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

Migraine and HA (Pathophysiology) - Block 2 Flashcards

(52 cards)

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Patients often do not respond to treatment until overused medication is withdrawn: withdrawal symptoms and increased headache, followed by improvement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

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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?

Study These Flashcards
A

HA is from sx of sub-acute toxicity

23
Q

Population more affected by migraine?

24
Q

What constitutes a chronic migraine?

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A

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

25
How does migraines impact livelihood?
Significant effect on physical, social and occupational functioning
26
What are the sx of migraines?
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
What occurs during the prodrome stage?
Vague premonitory sx 12-36 hrs before aura: * yoawning * excitiation * depression * lethargy * craving or distate for certain foods
27
What are the phases of a migraine?
1. Prodrome 2. Aura 3. Mild 4. Moderate-severe HA 5. Postdrome
28
What is the aura stage?
Visual distrubances (flashing lights or zigzag lines) * Tunnel vision * Unilaterl paresthesis
29
What occurs durikng postdrome?
1. Fatigue 2. Depression 3. Inability to concentrate 4. Severe exhaustion
30
How is seratonin synthesized?
Dietary tryptophan
31
What is the function of seratonin?
1. Platelet aggregation and homeostasis 2. Perstalsis 3. Stimulates vomiting (5HT3) 4. Stimulates peripheral nociceptive nerve endings vis inflammatory mediators in migraines
32
How does seratonin affect the vasculature?
High seratonin = vasoconstriction in neuorvasculature Low seratonin = vasodilation and increased trigeminal nerve activation = pain or HA
33
What is the the function of 5HT1B?
Walls of blood vessels: activation leads to constriction of cerebral and dura arteries
34
What is the function of 5HT1D?
Presynaptic receptors: inhibit rlease of pro-inflammatory neuropeptides and reduce inflammation of vessles
35
WHat is the function of 5HT1F?
Presynaptic receptor: inhibit trigeminal nerve activation
36
What are the CGRP isoforms?
a-CGRP: peripheral NS b-CGRP: enteric NS
37
What is the function of CGRP receptor stimulation?
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
Where are CGRP receptors expressed?
1. Trigeminovascular system 2. Smooth muscle 3. Satellite glial cells
39
Decribe how CGRP differ from seratonin?
1. Poten vasodilator that has longer DOA
40
How does CGRP cause vasodilation?
Trigeminal nucleus activates -> release of vasoactive neuropeptides including CGRP and vascular terminals -> Vasodilation
41
CGRP levels **decrease/increase** in blood and saliva duing acute migraines?
Increase
42
What are examples of food triggers?
1. Alcohol 2. Caffeine 3. Chocolate 4. Fermented 5. MSG 6. Nitrates
43
What are examples of environmental triggers?
1. Flickering lights 2. High altitude 3. Loud noise 4. Strong smells 5. Smoke 6. Weather
44
What are examples of beharioral triggers?
1. Lack of sleep 2. Fatigue 3. Menstruation 4. Skipped meals 5. Physical activity 6. Stress
45
Describe the mechanisms that may cause migraine pain
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
Describe the MOA of migraines?
1. Arterial activation -> Vasoconstriction 2. Compensatory vasodilation -> pounding HA 3. Inflammation and TG nerve activation -> activation of CNS pain centers and worsening pain
47
HA that affects more males?
CLuster
48
HA that affects more females?
Migraines
49
Duration of cluster HA?
15-180 min
50
DUration of migraine?
4h - 3 days
51
Duraation of tension HA? ## Footnote `
30 min - 7 days

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