Inflammation Flashcards

1
Q

What at some stimulants of acute inflammation

A
Microorganism 
Trauma
Ischeamic necrosis
radiation
Chemicals
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2
Q

What does acute inflammatory exudate contain

A
Blood components
Fluid
Neutrophils
Fibrin
Maybe macrophages and lymphocytes
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3
Q

What is the role of fluid in exudate

A

Dilutes toxins

Carries nutrients/mediators/antibodies

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4
Q

What is the role of fibrin in exudate

A

Induces migration- chemo taxis

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5
Q

What is the told of neutrophils in exudate

A

Phagocytise living tissue ( bacteria) and necrotic debris

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6
Q

What is the first step in exudate formation

A

Blood vessels near damage become dilated
Increased blood flow then slows
Turbulent flow-redness
Cellular contents in centre and plans and fluid at edges

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7
Q

What is the second step in exudate formation

A

Vessels become more permeable and endothelial cells swell and retract
Water/salts/protein leak into damaged area

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8
Q

What is the third step in exudate formation

A

Neutrophils marginate and emigrate,

Adhere to endothelial cells and migrate to damaged area under influence of chemotaxins

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9
Q

What types of exudate exist

A

Serous (pericardial sac)
Purulent (pus eg meninges)
Fibrinous (coagulates)
Fibrino-purulent

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10
Q

What is elevated ESR

A

Erythrocytes segmentation time, means increased viscosity

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11
Q

What are the possible outcomes from acute inflammation

A

Resolution
Abscess formation
Organisation and repair
Chronic inflammation

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12
Q

What processes lead to resolution

A

Damage neutralised/eliminated
Macrophages remove dead cells and exudate
Local cells re-grow
Tissue structure and function returns to normal

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13
Q

Give examples of resolution

A

Pneumonia
Tubular necrosis kidney
Sunburn

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14
Q

What are the processes that lead to abscess formation

A

Large accumulation of liquid purple my exudate in area of extensive necrosis due to tissue damage
especially caused by bacteria (necrotoxins)
Attempt to walk off and limit spread

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15
Q

What are stages of healing by repair

A

Vascular- macrophages and enzymes remove debris and new vessels grow and support cells (
Fibrovascular- fibroblasts proliferate and lay down collagen
Collagenous- mature collagen, granulation tissues mature to scar
Finally new capillaries regress

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16
Q

What does organisation always lead to

A

Scarring

17
Q

When does chronic inflammation occur. What does it always result in

A

Damaging stimulus persists. scarring

18
Q

What cell is the main effector of chronic inflammation

A

Macrophage activated by gamma interferon

19
Q

What are the roles of a macrophage

A

Phagocytise
Secretory- mediators on inflammation, oxygen metabolites, professes and hydrolases
Cytokines (il-1 and tnf-a)
Growth factors

20
Q

Why might a damaging stimuli persist

A

Gastric acid is repeatedly produced
Bacteria distance from neutrophils/antibiotics ( endocarditis)
Resistance to neutrophil phagocytosis

21
Q

What are the two outcomes from stalemate between gastric mucosa damage and repair

A

Better- gastric acid neutralised or removed and damages stops - scar
Worse- increased gastric acid or repair impaired- ulcer perforation

22
Q

What causes chronic inflammation

A

When damaging stimulus not eradicated

Stalemate between continuing damage and attempts to repairs by fibrous scar formation

23
Q

What is granulomatous inflammation.

A

Chronic inflammation in which neutrophils are ineffective so macrophages invoked as part of early immune response
Aggregates of macrophages around damaging agent, associated with surrounding lymphocytes and fibroblasts= granuloma

24
Q

What causes granulomatous inflammation

A
Low pathogenicity organisms which excite a type iv immune response 
Organic or inorganic foreign material
Fungi 
Sarcoidosis 
Parasites
25
Q

Give and example of granulomatous inflammation

A

Tuberculosis
Tuberuloculosis mycobacterium resistant to neutrophils
Type IV response- macrophages attracted by cytokines that T cells secrete

26
Q

How can TB get worse

A

Necrosis expands and cannot be contained in granuloma, may spread via lymphatic system/ veins/ bronchi

27
Q

What is first intention healing

A

Surgery, wound trauma minimised, edges closely appeared-minimal exudate
Collagenous scar by exudate and organisation

28
Q

What is second intention healing

A

Extensive damage, infection
Healing characterised by increased necrotic debris/ granulation tissue
Wound contraction

29
Q

What are the problems with acute inflammatory exudate

A

Causes symptoms- meningitis

Croup/diphtheria, pericarditis, pleurisy, peritonitis

30
Q

What is the problem with scar formation

A

Skin- unslightly,

not elastic not contractile not secretory not absorptive

31
Q

Name five factors that lead to inadequate healing

A
Continuing infection 
Foreign/uncleared necrotic material 
Ischaemia 
Diabetes
Steroid therapy 
Denervation of area
Irradiation previous
32
Q

How does the brain parenchyma heal

A

Doesn’t contain fibroblasts so cannot make collagen
Necrosis= liquifactive
A strictures proliferate and lay down glial fibres to walk off area- cystic

33
Q

Explain healing of a bone fracture

A
Defect filled with heamatoma
Phagocytosis of debris 
Heamatoma undergoes organisation
Vascular then fibrovascular granulation tissue 
Osteoprogenitor cells develop convert to osteoblasts
Synthesis of osteiod collagen
Calcified 
Woven bone links with old bone 
Active remodelling= strong lamellar bone
34
Q

What at the aims of acute inflammation

A

Destroy/neutralise
Liquefy/remove dead tissue
Prepare for healing