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2a - ICS > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Define adverse drug reactions (ADRs)

A

Unwanted or harmful reaction following administration of a drug or combination of drugs under normal conditions of use and is suspected to be related to the drug.

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2
Q

What is the key difference between side effects and ADRs

A

Side effects can have unintended effects which are beneficial whereas ADRs are never beneficial

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3
Q

What is the Rawlins Thompson (RT) system for ADRs (ABCDEs)

A

Augmented
Bizarre
Chronic use
Delayed
End of use

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4
Q

RT: Explain a type A ADR and give an example

A

Common, predictable and dose dependent
e.g morphine and constipation

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5
Q

RT: Explain a type B ADR and give an example

A

Not predictable and not dose dependent
e.g. anaphylaxis ad penicillin

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6
Q

RT: Explain a type C ADR and give an example

A

Long term use
e.g. osteoporosis and steroids

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7
Q

RT: Explain a type D ADR and give an example

A

Uncommon, usually dose related, show itself some time after use of drug
e.g malignancies after immunosuppression

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8
Q

RT: Explain a type E ADR and give an example

A

Occurs after abrupt drug withdrawal
e.g opiate withdrawal syndrome

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9
Q

When is the local route of administration used

A

When you want to target a specific area of pathology without exposing the rest of the system to drugs

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10
Q

Give 3 examples of drugs used for local administration

A

Topical steroid creams
Eye drops
Intranasal

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11
Q

What are the 2 classifications of systemic routes of administration

A

Enteral (GI tract)
Parenteral (not GI tract)

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12
Q

When would systemic routes of administration be used

A

When whole system coverage is wanted

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13
Q

Give 3 examples of enteral administration

A

Oral (PO)
Rectal (PR)

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14
Q

Give 3 examples of parenteral administration

A

Intravenous (IV)
Intramuscular (IM)
Subcutaneous (SC)

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15
Q

Are inhalation and transdermal routes systemic or local

A

They can be either depending on the drug

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16
Q

Define pharmacodynamics

A

Action of the drug on the body

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17
Q

Define pharmacokinetics

A

Action of the body on the drug (how it’s broken down)

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18
Q

How can a paracetamol overdose be treated

A

If the patient presents to the emergency department within 1 hour of the overdose, they can be given activated charcoal

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19
Q

How is activated charcoal delivered in a paracetamol overdose

A

Nasogastric tube

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20
Q

How does activated charcoal treat a paracetamol overdose

A

A.C has a sticky texture
A.C sticks to the paracetamol (adsorption) that is in the stomach and prevents it from being absorbed
It will then be excreted

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21
Q

What are the 4 stages of pharmacokinetics (ADME)

A

Absorption (route)
Distribution (systemic spreading)
Metabolism (1st pass met)
Excretion (hepatically/ renally)

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22
Q

Define bioavailability

A

Rate and extent to which an administered drug reaches the systemic circulation

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23
Q

What is the assumed bioavailability of a drug given intravenously

A

100%

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24
Q

Why is IV quicker than oral administration

A

IV is injected directly into the bloodstream so it doesn’t cross any membranes or encounter first pass metabolism

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25
Q

What is first pass metabolism

A

This happens when the gut and liver metabolise drugs given orally before they reach the circulation
This results in a reduced concentration of the drug in the systemic circulation

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26
Q

What is the therapeutic range of a drug

A

upper and lower bounds of safe doses of a drug
Narrower range = more care dispensing

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27
Q

Pharmacokinetics: What does distribution describe

A

The journey of the drug through the bloodstream into target tissue

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28
Q

Name 4 types of drug target types
Give examples of each

A
  • Cellular receptors (beta blockers)
  • Enzymes (ACE-I)
  • Membrane ion channels (Ca channel blockers)
  • Membrane transporters (proton pump inihibitors)
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29
Q

Pharmacokinetics: What 5 factors can affect distribution

A
  • Blood flow to area
  • Permeability of capillaries
  • Binding to proteins (albumin = slower)
  • Lipophilicity - penetrate cell membrane easily
  • Volume of distribution
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30
Q

What is the main route of elimination

A

The kidneys

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31
Q

What type of drug can the kidneys not eliminate

A

lipid soluble drugs

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32
Q

Where are lipid soluble drugs metabolised

A

Liver

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33
Q

Briefly describe how the liver converts lipid soluble drugs to water soluble drugs

A

Phase 1 - Make drug more hydrophilic (CYP450)
Phase 2 conjugation - If the drug is still too lipophilic, then add something to make it polar (acetylation)

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34
Q

How can an enzyme inducer and an inhibitor effect cytochrome p450

A

induction - other drugs are metabolised faster which can lead to sub-therapeutic overdose
Inhibition - other drugs are metabolised slowly and can reach toxic levels

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35
Q

What are the 2 main systems drugs are excreted by

A

Kidneys in urine
Liver in the bile and then faeces

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36
Q

State 4 types of receptors

A

Ligand-gated
G protein coupled
Kinase-linked
Cytosolic

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37
Q

Pharmacodynamics: describe signal transduction

A

Drug binds to extracellular or intracellular receptor
Leads to amplification or down-regulation of signals

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38
Q

What is an agonist

A

A compound that binds to a receptor and activates it ( full affinity and full efficacy)

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39
Q

What is an antagonist

A

A compound that binds to a receptor and prevents its activation (Full affinity and zero efficacy)

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40
Q

Define potency

A

concentration or amount of the drug required to produce a defined effect
i.e. lower dose needed for response = more potent

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41
Q

Define efficacy

A

How well the ligand (drug) successfully activates the receptor

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42
Q

What is EC50

A

the concentration that gives half the maximal response

43
Q

Define affinity

A

How well a ligand binds to its receptor

44
Q

Define tolerance in terms of drug response

A

Reduction in agonist effect over time
Repeated exposure to high concentrations

45
Q

What is inverse agonism

A

A drug that binds to the same receptor as an agonist but induces an opposite pharmacological response

46
Q

What is non-competitive inhibition

A

Inhibitor binds to an allosteric site on the receptor which alters the shape of the active site
* decreases efficacy irreversibly
* Affinity reduced

47
Q

What is competitive inhibition

A

Inhibitor binds to the same site as the ligand
* reversible
* Less affinity and no affect on efficacy

48
Q

Are ligands specific or selective to receptors

A

selective

49
Q

Rawlins-Thompson system: Describe a type A drug reaction

A

Augmented
* Predictable
* Dose dependent
* Common

50
Q

Rawlins-Thompson system: Describe a type B drug reaction

A

Bizarre
* Not predictable
* Not dose dependent
* e.g. anaphylaxis and penicillin

51
Q

Rawlins-Thompson system: Describe a type C drug reaction

A

Chronic
* Occurs after long term therapy

52
Q

Rawlins-Thompson system: Describe a type D drug reaction

A

Delayed
* Occurs many years after treatment

53
Q

Rawlins-Thompson system: Describe a type E drug reaction

A

End of treatment
* Withdrawal reaction after long term use; complication of stopping meds

54
Q

What is the yellow card scheme

A

ADR reporting scheme
Collects both spontaneous and suspected reactions

55
Q

What are cholinergic receptors

A

Receptors on the surface of cells that bind the neurotransmitter Acetylcholine (Ach)

56
Q

Name the 2 types of cholinergic receptors

A

Muscarinic (usually postsynaptic)
Nicotinic (usually presynaptic)

57
Q

Where are M2 receptors mainly found

A

Heart

58
Q

What happens when M2 receptors on hear SA and AV node are activated

A

SA node: decreases HR
AV node: decrease conduction velocity
Induces AV node block (increases PR interval)

59
Q

What happens when M3 receptors are stimulated in the respiratory system

A

Produces mucus
Bronchoconstriction

60
Q

What are adrenergic receptors

A

Receptors on the surface of cells that get activated when they bind a type of neurotransmitters called a catecholamine

61
Q

Give 2 examples of catecholamines

A

Adrenaline (epinephrine)
Noradrenaline (norepinephrine)

62
Q

Describe the length of pre and post ganglionic fibres in the parasympathetic NS

A

pre-ganglionic fibres are long
post-ganglionic fibres are long
This is opposite for the sympathetic NS

63
Q

What receptor does Ach released from the preganglionic neurons act on

A

Nicotinic

64
Q

In the sympathetic NS, what neurotransmitters are typically released by postganglionic neurons

