Acute inflamation mw % XXXXXXXXXXXXXXXXXXXXXXXXXXXX Flashcards

1
Q

What is the Definition of acute inflammation?

A

•Series of protective changes occurring in living tissue as a response to injury.

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2
Q

What are the important signs of inflammation?

A
  • Rubor - redness
  • Calor - heat
  • Tumor - swelling
  • Dolor - pain
  • Loss of function
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3
Q

What are the Causes - aetiology -
of acute inflammation?

A
  • Micro-organisms.
  • Mechanical - trauma - injury to tissue.
  • Chemical - upset stable environment
  • Physical - extreme conditions
  • Dead tissue
  • Hypersensitivity
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4
Q

Outline some feutures of acute inflammation?

A
  • Series of microscopic events
  • Localised to affected tissue
  • Take place in the microcirculation
  • Result in the clinical symptoms and signs of acute inflammation - the cardinal signs
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5
Q

What is the microcirculation?

A

•Capillary beds, fed by arterioles and drained by venules.

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6
Q

What are the overall steps in acute inflamation?

A
  • Changes in vessel radius - flow
  • Change in the permeability of the vessel wall - exudation
  • Movement of neutrophils from the vessel to the extravascular space
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7
Q

Explain the changes in vessel radius in acute inflamation?

A
  1. Transient arteriolar constriction.
  2. Local arteriolar dilatation- causes increased local tissue blood flow
  3. Relaxation of vessel smooth muscle
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8
Q

What is the advantage of increased permeability in acute inflamation?

A

•Locally produced chemical mediators cause an endothelial leak followed by the net movement of plasma from capillaries to extravascular space( Exudation).

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9
Q

What is the effect of exudation?

A
  • Oedema formed
  • Oedema is accumulation of fluid in the extravascular space
  • Explains swelling of tissue in acute inflammation
  • Swelling causes pain - reduce function
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10
Q

Describe the phases of emigration of neutraphils?

A
  • Margination - neutrophils move to endothelial aspect of lumen
  • Pavementing - neutrophils adhere to endothelium
  • Emigration - neutrophils squeeze between endothelial cells - active process - to extravascular tissues.
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11
Q

What is the resolution of acute inflammation?

A
  • Inciting agent isolated & destroyed
  • Macrophages move in from blood and phagocytose debris; then leave
  • Epithelial surfaces regenerate
  • Inflammatory exudate filters away
  • Vascular changes return to normal
  • Inflammation resolves
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12
Q

What are the benefits of acute inflammation?

A
  • Rapid response to non-specific insult
  • Cardinal signs and loss of function

–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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13
Q

What are the outcomes of acute inflamation?

A
  • Resolution
  • Suppuration-formation of pus.
  • Organisation
  • Chronic inflammation
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14
Q

Inflammation at various anatomical locations

A

•“structure”-itis

  • appendix -appendicitis
  • Lungs -pneumonia
  • Pleural cavity -pleurisy
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15
Q

What do neutrophils do?

A

•Mobile phagocytes

–recognise foreign antigen

–move towards it - chemotaxis

–adhere to organism

  • Release granule contents
  • Phagocytose & destroy foreign antigen
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16
Q

What are the Consequences of neutrophil action?

A
  • Neutophils die when granule contents released.
  • Produce a “soup” of fluid, bits of cell, organisms- pus.
  • Might extend into other tissues, progressing the inflammation
17
Q

What is the role of plasma proteins in inflammation?

A
  • Fibrinogen - coagulation factor - forms fibrin and clots exudate - localises inflammatory process
  • Immunoglobulins in plasma specific for antigen - humoural immune response
18
Q

Where do mediators of acute inflmation come from?

A
  • Endothelial cell surface membrane
  • Released from cells
  • In the plasma
19
Q

What are the collective effects of mediators?

A
  • Vasodilatation
  • Increased permeability
  • Neutrophil adhesion
  • Chemotaxis
  • Itch and pain
  • Mediators had positive and negative effects
  • Result is a dynamic balance
  • Favours and inhibits acute inflammation
  • relative to need
20
Q

What are the immediate systemic effects of inflammation?

A
  • Pyrexia - raised temperature
  • Feel unwell.
  • Neutrophilia - raised white cell count

–bone marrow releases/produces.

21
Q

What are the longer term effects?

A
  • Lymphadenopathy which is a regional lymph node enlargement–immune response
  • Weight loss - catabolic process
  • Anaemia
22
Q

Explain suppuration as an outcome to acute inflamation?

A

•Pus formation

–dead tissue, organisms, exudate, neutrophils, fibrin.

•pyogenic membrane(fibrin) surrounds pus

–capillary sprouts, neutrophils, fibroblasts

–Walls off pus

23
Q

What is an abscess?

A

•Collection of pus (suppuration) under pressure

•Single locule, multiloculated

  • “points” and discharges
  • Collapses - healing and repair
24
Q

Explain organisation as an outcome to acute inflamation?

A
  • Granulation tissue characteristic
  • Healing and repair
  • Leads to fibrosis and formation of a scar
25
Q

What is granulation tissue?

A
  • “universal patch” – repair kit – for all damage
  • Formed of:

–new capillaries - angiogenesis

–fibroblasts and collagen

–macrophages

26
Q

Explain dissemination as an outcome of acute inflammation ?

A
  • Spread to bloodsteam - patient “septic”
  • Bacteraemia - bacteria in blood
  • Septicaemia - growth of bacteria in blood
  • Toxaemia - toxic products in blood
27
Q

What are the effects of systemic infection?

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 haemorrhagic skin rash

28
Q

What are the outcomes of septic shock?

A
  • Rapidly fatal
  • Tissue hypoxia - cell death
  • Haemorrhage
  • Requires urgent intervention and support

–awareness and early recognition

–ability of young people to compensate

  • admit to hospital and intensive care