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HB 2 > Inflammation Cont’d > Flashcards

Inflammation Cont’d Flashcards

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?

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.

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?

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?

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?

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?

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
Q

What is the function of macrophages? How are they induced to form multinucleate giant cell?

A

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
Q

Describe the mechanism by classically activated macrophage M1 functions.

A

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
Q

Describe the mechanism by which alternatively activated macrophage (M2) functions.

A

Stimulated by IL-13, 14

Growth factors, TGF-b: tissue repair, fibrosis

IL-10, TGF-b: anti-inflammatory effects

28
Q

Describe the function of lymphocytes in chronic inflammation.

A

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
Q

E scribe the function of mast cells in chronic inflammation.

A

Found in CT
Express receptors that bind Fc portion of IgE
Participate in acute and chronic inflammation

30
Q

Describe the function of eosinophils in chronic inflammation.

A

Found in parasitic infection and allergic reaction mediated by IgE
Granules contains major basic protein: toxic to parasite and mammalian epithelial cells

31
Q

What is granulomatous inflammation?

A

Collections of activated macrophages, often with T lymphocytes, and sometimes associated with central necrosis

32
Q

What is a granuloma?

A

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
Q

What are two types of granuloma?

A

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
Q

Compare a caseating granuloma vs a non caseating granuloma.

A

Caseating: central caseous necrosis, lungs, response to infection

Non-caseating: no central necrosis, response to foreign material, sarcoidosis, or Crohn’s disease

35
Q

What are the system is effects of inflammation also known as? What are the most important mediators?

A

Known as “acute-phase” reaction

TNF, IL-1, and IL-6 are the most important mediators of the acute-phase reaction.

36
Q

What are the systemic effects of inflammation?

A

Fever, elevated plasma levels of acute-phase proteins, leukocytosis, increased heart rate and blood pressure, chills, cachexia, severe bacterial infection (sepsis, shock)

37
Q

Describe the mechanisms of a fever.

A

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
Q

Describe the mechanism of elevated plasma levels of acute phase proteins.

A

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
Q

Describe the mechanism of leukocytosis.

A

Cytokines stimulate production of leukocytes from precursors in the bone marrow

40
Q

What is cachexia?

A

Loss of weight, muscle atrophy, fatigue, weakness, and significant loss of appetite

41
Q

Describe the effects of severe bacterial infection (sepsis).

A

Disseminated intravascular coagulation

Hypotension

Metabolic disturbances including acidosis

42
Q

What are the diagnostic tests for inflammation?

A

ESR, CRP, SAA, Leukocyte count

43
Q

Describe the Erythrocyte sedimentation rate test (ESR).

A

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
Q

Describe the CRP test for inflammation.

A

CRP (acute phase protein, bind to phosphocholine on surface of dead or dying cells, activate complement system)

45
Q

What is SAA? (Diagnostic test for inflammation)

A

Serum amyloid A (acute phase protein, recruitment of immune cells to inflammatory site)

46
Q

What leukocytes are counted when testing for inflammation?

A

neutrophilia, eosinophilia, lymphocytosis

47
Q

What may be concluded when we see cells in the AC of the eye? Flare?

A

Cells- immune cells in AC

Flare- proteins leaked form inflamed blood vessels

HB 2 (17 decks)

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