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Step 1 12.31.12
Endocrine III
| Question | Answer |
|---|---|
| overload of what hormone is implicated in Cushing's syndrome? | cortisol |
| What is the major exogenous cause of Cushing's syndrome? What is the mech? | #1 cause = steroids, decr ACTH |
| What are 3 major causes of endogenous Cushing's syndrome? | 1. Cushing's disease 2. Ectopic ACTH 3. Adrenal- adenoma, carcinoma, nodular adrenal hyperplasia |
| How does Cushing's disease cause Cushing's syndrome? | due to ACTH secretion from pituitary adenoma; incr ACTH |
| How does Ectopic ACTH cause Cushing's syndrome? Where does it come from? | from nonpituitary tissue making ACTH (non small cell lung carcinoma, bronchial carcinoids), incr ACTH |
| What ACTH levels are seen in adrenal adenoma, carcinoma or nodular adrenal hyperplasia causing Cushing's syndrome? | low ACTH |
| What are the major findings in Cushing's syndrome? | hypertension, weight gain, moon facies, truncal obesity, buffalo hump, hyperglycemia (insulin resitance), skin changes (thinning, striae), osteoporosis, amenorrhea, immune surpression |
| What is the normal result of a dexamethazone test on cortisol? | low dose decr cortisol |
| What is the result of a dexamethazone test on cortisol in an ACTH pituitary tumor? | incr cortisol at low dose, decr cortisol at high dose |
| What is the result of a dexamethazone test on cortisol in an ectopic ACTH producing tumor? | incr cortisol at low dose and high dose |
| What is the result of a dexamethazone test on cortisol in a cortisol producing tumor? | incr in both low and high dose |
| What cuases primary hyperaldosteronism? | adrenal hyperplasia or aldosterone secreting adrenal adenoma( Conn's syndrome) |
| What are the Sx of primary hyper aldosteronism? | hypertension, hypokalemia metabolic alkalosis, low plasma renin. can be bilateral or unilateral |
| What is the Tx of primary hyperaldosteronism? | surgery to remove tumor and or spironolactone a K+ sparing diuretic that is an aldosterone antagonist |
| What is the mech and causes of secondary hyperaldosteronism? | renal artery stenosis, renal failure, CHF or cirrhosis, or nephrotic syndrome cause the kidney to perceive a low intravascular volume causing over activation of the RAS system |
| What is a key finding in secondary hyperaldosteronism? | high plasma renin |
| What is the mech of Addison's disease? | primary adrenal insufficiency due to adrenal atrophy or destruction by disease (AID, TB metastasis) |
| What hormones are deficienct in Addison's disease and what are the major Sx? | deficiency of aldosterone and cortisol. causes hypotension (hyponatremic volume contraction), hyperkalemia, acidosis, and skin hyperpigmentation |
| What causes the hyperpigmentation seen in Addison's disease? | due to MSH, a product of incr ACTH from POMC |
| What are the major ways to characterize Addison's disease? | Adrenal atrophy, absence of hormone production, involves all 3 cortical divisions (spares medulla) |
| How do you distinguish Addison's disease from secondary adrenal insufficency (decr pituitary ACTH production? | no skin hyperpigmentation and no hyperkalemia (Addison's= - (Cushing's + Conn's) |
| What is and what causes Waterhouse-Friderichesen's syndrome? | Acute primary adrenal insufficiency due to adrenal hemmorrhage associated with neisseria meningitidis, septicemia, DIC and endotoxic shock |
| What is the most common adrenal tumor in adults? From what cells is it derived? | pheochromocytoma derived from chromaffin cells |
| What is secreted by pheochromocytomas? What labs would be seen? | secrete epi, NE, and dopamine. urinary VMA (breakdown of NE) and plasma catecholamies are elevated |
| What are some major associations of pheochromocytoma? | neurofibratosis, MEN 2A types and 2B. |
| What is the tx for pheochromocytoma? | alpha antagonisits esp phenoxybenzamine, a non selective irreversible alpha blocker followed by surgery |
| What is the rule of 10's for pheochromocytoma? | 10% malignant, 10% bilateral, 10% extraadrenal, 10% calcify, 10% kids, 10% familial |
| How do the Sx in pheochromocytoma occur? | in spells, relapse and remit. |
