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Pathophysiology > inflammation > Flashcards

inflammation Flashcards

1
Q

clinical signs of acute inflammation

A

calor, dolor, rubor, tumor (swelling, edema), functio laesa (loss of fxn)

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2
Q

duration of acute vs chronic inflammation

A
  • acute: days to weeks

- chronic: weeks - months

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3
Q

specificity of acute vs chronic

A
  • acute: nonspecific

- chronic: specific (where immune response activated)

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4
Q

inflammatory cells of acute vs chronic

A
  • acute: neutrophils, macrophages

- chronic: lymphocytes, plasma cells, macrophages, fibroblasts

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5
Q

fluid exudation of acute vs chronic

A
  • acute: yes

- chronic: no

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6
Q

tissue necrosis acute vs chronic

A
  • acute: usually no

- chronic: yes (ongoing)

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7
Q

cardinal clinical signs acute vs chronic

A
  • acute: redness, swelling, pain, fever

- chronic: no

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8
Q

fibrosis (collagen deposition) acute vs chronic

A
  • acute: no

- chronic: yes

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9
Q

operative host responses acute vs chronic

A
  • acute: plasma factors (complement, immunoglobulins, neutrophils, non-immune phago)
  • chronic: immune response, phago, repair
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10
Q

systemic manifestation acute vs chronic

A
  • acute: fever (high)

- chronic: weight loss, anemia, low grade fever

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11
Q

WBC count acute vs chronic

A
  • acute: increase

- chronic: remain constant

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12
Q

vascular changes acute vs chronic

A
  • acute: vasodilation, increased permeability

- chronic: new vessel formation (granulation tissue)

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13
Q

exudate

A

inflammatory extravascular fluid containing increased protein, cellular debris (pus, WBCs)

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14
Q

exudation

A

escape of fluid, proteins and blood cells from vascular system into interstitial tissue or body cavities

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15
Q

transudate

A

ultra filtrate of plasma resulting from hydrostatic imbalance across vascular endothelium, no protein

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16
Q

transudation

A

process of which transudate is pushed across the endothelium because of hydrostatic pressure diffs

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17
Q

pus

A

purulent inflamm exudate rich in leukocytes and parenchymal cell debris

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18
Q

edema

A

XS fluid in interstitial areas from exudate or transudate (within tissue)

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19
Q

effusion

A

escape of fluid from anatomical vessels by exudation/rupture (pleural effusion, middle ear effusion), within a cavity

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20
Q

changes in vascular flow in acute inflammation

A
  • Initial transient vasoconstriction
  • Vasodilation, causing increased blood flow ->redness and increased temp
  • As blood flow increases, there is increased capillary pressure and permeability (results in net XS of fluid extravasated into interstitial tissues)
  • vascular perm increased = edema
21
Q

leukocyte extravasation

A
  • margination : stimulus (injury) activates endothelial cells which display selectins (adhesion molecules) on activated endothelial cells
  • rolling adhesion to endothelium (have integrins activated – adhesion receptors on leukocytes surfaces, which attach to endothelial cells)
  • trasmigration across endothelium and migration through interstitial tissues toward chemotactic stimulus
22
Q

chemotaxis

A
  • occurs after leukocyte extravasation
  • chemotactic agents for neutrophils include exogenous substances (bacterial products) as well as endogenous substances (complement, leukotrienes and cytokines) -> these activate leukocytes and cause them to release chemical mediators of inflammation
23
Q

neutrophils

A

-can be exogenous (bacteria) or endogenous (complement, leukotrienes, and cytokines) substances

24
Q

phagocytosis

A
  • once leaks have assume at inflamm site, neutrophils and macrophages work to eliminate invading matter:
  • recognition and attachment (opsonization, coat microbe with substance that increases efficiency of phago and IDs microbe as foreign)
  • engulfment
  • killing
25
Q

what are arachidonic acid metabolites?

A

-powerful mediators of endothelial injury & tissue damage, synthesized by two types of enzymes:

i. leukotrienes (made by lipooxygenases): potent chemotaxic agent involved in vasoconstriction, bronchospasm, & vascular permeability
ii. prostaglandins (made by cyclooxygenases): pathogenesis of pain and fever

26
Q

what are vasoactive amines?

A
  • histamine and seratonin

- vasodilation and increased vascular permeability

27
Q

histamine

A

mast cells (mediator released in response to physical injury, heat/cold, immune reactions

28
Q

seratonin

A

basophils, platelets

29
Q

complement system

A

20 component proteins found in plasma, function in innate and adaptive immunity, “complement cascade” affects multiple factors of acute inflammation: vascular permeability, vasodilation, leukocyte adhesion, chemotaxis, activation, phagocytosis

  • C3 and C5 are most important
  • acute inflammation
30
Q

kinin system

A
  • chemical mediator of acute inflamm
  • creates vasoactive peptides from plasma proteins that increase vascular permeability, contraction of smooth muscle, dilation of blood vessels and pain (side note: bradykinin effects similar to histamine)
31
Q

cytokines

A

proteins produced by many cell types (including lymphocytes and macrophages), regulate immune responses

  • chem mediators of acute inflammation
  • interleukin 1 and TNF
32
Q

interleukin 1

A

produced by macrophages and monocytes; activates T cells and macrophages, promotes inflammation
-effects: fever, pain, vasodilation, enabling transmigration

33
Q

TNF

A

cytotoxin from group of cytokines that cause cell death (adopt)
-derived from monocytes

34
Q

nitric oxide

A

powerful vasodilator

35
Q

oxygen derived free radicals

A

assist in killing foreign cells, unpaired electron (unstable, destructive)
-damages cell membranes of bacteria = lysis

36
Q

outcomes of acute inflammation

A
  • complete resolution (things return to normal)
  • suppuration/abscess formation (walled off)
  • repair (scarring)
  • progress to chronic inflammation
37
Q

granuloma

A
  • aggregation of macrophages that form a particular pattern. May also occur with foreign bodies and insoluble immune particles.
  • granulomatous inflammation: special type of chronic inflammation
38
Q

common causes of granulomas

A

syphilis TB, sarcoidosis

39
Q

lab diagnosis of inflammation - acute

A
  • Examination of exudate (high protein levels and specific gravity), presence of neutrophils(bacterial) lymphocytes (viral),Biopsy of tissue, culture, gram-stain, antibody levels, complement level (looking for C3 and C5)
  • CRP (c-reactive protein - acute)
  • ESR (erythrocyte sed rate = non specific marker for inflamm = acute)
40
Q

lab diagnosis of inflammation - chronic

A

-biopsy lesions, microbiologic cultures, immunologic studies, serologic studies for antibodies, skin tests for TB, fungus, serum autoantibody levels for autoimmune disease

41
Q

primary intention

A

brings wound edges together to encourage healing, most efficient and results in least amount of scarring.

42
Q

secondary intention

A

lesion is left open due to fear of infection, heals from inside out to prevent closing infection inside. Worst scaring but scar can be remodeled.

43
Q

tertiary intention

A

(delayed primary closure)- delayed primary closure for 4-6 days due to some concern for infection.

44
Q

phases of wound healing

A
  • inflammation
  • epithelization
  • collagen synthesis
  • scar maturation
45
Q

inflammation

A

process by which body responds to local injury by attempting to contain and isolate injury, destroy pathogens, inactivate toxins and repair. Occurs within 3-24 hours after injury.

46
Q

epithelization

A

Bridging to the wound with new epithelial cells, begins within about 12 hours from injury, new epithelial cells migrate from the wound edges. Wounds are sealed within 24-48 hours after injury

47
Q

collagen synthesis

A

Fibroblasts and collagen aggregate around the wound to make new tissue and repair damaged areas, occurs within 4 days - 6 weeks after injury,

48
Q

scar maturation

A

scar forms and remodels throughout the first year after the injury, takes a full year to come to final stage.

Pathophysiology (7 decks)

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