Brainscape's Knowledge GenomeTM

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


See full index

hlsc final > COX inhibits > Flashcards

COX inhibits Flashcards

1
Q

What enzymes to prostaglandins activate

A

COX-1

COX-2

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

What drugs counteract activity of COX-1 and 2

A

Aspiring
Ibuprofen
Celebrex
Acetaminophen

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

COX -1 effects on the body
(3)

A

Always active - housekeeping chores

  • Gastric protection (mucus production)
  • Promoting Platelet aggregation
  • Maintain Renal Vasodilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

COX-2 effects on the body
(4)

A

Activated by tissue damage

  • vasodilation
  • inflammation/ pain
  • fever
  • colorectal cancer promotion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

COX-1 inhibition drugs
Beneficial and Adverse

A

Beneficial Effect:

  • decrease platelet aggregation
  • protects against MI and stroke

Adverse:

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

COX 2 inhibition drugs
Beneficial and Adverse effects

A

Beneficial:

  • decreases inflammation, pain, fever
  • protection against collateral cancer

Adverse:

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

COX inhibitors: 2 groups

A

1) Anti-inflammatory properties
- NSAIDs (aspirin, ibuprofen, celecoxib)

2) Acetaminophen
- reduce pain and fever
- CANT SUPPRESS INFLAMMATION

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

NSAIDs 2 groups

A

1) first generation

  • inhibit both COX 1 and COX2
  • suppress pain and inflammation but SERIOUS SIDE EFFECTS

2) second generation

  • inhibit only COX 2
  • in theory can suppress pain and inflammation
    -FEWER adverse effects than first
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Chemistry of Aspirin

A

belongs to chemical family of salicylic acids

produced by substituting an acetyl group into salicylic acid
–> acetylsalicylic acid (ASA)

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

Mechanism of aspririn

A

inhibits COX-1 and COX-2

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

aspirin inhibition of COX-1
Positive and negative

A

Positive: protection against MI and stroke

Negative: gastric ulceration, bleeding and renal impairment

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

Inhibition of COX-2

A

Positive:
- decrease inflammation, pain, and fever
- vasoconstriction
- protection against colorectal cancer

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

Is aspirin a reversible or irreversible inhibitor of COX

A

irreversible inhibitor

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

Aspririn Pharmacokinetics

A

A: PO

D: ++ bound to albumin/ 20% delivered to body tissues and CNS

M: ASA reduced to salicylic acid in liver

E: salicylic acid excreted by the kidney

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

Plasma therapeutic and toxicity levels

A

low- 100 mcg/ml
therapeutic- 150-300 mcg/ml
severe toxicity- 400 mcg/ml

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

therapeutic uses aspirin (4)

A

1) mild moderate analgesia

2) fever reducer

3) rheumatoid arthritis and Osteoarthritis ** drug of choice

4) Suppression of platelet aggregation

  • aspirin binds to cox 1 = suppresses platelt aggregation
  • irreversible effect requires 8 days for platelets to reach normal levels
  • daily aspirin recommended for ischemic stroke, acute MI, chronic angina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

aspirin adverse effects

Short term
Long term
Salicylism
Pregnancy

A

short term- low AE

long-term high doses- toxicity

Salicylism- tinnitus, sweating, dizziness
- symptoms stop once aspirin stopped

pregnancy
- anemia from GI blood loss
- postpartum hemorrhage

18
Q

acute poisoning of aspirin

A

respiratory depression

adults lethal dose: 20-25 gm

children 4 gm

19
Q

dose/ administration of aspirin

A

always PO
- dose with food/water

20
Q

Non-aspirin first-generation NSAIDS

A

ibuprofen *prototype

21
Q

Non-aspirin First generation NSAIDS mechanism
Reversible?

A

inhibit COX 1 and COX 2
BUT REVERSIBLE INHIBITION

22
Q

Non-aspirin First generation NSAIDS therapeutic uses

A

similar to aspirin
- decreased inflammation, pain, fever

23
Q

Ibuprofen compared to Aspirin

A
  • less gastric bleeding
  • less inhibition of platelet aggregation = greater risk MI and stroke
24
Q

Non-aspirin First generation NSAIDS drug interaction

A

similar to aspirin

25
Q

Reye Syndrome

A

rare, serious, swelling of liver and brain

-affects children after viral infection

  • aspirin puts children at risk of these
26
Q

Second-Generation NSAIDs

A

COX-2 inhibitors

  • aka COXIBS
27
Q

why were COX 2 inhibitors developed

A

hypothesis that
- selective inhibition of COX-2 should be able to suppress pain/inflammation but no risk gastric ulcertaion

28
Q

Selective COX-2 Inhibitors drug

A

Celecoxib

29
Q

Selective COX-2 Inhibitors mech

A

selective inhibition of COX-2
- primarily reduces painand inflammation

30
Q

Selective COX-2 Inhibitors pharmacokinetics

A, D, Half life

A

PO- peaks in 3hours

Extensive (97%) binding to plasma proteins

Half-life 11 hours

31
Q

Selective COX-2 Inhibitors Adverse effects

A

well tolerated

dyspepsia (upset stomach) and stomach pain

pregnancy: don’t use third trimester

Cardiovasuvlar events

32
Q

how does celecoxib have increased risk MI and stroke?

A

1) does not inhibit COX-1
= does not inhibit platelet aggregation

2) does inhibit COX02 in blood vessels
- increased risk of vasoconstriction

Together = risk of vessel blockage, development of thrombis

33
Q

Second-Generation NSAIDs therapeutic uses

A

first selective COX-2 inhibitor to market

reduce pain and inflammation

indicated for RA, OA, juvenile idiopathic arthritis, pain and dysmenorrhea

doesn’t decrease aggregation = does not promote bleeding

34
Q

Acetaminophen

A
  • similar to aspirin
  • aceta has analgesic, antipyretic like aspirin
    –> doesnt have anti-inflammatory
35
Q

Mechanism of Action acetaminophen

A
  • limited to prostaglandin CNS inhibition of COX-1 and 2
    –> can reduce fever and pain but not inflammation
36
Q

acetaminophen pharmacokinetics

A,D, half life

A

PO/ peak in 3 hours

extensive plasma binding

Half-life 11 hours

37
Q

Drug interaction acetaminophen

A

Alcohol: regular alcohol consumption combined
= greater risk liver damage

Warfarin: increased bleeding

Vaccines: blunt immune response to childhood vaccines

38
Q

Acture Toxicity: Liver Damage with acetaminophen

A

overdose is leading cause of acute liver failure

low risk in normal therapeutic doses
- except for ppl who drink alcohol or have liver disease

39
Q

therapeutic uses acetaminophen

A

relief of pain and fever

Preferred to NSAIDs for children who have chickenpox or influenzas

40
Q
A

hlsc final (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions