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IHO Week 5 (MJ) > Anti-Inflammatory Drugs > Flashcards

Anti-Inflammatory Drugs Flashcards

1
Q

What is inflammation?

A

A process which begins following sublethal injury to tissue and ends with permanent destruction of tissue or complete healing

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2
Q

Mediators of the inflammatory response?

A

Endogenous substances that are stored or rapidly synthesized.
Act only at the site of injury.

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3
Q

Autacoids

A

An array of substances normally present in the body or formed there. Usually have a brief lifetime and act near their sites of synthesis.
Called local hormones or inflammatory mediators

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4
Q

Acute inflammation

A

Changes in blood vessel caliber and flow via:
-arteriolar dilation
-increased blood flow
slowing of flow, even to stasis

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5
Q

What is responsible for increased capillary permability

A

post capillary venules leak large molecules and contract the endothelium

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6
Q

How does leukocyte infiltration occur?

A

starts in postcapillary venules, leukocytes are paves and move into extracellular space.
Chemotaxis directs migration in response to stimuli.

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7
Q

Redness and heat occur because of…

A

vasodilation

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8
Q

Swelling occurs because of…

A

increased vascular permeability

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9
Q

Hypotension

A

widespread vasodilation, increased capillary permeability and fluid loss from circulation can contribute to decreased BP

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10
Q

Which mediators cause redness and vasodilation?

A

Histamine
PGE2
PGI2
Kinins

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11
Q

Which mediators cause swelling (increased vascular permeability)?

A

Histamine
Peptido leukotrienes (LTC4, LTD4, LTE4)
Kinins

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12
Q

Which mediators cause pain?

A

PGE
PGI
LTB4
Kinins

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13
Q

Chemotactic mediators?

A 
LTB4 (neutrophils)
Peptido leukotrienes (eosinophils)
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14
Q

Fever?

A

PGEs induce fever

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15
Q

Airway constriction?

A

Histamine
Peptidoleukotrienes
Kinins
PGD2

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16
Q

Hypotension

A

Kinins

Histamine

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17
Q

Histamine

A

Redness
Heat
Swelling
Airway constriction

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18
Q

What does histamine not cause?

A

chemotaxis

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19
Q

PGE2 and PGI2

A

Vasodilate
increase vascular permeability
Pain

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20
Q

PGD2 and thromboxane

A

bronchoconstriction

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21
Q

TXA2

A

Platelet aggregation (vasoconstriction)

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22
Q

PGI2

A

opposes platelet aggregation (vasodilation)

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23
Q

LTB4

A

chemotactic for PMNs

Reduce pain threshold

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24
Q

peptidoleukotrienes

A

bronchoconstriction
vascular perm.
chemotaxis (eosinophils)

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25
Q

Kinins

A

Everything

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26
Q

Kinins are a very strong…

A

vasodilator

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27
Q

Where is histamine found

A

high amounts in stomach, lung and skin

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28
Q

Histidine

A

AA, doesn’t do anthing

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29
Q

Histidine to Histamine via

A

L-histidine decarboxylase

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30
Q

Histamine on response curves

A

For most responses, antihistimines shift the agonist dose response curve right and look like a competitive antagonist

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31
Q

How many types of histamine receptors are there?

A

4 (H1 - H4)

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32
Q

H1

A 
bronchoconstriction
GI smooth muscle
capillary permeability
Pruritis
Catecholamine release
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33
Q

H2

A

Gastric acid secretion
Inhibition of IGE mediated basophil histamine release
Inhibition of t lyphocytes

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34
Q

Cardiac effects of H1 and H2

A

increased heart rate, force of contraction, increased arrhythmias and slow AV conduction

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35
Q

Vasodilator effects of H1 and H2

A

H1 - rapid and short lived

H2 - dilation develops slowly and is sustained

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36
Q

Triple response caused by histamine

A

Vasodilation (1 and 2), Flare (H1), wheal (H2), pain and itching (H1)

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37
Q

First generation antihistamines SE

A

Sedation
Dry secretions
GI disturbances

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38
Q

Overdose of FG antihistamine?

