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MA > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Who discovered Reserpine and when?

A

Kline in 1954

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2
Q

Who discovered Lithium and when?

A

In 1949, Cade in Australia discovered the use of lithium compounds in mania

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3
Q

Who discovered chlorpromazine and when?

A

Delay and Deniker’s team, and Charpentier 1950-1952

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4
Q

What was the first true antidepressant and when it discovered?

A

The first true antidepressant was discovered in 1952 Iproniazid (anti-TB treatment)
Iproniazid is a monoamine oxidase inhibitor.

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5
Q

Who discovered chlordiazepoxide and when?

A

Leo Sternbach in 1954

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6
Q

Who discovered the first TCA (what was it?) and when?

A

Kuhn discovered imipramine in 1958

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7
Q

Who synthesised butyrophenone haloperidol from pethidine and when?

A

In 1958, Janssen synthesised butyrophenone haloperidol from pethidine.

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8
Q

Who proposed the cheese reaction for MAOI associated hypertension?

A

1963 Cheese reaction was proposed to be the mechanism for MAOI associated
hypertension by Blackwell.

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9
Q

Who synthesised the first atypical agent?

A

Janssen synthesized an atypical agent RISPERIDONE in 1989

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10
Q

What was the first SSRI? Who synthesised it?

A

Carlssen synthesized purpose made SSRI Zimeldine – but this was withdrawn due to the
incidence of hypersensitivity syndrome and demyelinating disease that followed its use

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11
Q

What was the first SSRI on the market?

A

Fluoxetine

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12
Q

Who discovered Clozpaine and when?

A

Kane et al. 1988 rediscovered clozapine via a multicentre randomized design comparing
chlorpromazine vs. clozapine in ‘treatment resistant’ schizophrenia. 4% showed response
to chlorpromazine while 30% showed response to clozapine

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13
Q

Aliphatic phenothiazines is the chemical class of which drugs?

A

Chlorpromazine
Promazine
Triflupromazine

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14
Q

Piperidine derivatives is the chemical class of which drug?

A

Thioridazine

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15
Q

Piperazine derivatives is the chemical class of which drugs?

A

Trifluoperazine
Fluphenazine
Perphenazine
Thioridazine

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16
Q

Butyrophenones is the chemical class of which drugs?

A

Haloperidol

Droperidol

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17
Q

Thioxanthenes is the chemical class of which drugs?

A

Thiothixene
Flupenthixol
Zuclopenthixol

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18
Q

Dihydroindoles is the chemical class of which drug?

A

Molindone

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19
Q

Diphenylbutylpiperidine is the chemical class of which drug?

A

Pimozide (long t1/2)

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20
Q

Dibenzoxapine is the chemical class of which drug?

A

Loxapine

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21
Q

Benzisoxazole derivative is the chemical class of which drug?

A

Risperidone

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22
Q

Substituted benzamides is the chemical class of which drugs?

A

Amisulpride, Sulpiride

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23
Q

Dibenzodiazepine is the chemical class of which drug?

A

Clozapine

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24
Q

Dibenzothiazepine is the chemical class of which drug?

A

Quetiapine

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25
Q

Thienobenzodiazepine is the chemical class of which drug?

A

Olanzapine

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26
Q

Benzisothiazole is the chemical class of which drug?

A

Ziprasidone

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27
Q

Arylpiperidylindole (quinolone) is the chemical class of which drug?

A

Aripiprazole

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28
Q

Tertiary amines is the is the chemical class of which drugs?

A

Imipramine, Amitriptyline, Clomipramine, Dosulepin,
Trimipramine (also Venlafaxine)
The tertiary amines are thought to boost serotonin and noradrenaline.

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29
Q

Properties of secondary amines vs. tertiary amines?

A

more potent; less sedating; more noradrenergic, less antihistaminic or anticholinergic than tertiary

The secondary amines are said to have a lower side effect profile and to act primarily on noradrenaline

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30
Q

Secondary amines is the chemical class of which drugs?

A

Desipramine, Amoxapine, Nortriptyline and Protriptyline

also Duloxetine

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31
Q

Hydrazine derivatives is the chemical class of which drugs?

A

Phenelzine, Isocarboxazid (greater hepatotoxicity than

Tranylcypromine, a non hydrazine compound)

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32
Q

Aminoketone is the chemical class of which drug?

A

Bupropion

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33
Q

SSRIs

A

Citalopram, Paroxetine, Fluoxetine, Sertraline
and Fluvoxamine, S enantiomer of citalopram
- Escitalopram

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34
Q

SNRIs - serotonin and noradrenaline

reuptake inhibitor

A

Venlafaxine, Milnacipran, Duloxetine,

Sibutramine

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35
Q

NaSSA – Noradrenergic and specific

serotonergic antagonist

A

Mirtazapine and

Mianseri

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36
Q

NARI - Noradrenaline reuptake inhibitor

A

Reboxetine

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37
Q

NDDI - Noradrenaline Dopamine DisInhibitor -

A

Agomelatine

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38
Q

DARI – Dopamine reuptake inhibitor

*norepinephrine and dopamine re-uptake inhibitor

A

Bupropion

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39
Q

RIMA – reversible inhibitor of Monoamine A

oxidase

A

Moclobemide

brofaromine

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40
Q

SARI – serotonin antagonist and reuptake

inhibitors

A

Nefazodone, Trazodone

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41
Q

What is the novel agent Xanomeline?

A

A treatment option for schizophrenia. It acts via M1/M4
agonism
*also showed a trend toward improving cognitive function in Alzheimer’s

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42
Q

Which condition has ketamine been used in?

A

(NMDA) receptor antagonist that has shown

rapid antidepressant effects in treatment-resistant depression

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43
Q

What is the novel agent Pomaglumetad methionil?

A

a metabotropic glutamate receptor 2/3
agonist,

used to treat positive and negative symptom as an add-on therapy in schizophrenia.

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44
Q

What is deliquescence?

A

sensitivity to environmental moisture to such an extent that drugs turn from crystalline states into pastes or
liquids if left in contact with moist air even for a
short period of time.

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45
Q

Which drug has deliquescence?

A

Sodium valproate

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46
Q

What’s an active placebo?

A

An ‘active placebo’ has some activity inherently, but not against the treated condition.

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47
Q

What’s a nocebo?

A

When a substance administered for placebo effects produces prominent side-effects, it is
known as a ‘nocebo’.

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48
Q

What’s placebo sag?

A

Placebo sag is a term used to refer to decrease in placebo effect with repeated or chronic
administration of placebo drugs.

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49
Q

What is efficacy paradox?

A

The placebo effect may be disproportionately large for non-blinded therapies potentially
resulting in what has been called the efficacy paradox.

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50
Q

What do placebos work best for?

A

Placebos work best for pain, disorders of autonomic sensation, and disorders of factors
under neurohumoral control e.g. nausea, blood pressure, and bronchial asthma.

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51
Q

Placebo rates in psychiatric disorders

A

Depressive illness: 25 - 60%
Mania: up to 25%
Schizophrenia: 25 - 50%
Panic disorder: up to 70%

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52
Q

What colour tablets do anxiety and depression respond better to?

A

Anxiety symptoms responded better to green tablets and depressive symptoms responded
better to yellow tablets.

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53
Q

Why do placebos work?

A
  1. Natural remission theory
  2. Measurement regression (to the mean)
  3. Conditioning theory
  4. Endogenous opioids
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54
Q

Which medication form is associated with increased response?

