Clinical psychopharmacology Flashcards

Question

Tricyclic antidepressants - tertiary amines (8)

Answer 1

Amitriptyline Lofepramine Imipramine Clomipramine Dosulepin (Dothiepin) Doxepin Trimipramine Butriptyline

Answer 2

Protriptyline Amoxapine Nortriptyline Desipramine 'PAND'

Answer 3

drowsiness dry mouth blurred vision constipation urinary retention

Answer 4

**Irreversible MAOIs (traditional)** - *'PIT'* - Phenelzine - Isocarboxazid - Tranylcypromine **Reversible MAOIs** - Moclobemide (aka RIMA - Reversible Inhibitor of Monoamine oxidase type A) *- less likely to cause cheese reaction than the traditional MAOIs*

Answer 5

Venlafaxine Duloxetine Milnacipran

Answer 6

Reboxetine Atomoxetine

Answer 7

Mirtazepine Mianserin

Answer 8

Phenothiazine (aliphatic side chain)

Answer 9

Phenothiazine (piperidine side chain)

Answer 10

Phenothiazine (piperizine side chain)

Answer 11

Butyrophenone

Answer 12

Thioxanthene

Answer 13

Diphenylbutylpiperidine

Answer 14

Dibenzodiazepine

Answer 15

Benzoxasole

Answer 16

Thienobenzodiazepine

Answer 17

Dibenzothiazepine

Answer 18

Substituted benzamide

Answer 19

Arylpiperidylindole (quinolone)

Answer 20

Lofepramine

Answer 21

Amitriptylline Dosulepin

Answer 22

NICE guidelines recommend the use of clozapine to people with schizophrenia whose illness has not responded adequately to treatment despite the sequential use of adequate doses of **at least two different antipsychotic drugs**. They stipulated that at least one of the drugs should be a non-clozapine **second-generation antipsychotic.**

Answer 23

The average clozapine dose in the UK is **450 mg/day**. A 'therapeutic range' has not been established. It is generally accepted that **a level of 350 µg/L is necessary to achieve a therapeutic response**. **Levels greater than 500 µg/L should be treated with caution as there is a risk of seizures**. Lower doses may be required in non-smokers, the elderly, females, and in patients using enzyme inhibitors (e.g. SSRI's). Treatment should of course be guided by clinical response (treat the patient not the level).

Answer 24

Drowsiness/ sedation Dizziness Insomnia Salivation Nausea + Vomiting Dyspepsia Weight gain Constipation

Answer 25

Agranulocytosis Myocarditis Seizures Severe orthostatic hypotension with or without syncope Increased mortality in elderly patients with dementia related psychosis Colitis Pancreatitis Thrombocytopenia Thromboembolism Insulin resistance and diabetes mellitus ========================================== (Approx 33 percent developed diabetes mellitus over a ten year period (Henderson, 2005)) The BNF advices caution in the following circumstances: prostatic hypertrophy susceptibility to angle-closure glaucoma adult over 60 years

Answer 26

Agranulocyotosis occurs in **1-2%** of patients on clozapine It is **more common in the first 18 weeks** of treatment One-third of patients who stop clozapine due to neutropenia or agranulocytosis will develop a blood dyscrasia on rechallenge. In most cases, the second reaction will occur more rapidly, be more severe, and will last longer than the first

Answer 27

**Lithium** has been shown to independently raise the white cell count and has been used in this way successfully in combination with clozapine. Use of this combination can enable patients to continue on treatment when they develop neutropenia. Having said that there are case reports suggesting that the combined use of lithium and clozapine can result in toxicity and so this combination must be used with caution.

Answer 28

**Sulpride** and **amisulpride** are the favoured antipsychotics for augmentation with clozapine as their selectivity for D2 dopamine blockade compliments clozapine (which lacks high potency dopamine blockade). **Lamotrigine** has the best evidence of the mood stabilisers to support its use as an augmentation strategy.

Answer 29

Olanzapine Aripiprazole Risperidone - Risperdal Consta or Paliperidone 'OAR'

Answer 30

0.4 - 1.2 mmol/L

Answer 31

Drowsiness Dry mouth Polyuria Polydipsia Metallic taste Muscle weakness GI - Nausea + Diarrhoea Weight gain Fine tremor Worsening of psoriasis

Answer 32

Hypothyroidism Irreversible nephrogenic diabetes insipidus Reduced GFR (chronic kidney disease) Hyperparathyroidism

Answer 33

NSAIDs/COX-2 inhibitors ACE inhibitors Thiazide diuretics ==================================== NB: Loop diuretics (furosemide) generally have no effect on lithium levels

Answer 34

Cardiac (Ebstein's) anomalies The risk of Ebstein's in women taking lithium is 1 in 1000 (which is 20 times the normal level).

Answer 35

binds to sodium channels increases their refractory period

Answer 36

P450 enzyme inducer dizziness and ataxia drowsiness headache visual disturbances (especially diplopia) Steven-Johnson syndrome leucopenia and agranulocytosis syndrome of inappropriate ADH secretion (hyponatraemia)

Answer 37

Fingernail hypoplasia, craniofacial defects

Answer 38

GABA agonist NMDA antagonist

Answer 39

**1 - Semi-sodium valproate (Depakote)** (licensed for acute mania associated with bipolar disorder) **2 - Valproic acid** (licensed for acute mania associated with bipolar disorder) **3 - Sodium valproate** (licensed for epilepsy) [Note that the BNF 61 is not consistent with the Maudsley Guidelines 10th Edition which suggest valproic acid is not licensed for acute mania.]

Answer 40

Spina bifida, hypospadias

Answer 41

Tiredness Significant weight gain (30-50% of patients) Tremor (up to 25% of patients) Hair loss (5% to 10% of patients, with curly regrowth once valproate is stopped)

Answer 42

GABA agonist NMDA antagonist Na channel stabiliser

Answer 43

Refractory or rapid cycling bipolar affective disorder where lithium plus valproate has been ineffective

Answer 44

binds to sodium channels increasing their refractory period

Answer 45

Craniofacial defects limb defects cerebrovascular defects mental retardation

Answer 46

gingival hyperplasia (secondary to increased expression of platelet derived growth factor, PDGF) hirsutism coarsening of facial features drowsiness megaloblastic anaemia (2ndary to altered folate metabolism) peripheral neuropathy osteomalacia (enhanced vitamin D metabolism) lymphadenopathy dyskinesia

Answer 47

Potentiation of the GABA inhibitory effect on the CNS by increasing the number and frequency of chloride channel opening

Answer 48

- absorbed well following oral administration - they show high plasma protein binding (95% for diazepam) - mainly metabolised in the liver - they tend to be highly lipophilic and rapidly cross the blood brain barrier and placental barrier

Answer 49

20-100 hours

Answer 50

18-50 hours

Answer 51

5-30 hours

Answer 52

15-38 hours

Answer 53

8-22 hours

Answer 54

10-20 hours

Answer 55

10-15 hours

Answer 56

6-10 hours

Answer 57

2 hours (SPMM states 1-3 hours)

Answer 58

2 hours (SPMM states 1 hour)

Answer 59

5HT1A partial agonist Licensed for the short-term management of anxiety

Answer 60

Henry K. Beecher (1955)

Answer 61

a drug which has its own inherent effects but none for the condition for which it is being given. e.g. the use of atropine as the control drug in trials of antidepressants.

Answer 62

- Injections \> oral - brighter coloured tablets - larger tablets - status of the treating professional - branded \> unbranded

Answer 63

Pattern analyses have shown that the improvement as a result of placebo in depression tends to be **abrupt**, occurs **early** in treatment and is **less likely to persist**, whereas improvement in response to antidepressants tends to be gradual, occurs later and is more likely to persist.

