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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
is specific binding saturable
yes specific number of receptors | non specific is not
26
what is the scatchard equation
B/F = (Bmax - B) / Kd
27
what does the langmuir equation calculate
relationship between occupancy, affinity and drug conc
28
low Kd ? affinity
high
29
EC50 calculates
potency
30
efficacy measures
response
31
what are the 5 types of antagonism
``` chemical pharmacokinetic physiological competitive non-competitive ```
32
chemical antagonism
substances chemically altered by antagonist | e.g. heavy metals inactivated when adding chelating agent
33
pharmacokinetic antagonism
1. reduction in amount of drug absorbed 2. change in drug metabolism e.g. warfarin 3. change in excretion of agonist
34
physiological antagonism
interaction of 2 drugs with opposing effects e.g. noradreneline and histamine with BP
35
non-competitive antagonism
doesnt compete for active site but blocks a step in pathway
36
competitive antagonism
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
dose response =
conc of agonist with antagonist/conc of agonist | how much more agonist is needed in presence of antagonist
38
what does schild analysis measure
antagonist affinity
39
what are the major body compartments and there %
EC: plasma - 45%, interstitial fluid - 16%, lymph - 1-2% IC: 30-40% Trancellular fluid: 2.5% Fat: 20%
40
where will lipophilic drugs most likely end up
fat as highly lipid soluble
41
BBB?
blood brain barrier | endothelial cells lining blood vessels in CNS form tight junctions impermeable to water soluble molecules
42
when do the tight junctions become leaky
inflammation - allows entry of e.g. penicillin during meningitis
43
what are the 2 biochemical reactions in drug metabolism
phase 1 catabolic reactions produce more reactive drug | phase 2 synthetic anabolic reactions produce inactive drug through conjugation
44
what organ is the main site of drug metabolism and why
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
routes of drug administration
``` oral/rectal - gut precutaneous - skin intravenous - plasma intramuscular - muscle intrathecal - CSF inhalation - lungs ```
46
routes of drug excretion
urine - renal - 20% small molecules faeces - GI - bilebound expired air - lungs
47
NSAID?
non steroidal anti-inflammatory drug
48
what do they do
decrease production of inflammatory mediators e.g. prostaglandins bronchoconstriction promote platelet aggregation regulate contraction of uterus decrease sensitivity to pain by inhibiting nociceptors
49
how
PG12 + PGE2 decrease sensation of pain | PGD2 promotes platelet aggregation
50
COX1
ubiquitous constitutively active - all time maintains homeostasis common side effects are cause by this enzyme
51
COX2
only in inflammatory cells | induce transcription
52
COX3
splice varient of COX1 only in CNS paracetamol favours this one
53
what do NSAIDS do
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
structure of COX enxyme
2 subunits each with two catalytic sites
55
side effects of NSAIDS
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
symptoms of rheumatoid arthritis
swelling joints pain stiffness in morning poor sleep
57
what immunosuppressant drugs can treat RA
cyclosporin glucocorticoids they bind to proinflammatory cytokines IL-2
58
what biopharmaceutical can be used
humanised monoclonal antibodies | neutralise proinflammatory cytokines
59
what drugs treat asthma
bronchodilators - salbutamol
60
what phases
``` early/intermediate - reversible airway obstruction inflammation due to increased mast cells late phase - cytokines can develop chronic asthma ```
61
what cells are overactive in regards to asthma
TH2 cells
62
what increases your susceptibility to asthma`
``` genetic factors: IgE production environmental allegens pollutants ```
63
new therapies for treating asthma
humanised monoclonal antibodies | PGD2-R antagonists (small molecules)

BMS242- Physiology and Pharmacology (2 decks)

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