Medical Assessment and Management of the Surgical Patient

Question 1

45. Which of the following signs and/or symptoms are associated with venous thrombosis?

A. Homans sign
B. Levine’s sign
C. Quinke’s sign
D. Psoas sign

Answer 1

ANSWER: A

RATIONALE:
Homan’s sign: calf pain with forcible dorsiflexion of the foot, associated with lower extremity deep venous thrombosis. Levine’s sign: clenched fist over the chest while describing chest pain: associated with angina and acute myocardial infarction. Quinke’s sign: alternating blushing and blanching of the fingernail following light compression: seen in aortic regurgitation. Psoas sign (iliopsoas test): extension and elevation of the right leg produces pain in cases of inflammation of the psoas muscle: indicative of appendicitis.

REFERENCE:
Stedman’s Medical Dictionary 23rd ed., Williams & Wilkins, 1976 Bates B: A Guide To Physical Examination, 2nd ed. Lippincott, 1979

Question 2

46. In taking the blood pressure on an extremely obese patient, the standard size cuff would result in a blood pressure reading that is:

A. accurate
B. higher than the actual blood pressure
C. lower than the actual blood pressure
D. unreliable, since it is not possible to obtain an accurate blood pressure on an extremely
obese patient.

Answer 2

ANSWER: B

RATIONALE:
When considering the correct size of cuff, two pertinent points should be recalled: 1.) The inflatable bladder in the cuff should be able to completely encircle the arm with minimal overlap. 2.) The width of the bladder in the cuff should be approximately 20% greater than the diameter of the extremity used for the blood pressure cuff. Applying a cuff that is too small for an obese arm will produce a falsely elevated blood pressure reading; while applying too large a cuff on a thin arm will cause a falsely decreased blood pressure reading. Additionally, applying the cuff too loosely will produce a falsely elevated reading.

REFERENCE:
Malamed S: Sedation: A Guide To Patient Management. Mosby, 2003 p. 28

Question 3

47. Which of the following statements concerning cardiac output and myocardial work is true?

A. Preload represents passive ventricular wall stress and is best measured during systole
B. The primary determinants of afterload are the total peripheral resistance the heart muscle
must pump against and changes in intrathoracic pressure
C. Increasing heart rate is an efficient means of increasing myocardial work
D. Contractility is a direct measurement of the ability of the heart muscle to withstand
passive stretching

Answer 3

ANSWER: B

RATIONALE:
Cardiac afterload is indirectly measured through blood pressure and mean arterial
pressure. Increasing afterload (for example, via increasing peripheral vascular resistance or
intrathoracic pressure) or increasing heart rate increases myocardial oxygen consumption and work.
While preload does indeed represent passive ventricular wall stress, it is measured during diastole when the heart muscle wall is in its passive state. Preload is generally a reflection of the volume status of the patient. Increased heart rate is an inefficient means to increase cardiac output. Elevated heart rate is also potentially harmful in that it decreases the time that oxygen and nutrients can be delivered to the myocardial cells (diastolic perfusion time). Contractility is defined as the ability of the heart muscle to shorten with appropriate stimulation. With increased shortening of the muscle fibers during myocardial contraction, the heart can generate additional cardiac output more efficiently (an inotropic response) than by increases in heart rate (a chronotropic response).

REFERENCE:
Norton JM: Toward consistent definitions of preload and afterload. Adv Physiol Educ 25: 53-61, 2001.

Question 4

48. Which of the following concerning AV node conduction is true?

A. Modulation is achieved through nicotinic and cholinergic mechanisms.
B. AV conduction on the ECG is represented by the Q-T interval.
C. Digoxin enhances conduction speed.
D. No intrinsic automaticity is present at this node.

Answer 4

ANSWER: A

RATIONALE:
The vagus nerve provides cholinergic stimulation to the heart at the AV node and mediates a negative chronotropic effect. Catecholamines have the opposite effect and increase speed of impulse conduction through the AV node via nicotinic receptors. Catecholamines also cause an increase in myocardial inotropy.
In ECG tracings, the P-R interval represents the usual delay (0.20 secs) in conduction through the AV node. While digoxin is a positive ionotrope, it is also a negative chronotrope, decreasing the conduction velocity through the AV node. Although the automaticity of the AV node is usually masked by the more rapid impulses generated by the sino-atrial node, in the absence of atrial impulses the AV nodal junction often will generate depolarization at a rate of 40 to 60 impulses per minute.

REFERENCE:
Elamana V: Anesthetic considerations in patients with cardiac arrhythmias, pacemakers and AICDs. International Anes Clin 39(4): 21-42, 2001.

Question 5

49. Which of the following concerning Wolff-Parkinson-White Syndrome is true?

A. Sigma waves may alter the P-R interval on ECG.
B. Conduction is via the bundles of His.
C. Rapid ventricular response may be controlled with digitalis.
D. Procainamide may decrease conduction through accessory pathways.

Answer 5

ANSWER: D

RATIONALE:
WPW is a syndrome of rapid ventricular response to atrial stimulation by conduction through the accessory Bundle of Kent, bypassing the AV node and therefore the ability of the AV node to control over-rapid atrial impulse conduction to the ventricles. A gradual upslope of the P-R interval, the delta wave, is an ECG characteristic of this disorder. Emergent control of atrio- ventricular tachycardic conduction is by synchronized cardioversion if the patient is unstable. Medical management includes those drugs that can decrease impulse transmission through the accessory pathway (procainamide, amiodarone.) Digitalis and verapamil increase AV node refractoriness to conduction and can increase conduction through the aberrant pathway, which can cause serious deterioration in cases of tachycardia of supraventricular origin. Definitive treatment of the stable patient includes radiofrequency ablation of aberrant pathways.

REFERENCE:
Harrison’s Principles of Internal Medicine 13th ed., McGraw-Hill, 1994. pp1028-9 Guidelines 2000 For Cardiopulmonary Resuscitation and Emergency Cardiovascular Care, American Heart Association. P. 119
Dubin D: Rapid Interpretation of EKG’s, 4th ed. Cover Publishing, 1989 p. 157

Question 6

50. Non-pathological heart sounds, S1 and S2 can be characterized by:

A. left heart valve closure usually louder than right.
B. splitting of S1 during inspiration.
C. fixed splitting of S2 in the adolescent.
D. splitting of S2 on expiration.

Answer 6

ANSWER: A

RATIONALE:
Left (mitral) valve closure is louder due to the higher pressure in the aorta and left heart. S1 splitting, which represents a significant difference in the timing of closure of the mitral and tricuspid valves, is usually due to a pathologic process such as pulmonic stenosis or right bundle branch block. Non-pathologic split of S2 can occur on inspiration. Paradoxical S2 split occurs on expiration, with the most common associated pathology being left bundle branch block. Fixed S2 split can be indicative of atrial septal defect or right ventricular failure.

REFERENCE:
Bates, Barbara, MD. “A Guide to Physical Examination and History Taking” 4th ed. J.B. Lippincott Company pp 259-261
Stoelting RK, Miller RD. Basics of Anesthesia 4th ed. Churchill Livingstone pp 248-270

Question 7

51. Ventricular dilation in congestive heart failure is the result of:

A. increased cardiac output.
B. increase in circulating catecholamines.
C. decrease in ventricular afterload.
D. increase in end-diastolic ventricular volume.

Answer 7

ANSWER: D

RATIONALE:
Congestive heart failure is defined as the inability of the heart to maintain a cardiac output that meets the demands of peripheral organs. Catecholamine output is initially increased to attempt to increase heart rate and contractive force in order to maintain cardiac output. However, this is also accompanied by an increase in peripheral vascular resistance causing increased afterload. Eventually the myocardium cannot compensate and the end-diastolic ventricular volume is increased, due to decreased cardiac output and increased end-diastolic volume blood in left ventricle prior to systole. Myocardial failure can be secondary to coronary artery disease, non- ischemic cardiomyopathy, or longstanding valvular problems such as aortic incompetence.

REFERENCE:
Redding, S and Montgomery M. Dentistry in Systemic Disease. First edition JBK Publishing 1990 Pg 176-177.
Barash, Cullen, Stoelting : Clinical Anesthesia 2nd Edition J.B. Lippincott Company, Philadelphia 1992 pg 989-1017.

Question 8

52. Peripheral pedal edema and jugular venous distension are primarily characteristics of:

A. left heart failure
B. right heart failure
C. pulmonary edema
D. nephrotic syndrome

Answer 8

ANSWER: B

RATIONALE:
Right heart failure causes systemic venous congestion, resulting in jugular venous distension and causing peripheral edema from lymphatic stasis.
Left sided heart failure causes pulmonary vascular congestion, leading to pulmonary edema, dyspnea, orthopnea, and changes of pulmonary vasculature on chest radiographs. Nephrotic syndrome is a glomerulonephropathy causing severe proteinuria precipitating a large decrease in intravascular osmotic pressure and fluid loss to the interstitial tissue. While peripheral edema is a prominent symptom, intravascular volume depletion occurs and jugular venous distension is therefore not observed.

REFERENCE:
Redding, W., Montgomery M. : Dentistry in Systemic Disease, 1st ed. JBK Publishing 1990 pg 178-179
Barash, Cullen, Stoelting: Clinical Anesthesia 2nd Edition, J.B. Lippincott Company, Philadelphia pg 989-1017.

Question 9

53. Increased risk factors associated with patients diagnosed with congestive heart failure and managed with digitalis include all of the following except:

A. ejection fraction < 40%.
B. left atrial pressure > 20 mm Hg.
C. hyperkalemia
D. calcium channel blokers

Answer 9

ANSWER: C

RATIONALE:
Digitalis toxicity can be enhanced in the hypokalemic state and precipitate serious cardiac dysrhythmias.
Normal cardiac ejection fractions are 60-80%, and when < 50% constitute a risk of congestive failure. Normal left atrial pressure is 4-12 mm Hg; when elevated it represents increased preload and increases the work of a compromised myocardium, increasing risk. Calcium channel antagonists and beta blockers can decrease already impaired myocardial performance.

REFERENCE:
Rozien M, Fleisher L: Essence of Anesthesia Practice. WB Saunders, 1997
Yao F: Anesthesiology Problem Oriented Patient Management 4th ed., Lippincott, 1998

Question 10

54. When pre-operatively evaluating a patient that has an implanted permanent pacemaker, all of the following are true except:

A. Epicardial pacemakers do not require antibiotic prophylaxis for bacteremia-producing procedures.
B. A demand type pacemaker should be switched to a fixed rate mode to avoid interference of the pace making activity from intraoperative radiofrequency emitting equipment (example; electrocautery).
C. Dual chamber pacemakers can develop pacemaker-mediated tachycardia.
D. Patients with a pacemaker can not be defibrillated.

Answer 10

ANSWER: D

RATIONALE:
All current pacemakers allow defibrillation; however they should be checked for proper function after defibrillation. Demand pacemakers can undergo interference from any strong radiofrequency source, especially if it is grounded to the patient (such as electrocautery;) so demand pacemakers should be set on a fixed rate to avoid inappropriate interference with the demand function. Pacemaker-mediated tachycardia is a possible complication of dual- chamber(atrial and ventricular) pacing when the atrial lead senses retrograde depolarizations because of ventriculoatrial conduction. The resulting tachycardia often has a rate equal to the upper rate limit of the pacemaker. Pacemaker-mediated tachycardia can be eliminated by various reprogramming maneuvers, such as lengthening the post-ventriculoatrial refractory period.

REFERENCE:
Yao F: Anesthesiology Problem Oriented Patient Management 4th Ed. Lippincott-Raven 1998.
Goldman, Bennett (eds.): Cecil’s Textbook of Medicine 21st Edition.
Rozien M, Fleisher L: Essence of Anesthesia Practice, WB Saunders 1997. Advanced Cardiac Life Support Guidelines 1997, American Heart Association

Question 11

55. Which of the following statements regarding aortic stenosis is incorrect?

A. Aortic stenosis is typified by a midsystolic ejection murmur and a narrowed pulse pressure.
B. The triad of angina, syncope and congestive heart failure represents progression of symptoms associated with aortic stenosis.
C. The development of supraventricular arrhythmias including atrial fibrillation creates hemodynamic problems for the patient with aortic stenosis.
D. Hypotensive anesthesia for the aortic stenosis patient is cardioprotective by decreasing afterload and myocardial work.

Answer 11

ANSWER: D

RATIONALE:
Hypotension (reduced systemic vascular resistance ) does little to relieve the fixed afterload arising from a stenotic aortic valve; however hypotension lowers the diastolic coronary profusion gradient leading to myocardial ischemia. Therefore, induced hypotensive states are contraindicated in the patient with a stenoticaortic valve.
Aortic stenosis is characterized by a crescendo-decrescendo systolic murmur (which may radiate to the carotids) and narrowed pulse pressure. With left ventricular hypertrophy an apical thrust may be seen. The triad of angina, syncope and congestive heart failure correlate directly with mortality; the 50% survival data for these symptoms are 5,3, and 2 years respectively from the onset of symptoms without surgical treatment. Patients with aortic stenosis need the left ventricular filling obtained through a well timed atrial contraction. Supraventricular arrhythmias decrease ventricular filling (especially in the less compliant myocardium of left ventricular hypertrophy) and therefore decrease the amount of blood available for ejection past the stenotic aortic valve.

REFERENCE:
Yao F: Anesthesiology Problem Oriented Patient Management 4th Ed., Lippincott-Raven, 1998. Rozien M, Fleisher L: Essence of Anesthesia Practice, WB Sauders, 1997.
Advanced Cardiac Life Support Guidelines1997, American Heart Association

Question 12

56. Which of the following produces a diastolic murmur?

A. Aortic stenosis
B. Mitral regurgitation
C. Mitral valve prolapse
D. Mitral stenosis

Answer 12

ANSWER: D

RATIONALE:
Mitral stenosis produces a diastolic rumbling murmur. By auscultation one can hear an opening snap followed by a low-pitched diastolic rumble best heard at the apex. Diagnosis is confirmed by Doppler echocardiography. The most common cause of mitral stenosis is rheumatic fever. The first symptom of mitral stenosis is usually dyspnea on exertion as a result of pulmonary venous congestion secondary to elevated left atrial pressure.
The most common causes of aortic stenosis are rheumatic fever and congenital anomaly. Associated symptoms include syncope, dyspnea on exertion and angina. In the adult the physical findings are consistent with a systolic ejection (crescendo-decresendo) murmur and delayed pulse up-stroke. Diagnosis is confirmed with cardiac catheterization. Mitral regurgitation often is detected by a holosystolic rumbling murmur, while mitral valve prolapse yields a systolic click murmur.

REFERENCE:
Stoelting RK, Dierdorf ST: Valvular Heart Disease, in, Stoelting RK, Dierdorf ST(eds) Handbook for Anesthesia and Co-Existing Disease, Churchill Livingstone 1993
Kopitsky RG, Genton RE: Myocardial and Valvular Heart Diseases, in, Dungan WC, Ridner ML(eds) Manual of Medical Therapeutics 26 edition, Little Brown 1989
Campbell D: Aortic Stenosis, in, Abernathy CM, Harken AH (eds) Surgical Secrets, Mosby Yearbook 1991
Campbell D: Mitral Stenosis, in, Abernathy CM, Harken AH (eds) Surgical Secrets, Mosby Yearbook 1991

Question 13

57. Which of the following statements regarding premature ventricular contractions PVC’s are true?

A. Unifocal PVC’s in patients without a previous cardiac history may indicate early signs of myocardial infarction
B. Six or more PVC’s in a minute, especially if they are multifocal are considered ventricular tachycardia.
C. They should always be treated promptly to avoid the risk of ventricular tachycardia or fibrillation.
D. They rarely occur in a normal, healthy individual

Answer 13

ANSWER: B

RATIONALE:
Six or more PVC’s per minute are by definition ventricular tachycardia. Depending upon the clinical situation, antiarrhythmic therapy may be justified, especially if these are multifocal. Unifocal PVC’s in an otherwise healthy individual warrant investigation for nonspecific cardiac challenges such as hypoxemia, hypercarbia, acidemia, sympathetic surge, drug effects and electrolyte disturbances. They are, however, not indicative of impending myocardial infarction. Therefore an intelligent consideration of the clinical situation and a search for possible causes in the otherwise healthy patient should be performed rather than a “knee jerk” response of antiarrhythmic therapy.

REFERENCE:
Office anesthesia evaluation manual, AAOMS, 6th ed., p.31, 2000.
Elamana V: Anesthetic considerations in patients with cardiac arrhythmias, pacemakers and AICDs. International Anes Clin 39(4): 21-42, 2001.

Question 14

58. What is the maintenance fluid requirement of a healthy 70 kg adult who is restricted from oral intake NPO while awaiting surgery?

A. 60 cc/hr
B. 80 cc/hr
C. 110 cc/hr
D. 140 cc/hr

Answer 14

ANSWER: C

RATIONALE:
The calculation for fluid replacement for a healthy individual is as follows:

HOURLY CALCULATION
40 ml/hr for the first 10 kg of body weight
20 ml/hr for the 2nd 10 kg of body weight 10 ml/hr for each additional 10 kg
Total = 110 cc/hr

DAILY CALCULATION
1st 10kgx100ml=1000ml
2nd 10kgx50ml=500ml 50 kg x 20 ml = 1000 ml
Total = 2500 ml/24 hr = 104 ml/hr

REFERENCE:
Abubaker, A. and Benson, K.; Surgical Correction of Dentofacial Deformities, Vol. I, Bell, W., Proffit, W., White, R, 1980, pg. 223

Question 15

59. Initiators of hepatic cirrhosis include all of the following except:

A. Chronic cholestasis
B. Halothane
C. Uncontrolled diabetes mellitus
D. Right heart failure

Answer 15

ANSWER: C

RATIONALE:
Chronic biliary obstruction can cause cirrhotic liver changes. Halothane, by an immune- mediated reaction to metabolic byproducts, can cause a fulminant acute hepatic necrosis that may lead to cirrhosis in susceptible individuals. Prolonged severe right heart failure can lead to hepatic fibrosis and “cardiac cirrhosis.” Although the microangiopathy of uncontrolled diabetes mellitus can affect many organ systems, hepatic involvement is unusual.

REFERENCE:
OMS Knowledge Update Vol. I, Part 2 AAOMS 1995 p PEV 38
Harrison’s Principles of Internal Medicine, 13th ed. McGraw-Hill, 1994 pp 1478-1489

Question 16

60. A patient with a history of renal impairment and a measured glomerular filtration rate of 20 ml/min could be expected to manifest with which of the following?

A. Microcytic hypochromic anemia
B. Compensatory respiratory hypoventilation
C. Low anion gap
D. Hypertension tendency

Answer 16

ANSWER: D

RATIONALE:
Glomerular filtration of 20 ml/min would be considered to have moderate to severe renal failure. Moderate to severe renal failure affects the rennin-angiotensin system causing hypertension. Lack of renally-produced erythropoietin in renal failure yields a normochromic, normocytic anemia by decreased red blood cell production. Renal failure also causes a high anion-gap metabolic acidosis, which often is accompanied by a compensatory respiratory hyperventilation.

REFERENCE:
Petersen L, Indresano A, Marciani R, Roser S: Principles of Oral and Maxillofacial Surgery Volume I, Chapter 2 p. 31 1992

Question 17

61. Which medication should be avoided in the thyrotoxic patient?

A. atropine
B. methimazole
C. potassium iodide
D. propranolol

Answer 17

ANSWER: A

RATIONALE:
Thyrotoxicosis is manifested by a hyperadrenergic state including hypertension and tachycardia. Atropine would aggravate the cardiovascular effects of this disorder and should be avoided. Antithyroid medications such as methimazole and propothiouricil decrease thyroid hormone synthesis and decrease peripheral conversion of T4 to the more metabolically active T3. Initial intravenous potassium iodide actually decreases the acute release of T3 and T4 from the thyroid, although long-term it can increase iodine storage in the gland. Propranolol mitigates the cardiovascular effects of hyperthyroid activity and is used in acute management of the disease.

REFERENCE:
Pronovost P, Paris K: Perioperative management of thyroid disease. Postgrad Med 98:83-96, 1995
Gavin L: Thyroid crisis. Medical Clin N Amer 75:179-190, 1991

Question 18

62. All of the following conditions are seen in patients with severe untreated hypothyroidism except:

A. Dementia
B. Cardiac failure
C. Hypolipidemia
D. Coma

Answer 18

ANSWER: C

RATIONALE:
Untreated severe hypothyroidism manifests with altered mental status up to and including coma, heart failure, muscular weakness/lethargy, and hyperlipidemia especially low density lipoproteins often with advanced athlerosclerosis.

REFERENCE:
Vezeau PJ: Thyroid disorders. In: Bennett J (ed.): Medical Emergencies in Dentistry, WB Saunders, 2002. pp 374-5

Question 19

63. All of the following may be observed in the patient with untreated adrenal insufficiency except:

A. decreased systemic vascular resistance
B. peaked T waves on ECG
C. hypernatremia
D. rales

Answer 19

ANSWER: C

RATIONALE:
Adrenal insufficiency can include both cortisol and aldosterone production. Lack of cortisol can lead to decreased systemic vascular resistance and hypotension, especially under physiologic stressors. In the face of this challenge in a cardiac-debilitated patient, high-output congestive heart failure can lead to rales being auscultated. Physiologically, aldosterone release is under control of the rennin-angiotensin system; and aldosterone promotes renal sodium and water retention and potassium excretion. Conversely, hypoaldosteronism can lead to hyponatremia due to sodium losses, and to hyperkalemia, which is manifested by peaked T waves on ECG.

REFERENCE:
McKenna S: Adrenal Sufficiency. In: Bennett J (ed.): Medical Emergencies in Dentistry, WB Saunders, 2002. pp 379-387

Question 20

64. Which of the following is the initial treatment for diabetic ketoacidosis?

A. Insulin
B. Isotonic saline
C. Potassium chloride
D. Sodium bicarbonate

Answer 20

ANSWER: B

RATIONALE:
Restoration of fluids and electrolytes is the first resuscitative priority due to dehydration and sodium depletion. Initial hydration rapidly corrects plasma volume and increases the efficacy of later insulin therapy. Intracellular potassium depletion may be masked by near normal or slightly elevated serum potassium levels, especially in a volume-depleted patient. Therefore, following initial rehydration, insulin administration is also accompanied by titrated intravenous potassium with careful electrolyte measurements. Volume expansion and insulin administration usually resolves the metabolic acidosis from ketoacid production, and bicarbonate administration is not indicated in most cases.

REFERENCE:
Wall B: Diabetic ketoacidosis. Med Clin N Amer 79:9-37, 1995

Question 21

65. A normal glycosylated hemoglobin (Hemoglobin A1c) level is:

A. 4-6 %
B. 10-12 %
C. 15-18%
D. 20-25%

Answer 21

ANSWER: A

RATIONALE:
The major form of glycohemoglobin, termed hemoglobin A1c normally comprises only 4-6% of total hemoglobin. It would be higher in chronically hyperglycemic patients due to
condensation of glucose with free amino acids on the globin component of hemoglobin. Therefore, 2, 3, and 4 are too high for a healthy individual.

REFERENCE:
Little, J., Falace, D., Miller, C., and Rhodus, N: Dental Management of the Medically Compromised Patient, 5th edition, Elseiver Science,1997, pg. 397

Question 22

66. Which of the following would be considered the drug of choice for treatment of severe pseudomembranous colitis?

A. Vancomycin
B. Cefazolin
C. Clindamycin
D. Metronidazole

Answer 22

ANSWER: D

RATIONALE:
Metronidazole is an antibiotic which is effective against Clostridium difficile which causes pseudomembranous colitis. Vancomycin, due to its cost and concerns of promoting vancomycin microbiologic resistance (especially by Staphylococcus strains) has limited its oral use to very severe, metronidazole-resistant C. difficile enterocolitis infections. Cefazolin and clindamycin disturb the balance of intestinal flora and have been implicated as causative agents in the development of this infection.

REFERENCE:
Little, J., Falace, D., Miller, C., and Rhodus, N: Dental Management of the Medically
Compromised Patient, 5th edition, Elseiver Science, 1997 p. 306
Moyenuddin M, Williamson J, Ohl C: Clostridium difficile-associated diarrhea: Current strategies for diagnosis and therapy. Curr Gastrolenterol Rep 4(4):279-286, August 2002

Question 23

67. What endocrine abnormality is often an associated sequela of chronic renal failure?

A. Secondary hyperparathyroidism
B. Primary adrenal insufficiency
C. Hypothyroidism
D. Primary hyperaldosteronism

Answer 23

ANSWER: A

RATIONALE:
With renal failure there is decreased glomerular filtration which results in an increased level of serum phosphate. This tends to cause serum calcium to be deposited in bone leading to a decrease serum calcium level. In response to low serum calcium the parathyroid glands are stimulated to secrete parathormone (PTH) which results in secondary hyperparathyroidism. Primary adrenal insufficiency usually is a result of an autoimmune disorder but may also result from cancer, infection, or trauma. Hypothyroidism may result from any failure along the pituitary-thyroid axis (hypothalamus failure to release thyroid releasing hormone, adenohypophyseal failure to release thyroid stimulating hormone, or thyroid secretory failure.) Primary hyperaldosteronism results from adrenal cortical hyperplasia (specifically of the zona glomerulosa) or an aldosterone- secreting adenoma of the adrenal gland. None of the latter three states is a sequela of chronic renal failure.

REFERENCE:
Harrison’s Principles of Internal Medicine 13 ed., McGraw-Hill, 1994, pp. 2160-1

Question 24

68. Increased anion gap may be found in :

A. Hyperkalemia
B. Multiple myeloma
C. Hypoalbuminemia
D. Ketoacidosis

Answer 24

ANSWER: D

RATIONALE:
Anion gap gives information concerning “unmeasured” serum anions. Diabetic ketoacidosis is the most common cause of an increased anion gap. Hyperkalemia, increased proteinaceous cation in multiple myeloma, and decreased proteinacious anion in hypoalbuminemia will all cause a decreased anion gap.

REFERENCE:
Wallach J: Interpretation of Diagnostic Tests. Little, Brown, 1992. p. 396

Question 25

69. Which of the following concerning the management of the Parkinson’s disease patient is false?

A. Sialorrhea and cardiac sphincter dysfunction increase the incidence of pulmonary aspiration.
B. Ephedrine should be avoided if the patient takes selegiline.
C. Levodopa should be discontinued 24 hours prior to neuromuscular blocking agents.
D. Levodopa therapy may lead to hypovolemia and dyskinesia.

Answer 25

ANSWER: C

RATIONALE:
Levodopa has a short half-life and withdrawal prior to surgery can precipitate muscle rigidity and attendant difficulties in respiration and handling the patient. Sialorrhea, esophageal and laryngeal dysfunction increase aspiration risk in Parkinson’s patients. Selegiline is a monoamine oxidase-B inhibitor that decreases dopamine catabolism, and mitigates Parkinsonism’s decreases in dopamine in the caudate nucleus and the putamen. Ephedrine can precipitate an adrenergic crisis in MAO-B treated patients. Levodopa increases the activity of the rennin-angiotensin system, potentiating hypovolemia.

REFERENCE:
Benumof JL, Anesthesia & Uncommon Diseases, WB Saunders 1998 pp. 6-7; Atlee JL, Complications in Anesthesia WB Saunders 1999

Question 26

71. Which of the following statements regarding myasthenia gravis is incorrect?

A. Initial symptoms often include diplopia and ptosis.
B. The etiology involves decreased acetylcholine secretion at the neuromuscular junction.
C. Edrophonium is useful in diagnosis of this disorder.
D. Physiologic stress can exacerbate clinical symptoms, including respiratory muscle failure.

Answer 26

ANSWER: B

RATIONALE:
Myasthenia gravis is an autoimmune disease characterized by decreased acetylcholine receptors at the neuromuscular junction which leads to muscle weakness even with normal acetycholine secretion. . Ocular muscles are often the first affected, with diplopia and ptosis especially after repetitive eye activities. Stressors such as infection or surgery can exacerbate muscle weakness, including respiratory muscles. Edrophonium, an acetylcholinesterase inhibitor, often brings rapid relief from muscle weakness; however false negative and positive test results are not uncommon.

REFERENCE:
Goetz L, Textbook of Clinica Neurology 1st ed., WB Saunders, 1999 pp. 1024-1025 Cecil’s Textbook of Medicine, 21st ed., WB Saunders, 2000 pp 2221-2

Question 27

72. Which of the following statements concerning myotonic dystrophy is true?

A. ECG abnormalities are uncommon.
B. Inheritance is autosomal recessive.
C. Initial cardiac involvement most often is hypokinesis.
D. Extremity weakness progresses from distal to proximal

Answer 27

ANSWER: D

RATIONALE:
Distal-to-proximal weakness is the most common progression pattern, although myotonia and stiffness may occasionally predominate. The inheritance is autosomal dominant. Predominant cardiac involvement is by fatty degeneration and fibrosis of specialized cardiac conductive tissue (sino-atrial and atrio-ventricular nodes and His-Purkinje system.) This makes dysrhythmias the most common cardiac pathology accompanying myotonic dystrophy.

REFERENCE:
Braunwald E, Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed. WB Sauanders, 2001 p. 2265
Cecil’s Textbook of Medicine, 21st ed. WB Saunders, 2000 p. 2209
Miller, Anesthesia 5th ed. Churchill-Livingstone, 2000 p. 973

Question 28

73. Wernicke’s encephalopathy :

A. may be precipitated in susceptible individuals by saline infusion.
B. is due to folic acid deficiency.
C. is characterized by ophthalmoplegia and ataxia.
D. is often anteceded by mental status changes.

Answer 28

ANSWER: C

RATIONALE:
Often the initial presenting signs of Wernicke’s encephalopathy include abducens palsy, horizontal diplopia, nystagmus, and strabismus; and ataxia may cause ambulation difficulties. These neuromuscular signs often antecede mental changes. The disorder is caused by deficiency of thiamine (vitamin B1); administration of which can quickly reverse ocular symptoms but often has little effect on mental changes once they have occurred (such as anterograde and retrograde amnesia, apathy, drowsiness, confusion.) Glucose infusion into a thiamine-depleted individual (generally alcoholics) can precipitate Wernicke’s syndrome and all alcoholics receiving glucose infusions should have concomitant thiamine administration (50-100 mg immediately and then daily.)

