Module 5 EB #1 Flashcards
Red flag sx of acute HA
*what do these red flag sx exclude?
> 40yo
rapid onset
severe intensity
**thunderclap
-onset after trauma or during exertion
-brain tumor, meningitis, stroke, encephalitis, intercranial hemorrhage, temporal arteritis, acute angle glaucoma, raised ICP, CO poisoning, preeclampsia, aneurysm
When to transfer to the ED for acute HA (accompanying signs)?
-fever, vision change, neck stiffness
-neuro findings: mental status change, motor/sensory deficits, LOC
-past medical hx of HTN or HIV
SNOOOPPPPP
-sx of acute HA
-Systemic S or S (fever, wt loss)
-Neurologic S or S (confusion or impaired alertness)
-Onset (sudden)
-Older (>50yo)
-Occipital (back of head; occipital HA in children)
-Previous HA (new, worse, or different?)
-Progressive, persistent HA
-Precipitated by pressure (bearing down, coughing, sneezing)
-Postural HA (worse when supine, worse waking at night, worse in AM)
-Pregnancy
what is the most important component (what info is most important) in regards to acute HA?
onset of HA
-sudden, persistence = subarachnoid hemorrhage
–> especially when preceded by exertional activities
Elements to the neuro exam regarding acute HA
-VS
-Mental Status
-Motor and Sensory
-Reflexes
-Gait (rapid finger-nose testing)
Ottawa SAH clinical decision scale
100% sensitivity in predicting subarachnoid hemorrhage
-40 years or older
-neck pain/stiffness
-witnessed LOC
-onset during exertion
-thunderclap HA (pain peaks w/i 1 sec)
-Limited neck flexion (on exam)
Diagnostic imaging for acute HA
No contrast = visualize bone and surrounding soft tissue (blood vessels)
Migraine
-what type of dysfunction?
-neuronal dysfunction: a wave of activity by groups of excitable brain cells that trigger chemicals that cause dilation of blood cells –> creates HA
*pain felt by pt triggers more chemicals which leads to further dilation of blood vessels and more painT
Tension HA
-cause?
cause unclear
-derivative pain of tension HA has muscular origin
Cluster HA
-mechanism
vascular dilation trigeminal nerve stimulation, have circadian effects
-histamine release, inc mast cells, genetic factors, and autonomic NS activation may also contribute
Which HA does this describe?
Unilateral pain, throbbing, pulsitile
Migraine
Which HA does this describe?
worse with routine activity
Migraine
Which HA does this describe?
onset and duration of HA = 4-72hrs
Migraine
Which HA does this describe?
Accompanying sx: N/V, photophobia, phonophobia
Migraine
Which HA does this describe?
some have aura preceding AH (commonly visual aura)
Migraine
Which HA does this describe?
Family hx of this type of HA present
Migraine
Which HA does this describe?
Patient reports recent lack of sleep, missed meal, menstruation
Migraine
Which HA does this describe?
precranial tenderness with generalized apin described as vice-like, tight
tension
Which HA does this describe?
not pulsitile
tension
Which HA does this describe?
pain worse at base of neck or occipital area of head
tension
Which HA does this describe?
timing: constant daily HA
tension
Which HA does this describe?
no accompanying focal/neuro deficits = NO AURA
tension
Which HA does this describe?
episodes exacerbated by stress, fatigue, noise
tension
Which HA does this describe?
unilateral, temporal or periorbital pain with one or the following:
-ipsilateral sx: nasal congestion, rhinorrhea, lacrimation, redness of eye
cluster
Which HA does this describe?
pain often occurs at night (awakens patient), then have spontaneous remission
cluster
Which HA does this describe?
timing: episodic and last 15 min to 3 hours; then have spontaneous remission
cluster
Which HA does this describe?
commonly seen in middle aged men ages 20-40
cluster
Which HA does this describe?
no family hx of this HA or migraine present
cluster
Migraine:
patho
brain cells trigger release of chemicals that lead to blood vessel dilation and pain
Migraine:
-drug class most effective for symptomatic or abortive tx
- ergotamine (narrow blood vessels)
- triptans (acts like serotonin; quiets nerves) - constricts blood vessels in brain, slowing inflammation and blocks pain pathways
Migraine
-what should you do for a patient presenting with migraine before prescribing he/she ergotamine or triptans?
place pt in cool, dark room; give simple analgesic (tyl, ibup, naproxen) and reassess pain in 30 min
Tension HA
patho
muscular tension primarily in shoulders, neck leads to pain
Tension HA
-drug class most effective for symptomatic tx
No triptans; address comorbid issues, CBT, etc.
Similar to migraine tx –> prescribe simple analgesics
Cluster HA
-patho
myriad of reasons but similar to migraine HA etiology (brain cells trigger release of chemicals that lead to blood vessel dilation and pain)
Cluster HA
-Drug class most effective for symptomatic or abortive tx
TRIPTANS (sumatriptan SQ or intranasal)
O2 inhaled 100% in nonrebreather mask
Tension HA
-what medications can you consider?
muscle relaxers
-flexeril
-zanoflex
-robaxin
Can abortive drugs be given during pregnancy for HA?
