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Pharmacokinetics Flashcards

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1
Q

Define pharmacokinetics

A

Time course and disposition of drugs in the body (what the body does to the drug)

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2
Q

Processes of Pharmacokinetics?

A

Absorption
Distribution
Metabolism
Elimination

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3
Q

What influences a drugs absorption?

A

Form of drug
Rate of blood flow to site of administration
Solubility of drug (pH of drug, size of particles, pKA of drug - pH at which precisely half of drug is in its ionized form)
Route of administration

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4
Q

Negatives of oral administration of medication

A

Variable plasma concentration

Absorption may be erratic and subject to metabolism by liver and gut mocsa

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5
Q

What is first-pass effect?

A

Where a drug is metabolised by liver and gut mucosa

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6
Q

Mechanism of absorption of drugs from GI tract?

A

Active transport
Passive diffusion (most common)
Pore filtration

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7
Q

Factors influencing absorption of drugs from GI Tract?

A 
Intestinal motility
Gastric emptying
Gastric and intestinal pH
Intestinal microflora
Area available for absorportion
Integrity of blood flow
Presence/absence of food
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8
Q

What causes lower bioavailability or oral drugs?

A

Lack of absorption from GI tract

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9
Q

Affect of food on first–rate metabolism?

A

Delays gastric emptying

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10
Q

Which drugs can lead to delayed gastric emptying?

A

Those with anticholinergic effects - TCAs, opiates etc

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11
Q

Effect of grapefruit juice on drug absorptino

A

Grapefruit juice inhibits O-glycoprotein which increases absorption of certain medication, but downregulating intestinal CYP3A4 and CYP1A2.

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12
Q

Which drugs does grapefruit increases drug oral bioavailability?

A 
High first pass metabolism:
Calcium antagonists felodipine and Nimodipine
Terfenadine
Carbamazepine
Triazolam
Midazolam/diazepam
Simvastatin
Methyrlprednisolone
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13
Q

Where does most absorption of oral medication take place and why?

A

Small intestine - less acidic
Large surface area
long transit time

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14
Q

Where are slow or sustained release drugs mainly absorbed if taking orally?

A

Large bowel

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15
Q

Effect of enteric coating of capsules ?

A

Slow rate of disintegration so prolong effects of drug, reduce peak plasma concentration and thereby reduce SE.

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16
Q

Which type of oral preparation of drugs are absorbed quicker?

A

Liquid as disintegration is not required.

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17
Q

What is dissolution rate of oral medication dependent on?

A

Size of drug particle
Solubility of drug
Properties of intestinal fluid e.g. pH

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18
Q

When does absorption occur with IM medication?

A

10-30 minutes

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19
Q

Does first-pass metabolism occur with IM medication?

A

Rarely

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20
Q

What affects absorption of IM medications?

A

Blood flow
Aqueous solubility
Lipid soluble are absorbed quicker.
Low molecular weight are absorbed faster.

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21
Q

Which route results is the most rapid method of absorption?

A

IV

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22
Q

Which route is quickest for achieving therapeutic concentration?

A

IV

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23
Q

Bioavailability and first-pass metabolism of IV medications?

A

No first-pass metabolism

100% bioavailability

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24
Q

Which route has highest risk of life-threatening SE?

A

IV

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25
Q

Define permeation of a drug?

A

Lipid membrane permeability of drug molecule

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26
Q

Which type of drugs cannot cross lipid cell membrane?

A

Hydrophilic

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27
Q

Difficulty of lipophilic drugs?

A

Struggle to cross water layer in extracellular space

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28
Q

What factors affect permeation of a drug?

A

Lipid solubility

Concentration gradient

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29
Q

Which drug forms contribute to concentration gradient?

A

Free drug forms (i.e. not bound)

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30
Q

How can permeation take place?

A

Simple diffusion

Facilitated diffusion

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31
Q

What is simple diffusion?

A

Along concentration gradient w/o specific transport mechanism

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32
Q

What is active transport?

A

Transport against concentration gradient with ATP dependent energy expenditure

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33
Q

What form of a drug crosses the lipid membrane of a cell?

A

Non-ionized form

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34
Q

Which form of a drug is more water soluble; ionized or non?

A

Ionized

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35
Q

Consequence of ionized drug form being more water soluble?

A

Become trapped in glomerular filtrate and do not get reabsorbed. Therefore renal clearance is higher.

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36
Q

Which drug OD can be treated with alkalinization?

A

Aspirin

Barbituate

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37
Q

Acidification helps with elimination of which drug?

A

Amphetamines

Phencyclidine

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38
Q

What does distribution of a drug refer to?

A

Where in the body it can be found

Drug achieving equilibrium between different compartments

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39
Q

What factors influence drug distribution?

A 
Haemodynamic factors
Plasma protein binding
Permeability factors
Blood-brain barrier
Blood-CSF barrier
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40
Q

How do haeodynamic factors affect drug distribution?

A

Organs with high blood perfusion receive highest distribution and redistribution seen in second distribution phase to tissues.

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41
Q

Which organs have high blood perfusion?

A

Brain
Kidneys
Liver

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42
Q

Which route of administration leads to fastest distribution of a drug?

A

IV

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43
Q

Are bound or unbound parts of a drug the active part?

A

Unbound (unbound fraction)

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44
Q

What type of binding is plasma protein binding to drugs?

A

Reversible i.e. not covalent

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45
Q

When does protein binding of drugs become clinically relevant?

