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Pathophysiology > Inflammation & Repair -exam 1 > Flashcards

Inflammation & Repair -exam 1 Flashcards

1
Q

Acute inflammation definition

A

response to recent injury or infection

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2
Q

Key events of acute inflammation

A
  • vasodilation
  • profuse capillary leakage
  • infiltration of area by neutrophils
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3
Q

Chronic inflammation definition

A
  • more variable response to ongoing injury or infection

- T-cells, B-cells, macrophages, eosinophils, fibroblasts

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4
Q

Vasodilation

A

increased blood flow - redness and heat

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5
Q

Increased capillary permeability

A
  • leakage of fluid & proteins
  • osmotic water loss - swelling
  • leakage of fibrinogen leads to clotting
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6
Q

Neutrophil infiltration

A
  • margination, emigration, chemotaxix
  • phagocytosis & degranulation - pain
  • monocytes/macrophages appear later (3 days)
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7
Q

Margination

A

neutrophils adhere to capillary walls

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8
Q

Emigration (diapedesis)

A

neutrophils pass through capillary walls

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9
Q

Chemotaxis

A

neutrophils follow chemical signals to damage/infection

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10
Q

Phagocytosis

A

Neutrophils engulf pathogens & debris

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11
Q

Degranulation

A
  • neutrophils can’t engulf pathogen so it vomits it up
  • releases cytoplamic granules
  • frustrated phagocytosis
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12
Q

Diapedesis & chemotaxis driven by..

A

C5a and leukotrienes

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13
Q

Opsonins

A
  • makes pathogen appealing to neutrophils

- enhances phagocytosis

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14
Q

Degranulation releases

A
  • prostaglandins
  • leukotrienes
  • free radicals
  • lysosomal enzymes
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15
Q

Inflammatory mediators

A

chemicals responsible for aspects of inflammation

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16
Q

Inflammatory mediators derived from

A
  • histamine: released from tissue mast cells during injury or infection; vasodilation & capillary permeability
  • Bradykinin: kinin system; vasodilation & capillary permeability; causes pain (bee venoum)
  • complement system: collection of plasma proteins; classical & alternate pathways
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17
Q

Complement proteins

A
  • C3a/C5a - histamine release
  • C5a: chemotaxis
  • C3b: opsonin for phagocytosis
  • C5-C9: membrane attack complex
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18
Q

Arachidonic acid metabolites

A
  • derivative of cell membrane (phospholipids)

- can be converted to prostaglandins or leukotrienes

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19
Q

Prostaglandins causes ….

A
  • decreased vascular tone
  • increased pain
  • increased uterine tone
  • increased temperature
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20
Q

Types of prostaglandins

A
  • thromboxane A2
  • Prostacyclin (PGI2)
  • Prostaglandin E2
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21
Q

Thromboxane A2

A
  • produced by platelets

- vasoconstriction; platelet aggregation

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22
Q

Prostacyclin PGI2

A
  • produced by endothelial cells

- vasodilation, prevents platelet aggregation

23
Q

Prostaglandin E2

A

-vasodilation, potentiates bradykinin (pain), fever

24
Q

Leukotrienes causes…

A
  • smooth muscle contractions (bronchoconstriction)

- neutrophil chemotaxis

25
Q

Types of leukotrines

A
  • Leukotriene C4

- Leukotriene B4

26
Q

Leukotriene C4

A
  • increased capillary permeability
  • breaks down to LTD4 and LTE4
  • smooth muscle contractions
27
Q

Leukotriene B4

A
  • neutrophils & monocyte chemotaxis
28
Q

Monokines

A
  • released from monocytes/macrophages
  • causes a change in body metabolism that occurs during infection/injury -acute phage reaction
  • Interleukin 1 (fever) & tumor necrosis factor alpha (apoptosis)
29
Q

Acute phase reaction

A
  • “sick” from inflammatory illness

- shift in hepatic protein synthesis: increase complement, clotting, C-reactive protein

