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Repro Endo Drugs > edited drugs for repro_endo - Sheet1 > Flashcards

edited drugs for repro_endo - Sheet1 Flashcards

1
Q

amiloride

A

blocks Na channels -> decr MC effects in hyperaldosteronism *weaker effect than spirolactone

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2
Q

spironolactone: action, use and dosage (3 doses for 6 diseases)

A

antagonist at MC receptors (also androgen and progesterone receptors); 25-50 mg daily as K sparing diuretic for HTN and edematous states (CHF, cirrhosis, nephoris); 400 mg daily in primary hyperaldosteronism; 200 mg daily in PCOS (used off label for anti-androgen effects)

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3
Q

spironolactone side effects (4)

A

hyperkalemia, volume depletion, men: gynecomastia, impaired libido, impotence; women: mest. irregularities

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4
Q

eplerenone

A

highly selective (and expensive) MC antagonist (not androgens nor progesterone)

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5
Q

contraindications for spironolactone (3)

A

renal impairment, hyperkalemia, pregnancy

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6
Q

metyrapone

A

blocks 11-beta enzyme that converts 11-DOC -> cortisol; doesn’t interfere with aldosterone or androgen production (dx adrenal insufficiency as primary or central by seeing relative ACTH/11-DOC levels)

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7
Q

hydrocortisone dosing

A

physiological: 20-30 mg/day in the am; stress: 50 mg every 6-8 hrs; acute: 100 mg IV/IM every 6-8 hrs (don’t need MC replacement b/c hydrocortisone works as MC above 100 mg)

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8
Q

dex dosing

A

physiological: .5 mg daily; stress: 2 mg every 12 hrs; acute: 4 mg IV/IM

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9
Q

ketoconazole

A

non-specific inhibitor of cortisol synthesis (inhibits at 3 steps)

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10
Q

cabergoline

A

DA agonist used to tx somatotroph adenoma -> paradoxical effect

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11
Q

octreotide

A

STT analog used to tx somatotroph or thyrotroph adenoma

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12
Q

pegvisomant

A

GH anatagonist used to tx somatotroph adenoma -> binds only 1/2 receptor and thus blocks it

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13
Q

metformin: action, MOA, effect, metab, adverse effects (4), benefits (3), contraindications (5), misc (1)

A

prevents gluconeogenesis (and poss glycogenolysis); phosphorylation (activation) of AMPK; improves fasting glucose (little effect on postprandial); not metabolized, renally excreted unchanged (can accum. if renal insuff); adverse: anorexia, nausea, diarrhea, lactic acidosis; benefits: immed onset (altho need to titrate slowly to avoid GI effects), no hypoglycemia, weight neutral (poss loss) -> first drug of choice; contraindications: prone to acidosis, hypoxic states, renal failure, cardiac ischemia, T1DM; need insulin to work!

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14
Q

TZDs: action, MOA, effect, duration/onset, contraindications (3), adverse effects (3), benefits (3)

A

incr. periph tissue sensitivity to insulin; binds to nuclear PPAR-gamma receptor (incr. GLUT4 transcription); lowers fasting and post-meal glucose; slow onset of action (fasting gluc begins to decr w/in 5-7 days but doesn’t completely decline until 2-3 mons); contraindications: liver disease, heart failure, renal insuff.; side effects: weight gain (improved glyc. control and incr water due to Na reabs), hepatocellular injury, incr LDL; benefits: reduces TGs, raises HDL, no hypoglycemia

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15
Q

secretagogues: types (2), differences

A

sulfonylurea and meglitinides; both bind the beta cell ATP-dep K channel but meglitinide binds more quickly and dissociates more quickly (shorter duration -> 3-4 hrs vs 12-24)

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16
Q

sulfonylurea: action, MOA, duration, effect, metab, contraindications (3), adverse effects (3)

A

secretagogue; binds to sulfonyl receptor in beta cell causing depolarization of ATP-dependent K channels; 12-24 hrs duration; effect on fasting glucose; metab: excreted via kidney w/ active metabs (careful w/ renal probs); contraind: T1DM, DKA, sulfa allergy; adverse effects: hypoglycemia, weight gain, hunger

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17
Q

meglitinides: action, MOA, duration and onset, metab, contraindications (4), adverse effects (2), aka

A

secretagogue; binds to sulfonyl receptor in beta cell causing depolarization of ATP-dependent K channels; 3-4 hrs duration w/ fast onset (give w/ every meal -> hard for compliance); metab: hepatic (P450) w/ most metabs excreted GI; contraind: T1DM, liver failure, DKA, sulfa allergy; adverse effects: low glucose 2-4 hrs after meal, weight gain; aka glinides

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18
Q

alpha-glucoside inhibitors: MOA, effects, side effects (2), contraindications (1), metab

A

delay carbohydrate absorption (inhibits intestinal enzymes ability to break down sugars) and thus incr GLP-1; effects postprandial glucose only; side effects: flatulence, bloating -> titrate slowly to minimize; contraindications: GI disorders (esp IBD); metab: renally excreted unchanged

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19
Q

GLP-1 mimetic: names (2), comparison, contraindications (2), effect, metab, benefits (2), side effects (1)

A

exenatide (from Gila monster) and liraglutide; liraglutide is once daily injection b/c binds albumin vs. exenatide is twice daily (60 mins before each meal); avoid in pts with severe GI disease or on drugs that need rapid GI abs; effect on postprandial glucose; metab: renal after DPP-4 breakdown; benefit: weight loss, no hypoglycemia; side effects: GI

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20
Q

biguanides: names (1)

A

metformin

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21
Q

incretin enhancers: MOA, duration, effect, metab, contraind, adverse effects, benefits (2)

A

DPP-4 inhibitors; 80% inhib at 24 hrs (take 1 daily); immed effect on postprandial glucose; metab: renally excreted unchanged (dose adj for renal probs); contraindications: none; adverse effects: GI; benefits: weight neutral, no hypoglycemia

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22
Q

glimeperide: what is it, brand name

A

aka Amaryl, a sulfonyurea

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23
Q

bolus insulin types (3) and peak times

A

rapid: Aspart, Lipro (1 hr to peak); short-acting: regular (2-4 hrs to peak -> complexed w/ zinc)

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24
Q

basal insulin types (3) and dosing

A

intermediate: NPH (once or twice/day); long acting: glargine (once/day), detemir (once or twice/day)

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25
Q

rapid-acting insulin: names (3), kinetics (peak, onset, duration), vs. regular (2)

A

Aspart, Lispro, Glulisine; 1 hr peak (base substitutions disrupt monomer-monomer interactions and decr hexamer formation), 10-20 mins onset, 3-5 hr duration; 2x faster absorption and 2x higher peak concentration

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26
Q

NPH: what is it, duration, dosage, onset, peak

A

suspension of zinc insulin w/ protamine (positively charged peptide); 10-20 hrs duration; dosed once/twice daily; 1-2 hr onset, 4-8 hrs peak

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27
Q

glargine: what is it, dosage, onset

A

human analog insulin w/ base substitutions that cause it to exist at pH 4.0 -> when injected it forms microprecipate below skin that takes time to absorb (long lasting); dosed once daily; 1-2 hr onset (flat course)

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28
Q

detemir: what is it, dosage, duration, onset

A

insulin analog that is acylated w/ myristic acid (remains in solution after injection -> binds to albumin and slowly releases); dosed once or twice daily; duration is dose dependent (up to 24 hrs); .8-2 hr onset (flat course)

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29
Q

regular insulin kinetics (onset, peak, duration)

A

30-60 mins (complexed w/ zinc) onset, 2-4 hr peak, 6-10 hr duration

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30
Q

PARP inhibitors (olaparib)

A

used in BRCA1/2 mutation carriers to prevent ss break repair -> “two hit” hypothesis; tumors may restore BRCA1/2 function and thus become resistant to PARP inhibitors and cisplatin (but not taxane now!)

