Session 2 ILOs - Acute Inflammation Flashcards Preview

Sem 2 - Pathological Processes > Session 2 ILOs - Acute Inflammation > Flashcards

Flashcards in Session 2 ILOs - Acute Inflammation Deck (7)
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1
Q

What the common causes (aetiology) of acute inflammation?

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

Neutrophil emigrate:

  • Due to 4 step process (margination, rolling, adhesion and emigration/diapedis)
  • Can start to cause the immune response
3
Q

Describe how you can identify a neutrophil and describe its actions in mediating acute inflammation

A

Describe: multi-lobed nucleus

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
4
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

5
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 compression of tubes
  • Exudate can because 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.)
  • 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)
6
Q

Describe the features seen in some common clinical examples of acute inflammation: COVID-19 infection, lobar pneumonia, acute appendicitis, bacterial meningitis, ascending cholangitis and liver abscess

A

COVID-19 infection: Acute injury to the alveoli

  • 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

  • Productive cough
  • Dyspnoea
  • Pleuritic pain

Acute appendicitis: sudden inflammation of the appendix

  • 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

Bacterial meningitis: entry of bacteria into the CSF leading to inflammation and the adjacent brain tissue

  • 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

Ascending cholangitis: inflammation of the bile duct (cholangitis), usually caused by bacteria ascending from its junction with the duodenum (commonly with gallstones)

  • Right upper quadrant pain
  • Fever
  • Jaundice

Liver abscess

  • Can occur due to billary obstruction leading to inflammation which heads up into the liver
  • There is necrosis from infection
7
Q

Briefly describe the following 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:
- Definitely in alpha-1-anti-trypsin which is a protease inhibitor that breaks down bacteria that is released from neutrophils