Which cells are involved in acute inflammation?
- Neutrophils.
- Monocytes.
What are the microscopic features of acute inflammation?
- Vasodilation.
- Vascular leakage of protein rich fluid.
- Neutrophil polymorphs migrate to the site.
What are the clinical (macroscopic) features of acute inflammation?
- Rubor (redness)
- Tumour (swelling)
- Calor (hot).
- Dolar (pain).
- Loss of function.
What are the potential causes of acute inflammation?
- Trauma.
- Ischaemia.
- Chemicals.
- Microbial infection.
- Hypersensitivity.
Which cells are involved in chronic inflammation?
- Lymphocytes, macrophages and plasma cells.
What are the microscopic features of chronic inflammation?
- Evidence of continuous destruction.
- Necrosis.
What are the clinical (macroscopic) features of chronic inflammation?
- Chronic ulceration.
- Chronic abscess cavity.
- Granulomatous inflammation.
- Fibrosis.
What are the potential causes of chronic inflammation?
- Resistance of infective agent (e.g. TB)
- Endogenous materials (e.g. necrotic tissue).
- Exogenous materials (e.g. asbestos).
- Autoimmune conditions (e.g. RA).
- Primary granulomatous diseases (e.g. Crohn’s, sarcoidosis).
What is a granuloma?
- An aggregation of epithelioid histiocytes.
What is fibrosis? Which cells are involved?
- Excess deposition of ECM proteins.
- Carried out by myofibroblasts.
What is the process of scar tissue formation?
- Fibroblasts secrete collagen.
- The collagen cross-links and forms a pronounced alignment in a single direction.
- New tissue appears differently and has inferior function.
What are the four overarching stages of atherosclerosis?
1) Endothelial damage.
2) Fatty streak formation.
3) Plaque growth.
4) Plaque rupture (thrombus).
What is the detailed process of atherosclerosis?
1) Endothelium of vessel damaged.
2) LDL accumulates in the arterial wall.
3) Macrophages migrate to site and take up lipids to become FOAM CELLS.
4) Fatty streak forms (containing dead foam cells).
5) Macrophages release inflammatory cytokines and GF.
6) Smooth muscle in vessel wall proliferates.
6) Fibrin forms a fibrous cap over the atheroma.
7) Plaque continues to grow.
8) Eventually, the plaque ruptures which triggers thrombosis.
What are the three features in Virchow’s triad?
- Stasis of blood flow.
- Endothelial injury.
- Hypercoagulable state.
What is the difference between thrombosis and atherosclerosis?
- Atherosclerosis - Deposition of fatty materials int he arterial wall.
- Thrombosis - Coagulation/clotting of blood (platelet aggregation).
What is the process of thrombosis?
1) Endothelial injury.
2) Collagen exposed.
3) Platelets are activated and aggregate.
4) Clotting factors released/intrinsic pathway activated.
5) Fibrin meshwork forms and RBCs also become stuck in the atheroma.
6) Structure grows and protrudes further and further into the lumen of the vessel. This causes more turbulence of blood flow, and more platelet aggregation… (+ve feedback loop).
What are the 4 different fates of thrombosis?
1) Resolves - Body clears the thrombus/thrombus dissolves.
2) Organised - Becomes a scar.
3) Recanalisation - Intima proliferates and the thrombus becomes vascularised.
4) Embolus - Fragments of the thrombus break off into the circulation.
What is an embolus?
- Mass of material in the circulation lodges in a vessel, occluding the lumen.
What is ischaemia?
- Reduced blood flow to a tissue or body part caused by constriction or blockage of the vessels supplying it.
What is infarction?
- Necrosis of a tissue or body part when blood supply is compromised.
Is ischaemia reversible or non-reversible?
- Reversible.
Is infarction reversible or non-reversible?
- Non-reversible.
What is apoptosis?
- Controlled cell-death.
What are the two pathways for apoptosis?
- Extrinsic. Involves ligand binding (TNF/receptor binding)
- Intrinsic. Involves P53.
