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FM1- Pathology > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

(1) What are the 4 cardinal signs of inflammation?

A

rumor (redness), tumor (swelling), calor (heat), dolor (pain)

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2
Q

(1) Define inflammation.

A

a reaction to injurious agents that limits damage and promotes repair

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3
Q

(2) Cite the difference between innate and acquired immunity.

A

innate is a non-specific response like physical barrier or inflammation; acquired immunity is a response to a specific agent, mediated by antibodies

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4
Q

(3) List injurious agents that elicit inflammatory reactions. (6)

A 
trauma
physical and chemical toxins
tissue necrosis (powerful)
foreign bodies
immune reactions
on-going inflammation
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5
Q

(4) Describe the morphology, normal location, source and role in inflammation of a neutrophil.

A

a granulated cell with segmented nuclei, a motile phagocyte

are the primary cell responder of acute inflammation (neutrophilic infiltration within day(s))

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6
Q

(4) Describe the morphology, normal location, source and role in inflammation of a lymphocyte.

A

slightly bigger than RBC, with scant cytoplasm; several types include B, T and NK cells, their role is to produce antibodies, cytokines or toxic granules to eliminate invaders; primarily cell involved in chronic inflammation (help eliminate foreign material from the body through production of antibodies and toxic granules

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7
Q

(4) Describe the morphology, normal location, source and role in inflammation of a moncyte/macrophage.

A

granulated (toxic substances) cell with a horse-shoe shaped nucleus; represent a link between innate and acquired immune response as an antigen presenting cell; develop in bone marrow, migrate to tissues

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8
Q

(4) Describe the morphology, normal location, source and role in inflammation of a basophil/mast cells.

A

granulated cells with obscured bilobed nucleus, granules contain histamine (vasodilator), proteoglycans, protelytic enzymes and lipid mediators of inflammation (involved in anaphylaxis and allergic/hypersensitivity runs);

usually located near blood vessels and along mucoasae/dermis

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9
Q

(4) Describe the morphology, normal location, source and role in inflammation of a platelets.

A

formed form large megakaryocyte, (large nucleus, and large cytoplasm) in the bone marrow by production of anucleated cytoplasm fragments; platelets contain machinery and granules with platelet activating factor

primarily involved in hemostasis, contain platelet activating factor

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10
Q

(5) Name the two classes of chemical mediator of inflammation.

A 
plasma-derived (precursor forms that have to be activated)
cell derived (sequestered in cell organelles or produced upon stimulation)
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11
Q

(5) Name some examples of plasma-derived mediators of inflammation. (4)

A

factor 12, complement proteins, kinins, clotting proteins

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12
Q

(5) Name some examples of cell-derived mediators of inflammation. (5)

A

vasoactive amines (histamine, serotonin)
arachidonic metabolites (prostaglandins, leukotrienes, lipoxins)
cytokines and chemokines
nitric oxide
lysosomal contents (granules classified as azurophil/primary granules, spefici/secondary are phagolysosomes)
oxygen-derived free radicals

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13
Q

(6) How are acute and chronic inflammation differentiated?

A

by the cell type that predominates, neutrophils in acute, macrophages in chronic

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14
Q

(7) Discuss the two types of vascular change that are caused by inflammatory mediators.

A

changes in vascular caliber (and flow)

increased vascular permeability (contraction of epithelial cells due to histamine release)

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15
Q

(7) What causes the cardinal sign rumor?

A

stasis of blood in effective area due to dilation of pre and post capillaries

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16
Q

(7) Name 3 primary vasoactive mediators. (bonus name 3 cytokines that cause constriction of endothelial cells) ** know this**

A

histamine, bradykinin and substance P

IL-1, TNF, IFN-y

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17
Q

(8) Outline the basic cellular events in inflammation (5).

A
  1. leukocyte adhesion and transmigration
  2. chemotaxis
  3. Leukocyte activation
  4. phagocytosis
  5. release of leukocyte products
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18
Q

(8) Describe the steps of leukocyte adhesion, transmigration, and tissue migration.

A

in damaged tissue, blood stasis and loss of endothelial charge cause the leukocyte to roll across the endothelium

Sialyl-lewis X modified glycoprotein are low affinity and serve to slow the leukocyte down

cytokines released induce integrin ligands (ICAM-1, VCAM-1) and chemokines stimulate expression of proteoglycans on the endothelial surface

protoglycans induce integrins on leukocyte to become higher affinity causing a firm bond with selectin receptors

WBC squeezes into endothelial gaps (diapedesis) extending pseudopods, guided by PECAM-1 and migrate to the site of injury via chemotaxis which bind G protein coupled receptors in leukocyte cell membrane

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19
Q

(10) GIve 3 examples of chemicals sensed by WBC in chemotaxis.

A

complement products (C5a), products of lipoxygenase pathway (LTB4) and cytokines (IL-8)

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20
Q

(12) During leukocyte activation, the receptors on the cell surface can mediate the leukocyte response to injurious stimuli, including…

A

phagocytosis
secretion of cytokines
modulation of leukocyte adhesion molecules
production of arachidonic acid metabolites

(receptors include Toll-like receptors, Mannose receptor to initiate response)

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21
Q

(13) Describe the steps of phagocytosis. (3)

A
  1. mannose receptor recognizes antigens on microbial walls (glycoproteins and glycolipids); recognition and attachment are enhanced with opsonization by IgG or C3b or plasma lectins
  2. engulfment of foreign material creating a phagosome which fuses with lysosome for enzymatic digestion
  3. killing and degradation are accomplished by oxygen-dependent or independent mechanism (myloperoxidase creates free radical or by enzymatic digestion); degradation completed by acid hydrolyses
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22
Q

(14) Leukocyte products can be harmful to the host if released into the tissue in the following situations

A

regurgitation during feeding
frustrated phagocytosis
cytotoxic release (ingested damages cell membrane)
exocytosis –> can cause disease

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23
Q

(14) What diseases could result form the release of leukocyte products?

A

arthritis, acute transplant rejection, glomerulonephritis, vasculitis, atherosclerosis, asthma, gout

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24
Q

(9) List the leukocyte ligands for E-selectin, ICAM-1 and VCAM-1; describe the role of CD31.

A

Sialyl-lewis X modified glycoprotein and integrin ligands, PECAM-1 (CD31) is responsible for guiding the leukocyte out of the blood vessels

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25
Q

(15) Describe serous inflammation.

A

thin, watery fluid is exuded (plasma fluid that leaks from the vessel) at site of injury ie. burn blister

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26
Q

(15) Describe fibrinous inflammation.

A

clear fluid AND fibrinogen escape the vessel and the fibrinogen polymerizes to form a fibrin coat (common in body cavities- surface of cavity becomes rough and granular)

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27
Q

(15) Describe supurative/purulent inflammation.

A

a characteristic response to pygenic bacteria, results in production in large amounts of pus composed of neutrophils, necrotic cells and edema fluid

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28
Q

(15) Describe pseudomembranous inflammation.

A

overgrowth of C.diff or fungi, secondary to broad spectrum antibiotic use or immunosuppression in the colon where inflammatory cells, necrotic epithelium, fibrin and mucus form a thick film over the mucosa

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29
Q

(15) Describe an ulcer.

A

destruction of an epithelial lining, due to ischemia or infection

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30
Q

(15) Describe gangrene.

A

tissue necrosis secondary to interruption of the blood supply by trauma, infection or thrombosis; necrotizing bacterial infection can be superimposed

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31
Q

(15) Name some of the important characteristics of acute inflammation which are important in its termination.

A

mediator short half life
mediators are release in rapid bursts and rapidly degraded
mediators produce their own stop signals

32
Q

(17) Describe the relationship between acute and chronic inflammation.

A

if the offending agent is not cleared during acute response, chronic inflammation can persist ie. TB, diabetic foot ulcer; this also occurs with prolonged toxin exposure or autoimmune reaction.; chronic inflammation is the link between acute and acquired immunity responses

33
Q

(18/19) List the 3 main events of chronic inflammation and principle cell type involved.

A

mononuclear cell infiltration
tissue destruction
fibrosis

34
Q

(20) Describe how macrophages become activated, and what activated macrophages do. **

A

macrophages recognize antigens through cell surface receptors and are activated to act as antigen presenting cells

35
Q

(21) What is a granuloma?

A

distinct organization within the tissue of activated macrophages, surrounded by lymphocytes, may be necrotic at center; it is used to wall off foreign substances that cannot be destroyed; can be accompanied by giant cells

36
Q

(22) Identification of granulomas limits the diagnosis to which conditions?

A

infectious: TB, leprosy, brucellosis, cat-scratch disease or fungi
foreign (insoluble objects)
sarcoidosis

37
Q

(23) What are the causes and symptoms of sepsis?

