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Raynauds Syndrome 
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Raynaud's syndrome is vasospasm of parts of the hand in response to cold or emotional stress, causing reversible discomfort and color changes (pallor, cyanosis, erythema, or a combination) in one or more digits. 

Raynaud's syndrome is probably due to an exaggerated α2-adrenergic response that triggers vasospasm; the mechanism is not defined.

Primary Raynaud's syndrome is much more common (> 80% of cases) than secondary; it occurs without symptoms or signs of other disorders. In the remaining 20% of patients with Raynaud's symptoms, a causative underlying disease, most commonly systemic sclerosis - a connective tissue disease.

Secondary Raynaud's syndrome accompanies various disorders and conditions, mostly connective tissue disorders 

Nicotine commonly contributes to it but is often overlooked. Raynaud's syndrome may accompany migraine headaches, variant angina, and pulmonary hypertension, suggesting that these disorders share a common vasospastic mechanism.

Symptoms and Signs
Sensations of coldness, burning pain, paresthesias, or intermittent color changes of one or more digits are precipitated by exposure to cold, emotional stress, or vibration. All can be reversed by removing the stimulus. Rewarming the hands accelerates restoration of normal color and sensation.

Color changes are clearly demarcated across the digit. They may be triphasic (pallor, followed by cyanosis and after warming by erythema due to reactive hyperemia), biphasic (cyanosis, erythema), or uniphasic (pallor or cyanosis only). Changes are often symmetric. Raynaud's syndrome does not occur proximal to the metacarpophalangeal joints; it most commonly affects the middle 3 fingers and rarely affects the thumb. Vasospasm may last minutes to hours but is rarely severe enough to cause tissue loss.

Raynaud's syndrome secondary to a connective tissue disorder may progress to painful digital gangrene; Raynaud's syndrome secondary to systemic sclerosis tends to cause extremely painful, infected ulcers on the fingertips.

Diagnosis
Clinical criteria
Examination and testing for underlying disorder
Raynaud's syndrome itself is diagnosed clinically. Acrocyanosis also causes color change of the digits in response to cold but differs from Raynaud's in that it is persistent, not easily reversed, and does not cause trophic changes, ulcers, or pain.

Primary and secondary forms are distinguished clinically, supported by vascular laboratory studies and blood testing. Vascular laboratory testing includes digital pulse wave forms and pressures. The primary blood testing is the panel for collagen vascular diseases.

Clinical findings: A thorough history and physical examination directed at identifying a causative disorder are helpful but rarely diagnostic.

Findings suggesting primary Raynaud's syndrome are the following:

Age at onset < 40 (in 2/3 of cases)
Mild symmetric attacks affecting both hands
No tissue necrosis or gangrene
No history or physical findings suggesting another cause
Findings suggesting secondary Raynaud's syndrome are the following:

Age at onset > 30
Severe painful attacks that may be asymmetric and unilateral
Ischemic lesions
History and findings suggesting an accompanying disorder
Laboratory testing: Blood tests (eg, measurement of ESR, antinuclear antibodies, rheumatoid factor, anticentromere antibody, anti-SCL-70 antibody) are done to detect accompanying disorders.

Treatment
Trigger avoidance
Smoking cessation
Ca channel blockers or prazosin

Treatment of the primary form involves avoidance of cold, smoking cessation, and, if stress is a triggering factor, relaxation techniques (eg, biofeedback) or counseling. Drugs are used more often than behavioral treatments because of convenience. Vasodilating Ca channel blockers (extended-release nifedipine 60 to 90 mg po once/day, amlodipine 5 to 20 mg po once/day, felodipine 2.5 to 10 mg po bid, or isradipine 2.5 to 5 mg po bid) are most effective, followed by prazosin 1 to 5 mg po once/day or bid. 

Treatment of the secondary form focuses on the underlying disorder. 

VIGNETTES:

A young woman presents to her family physician with complaints of numbness, tingling, and burning of her fingers. She states that these symptoms are typically accompanied by "blanching" of her fingertips until they are nearly blue, followed by reddening as the episode resolves. The condition described is the initial presenting complaint in over 70% of patients with which of the following diseases?

A. Colonic polyposis
B. Congestive heart failure
C. Goodpasture's syndrome
D. Rheumatoid arthritis
E. Scleroderma

The correct answer is E. The finger color changes and pain are manifestations of Raynaud's phenomenon, which is often idiopathic, but can be related to many connective tissue diseases, notably progressive systemic sclerosis, also known as scleroderma (the initial complaint in over 70% of patients).

A 47 year old white female presents with severe Raynaud's phenomenon, dysphagia, sclerodactyly, and facial and palmar telangiectasias. Which of the following autoantibodies is most likely to be present in this patient?

A. Anti-centromere antibody
B. Anti-histone antibody
C. Anti-SS-A
D. Anti-SS-B
E. Rheumatoid factor

The correct answer is A. The symptoms described in the question are classic for CREST syndrome. CREST syndrome is the combination of calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia. Anti-centromere antibodies are reported in a high percentage of patients with CREST, but in a small percentage of pure scleroderma patients.
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Deep Venous Thrombosis (DVT) 
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Deep venous thrombosis (DVT) is clotting of blood in a deep vein of an extremity (usually calf or thigh) or the pelvis. DVT is the primary cause of pulmonary embolism. 

DVT occurs most commonly in the lower extremities. Lower extremity DVT is much more likely to cause pulmonary embolism (PE). The superficial femoral and popliteal veins in the thighs and the posterior tibial and peroneal veins in the calves are most commonly affected. About 50% of patients with DVT have occult PE, and at least 30% of patients with PE have demonstrable DVT.

Etiology: Virchow's Triad: Stasis, Endothelial Damage, Hypercoagulabiity

Stasis - venous stasis, prolonged immobility (as on a long plane or car ride, bed bound during hospitalization) and varicose veins. 

Endothelial injury or vessel wall injury - injuries and/or trauma to endothelium

Hypercoagulability (excessively easy clotting of blood) - hyperviscosity, deficiency of antithrombin III, protein C or S deficiency, Leiden V factor.

Cigarette smoking, Hormonal contraceptives, Cancer and pregnancy are also a risk factors for DVT.

Symptoms: Most deep vein thrombi occur in the small calf veins. Symptoms include vague aching pain, tenderness along the distribution of the veins, edema, erythema.
Dilated collateral superficial veins may become visible or palpable. Calf discomfort elicited by ankle dorsiflexion with the knee extended (Homans sign) occasionally occurs with distal leg DVT.

If Pulmonary Embolism (PE) occurs, symptoms may include shortness of breath and pleuritic chest pain.

Diagnosis
Lower Extremity Venous Doppler Ultrasound
Sometimes d-dimer testing
Diagnosis is typically by ultrasonography with Doppler flow studies (duplex ultrasonography). The need for additional tests (eg, d-dimer testing) and their choice and sequence depend on pretest probability and sometimes ultrasonography results. 

Ultrasonography: Ultrasonography identifies thrombi by directly visualizing the venous lining and by demonstrating abnormal vein compressibility or, with Doppler flow studies, impaired venous flow. The test is > 90% sensitive and > 95% specific for femoral and popliteal vein thrombosis but is less accurate for iliac or calf vein thrombosis.

d-Dimer: d-Dimer is a byproduct of fibrinolysis; elevated levels suggest recent presence and lysis of thrombi. d-Dimer assays vary in sensitivity and specificity; however, most are sensitive and not specific.

If symptoms and signs suggest PE, additional imaging (eg, ventilation/perfusion [V/Q] scanning or CT pulmonary angiography) is required.

Treatment
Anticoagulation

All patients with DVT are given anticoagulants, initially an injectable heparin (unfractionated or low molecular weight), followed by warfarin started within 24 to 48 h. Inadequate anticoagulation in the first 24 to 48 h may increase risk of recurrence or PE. 

In addition, elevation of legs (supported by a pillow or other soft surface to avoid venous compression) is recommended during periods of inactivity. 

LMWHs (eg, enoxaparin) are the initial treatment of choice because they can be given on an outpatient basis. 

Treatment is continued until full anticoagulation is achieved with warfarin. 

Duration of treatment varies. Patients with transient risk factors for DVT (eg, immobilization, surgery) can usually stop taking warfarin after 3 to 6 mo. Patients with nonmodifiable risk factors (eg, hypercoagulability), idiopathic (or unprovoked) DVT with no known risk factors, or recurrent DVT should take warfarin for at least 6 months and, in selected patients, probably for life unless complications occur.

Inferior vena cava filter (IVCF): An IVCF may help prevent PE in patients with lower extremity DVT who have contraindications to anticoagulant therapy or in patients with recurrent DVT (or emboli) despite adequate anticoagulation. An IVCF is placed in the inferior vena cava just below the renal veins via catheterization of an internal jugular or femoral vein. IVCFs reduce risk of acute embolic complications but can have longer-term complications (eg, venous collaterals can develop, providing a pathway for emboli to circumvent the IVCF, and increased risk of recurrent DVT). 

Prevention of DVT includes Prevention of immobility, Anticoagulation (eg, LMWH, warfarin), Intermittent pneumatic compression and IVCF.

Patients at low risk of DVT (eg, those who are undergoing minor surgery but have no clinical risk factors for DVT, those who must be temporarily inactive for long periods, as during an airplane flight) should be encouraged to walk or otherwise move their legs periodically; no medical treatment is needed. Dorsiflexion 10 times/h is probably sufficient.

Patients at higher risk of DVT (eg, those undergoing minor surgery if they have clinical risk factors for DVT; those undergoing major surgery, especially orthopedic surgery, even without risk factors; bedbound patients with major medical illnesses) require additional preventive treatment. Most of these patients can be identified and should receive DVT prophylaxis. Hospitalization itself is not considered a risk factor, and hospitalized patients not in one of these categories do not require routine DVT prophylaxis.

Intermittent pneumatic compression (IPC) uses a pump to cyclically inflate and deflate hollow plastic leggings, providing external compression to the lower legs and sometimes thighs. IPC may be used instead of or in combination with anticoagulants after surgery. IPC is recommended for patients undergoing surgery associated with a high risk of bleeding in whom anticoagulant use may be contraindicated. IPC is probably more effective for preventing calf than proximal DVT. IPC is contraindicated in some obese patients who may be unable to apply the devices properly.

The benefit of graded compression stockings is questionable except for low-risk surgical patients and selected hospitalized medical patients. However, combining stockings with other preventive measures may be more protective than any single approach.

VIGNETTES:

A 39 year old very healthy and functional woman is scheduled to undergo a right total hip replacement after she suffered a femoral head fracture 2 days ago during a fall while climbing a flight of stairs. She has no significant past medical history and takes no routine medications. She is scheduled to have her operation in the morning and you are called as a medicine consult to make any appropriate recommendations. Postoperatively, this patient is at greatest risk for developing

A. atrial fibrillation
B. confusion
C. a deep venous thrombosis
D. a myocardial infarction
E. a pulmonary embolism

The correct answer is C. Risk factors for deep venous thromboses (DVT) are both heritable as well as environmental. Among the latter, certain situations such as pregnancy, trauma, prolonged immobilization, orthopedic and certain neurosurgical procedures are associated with the greatest short-term risk. For this patient, with the risks of the fracture and the surgery being additive, some estimates place her risk of DVT at greater than 80%.

A 76 year old man is admitted to the medical ward 3 days status post subdural hematoma drainage, C3 cervical spine fracture, and fixation of multiple extremity fractures sustained in a motor vehicle accident. The patient is now awake and oriented to person, place, and time, but is a lower cervical spine incomplete quadriplegic. Physical examination reveals some minimal sensation in the legs, but no ability to move the extremities. There is a Foley catheter in place that is draining yellow colored urine. Doppler ultrasonography demonstrates a thrombus in the left popliteal vein. The most important next step in the management of this patient is

A. daily Doppler ultrasonography of the lower extremities
B. inferior vena cava filter placement
C. subcutaneous heparin
D. tissue plasminogen activator thrombolysis
E. warfarin

The correct answer is B. This patient has documented deep venous thrombosis (DVT) on ultrasonography and has had recent intracranial surgery. Intracranial surgery is an absolute contraindication to anticoagulation. Because the patient has a documented DVT, an inferior vena cava filter is necessary to prevent potentially fatal pulmonary emboli.

A 31 year old truck man is transferred to the general medical floor from the intensive care unit where he was being treated after sustaining multiple fractures from a motor vehicle accident. It is determined that the patient was under the influence of alcohol at the time of the accident. He has been in the intensive care unit for 20 days following open reduction and internal fixation of bilateral femur, tibia, and fibula fractures. The patient is otherwise doing well and has full use of his upper body. Legal proceedings will begin subsequent to discharge, and the patient states he is committed to ceasing alcohol consumption. Past medical history is significant for alcoholism. Medications include imipenem and morphine administered via patient-controlled analgesic pump. At this time, the patient is at greatest risk for

A. alcohol withdrawal
B. deep venous thrombosis
fat emboli to lungs
D. narcotic addiction from the morphine
E. suicide

The correct answer is B. This patient is profoundly immobile due to multiple fractures of both legs and he is at increased risk for developing a thrombus in the veins of his lower extremities. Deep venous thrombosis (DVT) prophylaxis with subcutaneous heparin should already have been started. DVT prophylaxis is necessary in all immobile patients, especially those who have sustained major orthopedic injury.
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Spontaneous bacterial peritonitis (SBP) 
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Waterhouse--Friderichsen syndrome (WFS) 
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Waterhouse–Friderichsen syndrome (WFS)

Waterhouse–Friderichsen syndrome (WFS) is defined as adrenal gland failure due to bleeding into the adrenal glands (adrenal gland hemorrhage), caused usually by severe bacterial infection by Neisseria meningitidis (meningococcus).

WFS is the most severe form of meningococcal septicemia. This bacterial infection leads to massive hemorrhage into one or (usually) both adrenal glands. It is characterized by overwhelming meningococcemia leading to massive blood invasion, organ failure, coma, low blood pressure and shock. 
WFS can also lead to disseminated intravascular coagulation (DIC) with widespread purpura, rapidly developing adrenocortical insufficiency and death.

Etiology
Bacteremia with Neisseria meningitidis (Meningococcus) is the underlying cause of WFS.
Other organisms that can cause WFS are:
Pseudomonas aeruginosa, Streptococcus pneumoniae, Mycobacterium tuberculosis, Staphylococcus aureus and Haemophilus influenzae. Cytomegalovirus can cause adrenal insufficiency, especially in the immunocompromised.

Prevention
Routine vaccination against meningococcus is recommended for all 11–18 year olds and people who have poor splenic function (who, for example, have had their spleen removed or who have sickle-cell disease which damages the spleen), or who have certain immune disorders, such as a complement deficiency.

Adrenal Gland Hormones
The outermost layer, the zona glomerulosa is the main site for production of mineralocorticoids, mainly aldosterone, which is largely responsible for the long-term regulation of blood pressure. Aldosterone's effects are on the distal convoluted tubule and collecting duct of the kidney where it causes increased reabsorption of sodium and increased excretion of both potassium.

The zona fasciculata of the adrenal gland is responsible for producing glucocorticoids, such as cortisol in humans. Its primary functions are to increase blood sugar through gluconeogenesis and aid in fat, protein and carbohydrate metabolism.

Symptoms:

The onset of the illness is nonspecific with fever, rigors, vomiting and headache and stiff neck. Soon a rash appears with diffuse petechial and purpuric lesions that can appear across the hands, face and arms.
Low blood pressure (hypotension) is the rule and rapidly leads to septic shock. The cyanosis of extremities can be impressive and the patient is very prostrated or comatose. 


Diagnosis:
Cultures and gran stains from blood and CSF can identify the Neisseria meningitidis (meningococcus) pathogen. Abdominal CT scan is done to show the bilateral adrenal hemorrhages. A random cortisol level also helps to confirm the diagnosis. 
Comprehensive metabolic profile to reveal hypoglycemia with hyponatremia and hyperkalemia which are all consistent with acute adrenal failure and low levels of cortisol and aldosterone.

Thrombocytopenia is sometimes extreme, with alteration in prothrombin time (PT) and partial thromboplastin time (PTT) suggestive of diffuse intravascular coagulation (DIC). Acidosis and acute renal failure can be seen as in any severe sepsis.

Treatment
Antibiotics | Steroids | IV Fluids
Fulminant meningococcemia is a medical emergency and needs to be treated with adequate antibiotics as fast as possible. Penicillin is used used with chloramphenicol as a good alternative in allergic patients. Ceftriaxone is an antibiotic commonly used also. Hydrocortisone can sometimes reverse the hypoadrenal shock. Catecholamines and IV Fluids for maintenance of blood pressure.

