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Inflammation Flashcards

Acute and chronic inflammation

1
Q

Features of acute vs chronic inflammation: onset, main cellular infiltrates, presence of tissue injury and fibrosis, local and systemic signs

A

Onset: acute - fast, minutes or hours; chronic- slow, days
Cellular infiltrates: acute - mostly neutrophils; chronic - monocytes/macrophages and lymphocytes
Tissue injury and fibrosis: acute - usually mild and self limited; chronic - often severe and progressive
Local and systemic signs: acute - prominent; chronic - less prominent

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2
Q

L-selectin (CD62L) - job, distribution

A

Job: adhesion molecule (mediates attachment of leukocytes to endothelial cells)
Distribution: neutrophils, monocyted, T cells, B cells

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3
Q

E-selectin (CD62E) - job, distribution

A

Job: adhesion molecule, mediates attachment of leukocytes to endothelium
Distribution: endothelium activated by cytokines (TNF, IL-1)

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4
Q

P-selectin - job, distribution

A

Job - adhesion molecule, mediates attachment of leukocytes to endothelium
Distribution - endothelium activated by cytokines (TNF, IL-1), histamine, thrombin

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5
Q

P-selectin - job, distribution

A

Job - adhesion molecule, mediates attachment of leukocytes to endothelium
Distribution - endothelium activated by cytokines (TNF, IL-1), histamine, thrombin

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6
Q

What are selectins and integrins, what are the main examples

A

Adhesion molecules, mediate attachment of leukocytes to the endothelium: P-selectin and E-selectin are expressed on activated endothelium; L-Selectin and integrins are expressed on leukocytes
The Ig CD31 is also an adhesion molecule and is expressed on both endothelium and leukocytes

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7
Q

Integrin LFA-1 - job, distribution

A

Job - integrin, adhesion molecule, mediates attachment of leukocytes to endothelium
Distribution - neutrophils, monocytes, T cells

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8
Q

MAC-1 - job, distribution

A

Job - adhesion molecule, mediates attachment of leukocytes to endothelium
Distribution - monocytes, dendritic cells

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9
Q

VLA-4 - job, distribution

A

Job - integrin, adhesion molecule, mediates attachment of leukocytes to endothelium
Distribution - monocytes, T cells

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10
Q

alpha4B7 - job, distribution

A

Job - integrin, adhesion molecule, mediates attachment of leukocytes to endothelium
Distribution - monocytes, T cells

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11
Q

CD31 - job, distribution

A

Job - Ig adhesion molecule, mediates attachment of leukocytes to endothelium
Distribution - endothelial cells, leukocytes

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12
Q

Neutrophils vs macrophages - origin

A

Neutrophils: haemopoietic stem cells in bone marrow
Macrophages: haemopoietic cells in bone marrow; many tissue resident macrophages are from stem cells in yolk sac or foetal liver early in development

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13
Q

Neutrophils vs macrophages - lifespan

A

Neutrophils: several days
Macrophages: inflammatory macrophages - days to weeks; tissue resident macrophages - years

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14
Q

Neutrophils vs macrophages - activation response, reactive oxygen species, nitrix oxide, degradation, cytokine production, NET formation, secretion of lysosymal enzymes

A

Activation response: neutrophils - rapid, short lived, mostly degranulation and enzymatic activity; macrophages- prolonged, slow, often dependent on gene transcription
ROS: neutrophils - rapidly induced by assembly of phagocyte oxidase (respiratory burst); macrophages - less prominent
NO: neutrophils - low levels or none; macrophages - induced following transcriptional activation of iNOS
Degranulation: neutrophils - major response, induced by cytoskeletal rearrangement; macrophages - not prominent
Cytokine production: neutrophils - low levels or none; macrophages - major functional activity, requires transcriptional activation of cytokine genes
NET formation: neutrophils - rapidly induced, by extrusion of nuclear contents; macrophages - no
Secretion of lysosomal enzymes: neutrophils - prominent; macrophages - less

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15
Q

Histamine - sources, actions

A

Sources: mast cells, basophils, platelets
Actions: vasodilation, increased vascular permeability, endothelial activation

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16
Q

Prostaglandins - generation, sources, actions, important examples and their specific actions

A

Generation - produced from arachidonic acid (AA) by cyclooxygenases COX-1 and COX-2 (produced from AA therefore are one of the lipid mediators)
Sources - mast cells, leukocytes, endothelial cells, other
Actions - mostly vasodilation, pain, fever
Important examples- PGE2, PGD2, PGF2a, PGI2 (prostacyclin), TxA2 (thromboxane)
*thromboxane produced in platelets and causes vasoconstriction and platelet aggregation
*prostacyclin is produced in endothelium and causes vasodilation and inhibits platelet aggregation
*imbalance of thromboxane:prostacyclin has been implicated as an early event in thrombus formation

