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232 Cards in this Set
- Front
- Back
what is a hardening of the arteries primarily characterized by thickening and loss of elasticity in the arterial walls
|
arteriosclerosis
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what type of arteriosclerosis is a chronic inflammatory response involving the wall of large and medium-sized muscular arteries and the large elastic arteries
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atherosclerosis
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what are the major risk factors for atherosclerosis
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hyperlipidemia (LDL), hypertension, smoking, and diabetes mellitus
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what are the minor risk factors for atherosclerosis
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severity increases with age, men, genetics, obesity, stress, and high carb intake
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Foam cells of atheromatous plaques are derived from what
|
activated macrophages and smooth muscle cells
|
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the extracellular lipid associated with atheromas is derived from what
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insiduation of cholesterol from the vessel lumen into the intima
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what type of arteriosclerosis is a ring like calcification within the media of medium-sized to small arteries of muscular type
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monckeberg medial calcific sclerosis
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with monckeberg medial calcific sclerosis is the calcification associated with inflammatory response? are the intima and adventitia affected
|
no to both
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what might cause MMCS
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prolonged vasotonic influences (vasoconstrictors)
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what type of arteriosclerosis is characterized by proliferative or hyaline thickening of the walls of small arteries and arterioles
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arteriolosclerosis
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what is a localized abnormal dilation of blood vessels or the wall of the heart
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aneurysm
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what are the 3 types of aneurysms discussed
|
arteriosclerotic, syphilitic, and dissecting hematoma
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what causes arteriosclerotic aneurysms
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atherosclerosis
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what kind of people get arteriosclerotic aneurysms
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hypertensive males over 50.
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what type of aneurysm involve the vasa vasorum of the thoracic aorta and arch
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syphilitic aneurysms
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what are the causes of dissecting hematomas
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cystic medial degeneration (associated with Marfan syndrome and other CT disorders) and hypertension
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what are abnormally dilated, tortuous veins produced by prolonged, increased intraluminal pressure
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varicose veins
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what are predisposing factors for varicose veins
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portal hypertension, obesity, aging and long periods of standing or sitting. (very common in obese women over ago of 50)
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what is thrombus formation in the veins, especially the deeper leg veins
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thrombophlebitis
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what are the predisposing factors for thrombophlebitis
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cardiac failure and venous stasis, neoplasia, pregnancy, post-op state, and prolonged bed rest
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what are the consequences of thrombophlebitis
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localized edema and cyanosis, and embolization to distant organs. embolization to the lungs may lead to acute cor pulmonale
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what are the mechanisms of cardiac dysfunction
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pump failure, obstruction to flow, regurgitant flow, cardiac conductive disorders, and disruption to the circulation
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pump failure is often associated with what and is referred to as what
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cardiogenic shock, associated with heart muscle damage where the cardiac muscle contracts weakly or inadequately and the chambers empty improperly
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valves failing to completely open is known as what
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stenosis
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valves failing to completely close causes what
|
regurgitant flow
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what is the end-point of all serious forms of heart disease
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congestive heart failure
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CHF is usually an acute/chronic condition?
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chronic
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what are the causes of left sided heart failure
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ischemic heart disease (atherosclerosis), hypertension, aortic and mitral valvular diseases (rheumatic heart disease, calcific aortic stenosis), and non-ischemic myocardial diseases
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what are the results of left sided heart failure
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increased pressure in the pulmonary vein and ca[illaries with resulting pulmonary congestion and edema, decreased renal perfusion (results in retention of water and salt), and cerebral hypoxia, coma, and death
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what are the causes of right sided heart failure
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secondary to left sided failure, cor pulmonale, cardiomyopathies and diffuse myocarditis, tricuspid or pulmonic valvular lesions, and constrictive pericarditis
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what are the results of right sided heart failure
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chronic passive congestion of liver, congestive splenomegaly, renal hypoxia (salt and water retention and pronounced prereenal azotemia), mild peripheral edema to anasarca, pleural effusion and ascites, and cerebral hypoxia due to venous congestion
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what is the most common cause of death in the US
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ischemic heart disease
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most cases of reduced coronary blood flow are related to what
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atherosclerotic narrowing of the epicardial coronary trunks associated with or without vasospasm or thrombosis
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how much narrowing of a vessel lumen is required before clinical symptoms are exhibited (usually during excercise)
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75%
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where are the most common sites of plaques in the coronary arteries
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LAD, LCX, and RCA
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what conditions cause an increased myocardial metabolic demand that may lead to periods of myocardial ischemia
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pregnancy, infection, excercise, hyperthyroidism, and tachycardia
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when might the availability of blood oxygen be reduced to the heart
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anemia, right-left heart shunts
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what are the mechanisms of acute plaque chance or disruption
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hemorrhage into the atheroma, rupture or fissuring, and erosion or ulceration
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unstable angina, acute myocardial infarction and sudden cardiac death are often referred to as what
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acute coronary syndromes
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what is a paroxysmal attack of chest pain, usually substernal or precordial, caused by myocardial ischemia that falls short of inducing myocardial infarction
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angina pectoris
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what are the causes of angina pectoris
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increased myocardial demand and decreased myocardial perfusion owing to fixed stenosing plaques, disrupted plaques, vasospasm, thrombosis, embolization and platelet aggregation
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what are the types of angina pectoris
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stable, unstable, and prinzmetals (variant)
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which type of agina pectoris is associated with an increased cardiac workload and is almost always associated with severe stenosing coronary atherosclerosis of the major trunks
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stable agina (tx is rest and vasodilators)
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what type of agina is uncommon and occurs at rest, and is thought to be associated with vasospasm and decreased coronary blood flor rather than increased cardiac demand and stenosing atherosclerosis
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prinzmetals agina
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what type of angina usually occurs at rest and involves prolonged pain, and is thought to be induced by plaque fissuring, ulceration, or rupture with superimposed partial thrombus formation and or vasospasm
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unstable agina
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which of the agina types is considered to be a preinfarctive clinical syndrome
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unstable angina
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most cases of myocardial infarction involve what as the cause
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severe coronary atherosclerosis
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myocardial infarction is also known as what
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heart attack
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what is the leading cause of death in the USA today
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heart attack
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what are the consequences from least to greatest for MI
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angina attack, ischemic myocardial necrosis limited to the inner one third to one half os eome portion of the left ventricular wall, ischemic necrosis that may traverse the entire thickness of some portion of the left ventricle or interventricular septum, or sudden cardiact death
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what are the 3 pathogenic mechanisms of MI
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thrombotic occlusion of a coronary artery overlying a stenosing complicated atheromatous plaque, vasospasm followed by a thrombosis, and sudden cardiac death associated with a fatal arrhthmia usually ventricular fibrillation (caused by some acute ischemic event)
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transmural infarcts usually involve what structures ofthe heart
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left ventricle and IV septum from endocardium to epicardium
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what are secondary complications involved with transmural infarcts
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infarcted papillary muscle and mitral valve incompetence, fibrinohemorrhagic pericarditis, mural thrombosis and peripheral embolism, ruptured infarct and pericardial tamponade, and ventricular aneurysm
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subendocardial infarcts usually involve what structures
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inner 1/3 to 1/2 of the ventricular wall
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what arteries are associated with MI and at what %
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LAD 40-50%, RCA 30-40%, and LCX 15-20%
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describe the evolution of morphologic changes that occur during MI
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20-40 minutes of total ischemia results in irreversible cell death, 1-3 days coagulative necrosis with neutrophil influx, 3-7 days macrophage influx to remove dead myofibers and neutrophils, 7-10 days early formation of fibrovascular granulation tissue, 2-8 weeks well established granulation tissue with decreased cellularity, more than 8 weeks dense scar tissue
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what are the causes of chronic ischemic heart disease
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slow, progressive, atherosclerotic, encroachment on the blood supply to the myocardium (this may lead to congestive heart failure)
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what is hypertensive heart disease
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a response of the heart to increased demands resulting from systemic hypertension
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what are the criteris for hypertensive heart disease
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left ventricular hypertrophy in the absenve of other cardiovascular pathology and a history of hypertension
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hypertension is defined as what
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140/90 or greater
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what is the second most common cause of cardiac death
|
hypertensive heart disease
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hypertension and diabetes strongly predisposes someone for what type of heart problem
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coronary atherosclerosis
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in hypertensive heart disease what is the weight of the heart and why
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500-700 grams usually due to left ventricular thickening
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in hypertensive heart disease the left side of the heart will always appear larger (T/F)
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F- enlargement is at the expense of the chamber volume so enlargement is not seen until decompensation and dilation occur
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what is cor pulomale
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right ventricular enlargement resulting from disorders that affect either the strucutre or function of the lungs
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what side of the heart is associated with cor pulmonale
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right
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are congenital heart disease and left-sided failure considered causes of cor pulmonale
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no
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what is an acute, recurrent inflammatory disease, principally of children that usually follows a pharyngeal infection with group A beta-hemolytic streptococci
|
rheumatic heart disease
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rheumatic heart disease is immune mediated T/F
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T
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in rheumatic heart disease what is the morphology of the pancarditis
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aschoff bodies, fibrinoid necrosis, fibrosis, and rheumatic valvulitis
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what is the most common cause of mitral stenosis
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rheumatic valvulitis
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what are the non-carditis findings of the rheumativ fever
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migratory polyarthritis of the large joints, subcutaneous nodules, erythema marginatum of the skin, and Sydenham chorea
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marfan syndrome can cause what valvular complication
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mitral valve prolapse
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what is the most common form of valvular heart disease in the industrialized world
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mitral valve prolapse
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what situations would cause death associated with mitral valve prolapse
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infective endocarditis, congestive heart failure, or ruptured chordae tendieae
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what is infective endocarditis characterized by
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colonization or invasion of the heart valves or the mural endocardium by a microbiologic agent leading to the formation of bulky friable vegetations composed of thrombotic debris and organsisms
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what are predisposing factors for infective endocarditis
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chronic alcoholism, intravenous drug abuse, cardiac surgery, intravascular indwelling catheters or prosthetic devices, and oral surgery
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what are the most commonly isolated organisms for IE
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s. viridans, staphylococcus aureus, and enterococci
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acute IE usually involve a previously normal/diseased valve and has high/low mortality with tx. what is it characterized by
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normal, high, characterized peripherally by leukocytosis
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what is myocarditis
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inflammatory disease of the heart
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most cases of myocarditis are of what origin
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viral
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what are 4 tyes of viral origins of myocarditis
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coxsackie A and B, ECHO, polio, influenza A and B
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viral forms of myocarditis are especially common in what groups
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infants, immunosuppressed and pregnant
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what is the pathogenisis for viral forms of myocarditis
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direct cytotoxicity and immune mediated (T-cell dependant) toxicity
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what are the types of bacterial myocarditis
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diphtheria, lyme disease, meningococcal, and leptospiral infections
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what are the types of mycotic and protozoal myocarditis
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aspergillosis and candidiasis in immunosuppressed pts, and trypanosoma cruzi (chagas disease)
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what are the most common primary tumors of the heart and where do they usually arise from
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myxomas in the left atrium
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what are the 3 tumors of the heart discussed
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myxomas, lipomas, and rhabomyomas
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how does the kidney acct as an endodcrine organ
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by secreting erythropoietin, renin, and prostaglandins
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can the capillaries and fenestrated endothelial cells of the glomerulus proliferate
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yes
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how many layers comprise the glomerular basement membrane
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3
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what cells of the kidney have foot processes and filtration slits
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parietal and visceral epithelial cells
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what cells of the glomerulus are contractile, phagocytic and can proliferate
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mesangial and matrix cells
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what tubules of the kidney are at greatest risk for ischemic and toxic injury
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proximal tubules
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what is the small endocrine organ of the kidney that produces renin and is embedded in the media of the afferent arterioles
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juxtaglomerular apparatus
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what structure is associated with the distal tubules
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macula densa
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what cells resemble mesangial cells
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lacis cells
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what comprises the interstitium of the kidney
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lymphatics, fenestrated peritubular capillaries and fibroblasts
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glomerular diseases often progress to involve what structures
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tubules, interstitium, and blood vessels
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glomerular diseases are not immune mediated T/F
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F
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what are the clinical features of acute glomerular injury
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hematuria, proteinuria, oliguria, azotemia, edema, and hypertension
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what are the effects associated with nephritic syndrome
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hematuria, proteinuria, oliguria and hypertension.
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nephritic syndrome is seen most in patients with type of glomerular disease
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proliferative or hypercellular glomerular diseases
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wht are the effects associated with nephrotic syndrome
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massive proteinuria with daily loss of 3.5 gm or more of protein, hypoalbuminemia with plasma albumin levels less then 3 gm per dl, generalized edema and hyperlipidemia. normotensive
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what type of glomerular disease is associated with the nephrotic syndrome
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membranous glomerular diseases in which the damaged capillary walls and or GBM develop an increased permeability to plasma proteins due to disruption of the size and charge barrier.
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in the nephrotic syndrome is there usually damage to the foot processes of the visceral epithelial cells
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yes
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what are the 3 causes of hypercellularity within the glomerulus
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cellular proliferation (due to prolif of endothelial or mesangial cells), leukocytic infiltration (neutrophils and monocytes), crescent formation
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whatis crescent formation
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accumulation of cells in the urinary space, mostly proliferating parietal epithelial cells, infiltrating leukocytes and fibrin
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the accumulation of a homogenous, eosinophilic material n the basement membrane or mesangium of the glomerulus is what
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hyalinization or sclerosis
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what is the most common etiology of human glomerulonephritis
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immune-complex nephritis
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with immunofluorescence the immune complexes along the GBM appears how
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granular lumpy bumpy deposits
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what infectious agents are implicated in immune-complex nephritis
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streptococcus, hepatitis viruses B and C, syphilis, malaria, etc
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in anti-GBM nephritis how does the deposits along the basement membrane appear
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linear and not granular
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what is an example of anti-GBM nephritis
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goodpasture's syndrome
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activation of the alternate complement pathway is involved in what type of glomerulonephritis
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membranoproliferative glomerulonephritis
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what are the cellular mediators of glomerular injury
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neutrophils, macrophages, lymphocytes, nk cells, platelets, and mesangial cells
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what are the soluble mediators of glomerular injury
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completement components, cytokines, chemokines, nitric oxide and the coagulation system
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what are the types of acute primary glomerulonephritis
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poststreptococcal (proliferative) glomerulonephritis, rapidly progressive (crescentric) glomerulonephritis, goodpasture's syndrome, membranous glomerulonephritis, lipid neprosis, and membranoproliferative glomerulonephritis
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poststreptococcal proliferative glomerulonephritis is most common in what group of people
|
most commonly in 6-10 year old children, 1-4 weeks after a group A beta-hemolytic streptococcal infection of the throat or skin.
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is poststreptococcal glomerulonephritis membranous or proliferative, and is it described as a nephritic or nephrotic syndrome
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proliferative, nephritic syndrome
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what characterizes rapidly progressive GN
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extensive proliferation of parietal epithelial cells, influx of monocytes and deposition of fibrin into bowman's space with crescent formation
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what is an anti-GBM form of rapidly progressive GN that is always preceded by pulmonary hemorrhage
|
goodpasture's syndrome
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what is a major cause of the nephrotic syndrome characterized primarily as a chronic immune-complex disorder with electron dense IgG and complement containing granular deposits along the subepithelial side of the GBM
|
membranous GN
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what does membranous GN result in
|
diffuse thickening of the GBM, effacement of the foot processes of the visceral eithelial cells, and subepithelial deposits containing immunoglobulins and complement without an increase in the number of cells
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what is a condition in which the nephrotic syndrome is associated with difuse effacement of foot processes of the visceral epithelial cells
|
lipoid nephrosis
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what is the most common cause of the nephrotic syndrome in 2-6 year old children
|
lipoid nephrosis
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is there GBM thickening or subepithelial deposits with lipoid nephrosis
|
no
|
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what type of GN is characterized by both a proliferation of mesangial cells and thickening of the capilary/GBM walls
|
membranoproliferative GN
|
|
what are the systemic diseases associated with glomerular damage
|
systemic lupus erythematosus, henoch-schonlein purpura, vegetative endocarditis, diabetis mellitus, amyloidosis, and plasma cell dyscrasias
|
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what type of GN progresses to end stage glomerular disease characterized by chronic renal failure
|
chronic GN
