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Principles > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Define Pharmacodynamics

A

Biological effects of drugs and mechanisms of action of a drug (what a drug does to the body)

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2
Q

Define Pharmacokinectics

A

Effect the body has on a drug (including; absorption, distribution, metabolism, elimination)

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3
Q

Define Efficacy

A

They ability of an agonist to evoke a response

Higher efficacy = larger response) (calculated by ß/a

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4
Q

Define Affinity

A

The strength of association between ligand and its receptor (it is determined by the chemical bonds between the two)

Greater affinity = greater duration of binding

Calculated by K+1/K-1

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5
Q

Define EC50

A

The concentration of agonist that results in a half maximal response (i.e. 50% of receptors are occupied)

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6
Q

If agonist A requires 0.01 concentration to elicit a response and agonist B requires 0.05 concentration to elicit a response.
Agonist A is more ____ than agonist B.

A

Potent

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7
Q

In the presence of a competitive antagonist, EC50 is unchanged. True/False?

A

False - EC50 increases

Increased concentration of agonist required to elicit same response

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8
Q

Both the ionised and unionised forms of a drug readily diffuse across the lipid bilayer. True/False?

A

False

Unionised form diffuses across more readily

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9
Q

Define pKa

A

The pH at which 50% of a drug is ionised and 50% is unionised

Therefore, when pH=pKa then 50% of drug is ionised and 50% is unionised

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10
Q

List 3 variations of the Henderson Hasselbach Equation

A

For weak acids:
pKa = pH + log[AH]/[A-]
pH - pKa = log[A-]/[AH]
10^(pKa-pH) = [AH]/[A-]

(For weak bases substitute AH for BH+ and A- for B)

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11
Q

Increasing the pH of an acidic drug causes it to become less ionised. True/False?

A

False

It becomes more ionised (acid drugs are less ionised in an acid environment)

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12
Q

Which administration routes by-pass first pass metabolism?

A

Sublingual, rectal, intravenous and intramuscular

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13
Q

Define the apparent volume of distribution (Vd)

How is it calculated?

A

Describes the extent to which a drug partitions between plasm and tissue compartments

Vd = Dose / [Drug]plasma

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14
Q

An apparent volume of distribution (Vd) closer to total body volume of water (~41L) suggests…

A

Drug is hydrophilic and contained within vascular compartment

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15
Q

An apparent volume of distribution (Vd) much greater than total body volume of water (~1000L) suggests…

A

Drug is lipophilic and can enter body tissue easily

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16
Q

Sympathetic preganglionic NT is?

A

Acetylcholine (cholinergic)

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17
Q

Sympathetic postganglionic NT is?

A

Noradrenline (adrenergic)

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18
Q

Parasympathetic pre and post ganglionic NT is acetylcholine. True/False?

A

True

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19
Q

Preganglionic neurone of sympathetic chain is long. True/False?

A

False - Preganglionic neurone of sympathetic chain is short

Note: preganglionic neurone of parasympathetic chain is long as ganglions are usually embedded in the target organ

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20
Q

Parasympathetic stimulation decreases force of heart contraction. True/False?

A

False

Has no effect on force of ventricular contraction, but does decrease heart rate

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21
Q

Components of a G-protein

A

α (contains guanine nucleotide binding site for GDP/GTP) and β + γ complex

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22
Q

M1 GPCR

Type: G_

Action: ___ acid secretion in stomach

A

Gq

  • Increased acid secretion in stomach
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23
Q

M2 GPCR

Type: G_

Action: ___ heart rate

A

Gi

  • Decreased heart rate (and heart force in atria only)

Remember: M2 is a presynaptic autoreceptor that modulates ACh release

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24
Q

M3 GPCR

Type: G_

Action: ___ of airways; ___ of specific vasculature; ____ mucus production; _____ intestinal motility and secretions; ____ bladder wall; ____ erection

A

Gq

  • Contraction of airways smooth muscle
  • Relaxation of vascular smooth muscle (in penis, salivary glands & pancreas)
  • Stimulates mucus production
  • Increases intestinal motility and secretions
  • Contracts bladder wall
  • Stimulates erection
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25
Q

Regarding the adrenergic transmission - NA Uptake 1 is located on the?

