A 2014 study classified cases into three types—epidermolysis bullosa simplex (EBS), junctional epidermolysis bullosa (JEB), and dystrophic epidermolysis bullosa (DEB) -- and reviewed their times of death. The first two types tended to die in infancy and the last in early adulthood.

Epidermolysis bullosa can be diagnosed either by a skin (punch) biopsy at the edge of a wound with immunofluorescent mapping, or via blood sample and genetic testing.

In most patients, the condition lasts only a matter of weeks; in some cases it can last longer (up to six months). The disease resolves completely without long-term effects. Two percent of patients have recurrence.

Experienced practitioners may make the diagnosis clinically. If the diagnosis is in doubt, tests may be performed to rule out similar conditions such as Lyme disease, ringworm, guttate psoriasis, nummular or discoid eczema, drug eruptions, other viral exanthems.The clinical appearance of pityriasis rosea is similar to that of secondary syphilis, and rapid plasma reagin testing should be performed if there is any clinical concern for syphilis. A biopsy of the lesions will show extravasated erythrocytes within dermal papillae and dyskeratotic cells within the dermis.

A set of validated diagnostic criteria for pityriasis rosea is as follows:

A patient is diagnosed as having pityriasis rosea if:

1. On at least one occasion or clinical encounter, he / she has all the essential clinical features and at least one of the optional clinical features, and

2. On all occasions or clinical encounters related to the rash, he / she does not have any of the exclusional clinical features.

The essential clinical features are the following:

1. Discrete circular or oval lesions,

2. Scaling on most lesions, and

3. Peripheral collarette scaling with central clearance on at least two lesions.

The optional clinical features are the following:

1. Truncal and proximal limb distribution, with less than 10% of lesions distal to mid-upper-arm and mid-thigh,

2. Orientation of most lesions along skin cleavage lines, and

3. A herald patch (not necessarily the largest) appearing at least two days before eruption of other lesions, from history of the patient or from clinical observation.

The exclusional clinical features are the following:

1. Multiple small vesicles at the centre of two or more lesions,

2. Two or more lesions on palmar or plantar skin surfaces, and

3. Clinical or serological evidence of secondary syphilis.

Epidermolysis bullosa dystrophica or dystrophic EB (DEB) is an inherited disease affecting the skin and other organs.

"Butterfly child" is the colloquial name for a child born with the disease, as their skin is seen to be as delicate and fragile as that of a butterfly.

The deficiency in anchoring fibrils impairs the adherence between the epidermis and the underlying dermis. The skin of DEB patients is thus highly susceptible to severe blistering.Collagen VII is also associated with the epithelium of the esophageal lining, and DEB patients may suffer from chronic scarring, webbing, and obstruction of the esophagus. Affected individuals are often severely malnourished due to trauma to the oral and esophageal mucosa and require feeding tubes for nutrition. They also suffer from iron-deficiency anemia of uncertain origin, which leads to chronic fatigue.

Open wounds on the skin heal slowly or not at all, often scarring extensively, and are particularly susceptible to infection. Many individuals bathe in a bleach and water mixture to fight off these infectionsThe chronic inflammation leads to errors in the DNA of the affected skin cells, which in turn causes squamous cell carcinoma (SCC). The majority of these patients die before the age of 30, either of SCC or complications related to DEB.

The chronic inflammatory state seen in recessive dystrophic epidermolysis bullosa (RDEB) may cause Small fiber peripheral neuropathy (SFN).; RDEB patients have reported the sensation of pain in line with neuropathic pain qualities.

Depending on the shape of the gum recession and the levels of bone around the teeth, areas of gum recession can be regenerated with new gum tissue using a variety of gum grafting "periodontal plastic surgery" procedures performed by a specialist in periodontics (a periodontist). These procedures are typically completed under local anesthesia with or without conscious sedation, as the patient prefers. This may involve repositioning of adjacent gum tissue to cover the recession (called a pedicle graft) or use of a free graft of gingival or connective tissue from the roof of the mouth (called a "free gingival graft" or a Subepithelial connective tissue graft). Alternatively, a material called acellular dermal matrix (processed donated human skin allograft) may be used instead of tissue from the patient's own palate.

If cause-specific measures are insufficient, soft-tissue graft surgery may be used to create more gingiva. The tissue used may be autologous tissue from another site in the patient's mouth, or it can be freeze-dried tissue products or synthetic membranes. New research is focused on using stem cells to culture the patients' own gums to replace receded gums.

Cystic nephromas are diagnosed by biopsy or excision. It is important to correctly diagnose them as, radiologically, they may mimic the appearance of a renal cell carcinoma that is cystic.

The characteristics of cystic nephromas are:

- Cysts lined by a simple epithelium with a "hobnail morphology", i.e. the nuclei of the cyst lining epithelium bulges into the lumen of the cysts,

- Ovarian-like stroma that has a:

- Spindle cell morphology, and has a

- Basophilic cytoplasm.

Cystic nephromas have an immunostaining pattern like ovarian stroma; they are positive for:

- Estrogen receptor (ER),

- Progesterone receptor (PR) and

- CD10.

The treatment of invasive amoebiasis should be directed to all sites where "E. histolytica" may be present. Hence the ideal amoebicide should be able to act within the intestinal lumen, in the intestinal wall, and systemically, particularly in the liver.

Systemic amoebicidal drugs include emetine, dehydroemetine, chloroquine diphosphate, metronidazole, and tinidazole.

Treatment must also include a lumenal amoebicide to prevent reinvasion of tissues by amoebae still in the intestines (see Amoebiasis). After completion of treatment with tissue amebicides, administer luminal amebicides for eradication of the asymptomatic colonization state. Failure to use luminal agents can lead to relapse of infection in approximately 10% of patients.

Breast cancer screening refers to testing otherwise-healthy women for breast cancer in an attempt to achieve an earlier diagnosis under the assumption that early detection will improve outcomes. A number of screening tests have been employed including clinical and self breast exams, mammography, genetic screening, ultrasound, and magnetic resonance imaging.

A clinical or self breast exam involves feeling the breast for lumps or other abnormalities. Clinical breast exams are performed by health care providers, while self-breast exams are performed by the person themselves. Evidence does not support the effectiveness of either type of breast exam, as by the time a lump is large enough to be found it is likely to have been growing for several years and thus soon be large enough to be found without an exam. Mammographic screening for breast cancer uses X-rays to examine the breast for any uncharacteristic masses or lumps. During a screening, the breast is compressed and a technician takes photos from multiple angles. A general mammogram takes photos of the entire breast, while a diagnostic mammogram focuses on a specific lump or area of concern.

A number of national bodies recommend breast cancer screening. For the average woman, the U.S. Preventive Services Task Force recommends mammography every two years in women between the ages of 50 and 74, the Council of Europe recommends mammography between 50 and 69 with most programs using a 2-year frequency, and in Canada screening is recommended between the ages of 50 and 74 at a frequency of 2 to 3 years. These task force reports point out that in addition to unnecessary surgery and anxiety, the risks of more frequent mammograms include a small but significant increase in breast cancer induced by radiation.

The Cochrane collaboration (2013) states that the best quality evidence neither demonstrates a reduction in cancer specific, nor a reduction in all cause mortality from screening mammography. When less rigorous trials are added to the analysis there is a reduction in mortality due to breast cancer of 0.05% (a decrease of 1 in 2000 deaths from breast cancer over 10 years or a relative decrease of 15% from breast cancer). Screening over 10 years results in a 30% increase in rates of over-diagnosis and over-treatment (3 to 14 per 1000) and more than half will have at least one falsely positive test. This has resulted in the view that it is not clear whether mammography screening does more good or harm. Cochrane states that, due to recent improvements in breast cancer treatment, and the risks of false positives from breast cancer screening leading to unnecessary treatment, "it therefore no longer seems beneficial to attend for breast cancer screening" at any age. Whether MRI as a screening method has greater harms or benefits when compared to standard mammography is not known.

Symptoms of pouchitis include Increased stool frequency, urgency, incontinence, nocturnal seepage, abdominal cramping, pelvic discomfort, and arthralgia.

Symptom severity does not always correlate with severity of endoscopically- or histologically-evaluated pouch inflammation. Additionally, these symptoms are not necessarily specific for pouchitis, asthey may arise from other inflammatory or functional pouch disorders such as Crohn's disease of the pouch, cuffitis, pouch sinus, or irritable pouch syndrome. The most reliable tool for diagnosis is endoscopy combined with histologic features (derived from tissue biopsies obtained during endoscopy).

Detection of antibodies (cold or warm) and /or complement system on RBC from the patient is a direct Coombs antiglobulin test

Detection of antibodies in serum of the patient (still circulating in the blood, that have not yet formed any complexes with RBC ) is an indirect Coombs antiglobulin test

The selective estrogen receptor modulators (such as tamoxifen) reduce the risk of breast cancer but increase the risk of thromboembolism and endometrial cancer. There is no overall change in the risk of death. They are thus not recommended for the prevention of breast cancer in women at average risk but may be offered for those at high risk. The benefit of breast cancer reduction continues for at least five years after stopping a course of treatment with these medications.

There is no clinically approved treatment for pouchitis.

First line treatment is usually with antibiotics, specifically with ciprofloxacin and metronidazole. Ampicillin or Piperacillin can also be considered as alternatives to empiric Ciprofloxacin and metronidazole). Administration of metronidazole at a high daily dose of 20 mg/kg can cause symptomatic peripheral neuropathology in up to 85% of patients. This can be a limiting factor in the use of maintenance metronidazole to suppress chronic pouchitis.

Other therapies which have been shown to be effective in randomised clinical trials include probiotic therapy, the application of which usually begins as soon as any antibiotic course is completed so as to re-populate the pouch with beneficial bacteria. Biologics, such as anti-TNF antibodies, may also be useful but the evidence for their use is largely anecdotal. In addition, discussion by patients using related internet forums appears to give evidence of benefits (again, after cessation of antibiotics) from certain diets, such as the Specific Carbohydrate Diet, Paleolithic Diet, and Low FODMAP Diet. In particular, attention has been drawn to the exclusion of complex carbohydrates, as well as other foods with high starch content (such as grains, rice, and potatoes) and certain dairy products including milk and soft cheese.

There are no specific guidelines for the treatment of diabetes and disordered eating, but the standard approach for treatment of two complex conditions as multidisciplinary team of professionals which in this case could include an endocrinologist, psychiatrist, psychologist, dietician, etc.

Due to the symptoms of palindromic arthritis and the nature of the attacks, diagnosis can be difficult or take a long time. The symptoms can be similar to many other forms of arthritis or other autoimmune diseases. It is often a case of eliminating the other conditions before getting the correct diagnosis due to there being no specific test for PR diagnosis.

No single test can confirm a diagnosis. A doctor may make a diagnosis based on medical history and signs and symptoms. Palindromic rheumatism must be distinguished from acute gouty arthritis and an atypical, acute onset of rheumatoid arthritis (RA). Without specific tests (such as analysis of joint fluid), it may be difficult to distinguish palindromic rheumatism from other episodic joint problems. It is important to note that a person may experience more than one autoimmune disorder at the same time. Laboratory findings are usually normal. Blood tests may show an elevation of the ESR and CRP, but are otherwise unremarkable. Rheumatoid factor may be present especially in the group that is likely to develop rheumatoid arthritis.

Triple-negative breast cancer accounts for approximately 15%-25% of all breast cancer cases. The overall proportion of TNBC is very similar in all age groups. Younger women have a higher rate of basal or BRCA related TNBC while older women have a higher proportion of apocrine, normal-like and rare subtypes including neuroendocrine TNBC.

Among younger women, African American and Hispanic women have a higher risk of TNBC, with African Americans facing worse prognosis than other ethnic groups.

In 2009, a case-control study of 187 triple-negative breast cancer patients described a 2.5 increased risk for triple-negative breast cancer in women who used oral contraceptives (OCs) for more than one year compared to women who used OCs for less than one year or never. The increased risk for triple-negative breast cancer was 4.2 among women 40 years of age or younger who used OCs for more than one year, while there was no increased risk for women between the ages of 41 and 45. Also, as duration of OC use increased, triple-negative breast cancer risk increased.

For acute pericarditis to formally be diagnosed, two or more of the following criteria must be present: chest pain consistent with a diagnosis of acute pericarditis (sharp chest pain worsened by breathing in or a cough), a pericardial friction rub, a pericardial effusion, and changes on electrocardiogram (ECG) consistent with acute pericarditis.

A complete blood count may show an elevated white count and a serum C-reactive protein may be elevated. Acute pericarditis is associated with a modest increase in serum creatine kinase MB (CK-MB). and cardiac troponin I (cTnI), both of which are also markers for injury to the muscular layer of the heart. Therefore, it is imperative to also rule out acute myocardial infarction in the face of these biomarkers. The elevation of these substances may occur when inflammation of the heart's muscular layer in addition to acute pericarditis. Also, ST elevation on EKG (see below) is more common in those patients with a cTnI > 1.5 µg/L. Coronary angiography in those patients should indicate normal vascular perfusion. Troponin levels increase in 35-50% of people with pericarditis.

