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patho exam 2
ch 23 - vascular disorders
| Question | Answer |
|---|---|
| tunica intima | single layer of epithelium |
| tunica intima contains | endothelium, subendothelial layer |
| tunica media | vascular smooth muscle, responsible for system BP |
| tunica media contains | smooth muscle and elastic fibers |
| tunica externa | aka adventitia, connective tissue |
| tunica externa contains | collagen fibers |
| central perfusion | blood flow pumped by heart to entire vascular system cardiav output and blood pressure pathologic processes affect entire body |
| local perfusion aka | microvascular perfusion |
| local perfusion | volume of bloody 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 |
| PVD is | conditions affecting circulation in tissues other than the brain or the heart |
| peripheral artery disease is | PVD affecting arteries, narrowed blood vessels reduce blood flow to the limbs |
| common types affecting veins | chronic venous insufficiency deep vein thrombosis leg ulcers varicose veins |
| PVD main drivers are | nutrition and disease |
| risk factors for PVD | smoking, hypertension, coronary heart disease, high cholesterol, diabetes, family history of vascular disease, obesity, sedentary lifestyle |
| who does PVD affect the most | affects adults over age of 50, men more than women |
| claudication | artery narrowed by plaque, cramping, aching, tingling or numbness in lower leg |
| what happens during claudication | person doing activity that requires O2 in an area where the artery is blocked |
| what artery is most commonly affected by claudication? | femoral artery |
| ateriosclerosis is | the thickening, hardening and loss of elasticity in arterial walls |
| what actually happens in arteriosclerosis | calcification of arterial walls, often due to aging |
| atherosclerosis | a form of arteriosclerosis caused by plaque buildup, can induce arteriosclerosis |
| risk factors of arteriosclerosis | lifestyle and genetic components smoking hypertension, heart disease high levels of cholesterol and LDLs diabetes, obesity advanced age, physical inactivity |
| arteriosclerosis lipid metabolism | dyslipidemia, hyperlipidemia, hypercholesterolemia, hypertriglyceridemia |
| dyslipidemia | abnormal balance of lipids (fats) in the bloodstream |
| hyperlipidemia | something high, LDL or HDL |
| hypercholesterolemia | high LDL |
| hypertriglyceridemia | high triglycerides |
| arteriosclerosis lipoproteins | low density lipoproteins high density lipoproteins triglycerides |
| low density lipoproteins | LDLs = bad, carries lipids from liver to peripheral tissue |
| high density lipoproteins | 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 |
| damage to endothelial cells examples | atheroma, chronic inflammatory response, ECM stabilizes plaque, atheroma intrudes on vessel lumen and impairs circulation |
| optimal LDL (mg/dL) | 100 |
| desirable LDL (mg/dL) | 100-129 |
| borderline high risk LDL (mg/dL) | 130-159 |
| high risk LDL (mg/dL) | 160-189 |
| very high risk LDL (mg/dL) | above 190 |
| desirable total cholesterol (mg/dL) | below 200 |
| borderline high risk total cholesterol (mg/dL) | 200-239 |
| high risk total cholesterol (mg/dL) | above 240 |
| desirable triglycerides (mg/dL) | below 150 |
| borderline high risk triglycerides (mg/dL) | 150-199 |
| high risk triglycerides (mg/dL) | 200-499 |
| very high risk triglycerides (mg/dL) | above 500 |
| arteriosclerosis CMs: major consequences | MI, stroke, PAD |
| arteriosclerosis CMs: other manifestations | arterial aneurysms, arterial dissection, acute arterial occlusion |
| arteriosclerosis: diagnosis | laboratory workup: hyperlipidemia, diabetes treadmill test with echocardiography ankle branch index (ABI) ultrasonography angiography (x-ray) |
| ankle brachial index | non-invasive test that measures blood flow in the arms and legs, helps detect PAD |
| ABI value greater than 1.4 | calcification/vessel hardening, refer to vascular specialist |
| ABI value 1.0-1.4 | normal, no recommendation |
| ABI value 0.9-1.0 | acceptable, no recommendation |
| ABI value 0.8-0.9 | some arterial disease, treat risk factors |
| ABI value 0.5-0.8 | moderate arterial disease, refer to vascular specialist |
| ABI value less than 0.5 | sever arterial disease, refer to vascular specialist |
| treatment for arteriosclerosis | lifestyle changes, medications, surgery to open occluded arteries (angioplasty, stent) |
| nonatherosclerotic peripheral arterial disease (NAPAD) | group of disorders in which blood flow is decreased for reasons other than plaque buildup |
| examples of nonatherosclerotic peripheral arterial disease (NAPAD) | coarction of aorta, thoracic outlet syndrome, raynaud disease |
| coarction 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 collarbone and first rib |
| raynaud disease | a condition that causes blood vessels narrow excessively in response to cold or stress |
| coarction of aorta CMs | depend of severity of deformity and how quickly symptoms manifest |
| coarction of aorta diagnosis | blood pressure taken on arms and legs |
| coarction of aorta treatment | surgery |
| thoracic outlet syndrome CMs | neck and shoulder region, and down region, pain, discoloration, tingling, weakness |
| thoracic outlet syndrome diagnosis | adson maneuver, measures to monitor blood flow |
| thoracic outlet syndrome treatment | physical therapy |
| raynaud disease CMs | pale skin, cyanosis, numbness, tingling, burning sensation, ischemia (may result in ulceration or tissue necrosis) |
| raynaud disease treatment | avoidance of triggers, anti-inflammatory medications, calcium channel blockers |
| chronic venous insufficiency is most common cause of | chronic venous disease |
| what is CVI | veins are unable to return adequate blood to the heart |
| CVI is caused by | DVT and 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 |
| pathogenesis of CVI | Low pressure in venous system Squeezing of skeletal muscles surrounding veins Stretching of veins Rupture of valves and clot formation |
| CMs of CVI | Leg cramps and pain Edema of leg or ankle Thickening or discoloration of skin on calves Heaviness or weakness in legs |
| common complications/associated conditions of CVI | Leg ulcers Varicose veins Deep vein thrombosis |
| diagnosis of CVI | Assessment of symptoms and triggers Ultrasound Venography D-dimer test (protein fragment that is formed when blood clots break down) |
| development of DVT | blood clot that leads to embolus |
| treatment of CVI | Preventive measures Sclerotherapy Radiofrequency Laser ablation Anticoagulants Filter in inferior vena cava to trap emboli |
| hypertension is | consistent elevation of BP |
| what pressure is HTN | systemic arterial pressure in brachial artery |
| where is systemic BP measured | brachial artery |
| HTN creates | excess pressure on arterial walls |
| causes of HTN | arteriosclerosis thickens the arterial wall |
| arteriosclerosis is induced by | aging and calcium accumulation |
| normal BP | less than 120 and less than 80 |
| elevated BP | 120-129 and less than 80 |
| stage 1 HTN | 130-139 or 80-89 |
| stage 2 HTN | 140 or higher or 90 or higher |
| sever HTN | no symptoms, higher than 180 and/or higher than 120 |
| HTN emergency | symptoms, higher than 180 and/or higher than 120 |
| primary HTN causes | no known cause (idiopathic) which makes it hard to treat |
| how common is primary HTN | makes up 90% of cases |
| influential factors of primary HTN | genetics (altered genes cause raised BP) age (higher age = higher risk for HTN) race (certain races are more prone) diet (bad diet = higher BP) smoking and alcohol consumption sedentary lifestyle (lazy) |
| any complication with what organ affects BP? | kidney |
| secondary HTN identifiable causes | diabetic nephropathy, chronic glomerulonephritis, glomerulosclerosis, autosomal dominant polycystic kidney disease (ADPKD) |
| secondary HTN: factors affecting BP | hormones - renin-angiotensin-aldosterone system (RAAS) nervous system |
| decrease of BP causes kidneys to | secrete renin into the blood |
| what is the primary role of kidneys | filter out blood |
| when renin is secreted into the blood, it becomes | angiotensin I in the blood |
| after renin is converted to angiotensin I, it is | converted by angiotensin II in the lungs |
| after angiotensin I is converted by angiotensin II in the lungs... | angiotensin II activates secretion of ADH and aldosterone |
| ADH function | increases water absorption |
| aldosterone function | increase sodium absorption |
| increase of H2O and Na absorption leads to | increase of BP |
| contributing factors of HTN | endothelial dysfunction - damage in epithelial cells (atherosclerosis) SNA - keeps HR and adrenaline raised which leads to higher BP alcohol - activates a system that increase BP lifestyle factors - induce water retention or dysfunction genetics |
| lifestyle factors that contribute to HTN | increased stress, high salt intake, lack of physical exercise, obesity |
| what race is more susceptible to accumulate lipids | african americans (also due to social aspects) |
| hypertension puts pt at risk for | further complications |
| clinical manifestations of HTN: long term | stroke, heart failure, heart attack, chronic kidney disease, vision loss, erectile dysfunction |
| clinical manifestations of HTN: short term | chest pain and dyspnea |
| controlling BP is key to | stopping many leading causes of death in the US |
| HTN diagnosis | measurement of BP |
| main treatment for HTN | related to diet |
| non pharm treatments for HTN | restrict Na consumption, limit alcohol consumption, stop smoking, maintain an optimal weight, reduced saturated fat/cholesterol and increase fruits and veggies, increase physical activity and reduce stress levels |
| ACE inhibitors stop | conversion of angio I to angio II |
| angiotensin receptor blockers stop | angio II from reaching its receptors |
| if trial and error drugs don't work, then | the HTN is not due to a mechanism in the body |
Created by:
leh195