Fa High Yield: Classic Findings

Front 1

Actinic keratosis

Back 1

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

Front 2

Addison's dz

Back 2

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

Front 3

Albright's syndrome

Back 3

=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.

Front 4

albuminocytologic dissociation

Back 4

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.

Front 5

Alport's syndrome

Back 5

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

Front 6

anti-basement membrane antibodies

Back 6

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.

Front 7

anticentromere antibodies

Back 7

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.

Front 8

anti-ds-DNA antibodies (ANA antibodies)

Back 8

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).

Front 9

anti-epithelial cell antibodies

Back 9

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.

Front 10

antigliadin antibodies

Back 10

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.

Front 11

antihistone antibodies

Back 11

drug-induced SLE

Front 12

anti-IgG antibodies

Back 12

rheumatoid arthritis

Front 13

antimitochondrial antibodies

Back 13

primary biliary sclerosis

Front 14

antineutrophil antibodies

Back 14

vasculitis

Front 15

antiplatelet antibodies

Back 15

idiopathic thrombocytopenic purpura (ITP)

Front 16

arachnodactyly

Back 16

Marfan's syndrome

Front 17

Argyll-Robertson pupil

Back 17

neurosyphilis

Front 18

Arnold-Chiari malformation

Back 18

cerebellar tonsillar herniation

Front 19

Aschoff bodies

Back 19

rheumatic fever

Front 20

atrophy of mammillary bodies

Back 20

Wernicke's encephalopathy: nystagmus, progressing ophthalmoplegia, truncal ataxia, confusion

Front 21

Auer rods

Back 21

acute myelogenous leukemia (especially promyelocytic type)

Front 22

autosplenectomy

Back 22

sickle cell anemia

Front 23

Babinski's sign

Back 23

UMN lesion

Front 24

Baker's cyst in popliteal fossa

Back 24

rheumatoid arthritis

Front 25

"bamboo spine" on X-ray

Back 25

ankylosing spondylitis

Front 26

Bartter's syndrome

Back 26

hyperreninemia

Front 27

basophilic stippling of RBCs

Back 27

lead poisoning

Front 28

Becker's muscular dystrophy

Back 28

defective dystrophin; less severe than Duchenne's

Front 29

Bell's palsy

Back 29

LMN CN VII palsy

Front 30

Bence Jones proteins

Back 30

multiple myeloma (kappa or lambda Ig light chains in urine), Waldenstrom's macroglobinemia (IgM)

Front 31

Berger's disease

Back 31

IgA nephropathy

Front 32

Bernard-Soulier disease

Back 32

defect in platelet adhesion

Front 33

bilater hilar adenopathy, uveitis

Back 33

sarcoidosis

Front 34

Birbeck granules on EM

Back 34

histiocytosis X (eosinophilic granuloma)

Front 35

bloody tap on LP

Back 35

subarachnoid hemorrhage

Front 36

"blue bloater"

Back 36

chronic bronchitis

Front 37

blue-domed cysts

Back 37

fibrocystic change of the breast

Front 38

Blue sclera

Back 38

osteogenesis imperfecta

Front 39

boot-shaped heart on X-ray

Back 39

tetralogy of Fallot; RVH

Front 40

Bouchard's nodes

Back 40

osteoarthritis (PIP swelling secondary to osteophytes)

Front 41

Boutonniere deformity

Back 41

rheumatoid arthritis

Front 42

branching rods in oral infection

Back 42

Actinomyces israelii

Front 43

"Brown tumor" of bone

Back 43

hemorrhage causes brown color of osteolytic cysts:
1. hyperparathyroidism
2. osteitis fibrosa cystica (von Recklinghausen's disease)

Front 44

Bruton's disease

Back 44

X-linked agammaglobinemia

Front 45

Budd-Chiari syndrome

Back 45

posthepatic venous thrombosis

Front 46

Buerger's disease

Back 46

small/medium-artery vasculitis

Front 47

Burkitt's lymphoma

Back 47

8:14 translocation; asociated w/ EBV

Front 48

Burton's lines

Back 48

lead poisoning

Front 49

c-ANCA,p-ANCA

Back 49

Wegener's granulomatosis, polyarthritis nodosa

Front 50

cafe-au-lait spots on skin

Back 50

neurofibromatosis

Front 51

Caisson disease

Back 51

Gas emboli

Front 52

Calf pseudohypertrophy

Back 52

Duchenne’s muscular dystrophy

Front 53

Call-Exner bodies

Back 53

Granulosa-theca cell tumor of the ovary

Front 54

Cardiomegaly with apical atrophy

Back 54

Chagas’ disease

Front 55

Cerebriform nuclei

Back 55

Mycosis fungoides (cutaneous T-cell lymphoma)

