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AGPCNP Board Prep > Ch8: Headaches > Flashcards

Ch8: Headaches Flashcards

1
Q

what is a primary headache

A

not associated with other diseases

likely a complex interplay of genetic, developmental, and environmental risks

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2
Q

(3) most common types of primary headaches

A
  • migraine
  • tension-type
  • cluster (less common)
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3
Q

what is a secondary headache

A

associated with or caused by other conditions, generally will not resolve until the specific cause is diagnosed and addressed

e.g., tumor, intracranial bleeding, increased intracranial pressure, use of select medications, meningitis, accelerated HTN, giant cell arteritis, acute sinusitits, viremia, etc.

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4
Q

most common (2) secondary headache causes seen in primary care

A
  • viremic (e.g., with the flu)
  • acute sinusitis

both are usually self-limiting

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5
Q

SNOOP mnemonic for red flags with headache

A

S - systemic symptoms (e.g., fever, unintended weight loss), secondary headache risk factors (e.g., >180/120, on anticoagulation)

N - neurologic signs (new-onset confusion, impaired alertness, nuchal rigidity, papilledema)

O - onset sudden or abrupt

O - onset age (>50yo)

P - prior headache history (change in quality or frequency), positional (worse with lying down), papilledema

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6
Q

only (2) neuro signs that are NOT red flags in headache presentation

A

photophobia, phonophobia

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7
Q

thunderclap headache, worry about…..

A

intracranial (subarachnoid) hemorrhage

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8
Q

headache that is worse with lying down, and worst in morning when waking up. worry about…..

A

increased intracranial pressure

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9
Q

how will papilledema usually present symptomatically

A

black spot in the middle of vision

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10
Q

acute headache with new onset neuro changes, what is your role as generalist NP?

A

send to ER

you won’t be the one ordering imaging because you can’t manage that acute care in primary care setting

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11
Q

giant cell arteritis, aka….

A

temporal arteritis

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12
Q

etiology of giant cell arteritis, generally

A

auto-immune

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13
Q

treatment for giant cell arteritis

A

co-managed with neurology

prednisone 60-80mg QD until inflammation is under control, and then systemic corticosteroids are continued for 6 months up to 18 months

while work-up and specialist consult is in the book, get them started on the high dose steroids

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14
Q

priority complication of giant cell arteritis, if untreated

A

blindness

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15
Q

at least ___% of people with giant cell arteritis will have a transient change in vision that will become permanent if not treated

A

50%

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16
Q

NSAIDs and corticosteroids, risk for ____ ulcers

A

gastric ulcers

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17
Q

most common med class to prevent NSAID and steroid-induced gastropathy

A

PPIs

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18
Q

H. pylori causes ____ ulcers

A

duodenal

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19
Q

long term use of systemic corticosteroids is prescribed for giant cell arteritis dx in older woman. what (2) medications should you consider to prevent sequela?

A
  • daily PPI to prevent gastritis/gastric ulcer

- bisphosphonates to counter bone loss

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20
Q

treatment for cluster headache

A

100% o2 inhaled

21
Q

headache associated with BP >180/>120. worry about….

A

intracranial hemorrhage

22
Q

headache unlikely to be caused by HTN unless the BP is above…..

A

> 180 / >120

23
Q

characteristics of TENSION headaches

A
  • lasts 30min - 7 days (typically 1-24hrs)
  • two or more of the following characteristics
    + pressing, non-pulsatile pain
    + mild to moderate intensity
    + usually bilateral
    + one or less of: nausea, photophobia, phonophobia

female:male ratio = 5:4

24
Q

characteristics of MIGRAINE headaches WITHOUT AURA

A
  • lasts 4-72 hrs
  • two or more of the following characteristics:
    + usually unilateral
    + pulsating quality
    + moderate to severe in intensity
    + aggravated by normal activities (e.g., walking)
  • during the headache, there are one or more of: nausea, vomiting, photophobia, phonophobia
  • positive family history in 70-90%

female:male ratio = 3:1

25
Q

characteristics of MIGRAINE headache WITH AURA

A

same symptoms as migraine without aura, except symptoms begin with or after aura onset

aura is caused by focal dysfunction of cerebral cortex or brain stem that causes 1 or more aura symptom developing over 4 minutes or in succession

symptoms include:

  • feeling dread or anxiety
  • unusual fatigue
  • unusual nervousness or excitement
  • GI upset
  • visual changes
  • olfactory alterations

no aura symptoms should last >1 hr

26
Q

aura symptoms typically last _____, no longer than ______

A

typically 20 min

no longer than 1 hr

27
Q

characteristics of CLUSTER headache

A
  • tends to occur daily in groups or clusters
  • clusters themselves last several weeks to months, then disappear for months to years
  • may occur at characteristic times of year such as vernal and autumnal equinox with 1-8 episodes/day, at the same time of day
  • most common time of day is 1 hr into sleep, described as “alarm clock headache” because the pain awakens person
  • headache is often located behind 1 eye with steady, intense pain (“hot poker in the eye”) sensation, severe pain in a crescendo pattern
  • pain episodes last 15 minutes to 3 hours, most commonly 30-45 minutes
  • pain is severe
  • may have ipsilateral autonomic signs such as lacrimation, conjunctival injection, ptosis, or nasal stuffiness

female:male ratio = 1:3 to 1:8

family history present in 20% of cases

28
Q

common triggers for primary headaches

A
  • chocolate
  • alcohol
  • certain cheeses
  • monosodium glutamate (MSG)
  • artificial sweeteners (e.g., aspartame)
  • perfume
  • stress
  • too much or too little sleep
  • altered routine
  • hunger
29
Q

OTC analgesics for the treatment of primary headaches

A
  • NSAIDs and acetaminophen most commonly
  • best effects if taken at headache onset
  • limit use to 2 days/week to avoid rebound headache
  • use WITH triptans for optimal relief
30
Q

limit use of NSAIDs and acetaminophen to _______ to avoid rebound headache syndrome

A

max 2 days/week

31
Q

migraine abortive prescription therapies

A
  • triptans (selective serotonin receptor agonists)
  • ergot derivatives (e.g., dihydroergotamine nasal spray or injection)
  • consider antiemetics PRN. consider opioids or systemic corticosteroids for severe symptoms refractory to first line therapies

Notes:

  • best effect if taken at onset of headache
  • do not use in pregnancy, CVD disease, poorly controlled HTN d/t vasoconstrictive effects
  • can also be used in tension and cluster headaches non-responsive to first-line therapies
32
Q

migraine preventive prescription therapies (5) classes

A
  • beta blockers (propanolol, metoprolol)
  • TCAs (amitriptyline, nortriptyline)
  • anticonvulsant drugs (divalproex sodium, valproate sodium [Depakote], topiramate [Topamax])
  • calcitonin gene-related peptide (CGRP) antagonists (monoclonal antibodies ending in –mab)
  • supplemental butterbur, feverfew, coenzyme Q10, magnesium, riboflavin

note: CCBs are old-school, used to be used, are NOT recommended and no longer considered effective

33
Q

nutritional supplements that can be used for migraine prevention (5)

A
  • butterbur
  • feverfew
  • coenzyme Q10
  • magnesium
  • riboflavin (B2)
34
Q

most common test performed in acute severe headache with new-onset abnormality on the neuroimaging, send to ER for this

A

CT without contrast

35
Q

CT without contrast is capable of revealing…..

A
  • acute or chronic hemorrhage, regardless of etiology

- stroke

36
Q

CT with contrast is capable of revealing….

A
  • tumor

- abscess

37
Q

MRI is capable of revealing…..

