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Exam Section 1: Item 1 of 50 National Board of Medical Examiners' Comprehensive Basic Science Self-Assessment
- Patients with prolonged starvation or untreated type 1 diabetes mellitus overproduce ketone bodies. Which of the following is a common factor that is responsible for ketosis in patients with these two conditions? A) Depletion of pentose phosphate pathway intermediates B) Increased availability of acetyl COA C) Inhibition of fatty acid oxidation D) Inhibition of gluconeogenesis E) Inhibition of glycogenolysis B. Increased availability of acetyl CoA is common to states of starvation and untreated type 1 diabetes mellitus. In starvation, glycogen stores are gradually depleted. The body then relies on the breakdown of fat through oxidation of fatty acids to provide energy. Fatty acid oxidation occurs in the mitochondria of the cell. In each cycle of oxidation, two-carbon fragments are cleaved to form acetyl CoA, which leaves the mitochondria via the carnitine shuttle. In addition to a molecule of acetyl CoA which then enters the citric acid cycle, a molecule of NADH is produced in each cycle. Ketogenesis occurs in starvation via two-carbon fragments, with formation of ketoacids such as acetoacetyl CoA and B-hydroxybutyrate. The ability to generate energy from adipose during a period of starvation is critical to maintaining the function of vital organs, such as the brain. In untreated type 1 diabetes mellitus, there is an absolute deficiency of insulin, which renders many cells incapable of shuttling glucose into the cell for use in cellular respiration. While there are several glucose transporters that do not require insulin for glucose entry, GLUT4 is commonly
expressed in many cell types and requires insulin to function. Patients with untreated type 1 diabetes mellitus will have serum glucose concentrations in the high-normal to high range as a result of ongoing gluconeogenesis and glycogenolysis, but insulin deficiency prevents entry of circulating glucose into cells through glucose transport proteins, effectively resulting in a state of starvation. This results in ketogenesis and accounts for the presence of ketone bodies in the blood and urine of patients with starvation or untreated type 1 diabetes mellitus. Incorrect Answers: A, C, D, and E. Depletion of pentose phosphate pathway intermediates (Choice A) is not correct. This pathway is active in many tissues including the liver, adrenal cortex, and in erythrocytes. It produces NADPH, ribose- 5 - phosphate, and erythrose- 4 - phosphate from glucose. Decreased activity of this pathway would not lead to generation of ketones. Inhibition of fatty acid oxidation (Choice C) is not correct. Fatty acid oxidation is increased during states of starvation or untreated type 1 diabetes mellitus. Inhibition of gluconeogenesis (Choice D) and inhibition of glycogenolysis (Choice E) are not features of starvation or untreated type 1 diabetes mellitus. In fact, these processes are accelerated in both states, although in starvation, this is caused by a deficiency of glucose. In untreated type 1 diabetes mellitus, these pathways are upregulated as a result of insulin deficiency, perceived by the cell as a hypoglycemic state. Educational Objective: Both starvation and untreated type 1 diabetes mellitus result in an increased rate of fatty acid oxidation, which generates acetyl CoA to be used in the citric acid cycle and NADH. Concomitant ketogenesis results in the formation of ketone bodies that can be detected in serum and urine. %3D Next Score Report Lab Values Calculator Help Pause 2 Exam Section 1: Item 2 of 50 National Board of Medical Examiners'
pancreas, spleen, kidneys, and adrenal glands. The vagus nerve serves as the efferent nerve for the gag reflex. The hypoglossal nerve (Choice E) is primarily a somatic efferent nerve to the tongue muscles, mediating tongue protrusion, depression, and retraction. The hypoglossal nerve does not innervate the pharynx. Educational Objective: The glossopharyngeal nerve (cranial nerve IX) contains somatic afferent fibers that control the sensation of the palate and upper pharynx, providing afferent information for the gag reflex. The efferent nerve for the gag reflex is the vagus nerve, which innervates the soft palate and pharyngeal muscles to control gagging and swallowing. Previous Next Score Report Lab Values Calculator Help Pause 3 Exam Section 1: Item 3 of 50 National Board of Medical Examiners' Comprehensive Basic Science Self-Assessment
- A 62-year-old man with a 4-year history of chronic angina pectoris comes to the emergency department because of severe chest and left shoulder pain. Physical examination shows bradycardia. An ECG shows ST-segment elevation in leads II, III, and aVF. Occlusion of blood flow in which of the following arteries is the most likely cause of the findings in this patient? A) Anterior interventricular (left anterior descending) B) Circumflex C) Left coronary D) Right coronary D.
The right coronary artery originates from the right aortic sinus and primarily provides blood flow to the right ventricle, right atrium, sinoatrial (SA) node, and atrioventricular (AV) node, and in a right-dominant circulation (-85% of patients), it provides a majority of the blood supply to the inferior heart through the posterior descending artery. Occlusion of the right coronary artery can result in infarction of myocardial tissue along the inferior portion of the heart, which leads to ST-segment changes in the inferior ECG leads II, III, and aVF. Impaired perfusion to the SA and AV nodes can also result in bradycardia or heart block. The patient requires admission to the hospital and emergent cardiac catheterization for revascularization or consideration of thrombolytics if not close to a center capable of percutaneous coronary intervention. Incorrect Answers: A, B, and C. The anterior interventricular (left anterior descending) (Choice A) artery branches from the left main coronary artery and provides perfusion to the anterior portion of the interventricular septum, the anterior left ventricle, and the anterolateral papillary muscle. Infarction of this territory may present with ST-segment changes in the precordial ECCG leads. The circumflex (Choice B) artery originates from the left main coronary artery and primarily provides perfusion to the lateral and posterior walls of the left ventricle, the anterolateral papillary muscle, and some blood flow to the AV node. It does not provide perfusion to the inferior heart unless the patient demonstrates a left-dominant circulation (~8% of patients). Infarction of this territory may result in ST-segment changes in the lateral, posterior, and/or inferior ECG leads. The left coronary (Choice C), or left main coronary, artery arises from the left aortic sinus and branches into the left anterior descending and left circumflex arteries. ST-elevation myocardial infarctions involving the left main coronary artery are associated with significant morbidity and mortality, as it would involve a majority of the myocardium. Educational Objective: The right coronary artery provides blood flow to the right ventricle, right atrium, SA node, and AV node, and in a right-dominant circulation (~85% of patients), it provides a majority of the blood supply to the inferior heart through the posterior descending artery. Myocardial infarction in this territory is associated with ST-segment changes in the inferior ECG leads and may also present with bradycardia or heart block. II Previous Next Score Report Lab Values Calculator
Decreasing VLDL production (Choice B) is one of the mechanisms of action of niacin (vitamin B3). VLDL is produced in the liver from cholesterol and niacin inhibits this catalytic conversion. Niacin also inhibits hormone-sensitive lipase and thus decreases lipolysis, the process by which triglycerides stored in adipose tissue are degraded. Inhibiting hepatic cholesterol synthesis (Choice C) is the mechanism of action of HMG-COA reductase inhibitors such as simvastatin, atorvastatin, and rosuvastatin. Statins inhibit the enzyme HMG-COA reductase, which catalyzes the rate limiting step in cholesterol biosynthesis, thereby resulting in decreased intrahepatic concentrations of cholesterol. As is the case when bile acid resins are used, decreased intrahepatic cholesterol concentrations lead to increased expression of LDL receptors on the surface of hepatocytes with a consequent decrease of circulating concentrations of LDL. Bile acid resins stimulate HDL production (Choice D) to a small degree. However, this is not the mechanism by which bile acid resins lower the total serum cholesterol. Educational Objective: Bile acid resins decrease serum cholesterol by inhibiting bile acid recycling through the intestinal lumen. The decreased reabsorption of cholesterol results in decreased intrahepatic cholesterol concentrations; this causes the liver to increase expression of the LDL receptors that bind plasma LDL and ultimately lower serum cholesterol. Previous Next Score Report Lab Values Calculator Help Pause 5 Exam Section 1: Item 5 of 50 National Board of Medical Examiners' Comprehensive Basic Science Self-Assessment
- A70-year-old woman comes to the physician for a follow-up examination. She had breast cancer 5 years ago and underwent partial mastectomy of the left breast at that time. She has received treatment with tamoxifen since then. Physical examination and mammography show no evidence of recurrence. Which of the following mechanisms most likely explains the
beneficial effect of tamoxifen in treating this patient? A) Competitive inhibition of estradiol activation of cyclin D1 and E2 proteins B) Competitive inhibition of estradiol binding to its receptor C) Competitive inhibition of estradiol synthase in ovaries and adrenal cortex D) Downregulation of bcl- 2 E) Downregulation of estrogen receptors F) Increased estradiol catabolism by CYP3A G) Increased renal excretion of synthesized estradiol B. Tamoxifen is a selective estrogen receptor modulator that is used in the treatment of breast cancer. It acts as an estrogen receptor antagonist in the breast but as an estrogen receptor agonist in the endometrium and bone. Because of its unopposed estrogen stimulation of the endometrium, it increases the risk for endometrial hyperplasia with the potential for atypia and consequent endometrial cancer. Other risks of tamoxifen use include deep venous thrombosis and pulmonary embolism as a result of the hypercoagulability caused by alterations to estrogen receptors. It decreases the risk for recurrent invasive breast cancer in bilateral breasts by approximately 30% to 50%, although it results in little difference in overall mortality. Incorrect Answers: A, C, D, E, F, and G. Competitive inhibition of estradiol activation of cyclin D1 and E2 proteins (Choice A) would decrease cell proliferation and the risk for recurrence of invasive breast carcinoma. Both cyclins are overexpressed or deregulated in tamoxifen-resistant breast cells. This is not the mechanism of tamoxifen. Competitive inhibition of estradiol synthase in ovaries and adrenal cortex (Choice C) is the mechanism of action of aromatase inhibitors, such as anastrozole, which are also used in the management of estrogen receptor-positive breast cancer. Downregulation of bcl-2 (Choice D) would decrease the risk for invasive carcinoma, since bcl-2 inhibits pro-apoptotic proteins, promoting cellular survival. However, this is not the mechanism of action of tamoxifen therapy. Downregulation of estrogen receptors (Choice E) would decrease the responsiveness of breast cancer cells to estradiol in the serum. This is not a mechanism currently employed in the hormonal treatment of breast cancer. Increased estradiol catabolism by CYP3A (Choice F) and increased renal excretion of synthesized estradiol (Choice G) would decrease the available estradiol to bind to estrogen receptor- positive breast cancer cells and would theoretically decrease the risk for recurrent breast carcinoma. They are not, however, mechanisms currently utilized by medications used to treat breast
and both the patients and investigators are blinded to the assignment (double-blinded). Controlled trials are the standard for medical research, and they generate more powerful evidence than other forms of observational or descriptive studies. In this case, the intervention is St. John's wort, and it is being compared with a placebo. A clinical trial typically utilizes a randomized, controlled design. There are four phases to clinical trials. In phase I, a small number of healthy volunteers are tested to determine if the drug is safe in healthy individuals. In phase II, a small number of diseased volunteers are tested to determine if the drug is effective in the disease population. In phase III, a large number of patients are assigned to receive either the drug or placebo to determine if the drug is better than the placebo or current standard of care. In phase IV, or post-market surveillance, patients who take the drug once it is approved are observed for any unpredicted adverse effects. Adverse results in a phase IV trial can result in a drug being removed from the market. Incorrect Answers: A, B, D, and E. A case-control study (Choice A) investigates an association between an exposure and an outcome. In this study design, a group of patients with the disease (cases) are identified. A group of patients without the disease (controls) are matched on baseline characteristics to the cases. Exposure data for the two groups is collected, and these data are compared to determine association with the outcome (disease) in question. An odds ratio may be calculated to compare exposures between groups. A cohort study (Choice B) identifies a group of patients with or without an exposure and follows them over time to identify whether an exposure is associated with an outcome of interest. Cohort studies may be retrospective or prospective in design. In a prospective design, the hypothesis and analysis protocols are established prior to the start of the study period. In a retrospective design, the hypothesis or question is designed after the study time period has passed. A crossover study (Choice D) is a type of controlled trial in which patients begin the study in either the intervention or placebo group and then cross over to the other group at a predetermined time point. For example, if this study had a crossover design, patients receiving St. John's wort would be followed until a given point in time, then switched to the placebo and followed to a second point in time. A cross-sectional study (Choice E) seeks to identify the prevalence of a condition at a particular point in time. An example of a cross-sectional study would be a single survey of a population inquiring whether patients have depression and concurrently inquiring about their use of St. John's wort. Thus, the risk factor and the outcomes are measured simultaneously. The study does not follow patients over time. All information is collected at a single point in time. Causation cannot be determined from a cross-sectional study, only correlation.
