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Pharmacology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What was the origin of aspirin? What is its effect?

A

Willow bark isolate; COX1/2 non-selective inhibitor

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2
Q

What is the target of NSAIDs?

A

COX 1 and COX 2

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3
Q

How many classes of NSAID are we looking at (there are more)?

A

Seven

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4
Q

What is the mechanism of aspirin’s action on COX?

A

Irreversible inhibtion via acetylation

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5
Q

What is the effect of acetylsalicylate’s byproduct following COX inhibition?

A

The remaining salicylate has a 30 minute half life as a competitive inhibitor

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6
Q

What are the therapeutic effects of acetylsalicylic acid?

A

Anti-inflammatory, analgesic, antipyretic, and anti-clotting (TxA2 inhibition in platelet aggregation)

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7
Q

What are the adverse effects of aspirin (and most NSAIDs)?

A

GI irritiation (PGE2 and PGI2 inhibition), Nephrotoxicity (too much use, or older patients), Bleeding/anemia (overuse with systemic or GI bleeding), Hypersensitivity reaction (0.2%), Salicylate toxicity (overdose, repiratory alkylosis, metabolic acidosis, coma, and death)

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8
Q

What is the MOA of diflunisal?

A

Competitive inhibition of COX1 and COX2

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9
Q

How do tolerability and half life of difluisal and aspirin compare?

A

Diflunisal is better at both; 3x potency in muscle

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10
Q

What is the MOA of acetaminophen on COX?

A

Competitive inhibition of COX1 and COX2 EXCEPT in presence of peroxides or within the CNS

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11
Q

How is acetominophen metabolized?

A

Phase 1 to excrete through the kidney; hepatotoxic by Phase 2 reaction in overdose that depletes glutathione

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12
Q

What is the antiinflammatory action of acetominophen? Why?

A

None - not yet known

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13
Q

When is acetominophen specifically used?

A

When a patient is intolerant to aspirin

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14
Q

What are the indole compounds? What class are they in?

A

Sulindac and Indomethacin; NSAIDs

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15
Q

What was the first use of indomethacin?

A

Gout

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16
Q

How do indole compounds compare to aspirin in potency and side effects?

A

10x the potency, but more and more serious side effects in chronic use

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17
Q

What is the most common NSAID?

A

Ibuprofen

18
Q

What are the propionic acid derivatives? What class of drug are they in?

A

Ibuprofen, naproxen, fenoprofen, ketoprofen, oxaprozin, and flurbiprofen; NSAIDs

19
Q

How do effectiveness and tolerability of Propionic acid derivatives compare to aspirin?

A

Both are better

20
Q

What is the general 1/2 life of propionic acid derivatives? What two differ?

A

Generally 1-2 hours, Naproxen=13hrs and Oxiprozin=50hrs

21
Q

What is the major enolic acid compound? What makes it good for MSK disorders?

A

Piroxicam for RA or OA or other inflammatory disorders; long (45hr) half life

22
Q

What is the use of ketorolac? What class is it in?

A

IM injection in post-op or topical for the eye; NSAID Heteroaryl Acetic Acid

23
Q

What are the coxibs?

A

COX2 inhibitors: Celecoxib and Etoricoxib

24
Q

How do the coxibs compare to general COX1/2 inhibitors in terms of efficacy and safety?

A

The lack of COX1 activity means no cardioprotective effects; some have high risk of MI and stroke and have been withdrawn; fewer GI side effects; Effecacy for anti-inflammatory, antipyretic and analgesic properties are similar to other NSAIDs

25
Q

What is the structural difference between coxibs and other NSAIDs?

A

Coxibs are larger to sterically hinder them from acting on the smaller COX1 active site

26
Q

What pathways (broader than COX1vsCOX2) are affected bt NSAIDs?

A

Prostaglandin, prostacyclin, and thromboxane synthesis; not leukotriene synthesis

27
Q

What is the only irrevesible NSAID?

A

Aspirin

28
Q

What are the three phases of inflammation?

A

Acute transient (local vasodilation/permeability), delayed subacute (infiltration by leukocytes), and chronic proliferative (tissue degeneration and necrosis)

29
Q

What is the effect of histamine?

A

local capillary dilation, edema due to permeability, and itching due to primary sensory neuron sensitization

30
Q

What are the effects of kinins?

A

pain from acute primary sensory neuron excitation and chronic arachidonic acid relase with pcv dilation

31
Q

When are COX1 and COX2 induced/active?

A

COX1 is constitutive in gastric/platelet/renal blood flow/parturition initiation and COX2 is inflammatory

32
Q

Match the prostaglandin/thromboxane with the cell source and major action: PGE2

A

Macrophages; protection of gastric mucosa, vasodilation, hyperalgesia

33
Q

What are eicosanoids?

A

arachidonic acid metabolites

34
Q

What is the source of arachidonic acid in inflammation? How is this relevant to injury response?

A

Arachidonic acid is derived from cell membrane phospholipids either during the injury (chemical/physical) process or within the kinin-mediated extracellular milieu

35
Q

What is the product of lipoxygenase metabolism of arachidonic acid?

A

leukotrienes

36
Q

What are the products of cyclooxygenase metabolism of arachidonic acid?

A

prostaglandins, prostacyclins, and thromboxanes

37
Q

Match the prostaglandin/thromboxane with the cell source and major action: PGD2

A

Mast cells; vasodilation and inhibition of platelet activation

38
Q

Match the prostaglandin/thromboxane with the cell source and major action: PGF2a

A

Mast cells; bronchoconstriction

39
Q

Match the prostaglandin/thromboxane with the cell source and major action: PGI2 (prostacyclin)

A

Endothelial cells; vasodilation and inhibition of platelet activation

40
Q

Match the prostaglandin/thromboxane with the cell source and major action: TxA2 (thromboxane)

A

Platelets; vasoconstriction, bronchoconstriction, and platelet aggregation

Pharmacology (5 decks)

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