Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Phase 2a NEW > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Physicochemical

A 
Drug reactions
Adsorption 
Precipitation
Chelation 
Neutralisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pharmacodynamics

A

drugs effect on the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Pharmacokinetics

A

body.’s effect on drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Treatment for paracetamol overdose

A

Activated charcoal - binds to paracetamol (adsorption) and then leaves the body like this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Treatment for opioid overdose

A

Naloxone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pharmacodynamics pathways

A

Summation
Synergism
Antagonism
Potentiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pharmacokinetics pathways

A

ADME - Absorption, Distribution, Metabolism, Excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Drugs tend to be metabolised in

A

Liver
Kidneys
Lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Codeine

A

Metabolised into morphine

Codeine is essentially low-dose and slow-releasing morphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Bioavailability

A

Comparison between how much oral drug vs IV drug makes it into the system (blood)
IV > Oral for bioavailability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Morphine side effects

A

Slows down gut motility and so level of adsorption (Para NS affected)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Acidity

A

Drug is split into 2 portions - ionised and unionised (tends to be equilibrium)
Unionised portion can coss through the phospholipid bilayer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Distribution - pathway of drug

A

Protein binding
Tissues
Effect sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Volume distribution

A

Bigger VD = not much in blood

Lower VD = mostly in blood so more reaches effect site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Protein binding

A

How much drug can bind to protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Metabolism

A

Morphine metabolised in Liver by CYP450 and then broken down into morphine-6-glucuronide (much more potent than morphine itself),

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Anti-epileptic drug (acute epilepsy)

A

Phenytoin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Enzyme inhibition and induction

A

counter mechanisms of enzyme action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Warfarin

A

Warfarin inhibits vitK factors in coag cascade
it is highly protein bound and is affected by enzyme induction which causes it to have less of an effect.
Metronidazole inhibits this and so more warfarin is about in blood which can be toxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

AKI (acute kidney injury) -causing drugs

A

NSAIDs, ACEi, Furosemide, Gentamicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Grapefruit juice

A

Interacts with warfarin by protein binding and CYP450 pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Excretion

A

Mostly extracted via kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Druggability

A

The ability of a protein target to bind small molecules ith high affinity
Also known as ligandability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Drug targets

A

Receptors
Enzymes
Transporters
Ion channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Receptors

A

Component of a cell that interacts with a specific ligand and initiates a chain of biochemical events leading to ligand observed effects
Chemicals communicate via receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Ligands can be

A

Exogenous (drugs)

Endogenous (hormones, neurotransmitter)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Neurotransmitters

A

Acetylcholine

Serotonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Hormones

A

Testosterone

Hydrocortisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Autacoids (local)

A

Cytokines

Histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Receptor types

A

Ligand-gated ion channels (Nicotonic ACh receptor)
G protein-coupled receptors (Beta-adrenoreceptors)
Kinase-linked receptors (Growth factor receptors)
Cytosolic/nuclear receptors (steroid receptors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

G protein-coupled receptors

A

One of the most common group of membrane receptors
7 membrane-spanning receptors
Ligands include light energy, peptides, lipids, sugars and proteins
G proteins (GTPases) act as molecular switches. (On when bound to GDP, off when bound to GTP)
G proteins are guanine-nucleotide binding proteins which transmit signals from GPCRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

GPCR pathway

A

Ligand
Receptor G protein
Coupled receptor
2nd messenger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Kinase linked receptors

A

Transmembrane receptors activated when the binding of an extracellular ligand causes enzymatic activity on the intracellular side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Nuclear receptors

A

Work by modifying gene transcription
Steroid hormones
Tamoxifen (breast cancer) acts as a selective oestrogen receptor modular (SERM), or as a partial agonist of the oestrogen receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Chemical imbalances can lead to pathology

A

Allergy - increased histamine

Parkinson’s - reduced dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Receptor ligands

A

Agonist - Compound that binds to and activates receptor

Antagonist - Compound that reduces the effect of an agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Potency

A

EC50 - Conc that gives half the maximal response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Full agonists

A

Complete saturation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Partial agonists

A

Never reaches complete saturation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Efficacy/Intrinsic activity

A

Max response achievable from a dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Potency vs efficacy

A

Drug may be potent but not efficacious and vice versa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Competitive antagonism

A

Antagonist reverses the effects of agonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Non-competitive antagonist

A

Molecule binds to an allosteric (non-agonist) site on the receptor to prevent activation of a receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Cholinergic receptor types

A

Nicotinic (agonist), curare (antag)

Muscarinic (agonist), atropine (antag)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Histamine receptor types

A 
All are GPCRs
H1 -
H2 - Contraction of ileum, acid secretion from parietal cells (agonist), Cimetidine (H2 antagonist)
H3 - 
H4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Affinity

A

How well a ligand binds to the receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Efficacy

A

How well a ligand activates a receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Antagonists

A

Have affinity but zero efficacy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Agonists

A

Have affinity and efficacy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Isoprenaline

A

Non-selective beta-adrenoreceptor agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Irreversible antagonist

A

BAAM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Receptor reserve

A

Where agonists need to activate only a small fraction of existing receptors to produce a maximal response, so spare receptors leftover (reserve)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Signal transduction (amplification)

A

Signaling cascade causes amplification of a signal and a response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Allosteric modulation

A

The ligand binds to site other than the active site of receptor and elicit a different response through a structural modification due to the binding at the allosteric site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Inverse agonism

A

When a drug binds to the same receptor as an agonist but induces a pharmacological response opposite to that of the agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Tolerance

A

Reduction in agonist effect over time

Continuous, repeated high concentrations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Desensitisation

A

Uncoupled protein is internalised and degraded

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Salbutamol

A

B2-adrenoreceptor agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Streptokinase

A

Clot buster - degrades a clot

Enzyme which is a drug product

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Statins

A

HMG-CoA reductase inhibitors
Block the rate-limiting step in the cholesterol pathway
A class of lipid-lowering medications that reduces the level of bad cholesterol
Primary prevention of CV disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

ACEi

A

Increased blood pressure via the RAAS pathway
Increases amount of salt and water retained by the body
Inhibiting ACE reduces AT2 production and therefore causes this reduction in BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Parkinson’s disease - Symptoms

A

Hypokinesia
Resting tremor
Muscle rigidity
Cognitive impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Parkinson’s disease - Treatment

A

Substrate - L-DOPA is a precursor for dopamine biosynthesis which crosses the blood-brain barrier (BBB)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Drugs and ion transport

A

Passive - Symporters, channels

Active - ATP-ases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Protein ports

A

Uniporters - uses ATP to pull molcules in
Symporters uses movement of a molecule to pull in another against conc grad
Antiporters - one substance moves against its gradient after the other moves down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Na-K-Cl cotransporter (NKCC)

A

Example of a symporter
Protein that transports Na, K and Cl into cells
Functions in organs that secrete fluids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Epithelial sodium channel

A

Membrane-bound ion channel
Causes reabsorption of Na+ ions at collecting ducts of kidneys nephrons
Blocked by high-affinity diuretic amiloride (often used with thiazide) - Anti-hypertensive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Voltage-gated calcium channels

A

Found in the membrane of excitable cells (muscle, glial, cells, neurons, etc)
At resting membrane potential, VDCCs are normally closed until activation resulting in depolarisation which then opens them
Amlodipine is an angioselective CCB that lowers BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Voltage-gated sodium channels

A

Conducts Na+ through plasma membrane

Lidocaine blocks transmission of action potentials

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Voltage-gated potassium channels

A

Sulfonylurea lowers blood glucose levels by blocking potassium channels (Treatment of T2DM)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Receptor-mediated chloride channel

A

GABA-A receptor

Barbiturates increase the permeability of channel to chloride ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Sodium-Potassium ATP-ase Pump