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31
Q

medical tx of impotence: what is it, how does it work, examples (3)

A

PDE5 inhibitors: sildenafil (Viagra) is prototype -> also vardenafil (Levitra) and tadalafil (Cialis); works by inhibiting breakdown of cGMP by PDE 5, thus incr cGMP and relaxing arteries/trabeculae smooth muscles; works to maintain vasodilatory response (cannot cause it)

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32
Q

PDE5 inhibitors pharmacokinetics: onset, metabolism, distribution, changes in metabolism due to… (4)

A

work quickly (peak plasma 30-90 mins after oral dose); metabolized by CYP3A4 to active metabolite (accounts for 20% activity); widely distributed throughout body tissues; incr. plasma levels (-> hypotension) in elderly (40% incr), liver disease (80%), severe renal disease (100%), w/ CYP3A4 inhibitors (100% incr -> macrolide antibiotics, antifungals, protease inhibitors, cimetidine - OOC for heartburn)

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33
Q

PDE5 inhibitors indications (4)

A

current: impotence, primary pulmonary hypertension; future: CF, BPH

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34
Q

PDE5 inhibitors side effects

A

PDE5 inhibitors prevent breakdown of cGMP, and cGMP is in several other pathways: sperm motility, test synthesis, vaginal smooth muscle, esophageal motility, retinal color vision, inhibition of platelet aggregation; side effects can be divided into four groups: vasodilation (headahce, flushing, rhinitis), CV (hypotension, tachycardia, platelet inhibition), GI (reflux), visual changes (blue green tinged vision, incr. light perception, blurred vision)

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35
Q

tx of female sexual dysfn (6)

A

educational: behavioral/sex therapy, anatomy arousal and response; HRT (estrogen, sometimes testosterone); vascular tx: PDE5 inhibitors (for SSRI induced dysfn only), Eros therapy (handheld device to incr clitoral blood flow), L-arginine tropical tx (Vigael, Sensua -> substrate for NO synthesis)

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36
Q

mifepristone

A

used for abortion up to 63 days (approved for 49 days); anti-progestin; take 4-6 hrs to complete abortion (needs 2 visits) * i think its approved longer now, up to ~10 weeks (70 d)

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37
Q

misoprostol

A

prostaglandin E1 analog (stimulates uterine contractions, softens/primes cervix); FDA approved for prevention and tx of gastric/duodenal ulcers; benefits: heat stable (no refrig), inexpensive, widely available; side effects: flu-like sx (diarrhea, nausea, vomiting, headaches); given vaginally or buccally

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38
Q

methotrexate

A

anti-folate (used off label for abortion - given IV); takes 3-45 days to complete abortion; slightly less effective than mifepristone (90-95% vs 93-98%); used where mifepristone isn’t approved and to end ectopic pregnancies (vs mifepristone, which only ends uterine pregnancies)

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39
Q

dosing of LT4

A

start: if under age 60 w/o cardiac disease -> 50-100 mcg, if over 60 or w/ cardiac disease -> 25 mcg; avg final dose (for pts w/o thyroid) = 1.6 mcg/kg PO qd (lower in elderly); give 75% of oral dose if given IV

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40
Q

methimazole: half life, dosing, protein bound? how long to see effects? side effects

A

half life 4-6 hrs (need 1x daily); starting does 10-30 mg QD; 2-4 weeks for improvement w/ 6-12 weeks to euthyroid; freq of side effects is dose related and there are fewer side effects than PTU; rare teratogenic effects -> use instead of PTU unless in pregnancy or thyroid storm

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41
Q

PTU: half life, dosing, protein bound? how long to see effects? side effects

A

half life 1 hr (need 3x daily); starting dose 100 mg TID; 2-4 weeks for improvement w/ 6-12 weeks to euthyroid; worse side effects than methimazole (i.e. severe hepatitis only seen w/ PTU) and no dose relationship of side effects; not teratogenic -> use only in pregnancy

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42
Q

when to use PTU

A

use methimazole in all Grave’s except: first trimester pregnancy, thyroid storm, adverse rxn to methimazole

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43
Q

side effects of antithyroid drugs (5)

A

most important side effect = agranulocytosis -> rare (.1-.5%) but severe -> can kill and can appear at any dose; severe hepatitis (PTU only at .1%, hence we don’t use it); cholestasis (not as severe as PTU hepatitis, seen w/ methimazole rarely); vasculitis (rare), severe polyarthritis (rare)

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44
Q

special instructions with antithyroid drugs

A

agranulocytosis is dangerous side effect, so tell pts to stop drug and check WBC for fever or sore throat; if granulocytes <500, hospitalize and give broad spectrum antibiotics, if not, resume drug

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45
Q

amiodarone

A

anti-arrhytmia drug w/ 37% weight iodine -> can cause hypothyroidism due to Wolf-Chakoff effect, or hyperthryoidism: type 1 due to Jod-Basedow phenomenon in pts w/ underlying thyroid nodular or Graves’ disease, type 2 due to toxic effect of amiodarone causing destructive thyroiditis in normal thyroids causing T3/4 release

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46
Q

raloxifene

A

type III SERM; competes with E2; acts as estrogen in bone and CVS but anti-estrogen in breast and uterus

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47
Q

type III SERM

A

raloxifene; competes with E2; acts as estrogen in bone and CVS but anti-estrogen in breast and uterus

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48
Q

tamoxifen

A

type IV SERM; competes with E2; acts as estrogen in bone, CVS, uterus, but anti-estrogen in breast

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49
Q

type IV SERM

A

tamoxifen; competes with E2; acts as estrogen in bone, CVS, uterus, but anti-estrogen in breast

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50
Q

RU-486 is what antagonist type?

A

type II antagonist

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51
Q

Equilin

A

ERT

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52
Q

Mestranol

A

estrogen -> inhibit lactation

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53
Q

letrozole

A

aromatase inhibitors -> use in breast cancer

54
Q

Norethindrone

A

progestin -> use in endometriosis

55
Q

finasteride

A

type II 5-alpha reductase inhibitor; used in BPH and baldness to prevent DHT from exerting its effects in the prostate and hair follicles (more dramatic effect on BPH then on baldness, however)

56
Q

flutamide

A

non-steroidal androgen receptor antagonist

57
Q

cyproterone acetate

A

steroidal androgen receptor antagonist

58
Q

Medroxyprogesterone acetate

A

aka MPA, progesterone-derived progestin in Depo-Provera -> only prog-derived on market

59
Q

Drosperinone

A

derived from 17-alpha spirolactone, used in Yaz/Yasmin b/c more mineralocorticoid activity

60
Q

bromocriptine

A

dopamine agonist; can be used to inhibit lactogenesis, treat lactotroph/somatotroph adenoma

61
Q

Herceptin

A

monoclonal antibody effective for breast cancer with HER-2/neu overexpression/amplification

65
Q

pegvisomat

A

gh receptor antagonist - GH adenomas

66
Q

eplereone

A

like spiralactone, exept only acts on MC – more expensive

67
Q

fludrocortisine

A

synthetic MC - side effect: hyperaldosteronism

68
Q

mitotane

A

adrenal cytotoxic (sometimes used for cushings)

69
Q

mifeprostone

A

GC receptor antagonist (also progesterone antagonist ) -s ometimes used for cushings

70
Q

metyrapone, ketoocnazole

A

inhibit steroidognesis enzymes - hypercortisolism ** hepatotoxic

71
Q

somatostatin analogue: pasireotide (anything ending in reotide)

A

inhibit ACTH secretion - used for hypercortisolism, doesnt work for acth-indepnedent adrenal adenomas

72
Q

methimazole/PTU (propylthiouracil)

A

antithryoid - try these before iodone’ 60% remissoin * do not use during pregnancy — inhibit intrathyroidal iodine utilization AND iodotyrosine coupling ** same mechanism: inhibit oxidation via thyroiperoxidase of iodine for addition to tg .. – use for graves disease (esp younger), acheive remission in adults, and to lwoer levels prior to surgery

73
Q

thyroid surgery

A

when thyroid is compresion OR pregnancy

74
Q

give T3

A

myxedema coma , thyroid cancer before radioactice iodine scans/therapy.. people with defects in enzyme st3–>t4

75
Q

Lt 4

A

hypothyroidism - need more still with: noncompliance, decreased absorption (iron, PPIs, bowel disease)), increased metabolism (anti-seizure), increased TBG (estrogen, hepatitis), worsening disease ;;; need less with - heart disease (dont want to overdo it)

76
Q

methimazole

A

preferred antithyroid - longer half life, fewer side effects more consistent dosing, NOT proteint bound - SE dose related - less drug inducedl upus, hepatits, vascultis

77
Q

PTU

A

binds protein - doesnt cross placenta well - use in first trimester pregnancy, thyroid storm (slows t4–> t3) and adverse reactions to methimazole

78
Q

anitthyroid side effects

A

AGRANULOCYTOSIS; ptu - hepatitis; both - cholestasis, vasculitis, skin rash, hives

79
Q

PTU, glucocorticoids, pronalol (beta -blockers)

A

inhibits t4 –> t3 ;; so does potassium iodine – faster effect – thyrotoxicosis

80
Q

amiadarone

A

used for arrthymias - lots of iodoine - causes hyper w/ graves, nodules; can cause hyper or hypo thyroidism — causes destructive thyroidiitis of normal thyroid –> hormone leakage –> hyperthyroidism

81
Q

rTSH

A

thyroid cancer diangosis and assessment - drives well differentiated thryoid cancers to take up more iodine - if you have I-131 can see where – helps AVOID hypo

82
Q

side effects from thyroid meds

A

inapporpriate dosing OR esnistivity to dyes

83
Q

treat thyroid storm

A

PTU, propranolol, hydrocortisone, potassium iodide drops ((block conversion !!)

84
Q

i-131

A

radioiodine - emits gamma rays/beta particles - higher doses for TX - kills off prolifeating cells (necrosis then fibrosis) - NOT pregnancy/KIDS

85
Q

lupron, suprellin

A

GnRH agonists, treat precocious puberty

86
Q

hypoPTH treament

A

give Calcium and Vitamin D .. target calcium level = low normal .. not REPLACING kidney effects so you dont want to spill too much into urine

87
Q

5 meds that cause osteoporosis

A

anticonvulsants, PPIs, aromatase inhibitors, depo-medroxyprogesterone, GC

88
Q

glucocrticoids…

A

cause fractures!

89
Q

rPTH

A

increase osteoblasts (osteoporosis)

90
Q

bisphosphobates, calcitonin, denosumab, Serm, estrogen

A

inhibit osteoclasts (osteoporosis!)

91
Q

bisphosphonate

A

binds to bone and prevents osteoclasts from working (osteoclasts die too) – short term effect: gi discomfort, ulcers constipation (ORAL) .. increase creatine (IV) .. flu like ilnness (IV) .. long term may actually weakne bones –> atypical femur fractures and osteonecrosis of jaw

92
Q

denosumab

A

osteporosis - blocks osteoclasts - mAb, soaks up RANKL - giving OPG basically .. can cause hypocalcemia, infections, and skin reactions

93
Q

teriparatide (rPTH)

A

OSTEOBLAST ACTIVATOR ! .. can only give 2 years , then stimulation of osteoclast > stimulation of osteoblast (don’t know why it doesn’t mimic hyperparathyroidism).. adverse effects; hypercalcemia, nausea, orthosatis - OSTEOSARCOMA (rats) .. dont give to people with exisitng bone prolif disease (ie pagets)

94
Q

calcitonin

A

acute fracture and pain - not good for prevention (another osteoclast inhibitor)

95
Q

raloxifene

A

SERM used for osteoporosis – reduces risk of reproductive cancers.. adverse: thromboembolism, menopause symptoms

96
Q

estrogen for osteoporosis

A

not really used anymore, risks > benefits

97
Q

rPTH, denosumabmab, bisphonates

A

best 3

98
Q

surgery for hyperPTH

A

younger than 50, severe hypercalcemia, reduced creatinie clearance (impaired kidney function); osteoporosis

99
Q

risk of overtreating hypothyroidism

A

high T4, which can lead to atrial fibrillatin

100
Q

reasons for high thyroid during thyroid treatment

A

doapmine, glucocorticoid, decreased binding protiens, taking more than they should for weight loss, reactivation of diseases like graves

101
Q

t3 on bone marrow

A

erythropoeies

104
Q

3 treatments for hypogonadism

A

Testosterone replacemnt (can worsen infertility), LH/FSH replacement, TESE

105
Q

treatment for BPH

A

alpha adrenergic blocker; 5alpha reductase inhibitor; surgical

106
Q

alkylating agents

A

do the worse damage to granulosa cells (chemo)

107
Q

misoprostol

A

“miso soup” - nausea/vomiting, diarrhea, feever/chills .. stimualtes uterine contractions, softens cervixs.. FDA approved for ulcers

108
Q

methotrexate

A

kills actively dividing cells - takes wayyyy longer than mifeprostone (blocks folate) - ..3-7 d for abotion, bleeding up to 45 d.

109
Q

cardioprotective effects of ERT

A

increase HDL, decrease LDL; delayed intimal thickening (but arteries thicker), dec angiotensin II; reverse ACh-induced vasoconstriction of carotid arteries

110
Q

aromatase inhibitors

A

block peripheral conversion of t–> e. … used in ER-positive cancers (breast and uterine)

111
Q

letrozole, anastrozole, exemestane

A

aromatase inhibitors

112
Q

estrogen effect on bone

A

promotes apoptosis of osteoclasts –> maintenance of bone density (why postmenopausal women lose bone density) .. ALSO CLOSURE OF EPHYSEAL PLATES

113
Q

ethinyl estradiol (EE)

A

used for hypogonadism and contraception

114
Q

mestranol

A

an estrogen; used for hypogonadism and contraception

115
Q

estradiol cypionate

A

longer duration than E2; used for ERT

116
Q

metabolic effects of estrogen

A

increase lepin (inhibit appetide), increase serum proteins including binding proteins and fibrinogen

117
Q

bisphenols, alkylphenols, phthalates (in plastic)

A

synthetic estrogenic compounds – implicated in precocious puberty, maybe.

118
Q

site of E1, E3 synthesis

A

liver (from E2), periphery (from andostenedione)

119
Q

estrogen inc coagulability

A

inc II, VII, IX, X and decrease antithrombin II

120
Q

non-genomic estrogen

A

binds uterine artery - promotes vasodilation - inc blood flow w/o transcriptional changes

121
Q

raloxifene

A

SERM - antagonist in breast AND uterus; agonist in bone and CV .. big downside: strokes, DVTs

122
Q

esterification in 17-beta - complete androgens

A

helps with cachexia to help gain lean mass , more like tesosterone - used for severe anorexia

123
Q

2-3 anti androgen drugs for prostate cancer

A

flutamide, nilutamie, cyproterone acetate

124
Q

flutamide

A

receptor antagonist

125
Q

nilutamide

A

receptor antagonist

126
Q

cyprotene acetate

A

receptor antagonist

127
Q

prostaglandin D2

A

more important for causing buildness then DHT

128
Q

aromatase locations

A

liver and periphery

129
Q

DHEA

A

hair growth, bone maturation, sense of well being

130
Q

finasteride

A

targets type 2 5a reductatse – bph, mpb

131
Q

alkylation at 17alpha

A

anabolic effects - commonly abused, in urine - increase RBC and muscle mass

132
Q

pentoxphylline

A

used to activate sperms from tese/pese

133
Q

clomiphene + FSH

A

treatment for intfertility in PCOS – but risk of eclampsia, gestational diabetes, premie, and perinatal motality if do get pregnant

134
Q

clomiphene

A

SERM (wikipedia: inhibits receptors in hypothalamus, releasing neg feedback, allowing FSH/LH to raise ..)

135
Q

PCOS treatment

A

OCPS/cyclic progesterone; anti-androgens; weight loss; insulin sensitizers

Repro Endo Drugs (1 decks)

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