Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Year 1: Patho/Pharm > Head Aches Patho > Flashcards

Head Aches Patho Flashcards

(55 cards)

Start Studying
1
Q

4 Types of Primary Head Aches

A
  1. Tension
  2. Migraine
  3. Cluster
  4. Medication overuse head ache
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Treatment Primary Head Aches

A
  1. Abortive therapy
    - non-specific
    - specific
  2. Preventative therapy
  3. Non pharmacological therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Tension Type Head Aches
Incidence, prevalence

A

Most common type of head ache
10-19 years
men = women

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

Tension Type Head Aches
Clinical S&S

A

Onset: gradual

Severity: mild to moderate

Quality: Tight band, bilateral, pressure, steady

Location: variable, usually temporal

Duration: hours to days

*Not aggravated by physical activity

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

Two types of tension type head aches

A
  1. Episodic
    < 15 days per month
  2. Chronic
    >/= 15 days per month for 3 months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Abortive Treatment
Tension Type Head Aches

A
  1. Non-Specific
    - Tylenol
    - NSAIDS
    - Ice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pathophysiology
Tension Type Head Aches

A

NOCICEPTORS and MUSCLES

  1. Hypersensitivity trigeminal nerve nociceptors
    - chronic
  2. Hypersensitivity myofacial sensory nerves
    - episodic
    - peri-cranial muscles

*NOT due to vasoconstriction
*TRIPTANS do not work

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

MOA
Abortive Treatment
Tension Type Head Ache

A

NSAIDS
Acetaminophen
Ice

  1. NSAIDs
  • block COX (periphery, central)
  • prevent formation prostaglandins
  • prostaglandins = fever (central)
  • prostaglandins = chemotaxis WBC
  • prostaglandins = vasodilation, vascular permeability -> edema, erythema, activation nociceptors
  1. Acetaminophen
    - block COX (central)
    - prevention fever and central pain
  2. ICE
    - Blocks pain signal? (see non pharm section)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Preventative Treatments
Tension Type Head Aches
Examples

A
  1. Tri-cyclic anti-depressants
  2. Serotonin norepinephrine reuptake inhibitors
  3. Tetracycline anti-depressants
  4. Botox
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Examples
Preventative Treatments
Tension Type Head Aches

A

Tricyclic anti-depressants
- Nortriptyline
- Amitriptyline

Serotonin norepineprhine reuptake inhibitors
- venlafaxine

Tetracycline anti-depressants
- mirtazapine

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

MOA
Preventative Treatments
Tension Type Head Aches

A

TCA
- Tri cyclic anti-depressants
- inhibit reuptake of NE and 5HT

SNRI
- serotonin norepinephrine reuptake inhibitors
- Inhibit reuptake of NE and 5HT

Tetracycline anti-depressants
- Increase release of serotonin and NE by inhibiting pre-synaptic receptor

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

Contraindications
Drug-Drug Interactions
TCA, SNRI, Tetracycline anti depressants

A

*All drugs increase serotonin and NE

Serotonin syndrome and hypertensive crisis

  • do not combine with
  • MAOinhibitors
  • Triptants
  • SSRIs
  • Together

Sedation

  • Do not combine with CNS sedating drugs (alcohol, benzodiazepines, phenobarb, etc.)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

SE
TCA

A

Tricyclic Antidepressants
- amytriptyline
- nortriptyline

MOA
- increase HT and NE by blocking reuptake
- *light effect on DA

SE
- ANTI CHOLINERGIC: dry mouth, urinary retention, constipation, gluacoma, sedation
- CARDIOTOXIC - dysrhythmias, conduction blocks
- SUICIDE

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

Prescribing considerations before starting TCA

A

ECG
- evaluation for bradycardia, branch blocks, dysrhythmias

TCAs can cause these
they are cardiotoxic

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

SE
SNRIs

A
  • better tolerated than TCA
  • *no anti-cholinergic
  • *not cardiotoxic

Examples
- venlafaxine

MOA
- block NE and serotonin reuptake

SE
- insomnia, sweating, head ache, nausea, anorexia
- weight loss, hyponatremia
SUICIDE

