Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

PR3153 Midterms > IC5 > Flashcards

IC5 Flashcards

(58 cards)

Start Studying
1
Q

what is the SNOOP10 guide? list the guide

A

red flags for secondary headaches:
SN2O2P10
systemic symptoms eg fever
neoplasm (abnormal mass)
neurologic deficit/dysfunction
onset sudden or abrupt
old age >50y/o
pattern change
positional headache
precipitated by sneezing, coughing, exercise
papilledema
progressive w/ atypical presentation
pregnancy/puerperium
painful eye w/ autonomic features
post traumatic onset
pathology of immune system (HIV/immunocompromised)
painkiller overuse/new drug.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

history taking for headache

A

LOTAARRRP
location
onset
type
associated = any weakness, dizziness, FEVER?
recurring = frequency? quality
precipitating = exercise, sneezing, coughing? recent injury? painkiller use?

get history of painkiller use.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

distinguishing features of primary headache (tension-type)
include pain location ,type, intensity, QOL, other symptoms, duration

A

bilateral pain
tightening
mild-moderate
does not affect/affected by daily activities
no other symptoms
30min to 7 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

distinguishing features of primary headache (migraine)
include pain location ,type, intensity, QOL, other symptoms, duration

A

unilateral pain
throbbing
moderate-severe
affects/affected by daily activities
nausea/vomiting, sensitivity to light, sight, aura
4-72hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

distinguishing features of primary headache (cluster headache)
include pain location ,type, intensity, QOL, other symptoms, duration

A

unilateral pain
variable
severe-VERY severe
restless/agitation
cranial autonomic symptoms on the side of the headache (runny nose, congestion, watery/swollen/red eye)
15-180min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the clinical presentation of TTH?

A

NO premonitory symptoms and aura

bilateral

non-pulsatile tightness or pressure

mild-moderate

pericranial/cervical muscle tenderness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

ICHD3 classification for infreq ETTH?

A

frequency of atleast 10 headache episodes occuring on avg <1 day/month (<12days/year)

duration 30min-7 days

and any of the following:
1) two of the following:
- bilateral
- pressing/tightening non pulsatile
- mild-moderate
- not aggravated by routine phy activity

2) both of the following
- no N/V
- no more than one of photophobia/phonophobia

3) not better accounted for by another ICHD3 diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

ICHD3 classification for frequent ETTH?

A

frequency of atleast 10 headache episodes occuring on avg 1-14 days/month (12-180days/year)

duration 30min-7 days

and any of the following:
1) two of the following:
- bilateral
- pressing/tightening non pulsatile
- mild-moderate
- not aggravated by routine phy activity

2) both of the following
- no N/V
- no more than one of photophobia/phonophobia

3) not better accounted for by another ICHD3 diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

ICHD3 classification for CTTH?

A

frequency of ≥15 days/month on avg >3 months (≥180days/year)

duration hours to days, or unremitting

and any of the following:
1) two of the following:
- bilateral
- pressing/tightening non pulsatile
- mild-moderate
- not aggravated by routine phy activity

2) both of the following
- neither moderate or severe N/V
- no more than one of photophobia/phonophobia/mild nausea

3) not better accounted for by another ICHD3 diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

triggers for TTH?

A

physical emotional stress
activities where head is held in one position for a long time
alcohol
caffeine
cold/flu or sinus infections
dehydration
hunger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

TTH pathophysiology?

A

myofascial mechanisms? = due to head being in the same position for long?

vascular mechanisms? = increased or abnormal blood flow in the cerebral arteries

= both peripheral sensitisation

genetic disposition/polymorphism?

central mechanisms? = altered pain perception and dysfunction in descending pain modulation?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

goals of therapy for TTH?

A

pain relieve

prevent progression to chronic TTH

consider patient education to identify triggers, eg. a headache diary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

acute phx management for TTH?

A

paracetamol (alone or with caffeine)
aspirin
NSAIDs: ibuprofen, naproxen, diclofenac, ketoprofen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

prophylactic phx management for TTH

A

amitriptyline (1st line) (TCA)

mirtazapine, venlafaxine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

non phx management for TTH?

A

cognitive behavioural therapy, biofeedback, relaxation

physical and/or occupational therapy

lifestyle modification (include sleep hygiene)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

proposed phases (and duration) of migraine attack?

A

prodrome
- hours to days

aura
- 5-60min

headache
- 4-72 hours

postdrome
- <12-24h

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are some prodrome symptoms in migraine

A

fatigue
cognitive difficulties
mood changes
food cravings
neck pain
yawning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

aura symptoms in migraine

A

related to cortex and cortical spreading
- visual aura
- sensory and speech disturbance
- motor symptoms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

headache symptoms in migraine

A

nausea with or without vomitting
photophobia
phonophobia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

post-drome symptoms in migraine

A

tired or weary

difficulty concentrating

neck stiffness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

ICHD3 criteria for migraine without aura

A

A. At least 5 attacks fulfilling criteria B-D

B. Headache attacks lasting 4–72 hours (when untreated or unsuccessfully treated)

C. Headache has at least 2 of the following 4 characteristics:
1. Unilateral location
2. Pulsating quality
3. Moderate or severe pain intensity
4. Aggravation by or causing avoidance of routine physical activity (e.g., walking or climbing stairs)

D. During headache at least 1 of the following:
1. Nausea and/or vomiting
2. Photophobia and phonophobia

E. Not better accounted for by another ICHD-3 diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

ICHD3 criteria for migraine with aura

A

A. At least 2 attacks fulfilling criteria B-C

B. At least 1 of the following fully reversible aura symptoms:
1. Visual
2. Sensory
3. Speech and/or language
4. Motor
5. Brainstem
6. Retinal

C. At least 3 of the following 6 characteristics:
1. At least 1 aura symptom spreads gradually over ≥5 minutes
2. 2 or more aura symptoms occur in succession
3. Each individual aura symptom lasts 5–60 minutes
4. At least 1 aura symptom is unilateral
5. At least 1 aura symptom is positive
6. The aura is accompanied, or followed within 60 minutes, by headache

D. Not better accounted for by another ICHD-3 diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

ICHD3 classification for chronic migraine

A

≥15 monthly headache days (MHD)
≥8 monthly migraine days (MMD)
for >3 months

criteria for MMD
≥2 migraine characterics: unilateral, pulsating, mod/severe, aggravated by QOL
AND if no aura, ≥1 of following
- photophobia/phonophobia, N/V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

nonphx management of migraine

Study These Flashcards
A

patient education and empowerment
- identify triggers
- headache diary
- adopt a healthy lifestyle (regular eating, sleep, exercise habits).

25
acute treatment goals for headache
rapid, consistent freedom from pain and associated symptoms, without recurrence restored ability to function minimal need for repeat dosing/resuce meds optimal self care and reduced subsequent use of resources minimal or no adr cost-effective tx
26
what are the drugs with established efficacy for migraine
triptans ergotamine derivatives gepants lasmiditan nonspecific: NSAIDs (eg diclofenac, ibuprofen, naproxen), paracetamol+caffeine
27
principles for acute treatment of migraine | what to consider for tx of acute migraine, eg treatment plan?
acute treatment should be taken as early as possible. =should have significant beneficial response in 2h, 24h pain free sustained response, and reduced disabiltiy during attacks stratified approach by starting with simple analgesics. (parecetamol > nsaids > triptans) consider anti emetics with N/V symptoms choose appropriate dosage forms and formulation eg nausea exacerbated with water= choose orally disintegrating tablets eg severe n/v or full-blown symptoms = parenteral formulation
28
MOA of NSAIDs for migraine
inhibit prostaglandin synthesis = prevent subsequent neurogenically mediated inflammation in the trigeminovascular system.
29
indication for NSAIDs in migraine (and ones with established efficacy)
aspirin diclofenac ibuprofen naproxen celecoxib
30
adr of NSAIDs in migraine
hypersx, GI (dyspepsia, N/V/D), CNS (drowsy/dizzy)
31
c/i or caution for nsaid in migraine
previous PUD, renal disease, severe CVD, hypersx
32
triptans MOA
5ht1b and 5ht1d selective receptor agonist - vasoconstriction of intracranial extracerebral blood vessels - inhibit vasoactive peptide released by trigeminal neurons - inhibit nociception transmission within trigeminocervical complex.
33
C/I for triptans
stroke/TIA ischemic CAD coronary artery vasospasm uncontrolled HTN PVD GI ischemia history of hemiplegic/basilar migraine
33
how to use triptans for migraine
take early in course of attack pain intensity is mild if there is lack of response, switch to another triptan some patients experience recurrence within 48h = take an additional dose
34
ADR triptans
pressure on chest nausea fatigue distal paraesthesia
35
DDI for triptans
concurrnet ergotamine/ergot type medication within 24h concurrent MAOi or within 2 weeks of discontinuation of MAOi therapy (sumatriptan broken down by MAOi)
36
ergotamine MOA and locally available drug
local: ergotamine1mg/caffeine100mg ergotamine: 1) 5ht1b/1d on intracranial vessel vasoconstriction 2) inhibit NE uptake at alpha-adrenoreceptor = prolonged vasoconstriction (more concern with ischemic ADR) caffeine: adenosine A1, A2A, A2B receptor antagonist = vasoconstriction cerebral vasculature may also enhance GI absorption of ergotamine by increase solubility of ergotamine and decrease GI pH.
37
ADR of ergotamine
N/V cramps insomnia, transient lower limb muscle pain
38
Contraindications of ergotamine
stroke/TIA ischemic CAD coronary artery vasospasm uncontrolled HTN PVD GI ischemia history of hemiplegic/basilar migraine
39
DDI or ergotamine (and outcome)
concurrent triptans 24h potent cyp3a4 inhiibtors increases the risk for vasospasm = cerebral ischemia AND/OR schema of extremities
40
opiod use in migraine?
not recommended due to lack of evidence, risk of dependence/abuse/withdrawal syndrome
41
criteria for initiating gepants and ditans for migraine?
prescription from licensed clinician patients atleast 18 y/o diagnosis by ICHD3 migraine with aura, migraine without aura, chronic migraine. either of the following: contraindicated to/unable to tolerate triptans, inadequate response to ≥2 triptans.
41
criteria for medication overuse headache
occuring ≥15days/month in patients with pre-existing headacheh and developing as consequence of regular overuse of acute or symptomatic hradahce medication paracetamol or ≥1 nsaid on ≥15 days/month for >3 months triptan or ≥1 opioid on ≥10 days/month for >3months
42
criteria for preventive treatment
AHS guideline prevention should be offered if ≥6 MHD, no degree of disability ≥4 MHD, some degree of disability ≥3 MHD, severe degree of disability EHF guideline prevention offered if 1) migraine impairs quality of life AND either 2a) attack cause disability on ≥2 days per month and optimised acute therapy does not prevent the above 2b) risk of over frequent use of acute therapy and patient willing to take daily medication.
42
what is CGRP involvement in migraine?
CGRP neuropeptide rises during migraine episodes = contribute to inflammatory processes, neurogenic inflammation, blood flow in the cerebral (smooth muscle) blood vessels, and pain transmission
42
what are the antiCGRP therapies
gepants anti-CGRP antibodies anti-CGRP receptor antibodies
42
medications with evidence of efficacy for **preventive** migraine treatment
parenteral: eptinezumab, erenumab, fremanezumab, galcanezumab oral: heart drugs: candesartan, metoprolol, timolol, propanolol anti seizure: valproate sodium, divalproex sodium antimigraine: frovitriptan
43
what is the mechanism of action of gepants
CGRP receptor antagonists, which bind to CGRP receptor and prevent signalling
43
what is the mechanism of action of antiCGRP antibodies and examples?
prevent CGRP from interacting with the receptor includes monoclonal antibodies like eptinezumab and other -nezumab drugs.
44
what is the MOA of antiCGRP receptor antibodies and any examples?
bind to CGRP receptor and prevent signalling monoclonal antibody = erenumab
45
what are some ADRs of CGRP blockade (including clinically reported and animal studies)
clinically reported: GASTRO: constipation, nausea BLOOD: raynaud (decreased blood flow to finger), hypertension BONE: joint pain THROAT: nasopharyngitis. animal studies - delayed wound healing - block cardiopulmonary protective effect - decreased survival in sepsis model - bone loss - reproductive toxicity
46
studies on long term use of CGRP receptors?
unknown. may not want to use long term because effects are unknown?
47
role of CGRP in the body
endogenous CGRP has multiple protective roles in CNS, immune, skin, GI, bone, pregnancy, endocrine, cardiovascular.
48
criteria for initiating CGRP mABs
meet 1 and 2 + either 3-5 1) prescribed by licensed clinician 2) ≥18 y/o 3) diagnosis of ICHD3 migraine with or without aura + inability to tolerate/inadequate RESPONSE to 8 WEEK trial dose to the other meds/treatment (4-7MMDs) 4) - ICHD3 migraine with or without aura .... (MIDAS or HIT) 5) ICHD3 chronic migraine and... contraindication or inability to tolerate 2 or more oral triptans
49
what is the criteria for continuing CGRP mABs
either 1) reduction in mean MHDs or headaches of at least moderate severity of ≥50% relative to the pretreatment baseline 2) clinically meaningful improvement in any specific outcome measureMENTS eg MIDAS decrease ≥5pts if 11-20 by 30% if >20
50
principles for preventive treatment of migraine
4S 1O 1) start low and titrate - if there is partial but suboptimal response or dose limiting ADR= consider combining preventive drugs from diff classes. 2) reaching therapeutic dose - set initial target dose and stop titration once maximal dose reached, efficacy optimal, AE become intolerable. 3) set adequate trial - minimum 8 wks at target therapeutic dose before effectiveness can be determined = switch if no response after the 8 weeks. - min 3 months for **monthly** injectable cgrp dosing and 6 months for **quarterly** dosing. 4) set realistic expectations - define treatment success for the patient: 50% reduction in freq, significant decrease in attack duration? severity? improved response to acute treatment? reduction in disability and improve in QOL? psychological distress? 5) optimise drug selection and maximise adherence - tolerability, headache subtype, concomitant meds, weight, ease of use, contra VS patient preferences... comorbis, preg, response, cost, insurance coverage.
51
how to assess treatment efficacy
headache diary disability assessment eg MIDAS grade: 0-5, 6-10, 11-20, 21+ ADR
52
migraine pathophysiology in depth (relate to prodromal symptoms):
prodrome - neuropeptides, hypothalamus activation - hypothalamus affects homeostatic functions resulting in changes in appetite, fatigue.. aura - cortical spreading depression. - due to hyperexcitation (depolarisaiton wave that inhibits cortical actvity = reduced blood flow) followed by depression in brain activity. headache - CGRP invovlement = sensitisation of peripheral/central trigeminovascular system= pain prodrome - similar to prodrome.

PR3153 Midterms (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions