Acute Inflammation Flashcards

0
Q

List the characteristic macroscopic features of acute inflammation

A

Calor (heat), rubor (redness), tumor (swelling), dolor (pain), loss of function

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1
Q

List the major causes and biological purposes of acute inflammation

A

Microbial infection, hypersensitivity reaction, physical agents, chemicals, tissue necrosis

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2
Q

Characterise the microscopic features of acute inflammation

A
  1. Transient vasoconstriction of arterioles
  2. Vasodilation of arterioles and capillaries
  3. Increased permeability of blood vessels
  4. Exudation of fluid
  5. Margination and emigration
  6. Macrophages and lymphocytes
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3
Q

Describe the action of some chemical mediators

A

Histamine - released from mast cells, basophils, causes vascular dilation, transient increase in vascular permeability, pain.
Proteases (plasma proteins, produced in liver) - kinins, complement system (C3a, C5a), coagulation system
Prostaglandins/Leukotrienes - increased blood flow
Cytokines/Chemokines - interleukins, TNF

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4
Q

Explain how formation of an exudate is brought about

A

Arteriolar dilation leads to increase in hydrostatic pressure
Increased permeability of a vessel leads to loss of protein into interstitium
Net flow of fluid out of vessel –> oedema

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5
Q

Explain the difference between exudate and transudate oedema

A

Exudate - high protein content e.g. inflammation
Transudate - low protein content, fluid loss due to hydrostatic pressure e.g. cardiac failure, venous outflow obstruction

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6
Q

Define the term ‘neutrophil leucocyte’

A

Neutrophil leucocyte - the primary type of white blood cell involved in inflammation, a type of granulocyte.

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7
Q

Explain what neutrophils do, and briefly how they do it

A
Margination - stasis causes neutrophils to line up at the edge of blood vessels along the endothelium
Rolling - neutrophils then roll along the endothelium, sticking to it intermittently 
Adhesion - neutrophils stick more avidly 
Emigration - neutrophils pass through vessel wall
Neutrophils phagocytose (contact, recognition, internalisation) facilitated by opsonins. They may release toxic metabolites and enzymes.
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8
Q

Explain the term ‘chemotaxis’

A

Neutrophils move by chemotaxis.
Chemotaxis - movement along a concentration gradient of chemoattractants
Chemotaxins include C5a, LTB4, bacterial peptides

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9
Q

Explain how the exudation of fluid, infiltration of cells, vasodilation and pain and loss of function help combat injury

A

Exudation of fluid - delivers plasma proteins to area of injury (immunoglobulins, inflammatory mediators, fibrinogen), dilutes toxins, increases lymphatic drainage (delivers microorganisms to phagocytes, antigens to immune system)
Infiltration of cells - removes pathogenic organisms, necrotic debris
Vasodilation - increases delivery (of fluid, cells) increases temperature
Pain and loss of function - enforces rest, reduces chance of further traumatic damage

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10
Q

Describe some possible local and systemic complications of acute inflammation

A

Local:
Swelling - blockage of tubes e.g. bile duct, compression of vital structures
Exudate - compression e.g. cardiac tamponade, serositis
Loss of fluid e.g. burns
Pain and loss of function especially if prolonged
Damage to normal tissue
Systemic:
Fever
Shock
Acute phase response - decreased appetite, raised pulse, altered sleep patterns
Acute phase proteins - C-reactive protein, a1 antitrypsin, fibrinogen, serum amyloid A protein

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11
Q

List the clinical sequelae of acute inflammation

A
  1. Complete resolution - exudate drains to lymphatics, fibrin is degraded by plasmin, neutrophils die and are phagocytosed, damaged tissue might regenerate
  2. Continued acute inflammation with chronic inflammation = abscess
  3. Chronic inflammation with fibrous repair, tissue regeneration
  4. Death
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12
Q

Explain how drugs may modify acute inflammation

A

Aspirin - lowers fever

Painkillers - reduce pain

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13
Q

Explain a few clinical examples of acute inflammation, including bacterial meningitis, lobar pneumonia, skin blisters, abscesses and acute appendicitis

A

Bacterial meningitis - acute inflammation in meninges can cause vascular thrombosis and reduce cerebral perfusion.
Lobar pneumonia - alveoli contain exudate, causative organism (streptococcus pneumoniae) leads to worsening fever, hypoxaemia, dry cough, breathlessness.
Skin blister - caused by heat, chemicals, collection of fluid strips off overlying epithelium, pain and profuse exudate.
Abscesses - inflammatory exudate forces tissues apart, liquefactive necrosis in centre
Acute appendicitis -

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14
Q

Give an example of one inherited disorder of the acute inflammatory process

A

a1 antitrypsin deficiency - a1 antitrypsin inhibits elastase, without this inhibition elastase breaks down lung/liver tissue –> emphysema, liver sclerosis

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