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Pharm 1 > Exam 1 > Flashcards

Exam 1 Flashcards

0
Q

insulin works via?

A

receptor tyrosine kinase

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1
Q

glucocorticoids work via?

A

intracellular receptors

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2
Q

platelet growth factors work via?

A

receptor tyrosine kinases

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3
Q

nerve growth factors work via

A

receptor tyrosine kinases

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4
Q

platelet-derived growth factors work via?

A

receptor tyrosine kinases

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5
Q

kinase activity is a separate protein for?

A

cytokine receptors

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6
Q

NO is synthesized via what signaling pathway

A

cyclic GMP/guanylyl cyclase

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7
Q

decreased response because the enzymes that metabolize the drug are induced
(increased drug metabolism = decreased response)
is??

A

pharmacokinetic tolerance

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8
Q

decreased response due to change in receptor # or function is?

A

pharmacodynamic tolerance

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9
Q

what is physiologic tolerance?

A

when 2 agents w/ opposing physiologic effects are administered together

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10
Q

what is competitive tolerance

A

receptor antagonist w/ an agonist

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11
Q

what is potency

A

the dose required to produce a particular effect

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12
Q

a basic drug in an acidic medium will…?

A

become ionized & accumulate

then be eliminated

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13
Q

drugs with high first pass metabolism?

A

lidocaine, morphine

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14
Q

how does first pass metabolism influence oral availability

A

decreases

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15
Q

drugs with low first pass metabolism

A

diazepam, digitoxin

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16
Q

CNS & autonomic drugs, cardiovascular drugs target?

A

G protein coupled receptor

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17
Q

local anesthetics and anticonvulsants target?

A

voltage-gated ion channels

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18
Q

nicotine targets?

A

ligand-gated ion channel

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19
Q

benzodiazepienes target?

A

ligand gated ion channels

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20
Q

MAO inhibitors and cholinesterase inhibitors target?

A

enzymes

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21
Q

antidepressants target? (and 2 examples?)

A

transport proteins (DAT, SERT)

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22
Q

anticancer and antiviral drugs target?

A

nucleic acids

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23
Q

codeine is metabolized to what?

A

morphine (active metabolite)

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24
Q

metabolism of diazepam

A

diazepam –> nordiazepam (longer half-life) –> oxazepam

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25
Q

acetaminophen metabolite?

A

N-acetyl-p-benzoquinone imine (toxic metabolite)

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26
Q

affinity is designated by?

A

Kd

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27
Q

what reactions are the most common phase I reactions?

A

oxidation

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28
Q

whats the most common phase II reaction?

A

conjugation

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29
Q

CYP2D6 polymorphism results in

A

decreased codeine metabolism to morphine –> less analgesic effect

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30
Q

acidic mediums trap which drugs?

A

basic drugs

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31
Q

basic mediums trap which drugs?

A

acidic drugs

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32
Q

what cytochrome metabolizes > 50% of drugs?

A

CYP 3A4

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33
Q

which CYP metabolizes alcohol?

A

CYP 2E1

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34
Q

alcohol’s effect of CYP2E1 (2)

A

induction- more activity —> EtOH tolerance

induction of CYP2E1 also increases acetaminophen metabolism

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35
Q

primary enzymes in Phase I metabolism?

A

Cytochrome P 450 (CYPs)

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36
Q

two CYP-independent oxidation reactions?

A

alcohol dehydrogenase

monoamine oxidase

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37
Q

grapefruit juice inhibits what enzyme?

A

CYP450 3A4

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38
Q

Examples of substrates inhibited by grapefruit juice?

A

Acetaminophen, diazepam, lidocaine

39
Q

Quinidine inhibits what enzyme?

A

CYP 2D6

40
Q

examples of substrates inhibited by quinidine?

A

Codeine, oxycodone

41
Q

what is a common endogenous compound used in Phase II conjugation reaction?

A

glucuronic acid

42
Q

Phase II conjugation reaction w/ glucuronic acid?

A

UDP-glucuronic acid + R-OH —> glucuronic acid-R + UDP

43
Q

renal excretion is influenced by 3 factors:

A

glomerular filtration rate
active tubular secretion or reabsorption
passive diffusion across tubular epithelium
(all of these can be impacted by pathology)

44
Q

describe enterohepatic circulation

A

conjugated metabolites released into the bile are cleaved by bacterial enzymes in the SI, releasing the drug for reabsorption

45
Q

effect of enterohepatic circulation on drug half-life

and an example?

A

increases the drug’s half-life

example: estrogen in BC

46
Q

biotransformation of drugs?

