Medical Assessment and Management of the Surgical Patient Flashcards
- 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: 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
- 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: 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
- 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: 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.
- 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: 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.
- 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: 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
- 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: 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
- 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: 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.
- 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: 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.
- 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: 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
- 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: 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
- 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: 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
- Which of the following produces a diastolic murmur?
A. Aortic stenosis
B. Mitral regurgitation
C. Mitral valve prolapse
D. Mitral stenosis
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
- 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: 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.
- 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: 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
- Initiators of hepatic cirrhosis include all of the following except:
A. Chronic cholestasis
B. Halothane
C. Uncontrolled diabetes mellitus
D. Right heart failure
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
- 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: 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
- Which medication should be avoided in the thyrotoxic patient?
A. atropine
B. methimazole
C. potassium iodide
D. propranolol
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
- All of the following conditions are seen in patients with severe untreated hypothyroidism except:
A. Dementia
B. Cardiac failure
C. Hypolipidemia
D. Coma
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
- 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: 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
- Which of the following is the initial treatment for diabetic ketoacidosis?
A. Insulin
B. Isotonic saline
C. Potassium chloride
D. Sodium bicarbonate
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
- A normal glycosylated hemoglobin (Hemoglobin A1c) level is:
A. 4-6 %
B. 10-12 %
C. 15-18%
D. 20-25%
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
- 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: 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
- 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: 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
- Increased anion gap may be found in :
A. Hyperkalemia
B. Multiple myeloma
C. Hypoalbuminemia
D. Ketoacidosis
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
