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Pathology > Products of acute inflammation > Flashcards

Products of acute inflammation Flashcards

1
Q

Fluidic phase

A

Dilute and localize the stimulus

  • increased blood flow –> mediators (histamine from mast cells and platelets) –> vasodilation of arterioles = opening of capillary beds = increased blood flow = head and redness (erythema)
  • increased permeability of capillaries and postcapillary venules –> loss of fluid and increased vessel diameter –> slower blood flow, concentration of RBCs and increased blood viscosity = swelling
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2
Q

Retraction of endothelial cells

A

Occurs mainly in venules (high density of histamine receptors)

  • induced by histamine, NO, etc
  • rapid and short lived (minutes)
  • retraction by contraction of actin/myosin filaments or reorganization of the cytoskeletal microtubule and proteins
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3
Q

Endothelial injury

A

Occurs in arterioles, capillaries, venules
- caused by burns, microbial toxins
- rapid, may be long lived (hours to days)
= endothelial cell necrosis and detachment
- activates clotting and complement

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4
Q

Serous fluid

A

Clear watery fluid, low concentration of plasma protein with no or low number of leukocytes (transudate)

  • results from increased vascular permeability, suggests injury is mild or peracute
  • may become cellular or rapidly resorbed by lymphatic drainage
  • mild skin injury, allergies, serosal surfaces
  • affected tissues spread apart by watery fluid
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5
Q

Fibrinous inflammation

A

Pattern of acute inflammation

  • caused by infectious agents
  • accumulation of fluid with a high concentration of plasma protein (can have high or low cellularity depending on duration/stimulus) = exudate
  • leakage of large molecular weight proteins (fibrinogen!!!)
  • fibrinogen polymerizes to form fibrin
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6
Q

Fibrinous exudate

A

Often in serous membranes of body cavities

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7
Q

Gross characteristics of fibrinous exudates

A
  • surface of affected tissue is red (hyperemic)
  • surface may be granular or dull
  • covered with thick, stringy, white gray to yellow material that is easily removed
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8
Q

Microscopic characteristics of fibrinous exudates

A

Eosinophilic proteinaceous material: fibrillary, along with edema
- rapidly becomes infiltrated by neutrophils = fibrinosuppurative exudate

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9
Q

Consequence of fibrinous inflammation

A

May resolve without any sequelae

- if extensive, fibroblasts may migrate in and begin organizing exudate = fibrous adhesions

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10
Q

Cellular phase

A

Delivers leukocytes to the site in order to kill and digest stimulus (neutrophils and macrophages)
- activated leukocytes cause tissue damage and prolong inflammation

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11
Q

Leukocyte adhesion cascade

A

Movement of leukocytes from vessel into the connective tissue

  • driven by chemokines, cytokines and chemoattractant substances
  • process initiated during fluidic phase: blood stasis –> leukocytes accumulate along vascular endothelium
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12
Q

Process of the cellular phase

A
  • margination: leukocytes move to periphery of vascular lumen in apposition with endothelial cell (pavementing)
  • rolling: leukocytes adhere transiently to endothelium
  • adhesion to endothelium: firm adhesion
  • migration: migration through the endothelium and then to the stimulus
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13
Q

Rolling and adhesion

A

Mediated by adhesion molecules expressed on leukocytes and endothelial cells
- expression enchanced by cytokines (TNF, IL-1/6)

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14
Q

Leukocyte migration through endothelium

A

Occurs mainly in post-capillary venules

  • chemokines stimulate cells to migrate
  • cells migrate toward stimulus due to chemical concentration gradient (chemotaxis)
  • pseudopodia from leukocytes extend between endothelial cells and contact the basement membrane and extracellular matrix proteins
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15
Q

Chemotaxis

A

Leukocytes move toward the site of injury

  • exogenous and endogenous substances act as chemoattractants
  • common exogenous: bacterial products, lipids
  • common endogenous: cytokines (IL-8), components of complement system, arachidonic acid metabolites (leukotriene B4)
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16
Q

Cellular infiltrate varies with _______

A

Age of response and type of stimulation

  • neutrophils: 6-24 hrs
  • monocytes: 24-48 hrs
17
Q

First cells to arrive depends on the stimulus

A
  • neutrophils in bacterial infection
  • lymphocytes and plasma cells in some hypersensitivity rxns
  • eosinophils in allergic rxns
  • lymphocytes in viral infection
18
Q

Purulent inflammation

A

Response consists of accumulation of fluid with high concentration of plasma protein and high number of neutrophils (exudate)

19
Q

What word is often used with purulent?

A

Suppurative

20
Q

Pus

A

Accumulation of dead neutrophils

21
Q

Plegmon

A

Pus distributed in tissue layers or along tissue layers

- cellulitis

22
Q

Gross purulent inflammation

A

Surface or CT is hyperemic with thick white to yellow material

  • white: neutrophils are predominant
  • yellow: lot of necrotic debris
  • consistency: may be water, creamy, or firm
  • odor: dependent of accompanying tissue necrosis and inciting agent
23
Q

Fibrinopurulent

A

When purulent inflammation is mixed with fibrin

24
Q

Microscopic purulent inflammation

A

Large numbers of neutrophils, many degenerate neutrophils and mixed with necrotic cellular debris, tissue debris, plasma proteins, fibrin

25
Q

Outcome of purulent inflammation

A
  • neutralize
  • form pus = resorption of pus
  • may progress to chronic inflammation –> abscess: circumscribed collection of pus surrounded by CT capsule
26
Q

Are abscesses acute or chronic?

A

Chronic!!

27
Q

TNF, IL-1, IL-6 result in _______

A

Fever

  • mediated by prostaglandins that are increased in the hypothalamus
  • cytokines increase cyclooxygenases that convert AA to PGE2
  • NSAIDS reduce fever by inhibiting prostaglandin synthesis
28
Q

TNF, IL-1 and IL-4

A

Increase production of leukocytes by the bone marrow

  • results from mobilization of neutrophils from storage pools in bone marow
  • increased neutrophils in the blood (neutrophilia)
29
Q

TNF

A

Energy balance

- promote lipid and protein metabolism and suppressing appetite = cachexia

30
Q

____ and ____ stimulate acute phase protein production by the liver

A

IL-1 and IL-6

31
Q

What are 3 acute phase proteins?

A
  • C reactive protein*
  • serum amyloid A*
  • fibrinogen
  • bind to microbial cell walls and activate complement
32
Q

How can prolonged production of acute phase proteins be deterimental?

A

Secondary amyloidosis

33
Q

What are systemic effects of cytokines and acute phase proteins?

A

Affect heart rate, blood pressure and body temperature

34
Q

Septicemia

A

Significant form of bacteremia complicated by toxemia, fever, malaise, shock

  • multiplication of microorganisms within blood
  • inflammation is not controlled locally, but is systemic
  • widespread endothelial damage
  • septic shock and DIC are sequelae of advanced bacterial septicemia
35
Q

LPS

A

Bacterial endotoxins and bacterial cell wall components

  • gains entry from microflora of the bowl (intestinal ischemia)
  • activates endothelial cells and leukocytes
  • activates factor XII to initiate intrinsic coagulation
  • directly activates complement
36
Q

Clinical manifestation of LPS

A

DIC, hypotension, metabolic disturbances, multiple organ failure and death

37
Q

Gross findings of septicemia

A

Fluid in body cavity, pulmonary edema, petechial hemorrhage, congestion of liver and intestine

38
Q

Histologic findings of septicemia

A

Acute necrosis of renal tubules, centrolobular hepatocytes and cardiac myocytes

Pathology (19 decks)

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