Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Semester 2 > M&R Session 8 > Flashcards

M&R Session 8 Flashcards

0
Q

What equation is used to calculate molarity?

A

Grams per litre/molecular weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Which drugs do not bind to proteins?

A

Anti microbial

Anti tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why must drug concentrations be considered in molarity?

A

Using equal weights of substances w/ different molecular weights leads to different concentrations of molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the critical determinant of drug action?

A

The molarity of drug molecules around receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What law does drug binding obey?

A

Mass action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What forms the dynamic equilibrium between ligand, receptors and the complex they form upon binding?

A

Association and dissociation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is related to the binding of drug molecules to receptors?

A

[reactants]
[products]
Le Chatelier’s principle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What two characteristics do agonists have?

A

Affinity

Intrinsic efficacy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What governs receptor activation to give intracellular effects?

A

Intrinsic efficacy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is intrinsic efficacy?

A

The ability to turn a receptor on by forming an activated receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is efficacy?

A

Ability to cause coupling leading to cellular action

Ability to generate a biological response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What determines efficacy?

A

Cell/tissue-dependent factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why can an antagonist not cause a response?

A

It only has affinity so cannot convert the receptor to an active form - no conformational change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do antagonists prevent receptors being turned on?

A

Prevent agonist binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What two methods are used to measure drug-receptor interactions?

A

Binding w/radioligand

Relation b/w [drug] and response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the process of radioligand binding.

A

Bind radioligand to cells/prepared membranes –> separate bound and free radioligand –> low [ligand] = low binding,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is B(max)?

A

The concentration at which all receptors are full

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is Kd?

A

The dissociation constant = 50% occupancy

Measure of affinity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Is Kd affected by receptor number?

A

Nope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does a low Kd indicate?

A

High affinity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is K(A)?

A

Index of affinity determined by functional assay

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the definition of a logarithm?

A

The exponent by which a fixed (base) value has to be raised to give a particular number

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How is [drug] usually expressed?

A

On a logarithmic scale giving a sigmoidal curve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Can Kd be used for agonists and antagonists?

A

Yes, it can be used for any type of ligand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What does receptor response require?

A

Efficacy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What type of ligand must be used to measure drug-receptor interactions by relation b/w [drug] and response?

A

An agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is E(max)?

A

Effect maximum; a tissue can only secrete/contract so much

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is EC50?

A

Effective concentration giving 50% of the maximal response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Define concentration in relation to drug action.

A

Known [drug] at site of action e.g. in cells and tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Define dose.

A

Concentration at an unknown site of action e.g. dose to a patient (mg or mg/kg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is potency?

A

How good a drug is at generating a biological response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What does potency depend on?

A

Affinity
Intrinsic efficacy
Efficacy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the key determinant of efficacy?

A

The number of receptors present

33
Q

What factors must be considered in drug action?

A 
Affinity
Efficacy
Selectivity
Pharmacokinetics
Physiochemical properties
34
Q

What is the therapeutic target used in asthma treatment?

A

Beta 2-adrenoreceptors

35
Q

Why do agonists for asthma treatment need to have specificity rather than just their usual high selectivity?

A

So they do not act on beta 1-adrenoreceptors in the heart

36
Q

What is functional antagonism?

A

Where the antagonist of the action not the receptor

37
Q

How is Salbutamol utility increased?

A

Beta 2-selective efficacy

Route of administration

38
Q

Describe the action of Salbutamol.

A

Binds slightly preferentially to beta 2 and is particularly good at turning beta 2 on

39
Q

Describe the action of Salmeterol.

A

Long acting

Selectivity based on affinity as it has no selective efficacy

40
Q

What problems are associated with Salbutamol and Salmeterol respectively?

A

Salbutamol: can act on beta 1-adrenoreceptors in heart –> increases HR –> angina (common in elderly w/asthma)
Salmeterol: insoluble so cannot be given IV when nebuliser no longer an option

41
Q

When are spare receptors often seen?

A

When receptors are catalytically active

42
Q

Give two examples of receptor types you would expect to see spare receptors with.

A

Tyrosine kinase

GPCRs

43
Q

Why do spare receptors exist?

A

B/c of amplification and response limited by post-receptor event

44
Q

In asthma what percentage of M3 muscarinic receptors are activated to give maximal contraction?