Front 56

Chagas’ disease

Back 56

Trypanosome infection

Front 57

Chancre

Back 57

1° syphilis (not painful)

Front 58

Chancroid

Back 58

Haemophilus ducreyi (painful)

Front 59

Charcot’s triad

Back 59

Multiple sclerosis (nystagmus, intention tremor, scanning speech), cholangitis
(jaundice, RUQ pain, fever)

Front 60

Charcot-Leyden crystals

Back 60

Bronchial asthma (eosinophil membranes)

Front 61

Chédiak-Higashi disease

Back 61

Phagocyte deficiency

Front 62

Cherry-red spot on macula

Back 62

Tay-Sachs, Niemann-Pick disease, central retinal artery occlusion

Front 63

Cheyne-Stokes respirations

Back 63

Central apnea in CHF and ↑ intracranial pressure

Front 64

“Chocolate cysts”

Back 64

Endometriosis (frequently involves both ovaries)

Front 65

Chronic atrophic gastritis

Back 65

Predisposition to gastric carcinoma

Front 66

Chvostek’s sign

Back 66

Hypocalcemia (facial muscle spasm upon tapping)

Front 67

Clear cell adenocarcinoma of the vagina

Back 67

DES exposure in utero

Front 68

Clue cells

Back 68

Gardnerella vaginitis

Front 69

Codman’s triangle on x-ray

Back 69

Osteosarcoma

Front 70

Cold agglutinins

Back 70

Mycoplasma pneumoniae, infectious mononucleosis

Front 71

Cold intolerance

Back 71

Hypothyroidism

Front 72

Condylomata lata

Back 72

2° syphilis

Front 73

Continuous machinery murmur

Back 73

Patent ductus arteriosus

Front 74

Cori’s disease

Back 74

Debranching enzyme deficiency

Front 75

Cotton-wool spots

Back 75

Chronic hypertension

Front 76

Cough, conjunctivitis, coryza
+ fever

Back 76

Measles

Front 77

Councilman bodies

Back 77

Toxic or viral hepatitis

Front 78

Cowdry type A bodies

Back 78

Herpesvirus

Front 79

Crescents in Bowman’s capsule

Back 79

Rapidly progressive crescentic glomerulonephritis

Front 80

Crigler-Najjar syndrome

Back 80

Congenital unconjugated hyperbilirubinemia

Front 81

Curling’s ulcer

Back 81

Acute gastric ulcer associated with severe burns

Front 82

Currant-jelly sputum

Back 82

Klebsiella

Front 83

Curschmann’s spirals

Back 83

Bronchial asthma (whorled mucous plugs)

Front 84

Cushing’s ulcer

Back 84

Acute gastric ulcer associated with CNS injury

Front 85

D-dimers

Back 85

DIC

Front 86

Depigmentation of neurons in substantia nigra

Back 86

Parkinson’s disease (basal ganglia disorder––rigidity, resting tremor, bradykinesia)

Front 87

Dermatitis, dementia, diarrhea

Back 87

Pellagra (niacin, vitamin B3 deficiency)

Front 88

Diabetes insipidus + exophthalmos + lesions of skull

Back 88

Hand-Schüller-Christian disease

Front 89

Dog or cat bite

Back 89

Pasteurella multocida

Front 90

Donovan bodies

Back 90

Granuloma inguinale

Front 91

Dressler’s syndrome

Back 91

Post-MI fibrinous pericarditis

Front 92

Dubin-Johnson syndrome

Back 92

Congenital conjugated hyperbilirubinemia (black liver)

Front 93

Duchenne’s muscular dystrophy

Back 93

Deleted dystrophin gene (X-linked recessive)

Front 94

Eburnation

Back 94

Osteoarthritis (polished, ivory-like appearance of bone)

Front 95

Edwards’ syndrome

Back 95

Trisomy 18 associated with rocker-bottom feet, low-set ears, heart disease

Front 96

Eisenmenger’s complex

Back 96

Late cyanosis shunt (uncorrected L →R shunt becomes R →L shunt)

Front 97

Elastic skin

Back 97

Ehlers-Danlos syndrome

Front 98

Erb-Duchenne palsy

Back 98

Superior trunk brachial plexus injury (“waiter’s tip”)

Front 99

Erythema chronicum migrans

Back 99

Lyme disease

Front 100

Fanconi’s syndrome

Back 100

Proximal tubular reabsorption defect

Front 101

“Fat, female, forty, and fertile”

Back 101

Acute cholecystitis

Front 102

Fatty liver

Back 102

Alcoholism

Front 103

Ferruginous bodies

Back 103

Asbestosis

Front 104

Gardner’s syndrome

Back 104

Colon polyps with osteomas and soft tissue tumors

Front 105

Gaucher’s disease

Back 105

Glucocerebrosidase deficiency

Front 106

Ghon focus

Back 106

1° TB

Front 107

Gilbert’s syndrome

Back 107

Benign congenital unconjugated hyperbilirubinemia

Front 108

Glanzmann’s thrombasthenia

Back 108

Defect in platelet aggregation

Front 109

Goodpasture’s syndrome

Back 109

Autoantibodies against alveolar and glomerular basement membrane proteins

Front 110

Gowers’ maneuver

Back 110

Duchenne’s (use of patient’s arms to help legs pick self off the floor)

Front 111

Guillain-Barré syndrome

Back 111

Idiopathic polyneuritis

Front 112

“Hair-on-end” appearance on x-ray

Back 112

β-thalassemia, sickle cell anemia (extramedullary hematopoiesis)

Front 113

Hand-Schüller-Christian disease

Back 113

Chronic progressive histiocytosis

Front 114

HbF

Back 114

Thalassemia major

Front 115

HbS

Back 115

Sickle cell anemia

Front 116

hCG elevated

Back 116

Choriocarcinoma, hydatidiform mole (occurs with and without embryo)

Front 117

Heberden’s nodes

Back 117

Osteoarthritis (DIP swelling 2° to osteophytes)

Front 118

Heinz bodies

Back 118

G6PD deficiency

Front 119

Henoch-Schönlein purpura

Back 119

Hypersensitivity vasculitis associated with hemorrhagic urticaria and URIs

Front 120

Heterophil antibodies

Back 120

Infectious mononucleosis (EBV)

Front 121

High-output cardiac failure (dilated cardiomyopathy)

Back 121

Wet beriberi (thiamine, vitamin B1 deficiency)

Front 122

HLA-B27

Back 122

Reiter’s syndrome, ankylosing spondylitis

Front 123

HLA-DR3 or -DR4

Back 123

Diabetes mellitus type 1 (caused by autoimmune destruction of β cells)

Front 124

Homer Wright rosettes

Back 124

Neuroblastoma

Front 125

Honeycomb lung on x-ray

Back 125

Interstitial fibrosis

Front 126

Horner’s syndrome

Back 126

Ptosis, miosis, and anhidrosis

Front 127

Howell-Jolly bodies

Back 127

Splenectomy (or nonfunctional spleen)

Front 128

Huntington’s disease

Back 128

Caudate degeneration (autosomal dominant)

Front 129

Hyperphagia + hypersexuality + hyperorality + hyperdocility

Back 129

Klüver-Bucy syndrome (amygdala)

Front 130

Hyperpigmentation of skin

Back 130

1° adrenal insufficiency (Addison’s disease)

Front 131

Horner’s syndrome

Back 131

Ptosis, miosis, and anhidrosis

Front 132

Howell-Jolly bodies: Spherical or ovoid nuclear fragments found in newly differentiated erythrocytes.

Back 132

Splenectomy (or nonfunctional spleen)

Front 133

Huntington’s disease

Back 133

Caudate degeneration (autosomal dominant)

Front 134

Hyperphagia + hypersexuality + hyperorality + hyperdocility

Back 134

Klüver-Bucy syndrome (amygdala)

Front 135

Hyperpigmentation of skin

Back 135

1° adrenal insufficiency (Addison’s disease)

Front 136

Horner’s syndrome

Back 136

Ptosis, miosis, and anhidrosis

Front 137

Howell-Jolly bodies: Spherical or ovoid nuclear fragments found in newly differentiated erythrocytes

Back 137

Splenectomy (or nonfunctional spleen)

Front 138

Hyperphagia + hypersexuality + hyperorality + hyperdocility

Back 138

Klüver-Bucy syndrome (amygdala)

Front 139

Hyperpigmentation of skin

Back 139

1° adrenal insufficiency (Addison’s disease)

Front 140

Hypersegmented neutrophils

Back 140

Macrocytic anemia

Front 141

Hypersegmented neutrophils

Back 141

Macrocytic anemia

Front 142

Hypertension + hypokalemia

Back 142

Conn’s syndrome

Front 143

Hypochromic microcytosis

Back 143

Iron deficiency anemia, lead poisoning

Front 144

Increased α-fetoprotein in amniotic fluid/maternal serum

Back 144

Anencephaly, spina bifida (neural tube defects)

Front 145

Increased uric acid levels

Back 145

Gout, Lesch-Nyhan syndrome, myeloproliferative disorders, loop and thiazide
diuretics

Front 146

Intussusception

Back 146

Adenovirus (causes hyperplasia of Peyer’s patches)

Front 147

Janeway lesions

Back 147

Endocarditis

Front 148

Jarisch-Herxheimer reaction

Back 148

Syphilis—overaggressive treatment of an asymptomatic patient that causes
symptoms due to rapid lysis

Front 149

Job’s syndrome

Back 149

Neutrophil chemotaxis abnormality

Front 150

Kaposi’s sarcoma

Back 150

AIDS in MSM (men who have sex with men)

Front 151

Kartagener’s syndrome

Back 151

Dynein defect

Front 152

Kayser-Fleischer rings

Back 152

Wilson’s disease

Front 153

Keratin pearls

Back 153

Squamous cell carcinoma

Front 154

Kimmelstiel-Wilson nodules

Back 154

Diabetic nephropathy

Front 155

Klüver-Bucy syndrome

Back 155

Bilateral amygdala lesions

Front 156

Koilocytes

Back 156

HPV

Front 157

Koplik spots

Back 157

Measles

Front 158

Krukenberg tumor

Back 158

Gastric adenocarcinoma with ovarian metastases

Front 159

Kussmaul hyperpnea

Back 159

Diabetic ketoacidosis

Front 160

Lens dislocation + aortic dissection + joint hyperflexibility

Back 160

Marfan’s syndrome (fibrillin deficit)

Front 161

Lesch-Nyhan syndrome

Back 161

HGPRT deficiency

Front 162

Lewy bodies

Back 162

Parkinson’s disease

Front 163

Libman-Sacks disease

Back 163

Endocarditis associated with SLE

Front 164

Lines of Zahn

Back 164

Arterial thrombus

Front 165

Lisch nodules

Back 165

Neurofibromatosis (von Recklinghausen’s disease)

Front 166

Low serum ceruloplasmin

Back 166

Wilson’s disease

Front 167

Lucid interval

Back 167

Epidural hematoma

Front 168

“Lumpy-bumpy” appearance of
glomeruli on immunofluorescence

Back 168

Poststreptococcal glomerulonephritis

Front 169

Lytic bone lesions on x-ray

Back 169

Multiple myeloma

Front 170

Mallory bodies

Back 170

Alcoholic liver disease

Front 171

Mallory-Weiss syndrome

Back 171

Esophagogastric lacerations

Front 172

McArdle’s disease

Back 172

Muscle phosphorylase deficiency

Front 173

McBurney’s sign

Back 173

Appendicitis

Front 174

MLF syndrome (INO)

Back 174

Multiple sclerosis

Front 175

Monoclonal antibody spike

Back 175

Multiple myeloma (called the M protein; usually IgG or IgA), MGUS (monoclonal
gammopathy of undetermined significance), Waldenström’s (M protein = IgM)
macroglobulinemia

Front 176

Myxedema

Back 176

Hypothyroidism

Front 177

Necrotizing vasculitis (lungs) and necrotizing glomerulonephritis

Back 177

Wegener’s and Goodpasture’s (hemoptysis and glomerular disease)

Front 178

Needle-shaped, negatively birefringent crystals

Back 178

Gout

Front 179

Negri bodies

Back 179

Rabies

Front 180

Nephritis + cataracts + hearing loss

Back 180

Alport’s syndrome

Front 181

Neurofibrillary tangles

Back 181

Alzheimer’s disease

Front 182

Niemann-Pick disease

Back 182

Sphingomyelinase deficiency

Front 183

No lactation postpartum

Back 183

Sheehan’s syndrome (pituitary infarction)

Front 184

Nutmeg liver

Back 184

CHF

Front 185

Occupational exposure to asbestos

Back 185

Malignant mesothelioma

Front 186

“Orphan Annie” nuclei

Back 186

Papillary carcinoma of the thyroid

Front 187

Osler’s nodes

Back 187

Endocarditis

Front 188

Owl’s eye

Back 188

CMV

Front 189

Painless jaundice

Back 189

Pancreatic cancer (head)

