- A 63 year old woman presents to your clinic with a 2 month history of increasing pain in his pelvis and front of his head ("not like a headache"). The pain is fairly constant, relieved somewhat with ibuprofen but less with acetaminophen, and does not change with motion or rest. She has a history of hypertension and is being treated with combination ACE inhibitor - diuretic. Physical exam is unremarkable: pain appears to be localized to the skull, pain in pelvis and skull are only mildly increased with pressure. Radiographs of the skull and pelvis are notable for increased density in the pelvis, and mixed increased bone density with areas of radiolucency in the skull. Laboratory results are notable for a normal complete blood count, an erythrocyte sedimentation rate of 40mm/hour, normal electrolytes and glucose, BUN 32mg/dL and creatinine 1.4mg/dL, normal transaminases, alkaline phosphatase 800 (normal <400), normal 5'-nucleotidase, albumin 3.9gm/dL, globulin 2.3gm/dL, and normal serum protein electrophoresis. Urine showed increased levels of collagen N-telopeptide and normal protein levels. The most likely diagnosis is [1]:
A. Multiple Myeloma
B. Breast Cancer with Bone Metastases
C. Osteoporosis
D. Paget's Disease
E. Waldenstrom's Macroglobulinemia - Which ONE of following symptoms is found only in primary adrenal insufficiency and not in secondary adrenal insufficiency [2] ?
A. Weakness
B. Hyperpigmentation
C. Hypotension
D. Weight Loss
E. Hyponatremia - The etiology of Type 2 Diabetes Mellitus is related to resistance of cells to insulin effects, so called insulin resistance. The defect most commonly found in the skeletal muscle of patients with Type 2 diabetes mellitus is [3]:
A. Glucose transport defects (GLUT-4 translocation abnormalities)
B. Abnormal fatty acid metabolism
C. Mutations in the insulin receptor
D. Failure of phosphorylation of myosin light chains
E. Failure of the skeletal muscle to utilize fatty acids for energy - All of the following are true concerning hyperaldosteronism EXCEPT [4]:
- A 46 year old man presents with 6 months of increasing fatigue, cold intolerance, thinning of his hair, decreased sexual interest with mild impotence, and intermittant constipation. He has no significant medical history except for a hernia repair at age 10. On examination, he appears tired but otherwise comfortable. His pulse lying down is 90 and standing is 110, blood pressure lying 110/70 and standing up he becomes dizzy and slightly nauseated with a blood pressure of 90/50. The dizziness is relieved on sitting down. His temperature is 37.6°C, and his respirations are normal at 18 per minute. He has a normal physical exam except for diffusely thin hair on his scalp. Electrocardiogram shows sinus tachycardia at 104 beats per minute, normal axis and intervals, slightly peaked T waves throughout. Laboratory tests are ordered and early results show a hematocrit of 34% (normal >36%), normal white cell counts with a mild eosinophilia, sodium 136mmol/L (normal 136-144mmol/L), potassium 5.6mmol/L (normal 3.5-5.5mmol/L), chloride 108mmol/L, bicarbonate 18mmol/L, glucose 85mg/dL, albumin 4.6gm/dL, globulins 2.5gm/dL. Additional studies are pending. The most likely diagnosis is [5]:
A. Hypogonadism
B. Testicular carcinoma
C. Hypothyroidism
D. Pituitary Insufficiency
E. Adrenal insufficiency - Which ONE of following is true concerning the diagnosis of Hashimoto's Thyroiditis [6] ?
A. Elevated TSH and reduced T4 levels are diagnostic
B. Combination of normal radioiodine uptake and elevated TSH is diagnostic
C. Elevated TSH with positive anti-thyroid microsomal antibodies is diagnostic
D. A free thyroxine index (FTI) more than 2 standard deviations above the mean is diagnostic
E. Presence of anti-thyroid microsomal and anti-thyroid peroxidase antibodies is diagnostic - All of the following are true concerning Protease Inhibitor associated lipodystrophy EXCEPT [7]:
A. Increased dorsocervical and breat fat with wasting of peripheral fat
B. Hyperlipidemia and insulin resistance (hyperglycemia) occur
C. Protease inhibitors are always implicated in the syndrome
D. Protease inhibitors bind to host cell proteins including CRABP-1 and LDL related protein
E. Inhibition of mitochondrial DNA polymerase gamma probably contributes to the syndrome - All of the following are complications of obesity EXCEPT [8]:
A. Hypertension
B. Cor PulmonaleC, OsteoarthritisD,.Insulin Resistance and Diabetes Mellitus
E. Osteoporosis - Which ONE of the following is true concerning the syndrome of inappropriate diuretic hormone (SIADH) ?
A. Serum osmolality is low and serum sodium is low
B. Urine sodium <20mmol/L but Urine Osmolarity > Serum Osm
C. Patient may be hypovolemic, euvolemic or slightly hypervolemic
D. Patients with uncorrected hypothyroidism can have SIADH
E. Serum ADH levels may be low, normal or elevated - A 65 year old woman with a history of osteoporosis based on a bone scan 4 years ago presents with new back pain. She had a histerectomy at age 55 for bleeding uterine fibroids and has been taking estrogen replacement therapy (ERT: Premarin 0.625mg po qd) since then and reports good compliance. She has been active with no weight loss, fevers, or other systemic symptoms. Physical examination is unremarkable. A radiograph of the spine shows new vertebral compression fractures V8-9 and L1 and osteopenic bones. Prescriptions for her ERT have been filled appopriately over the past several years. She has had no hot flashes or other symptoms compatible with estrogen deficiency. She takes hydrochlorothiazide for hypertension, calcium 1000mg per day with vitamin D 400 IU/day, a multivitamin and extra vitamin E 400 IU per day. There is no personal or family history of breast cancer. The most appropriate pharmacologic intervention next is [10]:
A. Discontinue Premarin® and begin raloxifene (Evista®)
B. Add calcitonin nasal (Miacalcin®) to her regimen, monitor urinary N-telopeptide levels, and change hydrochlorothiazide to a non-thiazide antihypertensive agent
C. Add cyclic etidronate to her regimen and change hydrochlorothiazide to a non-thiazide antihypertensive agent
D. Add alendronate (Fosamax®) to her regimen, monitor urinary N-telopeptide levels and change hydrochlorothiazide to a non-thiazide antihypertensive agent
E. Begin subcutaneous injections of parathyroid hormone
A. Aldosterone is mainly produced in the adrenal glomerulosa
B. In primary hyperaldosteronism, renin levels are suppressed
C. Hypokalemia is commonly seen in patients with aldosterone excess
D. Adrenal adenoma and hyperplasia are the most common causes of hyperaldosteronism
E. In the saline infusion test, infusion of 2L of saline will lead to increases in aldosteronelevels in normal persons; levels will not change in hyperaldosteronism