A

Capsules

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55
Q

Phases before drug approval

A
  1. Preclinical Animal Studies - Mutagenicity, carcinogenicity and organ system toxicity are studies at this phase
  2. Human trials – volunteers phase 1 (safety) - tolerability and pharmacokinetics of the
    drug are ascertained
  3. Human trials – patients phase 2 (effectiveness) - RCTs
  4. Human trials – patients phase 3 (superiority or equivalence to standard looking for
    comparative efficacy and tolerance profile). Extensive double blind RCT to determine how well does it work and what are the common side effects.
  5. Human trials – post-marketing surveillance phase 4:
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56
Q

Adverse effects detected by post marketing surveillance of psychotropic medications:

  1. Nefazadone
  2. Droperidol, Thioridazine
  3. Sertindole
  4. Thalidomide (analgesic)
  5. Nomifensine
  6. Zimeldine
  7. Remoxipiride(sulpiride group)
  8. Mianserin
  9. MAOIs
  10. Clozapine
A
  1. Nefazadone - Hepatotoxicity
  2. Droperidol, Thioridazine - prolonged QTc
  3. Sertindole - Sudden cardiac death
  4. Thalidomide (analgesic) - Phocomelia
  5. Nomifensine - Hepatotoxicity
  6. Zimeldine - Hypersensitivity reactions and Guillain-Barre syndrome
  7. Remoxipiride(sulpiride group) - Aplastic Anaemia
  8. Mianserin - Blood dyscrasias
  9. MAOIs - Cheese reactions
  10. Clozapine - Agranulocytosis
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57
Q

Non-adherence rates for antipsychotics?

A

40–60%
*Nonadherent patients with schizophrenia are 3.5 x
more likely to relapse within 2 years

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58
Q

Non-adherence rates for mood stabilisers?

A

18–56%

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59
Q

Non-adherence rates for antidepressants?

A

30–97% (median 63%)

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60
Q

Factors that reduce adherence

A 
•Asymptomatic stage of illness
•Cognitive deficits
•Comorbidity – alcohol and substance
misuse
•Devaluation of medication effects by
the physician
•Fear of side-effects.
•High frequency of daily doses
•Homelessness
•Lack of insight (most common cause)
•Long duration of illness (chronic
diseases)
•Oral formulations have poorer
adherence than depots
•Past history of non-adherence
•Polypharmacy
•Prophylactic or maintenance treatments
•Psychopathology of hostility,
suspiciousness and disorganization
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61
Q

Factors that improve adherence

A
  • Presence of family support
  • Liquid or sublingual forms
  • High enthusiasm fromclinican
  • Good patient-clinician relationship
  • Continued access to clincian
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62
Q

Factors that have no influence on adherence

A
  • Age at illness onset
  • Age at first hospitalization
  • Sex
  • Socioeconomic status,
  • Marital status
  • Ethnicity
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63
Q

What are the four main categories of the health belief model of adherence?

A
  1. Benefits
  2. Costs
  3. Susceptibility
  4. Secondary benefits of medication and adherence.
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64
Q

What are some methods of improving adherence?

A 
Psychoeducational programmes:
Cognitive-based interventions
Behaviour-modification interventions 
Motivational interviewing
Compliance therapy
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65
Q

What are pharmacokinetics?

A

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

*affected by the method of administration

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66
Q

What processes are involved in pharmacokinetics?

A

ADME; Absorption, Distribution, Metabolism,

and Elimination

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67
Q

Which factors affect the rate of absorption?

A
  • The form of the drug
  • The rate of blood flow at the site of administration
  • Solubility of the drug which depends on the pH of the drug, size of particles in the formulation and the pKa of the drug (pKa is the pH at which precisely half of the drug is in its ionised form)
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68
Q

What is first-pass effect?

A

metabolism by liver and gut

mucosa - drugs absorbed from the gut undergo extensive metabolism before entering the systemic circulation

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69
Q

What are the mechanisms of absorption of drugs from the GI tract?

A
  1. Active transport 2. Passive

diffusion (most common mechanism) 3. Pore filtration

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70
Q

Which factors influence absorption of drugs from GI tract?

A

Intestinal motility
Gastric emptying
Gastric and intestinal pH
Intestinal microflora e.g. Chlorpromazine is sulfated in the gut which reduces its absorption
Area available for absorption
Integrity of blood flow
Presence or absence of food (food delays gastric emptying)

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71
Q

What is dissolution rate dependent on?

A
  1. Size of drug particle
  2. Solubility of the drug
  3. Properties of intestinal fluid (e.g. p H)
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72
Q

How quickly does absorption happen with IM administration?

A

10-30 minutes (avoids most of the first pass

metabolism)

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73
Q

What factors influence the rate of absorption of drugs administered intramuscularly?

A

Blood flow and aqueous solubility.
Lipid soluble drugs are rapidly absorbed; drugs with a relative low molecular weight are better absorbed. Increased muscle blood flow e.g. after muscular exercise increases the rate of absorption

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74
Q

Which method of administration gives 100% bioavailability?

A

IV

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75
Q

Which factors affect permeation?

A

Lipophilicity
Concentration gradient - either simple or facilitated diffusion
Surface area and vascularity

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76
Q

Which is more water soluble the ionised or non-ionised form of a drug?

A

The ionized form is more water-soluble than the nonionized form

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77
Q

Is the renal clearance higher or lower for ionised drugs?

A

Renal clearance is higher for ionised drug (drug is “trapped” in the glomerular filtrate and does not get reabsorbed)

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78
Q

What is distribution of a drug?

A

to ‘where’ in the body it can be found.
Some drugs are confined to the body fluids only, but others accumulate in particular tissues.

*Distribution of a drug leads to a fall in
the plasma concentration (central to peripheral shift) and is most rapid after intravenous
administration

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79
Q

Which factors influence Drug distribution?

A
  1. Hemodynamic factors - cardiac output, regional blood flow. Organs with the highest blood perfusions such as the brain, kidneys, and liver receive the highest distribution
  2. Plasma protein binding
  3. Permeability factors- higher the lipid solubility of the drug, the greater its rate of entry into cells
  4. Blood-brain barrier
  5. Blood- CSF barrier
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80
Q

What are the two compartments the body is divided

into?

A

Central compartment - plasma

Peripheral compartment - fat and other tissues, which vary with age, sex and weight.

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81
Q

Which drugs are highly protein bound?

A

95 - 99% –> diazepam, chlorpromazine, amitriptyline and imipramine
90 - 95% –> Phenytoin, valproate and clomipramine

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82
Q

What can occur with drugs that are highly protein bound?

A

They are prone to interactions mediated b ythis mechanism
e.g. Diazepam displaces phenytoin from plasma proteins, resulting in an increased plasma concentration of free phenytoin and an increased risk of adverse effects.

*The effects of protein displacement are usually not of clinical significance, as the metabolism of the affected drug increases in parallel with the free drug concentration.

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83
Q

What are the plasma proteins responsible for binding to drugs?

A

acidic drugs - albumin.
alkaline drugs - α1-acid glycoprotein

*most psychotropic drugs are basic

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84
Q

Which factors can affect the permeability of the BBB?

A

fever, head injury, hypoxia, hypercapnia, retroviruses, inflammation, vasculitis, hypertension, cerebral irradiation and aging

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85
Q

What determined the ability of a drug to pass blood brain barrier?

A

molecular size, lipid solubility and ionic status (Unionized molecules that are freely available and less protein bound are transported across the barrier)

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86
Q

Which areas lack BBB?

A

Circumventricular organs - subfornical organ, area postrema of the medulla and the median eminence.

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87
Q

What is bioavailability of a drug?

A

how much of an administered drug reaches its target - affected by absorption, distribution and elimination

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88
Q

What is metabolism of a drug?

A

process that renders drug less lipid-soluble and more water-soluble so that products are more easily excreted from the body

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89
Q

What happens during phase 1 of metabolism?

A

oxidation, reduction and hydrolysis

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90
Q

What happens during phase 2 of metabolism?

A

conjugation - to produce a water soluble conjugate

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91
Q

Where can conjugated drugs be excreted through?

A

renal excretion if relative molecular mass < 300

bile excretion if relative molecular mass > 300

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92
Q

Most psychotherapeutic drugs are oxidized by which enzyme system?

