Brainscape's Knowledge GenomeTM

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


See full index

Semester 2 Year 1 > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

What does NSAIDs stand for?

A

Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

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

What are the main actions of NSAIDs?

A

1) Anti-inflammatory
2) Analgesic
3) Anti-pyretic

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

What is the primary physiological action of NSAIDs?

A

Inhibit prostaglandin biosynthesis by direct action on cyclo-oxygenase enzymes

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

What are the mechanisms of action of NSAIDs?

A

All inhibit cyclo-oxygenase (COX) but do so by two main mechanisms:

1) An irreversible, time-dependent inhibition of the enzyme
2) A rapid, reversible competitive inhibition of the enzyme

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

Describe the irreversible, time-dependent inhibition of the enzyme mechanism of action of NSAIDs

A

• e.g. aspirin
– inactivates the enzyme
– aspirin acetylates the a-amino group of the terminal serine of the enzyme forming a covalent bond
– further synthesis of prostaglandins requires synthesis of new enzyme

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

Describe the rapid, reversible competitive inhibition of the enzyme mechanism of action of NSAIDs

A

• e.g. ibuprofen
– binds reversibly to the enzyme
– competes with natural substrate, Arachidonic Acid

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

What are prostaglandins?

A

A family of compounds generated in tissues from a precursor (arachidonic acid) by cyclo-oxygenase enzymes

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

What are some prostaglandins?

A

– PGE2 and PGF2a were the first ones isolated and structures determined

– Thromboxanes, prostaglandins & leukotrienes all products of arachidonic acid metabolism

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

What are cyclo-oxygense enzymes?

A

A group of enzymes consisting of two main enzymes

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

What are the two main cyclo-oxygenase enzymes?

A

COX-1

COX-2

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

Describe COX-1

A

– Constitutive
– Important in maintain
GIT integrity

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

Describe COX-2

A

– Inducible
– Involved in
inflammatory response
– Implicated in cancer development

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

What is the role of prostaglandins in inflammation?

A

Inflammation always accompanied by release of prostaglandins

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

What are the prostaglandins released in inflammation?

A

– Predominantly PGE2 but also PGI2

– PGD2 from mast cells

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

What do the prostaglandins released in inflammation do?

A

PGE2, PGI2 and PGD2
– Act as potent vasodilators
– Also synergise with other inflammatory mediators (e.g. histamine and bradykinin)
– Potentiate histamine and bradykinin actions on postcapillary venule permeability and pain sensory nerves

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

Describe the anti inflammatory action of prostaglandins

A

Prostaglandins are important mediators of inflammation

– Particularly vasodilation and resultant oedema – Less effect on cellular accumulation or migration

17
Q

What is the impact of the role of prostaglandins in inflammation on the use of NSAIDs?

A

NSAIDs only effect aspects of inflammation in which prostaglandins play a significant part. NSAIDs can reduce many of the local signs and symptoms of inflammation:
– i.e. redness, heat, swelling, pain

18
Q

What is body temperature regulated by?

A

The hypothalamus

19
Q

How is a fever caused?

A

– Fever occurs when the hypothalamic thermostat “set point”
is raised
– Bacterial endotoxins cause release of factors (e.g.
interleukin 1) from macrophages
– Interleukin 1 causes generation of prostaglandins in the
hypothalamus (PGEs)
– Prostaglandins ↑ the thermostat “set point”

20
Q

How do NSAIDs have an anti-pyretic effect?

A

NSAIDs act by preventing the formation of prostaglandins and prevent the rise in temperature
– No effect on normal body temperature

21
Q

What causes pain in inflamed regions?

A

Inflamed regions painful due to histamine and bradykinin release
– activate nocioceptive afferent nerve terminals
– register a painful stimulus
Prostaglandins sensitise nocioceptive nerves to these compounds

22
Q

How do NSAIDs have an analgesic effect?

A

By preventing prostaglandin production NSAIDs prevent sensitisation to pain-producing compounds

23
Q

What is a famous example of salicylates

A

Also known as the aspirin family

Therefore: aspirin

24
Q

Describe aspirin physiologically

A

– pro-drug (acetylsalicylic acid)
—-• can directly acetylate COX enzyme
– also metabolised to active compound (salicylic acid) by plasma and tissue esterases
– salicylates found in plasma within 30 mins
– peak plasma concentrations within 1-2 hr

25
Q

What are the unwanted effects of salicylates?

A

Stomach
– bleeding, ulcers

Systemic
– tinnitus, dizziness, impaired hearing, nausea, vomiting, hypersensitivity

Metabolic changes
– acid/base balance affected

Haemostasis
– blood coagulation affected through and action on platelets

CNS effects
– stimulation initially, ultimately coma and respiratory depression

Renal
– insufficiency insusceptible patients and with chronic use and overdose

26
Q

What are propionic acids?

A

– e.g. ibuprofen, naproxen
– not prodrugs
– well absorbed
– last for 4-6 hours

27
Q

What are fenamates?

A

– e.g. mefenamic acid

28
Q

Describe the physiological effects of paracetamol

A

Good analgesic and antipyretic activity Poor anti-inflammatory
Well tolerated in GIT
Weak COX inhibitor

– May be selective inhibitor of CNS-specific COX, COX-3

29
Q

How is paracetamol given?

A

Given orally, well absorbed
– Peak plasma conc in 30-60 mins
– Half life in plasma 2-4 hr for therapeutic doses

30
Q

What is another name for paracetamol?

A

acetaminophen

31
Q

What is a benefit of paracetamol?

A

Fewer side effects than other NSAIDs (perhaps due to its selectivity for COX enzymes)

32
Q

What is a major issue with paracetamol?

A

Major issue is hepatotoxicity due to overdose
– Normally inactivated in the liver by glucoronate
and sulphate conjugation
– When these enzymes saturated, toxic metabolites are formed
– Result can be hepatic necrosis

33
Q

What are selective COX-2 inhibitors?

A

Coxibs
– e.g. celecoxib
– used for osteoarthritis and rheumatoid arthritis
– restricted for when traditional NSAIDs produce too severe GIT side effects
– cardiovascular risk needs to be assessed

34
Q

What are the clinical uses of the analgesic properties of NSAIDs?

A 
– headache
– dysmennorhea
– backache
– bony metastases of cancers 
– postoperative pain
35
Q

What NSAIDs should be used for short term analgesia?

A

– aspirin, paracetamol, ibuprofen

36
Q

What NSAIDs should be used for longer lasting analgesia for chronic pain?

A

– naproxen, diclofenac

37
Q

What are the clinical uses of the anti-inflammatory properties of NSAIDs?

A

– Both chronic or acute inflammatory conditions
– Dosage for chronic inflammatory disorders is high
– Therefore low incidence of side effects is important
—-• e.g.ibuprofen
– Coxibs sometimes used for osteoarthritis and rheumatoid arthritis

38
Q

What are the clinical uses of the anti-pyretic properties of NSAIDs?

A

– To lower temperature

– Paracetamol preferred because it lacks GIT side effects

Semester 2 Year 1 (82 decks)

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