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Z.Fiser > Fiser.07.Pharmacology > Flashcards

Fiser.07.Pharmacology Flashcards

1
Q

What is first-pass metabolism?

A

Metabolism through the liver

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2
Q

What two modes of administration avoid first-pass metabolism?

A

sublingual and rectal

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3
Q

what aspect of a drug determines its skin absorption?

A

based on lipid solubility through the epidermis

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4
Q

What types of drugs can be absorbed into CSF? (2 characteristics)

A

restricted to nonionized drugs & lipid soluble

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5
Q

Which blood component is largely responsible for binding drugs?

A

albumin

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6
Q

what percent of penicillin is albumin-bound?

A

90%

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7
Q

what percent of warfarin is albumin-bound?

A

90%

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8
Q

why should you avoid sulfonamides in newborns?

A

displaces unconjugated bilirubin from albumin in newborns

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9
Q

what body part is tetracycline stored in?

A

stored in bone

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10
Q

what body part are heavy metals stored in?

A

bone

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11
Q

define zero-order kinetics?

A

constant amount of drug eliminated regardless of dose

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12
Q

define first-order kinetics?

A

drug eliminated proportional to dose

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13
Q

how many half-lives does it take for a drug to reach steady state?

A

5

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14
Q

define volume of distribution (formula)

A

amount of drug in the body divided by the amount of drug in plasma/blood Vd = (Total Drug) / (Drug in Plasma/Blood)

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15
Q

Where do drugs with high volumes of distribution have higher [x]? (extravascular & intravascular)

A

higher [x] in extravascular tissue (ex: fat)

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16
Q

define bioavailability

A

the fraction of unchanged drug reaching the systemic circulation

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17
Q

what is the bioavailability of IV drugs? How does this compare to PO drugs?

A

IV drugs assumed to have 100% bioavailability, PO drugs are less bioavailable

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18
Q

Define ED50

A

median effective dose: drug level at which desired effect is attained in 50% of patients

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19
Q

Define LD50

A

lethal dose: drug level at which death occurs in 50% of patients

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20
Q

What does “hyperactive” mean in pharmacology?

A

effect at an unusually low dose

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21
Q

define “tachyphylaxis” in pharmacology

A

tolerance after only a few doses

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22
Q

define “potency” in pharmacology

A

dose required for effect

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23
Q

define “efficacy” in pharmacology

A

ability to achieve result without untoward effect

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24
Q

where in the hepatocyte does drug metabolism occur? (2)

A

smooth ER; P450 system

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25
Q

name four reactions that occur in Phase 1 of drug metabolism & 2 required substrates

A

demethylation; oxidation; reduction; hydrolysis mixed function oxidases, require NADPH / O2

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26
Q

name two reactions that occur in phase 2 of drug metabolism and its overall effect

A

glucuronic acid attaches; sulfates attach –> this results in a water-soluble metabolite to make it ready for excretion

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27
Q

Describe the process of enterohepatic circulation of drugs and give an example of a drug that undergoes it

A

biliary excreted drugs may become deconjugated in intestines with reabsorption, sometimes in active form. Ex: cyclosporine

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28
Q

name 11 inhibitors of P450

A

My - Macrolides; Sullen - Sulfonamides; Robot - Ritonavir; And Amiodarone; A cute - Acute alcohol abuse; Kangaroo - Ketoconazole; Couldn’t - Ciprofloxacin; Quickly - Quinidine; Get the - Gemfibrozil; Cement -Cimetidine; Gliding on - Grapefruit juice; Ice - Isoniazid

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29
Q

name 8 inducers of P450

A

Momma - Modafinil; Da - Dilantin; Grizzly - Griseofulvin; Bear - Barbituates; Cruelly - Chronic alcohol use; Steals - St. John’s wort / Cigarette Smoke; Phen-phen (and) - Phenytoin, Phenobarbital; While - Warfarin; Racing- Rifampin; Cars - Carbamazepine / Cruciform Vegetables

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30
Q

what is the most important organ for eliminating most drugs?

A

kidney

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31
Q

name two ways the kidney eliminates drugs

A

glomerular filtration; tubular secretion

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32
Q

which type of drug is water-soluble? (polar v. nonpolar)

A

polar drugs (ionized)

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33
Q

which type of drug is more likely to be fat-soluble (polar v. nonpolar)

A

nonpolar drugs (nonionized)

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34
Q

which type of drug is more likely to be eliminated in unaltered form? (polar v. nonpolar)

A

polar drugs (ionized)

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35
Q

which type of drug is more likely to be metabolized before excretion? (polar v. nonpolar)

A

nonpolar drugs (nonionized)

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36
Q

What metabolic process results in uric acid?

A

purine metabolism –> uric acid

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37
Q

what is the underlying (pathophys) of gout?

A

caused by uric acid buildup

38
Q

name four drugs that treat gout

A

colchicine; indomethacin; allopurinol; probenecid

39
Q

what is the MOA of colchicine?

A

antiinflammatory; binds tubulin & inhibits migration of WBCs

40
Q

what is the MOA of indomethacin?

A

NSAID, reversible COX inhibitor = reduced prostaglandin synthesis

41
Q

what is the MOA of allopurinol?

A

xanthine oxidase inhibitor, blocks uric acid formation from xanthine

42
Q

what is the MOA of probenecid?

A

increased renal secretion of uric acid

43
Q

what is the MOA of cholestyramine?

