Тесты - USMLE world step 1 medical Qbook (Questionnary book - банк тестов) - файл Patho physio 50q.doc

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Patho physio 50q.doc

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USMLE WORLD STEP 1 PATHOPHYSIOLOGY

Question List

Pathophysiology Q No:

1

Cardiology

Pathophysiology Q No:

42

Endocrinology

Pathophysiology Q No:

2

Pulmonology

Pathophysiology Q No:

43

Hepatobiliary system

Pathophysiology Q No:

3

Pulmonology

Pathophysiology Q No:

44

Cardiology

Pathophysiology Q No:

4

Cardiology

Pathophysiology Q No:

45

Cardiology

Pathophysiology Q No:

5

Renal

Pathophysiology Q No:

46

Gastrointestinal system

Pathophysiology Q No:

6

Hepatobiliary system

Pathophysiology Q No:

47

Pulmonology

Pathophysiology Q No:

7

Genitourinary

Pathophysiology Q No:

48

Hepatobiliary system

Pathophysiology Q No:

8

Renal

Pathophysiology Q No:

49

Musculoskeletal

Pathophysiology Q No:

9

Endocrinology

Pathophysiology Q No:

50

Endocrinology

Pathophysiology Q No:

10

Endocrinology

Pathophysiology Q No:

51

Endocrinology

Pathophysiology Q No:

11

Cardiology

Pathophysiology Q No:

52

Blood vessels

Pathophysiology Q No:

12

Endocrinology

Pathophysiology Q No:

53

Cardiology

Pathophysiology Q No:

13

Endocrinology

Pathophysiology Q No:

54

Endocrinology

Pathophysiology Q No:

14

Reproductive system

Pathophysiology Q No:

55

Cardiology

Pathophysiology Q No:

15

Pulmonology

Pathophysiology Q No:

56

Endocrinology

Pathophysiology Q No:

16

Pulmonology

Pathophysiology Q No:

57

Endocrinology

Pathophysiology Q No:

17

Endocrinology

Pathophysiology Q No:

58

Cardiology

Pathophysiology Q No:

18

Cardiology

Pathophysiology Q No:

59

Cardiology

Pathophysiology Q No:

19

Blood vessels

Pathophysiology Q No:

60

Endocrinology

Pathophysiology Q No:

20

Cardiology

Pathophysiology Q No:

61

Musculoskeletal

Pathophysiology Q No:

21

Endocrinology

Pathophysiology Q No:

62

Gastrointestinal system

Pathophysiology Q No:

22

Neurology

Pathophysiology Q No:

63

Musculoskeletal

Pathophysiology Q No:

23

Pulmonology

Pathophysiology Q No:

64

Cardiology

Pathophysiology Q No:

24

Pulmonology

Pathophysiology Q No:

65

Cardiology

Pathophysiology Q No:

25

Endocrinology

Pathophysiology Q No:

66

Endocrinology

Pathophysiology Q No:

26

Cardiology

Pathophysiology Q No:

67

Cardiology

Pathophysiology Q No:

27

Gastrointestinal system

Pathophysiology Q No:

68

Cardiology

Pathophysiology Q No:

28

Gastrointestinal system

Pathophysiology Q No:

69

Endocrinology

Pathophysiology Q No:

29

Cardiology

Pathophysiology Q No:

70

Endocrinology

Pathophysiology Q No:

30

Cardiology

Pathophysiology Q No:

71

Pulmonology

Pathophysiology Q No:

31

Endocrinology

Pathophysiology Q No:

72

Pulmonology

Pathophysiology Q No:

32

Blood vessels

Pathophysiology Q No:

73

Endocrinology

Pathophysiology Q No:

33

Cardiology

Pathophysiology Q No:

74

Genitourinary

Pathophysiology Q No:

34

Cardiology

Pathophysiology Q No:

75

Gastrointestinal system

Pathophysiology Q No:

35

Blood vessels

Pathophysiology Q No:

76

Endocrinology

Pathophysiology Q No:

36

Cardiology

Pathophysiology Q No:

77

Hepatobiliary system

Pathophysiology Q No:

37

Endocrinology

Pathophysiology Q No:

78

Endocrinology

Pathophysiology Q No:

38

Endocrinology

Pathophysiology Q No:

79

Endocrinology

Pathophysiology Q No:

39

Endocrinology

Pathophysiology Q No:

80

Gastrointestinal system

Pathophysiology Q No:

40

Gastrointestinal system

Pathophysiology Q No:

81

Gastrointestinal system

Pathophysiology Q No:

41

Endocrinology

Pathophysiology Q No:

82

Blood vessels



Pathophysiology Q No:

83

Cardiology

Pathophysiology Q No:

101

Blood vessels

Pathophysiology Q No:

84

Cardiology

Pathophysiology Q No:

102

Cardiology

Pathophysiology Q No:

85

Cardiology

Pathophysiology Q No:

103

Cardiology

Pathophysiology Q No:

86

Gastrointestinal system

Pathophysiology Q No:

104

Cardiology

Pathophysiology Q No:

87

Endocrinology

Pathophysiology Q No:

105

Gastrointestinal system

Pathophysiology Q No:

88

Musculoskeletal

Pathophysiology Q No:

106

Cardiology

Pathophysiology Q No:

89

Endocrinology

Pathophysiology Q No:

107

Cardiology

Pathophysiology Q No:

90

Genitourinary

Pathophysiology Q No:

108

Blood vessels

Pathophysiology Q No:

91

Blood vessels

Pathophysiology Q No:

109

Cardiology

Pathophysiology Q No:

92

Endocrinology

Pathophysiology Q No:

110

Cardiology

Pathophysiology Q No:

93

Endocrinology

Pathophysiology Q No:

111

Endocrinology

Pathophysiology Q No:

94

Hepatobiliary system

Pathophysiology Q No:

112

Musculoskeletal

Pathophysiology Q No:

95

Pulmonology

Pathophysiology Q No:

113

Endocrinology

Pathophysiology Q No:

96

Musculoskeletal

Pathophysiology Q No:

114

Hepatobiliary system

Pathophysiology Q No:

97

Gastrointestinal system

Pathophysiology Q No:

115

Endocrinology

Pathophysiology Q No:

98

Pulmonology

Pathophysiology Q No:

116

Pulmonology

Pathophysiology Q No:

99

Pulmonology

Pathophysiology Q No:

117

Endocrinology

Pathophysiology Q No:

100

Cardiology

 

 

 




Q NO 1: A 62-year-old Caucasian female hospitalized with acute myocardial infarction dies suddenly on day four of her hospitalization. The autopsy findings are pictured below (RV = right ventricle, LAD = left anterior descending coronary artery). The patient most likely died from which of the following?





A. Profound hypotension

B. Hypertensive emergency

C. Left-to-right shunt

D. Increased venous return

E. Right-to-left shunt

Explanation:

The gross autopsy specimen shows a ruptured left ventricular (LV) free wall. This complication of transmural (ST-elevation) myocardial infarction generally occurs 3 to 7 days after the onset of total ischemia, when coagulative necrosis neutrophil infiltration and enzymatic lysis of connective tissue have substantially weakened the infarcted myocardium (mean 4-5 days; range 1-10 days).

Free wall rupture causes cardiac tamponade, which greatly limits ventricular filling during diastole. As the pressure increases in the pericardial cavity, venous return to the heart is reduced. This leads to profound systemic hypotension and pulseless electrical activity. Failure to relieve the obstruction will lead to death.

Clinically, these patients present with profound hypotension and shortness of breath. On physical examination, the heart sounds are muffled and the jugular venous pressure is elevated.

(Choice C) Left-to-right shunting would occur as a result of ventricular septal rupture.

(Choice E) Right-to-left shunting is seen in patients with Eisenmenger syndrome, a complication of certain congenital heart diseases. This would be unusual as a complication of Ml.
Educational Objective:

The triad of muffled heart sounds elevated jugular venous pressure and profound hypotension indicates pericardial tamponade. Rupture of the ventricular free wall as a consequence of an acute transmural Ml can cause tamponade. Rupture usually occurs 3 to 7 days after the onset of total ischemia, when coagulative necrosis, neutrophil infiltration, and enzymatic lysis of connective tissue have sufficiently weakened the infarcted myocardium.


Q NO 2: A 65-year-old male presents to your office with exertional dyspnea. He has had four respiratory infections over the course of the past year. For the past 30 years he has smoked 1 Ѕ packs of cigarettes a day. Physical examination reveals diffusely decreased breath sounds, increased chest anteroposterior diameter, and decreased diaphragmatic excursion. Pulmonary function testing will most likely show which of the following patterns of findings (TLC total lung capacity; FEV 1 forced expiratory volume in 1 second; FVC forced vital capacity; RV, residual volume)?



Explanation:

This patient’s clinical picture is consistent with chronic obstructive pulmonary disease (COPD). COPD encompasses chronic bronchitis and emphysema. Heavy smoking is the most common cause. Chronic bronchitis and emphysema have similar effects on FEV1/FVC during pulmonary function testing (PFT). The hallmark of an obstructive PFT profile is decreased FEV1/FVC (FEV1%) due to expiratory airflow obstruction. Emphysema also causes a decrease in EVC and an increase in both TLC and RV due to destruction of interalveolar walls, decrease in lung elastic recoil, and distal airspace enlargement. Choice C is the only option with a decreased (FEV1%) and an increase in both TLC and RV.

(Choice E) This PFT profile is characteristic of restrictive lung disease (e.g. pulmonary fibrosis). In restrictive lung disease, lung volumes — particularly TLC and EVC — are decreased due to reduced lung expansion. FEV1/FVC may be increased above the normal value of approximately 80%. This FEV1% increase is the combined result of reduced FVC, decreased lung compliance, and increased elastic recoil.
Educational Objective:

Chronic obstructive pulmonary disease (COPD) in a heavy smoker may consist of both emphysema and chronic bronchitis and thus may present with both progressive exertional dyspnea (characteristic of emphysema) and frequent respiratory infections (characteristic of chronic bronchitis). On pulmonary function testing all COPD yields a decreased FEV1/FVC ratio. Emphysema also tends to increase TLC and RV. In contrast, restrictive lung diseases can cause reduced lung volumes and increased FEV1/FVC.


Q NO 3: A 45-year-old male presents to the ER with severe dyspnea of recent onset. He says he has never experienced symptoms like this before. Arterial blood gases show a Pa02 of 54 mmHg and a PaCO2 of 26 mmHg. The process most likely responsible for this patient’s condition is:


A. Upper airway obstruction

B. Poor respiratory drive

C. Respiratory muscle fatigue

D. Respiratory acidosis

E. Alveolar hyperventilation

r F. Decreased chest wall compliance
Explanation:

This patient has a combination of hypoxemia and hypocapnia. PaCO2 is inversely related to alveolar ventilation, and is considered the main indicator of alveolar ventilation. Assuming a normal rate of metabolic CO2 production, hypocapnia implies alveolar hyperventilation.

PaCO2 = Basal metabolic rate / alveolar ventilation

His hypoxia could be from pulmonary embolism pulmonary edema, pneumonia etc. All these conditions can cause tachypnea resulting in low PaCO2.

(Choice A) Significant upper airway obstruction would impair alveolar ventilation and would result in an increase in PaCO2 with a proportionate decrease in Pa02.

(Choice B) This patient’s degree of alveolar hyperventilation indicates that his peripheral arterial chemoreceptors sense the hypoxemia and are sending neural impulses to his CNS respiratory centers to increase respiratory drive above normal levels, resulting in hypocapnia.

(Choice C) Significant respiratory muscle fatigue would impair alveolar ventilation and would result in an increase in PaCO2.

(Choice D) Respiratory acidosis is caused by deficient alveolar ventilation, resulting in an increase in PaCO2 (hypercapnia).

(Choice F) A decrease in chest wall compliance could increase the work of breathing and thereby result in respiratory muscle fatigue. Alveolar hypoventilation and increased PaCO2 with a proportionate decrease in PaO2 could result.
Educational Objective:

Arterial PaCO2 is a direct indicator of the status of alveolar ventilation. Hypocapnia implies ongoing alveolar hyperventilation. Upper airway obstruction, reduced ventilatory drive, respiratory muscle fatigue, and decreased chest wall compliance are possible cause alveolar hypoventilation, which would cause hypercapnia.


Q NO 4: A 52-year-old Caucasian male presents to your office with two week history of progressive fatigue and exertional dyspnea. He brings with him the report from a recent cardiac catheterization (shown below). Cardiac auscultation reveals a murmur that is best heard when the patient sits up and leans forward. Which of the time points pictured below corresponds to the peak murmur intensity?





  1. A

  2. B

  3. C

  4. D

  5. E


Explanation:

Cardiac catheterization shows a hemodynamic profile consistent with aortic regurgitation (AR). Note the high peaking left ventricular and aortic pressures during systole and the steep diastolic decline in aortic pressure. A normal catheterization report is shown below for purposes of comparison:



The peak intensity of an AR murmur occurs after closure of the incompetent aortic valve, at the point when the pressure gradient between the aorta and the left ventricle is at its maximum i.e. time C.

(Choice A) This time point corresponds to the opening of the aortic valve during systole. The murmur of aortic stenosis would be heard best here.

(Choice B) This point corresponds to the closure of the aortic valve. The A2 heart sound is heard here. At this instant there is not yet regurgitant flow from the aorta to the left ventricle, so no murmurs are audible.

(Choice D) Time point D occurs in mid-diastole. The murmur of AR might be heard here, as there is a pressure gradient between the aorta and left ventricle (LV). However the intensity of the murmur would be less than at time C because the magnitude of the gradient is less. Because the AR murmur decreases in intensity with the falling aortic pressure, it is a “decrescendo” diastolic murmur.

(Choice E)Time E marks the onset of left atrial contraction at the end of ventricular diastole. If the murmur of AR were still audible at this time, its intensity would be further reduced by the increase in left ventricular end diastolic pressure.
Educational Objective:

The murmur of AR is a diastolic decrescendo murmur heard loudest in early diastole when the pressure gradient between the aorta and the left ventricle is maximal.


Q NO 5: A 34-year-old male who is being treated for acute leukemia develops oliguria. His serum creatinine level is 2.7 mg/dL. Renal biopsy reveals multiple uric acid crystals obstructing renal tubular lumen. The principal site of uric acid precipitation would be which of the following?


A. Proximal tubules due to high solute concentration

B. Proximal tubules due to impaired uric acid transport

C. Loop of Henle due to urine hyposmolarity

D. Distal tubules due to high urine flow rate

E. Collecting ducts due to low urine pH
Explanation:

Tumor lysis syndrome is an oncologic emergency. It often develops during chemotherapy for high-grade lymphomas, leukemias, and other tumors that have rapid cell turnover and high sensitivity to chemotherapy. When a large number of tumor cells are destroyed during chemotherapy, intracellular ions, such as potassium, phosphorous, and uric acid (a metabolite of tumor nucleic acid), are released into the serum and are then filtered by the kidneys.

Uric acid (pKa = 5.4) is soluble at physiologic pH, but precipitates in an acidic environment. The lowest pH along the nephron is found in the distal tubules and collecting ducts; so these are the segments of the nephron that become obstructed by uric acid crystals. Obstructive uropathy and acute renal failure follow.

The risk of tumor lysis syndrome can be reduced by urine alkalinization and hydration. Additionally allopurinol (a xanthine oxidase inhibitor) is used to reduce uric acid production during the breakdown of tumor cells.

(Choice D) Ignore the anatomy portion of choice D and evaluate the latter portion. A “high urine flow rate” would universally decrease uric acid crystallization and precipitation. Therefore, this cannot possibly be the correct answer.

(Choices A, B and C) Uric acid does not precipitate in proximal tubules or in Henle’s loop.
Educational Objective:

Tumor cell syndrome occurs when tumors with a high cell turnover are treated with chemotherapy. The lysis of tumor cells causes intracellular ions such as potassium and phosphorous, and uric acid (metabolite of tumor nucleic acid) to be released into serum. Uric acid is soluble at physiologic pH, but it can precipitate in the normally acidic environment of distal tubules and collecting ducts. The prevention of tumor lysis syndrome includes urine alkalinization and hydration, as high urine flow and high pH along the nephron prevents crystallization and precipitation of uric acid.


Q NO 6: A 54-year-old known alcoholic is brought to the emergency room because of hematemesis. By the following morning he has developed altered mental status. Physical examination shows abdominal distention, flapping tremor, and gynecomastia. Liver span is decreased. Which of the following is the most likely cause of his altered mental status?


A. Occlusion of the middle cerebral artery

B. Accumulation of blood urea nitrogen

C. Increased absorption of nitrogenous substances from gut

D. Decreased concentrations of y-aminobutyric acid (GABA)

E. Bacterial infection of the meninges
Explanation:

Hepatic encephalopathy is a reversible decline in neurologic function precipitated by hepatic damage. The pathogenesis of this condition is likely related to increased levels of ammonia in circulation which cause inhibitory neurotransmission via the GABA receptors in the central nervous system.

Ammonia initially enters circulation through the gastrointestinal tract, after having been created during the enterocytic catabolism of glutamine and the bacterial catabolism of dietary protein in the colon. The ammonia then enters the liver through the portal vein for detoxification to urea. Because the damaged liver has impaired detoxification ability however, ammonia accumulates in the blood instead. Frequently, hepatic encephalopathy is precipitated by a stressor that alters the ammonia balance (eg, hypovolemia, gastrointestinal bleeding hypokalemia, metabolic alkalosis, hypoxia, sedative usage, hypoglycemia, or infection).

Lowering of the blood ammonia level is typically accomplished with continuous administration of a disaccharidase such as lactulose. Bacterial action on the lactulose results in acidification of colonic contents, which converts the absorbable ammonia into nonabsorbable ammonium ion (an ammonia trap).

(Choice A) The middle cerebral artery is the largest cerebral artery and is most commonly involved in cerebrovascular accidents (CVAs). This patient’s presentation is suggestive of hepatic encephalopathy, however, and not stroke.

(Choice B) Accumulation of blood urea nitrogen is suggestive of renal failure, heart failure, or dehydration. Liver disease is associated with decreased blood urea nitrogen because less ammonia is converted to urea.

(Choice D) Increased (not decreased) activity of the GABA neurotransmitter system is thought to be directly responsible for the altered mental status seen in hepatic encephalopathy.

(Choice E) Bacterial infection of the meninges is characteristic of meningitis which does not fit this patient’s presentation as well as hepatic encephalopathy does.
Educational Objective:

Hepatic encephalopathy appears to be secondary to increased levels of ammonia in circulation which cause inhibitory neurotransmission via the GABA receptors in the central nervous system. Frequently hepatic encephalopathy is precipitated by a stressor that alters the ammonia balance (eg, gastrointestinal bleeding).

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