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FM 1 > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Inflammation

A
  • reaction to injurious agents that limits damage and promotes repair
  • mediated by blood vessels and blood cells
  • tightly regulated chain of molecular and cellular events
  • categorized as acute or chronic by the duration of the response and the type of cells involved
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2
Q

neutrophils

A
  • most common WBC in peripheral blood
  • segmented nucleus w/ 3-5 lobes and numerous cytoplasmic granules
  • motile phagocytes-move by pseudopods and digest foreign material via acid hyrolases from w/in granules
  • *Primary responder in acute inflammation
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3
Q

lymphocytes

A
  • single nucleus, scant cytoplasm
  • B-cells, T-cells, and NK cells
  • Primarily in chronic inflammation and acquired immunity
  • produce cytokines and help eliminate foreign material through production of antibodies and toxic granules
  • specialized lymphocytes can elaborate antibodies when stimulated
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4
Q

Monocytes

A

-produced in bone marrow, in circulation for ~1 day

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5
Q

Macrophages

A
  • monocytes in tissues
  • motile phagocytes, cytoplasmic granules containing toxic substances
  • acute and chronic inflammation: phagocytose foreign material, digest it, and present antigens via Class II MHC receptors
  • integral in transition from acute to chronic
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6
Q

Eosinophils

A
  • bi/tri lobed nucleus, cytoplasm full of pink (eosinophilic) granules that contain numerous chemical mediators of inflammation-histamine, proteolytic enzymes, major basic protein
  • primarily in rxns to allergens and parasites
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7
Q

Basophils

A
  • bilobed nucleus, cytoplasm filled w/ deep blue/purple (basophilic) granules-contain histamine, proteoglycans, proteolytic enzymes, and lipid mediators of inflammation (eg slow reacting substance of anaphylaxis)
  • allergic and hypersensitivity rxns
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8
Q

Mast cells

A

in tissues, identical to basophils

located near bv and along mucosa and dermis-interface between host and environment

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9
Q

Platelets

A
  • Small, anuclear discoid fragments of megakaryocyte cytoplasm, contains some cell machinery and numerous granules
  • primarily involved in hemostasis (blood clot formation)
  • granules contain numerous chemical mediators of inflammation (eg platelet activating factor-affects all cardinal features of inflammation)
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10
Q

Inflammatory changes in vascular flow

A
  • histamine mediates dilation of precapillary arterioles-increase vascular flow to capillary bed
  • postcapillary venule dilation -> stasis -> increased hydrostatic pressure in capillary bed
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11
Q

inflammatory changes in vascular permeability

A
  • gaps form between endothelial cells -> fluids, electrolytes, and/or blood can leak out of vessels into surrounding tissues
  • caused by: direct toxic injury to cells; constriction of endothelial cells and release of tight jxns due to vasoactive mediators of inflammation and cytokines
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12
Q

Leukocyte adhesion

A
  • stasis-blood flow slows
  • margination-anionic surface charge of endothelial cells decreases-leukocytes no longer repulsed-altered blood flow pushes leukocytes to periphery
  • adherence-leukocytes roll along endothelium and stick to it; mediated by expression of molecules and ligands on endothelial and leukocyte surfaces
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13
Q

Roll of macrophages in leukocyte adhesion

A

produce cytokines->

  • induce selectin transport to cell surfaces-bind Sialyl Lewis X-modified glycoprotein on leukocyte surfaces-slow leukocyte
  • induce expression of integrin ligands and proteoglycans -> induce leukocyte integrins to switch to high affinity state and bind integrin ligands
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14
Q

Transmigration

A

diapedesis-leukocytes extend pseudopods and squeeze through vessel wall-PECAM mediated
migration-leukocytes travel through extravascular space to site of injury along chemotactic gradient

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15
Q

Chemotaxis; 4 strong attractants of chemotaxis

A
  • movement of leukocytes along a chemical gradient-(LFB bacterial product, C5a complement protein, LTB4 arachadonic acid metabolite, IL-8 cytokine)
  • chemotactic agents bind g-protein coupled receptor -> polymerization of actin filaments and extension of filopodia
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16
Q