A

binds bile acids in gut –> forces body to resynthesize bile acid –> lowers total body cholesterol

44
Q

name one adverse effect of cholestyramine and how it occurs

A

cholestyramine can bind vitamin K in the gut –> increased bleeding tendency

45
Q

what is the MOA of statins?

A

HMG-CoA reductase inhibitor

46
Q

name two AEs of statins

A

liver dysfunction; rhabdomyolysis

47
Q

what is the MOA of niacin?

A

lipid lowering agent by inhibiting cholesterol synthesis

48
Q

name 1 AE of niacin and its tx

A

flushing, tx with ASA

49
Q

what is the MOA of promethazine?

A

phenergan is an antiemetic by inhibiting dopamine receptors

50
Q

name 1 AE of promethazine and its tx

A

AE: tardive dyskinesia; tx: diphenydramine (Benadryl)

51
Q

what is the indication and MOA of metoclopramide?

A

Reglan is a prokinetic, used to increase gut/gastric motility. MOA: inhibits dopamine Rs

52
Q

what is the MOA of ondansetron?

A

Zofran is an antiemetic that is a central-acting serotonin-R inhibitor

53
Q

what is the MOA of omeprazole

A

PPI, blocks H/K-ATPase in stomach parietal cells

54
Q

what is the MOA of cimetidine/ranitidine

A

H2-receptor (histamine) blocker, therefore reduce acid in the stomach

55
Q

what is the indication and MOA of octreotide?

A

long-acting somatostatin analogue, therefore reduce gut secretions

56
Q

name the MOA of digoxin

A

inhibits Na/K-ATPase, therefore increase myocardial calcium

57
Q

name 2 cardiac effects of digoxin

A

slows AV conduction, inotrope

58
Q

is digoxin cleared with hemodialysis?

A

nope

59
Q

why is digoxin a/w mesenteric ischemia?

A

digoxin can reduce blood flow to intestines = mesenteric ischemia

60
Q

name the electrolyte abnormality a/w digoxin & 2 resulting effects

A

digoxin –> hypokalemia –> increased cardiac sensitivity to digitalis –> can lead to arrhythmias/AV block

61
Q

name the 5 AEs a/w digoxin?

A

reduced blood flow to intestines; hypokalemia; visual changes (yellow hue); arrhythmias; fatigue

62
Q

name two indications to use amiodarone

A

acute atrial & ventricular arrhythmias

63
Q

name 3 AEs of amiodarone

A

pulmonary fibrosis with prolonged use; hypothyroidism; hyperthyroidism

64
Q

which arrhythmia can be treated with magnesium?

A

torsades de pointes (Vtach)

65
Q

what is the role of ACE-inhibitors in CHF patients

A

best single agent to increase survival in CHF patients

66
Q

what is the MOA of ACE inhibitors?

A

angiotensin-converting enzyme inhibitors

67
Q

why use ACE-inhibitors s/p MI?

A

prevents CHF s/p MI

68
Q

why are ACE inhibitors used in patients with HTN/DM?

A

prevents progression of renal dysfx in pts with HTN/DM

69
Q

why should you avoid ACE-inhibitors in patients with renal artery stenosis?

A

can precipitate renal failure

70
Q

why are beta blockers used s/p MI

A

best single agent to improve survival after MI

71
Q

why do you use beta blockers in patients with LV failure?

A

may prolong life in patients with severe LV failure

72
Q

what 2 postop complications are prevented by beta blockers

A

postop MI & Afib

73
Q

what is the MOA and effect of atropine

A

acethylcholine antagonist = increased HR

74
Q

what is the MOA and indication for metyrapone?

A

inhibits adrenal steroid synthesis; indicated for adrenocortical CA

75
Q

what is the MOA and indication for aminoglutethimide?

A

inhibits adrenal steroid synthesis; used for adrenocortical CA

76
Q

what is the pharmacologic structure of leuprolide

A

analogue of GnRH and LHRH

77
Q

what is the effect of continuous admin of leuprolide

A

paradoxic effect, inhibits release of LH/FSH from the pituitary

78
Q

which cancer is treated with leuprolide?

A

metastatic prostate CA

79
Q

what is the MOA of NSAIDs

A

inhibit prostaglandin synthesis

80
Q

name 3 ways NSAIDs increase risk of peptic ulcers

A

reduce mucus; reduce bicarb; increase acid production

81
Q

what is the MOA of misoprostol?

A

a PGE1 derivative, a protective prostaglandin

82
Q

what is misoprostol used to treat?

A

prevent peptic ulcer disease in patients on chronic NSAIDs

83
Q

what is the MOA of Haldol?

A

antipsychotic; inhibits dopamine receptors

84
Q

what is the 1 AE of Haldol and its tx

A

extrapyramidal sx; tx = Benadryl

85
Q

name of 4 S/Sx of ASA poisoning?

A

tinnitus; HA; nausea; vomiting

86
Q

what are the 1st and 2nd acid/base effects of ASA poisoning?

A

1st: respiratory alkalosis; 2nd: metabolic acidosis

87
Q

what is the MC side effect of gadolinium?

A

nausea

88
Q

what is the MC side effect of iodine contrast?

A

nausea

89
Q

what is the MC side effect of iodine contrast requiring medical treatment?

A

dyspnea

90
Q

what is the tx for tylenol overdose

A

N-acetylcysteine

Z.Fiser (22 decks)

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