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Pharmacology by Somebody > Deja Ch 2.3 Anti Inflamm > Flashcards

Deja Ch 2.3 Anti Inflamm Flashcards

1
Q

Eicosanoids (inflammatory mediators) are synthesized from what chemical compound?

A

Arachidonic acid

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2
Q

Give two examples of eicosanoids:

A
  1. Leukotrienes (LTs) 2. Prostaglandins (PGs)
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3
Q

How is arachidonic acid formed?

A

Phospholipase A2 acting on cell membrane phospholipids

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4
Q

Corticosteroids block what part of the inflammatory pathway?

A

Inhibition of phospholipase A2

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5
Q

Angiotensin and bradykinin have what effect on the inflammatory pathway?

A

Stimulation of phospholipase A2

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6
Q

What enzyme acts on arachidonic acid to form leukotrienes?

A

5-Lipoxygenase

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7
Q

Which leukotrienes is involved in neutrophil chemotaxis?

A

LTB4

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8
Q

Which leukotrienes are involved in anaphylaxis and bronchoconstriction?

A

LTA4; LTC4; LTD4

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9
Q

What drug inhibits 5-lipoxygenase, thereby inhibiting leukotriene synthesis?

A

Zileuton

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10
Q

What is zileuton used for?

A

Asthma; allergies

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11
Q

What two drugs act as lipoxygenase receptor antagonists and are used in the treatment of asthma and allergy?

A
  1. Montelukast 2. Zafirlukast
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12
Q

What are the adverse effects of zileuton and the leukotriene receptor antagonists?

A

Increased liver function tests (LFTs); headache; Churg-Strauss syndrome

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13
Q

5-Lipoxygenase is found in which cell types?

A

Neutrophils; eosinophils; basophils; mast cells

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14
Q

Which leukotrienes are considered the slow-releasing substances of anaphylaxis (SRS-A)?

A

LTA4; LTC4; LTD4

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15
Q

What enzyme acts on arachidonic acid to form PGs and thromboxanes (TXAs)?

A

Cyclooxygenase (COX)

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16
Q

Where is COX 1 found?

A

Platelets; gastrointestinal (GI) mucosa; vasculature

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17
Q

Where is COX 2 found?

A

Sites of inflammation; brain; kidney; GI tract (low amounts vs COX 1)

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18
Q

Is COX 1 a constitutive or inducible enzyme?

A

It is a constitutive enzyme, meaning that its concentration is not influenced by the concentration of substrate in the cell.

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19
Q

Is COX 2 a constitutive or inducible enzyme?

A

It is an inducible enzyme, meaning that in resting conditions the enzyme is present in only trace quantities in the cell. Upon entry of the enzyme’s substrate, the concentration of the enzyme increases exponentially.

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20
Q

Prostaglandin E1 (PGE1) does what to the following? Patent ductus arteriosus

A

Maintains patency

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21
Q

Prostaglandin E1 (PGE1) does what to the following? Uterine smooth muscle

A

Increases contraction; used as an abortifacient during pregnancy

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22
Q

Prostaglandin E1 (PGE1) does what to the following? Blood vessels

A

Vasodilation

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23
Q

Prostaglandin E1 (PGE1) does what to the following? Gastric mucosa

A

Cytoprotective effect (inhibition of HC1 secretion and stimulation of mucus and bicarbonate secretion)

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24
Q

What two PGF2_ analogs promote bronchiolar and uterine smooth muscle contraction?

A
  1. Carboprost 2. Dinoprost
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25
Q

Why are nonsteroidal anti-inflammatory drugs (NSAIDs) effective in the treatment of dysmenorrhea?

A

Inhibition of PGE2 and PGF2_ synthesis

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26
Q

What PGE1 analog is used for impotence due to its vasodilatory effects?

A

Alprostadil

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27
Q

What is another name for PGI2?

A

Prostacyclin

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28
Q

What are the actions of prostacyclin?

A

Inhibits platelet aggregation; vasodilation

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29
Q

What is the name of a prostacyclin analog and what is it used for?

A

Epoprostenol; pulmonary hypertension (HTN)

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30
Q

What are the actions of TXA2?

A

Promotes platelet aggregation; bronchoconstriction; vasoconstriction

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31
Q

Increasing cyclic adenosine monophosphate (cAMP) will do what to platelet aggregation?

A

Decrease platelet aggregation (mechanism of action of PGI2)

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32
Q

What is the mechanism of action of the nonselective NSAIDs?

A

Inhibit both COX 1 and COX 2, thereby inhibiting synthesis of PGs and TXAs

33
Q

Name the three COX 2-specific inhibitors:

A
  1. Celecoxib 2. Rofecoxib 3. Valdecoxib
34
Q

Do COX 2 inhibitors inhibit platelet aggregation?

A

No

35
Q

Which adverse effects of celecoxib have sparked debates about whether it should be pulled from the market or not?

A

Increased risk of cardiovascular events (myocardial infarction, stroke, and worsening of preexisting HTN)

36
Q

What are the main therapeutic effects of NSAIDs?

A

Anti-inflammatory; analgesic; antipyretic; antiplatelet

37
Q

What is the prototype NSAID?

A

Acetylsalicylic acid

38
Q

What is acetylsalicylic acid also known as?

A

Aspirin; ASA

39
Q

Does ASA act as a reversible or irreversible inhibitor of COX 1?

A

Irreversible

40
Q

How does ASA irreversibly inhibit COX?

A

Acetylates serine hydroxyl group near active site of COX, thereby forming an irreversible covalent bond

41
Q

What is the half-life of a platelet?

A

5 to 7 days

42
Q

Why can’t platelets produce more COX after ASA therapy?

A

Nonnucleated cells, therefore, lacking the capability of protein synthesis

43
Q

What laboratory test is prolonged after ASA therapy?

A

Bleeding time

44
Q

How does ASA work as an antipyretic?

A

Inhibits IL-1 stimulated synthesis of PGE2 in the hypothalamus, thereby inhibiting alteration of the temperature “set-point”

45
Q

Low-dose ASA does what to uric acid elimination?

A

Decreases tubular secretion (increases serum uric acid levels)

46
Q

High-dose ASA does what to uric acid elimination?

A

Decreases tubular reabsorption (decreases serum uric acid levels)

47
Q

What type of acid-base disturbance is seen in ASA overdose?

A

Mixed respiratory alkalosis with metabolic acidosis

48
Q

Does ASA overdose cause an anion gap or nonanion gap metabolic acidosis?

A

Anion gap metabolic acidosis

49
Q

What are the signs/symptoms of salicylism?

A

Decreased hearing; tinnitus; vertigo; nausea; vomiting; headache; hyperventilation; confusion; dizziness

50
Q

Why is ASA not given to children especially during times of viral (varicella and influenza) infections?

A

Reye syndrome

51
Q

What characterizes Reye syndrome?

A

Encephalopathy; hepatotoxicity

52
Q

How can excretion of ASA from the urine be expedited?

A

Alkalinization of urine with NaHCO3

53
Q

What should be given instead of ASA to children with fever?

A

Acetaminophen (or acetyl-para-aminophenol, APAP)

54
Q

What is the mechanism of action of acetyl-para-aminophenol?

A

The direct fashion in which acetaminophen produces analgesia is unknown. The drug inhibits synthesis of PGs (via COX 3 inhibition) in the central nervous system (CNS), the only place in the body COX 3 is found. It also blocks pain impulse generation peripherally. Antipyresis is achieved via inhibition of the hypothalamic heat regulating center.

55
Q

ASA can do what to asthmatics?

A

Exacerbate symptoms via bronchoconstriction due to unopposed production of leukotrienes

56
Q

What is the “triad” of ASA hypersensitivity?

A
  1. Asthma 2. Nasal polyps 3. Rhinitis
57
Q

What is the mechanism of ASA-induced hyperthermia at toxic doses?

A

Uncoupling of oxidative phosphorylation

58
Q

What are the GI adverse effects of NSAIDs?

A

Ulcers; gastritis; GI bleeding (via decreased PGs which act as GI mucosal protectants); nausea; abdominal cramping

59
Q

If a patient is taking ASA and warfarin concomitantly, what should the dose of ASA be?

A

81 mg daily

60
Q

ASA can do what to blood glucose?

A

Decrease blood glucose

61
Q

What type of kinetics does ASA follow?

A

Zero order

62
Q

Antiplatelet and analgesic effects of ASA occur at lower or higher doses than those required for anti- inflammatory effects?

A

Lower

63
Q

What is the drug of choice for closing a patent ductus arteriosus?

A

Indomethacin

64
Q

What is the mechanism of NSAID-induced renal failure?

A

Inhibition of PGE2 and PGI2 synthesis which are responsible for maintaining renal blood flow

65
Q

Give examples of nonselective NSAIDs other than ASA:

A

Ibuprofen; naproxen; diclofenac; indomethacin; ketorolac; piroxicam; oxaprozin; nabumetone; sulindac

66
Q

What are the major differences between nonselective NSAIDs and selective COX-2 inhibitors?

A

COX-2 inhibitors have less antiplatelet action and less GI adverse effects.

67
Q

Which COX-2 inhibitors are potentially cross-reactive in patients with sulfonamide allergy?

A

Celecoxib; valdecoxib

68
Q

Name two drugs that have antipyretic and analgesic effects yet lack anti-inflammatory and antiplatelet effects:

A
  1. APAP 2. Phenacetin
69
Q

acetyl-para-aminophenol inhibits COX centrally, peripherally, or both?

A

Centrally (inhibits PG synthesis in the CNS)

70
Q

Overdose of acetyl-para-aminophenol can potentially cause what life-threatening condition?

A

Hepatic necrosis

71
Q

How is acetyl-para-aminophenol predominantly metabolized?

A

Glucuronidation; sulfation

72
Q

Cytochrome P-450 2E1 metabolizes acetyl-para-aminophenol to which compound (this is a minor metabolic pathway)?

A

N-acetyl-benzoquinoneimine (NAPQI)

73
Q

Which metabolite of acetyl-para-aminophenol is hepatotoxic?

A

N-acetyl-benzoquinoneimine (NAPQI)

74
Q

Which compound binds to N-acetyl-benzoquinoneimine (NAPQI) and ultimately leads to its excretion?

A

Glutathione

75
Q

What happens to patients taking acetyl-para-aminophenol when glutathione stores run out?

A

Accumulation of NAPQI with subsequent hepatotoxicity

76
Q

What drug is used to replenish reduced glutathione during times of acetyl-para-aminophenol overdose?

A

N-acetylcysteine

77
Q

What is the maximum daily dose of acetyl-para-aminophenol in patients with normal hepatic function?

A

4 g per 24 hours

78
Q

What is the maximum daily dose of acetyl-para-aminophenol in patients with abnormal hepatic function?

A

2 g per 24 hours

Pharmacology by Somebody (25 decks)

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