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Pathology -- Gen Path > Chemical Mediators of Inflammation > Flashcards

Chemical Mediators of Inflammation Flashcards

1
Q

Examples of pre-formed mediators

A

Histamine, Serotonin, and some lysosomal enzymes.

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2
Q

Important categories of plasma proteins in inflammation?

A

Coagulation proteins – Hageman factor, plasmin
Fibrinopeptides (Fibrin Degredation products)
Complement Proteins (C3a, C5a, C3b)
Kinins
Immunoglobulins

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3
Q

Activation of ________ plays a key role in activating most of the other plasma proteins

A

Hageman Factor

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4
Q

Newly synthesized products in inflammation are usually made by….

A

Endothelial Cells
Monocytes
Fibroblasts

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5
Q

Clotting/Fibrinolytic System. Pre-formed and Newly synthesized messenger?

A

Pre – Histamne

New – Prostaglandins

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6
Q

Complement System. Pre-formed and Newly synthesized messenger?

A

Pre – Serotonin

New – Leukotrienes

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7
Q

Kinin System. Pre-formed and Newly synthesized messenger?

A

Pre – Lysosomal Enzymes

New – PAF, Cytokines

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8
Q

Where dos fast release histamine come from

A

lysis of mast cells, basophils

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9
Q

where does serotonin, thromboxane come from

A

Activation of platelets

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10
Q

How does rapid release Il-1 happen?

A

Activation of local sentry macrophages

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11
Q

WHy would a mast cell release its histamine?

A 
Trauma/Cold
Immunologic Rxn (IgE)
C3a, C5a
Histamine-releasing factors from neutrophils, monocytes, and platelets
Il-1, activation of Toll receptors
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12
Q

Over 90% of serotonin is found…

A

in enterochromaffin cells in the GI tract

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13
Q

What does Histamine/Serotonin do anyway? Unique activities of them individually?

A 
Vasodilation, increased permeability
Stim. of pain/itching
Contraction of smooth muscle
His -- Axonal reflex of flare response
Sero -- Aggregation of platelets
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14
Q

Preformed plasma protein pathways all turned on by activated Hageman Factor?

A

Fibrin Degradation Products
Anaphylaxis (via complement)
Kinin generation
Clot Formation

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15
Q

Important roles of Plasmin

A
  1. Cleaves fibrin into fibrin degradation products
  2. Cleaves complement components C5 and C3
  3. Activates Hageman, kininogens, and itself (amplifys the response)
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16
Q

The Kallikrein/Kinin system is important for…

A

Vascular permeability, contraction of SM, dilation of BV

PAIN

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17
Q

Important details on C5a

A

Chemotactic for PMNs
Neutrophil degranulation
Superoxide production

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18
Q

Early inflammation release of arachadonic acid leads to formation of…

A

Prostaglandins and Leukotrienes

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19
Q

Arachadonic Acid exposed to Cyclooxygenase (COX) will form…

A

Prostaglandins, Prostacyclins, or Thromboxane

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20
Q

Arachadonic Acid exposed to lipoxygenase will form…

A

Leukotrienes

SRS-A

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21
Q

Arachadonic Acid derivative formed in platelets

A

TXA2

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22
Q

Arachadonic Acid derivative formed in endothelial cells

A

PGI2, LTB4

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23
Q

Arachadonic Acid derivative formed in Mast Cells

A

SRS-A’s/LTC/LTE

PAF

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24
Q

Arachadonic Acid derivative formed in neutrophils

25
Q

Arachadonic Acid derivative formed in Macrophages

26
Q

Effects of PGD2 and PGE2

A

Produce vasodilation, increased vascuar permeability-, bronchoconstriction, hyperalgesia

27
Q

Effects of PGF2a

A

Vasodilation, Bronchoconstriction

28
Q

Effects of Prostacyclin (PGI2)

A

Vasodilation, Increased vascular permeability, inhibited PMNs, Inhibits platelet aggregation

29
Q

Effects of Thromboxane A2

A

Vasoconstriction, Bronchoconstriction, Platelet Aggregation

Antagonizes Prostacyclin

30
Q

What are the Slow Reacting Substances of Anaphylaxis (list the members)

A

LTC4, LTD4, LTE4

31
Q

What are the Slow Reacting Substances of Anaphylaxis (conceptually)

A

Mediators of responses to severe allergy: constriction of smooth muscle (vaso+broncho) and increased vascular permeability (vascular shock)

32
Q

Effects of LTB4

A

Primarily from PMNs, mediated their responses

Chemotaxis + Aggregation/Degranulation

33
Q

Effects of Platelet Activating Factor

A

Induces platelet aggregation and degranulation
Enhances the release of histamine and serotonin
Increased vascular permeability
Increases leukocyte adhesion, chemotaxis

34
Q

Effects of Lipoxins

A

Anti-inflammatory, Blockage of SRS-A receptor, promotes phagocytosis and cellular killing

35
Q

Early mediators of platelet aggregation…

A

PAF, Thromboxane A2 from mast cells + platelets

36
Q

Early mediators of vascular permeability…

A

SRS-As from mast cells, platelets

37
Q

Middle mediators of Chemotaxis…

A

LT B4, SRS-A, PAF from Mast Cells and PMNs

38
Q

Middle mediators of vascular permeability

A

SRS-A, LTB4 from PMNs

39
Q

Late mediators of vasodilation, vascular permeability…

A

SRS-A from PMNs, PGs from Macrophages

40
Q

What are interleukins?

A

Cytokines that communicate between different types of leukocytes, particularly mono and lymphs

41
Q

What is IL-2

A

T cell growth factor

Receptor induced by Il-1 from macrophages, Il2 production

42
Q

Which interleukins have systemic effects?

A

IL1, TNFa, IL6

43
Q

Primarily PMN chemokine?

44
Q

Role of IFNg in inflammation?

A

from T and NK, induces expression of MHC I and II, activates phagocytes, inhibits TH2, enhances leukocyte-endothelial adherence.

45
Q

M-CSF is made by ____. Its role is….

A

Macrophages

promote monocyte precursor growth

46
Q

G-CSF is made by ____. Its role is…

A

Mphages. Promote granulocyte prolif.

47
Q

GM-CSF is made by ______. Its role is…

A

T cells, Mphages, Fibroblasts, endothelial cells

Promotes granulocyte precursors

48
Q

TGFbeta is a potent stimulator of….

A

Fibrinogenesis and Scar Tissue

49
Q

IL1, TNF, IL6. Where do they come from? What do they do?

A

From – Mphages + inflam cells

Do – Fever, Acute Phase Proteins, Septic Shock

50
Q

Il2, Il12. Where do they come from? What do they do?

A

From - Lymphocytes

Do – Promote lymphocyte proliferation

51
Q

IFNg. Where do they come from? What do they do?

A

From – Lymphocytes
Do – MHC/Adhesion Molecule Expression
Activation of mp in granuloma formation

52
Q

IL8. Where do they come from? What do they do?

A

From – Activated inflamm. cells

Do – Neutrophil adhesion and migration

53
Q

MCP-1. Where do they come from? What do they do?

A

From – Activated Inflamm. cells

Do – Monocyte migration

54
Q

RANTES, MCP-3. Where do they come from? What do they do?

A

From – Inflamm. Cells

Do – Macrophages + Mast Cells for eosinophil migration

55
Q

GM-CSF. Where do they come from? What do they do?

A

From – Inflam. cell prolif and differentiation

Do – Expression of adhesion molecules, Cytokines

56
Q

Still even a little shakey on all of this?

A

Look at the summary on the last page

57
Q

IL receptors assocaited w/ Jak/Stat

A

2, 4, 7, 9, 15

58
Q

Type of mediator seen in minutes? minutes->hours? hours->days? Days->weeks?

A

Minutes – Preformed
Minutes/Hours – Plasma-Derived
Hours/Days – AA Metabolites
Days/Weeks – Cytokines, ILs, Chemokines, GFs

59
Q

Difference between Aspirin and NSAIDS

A

Aspirin – Irreversible Cox inhibition

Pathology -- Gen Path (17 decks)

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