A
  • tumor

- best for soft tissues

38
Q

(4) reasons for generalist NP to refer to a specialist (across body systems)

A
  1. requires a service the NP cannot provide or is beyond scope (e.g., needs a cholecystectomy so refer to a surgeon)
  2. a diagnosis that needs support or clarification by specialist (e.g., suspected autoimmune condition like RA or SLE)
  3. has an already-diagnosed health condition which needs ongoing input from a specialist (e.g., CHF, angina pectoris)
  4. fails to respond to standard first-line therapies (e.g., low back pain failed to respond to first line analgesics and PT)
39
Q

what is jaw claudication

A

pain in the jaw with chewing

40
Q

best FIRST test with suspected giant cell arteritis

A

ESR

ESR >100 mm/hr before biopsy is warranted

41
Q

ESR result that would warrant temporal artery bx in suspected giant cell arteritis

A

> 100 mm/hr

42
Q

definitive test for giant cell arteritis

A

arterial biopsy, done by a specialist

43
Q

management of suspected giant cell arteritis by the generalist NP

A
  • draw labs including ESR (>100, suspicious)
  • refer to neuro for arterial bx to confirm
  • in the interim, start on HIGH DOSE systemic corticosteroids (1-2mg/kg/day prednisone) until stabilized
  • anticipatory guidance that they will likely remain on lower-dose systemic steroids for 6 months - 2 years to prevent remission
  • consider starting aspirin to reduce stroke risk
  • consider GI protection with long-term steroid use such as a PPI
  • consider bone-protection such as bisphosphonates with long-term steroid use
44
Q

what is giant cell arteritis

A
  • autoimmune
  • vasculitis that affects the medium- and large-sized vessels including the temporal artery
  • inflammation and swelling of the arteries leads to decreased blood flow and associated symptoms
  • most commonly occurs in women 50-85yo
  • often seen comorbid to polymyalgia rheumatica
45
Q

giant cell arteritis (temporal arteritis) is commonly comorbid with…..

A

polymyalgia rheumatic (PMR)

46
Q

clinical presentation of giant cell arteritis

A
  • tender or nodular vessel, usually the temporal artery
  • pulseless vessel (d/t constriction)
  • accompanied by severe, unilateral headache
  • 50% will experience visual impairment including transient visual blurring, diplopia, eye pain, or sudden loss of vision
47
Q

how is giant cell arteritis diagnosed

A
  • ESR and CRP usually markedly elevated (ESR >100)
  • refer for arterial biopsy
  • color duplex US can be used to complement bx or as alternative
48
Q

common dietary triggers for migraines

A

…… refer to a nutritionist!

  • sour cream
  • ripened cheeses (e.g., cheddar, stilton, brie, camembert)
  • sausage, bologna, salami, pepperoni, summer sausage, hot dogs
  • pizza
  • chicken liver and pate
  • herring (pickled or dried)
  • any pickled, fermented, or marinated food
  • MSG commonly found in soy sauce, meat tenderizers, and seasoned salt
  • freshly-baked yeast products including sourdough bread
  • chocolate
  • nuts and nut butters like peanut butter
  • broad beans, lima beans, fava beans, snow peas
  • onions
  • figs, raisins, papaya, avocado, red plums
  • citrus fruits
  • bananas
  • caffeine (tea, coffee, cola, energy drinks)
  • alcohol
  • aspartame, phenylalanine-containing products
49
Q

possible lifestyle triggers for migraines

A

…. in general, people with chronic primary headaches have less issues when maintaining a regular schedule of sleep, nutrition, hydration, and exercise

  • menses, ovulation, or pregnancy
  • illness of any kind
  • intense or strenuous exercise
  • altered sleep patterns
  • altered eating patterns including fasting or missing meals
  • bright lights/flickering lights
  • excessive or repetitive noises
  • odors, fragrances, tobacco smoke
  • weather, seasonal changes
  • high altitudes
  • medications including SSRIs, SNRIs, analgesic overuse, hormonal contraception, MHT
  • stress

AGPCNP Board Prep (21 decks)

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