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Von Willebrand disease 
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Von Willebrand disease (VWD) is a hereditary deficiency of von Willebrand factor (VWF), which causes platelet dysfunction. Bleeding tendency is usually mild. Screening tests show a normal platelet count and, possibly, a slightly prolonged PTT. Diagnosis is based on low levels of VWF antigen and abnormal ristocetin cofactor activity. Treatment involves control of bleeding with replacement therapy (virally inactivated, intermediate-purity factor VIII concentrate) or desmopressin.

VWF is synthesized and secreted by vascular endothelium to form part of the perivascular matrix. VWF promotes the platelet adhesion phase of hemostasis by binding with a receptor on the platelet surface membrane (glycoprotein Ib/IX), thus connecting the platelets to the vessel wall. VWF is also required to maintain normal plasma factor VIII levels. Levels of VWF can temporarily increase in response to stress, exercise, pregnancy, inflammation, or infection.

VWD is classified into 3 types:

• Type 1: A quantitative deficiency of VWF, which is the most common form and is an autosomal dominant disorder
• Type 2: A qualitative impairment in synthesis of VWF that can result from various genetic abnormalities and is an autosomal dominant disorder
• Type 3: A rare autosomal recessive disorder in which homozygotes have no detectable VWF
Although VWD, like hemophilia A, is a hereditary disorder that may, when severe, cause factor VIII deficiency, factor VIII deficiency is usually only moderate.

Symptoms and Signs
Bleeding manifestations are mild to moderate and include easy bruising, mucosal bleeding, bleeding from small skin cuts that may stop and start over hours, sometimes increased menstrual bleeding, and abnormal bleeding after surgical procedures (eg, tooth extraction, tonsillectomy). Platelets function well enough that petechiae and purpura do not occur.

• Total plasma VWF antigen, VWF function, and plasma factor VIII level

Low levels of von Willebrand's factor cause a prolonged or normal APTT, a normal prothrombin time, and a prolonged bleeding time. Von Willebrand's disease is inherited in an autosomal dominant pattern with incomplete penetrance.

VWD is suspected in patients with bleeding disorders, particularly those with a family history of the disorder. Screening coagulation tests reveal a normal platelet count, normal INR, and sometimes a slightly prolonged PTT. Bleeding time testing is unreliable and no longer done.

Diagnosis requires measuring total plasma VWF antigen, VWF function as determined by the ability of plasma to support agglutination of normal platelets by ristocetin (ristocetin cofactor activity), and plasma factor VIII level. Stimuli that temporarily increase VWF levels can cause false-negative results in mild VWD; tests may need to be repeated.

In the common (type 1) form of VWD, results are concordant; ie, VWF antigen, VWF function, and plasma factor VIII level are equally depressed. The degree of depression varies from about 15 to 60% of normal and determines the severity of a patient's abnormal bleeding. Levels of VWF antigen can also be as low as 40% of normal in healthy people with type O blood.

Type 2 variants are suspected if tests are discordant, ie, VWF antigen is higher than expected for the degree of abnormality in ristocetin cofactor activity. (VWF antigen is higher than expected because the VWF defect in type 2 is qualitative, not quantitative.) Diagnosis is confirmed by demonstrating a reduced concentration of large VWF multimers on agarose gel electrophoresis. Four different type 2 variants are recognized, distinguished by different functional abnormalities of the VWF molecule.

Patients with type 3 VWD have no detectable VWF and a marked deficiency of factor VIII.

• Desmopressin
• VWF replacement when necessary
Patients are treated only if they are actively bleeding or are undergoing an invasive procedure (eg, surgery, dental extraction).

Desmopressin is an analog of vasopressin(antidiuretic hormone) that stimulates release of VWF into the plasma and may increase levels of factor VIII. Desmopressin can be helpful for type 1 VWD but is usually of no value in other types and may even be harmful in some. To ensure adequate response to the drug, physicians give patients a test dose and measure the response of VWF antigen. Desmopressin 0.3 mcg/kg given in 50 mL of 0.9% saline solution IV over 15 to 30 min may enable patients to undergo minor procedures (eg, tooth extraction, minor surgery) without needing replacement therapy. If a replacement product is needed, desmopressin may reduce the required dose. One dose of desmopressin is effective for about 8 to 10 h. About 48 h must elapse for new stores of VWF to accumulate, permitting a 2nd injection of desmopressin to be as effective as the initial dose. For many patients, intra-nasal desmopressin may be as effective as IV treatment.

For more significant procedures or for patients with types 2 or 3 VWD, treatment involves replacement of VWF by infusion of intermediate-purity factor VIII concentrates, which contain components of VWF. These concentrates are virally inactivated and therefore do not transmit HIV infection or hepatitis. Because they do not cause transfusion-transmitted infections, these concentrates are preferred to the previously used cryoprecipitate. High-purity factor VIII concentrates are prepared by immunoaffinity chromatography and contain no VWF and should not be used.

Key Points
• Patients have easy bruising and purpura, usually mucosal, and rarely joint bleeding.
• Screening tests reveal a normal platelet count, normal INR, and sometimes a slightly prolonged PTT.
• Confirming tests include total plasma VWF antigen, VWF function (VWF ristocetin cofactor assay), and plasma factor VIII level.
• Treatment, desmopressin or sometimes intermediate-purity factor VIII concentrate, is given for active bleeding and before an invasive procedure.


A 10 year-old child develops prolonged bleeding following a dental extraction. The child is referred to a hematologist; evaluation of the child's hematologic parameters demonstrates a prolonged partial thromboplastin time and an elevated bleeding time. Which of the following platelet abnormalities would most likely be found in this child?

A. Abnormal platelet morphology
B. Impaired platelet adhesion
C. Impaired platelet primary aggregation
D. Impaired release of platelet vesicles
E. Impaired secondary aggregation of platelets

The correct answer is B. This child probably has autosomal dominant von Willebrand's disease, in which an abnormal von Willebrand's factor (which also carries factor VIII in the blood) causes a defect in the initial adhesion of normal platelets to a damaged vessel wall. Since factor VIII levels are also consequently low, the partial thromboplastin time is also prolonged. Defects in platelet adhesion are also seen in Bernard-Soulier disease. 

Abnormal platelet morphology (choice A) is not seen in von Willebrand's disease, but may be observed with infiltration of the bone marrow by tumor or fibrosis, or after splenectomy.

Defects in primary platelet aggregation (choice C) are seen in thrombasthenia, which is caused by a deficiency or defect in the glycoprotein GpIIb-IIIa complex.

Defects of release of platelet vesicles (choice D) or secondary aggregation (choice E) are seen in storage pool disease and aspirin use.

A 27-year-old woman gave birth to a 7-pound 5-ounce baby boy. The vaginal birthing was normal and everything seemed fine, but 26 days after the baby was born the mother began to have heavy vaginal bleeding. Her husband called 911, and an ambulance brought her to a nearby trauma facility. They managed to stop the bleeding, but she had lost so much blood that they gave her two units of replacement blood and admitted her into the hospital. There, the attending physician noticed she had many bruises on her legs, arms, and trunk, making him think abuse. But he took a careful history, starting with the questions: How did you get these bruises? Have you or any of your family ever had a bleeding problem before? She replied, “The bruises just appeared, but I always did bruise easily. As to bleeding problems I can’t remember anything remarkable, except I used to have a bloody nose on a regular basis; so much so I some- times missed school; the school nurse told me to stop picking my nose, even though I didn’t think I did.” The physician also asked: “How about your menses?” She replied, “No real problem, they occurred on a regular basis with minimal cramping, but I did lose a lot of blood. However, my family’s doctor told me not to worry about it since my mother and grandmother also had heavy bleeding during their periods, thus it must simply be a familial trait.” On the basis of this information, which of the following conditions does this lady most likely have?

A. Hemophilia A
B. Hemophilia B
C. Hemophilia C
D. Bernard-Soulier syndrome 
E. Von Willebrand disease

The answer is E. Von Willebrand disease (choice E) is the most common of all the bleeding disorders; it affects both sexes equally, with a prevalence accounting for somewhat over 1% of the population. There are three major forms of the disease, types 1, 2, and 3, with four subsets of type 2: namely, 2A, 2B, 2M, and 2N. Patients with type 1 have less than the normal amount of von Willebrand’s factor (vWF), patients with type 2 disease have aberrant forms of vWF, and patient’s with type 3 disease have very little if any vWF. Types 1 and 2 are inherited as dominant traits; type 1 is the most common form, accounting for about 70% of case, and type 2A is the next most common form, making up about 17% of the cases. The type 3 disease is inherited as a recessive trait, is the most severe form, and is also not commonly encountered. During pregnancy, the levels of vWF normally rise throughout the third trimester and then decrease, normally to baseline about a mouth postpartum. 

However, in patients with von Willebrand disease, the decrease is exaggerated and levels of vWF decline even below the prepregnancy levels, which were already less than optimal. Consequently, as in the case described, a hemolytic crisis may take place some weeks after the birth (usually about a month). Recent National, Heart, Lung and Blood Institute (NHLBI) guidelines state that health care providers should remain in close contact with women with von Willebrand disease during this period. Although von Willebrand disease affects males and females to an equal extent, females more commonly become aware of otherwise borderline cases because of their menstrual periods. As in the case described, it is not uncommon for generations of women to have abnormally heavy menstrual flow, and while true that it runs in families, that does not make it normal. 

The function of vWF is to bind to other factors involved in coagulation and bring them to wound sites, thus permitting them to work together to inhibit bleeding. The basic vWF subunit is a 2,050 amino acid protein with specific domains for coagulation factor VIII, heparin, collagen, and platelet receptors and hence platelets. These monomers are N-glycosylated and converted into multimers in a process involving cysteine cross-linking at the C-terminus. These multimers are very large, containing up to 80 monomers, and only these larger forms of vWF are functional. Factor VIII is rapidly degraded when it is not bound to vWF, thus low circulating levels of vWF are accompanied by low levels of factor VIII. As mentioned, type 1 von Willebrand disease is due to reduced levels of functional vWF. Remember that, since this is a dominant condition, affected individuals all should have at least 50% of the normal levels of functional factor inherited from the normal parent. Variation in activity then depends upon residual activity remaining in the aberrant factor inherited from the other parent; thus, type 1 patients have half to near normal vWF levels and activity. In type 3 von Willebrand disease, a child inherits an aberrant factor from both parents; consequently, the type 2 diseases involve lack of functionality or hyperfunctionality in the factor that is synthesized.

Hemophilia A (choice A) and hemophilia B (choice B) are both sex-linked recessive conditions and con- sequently are rarely expressed in females; thus, they are clearly incorrect choices. Hemophilia A is the most common form, with a prevalence of about 1 case per 5,000 male births and results in a deficiency of blood coagulation factor VIII; hence, an alternate name, factor VIII deficiency. Patients may have cases that vary from severe to minor bleeding problems. Hemophilia B results in a deficiency of coagulation factor IX, and is also called factor IX deficiency or Christmas disease, after the first patient in whom the disease was described. It is less common than hemophilia A, with a prevalence of about 1 case per 25,000 male births. Hemophilia C (choice C) causes a deficiency of coagulation factor XI and affects members of both sexes. It is inherited in a recessive fashion and is quite rare, affecting about 1 person among 100,000 adults, almost only people of Ashkenazi or Iraqi Jewish decent, making it unlikely that this lady suffers from this disease. Bernard-Soulier syndrome (choice D) is a very rare condition, with an incidence of about 1 case per 1 million individuals; it is characterized by a thrombocytopenia. The biochemical cause is decreased expression of the glycoprotein complex Ib/IX/V on the surface of platelets. This complex normally serves as a vWF receptor, and when it is deficient, platelet adhesion to wound sites is inhibited. In vitro, this can be demonstrated by the lack of aggregation of platelets in response to ristocetin, an antibiotic that normally induces platelets to aggregate. A deficient number of platelets at the wound site inhibits formation of the primary platelet plug and causes an increased tendency to bleed. The thrombocytopenia may be due to decreased platelet half life.
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Systemic Lupus Erythematosus 
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Systemic lupus erythematosus (SLE) is a chronic, multisystem, inflammatory disorder of autoimmune etiology, occurring predominantly in young women. Common manifestations may include arthralgias and arthritis, malar and other rashes, pleuritis or pericarditis, renal or CNS involvement, and hematologic cytopenias. Diagnosis requires clinical and serologic criteria. Treatment of severe, ongoing, active disease requires corticosteroids, often hydroxychloroquine, and sometimes immunosuppressants.

Of all cases, 70 to 90% occur in women (usually of child-bearing age). SLE is more common among blacks and Asians than whites. Some drugs (eg, hydralazine, procainamide, isoniazid) cause a reversible lupus-like syndrome.

Symptoms and Signs
Malar rash
Discoid rash
Oral ulcer
Neurologic abnormality
Hematologic abnormality
ANA (+)
Immunologic abnormality
Renal involvement

Joint manifestations: Joint symptoms, ranging from intermittent arthralgias to acute polyarthritis, occur in about 90% of patients and may precede other manifestations by years. Most lupus polyarthritis is nondestructive and nondeforming.

Skin and mucous membrane manifestations: Skin lesions include malar butterfly erythema (flat or raised) that generally spares the nasolabial folds. The absence of papules and pustules helps distinguish SLE from rosacea. A variety of other erythematous, firm, maculopapular lesions can occur elsewhere, including exposed areas of the face and neck, upper chest, and elbows. Skin blistering and ulceration are rare, although recurrent ulcers on mucous membranes are common.

Neurologic manifestations: Neurologic symptoms can result from involvement of any part of the central or peripheral nervous system or meninges. Mild cognitive impairment is common. There may also be headaches, personality changes, ischemic stroke, subarachnoid hemorrhage, seizures, psychoses, organic brain syndrome, aseptic meningitis, peripheral and cranial neuropathies, transverse myelitis, or cerebellar dysfunction. 

Renal manifestations: Renal involvement can develop at any time and may be the only manifestation of SLE. It may be benign and asymptomatic or progressive and fatal. Renal lesions can range in severity from a focal, usually benign, glomerulitis to a diffuse, potentially fatal, membranoproliferative glomerulonephritis. Common manifestations include proteinuria (most often), an abnormal urinary sediment manifested by RBC casts and leukocytes, hypertension, and edema. 

Hematologic manifestations: Hematologic manifestations include anemia (autoimmune hemolytic), leukopenia (usually lymphopenia, with < 1500 cells/μL), and thrombocytopenia (sometimes life-threatening autoimmune thrombocytopenia). Recurrent arterial or venous thrombosis, thrombocytopenia, and a high probability of obstetric complications occur in patients with antiphospholipid antibodies. Thromboses probably account for many of the complications of SLE, including obstetric complications. 

GI manifestations: GI manifestations can result from bowel vasculitis or impaired bowel motility. In addition, pancreatitis can result from SLE or perhaps from its treatment with high-dose corticosteroids or azathioprine. Manifestations may include abdominal pain resulting from serositis, nausea, vomiting, manifestations of bowel perforation, and pseudo-obstruction. SLE rarely causes parenchymal liver disease. 

• Clinical criteria
• Cytopenias
• Autoantibodies
SLE should be suspected in patients, particularly young women, with any of the symptoms and signs. Laboratory testing differentiates SLE from other connective tissue disorders. Routine testing should include the following:

• Antinuclear antibodies (ANA) and anti–double-stranded (ds) DNA
• Chemistry profile including renal and liver enzymes

Fluorescent ANA: The fluorescent test for ANA is the best screen for SLE; positive ANA tests (usually in high titer: > 1:80) occur in > 98%. However, positive ANA tests can also occur in RA, other connective tissue disorders, cancers, and even in the general population. The false-positive rate varies from about 3% for ANA titers of 1:320 to about 30% for ANA titers of 1:40 among healthy controls. Drugs such as hydralazine, procainamide, and TNF-α antagonists can produce positive ANA results as well as a lupus-like syndrome; the ANA eventually becomes negative if the drug is stopped.

Other blood tests: Abnormal values in one or more of these assays suggest the presence of antiphospholipid antibodies (eg, anticardiolipin antibodies), which should then be measured directly by enzyme-linked immunosorbent assay (ELISA). Antiphospholipid antibodies are associated with arterial or venous thrombosis, thrombocytopenia, and, during pregnancy, spontaneous abortion or late fetal death but may be present in asymptomatic patients.

Renal involvement: Screening for renal involvement begins with urinalysis. RBC and/or WBC casts suggest active nephritis. Urinalysis should be done at regular intervals, even for patients in apparent remission, because kidney disease may be asymptomatic.

• NSAIDs and often antimalarials for mild disease
• Corticosteroids and often immunosuppressants for severe disease

Mild or remittent disease: Little or no therapy may be needed. Arthralgias are usually controlled with NSAIDs. Antimalarials help, particularly when joint and skin manifestations are prominent. Hydroxychloroquine 200 mg po once/day or bid reduces the frequency of SLE flares. Alternatives include chloroquine 250 mg po once/day and quinacrine 50 to 100 mg po once/day. Hydroxychloroquine can rarely cause retinal and skeletal or cardiac muscle toxicity. The eyes should be examined at 12-mo intervals. 

Severe disease: Corticosteroids are first-line therapy. A combination of prednisone and immunosuppressants is recommended in active, serious CNS lupus, vasculitis especially affecting viscera or nerves, or active lupus nephritis. Methylprednisolone 1 g by slow (1-h) IV infusion on 3 successive days is often the initial treatment. Then, prednisone given in doses of 40 to 60 mg po once/day can be maintained, but the dose may vary according to the manifestation of SLE. In severe renal involvement, cyclophosphamide is usually given in intermittent IV pulses instead of daily oral doses; eg, about 500 mg to 1 g/m2 IV (together with mesna and fluid loading to protect the bladder) monthly for 6 mo and then once q 3 mo for 18 mo. 

Key Points
• Joint and skin manifestations are classic in SLE, but the disorder can affect various organ systems, such as the skin, heart and lungs, lymphoid tissue, kidneys, and GI, hematologic, reproductive, and nervous systems.
• Among tests, use the highly sensitive ANA for screening, but use more specific autoantibodies (eg, anti-dsDNA, anti-Sm) for confirmation.
• Evaluate all patients for kidney involvement.
• Treat mild disease with an NSAID or an antimalarial such as chloroquine or hydroxychloroquine.
• Use corticosteroids for moderate or severe SLE and often an immunosuppressant for nephritis, CNS disease, and vasculitis or if corticosteroids are ineffective.
• Use corticosteroids at the lowest possible dose to maintain remission.


A 35-year-old black woman has complained of weight loss and fatigue for several weeks. In advising her on the phone as to measures to take before her appointment with you the following week, you asked her to keep a record of her temperature 4 times per day. She arrives for the appointment with the record. She also notes diffusely thinning hair. The temperature graph shows that her temperature has sometimes been as high as 101􏰃F. However, the high points of the daily graphs appear at various times in the early hours of the morning or late mornings, not in the afternoons or evenings. She complains also of arthralgia involving her metacarpophalangeal joints of the first and second fingers bilaterally, with 30 to 60 minutes of stiffness in the morning. A urinalysis yields microscopic hematuria and red cell casts. Which of the following diagnoses is most likely, given the combination of clinical findings?

A. Chronic glomerulonephritis 
B. Alopecia areata
C. Lupus
D. Chronic pyelonephritis
E. Pulmonary tuberculosis

The answer is C. Systemic Lupus Erythematosus occurs in black women 4 times as frequently as in white women and 23 times as frequently as in white men. The febrile course that does not follow the normal diurnal variation occurs in inflammatory processes not involving response to infection. Eventually, some two-thirds of patients have arthralgia or arthritis. Nearly 3 of 4 have skin manifestations, of which alopecia is fairly common; of course, the facial butterfly rash, not shown in this patient, is a hall- mark of the disease. Renal involvement is found in 16% to 38% of cases. Pulmonary tuberculosis would manifest not only pulmonary symptoms but also a febrile course with normal diurnal variation. Although each of the other choices may be characterized by at least one of the clinical findings in the vignette, none except lupus would mani- fest all of them.

A 28-year-old woman has had deep vein thrombosis in the past 3 years and is in the emergency department with a diagnosis of pulmonary embolism. Laboratory studies over the following 2 days revealed normal levels of Proteins C and S and antithrombin III. Further testing showed a positive lupus erythematosus preparation. Serologic test for syphilis is falsely positive. There is no rash; renal function is normal. Which of the following might be the most helpful laboratory test at this point?

A. Complete blood cell (CBC) 
B. Sedimentation rate
C. Anticardiolipin antibody level 
D. Prothrombin time
E. Hemoglobin A1C

The answer is C. Anticardiolipin antibodies are as close to specific as it gets in the murky field of autoimmune diseases, which virtually are all defined arbitrarily. The diagnosis is anti-phospholipid antibody disease. The most significant reason to be aware of this syndrome is the high risk of both intravenous and intra-arterial thromboses. The disease is basically a subset of LE.

A patient has fatigue and joint pain and is concerned about the possibility of systemic lupus erythematosus (SLE) after reading about this condition on the Internet. After taking a brief history you decide that further evaluation is appropriate. In addition to the history and physical findings, which one of the following laboratory findings would most support the diagnosis of SLE?

A. An abnormal C-reactive protein level
B. An erythrocyte sedimentation rate of 48 mm/hr
C. A positive antimicrosomal antibody test
D. A positive test for antiphospholipid antibodies
E. A positive test for rheumatoid factor

ANSWER: D. The criteria for the diagnosis of systemic lupus erythematosus (SLE) includes the presence of an immunologic disorder. Evidence of an immunologic disorder includes a positive finding of antiphospholipid antibodies, based upon one of the following: an abnormal serum level of immunoglobulin G or M anticardiolipin antibodies, a positive lupus anticoagulant test, or a false-positive serologic test for syphilis. The other test results listed are not criteria for the diagnosis of SLE.

For several years, a hypertensive 65-year-old female has been treated with hydrochlorothiazide, 25 mg/day; atenolol, 100 mg/day; and hydralazine, 50 mg 4 times/day. Her blood pressure has been well controlled on this regimen. Over the past 2 months she has experienced malaise, along with diffuse joint pains that involve symmetric sites in the fingers, hands, elbows, and knees. A pleural friction rub is noted on examination. Laboratory testing shows that the patient has mild anemia and leukopenia, with a negative rheumatoid factor and a positive antinuclear antibody (ANA) titer of 1:640. Which one of the following would be the most appropriate INITIAL step?

A. Replace hydrochlorothiazide with furosemide
B. Discontinue hydralazine
C. Start prednisone, 40 mg/day orally
D. Start hydroxychloroquine, 400 mg/day
E. Order renal function studies and anticipate that a renal biopsy will be needed

ANSWER: B. There are many drugs that can induce a syndrome resembling systemic lupus erythematosus, but the most common offenders are antiarrhythmics such as procainamide. Hydralazine is also a common cause. There is a genetic predisposition for this drug-induced lupus, determined by drug acetylation rates. Polyarthritis and pleuropericarditis occur in half of patients, but CNS or renal involvement is rare. While all patients with this condition have positive antinuclear antibody titers and most have antibodies to histones, antibodies to double-stranded DNA and decreased complement levels are rare, which distinguishes drug-induced lupus from idiopathic lupus.

The best initial management for drug-induced lupus is to withdraw the drug, and most patients will improve in a few weeks. For those with severe symptoms, a short course of corticosteroids is indicated. Once the offending drug is discontinued, symptoms seldom last beyond 6 months.
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Pericarditis is inflammation of the pericardium, often with fluid accumulation. Pericarditis may be caused by many disorders (eg, infection, MI, trauma, tumors, metabolic disorders) but is often idiopathic. Symptoms include chest pain or tightness, often worsened by deep breathing. Cardiac output may be greatly reduced if cardiac tamponade or constrictive pericarditis develops. Diagnosis is based on symptoms, a friction rub, ECG changes, and evidence of pericardial fluid accumulation on x-ray or echocardiogram. Finding the cause requires further evaluation. Treatment depends on the cause, but general measures include analgesics, anti-inflammatory drugs, colchicine, and rarely surgery.

Pericarditis may be i) Acute, ii) Subacute or iii) Chronic
Acute pericarditis develops quickly, causing an inflammatory reaction. Subacute (occurring within weeks to months of an inciting event) pericarditis and chronic pericarditis (defined as persisting > 6 mo) develop more slowly; their prominent feature is effusion. Acute disease may become subacute or chronic. Adverse hemodynamic effects and rhythm disturbance are rare, although cardiac tamponade is possible. Occasionally, pericarditis causes a marked thickening and stiffening of the pericardium (constrictive pericarditis). Pericarditis can lead to inflammation of the epicardial myocardium (myopericarditis).

Acute pericarditis may result from infection, autoimmune or inflammatory disorders, uremia, trauma, MI, cancer, radiation therapy, or certain drugs. Infectious pericarditis is most often viral. Purulent bacterial pericarditis is uncommon but may follow infective endocarditis, pneumonia, septicemia, penetrating trauma, or cardiac surgery. Often, the cause cannot be identified (called nonspecific or idiopathic pericarditis), but many of these cases are probably viral. Overall, the most common causes are viral and idiopathic. Acute MI causes 10 to 15% of cases of acute pericarditis.

Symptoms and Signs
Some patients present with symptoms and signs of inflammation (acute pericarditis); others present with those of fluid accumulation (pericardial effusion). Symptoms and signs vary depending on the severity of inflammation and the amount and rate of fluid accumulation. Even a large amount of pericardial fluid may be asymptomatic if it develops slowly (eg, over months).

Acute pericarditis: Acute pericarditis tends to cause chest pain and a pericardial rub, sometimes with dyspnea. The first evidence can be tamponade, with hypotension, shock, or pulmonary edema. 

Because the innervation of the pericardium and myocardium is the same, the chest pain of pericarditis is sometimes similar to that of myocardial inflammation or ischemia: Dull or sharp precordial or substernal pain may radiate to the neck, trapezius ridge (especially the left), or shoulders. Pain ranges from mild to severe. Unlike ischemic chest pain, pain due to pericarditis is usually aggravated by thoracic motion, cough, breathing, or swallowing food; it may be relieved by sitting up and leaning forward. Tachypnea and nonproductive cough may be present; fever, chills, and weakness are common. In 15 to 25% of patients with idiopathic pericarditis, symptoms recur intermittently for months or years (recurrent pericarditis). 

The most important physical finding is a triphasic or a systolic and diastolic precordial friction rub. However, the rub is often intermittent and evanescent; it may be present only during systole or, less frequently, only during diastole. If no rub is heard with the patient seated and leaning forward, auscultation may be attempted by listening with the diaphragm of the stethoscope while with the patient is on all fours. Sometimes, a pleural component to the rub is noted during breathing, which is due to inflammation of the pleura adjacent to the pericardium. 

• ECG and chest x-ray
• Echocardiography
Tests to identify cause (eg, pericardial fluid aspiration, pericardial biopsy)
Acute pericarditis: ECG and chest x-ray are done. Echocardiography is done to check for effusion (particularly loculated effusion with localized tamponade, which because of its atypical manifestations may not be suspected, and which may be suggested by indirect findings such as compression of chambers and characteristic respiratory variations), cardiac filling abnormalities, and wall motion abnormalities characteristic of myocardial involvement. Blood tests may detect leukocytosis and an elevated ESR, but these findings are nonspecific. 

The diagnosis is based on the presence of typical clinical findings and ECG abnormalities. Serial ECGs may be needed to show abnormalities. 

The ECG in acute pericarditis may show abnormalities confined to ST segments and T waves, usually in most leads. The ST segments in 2 or 3 of the standard leads become elevated but subsequently return to baseline. Unlike MI, acute pericarditis does not cause reciprocal depression in ST segments (except in leads aVR and V1), and there are no pathologic Q waves. The PR segment may be depressed. After several days or longer, T waves may become flattened and then inverted throughout the ECG, except in lead aVR; T wave–inversion occurs after the ST segment has returned to baseline and thus differs from the pattern of acute ischemia or MI. 

Echocardiography in acute pericarditis typically shows an effusion, which helps confirm the diagnosis, except in patients with purely fibrinous acute pericarditis in whom echocardiography is often normal. Findings indicating myocardial involvement include new focal or diffuse left ventricular dysfunction. 

Varies by cause
• NSAIDs, and sometimes colchicine or corticosteroids for pain and inflammation.
• Pericardiocentesis for tamponade and some large effusions
Sometimes intrapericardial drugs (eg, triamcinolone)
Sometimes pericardial resection for constrictive pericarditis
Treatment of cause
Hospitalization is warranted for most patients with an initial episode of acute pericarditis, particularly those with moderate or large effusions or with high-risk features, such as elevated temperature, subacute onset, immunosupression, recent trauma, oral anticoagulant therapy, failure to respond to an initial course of aspirin or NSAIDs, and myopericarditis. Hospitalization is needed to determine etiology and to observe for the development of cardiac tamponade. Close, early follow-up is important in patients who are not hospitalized. Possible causative drugs (eg, anticoagulants, procainamide, phenytoin) are stopped.

Pain can usually be controlled with colchicine or aspirin 325 to 650 mg po q 4 to 6 h or other NSAIDs (eg, ibuprofen 600 to 800 mg po q 6 to 8 h). The intensity of therapy is dictated by the patient's distress. Severe pain may require opioids. Colchicine 0.5 to 1 mg po once/day for 3 mo as an adjunct significantly decreases the recurrence rate and symptom persistence at 72 h in patients with a first episode of acute pericarditis and is increasingly being used as 1st-line therapy.

