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PathoPhysiology > Exam Two - Pain Management > Flashcards

Exam Two - Pain Management Flashcards

1
Q

NSAID stands for

A

Non-Steroidal Anti-Inflammatory Drugs

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2
Q

What are NSAIDs different classes?

A
  • Salicylates
  • Propionic Acid Derivatives
  • Oxicams
  • Acetic acid derivatives
  • Cox-2 Inhibitor
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3
Q

Examples of salicylates

A

aspirin (ASA)

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4
Q

Examples of Propionic Acid Derivatives

A

Ibuprofen
naproxen
ketoprofen
fenoprofen

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5
Q

Examples of Oxicams

A

meloxicam
piroxican

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6
Q

Examples of acetic acid derivatives

A

indomethacin
sulindac
tolmetin
ketorolac
etodolac (COOH)
diclofenac (phenylacetic acid)

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7
Q

Examples of Cox-2 Inhibitors

A

celecoxib

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8
Q

Most NSAIDS inhibit the _________ AND ___________ pathways

A

COX-1
COX-2

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9
Q

COX-1 is responsible for…

A

cytoprotective prostaglandins
- protect gastric mucosa
- aid platelet aggregation

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10
Q

COX-2 is responsible for…

A

imflammatory prostaglandins
- recruit inflammatory cells
- sensitize skin pain receptors
- regulate hypothalamic temperature control

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11
Q

Adverse effects of NSAIDs

A
  • increased GI bleed/ulcer risk
  • decreased renal perfusion
  • increased blood pressure
  • increase CV event risk…. other than Aspirin
  • increased bleeding risk
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12
Q

Which NSAIDs is safest to use in patients with CVD?

A

Naproxen

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13
Q

How close to surgery do you stop taking aspirin?

A

1 week

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14
Q

How close to surgery do you stop taking other NSAIDs?

A

1-2 days

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15
Q

Use NSAIDs with caution in patients with what diseases?

A

CVD, renal patients, HTN

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16
Q

How long can you use ketorolac (toradol)?

A

5 days! Black box warning

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17
Q

When we stay steroids, most often we’re referring to which kind?

A

Glucocorticoids

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18
Q

Uses of corticosteroids:

A

anti-inflammatory
anti-allergy
anti-rejection
Tx of Addisons DZ
Neonatology lung maturation

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19
Q

What are the routes of administration for corticosteroids

A

oral
inhaled
IV
IM
topical
eye drops
ear drops
rectal
intra-articular injection

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20
Q

Corticosteroids ____________ circulating lymphocytes

A

decrease

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21
Q

corticosteroids ___________ basophils, eosinophils, monocytes

A

decrease

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22
Q

corticosteroids ______ swelling.erythema/secretions

A

decrease

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23
Q

corticosteroids _____ PMN, Plts, RBCs, HGb/HCT

A

increase

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24
Q

corticosteroids ___ plasma glucose (GLC)

A

increase
increase hepatic HLC production

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25
Q

If you ______ mast cells, then you __________ histamine release

A

stabilize, decrease

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26
Q

if you __________ phospholipase A2, then you see a __________ in prostaglandins

A

inhibit, decrease

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27
Q

side effects for corticosteroids

A

hyperglycemia
increase appetite
steroid psychosis
impaired wound healing
hypertension and hypokalemia
risk of infection
osteoporosis
weight gain/fluid retention

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28
Q

common corticosteroids you should recognize:

A

prednisone (deltasone) 5mg
prednisolone (Pediapred) 5mg
Methyl-prednisolone (Solu-Medrol) 4mg
Dexamethasone (decadron) 1mg
triamcinolone (kenalog)
hydrocortisone (Solu-cortef)
betamethasone (celestone)

29
Q

spasmolytic

A

agent to treat spasticity resulting from upper motor neuron lesions such as MS, CP, CVA, spinal cord injuries, etc.

30
Q

anti-spasmodic

A

agent to treat spasms resulting from peripheral skeletal muscle conditions (local tissue injury)

31
Q

spasms =

A

muscle weakness related to sustained involuntary contraction of skeletal muscles, stiffness, impaired movement and increased basal muscle tone. May interfere with mobility and/or speech

32
Q

Spasmolytic agents you should know

A
  • baclofen (lioresal)
  • benzodiazepines (esp. diazepam)
  • tizanidine (zanaflex) alpha-2 agonist
33
Q

SE/risks of spasmolytics

A

fall, drowsiness/dizziness, N/V, impaired PT session

34
Q

centrally-acting anti-spasmodic agents you should recognize

A
  • cyclobenzaprine (flexeril)
  • methocarbamol (robaxin)
  • carisoprodol (Soma C-IV)
35
Q

Which two centrally-acting anti-spasmodic drugs are strong CNS depressors, incite drug seeking behavior, works at brainstem level, and are ineffective on spasms related to spinal cord injury or CP?

A

Methocarbamol (Robaxin) and carisoprodol (Soma C-IV)

36
Q

Which centrally acting anti-spasmodic drug has high abuse rates and patients ask for it by name?

A

Carisoprodol (Soma-IV)

37
Q

What is the MOA for centrally-acting anti-spasmodic agents?

A

still don’t know… general CNS depression?

38
Q

opiate

A

drug derived from the alkaloids of the opium poppy

39
Q

opioid

A

drugs that includes opiates, opiopeptins, and all synthetic/semisynthetic drugs that mimic the action of opiates

40
Q

opioid peptides

A

endogenous peptides that act on opioid receptors

41
Q

opioid agonist

A

drug that activates some or all opioid receptors and does not block any

42
Q

opioid partial agonist

A

drugs that can activate an opioid receptor to elicit a submaximal response

43
Q

opioid antagonist

A

drug that blocks some or all opioid receptors

44
Q

mixed agonist-antagonist

A

drug that activates some opioid receptors and blocks others

45
Q

narcotic

A

psychoactive compound with sedative properties, used in legal context to refer to substances with abuse/addictive potential

46
Q

What are the 3 types of opioid receptors?

A

mu
kappa
delta

47
Q

Mu receptors are responsible for…

A

analgesia
respiratory depression
euphoria
sedation
physical dependence
glowed GI tract
miosis
modulation of hormone & NT release

48
Q

kappa receptors are responsible for

A

analgesia
minimal respiratory depression
dysphoria
mild sedation
glowed GI transit
miosis
psychomimetic effects

49
Q

delta receptors responsible for

A

analgesia
modulation of hormone and &NT release

50
Q

Opiate overdose can kill why?

A

respiratory depression

51
Q

What are some CNS effects of opiates?

A

analgesia
euphoria
sedation
respiratory depression
cough suppression
miosis
truncal rigidity
N/V
reduced shivering
may increase ICP

52
Q

what are some PNS effects of opiates

A

bradycardia
hypotension
constipation
biliary colic
urinary retention
prolong labor
stimulate release of ADH, prolactin, somatotropin, and inhibit release of LH
pruritus (itching)
hives (increase HA release)

53
Q

What are the strong morphine like side effects?

A

respiratory depression
constipation
sedation
emesis N/V!
elevation of intracranial pressure
urinary retention
orthostatic hypotension
miosis (pinpoint pupils)
pruritus

54
Q

Morephine mnemonic stands for…

A

miosis
orthostatic hypotension
respiratory depression
physical dependency
histamine release
increased ICP
Nausea
Euphoria
Sedation

55
Q

Tolerance

A

a higher dose of drug is needed to achieve the same response

56
Q

What side effects of opiates have low tolerance build?

A

miosis and constipation

57
Q

Physical dependence

A

withdrawal symptoms occur if drug is abruptly stopped, should taper

58
Q

Opioid antagonist MOA?

A

antagonists at mu and kappa receptors

59
Q

What are examples of opioid antagonists?

A

naloxone (narcan) - short acting
naltrexone (ReVia) - oral
nalmefene (Revex) - long acting

60
Q

What are examples of common types of chronic neuropathic pain?

A
  • diabetic neuropathy
  • post-herpectic neuralgia
  • phantom limb pain
  • fibromyalgia
61
Q

What drugs are used to help chronic neuropathic pain?

A
  • TCA: tri-cyclic anti-depressants
  • SSRI (anti-depressant)
    -SNRI (anti-depressant)
  • Pregabalin (lyrica) anti-epileptic
  • Gabapentin (Neurontin) anti-ep
62
Q

Which drug has the longest track history in treating neuropathic pain?

A

TCA

63
Q

Which drugs are most commonly prescribed for neuropathic pain today?

A

pregabalin (lyrica) and gabapentin (neurontin)

64
Q

What is the MOA of TCA?

A

blocks re-uptake of NE, also blocks 5HT, alpha, HA and muscarinic receptors, analgesic actions still not clear

  • Fall risks and narrow TI
65
Q

gabapentin (Neurontin) MOA?

A

increases CNS GABA availability

66
Q

SE of gabapentin?

A

DZ, ataxia, sedation, mood changes, tremors

67
Q

Pregabalin (lyrica) MOA

A

MOA: similar to gabapentin

68
Q

How is pregabalin (lyrica) different from gabapentin?

A

much better bioavailability (F) = 0.9

69
Q

SNRIs appear ______ than SSRIs for chronic pain

A

more effective

MOA: inhibit reuptake of 5HT and NE

PathoPhysiology (29 decks)

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