Inflammation Flashcards

1
Q

What is inflammation?

A

defense reaction of living tissue against damage, aimed at removing the cause of injury and repairing the tissue
- plays an integral role in both innate and adaptive immunity

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2
Q

What are the types of inflammation? What do they do?

A
  • Acute - fights early stages of infection and prepares the process that leads to tissue repair
  • Chronic - characterized by the dominating presence of macrophages in the injured tissue
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3
Q

What are the exogenous causes of inflammation?

A
  • Physical agents - mechanical (fractures, foreign objects, sand, etc) and Thermal agents (burns, freezing)
  • Chemical agents - toxic gases, acids, bases
  • Biological agents - bacteria, viruses, parasites
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4
Q

What are endogenous causes of inflammation?

A
  • circulation disorders - thrombosis, infarction, hemorrhage

- metabolic products - uric acid, urea

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5
Q

What are the signs of acute inflammation?

A
  • calor (heat)
  • Rubor (redness)
  • tumor (swelling)
  • dolor (pain)
  • functio laesa (loss of function)
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6
Q

What are the mediators of inflammation?

A
  • pro-inflammatory cytokines (IL-1, IL-6, IL-8, TNFalpha)
  • complement components
  • prostaglandins
  • leukotrienes
  • Histamine
  • platelet-activating factor (PAF)
  • plasma proteases
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7
Q

How do prostaglandins contribute to inflammation?

A
  • contribute to vasodilation, capillary permeability, pain and fever during inflammation
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8
Q

How do leukotrienes contribute to inflammation?

A

induce smooth muscle contraction

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9
Q

How do histamines contribute to inflammation?

A
  • cause dilation and increased permeability of capillaries
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10
Q

How do platelet activating factor (PAF) contribute to inflammation?

A

induces platelet aggregation

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11
Q

How do plasma proteases contribute to inflammation?

A
  • kinins (particularly bradykinin) increase capillary permeability and pain
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12
Q

What happens during the vascular response of inflammation?

A
  • phase I - vasoconstriction
  • phase II - active vasodilation
  • phase III - passive dilation
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13
Q

What is included in the sequence of events of the cellular response of inflammation?

A
  • chemotaxis - of leukocytes
  • rolling - slow down leukocytes and increase their expression of adhesion molecules
  • migration - into tissue spaces
  • phagocytosis
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14
Q

What cells are the first to arrive at a site on infection?

A

cells of the innate immunity (neutrophils, macrophages, NK cells)

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15
Q

What are CAMs?

A

Cell adhesion molecules

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16
Q

What are the types of CAMs?

A
  • selectins
  • mucins
  • integrins
  • Ig-superfamily CAM
17
Q

What are the most important selectins and what do they bind?

A

selecin P, L, and E

- bind carbohydrate moieties on mucin-like molecules

18
Q

Where are the important selectins found?

A
  • Selectin L is expressed on leukocytes

- Selectin P and E are expressed on the endothelium during inflammation

19
Q

What are selectins responsible for?

A
  • leukocyte interaction with the endothelium during the initial phase of inflammation
20
Q

What are mucin CAMs?

A

group of heavily glycosylated, serine and threonine rich proteins that bind to selectins
- bind to selectins

21
Q

What are integrin CAMs?

A

heterodimeric proteins consisting of alpha and beta chains that are covalently joined at the cell surface
- bind to Ig superfamily domains

22
Q

What type of integrins do leukocytes express?

A

integrins with beta2 chains

23
Q

What happens if there is a defficiency in beta2 integrins?

A

leads to immunodeficiency call leukocyte adhesion deficiency (LAD) - an autosomal recessive disease manifested by recurrent bacterial infections
- neutrophils are unable to extravasate

24
Q

What do Ig-superfamily CAMs bind to?

A

integrins

25
Q

Where are Ig-superfamily CAMs expressed?

A

on endothelial cells

26
Q

What happens during the initiation of inflammation?

A

cytokines and other mediators of inflammation stimulate the endothelial cells, leading to increased expression of CAMs -> endothelial cell activation

27
Q

What are the four phases of leukocyte extravasation?

A
  • Phase I - rolling (leukocytes loosely bind to selectin E and P on endothelial cells. begins to roll on endothelium
  • Phase II - activation (increase in cytokine, especially chemokine secretion. increase in chemokine receptor expression on leukocytes -> activation of leukocytes
  • Phase III - Adhesion (integrins on leukocytes can now bind firmly to the endothelium)
  • Phase IV - transendothelial migration or diapedesis ( leukocytes squeeze through endothelium and use homotypic binding of platelet-endothelial-cell adhesion molecule 1 on the endothelium (self-to-self binding))
28
Q

What do effector lymphocytes do?

A

migrate to tissues where inflammation is taking place

29
Q

What do helper T lymphocytes do?

A

migrate to areas where they first encountered antigen