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HB 2 > Inflammation Cont’d > Flashcards

Inflammation Cont’d Flashcards

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1
Q

What are the sources of chemical mediator? What is their function/life span? (Inflammation)

A

Cell
Plasma (usually synthesized by liver)

Biological activity to regulate inflammatory response through receptor or direct acting

Short lived (inactivated by enzymes or inhibited)

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2
Q

Describe the cell derived chemical mediator-Histamine.

A

Preformed (mast cells, basophils, platelets, amoung first released)

Function- vasodilation and vascular permeability

Release from mast cells caused by:
Physical agents (trauma & heat)
Immunologic reactions involving binding of IgE antibodies to mast cells
Complement fragments C3a and C5a (anaphylatoxins) Neuropeptide (substance P)
Cytokines (IL-1 & IL-8)

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3
Q

What are arachidonic acid metabolites (eicosanoids)?

A

From leukocytes, mast cells, endothelial cells and platelets

Two major classes of enzymes
Cyclooxygenases: prostoglandins & thromboxanes Lipoxygenases: leukotrienes & lipoxins

Serve as short-range signaling agents

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4
Q

What is the first conversion of the arachidonic acid pathway? What can inhibit it?

A

Membrane bound phospholipids to arachidonic acid through phospholipase

Corticosteroids can inhibit

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5
Q

From arachidonic acid what two pathways arise? What can inhibits

A

Cyclooxygenase pathway (COX 1 and COX2) (NSAIDS can inhibit)

Lipoxygenase Pathway (lipoxygenase)

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6
Q

Describe the function of COX 1 and COX 2. How can NSAIDS inhibit COX 1 and COX2?

A

Cox-1: constituitive, prostaglandins protect stomach from acids, produced in inflammation
Cox-2: produced in inflammation
Most NSAIDS are non-specific COX- 1/COX-2 inhibitors

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7
Q

What are produced from the cyclooxygenase pathway?

A

Prostaglandins: vasodilation, inhibit platelets aggregation, pain (PGE2), fever (PGE2)

Thromboxanes: vasoconstriction, platelet aggregation

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8
Q

What is produced from the lipoxygenase pathway?

A

Leukotrienes: Bronchospasm, increase vascular permeability, increase leukocyte chemotaxis

Lipoxins: inhibit inflammation, decrease leukocyte chemotaxis

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9
Q

Describe platelet activating factor (chemical mediator of inflammation).

A

Derived from phospholipid
Produced by neutrophils, monocytes, basophils, endothelial cells, and platelets by the action of phospholipase A
Acts directly on target cells through the effects of a specific G protein-coupled receptors
Function: Bronchoconstriction, Vasodilation, Increased vascular permeability, Elicit enhanced leukocyte adhesion, chemotaxis, leukocyte degranulation

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10
Q

Describe cytokines.

A

Modulate function of other cell types
Bind to specific receptors on target cells
Transient response, regulated with Endo and exogenous signals

Major cytokines in acute inflammation are TNF, IL-1, IL-6 • Chronic inflammation: interferon-γ (IFN-γ), IL-17 and IL-12

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11
Q

Describe plasma proteases. (Chemical mediators of inflammation)

A

3 interrelated plasma-derived mediators that play a key role in inflammatory responses
1. Complement system
2. Kinin system
3. Clotting factor system

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12
Q

Principal mediators in vasodilation.

A

Histamine
Prostaglandins

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13
Q

Principal mediators in increased vascular permeability

A

Histamine and serotonin
C3a and C5a
Leukotrienes C4, D4, E4

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14
Q

Principal mediators in chemotaxis, leukocyte recruitment, and activation.

A

TNF, IL-1
chemokines
C3a, C5a
Leukotriene B4

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15
Q

Principal mediators in fever.

A

IL-1, TNF
Prostaglandins

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16
Q

Principal mediators in pain.

A

Prostaglandins
Bradykinin

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17
Q

Principal mediators in tissue damage.

A

Lysosomal enzymes of leukocytes
Reactive oxygen species

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18
Q

What is the function of bradykinin in the complement system?

A

Increased vascular permeability, arteriolar dilation, and bronchial smooth muscle contraction, pain

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19
Q

What is the function of factor 12 (Hageman factor) in the complement cascade?

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A

Clotting system- leads to thrombin formation and clotting

Kinin system- leads to formation of bradykinin and activates fibrinolytic system

Increases inflammation

20
Q

Define chronic inflammation.

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A

Inflammation of prolonged duration (weeks to years), continuing inflammation, tissue injury, attempts at healing occur simultaneously

21
Q

What kind of setting cause chronic inflammation?

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A

Persistent infection (TB or syphilis)
Immunity mediated inflammatory response (rheumatoid arthritis)
Prolonged exposure to potentially toxic agent (cholesterol crystals)

May develop with acute inflammation (sever persistent irritation)

22
Q

What are the characteristics of chronic inflammation?

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A

Tissue infiltration by mononuclear cells
• macrophages, lymphocytes, plasma cells

Tissue destruction
• largely induced by products of the inflammatory cells

Attempts at repair
• Increased connective tissue (fibrosis)
• Angiogenesis

23
Q

What pathology does chronic inflammation contribute to?

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A

Alzheimer’s
Pulmonary
Atherosclerosis
Rheumatoid arthritis
Tuberculosis
Cancer
Neurodengenerative
Diabetes

24
Q

Describe macrophages? What response are they dominant in? Where is the location of the mononuclear phagocytic system?

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A

Derived from peripheral blood monocytes
Transform into phag cell in extravascular space
Dominant in chronic inflammation

Mononuclear phagocyte system:
Normally scattered in connective tissue
Liver (Kupffer cells)
Spleen and lymph nodes (Sinus histiocytes)
CNS (microglial cells)
Lungs (alveolar macrophages)

25
What is the function of macrophages? How are they induced to form multinucleate giant cell?
Ingest and eliminate microbes and dead tissues Initiate the process of tissue repair Secrete mediators of inflammation Display antigens to T lymphocytes and respond to signals from T cells IFN-y can induce macrophages to fuse into large giant cell
26
Describe the mechanism by classically activated macrophage M1 functions.
Activated by IFN-1 (microbe) ROS, NO, lysosomal enzymes cause microbicidal actions: Phagocytosis and killing of bacteria and fungi IL-1, 12, 23 and chemokines: activate inflammation
27
Describe the mechanism by which alternatively activated macrophage (M2) functions.
Stimulated by IL-13, 14 Growth factors, TGF-b: tissue repair, fibrosis IL-10, TGF-b: anti-inflammatory effects
28
Describe the function of lymphocytes in chronic inflammation.
Major drivers of inflammation in many autoimmune and chronic inflammatory diseases CD4+ T cells –TH1 cells produce the cytokine IFN-γ, which activates macrophages in the classical pathway. –TH2 cells secrete IL-4, IL-5, and IL-13, which recruit and activate eosinophils and are responsible for the alternative pathway of macrophage activation. –TH17 cells secrete IL-17 and other cytokines that induce the secretion of chemokines responsible for recruiting neutrophils and monocytes into the reaction. B lymphocytes- May develop into plasma cells in tissues
29
E scribe the function of mast cells in chronic inflammation.
Found in CT Express receptors that bind Fc portion of IgE Participate in acute and chronic inflammation
30
Describe the function of eosinophils in chronic inflammation.
Found in parasitic infection and allergic reaction mediated by IgE Granules contains major basic protein: toxic to parasite and mammalian epithelial cells
31
What is granulomatous inflammation?
Collections of activated macrophages, often with T lymphocytes, and sometimes associated with central necrosis
32
What is a granuloma?
Formation is a cellular attempt to contain an offending agent that is difficult to eradicate Focal collections of macrophages (epithelioid macrophages) surrounded by a collar of mononuclear leukocytes, principally lymphocytes & occasionally plasma cells Giant Cell- Multinucleate cells made by fusion of macrophages, can be also be found in the granuloma
33
What are two types of granuloma?
Foreign body granuloma • foreign body in the absence of T cell–mediated immune responses – suture, talc, thorn, fibers etc Immune granuloma • Caused by a variety of agents that are capable of inducing a persistent T cell–mediated immune response – certain microbes, Self antigen eg. Crohn’s disease, unknown etiology, eg. Sarcoidosis, Wegener’s granulomatosis
34
Compare a caseating granuloma vs a non caseating granuloma.
Caseating: central caseous necrosis, lungs, response to infection Non-caseating: no central necrosis, response to foreign material, sarcoidosis, or Crohn’s disease
35
What are the system is effects of inflammation also known as? What are the most important mediators?
Known as “acute-phase” reaction TNF, IL-1, and IL-6 are the most important mediators of the acute-phase reaction.
36
What are the systemic effects of inflammation?
Fever, elevated plasma levels of acute-phase proteins, leukocytosis, increased heart rate and blood pressure, chills, cachexia, severe bacterial infection (sepsis, shock)
37
Describe the mechanisms of a fever.
In the hypothalamus the prostaglandins, especially PGE2, stimulate the production of neurotransmitters, which function to reset the temperature set point at a higher level
38
Describe the mechanism of elevated plasma levels of acute phase proteins.
C-reactive protein (CRP), fibrinogen, and serum amyloid A (SAA) protein Stimulated by IL-6 (for CRP and fibrinogen) and IL-1 or TNF (for SAA)
39
Describe the mechanism of leukocytosis.
Cytokines stimulate production of leukocytes from precursors in the bone marrow
40
What is cachexia?
Loss of weight, muscle atrophy, fatigue, weakness, and significant loss of appetite
41
Describe the effects of severe bacterial infection (sepsis).
Disseminated intravascular coagulation Hypotension Metabolic disturbances including acidosis
42
What are the diagnostic tests for inflammation?
ESR, CRP, SAA, Leukocyte count
43
Describe the Erythrocyte sedimentation rate test (ESR).
Finer in Ogden bind to erythrocytes and causes increase in ESR Measures distance RBC fall in one hr HIGH ESR: RBS settles quickly to bottom: nonspecific inflammation Different for men and women Age is a factor
44
Describe the CRP test for inflammation.
CRP (acute phase protein, bind to phosphocholine on surface of dead or dying cells, activate complement system)
45
What is SAA? (Diagnostic test for inflammation)
Serum amyloid A (acute phase protein, recruitment of immune cells to inflammatory site)
46
What leukocytes are counted when testing for inflammation?
neutrophilia, eosinophilia, lymphocytosis
47
What may be concluded when we see cells in the AC of the eye? Flare?
Cells- immune cells in AC Flare- proteins leaked form inflamed blood vessels

HB 2 (17 decks)

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