PP: Acute Inflammation Flashcards
What is acute inflammation?
Response of living tissue to injury.
Name 5 major causes and biological purposes of acute inflammation.
- Microbial infections
- Hypersensitivity reactions
- Physical agents (e.g. Heat, radiation)
- Chemicals
- Tissue necrosis
Name the 5 characteristic clinical signs of acute inflammation.
- Rubor (Redness)
- Calor (Heat)
- Dolor (Pain)
- Tumour (Swelling)
- Loss of function
How does blood flow change during acute inflammation?
- Transient vasoconstriction of arterioles
- Vasodilation of arterioles and then capillaries (this increases the blood flow)
- Increased vessel permeability (results in exudation of protein rich fluid into tissues and slowing of circulation STASIS which is why swelling is seen)
Where does fluid move if there is increased hydrostatic pressure inside the vessels?
Interstitial space
Where does the fluid move if the is increased osmotic pressure in the interstitium?
Increased flow out of the vessels into the interstitial space
What is the clinical consequence of vascular leakage?
Oedema
What is meant by exudate oedema?
Fluid loss in inflammation is due to a higher protein content in the interstitial spaces.
What is meant by transudate oedema?
Fluid is lost from the vessels due to increased hydrostatic pressure
Give 2 examples when transudate oedema would occur.
Cardiac failure or venous outflow obstruction
How do tissues change in acute inflammation in order to allow neutrophil emigration?
- Margination (status causes neutrophils to line up at the edge of vessels along the endothelium)
- Rolling (neutrophils roll along, sticking intermittently)
- Adhesion (They stick more avidly)
- Emigration
What is chemotaxis?
Movement along a concentration gradient of chemoattractants.
How do neutrophils phagocytose?
- Contact
- Recognition (facilitated by opsonins)
- Internalisation (Cytoskeletal changes, phagosomes fuse with lysosomes)
Name 2 killing mechanisms that neutrophils have.
- Oxygen dependant (produces superoxide and hydrogen peroxide)
- Oxygen independent (Lysozyme and hydrolases)
Which chemicals mediate increased blood flow?
Histamine and prostaglandins
Which chemicals mediate vascular permeability?
Histamine and leukotrienes
Which chemicals mediate neutrophil chemotaxis?
C5a, LTB4, bacterial peptides
Which chemicals mediate phagocytosis?
C3b
What could happen after acute inflammation?
- Complete resolution
- Chronic inflammation with abscess
- Chronic information with fiberous repair
- Death
What is the resolution of acute phase inflammation?
Changes gradually reverse and vascular changes stop.
- Neutrophils no longer migrate
- Vessel permeability returns to normal
- Vessel calibre returns to normal
Name 5 mechanisms of vascular leakage.
- Endothelial contraction
- Cytoskeleton reorganisation
- Direct injury
- Leukocyte dependant injury
- Increased transcytosis (channels across endothelial cytoplasm)
He does infiltration of cells combat injury?
Removes pathogenic organism and necrotic debris
He does vasodilation combat injury?
Increases delivery, increases temperature
He does exudation of fluid combat injury?
- Delivers plasma proteins to area of injury (immunoglobulins, inflammatory mediators, fibrinogen)
- Dilutes toxins
- Increases lymphatic drainage
He does pain and loss of function combat injury?
Enforces rest therefore reducing the chance of further traumatic damage.
Name 4 systemic effects of acute inflammation.
- fever
- leukocytosis
- acute phase response
- shock (clinical syndrome of circulatory failure)
Name 4 clinical examples of acute inflammation.
- Bacterial meningitis
- Lobar pneumonia
- Liver Abscess
- Acute appendicitis
What organism causes lobar pneumonia?
Strepococcus pneumoniae
What is an abscess?
When solid tissues undergo acute inflammation and the exudate forces the tissue apart. Liquefactive necrosis occurs at the centre.
Name 2 examples of acute inflammation disorders.
- Alpha-1 antitrypsin deficiency
2. Hereditary angio-oedema