A

10%

45
Q

Describe the relationship b/w drug concentration and its Kd if there are no spare receptors.

A

For full receptor response requires&raquo_space; Kd of drug

46
Q

What effect do spare receptors have on sensititvity?

A

Increase

47
Q

Describe the response when there are spare receptors present.

A

Occurs at lower [agonist]
Occurs at Kd
Decreased [drug] for full response

48
Q

What does changing receptor number do?

A

Changes agonist potency

Can affect the maximal response

49
Q

Describe the relationship b/w [drug], its effects and receptor number.

A

Same [drug] has different effects depending on receptor number

50
Q

What happens if receptor number is low?

A

There is 100% occupancy but insufficient receptors for a full response

51
Q

What can cause up-regulation of receptors w/low activity and down-regulation w/high activity?

A

Physiological, pathological or drug-induced changes

52
Q

What is tachyphylaxis?

A

Desensitised receptors

53
Q

How can partial agonists not elicit maximal response with full receptor occupancy?

A

Insufficient efficacy creates a different activated receptor so it is turned on but not fully

54
Q

What tends to happen with the binding curve and function curve for a partial agonist?

A

Overlap so EC50 ~ Kd

55
Q

What type of receptors do opioids primarily bind to?

A

Mu-opioid

56
Q

Why is buprenorphine sometimes used clinically instead of morphine?

A

It has a higher affinity but lower efficacy so can give sufficient pain control with a lower risk of breathing depression

57
Q

What type of agonist is heroin?

A

Full

58
Q

Which mixed agonist/antagonist is used to aid heroin withdrawal?

A

Buprenorphine

59
Q

What can cause a partial agonist to act as a full agonist?

A

Increased receptor number (low efficacy but enough receptors –> full response)

60
Q

What indicates intrinsic activity?

A

Maximal response

61
Q

Can full agonists w/identical intrinsic activities have different efficacies?

A

Yes

62
Q

What can be said about the response of two full agonists with equal intrinsic activity?

A

They have the same maximum response

63
Q

In which direction does the response curve of a drug move with increasing potency?

A

Left

64
Q

What does reversible competitive antagonism rely on?

A

A dynamic equilibrium b/w ligands and receptors

65
Q

What is K50?

A

The concentration of antagonist which gives 50% inhibition

Index of antagonist potency determined by [agonist]

66
Q

What is the difference between Kd and KB?

A 
Kd = antagonist affinity derived from radioligand
KB = antagonist affinity derived pharmacologically
67
Q

How do reversible competitive antagonists affect agonist concentration-response curves?

A

Cause parallel shift to right

68
Q

Which drug can be used clinically to reverse opioid-mediated respiratory depression?

A

Naloxone

69
Q

When does irreversible competitive antagonism occur?

A

When the antagonist dissociates slowly or not at all

70
Q

How does irreversible competitive antagonism affect the agonist concentration-response curve?

A

Parallel shift to right and suppresses maximal response

71
Q

How does irreversible competitive antagonism suppress maximal response?

A

Spare receptors are filled by antagonist therefore there are insufficient receptors for a full response

72
Q

How does phenoxybenzamine work?

A

Non-selective alpha 1 adrenoreceptor blocker that binds covalently so no matter how much adrenaline/NA present vasoconstriction is not caused

73
Q

What mechanism of action does Clopidogrel use to prevent thrombosis?

A

Irreversible P2Y12 antagonist which prevents cytochrome P450 metabolism

74
Q

What is non-competitive antagonism?

A

Endogenous ligand binds to orthosteric site on extracellular part of GPCR

75
Q

What are allosteric sites?

A

Binding sites for agonists and molecules that enhance or reduce ability of endogenous ligand to turn receptor on

76
Q

What type of antagonism does non-competitive antagonism resemble when comparing [agonist]-response curve?

A

Irreversible competitive antagonism

77
Q

Describe an NMDA (excitatory glutamate) receptor.

A

Inotropic receptor
Ligand gated ion channel
Distinct glutamate and ketamine binding sites

78
Q

What effects can binding at an NDMA produce?

A

Analgesia

Decreased central excitation

79
Q

Describe the allosteric sites of GPCRs.

A

High specificity

High receptor subtype selectivity

80
Q

Are GPCRs competitive?

A

No

81
Q

What do GPCRs often require to function?

A

Orthosteric ligand

Semester 2 (45 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions