Acute Inflammation Flashcards by Priyanka Bhandari

List the causes of acute inflammation.

micro-organisms such as bacteria since pathogenic organisms cause infection
mechanical (trauma) injury to tissue even sterile (eg surgery)
chemical - upset stable environment such as pH
physical - extreme conditions such as temperature or ionising radiaton.
dead tissue as cell necrosis irritates adjacent tissue
hypersensitivity have several classes of reaction

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Recognise the benefits of acute inflammation.

Effects of exudation
- oedema formed - accumulation of fluid formed in the
Rapid response to non-specific insult
Cardinal signs and loss of function through swelling of - extravascular provides transient protection of inflamed area
Neutrophils destroy organisms and denature antigen for macrophages
Plasma proteins localise process
Resolution and return to normal

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where does acute inflammation take place

in the microcirculation (series of microscopic events are localised to affected tissue)

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name the cardinal signs of inflammation

(local effects include)
rubor - redness
calor - heat
tumor - swelling
dolor - pain
loss of function

All of these are explained by the sequence of Pathological events taking place

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what is flush, flare and wheal

Transient arteriolar constriction
  - occurs for few moments, probably protective
Local arteriolar dilatation
  - active hyperaemia
Relaxation of vessel smooth muscle
  - ?autonomic NS or mediator derived

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exudation is

endothelial leak - fluid and protein not held in vessel lumen (imbalance of Starling forces)
localised vascular response

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exudate contains

fluid rich in protein - plasma - includes immunoglobulin and fibrinogen

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what is microcirculation

capillary beds, fed by arterioles and drained by venules

- lymphatic channels and drainage

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Describe the sequence of microvascular change.

what is flush, flare and wheal

Transient arteriolar constriction
  - occurs for few moments, probably protective
Local arteriolar dilatation
  - active hyperaemia
Relaxation of vessel smooth muscle
  - ?autonomic NS or mediator derived

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exudation is

endothelial leak - fluid and protein not held in vessel lumen (imbalance of Starling forces)
localised vascular response
net movement of plasma from capillaries to extravascular space

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exudate contains

fluid rich in protein - plasma - includes immunoglobulin and fibrinogen

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migration and neutrophils

neutrophils move to endothelial aspect of lumen

step 1

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pavementing and neutrophils

neutrophils adhere to endothelium

step 2

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migration of neutrophils

neutrophils move to endothelial aspect of lumen

step 1

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pavementing of neutrophils

neutrophils adhere to endothelium

step 2

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emigration of neutrophils

neutrophils squeeze between endothelial cells - active process - to extravascular tissues
(step 3)

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outcomes of cute inflammation

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resolution
suppuration
organisation
chronic inflammation

outcomes of acute inflammation

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resolution
suppuration
organisation
dissemination
chronic inflammation

list mediators of acute inflammation and describe functions

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Molecules on endothelial cell surface membrane (sticky)
Molecules released from cells
Molecules in the plasma
Molecules inside cells
effects include:
- vasodilatation
- increased permeability
- neutrophil adhesion
- chemotaxis
- itch and pain

inflammation of peritoneal cavity

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peritonitis

immediate systemic effects of acute inflammation

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pyrexia - raised temperature
- endogenous pyrogens from white cells act centrally
feel unwell
- malaise, anorexia, nausea
- abdominal pain and vomiting in children
neutrophilia - raised white cell count
- bone marrow releases/produces

explain the outcomes of acute inflammation - suppuration

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Pus formation
- dead tissue, organisms, exudate, neutrophils, fibrin, red cells, debris
Pyogenic membrane surrounds pus
- capillary sprouts, neutrophils, fibroblasts
- walls off pus
Abscess
- collection of pus (suppuration) under pressure
- single locule, multiloculated
- “points” and discharges
- collapses - healing and repair

Explain the systemic effects of acute inflammation.

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shock - inability to perfuse tissues
clinical picture of early septic shock
- peripheral vasodilatation
- tachycardia - high heart rate
- hypotension - low blood pressure
- often pyrexia
- sometimes hemorrhagic skin rash

Describe the complications of acute inflammation.

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raised HR insufficient to maintain cardiac output
SVR low; so BP falls
- BP = CO x SVR
- increasing heart rate insufficient (CO = SV x HR)
reduced perfusion of tissues
- tissue hypoxia
- loss of cell tissue and organ function

Summarise the mediators of acute inflammation.

histamine | maybe add more later?

Prostaglandins (arachidonic acid metabolites via cyclo-oxygenase pathway) and inflammation

- many cells (endothelium and leukocytes) - many promote histamine effects and inhibit inflammatory cells - thromboxane A2 promotes platelet aggregation and vasoconstriction – the opposite effect to PGD2, PGE2, etc - latter: effectiveness of non-steroidal anti-inflammatory drugs

Types of signalling in molecules inside cells: | pattern associated molecular patterns

- microbial antigen - genetically hard wired to recognise - innate and adaptive immunity

Types of signalling in molecules inside cells: | danger associated molecular patterns

- substances released in response to stimulus

Other types of signalling in molecules inside cells:

- stimulate pattern recognition receptors on cell membranes | - activate inflammatory response

Types of signalling in molecules inside cells: | pattern associated molecular patterns

- microbial antigen - genetically hard wired to recognise - innate (non-specific) and adaptive immunity

long term systemic effects of acute inflammation

lymphadenopathy - regional lymph node enlargement - immune response weight loss - catabolic process anaemia

what does 5-hydroxytryptamine (serotonin) do in inflammation

- preformed in platelets - released when platelets degranulate in coagulation - vasoconstriction

Pus in other places

empyema - in a hollow viscus - gall bladder - pleural cavity pyaemia - discharge to bloodstream

Outcomes of acute inflammation - organisation

- granulation tissue characteristic - healing and repair - leads to fibrosis and formation of a scar

What is granulation tissue?

``` “universal patch” – repair kit – for all damage formed of: - new capillaries - angiogenesis - fibroblasts and collagen - macrophages ```

Outcomes of acute inflammation - dissemination

- spread to bloodsteam - patient “septic” - bacteraemia - bacteria in blood - septicaemia - growth of bacteria in blood - toxaemia - toxic products in blood

Pathogenesis of septic shock

Systemic release of chemical mediators from cells into plasma Increased heart rate compensates - CO = SV x HR Bacterial endotoxin released Activation of coagulation

Systemic release of chemical mediators from cells into plasma causes

- mediators cause vasodilation causing loss of systemic vascular resistance (SVR) - BP = CO x SVR - results in catecholamine release - tachycardia (increased heart rate) follows to maintain (CO)

Bacterial endotoxin release causes

- interleukin-1 released | - acts on hypothalamus - pyrexia

Activation of coagulation causes

- disseminated intravascular coagulation - vasoactive chemical - vasodilatation - hemorrhagic skin rash

Systemic release of chemical mediators from cells into plasma causes

- mediators cause vasodilation causing loss of systemic vascular resistance (SVR) - BP = CO x SVR - results in catecholamine release - tachycardia (increased heart rate) follows to maintain (CO)

reduced perfusion of tissues in septic shock can lead to

tissue hypoxia | loss of cell tissue and organ function

Acute Inflammation Flashcards

(42 cards)