Acute inflammation is the bodys stereotypical response to tissue
injury. It is characterised by: Heat, pain, redness, swelling (calor, dolor, rubor, tumor) +/- loss of function (functio laesa) +/- secretions Chronic inflammation is present where there is active inflammation, tissue injury and healing at the same time. It is defined by the cells types present (macrophages and lymphocytes) and typically has a longer time course than acute inflammation A granuloma is a collection of epithelioid macrophages. Granulomatous inflammation is a form of chronic inflammation characterized by the presence of epithelioid macrophages, called such as they resemble epithelial cells. These can fuse to form multinucleate giant cells (Langhans cells) which are sometimes present in granulomatous inflammation. It can be classified as caseating (e.g. TB) or non-caseating (e.g. sarcoidosis, Crohns disease)
ASCITES
Ascites is the abnormal accumulation of fluid in the peritoneal cavity Causes can be split into transudates or exudates. Transudate is defined as protein content 30g/L. Another commonly used criteria is the SAAG (Serum-Ascites Albumin Gradient): A high gradient (>1.1 g/dL) indicates the ascites is due to portal hypertension. A low gradient (<1.1 g/dL) is suggestive of ascites of non-portal hypertensive aetiology. These can be split up into those with portal hypertension and those with hypoalbuminaemia: Increased portal venous pressure: Cirrhosis Right sided cardiac failure Constrictive pericarditis Budd Chiari syndrome (occlusion of hepatic veins) Thoracic duct obstruction Plasma oncotic changes due to hypoalbuminaemia: Liver failure Protein losing enteropathy Starvation or cachexia Nephritic and nephrotic syndromes Renal failure Causes of ascites classified as exudates: The main examples are inflammatory causes: these result in protein leakage (the 4 Ps) Peritonitis: bacterial or tuberculosis Post-irradiation Peritoneal metastases Pancreatitis
ATHEROSCLEROSIS
Atherosclerosis is a pathological process of the vasculature in which an artery wall thickens as a result of the accumulation of fatty materials such as cholesterol. Atherosclerosis begins with endothelial dysfunction, resulting in migration of macrophages, some of which form foam cells and a lipid core. There is migration of vascular smooth muscle cells to form a fibrous cap. This process ultimately results in stenosis of the vessel and rupture of the cap can lead to thrombosis and possible infarction of the supplied tissue. Risk factors for atherosclerosis include: Smoking Hypertension Diabetes mellitus types 1 and 2 Family history of atherosclerotic disease Increased cholesterol (in particular, increased LDL and decreased HDL) It can affect: The aorta Coronary arteries Carotid arteries and cerebral vasculature Popliteal and lower limb vasculature