A

In renal disease where proteinuria can occur, i.e. less protein for drugs to be bound, thereby higher concentration of active drug form.

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46
Q

Which plasma protein do acidic drugs mostly bind to?

A

Albumin

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47
Q

Which plasma protein do alkaline drugs mostly bind to?

A

Alpha1-acid glycoprotein

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48
Q

Which plasma protein do psychotropic drugs mainly bind to?

A

Most are basic, so alpha1acid glycoprotein and lipoproteins

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49
Q

What is the equation for volume distributino?

A

Vd =Q/Cp
Vd = volume distribution
Q = quantity of drug
Cp = plasma concentration at time of administration (zero time)

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50
Q

What does volume distribution refer to?

A

Apparent volume in which ingested drug is distributed in body.

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51
Q

What does a high volume distribution of a drug suggest?

A

Drug has high affinity for tissues outside body water such as brain and fat.

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52
Q

What does low Volume distribution suggest?

A

Drug is concentrated in blood

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53
Q

Plasma concentration of drug if drug is highly protein bound?

A

High (plasma protein exists in plasma)

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54
Q

What factors affect distribution of drug to the brain?

A

Brains regional blood flow
Blood-brain barrier
Drug’s affinity for receptors in brain

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55
Q

Composition of blood-brain barrier

A

Capillary endothelium of brain which contains tight junctions acting as a membrane/singe sheet.

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56
Q

What molecules does blood brain barrier prevent?

A

Proteins
Immunoglobulins
Bacteria
Viruses

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57
Q

Factors that can affect permeability of blood brain barrier?

A 
Fever
HI
Hypoxia
Hypercapnia
Retrovirusis
inflammation
HTN
Vasculitis
Cerebral irradiation
Ageing
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58
Q

How can you measure the integrity of the blood-brain barrier?

A

Measuring leakiness to labelled IgG olecules or gadonium

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59
Q

What types of molecules can easily pass the blood-brain barrier?

A

Unionized
Less protein bound
High lipid-water partition coefficient

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60
Q

Reason behind circumventricular organs?

A

Survival benefit as certain toxic substances stimulate postrema area and induce vomiting

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61
Q

Where is the blood-CSF barrier?

A

Choroid plexus

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62
Q

Structure of blood-CSF barrier?

A

Tight junctions between adjacent epithelial cells (as opposed to adjacent in blood brain barrier)

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63
Q

What is bioavailability?

A

How much of an administered drug reaches its target
The extent to which drug reaches systemic circulation compared with same quantity of drug taken IV i.e. fraction that circumvents first pass effect

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64
Q

How to measure PO bioavailability?

A

Plot plasma concentration against time for a given dose

Area under curve is proportional to amount of drug in plasma

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65
Q

How to measure bioavailability fraction between PO and IV medication

A

Plot plasma conc against time for a given dose for PO drug.

Divide area under curve for PO medication with area under curve for IV at same dose.

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66
Q

What determines bioavailability fraction?

A

Absorption
Distribution
Elimination

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67
Q

What is presystemic metabolism?

A

Reduction in amount of medication reaching systemic circulation due to absorption and first-pass metabolism

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68
Q

Where does first-pass metabolism occur?

A

Gut mucosa
Liver
Muscle tissue

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69
Q

What can reduce first pass metabolism?

A

Hepatic impairment

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70
Q

What is bioequivalence?

A

Measurement of comparability of plasma levels of two different formulations of same active compound when given at same dose and same route of administration.

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71
Q

When are two products said to be bioequivalent?

A

When graphical trace of heir plasma level plot against time are superimposible.

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72
Q

When is bioequivalence relevant?

A

When changing brands of same compound.

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73
Q

What is Xenobiotics?

A

Mechanism by which a foreign agent (such as drug molecule) is metabolized and eliminated from body.

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74
Q

What does metabolism/biotransformation do to the drug?

A

Renders it less lipid-soluble and more water-soluble.

Therefore more readily eliminated

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75
Q

Principle site of metabolism in body?

A

Liver

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76
Q

Where can metabolism of drugs occur?

A 
Liver
GI
Plasma
Lungs
Kidneys
Suprarenal cortex
Placenta
Skin
Lymphocytes
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77
Q

Main metabolic routes?

A

Oxidation
Reduction
Hydrolysis
Conjugation

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78
Q

What happens in phase 1 of drug metabolism?

A

Oxidation, reduction and hydrolysis, making molecule suitable for phase 2.

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79
Q

What happens in phase 2 of drug metabolism?

A

Conjugation reactions such as gluronidation resulting in polar compounds (mainly inactive) that are exrectable in bile or urine are formed.

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80
Q

What is needed for molecule to be renally excreted?

A

Relative molecular mass >300

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81
Q

How is a molecule excreted if its relative molecular mass is <300?

A

Excretion via bile

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82
Q

What enzymes are most psychotropic drugs oxidized by?

A

Hepatic cytochrome CYP-450

CYP3A4

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83
Q

What are CYP enzymes responsible for?

A

Inactivation for most psychotherapeutic drugs

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84
Q

Where do CYP enzymes mainly act?

A

Endoplasmic reticulum of hepatocytes and cells of intestines.

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85
Q

How can drug interactions influence the CYP system?

A

Induction
Non-competitive inhibition
Competitive inhibitino

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86
Q

How many caucasians lack the CYP2D6 enzyme?

A

5-10%

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87
Q

% of East Asians who lack CYP2C19 enzyme?

A

15-20%

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88
Q

Which drugs inhibit CYP system?

A

SSRIs - particularly fluoxetine.

