Session 2 ILOs - Acute Inflammation Flashcards
What the common causes (aetiology) of acute inflammation?
- Microbial infections
- Hypersensitivity reactions
- Physical and chemical agents
- Tissue necrosis
Explain the tissue changes that occur in acute inflammation
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
Describe how you can identify a neutrophil and describe its actions in mediating acute inflammation
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
Recognise and explain the action of some of the key chemical mediators involved in acute inflammation
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
Understand the local and systemic short and long term consequences of acute inflammation and interpret how these might affect organs
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:
- Could be completely resolved
- Repair with connective tissue (fibrosis) if there has been substantial destruction
- Progression to chronic inflammation (prolonged inflammation with repair)
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
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
Briefly describe the following clinical examples of inherited disorders of the acute inflammatory process: Hereditary angio-oedema, Alpha-1 antitrypsin deficiency, Chronic granulomatous disease
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