REFERENCE:
Textbook of Primary Care Medicine 3rd ed., Mosby, 2001 p 1479

Question 29

74. Which of the following concerning posttraumatic diabetes insipidus is true?

A. A hypertonic polyuria ensues.
B. Extreme dehydration may accompany hyponatremia.
C. An adenohypophyseal hormone analog is an effective treatment.
D. The targets of treatment are renal collecting ducts.

Answer 29

ANSWER: D

RATIONALE:
Traumatic diabetes insipidus results from a decreased secretion of antidiuretic hormone from the neurohypophysis (posterior pituitary.) The other neurohypophyseal hormone is oxytocin. Adenohypophyseal (anterior pituitary) hormones include follicle stimulating hormone, leuteinizing hormone, thyroid stimulating hormone, somatostatin, melanocyte stimulating hormone, and adrenocortical stimulating hormone.
Lack of ADH causes a decrease in water resorption from the renal collecting ducts, resulting in a voluminous hypotonic urine production, causing dehydration manifested by serum hyperosmolarity and hypernatremia. Treatment usually includes administration of intravenous or intranasal desmopressin, an analog of ADH that is almost devoid of vasopressor effects (unlike vasopressin.)

REFERENCE:
Harrison’s Principles of Internal Medicine, 13th ed., McGraw-Hill, 1994 pp1926-8 Guyton, AC: Textbook of Medical Physiology 6th ed, WB Saunders, 1981 pp. 429-430

Question 30

75. Which of the following may be indicated in the treatment of acute intracranial injury?

A. Ventilation-induced serum pCO2 < 25mm Hg
B. Intravenous glucocorticoids
C. IV administration of 10% dextrose in 0.45% saline
D. Mannitol 1 mg/kg initial bolus

Answer 30

ANSWER: D

RATIONALE:
Osmotic diuresis with IV mannitol is commonly used to decrease intracranial pressure from acute head injury. There are no studies confirming the benefit of glucocorticoid use in reducing elevated intracranial pressure from acute head injury. Judicious and limited hyperventilation may be used to temporarily bring pCO2 down to 30 mm Hg but prolonged periods of pCO2 < 25mm may cause significant cerebral vasoconstriction, worsening ischemia. Hypotonic fluids such as 0.45% normal saline may increase cerebral edema, and dextrose- containing fluids can contribute to hyperglycemia-induced cerebral injury.

REFERENCE:
ATLS Student Course Manual, 1997 American College of Surgeons pp 202-4

Question 31

76. The pathophysiology for Horner’s syndrome is:

A. interruption of preganglionic parasympathetic fibers.
B. Interruption of postganglionic sympathetic fibers.
C. aberrant conduction between motor branches of cranial nerve V and cranial nerve III.
D. traumatic or pathologic changes in the ciliary ganglion.

Answer 31

ANSWER: B

RATIONALE:
Horner’s syndrome is the result of disruption of sympathetic innervation to the orbital region characterized by miosis (unopposed parasympathetic-mediated papillary constriction;) upper lid ptosis (by loss of sympathetic innervation to Mueller’s muscle;) enophthalmos (either “apparent” by ptosis, or more rarely by atrophy of orbital contents if the syndrome occurs in a young patient or is longstanding;) and more inconsistently ipsilateral facial anhidrosis (lack of sweating.) Aberrant conduction (usually via a congential anomaly) between the motor branches cranial nerve V to the terminal branches of cranial nerve III produces Marcus Gunn syndrome (“jaw-winking” syndrome,) characterized by resting lid ptosis and upward motion of the superior lid with mandibular movement. Interruption of the parasympathetic fibers of the ciliary ganglion (where parasympathetic fibers to the orbit synapse) would result in pupillary dilation (mydriasis.)

REFERENCE:
Hollingshead WH: Anatomy for Surgeons, Volume 1. The Head and Neck, 2nd ed. Hoeber Medical, New York, 1968 pp 115, 172
Bullock JD: Marcus-Gun jaw- winking ptosis: Classification and surgical management. J Ophthomol Strabismus 17:375-9, 1980

Question 32

77. A patient with a left homonymous heminanopsia may indicate a lesion in the:

A. optic chiasm
B. right optic radiation
C. right optic nerve
D. left optic tract

Answer 32

ANSWER: B

RATIONALE:
Lesions of the optic radiation and of the optic tract produce a contralateral hemianopsia (loss of the contralateral field of vision in both eyes; in this case, a right optic radiation lesion causing a left homonymous hemianopsia.) Optic chiasm lesion produce a bitemporal hemianopsia (loss of temporal, i.e. lateral, field of vision in both eyes.) Lesions of the optic nerve produce an ipsilateral blind eye.

REFERENCE:
Alper’s and Mancalls’ Essentials of Neurologic Examination 2nd ed. DeGowan & DeGowan: Diagnostic Examination 6th ed.
Bates: A Guide to Physical Examination, 7th ed., Lipponcott, 1980

Question 33

78. Which medication is contraindicated for office-based anesthesia in a patient with partially controlled tonic-clonic seizure activity?

A. Propofol
B. Fentanyl
C. Ketamine
D. Methohexital

Answer 33

ANSWER: D

RATIONALE:
Although many thiobarbiturates decrease cerebral metabolism and electrical activity and are used as anticonvulsants, the oxybarbiturate methohexital has increased central nervous system excitatory effects and may precipitate seizures in epileptics. Propofol, fentanyl, and ketamine have no such pro-convulsant effects.

REFERENCE:
Weinberg G: Basic Science Review of Anesthesiology. McGraw-Hill, 1997 pp16-19

Question 34

79. At which parasympathetic ganglion do ocular preganglionic fibers synapse with postganglionic fibers?

A. Superior cervical
B. Pterygopalatine
C. Otic
D. Ciliary

Answer 34

ANSWER: D

RATIONALE:
Parasympathetic ganglia are present near the target organ, unlike sympathetic where the ganglia are near the spinal cord. Parasympathetics to the globe arise from cranial nerve III and synapse at the ciliary ganglion, just posterior to the globe. The otic ganglion synapses parasympathetic nervous system fibers from cranial nerve IX and supplies the parotid gland. The pterygopalatine ganglion receives presynaptic PSNS fibers from cranial nerve VII and supplies the secretory glands of the palate and nasal cavity. The superior cervical ganglion is sympathetic.

REFERENCE:
Vander S, Luciano T Human Physiology: The Mechanisms of Body Function. McGraw-Hill 1998 pp. 213-216
Romanes GJ, “Cunningham’s Manual of Practical Anatomy, Volume 3: Head & Neck. Oxford Medical Publications, 1986

Question 35

80. In comparing the characteristics of rheumatoid arthritis (RA) and osteoarthritis (OA), which of the following is incorrect?

A. RA has a significant inflammatory component while OA does not.
B. RA usually presents with multiple symmetric joint involvement; OA usually involves
only one or two joints initially.
C. Both processes have associated systemic manifestations, including fatigue, weakness, and
malaise.
D. There are no laboratory tests that are pathognomonic or accurately diagnostic for either
process.

Answer 35

ANSWER: C

RATIONALE:
Signs and symptoms of RA include multiple symmetric joint involvement, a significant inflammatory component, morning joint stiffness lasting more than one hour, symmetric swelling of the proximal interphalangeal joints, systemic manifestations of fatigue, weakness, and malaise. In comparison, OA is characterized by involvement of only one or two joints or joint groups (at least initially) morning stiffness lasting less than 15 minutes, and the initial hand lesions usually involve the distal interphalangeal joints. OA has no systemic involvement. There are no laboratory tests that are specifically pathogonomic for either process, although there area a number of serum markers that may accompany RA (such as elevations of rheumatoid factor, erythrocyte sedimentation rate; and a normochromic, microcytic anemia.)

REFERENCE:
Little and Falace: Dental Management of the Medically Compromised Patient6th ed. Harrison’s Principles of Internal Medicine, 15th ed., McGraw-Hill

Question 36

81. In obstructive pulmonary disease, which of the following changes in the total lung capacity (TLC) and residual volume (RV) occurs?

A. TLC is normal or decreased; RV is decreased
B. TLC is normal or decreased; RV is increased
C. TLC is normal or increased; RV is decreased
D. TLC is normal or increased; RV is increased

Answer 36

ANSWER: D

RATIONALE:
In obstructive pulmonary disease, total lung capacity may be normal or increased and residual volume is increased; both by air entrapment and emphysematous changes. Vital capacity is often decreased as the amount of nonventilated or poorly ventilated lung volume increases.

REFERENCE:
The ICU Book, 1991, p. 322

Question 37

83. Which of the following medication is least indicated for acute control of asthma?

A. Cromolyn sodium
B. Metaproterenol
C. Dexamethasone
D. Diphenhydramine

Answer 37

ANSWER: A

RATIONALE:
Chromolyn sodium is a mast cell stabilizer preventing the release of histamine in the mucosa of the tracheobronchial tree when used chronically, but acts too slowly to be useful on an emergent basis. Metaproterenol is a beta agonist used to dilate the airway and reverse bronchoconstriction. Dexamethasone may be used intravenously to control the mucosal inflammatory component of acute asthma. Diphenhydramine, a histamine antagonist, may be administered concomitantly with a beta agonist and a steroid to decrease histamine-mediated bronchoconstriction and mucosal edema.

REFERENCE:
Harrison’s Principles of Internal Medicine 13th ed., McGraw-Hill, 1994 pp 1170-2

Question 38

86. Which of the following is a form of restrictive lung disease?

A. Asthma
B. Bronchiectasis
C. Cystic fibrosis
D. Sarcoidosis

Answer 38

ANSWER: D

RATIONALE:
Sarcoidosis is restrictive because sarcoid lesions cause a decreased compliance of lung parenchyma, restricting the amount of lung capacity. Asthma, bronchiectasis, and cystic fibrosis increase airway ventilatory resistance (especially during exhalation) and air entrapment, and are therefore obstructive diseases.

REFERENCE:
Harrison’s Principles of Internal Medicine, 12th edition, p. 1036