury, there is often diffuse cerebral edema and blurring of the border between the grey and white matter. In some patients there may be discrete infarcts after a few days.

## Electroencephalogram
Most often the EEGs of patients in coma after cardiac arrest shows diffuse slowing of both the theta and delta waves, and periodic epileptiform firing. Severe slowing or a flat line appearance is associated with a poor prognosis.

## Other Diagnostic Studies
Other pertinent diagnostic studies in anoxic brain injury, include evoked-response testing, and the steps in diagnosing brain death.

# Treatment

## Medical Therapy
Medical therapy for anoxic brain injury, includes the use of therapeutic hypothermia. This has been associated with a reduction in ischemic brain injury, particularly in animal models. There are specific guidelines associated with the use of therapeutic hypothermia, as there can be significant complications and side effects from using this method of treatment.
Anterior corticospinal tract

# Overview
The anterior corticospinal tract (also called the ventral corticospinal tract, medial corticospinal tract, direct pyramidal tract, or anterior cerebrospinal fasciculus) is a small bundle of descending fibers that connect the cerebral cortex to the spinal cord. It is usually small, varying inversely in size with the lateral corticospinal tract, which is the main part of the corticospinal tract.
It lies close to the anterior median fissure, and is present only in the upper part of the medulla spinalis; gradually diminishing in size as it descends, it ends about the middle of the thoracic region.
It consists of descending fibers which arise from cells in the motor area of the cerebral hemisphere of the same side, and which, as they run downward in the medulla spinalis, cross in succession through the anterior white commissure to the opposite side, where they end, either directly or indirectly, by arborizing around the motor cells in the anterior column.
A few of its fibers are said to pass to the lateral column of the same side and to the gray matter at the base of the posterior column.
They conduct voluntary motor impulses from the precentral gyrus to the motor centers of the cord.

# Additional images
- Decussation of pyramids.
- The motor tract.
Anterior interosseous artery
The anterior interosseous artery (volar interosseous artery), passes down the forearm on the volar surface of the interosseous membrane.
It is accompanied by the volar interosseous branch of the median nerve, and overlapped by the contiguous margins of the Flexor digitorum profundus and Flexor pollicis longus, giving off in this situation muscular branches, and the nutrient arteries of the radius and ulna.
At the upper border of the Pronator quadratus it pierces the interosseous membrane and reaches the back of the forearm, where it anastomoses with the dorsal interosseous artery.
It then descends, in company with the terminal portion of the dorsal interosseous nerve, to the back of the wrist to join the dorsal carpal net-work.
The volar interosseous artery gives off a slender branch, the arteria mediana, which accompanies the median nerve, and gives offsets to its substance; this artery is sometimes much enlarged, and runs with the nerve into the palm of the hand.
Before it pierces the interosseous membrane the volar interosseous sends a branch downward behind the Pronator quadratus to join the volar carpal network.

# Additional images
- Cross-section through the middle of the forearm.
- Arteries of the back of the forearm and hand.
Aortoiliac occlusive disease

# Overview
Aortoiliac occlusive disease, also known as Leriche's syndrome or Leriche syndrome, is atherosclerotic occlusive disease involving the abdominal aorta and/or both of the iliac arteries.

# Etymology
The condition was first described by Robert Graham in 1814, but the condition with its triad of symptoms was ascribed to Rene Leriche. Leriche, a French surgeon, linked the pathophysiology with the anatomy of the condition. Leriche first published on the subject based on a patient he treated with the condition at the age of 30. Following treatment the 30 year old was able to walk without pain and maintain an erection.

# Symptoms
Classically, it is described as a triad of symptoms consisting of:
- absent or diminished femoral pulses,
- claudication or pain with walking in the buttocks and legs and
- penile impotence.

# Diagnostic Findings
Images courtesy of RadsWiki

# Treatment
- Aortoiliac bypass graft
- Axillofemoral and femoral-femoral bypass (sometimes abbreviated "ax-fem fem-fem")
Pica resident survival guide
Synonyms and keywords: Approach to pica, Pica workup, Pica management

# Overview
Pica is defined as the compulsive craving for or eating non-nutritive or non-food substances for at least a period of one month. Pica may be a part of a cultural phenomenon, during childhood, in persons or children who are mentally disabled or even in pregnancy. Iron deficiency anemia is also an important cause of pica. Pica is treated by a multifocal approach which includes reduction of cravings, addressing the social and emotional issues faced by the individual and treating the anemia if present. Pica is further divided based on the type of substance ingested such as ice, lead, soil, etc.

