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Vascular Disorders
| Question | Answer |
|---|---|
| Tunica intima | single layer on epithelium |
| Tunica media | vascular smooth muscle, responsible for systemic blood pressure |
| tunica externa | connective tissue |
| What does the tunica intima form on veins? | valves |
| Layers of the tunica intima | endothelium, subendothelial layer |
| What makes up the tunica media | smooth muscle and elastic fibers |
| What makes up the tunica externa | collagen fibers |
| Perfusion | ability of blood cells to deliver oxygen and nutrients to certain parts of the body |
| Central perfusion | blood flow pumped by heart to entire vascular system, cardiac output and blood pressure, pathologic processes affect entire body |
| Local perfusion (microvascular perfusion) | volume of blood flowing through specific tissue, controlled by capillaries serving region, pathologic processes affect specific tissues |
| Concepts and systems affecting and affected by impaired perfusion | cognition, comfort and pain, fluids and electrolytes, acid-base balance, nutrition, oxygenation |
| Peripheral Vascular Disease (PVD) | conditions affecting circulation in tissues other than brain or heart |
| Peripheral Artery Disease | PVD affecting arteries |
| Peripheral Vascular Disease common types affecting veins | chronic venous insufficiency, deep vein thrombosis, leg ulcers, varicose veins |
| Peripheral Vascular Disease risk factors | smoking, hypertension, coronary heart disease, high cholesterol, diabetes, family history of vascular disease, obesity, sedentary lifestyle |
| Who is more likely to develop PVD? | affects adults over age 50; men more often than women |
| Claudication | pain that happens when doing activity that requires increase in oxygen, associated with peripheral artery disease; artery narrowed by plaque |
| Claudication symptoms | cramping, aching, tingling or numbness in lower leg |
| Arteriosclerosis | thickening, loss of elasticity; calcification of arterial walls |
| Atherosclerosis | form of arteriosclerosis caused by plaque buildup |
| Arteriosclerosis risk factors | smoking, hypertension, heart disease, high levels of cholesterol and LDLs, diabetes, obesity, advanced age, physical inactivity |
| Arteriosclerosis lipid metabolism | dyslipidemia, hyperlipidemia, hypercholesterolemia, hypertriglyceridemia |
| dyslipidemia | increase in cholesterol and triglycerides |
| hyperlipidemia | increase in either triglycerides, LDL or cholesterol |
| hypercholesterolemia | high LDL |
| hypertriglyceridemia | high triglycerides |
| Arteriosclerosis Lipoproteins | Low-density lipoproteins (LDLs), High-density lipoproteins (HDLs), Triglycerides |
| LDLs | bad; carries lipids from liver to peripheral tissue |
| HDLs | good; takes lipids from tissue to target tissue and back to liver to be metabolized |
| When does atherosclerosis begin? | when endothelial cells are damaged- atheroma, chronic inflammatory response, extracellular matrix stabilizes plaque, atheroma intrudes on vessel lumen and impairs circulation, neutrophils and cytokines recruited to area causes buildup of plaque |
| thrombus | connected to wall of vessels |
| embolus | piece is unconnected and flows through artery |
| desirable total cholesterol | less than 200 mg/dL |
| borderline high risk total cholesterol | 200-239 mg/dL |
| high risk total cholesterol | more than 240 mg/dL |
| optimal LDL cholesterol | 100 mg/dL |
| desirable LDL cholesterol | 100-129 mg/dL |
| borderline high risk LDL cholesterol | 130-159 mg/dL |
| high risk LDL cholesterol | 160-189 mg/dL |
| very high risk LDL cholesterol | more than 190 mg/dL |
| desirable triglycerides | less than 150 mg/dL |
| borderline high risk triglycerides | 150-199 mg/dL |
| high risk triglycerides | 200-499 mg/dL |
| very high risk triglycerides | more than 500 mg/dL |
| Arteriosclerosis clinical manifestations major consequences | myocardial infarction, stroke, PAD |
| Arteriosclerosis other clinical manifestations | arterial aneurysms, arterial dissection, acute arterial occlusion |
| Arterial abnormalities | mycotic aneurysm, atherosclerotic aneurysm, saccular aneurysm, traumatic aneurysm |
| arteriosclerosis diagnosis | Laboratory workup (hyperlipidemia, diabetes), treadmill test with echocardiography, Ankle brachial index, ultrasonography, angiography (x-ray) |
| ABI value greater than 1.4 | calcification/vessel hardening |
| ABI value 1-1.4 | normal |
| ABI value less than 0.5 | severe arterial disease |
| Arteriosclerosis treatment | lifestyle changes, medications, surgery to occluded arteries (Angioplasty, stent) |
| Nonatherosclerotic peripheral artery disease | group of disorders in which blood flow is decreased for reasons other than plaque buildup |
| Nonatherosclerotic peripheral artery disease examples | coarctation of aorta, thoracic outlet syndrome, raynaud disease |
| coarctation of aorta | congenital heart defect where the aorta, the main artery carrying blood from the heart to the body, becomes narrowed |
| thoracic outlet syndrome | arteries/veins are compressed by collarbone and first rib |
| raynaud disease | a condition that causes blood vessels to narrow excessively in response to cold or stress |
| Nonatherosclerotic peripheral artery disease (coarctation of aorta) Clinical manifestations | depend on severity of deformity and how quickly symptoms manifest |
| Nonatherosclerotic peripheral artery disease (coarctation of aorta) diagnosis | blood pressure taken on arms and legs |
| Nonatherosclerotic peripheral artery disease (coarctation of aorta) treatment | surgery |
| Nonatherosclerotic peripheral artery disease (thoracic outlet syndrome) clinical manifestations | neck and shoulder region, and down extremity, pain, discoloration, tingling, weakness |
| Nonatherosclerotic peripheral artery disease (thoracic outlet syndrome) treatment | physical therapy |
| Nonatherosclerotic peripheral artery disease (Raynaud disease) clinical manifestations | pale skin, cyanosis, numbness, tingling, burning sensation, ischemia: may result in ulceration or tissue necrosis |
| Nonatherosclerotic peripheral artery disease (raynaud disease) treatment | avoidance of triggers, anti-inflammatory medications, calcium channel blockers |
| most common cause of chronic venous disease | chronic venous insufficiency |
| chronic venous insufficiency | veins unable to return adequate blood to heart |
| Causes of CVI | deep vein thrombosis, varicose veins |
| CVI associated conditions | genetic predisposition, female gender, pregnancy, age over 50, smoking, lack of physical activity, obesity, standing/sitting for long periods, oral contraceptive use |
| CVI pathogenesis | low pressure in venous systems, squeezing of skeletal muscles surrounding veins, stretching of veins, rupture of valves and clot formation |
| CVI clinical manifestations | leg cramps and pain, edema of leg or ankle, thickening or discoloration of skin on calves, heaviness or weakness in legs |
| CVI common complications/associated conditions | leg ulcers, varicose veins, deep vein thrombosis |
| CVI diagnosis | assessment of symptoms and triggers, ultrasound, venography, D-dimer test |
| D-dimer test | protein fragment that is formed when blood clots break down |
| CVI treatment | preventative measures, sclerotherapy, radiofrequency, laser ablation, anticoagulants, filter in inferior vena cava to trap emboli |
| hypertension | consistent elevation of blood pressure, systemic arterial pressure in brachial artery |
| causes of hypertension | creates excess pressure on arterial walls, arteriosclerosis thickens arterial wall |
| normal blood pressure | less than 120 and less than 80 |
| elevated blood pressure | 120-129 and less than 80 |
| stage 1 hypertension (high blood pressure) | 130-139 or 80-89 |
| stage 2 hypertension (high blood pressure) | 140 or higher or 90 or higher |
| severe hypertension (may not have symptoms) | higher than 180 and/or higher than 120 |
| hypertensive emergency (have symptoms) | higher than 180 and/or higher than 120 |
| symptoms of hypertension | chest pain, shortness of breath, back pain, numbness, weakness, change in vision or difficulty speaking |
| cause of primary hypertension | no known cause |
| What percent of cases are primary hypertension? | 90% |
| primary hypertension factors | genetics, age, race, diet, smoking and alcohol consumption, sedentary lifestyle |
| identifiable cause of secondary hypertension | diabetic nephropathy, chronic glomerulonephritis, glomerulosclerosis, and autosomal dominant polycistic kidney disease (ADPKD) |
| factors affecting blood pressure | hormones (renin-angiotensin-aldosterone system (RAAS)), nervous |
| Where are the major baroreceptors located? | aortic arch and carotid arteries |
| What happens when there is decreasing filtration in the kidneys? | they secrete renin |
| What happens when the kidneys secrete renin due to low blood pressure? | renin become angiotensin I which is then converted to angiotensin II in lungs; angiotensin II activates secretion of ADH and aldosterone |
| ADH | increases water absorption |
| aldosterone | increases sodium reabsorption into the bloodstream |
| contributing factors to hypertension | endothelial dysfunction (atherosclerosis), sympathetic nervous system (SNS), alcohol, lifestyle factors, genetics |
| lifestlye factors that contribute to hypertension | increased stress, high salt intake, lack of physical exercise, obesity |
| hypertension clinical manifestations | chest pain and dyspnea; long term consequences: stroke, heart failure, MI, chronic kidney disease, vision loss, erectile dysfunction |
| hypertension diagnosis | measurement of blood pressure |
| hypertension nonpharmacologic treatment | restrict sodium consumption, limit alcohol consumption, stop smoking, maintain an optimal weight, reduce saturated fat, cholesterol; increase fruits, vegetables, increase physical activity, reduce stress levels |
| beta blockers | decrease the heart rate and myocardial contractility, reducing cardiac output |
| diuretics | increase urine output and decrease fluid volume |
| ACE inhibitors | block formation of angiotensin II, causing vasodilation, and block aldosterone secretion, decreasing fluid volume |
| angiotensin receptor blockers | prevent angiotensin II from reaching its receptors, causing vasodilation |
| calcium channel blockers | block calcium ion channels in arterial smooth muscle, causing vasodilation |
| direct vasodilators | act on the smooth muscle of arterioles, causing vasodilation |
| alpha1 blockers | inhibit sympathetic activation in arterioles, causing vasodilation |
| hypertension pharmacologic treatment, first line antihypertensives | angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), calcium channel blockers (CCBs), thiazide diuretics |
| hypertension pharmacologic treatment, second line antihypertensives | adrenergic blockers, centrally, acting drugs, direct-acting vasodilators, direct renin inhibitors |
Created by:
camrynfoster