Тесты - Kaplan medical USMLE world step1 qbook General Pathology - файл Block 12.docприобрестиТесты - Kaplan medical USMLE world step1 qbook General Pathologyскачать
Доступные файлы (12):
USMLE WORLD STEP 1 PATHOLOGY MISS PRINT
Q NO 410: A 52-year-old Caucasian male presents to your office with periodic diarrhea and recent weight loss. His stools are foul smelling bulky, and frothy. His past medical history is insignificant. Physical examination findings are within normal limits. To confirm impaired nutrient absorption in this patient, you should do which of the following?
A. Draw blood
B. Collect stool
C. Perform duodenal aspiration
D. Schedule abdominal ultrasound
E. Schedule jejunal biopsy Explanation:
Impaired intestinal absorption of nutrients is called malabsorption. The main clinical manifestation of this syndrome is steatorrhea: foul-smelling bulky, greasy stool that contains large amounts of fat. Excess fat content will cause the stool to float in the toilet bowl. Weight loss and symptoms of various nutritional deficiencies are common. Anemia may result from iron folate, and/or vitamin B12 deficiency. Fat-soluble vitamins (K, A, D, and E) may also be lost. Vitamin K deficiency may cause petechiae and easy bruising. Decreased calcium and vitamin D absorption leads to bone pain. Muscle wasting and edema (protein deficiency) hyperkeratosis (vitamin A deficiency), and tetany (due to hypocalcaemia) can occur.
Multiple disorders that cause malabsorption are divided into the following major groups:
1. Pancreatic exocrine insufficiency: chronic pancreatitis and cystic fibrosis belong to this group of disorders. Diminished production of digestive pancreatic enzymes leads to impaired hydrolysis of nutrients in the small intestine.
2. Intestinal mucosal defects: examples are celiac disease tropical sprue Whipple disease Crohn disease and many others. Structural defect or injury to the intestinal epithelial cells hampers nutrient transport from the intestinal lumen and/or from intestinal cells to peripheral organs.
3. Bacterial proliferation in the small bowel occurs in afferent loop syndrome diverticulosis, and diabetic neuropathy. Bacteria compete for nutrients causing relative nutrient deficiency.
The first step in screening for malabsorption is Sudan lll stain which will identify the presence off a tin a stool sample. Quantitative analysis for fecal fat is used to confirm the diagnosis (>7gm/day of excreted fat is diagnostic for malabsorption). Further diagnostic steps are then taken to identify the primary cause of malabsorption.
(Choice A) While a CBC and serum chemistry in a patient with malabsorption may show anemia hypoalbuminemia, low serum levels of triglycerides cholesterol and carotene vitamin deficiencies and electrolyte abnormalities—these blood tests will not identify the cause of these abnormalities. There is no specific blood test for malabsorption.
(Choice C and E) Duodenal aspiration and jejunal biopsy are invasive tests and are never used to screen for malabsorption. While these two tests do help establish the definitive diagnosis of the primary condition causing malabsorption, a stool sample is a far more prudent first step. Crohn disease Whipple disease celiac sprue, and many other disorders can be diagnosed by small intestine aspiration and biopsy.
(Choice D) Imaging studies are very expensive and not very useful in the evaluation of malabsorption. Abdominal ultrasound is not likely to reveal much. A CT of the abdomen in a patient with chronic pancreatitis might show calcifications or atrophy of the pancreas.
Malabsorption is a syndrome of impaired intestinal digestion and absorption. Diarrhea, steatorrhea, weight loss, and vitamin and mineral deficiencies are common. Sudan lll stain of stool identifies fecal fat and is used to screen for malabsorption.
Q NO 417: A 34-year-old male returns from a trip to India and develops anorexia, mild nausea, and dark urine lasting two days. Physical examination reveals low-grade fever and mild right upper abdominal quadrant tenderness. A liver biopsy is most likely to show which of the following?
A. Liquefaction necrosis
B. Ballooning degeneration
C. Invasive cells
D. Fibrinoid necrosis
E. Regeneration nodules Explanation:
This patient has the classic symptoms of acute viral hepatitis: low-grade fever, anorexia, nausea, dark colored urine, and right upper quadrant tenderness. Hepatitis A virus (HAV) is most likely responsible since the patient has just returned from a region where it is endemic. HAV is the most common cause of acute viral hepatitis in young adults.
In all cases of acute viral hepatitis, diffuse ballooning degeneration (hepatocyte swelling), mononuclear cell infiltrates, and Councilman bodies (eosinophilic apoptotic hepatocytes) are seen histologically. (Liver biopsy is not needed to make the diagnosis of HAV infection, however.)
(Choice A) Prank hepatocyte necrosis, or coagulative necrosis, may occur in viral hepatitis. Liquefactive necrosis classically occurs in the CNS when ischemia causes cell death followed by enzymatic degradation of tissue.
(Choice C) HAV is not associated with an increased risk of hepatocellular cancer. Hepatitis B and C infections, aflatoxin B exposure, and all other forms of chronic hepatocyte injury are, however, associated with an increased incidence of hepatocellular carcinoma.
(Choice D) Fibrinoid necrosis is a histologic pattern of injury typically seen in the walls of blood vessels affected by immune complex and related forms of vasculitis.
(Choice E) Nodular regeneration of hepatocytes is generally found in patients with cirrhosis due to chronic hepatitis. HAV does not cause chronic hepatitis, while HBV and HCV are associated with chronic hepatitis leading to cirrhosis.
Anorexia, nausea, and low-grade fever followed by bilirubinuria and right upper quadrant tenderness suggest acute hepatitis which is most commonly caused by the Hepatitis A virus in young adults. Acute hepatitis due to most hepatotropic viruses causes hepatocyte ballooning degeneration and apoptosis on histologic exam.
Q NO 420: A 56-year-old male presents to clinic with a several week history of fatigue, palpitations and exertional dyspnea. His heart rate is irregular and measures 122/mm, while his blood pressure is 110/70mm Hg. Esophageal echocardiography reveals a thrombus in the dilated left atrium. If the thrombus enters circulation and obstructs a blood vessel which of the following organs is least likely to be affected by the infarction
E. Heart Explanation:
Infarcts in an otherwise normal liver are rare because it has a dual blood supply: the portal vein and hepatic artery. Should the hepatic artery be occluded the portal venous supply and retrograde arterial flow through accessory vessels is typically sufficient to sustain the liver parenchyma. The notable exception is when a transplanted liver undergoes hepatic artery thrombosis. In this case the liver can develop biliary tree infarction and organ failure because the collateral blood supply is severed during transplantation.
(Choice A) The spleen is relatively resistant to infarction after splenic artery occlusion because of its collateral blood flow and the potential for recruiting an additional blood supply from omentum adherent to the ischemic spleen. Nevertheless, wedge-shaped capsule-based splenic infarcts do occur and are a known complication of sickle cell anemia infective endocarditis, and cardiac mural thrombosis.
(Choice B) Irreversible damage appears to occur in the most vulnerable of neurons after approximately 5 minutes of complete ischemia.
(Choice C) The kidney is generally able to tolerate warm ischemia for several hours. Longer periods of complete ischemia result in immediate functional loss: late recovery of renal function is incomplete or absent.
(Choice E)The myocardium can endure complete arterial ischemia for twenty or thirty minutes without severe consequences. Briefer periods of ischemia do not result in necrosis but rather myocardial stunning.
Organ susceptibility to infarction after occlusion of a feeding artery is ranked from greatest to least as follows: central nervous system myocardium kidney spleen, and liver. The presence of a dual or collateral blood supply (as seen in the liver which is supplied by the hepatic artery and portal vein) enables organs to tolerate arterial occlusion.
Q NO 447: A 72-year-old male is brought to the ER with involuntary, wild, flinging movements of his right arm. Symptoms started several hours ago. His past medical history is significant or long-standing hypertension. Which of the following areas of the brain is most likely to be injured in this patient?
A. Lentiform nucleus
B. Substantia nigra
C. Caudate nucleus
D. Internal capsule
E. Subthalamic nucleus
F. Nucleus of the thalamus Explanation:
Wild flinging movements of the extremities on one side of the body (arm and/or leg) is called hemiballism. It occurs due to damage of the contralateral subthalamic nucleus—most commonly from a lacunar stroke. Patients suffering lacunar strokes usually have a long history of hypertension. The subthalamic nucleus is a component of the basal ganglia. It is ventral to the thalamus and superior to the internal capsule.
(Choice A) Involvement of the lentiform nucleus (globus pallidus and putamen) is characteristic of Wilson disease (hepatolenticular degeneration). Manifestations include wing-beating tremor psychosis and cirrhosis. Kayser Fleischer rings are seen in the cornea.
(Choice B) Damage to the substantia nigra occurs in Parkinson disease. Common symptoms are bradykinesia, rigidity, and resting tremor.
(Choice C) Atrophy of the caudate nucleus occurs in Huntington disease. Chorea, dementia, and behavioral abnormalities are typical.
(Choice D) Damage to the internal capsule occurs when perforating arteries are obstructed (lacunar infarcts) and results in pure motor or pure sensory deficits.
(Choice F) Lesions of the thalamus can cause thalamic syndrome. This syndrome of post-stroke pain occurs in about 2% of stroke victims and is often described as a burning or stabbing sensation of one half of the body (contralateral to the lesion).
The subthalamic nucleus is one of the components of the basal ganglia. Damage to this nucleus (most often due to lacunar stroke) leads to hemiballism. The involuntary flinging movements of one side of the body (arm and/or leg) that constitutes hemiballism are always contralateral to the lesion.
Q NO 448: A 38-year-old male who is hospitalized with a bleeding duodenal ulcer develops prolonged oliguria. Renal biopsy shows epithelial necrosis of the tubules tubulorrhexis, and intratubular casts. Which of the following is the most important threat in the recovers phase of this patient’s condition?
A. Metabolic acidosis
E. Volume overload Explanation:
Decreased renal blood flow triggers a chain of pathophysiologic changes in the nephron that cause tubular epithelial necrosis and acute renal failure. The initiating stage of ischemic ATN is usually unnoticed by clinicians as the symptoms of the main disorder (hemorrhage acute MI1 sepsis etc) prevail. If significant tubular damage occurs the oliguric stage (maintenance stage) follows in 24-36 hours. During this stage, urine output decreases, and metabolic changes of acute renal failure manifest. The most significant of these changes are detailed below:
1. Increased extracellular fluid volume can cause weight gain, edema, and pulmonary vascular congestion.
2. Hyperkalemia is usually asymptomatic when serum K concentration is <6.0 mEq/L. Above this level, peaked T waves are apparent on ERG, and potentially-fatal ventricular arrhythmias are possible.
3. Retention of both hydrogen and anions (sulfate, phosphate, and urate) will lead to high anion gap metabolic acidosis.
4. Other electrolyte changes include a decreased concentration of sodium and calcium and an increased level of phosphate and magnesium.
5. Urinalysis reveals pathognomonic muddy brown casts low urinary osmolarity (<350), high urinary sodium (>30), and high urinary fractional sodium excretion (Fe Na >1).
In spite of the seemingly-profound damage that occurs to nephrons in ATN tubular epithelial cells have an excellent regenerative capacity. If the patient survives the oliguric stage (by conservative management or dialysis) the recovery stage will follow in 1-2 weeks. It manifests by vigorous diuresis (sometimes >3 L/day). Because renal tubules cannot yet function fully electrolyte balance is still altered. High-volume hypotonic urine causes sodium retention and decreased concentrations of K, Mg1, P04, and Ca. Hypokalemia is one of the most serous complications of the recovery phase of ATN.
