15. Endocrine, Diabetes, Metabolism Flashcards
Weight gain, hirsutism/menstrual abnormalities (hyperandrogenism) mm weakness, HTN, easy bruisability, dermal atrophy, and striae are signs of what?
Cushing’s syndrome (hypercortisolism)
Dx - once hypercortisolism is confirmed (late-night salivary cortisol assay, 24-h urine free cortisol, overnight low-dose dexaethasone supp test), ACTH levels are measured to differentiate ACTH dependent and ACTH independent causes
How can chronic GI disease (eg steatorrhea, Celiac disease) cause vit D def?
Malabsorption –> hypocalcemia low phosphorus, elevated PTH
Most appropriate treatment for patient with central DI?
Desmopressin is first line for central DI. HCTZ is not as effective as monotherpay, but can be additive.
Note: can be used to differentiate central and nephro DI - central DI shows at least 50% inc in urine osm after admin.
Patient with weight loss, tachy, tremor, and lid retraction should be suspected of having what? What are the cardiovascular effects?
Thyrotoxicosis.
CV: afib/flutter, sinus tachy, premature AV complexes, inc myocardial o2 demand, widen pulse pressure
Systolic HTN is d/t hyperdynamic circulation from inc myocardial contractility and HR
Glucocorticoid deficiency, hypogonadism, and hypothyroidism characterize what condition?
sx include fatigue, cold intol, hypoglycemia, anorexia, low libido.
hypopituitarism.
Note: this contrasts from primary adrenal insuff in that ALDOSTERONE is normal in central adrenal insufficiency
How can high-volume blood transfusion cause symptomatic hypocalcemia?
Chelation of ionized calcium by citrate in transfused blood.
Sx: paresthesias, carpal spasm, hyperreflexia
A young patient with HTN, strong family hx of HTN and stroke, and easily induced hypokalemia after starting a thiazide diuretic suggests what?
Primary hyperaldosteronism.
Test renin and aldosterone
How does primary hyperparathyroidism (PHPT) cause HTN? What are common sx of PHPT?
Unclear
Bone pain, kidney stones, GI sx, neuropsych sx (bones, stones, abd moans, and psychiatric groans).
What test predicts the risk of future ulcers in patients with diabetic neuropathy
Monofilament test
Hypothyroidism can cause what additional metabolic abnormalities
Hypercholesterolemia (dt dec LDL surface receptors/receptor activity) +/- hypertriclyceridemia (d/t dec Lipoprotein lipase activity)
Hyponatremia
Elevated CK and transaminases
What are the lab findings in osteomalacia (calcium, phosphate, PTH) due to vit D def?
Sx?
Vit Def Ca: low Phosphate: low PTH: inc sx: Vit D def (eg d/t malabsorption, bypass surgery, celiac, chronic liver or kidney dz) --> asymp or bone pain, mm weakness or cramps
Premature sexual hormone activation (precocious puberty) can occur centrally or peripherally. Isolated premature adrenarche (body odor, oily hair, acne, pubic hair, and axillary hair) is caused by central or peripheral activation? Is bone age normal?
Peripheral - early activation of adrenal androgen release. Bone age normal
Note: obese children and of black or Hispanic ethnicities are at inc risk.
Premature thelarche (breast dev) also has normal bone age
Dry mucous membranes, polyuria, dec LOC, diffuse abd pain, metabolic acidosis, following an acute URI is most likely explained by what?
DKA from undiagnosed T1DM.
Infex –> systemic catecholamines and cortisol –> excess glucagon –> hyperglycemia, ketonemia, osmotic diuresis. Net renal loss of K+ with depletion of total K stores.
In determining central vs peripheral precocious puberty, what order should you measure bone age, LH, and GnRH?
Bone age first. If advanced, measure baseline LH, give GnRH, then remeasure LH.
Low LH = peripheral (gonadotropin-independent)
High LH = central (gonadotropin dependent)
If bone age normal - isolated breast or isolated pubic hair dev
weight loss, abdominal pain, fatigue, hyperpigmentation, hypotension, low serum cortisol, hyponatremia, and hyperkalemia, is suspicious of what? What is the MCC in developed countries?
Primary adrenal insufficiency - autoimmune adrenalitis is responsible for >90% of cases in developed countries.
Autoab against adrenal enzymes that make corticosteroids. Don’t make mineralocorticoids.