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Principles Em > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is pharmacodynamics?

A

What the drug does to the body

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2
Q

What is pharmacokinetics?

A

What the body does to a drug - ADME

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3
Q

What does ADME stand for?

A

Absorption
Distribution
Metabolism
Excretion

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4
Q

What is an agonist?

A

A drug which binds to a receptor to produce a cellular response

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5
Q

What is an antagonist?

A

A drug which binds to the same receptor as the agonist in order to block it

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6
Q

An agonist has both affinity and efficacy, true or false?

A

True

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7
Q

What is affinity?

A

The strength of association between a ligand and a receptor

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8
Q

What is efficacy?

A

The ability of an agonist to evoke a cellular response

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9
Q

What is the EC50?

A

The concentration that an agonist produces a half max response

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10
Q

What are the different types of receptor?

A

LGIC
GPCR
Kinase linked
Nuclear receptors

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11
Q

What nucleotide binding site is present on the G protein binding site?

A

Guanine

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12
Q

What is a receptor?

A

A macromolecule (mostly protein) on or within cells that mediate the biological actions of endogenous substances.

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13
Q

Give an example of an agonist

A

adrenaline - increases the cardiac rate

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14
Q

A high efficacy favours a bigger response, true or false?

A

True

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15
Q

What is the relationship between the concentration of the agonist and the effect this has, when plotted logarithmically?

A

Sigmoidal - s-shaped

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16
Q

if an agonist is more potent, what does this mean?

A

that it will carry out an effect over a smaller agonist concentration range

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17
Q

when is antagonism reversible?

A

when the agonist and antagonist bind to the same site - orthosteric - as this is competitive

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18
Q

when is antagonism non-reversible

A

in non-competative antagonism: the agonist and antagonist bind to different sites, meaning the agonist cannot activate as the agonist is bound

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19
Q

what effect does a non-competitive antagonism have graphically? (on a logarithmic plot)

A

the curve is decreased as the full effect of the agonist cannot be reached

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20
Q

what effect does competitive antagonism have graphically? (on a logarithmic plot)

A

the curve moves to the right but maintains the same height, meaning the agonist can still carry out its full effect, it just needs to be at a higher concentration

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21
Q

what are the different ways drugs can move around the body?

A
  • Bulk flow (via circulatory system)
  • Diffusion (only over short distances)
  • solubility (eg: lipid soluble molecules are more likely to diffuse across the lipid bilayer membranes)
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22
Q

what are the 4 ways something can cross the membrane?

A

endocytosis
passive diffusion
facilitated diffusion
active transport

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23
Q

Facilitated diffusion requires energy. True or false?

A

False

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24
Q

what is saturation kinetics?

A

A build up of drug in the extracellular compartment due to a limited amount of carrier proteins

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25
Q

Where in the body is there a high density of carrier proteins?

A 
blood brain barrier
GI tract
placenta
renal tubule
biliary tract
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26
Q

Ions/charged particles can easily cross the membrane. True or false?

A

False

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27
Q

what is pKa?

A

the pH where half of the drug is ionised and half is un-ionised

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28
Q

what is the Henderson Hasselbalch equation?

A

pH-pKa = log (A-/AH)
or
pH-pKa = log (B/BH+)

B= base
A = acid
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29
Q

what is the apparent volume of distribution?

A

Volume into which drug appears to be distributed with a concentration equal to that of plasma.
(REMEMBER: drug is not evenly distributed)

Eg: Lipophilic drugs cross membranes easily therefore Vd is normally greater than the total body volume

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30
Q

Where do low Vd drugs have access to?

A

the blood, normally retained in vascular compartments as it has high plasma protein binding, so has an increased drug plasma concentration

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31
Q

Where is the primary site for drug metabolism?

A

the liver

sometimes the kidney

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32
Q

what is drug metabolism?

A

the enzymatic conversion of the drug to form a metabolite that is normally less pharmacologically active than the OG compound.

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33
Q

what is bioavailability?

A

the amount of drug that is available in systemic circulation to do its job

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34
Q

why does IV give a higher bioavailability?

A

because it bypasses the liver

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35
Q

what happens during phase 1 metabolism?

A

the drug is either oxidised, hydrolysed or reduced forming a reactive metabolite that is pharmacologically active

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36
Q

what enzymes allow oxidation in phase 1 metabolism?

A

cytochrome P450 enzymes

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37
Q

what happens to aspirin during phase 1 metabolism?

A

it is hydrolised

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38
Q

what happens during phase 2 metabolism?

A

the drug combines with polar molecules (that are naturally present) to form a water soluble metabolite. This terminates biological activity

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39
Q

Give an example of a drug that bipasses phase 1 metabolism and goes straight to phase 2.

A

codeine

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40
Q

where can the drug or drug metabolites be excreted?

A

in the urine, faeces or bile

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41
Q

what role do the kidneys play in excretion of a drug?

A

this is the main organ where the drug is eliminated via renal filtration of the blood plasma

42
Q

What is clearance?

A

the volume of blood removed of drug per unit of time

43
Q

what determines the half life or a drug

A

its volume of distribution and its clearance

44
Q

What is the steady state of a drug?

A

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

45
Q

How can you figure out the dosage rate?

A

dosage rate = drug plasma concentration X the clearance

46
Q

How is the half life of a drug calculated?

A

half life = (0.693xVd)/CL

47
Q

what does the half life of a drug determine?

A

the time required for the drug plasma concentration to achieve the drug plasma concentration steady state

48
Q

what is the normal number of half lives needed for a drug to reach its steady state?

A

5 half lives

49
Q

what is oral availability?

A

the fraction of drug that reaches systemic circulation after oral ingestion

50
Q

what is systemic availability?

A

the fraction of drug that reaches systemic circulation after absorption

51
Q

The threapeutic ratio = MTC/MEC. What do these stand for and what does the ratio mean?

A 
MTC = maximum tolerated concentration
MEC = minimum effective concentration

the higher the TR, the safer the drug.

52
Q

what is first order kinetics of drug elimination?

A

the rate of elimination directly proportional to the drug concentration.
Half life is inversely proportional to elimination rate constant.

53
Q

What does clearance refer to in drug elimination?

A

The volume of plasma cleared of drug in unit time

54
Q

What is the equation for rate of elimination?

A

rate of elimination = clearance x plasma concentration

55
Q

what is a loading dose?

A

the initial higher dose of drug before stepping down to lower maintenance dose.

56
Q

what is the half life dependent on?

A

volume of distribution and clearance

57
Q

What 3 processes occur in the kidney to excrete drugs and drug metabolites?

A

Glomerular filtration
active tubular secretion
passive reabsorption across tubular epithelium.

58
Q

describe what happens in depolarisation and repolarisation.

A

Depolarisation: membrane potential becomes less negative (more positive)
Repolarisation: membrane potential returns to normal more -ve state.

59
Q

What way do Na ions move through Na channels?

A

Inwardly as there is a higher concentration of Na ions outside the cell, compared to inside the cell.

60
Q

What way do K ions move through K channels?

A

Outwardly

61
Q

What do voltage activated channels cause?

A

Depolarisation

62
Q

What do voltage activated K channels cause?

A

Hyperpolarisation

63
Q

How are voltage activated Na and K channels activated?

A

by membrane depolarisation

64
Q

Na channels activate more rapidly than K channels, true or false?

A

True

65
Q

In an AP what causes the upstroke and what causes the downstroke? And why is there an undershoot?

A

Upstroke due to cell becoming more +ve due to influx of Na ions.
Downstroke due to cell repolarising due to efflux of K ions.
Undershoot is due to delayed closure of K channels

66
Q

How can a Na channel go from being inactivated to closed?

A

Repolarisation of the cell

67
Q

What is the refractory period?

A

Time when the Na channels are inactivated, at this point they are non conducting, to close the cell needs to repolarise.

68
Q

What do oligodendrocytes do?

A

Produce myelinated cells in CNS

69
Q

What produces myelinated cells in the PNS?

A

schwann cells

70
Q

What are microglia?

A

Immune surveillance, the marcrophages of the CNS

71
Q

What are the pre and postganglionic neurones of the sympathetic system?

A 
Pre-ganglionic = acetyl choline (always)
Post-ganglionic = noradrenaline (usually)
72
Q

what does sympathetic stimulation do to the HR, bronchi, mucus production and arterioles?

A

increases HR
dilates/relaxed bronchi
decreases mucous production
vasoconstriction

73
Q

Ejaculation is regulated by which ANS response?

A

Sympathetic

74
Q

What are the pre and post-ganglionic neurones for the parasympathetic system?

A

Both acetyl choline

75
Q

From where do the sympathetic chains derive from?

A

Thoraco-lumbar outflow (T1-L2)

76
Q

Where does parasympathetic activity originate from?

A

CN 3, 7, 9 and 10

77
Q

What does parasympathetic stimulation cause on the heart, bronchi, and blood vessels?

A

Decreased HR
Bronchoconstriction
Stimulates mucus production
NO effect on blood vessels

78
Q

What type of ANS causes erection?

A

Parasympathetic

79
Q

Describe the chemical transmission allowing a sympathetic response.

A

AP from CNS
Travels to pre-synaptic terminal of perganglionic neuron.
Triggers Ca entry and ACh release
ACh opens ligand-gated ion channels in the postganglionic neurone.
This causes depolarisation and generation of APs which travel to the presynaptic terminal of the neurone triggering Ca entry and release of noradrenaline.

