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B33CNS > Migraine and Emesis (Prof Fone) > Flashcards

Migraine and Emesis (Prof Fone) Flashcards

1
Q

What is a migraine?

A

Painful, pulsating headache
4h - 3 days
Unilateral (affects one side of head) and associated photophobia.
7% men and 17% women have experienced a migraine in a year
Prevalence peaks in middle age

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2
Q

What is the incidence of migraine?

A

Women : Men 3.5:1
Episodic
16% of menstruating females

£1.5bn per anum cost in missed work or school.
No affect on life expectancy.

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3
Q

What is the symptomology of migraine?

A

Prodrome = yawning, mood or appetite change

  1. Aura - initial visual disturbances (30 min)
  2. Unilateral throbbing headache (4-72h)
    photophobia, nausea and vomiting prostrate
  3. Resolution - deep sleep and loss of headache
  4. Recovery - often get exhaustion
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4
Q

What is the dominant inherited disorder that can cause migraine?

A

Familial hemiplegic migraine (with aura)

Autosomal disorder

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5
Q

What is the most common point mutation that can cause genetically linked migraine disorder?

A

Point mutation in CACNA1A gene that encodes the pore forming alpha1A subunit of the P/Q voltage gated calcium channel.

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6
Q

Which mutation in potassium channel in spinal neurones is associated with common migraine?

A

TRESK K2P potassium channel in spinal neurones

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7
Q

What is the pathophysiology of migraine?

A

Multiple theories

Original theory =Vascular Origin (1940s)

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8
Q

What is the series of events in the Vascular Origin theory on the pathophysiology of migraine?

A

Humoral disturbances that lead to an abnormal cerebral blood flow

This leads to vascular disturbance; firstly this causes intracerebral vasoconstriction and aura, secondly this causes extracerebral vasodilatation and headache.

Blood flow doesn’t change in common migraine.

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9
Q

What is associated with the Cortical Spreading Depression theory?

A

A neuronal origin rather than vascular
Blood flow change does not correspond to intracranial artery distribution.
Vasoconstriction spreads from posterior of one hemisphere = neural mediation
May be the cause of aura but not the migraine

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10
Q

What is the pathophysiology of aura?

A

The aura usually involves a wave of electrical activity starting in the occipital cortex and spreading slowly. This is associated with visual hallucinations across the visual field that is reproducible in the same individual.

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11
Q

What is the Sensory Nerve theory of migraine cause?

A

Migraine = Enhanced Trigeminovascular Neuron Activity
The trigeminal nerve innervates, forehead, cheek, eye and lower face.
Neuronal activation is triggered in migraine.

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12
Q

How are migraines diagnosed?

A

No definitive test or diagnosis
Careful assessment of patient and history
Elimination of causes i.e. trauma or other drugs or rare disorders.

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13
Q

How are migraines classified according to the International Classification of Headache Disorders?

A

A At least 5 attacks fulfilling criteria in B - D
B Headache attacks lasting 4-72hours
C Headache has atleast two of the following criteria; unilateral, pulsating, moderate/severe pain, aggravation by or causing avoidance or daily routine
D nausea and vomiting OR photo/phonophobia
E Not attributed to a different disorder

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14
Q

What is the use in Migraine Diaries?

A

Encourage patients to record details of migraine attacks so that doctors can make a firm diagnosis, recognising warnings and triggers, assessing whether acute or preventative measures are working

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15
Q

What is recorded in Migraine Diaries?

A

When the pain begins and frequency
Symptoms
Length of attacks
Pain location and whether throbbing or piercing

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16
Q

How can a Migraine Diary be recorded with most effect?

A

Diet, medication, vitamins, health products, exercise, sleep duration, menstrual cycle.

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17
Q

What can be triggers to migraines?

A 
Stress
Refractory errors in glasses
Chocolate, eggs or fruit
Alcohol
Oral contraceptives
Time zone shifts
Physical exertion
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18
Q

What are the goals in migraine treatment?

A

Provide acute relief to recurrent attacks

Introduce effective prophylactic treatment

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19
Q

What is ‘Step 1’ in treating mild / occasional attacks?

A

Acute Tx = analgesics / NSAIDs and anti-emetics if nausea is a problem.
Most effective if taken early in the attack
GP can add an anti-emetic; domperidone, metoclopramide to enhance absorption as they accelerate gastric emptying.
Combine with rest and sleep.

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20
Q

What is ‘Step 2’ in treating mild / occasional attacks?

A

Triptans (sumatriptan, zolmitriptan etc) 5-HT1B and 5-HT1D receptor agonists. They cause constriction of cranial blood vessels and subsequently inhibition of neuropeptide (CGRP) release.
Cardiovascular risks
Available OTC 18-65 y/os
Short acting and poor CNS penetration
Chest pain, contraindicated in ischaemic heart disease
Will not prevent aura during the attack

(CGRP receptor antagonist in development)

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21
Q

What prophylactic / preventative migraine therapy is available?

A

Avoid known triggers such as stress or dietary factors.
B-blockers (propanalol, metoprolol) CCB (flunarizine) anticonvulsants (valproate, topiramate - caution pregnancy) or pre-menstrual oestrogen can be effective.

Acupuncture or gabapentin in treatment resistant cases

22
Q

What is emesis?

A 
a.k.a. vomiting 
Protective reflex (to expel ingested toxins) shown in man and most meal-feeding animals and is associated with nausea.
23
Q

What is nausea?

A

An unpleasant sensation that immediately precedes vomiting.
A cold sweat, pallor, salivation, self absorption, loss of gastric tone, duodenal contractions and reflux of intestinal contents into the stomach often accompany nausea.

24
Q

What is vomiting?

A

Co-ordinated involuntary reflex involving powerful, sustained contraction of the abdominal, chest wall and diaphragm muscles (greatly increases gastric pressure).
Opening of the cardioesphageal sphincter, glottis and jaw.
Rapid evacuation of the stomach contents up and out of the mouth.

25
Q

What prevents inhalation of vomit?

A

Breathing is suspended but at the same time the epiglottis closes over the trachea to avoid inhalation of vomit

26
Q

What is retching?

A

Incomplete reflex, when sphincter does not open and nothing is ejected; a preliminary phase to vomiting.

27
Q

Where is emesis controlled from?

A

The vomiting centre; functionally related group of neurones in the medullary reticular formation.

28
Q

What causes the motor components of the vomiting reflex?

A

Iatrogenic (chemotherapy, radiotherapy, opiates, antibiotics)
Motion sickness and Meniere’s disease (disorder of iddle ear)
Pregnancy
Poisoning e.g. ethanol
Gastroenteritis and stimulation of the pharynx
Meningitis and intracranial hemorrhage
Bulimia nervosa

29
Q

Which receptor is initially triggered in the vomiting centre?

A

The chemoreceptor trigger zone (CTZ) at base of 4th ventricle
Dopamine, serotonin, opioid and acetylcholine receptors

30
Q

What is the major output transmitter from the CTZ?

A

Neurokinin (substance P)

31
Q

Where are blood chemicals detected?

A

Area postrema

32
Q

What system plays a major role in motion sickness?

A

Vestibular system via vestibulocochlear (8th cranial nerve)

Muscarinic cholinergic and histamine receptors.

33
Q

What nerves are involved in the gag reflex?

A

Vagal nerve afferents activated when the pharynx is irritated leads to gag reflex
5-HT3 and NK1 receptors

34
Q

What do the gastrointestinal afferents do in emesis?

A

Gasterointestinal afferents respond to irritation of gastric mucosa by chemo, radiation, distention, acute gastroenteritis
Gut 5HT3 receptors

35
Q

What causes vomiting associated with psychological causes?

A

Descending inputs from higher centres - arise from sight or smell of vomit, association with vomit or psychiatric disorders.

36
Q

How and why can vomiting be induced?

A

If poisons swallowed; poison likely to still be in the stomach and the patients respiratory reflexes are not impaired i.e. the patient won’t inhale vomit.

37
Q

What anti-emetic can be swallowed to induce vomiting?

A

Ipecacuanha which directly activates the CTZ.

38
Q

Which 5-HT3 antagonists can be used as anti-emetics?

A

Ondansetron, granistron

39
Q

Which corticosteroids can be used as anti-emetics?

A

Dexamethasone

Eicosanoid synthesis inhibition

40
Q

Which NK1 antagonists can be used as anti-emetics?

A

Neurokinin 1
Aprepitant
Casopitant

41
Q

Which dopamine D2 antagonists can be used as anti-emetics?

A

Metoclopramide, domperidone, haloperidol

42
Q

Which anti-cholinergics can be used as anti-emetics?

A

Scopolamine

43
Q

Which anti-histamines can be used as anti-emetics?

A

Cinnarizine

44
Q

What can be used for vertigo nausea?

A

Betahistine

H3 antagonist

45
Q

Which cannabinoid agonists can be used as anti-emetics?

A

Nabilone

46
Q

How does olanzapine act as an anti-emetic?

A

Multiple receptor targets - dopamine, 5HT and muscarinic antagonist

47
Q

What is the best single agent therapy?

A

MK1 antagonism
APREPITANT
Because substance P is the major output transmitter from the vomiting centre and so by antagonising and stopping substance P, it is active against most causes of vomiting.

48
Q

What should be used to treat motion sickness?

A

H1 and H3 antagonists

49
Q

How can sickness be treated in chemotherapy?

A

Combination of corticosteroid and dopamine antagonist

OR 5HT3

50
Q

Why is nausea hard to treat?

A

Associated with higher centres and is partly learned or associated response rather than physiological

51
Q

How can some patients be resistant to all anti-emetics?

A

Due to a variant of 5-HT receptor.

B33CNS (20 decks)

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