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Physiology 2 > pharmacodynamics > Flashcards

pharmacodynamics Flashcards

1
Q

what are the 3 different types of naming for drugs?

A

chemical
generic
trade

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2
Q

drugs can be…

A

naturally occurring or synthetic

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3
Q

how do drugs work generally?

A

mimic or block the action of our own signalling molecules

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4
Q

what are the targets of drug action?

A

proteins - enzymes, transporters, ion channels and receptors
DNA

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5
Q

what are the receptor families?

A

ligand-gated ion channels
G protein coupled receptors (metabotropic)
kinase-linked receptors
nuclear receptors

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6
Q

how do kinase linked receptors work?

A

receptor > protein phosphorylation > gene transcription > protein synthesis > cellular effects

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7
Q

how do nuclear receptors work?

A

receptor in nucleus > binds to receptor > gene transcription > protein synthesis > cellular effects

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8
Q

specificity

A

drugs bind selectively to particular receptor types

no drug is 100% specific, only selective and bind to one receptor preferentially over another

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9
Q

What do agonist drugs do?

A

activate receptors

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10
Q

what do antagonist drugs do?

A

block receptors, often inhibit endogenous agonist action

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11
Q

how do agonist drugs work?

A

2 phases

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12
Q

what are the phases of agonist drugs

A
  1. drug binding/ affinity

2. receptor activation/ efficacy

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13
Q

Drug binding/ affinity

A

agonist/ drug binds to receptor forming a drug- receptor complex

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14
Q

receptor activation/ efficacy

A

activated D-R complex causes the biological effect

e.g. opens channel

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15
Q

what are the different agonist types?

A

full
partial
super
inverse

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16
Q

full agonists

A

cause 100% effect of the endogenous agonist

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17
Q

partial agonists

A

cause less than 100% of endogenous effect

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18
Q

super agonists

A

rarer

cause more than 100% of the endogenous effect

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19
Q

inverse agonists

A

reduce the basal receptor activity, by causing them to be inactive and so they cannot elicit a response

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20
Q

drug effect

A

is proportional to drug concentration

both agonists and antagonists elicit effects

21
Q

agonist drug potency

A

involves affinity and efficacy

22
Q

What is EC50

A

the concentration required to bring about a 50% response

23
Q

potency curve

A

further to the left on a % effect vs log[drug] conc. = more potent

24
Q

what is the target for botox?

A

glycoprotein, at presynaptic vesicle release of ACh

25
Q

how does Galpha q work?

A

activates Phospolipase C which produces DAG and IP3, activates Calcium release and Protein kinase C > vasoconstriction and smooth muscle contraction

26
Q

how do antagonist drugs work?

A

bind to receptor and form drug-receptor complex which makes the receptor inactive and prevents endogenous agonist binding causing the biological effect

27
Q

antagonist potency

A

only involves affinity not efficacy, as it blocks the receptor

28
Q

different types of antagonist

A

reversible/ irreversible
competitive
non-competitive
uncompetitive

29
Q

are competitive antagonists reversible or irreversible?

A

reversible

30
Q

what are uncompetitive antagonists?

A

requires agonist binding before it can bind to allosteric site of receptor/ enzyme. It then lessens the effect elicited by the substrate

31
Q

what are the non-receptor antagonists?

A

chemical antagonists
physiological antagonists
pharmacokinetic - influence the 4 processes

32
Q

what are chemical antagonists?

A

reduce concentration of agonist by binding

33
Q

occupancy and response

A

often not all receptors need to be occupied for maximum effect to be achieved - spare/ reserve receptors. Therefore a partial agonist may be sufficient over a full one

34
Q

tolerance

A

decrease in a drug’s effectiveness over days/ weeks

35
Q

resistance

A

adaptive changes making a drug less effective

36
Q

what causes changes in drug effectiveness?

A

desensitisation
tolerance
resistance

37
Q

how does resistance occur?

A 
change in receptors
loss of receptors
loss of mediators
enhanced drug metabolism
increased removal from site of action§
38
Q

pharmacogenomics

A

genetic variability in the way drugs behave in the body
PK = enzyme polymorphism
PD = receptor variants

39
Q

what factors are used to guid drug administration?

A

drug factors and patient factors

40
Q

what patient factors affect drug administration?

A

age
weight
gender
disease

41
Q

what drug factors affect drug administration?

A

pharmacokinetic and pharmacodynamics

42
Q

inpredictability

A

there is always unpredictability in PK and PD responses even if adjustments are made

43
Q

why might the outcome of drugs not be easily measured?

A

long delay in seeing result

multi-factorial condition

44
Q

Kd

A

relationship between the ability of a drug to bind and to dissociate
concentration required to occupy 50% of receptors

45
Q

when does EC50 = Kd

A

when all the receptors need binding to cause maximal response

46
Q

when there are spare receptors

A

the EC50 is much less than the Kd, provides degree of tolerance to things going wrong

47
Q

what happens when a competitive inhibitor and an agonist are used where there are spare receptors

A

more receptors need to be bound to elicit the 50% response but it can be done . Shifts EC50 to right

48
Q

what happens when a irreversible inhibitor and an agonist are used where there are spare receptors

A

shift in EC50 to right and loss of maximal response as receptor reserve is lost and receptors are no longer available so complex formation is reduced.

Physiology 2 (20 decks)

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