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Pance Endo combined
| Question | Answer |
|---|---|
| Rapid acting insulin: | Lispro; Aspart; Glulisine |
| Short acting insulin: | Regular |
| Intermediate acting insulin: | NPH |
| Basal insulin: | Glargine (Lantus); Detemir (Levemir) |
| Premixed insulin: | 70/30 regular; 70/30 aspart; 75/25 lispro; 50/50 |
| Action: Lispro, Aspart (rapid) | Onset of Action 5-15 min; Peak 30-90 min; Duration of Action 4-6 h |
| Glulisine (rapid) | Onset of Action 5-15 min; Peak 30-90 min; Duration of Action 6-8 h |
| Action: Regular (short acting) | Onset of Action 30-60 min; Peak 2-4 h; Duration of Action 6-10 h |
| Action: NPH (intermed acting) | Onset of Action 1-2 h; Peak 4-8 h; Duration of Action 10-20 h |
| Action: Glargine (basal) | Onset of Action 1-2 h; Peak: None; Duration of Action 24 h; do not mix with other human insulins |
| Action: Detemir (basal) | Onset of Action 1-2 h; Peak 6-8 h; Duration of Action 12-24 h |
| Fx on insulin absorption: Temperature | Heat increases, cold decreases |
| Fx on insulin absorption: Large doses (>80 units) | Delay onset and duration |
| Fx on insulin absorption: Certain insulin mixtures | Lente causes loss of rapid acting insulin action |
| Fx on insulin absorption: Large doses (>80 units) | Delay onset and duration |
| MOA: Alpha-glucosidase inhibitors (Precose, Glyset) | decrease glucose absorption in intestines |
| MOA: Biguanides | Decrease hepatic glucose output; increase glucose uptake |
| MOA: TZDs | Mx & adipose tissue: decrease insulin resistance; increase glucose uptake |
| MOA: Sulfonylurea & Repaglinide | Pancreas: increase insulin secretion |
| Use of sliding scale insulin: | should NOT be used as monotherapy |
| Hypoglycemia Tx: D50 | IV Dextrose (D50) Admin = most rapid method of alleviating hypoglycemia; appropriate for pts who are unconscious, severely symptomatic, or NPO |
| Rapid acting insulin: inject when: | within 15 min of meal; as rescue: w/o regard to meals |
| Glulisine (Apidra)(rapid): Dosing: | 15 min prior to meal OR within 20 min after starting a meal |
| Short acting insulin: inject when: | within 30 min of meal; as rescue: w/o regard to meals |
| NPH: typically inject how often: | x2 / day (depending on meal schedule) |
| Detemir is bound to ? and is good out of the fridge for: | bound to albumin; good for 42 days out of refrigerator |
| If change in basal insulin: BID NPH to long-acting: | Reduce TDD by 20%; administer total dose QD |
| 50/50 rule with NPH as basal: | Decrease amt used as bolus by 20% |
| Standard insulin split mix | 2/3 of TDD in AM (1/3 short acting; 2/3 intermed); 1/3 of TDD in PM (1/2 short acting, 1/2 intermed) |
| Rule of 1800 formula | 1800 / TDD = x (mg/dL changed by 1 unit insulin) = correction factor |
| Rule of 500: formula | 500 / TDD = x gm CHO covered by 1 unit insulin |
| Tx for impaired insulin secretion: | Sulfonylureas; meglitinides; insulin |
| Tx for insulin resistance: | biguanides; TZDs |
| Which insulins are cloudy? | NPH; mixes |
| Which insulin may be given IV? | Regular |
| Secondary hypothyroidism: Do not: | replete thyroid hormone before repleting cortisol; if pt adrenal/ cortisol deficient, & replete TH first, revs up metab, can lead to adrenal crisis (won't have enough cortisol to support metabm) |
| Acromegaly Tx | Surgical; Somatostatin Analogs: Sandostatin; poss dopamine agonists; XRT |
| Hypercalcemia: nonpharm tx | Tx underlying cause; enhance calciuresis: Fluids (2-3 L / day po for mild; IV saline for severe / Ca > 13); loop diuretics (only after volume repletion); furosemide |
| Hypercalcemia: Pharm tx: Inhibit osteoclastic resorption: | bisphosphonates; calcitonin; cinacalcet |
| Hypercalcemia: Pharm tx: Inhibit osteoclast resorption/ reduce GI absorption: | Glucocorticoids (prednisone; solumedrol) |