A

Digoxin - Inhibits this pump mainly in the myocardium

Mainly used for AF and heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Proton pump (stomach)

A

Omeprazole (PPI - 1st in class) - Inhibits acid secretion (finitely irreversible)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Irreversible enzyme inhibitors

A

Organophosphates (irreversible inhibitors of cholinesterase)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Xenobiotics

A

Compounds foreign to an organism’s normal biochemistry such as any drug or poison

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Cytochrome P450

A

Membrane-associated proteins located in the inner membrane of mitochondria or in the endoplasmic reticulum of cells
Major enzymes involved in drug metabolism
Most drugs undergo inactivation by CYPs
Many substances are bioactivated by CYPs to form their active compounds
CYPs metabolise thousands of endogenous and exogenous chemicals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Naturally occurring opioids

A

From opium poppy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Naturally occuring opioids from opium poppy

A

Moprhine - strong

Codeine - weak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Chemically modified (simple)

A

Diamorphine
Oxycodone
Dihydrocodeine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Synthetic opioids

A

Fentanyl
Pethidine
Allentanil
Remifentanil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Synthetic partial agonists

A

Buprenorhine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Synthetic partial antagonist

A

Naloxone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Bioavailability

A

First pass metabolism by liver

50% of oral is metabloised by first pass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Routes of admin

A

IV fastest

Oral slowest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

IV PCA

A

Patient-controlled analgesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Opioid receptors are located in

A

Epidural/CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Transdermal patches for lipid-soluble drugs such as

A

Fentanyl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Opium contains

A

Morphine

Codeine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Controlled drugs legislation

A

Opioids class A drugs
Secure storage
2 signatures required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Dihydrocodeine

A

1.5 times more potent than codeine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Oxycodone

A

1.5 times more potent than morphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Opioid pharmacodynamics

A

Natural endorphins (endogenous morphine) and enkephalins
GPCR - Via second messengers
Inhibit release of pain transmitters at spinal cord and midbrain - and modulate pain perception

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

How opioids work

A

Descending inhibition of pain
Part of fight or flight response
Never designed for sustained activation
Sustained activation leads to tolerance and addiction

94
Q

Opioid receptors

A

MOP
KOP
DOP
NOP

95
Q

Kappa agonists cause

A

Depression instead of euphoria

96
Q

All drugs currently used are

A

U agonists

97
Q

Potency vs efficacy

A

Potency - strong or weak, how well drug binds to receptor (binding affinity
Efficacy - Maximal response or not, Full or partial agonist

98
Q

Opioid potency examples

A

Diamorphine (strongest)
Morphine
Pethadine (weakest)

99
Q

Tolerance and dependence

A

Tolerance - down-regulation of receptors with prolonged use, need higher doses to achieve the same effect
Dependence - psychological (craving, euphoria), physical
Opioid withdrawal - lasts up to 72 hours

100
Q

Side effects

A 
Resp depression
Sedation
N and V
Constipation 
Itching
Immune suppression 
Endocrine effects
101
Q

Opioid-induced resp depression

A

Call for help
ABC
IV Naloxone (titrate to effect), has a short half-life so wears off.

102
Q

Opioids use in chronic non-cancer pain

A

Start to lose effectiveness quickly within weeks

103
Q

Common opioids

A

Fentanyl

Tramadol

104
Q

Pharmacogenetics

A

Codeine is a prodrug which needs to be metabolised by Cytochrome CYP2D6 to morphine to ork
CYP2D6 activity varies in the population - codeine will have a reduced or absent affect in some of the population

105
Q

Metabolism of morphine

A

Morphine is mebtaolised to Moprhine 6 glucuronide which is more potent than morphine and is renally excreted
In renal failure it will build up and may cause resp depression

106
Q

Tramadol

A 
Weak opioid agonist
Slightly stronger than codeine 
It is a Prodrug
Interacts with SSRIs, take care when prescribing to patients on antidepressants
Controlled drug
107
Q

Summary

A

Oral bioavilability is 50% for oral morphine
Titrate the dose to suit patient
Potentil for resp depression
POtential for addiciton - be careful for starting strong opioids for chronic backache
Dont issue repat prescription without seeing patient

108
Q

Blood pressure control

A

Raise it in shock

Lower it in hptn

109
Q

Heart rate control

A

Speed up bradycardias

Slow down tachycardias

110
Q

A drug to lower bp will

A

lower heart rate

111
Q

Nicotine and curare

A

Nicotine activates neuromuscular junction

Curare opposed this activation

112
Q

Vagal nerve stimulation

A

slows the heart

113
Q

NS

A

Somatic - skeletal muscle
Autonomic - involuntary
Enteric - gut

114
Q

PNS

A

Sympathetic

Parasympathetic

115
Q

Sympathetic NS

A

Release noradrenaline which activates adrenergic receptors (alpha and beta)

116
Q

Parasympathetic NS

A

Release ACh which acts on muscarinic receptors

117
Q

Sympa vs Para NS

A

Both NS first release ACh but then para fibres then release Noradrenaline whereas sympa fibres releases ACh

118
Q

Muscarinic receptors

A

M1-5
GPCRs
G proteins can activate second messengers
M1 - Brain
M2 - Heart (activation slows the heart)
M3 - Glandular and smooth muscle (bronchoconstriction)
M4/5 - CNS

119
Q

Atropine

A

For life-threatening bradycardias and cardiac arrest

120
Q

Muscarinic agonists

A

Pilocarpine - stimulates salivation (sjogrens syndrome),

121
Q

Muscarinic antagonists

A

Atropine

Hyoscine

122
Q

Hyoscine

A

Palliative care for drying secretions

123
Q

Bronchoconstriction treatment

A

Ipratropium bromide - short acting

Tiotropium - long acting

124
Q

Overactive bladder treatment

A

Solifenacin (anticholinergic)

125
Q

ACh

A

Major transmitter innervating skeletal muscle

126
Q

Anti-cholinergic side effects

A

Confusion
Constipation
Drying of mouth

127
Q

Catecholamines

A

Noradrenaline - management of shock in ICU
Adrenaline - Anaphylaxis management
Dopamine

128
Q

Signaling pathway

A

Receptor
Cell
G protein

129
Q

Signaling receptors

A

Alpha 1 and 2
Beta 1, 2 and 3
Beta 2 is the only receptor where Adrenaline dominates over NAd

130
Q

Alpha agonists

A

Septic shock treatment

Alpha 1 activation causes vasoconstriction

131
Q

Alpha 2

A

Clonidine - Alpha 2 agonist (lowers BP)

132
Q

Alpha 1 blockers

A

Blok alpha 1 to lower BP
Tamsulosin - treats prostatic hypertrophy
Doxazosin - Lowers BP
Alpha 2 blockers arent useful so dont learn them

133
Q

Beta agonists

A

Beta 2 activation, muscle relaxation in asthma

However beta agonists cause tachycardia and affect glucose metabolism in liver (increases glcuose production)

134
Q

Beta blockers

A

Propanolol - blocks Beta 1 and 2, slows HR, reduces tremor, may cause wheeze
Atenolol -Beta 1 selective, main effects on heart

135
Q

Beta 1 and 2

A

Beta 1 mainly affects heart

Beta 2 mainly affects lungs

136
Q

Uses of beta blockers

A 
Angina 
MI prevention
High BP
Arrhythmias 
Heart failure
137
Q

Beta blockers - side effects

A

Bronchoconstriction
Bradycardia
Hypoglycaemia
Cardiac depression

138
Q

hYPERSENSITIVTY

A

iMMEDIATE
aCUTE
DELAYED

139
Q

Antibodies

A

IgM - made at start of infection

IgE - allergies

140
Q

Type 1 reactions

A

Acute anaphylaxis
Hay fever
Asthma

141
Q

Atopy

A

An inherited tendency to exaggerated IgE response to antigen

Hay fever, eczema, asthma

142
Q

Skin prick test

A

Check for allergic responses

143
Q

Histamine

A

Drives allergic responsesT

144
Q

Histamine

A

Drives allergic responses

145
Q

Atopy diagnosis

A

Skin prick test

RAST test

146
Q

Hay fever treatment

A

Antihistamines

Steroids

147
Q

Anaphylaxis treatment

A 
Adrenaline
Fluids
Bronchodilators 
Steroids 
Anti-histamines
148
Q

Goodpastures syndrome

A

Autoantibodies formed - Type 2 reaction - Ig bound to surface antigens
Lung and kidney problems (pulmonary haemorrhage and glomeruloneprhtis (renal inflamamtion))
Treatment - remove anitbodies

149
Q

Mycoplasma pneumonia

A

Causes pneumonia
Type 2 reaction
Causes haemolytic anaemia

150
Q

Type 3 diseases

A

Endocarditis

Alveolitis

151
Q

Type 4 reactions

A

Formation of granulomas

Slow process

152
Q

Adverse drug reaction

A

Has to be noxious and unintended

153
Q

Side effect

A

An unintended effect of a drug that can be beneficial

Tend to be minor and predictable

154
Q

PDE5 inhibitors

A

Improve urinary flow

155
Q

Adverse drug reactions

A 
Toxic effects (beyond therapeutic range)
Collateral effects (therapeutic range)
Hypersusceptibility effects (below therapeutic range)
156
Q

Toxic effects

A

Nephrotoxicity with high doses of aminoglycosides such as gentamicin
Dysarthria and ataxia with lithium toxicity
Cerebellar signs and symptoms with xs phenytoin
Tend to occur if drug doses are too high or renal/hepatic issues

157
Q

Collateral effects

A

Standard therapeutic doses
Beta-blockers cause bronchoconstriction
Broad-spectrum antibiotics cause C difficile

158
Q

Hypersusceptibility reactions

A

Subtherapeutic effects

Anaphylaxis and penicillin

159
Q

Severity of ADRs

A

Mild - nausea, drowsiness, itching rash

Severe - Resp depression, neutropenia, haemorrhage, anaphylaxis

160
Q

Time independent reactions

A

Occur at any time during treatment

INR increase when erythromycin administered with warfarin

161
Q

Time-dependent reactions

A

Rapid reactions - red man syndrome due to histamine release with rapid administration of vancomycin
First dose reactions - Hypotension and ACEi
Early reactions - Nitrate induced headache
Intermediate reactions - delayed immunological reactions such as stevens-johnson syndrome with carbamazepine
Late reactions - adverse reactions of long term steroids

162
Q

Rawlins Thompson classification of ADRs

A

Type A - Predictable, dose dependent, common
Type B - Bizzare, not predictable, not dose depedent
Type C - Chronic, osteporosis and steroids
Type D - Delayed, maligancies after immunosuppression
Type E - End of treatment, occur after abrupt drug withdrawal - opiate withdrawal syndrome
Type F - Failure of therapy

163
Q

DoTS - ADRs classification

A

Dose relatedness
Timing
Patient susceptibility

164
Q

Risk factors for ADRs

A

Patient risk - F>M, Elderly and neonates, polypharmacy, genetic predisposition, hypersensitivity/allergy, hepatic/renal impairment
Drug risk - Low therapeutic index, a steep dose-response curve
Prescriber risks

165
Q

Causes of ADRs

A

Pharmaceutical variation
Receptor abnormality - malignant hyperthermia with general anesthetics
Abnormal biological system unmasked by drug - primaquine induced haemolysis
Abnormalities in drug metabolism
Immunological
Drug-induced interaction
Multifactorial - many reasons

166
Q

Type A - Augmented, predictable

A

Extension of primary effects - bradycardia and propanolol

167
Q

Type B - Bizzare, not predictable

A

Allergy

Hypersensitivity

168
Q

Idiosyncrasy

A

Inherent abnormal response to a drug

Rare but serious

169
Q

Types of allergic reaction

A

Type 1 - Immediate anaphylactic - IgE
Type 2 - Cytoxic antibody - IgG, IgM
Type 3
Type 4 - Delayed hypersensitivty - contact dermatitis

170
Q

Type C - Continuous

A

Steroids and osteoporosis
Analgesic nephropathy
Steroids and Iatrogenic Cushing’s syndrome
Colonic dysfunction due to laxatives

171
Q

Type D - Delayed

A

Teratogensis - drugs taken in the first trimester

172
Q

Type E - Ending of drug use

A

Withdrawal

173
Q

ADR suspicion

A

New drug
Dosage increase
Drug is stopped

174
Q

Most commons drugs with ADRs

A 
Antibiotics
Anti-neoplastics
NSAIDs
CNS drugs
Hypoglycaemics
Cardiovascular drugs
175
Q

Most common systems affected

A 
GI
Renal
Haemmorhagic 
Endocrine
Dermatological
176
Q

Common ADRs

A 
Confusion
Nausea
Balance problems
Diarrhea
Constipation
Hypotension
177
Q

Black triangle indicates a medicine

A

Undergoing additional monitoring

178
Q

Serious reactions

A

Fatal
Life-threatening
Disabling
Results in hospitalisation or prolongs it

179
Q

Allergic reactions to drugs

A

Interaction of drug/metabolite/non-drug element with patient and disease
Subsequent re-exposure
Exposure may not be medical - penicillin in dairy products`

180
Q

Intolerance is not same as

181
Q

Drug hypersensitivity

A

Immediate - anaphylaxis

Delayed - rahes, hepatitis, cytopenis

182
Q

Anaphylaxis can be

A

Immunological

Non-immunological

183
Q

Anaphylaxis is mediated by

184
Q

Type 1 hypersesnivity

A

Acute anaphylaxis
Prior exposure to antigen/drug
IgE antibodies formed and attach to agents and activate the release of histamine, prostaglandins etc

185
Q

Anaphyaxlsis

A 
Rapid onset
Vasodilaiton
Increased vascular permability 
Bronchoconstriciton
Urticaria 
Angeo-oedema
186
Q

Type 2 reactions

A

Antibody-dependent cytotoxicity

Drug or metabolite combines with protein

187
Q

Type 3 reactions

A

Antigen-antibody complexes and activate complement

Vasculitis

188
Q

Type 4 reactions

A

Lymphocyte mediated
Contact dermatitis
Stevens-Johnson syndrome

189
Q

Non-immune anaphylaxis

A

Due to direct mast cell dragranulation

No prior exposure

190
Q

Anaphylaxis main features

A

Exposure to the drug, immediate rapid onset
Rash
Swelling (lips, face, oedema, central cyanosis)
Wheeze/SOB
Hypotension (anaphylactic shock)
Cardiac arrest

191
Q

Shock

A

Lack of body organ perfusion

Leads to loss of consciousness

192
Q

Management of anaphylaxis

A 
ABC
Stop drug if infusion
Adrenaline IM/Epipen
High flow Oxygen
IV fluids
IV Antihistamine 
IV Hydrocortisone
IV Adrenaline for Anaphylactic shock
193
Q

Adrenaline

A

Vasoconstriction
Stimulation of B1 adrenoreceptors
Reduces oedema and bronchoconstriction

194
Q

Risk factors for hypersensitivity

A

Medicine factors - proteins or macromolecules

Host factors - F>M, HIV, Pred drug reaction, uncontrolled asthma

195
Q

ABC

A

ATP Binding Cassette

Carrier mediated transport

196
Q

SLC

A

Soluble carrier
OAT1 is an example - organic anion transporter, found in kidney and secretes penicillin and uric acid
Probenecid blocks it leading to uric acid excretion

