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Phase 2a Medicine (JH) > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Define pharmacology.

A

The study of the effects of drugs.

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2
Q

Define pharmacokinetics.

A

How the body affects the drug. (The study of absorption, distribution, metabolism and excretion of drugs.)

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3
Q

Define pharmacodynamics.

A

How the drug affects the body.

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4
Q

What is the main target of drugs?

A

Receptors.

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5
Q

What is the function of receptors?

A

They are the principal means by which chemicals communicate.

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6
Q

Give three examples of chemicals which communicate via receptors.

A

Neurotransmitters.
Autoacids (local hormones).
Hormones.

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7
Q

Give four examples of receptor.

A

Ligand-gated ion channels.
G protein coupled receptors.
Kinase-linked receptors.
Cytosolic/nuclear receptors.

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8
Q

Give an example of a ligand-gated ion channel.

A

Nicotinic ACh receptor.

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9
Q

Give an example of a G protein coupled receptor.

A

Beta-adrenoceptors.

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10
Q

What do kinase-linked receptors detect?

A

Growth factors.

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11
Q

What do cytosolic/nuclear receptors sense?

A

Steroids.

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12
Q

How do cytosolic/nuclear receptors respond to sensing steroids?

A

By modifying gene transcription.

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13
Q

Which part of cytosolic/nuclear receptor structure recognises discrete regions of DNA?

A

Zinc fingers.

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14
Q

Other than receptors, what three other things do drugs target?

A

Enzymes.
Transporters.
Ion channels.

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15
Q

An imbalance of chemicals / receptors can lead to what?

A

Pathology.

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16
Q

Allergy is a result of what chemical imbalance?

A

Increased histamine.

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17
Q

Parkinson’s is a result of what chemical imbalance?

A

Decreased dopamine.

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18
Q

Myasthenia gravis is a result of what receptor imbalance?

A

Loss of nicotinic ACh receptors.

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19
Q

What is myasthenia gravis?

A

A neuromuscular disease that leads to skeletal muscle weakness - commonly affecting the muscles of the eyes and face as well as those used for swallowing.

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20
Q

Mastocytosis is a result of what receptor imbalance?

A

Increase in C-kit receptor.

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21
Q

What is mastocytosis?

A

Mast cell disease that causes itching, hives and anaphylactic shock from the release of histamine.

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22
Q

What are receptor ligands?

A

Anything that acts at a receptor.

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23
Q

Define potency.

A

Measure of how well a drug works.

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24
Q

Define EC50.

A

The concentration of a drug that gives half the maximal response.

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25
Q

Define agonist.

A

A compound that binds to a receptor and activates it.

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26
Q

Normal response curves are usually two shapes, which?

A

Linear.

Sigmoidal.

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27
Q

A sigmoidal response curve uses what scale for the agonist?

A

A log scale.

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28
Q

What is a ‘full agonist’?

A

An agonist that has a response of 100%.

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29
Q

How do we describe a drug with a lower EC50 than another drug.

A

The drug with a lower EC50 is said to be more potent as it has a greater response at lower concentrations.

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30
Q

What is a ‘partial agonist’?

A

An agonist that has a maximum response of less than 100%.

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31
Q

Define efficacy (Emax).

A

The maximum response that is able to be achieved from an agonist.

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32
Q

How do we describe a drug with a higher Emax than another drug.

A

The drug with a higher Emax is said to be more efficacious.

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33
Q

Define intrinsic activity.

A

The relative ability of a drug-receptor complex to produce a maximum functional response.

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34
Q

How is intrinsic activity calculated?

A

(Emax of a partial agonist) / (Emax of a full agonist).

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35
Q

Define antagonist.

A

A compound that reduces the effect of an agonist (antagonists do not activate receptors).

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36
Q

The activity of an antagonist is affected by what?

A

The affinity of the antagonist for the receptor.

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37
Q

Describe competitive antagonism.

A

Antagonists compete with the agonists to bind (but not activate) receptors, thereby preventing the agonist from having an effect.

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38
Q

Describe how a dose response curve is affected by the addition of a competitive antagonist. .

A

The dose response curve shifts to the right.

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39
Q

The rightward shift of a dose response curve reflects what effect?

A

More agonist is required to illicit the same response.

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40
Q

Describe non-competitive antagonism.

A

Antagonists bind near the receptor and prevent activation of the receptor. As the antagonist does not bind directly, agonists are still able to bind (but not activate) the receptor.

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41
Q

Describe how a dose response curve is affected by the addition of a non-competitive antagonist.

A

The dose response curve shifts to the right and down.

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42
Q

The rightward and downward shift of a dose response curve reflects what effect?

A

More agonist is required to illicit the same response (more than with a competitive antagonist).

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43
Q

Give two types of cholinergic receptor.

A

Muscarinic (mAChR).

Nicotinic (nAChR).

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44
Q

Give the agonist and antagonist at a mAChR.

A

Agonist - muscarine.

Antagonist - atropine.

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45
Q

Give the agonist and antagonist at a nAChR.

A

Agonist - nicotine.

Antagonist - curare.

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46
Q

Give the agonist of a histamine receptor and the effect of that agonist.

A

Histamine. Histamine causes contraction of the ileum and acid secretion from parietal cells.

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47
Q

Give the antagonist of a histamine receptor and the effect of that antagonist.

A

Mepyramine. Mepyramine causes reversed contraction of the ileum and has no effect on acid secretion.

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48
Q

Give four factors that govern drug action.

A

Affinity.
Efficacy.
Number of receptors at tissue.
Signal amplification.

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49
Q

Define affinity.

A

Affinity describes how well a ligand binds to the receptor.

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50
Q

Define efficacy.

A

Efficacy describes how well a ligand activates the receptor.

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51
Q

Is affinity a property shown by agonists or antagonists?

A

Affinity is shown by both agonists and antagonists.

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52
Q

Is efficacy a property shown by agonists or antagonists?

A

Efficacy is shown by agonists and not antagonists.

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53
Q

Describe how the number of receptors at a tissues effects how much drug is required.

A

A decrease in the number of receptors at a tissue will increase the amount of drug required to illicit the same effect and vice versa.

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54
Q

Describe what is meant by ‘receptor reserve’.

A

Excess receptors on a cell surface than what is require to achieve a full effect thereby stimulation of only a fraction of the receptor population is enough to achieve maximum response.

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55
Q

Which agonists are receptor reserves available for?

A

Only full agonists.

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56
Q

Define signal amplification.

A

When a ligands binds to a receptor and triggers a signalling cascade.

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57
Q

Signal amplification determines what?

A

How powerful the response will be.

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58
Q

What determines signal amplification?

A

The type of tissue the receptor is based in.

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59
Q

Describe what is meant by ‘allosteric modulation’.

A

The binding of an allosteric ligand at a site on the receptor other than the primary (orthosteric) site. Allosteric modulation modifies the response by effecting the signalling cascade.

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60
Q

Describe inverse agonism.

A

An inverse agonist reduces receptor activation (as opposed to an antagonist - which has no effect).

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61
Q

Define tolerance.

A

The reduction in drug/agonist effect over time.

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62
Q

Under what conditions does tolerance develop?

A

Continuous, repeated high concentrations of drug use over time.

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63
Q

Give three examples how by receptors may become desensitised.

A

They become uncoupled and can no longer interact with G-protein.
The receptor is internalised in the vesicle of a cell.
The receptor becomes degraded.

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64
Q

Why is selectivity a better term to describe activity than specificity?

A

No compound is ever truly specific.

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65
Q

What kind of agonist is isoprenaline?

A

A non-selective B-adrenoceptor - it activates both B1 (heart) and B2 (lungs).

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66
Q

What kind of agonist is salbutamol?

A

A selective B2-adrenoceptor - but loses selectivity at very high concentrations.

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67
Q

Give two examples of NSAIDs.

A

Aspirin and ibuprofen.

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68
Q

Give three actions of NSAIDs.

A

Analgesic (pain relief).
Antipyretic (reduces fever).
Anti-inflammatory.

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69
Q

NSAIDs inhibit which enzyme in the pathway to reduce inflammation?

A

NSAIDs competitively inhibit the COX enzyme.

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70
Q

COX is an abbreviation of what?

A

Cyclooxygenase.

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71
Q

The COX enzyme is responsible for what conversion?

A

The breakdown of arachidonic acid to prostaglandin H2 (PGH2).

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72
Q

Give four examples of prostanoids that are produced from the action of specific syntheses on PGH2.

A 
Prostaglandin D2 (PGD2). 
Prostaglandin E2 (PGE2). 
Prostaglandin I2 (PGI2). 
Thromboxane A2 (TXA2).
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73
Q

The synthase that produces PGD2 is found where?

A

Mast cells.

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74
Q

The synthase that produces PGI2 is found where?

A

Vascular endothelial cells.

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75
Q

The synthase that produces PGE2 is found where?

A

Macrophages.

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76
Q

The synthase that produces TXA2 is found where?

A

Platelets.

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77
Q

By what mechanism does aspirin prevent the breakdown of arachidonic acid?

A

By irreversibly binding to the activate site of the COX enzyme (irreversible inactivation).

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78
Q

State and describe the two isoforms of the COX enzyme.

A

COX-1 is found normally and widely around the body.

COX-2 is induced and found in inflammation.

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79
Q

Does apirin act on COX-1 or COX-2?

A

Aspirin is non-selective so acts on COX-1 and COX-2.

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80
Q

Name a drug that is COX-2 selective.

A

Celecoxib.

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81
Q

Give two examples of ACE inhibitors.

A

Captopril.

Enalapril.

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82
Q

ACE inhibitors are an example of what type of drug?

A

Anti-hypertensives.

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83
Q

Inhibition of ACE prevents which conversion?

A

The conversion of angiotensin I to angiotensin II.

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84
Q

Explain the effect of less angiotensin II on hypertension.

A

Fewer angiotensin II receptors are activated therefore less vasoconstriction as well as less aldosterone released.

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85
Q

Give three examples of beta-lactam antibiotics.

A

Penicillins.
Amoxicillin.
Cephalosporins.

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86
Q

Describe how beta-lactam antibiotics work.

A

Inhibit the activity of certain enzymes to prevent the biosynthesis of peptidoglycan bacterial cell walls.

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87
Q

What drug type are not effectively removed from the kidneys and why?

A

Lipophilic drugs as they are passively absorbed due to the fact they can diffuse through cell membranes easily.

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88
Q

How can drugs be altered to enable them to be excreted more easily?

A

Cytochrome P450 introduces a hydroxyl group into the drug.

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89
Q

Give three examples of proton pump inhibitors.

A

Omeprazole.
Lansoprazole.
Pantoprazole.

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90
Q

Proton pump inhibitors are activated in what environment?

A

Acidic environments such as in the stomach.

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91
Q

What is the function of proton pump inhibitors?

A

PPIs act to inhibit acid secretion.

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92
Q

Stable stomach acidity is maintained through the action of which two ligands?

A

Prostaglandin E2.

Histamine.

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93
Q

How does PGE2 regulate stomach acidity?

A

PGE2 released from chromatin cells binds to EP3 receptors on parietal cells. PGE2 reduces the activity of the H+/K+ ATPase pump, inhibiting parietal cells.

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94
Q

How does histamine regulate stomach acidity?

A

Histamine released from histaminocytes binds to H2 receptors on parietal cells. Histamine increases the activity of the H+/K+ ATPase pump, activating parietal cells.

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95
Q

How do PPIs act to reduce stomach acidity?

A

PPIs irreversibly inactive the proton pump.

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96
Q

Diuretics act to inhibit which transport protein?

A

Symporters.

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97
Q

How does the drug furosemide act as a diuretic?

A

Furosemide inhibits the NKCC2 pump on the thick ascending limb of the loop of Henle.

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98
Q

What is the effect of the inhibition of the NKCC2 pump on the ascending limb of the loop of Henle?

A

The amount of Na+, Cl- and K+ ions able to enter the medullary interstitium is reduced, reducing hyperosmolarity therefore less water will diffuse out of the collecting ducts and into the blood.

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99
Q

How do thiazides act as diuretics?

A

Thiazides inhibit the Na+, Cl- cotransporter on the distal convoluted tubule, increasing water loss.

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100
Q

How can increased water excretion be useful?

A

In the treatment of hypertension and heart failure. Water loss reduces blood volume and blood pressure.

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101
Q

What is the function of neuronal uptake inhibitors?

A

Neuronal uptake inhibitors increase the concentration of neurotransmitter at a synapse by preventing their reuptake.

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102
Q

Give four examples of neurotransmitters subject to uptake.

A

Dopamine.
Noradrenaline.
Serotonin.
GABA.

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103
Q

Fluoxetine/Prozac inhibits the reuptake of what neurotransmitter?

A

Serotonin.

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104
Q

Imipramine inhibits the reuptake of what neurotransmitter?

A

Mostly inhibits the reuptake of noradrenaline and serotonin.

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105
Q

Cocaine inhibits the reuptake of what neurotransmitter?

A

Dopamine.

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106
Q

Tiagabin inhibits the reuptake of what neurotransmitter?

A

GABA.

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107
Q

Give three examples of calcium ion channel blockers.

A

Amlodipine.
Verapamil.
Diltiazem.

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108
Q

Amlodipine, verapamil and diltiazem are used in the treatment of what?

A

Hypertension.

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109
Q

How does amlodipine reduce hypertension?

A

Blocks the calcium channel (found in vascular smooth muscle), preventing the influx of Ca2+ after depolarisation of the membrane, therefore preventing vasoconstriction.

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110
Q

Give two examples of local anaesthetics.

A

Lidocaine.

Procaine.

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111
Q

How do local anaesthetics work?

A

By interrupting axonal neurotransmission in the sensory nerves.

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112
Q

How do local anaesthetics interrupt axonal neurotransmission?

A

By blocking voltage dependent sodium channels, preventing the depolarisation of neurones so threshold isn’t reached and no action potential is developed/propagated.

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113
Q

What is a drug?

A

A compound that is administered with an intended therapeutic effect.

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114
Q

What are the three phases of traditional pharmacokinetics?

A

Uptake into the plasma.
Distribution from the plasma.
Elimination from the plasma.

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115
Q

How are the phases of pharmacokinetics measured?

A

With concentration/time curves from serial plasma sampling.

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116
Q

The rate of diffusion of a dissolved drug into the plasma is affected by what three factors?

A

Concentration gradient.
Temperature.
Chemical reactions between the drug and the solute/plasma.

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117
Q

What is a first order reaction?

A

The rate is direction proportional to the concentration of the drug.

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118
Q

What is a second order reaction?

A

The rate is direction proportional to the square of the concentration of the drug.

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119
Q

What is a third order reaction?

A

The rate is direction proportional to the cube concentration of the drug.

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120
Q

What is a zero order reaction?

A

The rate is unrelated to the concentration of the drug.

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121
Q

What order process is diffusion?

A

First order.

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122
Q

What is plasma?

A

The fluid fraction (or aqueous solution) that remains when cells are removed from the blood.

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123
Q

Pharmacokinetic theory considers the body as three main compartments divided by what?

A

Tissue lipid rich barriers.

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124
Q

What are the three main compartments considered by pharmacokinetic theory?

A

Plasma.
Interstitial.
Intracellular.

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125
Q

What is the volume of the plasma?

A

5 litres.

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126
Q

What is the volume of the interstitial compartment?

A

15 litres.

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127
Q

What is the volume of the intracellular compartment?

A

45 litres.

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128
Q

Cellular tissue can be divided into which two types?

A 
Vessel rich (viscera). 
Vessel poor.
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129
Q

Name five ways a drug can move between compartments?

A 
Simple diffusion. 
Facilitated diffusion. 
Active transport. 
Through extracellular spaces. 
Non-ionic diffusion.
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130
Q

Describe movement by simple diffusion.

A

The movement of solutes from a region of high concentration to a region of low concentration - through a lipid barrier.

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131
Q

Describe movement by facilitated diffusion.

A

The movement of solutes from a region of high concentration to a region of low concentration - through protein channels.

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132
Q

Describe movement by active transport.

A

The movement of solutes from a region of low concentration to a region of high concentration - through protein carriers (requires energy).

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133
Q

Describe movement through extracellular spaces.

A

The movement of solutes through pores in a cell membrane.

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134
Q

Describe movement by non-ionic diffusion.

A

Ionic molecules become less ionic (more non-ionic) and thus more lipid soluble, enabling it to cross the lipid membrane and enter the cell.

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135
Q

Give an example of a drug that moves by non-ionic diffusion.

A

Aspirin.

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136
Q

How does a pH increase affect a weak acid?

A

The weak acid becomes more ionised.

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137
Q

How does a pH increase affect a weak base?

A

The weak base becomes less ionised.

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138
Q

Name a factor which has a large effect on uptake into the plasma.

A

The route of administration of the drug.

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139
Q

Define bioavailability.

A

The amount of drug taken up as a proportion of the amount administered.

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140
Q

What is an ideal bioavailability?

A

1 (100%).

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141
Q

Name ten routes of administration.

A 
Oral. 
Intramuscular. 
Intravenous. 
Subcutaneous
Transcutaneous. 
Intrathecal. 
Sublingual. 
Inhalation. 
Topical. 
Rectal.
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142
Q

What factor affects the amount of aspirin uptake?

A

Gastric pH.

143
Q

How does a raised pH affect the uptake of aspirin?

A

Reduced uptake of aspirin (a weak acid becomes more ionised) and thus a reduction in bioavailability.

144
Q

In which compartment(s) are proteins/large molecules active?

A

Plasma compartment.

145
Q

In which compartment(s) are water soluble molecules active?

A

Plasma and interstitial compartment.

146
Q

In which compartment(s) are lipid soluble molecules active?

A

Intracellular compartment.

147
Q

What is volume of distribution?

A

The volume (in litres) that the drug would occupy if it was distributed through all compartments as if they were all plasma.

148
Q

How is volume of distribution calculated?

A

Total amount of drug in the body / Concentration of drug in the plasma.

149
Q

The elimination of a drug is from where?

A

The plasma compartment.

150
Q

Which two routes of elimination are used for the majority of drugs?

A

Renal.

Hepatic.

151
Q

What is clearance?

A

The removal of a drug from the plasma by either the liver or kidneys.

152
Q

Define clearance.

A

The volume of plasma that can be completely cleared of a drug per unit time (ml/min).

153
Q

Clearance is measure of what?

A

Efficiency.

154
Q

What is assumed when measuring renal clearance?

A

The rate of elimination = the rate of appearance in urine.

155
Q

Name the marker substances used when measuring renal clearance.

A

Creatinine.

156
Q

Give the % of cardiac output that renal blood flow accounts for and the volume.

A

18% = 1L/min.

157
Q

Give the % of blood flow that renal plasma flow accounts for and the volume.

A

60% = 600mls/min.

158
Q

Give the % of blood flow that glomerular filtration accounts for and the volume.

A

12% = 130mls/min.

159
Q

Most drugs eliminated by the kidney are…

A

Water soluble and small molecules.

160
Q

Acute renal impairment is usually secondary to what?

A

Reduced pre-renal perfusion.

161
Q

Chronic renal impairment is usually caused by what?

A

Diabetes and hypertension.

162
Q

How may renal impairment affect drug choice for patients?

A

Drugs should be chosen that are eliminated by the liver instead.
Avoid nephrotoxic drugs.

163
Q

What % of cardiac output does hepatic blood flow account for?

A

24%.

164
Q

What is the hepatic extraction ratio?

A

The proportion of drug removed by one passage through the liver.

165
Q

When the hepatic extraction ratio is high, clearance is limited by…

A

Perfusion (hepatic blood flow).

166
Q

When the hepatic extraction ratio is low, clearance is limited by…

A

Diffusion.

167
Q

How does the liver respond to exposure to low HER drugs?

A

By producing more enzymes - which enable it to increase clearance.

168
Q

What is the aim of drug metabolism in the liver?

A

To make drugs more polar (so they can cross membranes less easily) and thus are more easily excreted.

169
Q

Drug metabolism in the liver occurs via which reactions?

A

Phase I and phase II reactions.

170
Q

What is the function of phase I and phase II reactions?

A

Phase I (functionalisations) reactions introduce a reactive group to the drug for phase II (conjugation) reactions.

171
Q

Functionalisation reactions can occur through the addition of which functional groups?

A
  • OH
  • SH
  • NH2
  • COOH
172
Q

Which enzyme are functionalisation reactions catalysed?

A

Cytochrome P450.

173
Q

What type of enzyme is CYP450?

A

A microsomal enzyme.

174
Q

What is a microsomal enzyme?

A

Enzymes attached to microsomes (particles consisting of ribosomes attached to a piece of endoplasmic reticulum).

175
Q

Describe how biliary secretion is used to excrete drugs.

A

Phase I water soluble metabolites and phase II glucuronides enter the bile and then the gut via the cystic duct.

176
Q

How is biliary secretion replaced during cholestasis?

A

Increased amounts are excreted by the kidneys.

177
Q

Describe how the enterohepatic circulation may prolong the action of some drugs.

A

Large bowel flora tend to metabolise glucuronic acid group on phase II glucuronide, liberating the drug and allowing it to be reabsorbed into the blood (where it has a prolonged effect) before going back to the liver and being reconjugated.

178
Q

What percentage of liver function has to be lost to have an effect on drug metabolism?

A

70%.

179
Q

Give three reasons why intravenous infusions are used for some drugs.

A

Highly accurate drug delivery (guarantees 100% bioavailability).
Quickest administration route.
Some drugs are ineffective when administered by other routes.

180
Q

Give an advantage and disadvantage of oral administration.

A

Adv: Excellent patient compliance with one tablet a day.
Dis: Bioavailability can be highly variable = uncertainty in treatment effectiveness.

181
Q

Give two disadvantages of intravenous infusion.

A

Requires constant monitoring.

Has the potential for serious calculation errors.

182
Q

Drug doses of intravenous infusion are given in what units?

A

mg/hour

183
Q

What factor is used when deciding IV drug dosage?

A

Body weight.

184
Q

When considering pharmokinetics, what does a high volume of distribution mean?

A

A small fraction of the drug will be in the plasma so it will take a long time to reach a steady state.

185
Q

What is meant by ‘steady state’?

A

Infusion dosage is equal to the rate of elimination from plasma.

186
Q

What is a loading/bolus dose of drug and why is it used?

A

A loading dose is an initial higher dose of drug given at the beginning of treatment. It is used to speed up the saturation of all the components.

187
Q

What is the risk of elimination becoming saturated?

A

Drug accumulation and thus toxicity.

188
Q

Give three qualities of drugs that are ideal for use in IV infusion.

A

Drugs with a small volume of distribution.
Drugs broken down by tissue/plasma enzymes irrespective of liver and renal function.
Drugs with a low risk of toxicity.

189
Q

Name the two parts that make up the peripheral nervous system.

A

Somatic.

Autonomic.

190
Q

State whether the somatic and autonomic nerve systems are voluntary or involuntary.

A

Somatic - voluntary.

Autonomic - involuntary.

191
Q

What neurotransmitter is used on the parasympathetic branch of the autonomic nervous system?

A

Acetylcholine.

192
Q

What neurotransmitter is used on the sympathetic branch of the autonomic nervous system?

A

Noradrenaline.

193
Q

ACh is the principal neurotransmitter in the body. What two types of cholinergic receptor does it act on?

A

Nicotinic (nAChR).

Muscarinic (mAChR).

194
Q

In the sympathetic nervous system: acetylcholine mediates the release of which other two chemical messengers?

A

Adrenaline.

Noradrenaline.

195
Q

In the parasympathetic nervous system: acetylcholine is mediated by which receptors?

A

Muscarinic ACh receptors (M1, M2, M3).

196
Q

Where are nicotinic ACh receptors found?

A

At the neuromuscular junction.

197
Q

In the somatic nervous system: acetylcholine is mediated by which receptors?

A

Nicotinic receptors at the neuromuscular junction.

198
Q

Name the enzyme required to make ACh from acetyl CoA and choline.

A

Choline acetyltransferase.

199
Q

ACh is broken down in the synaptic cleft after use by which enzyme?

A

Acetylcholinesterase.

200
Q

ACh is broken down by acetylcholinesterase into what?

A

Choline and acetate.

201
Q

Describe the effect of botulinum toxin on neurotransmitters at the neuromuscular junction.

A

Inhibits ACh release into the neuromuscular junction.

202
Q

Describe the mechanism by which botulinum toxin inhibits ACh release into the neuromuscular junction.

A

Uses protease to degrade vesicle proteins, preventing vesicle fusion and the release of ACh into the synaptic cleft.

203
Q

Give two medical uses of botulinum toxin.

A

Cosmetic (forehead wrinkles).

Spasticity (overactive muscle movement).

204
Q

Give a brand name of botulinum toxin.

A

Botox.

205
Q

Curare is an example of what kind of drug?

A

Competitive nAChR antagonist.

206
Q

Describe the mechanism by which curare results in a muscle relaxant effect.

A

Binds to nicotinic binding sites on nAChR preventing the binding of ACh.

207
Q

What is the effect of suxamethonium?

A

Causes short-term paralysis.

208
Q

Describe the mechanism by which suxamethonium results in short-term paralysis.

A

Essentially two ACh together. Acts to desensitise the receptor resulting in paralysis of the skeletal muscle.

209
Q

Sarin nerve gas is an example of what kind of drug?

A

Irreversible acetylcholinesterase inhibitor.

210
Q

Give seven adverse effects of muscarinic agents.

A 
Diarrhoea. 
Urination. 
Miosis. 
Bradycardia. 
Emesis. 
Lacrimation. 
Salivation.
211
Q

Parasympathetic nervous system: how does acetylcholine affect pupillary constriction?

A

Acetylcholine causes the pupils to constrict.

212
Q

Sympathetic nervous system: how does noradrenaline affect tears?

A

Noradrenaline inhibits tears.

213
Q

Parasympathetic nervous system: how does acetylcholine affect salivation?

A

Acetylcholine stimulates salivation.

214
Q

Sympathetic nervous system: how does noradrenaline affect heart rate?

A

Noradrenaline increases heart rate.

215
Q

Parasympathetic nervous system: how does acetylcholine affect respiration?

A

Acetylcholine reduces respiration.

216
Q

Sympathetic nervous system: how does noradrenaline affect digestion?

A

Noradrenaline inhibits digestion.

217
Q

Noradrenaline and adrenaline belong to what family?

A

Catecholamines.

218
Q

Noradrenaline and adrenaline are also known by which other names?

A

Norepinephrine (noradrenaline).

Epinephrine (adrenaline).

219
Q

Name the precursor of noradrenaline and adrenaline.

A

Tyrosine.

220
Q

Give the intermediaries involved in the production of adrenaline from tyrosine.

A

Tyrosine > DOPA > Dopamine > Noradrenaline > Adrenaline.

221
Q

MonoAmine Oxidase and Catechol-O-Methyl Transferase have what effect on catecholamines?

A

They both inactivate catecholamines by metabolising them and reducing their stimulant effect.

222
Q

Name five classes of adrenoceptor.

A 
Alpha-1
Alpha-2
Beta-1
Beta-2
Beta-3
223
Q

Alpha-1 adrenoceptors primarily mediate what?

A

Smooth muscle contraction.

224
Q

Give three effects of the activation of alpha-1 adrenoceptors.

A

Vasoconstriction of blood vessels.
Pupil dilation.
Bladder contraction.

225
Q

Alpha-2 adrenoceptors have which primary function?

A

Presynaptic inhibition of noradrenaline in a form of negative feedback.

226
Q

Give five effects of the activation of beta-1 adrenoceptors.

