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Pathophysiology > Unit I - Inflammation & Healing > Flashcards

Unit I - Inflammation & Healing Flashcards

1
Q

natural cycle of inflammatory process

A

cellular injury, acute inflammation, chronic inflammation with granuloma
*healing can occur at any stage

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2
Q

granuloma

A

inflammatory nodule

  • granular, firm
  • contains macrophages, epithelia cells and necrotic tissue
  • persistent antigens
  • surrounded by WBCs
  • can lead to chronic inflammatory disease
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3
Q

dilution phase - 5 cardinal signs

A
  1. Redness (hyperemia -capillary dilation)
  2. Swelling (edema - increased capillary fluid permeability)
  3. Heat
  4. Pain
  5. Loss of function
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4
Q

dilution phase - process

A

starts with mast cells (degranulates), release pro inflammatory mediators, which initiate the inflammatory process, fluid exudate dilutes affected area, fibrin isolates the inflamed area

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5
Q

mast cell pro inflammatory mediators

A

vasoactive amines - cause vasodilation and increase vessel permeability

(histamine, serotonin, bradykinin)

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6
Q

pro inflammatory cytokines

A

signaling molecules that mobilize white blood cell communication

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7
Q

example of skin inflammation

A

Roasacea, nasal polyp

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8
Q

demolition phase

A

proliferation of white blood cells

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9
Q

most abundant WBCs are

A

neutrophils (PMNs)

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10
Q

diapedesis

A

process in which spaces between endothelial cells enlarge and neutrophils squeeze through

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11
Q

causes PMNs to migrate toward foreign body

A

chemotaxis

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12
Q

as PMNs proliferate, they must be transferred from the blood to the

A

ECF

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13
Q

WBC pavementation (margination) occurs because of loss of

A

laminar flow

allows things to get where they need to be (without it, could not fight off infection)

In laminar flow, most WBC (and RBC) are traveling in the area of highest velocity, i.e. the center of the blood vessel. As the velocity of blood flow decreases, more and more blood cells migrate to the edges of the blood vessel positioning them to marginate at the edges
As PMNs proliferate, they must be transferred from blood to ECF via Laminar flow; longest arrows in the center flow fastest, more to the periphery it is slower; difference in velocity causes the WBC to congregate at the center of the cell because that is where the blood is flowing fastest

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14
Q

phagocytosis

A

ingestion of foreign material (necrotic tissue, pathogens)

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15
Q

types of cytokines

A

eosinophil chemotactic factor (ECF), neutrophil chemotactic factor (NCT), tumor necrosis factor (TNF), platelet activating factor (PAF), interleukins

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16
Q

end result of phagocytosis (2 things)

A

colliquative necrosis with supportive drainage

suppuration - pus

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17
Q

after phagocytosis

A

fluid dilutes bad substance and fibrin in the plasmin limits the spread

18
Q

acute inflammation (3 things)

A
  • less than 2 weeks
  • PMNs dominate/increase - “shift to the left” (70% to 90%)
  • WBC count above normal (4000-8000 WBC)
19
Q

chronic inflammation

A
  • more than 2 weeks
  • fatigue, weight loss, cognitive loss
  • elevated monocytes and lymphocytes
  • PMNs normalize/decrease - “shift to the right”
  • mild leukocytosis or leukcytopenia
20
Q

desirable effects of inflammation

A
  • walls off an invading foreign body via fibrin in the exudate
  • dilutes the concentration of the foreign body
  • kills it with WBCs
21
Q

undesirable effects of inflammation

A
  • lassitude (fatigue)
  • anorexia
  • fever
  • prostration
  • acute phase response
22
Q

acute phase proteins (synthesized by the liver)

A

25+
positive APPs: protein increases during acute phase response
negative APPs: protein decreases during acute phase response

23
Q

**tests for inflammation with APPs (and what a positive test looks like)

A

increased erythrocyte sedimentation rate (ESR): attach to red blood cells, inc blood viscosity, look for inflammation
*POSITIVE TEST: blood separates faster than normal

24
Q

type of healing - labile

A

(vegetative intermitotics)

  • cells replace on periodic basis
    ex: bone marrow, lining of GI tract, skin
25
Q

type of healing - stable

A

(vegetative post-mitotics)

  • cells replace only after injury
    ex: liver
26
Q

type of healing - permanent

A

(fixed post-mitotics)

  • cells hypertrophy to take place of loss cells
    ex: CNS, cardiac mx, kidney
27
Q

regeneration/resolution of tissue injury

A

regrowth of original tissue (so must be irreversible injury)
NO destruction of tissue
(sunburn, cold)

28
Q

replacement (2 kinds)

A
  1. replacement with different tissue (metaplasia) NO scar - barretts esophagus
  2. replacement with scar tissue: not functional and doesn’t perfuse blood well
29
Q

repair healing - 2 ways

A

primary intention or secondary intention

30
Q

primary intention

A

edges of a wound are in close approximation to each other
minimal scarring/loss of function

  • bound by blood clot, inflammatory reaction and WBCs kill foreign bodies, fibroblasts/collagen and scar
  • re-epithelialization must occur over an organized clot
31
Q

secondary intention

A

wound edges NOT close together
takes much longer to heal, larger scar is formed, possible dysfunction
- collagen is different (may cause keloids)

32
Q

keloid formation (hypertrophic scarring)

A

severe scarring due to deposition of type 3 collagen rather than type 1

33
Q

redness

A
  • capillary sphincter contracts
  • blood flow decreases
  • huge blood volume, low flow
    (Rosacea)
34
Q

swelling

A
  • pro-inflammatory mediators (increase capillary permeability so it swells bc lots of fluid in it)
  • increased hydrostatic pressure
  • increased extracellular fluid
35
Q

heat

A

increased blood volume in the area causes warmth

36
Q

pain

A
  • pressure on pain sensory endings
  • increased acidity of extracellular fluid
  • histamine, prostaglandins, bradykinin release
37
Q

loss of function

A

due to all of the other symptoms

38
Q

dystrophic calcification

A

common in bigger mx like quads

39
Q

super infection forming gangrene

A

poor circulation impeding fast healing to injury, can lose limb

40
Q

2 positive APPs to know:

A

CRP: binds to dead/dying cells
SAAP: recruits PMN’s and macrophages to sites with inflammation

41
Q

negative APPs to know

A

-

Pathophysiology (27 decks)

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