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Year 2 - Pharmacology and Therapeutics > Drug Mechanism & Receptor Interactions > Flashcards

Drug Mechanism & Receptor Interactions Flashcards

1
Q

Pharmacokinetics

A

what the body does/responds to the drugs - refers to the drugs movement into, through and out of the body

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2
Q

Pharmacodynamics

A

the effects of drugs and their mechanism of action

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3
Q

Drug

A

Chemical substance that interacts with a biological system to produce a physiological effect

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4
Q

What are the 4 drug target sites and what are they all?

A

Receptors
Ion channels
Transport systems
Enzymes

They’re all proteins

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5
Q

What is the most common drug target site and its properties?

A

Receptors - 4 types (Type 1-4)
Usually on CSM (NOT Type 4)
Activated by NT/hormone
Defined via. agonist & antagonist

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6
Q

Atropine?

A

Antagonist
Muscarinic Ach
Competitive & Selective

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7
Q

Ach?

A

Agonist

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8
Q

Ion channels?

A

Drug target site

Selective pores - voltage-sensitive (membrane potential) OR receptor-linked (conformational change)

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9
Q

Examples of drugs working on ion channels?

A

LAs - interact w VSSCs (block it)

Ca2+ channel blockers (if end in -dipine)

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10
Q

Transport Systems and examples?

A

AGAINST [gradient]
Specific for certain species
Require ATP

Examples - Na+/K+ ATPase
NA uptake 1

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11
Q

Examples of drugs working on transport systems

A

TCAs (anti-depressant drugs work on NA uptake proteins)

Cardiac glycosides

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12
Q

Enzymes as drug target sites?

A

Drug can have 3 interactions:
Enzyme inhibitors
False substrates
Prodrugs

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13
Q

Explain how enzymes as drug target sites can give rise to unwanted effects

A

Paracetamol
Becomes saturated in the body, overloading the metabolising enzymes = switches to another enzymes giving rise to toxic by-products = affects liver/kidneys

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14
Q

NSDA?

A

Non-specific drug action

Action produced via. non-protein receptor interactions

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15
Q

Examples of NSDAs?

A

Antacids - addition of base

Osmotic purgatives - laxatives work by drawing H20 into the gut

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16
Q

PPB?

A

Plasma protein binding - acts as reservoir of inactive drugs

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17
Q

Agonist

A

Ligand that stimulates/activates a receptor

e.g. Ach, nicotine

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18
Q

Antagonist

A

Ligand that binds to receptors (Affinity) but does nothing only blocks it (NO efficacy)

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19
Q

Full agonist

A

can stimulate full/maximal response

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20
Q

Partial agonist

A

If given with full agonist, can produce some antagonist activity

21
Q

Selectivity

A

NOT SPECIFIC as when increase drug dose, can overlap with other receptor populations (giving rise to unwanted side-effects)

22
Q

Drug-receptor structure-activity relationship?

A

Stringent relationship between the activity of drug & its chemical structure

Can form antagonists from agonists (altering structure)

23
Q

What is required for efficacy?

A

A transducer!

Could include opening a ion-channel OR linking to an enzyme etc.

24
Q

Dose-response curve for full/partial agonist?

A

Partial agonist has a LOWER max - this is as it has a reduced efficacy

25
Q

2 types of receptor antagonist

A

Competitive & Irreversible

26
Q

Competitive?

A

Competes for same site as agonist
Surmountable - can be overcome by higher [agonist]
D-R curve shifts to right

27
Q

Examples of competitive?

A

Atropine

Propranolol - beta1 and 2 (non-selective)

28
Q

Irreversible?

A 
Binds tightly to site 
OR
binds to a different site
Unsurmountable
LONGER duration of action
29
Q

Examples of irreversible?

A

Hexamethonium

30
Q

Effects of antagonist on D-R curve?

A

Competitive shifts to R as higher [agonist] required for same response
Irreversible has a LOWER response as blocking receptors so cannot have the same response as before

31
Q

4 types of drug antagonism?

A

Receptor blockade
Physiological antagonism
Chemical antagonism
Pharmacokinetic antagonism

32
Q

Drug antagonism?

A

the way in which drugs can interact to diminish the effect of the other

33
Q

Receptor blockade?

A

Competitive and irreversible

Can also have ‘use-dependency’ of ion channel blockers - the more the cell is active, the more it is blocked

34
Q

Physiological antagonism?

A

Drugs interact w DIFFERENT receptors producing OPPOSITE effects in same tissue
e.g. NA and histamine on BP

35
Q

Chemical Antagonism

A

Interact in solution to antagonise a REACTION (rather than binding to specific receptor)
e.g. heavy metal complexed are collated, forming non-toxic clumps that can be excreted

36
Q

Pharmacokinetic antagonism

A

Agonists that are administered and antagonised by the body itself, reducing [active drug] at site of action
Could reduce absorption, increase metabolism & excretion

37
Q

Barbiturates?

A

pharmacokinetic antagonism
If taken for a long time = enzyme-induced so metabolised quickly in the liver which can affect other drugs that are metabolised by same enzyme e.g. Warfarin

38
Q

Drug tolerance?

A

Gradual decrease in responsiveness to drug with repeated administration

39
Q

5 reason for drug tolerance?

A 
Pharmacokinetic factors
Loss of receptors
Change in receptors
Exhaustion of mediator stores
Physiological adaption
40
Q

Pharmacokinetic Factors

A

Enzyme-induced

Increased rate of metabolism

41
Q

Loss of receptors?

A

Receptor ‘down-regulation’ via. endocytosis

e.g. beta-adrenoceptors

42
Q

Denervation supersensitivity?

A

Up-regulation of receptors (NOT for drug tolerance)

43
Q

Change in receptors?

A

Receptor desensitisation - conformational change SO affinity BUT NO efficacy
e.g. nAchR at NMJ

44
Q

Exhaustion of mediator stores?

A

What the name says e.g. amphetamine and NA (less NA so amphetamine cannot work [OneNote!!])

45
Q

Physiological adpation

A

Body physiologically adapts to the administration of the drug over time e.g. BP dropping drug could cause the activation of RAS

46
Q

Type 1?

A 
Ion-channel linked receptor
Location is CSM and effector is the channel
Direct coupling
x4 or 5 domains in subunit
e.g. nAchR and GABAa
47
Q

Type 2?

A 
G-protein coupled receptor
Location is CSM and effector can be enzyme or channel
G-protein coupling
7-TM structure
e.g. mAchR e.g. alpha1/2 and beta1/2
48
Q

Type 3?

A 
Kinase-linked receptors
Location is CSM and effector is enzymes
Direct coupling - protein phosphorylation (tyrosine kinase)
Only one subunit - alpha-helix
e.g. Insulin/growth receptors
49
Q

Type 4?

A

IC steroid type receptors
Located IC and effector is gene transcripts
Couple via. DNA
NO subunits - have DNA binding domain instead
e.g. steroid/thyroid receptors

Year 2 - Pharmacology and Therapeutics (9 decks)

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