NMS Q&A Family Medicine

212 NMS Q&A Family MedicineExamination Answers1. The answer is C. Prolonged P-R interval on restingECG with total calcium level of 12 mg and PTH of 40 ngis virtually certain to be caused by hyperparathyroidism,which is not the same as saying all cases of hyperparathyroidismexhibit this combination of factors and othersthat follow in this discussion; that is, high specificity doesnot translate to high sensitivity. The main message here isthat any measurable level of PTH in the presence of hypercalcemiasignifies that PTH is the driver. Each of the othersymptoms listed as well as calcium-containing renalstones and decreased deep tendon reflexes are found inhyperparathyroidism but are not specific. Other findingsand symptoms include prolonged Q-T interval anddecreased P-R intervals on ECG, pruritus, intellectualfatigue, and depression. It has been said that hyperparathyroidismcauses problems with “bones, stones andabdominal groans, psychic moans.”2. The answer is D. Carpopedal spasm. That is, it is not arequired characteristic by NIH consensus for diagnosis ofhyperparathyroidism. Actually, carpopedal spasm is asequela of hypocalcemia. Hyperparathyroidism causeshypercalcemia. Each of the other characteristics must bepresent by those criteria: serum calcium 1 mg/dL abovenormal; urinary Ca 400 mg/dL; abnormally low bonedensity; age less than 60 years.3. The answer is D. Anorexia nervosa is characterized byincreased urinary cortisol but not elevated serum cortisol.Ingestion of gamma-hydroxybutyrate occurs in its use asa party drug and results in ACTH-dependent reversibleCushing syndrome. In familial cortisol resistance, serumcortisol is elevated, but by definition, relatively ineffectiveand the resultant errors of metabolism lead to hypergonadismand hypertension. Factitious hypercortisolism isby definition caused by planned deception. In this case,when elevated cortisol level is encountered, it is mostlikely due to factitious self-treatment with ACTH and canbe very difficult to prove.4. The answer is D. Acute adrenal insufficiency may beprecipitated by hypotension, trauma, or hemorrhage. Thefact that this is an acutely ill patient, who is a type I diabeticyet manifests hypoglycemia, as opposed to markedlyincreased insulin requirements, rules against, if not eliminates,sepsis or other infectious causes. Neurologic sequelaefrom trauma would be unexpected in a person whosuffered neither loss of consciousness nor symptoms ofconcussion.5. The answer is E. Hypovolemia, normal sodium concentration,normal serum potassium, and normal skincolor, in association with abnormally low levels of cortisol,are all signs of adrenal insufficiency that is due topituitary failure as opposed to primary adrenal insufficiency.In primary disease, ACTH is elevated, andincreased skin pigmentation is an indirect result of this.Also, in primary adrenal insufficiency, most often as aresult of destructive processes in the physical site of theadrenal glands, the zona glomerulosa is destroyed as wellso that hyperkalemia, resulting from absence of aldosterone,occurs; this is not so in secondary adrenal insufficiency.Peripheral blood cell changes, neutropenia, relativeeosinophilia, and lymphocytosis occur in primary or secondaryadrenal insufficiency.6. The answer is C. Hyrocortisone 24 mg daily, given as16 mg in the morning and 8 mg in the afternoon, plusfludrocortisone 0.3 mg daily. Important points to rememberare (a) that the glucocorticoid should be given as twothirdsof the replacement dosage in the morning with theremainder in the afternoon and (b) that many patientswith primary adrenal insufficiency require replacementof the mineralocorticoid as well. In this example, fludrocortisonereplaces aldosterone. The dexamethasonereplacement dosage is 0.75 mg daily in divided doses, withtwo-thirds in the morning and one-third in the afternoon.However, as the most pure synthetic product among thosepresented, it has the least mineralocorticoid activity. Thus,nearly always there must be mineralocorticoid replacement,if dexamethasone is used to treat primary adrenalinsufficiency. If prednisone is used for glucocorticoidreplacement, then the dosage is 5 mg, but also in divideddoses (two-thirds and one-third). From the foregoing, itis easily inferred that prednisone is five times as potent,milligram for milligram, as hydrocortisone and that dexamethasonehas 33 times the potency of hydrocortisone.7. The answer is C. Hydrocortisone in replacement dosagesnot only repletes the serum cortisol that tends to beinsufficient but, through negative feedback, suppressesACTH, removing the stimulus driving the aberrantpathway. About 50% of cases lack also minealocorticoid(salt wasting) and bear treatment with fludrocortisone.Little is known about that polyuria and polydipsia mayaccompany this disease. Three other types, all rare, manifestelevated 17-hydroxypregnenolone (3-beta-hydroxy)and decreased 17-alpha-hydroxy steroid (17-hydroxylasedeficiency).