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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
Q

main cell type in acute inflammation

A

leukocytes or PMNs

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26
Q

3 triggers of acute inflamation

A

infection by toxins
tissue necrosis, irradiation
foreign bodies

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27
Q

Propagation of disease typically occurs as result of autoimmune response, including a self-amplyfing cycle of damage

A

Chronic inflammation

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28
Q

main cell type for chronic inflammation______

main characteristic______

A

Monocytes

fibrosis

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29
Q

Atherosclerosis is a chrnoic inflammatory process of the arterial wall that is induced by a _______ toxic plasma lipid component

A

endogenous

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30
Q

Triggers of chronic inflammation include

A
  1. autoimmune disease: RA or MS
  2. unregulated immune response against microbes : IBS
  3. Immune response against common envir substanses: allergies or bronchial asthma
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31
Q

Inflammation is a defenisive host response to foreign invaders and necrotic tissue but itself is….

A

capable of causing tissue damage

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32
Q

Mediators can be effective targets to tx inflammation but because there is a multitide of them….

A

there is not one that will take care of everything

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33
Q

Pharmacology of Histamine

A

Antihistamine/H1 receptor antagonist:

diphenhydramine

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34
Q

Cell source of Bradykinin

A

endothelial cells

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35
Q

Response to bradykinin

A

The 3 Vs

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36
Q

Mechanism of action of bradykinin

A

Activated GCPR–> B2 receptor for pro-inflamation

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37
Q

Pharmacology of Bradykinin

A
  1. BK2 receptor antagonist
38
Q

What do we use a BK2 receptor antagonist for

A
  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
Q

Complement system (pls proteins) cell source

A

made by liver, circulates in blood

40
Q

Physio response to complement

A

chemotaxis
promote release of mediators from PMNs
increase vascular permeability
(if too much–tissue injury)

41
Q

Mech of Complement

A

Complexes of complement protein aggregate to cell surface mmb and cause osmotic lysis
-specific complement R’s result in mast cell degranulation

42
Q

What is acute phase reaction

A

in response to injury.. local inflammation cells secrete cytokines–> cause liver to increase/decrease production of proteins

43
Q

a protein whose plasma conc changes from baseline by at least 25% during inflammation

A

Acute Phase Protein

44
Q

C-reacitve Protein (plasma protein) cell source

A

made by liver and fat cells

-protein that bind to the “C” polysach of bacterial cell wall

45
Q

Respones of C reactive protein

A

acute phase reactant
activates complement
mediates phagocytosis
marker of inflammation

46
Q

Mech of C reactive proteins

A

bind to phosphotidylcholine containing substantces in bacteria and damaged cells
***Ca++ dependent binding

47
Q

Too much _____ associated to increased risk of diabetes, hypertension, and CV disease

A

CRP

this is a marker to know if you are at increased risk for certain disease states

48
Q

Statins work to:

A

reduced CRP levels

49
Q

Cytokines are

A

secreated proteins: souce = nearly all cells

50
Q

IL-1 (IL-alpha and IL-beta) and TNF alpha are

A

pro-inflammatory cytokines

51
Q

Physiological response of cytokines
IL-1:
TNF:

A

IL1 is acute phase rxn, fibroblast and lymphocyte proliferation, fever
TNF: acute phase rxn, fever, and sepsis

52
Q

Mech of cytokines

A

Bind to receptor to induce gene expression via activation of NFkB and AP-1

53
Q

Activation of NFkB and AP-1 result in:

A 
increased COX (fever) and lipoxygenases
increase adhesion molecule expression
include collagenase (fibrosis)
54
Q

Two drugs to block cytokines are:

A

Etanercept

Infliximab

55
Q

purine nucleoside formed from breakdown of ATP

A

Adenosine~ all cells

56
Q

Physiological response to adenosine

A

increased extracellulary during injury… key ANTIINFLAMMATORY
inhibits cytokine action

57
Q

-increased extracellulary during injury… key ANTIINFLAMMATORY
inhibits cytokine action

A

adenosine

58
Q

Mech of adenosine

A

activation of GPCRs

59
Q

Pharmacology of adenosine:

A

Adenosine A2 agonists
Methotrexate~ increases adenosine release~ use to tx RA
Adenosine A3 antagonists in asthma/inhibit mediator release

60
Q

Adenosine is/is not receptor specific

A

Is receptor specific

61
Q

Cell source of CAMs

A

endothelial cells, platelets, leukocytes

62
Q

integrins, selectins, cadherins are examples of

A

CAMs

63
Q

Physiological response to CAMS

A
  1. Leukocyte adhesion to endothelium… necessary for repair process
  2. endothelial adhesion molecules help recruit activated platelets
64
Q

Mech of CAMs

A

Glycoproteins on cell surface mediate contact btwn 2 cells or btwn cells and ECM
~ act like ‘contact molecules’

65
Q

Oxygen derived free radicals are

A

superoxide and hydroxy radicals in nearly all cells

66
Q

Physio response to O2 derived free rads

A

intracellular killing of bacteria by neutrophils

67
Q

Mech of O2 derived free radicals

A

protein oxidation
lipid peroxidation
DNA mutations

68
Q

Pharm of oxygen derived free radicals

A

Vit C and E anti-oxidants

69
Q

three examples of lipid mediators

A

Prostaglandins
Leukotrienes
Glucocorticoids

70
Q

Cell source of PGs

A

nealy all cells

71
Q

Physio response to PGs

A

Vasodialation/or constiction
pain
fever
platet aggregation via thromboxane

72
Q

Mech of oxygen derived free radicals

A

protein oxidation, lipid peroxidation, DNA mutation

73
Q

PGE2 and PGI2 directly….

and indirectly

A

increase blood flow and indirectly enhance edema formation and leukocyte infiltration

74
Q

slow reacting subastance of anaphylaxis (SRS-A) released from mast cells

A

Leukotrienes

75
Q

Leukotrienes are:

released from:

A

slow reacting subastance of anaphylaxis (SRS-A) released from mast cells (macrophages and neutrophils)

76
Q

What do LTC4/LTD4 do?

A

increase vascular permeability

77
Q

What does the LTB4 leukotriene do?

A

chemoattractant for neutrophils

78
Q

Leukotrienes are increased in:

A

allergies/asthma

79
Q

physiological response to leukotrienes

A

increase vascular permeabilty

bronchoconstriction

80
Q

Mech of Leukotrienes

A

activaes GCPRs

81
Q

Steroids bind to:

A

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
Q

Fnx of steroids

A

increase anti-inflammatory genes

Decrease pro-inflammatory genes

83
Q

Most patients do/do not respond to steroids

A

do

84
Q

If indi has steroid resistanc, this is dt

A

cellular defect in steroid responsiveness

85
Q

Zileuton is:

A

5-lipoxygenase inhibitor

–antagonist to leukotrienes

86
Q

NSAIDs will:

A

inhibit COX and reduce production of inflammatory prostaoids

87
Q

Physio response of glucocorticoids:

A

inhibit cytokines
inhibit phospholipase A2
Inhibit COX2
inhibits CAMs

88
Q

potentially our most effective agent for controlling chronic inflammatory disease

A

steroids

89
Q

we can inhale these as a first line tx for chronic asthma

A

steroids

90
Q

Leukotriene antagonists

A

Zafirlukast: competitive antagonist of leukotriene R
Zileuton: inhibit synthesis of leukotrienes

91
Q

Two cytokine inhibitors

A

Etanercept

Infliximab

Pharm: block 2 week 1 (4 decks)

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