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General Pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Purpose of inflammation

A

-Isolate, dilute, neutralize, confine, and remove offending agent
-Clear area of debris
-Initiate healing and repair

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2
Q

Outcomes of inflammation

A

-Eliminate agent and return to normal
-Stalemate: ongoing
-Death of host

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3
Q

Cardinal sings of inflammation

A

-Rubor(redness)
-Tumor (swelling)
-Calor (heat)
-Dolor (pain)
-Function laesa (loss of function)

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4
Q

Vascular events in inflammation (7)

A
  1. Transient arteriolar vasoconstriction
  2. Arteriolar vasodilation
  3. Capillary congestion
  4. Increased vascular permeability
  5. Slowing blood flow
  6. Redistribution of blood cell elements
  7. Blood flow stasis
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5
Q

Transient arteriolar vasoconstriction

A

Caused by stimulus on smooth muscle regulated by local mediators. Doesn’t occur with all stimuli. Can last several seconds up to 5 minutes

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6
Q

Arteriolar vasodilation

A

A wave starting at arteriole to venule. Causes hypermia. Mediators include: histamine, bradykinin, Prostacyclin, NO etc

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7
Q

Increased vascular permeability

A

Endothelial junctions become leaky resulting in fluid loss. Mediators from immediate transient response and delayed sustained response (TNF, IL1 etc). Results in edema

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8
Q

Edema from vascular permeability

A

Fluid in ECM contains proteins involved in inflammation and helps dilute inciting stimulus Starts as a transudate(basically water) to an exudate

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9
Q

Slowing of blood flow

A

-Large vascular diameter and increased number of blood cells (congestion)
-Increased blood viscosity due to plasma loss
-Increased adhesiveness of erythrocytes

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10
Q

Redistribution of blood cell elements

A

-Laminar flow is disrupted due to vasodilation and congestion
-Erythrocytes centrally located
-Leukocytes move to periphery along endothelial

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11
Q

End goal

A

-Dilution of inflammatory stimulus
-Movement and concentration of plasma mediators at inflammation
-Intravascular leukocytes are poised to leave vessel

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12
Q

Cellular events major steps

A
  1. Margination and adhesion to endothelium
  2. Emigration
  3. Chemotaxis
  4. Accumulation
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13
Q

Margination

A

Leukoctes move to periphery of vessels generally post capillary venules
-Roll along endothelium by binding to selectins then firmly bind through ICAM and VCAM and B-2 integrins

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14
Q

Emigration

A

Leukocytes move from endothelial surface into the ECM
-Go through endothelial pores
-More receptors within the interendothelial junction (PECAM-1 and JAMs)
-Leukocytes exert pseudopods (Ca mediated) into junction and pulls them through to the outside

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15
Q

Order of emigration

A

-Neutrophils
-Monocytes
-Lymphocytes

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16
Q

Chemotaxis

A

Leukocytes directed to site of inflammatory stimulus.
-Occurs in response to a concentration gradient of a chemical attractant

17
Q

Chemotactic factors

A

-Complement components
-Bacterial products
-Arachidonic acid metabolites
-Kinins
-Collagen and fibrin breakdown products
-Cytokines
-Chemokines

18
Q

Mechanism of chemotaxis

A

-Chemotactic factors interact with specific leukocytes membrane receptors
-Phospholipase C activated and get localized release of cytoplasm Ca that causes assembly and disassembly of microtubules
-B1-integrins bind to ECM components and pull to stimulus

19
Q

Accumulation

A

-Neutrophils accumulate first byt they are short-lived
-Macrophages more numerous after 24-48hrs but are long lived
-Lymphocytes may persist later in persistent stimuli

20
Q

Events of phagocytosis

A

-Opsonization
-Attachment
-Ingestion
-Killing and degradation
-Oxygen independent killing
-Oxygen dependent killing

21
Q

Most important phagocytes in inflammation

A

Neutrophils and macrophages

22
Q

Opsonization

A

Coat foreign material with opsonin to enhance phagocytosis (C3b, IgG, collectins)

23
Q

Attachment

A

Phagocyte attaches to foreign material thanks to opsonins
-Can attach to unopsonized material but less efficiently

24
Q

Ingestion

A

Cell membrane pseudopods extend around material and internalize it into an intra-cytoplasmic vacuole (phagosome)
-Ca fluces regulate cytoskeletal changes

25
Q

Killing and degredation

A

A lysosome fuses to phagosome to form phagolysosome enzymes released (degranulation)
-Then kill with either oxygen dependent or independent killing
-Degrade and digest material

26
Q

O2 independent killing

A

Acid hydrolases
-Bactericidal permeability increasing protein
-Lysozyme
-Lactoferrin
-Defensins
etc

27
Q

O2 dependent killing

A

Use Oxygen metabolites that are highly reactive 2 paths: myeloperoxidase independent and dependent pathway

28
Q

Myeloperoxidase independent path

A

-Superoxide anion, hydrogen peroxide, and hydroxyl radical
-Form NADPH oxidase during respiratory burst initiates process

29
Q

Myeloperxidase dependent

A

Make hypochlorous acid (bleach)
-Most potent killing mechanisms
-In neutrophils

General Pathology (30 decks)

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