A

Hepatic cytochrome P-450 enzyme system

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93
Q

Between 5and 10% of Caucasians lack which P-450 enzyme and are poor metabolisers of corresponding substrates?

A

CYP2D6

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94
Q

Up to 15-20% of East Asians are poor metabolisers of substrates of which P-450 enzymes?

A

CYP2C19

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95
Q

Which psychotropic medications are metabolised by CYP2D6?

A

All TCAs, fluoxetine, paroxetine, trazodone, nefazodone, valproate, antipsychotics, risperidone, carbamazepine

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96
Q

Which psychotropic medications inhibit CYP2D6?

A

Paroxetine, to some extent fluoxetine, antipsychotics, amitriptyline and clomipramine

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97
Q

Which psychotropic medications are metabolised by CYP3A4?

A

Clomipramine, fluvoxamine, mirtazapine, nefazodone, Carbamazepine, most benzodiazepines.

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98
Q

Which psychotropic medications stimulate CYP3A4?

A

Carbamazepine and barbiturates

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99
Q

Which psychotropic medications inhibit CYP3A4?

A

Calcium channel blockers, fluoxetine and nefazodone.

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100
Q

What does smoking do to CYP1A2?

A

Inhibits

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101
Q

What does Fluvoxamine do to plasma Clozapine concentrations?

A

Increases plasma clozapine concentrations (by inhibiting CYP system)

*Clozapine levels may be increased 10-fold by the addition of fluvoxamine, which can induce seizures.

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102
Q

What does Fluoxetine do to plasma TCA levels?

A

Fluoxetine increases plasma tricyclic antidepressants via 2D6 and 2C19

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103
Q

What does carbamazepine do to the plasma concentration of the oral contraceptive?

A

Decreases the plasma concentration of several drugs including contraceptive pills.

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104
Q

Which drugs undergo autoinduction?

A

Carbamazepine and phenobarbitone

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105
Q

How does carbamazepine undergo autoinduction?

A

Carbamazepine is metabolised by CYP2D6, synthesis of which in turn is induced by carbamazepine

As a result of this autoinduction, the rate of metabolism of carbamazepine (and other P450 substrates) gradually increases over the first several weeks of treatment.

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106
Q

Which enzyme do smoking and caffeine affect?

A

Smoking and caffeine affect glucuronidation reaction via UGT enzyme and CYP1A2

  • caffeine competitively inhibits CYP1A2
  • Polyaromatic Hydrocarbons (PAH)in cigarettes induce CYP1A2
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107
Q

What are aripiprazole and risperidone metabolised by?

A

CYP2D6 and CYP3A

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108
Q

What are Quetiapine and ziprasidone metabolised by?

A

mainly metabolized by CYP3A

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109
Q

What are Olanzapine and Clozapine metabolised by?

A

CYP1A2 and UGTs

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110
Q

What’s the effect of caffeine on Clozapine/olanzapine?

A

increases levels

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111
Q

What’s the effect of caffeine on Clozapine/olanzapine?

A

decreases levels

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112
Q

What are the major routes of drug excretion?

A

urine, faeces and bile

*may also be excreted in sweat, sebum, tears, saliva and breast milk

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113
Q

What are the factors that influence excretion?

A
  • Increased age (decreases excretion)
  • Reduction in renal blood flow e.g. dehydration
  • Renal impairment leading to decreased renal function
  • Alterations in re-absorption: urine pH
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114
Q

Which drugs undergo renal elimination without significant liver breakdown?

A

lithium, amisulpride, sulpiride, gabapentin, acamprosate and amantadine.

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115
Q

What’s the half life of a drug?

A

The time taken for the plasma concentration of a drug to halve

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116
Q

What is first order kinetics?

A

a constant fraction of drug is cleared per unit time
(the higher the amounts of a drug present, the faster the elimination)

e.g. 100mg/ml (2hours) -> 50mg/ml (2hours) -> 25mg/ml (2hours) -> 12.5mg/ml

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117
Q

What is zero-order kinetics?

A

a constant amount, not a fraction, of the drug is cleared per unit time

e.g. 100mg (2hours) -> 80mg (2hours) -> 60mg (2hours) -> 40mg

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118
Q

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

A

4-5 half lives

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119
Q

What is the median toxic dose?

A

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

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120
Q

What is the median effective dose?

A

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

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121
Q

What is the therapeutic index?

A

measure of the toxicity or safety of a drug

ratio of the median toxic dose to median effective dose

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122
Q

Changes in body composition in the elderly?

A

Increase in total body fat
Decrease in total muscle mass (lean body mass)
Decrease in total body water

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123
Q

What’s the effect of changes in body composition in the elderly?

A

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

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124
Q

Changes in plasma protein in the elderly?

A

Decrease in plasma protein binding capacity

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125
Q

What’s the effect of changes in plasma protein in the elderly?

A

15-25% decrease in protein binding due to higher proteinuria and lesser plasma protein synthesis by the liver.

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126
Q

Changes in the liver in the elderly?

A

Decreased hepatic blood flow occurs.

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127
Q

What’s the effect of changes in the liver in the elderly?

A

After 80, CYP system declines.

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128
Q

Changes in the kidney in the elderly?

A

Decreases in renal blood flow have been approximated at 10% per decade beginning after the fourth decade - leads to reduced creatinine clearance and GFR.

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129
Q

What’s the effect of changes in the kidney in the elderly?

A

More frequent toxicity of renally eliminated agents(e.g. lithium).

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130
Q

Changes in the GI tract in the elderly?

A
  • GI blood flow is diminished

- Gastric pH is increased as acidity drops

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131
Q

What’s the effect of changes in the GI tract in the elderly?

A
  • Slower but nearly equal absorption of oral administered drugs
  • Decreased gastric first pass metabolism noted

A reduction in the gastric wall content of dopa decarboxylase leads to a 3-fold increase in the concentration of levodopa in the elderly

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132
Q

Changes in the brain receptors in the elderly?

A
  • Decreased number of brain acetylcholine postsynaptic receptors
  • choline acetyltransferase is diminished
  • brain acetylcholinesterase decreased
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133
Q

What’s the effect of changes in the brain receptors in the elderly?

A

Anticholinergic side effects more pronounced leading to increased frequency of delirium on polypharmacy.

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134
Q

Pharmacokinetic changes in neonates

A
  • higher proportion of total body water and extracellular body water
  • lower proportion of adipose tissue
  • glomerular filtration rate is lower in those aged less than 3-5 months
  • lower gastric acidity and have an increased gastric emptying time
  • more permeable blood—brain barrier
  • microsomal enzyme activity in the liver is lower in those than 2 months
  • lower plasma concentration of albumin
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135
Q

Pharmacokinetic changes in pregnancy

A
  • Delayed gastric emptying
  • Decreased GIT motility
  • Increased volume of distribution (5%)
  • Decreased drug-binding capacity
  • Decreased albumin level
  • Induced liver metabolic pathway
  • Increased GFR & renal clearance.
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136
Q

Pharmacokinetic changes in renal impairment (benzos)

A
  • Benzodiazepines should be used with caution
  • half-life of diazepam remains unchanged in end-stage renal disease, but its metabolite, desmethyldiazepam, may accumulate, causing excessive sedation
  • The half-life of lorazepam is increased from 8–25 hours in healthy adults to 32–72 hours in end-stage renal disease
  • At a low level of renal function, lorazepam dosage should be reduced by 50% to avoid excessive sedation
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137
Q

Pharmacokinetic changes in renal impairment (antidepressants)

A
  • Imipramine and amitriptyline can be given at their usual dosage
  • Dosage of fluoxetine and fluvoxamine does not have to be reduced
  • Half normal dose is used for citalopram in patients with renal impairment or in elderly
  • Half-life of paroxetine is increased with severe renal impairment, requiring dosage reduction
  • Sertraline is not recommended in renal impairment
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138
Q

Pharmacokinetic changes in renal impairment (antipsychotics)

A
  • Haloperidol does not require a dose reduction in renal impairment unless excessive sedation or hypotension occurs -Amisulpride is renally excreted almost exclusively so relatively contraindicated in renal failure
  • Risperidone and its active metabolite 9-hydroxy-risperidone are substantially excreted in the urine so in renal impairment the elimination half-life is prolonged
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139
Q

Active metabolite of Imipramine

A

desipramine

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140
Q

Active metabolite of Amitriptyline

A

nortriptyline

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141
Q

Active metabolite of Trazodone, nefazodone

A

mCPP

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142
Q

Active metabolite of Fluoxetine

A

norfluoxetine

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143
Q

Active metabolite of Sertraline

A

desmethylsertraline

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144
Q

Which drugs inhibit TCA metabolism and therefore increase TCA plasma concentrations?

