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MSII Pathology > Chapter 2. Inflammation and Repair - Acute Inflammation > Flashcards

Chapter 2. Inflammation and Repair - Acute Inflammation Flashcards

1
Q

what is the definition of acute inflammation?

A

transient and early response to injury; chemical, vascular, and cellular

  • involves release of chemical mediators
  • leads to sterotypic vessel and leukocyte responses
  • NOT synonym for infection, but can be a side efffect
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2
Q

what are cardinal signs of inflammation? the pathology behind it?

A
  1. rubor (readness) and calor (heat)
    - histamine-mediated vasodilation of arterioles
  2. tumor (swelling/edema)
    - histamine-mediated increase in permeability of venules causing increased fluid in interstitial space
  3. dolor (pain)
    - PGE2 sensitizes specialized nerve endings to effects of bradykinin and other pain mediators
  4. functio laesa (loss of function)
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3
Q

what are stimuli for acute inflammation?

A
  1. infections
  2. immune reactions
  3. tissue necrosis, trauma, radiation, burns, foreign bodies, etc.
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4
Q

what is the sequence of vascular events in acute inflammation?

A
  1. vasoconstriction of arterioles (neurogenic reflex that lasts only seconds)
  2. vasodilation of arterioles
    - histamine and other vasodilators relax smooth muscle, causing increased blood flow, which increases hydrostatic pressure
  3. increased permeability of venules
    - histamine and other mediators contract endothelial cells, producing endothelial gaps
    - -tight junctions are simpler in venules than arterioles
    - transudate )protein and cell-poor fluid) moves into interstitial tissue
  4. swelling of tissue (edema) due to net outflow of fluid surpassing lymphatic ability to remove fluid
  5. reduced blood flow (decrease in hydrostatic pressure caused by outflow of fluid into interstitial tissue
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5
Q

what is the sequence of cellular events in response to bacterial infection?

A

neutrophils are primary leukocytes in acute inflammation

  1. marginization (RBC aggregate into rouleaux in venules, and neutrophils are pushed from central axial column to periphery)
  2. rolling (due to activation of selectin adhesion molecules on surface of neutrophils and endothelial cells; bind to selectins)
  3. adhesion (adhesins like integrin firmly binds neutrophils to endothelial cells’ ICAM and VCAM)
  4. transmigration (diapedesis); neutrophils dissolve basement membrane to enter interstitial tissue
  5. chemotaxis (neutrophils follow chemical gradients that lead to infection site)
  6. phagocytosis
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6
Q

what activates adhesion molecules?

A

C3a and LTB4 (leukotriene)

-endotoxins enhance activation to cause neutropenia (decreased peripheral blood count)

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7
Q

what inhibits activation of adhesion molecules?

A

catecholamines, corticosteroids, and lithium

-neutrophil count increases (neutrophil leukocytosis)

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8
Q

what are ICAM and VCAM? what are they activated by?

A

endothelial cell adhesion molecules (intracellular and vascular cell adhesion molecules)
-activated by IL-1 and TNF

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9
Q

what is leukocyte adhesion deficiency (LAD)?

A

autosomal recessive disorders

  • LAD1 is deficiency of CD11a:CD18
  • LAD2 is deficiency of selectin that binds neutrophils
  • have delayed separation of umbilical cord (neutrophil enzymes important in separation) and severe gingivitis, poor wound healing, neutrophilic leukocytosis (loss of marginating pool)
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10
Q

what is exudate?

A

fluid rich in proteins and cells that accumulates in interstitial tissue during diapedesis
-dilutes bacterial toxins and provides opsonins to assist in phagocytosis

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11
Q

what are chemotactic mediators?

A

C5a, LTB4, bacterial products, and IL-8

-these bind to neutrophil receptors, which releases Ca to increase neutrophil motility

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12
Q

what are the 3 steps of phagocytosis?

A
  1. opsonization
  2. ingestion
  3. killing
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13
Q

what are important opsonins?

A

IgG and C3b, along with other proteins like C-reactive protein
-but neutrophils only have receptors for IgG and C3b

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14
Q

what is Bruton’s agammaglobulinemia?

A

opsinization defect

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15
Q

what is Chediak-Higashi syndrome?

A

defect in microtuble function that prevents phagolysosomes formation

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16
Q

what is the O2-dependent myeloperoxidase (MPO) system? what are

A

most potent microbicidal system only present in neutrophils and monocytes

  • production of superoxide free radicals (NADPH oxidase converts O2 to -O2., which releases energy as respiratory/oxidative burst
  • production of peroxide (superoxide dismutase converts -O2. to H2O2, which is neutralized by glutathione peroxidase
  • -some peroxide is converted to hydroxyl FR by Fe
  • production of bleach (MPO combines H2O2 with Cl- to form HOCl. FR to kill bacteria)
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17
Q

what is chronic granulomatous disease? what are some signs?

A

XLR or AR disease

  • absent NADPH oxidase and reduced -O2. production causes absent respiratory burst
  • macrophages fuse together to form multinucleated giant cells to take over neutrophil function
  • severe infections involving lungs, skin, visceral organs, bones
  • classic screening test is colorless NBT dye, which becomes blue if respiratory burst intact (negative CGD)
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18
Q

what is MPO deficiency?

A

AR that has normal respiratory burst (both .O2- and H2O2 are made), but HOCl. is not

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19
Q

what is the O2-independent system? two examples?