# Causes
- Pica is commonly seen in children over 2 years of age.
- Iron deficiency anemia
- Pregnancy
- Autism and other developmental disabilities
- Lower socioeconomic status
- Epilepsy
- Schizophrenia
- Recently, obsessive compulsive disorder has also been implicated as a cause .

# Diagnosis
- The diagnosis of pica includes a detailed history and physical examination, appropriate laboratory investigations.

# Treatment
Management of pica is summarised in the algorithm below.

# Do's
- Check for lead levels in children with pica, particularly those living in houses built during and before 1960.
- Screen for parasitic infections such as Toxocara and Ascaris in people exhibiting geophagia (ingestion of soil, sand or clay).
- Basic metabolic tests should be done, particularly when hypokalemia is suspected as it is seen in people ingesting clay or chalk.
- Rule out substance abuse in adults with pica.

# Don'ts
- Don't forget to educate patients about healthy eating habits.
- Don't make a diagnosis of pica where cultural traditions such as clay eating are normative.
Arcanobacterium haemolyticus

# Treatment
- Arcanobacterium haemolyticum treatment
- Preferred regimen: Erythromycin Base: 333 mg PO q8h; estolate/stearate/base: 250-500 mg q6h PO
- Alternative regimen: Benzathine Penicillin G 1.2 MU IM q3-4 weeks
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Asherman's syndrome overview

# Overview
Asherman's syndrome, also called "uterine synechiae" or intrauterine adhesions, presents a condition characterized by the presence of scars within the uterine cavity.
An artificial form of Asherman's syndrome can be surgically induced by endometrial ablation in women with excessive uterine bleeding, in lieu of hysterectomy.

# Historical Perspective
The Israeli gynecologist Joseph Asherman is credited with describing and characterizing the disease, hence it is called Asherman syndrome.

# Classification
Classification of Asherman's syndrome takes into account the amount of functional endometrium present, the menstrual pattern, obstetric history, and more recently the location and severity of adhesions inside the uterus. There is no data showing superiority of one system over the other.

# Pathophysiology
Asherman syndrome most often is the result of vigorous scraping and damage to the basal layer of the endometrium during a dilation and curettage, which may be done for a variety of reasons. It may also occur after delivery, especially if there is uncontrolled hemorrhage, or after the elective termination of a pregnancy. Less often, it is due to sampling for endometrial cancer, or removal of endometrial polyps. It may also occur after surgery to remove uterine fibroids.

# Causes
Asherman's syndrome is most commonly linked to obstetric procedures that cause abrasion of the basal layer of the endometrium. Other causes include caesarian sections, infections or pelvic radiation therapy.
Intrauterine devices have not been linked to Asherman's syndrome.

# Differentiating Asherman's Syndrome from other diseases
Asherman Syndrome must be differentiated from other conditions that may cause amenorrhea and pregnancy loss, and may cause infertility.

# Epidiology and Demographics
Asherman's Syndrome may occur in up to 13% of women undergoing a termination of pregnancy during the first trimester, and 30% in women undergoing a dilation and curettage (D and C) after a late spontaneous abortion. Structural placental abnormalities and previous procedures done in the uterus increase the risk.

# Risk Factors
The strongest risk factors for developing Asherman Syndrome is previous obstetric curettage procedures and infections.

# Screening
No screening guidelines exist for Asherman's Syndrome.

# Natural History, Complications and Prognosis
Asherman's syndrome typically occurs after a triggering event such as an infection or a procedure, and is a cumulative process which may lead to infertility. Damage to the uterine cavity may also cause pain, congestion and endometriosis.
Atovaquone drug interactions

# Drug Interactions

### Rifampin
In a study with 13 HIV-infected volunteers, the oral administration of rifampin 600 mg every 24 hours with MEPRON Suspension 750 mg every 12 hours resulted in a 52%  13% decrease in the average steady-state plasma atovaquone concentration and a 37%  42% increase in the average steady-state plasma rifampin concentration. The half-life of atovaquone decreased from 82  36 hours when administered without rifampin to 50  16 hours with rifampin.
Rifabutin, another rifamycin, is structurally similar to rifampin and may possibly have some of the same drug interactions as rifampin. No interaction trials have been conducted with MEPRON and rifabutin.