A

Quinidine, cimetidine, fluoxetine, paroxetine, phenothiazines, disulfiram, methylphenidate

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145
Q

Which drugs induce TCA metabolism and therefore decrease TCA plasma concentrations?

A

Smoking, phenytoin, carbamazepine, OC pills and barbiturates

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146
Q

What are the effects of TCAs on warfarin?

A

TCAs increase warfarin levels so there is a high risk of bleeding

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147
Q

What are the effects of TCAS on clonidine?

A

TCAs reduce clonidine levels and can cause Hypertensive crisis

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148
Q

What are the effects of TCAs on MOAIs?

A
  • Synergistic serotonergic enhancement esp. with clomipramine
  • TCAs reduce tyramine entry via monoamine reuptake channels
  • There is a higher risk of serotonin syndrome but lower risk of cheese reaction
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149
Q

What are the effects of TCAS on ldopa?

A

TCAs reduce absorption of l-dopa and so lower l-dopa efficacy in Parkinsonism

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150
Q

What are the effects of TCAS on morphine?

A

Amitriptyline and clomipramine decrease the metabolism through UDP glucuronyl transferase interaction leading to increased opioid toxicity

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151
Q

What are the effects of TCAS on Phenothiazines?

A

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

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152
Q

Which SSRI is the least protien bound?

A

Escitalopram (56%)

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153
Q

What’s the half-life of norfluoxetine?

A

4–16 days

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154
Q

What’s the half-life of fluoxetine?

A

4-6 days

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155
Q

Which SSRIs do not have active metabolites?

A

Fluvoxamine and paroxetine

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156
Q

Which is the most selective SSRI?

A

Citalopram

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157
Q

Which is the most potent SSRI?

A

Paroxetine

158
Q

What’s the relationship between fluvoxamine and diazepam?

A

Fluvoxamine reduces the clearance of both diazepam and its active metabolite

159
Q

CYP450 profile of fluoxetine

A

metabolised by 2D6

Inhibits 2C19, 2D6.

160
Q

Which drugs does fluoxetine interact with?

A

All TCAs especially Clomipramine and Imipramine (both 2C19 & 2D6),
Citalopram, Sertraline, Moclobemide, Duloxetine, Mirtazapine Venlafaxine

*levels of these drugs are increased

161
Q

CYP450 profile of paroxetine

A

Metabolised by 2D6

Inhibits 2D6

162
Q

Which drugs does paroxetine interact with?

A

All TCAs
Citalopram, Fluoxetine, Fluvoxamine, Duloxetine, Mirtazapine, Venlafaxine

*levels of these drugs are increased

163
Q

CYP450 profile of fluvoxamine

A

Inhibits 1A2, 2C19, 3A4

164
Q

Which drugs does fluvoxamine interact with?

A

Clomipramine, Doxepine, Trimipramine, Duloxetine, Mirtazapine, Citalopram, Escitalopram, Sertraline, Trazodone

theophylline (via CYP1A2 inhibition)

*levels of these drugs are increased

165
Q

CYP450 profile of duloxetine

A

Inhibits 2D6

166
Q

Which drugs does duloxetine interact with?

A

All TCAs
Citalopram, Fluoxetine, Paroxetine, Fluvoxamine, Mirtazapine, Venlafaxine.

*levels of these drugs are increased

167
Q

CYP450 profile of Desipramine and Clomipramine

A

Inhibits 2D6

168
Q

Which drugs do Desipramine and Clomipramine interact with?

A

All TCAs
Citalopram, Fluoxetine, Fluvoxamine, Duloxetine, Mirtazapine, Venlafaxine

*levels of these drugs are increased

169
Q

What’s the half life of:

  1. paroxetine?
  2. fluvoxamine?
  3. sertraline?
  4. citalopram?
  5. fluoxetine?
  6. Venlafaxine?
  7. Duloxetine?
  8. Buspirone?
A
  1. 10 hours
  2. 11 hours
  3. 26 hours
  4. 33 hours
  5. 1.9 days
  6. 3.5 hours
  7. 8 hours
  8. 2-11 hours (given TDS)
170
Q

Which drug when used with MAOIs may cause a fatal excitatory reaction?

A

Pethidine/meperidine

171
Q

What’s the effect of st john’s wort on CYP?

172
Q

which enzymes mediate Mirtazapine metabolism?

A

CYP2D6 and CYP3A4

173
Q

which enzymes mediate Agomelatine metabolism?

A

CYP1A2 (90%) and CYP2C9 (10%)

174
Q

What is the effect of loss of sodium on lithium levels?

A

loss of body sodium can increase lithium reabsorption as compensation in error leading to toxicity.

175
Q

Which agents increase lithium levels?

A

ACE inhibitors
Fluoxetine
NSAIDs
Thiazide diuretics

176
Q

Which agents decrease lithium levels?

A 
Osmotic diuretics
Caffeine
Aminophylline
Theobromine, Theophylline 
Carbonic anhydrase inhibitors
177
Q

Which agents can cause toxicity of lithium at normal levels?

A 
Carbamazepine
Atracurium
Haloperidol, clozapine
Calcium channel blockers
metronidazole
178
Q

What happens to the bioavailability of gabapentin as the dose increases?

A

It decreases

179
Q

Kinetics of Flupenthixol decanoate

A

Peak levels 3–7 days post IM.

Apparent half-life of 17 days

180
Q

Kinetics of Fluphenazine decanoate

A

Peak levels are 24h post-IM.

The apparent half-life of 7-14 days. Smoking reduces levels

181
Q

Kinetics of Haloperidol decanoate

A

Peak levels 7 days post IM.

The apparent half-life of 3 weeks. Smoking reduces levels

182
Q

Kinetics of Perphenazine decanoate

A

Peak levels 1-7 days post IM.

Apparent half-life of 2 weeks

183
Q

Kinetics of Pipotiazine palmitate

A

Peak levels 1-2 weeks post IM.

Apparent half-life of 2 weeks

184
Q

Kinetics of Zuclopenthixol decanoate

A

Peak levels 1 week post IM.

The apparent half-life of 7-20 days.

185
Q

What’s the half life of:

  1. Risperidone?
  2. Quetiapine?
  3. Aripiprazole?
A
  1. 15 hours
  2. 6 hours
  3. 75 hours - 96 hours (~3 days) –> active metabolite dihydroaripiprazole - 94 hours
186
Q

What’s the major active metabolite of risperidone?

A

Paliperidone

187
Q

What’s the active metabolite formed when risperidone undergoes first-pass hepatic metabolism?

A

9-hydroxyrisperidone (by CYP2D6)

188
Q

Aripiprazole is metabolised by which enzymes?

A

CYP 3A4 and CYP2D6

189
Q

What % of Aripiprazole is protein bound?

190
Q

What % of Risperidone is protein bound?

191
Q

How long should deport risperidone be supplemented with oral risperidone?

192
Q

What is the oral bioavailability of Donepezil?

193
Q

Is donepezil protein bound?

194
Q

What’s the half life of donepezil?

195
Q

What’s the half life of methypenidate?

196
Q

What are the long acting benzos?

