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Neurology > Pharm 32 > Flashcards

Pharm 32 Flashcards

1
Q

o MOA: agonize 5-HT1 receptors

○ Leads to vasoconstriction of painfully dilated meningeal, dural, cerebral, and pial vessels

○ Inhibits dural vasodilation and inflammation

○ Inhibits trigeminal nuclear excitability

A

triptan MOA

sumatriptan, frovatriptan, zolmitriptan

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2
Q

triptan drugs

sumatriptan, frovatriptan, zolmitriptan

A

o Minor differences in pharmacokinetic or receptor affinity exist across these drugs, but for most patients, the agents are interchangeable
o Choice is usually dictated by cost/formulary availability

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3
Q

When are triptan drugs most effective

A

○ Taken at onset of migraine
○ Combined with an NSAID
○ NOT overused
○ No opioid use recently

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4
Q

Sumatriptan

A

used most often - rapid and short acting

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5
Q

Frovatriptan

A

used for menstrual migraines

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6
Q

Ergot alkaloids use

A

acute migraine treatment

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7
Q

Potent vasoconstrictor MOA

A

ergot alkaloids

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8
Q

Formulations of ergot alkaloids

A

always include caffeine to improve bioavailability

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9
Q

○ DO NOT combo with other vasoconstrictors or use on anyone who cannot tolerate a vasoconstrictor
§ Such as in peripheral vascular disease
§ Individuals already on “triptans”
§ Must monitor BP and for angina/peripheral vascular ischemia
○ Cold fingers and toes!

A

Ergot alkaloids ADE

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10
Q 
○ Dysphoria
○ Nausea
○ Vomiting
○ Cardiovascular effects
○ Greater cost of oral formulations
A

Ergot alkaloids ADE

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11
Q

Primary role of muscle relaxants in spasticity

A

pts with underlying spastic syndromes

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12
Q

muscle relaxants role in musculoskeletal pain

A

Adjunct to NSAIDs, and/or opioids for MSK pain

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13
Q

Peripheral GABA receptors

A

Baclofen

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14
Q

Alpha 2 adrenergic agonist MOA

A

tizanidine

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15
Q

GABA-A and GABA-B allosteric agonists (opens Cl- channels)

A

diazepam

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16
Q

general CNS depressant

A

methocarbamol

cyclobenzaprine

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17
Q

Interferes with the release of calcium ions from the sarcoplasmic reticulum

A

dantrolene

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18
Q

□ Administered via intrathecal route for severe spasticity

Reduces motor neuron excitability/spasticity; relieves clonus, flexor spasms, muscle rigidity

A

baclofen

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19
Q

Management of spasticity
Similar uses as baclofen
Common OFF LABEL use is for acute low back pain

A

tizanidine

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20
Q

Chronic spastic syndromes (usually oral) and malignant hyperthermia (IV)

Not a regular go-to for lower spastic back pain due to HEPATOTOXICITY

A

dantrolene

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21
Q

Acute, painful muscle spasms associated with musculoskeletal conditions

□ DO NOT combine with TCAs due to similar structure –> toxicity
□ STRONG anticholinergic
□ Sedation

A

cyclobenzaprine

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22
Q

Adjunctive treatment of muscle spams associated with acute painful musculoskeletal conditions

A

methocarbamol

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23
Q

§ Use: Muscle spasms, Spasticity

§ ADE: Tolerance, dependence, CNS depression, abuse

§ PKs: Unpredictable and undergo a variable duration of action; Accumulates in tissues

A

diazepam

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24
Q

Schedule 4 drug

§ ADE
□ Tolerance, dependence, CNS depression, abuse
□ MAX recommendation in therapy length: 2-3 weeks
□ Longer treatments are associated with withdrawal

A

carisoprodol

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25
Q

Activates peripheral nociceptors on primary sensory neurons to temporary increase release of substance P

Eventually leads to depletion of substance P in neurons to relieve neuronal firing

A

capsaicin

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26
Q

good for insect bites, minor burns/cuts/scrapes, poison oak/ivy/sumac, eczema, psoriasis, dry skin

A

menthol

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27
Q

Methyl salicylate

A

§ Combined with trolamine salicylate to form “Aspercreme”
□ Intraarticular salicylic acid concentrations can reach 60% of those provided by large systemic doses of ASA –> CHEAP
□ Useful for mild musculoskeletal and arthritic pain