A

Increased force of heart contraction.
Increased heart rate.
Increased electrical conduction in the heart.
Increased renin release from the kidney.
Increased blood pressure.

227
Q

Name the large plasma protein cleaved by renin.

A

Angiotensinogen.

228
Q

Where is angiotensinogen produced?

A

In the liver.

229
Q

Angiotensinogen is cleaved by renin to produce a smaller popylpetide called what?

A

Angiotensin I.

230
Q

Where is renin released from?

A

The juxtaglomerular cells in the afferent arterioles that supply the nephrons in the kidneys.

231
Q

Angiotensin I is converted to angiotensin II by what enzyme?

A

Angiotensin-converting-enzyme (ACE).

232
Q

Where is ACE produced?

A

The lungs.

233
Q

Angiotensin II stimulates which cells?

A

Cells of the zona glomerulosa.

234
Q

Where are the cells of the zona glomerulosa located?

A

In the adrenal cortex of the adrenal glands.

235
Q

Name the hormone secreted by the cells of the zona glomerulosa when stimulated by angiotensin II.

A

Aldosterone.

236
Q

Give two ways by which aldosterone increases blood pressure.

A

By stimulating vasopressin release (which causes water retention).
By stimulating the transcription of epithelial sodium channels resulting in increased Na+ reabsorption and also H2O reabsorption.

237
Q

Give three effects of the activation of beta-2 adrenoceptors.

A

Bronchodilation.
Vasodilation.
Reduced GI motility.

238
Q

Give two effects of the activation of beta-3 adrenoceptors.

A

Increased lipolysis.

Relaxation of bladder.

239
Q

What is lipolysis?

A

Breakdown of lipids (hydrolysis of triglycerides into glycerol and free fatty acids).

240
Q

What type of agonist is adrenaline?

A

Non-selective agonist.

241
Q

What is meant by the term ‘non-selective agonist’?

A

Works at any alpha or beta adrenoceptor.

242
Q

Give examples of three clinical conditions under which adrenaline used?

A

Anaphylaxis.
Cardiac arrest.
Acute hypotension.

243
Q

Which adrenoceptors are targeted by adrenaline?

A

Alpha-1 (blood vessels).
Beta-1 (heart).
Beta-2 (bronchial smooth muscle).

244
Q

Describe how the effects of adrenaline can help treat anaphylaxis.

A

Anaphylaxis characterised by reduced blood pressure and increased bronchoconstriction. Adrenaline causes vasoconstriction and increases the force of heart contraction (increasing blood pressure). Adrenaline also causes bronchodilation.

245
Q

Name two drugs which are alpha-1 adrenergic agonists.

A

Phenylephrine.

Oxymetazoline.

246
Q

Give a clinical use for phenylephrine and oxymetazoline.

A

Useful as a nasal decongestant (as they shrink nasal blood vessels - less fluid leakage).

247
Q

Name a drug that is an alpha-2 adrenergic agonist.

A

Clonidine.

248
Q

Give a clinical use for clonidine.

A

Useful as an anti-hypertensive (as it inhibits noradrenaline release - slower heart rate).

249
Q

Name a drug that is a beta-1 adrenergic agonist.

A

Dobutamine.

250
Q

Give a clinical use for dobutamine.

A

Cardiac stimulant (positive inotropic effect).

251
Q

What is meant by the term ‘positive inotropic effect’?

A

The effect is increased force of cardiac muscle contraction.

252
Q

Name a drug that is a beta-2 adrenergic agonist.

A

Salbutamol.

253
Q

Give a clinical use for salbutamol.

A

Asthma (causes bronchodilation).

254
Q

Name a drug that is a beta-3 adrenergic agonist.

A

Mirabegron.

255
Q

Give a clinical use for mirabegron.

A

Useful in the treatment of overactive bladder (as it causes bladder relaxation).

256
Q

Describe the effect of amphetamines and cocaine as indirect-acting adrenergic agonists.

A

Inhibit the noradrenaline transporter on the pre-synaptic neurone, causing a build up of catecholamines (notably noradrenaline) in the synapse. Results in CNS overstimulation.

257
Q

Give examples of two conditions that are treated by the use of MAO and COMT.

A

Parkinson’s.

Depression.

258
Q

Describe the effect of MAO and COMT as indirect-acting adrenergic agonists.

A

Result in a buildup of noradrenaline + other catecholamines such as dopamine.

259
Q

Name a drug that is an alpha-1 adrenergic antagonist.

A

Doxazosin.

260
Q

Give a clinical use for doxazosin.

A

Reduces blood pressure (as is a vasodilator).

261
Q

Name a drug that is an alpha-2 adrenergic antagonist.

A

Yohimbine.

262
Q

Give a clinical use for yohimbine.

A

Blocks the alpha-2 receptor therefore no noradrenaline inhibition - raise blood pressure.

263
Q

Why shouldn’t beta blockers be used for patients with asthma?

A

Most will be on beta-2 agonists.

264
Q

Give a clinical use for propranolol.

A

Treatment of arrhythmia. Propranolol have membrane stabilising activity (MSA) which means it can inhibit the propagation of action potentials across a membrane.

265
Q

Define druggability.

A

The ability of a protein target to bring small molecules with high affinity.

266
Q

What are stereoisomers?

A

Compounds with the same molecular formula and structural formula but have a different arrangement of their atoms in space.

267
Q

What is meant by ‘rational drug design’?

A

Rational drug design is the process of finding new medications based on the knowledge of a biological target.

268
Q

What is the purpose of high-throughput screening?

A

Rapidly identifies active compounds, antibodies or genes that modulate a particular biomolecular pathway.

269
Q

Define pain.

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage.

270
Q

What are the three components of pain?