A

lipid-soluble, non-ionized —> water-soluble, ionized metabolites

47
Q

large Vd signifies? re: distribution

A

extensive distribution, binds to peripheral tissues (not plasma- not bioavailable)

48
Q

small Vd signifies? re: distribution

A

drugs that are highly concentrated in the plasma

49
Q

examples of drugs with large Vd?

A

Acetaminophen, Propranolol

50
Q

examples of drugs with small Vd?

A

Heparin, Warfarin

51
Q

spare receptors effect on the concentration-response curve

A

shifted left to smaller concentrations

52
Q

competitive antagonist effect on the curve

A

dose response curve shifts to the right

53
Q

noncompetitive agonist effect on the curve

A

Emax and Bmax decrease

54
Q

partial agonist effect on curve

A

lower Bmax and Emax than the full agonist

55
Q

graded dose response curve measures?

A

response in an individual

56
Q

on a graded dose response curve, the position on the X-axis indicates

A

potency

57
Q

contraindications for gastric lavage (4)

A

more than 4 hours since ingestion of most poisons
more than 30 min since ingestion of corrosive
not used for hydrocarbon solvents
or if coma, stupor, delirium are present

58
Q

methods of increasing excretion rate to treat toxicity (4)

A

osmotic diuretics, alter urine pH, hemodialysis, hemoperfusion

59
Q

single/multiple exposure to a poison over 1-2 days

A

acute toxicity

60
Q

repeated exposures to a poison <3 mo.

A

subacute toxicity

61
Q

repeated exposures to a poison > 3 mo.

A

chronic toxicity

62
Q

nicotine toxicity mechanism

A

interference w/ receptor-ligand interactions

63
Q

local anesthetic toxicity mechanism

A

interference w/ membrane fxn

64
Q

toxicity mechanism of cyanide

A

interference w/ cellular energy fxn

65
Q

toxicity mechanism of organophosphates

A

binding to biomolecules

66
Q

toxicity mechanism of ethylene glycol

A

perturbation in calcium homeostasis

67
Q

toxicity mechanism of MPTP

A

toxicity from selective cell loss

68
Q

toxicity mechanism of carcinogens

A

non-lethal alterations in somatic cells

69
Q

toxicity mechanism of dioxins

A

interference w/ cellular transcription factors

70
Q

toxicity mechanism of Acetaminophen

A

induction of programmed cell death

71
Q

Poisoning treatments that reduce absorption or increase elimination (3)

A 
Activated charcoal
Ammonium chloride (acidifies urine- basic drugs)
Sodium bicarbonate (alkalinizes the urine- acidic drugs)
72
Q

chelator of arsenic, gold, mercury, and acute lead

A

Dimercaprol

73
Q

chelator of copper

A

Penicillamine

74
Q

chelator of iron

A

Deferoxamine

75
Q

tx for lead poisoning

A

calcium disodium edatate

76
Q

tx for acetaminophen poisoning (drug)

A

Acetylcysteine

77
Q

antidote for cholinesterase inhibitor

A

Atropine

78
Q

sx of organophosphate poisoning

A

SLUD

Salivation, Lacrimation, Urination, Defecation

79
Q

Kayser-Fleischer rings indicate?

A

copper accumulation

80
Q

competitive agonist effect on curve (2)

A

increased Kd

right shift

81
Q

noncompetitive antagonist effect on curve (2)

A

Emax and Bmax decrease

82
Q

efficacy of partial agonists?

A

lower

83
Q

Administration of agonist and allosteric activator effect the curve how?

A

same Emax, shift left

84
Q

Administration of agonist and competitive antagonist affect the curve how?

A

shift right

No Emax

85
Q

Administration of Agonist & Noncompetitive Antagonist affect the curve how?

A

No Emax

86
Q

decreased response because the enzymes that metabolize the drug are induced

A

pharmacokinetic tolerance

87
Q

examples of pharmacokinetic tolerance

A

barbiturates, EtOH, warfarin

88
Q

decreased response due to change in receptor number or function

A 
pharmacodynamic tolerance
(desensitization, receptor down-regulation)
89
Q

example of pharmacodynamic tolerance

A

B-adrenergic agonists (Albuterol)

90
Q

occurs when two agents with opposing physiologic effects are administered together

A

physiologic tolerance

91
Q

example of physiologic tolerance?

A

histamine and norepinephrine

vasodilation and vasoconstriction

92
Q

administration of receptor antagonist along with receptor agonist results in?

A

competitive tolerance

93
Q

example of competitive tolerance

A

Yohimbe & clonidine

94
Q

two methods of desensitization?

A
  1. continuous exposure to an agonist –> conversion of an ion channel to an altered, closed state
  2. receptor coupling effector is phosphorylated to an inactive form
95
Q

chronic administration of agonists can result in?

A

down-regulation = degradation of receptors

Pharm 1 (3 decks)

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