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

Anti-Inflammatory Drugs Flashcards

(101 cards)

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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
Kinins
Everything
26
Kinins are a very strong...
vasodilator
27
Where is histamine found
high amounts in stomach, lung and skin
28
Histidine
AA, doesn't do anthing
29
Histidine to Histamine via
L-histidine decarboxylase
30
Histamine on response curves
For most responses, antihistimines shift the agonist dose response curve right and look like a competitive antagonist
31
How many types of histamine receptors are there?
4 (H1 - H4)
32
H1
``` bronchoconstriction GI smooth muscle capillary permeability Pruritis Catecholamine release ```
33
H2
Gastric acid secretion Inhibition of IGE mediated basophil histamine release Inhibition of t lyphocytes
34
Cardiac effects of H1 and H2
increased heart rate, force of contraction, increased arrhythmias and slow AV conduction
35
Vasodilator effects of H1 and H2
H1 - rapid and short lived | H2 - dilation develops slowly and is sustained
36
Triple response caused by histamine
Vasodilation (1 and 2), Flare (H1), wheal (H2), pain and itching (H1)
37
First generation antihistamines SE
Sedation Dry secretions GI disturbances
38
Overdose of FG antihistamine?
Resembles atropine poisoning - dilated pupils, flushed face and fever with dry mouth.. etc.
39
Name FG antihistamine?
Diphenhydramine | Chlorpheniramine
40
CNS in first vs. second generation antihistamines?
Only a small amount of the second generation drugs cross BBB because they have affinity for the P-glycoprotein efflux pump.
41
Names of SG antihistamines?
Cetirizine Fexofenadine Loratadine
42
Therapeutic uses of H1 antihistamines?
Allergies, urticaria, atopic dermatitis
43
Should you use an anti-histamine in an asthma attack?
NO
44
H2 antihistamines
used in gastric stuff. Inhibit gastric acid secretion
45
Phospholipids are converted to AA via?
Phospholipase A2
46
AA to prostanoids via?
Cyclooxygenase (COX)
47
AA to leukotrienes via?
Lipoxygenase (LOX)
48
Control step in ability to produce prostaglandins and thromboxanes?
Availability of AA
49
COX1
constitutive Found in platelets Expressed in most cells Gastric muscosa
50
COX2
Induced Not found in platelets Brain and kidney constitutively; induced by serum factors, cytokines and growth factors via inflammation
51
What is the most important isozyme in the production of prostaglandins and thromboxane in inflammation?
COX2
52
How is COX degraded?
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
Thromboxane is a vaso_____
constrictor
54
Prostacyclin is a vaso_____
dilator
55
COX receptors
g protein coupled receptors with various second messengers
56
List the COX receptors
``` DP (PGD) FP (PGF) IP (PGI2) TP (TXA2) EP (PGE) --> 4 subtypes EP1 through EP4 ```
57
How is fever induced?
IL-1 induces PGEs
58
Vasodilation induced via?
PGEs and PGI2
59
Increased vascular permeability induced via?
PGEs and PGI2
60
How is pain induced?
PGEs | PGEs and PGI2 lower the threshold of pain or sensitize pain receptors and synergize with other mediators to cause pain
61
What other mediators can cause PG production and result in pain?
Cytokines Bradykinin Other mediators
62
What do NSAIDS inhibit?
Cyclooxygenase
63
Three AAAs of NSAIDS?
Analgesia Anti-inflammatory Anti-pyretic
64
Mechanism of fever?
Inflammation - IL-1 - PGE2 in circumventricular organs in and near the hypothalamus - Fever via resetting of the thermal set point
65
Aspirin
Irreversibly inhibits COX via actylation
66
Ibuprofen
NSAID
67
Naproxen
NSAID, Longer half life than Ibuprofen
68
Indomethacin
most potent NSAID
69
Piroxicam
once a day administration NSAID, GI bleeding
70
Celecoxib
More selective for COX-2 (Less GI effect)
71
Acetaminophen
NOT a NSAID because NOT anti-inflammatory
72
Acetaminophen is a weak ___ Inhibitor
COX
73
Acetaminophen overdose can cause serious _____ injury
hepatic
74
SE of COX inhibitors
``` GI ulceration (inhibition of PG syntehsis) Prolongation of gestation (PG initiates labor) Renal function Hepatic function Increased bleeding time ```
75
Bleeding and COX inhibitors
Inhibiting COX1 in the platelets prevents platelet aggregation and TX formation
76
Aspirin Hypersensitivity
atopic individuals No AB to aspirin - hypersensitivity like rxn Sx: rhinitis, urticaria, asthma, laryngeal edema
77
Mechanism of aspirin hypersensitivity (1)
Blockade of COX shifts arachidonate utilization to the lipoxygenase pathway - increased leukotriene production Upregulation of Cys LTR1
78
Mechanism of aspirin hypersensitivity (2)
Inhibition of COX1 results in declining PGE2. Removing PGE2 eliminates the blocking of 5-lipoxygenase and allows for rapid synthesis of leukotrienes.
79
COX2 inhibitors and aspirin hypersensitive individuals?
Initial reports suggest they are safe
80
When would COX2 be ideal?
GI irritation Decreased platelets funciton Aspirin Hypersensitvity
81
Why are COX2 inhibitors bad for the CV system?
reduce the production of Prostacyclin which inhibits platelet aggregation - may increase risk of thrombotic CV events.
82
5-Lipoxygenase
converts 5-HPETE to Leukotriene A4 (LTA4)
83
LTA4 to LTB4 via....
LTA hydrolyase
84
LTA4 to LTC4
``` LTC4 synthase (Mast cell or basophil) Glutathione S transferase (endothelial cell, smooth muscle) ```
85
LTA4 + (LTC4 synthase or Glutathione S transferase)
LTC4 - LTD4 - LTE4
86
LTB4
chemotaxis
87
LTC4, LTD4, LTE4
airway constriction
88
receptors LTC4
``` Cys LTR2 (mostly) Cys LTR1 (some) ```
89
Receptors LTB4
LTB4 receptor
90
Receptor LTD4
``` cys LTR1 (mostly) cys LTR2 (some) ```
91
Leukotriene inhibitor mechanism
used in treatment of asthma (chronic) | not recommended for acute
92
Name 3 LT inhibitors
Zileuton Zafirlukast Montelukast
93
Zileuton mechanism
``` 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
Zafirlukast
Leukotriene receptor antagonist (LTD4, Cys LTR1) | Inhibits cytochrome p450
95
Montelukast
Leukotriene receptor antagonist (LTD4, Cys LTR1)
96
Kallikrein
converts kininogen to bradykinin (9 aa) or kallidin (10aa)
97
ACE functions
angiotensin I to Angiotensin II (vasoconstriction) | bradykinin to inactive kinin (decreases dilation)
98
Why do ACE inhibitors work?
``` Decreases vasoconstriction (via angiotensin) Increases dilation (by maintaining bradykinin) ```
99
ACE
Angiotensin converting enzyme | Kininase II
100
Kinins and B2 receptors (terminal arginine)
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
Kinins and B1 receptors (no terminal arginine)
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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