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cardiovascular
Stack #164775
| Question | Answer |
|---|---|
| The development of the ____________is mandatory in early gestation in order to supply oxygen and essential nutrients to, and remove waste products from, the rapidly developing tissues. | cardiovascular system |
| the circulatory pattern can divided into two systems: | the right-sided pulmonary circulation and the left-sided systemic circulation. |
| Inutero, instead of circulating through the pulmonary circuit, blood needs to be transferred to the left side of the heart so that it can be pumped into the systemic circulation. This is accomplished by | right to left shunt |
| These are examples of what type of shunts? truncus arteriosus, transposition of the great vessels, tetralogy of Fallot, tricuspid atresia | RIGHT-TO-LEFT SHUNTS |
| In general, these types of shunts divert non-oxygenated blood away from the pulmonary circuit and into the systemic circulation, reducing the oxygen saturation of the arterial blood. | right to left |
| Type of shunt that results in cyanosis (a bluish discoloration of the skin due to accumulation of reduced hemoglobin in capillary beds and seen most readily around the lips and nail beds) at or soon after birth. | Right to left |
| atrial septal defect, ventricular septal defect, patent ductus arteriosus | LEFT-TO-RIGHT SHUNTS |
| In general,__________ shunts divert oxygenated blood from the systemic circulation (including the myocardial circulation) and into the pulmonary circulation, depriving the systemic tissues of oxygen. | left to right |
| the excess blood flowing through the pulmonary circulation in a left to right shunt produces | pulmonary hypertension |
| coarctation of the aorta, valvular stenosis | OBSTRUCTIVE DISORDERS |
| These are physical barriers to blood flow and generally do not cause cyanosis. | OBSTRUCTIVE DISORDERS |
| Obstructive disorders lead to | hemodynamic disturbances. |
| This encompasses a group of vascular disorders which are characterized by thickening and loss of elasticity of arterial walls. | Arteriosclerosis |
| This is a slow progressive disease of the large elastic and large and medium sized muscular arteries characterized by the formation of atherosclerotic plaques. | Atherosclerosis |
| What percent of all deaths in the U.S. are related to cardiovascular disease | 50 |
| primarily transport dietary triglycerides and, to a lesser extent, dietary cholesterol | chylomicrons |
| hyperlipidemia, hypertension, cigarette smoking, and diabetes mellitus. | Major risk factors for atherosclerosis |
| physical inactivity, stress and behavior patterns, obesity, and long term oral contraceptive use. | Minor risk factors for atherosclerosis |
| vital for the synthesis of cellular membranes, steroid hormones, and bile acids. | cholesterol |
| are primarily derived from exogenous dietary cholesterol & triglycerides that are absorbed across the intestinal mucosa | Plasma lipids |
| triglycerides that are absorbed across the | intestinal mucosa |
| Cholesterol and triglycerides are ____ in blood | insoluble |
| Cholesterol and triglycerides complexed with a variety of specific proteins to form | soluble lipoproteins |
| primarily transport dietary triglycerides and, to a lesser extent, dietary cholesterol | chylomicrons |
| primarily transport endogenously produced hepatic triglycerides to adipose and muscle tissue | pre-beta lipoproteins ("very low density lipoprotein", VLDL) |
| chylomicrons beta ,lipoproteins, pre-beta lipoproteins ,alpha lipoproteins | specific proteins that join with chlolesterol and triglycerides to form soluble lipoproteins |
| transport dietary triglycerides and, to a lesser extent, dietary cholesterol | chylomicrons |
| primarily transport endogenous cholesterol and are the major plasma cholesterol carriers; | beta lipoproteins ("low density lipoprotein", LDL) |
| primarily transport endogenously produced hepatic triglycerides to adipose and muscle tissue | pre-beta lipoproteins ("very low density lipoprotein", VLDL) |
| primarily transport endogenous cholesterol acquired from extrahepatic tissues and returns it to the liver. | alpha lipoproteins ("high density lipoprotein", HDL) |
| major clearance mechanism for cholesterol | RECEPTOR PATHWAY |
| Receptor pathway, The LDL is cleared from the plasma by incorporation into the liver cell where it can then be can be excreted into the | bile |
| In cells outside of the liver, excess free cholesterol is stored in the | cytoplasm |
| can extract cholesterol from the cell and transfer it to the liver where it can then be excreted | HDL |
| What tpye of levels of plasma LDL are directly related to the development of clinically significant atherosclerosis | Elevated |
| elevated levels of ___ seem to have a protective effect from atherosclerosis | HDL |
| RECEPTOR-INDEPENDENT PATHWAY related to plasma clearance of ldl | PHAGOCYTIC |
| normally clears approximately one third of the plasma LDL | phagocytic |
| high levels of plasma LDL the cells become overstuffed and lead to the development of | xanthomas. |
| Two pathways of plasma clearance of LDL | Phagocytic & Receptor |
| The vast majority of cases of hypercholesterolemia, however, are due to | dietary excess |
| excessive caloric intake, excessive dietary cholesterol, and saturated fatty acids. | major contributors to hypercholesterolemia |
| Initial screening for atherosclerotic risk involves measurement of | total serum cholesterol |
| In middle aged adults (>40), a value between ___ mg/dl and ___ mg/dl is considered borderline | 200 & 240 |
| overt hypercholesterolemia is considered to be a plasma cholesterol >____ mg/dl | 240 |
| A "good" ratio would be___ or less. TC/HDL-C RATIO | 4:1 |
| increased plasma total homocysteine level is an independent risk factor for __________whether or not serum cholesterol is elevated. | atheroscloticc disease |
| methionine, homocysteine impairs | endothelial function |
| deficiencies of these vitamins lead to elevated homocysteine levels. | vit. B12, vit. B6 and folic acid |
| CHLAMYDIA PNEUMONIAE AND CYTOMEGALOVIRUS INFECTIONS, do these independently increase risk of atherosclerosis? | NO |
| These are probably reversible lesions and may or may not represent precursor lesions of adult plaques. | FATTY STREAKS |
| These appear as multiple, essentially flat yellow streaks on the inner surface of vessels. | FATTY STREAKS |
| These appear as multifocal asymmetric elevations of the vessel lining. | ATHEROSCLEROTIC PLAQUES |
| plaques which contain a large amount of collagen | fibrous |
| plaques which contain abundant lipid material | soft (atheromatous) |
| CLINICAL SIGNIFICANCE of atheroscleroses is related to what three things? | physical obstruction to blood flow, the risk of thrombosis, and alteration of the normal activity of endothelial cells. |
| clinical symptoms of atherosclerotic plaques generally related to the hemodynamic effects on | the heart, brain, kidney, small bowel, and lower extremities. |
| IHD is responsible for approximately % of the total mortality in the U.S. | 30 |
| IHD is responsible for approximately % of the deaths due to heart disease | 75 |
| IHD results from an imbalance between the availability of _____ and the metabolic demand of the heart | oxygen |
| The availability of oxygen to the heart may be affected by what three things? | reduced coronary flow, increased metabolic demand, or decreased saturated hemoglobin availability. |
| acute IHD is manifested as | angina pectoris |
| This is not a disease in itself but a symptom complex manifested by paroxysmal attacks of substernal or precordial chest discomfort | ANGINA PECTORIS |
| IHD is manifested as | angina pectoris, myocardial infarct, or occasionally sudden cardiac death. |
| chest discomfort often described as a pressure, constriction, or heaviness which may extend into the neck, left jaw, left shoulder, and left arm. | Clinical symptoms of angina pectoris |
| It is often induced or aggravated by cold weather, exercise, heavy meals, cigarette smoking, or emotional stress. | Angina Pectoris |
| The discomfort arises from a temporary inability to supply sufficient oxygen to the heart muscles, | Angina Pectoris |
| In the vast majority (99%) of cases, angina is the result of | atherosclerotic stenosis (narrowing) of the coronary arteries. |
| There are no significant permanent morphological changes in the myocardium, but there is an increased risk of myocardial infarction with this type of IHD | Angina Pectoris |
| This causes 60% of the deaths related to ischemic heart disease | ACUTE MYOCARDIAL INFARCTION |
| is due to irreversible myocardial damage resulting from inadequate oxygenation of myocardial fibers. | ACUTE MYOCARDIAL INFARCTION |
| in most instances, is due either to occluded or markedly reduced blood flow rather than increased metabolic demand | ACUTE MYOCARDIAL INFARCTION |
| The risk of acute thrombosis depends, therefore, more on the _________ of the plaque than it does on the size. | biology |
| gradually enlarging plaques will produce stable angina and allow time for | a collateral circulation to develop |
| typical presentation is a crushing, substernal chest pain unrelieved by rest or nitroglycerin and accompanied by nausea, vomiting, diaphoresis, arrhythmias, hypotension and shock. | Acute MI |
| Most infarcts occur in the distribution of the | left anterior descending coronary artery |
| the anterior interventricular septum and the anterior and lateral left ventricular wall | left anterior descending coronary artery |
| No changes are grossly visible from MI, until about | one day after the infarct when the affected area becomes pale. |
| When the myocardial cells die, they release _____________ into the circulation | cytoplasmic enzymes |
| there is elevation of serum CPK during the first | 24 hours |
| CPK will return to normal, how many days after MI? | 3-5 days |
| slower rise in serum LDH post MI, which persists | 7-12 days |
| which are part of the contractile proteins of skeletal and myocardial muscle that are released into the serum when muscle necrosis occurs | serum troponins |
| These are released into the serum when muscle necrosis occurs | serum troponins |
| the most cardiac specific. | troponin-I (cTn-I |
| Does Troponin I rise in response to skeletal injury? | no |
| When does troponin I rise related to cardiac injury and how long does it stay elevated? | 2 hours, 2 weeks |
| 3 MODES OF INTERVENTION for acute MI | Thrombolytic therapy,Angioplasty,Coronary bypass |
| Can sudden cardiac death occur without clinical or morphologic evidence of coronary disease. | Yes |
| 40% of deaths from IHD is caused by | CHRONIC ISCHEMIC HEART DISEASE |
| become manifested by the insidious onset of congestive heart failure as the cardiac reserve is slowly depleted. | Chronic ischemic heart disease |
| is characterized by diffuse myocardial atrophy, spotty loss of myocardial cells (myocytolysis), diffuse fibrosis, and possible scarring from previous infarcts. | Chronic ischemic heart disease |
| implies failure of a valve to open properly thereby creating obstruction to the forward flow of blood. | Valvular stenosis |
| almost always due to a primary abnormality of the cusps or leaflets. | Acquired stenosis |
| inability of a valve to close properly and thereby allows for the backward flow of blood. | Insufficiency |
| This is a consequence of cardiac involvement in a systemic inflammatory disease | RHEUMATIC HEART DISEASE |
| Rheumatic fever may follow an infection by | ß-hemolytic streptococci |
| clinically characterized by one or more of the following: migratory polyarthritis, carditis, erythema marginatum, subcutaneous nodules, and Sydenham chorea | RHEUMATIC HEART DISEASE |
| Rheumatic fever is much more common in children or adults | children |
| Rheumatic fever: % of first attacks occur between 5 and 15 | 90 |
| with age, the signs and symptoms of Rheumatic fever are more likely to be milder and related primarily to | arthritis. |
| Symptoms of rheumatic fever are due to immunologic cross reactivity between | streptococcal antigens and host tissue antigens |
| Rheumatic fever induces an inflammatory reaction in ____layers of the heart (pancarditis) | all |
| Acute fibrinous inflammation of the pericardium, with rheumatic heart disease may cause a ____________on auscultation. | friction rub |
| Focal necrosis and inflammation of the myocardium, with rheumatic heart disease may lead to | cardiac arrhythmias. |
| This is the most crippling and destructive aspect of rheumatic heart disease. | ENDOCARDITIS |
| Healing of the inflammation, due to rheumatic heart disease, that occurs in the heart valves results in | fibrous, thickened, rigid valves whose leaflets or cusps become fused and calcified. This leads to valvular stenosis and insufficiency. |
| What valves in the heart are generally effected by endocarditis resulting from rheumatic heart disease? | primarily involving the mitral valve and, in some cases, the aortic valve |
| Causes of death, related to what disease, include cardiac failure, mural thrombosis and embolization, and bacterial endocarditis. | rheumatic fever |
| most often seen in elderly patients and may be the result of chronic, "wear and tear" valvular damage. Unlike rheumatic valves, however, there is little or no fusion of the valve cusps or leaflets. | Calcific Aortic Stenosis |
| Symptoms (dyspnea, angina, syncope, etc.) generally are referable to left heart failure or inadequate cardiac output.What type of heart disease? | calcific aortic stenosis |
| Survival rate of calcific aortic stenosis | 2-3 years unless valve replacement |
| This is a common condition (5-7% of general population, more frequent in young women) which may in some cases be congenital in origin | MITRAL VALVE PROLAPSE |
| Type of valvular disease: may be related to a metabolic defect in connective tissue metabolism | MITRAL VALVE PROLAPSE |
| Type of valvular disease: Prolapse is characterized by enlarged mitral leaflets and/or elongated chordae. Eventually, possibly from long standing trauma, the leaflets thicken as do the chordae, which may also fuse | MITRAL VALVE PROLAPSE |
| What causes death related to mitral valve prolapse? | death can result from complications of infective endocarditis, from chronic congestive failure, from chordal rupture or from arrhythmia. |
| What are symptoms of mitral valve prolapse | none |
| This valvular heart disease involves the development of friable septic vegetations (thrombi with embedded bacteria) on heart valves or endocardial surfaces | INFECTIVE ENDOCARDITIS |
| two clinical categories of inefective endocarditis | acute and subacute |
| In this form of inefective endocarditis, virulent organisms such as Staphylococcus aureus can directly damage the heart valves and promote thrombus formation. | ACUTE ENDOCARDITIS |
| This type of inefective endocarditis may be seen in IV drug users or chronic alcoholics whose hearts usually do not have underlying abnormality | acute endocarditis |
| patients on whom previous cardiac surgery has been performed; or in patients who have had "foreign bodies" introduced into the cardiovascular system would have what type of inefective endocarditis | acute |
| , I.V. drug users inject microorganisms directly into veins, hence the endocarditis tends to predominantly affect what heart valves | right-sided valves |
| Clinically, there is an abrupt onset of high fever, shaking chills, and profound weakness. Type of inefective endocarditis | acute |
| As many as 70% of these patients may die as a result of heart failure, emboli, arrhythmias, or uncontrolled sepsis. Type of inefective endocarditis | acute |
| In this form of inefective endocarditis, hearts characteristically have some underlying disease with either valvular or congenital abnormalities that predisposes to thrombus formation on the endocardial surfaces. | SUBACUTE ENDOCARDITIS |
| What is the predominant organism and the valves most commonly affected in subacute endocarditis? | Streptococcus viridans, mitral and/or aortic |
| Clinically, the onset is usually insidious with progressive weakness, weight loss, anemia, fever, occasional night sweats. Type of inefective endocarditis. | subacurte |
| Initial manifestations of subacute endocarditis, may be due to embolization of vegetations to the | brain or other organs. |
| Mortality from subacute endocarditis ranges up to | 15%. |
| blood pressure > 140/90 | HYPERTENSIVE HEART DISEASE |
| Most hypertension is of __________etiology | unknown |
| Blood pressure is principally governed by | cardiac volume output and the peripheral arteriolar resistance. |
| The heart responds to a pressure overload by _____________ of the ventricle which thickens the wall | concentric hypertrophy |
| In the absence of any other abnormality that might produce left ventricular hypertrophy (i.e. valve disease), this is the identifying hallmark of hypertension. | concentric hypertrophy |
| thickens the wall of ventricle, increases heart weight (without significant increase in size), and decreases ventricular volume | concentric hypertrophy |
| When it is no longer able to adapt to the change in work load, the heart begins to | decompensate |
| hypertension is generally asymptomatic until what occurs? | cardiac decompensation |
| What symptoms occur with hypertension after cardiac decompensation occurs? | an insidious onset of symptoms of left heart failure. |
| This refers to any inflammatory condition (microbiologic, immunologic, etc.) that involves the myocardium. | MYOCARDITIS |
| Over half of the cases of myocarditis are caused by ________ and are most frequently seen in infants, pregnant women, and immunosuppressed patients | virsus, |
| Type of myocardial heart disease: , the clinical manifestations usually include tachycardia, arrhythmias, low grade fever, dyspnea and malaise | myocarditis |
| The inflammation from myocarditis, usually resolves in ___ weeks but may progress to chronic disease requiring heart transplantation | 6-8 |
| This term refers to non-inflammatory disorders of the myocardium. | CARDIOMYOPATHY |
| Three types of cardiomyopathy | dileated, hypertrophic, restrictive |
| CARDIOMYOPATHY This may simply represent a common end point of a variety of previously undiagnosed cardiac diseases and can occur at any age. | DILATED (CONGESTIVE) |
| Type of cardiomyhopathy:Some are of known cause (alcoholic, familial, peripartum, nutritional, and post-infectious cardiomyopathies), but the large majority must be classified as idiopathic. | Dilated (Congestive) |
| Type of cardiomyopathy: These are characterized by dilatation and hypertrophy of all chambers of the heart with impairment of ventricular contraction and congestive heart failure. | dilated congestive |
| Type of cardiomyopathy:There is always increased heart weight due to ventricular hypertrophy, but grossly the hypertrophy may be obscured by the ventricular dilatation. | dilated congestive |
| Dilated congestive-The myocardium shows diffuse interstitial fibrosis withor without evidence of inflammation or severe coronary atherosclerosis | without |
| Due to poor contractility, with dilated congestive cardiomyopthay, mural thrombi are prone to develop where? | most frequently in the left ventricle. |
| Type of cardiomyopathy:Patients generally present with signs and symptoms of congestive heart failure. | dilated congestive |
| What causes death with dilated congestive myopathy? | Progressive heart failure usually culminates in death unless patients first succumb to arrhythmias or the effects of systemic emboli. |
| In most instances, it probably represents an inherited condition (particularly in patients with a family history of sudden unexplained deaths, dilated atria, disproportional hypertrophy of the interventricular septum with myofiber disarray, decreased vent | hypertrophic obstructive cardiomyopathy |
| Symptoms of cardiomyopathy:systolic murmurs of aortic outflow obstruction and mitral insufficiency) and symptoms (angina, syncope, dyspnea | hypertrophic obstructive cardiomyopathy |
| Outcome of hypertrophic obstructive cardiomyopathy | The clinical course is variable with some patients able to be helped by medical therapy. Others, however, develop arrhythmias or progressive heart failure complicated by embolization from atrial thrombi or infective endocarditis. |
| Type of cardiomyopathy: These are rare conditions characterized by restriction of ventricular filling. | RESTRICTIVE/INFILTRATIVE |
| Type of cardiomyopathy: the clinical signs and symptoms are essentially the same as dilated cardiomyopathy. | RESTRICTIVE/INFILTRATIVE |
| Amyloidosis, sarcoidosis, hemochromatosis, Pompe disease, result in diffuse infiltration of the myocardium by abnormal substances thereby restricting normal myocardial compliance and ________ the ventricular filling pressures. | elevating |
| Type of pericardial disease: This is generally due to infectious organisms or irritation of the pericardium and can lead to the accumulation of either fibrinous, serous, purulent, or hemorrhagic fluid. | ACUTE PERICARDITIS |
| acute pericarditis, Clinical significance depends on the type of _________ that accumulates and the ________ with which it accumulates. | fluid, rapidity |
| rapid fluid buildup in acute pericarditis (effusions, exudates, blood, etc) will compress the heart, prevent venous blood from entering, and therefore decrease | cardiac output (cardiac tamponade). |
| Type of pericarditis: This may lead to obliteration of the pericardial sac which can interfere with the ability of the heart to contract normally and thereby interfere with cardiac output. | CHRONIC PERICARDITIS |
| Type of aortic aneurysms: These are the most commonly encountered aortic aneurysms and almost all are the result of atherosclerotic weakening of the aortic wall. | ABDOMINAL |
| abdominal aortic aneurysms generally occur in _____________, half of whom are hypertensive. | middle-aged to elderly males |
| Where do abdominal aortic aneurysms occur? Why? | distal abdominal aorta where atherosclerosis tends to be most severe |
| Type of aortic aneurysms:They develop slowly over time and do not produce clinical symptoms until they become large or until they rupture (the risk of rupture increases as the size increases). | abdominal |
| Type of aortic aneurysm: Due to their location, clinical symptoms are more common | thoracic |
| Type of thoracic aneurysm:Compression of lungs, trachea or bronchi may lead to respiratory problems; compression of the esophagus may lead to dysphagia; compression of the recurrent laryngeal nerve may lead to hoarseness; and erosion of bony structures ma | thoracic |
| Type of thoracic aortic aneurysms:This disorder is responsible for the majority of thoracic aortic aneurysms. | CYSTIC MEDIAL NECROSIS |
| Type of thoracic aortic aneurysms:a chronic degenerative process of unknown etiology that results in focal destruction of the media of the thoracic aorta. | cystic medial necrosis |
| What causes cystic medical necrosis? | metabolic defect in the synthesis of collagen and elastin and is frequently associated with Marfan syndrome |
| What causes death in people with syphilis thoracic aortic aneurysms? | of heart failure, but the aneurysm may rupture |
| This is more common than rupture of atherosclerotic aneurysms and involves tearing of the inner lining of the aorta with dissection of blood into and along the wall. | AORTIC DISSECTION |
| What is frequently associated with aortic dissection? | hypertension |
| these present as a "tearing" pain in anterior chest radiating into and down the back. | aortic dissections |
| The clinical presentation of aortic dissection may be very similar to | myocardial infarction or perforated peptic ulcer. |
| Causes of death with aortic dissections | When they occur in the proximal aorta, a major cause of death is retrograde dissection, rupture into the pericardial cavity, and cardiac tamponade. |
| This occurs as a result of gradual buildup of atherosclerotic plaques (often as a complication of diabetes) | PERIPHERAL VASCULAR DISEASE |
| With PVD As the arteries are narrowed by atherosclerosis, there will be eventual ulceration and _______necrosis of the skin and underlying tissues. | gangrenous |
| A varix refers to any venous dilatation that results from chronic elevation of intravascular hydrostatic pressure. | VARICOSE VEINS |
| Varicous veins are most commonly seen in the | superficial leg veins |
| The overall effect of varicous veins is to | create chronic soft tissue edema, venous stasis, and thrombosis. |
| Clincial significance of varicous veins | stasis dermatitis and chronic ulcerations. |
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