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150 Cards in this Set
- Front
- Back
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zona glomerulosa
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secretes aldosterone (mineralocorticoids)
under control of renin-angiotensin |
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zona fasiculata
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secretes cortisol (glucocorticoids), sex hormones
controlled by ATCH, CRH |
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zona retriularis
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secretes sex hormones (androgens)
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adrenal medulla
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middle of adrenal gland derived from neural crest cells, regulated by preganglionic sympathetic fibers
secretes catecholamines (epi, and NE) - from chromaffin cells |
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adrenal cortex
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from mesoderm
3 layers: zona granulosa zona fasiculata zona reticularis GFR (glomerulosa, fasiculata, restularis) coresponds with salt (aldosterone), sugar (glucocorticoids), and sex (androgens) |
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pheochromocytoma vs neuroblastoma
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pheochromocytoma most common tumor of adrenal medulla in adults
pheochromocytoma causes hypertension neruoblastoma is most common adrenal medulla tumor in children neuroblastoma does not cause hypertension |
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adrenal gland drainage
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left adrenal -> left adrenal vein -> left renal
right adrena -> right adrenal vein -> IVC |
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posterior pituitary hormones
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ADH, oxytocin
made in hypothalamus, STORED in the posterior pituitary |
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posterior pituitary is derived from what tissue
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neruoectoderm
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anterior pituitary hormones
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FLAT PiG
FSH LH ACTH TSH Prolactin i Growth hormone Melanotropin (MSH) |
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acidophils of pituitary gland forms
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GH and prolactin
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basophils of pituitary gland forms
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FSH, LH, ACTH, TSH
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anterior pituitary hormone is derived from what tissue
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oral ectoderm (rathke's pouch)
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T/F TSH, LH, FSH, and hCG have a common beta subunit
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False, they have a common alpha subunit
beta subunit determines activity/specificity |
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pancreatic endocrine cells
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alpha cells located peripherally in islets - glucagon
beta cells located centrally in islets - isulin gamma cells interspersed in islet - somatostatin highest concentration of endocrine cells are in the tail of the pancreas |
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insulin is required for which cells to uptake glucose
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required for muscle and adipose cells
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insulin independent cells (does not need insulin for glucose uptake)
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BRICK L
Brain RBC Intestine Cornea Kidney Liver |
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anabolic effects of insulin (6)
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increased glucose transport
increased glycogen synthesis increased triglyceride synthesis and storage increased Na+ retention increased protein synthesis increased cell uptake of K+ and aminoacids |
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mechanism of secretion of insulin and regulation
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Beta cells respond to ATP from glucose metabolism
closed K channels -> cell depolarization->opens Ca++ channels->Ca facilitates insulin vesicle exocytosis reg: hyperglycemia, GH, Beta2-antagonists increase; hypoglycemia, somatostatin, alpha-2-agonists decrease |
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GLUT channel locations
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GLUT1 - RBC, Brain
GLUT2 - beta-islet cells, liver, kidney, small intestine GLUT4 - adipose tissue, skeletal muscle (insulin responding) |
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Glucagon
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made by alpha cells of pancreas, secreted in response to hypoglycemia
inhibited by insulin, hyperglycemia, somatostatin 1. promotes glycogenolysis, gluconeogenesis 2. lipolysis and ketone production 3. inhibition of insulin and further glucagon release |
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hypothalamic control of TSH, prolactin secretion
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TRH release by hypothalamus
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how does the hypothalamus negatively regulate prolactin
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dopamine
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prolactin relationship with GnRH
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prolactin inhibits GnRH
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somatostatin effect on hypothalamus
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negatively regulates GH, TSH
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GnRH on pituitary
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causes secretion of FSH, LH from anterior pit
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how does prolactin regulate itself
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increases dopamine synthesis and secretion from hypothalamus
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function of prolactin, regulation
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inhibited by dopamine, TRH promotes prolactin secretion (can be depressed in hypothyroidism)
stimulates milk production in breast inhibits ovulation and spermatogenesis by inhibiting GnRH |
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drugs that inhibit prolactin
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dopamine agonist
bromocriptine treatment for hyperprolactinemia |
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drugs that stimulate prolactin secretion
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dopamine antagonist
antipsychotics, estrogens |
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Growth hormone (somatotropin)
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from anterior pituitary
regulation: released in pulses in response to GHRH, increased during sleep/excercise inhibited by glucose and somatostatin Function: stimulates linear growth and muscle mass through somatomedin secretion - increased AA uptake stimulates production of peptide growth factors, insulin-like growth factor JAK/Stat pathways -> tyrosine kinase activated -> MAP kinase increases insulin resistance, decreased uptake of glucose by fat/muscle excess -> acromegaly or gigantism |
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17alpha hydroxylase deficiency
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need 17alpha hydroxylase for conversion to cortisol and testosterone precursors
deficiency -> decreased sex hormones decreased cortisol increased mineralocorticoids symptoms: *hypertension* hypokalemia males - decreased DHT -> pseudohermphroditism (ambiguous genitalia, undescended testes) females - lack 2ndary sex characteristics |
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21 hydroxylase deficiency
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most common congenital bilateral adrenal hyperplasia
can't make cortisol, aldosterone decreased cortisol decreased mineralocorticoids increased sex hormones increased renin symptoms: HYPOtension hyperkalemia masculinization feminine pseudohermaphroditism in babies - hypovolemic shock |
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11beta hydroxylase deficiency
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decreased cortisol
decreased aldosterone increased sex hormones symptoms: HYPERtension masculinization hypertension is caused by 11-deoxycoticosterone (aldosterone precursor) |
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decreased sex hormones
increased aldosterone decreased cortisol which congenital bilateral adrenal hyperplasia? |
17alpha hydroxylase deficiency
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decreased cortisol
increased sex hormones decreased aldosterone which congenital bilateral adrenal hyperplasia? |
21 hydroxylase deficiency
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decreased aldosterone
decreased cortisol increased sex hormones which congenital bilateral adrenal hyperplasia? |
if hypertension then 11beta hydroxylase deficiency
if hypotension then 21 hyroxylase deficiency |
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what is common to all congenital bilateral adrenal hyperplasias?
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decreased cortisol
increased ACTH -> hyperplasia |
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function of cortisol (5)
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maintains blood pressure - upregulates alpha 1 receptors for NE to work on
decreased bone - osteoporosis, avascular necrosis with excess anti-inflammatory -decreases phospholipase A2 activity -> decreased leukotriene and prostaglanding production -inhibits leukocyte adhesion -> neutrophilia -blocks histamine release from mast cells -reduces eosinophils -blocks IL-2 production increases insulin resistance gluconeogenesis, lipolysis, proteolysis promotes activity of glucagon - absence is associated with hypoglycemia |
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Cortisol regulation
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released in a pulsatile fashion
CRH from hypothalamus stimulates ACTH release from pituitary -> production of cortisol in zona fasciculata cortisol decreases CRH, ACTH, and cortisol secretion |
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parathyroid hormone function (4)
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increased bone resorption of calcium and phosphage
increased kidney reabsorption of calcium in distal convoluted deceased kidney resorption of phosphate increased 1,25 vit D (stimulates 1alpha hydroxylase) -> increased Ca, Pi, bone deposition overall: increased serium Ca++, decreased serum PO4-, increased URINE PO4- |
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regulation of PTH secretion
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decreased serum Ca++ increases PTH secretion
decreased free serum Mg++ decreases PTH 1,25(OH)2-D negatively regulates released from chief cells superior 2 from 3rd pharyngeal pouch, inferior from 4th |
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T/F PTH acts directly on osteoclasts to increases bone resportion
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False
works directly on osteoBLASTS, which release chemical mediators to stimulate osteoCLASTS indirectly |
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1,25 vitamin D function, regulation
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increased Ca++ and PO4- absorption in intestines
released calcium and phosphate from bone matrix increased PTH, decreased Ca, Pi increase 1,25(OH)2-D production negative feedback loop on self |
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vitamin D deficiency
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rickets in children
osteomalacia in adults |
