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Block Two > SFP: Inflammation II > Flashcards

SFP: Inflammation II Flashcards

1
Q

Identify the cascades activated by Factor XII.

A

Complement, kinins, and coagulation by products

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2
Q

what are systemic mediators? give examples

A

they circulate as inactive precursors that require cleavage for activation. examples are complement, kinins, and coagulation factors

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3
Q

Describe the kinin cascade: final product and its effects

A

Produces bradykinin

Increases vascular permeability, dilates arterioles, contracts bronchial smooth muscle, and causes pain

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4
Q

Name the steps of the kinin cascade

A

-XIIa converts prekallikrein to kallikrein
-Kallikrein converts high MW kininogen to active bradykinin

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5
Q

What does the clotting cascade produce?

A

a clot

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6
Q

describe the steps of the clotting cascade

A

-XIIa activates a series of inactive to active conversions

-Thrombin is produced, which enhances leukocyte adhesion and cleaves C5

-Thrombin converts soluble fibrinogen to a fibrin clot.

-Making a fibrin clot produces fibrinopeptides that increase vascular permeability

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7
Q

Describe the fibrinolytic cascade

A

-Plasminogen is cleaved by a plasminogen activator or kallikrein to form active protease plasmin

-Plasmin cleaves the fibrin clot

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8
Q

what can plasmin activate

A

XIIa and complement cascade

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9
Q

What is the purpose of fibrin degradation products?

A

increase vascular permeability

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10
Q

what is the purpose of factor Xa in the clotting cascade

A

increases vascular permeability and leukocyte emigration

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11
Q

what is the purpose of thrombin

A

enhances leukocyte adhesion to endothelial cells and cleaves C5

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12
Q

What is the membrane attack complex?

A

It is formed from the complement cascade and punches holes in microbial membranes

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13
Q

What are some functions of components of complement cascade

A

-Forming MAC
-Opsonize for phagocytosis
-Alter vascular permeability
-Leukocyte activation, adherence, and chemotaxis

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14
Q

What cleaves C3 and C5?

A

Plasmin cleaves C3, thrombin cleaves C5

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15
Q

What do C3a and C5a do?

A

They act as anaphylatoxins. They encourage mast cell release of histamine and increase vascular permeability

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16
Q

what is a special function of C5a

A

arachidonic acid metabolism

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17
Q

What cell-derived local mediators come from preformed granules?

A

Vasoactive amines like histamine, serotonin, and lysosomal enzymes

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18
Q

What cell derived local mediators are synthesized de novo?

A

Products of membrane phospholipids (prostaglandins, leukotrienes, lipotoxins, PAF), cytokines, and free radicals (nitric oxide and substance P)

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19
Q

Describe the origin and actions of histamine

A

Comes from mast cells near vessels and basophils/platelets. It dilates arterioles, constricts large arteries, contracts venular endothelial cells to form gaps, and is the principal mediator if immediate increased permeability

20
Q

What is the principal mediator of immediate increased permeability

A

Histamine

21
Q

Describe the origin and actions of serotonin

A

Originates from delta granules in platelets, and platelet aggregation stimulates their release. They dilate arterioles, constricts large arteries, contracts venular endothelial cells to form gaps

22
Q

What are the lysosomal enzymes?

A

Inactive acid proteases and active neutral proteases

23
Q

What is the function of alpha 1 antitrypsin

A

They degrade neutral proteases and keep them from damages normal tissue adjacent to inflammation

24
Q

Describe the origin of arachidonic acid.

A

They’re derived from broken membranes at the site of tissue damage.

25
Q

What activates phospholipases that form arachidonic acid

A

Injury and/or C5a

26
Q

What pathways metabolize arachidonic acid and what do they form?

A

Cyclooxygenase: forms prostaglandins TXA2 and PGI2

Lipoxygenase: creates leukotrienes and lipoxins

27
Q

Common anti-inflammatory drugs target what parts of the arachidonic acid metabolism

A

Phospholipases or the cyclooxygenase pathway

28
Q

What are eicosanoids? What do they do?

A

Products of arachidonic acid metabolism; they lead to swelling and edema

29
Q

What are the main products formed by the cyclooxygenase pathway and lipoxygenase pathway?

A

Cyclooxygenase: thromboxane A2 and prostacyclin

Lipoxygenase: leukotrienes and lipotoxins

30
Q

Describe the formation of the two main products in the cyclooxygenase pathway and their functions

A

-Cyclooxygenase forms PGG2 followed by PGH2

-Platelets form thromboxane A2
(TXA2) from PGH2. TXA2 causes vasoconstriction and promotes platelet aggregation

-Endothelium forms prostacyclin (PGI2) from PGH2. PGI2 causes vasodilation and inhibits platelet aggregation

31
Q

What other molecules can process PGH2? What is their effect?

A

PGD2, PGE2, and PGF2a. they cause vasodilation and potentiate edema

32
Q

Describe the formation of the main products in the lipoxygenase pathway and their functions

A

-5-lipoxygenase metabolizes arachidonic acid and forms 5-HPETE

-5-HPTE converts to various leukotrienes via 5-lipoxygenase

-Neutrophils transfer LTA4 (a leukotriene) to platelets to allow them to make lipoxins

-12-lipoxygenase can form
lipotoxins from 5-HPETE

33
Q

What do leukotrienes do?

A

Cause vasoconstriction, bronchospasm, and increased permeability

34
Q

What do lipoxins do?

A

Cause vasodilation, inhibit neutrophil chemotaxis, and stimulate monocyte adhesion. Tends to stop certain parts of inflammation!

35
Q

What is the issue with cox2 inhibitors?

A

They promote clots and lead to increased coronary artery events because they inhibit prostacyclins more than thromboxane.

36
Q

Describe platelet activating factor

A

It leads to platelet aggregation, vasoconstriction and bronchiconstriction

37
Q

What classes of cytokines are associated with acute inflammation

A

Inflammatory cytokines: TNF and IL-1

Chemokines: colony stimulating chemokines

38
Q

What are the functions of TNF and IL-1

A

-They stimulate endothelial cells, neutrophils, and fibroblasts. Stimulating endothelial cells results in increased expression of adhesion factors, increased cytokine and growth factor secretion, and production of eicosacoids and NO.

-they stimulate neutrophils to aggregate and activate. They stimulate fibroblasts to secrete proteolytic enzymes and produce matrix proteins

39
Q

TNF and IL-1 lead to the production of which interleukin? what is the impact of this?

A

IL-6; this leads to systemic effects of inflammation (fever, loss of appetite, etc.)

40
Q

What are the acute phase reactions of systemic effects of acute inflammation

A

-Acute phase reactions via TNF, IL-1, and IL-6 that cause fever and increased SED rate
-Leukocytosis and increased WBC count from IL-1 and TNF causing increased release from bone marrow

41
Q

Describe the role of NO in inflammatory events in various tissues.

A

NO can kill microbes and cause vasodilation. It will reduce leukocyte recruitment and platelet aggregation, which mediates the effects of acute inflammation. It can, however, lead to complete vasodilation and shock.

42
Q

Describe the origin and actions of substance P

A

Secreted by nerve fibers in the lungs and GI tract. They initiate inflammation, transmit pain signals, regulates vessel tone, and modulates vascular permeability.

43
Q

What terminates acute inflammation

A

Removal of stimulus, the short lifetime of neutrophils, and production of anti-inflammatory mediators like lipoxins, TGF-beta, and IL-10

44
Q

C reactive protein is made in the ___ and is indicative of the ____ reaction

A

Liver; acute phase reaction

45
Q

Production of C reactive protein is induced by what 3 factors?

A

TNF, IL-1, and IL-6

Block Two (30 decks)

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