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Neuro Block 2 > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

What sorts of pain will NSAIDs be effective for?

A

pain due to inflammation - only works for mild to moderate pain, but there’s fewer adverse effects

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2
Q

What biochemical pathway is affected by NSAIDs?

A

the arachidonic acid pathway

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3
Q

Describe the arachidonic acid pathway

A

trigger activates phospholipase, which releases an arachidonic acid from the membrane phospholipids

arachidonic acid is acted on by loposygenase or cyclooxygenase

lipoxygenase creates leukotrienes

cyclooxygenase makes prostaglandins, thromboxanes and prostacyclins

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4
Q

What enzyme in the arachidonic acid pathway is blocked by NSAIDs?

A

COX1 and COX2

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5
Q

How are COX1 and COX2 different?

A

COX1 is active under normal physiology - promotes prostaglandin production that provide gastric cytoprotection, vasodilation, and platelet aggregation

COX2 is inducible in response to inflammation

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6
Q

What effect do thromboxanes have on platelet? How about prostacylincs?

A

thomboxanes promote platelet aggregation

prostacyclins inhibit platelet aggregation

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7
Q

How are prostaglandins related to pain and why does blocking their production make pain better?

A

they modify te nociception threshold by making the threshold for activation lower - more sensitive to pain

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8
Q

What is special about aspirin among the NSAIDs?

A

It irreverisbly inhibits both COX1 and COX2, while the other NSAIDs reversibly inhibit them

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9
Q

What three things are all NSAIDS capable ot?

A

analgesic

antipyretic

anti-inflammatory

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10
Q

How is the antipyretic effect of NSAIDs mediated?

A

PGE2 is what triggers the hypothalamus to increase the body temp set point - that’s why you get fever in inflammation

if you use NSAIDs to block PGE2 production, body temp normalizes

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11
Q

What are the adverse effects of the NSAIDS - especially aspirin?

A

It causes gastrointestinald istress

the prostaglandins that were made by COX1 and had protective effects in the GI system are no longer synthesized, so you get increased gastric acid secretion and decreased mucous secretion, leading to capillary damage, necrosis and bleeding - iron deficiency anemia

increased clotting time

respiratory and electrolyte disturbances

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12
Q

How significant is aspirin’s impact on clotting time?

A

you get a 2x increase in clotting time for a week after a single dose of aspirin because of the irreversible inhibition of COX (thromboxane synthesis) in platelets

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13
Q

When should you stop NSAIDS before elective surgery? Aspirin specifically

A

stop NSAIDs 2 days before and aspirin 1 week before

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14
Q

How do the NSAIDs lead to respiratory and electrolyte disturbances?

A

high doses stimualte respiratory center int he medulla, leading to hyperventilatoin

this hyperventilation causes respiratory alkalosis (increase blood pH)

It can also cause metabolic acidosis because toxic doses of aspirin can uncouple oxidative phosphorylation such that lactic acid accumulates in the serum, decreasing blood pH - this is the bigger deal than above

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15
Q

What are the mild toxicity symptoms with aspirin OD?

A

tinnitus

headache

nausea, vomiting

sweating, thirst, hyperventilation

hearing loss

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16
Q

What are the most severe toxicity symptoms in aspirin OD?

A

hyeprventilation

acid/base imbalance

dehydration

agitation, hyperactivity, slurred speech, tremor, seizures, coma

fever (especially in children)

17
Q

How do you treat an aspirin overdose?

A

gastric decontamination: induce vomiting, gastric lavage, activated charcoal

correct the acid base imbalance by giving sodium bicarb

maybe blood transfusion and dialysis to clear the system

full reovery IS possible if treated

18
Q

What happens in an aspirin hypersensitivity?

A

rhinitis, profuse secretions, branchial asthma, bronchoconstruciton, hypotension, vasomotor collaspe, copa

It is NOT immune mediated though - they think it’s because the arachidonic acid that can’t be acted on by COX is shunted into the liposygenase pathway, yielding excess leukotrienes

19
Q

What is the treatment for an acute aspirin hypersensitivity reaction?

A

epinephrine (same as an anaphylaxis)

avoid NSAIDs and other salicilates in the future

20
Q

What is Reye’s syndrome?

A

It’s a fatal condition associated with aspirin use in the presence of viral infection - so don’t give to kids with chidken pox

21
Q

Why do you want to avoid concurrent aspirin use with other NSAIDS?

A

Because prophylactic aspirin targets thromboxanes first, so you get reduced clotting

However, if given with other NSAIDs, this can also target the proctacyclin production, so clotting actually can be increased!

22
Q

Why is ibuprofen nice compared to aspirin?

A

it has fewer GI adverse effects and the clotting effects are reversible

23
Q

What is special about indomethacin? WHy is it not used often?

A

It’s the most potent COX inhibitor

It has significant toxicity, so it’s usually only used if other NSAIDS have been ineffective

24
Q

What congenital disorder is indomethacin used to treat?

A

patent ductus arteriosus

25
Q

What ist he NSAID that can be injected and replace morphine if opioid addiciton is an issue?

A

ketorolac

26
Q

What is special about celecoxib?

A

it is a selective COX2 inhibitor, so you get the inflammation reduction without the harmful GI effects

27
Q

Why is acetaminophen NOT an NSAID?

A

It doesn’t have anti-inflammatory effects although it is analgesic and antipyretic

28
Q

What are the pros of taking acetaminophen besides the minimal effect on GI?

A

it also has no effec ton bleeding or on respiration

29
Q

What is the major issue with tylenol toxicity though?

A

It’s therapeutic index is much lower than other OTC meds because a toxic free radical metabolite is formed in the liver and can cause hepatic necrosis

30
Q

Why should you not drink alcohol with tylenol?

A

ethanol will shift liver metabolism to the toxic metabolite, thus increasing risk of hepatotoxicity

31
Q

What is the treatment for a tylenol overdose?

A

N-acetylcysteine works as a scavenger drug so that is picks up all the qhinone free radical product

(basically an exogenous equivalent of glutathione)

32
Q
A

Neuro Block 2 (19 decks)

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