VIGNETTES:

A 25 year old summer camp counselor complains of a severe headache and weakness. His condition rapidly deteriorates over a period of hours, and he is airlifted to a nearby hospital. A lumbar puncture is performed and a Gram's stain of spinal fluid reveals gram-negative diplococci. Infection with this organism is also associated with which of the following?

A. Dysentery
B. Erythema chronicum migrans
C. Myocarditis
D. Ophthalmia neonatorum
E. Waterhouse-Friderichsen syndrome

The correct answer is E. The Neisseria are gram-negative diplococci, and have two clinically important species, N. meningitidis and N. gonorrhoeae. N. meningitidis can either cause a sudden, fulminant, life-threatening meningitis or meningococcemia with a vasculitic purpura and disseminated intravascular coagulation. The latter presentation may be complicated by adrenal involvement, precipitating the usually fatal Waterhouse-Friderichsen syndrome with coagulopathy, hypotension, adrenal cortical necrosis, and sepsis. N. gonorrhoeae causes gonorrhea and ophthalmia neonatorum (choice D), a neonatal eye infection.

Classical dysentery (multiple, small-volume stools with blood, mucus, and pus associated with abdominal cramps and tenesmus); (choice A) is caused by Shigella dysenteriae. A similar syndrome can be caused by other bacteria or amoebae as well.

Erythema chronicum migrans (choice B) is the pathognomonic dermatologic manifestation of Lyme disease. This skin lesion consists of an expanding erythematous lesion, with central clearing.

Bacterial myocarditis (choice C) is uncommon, and when it does occur, it usually involves Staphylococcus aureus or Corynebacterium diphtheriae.

A previously healthy 22 year old man comes to his college medical clinic for headaches and low-grade fevers. He is discharged home with the diagnosis of a "viral syndrome" and instructed to get ample rest. Approximately three hours later his roommate calls 911 reporting that his friend is unconscious and not arousable. On arrival the paramedics find a lethargic, febrile man lying on the floor and unresponsive. The patient is stabilized and he is rushed emergently to the local hospital where an abdominal CT scan shows bilateral adrenal hemorrhages. His blood pressure is 80/40 mm Hg and his pulse is 110/min. He appears very ill and continues to be non-responsive. The most appropriate study at this time is a/an

A. Cort-Stim test
B. cortisol level
C. high-dose ACTH stimulation test
D. insulin response test
E. low-dose ACTH stimulation test

The correct answer is B. This patient has bilateral adrenal hemorrhages in the setting of fulminant disseminated Neisseria sepsis. This is called the Waterhouse-Friderichsen Syndrome. The patient therefore almost certainly has acute adrenal insufficiency. In a critically ill patient, a random cortisol level that is low confirms this diagnosis.

A Cort-Stim test (choice A) is a test whereby synthetic ACTH is administered and the cortisol response is measured one hour later. It is more sensitive at detecting adrenal insufficiency but is both too time-consuming and unnecessary in this patient. The threshold for supplying exogenous steroids is very low so all that is needed is a suspicion for insufficiency that a random cortisol level can easily provide.

A high-dose ACTH stimulation test (choice C) or low-dose ACTH stimulation test (choice E) are both very sensitive tests that require 24 hours to perform. They both are useful at quantifying adrenal function so that differentiation between various causes of adrenal insufficiency can be made. However, they are not the most appropriate studies in this acute situation.

The insulin response test (choice D) is another method used to indirectly assess adrenal function but will not be useful in this patient since the goal is rapid direct assessment of her adrenal function.

A 23 year old woman is brought to the emergency department by ambulance. She is accompanied by her roommate who states that the patient developed a fever and some confusion 3 hours before, and approximately 30 minutes ago became unconscious. The roommate reports that the patient was complaining of a stiff neck and headache a few hours before she became ill. The roommate knows of no significant medical history but reports that the patient is a volunteer at a local children's hospital. Initial examination shows the patient to be non-responsive. Her temperature is 40.4 C (104.7 F), blood pressure is 70/40 mm Hg, pulse is 140/min, and respirations are 32/min. There are diffuse petechial and purpuric lesions across the hands, face, and arms. After tracheal intubation, infusion of pressors fails to augment the blood pressure and it remains at 65/35 mm Hg. The most appropriate next step in this patient's care is to

A. begin heparin therapy only
B. give her high-dose corticosteroids, intravenously
C. initiate chest compressions
D. perform a lumbar puncture
E. transfer her to the intensive care unit

The correct answer is B. This patient almost certainly has meningococcal sepsis and Waterhouse-Friderichsen syndrome (meningococcemia and adrenal hemorrhage). These patients require exogenous steroids for acute adrenal insufficiency, although they have not been shown to alter survival outcomes. This is presumably due to the fact that these patients are critically ill and are at grave risk for renal and pulmonary failure, massive coagulopathy, and irreversible septic shock. She requires high doses of intravenous corticosteroids and saline and antibiotics.

A characteristic of all sepsis syndromes is disseminated intravascular coagulation (DIC), a consumptive coagulopathy. This patient also has microangiopathic hemolysis secondary to massive small vessel clotting. The correction of her coagulation disorder requires coagulation factors and resolution of her sepsis. Heparin (choice A) may be necessary, but it should only be used in combination with cryoprecipitate and platelets because it may cause bleeding if given alone.

There is no need to initiate chest compressions (choice C) since the patient has a blood pressure, albeit a very weak one. She is in profound septic shock with concomitant adrenal insufficiency and requires catecholamines and steroids.

There is no need for a lumbar puncture (choice D) since this patient has disseminated disease and blood cultures will certainly reveal the presence of the organism.

It is appropriate to transfer the patient to an intensive care unit (choice E) once her condition is stabilized.
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Celiac Disease 
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Celiac disease is an immunologically mediated disease in genetically susceptible people caused by intolerance to gluten, resulting in mucosal inflammation and villous atrophy, which causes malabsorption. 

Etiology
Celiac disease is a hereditary disorder caused by sensitivity to the gliadin component of gluten, a protein found in wheat; similar proteins are present in rye and barley. In a genetically susceptible person, gluten-sensitive T cells are activated when gluten-derived peptide epitopes are presented. The inflammatory response causes characteristic mucosal villous atrophy in the small bowel.

Epidemiology: Celiac disease mainly affects people of northern European descent. Prevalence estimates based on serologic screens among blood donors (sometimes confirmed by biopsy) indicate the disorder may be present in about 1/300 in Europe, especially in Ireland and Italy, and perhaps 1/250 in some parts of the US. 

The disease affects about 10 to 20% of 1st-degree relatives. Female:male ratio is 2:1. Onset is generally in childhood but may occur later.

Symptoms: the clinical presentation varies; no typical presentation exists. Some patients are asymptomatic or have only signs of nutritional deficiency. Others have significant GI symptoms.

Celiac disease can manifest in infancy and childhood after introduction of cereals into the diet. The child has failure to thrive, apathy, anorexia, pallor, generalized hypotonia, abdominal distention, and muscle wasting. Stools are soft, bulky, clay-colored, and offensive. Older children may present with anemia or failure to grow normally.

In adults, lassitude, weakness, and anorexia are most common. Mild and intermittent diarrhea is sometimes the presenting symptom. Steatorrhea ranges from mild to severe (7 to 50 g of fat/day). Some patients have weight loss, rarely enough to become underweight. Anemia, glossitis, angular stomatitis, and aphthous ulcers are usually seen in these patients. Manifestations of vitamin D and Ca deficiencies (eg, osteomalacia, osteopenia, osteoporosis) are common. Both men and women may have reduced fertility; women may not have menstrual periods.

About 10% of patients have dermatitis herpetiformis, an intensely pruritic papulovesicular rash that is symmetrically distributed over the extensor areas of the elbows, knees, buttocks, shoulders, and scalp. This rash can be induced by a high-gluten diet. Celiac disease is also associated with diabetes mellitus, autoimmune thyroid disease and Down syndrome.

Diagnosis
Serologic markers
Small-bowel biopsy
The diagnosis is suspected clinically and by laboratory abnormalities suggestive of malabsorption. Family incidence is a valuable clue. Celiac disease should be strongly considered in a patient with iron deficiency without obvious GI bleeding.