A

Post-ganglionic neurone

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26
Q

Regarding the adrenergic transmission - NA Uptake 2 is located on the?

A

Effector cell

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27
Q

NA taken up by U1 is broken down by which enzyme?

A

Monoamine Oxidase - MAO - in the post-ganglionic neurone

N.B. MAO is a target of some anti-depressant drugs

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28
Q

NA taken up by U2 is broken down by which enzyme?

A

Catechol-O-methyltransferase - COMT - in the effector cell

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29
Q

ß1 GPCR

Type: G_

Action: ____ heart rate and force

A

Gs

Increased heart rate and force (in both atria and ventricles)

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30
Q

ß2 GPCR

Type: G_

Action: ___ of airways and vasculature

A

Gs

Relaxation of airway and vascular smooth muscle

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31
Q

α1 GPCR

Type: G_

Action: ____ of vasculature

A

Gq

Contraction of vascular smooth muscle

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32
Q

α2 GPCR

Type: G_

Action: ____ NA release

A

Gi

Decreased NA release

Remember: α2 is a presynaptic autoreceptor that modulates release of NA

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33
Q

ACh binding to post-ganglionic M2 receptor causes ____ Ca2+ entry, which results in ___ NT release

A

Reduced, less

Remember: M2 is a presynaptic autoreceptor that modulates ACh release

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34
Q

NA binding to post-ganglionic α2 receptor causes increased Ca2+ entry, resulting in more NT release. True/False?

A

False
Decreased Ca2+ entry, resulting in less NT release

Remember: α2 is a presynaptic autoreceptor that modulates release of NA

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35
Q

Cocaine blocks U_, causing an ___ in NA in the synaptic cleft

What effect does cocaine have via α1 and ß1 GPCRs?

A

Cocaine blocks U1, causing an increase in NA in the synaptic cleft

Overstimulation - α1 - increases vasoconstriction
Overstimulation - ß1 - arrhythmia (increased heart rate)

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36
Q

Amphetamine enters the postganglionic neurone via ___ and inhibits the enzyme ___, resulting in ___ in NA in the cytoplasm. It also displaces ___ from _____ to cytoplasm which then exits via ___.

A

Amphetamine enters the postganglionic neurone via U1 and inhibits the enzyme MAO, resulting in increase in NA in the cytoplasm. It also displaces NA from vesicles to cytoplasm which then exits via U1

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37
Q

Which subunits form the PNS ganglionic nicotinic receptors?

A

3 x B4

2 x α3

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38
Q

What term is given to the concentration that a drug must reach in the plasma to achieve an effect?

A

Minimum effective concentration

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39
Q

Define the maximum tolerated concentration as…

A

The drug concentration in the plasma which must not be exceeded to prevent toxic effects

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40
Q

Therapeutic ratio/index is given by…

A

MTC/MEC

MTC = maximum tolerated concentration
MEC = minimum effective concentration
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41
Q

How can drug plasma concentration be calculated?

A

Dose/Vd

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42
Q

What is first order kinetics in terms of elimination?

A

Rate of elimination is proportional to drug concentration

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43
Q

How is drug half life calculated?

A

0.693*Vd/CL

CL= rate of clearance

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44
Q

For drugs exhibiting 1st order kinetics, the dose administered changes __ directly, but has no effect upon __ or __

A

Plasma concentration, half-life, rate of elimination

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45
Q

Plasma clearance is given by…

A

Vd x rate of elimination

or

Rate of elimination / [Drug] plasma

46
Q

Rate of 1st order kinetic drug elimination is given by…

A

Cp x Clp

47
Q

Css (steady state concentration) is normally achieved after _ half lives

A

5

48
Q

The time to reach Css is determined by the infusion rate but not the half life. True/False?

A

False

Css is determined by the half life, not infusion rate

49
Q

Depolarisation is when the membrane potential becomes more negative. True/False?

