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Patho/Pharm 2 > Neuro > Flashcards

Neuro Flashcards

1
Q

what is transduction

A

process of converting a painful stimulus into an electrical signal that is transmitted to the CNS

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2
Q

what are the two fibre types that are involved with transduction

A

delta fibres (fast, sharp) & C fibres (dull, slow)

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3
Q

what is transmission

A

the conduction of pain impulses along delta and C fibres to the dorsal horn of the spinal cord

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4
Q

what is perception

A

conscious awareness of pain

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5
Q

where does perception occur in the brain

A

reticular and limbic systems and cerebral cortex

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6
Q

what 3 systems interact to produce perception of pain

A

sensory-discriminiative, affective-motivational, and cognitive-evaluative system

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7
Q

what is pain threshold

A

lowest intensity of pain that a person can recognize

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8
Q

what is pain tolerance

A

greatest intensity of pain that a person can endure

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9
Q

what is modulation

A

the different ways that the transmission of pain through the nervous system can be increased or decreased (analgesic drugs, endogenous opioids)

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10
Q

what is PQRST assessment for pain

A

precipitators, quality, region/radiation, subjective severity, temporal nature/timing

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11
Q

what is the MOA for opioid receptor agonists

A

activate µ(mu) receptors ; weak activation of kappa receptors

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12
Q

which receptors are most responsible for respiratory depression

A

µ (mu) receptors

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13
Q

what is black box warning for opioid receptor agonists

A

respiratory depression

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14
Q

what can you use to reverse effects of opioid receptor agonists in the event of overdose/toxicity

A

naloxone

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15
Q

what are common AEs of opioid receptor agonists

A

constipation, urinary retention, orthostatic hypotension, pruritis, N/V, confusion, sedation, addiction/dependence , toxicity

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16
Q

what is black box for codiene

A

resp depression or death –> caution for people who are ultra metaboliers

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17
Q

what is important consideration for fentanyl

A

increased risk of toxicity if taking CYP3A4 inhibitors (Ritonavir); not used for acute post-op pain but better for chronic pain

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18
Q

what is black box warning for methadone

A

QT prolongation/lethal arrhythmia

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19
Q

what is the MOA for agonsit-antagonist opiods

A

work at µ and K receptors, less effective than agonist or antagonists; good for mild to moderate pain

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20
Q

what are examples of agonist-antagonist opiods

A

nalbuphine (pruritis) & buprenorphine (opioid use disorder)

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21
Q

what is the MOA for pure opioid antagonists

A

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

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22
Q

can naloxone be given orally

A

NO – big first pass effect, only give subq or intranasal

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23
Q

what is the MOA for tramadol

A

non-opioid centrally acting analgesic (synthetic opioid) that works at µ receptors to block reuptake of NE and serotonin

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24
Q

what are AEs of tramadol

A

seizures, serotonin syndrome, sedation/dizzinesss/HA/dry mouth, hypertensive crisis (if used with MOA inhibitors)

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25
Q

what is the MOA of tricyclic antidepressents (amitriptyline, nortriptyline, imipramine)

A

block neuronal reuptake fo monoamine transmitters NE and serotonin -> intensity their effect

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26
Q

what med is first line for neuropathic pain and fibromyalgia

A

tricyclic antidepressants

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27
Q

what is black box for tricyclic antidepressants

A

seizures –> use with caution if person has seizure disorder

avoid with MAOIs due to risk of hypertensive crisis

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28
Q

what is MOA for tylenol

A

inhibition of COX in CNS only, no antiinflammatory effect

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29
Q

what is major AE for tylenol

A

liver injury (symptoms NVD, swating, abdominal pain)

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30
Q

what is the antidote for tylenol

A

acytylcysteine

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31
Q

what is MOA of NSAIDs

A

1st gen (1st line): ASA irreversibly inhibits COX & suppress platelet aggregation, others reversibly inhibit COX

2nd gen: selectively inhibit COX-2

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32
Q

what are AEs for NSAIDs

A

1st gen: renal injury, SJS
2nd gen: GI ulceration, CV events

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33
Q

what is breakthrough pain

A

transient episodes of mod/severe pain

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34
Q

what is the best med for breakthrough pain

A

strong opioid with rapid onset & short duration

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35
Q

what is multmodal/balanced analgesia

A

using analgesics that have different MOA together

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36
Q

what are medication options for multimodal/balanced analgesia

A

non-opioid (Tylennol & NSAIDs), long-acting opioids (stable release of opioid) and break through opioids (immediate acting to treat acute pain episode)

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37
Q

what are complementary therapies to treat pain

A

massage, CBT, mindfulness, exercise, acupuncture

38
Q

what is patho of tension type headaches

A

not well understood, thought to be tight muscles & hypersensitivity to nociceptors –> most common primary HA

39
Q

what cranial nerve is most involved with tension headaches

A

trigeminal nerve (V)

40
Q

what is the clinicla presentation for tension headaches

A

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

41
Q

what is treatment for tension headaches

A

ice, NSAIDs/Tylenol
chronic: TCAs, behavioural relaxation

avoid long term analgesics and triptans

preventative: tricyclic antidepressents, venlafaxine (SNRI) –> caution with venlafaxine in pts <18

42
Q

what is patho of migraines

A

not well understood, neurovascular disorder involving dilation and inflammation of intracranial blood vessels and activation of trigeminal nerve

43
Q

what two neurotransmitters play a role in migraines

A

serotonin (supresses) and calcitonin gene related peptide (promotes)

44
Q

what are the three classifications of migraines

A
  1. migraine with aura (visual, sensory, motor)
  2. without aura (most common)
  3. chronic (15+ days/month)
45
Q

what is the criteria for classification of non aura migraines

A

2 of:
1.unilateral location
2. pulsating
3. aggravation with activity
4. mod/severe intensity

PLUS 1 of

  1. N +/- V
  2. photophobia/phonophobia
46
Q

what are three phases of migraines

A
  1. premonitory phase (days/hours before)
  2. migaine aura (1/3 of patients, up to 1hr)
  3. headache phase - begins on one side adn spreads to entire head, possible hypersensitivity to anything touching head
  4. recovery phase
47
Q

what is treatment for active migraines

A

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

48
Q

what is preventative treatment for migraines

A

b-blockers, anti-epilptics, TCAs, estrogen & triptans, localized injections, CGRP monoclonal antibodies

49
Q

how do triptans treat migraines?

A

relieve pain by constricting intracranial blood vessels and reducing inflammation by selectively activating serotonin receptors

50
Q

what is the patho for cluster HA

A

not understood, trigeminal nerve activation w/ hypothalamus involvement; vasoactive peptide release & formation of neurogenic inflammation

51
Q

what is the presentation of cluster headaches

A

sudden, extreme pain & short duration, severe throbbing, stabbing pain in temporal-orbital region

52
Q

how do cluster headaches differ from migraines

A

no aura, no n/v, more debilitating, not associated with fam hx

53
Q

what are treatments for cluster headaches

A

triptans, oxygen, glucocortiods, CCBs, neurostabalizer (lithium)

54
Q

what can occur with medication overuse in treatment/prevention of headaches

A

rebound/drug-induced HA, develops in response to frequent use of abortive HA meds (tylenol, NSAIDs, triptans & opioids)

55
Q

what is treatment for rebound headache

A

stop all HA meds (days to weeks), limit abortive meds to 2-3x/week and start preventative meds if HA 2-3+ times/month

56
Q

what are abortive meds for tension type headaches

A

NSAIDs, Acetaminophen

57
Q

what are abortive meds for mild/mod migraines

A

NSAIDs, Acetaminophen, Triptans

58
Q

what are abortive meds for mod/severe migraines

A

triptans, ergot, opiods (if all else fails)

59
Q

what are considerations for tylenol for headaches

A

always take in combo with other meds (aspirin, caffeine)

60
Q

what is a common side effect of triptans

A

unpleasant pressure on chest (unrelated to ischemic heart disease), coronary vasospasm

61
Q

what are CIs for triptans

A

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

62
Q

what is the MOA for ergot in treatment of migraines

A

alter transmission at serotonergic, dopaminergic, and alpha adrenergic juntions

63
Q

what is black box for ergot

A

vasoconstriction

64
Q

what are CIs for ergot

A

hepatic or renal impairment, sepsis, CV disease, concurrent use of CYP3A4

65
Q

what is the MOA for Calcitonin gene related peptide receptor antagonist

A

CGRP generates inflammatory mediators that activate trigeminovascular system –> this blocks that

66
Q

what is the moa for opioid nasal spray (butorphanol) and when should it be used

A

agonist-antagonist opioid; works at mu and kappa receptors - only use as last resort when all other treatment options fail

67
Q

what are meds for tension-type headache prophylaxis

A

tricyclic antidepressants, Venlafaxine (SNRI)

68
Q

what meds are used for migraine prophylaxis

A

B-blockers (1st line), antiepileptics, tricyclic antidepressants, estrogens, CGRP antagonists

69
Q

what meds are used to prevent cluster headaches

A

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

70
Q

what are indications for putting somebody on preventative migraine medication

A

> 3 episodes per month, attacks are severe, attacks do not respond to abortive meds

71
Q

what is Divalproex

A

effective antiepileptic used for migraine prophylaxis, is a form of valproic acid (CI in pregnancy)

72
Q

what is topiramate

A

effective antiepileptic used for migraine prophylaxis, more expensive

73
Q

what is amitriptyline

A

tricyclic antidepressant used for migraine prophylaxis

74
Q

what are AEs of tricyclic antidepressants

A

anticholenergic (dry mouth, constipation, urinary retention, blurred vision, tachycardia), hypotension

75
Q

what is the MOA for estrogen and what is it used for

A

supplement to counter decline in estrogen levels preceding menstruation which can trigger migraine (prophylaxis for migraine)

ex) divigel, climara

76
Q

what are alternatives to estrogen for menstrually associated migrianes

A

tryptans, naproxen

77
Q

what is erenumab

A

CGRP monoclonal antibodies used for migraine prophylaxis

78
Q

what is erenumab

A

CGRP monoclonal antibodies used for migraine prophylaxis

79
Q

what is verapamil and what is is used for

A

CCB - first line for prevention of cluster headaches

80
Q

what is an important consideration for Verapamil

A

it is a cyp3a4 inhibitor - caution with ergot and fentanyl

81
Q

what are AEs of verapamil

A

cardiac arrhythmias, bradycardia, prolonged PR interval –> need ECG q6months

82
Q

what is lithium & what is it used for

A

neurostabilizers second line for prophylaxis of cluster HA

83
Q

what is important consideration for lithium

A

narrow therapeutic window –> need drug monitoring

84
Q

what are AEs of lithium

A

cognitive disturbance, tremor, dizziness

85
Q

what are glucocorticoids used for

A

prevention of cluster headaches through suboccipital injection or treatment thrugh prednisone/dexamethasone

86
Q

what are non pharm treatment for HA

A

stress reduction, sleep, relaxation techniques, avoidance of triggers (strong smells, missed meals, overexertion, bright lights etc)

87
Q

what is thought to be the most effective med at stopping cluster headache attacks but is at high risk for overuse

A

sumatriptan

88
Q

when should you use abortive meds for migraine

A

at earliest sign of attack –> if taken to late GI disturbance resulting from migraine may impact absorption

89
Q

are triptans used for tension headaches?

A

NO

90
Q

what are abortive meds for cluster headaches

A

triptans, oxygen

Patho/Pharm 2 (7 decks)

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