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Pathology > Inflammation and repair > Flashcards

Inflammation and repair Flashcards

1
Q

describe the classic vascular changes and cellular events of the inflammatory rxn

A

vasodilation
increased vascular permeability
accumulation and activation of leukocytes at site of injury

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2
Q

what are the alterations in endothelial barrier during acute inflammation

A

-endothelial contraction (post cap venules )
-endothelial cell retraction ( structural rearrangement of cytoskeleton)
- direct endothelial injury ( necrosis due to bacterial enzymes)
-delayed prolonged response (mech unknown)
-

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3
Q

Mediators of increased vascular permeability : Endothelium derived

A

nitrous oxide -relaxing factor

  • platelet-activating factor
  • prostaglandins
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4
Q

Mediators of increased vascular permeability: mast cell/ basophil degranulation

A

histamine

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5
Q

Mediators of increased vascular permeability: platelets

A

serotonin

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6
Q

Mediators of increased vascular permeability: inflammatory cells

A
  • platelet activating factor , PG and leukotrienes
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7
Q

Rubor and Calor

A

Redness and warmth :

  • due to vasodilation of arterioles which increases blood flow
  • key mediator is histamine which causes a relaxation of arteriolar smooth muscle
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8
Q

Tumor

A

swelling :

due to leakage of fluid from postcapillary venules into the interstitial space (exudate)

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9
Q

dolor

A

pain

bradykinin and PgE2, sensitize sensory nerve ending

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10
Q

Fever

A

pyrogens (LPS from bacteria) cause macrophages to release IL-1 and tNF which increase cyclooxygenase activity in perivascular cells of the hypothalamus
- increase in PGE2 raises temperature set point

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11
Q

describe the steps involved with isolation and destruction of an infectious agent by neutrophils

A
  1. margination -( vasodilation slows blood flow and cells start to flow from center to periphery)
  2. rolling -( selectin “speed bumps” are upregulated on endothelial cells, sialyl Lewis X on Leukocytes bind to the selectin)
  3. Adhesion -( ICAM and VCAM are upregulated on endothelial (TNF and IL-1) . integrins are upregulated on leukocytes (C5a and LTB4) . interact and firm adhesion
  4. transmigration and chemotaxis -( migrate across postcapul venules toward chemotaxis ( IL-8, C5a, LTB4)
  5. phagocytosis -( enhanced by opsonins IgG and C3b)
  6. destruction of phagocytosed material - ( O2 dependent killing is the most effective HOCl from oxidative burst kills microbes . O2 independent killing - enzymes present in leukocyte secondary granules
  7. resolution
    - neutrophils undergo apoptosis and disappear within 24 hrs after resolution of the inflammatory stimulus
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12
Q

mediators of acute inflammation

A 
Toll like receptors ( TLRs) 
Arachidonic acid metabolites 
mast cells 
complement 
Hageman factor (XII)
neutrophils
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13
Q

mediators of acute inflammation : TLRS

A
  • present on cells of the innate immune system ( macro, dendritic)
  • activated by PAMPs
  • CD-14 -> LPS on gram -
  • TLR activation -> upregulation of NK-kappa beta
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14
Q

mediators of acute inflammation - arachidonic acid metabolites

A

AA released from phospholipid cell membrane by phospholipase A2 and acted upon by COX or 5-lipoxygenase
-> COX -> PG
PGI1,PGD2, PGE2 mediate vasodilation and increased vascular perm.

5-lipoxygenase produces leukotrienes
-> LTB4 attracts and activates neutrophils
LTC4, LTD4, LTE4 mediate vasoconstriction, bronchospasm, increase vascular permeability

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15
Q

mediators of acute inflammation : mast cells

A

activated by tissue trauma, complement C3a, C5a or crosslinking of cell surface IgE antigen
immediate response: histamine -> vasodil arterioles, increased vascular perm
delayed response: produced of arachidonic acid metabolites .

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16
Q

mediators of acute inflammation : hageman factors

A

when activated activates coagulation and fibrinolytic systems, complement, kinin system

17
Q

Transudate vs exudate

A

exudate is due to increase capillary permeability ( cloudy a bunch of cells)
transudate is due to increased hydrostatic pressure (clear no cells)

18
Q

Chronic inflammation

A

lymphocytes and plasma cells in tissue

- delayed by more specific

19
Q

granulomatous inflammation

A
  • granuloma - collection of epithelioid histiocytes usually surrounded by giant cells ( langerhans or foreign body) and a rim of lymphocytes
20
Q

repair

A

replacement of dead or damaged cells with vital tissue

21
Q

Labile cells

A

multiply throughout life , epithelial surface cells, lymphoid and hematopoietic cells
small and large bowel ( stem cells in mucosal crypts )

22
Q

stable cells

A

latent capacity to regenerate parenchymal cells of all glands, mesenchymal cells, endothelial ells and smooth muscle cells , liver

23
Q

permanent cells

A

DO NOT DIVIDE after development proliferation has stopped - neurons, myocardial cells

24
Q

granulation tissue

A

macrophages secrete angiogenesis factors which stimulate the growth of solid capillary buds which later form a lumen - edematous tissue rich in nutrients

  • chemotactic and growth factors stimulate the ingrowth and activation of fibroblasts
  • with time inflammatory cells decrease and collagen is laid down, capillaries become less prominent
25
Q

regeneration

A
26
Q

repair

A

replacement of damaged tissue with fibrous scar

  • occurs when regenerative stem cells are lost or when a tissue lacks regenerative capacity
  • granulation tissue is the initial phase of repair
    - fibroblast ( Type III collagen), capillaries ( provide nutrients) , and myofibroblasts ( contract wound)
  • results in scar formation -> Type III-> I
27
Q

mechanism of tissue regeneration

A

paracrine signalling via growth factors ( macrophages secrete growth factors that target fibroblasts)

  • interaction of growth factors with receptors results in gene expression and cellular growth
  • TGF-alpha -> epithelial and fibroblast growth factor
  • TGF-beta -> important fibroblast growth factor; also inhibits inflammation
  • platelet derived growth factor - GF for endothelium, smooth muscle and fibroblasts
  • fibroblast growth factor- important for angiogenesis and skeletal development
  • vascular endothelial growth factor (VEGF)- angiogenesis
28
Q

Basement Membrane VI

A

ubiquitous in microfibrils

29
Q

Basement Membrane VII

A

anchoring fibrils at dermal-epidermal junctions

30
Q

basement membrane IX

A

cartilage , intervertebral disks

31
Q

basement membrane XVII

A

transmembrane collagen in epidermal cells

32
Q

basement membrane V and XVIII

A

endostatin-forming collagens , endothelial cells

33
Q

time course for wound strength

A
  • 7 days post wounding: 5-10% tensile strength of unwounded skin- low collagen content
  • 60-70 days post wounding: 100% collagen but only 30% tensile strength ( type III prominent)
  • 100 days post-wounding: 100% collagen content and 80% if tensile strength increase type I but will never return to organized strength
34
Q

healing by primary union - time course

A

Day 1- blood clot, acute inflammation
Day 2- re-epithelialization of fibrin clot; fibroblast activation
Day 3 - neutrophils replaced by macrophages which debride wound
Day 7- wound covered with normal thickness epidermis; collagenization in granulation tissue
second week- fibroblasts; vessels and collagenization-> wound is red , most inflammatory cells are gone
after second week: increase in collagenization and tensile strength but less strength and elasticity than normal skin

35
Q

Defects in leukocyte adhesion

A

LAD 1 : beta 2 chain of CD11 & CD18 intergins
LAD 2: ligand for E-selectin (sialyl lewix X)

both result in reccurent bacterial infections and impaired wound healing

36
Q

Defects in chemotaxis

A

chediak-higashi( rare, autosomal recessive) disordered microtubule assembly -> impaired locomotion, neutropenia, and defective degranulation

-diabetes mellitus
complement deficiency (C5a)
-chronic renal failure

37
Q

defects in leukocyte function

A

bone marrow suppression leading to leukopenia

38
Q

defects in phagocytosis

A

diabetes mellitus

- deficiency in opsonins -> immunoglobulins or complement ( C3b)

39
Q

defects in microbicidal activity

A

chronic granulomatous disease : nadph oxidase deficiency- cant make superoxide or H202
- x-linked, autosomal recessive

chediak- higashi -> defective granulation
myeloperoxidase deficiency -> mild other routes of killing
severe G6PD deficiency blocks synthesis of NADPH

Pathology (12 decks)

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