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APPLIED PHARMACOLOGY💊 > Nervous System > Flashcards

Nervous System Flashcards

1
Q

Paracetamol - Indications

A

1) Acute and Chronic pain

2) Antipyretic

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2
Q

Paracetamol - MOA

A
  • Poorly understood
  • Weak inhibitor of cyclo-oxygenase (COX) : enzyme involved in prostaglandin metabolism
  • COX inhibition, increase pain threshold and reduce prostaglandin concentration s in thermoregulation pathway –> controlling fever
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3
Q

Paracetamol - Side Effects

A

Few SE

Overdose : causes liver failure

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4
Q

Paracetamol - Contraindication

A

None

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5
Q

Paracetamol - Caution

A
  • Chronic excessive alcohol use

- Liver toxicity, Hepatic impairment

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6
Q

Paracetamol - Interactions

A

CYP inducers - increase risk of liver toxicity after overdose

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7
Q

Paracetamol - Max dose

A

4g / day

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8
Q

Weak/ Moderate Opioids - Examples

A

Tramadol
Codeine
Dihydrocodeine

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9
Q

Weak/ Moderate Opioids - Indication

A

1) Mild - to - Moderate pain

- -> 2nd line

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10
Q

Weak/ Moderate Opioids - MOA

A

They are metabolised by the liver to produce small amounts of morphine.
- These are agonists of opioid µ (mu) receptors. Thus have an analgesic effect

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11
Q

Weak/ Moderate Opioids - Side Effects

A
  • Nausea
  • Constipation
  • dizziness
  • drowsiness
  • Neurological and respiratory depression in overdose
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12
Q

Weak/ Moderate Opioids - Contraindications

A
  • Avoided in epilepsy and controlled epilepsy
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13
Q

Weak/ Moderate Opioids - Caution

A
  • Respiratory disease

- Reduced dose in renal and hepatic impairment + elderly

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14
Q

Weak/ Moderate Opioids - Interactions

A

-Should not be used with other sedating drugs : antipsychotic, benzodiazepine, tricyclic antidepressants

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15
Q

Weak/ Moderate Opioids - Patient education

A

Avoid driving or operating heavy machinery if they become drowsy or confused

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16
Q

Strong Opioids - Examples

A
  • Morphine

- Oxycodone

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17
Q

Strong Opioids - Indications

A

1) Rapid relief of acute sever pain
2) Relief of chronic pain
3) Relief of SOB in end-of-life care & acute pulmonary oedema

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18
Q

Strong Opioids - MOA

A
  • The therapeutic action of opioids arises from activation of opioid µ receptors in the central nervous system (CNS).
  • Activation of these G protein-coupled receptors has several effects that, overall, reduce neuronal excitability and pain
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19
Q

Strong Opioids - Side Effects

A
  • Euphoria & detachment
  • Nausea & vomiting
  • Constipation
  • Itching, urticaria, sweating
  • Tolerance & dependence
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20
Q

Strong Opioids - Contraindications

A
  • Respiratory Failure

- Biliary colic

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21
Q

Strong Opioids - Caution

A
  • Hepatic + Liver Failure

- Elderly

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22
Q

Strong Opioids - Interactions

A
  • Should not be used with other sedating drugs (e.g. antipsychotics, benzodiazepines & tricyclic antidepressants)
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23
Q

Carbamazepine - Indications

A

1) Epilepsy = seizure prophylaxis

2) Trigeminal neuralgia –> 1st line

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24
Q

Carbamazepine - MOA

A
  • Inhibits neuronal sodium channels.

- This stabilises RMP and reduces neuronal excitability

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25
Q

Carbamazepine - Side Effects

A
  • GI Upset : N & V
  • Neuro effects : dizziness & ataxia
  • Carbamazepine hypersensitivity
  • Oedema + Hyponatraemia
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26
Q

Carbamazepine - Contraindications

A
  • Prior antiepileptic hypersensitivity syndrome
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27
Q

Carbamazepine - Caution

A

Hepatic + renal or cardiac disease –> due to increased toxicity

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28
Q

Carbamazepine - Interactions

A
  • Carbamazepine induces CYP enzyme which reduces plasma conc and efficacy of drugs that are metabolised by CYP enzymes (e.g. warfarin + oestrogen)
  • CYP inhibitors : increased conc and adverse effects as carbamazepine is metabolised by CYP enzymes.
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29
Q

Carbamazepine - Patient Education

A
  • Started at low dose (100-200mg) and then increased as tolerance to SE develops.
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30
Q

Valproate - Examples

A

Sodium valproate

Valproic acid

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31
Q

Valproate - Indications

A

1) Epilepsy - seizure prophylaxis
2) Certain cases of established convulsive status epilepticus
3) Bipolar disorder

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32
Q

Valproate - MOA

A
  • Weak inhibitor of neuronal sodium channels, stabilising RMP and reducing neuronal excitability
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33
Q

Valproate - Side Effects

A

Common:

  • GI upset : Nausea, diarrhoea
  • Neuro /psychiatric : tremor, behavioural disturbances
  • Thrombocytopenia

Life-threatening:
- Severe liver injury, bone marrow failure

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34
Q

Valproate - Contraindications

A
  • Women of child-bearing age

- 1st trimester of pregnancy

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35
Q

Valproate - Caution

A
  • Hepatic impairment

- Severe renal impairment

36
Q

Valproate - Interactions

A
  • With Lamitrigine & drugs metabolised by CYP enzymes (warfarin) : inhibit liver enzymes, risk of toxicity and increase plasma conc
  • CYP inducers (carbamezepine) : because valproate is metabolised by CYP enzymes, so inducers reduce conc and increase risk of seizures
37
Q

Valproate - Patient Education

A
  • Take tablets with food to reduce GI irritation
38
Q

Lamotrigine - Indications

A

1) Epilepsy : seizure prophylaxis
- -> focal, tonic-clonic, absence

2) Bipolar disorder

39
Q

Lamotrigine - MOA

A
  • It binds to voltage-sensitive neuronal Na+ channels, interfering with Na+ influx into the neuron.
  • This prevents repetitive neuronal firing, which is a characteristic of seizure activity
40
Q

Lamotrigine - Side Effects

A

Common:

  • headache
  • drowsiness
  • Irritability
  • Blurred vision
  • dizziness
  • GI symptoms

RASH: urgent review and may need to discontinue due to severe hypersensitivity reaction

41
Q

Lamotrigine - Contraindications

A
  • Prior hypersensitivity to other anti-epileptic drugs
42
Q

Lamotrigine - Caution

A
  • Hepatic impairment - metabolised by liver
43
Q

Lamotrigine - Interactions

A
  • Carbamazepine, phenytoin, oestrogens, rifampicin –> reduce lamotrigine conc –> treatment failure
  • Valproate –> increase conc to rise –> toxicity
44
Q

Lamotrigine - Patient Education

A
  • try not to miss dose
  • do not stop treatment abruptly
  • Driving is prohibited unless they have been seizure-free for 12 months, and for 6 months after changing or stopping treatment.
45
Q

Levetiracetam - Indications

A

1) Epilepsy : seizure prophylaxis

2) Selected cases of established convulsive status epilepticus

46
Q

Levetiracetam - MOA

A
  • The molecular target of levetiracetam is synaptic vesicle protein 2A (SV2A).
  • SV2A is expressed throughout the brain, in both excitatory and inhibitory synapses, as a glycoprotein located within the membranes of synaptic vesicles.
  • It is presumably through interfering with synaptic vesicle function that levetiracetam modulates neuronal excitability and reduces the risk of seizures.
47
Q

Levetiracetam - Side Effects

A

Most people usually have none.

  • Drowsiness
  • Weakness
  • Dizziness
  • Headache

Rare:
- Suicidal ideation

48
Q

Levetiracetam - Caution

A
  • Renal impairment
49
Q

Levetiracetam - Interactions

A

Ver few

50
Q

Levetiracetam - Patient Education

A
  • try not to miss dose
  • do not stop treatment abruptly
  • Driving is prohibited unless they have been seizure-free for 12 months, and for 6 months after changing or stopping treatment.
51
Q

Benzodiazepine - Examples

A
  • Diazepam
  • Temazepam
  • Lorazepam
  • Chlordiazepoxide
  • Midazolam
52
Q

Benzodiazepine - Indications

A

1) Seizure & SE : 1st line
2) Alcohol withdrawal : 1st line
3) Sedation for interventional procedures
4) Anxiety or insomnia : short-term

53
Q

Benzodiazepine - MOA

A
  • Benzodiazepines are gamma-aminobutyric acid (GABA) receptor agonists. They enhance the binding of GABA to the GABA receptor
  • Benzodiazepine drugs increase the effects of GABA on your brain and body.
54
Q

Benzodiazepine - Side Effects

A
  • Drowsiness
  • Coma

Overdose:
- airway obstruction & death

Repeated:
- dependence

55
Q

Benzodiazepine - Contraindication

A

None

56
Q

Benzodiazepine - Caution

A
  • Elderly

Avoid in:

  • Resp impairment
  • Neuromuscular disease
  • Liver failure
57
Q

Benzodiazepine - Interactions

A
  • Additive with other sedating drugs - alcohol & opioids
  • CYP inhibitors - increase effects
  • -> (e.g. amiodarone, diltiazem, macrolides, fluconazole, protease inhibitors)
58
Q

CYP inhibitors

A
  • amiodarone
  • diltiazem
  • macrolides
  • fluconazole
  • protease inhibitors
59
Q

Benzodiazepine - Patient Education

A
  • Should not drive or operate complex or heavy machinery after taking the drug
  • caution them that sometimes sleepiness may persist the following day.
60
Q

Benzodiazepine - Monitoring

A
  • Pre-treatment: ECG, LFTs, U&Es

- Ongoing: LFTs, U&Es Monitor potential for addiction – lowest possible dose for the shortest time should be given

61
Q

Serotonin 5-HT1-receptor agonists - Examples

A

Sumatriptan

62
Q

Triptan - Indications

A

1) Acute migraine with or without aura

63
Q

Triptan - MOA

A

Triptans constrict cranial blood vessels and inhibit neurotransmission in the peripheral trigeminal nerve and in the trigeminocervical complex.

64
Q

Triptan - Side Effects

A

Common:

  • Pain or discomfort in the chest and throat
  • -> intense but resolve quickly
  • N & V
  • Tiredness
  • Dizziness

RARE: MI

65
Q

Triptan - Contraindications

A
  • Coronary Artery disease + Cerebrovasulcar disease due to its vasoconstrictor properties
  • Hemiplegic or basilar migraines
66
Q

Triptan - Caution

A

None

67
Q

Triptan - Interactions

A
  • Monoamine oxidase inhibitors (e.g. tramadol, SSRI, tricyclic antidepressants) increase the risk of serotonin toxicity
68
Q

Triptan - Patient Education

A
  • Can be taken with NSAIDs

- Only works when taken after the start of migraine (no preventative of an attack)

69
Q

Antiemetics, dopamine D2-receptor antagonists - Examples

A
  • metoclopramide

- domperidone

70
Q

Dopamine D2-receptor antagonists - Indications

A

Prohpylaxis & treatment of N & V

–> specifically regarding reduced gut motility

71
Q

Dopamine D2-receptor antagonists - MOA

A

+ First, the D2 receptor is the main receptor in the chemoreceptor trigger zone (CTZ), which is the area responsible for sensing emetogenic substances in the blood.
+ D2-receptor antagonists are therefore effective in nausea and vomiting caused by CTZ stimulation (e.g. by emetogenic drugs).

+ Second, dopamine is an important neurotransmitter in the gut, where it promotes relaxation of the stomach and lower oesophageal sphincter and inhibits gastroduodenal coordination.
+ D2-receptor antagonists therefore have a prokinetic effect, promoting gastric emptying, which contributes to their antiemetic action in conditions associated with reduced gut motility

72
Q

Dopamine D2-receptor antagonists - Side Effects

A

Common: Diarrhoea

-QT-interval prolongation & arrhythmias

73
Q

Dopamine D2-receptor antagonists - Contraindications

A

Should not be prescribed for more than 5 days.

Avoid:

  • neonates, children, young adults
  • Intestinal obstruction
  • perforation

Avoid metoclopramide:
- Parkinson’s disease

Avoid Domperidone:

  • cardiac conduction abnormalities
  • severe hepatic impairmentt
74
Q

Dopamine D2-receptor antagonists - Interaction

A
  • Increased SE with antipsychotics.
  • Avoid with dopaminergic agents for parkinson’s
  • Avoid with CYP inhibitors - increase SE.
75
Q

Antiemetics, Histamine H1-receptor antagonists - Examples

A
  • cyclizine
  • cinnarizine
  • promethazine
76
Q

Histamine H1-receptor antagonists - Indications

A

Prohpylaxis & treatment of N & V.

–> especially motion sickness or vertigo

77
Q

Histamine H1-receptor antagonists - MOA

A

Nausea and vomiting are triggered by gut irritation, drugs, motion and vestibular disorders, as well as higher stimuli (sights, smells, emotions).

  • The various pathways converge on a ‘vomiting centre’ in the medulla, which receives inputs from the chemoreceptor trigger zone (CTZ), & other centres.
  • Histamine (H1) and acetylcholine (muscarinic) receptors predominate in the vomiting centre and in its communication with the vestibular system.
  • Drugs such as cyclizine block both receptors.
  • This makes them useful treatments for nausea and vomiting in a wide range of conditions, particularly when associated with motion or vertigo.
78
Q

Histamine H1-receptor antagonists - Side Effects

A

Common: Drowsiness, dry throat and mouth.

  • After IV tachycardia, palpitations
79
Q

Histamine H1-receptor antagonists - Contraindications

A
  • Hepatic encephalopathy

- Prostatic enlargement

80
Q

Histamine H1-receptor antagonists - Interaction

A
  • Other sedative drugs (benzo , opioids)

- Ipratropium or tiotropium

81
Q

Antiemetics, serotonin 5-HT3-receptor antagonists - Examples

A
  • ondansetron

- granisetron

82
Q

Serotonin 5-HT3-receptor antagonists - Indications

A

Prohpylaxis & treatment of N & V.

–> especially in context of general anaesthesia and chemotherapy

83
Q

Serotonin 5-HT3-receptor antagonists - MOA

A
  • First, there is a high density of 5-HT3 receptors in the CTZ, which are responsible for sensing emetogenic substances in the blood (e.g. drugs).
  • Second, 5-HT is the key neurotransmitter released by the gut in response to emetogenic stimuli.
  • Acting on 5-HT3 receptors, it stimulates the vagus nerve, which in turn activates the vomiting centre.
  • Thus 5-HT3 antagonists are effective against nausea and vomiting as a result of CTZ stimulation (e.g. drugs) and visceral stimuli (gut infection, radiotherapy).
84
Q

Serotonin 5-HT3-receptor antagonists - Side Effects

A

SE are rare

  • Constipation
  • Diarrhoea
  • Headaches
85
Q

Serotonin 5-HT3-receptor antagonists - Contraindications

A

Avoid in pt with prolonged AT interval

86
Q

Serotonin 5-HT3-receptor antagonists - Interactions

A

Drugs that prolong the QT interval : antipsychotics, quinine, SSRI

APPLIED PHARMACOLOGY💊 (11 decks)

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