S2) Acute Inflammation Flashcards by Vinay Tanna

What is inflammation?

Response of living tissue to injury

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Causes of acute inflammation (5)

Microbial infections

Hypersensitivity reactions

Physical agents

Chemicals

Tissue necrosis

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Clinical signs of AI (5)

Rubor = redness

Tumor = swelling

Calor = heat

Dolor = pain

Loss of function

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4 stages of vascular response

1) Arterioles vasoconstrict
2) Arterioles and capillaries vasodilate causing heat and redness

3) Permeability of blood vessels increases
- exudate formed

4) Stasis caused by increased concentration of RBCs and increased viscosity of the blood

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Where is histamine released from?

What does it do? (3)

Mast cells, basophils and platelets

Vasodilation, increased permeability and pain

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Transudate vs exudate

Transudate caused by change in hydrostatic pressure

Exudate has a high protein content

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How does the exudate leave the vessels? (5)

Contraction of epithelia

Cytoskeletal reorganisation

Direct injury

Increased transcytosis eg vegF channels

Leukocyte dependent injury

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Which two mediators cause epithelia to contract

Histamine and leukotrienes

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4 stages of neutrophil infiltration

1) Margination caused by stains
2) Rolling - intermittent sticking
3) Adhesion
4) Emigration

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How do neutrophils migrate from the vessels? (2)

Relaxation of tight junctions

Digestion of basement membrane

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4 stages of neutrophil movement inside tissue

1) Chemotaxis - attracted by C5a, LTB4 and bacterial peptides
2) Receptor binds to ligands
3) Cytoskeleton rearranges
4) Pseudopod forms (cytoplasm filled projection)

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What do neutrophils do? (4)

1) Contact, recognition and internalisation
2) Facilitated by opsonins
3) Cytoskeletal changes
4) Phagosomes fuse with lysosomes to make secondary lysosomes

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What are the two mechanisms of destruction?

Oxygen dependent

Oxygen independent

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Describe oxygen independent mechanisms (3)

Lysozymes and hydrolases

Bactericidal permeability increasing protein (BPI)

Cationic proteins (defensins)

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Which chemical mediators increase blood flow? (2)

Histamine and prostaglandins

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Which chemical mediators increase vascular permeability? (4)

Histamine
Leukotrienes
Serotonin
Bradykinin

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Which mediators cause neutrophil chemotaxis? (3)

C5a, LTB4 and bacterial peptides

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How does the following combat injury:

Exudate (3)

Delivers protein to areas of injury eg mediators and fibrinogen

Dilutes toxins

Increases lymphatic drainage

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How does the following combat injury:

Infiltration of cells

Removes organisms and debris

How does the following combat injury:

Vasodilation

Increases delivery and temperature

How does the following combat injury:

Pain and loss of function

Enforces rest, reducing chance of further damage

4 local complications of acute inflammation?

Swelling can block tubes eg bile duct or intestine

Exudate can compress pericardium causes cardiac tamponade

Loss of fluid eg in burns

Pain

How is fever caused?

Macrophages produce pyrogenic cytokines (TNF, interleukin 1) when stimulated by excess pyrogens

Cytokines cause increase in synthesis of prostaglandin E2

Anterior hypothalamus set point increases

How is prostaglandin synthesis inhibited?

Aspirin or NSAIDS inhibit cyclo-oxygenase which produces prostaglandins from arachadonic acid

What is leukocytosis? Which mediators cause it to occur?

Accelerated release of cells from bone marrow 1l-1 and TNFa

Which proteins are acutely affected by AI in the serum

CRP, a1-antitrypsin, fibrinogen, amyloid A protein

How are mediators inactivated? (5)

Short half lives Enzymes eg heparinase Inhibitors may bind eg antiproteases Specific inhibitors eg lipoxins and endothelin (peptides which constrict blood vessels) Diluted by the exudate

Bacterial meningitis: What causes it? Symptoms? How does it cause death?

Infection of the meninges - protective layers of the spinal cord and brain Stiff neck, non-blanching rash, fever Inflammation causes vascular thrombosis and reduced cerebral perfusion

4 stages of lobar pneumonia:

1) Congestion - fluid build up, heavy lungs 2) Red hepatisation 3) Grey hepatisation 4) Resolution

Skin blisters: What causes them? Why is the exudate clear? What happens after?

Heat, sunlight or chemicals - fluid strips away epithelium Few inflammatory cells Resolvable or scars over

Describe what is in an abscess

Inflammatory exudate forces tissues apart with liquefactive necrosis in the centre Causes high pressure and pain

3 types of exudate into serous cavities

Ascites (abdomen) Pleural effusion Pericardial effusion

Other inherited disorders:

Angio-oedema Complement deficiencies Chronic granulomatous disease

How are prostaglandins made and what do they do?

Made from cell membrane phospholipids and causes vasodilation, fever and increased pain sensitivity

Fresh blood isn't chemotactic - why is clotted blood?

Breakdown products of thrombin and fibrin and chemotactic

How do cells respond to chemotaxins?

Chemotaxin binds to cell receptor Ca and Na rush into cell Cell swells and reorganises its cytoskeleton Cell assumes a triangular shape pointing in the direction of the chemotactic stimulus - sending out pseudopod

What is the difference between rolling and adhesion?

Rolling - neutrophils bind to selectins Adhesion - neutrophils bind to intergrins

Which chemical mediators causes chemotaxis (5)

Leukotriene b4 C5a C3a Chemokines Endotoxins

What is shock? What causes it?

Dramatic drop in BP due to widespread vasodilation and increased vascular permeability Bacterial products or inflammatory mediators spreading around the body

Sequelae to AI (4)

Pus/ abscess (purulent exudate) Haemorrhagic exudate Serous exudate Fibrinous exudate

What is purulent exudate?

Cream/white exudate rich in neutrophils

What is a haemorrhagic exudate?

Red bloody exudate because of RBCs released from ruptured blood vessels Seen in destructive infections and malignant tumours

What is a serous exudate? What protein doesn't it contain?

Clear exudate with plasma proteins but few leucocytes so infection unlikely Seen in blisters Fibrinogen

What is a seroma?

A tissue space filled with clear, sterile fluid Seen as a post-operative complication

What is a fibrinogen exudate?

Exudate with significant deposition of fibrin

Hereditary angio-oedema: What causes it? Symptoms

C1-esterase inhibitor deficiency Itchy cutaneous angio-oedema Recurrent abdominal pain due to intestinal oedema

Complications of pneumonia: (5)

Bacteraemia leading to meningitis, arthritis or endocarditis Lung abscesses Empyema Pleural effusion Lung fibrosis