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DWT exam 2 > pathology acute inflammation > Flashcards

pathology acute inflammation Flashcards

1
Q

inflammation definition

A

A well organized cascade of fluid and cellular changes within vascularized tissue

Host response to remove damaged/necrotic tissue or foreign invaders

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2
Q

5 cardinal signs of inflammation

A
  1. heat
  2. redness
  3. swelling
  4. pain
  5. loss of function
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3
Q

purpose of inflammation

A

Inflammation is part of the process of repair and healing
* destroys, dilutes, or walls off injurious agents
* initiates healing and tissue repair

Fundamentally a protective response
* Get rid of pathogens
* Remove necrotic debris (phagocytosis)
* Repair the damage = return to normal structure/function

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4
Q

acute inflammation

A

Rapid
Short Duration
minutes to days
Characterized by exudation of fluid and plasma protein (edema) and emigration of leukocytes (mostly neutrophils)

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5
Q

chronic inflammation

A

Longer duration: days to years
Macrophages and lymphocytes **
Proliferation of blood vessels and connective tissue (fibrosis**)

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6
Q

3 main components of acute inflammation

A

1) Vascular alteration (vasodilation) leading to increased blood flow (hyperemia)

2) Changes in microvasculature permeability (leaky) that allow plasma proteins and leukocytes to leave the circulation

3) Emigration of leukocytes into the perivascular area

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7
Q

exudate

A

Inflammatory extravascular fluid with
* high protein concentration (>5 g/dL)
* high cell content (>5000 leukocytes/mL)
* high specific gravity >1.020

Formed when there is significant alteration in small blood vessel permeability at the site of injury
ex: pus

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8
Q

transudate

A

Extravascular fluid with
* low protein concentration (<2 g/dL)
* low cell content (<1500 leukocytes/mL)
* low specific gravity <1.012

An ultrafiltrate of blood
Increased hydrostatic pressure (ie. congestive heart failure)
Decreased oncotic pressure (hypoproteinemia)

looks like serum (clear, straw colored)

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9
Q

effusion

A

fluid accumulates in body cavity

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10
Q

edema

A

An accumulation of fluid in interstitial or serous cavities

Increased vascular permeability
Increased intravascular hydrostatic pressure
Decreased intravascular osmotic pressure
Decreased lymphatic drainage

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11
Q

pus

A

Pus - a purulent exudate rich in leukocytes (mostly neutrophils) and cell debris
purrulent = adjective!!

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12
Q

vascular changes with acute inflammation

A
  1. Vasodilation – involves arterioles first, then results in opening new capillary beds; mainly induced by histamine and nitric oxide acting on vascular smooth muscle
  2. Increased permeability of microvasculature – protein rich fluid pours out into extravascular tissue
  3. Loss of fluid results in concentration of red cells in small vessels, increased blood viscosity and blood stasis
  4. Stasis – allows leukocytes to accumulate along the endothelium and stick to it (leukocyte emigration/diapedesis)
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13
Q

4 mechanisms for vasular leakage:

A
  1. endothelial contraction: Endothelial cells contract –> increase in interendothelial space (mediated by histamine, bradykinins, leukotrienes), Rapid and short-lived (15-30 minutes)
  2. direct endothelial injury: Direct damage to endothelium causes necrosis and detachment (burns, lytic bacteria), Starts immediately, lasts until thrombosis occurs or endothelium repaired
  3. leukocyte-dependent injury: Activated leukocytes may secrete free radicals and proteolytic enzymes, leading to cell damage
  4. Increased transcytosis: Increased transport of fluid and protein through endothelial cells
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14
Q

endothelial contraction

A

1st mechanism for vasular leakage
Endothelial cells contract –> increase in interendothelial space
mediated by histamine, bradykinins, leukotrienes

Rapid and short-lived (15-30 minutes)

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15
Q

endothelial direct injury

A

2nd mechanism for vasular leakage
Direct damage to endothelium causes necrosis and detachment (burns, lytic bacteria)
Starts immediately, lasts until thrombosis occurs or endothelium repaired

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16
Q

leukocyte mediated injury endothelial changes

A

3rd mechanism for vasular leakage
Activated leukocytes may secrete free radicals and proteolytic enzymes, leading to cell damage

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17
Q

transcytosis

A

4th mechanism for vasular leakage
Increased transport of fluid and protein through endothelial cells

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18
Q

Leukocyte Extravasation Stages

A
  1. Margination, rolling, and adhesion: in normal blood flow endothelium does not “catch” cells, it must be activated by cytokines to do so
  2. Transmigration across endothelium (mainly venules), also called diapedesis
  3. Migration – in interstitial tissue toward a chemotactic stimulus
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19
Q

selectins

A

initiate low affinity rolling of leukocytes
binds and releases like velcro

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20
Q

Margination, Rolling, and Adhesion in leukocyte extravasation

A

Blood stasis
* helps leukocytes stack up at periphery (against vessel wall)

Rolling
* leukocytes adhere transiently to endothelium
* roll until becoming firmly attached to endothelium

Neutrophils, monocytes, eosinophils, basophils, lymphocytes all use the same method described above

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21
Q

integrins

A

high affinity binding

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22
Q

low affinity binding of leukocytes extravasation

A

Mediated by selectins expressed on surface of endothelium and leukocytes

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23
Q

high affinity binding of leukocyte extravasation

A

Integrins on leukocytes bind to immunoglobulin family receptors on endothelial cells

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24
Q

genetic deficiencies in leukocyte adhesion

A

Heritable deficiencies in type and amount of adhesion molecules (selectins/integrins) can inhibit leukocyte transmigration and acute inflammation

This may result in poor inflammatory response to pathogens and dead tissue

Causes recurrent infections

25
Q

transmigration of leukocyte extravasation

A

Leukocyte inserts a pseudopod into the junction between endothelial cells and squeezes through

Made possible by adhesion molecules located on leukocytes and endothelial cells

26
Q

chemotaxis of leukocyte extravasation

A

Movement of leukocytes in tissue along a chemical gradient
can be due to:
* Exogenous products – bacteria
* Endogenous products – complement system components (C5a, leukotriene B4, cytokines)

Cell moves by extending a filopodia that pulls the back of the cell forward.

27
Q

steps of phagocytosis

A
  1. Recognition and Attachment
  2. Engulfment
  3. Killing or degradation of ingested material
28
Q

recognition and attachment in phagocytosis

A

microbe binds to phagocytic receptor

29
Q

engulfment in phagocytosis

A

phagocyte membrane zips up around membrane and makes pseudopods

Pseudopods flow around particle to form a phagosome

Phagosome fuses with lysosome in cell creating the phagolysosome

30
Q

killing and degredation in phagocytosis

A

Reactive oxygen species (ROS)
* Produced within the lysosome
* Respiratory burst – rapid oxidative reaction
* Primary mode of microbial killing

Lysosomal enzymes

31
Q

Release of Leukocyte Products During Killing (phagocytosis)

A

Collateral damage
when neut dies while killing in a phagolysosome
Release of lysosomal enzymes and ROS into extracellular space

Cytotoxic release – crystals (eg. urates) can puncture the cell during phagocytosis and lead to leakage of enzymes and other leukocyte products

32
Q

Neutophil extracellular traps (NETs)

A

Produced by neutrophils in response to infectious pathogens and inflammatory mediators

Mechanism of killing microbes

Extracellular fibrillar network composed of:
* Meshwork of nuclear chromatin
* Antimicrobial peptides and enzymes

33
Q

genetic defects in leukocyte function

A

Inherited defects in leukocyte adhesion
* Leukocyte Adhesion Deficiencies (LAD)

Inherited defects in phagolysosome fusion
* Chediak–Higashi syndrome

Inherited defects in microbicidal activity

ALL CAUSE RECURRENT INFECTIONS

33
Q

genetic defects in leukocyte function

A

Inherited defects in leukocyte adhesion
* Leukocyte Adhesion Deficiencies (LAD)

Inherited defects in phagolysosome fusion
* Chediak–Higashi syndrome

Inherited defects in microbicidal activity

ALL CAUSE RECURRENT INFECTIONS

34
Q

Cell derived mediators

A

Vasoactive amines (Histamine, Seratonin)
Arachidonic acid metabolites
Nitric oxide (NO)
Cytokines

35
Q

Plasma derived mediators

A

complement system

36
Q

histamine

A
  • vasoactive amine
  • Present in a PREFORMED state in mast cells, basophils and platelets in cytoplasmic granules
  • can be released instantly, as needed
  • mast cells typically are found in connective tissue near blood vessels
37
Q

Histamine is released in response to:

A
  • physical injury (heat, cold, trauma)
  • immune reactions (IgE binding, type 1 hypersensitivity)
  • presence of complement fragments C3a and C5a (anaphylatoxins)
38
Q

Actions of histamine

A

vasoactive amine
* dilatation of arterioles
* increases vascular permeability of venules
* causes endothelial contraction in venules

39
Q

serotonin

A

vasoactive amine
also known as 5-hydroxytryptamine
preformed in platelets
Released in response to platelet aggregation
actions are similar to histamine in acute inflammation

40
Q

Arachidonic acid metabolites

A

The degradation of cell membrane phospholipids by phospholipases yields AA

Eicosanoids
* Products of AA metabolism
* regulate inflammation and hemostasis

Two primary classes of inflammatory metabolites
* prostaglandins
* leukotrienes

41
Q

Eicosanoids

A
  • Products of AA metabolism
  • regulate inflammation and hemostasis
42
Q

Arachidonic acid cascase

A
  1. cell membranes broken into arachidonic acid by phospholipase (glucocorticoids inhibit)
  2. arachidonic acid turned into prostaglandin by cyclooxygenase (NSAIDS inhibit)
  3. lipooxygenases cleave arachidonic acid into leukotrienes
43
Q

lipoxygenase

A

Enzyme that produces leukotrienes and lipoxins from AA

44
Q

leukotrienes

A

Chemotactic for leukocytes
Vascular effects: vasoconstriction, ↑ vascular permeability
produced from arachidonic acid by lipoxygenase

45
Q

lipoxins

A

produced from arachidonic acid by lipoxygenase
Lipoxins inhibit inflammation
Inhibit leukocyte recruitment and cellular components of inflammation

46
Q

Nitric oxide

A
  • Produced by endothelial cells, macrophages, neurons
  • Synthesized by nitric oxide synthase

NO: 2 functions in inflammation
* Vasodilation (contributes to vascular reaction)
* Inhibits cellular inflammatory response
* reduces platelet aggregation and adhesion (anti-inflammatory)
* inhibits leukocyte recruitment (anti-inflammatory)

As a free radical kills microbes

47
Q

cytokines

A

polypeptides produced primarily by macrophages and lymphocytes

Primary action is modulation of activities of other cells

The main cytokines involved in acute inflammation are IL-1 (interleukin-1) and TNF (tumor necrosis factor)

48
Q

The main cytokines involved in acute inflammation

A

IL-1 (interleukin-1) and TNF (tumor necrosis factor)

49
Q

TNF/IL-1 actions

A

vascular:
* leukocyte adhesion molecules
* procoagulant activity

leukocytes:
* activate
* produce cytokines

fibroblasts
* proliferate, repair
* increase collagen synthesis

systemic
* fever
* leukocytosis
* decrease appetite
* increase sleep

50
Q

complement

A

Defense against microbes
* formation of MAC - membrane attack complex

Complement activation causes
* ↑ vascular permeability
* Chemotaxis
* Opsonization

Main components are present as inactive plasma precursors (C1-9)

51
Q

complement activation pathways

A

alternate: microbe antigens directly activate c3 convertase
classical: antibodies bind to antigens activating c3 convertase
lectin: mannose-binding lectin binds to antigen activating c3 convertase

c3b causes:
* recruitment lymphocytes
* phagocytosis
* formation of MAC

52
Q

classical complement pathway

A

reaction with IgG or IgM containing antigen-antibody complex

53
Q

alternate complement pathway

A

contact with microbial surfaces and polysaccharides (cobra venom, endotoxin)

54
Q

lectin complement pathway

A

plasma mannose-binding lectin binds to microbes

55
Q

C3 convertase

A

The initial steps in complement activation lead to formation of an enzyme - C3 convertase - which cleaves C3
C3 cleavage leads to:
* release of C3a (anaphylatoxin)
* covalent attachment of C3b (initiates formation of C5 convertase)
* formation of C5-9 (MAC)

56
Q

C5a

A

facilitate histamine release from mast cells (vasodilate, increase permeability)

activates lipoxygenase pathway of AA metabolism in neutrophils and monocytes
chemotactic for neutrophils, monocytes, eosinophils, basophils

complement

57
Q

C3b

A

act as opsonins when fixed to bacteria; facilitate phagocytosis by neutrophils and macrophages (receptor)

complement

DWT exam 2 (22 decks)

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