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MSK/Derm > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

How are NSAIDs related?

A

only in the fact that they inhibit cyclooxygnase (COX), which makes prostaglandins

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2
Q

What is the mechanism of creation of tissue specific prostaglandins?

A

cell injury (or other trigger) -> phospholipase A2 -> arachidonic acid -> cyclooxygnase -> prostaglandin H2 -> tissue specific PG synthase -> tissue specific prostaglandins

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3
Q

What are the two types of COX?

A

each has its own gene, both make PGs from AA

COX1 - the “housekeeping” one and present in most tissues all the time

COX2 - the “inflammatory” one and appears with inflammation and injury, which is the cause of the pain except in the CNS, kidney, and uterus

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4
Q

What systems are affected by prostaglandins?

A

PNS and CNS (pain)

GI

renal (and CV)

platelets (hemostasis)

other - bone, reproductive

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5
Q

How do prostaglandins affect pain?

A

causes allodynia and hyperalgesia

  • sensitize pain in nerve endings
  • enhance pain in CNS
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6
Q

What is the role of COX-2 in peripheral mechanisms of pain?

A

ramp up PGE2, which bind to prostaglandin receptors

these ramp up PKA and PKC, which causes nociceptors leaky to sodium

resting membrane potential goes up and firing potential goes up

now instead of having a crush, cut, or burn trigger, touch will trigger firing of the nerve

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7
Q

Why do NSAIDs work when there is no inflammation?

A

headaches

osteoarthritis

hangovers

postop pain (third molar extraction)

work when there is no inflammation - due to role in CNS

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8
Q

How do PGs enhance pain in the CNS?

A

enhance pain in CNS

increase SP and glutamate release

increase sensitivity 2nd order neurons

decrease release of inhibitory transmitters

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9
Q

Why are NSAIDs not true analgesics?

A

they only blunt PNS/CNS sensitization

they do not block pain transmission - can still feel acute pain and prevent self-injury

are actually anti-hyperalgesics

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10
Q

What does COX-1 do in the GI system?

A

protects the GI system

increases mucous layer thickness

decrease pH gradient

increase bicarbonate secretion

incrase mucosal blood flow

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11
Q

What are the NSAID GI toxicities?

A

two mechanisms:

1) direct gastric irritation (all but 1 acids)
2) decreased cytoprotection in stomach - bicarbonate secretion, blood flow, epithelial cell turnover, mucosal immunocyte function

not often associated with dyspepsia - silent ulceration in 70%

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12
Q

misoprostol

A

protects GI tract

a synthetic PGE1

increases nucous formation

problem - big time diarrhea

sold as combo drug with diclofenac

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13
Q

What is the role of PG in the kidneys?

A

renal PGs from COX1 and COX2

affect NA+ and water balance - affects BP

in decreased perfusion states, PGs dilate afferent blood vessels and are needed to prevent ischemia when low volume/BP/cardiac output

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14
Q

What is the effect of NSAIDs in treated hypertensives?

A

increases BP in treated HTN

increases systolic BP and increases MI risk

normotensives unaffected

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15
Q

What are renal affects of NSAIDs?

A

BP elevation/diuretic interaction by messing with PG Na+/water balance

ischemic acute tubular necrosis by preventnig PG afferent blood vessel dilation in lower perfusion states

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16
Q

How does PG cause hemostasis?

A

platelets only contain COX1

forms thromboxane and leads to aggregation

NSAIDS lead to decreased clotting

17
Q

What is the effect of aspirin on COX1 and 2?

A

blocks function of the enzyme and irreversibly acetlyates it

platelets can’t make more due to lack of nucleus

7-10 days of protection because that’s how long it takes to make new platelets

to recover need to take more COX

18
Q

What are the pharmacokinetics of NSAIDs?

A

all are rapidly absorbed orally

all highly protein bound - relevant in elderly with decreased albumin and can displace warfarin and leed to BLEEDING

all mostly metabolized in liver

different half lives

19
Q

What are the pharmokinetics of aspirin?

A

salicylate so irritating that it can only be used externally - methyl salicylate is oil of wintergreen

aspirin is an ester of the salicylic acid - acetylsalicylic acid has a T1/2 of 15 min becoming salicylate

salicylate has T1/2 of 2-3 hours at normal doses

all other NSAIDs are >6 hours, some 24 hours

20
Q

What are the effects of ASA on NSAIDs?

A

displaces NSAIDs from albumin

increases toxicity risk

21
Q

What are pertinent histories that should caution use of NSAIDs?

A

ulcers

coagulopathy

renal disease

hepatic disease

CV disease - ASA ok (low dose)

22
Q

What is Reye’s syndrome?

A

after viral illness in chldren, aspirin causes hepatotoxicity, siezures, coma, and death

ex. URI, chickenpox, etc.

23
Q

acetaminophen (paracetamol)

A

the active metabolite of phenacetin

weak anti-inflammatory and no peripheral COX inhibition

reasonable antipyretic and analgesic - mechanisms unclear

24
Q

What are the side effects of acetaminophen?

A

no effect on GI, platelet, and renal

max daily dose is 4g (12 pills)

less in drinkers and liver pts

25
Q

NSAID names to know

A

Ibuprofen (Motrin)

Naprosyn (Naproxen, Alleve)

Indomethacin (Indocin)

Diclofenac (Voltaren)

Nabumetone (Relafen)

Ketorolac (Toradol)

Acetylsalicylic acid (ASA)

Melixicam (Mobic)

Celoxib (Celebrex)

Acetaminophen

26
Q

Celecoxib

A

COX2 specific inhibitor

GI ulcers reduced by half

same as NSAIDS - increased BP and increased CVA

no effect on platelets - can use during surgery, no interference with low dose ASA

27
Q

IV NSAIDs in the US

A

ketorolac

ibuprofen

acetaminophen

28
Q

ketorolac

A

generic, potent analgesic

minimal inflammatory effect

worthless orally

limited to 5 days due to toxicity

not as potent as acetaminophen IV

29
Q

topical NSAIDs in the US

A

diclofenac - gel or ointment or patch

useful on superifical joints

less toxicity - no platelet effects, minimal GI effects, and FDA warnings are all the same

30
Q

What are the limits to opioid therapy?

A

opioids slow GI tract peristalsis via direct ation on gut and CNS

causes constipation in outpatients

after GI surgery, means longer ileus - patient can’t take orals or leave with ileus, pain can slow GI function, if severe pain and ileus, opioids are a poblem!

31
Q

What is incident pain?

A

pain only presents when patient moves (ex. coughing after thoracotomy)

opioid doses to control pain when present causes side effects when pain is not present

ideal for NSAIDs (blunt the hyperalgesia of coughing, no sedation when not coughing)

32
Q

Keterolac

A

in the past, NSAIDs can’t cover more severe pain but can cover pains that opioids can’t

the solution was to combine NSAIDs and opioids

this drug is a combination of the two that can be administered IV and IM

33
Q

What are the problems of administering perioperative NSAIDs?

A

not popular after surgery because of increased bleeding

stress ulcers are worsened

renal compromise - anesthesia and surgery decreases renal blood flow and some antibiotics further stress the kidneys

bone healing is slowed

IV acetaminophen has none of these issues!

MSK/Derm (54 decks)

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