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CPT Drugs > CNS Drugs > Flashcards

CNS Drugs Flashcards

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1
Q

Hyoscine hydrobromide drug class

A

Muscarinic antagonist

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2
Q

Hyoscine hydrobromide indications

A

Motion sickness

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3
Q

Hyoscine hydrobromide mechanism of action

A

It competitively blocks Muscarinic acetylcholine receptors in the vestibular nuclei and chemoreceptor trigger zone.

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4
Q

Hyoscine hydrobromide ADR

A 
Sedation 
Memory problems
Glaucoma
Dry mouth
Constipation
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5
Q

Cyclizine drug class

A

Histamine 1 receptor antagonists

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6
Q

Cyclizine indications

A

Motion sickness

Morning sickness

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7
Q

Cyclizine mechanism of action

A

It acts centrally on the vestibular nuclei and inhibits histaminergic signals from the vestibular system to the chemoreceptor trigger zone in the medulla.

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8
Q

Cyclizine ADR

A 
Sedation 
Excitation 
Dry mouth 
Constipation 
Urinary retention 
Cardiac toxicity - long QT interval
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9
Q

Cyclizine caution

A

Elderly

Children

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10
Q

Ondansetron drug class

A

5-HT3 receptor antagonist

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11
Q

Ondansetron indications

A

Nausea and vomiting

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12
Q

Ondansetron mechanism of action

A

It can centrally on the chemoreceptor trigger zone and peripherally to reduce GI motility and secretions

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13
Q

Ondansetron ADR

A 
Constipation 
Headache
Elevated liver enzymes 
Long QT syndrome 
Extra-pyramidal effects - Dystonia, Parkinsonism
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14
Q

D2 receptor antagonists examples

A

Metoclopramide
Domperidone
Haloperidol

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15
Q

D2 receptor antagonist indications

A

Nausea and vomiting
Motion sickness
Vertigo

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16
Q

D2 receptor antagonists mechanism of action

A

It increases acetylcholine at Muscarinic receptors in the gut. It promotes gastric emptying by increasing tone of lower oesophageal sphincter, tone of gastric contractions and decreasing the tone of the pylorus.

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17
Q

Metoclopramide ADR

A

Galactorrhoea
Extra-pyramidal effects - Dystonia and Parkinsonism
Sedation
Hypotension

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18
Q

Domperidone ADR

A

Sudden cardiac death due to long QT and VT

Galactorrhoea

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19
Q

Dexamethasone drug class

A

Corticosteriod

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20
Q

Dexamethasone indications

A

Nausea and vomiting

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21
Q

Dexamethasone mechanism of action

A

May act on the chemoreceptor tigger zone

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22
Q

Dexamethasone ADR

A

Insomnia
Increased appetite
Increased blood sugar

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23
Q

Nabilone drug class

A

Cannabinoid

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24
Q

Nabilone ADR

A

Dizziness

Drowsiness

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25
Q

Aprepitant drug class

A

Neurokinin 1 receptor antagonist

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26
Q

Aprepitant indications

A

Nausea and vomiting

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27
Q

Aprepitant mechanism of action

A

It prevents the action of substance P at the chemoreceptor trigger zone and in peripheral nerves. It boosts the effects of 5HT3 receptor antagonists.

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28
Q

Aprepitant ADR

A

Headache
Diarrhoea
Constipation
Stevens-Johnson syndrome - skin reaction

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29
Q

First line drug for motion sickness

A

Hyoscine hydrobromide

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30
Q

D2 receptor antagonist cautions

A

Obstruction

Risk of perforation

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31
Q

First line for Morning sickness in pregnancy

A

H1 receptor antagonist or D2 receptor antagonist

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32
Q

First line for emesis in chemotherapy

A

Dexamethasone then Ondansetron

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33
Q

Nociception definition

A

The non-conscious neural traffic due to trauma or potential trauma to tissue

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34
Q

Pain definition

A

A complex, unpleasant awareness of sensation modified by experience, expectation, immediate context and culture.

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35
Q

Describe the pain reflex ?

A 
Nociceptors stimulated 
Release of substance P and glutamate
Afferent nerve stimulated 
Fibres decussate 
Action potential ascends
Synapse in thalamus 
Projects to post central gyrus
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36
Q

Opioid mechanism of action

A

Agonist binds which leads to a decreased in cAMP. This causes an efflux of potassium. The membrane then becomes hyper polarised. There is decreased production of substance P and GABA which increases dopamine release causing a euphoric effect.

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37
Q

What are some strong opioid agonist ?

A

Morphine
Fentanyl
Heroin
Oxycodone

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38
Q

What are some moderate opioid agonist ?

A

Codeine

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39
Q

What is a partial opioid agonist ?

A

Buprenorphine

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40
Q

What is a opioid antagonist ?

A

Naloxone

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41
Q

Which receptor does Morphine have a strong affinity to ?

A

Mu receptors

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42
Q

Morphine ADR

A 
Respiratory depression 
Emesis
GI tract side effects
Cardiovascular side effects
Miosis
Histamine release
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43
Q

Potency and affinity of Fentanyl compared to morphine

A

More potent

Higher affinity

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44
Q

Morphine actions

A

Analgesia

Euphoria

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45
Q

Fentanyl actions

A

Analgesia

Anaesthetic

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46
Q

Fentanyl ADR

A

Respiratory depression
Constipation
Vomiting

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47
Q

Potency of Codeine compared to morphine

A

Less potent

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48
Q

Codeine actions

A

Mild to moderate analgesia

Cough depressant

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49
Q

Codeine ADR

A

Constipation

Respiratory depression

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50
Q

Buprenorphine affinity compared to morphine

A

Very high so not easily displaced

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51
Q

Buprenorphine actions

A

Moderate to severe pain

Opioid addiction treatment

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52
Q

Buprenorphine ADR

A

Respiratory depression
Low BP
Nausea
Dizziness

53
Q

Naloxone affinity compared to morphine and Buprenorphine

A

Greater than morphine but less than Buprenorphine

54
Q

Overdose effects

A 
Dependence 
Vomiting
Constipation 
Hypotension 
Bradycardia 
Histamine release 
Miosis 
Drowsiness
Respiratory depression
55
Q

Opioid contraindications

A 
Hepatic failure
Acute respiratory distress
Comatose
Head injuries 
Raised ICP
56
Q

What does PGE2 contribute to ?

A

Regulation of acid secretion in parietal cells

57
Q

What does prostacyclin - PGI2 - contribute to ?

A

Maintenance of blood flow and mucosal repair

58
Q

What can enhance prostanoids ?

A

Autacoids such as bradykinin and histamine

59
Q

What can a disturbance of prostanoids lead to ?

A

Hypertension
MI
Stoke

60
Q

What homeostatic functions does COX-1 do ?

A

GI protection
Platelet aggregation
Vascular resistance

61
Q

What homeostatic functions does COX-2 do ?

A

Renal homeostasis
Tissue repair and healing
Reproduction
Inhibition of platelet aggregation

62
Q

How do NSAIDs have analgesic effects ?

A

It blocks PGE2 which reduces peripheral pain fibre sensitivity. This can result in decreased PGE2 synthesis in the dorsal horn causing a decrease in neurotransmitter release. This decreases excitability of neurons in the pain relay pathway.

63
Q

How do NSAIDs have an anti-inflammatory effect ?

A

NSAIDs reduce production of prostaglandins released at the site of injury. This decreases vasodilation and capillary permeability reducing local swelling.

64
Q

How do NSAIDs have an anti-pyretic effect ?

A

NSAIDs inhibit the hypothalamic COX-2 where cytokine induced prostaglandin synthesis is elevated results in a reduction in temperature.

65
Q

What has COX-1 selectivity ?

A

Aspirin

66
Q

Order of increasing COX-2 selectivity (least to most)

A 
Ibuprofen 
Naproxen 
Diclofenac
Celecoxib
Etoricoxib
67
Q

NSAIDs ADR

A 
Dyspepsia 
Nausea
Peptic ulceration 
Bleeding 
Perforation
Decreased GFR
68
Q

NSAIDs cautions

A 
Elderly 
Prolonged use
Smoking
Alcohol 
History of peptic ulceration 
H.Pylori infection
Heart failure
Underlying CKD
69
Q

NSAIDs DDI

A 
Aspirin 
Glucocorticoid steriods 
Anti-coagulants 
ACEi
ARB
Diuretics
Warfarin - increased risk of bleeding 
Methotrexate
70
Q

NSAIDs indications

A

Inflammatory conditions
Osteoarthritis
Postoperative pain
Menorrhagia

71
Q

Paracetamol indications

A

Mild to moderate pain

Fever

72
Q

Paracetamol mechanism of action

A

COX-2 selective inhibition in the CNS which decreases pain signals to higher centres

73
Q

Paracetamol overdose effects

A

Nausea
Vomiting
Abdominal pain
Liver damage

74
Q

Paracetamol overdose treatment

A

Activated charcoal is overdose is very recently

Give N-acetylcysteine

75
Q

Seizure definition

A

A transient occurrence of signs and symptoms due to abnormal electrical activity in the brain, leading to a disturbance of consciousness, behaviour, emotion, motor function or sensation.

76
Q

Most important excitatory neurotransmitter and the receptor is acts on ?

A

Glutamate on the NMDA receptor

77
Q

Most important inhibitory neurotransmitter and the receptor it acts on ?

A

GABA on GABA alpha receptors

78
Q

What can cause a seizure ?

A

Loss of inhibitory signals or too strong an excitatory ones

This imbalance can happen in any point in the brain and local changes can lead to generalised effects.

79
Q

What can cause an imbalance in the brain to cause a seizure ?

A

Genetic differences in brain chemistry / receptor structure
Drugs
Drug withdrawal
Strokes and tumours

80
Q

Signs and symptoms of seizures

A

Shaking and jerking
Loss of consciousness
Tongue biting
Possible aura prior

81
Q

Epilepsy definition

A

Epilepsy is a tendency towards recurrent seizures unprovoked by a systemic or neurological insult.

82
Q

Potential stimuli for seizures

A 
Photogenic 
Musicogenic 
Thinking 
Eating
Hot water immersion 
Reading 
Orgasm
Movement
83
Q

Where do generalised seizures originate ?

A

Originate at a point and rapidly engage both hemispheres

84
Q

Where do focal seizures originate ?

A

Originate within networks limited to one hemisphere. May be discretely localised or more widely distributed

85
Q

What is a provoked seizure ?

A 
Seizures that result from another medical condition such as :
Drug use or withdrawal 
Alcohol withdrawal 
Head trauma 
Metabolic disturbances 
CNS infections
86
Q

How to manage a seizure under 5 mins ?

A

Start a timer and usually seizures will self-terminate without use of drugs

87
Q

What is status epilepticus ?

A

A seizure lasting more than 5 minutes or more, or multiple seizures without a complete recovery between them.

88
Q

Drug management for Status epilepticus

A

0-5 mins - Full dose of benzodiazepine
0-15 mins - 2nd full dose of benzodiazepine
15-45 mins - phenytoin or levetiracetam
45 mins + - thiopentone / anaesthesia

89
Q

Investigations for a diagnosis of epilepsy

A

EEG- record the electrical pattern of activity in the brain

Imaging - MRI

90
Q

Benzodiazepine drug class

A

GABA alpha agonist

91
Q

Benzodiazepine indications

A

Termination of a seizure

92
Q

Benzodiazepine mechanism of action

A

There is increased chloride conductance resulting in more negative resting potential so the action potential is less likely to fire.

93
Q

Benzodiazepine examples

A

IV lorazepam
Diazepam rectally
Buccal or intranasal midazolam

94
Q

Carbamazepine drug class

A

Sodium channel blocker anti-epileptic drug

95
Q

Carbamazepine indication

A

Epilepsy

96
Q

Carbamazepine mechanism of action

A

Blocking sodium channels in the central neurones which slows recovery of neurones from inactive to closed states. This reduces neuronal transmission.

97
Q

Carbamazepine ADR

A

Suicidal thoughts
Joint pain
Bone marrow failure

98
Q

Phenytoin drug class

A

Sodium channel blocker anti - epileptic drug

99
Q

Phenytoin indications

A

Epilepsy

Mainly used in status epilepticus

100
Q

Phenytoin cautions

A

Exhibits zero order kinetics so there must be care in adjusting doses

101
Q

Phenytoin ADR

A

Bone marrow supression
Hypotension
Arrhythmia with IV use

102
Q

Sodium valproate drug class

A

Anti - epileptic

103
Q

Sodium valproate indications

A

1st line for generalised epilepsies

104
Q

Sodium valproate ADR

A

Liver failure
Pancreatitis
Lethargy

105
Q

Sodium valproate mechanism of action

A

Mixed GABA alpha effects and sodium channel blockade

106
Q

Lamotrigine drug class

A

Sodium channel blocker anti - epileptic drugs

107
Q

Lamotrigine indications

A

Focal epilepsy

Used for generalised epilepsy when sodium valproate is contraindicated

108
Q

Levetiracetam indications

A

Focal seizures

Generalised seizures

109
Q

Positives of levetiracetam

A

Safe in pregnancy

110
Q

Levetiracetam mechanism of action

A

It stops the release of neurotransmitters into synapse and reduces neuronal activity.

111
Q

Levetiracetam drug class

A

Synaptic vesicle glycoprotein binder - AED

112
Q

Anti-epileptic drug ADR

A 
Tiredness 
Drowsiness
Nausea
Vomiting
Mood changes
Suicidal ideation 
Osteoporosis
113
Q

AED DDI

A

Warfarin
Alcohol
Decreases effectiveness of oral contraceptive pill and antibiotics
CYP inducers - phenytoin, carbamazepine and barbiturates
CYP inhibitors - valproate

114
Q

Dopamine receptor agonist examples

A

Levodopa
Co-careldopa
Amantadine

115
Q

What is special about co-careldopa ?

A

Levodopa is used in combination with a peripheral dopa decarboxylase inhibitor. This reduces the dose and side effects. It also increases levodopa reaching the brain.

116
Q

Dopamine receptor agonist indications

A

Parkinson’s disease

117
Q

Levodopa side effects

A

Nausea
Hypotension
Psychosis
Tachycardia

118
Q

Levodopa mechanism of action

A

Levodopa is a prodrug that is converted to dopamine by DOPA decarboxylase. It crosses the blood brain barrier and is decarboxylase to dopamine where it stimulates dopaminergic receptors.

119
Q

Levodopa DDI

A

Pyridoxine ( vitamin B6 ) increases peripheral breakdown of levodopa.
MAOI and levodopa increase risk of hypertensive crisis.
Many anti-psychotic drugs block dopamine receptors and have Parkinsonism as a side effect.

120
Q

COMT inhibitor examples

A

Entacapone

Opicapone

121
Q

COMT inhibitors mechanism of action

A

No therapeutic effect alone and used alongside levodopa. They reduce the breakdown of levodopa so prolong motor response to levodopa.

122
Q

COMT inhibitor indications

A

Used alongside levodopa for Parkinson’s disease

123
Q

Examples of impulse control disorders

A

Pathological gambling
Hyper-sexuality
Compulsive shopping
Punding

124
Q

Dopamine receptor agonist ADR

A 
Sedation 
Hallucinations 
Confusion 
Nausea
Hypotension
125
Q

MAOI examples

A

Selegiline

Rasagiline

126
Q

MAOI actions

A

Can be used alone
Prolongs the action of levodopa
Smooths out motor response

127
Q

Anti-cholinergics examples

A

Orphenadrine

Procyclidine

128
Q

Anti-cholinergic ADR

A

Confusion

Drowsiness

129
Q

Anti-cholinergic positive

A

Treats the tremor

CPT Drugs (9 decks)

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