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NMS Q&A Family Medicine

NMS Q&A Family Medicine

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116 <strong>NMS</strong> Q&A <strong>Family</strong> <strong>Medicine</strong>Examination Answers1. The answer is D. Arteriolonephrosclerosis is the irreversiblecause of ARF among the listed choices. Arteriolonephrosclerosisis late stage renal disease attributable tolongstanding poorly controlled hypertension. Symptoms ofmalaise occur in ARF when the BUN rises to 50 to 60 mg/dL, and to be sure, irreversible ARF is a medical emergencyto avert irreversible renal failure. In CRF, symptoms do notoccur until the BUN approaches 100 mg/dL. Fluid depletiongenerally first shows a rising BUN out of proportion tothe rise in creatinine, that is, the “prerenal” pattern. Normally,the BUN is found to be about 10 times the creatininelevel. Obviously, this form of ARF is amenable to rapid fluidtherapy. ARF due to toxic medications has been proven tobe reversible with withdrawal of the drug in the vast majorityof cases. Loop diuretics occasionally cause ARF thatresembles and actually is fluid depletion in form. Contrastmedia are to be avoided stringently in the face of baselineelevated creatinine, but the ARF that may ensue can beavoided and treated by fluid therapy. ACE inhibitors andangiotensin converting enzyme receptor blockers may causeARF but rarely and easily diagnosable early and reversed.2. The answer is E. The patient in uremia with small“end-stage kidneys” is not a candidate for renal biopsy.Each of the other choices is an indication for renal biopsyon the basis of possible treatable and reversible causes.3. The answer is E. Metformin, despite its benefit in controlof type 2 diabetes, hence theoretically instrumental inpreventing renal failure, is nephrotoxic in the presence ofpreexisting reduced renal function. Each of the othersmentioned in the choices is helpful in the retardation ofthe advance of CRF.4. The answer is B. Antiglomerular membrane antibodies(anti-AGB AB). The combination of glomerulonephritisand pulmonary hemorrhage along with anti-AGBAB antibodies defines Goodpasture disease. This a seriousand potentially fatal disease whose treatment is best left tothose who are experienced in critical care. In 90% of cases,anti-AGB AB antibodies are present. ANCAs are present inabout 15%. Iron deficiency anemia is common, reflectingthe significance of the blood loss through the lungs. Whileneither one is particularly specific, Goodpasture is the onlyacute autoimmune disease that involves both the kidneysand the lungs. Diabetes is not associated statistically. BUNand ASO are entirely nonspecific, albeit sensitive indicatorsof inflammation with autoimmune components.5. The answer is A. The 24-hour urine specimen thatshows 250 mg of albumen falls within the definition ofmicroalbuminuria for a diabetic, which is 30 to 300 mg ofalbumen in 24 hours. Other, quick methods of detectionof microalbuminuria include a urine spot albumenspecificdipstick finding of 3 mg/dL and spot urine albumen-to-creatinineratio of 17 to 250 mg of albumen to 1 gof creatinine (men) or 25 to 355 mg of albumen to 1 gcreatinine (women). Because small amounts of proteinmay appear in the urine for brief periods, microalbuminuriashould be confirmed after a delay of 2 to 3 weeks. Ifproteinuria persists, the patient should be evaluated forkidney disease, with attention to diabetes, hypertension,and various causes of glomerular disease. Nephrotic syndromeis entirely different, foremost in that the definitionof nephrotic syndrome is 3 g of total protein (both albumenand globulin) per 24-hour period.6. The answer is D. ACEIs as well as angiotensin receptorblocking agents (ARBA) protect against renal damage byreducing the GFR per nephron. GFRs per unit number ofsurviving glomeruli increase as creatinine clearancedecreases. An elevated GFR leads to proteinuria. Deteriorationof renal function is retarded by control of either BPin hypertensive patients or blood sugar in diabetic patients(see discussion of Question 2). Thus, the other choices,insofar as they are antihypertensive agents, do serve toprevent loss of renal function to the extent that they succeedin control of BP. ACEIs and ARBAs are antihypertensiveagents, particularly in patients whose hypertensionis driven to a significant degree by the rennin–angiotensinsystem. Thus, ACEIs and ARBAs protect renal function inhypertensive patients in two ways and in diabetics solelythrough the effect to reduce the GFR.7. The answer is E. When creatinine clearance falls tobelow 60 mL/minute, phosphates are retained and a relativehyperphosphatemia results. The reciprocal relationshipbetween serum phosphates and serum calcium givesrise to hypocalcemia, to which the parathyroid glandsrespond by increasing the output of parathormone. Negativecalcium balance is thus a part of the pathophysiologyof CRF and results in a loss of bone density. Failure ofcalcium absorption occurs secondary to loss of estrogensupport in menopause because of the loss of theparathormone-inhibiting effects of estrogen, relevant inChoices C and D but not in renal failure. The postmenopausalstate is associated with hyperparathyroidism for adifferent reason, which in turn contributes to postmenopausaldecrease in postmenopausal bone density.8. The answer is C. Creatinine clearance is the measureof renal function. The stages of kidney disease are defined

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