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28
Q

NSAID that is topical and transdermal

A

diclofenac

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29
Q

§ VERY low doses of an NSAID, but still warned about the systemic effects of taking an NSAID
□ CV thrombotic events, GI effects (ulcers, bleeding, perfs), renal, HTN, CHF, pregnancy, liver warnings
□ PREGNANCY: may cause premature closure of ductus arteriosus

A

diclofenac

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30
Q

ASA triad

A

chronic rhinosinusitis, nasal polyps, severe bronchial asthma

31
Q

local anesthetics MOA

A

blocks sodium channels to prevent the pain signal impulse from conducting along the afferent nerve

Suppresses the perception of the pain occurring

32
Q

○ Why the anesthesia may fail

§ Pharmacokinetic reasons

A

□ Increased local blood flow/distribution away from site of injection
□ Local tissue acidosis/edema - like during infections
□ Patients with higher rates of metabolism

33
Q

○ Why the anesthesia may fail

§ Pharmacodynamic reasons

A

□ Effects of inflammation on peripheral and central sensitization of nerves
□ Patients with less susceptible nerve fibers

34
Q

ADE: cardiac of local anesthetics

A

□ AV block
□ Dysrhythmias
□ Bradycardia/Hypotension
□ Cardiac arrest

35
Q

ADE: neurological of local anesthetics

A

□ CNS excitation followed by depression
□ Spinal HA
□ Autonomic blockades results in urinary/fecal incontinence

36
Q

Lidocaine vs. ropivacaine

A

lidocaine: faster acting
ropivacaine: longer acting with half life >4hrs

37
Q

benzocaine vs. tetracaine

A

benzocaine more prone to methemoglobinemia

38
Q

Any history of CV disease, heart disease, or hepatic impairment, contraindicates this use

A

ergotamine/dihydroergotamine

39
Q

Why is caffeine in ergotamine for migraine treatment?

A

Caffeine increases the bioavailability of ergotamines

Caffeine can help with the migraine

40
Q

Factors that increase triptan effectiveness to treat migraine

A

a. Taken at very onset of migraine
b. Combined with an NSAID
c. Not overused
d. Opioid use not recent

41
Q

Factors that decrease triptan effectiveness to treat migraine

A

a. Waiting to take the med
b. Not combined with an NSAID
c. Used frequently already
d. Have a contraindication

42
Q

Rapid-acting, and therefore potentially more effective as migraine and cluster headache abortive therapies

A

sumatriptan

43
Q

Longer-acting, and therefore potentially more useful for menstrual or other similarly timed recurring migraines

A

frovatriptan

44
Q

Describe and compare contraindications of the ergot alkaloids and -triptans

A

A. Cardiovascular, coronary heart disease
B. HTN, uncontrolled
C. Hepatic impairment (as are liver metabolized!)
D. Peripheral vascular disease - ANY HISTORY, symptoms, or signs
E. Hypersensitivity to drug or components

45
Q

ergotism from moderate ingestion

A

n/v

46
Q

ergotism from higher ingestion levels

A

i. Distal vasoconstriction - check for peripheral vascular ischemia! (cold fingers and toes)
ii. Itching/burning limb pain
iii. Loss of limb sensation
iv. Gangrene/auto-amputation of charcoal-black limbs

47
Q

ergotism from convulsive levels

A

i. Flexion of fingers/wrists/ankles
ii. Double vision
iii. Altered mental state/mania
iv. Hallucinations and diaphoresis

48
Q

OTC analgesics for tension HA tx

A

i. 1,000mg acetaminophen

ii. Ibuprofen, ASA, naproxen

49
Q

prevention of tension HA

A

i. can include amitriptyline, PT
ii. PT will strengthen muscle/reduce tension, address postural deficits
iii. Trigger management

50
Q

prevention of cluster HA

first choice

A

i. Verapamil is first choice for prevention
1) Does not readily cross the BBB so much have larger doses
a) Do have to watch for BP dropping, swelling/edema

51
Q

prevention of cluster HA

second choice

A

ii. Lithium is first or second choice

52
Q

prevention of cluster HA

other choice

A

iii. Others:

1) Glucocorticoids, Warfarin, Melatonin

53
Q

treatment of cluster HA

A

i. “Triptan” - rapid onset formulation –> sumatriptan

ii. Oxygen: 7 - 12 L/min by a non-rebreather mask

54
Q

reduced HA incidence

A

HTN meds

55
Q

Sources of pain relieved by Tylenol

A

a. Frequent episodic tension type HA (1,000mg) and other general Has
b. Osteoarthritis pain
i. NSAIDs are recommended as initial therapy for OA
1) Oral NSAIDs for hand, knee, hip OA
2) Topical NSAIDs for hand and knee OA and >75yrs

