NMS Q&A Family Medicine

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198 NMS Q&A Family Medicine18 You order a serum creatinine and 24-hour urinefor creatinine and for total and complete proteinfor an 40-year-old Caucasian diabetic type 1 male.His height is 6 ft 1 in. and he weighs 180 lb. Fromthese data, you calculate a creatinine clearance of50 mL/hour. Each of the following statements isrelevant regarding this finding except for (which)statement?(A) Closer blood sugar control is indicated.(B) Among cases of this condition, more are causedby type 2 diabetes than by type 1.(C) Blood pressure control is important.(D) Pharmacological means to raise the glomerularfiltration rate is indicated.(E) Dietary protein control is indicated.
Diabetes Mellitus 199Examination Answers1. The answer is B. Asian. This group develops type 2 diabetesat lower BMIs and lower ages than other groups. Furthermore,they appear to be most subject to renal diseasedue to diabetes. This may be surprising because Latinosand blacks are known to be developing diabetes at increasinglylower ages but that is clearly because of the appearanceof increasingly lower ages of obesity. The same maybe said for Latino-Americans and some aboriginal tribes.As for blacks in America, insulin resistance is greater forgiven levels of BMI (but without a commensurate increasein atherosclerotic risk, as compared to Caucasians).2. The answer is B. The incorrect statement is thatexenatide reduces insulin resistance in type 2 diabetes.Each of the other statements about the much-laudedexenatide (Byetta) is true. Suppression of glucagonappears to be somewhat clinically significant in that bloodsugar control is improved and HgbA1c adequately controlled.Perhaps more important is that a side effect isweight loss. Exenatide must be delivered by subcutaneousinjection twice daily, promotes a higher insulin responsethan an equivalent dose of glucose, and carries a lowerrisk of hypoglycemic reaction than sulfonylureas.3. The answer is A. Glargine (Lantus by Sanofi-Aventis),the longest acting of the insulins presented. Its onset occursat about 1.5 hours after injection and lasts for 24 hours.As to lispro (Humalog by Lilly), glulisine (Apidra bySanofi Aventis), and Aspart insulin (Novolog by NovoNordisk), all have onsets of action within 5 to 15 minutespeaking at 1 to 1.5 hours and lasting 3 to 4 hours. Regularinsulin sets on in 30 to 60 minutes, peaks in 2 hours andlasts 6 to 7 hours.4. The answer is C. HHS precipitated by dehydration isthe best description of the pathophysiology of thispatient’s condition. Required for this development is type2 diabetes, a measure of at least temporary poor control,and a clinical stimulus for dehydration. As serum osmolalityexceeds 310 mosm/kg, the patient develops lethargyand confusion with coma supervening at 320 to 330. DKA,found virtually only in type 2 diabetes, is ruled out by thelack of ketosis. The hyperosmolar state is certainly somewhatrelated to diabetes control, but the latter is not theproximate cause. In the present case, dehydration wouldhave been caused by the gastroenteritis. Even egregiouslynoncompliant or poorly controlled patients seldomdevelop the hyperosmolar state. The BUN of 110 mg/dL iscommon in the hyperosmolar state and does not denoterenal failure. The azotemia will respond to aggressive fluidand electrolyte repletion therapy.5. The answer is C. The major precipitants of HHS,although the final common pathway is dehydration, aremedication noncompliance and ethanol and cocaine use.Although it has been written that “causes” include myocardialinfarction, stroke, hyperthermia and hypothermia,pulmonary embolus, and many other diseases, no onedevelops HHS who does not have a type 2 diabetic diathesis.According to the article by Stoner cited in the references,the case mortality of this syndrome is greater thanthat of DKA. A significant anion gap is more characteristicof DKA, and infarct is not a particular characteristic ofHHS. Although gastroparesis is generally thought of as acomplication of type 2 diabetes, it may be found in HHSduring the acute phase when dehydration is marked.Because the basic pathophysiology of HHS is dehydration,that is, neither hyperglycemia per se nor acidosis, thequickest response is fluid therapy while using modestmeans to reduce the blood sugar level, which will fall evenwithout insulin as fluid and sodium repletion proceeds.6. The answer is B. Only the biguanides, of which theonly presently approved example is metformin, facilitateweight loss while reducing blood sugar without stimulatinginsulin production. It accomplishes the latter bydecreasing hepatic glucose production, mainly throughreduction of gluconeogenesis. Because of its ability toreduce blood sugar without stimulating insulin production,it functionally reduces insulin resistance. Sulfonylureaagents decrease blood sugar levels by stimulatingproduction of insulin (i.e., they are secretagogues forinsulin), hence contributing to higher insulin levels andultimate exhaustion of the beta-cells of the pancreas.Non-sulfonylurea secretagogues work similarly to sulfonylureasecretagogues but more rapidly. Thiazolidinedionesenhance insulin sensitivity by activating a nucleartranscription factor and modulating many genes that regulateCHO metabolism. The net effect is to increase insulinsensitivity. Alpha-glucosidase inhibitors work bydelaying intestinal absorption of CHOs and thus reducingPP glucose levels. Their effectiveness is not impressive,and the side effect of flatulence has made the agent acarboseless popular with time.7. The answer is D. The pains are caused by long-standinghyperglycemia. The patient has diabetic neuropathy (i.e.,neuropathy did not cause the pains; the pains wereevidence, part and parcel, of diabetic neuropathy). TheUnited Kingdom Prospective Diabetes Study Groupresults published in four separate journal articles (two inLancet and two in the British Medical Journal , all in 1998)showed for type 2 diabetes the same as the DCCT Group
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NMS Q&AFamily Medicine3rd EDITION
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Acquisitions Editor: Susan RhynerPr
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Foreword to the First EditionFamily
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AcknowledgmentsFor the contribution
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xivContentsChapter 15 Surgical Issu
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SECTION IUrgent Carechapter 1Urgent
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Urgent Care in Family Practice 3(A)
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Urgent Care in Family Practice 5Exa
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Urgent Care in Family Practice 7rem
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10 NMS Q&A Family Medicine(A) To pl
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12 NMS Q&A Family MedicineExaminati
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chapter 3Otolaryngology inPrimary C
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Otolaryngology in Primary Care 17tr
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Otolaryngology in Primary Care 1924
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Otolaryngology in Primary Care 21of
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Otolaryngology in Primary Care 23co
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30 NMS Q&A Family MedicineQuestions
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36 NMS Q&A Family Medicine80 mm Hg.
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SECTION IIICardiovascular Diseasesi
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Cardiology 41(A) Systolic crescendo
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Cardiology 43Examination Answers1.
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Cardiology 4516. The answer is C. T
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chapter 7Peripheral Vascular Diseas
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Peripheral Vascular Disease 49would
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Peripheral Vascular Disease 51Exami
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Peripheral Vascular Disease 53right
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chap ter 8Cerebrovascular DiseaseEx
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Cerebrovascular Disease 57(A) A non
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Cerebrovascular Disease 59ventricul
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chap ter 9Pediatric CardiologyExami
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Pediatric Cardiology 6315 You hear
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Pediatric Cardiology 65by placing o
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chap ter 10HypertensionExamination
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Hypertension 6915 In hypertensive p
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Hypertension 71systolic hypertensio
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74 NMS Q&A Family Medicine(A) Right
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Neurology 778. The answer is A. The
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SECTION VRespiratory Diseasesin Pri
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Pneumonia and Bronchitides 81(C) Co
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Pneumonia and Bronchitides 836. The
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chapter 13Respiratory Diseasesin Ch
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Respiratory Diseases in Children 87
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SECTION VIThe Gastrointestinal Trac
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Medical Problems of the Gastrointes
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Medical Problems of the Gastrointes
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chap ter 15Surgical Issues of theGa
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Surgical Issues of the Gastrointest
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Surgical Issues of the Gastrointest
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chap ter 16Problems of the LiverExa
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Problems of the Liver 103level, whe
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Problems of the Liver 105been inves
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SECTION VIIUrology and Nephrologyin
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Problems of the Urinary Tract 10913
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Problems of the Urinary Tract 11110
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114 NMS Q&A Family Medicine7 Which
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116 NMS Q&A Family MedicineExaminat
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118 NMS Q&A Family Medicineof malig
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124 NMS Q&A Family MedicineReferenc
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chapter 21Gynecology in Mature Adul
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Gynecology in Mature Adults 133amen
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Gynecology in Mature Adults 1357. T
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chapter 22Diseases of the Female Br
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Diseases of the Female Breast 139Ex
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Diseases of the Female Breast 141Re
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144 NMS Q&A Family Medicine(B) Long
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146 NMS Q&A Family Medicine(D) PIP
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Page 207 and 208: chap ter 31Other Infectious Disease
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Page 213 and 214: SECTION XIEndocrinology inPrimary C
Page 215: Diabetes Mellitus 197normal saline
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Page 249 and 250: Preoperative Clearance 23121 Prophy
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Page 253 and 254: chap ter 38Obesity and Dyslipidemia
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chapter 41Concepts in Epidemiologya
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Concepts in Epidemiology and Resear
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Concepts in Epidemiology and Resear
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chapter 51Anxiety and PhobiasExamin
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Anxiety and Phobias 297Examination
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chapter 52Somatic Symptoms withoutO
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Somatic Symptoms without Organic Ba
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Somatic Symptoms without Organic Ba
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chapter 54GeriatricsExamination que
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Geriatrics 315Examination Answers1.
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chapter 55HematologyExamination que
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Hematology 31915 A 45-year-old busy
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Hematology 321Mean cell hemoglobin
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Hematology 323whereas in multiple m
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