Corticosteroids (eg, prednisone 60 to 80 mg po once/day for 1 wk, followed by rapid tapering of the dose) may be used in patients with specific indications (eg, connective tissue disorder, autoimmune or uremic pericarditis, failure to respond to colchicine or NSAIDs) but are not given routinely because they enhance viral multiplication and recurrence is common when the dosage is tapered; colchicine may be particularly useful during the taper.


A 40-year-old man comes to the office complaining of a 3-day history of midsternal chest pain, non-radiating that is worse with inspiration and relieved by sitting forward. He has no past medical history, is on no medications, does not smoke, and has no known drug allergies. He leads an active lifestyle, and had been running about 10 miles a week without problem until a week ago when he developed a “viral syndrome.” His temperature is 38.4 C (100 F), blood pressure is 130/70 mm Hg, pulse is 100/min and regular, and respiratory rate is 20/min. He has a high pitched, grating sound that can be auscultated throughout the cardiac cycle over his precordium. An electrocardiogram shows diffuse ST elevation, diffuse PR depression with PR elevation in lead aVR. The most likely diagnosis is

A. angina
B. myocardial infarction
C. pericarditis
D. pneumonia
E. pulmonary embolism

The correct is answer is C. A chest pain that is pleuritic and improves with sitting up and leaning forward is a classic description of the chest pain associated with pericarditis, as is the precordial rub auscultated on physical exam. Diffuse ST elevations with diffuse PR depressions and PR elevation in lead aVR is also the classic description of the EKG findings associated with pericarditis.

Angina (choice A) or myocardial infarction (choice B) are less likely given that the patient has no risk for coronary artery disease (hypertension, hyperlipidemia, diabetes, tobacco). He also describes a very active lifestyle without symptoms, suggestive of no cardiac pathology prior to the onset of these symptoms. The ST changes on EKG, that alone would suggest ischemia, become more consistent with pericarditis since they are associated with PR segment changes that are classically associated with this particular disease process.

Pneumonia (choice D) is unlikely since there is no history of cough or dyspnea, and there is no mention of findings on the chest exam consistent with such a process (e.g., findings suggesting a consolidative process such as decreased breath sounds, increased fremitus, and egophony over the affected area).

Pulmonary embolism (choice E) is less likely, given that there are no apparent risk factors such as a history of hypercoagulability or poor activity. The EKG findings are also not consistent with a pulmonary embolism, where one would classically see an S wave in lead I, Q wave and T wave inversion in lead III, or ST-T wave changes in leads V1 through V4.

A 17-year-old boy who is hospitalized for depression on the general psychiatric unit complains of severe chest pain. The pain is worse on inspiration and has been present for about 2 weeks. His past medical history is significant for depression with multiple suicide gestures for the past 5 years and seasonal allergies. Review of systems is significant for a recent bronchitis. Vital signs are temperature 37.2 C (99 F), blood pressure 120/70 mm Hg, pulse 92/min, and respirations 10/min. The patient is disheveled, but well developed. Cardiac examination reveals a leathery sound on systole and diastole. An electrocardiogram reveals normal sinus rhythm at a rate of 95/min. Chest x-ray reveals moderate cardiomegaly. A prior report from a chest x-ray taken 8 months ago states that the heart size was normal. The next step in managing this patient would be to

A. begin therapy with ibuprofen
B. begin therapy with prednisone
C. obtain permission for an HIV test
D. order a cardiac perfusion scan
E. send cardiac enzymes to rule out a myocardial infarction

The correct answer is A. This patient is presenting with inspiratory chest pain, a leathery rub on systole and diastole, and a newly enlarged heart. This is consistent with postviral pericarditis, the most common form of pericarditis. Treatment includes nonsteroidal antiinflammatory medication and in refractory cases, steroids. Other causes of pericarditis not apropos to this case include myocardial infarction, connective tissue disease such as rheumatoid arthritis and lupus, drugs such as procainamide, hydralazine, and isoniazid, metastatic cancer such as lung and breast cancer, and renal failure.

Steroid treatment such as prednisone (choice B) is prescribed only after an aggressive course of antiinflammatory treatment has failed given the many side effects of steroid medication.

An HIV test (choice C) is unnecessary given the low-risk social history of this patient. Evaluation and treatment for pericarditis is the most appropriate next step.

A cardiac perfusion scan (choice D) would only be appropriate for a postmyocardial infarction. Evaluation and treatment for pericarditis is the most appropriate next step.

Cardiac enzymes (choice E) are unnecessary given the patient's age and lack of electrocardiographic findings to suggest a myocardial infarction. This patient is presenting with inspiratory chest pain, a leathery rub on systole and diastole and a newly enlarged heart. This is consistent with postviral pericarditis, the most common cause of pericarditis.

A 35-year-old man comes to the emergency department with a 2-day history of sharp chest pain that has been getting progressively worse. The pain increases when he is supine and improves when he sits upright. He has never had pain like this before and he denies dyspnea, diaphoresis, nausea, or presyncope. Upon further questioning, you discover that he had a recent upper respiratory tract infection that resolved approximately 5 days ago. His temperature is 37.6 C (99.7 F), blood pressure is 120/82 mm Hg, pulse is 95/min, and respirations are 14/min. Physical examination shows a triphasic cardiac rub. A chest x-ray is normal and an electrocardiogram shows diffuse ST segment elevation with ST segment depression in aVR. The most appropriate next step in management is to

A. administer nonsteroidal antiinflammatory agents
B. obtain an echocardiogram
C. obtain serial cardiac enzymes
D. order serologies for coxsackie B virus

The correct answer is A. The patient has acute pericarditis, which is purely a clinical diagnosis. There is no single serologic or imaging test that confirms the diagnosis. The classic pleuritic chest pain that worsens when supine, the pericardial friction rub on exam, and the diffuse ST segment elevation on ECG together make the diagnosis. Acute pericarditis may occur around the time of a known viral or upper respiratory tract infection and may itself be accompanied by fever. If the diagnosis remains uncertain, serologic markers of inflammation (such as an elevated white count, erythrocyte sedimentation rate, or C-reactive protein) may help make the diagnosis. The pericardial rub is classically "triphasic". The three components come from atrial systole, ventricular systole, and ventricular relaxation during ventricular diastole. The treatment is nonsteroidal antiinflammatory drugs (NSAIDs). Naproxen and indomethacin are most often used, but there is no data to demonstrate that any one NSAID is superior to another. There is also little data on duration of therapy, but a 7- to 14-day course is reasonable. The patient should follow up with a physician during that time frame to assure that the pericarditis has resolved.

An echocardiogram (choice B) is incorrect because there is no evidence of congestive heart failure or hemodynamic compromise. Echocardiogram is neither sensitive nor specific for the diagnosis of acute pericarditis and should therefore not be used to rule in or rule out the disease. While pericarditis can sometimes lead to a significant pericardial effusion and rarely to pericardial tamponade, the patient had no evidence of pericardial tamponade on history, no shortness of breath on exam, no hypotension, distended neck veins, or pulsus paradoxus.

While myocardial infarction should always be on the differential diagnosis for any patient presenting with chest pain, obtaining serial cardiac enzymes (choice C) is incorrect for several reasons. First, he has no risk factors for coronary artery disease. He is young, has no known hypertension or high cholesterol, does not smoke, nor does he have a family history of coronary artery disease. He jogs regularly without difficulty. The quality of his chest pain (sharp and changing with position) would be atypical for ischemic pain. The diffuse ST segment elevation on electrocardiogram is classic for pericarditis and would have to represent the unlikely, simultaneous involvement of several coronary arteries to reflect an acute myocardial infarction.

In the majority of cases, acute pericarditis is idiopathic. Obtaining serologies for coxsackie B virus (choice D) is incorrect because, while coxsackie B is the most common known infectious etiology of acute pericarditis, the presence or absence of the disease does not change management.
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Testicular Torsion
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Testicular torsion is an emergency condition due to rotation of the testis and consequent strangulation of its blood supply. Symptoms are acute scrotal pain and swelling, nausea, and vomiting. Diagnosis is based on physical examination and confirmed by color Doppler ultrasonography. Treatment is immediate manual detorsion followed by surgical intervention.

Anomalous development of the tunica vaginalis and spermatic cord can lead to incomplete fixation of the testis to the tunica vaginalis. This anomaly predisposes the testis to twisting on its cord spontaneously or after trauma. The predisposing anomaly is present in about 12% of males. Torsion is most common between the ages of 12 and 18, with a secondary peak in infancy. It is uncommon in men > age 30. It is more common in the left testis.

Symptoms and Signs
Immediate symptoms are rapid onset of severe local pain, nausea, and vomiting, followed by scrotal edema and induration. Fever and urinary frequency may be present. The testis is tender and may be elevated and horizontal. The contralateral testis may also be horizontal because the anatomic defect is usually bilateral. The cremasteric reflex is usually absent on the affected side. Sometimes, torsion can spontaneously resolve and then recur, which may appear to suggest a less acute onset. Usually, however, the onset and resolution of pain is very rapid with each episode.

• Clinical evaluation
• Often color Doppler ultrasonography
Torsion must be rapidly identified. Similar symptoms result mainly from epididymitis. With epididymitis, pain and swelling are usually less acute and initially localized to the epididymis. However, in both conditions, generalized swelling and tenderness often develop, making it difficult to distinguish torsion from epididymitis. A clinical diagnosis usually is sufficient to proceed to treatment. An equivocal diagnosis may be resolved by immediate imaging if available. Color Doppler ultrasonography of the scrotum is preferred. Radioisotope scrotal scanning is also diagnostic but takes longer and is less useful.

• Manual detorsion
• Surgery: Urgently if detorsion is unsuccessful, otherwise electively
Immediate manual detorsion without imaging can be attempted on the initial examination; its success is variable. Because testes usually rotate inward, for detorsion the testis is rotated in an outward direction (eg, for the left testis, detorsion is clockwise when viewed from the front—underneath the testis). More than one rotation may be needed to resolve the torsion; pain relief guides the procedure. If detorsion fails, immediate surgery is indicated, because exploration within a few hours offers the only hope of testicular salvage. Testicular salvage drops rapidly from 80 to 100% at 6 to 8 h to near zero at 12 h. Fixation of the contralateral testis is also done to prevent torsion on that side. When manual detorsion is successful, bilateral testicular fixation is done electively.

Key Points
• Testicular torsion typically causes rapid onset of severe scrotal pain, nausea, and vomiting, followed by scrotal edema and induration.
• Neither urinary frequency or fever rule out testiculartorsion, but the cremasteric reflex is usually absent.
• Treat patients with suggestive clinical findings; reserve imaging studies for cases with equivocal findings.
• Rotate the affected testicle outward and, if not successful, arrange for immediate surgery.


Typically, the anterior two thirds of each testis is covered by the tunica vaginalis, where fluids can accumulate. The tunica vaginalis attaches to the posterolateral surface of the testes and limits their movement within the scrotum. If the fixation is too high (anterior and cephalad), the testes can move more freely and torsion is more likely. A: Fixation is normal. B: Fixation is too high, allowing the testis to rotate transversely and resulting in torsion.


A previously healthy 15-year-old boy is brought to your emergency department with a 3-hour history of right testicular pain. He states that the pain began after football practice this afternoon. He does not remember any trauma to the area during practice. He appears to be in a significant amount of pain. His blood pressure is 128/80 mm Hg and his pulse is 110/min. Physical examination shows an erythematous, swollen right scrotum with significant tenderness to palpation on that side. You also note that the cremasteric reflex is absent on the right side. A urinalysis was sent from triage and is negative. The most appropriate next step is a

A. CT of the abdomen
B. surgical consultation
C. urine for gonorrhea and chlamydia
D. testicular biopsy
E. voiding cystourethrogram

The correct answer is B. The patient in this vignette has torsion of the right testicle. In any patient with testicular swelling and pain, surgical consultation should be sought as soon as possible because delay in the diagnosis of testicular torsion can result in loss of that testis due to absent blood flow. If the diagnosis is delayed >6 hrs without intervention, there is a significant risk of necrosis of that testis. An ultrasound with color Doppler will evaluate the blood flow to the affected testis and also assess the morphology of the testicle. However, it often delays the management of the condition, which could have disastrous effects.

A CT scan of the abdomen (choice A) will not be helpful in assessing this patient's scrotum.

Sending urine for gonorrhea and chlamydia (choice C) is an important consideration in a sexually active adolescent who presents with symptoms of epididymitis. Epididymitis is one of the main causes of acute painful scrotal swelling in sexually active young men. Usually the urinalysis will reveal pyuria. This is not a diagnostic test that should supercede the ultrasound with the Doppler, due to the importance of early identification of reduced/absent blood flow.

Testicular biopsy (choice D) is not part of the evaluation of testicular torsion.

A voiding cystourethrogram (choice E) is a procedure used to diagnose vesicoureteral reflux. This test is used as part of the work-up of a child with a urinary tract infection.

A 27-year-old man comes to the emergency department because of an "exquisitely painful" scrotum. He says that he was walking to lunch with friends when the pain hit him "like a thunderclap." He says that he has a steady girlfriend and that they have an "active sex life." He is "very healthy" and has never experienced pain like this before. He regularly checks himself "there" after that young comedian underwent testicular surgery on television. His temperature is 37 C (98.6 F), blood pressure is 130/85 mm Hg, pulse is 86/min, and respirations are 19/min. Physical examination shows severe scrotal tenderness that is not relieved when the scrotum is elevated. The right testes is high in the scrotum and riding in a horizontal position. The cord above the testes is not tender. A urinalysis shows:

Color straw/light Microscopic
Specific gravity 1.020 WBC 4/hpf
pH 5.8 Glucose absent
Protein absent Bacteria absent

The most appropriate next step is to
A. administer ciprofloxacin, intravenously
B. apply ice packs and observe in the emergency department
C. measure serum HCG and AFP
D. perform a trans-scrotal testicular biopsy
E. request a urology consultation, STAT

The correct answer is E. This patient has the classic presentation of testicular torsion, which is a surgical emergency, and therefore requires an immediate urologic consultation. He requires surgical intervention to reverse the spermatic cord torsion and restore blood flow.

Antibiotics, such a ciprofloxacin (choice A) are necessary to treat epididymitis, which typically presents with scrotal pain, fever, pyuria, a tender cord, and a normal positioned testes. Elevation of the testes may somewhat relieve the pain. Ice packs, bed rest, antiinflammatory agents, and scrotal support are typically used in conjunction with the antibiotics.

Applying ice packs and observing him in the emergency department (choice B) is inappropriate management of testicular torsion, which requires immediate urologic consultation.

Measuring serum HCG and AFP (choice C) is part of the evaluation for testicular cancer, which typically presents as a painless mass. If tenderness is present, it is often dull and aching, rarely acute and "exquisitely painful."

Performing a trans-scrotal testicular biopsy (choice D) is not useful in testicular torsion, which is a surgical emergency, and therefore requires an immediate urologic consultation. A trans-scrotal testicular biopsy is usually avoided, even if a testicular malignancy is suspected, to prevent potential tumor contamination of the lymphatics.
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Coarctation of the Aorta 
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Coarctation of the aorta is a localized narrowing of the aortic lumen that results in upper-extremity hypertension, left ventricular hypertrophy, and malperfusion of the abdominal organs and lower extremities. Symptoms vary with the anomaly's severity and range from headache, chest pain, cold extremities, fatigue, and leg claudication to fulminant heart failure and shock. A soft bruit may be heard over the coarctation site. Diagnosis is by echocardiography or by CT or MR angiography. Treatment is balloon angioplasty with stent placement, or surgical correction.

Coarctation of the aorta accounts for 6 to 8% of congenital heart anomalies. It occurs in 10 to 20% of patients with Turner syndrome. The male:female ratio is 2:1.

Coarctation of the aorta usually occurs at the proximal thoracic aorta just beyond the left subclavian artery and before the opening of the ductus arteriosus. Coarctation rarely involves the abdominal aorta. Thus, in utero and before the patent ductus arteriosus (PDA) closes, much of the cardiac output bypasses the coarctation via the PDA. Coarctation may occur alone or with various other congenital anomalies (eg, bicuspid aortic valve, ventricular septal defect, aortic stenosis, patent ductus arteriosus, mitral valve disorders, intracerebral aneurysms).

Physiologic consequences involve 2 phenomena:

• Pressure overload in the arterial circulation proximal to the coarctation
• Hypoperfusion distal to the coarctation
• Pressure overload causes left ventricular hypertrophy and hypertension in the upper part of the body including the brain.

Hypoperfusion affects the abdominal organs and lower extremities. Malperfusion of the intestines increases the risk of sepsis due to enteric organisms.

Ultimately, the pressure gradient increases collateral circulation to the abdomen and lower extremities via intercostal, internal mammary, scapular, and other arteries.

Untreated coarctation may result in left ventricular failure, rupture of the aorta, intracranial hemorrhage, hypertensive encephalopathy, and hypertensive cardiovascular disease during adulthood.

Symptoms and Signs
If coarctation is significant, circulatory shock with renal insufficiency (oliguria or anuria) and metabolic acidosis may develop in the first 7 to 10 days of life and may mimic findings of other systemic disorders such as sepsis. Infants with critical (severe) coarctation are likely to become acutely ill as soon as the ductus arteriosus constricts or closes.

Less severe coarctation may be asymptomatic during infancy. Subtle symptoms (eg, headache; chest pain, fatigue, and leg claudication during physical activities) may be present as children age. Upper-extremity hypertension is often present, but heart failure (HF) rarely develops after the neonatal period.

Typical physical examination findings include strong pulses and hypertension in the upper extremities, diminished or delayed femoral pulses, and a BP gradient, with low or unobtainable arterial BP in the lower extremities. A grade 2 to 3/6 ejection systolic murmur is often present at the upper left sternal border, left axilla, and sometimes most prominently in the left interscapular area. An apical systolic ejection click is present if a bicuspid aortic valve is also present. Dilated intercostal collateral arteries may cause a continuous murmur in the intercostal spaces. Affected females may have Turner syndrome, a congenital disorder causing lymphedema of the feet, webbed neck, squarely shaped chest, cubitus valgus, and widely spaced nipples.

• Chest x-ray and ECG
• Echocardiography or CT or MR angiography
Diagnosis is suggested by clinical examination (including BP measurement in all 4 extremities), supported by chest x-ray and ECG, and established by 2-dimensional echocardiography with color flow and Doppler studies or, in older patients with a suboptimal echocardiographic window, with CT or MR angiography.

Chest x-ray shows coarctation as a “3” sign in the upper left mediastinal shadow. Heart size is normal unless HF supervenes. Dilated intercostal collateral arteries may erode the 3rd to 8th ribs, causing rib notching, but this is seldom seen before age 5 yr.

ECG usually shows left ventricular hypertrophy but may be normal. In neonates and small infants, ECG usually shows right ventricular hypertrophy rather than left ventricular hypertrophy.

• For symptomatic neonates, prostaglandin E1 infusion
• For hypertension, β-blockers
• Surgical correction or balloon angioplasty (sometimes with stent placement)

Symptomatic neonates require cardiopulmonary stabilization with infusion of prostaglandin E1 (0.01 to 0.10 mcg/kg/min—titrate to the lowest effective dose) to reopen the constricted ductus arteriosus. Opening the ductus and its aortic ampulla provides some relief by allowing pulmonary artery blood to bypass the aortic obstruction via the ductus and increase perfusion of the descending aorta, improving systemic perfusion and reversing metabolic acidosis. Diuretics can help treat HF symptoms. Supplemental O2 should be used with caution in neonates because the resulting decrease in pulmonary vascular resistance may increase pulmonary blood flow at the expense of systemic blood flow.

In nonemergent situations, patients with hypertension may be treated with β-blockers; ACE inhibitors may adversely affect renal function. After repair of the coarctation, hypertension may persist or develop years after repair and can be treated with β-blockers, ACE inhibitors, angiotensin II receptor blockers, or Ca channel blockers.

The preferred definitive treatment is controversial. Some centers prefer balloon angioplasty with or without stent placement, but most prefer surgical correction and reserve the balloon procedure for recoarctation after surgical correction or for primary treatment of discrete coarctation in older children or adolescents.

Surgical options include resection and end-to-end anastomosis, patch aortoplasty, and left subclavian flap aortoplasty. Choice of surgical technique depends on anatomy and center preference.

Key Points
• Coarctation of the aorta is a localized narrowing of the lumen, typically in the proximal thoracic aorta just beyond the left subclavian artery and before the opening of the ductus arteriosus.
• Manifestations depend on severity of coarctation but typically involve pressure overload proximal to the coarctation, leading to heart failure, and hypoperfusion distal to the coarctation.
• Severe coarctation can manifest in the neonatal period with acidosis, renal insufficiency, and shock, but mild coarctation may not be apparent until an adolescent or adult is evaluated for hypertension.
• There is typically a BP gradient between upper and lower extremities and a grade 2 to 3/6 ejection systolic murmur, sometimes most prominent in the left interscapular area.
• For symptomatic neonates, infuse prostaglandin E1 to reopen the constricted ductus arteriosus.
• Correct coarctation surgically or using balloon angioplasty with or without stent placement.


On a routine examination of a new patient, diminished blood pressure readings are found in an adolescent’s legs, relative to that found in the upper extremities. You suspect coarctation of the aorta. Each of the following may be associated with coarctation EXCEPT for which factor?

A. This may be an XO female patient.
B. There may be notching of the ribs seen on x-ray. 
C. A delay in the femoral pulse may be found.
D. Cyanosis of the lips and clubbing of the fingernails may be observed.
E. The patient is more likely to be male than female.

The answer is D. Cyanosis of the lips and clubbing of the fingernails will not be observed in coarctation. Male individuals are significantly more often affected than female individuals. However, if a phenotypic female is affected, she is quite likely to be an XO genotype. The femoral pulse delay and collateral formation are usually not evident in children. Although delayed femoral pulses are not usually found in children, by the age of adolescence this finding is common. Also, by adulthood, rib notching is commonly found in coarctation. The most common locus of coarctation is the thoracic aorta just distal to the origin of the left subclavian artery.

A 22-year-old woman presented as a new patient for general medical care 7 months ago. She had a blood pressure of 180/110 mm Hg. One month after initiation of hydrochlorothiazide, her blood pressure was 175/110 mm Hg. Two other antihypertensive medications were added during the next 6 months with little success. Her social history reveals that she has many sexual partners and does not use contraception; she is G0P0. On physical examination, she has short stature as well as cubitus valgus. Which of the following conditions is the most likely cause of the woman’s hypertension?

A. Primary aldosteronism
B. Primary hyperparathyroidism 
C. Coarctation of the aorta
D. Pheochromocytoma
E. Hyperthyroidism

Which of the following tests might provide useful information?

A. Chest radiograph  |  B. TSH
C. Urine metanephrine  |  D. Parathyroid hormone 
E. Plasma renin activity

The answers are: C, A. In the evaluation of a patient with early onset of hypertension, it is essential to consider secondary causes of the condition. The differential diagnosis includes renal parenchymal disease, renovascular disease, primary aldosteronism, hyperparathyroidism, coarctation of the aorta, pheochromocytoma, and Cushing syndrome. This patient may have Turner syndrome; her short stature and cubitus valgus are consistent with this condition. Other features of this 45,X disease are low hairline, shield chest, widely spaced nipples, and a webbed neck. Patients are infertile; despite frequent, unprotected sexual encounters, this patient is G0P0, which might raise the suspicion for infertility. Amenorrhea is also present. Cardiac abnormalities include bicuspid aortic valve and coarctation of the aorta. None of the conditions named are present, so coarctation of the aorta is the cause of this patient’s hypertension.

A chest radiograph might show rib notching secondary to erosion by collateral vessels, as well as the “3 sign” in the paramediastinal shadow secondary to aortic indentation with prestenotic and post- stenotic dilatation of the vessel. Urine metanephrines are useful in the diagnosis of pheochromocytoma, parathyroid hormone is useful in the diagnosis of hyperparathyroidism, and plasma renin activity– aldosterone level is useful in the diagnosis of primary aldosteronism.
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Genital Warts (Condylomata Acuminata) 
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Genital Warts (Condylomata Acuminata) are lesions of the skin or mucous membranes of the genitals caused by certain types of human papillomavirus (HPV). Some types of HPV cause flat warts in the cervical canal or anus; infection with certain HPV types can lead to cancer. Diagnosis of external warts is based on their clinical appearance. Multiple treatments exist, but few are highly effective unless applied repeatedly over weeks to months. Genital warts may resolve without treatment in immunocompetent patients but may persist and spread widely in patients with decreased cell-mediated immunity (eg, due to pregnancy or HIV infection).

There are > 100 known types of HPV. Some cause common skin warts. Some infect primarily the skin and mucosa of the anogenital region. Important manifestations of anogenital HPV include

• Genital warts (condyloma acuminatum)
• Intraepithelial neoplasia and carcinoma of the cervix, anus, or penis
• Bladder and oral cancers
• Bowenoid papulosis
Condylomata acuminata are benign anogenital warts most often caused by HPV types 6 and 11. Low- and high-grade intraepithelial neoplasia and carcinoma may be caused by HPV. Virtually all cervical cancer is caused by HPV; about 70% is caused by types 16 and 18, and many of the rest result from types 31, 33, 35, and 39. HPV types that affect mainly the anogenital area can be transmitted to the oropharynx by orogenital contact; type 16 appears responsible for many cases of oropharyngeal cancer. HPV types 16 and 18 can also cause cancer in other areas, including the vulva, vagina, and penis.

HPV is transmitted from lesions during skin-to-skin contact. The types that affect the anogenital region are usually transmitted sexually by penetrative vaginal or anal intercourse, but digital, oral, and nonpenetrative genital contact may be involved.

Genital warts are more common among immunocompromised patients. Growth rates vary, but pregnancy, immunosuppression, or maceration of the skin may accelerate the growth and spread of warts.

Symptoms and Signs
Warts appear after an incubation period of 1 to 6 mo. Visible anogenital warts are usually soft, moist, minute pink or gray polyps (raised lesions) that enlarge, may become pedunculated, have rough surfaces, and may occur in clusters. They are usually asymptomatic, but some patients have itching, burning, or discomfort.

In men, warts occur most commonly under the foreskin, on the coronal sulcus, within the urethral meatus, and on the penile shaft. They may occur around the anus and in the rectum, especially in homosexual men. In women, warts occur most commonly on the vulva, vaginal wall, cervix, and perineum; the urethra and anal region may be affected. HPV types 16 and 18 usually cause flat endocervical or anal warts that are difficult to see and diagnose clinically.

• Clinical evaluation, sometimes including colposcopy, anoscopy, or both
• Genital warts are usually diagnosed clinically. Their appearance usually differentiates them from condyloma lata of secondary syphilis (which are flat-topped) and from carcinomas. However, serologic tests for syphilis (STS) should be done initially and after 3 mo. Biopsies of atypical, bleeding, ulcerated, or persistent warts may be necessary to exclude carcinoma.

Endocervical and anal warts can be visualized only by colposcopy and anoscopy. Applying a 3 to 5% solution of acetic acid for a few minutes before colposcopy causes warts to whiten and enhances visualization and detection of small warts.

• Mechanical removal (eg, by cryotherapy, electrocauterization, laser, or surgical excision)
• Topical treatment (eg, with antimitotics, caustics, or interferon inducers)
No treatment of anogenital warts is completely satisfactory, and relapses are frequent and require retreatment. In immunocompetent people, genital warts may resolve without treatment. In immunocompromised patients, warts may be less responsive to treatment.

Genital warts may be removed by cryotherapy, electrocauterization, laser, or surgical excision; a local or general anesthetic is used depending on the size and number to be removed. Removal with a resectoscope may be the most effective treatment; a general anesthetic is used.

Topical antimitotics (eg, podophyllotoxin, podophyllin, 5-fluorouracil), caustics (eg, trichloroacetic acid), interferon inducers (eg, imiquimod), and sinecatechins (a newer botanical product with an unknown mechanism) are widely used but usually require multiple applications over weeks to months and are frequently ineffective. Before topical treatments are applied, surrounding tissue should be protected with petroleum jelly. Patients should be warned that after treatment, the area may be painful.

Interferon alfa (eg, interferon alfa-2b, interferon alfa-n3), intralesionally or IM, has cleared intractable lesions on the skin and genitals, but optimal administration and long-term effects are unclear. Also, in some patients with bowenoid papulosis of the genitals (caused by type 16 HPV), lesions initially disappeared after treatment with interferon alfa but reappeared as invasive cancers.

For intraurethral lesions, thiotepa (an alkylating drug), instilled in the urethra, is effective. In men, 5-fluorouracil applied bid to tid is highly effective for urethral lesions, but rarely, it causes swelling, leading to urethral obstruction. Endocervical lesions should not be treated until Papanicolaou (Pap) test results rule out other cervical abnormalities (eg, dysplasia, cancer) that may dictate additional treatment.

By removing the moist underside of the prepuce, circumcision may prevent recurrences in uncircumcised men.

Sex partners of women with endocervical warts and of patients with bowenoid papulosis should be counseled and screened regularly for HPV-related lesions. A similar approach can be used for HPV in the rectum.

Current sex partners of people with genital warts should be examined and, if infected, treated.

A quadrivalent vaccine that protects against the 2 types of HPV (types 6 and 11) that cause > 90% of visible genitalwarts is available. This vaccine also protects against the 2 types of HPV (types 16 and 18) that cause most cervical cancers. A bivalent vaccine that protects against types 16 and 18 is also available.