A

Resembles atropine poisoning - dilated pupils, flushed face and fever with dry mouth.. etc.

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39
Q

Name FG antihistamine?

A

Diphenhydramine

Chlorpheniramine

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40
Q

CNS in first vs. second generation antihistamines?

A

Only a small amount of the second generation drugs cross BBB because they have affinity for the P-glycoprotein efflux pump.

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41
Q

Names of SG antihistamines?

A

Cetirizine
Fexofenadine
Loratadine

42
Q

Therapeutic uses of H1 antihistamines?

A

Allergies, urticaria, atopic dermatitis

43
Q

Should you use an anti-histamine in an asthma attack?

A

NO

44
Q

H2 antihistamines

A

used in gastric stuff. Inhibit gastric acid secretion

45
Q

Phospholipids are converted to AA via?

A

Phospholipase A2

46
Q

AA to prostanoids via?

A

Cyclooxygenase (COX)

47
Q

AA to leukotrienes via?

A

Lipoxygenase (LOX)

48
Q

Control step in ability to produce prostaglandins and thromboxanes?

A

Availability of AA

49
Q

COX1

A

constitutive
Found in platelets
Expressed in most cells
Gastric muscosa

50
Q

COX2

A

Induced
Not found in platelets
Brain and kidney constitutively; induced by serum factors, cytokines and growth factors via inflammation

51
Q

What is the most important isozyme in the production of prostaglandins and thromboxane in inflammation?

A

COX2

52
Q

How is COX degraded?

A

Spontaneous chemical hydrolysis or enzymatic degradation
Uptake into cells by a transport protein and subsequent enzymatic degradation
COX products have short half lives to limit systemic effects

53
Q

Thromboxane is a vaso_____

A

constrictor

54
Q

Prostacyclin is a vaso_____

A

dilator

55
Q

COX receptors

A

g protein coupled receptors with various second messengers

56
Q

List the COX receptors

A 
DP (PGD)
FP (PGF)
IP (PGI2)
TP (TXA2)
EP (PGE) --> 4 subtypes EP1 through EP4
57
Q

How is fever induced?

A

IL-1 induces PGEs

58
Q

Vasodilation induced via?

A

PGEs and PGI2

59
Q

Increased vascular permeability induced via?

A

PGEs and PGI2

60
Q

How is pain induced?

A

PGEs

PGEs and PGI2 lower the threshold of pain or sensitize pain receptors and synergize with other mediators to cause pain

61
Q

What other mediators can cause PG production and result in pain?

A

Cytokines
Bradykinin
Other mediators

62
Q

What do NSAIDS inhibit?

A

Cyclooxygenase

63
Q

Three AAAs of NSAIDS?

A

Analgesia
Anti-inflammatory
Anti-pyretic

64
Q

Mechanism of fever?

A

Inflammation - IL-1 - PGE2 in circumventricular organs in and near the hypothalamus - Fever via resetting of the thermal set point

65
Q

Aspirin

A

Irreversibly inhibits COX via actylation

66
Q

Ibuprofen

A

NSAID

67
Q

Naproxen

A

NSAID, Longer half life than Ibuprofen

68
Q

Indomethacin

A

most potent NSAID

69
Q

Piroxicam

A

once a day administration NSAID, GI bleeding

70
Q

Celecoxib

A

More selective for COX-2 (Less GI effect)

71
Q

Acetaminophen

A

NOT a NSAID because NOT anti-inflammatory

72
Q

Acetaminophen is a weak ___ Inhibitor

A

COX

73
Q

Acetaminophen overdose can cause serious _____ injury

A

hepatic

74
Q

SE of COX inhibitors

A 
GI ulceration (inhibition of PG syntehsis)
Prolongation of gestation (PG initiates labor)
Renal function
Hepatic function
Increased bleeding time
75
Q

