SBI 241 - Week 6.docx

**SBI 241 -- Week 6** **Atherosclerosis and Hypertension** *[Vascular bed]* Blood vessels can dilate, constrict, pulsate and form a closed delivery system for the blood, which begins and ends at the heart. [STRUCTURE:] *[Blood vessels]*, except capillaries, are composed of three distinct layers...

**SBI 241 -- Week 6** **Atherosclerosis and Hypertension** *[Vascular bed]* Blood vessels can dilate, constrict, pulsate and form a closed delivery system for the blood, which begins and ends at the heart. [STRUCTURE:] *[Blood vessels]*, except capillaries, are composed of three distinct layers: - [Tunica externa/tunica adventitia] -- Outer layer, largely composed of collagen fibres that protect and support the blood vessels and secure them to the surrounding tissues. Supplied with sympathetic nerve fibres and lymphatic vessels. - [Tunica media] -- middle layer, contains smooth muscle and elastic tissue. Sympathetic nervous system also innervates the smooth muscle layer and controls the diameter of the blood vessel. Constriction and dilation causes blood pressure to increase or decrease. - [Tunica interna] -- inner layer and lined with endothelium. Makes the inner surface smooth, thus minimising friction as blood flows through the vessel. *[Endothelium]*, lines all vessels and make up the main part of the capillary wall, has dynamic function: - Endothelium is involved in both coagulation and antithrombosis, as well as fibrinolysis, immune function, vasodilation or constriction, tissue growth and wound healing. - In particular, the endothelium is involved in a delicate balance between coagulation and anticoagulation as a result of the production of many chemical mediators. Some of this cause vasodilation, such as prostacyclin, nitric oxide and endothelium‐derived relaxing factor, and some cause vasoconstriction, such as endothelin, angiotensin II and thromboxane. - A healthy intact endothelium tends toward anticoagulation, but if damaged, the balance switches in favour of clot formation. This arrangement generally works well with clots forming where blood vessels are damaged, thus preventing blood loss and enabling the repair process to begin. *[Arteries]* -- thick walls and narrow lumen, responds to hormonal and neural signals. 3 groups are: 1. Elastic arteries 2. Muscular arteries 3. Arterioles *[Veins]* -- Thinner walls, contain fewer elastic and collagen fibres and less smooth muscles. Lumen is larger. *[Arteriosclerosis]* -- abnormal thickening and hardening of artery walls, lipids may be present. *[Atherosclerosis]* -- Form of arteriosclerosis with soft deposits of intra-arterial fat and other variations depending on the severity of condition. = Causes coronary heart disease and cerebrovascular disease. Risk factors: - Hypertension - Obesity - Smoking - Alcohol - Diabetes - Male gender **Pathophysiology of Atherosclerosis** *[Endothelial injury]* Endothelium becomes inflamed Smooth muscle cell and collagen migrate over the fatty streak = forms a fibrous plaque. - inflammatory cells → further inflammation → more endothelial damage - macrophages become foam cells and form fatty streaks - endothelium changes → platelet aggregation and vasoconstriction →decreased blood flow The fibrous plaque now formed may calcify, protrude into the lumen, obstruct blood flow, and become an 'unstable' plaque. An unstable plaque is prone to rupture and thus become a 'complicated' plaque. After rupture platelet adhesion occurs and tissue clotting factors are also released. A thrombus rapidly forms and may cause complete blockage of the vessel. **Clinical manifestations of atherosclerosis** [Partial obstruction] = transient ischaemic events, stress or exercise. [Further obstruction] = Infarction with manifestations depend on the vessels involved e.g. [coronary and cerebral vessels] = heart attack and stroke. [Peripheral artery obstruction] = associated with pain and disability especially lower limbs. **Management of atherosclerosis** Modification of lifestyle factors + Control of diabetes and HT + improvement of serum lipids + aspirin may be indicated. [Dyslipidaemia] metabolic disorder characterised by increased concentrations of plasma cholesterol and triglycerides. Primary lipoproteins found in blood of fasting individuals = VLDL, LDL (bad) and HDL (good). **Deep Vein Thrombosis (DVT)** [Thrombus] - develop in the superficial or deep veins of the legs. The blood flow is sluggish in the affected vessels, and the clotting cascade takes place. Triggers the inflammatory response, causing tenderness, swelling and erythema at the affected site. Thrombus can become loose and travel through the circulation as an embolus, may travel to the lungs causing = pulmonary embolism. [Hypertension] -- repeated measurements of over 140/90 [Secondary h]ypertension is caused by: Kidney disease, endocrine imbalance [Malignant hypertension] -- Occurs in younger groups with renal and collagen disease [Isolated systolic hypertension] -- occurs when combination of factors is seen in the elderly and is due to the increase in cardiac output, increased peripheral resistance and renal vascular resistance. [Risk factors for hypertension:] - family history - age and gender - abdominal obesity - Alcohol intake - Glucose intolerance - High sodium intake - Sedentary lifestyle - Low potassium, calcium and magnesium intake. [Clinical Manifestations of hypertension:] Considered as a silent condition, early on. Symptoms arise due to associated damage of organs as well as vascular changes: - Heart disease - Renal insufficiency - Brain dysfunction - Impaired vision - Impaired mobility - Vascular occlusion and oedema [Chronic hypertension leads to:] 1. Vascular remodelling 2. Renal changes 3. Cardiac hypertrophy These causes increased risk of, Myocardial infarction, kidney disease and stroke. [Evaluation of hypertension] 1. Repeated high BP measurement 2. History and physical examination 3. Blood analysis - Na+, K+, Cl-, HCO3- - Urea, creatinine, uric acid - Haemoglobin - Fasting glucose - Total cholesterol, LDL, HDL 4. ECG Hypertension: Management