Inflammation and Healing Flashcards

1
Q

What is acute inflammation?

A

Initial and transient series of tissues reactions to injury

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2
Q

5 causes of acute inflammation

A

Trauma, heat, cold, UV, radiation, microbial infections, chemicals, tissue necrosis, hypersensitivity reactions

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3
Q

4 outcomes of acute inflammation

A

Resolution, progression, suppuration, organisation

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4
Q

3 processes involved in acute inflammation

A

Changes in vessel calibre, increased vascular permeability and formation of fluid exudate, formation of cellular exudate - emigration of neutrophil polymorphs into extravascular space

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5
Q

4 physical characteristics of acute inflammation

A

Rubor, calor, tomur, dolor (also loss of function)

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6
Q

Features of the fluid exudate and what it contains

A

High protein content - up to 50g/L - immunoglobulins, coagulation factors such as fibrinogen

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7
Q

4 steps of neutrophil emigrations

A

Margination into plasmatic zone, adhesion to endothelial cells, pass between endothelial cells, pass through basal lamina and migrate into adventitia

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8
Q

6 chemical mediators released by cells

A

Histamine, lysosomal compounds, prostaglandins, leukotreines, serotonin, chemokines

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9
Q

What effects does histamine have in acute inflammation?

A

Causes vascular dilatation and the immediate transient phase of increased vascular permeability

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10
Q

Where is histamine stored?

A

Stored as preformed granules mainly in mast cells but also in basophil and eosinophil leucocytes and platelets

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11
Q

Name the 4 enzymatic cascade systems present in plasma

A

Coagulation factors, kinin system, complement and the fibrinolytic system

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12
Q

4 advantages of these systems

A

Each step results in amplification of the response, it is safer to have inactive precursors than active mediators, more regulators can modulate response, each step results in end products with possible different activities

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13
Q

3 ways the complement system can be activated

A

In tissue necrosis enzymes capable of activating it are released, during infection formation of antigen-antibody complexes activate it via the classical pathway, endotoxins of Gram negative bacteria can activate it via the alternative pathway, products of kinin and fibrinolytic pathway

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14
Q

2 features of a neutrophil polymorph

A

Multilobulated nucleus, fine granules

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15
Q

Define organisation

A

Organisation of tissues is their replacement by granulation tissue as part of the repair process

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16
Q

4 causes of chronic inflammation

A

Progression from acute, primary chronic inflammation (crohns/sarcoidosis/autoimmue diseases), transplant rejection, organisms that are resistance to phagocytosis

17
Q

3 characteristic cells of chronic inflammation

A

Lymphocytes, plasma cells and macrophages

18
Q

5 activities of cytokines

A

Recruitment of macrophages, production of inflammatory mediators, recruitment of other lymphocytes, destruction of target cells, interferon production

19
Q

What is a granuloma?

A

An aggregate of epithelioid histiocytes

20
Q

What is an epithelioid histiocyte?

A

Activated macrophage with large vesicular nucleus and eosinophilic cytoplasm

21
Q

When do histiocytic giant cells form?

A

When particulate matter which is indigestible by macrophages accumulates (silica or bacteria such as tubercle bacilli)

22
Q

3 types of histiocytic giant cells and one characteristic or each

A

Langhans giant cells - horseshoe arranged nuclei, Foreign body giant cells - randomly scattered nuclei, Touton giant cells - central ring of nuclei/clear peripheral cytoplasm due to accumulated lipid

23
Q

What are the 3 populations of cells according to their potential for renewal and an example of where you would find each

A

Labile - good capacity to regenerate, eg surface epithelium
Stable - divide at slow rate normally but retain ability to divide when necessary, eg hepatocytes
Permanent - no effective regeneration, eg nerve cells

24
Q

3 mechanisms of pain associated with acute inflammation

A

Distortion of tissues due to oedema, pus under pressure in an abscess cavity, chemical mediators (bradykinin/prostaglandins/serotonin)

25
Q

2 beneficial effects of inflammation

A

Walling off of an abscess cavity (reducing the spread of infection) and the destruction of invading microorganisms

26
Q

5 systemic effects of inflammation

A

Pyrexia, weight loss, reactive hyperplasia of the reticuloendothelial system, haematological changes, amyloidosis

27
Q

What can be measured in the blood that acts as a marker for systemic granulomatous disease?

A

ACE - secretory product of epithelioid histiocytes

28
Q

2 features of granulation tissue

A

loops of capillaries supported by myofibroblasts

29
Q

What is healing by first intention?

A

Narrow wounds, fibrin links both sides, coagulated blood forms scab, capillaries proliferate, fibroblasts secrete collagen, basal epidermal cells proliferate,

30
Q

What is healing by second intention?

A

Phagocytosis to remove debris, granulation tissue to fill in defects, organisation, early fibrous scar, scar contraction,