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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
Neuronal NO (nNOS):
made in neurons, no role in inflam
26
Inducible NO(iNOS)
made by macrophage, PMN, endothelial cells when stimulated with IL-1, TNF and Interfeuron Gamma and bacterial endotoxin
27
Role of NO in phagocytic cells during inflam
Kill microbes through Free radical form
28
Endothelial NOS
made primarily in endothelial
29
Functions of NO
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.
30
What does histamine do?
increase vasopermiability, vasodilation, bronchoconstriction, eosinophils chemotaxis
31
What induces histamine production?
Leukocytes: Il-1 and Il-8 Physical: trauma, cold and heat Allergy: IgE binding Complement: anaphylatoxins (C3a and C5a)
32
Cell source of histamine?
Mostly mast cells, basophils and platelets
33
Plasma derived inflamm mediators
Synth in liver, end product of serine proteases, zymogen are activated in step wise manner, circulating in matrix of tissues
34
What do complement products do?
increase vasopermeability, chemotaxis, opsonization
35
How is classical complement pathway triggered?
fixing C1 to IgG or IgM bound to antigen
36
How is lectin complement pathway triggered?
plasma mannose binding protein binds to carbs on microbes and activates another complement molecule
37
How is alternate complement pathway triggered?
microbial surface molecules such as LPS, endotoxin in the absence of antibody
38
For which cell is C5a a chemotactic agent for?
monocytes, eosinophils, basophils, neutrophils
39
What pathway can C5a activate?
Lipoxygenase pathway in AA metabolism in neut and monocytes--release more mediators, and thrombins effect on endothelial cells
40
What do C5a and C3a do?
They are anaphylatoxins--stimulate mast cell to release histamine--increase vaso permeability and vasodilation
41
How does C3b work?
Coats microbes and Neut. and macro have CR1 which binds with C3b and phagocytoze the microbe
42
What does C5b do?
Make membrane attack complex with C6-9 on microbes, make the membrane permeable to water and ions--cell death and lysis
43
What are kinins?
Vasoactive peptides from plasma kininogen when cleaved by kallikrens
44
What does bradykinin do?
Increase vasopermeability, vasodilation, smooth muscle contraction (bronchi and uterus) and mediates pain
45
Which receptor does bradykinin bind to?
B1 and b2 G-coupled receptors in various cells
46
How is B1 receptor expression induced?
binding of cytokines: IL-1, TNF-a, IFN gamma
47
What does bradykinin binding with B1 and B2 receptor do?
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
What are the side effects if ACEi is taken for hypertension?
As bradykinin is not broken down, Edema due to vasopermeability and vasodilation, and persistant cough due to bronchoconstriction
49
What releases plasminogen activator?
endothelial cells, leukocytes, and other cells
50
What can plasmin do?
Primarily cleave fibrin, cleave C3 and generate fibrin split product that results from cleavage if fibrin--increase vascular permeability, activate XII to XIIa
51
What can presence of thrombin do to endothelial cells?
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
How does C-reactive protein affect macrophages?
activates synthesis of cytokines, and binds to Fc and acts as an opsonin.
53
How does C-reactive protein activate complement pathway?
Through classical and alternative pathway
54
How does C-reactive protein recognize altered self and foregin materials?
binding to cell walls of bacteria and fungi, damaged or dead cell
55
What can C-reactive protein level indicate? where is it produced?
non-specific marker of inflam; liver
56
Where is Serum amyloid A produced and what is it associated with?
Liver and with high density lipoprotein
57
How does SAA activate cells?
toll-like receptor binding
58
How does SAA effect neutrophils and mast cell?
Chemotactic agent
59
Which disease is SAA involved in?
Amyloid A-type amyloidosis and chronic inflam
60
What does mannose-binding lecti (MBL) do?
binds to mannose on bacteria and acts as an opsonin and activate complement via lectin binding pathway; crucial in resolution of infection
61
What does a-2-macroglobulin do?
inhibits proteases involved in coagulation and fibrinolysis
62
What are some protein that reduces Fe for bacteria?
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
What do a-1 anti-trypsin and a1chymotrypsin do?
downregulate inflammation
64
What does erythrocyte sedimentation rate show?
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
What are coagulation proteins involved in acute phase response?
prothrombin, vWF, fibrinigen, FVIII, plasminogen
66
Three phases of fever?
Initial: shivering, chills, rigors Plateau phase: core body temp = set point Defervecence: when body temp> set point patient feels warm--> sweating
67
Positive aspect of fever?
enhance immune response and increase cell death to prevent viral replication
68
Negative aspect of fever?
Decrease cardiac output, decrease blood flow to brain (seizure and damage CNS), acidosis (increase repiratpru rate and o2 consumption and increase metabolic rate.
69
Which PG leads to sleepiness?
PGD2
70
What does Il-1 and TNF-a do in fever?
malaise and decrease appetite and sleepiness
71
When does neutrophils increase in peripheral tissues?
bacterial infection
72
When does Lymphocyte increase in peripheral tissues?
viral infection
73
When does esoinophils increase in peripheral tissues?
parasite infection, asthma, hay fever, autoimmune process
74
When does leukopenia happen?
Viral infection, rickettsia, protozoa, TB and cancer
75
Normal range of WBC? Neutrophils make up what percentage of WBC? Bands are precursur to what cells?
5,000-10,000, 57-63%, neutrophils--refer to bandemia when there are a lot of it
76
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
Leukocyte Adhesion deficiency I
77
Mode of transmission of LADI and what it is defective in?
Aut recessive, integrins of Leukocyte
78
Lab for LAD1
Neutrophils, but lack CD18 ells and mut analysis
79
Treatment of LAD1
antibiotics and BMT (severe LAD1)
80
What is defective in LADII?
specific golgi GDP-fucose transporter that leads to absence in fucosyl moieties and absence of selectin ligan on leukocyte surface--defective rolling
81
What is defective in LADIII?
Integrin activation
82
What mut leads to Chronic granulomatous disease
NADPH Oxidase--so lack of respiratory bursts as no ROS
83
How is CGD diagnosed?
Neutrophils function test
84
CGD common sites of infection?
skin, lung, lymph nodes, and liver and patients have normal response to viral infection
85
Which bacterial infection is common in CGD
catalse producing staphylococcus aureus and aspergillus (with minimal fever and lower leukocytosis)
86
How to diagnose CGD effectively?
Tissue biopsy: look for granulomata in CGD | Oxidative bursts test: Nitroblue tetrazolium test (NBT)
87
Treatment of CGD?
antibiotics and antifungal prophylaxis, INF-gamma or bone marrow transplant
88
Sx: 70% x-linked, fungal and bacterial infection, granuloma formation, defects in phagocytes NADPH oxidase?
CGD
89
Fluid encountered in pleural or pericardial effusions, erythematous vesicles and autoimmune or viral in etiology, yellowish, no mononuclear cell and little protein
Serous inflam--transudate
90
Where does serous fluid accumulate?
Between epidemris and dermis
91
Irrefular surface with fibrinous inflammation in heart or abdominal lining; meshwork of fibers
fibrinous inflammation
92
Days of infiltration of leukocytes:
Hours: edema, 1 day: neutrophils and Day 2: monocytes and macrophages
93
Where can you see suppurative inflammation:
acute bronchopneumonia (exudate) amd typically bacterial and has neutrophils (streptoccoci pyogenes, pneumoniae, e coli and meningitidis, and gonorrhoeae).
94
Cellulitis: acute inflammation of skin
bacterial: staphylococcus and streptococcus, secondary to trauma or surgery, travels along between dermis and subcut
95
Sx: fever, headache, nausea, vomiting, neck stiff, photophobia, and confusion
Purulent leptomeningitis
96
Charactertistics lab finding of Purulent leptomeningitis
increase in pressure, increase in proyein WBC, and decrease glucose vs serum, (and bacteria and PMNs)
97
Pulmonary abscess?
walled off with fibrin wall, etiology is bacterial (staph and strep) and some fungi
98
Location of pseudomembranous inflammation? Exudate involved?
colon and pharynx, yes, mushroom shaped , yellowish-gray, plaque like
99
Where is ulcer common and what happens?
skin, GI and urinary bladder, and eroding epithelial cells due to trauma, toxins and ischemia
100
Common etiologies of chronic inflammation?
persistent inflammation, hypersenstive immune response, exogenous (silica) and endogenous (cholestrol) toxic agents
101
Features of chronic inflam?
collection of chronic inflam cells (lympp ad macro) and parenchymal destruction --organ function loss Viral infection--almost always involve chronic inflam
102
Types of chronic inflam?
Inflitritive; thyroid and prostate | Granulomatous
103
Noncaseating Granulomatous etiology
Foregin body, fungus, parasite and immune and most common
104
caseating Granulomatous etiology
TB and Bartonella henselae, seen in chest on radiographs
105
necrotizing Granulomatous etiology
fungus and immune
106
Granulomatous image looks like
multinucleated cells and peripheral nuclei
107
example of non caseating granulomas
sarcoidosis, autoimmune disorders

Foundations 2 (15 decks)

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