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Step 1 Andre > Pharmacology: kinetics/dynamics + some drugs > Flashcards

Pharmacology: kinetics/dynamics + some drugs Flashcards

1
Q

Enzyme kinetics

- 3 types and their axes and their shapes

A
  1. Michaelis-Menten: Velocity vs. [Substrate] - hyperbole
  2. Lineweaver-Burk: 1/V vs. 1/[S] - linear
  3. Enzyme inhibition: 1/V vs. 1/[S] - linear
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2
Q

Km and affinity

A

inversely related to affinity of enzyme for substrate

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3
Q

Vmax and enzyme concentration

A

Vmax directly proportional to enzyme concentration

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4
Q

sigmoid curve indicative of what?

A

cooperative kinetics, like Hb

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5
Q

Kinds of enzyme inhibitors (3)

A

reversible competitive
irreversible competitive
noncompetitive

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6
Q

which ones bind to active sites

A

the competitive ones

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7
Q

how does Vmax change with inhibitors

A

unchanged with reversible competitive

you need less enzyme for irreversible and noncompetitive inhibition b/c less substrates to act at

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8
Q

how does Km change with inhibitors

A

increased with reversible competitive b/c that’s how reversible compt acts, by being more affinitive for substrate
unchanged for irreversible and noncompetitive inhibition

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9
Q

how does pharmacodynamics change with inhibitors

A

reversible: decreased potency
irreversible: decreased efficacy
noncompetitive: decreased efficacy

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10
Q

Pharmacokinetics: what is it

A

what the body does with drugs

absorb, distribute, metabolize, excrete

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11
Q

Pharmacodynamics: what is it

A

how the body is affected by drugs

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12
Q

Bioavailability

  • IV
  • PO
A

fraction of unchanged drug in systemic circulation

  • IV: 100%
  • PO: < 100% 2/2 incomplete absorption and first-pass metabolism
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13
Q

Vd (volume of distribution)

A

amount of drug in body / plasma drug concentration

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14
Q

where is it low Vd
medium Vd
high Vd?

A

low: blood
medium: ECF
high: all tissues, including fat

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15
Q

half life

A

t = (0.693 x Vd) / CL

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16
Q

how many half-lives does it take at costant infusion to ready steady state

A

4-5

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17
Q

Clearance (CL)

  • what is it
  • equation
  • what can affect it
A
  • volume of plasma cleared of drug per unit time
  • CL = Vd x Ke (elimination constant)
  • CL = (rate of elimination) / (plasma drug concentration)
  • renal, hepatic, or cardiac f(x)
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18
Q

Loading dose calculation

A

(Cp x Vd) / F

Cp = target plasma concentration at steady state
F= dosing frequency
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19
Q

Maintenance dose calculation

A

(Cp x CL x tau) / F

tau = dosage interval

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20
Q

Time to reach steady state dependent on?

A

only half life

independent of dose and dosing frequency

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21
Q

zero-order elimination

A

constant amount of drug eliminated per time

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22
Q

examples of zero-order elimination meds

A

Phenytoin
Ethanol
ASA

PEA is round, like 0

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23
Q

first-order elimination

A

rate directly proportional to drug present
constant proportion of drug eliminated per time
exponential curve

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24
Q

what is each elimination process “limited/dependent on?

A

zero-order is capacity limited

first-order s flow-dependent

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25
Q

urine clears ionized or neutral forms

A

ionized

neutral ones reabsorbed

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26
Q

weak acids

  • trapped where?
  • examples
  • treat overdose with?
A
  • basic environments
  • Phenobarbital, MTX, ASA
  • bicarbonate to pull off the proton from the toxin and make it ionic so it stays in urine for excretion
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27
Q

weak bases

  • trapped where
  • examples
  • treat overdose with?
A
  • acidic environments
  • amphetamines
  • ammonium chloride to add proton to base and make it ionic so it stays in urine for excretion
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28
Q

phase I drug metabolism

  • steps
  • who loses it
  • what does it yield
A
  • Reduction
  • Oxidation
  • ## Hydrolysiswith Cyt P-450
  • geriatrics lose phase I
  • usu yields slightly polar, water-soluble metabolites (often still active)
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29
Q

phase II drug metabolism

  • steps
  • what does it yield
A
  • Conjugation:
    1. Glucoronidation
    2. Acetylation
    3. Sulfation
  • usu yields very polar, inactive metabolites that are renally excreted
  • geriatrics still have this phase of drug metabolism
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30
Q

efficacy vs. potency

A
  • efficacy: maximal EFFECT a drug can produce

- potency: AMOUNT needed for given effect

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31
Q

high efficacy drugs classes (4)

A
  1. analgesia meds
  2. abx
  3. anti-histamine
  4. decongestant
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32
Q

highly potent drug classes (3)

A
  1. chemo
  2. anti-htn
  3. lipid-lowering
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33
Q

reversible competitive antagonist for Diazepam

- which receptor

A

flumazenil on GABA rec

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34
Q

noncomp antagonist for glutamate

- which receptor

A

ketamine on NMDA rec

35
Q

irreversible competitive antag for NE

- which receptor

A

phenoxybenzamine on alpha-receptors

36
Q

partial agonist for morphine

- which receptor

A

buprenorphine on opioid mew-rec

37
Q

which affects potency and which affects efficacy

A
  • reversible competitive antagonists affect potency b/c you can overcome the competition by adding more substrate
  • irreversible competitive antagonists and noncompetitive antagonists affect efficacy b/c no matter how much more you put in, you can’t get the same effect
38
Q

Therapeutic index equation

safer drugs have higher or lower TI?

A

TD50 / ED 50

TD50 = median toxic dose
ED50 = median effective dose

safer drugs have higher TI b/c greater difference b/w toxic and effective dose

39
Q

examples of low TI drugs

A

digoxin
lithium
theophylline
warfarin

40
Q

parasympathetic NS

  • pre-/post-ganglionic NTs and the receptors
  • exceptions
  • what cells are targets
A
  • Pre releases Ach onto nAchR of post
  • Post releases Ach onto mAchR of targets
  • no exceptions
  • cardiac muscle, smooth muscle, glands, nerve terminals
41
Q

sympathetic NS

  • pre/postG NTs and receptors
  • exceptions
  • what cells are targets
A
  • Pre releases Ach onto nAchR of post
  • Post releases NE to alpha and betas
    UNLESS
  • Post releases D to D1 recetors
  • Post release Ach to mAchR at sweat glands
  • Adrenal medulla receives only Ach onto nAchR from preG and itself releases Epi, NE
  • NE targets: cardiac muscle, smooth muscle, glands, nerve terminals
  • D targets: renal vasculature, smooth muscle
42
Q

botulinum blocks what

A

release of Ach at all terminals

43
Q

how many muscarinic AchRs?

44
Q

examples of GPCR’s (13)

A
  • adrenergics: alpha-1 and 2 + beta-1 and 2
  • muscarinics: M1-3
  • Dopamine: D1 and 2
  • Histamine: H1 and 2
  • Vasopressin: V1 and 2
45
Q

alpha-1 = which GPCR

46
Q

alpha-2 = which GPCR

47
Q

beta-1 = which GPCR

48
Q

beta-2 = which GPCR

49
Q

M1 = which GPCR

50
Q

M2 = which GPCR

51
Q

M3 = which GPCR

52
Q

D1 = which GPCR

53
Q

D2 = which GPCR

54
Q

H1 = which GPCR

55
Q

H2 = which GPCR

56
Q

V1 = which GPCR

57
Q

V2 = which GPCR

58
Q

summary of GPCR from adrenergic, muscarinic, dopa, hista, vaso

A

QISS, QIQ, SI, QS, QS

kiss quick, yes, ks, ks

59
Q

Gq’s

A

alpha-1, M1, M3, H1, V1

60
Q

Gs’s

A

beta-1, beta-2, D1, H2, V2

61
Q

Gi’s

A

alpha-2, M2, D2

62
Q

actions of alpha-1

A
  • vascular smooth muscle contraction
  • pupillary dilator muscle contraction (mydriasis)
  • intestinal and bladder sphincted muscle

Gq, so muscle contractions

63
Q

actions of alpha-2

A
  • decreased sympathetic outflow
  • decreased insulin release
  • decrease lipolysis
  • decreased blood flow (increased plt aggregation)

Gi, so decreases stuff

64
Q

actions of beta-1

A
  • increased HR
  • increased contractility
  • increased renin
  • increased lipolysis

Gs, so increases stuff

65
Q

actions of beta-2

A
  • increases blood flow (vascodilation)
  • increases breathing (bronchodilation)
  • increases HR
  • increases contractility
  • increases lipolysis
  • increases insulin release
  • increases aqueous humor production
  • ciliary muscle relaxation - impedes aqueous humor flow … creates pressure in eye for functioning?
  • decrease uterine tone … don’t want to be delivering in fight-flight situation

Gs, so increases stuff beta-2, so increases more stuff than beta-1

66
Q

actions of M1

A

CNS and enteric NS

Gq

67
Q

actions of M2

A

decrease HR and atria contractility

Gi, so decreases stuff

68
Q

actions of M3

A
  • increase exocrine gland secretions w/muscle contractions
  • increase gut peristalsis w/muscle contractions
  • increase bladder muscle contraction
  • increase bronchomuscle contraction (bronchoconstriction)
  • increase pupillary sphincter muscle contraction (miosis)
  • increases ciliary muscle contraction (accomodation and allows flow of aqueous humor)

Gq, so muscle contractions

69
Q

actions of D1

A

relaxes renal vascular smooth muscle

70
Q

actions of D2

A

modulates NT release, esp in brain

71
Q

actions of H1

A
  • increase nasal and bronchial mucus production
  • increase vascular permeatbility
  • contraction of bronchioles
  • pruritus
  • pain
72
Q

actions of H2

A
  • increases gastric acid secretion by parietal cells
73
Q

actions of V1

A
  • increase vascular smooth muscle contraction

Gq, so muscle contraction

74
Q

actions of V2

A
  • increase water permeability and reabsorption in collecting tubules

Gs, so increases stuff (2 b/c 2 kidneys)

75
Q

What happens to NE once it gets into the synaptic space (3) things

A
  1. diffusion, metabolism
  2. immediate reuptake via transporter
  3. negative feedback by action on pre-syn alpha-2
76
Q

choline transporter inhibitor

A

Hemicholinium

77
Q

Ach vesicule loading inhibitor

A

Ves.ami.col

78
Q

Ach release inhibitor

79
Q

Tyrosine hydroxylase inhibitor

A

Metyrosine

80
Q

Dopamine vesicle loading inhibitor

81
Q

vesciular NE release inhibitor

A

Bretylium

Guanethidine

82
Q

vesicular NE release stimulator

A

amphetamines

83
Q

NE reuptake inhibitor

A

coke, TCA, amphetamines

84
Q

Cholinomimetic agents (4)

A

Bethanechol
Cabachol
Pilocarpine
Metacholine

Step 1 Andre (42 decks)

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