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IPAP PHARM II TEST 3: HEADACHES QUESTIONS AND ANSWERS WITH SOLUTIONS 2024
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IPAP PHARM II TEST 3: HEADACHES QUESTIONS AND ANSWERS WITH SOLUTIONS 2024
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IPAP PHARM II TEST 3: HEADACHESQUESTIONS AND ANSWERS WITH
SOLUTIONS 2024
What is the difference between a primary and secondary headache? - ANSWER Without an underlying
cause (*primary* headache)
Secondary a distinct pathologic process (*secondary* headache)
What does it mean to *SNOOP* for secondary headaches? - ANSWER
Why go *SNOOP*ing? - ANSWER
What is the difference between a migraine headache *with* & *without* aura? - ANSWER (don't
memorize, just be aware)
Do migraines have a *definite genetic predisposition*? - ANSWER Yes!
~ 50 percent of cases of familial hemiplegic migraine (FHM) are caused by mutations within the
CACNL1A4 gene on chromosome 19 (don't memorize the gene)
What is an important mediator for headaches? - ANSWER *Serotonin (5-HT)*
Supported by observations of drugs that stimulate *5-HT1* receptors (e.g., triptans), antagonize *5-HT2*
receptors (e.g., methysergide), prevent *5-HT* reuptake (e.g., TCAs) or release (e.g., CCBs), or inhibit
brainstem serotonergic raphe neurons (e.g., valproate)
What is the *vascular hypothesis* (1938)? - ANSWER Migraine aura is caused by intracerebral arterial
vasoconstriction that is followed by a reactive extracranial vasodilation and an associated headache
Not completely supported by regional blood flow studies
,-In migraine with aura, there is modest cortical hypoperfusion (25 to 30 percent decrease) that is
insufficient to explain symptoms based on ischemia
-In migraine without aura, few patients demonstrate flow abnormalities
What theory explains the migraine aura? - ANSWER Migraine aura may be explained by the *neuronal
theory* in that the positive (e.g., light around the edges of the field of vision) and negative (e.g., blind
spots or tunnel vision) *symptoms of the migraine aura are caused by neuronal dysfunction, not
ischemia*
Migraine pain results from activity within what system? - ANSWER *Trigeminovascular system*
Activation of trigeminal sensory nerves triggers the release of vasoactive neuropeptides (calcitonin gene-
related peptide [CGRP], substance P, neurokinan A), which interact with dural blood vessels to produce
vasodilation and dural plasma extravasation leading to neurogenic inflammation
Activity within the trigeminovascular system may in part be regulated by serotonergic neurons
What are the 4 potential phases of a headache? - ANSWER 1. Premonitory symptoms
2. Aura
3. Headache
4. Resolution phase
What occurs in *phase 1*? - ANSWER *Premonitory symptoms*
What occurs in *phase 2*? - ANSWER *Aura*
Experienced by up to 31 percent
-64 percent do not experience an aura
, -18 percent experience an aura
-13 percent experience both aura/without aura headaches
Positive or negative visual *(most often)*, sensory, or motor symptoms that develop over 5 to 20
minutes and last for usually 60 minutes, with the headache usually following within 60 minutes
What occurs in *phase 3*? - ANSWER *Headache*
Most often occurs in the early morning hours on awakening
90 percent experience *nausea*; 1/3 will vomit
*Sensory hypersensitivity* results in subjects seeking a dark, quiet place
Generally begins with a *dull ache that intensifies* over a period of minutes to hours to a throbbing
headache, which *worsens with each arterial pulse*
*Often confused with tension-type headaches*
What occurs in *phase 4*? - ANSWER Fatigue, irritable, impaired concentration, scalp tenderness, mood
changes (e.g., refreshed and euphoric or malaise and depression)
What can trigger a headache? - ANSWER
What are the *most important attributes of a headache*? - ANSWER *Chronologic pattern and severity *
Pursue the seven key attributes of a symptom AKA *OLD CART*
*O*nset
*L*ocation
*D*uration
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