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USMLE2 Medicine 02
Endocrine
| Question | Answer |
|---|---|
| tx for a prolactinoma | dopamine agonist: cabergoline or bromocriptine |
| order of intervention for prolactinoma | dopamine agonist first, then surgery esp if compression of other structures or neuro sx's, last radiation |
| Non pregnant woman with elevated prolactin level. What to do? | If >100, get MRI of pituitary. |
| what is acromegaly? | excessive GH secretion from ant pituitary |
| acromegaly increases risk for what? | DM |
| What is the best initial test for acromegaly? what is confirmatory test? | IGF-1. Need to confirm with oral glucose challenge (100g glucose) --> then check GH. Confirmed is high GH since glucose load should normally suppress GH. |
| How to follow disease in acromegaly? | IGF (also called somatomedin) |
| How to tx acromegaly | 1. transphenoidal surgery, then 2. octreotide (somatostatin; blocks GH) - BEST medical therapy, then 3. bromocriptine/cabergoline (dopamine agonists; dopamine inhibits GHRH), then 4. pegvisomant (block GH from binding to its receptor peripherally) |
| what is the most common cause of death in acromegaly? | cardiac failure |
| severe HA, n/v, depression of consciousness, pt w h/o pituitary adenoma | pituitary aPOPlexy - acute hemorrhagic infarction of adenoma --> EMERGENCY! The adenoma POPs! |
| post-partum pt won't lactate. what should you check? | pituitary function (think: Sheehan post-partum necrosis) |
| what is the most important thing to replace in pan-hypo-pituitarism? | cortisol |
| What is the order that anterior pituitary hormones disappear? | 1. LH/FSH, 2. GH, 3. TSH, 4. ACTH |
| 3 drugs to test for ACTH deficiency | 1. insulin (stimulates ACTH so should see increase in cortisol if nl), 2. metyrapone (blocks cortisol --> dec neg FB on ACTH --> should see increase in ACTH if nl), 3. cosyntropin (ACTH analog) --> if low cortisol, then adrenal atrophy from pit insuff |
| obese multiparous pt with HA and no visible pituitary gland on CT/MRI. what is the dz and what is the treatment? | empty sella syndrome (subarachnoid space gets into the sella and pushes on anterior pituitary causing enlarged sella). tx is reassurance. |
| what is SIADH | syndrome of inappropriate secretion of ADH - excess secretion of ADH from posterior pit |
| what is DI | diabetes insipidus - deficiency of ADH release from posterior pit. Decrease in ANTI-diuretic hormone causes increased diuresis --> excessive dilute urine, hypernatremia, and increased thirst (polydipsia) |
| central vs. nephrogenic DI | central is a problem with ADH production in hypothalamus or with ADH secretion from posterior pit. nephrogenic is faulty kidney response to ADH. |
| treatment for central DI; for nephrogenic DI | central is just replacement of ADH (aka vasopressin); for nephrogenic, use HCTZ +/- amiloride (K sparing diuretic) - decreases excretion rate and increases urine osmolarity |
| pt with really high urine osmolarity, no signs of edema/HTN/dehydration, Na<120, and irritability, confusion, sz | cerebral edema from excess ADH --> hyponatremia 2/2 increased water retention and Na excretion |
| how to tx SIADH | 1. fluid restriction to <1L/24h, 2. demeclocycline (inhibits action of ADH on kidney) |
| What happens to thyroid levels in pregnancy? with use of OCPs? | increase in thyroxine binding globulin --> increased binding of T4, increases total T4, but normal free T4. both pregnancy and OCP usage cause this. |
| What happens to thyroid levels in nephrotic syndrome? with use of androgens? | decreased thyroxine binding globulin --> decreases total T4, but normal free T4. pt is still euthyroid. |
| antimicrosomal and antithyroglobulin antibodies | Hashimoto thyroiditis |
| Anti thyroid stimulating immunoglobulin (TSI) | Graves |
| how to follow the adequacy of treatment in thyroid CA? | thyroglobulin levels |
| decreased TSH, elevated T3/T4, increased radioactive iodine uptake | primary hyperthyroidism |
