Headache Active Learning Flashcards

1
Q

What are the 3 main types of primary headache?

A

tension

cluster

migraine

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2
Q

What is hte most common type of primary headache? What is the most common one you’ll see in a primary care office?

A

tension headaches are most common overall, but migraines will predominate in-office

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3
Q

FOr tension headaches… age of onset? gender difference? other social factors?

A

under 40 yrs of age

women

increased with higher educational attainment

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4
Q

When do you consider tension headaches chronic?

A

when they happen every other day or more often

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5
Q

What is the pathophysiology behind tension headaches?

A

muscle contraction of neck and upper back

greater occipital nerve compression

irritation of nerve causing pain that starts in back and wraps around the sides like a headband

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6
Q

How will tension headahces present?

A
  • last 30 min to a week
  • pressing/tighening/constant pain (not throbbing)
  • mild to moderate intensity
  • bilateral
  • not aggreavated by routine physical activity
  • NO nausa or vomiting
  • can hav ephono or photphobia but not both
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7
Q

True or false: physical therapy is very effective at eliminating tension headaches.

A

false

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8
Q

Who is at higher risk for cluster headaches?

A

young males

male: female is 4:1

mean age of onset is 27-31

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9
Q

What do they think causes cluster headache?

A

posibly hypothalamic activation of the trigeminovascular autonomic system, innervating the dura and cerebral vasculature and other targets

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10
Q

What is the clinical presentation for a cluster headache?

A

severe, unliteral orbital/supraorbital/temporal pain lasting 15-180 minutes

circadian periodicity

frequency is every other day to 8/day during a cluster

associated with autonomic symptoms: lacrimation, nasal congestion, rhinorrhea, forehad sweating, miosis, ptosis, eyelid edema, conjunctival injection

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11
Q

What is the treatment for cluster headches?

A

Oxygen at high levels thorugh a nonrebreathing mask for 15 minutes

triptan medications - SUBQ OR NASAL - oral won’t reach high enough plasma levels to be effective in the amount of time the headache lasts

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12
Q

WHo gets migraines most often?

A

females (3 to 1)

onset before 40 yrs of age

prevalence is 18% in women and general lifetime prevalence is 25%

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13
Q

What are some theories as to the cause of migraines?

A

spreading cortical depressoin

possible neurotransmitter dysfunction (NO or CGRP)

Dorsal pontine activation

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14
Q

What is the typical clinical presentation for a migraine headache?

A

gradual onset..

can be associated with aura first, sometimes photophobia, and phonophobia

intermittent, unilateral throbbing headache lasting hours to days. Can generalize to both sides if not treated

nausea and vomiting often

exacerbated by activity - typically makes normal daily life impossible

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15
Q

True or false: there is no genetic component to migraines.

A

false

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16
Q

What should you really thinking about in a young sexually active women with migraines + aura?

A

If they’re on an estrogen-containing birth control, they’re at higher risk for stroke

17
Q

What affect might Viagra have on migraines?

A

if a guy already has migraines, taking viagara may increase the risk of a migraine attack occurring

18
Q

What is the first line of drugs for the treatment of migraine attacks?

A

triptans or DHE if those don’t work

also antiemetics - perchlorperaxine or metoclopramide

aspirin, ibuprofen and naproxen may be helpful

desamethasone

19
Q

What is the counterintuitive effect over extensive medication use in migraine treatment?

A

frequent use of OTC analgeis, triptans, and opioids significantly increase the risk for medication overuse headache

20
Q

What medications are best for prophylactic medications in migraine headache treatment?

A

amitriptyline

divalproex sodium

propanalol beta blockers

timolol

21
Q

What neurotransmitter is largely targetted in treatment of migraine headaches?

A

serotonin

22
Q

How is 5HT synthesized, stored and metabolized?

A

made from tryptophan

stored in vesicles at pre-synaptic terminal

brought back in thorugh a reuptake transporter and broken down by MAO

23
Q

WHere else does 5HT work esides the CNS?

A

in the GI tract

its produced and stored in enterochromaffin cells of gastric mucosa and will be released in response to mechanical stretch from eating

metabolized by MOA in the liver

24
Q

In the vascular system, what does 5HT do?

A

it produces vascoconstriction of the cerebral vasculature and splanchnic/renal/pulmonary vasculature

25
Q

Which 5HT receptors are targeted for migraine treatment?

A

5HT 1B and 1D

26
Q

What happens to 5HT levels as a trigger for migraine?

A

increases - so it starts with vasoconstriction

27
Q

Are migraine treatments 5HT receptor agonists or antagonists? Why is this weird?

A

agoanists - weird because a spike in sterotonin was the trigger for the migraine

28
Q

What ion channels are affected by 5HT 1Ba nd D receptors and what does this mean for the membrane?

A

activates K+ channels

inhibits Ca2+ channels

this means the membrane becomes hyperpolarized

29
Q

If Tritans are 5HT 1b and 1d receptor agonists, what do they do?

A

they cause vasoconstriction

autoregulation

and decreased release of pro-inflammatory neuropeptides

30
Q

What are the general pharmacokinetics of triptans?

A

metabolized by MOA

1-3 hour half-life

urinary and fecal excretion

31
Q

When woul dyou NOT want to prescribe triptans and why?

A

In cariovascular disease, uncontrolled HTN, current use of Ergots, liver disease

vascular stuff because it increases risk of stroke or heart attack due to the vasoconstrictive/vasospasmic effects

32
Q

How does Ergot work in treatment of migraines? Why are they given less often?

A

same way as the triptans - agonist for the 5HT 1B and 1D receptors

not used as often because they can cause severe nausea and vomiting

33
Q

Why do you need to be careful about drug interactions with Ergots like DHE?

A

It is metabolized by the CYP3A4 pathway in the liver, so if they’r eon drugs that reduce this, ergot iwll build up to dangerous levels quickly

34
Q

What are the headache red flags for life threatening underlying causes?

A

sudden onset of severe thunderclap headache = subarachnoid

headache with exercise = ruptured aneurysm

new HA onset after age 50 = temporal arteritis or mass

HA with fever, nucla rigidity, etc = meningitis

HA onset hours to weeks after trauma = subdural

HA with focal neurological signs, papilledema = tumor, subdural, epidural

multiple people with similar new onset HA = environmental exposure like CO

35
Q

Wheen do you order neuroimaging in headche?

A

with focal neuro exam findings

abrupt onset of headaches

change in character/intensity/frequency

Tx failure

36
Q
A