Educational Objective: A randomized, blinded, controlled trial is the standard for medical research. Subjects are randomly assigned to receive either the intervention or placebo, and their outcomes are closely measured. These studies generate the most compelling evidence that a given intervention has an effect on a given outcome, and they compare that effect to either a placebo or the current standard of care. Previous Next Score Report Lab Values Calculator Help Pause 7 Exam Section 1: Item 7 of 50 National Board of Medical Examiners' Comprehensive Basic Science Self-Assessment
- A 60-year-old woman comes to the physician because of intermittent joint pain during the past 5 years. The pain is abrupt in onset and involves principally her hands, knees, and toes. She has a history of pyelonephritis; there is no history of trauma. Examination of the left knee shows tenderness, swelling, and warmth with dusky, erythematous overlying skin. A photograph of the left hand is shown, along with a photomicrograph of joint fluid aspirate. Which of the following is most likely in excess concentration in the joint fluid of this patient? A) Calcium apatite B) Calcium oxalate C) Calcium pyrophosphate D) Cholesterol E) Sodium chloride F) Sodium monourate F.
Previous Next Score Report Lab Values Calculator Help Pause 8 Exam Section 1: Item 8 of 50 National Board of Medical Examiners' Comprehensive Basic Science Self-Assessment
- A 12-year-old boy is brought to the office by his mother for an annual well-child examination. He has asthma well controlled with inhaled budesonide. The mother says that the boy recently has voiced concern about his height and is bothered by the fact that he is considerably shorter than the other boys on his basketball team. The patient's father is 182 cm (6 ft) tall and his mother is 168 cm (5 ft 6 in) tall. The patient is 135 cm (4 ft 5 in; 3rd percentile) tall and weighs 32 kg ( lb; 10th percentile); BMI is 17 kg/m2 (35th percentile). The patient's growth has remained steady at the 3rd percentile during the past 8 years. Vital signs are within normal limits. Sexual maturity rating is 1 for pubic hair and genital development. The remainder of the physical examination shows no abnormalities. Which of the following is the most likely diagnosis? A) Constitutional growth delay B) Familial short stature C) Growth hormone deficiency D) Hypopituitarism E) Hypothyroidism F) Steroid-induced growth failure A. Short stature can be hereditary, or a result of a variety of causes, such as constitutional growth delay, chronic steroid use, endocrine abnormalities, cardiopulmonary disease, and genetic
disorders. Familial (hereditary) short stature and constitutional growth delay are the most common causes of short stature. Familial short stature is associated with short stature in both parents, a normal gain of height velocity, and a bone age that corresponds with chronological age, whereas a constitutional growth delay is independent of parental stature, has a decreased growth velocity, and a bone age younger than the patient's chronological age. Those with constitutional growth delay typically reach a normal adult height, with more rapid increases in height gain velocity after they reach puberty. Other causes of short stature include growth hormone deficiency, hypothyroidism, cystic fibrosis, severe congenital heart disease, Turner syndrome, and Down syndrome. This patient has parents with normal stature and has had a decreased growth velocity but does not have other signs or symptoms to suggest another cause of short stature, making constitutional growth delay the most likely diagnosis. Incorrect Answers: B, C, D, E, and F. Familial short stature (Choice B) typically presents in a patient whose parents are both of short stature with a normal growth velocity and bone age consistent with chronological age. They will remain of short stature into adulthood. This patient has a diminished growth velocity, making this answer less likely. Growth hormone deficiency (Choice C) can present in infancy or childhood, depending on the severity of deficiency. Acquired growth hormone deficiency is typically caused by a nonfunctional pituitary tumor and presents with severe growth delay and a bone age younger than chronological age. It is associated with a rapid decline in the height-for-age curve, crossing percentiles. This patient's growth velocity has been slow but consistent, making growth hormone deficiency a less likely cause of his short stature. Hypopituitarism (Choice D) presents with short stature, fatigue, hypotension, cold intolerance, constipation, amenorrhea or oligomenorrhea in women, and decreased libido in men, as well as decreased development of secondary sexual characteristics. This patient does not have signs or symptoms to suggest hypopituitarism. Hypothyroidism (Choice E) in adolescents can present with short stature and growth delay, but it would be expected to present with other signs of hypothyroidism, such as fatigue, weight gain, cold intolerance, and constipation. Steroid-induced growth failure (Choice F) is seen in patients on chronic systemic steroid therapy as a result of the negative feedback on growth hormone secretion and inhibition of collagen and bone formation. While this patient takes daily inhaled steroids, this local delivery of steroids to the respiratory tract would be unlikely to cause steroid-induced growth failure. Educational Objective: Constitutional growth delay presents in a patient who has parents of normal stature and demonstrates short stature, delayed pubertal development, slow but consistent
activate complement, which attracts neutrophils. The neutrophils set into motion an inflammatory cascade and release lysosomal enzymes, causing inflammation and degradation of the surrounding healthy tissue. Another example of type III hypersensitivity is serum sickness. Serum sickness occurs when a drug, such as anti-thymocyte globulin, acts as a hapten to the immune system, triggering antibody formation. The antibodies then bind the drug, deposit in tissue, and attract and activate complement. The result is fever, rash, and arthralgias. Serum sickness reaction usually occurs 1 to 2 weeks after the initial exposure to the drug, reflecting the time required to mount an immune response. Incorrect Answers: A, C, D, and E. Acute rheumatic fever (Choice A) is a late complication of untreated Group A Streptococcus infection characterized by carditis, subcutaneous nodules, erythema marginatum, Sydenham chorea, and migratory polyarthritis. The cause is related to immune cross-reactivity caused by molecular homology between streptococcal M protein and human cardiac myosin proteins. It is a type II (complement-mediated cytotoxic) hypersensitivity reaction. Graft-versus-host disease (Choice C) and immune response to PPD skin testing (Choice D), or tuberculin reaction, are examples of type IV (delayed) hypersensitivity reactions. Type IV hypersensitivity is characterized by a cell-mediated response that involves the maturation of antigen- specific CD4+ or CD8+ T lymphocytes to a specific antigen. When the antigen is encountered, ČD4+ T lymphocytes release cytokines leading to inflammation and macrophage activation, while CD8+ T lymphocytes directly kill cells expressing the antigen. This type of hypersensitivity takes several days to manifest. Allergic contact dermatitis is another example of a type IV hypersensitivity reaction. Peanut allergy (Choice E) is an example of a type I (immediate) hypersensitivity reaction. Type I hypersensitivity occurs when preformed IgE on the surface of mast cells and basophils is crosslinked by an antigen, leading to immediate degranulation and release of histamine. This results in vasodilation, vascular pooling, and increased vascular permeability, which clinically manifests as urticaria, angioedema, or anaphylaxis. Educational Objective: Type III hypersensitivity is defined by the presence of circulating antigen- antibody-complement complexes that deposit in tissues and cause inflammation and destruction. SLE, serum sickness reaction, polyarteritis nodosa, and poststreptococcal glomerulonephritis are all examples of type III hypersensitivity reactions. Previous Next Score Report Lab Values
Calculator Help Pause 10 Exam Section 1: Item 10 of 50 National Board of Medical Examiners' Comprehensive Basic Science Self-Assessment
- A 33-year-old woman comes to the physician because of fatigue for 2 months; she feels well otherwise. She has a 10-year history of systemic lupus erythematosus treated with prednisone. Physical examination shows no abnormalities. Laboratory studies show: 9.0 g/dL 27% 8500/mm 0.2% Hemoglobin Hematocrit Leukocyte count Reticulocyte count Platelet count 190,000/mm Serum Ferritin Iron Total iron-binding capacity Red cell morphology 250 ng/mL 10 pug/dL 100 ug/dL (N=250-400)