| What are the 5 Ps of the presentation of pheochromocytoma? | 1. Pressure (elevated BP) 2. Pain (HA) 3. perspiration 4. Palpitations (tachycardia) 5. Pallor |
| What is the mech of getting phenylalainie to Dopamine? | phenylalanine-->tyrosine-->L-dopa--Dopa |
| What is the source of HVA? | dopamine |
| What is the source of VMA? | Dopamine-->NE--> VMA |
| What is the source of metepinephrine? | Dopamine--NE--Epi-->metanephrine |
| What is the most common tumor of adrenal medulla in children? | neuroblastoma |
| What is a major lab seen in neuroblastoma? | homovanillic acid (HVA) breakdown product of dopamine is elevated in the urine |
| What is a major genetic marker for rapid progression of neuroblastoma? | N-myc= rapid tumor progression |
| What are the major Sx of hypothyroidism? | 1. cold intolerance due to decr heat production 2. weight gain, decr appetitie 3. hypoactivty, lethargy, fatigue, weakenss 4. constipation 5. decr reflexes 6. myxedema (facial/periorbital) 7. dry cool skin, corse brittle hair 8. bradycardia, DOE |
| What are the major Sx of hyperparathyroidism? | 1. heat intolerance due to incr heat production 2. weight loss, incr appetitie 3. hyperactivity 4. diarrhea 5. incr reflexes 6. pretibila myxedema (Grave's disease) 7. warm, moist skin, fine hair 8. CP, palpitation, arryhtmia, incr Beta adrenergic recpet |
| What are the key lab findings in hypothyroidism? | incr TSH (sensitive for primary hypothyroid), decr total T4, decr free T4, decr T3 uptake |
| What are the key lab findings in hyperthyroidism? | decr TSH (if primary), incr total T4, incr free T4, incr T3 uptake |
| What is Hashimoto's thyroiditis? What are some major associations? | common cause of hypothyroidism. Can be hyper early in course due to follicular rupture AID. Associated with HLA-DR5. incr risk of NHL. |
| What are the major histiological findings in Hashimoto's thyroiditis? | Hurthle cells: lyphocyttic infiltrate with germinal centers |
| What are the key findings in Hashimoto's throiditis? | moderately enlarged, non tender thyroid. antimicrosma, antithyroglobulin Ab |
| What is and what causes cretinism? | due to severe fetal hypothyroidism. occure when endemic goiters occur (low iodine consumption). sporadic cretinism is caused by a defect in T4 formation or developmental failure in thyroid formation |
| What are are the major findings in cretinism? | pot bellied, pale, puffy faced child with protrudiding umbilicus, and protuberant tongue |
| What is Subacute thyroditis (de Quervain's)? | self limited hypothyroidism following flulike illness |
| What is seen in the histology of Subacute thyroditis (de Quervain's)? | granulomatous inflammation |
| What are the key findings in Subacute thyroditis (de Quervain's)? | incr ESR, jaw pain, early inflmmation, very tender thyroid. can be hyperthyroid early in course |
| What is Riedel's thyroiditis? | thyroid is replaced by fibrous tissue (hypothyroid). Others: iodine deficiency, thyroglossal cut cyst, goitrogens, Wolff-Chaikoff effect |
| What are the major findings in Ridel's thyroditis? | fixed, hard ( rock like), and painless gioter |
| What are 4 major causes of hypothyrodism? | Hashimoto's thyroditis, cretinism, subacute thyroiditis , Riedel's thyroiditis |
| What are 3 major causes of hyperthyroidism? | Grave's disease, Thyroid strom, Toxic multinodular goiter |
| What is the cause of Grave's disease? | AID hyperthyroidism due to thyroid stimulating/TSH receptor Ab |
| What findings are seen in Graves disease? | ophthalmopathy (proptosis, EOM swelling), pretibial myxedema, incr in CT deposition, diffuse goiter. |
| When does Graves disease present? | often during stress e.g childbirth |
| What is a thyroid storm? | stress induced catecholamine surge leading to death by arrythmia. seen as serious complication of graves disease. might see incr ALP due to incr bone turnover |
| What is a toxic multinodular goiter? | focal patches of hyperfunctioning follicular cells working independently of TSH due to mutation in TSH receptor. incr relase of T4 and T3 |
| What is the Jod-Basedow phenomdeficiency goiter is made iodine repleterenon of a toxic multinodular goiter? | thyrotoxicosis if a patient with an iodine |
| What is seen in a papillary carcinoma of the thyroid? | most common, excellent prognosis, ground glass nuclei (oprhan annie), psammoma bodies, nuclear grooves. incr risk with childhood radiation |
| What is seen in follicular carcinoma of the thyroid? | good prognosis, uniform follicles |
| What is seen in a medullary carcinoma of the thyroid? | from parafollicular C cells; produces calcitonin, sheets of cells in amyloid stroma. associated with MEN 2A and 2B |
| What is seen in undifferentiated/anaplastic thyroid cancer? | older patients, very poor prognosis |
| What is seen in lymphoma of the thyroid? | associated with hashimotos thyroiditis |
| What usually causes primary hyperparathyroidism? | usually an adenoma |
| What are the major findings in primary hyperparathyroidism? | hypercalcemia, hypercalciuria (renal stones), hypophosphatemia, incr PTH, incr alkaline phosphatase, incr cAMP in urine |
| How does primary hyperparathyroidism present? | often asx or may present with weakness and constipation |
| What is a menomonic for the problems associated with primary hyperparathyroidism? | Stones, bones, groans. can cause ostetitis fibrosa cystic= cystic space filled with brown fibrous tissue |
| What causes secondary hyperparathyroidism? | secondary hyperplasia due to decr gut Ca++ absorbtion and incr phosphorus. most often in chronic renal disease |
| What are the major findings in secondary hyperparathyroidism? | hypocalcemia, hyperphosphatemia, incr alkaline phosphatase, incr PTH |
| What is renal osteodystrophy? | bone lesions due to secondary or tertiary hyperparathyroidism due in turn to renal disease |
| What is the cause and findings of tertiary hyperparathyroidism? | refractory hyperparathyroidism due to chronic renal disease. very incr PTH, incr Ca++ |
| What causes hypoparathyroidism? | accidental surgical excision, AID, or DiGeorge |
| What are the major findings in hypoparathyroidism?> | hypocalcemia, tetany |
| What is Chovstek's sign? | tapping of facial nerve elicits contraction of facial muscles in hypoparathyrodisim |
| What is Tousseaus sign? | occlusion of brachial artery qwith BP cuff-->carpal spasm in hypoparathyroidism |
| What causes pseudohypoprathyroidism (Albright's hereditary osteodystrophy)? | autosomal dominant kidney unrepsonsiveness to PTH |
| What are the major findings in pseudohypoparathyroidism? | hypocalcemia, shortened 4th/5th digits, short stature |
| What does a PTH of 1-10 and a Ca++ 4-8 suggest? | hypoprathyroidism due to surgical removal or AID |
| What does a PTH near 100 and a calcium of 4-8 suggest? | secondary hyperparathyroidism due to renal failure |
| What does a PTH near 100 and a calcium 12-14 suggest? | primary hyperparathyrodism due to hyperplasia, adenoma, carcinoma |
| What does a PTH 1-10 and a calcium 12-14 suggest? | PTH independent hypercalcemia (excess calcium ingestion, cancer) |
| What is a pituitary adenoma and what are the major findings? | most common prolactinoma. findings: amenorrhea, galactorrhea, low libido, infertility (decr GnRH), |
| What is the reaction of a pituitary adenoma to bromocriptine or cabergoline? | these dopamine agonists cause shrinkage of the prolactinoma |
| What nerve structure might a pituitary adenoma impinge on causing what? | can impinge on optic chiasm--> bitemporal hemianopia |
| What is and what are the major findings of acromegaly? | excess GH in adults. see large tongue, with deep furrows, deep voice, large hands, coarse facial features, imparied glucose tolerance (insuling resistance) |
| What happens when GH in incr in children? | gigantism with incr linear bone growth |
| In what conditions is incr GH normal? | stress, exercise, hypoglycemia |
| How do you treat acromegaly? | pituitary ademonaa resection followed by octreotide administration |
| How do you Dx acromegaly? | incr serum IGF-1. failure to surpress serum GH following oral glucose tolerance test |
| What are the main characteristics and causes of diabetes insipidus? | characterized by intense thirst and polyuria together with an inability to concentrate urine due to lack of ADH or lack of renal response to ADH |
