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285 Cards in this Set

  • Front
  • Back
Actinic keratosis
Often preceeds SCC*

-aka solar keratosis; premalignant condition of thick scaly, or crusty patches of skin
-more common in fair skinned people who are frequently exposed to the sun, b/c their pigment isn't protective
-accompanied by solar damage (appears on sun exposed areas)
-they should be treated b/c they can progress to SCC
-people with skin phototypes 1&2 are mosre likely to be affected (as well as albinos and immunosuppressed)
-diagnosis: exam or biopsy

-Seborrheic keratoses are other bumps that appear in groups like the actinic keratosis but are not caused by sun exposure, and are not related to skin cancers. Seborrheic keratoses may be mistaken for an actinic keratosis

-tx: cryosurgery; 5-fluorouracil (a chemotherapy agent): a cream that contains this medication causes AKs to become red and inflamed before they fall of
Addison's dz
primary adrenocortical deficiency (autoimmune)*

-aka chronic adrenal insufficiency, or hypocortisolism
-rare endocrine disorder in which the body produces insufficient amounts of adrenal steroid hormone (glucocorticoids and often mineralocorticoids)
-In primary adrenal insufficiency (classic Addison's disease) the hormone aldosterone is also deficient. Many of the symptoms of Addison's disease arise due to the hyposecretion of aldosterone leading to hyperkalemia (high blood potassium levels) and metabolic acidosis (increased acidity of the blood due to decreased bicarbonate levels). Often the production of adrenaline is also diminished.
-Addison's disease usually effects the body slowly (over several months). The symptoms tend to be non-specific, and may not be noticed until some stressful intercurrent illness or situation occurs

-common symptoms: chronic fatigue that gradually worsens; Muscle weakness; Weight loss and loss of appetite; Nausea, diarrhea, or vomiting; Areas of hyperpigmentation (darkened skin), known as melasma suprarenale, caused by increases in pro-opiomelanocortin.

Although cutaneous pigmentation will most likely disappear following therapy, pigmentation of the oral mucosa tends to persist.

more symptoms: Irritability; Depression; Craving for salt and salty foods; Polyuria (increased urine production); For women, menstrual periods that become irregular or cease

-On examination, the following may be noticed: Low blood pressure that falls further when standing (orthostatic hypotension); Tetany (particularly after drinking milk) due to phosphate excess; Numbness of the extremities, sometimes with paralysis, due to potassium excess; Hypovolemia (decreased blood volume); Dehydration; Hypotension (abnormally low blood pressure); Tremors; Tachycardia (abnormally rapid beating of the heart); Restlessness; Diaphoresis (excessive sweating); Axillary or pubic hypotrichosis (decreased hair growth)

-routine investigation may show: hypoglycemia, eosiophilia, hyponatremia, hyperkalemia
Albright's syndrome
=polyostotic fibrous dysplasia; patients have precocious puberty, cafe-au-lait spots, short stature, occurs in young girls*

-a genetic disorder of bones, skin pigmentation and hormonal problems along with premature puberty

-Within the syndrome there are bone fractures and deformity of the legs, arms and skull, different pigment patches on the skin, and early puberty with increased rate of growth.

-Polyostotic fibrous dysplasia is usually caused by mosaicism for a mutation in a gene called GNAS1 (Guanine Nucleotide binding protein, Alpha Stimulating activity polypeptide 1).
-syndrome shows a broad spectrum of severity
-the disease frequently involves the skull and facial bones, pelvis, spine and shoulder girdle
-the sites of involvement are the femur (91%), tibia (81%), pelvis (78%), ribs, skull and facial bones (50%), upper extremities, lumbar spine, clavicle, and cervical spine, in decreasing order of frequency.
albuminocytologic dissociation
Guillain-Barre (inc protein in CSF w/ only modest inc in cell count)*

Guillain-Barré syndrome (GBS) is an acute, autoimmune, polyradiculoneuropathy affecting the peripheral nervous system, usually triggered by an acute infectious process. It is included in the wider group of peripheral neuropathies. There are several types of GBS, but unless otherwise stated, GBS refers to the most common form, acute inflammatory demyelinating polyneuropathy (AIDP).

-It is frequently severe and usually exhibits as an ASCENDING paralysis noted by weakness in the legs that spreads to the upper limbs and the face along with complete loss of deep tendon reflexes. With prompt treatment of plasmapheresis followed by immunoglobulins and supportive care, the majority of patients will regain full functional capacity. However, death may occur if severe pulmonary complications and dysautonomia are present.

-All forms of Guillain-Barre syndrome are due to an immune response to foreign antigens (such as infectious agents or vaccines) but mistargeted to host nerve tissues instead (a form of antigenic mimicry). The targets of such immune attack are thought to be gangliosides, which are complex glycosphingolipids present in large quantities on human nerve tissues, especially in the nodes of Ranvier. An example is the GM1 ganglioside, which can be affected in as many as 20-50% of cases, especially in those preceded by Campylobacter jejuni infections.

-Recent studies on the disease have demonstrated that approximately 80% of the patients have myelin loss, whereas, in the remaining 20%, the pathologic hallmark of the disease is indeed axon loss.

