Inflammation & Repair -exam 1 Flashcards
1
Q
Acute inflammation definition
A
response to recent injury or infection
2
Q
Key events of acute inflammation
A
- vasodilation
- profuse capillary leakage
- infiltration of area by neutrophils
3
Q
Chronic inflammation definition
A
- more variable response to ongoing injury or infection
- T-cells, B-cells, macrophages, eosinophils, fibroblasts
4
Q
Vasodilation
A
increased blood flow - redness and heat
5
Q
Increased capillary permeability
A
- leakage of fluid & proteins
- osmotic water loss - swelling
- leakage of fibrinogen leads to clotting
6
Q
Neutrophil infiltration
A
- margination, emigration, chemotaxix
- phagocytosis & degranulation - pain
- monocytes/macrophages appear later (3 days)
7
Q
Margination
A
neutrophils adhere to capillary walls
8
Q
Emigration (diapedesis)
A
neutrophils pass through capillary walls
9
Q
Chemotaxis
A
neutrophils follow chemical signals to damage/infection
10
Q
Phagocytosis
A
Neutrophils engulf pathogens & debris
11
Q
Degranulation
A
- neutrophils can’t engulf pathogen so it vomits it up
- releases cytoplamic granules
- frustrated phagocytosis
12
Q
Diapedesis & chemotaxis driven by..
A
C5a and leukotrienes
13
Q
Opsonins
A
- makes pathogen appealing to neutrophils
- enhances phagocytosis
14
Q
Degranulation releases
A
- prostaglandins
- leukotrienes
- free radicals
- lysosomal enzymes
15
Q
Inflammatory mediators
A
chemicals responsible for aspects of inflammation
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
17
Q
Complement proteins
A
- C3a/C5a - histamine release
- C5a: chemotaxis
- C3b: opsonin for phagocytosis
- C5-C9: membrane attack complex
18
Q
Arachidonic acid metabolites
A
- derivative of cell membrane (phospholipids)
- can be converted to prostaglandins or leukotrienes
19
Q
Prostaglandins causes ….
A
- decreased vascular tone
- increased pain
- increased uterine tone
- increased temperature
20
Q
Types of prostaglandins
A
- thromboxane A2
- Prostacyclin (PGI2)
- Prostaglandin E2
21
Q
Thromboxane A2
A
- produced by platelets
- vasoconstriction; platelet aggregation
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
Types of leukotrines
- Leukotriene C4
| - Leukotriene B4
26
Leukotriene C4
- increased capillary permeability
- breaks down to LTD4 and LTE4
- smooth muscle contractions
27
Leukotriene B4
- neutrophils & monocyte chemotaxis
28
Monokines
- 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
Acute phase reaction
- "sick" from inflammatory illness
| - shift in hepatic protein synthesis: increase complement, clotting, C-reactive protein
30
SIRS
- systemic inflammatory response syndrome
| - exuberant production of inflammatory mediators: results in multisystem organ failure due to normal tissue damage
31
SIRS criteria
- 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
Acute inflammation outcomes
- 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
Granulomas
- bodies attempt to wall something off that it can't destroy
| - macrophages adhere to each other to wall off stuff
34
Neutrophils predominant in?
infections by common bacteria
35
Lymphocytes predominant in?
viral infections
36
Plasma cells predominant in?
spirochete diseases (syphilis & lymph disease)
37
Monocyte/macrophages predominant in?
tuberculosis and fungal infections
38
Eosinophils predominant in?
infection caused by worms
39
Two routes of healing
- regeneration
| - repair by fibrous tissues (scar)
40
Regeneration
normal cells that were destroyed gets replaced by new normally functioning cells
41
Repair by fibrous tissues
normal cells that were destroyed get replaced by new tissue that is not normally functioning cells
42
Labile cells
- constantly divide
| - most epithelium
43
Stable cells
- don't regenerate constantly as part of normal cycle, but can regenerate if needed
- glandular cells, fibroblasts, endotherlium, osteroblasts, liver cells
44
Permanent cells
- do not regenerate
| - gila, neurons, heart
45
Damaged epithelium repair
-stimulates mitosis to grow towards each other
46
How connective tissue replaces permanent cells
1. fibroblasts proliferate
2. endothelial cells proliferate
3. both invade and displaces the clot that forms on top
47
Maturing scar
- 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
Primary intention repair
- 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
Secondary intention repair
- 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
Types of wound healing alterations
- 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
Hindrances to healing
- Not old age alone
- inadequate nutrition
- poor blood supply
- foreign bodies
- infection
- Glucocorticoid (steroid) therapy
52
Phospholipase A2
- liberates arachiodonic acid to from cell membrane
| - inhibited by steroids
53
Cyclooxygenase
- converts arachiodonic acid to prostaglandins
| - inhibited by aspirin and NSAIDs
54
5-lipoxygenase
- converts arachiodonic acid to leukotrienes
| - various inhibitors
