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Pharm: block 2 week 1 > Inflammation > Flashcards

Inflammation Flashcards

1
Q

body’s mechanism for handling agents that could damage it

A

Inflammation

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2
Q

________ protective mechanism to rid body of cause of cell injury and resultant necrotic cells that injury produces

A

inflammation

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3
Q

5 signs of acute inflammation

A 
red discoloration
heat
pain
mass effect
LOF
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4
Q

Three physiological processes that occur during acute inflammation

A

vasodialation
increased vascular permeability
recruitment of neutrophils

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5
Q

Duration of chronic inflammation

A

prolongued: weeks, months or indefinate

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6
Q

main players in chronic inflammation

A

lymphocytes, plasma cells, MACROPHAGES, fibroblasts and angioblasts

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7
Q

What happens to a capillary bed during inflammation

A
  1. increased BF
  2. leakage of plasma proteins–> edema
  3. neutrophil emigration
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8
Q

Key point on inflammation:
under normal circumstances, body can _____ inflammation thus may not be seen at all while in other cases is never resolved

A

moderate

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9
Q

Inflammation is can be controlled by many or one path?

A

many

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10
Q

to rid organism of intial cuase of cell injury and the consequences of the injury is:

A

self protection

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11
Q

repairs begin during inflammation but reach completion after injurious influence has been neutralized

A

healing process

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12
Q

in process of repair, injured tissue is replace via _______ of native parenchymal cells or by filling defect with ________

A

regeneration

fibrous tissue

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13
Q

What does an ideal anti-inflammatory do?

A

controls harmful effects of inflammation but doesn’t interfere with it’s benefits

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14
Q

non-adaptive immune response to microbial pathogens (recognized by specific Rs) and nonmicrobials that are released during injury

A

Innate immunity

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15
Q

players in innate immunity

A

NK cell, macrophages, DCs

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16
Q

antiG produced by microbial pathogens are recognized by B and T lymphs which then eliminate microbial agetn

A

Adaptive or aquired immunity

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17
Q

Two potential harmful effects of inflammation

A
  1. inflam cells release lysosomal enZ that can digest normal tissue
  2. inflammatory swelling may result in death, obstruct airways or swelling w/in cranial cavity
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18
Q

What is the mediator theory

A

signs and symptoms of inflammation care caused by release of chemicals

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19
Q

Histamine is a

A

inflammatory mediator

biogenic amine

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20
Q

inflammatory mediator

biogenic amine

A

histamine

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21
Q

What is the cell source for histamine

A

mast cells and basophils

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22
Q

What is the physiological response caused by histamine

A

vasodialation
increased vascular permeability
very painful (the 3 Vs)

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23
Q

Mechanis of Histamine

A

Activates GPCRs

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24
Q

main characteristic of acute inflammation

A

edema

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25
main cell type in acute inflammation
leukocytes or PMNs
26
3 triggers of acute inflamation
infection by toxins tissue necrosis, irradiation foreign bodies
27
Propagation of disease typically occurs as result of autoimmune response, including a self-amplyfing cycle of damage
Chronic inflammation
28
main cell type for chronic inflammation______ | main characteristic______
Monocytes | fibrosis
29
Atherosclerosis is a chrnoic inflammatory process of the arterial wall that is induced by a _______ toxic plasma lipid component
endogenous
30
Triggers of chronic inflammation include
1. autoimmune disease: RA or MS 2. unregulated immune response against microbes : IBS 3. Immune response against common envir substanses: allergies or bronchial asthma
31
Inflammation is a defenisive host response to foreign invaders and necrotic tissue but itself is....
capable of causing tissue damage
32
Mediators can be effective targets to tx inflammation but because there is a multitide of them....
there is not one that will take care of everything
33
Pharmacology of Histamine
Antihistamine/H1 receptor antagonist: | diphenhydramine
34
Cell source of Bradykinin
endothelial cells
35
Response to bradykinin
The 3 Vs
36
Mechanism of action of bradykinin
Activated GCPR--> B2 receptor for pro-inflamation
37
Pharmacology of Bradykinin
1. BK2 receptor antagonist
38
What do we use a BK2 receptor antagonist for
1. antagonizer of bradykinin 2. tx acute attacks of heriditary angioedema (HAE) that has increased production of bradykinin 3. tx symptoms of localized swelling, inflammation and pain
39
Complement system (pls proteins) cell source
made by liver, circulates in blood
40
Physio response to complement
chemotaxis promote release of mediators from PMNs increase vascular permeability (if too much--tissue injury)
41
Mech of Complement
Complexes of complement protein aggregate to cell surface mmb and cause osmotic lysis -specific complement R's result in mast cell degranulation
42
What is acute phase reaction
in response to injury.. local inflammation cells secrete cytokines--> cause liver to increase/decrease production of proteins
43
a protein whose plasma conc changes from baseline by at least 25% during inflammation
Acute Phase Protein
44
C-reacitve Protein (plasma protein) cell source
made by liver and fat cells | -protein that bind to the "C" polysach of bacterial cell wall
45
Respones of C reactive protein
acute phase reactant activates complement mediates phagocytosis marker of inflammation
46
Mech of C reactive proteins
bind to phosphotidylcholine containing substantces in bacteria and damaged cells ***Ca++ dependent binding
47
Too much _____ associated to increased risk of diabetes, hypertension, and CV disease
CRP | this is a marker to know if you are at increased risk for certain disease states
48
Statins work to:
reduced CRP levels
49
Cytokines are
secreated proteins: souce = nearly all cells
50
IL-1 (IL-alpha and IL-beta) and TNF alpha are
pro-inflammatory cytokines
51
Physiological response of cytokines IL-1: TNF:
IL1 is acute phase rxn, fibroblast and lymphocyte proliferation, fever TNF: acute phase rxn, fever, and sepsis
52
Mech of cytokines
Bind to receptor to induce gene expression via activation of NFkB and AP-1
53
Activation of NFkB and AP-1 result in:
``` increased COX (fever) and lipoxygenases increase adhesion molecule expression include collagenase (fibrosis) ```
54
Two drugs to block cytokines are:
Etanercept | Infliximab
55
purine nucleoside formed from breakdown of ATP
Adenosine~ all cells
56
Physiological response to adenosine
increased extracellulary during injury... key ANTIINFLAMMATORY inhibits cytokine action
57
-increased extracellulary during injury... key ANTIINFLAMMATORY inhibits cytokine action
adenosine
58
Mech of adenosine
activation of GPCRs
59
Pharmacology of adenosine:
Adenosine A2 agonists Methotrexate~ increases adenosine release~ use to tx RA Adenosine A3 antagonists in asthma/inhibit mediator release
60
Adenosine is/is not receptor specific
Is receptor specific
61
Cell source of CAMs
endothelial cells, platelets, leukocytes
62
integrins, selectins, cadherins are examples of
CAMs
63
Physiological response to CAMS
1. Leukocyte adhesion to endothelium... necessary for repair process 2. endothelial adhesion molecules help recruit activated platelets
64
Mech of CAMs
Glycoproteins on cell surface mediate contact btwn 2 cells or btwn cells and ECM ~ act like 'contact molecules'
65
Oxygen derived free radicals are
superoxide and hydroxy radicals in nearly all cells
66
Physio response to O2 derived free rads
intracellular killing of bacteria by neutrophils
67
Mech of O2 derived free radicals
protein oxidation lipid peroxidation DNA mutations
68
Pharm of oxygen derived free radicals
Vit C and E anti-oxidants
69
three examples of lipid mediators
Prostaglandins Leukotrienes Glucocorticoids
70
Cell source of PGs
nealy all cells
71
Physio response to PGs
Vasodialation/or constiction pain fever platet aggregation via thromboxane
72
Mech of oxygen derived free radicals
protein oxidation, lipid peroxidation, DNA mutation
73
PGE2 and PGI2 directly.... | and indirectly
increase blood flow and indirectly enhance edema formation and leukocyte infiltration
74
slow reacting subastance of anaphylaxis (SRS-A) released from mast cells
Leukotrienes
75
Leukotrienes are: | released from:
slow reacting subastance of anaphylaxis (SRS-A) released from mast cells (macrophages and neutrophils)
76
What do LTC4/LTD4 do?
increase vascular permeability
77
What does the LTB4 leukotriene do?
chemoattractant for neutrophils
78
Leukotrienes are increased in:
allergies/asthma
79
physiological response to leukotrienes
increase vascular permeabilty | bronchoconstriction
80
Mech of Leukotrienes
activaes GCPRs
81
Steroids bind to:
cytoplasmic receptors--> form activated Recpetor-Steroid complex--> localize to nucleus and binds to steroid response elements in DNA: will induce or repress transcription of target genes
82
Fnx of steroids
increase anti-inflammatory genes | Decrease pro-inflammatory genes
83
Most patients do/do not respond to steroids
do
84
If indi has steroid resistanc, this is dt
cellular defect in steroid responsiveness
85
Zileuton is:
5-lipoxygenase inhibitor | --antagonist to leukotrienes
86
NSAIDs will:
inhibit COX and reduce production of inflammatory prostaoids
87
Physio response of glucocorticoids:
inhibit cytokines inhibit phospholipase A2 Inhibit COX2 inhibits CAMs
88
potentially our most effective agent for controlling chronic inflammatory disease
steroids
89
we can inhale these as a first line tx for chronic asthma
steroids
90
Leukotriene antagonists
Zafirlukast: competitive antagonist of leukotriene R Zileuton: inhibit synthesis of leukotrienes
91
Two cytokine inhibitors
Etanercept | Infliximab

Pharm: block 2 week 1 (4 decks)

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