APEX- NSAIDS Flashcards
All of the following are associated with Samter’s triad EXCEPT:
A. Allergic rhinitis
B. Bronchospasm
C. Nasal polyps
D. Hypertension
D. Hypertension
Samter’s triad is associated with Aspirin exacerbated resp disease
Samter’s triad is associated with what
3 components
what can happen
Aspirin exacerbated respiratory disease
- Asthma
- Allergic rhinitis
- Nasal polyps
pts can develop life-threatening bronchospasm following aspirn administration
How do NSAIDs reduce pain
they inhibit cyclooxygenase enzyme and reduce the production of prostaglandins
What is diclofenac
a non-selective COX inhibitor
NSAID
prevents the formation of prostaglandins by inhibiting cylooxygenase
brand names: voltaren
What is indomethacin
“a non-selective COX inhibitor “
+
“prostaglandin synthase inhibitor” - used to close PDA
NSAID
preents the formation of prostaglandins by inhibiting cylooxygenase
What is a drug with the suffix -coxib
selective COX-2 inhbitior
inhibits the inducible prostaglandins which produce inflammation, pain, and fever
Describe the arachidonic acid pathway
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
Is there a ceiling effect on analgesia with NSAIDS or Opioids?
ceiling effect with nsaids for analgesia
no ceiling effect for analgesia with opioids
3 downfalls of cox 1 inhibition
gastric irritation
impaired platelet function
reduced renal blood flow
selective COX-2 inhibitors seem great…but why arent they
they increase the risk of HTN, MI, and HF moreso than COX-1
screwed either way
How might COX inhibitors produce bronchospasm
decreased prostaglandins > leukotrienes > bronchospasm
why to avoid NSAIDs in pts with renal disease
because blocking prostaglandins reduces renal blood flow
cox-1 prostaglinds responsible for : platelet function, gastri mucosa, and renal blood flow
You always know there is something with nsaids and ortho that you question… what is it?
they decrease osteoclast and osteoblast activity and may impair bone healing
no one seems to care though lol
Key drug interactions with NSAIDs
Alter highly bound protein drugs (increase their plasma concentration)
>NSAIDS displace albumin, bound drugs
»Warfarin, phenytoin, valproic acid
30mg of Ketorolac is equivilant analgesia provided by how many mg of IV Morphine
10mg
i call bullshit
Ketorolac can only be taken for how many days
5
how does aspirin work
it irreversibly inhibits COX-1 and COX-2
platelets are inhibited for the life of the platelet
aspirin toxicity can cause a (gap/non-anion gap) metabolic acidosis
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
How is acetaminophen similar and different compared to NSAIDS
+analgesic and antipyretic
NOT antiinflammatory
T/F: tylenol has antiinflammatory properties
false,
just antipyretic and analgesic
What is the most common cause of acute liver failure in the US
chronic liver failure?
Tyelnol - max is 4g/day
alcohol abuse
2 theories for how tylenol works
exact mechanism is unclear
possibily inhibits prostaglandins by a Cox-3 pathway?
may activate the descending inhibitory pain pathway in the spinal cord
Membrane phospholipids are converted to arachadonic acid by what
what is arachadonic acid converted to?
Phospholiapase A2
prostaglandins
What is phospholiapase A2 responsible for?
i
converting membrane phospholipids to arachodonic acid > prostaglandins needed for GI mucuosa, renal blood flow, and platelet function