Carbamazepine

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89
Q

Which drug an increase clozapine levels by x0?

A

Fluvoxamine, which can induce seizures

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90
Q

Effect of Fluoxetine on other drugs

A

Fluoxetine increases TCAs via 2D6 and 219.

Fluoxetine increases clozapine plasma conc.

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91
Q

Effect of Carbamazepine on other drugs

A

Decreases plasma conc of COCp

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92
Q

Affect of antidepressants on warfarin?

A

Antidepressants can inhibit metabolism of warfarin leading to bleeding.

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93
Q

Which antipsychotic and antidepressant compete with each other for same metabolic enzymes?

A

TCAs and Haloperidol

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94
Q

Which two medications induce their own metabolism?

A

Carbamazepine and phenobarbitone

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95
Q

Non-medical CYP inducers?

A

Brussel sprouts
EtOH
Smoking

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96
Q

Non-medication CYP inhibitors?

A

Grapefruit juice

Caffeine

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97
Q

Psychotropics metabolized by CYP2D6?

A 
All TCAs
Fluoxetine
Paroxetine
Trazadone
Nefazodone
Valproate
All neuroleptics
Risperidone
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98
Q

What psychotropics inhibit CYP2D6

A 
Paroxetine
Fluoxetine
Neuroleptics
Amitriptyline
Clomipramine
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99
Q

Which CYP enzyme is most prominent in gut wall mucosa?

A

CYP3A4

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100
Q

Which psychotropics are metabolized by CYP3A4?

A 
Clomipramine
Fluvoxamine
Mirtazapine
Nefazodone
Carbamazepine
Most benzos
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101
Q

What stimulates CYP3A4?

A

Carbamazepine

Barbituates

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102
Q

What inhibits CYP3A4?

A

Ca channel blockers
Fluoxetine
Nefazodone

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103
Q

Describe autoinduction in Carbamazepine

A

Carbamazepine is metabolized by hepatic CYP2D6, which in turn induces carbamazapines.

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104
Q

Impact of autoinduction on Carbamazapine

A

Rate of metabolism of carbazapine (and other P450 substrates) increases over first several weeks of treatment.
This can delay final steady state until 3-4 weeks after initiation.
Hence level must be monitored and dose often raised during early phase of treatment.

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105
Q

Which enzyme is affected by smoking and caffeine?

A

They affect glucoronidation reaction via UGT enzyme and CYP1A2.

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106
Q

Which drugs are metabolised by CYP1A2 and thereby affected by smoking and caffeine?

A

Clozapine

Olanzapine

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107
Q

Effect of caffeine on CYP1A2

A

Competitive inhibition

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108
Q

Effect of caffeine on clozapine and olanzapine

A

Increases levels

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109
Q

Effect of smoking on CYP1A2

A

Polyaromatic hydrocarbons in cigarrettes induce the enzyme.

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110
Q

Which effects are seen sooner of CYP1A2; inducers or inhibitors?

A

Inhibitors (caffeine)

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111
Q

Major routes of drug excretion

A 
Urine
Faeces
Bile
Sweat
Tears
Saliva
Sebum
Breast milk
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112
Q

Most suited compounds for renal excretion?

A

Ionized

Non-lipid soluble

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113
Q

Factors that influence drug excretion?

A 
Increased age = decreased excretion
Reduction in renal blood flow
Renal impairment
Alterations in re-absorption: urine pH
Low Na
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114
Q

What is pH of normal urine?

A

Weakly acidic

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115
Q

Affect of Low Na Urine on Lithium?

A

Increases lithium reabsorption and decreases excretion, leading to toxicity

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116
Q

What is clearance?

A

Volume of blood cleared of a particular drug in unit time

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117
Q

What is clearance directly proportional to?

A

Volume of distribtuion

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118
Q

What is the equation for clearance?

A

Cl=kxVd
Cl = clearance
k = constant of proportionality (first order elimination constant)

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119
Q

Relationship between clearance and drugs with first order kinetics?

A

Clearance is constant irrespective of dose as rate of elimination is directly proportional to plasma level

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120
Q

Which drugs have renal elimination?

A 
Lithium
Amisulpride
Sulpride
Gabapentin
Acamprosate
Amantadine
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121
Q

What is the half-life of a drug?

A

Time taken for plasma concentration of a drug to have = t1/2

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122
Q

What is the distribution half-life?

A

Following IV injection, rapid fall in plasma drug conc caused by redistribution of drug into tissues.
Distribution half life = time taken for this redistribution to halve the inital peak conc.

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123
Q

What is the elimination half life?

A

Time taken for elimination process to halve plasma drug conc

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124
Q

What type of elimination can drugs undergo?

A

First order kinetics

Zero order kinetics

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125
Q

What is first order kinetics?

A

When constant fraction of drug is cleared per unit time

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126
Q

Affect of first order kinetics on dose of drugs and its subsequent clearance?

A

When amount of drug in plasma/dose administered increases, clearance proportionally increases.

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127
Q

What would a graph of first-order kinetics look like?

A

Exponential decay versus time.

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128
Q

What is the elimination half life in first order kinetics?

A

Time to eliminate 50% of a given amount, or time to achieve a decrease in plasma level to 50% of original

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129
Q

In first order kinetics, what does rate of elimination depend on?

A

Drug concentration

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130
Q

What is zero-order kinetics?

A

Constant amount of drug is cleared per unit time, irrespective of amount of drug in plasma concernation/dose.

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131
Q

Danger of zero-order kinetics?

A

Increasing dose may result in toxicity.

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132
Q

What does rate of elimination depend on in zero-order kinetics?

A

Availability of enzymes, slow release formula etc

NOT dose of drug

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133
Q

What is a steady state?

A

When rate of drug going in = rate of drug going out. Fluctuations in plasma level do not get eliminated.

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134
Q

How long does it take for a drug to reach steady plasma level?

A

4-5 t1/2

Dependent on elimination t1/2 of drug.

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135
Q

What does steady state depend on?

A

Dose administered

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136
Q

What can help reach steady state more rapidly?

A

Loading dose

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137
Q

What is a quantal curve?

A

Dose-response curve:
Plots the percentage of a population showing a specified, pre-defined categorical drug effect against dose administered.
Plots drug conc against continuous effects of the drug.

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138
Q

What can be determined from a quantal curve?

A

Median effective dose or median toxic dose.

Therapeutic index

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139
Q

What is the median toxic dose?

A

Dose at which 50% of patients experience a specific toxic effect

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140
Q

What is the median effective dose?

A

Dose at which 50% of patients have a specified therapeutic effect.

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141
Q

What does a steep drug-response curve suggest?

A

Little variability

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142
Q

Which type of curve in a quantal curve plot suggests great variability in patient sensitivity to the effects of a drug?

A

Flat curve

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143
Q

What is the therapeutic index?

A

Relative measure of toxicity or safety of a drug.
Defined as the ratio of the median toxic dose to median effective dose.
Or: ratio of minimum plasma conc causing toxic effects to that causing a therapeutic effect.

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144
Q

What is therapeutic index only useful for?

A

Dose-dependent side effects

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145
Q

What is the therapeutic window?

A

A specified plasma conc value, only within which certain drugs appear to have therapeutic efficacy.

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146
Q

What happens to the elderly in terms of body composition?

A

Increase in total body fat.
Decrease in total muscle mass.
Decrease in total body water.

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147
Q

Effect of changes in body composition in the elderly on drugs?

A

Larger volume of distribution and longer half-life of lipophilic chemicals because of their increased sequestration in fat. e.g. benzo excretion is slower in the elderly.

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148
Q

What happens to plasma proteins in the elderly?

A

Decreased plasma protein binding capacity

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149
Q

Effect of decreased plasma protein binding efficacy in the elderly on dugs?

A

Higher proteinuria
Reduced plasma protein synthesis by liver - reduced albumin, protein affinity decreased, acid glycoprotein increased.
Higher free drug plasma conc - increased metabolism and clearance of free drug.
More frequent protein binding interactions.
Phenytoin is affected.

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150
Q

Effect of ageing on the liver?

A

Decreased hepatic blood flow.

No change in metabolism.

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151
Q

Impact of liver changes in the elderly on drug kinetics?

A

> 80 y/o, CYP system declines.
Decreased hepatic first pass effect.
Lorazepam>Diazepam in elderly.

152
Q

Effect of ageing on the kidneys?

A

Decreased in renal blood flow - 10% per decade after 4th decade.
Reduced eGFR.

153
Q

Impact of kidney changes in the elderly on drug kinetics?

A

Frequent toxicity of renally eliminated drugs.

154
Q

Impact of age on the GI tract?

A

GI blood flow decreases.

Gastic pH increases as acidity drops.

155
Q

Impact of age-related changes in GI tract on drug kinetics?

A

Decreased gastric first pass metabolism.

Reduction in gastric wall content of dopa decarboxylase = 3-fold increase in conc of levodopa in elderly.

156
Q

Impact of age on the brain?

A

Decreased number of brain Ach postsynaptic receptors.
Choline acetyltransferase is diminished.
Level of brain Acetylcholinestrase decreased.

157
Q

Impact of age-related changes in the brain on drug kinetics?

A

Anticholinergic SEs are more pronounced = increased delirium.

158
Q

Changes in neonates body composition?

A

Higher proportion of total body water and extracellular body water
Lower proportion of adipose tissue

159
Q

Changes in neonates renal function?

A

eGFR is lower in those <3-5 months old

160
Q

GI changes in neonates?

A

Lower gastric acidity

Increased gastric emptying time

161
Q

Brain changes in neonates?

A

More permeable blood-brain barrier

162
Q

Liver changes in neonates?

A

Microsomal enzyme activity in liver is lower in those <2 months old
Lower plasma conc of albumin in neonates

163
Q

Affect of pregnancy on GI tract?

A

Delayed gastric emptying

Decreased GIT motility

164
Q

Affect of pregnancy on body composition?

A

5% increased volume of distribution

Decreased drug-binding capacity

165
Q

Affect of pregnancy on the kidneys?

A

Increased renal clearance & eGFR

166
Q

Affect of pregnancy on the liver?

A

Decreased albumin level

Induced liver metabolic pathway

167
Q

Affect of reduced renal function on diazepam?

A

Half-life unchanged

Metabolite, desmethyldiazepam may accumulate, causing excessive sedation.

168
Q

Affect of reduced renal function on lorazepam?

A

Half life increased from 8-25 hours to 32-72 hours

Dose should be reduced by 50% to avoid excessive sedation

169
Q

Affect of reduced renal function for SSRIs?

A

Citalopram: half normal dose
Paroxetine: reduce dose
Sertraline: do not use in renal impairment
Fluoxetine: continue normal dose

170
Q

Affect of renal impairment in Amisulpride dose?

A

This is renally excreted, and is therefore contra-indicated.

171
Q

Affect of renal impairment on Risperidone?

A

Risperidone and its active metabole are excreted in urine so renal impairment leads to prolonged elimination half-life

172
Q

How long does it take for TCAs to reach peak plasma conc?

A

1-12hours

173
Q

Why are 7-9% of caucasians slow metabolisers of TCAs?

A

CYP2D6 polymorphism

174
Q

Affect of clearance of TCAs in kids and the elderly?

A

Children: clear more TCAs from body
Elderly: less

175
Q

Half-life of TCAs?

A

Close to 24h

176
Q

Can TCAs cross blood-brain barrier?

A

Yes

177
Q

Binding of TCAs on plasma proteins?

A

Significant - 80-95%

178
Q

What is measured to assess therapeutic dosing of TCAs?

A 
Plasma levels (not serum).
Determined after 5-7days when steady state is reached, and 8-12 hours after last dose to avoid false peaks.
179
Q

When is clear therapeutic window seen for nortriptyline?

A

Between 50-150 ng/ml

180
Q

Active metabolite for Imipramine?

A

Desipramine

181
Q

Active metabolite for Amitriptyline?

A

Notriptyline

182
Q

Active metabolite for Trazadone and Nefazodone?

A

mCPP

183
Q

Active metabolite for Fluoxetine?

A

Norfluoxetine

184
Q

Active metabolite for Sertraline?

A

Desmethylsertraline

185
Q

Which psych medications decrease metabolism of morphine and thereby contribute to opioid toxicity?

A

Amitriptyline
Clomipramine
Through UDP glucuronyl transferase interaction

186
Q

What induces metabolism of TCA and thereby reduces its levels?

A 
Smoking
Phenytoin
Carbamazepine
OC pills
Barbituates
187
Q

Impact of smoking on TCAs?

A

Induces metabolism, thereby reducing TCA levels.

188
Q

Impact of phenothiazines on TCA levels?

A

Mutual inhibition of metabolism, thereby increases both TCA and antipsychotic levels

189
Q

What drugs inhibit TCA metabolism and thereby increase TCA plasma levels?

A 
Quinidine
Cimetidine
Fluoxetine
Paroxetine
Phenothiazine
Disulfiram
Methylphenidate
190
Q

Affect of TCA on warfarin?

A

TCAs increase warfarin levels = increased risk of bleeding

191
Q

Affect of TCAs on Clonidine?

A

TCAs reduce clonidine levels, thereby can lead to hypertensive crises

192
Q

Affect of TCAs on MAOIs?

A

Reduce tyramine entry via monoamine reuptake channels.
Synergistic serotonergic enhanceent (esp clomipramine).
Thereby higher risk of seretonin syndrome and lower risk of cheese reaction.

193
Q

Affect of TCAs on L-Dopa?

A

Reduce absorption of L-dopa, thereby lower l-dopa efficacy in Parkinsons

194
Q

Affect of TCAs on morphine?

A

Amitroptyline and clomipramine decrease metabolism of morphine through UDP glucuronyl transferase interaction, thereby increase opioid toxicity

195
Q

Impact of food on sertraline?

A

Sertraline availability increased by presence of food

196
Q

Protein binding ability of SSRIs?

A

Most are highly protein bound except for escitalopram (56% bound)

197
Q

What metabolizes fluoxetine?

A

Norfluoxetine - similar activity on 5-HT reuptake as fluoxetine.

198
Q

Half-life of fluoxetine?

A

4-6 days

199
Q

Half-life of norfluoxetine?

A

4-16 days

200
Q

Active metabolites of fluvoxamine and paroxetine?

A

None

201
Q

Pharmacokinetics of Fluoxetine and paroxetine?

A

Nonlinear; changes in dose can produce proportionally large plasma levels. This is because they can both inhibit their own clearance at clinically relevant doses.

202
Q

Which SSRI is most selective?

A

Citalopram

203
Q

Which SSRI is most potent?

A

Paroxetine

204
Q

How does Fluoxetine work?

A

Weakly inhibits noradrenaline reuptake and binds to 5-HT2C receptors.

205
Q

How does sertraline work?

A

Weakly inhibits noradrenaline and dopamine reuptake.

206
Q

Impact of high dosage of Paroxetine?

A

Significant anticholinergic activity - binds to nitric oxide synthase.

207
Q

Impact of fluoxetine and olanzapine taken together?

A

Increase brain concentrations of noradrenaline.

208
Q

Which disorders respond to SSRIs?

A 
Depression
GAD
Panic disorder
OCD
Bulimia
PMD - if sertraline/paroxetine produces positive effect.
209
Q

What can fluvoxamine reduce clearance of?

A

Diazepam and its active metabolite, N-desmethyl diazepam, thus can cause accumulation.

210
Q

What metabolises citalopram?

A

CYP2C19, and then CYP2D6.

211
Q

What metabolizes sertraline?

A

Demethylation by CYP3A3 and CYP3A4

212
Q

Enzyme profile of Fluoxetine

A

Inhibits 2C19, 3D6.

Partially metabolized by 2D6

213
Q

What does Fluoxetine interact with?

A 
Increases:
All TCAs - particularly Clomipramine and Imipramine (both 2C19 and 2D6).
Citalopram
Sertraline
Moclobemide
Duloxetine
Mirtazapine
Velafaxine
214
Q

Enzyme profile of Paroxetine?

A

Metabolized by 2D6

Inhibits 2D6

215
Q

Which drugs does Paroxetine increase?

A 
All TCAs
Citalopram
Fluoxetine
Fluvoxamine
Duloxetine
Mirtazapine
Venlafaxine
216
Q

Enzyme profile of Fluvoxamine

A

Inhibits 1A2, 2C19, 3A4

217
Q

Which drugs does Fluvoxamine increase?

A 
Clomipramine
Doxepine
Trimipramine
Duloxetine
Mirtazapine
Citaloprame
Escitaloprame
Sertraline
Trazadone
218
Q

Enzyme profile of Duloxetine?

A

Inhibits 2D6

219
Q

Which drugs does Duloxetine increase?

A 
All TCAs
Citalopram
Fluoxetine
Paroxetine
Fluvoxamine
Mirtazapine
Venlafaxine
220
Q

Enzyme profile of Desipramine and Clomipramine?

A

Inhibits 2D6

221
Q

Which drugs do Desipramine and Clomipramine increase?

A 
All TCAs
Citalopram
Fluoxetine
Fluvoxamine
Duloxetine
Mirtazapine
Venlafaxine
222
Q

Which drugs lead to potential serotonin toxicity?

A

Desipramine

Clomipramine

223
Q

What causes nonlinear pharmacokinetics of paroxetine and fluoxetine?

A

Autoinhibition of CYP2D6

224
Q

Effect of Fluvoxamine on Theophylline?

A

Reduces clearance 3-fold via CYP1A2 inhibition.

225
Q

What do you need do if prescribing theophylline with fluvoxamine?

A

Theophylline dose reduced by 1/3.

Monitor plasma conc of theophylline.

226
Q

Plasma elimination half-life of Paroxetine for single dose?

A

10h

227
Q

Plasma elimination half-lifeof Paroxetine for multiple doses?

A

21h

228
Q

Pharmacokinetics of Paroxetine?

A

Nonlinear

229
Q

Plasma elimination half-life of single dose of Fluvoxamine?

A

11h

230
Q

Plasma elimination half-life of multiple dose of Fluvoxamine?

A

14h

231
Q

Pharmacokinetics of Fluvoxamine?

A

Nonlinear

232
Q

Plasma elimination half-life of Sertraline (single dose)?

A

26h

233
Q

Pharmacokinetics of Sertraline?

A

Linear

234
Q

Plasma elimination half-life of single dose of Citalopram?

A

33h

235
Q

Pharmacokinetics of Citalopram?

A

Linear

236
Q

Pharmaco-kinetics of single dose of Fluoxetine?

A

Nonlinear

237
Q

Plasma elimination of half-life of single dose of FLuxoetine?

A

1.9 days

238
Q

Plasma elimination half-life of multiple doses of Fluoxetine?

A

5.6 days (7-15 days)

239
Q

Impact of Fluvoxamine on Warfarin?

A

Warfarin plasma conc increases by 98% and prothrombin time is prolonged.

240
Q

What is the advice regarding starting medications that interact irreversibly with MAOIs?

A

Wait 2 weeks before starting

241
Q

Affect of prescribing MAOIs and Pethidine?

A

Depressive (pronounced sedation due to opioid toxicity)

Excitatory (serotonin excess)

242
Q

Symptoms of serotonin excess?

A 
Agitation
Hyperpyrexia
Cardiovascular collapse
Coma
Death
243
Q

Important characteristics of Pethidine?

A

Serotonin releasing property

Reuptake inhibitino property

244
Q

Which drug must never be used with MAOIs?

A

Pethidine

245
Q

Impact of Amphetamine and Methylphenidate?

A

Amphetamine induces serotonin release

Methylphenidate does not

246
Q

Protein binding of Venlafaaxine?

A

Low protein binding

247
Q

Half life of Vanlafaxine?

A

3.5 ours

248
Q

What is the metabolite of Venlafaxine?

A

O-desmethyl venlafaxine

249
Q

Half-life of metabolite of venlafaxine?

A

9 hours

250
Q

What metabolises the metabolite of venlafaxine?

A

P450 CYP 2D6

251
Q

Half-life of Duloxetine?

A

12 hours

252
Q

What metabolizes Duloxetine?

A

CYP450 (hepatic)

253
Q

Protein binding of Duloxetine?

A

Highly protein bound

254
Q

Metabolism of Trazadone and Nefazodone?

A

Extensive hepatic metabolism

255
Q

Metabolite of Trazadone and Nefazadone?

A

M-chlorophenylpiparazine; stimulates 5-HT receptors

256
Q

Half-life of Trazadone?

A

5-9 hours

257
Q

Affect of Trazadone on receptors?

A

Weak inhibitor of serotonin reuptake

Antagonist of serotonin 5-HT2A and 5HT2C

258
Q

Active metabolite of Trazadone?

A

M-chlorophenylpiperazine - 5-HT2C agonist

259
Q

Half-life of active metabolite of Trazadone?

A

14 hours

260
Q

Clinical impact of Trazadone metabolite?

A

Migraine
Anxiety
Weight loss

261
Q

Sedation affects of Trazadone?

A

Acute sedative effects

262
Q

Impact of Trazadone on other drugs?

A

Increase levels of digoxin, phenytoin and warfarin

263
Q

What results in increased SE of trazadone?

A

CYP3A4 inhibitors can increase the metabolite but reducing its breakdown

264
Q

Half life of buspirone?

A

2-11 hours

265
Q

Metabolite of Buspirone?

A

1-pyrimidinylpiperazine

266
Q

DIfference between Buspirone and its metabolite?