Signs and symptoms: The disease is characterized by weakness which affects the lower limbs first, and rapidly progresses in an ascending fashion. Patients generally notice weakness in their legs, manifesting as "rubbery legs" or legs that tend to buckle, with or without dysthesias (numbness or tingling). As the weakness progresses upward, usually over periods of hours to days, the arms and facial muscles also become affected. Frequently, the lower cranial nerves may be affected, leading to bulbar weakness (causing difficulty with eye movements, double vision), oropharyngeal dysphagia (difficulty with swallowing, drooling, and/or maintaining an open airway). Most patients require hospitalization and about 30% require ventilatory assistance.
-Sensory loss, if present, usually takes the form of loss of proprioception (position sense) and areflexia (complete loss of deep tendon reflexes), an important feature of GBS. Loss of pain and temperature sensation is usually mild. In fact, pain is a common symptom in GBS, presenting as deep aching pain usually in the weakened muscles, which patients compare to the pain from overexercising. These pains are self-limited and should be treated with standard analgesics. Bladder dysfunction may occur in severe cases but should be transient. If severe, spinal cord disease should be suspected.

-The diagnosis of GBS usually depends on the typical clinical findings such as rapidly evolving flaccid paralysis, areflexia, absence of fever, and a likely inciting event. CSF and electrodiagnostics may be useful, but because of the acute nature of the disease, they may not become abnormal until the end of the first week. CSF - typical CSF findings include an elevated protein level (100 - 1000 mg/dL) without an accompanying pleocytosis (increased cell count). A sustained pleocytosis may indicate an alternative diagnosis such as infection. Anyway the diagnosis is confirmed by the presence of Albuminocytological dissociation in the CSF.
Alport's syndrome
hereditary nephritis w/ nerve deafness*

Alport syndrome is a genetic condition characterized by the progressive loss of kidney function and hearing. Alport syndrome can also affect the eyes. The presence of blood in the urine (hematuria) is almost always found in this condition.

Alport syndrome is caused by mutations in COL4A3, COL4A4, and COL4A5, collagen biosynthesis genes. Mutations in any of these genes prevent the proper production or assembly of the type IV collagen network, which is an important structural component of basement membranes in the kidney, inner ear, and eye. Basement membranes are thin, sheet-like structures that separate and support cells in many tissues. When mutations prevent the formation of type IV collagen fibers, the basement membranes of the kidneys are not able to filter waste products from the blood and create urine normally, allowing blood and protein into the urine. The abnormalities of type IV collagen in kidney basement membranes cause gradual scarring of the kidneys, eventually leading to kidney failure in many people with the disease.

Alport syndrome can have different inheritance patterns that are dependent on the genetic mutation.
--In most people with Alport syndrome, the condition is inherited in an X-linked pattern, due to mutations in the COL4A5 gene.
--Alport syndrome can be inherited in an autosomal recessive pattern if both copies of the COL4A3 or COL4A4 gene, located on chromosome 2, have been mutated
anti-basement membrane antibodies
Goodpasture's syndrome*

Goodpasture’s syndrome (also known as Goodpasture’s disease and anti-glomerular basement membrane disease) is a rare condition characterised by rapid destruction of the kidneys and haemorrhaging of the lungs. Although many diseases can present with these symptoms, the name Goodpasture’s syndrome is usually reserved for the autoimmune disease produced when the patient’s immune system attacks cells presenting the Goodpasture antigen, which are found in the kidney and lung, causing damage to these organs.

Most patients present with both lung and kidney disease, however, some patients present with one of these diseases alone. The first lung symptoms usually develop days to months before kidney damage is evident. There is an increased incidence of syndactly.

The kidney disease mostly affects the glomeruli causing a form of nephritis. It is usually not detected until a rapid advance of the disease occurs so that kidney function can be completely lost in a matter of days, a condition known as rapidly progressive glomerulonephritis, or RPGN. Blood leaks into the urine causing hematuria, the volume urinated decreases and urea and other products usually excreted by the kidney are retained and build up in the blood. This is acute renal failure. Renal failure does not cause symptoms until more than 80% of kidney function has been lost. Symptoms include loss of appetite and sickness at first and then, when the damage is more advanced, breathlessness, high blood pressure and edema (swelling caused by fluid retention). The kidney involvement usually presents as nephritic syndrome, i.e. hematuria, a reduced glomerular filtration rate, and high blood pressure. This is in contrast to nephrotic syndrome, a more rare outcome of Goodpasture's, characterized by an abnormally large amount protein in the urine (proteinuria), coupled with severe edema.

Because of the vagueness of early symptoms and rapid progression of the disease, diagnosis is often not reached until very late in the course of the disease. Kidney biopsy is often the fastest way to secure the diagnosis and gain information about the extent of the disease and likely effect of treatment. Tests for anti-GBM antibodies may also be useful, combined with tests for antibodies to neutrophil cytoplasmic antigens, which are also directed against the patient’s own proteins.

As with many autoimmune conditions, the precise cause of Goodpasture’s Syndrome is not yet known. It is believed to be a type II hypersensitivity reaction to Goodpasture’s antigens on the cells of the glomeruli of the kidneys and the pulmonary alveoli, whereby the immune system wrongly recognizes these cells as foreign and attacks and destroys them, as it would an invading pathogen.

Like many autoimmune diseases, Goodpasture’s syndrome responds well to treatment with corticosteroids and immunosuppressants, however, the side effects of these can be serious, including as they do increased risk of infection, which may accelerate the progression of the disease. The concentration of anti-GBM antibodies in the blood may be reduced by apheresis to remove blood plasma and its replacement with an isotonic salt and protein solution. This course of treatment usually lasts between three and six months.

Very rare disease: 1 out of a million. It is most common between ages 18 and 30 and again between 50 and 65. Men and women are equally affected.
anticentromere antibodies
scleroderma (CREST)*

Scleroderma is a rare, chronic disease characterized by excessive deposits of collagen in the skin or other organs. The localized type of the disease tends not to be fatal. Diffuse scleroderma or systemic sclerosis, the generalized type of the disease, can be fatal as a result of heart, kidney, lung or intestinal damage.

Scleroderma affects the skin, and in more serious cases it can affect the blood vessels and internal organs. The most evident symptom is the hardening of the skin and associated scarring. Typically, the skin appears reddish or scaly in appearance. Blood vessels may also be more visible. Where large areas are affected, fat and muscle wastage will weaken limbs and affect appearance.

There is discoloration of the hands and feet in response to cold. Most patients (over 80%) have Raynaud's phenomenon, a vascular symptom that can affect the fingers and toes. Systemic scleroderma and Raynaud's can cause painful ulcers on the fingers or toes which are known as digital ulcers. Calcinosis is also common in systemic scleroderma, and is often seen near the elbows, knees or other joints.

Diagnosis is by clinical suspicion, presence of autoantibodies (specifically anti-centromere and anti-scl70/anti-topoisomerase) and occasionally by biopsy. Of the antibodies, 90% have a detectable anti-nuclear antibody. Anti-centromere is more common in the limited form (80-90%) than in the systemic form (10%), and anti-scl70 is more common in the diffuse form (30-40%) and in African-American patients (who are more prone to the systemic form).

There are three major forms of scleroderma: diffuse, limited (CREST syndrome) and morphea/linear. Diffuse and limited scleroderma are both a systemic disease, whereas the linear/morphea form is localized to the skin. (Some physicians consider CREST and limited scleroderma one and the same, others treat them as two separate forms of scleroderma.) There is also a subset of the systemic form known as "systemic scleroderma sine scleroderma", meaning the usual skin involvement is not present.

The limited form is often referred to as CREST syndrome. "CREST" is an acronym for: Calcinosis, Raynaud's syndrome, Esophageal dysmotility, Sclerodactyly, Telangiectasia

The overproduction of collagen is thought to result from an autoimmune dysfunction, in which the immune system would start to attack the kinetochore of the chromosomes. This would lead to genetic malfunction of nearby genes. T cells accumulate in the skin; these are thought to secrete cytokines and other proteins that stimulate collagen deposition. Stimulation of the fibroblast, in particular, seems to be crucial to the disease process, and studies have converged on the potential factors that produce this effect.
anti-ds-DNA antibodies (ANA antibodies)
SLE (type III hypersensitivity)*

Systemic lupus erythematosus (SLE or lupus) is a chronic autoimmune disease that is potentially debilitating and sometimes fatal as the immune system attacks the body’s cells and tissue, resulting in inflammation and tissue damage. SLE can affect any part of the body, but most often harms the heart, joints, skin, lungs, blood vessels, liver, kidneys and nervous system. The course of the disease is unpredictable, with periods of illness (called flares) alternating with remission. Lupus can occur at any age, but is most common in women, particularly of non-Caucasian descent.[1] Lupus is treatable symptomatically, mainly with corticosteroids and immunosuppressants, though there is currently no cure. The origins of the name are uncertain, but may derive from a characteristic reddish rash that purportedly resembles a wolf's face. The term "lupus", from the Latin for wolf, may derive from the rapacity and virulence of the disease; a 1590 work described it as "a malignant ulcer quickly consuming the neather parts; ... very hungry like unto a woolfe".

Lupus is a chronic autoimmune disease in which the body's own defense system attacks otherwise healthy tissue. Clinically, it can affect multiple organ systems including the heart, skin, joints, kidneys and nervous system. There are several types of lupus; generally when the word 'lupus' alone is used, it refers to the systemic lupus erythematosus or SLE as discussed in this article. Other types include:
-Drug-induced lupus erythematosus, a drug-induced form of SLE; this type of lupus can occur equally for either gender
-Lupus nephritis, an inflammation of the kidneys caused by SLE
-Discoid lupus erythematosus, a skin disorder which causes a red, raised rash on the face, scalp or rest of the body, which can develop into SLE
-Subacute cutaneous lupus erythematosus, which causes non-scarring skin lesions on patches of skin exposed to sunlight
-Neonatal lupus, a rare disease affecting babies born to women with SLE, Sjögren's syndrome or sometimes no autoimmune disorder. It is theorized that maternal antibodies attack the fetus, causing skin rash, liver problems, low blood counts (which gradually fade) and rarely bradycardia.

SLE is one of several diseases known as the great imitator because its symptoms vary so widely it often mimics or is mistaken for other illnesses, and because the symptoms come and go unpredictably. Diagnosis can be elusive, with patients sometimes suffering unexplained symptoms and untreated SLE for years. Common initial and chronic complaints are fever, malaise, joint pains, myalgias and fatigue. Because they are so often seen with other diseases, these signs and symptoms are not part of the diagnostic criteria for SLE.

Effects pretty much every organ system.

Lupus research has dramatically increased in recent years but the exact cause of the disease is unknown and there is still no consensus on whether it is a single condition or a group of related diseases. SLE is a chronic inflammatory disease believed to be a type III hypersensitivity response with potential type II involvement,[7] characterised by the body's production of antibodies against the nuclear components of its own cells. There are three mechanisms by which lupus is thought to develop: genetic predisposition, environmental triggers and drug reaction (drug-induced lupus).