The HPV vaccine is recommended for girls and women aged 9 to 26 yr for prevention of initial infection. Three doses are given, preferably at age 11 to 12 yr. The vaccine should be administered before onset of sexual activity, but girls and women who are sexually active should still be vaccinated.

Only the quadrivalent vaccine is recommended for males. Three doses of the vaccine are recommended for boys at age 11 to 12; boys aged 13 to 21 who have not completed the 3-dose series should also be given the vaccine. The vaccine is also recommended for men up to age 26 who have sex with men or whose immune system is compromised; it may be given to men aged 22 to 26 if they have not completed the 3-dose series.

Because of the location of these warts, condoms may not fully protect against infection.

Key Points
• Genital warts are caused by a few types of human papillomavirus (HPV).
• HPV types 16 and 18 cause about 70% of cervical cancers and can cause cancer in other areas, including the vulva, vagina, penis, and oropharynx.
• Diagnose warts by inspection; HPV testing is available, but its role in HPV management is unclear.
• Remove warts mechanically or using various topical treatments.
• HPV vaccination is recommended for children and young adults of both sexes.


A 24-year-old man comes to the clinic because of 2 "bumps" on his penis and scrotum. The lesions have been there for approximately 7 months and have been getting progressively larger. They are not painful. He is sexually active with 2 female partners, who are both on oral contraceptive pills and so they do not use barrier contraception. He had chlamydial urethritis last year. His temperature is 37.0 C (98.6 F). Physical examination shows a 3 mm flesh-colored, non-tender, lesion with a "heaped-up" appearance on the shaft of the penis and a 4 mm lesion with a similar appearance on his scrotum. The remainder of the examination is unremarkable. A rapid plasma regain (RPR), VDRL, and fluorescent treponemal antibody absorption (FTA-ABS) test are all nonreactive. In addition to providing the appropriate treatment, he should be told that:

A. Condoms will prevent the spread of this disease to future sexual partners
B. His sexual partners should be evaluated because they may be at an increased risk for cervical cancer
C. Oral suppressive therapy will decrease the frequency of recurrences
D. The state health department will be contacted because this is a notifiable infectious disease
E. Treatment will eradicate the infection

The correct answer is B. This patient has an anogenital human papillomavirus (HPV) infection (also known as genital warts). These lesions may be confused with condyloma lata (secondary syphilis). However, the "heaped-up" appearance of the flesh colored lesions are more characteristic of HPV and the serology for syphilis is negative. The treatment options for HPV include podophyllin application, cryotherapy, trichloroacetic acid, imiquimod, electrocautery, laser surgery, or surgical excision. This patient needs to tell his sexual partners to be evaluated because HPV infection is associated with cervical cancer.

Condoms may help to decrease the spread of this disease to future sexual partners, but it will not prevent it (choice A) because the treatment does not eradicate the infection from the surrounding tissues. He still should be advised to use condoms.

If this patient had a herpes infection (vesicles and ulcers), oral suppressive therapy would decrease the frequency of recurrences. However, he has an HPV infection, which is not usually treated with oral suppressive therapy (choice C).

It is incorrect to tell him that the state health department will be contacted because this is not a notifiable infectious disease (choice D). Notifiable sexually transmitted diseases are syphilis, chlamydia, gonorrhea, and AIDS.

It is incorrect to tell him that treatment will eradicate the infection (choice E) because while treatment may initially remove the wart, it does not eradicate the HPV from the surrounding tissues.

A 24-year-old woman comes to the clinic for a periodic health maintenance examination. She has no complaints. She exercises daily, eats a low fat diet, drinks "a couple of beers" with friends on the weekends, and is a "social" cigarette smoker. She has multiple sexual partners and uses oral contraceptive pills as birth control. She does not use condoms because "it is not as pleasurable." Her blood pressure is 110/70 mm Hg and pulse is 60/min. Her physical examination is unremarkable. You perform a pelvic examination and send a Pap smear to the laboratory for evaluation. The results, which return 5 days later, show two superficial squamous cells with sharply demarcated, large perinuclear vacuoles and alterations in the chromatin pattern. They use the term "koilocytic atypia." At this time the most correct statement about her condition is:

A. Acyclovir will decrease the shedding of the organism
B. Her Pap smear findings are unrelated to her sexual activity
C. She and her sexual partners should be treated with metronidazole
D. She may be at an increased risk for developing cervical cancer

The correct answer is D. This patient most likely has an infection with the human papilloma virus (HPV) and depending on the viral subtype (types 16, 18, 31 and 33), she may be at an increased risk for developing cervical carcinoma. Subtypes 6 and 11 are associated with condyloma acuminata which manifests as genital warts. The typical Pap smear findings of a HPV infection include a perinuclear halo and a wrinkled nucleus. HPV infection is associated with cervical dysplasia which may progress to invasive squamous cell carcinoma.

Acyclovir may decrease the shedding of the organism (choice A) if this patient has a herpes infection. A Pap smear of a patient with herpes typically shows giant multinucleated cells with eosinophilic intranuclear inclusions. This patient most likely has an HPV infection, not a herpes infection.

Her Pap smear findings are unrelated to her sexual activity (choice B) is incorrect because she most likely has an HPV infection, which is a sexually transmitted disease.

If this patient had a trichomonas infection, she and her sexual partners should be treated with metronidazole (choice C). However, she most likely has an HPV infection. Trichomonas often presents with a frothy vaginal discharge. A wet mount of the discharge will show motile, flagellated organisms.

A 37-year-old man comes to the clinic because of bright red blood on the toilet paper with bowel movements. He can also feel "bumps" around his anus and wonders if they are hemorrhoidal masses. He tells you that he has had difficulty gaining weight in the past few years and admits to occasional heroin usage and multiple sexual partners. On examination, he appears emaciated with temporal wasting and lipodystrophy of the face. There are multiple moist, pink cauliflower-like 0.2 - 0.5 cm papules surrounding the anus. Digital rectal examination reveals guaiac-negative, brown stool. He consents to whatever you think is appropriate management. At this time you should

A. perform anoscopy
B. recommend increased fluid intake and a high fiber diet
C. refer him for resection of condylomata acuminata
D. refer him for resection of hemorrhoids
E. send studies for sexually transmitted diseases including HIV

The correct answer is E. You should send studies for sexually transmitted diseases, is correct because his complex sexual history, temporal wasting, lipodystrophy of face, and genital warts (condylomata acuminata) all point toward high risk for HIV. Condylomata acuminata occur in men anywhere on the penis or about the anus. When perianal lesions occur, a prior history of receptive anal intercourse will usually predict whether intra-anal warts are present and will help to determine the need for anoscopy. Genital warts are sexually transmitted. A complete history should be taken and the patient should be screened for other sexually transmitted diseases as appropriate.

Anoscopy (choice A) is unnecessary at this time. The bright red blood on the toilet paper for this patient is most likely secondary to irritation of the friable genital warts.

Increased fluid intake and a high fiber diet (choice B) are appropriate for hemorrhoids, not HPV.

Referral for general surgery for resection of condylomata acuminata (choice C) is incorrect. This may be appropriate as follow-up care for this patient, but the most important first step is to work him up for HIV.

Referral to general surgery for resection of hemorrhoids (choice D) is incorrect because this patient has HPV, not hemorrhoids.
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Polycystic Ovary Syndrome (PCOS)
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Polycystic ovary syndrome is a clinical syndrome characterized by mild obesity, irregular menses or amenorrhea, and signs of androgen excess (eg, hirsutism, acne). In most patients, the ovaries contain multiple cysts. Diagnosis is by pregnancy testing, hormone measurement, and imaging to exclude a virilizing tumor. Treatment is symptomatic.

Polycystic ovary syndrome (PCOS) occurs in 5 to 10% of women. It is a most common cause of infertility. It is usually defined as a clinical syndrome, not by the presence of ovarian cysts. But typically, ovaries contain many 2- to 6-mm follicular cysts and sometimes larger cysts containing atretic cells. Ovaries may be enlarged with smooth, thickened capsules or may be normal in size.

This syndrome involves anovulation or ovulatory dysfunction and androgen excess of unclear etiology. However, some evidence suggests that patients have a functional abnormality of cytochrome P450c17 affecting 17-hydroxylase (the rate-limiting enzyme in androgen production); as a result, androgen production increases.

PCOS has several serious complications. Estrogen levels are elevated, increasing risk of endometrial hyperplasia and, eventually, endometrial cancer. Androgen levels are often elevated, increasing the risk of metabolic syndrome and causing hirsutism. Hyperinsulinemia due to insulin resistance may be present and may contribute to increased ovarian production of androgens. Over the long term, androgen excess increases the risk of cardiovascular disorders, including hypertension.

Symptoms and Signs
Symptoms typically begin during puberty and worsen with time. Premature adrenarche, characterized by excess dehydroepiandrosterone sulfate (DHEAS) and often early growth of axillary hair, body odor, and microcomedonal acne, is common. Typical symptoms include mild obesity, slight hirsutism, and irregular menses or amenorrhea. Body hair may grow in a male pattern (eg, on the upper lip and chin, around the nipples, and along the linea alba of the lower abdomen). Some women have other signs of virilization, such as acne and temporal balding. Areas of thickened, darkened skin (acanthosis nigricans) may appear in the axillae, on the nape of the neck, in skinfolds, and on knuckles and/or elbows; the cause is high insulin levels due to insulin resistance.

• Clinical criteria
• Serum testosterone, follicle-stimulating hormone, prolactin, and thyroid-stimulating hormone levels
• Pelvic ultrasonography
Ovulatory dysfunction is usually present at puberty, resulting in primary amenorrhea; thus, this syndrome is unlikely if regular menses occurred for a time after menarche.

Examination usually detects abundant cervical mucus, reflecting high estrogen levels. PCOS is suspected if women have at least two typical symptoms.

Testing includes pregnancy testing; measurement of serum total testosterone, follicle-stimulating hormone (FSH), prolactin, and thyroid-stimulating hormone (TSH); and pelvic ultrasonography to exclude other possible causes of symptoms. Serum free testosterone is more sensitive than total testosterone but is technically more difficult to measure. Normal to mildly increased testosterone and normal to mildly decreased FSH levels suggest PCOS.

LH/FSH ratio - This ratio is normally about 1:1 in premenopausal women, but with PCOS a ratio of greater than 2:1 or 3:1 may be considered diagnostic.

The diagnosis requires at least two of the following three criteria:

i) Ovulatory dysfunction causing menstrual irregularity
ii) Clinical or biochemical evidence of hyperandrogenism
iii) > 10 follicles per ovary (detected by pelvic ultrasonography), usually occurring in the periphery and resembling a string of pearls
In women meeting these criteria, serum cortisol is measured to exclude Cushing syndrome, and early-morning serum 17-hydroxyprogesterone is measured to exclude adrenal virilism. 
Serum DHEAS is measured. If DHEAS is abnormal, women are evaluated as for amenorrhea. Adult women with PCOS are evaluated for metabolic syndrome by measuring BP and usually serum glucose and lipids (lipid profile).

Intermittent progestins or oral contraceptives
Management of hirsutism and, in adult women, long-term risks of hormonal abnormalities
Infertility treatments in women who desire pregnancy
Treatment aims to relieve symptoms and to correct hormonal abnormalities and thus reduce risks of estrogen excess (eg, endometrial hyperplasia) and androgen excess (eg, cardiovascular disorders).

Women who do not desire pregnancy are usually given an intermittent progestin (eg, medroxyprogesterone 5 to 10 mg po once/day for 10 to 14 days every 1 to 2 mo) or oral contraceptives to reduce the risk of endometrial hyperplasia and cancer. These treatments also reduce circulating androgens and usually help make menstrual cycles more regular.

For hirsutism, physical measures (eg, bleaching, electrolysis, plucking, waxing, depilation) can be used. Eflornithine cream 13.9% bid may help remove unwanted facial hair. In adult women who do not desire pregnancy, hormone therapy that decreases androgen levels or spironolactone can be tried. Acne can be treated with the usual drugs (eg, benzoyl peroxide, tretinoin cream, topical and oral antibiotics).

Weight loss is encouraged. It may help induce ovulation, make menstrual cycles more regular, increase insulin sensitivity, and reduce acanthosis nigricans and hirsutism.

Metformin 500 to 1000 mg bid is used to help increase insulin sensitivity if weight loss is unsuccessful or menses do not resume. Metformin can also reduce free testosterone levels. When metformin is used, serum glucose should be measured, and kidney and liver function tests should be done periodically. Because metformin may induce ovulation, contraception is needed if pregnancy is not desired.

For women who desire pregnancy, infertility treatments (eg, clomiphene, metformin) are used. Weight loss may also be helpful. Hormone therapy that may have contraceptive effects is avoided.

Key Points
• PCOS is a common cause of ovulatory dysfunction.
• Suspect PCOS in women who have irregular menses, are mildly obese and slightly hirsute.
• Test for serious disorders (eg, Cushing syndrome, tumors) that can cause similar symptoms and for complications (eg, metabolic syndrome).


A 24-year-old female comes in for a new patient visit with the complaint of missed menstrual cycles. She states her period has never been regular, and that in the past it was common for her to skip a month or two between cycles. Now, however, she has not had a period in the past 7 months. She denies sexual activity, reports no medical problems, and her only prescribed medication is a face wash for acne. On review of systems she reports a weight gain of 10 lb over the past year. Her laboratory test reveals an FSH level of 8.7 mIU/mL, LH of 22.2 mIU/mL, estradiol of 45 pg/mL, TSH of 2.2 mIU/mL, prolactin of 12 ng/mL, and total testosterone of 98 ng/dL. The most likely diagnosis is:

A. Premature ovarian insufficiency
B. Polycystic ovary syndrome
C. Prolactinoma
D. Functional hypothalamic amenorrhea
E. Hypothyroidism

The answer is B. This woman fits the criteria for PCOS with her amenorrhea and clinical (acne) and biochemical hyperandrogenism (testosterone is elevated). Premature ovarian insufficiency would be suggested by elevated FSH, not LH. Her LH is elevated, but this elevated LH to FSH ratio is often seen with PCOS. Her laboratory test is not consistent with hypothyroidism, a prolactinoma or hypothalamic amenorrhea.

A 30-year-old woman presents to your office with an ultrasound report stating she has “polycystic- appearing ovaries.” She has a friend who has PCOS and is currently having trouble conceiving and wants to know what this means for her. You tell her that she may have PCOS if she also

A. Occasionally skips a menstrual cycle
B. Is obese
C. Is hirsute
D. Has diabetes
E. Has elevated LH levels

The answer is C. PCOS is diagnosed when a patient has two of the following three criteria (ovulatory dysfunction, hyperandrogenism, or polycystic ovaries) in addition to ruling out other causes for her symptoms. This patient has polycystic ovaries on ultrasound, but only answer C is hirsute fulfills the criteria for hyperandrogenism. Occasionally skipping a menstrual cycle does not fulfill the definition of amenorrhea or oligomenorrhea. Amenorrhea is lack of menses and oligomenorrhea is defined as 35 or more days between menses, or less than ten menses per year. Obesity, diabetes, and elevated LH levels are all associated with PCOS, but are not diagnostic.

