Chronic inflammation occurs when there is persistence of damaging stimulus or injury so that complete healing cannot occur.
Chronic inflammation is characterized by infiltration of mononuclear cells, including macrophages, lymphocytes, and plasma cells.
Chronic inflammation leads to tissue destruction and attempts at healing.
Granulomatous inflammation is characterized by the formation of granulomas, composed of epithelioid cells, multinucleate giant cells, lymphocytes, and often seen in type 4 hypersensitivity reactions in which cell-mediated immunity is involved.
Hyperaemia and Congestion are haemodynamic disorders (disorders of circulation).
Peripheral Nerve Injury involves distal end degeneration, sprouts arising from severed axon, slow growth, haphazard growth, and loss of neurons that cannot be regenerated.
Aortic valve stenosis is a pathology due to scarring.
Fibrosis often refers to the abnormal deposition of collagen that occurs in internal organs in chronic diseases.
Stomach outlet stenosis is a pathology due to scarring.
Healing of Myocardial Infarct involves the healing of cardiomyocytes by fibrosis and compensation for loss of myocardium by hypertrophy of surviving myocardial fibres.
Healing of a bone fracture involves initial bridging by hematoma, forming granulation tissues to form the woven bone "callus" remodeling with formation of cancellous bone, and increasing tensile strength.
Constrictive pericarditis is a pathology due to scarring.
Liver cirrhosis is a pathology due to scarring.
Hyperaemia is defined as arterial vasodilation resulting in more blood in the blood vessels.
Congestion is defined as venous outflow obstruction resulting in more blood in the blood vessels.
Local factors that affect wound healing include infection, mechanical factors, foreign bodies, and the size, location, and type of wound.
Hormones: Glucocorticoids have an anti-inflammatory effect and inhibit healing.
Complications of wound healing include deficient scar formation, wound dehiscence (splitting open), ulceration, incisional hernias, and the formation of contractures following severe burns and chemical injury.
Nutrition: Protein and vitamin C deficiency inhibit collagen synthesis.
Systemic factors that affect wound healing include age, nutrition, metabolicstatus, and hormones.
Generalised oedema can be caused by cardiac, renal, or hepatic causes.
Haemorrhage can be caused by traumatic or spontaneous factors, and can be due to abnormal vessels or platelets.
Congestion can be localised, in deep leg veins with blood clot, or generalised, as in congestive heart failure.
Cardiac oedema is due to heart failure.
Physiological hyperaemia is caused by nervous impulses and functional demands on muscles during exercise.
Localised oedema can be caused by impaired venous drainage, venous occlusion due to thrombosis, increased vascular permeability and hyperaemia, inflammation, obstruction or destruction of lymphatics, and filariasis or cancer.
Nephrotic syndrome is characterised by protein loss in urine due to glomerular disease, which results in reduced plasma oncotic pressure and activation of the renin-angiotensin-aldosterone system (kidney retains Na+ and water).
Oedema is an excessive extravascular accumulation of fluid in interstitial tissues and body cavities.
The primary causes of oedema are changes in Starling’s forces, including increased hydrostatic pressure, reduced oncotic (osmotic) pressure, increased endothelial permeability, lymphatic obstruction, and sodium and water retention.
Pathological hyperaemia is associated with acute inflammation.
Cancer, pneumonia, ischaemic heart disease, cerebrovascular disease, accidents, hypertensive diseases, kidney diseases, urinary tract infections, and other heart diseases are the top causes of death in Singapore.
Septic emboli are a type of embolism that spread infection.
Fat, air, and amniotic fluid are examples of liquid, gaseous, and solid types of embolisms respectively.
Factors affecting the development of an infarct include the anatomy of the arterial blood supply, the rate of development of vascular occlusion, tissue vulnerability, and prior hypoxia.