A

Sensory.
Emotional.
Actual/potential tissue damage.

271
Q

Give three examples of pain’s positive role.

A

Warning of tissue damage.
Immobilisation for healing.
Protection of the species

272
Q

Give three physiological effects of pain.

A

Increased heart rate.
Increased blood pressure.
Increased respiratory rate.

273
Q

Give five classifications of pain.

A 
Acute pain. 
Cancer pain. 
Chronic non-cancer pain. 
Nociceptive pain. 
Neuropathic pain.
274
Q

What is nociceptive pain?

A

Pain brought about when inflammatory chemicals reach nerves to stimulate pain.

275
Q

What is neuropathic pain?

A

Pain brought about when a nerve is directly damaged causing pain to originate within the nervous system.

276
Q

How long does acute pain generally last?

A

Less than a week.

277
Q

Acute pain results from the activation of which receptors?

A

Nociceptors.

278
Q

What are nociceptors?

A

The nerve endings of sensory nerve fibres of the peripheral nervous system.

279
Q

The pain pathway begins when noxious stimulus is detected by nociceptors and passed where?

A

To the ascending pathway of the spinal cord.

280
Q

From the spinal cord, the pain pathway goes where?

A

The thalamus.

281
Q

From the thalamus, the pain pathway is directed to which three areas of the brain?

A

Cortical areas.
Somatosensory cortex.
Prefrontal cortex.

282
Q

What excitatory neurotransmitter is used in the pain pathway?

A

Glutamate.

283
Q

Give three types of noxious stimulus.

A

Mechanical.
Thermal.
Chemical.

284
Q

Describe how the breakdown of membrane lipids leads to pain.

A

The breakdown of membrane lipids leads to the formation of arachidonic acid (under the action of phospholipase A2). Arachidonic acid is converted to prostaglandins by COX and prostaglandins stimulate pain.

285
Q

Nociceptors are the endings of which two types of nerve fibre?

A

C fibres.

A delta fibres.

286
Q

How are C fibres and A delta fibres structurally different?

A

C fibres are unmyelinated while A delta fibres are myelinated.

287
Q

How C fibres and A delta fibres conduct pain differently.

A

C fibres are characterised by diffuse dull intense pain while A delta fibres conduct localised sharp sensation.

288
Q

What is chronic pain?

A

Ongoing persistent pain for greater than 3-6 months.

289
Q

What is the function of chronic pain?

A

No useful biological function.

290
Q

Give four effects of chronic pain on the individual suffering.

A

Physical immobility.
Emotional distress.
Isolation (little social interaction).
Job issues.

291
Q

What is an adverse drug reaction (ADR)?

A

A response to a drug which is noxious and unintended.

292
Q

What are the five types of adverse drug reaction (ADR)?

A 
A - Augmented. 
B - Bizarre. 
C - Chronic. 
D - Delayed. 
E - End of use.
293
Q

What is a Type A ADR?

A

An extension of the clinical effect. It is predictable and dose related.

294
Q

Which patients are at higher risk of ADR?

A

Those with renal or hepatic impairment due to elimination difficulties.
Elderly patients who have reduced glomerular filtration and hepatic impairment.

295
Q

What is a Type B ADR?

A

Unexpected and unrelated to the dosage. Mostly due to immunological mechanisms (hypersensitivity).

296
Q

What is a Type C ADR?

A

Occurs after long term therapy. May not be immediately obvious with new medicines.

297
Q

What is a Type D ADR?

A

Occurs after a long period of time after treatment.

298
Q

What is a Type E ADR?

A

Withdrawal reactions after relatively long term use.

299
Q

What five questions should you ask to determine the type of ADR?

A

Is there a history of allergy? (B).
Is it predictable from mechanism of action? (A).
Has the patient been on the medication for a long time? (C).
Is the patient withdrawing from medication? (E).
Has the patient used a drug in the past that could be a problem now? (D).

300
Q

What are the five types of hypersensitivity?

A 
Type I (immediate). 
Type II (cytotoxic). 
Type III (immune complex). 
Type IV (delayed).
301
Q

Describe Type I hypersensitivity.

A

The result of exposure to allergens. It is IgE mediated and results in anaphylaxis.

302
Q

Describe Type II hypersensitivity.

A

IgG mediated. Drug combines with protein and body treats protein as foreign, produces antibodies against the antigen, complement activation causes cell death.

303
Q

Describe Type III hypersensitivity.

A

Small immune complexes form that cannot be cleared by macrophages. The complexes accumulate and insert themselves into the walls of blood vessels, glomeruli etc. Complexes attract leukocytes - causing inflammation.

304
Q

Describe Type IV hypersensitivity.

A

T-cell mediated.

305
Q

What causes mast cells to degranulate?

A

Cross linking with IgE receptors.

306
Q

What is release during mast cell degranulation.

A

Histamine.
Thromboxanes and prostaglandins.
Tumour necrosis factor.

307
Q

What are mast cells?

A

A type of granulocyte.

308
Q

Give seven features of anaphylaxis.

A 
Rash with blotches. 
Swelling of lips and face. 
Oedema. 
Central cyanosis. 
Wheeze. 
Hypotension. 
Cardiac arrest
309
Q

What is central cyanosis?

A

Bluish discolouration of the skin and mucous membranes around the core, lips and tongue.

310
Q

How is anaphylaxis managed?

A 
Basic life support (ABCs). 
Stop drug if infusion. 
Adrenaline. 
IV Anti-histamine. 
IV Hydrocortisone.
311
Q

What are the three groups of risk factor for drug hypersensitivity?

A

Medicine factors.
Host factors.
Genetic factors (certain HLA groups).

312
Q

What is the protocol if ADR is suspected?

A

Full medication history and previous reactions. Check useful sources to see if ADR is described.

313
Q

What marker can be used to identify Type A ADR?

A

Serum concentration of drug (if high, suspect drug as cause).

314
Q

What marker can be used to identify Type B ADR?

A

Tryptase - only released from mast cells (best confirmation of allergy-based ADR).

315
Q

What are the three options in the management of care for patients with ADR?

A

Continue the drug and manage the ADR by other means.
Reduce the dose of the drug.
Stop the drug.

316
Q

How are Type A ADRs managed?

A

Dose-related therefore may respond to dose reduction or temporary withdrawal.

317
Q

How are Type B ADRs managed

A

Not usually dose-related therefore should withdraw the medicine immediately and give supportive treatment if reaction is severe.

318
Q

How are ADRs reported?

A

MHRA Yellow Card Scheme.

319
Q

What should be reported to the MHRA Yellow Card Scheme?

A

All suspected ADRs for new medicines.
All ADRs in children.
All serious reactions, even if well documented.

320
Q

What is meant by the term ‘serious reaction’?

A

Fatal.
Life threatening.
Disabling.
Result in or prolong hospitalisation.

321
Q

Describe what synergy is in the context of drug interactions.

A

When the actions of two drugs combine.

322
Q

Describe what antagonism is in the context of drug interactions.

A

Where one drug block the action of the other.

323
Q

Give an example of positive synergy.

A

Paracetamol and codeine (co-codamol) together have an increased analgesic effect

324
Q

What are patient risk factors for drug interaction?

A

Polypharmacy.
Old age.
Genetics.

325
Q

What are pharmacological risk factors for drug interaction?

A

Narrow therapeutic index.

Steep dose / response curve.

326
Q

What is a therapeutic index?

A

Difference between the amount of therapeutic agent that causes the therapeutic effect and the amount that causes the toxic effect.

327
Q

What are the four pharmacokinetic mechanisms of drug interaction?

A

Absorption.
Distribution.
Metabolism.
Excretion.

328
Q

State five factors that affect absorption (w/ respect to drug interaction)?

A 
Motility. 
Acidity. 
Solubility. 
Non-absorbed complex formation. 
Direct action on enterocytes.
329
Q

State what factor affects distribution (w/ respect to drug interaction)?

A

Protein binding. By affecting drug concentration in the plasma thus reducing distribution - less available to have an effect.

330
Q

What factors affect metabolism (w/ respect to drug interaction)?

A

CYP450 inducers and inhibitors. CP450 are a family of proteins that metabolise many substrates (including drugs).

331
Q

How does the increased metabolism of a pro-drug alter its therapeutic effects?

A

Increased therapeutic effect (increased concentration of the active form of the drug).

332
Q

Describe how grapefruit juice can change drug effectiveness.

A

Grapefruit juice affect CYP3A4 resulting in increased bioavailability - thus drug more effective.

333
Q

What two factors make up the excretion (w/ respect to drug interaction)?

A

Renal excretion.

Biliary excretion.

334
Q

Under what conditions are weak acids/bases cleared faster?

A

Weak acids cleared faster if urine is alkaline.

Weak bases cleared faster is urine is acidic.

335
Q

Renal excretion is dependent on what factor?

A

pH.

336
Q

Give examples of drugs that are weak acids.

A

Aspirin.
Ibuprofen.
Paracetamol.
Warfarin.

337
Q

Give examples of drugs that are weak bases.

A

Amphetamine.
Atropine.
Propranolol.
Salbutamol.

338
Q

Give three common parenteral routes of drug administration.

A

Subcutaneous.
Intramuscular.
Intravenous.

339
Q

Describe the term ‘respiratory depression’.

A

Hypoventilation - when ventilation is inadequate causing increased CO2 concentration and respiratory acidosis.

340
Q

What is the relative dose of morphine that should be given parenterally rather than orally?

A

Half dose if giving parenterally.

341
Q

Describe the difference between morphine and diamorphine.

A

Diamorphine is more potent and faster acting.

342
Q

Give another name for diamorphine.

A

Heroin.

343
Q

How do opioids work?

A

Inhibit the release of pain transmitters at the spinal cord and midbrain and modulate pain perception in higher centres.

344
Q

Sustained activation with opioids leads to what?

A

Tolerance and addiction.

345
Q

Dependence comes in which two forms?

A

Psychological - craving euphoria.

Physical.

346
Q

Given that codeine is a prodrug explain why it is difficult to control its activity.

A

Codeine must be metabolised by CYP2D6 which has varying degrees of activity in the population.

347
Q

Why is codeine banned from being given to children and breast feeding mothers.

A

Risk of being in 5% of population that have overactive CYP2D6 and are therefore at risk of respiratory depression.

348
Q

Describe IgA antibodies.

A

IgA antibodies are found in mucosal areas such has the gut, respiratory tract and urogenital tract. IgA prevents colonisation by pathogens, it is also found in saliva, tears and breast milk.

349
Q

Describe IgD antibodies.

A

IgD antibodies are found on B cells that have not been exposed to antigens.

350
Q

Describe IgG antibodies.

A

IgG antibodies are the most abundant type of antibodies and are responsible for the secondary response.

351
Q

Describe IgM antibodies.

A

IgM antibodies are the most primitive antibody and eliminates pathogens in the early stages of B cell-mediated immunity (humoral, primary immunity) before there are sufficient IgG.

352
Q

Describe IgE antibodies.

A

IgE antibodies are in response to parasites and responsible for anaphylaxis.

353
Q

Define the half life of a drug.

A

The time taken for the plasma drug concentration to fall to half of its original value.

Phase 2a Medicine (JH) (7 decks)

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