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Foundations 2 > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Cyclooxygenase produces

A

PGI2, TxA2, PGD2, PGE2 (pain and fever)

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2
Q

What does PGI2 do? Where is it mostly made?

A

potent vasoconstrictor and inhibits platelet aggregation, and potentiates membrane permeability and chemotactic; endothelial cells

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3
Q

What does TxA2 (Thromoboxane) do? Where is mostly expressed?

A

potent platelet aggregator and vasoconstrictor, bronchoconstriction; platelets

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4
Q

What does PGD2 do?

A

major PG of mast cell, bronchoconstriction, vasodilation, increase vascular permeability and recuritment of eosinophils

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5
Q

What does PGF2alpha do?

A

uterine smooth muscle contraction, bronchoconstriction, intiates parturition (labor)

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6
Q

What does PGE2 do?

A

Vasodilation, increase vaso permeability, pain and fever

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7
Q

What cells synthesize PG? what are they involved in?

A

mast cell, macrophage, enothelial cells; systemic inflammation

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8
Q

What is LTB4 for?

A

PMN chemotaxis and activation of PMN: so aggregation and adhesion, ad also generate reactive oxygen species

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9
Q

What us LTC4, LTD4, AND LTE4 for?

A

induce bronchoconstriction and vasoconstriction, increase vascular permeability in venules–more potent than histamine.

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10
Q

What is 5-HETE for and what produces it?

A

Chemotactic factor for PMNs and produced in PMNs

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11
Q

What is lipoxin production an example of?

A

As leukocytes and platelets need to make it together: trancellular biosythesis

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12
Q

What does lipoxin do?

A

inhibits leukocytes recruitment, neutrphil chemotaxisand adhesion to cell wall

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13
Q

What is endogenous negative regulators of Leukotriene?

A

Lipoxins

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14
Q

What inhibits PG synthesis?

A

Aspirin and NSAIDs

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15
Q

What do lipoxygenase inhibitors do?

A

diminish LT production–treats Asthma

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16
Q

What does corticosteroids do?

A

reduce transcription of COX-2, PLA2, and proinflam cytokines such as IL-1 and TNF

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17
Q

What favors the production of anti-inflammatory lipid mediators? (resolvins and protectins)

A

fish oil

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18
Q

Where is PAF derived from?

A

PM of neutrophils, monocytes, activated endothelial cells and basophils, and platelets

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19
Q

Where does PAF bind?

A

Bind to G-protein coupled receptor (PAFR) which is always expressed in endothelial cells, platelets, and leukocytes

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20
Q

What does PAF do?

A

Enchance platelet aggregation and degranulation, activates leukocytes–promoting adherence as well as ROS, lipid mediators and TNF-a and IL-6, motility, chemotaxis, invasion; also endothelial cells increase vasocular permeability and vasodilation–and stimulates production of eicosanoids and cytokines from platelets and other cells.

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21
Q

What do lipid mediators do? where are they stored?

A

Only potentiate the inflam response and they are not stored and only released in response to bradykinin and cytokines–which stimulate PKA2

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22
Q

What produces NO?

A

Endothelial cells, macrophages and some neurons

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23
Q

How is NO produced?

A

L-arginine, oxygen, NADPH by Nitric Oxide synthase

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24
Q

Types of NO

A

Neuronal, Inducible and endothliel

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25
Q

Neuronal NO (nNOS):

A

made in neurons, no role in inflam

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26
Q

Inducible NO(iNOS)

A

made by macrophage, PMN, endothelial cells when stimulated with IL-1, TNF and Interfeuron Gamma and bacterial endotoxin

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27
Q

Role of NO in phagocytic cells during inflam

A

Kill microbes through Free radical form

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28
Q

Endothelial NOS

A

made primarily in endothelial

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29
Q

Functions of NO

A

1) relaxes smooth muscles: dilation through cGMP
2) inhibits inflammation by reducing platelet agg. and inhibiting mast cell -induced inflam and leukocyte recruitment
3) antomicrobial: kills microbes through free radical in macro and neut.

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30
Q

What does histamine do?

A

increase vasopermiability, vasodilation, bronchoconstriction, eosinophils chemotaxis

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31
Q

What induces histamine production?

A

Leukocytes: Il-1 and Il-8
Physical: trauma, cold and heat
Allergy: IgE binding
Complement: anaphylatoxins (C3a and C5a)

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32
Q

Cell source of histamine?

A

Mostly mast cells, basophils and platelets

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33
Q

Plasma derived inflamm mediators

A

Synth in liver, end product of serine proteases, zymogen are activated in step wise manner, circulating in matrix of tissues

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34
Q

What do complement products do?

A

increase vasopermeability, chemotaxis, opsonization

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35
Q

How is classical complement pathway triggered?

A

fixing C1 to IgG or IgM bound to antigen

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36
Q

How is lectin complement pathway triggered?

A

plasma mannose binding protein binds to carbs on microbes and activates another complement molecule

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37
Q

How is alternate complement pathway triggered?

A

microbial surface molecules such as LPS, endotoxin in the absence of antibody

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38
Q

For which cell is C5a a chemotactic agent for?

A

monocytes, eosinophils, basophils, neutrophils

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39
Q

What pathway can C5a activate?

A

Lipoxygenase pathway in AA metabolism in neut and monocytes–release more mediators, and thrombins effect on endothelial cells

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40
Q

What do C5a and C3a do?

A

They are anaphylatoxins–stimulate mast cell to release histamine–increase vaso permeability and vasodilation

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41
Q

How does C3b work?

A

Coats microbes and Neut. and macro have CR1 which binds with C3b and phagocytoze the microbe

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42
Q

What does C5b do?

A

Make membrane attack complex with C6-9 on microbes, make the membrane permeable to water and ions–cell death and lysis

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43
Q

What are kinins?

A

Vasoactive peptides from plasma kininogen when cleaved by kallikrens

44
Q

What does bradykinin do?

A

Increase vasopermeability, vasodilation, smooth muscle contraction (bronchi and uterus) and mediates pain

45
Q

Which receptor does bradykinin bind to?

A

B1 and b2 G-coupled receptors in various cells

46
Q

How is B1 receptor expression induced?

A

binding of cytokines: IL-1, TNF-a, IFN gamma

47
Q

What does bradykinin binding with B1 and B2 receptor do?

A

endothelial cells activated and produce nO and prostaglandin synthesis which increases vasopermeability, vasodilation and constriction of non vascular smooth muscles in uterus and bronchi

48
Q

What are the side effects if ACEi is taken for hypertension?

A

As bradykinin is not broken down, Edema due to vasopermeability and vasodilation, and persistant cough due to bronchoconstriction

49
Q

What releases plasminogen activator?

A

endothelial cells, leukocytes, and other cells

50
Q

What can plasmin do?

A

Primarily cleave fibrin, cleave C3 and generate fibrin split product that results from cleavage if fibrin–increase vascular permeability, activate XII to XIIa

51
Q

What can presence of thrombin do to endothelial cells?

A

promote inflammation by inducing exp. of CAMs, cytokines, chemokines, prostaglandins, NO and platelet activating factor–these recruit leukocytes and support other events in inflam.

52
Q

How does C-reactive protein affect macrophages?

A

activates synthesis of cytokines, and binds to Fc and acts as an opsonin.

53
Q

How does C-reactive protein activate complement pathway?

A

Through classical and alternative pathway

54
Q

How does C-reactive protein recognize altered self and foregin materials?

A

binding to cell walls of bacteria and fungi, damaged or dead cell

55
Q

What can C-reactive protein level indicate? where is it produced?

A

non-specific marker of inflam; liver

56
Q

Where is Serum amyloid A produced and what is it associated with?

A

Liver and with high density lipoprotein

57
Q

How does SAA activate cells?

A

toll-like receptor binding

58
Q

How does SAA effect neutrophils and mast cell?

A

Chemotactic agent

59
Q

Which disease is SAA involved in?

A

Amyloid A-type amyloidosis and chronic inflam

60
Q

What does mannose-binding lecti (MBL) do?

A

binds to mannose on bacteria and acts as an opsonin and activate complement via lectin binding pathway; crucial in resolution of infection

61
Q

What does a-2-macroglobulin do?

A

inhibits proteases involved in coagulation and fibrinolysis

62
Q

What are some protein that reduces Fe for bacteria?

A

Haptoglobin (binds Hb), ferritin (binds Fe), Hepcidin ( prevents Fe release from ferritin in macro and intestine) and Ceruloplasmin (oxidizes iron); some of them associated with anemia

63
Q

What do a-1 anti-trypsin and a1chymotrypsin do?

A

downregulate inflammation

64
Q

What does erythrocyte sedimentation rate show?

A

nonspecific test that measures presence of inflamm and acute phase response, tendency of blood to settle when there is more plasma fibrin, Ig. RBC have Rouleaux form, when value over 20mm/hr–inflammation

65
Q

What are coagulation proteins involved in acute phase response?

A

prothrombin, vWF, fibrinigen, FVIII, plasminogen

66
Q

Three phases of fever?

A

Initial: shivering, chills, rigors
Plateau phase: core body temp = set point
Defervecence: when body temp> set point
patient feels warm–> sweating

67
Q

Positive aspect of fever?

A

enhance immune response and increase cell death to prevent viral replication

68
Q

Negative aspect of fever?

A

Decrease cardiac output, decrease blood flow to brain (seizure and damage CNS), acidosis (increase repiratpru rate and o2 consumption and increase metabolic rate.

69
Q

Which PG leads to sleepiness?

A

PGD2

70
Q

What does Il-1 and TNF-a do in fever?

A

malaise and decrease appetite and sleepiness

71
Q

When does neutrophils increase in peripheral tissues?

A

bacterial infection

72
Q

When does Lymphocyte increase in peripheral tissues?

A

viral infection

73
Q

When does esoinophils increase in peripheral tissues?

A

parasite infection, asthma, hay fever, autoimmune process

74
Q

When does leukopenia happen?

A

Viral infection, rickettsia, protozoa, TB and cancer

75
Q

Normal range of WBC? Neutrophils make up what percentage of WBC? Bands are precursur to what cells?

A

5,000-10,000, 57-63%, neutrophils–refer to bandemia when there are a lot of it

76
Q

bacterial infections primarily in skin and mucosal surfaces, omphalitis and delayed separation of umbilical chord; absence of pus formation at site of infection, gingaivits and periodontits, leukocytosis and neutrophils predominate

A

Leukocyte Adhesion deficiency I

77
Q

Mode of transmission of LADI and what it is defective in?

A

Aut recessive, integrins of Leukocyte

78
Q

Lab for LAD1

A

Neutrophils, but lack CD18 ells and mut analysis

79
Q

Treatment of LAD1

A

antibiotics and BMT (severe LAD1)

80
Q

What is defective in LADII?

A

specific golgi GDP-fucose transporter that leads to absence in fucosyl moieties and absence of selectin ligan on leukocyte surface–defective rolling

81
Q

What is defective in LADIII?

A

Integrin activation

82
Q

What mut leads to Chronic granulomatous disease

A

NADPH Oxidase–so lack of respiratory bursts as no ROS

83
Q

How is CGD diagnosed?

A

Neutrophils function test

84
Q

CGD common sites of infection?

A

skin, lung, lymph nodes, and liver and patients have normal response to viral infection

85
Q

Which bacterial infection is common in CGD

A

catalse producing staphylococcus aureus and aspergillus (with minimal fever and lower leukocytosis)

86
Q

How to diagnose CGD effectively?

A

Tissue biopsy: look for granulomata in CGD

Oxidative bursts test: Nitroblue tetrazolium test (NBT)

87
Q

Treatment of CGD?

A

antibiotics and antifungal prophylaxis, INF-gamma or bone marrow transplant

88
Q

Sx: 70% x-linked, fungal and bacterial infection, granuloma formation, defects in phagocytes NADPH oxidase?

A

CGD

89
Q

Fluid encountered in pleural or pericardial effusions, erythematous vesicles and autoimmune or viral in etiology, yellowish, no mononuclear cell and little protein

A

Serous inflam–transudate

90
Q

Where does serous fluid accumulate?

A

Between epidemris and dermis

91
Q

Irrefular surface with fibrinous inflammation in heart or abdominal lining; meshwork of fibers

A

fibrinous inflammation

92
Q

Days of infiltration of leukocytes:

A

Hours: edema, 1 day: neutrophils and Day 2: monocytes and macrophages

93
Q

Where can you see suppurative inflammation:

A

acute bronchopneumonia (exudate) amd typically bacterial and has neutrophils (streptoccoci pyogenes, pneumoniae, e coli and meningitidis, and gonorrhoeae).

94
Q

Cellulitis: acute inflammation of skin

A

bacterial: staphylococcus and streptococcus, secondary to trauma or surgery, travels along between dermis and subcut

95
Q

Sx: fever, headache, nausea, vomiting, neck stiff, photophobia, and confusion

A

Purulent leptomeningitis

96
Q

Charactertistics lab finding of Purulent leptomeningitis

A

increase in pressure, increase in proyein WBC, and decrease glucose vs serum, (and bacteria and PMNs)

97
Q

Pulmonary abscess?

A

walled off with fibrin wall, etiology is bacterial (staph and strep) and some fungi

98
Q

Location of pseudomembranous inflammation? Exudate involved?

A

colon and pharynx, yes, mushroom shaped , yellowish-gray, plaque like

99
Q

Where is ulcer common and what happens?

A

skin, GI and urinary bladder, and eroding epithelial cells due to trauma, toxins and ischemia

100
Q

Common etiologies of chronic inflammation?

A

persistent inflammation, hypersenstive immune response, exogenous (silica) and endogenous (cholestrol) toxic agents

101
Q

Features of chronic inflam?

A

collection of chronic inflam cells (lympp ad macro) and parenchymal destruction –organ function loss
Viral infection–almost always involve chronic inflam

102
Q

Types of chronic inflam?

A

Inflitritive; thyroid and prostate

Granulomatous

103
Q

Noncaseating Granulomatous etiology

A

Foregin body, fungus, parasite and immune and most common

104
Q

caseating Granulomatous etiology

A

TB and Bartonella henselae, seen in chest on radiographs

105
Q

necrotizing Granulomatous etiology

A

fungus and immune

106
Q

Granulomatous image looks like

A

multinucleated cells and peripheral nuclei

107
Q

example of non caseating granulomas

A

sarcoidosis, autoimmune disorders

Foundations 2 (15 decks)

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