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BDS2 PMI > PMI03-2012 > Flashcards

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
Q

What causes redness in inflammation?

A

Vasodilatation

Increased blood flow

26
Q

What causes swelling in inflammation?

A

Exudation (increased vascular permeability)

27
Q

What causes pain in inflammation?

A

Release of mediators

Exudation

Inflammatory cell influx

28
Q

What are the beneficial effects of acute inflammation?

A

Dilution of toxins

Entry of antibodies and immune cells

Nutrient and drug transport

Fibrin formation

29
Q

What are the adverse effects of acute inflammation?

A

Tissue damage

Swelling

Pyrexia

(Asthma and autoimmunity)

BDS2 PMI (21 decks)

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