Lupus research has dramatically increased in recent years but the exact cause of the disease is unknown and there is still no consensus on whether it is a single condition or a group of related diseases. SLE is a chronic inflammatory disease believed to be a type III hypersensitivity response with potential type II involvement,[7] characterised by the body's production of antibodies against the nuclear components of its own cells. There are three mechanisms by which lupus is thought to develop: genetic predisposition, environmental triggers and drug reaction (drug-induced lupus).

Genetics: The first mechanism may arise genetically. Research indicates that SLE may have a genetic link. Lupus does run in families, but no single "lupus gene" has yet been identified. Instead, multiple genes appear to influence a person's chance of lupus developing when triggered by environmental factors. The most important genes are located on chromosome 6, where mutations may occur randomly (de novo) or be inherited. Additionally, people with SLE have an altered RUNX-1 binding site, which may be either cause or contributor (or both) to the condition. Altered binding sites for RUNX-1 have also been found in people with psoriasis and rheumatoid arthritis.
Environmental triggers: The second mechanism may be due to environmental factors. These factors may not only exacerbate existing lupus conditions, but also trigger the initial onset. They include certain medications (such as some antidepressants and antibiotics), extreme stress, exposure to sunlight, hormones, and infections. Some researchers have sought to find a connection between certain infectious agents (viruses and bacteria), but no pathogen can be consistently linked to the disease. UV radiation has been shown to trigger the photosensitive lupus rash, but some evidence also suggests that UV light is capable of altering the structure of the DNA, leading to the creation of autoantibodies. Some researchers have found that women with silicone gel-filled breast implants have produced antibodies to their own collagen, but it is not known how often these antibodies occur in the general population and there is no data that show these antibodies cause connective tissue diseases such as lupus.

Drug reactions: Drug-induced lupus erythematosus is a reversible condition that usually occurs in patients being treated for a long-term illness. Drug-induced lupus mimics systemic lupus. However, symptoms of drug-induced lupus generally disappear once a patient is taken off the medication which triggered the episode. There are about 400 medications currently in use that can cause this condition, though the most common drugs are procainamide, hydralazine and quinidine.

Non-SLE forms of lupus: Discoid (cutaneous) lupus is limited to skin symptoms and is diagnosed via biopsy of skin rash on the face, neck or scalp. Often an anti-nuclear antibody (ANA) test for discoid patients is negative or a low-titre positive. About 10% of discoid lupus patients eventually develop SLE.

Diagnosis: Anti-nuclear antibody testing and anti-extractable nuclear antigen (anti-ENA) form the mainstay of serologic testing for lupus. Antiphospholipid antibodies occur more often in SLE, and can predispose for thrombosis. More specific are the anti-smith and anti-dsDNA antibodies. Other tests routinely performed in suspected SLE are complement system levels (low levels suggest consumption by the immune system), electrolytes and renal function (disturbed if the kidney is involved), liver enzymes and a complete blood count.

For inclusion in clinical trials, patients must meet the following three criteria to be classified as having SLE: (i) patient must present with four of the below eleven symptoms (ii) either simultaneously or serially (iii) during a given period of observation.

A useful mnemonic for these 11 criteria is "SOAP BRAIN MD": Serositis (8), Oral ulcers (4), Arthritis (5), Photosensitivity (3), Blood Changes (9), Renal involvement (proteinuria or casts) (6), ANA (10), Immunological changes (11), Neurological signs (seizures, frank psychosis) (7), Malar Rash (1), Discoid Rash (2).
anti-epithelial cell antibodies
pemphigus vulgaris*

Pemphigus is an autoimmune disorder that causes blistering and raw sores on skin and mucous membranes. As with other autoimmune disorders, it is caused when the body's defenses mistake its own tissues as foreign, and attack the cells. Pemphigus is derived from the Greek pemphix, meaning bubble or blister.

There are three types of pemphigus which vary in severity: pemphigus vulgaris, pemphigus foliaceus, and paraneoplastic pemphigus.

The most common form of the disorder is pemphigus vulgaris (ICD-10 L10.0). It occurs when antibodies attack Desmoglein 3, a protein that keeps cells bound together. Thus, cells simply fall apart, causing skin to slough off. Although pemphigus vulgaris may occur at any age, it is quite rare in children, and most common in the middle aged and elderly. Sores often originate in the mouth, making eating difficult and uncomfortable. Pemphigus vulgaris often affects people between the ages of 40-60, and mainly of Jewish or Mediterranean descent. Some patients are associated with myasthenia gravis, but it's unusual.

Foliaceus is the least severe of the three varieties. Desmoglein 1, the protein that is destroyed by the body's immune system is only found in the top dry layer of the skin, so mouth sores do not occur. Pemphigus foliaceus is characterized by crusty sores that often begin on the scalp, and may move to the chest, back, and face. It is not as painful as pemphigus vulgaris, and is often mis-diagnosed as dermatitis or eczema.

