APEX- NSAIDS Flashcards

1
Q

All of the following are associated with Samter’s triad EXCEPT:
A. Allergic rhinitis
B. Bronchospasm
C. Nasal polyps
D. Hypertension

A

D. Hypertension

Samter’s triad is associated with Aspirin exacerbated resp disease

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2
Q

Samter’s triad is associated with what

3 components

what can happen

A

Aspirin exacerbated respiratory disease

  1. Asthma
  2. Allergic rhinitis
  3. Nasal polyps

pts can develop life-threatening bronchospasm following aspirn administration

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3
Q

How do NSAIDs reduce pain

A

they inhibit cyclooxygenase enzyme and reduce the production of prostaglandins

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4
Q

What is diclofenac

A

a non-selective COX inhibitor

NSAID

prevents the formation of prostaglandins by inhibiting cylooxygenase
brand names: voltaren

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5
Q

What is indomethacin

A

“a non-selective COX inhibitor “
+
“prostaglandin synthase inhibitor” - used to close PDA

NSAID

preents the formation of prostaglandins by inhibiting cylooxygenase

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6
Q

What is a drug with the suffix -coxib

A

selective COX-2 inhbitior

inhibits the inducible prostaglandins which produce inflammation, pain, and fever

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7
Q

Describe the arachidonic acid pathway

A

when cells break down, the phospholipids in their membrane are converted to arachadonic acid by Phospholiapase A2

Arachiodnic acid is then broke ndown into Prostaglandins by 1 of 2 pathways

COX 1 (always present)- breaks it down to prostagladins needed for GI mucousa, platelet function, and renal blood flow

COX 2 (inducible)- breaks it down to prostaglandins that are needed for inflammation, pain, and fever

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8
Q

Is there a ceiling effect on analgesia with NSAIDS or Opioids?

A

ceiling effect with nsaids for analgesia

no ceiling effect for analgesia with opioids

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9
Q

3 downfalls of cox 1 inhibition

A

gastric irritation
impaired platelet function
reduced renal blood flow

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10
Q

selective COX-2 inhibitors seem great…but why arent they

A

they increase the risk of HTN, MI, and HF moreso than COX-1

screwed either way

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11
Q

How might COX inhibitors produce bronchospasm

A

decreased prostaglandins > leukotrienes > bronchospasm

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12
Q

why to avoid NSAIDs in pts with renal disease

A

because blocking prostaglandins reduces renal blood flow

cox-1 prostaglinds responsible for : platelet function, gastri mucosa, and renal blood flow

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13
Q

You always know there is something with nsaids and ortho that you question… what is it?

A

they decrease osteoclast and osteoblast activity and may impair bone healing

no one seems to care though lol

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14
Q

Key drug interactions with NSAIDs

A

Alter highly bound protein drugs (increase their plasma concentration)
>NSAIDS displace albumin, bound drugs
»Warfarin, phenytoin, valproic acid

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15
Q

30mg of Ketorolac is equivilant analgesia provided by how many mg of IV Morphine

A

10mg

i call bullshit

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16
Q

Ketorolac can only be taken for how many days

A

5

17
Q

how does aspirin work

A

it irreversibly inhibits COX-1 and COX-2
platelets are inhibited for the life of the platelet

18
Q

aspirin toxicity can cause a (gap/non-anion gap) metabolic acidosis

A

gap acidosis

salacylic acid ↔ Salisil**ate **& H+

non gap = loss of bicarb (gain of chloride (hydrochloric acid) to compensate)
+gap = gain of acid (anything that results in gaine of something adding in ate

MUDPILES
Methanyl ↔ formic acid > formate
Uremia ↔ causes accumulation of sulfates and phosphates
Dka ↔ betahydroxyentric acid ↔ betahydroxybuterate
P
Ishemia/Iron : lactic acid ↔ H+ and Lactate
Ethanol/Tthylane glycol
Salicilates

HA ↔ H+ & A-
H+ proton combines with bicarb > H20 + CO2

19
Q

How is acetaminophen similar and different compared to NSAIDS

A

+analgesic and antipyretic
NOT antiinflammatory

20
Q

T/F: tylenol has antiinflammatory properties

A

false,

just antipyretic and analgesic

21
Q

What is the most common cause of acute liver failure in the US

chronic liver failure?

A

Tyelnol - max is 4g/day

alcohol abuse

22
Q

2 theories for how tylenol works

exact mechanism is unclear

A

possibily inhibits prostaglandins by a Cox-3 pathway?
may activate the descending inhibitory pain pathway in the spinal cord

23
Q

Membrane phospholipids are converted to arachadonic acid by what

what is arachadonic acid converted to?

A

Phospholiapase A2

prostaglandins

24
Q

What is phospholiapase A2 responsible for?

i

A

converting membrane phospholipids to arachodonic acid > prostaglandins needed for GI mucuosa, renal blood flow, and platelet function

25
Q

when can the administration of aspirin lead to life threatening bronchospasm?

can other nsaids cause it?

A

if the pt has Samter’s Triad:

Asthma, allergic rhinitis, nasal polyps

yes! ketorolac, ibuprofen, or naproxen