Anti-Inflammatory Drugs Flashcards

(31 cards)

1
Q

When are mediators recruited

A

Within the first 24 hours

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2
Q

Pruritis

A

Itchy skin

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3
Q

Cytokines

A

Peptides that often work in the medium-long term. Cause production of acute-phase proteins when released into the circulation (inflammatory proterties) and elevate temp through liver

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4
Q

Chemokines

A

Chemoattractant cytokines that cause inflammatory cell recruitment

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5
Q

Cytokine and chemokine action

A

Increase blood flow and vascular permeability but MAINLY cause cell recruitment and activation

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6
Q

Stored in Mast Cells

A

Histamine

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7
Q

Histamine inflammation receptor type and anti-inflammatory drug type

A

H1 histamine receptor. Anti-histamine antagonist

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8
Q

Emetic

A

Vomiting

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9
Q

Lipid Mediators causing inflammation

A

Prostaglandin, leukotrienes, and Platelet-activating factors (PAF)

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10
Q

Prostaglandin Synthesis

A

Cell membrane phospholipid + phospholipase A2 -> arachidonic acid, this is acted on by COX to create prostaglandin

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11
Q

NSAIDs

A

Non-Steroidal Anti-Inflammatory Drugs

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12
Q

How do NSAIDs block inflammation

A

They block COX from acting on arachidonic acid, the last step in prostaglandin synthesis

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13
Q

Synthesis of Leukotrienes (LTs)

A

Arachidonic acid acted on by 5-LO

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14
Q

How to block leukotrienes (LTs) Inflammation

A

Leukotriene D4 (LD4) receptor antagonist

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15
Q

What are the main Leukotriene receptor antagonists

A

Monolukast and Zafirlukast. Reduce bronchoconstriction/asthma

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16
Q

Analgesia

A

Relieves pain

17
Q

What does COX inhibition lead to

A

Decreased vasodilation/swelling/fever, analgesia, and has little effect on the cellular changes in inflammation

18
Q

Cox-1

A

Constitutive type that drives the physiological response. Does not specifically target the inflammatory response

19
Q

Selective Cox-2 inhibitors

A

Inducible type. Block inflammation at specific sites

20
Q

Examples of NSAIDs used in Large and Small Vet Med

A

Carprofen, ketoprofen, meloxicam

21
Q

Pharmacokinetic considerations of NSAIDs

A

Highly protein plasma bound. Do not use an NSAID within 24 hrs of another NSAID. Avoid use in dehydrated patients

22
Q

Side Effects of NSAID

A

Damage to GIT, Nephrotoxicity, Hepatotoxicity

23
Q

What do glucocorticoids mimic

A

The actions of cortisol

24
Q

What is cortisol

A

The natural inhibitor of the inflammatory response

25
Glucocorticoids mechanism of action
Decrease the production of pro-inflammatory mediators, release of inflammatory mediators/cells, and circulating complement components
26
Clinical uses of corticosteroids
Allergic disease or anaphylaxis, topical, or chronic inflammation. Immunosuppression
27
Contra-indicators using corticosteroids
Renal disease or diabetes mellitus
28
Avoid corticosteroid use in...
Pregnant animals, immediately after surgery, or without being paired with an antibacterial in animals with bacterial infections
29
#1 Side effect of Corticosteroids
Suppression of wound healing, induction of iatrogenic Cushings syndrome in long term use
30
#2 Side Effects of Corticosteroids
Suppression of endogenous steroid production.
31
Attention Points of Lecture
Most anti-inflammatory drugs only provide symptomatic relief. They have long-term side effects. Focus and treat the underlying causes of the clinical problem