The least common and most severe type of pemphigus is the neoplastic variety, also known as paraneoplastic pemphigus. This disorder is usually found in conjunction with an already-existing malignancy. Very painful sores appear on the mouth, lips, and the esophagus. In this variety of pemphigus, the disease process often involves Bronchiolitis obliterans, a fatal destruction of alveoli in lung tissue. A diagnosis of neoplastic pemphigus may prompt a search for an existing tumor. Sometimes, the tumor is not malignant. In these cases, tumor removal may lead to a remission of the pemphigus. However, any decline in pulmonary function is generally irreversible. With Intravenous Immunoglobulin (IVIG) treatment and aggressive chemotherapy for the underlying lympoma, V Kingsley is now one known survivor of Paraneoplastic Pemphigus with pulmonary involvement.

Diagnosis relies on microscopic examination of skin lesion samples. A biopsy of a suspected lesion is taken: a sample of the blistered skin is removed and examined under the microscope to determine if the cells are separated in the manner characteristic of pemphigus. Unlike in the related pemphigoid, pemphigus manifests as intra-epithelial clefting, meaning the spinous cells of the epithelium break apart, a phenomenon known as acantholysis. This is because the desmosomes are attacked. In pemphigoid, the epitheium remains intact, but is entirely "unzipped" from the underlying connective tissue bed, or lamina propria, because the hemidesmosomes are attacked. Also apparent in pemphigus is a "tombstone appearance" of the basal cell layer and Tzanck cells.
Direct immunoflourescence on the biopsy skin sample can be used to detect desmoglein antibodies in the skin. The presence of these antibodies indicates pemphigus. Indirect immunofluorescence and ELISA can measure desmoglein antibodies in blood serum.
antigliadin antibodies
celiac disease*

Celiac disease is an autoimmune disorder of the small bowel that occurs in genetically predisposed individuals in all age groups after early infancy. Symptoms may include diarrhoea, failure to thrive (in children) and fatigue, but these may be absent and associated symptoms in all other organ systems have been described. It affects approximately 1% of Indo-European populations, though it is significantly underdiagnosed. A growing portion of diagnoses are being made in asymptomatic persons as a result of increasing screening.

Coeliac disease is caused by a reaction to gliadin, a gluten protein found in wheat (and similar proteins of the tribe Triticeae which includes other cultivars such as barley and rye). Upon exposure to gliadin, the enzyme tissue transglutaminase modifies the protein, and the immune system cross-reacts with the bowel tissue, causing an inflammatory reaction. That leads to flattening of the lining of the small intestine, which interferes with the absorption of nutrients. The only effective treatment is a lifelong gluten-free diet.

Classic symptoms of coeliac disease include diarrhoea, weight loss (or stunted growth in children) and fatigue, but while coeliac disease is primarily a bowel disease, bowel symptoms may also be limited or even absent. Some patients are diagnosed with symptoms related to the decreased absorption of nutrients or with various symptoms which, although statistically linked, have no clear relationship with the malfunctioning bowel. Given this wide range of possible symptoms, the classic triad is no longer a requirement for diagnosis.

The changes in the bowel make it less able to absorb nutrients, minerals and the fat-soluble vitamins A, D, E and K.

Coeliac disease has been linked with a number of conditions:
--IgA deficiency is present in 2% of patients with coeliac disease, and in turn this condition features a tenfold increased risk of coeliac disease
--Dermatitis herpetiformis; this itchy cutaneous condition has been linked to a transglutaminase enzyme in the skin, features small bowel changes identical to those in coeliac disease and occurs more often (2%) in patients with coeliac disease.

