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2a - ICS > Pharmacology > Flashcards

Pharmacology Flashcards

(103 cards)

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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
What is first pass metabolism
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
26
What is the therapeutic range of a drug
upper and lower bounds of safe doses of a drug Narrower range = more care dispensing
27
Pharmacokinetics: What does distribution describe
The journey of the drug through the bloodstream into target tissue
28
Name 4 types of drug target types Give examples of each
* Cellular receptors (beta blockers) * Enzymes (ACE-I) * Membrane ion channels (Ca channel blockers) * Membrane transporters (proton pump inihibitors)
29
Pharmacokinetics: What 5 factors can affect distribution
* Blood flow to area * Permeability of capillaries * Binding to proteins (albumin = slower) * Lipophilicity - penetrate cell membrane easily * Volume of distribution
30
What is the main route of elimination
The kidneys
31
What type of drug can the kidneys not eliminate
lipid soluble drugs
32
Where are lipid soluble drugs metabolised
Liver
33
Briefly describe how the liver converts lipid soluble drugs to water soluble drugs
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)
34
How can an enzyme inducer and an inhibitor effect cytochrome p450
induction - other drugs are metabolised faster which can lead to sub-therapeutic overdose Inhibition - other drugs are metabolised slowly and can reach toxic levels
35
What are the 2 main systems drugs are excreted by
Kidneys in urine Liver in the bile and then faeces
36
State 4 types of receptors
Ligand-gated G protein coupled Kinase-linked Cytosolic
37
Pharmacodynamics: describe signal transduction
Drug binds to extracellular or intracellular receptor Leads to amplification or down-regulation of signals
38
What is an agonist
A compound that binds to a receptor and activates it ( full affinity and full efficacy)
39
What is an antagonist
A compound that binds to a receptor and prevents its activation (Full affinity and zero efficacy)
40
Define potency
concentration or amount of the drug required to produce a defined effect i.e. lower dose needed for response = more potent
41
Define efficacy
How well the ligand (drug) successfully activates the receptor
42
What is EC50
the concentration that gives half the maximal response
43
Define affinity
How well a ligand binds to its receptor
44
Define tolerance in terms of drug response
Reduction in agonist effect over time Repeated exposure to high concentrations
45
What is inverse agonism
A drug that binds to the same receptor as an agonist but induces an opposite pharmacological response
46
What is non-competitive inhibition
Inhibitor binds to an allosteric site on the receptor which alters the shape of the active site * decreases efficacy irreversibly * Affinity reduced
47
What is competitive inhibition
Inhibitor binds to the same site as the ligand * reversible * Less affinity and no affect on efficacy
48
Are ligands specific or selective to receptors
selective
49
Rawlins-Thompson system: Describe a type A drug reaction
Augmented * Predictable * Dose dependent * Common
50
Rawlins-Thompson system: Describe a type B drug reaction
Bizarre * Not predictable * Not dose dependent * e.g. anaphylaxis and penicillin
51
Rawlins-Thompson system: Describe a type C drug reaction
Chronic * Occurs after long term therapy
52
Rawlins-Thompson system: Describe a type D drug reaction
Delayed * Occurs many years after treatment
53
Rawlins-Thompson system: Describe a type E drug reaction
End of treatment * Withdrawal reaction after long term use; complication of stopping meds
54
What is the yellow card scheme
ADR reporting scheme Collects both spontaneous and suspected reactions
55
What are cholinergic receptors
Receptors on the surface of cells that bind the neurotransmitter Acetylcholine (Ach)
56
Name the 2 types of cholinergic receptors
Muscarinic (usually postsynaptic) Nicotinic (usually presynaptic)
57
Where are M2 receptors mainly found
Heart
58
What happens when M2 receptors on hear SA and AV node are activated
SA node: decreases HR AV node: decrease conduction velocity Induces AV node block (increases PR interval)
59
What happens when M3 receptors are stimulated in the respiratory system
Produces mucus Bronchoconstriction
