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Pharmacology > Opoids, NSAIDS, Acetaminophen > Flashcards

Opoids, NSAIDS, Acetaminophen Flashcards

1
Q

What receptors do opioids act on?

A

Mu, Kappa, Delta

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2
Q

What are mu receptors for?

A

kind of everything

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3
Q

what are Kappa receptors for?

A

sleepiness, pain relief, slowing down the gut

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4
Q

What are delta receptors for?

A

we don’t really know

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5
Q

Effects of Opioids

A

Analgesia, respiratory depression, sedation, euphoria, physical dependence, decreased gut motility

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6
Q

What is the most dangerous effect of Opioids?

A

respiratory depression

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7
Q

How do pure agonists work

A

bind to activate receptors

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8
Q

How do pure antagonists work

A

bind to receptors and block them

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9
Q

what is the main cause of death from opoids?

A

decreases the sensitivity of respiratory center in the brain causing a build up of CO2

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10
Q

What can increase respiratory depression?

A

when mixed with other cns depressants ie: alcohol, benzos, muscle relaxers, gabapentin

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10
Q

You will build a tolerance to all but what 2 things?

A

constipation, miosis

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11
Q

Physical dependence

A

happens to anyone using opioids for 2 or more weeks

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11
Q

what is the general rule for cross tolerance?

A

reduce equanlgesic dose by 25-50%

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12
Q

First signs of with drawl

A

yawning, rhinorrea, sweating

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13
Q

progressing withdrawl

A

anorexia, irritability, tremor

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14
Q

Severe withdrawl symptoms,

A

violent sneezing, cramps, NV, weakness, diarrhea, muscle spasms

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15
Q

Morphine drug class

A

Pure agonist

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16
Q

What route is the worst for morphine and why?

A

Oral; because absorption varies

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17
Q

Who needs special dosing with morphine?

A

older pts need doses decreased by 33%; can accumulate with low renal function

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18
Q

Other agonists related to morphine (4)

A

Codeine, Hydromorphone, Hydrocodone, Oxycodone

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19
Q

What is essential for codeine?

A

CYP2D6

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20
Q

what is CYP2D6?

A

enzyme that breaks down fat soluble drugs in the liver

21
Q

Why does codeine work?

A

because 15% of it gets turned into morphine

22
Q

Tramadol

A

half opioid agonist, half antidepressant

23
Q

What receptor does Tramadol bind to?

A

Mu receptor

24
Q

What does tramadol block?

A

the reuptake of serotonin and epinephrine

25
Q

who would tramadol benefit

A

People experiencing nerve pain

26
Q

Mixed agonist-antagonist

A

lower risk for respiratory depression and abuse

27
Q

what is an analgesic ceiling

A

they can only provide so much relief

28
Q

what drug class has an analgesic ceiling?

A

mixed agonist-antagonist

29
Q

Buprenophrine drug class

A

mixed

30
Q

what side effects are to mixed aginist-antagonists?

A

psychotomimetic- hallucinations and dysphoria

31
Q

what can mixed drug class cause?

A

opioid withdrawl

32
Q

Antagonists (central acting)

A

OD and abuse deterrent- Naloxone

33
Q

Antagonists (peripheral)

A

treatment of opioid related constipation: methylnaltrexone

34
Q

NSAIDS

A

inhibit central and peripheral prostaglandin synthesis

35
Q

what stimulates COX 2

A

process of injury

36
Q

What NSAIDS are non specific to Cox 1 or 2

A

ibuprofen, meloxicam, naproxen, diclofenac

37
Q

What NSAID is specific to COX2

A

celoxib

38
Q

What is the highest risk of NSAID use?

A

GI bleeding and ulcers

39
Q

Why do NSAIDS cause gi bleeds?

A

because they inhibit prostaglandins so the stomach lining isnt protective against the acid

40
Q

What is decreased especially if someone is dehydrated or taking an ace inhibitor?

A

Renal function

41
Q

Why do NSAIDS lower platelet fxn?

A

makes them less able to stick together, easy bruising and bleeding

42
Q

Cardiac toxicity (NSAID)

A

only related to COX2

43
Q

Who is at high risk for GI bleeds with NSAID use

A

people with a history, on aspirin, warfarin, steroids, over the age of 65

44
Q

Treatment for GI bleeds with NSAID use

A

concurrent PPI use, change to celoxib

45
Q

Ketorolac

A

max of 5 day use in all forms, has dose adjustments for people over the age of 65 and that weigh less than 50 kg

46
Q

Contraindications of Ketorolac

A

prior or active ulcer, advanced renal disease, high bleeding risk, concurrent aspirin use, NSAID or probenecid (gout drug)

47
Q

Acetaminophen

A

inhibits central prostaglandin synthesis- does not work outside the brain

48
Q

what does acetaminophen not help with

A

swelling

49
Q

what toxic substance does acetaminophen get turned into when metabolized by the liver?

A

NAPQI

50
Q

What is acetaminophen the biggest cause of

A

acute liver failure

51
Q
A

Pharmacology (2 decks)

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