Session 2 ILO's Acute inflammation Flashcards

1
Q

Describe the common causes (aetiology) of acute inflammation

A
  • Microbial infections
  • Hypersensitivity reactions
  • Physical and chemical agents
  • Tissue necrosis
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2
Q

Explain the tissue changes that occur in acute inflammation

A

Changes to vascular flow:
- Initial vasoconstriction at initial injury site (seconds)
- Then vasodilation occurs, allowing more blood (fluid and leukocytes) to flow to the affected area
CAUSES heat and redness

Fluid exudate is formed:

  • Permeability increases as well to allow: fluid, cells and proteins to escape
  • Exudate is a protein rich fluid, containing red and white cells

Neutrophil emigration:
- Neutrophils Rapidly migrate to site of infection for phagocytosis / to cause the immune response

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3
Q

Evaluate how these tissue changes (including vascular flow, formation of a fluid exudate, neutrophil emigration) constitute an effective response to injury

A

Increase delivery of:

  • Nutrients
  • Oxygen
  • Antibodies
  • Inflammatory cells

Cause:

  • Dilution of toxins
  • Stimulation of immune response
  • Destruction and removal of dead or foreign material

All of which constitute an effective response to injury

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4
Q

Recognise what a neutrophil is and describe its actions in mediating acute inflammation.

A

Describe: multi-lobed nucleus - they form pus

Actions in mediating acute inflammation:

  • Phagocytose - the phagosome fuses with the lysosome and also release inflammatory mediators
  • Directed to the correct substance via opsonisation
  • Kill the pathogens, either through oxygen dependant (respiratory burst) or oxygen independant (lysozyme, hydrolytic enzymes, defensins) mechanisms
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5
Q

Recognise and explain the action of some of the key chemical mediators involved in acute inflammation

A

Vasoactive amines, e.g. histamine

  • Increase vasodilation
  • Increase vascular permeability

Vasoactive peptides, e.g. bradykinin

  • Increase vascular permeability
  • Increase pain response

Mediators derived from phospholipids, e.g. prostaglandin

  • Increase vasodilation
  • Increase temperature
  • Increase pain response

Complement components, e.g. C3a

  • Increase vascular permeability
  • Help with chemotaxis

Cytokines and chemokines, e.g. tumour necrosis factor (TNF)

  • Help with chemotaxis
  • Increase temperature

Exogenous mediators, e.g. endotoxin
- Help with chemotaxis

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6
Q

Define inflammation

A

Response of living tissue to injury controlled by chemical mediators
Consists of vascular phase(changes in blood flow&accumulation of exudate) and cellular phase(delivery of neutrophils)

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7
Q

Recognise and interpret the clinical signs of acute inflammation and how these relate to tissue changes.

A

rubor - redness - increased blood flow due to vascular phase
tumour - swelling- increased capillary permeability and hydrostatic pressure increase
calor - heat - vasodilation from vascular phase
dolor - pain
loss of function - this enforces rest and reduces the chance of further damage

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8
Q

Understand the local and systemic short and long term consequences of acute inflammation and interpret how these might affect organs.

A

Local acute inflammation:

  • Local swelling, could lead to obstruction and compression of tubes
  • Exudate can cause compression of organs
  • Loss of fluid (e.g. burns)
  • Pain (muscle atrophy)

Systemic acute inflammation:

  • Fever
  • Leucocytosis (increased production of WBC)
  • Acute phase response (feeling generally unwell e.g. reduced appetite, altered sleep etc.) it induces rest
  • Acute phase proteins (e.g. CRP, fibrinogen, alpha-1 antitrypsin)
  • SEPTIC SHOCK risk factor

Long term consequences:

  1. Could be completely resolved
  2. Repair with connective tissue (fibrosis) if there has been substantial destruction
  3. Progression to chronic inflammation (prolonged inflammation with repair)
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9
Q

Describe the features seen in some common clinical examples of acute inflammation: COVID-19 infection, lobar pneumonia, acute appendicitis

A

COVID-19 infection: Acute injury to the alveoli (4)

  • Thrombus production
  • Fever or chills
  • Cough
  • Shortness of breath or difficulty breathing

Lobar pneumonia: inflammatory exudate within the intra-alveolar space resulting in consolidation that affects a large and continuous area of the lobe of a lung (4)

  • Productive cough
  • Dyspnoea
  • Pleuritic pain
  • Sputum

Acute appendicitis: sudden inflammation of the appendix (4)

  • Initial pain starts in the middle of your tummy before moving towards the right iliac fossa region
  • Low-grade fever that may worsen as the illness progresses
  • loss of appetite
  • vomitting
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10
Q

Understand a few clinical examples of inherited disorders of the acute inflammatory process: Hereditary angio-oedema, Alpha-1 antitrypsin deficiency, Chronic granulomatous disease.

A

Hereditary angio-oedema:

  • Deficiency in the C1 esterase inhibitor of the complement pathway
  • Leads to reduced C2 and C4
  • Rapid swelling and oedema of the skin randomly, with no clear trigger

Chronic granulomatous disease:

  • Deficiency in NADPH oxidase
  • No respiratory burst defence so can engulf pathogens, but cannot kill them
  • Granulomas form (accumulations of neutrophils/macrophages with trapped bacteria)

Alpha-1 antitrypsin deficiency:
- Deficiency in alpha-1-anti-trypsin which is a protease inhibitor that breaks down bacteria that is released from neutrophils

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11
Q

Describe the features seen in some common clinical examples of acute inflammation: bacterial meningitis, ascending cholangitis and liver abscess.

A

Bacterial meningitis: entry of bacteria into the CSF leading to inflammation of the adjacent brain tissue (5)

  • Fever of 38C or above
  • Rash that does not fade when a glass is rolled over it (but a rash will not always develop)
  • Dislike of bright lights
  • Intense headache
  • Stiff neck

Ascending cholangitis: is an infection of the biliary tree, most commonly caused by obstruction with inflammation and bacterial seeding and growth (less severe form.) (3)

  • Right upper quadrant pain
  • Fever
  • Jaundice

Liver abscess

  • collections of thick fluid or pus containing blood, dead cells and germs that develop after infections affecting the liver, bile ducts or other sites in the body (8)
  • There is necrosis from infection
  • Chest &upper abdomen pain
  • Dark urine
  • Fevers
  • night sweats
  • nausea
  • vomiting
  • weight loss
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