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Hailey - IHO > Anti-inflammatory Agents > Flashcards

Anti-inflammatory Agents Flashcards

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1
Q

Inflammation: _____ > _____ > ______

A

Injury –> Mediators –> Inflammation

Inflammation:
redness
swelling 
heat
pain
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2
Q

Autacoids:

A 
array of substances normally present in then body
brief lifetime
act near sites of synthesis
lcoal hormaones
inflammatory mediators
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3
Q

Acute Inflammation physiology:

A

Changes in blood vessel caber and flow
Increased vascular permeability
Leuocytic infiltration

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4
Q

Which mediators COULD cause vasodilatation, increased permeability, migration of WBC?

A 
histamine
PGs
LTs
PAF platelet activiating facotor
kinis
products of complement system activation
cytokines
chemokines
interleukins
adehsions molecules
etc.
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5
Q

Histamine major activities

A

Redness
Heat
Swelling
Airway constriction

NOT CHEMOTAXIS

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6
Q

Prostaglandin and thromboxane major activities

A

opposing effects often

See individual: PGE, PGI, PGD, thromboxane, TXA, PGI

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7
Q

Leukotriene major activities

A

LTB4 is chemotactic (PMNs)
Reduces pain threshold

Peptido LTs:
Bronchoconstriction
Increased vascular permeability
Chemotaxis (eosinophils)

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8
Q

Kinis (bradykinin and kallidin) major activities

A

everything
Very STRONG VASODILATOR
–> hypotension
NOT chemotactic

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9
Q

Redness/vasodilation

A

Histamine
PGE2
PGI2
Kinins

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10
Q

Swelling/increased vascular permeability

A

Histamine
Peptide leukotrienes (LTC4, LTD4, LTE4)
Kinins

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11
Q

Pain/reduces pain threshold or causes pain

A

PGE
PGI
LTB4
Kinins

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12
Q

Chemotactic/directic migration of WBCs

A 
LTB4 (neutrophis)
Peptido leukotrienes (eosinophils)
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13
Q

Fever

A

PGEs

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14
Q

Airway constriciton/broncoconstriction

A

Histamine
Peptido leukotrienes
Kinins
PGD2

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15
Q

Hypotension

A

Kinins*

Histamine

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16
Q

Intracutaneous histamine “triple response”

A

itching
pain
urticaria/hives

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17
Q

IV histamine

A 
decreased BP
tachycardia (response to dec BP)
bronchoconstriction
HA
flushing of false
urticaria (wheal and flare)
mucus secretion
gastric acid secretion
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18
Q

Antihistamines mech

A

inverse agonists

shift agonist dose-response curve to the right = look like a competitive antagonist

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19
Q

H1 receptor

histamine-induced…

A 
Bronchoconstriction
Contraction of GI smooth muscle
Increased capillary permeability (wheal)
Pruritis (itch) and pain
Release of catecholamines from adrenal medulla
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20
Q

H2 receptor

histamine-induced…

A

GASTRIC ACID SECRETION
Inhibition of IgE-mediated basophilic histamine release
Inhibition of T lymphocyte mediated cytotoxicity
Suppression of Th2 cells and cytokines

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21
Q

H3 receptor

histamine-induced…

A

Present on histaminergic nerve terminals

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22
Q

H4 receptor

histamine-induced…

A

Present on many immune cells (eosinophils, DCs, T cell, neutrophils)

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23
Q

Mixed H1 and H2 receptor mediated responses

A

Cardiac effects (H1 and H2): increased HR, arr
Vasodilator effects (H1 at low dose hist, 1 and 2 at high hist): H1 rapid dilation short lived, H2 develops slowly dilation sustained
Triple response: vasodiation (H1 and H2), flare and wheal (H1 primarily), pain and itching (primarily H1)
Nasal symptoms: H2 –> itching, sneezing, hypersecretions, nasal bloakage,
H2 mucus production

