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PED1003 pharmacology > intro L1-8 > Flashcards

intro L1-8 Flashcards

1
Q

pharmacodynamics

A

effect of drug on body

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2
Q

pharmacokinetics

A

effect of body on drug

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3
Q

pharmacokinetics factors

A

adsorption
distribution
metabolism
excretion

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4
Q

antihistimine action

A

cross blood-brain barrier into CNS, antagonizing H1 receptors and blocking histimine

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5
Q

antihistimine class

A

reversible competitive inhibitors, therefore can be overridden

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6
Q

drug-interaction factors

A

shape
charge distribution
hydrophobicity
ionisation of drug
conformation of target
stereochemistry of drug molecule

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7
Q

drug action targets

A

receptors
ion channels
enzymes
carrier molecules

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8
Q

drugs acting via physico-chemical properties

A

antacids
laxatives
antidotes

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9
Q

agonist

A

drug mimicking endogenous chemical messengers, eliciting a cellular response

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10
Q

antagonist

A

drug blocking chemical messengers

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11
Q

NSAID’s

A

non-steroidal anti-inflammatory drugs

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12
Q

Benzodiazepine action

A

bind to GABAa at B-2 binding site

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13
Q

signal receptor transduction

A

receptor binds agonist
altered physical/ biochemical properties of receptor

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14
Q

4 drug-responding receptor types

A

ligand-gated ion
G-protein coupled
enzyme-linked
intracellular

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15
Q

nicotinic ACh receptors

A

at skeletal muscle
antagonists used as muscle relaxants

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16
Q

heterotrimeric G-proteins

A

coupled to effectors producing 2nd messengers

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17
Q

Gi

A

inhibits adenlyl cyclase

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18
Q

Gq

A

activates phospholipase C

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19
Q

Gs

A

activates adenlyl cyclase

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20
Q

kinase-linked receptor

A

ligand-binding extracellular domain attached to intracellular by single span membrane helix
ligand binding> dimerisation> auto-phosphorylation

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21
Q

insulin receptorq

A

tyrosine kinase activity in beta sub unit increase> autophosphorylating and promoting other kinase phosphorylation

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22
Q

action of nuclear intracellular receptor

A

enters nucleus and binds to receptor for txn
CLASS II
e.g. heterodimers and lipid ligands

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23
Q

CLASS I intracellular receptors

A

in cytoplasm
e.g. homodimers and endocrine

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24
Q

graded dose-response curve

A

response of a particular system

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25
Q

quantal dose-response curve

A

drug dose for a specified response

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26
Q

functions of dose-response curve

A

allow estimation of Emax/ EC50
efficacy/ potency determination

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27
Q

affinity

A

strength w which agonist/ drug binds to receptor
tendency of ligand to form stable complex w receptor

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28
Q

K1

A

rate of receptor against association

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29
Q

K-1

A

rate of AR complex dissociation

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30
Q

affinity formula

A

K1/K-1
association rate/ complex dissociation rate

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31
Q

Bmax

A

max number of binding sites

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32
Q

Kd

A

equilibrium dissociation constant
concentration of ligand when 50% of receptors occupied
(lower=higher affin)

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33
Q

Kd functions

A

receptor identification
quantitative comparison of drug affinity

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34
Q

affinity factors

A

no./nature of bonds
level of fit
Kd

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35
Q

potency

A

amount of drug required to
produce given effect

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36
Q

potency factors

A

affinity
efficacy
receptor density
affinity of stimulus-response mechanisms used

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37
Q

when is Kd = EC50

A

if occupation and bio effect is linear

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38
Q

receptor property meaning only fractional occupancy is required for max effect

A

receptors can amplify signal duration and intensity

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39
Q

efficacy

A

ability of an agonist to activate a receptor

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40
Q

efficacy determination

A

max effect agonist can produce regardless of dose
nature of receptor-effector system

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41
Q

full agonist

A

high efficacy
max response w partial occupancy

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42
Q

partial agonist

A

max response not available even with full occupancy

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43
Q

inverse agonist

A

higher affinity for AR state than AR*

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44
Q

positive allosteric modulators

A

not active alone
high affin/ efficacy of endogenous agonist

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45
Q

negative allosteric modulators

A

not active alone
low affin/ efficacy of endogenous agonist

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46
Q

receptor desensitization

A

effect reduction with continual/ repeated administration

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47
Q

factors of receptor desensitization

A

conformational changes in receptor
receptor internalization
mediator depletion
altered drug metabolism
other physio responses

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48
Q

types of antagonist

A

chemical
physiological
pharmacological

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49
Q

chemical antagonist

A

binding of 2 agents rendering inactivity of drug
cholating agent

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50
Q

physiological antagonist

A

2 agents with opposite effects cancelling each other out

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51
Q

pharmacological antagonist

A

receptor binding blocking action

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52
Q

types of pharmacological antagonist

A

competitive
irreversible
non-competitive

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53
Q

competitive pharmacological

A

binds and prevents
overcome w ^ agonist conc
right parallel shifyt
common

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54
Q

irreversible pharmacological

A

covalent irreversible binding
parallel right shift and decreasing asymptote
less common

