PMI03-2012 Flashcards

1
Q

Define inflammation.

A

Complex response of vascularised tissues to infections and tissue damage

Involves cells and molecules of host defence from the circulation

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2
Q

How long does acute inflammation take to develop?

A

Minutes to hours

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3
Q

How do acute and chronic inflammation differ?

A

Tissue composition

CAN OCCUR SIMULTANEOUSLY

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4
Q

What is the purpose of acute inflammation?

A

Destroy/contain noxious stimuli by dilution and phagocytosis

Initiate repair and return function by fibrin formation and nutrient transport

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5
Q

What agents can cause damage?

A

Physical = trauma, thermal, radiation

Chemical = CO, cigarette smoke, ethanol

Infectious = toxins, metabolic products, lysis, DNA damage

O2 deprivation = hypoxia, ischaemia

Immunologic = autoimmunity

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6
Q

What vascular events take place in inflammation?

A

Vasodilatation

Increased vascular permeability

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7
Q

Which mediators are responsible for the vascular events that occur in inflammation?

A

Histamine

Prostaglandins

Platelet activating factor

Kinins

Leukotrienes

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8
Q

What is the purpose of vasodilatation in inflammation?

A

Decreased flow rate so cells pack/vascular congestion and escape vessels more easily

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9
Q

What is the purpose of increased vascular permeability in inflammation?

A

Allows exudation of fluid, molecules and immune cells

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10
Q

Which cell is predominant in acute inflammation?

A

Neutrophil/polymorphonuclear leukocyte (PMN)

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11
Q

How do neutrophils reach the site of injury/infection from the blood?

A

Margination at site where vascular events have occurred

Receptors detect endothelial ligands (and vice versa) = rolling adhesion with selectins

Arrest of rolling with integrins (PMN) and ICAM-1 (endothelial)

Transmigration/diapedesis

Chemotaxis

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12
Q

Describe the process of rolling adhesion of neutrophils in acute inflammation.

A

L-selectin of neutrophils weakly binds P-selectin of endothelial cells

Attaching and detaching = rolling

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13
Q

Which molecules upregulate selectins?

A

IL-1

TNF

(released following tissue damage)

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14
Q

What molecules can contribute to chemotaxis of neutrophils?

A

Bacterial products

Chemokines

C5a/anaphylatoxins

Leukotriene B4

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15
Q

What are the three types of exudate?

A

Serous

Fibrinous/fibrin

Purulent/suppurative

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16
Q

Describe serous exudate.

A

Least common type of exudate

Cell-poor

Found in mucosal or skin blisters

Feature of certain viral infections

17
Q

Describe fibrinous exudate.

A

Pinky-orange with H&E

Occurs where there has been significant vascular damage

Fibrinogen leaks out to form fibrin

18
Q

Describe purulent exudate.

A

Cell-rich - usually with neutrophils

Found commonly in abscesses

Especially common in pyogenic bacterial infections (Staphylococcus)

19
Q

Give some examples of plasma-derived mediators.

A

Kinins

Complement

Fibrin

20
Q

Give some examples of inflammatory cell-derived mediators.

A

Histamine

Serotonin

Prostaglandins

Leukotrienes

Nitric oxide

Platelet activating factor

21
Q

Describe how neutrophils carry out their actions.

A
  1. Adherence and ingestion with extension of pseudopodia into a phagosome - aided by opsonisation
  2. Phagosome fuses with lysosome to form phagolysosome
  3. Digestion
  4. Residual body is discharged or sequestered
22
Q

How are the killing species/compounds created for digestion in a neutrophil?

A

Reduction of NADP+ to NADPH in formation of superoxide anion (ROS)

ROS converted to hydrogen peroxide

Myeloperoxidase converts H2O2 to hypochlorite in the presence of Cl-

23
Q

What are the cardinal signs of inflammation?

A

Heat/calor

Redness/rubor

Swelling/tumor

Pain/dolor

Loss of function/functio laesa

24
Q

What causes heat in inflammation?

A

Vasodilatation

Increased blood flow

25
What causes redness in inflammation?
Vasodilatation Increased blood flow
26
What causes swelling in inflammation?
Exudation (increased vascular permeability)
27
What causes pain in inflammation?
Release of mediators Exudation Inflammatory cell influx
28
What are the beneficial effects of acute inflammation?
Dilution of toxins Entry of antibodies and immune cells Nutrient and drug transport Fibrin formation
29
What are the adverse effects of acute inflammation?
Tissue damage Swelling Pyrexia (Asthma and autoimmunity)