A

bacterial killing from substances in leukocyte granules
-ex: lactoferrin (binds Fe necessary for bacterial reproduction) and major basic protein (eosinophil product cytotoxic to helminths)

20
Q

what are chemical mediators?

A

derive from plasma, leukocytes, local tissue, and bacterial products

  • have short lives (seconds to minutes)
  • have local and systemic effects, with many diverse functions
21
Q

what is the most important chemical mediator of acute inflammation?

A

histamine

22
Q

what are types of acute inflammation?

A
  1. purulent (suppurative) inflammation
  2. fibrinous inflammation
  3. serous inflammation
  4. pseudomembranous inflammation
23
Q

what is purulent inflammation and an example?

A

suppurative; localized proliferation of pus-forming organisms (like S. aureus, that has coagulase that cleaves fibrinogen into fibrin and traps bacteria and neutrophils)

24
Q

what is fibrinous inflammation

A

due to increased vessel permeability, with deposition of fibrin-rich exudate
-often on serosal lining of pericardium, peritoneum, or pleura (danger of adhesions)

25
Q

what is the most common cause of a skin abscess?

A

Staphylococcus aureus

26
Q

what are the three arachidonic acid metabolites that act as chemical mediators?

A

prostaglandins, thromboxane A2, and leukotrienes

27
Q

what is the source and function of prostaglandins?

A

source: macrophages, endothelial cells, and platelets
- PGH2 is the major precursor of PGs and thromboxanes

PGE2: vasodilation, pain, and fever
PGI2: vasodilation, and inhibition of platelet aggregation

28
Q

what is the source and function of thromboxane A2?

A

from platelets, and converted from GH2 by thromboxane synthase

for vasoconstriction and platelet aggregation

29
Q

what is the source and function of leukotrienes (LTs)

A

leukocytes, and lipoxygenase-mediated hydroxylation

LTB4: chemotaxis and activation of neutrophil adhesion molecules
LTC4, LTD4, LTE4: casoconstriction, increased venular permeability, bronchoconstriction

30
Q

what does zileuton do?

A

inhibits 5-lipoxygenase to decrease synthesis of LTB4, LTC4, LTD4, and LTE4

31
Q

what does montelukast leukotriene receptor antagonist do?

A

decrease synthesis of LTC4, LTD4, and LTE4

32
Q

what is the source and function of bradykinin?

A

product of kinin system activation by activated factor XII

vasodilation, increased venular permeability, and pain

33
Q

what is the source and function of chemokines?

A

leukocytes, endothelial cells

activate neutrophil chemotaxis

34
Q

what is the source and function of complement?

A

synthesized in liver as acute phase reactant

C3a, C5a: anaphylatoxins: stimulate mast cell release of histamine
C3b: opsonization
C5a: activation of neutrophil adhesion molecules, chemotaxis
C5-9: (membrane attack complex) cell lysis

35
Q

what are important chemical mediator cytokines?

A

IL1/6/8, TNF

36
Q

what is the source and function of IL-1, TNF?

A

macrophages (main source), monocytes, dendritic cells, and endothelial cells

  • initiate PGE2 synthesis in anterior hypothalamus, leading to fever
  • activate endothelial cell adhesion molecules
  • increase liver synthesis of acute-phase reactants like ferritin, coagulation factors, and C-reactive PRO
  • TNF is promotor of apoptosis
37
Q

what is the source and function of IL-6

A

macrophages (main source), monocytes, dendritic cells, and endothelial cells

increase liver synthesis of acute phase reactants

38
Q

what is the source and function of IL-8

A

macrophages (main source), monocytes, dendritic cells, and endothelial cells

chemotaxis

39
Q

what is the source and function of histamine

A

mast cells (primarily), platelets, enterochromaffin cells

for vasodilation, increased venular permeability

40
Q

what is the source and function of NO

A

macrophages, endothelial cells; also a FR gas released during conversion of arg to citrulline by NO synthase

for vasodilation, and bactericidal

41
Q

what is the source and function of serotonin

A

platelets

vasodilation, increased venular permeability, increases collagen synthesis

42
Q

what is serous inflammation?

A

thin, watery exudate due to insufficient fibrinogen to make fibrin
-in 2nd degree burns, viral pleuritis

43
Q

what is pseudomembranous inflammation

A

bacterial toxin-induced damage of mucosal lining, producing shaggy membrane composed of necrotic tissue
-in C. difficile in psuedomembranous colitis, diptheria, and noninvasive bacteria

44
Q

what is the role of fever in inflammation?

A

right-shifts in O2-binding curve

  • more O2 is available for O2-dependent MPO system
  • provides histile environment for bacterial and viral reproduction
45
Q

what are factors involved in the termination of acute inflammation (4)?

A
  1. short half-life of inflammatory mediators
  2. lipoxins (anti-inflammatory mediators)
    - derived from AA metabolites
    - inhibit transmigration and chemotaxis
    - signal macrophages to phagocytose apoptotic bodies
  3. resolvins
    - made from omega-3 FA
    - inhibit production and recruitment of inflammatory cells to site of inflammation
  4. clearance of neutrophils by apoptosis
46
Q

that are the possible consequences of acute inflammation?

A
  1. complete resolution
    - occurs with mild injury to cells that have the capacity to enter the cell cycle (first degree burns, bee stings)
  2. tissue destruction and scar formation
    - occurs with extensive injury or damage to permanent cells (third degree burns)
  3. formation of abscesses
  4. progression to chronic inflammation

MSII Pathology (11 decks)

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