A 28-year-old female sees you with a complaint of irregular menses. She has not had a menstrual period for 6 months. She is also concerned about weight gain, worsening acne, and dark hair on her upper lip, chin, and periareolar region. She is also interested in becoming pregnant soon. The patient tells you she has started an exercise program, which has helped with weight loss, but she continues to have amenorrhea. She has a negative urine 6-hCG test, a mild elevation in free testosterone levels, and glucose intolerance. Which one of the following would you consider initially for inducing ovulation?

A. Insulin
B. Metformin (Glucophage)
C. Ethinyl estradiol/norgestimate (Ortho Tri-Cyclen)
D. Glipizide (Glucotrol)
E. Spironolactone (Aldactone)

ANSWER: B. First-line agents for ovulation induction and treatment of infertility in patients with polycystic ovary syndrome (PCOS) include metformin and clomiphene, alone or in combination, as well as rosiglitazone. In one study of nonobese women with PCOS, metformin was found to be more effective than clomiphene for improving the rate of conception. However, the treatment of infertile women with PCOS remains controversial. One recent group of experts recommended that metformin use for ovulation induction in PCOS be restricted to women with glucose intolerance.
Oral contraceptives are commonly used to treat menstrual irregularities in women with PCOS; however, there are few studies supporting their use, and they would not be appropriate for ovulation induction. Spironolactone is a first-line agent for treatment of hirsutism (SOR A) and has shown promise in treating menstrual irregularities, but is not commonly recommended for ovulation induction. There is a high prevalence of insulin resistance in women with PCOS, as measured by glucose intolerance; insulin-sensitizing agents are therefore indicated, but not insulin or sulfonylurea medications.

An obese 32-year-old female has not conceived after more than 4 years of unprotected intercourse. You perform an appropriate workup and diagnose polycystic ovary syndrome.
Of the following, the most effective management for her infertility would be

A. spironolactone (Aldactone) 
B. luteinizing hormone
C. basal body temperature monitoring 
D. clomiphene (Clomid) 
E. bromocriptine (Parlodel)

ANSWER: D. Polycystic ovary syndrome may be the most common cause of female infertility, affecting 6%–8% of women. Some patients with polycystic ovary syndrome have hyperandrogenism, elevated levels of luteinizing hormone, and hyperinsulinemia. While early studies supported the use of metformin to increase fertility, a more recent study has shown that only 7% of women treated with metformin were able to conceive, whereas 22% of women treated with clomiphene citrate had a live birth. Spironolactone is useful for treating hirsutism, but not infertility. Since levels of other hormones are already elevated, the other measures listed would not be of benefit.
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Candida Esophagitis
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Esophagitis is an inflammation of the lining of the esophagus. If left untreated, this condition can cause problems with swallowing, ulcers, and scarring of the esophagus. In some instances, a condition known as Barrett's esophagus may develop, which is a risk factor for esophageal cancer.

Esophagitis is caused by an infection or irritation in the esophagus. An infection can be caused by bacteria, viruses, fungi, or diseases that weaken the immune system. Infections that cause esophagitis include:

Candida. This is a yeast infection of the esophagus caused by the same fungus that causes vaginal yeast infections. The infection develops in the esophagus when the body's immune system is weak, such as in people with diabetes or HIV. It is usually very treatable with antifungal drugs.
Herpes. Like Candida, this viral infection can develop in the esophagus when the body's immune system is weak. It is treatable with antiviral drugs.

Irritation leading to esophagitis may be caused by any of the following:

• GERD, or gastroesophageal reflux disease
• Vomiting
• Surgery
• Medications such as aspirin and other anti-inflammatory drugs
• Difficult and/or painful swallowing
• Heartburn
• Mouth sores
• A feeling of something of being stuck in the throat
• Nausea/Vomiting

• Esophagogastroduodenoscopy (EGD) - Upper endoscopy. A test in which a long, flexible lighted tube, called an endoscope, is used to view the esophagus.
• Biopsy. During this test, a small sample of the esophageal tissue is removed and then sent to a laboratory to be examined under a microscope.
• Upper GI series (or barium swallow) . During this procedure, X-rays are taken of the esophagus after drinking a barium solution. Barium coats the lining of the esophagus and shows up white on an X-ray. This characteristic enables doctors to view certain abnormalities of the esophagus.

Treatment for esophagitis depends on its cause. Possible treatments include:

• Medications that block acid production such as heartburn drugs.
• Antibiotics, anti-fungals, or antivirals to treat an infection.
• Pain medications that can be gargled or swallowed.
• Corticosteroid medication to reduce inflammation.



Candida esophagitis has received special attention ever since the beginning of the HIV epidemic. Between 3 and 10% of HIV-infected patients will first come to medical attention as the result of their first episode of candida esophagitis. The incidence of overall rate of esophagitis among patients infected with HIV has been reported to be as high as 15 to 20%. These rates are very much affected by use of effective anti-retroviral therapy. However, even with such therapy, patients with advanced AIDS often suffer tremendously with candida esophagitis.

Candida albicans is responsible for the vast majority of cases of symptomatic infection.

Patients with candidal esophagitis will usually have some, if not all, of the following symptoms: dysphagia (a perception of difficulty with swallowing), odynophagia (pain during swallowing), substernal chest pain that is not clearly related to swallowing, and/or a feeling of obstruction in the chest. Candidal esophagitis has been associated with fever, but this is uncommon.

Candidal esophagitis in patients with HIV/AIDS is sometimes said to be the "most frequent invasive candidal disease in patients with AIDS". However, biopsy studies have shown that Candida in the esophagus is never invasive in the true sense of the word. Rather the process is limited to the surface of the esophagus. Candidal esophagitis is, however, a significant disease and was the most common AIDS-defining disease in two cohorts of HIV-infected women. Candidal esophagitis usually occurs when CD4+ counts are below 100 cell/mm3, although it can also be seen during the transient immunosuppresion of acute HIV infection.

The best test for Candida esophagitis is upper gastrointestinal endoscopy. However, it has been clearly demonstrated that this expensive and invasive procedure is unnecessary in most cases. In this setting, a therapeutic trial of an ‘azole’ is an appropriate diagnostic and therapeutic strategy. Endoscopy is reserved for patients who fail to respond to this therapeutic trial.

Blind brushing of the esophagus via nasogastric tube has been shown to have a sensitivity of 96% and a specificity of 87%. Barium swallow can also show lesions that are suggestive of esophageal candidiasis, but is less sensitive (80%), even if done with a double-contrast technique (sensitivity of 88%). However, all of these approaches are inferior to endoscopy.

Systemically active therapy is needed for effective treatment of candidal esophagitis. The length of therapy depends on the clinical response. Ideally a course of therapy should last until 2 weeks after resolution of symptoms.

Medications include: fluconazole and itraconazole.

Difficult Clinical Situations

The principle difficulty with candidal esophagitis is its tendency to recur in patients with advanced and uncontrolled HIV. Such relapses require either intermittent retreatment or continuous suppression.


A male homosexual patient who has tested positive for HIV infection complains of painful swallowing, and endoscopy shows white, adherent plaques that leave beefy red denuded areas when removed. The examination is negative except for white exudates in the oral cavity that leave a raw, slightly bleeding base. Which of the following is a clearly relevant statement regarding this patient’s physical findings?

A. He is presumed to have Ludwig angina due to beta-hemolytic streptococcal infection.
B. The patient has esophageal herpes simplex related to his immunodeficient status.
C. The patient has aphthous esophagitis related to his immunodeficient status.
D. The patient has candidiasis of no more significance than coincidence as there is no oral thrush.
E. The patient has esophageal candidiasis, of significance in an HIV-infected patient.

The answer is E. Candidiasis is highly suggestive of immunoincompetence in adults, particularly in the esophagus, trachea, bronchi, or lungs. Of interest is that even oral candidiasis in an HIV-infected person strongly presages progression to AIDS, even correcting for CD4 count. Only 75% of patients with esophageal candidiasis have oral candidiasis so that oral candidiasis is not a reliable confirmatory indicator for esophageal candidiasis. Luwig angina is unusual and may well be suspicious for immunoincompetence but presents with a cellulitis apparent by external examination of the neck. The clinical picture does not include a description of herpetic or aphthous ulcers.

A 43-year-old man with acquired immunodeficiency syndrome (AIDS) is in the hospital for pneumonia. On his second hospital day, he reports difficulty swallowing his meals. He says that for the last month he has had difficulty swallowing food and medications. He also occasionally feels a burning pain in his upper chest when swallowing. He denies abdominal pain, nausea, or vomiting. Vital signs are: 37.0 C (98.6 F), blood pressure 129/88 mm Hg, pulse 80/min. Examination of his mouth reveals pink oral mucosa and a normal tongue. He has no significant cervical lymphadenopathy. Abdominal examination is normal. The patient's last CD4 count was performed 5 months ago and at that time was 190/mm3. The most appropriate next step in the management of this patient is to

A. order esophagogastroduodenoscopy (EGD)
B. order a Helicobacter pylori antibody test
C. prescribe a trial of antacids and schedule a follow-up appointment
D. prescribe oral acyclovir
E. prescribe oral fluconazole

The correct answer is A. The symptoms of dysphagia and odynophagia in a patient with AIDS are highly suspicious for esophagitis. The causes of esophagitis in the setting of AIDS or other immunocompromised states include Candida albicans, cytomegalovirus (CMV), and herpes simplex virus (HSV). The most frequent cause is C. albicans, which accounts for 50-70% of all cases. Esophagogastroduodenoscopy (EGD) is the best way to diagnose the etiology of esophagitis by providing both direct visualization of the esophageal lesions and the ability to obtain biopsies. If the patient has oral thrush and symptoms of esophagitis, the most likely etiology is C. albicans and treatment with fluconazole can be initiated empirically. This patient, however, has normal oral mucosa and needs an EGD prior to treatment.

The Helicobacter pylori antibody test (choice B) is used to determine the etiology of gastric ulcers. This test is not indicated in this patient because he does not have symptoms of ulcer disease. The symptoms of dysphagia and odynophagia in a patient with AIDS are highly suspicious for a fungal or viral esophagitis.

A trial of antacids (choice C) is inappropriate for this patient. The symptoms of dysphagia and odynophagia in a patient with AIDS are highly suspicious for fungal or viral esophagitis. Antacids are used primarily for gastroesophageal reflux disease and will not help in this case. A follow-up appointment is important, however, after the patient has an esophagogastroduodenoscopy (EGD) and is started on appropriate medications.

Treatment with acyclovir (choice D) is premature at this time. There are multiple causes of esophagitis in patients with AIDS and an esophagogastroduodenoscopy (EGD) should be performed to evaluate the esophageal lesions as well as to obtain biopsies. If the esophagitis is caused by herpes simplex virus (HSV), acyclovir is the anti-viral medication of choice.

Treatment with fluconazole (choice E) is premature at this time. There are multiple causes of esophagitis in patients with AIDS and esophagogastroduodenoscopy (EGD) should be performed to evaluate the esophageal lesions as well as to obtain biopsies. If the esophagitis is caused by Candida albicans, fluconazole is the anti-fungal medication of choice.
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Acute bacterial meningitis is rapidly progressive bacterial infection of the meninges and subarachnoid space. Findings typically include headache, fever, and nuchal rigidity. Diagnosis is by CSF analysis. Treatment is with antibiotics and corticosteroids given as soon as possible.

Most commonly, bacteria reach the subarachnoid space and meninges via hematogenous spread. Bacteria may also reach the meninges from nearby infected structures (eg, sinuses, the middle ear) or through a congenital or acquired defect in the skull or spine (eg, a penetrating head wound, a neural tube defect, an opening made during neurosurgery).

Because WBCs, immunoglobulins, and complement are normally sparse or absent from CSF, bacteria initially multiply without causing inflammation. Later, bacteria release endotoxins, teichoic acid, and other substances that trigger an inflammatory response with mediators such as WBCs and TNF. Typically in CSF, levels of protein increase, and because bacteria consume glucose and because less glucose is transported into the CSF, glucose levels decrease.

Likely causes depend on i) Patient age, ii) Route of entry, iii) Immune status of the patient.

Age: In children and young adults, the most common causes are 

• Neisseria meningitidis
• Streptococcus pneumoniae
• Haemophilus influenzae type B

In middle-aged adults and in the elderly, the most common cause of meningitis is 

• S. pneumoniae
• Less commonly, N. meningitidis causes meningitis in middle-aged and older adults.

Route: Routes of entry include the following: 

By hematogenous spread (the most common route)
From infected structures in or around the head (eg, sinuses, middle ear, mastoid process), sometimes associated with a CSF leak
Through a penetrating wound
After a neurosurgical procedure (eg, if a ventricular shunt becomes infected)
Through congenital or acquired defects in the skull or spine
Having any of the above conditions increases the risk of acquiring meningitis. 

Immune status: Overall, the most common causes in immunocompromised patients are 

S. pneumoniae
L. monocytogenes
Pseudomonas aeruginosa
Mycobacterium tuberculosis
N. meningitidis
Gram-negative bacteria

Symptoms and Signs
In most cases, bacterial meningitis begins with 3 to 5 days of insidiously progressive nonspecific symptoms including malaise, fever, irritability, and vomiting. However, meningitis may be more rapid in onset and can be fulminant, making bacterial meningitis one of the few disorders in which a previously healthy young person may go to sleep with mild symptoms and never awaken.

Typical meningeal symptoms and signs include fever, tachycardia, headache, photophobia, changes in mental status (eg, lethargy, obtundation), nuchal rigidity (although not all patients report it), and sometimes, when Staphylococcus aureus is the cause, back pain.

Kernig's sign 
• An indication of meningitis in which complete extension of the leg at the knee is impossible when the individual lies on the back and flexes the thigh at a right angle to the axis of the trunk.

Brudzinski's sign
• An indication in which passive flexion of the neck causes flexion of the legs.

Seizures occur early in up to 40% of children with acute bacterial meningitis and may occur in adults. Up to 12% of patients present in coma. Severe meningitis may cause papilledema, but papilledema may be absent early, even when ICP is increased.

Accompanying systemic infection by the organism may cause rashes, petechiae, or purpura (which suggest meningococcemia); pulmonary consolidation (often in meningitis due to S. pneumoniae); or heart murmurs (which suggest endocarditis—eg, often caused by S. aureus or S. pneumoniae).

Blood Cultures
CSF analysis via Lumbar Puncture
As soon as acute bacterial meningitis is suspected, blood cultures and lumbar puncture for CSF analysis (unless contraindicated) are done. If the patient is very ill, antibiotics are given immediately. The need for confirmation should not delay treatment.

Clinicians should suspect bacterial meningitis in patients with typical symptoms and signs, usually fever, changes in mental status, and nuchal rigidity. However, clinicians must be aware that symptoms and signs are different in neonates and infants and may be absent or initially mild in the elderly, alcoholics, and immunocompromised patients. Diagnosis can be challenging in patients who have had a neurosurgical procedure (because such procedures can also cause changes in mental status and neck stiffness) and in the elderly and alcoholics (because changes in mental status may be due to falls and subdural hematomas).

Because untreated bacterial meningitis is lethal, tests should be done if there is even a small chance of meningitis. Testing is particularly helpful in infants, the elderly, alcoholics, immunocompromised patients, and patients who had neurosurgical procedure because symptoms may be atypical.

If findings suggest acute bacterial meningitis, routine tests include

• CSF analysis
• CBC and differential
• Metabolic panel
• Blood cultures plus PCR (if available)
• Lumbar puncture: Unless contraindicated, lumbar puncture is done immediately to obtain CSF for analysis, the mainstay of diagnosis. 

Contraindications to immediate lumbar puncture are signs suggesting markedly increased ICP or a mass; typically, these signs include focal deficits, papilledema, deterioration in consciousness, and seizures. In such cases, lumbar puncture may cause brain herniation and thus is deferred until neuroimaging (typically contrast-enhanced CT or MRI) is done to check for increased ICP or a mass. When lumbar puncture is deferred, treatment is best begun immediately (after blood sampling for culture and before neuroimaging). After ICP, if increased, has been lowered or if no mass is detected, lumbar puncture can be done. 

CSF should be sent for analysis: cell count, protein, glucose, Gram staining, culture, PCR (if available), and other tests as indicated clinically. Simultaneously, a blood sample should be drawn and sent to have the CSF:blood glucose ratio determined.

Typical CSF findings in bacterial meningitis include increased pressure, fluid that is often turbid, a high WBC count (consisting predominantly of PMNs), elevated protein, and a low CSF:blood glucose ratio. A CSF glucose level of ≤ 18 mg/dL or a CSF:blood glucose ratio of < 0.23 strongly suggests bacterial meningitis.

• Antibiotics
Antibiotics are the mainstay of therapy. In addition to antibiotics, treatment includes measures to decrease brain and cranial nerve inflammation and increased ICP. Most patients are admitted to an ICU.

Antibiotics: Antibiotics must be bactericidal for the causative bacteria and must be able to penetrate the blood-brain barrier. 

If patients appear ill and findings suggest meningitis, antibiotics are started as soon as blood cultures are drawn. If lumbar puncture is delayed pending neuroimaging results, treatment begins before neuroimaging. If patients do not appear very ill or have atypical symptoms and the diagnosis is less certain, antibiotics can wait until CSF results are known. 

Appropriate empiric antibiotics depend on the patient's age and immune status and route of infection. In general, clinicians should use antibiotics that are effective against S. pneumoniae, N. meningitidis, and S. aureus. Antibiotic therapy may need to be modified based on results of culture and sensitivity testing. Commonly used antibiotics include 3rd-generation cephalosporins for S. pneumoniae and N. meningitidis, ampicillin for L monocytogenes, and vancomycin for penicillin-resistant strains of S. pneumoniae and for S. aureus. 


A 25-year-old male graduate student develops an acute headache, fever, and rash while visiting his parents during fall break. When he comes to the emergency department he has a widespread petechial rash and a stiff neck, and his blood pressure is 78/40 mm Hg. He is treated with appropriate empiric antibiotics, and the spinal fluid from a tap reveals a large number of polynuclear leukocytes and gram-negative diplococci. What is the most likely diagnosis?

A. Meningitis
B. Lyme Disease
C. Tuberculosis
D. Bells Palsy
E. Sarcoidosis

ANSWER: A. This patient likely has meningitis due to Neisseria meningitidis. 

A 41-year-old woman who had "flu like symptoms" last week comes to the emergency department because of a 48-hour history of " tongue numbness" and "a bit of tingling in her fingertips." A few hours ago she began having trouble moving her mouth and difficulty swallowing because the water would "drool out" of her mouth. She also says that her "eyes feel like they feel when they're dilated." She tells you that she also has "some neck ache and back ache" and pain in her eyes with movement. Her temperature is 38.3 C (101.0 F). Examination shows bilateral lower motor neuron seventh nerve palsy, absent gag bilaterally, slow and weak tongue movement, and decreased taste bilaterally. She complains of pain and attempts to resist motion when you try to flex her neck as she is lying on her back and when you flex her left leg at the hip and try to straighten her knee. Routine laboratory studies and a CT scan of the head are normal. The most appropriate next step in management is to

A. get an MRI of the head
B. obtain an otolaryngology consult
C. perform a lumbar puncture
D. prescribe acyclovir and prednisone
E. send the patient home to follow up in clinic in 1 month

The correct answer is C. This patient probably has some type of meningitis. Possible etiologies include lyme, tuberculosis, sarcoid, viral, or pharmacologic. Inflammatory cells should be present in the cerebrospinal fluid and specific tests sent. A lumbar puncture can also rule out bacterial meningitis.

A brain MRI (choice A) may be useful, but a lumbar puncture should be done first. An otolaryngology consult (choice B) will probably not be helpful in this case. Acyclovir and prednisone (choice D) may be used to treat an uncomplicated case of unilateral Bell palsy. The patient should not be sent home (choice E) without ruling out infectious meningitis.

A 36-year-old woman comes to the emergency department because of a severe headache. She states that the headache woke her up from sleep 6 hours ago, and was not relieved by aspirin or acetaminophen. She also noticed that she has neck stiffness and that "it hurts" during neck extension and flexion. She was recently diagnosed with Hodgkin's disease, but before that, she was usually "pretty healthy," except for a few urinary tract infections and hypertension. Her temperature is 39.0 C (102.2 F), blood pressure is 130/80 mm Hg, pulse is 75/min, and respirations are 17/min. Physical examination shows nuchal rigidity. Funduscopic examination shows bilateral optic disc swelling. She appears lethargic, has eye tenderness with movement, mild photosensitivity. After blood cultures are obtained the most appropriate next step is to

A. administer ceftriaxone, intravenously
B. order a CT scan of the head
C. order a MR angiogram of the head
D. order an MRI of the head
E. perform a lumbar puncture

The correct answer is A. This patient has the signs and symptoms that are suggestive of meningitis, but she also has papilledema (optic disc swelling), which means that an intracranial mass must be ruled out before performing a lumbar puncture (to reduce the risk for brain herniation). However, empiric antimicrobial therapy should be started before the neuroimaging study so that clinical deterioration does not occur.

A CT scan of the head (choice B) is the appropriate next diagnostic procedure in this patient with suspected meningitis and papilledema, but it should be done only after empiric antimicrobial therapy is started. A mass lesion must be ruled out with the CT, but also this patient may have a subarachnoid hemorrhage in which case a CT scan is also indicated (usually before the lumbar puncture).

An MR angiogram (choice C) is sometimes used later on in the evaluation of the patient with papilledema, after a CT scan and MRI have ruled out a brain tumor, to evaluate the patient for an arteriovenous shunt or a dural venous sinus occlusion.

An MRI of the head (choice D) is part of the evaluation of papilledema, however in this patient with suspected meningitis, an empiric antibiotic should be given before any diagnostic procedure is performed.

A lumbar puncture (choice E) is the most important study to evaluate meningitis, however this patient has papilledema (optic disc swelling), and therefore a CT scan must be performed to rule out a mass lesion. Antibiotics should be initiated even before the CT scan, to prevent even further clinical deterioration if the patient does have meningitis. This patient may also have a subarachnoid hemorrhage, which sometimes requires an LP after a CT scan to establish the diagnosis.
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Schizophrenia is characterized by psychosis (loss of contact with reality), hallucinations (false perceptions), delusions (false beliefs), disorganized speech and behavior, flattened affect (restricted range of emotions), cognitive deficits (impaired reasoning and problem solving), and occupational and social dysfunction. The cause is unknown, but evidence for a genetic component is strong. Symptoms usually begin in adolescence or early adulthood. One or more episodes of symptoms must last ≥ 6 mo before the diagnosis is made. Treatment consists of drug therapy, psychotherapy, and rehabilitation.

Worldwide, the prevalence of schizophrenia is about 1%. The rate is comparable among men and women and relatively constant cross-culturally. The rate is higher among lower socioeconomic classes in urban areas, perhaps because its disabling effects lead to unemployment and poverty. The average age at onset is early to mid 20s in women and somewhat earlier in men; about 40% of males have their first episode before age 20.

Although its specific cause is unknown, schizophrenia has a biologic basis, as evidenced by alterations in brain structure (eg, enlarged cerebral ventricles, thinning of the cortex, decreased size of the anterior hippocampus and other brain regions) and by changes in neurotransmitters, especially altered activity of dopamine and glutamate.

Neurodevelopmental vulnerability: Vulnerability may result from genetic predisposition; intrauterine, birth, or postnatal complications; or viral CNS infections. Maternal exposure to famine and influenza during the 2nd trimester of pregnancy, birth weight < 2500 g, Rh incompatibility during a 2nd pregnancy, and hypoxia increase risk. 

Although most people with schizophrenia do not have a family history, genetic factors have been implicated. People who have a 1st-degree relative with schizophrenia have about a 10% risk of developing the disorder, compared with a 1% risk among the general population. Monozygotic twins have a concordance of about 50%.

Environmental stressors: Stressors can trigger the emergence or recurrence of symptoms in vulnerable people. Stressors may be primarily biochemical (eg, substance abuse, especially marijuana) or social (eg, becoming unemployed or impoverished, leaving home for college, breaking off a romantic relationship, joining the military).

Symptoms and Signs
Symptom categories: Generally, symptoms are categorized as 

• Positive: An excess or distortion of normal functions
• Negative: Diminution or loss of normal functions
• Disorganized: Thought disorders and bizarre behavior
• Cognitive: Deficits in information processing and problem solving
Patients may have symptoms from one or all categories. 

Positive symptoms can be further categorized as 

• Delusions
• Hallucinations
Delusions are erroneous beliefs that are maintained despite clear contradictory evidence. In persecutory delusions, patients believe they are being tormented, followed, tricked, or spied on. In delusions of reference, patients believe that passages from books, newspapers, song lyrics, or other environmental cues are directed at them. In delusions of thought withdrawal or thought insertion, patients believe that others can read their mind, that their thoughts are being transmitted to others, or that thoughts and impulses are being imposed on them by outside forces. Delusions in schizophrenia tend to be bizarre—ie, clearly implausible and not derived from ordinary life experiences (eg, believing that someone removed their internal organs without leaving a scar). 

Hallucinations are sensory perceptions that are not perceived by anyone else. They may be auditory, visual, olfactory, gustatory, or tactile, but auditory hallucinations are by far the most common. Patients may hear voices commenting on their behavior, conversing with one another, or making critical and abusive comments. Delusions and hallucinations may be extremely vexing to patients. 

Negative (deficit) symptoms include blunted affect, poverty of speech, anhedonia, and asociality. With blunted affect, the patient's face appears immobile, with poor eye contact and lack of expressiveness. Poverty of speech refers to decreased speech and terse replies to questions, creating the impression of inner emptiness. Anhedonia may be reflected by a lack of interest in activities and increased purposeless activity. Asociality is shown by a lack of interest in relationships. Negative symptoms often lead to poor motivation and a diminished sense of purpose and goals. 

Disorganized symptoms: which can be considered a type of positive symptom, involve thought disorders and bizarre behaviors. Thinking is disorganized, with rambling, non–goal-directed speech that shifts from one topic to another. Speech can range from mildly disorganized to incoherent and incomprehensible. Bizarre behavior may include childlike silliness, agitation, and inappropriate appearance, hygiene, or conduct. Catatonia is an extreme behavior that can include maintaining a rigid posture and resisting efforts to be moved or engaging in purposeless and unstimulated motor activity. 

Cognitive deficits: include impairment in attention, processing speed, working memory, abstract thinking, problem solving, and understanding of social interactions. The patient's thinking may be inflexible, and the ability to problem solve, understand the viewpoints of other people, and learn from experience may be diminished. Severity of cognitive impairment is a major determinant of overall disability. 

Suicide: About 5 to 6% of patients with schizophrenia commit suicide, and about 20% attempt it; many more have significant suicidal ideation. Suicide is the major cause of premature death among people with schizophrenia and explains, in part, why on average the disorder reduces life span by 10 yr. Risk may be especially high for young men with schizophrenia and substance abuse. Risk is also increased in patients who have depressive symptoms or feelings of hopelessness, who are unemployed, or who have just had a psychotic episode or been discharged from the hospital. Patients who have late onset and good premorbid functioning—the very patients with the best prognosis for recovery—are also at the greatest risk of suicide.

• Combination of history, symptoms, and signs
No definitive test for schizophrenia exists. Diagnosis is based on a comprehensive assessment of history, symptoms, and signs. Information from collateral sources, such as family members, friends, teachers, and coworkers, is often important. The diagnosis requires both of the following:

• ≥ 2 characteristic symptoms (delusions, hallucinations, disorganized speech, disorganized behavior, negative symptoms) for a significant portion of a 1-mo period (symptoms must include at least one of the first 3)
• Prodromal or attenuated signs of illness with social, occupational, or self-care impairments evident for a 6-mo period that includes 1 mo of active symptoms
• Psychosis due to other medical disorders or substance abuse must be ruled out by history and examination that includes laboratory tests and neuroimaging. Although some patients with schizophrenia have structural brain abnormalities present on imaging, these abnormalities are insufficiently specific to have diagnostic value.

• Antipsychotic drugs
• Rehabilitation, including community support services
• Psychotherapy

Drugs are divided into conventional antipsychotics and 2nd-generation antipsychotics (SGAs) based on their specific neurotransmitter receptor affinity and activity.

Conventional antipsychotics (eg: Haloperidol, Thioridazine): These drugs act primarily by blocking the dopamine receptor (dopamine blockers). Extrapyramidal symptoms (EPS) include:

• Acute Dystonia - is an extrapyramidal movement disorder that occurs in the first few hours or days of treatment with an antipsychotic medication. Patients develop muscle spasms or stiffness (e.g., torticollis, trismus), tongue protrusions and twisting, opisthotonos (great rigid spasm of the body, with the back fully arched and the heels and head bent back), and oculogyric crisis (forced sustained deviation of the head and eyes). Treat with antihistamines (e.g., diphenhydramine) or anticholinergics (e.g., benztropine, trihexyphenidyl). Benztropine is often given as an IM injection.