### Trimethoprim/Sulfamethoxazole (TMP-SMX)
The possible interaction between atovaquone and TMP-SMX was evaluated in 6 HIV-infected adult volunteers as part of a larger multiple-dose, dose-escalation, and chronic dosing study of MEPRON Suspension. In this crossover study, MEPRON Suspension 500 mg once daily, or TMP-SMX tablets (160 mg trimethoprim and 800 mg sulfamethoxazole) twice daily, or the combination were administered with food to achieve steady state. No difference was observed in the average steady-state plasma atovaquone concentration after coadministration with TMP-SMX. Coadministration of MEPRON with TMP-SMX resulted in a 17% and 8% decrease in average steady-state concentrations of trimethoprim and sulfamethoxazole in plasma, respectively. This effect is minor and would not be expected to produce clinically significant events.

### Zidovudine
Data from 14 HIV-infected volunteers who were given atovaquone tablets 750 mg every 12 hours with zidovudine 200 mg every 8 hours showed a 24%  12% decrease in zidovudine apparent oral clearance, leading to a 35%  23% increase in plasma zidovudine AUC. The glucuronide metabolite:parent ratio decreased from a mean of 4.5 when zidovudine was administered alone to 3.1 when zidovudine was administered with atovaquone tablets. This effect is minor and would not be expected to produce clinically significant events. Zidovudine had no effect on atovaquone pharmacokinetics.
Autoimmune inner ear disease

# Overview
Autoimmune inner ear disease is a suspected autoimmune disease characterized by rapidly progressive bilateral sensorineural hearing loss. It occurs when the body's immune system attacks cells in the inner ear that are mistaken for a virus or bacteria. Autoimmune inner ear disease was first described by Dr. Brian McCabe of the University of Iowa in 1979.

# Historical Perspective

# Classification

# Pathophysiology

# Causes
AIED is generally caused by  either antibodies or immune cells that cause damage to the inner ear. There are several autoimmune disorders to which AIED is related:
- Bystander damage
- Cross-reactions
- Genetic factors
- Drug Use (opiate-based painkillers like OxyContin)  
Research has found that long term abuse of opiate-based painkillers (such as OxyContin and Hydrocodone) can lead to profound hearing loss caused by damage to the inner ear, according to Dr. Gail Ishiyama, an assistant professor at the UCLA department of neurology.

# Differentiating Autoimmune Inner Ear Disease from other Diseases
- The symptoms can be easily mistaken for Otitis Media. .

# Epidemiology and Demographics

## Age

## Gender

## Race

# Risk Factors

# Natural History, Complications and Prognosis

# Diagnosis

## Diagnostic Criteria

## Symptoms
- Symptoms of AIED are:
A sudden loss of hearing in one ear, followed by a gradual loss of hearing in the second ear.
A Feeling of fullness in one ear
Vertigo
Tinnitus
- A sudden loss of hearing in one ear, followed by a gradual loss of hearing in the second ear.
- A Feeling of fullness in one ear
- Vertigo
- Tinnitus

## Physical Examination

## Laboratory Findings

## Imaging Findings

## Other Diagnostic Studies

# Treatment

## Medical Therapy
AIED treatment is a rapidly changing field. Steroids are often used in the treatment of AIED, as well as cytotoxic agents such as Cyclophosphamide and Methotrexate.
More recently, in order to avoid many of the side effects of steroids, alternative medications and surgical procedures are used.
Since these change quite frequently, it is a good idea to check many sources in locating the most cutting-edge procedure for treating autoimmune inner ear disease.

## Surgery

## Prevention
Bone morphogenetic protein 1
Bone morphogenetic protein 1, also known as BMP1, is a protein which in humans is encoded by the BMP1 gene. There are seven isoforms of the protein created by alternate splicing.

# Function
BMP1 belongs to the peptidase M12A family of bone morphogenetic proteins (BMPs). It induces bone and cartilage development. Unlike other BMPs, it does not belong to the TGF superfamily. It was initially discovered to work like other BMPs by inducing bone and cartilage development. It however, is a metalloprotease that cleaves the C-terminus of procollagen I, II and III. It has an astacin-like protease domain.
It has been shown to cleave laminin 5  and is localized in the basal epithelial layer of bovine skin.
The BMP1 locus encodes a protein that is capable of inducing formation of cartilage in vivo.  Although other bone morphogenetic proteins are members of the TGF-beta superfamily, BMP1 encodes a protein that is not closely related to other known growth factors. BMP1 protein and procollagen C proteinase (PCP), a secreted metalloprotease requiring calcium and needed for cartilage and bone formation, are identical. PCP or BMP1 protein cleaves the C-terminal propeptides of procollagen I, II, and III and its activity is increased by the procollagen C-endopeptidase enhancer protein.  The BMP1 gene is expressed as alternatively spliced variants that share an N-terminal protease domain but differ in their C-terminal region

# Structure
The structure of BMP1 was determined through X-Ray diffraction with a resolution of 1.27 A.  Crystallization experiments were done by vapor diffusion at a pH of 7.5.  This is important because it is close to the pH of the human body, where BMP1 resides in vivo.  BMP1 is 202 residues in length. Its secondary structure is made up of 30% helices, or 10 helices, 61 residues in length, and 15% beta sheets, or 11 strands, 32 residues in length.  It contains ligands of an acetyl group and a Zinc ion.
A Ramachandran plot was constructed for BMP.  This plot shows that BMP1 most prefers Phi and Psi angles (Phi, Psi) of around (-60,-45) and (-60, 140). These preferred angles are an estimate of the most clustered data of the Ramachandran plot.  The preferred region is much greater in range.  97% of the residues were in preferred regions and 100% of the residues were in the allowed region, with no outliers.
Bone morphogenetic protein 2
Bone morphogenetic protein 2 or BMP-2 belongs to the TGF- superfamily of proteins.

# Function
BMP-2 like other bone morphogenetic proteins, plays an important role in the development of bone and cartilage. It is involved in the hedgehog pathway, TGF beta signaling pathway, and in cytokine-cytokine receptor interaction. It is also involved in cardiac cell differentiation and epithelial to mesenchymal transition.
Like many other proteins from the BMP family, BMP-2 has been demonstrated to potently induce osteoblast differentiation in a variety of cell types.

# Interactions
Bone morphogenetic protein 2 has been shown to interact with BMPR1A.

# Clinical use and complications
Bone morphogenetic protein 2 is shown to stimulate the production of bone. Recombinant human protein (rhBMP-2) is currently available for orthopaedic usage in the United States. Implantation of BMP-2 is performed using a variety of biomaterial carriers ("metals, ceramics, polymers, and composites") and delivery systems ("hydrogel, microsphere, nanoparticles, and fibers"). While used primarily in orthopedic procedures such as spinal fusion, BMP-2 has also found its way into the field of dentistry.
The use of dual tapered threaded fusion cages and recombinant human bone morphogenetic protein-2 on an absorbable collagen sponge obtained and maintained intervertebral spinal fusion, improved clinical outcomes, and reduced pain after anterior lumbar interbody arthrodesis in patients with degenerative lumbar disc disease. As an adjuvant to allograft bone or as a replacement for harvested autograft, bone morphogenetic proteins (BMPs) appear to improve fusion rates after spinal arthrodesis in both animal models and humans, while reducing the donor-site morbidity previously associated with such procedures.
A study published in 2011 noted "reports of frequent and occasionally catastrophic complications associated with use of  in spinal fusion surgeries", with a level of risk far in excess of estimates reported in earlier studies. An additional review by Agrawal and Sinha of BMP-2 and its common delivery systems in early 2016 showed how "problems like ectopic growth, lesser protein delivery,  inactivation of the protein" reveal a further need "to modify the available carrier systems as well as explore other biomaterials with desired properties."