Leukocyte activation

A

-modulate leukocyte adhesion molecules
-ingest and degrade foreign substances scavenged from tissue
-degranulate
-secrete cytokines that amplify and regulate inflammation
-produce arachidonic acid metabolites
-aggregate platelets
(activators include antibodies, thrombin, bacterial products, etc)

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17
Q

Phagocytosis-recognition and attachment

A
  • macrophage mannose receptor recognizes terminal mannose and fucose residues of glycoproteins and glycolipids on microbial cell walls
  • recognition and attachment enhanced if foreign object opsonized
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18
Q

Phagocytosis-engulfment

A
  • cytoplasm extends around foreign complex and forms intracellular phagosome
  • phagosome fuses w/ lysosome
  • contents mix and enzymes activate
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19
Q

Phagocytosis-killing and degradation

A
  • oxygen dependent mechanism-H2O2 and HOCl destroy microbes by halogenation or lipid peroxidation
  • oxygen independent mechanism-acid hydrolases in leukocyte granules toxic to phagolysosome contents
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20
Q

Leukocyte product leak

A
  • regurgitation during feeding
  • frustrated phagocytosis (complex fixed on tissue)
  • cytotoxic release (damage own cell membrane eg gout crystals)
  • active exocytosis
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21
Q

Chemical mediators of inflammation

A

Histamine
bradykinin
substance P
cytokines-IL-1, TNF, IFN-gamma

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22
Q

Integrin Ligands

A
  • ICAM-1 and VCAM-1
  • cytokines from macrophages induce their expression on endothelial cells
  • bind integrins on leukocyte cell surface for leukocyte adherence
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23
Q

PECAM-1

A

Integrin ligand on endothelial cell surface that mediates leukocyte diapedesis

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24
Q

Defects in leukocyte adhesion

A
  • genetic deficiency in leukocyte adhesion molecules (LAD 1 and 2)
  • susceptible to recurrent bacterial infections and have impaired wound healing
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25
Q

defects in phagolysosome function

A
  • Chediak-Higashi syndrome: autosomal recessive, neutropenia, defective granulation, defective ROS microbicides; albinism, nerve defects, bleeding disorders
  • Chronic granulomatous disease-defect in genes encoding NADPH oxidase
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26
Q

Bone Marrow suppression

A

->decreased leukocyte activity due to primary or secondary ds of bone marrow

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27
Q

aberrant release of leukocyte products

A

underlies many severe and chronic inflammatory diseases, such as arthritis, asthma, atherosclerosis.

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28
Q

Serous inflammation

A

thin watery fluid (transudate) exuded at site of injury eg burn blister

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29
Q

fibrinous inflammation

A

clear fluid and fibrinogen escape vessel; fibrinogen polymerizes to form thick fibrin coat of tan-pink, stringy material; lining of body cavities

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30
Q

suppurative/purulent inflammation

A

production of large amounts of pus (neutrophils, necrotic cells, edema fluid); characteristic of pyogenic bacteria infection; eg acute appendicitis, abscess, empyema

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31
Q

pseudomembranous inflammation

A

overgrowth of colonic mucosa by C. dif or fungi, secondary to broad spectrum antibiotic use or immunosuppression; film of inflammatory cells, necrotic epithelium, fibrin and mucus cover mucosa

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32
Q

ulcerative inflammation

A

destruction of epithelial lining due to ischemic damage or infection

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33
Q

Gangrenous inflammation

A

tissue necrosis secondary to interruption of blood supply

  • dry-w/o superinfection
  • wet-leads to liquefactive necrosis
  • gas-superinfection with gas forming organisms
  • necrotizing fasciitis-deep tissues
  • Fournier’s-scrotum
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34
Q

Resolution

A
  • replacement of dead cells by cells that were normally there before inflammatory process took place
  • effects of inflammation completely reversed-resume normal tissue
  • can only occur in tissues w/ regenerative capacity
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35
Q

Scar formation

A
  • replacement of damaged tissue by fibrous tissue

- tissue injury is extensive or involves cells that have limited regenerative capacity

