NMS Q&A Family Medicine

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