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24
Q

Older anti-histamines pearls

A

Diphenhydramine (Benadryl)
Chlorpheniramine (Chlor-tabs)
and others

  • BLOCK H1, muscarinic, alpha adrenergic, AND 5HT receptors
  • Cross BBB, no efflux
  • sedating and dry secretions
  • CARDIOTOXIC
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25
Newer anti-histamines pearls
Cetirizine (Zyrtec) Fexofenadine (Allegra) Loratadine (Claritin) - BLOCK H1 receptors, minimal anticholinergic properties - Do not cause sedation and drying of secretions - Cross BBB, BUT EFFLUXED OUT - NOT cardiotoxic
26
Anti-histamine TU
Allergy (uricaria, poison ivy, etc., not asthma) Motion sickness Sleep aid (diphenhydramine) May reduce rhinorrhea of common cold
27
H2 anti-histamines (for next year)
Cimetidine Ranitidine Famotidine Nizatidine
28
Prostainoid synthesis
Phospholipis in cellmembrane (phospholipase A2) --> arachidonic acid --> (COX) > Prostaglandins and Thromboxanes OR (LOX) > Leukotrienes
29
COX-1
constitutive constitutively expressed in most cells protects gastric mucosa (because allows mucosal secretion fro certain PG) found in platelets
30
COX-2
induced constitutively expressed in brain and kidney induced by certain serum factors, cytokines, GFs in tissues and site of inflammation* NOT found in platelets
31
Cyclooxygenase produces
Inflammation (redness, swelling, heat, pain) Fever Cardiovascular disease (PGs and TXA important in balance of platelet aggregation)
32
Action of cyclooxygenase product depends on...
which prostanoid receptor is in that tissue
33
Receptors for prostaglandins
Seven transmembrane G protein coupled receptors with various 2nd messengers ``` DP (PGD) FP (PGF) IP (PGI2) TP (TXA2) EP (PGE) EP1-4 ```
34
Characteristics of PG receptors (platelet aggregation, smooth muscle tone, natural agonist, G protein, second messenger)
``` DP (-, +/-, PGD2, Gs, cAMP) FP (-, +, PGF2a, Gq, IP3/DAG/Ca2+) IP (-, -, PGI2 (PGE1), Gs, cAMP) TP (+, +, TXA2, PGH2, Gq, IP3/DAG/Ca2+) EP1 (-, +, PGE2, Gq, IP3/DAG/Ca2+) EP2 (-, -, PGE2, Gs, cAMP) EP3 (-, +, PGE2) Gi Gs Gq, cAMP, IP3/DAG/Ca2+) EP4 (-, -, PGE2, Gs, cAMP) ```
35
DP
(-, +/-, PGD2, Gs, cAMP)
36
FP
(-, +, PGF2a, Gq, IP3/DAG/Ca2+)
37
IP
(-, -, PGI2 (PGE1), Gs, cAMP)
38
TP
(+, +, TXA2, PGH2, Gq, IP3/DAG/Ca2+)
39
EP1, 2, 3, 4
EP1 (-, +, PGE2, Gq, IP3/DAG/Ca2+) EP2 (-, -, PGE2, Gs, cAMP) EP3 (-, +, PGE2) Gi Gs Gq, cAMP, IP3/DAG/Ca2+) EP4 (-, -, PGE2, Gs, cAMP)
40
Inflammatory effects of PGs:
Fever (PGEs) Vasodilation (PGEs and PGIs) Increased vascular permeability (PGEs and PGIs) Pain (PGEs cause pain, PGEs and PGI2 sensitize pain receptors)
41
Shared therapeutics of COX1/2 inhibitors
analgesia antipyretics anti-inflammatory
42
Aspirin
Irreversibly binds/acetylated COX
43
Ibuprofen
(-) COX1/2 | fewer GI SE
44
Naproxen
(-) COX1/2
45
Ketorolac
(-) COX1/2 | promoted primarily for analgesia, also anti-inflammatory
46
Ketoprofen
(-) COX1/2
47
Indomethacin
(-) COX1/2 Most potent NSAID SEVERE FRONTAL HA and BLOOD DISORDERS
48
Sulindac
(-) COX1/2
49
Piroxicam
(-) COX1/2 only QD admin cause SERIOUS GI BLEED
50
Celecoxib
Celebrex | (-) COX 2***
51
Acetaminophen
``` NOT A NSAID analgesic antipyretic NOT ANTI-INFLAMMATORY effectively inhibits COX in brain, but not at sites of inflammation ```
52
SE (-) COX
``` Gastric or intestinal ulcertain Prolongation of gestation Renal dysfunction Hepatic dysfunction Increased bleeding time (inhibition of COX1 in platelet prevents platelet aggregation and TXA formation) Aspirin hypersensitivity ```
53
Aspiring hypersensitivity
3-10% of asthmatics Atopic individuals No antibody to aspirin, so hypersensitivity reaction Sx: rhinitis, urticaria, asthma, laryngeal edema **COX2 are save in aspirin hypersensitive individuals
54
Selective COX-2 inhibitor SE
inhibition of induction of labor alterations in renal function ***reduce production of PROSTACYCLIN (inhibits platelet aggregation) by endothelial cells --> longterm --> increase risk of thrombotic CV events less likely: gastric ulceration or aspirin hypersensitivity
55
Aspirin and Reye syndrome
encephalopathy and fatty liver following viral infection in children (use acetaminophen)
56
Aspirin TI
LOW TI anti-inflammatory doses for aspirin are close to toxic doses borderline: anti-inflam and tinnitus
57
Leukotriene synthesis and limitation in pathway
AA --> 5-HPETE --> LTA --> LTB OR LTC --> D E **AA availability is limitation in pathway
58
Degradation of LOX products
LTA4: short half life LTB4: oxidized by enzymes in PMNs LTE4: excreted in urine OR acetylated and excreted in bile
59
SRS-As
slow reacting substance of anaphylaxis LTC4, LTD4, LTE4 = peptidoleukotrience or cysteinyl leukotrienes
60
5-lipoxygenase
5-LOX is a cytosolic enzyme that is translocated from the cytosol to membranes by binding to the protein FLAP (5-lipoxygenase activating protein)
61
Leukotrienes are primarily generated in...
leukocytes. PMNs primarily make LTB4 Mast cells and basophils primarily make peptide-leukotriends
62
PMN
LTB4
63
RBC
LTB4
64
Platelet
LTB4
65
Endothelial cell, smooth muscle cell
LTC4
66
Mast cell, basophil
LTC4 | LTD4
67
LTB4 receptor
LTB4 only
68
CysLTR1 peptidoleukotriene receptor
CysLTR1 OR LTD4 Rec 1st LTD4, 2nd LTC4/LTE4
69
CysLTR2 peptidoleukotriene receptor
CysLTR2 OR LTDC4 Rec 1st LTC4, 2nd LTD4/LTE4
70
Leukotriene inhibitors used in treatment of...
bronchial asthma | chronic asthma
71
Zileuton mech
Inhibits 5-LOX | Prevents synthesis of LTB4 and peptide-leukotrienes
72
Zileuton use and tox
cytoP450 --> drug interactions decrease need for beta-agonstis in asthma HEPATIC TOXICITY
73
Zafirlukast/Montelukast mech
Leukotriene receptor antagoneis (LTD4 receptor, CysLTR1)
74
Zafirlukast/Montelukast use and tox
Zafirlukast: inhibits cyto P450 --> significant drug interactions Montelukast: QD admin** both used in chronic asthma
75
Kinins
bradykinin kallidin redness swelling, heat, pain
76
Kinin synthesis
extracellular synthesis | Kininase I and II
77
Hfa
activated Hageman factor, part of clotting cascade
78
Plasmin
enzyme that digests fibrin
79
Kininase I
carboxypeptidase N removes carboxy terminal arginine
80
Kininase II
angiotensin converting enzyme (ACE) removes terminal phe and arg
81
bradykinin and kallidin are the ___________
mediators with inflammatory activities
82
Actions of kinins (kallidin and bradykinin = plasma kinins) via B2 receptor
kallidin and bradykinin: more active > bradykinin and kallidin without the terminal arg ``` HYPOTENSION EDEMA capillary permeabiity PAIN stimulate nerve endings contract gut smooth muscle contract airway smooth muse relaes catecholamines release prostaglandins ```
83
Actions of kinins (kallidin and bradykinin = plasma kinins) via B1 receptor
bradykinin and kallidin without the terminal arg: more active > bradykinin or kallidin chronic inflammatory effects INDICTED after trauma Hypotension pain
84
Interrelationship between __, __, __, and __.
kinin complement coagulation fibrinolytic pathways

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