80
Q

What are the two key differences in chemical transmission in the sympathetic vs parasympathetic system?

A

In parasympathetic ACh is released by both pre and post-ganglionic neurones.
ACh (para) activates muscarinic G-protein receptors.
Noradrenaline actives G- protein adrenoceptors

81
Q

Describe the structure of G-protein coupled receptor in response to the receptor part.

A

It is an integral membrane protein.
Has extracellular NH2 and intracellular COOH termini.
7 transmembrane spanse joined by 3 extracellular and 3 connecting loops.

82
Q

Describe the structure of the G-protein part of the GPCR.

A

Peripheral membrane protein.
3 polypeptide subunits (alpha = binding site)
Contains guanine nucleotide binding site which holds GTP.

83
Q

How do GPCR work when there is no signalling?

A

The receptor is unoccupied.
G protein binds GDP.
Effector not modulated

84
Q

How is the signal turned on in a GPCR?

A

Agonist activates receptor.
G protein couples with receptor.
GDP dissociated and GTP binds instead to alpha subunit
G protein dissociates.
Alpha subunit combines with and modifies activity of effector.
(agonist may dissociate from receptor but signalling continues)

85
Q

Describe how the signal is turned off in a GPCR?

A

Alpha subunit hydrolyses GTP -> GDP.

It then rejoins the beta gamma subunit

86
Q

what do nicotinic acetylcholine receptors consist of?

A

5 glycoprotein subunits that form a central, cation conducting channel

87
Q

describe what happens during the cholinergic (ACh) transmission at parasympathetic neuroeffector junctions

A

Uptake of chlorine, synthesising and storing ACh.
Depolarisation by AP, causing Ca influx and Ca induced release of ACh.
ACh muscarinic receptors (M1-3) are activated causing a cellular response.
ACh is degraded to choline and acetate by AChE which terminates transmissions.
Reuptake and reuse of choline.

88
Q

What degrades ACh?

A

AChE

89
Q

Describe what G-protein muscarinic ACh receptor subtype M1 does and its alpha subunit’s name.

A

Alpha subunit Gq

Stinulates phopholipase C causing increased stomach acid secretion.

90
Q

Describe what G-protein muscarinic ACh receptor subtype M2 does and its alpha subunit’s name.

A

Alpha subunit Gi.

Inhibits adenylyl cyclase, opening K channels, causing decreased HR

91
Q

Describe what G-protein muscarinic ACh receptor subtype M3 does and its alpha subunit’s name.

A

Alpha subunit Gq

Stimulates phospholipase C, causing increased saliva secretion and bronchoconstriction

92
Q

Describe what happens in noradrenergic transmission at sympathetic neuroeffector junctions.

A

Synthesis and storage of NA
Depolarization by AP
Ca influx causing release of NA.
Activation of adrenoceptor subtypes causing cellular response.
Reuptake of NA by transporters.
Metabolism of NA by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT)

93
Q

What are the adrenoceptor subtypes at sympathetic neuroeffector junctions?

A

beta 1 and 2 and alpha 1 and 2

94
Q

What is adrenoceptor beta 1’s alpha subunit called and what does it do?

A

Gs alpha subunit

Stimulation of adenylyl cyclase causing increased HR and force

95
Q

What is adrenoceptor beta 2’s alpha subunit called and what does it do?

A

Gs alpha subunit.

Stimulates adenylyl cyclase causing relaxation of bronchial and vascular smooth muscle

96
Q

What is adrenoceptor alpha 1’s alpha subunit called and what does it do?

A

Gq alpha subunit

Stimulation of phospholipase C causing contraction of vascular smooth muscle

97
Q

What is adrenoceptor alpha 2’s alpha subunit called and what does it do?

A

Gi

Inhibition of adenylyl cyclase causing inhibition of NA release.

98
Q

Describe what amphetamine is and what it does.

A

Is a U1 substrate.
Works by inhibiting MAO, which displaces NA into the cytoplasm.
NA accumulates in synaptic cleft causing increased adrenoceptor stimulation

99
Q

describe what prazosin is and what it is used for.

A

Selective, competative antagonist of alpha 1 adrenoceptors. Causes vasodilation and used as anti-hypertensive

100
Q

describe what atenolol is and what it does.

A

Selective, competative antagonist of beta 1. Therefore will decrease HR and so used as anti-anginal and anti-hypertensive agent.

101
Q

Describe what salbutamol is and used for.

A

Selective agonist for beta 2 adrenoceptor. Used as a bronchodilator in asthma as will increase the relaxation action of the sympathetic adrenoceptor

102
Q

describe what atropine is and what it does.

A

Competitive antagonist of muscarinic ACh receptors, blocks the parasympathetic division of ANS. So is used to reverse bradycardia post MI

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