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Primary Pharmacology > Cns Pharmacology > Flashcards

Cns Pharmacology Flashcards

1
Q

What sites are involved in N/V
Where are they
Receptors at them

A

CTZ - postrema outside bbb, D2, 5HT3
Vomiting centre - dorsolateral reticular formation of brainstem - D2, 5HT3, M3,
Nucleus of tractus solarius (intergrates afferent signals) - H1, NK1

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2
Q

Causes of nausea and vomiting

A

Drug induced
Pregnancy
Radiotherapy
Psychogenic
Vestibular
Motion sickness
Hypotension’s
Migraine
Abdominal pathological
Raise ICP

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3
Q

Categories of antiemetics and examples

A

Anti cholinergic - atropine, hyoscine
Phenothiazines - prochlorpherazine, promethazine
Butyrophenones - droperidol, haloperidol
Antihistamines - cyclizine, buclizine
5HT3 antangonists - ondansetron, granisetron
Cannaboids - nabilone
NK1 antagonist - aprepitant
Peripherally acting - metoclopramide, domperidone
Steroid - dexamethasone
Miscellaneous - betahistine, sedatives, anxiolytics

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4
Q

Example and method of action of anticholinergic antiemetics

A

Atropine, hyoscine
Cross BBB, act on mACh receptors in vomiting centre and in GI tract
Reduce GI tract tone, increase sphincter tone, reduce gastric secretions

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5
Q

When to use anticholinergic antiemetics
Side effects

A

Motion sickness
Opioid induced nausea

Sedation, dry mouth, blurred vision, pupillary dilation, central anticholinergic syndrome

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6
Q

What is central anticholinergic syndrome
Management

A

Muscurinic antagonists cross bbb causing
Excitement
Drownsiness
Ataxia
Coma

An anticholinesterase that can cross the bbb eg physostigmine

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7
Q

Example and method of action of phenothiazine antiemetics

A

Prochlorperazine, premethazine
Antagonise D2 receptors in CTZ
Antagonise M3 receptors much like anticholinergic antiemetics
Antagonise H1 receptors

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8
Q

Main side effect of phenothiazine antiemetics

A

Sedation

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9
Q

Example and method of action of butyrophenone antiemetics

A

Haloperidol, droperidol
D2 antagonist at CTZ

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10
Q

Main side effects of butyrophenone antiemetics

A

Dissociative phenomenon
QT prolongation
Postural hypotension
Extrapyramidal effects
Neuroleptic malignant syndrome
Hyperprolacinaemia and gynaecomastia

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11
Q

Other effects of haloperidol that aren’t antiemetics

A

Antipsychotic
Anticonvulsant

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12
Q

Why does haloperidol cause postural hypotension

A

Alpha 1 adrenoreceptor block

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13
Q

Example and method of action of antihistamine antiemetics

A

Cyclizine, cinnarizine
H1 antagonism at CTZ

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14
Q

Best type of nausea and vomiting effected by antihistamines

A

Motion sickness

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15
Q

Side effects of cyclizine
Why

A

Dry mouth, tachycardia
Anti muscurinic properties

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16
Q

How do 5HT3 receptor antagonists work for antiemetics, examples

A

Ondansetron tropisetron
Antagonism of 5HT at posteraema, nucleus tractus solitarius, vagus nerve and gi tract

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17
Q

Side effects of ondansetron

A

Headaches
Constipation
QTc prolongation

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18
Q

How do cannabinoids work for antiemetics, examples

A

Antagonism of cannabinoid receptor at CTZ

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19
Q

When are cannabinoids most useful for nausea and vomiting

A

Opioids, cytotoxic chemotherapy and radiotherapy

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20
Q

Side effects of a cannabinoids

A

Hallucinations
Psychosis
Dizziness
Dry mouth

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21
Q

How do neurokinin receptor antagonists work for antiemetics, examples

A

Aprepitant
Act at nucleus of tractus solitarius and dorsal motor nucleus of vagus nerve

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22
Q

Comparison of aprepitant to ondansetron
Half life
Presentation

A

Broader spectrum of activity
11 hours
Oral capsule - prodrug fosaprepitant is available IV

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23
Q

How does dex work as an antiemetic

A

Maybe prostaglandin inhibition
Maybe inhibition of gut or neuronal 5Ht release

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24
Q

What is in a ml vial of dexamethasone

A

3.3mg dex
Sodium
Phosphate
Overall contains between 4mg dex phosphate or 4.3mg dex sodium phosphate

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25
Q

Examples of peripherally acting antiemetic drugs and how they work

A

Domperidone, metoclopramide
D2 antagonism at CTZ, inhibits emetic effects of gastric irritants
Antagonises H1 and 5HT
Promotes gastric emptying

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26
Q

Why do we tend to give metoclopramide not domperidone

A

Can’t be given paraetnrally
Causes qt prolongation, arrhythmia, sudden death has been reported

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27
Q

When are metoclopramide particularly useful

A

Cytotoxic and radiotherapy n and v
Impaired gastric transit eg diabetes

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28
Q

Bioavailability of cyclizine

A

80%

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29
Q

Side effects of dexamthasone

A

Increased post op infection and bleeding in the vulnerable
Increased convulsions and increased ICP

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30
Q

How is cyclizine metabolised

A

To norcyclizine

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31
Q

How is dex metabolised

A

Hepatic

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32
Q

Protein binding of metoclopramide

A

18%

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33
Q

Elimination of metoclopramide

A

80% in urine - either unchanged or conjugated

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34
Q

Side effects metoclopramide

A

Drowsiness, dizziness, extrapyramidal

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35
Q

Oral bioavailability of ondansetron

A

60%

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36
Q

Metabolism of ondansetron

A

Hepatic
Main metaboilte 8-hydroxyondansetron
Excreted in urine

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37
Q

Medications for status epilepticus

A

First line benzos
Second line - phenytoin, phenobarbital, chlormethazole, paraldehyde

38
Q

Agent of choice for petimal seizure

A

Ethosuximide
Valproate

39
Q

Agent of choice for tonic clinic seizures

A

Carbamazepine
Lamotrigine
Phenytoin
Valproate
Phenobarbital

40
Q

Agents of choice for myoclonus seizure

A

Valproate
Clonazepam
Lamotrigine
Ethosuximide

41
Q

Agents of choice for atypical seizures

A

Clonazepam
Ethosuximide
Lamotrigine
Phenobarbital
Phenytoin
Valproate

42
Q

Risks of antiepileptic medications in pregnancy

Mitigation stratergies

A

Teratogenic
Neural tube deficits
Coagulation disorders in newborn
Incompliance with meds causing seizure!

Coucelling and antenatal screening
Folate supplementation
Pre delivery Vit k

43
Q

How do benzos work in epilepsy

A

Attach to gaba increasing activity

44
Q

How do barbiturates work in epilepsy

A

Binds to gaba and facilitates chloride conduction - similar to benzos but different site

45
Q

What class of drug is phenytoin
How does it work

A

A hydantoin
Fast sodium channels responsible for depolarisation during APs
Bins when refractory so is use dependant

46
Q

Side effects of phenytoin

A

Hirsuitism
Gum hyperplasia
Megaloblastic anaemia
Fetal malformations

47
Q

Why does phenytoin interact with so many other drugs

A

85% protein binding - complete with aspirin, phenylbutazone, valproate
Enzyme induction - steroids, coumarins, oestrogens, phenobarbitol

48
Q

What is special about phenytoin metabolism

A

Zero order kinetics - enzyme pathway very rapidly saturated, so half life increases with dose.

49
Q

How does carbamazepine work

A

Use dependant voltage gated sodium channel blockade
Agonist at postsynaptic gaba receptor

50
Q

What is special about carbamazepine metabolism

A

Half life drops from 30-15hrs due to enzyme induction

51
Q

What is gabapentin
How does it work

A

An amino acid!
Competes with amino acids for specific transmembrane transporters
Increases concentration and synthesis of gaba
Binds to voltage sensitive ca channels
Reduces release of na, dopamine and 5Ht
Inhibits voltage sensitive na channels
Increases 5Ht
Prevents neuronal death by inhibition of glutamate synthesis

52
Q

How does valproate work
Main uses

A

Inhibits gaba transaminase increasing gaba levels
Peti mal, myoclonus epilepsy, infantile spasm

53
Q

Main issues with valproate

A

Neural tube deficits
Platelet number decrease

54
Q

How does lamotrigine work
Main uses

A

Stabilises inactive presynaptic sodium channels reducing neurotransmitter release
Partial seizures, tonic clinic seizures and myoclonic seizures

55
Q

How does levetiracetam work

A

Thought to bind selectively on epleptigenic neuronal tissue

56
Q

How does vigabactrin work
Issues

A

Inhibits gaba transaminase
Causes visual field deficit in 1/3rd of patients
Behavioural problems

57
Q

Classes and Examples of tricyclic antidepressants.

A

Dibenzazepines - clomiparamine, imipramine
Dibenzocycloheptanes - amitryptyline, nortriptyline

58
Q

How do TCAs work

A

Prevent reuptake of neurotransmitters, primerally noradrenaline, but also serotonin and dopamine
Acts on presynaptic alpha 2 receptors to increase neurotransmitter release
Antagonise mACh, H1, and alpha1 receptors

59
Q

Side effects of TCAs

A

Sedation
Weakness
Fatigue
Postural hypotension
Sinus tachycardia
PR and QT prolongation

60
Q

Protein binding of TCAs

A

95% to albumin

61
Q

Tca metabolism

A

Hepatic microsomal enzymes
N demethylation
Ring hydroxylation

62
Q

Classification and examples of MAOIs

A

Cyclopropylamines - transcypromine
Hydrazines - iproniazid, phenelzine
Propargylamines - pargyline, selegiline

63
Q

What is the distinction between mao-a and mao-b?

A

A is more effective at oxidising na and 5Ht
Equally effective at metabolising dopamine and tyramine

64
Q

How do MAOIs confir antidepressant effect

A

Inhibition of mao-a

65
Q

What sort of inhibition do MAOIs confir

A

Irreversible

66
Q

What do the different MAOIs inhibit

A

Phenelzine, transcypromine and iproniazid inhibit both isoenzymes non selectively
Clorygyline is selective to mao-a
Selegiline is selective to mao-b

67
Q

How does selegiline work

A

Mao-b inhibition thus not antidepressant but raises dopamine levels

68
Q

How long does it take MAOIs to work

A

Action immediately but no sign of antidepressant action for a few weeks

69
Q

Issues with MAOIs

A

Unable to metabolise exogenous amines properly thus get pressor effects from tyramine (found in cheese, red wine, marmite) and indirect sympathomimetic drugs including cough medicines.
Interaction with pethadine can cause coma

70
Q

What is the only reversible MAOI
What does it do
Advantage

A

Moclobemide
Reversibley inhibits mao-a
Can stop to reverese without haveing to await new mao enzyme formation

71
Q

Common side effects of ssris

A

Diarrhoea
Nausea vomiting
Headaches
Restlessness
Anxiety
Withdrawal

72
Q

How long between Ssri and maoi

A

MAOI 2-5 weeks post stopping ssri
Ssri 2 weeks after stopping MAOI

73
Q

Example of Snri

A

Venlafaxine

74
Q

Example of a selective noradrenaline reuptake inhibitor

A

Reboxetine

75
Q

What is mirtazapine
Effects

A

A noradrenergic and specific serotonergic antidepressant

Increases na and 5Ht
Blockades alpha 2 adrenoreceptors

76
Q

Why does lithium accumulate intracellular
Effect of this

A

It is 1A on the periodic table with atomic number 3 and molecular weight 7
Mimics sodium but smaller so can pass through fast sodium channels into cells but not out through the NaKATPase
Displaces potassium reducing outward leakage of potassium reducing transmembrane potential (more positive) facilitating depolarisation

77
Q

Target lithium plasma levels

A

0.4 to 1.0

78
Q

Lithium half life
Implication for anaesthesia

A

12 hours
Should be stopped 2-3 days before using a muscle relaxant
Especially non-depolarising muscle relaxants which are potentiated.
May delay onset and prolong relaxation of sux.

79
Q

Effect of lithium on vasopressin p

A

Inhibits activity in the kidneys

80
Q

Other hormones effected by lithium

A

Increases aldosterone secretion
Inhibits thyroid hormone release

81
Q

Neurological effects of lithium

A

Thirst, tremor, muscle weakness, confusion, seizures

82
Q

Side effects of antipsychotics

A

Extrapyramidal side effects (facial grimace, incoluntary movement, oculogyric crisis, torsion, spams, Parkinsonism, tardive dyskinesia)
Increased prolactin secretion
Antimuscarinic (dry mouth, constipation, urinary retention, blurred vision
Alpha adrenergic - postural hypotension
Antihistaminergic - sedation
Qt prolongation
Agranulocytosis (clozapine)

83
Q

Mechanisms of drugs for Parkinson’s, example

A

Increase dopamine synthesis - levodopa
Decreased peripheral conversions of levodopa - carbidopa
Decreased dopamine breakdown - selegiline
Dopamine receptor agonists - bromocriptine
Dopamine receptor facilitators - amantadine
ACh antagonists - benztropine

84
Q

How does levodopa work in Parkinson’s

A

Racemic dopa has many side effects without being useful, Dopamine can’t cross bbb
Give levodopa, we’ll absorbed orally, crosses bbb and converted to dopamine which has effect.

85
Q

What does carbidopa do in Parkinson’s

A

Give with levodopa
Inhibits peripheral conversion of levodopa to dopamine so less systemic side effects and more enters brain.

86
Q

What does domperidone do in Parkinson’s

A

Dopamine anatagoinst that only slowly crosses bbb so reduces peripheral side effects of dopamine thus permitting use of larger doses than would otherwise be tolerated.

87
Q

How does selegiline work in parkinsons

A

Selective maob inhibitor
Decreases dopamine breakdown

88
Q

Examples and effects of dopaminergic drugs in Parkinson’s
Side effects

A

Bromocriptine, cabergoline
Stimulate central d2 receptors
Used when levodopa ineffective
Side effects of prolactin inhibition, ergot derived so retroperitonal, cardiac and pulmonary fibrosis

89
Q

Use of amantidine in Parkinson’s

A

Possible facilitation of dopamine release and inhbition of metabolism

90
Q

Use of ach antagonists in Parkinson’s
Examples

A

Benhexol, procyclidine
Cross bbb
Restore imbalance between cholinergic and dopimanergic effects in brain
Antagonise pre synaptic inhibition of dopamine release

Primary Pharmacology (18 decks)

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