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Yr 2 Pharm + Therapeutics > 2+3: Drug Mechanisms + Receptor Interactions > Flashcards

2+3: Drug Mechanisms + Receptor Interactions Flashcards

1
Q

Define pharmacodynamics

A

the effect of the drug on the body (responses produced, mechanism of action)

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2
Q

Defime pharmacokinetics

A

the effect of the body on the drug (e.g. absorption, distribution, metabolism, excretion).

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3
Q

Define drug

A

chemical substance that interacts with a biological system to produce a physiological effect.

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4
Q

4 main drug target sites

A

Receptors
Ion channels
Transport systems
Enzymes

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5
Q

What do all 4 drug target sites have in common

A

proteinacious binding sites

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6
Q

What are receptors activated by

A

NTs + hormones

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7
Q

Example of agonist and what it stimualtes

A

ACh - nonselective agonist stimulating nicotiic + muscarinic

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8
Q

Example of antagonist and what it blocks

A

Atropine - muscarinic antagonist

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9
Q

Uses of atropine

A

used as anaesthetic premediation to dry up secretions

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10
Q

2 types of ion channels

A

Voltage-sensitive (VGCC) - affected by memb potential

Receptor-linked (nicotine-ACh receptor is linked with cation channels)

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11
Q

How do local anaesthetics work

A

Block VGSCs in sensory axons, blocking Na passage. Fewer APs propagated along these axons so pain perception reduced
Nocicpetor neurons are also inhibited

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12
Q

How do ca channel blockers work

A

Block VGCCs stop Ca influx into SM of vasculature which relaxes muscle, reducing TPR thus BP

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13
Q

What is amlodipine

A

Ca channel blocker

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14
Q

What are transport systems

A

Systems of carrier proteins and molecules using ATP to carry substances against conc grad. They’re specific for certain species. They dont mediate a response

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15
Q

Examples of transport systems

A

Na/K ATPase transports Na out and K into cells.

NA and Uptake 1 - SNS releases NA into synapse, binds postsynaptic adrenoreceptors. Main uptake when inactivating NA is into presynpatic nerve terminal via Uptake 1

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16
Q

How do tricyclic anti-depressants work

A

Interfers w NA Uptake 1 system. Downregulate NA and 5HT transmission in the brain. transmission in brain. TCAs bind NA transporter and slow transporter. This increases NA conc in synapse = enhanced NA effect postsynaptically in brain. (Same w 5HT)

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17
Q

What are cardiac glycosides

A

cardiac stimulant drugs increase heart contractility: interferes w Na/K ATPase

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18
Q

What is digoxin and how it works

A

Cardiac glycoside.
Used to treat HF
Binds to the Na/K ATPase on the cardiac myocytes and slows it so there is a slightly increased intracellular Na concentration which has a knock on effect on the intracellular Ca in the cardiomyocyte. Thus improved contraction and cardiac output. Gives an increased force of contraction too.

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19
Q

3 ways that drugs interact w enzymes

A
  1. Enzyme inhibitors
  2. False Substrates
  3. Prodrug
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20
Q

Example of enzyme inhibitor

A

Anticholinesterases like neostigmine. Increase [ACh] in synapsen by slowing acetylcholinesterase by binding it.
Used to treat muscle disorders

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21
Q

Example of false substrate

A

methyldopa takes place of DOPA - taken into S neurons, folows same S pathway as NA but generates methyl NA. Less effective alpha-1 receptor action causing less effective vasoconstriction

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22
Q

Example of prodrug

A

Chloral hydrate w is converted to trichloroethanol in the liver. This has hypnotic effects
It’ds a sleeping pill.

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23
Q

Unwanted effects of paracetamol

A

If too much, can saturate microsomal enzymes so another set of enaymes, P450, have to metabolise and this generates toxic substances = irreversible damage to liver + kidney

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24
Q

How do gnereal anaesthetics work

A

dampen synaptic transmission but dont interact w specific transport system/receptor.

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25
Q

How do antacids work

A

reduce stomach acidity as they are basic so can neutralise stomach acid

26
Q

How do osmotic purgatives work

A

they stimulat voiding of gut contents - they draw water into stomach contents and this softens stool and stimualtes voiding.

27
Q

Define potency

A

how powerful the drug is. It depends on affinity and efficacy

28
Q

Define affinity

A

how willingly the drug binds to its receptor (refers to avidity)

29
Q

What does affinity of drug to receptor depend on?

A 
Electrostatic forces
intermolecular forces
H-bonding
VDWs 
Hydrophobic interactions
30
Q

Define efficacy

A

also called intrinsic activity - the ability of a drug to generate a response once it has bound to the receptor - usually involves some sort of conformational change

31
Q

Define full agonist

A

Full Agonist: an agonist that generates the maximal response

32
Q

Define partial agonist

A

Partial Agonist: an agonist that generates less than the maximal response

33
Q

What happens when you administer partial agonist w full agonist

A

you will get an effect similar to an antagonist because the partial agonist interferes with the ability of the full agonist to generate a response

34
Q

Antagonists have ____ but no ____

A

Affinity

Efficacy

35
Q

2 main types of antagonist

A

Competitive

Irreversible

36
Q

Competitive antagonists

A

bind to same site as agonist on receptor = responses are surmountable (they can be overcome by increasing agonist)

37
Q

What do competitive antagonists do to D-R curve

A

shift to right

38
Q

Irreversible antagonists

A

binds tightly w covalent bonds. They could also bind at diff sites which = responses are insurmountable so cant be overcome by increasing agonist as no competition.

39
Q

Example of irreversible antagonist

A

Hexmethonium - irreversible nicotinic cholinoceptor antagonist (blocks ion channel rather than recepto)

40
Q

4 main families of receptors:

A

Type 1: Ionotropic
Type 2: G-protein coupled
Type 3: Tyrosine kinase-linked
Type 4: Intracellular Steroid Type receptors

41
Q

Location of the diff receptor families

A

Types 1-3: membrane

Type 4: intracellular

42
Q

Structure of ionotropic receptors

A

4/5 subunits
Defining feature: transmemb sections have alpha helices
There’s an external binding domain which will stimulate and open ionchannels

43
Q

Structure of type 2 receptors

A

1 subunit

7 transmemb domains (7 alpha helices

44
Q

Type 3 receptor structure

A

Single protein
1 transmemb domain.
Inside the cell is intracellular domain.

45
Q

Type 4 receptor structure

A

The DNA binding domain is called zinc fingers. When receptor stimulated, zinc fingers uncovered = DNA binding and increased transcription

46
Q

Effectors of the receptor families

A

Type 1 - channel
Type 2- enzyme/channel
Type 3: enzyme
Type 4: gene transcription

47
Q

Example of type 1 receptor

A

nicotnic acetylcholine receptor

GAB A

48
Q

Eg of Type 2 recpetor

A

B1 adrenoreceptor in heart

muscarinic acetylcholine receptor

49
Q

Eg of Type 3 receptor

A

insulin receptor

Growth factor + cytokine receptors

50
Q

Eg of type 4 receptor

A

steroid/thyroid receptors

51
Q

4 types of drug antagonism

A
  • Receptor Blockade
  • Physiological Antagonism
  • Chemical Antagonism
  • Pharmacokinetic Antagonism
52
Q

How does receptor blockade work

A

An antagonist binds receptor and prevents the binding of an agonist.
‘Use Dependency’ - this refers to ion channel blockers; more the tissue on which drug is acting is being used (more active they are), more effective this type of blocker will be.

E.g. local anaesthesia

53
Q

What is physical antagonism

A

When 2 drugs act at different receptors to have opposite effects in the same tissue.
E.g. NA on the vasculature binds to adrenoreceptors = vasoconstriction, increasing BP. If we coadminister histamine - it acts on different receptors (H1 receptors) on vasculature = vasodilation, reducing BP.

54
Q

What is pharmacokinetic antagonism

A

When one drug reduces the concentration of the other drug at the site of its action. It may reduce the absorption, increase the metabolism or increase the excretion of another drug.

55
Q

Eg of pharmacokinetic antagonism

A

Repeated administration of barbiturates increases production of microsomal enzymes so if we administer another drug that is metabolised by the same enzymes then it is going to be metabolised more quickly and its effect will be reduced

56
Q

Define drug tolerance

A

the gradual decrease in responsiveness to a drug w repeated administration
E.g. benzodiazepines

57
Q

5 potential causes of drug intolerance

A
  • Pharmacokinetic Factors
  • Loss of Receptors
  • Change in Receptors
  • Exhaustion of Mediator Stores
  • Physiological Adaptation
58
Q

Describe how pharmacokinetic factors cause drug intolerance

A

Metabolism of the drug increases when it is given repeatedly over a period of time. Barbiturates and alcohol are good examples

59
Q

Describe how loss of receptors cause drug intolerance

A

The cell takes receptors off its membrane via membrane endocytosis. If the cell repeatedly stimulated by agonist, the cell will endocytose some receptors so there are fewer available on the cell surface – aka receptor downregulation.

60
Q

Describe how change in receptors cause drug introlerance

A

number of receptors on the cell surface doesn’t change but the receptors themselves undergo desensitisation due to continued stimulation over a long period of time. This method involves a conformational change so a proportion of the receptors are no longer effective.

61
Q

Describe how exhaustion of mediator stores causes drug intolerance

A

Amphetamine is an example - is a CNS stimulant and acts on noradrenergic neruosn in brains.

62
Q

Describe how physiological adaptation causes drug introlerance

A

Homeostatic response - body atempts to maintain stable internal env by developing tolerance to drug side effects

Yr 2 Pharm + Therapeutics (9 decks)

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