Confirmation requires a small-bowel biopsy from the second portion of the duodenum. Findings include lack or shortening of villi (villous atrophy), increased intraepithelial cells, and crypt hyperplasia. However, such findings can also occur in tropical sprue, severe intestinal bacterial overgrowth, eosinophilic enteritis, lactose intolerance, and lymphoma.

Because biopsy lacks specificity, serologic markers can aid diagnosis. Anti-tissue transglutaminase antibody (AGA) and anti-endomysial antibody (EMA—an antibody against an intestinal connective tissue protein) have sensitivity and specificity > 90%. These markers can also be used to screen populations with high prevalence of celiac disease, including 1st-degree relatives of affected patients and patients with diseases that occur at a greater frequency in association with celiac disease. If either test is positive, the patient should have a diagnostic small-bowel biopsy. If both are negative, celiac disease is extremely unlikely. 

Other laboratory abnormalities often occur and should be sought. They include anemia (iron-deficiency anemia in children and folate-deficiency anemia in adults); low albumin, Ca, K, and Na; and elevated alkaline phosphatase and PT.

Treatment
Gluten-free diet
Supplements to replace any serious deficiencies
Treatment is a gluten-free diet (avoiding foods containing wheat, rye, or barley). Gluten is so widely used (eg, in commercial soups, sauces, ice creams, hot dogs) that a patient needs a detailed list of foods to avoid. Patients are encouraged to consult a dietitian and join a celiac support group. The response to a gluten-free diet is usually rapid and symptoms resolve in 1 to 2 weeks. Ingesting even small amounts of food containing gluten may prevent remission or induce relapse.

Small-bowel biopsy should be repeated after 3 to 4 months of a gluten-free diet. If abnormalities persist, other causes of villous atrophy (eg, lymphoma) should be considered. Lessening of symptoms and improvement in small-bowel morphology are accompanied by a decrease in AGA and EMA titers.

Supplementary vitamins, minerals may be given, depending on the deficiencies. Mild cases may not require supplementation, whereas severe cases may require comprehensive replacement. For adults, replacement includes ferrous sulfate 300 mg po once/day to tid, folate 5 to 10 mg po once/day, Calcium supplements and any standard multivitamin. 



VIGNETTES:

A 33 year old man presents with weight loss, diarrhea, and flatulence. Jejunal biopsy demonstrates marked atrophy of villi. This patient's condition may improve with removal of which of the following from the diet?

A. Beef
B. Eggs
C. Potatoes
D. Tomatoes
E. Wheat

The correct answer is E. The patient probably has celiac sprue (celiac disease), which is caused by an allergic, immunologic, or toxic reaction to the gliadin component of gluten (from wheat). The symptoms and pathologic changes usually reverse with complete removal of gliadin from the diet. Therapeutic failures are frequently due to hidden wheat in the diet. Patients with celiac disease have an increased risk of developing gastrointestinal lymphoma.

A patient complains of crampy abdominal pain, diarrhea, fatigue, and weight loss over the past 12 months. Each day, she passes 4-5 loose, malodorous stools that float in the toilet. Fecal fat content is increased. A biopsy of duodenal mucosa reveals loss of villi and intraepithelial lymphocytic infiltration; smooth muscle layers appear normal. Which of the following is the most likely diagnosis? 

A. Celiac sprue
B. Irritable bowel syndrome
C. Lactose intolerance
D. Scleroderma

The correct answer is A. Celiac sprue, or gluten-sensitive enteropathy, results from destruction of the intestinal epithelium by antibodies against the gliadin component of gluten (from wheat, oats, barley and rye). It results in flattening of the villi of the small intestine, beginning in the duodenum and gradually involving more distal parts of the small intestine. Enterocytes also show lymphocytic infiltration suggestive of an immune reaction. The loss of surface area for digestion and absorption results in a generalized malabsorption with malnutrition and weight loss. The absorption of iron and folic acid is usually diminished as well. Steatorrhea (fat in the stool) contributes to diarrhea because of an action of colonic bacteria to produce metabolites of the undigested fat that stimulate electrolyte and water secretion. Removal of gluten from the diet will allow the villi to regenerate and restore normal absorptive function.
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Normal Pressure Hydrocephalus
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Normal Pressure Hydrocephalus (NPH) is characterized by gait disturbance, urinary incontinence, dementia, enlarged brain ventricles due to an abnormal accumulation of cerebrospinal fluid (CSF) in the ventricles of the brain, which can cause ventriculomegaly, and normal or slightly elevated CSF pressure.

Normal-pressure hydrocephalus is thought to result from a defect in CSF resorption in arachnoid granulations. This disorder accounts for up to 6% of dementias.

Symptoms and Signs
Most commonly, the gait disturbance is nonspecific unsteadiness and impaired balance, although a magnetic gait (the feet appear to stick to the floor) is considered the characteristic gait disturbance. Dementia may not occur until late in the disorder. The most common early symptoms of dementia are disturbances of executive function and attention; memory tends to become impaired later. Urinary incontinence is common.

Diagnosis
Clinical evaluation
Neuroimaging (CT or MRI)
Sometimes removal of CSF
The classic symptoms (gait disturbance, urinary incontinence, and dementia), even combined, are nonspecific for normal-pressure hydrocephalus, particularly in the elderly. For example, some forms of vascular dementia can cause dementia, gait disturbance, and, less commonly, urinary incontinence. Brain imaging may show ventricular enlargement disproportionate to cortical atrophy; this finding is nonspecific but may support the diagnosis of normal-pressure hydrocephalus.

Lumbar puncture with removal of 30 to 50 mL of CSF can be done as a diagnostic trial. Improvement in gait, continence, and cognition after removal helps confirm the diagnosis, but improvement may not be evident until several hours after removal. Additional CSF may leak out after lumbar puncture, sometimes contributing to neurologic improvement.

Treatment
Sometimes ventriculoperitoneal shunting
Ventriculoperitoneal shunting is useful for patients with acceptable surgical risks. Improvements after lumbar puncture to remove CSF, done during diagnosis, may predict the response to shunting. In several case series (but in no randomized trials), patients improved substantially, typically in gait, continence, and daily functioning, after shunting; improvement in cognition was less common.

VIGNETTES:

A 70 year old man is admitted to the hospital for delirium associated with a urinary tract infection. Upon adequate treatment of the infection, the patient's mental status improves significantly, though he is noted to remain partly disoriented. He also has an impairment in short-term memory, difficulties in naming simple objects, and impaired concentration. His family members confirm an 8 month history of gradual progressive decline in cognitive abilities, which they attribute to old-age. However, the man is no longer able to manage his finances and has gotten lost while driving to the grocery store on two occasions. Prior to discharge from the hospital, the nursing staff reports that the patient continues to have urinary incontinence, though his infection has resolved. He is also noted to have a very unsteady gait, requiring assistance when walking. No other obvious signs or symptoms are present. Which disorder most likely accounts for this patient's dementia?

A. Creutzfeldt-Jakob disease
B. Huntington disease
C. Normal pressure hydrocephalus
D. Parkinson disease
Pick disease

The correct answer is C. Normal pressure hydrocephalus is a potentially reversible cause of dementia that causes gait disturbances (unsteady or shuffling gait), urinary incontinence, and dementia. Enlargement of the ventricles with increased cerebrospinal fluid (CSF) pressure is found, and therapeutic lumbar punctures may significantly improve symptoms.

A 72 year old man comes to clinical attention with progressive memory loss, urinary incontinence, and gait instability. MRI of the brain shows dilatation of the ventricular cavities, while the cerebral cortex appears normal. No infarcts are seen. Repeated lumbar punctures reveal occasional increases in cerebrospinal fluid (CSF) pressure. A biopsy of the frontal cortex demonstrates the absence of neurofibrillary tangles and senile plaques. Which of the following is the most appropriate treatment?

A. Acetylcholinesterase inhibitors such as tacrine
B. Aspirin
C. L-DOPA
D. Ventricular shunt
Vitamin B1 (Thiamine)

The correct answer is D. This is an "interdisciplinary" question, which begins with a clinical scenario and ends by testing your knowledge of pathophysiology and pharmacology. The clinical presentation has the classic triad of memory loss, urinary incontinence, and gait abnormalities characteristic of normal pressure hydrocephalus (recently renamed intermittently raised pressure hydrocephalus). This condition results from intermittent increases in CSF pressure, leading to progressive damage to cerebral white matter and dilatation of the ventricles. No significant cortical atrophy is present. The lack of Alzheimer-related changes in the biopsy and the measurements of CSF pressure support the diagnosis. Relief of CSF pressure can be obtained by placing a ventricular shunt, which usually improves clinical symptomatology.
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Glaucoma 
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Glaucomas are a group of eye disorders characterized by progressive optic nerve damage at least partly due to increased intraocular pressure (IOP). Glaucoma is the 3rd most common cause of blindness worldwide. 

