Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology > Anti-Inflammatory Drugs > Flashcards

Anti-Inflammatory Drugs Flashcards

1
Q

What are the autacoids that contribute to inflammation?

A

Eicosanoids (20-chain FA)
Histamine
Serotonin
Bradykinin

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

List non-autacoid mediators of inflammation.

A

Cytokines, complement, platelet activating factor, free radicals.

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

Which enzyme converts membrane phospholipids to arachidonic acid?

A

Phospholipase A

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

Which eicosanoids are reduced with COX inhibitors?

A

Thromboxane (TxA2, TxB2), PGI2 (6-keto PGF1alpha), PGD2, PGE2, PGF2.

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

What are some functions of eicosanoids?

A

Inflammation, allergies, platelet aggregation, uterine motility, vasoconstriction/dilation, bronchoconstriction/dilation, gastric function (reduced acid and increased mucous secretion).

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

What are the clinical uses of NSAIDs?

A 
Mild-moderate pain caused by inflammation and tissue injury
Fever (antipyretic effect)
Oppose platelet aggregation
Migraine
Arthritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Of COX-1 and COX-2, which is constitutive and which is synthesised de-novo in inflammation?

A

COX-1 is constitutive and COX-2 is synthesised de-novo when required.

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

At which doses is aspirin selective for which COX enzyme?

A

Selective for COX-1 at low doses and non-selective at high doses.

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

What are the major ADRs associated with NSAIDs?

A

GI tract: increased acid and reduced mucous
Increased bleeding due to reduced platelet aggregation
Renal impairment (failure with chronic use) due to Na+ and fluid retention and PGs involvement in renal blood flow modulation
Allergic reactions due to increased leukotriene

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

Which NSAIDs are non-selective COX inhibitors?

A

Most classic NSAIDs, high dose aspirin

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

What are the benefits and risks of COX-2 selective NSAIDs?

A

Selective for eicosanoids increased in inflammation, lower GI ADRs.
Greater risk of CVS ADRs

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

What feature makes new NSAIDs selective for COX-2?

A

Contain a side pocket that interacts with COX-2 only.

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

How to classic NSAIDs interact with COX enzymes?

A

Enter the hydrophobic channel, forming reversible AA bonding, blocking the catalytic site.

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

Describe the order kinetics of aspirin.

A

First order kinetics at low doses, zero order kinetics at high doses.

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

Is aspirin reversible or irreversible?

A

Irreversible

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

Which therapeutic effects occur at which doses of aspirin?

A

Antiplatelet - low doses (0.5-1mg/kg)
Analgesic and antipyretic - medium doses (5-10mg/kg)
Anti-inflammatory at high doses (30mg+/kg), GI ADRs seen.

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

List the ADRs of aspirin that occur at high doses.

A

Salicylism (high acidity(, tinitus, deafness, headache, confusion, convulsions

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

What is the function of mineralocorticoids, e.g. aldosterone?

A

Fluid and electrolyte balance

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

What is the function of glucocorticoids, e.g. hydrocortisone (cortisol)?

A

Carbohydrate and proteins metabolism, some fat metabolism.

Brain-sparing, ensure enough glucose for the brain.

20
Q

What is the function of gonadocorticoids, e.g. androgens?

A

Contribute to pre-puberty priming of the body, hair distribution.

21
Q

What is the route of administration of glucocorticoids?

A

Systemic - oral, i.m., i.v.

Topical

22
Q

What kind of receptor is the glucocorticoid receptor?

A

Nuclear receptor

23
Q

What is the mechanism of action of glucocorticoids?

A

Increase annexin-1 (lipocortin), which inhibits phospholipase A.

24
Q

What are the treatment outcomes for corticosteroid use?

A 
Decreased: 
vasodilation, oedema,
leukocyte number and activity
fibroblast function
eicosanoid, cytokine NO synthesis
histamine release from mast cells/basophils via membrane stabilisation
25
Q

List the ADRs of glucocorticoid’s

A 
Cushing's-like syndrome 
Moon face, buffalo hump, SC fat and central obesity- fat redistribution 
Euphoria at peak, followed by depression
Hypertension
Skin thinning - protein use
Easy bruising, poor wound healing
Avascular necrosis of humeral head
Osteoporosis
26
Q

What are some clinical considerations for glucocorticoids?

A

Delayed effect, 4-6 hours
Best for one off treatment
Sudden withdrawal after extended treatment can cause adrenal insufficiency
Problematic with long therapy
Need to use the lowest done for the shortest period.

27
Q

What are the advantages of NSAID therapy?

A

Effective control of inflammation and pain, reduction in swelling
Improves mobility, flexibility, range of motion
Improve quality of life
Low-cost

28
Q

What are the disadvantages of NSAID therapy?

A 
Does not affect disease progression
GI toxicity
Renal complications 
Hepatic dysfunction
CVS complications particularly heart attacks and particularly with COX-2 selective.
29
Q

What are the advantages of corticosteroid therapy?

A

Anti-inflammatory and immunosuppressive
Bridge gap between DMARD initiation and onset
Intra-articular injections can be used for individual joint flares.

30
Q

What are the disadvantages of corticosteroid therapy?

A

Steroid-induced, osteopenia, Cushing’s-like syndrome
Unsuccessful with tapering and discontinuation
No evidence of effect on disease progression

31
Q

How long does it take for DMARDs to become effective?

A

6-8 weeks, up to 6 months for some

32
Q

Which anti-inflammatory drug group slows disease progression?

A

DMARDs

33
Q

What are the clinical benefits of DMARDs?

A

Improve functionD
Decrease pain, although analgesics are often still required
Interfere with inflammation and joint erosion

34
Q

When are bDMARDs introduced into care?

A

When DMARDs fail or are too toxic.

35
Q

Give three examples of DMARDs

A

Antimalarials, sulfasalazine, methotrexate/leflunomide

36
Q

Which immune cell do antimalarials target?

A

Antigen presenting cells

37
Q

What immune cells does sulfasalazine target?

A

Antigen presenting cells and T cells

38
Q

What immune cells does methotrexate target?

A

B cells, reducing ACPA and rheumatoid factor production.

39
Q

What cytokines are produced by antigen-presenting cells?

A

GM-CSF, TNF, IL-1, IL-6, IL-7

40
Q

Which cytokine produced by T cells is reduced with DMARDs?

A

IL-17

41
Q

List the four effects of IL-1 in rheumatoid arthritis.

A

Activates monocytes/macrophages, induces fibroblast proliferation, activates chondrocytes, activates osteoclasts.

42
Q

Which three cells are activated by TNF-alpha by rheumatoid arthritis?

A

Osteoclasts, synoviocytes, cartilage

43
Q

What is the mechanism of action of TNF-alpha inhibitor DMARDs?

A

Prevent binding of TNF-alpha to TNF receptors, suppressing downstream cytokines and leukocyte migration and activation.

44
Q

Give three examples of anti-TNF bDMARDs.

A

Etanercept, infliximab, adalimumab

45
Q

Name the bDMARD that targets B cells.

A

Rituximab

46
Q

Name the bDMARD that targets IL-2

A

Basiliximab

Pharmacology (14 decks)

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