• Akathisia - occurs in the first few days of treatment. The patient has a subjective feeling of restless and may pace constantly, alternate sitting and standing, and be unable to sit still. Treat with beta blockers or benzodiazepines (e.g., lorazepam).

• Parkinsonism - Parkinsonism usually occurs in patients taking antipsychotics within the first few months of treatment. The patient develops stiffness, cogwheel rigidity, shuffling gait, mask-like facies and drooling.  Treat with antihistamines (e.g., diphenhydramine) or anticholinergics (e.g., benztropine, trihexyphenidyl).

• Tardive Dyskinesia - Most commonly the patient develops abnormal involuntary movements usually involve orofacial muscles. The perioral movements (darting, protruding movements of the tongue, chewing, grimacing, puckering). There is no known treatment for tardive dyskinesia. Options are to discontinue the current antipsychotic and consider switching to clozapine or risperidone.

Second-generation antipsychotics (eg. Clozapine, Risperidone): SGAs block dopamine receptors more selectively than conventional antipsychotics, decreasing the likelihood of extrapyramidal (motor) adverse effects. Although greater binding to serotonergic receptors was initially thought to contribute to the efficacy of SGAs, studies suggest this binding is unrelated to efficacy or adverse effect profile.


A 36-year-old man is admitted to the hospital for acute management of his schizophrenia. He is a homeless man that you often see hanging out around the neighborhood. He has had multiple hospitalizations over the past 5 years and they usually occur when he stops taking his medications. He usually believes that his dead cousin speaks directly to him through fire hydrants and that she tells him that he does not need to take any medication. Unfortunately, she is the only person that he listens to. You are called to see him because you have treated him many times in the past. When you get to the floor, the nurse tells you that you should be careful when you enter the room because orders for the medication have not been written yet. You hear howling as you are talking to the nurse and when you get to his room you see that he is kneeling at the window "howling at the moon." He becomes angry and violent when you try to enter his room. You go back to the nurse station and tell her to give him an injection of haloperidol and diazepam. In addition, at this time you should

A. begin psychosocial treatment with behavior skills training
B. give dantrolene to prevent neuroleptic malignant syndrome
C. prescribe benztropine to prevent parkinsonian-like symptoms
D. prescribe clozapine to treat his negative symptoms

The correct answer is C. In acute psychiatric emergencies, a neuroleptic agent (haloperidol) and a benzodiazepine (diazepam) are typically given to control the patient and aid in sedation. An anticholinergic agent, such as benztropine, should be added to prevent parkinsonian-like symptoms (rigidity and akinesia) that may occur in patients treated with high-potency antipsychotic agents (haloperidol).

In this acute situation, it is inappropriate to begin psychosocial treatment with behavior skills training (choice A). Psychosocial treatment, including behavior skills training, multi-family groups, vocational training, and workshops, is very important in the long-term management of schizophrenia. During the patient's hospitalization, after the patient is stabilized, the treatment plan should focus on practical issues, and set the stage for outpatient psychosocial issues.

Dantrolene is the treatment for neuroleptic malignant syndrome (choice B), which may be caused by high-potency antipsychotic agents (haloperidol). It is not routinely given to prevent this condition. NMS is associated with a high fever, autonomic instability, rigidity, behavioral changes, and laboratory abnormalities such as elevated white blood cell count, creatine kinase, and abnormal liver function tests.

Clozapine (choice D) is used as a second-line antipsychotic agent for patients who do not respond to the typical antipsychotic medications and have prominent negative symptoms (flat affect, poverty of speech, and asociality). It is not typically the first agent given in an acute psychiatric emergency. It is associated with agranulocytosis (1%) and requires weekly monitoring of the white blood cell count.

A 28-year-old woman is brought to the clinic by a friend. She is a corporate attorney but has been missing from work on and off for the past 3 months. Her friends believe that she has been agitated and that her personality has changed. Prior to her absence, her performance at the office had been “slipping.” On examination, she appears disheveled but is alert and oriented. The rest of the examination is normal.

Which of the following conditions likely explains the woman’s symptoms?

A. Major depressive disorder 
B. Drug abuse
C. Brief psychotic disorder 
D. Schizoaffective disorder 
E. Schizophrenia

Which of the following measures is the most important next step?

A. Assess suicide risk
B. Screen for drugs of abuse
C. Obtain a medication list
D. Order a thyroid-stimulating hormone (TSH) level
E. Order chemistries

Which of the following properties is associated with this disorder?

A. Affects approximately 5% of the population 
B. More common in women
C. High levels of TSH
D. More common in lower socioeconomic groups 
E. Has no “season of birth” correlation

Which of the following neurotransmitters/hormones is intimately involved with this disease?

A. Triiodothyronine (T3)  |  B. Serotonin  |  C. Norepinephrine
D. Dopamine hydrochloride  |  E. Acetylcholine chloride

The answers are: E, A, D, D. Schizophrenia is characterized by alterations in perception, thinking, social activity, and affect. This dis- order, which often begins in late adolescence, starts with social withdrawal and perceptual distortions and progresses to a state of delusions and hallucinations. The age of onset is 15 to 25 years for men and 25 to 35 years for women. Presenting symptoms may be positive (delusions, hallucinations) or negative (anhedonia, decreased emotion, impaired concentration, social withdrawal). The more severe the negative symptoms, the poorer the outcome. The four symptom subtypes of schizophrenia are catatonic, paranoid, disorganized, and residual.

The feature of this patient’s presentation that points toward schizophrenia is her previous success and the deterioration that has lasted for more than 6 months. Her agitation, personality change, and lack of interest in her appearance is typical as well. Other disorders may present with psychotic symptoms. However, these should be differentiated from schizophrenia. Schizophreniform disorder satisfies the criteria for schizophrenia, but affected patients have had symptoms for less than 6 months. Schizoaffective disorder is characterized by psychosis resembling schizophrenia but with predominant mood disturbances. Brief psychotic disorder involves the experiencing of a full psychotic episode that is short-lived and often temporally related to a stressor (e.g., pregnancy).

Because individuals with schizophrenia are at high risk for suicide, it is important to assess this patient’s suicide risk. One third of persons with schizophrenia attempt suicide; 10% are successful. Risk factors for suicide include male gender, age older than 30 years, and recent hospital discharge. All of the other choices in Question 16 represent appropriate measures in the evaluation of the patient. However, the most emergent issue and the one that will alter the therapy is determination of the likelihood that this patient will commit suicide.

Schizophrenia affects 1% of the population. There is no significant gender difference in prevalence of disease. It is diagnosed disproportionately among the lower socioeconomic classes. More individuals with schizophrenia are born during cold weather months. In addition, dopamine appears to be directly associated with schizophrenia. Dopamine receptor blockers are useful in its treatment. As yet, there is no evidence that other neurotransmitters play a therapeutic role.
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Tinea Versicolor
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Tinea versicolor is skin infection with Malassezia furfur that manifests as multiple asymptomatic scaly patches varying in color from white to tan to brown to pink. Diagnosis is based on clinical appearance and potassium hydroxide wet mount of skin scrapings. Treatment is with topical or sometimes oral antifungals. Recurrence is common.

Malassezia furfur is a dimorphic fungus that is normally a harmless component of normal skin flora but that in some people causes tinea versicolor. Most affected people are healthy. Factors that may predispose to tinea versicolor include heat and humidity and immunosuppression due to corticosteroids, pregnancy, undernutrition, diabetes, or other disorders. Hypopigmentation in tinea versicolor is due to the inhibition of tyrosinase caused by M. furfur production of azelaic acid.

Symptoms and Signs
Tinea versicolor usually is asymptomatic. Classically, it causes the appearance of multiple tan, brown, salmon, pink, or white scaling patches on the trunk, neck, abdomen, and occasionally face. The lesions may coalesce. In light-skinned patients, the condition is often diagnosed in summer months because the lesions, which do not tan, become more obvious against tanned skin. Tinea versicolor is benign and is not considered contagious.

• Clinical appearance
• Potassium hydroxide wet mount
• Sometimes Wood light examination

Diagnosis is based on clinical appearance and by identification of hyphae and budding cells (“spaghetti and meatballs”) on potassium hydroxide wet mount of fine scale scrapings. A Wood light examination reveals golden-white fluorescence.

• Topical antifungals
• Sometimes oral antifungals
• Treatment is any topical antifungal drug. Examples include selenium sulfide shampoo 2.5% (in 10-min applications daily for 1 wk or 24-h applications weekly for 1 mo); topical azoles (eg, ketoconazole 2% daily for 2 wk); and daily bathing with zinc pyrithione soap 2% or sulfur-salicylic shampoo 2% for 1 to 2 wk.

Oral treatment is indicated for patients with extensive disease and those with frequent recurrences. Two convenient regimens are a single 400-mg dose of ketoconazole or fluconazole 150 mg/wk for 2 to 4 wk.

Hypopigmentation from tinea versicolor is reversible in months to years after the yeast has cleared. Recurrence is almost universal after treatment because the causative organism is a normal skin inhabitant. Fastidious hygiene, regular use of zinc pyrithione soap, or once-monthly use of topical antifungal therapy lowers the likelihood of recurrence.

Key Points
• Although tineaversicolor can occur in immunosuppressed patients, most affected patients are healthy.
• The disorder is frequently diagnosed in the summer, but mainly because hypopigmented lesions become more obvious against tanned skin.
• Try to confirm the diagnosis by finding hyphae and budding cells on potassium hydroxide wet mount of fine scale scrapings.
• Treat with topical or oral antifungals.


A 29-year-old man comes to the office because of a recurrent rash that worsens in the summer season and recurs more frequently with humid weather. Usually the rash involves his upper back and occasion spreads to the shoulders and proximal arms. It is occasionally pruritic. Physical examination shows multiple hypopigmented oval macules and patches on his upper back. His hands and feet are not involved and all nails appear normal. You examine scrapings of the scale with potassium hydroxide under the microscope and find numerous short hyphae with multiple round spores in clumps. You should tell the patient that he has

A. tinea corporis and should be treated with oral terbinafine
B. tinea corporis and should be treated with topical ketoconazole
C. tinea corporis and should be treated with topical terbinafine
D. tinea versicolor and should be treated with oral terbinafine
E. tinea versicolor and should use ketoconazole shampoo

The correct answer is E. This patient has tinea versicolor and he should be treated with ketoconazole shampoo. Tinea versicolor, also known as pityriasis versicolor, usually presents on the upper trunk and extends onto the upper arms, finely scaling, guttate, or nummular patches appear, particularly on young adults who perspire freely. The individual patches are yellowish or brownish macules in pale skin or hypopigmented macules in dark skin, with delicate scaling. Mild itching and inflammation may be present. This common disease is most prevalent in the tropics, where there is high humidity, high temperatures and frequent exposure to sunlight. The fungus is easily demonstrated in scrapings of the scales. Microscopically, there are short, thick fungal hyphae and large numbers of variously sized spores. This combination is commonly referred to as "spaghetti and meatballs". Treatment is accomplished with topical imidazoles, oral ketoconazole, or itraconazole. Oral terbinafine (choice D) has been shown to be ineffective.

Tinea corporis (choices A, B, C) are all incorrect, because the lesions described on this young man are not consistent with tinea corporis. Typical tinea corporis lesions (also known as ring worm) are round, erythematous borders with central clearing and superficial scales. The borders tend to be elevated rather than flat.

A 25-year-old man comes to the clinic complaining of an itchy rash for 2-3 weeks on his chest and upper back. He is otherwise healthy and is not taking any medications. On physical examination, there are numerous hypopigmented macules, some coalescing into patches on his chest wall, upper back, and proximal arms bilaterally. There is superficial scaling on some of the lesions, but no erythema or violaceous borders. Wood's lamp on the lesions revealed yellow-white fluorescence. A scraping of the skin with potassium hydroxide, under the microscope, reveals short hyphae with numerous round spores. The correct diagnosis and treatment is

A. erythrasma and topical cleomycin
B. erythrasma and topical ketoconazole
C. tinea corporis and topical terbinafine
D. tinea versicolor and topical cleomycin
E. tinea versicolor and topical ketoconazole

The correct answer is E. Tinea versicolor and topical ketoconazole is the correct answer because this is a common skin disorder caused by Malassezia furfur (also known as Pityrosporum ovale). The disease may occur at any age, but it is much more common during the years of higher sebaceous activity (i.e., adolescence and young adulthood). The lesions begin as multiple small, circular macules of various colors (white, pink, or brown) that enlarge radially. The hypopigmented lesions are caused by alterations in melanosome formation and transfer to keratinocytes. The upper trunk is most commonly affected. Diagnosis is confirmed by potassium hydroxide examination of the scale which shows numerous hyphae that tend to break into short, rod-shaped fragments intermixed with round spores in grapelike clusters, giving the so-called "spaghetti and meatballs" pattern. Wood's light examination shows irregular, pale, yellow-to-white fluorescence that fades with improvement. Treatment includes a a topical selenium sulfide suspension, ketoconazole, zinc pyrithione shampoo, or oral ketoconazole, itraconazole, or fluconazole.

Erythrasma with topical cleomycin (choice A) and erythrasma with topical ketoconazole (choice B) are both incorrect because erythrasma is caused by Corynebacterium species. Therefore, it should not have any hyphae on scraping. It is a disorder characterized by red to brown scaling patches affecting the intertriginous areas such as the groin, submammary regions, axillae, and toe webs. The correct treatment for erythrasma is either topical erythromycin or cleomycin

Tinea corporis(choice C) is incorrect because tinea corporis lesions, also known as ring worm, tend to be round with elevated erythematous borders that have a central clearing and superficial scales. In addition, tinea corporis is usually caused by the Trichophyton species which do not fluoresce with wood's lamp examination.

A middle-aged man presents with a rash on his back. Examination shows multiple, asymptomatic, scaly patches varying from white to brown. The patient states that he notices the condition only in the summer because the lesions do not tan. A potassium hydroxide preparation from a scraping shows spores and nonbranched hyphae. What is the most accurate diagnosis?

A. Candidiasis
B. Tinea versicolor
C. Herpes simplex
D. Tinea capitis
E. Tinea corporis

The answer is B. Tinea versicolor produces confluent, scaling macules on the trunk, and KOH examination shows spores and nonbranched hyphae.

Dermatophyte infection of the body (tinea corporis) typically produces annular lesions that, on potassium hydroxide (KOH) preparation, show branched hyphae. Candidiasis produces pustules that form coalescent areas of erythema, typically in intertriginous areas, and KOH examination shows budding spores. Herpes simplex is a blistering eruption, and a Tzanck smear shows multinucleated giant cells. Tinea capitis is a dermatophyte infection that affects the scalp.
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I sold my 2012 Hyundai Accent today at Village Luxury Cars. The process was explained to me clearly by the sales person Omid Fard. The check was made out to me the same day. Very easy and pleasant experience. Great place to sell your car. They also have a very nice selection of vehicles, if you want to buy.
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