Endoscopy with biopsy is still considered the gold standard in the diagnosis of coeliac disease.
antihistone antibodies
drug-induced SLE
anti-IgG antibodies
rheumatoid arthritis
antimitochondrial antibodies
primary biliary sclerosis
antineutrophil antibodies
antiplatelet antibodies
idiopathic thrombocytopenic purpura (ITP)
Marfan's syndrome
Argyll-Robertson pupil
Arnold-Chiari malformation
cerebellar tonsillar herniation
Aschoff bodies
rheumatic fever
atrophy of mammillary bodies
Wernicke's encephalopathy: nystagmus, progressing ophthalmoplegia, truncal ataxia, confusion
Auer rods
acute myelogenous leukemia (especially promyelocytic type)
sickle cell anemia
Babinski's sign
UMN lesion
Baker's cyst in popliteal fossa
rheumatoid arthritis
"bamboo spine" on X-ray
ankylosing spondylitis
Bartter's syndrome
basophilic stippling of RBCs
lead poisoning
Becker's muscular dystrophy
defective dystrophin; less severe than Duchenne's
Bell's palsy
LMN CN VII palsy
Bence Jones proteins
multiple myeloma (kappa or lambda Ig light chains in urine), Waldenstrom's macroglobinemia (IgM)
Berger's disease
IgA nephropathy
Bernard-Soulier disease
defect in platelet adhesion
bilater hilar adenopathy, uveitis
Birbeck granules on EM
histiocytosis X (eosinophilic granuloma)
bloody tap on LP
subarachnoid hemorrhage
"blue bloater"
chronic bronchitis
blue-domed cysts
fibrocystic change of the breast
Blue sclera
osteogenesis imperfecta
boot-shaped heart on X-ray
tetralogy of Fallot; RVH
Bouchard's nodes
osteoarthritis (PIP swelling secondary to osteophytes)
Boutonniere deformity
rheumatoid arthritis
branching rods in oral infection
Actinomyces israelii
"Brown tumor" of bone
hemorrhage causes brown color of osteolytic cysts:
1. hyperparathyroidism
2. osteitis fibrosa cystica (von Recklinghausen's disease)
Bruton's disease
X-linked agammaglobinemia
Budd-Chiari syndrome
posthepatic venous thrombosis
Buerger's disease
small/medium-artery vasculitis
Burkitt's lymphoma
8:14 translocation; asociated w/ EBV
Burton's lines
lead poisoning
Wegener's granulomatosis, polyarthritis nodosa
cafe-au-lait spots on skin
Caisson disease
Gas emboli
Calf pseudohypertrophy
Duchenne’s muscular dystrophy
Call-Exner bodies
Granulosa-theca cell tumor of the ovary
Cardiomegaly with apical atrophy
Chagas’ disease
Cerebriform nuclei
Mycosis fungoides (cutaneous T-cell lymphoma)
Chagas’ disease
Trypanosome infection
1° syphilis (not painful)
Haemophilus ducreyi (painful)
Charcot’s triad
Multiple sclerosis (nystagmus, intention tremor, scanning speech), cholangitis
(jaundice, RUQ pain, fever)
Charcot-Leyden crystals
Bronchial asthma (eosinophil membranes)
Chédiak-Higashi disease
Phagocyte deficiency
Cherry-red spot on macula
Tay-Sachs, Niemann-Pick disease, central retinal artery occlusion
Cheyne-Stokes respirations
Central apnea in CHF and ↑ intracranial pressure
“Chocolate cysts”
Endometriosis (frequently involves both ovaries)
Chronic atrophic gastritis
Predisposition to gastric carcinoma
Chvostek’s sign
Hypocalcemia (facial muscle spasm upon tapping)
Clear cell adenocarcinoma of the vagina
DES exposure in utero
Clue cells
Gardnerella vaginitis
Codman’s triangle on x-ray
Cold agglutinins
Mycoplasma pneumoniae, infectious mononucleosis
Cold intolerance
Condylomata lata
2° syphilis
Continuous machinery murmur
Patent ductus arteriosus
Cori’s disease
Debranching enzyme deficiency
Cotton-wool spots
Chronic hypertension
Cough, conjunctivitis, coryza
+ fever
Councilman bodies
Toxic or viral hepatitis
Cowdry type A bodies
Crescents in Bowman’s capsule
Rapidly progressive crescentic glomerulonephritis
Crigler-Najjar syndrome
Congenital unconjugated hyperbilirubinemia
Curling’s ulcer
Acute gastric ulcer associated with severe burns
Currant-jelly sputum
Curschmann’s spirals
Bronchial asthma (whorled mucous plugs)
Cushing’s ulcer
Acute gastric ulcer associated with CNS injury
Depigmentation of neurons in substantia nigra
Parkinson’s disease (basal ganglia disorder––rigidity, resting tremor, bradykinesia)
Dermatitis, dementia, diarrhea
Pellagra (niacin, vitamin B3 deficiency)
Diabetes insipidus + exophthalmos + lesions of skull
Hand-Schüller-Christian disease
Dog or cat bite
Pasteurella multocida
Donovan bodies
Granuloma inguinale
Dressler’s syndrome
Post-MI fibrinous pericarditis
Dubin-Johnson syndrome
Congenital conjugated hyperbilirubinemia (black liver)
Duchenne’s muscular dystrophy
Deleted dystrophin gene (X-linked recessive)
Osteoarthritis (polished, ivory-like appearance of bone)
Edwards’ syndrome
Trisomy 18 associated with rocker-bottom feet, low-set ears, heart disease
Eisenmenger’s complex
Late cyanosis shunt (uncorrected L →R shunt becomes R →L shunt)
Elastic skin
Ehlers-Danlos syndrome
Erb-Duchenne palsy
Superior trunk brachial plexus injury (“waiter’s tip”)
Erythema chronicum migrans
Lyme disease
Fanconi’s syndrome
Proximal tubular reabsorption defect
“Fat, female, forty, and fertile”
Acute cholecystitis
Fatty liver
Ferruginous bodies
Gardner’s syndrome
Colon polyps with osteomas and soft tissue tumors
Gaucher’s disease
Glucocerebrosidase deficiency
Ghon focus
1° TB
Gilbert’s syndrome
Benign congenital unconjugated hyperbilirubinemia
Glanzmann’s thrombasthenia
Defect in platelet aggregation
Goodpasture’s syndrome
Autoantibodies against alveolar and glomerular basement membrane proteins
Gowers’ maneuver
Duchenne’s (use of patient’s arms to help legs pick self off the floor)
Guillain-Barré syndrome
Idiopathic polyneuritis
“Hair-on-end” appearance on x-ray
β-thalassemia, sickle cell anemia (extramedullary hematopoiesis)
Hand-Schüller-Christian disease
Chronic progressive histiocytosis
Thalassemia major
Sickle cell anemia
hCG elevated
Choriocarcinoma, hydatidiform mole (occurs with and without embryo)
Heberden’s nodes
Osteoarthritis (DIP swelling 2° to osteophytes)
