Acute/chron Inflamm Flashcards

0
Q

Acute vs chronic

A

Short duration : long
Fast onset: slow
Infiltrated w granulocytes(neutrophils): agranulocytes (macrophage, lymphocyte, plasma cells)
Acute onset/fast rising fever: low grade/slow rising fever
Increase WBC count:no change in WBC count
Shows cardinal signs : slow progressive tissue necrosis, fibrosis
Vasodilation, increased permea: new vessel formation (granulation tissue)

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1
Q

Clinical signs of acute inflamm

A
Calor
Rubor
Tumor
Dolor
Functio laesa
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2
Q

systemic manifestations that indicate presence of inflamm

A

fever (due to vasodilation); increase in peripheral WBCs (WBC emigration to injury site); increase plasma pro levels

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3
Q

exudate

A

inflamm extravasc fluid containing increased protein, cellular debris and having spec gravity of >1.020

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4
Q

transudate

A

ultra filtrate of plasma resulting from hydrostatic imbalance across vascular endothelium containing decreased protein (specific gravity <1.012)

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5
Q

edema

A

excess fluid in interstitial areas/body cavity due to exudate OR transudate

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6
Q

effusion

A

escape of fluid from anatomical vessels by exudation/rupture

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7
Q

changes in vascular flow that occur in acute inflamm

A
  1. initial transient vasoconstriction
  2. subsequent vasodilation causing increased blood flow, heat, redness
  3. increased mean capillary pressure, hydrostatic pressure (cap bed now has overflow of fluid), and decreased colloid pressure
  4. exudates escape into interstitium (to compensate for overload of pressure) resulting in excess of fluid in interstitial tissues
  5. vascular permeability increasing= edema
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8
Q

emigration of leukocytes to injury site

A

designed to ingest offending agents, kill bacteria, and degrade necrotic tissues and foreign antigens

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9
Q

cell events resulting in leukocytes to injury site: leukocyte extravasation

A
  1. margination
  2. rolling
  3. adhesion
  4. transmigration
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10
Q

cell events resulting in leukocytes to injury site: chemotaxis

A

occurs after leukocyte extravasation; chem gradients signal leukocytes to move toward injury

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11
Q

cell events resulting in leukocytes to injury site: phagocytosis

A

once leukocytes have accumulated at inflamm site, neutrophils and macrophages work to eliminate the invading matter:

  1. recognition and attachment of the particle to be ingested (opsonization)
  2. engulfment
  3. killing
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12
Q

chemical mediators: arachadonic acid metabolites

A

located on lipid membrane:

  1. leukotrienes (synthesized by lipooxygenases; involved in vasoconstriction, bronchospasm, vascular permeability)
  2. prostaglandins/thromboxanes (synth by cycooxygenases; cause pain/fever)
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13
Q

chem mediators: vasoactive amines: histamine/seratonin

A

found in basophils, platelets, mast cells; cause vasodilation and increased vascular permeability

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14
Q

chem mediators: complement system

A

protein cascade that assists the antibodies destroy bacteria, ends in lysis of bacteria. cascade properties enable massive response/amplification to original signal

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15
Q

chem mediators: kinin system

A

increase vasc permeability; constrict smooth musc; vasodilate; cause pain

16
Q

chem mediators: cytokines

A

cell signaling proteins. include chemokines, interferons, interleukins, lymphokines, and TNF – involved in “acute phase” rxns –“I’m feeling sick”:

  1. interleukin
  2. tumor necrosis factor
17
Q

chem mediators: nitric oxide

A

released from macrophages and endothelial cells. involved in tissue destruction and vasodilation

18
Q

chem mediators: oxygen-derived free radicals

A

“active form” of oxygen; damages cell membrane of bacteria

19
Q

possible outcomes of acute inflamm

A
  1. complete resolution
  2. supporation/abscess formation
  3. repair
  4. progress to chronic inflamm
20
Q

granulatomas inflamm

A

cluster of macrophages surrounding necrosis w a rim of lymphocytes. some of these macrophages fuse (giant cells). happens when phagocytosis cannot occur.

21
Q

acute phase reactants

A

C-Reactive Protein; Erythrocyte Sedimentation Rate

22
Q

acute vs chronic inflamm on lab. eval

A

acute: will see exudate, neutrophils, lymphocytes
chronic: will see macrophages

23
Q

phases of wound healing

A
  1. inflamm
  2. epithelialization (to help keep out bacteria)
  3. collagen synthesis (produced by myofibroblasts)
  4. scar maturation
  5. organization