Glaucomas are categorized as open-angle or closed-angle (angle-closure). The “angle” refers to the angle formed by the junction of the iris and cornea at the periphery of the anterior chamber. The angle is where > 98% of the aqueous humor exits the eye via either the trabecular meshwork and Schlemm's canal (the major pathway, particularly in the elderly) or the ciliary body face and choroidal vasculature. 

Pathophysiology
Axons of retinal ganglion cells travel through the optic nerve carrying images from the eye to the brain. Damage to these axons causes ganglion cell death with resultant optic nerve atrophy and patchy vision loss. Elevated IOP (in unaffected eyes, the average range is 11 to 21 mm Hg) plays a role in axonal damage, either by direct nerve compression or diminution of blood flow. 

IOP is determined by the balance of aqueous humor secretion and drainage. Elevated IOP is caused by inhibited or obstructed outflow, not oversecretion. In open-angle glaucoma, IOP is elevated because outflow is inadequate despite an angle that appears unobstructed. In angle-closure glaucoma, IOP is elevated when a physical distortion of the peripheral iris mechanically blocks outflow.

Open Angle Glaucoma

Aqueous humor drainage is inadequate, whereas production by the ciliary body is normal. Identifiable mechanisms for inadequate drainage include developmental anomalies, scarring caused by trauma or infection, and plugging of channels by detached iris pigment (ie, pigment dispersion syndrome) or abnormal protein deposits (eg, pseudoexfoliation syndrome).

Angle-Closure Glaucoma

Angle-closure glaucoma is glaucoma associated with a physically obstructed anterior chamber angle, which may be chronic or, rarely, acute. 

Angle-closure glaucoma is caused by factors that either pull or push the iris up into the angle (ie, junction of the iris and cornea at the periphery of the anterior chamber), physically blocking drainage of aqueous humor (fluid between the lens and cornea) and raising IOP. Elevated IOP damages the optic nerve.

Pathophysiology
Angle closure may be primary (cause is unknown) or secondary to another condition  and can be acute, subacute (intermittent), or chronic.

Primary angle-closure glaucoma: Narrow angles are not present in young people. As people age, the lens of the eye continues to grow. In some but not all people, this growth pushes the iris forward, narrowing the angle. Risk factors for developing narrow angles include Asian ethnicity, hyperopia, family history and advanced age.

In people with narrow angles, the distance between the pupillary iris and the lens is also very narrow. When the iris dilates, forces pull it centripetally and posteriorly causing iris–lens contact, which prevents aqueous from passing between the lens and iris into the anterior chamber (this mechanism is termed pupillary block). Pressure from the continued secretion of aqueous into the posterior chamber by the ciliary body pushes the peripheral iris anteriorly (causing a forward-bowing iris called iris bombe), closing the angle. This closure blocks aqueous outflow, resulting in rapid (within hours) and severe (> 40 mm Hg) elevation of IOP. Because of the rapid onset, this condition is called primary acute angle-closure glaucoma and is an ophthalmic emergency requiring immediate treatment.

Intermittent angle-closure glaucoma occurs if the episode of pupillary block resolves spontaneously after several hours, usually after sleeping supine.

Chronic angle-closure glaucoma occurs if the angle narrows slowly, allowing scarring between the peripheral iris and trabecular meshwork; IOP elevation is slow.

Symptoms and Signs
Acute angle-closure glaucoma: Patients have severe ocular pain and redness, decreased vision, colored halos around lights, headache, nausea, and vomiting. The systemic complaints may be so severe that patients are misdiagnosed as having a neurologic or GI problem. Examination typically reveals conjunctival hyperemia, a hazy cornea, a fixed mid-dilated pupil, and anterior chamber inflammation. Vision is decreased. IOP is usually 40 to 80 mm Hg. The optic nerve is difficult to visualize because of corneal edema, and visual field testing is not done because of discomfort.

Chronic angle-closure glaucoma: This type of glaucoma manifests similarly to open-angle glaucoma. Some patients have ocular redness, discomfort, blurred vision, or headache that lessens with sleep (perhaps because of sleep-induced miosis and posterior displacement of the lens by gravity). On gonioscopy, the angle is narrow, and peripheral anterior synechiae (PAS) may be seen. IOP may be normal but is usually higher in the affected eye.

Diagnosis
Acute: Measurement of IOP and clinical findings
Chronic: Gonioscopy showing peripheral anterior synechiae and characteristic optic nerve and visual field abnormalities
Diagnosis of acute angle-closure glaucoma is clinical and by measurement of IOP. Gonioscopy may be difficult to do in the involved eye because of a clouded cornea with friable corneal epithelium. However, examination of the other eye reveals a narrow or occludable angle. If the other eye has a wide angle, a diagnosis other than primary angle-closure glaucoma should be considered.

Diagnosis of chronic angle-closure glaucoma is based on the presence of PAS on gonioscopy and characteristic optic nerve and visual field changes.

Treatment
Acute: Timolol, pilocarpine, and apraclonidine drops and a systemic osmotic drug followed promptly by laser peripheral iridotomy
Chronic: Similar to primary open-angle glaucoma except that laser peripheral iridotomy may be done if the clinician feels that the procedure may slow mechanical closing of the angle

Acute angle-closure glaucoma: Treatment must be initiated immediately because vision can be lost quickly and permanently. The patient should receive several drugs at once. A suggested regimen is timolol 0.5% one drop q 30 min for 2 doses; pilocarpine 2 to 4% one drop q 15 min for the first 1 to 2 h; and an osmotic agent, such as mannitol 1.0 to 1.5 mg/kg IV, or isosorbide 100 g po. Response is evaluated by measuring IOP.

Definitive treatment is with laser peripheral iridotomy (LPI), which opens another pathway for fluid to pass from the posterior to the anterior chamber, breaking the pupillary block. 

Chronic angle-closure glaucoma: Patients with chronic, subacute, or intermittent angle-closure glaucoma should also have LPI. Additionally, patients with a narrow angle, even in the absence of symptoms, should undergo prompt LPI to prevent angle-closure glaucoma.

The drug and surgical treatments are the same as with open-angle glaucoma. Laser trabeculoplasty is relatively contraindicated if the angle is so narrow that additional PAS may form after the laser procedure.

VIGNETTES:

A 59 year old man comes to the emergency department because of a severe headache. The headache came on suddenly as he was leaving the light show at the planetarium. He also has right eye pain and nausea and he vomited twice during the car ride over to the hospital. He has no significant past medical history. He has had other headaches in the past, but has never experienced anything like this. His temperature is 36.7 C (98.0 F), blood pressure is 130/90 mm Hg, pulse is 75/min, and respirations are 18/min. Physical examination shows a tender red right eye with a partially dilated pupil, but is otherwise unremarkable. The most appropriate next step is to

A. administer glucocorticoids, intravenously
B. administer sumatriptan, intramuscularly
C. give him oxygen therapy, 100% for 15 minutes
D. measure intraocular pressure
E. order a CT scan of the head

The correct answer is D. This patient with a headache and a red eye either has acute glaucoma or a cluster headache. The partially dilated pupil is more consistent with acute glaucoma. Acute glaucoma, which is caused by increased intraocular pressure, often presents with abdominal pain, nausea, vomiting, and a headache. It is an ophthalmologic emergency that may lead to blindness, so this diagnosis should be included in your differential when a patient presents with these other symptoms. The patient usually has eye pain, but it may be overshadowed by the other symptoms. The diagnosis is established by measuring intraocular pressure. You should call for an immediate ophthalmologic consultation and possibly administer acetazolamide, topical beta blockers, mannitol, and pilocarpine. A cluster headache is an episodic headache that typically presents with a few short headaches a day for a few weeks that is associated with periorbital pain, reddening of the eye, and lacrimation. 

A 45 year old woman is brought to the emergency department by her husband because of an "excruciatingly painful left eye." They were at the movies when she began to complain of blurry vision, a severe headache, and she had to run to the restroom to throw-up. The pain "settled into her eye" on the ride over to the hospital. She is now complaining of seeing "halos" around lights. Her ophthalmologic history is significant for several dendritic herpetic ulcers over the past few years. Physical examination shows conjunctival hyperemia with an edematous left eyelid. The cornea appears "steamy" and the pupil is fixed and mid-dilated. The left eye is tender and firm on palpation and tonometric testing reveals an intraocular pressure (IOP) of 67mm Hg. Immediate management would be to

A. administer mannitol, intravenously
B. order a CT scan of the head
C. perform a lumbar puncture
D. perform a peripheral iridotomy
E. treat the patient with corticosteroids, topically

The correct answer is A. This patient most likely has acute angle-closure glaucoma, which is an ocular emergency that requires immediate treatment to prevent blindness. It is characterized by a rapid increase of IOP, often occurring when the pupil is dilated (such as in a dark movie theater). The symptoms include severe eye pain, blurry vision, a headache, nausea, and vomiting. The physical examination usually shows a tender, firm eye with conjunctival hyperemia, lid edema, a hazy cornea, and a fixed, mid-dilated pupil. Immediate treatment includes mannitol (to reduce vitreous humor volume), acetazolamide and topical beta-blockers, such as timolol (to block aqueous production), and pilocarpine (to facilitate aqueous outflow). Ophthalmologic consultation should also be sought as soon as possible. A peripheral laser iridectomy is the definitive procedure and is usually performed after the IOP is controlled.
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Bells Palsy 
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Facial nerve (7th cranial nerve) palsy is often idiopathic (formerly called Bell palsy). Idiopathic facial nerve palsy is sudden, unilateral peripheral facial nerve palsy. 

Etiology
Historically, Bell palsy was thought to be idiopathic facial nerve (peripheral 7th cranial nerve) palsy. About half the cases of facial nerve palsy are idiopathic. The mechanism for idiopathic facial nerve palsy is presumably swelling of the facial nerve due to an immune or viral disorder. Recent evidence suggests that herpes simplex virus infection is the most common cause and that herpes zoster may be the second most common viral cause. Other viral causes include coxsackievirus, cytomegalovirus, adenovirus, and the Epstein-Barr, mumps, rubella, and influenza B viruses. The swollen nerve is maximally compressed as it passes through the labyrinthine portion of the facial canal, resulting in ischemia and paresis.

Symptoms and Signs
Pain behind the ear often precedes facial paresis in idiopathic facial nerve palsy. Paresis, often with complete paralysis, develops within hours and is usually maximal within 48 to 72 h. Patients may report a numb or heavy feeling in the face. The affected side becomes flat and expressionless; the ability to wrinkle the forehead, blink, and grimace is limited or absent. In severe cases, the palpebral fissure widens and the eye does not close, often irritating the conjunctiva and drying the cornea.

Sensory examination is normal, but the external auditory canal and a small patch behind the ear (over the mastoid) may be painful to the touch. If the nerve lesion is proximal to the geniculate ganglion, salivation, taste, and lacrimation may be impaired, and hyperacusis may be present.

Diagnosis
Clinical evaluation
Other testing if indicated by clinical findings
Facial nerve palsy is diagnosed based on clinical evaluation. There are no specific diagnostic tests. Facial nerve palsy can be distinguished from a central facial nerve lesion (eg, due to hemispheric stroke or tumor), which causes weakness primarily of the lower face, sparing the forehead muscle and allowing patients to wrinkle their forehead; also, patients with central lesions can usually furrow their brow and close their eyes tightly.

Treatment
Supportive measures
Corneal drying must be prevented by frequent use of natural tears, isotonic saline, or methylcellulose drops and by intermittent use of tape or a patch to help close the eye, particularly during sleep. 

In idiopathic facial nerve palsy, corticosteroids, if begun within 48 h after onset, result in faster and more complete recovery. Prednisone 60 to 80 mg po once/day is given for 1 wk, then decreased gradually over the 2nd wk. Antiviral drugs effective against herpes simplex virus (eg, valacyclovir 1 g po tid for 7 to 10 days, famciclovir 500 mg po tid for 5 to 10 days, acyclovir 400 mg po 5 times/day for 10 days) have been prescribed, but recent data suggest that antiviral drugs provide no benefit.

VIGNETTES:

You are working in the emergency department evaluating a 36 year old left-handed man who presents with right ear pain and facial weakness. Yesterday, he woke up in the morning and noticed that his "right face looked different" and that he also had slurred speech. He denies weakness or numbness of the rest of his body. The ear pain began about 3 days earlier. His blood pressure is 167/90 mm Hg. Otoscopic exam is unremarkable. There is equal weakness of the upper and lower face on the right. Taste is decreased on the right half of the tongue. Motor and sensory examination of the extremities is normal. The most appropriate next step is to

A. admit the patient for a cerebrovascular evaluation
B. get a head CT
C. get an otolaryngology consult
D. prescribe acyclovir and prednisone
E. start therapy with heparin

The correct answer is D. This patient has an isolated cranial nerve VII deficit (Bell palsy), which is most likely caused by inflammation of the facial nerve. Some believe that is caused by the reactivation of herpes virus, and so it may be treated with acyclovir and prednisone.
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Spontaneous bacterial peritonitis (SBP) 
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Spontaneous bacterial peritonitis (SBP) is infection of ascitic fluid without an apparent source. Manifestations may include fever, malaise, and symptoms of ascites and worsening hepatic failure. 

SBP is particularly common in cirrhotic ascites, especially among alcoholics. This infection can cause serious sequelae or death. The most common bacteria causing SBP are gram-negative Escherichia coli and Klebsiella pneumoniae and gram-positive Streptococcus pneumoniae; usually only a single organism is involved.

Symptoms and Signs
Patients have symptoms and signs of ascites. Discomfort is usually present; it typically is diffuse, constant, and mild to moderate in severity.

Signs of SBP may include fever, malaise, encephalopathy, worsening hepatic failure, and unexplained clinical deterioration. Peritoneal signs (eg, abdominal tenderness and rebound) are present but may be somewhat diminished by the presence of ascitic fluid.

Diagnosis
Diagnostic abdominal paracentesis
Clinical diagnosis of SBP can be difficult; diagnosis requires a high index of suspicion and liberal use of diagnostic abdominal paracentesis, including culture. Transferring ascitic fluid to blood culture media before incubation increases the sensitivity of culture to almost 70%. PMN count of > 250 cells/μL is diagnostic of SBP. Blood cultures are also indicated. Because SBP usually results from a single organism, finding mixed flora on culture suggests a perforated abdominal viscus or contaminated specimen.

Treatment
Cefotaxime or another antibiotic
If SBP is diagnosed, an antibiotic such as cefotaxime 2 g IV q 4 to 8 h (pending Gram stain and culture results) is given for at least 5 days and until ascitic fluid shows < 250 PMNs/μL. Antibiotics increase the chance of survival. Because SBP recurs within a year in up to 70% of patients, prophylactic antibiotics are indicated; quinolones (eg, levofloxacin) are most widely used.

Antibiotic prophylaxis in ascitic patients with variceal hemorrhage decreases the risk of SBP.

VIGNETTES:

A 56 year old man is admitted to the hospital for fever and abdominal pain. He has a history of cirrhosis and is known to be hepatitis C positive. He was diagnosed with cirrhosis four years ago. He denies any alcohol or tobacco use. His only medications are spironolactone and propranolol. He reports that five days ago, he had fever to 102 degrees F and the gradual onset of diffuse abdominal pain. On examination, his temperature is 38.3 C (101 F), his blood pressure is 100/50 mm Hg, and his pulse is 110/min and regular. His lungs are clear, he has numerous spider angiomata on his thorax and back, and his abdomen is massively distended, with shifting dullness by percussion. Laboratory studies show: Leukocytes 13,200/mm3 Hematocrit 33% Prothrombin time 15.2 seconds Albumin 0.1 g/dL Sodium 135 mEq/L Potassium 4.7 mEq/L Which of the following is the most appropriate next step in diagnosis?

A. Abdominal ultrasound 
B. Abdominal CT scan 
C. Electrocardiogram 
D. Abdominal paracentesis 
E. Lumbar puncture 

D. The prevalence of infection of ascites fluid, so called spontaneous bacterial peritonitis (SBP), is estimated at 50% in hospitalized cirrhotics. ALL febrile patients admitted with ascites must have an abdominal paracentesis performed to both determine the cause for the ascites and rule out infection of the ascites. The diagnosis of SBP is made when there is an elevated ascitic fluid absolute neutrophil count (> 250 cells/mm3) without an evident intra-abdominal or surgically treatable cause for the infection. SBP most often occurs with portal hypertensive ascites. The most sensitive marker available for such ascites is a serum/ascites albumin gradient > 1.1 g/dL.

A 62 year old woman is admitted to the hospital with severe ascites and fever. She has a 2 year history of portal hypertension secondary to hepatitis C-induced cirrhosis. The patient was placed on the liver transplant waiting list 3 months ago. Four months prior to admission she suffered an upper gastrointestinal bleed secondary to esophageal varices, which was subsequently banded via endoscopy. Two days ago, the patient developed abdominal pain, increasing abdominal girth, and fever. She was admitted to the hospital with the diagnosis of spontaneous bacterial peritonitis. The appropriate therapy is initiated and over the course of the next 4 days the patient appeared to be responding well. On the day of discharge you begin to plan her outpatient management and follow-up care. To prevent further disability from her current acute condition, you should prescribe

A. hydrochlorothiazide
B. lactulose
C. levofloxacin
D. oral protein supplements
E. propranolol

The correct answer is C. The 1-year risk of recurrent infection in patients surviving spontaneous bacterial peritonitis (SBP) is as high at 70%. Prophylaxis has been tested in this group and shown to be efficacious. The rate of recurrence is less with therapy, although there is no survival benefit. The agents tested have mostly been fluoroquinolone antibiotics. Levofloxacin is now the preferred agent in that class.
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Vitamin B12 Deficiency 
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Vitamin B12 Deficiency

Vitamin B12 (also called Cobalamin) is necessary for the formation of normal RBCs. Intrinsic factor, secreted by parietal cells in the gastric mucosa, binds with vitamin B12. Intrinsic factor is required for absorption of vitamin B12, which takes place in the terminal ileum.

The liver stores large amounts of vitamin B12. Enterohepatic reabsorption helps retain vitamin B12. Liver vitamin B12 stores can normally sustain physiologic needs for 3 to 5 years if B12 intake stops (eg, in people who become vegans).

Dietary vitamin B12 deficiency usually results from inadequate absorption, but deficiency can develop in vegans who do not take vitamin supplements. Deficiency causes megaloblastic anemia, damage to the white matter of the spinal cord and brain, and peripheral neuropathy. 

Causes of Vitamin B12 Deficiency:

Inadequate diet: Vegan diet

Impaired absorption (most common cause): Lack of intrinsic factor (due to autoimmune metaplastic atrophic gastritis, destruction of gastric mucosa, gastric surgery, or gastric bypass surgery) |
Small-bowel disorders (eg, inflammatory bowel disease, celiac disease, cancer, biliary or pancreatic disorders)

Inadequate utilization: Enzyme deficiencies | Liver disorders | Transport protein abnormality

Medications: Antacids | Metformin | Nitrous oxide (repeated exposure)

Vitamin B12 absorption may be inadequate if ileal absorptive sites are destroyed by inflammatory bowel disease or are surgically removed. 

Pernicious anemia is often used synonymously with vitamin B12 deficiency. However, pernicious anemia specifically refers to anemia resulting from vitamin B12 deficiency caused by an autoimmune metaplastic atrophic gastritis with loss of intrinsic factor. Patients with classic pernicious anemia, most commonly younger adults, are at increased risk of stomach cancers.

Symptoms:
Various GI symptoms, including weight loss and poorly localized abdominal pain, may occur. 

Neurologic symptoms develop independently from and often without hematologic abnormalities.

Subacute combined degeneration refers to degenerative changes in the nervous system due to vitamin B12 deficiency; they affect mostly brain and spinal cord white matter. Demyelinating or axonal peripheral neuropathies can occur.

In early stages, decreased position and vibratory sensation in the extremities is accompanied by mild to moderate weakness and hyporeflexia. In later stages, spasticity, extensor plantar responses, greater loss of position and vibratory sensation in the lower extremities, and ataxia emerge. These deficits may develop in a stocking-glove distribution. 

Diagnosis
CBC, MCV and vitamin B12 and folate levels
Sometimes methylmalonic acid levels or Schilling test

Diagnosis is based on CBC and vitamin B12 and folate levels. CBC usually detects megaloblastic anemia. Tissue deficiency and macrocytic indexes may precede the development of anemia. A vitamin B12 level < 200 pg/mL (< 145 pmol/L) indicates vitamin B12 deficiency. The folate level is measured because vitamin B12 deficiency must be differentiated from folate deficiency as a cause of megaloblastic anemia; 

Schilling test: The Schilling test is useful only if diagnosing intrinsic factor deficiency is important, as in classic pernicious anemia. The Schilling test measures absorption of free radiolabeled vitamin B12. Radiolabeled vitamin B12 is given orally. Absorbed radiolabeled vitamin B12 is excreted in urine, which is collected for 24 h. The amount excreted is measured, and the percentage of total radiolabeled vitamin B12 is determined. If absorption is normal, ≥ 9% of the dose given appears in the urine. Reduced urinary excretion (< 5% if kidney function is normal) indicates inadequate vitamin B12 absorption. Improved absorption with the subsequent addition of intrinsic factor to radiolabeled vitamin B12 confirms the diagnosis of pernicious anemia.

Treatment
Supplemental vitamin B12
Vitamin B12 1000 to 2000 μg po can be given once/day to patients who do not have severe deficiency or neurologic symptoms or signs. For more severe deficiency, vitamin B12 1 mg IM is usually given 1 to 4 times/wk for several weeks until hematologic abnormalities are corrected; then it is given once/mo.

Although hematologic abnormalities are usually corrected within 6 wk (reticulocyte count should improve within 1 wk), resolution of neurologic symptoms may take much longer. Neurologic symptoms that persist for months or years become irreversible. 





VIGNETTES:

A 46 year old woman is seen by her family physician because she is feeling poorly. The woman has a known history of severe chronic gastritis. Physical examination demonstrates pallor of skin and mucosal membranes; no other positive findings are noted. A hematocrit of 33% is demonstrated in the physician's office. Blood smear performed and reviewed in the office shows enlarged erythrocytes that have enlarged central pale areas. Neutrophils and other white cells are present in normal numbers. Some of the neutrophils have hypersegmented nuclei. Which of the following is the most likely diagnosis?

A. Beta thalassemia trait
B. Folate deficiency anemia
C. Iron deficiency anemia
D. Sickle cell anemia
E. Vitamin B12 deficiency anemia

The correct answer is E. While either folate deficiency or vitamin B12 deficiency could produce a megaloblastic anemia such as that seen in this patient, the specific hint of chronic gastritis should suggest insufficient synthesis of the intrinsic factor needed for Vitamin B12 absorption by the small intestine. For classic pernicious anemia, autoantibodies directed against parietal cells and intrinsic factor are documented, but some physicians use the term pernicious anemia to also include vitamin B12-deficient anemic states in which another process, such as chronic gastritis (as in this case), has destroyed large amounts of gastric mucosa. Vitamin B12 deficiency anemia can also be seen as a result of inadequate diet (particularly among vegetarians) and small intestinal disease. Additionally, inadequate utilization of B12 can occur in many severely ill patients. The diagnosis of vitamin B12 deficiency can be confirmed with a serum vitamin B12 assay. Supplemental vitamin B12 is given as an IM injection. 

A patient develops a persistent macrocytic anemia. Serum folate levels are normal, but serum vitamin B12 levels are low. Oral vitamin absorption studies demonstrate that the patient is unable to absorb vitamin B12 in adequate amounts. Cancer of which of the following organs is most strongly associated with this patient's condition?

A. Colon
B. Duodenum
C. Esophagus
D. Ileum
E. Stomach

The correct answer is E. Megaloblastic anemia with poor vitamin B12 absorption suggests pernicious anemia. In this condition, an autoimmune attack on gastric parietal cells leads to atrophic gastritis with deficient synthesis of the intrinsic factor needed for vitamin B12 absorption. Vitamin B12 is required for DNA synthesis in blood cell precursors; deficiency produces megaloblastic anemia. Chronic atrophic gastritis predisposes an individual to the development of gastric carcinoma.

A 35 year old woman comes to the office because of generalized weakness and a "pins and needles" feeling in her lower extremities for the past 3 weeks. She states that she feels "unsteady" on her feet. She exercises daily, rarely drinks alcohol, and is a strict vegetarian. Since this is the first time you have met this woman, she tells you that she has not had any major illnesses, but has been hospitalized multiple times over the past few years for anorexia nervosa. Her temperature is 37 C (98.6 F), blood pressure is 110/70 mm Hg, pulse is 60/min, and respirations are 18/min. Examination shows weakness of the proximal and distal muscles of the lower extremities. There is impaired proprioception and vibratory sensation. Deep tendon reflexes are increased. The gait is ataxic. The most likely diagnosis is

A. Guillain-Barre syndrome
B. Lambert-Eaton syndrome
C. myasthenia gravis
D. polymyositis
E. subacute combined degeneration of the spinal cord

The correct answer is E. This patient most likely has subacute combined degeneration of the spinal cord, which is a condition caused by vitamin B12 deficiency. It is most often caused by pernicious anemia, but it may be acquired in patients with strict vegetarian diets or small bowel disease. The clinical manifestations include weakness, paraesthesias, loss of vibratory sensation, increased deep tendon reflexes, and extensor plantar responses. The gait is ataxic. Mental changes may also occur. The diagnosis is usually established by measuring serum vitamin B12 levels. The treatment is vitamin B12 replacement.
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Pelvic Inflammatory Disease (PID) 
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Pelvic inflammatory disease (PID)

Pelvic inflammatory disease (PID) is infection of the upper female genital tract: the cervix, uterus, fallopian tubes, and ovaries; abscesses may occur. Common symptoms and signs include lower abdominal pain, cervical discharge, and irregular vaginal bleeding. Long-term complications include infertility, chronic pelvic pain, and ectopic pregnancy. 

Etiology
PID results from microorganisms ascending from the vagina and cervix into the endometrium and fallopian tubes. Neisseria gonorrhoeae and Chlamydia trachomatis are common causes of PID; they are transmitted sexually. PID usually also involves other aerobic and anaerobic bacteria, including pathogens that are associated with bacterial vaginosis.

Risk factors: PID commonly occurs in women < 35. It is rare before menarche, after menopause, and during pregnancy. Risk factors include previous PID and presence of bacterial vaginosis or any sexually transmitted disease. Other risk factors, particularly for gonorrheal or chlamydial PID, include younger age, nonwhite race, low socioeconomic status, and multiple or new sex partners.

Symptoms and Signs
Lower abdominal pain, fever, cervical discharge, and abnormal uterine bleeding are common, particularly during or after menses.

Cervicitis: The cervix appears red and bleeds easily. Mucopurulent discharge is common; usually, it is yellow-green and can be seen exuding from the endocervical canal.

Acute salpingitis: Lower abdominal pain is usually present and bilateral but may be unilateral, even when both tubes are involved. Pain can also occur in the upper abdomen. Nausea and vomiting are common when pain is severe. Irregular bleeding (caused by endometritis) and fever each occur in up to one third of patients. In the early stages, signs may be mild or absent. Later, cervical motion tenderness, guarding, and rebound tenderness are common. 

Salpingitis may cause tubal scarring and adhesions, which commonly result in chronic pelvic pain, infertility, and increased risk of ectopic pregnancy.

Diagnosis:
PCR or Culture
Pregnancy test
PID is suspected when women of reproductive age, particularly those with risk factors, have lower abdominal pain or cervical or unexplained vaginal discharge. PID is considered when irregular vaginal bleeding, dyspareunia, or dysuria is unexplained. PID is more likely if lower abdominal, unilateral or bilateral adnexal, and cervical motion tenderness are present. 

If PID is suspected, PCR of cervical specimens for N. gonorrhoeae and C. trachomatis (which is about 99% sensitive and specific) and a pregnancy test are done. If PCR is unavailable, cultures are done. At the point of care, cervical discharge is usually examined to confirm purulence; a Gram stain or saline wet mount is used, but these tests are neither sensitive nor specific. If a patient cannot be adequately examined because of tenderness, ultrasonography is done as soon as possible. WBC count may be elevated but is not helpful diagnostically.

If the pregnancy test is positive, ectopic pregnancy, which can produce similar findings, should be considered. Other common causes of pelvic pain include endometriosis, adnexal torsion, ovarian cyst rupture, and appendicitis. 

Treatment
Parenteral (IV): 
Regimen A: Cefotetan or Cefoxitin plus Doxycycline, OR
Regimen B: Clindamycin plus Gentamicin
Oral: 
Ceftriaxone IM plus Doxycycline with or without Metronidazole, OR
Cefoxitin IM with probenecid plus Doxycycline with or without Metronidazole

Antibiotics to cover N. gonorrhoeae, C. trachomatis, and sometimes other organisms like Trichomonas.
Antibiotics are given empirically to cover N. gonorrhoeae and C. trachomatis and are modified based on laboratory test results. Empirical treatment is needed whenever the diagnosis is in question for several reasons:

Sex partners of patients with N. gonorrhoeae or C. trachomatis infection should be treated.

VIGNETTES:

A 16 year old runaway comes to the emergency department because of a 24 hour history of lower abdominal pain and vomiting. She tells you that she hates doctors and hospitals and is only here because another girl on the street told her that "this may be serious." She asks you to give her medicine quickly so she can leave. She is sexually active with multiple partners and she "occasionally" uses condoms for contraception. She lives "on the streets" and begs for money at the doorways of banks. She has not received any medical care in 6 years. Her last menstrual period was 9 days ago. She is unsure if she ever had a sexually transmitted disease in the past. Her temperature is 38.8 C (101.8 F), blood pressure is 110/70 mm Hg, and pulse is 65/min. Physical examination shows bilateral lower abdominal tenderness, but rebound tenderness and guarding are absent. Pelvic examination shows cervical motion tenderness, adnexal tenderness, and a yellowish-white cervical discharge. There are no palpable masses. A urine pregnancy test is negative. Cervical cultures are taken and sent to pathology for evaluation. The erythrocyte sedimentation rate and C-reactive protein level are elevated. The most appropriate next step is to

A. admit her to the hospital and begin cefoxitin and doxycycline therapy, intravenously
B. admit her to the hospital and prepare her for an immediate operation
C. do a culdocentesis
D. prescribe ofloxacin and metronidazole therapy, orally, and discharge her
E. try to contact her male sexual partners for evaluation and treatment

The correct answer is A. The diagnosis of pelvic inflammatory disease (PID) is typically based on clinical findings such as lower abdominal tenderness, cervical motion tenderness, adnexal tenderness, a vaginal or cervical discharge, fever >38.3 C, (101.0 F), elevated erythrocyte sedimentation rate and C-reactive protein, and laboratory documentation of N. gonorrhoeae or C. trachomatis. Treatment should be given even before the culture results return to reduce the risks of infertility and progressive infection. Admission to the hospital is important for this patient because compliance and follow-up cannot be assured since she is homeless and has already said that she hates doctors and hospitals. There is a chance that this patient may take the prescription and not return, so admission is indicated.

A 24 year old woman complains of abdominal pain of rapid onset in the right lower quadrant. She subsequently undergoes surgery for suspected acute appendicitis. At surgery, however, a tubal pregnancy is discovered. The most frequent predisposing factor for this condition is

A. endometriosis
B. an intrauterine device
C. leiomyomas of the uterus
D. pelvic inflammatory disease
E. previous surgery

The correct answer is D. The great majority of ectopic pregnancies (90%) occur in the fallopian tubes. The other sites are the ovaries, abdominal cavity, and the intrauterine segment of the fallopian tubes. Any condition that leads to anatomical abnormalities of the uterus and fallopian tubes may predispose to ectopic pregnancy. The most frequent of such conditions is pelvic inflammatory disease (PID), which is usually associated with
salpingitis. PID is a common infectious condition most frequently caused by Neisseria gonorrhoeae and Chlamydia trachomatis, both sexually transmitted. Other cases are due to a polymicrobial population, including staphylococci, streptococci, coliform bacteria, and Clostridium perfringens, acquired during abortion or delivery. PID leads to acute purulent salpingitis. If this is untreated or inadequately treated, it progresses to salpingo-oophoritis, tubal abscesses, pyosalpinx, or hydrosalpinx. Even milder cases may cause adhesions within the tube or between the tube and the ovary that interfere with implantation of the ovum and result in tubal pregnancy. All the remaining conditions listed above may also predispose to ectopic pregnancy.
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