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Immunity > Inflammation and Anti-inflammatory Drugs > Flashcards

Inflammation and Anti-inflammatory Drugs Flashcards

1
Q

Inflammation results in

A

Vasodilation

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2
Q

Occurs immediately after trauma to prevent the spread of pathogens, minimize further tissue damage, and promote healing and repair

A

Inflammatory Response

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3
Q

The inflammatory response involves which three key processes?

A
  1. ) Vasodilation
  2. ) Increased vascular permiability
  3. ) Migration of neutrophils
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4
Q

First WBCs to arrive at injury site

  • infiltrate injured tissues
  • remove damaged tissue through phagocytosis
A

Neutrophils

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5
Q

More long lived than neutrophils

  • phagocytose pathogens and cellular debris
  • engulf neutrophils during resolution of inflammaiton
A

Macrophages

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6
Q

Mediate wound healing and defense against pathogens

A

Mast cells

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7
Q

Mast cells play a major role in allergy, eczema, and anaphylaxis by releasing the vasodilator

A

Histamine

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8
Q

Cause vasodilation, increase the permeability of blood vessels, lower blood pressure, and stimulate pain receptors

A

Kinins

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9
Q

Prostaglandins produced in inflammation potentiate the action of

A

Bradykinin

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10
Q

Members of a large family of chemical mediators derived from arachidonic acid (a fatty acid) and are found in all tissues of the body

A

Prostaglandins

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11
Q

Prostaglandins belong to the eicosanoid family that includes

A

Prostaglandins, thromboxanes, and leukotrienes

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12
Q

Prostaglandins and thromboxanes are collectively known as

A

Prostanoids

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13
Q

Functions in the promotion of gastric mucus secretion and inhibition of gastric acid secretion

-protects stomach lining from erosive effects of gastric acid

A

Prostaglandin E2 (PGE2)

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14
Q

Functions in the inhibition of platelet aggregation in the clotting process and vasodilation

A

Prostaglandin I2 (PGI2, aka Prostacyclin)

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15
Q

Promotes platelet aggregation in the clotting process and vasoconstriction

A

Thromboxane A2 (TXA2)

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16
Q

Counterbalance each other in many respects

A

PGI2 and TXA2

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17
Q

The main prostanoid involved in inflammation

A

PGE2

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18
Q

Mast cells and macrophages produce large amounts of PGE2 that is released into the

A

Inflamed area

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19
Q

Increased synthesis of PGE2 results from the upregulation of an enzyme called

A

COX-2

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20
Q

Part of a family of cyclo-oxygenase enzymes

A

COX-2

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21
Q

Perhaps the most common, being produced constitutively in most cells of the body and producing the prostaglandins involved in normal homeostasis (“housekeeping” functions)

A

COX-1

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22
Q

COX-2 expression is induced by

A

Inflammation

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23
Q

Provide analgesic (pain-killing) and antipyretic (feverreducing) effects, and, in higher doses, anti-inflammatory effects

A

NSAIDs

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24
Q

An example of a steroidal anti-inflammatory is

A

Hydrocortisone

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25
Q

Reduce the production of inflammatory prostaglandin E2 (PGE2) and so they attenuate inflammatory effects

A

NSAIDs

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26
Q

All NSAIDs (aspirin, ibuprofen ( Advil ® ), naproxen ( Aleve® ), diclofenac and indomethacin, etc.) have similar actions, inhibiting the

A

COX-2 Enzyme

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27
Q

60% of patients will respond to any

A

NSAID

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28
Q

The full analgesic effect of an NSAID should be obtained within a

-anti-inflammatory action may take longer

29
Q

Anti-inflammatory drugs that target COX-2 are likely to also bind to

30
Q

COX-2 inhibitors decrease the levels of

31
Q

Since NSAIDs also bind COX-1, the reduction in levels of “housekeeping” prostaglandins can produce disturbances in

A

Homeostasis

32
Q

The most common side affect of NSAIDs is

A

GI discomfort

33
Q

Contra-indicated in patients with peptic ulcers, hypersensitivity reactions to aspirin, coagulation defects, severe heart failure, etc

34
Q

Has the potential to induce asthma via the increased production of leukotrienes LTC4,LTD4, and LTE4

35
Q

Relatively selective for COX-1 and less popular now as an anti-inflammatory due to GI effects and Reye syndrome

