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

Head Aches Patho Flashcards

1
Q

4 Types of Primary Head Aches

A
  1. Tension
  2. Migraine
  3. Cluster
  4. Medication overuse head ache
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2
Q

Treatment Primary Head Aches

A
  1. Abortive therapy
    - non-specific
    - specific
  2. Preventative therapy
  3. Non pharmacological therapy
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3
Q

Tension Type Head Aches
Incidence, prevalence

A

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

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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

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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
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5
Q

Abortive Treatment
Tension Type Head Aches

A
  1. Non-Specific
    - Tylenol
    - NSAIDS
    - Ice
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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

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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)
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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
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7
Q

Examples
Preventative Treatments
Tension Type Head Aches

A

Tricyclic anti-depressants
- Nortriptyline
- Amitriptyline

Serotonin norepineprhine reuptake inhibitors
- venlafaxine

Tetracycline anti-depressants
- mirtazapine

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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

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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.)
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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

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11
Q

Prescribing considerations before starting TCA

A

ECG
- evaluation for bradycardia, branch blocks, dysrhythmias

TCAs can cause these
they are cardiotoxic

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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

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13
Q

SE
Tetracycline anti-depressants

A

Examples
- mirtazapine

MOA
- increases release of NE and serotonin

SE
- Hypercholesterolemia
- weight gain
- agranulocytosis
- CNS sedation

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14
Q

Why are preventative therapies not prescribed for children < 18 years

A

Increase risk of suicide

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15
Q

Botox
MOA, therapeutic effect, SE

A

Neuromuscarinic blockage

reduce HA by 2 / month

SE
paralysis
dysphagia

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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

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17
Q

Migraine HA
Incidence, prevalence

A

more common females

18-44 years of age

family history

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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)
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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

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20
Q

4 Phases of Migraine HA

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

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
Q

tension type head ache vs. migraine head ache

A

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
Q

Migraine HA
Trigeminovascular activation

A
  1. inflammation
  2. vasodilation
  3. hypersensitivity nociceptors
  4. pain
24
Q

Abortive treatment
migraine head aches

A
  1. NSAIDS, tylenol (moderate)

Severe
1. triptans
2. ergot alkaloids
3. Calcitonin gene related protein blockers
4. opioids (last resort)

25
Q

Preventative treatment
mIgraine head aches

A
  1. triptans
  2. beta blockers
  3. TCAs, SNRIs
  4. AEDs (gabapentin, topiramate, divalproex)
  5. estrogens
  6. injections
26
Q

Example Triptans

A

Almotriptan
sumatriptan

Almotriptan
*approved for children in canada > 12 years

27
Q

Serotonin syndrome
S&S

A

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
Q

Ergot Alkaloids
Indication and examples

A

Abortive therapy
Second line
if triptans do not work

Examples
- Ergotamine
- Dihydroergotamine (canada)

29
Q

MOA
ergot alkaloids

A

Unknown
increase transmission at serotonin, dompamin and alpha adrenergic nerons

decrease release of pro-inflammatory NT (CRGP) from trigeminovascular ssystem

decrease vasomotor centres

30
Q

ERgot alkaloids
SE

A

VASOCONSTRICTION

GI: n/v

Cardio: HTN, vasoconstriction, angina, dysrhythmias

PVS: vasoconstriction, ischemia, gangrene

Teratogenic

31
Q

Ergot alkaloids
Contraindications

A

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
Q

Pharmacokinetics
ergot alkaloids

A

IN, IM, Subcutaneous

Not PO - 100% first pass effect

33
Q

Black box warning
Ergot alkaloids

A

ischemia and gangrene

increase risk
- increase use, longer duration
- CYP3A4inhibitors
- hepatic or renal disease
- CAD or peripheral vascular disease
- HTN
- sepsis

34
Q

Calcitonin gene related peptide (CGRP) receptor antagonists
Examples

A

Ubrogepant
Atogepant

35
Q

CGRP receptor antagonists
MOA

A

bind to receptor
block effect of CGRP (pro-inflammatory, released from trigeminovascular system)

36
Q

CGRP receptor antagonists
SE

A

nausea, vomiting
teratogenic

37
Q

Preventative Therapy
Migraine HA
Qualifications

A

Any age

> 3 HA in a month
Severe in quality
do not respond to abortive therapy

38
Q

Preventative therapy
Migraine HA
Examples

A
  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
  1. TCA
    - amitriptyline
    - SE: anti-cholinergic, anti-histamine, suicide, cardiotoxicity (dysrhtyhmias, HTN), serotonin syndrome, hypertensive crisis
    - ECG before you start
  2. estrogens / Triptans - menstruation induced
  3. injections
    - botox
    - lidocaine/bupivicane nerve block
  4. CGRP monoclonal antibodies
    SE: immunogenicity, hypersensitivity, skin/GI, hepatotoxicity
39
Q

Pathophysiology
Cluster head aches

A
  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
Q

Cluster head aches
Are also known as

A

Trigeminal Autonomic cephalalgias

41
Q

Cluster head ache
incidence, prevalence, triggers

A

men > women
onset 20-50 years of age
triggers: alcohol, smoking, caffiene
no family history

42
Q

Cluster head aches
clinical signs and symptoms

A

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
Q

Treatment
Cluster head aches
abortion

A

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
Q

Preventative treatment
Cluster HA

A
  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)
  1. Lithium
  2. Suboccipital glucocorticoid injections
    - decrease severity frequency
    - repeat every 3 months
45
Q

Lithium
MOA, therapeutic index, SE, contraindications

A

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
Q

verapamil
MOA, SE, contraindications, monitoring

A

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
Q

Medication over use head aches
Example medications

A

NSAIDS
Tylenol
Opioids
Triptans (mild, for days)
Ergot alkaloids (severe, for weeks)

48
Q

Medicaiton over use head aches
when are you at risk?

A

> 2 x per week using abortive medications

  • start preventative treatment to decrease amount of times having to use abortive medications
  • higher dosages
49
Q

Medication over use head aches are also known as

A

rebound head aches
drug induced head aches

50
Q

MOA
medication induced head aches

A

unknown

51
Q

Treatment
medication over use headaches

A

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
Q

Non pharmacological therapy for HA prevention

A

stress

eating regular intervals

exercise

water

CBT, accupuncture, biofeedback

HA diary to identify triggers, avoid triggers

sleep

Year 1: Patho/Pharm (39 decks)

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