A

Metabolite achieves higher brain conc in brain

267
Q

Receptor action of Buspirone?

A

Partial agonist on 5-HT1A receptors - presynaptic agonism leads to inhibition of release of serotonin with consequent anti-anxiety effects.
Postsynaptic agonism leads to antidepressant acitivity.

268
Q

How does Buspirone lead to antidepressant acitivity?

A

Postsynaptic agonism of 5HT-1A receptors.

269
Q

Action of St johns wort?

A

CYP inducer

270
Q

Which receptors does st johns worst act on?

A

Multiple monoamine ruptake inhibition

271
Q

Which drugs does St Johns Worst decrease efficacy of?

A

Warfarin
OCPs
Anti-epileptics

272
Q

What does non-response mean for antidepressants?

A

Minimal or <25% decrease in baseline severity of sx

273
Q

What does partial response mean for antidepressants?

A

25-50% reduction in baseline severity

274
Q

What does partial remission mean for antidepressant use?

A

> 50% reduction but still some sx evident

275
Q

What does remission mean in antidepressant use?

A

No sx; returning to normal function (<6 months from last episode)

276
Q

What does relapse mean in antidepressant function?

A

Return to fully sx state when in remission

277
Q

What does recovery mean in antidepressant use?

A

Extended remission sustained for longer than 6-12 months

278
Q

What does recurrence mean in antidepressant use?

A

Onset of new episode of depression when in recovery

279
Q

When does Mirtazapine reach peak plasma conc?

A

Within 2 hours

280
Q

Protein binding of Mirtazapine?

A

85% binds to plasma proteins

281
Q

Bioavailability of Mirtazapine?

A

50% due to first-pass metabolism

282
Q

Pharmacokinetics of Mirtazapine?

A

First-order linear elimination over dose of 15-80mg

283
Q

Elimination rate of Mirtazapine?

A

20-40 hours

284
Q

What mediates metabolism of Mirtazapine?

A

CYP2D6

CYP3A4

285
Q

What drugs can increase plasma conc of Mirtazapine?

A

Paroxetine and Fluoxetine - inhibit CYP system.

286
Q

What drug decreases Mirtazapine plasma conc>?

A

Carbamazepine - 60% decrease

287
Q

Meabolism of Agomelatine?

A

First-pass metabolism
CYP1A2 (90%)
CYP2C( (10%

288
Q

Bioavailability of Agomelatine?

A

Low

289
Q

Protein binding of aAgomelatine?

A

95%

290
Q

Haf-life of Agomelatine?

A

2.3 hours

291
Q

Are lithium carbonate and citrate the same?

A

No

292
Q

How long does it take for Lithium to reach a steady sate?

A

4-5 days

293
Q

Protein binding of Lithium?

A

Not protein bound

294
Q

Half-life of plasma Lithium?

A

18 years inititally, 1 year of chronic use increases this to 26 hours

295
Q

Where is lithium excreted?

A

Proximal tubules in kidney - where sodium is filtered

296
Q

Impact of loss of body sodium on lithium?

A

Increase lithium reabsorption as compensation in error - leads to toxicity

297
Q

What drugs can increase lithium?

A 
ACE inhibitors
Loop diuretics
Fluoxetine
NSAIDs
Thiazides
298
Q

What drugs can decrease lithium levels?

A 
Osmotic diuresis
Caffeine
Aminophylline
Theobromine, Theophylline
Carbonic anyhdrase inhibitors
299
Q

Which medications can cause lithium toxicity within normal levels?

A 
Carbamazepine
Atracurium
Haloperidol, clozapine
Calcium channel blockers
Metronidazole
300
Q

How does carabimazepine cause lithium toxicity?

A

Increased antithyroid effect and neurotoxicity

301
Q

How does Atracurium cause lithium toxicity?

A

Increased neuromuscular blockade

302
Q

How do haloperidol and clozapine cause lithium toxicity?

A

Increased neurotixic effects

303
Q

How do calcium channel blockers cause lithium toxicity?

A

Increased neurotoxicity

304
Q

How does metronidazole cause lithium toxicity?

A

Increased neurotoxicity

305
Q

What is Divalproex?

A

Semisodium compound of Valproate

306
Q

What is Divalproex made of?

A

Half valproic acid

Half sodium valproate

307
Q

Bioavailability of valproate?

A

Close to 100%

308
Q

Characteristics of valproate?

A

Hydrophilic

Low volume of distribution

309
Q

Half life of valproate?

A

9-16 hours

310
Q

Protein binding of valproate?

A

90%

311
Q

Characteristics of valproate at higher doses?

A

Increased free fraction may remain in plasma (rather than escaping to tissues) and thus be cleared by liver, leading to sublinear kinetics so that with highe rplasma conc, greater in creases in dose may be needed to yield desired increase in plasma levels.

312
Q

Impact of valproate on diazepam?

A

Binding interaction so that valproate can increase free diazepam

313
Q

Structure of carbamazepine?

A

Tricyclic structre

314
Q

Metabolism of Carbamazepine?

A

Hepatic

Induces its own breakdown

315
Q

Bioavailability of Carbamazapine?

A

80%

316
Q

Plasma protein binding of Carbamazapine?

A

75%

317
Q

Breakdown of Carbamazapine

A

Autoinduction of epoxide pathway via induction of CYP3A3/4

318
Q

Half life of carbamazapine before autoinduction?

A

24 hours

Clearance: 25ml/min

319
Q

Half life of Carbamazapine after autoinduction?