Answer 64

a situation where the placebo effect is diminished (attenuated) with repeated use

Answer 65

Depression - 60% Schizophrenia - 30%

Answer 66

Animal studies Phase 1 clinical trials - **safety** Phase 2 clinical trials - **effectiveness** Phase 3 clinical trials - **superiority** Phase 4 clinical trials - **post-marketing surveillance**

Answer 67

Phase 4 (post-marketing trials)

Answer 68

Absorption Distribution Metabolism Elimination 'ADME'

Answer 69

The process by which a drug enters the bloodstream

Answer 70

Inhalation

Answer 71

the fraction of an administered dose of a drug that reaches the systemic circulation in an unchanged form (by definition, when a medication is administered intravenously, its bioavailability is 100%)

Answer 72

**the reversible transfer of a drug from one location to another within the body** 2 important factors affecting this are: * tissue perfusion * drug lipophilicity

Answer 73

the biotransformation of compounds into new compounds, in order that they are made more water-soluble and can be more easily excreted from the body

Answer 74

how a drug is removed from the body, whether unaltered or in the form of its metabolites

Answer 75

aka prehepatic/presystemic metabolism the intestinal and hepatic degradation or alteration of a drug or substance taken by mouth, after absorption, that removes some of the active substance from the blood before it enters the general circulation

Answer 76

the time taken to eliminate 50% of the absorbed dose of a drug from a person's plasma

Answer 77

the time taken for a drug to lose half of its pharmacologic activity

Answer 78

the volume of plasma (or blood) from which the drug is completely removed, or cleared, in a given time period [aka renal clearance or renal plasma clearance where referring specifically to the kidneys]

Answer 79

a barrier separating the circulating blood flow in the human body from the extracellular fluid in the brain. * it consists of **capillary endothelial cells** tightly packed together * lipid soluble molecules pass through relatively easily whereas water soluble ones do not * Large molecules do not pass through the easily * Molecules that are highly charged struggle to pass through * The permeability of the BBB increases when it is inflamed * Nasally administered drugs can theoretically bypass the BBB * At several areas the BBB is fenestrated to allow neurosecretory products to enter the blood * Posterior pituitary * Area postrema

Answer 80

- an evolved mechanism that deals with exogenous toxins and is therefore essential in the metabolism of drugs - comprises about fifty separate enzymes - the enzymes are located on the **endoplastic reticulum** of cells and are mainly found in the **liver** and **small intestine**

Answer 81

**Inhibits CYP3A4** Increases levels of: - carbamazepine - benzos: diazepam, nitrazepam - neuroleptics: aripiprazole, quetiapine - antidepressants: sertraline, trazodone **Inhibits CYP1A2** Increases levels of: - clozapine

Answer 82

**Inhibits CYP1A2** Increases levels of: - clozapine

Answer 83

**Induces CYP1A2** Reduces levels of: - clozapine - olanzapine - fluvoxamine

Answer 84

This refers to the situation where the intake of a drug is at the same overall rate as its elimination from the body, so that there is no net change in the amount of drug in the person's system. It is usually reached after **4-5 times the half-life** of the drug has elapsed after commencement of regular dosing.

Answer 85

aka **Linear kinetics** **elimination of the drug takes place at a rate proportional to the plasma concentration** * a constant fraction of the drug is eliminated per unit time, but the actual amount of drug eliminated per unit time varies (reduces with plasma concentration) * drugs that follow linear kinetics have a fixed half-life * most drugs undergo linear kinetics

Answer 86

aka **non-linear kinetics** **elimination of the drug take place at a constant rate, regardless of the plasma concentration** * the fraction of the drug eliminated per unit time varies, but the actual amount of drug eliminated per unit time stays the same * drugs that follow non-linear kinetics do not have a fixed half-life (the half-life will be longer at the beginning and get shorter as the total amount of drug in the body decreases)

Answer 87

**More fat, less water** - lipid-soluble drugs are more widely distributed, therefore decreased plasma levels - water-soluble drugs are less well-distributed, therefore increased plasma levels **Less albumin** - greater unbound free fraction (increased amounts of active drug)

Answer 88

Reduced liver activity -\> reduced first-pass metabolism

Answer 89

**More fat, less water** - half-life of lipid-soluble drugs is increased

Answer 90

Asian \< Caucasian \< African American

Answer 91

Middle Eastern and North African

Answer 92

D - increased water and fat content leads to dilution and hence **lower plasma levels of drug** E - increased blood flow leads to **increased renal clearance** of many drugs

Answer 93

thioridazine droperidol

Answer 94

An assumption made in therapeutic drug monitoring that plasma drug concentration is roughly equal to the concentration at the site of action.

Answer 95

TD50: ED50 The ratio of the median toxic dose (TD50) and the median effective dose of a drug (ED50)

Answer 96

The difference between the minimum effective concentration and the minimum toxic concentration of a drug

Answer 97

Carbamazepine Lithium Phenytoin

Answer 98

Desmethyldiazepam

Answer 99

Dothiepinsulfoxide

Answer 100

Fluoxetine half-life - 4-6 days Fluoxetine's active metabolite is **norfluoxetine** - has a similar activity on 5-HT reuptake - half-life of 4-16 days

Answer 101

Desimipramine

Answer 102

9-Hydroxyrisperidone

Answer 103

Nortriptyline

Answer 104

**D2/D3 selective antagonist** cause substantial increase in prolactin less likely to produce EPSEs lack sedative and anticholinergic properties ---------------------------------------------------- low affinity selective antagonist of 'D2 like' receptors (D2=D3\>D4) - little affinity for D1 like receptors (D1 and D5) or non dopaminergic receptors (serotonin, histamine, adrenergic, and cholinergic)

Answer 105

**D2 partial agonist** **5HT1A partial agonist** **5HT2A antagonist** activating profile prodopaminergic SEs - insomnia, nausea, vomiting less likely to cause weight gain

Answer 106

**D2 antagonist** **5HT2A antagonist** **alpha-2 adrenoceptor antagonist** requires sublingual administration in UK licensed for mania but no schizophrenia

Answer 107

**D2 antagonist** **alpha-1 adrenoceptor antagonist** -\> hypotension **H1 antagonist** -\> sedating **muscarinic acetylcholin receptor antagonist** -\> dry mouth, urinary difficulties, constipation

Answer 108

**D2 antagonist (weak)** **D4 antagonist** **5HT2 antagonist (high affinity)** **5HT6 antagonist** **H1 antagonist** **Alpha-1 antagonist** **Muscarinic cholinergic receptor antagonist**

Answer 109

**D2 antagonist (potent)** **5-HT2 antagonist (potent)** Binds only weakly to H1 and and alpha-1 receptors, therefore less sedation, weight gain, and orthostatic hypotension

Answer 110

**High 5HT2/D2 blocking ratio** **Potent D4 and 5HT6 blockade** Significant anticholinergic and H1-antagonism, therefore strongly sedating

Answer 111

**D2 antagonist (weak)** **5-HT2 antagonist (weak)** H1 antagonist and anticholinergic Highly sedating

Answer 112

**D2 antagonist (potent)** **5-HT2 antagonist (potent)** alpha-1 antagonist mild sedation and hypotension in higher therapeutic doses can lead to EPSEs and hyperprolactinaemia similar to typicals

Answer 113

**Selective D2 antagonism** causes substantial increase in prolactin less likely to produce EPSEs lack sedative and anticholinergic properties

Answer 114

**D2 antagonist** **5HT2 antagonist** **5HT1a agonist** **Noradrenaline reuptake inhibitor** Not licensed in UK QT interval prolongation

Answer 115

**Melatonergic receptor agonist (MT1 and MT2)** **5-HT2C antagonist**

Answer 116

**Norepinephrine-dopamine reuptake inhibitor (NDRI)** **Nicotinic acetylcholine receptor antagonist** Used in smoking cessation and depression ===================================== Class - Aminoketone Increases seizure risk and is contraindicated in seizure disorders

Answer 117

**5HT1A partial agonist** Effective in generalised anxiety disorder but not panic disorder. Unlike benzodiazepines, the anxiolytic effects take several days to develop.

