NSAIDs/Pain Management Flashcards

1
Q

NSAIDs only relate in the fact that they all

A

Inhibit the enzyme making prostaglandins- cyclooxygenase

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2
Q

Mechanism of NSAIDs- two step process

A

COX breaks down arachidonic acid–> prostaglandin G2–>prostaglandin H2–> tissue specific prostaglandins.

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3
Q

Two types of COX

A

Both make PGs from AA
Each has its own gene
COX1 is the housekeeping one- present in most tissues all the time
COX2 is the inflammatory one- appears when injury/inflammation occurs, one causing pain, except in CNS, kidney, uterus

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4
Q

Prostaglandins and pain

A

Allodynia/hyperalgesia
Sensitize nerve endings- touch triggers them now
Enhance pain in CNS (amplifies pain by hyperalgesia) and PNS

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5
Q

How do prostaglandins enhance pain in CNS

A

Increase SP and glutamate release
Increase sensitivity of 2nd order neurons
Decreased release of inhibitory transmitters descending

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6
Q

NSAIDs and pain

A

They simply blunt PNS/CNS sensitization, so they are anti-hyperalgesics, not anti-inflammatories.
They can act without inflammation: CNS action, hangover, headache, postop pain, molar extractions, sunburn
Need an upregulation of PGs to have benefit
‘Afterward’ pain is blunted, not initial pain.

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7
Q

Normal gastric protective mechanisms

A

PG-dependent protective factors that increase mucous layer thickness, pH gradient, bicarbonate secretion, and mucosal blood flow. Mostly COX-1
Why NSAIDs are an indirect cause of stomach ulcers

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8
Q

GI toxicity

A

Not often associated with dyspepsia- usually a silent ulceration in 70%

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9
Q

NSAID renal concerns- 1st

A

BP elevation/diuretic interaction- because they are highly protein bound, they cannot be dialyzed. NSAIDs enhance the ability to absorb sodium concentrate, so we hold onto more water. Edema, stroke, heart attacks. Caution of those who are HTN/renal issues

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10
Q

Renal concerns- 2nd

A

Decreases perfusion states, PGs normally dilate afferent blood vessels. NSAIDs choke off blood supply- ischemia, renal failure
Caution in patients with: Dehydration, blood loss, reduced cardiac output (CHF), and low blood pressure

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11
Q

NSAIDs and CV

A

They all have a CV risk but:
Naproxen is the lowest
Diclofenac is the highest

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12
Q

PGs and hemostasis

A

Prostacyclin (PGI2) made by COX2- made in endothelium which have nuclei, platelet inhibitor and vasodilator.
Thromboxane A2 made by COX1- made in platelets which do not have nuclei. Platelet activator and vasoconstrictor.
The platelet side is usually very inactive, endothelial side is minimally active.

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13
Q

NSAIDs and hemostasis

A

Blocks formation of COX1 making TXA2 more so, since this one is more active during bleeding/injury in platelets. Inhibiting it= decreasing clotting (bad if undergoing surgery)
Since the endothelial COX2 and PGI2 are minimally active, no big change is seen from blocking it.

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14
Q

Hematologic toxicity- NSAIDs vs ASA

A

NSAIDs reversibly bind COX, so coagulation normalizes after a couple half lives
ASA irreversibly acetylates COX, so since platelets do not have nuclei, have to make completely new platelets before coagulation can recover: 7-10 days. Endothelium has nuclei and can recover

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15
Q

COX-2 inhibitor

A

Have no platelet affects

*celecoxib

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16
Q

NSAID side effects

A
Stomach/duodenal ulceration 
Decrease platelet clotting function
Decrease blood flow in kidneys
Edema and HTN- in at risk patients only, it will increase CV risk (high BP and CAD)
Reports of hepatic dysfunction
17
Q

NSAID cautions

A

Wary of using in history of- ulcers, coagulopathy, renal disease, hepatic disease
CV disease: ASA okay on low dose

18
Q

Reye’s Syndrome

A

ASA (aspirin) given to children with a viral illness- causes hepatotoxicity, lactic acidosis, seizures, coma, death
Dose related risk increase

19
Q

NSAIDs to know

A
Ibuprofen (Motrin)
Naprosyn (naproxen, alleve)
Indomethacin
Diclofenac
Nabumetone
Ketorolac
Acetylsalicylic acid
Meloxicam
Celecoxib
Acetaminophen
20
Q

ASA and platelet inhibition is useful for

A

Cardioprotection and stroke protection

21
Q

Generic IV NSAID

A

Ketorolac- potent analgesic, hospital use, multimodal analgesia when IV opioids are not working, works on CNS

22
Q

An opioid resistant pain that NSAIDs are good for

A

Incident pain- pain only present when patient moves

Nerve pain- not C fiber mediated (which opioids primarily act on)

23
Q

What is neuropathic pain?

A

After a PNS/CNS injury- wiring damage
Opioid resistant- hard to treat
Shooting, burning with sensory changes.

24
Q

Acute pain medications

A

Non-opioid: NSAIDs/APAP, muscle relaxants, topical (lidocaine)
Opioid: tramadol, opioids

25
Q

IV benzodiazepines for muscle spasms warning

A

Warning with opioids*

26
Q

PCA continuous infusion option

A

For patients on chronic preop opioids ONLY

Tolerant to analgesia and hypovolent

27
Q

Muscle relaxants- antispasticity

A

Baclofen- GABA pre and post receptor for muscle pain and neuropathic pain
Tizanidine- alpha-2 receptor agonist to blunt sympathetic outflow, sedation and hypotension possible

28
Q

Muscle relaxants- MSK pain disorders

A

Cyclobenzaprine- only one that can be used daily, TCA like action
Carisoprodol- aka soma, metabolized to meprobamate, withdrawal from this can kill you, sedative and habituative, barbiturate metabolite, DO NOT USE

29
Q

Multimodal analgesia

A

Two work by DIFFERENT mechanisms

Synergy, reduced side effects

30
Q

Chronic pain management meds

A

Daily-Antidepressants, anticonvulsants, debatable are NSAIDs and opioids.
Acute on chronic- NSAIDs, muscle relaxants, opioids

31
Q

Antidepressants

A
TCAs and SNRIs are analgesic- block reuptake of both 5-HT and NE
Enhance descending inhibitory system
NOT via Rx of depression
Need 2-4 weeks to see effects
NO TOLERANCE
32
Q

Antiepileptic drugs

A

Gabapentin- best for shooting, intermittent stabbing pain.