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Phase 2a Medicine > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is pharmacodynamics?

A

Effect of a drug on the body

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2
Q

What is pharmacokinetics?

A

Effect of the body on a drug

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3
Q

What are the 4 physicochemical reactions?

A
  1. Adsorption
  2. Precipitation
  3. Chelation
  4. Neutralisation
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4
Q

What is summation?

A

If 2 half doses of drugs are given at the same time, can get a full dose as a result of the combination

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5
Q

What is synergy?

A

When a dose is more than expected when a combined dose is given

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6
Q

What is potentiation?

A

Drug A stays the same but causes drug B to have an increased effect

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7
Q

What are the patient risk factors for drug interactions?

A
  1. Polypharmacy
  2. Old age
  3. Genetics
  4. Hepatic disease
  5. Renal disease
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8
Q

What are the drug risk factors for drug interaction?

A
  1. Narrow therapeutic index
  2. Step dose/response curve
  3. Saturable metabolism
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9
Q

What are the mechanisms of pharmacokinetics?

A
  1. Absorption
  2. Distribution
  3. Metabolism
  4. Excretion (ADME)
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10
Q

What are the mechanisms of pharmacodynamics?

A
  1. Receptor based
  2. Signal transduction
  3. Physiological systems
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11
Q

Describe the absorption of IV drugs

A

Starts low then get quick increase in blood concentration of a drug, which exponentially goes down after it peaks

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12
Q

Describe the absorption of oral drugs

A

Low peak which is reached slowly but takes longer to get rid of as it is still being absorbed from the gut even as it is being excreted

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13
Q

What is bioavailability?

A

How much of a dose of a drug you get

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14
Q

What type of drug is given in ICU to increase feed of pt.?

A

Drugs to increase gut motility

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15
Q

What effect does changing the pH of a drug environment have?

A

Changes portion of ionised: non-ionised drug

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16
Q

What does it mean if there’s a big volume of distribution?

A

Most of the drug will not go to the effector site

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17
Q

What happens if there is a low volume of distribution?

A

The drug is fairly targeted to the effector site

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18
Q

What happens in enzyme induction?

A

Drug A increases the effect of CYP450 to make drug B more potent

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19
Q

What is enzyme inhibition?

A

Drug A reduces the effect of CYP450 to make drug B less potent

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20
Q

What is given to overcome aspirin overdose?

A

NaCO3 which causes excretion of aspirin to happen faster

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21
Q

What drugs cause AKI?

A

NSAIDs, furosemide

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22
Q

What is the effect of grapefruit juice?

A

Affects CYP3A4 to increase bioavailability

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23
Q

What are the routes of excretion?

A

Renal, biliary

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24
Q

What is a drug?

A

Medicine or other substance which has a physiological effect when ingested or otherwise introduced into body

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25
Q

What is druggability?

A

Ability of a protein target to bind small molecules with high affinity

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26
Q

What are the 4 common drug targets?

A
  1. Receptors
  2. Enzymes
  3. Transporters
  4. Ion channels
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27
Q

What is a receptor?

A

A component of a cell that interacts with a specific ligand and initiates a change of biochemical events leading to ligands observed effects

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28
Q

What are the 4 common receptors?

A
  1. Ligand-gated ion channels
  2. G protein coupled receptors
  3. Kinase-linked receptors
  4. Cytosolic/nuclear receptors
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29
Q

What do the majority of GPCRs interact with?

A

PLC or adenylyl cyclase

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30
Q

What can change the way a receptor responds?

A

Polymorphisms

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31
Q

What happens when a ligand binds a kinase linked receptor?

A

Causes polymorphism of components which then recruit molecules which only interact with phosphorylated component of receptor to amplify signal on IC side

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32
Q

What is a receptor ligand?

A

A molecule that binds to another molecule

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33
Q

What is an agonist?

A

A compound that binds to a receptor and activates it

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34
Q

What is an antagonist?

A

A compound that reduces the effect of an agonist

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35
Q

What is potency?

A

EC50, concentration that gives half the maximal response

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36
Q

What is efficacy (Emax)?

A

Maximum response achievable from a dose

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37
Q

What is intrinsic activity?