| What causes a lack of ADH (Central DI)? | pituitary tumor, trauma, surgery, histiocytosis X |
| What can cause nephrogenic DI? | hereditary or secondary to hypercalcemia, lithium, or democlocycline (ADH antagonist) |
| How do you Dx DI? | water deprivation test, urine osm doesnt incr. response to desmopressin distinguishes b/w central and nephrogenic |
| What are the major findings in DI? | urine specific gravity < 1.006; serum osmolarity > 290 mOsm |
| How do you tx DI? | adequate fluid intake. if central: intranasal desmopressin (DH analog). if nephrogenic: HCTZ, indomethacin, amiloride |
| What is and what are the major characteristics of SIADH? | syndrome of inappropriate antidiuretic hormone secretion. 1. excessive water retention 2. hyponatremia 3. uirne osmolarity > serum osmolarity |
| What are some major causes of SIADH? | 1. ectopic ADH (small cell lung cancer) 2. CNS disorders/head trauma 3. pulmonary disease 4. dugs (cyclophosphamide) |
| How does the body respond in SIADH? What can it lead to? | body responds with decr aldosterone (hyponatermia) to maintain near normal volume status. very low serum sodium levels can lead to seizures (correct slowly) |
| How do you tx SIADH? | demeclocycline or H20 restriction |
| What are 5 causes of hypopituitarism? | 1. nonsecreting pituitary adenoma, craniopharyngioma 2. Sheehan's syndrome (infarct of pituitary following post partum bleeding ; present with failure to lactate) 3. empty sella syndrome: unexplained atrophy of pituitary 4.brain injury 5. radiation |
| What are the acute manifestations of dibetes mellitus (DM)? | polydipsia, polyuria, polyphagia, weight loss, DKA (type I), hyperosmolar coma (type 2), unopposed secretion of GH and epinephrine (exacerbates hyperglycemia) |
| What are the 3 major things that insulin deficiency (gulcagon excess) lead to? | decr glucose uptake, incr protein catabolism, incr lipolysis |
| How does nonenzymatic glycosylation manifest in chronic DM? | small vessel and large vessel disease |
| What small vessel disease can be seen in chronic DM? | diffuse thickening of BM--> retinopathy (hemmorhages, exudates, microaneurysms, vessel proliferation) glaucoma, nephropathy ( nodular sclerosis, progressive proteinuria, chronic renal failure, arteriosclerosis leading to HTN, Kimmelsteil- WIlson nodules) |
| What large vessel disease can be seen in chronic DM? | atherosclerosis, CAD, periveral vascular occlusive disease, gangrene-->limb loss, cerebrovascular disease |
| What can osmotic damage manifest as in chronic DM? | 1. neuropathy (motor, sensory, autonomic) 2. cataracts (sorbitol accumulation) |
| What tests are used in DM? | fasting serum glucose, glucosetolerance test HbA1c (meaures long term diabetic control) |
| What is the primary defect in type 1 vs Type 2 DM? | 1: AID destruction of beta cells after infection. 2: incr resistance to insulin |
| What is the neccessity of insulin in tx in type 1 vs Type 2 DM? | 1: always needed 2: sometimes |
| What is the age of onset in type 1 vs Type 2 DM? | 1: <30 2:>40. exceptions commonly occur |
| Which is associated with obesity type 1 vs Type 2 DM? | type 2 |
| What is the genetic disposition in type 1 vs Type 2 DM? | 1:weak, 50% in identical twins, polygenic 2: relatively strong, 90% in twins, polygenic |
| What is the association of the HLA system in type 1 vs Type 2 DM? | 1: HLADR3,4. 2: none |
| What is the glucose intolerance in type 1 vs Type 2 DM? | 1: severe 2: low |
| What is the insulin sensitivity in type 1 vs Type 2 DM? | 1: high 2: low |
| What is the ketoacidosis in type 1 vs Type 2 DM? | 1: common 2:rare |
| What is the beta cell numbers in the islets in type 1 vs Type 2 DM? | 1: decr 2: variable with amyloid depostis |
| What is the serum insulin levels in type 1 vs Type 2 DM? | 1: decr 2: variable |
| What is the commoness of the classic sx of polyuria, polydipsia, thrist and weight loss in type 1 vs Type 2 DM? | 1: common 2: sometimes |
| What is the histology in type 1 vs Type 2 DM? | 1: islet leukoctic infiltrate 2: islet amyloid deposit |
| What is the cause and mech of diabetic ketoacidosis? | due to incr insulin requirments from incr stress, infection. excess fat breakdown and icr ketogenesis from incr free fatty acids which are made into ketone bodies ( beta hydroxybutyrate>acetoacetate) |
| What are the signs and sx of diabetic ketoacidosis? | Kussmaul respirations (rapid + deep breathing), n/v, abdominal pain, psychosis/delirium, dehydration, fruity breath odor (exhaled acetone) |
| What labs are seen in diabetic ketoacidosis? | hyperglycemia, incr H+, decr HCO3 (anion gap met ac), incr blood ketone levels, leukocytosis, hyperkalemia but depleted intracellular K due to transcellular shift due to decr insulin |
| What are the major complications of diabetic ketoacidosis? | life threatening mucormycosis, Rhizopus infection, cerebral edema, cardiac arryhtmias, heart failure |
| What is the Tx of diabetic ketoacidosis? | IV fluids, IV insulin, and K + to replete intracellular stores, glucose if neccessary |
| What is the cause of carcinoid syndrome? | rare syndrome caused by carcinoid tumors (neuroendocrine cells) especially metastatic small bowel tumors whcih secrete 5-HT. not seen if tumor limited to GI tract |
| What are the sx of carcinoid syndrome? | recurrent diarrhea, cutaneous flushing, asthmatic wheezing, right sided valvular disease. most common tumor of appencix |
| What labs are seen in carcinoid syndrome? | incr 5-HIAA in urine |
| What is the rule of 1/3 for carcinoid syndrome? | 1/3 metastasize, 1/3 present with secondary malignancy, 1/3 are multiple |
| How do you treat carcinoid syndrome? | octreotide |
| What is Zollinger-Ellison syndrome? | gastrin secreting tumor of pancreas or duodenum. stomach shows rugal thickening with acid hypersecretion. causes reccurrent ulcers. may be associated wiht MEN type 1 |
| What are the characteristics of Multiple endocrine neoplasias (MEN) 1 (Wermer's syndrome)? | parathyroid tumors, pituitary tumors (prolactin of GH), pancreatic endocrine tumors ( Zollinge-Ellison, insulinomas, VIPomas, glucagonomas, |
| What is a common presentation of MEN 1 neoplasia? | kidney stones and stomach ulcers |
| What are the general types of MEN 2A (Sipple's syndrome) neoplasia? | medullary thyrodi carcinoma (secretes calcitonin), heochromocytoma, parathyroid tumors |
| What are the general types of MEN 2B neoplasia? | medullary thyroid carciomas (secers calcitonin, pheochromocytoma, oral/intestinal gangliponeuromatosis (associated with marfinoid habitus) |
| What are the 3Ps of MEN 1? | pituitary, parathyroid, pancreas |
| what are the 2 Ps of MEN 2A? | parathyroid and pheochromocytoma |
| What is the 1 P of MEN 2B? | pheochromocytoma |
| What is the inheritance of all MEN syndromes? | autosomal dominant inheritance |
| What MEN are associated with the ret gene? | MEN 2A and 2B |
| What is the Tx strategy for Type I DM? | low sugar diet, insulin replacement |
| What is the Tx strategy for type II DM? | dietary modification and exercise for weight loss. oral hypoglyemics, and insulin replacements |
| What is the class of lispro, aspart, regular NPH, glargine, detemir? | insulins |
| Which insulins are long vs shirt vs intermediate, vs rapid? | lispro, aspart: rapid. regular: short. NPH: intermediate. Glargine, detemir (long acting) |
| What is the action of the lispro, aspart, regular NPH, glargine, detemir on liver, muscle and fats? | binds insuling receptor. liver: incr glucose stored as glycogen. muscle: incr glycogen and protein synth, K+ uptake. fat: aids TG storage |
| What is the clinical use of lispro, aspart, regular NPH, glargine, detemir? | Type 1, 2 DM, gestational diabetes, life threatening hyperkalemia, stress induced hyperglycemia |
| What are the major SE of lispro, aspart, regular NPH, glargine, detemir? | hypoglycemia, hypersensitivity reaction (very rare) |
| What is the class of 1st Gen: tolbutamide, chlropropamide. 2nd: glyburide, glimepiride, Glipizide? | sulfonylureas |
| What is the action of 1st Gen: tolbutamide, chlropropamide. 2nd: glyburide, glimepiride, Glipizide? | close K+ channel in Beta cell membrane so cell depolarizes--> triggers insulin release via Ca++ influx |
| What is the clinical use of 1st Gen: tolbutamide, chlropropamide. 2nd: glyburide, glimepiride, Glipizide? | stimulate release of endogenous insulin in type II DM. useless in type I |
