Acute Inflammation Flashcards
List the characteristic macroscopic features of acute inflammation
Calor (heat), rubor (redness), tumor (swelling), dolor (pain), loss of function
List the major causes and biological purposes of acute inflammation
Microbial infection, hypersensitivity reaction, physical agents, chemicals, tissue necrosis
Characterise the microscopic features of acute inflammation
- Transient vasoconstriction of arterioles
- Vasodilation of arterioles and capillaries
- Increased permeability of blood vessels
- Exudation of fluid
- Margination and emigration
- Macrophages and lymphocytes
Describe the action of some chemical mediators
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
Explain how formation of an exudate is brought about
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
Explain the difference between exudate and transudate oedema
Exudate - high protein content e.g. inflammation
Transudate - low protein content, fluid loss due to hydrostatic pressure e.g. cardiac failure, venous outflow obstruction
Define the term ‘neutrophil leucocyte’
Neutrophil leucocyte - the primary type of white blood cell involved in inflammation, a type of granulocyte.
Explain what neutrophils do, and briefly how they do it
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.
Explain the term ‘chemotaxis’
Neutrophils move by chemotaxis.
Chemotaxis - movement along a concentration gradient of chemoattractants
Chemotaxins include C5a, LTB4, bacterial peptides
Explain how the exudation of fluid, infiltration of cells, vasodilation and pain and loss of function help combat injury
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
Describe some possible local and systemic complications of acute inflammation
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
List the clinical sequelae of acute inflammation
- Complete resolution - exudate drains to lymphatics, fibrin is degraded by plasmin, neutrophils die and are phagocytosed, damaged tissue might regenerate
- Continued acute inflammation with chronic inflammation = abscess
- Chronic inflammation with fibrous repair, tissue regeneration
- Death
Explain how drugs may modify acute inflammation
Aspirin - lowers fever
Painkillers - reduce pain
Explain a few clinical examples of acute inflammation, including bacterial meningitis, lobar pneumonia, skin blisters, abscesses and acute appendicitis
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 -
Give an example of one inherited disorder of the acute inflammatory process
a1 antitrypsin deficiency - a1 antitrypsin inhibits elastase, without this inhibition elastase breaks down lung/liver tissue –> emphysema, liver sclerosis