| Hypocalcemia Tx | Vit D (25 OH D deficiency): Calcium (2000-4000 mg/day); ergocalciferol / cholecalciferol if 25 OH D deficient; Calcitriol if 25 OH D sufficient |
| Osteomalacia: Tx | Ergocalciferol (D2-Drisdol) 50K U BID x 6-12 mos; Vitamin D (25 OH D def): Ca (1500-2000 mg/day); cholecalciferol (D3); Calcitriol (for hypophosphatemic osteomalacia) |
| Skeletal response to continuously delivered PTH | inc osteoclasts, inc resorption, inc serum Ca |
| Skeletal response to once-daily delivered PTH | inc osteoblasts, inc bone formation, inc bone mass/ strength |
| Adrenal crisis tx | Tx HYPOTENSION w/ volume (2 to 3 L of NS or D5NS); Give IV DEXAMETHASONE 4mg or IV HYDROCORTISONE 100mg (Dex preferred bc it won't interfere w/ further dx testing & is long acting) |
| Chronic adrenal insuff: maint tx | Hydrocortisone 20mg AM / 10mg PM; Dex; prednisone |
| Cushing syn: tx | Surg Resection; Transphenoidal microsurgical removal (if sure Cushing dz); Bilateral Adrenalectomy (uncommon); Pharmacologic adrenal blockade |
| Primary hyperaldosteronism: Tx: Aldosterone Producing Adenoma: | surgical (effective only in patients with unilateral disease) |
| Primary hyperaldosteronism: Tx: IHA or poor surgical candidate: | med tx: Mineralocorticoid receptor antagonists: Spironolactone (DOC) or Eplerenone; CCB; ACEI |
| Pheochromocytoma: Tx : First: | Alpha Adrenergic-Blockade first; Beta-blockade next if nec; NEVER start before alpha-blockade (can lead to worsened hypertensive crises); CCB (may be better tolerated than alpha-blockade) |
| Pheochromocytoma: Tx: | Surgical resection is tx of choice (May req open lap); Need adequate a-blockade pre-op; Watch for post-op comps(Labile BP; Post-resection hypoTN/ shock; Hypoglycemia) |
| toxic multinodular goiter Tx | Rx RAI |
| subacute thyroiditis: Tx | ASA/ NSAIDs; prednisone |
| Multinodular goiters: tx | thyroxine suppression of TSH; surg if obstruction |
| Tx for Graves dz | PTU (esp for PG/BF)(TID); Tapazole (qd) |
| PTU works within: | 17 weeks |
| Surgery for hyperthyroid: subtotal or total thyroidectomy: indicated in: | pts with obstructions (lg goiters), malignancy, pregnancy in 2nd trimester, or those with contraindications to RAI or thioamides |
| Tx of choice for hyperthyroid in US: | radioactive I ablation (CI in PG) |
| Hyperthyroid tx adjuncts: | beta-blockers (propranolol); c'steroids (dec action of thy hormone & imm response in Graves); Iodine (blocks thy hor release) |
| Tx for thyroid storm | First: Propranolol, hydrocortisone; PTU/methimazole, Iodide; Supportive measures; mortality 20% |
| Myxedema Coma: tx | stat IV levothyroxine; then check labs |
| thyroid replacement tx dosing | <45 yo 100%; > 45 or LT/severe dz 50%; CVD or >65 25%; PG: inc dose by 50% |
| hyperthyroid ophthalmopathy tx: | IV methylprednisolone |
| hyperthyroid drug of choice for PG & breastfeeding pts = | PTU |
| hypoPTH tx: | airway, IV Ca gluconate; maintenance oral Ca, vit D, calcitriol, Mg; poss PTH tissue txp |
| T1DM diet recs | 45-65% CHO, 10-35% pro, 25-35% fat; <33 mg/day chol |
| Gastroparesis, impotence, recurrent infections, stocking-glove paresthesia = | Diabetic neuropathy (Treat w/ TCA (amitriptyline) |
| Hypoglycemia despite glucose administration; increased C-peptide; may be due to: | Insulinoma or extrapancreatic tumor |
| Hypoglycemia in alcoholic: give: | Give Thiamine before glucose to prevent Wernicke encephalopathy |
| DM complications: chronic hyperglycemia leads to: | nonenzymatic glycation of proteins & produces tissue damage |
| Pronounced hyperglycemia with insulin deficiency = | DKA |
| DM: Ocular Complications | Retinopathy; Cataracts; Glaucoma; pts w/ DM need an annual ophthalmologic exam |
| Diabetic Retinopathy: microaneurysms = | Small blow-out swellings of blood vessels |