Electrocardiogram (ECG) changes in acute pericarditis mainly indicates inflammation of the epicardium (the layer directly surrounding the heart), since the fibrous pericardium is electrically inert. For example, in uremia, there is no inflammation in the epicardium, only fibrin deposition, and therefore the EKG in uremic pericarditis will be normal. Typical EKG changes in acute pericarditis includes

- stage 1 -- diffuse, positive, ST elevations with reciprocal ST depression in aVR and V1. Elevation of PR segment in aVR and depression of PR in other leads especially left heart V5, V6 leads indicates atrial injury.

- stage 2 -- normalization of ST and PR deviations

- stage 3 -- diffuse T wave inversions (may not be present in all patients)

- stage 4 -- EKG becomes normal OR T waves may be indefinitely inverted

The two most common clinical conditions where ECG findings may mimic pericarditis are acute myocardial infarction (AMI) and generalized early repolarization. As opposed to pericarditis, AMI usually causes localized convex ST-elevation usually associated with reciprocal ST-depression which may also be frequently accompanied by Q-waves, T-wave inversions (while ST is still elevated unlike pericarditis), arrhythmias and conduction abnormalities. In AMI, PR-depressions are rarely present. Early repolarization usually occurs in young males (age <40 years) and ECG changes are characterized by terminal R-S slurring, temporal stability of ST-deviations and J-height/ T-amplitude ratio in V5 and V6 of <25% as opposed to pericarditis where terminal R-S slurring is very uncommon and J-height/ T-amplitude ratio is ≥ 25%. Very rarely, ECG changes in hypothermia may mimic pericarditis, however differentiation can be helpful by a detailed history and presence of an Osborne wave in hypothermia.

Another important diagnostic electrocardiographic sign in acute pericarditis is the Spodick sign. It signifies to the PR-depressions in a usual (but not always) association with downsloping TP segment in patients with acute pericarditis and is present in up to 80% of the patients affected with acute pericarditis. The sign is often best visualized in lead II and lateral precordial leads. In addition, Spodick’s sign may also serve as an important distinguishing electrocardiographic tool between the acute pericarditis and acute coronary syndrome. The presence of a classical Spodick’s sign is often a giveaway to the diagnosis.

Rarely, electrical alternans may be seen, depending on the size of the effusion.

A chest x-ray is usually normal in acute pericarditis, but can reveal the presence of an enlarged heart if a pericardial effusion is present and is greater than 200 mL in volume. Conversely, patients with unexplained new onset cardiomegaly should always be worked up for acute pericarditis.

An echocardiogram is typically normal in acute pericarditis but can reveal pericardial effusion, the presence of which supports the diagnosis, although its absence does not exclude the diagnosis.

A stress test, is just that, a test to put stress on the heart through exercise. A doctor will put a patient through a series of exercises to measure the tolerance for stress on the heart. This test uses an ECG to detect the electrical impulses of the heart during physical exertion.

During this test a patient is put on a treadmill or a stationary bike. The incline or resistance of the bike are steadily increased until the patient reaches the target heart rate for the patient's age and weight.

An exercise stress test is not always accurate in determining if one has a blockage in the arteries. Women and those who are young may show abnormalities on their test even though no signs of coronary ischemia or CAD are present.

If there is a suspicion that one may have coronary ischemia, a doctor will administer a series of tests to confirm the diagnosis.. The most common tests today are an electrocardiogram, an exercise stress test, and a coronary angiography.

The doctor will also ask a series of questions to determine the medical history of the patient, including past incidences of chest pain or shortness of breath. He may also inquire about the duration of symptoms, how often they occur and any measures taken in attempts to relieve them.

Cold agglutinin disease can be either primary (arising spontaneously) or secondary (a result of another pathology).

- The primary form is caused by excessive cell proliferation of B lymphocytes.

- Secondary cold agglutinin disease is a result of an underlying condition.

- In adults, this is typically due to a lymphoproliferative disease such as lymphoma and chronic lymphoid leukemia, or infection. Waldenström's macroglobulinemia may also be positive for cold agglutinins.

- In children, cold agglutinin disease is often secondary to an infection, such as "Mycoplasma" pneumonia, mononucleosis, and HIV.

Genetic testing for Brugada syndrome is clinically available and may help confirm a diagnosis, as well as differentiate between relatives who are at risk for the disease and those who are not. Some symptoms when pinpointing this disease include fainting, irregular heartbeats, and chaotic heartbeats. However, just detecting the irregular heartbeat may be a sign of another disease, so the doctor must detect another symptom as well.