Bleeding and COX inhibitors

A

Inhibiting COX1 in the platelets prevents platelet aggregation and TX formation

76
Q

Aspirin Hypersensitivity

A

atopic individuals
No AB to aspirin - hypersensitivity like rxn
Sx: rhinitis, urticaria, asthma, laryngeal edema

77
Q

Mechanism of aspirin hypersensitivity (1)

A

Blockade of COX shifts arachidonate utilization to the lipoxygenase pathway - increased leukotriene production
Upregulation of Cys LTR1

78
Q

Mechanism of aspirin hypersensitivity (2)

A

Inhibition of COX1 results in declining PGE2. Removing PGE2 eliminates the blocking of 5-lipoxygenase and allows for rapid synthesis of leukotrienes.

79
Q

COX2 inhibitors and aspirin hypersensitive individuals?

A

Initial reports suggest they are safe

80
Q

When would COX2 be ideal?

A

GI irritation
Decreased platelets funciton
Aspirin Hypersensitvity

81
Q

Why are COX2 inhibitors bad for the CV system?

A

reduce the production of Prostacyclin which inhibits platelet aggregation - may increase risk of thrombotic CV events.

82
Q

5-Lipoxygenase

A

converts 5-HPETE to Leukotriene A4 (LTA4)

83
Q

LTA4 to LTB4 via….

A

LTA hydrolyase

84
Q

LTA4 to LTC4

A 
LTC4 synthase (Mast cell or basophil)
Glutathione S transferase (endothelial cell, smooth muscle)
85
Q

LTA4 + (LTC4 synthase or Glutathione S transferase)

A

LTC4 - LTD4 - LTE4

86
Q

LTB4

A

chemotaxis

87
Q

LTC4, LTD4, LTE4

A

airway constriction

88
Q

receptors LTC4

A 
Cys LTR2 (mostly)
Cys LTR1 (some)
89
Q

Receptors LTB4

A

LTB4 receptor

90
Q

Receptor LTD4

A 
cys LTR1 (mostly)
cys LTR2 (some)
91
Q

Leukotriene inhibitor mechanism

A

used in treatment of asthma (chronic)

not recommended for acute

92
Q

Name 3 LT inhibitors

A

Zileuton
Zafirlukast
Montelukast

93
Q

Zileuton mechanism

A 
inhibits 5-lipoxygenase and prevents synthesis of LTB4 as well as leukotrienes
Metabolized by cytochrome p450
decrease need of b agonists in asthma
Chronic asthma
Hepatic toxicity
94
Q

Zafirlukast

A

Leukotriene receptor antagonist (LTD4, Cys LTR1)

Inhibits cytochrome p450

95
Q

Montelukast

A

Leukotriene receptor antagonist (LTD4, Cys LTR1)

96
Q

Kallikrein

A

converts kininogen to bradykinin (9 aa) or kallidin (10aa)

97
Q

ACE functions

A

angiotensin I to Angiotensin II (vasoconstriction)

bradykinin to inactive kinin (decreases dilation)

98
Q

Why do ACE inhibitors work?

A 
Decreases vasoconstriction (via angiotensin)
Increases dilation (by maintaining bradykinin)
99
Q

ACE

A

Angiotensin converting enzyme

Kininase II

100
Q

Kinins and B2 receptors (terminal arginine)

A

vasodilators
increase permeability of capillaries (edema)
algesic agents (pain)
Contract gut smooth muscle
Constrict airway smooth muscle
release catecholamines from adrenal medulla
release PGs

101
Q

Kinins and B1 receptors (no terminal arginine)

A

inflammatory effects (chronic)
Induced after trauma
Hypotension and pain
May be involved with cytokine production and long term effects

IHO Week 5 (MJ) (4 decks)

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