| DM Retinopathy: Exudates = | Small leaks of fluid from damaged blood vessels |
| DM Retinopathy: hemorrhages | Small bleeds from damaged blood vessels |
| DM Retinopathy: Blood vessels: | may become blocked => reduced blood & oxygen to small sections of retina; New abnormal vessels may grow from damaged vessels (AKA proliferative retinopathy); new vessels are delicate & bleed easily |
| Treatment of renal failure due to DM: | renal transplant more promising than dialysis (if patient eligible) |
| Most common complication of DM: | Neuropathy |
| Characterize DM Neuropathy | Distal symmetrical polyneuropathy with loss of motor & sensory function, esp. of long nerves |
| DM Neuropathy clinical features | Painful diabetic neuropathy with hypersensitivity to light touch; Diabetic gastroparesis; Erectile dysfunction |
| Test for Diabetic Foot Ulcer with: | 10g monofilament test ; Comprehensive foot exam |
| Major metabolic defects in T2DM | Peripheral insulin resistance in mx & fat; Decreased pancreatic insulin secretion; Increased hepatic glucose output |
| DM risk factors | FH; Age > 45; High-risk ethnic pop; Habitual physical inactivity; Meds (transplant, HIV, anti-psychotics); Obesity |
| Obesity & DM | fat cells = endocrine organs |
| Glycemic recommendations for non-PG adults w/ DM | A1C <7.0%; FPG 70-130 mg/dL; Peak postprandial glu <180 (1 hr) & <150 (after 2 hrs) |
| HbA1c & DM dx | Dx s/b made if A1c <6.5; s/b confirmed w/ repeat test; not nec for sx pt w/plasma glu ≥200 mg/dL |
| DM clinical features | Polyuria; Polydipsia; Wt loss; Fatigue; blurred vision; Suscept to infxn; May be asymptomatic, esp Type 2 |
| DM: Polyuria occurs when: | serum glu >180 mg/dL (exceeds renal threshold for glu, which leads to increased urinary glu excretion) |
| DM: Glycosuria causes: | osmotic diuresis (ie, polyuria) and hypovolemia |
| DM & wt loss | 2/2 hypovolemia and increased catabolism; insulin def in DM kids impairs glucose utilization in sk mx & increases fat / mx breakdown; initially, appetite is inc; over time, kids may become anorexic |
| DM: Wt loss: Less common in: | Type 2 DM |
| Acute life threatening complications of DM: | DKA; Nonketotic hyperosmolar syndrome |
| DKA: Dx | Hyperglycemia; Ketonemia; Acidemia |
| Ketones: Why | Insulin def: Inc lipase activity increases breakdown of TGs to glycerol & free fatty acids (= precursors to ketone bodies) |
| DKA mgmt | continuous insulin drip (monitor) (MOST IMPORTANT); Fluids; Potassium; EKG; |
| Major cause of mortality for DM pts: | CVD |
| Leading cause of ESRD: | Diabetic nephropathy (occurs in 20-40% of DM pts) |
| Most common cause of new blindness in pts 20-74 yo: | Diabetic retinopathy |
| DM & ABCs of CHD prevention: A = | Aspirin; ACEI; A1C control |
| DM & ABCs of CHD prevention: B = | Beta-blockade; BP control |
| DM & ABCs of CHD prevention: C = | Chol mgmt |
| DM & ABCs of CHD prevention: D = | Diet; do not smoke; decrease DM risk |
| DM & ABCs of CHD prevention: E = | Exercise |
| GLP-1 is secreted from: | L-cells of the jejunum & ileum |
| GLP-1 functions | stimulates glucose-dependent insulin secretion; suppresses glucagon secretion; slows gastric emptying; leads to reduction in food intake; increases insulin sensitivity |
| Target/recommendations: HbA1c | target <7.0; <6.0 if poss w/o inducing hypoglycemia |
| T2DM Target: BP | <130/80 (ACEI / ARB) |
| T2DM Target: Lipids | LDL <100 (<70 optimal); HDL >40 M, >50 F; TG <150; statin for CV hx or >40 yo to lower LDL 30-40% |
| T2DM recommendations: ASA | >40 yo or other risk factors; all w/ CV hx |
| T2DM recommendations: ACEI | > 55 yo w/ other CV risk factor |
| Metabolic syndrome: Dx: | 3 of 5: Waist circum >40 (M) / >35 (F); TG ≥150; HDL <40 (M) / <50 (F); BP ≥ 130/85; FPG ≥110 |
| Somogyi | hypoglycemia triggers counter-reg hormones; causes hyperglycemia; manage insulin to prevent hypoglycemia |