60
What are adrenergic receptors
Receptors on the surface of cells that get activated when they bind a type of neurotransmitters called a catecholamine
61
Give 2 examples of catecholamines
Adrenaline (epinephrine) Noradrenaline (norepinephrine)
62
Describe the length of pre and post ganglionic fibres in the parasympathetic NS
pre-ganglionic fibres are long post-ganglionic fibres are long This is opposite for the sympathetic NS
63
What receptor does Ach released from the preganglionic neurons act on
Nicotinic
64
In the sympathetic NS, what neurotransmitters are typically released by postganglionic neurons
adrenaline and noradrenaline
65
What are the 2 main types of adrenergic receptors
alpha and beta
66
In the PNS, postganglionic neurons release Ach. Name the receptor it binds to
muscarinic receptor
67
Symptoms of a cholinergic crisis (SLUDGE)
Salivation Lacrimation Urination Defecation GI upset Emesis (vomiting)
68
What are cholinergic agonists
Mimic or enhance the action of ACh at the neuromuscular junction
69
What type of receptor is an adrenergic receptor
G-protein coupled receptor
70
Where is adrenaline released from
Adrenal glands
71
Where is noradrenaline released from
Sympathetic nerve fibre ends
72
Where are alpha 1 receptors mainly found
vascular smooth muscle and sphincters
73
Where are alpha 2 receptors mainly found
Brain and peripherally
74
Give 2 functions of alpha 1 receptors
Vasoconstriction Increased bp
75
Name the drug that is used in benign prostatic hyperplasia
Tamsulosin Block alpha 1 receptor in prostate
76
Give 2 functions of alpha 2 receptors
Inhibition of noradrenaline Inhibition of Ach release
77
Where are B1 receptors mainly found
Heart Kidneys Fat cells
78
Give 2 functions of ß1 receptors
Increased myocardial contractility Increased renin secretion
79
When are beta blockers contraindicated
In absolute asthma
80
Where are B2 receptors mainly found
lungs
81
Give 3 functions of ß2 receptors
Vasodilation Bronchodilation Increased release of glucagon
82
Give an example of a B2 agonist and which 2 conditions may they be prescribed
Salbutamol COPD and Asthma
83
Give 2 functions of B3 receptors
Increased lipolysis Relaxes bladder detrusor
84
What are NSAIDs
Non-steroidal anti-inflammatory drugs
85
Describe the difference between selective and non-selective NSAIDs
Non-selective: competitive reversible inhibitors of COX1 and 2 Selective: selectively inhibit COX 2
86
How do NSAIDs relieve inflammation
COX2 is needed for prostaglandin synthesis Prostaglandins are responsible for pain and inflammation NSAIDs reduce symptoms of pain and inflammation
87
Give 2 examples of non-selective NSAIDs
ibuprofen naproxen
88
Give 2 examples of COX2-selective NSAIDs
celecoxib Rofecoxib
89
Disadvantage of long term NSAID use
Can cause gastric bleeding Prostaglandins are needed for gastric mucus production Some NSAIDs inhibit COX 1 which is needed for prostaglandin synthesis
90
Define pro-drugs
Drugs that are not active until they are metabolised
91
What drug acts as an antagonist at the morphine receptor
Naloxone
92
What enzyme is needed to metabolise codeine
Codeine is a pro drug and is metabolised by CYP2D6
93
What is the bioavailability of morphine taken orally
50%
94
10mg of morphine is taken orally. What is the equivalent dose if given parenterally?
5mg
95
When are opioids used
Chronic severe pain relief - mostly cancer pain ana
96
Where might opioid receptors be found
Epidural space and CSF
97
physiological characteristics of diamorphine
More potent and faster acting as it crosses the blood brain barrier quickly
98
Give 5 side effect of opioids
Respiratory depression Sedation Nausea Vomiting Constipation (main)
99
What is released in the presence of pain
Endorphins
100
Describe the difference in potency between diamorphine and morphine
Morphine is half as potent as diamorphine so double the dose would be needed 5mg diamorphine = 10mg morphine = 100mg pethidine
101
Describe the dose-response curve for morphine
As dose increases, response increases. The association is initially rapid and the plateaus
102
4 classes of diuretics
* Thiazide - hydrochlorothiazide * Loop diuretics - furosemide * K-sparing diuretics - spironolactone * Aldosterone antagonists
103
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2a - ICS (4 decks)

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