Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology Block 2 > Aspirin/NSAIDS > Flashcards

Aspirin/NSAIDS Flashcards

1
Q

What are the general indications for NSAIDS?

A

Pain Relief
Reduce Inflammation
Fever REduction

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

What are Aspiring specific indications?

A

Stroke/MI prevention

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

How do NSAIDs work?

A

Block COX enzymes -> prevent prostaglandin production -> dec inflammation, pain, fever

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

How do NSAIDs block COX enzymes?

A

All NSAIDS except Aspirin act as competitive inhibitors for the COX enzyme

Aspirin blocks as an irreversible non-competitive COX enzyme inhibitor via covalent modification of the active site

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

Where are COX1 enzymes found and what do they do?

A

Constitutively expressed in most tissues

General housekeeping role

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where are COX2 enzymes found and what do they do?

A

Induced in macrophages, monocyte
Constitutive in kidney and endothelium at low levels
Pro inflammatory responses

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

What are the housekeeping functions of COX1 in the GI tract?

A 
PG production provides cytoprotective functions to stomach
Dec acid secretion
Inc gastric bicarb production
Inc gastric mucous production
Vasodilate-> gastric blood flow inc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do NSAIDS reduce fever?

A

Blocking PG production and thus no action on CNS at the thermoregulatory center of the hypothalamus for fever

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

What are the housekeeping functions of COX1 i the CV system?

A

Platelets expresss only COX-1 => produce TXA2 (thromboxane) => vasoconstriction + platelet aggregation

Endothelial cells => COX1 and COX2 => no TXA2 synthase => produce PGI2 (prostacyclin) => vasodilation and inhibit platelet aggregation

Balance between the two can have differing results

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

What are hte functions of COX enzymes in the kidney?

A

Both COX1 and COX2 => PGs promote vasodilation to prevent renal ischemia
*Important in diseased state to counter vasoconstrictors

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

How can NSAIDs be used during labor?

A

It would delay it as PG production stimulates uterine contraction and NSAIDs would block this

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

What can happen if a women is treated with NSAID during pregnancy?

A

Premature closure of hte ductus arteriousus -> deleterious to fetal circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What can be done with patent ductus?

A

Treat with NSAID to inhibit fetal PGs that are keeping hte ductus open

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

How are Coxibs differnt from Aspirin/NSAIDs?

A

Coxib only inhibits COX-2

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

Why does aspirin block COX1 better than COX2?

A

COX2 has a larger binding site so it can partially bind arachidonic acid

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

How does aspirin block the COX enzymes?

A

Irreversibly acetylates a serine residue in the actie site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the unique indication for aspirin?

A

prophylactc prevention of CV events via low dose (81mg) aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why should you not give more aspirin for the protective CV effects?

A

At high doses the anti platelet effect of inhibiting TXA2 in platelets is offset by increased inhibition of PGI2 from the endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why don’t other NSAIDs show the same protective effects of low dose aspirin?

A

They are reversible inhibitors while aspirin is irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does low dose aspirin help treat CVD?

A

Aspirin acetylates COX1 in platelets permanently -> dec TXA2 (Platelets have no nucleus so more permanent)

Endothelial cells have nucleus -> COX1 inhibition is minimal -> produce PGI2

Result: More Anti thrombotic environment with PGI2>TXA2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are some other salicylates and their unique properties?

A

Diflusinal: does not cross BBB -> no anti fever properties

Methyl Salicylate: bengay/icy hot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What kind of inhibitors are hte salicylates (except for aspirin)

A

Competitive inhibtor

23
Q

When should salicylates be used over aspirin?

A

Pts at inc risk for GI problems or bleeding

24
Q

Why do we see aspirin/salicylate toxicities?

A

At low dose its fine with 1st order kinetics

High dose -> metabolic enzymes in liver are overwhelmeed -> get 0 order kinetics

25
Q

What are the sx of salicylate intoxication?

A

COMA, DEATH, hyperthermia, hyperventilation, acidosis, eetc

26
Q

What is the treatment for salicylate toxicity/OD

A

Alkalinization of urine with sodium bicarb => inc ionized form in urine -> prevents reabsorptionand inc excretion

27
Q

What is an indication for traditional NSAIDs but not Aspirin/salicylates?

A

Treatment of Gout

28
Q

What is unique about ibuprofen as a NSAID?

A

Equipotent to Aspirin and better tolerated

Rapid onset of action (15-30mins)

29
Q

What is unique about Naproxen as an NSAID?

A

More potent than aspirin
Rapid onset of action (60 mins)
Long serum half life -> allows 2x daily dosing

30
Q

What is unique about oxaprozin as an NSAID?

A

Slow onset of action

Very long serum half life -> allows 1x daily dosing

31
Q

What is unique about indomethacin as an NSAID

A

10-40x more potenet than Aspirin for antiinflammatory
Not tolerated as well as ibuprofen
used to promote closure of patent ductus

32
Q

What is Ketorolac used for?

A

Weak anti inflammatory NSAID
Used as IV analgesic for post surgery pain
Can be used as replacement for opioid analgesics

33
Q

What is unique about Diclofenac as an NSAID?

A

More selective for COX2

Increasesd heart and stroke risk

34
Q

What are the adverse effects seen with Aspirin and tNSAIds?

A 
Gi toxicity
Kidney Impairment
Risk of bleeding
Exacerbate HTN and heart disease
NSAID hypersensitivity
Pregnancy issues
35
Q

What are adverse effects only specific for Aspirin?

A

Increased Gout

Reye’s Syndrome

36
Q

How does NSAID induce GI toxicity?

A

Direct damage to gastric epithelial cells via ion trapping of aspirin/NSAIDs
Inhibiton of COX1 in stomach -> losss of gastric proective PG effects

Can lead to GI bleesd and ulcers

37
Q

How can the sx of NSAID induced GI toxicity be relieved?

A

Misprostol

Omeprazole

38
Q

How does NSAID induce adverse effects on kidney funciton?

A

Usually caused in pts with underlying kidney disease -> NSAIDS block production of vasodilatory PGs -> vasoconstriciton of renal arteries > ischemia

Only seen with sick ppl but not in normal

Also dec GFR and H2O/Na+ excretion
Exacerbate HTN and HF

39
Q

What is another effect that NSAIDs can have on the kidney?

A

Acute interstitial Nephritis and NEphrotic syndrome due to prolonged exposure -> recover with drug removal

Analgesic Nephropathy/Chronic Interstitial Nephritis: due to chronic daily overuse over years -> can lead to end stage renal disease from renal ischemia

40
Q

What are the CV adverse effects of NSAIDs

A

Increased risk of heart attack and stroke (NOT ASPIRIN)

Exacerbate HTN and HF due to vasoconstriciton promotion

41
Q

What hemodyanmic adverse effects are possible with NSAIDs?

A

Increased risk of bleeding
Avoid in pts with preexisting platelet deficiency
Avoid in pts prior to surgery

42
Q

What happens if a patient shows hypersensitivity to NSAID?

A

Probably will be reactive to other NSAIDs as well

43
Q

What is REye’s Syndrome?

A

Rare, fatal liver degenerative disease associated with aspirin given to children during febrile viral infections

44
Q

What should be given and not given with rEye’s syndrome?

A

DO NOT GIVE ASPIRING

Use NSAID or acetaminophen

45
Q

Does Aspirin or NSAId lead to increased risk of gout?

A

Aspirin

46
Q

what are COXIBs?

A

Selective COX-2 Inhibitors that do not exhbiti adverse effects of inhibiting COX-1

47
Q

What is Celecoxib?

A

COXIB that competitively inhibits COX-2

48
Q

What are hte indications for Celecoxib?

A

Rheumatoid Arhtritis and Osteoarthritis
Pts with increased risk of GI problems
Pts with increased risk of bleeding

49
Q

What are the side effects of Celecoxib?

A

Increased CVD risk!!!

As a result dont want to use this as 1st choice med

50
Q

How does Celecoxib promote CVD problems?

A

Inhibits COX2 -> dec level of PGI2 -> TXA2 > PGI2 -> pro thrombotic state along with vasoconstrictions

51
Q

What are general contraindications for NSAIDs?

A 
GI Ulcers
Renal Disorders
Bleeding Disorders/Anticoagulants
History of CVD/HTN/HF
Pregnancy
Hypersensitivity to NSAID
52
Q

How does NSAIDs interact with lithium, methotrexate, and aminoglycosides?

A

NSAIDs impair renal function -> decreased renal clearance -> lithium, methotrexate, or aminoglycoside toxicity seen

53
Q

Why should you not take both NSAIDs and Anti HTN drugs together?

A

NSAIDs promote vasoconstriction -> counteract anti HTN effects

54
Q

What happens when NSAIDs are given with anti coagulants?

A

NSAIDs displace warfarin from albumin -> NSAIDs prevent platetelet COX1 -> inc risk for bleeding

Pharmacology Block 2 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions