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U8 Pathology > Inflammation and Repair > Flashcards

Inflammation and Repair Flashcards

1
Q

What does the presence of exudate imply?

A

there is an increase in the permeability of small blood vessels triggered by some sort of tissue injury and ongoing inflammation reaction

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2
Q

What is transudate?

A

fluid with low protein content

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3
Q

What promotes vascular leakage when released?

A

Vascular Endothelial growth factor–VEGF

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4
Q

What are Weibel -Palade Bodies and what do they produce?

A

Located in venular endothelial cells–glue factory of endothelial cells

Synthesize

  • -P-selection- adhesion molecule for leukocytes
  • -von Willebrand factor- adhesion molecule of the platelet
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5
Q

What do IL-1 and THF cytokines cause?

A

expression of L-selectins on surface of neutrophils and E/P-selectins on venular endothelial cells

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6
Q

What does C5a and LTB4 activate?

A

B2-integrins on the surface of neutrophils

also attracts neutrophils

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7
Q

What is neutrophilic leukocytosis and how does it occur?

A

Increase in peripheral blood neutrophils caused by inhibition of neutrophil B2-integrins

–Catecholamines and corticosteroids cause this

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8
Q

What causes adhesion of the leukocyte to the endothelial wall?

A

Expression of B2-integrins(Ligand) on the neutrophil and expression of VCAM/ICAM on endothelial surface

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9
Q

What is Leukocyte adhesion deficiency Type 1?

A

Deficiency of B2-integrin–neutrophils can’t adhere to endothelium

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10
Q

What is Leukocyte adhesion deficiency Type 2?

A

deficiency of an endothelial cell selection that normally binds neutrophils

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11
Q

What are the clinical findings seen in leukocyte adhesion deficiency?

A

Early sign–Delayed separation of umbilical cord–neutrophil enzymes important in cord separation
Other findings– gingivitis/poor wound healing/peripheral blood neutrophilic leukocytosis

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12
Q

What are some chemotaxis that attract neutrophils after transmigration?

A

IL-8/C5a/LTB4

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13
Q

What is Bruton agammaglobulinemia?

A

opsonization defect–pre-B cells cannot mature to B-cells–cannot synthesize IgG

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14
Q

What is Chediak-Higshi syndrome?

A

defect in microtubule function–prevents lysosomes from fusing with phagosomes to produce a phagolysosome

  • -increased risk of pyogenic infections
  • -Neutropenia
  • -Giant granules in leukocytes
  • -Albinism
  • -Peripheral neuropathy
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15
Q

What is Chronic granulomatous disease and what does it lead to?

A

NADPH oxidase defect– leads to recurrent infection and granuloma formation with catalase-positive organisms

  • -Staph aureus
  • -Pseudomonas cepacia

NBT– abnormal–colorless because superoxide cannot be formed

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16
Q

What is MPO deficiency and what are pts at increased risk of?

A

defective conversion of H2O2 to HOCl
–increased risk for Candida infections

NBT test normal–turns blue because superoxide can be formed

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17
Q

What are the plasma derived factors that cause increased vascular permeability?

A

Hageman factor activation

Complement system activation

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18
Q

What are the cell derived factors that cause increased vascular permeability?

A

Mast cell degranulation–histamine
platelets–serotonin
inflammatory cells
endothelium

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19
Q

What acute inflammatory mediators cause Vasodilation?

A

Histamine
NO
PGI2

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20
Q

What acute inflammatory mediators cause vasoconstriction?

A

TXA2

LTC4/D4/E4

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21
Q

What acute inflammatory mediators cause increased venular permeability?

A 
histamine
bradykinin
LTC4
LTD4
LTE4
C3a
C5a
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22
Q

What acute inflammatory mediators cause pain?

A

PGE2

Bradykinin

23
Q

What acute inflammatory mediators cause fever?

A

PGE2
IL-1
TNF

24
Q

What acute inflammatory mediators are chemotaxis?

A

C5a/LTB4/IL-8

25
Q

What mediates liver synthesis of acute phase reactants?

A

IL-6

26
Q

What are the 3 complement pathways and how do each function?

A

Classical– Cl binds IgG and IgM
Alternative– microbe activates complement
Lectin– Mannose binds MBL–activates complement

27
Q

What complement is responsible for opsonin for phagocytosis?

A

C3b

28
Q

What complement is responsible for chemotaxis for neutrophils?

A

C5a

29
Q

What complements are responsible for anaphylatoxins–histamine-mediated vasodilation and vascular permeability?

A

C3a

C5a

30
Q

What complement is responsible for Mac–lysis of microbe?

A

C5b

31
Q

What is serous inflammation and what are examples?

A

exudation of cell-poor fluid

Blister in 2nd degree burns and viral pleuritis

32
Q

What is Fibrinous inflammation and what are examples?

A

increased vessel permeability–>deposition of a fibrin-rich exudate on surface of tissue

Leads to scar tissue formation in pericardium/peritoneum/pleura

33
Q

What is Purulent inflammation and what are examples?

A

localized proliferation of pus-forming organisms—s.aureus
—exudate consisting of–neutrophils/liquefied debris of necrotic cells/edema fluid

Appendicitis and abscesses

34
Q

What is Pseudomembranous inflammation and what are examples?

A

ulcer–bac toxin-induced damage to the mucosal lining —shedding of inflamed necrotic tissue

Peptic ulcers in stomach/duodenum
C. Diff infection

35
Q

What are the 3 typical outcomes to acute inflammation?

A

resolution
scar formation
progression into chronic inflammation

36
Q

What are the two pathways of macrophage activation and what does each do?

A

Classical–kill ingested organism

Alternative– tissue repair

37
Q

What is noncaseating granulomas and what are examples?

A

Lack central necrosis

Cat scratch dz/ sarcoidosis/crohns dz

38
Q

What is caseating granulomas and what are examples?

A

Exhibit central caseous necrosis due to lipid released from cell wall of dead pathogens

TB and fungi infection

39
Q

What is VEGF and how is it stimulated?

A

Stimulates angiogenesis —stimulated by TNF released from macrophages–hypoxia inducible factor released by cells

40
Q

What is Fibroblast growth factor (FGF)?

A

Chemotactic for fibroblasts

41
Q

What is Epidermal growth factor (EGF)?

A

Stimulates keratinocyte migration

granulation tissue formation

42
Q

What is Platelet-derived growth factor (PDGF)?

A

Chemotactic for neutrophils/macrophages/fibroblasts/endothelial cells/smooth muscle cells

43
Q

What is Transforming growth factor-B (TGF-B)?

A

Chemotactic for macrophages/lymphocytes/fibroblasts/smooth muscle cells

44
Q

What are the components of granulation tissue?

A

Fibroblasts– deposit type 3 collagen
capillaries– supply nutrients
myofibroblasts– contract wound

45
Q

What is required for dense scar tissue production–Collagen III–> collagen I?

A

Metalloproteinase–collagenase+ zinc

46
Q

What is wound healing by primary intention?

A

wound edges brought together–suturing

47
Q

What is would healing by secondary intention?

A

edges not approximated and granulation tissue fills defect–myofibroblasts contract wound and scar forms

48
Q

What is would healing by tertiary intention?

A

contaminated wound–stays open for debridement and antibiotic treatment–then closed

49
Q

How does a Vit C deficiency affect wound healing?

A

important cofactor in hydroxylation which is necessary for collagen cross-linking

50
Q

How does a copper deficiency affect wound healing?

A

important cofactor for lysyl oxidase–cross links lysine to hydroxylysine to form stable collagen

51
Q

How does a zinc deficiency affect would healing?

A

Zinc cofactor for collagenase–replaces type III collagen with type I collagen

52
Q

What is Dehiscence?

A

rupture of a wound–most commonly seen after abdominal surgery

53
Q

What does corticosteroid therapy cause and why?

A

Absolute neutrophilic leukocytosis–they inhibit activation of neutrophilic adhesion molecules

54
Q

What is C-reactive protein and what is it used for?

A

Acute phase reactant

Very sensitive indicator of necrosis associated with AI

U8 Pathology (3 decks)

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