Heinz bodies
G6PD deficiency
Henoch-Schönlein purpura
Hypersensitivity vasculitis associated with hemorrhagic urticaria and URIs
Heterophil antibodies
Infectious mononucleosis (EBV)
High-output cardiac failure (dilated cardiomyopathy)
Wet beriberi (thiamine, vitamin B1 deficiency)
Reiter’s syndrome, ankylosing spondylitis
HLA-DR3 or -DR4
Diabetes mellitus type 1 (caused by autoimmune destruction of β cells)
Homer Wright rosettes
Honeycomb lung on x-ray
Interstitial fibrosis
Horner’s syndrome
Ptosis, miosis, and anhidrosis
Howell-Jolly bodies
Splenectomy (or nonfunctional spleen)
Huntington’s disease
Caudate degeneration (autosomal dominant)
Hyperphagia + hypersexuality + hyperorality + hyperdocility
Klüver-Bucy syndrome (amygdala)
Hyperpigmentation of skin
1° adrenal insufficiency (Addison’s disease)
Horner’s syndrome
Ptosis, miosis, and anhidrosis
Howell-Jolly bodies: Spherical or ovoid nuclear fragments found in newly differentiated erythrocytes.
Splenectomy (or nonfunctional spleen)
Huntington’s disease
Caudate degeneration (autosomal dominant)
Hyperphagia + hypersexuality + hyperorality + hyperdocility
Klüver-Bucy syndrome (amygdala)
Hyperpigmentation of skin
1° adrenal insufficiency (Addison’s disease)
Horner’s syndrome
Ptosis, miosis, and anhidrosis
Howell-Jolly bodies: Spherical or ovoid nuclear fragments found in newly differentiated erythrocytes
Splenectomy (or nonfunctional spleen)
Hyperphagia + hypersexuality + hyperorality + hyperdocility
Klüver-Bucy syndrome (amygdala)
Hyperpigmentation of skin
1° adrenal insufficiency (Addison’s disease)
Hypersegmented neutrophils
Macrocytic anemia
Hypersegmented neutrophils
Macrocytic anemia
Hypertension + hypokalemia
Conn’s syndrome
Hypochromic microcytosis
Iron deficiency anemia, lead poisoning
Increased α-fetoprotein in amniotic fluid/maternal serum
Anencephaly, spina bifida (neural tube defects)
Increased uric acid levels
Gout, Lesch-Nyhan syndrome, myeloproliferative disorders, loop and thiazide
Adenovirus (causes hyperplasia of Peyer’s patches)
Janeway lesions
Jarisch-Herxheimer reaction
Syphilis—overaggressive treatment of an asymptomatic patient that causes
symptoms due to rapid lysis
Job’s syndrome
Neutrophil chemotaxis abnormality
Kaposi’s sarcoma
AIDS in MSM (men who have sex with men)
Kartagener’s syndrome
Dynein defect
Kayser-Fleischer rings
Wilson’s disease
Keratin pearls
Squamous cell carcinoma
Kimmelstiel-Wilson nodules
Diabetic nephropathy
Klüver-Bucy syndrome
Bilateral amygdala lesions
Koplik spots
Krukenberg tumor
Gastric adenocarcinoma with ovarian metastases
Kussmaul hyperpnea
Diabetic ketoacidosis
Lens dislocation + aortic dissection + joint hyperflexibility
Marfan’s syndrome (fibrillin deficit)
Lesch-Nyhan syndrome
HGPRT deficiency
Lewy bodies
Parkinson’s disease
Libman-Sacks disease
Endocarditis associated with SLE
Lines of Zahn
Arterial thrombus
Lisch nodules
Neurofibromatosis (von Recklinghausen’s disease)
Low serum ceruloplasmin
Wilson’s disease
Lucid interval
Epidural hematoma
“Lumpy-bumpy” appearance of
glomeruli on immunofluorescence
Poststreptococcal glomerulonephritis
Lytic bone lesions on x-ray
Multiple myeloma
Mallory bodies
Alcoholic liver disease
Mallory-Weiss syndrome
Esophagogastric lacerations
McArdle’s disease
Muscle phosphorylase deficiency
McBurney’s sign
MLF syndrome (INO)
Multiple sclerosis
Monoclonal antibody spike
Multiple myeloma (called the M protein; usually IgG or IgA), MGUS (monoclonal
gammopathy of undetermined significance), Waldenström’s (M protein = IgM)
Necrotizing vasculitis (lungs) and necrotizing glomerulonephritis
Wegener’s and Goodpasture’s (hemoptysis and glomerular disease)
Needle-shaped, negatively birefringent crystals
Negri bodies
Nephritis + cataracts + hearing loss
Alport’s syndrome
Neurofibrillary tangles
Alzheimer’s disease
Niemann-Pick disease
Sphingomyelinase deficiency
No lactation postpartum
Sheehan’s syndrome (pituitary infarction)
Nutmeg liver
Occupational exposure to asbestos
Malignant mesothelioma
“Orphan Annie” nuclei
Papillary carcinoma of the thyroid
Osler’s nodes
Owl’s eye
Painless jaundice
Pancreatic cancer (head)
Palpable purpura on legs and buttocks
Henoch-Schönlein purpura
Pancoast’s tumor
Bronchogenic apical tumor associated with Horner’s syndrome
Rheumatoid arthritis
Parkinson’s disease
Nigrostriatal dopamine depletion
Periosteal elevation on x-ray
Pyogenic osteomyelitis
Peutz-Jeghers syndrome
Benign polyposis
Peyronie’s disease
Penile fibrosis
Philadelphia chromosome (bcr-abl)
CML (may sometimes be associated with AML)
Pick bodies
Pick’s disease
Pick’s disease
Progressive dementia, similar to Alzheimer’s
“Pink puffer”
1. centroacinar: smoking
2. panacinar: α1-antitrypsin deficiency
Plummer-Vinson syndrome
Esophageal webs with iron deficiency anemia
Gout (MP joint of hallux)
Podocyte fusion
Minimal change disease
Polyneuropathy, cardiac pathology, and edema
Dry beriberi (thiamine, vitamin B1 deficiency)
Polyneuropathy preceded by GI or respiratory infection
Guillain-Barré syndrome
Pompe’s disease
Lysosomal glucosidase deficiency associated with cardiomegaly
Port-wine stain
Positive anterior “drawer sign”
Anterior cruciate ligament injury
Pott’s disease
Vertebral tuberculosis
Pseudopalisade tumor cell arrangement
Glioblastoma multiforme
Ewing's sarcoma
Ptosis, miosis, anhidrosis
Horner's syndrome (Pancoast's tumor)
Rash on palms and soles
2° syphilis, Rocky Mountain spotted fever
Raynaud’s syndrome
Recurrent vasospasm in extremities
RBC casts in urine
Acute glomerulonephritis
Recurrent pulmonary Pseudomonas and S. aureus infections
Cystic fibrosis
Red urine in the morning
Paroxysmal nocturnal hemoglobinuria
Reed-Sternberg cells
Hodgkin’s lymphoma
Reid index (increased)
Chronic bronchitis
Reinke crystals
Leydig cell tumor
Reiter’s syndrome
Urethritis, conjunctivitis, arthritis

"Can't see, can't pee, can't climb a tree."
Renal cell carcinoma + cavernous hemangiomas + adenomas
von Hippel–Lindau disease
Renal epithelial casts in urine
Acute toxic/viral nephrosis
Rhomboid crystals, positively birefringent

"p = positive"
Rib notching
Coarctation of aorta
Roth’s spots in retina
Rotor’s syndrome
Congenital conjugated hyperbilirubinemia
Rouleaux formation (RBCs)
Multiple myeloma
Russell bodies
Multiple myeloma
1. Left-to-right shunt (VSD, PDA, ASD)
2. mitral regurgitation
3. LV failure (CHF)
1. Aortic stenosis
2. Hypertrophic subaortic stenosis
Schiller-Duval bodies
Yolk sac tumor
Senile plaques
Alzheimer’s disease
Sézary syndrome
Cutaneous T-cell lymphoma
Sheehan’s syndrome
Postpartum pituitary necrosis
Shwartzman reaction
Neisseria meningitidis
Signet-ring cells
Gastric carcinoma
Simian crease
Down syndrome
Sipple’s syndrome
MEN type IIa
Sjögren’s syndrome
Dry eyes, dry mouth, arthritis
Skip lesions
Crohn's disease
Slapped cheeks
Erythema infectiosum (fifth disease)
Smith antigen
“Smudge cell”
Soap bubble on x-ray
Giant cell tumor of bone
Spike and dome on EM
Membranous glomerulonephritis
Spitz nevus
Benign juvenile melanoma
Splinter hemorrhages in fingernails
Starry-sky pattern
Burkitt’s lymphoma
“Strawberry tongue”
Scarlet fever
Streaky ovaries
Turner's syndrome
String sign on x-ray
Crohn's disease
Subepithelial humps on EM
Poststreptococcal glomerulonephritis
Suboccipital lymphadenopathy
Sulfur granules
Actinomyces israelii
Swollen gums, bruising, poor wound healing, anemia
Scurvy (ascorbic acid, vitamin C deficiency)—vitamin C is necessary for hydroxylation of proline and lysine in collagen synthesis
Systolic ejection murmur (crescendo-decrescendo)
Aortic valve stenosis
Burkitt’s lymphoma (c-myc activation)
Philadelphia chromosome, CML (bcr-abl hybrid)
Follicular lymphomas (bcl-2 activation)
Tabes dorsalis
3° syphilis
Tendon xanthomas (classically Achilles)
Familial hypercholesterolemia
Thumb sign on lateral x-ray
Epiglottitis (Haemophilus influenzae)
Thyroidization of kidney
Chronic bacterial pyelonephritis
“Tram-track” appearance on LM
Membranoproliferative glomerulonephritis
Trousseau’s sign
Visceral cancer, pancreatic adenocarcinoma (migratory thrombophlebitis),hypocalcemia (carpal spasm)
Virchow’s node
Left supraclavicular node enlargement from metastatic carcinoma of the stomach
Virchow’s triad
Pulmonary embolism (triad = blood stasis, endothelial damage, hypercoagulation)
von Recklinghausen’s disease
Neurofibromatosis with café-au-lait spots
von Recklinghausen’s disease of bone
Osteitis fibrosa cystica (“brown tumor”)
Wallenberg’s syndrome
PICA thrombosis
Waterhouse-Friderichsen syndrome
Adrenal hemorrhage associated with meningococcemia
Waxy casts
Chronic end-stage renal disease
WBC casts in urine
Acute pyelonephritis
WBCs in urine
Acute cystitis
Wermer’s syndrome
Whipple’s disease
Malabsorption syndrome caused by Tropheryma whippelii
Wilson’s disease
Hepatolenticular degeneration
“Wire loop” appearance on LM
Lupus nephropathy
“Worst headache of my life”
Berry aneurysm—associated with adult polycystic kidney disease
Xanthochromia (CSF)
Subarachnoid hemorrhage
Xerostomia + arthritis + keratoconjunctivitis sicca
Sjögren’s syndrome
Zenker’s diverticulum
Upper GI diverticulum
Zollinger-Ellison syndrome
Gastrin-secreting tumor associated with ulcers