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Pharmaceutical factors Flashcards

1
Q

What is a double blind clinical trial?

A

Neither the participants nor the experimenters know who is receiving treatment

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2
Q

What is the MCC?

A

Medicine controls council

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3
Q

What is triptorelin?

A

An LHRH agonist

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4
Q

What is rifapentine?

A

Anti-TB drug

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5
Q

Name obstacles in the international pharmaceutical industry

A 
Patents 
Payor pressure
Generic competition
Safety concerns
Reputation
Earnings pressure
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6
Q

Which experimental heart pill created by Pfizer failed?

A

Torcetrapib

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7
Q

What is torcetrapib?

A

Cholesteryl ester transfer protein (CETP) inhibitor

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8
Q

What are pharmacokinetics?

A

Study of time course of drug concentration in the body

“What body does to the drug”

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9
Q

Name the aspects of drug input and output

A 
LADMET
Liberation
Absorption
Distribution
Metabolism
Excretion
Toxicity
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10
Q

Which pharmacokinetic factors are most important to determine dose?

A

Volume of distribution (Vd)
Half life (t1/2)
Clearance (CL)

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11
Q

What is absorption?

A

Movement of drug from site of administration to target site

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12
Q

What is distribution?

A

Diffusion/transport of drug from intravascular space to extravascular space

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13
Q

What is metabolism?

A

Chemical conversion/transformation of drugs into compounds for easier elimination

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14
Q

What is excretion?

A

Elimination of unchanged drug/metabolite from body via excretory system

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15
Q

What is bioavailability?

A

The fraction of administered dug that reaches the systemic circulation unchanged

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16
Q

What is the formula for bioavailability and why?

A

AUCoral/AUCIV

Because IV is always 100% bioavailable

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17
Q

Which factors affect bioavailability and how?

A

All ADME processes
Poor absorption = low bioavailability
High first-pass metabolism = low bioavailability

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18
Q

When is steady state achieved?

A

Rate of drug absorption = drug elimination

Cp plateaus

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19
Q

Which drugs will a missed dose affect?

A

Narrow therapeutic index drugs

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20
Q

How do you calculate Vd?

A

Total amount of drug in body (mg)/drug Cp (mg/L)

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21
Q

What is Vd an indication of?

A

Lipophilicity

Plasma protein binding

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22
Q

What is the relationship between Vd and Cp?

A

Inverse

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23
Q

What is the relationship between Vd and half life?

A

Direct

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24
Q

As Cp increases, what happens to Vd?

A

Decrease

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25
Q

As Cp decreases, what happens to Vd?

A

Increases

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26
Q

As half life increases, what happens to Vd?

A

Increases

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27
Q

As half life decreases, what happens to Vd?

A

Decreases

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28
Q

What if half life?

A

The time necessary for the drug’s plasma concentration to decrease by 1/2

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29
Q

What is the therapeutic range?

A

Above minimum therapeutic concentration

Below minimum toxic concentration

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30
Q

What does half life provide an index for?

A

Time-course of drug accumulation
Time-course of drug elimination
Dosing interval

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31
Q

Which factors influence half life?

A

Elimination rate
Vd
Patient factors

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32
Q

What effect does a higher clearance have on half life?

A

Decreased half life

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33
Q

What is the effect of a short half life on duration of action, dosing frequency, compliance, steady state and side effects

A 
Short duration
Increased dosing
Lower compliance
Earlier steady state
Quicker side effects
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34
Q

What is the effect of a short long life on duration of action, dosing frequency, compliance, steady state and side effects

A 
Long duration
Decreased dosing
Higher compliance
Later steady state
Longer side effects
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35
Q

What are first order kinetics?

A

The constant fraction of drug eliminated per unit of time

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36
Q

In first order-kinetics, half life is constant/variable?

A

Constant

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37
Q

In first-order kinetics, half life is concentration dependent/independent

A

Concentration independent

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38
Q

What are zero order kinetics?

A

The constant amount of drug eliminated per unit of time

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39
Q

In zero-order kinetics, half life is constant/variable?

A

Variable

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40
Q

In zero-order kinetics, half life is concentration dependent/independent?

A

Independent

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41
Q

Name drugs that undergo zero-order kinetics

A

Phenytoin
Warfarin
Alcohol

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42
Q

Name rate-limiting factors

A

Absorption
Distribution
Metabolism
Excretion

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43
Q

What is clearance (CL)?

A

Volume of plasma cleared of drug per unit time

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44
Q

What is the equation for clearance?

A

Rate of elimination/drug Cp

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45
Q

How do you determine clearance in IV dosing?

A

dose/AUC

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46
Q

How do you determine clearance in oral dosing?

A

bioavailability x dose/AUC

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47
Q

How do you determine clearance in with Vd and half life?