-One of the oldest analgesics

36
Q

Aspirin is increasingly popular as an anti-platelet drug for patients with CAD at risk for

A

Thrombosis

37
Q

Aspirin is unique among the NSAIDs in that it binds covalently (irreversibly) to the

A

COX-1 and COX-2 active sites in platelets

38
Q

Inhibits thromboxane (TXA2) production in platelets and reduces their ability to coagulate with fibrin

39
Q

These drugs are highly selective for COX-2 enzyme over COX-1, thereby selectively inhibit production of proinflammatory prostaglandins

A

Selective COX-2 inhibitors

40
Q

Long-term use of selective COX-2 inhibitors was believed possible with less chance of side-effects, particularly

A

GI problems

41
Q

Selective COX-2 inhibitors were also believed useful in the treatment of chronic inflammatory diseases such as

42
Q

Rofecoxib( Vioxx ® ) was withdrawn from the US market in 2004, after long-term studies revealed increased risk of cardiovascular events. The only selective COX-2 inhibitor still available in the US is

A

Celecoxib (Celebrex)

43
Q

Selective COX-2 inhibitors slightly increase the risk of

A

MI and Stroke

44
Q

Why do selective COX-2 inhibitors increase the risk of MI?

A

They inhibit PGI2 but not TXA2

45
Q

On the other hand, low-dose aspirin is beneficial for the prevention of coronary heart disease (CHD). This is because it

A

Blocks synthesis of TXA2 but not PGI2 as much

46
Q

Strong evidence suggests that Celecoxib (Celebrex™) and low/moderate dose Aspirin are effective in dramatically reducing the risk and severity of

A

Colorectal Cancer (CRC)

47
Q

The net effect of selective COX-2 inhibitors is an excess of

48
Q

81 mg of “baby” Aspirin inhibits both

-provides a positive cardiovascular effect

A

COX-1 and COX-2

49
Q

Has anti-pyretic and analgesic properties, but it is not an anti-inflammatory drug (therefore, it is not an NSAID)

A

Acetaminophen (Tylenol)

50
Q

Acetaminiphens mechanism of action is subject to much pharmacological speculation but somehow it reduces

A

Prostaglandin synthesis

51
Q

A reduction in prostaglandins in the hypothalamus (CNS) reduces

52
Q

Hepatotoxicity can occur at only 2-3 times the therapeutic dose of tylenol. This is because at this dose we see production of the toxic metabolite

53
Q

Given via IV to treat acetaminophen overdose

A

N - Acetylcysteine (NAC)

54
Q

Increases stores of antioxidant glutathione in liver → promotes metabolism/excretion of drug

55
Q

What is the maximum recommended daily dose of Acetaminophen?

A

4g per day

56
Q

What is the minimum toxic single dose in healthy adults?

57
Q

Involved in a wide range of physiological processes, including stress response, immune response, and regulation of inflammation, carbohydrate metabolism, protein catabolism, fat distribution, blood electrolyte levels, and behavior

58
Q

Synthetic corticosteroid drugs include

A

Hydrocortisone,
prednisolone, dexamethasone
and betamethasone

59
Q

Steroids have antiinflammatory effects by down-regulating the production of

60
Q

Reduces activity of immune cells including mast cells and macrophages

A

Immunosuppressive effects of steroid anti-inflammatories

61
Q

These immunosuppressive effects reduce the production of

62
Q

Particularly useful when inflammatory response is a major manifestation of the disorder

A

Corticosteroids

63
Q

The chronic side effects of steroids are what might be expected from immunosuppressive drugs that reduce

A

Protein synthesis

64
Q

Not usually curative and can be dangerous

A

Corticosteroids

65
Q

Stimulate gluconeogenesis and glycogen synthesis. Inhibit glucose uptake by muscle cells. Net effect is increased serum glucose levels, hyperglycemia, weight gain, diabetes, need for insulin

A

Corticosteroids

66
Q

Corticosteroids affect lipid levels by stimulating

A

Hormone-sensitive lipase (thus lipolysis)

67
Q

Corticosteroids also promote

A

Protein Catabolism

68
Q

What are two common physical side effects of the fat redistribution seen with corticosteroids?

A

Moon facies and buffalo hump

Immunity (33 decks)

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