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calcitonin source and function
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secreted from parafollicular cells of thyroid
decreases bone resorption of calcium (calciTONin TONES down calcium) opposes PTH stimulated by increased serum Ca++ |
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cAMP mediated hormones
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FLAT CHAMP
FSH LH ACTH TSH CRH hCG ADH (V2 receptor) MSH PTH + calcitonin, FHRH, glucagon |
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cGMP mediated hormones
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ANP, NO
vasodilators |
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IP3 mediated hormones
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GOAT
GnRH Oxytocin ADH (V1 receptor) TRH |
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hormones that use cytosolic steroid recptors
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VET CAP
Vit D Esterogen Testosterone Cortisol Aldosterone Progesterone |
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hormones that use nuclear steroid receptors
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T3/T4
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tyrosine kinase (MAP kinase) mediated hormones
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insulin, IGF-1, FGF, PDGF
think growth receptors |
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JAK/STAT, receptor associated tyrosine kinase mediated hormones
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GH, prolactin, IL-2
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steroid hormone mechanism (name the steps)
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hormone diffuses through cell membrane
binding to receptor located in nucleus or cytoplasm binding to enhance like element in DNA effect on transcription transformation of receptor to expose the DNA binding domain transformation of receptor to expose DNA binding domain |
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sex hormone binding globuilin (SHBG)
1. effect when increased in men 2. effect when decreased in women |
1. increased SHBG -> lower free testosterone -> gynecomastia
2. decreased SHBG -> increased testosterone -> hirsutism |
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function of T3
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4 Bs
Brain maturation Bone growth Beta-adrenergic effect (heart rate, contractility) Basal Metabolic Rate increase (via increased Na/K ATPase -> O2 consumption, respiratory rate, temp) also: glyucogenolysis, glyuconeogenesis, lipolysis T3/T4 - bind nuclear receptros to activate and enhancer -> expression of DNA -> protein synthesis |
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Thyroid hormone regulation
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TRH (hypothalamus) stimulates TSH from pituitary which activates follicular cells
negative feedback from T4 |
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what binds T3/T4 in the blood
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thyroixin binding globulin
only free hormone is active see decrease in TBG in hepatic failure see increase TBG in pregnancy or oral contraceptive |
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T3 or T4 has higher affinity
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T3
T4 is converted to T3 at target tissues |
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purpose of peroxidase in the thyroid
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oxidation of organification of iodide and coupling MIT and DIT for thyroid hormone production
inhibited by propylthiouracil (also 5'-deiodinase) methimazole inhibits peroxidase |
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Wolff-chaikoff effect
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transient decrease in T3/T4 due excess igenestion of iodide -> inhibts thyroid peroxidae -> decreased iodide organification
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dexamethasone challenge test
for healthy for ACTH producing pituitary tumor for ectopic ACTH producing tumor for cortisol producing tumor |
1. healthy - see decreased cortisol after low dose
2. ACTH producing pituitary tumor - increased cortisol after low dose, DECREASED after big dose 3. ectopic ACTH tumor - increased cortisol for high and low dose 4. cortisol producing tumor - increased cortisol after low and high dose |
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Cushing's Syndrome exogenous causes
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corticosteroid use - number 1 cause
decreased ACTH |
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Cushing's Syndrome endogenous causes (3)
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1. Cushing's DISEASE - 70% of endogenous causes - ACTH secreted from pituitary adenoma - increased ACTH
2. Ectopic ACTH - non pituitary source of ACTH - see increased ACTH (small cell lung cnacer, bronchial carcinoid) 3. Adrenal cause - adenoma, carcinoma, nodular hyperplasia - see decreased ACTH |
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symptoms of Cushing's Syndrome
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hypertension
weight gain moon facies truncal obesity buffalo hump hyperglycemia (insulin resist) skin changes - thinning, striae osteoporosis amenorrhea immune supression hypokalemic alkalosis |
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primary hyperaldosteronism (conn's syndrome)
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adrenal hyperplasia, aldosterone secreting adrenal ademoa
hypertension, hypokalemia, metabolic alkalsosis, *low plasma renin* can be bilateral or unilateral |
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secondary hyperaldosteronism
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kidney preception of low intravascular volume -> overactive Renin-angiotensin system
causes: renal artery stenosis, chronic renal failure, CHF, cirrhosis, or nephrotic syndrome high plasma renin |
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treatment for hyperaldosteronism
