Ch 13.6: Blood Vessels 13.7: Athrosclerosis and Cardiac Arrhythmias Transportation Respiratory gases, nutrients, and wastes Regulation Hormonal and temperature Protection Clotting and immunity

SLOs Compare the structure and function of arteries and veins Explain venous return and what happens when valves become incompetent Explain Angiogenesis and why understanting of it is relevant to medicine Review the structures and functions of different types of capillaries Describe how atherosclerosis develops and how it contribute to disease and death

Blood Vessel Structure Review Exchange Takes Place in the Capillaries Compare to Figs 13-26 & 27

Clinical Application: Aneurism Arteries Vasoconstriction and Vasodilation influence resistance Clinical Application: Aneurism Weakening of arterial walls  Risk: May lead to _______________________ Causes? Where is this?

Clinical Application cont. Cerebral aneurisms that rupture lead to _________________________

Capillaries Capillary types Tight leaky Diameter of these smallest blood vessels: ____________ Structure? Function? Regulation of Blood flow to capillaries: Vasoconstriction and vasodilation of arterioles Precapillary sphincters Capillary types Tight leaky Skin Muscle Lung CNS Exocrine glands Kidneys GI tract Liver Spleen BM

Clinical Application: Angiogenesis Growth of new blood vessels – occurs during Normal body maturation and growth Monthly re-growth of functional endometrium Wound healing Endurance training Cancer growth Macular Degeneration Clinical implications: Promote or inhibit angiogenesis with relevant cytokines

Veins Most of the total blood volume is in veins Lower pressure (2 mmHg compared to 100 mmHg average arterial pressure) Thinner walls than arteries, larger lumen; collapse when cut help return blood to heart Compare to Fig 13-29

Clinical Application: Varicose Veins Other vein pathologies: Deep vein thrombosis, leading to thrombo____________

Atherosclerosis Most common form of arteriosclerosis (hardening of the arteries) Contributes to 50% of deaths due to MI and stroke Plaque form in response to damage to endothelium of blood vessel. Caused by smoking, high blood pressure, diabetes, high cholesterol

Steps of Atherosclerosis LDLs vs. HDLs People who consume or produce a lot of cholesterol have more LDLs When endothelial cells engulf LDLs, they become oxidized LDLs that damage the endothelium Macrophages ingests LDL-cholesterol just under intima  Foam cells Macrophage paracrines cause smooth muscle cell proliferation  Fatty streaks  Plaques Cap of connective tissue covers layers of smooth muscle, lipids, and cellular debris.

Atherosclerosis is Inflammatory Process C-reactive protein (CRP): Produced by liver, increased in the presence of inflammation Blood tests can detect elevated C-reactive protein levels  considered non-specific “marker” for disease C-reactive protein is better predictor for athero- sclerosis than LDL levels Atherosclerosis is promoted by inflammation, Many cytokines and other paracrine regulators are involved

Inflammation converts stable plaques to vulnerable plaques Cerebral and coronary thrombi and emboli  ? Plaques can also weaken artery walls  ? Fig 13-31

Cardiovascular Disease (CVD) Not in book! Cardiovascular Disease (CVD)  1/2 of deaths in US – most common: CAD or CHD Uncontrollable vs. controllable risk factors Gender, age, genetics Cigarette smoking, obesity, Both: DM, high BP, high cholesterol

Cigarette Smoking Not in book! Nicotinic cholinergic receptors stimulate sympathetic neurons where? Vasoconstriction  BP ?  Risk for atherosclerosis  Carbon monoxide (myocardium extracts most of O2 brought to it under resting conditions)

Ischemic Heart Disease Ischemia means? Atherosclerosis most common cause Associated with increased production of lactic acid and resulting pain  angina pectoris (= type of ________ _____) Consequence of sustained ischemia? Nitroglycerin produces vasodilation

Detecting Ischemia Depression of the S-T segment of an electrocardiogram Plasma concentration of blood enzymes CPK – 3-6 hours, return to normal in 3 days LD – 48-72 hours, elevated about 11 days Troponin I – today’s most sensitive test

Heart Arrhythmias Detected by ECG see lab! The End