NO
Which type(s) of HA can recur?
Migraine and cluster
-HA that occurs 2-3x/MO or significant disability associated with attack
Migraine HA
-prescribe prophylactic/preventative med (how many options total?)
Topiramate
Valproic acid
Propanolol
Verapamil
Amitriptyline
Botox
Riboflavin
(7)
Cluster HA
-prescribe prophylactic/preventative med
Lithium
Topiramate
Verapamil
foods that trigger migraine or cluster AH
chocolate and ETOH
Considerations in HA management
avoid opioid meds d/t SE (including rebound HA)
keep HA diary to identify triggers and avoid any precipitating factors if known
Other HA disorders
-posttraumatic HA
-analgesic rebound HA
-primary cough HA
-HA d/t intracranial mass
Posttraumatic HA
-def
-how quickly does HA appear? does it worsen?
-sx
-tx
-HA following closed head injury regardless of LOC
-pain appears w/i 24 hours; worsens over weeks but gradually subsides
-constant dull ache; can be localized, lateralized or generalized; associated with N/V, seeing black spots - scintillating scotoma
-simple analgesics (tyl, ibup)
Analgesic rebound HA
-def
-how long do these meds need to be used to become a risk factor?
-simple analgesic effects (timeline)
-tx
-using ergotamines, triptans, opioids, and meds containing butalbital (fioricet)
-for more than 10 days per MO
-simple analgesics (tyl, acetylsalicylic acid, NSAIDs) taken more than 15 days per MO
-“fix the why” - prescribe preventative tx for migraines so they will stop using these meds as frequently (topiramate, valproic acid, verapamil, amitriptyline, botox, riboflavin, propanolol)
Primary cough HA
-def
-what should you be thinking? what should you order?
-tx
-pain with coughing, straining, sneezing, laughing (only lasts a few minutes)
-THINK BRAIN TUMOR. Order CT or MRI
-once brain tumor is r/o, NSAID (indomethacin)
HA d/t intracranial mass
-when does this tend to occur (age)? what should you order?
-aggravating factors
-how does body counteract inc ICP in this state?
-associated systemic signs that may be associated w/ this?
-new or worsening HA in middle or later life; order MRI or CT
-worse when lying down; awakens the patient at night (same as cluster HA :) ); peaks in the AM after overnight recumbency
*lying down increases CIP but our SCF and spine can adjust for this; with a tumor, prevents feedback system from operating as normal and leads to inc ICP
-body’s natural response to counteract inc ICP is to keep you upright
-fever, night sweats, weight loss
facial pain: trigeminal neuralgia
-where is the pain felt? descriptor of pain?
-what makes this pain worse?
-is neuro exam abnormal or normal?
-can remission occur?
-effect women or men more? at what point of life does this tend to occur?
-unilateral stabbing pain localized to the second and third division of the trigeminal nerve = pain arising at one side of the mouth and shoots toward the eye, ear, or nostril ON THAT SIDE
-with touch (even air hitting face)
-normal
-yes
-women; middle and later life
Facial pain: trigeminal neuralgia
-why does this occur?
-tx
-impinging of trigeminal nerve leads to misfiring and nerve pain
-carbamazepine - decreases nerve impulses that cause seizures and pain (anticonvulsant)
Facial pain: trigeminal neuralgia
-when to expect MS with these sx?
-drug of choice for MS and trigeminal neuralgia
-<40yrs
-gabapentin
Facial pain: posttherpetic neuralgia
-what should we be thinking?
-who is this common in (what population)?
-sx
-what aids in dx?
-tx
-prevention
*what NOT TO DO
-herpes zoster (singles)
-elderly/immunocompromised; when first division of trigeminal nerve is affected
-severe visible rash (when first division of trigeminal nerve is affected - rash on forehead, bridge of nose)
-hx of shingles and presence of cutaneous scaring
-acyclovir or valacyclovir when given >3hrs after rash onset
-shindrix vaccine
*DO NOT ADMINISTER SYSTEMIC CORTICOSTEROIDS: weakens immune system, makes virus/rash worse
Facial Pain: TMJ
-def
-sx
-tx
-due to injury to jaw, joint, or muscles of head and neck; grinding/clenching of teeth, or stress causing one to tighten facial/jaw muscles
-pain, tenderness in face, jaw joint area, around ear w/ chewing, speaking, opening mouth wide; jaw can get struck; clicking, popping, grinding sounds of jaw with opening/losing/chewing = can be painful
-simple analgesics; sometimes muscle relaxants (refer to dentist - mouthguard?
Facial pain: SAH
-most common cause?
-other causes?
-risk factors?
-what do patients present with?
-role of NP
-med
-trauma
-rupture of arterial saccular “berry” aneurysm or an AVM (from high BP?)
-older age, female, nonwhite ethnicity, HTN, smokier, consuming large amounts of alc
-present with sudden severe HA (WORST HA they have ever experienced); proceed to vomit
*signs of meningeal irritation (stiff neck, dec neck flexion are common): transient LOC, appear confused/irritable, progresses to coma; focal neuro deficits are ABSENT
-stat transfer to ER for CT; neuro surgery consult; ICU admission
-nimodipine = reduces iscehmic deficits from arterial vasospasm
Facial pain: pseudotumor cerebri - “Idiopathic Intracranial HTN”
-def
-RF
-etiology (most common)
-S/S
-NP role
-meds
“False Brain Tumor”
-pressure around brain inc; causes HA and vision problems (double vision)
-overweight women 20s-40s
-(many) - thrombosis of transverse sinus (complication of otitis media) is the most common; abrupt cessation of PO steroids; long-term use tetracycline or PO contraceptives
-worsened by straining; fondoscopic exam reveals edema and abducens palsy (causes eyes to turn out); chronic IH will cause pulse incronis tinnitis
-REFER to ER for CT; r/o emergent HA causes including space occupying lesions of the brain
-initiated and managed by neuro
Adjustment disorders
-def (when did stressor occur?)
-common rxns to stress
*does this resolve?
-tx
-signs of anxiety/depression d/t identifiable stressor that has occurred in past 3MO; sx are out of proportion to the severity of the stressor but not as severe as major depression or GAD
-manifests as developing somatic complaints: running away, drinking ETOH excessively, over eating, starting an affair
-this condition is completely situational; usually resolves when stressor resolves or when individual effectively adapts to situation
-behavioral techniques: CBT with emphasis on strengthening existing coping methods); lorazepam (for limited time)
trauma and stressor-related disorders: PTSD
-key to dx
-sx
-more common in which sex?
-tx
-establish if pt experienced a traumatic or life threatening event
-flashbacks, obtrusive images/intrusive thoughts, nightmares; pt feels like they experience moment repeatedly; causes pt to avoid stimuli that could be associated with the event
-more common in women and when event is associated with physical injury
-centered around interventions that will help pt integrate the event in an adaptive way
*psychotherapy: initiate ASAP; brief 8-12 sessions
*drug of choice: SSRIs: sertraline and paroxetine + others
Anxiety
-sympathomimetic sx of anxiety
-impact of trigger avoidance
-what is a contributing factor to anxiety?
-response to a CNS state that perpetuates further anxiety (fight or flight) –> anxiety can be self-perpetuating
-reinforcement of the anxiety (person continues to associate trigger w/ anxiety and never relearns through experience that the trigger need not always result in fear, or that anxiety will naturally improve with prolonged exposure to an objectively neutral stressor)
-lack of structure is frequently a contributing factor; no thoughts to occupy their time leads to over-thinking
Generalized Anxiety Disorder
-short term or chronic? which sex is this more common?
-sx + how long do sx need to be present for dx
-triggers
-physical manifestations
-tx
-chronic, women
-apprehension, worry, irritability, difficulty concentrating, insomnia; must be present (more days than not) for at least 6MO
-everyday activities
-tachycardia, HTN, nausea, epigastric pain, HA, near-syncope
-SSRI (venlafaxine, duloxetine) or SNRI (escitalopram, paroxetine)
Phobia disorder
-short term or chronic?
-def
-debilitating fears
-tx
-chronic, specific object or situation
-fear out of proportion to the danger posed
-debilitating fears: social phobia - patient remains isolated at home
-desensitization; SSRI (venlafaxine, duloxetine) or SNRI (escitalopram, paroxetine)
Panic disorder: panic attack
-def
-sx
-key to dx
-recurrent, unpredictable episodes of intense surges of anxiety and marked physiologic manifestations = impending doom
*pt appears dyspneic, tachycardic, report palpitations, HA, dizziness, numbness of extremities, feeling smothered or nauseous, bloating
-psychic pain and suffering the individual expresses
Panic disorder: panic disorder
-def
-RF
-what can this presentation mimic?
-tx
-dx when panic attacks are accompanied by a chronic fear of the recurrence of an attack or a maladaptive change in behavior = try to avoid potential triggers of the panic attack
-family hx, female, premenstrual period, mitral valve prolapse
-MIMIC a cardiac event = MI must be ruled out w/ EKG and cardiac enzymes
-SSRI (venlafaxine, duloxetine) and SNRI (escitalopram, paroxetine)
Panic disorder
-2 categories
-complications
-must R/O what?
-first line tx:
-first line drug class
-panic attack, panic disorder
-inc risk of major depression or suicide attempts; ETOH abuse and dependence on sedatives
-cardiovascular, endocrine, respiratory, neurologic, substance related syndromes
-psychotherapy (CBT)
-SSRIs (venlafaxine, duloxetine) or SNRIs (escitalopram, paroxetine)
**antidepressants take approx 2-4 weeks before effective
**abrupt withdrawal can lead to suicidal thoughts