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BMS242- Physiology and Pharmacology > core pharmacology > Flashcards

core pharmacology Flashcards

1
Q

what are the 4 main classes of proteins targeted by drugs

A

receptor
enzyme
channel
transporter

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2
Q

if you increase drug concentration enough it will have an effect

A

true drugs are never completely specific

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3
Q

in terms of channels what is a modulator and what is a blocker

A

modulator - drug binds to allosteric site and changes behaviour of channel
blocker - drug binds to active site blocking channel

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4
Q

what is a pro-drug

A

a drug that needs to be metabolised in order to produce active form

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5
Q

what are the 4 receptor families and how many TMDs

A

ion channels - 4/5 TMD
GPCR - 7 TMD
kinase linked - 1 TMD
nuclear receptors - 1 TMD

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6
Q

how many phases in drug development

A

6

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7
Q

what is lead development

A

find key target of drug

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8
Q

what is preclinical development

A

safety margin
define max dose/conc
rescue treatments
obtain regulatory approval

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9
Q

exploratory studies

A

in vitro - mutagenecity testes by Ames test
arrythmia biomarker with hERG potassium ion channel
in vivo - repeat administration for 14 days

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10
Q

describe 3 phases of clinical trial

A

phase 1 - is it safe? how well is it tolerated? what are the pharacokinetic properties?
phase 2 - proof of concept? how much so its effective? how well does it work/
phase 3 - 1000+ patients

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11
Q

how many make it past clinical trial

A

11%

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12
Q

similarities in small molecule and biomolecule trials

A

1-, 3- ,6- month studies

developmental toxicity studies done

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13
Q

differences

A

small molecule shorter half life, more toxic metabolites as it can enter cell, can create mutants

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14
Q

occupancy =

A

No. of receptors occupied/No. of receptors - between 0-1

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15
Q

how do we measure occupancy

A

radioligand binding assay

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16
Q

what radioactive compound do we use

A

125I or 3H

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17
Q

stages of assay

A 
tissue prep + ligand - create cell line
mix
incubate to reach equilibrium
filter
rinse - non bound ligands
measure radioactivity
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18
Q

how can you reduce non specific binding

A

use anti-absorbant e.g. albumin/collagen

does not reduce non specific tissue binding

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19
Q

what must a radio ligand be

A

biologically active
pure
not easily degraded
labelled

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20
Q

how would you reduce degradation of ligand

A

free radical scavenger i.e. ethanol
store at low temp
avoid light
incorporate anti-oxidant such as ascorbic acid

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21
Q

advantages and disadvantages of H/I

A 
H - indistinguishable from native compound
very specific activity 
good stability when stored properly
long half life 
need specialist labs
expensive and difficult to label

I- higher specific activity if aromatic OH group added
easy and cheap
more readily degraded
short half life

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22
Q

main way of separating bound ligand from free

A

centrifugation

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23
Q

why is rate of dissociation a problem

A

if there is a low affinity then a quick separation time is needed or else all ligand will separate
very low affinity is too fact to calculate

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24
Q

how do you calculate specific binding

A

scatchard plot

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25
Q

is specific binding saturable

A

yes specific number of receptors

non specific is not

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26
Q

what is the scatchard equation

A

B/F = (Bmax - B) / Kd

27
Q

what does the langmuir equation calculate

A

relationship between occupancy, affinity and drug conc

28
Q

low Kd ? affinity

A

high

29
Q

EC50 calculates

A

potency

30
Q

efficacy measures

A

response

31
Q

what are the 5 types of antagonism

A 
chemical
pharmacokinetic
physiological
competitive
non-competitive
32
Q

chemical antagonism

A

substances chemically altered by antagonist

e.g. heavy metals inactivated when adding chelating agent

33
Q

pharmacokinetic antagonism

A
  1. reduction in amount of drug absorbed
  2. change in drug metabolism e.g. warfarin
  3. change in excretion of agonist
34
Q

physiological antagonism

A

interaction of 2 drugs with opposing effects e.g. noradreneline and histamine with BP

35
Q

non-competitive antagonism

A

doesnt compete for active site but blocks a step in pathway

36
Q

competitive antagonism

A
  1. reversible
    can be overcome e.g. atropine in response to Ach
    parallel right shift no change in max
  2. irreversibe
    cannot be reversed by adding more agonist
    decreases max response
37
Q

dose response =

A

conc of agonist with antagonist/conc of agonist

how much more agonist is needed in presence of antagonist

38
Q

what does schild analysis measure

A

antagonist affinity

39
Q

what are the major body compartments and there %

A

EC: plasma - 45%, interstitial fluid - 16%, lymph - 1-2%
IC: 30-40%
Trancellular fluid: 2.5%
Fat: 20%

40
Q

where will lipophilic drugs most likely end up

A

fat as highly lipid soluble

41
Q

BBB?

A

blood brain barrier

endothelial cells lining blood vessels in CNS form tight junctions impermeable to water soluble molecules

42
Q

when do the tight junctions become leaky

A

inflammation - allows entry of e.g. penicillin during meningitis

43
Q

what are the 2 biochemical reactions in drug metabolism

A

phase 1 catabolic reactions produce more reactive drug

phase 2 synthetic anabolic reactions produce inactive drug through conjugation

44
Q

what organ is the main site of drug metabolism and why

A

liver
contains microsomal enzymes such as P450, alcohol dehydrogenase and MAO
must be lipid soluble to cross membrane
produgs become activated
metabolism can alter or prolong pharmacological actions of drug

45
Q

routes of drug administration

A 
oral/rectal - gut
precutaneous - skin
intravenous - plasma
intramuscular - muscle
intrathecal - CSF
inhalation - lungs
46
Q

routes of drug excretion

A

urine - renal - 20% small molecules
faeces - GI - bilebound
expired air - lungs

47
Q

NSAID?

A

non steroidal anti-inflammatory drug

48
Q

what do they do

A

decrease production of inflammatory mediators e.g. prostaglandins
bronchoconstriction
promote platelet aggregation
regulate contraction of uterus
decrease sensitivity to pain by inhibiting nociceptors

49
Q

how

A

PG12 + PGE2 decrease sensation of pain

PGD2 promotes platelet aggregation

50
Q

COX1

A

ubiquitous
constitutively active - all time
maintains homeostasis
common side effects are cause by this enzyme

51
Q

COX2

A

only in inflammatory cells

induce transcription

52
Q

COX3

A

splice varient of COX1
only in CNS
paracetamol favours this one

53
Q

what do NSAIDS do

A

decrease vasodilation therefore oedema
cannot be used against pre-existive mediators
analgesic -reduce pain
antipyretic - lower temp via IL-1 inducing COX2 production of PGE

54
Q

structure of COX enxyme

A

2 subunits each with two catalytic sites

55
Q

side effects of NSAIDS

A

PGs inhibit acid excretion in gut - GI problems
PGs maintain renal blood flow - renal failure
liver damage if take too much as intermediate is hight toxic and can build up
bronchospasm in asthmatics
rashes

56
Q

symptoms of rheumatoid arthritis

A

swelling joints
pain
stiffness in morning
poor sleep

57
Q

what immunosuppressant drugs can treat RA

A

cyclosporin
glucocorticoids
they bind to proinflammatory cytokines IL-2

58
Q

what biopharmaceutical can be used

A

humanised monoclonal antibodies

neutralise proinflammatory cytokines

59
Q

what drugs treat asthma

A

bronchodilators - salbutamol

60
Q

what phases

A 
early/intermediate 
 - reversible airway obstruction 
inflammation due to increased mast cells
late phase
- cytokines 
can develop chronic asthma
61
Q

what cells are overactive in regards to asthma

A

TH2 cells

62
Q

what increases your susceptibility to asthma`

A 
genetic factors:
IgE production
environmental 
allegens 
pollutants
63
Q

new therapies for treating asthma

A

humanised monoclonal antibodies

PGD2-R antagonists (small molecules)

BMS242- Physiology and Pharmacology (2 decks)

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