| decreased TSH, elevated T3/T4, decreased radioactive iodine uptake | factitious hyperthyroidism (taking too much thyroid hormone medication) or subacute thyroiditis (inflammation/destruction of thyroid gland --> releasing preformed T3/T4 into circulation) |
| decreased TSH, decreased T3/T4, decreased radioactive iodine uptake | 2nd or 3iary hypothyroidism (hypothalamus secretes decrease TRH, causing decreased TSH and therefore low levels of T3/T4) |
| what drug can cause thyrotoxicosis? | amiodarone |
| etiology of Graves | autoAb that bind to TSH receptor on thyroid gland |
| what is a complication of thyroid drugs PTU and methimazole? | liver damage and agranulocytosis (failure of bone marrow to make enough WBCs -- usually causing neutropenia) |
| treatment for thyroid storm | 1. IVF, steroids, cooling of fever, 2. PTU/methim to lower T3/T4, 3. iodine to inhibit hormone release, 4. B blockers, 5. dexamethasone to inhibit hormone release, impair T3/T4 production, renal support |
| what drugs can cause hypothyroidism? | lithium and ASA |
| increased TSH, decreased T4 and FT4, lesser decrease in T3 | primary hypothyroidism |
| nl or decreased TSH, decreased T4 and FT4, decrease in other hormones | 2 or 3 hypothyroidism |
| if strong suspicion of 2 or 3 hypothyroidism, how to manage? | give hydrocortisone first, then replace thyroid hormone. |
| what is myxedema coma and how to treat? | long-standing hypothyroidism, untreated. cold exposure/trauma/infxn/CNS depressants --> hypothermia, stupor --> CO2 retention --> respiratory depression --> fatal. tx with very high T3 and T4 |
| pain over the thyroid gland | subacute thyroiditis, usu after viral URI, enlarged firm painful gland |
| tx of subacute thyroiditis | ASA, prednisone, propranolol; will eventually return to nl function |
| most common cause of sporadic goiter in children | Hashimoto Thyroiditis |
| painless goiter, rubbery, can be asymmetric | Hashimoto Thyroiditis |
| Types of thyroid CA | Pham FAMily - papillary, follicular, anaplastic, medullary |
| Tx of papillary thyroid CA | surg if small and resectable, surg + radiation if big; levothyroxine to suppress TSH |
| most common thyroid CA | papillary |
| thyroid CA associated with radiation exposure | papillary |
| thyroid CA more common in elderly | follicular and anaplastic |
| how does papillary CA of thyroid spread? follicular? anaplastic | by lymphatics for papillary; hematogenously for follicular, anaplastic by direct extension |
| tx for follicular thyroid CA | near total thyroidectomy + post op radioiodine ablation |
| most malignant thyroid CA | anaplastic, most die within 1 year of dx |
| thyroid CA that produces calcitonin | medullary |
| MEN I | PPP - pan pit pth. pancreatic tumor (insulinoma, gastrinoma, vipoma), pituitary adenoma, PTH hyperplasia. |
| MEN IIa (Sipple Syndrome) | P [PA] T: PTH hyperplasia, Pheo OR Adrenal medullary hyperplasia, Thyroid CA (medullary) |
| MEN IIb | PNT (rhymes): Pheo, Neuroma, Thyroid medullary CA |
| Tx for medullary CA | thyroidectomy |
| elevated calcitonin | think CA; if thyroid, then can only be medullary |
| recent growth of nontender thyroid mass, no hoarseness | think thyroid CA |
| psmmoma bodies | papillary CA |
| hyperfunctioning thyroid is never what? | CA |
| what to do first if you have pt with solitary nonfunctioning thyroid nodule? | TSH --> if nl TSH, then U/S, then FNA for cytology |
| PTH effect on Ca Phos and Vit D | increases Ca and Vit D, decreases Phos |
| Vit D effect on Ca and Phos | increases Ca PO4 absorption from intestines, increases PO4 absorption from kidney |
| hyperCa most likely caused by what? | hyper PTH (malignancy produces a protein that looks like PTH) |
| neuro consequences of hyperCa | lethargy, confusion |
| GI consequences of hyperCa | constipation, anorexia, n/v; precipitation of Ca in pancreas --> pancreatitis; ulcer creation |
| renal consequences of hyperCa | Ca --> induction of nephrogenic DI (kidney doesn't respond to ADH) --> polyuria, polydipsia; nephrolithiasis |
| cardiovascular consequences of hyperCa | HTN, short QT on EKG |
