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Anti-Inflammatory Drugs Flashcards

1
Q

What are the autacoids that contribute to inflammation?

A

Eicosanoids (20-chain FA)
Histamine
Serotonin
Bradykinin

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2
Q

List non-autacoid mediators of inflammation.

A

Cytokines, complement, platelet activating factor, free radicals.

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3
Q

Which enzyme converts membrane phospholipids to arachidonic acid?

A

Phospholipase A

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4
Q

Which eicosanoids are reduced with COX inhibitors?

A

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

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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).

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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
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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.

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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.

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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

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10
Q

Which NSAIDs are non-selective COX inhibitors?

A

Most classic NSAIDs, high dose aspirin

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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

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12
Q

What feature makes new NSAIDs selective for COX-2?

A

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

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13
Q

How to classic NSAIDs interact with COX enzymes?

A

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

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14
Q

Describe the order kinetics of aspirin.

A

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

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15
Q

Is aspirin reversible or irreversible?

A

Irreversible

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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.

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17
Q

List the ADRs of aspirin that occur at high doses.

A

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

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18
Q

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

A

Fluid and electrolyte balance

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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
List the ADRs of glucocorticoid's
``` 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
What are some clinical considerations for glucocorticoids?
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
What are the advantages of NSAID therapy?
Effective control of inflammation and pain, reduction in swelling Improves mobility, flexibility, range of motion Improve quality of life Low-cost
28
What are the disadvantages of NSAID therapy?
``` Does not affect disease progression GI toxicity Renal complications Hepatic dysfunction CVS complications particularly heart attacks and particularly with COX-2 selective. ```
29
What are the advantages of corticosteroid therapy?
Anti-inflammatory and immunosuppressive Bridge gap between DMARD initiation and onset Intra-articular injections can be used for individual joint flares.
30
What are the disadvantages of corticosteroid therapy?
Steroid-induced, osteopenia, Cushing's-like syndrome Unsuccessful with tapering and discontinuation No evidence of effect on disease progression
31
How long does it take for DMARDs to become effective?
6-8 weeks, up to 6 months for some
32
Which anti-inflammatory drug group slows disease progression?
DMARDs
33
What are the clinical benefits of DMARDs?
Improve functionD Decrease pain, although analgesics are often still required Interfere with inflammation and joint erosion
34
When are bDMARDs introduced into care?
When DMARDs fail or are too toxic.
35
Give three examples of DMARDs
Antimalarials, sulfasalazine, methotrexate/leflunomide
36
Which immune cell do antimalarials target?
Antigen presenting cells
37
What immune cells does sulfasalazine target?
Antigen presenting cells and T cells
38
What immune cells does methotrexate target?
B cells, reducing ACPA and rheumatoid factor production.
39
What cytokines are produced by antigen-presenting cells?
GM-CSF, TNF, IL-1, IL-6, IL-7
40
Which cytokine produced by T cells is reduced with DMARDs?
IL-17
41
List the four effects of IL-1 in rheumatoid arthritis.
Activates monocytes/macrophages, induces fibroblast proliferation, activates chondrocytes, activates osteoclasts.
42
Which three cells are activated by TNF-alpha by rheumatoid arthritis?
Osteoclasts, synoviocytes, cartilage
43
What is the mechanism of action of TNF-alpha inhibitor DMARDs?
Prevent binding of TNF-alpha to TNF receptors, suppressing downstream cytokines and leukocyte migration and activation.
44
Give three examples of anti-TNF bDMARDs.
Etanercept, infliximab, adalimumab
45
Name the bDMARD that targets B cells.
Rituximab
46
Name the bDMARD that targets IL-2
Basiliximab

Pharmacology (14 decks)

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