56
Q

Source of pain NOT relieved by Tylenol

A

low back pain

57
Q

A. Acute pain treatment for muscle relaxants

A

a. Methocarbamol
b. Diazepam - risk for tolerance, abuse, and dependence
c. Carisoprodol - risk for tolerance, abuse, and dependence
d. Tizanidine - off label
e. Diclofenac 1% gel for acute pain of strains, sprains, and contusions of 2-4 grams to skin of the affected areas

58
Q

B. Chronic pain treatment for muscle relaxants

A

a. Baclofen

b. Dantrolene - watch hepatotoxicity

59
Q

Capsaicin use

A

i. Post herpetic neuralgia

ii. Minor aches/pains of muscles/joints - arthritis, backache, sprains

60
Q

menthol use

A

sore throats

MSK aches/pains

61
Q

methyl salicylate use

A

arthritis

mild MSK pain

62
Q

diclofenac use

A

upper/lower extremity joint arthritis

acute pain of strains/sprains/contusions

63
Q

capsaicin SE

A

i. Dose must be titrated up and can produce a burning sensation for the first few days of application
ii. Lower doses produce less burning

64
Q

diclofenac SE

A

i. All indications with NSAIDs
1) CV thrombotic events, CHF, renal, liver toxicities, GI effects (ulcers, perforations, bleeds), pregnancy (premature closure of ductus arteriosus)
2) Increased sun sensitivity

65
Q

MOA of local anesthetics

A

Suppress pain by blocking the sodium channels on afferent nerves to suppress pain impulse conduction signals at the administration site to reduce the body’s awareness of the pain

66
Q

local anesthetics clinical use

A

Suppresses pain without generalized depression of nervous system at correct doses and route/site of administration

67
Q

Chronological onset of local anesthetic action (5 steps to know)

A
  1. anesthetic is injected near a nerve
  2. local anesthetic permeates axonal neuronal membranes
  3. binding of local anesthetic to sites on voltage-gated sodium channels
  4. period of time when only a few sodium channels are blocked -> results are insufficient for full anesthesia
  5. clinically observed rates of onset and recovery from blockade due to relatively slow diffusion of local anesthetic molecules into and out of the whole nerve.
68
Q

ester-type anesthetics (4)

A

cocaine
procaine
tetracaine
benzocaine

69
Q

amide-type anesthetics (5)

A 
lidocaine
mepivaciane
articaine
bupivacaine
ropivacaine
70
Q

Ester-type anesthetics metabolism

A

Very short plasma half-life:

Therefore only administered locally and are broken down quite quickly

1/2 life renders them ineffective for systemic / significant tissue distribution

71
Q

Amide-type anesthetics metabolism

A

b. Has a much larger tissue distribution and can therefore be administered over a greater area
c. Metabolized by the liver
d. Great choice for wanting a longer duration of anesthetic

72
Q

cross allergenic potential with ester and amide anesthetics

A

a. If allergic to a specific ester, cannot use other ester anesthetics
i. CAN use an amide-type however
ii. And vice-versa
b. Esters are metabolized to PABA and some individuals have a reaction to this

73
Q

adverse effects of local anesthetics that are an extension of the MOA

A

a. Difficult to control toxicity of agents due to sodium channels being required for normal function of neurons
i. Blockage can result in…
1) Cardiac effects: potentially dysrhythmias
2) Central nervous system adverse effects
3) Induce seizures
4) Systemic effects when absorbed systemically/administered into highly perfused tissues

74
Q

use of epi in local anesthetics

A
  • a vasoconstrictor that helps to reduce the systemic effects and prolong the local effects
  • helps with bleeding at the site
  • decreases rate of vascular absorption
  • increases anesthetic molecules at targeted nerve membrane
  • deeper and longer duration of anesthesia achieved
  • provides a marker for inadvertently entering a vascular vessel due to CV excitability
  • May have ability to activate endogenous analgesic mechanisms and produce a deeper state of anesthesia through activation and binding of alpha2 adrenergic receptors

(Absorption of a vasoconstrictor itself can cause palpitations, tachycardia, nervousness, HTN)

Neurology (12 decks)

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