| neuro consequences of hyperCa | lethargy, confusion, weakness |
| GI consequences of hyperCa | constipation, anorexia, n/v; precipitation of Ca in pancreas --> pancreatitis; ulcer creation |
| renal consequences of hyperCa | Ca --> induction of nephrogenic DI (kidney doesn't respond to ADH) --> polyuria, polydipsia; nephrolithiasis |
| cardiovascular consequences of hyperCa | HTN, short QT on EKG |
| how to manage HyperCa | 1. IVF (NS), 2. furosemide --> promotes Ca loss, 3. bisphosphonates (i.e. pamidronate) --> inhibit osteoclasts and promote osteoblasts to use Ca to build bone (takes 2-3 d), 4. calcitonin (inhibits osteoclasts) if can't wait 2-3 d for alendronate to work |
| pt with bone pain, areas of demineralization, bone cysts, and brown tumors (punched out lesions on bone producing a salt and pepper like appearance) | hyperPTH --> increased rate of bone resorption --> osteitis fibrosa cystica |
| high PTH and high serum Ca | primary hyperPTH |
| how to diagnose hyperPTH? | neck exploration; no imaging |
| tx of hyperPTH | 1. pamidronate (bisphosphonate) if Ca <11.5 and asympt; 2. resection of that part of the gland if Ca is >11.5; 3. restriction of dietary Ca; 4. oral hydration; 5. phosphate supplementation, 6. estrogen in post-menopause |
| PTH-dectomy indications | sx's, organ damage, or pregnant |
| most common causes of hypoCa | 1. hypoPTH, 2. renal failure (no VitD-mediated Ca absorption), 3. hyperPhos (Phos and Ca are opposite, causes precipitation of Ca in tissues), 4. and hypoMg --> prevents release of PTH |
| how does alkalosis affect Ca levels? | causes increased binding of Ca to albumin --> decreased Ca in blood |
| how does low albumin affect Ca levels? | causes pseudo hypoCa: low albumin will decrease total Ca because albumin binds calcium, but level of free Ca will remain same. |
| how does blood transfusion affect Ca levels? | Ca binds to citrate in the transfused units --> hypoCa |
| clinical effects of hypoCa | increased neuro hyperexcitability --> sz, tetany, circum-oral numbness, tingling; prolonged QT --> arrythmias; cataracts |
| tx of hypoCa | IV CaGluconate and Vit D, maintenance with Ca PO and Vit D PO, restriction of dietary PO4 and phosphate binding agents (i.e. CaCO3 or aluminum OH) |
| most common cause of hypoPTH | removal of the gland |
| how does Mg level affect PTH | Mg deficiency prevents release of PTH |
| what causes hypoMg? | decreased GI absorption or alcoholism |
| what causes secondary hyperPTH? | chronic renal failure, decreased active Vit D |
| chvostek sign | percussion of facial nerve in front of ear --> contraction of facial muscles and upper lip; indicates hypo Ca or hypo PTH |
| Trousseau sign | a blood pressure cuff inflated to P > SBP for 3 min --> occlusion of brachial artery --> hypocalcemia and subsequent neuromuscular irritability will induce spasm of the muscles of the hand and forearm; indicates hypoCa |
| low Ca with hi phos | 1. renal failure (dec vit D --> dec Ca, hi phos), 2. massive tissue destruction, 3. hypoPTH, 4. pseudohypoPTH |
| low Ca, low phos | absent or ineffective VitD (Vit D increases both) |
| which type of DM has more genetics associated with it? | Type 2 - >20% first degree relatives are affected with 90-100% occurrence in identical twins. |
| what are the physiologic defects of NIDDM? | 1. abnormal insulin secretion, 2. insulin resistance in target tissues |
| NIDDM (Type 2) associated DKA. What is the counterpart for IDDM (Type 1)? | Hyperosmolar coma |
| Criteria to diagnose DM | 1. sx's and plasma glucose >200, 2. FPG >126 x 2 |
| what is DOC for DM Type 2 pts who are not obese? | sulfonylureas (glyburide, glipizide) |
| what is DOC for DM Type 2 pts who are obese? | metformin |
| who should not use metformin? | pts with renal insuff |
| what is the advantage of using metforming to tx DM? | no a hypoglycemic agent (suppresses hepatic gluconeogenesis) |
| how to start insulin therapy for a DM pt | 0.5 U/kg. 2/3 in AM (2/3 intermediate, 1/3 regular). 1/3 in PM (half intermediate, half regular). FSBG before meals and at bedtime. |
| insulin prescription with glargine | glargine one a day injection; 2-3x/d ultra short-acting (lispro or aspart) before meals |
| glargine vs. NPH | glargine causes fewer episodes of hypoglycemia |
| give types of insulin in order of peak of action | lispro/aspart (ultra short-acting, peak 30-60 min, 3-6h duration); regular (rapid, 2-6 hr peak, 6-8h duration); NPH (intermediate, peak 6-12h, 12-18h duration); glargine (long-acting, peak 2h, 24h duration) |
| What causes DKA? | severe insulin insuff, precipitated by no meds, infxn, stress, EtOH |
| What is the main problem in DKA? | anion gap acidosis and dehydration |
| Person comes in with anorexia, n/v, abd pain, Kussmaul respiration, dry mucous membranes, and fruity breath | DKA |
| DKA associated with hyper or hypo K? | K+ goes in same direction as H+ --> acidosis is high H+ so DKA is high K+ (hyperkalemia), tho the total body level of K decreases because of urinary losses |
| Dx DKA | 1. hyperglycemia, 2. hi acetoacetate/acetone/hydroxybutyrate, 3. anion gap metabolic acidosis |
| formula for anion gap | sodium - bicarb + Chloride. nA B C |
| how to tx DKA? | 1. insulin, 2. IVF, 3. replace electrolytes |
| pt with weakness, polyuria, polydipsia, lethargy, confusion, convulsions, and coma | hyperosmolar nonketotid coma (HONK) |
| HONK | severe hyperglycemia --> sustained hyperglycemic diuresis --> profound dehydration |
| Pt comes in with weakness, polyuria, polydipsia, lethargy, confusion, convulsions, elevated blood glucose and high serum osmolarity | HONK. mild met acidosis, but NO ketosis! |
| Management of HONK | 1. IVF, 2. electrolytes, 3. insulin |
| Diabetics should be screened for what | 1. retinopathy q year (Type 1 can start 5 years after dx), 2. proteinuria (suggesting renal disease) q year, 3. foot exam |
| Indications for ACEi in DM pt | 1. HTN, 2. proteinuria >300mg/d, 3. microalbuminuria >30mg/d |
| 75% of deaths in DM are due to what? | MI, CHF or stroke |
| 1% reduction in HbA1C --> how does this affect risk of MI? | decreases MI risk by 14% |
| 10 pt reduction in BP --> how does this affect risk of MI? | decreases MI risk by 12% |
| When is CABG indicated in DM pt? | 2-vessel disease (instead of 4-vessel) |
| What is the LDL target for a DM pt? | <100; if >100, should start lifestyle modifications and statin. Definite drug therapy when LDL>130. |
| How to treat gastroparesis in DM? | metoclopramide or erythromycin |
| how common is erectile dysfxn in DM? how to tx? | 50% after 10 years of DM. tx with sildenafil |
| peripheral neuropathy in DM | 1. symmetric, 2. numbness, paresthesia, pain, 3. absent reflexes, 4. loss of vibratory sense |
| mononeuropathy in DM | affects single nerve or nerve trunk; vascular origin; foot drop, wrist drop or defect in EOM (CN 3, 4, 6) |
| pt with DM comes in with orthostatic hypoTN, syncope | autonomic dysfunction. can also include gastroparesis, dysphagia, constipation, diarrhea, urinary retention (in general, state of STASIS), impotence, retrograde ejaculation |
| How to manage peripheral neuropathy in DM pt? | gabapentin or pregabalin |
| Somogyi effect | rebound hyperglycemia in the AM because of counterregulatory hormone release after hypoglycemia at night |
| dawn effect | early morning rise in glucose requiring increased insulin |
| Causes of hypoglycemia in DM | 1. glucose underproduction, 2. hyperinsulin, 3. excessive epinephrine --> sweating, tremor, tachy, anxiety, hunger, 4. CNS dysfxn --> dizziness, HA, cloudy vision, confusion, convulsions, LOC. |
| Pt comes in with blurred vision, HA, feelings of detachment, slurred speech, weakness, low blood sugar, sx's in early AM or late afternoon or after fasting or exercise | insulinoma or factitious insulinoma (insulin injection) |
| hypoglycemia, high immunoreactivity, insulin, and suppressed plasma C peptide | --> pathognomonic of exogenous insulin administration |
| How does EtOH induce hypoglycemia? | at 45mg/dL, etOH induces hypoglycemia by blocking gluconeogenesis |
Created by:
christinapham
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