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Drug Action III > Migraine and HA (Pathophysiology) - Block 2 > Flashcards

Migraine and HA (Pathophysiology) - Block 2 Flashcards

1
Q

What is a sinus HA?

A

Caused by sinusitis, pain and pressure behind the eyes, along the nose and behind the cheeks

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2
Q

What is a tension HA?

A

Most common kind, caused by muscle contractions and described as tightening or constricting of the head

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3
Q

What is a cluster HA?

A

Unilateral, severe throbbing pain. Occurs in clusters, several days/week for 2 -3 months

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4
Q

What are the types of HA?

A
  1. Tension
  2. Sinus
  3. Cluster
  4. Migrain with or without aura
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5
Q

How does a HA occur if there are no pain receptors in the brain tissue?

A

Pain receptors are in:
* BV
* Mininges
* Scalp
* Skull

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6
Q

What are the contributing facotrs of chronic HA?

A
  1. Overuse or misuse of certain meds
  2. Other diseases (Depression, anxiety, sinus)
  3. Stress
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7
Q

What is a rebound HA?

A

Med Overuse HA: Chronic daily with regular overuse for > 3 months of ≥ 1 drug(s) that can be taken for acute and/or symptomatic treatment of headache

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8
Q

How is a rebound HA treated?

A

Headache developed or worsened during medication overuse

Patients often do not respond to treatment until overused medication is withdrawn: withdrawal symptoms and increased headache, followed by improvement

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9
Q

Describe the overuse thresholds by meds?

A
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10
Q

What is the most common primary HA?

A

Tension type HA

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11
Q

What are the features of tension HA?

A

Chronic head-pain syndrome:
1. Bilateral tight, bandlike discomfort (nonpulsating)
2. Mild – moderate intensity
3. Head pain without any accompanying features

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12
Q

What are the features of cluster HA?

A
  1. Deep, unilateral (periorbital or temporal)
  2. Excruciating, nonfluctuating, explosive pain
  3. Periodicity: happens at the same time every day
  4. Onset of attacks is nocturnal in 50% of patients
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13
Q

What are the the sx of cluster HA?

A

ipsilateral: conjunctival injection or lacrimation, aural fullness, eyelid edema, facial sweating, rhinorrhea or nasal congestion or cranial sympathetic dysfunction

  • Photophobia or phonophobia
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14
Q

What are the triggers of cluster HA?

A
  1. Alcohol
  2. REM sleep
  3. diurnal or annual cycles
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15
Q

What is SAH?

A

Subarachnoid hemorrhage: sudden onset of very sevee HA
* neck stiffness
* “thunderclap”

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16
Q

Sx of meningitis?

A
  • Generalized or frontal HA
  • Fever/neck stiffness, N, and disturbed consciousness
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17
Q

Sx of intracranial tumors?

A

Cardinal sx = epilepsy

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18
Q

Ex of life threatening HA?

A
  1. Subarachnoid hemorrhage
  2. Meningitis
  3. Intracranial tumors
  4. Primary angle closure glaucoma
  5. Idiopathic intracranial HTN
  6. Temporal arteritis
  7. Carbon monoxide poisoning
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19
Q

Sx of primary angle closure glaucoma?

A
  1. Rare before middle age
  2. Dramatic or episodic and mild, HA and eye pain
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20
Q

Sx of Idiopathic intracranial hypertension?

A

Raised intracranial pressure

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21
Q

Sx of temporal arteritis?

A

chronic inflammation of large and medium arteries of the head -> scalp tenderness

Sx persist worst at night

22
Q

How does carbon monoxide poisoning contribute to HA?

A

HA is from sx of sub-acute toxicity

23
Q

Population more affected by migraine?

A

Women
25-55YO

24
Q

What constitutes a chronic migraine?

A

≥8 migraine episodes/month and ≥ 15 HA days/month

25
Q

How does migraines impact livelihood?

A

Significant effect on physical, social and occupational functioning

26
Q

What are the sx of migraines?

A
  1. One side of head but can become bilateral
  2. Begins as dull ache, intensifies to severe pulsating pain
  3. Photophobia
  4. Phonophobia
  5. N/V
27
Q

What occurs during the prodrome stage?

A

Vague premonitory sx 12-36 hrs before aura:
* yoawning
* excitiation
* depression
* lethargy
* craving or distate for certain foods

27
Q

What are the phases of a migraine?

A
  1. Prodrome
  2. Aura
  3. Mild
  4. Moderate-severe HA
  5. Postdrome
28
Q

What is the aura stage?

A

Visual distrubances (flashing lights or zigzag lines)
* Tunnel vision
* Unilaterl paresthesis

29
Q

What occurs durikng postdrome?

A
  1. Fatigue
  2. Depression
  3. Inability to concentrate
  4. Severe exhaustion
30
Q

How is seratonin synthesized?

A

Dietary tryptophan

31
Q

What is the function of seratonin?

A
  1. Platelet aggregation and homeostasis
  2. Perstalsis
  3. Stimulates vomiting (5HT3)
  4. Stimulates peripheral nociceptive nerve endings vis inflammatory mediators in migraines
32
Q

How does seratonin affect the vasculature?

A

High seratonin = vasoconstriction in neuorvasculature
Low seratonin = vasodilation and increased trigeminal nerve activation = pain or HA

33
Q

What is the the function of 5HT1B?

A

Walls of blood vessels: activation leads to constriction of cerebral and dura arteries

34
Q

What is the function of 5HT1D?

A

Presynaptic receptors: inhibit rlease of pro-inflammatory neuropeptides and reduce inflammation of vessles

35
Q

WHat is the function of 5HT1F?

A

Presynaptic receptor: inhibit trigeminal nerve activation

36
Q

What are the CGRP isoforms?

A

a-CGRP: peripheral NS
b-CGRP: enteric NS

37
Q

What is the function of CGRP receptor stimulation?

A

Involved in trigeminal sensitization and migraine pathology

  • trigeminal ganglion is found outside the BBB, therefore therapeutic agents don’t need to cross the BBB
38
Q

Where are CGRP receptors expressed?

A
  1. Trigeminovascular system
  2. Smooth muscle
  3. Satellite glial cells
39
Q

Decribe how CGRP differ from seratonin?

A
  1. Poten vasodilator that has longer DOA
40
Q

How does CGRP cause vasodilation?

A

Trigeminal nucleus activates -> release of vasoactive neuropeptides including CGRP and vascular terminals -> Vasodilation

41
Q

CGRP levels decrease/increase in blood and saliva duing acute migraines?

A

Increase

42
Q

What are examples of food triggers?

A
  1. Alcohol
  2. Caffeine
  3. Chocolate
  4. Fermented
  5. MSG
  6. Nitrates
43
Q

What are examples of environmental triggers?

A
  1. Flickering lights
  2. High altitude
  3. Loud noise
  4. Strong smells
  5. Smoke
  6. Weather
44
Q

What are examples of beharioral triggers?

A
  1. Lack of sleep
  2. Fatigue
  3. Menstruation
  4. Skipped meals
  5. Physical activity
  6. Stress
45
Q

Describe the mechanisms that may cause migraine pain

A

Neurovascular process leading to the activity of the trigeminovascular system
* Vasoconstriction due to TG activation
* Released neuropeptides interact with dural BV -> vasodilation -> neurogenic inflammation
* Orthodromic conduction along TGV fibers transmits pain impulses to tTG nucleus caudalis then to higher cortical pain centers
* During migraine, seratonin and magnesium leves drop

46
Q

Describe the MOA of migraines?

A
  1. Arterial activation -> Vasoconstriction
  2. Compensatory vasodilation -> pounding HA
  3. Inflammation and TG nerve activation -> activation of CNS pain centers and worsening pain
47
Q

HA that affects more males?

A

CLuster

48
Q

HA that affects more females?

A

Migraines

49
Q

Duration of cluster HA?

A

15-180 min

50
Q

DUration of migraine?

A

4h - 3 days

51
Q

Duraation of tension HA?

`

A

30 min - 7 days

Drug Action III (23 decks)

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