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Immunology > Inflammation #2 > Flashcards

Inflammation #2 Flashcards

1
Q

Early inflammatory mediators?

A

Histamine, Plasma Proteins, Eicosanoids

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2
Q

late inflammatory mediators?

A

Cytokines, Growth Factors

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3
Q

Three (broad) ways in which inflammation can be inhibited?

A

Blocking mediator synthesis
Block mediator receptor
Anti-mediator block antibodies

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4
Q

How can mast cells release so quickly?

A

They’re full of pre-formed histamine

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5
Q

Types of serum proteins involved in inflamm response

A

Complement proteins
Coagulation proteins
Kinins (pain)

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6
Q

Why is only low-dose aspirin useful?

A

Inhibits only thromboxane without inhibiting prostacyc.

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7
Q

Two important Arachadonic acid metabolites of inflammation

A

Prostaglandins and Leukotrienes

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8
Q

What do the AA metabolites to (in general)

A

Help maintain inflammatory state over hours-days

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9
Q

Where is AA found?

How is it released?

A

Cell membranes

Cleavage by phospholipases

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10
Q

AA is located in the ____ position in phosopholipids

A

2nd

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11
Q

Two ways that AA clevage can go down?

A
  1. Clevage by PLA2

2. Clevage by PLC, DAG lipase

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12
Q

Cells with what enzyme make prostaglandins? Which cell types?

A

Cyclo-oxygenase

Mac (PGE/F), Platelets (Thromboxane), Endothelials (Prostacyclin)

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13
Q

Cells with what enzymes make leukotrienes? Which cell types?

A

Lipoxygenase
Neutro (LTB4)
Mast Cells (LTC, D, E)

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14
Q

LTC, LTD, and LTE are also called

A

Slow Reacting Substrate of Anaphylaxis (SRSA)

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15
Q

What happens with SRSAs hit the circulation?

A

Anaphylactic Shock

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16
Q

Asprin/NSAIDs inhibit…

A

Cyclo-oxygenase

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17
Q

Prostagandins made by macros?

A

PGD and PGE/F

18
Q

Who makes LTB4? What does it do?

A

Neutrophils to recruit more neutrophils

19
Q

Why might a person use a leukotriene inhibitor? Why might this be a problem?

A

To treat asthma/allergies

Increased infection from LTB4/neutrophil block

20
Q

Inflammatory cytokines may serve as _____ or ____

A

Chemokines

GFs

21
Q

Which one is T cell growth factor?

A

IL2

22
Q

Macrophage inflammatory cytokines?

A

IL-1
TNF-a
IL-6

23
Q

Systemic effects of inflammation?

A

Fever, APP synthesis, Inc. in WBCs

24
Q

Two listed types of Acute Phase Proteins?

A

C-reactive

Mannose-binding lectin

25
Q

What does C-reactive protein do?

A

Binds to cell surfaces and results in increased complement binding

26
Q

What does mannose-bindin lectin do?

A

Activates alternate completment pathway

27
Q

Chemokines share two ________ ________.

A

Conserved Cysteines

CC or CXC chemokines

28
Q

Who is the protoptype CXC Chemokine? What does it do?

A

IL-8
From Mac, Endo
Usef in neutrophil chemotaxis

29
Q

What do RANTES and MIP-1 cause?

A

Eosinophil chemotaxis

30
Q

What does MCP-1 do?

A

Monocyte chemotaxis

Mast cell release

31
Q

Well known inflammatory growth factors.

A

Colony Stimulating Factors
FGF
VEGF

32
Q

Adhesion molecules are activated in inflammation by

A

LTB4, C5A, HIS – P-sel
IL1, TNF – E Sel
IL-8 – Neu

33
Q

Signalling pathway used by Toll-Like Receptors?

A

NFkB signaling

34
Q

Systemic activation of inflammation can occur in a

A

cytokine storm

35
Q

What is Septic Shock

A

Systemic inflammatory rxn from bacteremia with an organism expressing LPS or LOS

36
Q

What is Systemic Inflammatory Response Syndrome?

A

Overproduction of Inflamm. cytokines and mediators

37
Q

Important role of IL-4

A

IgE, Mast Cell, and EOSINOPHIL activation

38
Q

Important role of IL-5

A

IgA and promoter or EOSINOPHILS

39
Q

What does IFN-g do?

A 
Activate Macro
Induce MHC I/II
Granuloma Fomration
Enhances Adherance
Inhib TH2
40
Q

What causes granulomas?

A

Specific immune response to persistent infection of macrophages. CD4 mediated

41
Q

Defining cell of a granuloma?

A

Epithelioid Cell – Flattened plump macrophages

Immunology (10 decks)

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