A

Diazepam,
chlordiazepoxide,
clonazepam,
flurazepam

197
Q

What are the short acting benzos?

A

Lorazepam, oxazepam,
temazepam,
Alprazolam

198
Q

What is a Very short acting benzo?

199
Q

Onset and half life of:

  1. Zopiclone
  2. Zaleplon
  3. Zolpidem
A
  1. Onset within 45 mins; half-life 3 to 6 hours (acts
    up to 8 hours)
  2. Onset within 30 mins; half-life 1 hour (acts
    up to 4 hours).
  3. Onset within 30 mins; half-life 1 to 3 hours (acts up to 6 hours).
200
Q

What are pharmacodynamics?

A

What the drug does to the body

201
Q

What are Ionotropic receptors?

A

ligand-gated ionic channels

*Their activation leads to a rapid
transient increase in membrane permeability to ions
e.g. nicotinic acetylcholine receptors, GABA-A
receptors, glutamate receptors and serotonin 5HT 3

202
Q

What are Metabotropic receptors?

A

G-proteins bind to the intracellular portion of the receptor and activate a second messenger

*slow response
e.g. Dopamine (D1-5), Noradrenaline, and
Serotonin 5HT1-7 except 5-HT 3, muscarinic acetylcholine receptors and opioid receptors

203
Q

What is a full agonist?

A

produces a maximal response

204
Q

What is a partial agonist?

A

cannot elicit a maximal response and are less effective than full agonists -> have a ceiling effect

205
Q

What is an inverse agonist?

A

binds to the same receptor but produces the opposite

pharmacological effect

206
Q

What is an antagonist?

A

drugs that interact with receptors to interfere with their activation by neurotransmitter or other agonistic molecules

  • competitive (can be reversed)
  • non competitive (change the receptor site)
  • ->the effects can be reversed only partially by increasing the dose of the agonist drug (reduces both the potency and the efficacy of agonists)
  • irreversible
207
Q

What is Pharmacological antagonism?

A

opposing action of two molecules by acting via

same receptors

208
Q

What is physiological antagonism?

A

opposing action of two molecules by acting via

same receptors

209
Q

What is chemical antagonism?

A

opposing action of two molecules by acting via

chemical reactions

210
Q

What’s the law of mass action?

A

drug response is proportional to the fraction of

receptors occupied - as the concentration of drug increases, the responses increases until all receptors are occupied

211
Q

How may receptor be up-regulated or down-regulated by drugs?

A

agonists may cause down-regulation (desensitivity) or reduction in receptor numbers

antagonists may cause upregulation (hypersensitivity) or increase in receptor numbers.

212
Q

What’s the potency of a drug?

A

the amount of the drug needed to

produce a particular effect compared to another standard drug with similar receptor profile

213
Q

Which factors affect the potency of a drug?

A

a. The proportion of the drug reaching the receptor
b. The affinity for the receptor
c. Efficacy

214
Q

What’s the affinity of a drug?

A

ability of the drug to bind to its appropriate receptor (‘affection’)

215
Q

What’s the efficacy of a drug?

What else might it be referred to as?

A

refers to how well the drug produces the expected response i.e. the maximum clinical response produced by a drug

The intrinsic activity

216
Q

Which receptors do atypical antipsychotics work on?

A

.Atypical drugs show selectivity for D2

receptors and also show high 5HT2: D2 blocking ratio

217
Q

Amisulpride mechanism of action

A

D2 and D3 antagonism

Some 5HT7 activity

218
Q

Aripiprazole mechanism of action

A

Partial dopamine agonist at D2
5HT2A antagonist
Exhibits a Goldilocks’ phenomenon - stabilising action wherein anatagonising DA at sites of excessive
dopamine such as mesolimbic zones while mimicking DA (agonism) at dopamine deficient zones such as mesocortical areas that are linked negative symptoms.

219
Q

Asenapine mechanism of action

A

D2 antagonist and serotonin 5HT2A blocker

alpha-2 blockade effect

220
Q

Chlorpromazine and promazine mechanism of action

A

moderate antimuscarinic effect in addition to D2 blockade

221
Q

Clozapine mechanism of action

A 
Low D2/high 5HT2 ratio activity
blocks D4 and 5HT6 receptors
 alpha 1 antagonism and anticholinergic and antihistaminic properties
Weak D1 and D2 affinity
binds 5HT3
222
Q

Lurasidone mechanism of action

A

D2 antagonist and serotonin 5HT2A blocker
high affinity for serotonin 5HT7
partial agonist at 5HT1A receptor

223
Q

Olanzapine mechanism of action

A

Has high 5HT2 / high D2 blockade ratio.

Potent D4 blockade and 5HT6 blockade also noted.

224
Q

Quetiapine mechanism of action

A

lowD2/low 5HT2 activity

225
Q

Risperidone mechanism of action

A

Has high 5HT2A antagonistic property

High D2/high 5HT2 activity

226
Q

Sulpiride mechanism of action

A

Pure D2 antagonist.

227
Q

Thioridazine, pericyazine and pipotiazine mechanism of action

A

D2 antagonists. Marked antimuscarinic effect. Less EPSEs than other typicals.

228
Q

Thioxanthenes mechanism of action

A

D2 antagonists

229
Q

Ziprasidone mechanism of action

A

5-HT2A and D2 blockade

Antagonizes 5-HT1D, 5-HT2C, D3, D4 receptors.

230
Q

Zotepine mechanism of action

A

5HT2A, 5HT2C, D1, D2, D3, D4 antagonism.

Potent noradrenaline reuptake inhibitor. Potent antihistaminic activity and some NMDA antagonism

231
Q

Buspirone belongs to the chemical class of

A

Azaspirones

232
Q

Which class of antidepressants can increase seizure risk heavily?

A

Aminoketone (Bupropion) is contraindicated in seizure disorder

233
Q

Which antidepressant is an enantiomer of another antidepressant drug?

A

enantiomer = mirror image

Escitalopram

234
Q

Zopiclone belongs to the chemical class of

A

Cyclopyrrolones

235
Q

Buspirone mechanism of action

A

partial agonist at the 5-HT1A autoreceptor

236
Q

Why may escitalopram be more effective than citalopram?

A

Escitalopram binds to both the re-uptake site and an allosteric site causing conformational changes in the 5-HT Transporter and enhancing re-uptake blockade

*May also have earlier onset of action

237
Q

Acamprosate is a

A

synthetic taurine analogue, which appears to act centrally on glutamate and GABA neurotransmitter systems

238
Q

Triazolopyridine is the chemical class of which drugs?

A

Trazodone, Nefazodone

239
Q

Imidazopyridine is the chemical class of which drug?

240
Q

Pyrazolopyrimidine is the chemical class of which drug?

241
Q

Benzothiazolyl piperazine is the chemical class of which drug?

A

Ziprasidone

242
Q

Lofexidine mechanism of action

A

Alpha-2 agonist
(In opioid detoxification, if short duration of treatment is desirable, a2 adrenergic agonists such as lofexidine and clonidine are preferred to methadone)

243
Q

What’s the ‘standardised difference in effectiveness’?

A

The difference in the effect of treatment in the active treatment group compared to the placebo group after taking into account the variation in the treatment effect

244
Q

Which drugs were nown as major tranquilisers?

A

Antipsychotics came to be known as major tranquilizers while barbiturates and benzodiazepines were called minor tranquilizers

245
Q

Which psychotropic is well known to cause sudden death?

A

thioridazine, droperidol - via cardiac arryythmias

246
Q

Ethnic differences in psychiatric drug effects are noted in which pharmacological actions?

A
  1. Blood levels of haloperidol - Maximal haloperidol concentration in plasma after rapid tranquillisation is significantly high for Asians than Caucasians.
  2. Hydroxylation of tricyclics - Caucasians appear to have lower plasma levels of tricyclic antidepressants and attain plasma peaks later when compared with Asians. These differences have been attributed to a greater incidence of slow hydroxylation among Asians when compared with Caucasians
  3. Prolactin response to antipsychotics - Asian subjects were reported to produce greater serum prolactin levels than Caucasian subjects.
  4. Alcohol metabolism - Nearly 40% Asians and around 60% South American Native Indians lack Aldehyde dehydrogenase enzyme in sufficient amounts to metabolise alcohol.
247
Q

Who is associated with the use of valproate in mania?

A

Bowden in 1994

248
Q

Placebo response is likely if patient is of lower social class T/F?

249
Q

Which drug could be used for the treatment of mixed affective episodes of bipolar disorder?

250
Q

What is cyproterone acetate?

A

Testosterone antagonist

251
Q

What is linked with intentional nonadherence?

A

A desire for self-efficacy

252
Q

Reserpine is extracted from which plant?

A

Rauwolfia serpentina

253
Q

Which hormone is most commonly used in the treatment of depression?

254
Q

A potential advancement in the treatment of dementia is

A

Drugs acting on intracellular mechanisms - Drugs acting on ß-secretase are promising candidates to enter clinical trial for Alzheimer’s disease as of now

255
Q

Advantages of buspirone over benzodiazepines when used for anxiety

A

Buspirone cause no dependence
Buspirone can be withdrawn more easily
Buspirone has no street value
Buspirone causes no tolerance usually

256
Q

Which drug undergo direct phase 2 metabolism reactions?

A

lorazepam, temazepam and oxazepam

257
Q

Which drug is excreted unchanged in urine?

A

Gabapentin

258
Q

Is lithium protein bound?

259
Q

What happens to lithium clearance when sodium is depleted?

A

It’s reduced

260
Q

Which drugs act on presynaptic receptors as the main mechanism of action?

A

Clonidine, lofexidine act at alpha2 presynaptic receptor.

261
Q

Urinary acidification can help eliminate which medications on overdose?

A

amphetamines and phencyclidine

262
Q

Volume of distribution

A
  • Drugs with high affinity for tissues such as fat have high volume of distribution
  • The drug distribution in plasma to various tissues depends on plasma protein binding
  • The drug distribution in plasma to various tissues depends on tissue permeability
  • Tissue distribution leads to a fall in plasma concentration
263
Q

How many minimum weeks of interval should be given between fluoxetine and phenelzine when switching from the SSRI to the MAOI?

264
Q

Drugs eliminated by zero order kinetics

A

Ethanol, Phenytoin, high dose Salicylates, high dose Fluoxetine, high dose Omeprazole.
Venlafaxine XL
Depot antipsychotics

265
Q

The enhancement of drug effects following the repeated administration of the same dose of a drug is called

A

sensitisation

266
Q

Valproate levels are decreased by

A

Carbamazepine

267
Q

Which drugs are enzyme inducers?

268
Q

Which drugs are enzyme inhibitors?

A

Caffeine is an inhibitor. Paroxetine, to some extent fluoxetine, neuroleptics, amitriptyline and clomipramine inhibit

269
Q

What is true about the use of TCAs in children compared to adults?

A

Due to more extensive metabolism, young people require higher mg/kg doses than adults.

270
Q

Which drug has its plasma levels reduced even after regular administration of the same dose for a month?

A

Carbamezapine - due to autoinduction

271
Q

The area under the curve after a single dose allows determination of the

A

Bioavailability of the drug

272
Q

What is clearance?

A

Clearance is defined as the volume of blood cleared of a particular drug in unit time - It helps calculating half life of a drug in the body

273
Q

Enzyme autoinhibition is most likely to be seen with which antidepressants?

A

fluoxetine, paroxetine and sertraline show autoinhibition of CYP2D6 though paroxetine is the one that is most affected.

274
Q

Formula for volume of distribution

A

(Volume of distribution) Vd =Q/Cp, where Vd-volume of distribution, Q-quantity of drug and Cp-plasma

275
Q

There is poor oral absorption of most psychotropics in which part of the gastrointestinal system?

276
Q

Which medications have low protein-binding?

A

Venlafaxine (25%-30%)

277
Q

TCAs may reduce their own absorption T/F?

A

T

Due to anticholinergic effects, they may reduce their own absorption (delayed gastric emptying esp. amitryptiline)

278
Q

Some drugs such as fluoxetine move from first order to zero order kinetics in supratherapeutic doses. What happens to their t1/2 in such cases?

A

t1/2 becomes dependent on doset1/2 becomes dependent on dose

279
Q

interaction of fluoxetine with other drugs

A

Fluoxetine increases concentration of haloperidol, carbamazepine and phenytoin. Fluoxetine enhances the effects of oral anticoagulants and propranolol.

280
Q

Which of the following can be given as a loading dose in acute mania?

281
Q

Tyramine gains neuronal access and releases stored catecholamines via which route?

A

Catecholamines reuptake channels

282
Q

The pharmacological activity of benzodiazepines depends on its action on which of the following receptors?

A

GABA-a receptor complex

283
Q

Which drug is not suitable for treating acute mania?

A

Topiramate

284
Q

Gabapentin has antiepileptic properties T/F?

285
Q

Receptor blockade in which dopaminergic pathway results in increased prolactin levels in the body?

A

Tuburoinfundibular pathway

286
Q

Receptor blockade in which dopaminergic pathway results in the therapeutic effects of antipsychotics?

A

Blockade of dopamine-2 receptors in the mesolimbic pathway leads to the therapeutic effects

287
Q

The mechanism of action of varenicline tartrate is

A

Partial nicotinic agonism - relieves symptoms of nicotine withdrawal and cigarette craving through its agonist actions while blocking the reinforcing effects of continued nicotine use through an antagonist action.

288
Q

Which SSRIs are potent enzyme inhibitors?

A

Fluoxetine, Fluvoxamine and Paroxetine are potent inhibitors of several hepatic cytochrome enzyme

289
Q

Which SSRI is a weak enzyme inhibitors?

A

Citalopram

290
Q

The enzyme/s that metabolise/s most of the body dopamine:

A

MAO-B and COMT

291
Q

Which actions can cause anorgasmia?

A

Alpha 1 antagonism

5HT2A/2C stimulation (delayed ejaculation in SSRIs)

292
Q

Which neurotransmitter receptor explains Mirtazapine’s sedative effects?

A

5HT Type 2 receptors

293
Q

Mechanism of action of buprenorphine is via partial agonism at

A

µ-opioid receptors

294
Q

What increases the risk of withdrawal reactions to therapeutic drugs?

A

The drug having anticholinergic properties

295
Q

The mechanism of action for Sodium valproate

A

GABA potentiation

296
Q

Which antidementia drug acts directly on nicotine receptors?

A

Galantamine

It is a reversible, competitive inhibitor of acetylcholinesterase with some inhibitory action on butyrylcholinesterase. It is also an agonist at nicotinic receptor sites.

297
Q

The mechanism of action of cyproheptadine is

A

Histamine H1 receptor blockade

298
Q

Which drug acts as a full agonist at Mu receptor and has a long half-life?

299
Q

Least sedative of tricyclic antidepressants?

A

Nortriptyline

300
Q

Most sedative of tricyclic antidepressants?

A

trimipramine

301
Q

Which of the following groups of medications are associated with bruxism?

A

Stimulants

302
Q

What is a potentially life-threatening side effect of mirtazapine, occurring with a risk of up to 1 in 1,000 instances?

A

Severe neutropenia,

303
Q

trazodone mechanism of action

A

It is a mixed serotonin antagonist/agonist.

304
Q

Endogenous substrates for monoamine oxidase (MAO) isoenzymes include

A

Epinephrine, dopamine, and serotonin

MAO-A is more selective for serotonin while MAO-B is more so for dopamine.

305
Q

Haloperidol acts on which receptors?

A

Haloperidol has a High D2/low 5HT2 activity

306
Q

Evidence-based support when prescribing antidementia drug donepezil

A

Reduces caregiver burden
Improves the amount of daily activities in some patients
Improves neuropsychiatric symptoms
Reduces the progression of cognitive decline

307
Q

Which medication has been found to be effective in patients with premature ejaculation?

A

Due to the inhibitory effects of serotonin on the central ejaculatory reflex, selective serotonin reuptake inhibitors (SSRIs) are useful in the treatment of Premature Ejaculation.

308
Q

The mechanism of action of barbiturates is by

A

Barbiturates act on GABA receptors and serve to increase the duration of chloride channel opening.

309
Q

How much Zuclopenthixol depot is equivalent to 50mg of haloperidol given every four weeks?

A

200mg / 2 weeks or 400mg/4 weeks of zuclopentixol depot

310
Q

What leads to worsening of negative symptoms in schizophrenia?

A

Blockade of dopamine-2 receptors in the mesocortical pathway leads to production or worsening of negative symptoms.

311
Q

What leads to EPSEs in schizophrenia?

A

Blockade of dopamine-2 receptors in the nigrostriatal pathway leads to EPSEs

312
Q

Excitotoxicity that is secondary to glutamatergic overstimulation results in neuronal damage. This is the basis of treating patients with neurodegenerative disorders with which medication?

313
Q

Which TCA has a stimulant effect?

A

Desipramine

314
Q

What has been postulated as the pharmacological basis of clozapine related hypersalivation?

A

Muscarinic M-4 agonism

315
Q

The chronic administration of tricyclics results in

A

Downregulation of beta-adrenergic receptors

316
Q

Which class of antidepressant drugs must be avoided while treating depression in a patient who does not want to gain weight?

317
Q

Which drug is associated with nephrolithiasis?

A

Topiramate

318
Q

Antibiotic that can cause serotonin syndrome if combined with MAOIs:

319
Q

common side effect of MAOIs

A

Postural hypotension

320
Q

Which AED may cause appetite suppression and weight loss?

A

Topiramate

321
Q

What is an important difference between NMS and serotonin syndrome clinically?

A

Symptoms such as hyperreflexia and myoclonus are attributed to the enhanced release of serotonin in serotonin syndrome and are not seen in NMS.

322
Q

Which mood stabiliser can cause SJS?

A

Lamotrigine (1% of the population with the risk being greatest in the first 8 weeks)

323
Q

treatment of clozapine-induced hypersalivation

A

Pirenzepine is a selective M1, M4 antagonist. Other drugs of use include benzhexol (trihexyphenidyl), hyoscine, Amitriptyline, and combination of benztropine and terazosin.

324
Q

Which of the following diuretics can be used to control lithium-induced polyuria without causing lithium toxicity?

A

Amiloriide

325
Q

The most common side effects with methylphenidate

A

nervousness, agitation, anxiety, and insomnia.

326
Q

common side effect of rivastigmine

A

nausea, vomiting, diarrhea, high blood pressure and hallucinations

327
Q

Which antidepressant is contraindicated in closed-angle glaucoma?

A

Paroxetine

328
Q

The mechanism by which weight gain occurs during treatment with psychotropics

A

5HT2-c antagonism
Hyperprolactinaemia
H-1 antagonism
Increased serum leptin leading to leptin desensitisation.

329
Q

The tricyclic with highest antihistaminic activity is

330
Q

A specific side effect of mianserin that requires regular monitoring is

A

A specific side effect of mianserin that requires regular monitoring is

331
Q

In treating serotonin syndrome which receptor antagonism is useful for controlling neurological signs

332
Q

Lithium induced hypothyroidism is much more common in

A

Young females

333
Q

Postural hypotension as a side effect of tricyclic antidepressants are related to

A

Alpha-adrenergic blockade

334
Q

Risk factors for TD

A

Older patients, females, patients with organic brain damage and patients with affective disorders, and those who have had acute EPSEs (Extra pyramidal side effects) early on treatment.

335
Q

The CNS side effects like anxiety and agitation in the initial few weeks of treatment with SSRIs are proposed to be due to

A

Over stimulation of 5HT2 receptors in the limbic system

336
Q

The sexual side effects caused by SSRI antidepressants are related to the consequence of stimulating which receptors?

A

5HT-2 receptors

337
Q

Which benzodiazepine is more toxic than others in overdose?

A

Alprazolam

338
Q

Symptoms of anticholinergic delirium

A

hot, dry skin; dry mucous membranes; dilated pupils; absent bowel sounds; and tachycardia.

339
Q

Management of of anticholinergic delirium

A

Discontinue anticholinergic drugs

Atropine can be used to treat anticholinergic delirium symptoms once the agent has been removed.

340
Q

The toxic confusional state caused by antipsychotics is mainly due to which mechanism?

A

Muscarinic receptor blockade

341
Q

Which SSRI is relatively unsafe for post-MI patients?

A

Citalopram

342
Q

Most common adverse effect of valproate?

343
Q

Which SSRI is present in high concentrations in breast milk?

A

Fluoxetine

344
Q

In managing the hypertensive crisis associated with monoamine oxidase (MAO) inhibitors and the ingestion of food with tyramine, the agent of choice is:

A

phentolamine or phenoxybenzamine

345
Q

Agranulocytosis as a side effect of Clozapine occurs most commonly during the

A

First 18 weeks of treatment

346
Q

Drugs with a high effect on QTc include

A

sertindole, thioridazine, pimozide and droperidol (and haloperidol)

347
Q

What is a prominent side effect of venlafaxine controlled by terazosin, alpha-adrenergic blocker?

348
Q

What percentage of patients with Tardive Dyskinesia may show recovery within a year with antipsychotic reduction?

A

Approximately 50-55%

349
Q

The patients who are prescribed clozapine or olanzapine should have their serum lipids measured every

A

3 months for the first year of treatment

350
Q

Sustained abnormal postures or positions called tardive dystonias are sometimes seen during neuroleptic treatment. Tardive dystonia occurs after

A

Months to years of antipsychotic treatment

351
Q

Urinary hesitancy can be an uncomfortable side effect during treatment with antidepressants such as the selective noradrenaline reuptake inhibitor reboxetine.

A

The use of selective a1A-adrenoceptor antagonists such as doxazosin or tamsulosin can treat the urinary hesitancy - especially in the elderly with associated prostate enlargement.

352
Q

the receptors responsible for side effects by psychotropic medications?
1 . weight gain caused by antipsychotics
2. hyperprolactinemia induced by antipsychotics
3. EPSEs of antipsychotics
4. Gastrointestinal discomfort caused by SSRIs
5. Postural hypotension induced by antipsychotics

A
  1. 5HT2C Antagonism
  2. D2 blockade
    3 D2 blockade
  3. 5HT3 stimulation
  4. Alpha-1 antagonism
353
Q

Drugs most likely to cause the following adverse effects:

  1. Seizures
  2. Ovarian cysts
  3. SJS
  4. Prolonged qTC
A
  1. Bupropion (doses >400mg/day)
  2. valproate
  3. lamotrigine, carbamazepine
  4. Ziprasidone (more than other atypicals)
354
Q

Psychiatric side effects of non-psychiatric medications

  1. Treatment for resting tremors that results in acute confusional state with paranoia and visual hallucinations
  2. Treatment for swollen legs that results in visual halos, which are green in colour and confusion
  3. Treatment for polymyalgia rheumatica that results in hypomania and confusion
A
  1. Levedopa
  2. Digoxin
  3. Prednisolone
355
Q

Sexual side effects

  1. Painfully prolonged erection caused by treatment for low mood and insomnia
  2. Decreased sexual interest, abnormal ejaculation caused by treatment for chronic auditory hallucinations
  3. New onset pain during intercourse caused treatment for depression.
A
  1. Trazodone
  2. Risperidone
  3. Paroxetine
356
Q

