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Patho

heart and lymphatics

TermDefinition
Circulatory System Main goal is to transport oxygen and nutrients and the removal of metabolic waste products within the body
Capillaries Single layer of endothelial cells
Lymphatics Reabsorb fluid that leaks out of vascular network. Deep in connective tissue
Intima Layer of endothelial cells. Direct contact with blood
Media Smooth muscle and elastin. Ticker in arteries.
Adventitia Supportive connective tissue.
Extrinsic Vasoconstriction.
Intrinsic Autoregulation.
Thrombus-stationary blood clot Blood clots composed of aggregated platelets, clotting platelets, fibrin. Form in chambers of the heart.
Thrombus Intermittent claudication, cool to touch, calf or groin tenderness
Embolus-traveling blood clot Dislodged thrombus, from heart, from deep veins of pelvis and lower extremities.
Vasospasm Sudden constriction of smooth muscle, angina
Vasculitis Inflammation of an artery
Phlebitis inflammation of an artery
Atherosclerosis most common form Most common cause of CHRONIC arterial obstruction Risk factor for cardiovascular disease
Plaque muscle cells, lipoproteins, inflammatory debris
LDL cholesterol “bad” because it attaches to and is toxic to vessel walls
HDL cholesterol “good” because it stimulates the mobilization of cholesterol from the periphery to the liver where it is broken down
Peripheral Arterial Disease PAD Disease of superficial vessels (usually legs) Seen most in older men Risk factors are the same as for atherosclerosis
Raynaud Syndrome Vasospasms of the small vessels in the digits Begins in adolescence Most common in women Precipitated by cold or emotional stress
Aneurysms Localized arterial dilations Arterial wall deteriorates until it bulges out Due do vascular structure that has lost elasticity and has weakened.
Vascular Incompetence Results in venous insufficiency Overstretching of the valves The valve cusps can no longer meet Backflow results in engorgement of involved veins
Varicose Veins Develop when return flow is blocked Valvular incompetence involving superficial veins Varicosities develop-superficial, darkened, raised, tortuous veins
Chronic Venous Insufficiency Valvular incompetence involving deep veins Pressure elevated for long periods/deep veins affected Previous DVT is a risk factor
Deep Vein Thrombosis (DVT) Stasis of blood in an extremity Immobility Impaired heart function Increased blood viscosity Dehydration Increased coagulation
Arterial Blood Pressure Provides the momentum for adequate blood flow to meet the body’s needs for delivery of oxygen and nutrients.
Normal Blood pressure SBP= <120 DBP= <80
BP regulations. Short-term Sympathetic nervous system, Barocreceptors
BP regulations. Long-term Nervous system, hormones, Kidneys. Fluid balance, RAAS, ADH
Fluid volume. Increase in extracellular fluid results in Increased CO
Renin-angiotensin-aldosterone system (RAAS) Renin is an enzyme made and controlled in the kidneys Renin forms angiotensin I
Vasopressin Antidiuretic Hormone (ADH). Released from the pituitary because of: Decreased BP, Decreased Blood volume, Increased osmolarity
Essential Hypertention Silent killer. Generally asymptomatic, Leads to many cardiovascular disorders. Causes trauma to the intima of the vessels.
Pheochromocytoma Tumor of adrenal medulla. Hypersecreting benign adenoma
Hypertensive Crisis (AKA Malignant HTN) uncontrolled primary HTN. Hypertensive Crisis is a life threatening elevation of BP and is often drug induced Diastolic >120 mm HG
Orthostatic Hypotension Decreased BP that occurs when position is changed quickly to upright
Coronary Heart Disease (CHD) Leading cause of death in the US.
Atherosclerosis Harding of the arteries. Generally the underlying cause of CHD. Plaque build up from earlier.
Ischemia Inadequate oxygen supply to the myocardium as a result of the impaired blood flow.
Myocardial Ishcemia: Acute Coronary Syndrome occurs when sudden obstruction of coronary blood flow results in acute myocardial ischemia
chronic coronary syndrome Plaque build up progresses slowly so the heart has time to develop other pathways (collateral circulation)
Angina Pectoris Chest Pain. Crushing or squeezing.
Stable Angina Classic or typical. Results from narrowing and stiffening of the coronary vessels. Cant respond to increased O2 demand.
Variant Angina Prinzmetal's Results from coronary vasospasms (unrelated to increased O2 demand)
Unstable Angina Acute coronary syndrome. Cannot distinguish from MI w/o labs EKG
Myocardial Infarction Results from prolonged or total disruption of blood flow to the myocardium. Thrombus formation on a rough spot or rupture site on an atherosclerotic plaque ECG/EKG
Time you are susceptible to a rupture after a myocardial infarction 1-2 weeks
Valvular Disease- Stenosis Failure of a valve to open completely. Increased work because blood must be forced through high resistance. Hypertrophy
Valvular Disease- Regurgitation Failure of a valve to completely close. Back flow of blood into previous chambers. Hypertrophy
Valvular Disease- Prolapse Valve balloons backward into the supplying chamber.
Aortic Stenosis Calcium deposits on the aortic cusps. Obstructs aortic flow. Increase in left ventricle pressure.
Aortic Regurgitation Blood leaks from aorta back to left ventricle. Increase left ventricle pressure.
Endocardium Layer of endothelial cells that lines the chambers of the heart.
Rheumatic Heart Disease (RHD) May acquire if had Rheumatic Fever in childhood from strep infection. Heart damage due to immune attack on individual's own tissues. Incompletely understood.
Infective Endocarditis Infection of the endocardial structures by microorganisms which results in inflammation Strep. and Staph. Flu-like symptoms
Myocarditis Inflammation and necrosis of the cardiac muscle cells. May be caused by bacteria, viruses, immune-mediated diseases and physical agents.
Pericardium Protective covering of the heart that is made of 2 layers.
Pericardium Visceral Layer attached to heart itself
Pericardium parietal layer Layer that forms a sac around the heart
Created by: whitneydpugh