Front 190

Palpable purpura on legs and buttocks

Back 190

Henoch-Schönlein purpura

Front 191

Pancoast’s tumor

Back 191

Bronchogenic apical tumor associated with Horner’s syndrome

Front 192

Pannus

Back 192

Rheumatoid arthritis

Front 193

Parkinson’s disease

Back 193

Nigrostriatal dopamine depletion

Front 194

Periosteal elevation on x-ray

Back 194

Pyogenic osteomyelitis

Front 195

Peutz-Jeghers syndrome

Back 195

Benign polyposis

Front 196

Peyronie’s disease

Back 196

Penile fibrosis

Front 197

Philadelphia chromosome (bcr-abl)

Back 197

CML (may sometimes be associated with AML)

Front 198

Pick bodies

Back 198

Pick’s disease

Front 199

Pick’s disease

Back 199

Progressive dementia, similar to Alzheimer’s

Front 200

“Pink puffer”

Back 200

Emphysema
1. centroacinar: smoking
2. panacinar: α1-antitrypsin deficiency

Front 201

Plummer-Vinson syndrome

Back 201

Esophageal webs with iron deficiency anemia

Front 202

Podagra

Back 202

Gout (MP joint of hallux)

Front 203

Podocyte fusion

Back 203

Minimal change disease

Front 204

Polyneuropathy, cardiac pathology, and edema

Back 204

Dry beriberi (thiamine, vitamin B1 deficiency)

Front 205

Polyneuropathy preceded by GI or respiratory infection

Back 205

Guillain-Barré syndrome

Front 206

Pompe’s disease

Back 206

Lysosomal glucosidase deficiency associated with cardiomegaly

Front 207

Port-wine stain

Back 207

Hemangioma

Front 208

Positive anterior “drawer sign”

Back 208

Anterior cruciate ligament injury

Front 209

Pott’s disease

Back 209

Vertebral tuberculosis

Front 210

Pseudopalisade tumor cell arrangement

Back 210

Glioblastoma multiforme

Front 211

Pseudorosettes

Back 211

Ewing's sarcoma

Front 212

Ptosis, miosis, anhidrosis

Back 212

Horner's syndrome (Pancoast's tumor)

Front 213

Rash on palms and soles

Back 213

2° syphilis, Rocky Mountain spotted fever

Front 214

Raynaud’s syndrome

Back 214

Recurrent vasospasm in extremities

Front 215

RBC casts in urine

Back 215

Acute glomerulonephritis

Front 216

Recurrent pulmonary Pseudomonas and S. aureus infections

Back 216

Cystic fibrosis

Front 217

Red urine in the morning

Back 217

Paroxysmal nocturnal hemoglobinuria

Front 218

Reed-Sternberg cells

Back 218

Hodgkin’s lymphoma

Front 219

Reid index (increased)

Back 219

Chronic bronchitis

Front 220

Reinke crystals

Back 220

Leydig cell tumor

Front 221

Reiter’s syndrome

Back 221

Urethritis, conjunctivitis, arthritis

"Can't see, can't pee, can't climb a tree."

Front 222

Renal cell carcinoma + cavernous hemangiomas + adenomas

Back 222

von Hippel–Lindau disease

Front 223

Renal epithelial casts in urine

Back 223

Acute toxic/viral nephrosis

Front 224

Rhomboid crystals, positively birefringent

Back 224

Pseudogout

"p = positive"

Front 225

Rib notching

Back 225

Coarctation of aorta

Front 226

Roth’s spots in retina

Back 226

endocarditis

Front 227

Rotor’s syndrome

Back 227

Congenital conjugated hyperbilirubinemia

Front 228

Rouleaux formation (RBCs)

Back 228

Multiple myeloma

Front 229

Russell bodies

Back 229

Multiple myeloma

Front 230

S3

Back 230

1. Left-to-right shunt (VSD, PDA, ASD)
2. mitral regurgitation
3. LV failure (CHF)

Front 231

S4

Back 231

1. Aortic stenosis
2. Hypertrophic subaortic stenosis

Front 232

Schiller-Duval bodies

Back 232

Yolk sac tumor

Front 233

Senile plaques

Back 233

Alzheimer’s disease

Front 234

Sézary syndrome

Back 234

Cutaneous T-cell lymphoma

Front 235

Sheehan’s syndrome

Back 235

Postpartum pituitary necrosis

Front 236

Shwartzman reaction

Back 236

Neisseria meningitidis

Front 237

Signet-ring cells

Back 237

Gastric carcinoma

Front 238

Simian crease

Back 238

Down syndrome

Front 239

Sipple’s syndrome

Back 239

MEN type IIa

Front 240

Sjögren’s syndrome

Back 240

Dry eyes, dry mouth, arthritis

Front 241

Skip lesions

Back 241

Crohn's disease

Front 242

Slapped cheeks

Back 242

Erythema infectiosum (fifth disease)