A

Ability of a drug-receptor complex to produce a maximal functional response

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38
Q

How do you determine intrinsic activity (IA)?

A

IA = Emax of a partial agonist ÷ Emax of full agonist

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39
Q

What is competitive antagonism?

A

Directly competes for binding to receptor

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40
Q

What is non-competitive antagonism?

A

Binds to an allosteric site of receptor to prevent activation of receptor

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41
Q

What are the 2 categories of cholinergic receptor?

A

Nicotinic and muscarinic

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42
Q

What factors govern drug action?

A
  1. Affinity
  2. Efficacy
  3. Receptor number
  4. Signal amplification
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43
Q

What is affinity?

A

Describes how well a ligand binds to receptor

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44
Q

What is efficacy?

A

Describes how well a ligand activates a receptor

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45
Q

What is receptor reverse?

A

Where an agonist needs to activate only a small fraction of existing receptors to produce a maximal system response

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46
Q

What is a signal cascade?

A

Response following ligand binding a receptor by causing a number of amplification steps

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47
Q

What is allosteric modulation?

A

Where antagonist (or ligand) binds to a site which isn’t the active site of that receptor

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48
Q

What is inverse agonism?

A

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

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49
Q

What is tolerance?

A

Reduction in agonist effect over time

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50
Q

When does desensitisation occur?

A

When proteins are uncoupled, internalised or degraded

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51
Q

What is an enzyme inhibitor?

A

A molecule that binds to an enzyme and decreases its activity

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52
Q

How do enzyme inhibitors work?

A

Prevent substrate from entering enzyme’s active site and prevents it from catalysing its reaction

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53
Q

What are the types of enzyme inhibitor?

A
  1. Irreversible inhibitors

2. Reversible inhibitors

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54
Q

How do irreversible inhibitors bind?

A

Covalent bond

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55
Q

What are the symptoms of Parkinson’s?

A 
Hypokinesia
Tremor at rest
Muscle rigidity, motor inertia
Cognitive impairment
Degenerative disease of basal ganglia
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56
Q

What is the pathway for Parkinson’s?

A

Early degeneration of dopaminergic in nigrostriatial pathway leading to autonomic dysfunction and dementia

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57
Q

What are the 3 main protein ports?

A
  1. Uniporter
  2. Symporter
  3. Antiporter
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58
Q

How do uniporters work?

A

Use energy from ATP to pull molecules in

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59
Q

How do symporters work?

A

Use movement in of one molecule to pull in another molecule against a concentration gradient

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60
Q

How do antiporters work?

A

One substance moves against its gradient, using energy from second substance moving down its gradient

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61
Q

What is the mechanism of action for furosemide?

A

Inhibits luminal NKCC co-transporter in thick ascending limb of loop of Henle to cause loss of Na, Cl and K in urine

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62
Q

What is ENaC?

A

An apical membrane-bound heterotrimeric ion channel selectively permeable to Na ions

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63
Q

What high affinity diuretic blocks ENaC?

A

Amiloride

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64
Q

Where are voltage gated Ca channels found?

A

Membrane of excitable cells

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65
Q

How do voltage gated Ca channels work?

A

Ca enters cell, resulting in activation of Ca-sensitive K channels, muscular contraction, excitation of neurons etc.

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66
Q

What is amlodipine?

A

An angioselective Ca channel blockers that inhibits the movement of Ca ions into vascular smooth muscle cells and cardiac muscle celsl

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67
Q

How does amlodipine work?

A
  1. Inhibits Ca ion influx across cell membranes with greater effect on vascular SMC.
  2. Causes vasodilation and a reduction in peripheral vascular resistance.
  3. Lowers BP and prevents excessive constriction in coronary arteries
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68
Q

What is the main inhibitory neurotransmitter in the CNS?

A

GABA

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69
Q

What drug inhibits Na/K ATPase?

A

Digoxin

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70
Q

What is a heterodimeric protein?

A

Where 2 distinct proteins come together and assemble in the membrane

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71
Q

What is H/K ATPase responsible for?

A

Acidification of the stomach, activation of the digestive enzyme pepsin

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72
Q

What is the ideal target for inhibiting acid secretion?

A

Proton pump

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73
Q

What are the symptoms of irreversible inhibition of muscarinic receptors?

A 
Salivation
Defecation
Urination
Bradycardia
Hypotension
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74
Q

What are the symptoms of irreversible inhibition of nicotinic receptors?

A

Twitching
Severe weakness
Paralysis of diaphragm

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75
Q

What are the symptoms of irreversible inhibition of the CNS?

A

Confusion
Loss of reflexes
Convulsions
Coma

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76
Q

What are xenobiotics?

A

Compounds foreign to an organism’s normal biochemistry

77
Q

How much oral morphine is metabolised by first pass metabolism in the liver?

78
Q

What method is used for morphine release in palliative care?

A

MST continus

79
Q

Why is diamorphine more potent and faster acting than morphine?

A

It crosses the BBB faster

80
Q

What are the practical issues with controlled drugs?

A

Secure storage, CD books that need 2 signatures, prescription regulations

81
Q

In what proportion of people is codeine not metabolised?

82
Q

What receptor type do opioids act on?

A

GPCRs via 2nd messengers

83
Q

How do opioids work?

A

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

84
Q

What are the 4 main opioid receptors?

A

MOP (mu), KOP (kappa), DOP (delta), NOP (nociception)

85
Q

What is the side effect of activating kappa OP?

A

Depression instead of euphoria

86
Q

What opioid receptor do all current drugs target?

87
Q

What is tolerance?

A

Downregulation of receptors with prolonged use

88
Q

What is dependence?

A

A psychological response to drugs with cravings and euphoria

89
Q

How long until opioid withdrawal sets in?

90
Q

What are the side effects of opioids?

A
  1. Respiratory depression
  2. Sedation
  3. Nausea and vomiting
  4. Constipation
  5. Itching
  6. Immune suppression
  7. Endocrine effects
91
Q

What drug is given as treatment for respiratory repression?

92
Q

What metabolises codeine to work?

93
Q

Why might someone be at increased risk of respiratory depression with codeine?

A

Overactive CYP2D6

94
Q

What builds up to cause respiratory depression when taking morphine with renal failure?

A

Morphine 6 glucuronide

95
Q

What alternative to morphine is used in patients with renal failure?

96
Q

What is the secondary effect of tramadol?

A

Serotonin and noradrenaline reuptake inhibitor

97
Q

What does tramadol interact with?

A

SSRIs, tricyclic antidepressants, MAOIs

98
Q

Why can nicotinic receptors not be targeted for the nervous systems?

A

It is used in both sympathetic and parasympathetic pathways

99
Q

What pathway does cholinergic pharmacology target?

A

Parasympathetic

100
Q

What does nicotine stimulate?

A

All autonomic ganglia via specific ganglionic nicotinic receptors

101
Q

What does muscarine activate?

A

Muscarinic receptors of parasympathetic nervous system

102
Q

What is targeted in cholinergic pharmacology?

A

Muscarinic receptors

103
Q

What are the muscarinic receptors?

104
Q

Where is M2 found?

105
Q

What are drugs which target M2 used for?

A

Life-threatening bradycardia, cardiac arrest

106
Q

Where are M3 found?

A

Glandular and smooth muscle

107
Q

What do M3 cause?

A

Bronchoconstriction, sweating, salivary gland secretion

108
Q

What is hyoscine used for?

A

To reduce respiratory secretions in palliative care

109
Q

Give 5 side effects of anti-cholinergic drugs

A
  1. Confusion
  2. Constipation
  3. Dry mouth
  4. Blurred vision
  5. Glaucoma
110
Q

Give 4 side effects of cholinergic drugs

A
  1. Muscle paralysis
  2. Twitching
  3. Salivation
  4. Confusion
111
Q

Which receptors is NA the agonist for?

A

Alpha 1, Beta 3

112
Q

Which receptors is Adr the agonist for?

113
Q

Which receptors are NA and Adr the agonists for?

A

Alpha 2, Beta 1

114
Q

What is the mechanism of alpha 1?

A

Increases intracellular Ca, Gq signalling

115
Q

What is the consequence of alpha 1?

A

Contracts smooth muscle

116
Q

What is the mechanism of alpha 2?

A

Gi signalling, inhibition of cAMP generation

117
Q

What is the consequence of alpha 2?

A

Mixed effects on smooth muscle

118
Q

What is the mechanism of the beta receptors?

A

Gs, raises cAMP

119
Q

What is the consequence of beta 1?

A

Chronotropic and inotropic effects on heart (increase strength and stroke volume)

120
Q

What is the consequence of beta 2?

A

Relaxes smooth muscle (premature labour, asthma)

121
Q

What is the consequence of beta 3?

A

Enhances lipolysis, relaxes bladder detrusor

122
Q

Name a drug control-indicated in asthma which blocks beta 1/2

A

Propranolol

123
Q

Give 5 uses of beta blockers

A
  1. Angina
  2. MI prevention
  3. High BP
  4. Anxiety
  5. Arrhythmias
  6. HF
124
Q

Give 5 side effects of beta blockers

A
  1. Tiredness
  2. Cold extremities
  3. Bronchoconstriction
  4. Bradycardia
  5. Hypoglycaemia
  6. Cardiac depression
125
Q

What % of hospital admissions do adverse drug reactions account for?

126
Q

What is an adverse drug reaction?

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 drug

127
Q

What are the requirements for an adverse drug reaction?

A

Noxious and unintended

128
Q

What is a side effect?

A

An unintended effect of a drug related to its pharmacological properties and can include unexpected benefits of treatment

129
Q

What causes adverse drug reactions (ADRs)?

A
  1. Toxic effects
  2. Collateral effects
  3. Hypersusceptibility effects
130
Q

When can toxic effects occur?

A
  1. If dose is too high
  2. If drug excretion is reduced
  3. Interaction with other drugs
131
Q

What is a type A ADR?

A

Augmented pharmacological - predictable, dose dependent, common

132
Q

What is a type B ADR?

A

Bizarre or idiosyncratic - not predictable and not dose dependent

133
Q

What is a type C ADR?

134
Q

What is a type D ADR?

135
Q

What is a type E ADR?

A

End of treatment - occur after abrupt drug withdrawal

136
Q

What is a type F ADR?

A

Failure of therapy

137
Q

What is DoTS in relation to ADR causes?

A

Dose relatedness, Timing, patient Susceptibility

138
Q

What are 5 patient risk factors for ADRs?

A
  1. Female
  2. Elderly
  3. Polypharmacy
  4. Genetic predisposition
  5. Renal impairment
139
Q

What are 3 drug risk factors for ADRs?

A
  1. Steep dose-repense curve
  2. Low therapeutic index
  3. Commonly causes ADRs
140
Q

What are the main causes for ADRs?

A
  1. Pharmaceutical variation
  2. Receptor abnormality
  3. Abnormal biological system unmasked by drug
  4. Abnormalities in drug metabolism
  5. Immunological
  6. Drug-drug interactions
  7. Multifactorial
141
Q

What is idiosyncrasy?

A

Inherent abnormal response to a drug

142
Q

When should an ADR be suspected?

A
  1. Symptoms soon after a new drug is started
  2. Symptoms after a dosage increase
  3. Symptoms disappear when drug is stopped
  4. Symptoms reappear when drug is restarted
143
Q

Give 5 common symptoms of ADRs

A
  1. Confusion
  2. Nausea
  3. Balance problems
  4. Diarrhoea
  5. Constipation
  6. Hypotension
144
Q

What is the yellow card scheme?

A

ADR reporting scheme

145
Q

Give 2 advantages of the yellow card scheme

A
  1. Early warning system for identifying reactions

2. Provides info about what factors predispose patients to ADRs

146
Q

Give 2 disadvantages of the yellow card scheme

A
  1. Not all ADRs are reported

2. Relies on ADR being recognised

147
Q

What is a black triangle drug?

A

A medicine which is undergoing additional monitoring

148
Q

What is hypersensitivity?

A

Objectively reproducible symptoms or signs, initiated by exposure to a defined stimulus at a dose tolerated by normal subjects and may be caused by immunologic or non-immunologic mechanisms

149
Q

What are 5 symptoms of anaphylaxis?

A
  1. Rash
  2. Oedema/swelling
  3. Shortness of breath
  4. Hypotension
  5. Cardiac arrest
150
Q

What causes non-immune anaphylaxis?

A

Direct mast cell degranulation

151
Q

How much adrenaline is given in anaphylaxis?

152
Q

How does adrenaline work?

A

Stimulates Beta1-adrenoceptors to give positive ionotropic and chronotropic effects on heart

153
Q

What are the actions of drugs in the body?

A
  1. Absorption
  2. Distribution
  3. Metabolism
  4. Excretion
154
Q

What is absorption?

A

The process of transfer from the site of administration into the general or systemic circulation

155
Q

How can drugs cross membranes?

A
  1. Passive diffusion
  2. Diffusion through pores or ion channels
  3. Carrier mediated
  4. Pinocytosis
156
Q

What is required to passively diffuse over the lipid bilayer?

A

Degree of lipid solubility

157
Q

What is pinocytosis involved in?

A

Uptake of endogenous macromolecules, can be involved in uptake of recombinant therapeutic proteins

158
Q

Why are ionisable groups essential for most drug mechanisms?

A

Ionic forces are part of ligand receptor interaction

159
Q

What does the extent of ionisation depend on?

A
  1. Strength of ionisable group

2. pH of solution

160
Q

What affects the speed of oral absorption?

A
  1. Drug structure
  2. Drug formulation
  3. Gastric emptying
  4. First pass metabolism
161
Q

What metabolic barriers must drugs taken orally pass to reach circulation?

A
  1. Intestinal lumen
  2. Intestinal wall
  3. Liver
  4. Lungs
162
Q

How can hepatic first pass metabolism be avoided?

A

Give drug to region of gut not drained by splanchnic

163
Q

How are inhalation drugs limited?

A
  1. Risks of toxicity to alveoli

2. Delivery of non-volatile drugs

164
Q

What is distribution?

A

The process by which the drug is transferred reversibly from the general circulation to the tissues as the blood concentration increases and then returns from the tissues to the blood when the blood concentration falls

165
Q

What type of drugs easily pass from blood to brain?

A

Lipid soluble drugs

166
Q

What protects the brain by returning drug molecules to the circulation?

A

Efflux transporters

167
Q

What is elimination

A

Removal of drugs activity from body

168
Q

What may elimination consist of?

A

Metabolism and excretion

169
Q

What is metabolism re. drugs?

A

Transformation of drug molecule into a different molecule

170
Q

What is excretion re. drugs?

A

Molecule is expelled in liquid, solid or gaseous waste

171
Q

What does phase 1 of drug metabolism involve?

A

Transformation of drug to a more polar metabolite by unmasking or adding a functional group

172
Q

What catalyses most phase 1 reactions?

A

Cytochrome P450

173
Q

What can induce P450?

A

Smoking and alcohol

174
Q

What can inhibit P450?

A

Drugs and food e.g. cimetidine and grapefruit

175
Q

What does phase 2 drug metabolism involve?

A

Formation of covalent bond between drug or its phase 1 metabolite and an endogenous substrate

176
Q

What are the processes in renal drug processing?

A
  1. Glomerular filtration
  2. Tubular secretion
  3. Reabsorption
177
Q

What is zero order kinetics?

A

The change in concentration per time is a fixed amount of drug per time, independent of concentration

178
Q

What is first order kinetics?

A

Change in concentration at any time is proportional to the concentration

179
Q

What is half-life?

A

Time taken for a concentration to reduce by one half

180
Q

What is half-life used for in practice?

A

Elimination rate from plasma

181
Q

What is bioavailability?

A

The fraction of the administered drug that reaches the systemic circulation unaltered

182
Q

What is the bioavailability of IV drugs?

183
Q

What is distribution?

A

Rate and extent of movement of a drug into and out of tissues from blood

184
Q

What does drug distribution determine?

A

Total amount of drug that has to be administered to produce a particular plasma concentration

185
Q

What is clearance?

A

Volume of blood or plasma cleared of drug per unit time

186
Q

What are repeated drug doses used to maintain?

A

A constant drug conc. in the blood and at the site of action for therapeutic effect

187
Q

What is steady state?

A

Balance between drug input and elimination

188
Q

How can plasma steady state be altered in oral drugs?

A

Change dose or interval

Phase 2a Medicine (15 decks)

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