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Principles of Disease > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

List the causes of acute inflammation.

A
  • 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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2
Q

Recognise the benefits of acute inflammation.

A
  • 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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3
Q

where does acute inflammation take place

A

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

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4
Q

name the cardinal signs of inflammation

A 
(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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5
Q

what is flush, flare and wheal

A 
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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6
Q

exudation is

A

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

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7
Q

exudate contains

A

fluid rich in protein - plasma - includes immunoglobulin and fibrinogen

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8
Q

what is microcirculation

A

capillary beds, fed by arterioles and drained by venules

- lymphatic channels and drainage

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9
Q

Describe the sequence of microvascular change.

what is flush, flare and wheal

A 
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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10
Q

exudation is

A

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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11
Q

exudate contains

A

fluid rich in protein - plasma - includes immunoglobulin and fibrinogen

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12
Q

migration and neutrophils

A

neutrophils move to endothelial aspect of lumen

step 1

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13
Q

pavementing and neutrophils

A

neutrophils adhere to endothelium

step 2

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14
Q

migration of neutrophils

A

neutrophils move to endothelial aspect of lumen

step 1

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15
Q

pavementing of neutrophils

A

neutrophils adhere to endothelium

step 2

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16
Q

emigration of neutrophils

A

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

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17
Q

outcomes of cute inflammation

A

resolution
suppuration
organisation
chronic inflammation

18
Q

outcomes of acute inflammation

A 
resolution
suppuration
organisation
dissemination
chronic inflammation
19
Q

list mediators of acute inflammation and describe functions

A 
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
20
Q

inflammation of peritoneal cavity

A

peritonitis

21
Q

immediate systemic effects of acute inflammation

A

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

22
Q

explain the outcomes of acute inflammation - suppuration

A

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

23
Q

Explain the systemic effects of acute inflammation.

A 
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
24
Q

Describe the complications of acute inflammation.

A

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

25
Q

Summarise the mediators of acute inflammation.

A

histamine

maybe add more later?

26
Q

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

A
  • 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
27
Q

Types of signalling in molecules inside cells:

pattern associated molecular patterns

A
  • microbial antigen
  • genetically hard wired to recognise
  • innate and adaptive immunity
28
Q

Types of signalling in molecules inside cells:

danger associated molecular patterns

A
  • substances released in response to stimulus
29
Q

Other types of signalling in molecules inside cells:

A
  • stimulate pattern recognition receptors on cell membranes

- activate inflammatory response

30
Q

Types of signalling in molecules inside cells:

pattern associated molecular patterns

A
  • microbial antigen
  • genetically hard wired to recognise
  • innate (non-specific) and adaptive immunity
31
Q

long term systemic effects of acute inflammation

A

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

32
Q

what does 5-hydroxytryptamine (serotonin) do in inflammation

A
  • preformed in platelets
  • released when platelets degranulate in coagulation
  • vasoconstriction
33
Q

Pus in other places

A

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

34
Q

Outcomes of acute inflammation - organisation

A
  • granulation tissue characteristic
  • healing and repair
  • leads to fibrosis and formation of a scar
35
Q

What is granulation tissue?

A 
“universal patch” – repair kit – for all damage
formed of:
- new capillaries - angiogenesis
- fibroblasts and collagen
- macrophages
36
Q

Outcomes of acute inflammation - dissemination

A
  • spread to bloodsteam - patient “septic”
  • bacteraemia - bacteria in blood
  • septicaemia - growth of bacteria in blood
  • toxaemia - toxic products in blood
37
Q

Pathogenesis of septic shock

A

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

38
Q

Systemic release of chemical mediators from cells into plasma causes

A
  • 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)
39
Q

Bacterial endotoxin release causes

A
  • interleukin-1 released

- acts on hypothalamus - pyrexia

40
Q

Activation of coagulation causes

A
  • disseminated intravascular coagulation
  • vasoactive chemical - vasodilatation
  • hemorrhagic skin rash
41
Q

Systemic release of chemical mediators from cells into plasma causes

A
  • 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)
42
Q

reduced perfusion of tissues in septic shock can lead to

A

tissue hypoxia

loss of cell tissue and organ function

Principles of Disease (27 decks)

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