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spironolactone or other aldosterone antagonist
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addison's disease
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chronic PRIMARY adrenal insufficiency due to adrenal atrophy or destruction by disease
lack aldosterone and cortisol => hypotension (hyponatremic volume contraction), hyperkalemia, acidosis, and skin hyperpigmentation (MSH an ACTH byproduct) high ACTH due to lack of feed back increased MSH causes hyperpigmentation involves cortical divisions but not the medulla |
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addisons disease vs 2ndary adrenal insufficiency
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2ndary adrenal insufficiency characterized by LOW ACTH thus no hyperpigmentation
zona glomoerulosa is preserved -> normal aldosterone -> normal K usually due to exogenous glucocorticoid treatment |
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waterhouse-Friederichsen syndrome
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ACUTE primary adrenal insufficiency due to adrenal hemorrhage due to neisseria meningitidis septicemia, DIC, or endotoxic shock
(addison's disease is chronic) |
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most common tumor of the adrenal medulla in adults
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pheochromocytoma - arises from chromaffin cells
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rules of 10 for pheochromocytoma
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10% maliginalt
10% bilateral 10% extra-adrenal 10% calcify 10% kids 10% familial - MEN 2A/2B |
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pheochromocytoma pathophysiology
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usually secrete epinephrine, NE, dopamine -> hypertension
look EPISODIC symptoms (5 Ps): pressure (blood) pain (headache) perspiration palpitations (tachycardia) pallor look for VMA, HVA, metanephrine in urine and increased plasma catecholamines associated with neurofibromatosis, MEN 2A and 2B treat with alpha-antagonist -phenoxybenzamine (irreversible alpha-blocker -prophylaxis before surgery) |
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vanillylmandelic acid (VMA)
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break down product of norepinephrine found in urine
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homovanillic acid (HVA)
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dopamine breakdown product in the urine
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metanephrine
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epinephrine breakdown product in the urine
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most common tumor of adrenal medulla in children
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neuroblastoma
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Neuroblastoma
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N-myc oncogene - 20% new mutation, 70-80% deletion of short arm of CHR1 or gain of long arm of Chr 17
amplifies N-myc oncogene (nuclear transcription factor) often produce catecholamines, vasoactive intestinal peptide (watery diarrhea, hypokalemia, achlorhydria) |
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lab findings for hypothyroidism
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increased TSH (primary hypothyroidism)
decreased total T4 decreased free T4 decreased T3 uptake |
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lab findings for hyperthyorisim
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decreased TSH (primary hyperthyroidism)
increased total T4 incresed free T4 increased T3 uptake |
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hypothyroidism symptoms
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cold intolerance (decreased heat production)
weight gain (decreased appetite) lethargy, fatigue, weakness constipation decreased reflex myxedema (facial, peirorbital) dry, cool skin coarse, brittle hair bradycardia, dyspnea on exertion |
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hyperthyroidism symptoms
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heat intolerance
weight loss (increased appetite) hyperactivity diarrhea increased relfex pretibial myxedema warm, moist skin fine hair chest pain, tachycardia, palpitation, arrhythmia |
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causes of hypothyroidism
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hashimoto's thyroiditis
cretinism subacute thyroiditis riedel's thyroiditis |
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hashimoto's thyroiditis
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most common of hypothyroidism
autoimmune dmg to thyroid, (antimicrosomal TPO, antithyroglobulin antibodies) HLA-DR5 associated look for hurthle cells, lymphocytic infiltrate with germinal centers (can begin as hyperthyroidism due to damage rupture of follicles) |
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cretinism
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due to severe fetal hypothyroidism
endemic cretinism - associated with endemic goiter (lack of dietary iodine) sporatic cretinism - defect in T4 formation or developmental failure in thyroid pot bellied, pale, puffy faced child with protruding umbilicus and tongue |
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subacute thyroiditis
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self limited hypothyroidism
follows flu like illness see granulomatous inflammation, increased ESR, jaw pain, early inflam, tender thyroid (may begin as hyperthyroid) |
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riedel thyroiditis
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thyroid replaced by fibrous tissue -> hypothyroidism
findings are fixed, hard, rock like painless goiter |
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causes of hyperthyroidism
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graves' disease
thyrotoxicosis toxic multinodular goiter |
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Thyroglossal cyst
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endodermal diverticulum of floor of pharynx
thyoglossal duct reamins foramen cecum marks form site of duct |
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grave's disease
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autoimmune hyperthyroidism due to thyroid stimulating/TSH receptor antibodies
see ophthalmopathy, pretibial myxedema, diffuse goiter see with stress type II hypersensitivity |
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thyrotoxicosis
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stress induced catecholamine surge -> arrhythmia -> death
see with graves and other hyperthyroid disorders |
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toxic multinodular goiter
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focal patches of hyperfunctioning follicular cells work independent of TSH due to mutation in TSH receptor
increased release of T3 and T4 hot nodules are rearely malignant jod-basedow phenomenon - if patient iwth iodeine deficiency is made iodine replete can get thyrotoxicosis |
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thyroid cancers different kinds (5)
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1. papillary carcinoma - most common
2. follicular carcinoma 3. medullary carcinoma 4. undifferentiated/anaplastic 5 associated with hashimoto's thyroiditis |
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papillary thyroid cancer
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most common
excellent prognosis ground glass nuclei (Orphan Annie) psammoma bodies nuclear grooves increased risk with childhood radiation |
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follicular thyroid carcinoma
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good prognosis
see uniform follicles hematogenous spread of mets to bone/lung |
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medullary thyorid carcinoma
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from parafollicular C cells
produces calcitonin sheets of cells in amyloid stroma associated with MEN 2A and 2B - ret gene |
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undifferentiated/anaplastic thyroid carcinoma
- what patients - prognosis? |
older patients
bad prognosis |
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what is lymphoma thyroid associated with
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hashimotos
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primary hyperparathyroidism
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usually adenoma
see hypercalcemia, hypercalciuria (renal stones), hypophosphatemia increased PTH increased alk phos increased cAMP in urine asymptomatic usually, but can see with weakness and constipation "stones bones and groans" stones - renal stones bones - osteitis fibrosa cystica groans - weakness/constipation osteitis fibrosis cystica - spaces filled with brown fibrous tissus = painful |
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secondary hyperparathyroidism
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2ndary hyperplasia due to decrased Ca++ absorption in gut and increased phosphorus
see with chronic renal disease -> hypovitaminosis D renal osteodystrophy hypocalcemia, hyperphosphatemia increased alk phos increased PTH |
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tertiary hyperparathyroidism
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refractory hyperthyroidism resulting from chronic renal disease
very high increased PTH increased Ca++ |
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renal osteodystrophy
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bone lesions due to 2ndary or tert hyperparathyroidism due to renal disease
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hypoparathyoridism
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often due to accidental surgical excisions during thyroid surgery, autoimmune dmg, or DiGeorge syndrome
findings: hypocalcemia, tetany. cardiac conduction deects, increased QT chovostek sign trousseau sign |
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chovostek sign
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tapping of facial nerve -> contraction of facial muscle
see with hypoparathyroidism |
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trousseau's sign
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occlusion of vrachial artery with BP cuff -> carpal spasm
see with hypoparathyroidism |
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DiGeorge syndrome
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failure of development of 3rd/4th pharyngeal pouch
absence of parathyroid and thymus deletion of chromsome 22 at q11.2 hypocalcemia/tetany T-cell deficiency with recurrent viral/fungal infections may have cardiac defects |
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pseudohypoparathyroidism
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albright's hereditary osteodystrophy
autosomal dominant - kidney is unresponsive to PTH hypocalcemia, shortened 4th/5th digits, short stature |
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pituitary adenoma
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most often a prolactinoma
see amenorrhea, glactorrhea, low libido, infertility (low GnRH) can impinge on optic chiasm -> bitermporal hemianopia |
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bromcriptine, cabergoline
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dopamine agonist
treats prolacinomas |
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acromegaly
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excess growth hormone
large tongue, deep furrows, deep voice, large hands and feet, coarse facial features, insulin resistance in children refered to gigantism (increased linear bone growth) treat with pituitary adenoma resection followed by octreotide |
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when is it normal to have high growth hormone
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stress, exercise, hypoglycemia
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diabetes insipidus
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characterized by intense thirst and polyuria
lack or can't respond to ADH - can't concentrate urine |
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causes of central diabetes insipidus
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pituitary tumor, trauma, surgery, histiocytosis X
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causes of nephrogenic diabetes insipidus
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hereditary, or 2ndary to hypercalcemia, lithium, demeclocycline
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diagnosis of diabetes insipidus
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water deprivation test
should see increase in urine osmolality when water restricted use demopressin to distinguish between central and nephrogenic (desmopressin with cause response in people with central DI) urine specific gravity < 1.006, serum osmolality > 290 |
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treatment of central DI and nephrogenic DI
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central DI - ADH analog (desmopressin)
nephrogenic DI - hydrochlorothiazide, indomethacin, amiloride |
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SIADH
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syndrome of inappropriate antidiuretic hormone
see: excessive water retention hyponatremia urine osmolarity > serum osmolarity decreased aldosterone low sodium -> seizures, correct slowly to prevent pontine myelonolysis |
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treatment of SIADH
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demeclocycline or water restrict
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causes of SIADH
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ectopic ADH
CNS disorders/head trauma pulmonary disease drugs - cyclophosphamide |
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diabetes mellitus
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polydipsia, polyuria, polyphagia, weight loss
unopposed secretion of GH and epinephrine worsens hyperglycemia insulin deficiency, glucagon excess -> increased glucose uptake, increased protein catabolism, and increased lipolysis chronic: non-enzymatic glycolsylation -> small vessel disease -> retinopathy, glaucoma, nephropathy non-enzymatic glycolsylation -> large vessel disease -> CAD, peipheral vascular occlusive disease, gangrine -> limb loss, cardiovascular disease |
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DKA is seen in type 1 or 2 diabetes most often
hyperosmolar coma seen in type 1 or type 2 most often |
DKA -type 1
hyperosmolar coma - type 2 |
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type 1 or 2 diabetes is associated with strong genetic predisposition
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type 2
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type 1 or 2 diabetes is associated with HLA system
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type 1 - HLA-DR3 and 4, DQ
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histology of type 1 diabetes
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islet leukocytic infiltrate
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histology of type 2 diabetes
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islet amyloid deposit
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diabetic ketoacidosis
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complication of type 1 diabetes
usually due to increased insulin due to STRESS -> use fat -> ketogenesis Beta-hydroxybutyrate > acetoacetate see: kussmaul respiration, nausea, abdominal pain, psychosis, dehydration, fruity breath odor labs - hyperglycemia, anion gap metabolic acidosis, increased blood ketones, leukocytosis, hyperkalemia with decreased intracellular K+ tx: IV fluids, insulin, K+, glucose if necessary |
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diabetic ketoacidosis complications
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mucormycosis, rhizopus, cerebral dema, cardiac arrhythmias, heart failure
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Hyperosmolar nonketotic state
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type 2 DM complication -> severe hyperglycemia without ketoacidosis
hyperglycemia -> glucosuria -> osmotic diuresis leads to volume depletion, hyperosmolarity, intracellular dehyrdration, hemoconcentration, electrolyte loss |
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carcinoid syndrome
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caused by carcinoid tumors derived from neuroendocrine cells - especially metastatic small bowel tumors -> secrete high levels of serotonin
see diarrhea, cutaneous flushing, asthmatic wheezing, right sided valvular disease rules of 1/3: 1/3 metastasize 1/3 present with 2nd malignancy 1/3 are multiple see 5-HIAA in urine |
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zolinger elson syndrome
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gastin secreting tumor of pancreas or duodenum
stomach shows rugal thickening with acid hypersecretion - associated with MEN 1 |
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MEN 1 (wermer's syndrome)
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3 Ps
pancreas tumor - ZE syndrome, insulinoma, VIPoma, glucagomoas pituitary tumors parathyroid tumors mutation in the menin tumor suppressor gene |
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MEN 2a (sipple's syndrome)
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2 Ps
pheochromocytoma parathyroid tumor + medullary thyroid carcinoma (secretes calcitonin) |
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MEN 2b
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1 P
pheochromocytoma + medullary thyroid carcinoma (secretes calcitonin) + oral.intestinal ganglioneuromatosis (w/ marfan habitus) |
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MEN syndromes are auto dom or auto rec?
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autosomal dominant
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what gene is associatd with MEN 2A and 2B`
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ret gene
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oxytocin
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secreted from paraventricular nucleus of hypothalamus
induces uterine contractions during labor, coordinated myometrial contractions -> induce parturion lesser effects - increase synthesis of uterine prostaglandin - contractions contraction of myoepithelial cells of breast during lactation - in response to suckling of nipple |
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Insulin-mimetics
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rapid acting - lispro, aspart
short-acting - regular intermediate -NPH long - glargine detemir bind insulin receptor used primarily in type 1, but can be used in late type 2 |
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sulfonylureas
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first generation: tolbutamide, chlorpropamide
second generation: glyburide, glimepiride, glipizide close K+ channel in beta-cell membrane -> cell depolarizes -> triggers insulin release via Ca influx type 2 first generation SE: disulfiram-like effects second: hypoglycemia hepatic metabolism |
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Biguanide
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metformin - exact mechanism unknown
decreases gluconeogeneis, increases glycolysis, increased peripheral glucose uptake (insulin sensitivity) first line for type 2, pts. without islet function lactic acidosis - contraindicated in renal failure |
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glitazones/thiazolidinediones
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pioglitazone, rosiglitazone
increased insulin sensitivity in peripheral tissue - binds PPAR-gamma nuclear transcription regulator - PPAR-y regulates fatty acid stoarge and glucose metabolism, increases insulin sensitivity |
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alpha-glucosidase inhibitors
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acarbose, miglitol
inhibit intestinal brush-border alpha-glucosidases to prevent sugar hydrolysis and absorption SE: GI disturbances |
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Pramlintide
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decreases glucagon
can cause hypoglycemia, nausea, diarrhea |
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GLP-1 analogs
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exenatide - increases insulin and decreases glucagon release
nasuea, vomiting, pancreatitis |
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Sitagliptin
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inhibits dipeptidyl peptidase (DPP-4) preventing deactivation of GLP-1
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propylthiouracil, methimazole
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block peroxidase -> inhibits organification of iodide and coupling of thyroid hromone
propylthiouracil also blocks 5'-deiodinase which decreases peripheral conversion of T4 to T3 used for hyperthyroidism SE: rash, aplastic anemia, hepatoxicity, methimazole is maybe a teratogen |
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Levothyroxine, triiodothyronine
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thyroxine replacement
used for hypothyroidism, myxedema SE: tachycardia, heat intolerance, tremores, arrhythmias |
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Somatostatin (octreotiide) as a drug
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treat acromegaly, carcinoid, gastrinoma, glucagonoma
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oxytocin as a drug
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stimulates labor, uterine contractions, milk let-down, controls uterine hemorrhage
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Demeclocycline
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ASH antagonist (member of tetracycline family)
used for SIADH SE: nephrogenic DI, photosensitivty, abnormalities of bone and teeth |