A

False

More positive

50
Q

Resting membrane potential, Vm, is normally approx…

A

-70mV

51
Q

Activation of Na+ channels and subsequent Na+ channels is an example of ____ feedback

A

Positive

52
Q

Refractory period of the AP describes…

A

The inactivated state of sodium channels, ultimately causing repolarisation to closed state

53
Q

In the relative refractory period, a strong enough stimulus can elicit the generation of a new AP. True/False?

A

True

54
Q

What is the function of Schwann cells?

A

Wrap around axons in a “myelin sheath” to provide insulation and speed up electrical conduction

55
Q

Saltatory conduction describes…

A

APs jumping between gaps between adjacent nodes of Ranvier

56
Q

Where does reversible competitive antagonism occur?

A

Orthosteric site

57
Q

Where does reversible non-competitive antagonism occur?

A

Allosteric site

58
Q

Define oral availability

A

Fraction of drug reaching systemic circulation after orl ingestion

59
Q

Define systemic availability

A

Fraction of drug reaching systemic circulation after absorption

60
Q

Define Drug Clearance

A

Volume of blood removed (or cleared) of drug per unit of time

61
Q

Define Steady state

A

When the rate of drug administration is equal to the rate of elimination

62
Q

What is the shape of the agonist -receptor saturation curve?

A

Hyperbolic relationship

63
Q

What is the shape of the agonist -receptor saturation curve in a semi-logarithmic plot?

A

Sigmoidal

64
Q

How does the addition of a competitive antagonist effect the agonist -receptor saturation curve in a semi-logarithmic plot?

A

Shift of sigmoidal curve to the right

Equal efficacy to agonist alone, however agonist alone is more potent (lower EC50)

65
Q

How does the addition of a non-competitive antagonist effect the agonist -receptor saturation curve in a semi-logarithmic plot?

A

Small curve in same position

Same potency as agonist alone, however less efficacy

66
Q

What is the difference between autocrine and paracine chemical signalling?

A

Autocrine - cells release chemical signals that affect itself
Paracrine - cells release chemical signals that affect neighbouring cells

67
Q

What is the difference between speed of transmission of ligand-gated ion channels, GPCR, Kinase-linked receptors and nuclear receptors?

A

LGIC - miliseconds
GPCR - seconds
Kinase-linked - hours
Nuclear - hours/days

68
Q

List typical ligands for ionotropic LGIC receptors

A

ACh, AAs, rarely amines

69
Q

List typical ligands for metabotropic GPCR receptors

A

ACh, AAs, amines, peptides and adrenaline

70
Q

List typical ligands for kinase-linked receptors

A

Insulin, Growth factors immune signals

71
Q

List typical ligands for nuclear receptors

A

steroid hormones and thyroid hormones

72
Q

Which type of receptor is targeted by hydrophobic signalling molecules?

A

Nuclear receptors

73
Q

Which types of receptor are targeted by hydrophilic signalling molecules?

A

LGICs, GPCRs, Kinase-linked receptors

74
Q

Describe the action of insulin kinase-linked receptors

A

Insulin causes autophosphorlyation of intracellular tyrosine residues which recruits proteins i.e. insulin receptor substrate 1

75
Q

Describe the action of nuclear receptors

A

Lipophilic steroid hormone diffuses across plasma membrane then combines with intracellular receptor (causing dissociation of HSP). Receptor-steroid complex travels to nucleus and forms a dimer which binds DNA to switch on/off genes.

76
Q

How is the GPCR signal turned off?

A

Alpha subunit hydrolyses GTP to GDP

77
Q

What are the steps involved in GPCR activation?

A

Agonist binds transmembrane receptor causing conformational change which in turn causes alpha subunit to release GDP and pick up GTP.
Activated alpha subunit separates from the beta-gamma dimer and combines with effector channel

78
Q

How do Gs type GPCRs work?

A

Stimulates AC ⮕ upregulates cAMP ⮕increased PKA ⮕ Phosphorylation

79
Q

How do Gi type GPCRs work?

A

Inhibits AC ⮕ downregulates cAMP ⮕ decreased PKA ⮕ inhibited phosphorylation

80
Q

How do Gq type GPCRs work?

A

Stimulates PLC ⮕ upregulates the conversion of PIP2 to IP3 and DAG ⮕ IP3 binds receptor (causing calcium influx from ER) and DAG causes phosphorylation

81
Q

Where do drugs that are weak bases accumulate?

A

In compartments with low pH (acidic)

82
Q

Where do drugs that are weak acids accumulate?

A

In compartments with high pH (basic)

83
Q

Where does most drugs get absorbed regardless of pH?

A

Small intestine - due to large surface area

84
Q

How can volume of distribution be calculated when giving IV fluids?

A

Dose = Vd

85
Q

What is the most abundant plasma protein?

A

Albumin

86
Q

How does plasma protein binding affect drug availability for diffusion to target organ?

A

Reduced

87
Q

Describe the therapeutic window of a safe dug

A

High therapeutic ratio = large therapeutic window

88
Q

Where are the drug-metabolising enzymes in hepatocytes found?

A

Bound to SER

89
Q

Describe Phase 1 Drug Metabolism

A

Change drug via catabolic reactions (i.e. oxidation, reduction or hydrolysis)
- Oxidation via CYP450 produces more chemically active (or toxic) metabolites by introducing a reactive species

90
Q

Describe Phase 2 Drug Metabolism

A

Anabolic reactions involving conjugation to form a water soluble metabolite, usually result in inactive products
- Conjugated species are usually readily excreted via kidneys

91
Q

What types of metabolites are readily excreted by the kidneys?

A

Charged metabolites

92
Q

How are unbound drugs filtered by the kidneys?

A

Passive glomerular filtration

93
Q

How are acidic drugs filtered by the kidneys?

A

Active OAT

94
Q

How are basic drugs filtered by the kidneys?

A

Active OCT

95
Q

Describe zero-order elimination kinetics

A

When Vmax is reached and rate of elimination is constant

96
Q

How can the rate of drug elimination be calculated?

A

Rate = (Vmax x [Drug]plasma) / (Km + [Drug] plasma)

97
Q

Does changing rate of administration change the time to steady state?

A

No, but it does alter the [ss]

98
Q

How can steady state dosage be calculated?

A

Dosage rate = [Drug]plasma x Clearance rate

99
Q

What does a loading does do?

A

Decreases time to steady state

100
Q

How can Loading doses be calculates?

A

IV: LD = Vd x target [plasma]
PO: LD = (Vd x target [plasma]) x F

(where F = oral bioavailability)

101
Q 
What effect does; 
- ageing, 
- obesity, 
- pathological fluid 
...have on drug half life?
A
  • decreases
  • increases
  • increases
102
Q

Name factors that effect the volume of distribution

A

Ageing and obesity

103
Q

Name factors that effect clearance rate

A

CYP450 concentration, renal failure, cardiac failure and hepatic failure

104
Q 
What effect does; 
- increased CYP450, 
- decreased CYP450, 
- renal failure, 
- cardiac failure, 
- hepatic failure, 
...have on drug half life?
A
  • decreased
  • increased
  • increased
  • increased
  • increased
105
Q

Which NTs modulate activity in the sympathetic nervous system?

A

Main: NA

Additional modulators: ATP and NPY

106
Q

Which NTs modulate activity in the parasympathetic nervous system?

A

Main: ACh

Additional modulators: NO and VIP

107
Q

Which subunits form the PNS skeletal muscle nicotinic receptors?

A

(alpha1) x2
Beta1
Gamma
Epsilon

108
Q

Which subunits form the CNS nicotinic receptors?

A

(alpha7) x5

or

(alpha4) x2
(beta2) x3

109
Q

What is the effect of prazosin on alpha1 ADRs?

A

Antagonist - causing vasodilation

Therefore, used as an anti-hypertensive

110
Q

What is the effect of atenolol on ß1 ADRs?

A

Antagonist

Used as an anti-anginal and anfti-hypertensive

111
Q

What is the effect of atropine on M1-3 GPCRs?

A

Widespread parasympathetic blockade

Used in decreasing heart rate following MI and also used in acetylycholinesterase poisoning

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