A

2-4 weeks into therapy:
half life is 8 hours
Clearance is 75ml/min

320
Q

Active metabolite of carbamazpine?

A

CBZ-10,11-epoxide

321
Q

Half-life of Carbamazpine metabolite?

A

6 hours

322
Q

What steady state plasma conc of Carbamazpine is therapeutic?

A

4-12 ng/ml

323
Q

What drugs can increase carbamazapine levels?

A

Verapamil
Diltiazem
Erythromycin can cause toxicity

324
Q

What drug levels does Carbamazapine decrease?

A

Nimodipine

Felodipine

325
Q

Affect of Valproate on Carbamazapine?

A

Valproate inhibits epoxide hydrolase, increasing plasma carbamazepine-epoxide levels without altering total plasma carbamazepine levels.
Displaces carbamazepine from plasma proteins, increasing free carbamazepine.

326
Q

Affect of carbamazepine on warfarin?

A

Reduces warfarin efficacy

327
Q

Mood stabilizing effects of Gabapentin?

A

None

328
Q

Which psych disorders is Gabapantin used in?

A

Anxiety

Bipolar

329
Q

Plasma protein binding of Gabapentin?

A

Not bound to plasma protein

330
Q

Where is gabapentin excreted?

A

100% in urine

331
Q

Half life of Gabapentin?

A

4-9 hours

332
Q

What can increase gabapentin clearance?

A

Increased physical activity

333
Q

Bioavailability of Gabapentin?

A

Decreases as dose increases

334
Q

Bioavailability of Gabapentin given at 900mg per day?

A

60%

335
Q

Bioavailability of Gabapentin when given at 2400mg per day?

A

34%

336
Q

Bioavailability of Gabapentin when given at 4800mg per day?

A

27%

337
Q

Affect of hepatic metabolism on Gabapentin?

A

None

338
Q

When is Gabapentin steady state reached?

A

1-2 days

339
Q

When does Lamotrigine reach peak conc?

A

Within 3 hours postdose

340
Q

Oral availability of Lamotrigine?

A

98%

341
Q

Plasma protein binding of Lamotrigine?

A

56%

342
Q

Half life of Lamotrigine?

A

24-36 hours

343
Q

Which drugs reduce half life of lamotrigine?

A

Enzyme-inducing drugs:

Phenytoin, phenobarbital, carbamazepine

344
Q

Which drugs increase half-life of Lamotrigine?

A

Valproate

345
Q

Impact of Lamotrigine on Carbamazepine?

A

Lamotrigine increases carbamazepine-10,11-epoxide

346
Q

When are peak plasma levels of typical antipsychotics reached, given as IM?

A

30 mins

347
Q

When are peak plasma levels of typical antipsychotics reached when given orally?

A

1-4 hours

348
Q

When is the steady state of antipsychotic reached?

A

3-5 days

349
Q

Half life for elimination of antipsychotics?

A

10-30 hours

350
Q

How long can depot forms of Haloperidol and Fluphenazine persist?

A

1-3 months if lipid storage and brain retention

351
Q

Active matabolite of Thioridazine?

A

Mesoridazone

352
Q

Active metabolite of Loxapine?

A

7-hydroxyloxapine

353
Q

What are typical antipsychotics mainly substrates of?

A

CYP1A

CYP2D6

354
Q

Which enzyme do typical antipsychotics inhibit?

A

2D6

355
Q

Bioavailability of Chlorpromazine?

A

37%

356
Q

What can decrease absorption of phenothiazines?

A

Antacids

357
Q

What drugs reduce antipsychotic levels (typical)?

A 
Enzyme inducers:
Carbamazepine
Phenytoin
Ethambutol
Barbituates
358
Q

What drugs increase typical antipsychotic levels?

A 
Clearance inhibitors:
SSRIs
TCAs
Cimetidine
Erythromycin
Ciprofloxacin
Ketoconazole
359
Q

Kinetics of Fluophenthixol decanoate depot?

A

Peak levels 3-7 days post IM

Half-life 17 days

360
Q

Kinetics of fluphenazine decanoate depot?

A

Peak levels 24 hours post-IM

Apparant half-life of 7-14 days

361
Q

Affect of smoking on Fluphenazine decanoate and Haloperidol depot?

A

Reduces levels

362
Q

Kinetics of Haloperidol decanoate depot?

A

Peak levels 7 days post IM

Half-life 3 weeks

363
Q

Kinetics of Perphenazine decanoate depot?

A

Peak levels 1-7 days post IM

Half-life of 2 weeks

364
Q

Kinetics of Pipotiazine palmitate depot?

A

Peak levels 1-2 weeks post IM

Half-life 2 weeks

365
Q

Kinetics of Zuclopenthixol decanoate depot?

A

Peak levels 1 week post IM

Half-life 7-20 days

366
Q

Half life of Risperidone?

A

15 hours

367
Q

Chlorpomazine equivalent of Risperidone?

A

2mg/day

368
Q

Half life of Clozapaine?

A

16 hours

369
Q

Chlorpromazine equivalent of clozapine?

A

50mg/day

370
Q

Half life of Quetiapine

A

6 hours

371
Q

Chlorpromazine equivalent of Quetiapine?

A

75mg/day

372
Q

Half life of Olanzapine?

A

30 hours

373
Q

Chlorpromazine equivalent of Olanzapine?

A

5mg/day

374
Q

Half life of Aripiprazole?

A

90 hours

375
Q

Chlorpromazine equivalent of Aripiprazole?

A

7.5mg/day

► Med - MRC Psych (21 decks)

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