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Pance Endo combined

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