Lecture 15 Flashcards
(20 cards)
Systolic pressure
pressure in arteries when heart contracts
diastolic pressure
pressure in arteries when heart relaxes
isolated systolic hypertension
elevated systolic ONLY
isolated diastolic hypertension
elevated diastole ONLY
Factors influencing HR
CO, blood volume and peripheral resistance
Hypertension prevalence
over 1B people globally (>25% Aussies). More prevalent in males
primary hypertension
90% cases. Clinically silent. Risk factors incl. age, male, family history, diabetes, stress, smoking, Na+, alcohol, obesity, sedentary lifestyle
secondary hypertension
caused be decreased renal blood flow, primary aldosteronism or tumours on the adrenal gland/neuroendocrine glands. All owing to renin-angiotensin-aldosterone system. Angiotensin II is involved in vasoconstriction of arteries, increases peripheral resistance and BP. It targets aldosterone and vasopressin release which can influence the kidney and it’s capability to hold Na+ and K+. decrease salt clearance = increase salt retention = increase H2O retention = increase blood volume.
underlying issue with hypertension
Prolonged exertion of high pressure on the artery wall = fibrotic changes (decrease elasticity) and endothelial damage. Hypertension = risk of CVD
Atherosclerosis
Med to large arteries. Hardening result from plaque development (lipid plaque)
Arteriosclerosis
Arterioles. Not related to a plaque. Lumen size decreases due to protein or cellular buildup
Atherosclerosis risk factors
Develops silently therefore, not diagnosed until clinical event. Smoking, hypertension, dislipidemia, diabetes, age, race, male, family history
Estrogen
Anti-atherogenic. Involved in vasodilation and prevents plaque progression as long as endothelial layer is intact. Phytoestrogens provide similar protection. After menopause, risk of CVD significantly increases
Intima
inner most. Endothelial mesh and minimal subendothelial CT
Media
Layers of vascular SM cells that provide elasticity
Adventitia
Small BV, loose CT and collagen. structural integrity.
Preclinical phase
Hypertension -> endothelial damage. toxins from smoking, LDLs. All disrupt endothelial layer = release of cytokines = stimulate inflammation = attempted phagocytosis of LDLs= formation of foam cells = increase cytokines = increase monocytes = increase foam cells. Over time, platelets come and cause SMC migration from media to intima. They produce collagen which composes fibrous cap.
Plaque components
Fatty streak (foam cells + LDLs) + fibrous cap
Clinical phase
Plaques can remain stable for yonks. But, the inflammatory cells sitting in the plaque can secrete enzymes that break down fibrous cap, weakening it and impacting outer layer of the vessels, As FC decreases, it can make the plaque vulnerable. At this point, FC is thin and there is a large lipid-filled necrotic core. As soon as lipid core is exposed to the blood, it can be thrombogenic where platelets form a plug which eventually becomes a blood clot. BC decreases blood flow risking ischaemia. These enzymes can also lead to embolism where artery ruptures leading to aneurysm. Can also risk embolism
Atherosclerotic CVD
Leading cause of VD worldwide as it can lead to coronary artery disease, cerebrovascular disease, peripheral artery disease, aneurysms
