NSAIDS And Non Narcotics Flashcards

1
Q

6 common indications for NSAIDS?

A
Osteoarthritis
Bursitis
Gout Flare up
AS
Dysmenorrhea
HA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

4 similarities of COX1 and COX 2?

A

Use same substrates, AA
Both make the same products, PGs
Both have role in inflammation
Both have role in renal function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where is COX1 and COX2 expressed in the body? Where in the body does COX 2 have a prominent physiological role?

A

COX 1 in all tissues all the time
COX2 in some tissues and sometimes.
COX2 has a big role in kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

3 step sequence to go from inflammation to symptoms with COX1?

A
  1. Inflammation stimulates AA release
  2. COX1 converts AA into PGE2
  3. PGE2 causes symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Same question, 3 step sequence from inflammation to symptoms for COX2?

A
  1. Inflammation induces COX2 expression and AA release
  2. COX2 also converts AA into PGE2
  3. COX2 derived PGE2 amplifies symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the 1 benefit we are looking for when giving a COX1 and 2 inhibitor?
What are risks of giving COX inhibitors?

A

Block inflammation

COX1 mucosal integrity
COX1 hemostasis
COX1 and 2 sodium and water excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

4 major beneficial actions of inhabiting both Cox 1 and 2 and one beneficial action that is inhibiting only COX 1, all by aspirin?

A

Suppress inflammation
Relief of mild to moderate pain
Reduce fever

Prevent of MI and stroke by suppresses platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

3 major risks of inhabiting cox 1 and 2 by aspirin?

A

Gastric ulcer, bleeding and renal impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

MOA of aspirin?

A

Irreversible inhibition of cyclooxygenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

3 things he mentioned that aspirin is really good at treating?

A

Pain, RA, and chronic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What 2 things we can go to minimize risk of aspirin induced ulcers?

A

Test/get rid of H pylori before therapy

Give a proton pump inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

3 other clinical conditions we are mindful about giving aspirin?

A
  1. People on anticoagulants because of its anti platelet effects
  2. Implied renal function can cause retention of sodium and water, so heart or HTN patients
  3. Aspirin induced asthma, causes more LT doing its inflammatory thing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What can long term aspirin use lead to in the kidney and what are we worried about with aspirin and children?

A

Renal papillary necrosis

Reye syndrome in kids with chick pox or the flu

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

2 big differences between aspirin and other NSAIDS?

A

They reversibly block, so their effects decline as blood levels decline
Increase risk for MI and Stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which COX does celecoxib block?
What does it cause less of than other NSAIDS?
What does it not inhibit?

A

Blocks COX2
Less gastric ulceration
Does not inhibit platelet aggregation, so does not cause bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Coxibs, or second generation NSAIDS block which Cox?

A

2

17
Q

3 general consensus for NSAIDS and patients with cardiovascular risk?

A
  1. All NSAIDS used at lowest dose
  2. Goal is to avoid NSAIDS and cox 2 inhibitors all together
  3. If need to use NSAID therapy with a patient who has cardiovascular risk, use Naproxen
18
Q

5 contraindications for NSAID use?

A
  1. Chronic kidney disease with creatinine clearance less than 60
  2. Ulcers
  3. CV disease, particularly HR and HTN
  4. NSAID allergy
  5. Anticoagulant
19
Q

4 things that acetaminophen doesn’t do that NSAIDS do?

A

No Anti-inflammatory action
doesn’t cause ulcers
Does not suppress platelet aggregation
Does not impair renal function

20
Q

2 complications of acetaminophen?

A

Hepatic necrosis when glutathione is depleted

Inhibits metabolism of warfarin, so bleeding

21
Q

Step 1-5 of aspirin toxicity progression?

A
  1. Uncoupled mitochondrial oxidative phos in CNS
  2. Respiratory center registers the low ATP as hypoxemia, so hyperventilation is turned on
  3. This leads to respiratory alkalosis which tells the kidney to ditch its bicarb
  4. Acids accumulate because ATP is not being made
  5. Severe metabolic acidosis
22
Q

3 first line agents for neuropathic pain?

A

Calcium channel alpha 2 delta ligand, gabapentin
SNRI
TCA

23
Q

2 beneficial effects of TCA?

A

Pain relief and depression relief

24
Q

2 beneficial effects of SNRIS and MOA?

A

Pain relief and relief of concurrent depression

Inhibit serotonin and norepinephrine

25
Q

MOA for pregabalin?

4 approved indications for pregabilin?

A

GABA analog that binds to the alpha 2 delta submit of voltage gated calcium channels in the CNS and not allowing as much calcium in, thereby inhibiting NT release.

Neuropathic pain with diabetic neuropathy, postherpatic neuralgia, partial seizures, and fibromyalgia

26
Q

MOA for gabapentin?
Approved use?
Off label uses?

A

Same as pregablin
Broad spectrum seizure med
Same 4 but also RLS and migraine

27
Q

What are 3 second line agents for neuropathic pain?

A

Other antiepileptics
Opioids
Tramadol

28
Q

MOA of tramadol?
Clinical indication?
5 adverse effects?

A

Weak mu analog that primarily blocks NE and 5HT reuptake
Moderate to moderately server pain
Sedation, dizziness, headache, dry mouth, and constipation

29
Q

MOA of tapentadol?

Adverse effect?

A

Moderate to strong mu agonist and blocks re uptake of NE

Causes less constipation