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Phase 2 Quick > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is Pharmacodynamics?

A

How the drug affects the body

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2
Q

What is pharmacokinetics?

A

How body affects the drug

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3
Q

Describe the 4 aspects of Pharmacokinetics

A

ADME
Administration - route
Distribution - systemic spread
Metabolism - 1st pass metabolism, IV skips this!
Excretion - hepatically or renally

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4
Q

Drug Receptor types

A

Ligand-gated ion channels - nicotinic ACh receptors

G Protein Coupled receptors (GPCR’s) - beta-adrenoceptors

Kinase-linked receptors - for growth factors

Cytosolic/nuclear receptors - steroid

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5
Q

What questions should you ask when prescribing a drug, with pharmacokinetics in mind?

A

How quickly will drug reach its site of action? How quickly will I see a response?
Drug interactions likely?
Is a dose adjustment needed in certain disease states?
What monitoring is required?

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6
Q

What mechanisms do drugs use to permeate membranes?

A
  1. Passive diffusion through hydrophobic membranes - lipid soluble molecules
  2. Passive diffusion through aqueous pores - only v small soluble drugs, e.g. lithium
  3. Carrier mediated drugs - quite unusual, basically when proteins that usually transport sugars, amino acids etc transport drugs
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7
Q

How does drug ionisation affect drug absorption?

A

Ionised drugs have poor lipid solubility
∴ only unionised drugs can pass

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8
Q

Why are the majority of medications PO?

A

Convenient
Cost-effective

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9
Q

Where are medications that are weak bases best absorbed? Why?

A

In the small intestine
bc small intestine has a pH of ~ 6.5 ∴ more likely to be similar pH to pKa of medication (the pH at which ionised & unionised drug is 50/50)

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10
Q

Where are medications that are weak acids best absorbed? Why?

A

In stomach
bc stomach has a pH of ~ 3 ∴ more likely to be similar pH to pKa of medication (the pH at which ionised & unionised drug is 50/50)

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11
Q

What factors affect the oral drug absorption in the stomach?

A

Gastric enzymes - digest the drug, esp large protein drugs e.g. insulin (∴ never given orally)

Low pH - can degrade

Full stomach = slower absorption

Gastric motility - can be altered by drugs/disease

Prev. surgery

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12
Q

What factors affect the oral drug absorption in the small intestine?

A

Drug structure - large/hydrophillic molecules are poorly absorbed

Medicine formulation - i.e. capsule has a coating to control release
Modified release slows rate of absorption (bc less freq dosing)

P-glycoprotein - will remove substrates from endothelial cells back into lumen lol

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13
Q

What is first pass metabolism?

A

Metabolism of drugs which prevents them from reaching systemic circulation
(The fraction of drug lost at absorption)

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14
Q

What happens during first-pass metabolism?

A

Degradation by enzymes in intestinal wall
&
Absorption from intestine into hepatic portal vein and metabolism via liver enzymes

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15
Q

What is bioavailability?

A

Proportion of administered dose which reaches the systemic circulation

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16
Q

What is bioavailability (F) dependent on?

A

Extent of absorption and first pass metabolism
NOT on rate of absorption

Varies w/ route of administration and between Px

e.g. tablet has lower bioavailability (F) than IV

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17
Q

What is bioavailability expressed as?

A

% or fraction

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18
Q

Pros of PR route

A

Local administration
Avoids first pass metabolism
Helps if patients has severe N/V ∴ can’t take meds orally

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19
Q

Cons of PR route

A

Absorption is variable
Patient preference

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20
Q

Example of PR medication

A

Diazepam suppositories for epileptic seizures

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21
Q

Pros of INH route

A

Well perfused large SA
Local administration

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22
Q

Cons of INH route

A

Inhaler technique might be ineffective

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23
Q

Example of INH route meds

A

Gaseous anaesthetic
Salbutamol inhaler

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24
Q

Pros of SC route

A

Faster onset than PO
Formulation can be changed to control absorption rate

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25
Q

Cons of SC route

A

Not as rapid as IV

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26
Q

Examples of SC route meds

A

Long acting insulin for T1DM and T2DM

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27
Q

Pros of TD route

A

Provides continuous drug release
Avoids first pass metabolism

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28
Q

Cons of TD route

A

Only suitable for lipid soluble drugs
Slow onset of action

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29
Q

Examples of TD route medication

A

Fentanyl patches for severe chronic pain

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30
Q

What factors influence distribution?

