Lecture 19: Acute Inflammation Flashcards
What is inflammation?
“Local physiological response to tissue injury”
What are the two types of inflammation?
Acute (Initial)
Chronic (Prolonged)
What can be causes of acute inflammation?
Microbial infection
Hypersensitivity reactions (Sun, Acids, Allergic reactions)
What are some symptoms of acute inflammation?
- Redness
- Heat
- Swelling
- Pain
- Loss of function
What causes redness during inflammation?
Dilation of small blood vessels
What causes heat during inflammation?
Peripheries
Hyperaemia -> vascular dilation
Fever
What swelling occurs during inflammation?
Oedema
Exudate
(inflammatory cells)
New connective tissue
Why does pain occur during inflammation?
Stretching/distortion of tissue
Bradykinin, prostaglandins, serotonin
Why does loss of function occur during inflammation?
Movement inhibited by pain
Severe swelling
What are the 3 steps to acute inflammation?
- Changes in vessel calibre (and flow)
- Increase vascular permeability -> formation of fluid exudate
- of cellular exudate
What allows increased/ diversion of blood flow in acute inflammation?
Opening of precapillary sphincter
Why is vascular permeability increases during acute inflammation?
Fluid escapes from vessels as does proteins (Fluid exudate) which leads to odema
What are 3 features of fluid Exudate?
High protein content 50g/L
Contains fibrinogen -> fibrin deposition
High turnover
How does fluid escape leading to increased vascular permeability in acute inflammation?
Gaps appear between endothelial cells of veins and venules
histamine acts on Contractile proteins (actin)
What are features of delayed prolonged leakage?
Heat, cold, radiation, bacterial toxins, corrosive chemicals
What is the mechanism for immediate transient reactions?
Chemical mediators
Histamine, bradykinin, NO, C5a, lecotriene B4, Platelet activating factor
What is the mechanism for immediate sustained reactions?
Severe direct vascular injury e.g. trauma
What is the mechanism for delayed prolonged reactions?
Endothelial cell injury
What is a Diagonostic histological feature of acute inflammation?
accumulation of neutrophil polymorphs within extracellular space (Cellular Exudate)
3 marginations of neutrophils?
Loss of intravascular fluid
Increase of in plasma viscosity
Slowing of flow
How does adhesion of neutrophils occur during acute inflammation?
“pavementing” of neutrophils in venules
Normally random contact does not cause adhesion
Site of inflammation, early process independent of flow
Interaction of adhesion molecules
What happens after adhesion of neutrophils?
Neutrophil Emigration (Diapedesis)
What is Neutrophil Emigration (Diapedesis)?
Migration by active amoeboid movement
Venules and small veins
What might also escape from vessels during acute inflammation aside from fluid and proteins?
Red cells may also escape
Passive process
Hydrostatic pressure
What is chemotaxis?
the attraction of neutrophils towards chemicals
What chemical substances are released by injured tissues early on?
Histamine, thrombin
What does histamine and thrombin release from injured tissue cause?
increase of adhesion molecules on endothelial cells
What cells produce histamine?
Mast cells
Basophils
Eosinophils
Platelets
Release stimulated by complement C3a and C5a, neutrophil lysosomal proteins
Repercussions of histamine and thrombin being released from injured cells.
Vasodilation
Emigration of neutrophils
Chemotaxis
Increased vascular permeability
Itching and pain
What does plasma contain? (Chemical mediators)
Plasma contains 4 enzymatic cascade systems that produce inflammatory mediators
(complement, kinins, coagulation factors, fibrinolytic system)
What do macrophages secrete during an acute response?
Secrete chemical mediators (IL1,TNF-alpha)
Effects on endothelial cells
Occur after histamine and thrombin
E-selectin (adhesion molecule), IL-8 (chemotaxin for neutrophils)
What are the roles of neutrophil polymorph?
Movement (Contraction of microtubules
Chemotaxis – directional response to chemical mediators)
Adhesion
(Opsonised by immunoglobulins or complement
Allows for neutrophils to bind)
Phagocytosis
Describe phagocytosis?
The process where cells ingest solid particles
Adhesion (facilitated by opsonisation)
Ingestion (pseudopodia)
Phagasome
Lysosomes fuse
What are 6 beneficial effects of acute inflammation?
Dilution of toxins
– carried away by lymphatics
Entry of antibodies
– Increased vascular permeability
Transport of drugs
– Especially antibiotics
Fibrin formation
– Impedes movement of microorganisms, trapping for phagacyotsis, matrix for granulation tissue
Delivery of nutrients and oxygen
– Essential for cells with high metabolic activity (neutrophils)
Stimulate the immune response
– Fluid drains to local lymph nodes with soluble antigens
What are some harmful effects of acute inflammation?
Digestion of normal tissues
– collagenases and proteases
Swelling
– epiglottitis, cranial cavity
Inappropriate inflammatory response
– type I hypersensitivity
What is resolution?
“complete restoration of tissues to normal after an episode of acute inflammation”
What happens in the body during resolution?
Minimal cell death/tissue damage
Occurrence in organ/tissue with regenerative capacity
Rapid destruction of causal agent
Rapid removal of fluid by vascular drainage
What is suppuration?
Formation of pus
What 5 cells aid suppuration?
Living neutrophils
Dead neutrophils
Bacteria
Cellular debris
Globules of liquid
What is an abscess?
Collection of pus, bacteria often inaccessible to antibodies and antibiotics
How can abscesses be drained?
Can form a “point” and burst
Cavity collapses -> organisation, fibrosis, scar
What is Empyema?
Empyema = collection of pus in a body cavity e.g. pleural space, gallbladder
What is a fistula?
abnormal connection between 2 mucosal surfaces or a mucosal surface to the skin
What is organisation?
Replacement of tissue by granulation tissue
New capillaries grow into the inflammatory exudate
Macrophages migrate
Fibroblasts proliferate
how does acute inflammation migrate into chronic inflammation?
Causative agent not removed - > progression to chronic inflammation
Change in character of exudate
Lymphocytes, Plasma cells, macrophages
Can you have chronic inflammation without a period of acute inflammation?
Yes
Systemic effects of inflammation?
Pyrexia
Constitutional symptoms (Malaise, anorexia, nausea)
Reactive hyperplasia of reticuloendothelial system
Enlarged lymph nodes, splenomegaly
Haematological changes
Increased ESR, leucocytosis, anaemia