Decreased uptake of iron by bone marrow macrophages (Choice D) does not occur in ACD. Macrophages in this condition have a tendency to store iron; an increased concentration of hepcidin, which is the primary pathologic change in ACD, inhibits the release of iron from macrophages. Educational Objective: ACD is common in patients with rheumatologic diseases such as SLE; itis the result of increased hepcidin secretion mediated by increased concentrations of inflammatory cytokines. This results in the increased retention of iron within the RES and impaired iron exportation for use in erythropoiesis with consequent anemia. Ferritin concentrations are normal to increased, and serum iron concentrations and TIBC are decreased. Previous Next Score Report Lab Values Calculator Help Pause 11 Exam Section 1: Item 11 of 50 National Board of Medical Examiners' Comprehensive Basic Science Self-Assessment
- A 47-year-old man comes to the emergency department because of the sudden onset of severe pain of his lower chest and upper abdomen, and dry heaves. He also has a 4-year history of intermittent heartburn. His pulse is 118/min, and blood pressure is 80/50 mm Hg. Physical examination shows epigastric tenderness. A nasogastric tube cannot be passed into the stomach. The diagnosis of gastric volvulus is made, and appropriate treatment is begun. This patient most likely also has which of the following underlying conditions? A) Cholecystitis B) Duodenal ulcer C) Gastric cancer D) Pancreatitis E) Paraesophageal hernia
E.
Gastric volvulus occurs when the stomach rotates along its short or long axis causing obstruction. It may be caused by anomalies of the gastric ligaments (primary gastric volvulus) or anatomic abnormalities (eg, paraesophageal hernia). An acute gastric volvulus presents with severe abdominal pain and nonproductive vomiting or heaving. These symptoms with the inability to pass a nasogastric tube into the abdomen are called the Borchardt triad and are present in - 70% of patients with gastric volvulus. The most common cause of secondary gastric volvulus is a paraesophageal hernia, followed by a diaphragmatic hernia or phrenic nerve paralysis. In children, a congenital diaphragmatic hernia is the most commonly associated abnormality. In the case of a paraesophageal hernia, the stomach rotates on its long axis, which can be imagined as a line from the gastroesophageal junction to the pyloric sphincter. This causes the greater curvature of the stomach to be superior to the inferior curvature of the stomach and obstructs the gastric outlet. With prolonged volvulus, strangulation of the stomach can occur, which is followed by ischemia, necrosis, perforation, and finally peritonitis. The first step in treatment is to attempt decompression via a nasogastric tube to decrease pressure on the gastric mucosa and prevent ischemia. However, if unsuccessful, surgical intervention is required. Incorrect Answers: A, B, C, and D. Cholecystitis (Choice A) occurs secondary to obstruction of the cystic duct from a gallstone, which results in subsequent inflammation of the gallbladder wall. It typically presents with fever, abdominal pain, and tenderness to palpation in the right upper quadrant, often in a patient with a history of biliary colic and cholelithiasis. The pain may also radiate to the right shoulder or interscapular region. It would not contribute to the development of gastric volvulus. Duodenal ulcer (Choice B) classically presents with worsening abdominal pain related to a lack of consumption of food. The most common cause of duodenal ulcers is infection with the bacterium Helicobacter pylori. Persistent inflammation related to a duodenal ulcer can result in complications including fibrosis, stricture, and hemorrhage. Perforation is another potential complication, which commonly presents with acute abdominal pain, peritonitis, fever, and free air on x- rays and CT. While a stricture or fibrosis from a duodenal ulcer could cause a small bowel obstruction or be a lead point for intussusception, it would not cause gastric volvulus. Gastric cancer (Choice C) would be more likely to manifest with weight loss, early satiety, gastrointestinal bleeding, and systemic symptoms such as fatigue and malaise. Gastric cancer is less likely to cause gastric volvulus than a paraesophageal hernia since it is usually confined to the lumen of the stomach and does not cause redundancy in the gastric wall or an anatomic change that allows the stomach to rotate on its axis.
