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General Pathology > Exam #1: Acute Inflammation II > Flashcards

Exam #1: Acute Inflammation II Flashcards

1
Q

Generally, how are organisms phagocytosed?

A

1) Recognition of the offending agent & activation of leukocytes
2) Engulfment

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2
Q

What are the mediators of recognition and attachment.

A
  • Mannose receptors= recognize mannose and fucose on microbial cell walls
  • Scavenger receptors
  • Opsonins= IgG & C3b
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3
Q

Describe the process of engulfment.

A

After a microbe has bound to a phagocyte receptor:

1) Pseudopods, or extensions of the cytoplasm, surround the object forming a phagosome
2) Phagosome that fuses with the lysosome, creating a phagolysosome

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4
Q

What are the two systems for killing organisms?

A

Once the phagolysosome has formed, killing is mediated by two pathways:

1) Oxygen-dependent
2) Oxygen-independent

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5
Q

What is the oxygen-dependent/ aerobic process for killing organisms?

A

Respiratory burst

1) Oxygen–>superoxide via NADPH oxidase
2) Superoxide–>Hydrogen peroxide via superoxide dismutase
3) Myelo-peroxidase from neutrophilic granules catalyzing reaction between Cl- & Hydrogen peroxide, forming hypochlorus acid

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6
Q

What reaction is carried out by NADPH oxidase?

A

Oxygen–>Superoxide

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7
Q

What reaction is carried out by Superoxide Dismutase?

A

Superoxide–>Hydrogen peroxide

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8
Q

What is myelo-peroxidase from? What reaction does it catalyze?

A

Neutrophils
CL- & H2O2–>HOCl

(Hypochlorous acid i.e. bleach)

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9
Q

Describe the oxygen-independent mechanism for killing organisms.

A

The oxygen-independent mechanisms of killing include leukocyte granule proteins and enzymes

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10
Q

What is leukocyte activation?

A

Initiating secretion or production of cell surface proteins by leukocytes

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11
Q

What are the functional responses induced on leukocytes upon activation?

A

1) Production of arachidonic acid (AA) metabolites
2) Degranulation & secretion of lysosomal enzymes & activation of oxidative burst
3) Secretion of cytokines
4) Modulation of adhesion molecules

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12
Q

List the general characteristics of inflammatory mediators.

A
  • Originate from plasma proteins or cells
  • Bind to specific receptors on target cells
  • Can stimulate the release of other mediators from target cells
  • Most are short lived
  • Most have the potential to cause harmful effects
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13
Q

What are the vasoactive amines?

A

Histamine

Serotonin

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14
Q

What is the function of the vasoactive amines?

A
  • ARTERIOLAR dilation (vasodilation)

- Increased permeability of POSTCAPILLARY VENULES

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15
Q

Where do the vasoactive amines come from?

A

Stored in preformed granules of mast cells, basophils, and platelets

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16
Q

What causes the release of vasoactive amines from mast cells?

A
  • Trauma
  • Platelet aggregation
  • C3a, C4a, C5a
  • Neuropeptides
  • Cytokines
  • Histamine releasing proteins
  • IgE binding to mast cells
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17
Q

Review the three pathways of complement activation.

A

1) Classic= binding of antigen- antibody complex to C1
2) Alternate= C3 directly activated by bacterial endotoxins, complex polysaccharides, & aggregated globulins
3) Lectin= C1 activation by mannose

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18
Q

What is the center of complement activation?

A

C3

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19
Q

What is the function of C3a, C4a, and C5a in imflammation?

A

Stimulate histamine release from mast cells leading to increased vascular permeability & vasodilation

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20
Q

What is the function of C5a?

A
  • Chemotaxis of monocytes & granulocytes
  • Increases surface expression of leukocyte CAM
  • Activates LOX pathway in neutrophils & monocytes
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21
Q

What is the function of C3b?

A

Opsonization

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22
Q

What is the function of C5-9?

A

Membrane attack complex (MAC) that inserts into the lipid bilayer forming macropores tha ticnrease the cell permeability & leads to lysis

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23
Q

What is Hageman Factor?

A

Factor XII of the intrinsic clotting system
- Activated by direct contact with endotoxins, collagen, basememnt membrane i.e. any NEGATIVELY charged surface

Triggers:

  • Kinin system
  • Clotting cascade
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24
Q

Outline the Kinin System.

A

1) Activated Hageman Factor (XII) converts Prekallikrein to Kallikrein
2) Kallikrein:
- Amplifies activation of Hageman Factor
- Cleaves kininogen to form kinins including bradykinin
- Converts plasminogen to plasmin
- Converts C5 to C5a, a chemoattractant for luekocytes
- Increases cell adhesion molecule expression

25
Q

What is bradykinin? What is the function of bradykinin?

A

Bradykinin= a short-lived vasoactive peptide

  • Increases vascular permeability
  • Dilates blood vessels
  • Contracts non-vascular smooth muscle
  • Causes pain

*Note that bradykinin is inactivated by plasma kininase

26
Q

What is thrombin?

A
  • Thrombin is a protease that cleaves fibrinogen to generate insoluble fibrin
  • It is the link between inflammation and coagulation
27
Q

What is the function of thrombin?

A

Binds protease-activated receptors (PARs) that

  • Mobilize P-selectin
  • Produce chemokines, PAF, and NO
  • Stimulate enothelial adhesion molecule formation
  • Induce COX-2 and production of prostaglandins
  • Induces changes in endothelial shape
28
Q

What is plasmin?