| Dawn phenomenon | d/t waning insulin levels; causes hyperglycemia; manage with insulin, or move peak to more physiologic time |
| Nonketotic hyperosmolar syndrome = | high blood viscosity; glu > 600, osmo >350, oliguria |
| DM dx criteria | [A1c ≥6.5% ; FPG ≥ 126 mg/dL; 2 hour GTT ≥ 200 mg/dL (75g load); or RPG ≥ 200 mg/dL] PLUS DM sxs (polyuria, polydipsia, wt loss, blurred vision) |
| Alert Values: FBS (female) | < 40 and > 400 mg/dL |
| Prediabetes / impaired fasting glucose (IFG) lab value: | FPG 100 - 125 mg/dL |
| Values assoc w/ diabetic retinopathy | FBS 126 mg/dL; 2 hr GTT 200 mg/dL; HgbA1c of 7% |
| Created when proinsulin splits into insulin & this product | C-peptide (connecting peptide); used mostly in newly diagnosed diabetics |
| C-peptide: Type 1 diabetes: | decreased levels |
| C-peptide: Type 2 diabetes: | normal or high levels |
| C-peptide: can be used to identify: | gastrinoma spread or malingering (low C-peptide with hypoglycemia may reflect abuse of insulin) |
| Glucose Testing: Urine: Requires: | normal renal glucose threshold |
| Fasting blood glucose (FPG or FBS): lab testing requires: | No caloric intake for at least 8 hours |
| Types of stress that increase glucose | trauma, acute illness, general anesthesia, burns |
| 2 hour GTT Interp: FPG (mg/dL) | Normal GTT <100; Impaired Glucose Tolerance 100-125; DM ≥ 126 |
| 2 hour GTT Interp: 2 hrs after glucose load | Normal GTT <140; Impaired Glucose Tolerance 140-199; DM ≥ 200 |
| Diabetic control correlates highly with: | pt education & motivation |
| HbA1c: In normal people: | 3-6% of hemoglobin is glycosylated in the form A1c |
| HbA1c: Normalizes within: | within 3 weeks of normoglycemic levels |
| HbA1c & RBCs: | Older RBCs have higher HbA1c levels; pts w/ episodic or chronic hemolysis who have larger proportion of young RBCs might have spuriously low levels |
| If HbA1c if > 7% : | adjust therapy |
| HbA1c: If good DM control: | check HbA1c 1-2 times yearly |
| HbA1c: If suboptimal DM control: | check HbA1c every 3 months |
| DKA: lab values | Hyperglycemia > 250 mg/dL or glycosuria 4+ ; Acidosis with blood pH < 7.3; Serum bicarb < 15 mEq/L; Serum positive for ketones |
| Test for DM Nephropathy: | urine microalbumin; more sensitive than dipstick protein |
| Urine microalbumin: May use: | albumin:creatinine (A:C) ratio |
| Urine microalbumin: Correlates with: | nocturnal systolic blood pressure |
| T1DM ID'd by: | sero autoimmune markers of pancreatic islet dysfn and genetic markers |
| impaired fasting glucose = | FBS = 100 - 125 mg/dL |
| impaired glucose tolerance (at 2 hrs) = | 140-199 mg/dL 2 hrs after OGTT (75 g oral glu) |
| Decreased radioactive iodine uptake, decreased free T4, increased TSH | Hashimoto thyroiditis |
| Female, weight loss, palpitations, atrial fibrillation | Hyperthyroid (work it up with TSH, T4) |
| Exopthalmos, palpitations, wt. loss. Elevated radioactive idodine uptake | Hyperthyroid, Graves Dx: tx w/radioactive iodine |
| Post thyroidectomy - most likely injury | Recurrent laryngeal nerve = hoarseness |
| Post thyroidectomy - electrolyte watch | Hypocalcemia |
| Infant w/ round face, large protruding tongue, dry skin, umbilical hernia, constipation, enlarged abdomen, poor feeding, delayed devt milestones = | Congenital Hypothyroidism |
| Wt gain, edema, coarse dry skin, hair, menorrhagia, cold intolerance, h/o transphenoidal surgery & radiation | Hypothyroidism |
| Primary hypothyroidism | Thyroid gland fails to make T4; TSH is HIGH; FREE T4 is LOW |
| Secondary hypothyroidism: | Pituitary gland fails to make TSH; poss sequela of panhypopituitarism; TSH is inappropriately LOW; FREE T4 is LOW |
| Hypothyroid S/S | Cold intolerance; Fatigue; Heavy Menstrual Bleeding; Wt Gain; Myxedema Coma |
| Secondary hypothyroidism: you cannot: | Follow TSH to adjust thyroid hormone replacement (must also follow Free T4) |
| hypothyroidism & low normal TSH, low normal T4: consider: | Secondary hypothyroidism |
| TSH levels don't rise in: | primary hypopituitarism & states of altered thyroid homeostasis |
| hypometabolism with low T3/T4; +/- low FTI & nml TSH | euthyroid sick syndrome |
| Graves dz: predictors of remission | small goiter (decreases w/thioamides, eg, PTU); FT3 predominance; neg TSI titer (IgG Ab vs thyroid cell TSH rec) |
| Graves dz: etiology | Auto-antibody reacting with the TSH receptor (TSI, 80-95% pos) |
| Graves dz: eval | Symmetric non-tender goiter (80%) (bruit is pathognomonic); Ocular findings (30%); Pretibial myxedema; TSH, Free T4, Free T3; Thyroid uptake and scan |
| thyroiditis (early): course: | hyperthy (1-3 mo); then hypothy (1-3 mo); then euthyroid |
| Hypothyroid etiology (3) | Primary; goiterous; central |
| Hashimoto etiology | cytotoxic anti-thy Ab's (80-90% antithyroglobulin); >50 yo |
| toxic multinodular goiter etiology | multicell autonomic fn |
| toxic multinodular goiter exam | >50 yo; lg irreg nod thy; TSH, FT4, FT3, uptake & scan |
| Toxic thyroid nodule: etiology | activation of TSH receptors via rec gene mutation |
| Toxic thyroid nodule: exam | 30-40 yo; lg irreg nod thy; onycholysis; TSH, FT4, uptake & scan; Rx RAI |
| Multinodular goiters | 2-4% prev in iodine-sufficient areas; F 5-15 x M; multifactorial; genetic cause? |
| Myxedema Coma: findings | Emergency: elderly in winter; Hypothermia; Resp depression; Unconsciousness |
| osteoporosis, clubbing, finger swelling may be 2/2: | chronic thyrotoxicosis |
| thyroid neoplasm RF | childhood head/neck radiation or radio-I exp; then ca 20 yrs later |
| thyroid neoplasm s/s | painless neck swelling; single firm nontender nodule: stony, hard gland; medullary: flushing, Cushing; anaplastic: hoarse (recurrent laryng n.) |
| Hypercalcemia pathogenesis | accel bone resorption by osteoclasts (PTH, 1,25 (OH)D, IL-1, IL-6, TNF-alpha); enhanced GI absorption of Ca (vit D); hypercalcemia = eclipsed renal capacity to excrete Ca load (ie, hypercalciuria also present) |
| Hypercalcemia: causes | inc skeleton resorption (primary hyperPTH; malig); inc GI absorption (milk-alk syn); both inc skel resorp & GI absorption (granulomatous: sarcoid, TB, fungal) |
| Chvostek sx = | twitching of face and upper lip in response to tapping inferior to TMJ joint |
| Trousseau sx = | inflate BP cuff, leave it there; pt gets carpal spasm |
| Acute Hypocalcemia S/S | tetany, twitching, paresthesia; Chvostek sx; Trousseau sx; seizures; laryngo or bronchospasm; long QT; arrhythmia; hypotension |
| Chronic Hypocalcemia S/S | ectopic calcification (basal ganglia); EPS; parkinsonism; dementia; cataracts; abnml teeth; dry skin |
| Most common cause of hypocalcemia | surgically induced hypoPTH |
| Osteomalacia = | Defective bone matrix mineralization d/t: inadequate vit D/Ca & phosphorus; deficient mineralizn mechm in presence of normal Ca / phosphorus |
| Osteomalacia in childhood is: | rickets |
| Osteomalacia symptoms | diffuse bone pain (esp pelvis), waddling gait, mx weakness, fractures & pseudofractures (Looser's zones) of long bones, ribs, pelvis |
| Osteomalacia: causes | Vitamin D def; Hypophosphatemia (inherited disorders); Mineralization disorders |
| GH deficiency seen in: | obesity & cortico-steroid therapy |
| 3 causes of pituitary dwarfism: | pit tumor (1/3); pit damage (1/3); Pure GH deficiency (1/3) |
| Most common disorder involving excess pituitary secretion | Prolactinomas |
| Osteoporosis risk factors | Personal hx of fx as adult; Hx of fx in 1st degree relative; current SMK; wt < 127 lb |
| Bone mineral density (BMD) values | T score: BMD > -1SD below YN = nml; severe osteo = BMD <-2.5 |
| best predictor of bone fx risk | bone density (75-85% of variance in bone strength) |
