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Hailey - IHO > Anti-inflammatory Agents > Flashcards

Anti-inflammatory Agents Flashcards

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
Q

Newer anti-histamines pearls

A

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
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26
Q

Anti-histamine TU

A

Allergy (uricaria, poison ivy, etc., not asthma)
Motion sickness
Sleep aid (diphenhydramine)
May reduce rhinorrhea of common cold

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27
Q

H2 anti-histamines (for next year)

A

Cimetidine
Ranitidine
Famotidine
Nizatidine

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28
Q

Prostainoid synthesis

A

Phospholipis in cellmembrane (phospholipase A2) –> arachidonic acid –> (COX) > Prostaglandins and Thromboxanes OR (LOX) > Leukotrienes

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29
Q

COX-1

A

constitutive
constitutively expressed in most cells
protects gastric mucosa (because allows mucosal secretion fro certain PG)
found in platelets

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30
Q

COX-2

A

induced
constitutively expressed in brain and kidney
induced by certain serum factors, cytokines, GFs in tissues and site of inflammation*
NOT found in platelets

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31
Q

Cyclooxygenase produces

A

Inflammation (redness, swelling, heat, pain)
Fever
Cardiovascular disease (PGs and TXA important in balance of platelet aggregation)

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32
Q

Action of cyclooxygenase product depends on…

A

which prostanoid receptor is in that tissue

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33
Q

Receptors for prostaglandins

A

Seven transmembrane G protein coupled receptors with various 2nd messengers

DP (PGD)
FP (PGF)
IP (PGI2)
TP (TXA2)
EP (PGE) EP1-4
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34
Q

Characteristics of PG receptors (platelet aggregation, smooth muscle tone, natural agonist, G protein, second messenger)

A 
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
Q

DP

A

(-, +/-, PGD2, Gs, cAMP)

36
Q

FP

A

(-, +, PGF2a, Gq, IP3/DAG/Ca2+)

37
Q

IP

A

(-, -, PGI2 (PGE1), Gs, cAMP)

38
Q

TP

A

(+, +, TXA2, PGH2, Gq, IP3/DAG/Ca2+)

39
Q

EP1, 2, 3, 4

A

EP1 (-, +, PGE2, Gq, IP3/DAG/Ca2+)
EP2 (-, -, PGE2, Gs, cAMP)
EP3 (-, +, PGE2) Gi Gs Gq, cAMP, IP3/DAG/Ca2+)
EP4 (-, -, PGE2, Gs, cAMP)

40
Q

Inflammatory effects of PGs:

A

Fever (PGEs)
Vasodilation (PGEs and PGIs)
Increased vascular permeability (PGEs and PGIs)
Pain (PGEs cause pain, PGEs and PGI2 sensitize pain receptors)

41
Q

Shared therapeutics of COX1/2 inhibitors

A

analgesia
antipyretics
anti-inflammatory

42
Q

Aspirin

A

Irreversibly binds/acetylated COX

43
Q

Ibuprofen

A

(-) COX1/2

fewer GI SE

44
Q

Naproxen

A

(-) COX1/2

45
Q

Ketorolac

A

(-) COX1/2

promoted primarily for analgesia, also anti-inflammatory

46
Q

Ketoprofen

A

(-) COX1/2

47
Q

Indomethacin

A

(-) COX1/2
Most potent NSAID
SEVERE FRONTAL HA and BLOOD DISORDERS

48
Q

Sulindac

A

(-) COX1/2

49
Q

Piroxicam

A

(-) COX1/2
only QD admin
cause SERIOUS GI BLEED

50
Q

Celecoxib

A

Celebrex

(-) COX 2***

51
Q

Acetaminophen

A 
NOT A NSAID
analgesic
antipyretic
NOT ANTI-INFLAMMATORY
effectively inhibits COX in brain, but not at sites of inflammation
52
Q

SE (-) COX

A 
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
Q

Aspiring hypersensitivity

A

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
Q

Selective COX-2 inhibitor SE

A

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
Q

Aspirin and Reye syndrome

A

encephalopathy and fatty liver following viral infection in children
(use acetaminophen)

56
Q

Aspirin TI

A

LOW TI
anti-inflammatory doses for aspirin are close to toxic doses
borderline: anti-inflam and tinnitus

57
Q

Leukotriene synthesis and limitation in pathway

A

AA –> 5-HPETE –> LTA –> LTB OR LTC –> D E

**AA availability is limitation in pathway

58
Q

Degradation of LOX products

A

LTA4: short half life
LTB4: oxidized by enzymes in PMNs
LTE4: excreted in urine OR acetylated and excreted in bile

59
Q

SRS-As

A

slow reacting substance of anaphylaxis
LTC4, LTD4, LTE4
= peptidoleukotrience or cysteinyl leukotrienes

60
Q

5-lipoxygenase

A

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
Q

Leukotrienes are primarily generated in…

A

leukocytes.

PMNs primarily make LTB4
Mast cells and basophils primarily make peptide-leukotriends

62
Q

PMN

A

LTB4

63
Q

RBC

A

LTB4

64
Q

Platelet

A

LTB4

65
Q

Endothelial cell, smooth muscle cell

A

LTC4

66
Q

Mast cell, basophil

A

LTC4

LTD4

67
Q

LTB4 receptor

A

LTB4 only

68
Q

CysLTR1 peptidoleukotriene receptor

A

CysLTR1 OR LTD4 Rec

1st LTD4, 2nd LTC4/LTE4

69
Q

CysLTR2 peptidoleukotriene receptor

A

CysLTR2 OR LTDC4 Rec

1st LTC4, 2nd LTD4/LTE4

70
Q

Leukotriene inhibitors used in treatment of…

A

bronchial asthma

chronic asthma

71
Q

Zileuton mech

A

Inhibits 5-LOX

Prevents synthesis of LTB4 and peptide-leukotrienes

72
Q

Zileuton use and tox

A

cytoP450 –> drug interactions
decrease need for beta-agonstis in asthma
HEPATIC TOXICITY

73
Q

Zafirlukast/Montelukast mech

A

Leukotriene receptor antagoneis (LTD4 receptor, CysLTR1)

74
Q

Zafirlukast/Montelukast use and tox

A

Zafirlukast: inhibits cyto P450 –> significant drug interactions

Montelukast: QD admin**

both used in chronic asthma

75
Q

Kinins

A

bradykinin
kallidin

redness swelling, heat, pain

76
Q

Kinin synthesis

A

extracellular synthesis

Kininase I and II

77
Q

Hfa

A

activated Hageman factor, part of clotting cascade

78
Q

Plasmin

A

enzyme that digests fibrin

79
Q

Kininase I

A

carboxypeptidase N removes carboxy terminal arginine

80
Q

Kininase II

A

angiotensin converting enzyme (ACE) removes terminal phe and arg

81
Q

bradykinin and kallidin are the ___________

A

mediators with inflammatory activities

82
Q

Actions of kinins (kallidin and bradykinin = plasma kinins) via B2 receptor

A

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
Q

Actions of kinins (kallidin and bradykinin = plasma kinins) via B1 receptor

A

bradykinin and kallidin without the terminal arg: more active > bradykinin or kallidin

chronic inflammatory effects
INDICTED after trauma
Hypotension
pain

84
Q

Interrelationship between __, __, __, and __.

A

kinin
complement
coagulation
fibrinolytic pathways

Hailey - IHO (5 decks)

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