A

Protease formed by cleaving plasminogen by kallikrein or plasminogen activator released by endothelium and leukocytes

29
Q

What is the function of plasmin?

A

Lyses fibrin clots

  • Activates Hageman Factor (XII)
  • Cleaves C3 to C3a
  • Degrades fibrin to form fibrin split products that increase vascular permeability in skin and lung
30
Q

What is Arachidonic acid?

A
  • Normally bound to cell membrane phospholipids

- Released by the action of cellular phospholipases

31
Q

What are the two key pathways that stem from AA?

A

1) COX

2) LOX

32
Q

Outline the COX pathway.

A

COX converts AA into protaglandin intermediates that form several inflammation related products including:

  • Thromboxane A2 (TXA2)
  • Prostacyclin (PGI2)
  • PGE2
  • PGD2, PGF2a, PGE2
33
Q

What is TXA2 & what is its function?

A

Thromboxane A2= potent platelet aggregator and vasoconstrictor

34
Q

What is PGI2 & what is its function?

A

PGI2= protacyclin, a vasodilator and inhibitor of platelet aggregation

35
Q

What is the function of PGD2, PGF2a, and PGE2? What is unique about PGE2?

A

All three cause vasodilation and potentiate edema

  • pGE2= also sensitizes skin to painful stimuli and plays a role in cytokine induced fever
36
Q

What is the mechanism of action of aspirin? What is the mechanism of action of glucocorticoids?

A

Aspirin & NSAIDS= inhibits COX-1 & OCX-2, reducing platelet aggregation & vasoconstriction

Clucocorticoids= inhibit phospholipases and the release of AA

37
Q

Outline the LOX pathway.

A

Lipoxygenase converts AA into HPETE compounds, and then leukotrienes & lipoxins

38
Q

What is the function of Leukotriene B4 (LTB4)?

A

Potent chemoattractant causing

  • neutrophil aggregation & adhesion to endothelial cells
  • generation of ROS
  • release of lysosomes
39
Q

What is the function of Leukotrienes C4, D4, E4?

A

Cause intense vasoconstriction, bronchopasm & increase vascular permeability

*Allergic reaction

40
Q

What are lipoxins?

A
  • Endogenous negative regulators of leukotriene action

- Principal actions are to inhibit leukocyte recruitment and the cellular activities of inflammation

41
Q

What is the function of Lipoxin L4 & B4?

A

Inhibition of neutrophil adhesion to endothelium and neutrophil chemotaxis

42
Q

What is PAF?

A

Platelet Activating Factor

  • Causes platelet aggregation
  • Has multiple inflammatory effects
43
Q

What is the function of PAF dependent on?

A

Concentration- dependent:

  • Low= vasodilation & venular permeability
  • High= vasoconstriction & bronchoconstriction
44
Q

What are cytokines?

A

Polypeptides that function as cellular hormones or locally acting cell-to-cell mediators

45
Q

What are chemokines?

A

Cytokines with strong chemotactic properties

46
Q

What cells produce IL-1 & TNF-a?

A

Activated macrophages

47
Q

What are the functions of IL-1 & TNF-a?

A

These are two cytokines that work synergistically to mediate inflammation, including:

  • Acute phase reactions
  • Endothelial effects
  • Fibroblast effects
  • Leukocyte effects
48
Q

What are the acute phase reactions produced by IL-1 & TNF-a?

A
  • Fever
  • Affect sleep and appetite
  • Acute phase proteins
  • Neutrophilia
  • Hemodynamic effects in shock
49
Q

What are the endothelial effects of IL-1 & TNF-a?

A
  • Increased expression of leukocyte adhesion molecules
  • Stimulate PGI synthesis
  • Increase procoagulant activity
  • Increased production of IL1, IL-6, IL-8, and PDGF
50
Q

What Fibroblast effects of IL-1 & TNF-a?

A
  • Increases proliferation, collagen synthesis, and PGE synthesis
  • Increases protease and collagenase production
51
Q

What are the Leukocyte effects of IL-1 & TNF-a?

A

Increased cytokine secretion (IL-1 & IL-6)

52
Q

How are chemokines classified?

A

Classified according to conserved cysteine residues in the protein

53
Q

What is the difference between C-X-C or alpha chemokines, C-C or beta-chemokines, C or gamma chemokines, and CX3C?

A

Alpha= act primarily on neutrophils e.g. IL-8, which is important for neutrophil chemotaxis

Beta= attract monocytes, eosinophils, basophils, and lymphocytes, but NOT NEUTROPHILS

Gamma= specific for lymphocytes

CX3C= attractant for monocytes and T-cells

54
Q

What is NO? List the functions of NO.

A

Nitric Oxide

  • Soluble free radical gas that is produced by: macrophages, endothelium, and some neurons
  • Strong vasodilator
  • Reduces platelet aggregation
  • Microbicidal
55
Q

What are ROS?

A

Reactive Oxygen Species released from neutrophils & macrophages

56
Q

What is the function of antioxidants?

A

Protection from free radicals

57
Q

What are neuropeptides?

A

Substance P & Neurokinin A

58
Q

What are the biological functions of substance P?

A
  • Transmission of pain signals
  • Regulation of blood pressure
  • Increasing vascular permeability

General Pathology (33 decks)

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