Neuro Flashcards
what is transduction
process of converting a painful stimulus into an electrical signal that is transmitted to the CNS
what are the two fibre types that are involved with transduction
delta fibres (fast, sharp) & C fibres (dull, slow)
what is transmission
the conduction of pain impulses along delta and C fibres to the dorsal horn of the spinal cord
what is perception
conscious awareness of pain
where does perception occur in the brain
reticular and limbic systems and cerebral cortex
what 3 systems interact to produce perception of pain
sensory-discriminiative, affective-motivational, and cognitive-evaluative system
what is pain threshold
lowest intensity of pain that a person can recognize
what is pain tolerance
greatest intensity of pain that a person can endure
what is modulation
the different ways that the transmission of pain through the nervous system can be increased or decreased (analgesic drugs, endogenous opioids)
what is PQRST assessment for pain
precipitators, quality, region/radiation, subjective severity, temporal nature/timing
what is the MOA for opioid receptor agonists
activate µ(mu) receptors ; weak activation of kappa receptors
which receptors are most responsible for respiratory depression
µ (mu) receptors
what is black box warning for opioid receptor agonists
respiratory depression
what can you use to reverse effects of opioid receptor agonists in the event of overdose/toxicity
naloxone
what are common AEs of opioid receptor agonists
constipation, urinary retention, orthostatic hypotension, pruritis, N/V, confusion, sedation, addiction/dependence , toxicity
what is black box for codiene
resp depression or death –> caution for people who are ultra metaboliers
what is important consideration for fentanyl
increased risk of toxicity if taking CYP3A4 inhibitors (Ritonavir); not used for acute post-op pain but better for chronic pain
what is black box warning for methadone
QT prolongation/lethal arrhythmia
what is the MOA for agonsit-antagonist opiods
work at µ and K receptors, less effective than agonist or antagonists; good for mild to moderate pain
what are examples of agonist-antagonist opiods
nalbuphine (pruritis) & buprenorphine (opioid use disorder)
what is the MOA for pure opioid antagonists
acts of µ adn K receptos, no analgesic effect but used to reverse CNS/resp depression (naloxone)
–> can cause withdrawal, but no harm from administered unnecessarily if unsure
can naloxone be given orally
NO – big first pass effect, only give subq or intranasal
what is the MOA for tramadol
non-opioid centrally acting analgesic (synthetic opioid) that works at µ receptors to block reuptake of NE and serotonin
what are AEs of tramadol
seizures, serotonin syndrome, sedation/dizzinesss/HA/dry mouth, hypertensive crisis (if used with MOA inhibitors)
what is the MOA of tricyclic antidepressents (amitriptyline, nortriptyline, imipramine)
block neuronal reuptake fo monoamine transmitters NE and serotonin -> intensity their effect
what med is first line for neuropathic pain and fibromyalgia
tricyclic antidepressants
what is black box for tricyclic antidepressants
seizures –> use with caution if person has seizure disorder
avoid with MAOIs due to risk of hypertensive crisis
what is MOA for tylenol
inhibition of COX in CNS only, no antiinflammatory effect
what is major AE for tylenol
liver injury (symptoms NVD, swating, abdominal pain)
what is the antidote for tylenol
acytylcysteine
what is MOA of NSAIDs
1st gen (1st line): ASA irreversibly inhibits COX & suppress platelet aggregation, others reversibly inhibit COX
2nd gen: selectively inhibit COX-2
what are AEs for NSAIDs
1st gen: renal injury, SJS
2nd gen: GI ulceration, CV events
what is breakthrough pain
transient episodes of mod/severe pain
what is the best med for breakthrough pain
strong opioid with rapid onset & short duration
what is multmodal/balanced analgesia
using analgesics that have different MOA together
what are medication options for multimodal/balanced analgesia
non-opioid (Tylennol & NSAIDs), long-acting opioids (stable release of opioid) and break through opioids (immediate acting to treat acute pain episode)
what are complementary therapies to treat pain
massage, CBT, mindfulness, exercise, acupuncture
what is patho of tension type headaches
not well understood, thought to be tight muscles & hypersensitivity to nociceptors –> most common primary HA
what cranial nerve is most involved with tension headaches
trigeminal nerve (V)
what is the clinicla presentation for tension headaches
mild/mod BILATERAL headache that feels like tight band or pressure sensation around the head - stready with gradual onset
episodic = <15days/month
chronic=>15days/month for 3+months
what is treatment for tension headaches
ice, NSAIDs/Tylenol
chronic: TCAs, behavioural relaxation
avoid long term analgesics and triptans
preventative: tricyclic antidepressents, venlafaxine (SNRI) –> caution with venlafaxine in pts <18
what is patho of migraines
not well understood, neurovascular disorder involving dilation and inflammation of intracranial blood vessels and activation of trigeminal nerve
what two neurotransmitters play a role in migraines
serotonin (supresses) and calcitonin gene related peptide (promotes)
what are the three classifications of migraines
- migraine with aura (visual, sensory, motor)
- without aura (most common)
- chronic (15+ days/month)
what is the criteria for classification of non aura migraines
2 of:
1.unilateral location
2. pulsating
3. aggravation with activity
4. mod/severe intensity
PLUS 1 of
- N +/- V
- photophobia/phonophobia
what are three phases of migraines
- premonitory phase (days/hours before)
- migaine aura (1/3 of patients, up to 1hr)
- headache phase - begins on one side adn spreads to entire head, possible hypersensitivity to anything touching head
- recovery phase
what is treatment for active migraines
avoid trigger
abortive therapy at earliest sign:
- first line NSAIDs, selective serotonin agonists/triptans,
-ibuprofen 1st line for children
-second line ergot alkaloids –> black box warning for vasoconstriction
- calcitonin gene related peptide (CGRP) rc antagnosit
opioids not recommended unless other treatments fail
what is preventative treatment for migraines
b-blockers, anti-epilptics, TCAs, estrogen & triptans, localized injections, CGRP monoclonal antibodies
how do triptans treat migraines?
relieve pain by constricting intracranial blood vessels and reducing inflammation by selectively activating serotonin receptors
what is the patho for cluster HA
not understood, trigeminal nerve activation w/ hypothalamus involvement; vasoactive peptide release & formation of neurogenic inflammation
what is the presentation of cluster headaches
sudden, extreme pain & short duration, severe throbbing, stabbing pain in temporal-orbital region
how do cluster headaches differ from migraines
no aura, no n/v, more debilitating, not associated with fam hx
what are treatments for cluster headaches
triptans, oxygen, glucocortiods, CCBs, neurostabalizer (lithium)
what can occur with medication overuse in treatment/prevention of headaches
rebound/drug-induced HA, develops in response to frequent use of abortive HA meds (tylenol, NSAIDs, triptans & opioids)
what is treatment for rebound headache
stop all HA meds (days to weeks), limit abortive meds to 2-3x/week and start preventative meds if HA 2-3+ times/month
what are abortive meds for tension type headaches
NSAIDs, Acetaminophen
what are abortive meds for mild/mod migraines
NSAIDs, Acetaminophen, Triptans
what are abortive meds for mod/severe migraines
triptans, ergot, opiods (if all else fails)
what are considerations for tylenol for headaches
always take in combo with other meds (aspirin, caffeine)
what is a common side effect of triptans
unpleasant pressure on chest (unrelated to ischemic heart disease), coronary vasospasm
what are CIs for triptans
cardiac disease (ischemic heart disease, prior MI, uncontrolled HTN), pregnancy, concurrent use of SSRI, SNRI (serotonin syndrom), MAOIs (toxicity), children under 12
do not use within 24hrs of another triptan or ergot
what is the MOA for ergot in treatment of migraines
alter transmission at serotonergic, dopaminergic, and alpha adrenergic juntions
what is black box for ergot
vasoconstriction
what are CIs for ergot
hepatic or renal impairment, sepsis, CV disease, concurrent use of CYP3A4
what is the MOA for Calcitonin gene related peptide receptor antagonist
CGRP generates inflammatory mediators that activate trigeminovascular system –> this blocks that
what is the moa for opioid nasal spray (butorphanol) and when should it be used
agonist-antagonist opioid; works at mu and kappa receptors - only use as last resort when all other treatment options fail
what are meds for tension-type headache prophylaxis
tricyclic antidepressants, Venlafaxine (SNRI)
what meds are used for migraine prophylaxis
B-blockers (1st line), antiepileptics, tricyclic antidepressants, estrogens, CGRP antagonists
what meds are used to prevent cluster headaches
CCBs (verapamil 1st line), neurostabalizers (lithium), glucocorticoids
*note - all prophylactic therapy for cluster headaches should be limited to cluster cycle and d/c’d when cycle is over
what are indications for putting somebody on preventative migraine medication
> 3 episodes per month, attacks are severe, attacks do not respond to abortive meds
what is Divalproex
effective antiepileptic used for migraine prophylaxis, is a form of valproic acid (CI in pregnancy)
what is topiramate
effective antiepileptic used for migraine prophylaxis, more expensive
what is amitriptyline
tricyclic antidepressant used for migraine prophylaxis
what are AEs of tricyclic antidepressants
anticholenergic (dry mouth, constipation, urinary retention, blurred vision, tachycardia), hypotension
what is the MOA for estrogen and what is it used for
supplement to counter decline in estrogen levels preceding menstruation which can trigger migraine (prophylaxis for migraine)
ex) divigel, climara
what are alternatives to estrogen for menstrually associated migrianes
tryptans, naproxen
what is erenumab
CGRP monoclonal antibodies used for migraine prophylaxis
what is erenumab
CGRP monoclonal antibodies used for migraine prophylaxis
what is verapamil and what is is used for
CCB - first line for prevention of cluster headaches
what is an important consideration for Verapamil
it is a cyp3a4 inhibitor - caution with ergot and fentanyl
what are AEs of verapamil
cardiac arrhythmias, bradycardia, prolonged PR interval –> need ECG q6months
what is lithium & what is it used for
neurostabilizers second line for prophylaxis of cluster HA
what is important consideration for lithium
narrow therapeutic window –> need drug monitoring
what are AEs of lithium
cognitive disturbance, tremor, dizziness
what are glucocorticoids used for
prevention of cluster headaches through suboccipital injection or treatment thrugh prednisone/dexamethasone
what are non pharm treatment for HA
stress reduction, sleep, relaxation techniques, avoidance of triggers (strong smells, missed meals, overexertion, bright lights etc)
what is thought to be the most effective med at stopping cluster headache attacks but is at high risk for overuse
sumatriptan
when should you use abortive meds for migraine
at earliest sign of attack –> if taken to late GI disturbance resulting from migraine may impact absorption
are triptans used for tension headaches?
NO
what are abortive meds for cluster headaches
triptans, oxygen