Answer 118

**Selective Serotonin Re-uptake Inhibitor (SSRI)** Associated with QT interval prolongation

Answer 119

**5HT reuptake inhibitor** (most potent of the tricyclics) Its metabolite desmethylclomipramine is an effective **noradrenaline reuptake inhibitor** *Only tricyclic effective in OCD*

Answer 120

Serotonin and noradrenaline reuptake inhibitor (SNRI)

Answer 121

**Noradrenaline and serotonin specific antidepressant (NaSSa)** 5HT2 antagonist 5HT3 antagonist H1 antagonist alpha 1 and alpha 2 antagonist muscarinic antagonist (moderate) Sedating profile

Answer 122

**Serotonin and noradrenaline reuptake inhibitor (SNRI)** - potent 5HT reuptake inhibition - noradrenaline reuptake inhibition only apparent at higher doses * negligible affinity for other receptors, therefore lacks sedative and anticholinergic properties*

Answer 123

**Selective Noradrenaline Re-uptake Inhibitor (NARI)** No clinically significant effects on other receptors

Answer 124

Weak MAOI Weak SNRI (also considered by some to be a weak SSRI)

Answer 125

**SARI (Serotonin antagonist and reuptake inhibitor)** 5HT2 antagonism 5HT reuptake inhibition (weak) alpha-1 antagonism *Distinct sedating profile*

Answer 126

**Reversible inhibitor of monoamine oxidase type A** No tyramine reaction, making it advantages compared with conventional MAOIs. However, therapeutic efficacy not well established.

Answer 127

**Reversible acetylcholinesterase inhibitor** (all) Rivastigmine is additionally a **butyrylcholinesterase inhibitor** Galantamine is additionally a **nicotinic acetylcholine receptor agonist**

Answer 128

**NMDA (glutamate) receptor antagonist**

Answer 129

Unknown. However, according to MRCPsych mentor: **GABA agonist** **NMDA antagonist**

Answer 130

Mechanism unclear - known to inhibit voltage activated calcium channels but it is not clear if this is how it exerts its therapeutic effect * Sedating* * Not licensed for the treatment of mood disorders*

Answer 131

**GABA agonist** **NMDA antagonist** **Na channel stabiliser**

Answer 132

Stabilises Na channels

Answer 133

Stabilises Na channels

Answer 134

**Blocks voltage-dependent sodium channels** **Reduces excitatory neurotransmitter release - esp. glutamate** * not licensed in UK for mood disorders.* * some evidence of benefit in bipolar depression, but not mania*

Answer 135

**Inhibition of the alpha-2-delta subunit of voltage-gated calcium channels in the central nervous system** *licensed for generalised anxiety disorder and neuropathic pain*

Answer 136

Facilitate GABA transmission by acting as **agonists on the omega site within the GABA-A complex** (all are agonists except clonazepam which is a partial agonist) They therefore facilitate inhibitory neurotransmission via chloride ions - they increase the frequency and duration (not number) of chloride channel openings

Answer 137

**GABA-A agonists** (but act on different parts of the GABA-A complex to benzodiazepines)

Answer 138

NMDA antagonist

Answer 139

NMDA antagonist

Answer 140

(presynpatic) Alpha 2 adrenoceptor agonist historically used to treat high blood pressure, but more commonly used to help with the physical symptoms of opioid withdrawal

Answer 141

(presynaptic) Alpha 2 adrenoceptor agonist Hypertension Prevention of recurrent migraine, Prevention of vascular headache, Menopausal symptoms, particularly flushing and vasomotor conditions

Answer 142

**Partial agonist at the mu-opioid receptor** Adjunct in the treatment of opioid dependence

Answer 143

Short-acting mu opioid antagonist

Answer 144

**Mu opioid receptor agonist** Adjunct in treatment of opioid dependence Longer acting than heroin

Answer 145

Noradrenaline reuptake inhibitor (NARI) used in ADHD

Answer 146

**selective nicotine-receptor partial agonist.** used in smoking cessation

Answer 147

**Irreversibly inhibits aldehyde dehydrogenase** Adjunct in the treatment of alcohol dependence

Answer 148

**Metabotropic glutamate receptor antagonist** **GABA-A agonist** a synthetic taurine analogue Maintenance of abstinence in alcohol-dependent patients

Answer 149

**selective, irreversible inhibition of monoamine oxidase type B** (also inhibits MAO-A at higher doses) Parkinson's disease