A
  1. Molecule size (small, ↑ distribution)
  2. Lipid solubility (if lipophillic, ↑ distribution)
  3. Protein binding (if NOT protein bound, ↑ distribution)
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31
Q

What is the volume of distribution (Vd)?

A

Also sometimes known as apparent volume of distribution

Theoretical vol a drug will be distributed in the body
Vol of plasma required to contain the total administered dose

If well distributed, high Vd
If poorly distributed, low Vd

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32
Q

What is the blood brain barrier?

A

Membrane that separates foreign substances in blood from CNS

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33
Q

Describe the physical aspect of the BBB

A

Continuous layer of endothelial cells with tight junctions
Has high number of efflux pumps that remove water soluble molecules

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34
Q

How can drugs reach the CNS?

A

High lipid solubility - can permeate and diffuse across BBB
Intrathecal route
Inflammation - causes BBB to be leaky ∴ drugs can cross

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35
Q

In actuality, what must you think about when prescribing drugs, in relation to distribution?

A

Careful w dosing drugs with a small Vd - using actual body weight in obese patients
e.g. Aciclovir NOT distributed to fat ∴ should be dosed based on ideal body weight, not actual

Distribution changes in diff disease states (i.e. sepsis = leaky blood vessels = BBB penetration)

Age changes body composition, which changes Vd of water soluble drugs

Drugs that can cross BBB have CNS s/e

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36
Q

What is drug elimination?

A

The process by which the drug becomes no longer available to exert its effect on the body

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37
Q

Name 2 methods of drug elimination

A

Metabolism - modification of drug to new chemical entity
Excretion of unchanged drug

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38
Q

What are the 2 phases of metabolism?

A
  1. Oxidation / Reduction / Hydrolysis to introduce reactive group to chemical structure. Slightly increase hydrophilicity
    By microsomal enzymes e.g. CYP450
  2. CONJUGATION. Adds functional group to produce hydrophilic, inert molecule.
    e.g. glucuronidation

then excreted

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39
Q

What cytochrome is mainly responsible for Phase 1 metabolism? Where are these located?

A

Cytochrome P450 (CYP450)
Mostly in liver (also small intestine, lung)

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40
Q

When will CYP enzyme function vary?

A

Genetic variation
↓ Function in severe liver disease
Interactions w/ drugs/foods which can ↑ or ↓ activity

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41
Q

How many CYP450 enzymes are there?

A

57

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42
Q

What CYP enzyme has the substrates caffeine, paracetamol, theophylline and warfarin?

A

CYP 1A2

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43
Q

What CYP enzyme has the substrates ibuprofen and warfarin?

A

CYP 2C9

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44
Q

What CYP enzyme has the substrates codeine and warfarin?

A

CYP 2D6

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45
Q

What CYP enzyme has the substrates simvastatin, warfarin, DOACs, carbamazapine and diltiazem?

A

CYP 3A4

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46
Q

What substrates are associated with CYP1A2?

A

Caffeine, paracetamol, theophylline, warfarin

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47
Q

What substrates are associated with CYP2C9?

A

Ibuprofen, warfarin

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48
Q

What substrates are associated with CYP2C19?

A

Omeprazole, phenytoin

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49
Q

What substrates are associated with CYP2D6?

A

Codeine, warfarin

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50
Q

What substrates are associated with CYP3A4?

A

simvastatin, warfarin, DOACs, carbamazapine and diltiazem

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51
Q

Which are the most signif CYP for drug metabolism?

A

3A4, 2C9, 2C19, 1A2, 2D6

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52
Q

In actuality, what must you think about when prescribing drugs, in relation to metabolism?

A

If severe liver impairment, is metabolism reduced?
∴ reduced dose? additional monitoring? avoid??

Drug interactions

Saturation of metabolic pathways can lead to accumulation or toxicity (paracetamol overdose)

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53
Q

If normal dose of paracetamol, how is it metabolised?

A

Via glucuronidation and sulphation to form a non-toxic metabolite

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54
Q

If paracetamol overdose, how is it metabolised? What is the result? How do we treat this?

A

Normal pathway is saturated
∴ Oxidation by CYP2E1

Forms NAPQI (v toxic)
Causes hepatocyte necrosis ∴ liver failure

We would give IV n-acetyl cysteine (NAC)
Replenishes body’s stores of glutathione
∴ glutathione conjugation
∴ produces a non-toxic metabolite :)

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55
Q

When would we give a reduced paracetamol dose?

A

In low body weight patients
Or if severe hepatic impairment

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56
Q

In what forms can drugs/metabolites be excreted?

A

Liquids - small polar molecules e.g. urine, bile, sweat, tears, breast milk

Solids - large molecules e.g. faeces (thru biliary excretion)

Gases - volatiles e.g. expired air

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57
Q

What is the first process that accounts for renal excretion?

A
  1. Glomerular filtration
    Free/unbound drug molecules will pass through
    V large molecules will be excluded and will go thru efferent arteriole
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58
Q

What is the 2nd process of renal excretion?

A
  1. Active tubular secretion
    Drug molecules transported from blood into renal tubule thru carriers
    (organic anion transporter (OAT) & organic cation transporter (OCT))

Can clear protein bound drugs

Most effective renal clearance mechanism

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59
Q

What is the 3rd process of renal excretion?

A
  1. Passive reabsorption
    Diffusion down conc gradient from tubule into peritubular capillaries

Hydrophobic drugs diffuse easily
Highly polar drugs will be excreted

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60
Q

Types of Adverse drug reactions

A

ABCDEFG

Augmented
Bizarre
Chronic/continuing
Delayed
End of use/withdrawal
Failure of treatment
Genetic

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61
Q

What should you do if a patient has a Adverse Drug reaction?

A

Report to MHRA using the YELLOW CARD SCHEME

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62
Q

What is Augmented ADR caused by?

A

Exaggerated effect of drugs pharmacology at therapeutic dose
Usually not fatal

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63
Q

What is the most common ADR?

A

Augmented (80%)

64
Q

When is Augumented ADR dependent on?

A

Dose dependent
Reversible when drug is withdrawn

65
Q

Give some examples of Augmented ADR

A

AKI w/ ACE-i
Bradycardia w/ beta blockers
Hypoglycaemia w/ gliclazide, insulin
Resp depression w/ opiates
Bleedings w/ anticoag

66
Q

Describe Bizarre ADRs

A

Not related to pharm
Not dose related
Can cause serious illness/death
Symptoms don’t always resolve when stopping drug

67
Q

Give examples of a Bizarre ADR

A

Anaphylaxis w/ penicillin
Tendon rupture w/ quinolone abx
Steven Johnson Syndrome w/ IV vancomycin

68
Q

What is a Chronic/Continuous ADR?

A

An ADR that continues after drug has been stopped

69
Q

Give examples of Chronic/Continuing ADR

A

Osteonecrosis of the jaw w/ bisphosphonates
HF w/ pioglitazone

70
Q

What is a delayed ADR?

A

ADRs that become apparent some time after stopping drug

71
Q

Give an example of a delayed ADR

A

Leucopenia w/ chemo

72
Q

What is an End of Use/Withdrawal ADR?

A

ADR that develops after drug has been stopped

73
Q

Give examples of End of Use/Withdrawal ADR

A

Insomnia after stopping benzodiazepine
Rebound tachycardia after stopping BB

74
Q

What could cause a Failure of treatment ADR?

A

Drug-drug or drug-food interaction
Poor compliance with administration instructions

75
Q

Give examples of a Type F ADR

A

Failure of bisphosphonates due to taking w/ food
Failure of DOAC due to enzyme inducer (e.g. carbamazepine)

76
Q

What is a Genetic ADR?

A

When drug causes irreversible damage to genome

77
Q

Give an example of a Genetic ADR

A

Phocomelia in children of women taking thalidomide

78
Q

Other than the ABCDEFG classification, what is another way of classifying ADRs?