(Choices A, B and E) Anion gap metabolic acidosis hyperphosphatemia and volume overload occurs in the oliguric stage of ATN. During the recovery phase patients can become dehydrated. Careful volume replacement is prudent during this phase.
(Choice D) Hypercalcemia doesn’t occur in ATN. Instead there is hypocalcemia, due to both the deposition of calcium phosphate and reduced levels of 1,25 dihydroxyvitamin D.
During the recovery phase (polyuric phase) of ATNI patients can become dehydrated and can develop severe hypokalemia due to high-volume hypotonic urine.
Q NO 449: A 42-year-old female with primary pulmonary hypertension undergoes lung transplantation. Although she did well at first, the patient now complains of fatigue and exertional dyspnea. Lung biopsy shows areas of total fibrotic obstruction of the terminal bronchioles. This patient’s condition is most likely explained by:
A. Ischemia-reperfusion injury
B. Disease recurrence
C. Acute rejection
D. Chronic rejection
E. Opportunistic infection Explanation:
Lung transplantation may be complicated by both acute and chronic rejection. Acute rejection can be effectively treated with immunosuppressants. Chronic rejection, however, is a major cause of morbidity and mortality among transplant patients. Chronic rejection affects the small bronchioli producing the obstructive lung disease known as bronchiolitis obliterans.
The pathologic basis of this condition is lymphocytic inflammation and necrosis of the bronchiolar walls. Early on, fibrinopurulent exudate and granulation tissue are found in the lumen of the bronchioli. They are later replaced by connective tissue. Scarring leads to progressive obliteration of small airway lumens.
(Choice A) Ischemia-reperfusion injury (or reperfusion edema) is a form of noncardiogenic pulmonary edema that can occur in the allograft due to surgical trauma, organ ischemia, denervation, or interruption of lymphatic outflow. Reperfusion edema is seen during the first few days following transplantation.
(Choice B) Primary lung disease may recur in the lung allograft. However, the biopsy would have shown disease in the pulmonary arteries consistent with pulmonary hypertension.
(Choice C) Acute rejection occurs within days to weeks of transplantation. There are perivascular mononuclear infiltrates on histologic examination. The symptoms of acute rejection include dry cough, dyspnea, and fever. Parenchymal infiltrates are seen on chest x-ray.
(Choice E) Infection is the leading cause of death in lung transplant recipients. CMV is the most significant opportunistic infection in lung transplant recipients. Infected cells have a characteristic intranuclear inclusion surrounded by a clear halo (owl’s eye inclusion).
Chronic rejection is a major problem in lung transplant recipients. It affects small airways, causing bronchiolitis obliterans. Lymphocytic inflammation, necrosis, and fibrosis of the bronchiolar wall occur. Ultimately, there is occlusion of the bronchiolar lumen.
Q NO 450: A 55-year-old male who recently moved to your community comes to your office for a routine checkup. Upon review of his medical records you find that he has multiple medical problems. He has smoked one pack of cigarettes daily for the last 20 years and consumes 2-3 bottles of beer every day. Physical examination findings are shown on the slide below. Which of the following diseases should be considered as a cause of this patient’s findings?
A. Rheumatoid arthritis
B. Bronchial asthma
D. Mitral valve prolapse
E. Iron deficiency anemia
F. Patent foramen ovale Explanation:
Thickening of the distal portion of the distal phalanges shown on the image above is called clubbing. This deformity of the fingers and fingernails is associated with a number of chronic diseases causing hypoxia. On physical exam, the fingers will have a “drumstick” appearance due to thickening of the distal phalanges. Flattening of the nail folds and shininess of the nail and distal portion of the finger will also be evident. Pressing on the nails reveals a spongy fluctuant sensation of the nailbeds.
Clubbing develops insidiously and is a sign of chronic hypoxic disease most commonly. The pathophysiology of digital clubbing has yet to be completely elucidated but it is thought to be caused by vasodilatation of the capillaries in the distal phalangeal region leading to increased blood flow to the distal portion of the finger, interstitial edema and increased growth of fibrovascular tissue. A number of circulating vasodilators have also been implicated in the development of clubbing. The following conditions commonly cause digital clubbing:
1. Lung diseases: lung cancer (especially large-cell carcinoma), tuberculosis, cystic fibrosis bronchiectasis (Choice C) pulmonary hypertension empyema and many other chronic lung diseases associated with hypoxia.
2. Heart diseases: cyanotic congenital heart diseases (five T’s, especially tetralogy of Fallot).
3. Other: Inflammatory bowel diseases (Crohn, ulcerative colitis) hyperthyroidism, malabsorption.
(Choice A) Swelling of the metacarpophalangeal and proximal interphalangeal (not distal) joints of the hands along with atrophy of interosseous muscles is a common finding in patients with rheumatoid arthritis.
(Choice B) Bronchial asthma is not associated with clubbing. Physical exam will reveal musical wheezes and possibly signs of other atopic disease such as atopic dermatitis nasal polyps or hives.
(Choice D) Mitral valve prolapse is associated with a midsystolic click and a late systolic murmur best heard over the apex of the heart.
(Choice E) Iron deficiency anemia may result in physical exam findings of pallor and koilonychia (spoon shaped nails).
Digital clubbing is often associated with prolonged hypoxia. It accompanies large-cell lung cancer tuberculosis cystic fibrosis bronchiectasis and suppurative lung diseases such as empyema and chronic lung abscesses as well as other conditions.