Teratogenicity of psychotropics

  1. Newborn with anencephaly
  2. Newborn with defect of the tricuspid valve
  3. Newborn with spina bifida
A
  1. Valproate
  2. lithium
  3. Valproate
357
Q

antidepressant drug that is most likely to interact and should be avoided in the following situations

  1. A 33-year-old woman treated for mixed anxiety & depressive disorder. She is on diazepam, started by her GP
  2. A 21-year-old asthmatic on theophylline is suffering from depression
  3. A 67-year-old gentleman with a previous history of stroke and is now depressed. He is on regular warfarin.
A
  1. Fluvoxamine reduces the clearance of both diazepam and its active metabolite, N-desmethyldiazepam
  2. Fluvoxamine reduces the clearance of theophylline approximately 3-fold via CYP1A2 inhibition
  3. When fluvoxamine is administered with warfarin, warfarin plasma levels increases by 98% and prothrombin times are prolonged.
358
Q

appropriate treatment option for the toxic symptoms produced by psychotropic drug

  1. Aspirin overdose
  2. Amphetamine overdose
  3. Diazepam overdose
  4. Amitryptyline overdose
  5. lithium toxicity following diarrhoea and presents with tremors and ataxia
  6. Methadone overdose
  7. Phenelzine (MAOI) + cheese and wine - high BP
  8. Barbiturate overdose
A
  1. Alkalinisation of urine - for salicylate (aspirin) overdose, and barbiturate overdose
  2. Acidification of urine - for amphetamines and phencyclidine
  3. Flumazenil
  4. Diazepam
  5. Haemofyalisis
  6. Naloxone
  7. phentolamine
  8. Alkalinisation of urine
359
Q

target plasma levels.

  1. sodium valproate
  2. Clozapine
  3. Lithium
  4. Carbamazepine
  5. Pehytoin
  6. Amitriptyline
A
  1. 50-100mg/L
  2. 350-500 mcg/L
  3. 0.6-1 mmol/L
  4. > 7 mg/L
  5. 10-20mg/L
  6. 100-200 mcg/L
360
Q

primary mechanism of action for:

  1. Ramelteon
  2. Riluzole
  3. Atomoxetine
  4. Clonidine
  5. Varenicicline
A
  1. MT1/MT2 receptor agonist
  2. NMDA glutamate receptor antagonist
  3. Selective presynaptic norepinephrine reuptake inhibition
  4. Presynaptic alpha-2 agonist
  5. Partial agonist at the α4β2 unit of nicotinic acetylcholine receptor
361
Q

In addition to a marked ST elevation in inferior leads, what other feature can be expected in case of acute myocardial infarction presenting with bradycardia?

A

RR interval is prolonged reflecting the bradycardia.

362
Q

most significant effect of these receptors

  1. Blockade of postsynaptic alpha-1 adrenoreceptor
  2. Blockade of M3 cholinergic receptors
  3. Blockade of H1 histamine receptors
  4. Downregulation of 5-HT2A receptors.
  5. D-2 receptor blockade
  6. SSRI-induced nausea
  7. Lower incidence of EPSEs of newer atypical antipsychotics
A
  1. Sedation and orthostatic hypotension,
  2. Dry mouth, constipation
  3. Sedation and weight gain
  4. Tolerance to hallucinogenic drugs
  5. Neuroleptic malignant syndrome
    6 gastrointestinal side effects like nausea, vomiting, anorexia, and diarrhoea
  6. Serotonin 5HT2 receptor blockade
363
Q
  1. Noncompetitive antagonist
  2. Competitive antagonist
  3. Partial agonist
A
  1. Ketamine at NMDA receptors
  2. Propranalol at beta adrenergic receptors
  3. Buprenorphine
364
Q

Active metabolite of:

  1. Amitriptyline
  2. Clomipramine
  3. Dosulepin
  4. Doxepin
  5. Imipramine
  6. Lofepramine
  7. Fluoxetine
  8. Trazodone
  9. Mirtazapine
  10. Venlafaxine
A
  1. Nortriptyline
  2. Desmethyl-clomipramine
  3. Desmethyldosulepin
  4. Desmethyldoxepin
  5. Desipramine
  6. Desipramine
  7. Norfluoxetine
  8. mCPP
  9. Demethyl-mirtazapine
  10. O-desmethyl-venlafaxine
365
Q

Common side-effects of TCAs include:

A 
drowsiness
dry mouth
blurred vision
constipation
urinary retention
366
Q

Drugs with a low effect on QTc include

A 
Amisulpride	Low
Clozapine	Low
Olanzapine	Low
Risperidone	Low
Aripiprazole	None
Palperidone	None
367
Q

Anticholinergic (antimuscarinic) effects

A

Dry mouth, blurred vision, urinary retention, constipation

368
Q

Antidopaminergic effects

A

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

369
Q

Antiadrenergic effects

A

Postural hypotension, ejaculatory failure

370
Q

Histaminergic effects

A

Drowsiness

371
Q

alternative routes of administration of:

  1. fluoxetine
  2. citalopram
  3. Mirtazapine
  4. Amitriptyline
  5. clomipramine
  6. Selegiline
A
  1. Sublingual
  2. IV
  3. IV
  4. IV/IM
  5. IV
  6. Transdermal
372
Q

Drugs unsuitable for compliance aids include

A 
Sodium valproate
Zopiclone
Venlafaxine
Topiramate
Methylphenidate
Mirtazapine
Olanzapine
Amisulpride
Aripiprazole
373
Q

Which drug exerts its action through the action on the alpha-2-delta subunit of voltage-gated calcium channels in the central nervous system?

A

Pregabalin

374
Q

What’s the half life of:

  1. Diazepam
  2. Lorazepam
  3. Chlordiazepoxide
  4. Nitrazepam
  5. emazepam
A
  1. Diazepam 20-100 hrs (36-200 hrs for active metabolite)
  2. Lorazepam 10-20hrs
  3. Chlordiazepoxide 5-30 hrs (36-200 hrs for active metabolite)
  4. Nitrazepam 15-38 hrs
  5. Temazepam 8-22 hrs
375
Q

Types of adverse reactions

A 
Type I (IgE-mediated) reactions
Type II (cytotoxic) reactions
Type III (immune complex) reactions
Type IV (cell mediated) reactions
376
Q

What’s Memantine’s MOA?

A

Non competitive NMDA receptor agonist

5HT2 receptor antagonist

377
Q

What’s Galantamine’s MOA?

A

Nicotinic receptor modulator

Selective and reversible AChe

378
Q

What’s Rivastigmine’s MOA?

A

Pseudo irreversible AChe

Butyrylcholinesterase inhibitor

379
Q

The somatodendriric inhibition of 5HT is regulated by which receptors?

380
Q

What increases the incidence of cleft palate in baby when used in pregnancy?

A

SSRIs

Lamotrigine

381
Q

Which side effect has not been reported in association with therapeutic doses of SSRIs?

Which have been?

A

Hypertension

Hallucinations, akathisia, galactorrhoea, photosensitivity

382
Q

The risk of developing seizures with the use of clozapine is increased by?

383
Q

Which AP is fastest to dissociate from D2 receptors?

384
Q

What’s the explanation for Chlorpromazine antiemetic property?

A

D2 blockade in the chemoreceptor trigger zone

385
Q

Which drugs should be avoided with cyclosporine use?

A

Fluoxetine Fluvoxamine and Trazodone

They are potent CYP34A inhibitors and can affect the levels

386
Q

Which diuretics can be used with lithium?

A

Furosemide is safest

387
Q

Which antidepresant’s plasma levels correlate with therapeutic response?

A

Imipramine

388
Q

Most important side effect associated with Galantamine?

A

Bradycardia

389
Q

Most important side effect associated with Venlafaxine?

A

Diastolic hypertension

390
Q

Most important side effect associated with Topiramate?

A

Weight loss

391
Q

Which drugs can cause nocturnal myoclonus?

MA (5 decks)

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