30
Q

SIRS

A
  • systemic inflammatory response syndrome

- exuberant production of inflammatory mediators: results in multisystem organ failure due to normal tissue damage

31
Q

SIRS criteria

A
  • temp: > 38 C or < 36 C
  • heart rate: >90bpm
  • Respiratory rate: >20/min or Pco2 less than 32 mmHg
  • WBC: > 12,000 or < 4,000
32
Q

Acute inflammation outcomes

A
  • complete resolution: no tissue damage
  • healing by scarring: destroyed tissues replaced by connective tissue (scar)
  • abscess formation: neutrophils wall off infection
  • progression to chronic: neutrophils loose
33
Q

Granulomas

A
  • bodies attempt to wall something off that it can’t destroy

- macrophages adhere to each other to wall off stuff

34
Q

Neutrophils predominant in?

A

infections by common bacteria

35
Q

Lymphocytes predominant in?

A

viral infections

36
Q

Plasma cells predominant in?

A

spirochete diseases (syphilis & lymph disease)

37
Q

Monocyte/macrophages predominant in?

A

tuberculosis and fungal infections

38
Q

Eosinophils predominant in?

A

infection caused by worms

39
Q

Two routes of healing

A
  • regeneration

- repair by fibrous tissues (scar)

40
Q

Regeneration

A

normal cells that were destroyed gets replaced by new normally functioning cells

41
Q

Repair by fibrous tissues

A

normal cells that were destroyed get replaced by new tissue that is not normally functioning cells

42
Q

Labile cells

A
  • constantly divide

- most epithelium

43
Q

Stable cells

A
  • don’t regenerate constantly as part of normal cycle, but can regenerate if needed
  • glandular cells, fibroblasts, endotherlium, osteroblasts, liver cells
44
Q

Permanent cells

A
  • do not regenerate

- gila, neurons, heart

45
Q

Damaged epithelium repair

A

-stimulates mitosis to grow towards each other

46
Q

How connective tissue replaces permanent cells

A
  1. fibroblasts proliferate
  2. endothelial cells proliferate
  3. both invade and displaces the clot that forms on top
47
Q

Maturing scar

A
  • enough collagen to fill the void
  • re-epithelialization completes
  • Type III collagen replaced by type I
  • Fibroblasts contract and return to rest (reduction of scar)
  • most new vessels resorb
48
Q

Primary intention repair

A
  • ideal situation for wound healing
    1. minutes: clotting cascade activated, stops the bleeding
    2. 24 hrs: neutrophils enter, epithelial cells are regenerating from the edges
    3. 3 days: macrophages enter, granulation tissue appears, epithelial cells now cover the wound surface
    4. 5 days: granulation tissue fills the entire wound
    5. 2 weeks: fibroblasts multiply, collagen accumulates
    6. 4 weeks: overlaying epidermis complete scans adnexal structures, capillary involved and scar contraction occurring, red scar turns white
49
Q

Secondary intention repair

A
  • no approximation
  • larger scab, more inflammation, possible infection, more granulation
  • complete re-epithelialization pushes off scab
  • much longer to complete healing
  • always produces deformity
50
Q

Types of wound healing alterations

A
  • contracture: fibroblasts contract too much (burn)
  • hypertophic scar: exuberant scar tissue formation; stays within original wound margin
  • keloids: exuberant scar tissue formation; goes beyond wound margins; more prevalent in darker skin tones
51
Q

Hindrances to healing

A
  • Not old age alone
  • inadequate nutrition
  • poor blood supply
  • foreign bodies
  • infection
  • Glucocorticoid (steroid) therapy
52
Q

Phospholipase A2

A
  • liberates arachiodonic acid to from cell membrane

- inhibited by steroids

53
Q

Cyclooxygenase

A
  • converts arachiodonic acid to prostaglandins

- inhibited by aspirin and NSAIDs

54
Q

5-lipoxygenase

A
  • converts arachiodonic acid to leukotrienes

- various inhibitors

Pathophysiology (5 decks)

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