A

DoTS

Dose-relatedness
Timing
Susceptibility

79
Q

Describe the Do in DoTS

A

Dose relatedness
Looks at the dose you might get a ADR

//
Hypersusceptibility reaction
When you get an ADR at a subtherapeutic dose
e.g. anaphylaxis w/ penicillin

Collateral effect
ADR at a therapeutic dose
e.g. hypokalaemia w/ loop diuretic

Toxic effects
ADR at subpratherapeutic dose
e.g. liver damage w/ paracetamol

80
Q

Describe the T in DoTS

A

Timing
When does ADR develop in relation to the drug taken

TYPES :
Rapid
First dose
Early
Intermediate
Late
Delayed

81
Q

Describe the S in DoTS

A

Susceptibility
Certain patients/groups have specific susceptibility to ADRs

Could be due to :
Age
Gender
Disease states
Physiological states

82
Q

Define Agonist

A

Have full affinity and FULL efficacy
∴ ↑ Activation of the receptor

83
Q

Define Antagonist

A

Full affinity and ZERO efficacy
∴ ↓ Activation of the receptor

84
Q

Define affinity

A

How well a ligand binds to its receptors

85
Q

Define efficacy

A

How well a ligand successfully activates its receptors

86
Q

Define Potency

A

Relative strength of the drug
i.e. lower dose needed for response

87
Q

Define a Competitive inhibitor

A

Binds AT active site
↓ Efficacy reversibly
Affinity is unchanged

88
Q

Define a Non-Competitive inhibitor

A

Binds AWAY from active site, changes its shape
↓ Efficacy irreversibly
↓ Affinity

89
Q

In terms of the Dose/Response curve, describe competitive inhibitors

A

Curve shifts to the RIGHT
Drug has less affinity but same efficacy
Same EC50

DRUG IS LESS POTENT

90
Q

What is Ec50?

A

The conc required for a 50% effect

91
Q

In terms of the Dose/Response curve, describe non-competitive inhibitors

A

Curve shifts RIGHT & DOWN
Drug has less affinity and less efficacy
EC50 decreases

DRUG IS LESS POTENT

92
Q

Define Bioavailability

A

How much drug is uptaken systemically for effect
e.g. IV = always 100%

93
Q

What is the therapeutic range?

A

Upper and lower bounds of safe dose of a drug
(if narrower range, needs more care in dispensing)

94
Q

Drug Targets for drugs
Examples of each

A

Receptor action (MC!!) - Beta blockers
Enzymes - ACEi
Ion channels - CCB
Transporters - PPI

95
Q

Where does metabolism of drugs occur?

A

GIT - mechanical & chemical digestion, for majority of food

Renal - simple, already soluble molecules.

Hepatic - more complex, hydrophobic molecules. Undergoes Phase 1 +/- Phase 2 reactions

96
Q

Autonomic vs Somatic?
What transmission falls under what?

A

Autonomic - automatically, no conscious effort
Parasympathetic and Sympathetic

Somatic - voluntary
Skeletal muscle motor

97
Q

Parasympathetic pre and post synpatic?

A

ACH - pre
ACH - post

98
Q

Sympathetic pre and post synaptic?

A

AcH - pre
Noradrenaline - post

99
Q

Skeletal muscle motor what neurotransmitter?

A

Ach at the NMJ

100
Q

2 Main receptors in Cholinergic Pharm?
Where are they - in reference to synapse?

A

Nicotinic - Presynaptic
Muscarinic - Postsynaptic

101
Q

Name the main muscarinic receptors
Where do you find them?

A

M1 - Brain
M2 - Heart
M3 - Lungs!

102
Q

Which condition is related to disrupted Ach Transmission at the NMJ?

A

Myasthenia Gravis

103
Q

Tx Myasthenia Gravis

A

Neostigmine
Pyridostigmine

104
Q

S/E of XS Acetylcholine stimulation

A

SLUDGE

Salivation
Lacrimation
Urination
Defecation
Gastric distress
Emesis

105
Q

Where do we find Alpha 1 & Alpha 2 receptors?

A

Vessels and sphincters e.g. bladder neck
(Distal circulation)

106
Q

Where do we find Beta 1 receptors?

A

Heart

107
Q

Where do we find Beta 2 receptors?

A

Lungs

108
Q

What is tamsulosin?

A

Alpha 1 blocker

109
Q

Name a Beta 1 agonist
When is it used?

A

Dobutamine
Cardiogenic shock!!

110
Q

What does a Beta 1 AGONIST do?

A

INCREASES force (inotropy) and rate (chronotropy) of cardiac contractions

111
Q

What does a Beta 1 ANTAGONIST do?