| What are the major SE of 1st Gen: tolbutamide, chlropropamide. 2nd: glyburide, glimepiride, Glipizide? | 1st gen: like disulfram. 2nd: hypoglycemia |
| What is the class of metformin? | biguanide |
| What is the action of metformin? | ukn mech.decr gluconeogenesis, incr glycolysisz, incr peripheral glucose uptake (insulin sensitivity) |
| What is the clinical use of metformin? | First line in DM 2. can be used in pt w/o islet fx |
| What is the major SE of metformin? | lactic acidosis so CONTRAI in renal failure |
| What is the class of pioglitazone, rosiglitazone? | glitazones/thiazolidinediones |
| What is the mech of pioglitazone, rosiglitazone? | incr insulin sensitivity in peripheral tissue. binds to PPAR-gamma nuclear transcription factor which regulates FA stroage and glucose metabolism |
| What is the clinical use of pioglitazone, rosiglitazone? | used as monotherapy in type 2 DM |
| What are the major SE of pioglitazone, rosiglitazone? | weight gain, edema, hepatotoxicity, heart failure |
| What is the class of acarbose, miglitol? | alpha glucosidase inhibitors |
| What is the mech of acarbose, miglitol? | inhibit intestinal brush border alpha glucosidases. delayed sugar hydrolysis and glucose absorbtion--> decr postprandial hyperglycemia |
| What is the clinical use of acarbose, miglitol? | used as monotherapy in type 2 DM or in combination with above agents |
| What are the major SE of acarbose, miglitol? | GI disturbances |
| What is the class of pramlintide? | mimetic |
| What is the mech of pramlintide? | decr glucagon |
| What is the clinical use of pramlintide? | type 2 DM |
| What are the major SE of pramlintide? | hypoglycemia, nausea, diarrhea |
| What is the class of exenatide? | GLP-1 analog |
| What is the mech of exenatide? | incr insulin, decr glucose release |
| What is the use of exenatide? | type 2 DM |
| What are the major SE of exenatide? | n/v, pancreatitis |
| What is the mech of the propylthiouracil, methimazole? | block peroxidase thereby inhibitng organification of iodine and coupling of thyroid hormone synthesis. propylthiouracil alos blocks 5'deiodinase which decr peripheral conversion of T4 to T3 |
| What is the clinical use of propylthiouracil, methimazole? | hyperthyroidism |
| What are the major SE of propylthiouracil, methimazole? | skin rash, agranulocytosis (rare), aplastic anemia, heptaotoxicity (propyl), methimazole might be a teratogen |
| What is the mech of levothroxine, triiodothyronine? | thyroxine replacement |
| What is the use of levothroxine, triiodothyronine? | hypothyroidism, myxedema |
| What are the major SE of levothroxine, triiodothyronine? | tachycardia, heat intolerance, tremors, arrythmias |
| What is the clinical use of GH? | GH deficiency, turner syndrome |
| What is the clinical use of somatostatin (octreotide)? | acromegaly, carcinoid, gastrinoma, glucagonoma |
| What is the clinical use of oxytocin? | stimulates labor, uterine contractions, milk let down, controls uterine hemmorrhage |
| What is the the clinical use of ADH (desmopressin) ? | pituitary (central, not nephrogenic) DI |
| What is the mech of demeclocycline? | ADH antagonist (member of tetracyclines) |
| What is the clinical use fo demeclocycline? | SIADH |
| What are the major SE of demeclocycline? | nephrogenic DI, photosensitivity, abnormalities of bone and breath |
| What are the class of hydrocortisone, predisone, triamcinolone, dexamethasone. beclomethasone? | glucocorticoids |
| What is the mech of hydrocortisone, predisone, triamcinolone, dexamethasone. beclomethasone? | decr production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX2 |
| What is the clinical use of hydrocortisone, predisone, triamcinolone, dexamethasone. beclomethasone? | Addison's disease, inflammation, immune surpression, asthma |
| What are the major SE of hydrocortisone, predisone, triamcinolone, dexamethasone. beclomethasone? | iatrogenic Cushing's syndrome- buffalo hump, moon facies, truncvcal obesity, muscle wasting, thin skin, brusability, osteoporosis, adrenocrotical atrophy, peptic ulcers, diabetes (if chronic), adrenal insufficiency when drug stopped after chronic use |
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