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Pathology > Acute and chronic inflammation > Flashcards

Acute and chronic inflammation Flashcards

1
Q

Inflammation

A

Reaction to injurious agents that limits damage and promotes repair, mediated by vessels and blood cells, tightly regulated chain of molecular and cellular events, categorized as acute or chronic based on duration of response and types of cells involved

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2
Q

Neutrophils

A

Major constituent of white blood cells
Segmented nuclei
Motile, granular phagocytes
Primary responder in acute inflammation

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3
Q

Leukocytes

A

Single nucleus, scant cytoplasm
Divided into B cells, T cells, NK cells
Produce antibodies, cytokines, toxic granules
Primary cell type in chronic inflammation

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4
Q

Macrophages

A

Motile phagocytes

Bridge innate-> acquired inflammation by recognizing opsonized particles and presenting via MHC Class II receptors

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5
Q

Macrophage activation

A

Non-immune: activation by endotoxin, fibronectin, chemical mediators of inflammation
Also activated by cytokine IFN-y

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6
Q

Eosinophils

A

Bi- or tri-lobed nucleus, cytoplasm with eosinophilic granules
Granules contain histamine, proteolytic enzymes, major basic protein
Involved in inflammatory reactions to allergens and parasites

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7
Q

Basophils (mast cells)

A

Bilobed nucleus obscured by basophilic granules containing histamine, proteoglycans, proteolytic enzymes

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8
Q

Granulocytes

A

Neutrophils, eosinophils, basophils

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9
Q

Mononuclear cells

A

Lymphocytes, macrophages

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10
Q

Steps in acute inflammation

A
  1. changes in vascular flow and permeability
  2. leukocyte recruitment and activation (adhesion, transmigration, activation, phagocytosis, release of products)
  3. Sequelae of inflammation (resolution, scar formation, chronic inflammation)
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11
Q

Vasoactive mediators of vascular permeability

A

histamine, bradykinine, substance P, IL-1, TNF, IFN-y

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12
Q

Leukocyte adhesion

A

Stasis, margination, adherence (selectins on endothelium loosely bind to S-L X mod glycoprotein then ICAM1/ VCAM1 on endothelium loosely bind to intigrins)

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13
Q

Leukocyte chemotactic agents

A

exogenous agents, C5a, LTB4, IL-8

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14
Q

Phagocytosis: regognition

A

mannose and fucose residues on microbial cell walls but not host cells; opsonization by IgG or C3b aids

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15
Q

Phagocytosis: killing

A
  • oxygen dependent: NADPH oxidation produces hydroxyl radical that is converted to hypochlorite by myeloperoxidase
  • oxygen independent: substances in leukocyte granules
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16
Q

regurgitation during feeding

A

phagolysosome remains open to outside after fusion

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17
Q

frustrated phagocytosis

A

leukocyte attaches to immune complexes fixed on tissues, so they cannot be phagocytosed

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18
Q

cytotoxic release

A

leukocyte ingests a substance that damages its cell membrane (ex uric acid crystals)

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19
Q

exocytosis

A

lysosomal granules secreted to outside of cell

20
Q

serous inflammation

A

thin watery transudate exuded at site of injury

21
Q

fibrinous inflammation

A

clear fluid plus fibrinogen escapes the vessel causing polymerization to form a thick fibrin coat. characteristic of inflammation of lining of body cavities

22
Q

suppurative/ purulent inflammation

A

production of pus composed of neutrophils, necrotic cells, and edema fluid. characteristic in infection with pyogenic bacteria

23
Q

pseudomembranous inflammation

A

characteristic overgrowth of colonic C diff or fungi (secondary to antibiotics/ immunosuppression) causing a film over mucosa made up of inflammatory cells, necrotic epithelium, fibrin, mucus

24
Q

ulcer

A

destruction of an epithelial lining due to ischemic damage or infection

25
Q

gangrene

A

tissue necrosis secondary to interruption of blood supply due to trauma, infection, or thrombosis

26
Q

non-specific chronic inflammation

A

mononuclear cell infiltration, tissue destruction, fibrosis

27
Q

granuloma

A

collection of activated macrophages (“epithelialized”) surrounded by a collar of lymphocytes with or without central caseation and giant cells
- limited ddx: TB, leprosy, brucellosis, cat scratch disease, fungi, foreign insoluble objects, sarcoidosis

28
Q

Complement system: classical pathway

A

antigen-antibody complex activates C1, initiating complement cascade

29
Q

Complement system: alternative pathway

A

microbial surface molecules or Factor XII directly activate C3

30
Q

Complement system: lectin pathway

A

plasma lectin bound to mannose on bacterial surface activates C1, initiating the complement cascade

31
Q

C5a

A

chemotactic; causes vasodilation by stimulating histamine release

32
Q

C3a

A

causes vasodilation by stimulating histamine release

33
Q

C3b

A

opsonin

34
Q

kalikrein

A

converts high molecular weight kininogen to bradykinin; directly activates C5 to C5a; activates Factor XII (autocatalytic amplifiers)

35
Q

thrombin

A

links the clotting cascade and inflammation: causes mobilizaation of selectins, change in endothelial cell shape, production of chemokines, induction of arachidonic acid pahtway, production of platelet factor and NO

36
Q

plasmin

A

fibrinolytic and inflammatory roles:

  • directly cleaves C3 to form C3a
  • activates Factor XII, promoting kinin and clotting cascades
  • forms fibrin split products by breaking fibrin, which augment vascular permeability
37
Q

platelet activating factor

A
  • derived from phospholipids, produced in platelets, macrophages, neutorphils, basophils, endothelial cells
  • cause platelet aggregation, vasodilation, bronchoconstriction, leukocyte adhesion, chemotaxis, degranulation, oxidative burst, potentiation of arachidonic acid metabolism
38
Q

primary lysosomal granules

A

contain myeloperoxidase, definsins, elastase, lysozyme, acid hydrolases, collagenases.
release contents into lysosomes

39
Q

secondary lysosomal granules

A

contain lysozyme, gelatinase, histaminase, alkaline phosphatas, collagenase, lactoferrin, plasminogen activator
release to extracellular space more readily than primary granules

40
Q

defects in leukocyte adhesion

A
  • genetic deficiencies LAD types 1 and 2 –> recurrent bacterial infection, impaired wound healing
41
Q

Chediak-Higashi syndrome

A
  • neutropenia, defective granulation, delayed microbial killing
  • abnormalities in melanocytes (albanism), nerve cells, platelets (bleeding disorders)
  • giant lysosomal granules in neutrophils
42
Q

chronic granulomatous disease

A

defects in oxygen-dependent microbicidal activity due to defect in genes encoding for NADPH oxidase-> recurrent bacterial infection

43
Q

Complement C3 deficiency

A

increased susceptibility to infection; inability to form MAC-> unable to clear infection by Neisseria

44
Q

paroxysmal nocturnal hemoglobinuria

A
  • mutation in genese controlling complement activation

- recurrent complement-mediate intravascular hemolysis, hemolytic anemia

45
Q

hereditary angioneurotic edema

A
  • genetic deficiency of C1 inhibitor

- edema of skin and mucosa of larynx and GI tract provoked by emotional stress or trauma

46
Q

a1-antitrypsin deficiency

A
  • a1-antitrypsin is a major inhibitor of elastase, proteases from neutorphils
  • lack of antiprotease-> digestion of extracellular tissue-> emphsema, cholestatic hepatitis leading to cirrhosis, variable expression

Pathology (7 decks)

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