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97 Cards in this Set
- Front
- Back
MCC of Cushing's syndrome
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exogenous (iatrogen) steroid use (decreased ACTH)
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Cushing's disease
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70% of endogenous causes; due to ACTH secretion from pituitary adenoma (increased ACTH)
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ectopic ACTH as cause of Cushing's
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15%; nonpituitary tissue making ACTH ex. small cell lung cancer, bronchial carcinoids (increased ACTH)
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adrenal cause of Cushing's
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15%; adenoma, carcinoma, nodular adrenal hyperplasia (decreased ACTH)
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dexamethasone suppression test - healthy person
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decreased cortisol level after low dose
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dexamethosone suppression test - ACTH producing pituitary tumor (Cushing's disease)
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increased cortisol after low dose; decreased cortisol after high dose
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dexamethosone suppression test - ectopic ACTH producing tumor
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increased cortisol after both low and high doses
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dexamethasone suppression test - cortisol-producing tumor
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increased cortisol after low and high dose
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clinical findings in Cushing's syndrome
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HTN, weight gain, moon facies, truncal obesity, buffalo hump, hyperglycemia, skin changes, osteoporosis, amenorrhea, immune suppression
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primary hyperaldosteronism (Conn's syndrome)
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unilateral/bilateral aldosterone-secreting tumor
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findings in Conn's syndrome
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hypertension (Na+ and H20 retention), hypokalemia, metabolic alkalosis (H+, K+ secretion), low plasma renin
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treatment of Conn's syndrome
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(1) surgery to remove tumor (2) spirinolactone - K+ sparing diuretic that is an aldosterone antagonist
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secondary hyperaldosteronism
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kidney perception of low IV volume results in overactive renin-angiotensin system; associated with high plasma renin
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causes of secondary hyperaldosteronism
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CHF, renal artery stenosis, chronic renal failure, cirrhosis, nephrotic syndrome
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Addison's disease
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chronic primary adrenal insufficiency due to adrenal atrophy or destruction by disease resulting in deficiency of aldosterone and cortisol
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findings in Addison's disease
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hypotension, hyperkalemia, metabolic acidosis, skin hyperpigmentation, adrenal atrophy of all 3 layers
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secondary adrenal insufficiency
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decreased pituitary ACTH production which has no skin hyperpigmentation and no hyperkalemia
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waterhouse-friedrichson syndrome
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acute primary adrenal insufficiency due to adrenal hemorrhage
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causes of waterhouse friedrichson syndrome
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Neisseria meningitidis, DIC, endotoxic shock
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MC tumor of adrenal medulla in adults
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pheochromocytoma
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which cells does a pheochromocytoma arise from?
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chromaffin cells (neural crest)
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findings in pheochromocytoma
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(1) episodic HTN - due to E, NE and DA release (2) urinary VMA elevated (3) plasma catecholamines elevated
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pheochromocytomas are associated with..
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neurofibromatosis, MEN types 2a and 2b
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rule of 10s (pheochromocytoma)
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10% malignant, 10% bilateral, 10% extraadrenal, 10% calcify, 10% kids, 10% familial
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pheochromocytoma symptoms
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episodic: Pressure (BP), Pain (headache), Perspiration, Palpitations (tachycardia), Pallor
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breakdown productions of DA (1), NE (2) and E (3)
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(1) DA - HVA (2) NE - VMA (3) E - metanephrine
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MC tumor of adrenal medulla in children
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neuroblastoma
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neuroblastoma
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can occur anywhere along sympathetic chain, elevated HVA in urine, overexpression of N-myc oncogene associated with rapid tumor progression
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signs/symptoms of hypothyroidism
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cold intolerance, weight gain (decreased appetite), lethargy/fatigue, constipation, decreased reflexes, myxedema, dry cool skin, bradycardia, dyspnea on exertion
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signs/symptoms of hyperthermia
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heat intolerance, weight loss, increased appetite, hyperactivity, diarrhea, increased reflexes, pretibial myxedema, warm moist skin, fine hair, chest pain, palpitations, arrhythmias
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lab findings in hypothyroidism
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increased TSH, decreased total T4, free T4, T3 uptake
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lab findings in hyperthyroidism
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decreased TSH, increased total T4, freeT4 and T3 uptake
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MCC of hypothyroidism
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Hashimoto's thyroiditis
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Hashimoto's thyroiditis
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autoimmune disorder; antimicrosomal and antithyroglobulin ab's with association to HLA-DR5
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histology in Hashimoto's
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Hurthle cells, lymphocytic infiltrate with germinal centres
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findings in Hashimoto's
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moderately enlarged, nontender thyroid
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Cretinism
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severe fetal hypothyroidism
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endemic Cretinism
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endemic goiter is prevalent ex. lack of dietary iodine
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sporadic cretinism
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defect in T4 formation or developmental failure in thyroid function
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findings in Cretinism
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pot bellied, pale, puffy-faced child with protruding umbilicus and protuberant tongue; mental retardation
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subacute thyroiditis (de Quervain's)
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self-limited hypothyroidism following a flu-like illness; may initially be hyperthyroid
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histology of subacute thyroiditis
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granulomatous inflammation
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findings in subacute thyroiditis
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increased ESR, jaw pain, early inflammation, very tender thyroid
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Reidel's thyroiditis
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thyroid replaced by fibrous tissue (hypothyroid)
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findings in Riedel's thyroiditis
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fixed, hard (rock-like) and painless goiter
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Grave's disease
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type II HS, autoimmune hyperthyroidism with thyroid stimulating/TSH receptor antibodies
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signs/symptoms of Grave's disease
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ophthalmopathy - proptosis, EOM swelling; pretibial myxedema, diffuse goiter; often presents during stress
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thyrotoxicosis
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stress-induced catecholamine surge leading to death by arrhythmia; serious complication of Grave's disease
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toxic multinodular goiter
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focal patches of hyperfunctioning follicular cells working independently of TSH due to mutation of TSH receptor; increased release of T3/T4
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Jod-Basedow phenomenon
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thyrotoxicosis if a patient with iodine deficiency goiter is made iodine replete
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treatment strategy for type 1 DM
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low sugar diet, insulin replacement
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tx strategy for type 2 DM
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dietary modification, exercise, oral hypoglycemics, insulin replacement
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rapid acting insulin (3)
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Lispro, Aspart, Regular
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intermediate acting insulin (1)
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NPH
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long-acting insulin (2)
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glargine, detemir
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MOA of insulin
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(1) liver - increases glucose stored as glycogen (2) muscle - increases glycogen and protein synthesis; K+ uptake (3) fat - aids in TG storage
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clinical uses of insulin
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(1) type 1 DM/type 2 DM (2) DKA (3) gestational diabetes (4) stress-induced hyperglycemia
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toxicities of insulin
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(1) hypoglycemia (2) hypersensitivity - very rare
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first generation sulfonylureas
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tolbutamide, chlorpropamide
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second generation sulfonylureas
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glyburide, glimepiride, glipizide
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MOA of sulfonylureas
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close K+ channel in B-cell membrane which depolarizes cells and insulin is released via influx of Ca2+
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clinical use of sulfonylureas
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stimulate release of endogenous insulin in DM2
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side effects of first generation sulfonylureas
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disulfuram-like effects
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side effects of second generation sulfonylureas
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hypoglycemia
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ex of biguanide drug
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metformin
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MOA of metformin
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unknown - decreases gluconeogenesis, increases glycolysis and peripheral glucose uptake
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clinical uses of metformin
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taken orally; can be used in pts without islet function
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side effects of metformin
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(1) lactic acidosis (2) C/I in renal failure
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glitazones/thiazolidinediones
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pioglitazone, rosiglitazone
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MOA of glitazones
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increase insulin sensitivity in peripheral tissue; bind to PPAR-y nuclear transcriptor regulator
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clinical use of glitazones
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monotherapy in type 2 DM or combined with above agents
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side effects of glitazone drugs
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(1) weight gain (2) edema (3) hepatotoxicity (4) CV toxicity
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alpha-glucosidase inhibitors
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acarbose, miglitol
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MOA of acarbose/miglitol
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inhibit intestinal brush border a-glucosidase = delayed sugar hydrolysis and glucose absorption = decreased post-prandial hyperglycemia
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clinical uses of acarbose/miglitol
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monotherapy in type 2 DM or combined with above agents
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side effects of acarbose/miglitol
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GI disturbance - flatulence, diarrhea; potentially hepatotoxic
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pramlintide
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mimetic that decreases glucagon
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clinical uses of pramlintide
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type 2 DM
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side effects of pramlintide
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hypoglycemia, nausea, diarrhea
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exenatide
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GLP-1 analog that increases insulin and decreases glucagon release
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clinical uses of exenatide
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type 2 DM
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side effects of exenatide
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nausea, vomiting, pancreatitis
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MOA - propylthiouracil/methimazole
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inhibit organification of iodide and coupling of thyroid hormone synthesis; PTU decreased peripheral conversion of T4 to T3
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clinical uses of propylthiouracil/methimazole
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hyperthyroidism
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toxicity of propylthiouracil/methimazole
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(1) skin rash (2) agranulocytosis (3) aplastic anemia (4) methimazole = teratogen
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which drugs can be used for thyroxine replacement?
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levothyroxine/ triiodothyronine
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clinical uses of levothyroxine/triiodothyronine
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hypothyroidism, myxedema
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toxicity of levothyroxine/triiodothyronine
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tachycardia, heat intolerance, tremors, arrhythmias
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clinical use of GH
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GH deficiency, Turner's syndrome
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clinical use of somatostatin (octreotide)
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acromegaly, carcinoid, gastrinoma, glucagonoma
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clinical use of oxytocin
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stimulates labor, uterine contractions and milk-letdown; controls uterine hemorrhage
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clinical use of desmopressin
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ADH analog used to treat central/pituitary diabetes insipidus
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demeclocycline - MOA
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ADH antagonist (member of tetracycline family)
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MOA of glucocorticoids
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decreases production of leukotrienes and PGs by inhibiting PLA2 and expression COX2
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clinical uses of glucocorticoids
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Addison's disease, inflammation, immune suppression, asthma
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Iatrogenic Cushing's syndrome
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buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes
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toxicity of glucocorticoids
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adrenal insufficiency if drug stopped abruptly after chronic use
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