197
Q

Pinocytosis

A

Carrier mediated entry into the cytoplasm

198
Q

Amphotericin

A

Antifungal

199
Q

Drug absorption in gut

A

Drug needs to be lipid-soluble to be absorbed into gut

200
Q

Drug formulation

A

Some formulated to dissolve slowly (modified release) or have an enteric coating that is resistant to stomach acidity - Aspirin has an EC

201
Q

First pass metabolism - Barriers

A

Intestinal lumen
Intestinal wall
Liver
Lungs

202
Q

Intestinal lumen

A

Digestive enzymes

203
Q

Intestinal wall

A

Cellular enzymes - MAO

Efflux transporters - P-gp which limits absorption by transporting drug back into gut lumen

204
Q

Liver

A

Major site of drug metabolism

205
Q

Transcutaenous

A

Transdermal patches - Fentanyl patches

206
Q

Thiopental

A

Rapid anaesthetic because of initial high brain conc, but is short-lived as continued muscle uptake lowers blood conc and indirectly the brain conc

207
Q

Protein binding

A

Commonest reversible binding occurs with plasma protein albumin

208
Q

Lipid soluble drugs

A

Pass easily through BBB

209
Q

CYP450

A

Membrane bound isoenzyme
Present in smooth endoplasmic reticulum
Largely in livet tissue
Cimetidine and grapefruit induce/inhibit CYP450
Smoking and alcohol increase drug metabolism rapidly which can lead to consequences

210
Q

Phase 1 reaction

A

Breaking drug down

Introduction of a functional group

211
Q

Phase 2 reaction

A

Building drug up with functional active chemical groups (such as methyl group)

212
Q

Excretion

A

Fluids - urine, bile, sweat, breast milk
Solids - faeces, hair
Gases - expired air (volatiles)

213
Q

Total urine excretion determined by

A

Glomerular filtration
Tubular secretion
Reabsorption

214
Q

Ethanol enzyme system

A

Alcohol dehydrogenase

215
Q

Ciprofloxacin

216
Q

Lipid vs water-soluble drugs

A

Lipid soluble faster than water-soluble drugs

217
Q

Opiates

A

Analgesia

Codeine, tramadol

218
Q

Depressants

A

Sedation

Benzodiazepines, gabapentinoids, alcohol

219
Q

Stimulants

A

Increase alertness

Amphetamines, cocaine, caffeine, ecstasy/MDMA

220
Q

Cannabinoids

A

Relaxation, euphoria

Cannabis, spice

221
Q

Hallucinogens

A

Altered sensory perceptions

LSD, magic mushrooms

222
Q

Anaesthetic

A

Anaesthesia, sedative

Ketamine, NOX

223
Q

New psychoactive substances

A

Legal high

Tend to be used in clubs

224
Q

Substance use disorder (addiction)

A

Compulsive use of a substance despite harmful consequences

225
Q

Alcohol units guidelines

A

14 units per week spread over 3 days or more

226
Q

Alcohol specific deaths by condtition

A

Alcoholic liver disease
Alcoholic cardiomyopathy
Alcohol induced acute pancreatitis

227
Q

Alcohol withdrawal

A 
Tremors
Agitation
Tachycardia
Hptn
Seizures 
Hallucination - visual/tactile
228
Q

Alcohol and pregnancy

A

Foetal alcohol syndrome - Pre/postnatal growth retardation, Craniofacial abnormalities

229
Q

Psychosocial effects of excessive alcohol consumption

A

Interpersonal relationships - violence, rape, depression/anxiety
Work problems
Poverty
Driving incidents/offences

230
Q

Alcohol-use disorders - Primary prevention

A

Pricing - Make less affordable (MUP - minimum unit pricing)
Availability - Licensing
Marketing - Limit exposure to young children
Campaigns - Drinkaware

231
Q

Alcohol-use disorders - Screening

A

Clinical interview as part of routine exam in patients who are pregnant, smoking, health problems that are likely alcohol-induced
FAST - Fast alcohol screening test

Phase 2a NEW (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions