Chapter 15_1 flashcards
(27 cards)
Arteries: Basic Definition & Function
Muscular-walled blood vessels with elastic fibers that move blood away from the heart under high pressure. Greater arterial pressure means greater resistance the heart must pump against.
Arteriosclerosis vs. Atherosclerosis: General Definitions
Arteriosclerosis: Hardening and narrowing of arteries. Atherosclerosis: Plaque build-up on the arterial wall, restricting blood flow.
Arterial Wall Composition: Tunica Intima
Innermost layer, composed of endothelial cells in contact with blood. Primary site of damage in arteriosclerosis/atherosclerosis.
Arterial Wall Composition: Tunica Media
Middle layer, composed of smooth muscle that constricts/dilates to change artery diameter. Innervated by autonomic nerves (alpha-adrenergic for vasoconstriction, beta-adrenergic for vasodilation). Calcium entry causes vasoconstriction.
Arterial Wall Composition: Tunica Externa (Adventitia)
Outermost covering, largely composed of connective tissue providing support.
Endothelium: Key Functions Overview
Metabolically active tissue involved in: fluid filtration, blood vessel tone maintenance, hemostasis, angiogenesis (new blood vessel growth), neutrophil chemotaxis, and hormone secretion.
Endothelial Substances: Nitric Oxide (NO) vs. Endothelin
Nitric Oxide (NO): Stimulates vessel vasodilation. Endothelin: Stimulates vessel vasoconstriction.
Endothelial Substances: VEGF, C-type Natriuretic Peptide, Prostacyclin, Thromboxane A2, vWF
VEGF: Vascular Endothelial Growth Factor, stimulates angiogenesis. C-type Natriuretic Peptide: Causes diuresis. Prostacyclin: Inhibits clotting. Thromboxane A2: Activates clotting. von Willebrand factor (vWF): Activates clotting.
Endothelial Injury: Consequences
Key early event in arteriosclerosis/atherosclerosis. Incites inflammation, attracts WBCs, vWF released (increases platelet aggregation), foam cells form, NO release inhibited (vasoconstriction), leads to plaque formation.
Blood Flow Regulation: Relationship between Flow, Pressure, Resistance
Blood flow is inversely related to vessel diameter (smaller diameter = reduced flow, increased pressure). Resistance affected by vessel diameter, length, blood viscosity. Equation: Blood Flow = Blood Pressure / Resistance (CO = BP / PVR).
Blood Pressure (BP) Equation & Factor Adjustment
BP = CO (Cardiac Output) x PVR (Peripheral Vascular Resistance). Body can adjust CO and PVR independently to maintain BP. To raise BP, increase CO and/or PVR.
Laminar vs. Turbulent Blood Flow
Laminar Flow: Smooth flow, parallel to vessel walls (healthy endothelium). Turbulent Flow: Rough flow, perpendicular to vessel walls (occurs with endothelial injury, plaque); produces “whooshing” sound (bruit); increases thrombus formation risk.
Arterial Wall Tension & Laplace’s Law
Wall Tension: Force in vessel wall opposing distending pressure inside. Laplace’s Law: Intraluminal pressure = Tension / Radius (P = T/r). Thicker wall = lower tension.
Arterial Compliance: Definition
The distending capacity of a blood vessel; allows accommodation of blood flow with pressure changes.
Blood Pressure: Systole, Diastole, Pulse Pressure
Systole: Period of cardiac contraction. Diastole: Period of cardiac relaxation. Pulse Pressure: Difference between Systolic BP (SBP) and Diastolic BP (DBP); ideally ~40 mm Hg.
Stroke Volume (SV) & Cardiac Output (CO): Definitions & Relation
Stroke Volume (SV): Amount of blood ejected per beat (approx. 70 mL in healthy adult). Cardiac Output (CO): Volume of blood ejected by left ventricle per minute (approx. 5 L/min at rest). CO = Heart Rate (HR) x SV.
Blood Pressure Regulation: Baroreceptors
Short-term BP regulation. Located in walls of aorta and carotid arteries. Sense stretch/drop in BP. If BP drops, stimulate SNS (increase HR, contractility, vasoconstriction). If BP high, stimulate PNS (decrease HR, contractility, cause vasodilation).
Blood Pressure Regulation: Renin-Angiotensin-Aldosterone System (RAAS)
Triggered by low renal perfusion/BP. Renin (kidney) converts Angiotensinogen (liver) to Angiotensin I. ACE (lungs) converts Angiotensin I to Angiotensin II. Angiotensin II: potent vasoconstrictor, stimulates adrenal gland for Aldosterone release. Aldosterone: increases Na+ and water reabsorption, increasing blood volume/BP.
Blood Pressure Regulation: Antidiuretic Hormone (ADH/Vasopressin)
Released from posterior pituitary in response to drop in BP/blood volume or increased blood osmolarity. Increases water reabsorption by kidneys, raising blood volume and BP.
Blood Pressure Regulation: Natriuresis (ANP & BNP)
Excretion of Na+ and water by kidneys in response to elevated blood volume. Atrial Natriuretic Peptide (ANP) released from atria, B-type Natriuretic Peptide (BNP) from ventricles when overstretched. Promote natriuresis by increasing GFR, reducing blood volume/BP.
Lipids in Blood: Cholesterol & Triglycerides
Cholesterol: Ingested from diet & made by liver; used in cell membranes, hormone synthesis. Triglycerides: Ingested in diet, stored in adipose tissue.
Lipoproteins: LDL vs. HDL
Transport lipids. LDL (Low-Density Lipoprotein): “Bad” cholesterol; involved in plaque formation in arteries. HDL (High-Density Lipoprotein): “Good” cholesterol; helps excrete cholesterol via “reverse cholesterol transport.”
Effect of Glucose on Arteries
High glucose injures endothelial cells via glycosylation (glycation), forming Advanced Glycosylation End Products (AGEs). AGEs damage endothelium, increase endothelin release (vasoconstriction), contributing to atherosclerosis.
Effect of Free Radicals on Arteries
Damage cell membrane of endothelial cells, causing inflammation and initiating atherosclerosis.