A

adrenaline and noradrenaline

65
Q

What are the 2 main types of adrenergic receptors

A

alpha and beta

66
Q

In the PNS, postganglionic neurons release Ach. Name the receptor it binds to

A

muscarinic receptor

67
Q

Symptoms of a cholinergic crisis (SLUDGE)

A

Salivation
Lacrimation
Urination
Defecation
GI upset
Emesis (vomiting)

68
Q

What are cholinergic agonists

A

Mimic or enhance the action of ACh at the neuromuscular junction

69
Q

What type of receptor is an adrenergic receptor

A

G-protein coupled receptor

70
Q

Where is adrenaline released from

A

Adrenal glands

71
Q

Where is noradrenaline released from

A

Sympathetic nerve fibre ends

72
Q

Where are alpha 1 receptors mainly found

A

vascular smooth muscle and sphincters

73
Q

Where are alpha 2 receptors mainly found

A

Brain and peripherally

74
Q

Give 2 functions of alpha 1 receptors

A

Vasoconstriction
Increased bp

75
Q

Name the drug that is used in benign prostatic hyperplasia

A

Tamsulosin
Block alpha 1 receptor in prostate

76
Q

Give 2 functions of alpha 2 receptors

A

Inhibition of noradrenaline
Inhibition of Ach release

77
Q

Where are B1 receptors mainly found

A

Heart
Kidneys
Fat cells

78
Q

Give 2 functions of ß1 receptors

A

Increased myocardial contractility
Increased renin secretion

79
Q

When are beta blockers contraindicated

A

In absolute asthma

80
Q

Where are B2 receptors mainly found

A

lungs

81
Q

Give 3 functions of ß2 receptors

A

Vasodilation
Bronchodilation
Increased release of glucagon

82
Q

Give an example of a B2 agonist and which 2 conditions may they be prescribed

A

Salbutamol
COPD and Asthma

83
Q

Give 2 functions of B3 receptors

A

Increased lipolysis
Relaxes bladder detrusor

84
Q

What are NSAIDs

A

Non-steroidal anti-inflammatory drugs

85
Q

Describe the difference between selective and non-selective NSAIDs

A

Non-selective: competitive reversible inhibitors of COX1 and 2
Selective: selectively inhibit COX 2

86
Q

How do NSAIDs relieve inflammation

A

COX2 is needed for prostaglandin synthesis
Prostaglandins are responsible for pain and inflammation
NSAIDs reduce symptoms of pain and inflammation

87
Q

Give 2 examples of non-selective NSAIDs

A

ibuprofen
naproxen

88
Q

Give 2 examples of COX2-selective NSAIDs

A

celecoxib
Rofecoxib

89
Q

Disadvantage of long term NSAID use

A

Can cause gastric bleeding
Prostaglandins are needed for gastric mucus production
Some NSAIDs inhibit COX 1 which is needed for prostaglandin synthesis

90
Q

Define pro-drugs

A

Drugs that are not active until they are metabolised

91
Q

What drug acts as an antagonist at the morphine receptor

A

Naloxone

92
Q

What enzyme is needed to metabolise codeine

A

Codeine is a pro drug and is metabolised by CYP2D6

93
Q

What is the bioavailability of morphine taken orally

A

50%

94
Q

10mg of morphine is taken orally. What is the equivalent dose if given parenterally?

A

5mg

95
Q

When are opioids used

A

Chronic severe pain relief - mostly cancer pain ana

96
Q

Where might opioid receptors be found

A

Epidural space and CSF

97
Q

physiological characteristics of diamorphine

A

More potent and faster acting as it crosses the blood brain barrier quickly

98
Q

Give 5 side effect of opioids

A

Respiratory depression
Sedation
Nausea
Vomiting
Constipation (main)

99
Q

What is released in the presence of pain

A

Endorphins

100
Q

Describe the difference in potency between diamorphine and morphine

A

Morphine is half as potent as diamorphine so double the dose would be needed
5mg diamorphine = 10mg morphine = 100mg pethidine

101
Q

Describe the dose-response curve for morphine

A

As dose increases, response increases. The association is initially rapid and the plateaus

102
Q

4 classes of diuretics

A
  • Thiazide - hydrochlorothiazide
  • Loop diuretics - furosemide
  • K-sparing diuretics - spironolactone
  • Aldosterone antagonists
103
Q

2 examples of

A

2a - ICS (4 decks)

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