Answer 150

Phenothiazines SSRI: fluoxetine, paroxetine Disulfiram Methylphenidate Quinidine Cimetidine

Answer 151

Smoking Phenytoin Carbamazepine Contraceptive pill Barbiturates

Answer 152

Mutual inhibition of metabolism -\> increase in levels of both antipsychotic and TCA

Answer 153

TCAs increase warfarin levels - high risk of bleeding

Answer 154

TCAs reduce clonidine levels - risk of hypertensive crisis

Answer 155

Synergistic serotonergic enhancement (especially with clomipramine) -\> increased risk of serotonin syndrome TCAs reduce tyramine entry via monoamine reuptake channels -\> lower risk of cheese reaction

Answer 156

Both are capable of inhibiting their own clearance at clinically relevant doses - they therefore have nonlinear pharmacokinetics - changes in dose can produce proportionately large changes in plasma level

Answer 157

Citalopram | (and escitalopram)

Answer 158

33 hours Not a potent inhibitor of most cytochrome enzymes

Answer 159

30 hours Not a potent inhibitor of most cytochrome enzymes

Answer 160

4-6 days Inhibits CYP2D6, CYP3A4. Increases levels of some antipsychotics, some benzodiazepines, carbamazepine, ciclosporin, phenytoin, tricyclics Never use with MAOIs Avoid selegiline and St John's Wort

Answer 161

17-22 hours Inhibits CYP1A2/2C9/3A4. Increases levels of some benzodiazepines, carbamazepine, ciclosporin, phenytoin, some tricyclics, methadone, olanzapine, clozapine, propanolol, theophylline, warfarin

Answer 162

24 hours antimuscarinic effects and sedation more common Potent inhibitor of CYP2D6/3A4. Increases levels of some antipsychotics and tricyclics Never use with MAOIs. Avoid St John's Wort

Answer 163

26 hours Inhibits CYP2D6. Increases levels of some antipsychotics and tricyclics Avoid St John's Wort

Answer 164

The combination of **MAOIs and TCAs**, appears safe if both treatments are initiated in low doses simultaneously and are gradually increased together. The combination of **MAOIs and SSRIs (or clomipramine)** is generally contraindicated, because it can cause potentially fatal reactions such as serotonin syndrome.

Answer 165

rapidly absorbed following oral administration does not bind to plasma proteins it is not metabolised so does not have an active metabolite it is almost exclusively excreted by the kidneys unchanged ======================== Blood samples for lithium should be taken 12 hours post dose (for people prescribed a single daily dose).

Answer 166

Lithium blood level should 'normally' be checked every 3 months Thyroid and renal function should be checked every 6 months

Answer 167

**Type A (pharmacological)** can be predicted from the pharmacology of the drug involved. They are dose dependent and so are reversible on withdrawal of the drug. **Type B reactions (idiosyncratic)** cannot be predicted from the known pharmacology of the drug. Type B reactions include allergic reactions. ======================= Type A accounts for 80% of all ADRs

Answer 168

Galactorrhoea, gynecomastia, menstrual disturbance, lowered sperm count, reduced libido, Parkinsonism, dystonia, akathisia, tardive dyskinesia

Answer 169

Memory impairment, confusion

Answer 170

Dry mouth, blurred vision, glaucoma, tachycardia, urinary retention, constipation, ataxia

Answer 171

Weight gain, sedation

Answer 172

Orthostatic hypotension, sedation, sexual dysfunction, priapism

Answer 173

Haloperidol Amisulpride Sulpiride

Answer 174

Imipramine Paroxetine Citalopram

Answer 175

Lorazepam Oxazepam Temazepam Zopliclone 3.75mg (with care)

Answer 176

Histamine H1 antagonism Serotonin 5-HT2C antagonism

Answer 177

Over stimulation of 5HT2 receptors in the limbic system

Answer 178

muscarinic M4 agonism adrenergic alpha 2 antagonism inhibition of the swallowing reflex

Answer 179

Fluoxetine

Answer 180

Licensed in UK for treatment of moderate to severe tardive dyskinesia

Answer 181

alpha 1 adrenoceptor antagonist effective in reducing excessive sweating caused by antidepressant treatment, especially venlafaxine and SSRIs

Answer 182

appetite suppression sleep disturbance abdominal pain

Answer 183

weight loss restricted growth headache worsening of tics behavioural rebound significantly raised blood pressure

Answer 184

Long QT syndrome Bradycardia Ischaemic heart disease Myocarditis Myocardial infarction Left ventricular hypertrophy

Answer 185

Hypokalaemia Hypomagnesaemia Hypocalcaemia

Answer 186

Extreme physical exertion Stress or shock Anorexia nervosa Extremes of age (old or young) Female gender

Answer 187

Antibiotics * Ampicillin * Erythromycin Antiarrthythmics * Amiodarone * Sotalol Antimalarials * Chloroquine * Quinine Others * Methadone * Tamoxifen * Amantadine

Answer 188

normal \<440 borderline 440-450 prolonged \>450

Answer 189

normal \<440 borderline 440-460 prolonged \>460

Answer 190

No action required unless T-wave morphology

Answer 191

Consider reducing dose or switching to drug of lower QTc effect, repeat ECG and refer to cardiology

Answer 192

Stop causative drug, switch to drug of lower effect refer to cardiology

Answer 193

Haloperidol Pimozide

Answer 194

Quetiapine Chlorpromazine Zotepine Ziprasidone

Answer 195

Amisulpride Clozapine Olanzapine Risperidone

Answer 196

Aripiprazole Paliperidone

Answer 197

Type A (**pharmacological**) reactions can be predicted from the pharmacology of the drug involved. They are dose dependent and so are reversible on withdrawal of the drug. Type B (**idiosyncratic**) reactions cannot be predicted from the known pharmacology of the drug. Type B reactions include allergic reactions. ==================================== Type A account for up to 80% of all ARDs.

Answer 198

how avidly the drug binds to the receptor

Answer 199

the concentration or dose of a drug required to produce 50% of the drug's maximal effect. Potency depends on both the **affinity** of a drug for its receptor, and the **efficiency** with which drug-receptor interaction is coupled to response

Answer 200

also referred to as '**intrinsic activity**' the ability of the drug to elicit a response when it binds to the receptor

Answer 201

**Parkinsonism** - characterized by the triad of tremor, rigidity (lead pipe or cogwheel), and bradykinesia **Akathisia** - a subjective sense of restlessness, along with such objective evidence of restlessness as pacing or rocking **Dystonias** - prolonged and unintentional muscular contractions of voluntary or involuntary muscles **Tardive dyskinesia -** involuntary, repetitive body movements. This may include grimacing, sticking out the tongue, or smacking the lips 'PAD-T'

Answer 202

10% More common in: * young males * neuroleptic-naive * high potency drugs (e.g. haloperidol) develops within minutes or hours of starting antipsychotics Treatments: * anticholinergic drugs * switch antipsychotic * botulinum toxin * rTMS

Answer 203

**Torticollis** - cervical muscles spasms, resulting in a twisted posturing of the neck. **Trismus** - contraction of the jaw musculature and can result in lockjaw. **Opisthotonus** - arched posturing of the head, trunk, and extremities. **Laryngeal dystonia** - difficulty in breathing **Oculogyric crises** - involuntary contraction of one or more of the extraocular muscles, which may result in a fixed gaze with diplopia

Answer 204

20% more common in * elderly females * those with pre-existing neuro damage (e.g. stroke) Days to weeks after antipsychotic started or dose increased Treatments * reduce dose/switch * anticholinergic drugs

Answer 205

25% Hours to weeks Treatments: * reduce dose/switch * propranolol * clonazepam * mirtazepine * trazodone * mianserin * cyproheptadine * diphenhydramine

Answer 206

5% of patients per year of antipsychotic exposure More common in * elderly women * those with affective illness * those who have had EPSE early on in treatment develops over months to years Treatments * **stop** anticholinergic * reduce dose/switch to an atypical (clozapine/quetiapine) * tetrabenazine

Answer 207

liquid - Fluoxetine patch - Selegeline

Answer 208

Citalopram Mirtazepine Amitriptyline Clomipramine

Answer 209

Being elderly Being female Being a smoker Having medical co-morbidity Polypharmacy Low body weight Low baseline sodium concentration Reduced renal function Warm weather

Answer 210

* Absorption by oral administration occurs primarily in the **small bowel** * Absorption of many slow or sustained release drugs occurs in the **large bowel.** * There is poor absorption in the acidic stomach but conversely good absorption in the alkaline jejunum, ileum, colon and rectum.

