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

Pharmacology: kinetics/dynamics + some drugs Flashcards

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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
urine clears ionized or neutral forms
ionized neutral ones reabsorbed
26
weak acids - trapped where? - examples - treat overdose with?
- 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
27
weak bases - trapped where - examples - treat overdose with?
- acidic environments - amphetamines - ammonium chloride to add proton to base and make it ionic so it stays in urine for excretion
28
phase I drug metabolism - steps - who loses it - what does it yield
- Reduction - Oxidation - Hydrolysis ------------------------------- with Cyt P-450 - geriatrics lose phase I - usu yields slightly polar, water-soluble metabolites (often still active)
29
phase II drug metabolism - steps - what does it yield
- 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
30
efficacy vs. potency
- efficacy: maximal EFFECT a drug can produce | - potency: AMOUNT needed for given effect
31
high efficacy drugs classes (4)
1. analgesia meds 2. abx 3. anti-histamine 4. decongestant
32
highly potent drug classes (3)
1. chemo 2. anti-htn 3. lipid-lowering
33
reversible competitive antagonist for Diazepam | - which receptor
flumazenil on GABA rec
34
noncomp antagonist for glutamate | - which receptor
ketamine on NMDA rec
35
irreversible competitive antag for NE | - which receptor
phenoxybenzamine on alpha-receptors
36
partial agonist for morphine | - which receptor
buprenorphine on opioid mew-rec
37
which affects potency and which affects efficacy
- 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
Therapeutic index equation safer drugs have higher or lower TI?
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
examples of low TI drugs
digoxin lithium theophylline warfarin
40
parasympathetic NS - pre-/post-ganglionic NTs and the receptors - exceptions - what cells are targets
- Pre releases Ach onto nAchR of post - Post releases Ach onto mAchR of targets - no exceptions - cardiac muscle, smooth muscle, glands, nerve terminals
41
sympathetic NS - pre/postG NTs and receptors - exceptions - what cells are targets
- 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
botulinum blocks what
release of Ach at all terminals
43
how many muscarinic AchRs?
5, M1-5
44
examples of GPCR's (13)
- 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
alpha-1 = which GPCR
Gq
46
alpha-2 = which GPCR
Gi
47
beta-1 = which GPCR
Gs
48
beta-2 = which GPCR
Gs
49
M1 = which GPCR
Gq
50
M2 = which GPCR
Gi
51
M3 = which GPCR
Gq
52
D1 = which GPCR
Gs
53
D2 = which GPCR
Gi
54
H1 = which GPCR
Gq
55
H2 = which GPCR
Gs
56
V1 = which GPCR
Gq
57
V2 = which GPCR
Gs
58
summary of GPCR from adrenergic, muscarinic, dopa, hista, vaso
QISS, QIQ, SI, QS, QS kiss quick, yes, ks, ks
59
Gq's
alpha-1, M1, M3, H1, V1
60
Gs's
beta-1, beta-2, D1, H2, V2
61
Gi's
alpha-2, M2, D2
62
actions of alpha-1
- vascular smooth muscle contraction - pupillary dilator muscle contraction (mydriasis) - intestinal and bladder sphincted muscle Gq, so muscle contractions
63
actions of alpha-2
- decreased sympathetic outflow - decreased insulin release - decrease lipolysis - decreased blood flow (increased plt aggregation) Gi, so decreases stuff
64
actions of beta-1
- increased HR - increased contractility - increased renin - increased lipolysis Gs, so increases stuff
65
actions of beta-2
- 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
actions of M1
CNS and enteric NS Gq
67
actions of M2
decrease HR and atria contractility Gi, so decreases stuff
68
actions of M3
- 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
actions of D1
relaxes renal vascular smooth muscle
70
actions of D2
modulates NT release, esp in brain
71
actions of H1
- increase nasal and bronchial mucus production - increase vascular permeatbility - contraction of bronchioles - pruritus - pain
72
actions of H2
- increases gastric acid secretion by parietal cells
73
actions of V1
- increase vascular smooth muscle contraction Gq, so muscle contraction
74
actions of V2
- increase water permeability and reabsorption in collecting tubules Gs, so increases stuff (2 b/c 2 kidneys)
75
What happens to NE once it gets into the synaptic space (3) things
1. diffusion, metabolism 2. immediate reuptake via transporter 3. negative feedback by action on pre-syn alpha-2
76
choline transporter inhibitor
Hemicholinium
77
Ach vesicule loading inhibitor
Ves.ami.col
78
Ach release inhibitor
botulinum
79
Tyrosine hydroxylase inhibitor
Metyrosine
80
Dopamine vesicle loading inhibitor
Reserpine
81
vesciular NE release inhibitor
Bretylium | Guanethidine
82
vesicular NE release stimulator
amphetamines
83
NE reuptake inhibitor
coke, TCA, amphetamines
84
Cholinomimetic agents (4)
Bethanechol Cabachol Pilocarpine Metacholine

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