A

? sepsis is system level inflammatory response, characterized by high fever, increase HR and respiratory rate, signs of organ failure

38
Q

(24) Compare and contrast resolution and scar.**

A

resolution is replacement of dead cells by cells that were normally there before the inflammatory process, scar is replacement of damaged tissue by fibrous tissue

39
Q

(25) Describe what types of cells release histamine and seratonin and what are the effects? (vasoactive amines)

A

histamine by mast cells, basophils or platelets, causes dilation and permeability of vessels

seratonin by platelets and enterochromaffin cells, released when platelets aggregate and causes increased vessel permeability

40
Q

(25) What three interrelated systems participate in plasma protein mediation of inflammation.

A

complement system, kinin system, and clotting system

41
Q

(25) Arachidonic acid metabolites

A

produced by platelets, vascular edothelilum and mast cells; leukotrienes are more potent than histamine in promoting vascular permeability; metabolites contribute to all 4 cardinal signs

42
Q

(25) platelet activating factor

A

PAF is derived from phospholipids and is produced by platelets, basophils/mast cells, neutrophils, monocytes/macrophages and endothelial cells

action is via a specific G-protein coupled receptor on effecter cells (elicits most of the cardinal features of inflammation)

43
Q

(25) Contrast cytokines and chemokines.

A

cytokines are proteins that modulate the function of there cell types (in inflammation TNF-1, IL-1); chemokine stimulates leukocyte recruitment and migration (maybe expressed constitutively or specifically)

44
Q

(25) Nitric oxide

A

NO by endothelial cells causes constitutive dilation
NO by phagocytes is a free radical
NO is also produced in the brain

45
Q

(25) How do hypoxia and necrotic cells act in the inflammatory process?

A

they are powerful pro-inflammatory stimulants

46
Q

(25/29) Oxygen-derived free radicals

A

produced by leukocytes in response to microbes, chemokines, or immune complexes; causes destruction of phagocytose microbes and potentiation of inflammatory response

47
Q

(25) Neuropeptides mediate the degranulation of macrophages and mast cells in neurogenic inflammation, name their names.

A

in response to psychological stress small sensory nerves release pro-inflammatory neuropeptides (substance P, calcitonin gene related protein) and is linked to systemic stress response mediated by CRF

48
Q

(26) What role does the complement system play in inflammatory response?

A

20 proteins produced in the liver which circulate in their inactive form in the plasma;
can be activated by classical (antigen-antibody/C1q binding), lectin (lectin bound to mannose on bacteria surface) or alternative pathways (microbial surface molecules direct C3 activation) which converge on C3 convertase

C3 convertase generates C3a, C3b and C5a which amplify the response and can generate an attack complex

49
Q

(26) What are the roles of C3b, C5a and C3a in the inflammation process.

A

C3b participates in opsonization
C5a and C3a (anaphylatoxins) have action in vasodilation and permeability
C5a in chemotaxis and activation of arachidonic acid metabolism

50
Q

(26) Where do most complement control proteins act?

A

at the level of convertase

51
Q

(26) Discuss the molecules and enzymes in the kinin system.

A

prekallikrein is converted to kallikerin by factor XII

high molecular weight kininogen is converted to bradykini by kallikrein

52
Q

(26) What is the activity of bradykinin

A 
dilates vessels and increases permeability
causes pain  (bradykinin is very potent, cleared by kinases such as ACE in the lung)

*not kallikrein directly activates C5 and C5a in the complement pathway and acts as a autocatalytic amplifier

53
Q

(26) Describe the activation and product of the clotting system.

A

factor XII is activated by collagen, injured basement membrane and activated platelets;

the product is thrombin which binds to G-protein coupled receptors on platelets, endothelial cells and smooth muscle causing mobilization of selections, change in endothelial shape, production of chemokines and induction of arachidonic acid, production of PAF an NO

54
Q

(26) Name 4 enzymes that inhibit the activity of various enzymes in the clotting cascade.

A

antithrombins, protein C and S and tissue factor pathway inhibitor

55
Q

(26) Name the 4 most important mediators of inflammation in vivo.

A

bradykinin, C3a, C5a and thrombin (kallikrein and plasmin amplify the inflammatory response by activating factor XII)

56
Q

(27) Name the 4 systems of inflammation initiated by factor XII.

A

kinin, clotting, fibrinolytic and complement systems

57
Q

(26) What role do arachidonic acid metabolites play in inflammation?

A

synthesized from cell membrane lipids, metabolites bind G-coupled receptors; they are produced by the cyclooxygenase or lipoxygenase pathways and are blocked by steroids (de-esterifyies arachidonic acid), aspirin, NSAIDs and COX-2 inhibitors (inhibit the cyclooxygenase pathway)

58
Q

(23) Which compounds mediate the hemodynamic effects of sepsis specifically?

A

IL1 and TNF (TNF is also responsible for cachexia)

59
Q

(23) What are the symptoms of sepsis?

A

fever, acute phase proteins, leukocytosis, increased pulse, pressure, wetting, rigors, chills, lethargy

60
Q

(31) Discuss several examples of deranged inflammation.

A

defects in leukocyte adhesion, defects in phagolysosome function (ie.Chediak-Higashi syndrome), defects in oxygen dependent microbicidal activity (chronic granulomatous disease), bone marrow suppression (primary or secondary)

61
Q

(31) Discuss anaphylaxis.

A

inappropriate engagement of the inflammation in reaction to allergens- type I hypersensitivity allergic reaction due to the massive release of histamine (vasodilation and bronchoconstriction)

62
Q

(31) What occurs in complement deficiencies?

A

decreased C3 means increased susceptibility to infection, can lead to defective formation of membrane attach complex

63
Q

(31) What occurs during complement inhibitor deficiencies (ie. paroxysmal nocturnal hemoglobinura or hereditary angioneurotic edema)?

A

mutation in genes controlling complement activation leading to recurrent complement mediated intravascular hemolysis

genetic deficiency of C1 inhibitor causes edema of skin and mucosa of larynx/GI tract due to emotional stress or trauma

64
Q

(31) What is a1-antitrpysin deficiency

A

normally acts as a anti protease, so sustained action of elastases causes digestion of extracellular tissues (often effecting the lungs- panacinar emphysema and liver-cholestatic hepatitis)

65
Q

(32) Efforts to treat allergic diseases have resulted in what treatments?

A

blocking of histamine release (cromolyn sodium) or blocking of histamine receptor (loratadine)

66
Q

(32) How have treatments been developed to stop the metabolism of arachidonic acid?

A

steroids used in autoimmune, transplantation and allergy
aspirin and NSAIDs use din arthritis etc.
COX-2 inhibitors are also used in arthritis (IL-1 blockers may also treat)

67
Q

(32) What are the clinical effects of trying to block the effects of TNF?

A

used to treat autoimmune diseases like Chron’s or rheumatoid arthritis

68
Q

(4) Describe the morphology, normal location, source and role in inflammation of a eosinophil.

A

bi or trilled nucleus, cytoplasm filled with granules of mediators of inflammation and proteolytic enzymes, involved primarily in run to allergens and parasites

69
Q

(6) What class of immune cells are characteristic of acute v. chronic inflammation?

A

acute: granulocytes (neturophils, eosinophils, basophils/mast cells)

chronic inflammation: mononuclear cells (macrophages, lymphocytes and plasma cells)

70
Q

(8) What induces the transport of selections of endothelial cells from intracellular organelles to the cell surface

A

cytokines produced by macrophages at the site of inflammation induce transportation of selectins

71
Q

(26) What does activation of thrombin induce in the vascular system?

A

mobilization of selectins to endothelial cells
change in endo cell shape to open gap junctions
metabolism of arachidonic acid
production of cytokines, PAC and NO

72
Q

(26) Plasmin as part of fivrinolytic system causes what other actions within the inflammatory reaction?

A

directly cleaves C3
activates Factor XII
splits fibrin products, augmenting vascular permeability

73
Q

(30) Which leukotrienes are known as the slow-reacting substances of anaphylaxis?

A

leukotrienes C4,D4 and E4, important in inflammatory process of allergic reactions (can cause bronchospasm)

74
Q

(26) Name the two pathways to eicosanoid production.

A

cyclooxygenase pathway (produces prostaglandins and thromboxane)

lipozygenase pathway (produces leukotrienes and lipoxins

75
Q

(30) Name pyrogens produce by macrophages to stimulate the release of prostaglandin’s in the hypothalamus in stimulating fever.

A

IL-1 and TNF-a

76
Q

(30) Name 3 serum non-specific acute phase reactants use in markers of inflammation. (produces primarily in response it IL-6)

A

c-reactive protein
fibrinogen/erythrocyte sedimentation rate
serum amyloid protein

77
Q

(33) Define leukocytosis, left shift and leukopenia.

A

leukocytosis: elevated WBC count
left shift: in severe inflm. response, the increased presence of immature WBC
leukopenia- decrease WBC

FM1- Pathology (6 decks)

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