Answer 211

excess serotonergic activity in the CNS most frequent cause of severe reaction is the co-administration of an MAOI with an SSRI typically acute and rapidly progressive, following shortly after one or two doses of the offending medication. clinical triad: * neuromuscular abnormalities * clonus * hyperreflexia * muscular rigidity * altered mental state * autonomic dysfunction * hyperthermia

Answer 212

almost exclusively caused by antipsychotics (but is also associated with antidepressants and lithium). Rapid and large dose increases often trigger it, along with rapid dose reductions, and abrupt withdrawal of anticholinergics. typically develops **within 2 weeks of initial treatment** but may occur at any time the drug is being taken. Presentation * hyperthermia * muscle rigidity -\> rhabdomyolysis, elevated CPK * altered consciousness

Answer 213

Common features include alteration in consciousness, sweating, autonomic instability, hyperthermia, and elevated CPK levels. Serotonin syndrome typically has an acute onset (within 24 hours of drug administration), whereas that of NMS is more insidious (typically taking up to 2 weeks to appear).

Answer 214

Amitriptyline Imipramine Nortriptyline

Answer 215

Clomipramine

Answer 216

Clomipramine [Cataplexy - 'C' for 'Clomipramine']

Answer 217

Citalopram Escitalopram Sertraline Paroxetine Venlafaxine

Answer 218

Escitalopram Paroxetine Sertraline Moclobemide Venlafaxine

Answer 219

Escitalopram Paroxetine Duloxetine Venlafaxine

Answer 220

Escitalopram Fluoxetine Fluvoxamine Paroxetine Sertraline

Answer 221

Fluoxetine

Answer 222

Paroxetine Sertraline

Answer 223

psychostimulant enhances wakefulness, attention, and vigilance. It is similar to amphetamines apart from that it tends to lack the euphoric effects, does not seem to be associated with dependence or tolerance, and does not tend to precipitate psychosis. licensed for: * narcolepsy * obstructive sleep apnea * chronic shift work * also suggested as an adjunctive treatment for depression (in the Maudsley). More recently it has also been used as a 'smart drug' in the hope that it will boost normal cognitive functioning.

Answer 224

Inform the service user that there is a high risk of relapse if they stop medication in the next 1-2 years. (NICE guidelines)

Answer 225

14-28 days

Answer 226

31% of patients using clozapine develop hypersalivation (silarrhoea)

Answer 227

Suboxone is a combination of four parts **buprenorphine** to one part **naloxone**. The latter is added to prevent addicts from injecting the tablets, as this was common when addicts were given pure buprenorphine tablets. Because it contains naloxone it is likely to produce intense withdrawal symptoms if injected, this does not occur when the tablet is swallowed as naloxone is not absorbed by the gut.

Answer 228

buprenorphine

Answer 229

14-16 days

Answer 230

Race - Afro-Caribbean 77% increase in risk Age - risk decreases as age increases Low baseline white cell count

Answer 231

absolute neutrophil count (ANC) of less than 0.5 \* 10^9/L Ethnicity - Asians are 2.4 times more likely than Caucasians to develop agranulocytosis on clozapine Age - risk increases with age

Answer 232

Advancing age Female Ethnicity - higher rates in African Americans Affective disorder 1st gen \> 2nd antipsychotics Mental retardation Substance abuse

Answer 233

Sodium valproate Zopiclone Venlafaxine Topiramate Methylphenidate Mirtazapine Olanzapine Amisulpride Aripiprazole

Answer 234

CYP2D6 is inactive in 6-10% of white people, and 2% of Asians.

Clinical psychopharmacology Flashcards

(288 cards)