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55
Q

non-competitive pharmacological

A

allosteric blocking downstream effects
decreasing slope and max dose-response curve

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56
Q

dose ratio formulae

A

(agonist + antagonist EC50)/ agonist EC50

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57
Q

Schild equation

A

dose ratio -1 = antagonist conc/ antagonist dissociation constant

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58
Q

pA2 values

A

describe receptor antagonist activity

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59
Q

pA2 formula

A

-logKb
*only if linear relationship and schild plot =1

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60
Q

therapeutic window index

A

defines dose range between therapeutic and toxic effects

61
Q

types of drug movement

A

bulk flow (e.g. blood stream/ lymphatics.)
barrier diffusion (e.g. blood-brain barrier gastrointestinal mucosa…)

62
Q

drug administration routes (quickest first)

A

IV
oral
dermal

63
Q

IV event

A

rapid action
high dose control
drug poorly absorbed otherwise

64
Q

types of injection

A

IV
Intramuscular
subcutaneous

65
Q

what does rate of injection diffusion depend on

A

tissue diffusion
blood flow removal

66
Q

stomach conditions for drugs

A

low pH
pH partitioning as drugs ionize

67
Q

small intestine conditions for drugs

A

large sa
v permeable
large blood supply
enterocytes have metablic enzymes/ transporters for uptake and efflux

68
Q

enterohepatic recirculation

A

moves through gut
blood absorption
hepatic portal vein entrance
liver transport
gall bladder transport

69
Q

sublingual GI routes

A

network of capillaries under tongue, drug bypasses 1st pass metabolism straight into bloodstream

70
Q

rectal GI route

A

local effects
avoids 2/3 1st pass metabolism
:(unreliable

71
Q

examples when rectal GI should be used

A

opioid withdrawal
travel sickness
status epilepticus in children

72
Q

parenteral routes

A

inhalation
topical drugs
cornea
nasal mucosa
vaginal
transdermal

73
Q

inhalation GI route

A

skips 1st pass
rapid action

74
Q

factors affecting drug absorption

A

metabolism
pKa
drug molecule size
membrane permeability
skin hydration
lipid solubility
stratum corneum reservoir

75
Q

ionized form of drug vs unionized

A

not lipid-soluble
vs lipid-soluble

76
Q

oral absorption factors

A

gastric motility
food splanchnic blood flow
particle size
capsules

77
Q

Cmax

A

max conc of drug after dosing

78
Q

Tmax

A

time taken to reach Cmax

79
Q

bioavailability

A

fraction of drug administered absorbed and available to have effect

80
Q

factors of drug distribution

A

perfusion
cell membrane crossing
protein binding ability

81
Q

albumin

A

binds mostly acidic and some basic drugs

82
Q

AAG

A

A1 acid glycoprotein
binds basic drugs
^ inflam effects

83
Q

bioavailiability factors

A

free drug available
affinity
protein conc

84
Q

Vd

A

volume of fluid required to contain total amount of drug in body Q at same conc present in plasma

85
Q

Vd formulae

A

Q/Cp

86
Q

why do drugs need to be metabolized

A

lipophilic drugs not eliminated by kidney and therefore need further metabolism to more polar/ water-soluble products prior to excretion

87
Q

metabolism phase 1

A

enzymatic reactions exposing/introducing functional groups (e.g. hydroxyl/ amino/ sulphydryl/ carboxyl)
decreasing lipid solubility and ^ pharmcological activity

88
Q

hydroxylation

A

conversion of hydrogen to hydroxyl

89
Q

deamination

A

conversion of an amino group to a carbonyl group

90
Q

dehydrogenisation

A

conversion of a hydroxyl group to a carbonyl group

91
Q

xenobiotic metabolism behaviour

A

undergo oxidation

92
Q

CYP450

A

embedded inSER
combine w pink compound to produce pink compound

93
Q

variations in P450

A

species differences
genetic polymorphisms
drugs
environmental factors

94
Q

butrylcholinesterase

A

hydrolyzes suxamethonium, overactivating cholinergic receptors on muscles, causing paralysis

95
Q

alcohol dehydrogenase

A

hepatocyte cytoplasm oxidation of ethanol to acetaldehyde
requires NAD+

96
Q

aspirin esterase

A

aspirin hydrolysis to salicylate
found in plasma

97
Q

metabolism phase 2

A

conjugation occurs in liver/ kidney/ lung
further decrease in lipid solubility

98
Q

functionalisation

A

reactive group introduction
products more reactive/ toxic

99
Q

total clearance

A

vol of plasma/ blood cleared of drug per unit time to achieve overall elimination of drug from body

100
Q

Kel

A

elimination rate constant
fraction of drug eliminated per unit time at any point

101
Q

Kel formula

A

total clearance / volume of distribution

102
Q

glucaronidation

A

UDP-glucaronyl transferase (broad substrate specificity mediation)
glucaronides pharamcologically inactive and excreted

103
Q

therapeutic paracetamol metabolism

A

conjugation w sulphate and glucoronic acid
minor proportion metabolized by CYP450 to toxic metabolite

104
Q

paracetamol overdose

A

saturated conjugation pathways and toxic metabolite reacts w liver proteions not depleted glutathione
tissue damage occurs and hepatic necrosis

105
Q

exogenous drug metabolism factors

A

drugs
smoking/ alcohol
environmental

106
Q

endogenous drug metabolism factors

A

genetics
age
disease

107
Q

fast metabolizer genetic constitution

A

normal enzyme activity
decreasing plasma conc
^metabolite conc
normal therapeutic response

108
Q

slow metabolizer genetic constitution

A

decreasing enzyme activity
^ plasma conc
decreasing metabolite conc
exaggerated therapeutic response

109
Q

pharmacogenomic factors

A

decreasing CYP w age
half-life variability

110
Q

drug induction
examples?

A

^ synthesis of enzymes
^ metabolism of inducing agent
e.g. smoking/ ethanol

111
Q

3 processes of renal excretion

A

glomerular filtration
tubular reabsorption
tubular secretion

112
Q

water-soluble drug excretion

A

unchanged passed through kidneys

113
Q

lipid-soluble excretion

A

glomerular filtration, tubular reabsorption, metabolism to more polar, urine excretion

114
Q

do lipid solubility and pH affect glomerular filtration?

A

no

115
Q

entry rate factors

A

molecular weight
conc of free drug in plasma

116
Q

2 drug carrier systems to tubular lumen against echem gradient

A

acidic drugs
organic bases (most effective)

117
Q

lipid-soluble drug effect on tubular reabsorption

A

^tubular permeability and slow excretion

118
Q

water-soluble effect on tubular reabsorption

A

decreasing tubular permeability and decreasing urine concentration

119
Q

tubular reabsorption factors

A

drug lipid-solubility
tubular fluid pH > affects ionization

120
Q

what happens when solution pH = drug pKa

A

50% drug ionized

121
Q

pH partitioning

A

acidic drugs accumulating in basic fluid compartments and vice versa

122
Q

weak acid ionization max

A

at alkaline pH
* therefore more rapidly excreted in opposing pH urine

123
Q

weak alkaline ionization max

A

at acid pH
* therefore more rapidly excreted in opposing pH urine

124
Q

pharmacokinetic parameters

A

bioavailability
distribution volume
elimination half-life
clearance

125
Q

one-compartment model

A

simplified model demonstrating human as single, well-stirred compartment

126
Q

kinetic order

A

relates plasma conc of a drug and rate of elimination from the body

127
Q

1st order

A

rate of drug decrease dependent on plasma conc
rate-limiting factor= drug concentration

128
Q

2 comppartment model

A

drugs only enter body tissues via plasma (peripheral/ central comp)

129
Q

0 order

A

drug decrease independent of plasma conc
constant rate due to limiting factor

130
Q

Vd

A

volume of distribution
used to calculate drug dose / loading

131
Q

Vd formula

A

dose/ C0

132
Q

Vd effect on plasma concentration

A

inverse

133
Q

4 phases of uk drug development

A

target discovery
lead identification
lead optimization
clinical candidate

134
Q

high throughput screening

A

global protein profiling, protein-protein interaction

135
Q

structure activity relationships

A

predicting biological activity from molecular structures

136
Q

chemoproteomics

A

selectivity/ drug affinity profiling

137
Q

GLP

A

Good lab practice
managerial quality control system

138
Q

FDA modernisation act 2.0

A

no longer requires all drugs to be tested on animals before human trials

139
Q

2 regulation authorities in UK

A

MHRA
European medicines agency

140
Q

drug manufacturing authorization stages

A

product identification]
product maufacture
pre clinical data
clinical results

141
Q

therapeutic trial

A

ethically designed experiment addressingrecisely-framed questions

142
Q

trial question framework

A

treatment
prevention
diagnostic
QOL

143
Q

factors affecting reliability

A

bias
controls
blinding

144
Q

placebo effect causes

A

natural remission
regression to mean
classical conditioning
‘nocebo effect’ neurochemistry

145
Q

clinical trial endpoint measures

A

clinical measures (liver/ kidney function, blood/urine chemistry/ eye testing)
PK measures (e.g. Cmax, Tmax, bioavailability)
PD measures (e.g. target affinity/ biomarkers)

146
Q

phase 1 trials

A

establishes:
PK/PD properties of drug
toxicological properties
* roughly 1 year

147
Q

phase 2 trials

A

establishes:
- pharmacodynamics
- clinical effectiveness
- dose ranging

148
Q

phase 3 trials

A

establishes:
efficacy
safety
comparison to other therapeutic alternatives

PED1003 pharmacology (6 decks)

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