| T-score: osteopenia | -1 to -2.5 SD below YN |
| Primary adrenal insufficiency AKA ____ involves: | AKA Addison dz; all 3 zones of adrenal (so potl insuff of cortisol & aldosterone) |
| Primary adrenal insuff: abrupt onset: etiology | Adrenal hemorrhage, necrosis, thrombosis; meningococcal sepsis (Waterhouse-Friderichsen Syn); pseudo; coag dz; mets ca w/ bleed |
| Primary adrenal insuff: slow onset: etiology | Auto-immune Adrenalitis; infxs Adrenalitis; Mets ca; congenital Adrenal Hyperplasia (CAH); Adrenomyeloneuropathy |
| Primary adrenal insuff: clin findings | Hyperpigmentation (due to xs ACTH); Salt craving; Hyponatremia; Hyperkalemia; Vitiligo, pallor; auto-immune thyroid dz; CNS sx in adrenomyeloneuropathy |
| Secondary/tert adrenal insuff: slow onset: etiology | Pit tumor / surgery / rad; Craniopharyngioma ; Isolated ACTH def; Megace (glucocorticoid-like action); LT g'corticoid tx; Sarcoidosis; Hypothalamic tumor |
| Hirsutism / virilization: etiology | Idiopathic (Familial); PCOS; Androgen-secreting adrenal adenomas or carcinoma; Ovarian tumors; Glucocorticoid resistance |
| Hirsutism / virilization: etiology: ACTH-dependent causes | Congenital Adrenal Hyperplasia; ACTH-dependent Cushing Syn |
| Androgen-secreting adrenal adenomas | Rare; serum androgen remain elevated despite Dex suppression |
| Androgen-secreting adrenal carcinomas | usu > 5 cm at dx; Very high DHEA, DHEA sulfate; No response to HD Dex Suppression |
| Congenital adrenal hypertrophy: etio | Enzyme defects in adrenal steroid hor synth => insuff cortisol +/-mineralocorticoid; classically with an assoc androgen excess |
| Congenital adrenal hypertrophy: classical forms | Salt-wasting form; Virilizing Syndromes |
| Primary hyperaldosteronism: clin findings | Hypertension; Mx Sx (d/t hypokalemia): cramping, weakness, periodic paralysis; Often few clinical findings at all (often suspected after lab abnormalities) |
| Primary hyperaldosteronism: issues in eval | S/b off Aldactone; CCB; ACEI (consider in-house eval); At least 150mEq of sodium intake daily (to suppress aldosterone prodn) |
| Primary hyperaldosteronism: presenting forms | Aldosterone-Producing Adenoma (Conn syndrome); Bilateral Hyperplasia of the Zona Glomerulosa (need remove both); Primary adrenal hyperplasia; Adrenal carcinoma |
| Pheochromocytoma = | dz of adrenal medulla (site of catecholamine prodn) |
| Pheochromocytoma: 5 P's | pain; pallor (ortho hypoTN); palpitations; pressure (HTN); perspiration |
| Pheochromocytoma; rule of 10 | 10% of dz are: extra-adrenal; bilateral; familial; malignant; not assoc w/ HTN |
| Cushing: lab dx | 24 hr urine cort; Dex suppression test; high PM cortisol |
| Asian M (15%), post high CHO or exercise, thyrotoxicosis => | hypokalemic periodic paralysis |
| Secondary hyperaldosteronism is: | more common than primary; usu d/t renal artery stenosis (curable by surg/angioplasty) |
| Recurrent HA, HTN not responding to meds, sweating; Attacks of severe HA, HTN, glucosuria; Urinary catecholamines & metanephrines | Pheochromocytoma (tx pre-op w/ alpha blocker) |
| HTN not responsive to meds | Renal artery stenosis (Infrarenal artery) |
| HTN w/ hypernatremia, hypokalemia | Primary Aldosteronism |
| Tetany, carpopedal spasm, hypocalcemia, cataracts; Chvostek & Trousseau sxs | Hypoparathyroidism |
| Exogenous corticosteroid use | Cushing syndrome |
| Dexamethasone suppression test | Cushing syndrome |
| Central obesity, abdominal stria, hyperglycemia, moon facies, buffalo hump, easy bruising | Cushing syndrome |
| Acute steroid withdrawal | Addison dz, crisis |
| Hyperpigmentation, hypoglycemia, orthostatic hypotension, hypotension not responsive to fluids, hypotension following an illness, trauma, or surgery | Addison dz, crisis (Low aldosterone; get Random or AM cortisol, ACTH stimulation test) |
| Worsening fatigue, wt loss, weakness, recurrent abdominal pain, hair loss, hyperpigmentation. Hyponatremia, hyperkalemia | Addison dz, crisis (Low aldosterone; get Random or AM cortisol, ACTH stimulation test) |
| Hyponatremia, hyperkalemia | Acute adrenal insufficiency (Addison crisis) |
| XXY male - short stature, low intelligence; small firm testes, gynecomastia, abn arm-body length | Klinefelter (hypogonadism) |
| Adrenal Insufficiency (AI) is: | Cortisol Deficiency |
| Primary Adrenal Insuff = | Addison Dz; adrenal gland does not respond to ACTH & not make adrenal hormones; 80% 2/2 autoimmune destn of adrenal cortex |
| Secondary Adrenal Insuff = | Pit does not make ACTH; adrenal is not stimulated to make cortisol |
| Tertiary Adrenal Insuff = | Suppression of CRH & ACTH by exogenous cortisol use |
| Primary Adrenal Insuff: Sx | Fatigue, hyponatremia, Hyperkalemia; ortho hypotension; delayed DTRs; Hyperpigmentation (from ACTH, only in primary AI); |
| Secondary adrenal insuff & RAAS | b/c secondary & tertiary adrenal insuff only involve low ACTH levels, the RAAS is still intact; Only cortisol is deficient. |
| Secondary adrenal insuff: Sx | Hyperkalemia & Hypotension are rarely seen; hyperpigmentation is not seen |
| Sx of Hypopituitarism | Secondary Hypothyroidism; Hypocortisolism (secondary adrenal insuff); Amenorrhea, Menopause, Erectile Dysfunction, Infertility; Polyuria/Polydipsia |
| Hyperprolactinemia: Sx (Women) | Galactorrhea; Amenorrhea; Infertility |
| Hyperprolactinemia: Sx (Men) | ED; Infertility; HA; Mass Effect (eg, from tumor in head); Galactorrhea (Pathognomonic) |
| Prolactinoma: tx w/ Dopaminergic Drugs if: | Macroadenoma; Mass Effect; Visual Field Deficit; Fertilty Desired |
| Prolactinoma: tx w/ Hormone Replacement if: | No Fertility Desired; Microadenoma; Visual Field Full; No Mass Effect; Estrogen or Testosterone is low |
| Acromegaly vs Gigantism | Acromeg: pit tumor secreting GH in adulthood; Gigantism: pit tumor secreting GH during PUBERTY before epiphyseal plate fusion; rapid linear growth, heights up to 8ft 11 in |
| When to Suspect Acromegaly | MEN-1/other FH; Prominent brow; enlarged soft tissue of hands/ft, doughy handshake; splayed teeth, macroglossia; DM; HTN/ LVH; |
| Cushing syndrome | XS cortisol prodn; Exogenous (Use of synthetic Glucocorticoids); Endogenous = Cushing Dz; poss 2/2 adrenocortical tumor or nonpit ACTH-producing tumor (eg, SCLC) |
| Cushing syndrome: Sx | DM; HTN; Osteoporosis; Psychosis; Easy Bruising; central Obesity; Hyponatremia; Moon Facies; Buffalo Hump; prox Mx Wasting/weakness; Hirsutism; Purple Striae; Supraclavicular Fat; Infections; amenorrhea |
| Cushing Dz may be due to: | Pit ACTH overprodn; Ectopic ACTH Prodn; or Pit/Adrenal Adenoma producing cortisol |
| Cushing Dz: endogenous cortisol excess: | 75-80 % of cases; elevated cortisol levels do not suppress hypothalamic & ant pit secretion of CRH & ACTH |
| Ectopic ACTH production = | Nonpituitary Tumors secrete ACTH and do not respond to negative inhibition of high cortisol levels |
| Ectopic ACTH production poss d/t: | Small Cell Lung Ca; Carcinoid Tumors; Pheochromocytoma; Thymoma; Pancreatic Cell tumors; Medullary Ca of the Thyroid |
| Adrenal Hypercortisolism | ACTH & CRH are suppressed; Caused by: Adrenal Adenomas; Adrenal Ca; Micronodular or Macronodular Hyperplasia |
| Lack of stimulating hormone: causes | Pituitary (PanHypopituitarism); Hypothalamus (Stress, Tumor) |
| Hyperfunctioning of Endocrine Gland | Autonomous Fn of Primary Gland (Thyroid Toxic Adenoma); Autonomous Fn of Gland making Stim Hormone (Cushing Dz: ACTH); Ab's that Stim Hor Receptor (Graves / TSI); Ectopic Prod Stim Hormone (Ectopic ACTH) |
| Hypercalcemia S/S | serum Ca >10.5 mg/dL; altered mentation, N/V; polyuria, polydipsia, stones |
| Adrenal insuff dx: labs | AM cortisol (low); ACTH stim (low); plasma ACTH (>100: primary AI) (nml: 5-45 R/O primary AI; find cause of secondary/tert AI) |
| Cushing syn: ACTH-indept: | Adrenal lesion/tumor: next step is adrenal CT; exogenous source; Plasma ACTH level is low (< 5 pg/mL) |
| Cushing syn: ACTH-dependent: | Plasma ACTH level is normal or high (>15 pg/mL); Either ectopic production OR Pituitary adenoma = Cushing dz |
| Diagnosis: ACTH-dept: distinguish btw ectopic vs pituitary: | CRH-Stimulation test; HD Dex suppression; Petrosal Sinus Sampling; Octreotide scintigraphy to localize ectopic source; MRI |
| Primary hyperaldosteronism: labs | Chem7 (Hypokalemia, Metab alkalosis); Serum renin & aldosterone ( Aldo/renin ratio >20 is suspicious); 24-hr urine aldost (high in setting of low renin (<5mcg/dL) suspicious); Saline-loading; 18-OH corticosterone |
| Primary hyperaldosteronism: labs: 18-OH corticosterone | indicative of aldosterone producing adenoma (APA) |
| Primary hyperaldosteronism: imaging | Abd CT (esp of adrenals); Adrenal vein sampling: for localization (cath of left an&d right adrenal veins & the IVC, looking for lateralization of elevated aldosterone level |
| Pheochromocytoma: Dx | 24 hr urine (for Catecholamines & Metabolites: Metanephrines / VMA); Serum metanephrines/ plasma catecholamines; Imaging |
| Thyroid imaging | Thyroid scan (99m Tc) (hot nodule = benign); US (good for nodules); CT; MRI; PET |
| Thyroid nodule: eval for neoplasm | TSH; FNA/bx essential; US (80%) |
| Preferred test for Cushing syndrome | 24 hr urine cortisol (>125 mg/dL per 24 hr) |
| Increased ACTH is due to: | Cushing dz; Addison; ectopic ACTH-producing tumors |
| Decreased ACTH is due to: | secondary AI: adrenal tumor; steroid medication; hypopituitarism |
| Acute Adrenal insuff: lab findings | Low cortisol; Hyperkalemia; Hyponatremia; Elevated BUN; Hypoglycemia |
| Renin & aldosterone: body position | levels rise following assumption of an upright position |
| Elevation of 17-KS indicates: | tumor or hyperplasia of adrenal cortex |
| adrenal x-rays to: | look for calcifications (poss d/t TB) |
| adrenal CT/MRI to: | evaluate the size & shape of the adrenal glands & pituitary |
| medullary thyroid tumor labs | high calcitonin & CEA |
| hypoparathyroid labs | Low serum & urine ca, PTH, Mg; high PO4, nl alk phos |
| hypoparathyroid imaging | CT/MRI: dense bones & basal ganglia calcifications; xray: bone mineral density at L-spine |
| Cushing imaging | MRI for pit tumor; CT for adrenocortical tumor |
| Acromegaly Dx | Elevated IGF-1; GH Fails to Suppress <2 ng/mL after 75 g CHO load |
| Hypercortisolism: Dx | 24 hr urine for free cortisol (if >100, prob Cushing, if >300, def Cushing; Check Cortisol at night; Suppressing Cortisol with oral dex; checking ACTH levels |
| Hypercortisolism: Dx: why suppress cortisol w/Dex | if suppress to <5, then do not have Cushing (dex provided enough glucocorticoid to pit, signals need not prod cortisol); if ACTH >10, prob has tumor that does not respond to dex |
| Hypercortisolism: Dx: radiography | Do not do radiographic studies prior to lab studies (poss Incidental Tumors, False Negative Scans) |
| If suspect pt is hypocalcemic, measure 1,25-D? | No; measure 25-OH D |
| Hyperthyroidism labs | Low TSH; Elevated FT4, T3 Uptake, FTI |
| Hypothyroidism labs | High TSH; Low FT4, T3 Uptake, FTI |
| Pituitary adenoma diagnosed by: | CT or MRI of brain to evaluate sella turcica |
| GH lab testing | GH on fasting AM samples (often not diagnostic); GH Stim tests (hyperglycemia normally suppresses GH secretion); GH remains elevated in acromegaly |
| IGF-1 levels influenced by: | nutrition (low in malnutrition) |
| DEXA used for: | PA spine, lateral spine, hip, forearm, total body |
Created by:
duanea00
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