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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
Reduce the production of inflammatory prostaglandin E2 (PGE2) and so they attenuate inflammatory effects
NSAIDs
26
All NSAIDs (aspirin, ibuprofen ( Advil ® ), naproxen ( Aleve® ), diclofenac and indomethacin, etc.) have similar actions, inhibiting the
COX-2 Enzyme
27
60% of patients will respond to any
NSAID
28
The full analgesic effect of an NSAID should be obtained within a -anti-inflammatory action may take longer
Week
29
Anti-inflammatory drugs that target COX-2 are likely to also bind to
COX-1
30
COX-2 inhibitors decrease the levels of
PGE2
31
Since NSAIDs also bind COX-1, the reduction in levels of “housekeeping” prostaglandins can produce disturbances in
Homeostasis
32
The most common side affect of NSAIDs is
GI discomfort
33
Contra-indicated in patients with peptic ulcers, hypersensitivity reactions to aspirin, coagulation defects, severe heart failure, etc
NSAIDs
34
Has the potential to induce asthma via the increased production of leukotrienes LTC4,LTD4, and LTE4
Aspirin
35
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
Aspirin
36
Aspirin is increasingly popular as an anti-platelet drug for patients with CAD at risk for
Thrombosis
37
Aspirin is unique among the NSAIDs in that it binds covalently (irreversibly) to the
COX-1 and COX-2 active sites in platelets
38
Inhibits thromboxane (TXA2) production in platelets and reduces their ability to coagulate with fibrin
Aspirin
39
These drugs are highly selective for COX-2 enzyme over COX-1, thereby selectively inhibit production of proinflammatory prostaglandins
Selective COX-2 inhibitors
40
Long-term use of selective COX-2 inhibitors was believed possible with less chance of side-effects, particularly
GI problems
41
Selective COX-2 inhibitors were also believed useful in the treatment of chronic inflammatory diseases such as
RA
42
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
Celecoxib (Celebrex)
43
Selective COX-2 inhibitors slightly increase the risk of
MI and Stroke
44
Why do selective COX-2 inhibitors increase the risk of MI?
They inhibit PGI2 but not TXA2
45
On the other hand, low-dose aspirin is beneficial for the prevention of coronary heart disease (CHD). This is because it
Blocks synthesis of TXA2 but not PGI2 as much
46
Strong evidence suggests that Celecoxib (Celebrex™) and low/moderate dose Aspirin are effective in dramatically reducing the risk and severity of
Colorectal Cancer (CRC)
47
The net effect of selective COX-2 inhibitors is an excess of
TXA2
48
81 mg of "baby" Aspirin inhibits both -provides a positive cardiovascular effect
COX-1 and COX-2
49
Has anti-pyretic and analgesic properties, but it is not an anti-inflammatory drug (therefore, it is not an NSAID)
Acetaminophen (Tylenol)
50
Acetaminiphens mechanism of action is subject to much pharmacological speculation but somehow it reduces
Prostaglandin synthesis
51
A reduction in prostaglandins in the hypothalamus (CNS) reduces
Pyresis
52
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
NAPQI
53
Given via IV to treat acetaminophen overdose
N - Acetylcysteine (NAC)
54
Increases stores of antioxidant glutathione in liver → promotes metabolism/excretion of drug
NAC
55
What is the maximum recommended daily dose of Acetaminophen?
4g per day
56
What is the minimum toxic single dose in healthy adults?
7.5-10 g
57
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
Cortisol
58
Synthetic corticosteroid drugs include
Hydrocortisone, prednisolone, dexamethasone and betamethasone
59
Steroids have antiinflammatory effects by down-regulating the production of
COX-2
60
Reduces activity of immune cells including mast cells and macrophages
Immunosuppressive effects of steroid anti-inflammatories
61
These immunosuppressive effects reduce the production of
Histamine
62
Particularly useful when inflammatory response is a major manifestation of the disorder
Corticosteroids
63
The chronic side effects of steroids are what might be expected from immunosuppressive drugs that reduce
Protein synthesis
64
Not usually curative and can be dangerous
Corticosteroids
65
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
Corticosteroids
66
Corticosteroids affect lipid levels by stimulating
Hormone-sensitive lipase (thus lipolysis)
67
Corticosteroids also promote
Protein Catabolism
68
What are two common physical side effects of the fat redistribution seen with corticosteroids?
Moon facies and buffalo hump

Immunity (33 decks)

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