A

0.693 x Vd/half life

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48
Q

How do you calculate maintenance dose rate?

A

CL x Css

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49
Q

When is steady state reached with every single drug?

A

4-5 x t1/2

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50
Q

A drug with a Vd <15L is likely…?

A

Hydrophilic

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51
Q

A drug with a Vd >40L is likely…?

A

Lipophilic

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52
Q

Name reasons for polypharmacy

A

Multiple diseases
Combination therapy
Complementary therapy

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53
Q

What does terfenadine interact with and why was it withdrawn?

A

Macrolides
Grapefruit juice
-> fatal arrythmias

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54
Q

What is terfenadine?

A

An antihistamine

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55
Q

What does astemizole interact with and why was it withdrawn?

A

Macrolides
Grapefruit juice
-> fatal arrythmias

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56
Q

What is astemizole?

A

An antihistamine

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57
Q

What does mibefradil interact with and why was it withdrawn?

A

Beta blockers

-> cardiogenic shock

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58
Q

What is mibefradil?

A

Non-selective calcium channel blocker

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59
Q

What does it mean if a drug has a narrow therapeutic index?

A

Therapeutic effects is close to the adverse effect threshold

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60
Q

What factors make a drug most suceptible to drug interactions?

A

Narrow therapeutic index
High 1st pass metabolism
Single route of elimination

61
Q

Name the two types of drug interactions

A

Pharmacodynamic

Pharmacokinetic

62
Q

Name the kinds of pharmacodynamic interactions

A

Additive (sum of)
Synergistic (>sum of)
Antagonistic

63
Q

Give an example of additive/synergistic anticoagulants

A

Warfarin + aspirin

64
Q

Give an example of antagonistic drugs

A

Bronchodilator + antihypertensive

Flumazenil + benzodiazepine

65
Q

Why do bronchodilators and antihypertensives result in an antagonistic effect?

A 
Bronchodilator = beta adrenergic activation
Antihypertensive = beta adrenergic inhibition
66
Q

What is a substrate?

A

Competes for same binding site

67
Q

Name factors that affect drug absorption

A 
Drug solubility
Gut flora
Protein carriers
Gut pH
Gastric motility
Transporter function
68
Q

Give an example of how adsorption agents play a role in drug interaction

A

Activated charcoal -> reduced toxin levels

Tetracycline failure due to dairy/antacids (insoluble complex forms)

69
Q

Give an example of how gut flora plays a role in drug interaction

A

Macrolide antibiotics kill gut flora -> digoxin-induced toxicity (incr bioavailbility)

70
Q

Give an example of how gut pH plays a role in drug interaction

A

Antacids -> incr gut pH -> ketoconazole failure

71
Q

Comment on ionized vs unionized drugs crossing plasma membranes

A 
Ionized = struggles to cross plasma membrane
Uncharged = crosses plasma membrane easily
72
Q

Give an example of how gastric motility plays a role in drug interaction

A

Prokinetic -> metformin antidiabetic effect reduced

73
Q

What are p-gp transporters and why are they important in drug interactions?

A

P-glycoprotein transporters
Protective measure to efflux cytotoxins from intracellular compartment -> extracellular space/gastric lumen
Inducing leads to increased efflux and therapeutic failure
Blocking leads to higher accumulation and bioavailibility -> adverse effects

74
Q

Give an example of how blocking p-gp transporters plays a role in drug interaction

A

Macrolide antibiotics prevent p-gp efflux of digoxin -> digoxin toxicity

75
Q

Why are p-gp transporters important in cancer treatment?

A

Higher p-gp expression = higher cancer resistance

Block the p-gp -> higher anticancer activity

76
Q

Which plasma protein binds acidic and basic drugs?

77
Q

Which plasma protein binds only basic drugs?

A

Alpha-acid glycoprotein

78
Q

Comment on plasma-bound drugs

A

Pharmacologically inert
Cannot be filtered by kidney
Free fraction = bioactive and can be metabolised and removed

79
Q

Give an example of how plasma proteins play a role in drug interaction

A

Streptozocin induces hypoalbuminaema -> incr adverse effects of other drugs

Ibuprofen displaces methotrexate from albumin -> incr methotrexate toxicity

80
Q

What is phase I metabolism?

A

CYP450 monooxidase system prepares drugs for further chemical conversion

81
Q

What is phase II metabolism?

A

Inactivation of drug

Increases hydrophilicity

82
Q

Comment on how enzyme induction plays a role in drug interaction

A

Decr drug plasma concentrations -> treatment failure

Incr pro-drug conversion/toxic metabolite formation -> adverse effects

83
Q

Give an example of how enzyme induction plays a role in drug interaction

A

Macrolide antibiotics reduce OCP fficacy

84
Q

Comment on how enzyme inhibition plays a role in drug interaction

A

Higher plasma [ ] -> adverse effects

Decr active metabolites -> treatment failure

85
Q

Give an example of how enzyme inhibition plays a role in drug interaction

A

Grapefruit juice inhibits CYP3A4 metabolism -> incr diazepam toxicity

86
Q

Which organ is the main excretory organ?

87
Q

Which factors affect kidney excretion?

A

Urinary pH
Transporter competition
Renal blood flow
Active tubular secretion

88
Q

What is the affect of acidic urine on excretion?

A

Higher weak base excretion

89
Q

What is the affect of alkaline urine on excretion?

A

Higher weak acid excretion

90
Q

Give an example of how active tubular secretion plays a role in drug interaction

A

Probenecid excreted > penicillin -> incr penicillin [ ]

Ibuprofen excreted > methotrexate -> incr methorexate [ ]

91
Q

What is the mechanism of drug interaction due to fatty meals and what is the result?

A

Increased absorption of lipophilic drugs

Increased bioavailibility of griseofulvin

92
Q

Griseofulvin is lipophilic/lipophobic

A

Lipophilic

93
Q

What is the mechanism of drug interaction due to fibre-rich meals and what is the result?

A

Increased adsorption of drugs

Decreased bioavailbility of digoxin

94
Q

What is the mechanism of drug interaction due to pressor/tyramine-rich meals and what is the result?

A

Increased catecholamine release due to tyramine

Hypertensive crisis with selegiline

95
Q

What is the mechanism of drug interaction due to sodium-rich meals and what is the result?

A

Increased sodium [ ]

Increased absorption of lithium

96
Q

What is the mechanism of drug interaction due to potassium-rich meals and what is the result?

A

Increased potassium [ ]

Cardiac arrythmias w/ potassium sparing diuretics

97
Q

What is the result of an interaction with alcohol and hepatotoxins?

A

Increased hepatotoxicity of acetominophen

98
Q

What is the result of an interaction with alcohol and acetaldehyde dehydrogenase inhibitors?

A

Severe hangover effect with disulfarim

99
Q

What is the result of an interaction with alcohol and NSAIDs?

A

Increased mucosal damage with aspirin

100
Q

What is the result of an interaction with caffeine-rich drinks and anxiolytics?

A

Antagonism of diazepam therapeutic effects

101
Q

What is the result of an interaction with caffeine-rich drinks and stimulants?

A

Stimulant-toxicity with theophylline

102
Q

What is the result of an interaction with grapefruit juice and cyclosporine?

A

Decreased metabolism of cyclosporine (CYP3A4)

103
Q

What is warfarin?

A

A vitamin K epoxide reductase inhibitor

104
Q

What is the intended INR with warfarin use?

A

INR stable 2-4

105
Q

How is warfarin metabolised?

A

CYP450 metabolism esp CYP2C9

106
Q

What is the mechanism of interaction of warfarin with oral antibiotics and what is the result?

A

Inhibition of CYP2C9
Kills gut flora

Increased bleeding

107
Q

What is the mechanism of interaction of warfarin with NSAIDs and what is the result?

A

Additive/synergistic anticoagulant effect

Increased bleeding

108
Q

What is the mechanism of interaction of warfarin with antiplatelet drugs and what is the result?

A

Additive/synergistic anticoagulant effect

Increased bleeding

109
Q

What is the mechanism of interaction of warfarin with ginger/garlic and what is the result?

A

Additive/synergistic anticoagulant effect

Increased bleeding

110
Q

What is the mechanism of interaction of warfarin with vitamin K and what is the result?

A

Oversaturates the coagulation cascade

Treatment failure -> thromboses

111
Q

What is the mechanism of interaction of warfarin with St John’s wort and what is the result?

A

Induction of CYP3A4 and CYP2C19

Treatment failure -> thromboses

112
Q

What is the mechanism of interaction of macrolides with other drugs?

A

Potent CYP4A inhibitors

Gut flora destruction

113
Q

What is the mechanism of interaction of macrolides with digoxin and what is the result?

A

P-gp inhibition
Gut flora destruction

Digoxin toxicity

114
Q

What is the mechanism of interaction of macrolides with clozapine and what is the result

A

CYP3A4 inhibition

Seizures and disorientation

115
Q

What is the mechanism of interaction of macrolides with midazolam and what is the result

A

CYP3A4 inhibition

Increased hypnotic effect

116
Q

What is the mechanism of interaction of macrolides with theophylline and what is the result

A

CYP3A4 inhibition

Tremors and tachycardia

117
Q

What is the mechanism of interaction of macrolides with quinidine and what is the result

A

P-gp inhibition
CYP3A4 inhibition

Prolonged QT interval
Ventricular dysrhythmias

118
Q

How do MAO-I increase serotonin concentrations?

A

Reduce serotonin degradation

119
Q

What is the mechanism of interaction of monoamine oxidase inhibitors with SSRIs and what is the result

A

Increased serotonin levels

Serotonin syndrome

120
Q

What is the mechanism of interaction of monoamine oxidase inhibitors with TCAs and what is the result

A

Increased catecholamine levels

Hypertensive crises
Psychoses
Serotonin syndrome

121
Q

What is the mechanism of interaction of monoamine oxidase inhibitors with catecholamine releasers/reuptake inhibitors and what is the result

A

Increased catecholamine levels

Hypertensive crises
Psychoses
Serotonin syndrome

122
Q

What is the mechanism of interaction of monoamine oxidase inhibitors with local anaesthetics and what is the result

A

Increased blood pressure

Hypertensive crises

123
Q

What is the mechanism of interaction of monoamine oxidase inhibitors with tyramine-containing food and what is the result

A

Increased catecholamine release

Hypertensive crises

124
Q

Explain the interaction of tyramine with MOA-I

A

Tyramine in foods = catecholamine releasing agent -> noradrenaline release
Noradrenaline metbaolised by MOA
MOA-I -> incr noradrenaline -> advers effects eg incr blood pressure

125
Q

What tyramine intake is enough to interact with a MOA-I?

126
Q

What occurs in chronic tyramine intake with MOA-I?

A

Tyramine releases octopamine and noradrenaline -> less catecholamines -> less adverse effects

127
Q

How do NSAIDs work?

A

Inhibit COX -> decr prostaglandin synthesis

128
Q

What is the mechanism of interaction of NSAIDs with warfarin and what is the result

A

Increased anticoagulant effect

Increased bleeding

129
Q

What is the mechanism of interaction of NSAIDs with methotrexate and what is the result

A

Displaced methotrexate from albumin + decrease renal clearance

Methotrexate toxicity

130
Q

What is the mechanism of interaction of NSAIDs with digoxin and what is the result

A

Reduced renal clearance

Digoxin toxicity

131
Q

What is the mechanism of interaction of NSAIDs with lithium and what is the result

A

Reduced renal clearance

Tremors and seizures

132
Q

What is the mechanism of interaction of NSAIDs with ACE-I and what is the result

A

Inhibition of prostaglandin-mediated vasodilation

Treatment failure: hypertension

133
Q

What is the mechanism of interaction of NSAIDs with diuretics and what is the result

A

Salt and water retention

Treatment failure: hypertension

134
Q

What is the mechanism of interaction of grapefruit juice with amiodarone and what is the result

A

CYP3A4 inhibition and reduced mRNA expression

Arrythmias

135
Q

What is the mechanism of interaction of grapefruit juice with cyclosporine and what is the result

A

CYP3A4 inhibition and reduced mRNA expression

Immunosuppression

136
Q

What is the mechanism of interaction of grapefruit juice with diazepam and what is the result

A

CYP3A4 inhibition and reduced mRNA expression

Increased sedation

137
Q

What is the mechanism of interaction of grapefruit juice with quitapine and what is the result

A

CYP3A4 inhibition and reduced mRNA expression

Hallucinations
Hypotension

138
Q

What is the mechanism of interaction of grapefruit juice with loperamide and what is the result

A

CYP3A4 inhibition and reduced mRNA expression

Severe GI pain

139
Q

What is the mechanism of interaction of grapefruit juice with oxycodone and what is the result

A

CYP3A4 inhibition and reduced mRNA expression

Bradycardia
Hallucinations

140
Q

How does grapefruit juice work?

A

Potent CYP3A4 inhibitor

141
Q

How does St John’s wort work?

A

CYP450 inducer

142
Q

What is St John’s wort used for?

A

Hypericum perforatum preparation -> anxiety and depression

143
Q

What is the mechanism of interaction of St John’s wort with warfarin and what is the result

A

Induction of CYP3A4 and CYP2C19

Treatment failure: increased coagulation

144
Q

What is the mechanism of interaction of St John’s wort with cyclosporine and what is the result

A

Induction of CYP3A4 and CYP2C19

Treatment failure: organ rejection

145
Q

What is the mechanism of interaction of St John’s wort with contraceptives and what is the result

A

Induction of CYP3A4 and CYP2C19

Treatment failure: failed contraception

146
Q

What is the mechanism of interaction of St John’s wort with ARVs and what is the result

A

Induction of CYP3A4 and CYP2C19

Treatment failure: viral replication

147
Q

What is the mechanism of interaction of St John’s wort with SSRIs and what is the result

A

Increased plasma serotonin levels

Serotonin syndrome

148
Q

What is the mechanism of interaction of St John’s wort with aminolevulinic acid and what is the result

A

Increased photosensitvity

Skin irritation

Pharmacology (32 decks)

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