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36
Q

Chronic inflammation

A
  • injurious agent persist/cannot be removed by neutrophils alone
  • acquired immune system activated
  • primary response to things like autoimmune ds, some viral infections, some malignancies (TB, syphilis, DM foot ulcers, HepC)
  • Macrophages present digested material or antigens to lymphocytes
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37
Q

Non-specific chronic inflammation

A
  • mononuclear cell infiltration (macrophages, lymphocytes, and plasma cells) dominate
  • cause tissue destruction and lead to scar (fibrosis)
  • often w/ reparative process (granulation tissue)
38
Q

Granulomatous inflammation

A
  • granuloma formation-collection of activated (plump epithelioid) macrophages surrounded by a collar of chronic inflammatory cells, w/ or w/o central necrosis (caseation) and/or giant cells
  • caused by certain infectious agents (TB, leprosy, brucellosis, cat-scratch, fungi), insoluble foreign objects, or sarcoidosis
  • seal off injurious agent
39
Q

chemical mediators of inflammation

A
  • activated or released in response to particular stimuli
  • rapidly released and rapidly cleared
  • mediate effects through specific receptors on target cells
40
Q

Plasma derived chemical mediators of inflammation

A
  • produced in liver and circulate in serum as precursor forms
  • factor XII (Hageman factor)
  • complement proteins
  • kinins
  • clotting proteins
41
Q

Cell derived chemical mediators of inflammation

A
  • sequestered in cell organelles of produced by effector cells upon stimulation
  • vasoactive amines (histamine, serotonin)
  • Arachidonic acid metabolites (prostaglandins, leukotrienes, lipoxins)
  • cytokines and chemokines (IL-1, TNF)
  • nitric oxide
  • lysosomal contents
  • O2 derived free radicals
42
Q

Vasoactive amines

A
  • histamine and serotonin
  • primarily affect altered flow and permeability of vessels
  • stored in intracellular granules and rapidly released in response to injurious stimuli
  • 1st mediators released
43
Q

histamine

A
  • in mast cells, basophils, and platelets
  • dilation of arterioles and increased permeability of postcapillary venules
  • principle mediator of immediate transient response
44
Q

serotonin

A
  • in platelets

- released when platelets aggregate and causes vessel permeability

45
Q

C5a

A
  • plasma protein
  • complement system
  • potent chemotactic agent-attract leukocytes; also adhesion and activation
  • anaphyltoxin->vascular dilation by stimulating histamine response
46
Q

C3a

A
  • plasma protein
  • complement system
  • anaphyltoxin->vascular dilation by stimulating histamine release; also vascular leakage
47
Q

C3b

A
  • complement system

- opsonin-target bacteria for phagocytosis

48
Q

Complement system

A

activation leads to inflammation, phagocytosis, and lysis of microbes

49
Q

Factor XII (Hageman factor)

A
  • plasma protein
  • activated at site of tissue injury by exposed collagen, BM, and activated platelets
  • activates prekallikrein-> kallikrein; kallikrein is enzyme to make bradykinin
  • also initiates clotting cascade -> thrombin
  • fibrinolytic system -> plasmin activation
  • complement system
50
Q

bradykinin

A
  • plasma protein
  • increases vascular permeability and pain
  • rapidly cleared by kinases such as ACE in lung
51
Q

Thrombin

A
  • plasma protein
  • activated by clotting cascade
  • links clotting cascade to inflammation by activating platelets, endothelial cells, and smooth muscle cells
52
Q

Thrombin activates:

A
  • mobilization of selectins to endothelial cell surfaces
  • change in endothelial shape-gap jxns open
  • induction of metabolism of arachidonic acid
  • production of cytokines, platelet activating factor, and nitric oxide
53
Q

Fibrinolytic system

A
  • component of clotting system
  • antagonizes clotting cascade by breaking up fibrin clots once formed
  • plasminogen incorporated into blood clots as they form -> gets converted to plasmin by tissue plasminogen factor, kallikrein, and factor 12 -> catalyze breakdown of fibrin
54
Q

Plasmin

A
  • plasma protein
  • directly cleaves C3 to form anaphylatoxin C3a
  • activates factor XII-> promotes activation of kinin and clotting cascades
  • products of action on fibrin (fibrin split products) augment vascular permeability
55
Q

most important plasma protein mediators of inflammation in vivo

A
  • bradykinin
  • C3a
  • C5a
  • thrombin
56
Q

Kallikrein

A
  • plasma protein
  • convert C5 to C5a
  • amplify inflammatory response by activating factor XII
  • convert plasminogen -> plasmin
  • activate bradykinin
57
Q

Arachidonic acid metabolites

A
  • arachidonic acid esterified in cell membrane -> metabolites synthesized in response to external stimuli -> eicosanoids
  • bind G-protein coupled receptors
  • chemotaxis, vasoconstriction, bronchospasm, increase permeability, vasodilation, inhibit neutrophil chemotaxis, stimulate monocyte adhesion, inhibit platelet aggregation, promote platelet aggregation, potentiate edema
58
Q

leukotrienes

A
  • more potent in promoting vascular permeability than histamine
  • act on bronchial tree to cause bronchospasm
  • C4, D4, and E4 -> slow reacting substances of anaphylaxis
  • inflammatory mediators in allergic reactions
59
Q

cyclooxygenase pathway

A 
make prostaglandins (mast cells, vascular epithelium) and thromboxane (platelets)
-inhibited by acetaminophen, NSAIDs, and COX inhibitors
60
Q

lipoxygenase pathway

A

make leukotrienes and lipoxins (neutrophils)

61
Q

steroids

A

inhibit phospholipases -> can’t metabolize arachidonic acid

62
Q

Platelet activating factor

A
  • platelet aggregation and degranulation
  • increased leukocyte adhesion
  • chemotaxis
  • oxidative burst
  • changes in vascular permeability
  • augmentation of arachidonic acid metabolism in phagocytes
  • bronchoconstriction
  • boosts synthesis of other chemical mediators of inflammation
  • produced from membrane phospholipids of many cell types
  • G-protein coupled receptors
63
Q

cytokine

A
  • protein that modulates the fxn of other cell types (ie messenger)
  • interleukins, growth factors, tumor necrosis factors
  • integral to cell growth and differentiation, inflammation, immunity and repair
64
Q

chemokine

A
  • proteins that stimulate recruitment and migration of leukocytes
  • produced by leukocytes
65
Q

TNF-a

A
  • one of most important cytokines for inflammation
  • from macrophages
  • hemodynamic effects of septic shock
  • cachexia in chronic illnesses
  • elicit acute phase reactions, activate endothelial cells, recruit and activate lymphocytes
  • vascular leakage, chemotaxi
66
Q

IL-1

A
  • one of most impt cytokines in inflammation
  • from macrophages
  • elicit acute phase reaction, activate endothelial cells, recruit and activate lymphocytes
  • vascular leakage, chemotaxis
67
Q

Nitric oxide

A
  • produced by endothelial cells and macrophages in response to an increase in cytosolic calcium or stimulation by cytokines
  • vasodilation, vascular leakage, chemotaxis
  • microbicidal via production of reactive O2 intermediates
68
Q

Lysosomal enzymes

A
  • present in phagocytes
  • primary/azurophil granules-myeloperoxidase, defensins, elastase, lysozyme, acid hydrolases, collagenases
  • secondary/specific granules-lysozyme, gelatinase, histaminase, alkaline phosphatase, collagenase, lactoferrin, plasminogen activator
69
Q

Oxygen derived free radicals

A
  • produced by NADPH system in leukocytes in response to microbes, chemokines, or immune complexes
  • superoxide anion, H2O2, hydroxyl radical, reactive nitrogen intermediates
70
Q

antioxidants

A

ceruloplasmin, superoxide dismutase, and catalase-neutralize oxygen derived free radicals

71
Q

neuropeptides

A
  • stress activates release of neuropeptides from small, unmyelinated sensory fibers
  • substance P and calcitonin gene-related peptide
  • mediate degranulation of macrophages and mast cells -> increase local cytokine [ ] and induce vascular permeability and dilation
  • migraine, asthma, fibromyalgia, derm, pancreatitis, chronic pelvic pain
72
Q

fever

A
  • pyrogens (IL-1 and TNF-a) produced by macrophages induce prostaglandin release by hypothalamus -> reset temp set point
  • may help clear infection
73
Q

Acute phase reactants

A
  • non-specific markers of inflammation

- IL-6 from activated macrophages -> synthesis, primarily in liver

74
Q

C-reactive protein

A
  • acute phase reactant

- marker for acute MI and and other causes of inflammation

75
Q

Fibrinogen

A
  • acute phase reactant
  • makes erythrocytes stick together -> form stacks, fall to bottom of test tube
  • erythrocyte sedimentation rate - increase ESR= more fibrinogen= more inflammation
76
Q

Serum amyloid protein

A
  • acute phase reactant

- brings HDL to macrphages for metabolism (if high, then high macrophage activity)

77
Q

leukocytosis

A
  • elevated WBC (primarily leukocytes) in peripheral blood due to increased release from bone marrow
  • if inflammation severe, may get left shift- presence of immature WBC in circulation
  • mediated by IL-1 and TNF-a from macrophages
  • occasionally see leukopenia
78
Q

Acute phase reaction

A
  • increased pulse, increased BP, sweating, rigor, chills, fever, anorexia, somnolence, and malaise
  • accompany acute inflammatory response and increased acute phase reactants in blood
79
Q

sepsis

A
  • clinical syndrome w/ overwhelming bacterial infection or release of bacterial toxins into blood
  • mediated by certain cytokines (TNF, IL-1)
  • characterized by tachycardia, fever or hypothermia, hyperventilation, and leukocytosis or leukopenia
80
Q

anaphylaxis

A
  • type 1 hypersensitivity allergic reaction to foods, insect, stings, drugs, latex, etc
  • IgE receptor cross linking on mast cells -> degranulation -> increased histamine -> vasodilation (rash, redness, edema) and bronchoconstriction (respiratory distress)
  • medical emergency-epinephrine to bronchodilate and regulate heartbeat
81
Q

Complement deficiencies

A
  • C3-> increased susceptibility to infection

- defective MAC formation -> unable to clear Neisseria infection

82
Q

paroxysmal nocturnal hemoglobinuria

A
  • complement inhibitor deficiency
  • gene mutation controlling complement activation
  • recurrent complement mediate intravascular hemolysis -> chronic hemolytic anemia
83
Q

hereditary angioneurotic edema

A
  • complement inhibitor deficiency
  • C1 inhibitor deficiency
  • skin edema, edema of mucosa of larynx and GI tract
  • provoked by emotional stress or trauma
84
Q

-a1-antitrypsin deficiency

A
  • complement inhibitor deficiency
  • antiprotease in tissues-major inhibitor of neutrophil elastase and others
  • proteases damage tissues-lung-panacinar emphysema- and liver-cholestatic hepatitis-cirrhosis
  • genetic, autosomal recessive mutation in protease inhibitor gene
85
Q

block histamine

A
  • allergic diseases-asthma, allergic rhinitis
  • cromolyn sodium-block histamine release
  • loratadine-block histamine receptor
86
Q

Block arachidonic acid metabolism

A
  • steroids-autoimmune ds, transplantation, asthma
  • acetaminophen, NSAIDs-lots
  • COX-2 inhibitors (Vioxx, celebrex, bextra)-arthritis
87
Q

Block effect of TNF

A

infliximab, etanercept-autoimmune disease (crohns, rheumatoid arthritis)

88
Q

block angiogenesis (VEG-F)

A

bevacizumab-solid tumors (metastatic colorectal cancer, lung cancer)

89
Q

block effect of leukotrienes

A

zafirlukast, montelucast-asthma

90
Q

prostaglandins

A
  • from membrane phospholipids
  • vasodilation, pain, fever
  • potentiate other mediators
91
Q

leukotriene B4

A
  • from leukocytes

- chemotaxis, leukocyte adhesion, activation

92
Q

Leukotriene C4, D4, E4

A
  • from leukocytes, mast cells
  • vascular leakage
  • bronchoconstriction

FM 1 (9 decks)

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