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17
Q

Leukotrienes - generation, sources, actions, important examples and their specific actions

A

Generation - produced from arachidonic acid (AA) from lipoxygenases (produced from AA and therefore one of the lipid mediators)
Sources - mast cells, leukocytes
Actions - increased vascular permeability, chemotaxis, leukocyte adhesion and activation
Important examples:
LTB4 - potent chemotactic agent and activator of neutrophils, causes aggregation and adhesion to endothelium, generation of ROS and release of lysosomal enzymes
LTC4, LTD4, LTE4 - cystienyl containing leukotrienes, cause intense vasoconstriction, bronchospasm and increased permeability of venules
*montelukast is a leukotrine receptor antagonist

18
Q

Cytokines - sources, actions, important examples and their specific actions

A

Sources - macrophages, endothelial cells, mast cells
Actions - local endothelial activation (expression of adhesion molecules), fever, metabolic changes, shock (hypotension)
Important examples:
TNF and Interleukin-1- produced mainly by activated macrophages and dendritic cells, TNF also produced by T lymphocytes, IL1 also produced by some epithelial cells, production is induced by signals through TLRs and other microbial sensors, generation of the biologically active form of IL1 is also dependent on the inflammasome, critical in endothelial activation and leukocyte recruitment (promote adhesion and migration), leukocyte activation, systemic acute phase response
*infliximab is a TNF inhibitor

19
Q

Chemokines - sources, actions, examples

A

Sources: leukocytes, activated macrophages
Actions: chemotaxis, leukocyte activation; mediate their activities via seven-transmembrane G protein-coupled receptors; have roles in acute inflammation and in homeostatic maintenance of tissue architecture
Examples:
C-X-C chemokines, typical example is CXCL8 (prev called IL8), secreted mostly by activated macrophages and endothelial cells, causes activation and chemotaxis of neutrophils with some activity on monocytes and eosinophils, important induces are microbial products and other cytokines especially TNF and IL1
C-C chemokines, eg monocyte chemoattractant protein (MCP1 or CCL2) eotaxin (CCL11) macrophages inflammatory protein 1alpha (MIP-1alpha or CCL3), generally attract monocytes eosinophils basophils lymphocytes but less potent chemoattractants for neutrophils, most have overlapping actions but eotaxin specific for recruiting eosinophils
C chemokines, egs lymphotaxin XCL1, relatively specific for lymphocytes
CX3C chemokines, only known member is fractalkine (CX3CL1), exists in two forms which are a surface bound form on endothelial cells and a free form derived from proteolytic of the membrane bound form, promotes strong adhesion (membrane form) and chemoattractant activity (free form) of monocytes and T cells

20
Q

Complement system - description, generation, activation pathways, effector functions, important complement proteins and their specific actions

A

Description: collection of plasma proteins that function in host defense against microbes and pathologic inflammatory reactions
Generation: complement proteins present in inactive forms in plasma
Activation pathways: critical step in complement activation is proteolytic of C3 (most abundant component), can occur by three pathways; classical pathway - triggered by binding of C1 to antibody (IgM or IgG) that has bound to an antigen; alternative pathway - triggered by microbial surface molecules/ complex polysaccharides / cobra venom / other substances in the absence of antibodies; lectin pathway, plasma mannose-binding lectin binds to carbohydrates on microbes and directly activates C1; all three pathways lead to formation if C3 convertase which splits C3 into C3a and C3b
Effector functions: inflammation - mediated by C3a and C5a (formed by C5 convertase which is formed from C3b), these are anaphylatoxins, stimulate histamine release from mast cells and thereby increase vascular permeability and cause vasodilation, C5a also chemotactic for neutrophs monocytes eosinophils basophils and activates lipoxygenase pathway of AA metabolism; opsonisation and phagocytosis - some C3b is fixed to microbial cell walls and acts as opsonins promoting phagocytosis by neutrophils and macrophages; cell lysis - membrane attack complex (MAC) is formed on surface of microbes allowing water and electrolytes free passage across cellular membrane leading to lysis of the microbe

21
Q

Important regulators of complement system

A 
C1 inhibitor (C1 INH): blocks activation of C1 which is the first protein of the classicL complement pathway, inherited deficiency is cause of hereditary angioedema
Decay accelerating factor (DAF) and CD59: proteins linked to plasma membranes by GPI anchors; DAF prevents formation of C3 convertases; CD59 inhibits formation of the membrane attack complex; acquired deficiency of the enzyme that creates GPI anchors leads to paroxysms nocturnal haemoglobinuria (due to excessive complement activation and lysis of red cells)
Complement factor H: circulating glycoprotein that inhibits alternative complement activation pathway; deficiencies in factor H lead to atypical haemolytic uremic syndrome caused by complement deposits in glomerular vessels leading to endothelial damage and thrombi formation; factor H gene polymorphism also linked to age related macular degeneration
22
Q

Kinins - generation, actions, examples

A

Vasoactive peptides derived from kininogens (which are plasma proteins) by action of proteases called kallikreins
Cleavage of high-molecular-weight kininogen forms bradykinin which causes increased vascular permeability, contraction of non-vascular smooth muscle, dilation of blood vessels, and pain when injected into skin

23
Q

Platelet activating factor - sources, actions

A

Sources - leukocytes, mast cells

Actions - vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst

24
Q

Principal mediators of vasodilation

A

Histamine, prostaglandins

25
Q

Principal mediators of increased vascular permeability

A

Histamine, serotonin, complement proteins C3a and C5a (by liberating vasoactibe amines from mast and other cells), leukotrienes LTC4 LTD4 LTE4

26
Q

Principal mediators of chemotaxis, leukocyte recruitment and activation

A

TNF, IL-1, chemokines, complement proteins C3a C5a, leukotriene LTB4

27
Q

Principal mediators of fever

A

IL-1, TNF, prostaglandins

28
Q

Principal mediators of pain related to inflammation

A

Prostaglandins, bradykinin, substance P

29
Q

Principal mediators of tissue damage related to inflammation

A

Lysosomal enzymes of leukocytes, ROS

30
Q

Neuropeptides - description, sources, examples, actions

A

Small peptides secreted by sensory nerves and various leukocytes, produced in central and peripheral nervous system
Play a role in initiation and regulation of inflammatory responses, could provide mechanism for cross talk between nervous system and immune/inflammatory reactions
Egs:
Substance P, substance P containing nerves prominent in lung and GI tract, many activities important to inflammation including pain signal transmission and vascular permeability
Neurokinin A

31
Q

Morphological patterns of acute inflammation

A

Serous inflammation - marked by exudate of cell-poor fluid, eg effusions (not always from inflammation), blisters
Fibrinous inflammation - fibrinous exudate develops when vascular leaks are large allowing fibrinogen to pass out of blood or there is local procoagulant stimulus, characteristic of inflammation in lining of body cavities such as meninges pericardium pleura, fibrinous exudates may be dissolved and cleared by macrophages or may lead to fibrosis
Purulent (suppurative) inflammation and abscess - characterised by production of pus which is an exudate consisting of neutrophils liquefied debris of necrotic cells and oedema fluid, most frequent cause is bacteria that cause liquefactive tissue necrosis eg staphylococci
Ulcers - sloughing of inflammation necrotic tissue on surface of an organ or tissue, often acute and chronic inflammation coexist

32
Q

Possible outcomes of acute inflammation

A

Complete resolution, healing by connective tissue replacement (scarring, fibrosis), progression to chronic inflammation

33
Q

Acute vs chronic inflammation - typical associated injuries and responses (brief)

A

Injuries: acute - infarction, bacterial infection, toxins, trauma; chronic - viral infections, chronic infections, persistent injury, autoimmune disease
Responses: acute - vascular changes, neutrophil recruitment, mediators; chronic - angiogenesis, mononuclear cell infiltration, fibrosis

34
Q

Cardinal signs of inflammation

A

Rubor, calor, tumor, dolor
Redness, warmth, swelling, pain
Rubor calor tumor due to increased blood flow and oedema
Dolor due to tissue damage and liberation of prostaglandins, neuropeptides and cytokines

35
Q

Main prostaglandins

A

PGE1, PGE2, PGD2, PGF2a, PGI2 (prostacyclin), TxA2 (thromboxane A2)

36
Q

Main leukotrienes

A

LTB4, LTC4, LTD4, LTE4

37
Q

Main cytokines

A

TNF, IL1, IL6

38
Q

Main chemokines

A 
CXC chemokines (eg CXCL8 prev called IL8)
CC chemokines (eg monocyte chemoattractant protein MCP1 aka CCL2, eotaxin CCL11, macrophage inflammatory protein 1 alpha MIP1alpha aka CCL3)
C chemokines (eg lymphotactin XCL1)
CX3C chemokines (eg fractalkine CX3CL1)
39
Q

Main complement proteins

A

C1, C3 C3a C3b, C5a C5b

40
Q

Main complement regulatory proteins

A

C1 inhibitor (C1 INH), decay accelerating factor (DAF), CD59, complement factor H

41
Q

Main neuropeptides

A

Substance P, neurokinin A

42
Q

Main adhesion molecules

A

Selectins: E-selectin, P-selectin, L-selectin
Integrins: LFA1, MAC1, VLA4, alpha4beta7
Ig: CD31

My Cards- Pathology (3 decks)

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