Q NO 451: A 50-year-old Caucasian female with severe upper abdominal pain, vomiting and low-grade fever is admitted to the hospital for work-up. Her serum bilirubin level is 1.2 mg/dL and serum alkaline phosphatase level is 300 U/L. Which of the following test results is most suggestive of acute cholecystitis as the cause of this patient’s complaints?
A. Opacities in the right subcostal area revealed on the abdominal X-ray
B. Increased serum AST and ALT levels
C. Failed gallbladder visualization on radionuclide biliary scan
D. Highly reflective structures seen inside the gallbladder on abdominal ultrasonography
E. Distended duodenum on upper 01 series Explanation:
Acute calculous cholecystitis is secondary to gallstone formation in over 90% of cases, most commonly arising when a gallstone impacts in the cystic duct. Ingestion of fatty foods then stimulates the contraction of the gallbladder against the obstructed cystic duct, causing severe colicky pain. The tissue behind the duct obstruction becomes inflamed, typically as a result of prostaglandin release and stony disruption of the mucosal layer. Ischemic changes ensue in the edematous and distended organ, followed shortly by bacterial invasion. Potential complications include gangrene and perforation, with generalized peritonitis or a well-circumscribed abscess the more common outcome.
This condition typically develops after ingestion of a large or fatty meal and is characterized by the sudden appearance of steady pain in the epigastrium or right upper quadrant. The pain may radiate to the right scapula or be accompanied by Murphy’s sign, which is the sharp arrest of inspiration with gallbladder palpation. Other classical findings include fever, vomiting, and leukocytosis. Total serum bilirubin may range from 1-4 mg/dL, and serum aminotransferases and alkaline phosphatase are often elevated. The diagnosis can be confirmed with cholescintigraphy (HIDA scan), which uses an intravenously injected radiolabeled agent that is taken up by hepatocytes and excreted into bile. If the cystic duct is patent the radiolabeled agent will enter the gallbladder and the organ is visualized. If the cystic duct is obstructed (as in cases of acute calculous cholecystitis), the radiolabeled agent cannot enter the gallbladder and the organ is not visualized.
(Choice A) Most patients have insufficient calcium in their gallstones to be visualized on an abdominal x-ray.
(Choice B) Increased serum AST and ALT levels are common findings in acute calculous cholecystitis, but are not diagnostic.
(Choice D) Gallstones visualized on ultrasound examination in the clinical context of right upper quadrant abdominal pain and fever are suggestive but not diagnostic of acute calculous cholecystitis.
(Choice E) Distended duodenum on upper GI would be suggestive of small bowel obstruction, as seen with gallstone ileus.
Positive HIDA scan confirms cystic duct obstruction, which is necessary for a definitive diagnosis of acute calculous cholecystitis. The mere presence of non-obstructing biliary stones, in contrast, is suggestive but not diagnostic of the condition.
Q NO 452: A 3-week-old male born to a 23-year-old Caucasian primigravida develops projectile non-bilious vomiting after every meal. Abdominal inspection reveals prominent peristalsis in the epigastrium and an olive-sized mass is felt on deep palpation of the right upper abdomen. The mass most likely represents:
A. Infection focus
B. Neoplastic cell proliferation
C. Smooth muscle hypertrophy
D. Pancreatic juice accumulation
E. Biliary duct distension Explanation:
Congenital pyloric stenosis is a relatively common disorder that is encountered primarily in male infants (at a 3:1 ratio) and characterized by a multifactorial pattern of inheritance. Infants typically present with recurrent projectile nonbilious vomiting, and physical examination demonstrates visible peristalsis and the presence of an olive-sized mass in the distal stomach or pyloric region. The mass is thought to develop secondary to hypertrophy of the pyloric muscularis mucosae. The narrowing of the pyloric channel is thought to be exacerbated by localized edema and inflammation. The stenosis is relieved by surgical splitting of the muscle.
(Choices A, D, and E) Infection, pancreatic juice accumulation, and biliary duct distension are not associated with pyloric stenosis.
(Choice B) Acquired pyloric stenosis occurs in adults and is associated with gastritis, peptic ulcers in the pylorus, or a neoplastic process (eg, carcinoma of the pyloric region or lymphoma). Neoplasm in this area would not be expected in an infant, however.
Congenital pyloric stenosis arises secondary to hypertrophy of the pyloric muscularis mucosae.
Q NO 453: A 21-year-old male with chronic headaches and ataxia is found on MRI to have low-lying cerebellar tonsils extending into the vertebral canal. This patient’s condition is most likely:
A. Single gene disorder
B. Congenital malformation
C. Secondary to trauma
D. Secondary to neoplasia
E. Autoimmune disease
F. Vascular disease Explanation:
Arnold-Chiari malformation is a congenital disease due to underdevelopment of the posterior fossa. The small size of the fossa causes parts of the cerebellum and medulla to herniate through the foramen magnum.
There are two types of Arnold-Chiari malformations. In Arnold-Chiari malformation type I, low-lying cerebellar tonsils extend below the foramen magnum into the vertebral canal. It may be asymptomatic in infants, but in adults manifests with headaches and cerebellar symptoms (such as ataxia).
Arnold-Chiari malformation type II is more severe and becomes symptomatic in the neonatal period. It is characterized by an abnormally formed cerebellum and medulla. Both the cerebellar vermis and medulla extend downward through the foramen magnum. Lumbar myelomeningocele and hydrocephalus (due to aqueductal stenosis) are almost always present in these patients.
Arnold-Chiari type II causes symptoms of compression of the medulla such as difficulty swallowing, dysphonia, stridor, and apnea. Lumbar myelomeningocele usually leads to leg paralysis. If untreated, hydrocephalus can cause mental impairment.
The other choices are not related to the pathogenesis of Arnold-Chiari malformation.
Arnold-Chiari malformations are congenital abnormalities. They are caused by impaired development of the posterior fossa. Arnold-Chiari type 1 is relatively benign and may manifest in adulthood. Arnold-Chiari type II is severe and is evident in the newborn.
Q NO 489: A 52-year-old Caucasian female with intense generalized pruritus is found to have high alkaline phosphatase level and high titers of antimitochondrial antibodies. Liver biopsy is performed in this patient. Morphologic findings on this patient’s liver biopsy are likely to resemble:
A. Alcoholic hepatitis
B. Acetaminophen toxicity
C. Reye’s syndrome
D. Graft-vs-host disease
F. Budd-Chiari syndrome Explanation:
Primary biliary cirrhosis (PBC) is a chronic liver disease characterized by autoimmune destruction of the intrahepatic bile ducts and cholestasis.
Histologically, the disease is focal and variable with a wide range in severity evident in different portions of the liver. In the precirrhotic stage, the interlobular bile ducts are destroyed by granulomatous inflammation (“florid duct lesion”) and a heavy portal tract infiltrate of macrophages, lymphocytes, plasma cells, and eosinophils is present. The similarity of these findings to those seen in graft versus host disease suggests that immunologic injury is responsible for disease manifestations.
Eventually, progressive hepatic damage secondary to the obstruction in intrahepatic bile flow is observed. Upstream portal tracts undergo bile ductular proliferation, inflammation, and necrosis of adjacent parenchyma. Generalized cholestasis develops, and the liver gradually becomes grossly stained green and uniformly micronodular. Ultimately, the end-stage liver findings in PBC cannot be distinguished from those in secondary biliary cirrhosis or chronic hepatitis.
(Choice A) Alcoholic hepatitis is characterized by hepatocellular swelling and necrosis, Mallory bodies, neutrophilic infiltration, and fibrosis.
(Choice B) Serious acetaminophen overdose is characterized by liver failure and centrilobular necrosis that can extend to include the entire lobule.
(Choice C) Reye’s syndrome is characterized by microvesicular steatosis.
(Choice E) Hemochromatosis is characterized by the deposition of hemosiderin in the liver. Cirrhosis may eventually ensue if the condition is left untreated.
(Choice F) The increased intrahepatic blood pressure associated with Budd-Chiari syndrome often causes hepatomegaly, abdominal pain, and ascites secondary to thrombosis of the hepatic vein. Typically, the liver becomes grossly swollen, reddish purple, and develops a tense capsule. Severe centri lobular congestion and necrosis are observed microscopically.
Primary biliary cirrhosis and graft versus host disease have similar histologic findings, including granulomatous bile duct destruction and a heavy lymphocyte-predominant portal tract infiltrate.
Q NO 492: A 62-year-old Caucasian female presents with dilated and tortuous superficial veins in her lower legs. She says that her mother and grandmother had the same problem. The most likely complication of her condition would be which of the following?
A. Myocardial infarction
B. Skin ulcerations
C. Pulmonary embolism
D. Intermittent claudication
E. Ischemic stroke
F. Phlegmasia alba dolens Explanation:
Varicose veins are dilated, tortuous veins resulting from prolonged increases in intraluminal pressure and from loss of vessel-wall tensile strength. The predominant location of varicosities are in superficial veins of the leg. Risk factors are all related to a chronic increase in lower extremity venous pressure and include long periods of standing age greater than 50, obesity, and multiple pregnancies. Defective venous wall development may account for a familial tendency. Varicose dilation of veins leads to incompetent venous valves, venous stasis/congestion, edema, and an increased incidence of thrombosis. Complications result from the poor blood flow—painful thromboses, stasis dermatitis, skin ulcerations, poorly healing wounds, and superficial infections that may promote chronic varicose ulcers. Although deep venous thromboses (DVTs) are the number one cause of pulmonary emboli varicose vein thromboses are restricted to the superficial venous system; therefore thromboembolism is very infrequent with varicose veins.
(Choice A) Although obesity and age are coronary artery disease risk factors varicose veins themselves are not thought to be related to coronary artery atherosclerosis.
(Choice C) This choice is probably the most tempting wrong answer. Deep venous thrombosis is very commonly associated with pulmonary embolism. Thrombosis in superficial varicose veins, however very rarely causes pulmonary embolism.
(Choice D) Claudication is a term that describes a pain and weakness that is associated with exertion and that disappears after rest. Claudication usually refers to the legs, especially the calves, and most commonly stems from inadequate blood supply to the muscles. Peripheral artery disease is the principal cause of claudication. Patients with chronic venous insufficiency (which may present as superficial varicosities) may uncommonly report leg discomfort with exertion. A possible pathogenesis of this discomfort is that venous hypertension during exercise may diminish the capillary perfusion to exercising muscles.
(Choice E) The presence of lower extremity varicose veins is not known to have a direct influence on the incidence of stroke. Stroke and varicose veins share only one major risk factor advanced age.
(Choice F) Phlegmasia alba dolens (painful white leg, “milk leg”) is a consequence of iliofemoral venous thrombosis occurring in peripartum women. Venous stasis due to the pressure of the gravid uterus on deep pelvic veins and the hypercoagulable state inherently present during pregnancy can result in deep venous thrombosis.
Varicose veins are dilated, tortuous veins resulting from prolonged increases in intraluminal pressure and loss of vessel wall tensile strength. Incompetent venous valves venous stasis/congestion, edema, and an increased incidence of superficial venous thrombosis may result. However thromboembolism is a very infrequent complication of varicose veins. Venous stasis ulcers are very common and often occur over the medical malleolus.
Q NO 494: A 70-year-old Caucasian female presents to your office with back pain. Physical examination reveals local tenderness over two lumbar vertebrae, but no abnormal neurological findings. The woman’s past medical history is non-contributory. She is not taking any medications except an over-the-counter multivitamin. X-ray findings are consistent with a vertebral compression fracture. Which of the following changes in bone structure is most likely responsible for this patent’s condition?
. Osteoid matrix accumulation around trabeculae
B. Trabecular thinning with fewer interconnections
C. Subperiosteal resorption with cystic degeneration
D. Lamellar bone structure resembling a mosaic
E. Spongiosa filling the medullary canal with no mature trabeculae Explanation:
Osteoporosis is predominantly a disease of postmenopausal, white females. White females have lower bone mass compared to black females. After menopause declining estrogen levels accelerate the loss of bone mass mainly through a decrease in osteoblastic activity and an increase in osteoclastic activity.
The two major types of bone present in an adult skeleton are trabecular and cortical. Trabecular bones are also called spongy or cancellous bones. Trabecular bone composes only 15% of the total skeleton, by weight but trabecular bone is metabolically more active because of its large surface area. Cortical bones (long bones) contribute by serving as mechanical support and sites of muscle attachment. Most of the appendicular skeleton (the limbs) is cortical bone. Osteoporosis primarily involves trabecular, or spongy bone. The most prominent changes in osteoporosis occur in dorsolumbar vertebral bodies as vertebrae are predominantly trabecular. The neck of the femur consists of 50% of trabecular and 50% of cortical bone. Osteoporotic fractures are most common at vertebral bodies and second most common at the neck of the femur.
(Choice A) Increased deposition of un mineralized osteoid is very characteristic of vitamin D deficiency. Vitamin D is important for the absorption of calcium and phosphorus from the gastrointestinal tract and for bone mineralization.
(Choice C) Hyperparathyroidism increases osteoclastic activity, which results in increased bone resorption. Bone resorption in hyperparathyroidism primarily involves cortical bones (bone loss in postmenopausal osteoporosis is trabecular). Increased resorption of cortical bones results in subperiosteal thinning, a very characteristic feature of hyperparathyroidism.
(Choice D) Paget’s disease of the bone involves only focal areas of the skeleton. The disease process starts as marked osteoclastic activation in particular locations followed by increased osteoblastic activity. The net result is a focal formation of abnormal bone. The new collagen is laid down in a haphazard manner in lieu of the linear deposition in normal bones. The end product is a mosaic pattern of lamellar bone where irregular sections of lamellar bone are linked by cement lines. Cement lines represent previous areas of bone resorption.
(Choice E) Histologically osteopetrosis is characterized by the persistence of primary, un mineralized spongiosa in the medullary canals. In normal individuals the primary spongiosa is replaced by bone marrow.
Osteoporosis (porous bones) represents loss of total bone mass” that results in trabecular thinning. Subperiosteal resorption with cystic degeneration is characteristic of hyperparathyroidism. Vitamin D deficiency results in “excessive un mineralized osteoid” resulting in low mineral density. Osteopetrosis is characterized by ‘the persistence of primary, un mineralized spongiosa in the medullary canals.”
Q NO 495: A 34-year-old Caucasian male is receiving total parenteral nutrition after extensive jejunal resection. Several months later he is found to have biliary stones on abdominal ultrasonography. Which of the following is most likely responsible for the new finding in this patient?
A. High cholesterol content of the nutritional fluids
B. Impaired cholesterol esterification in the liver due to low phospholipid supplementation
C. Increased gastrin release in response to parenteral amino acids
D. Decreased cholecystokinin release due to the lack of enteral stimulation
E. Decreased cholesterol conversion by bile acids due to liver dysfunction Explanation:
A prolonged course of total parenteral nutrition (TPN) is often complicated by the formation of gallstones with one study suggesting the incidence is as high as 44% in this patient population. The pathogenesis of TPN-induced gallstones is thought to include: 1) biliary stasis from absent enteral stimulation secondary to decreased cholecystokinin release: and 2) in those with ileal resection, disturbance of the enterohepatic bile acid circulation resulting in supersaturation of hepatic bile with cholesterol. Exogenous cholecystokinin administration will typically prevent gallstone formation in patients on TPN.
(Choice A) Total parenteral nutrition comes in various formulas, with different proportions of glucose, amino acids, and fats provided based on the individual patient’s needs. Electrolytes, vitamins, minerals, and trace elements are added in carefully calculated amounts. Therefore it is highly unlikely that the TPN would have excessive fats or inappropriate cholesterol content.
(Choice B) Excess intracellular cholesterol is esterified by acyl-CoA-cholesterol acyltransferase (ACAT) for storage within the cell. Disruptions in this process are not a significant cause of gallstone formation in patients on TPN.
(Choice C) Parenteral nutrition typically results in decreased, not increased gastrin release. Moreover gastrin is not a significant factor in the formation of gallstones.
(Choice E) Liver disease can result in impaired enterohepatic recirculation of bile acids, as injured hepatocytes have a diminished ability to extract bile acids from portal blood. There is no indication that this patient has liver disease, however.
Total parenteral nutrition can induce gallstone formation secondary to biliary stasis from absent enteral stimulation or disturbance of the enterohepatic bile acid circulation in those with ileal resections.
Q NO 498: A 57-year-old Caucasian male died in his car on his way to the emergency room, 30 minutes after the onset of chest pain. His past medical history is significant for hypertension, diabetes, and hypercholesterolemia. His medications included metformin, simvastatin, and enalapril. A cross-section of his left anterior descending coronary arteri is shown on the slide below. Which of the following is the most likely cause of death of this patient?
A. Contractile dysfunction
B. Ventricular septal rupture
C. Cardiac free wall rupture
D. Ventricular fibrillation
E. Embolic stroke
F. Atrial fibrillation Explanation:
This patient’s LAD coronary artery shows an acute plaque change. There is a ruptured atheromatous plaque with superimposed thrombosis. The vessel lumen is completely occluded by the thrombus. Thus, it appears an acute coronary syndrome caused sudden cardiac death (SCD).
SCD is defined as cardiac arrest that begins within one hour of the precipitating event and ultimately proves fatal. Approximately 80% of SCDs are due to coronary artery disease (CAD). In the majority of CAD-related SCDI the pathogenesis is acute plaque change producing acute myocardial ischemia. Ischemia produces electrical instability in the heart and can generate a potentially lethal arrhythmia. Ventricular fibrillation is usually the first arrhythmia to appear as a result of acute myocardial ischemia, and is the most common cause of lethal cardiac arrest in CAD-related SCD. Ventricular fibrillation is also the most common cause of death from myocardial infarction in the pre-hospital phase (i.e. prior to arrival in the emergency room).
Ventricular tachycardia and ventricular fibrillation are the most lethal arrhythmias in patients with acute Ml. Atrial flutter and atrial fibrillation are arrhythmias that do not usually result in sudden cardiac death.
(Choice A) Extensive myocardial infarction (Ml) may result in terminal ventricular failure. However, death due to heart failure caused by an Ml usually does not occur suddenly. Ventricular failure is the most common cause of death due to Ml during the in-hospital phase.
(Choices B and C) When a patient sustains this sort of occlusion, death can result from complications of myocardial infarction. Extracardiac obstructive shock, due to left ventricular free wall rupture and cardiac tamponade, is a less common cause of death in such instances. This is an unlikely explanation for the patient in the vignette however, because LV rupture generally does not occur until 3 to 7 days after the onset of infarction. Similarly, death may result due to ventricular septal rupture but this also does not occur until 3-7 days after the onset of infarction.
(Choice E) Following a myocardial infarction (MI) there may be ventricular mural thrombosis and cerebral thromboembolism. However it is unusual to have significant mural thrombosis prior to 48 hours after the Ml.
Coronary artery disease is the underlying etiology in most cases of sudden cardiac death. Typically an acute plaque change will result in acute myocardial ischemia, which may precipitate ventricular fibrillation. Cardiac arrhythmia is the most common cause of death in Ml patients in the pre-hospital phase. Ventricular failure is the most common cause of death during the in-hospital phase of Ml. Other later-onset potentially lethal complications include ventricular rupture and mural thrombosis with thromboembolism.
Q NO 502: A 23-year-old male is brought to the ER with a Mo-day history of fever, headaches, and confusion. The patient slips into a coma and dies several days after admission. Autopsy reveals intense, bilateral, hemorrhagic necrosis of the inferior and medial temporal lobes. This patient’s condition was most likely caused by which of the following?
B. Herpesvirus infection
C. Enterovirus infection
D. Polyomavirus infection
E. Spirochetal infection
F. Mycobacterial infection
G. Fungal infection
H. Protozoal disease Explanation:
HSV-1 mostly affects teenagers and young adults and is the most common cause of sporadic encephalitis. Encephalitis results from the reactivation of latent virus “living” in the trigeminal ganglion and the virus spread along this nerve into the cerebral vault. Temporal lobe involvement is characteristic of HSV-1 encephalitis.
The most common early symptoms of acute encephalitis are headache and fever. Mental status changes (lethargy, confusion), cranial nerve deficits, and seizures may follow. Specific symptoms of herpetic encephalitis are related to HSV-1’s predilection for the temporal lobe including aphasia (damage of speech areas), olfactory hallucinations (olfactory cortex involvement), and personality changes (amygdala damage).
Macroscopic brain examination reveals edema and hemorrhagic necrosis of the temporal lobes. Eosinophilic intranuclear inclusions (Cowdry type A) are present in glial cells and neurons. Multinucleated giant cells may also be found.
EEG can reveal focal temporal abnormalities. CT or MRI detect edema and hemorrhage in the temporal lobe. CSE has a typical “viral pattern with lymphocytic pleocytosis, normal glucose, and elevated protein levels.
(Choice C) Enterovirus infection causes viral meningitis. Patients present with headache, nausea, vomiting, and confusion. Meningeal signs are positive. The inflammatory process is confined to the meninges and does not specifically involve the temporal lobe.
(Choices F and G) Both mycobacteria and fungi can cause meningoencephalitis, but neither shows a predilection for the temporal lobe.
HSV-1 encephalitis has a predilection for the temporal lobe. This site-specific damage causes restricted symptoms, including aphasia (damage of speech areas), olfactory hallucinations (olfactory cortex involvement), and personality changes (amygdala involvement). Macroscopic brain examination reveals edema and hemorrhagic necrosis of the temporal lobes.
Q NO 505: A 65-year-old male is being evaluated for fatigue mild normocytic anemia and anorexia. He has lost 10 pounds over the last two months. Chest X-ray reveals an irregular perihilar mass in the right lung field. This patient’s symptoms can be mimicked in experimental animals by administration of which of the following?
F. Vasopressin Explanation:
Cachexia is a syndrome that encompasses anorexia, malaise, anemia, weight loss and generalized wasting due to underlying systemic disease. Cachexia in the patient described above is a manifestation of the lung neoplasm revealed on his chest X-ray. Tumor necrosis factor-alpha is a cytokine that causes necrosis of some tumors in vitro. In experimental animals it also produces symptoms of cachexia. For this reason TNF-? is also called cachectin and is considered a main mediator of paraneoplastic cachexia.
TNF-? is produced by macrophages in response to infection as well as by some neoplastic cells. Its role in cachexia is explained by its influence on hypothalamus that leads to appetite suppression.
In bacterial infections, TNF-? produces fever along with IL-1 mediates many of the symptoms of septic shock and causes hepatic release of acute-phase reactants such as C-reactive protein and fibrinogen.
(Choice A) Interferon-? is synthesized by leukocytes and has antiviral as well as anti-tumor activity.
(Choice B) IL-3 is produced by activated CD4+ TH cells. It stimulates growth and differentiation of immature T cells in the bone marrow.
(Choice C) The main function of transforming growth factor-beta is inhibition of the inflammatory response. It decreases T cell proliferation and cytokine production
(Choice D) PTHrP (parathyroid hormone-related peptide) is produced by tumor cells and causes paraneoplastic hypercalcemia.
(Choice F) Production of vasopressin by some tumors results in SIADH (syndrome of inappropriate ADH secretion).
TNF-? was shown to induce a wasting syndrome (cachexia) in experimental animals. It is thought to mediate paraneoplastic cachexia in humans by suppressing appetite, inhibiting lipoprotein lipase and increasing insulin resistance of peripheral tissues.
Q NO 509: A 46-year-old male presents to the emergency room after an episode of large-volume hematemesis. Physical examination reveals a palpable spleen and mild ascites. Endoscopy is performed and reveals bleeding esophageal varices. A liver biopsy performed two days later reveals no abnormalities. Which of the following is the most likely cause of this patient’s condition?
A. Acetaminophen toxicity
B. Long-term alcohol consumption
C. Budd-Chiari syndrome
D. Constrictive pericarditis
E. Portal vein thrombosis Explanation:
This patient is exhibiting signs of portal hypertension, including: ascites, hematemesis (from esophageal varices), and splenic enlargement. Varices form in portal hypertension because increased hydrostatic pressure in the portal system causes blood to be shunted through portocaval anastomoses. This patient’s normal liver biopsy indicates that the process responsible for the portal hypertension occurred distal to the liver in the portal circulation. Portal vein thrombosis is the only process listed that occurs distal to the liver and causes portal hypertension while leaving the liver unaffected.
(Choice A) Acetaminophen toxicity causes centrilobular hepatic necrosis and liver failure 24-48 hours following ingestion, depending on the amount consumed. This process would be obvious on liver biopsy.
(Choice B) Long-term alcohol consumption causes hepatic cirrhosis, where hepatocyte damage and death stimulate fibroblast proliferation and fibrosis. With continued alcohol consumption, fibrosis outpaces the liver’s regenerative capacity. This process would be evident on liver biopsy.
(Choice C) In Budd-Chiari syndrome there is occlusion of the hepatic vein the vein that drains blood from the liver and portal circulation into the systemic circulation. Liver biopsy shows centrilobular congestion and fibrosis.
(Choice D) Constrictive pericarditis causes blood to back up in the systemic venous circulation due to decreased cardiac output. This increases pressure within the liver in much the same way that Budd-Chi an syndrome does.
Portal vein thrombosis causes portal hypertension, splenomegaly, ascites and varicosities in portocaval anastomoses. It does not cause histologic changes to the hepatic parenchyma.
Q NO 510: A 35-year-old previously healthy male is brought to the ER after being involved in a motor vehicle accident. The patient has suffered significant blunt chest and head trauma. In the ER, his blood pressure drops suddenly and he begins experiencing respiratory distress. On physical examination, the patient is tachycardic and tachypneic. His systolic blood pressured falls 20mm Hg with inspiration, and jugular venous distention is present. His breath sounds are clear to auscultation. The most likely cause of this patient’s deterioration is:
A. Tension pneumothorax
B. Epidural hematoma
D. Aortic rupture
E. Cardiac tamponade Explanation:
On physical examination this patient has pulsus paradoxus (a fall in systolic blood pressure of more than 10 mmHg on inspiration), jugular venous distention, and tachycardia. Based on his history and physical exam findings, cardiac tamponade is the most likely diagnosis. Cardiac tamponade should be suspected in any patient who has the characteristic triad of muffled heart sounds jugular venous distention, and hypotension.
During normal inspiration, the pressure in the pleural space and lung interstitium decreases, increasing pulmonary vascular capacitance. This results in a fall in venous inflow to the left heart and a drop in cardiac output (CO). Increased venous return to the right heart and an increased heart rate during inspiration tend to offset this decrease in CO by increasing right ventricular output and pulmonary venous inflow into the left heart. Conditions that limit the compensatory increase in right ventricular filling and output during inspiration can exaggerate this normal inspiratory drop in left sided CO and systolic blood pressure. These conditions include: pericardial tamponade, constrictive pericarditis, emphysema with cor pulmonale, asthma, and pulmonary embolism.
(Choice A) Tension pneumothorax can cause hypotension, tachycardia, tachypnea, and jugular venous distension (JVD). Tension pneumothorax can result from blunt or penetrating chest trauma that injures the visceral pleura or tracheobronchial tree but the findings of absent breath sounds and hyperresonance to percussion on the affected side would also be observed.
(Choice B) An epidural hematoma (EDH) may initially cause hypertension and bradycardia due to the Cushing reflex to increased intracranial pressure. If an EDH progresses to cause herniation, hypotension may follow. An EDH would not cause elevated JVD or pulsus paradoxus.
(Choice C) Blunt or penetrating chest trauma could cause a massive hemothorax with hemorrhagic hypotension, tachycardia, and tachypnea. However the findings of absent breath sounds and dullness to percussion on the affected side would also be observed.
(Choice D) An aortic rupture would cause hypovolemic shock not elevated JVD.
The combination of jugular venous distension (reflective of elevated central venous pressure) and hypotension together with pulsus paradoxus in a previously healthy patient who has suffered penetrating or blunt chest trauma to the precordial region is highly suggestive of tamponade. Tension pneumothorax and hemothorax are relatively unlikely to cause pulsus paradoxus. Breath sounds are normal in tamponade and absent in tension pneumothorax.