Front 243

Smith antigen

Back 243

SLE

Front 244

“Smudge cell”

Back 244

CLL

Front 245

Soap bubble on x-ray

Back 245

Giant cell tumor of bone

Front 246

Spike and dome on EM

Back 246

Membranous glomerulonephritis

Front 247

Spitz nevus

Back 247

Benign juvenile melanoma

Front 248

Splinter hemorrhages in fingernails

Back 248

Endocarditis

Front 249

Starry-sky pattern

Back 249

Burkitt’s lymphoma

Front 250

“Strawberry tongue”

Back 250

Scarlet fever

Front 251

Streaky ovaries

Back 251

Turner's syndrome

Front 252

String sign on x-ray

Back 252

Crohn's disease

Front 253

Subepithelial humps on EM

Back 253

Poststreptococcal glomerulonephritis

Front 254

Suboccipital lymphadenopathy

Back 254

Rubella

Front 255

Sulfur granules

Back 255

Actinomyces israelii

Front 256

Swollen gums, bruising, poor wound healing, anemia

Back 256

Scurvy (ascorbic acid, vitamin C deficiency)—vitamin C is necessary for hydroxylation of proline and lysine in collagen synthesis

Front 257

Systolic ejection murmur (crescendo-decrescendo)

Back 257

Aortic valve stenosis

Front 258

t(8;14)

Back 258

Burkitt’s lymphoma (c-myc activation)

Front 259

t(9;22)

Back 259

Philadelphia chromosome, CML (bcr-abl hybrid)

Front 260

t(14;18)

Back 260

Follicular lymphomas (bcl-2 activation)

Front 261

Tabes dorsalis

Back 261

3° syphilis

Front 262

Tendon xanthomas (classically Achilles)

Back 262

Familial hypercholesterolemia

Front 263

Thumb sign on lateral x-ray

Back 263

Epiglottitis (Haemophilus influenzae)

Front 264

Thyroidization of kidney

Back 264

Chronic bacterial pyelonephritis

Front 265

Tophi

Back 265

Gout

Front 266

“Tram-track” appearance on LM

Back 266

Membranoproliferative glomerulonephritis

Front 267

Trousseau’s sign

Back 267

Visceral cancer, pancreatic adenocarcinoma (migratory thrombophlebitis),hypocalcemia (carpal spasm)

Front 268

Virchow’s node

Back 268

Left supraclavicular node enlargement from metastatic carcinoma of the stomach

Front 269

Virchow’s triad

Back 269

Pulmonary embolism (triad = blood stasis, endothelial damage, hypercoagulation)

Front 270

von Recklinghausen’s disease

Back 270

Neurofibromatosis with café-au-lait spots

Front 271

von Recklinghausen’s disease of bone

Back 271

Osteitis fibrosa cystica (“brown tumor”)

Front 272

Wallenberg’s syndrome

Back 272

PICA thrombosis

Front 273

Waterhouse-Friderichsen syndrome

Back 273

Adrenal hemorrhage associated with meningococcemia

Front 274

Waxy casts

Back 274

Chronic end-stage renal disease

Front 275

WBC casts in urine

Back 275

Acute pyelonephritis

Front 276

WBCs in urine

Back 276

Acute cystitis

Front 277

Wermer’s syndrome

Back 277

MEN I

Front 278

Whipple’s disease

Back 278

Malabsorption syndrome caused by Tropheryma whippelii

Front 279

Wilson’s disease

Back 279

Hepatolenticular degeneration

Front 280

“Wire loop” appearance on LM

Back 280

Lupus nephropathy

Front 281

“Worst headache of my life”

Back 281

Berry aneurysm—associated with adult polycystic kidney disease

Front 282

Xanthochromia (CSF)

Back 282

Subarachnoid hemorrhage

Front 283

Xerostomia + arthritis + keratoconjunctivitis sicca

Back 283

Sjögren’s syndrome

Front 284

Zenker’s diverticulum

Back 284

Upper GI diverticulum

Front 285

Zollinger-Ellison syndrome

Back 285

Gastrin-secreting tumor associated with ulcers