A

DECREASES force (inotropy) and rate (chronotropy) of cardiac contractions

112
Q

Name a Beta 1 antagonist

A

Beta blocker!

113
Q

When are BB CI?

A

Absolute asthma

114
Q

What does a Beta 2 AGONIST do?

A

Bronchodilate airways

115
Q

Example of Beta 2 agonist

A

SABA - salbutamol

116
Q

What is a cardioselective drug?
Give an example

A

Only act on cardiac tissue
Beta blockers (beta 1 only)

117
Q

Examples of opioids

A

Morphine
Diamorphine (heroin)
Codeine
Pethidine

118
Q

What is the bioavailability if you take opioids PO?

A

50%

119
Q

When do you tend to use opioids?

A

For chronic severe pain relief
Mostly cancer pain

120
Q

5mg diamorphine =

A

10mg morphine = 100mg pethidine

121
Q

Main S/E of opiate use?

A

Constipation

122
Q

Opiate over can cause ?
Treatment for this and Route of administration?

A

Respiratory depression
IV Naloxone

123
Q

Give examples of when you would use blood thinners?

A

DVT/PE
AF
Prosthetic valves
Bleeding disorders
Ischaemic stroke
MI

124
Q

Give examples of blood thinners

A

DOACs - Apixaban, Rivaroxaban
Warfarin
LMWH
Alteplase IV
Antiplatelets - Clopidogrel, ticagrelor

125
Q

Warfarin inhibits?

A

Vit K
Clotting factors 10, 9, 7, 2

126
Q

LMWH inhibits?

A

Clotting factors 3, 10

127
Q

What does COX-1 do?

A

Involved in Prostaglandin synthesis
which protects gastric mucosa

128
Q

S/E COX-1 inhibition

A

Peptic ulcer

129
Q

NSAID MOA?

A

Inhibits arachidonic acid pathyway COX-1 and COX-2

130
Q

What does COX-2 do?

A

Involved in inflammation

131
Q

Example of a selective COX-2 inhibitor?

A

Celecoxib

132
Q

Why don’t we use COX-2 selective drugs?

A

Not as effective
Also expensive

133
Q

Where do Loop diuretics act upon?

A

Ascending limb

134
Q

MOA Loop diuretics

A

Na-K-Cl contransporter channels

135
Q

Example Loop diuretic

A

Furosemide

136
Q

Where do Thiazide Diuretics act on?

A

DCT

137
Q

Thiazide diuretic MOA

A

Na-Cl co-transporter

138
Q

Example of Thiazide diuretic

A

Bendroflumethiazide

139
Q

Where do Aldosterone antagonists act upon?

A

Collecting duct

140
Q

MOA Aldosterone antagonist

A

Increases Na+ excretion and retains K+ but acting on aldosterone receptors

141
Q

What is an aldosterone antagonist also known as?

A

K+ sparing diuretic

142
Q

PPI e.g.

A

Lansoprazole

143
Q

What does PPI do?

A

↓ Acidity of GI lumen

144
Q

Nicotinic is assoc w?

A

CNS

145
Q

Muscurinic is assoc w?

A

PNS

146
Q

Main S/E of ACEi
Why?

A

Dry cough
Bc build up of bradykinin in airways

147
Q

Difference between tolerance and dependence?

A

Tolerance is physiological while dependence is psychological

148
Q

Main S/E of CCB
What condition might this be mistaken for?

A

Oedema - Ankle swelling
HF

149
Q

What is the first line treatment for Anaphylaxis?

A

IM 500 micrograms Adrenaline

150
Q

Metformin S/E

A

GI distress
Stomach pain

151
Q

S/E Sulphonylurea

A

Hypoglycaemic episodes
Weight gain

152
Q

What is Metformin?

A

Biguanide

153
Q

S/E Spironolactone

A

Hyperkalaemia
Stomach cramps

154
Q

S/E Amiodarone

A

Clubbing
Non-productive cough
Fine crackles on ausc
Reduced chest expansion

Thyroid disease
Corneal deposits

155
Q

S/E Statin

A

Myalgia
Liver impairment

156
Q

S/E BB

A

Bradycardia
Bronchospasm
Cold peripheries

157
Q
A

Phase 2 Quick (18 decks)

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