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

SE
Tetracycline anti-depressants

A

Examples
- mirtazapine

MOA
- increases release of NE and serotonin

SE
- Hypercholesterolemia
- weight gain
- agranulocytosis
- CNS sedation

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

Why are preventative therapies not prescribed for children < 18 years

A

Increase risk of suicide

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

Botox
MOA, therapeutic effect, SE

A

Neuromuscarinic blockage

reduce HA by 2 / month

SE
paralysis
dysphagia

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

Normal physiological effect of NE and serotonin

A

Neuromodulators
Decrease pain transmission in the spinal cord

Therapies
- increase NE and serotonin = decrease pain transmission = decrease pain signals to the brain

ex.
TCAs
SNRIs
mirtazapine

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

Migraine HA
Incidence, prevalence

A

more common females

18-44 years of age

family history

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

MIgraine HA
Triggers

A
  • Stress (before/after)
  • weather
  • periods
  • food (tyramines - aged wine, cheese, smoked fish; nitrates - bacon; caffiene; chocolate)
  • sleep (too much, too little)
  • sensory overload (lights, smells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Diagnostic criteria
Migraine HA

A

5 episodes, 4 hours - 72 hours duration, with at least 2:

  • unilateral pain
  • thobbing/pulsing
  • moderate to severe
  • avoidance / aggrevated by activity

at least 1 of the following:
- nausea/vomiting
- photophobia or phonophobia

REMEMBER
Tension head aches
- bilateral
- steady pain
- not aggrevated by activity
- mild to moderate
- gradual onset

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

4 Phases of Migraine HA

Study These Flashcards
A
  1. Premonitory phase
    - hours to days before
  • tired, irritable, concentration, hunger
  • PATHO: increased blood flow hypothalamus
  1. Aura phase (1/3 people)
    - 1 hour before
  • cortical spreading depression (CSD)
  • depolarization from occiput across cortex
  • depresses the threshold for firing (hyperactivity)
  1. Head ache phase (2/3)
    - 4 hours to 72 hours
  • Activation trigeminovascular system
  • Trigeminal nerve hyperactivity -> projections dural intracranial blood vessels –>
    inflammation
    vasodilation
    pain
  1. Recovery
    - hours to days
    - irritability, fatigue, depression
21
Q

Neuromodulators
Protective vs. Not during HA phase

Study These Flashcards
A

Serotonin

  • neuromodulator
  • protective
  • vasoconstriction of the (trigeminovascular system)

*protective before, during, afterwards

Example medications
- SNRI
- TCA
- mirtazipine (tricyclic antidepressant)
- triptans

Calcitonin gene related protein (CGRP)

  • released by trigeminovascular system
  • increase inflammation and vasodilation
  • worsen head aches
  • calcium increases calcitonin release from thyroid (this is why dairy increases migraine head aches)

*increases during migraine
*caused by infusing it

22
tension type head ache vs. migraine head ache
tension type head ache - hypersensitivity nociceptors trigeminal nerve - hypersensitivity myofacial afferent nerves migraine type head ache - trigeminovascular system - inflammation, vasodilation, irritation of meningeal vessels
23
Migraine HA Trigeminovascular activation
1. inflammation 2. vasodilation 3. hypersensitivity nociceptors 4. pain
24
Abortive treatment migraine head aches
1. NSAIDS, tylenol (moderate) Severe 1. triptans 2. ergot alkaloids 3. Calcitonin gene related protein blockers 4. opioids (last resort)
25
Preventative treatment mIgraine head aches
1. triptans 2. beta blockers 3. TCAs, SNRIs 4. AEDs (gabapentin, topiramate, divalproex) 5. estrogens 6. injections
26
Example Triptans
Almotriptan sumatriptan Almotriptan *approved for children in canada > 12 years
27
Serotonin syndrome S&S
Neuro: aggitation, delirium, hallucinations Heart: tachycardia, dysrhythmias MSK: myocolonus, ataxia, tremors, hyperreflexia GI: N/V/D DEATH Do not combine - triptans - ergot alkaloids - SNRI - SSRIs - MAOinhibitors
28
Ergot Alkaloids Indication and examples
Abortive therapy Second line if triptans do not work Examples - Ergotamine - Dihydroergotamine (canada)
29
MOA ergot alkaloids
Unknown increase transmission at serotonin, dompamin and alpha adrenergic nerons decrease release of pro-inflammatory NT (CRGP) from trigeminovascular ssystem decrease vasomotor centres
30
ERgot alkaloids SE
VASOCONSTRICTION GI: n/v Cardio: HTN, vasoconstriction, angina, dysrhythmias PVS: vasoconstriction, ischemia, gangrene Teratogenic
31
Ergot alkaloids Contraindications
pregnancy - causes uterine contractions and labour hepatic or kidney disease CYP3A4 inhibitors HTN, dysrhythmias CAD, PVD sepsis *ischemia and gangrene Drugs - triptans - washout of 24 hours needed
32
Pharmacokinetics ergot alkaloids
IN, IM, Subcutaneous Not PO - 100% first pass effect
33
Black box warning Ergot alkaloids
ischemia and gangrene increase risk - increase use, longer duration - CYP3A4inhibitors - hepatic or renal disease - CAD or peripheral vascular disease - HTN - sepsis
34
Calcitonin gene related peptide (CGRP) receptor antagonists Examples
Ubrogepant Atogepant
35
CGRP receptor antagonists MOA
bind to receptor block effect of CGRP (pro-inflammatory, released from trigeminovascular system)
36
CGRP receptor antagonists SE
nausea, vomiting teratogenic
37
Preventative Therapy Migraine HA Qualifications
Any age > 3 HA in a month Severe in quality do not respond to abortive therapy
38
Preventative therapy Migraine HA Examples
1. beta blockers - propranolol - SE: heart block, bradycardia, hypotension, HF, hypoglycemia, rebound tachycardia, bronchoconstriction - ECG before start 2. AEDs - divalproex (VPA) - SE: teratogenic, hepatitis, pancreatitis, GI upset, ammonia - topiramate - SE: metabolic acidosis - gabapentin 3. TCA - amitriptyline - SE: anti-cholinergic, anti-histamine, suicide, cardiotoxicity (dysrhtyhmias, HTN), serotonin syndrome, hypertensive crisis - ECG before you start 4. estrogens / Triptans - menstruation induced 5. injections - botox - lidocaine/bupivicane nerve block 6. CGRP monoclonal antibodies SE: immunogenicity, hypersensitivity, skin/GI, hepatotoxicity
39
Pathophysiology Cluster head aches
1. trigeminovascular system - inflammation - vasodilation 2. autonomic division trigeminal nerve - occiput, cheek, temple - dysfunciton ANS: rhinorrhea, lacrimnation, Horner's sydnrom (Ptosis, anhydrosis, mydriasis) 3. hypothalamus - pattern of attacks
40
Cluster head aches Are also known as
Trigeminal Autonomic cephalalgias
41
Cluster head ache incidence, prevalence, triggers
men > women onset 20-50 years of age triggers: alcohol, smoking, caffiene no family history
42
Cluster head aches clinical signs and symptoms
sudden onset unilatera severe stabbing pain (more debilitating than migraine) clusters in time 8x per day, for hours to days, remission for years associated: horner's syndrome, ipsilateral lacrimation rhonorrhea
43
Treatment Cluster head aches abortion
First line: Triptan + oxygen + glucocorticoid 1. First line: tripans - Somatotriptan - SE: vasoconstriction, angina, vasospastic angina, crushing chest pain (bronchoconstriction, pulmonary constriction, esophageal spasms, intercostal muscles, HTN, teratogenic 2. Second line: ergot alkaloids - dihydroergotamine - SE: black box warning vasoconstriction and gangrene, HTN, angina, muscular weakness/numbness/tingling, N/V 3. glucocorticoid - methylprednisone, dexmethasone - SE: GI ulcers, infection, hypernatremia, FVO, hypokalemia, osteoporosis, adrenal supression, hyperglycemia, striations, etc.
44
Preventative treatment Cluster HA
1. non-dihydropyridine calcium channel blockers - Heart: decrease HR, conduciton, contraction - VSM: prevent calcium influx and contraction, vasodilation - SE: heart block, bradycardia, hypotension, flushing, HA, fainting, edema, eczema, constipation (ECG before administer) 2. Lithium 3. Suboccipital glucocorticoid injections - decrease severity frequency - repeat every 3 months
45
Lithium MOA, therapeutic index, SE, contraindications
MOA: unknown Therapeutic index: narrow 0.6-0.8 (toxicity 1.5) SE: toxicity N/V/D, polyuria (blocks ADH), tremors, stupor, coma, teratogenic Contraindications: diuretics
46
verapamil MOA, SE, contraindications, monitoring
MOA: unclear for migraines SE: heart block , bradycardia, heart failure, flushing, head ache, dizziness, eczema, constipatoin monitoring; ECG before start, every 6 months of therapy
47
Medication over use head aches Example medications
NSAIDS Tylenol Opioids Triptans (mild, for days) Ergot alkaloids (severe, for weeks)
48
Medicaiton over use head aches when are you at risk?
> 2 x per week using abortive medications - start preventative treatment to decrease amount of times having to use abortive medications - higher dosages
49
Medication over use head aches are also known as
rebound head aches drug induced head aches
50
MOA medication induced head aches
unknown
51
Treatment medication over use headaches
D/C medications inform client HA will get worse ergot alkaloids (severe, for weeks) triptans (mild and for days) lower dosage start preventative therapy addition non pharmacological therapy
52
Non pharmacological therapy for HA prevention
stress eating regular intervals exercise water CBT, accupuncture, biofeedback HA diary to identify triggers, avoid triggers sleep

Year 1: Patho/Pharm (45 decks)

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