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what GN is characterized by uremia, elevated blood BUN and creatinine levels, deranged blood volume (resulting in dehydration, edema, and hyperkalemia, acid-base imbalance, GI ulceration and hemorrhage, hypertension, anemia and bleeding diathesis, and abnormalities of calcium, phosphorous, and bone metabolism
|
chronic GN
|
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what is an acute bacterial infection of the kidney and renal pelvis associated with urinary tract infections
|
pyelonephritis
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most infections causing pyelonephritis arise from what type of bacteria
|
intestinal gram negative bacteria
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what is the end stage kidney disease with scarring of the calyces and pelvis. tubules may be cast-filled and dilated producing a morphology described as thyroidization
|
chronic tubulointestinal nephritis
|
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what type of nephropathy is caused by extensive intake of analgesiv mixtures and characterized by chronic interstitial nephritis with renal papillary necrosis
|
chronic analgesiv nephropathy
|
|
what is the most common cause of acute renal failure, due to destruction of tubular epithelium
|
acute tubular necrosis
|
|
what are the causes of acute tubular necrosis
|
ischemia, and nephrotoxic effects of heavy metals, ethylene glycol, and other organic compounds
|
|
what is hyalinization of the small renal arteries and arterioles with narrowing of the lumen, resulting in a variety of glomerular alterations, interstitial fibrosis, and patchy ischemic tubular atrophy
|
benign nephrosclerosis
|
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what is characterized by fibrinoid necrosis of arterioles and necrotizing or hyperplastic arteriolitis, and can progress to malignant hypertension
|
malignant nephrosclerosis
|
|
what are the two pathogenic processes of thrombotic microangiopathies
|
endothelial injury and platelet aggregation, which lead to tubular ischemia (coagulative necrosis) as a result of vascular obstruction and vasoconstriction
|
|
what is the etiology for thrombotic microangiopathies
|
those things that induce disseminated intravascular coagulation
|
|
what is a dilation of the renal pelvis and calyces associated with progressive atrophy of the kidney due to obstruction to the urine outflow
|
urinary tract obstruction (hydronephrosis)
|
|
what are the benign renal tumors
|
papillary adenoma, fibroma, hamartoma, angiomyolipomas, and oncocytoma
|
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what renal tumor arise from the cortical tubular epithelium
|
pappilary adenoma
|
|
what renal tumors are found within the pyramids
|
fibroma or hamartoma
|
|
what reanl tumors consist of blood vessels, smooth muscle and fat cells
|
angiomyolipomas
|
|
what renal tumor arises from the medullary collecting tubules
|
oncocytoma
|
|
what is the most common renal cancer seen in older male patients. tubular epithelial origin
|
renal cell carcinoma
|
|
what is the most important risk factor for renal cell carcinoma
|
tobacco, genetics
|
|
what is the most common organ cancer of children under 10
|
nephroblastoma (Wilms tumor)
|
|
what are the types of malignant renal tumors
|
urothelial carcinoma, nephroblastoma, and renal cell carcinoma
|
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what is a chronic disorder of carbohydrate, fat, and protein metabolism characterized in its fully expressed clinical form by fasting hyperglycemia (more than 126 mg/dl on more than one occasion), glycosuria, and a striking tendency toward dev't of atherosclerosis, microangiopathy, nephropathy, and neuropathy
|
diabetes mellitus
|
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what is the leading cause of end-stage renal disease, adult-onset blindness and non-traumatic lower leg amputation in the US
|
diabetes mellitus
|
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what type of diabetes is transmitted as an autosomal dominant and accounts for less than 5% of the cases of primary diabetes. it manifests clinically as only a mild hyperglycemia. pts have a primary defect in beta cell function without loss of beta cell mass or insulin production
|
maturity-onset diabetes of the young
|
|
insulin is released by what
|
beta cells of pancreas
|
|
in type 1 diabetes what is the main cause of destruction of beta cells
|
t-lymphocytes reacting against poorly defined beta cell antigens
|
|
diabetic microangiopathy is seen in what sites with diabetes
|
skin, skeletal muscle, retin, renal glomeruli/tubules, bowman's capsule, and peripheral nerves
|
|
most diabetic type 1 or 2 patients that have suffered for more than 10 years have what associated problems
|
severe accelerated atherosclerosis leading to myocardial infarction, cerebral stroke, and gangrene of the lower extremities
|
|
thickening of arteriolar walls is due to what in diabetic patients
|
amorphous hyalinization, BM thickening, endothelial proliferation, and deposition of PAS-positive mucopolysaccharides
|
|
what changes are seen in the pancreas in diabetes
|
reduction in size and number of islets, beta cell degranulation, glycogen cytoplasmic vacuolation, hyalin repacement of islets, fibrous ct or amyloid and leukocytic infiltration
|
|
amyloid replacement of the islets is more common in what type of diabetes
|
type 2
|
|
what is the most severely damaged organ in diabetes
|
kidneys
|
|
what is the second most common cause of death in diabetic pts
|
renal failure
|
|
what is the most common renal lesion in chronic diabetics, comprised by an overall thickening of the BM of the capillaries throughout their entire length, associated with the proliferation of mesangial cells and the deposition of excess amounts of mesangial matrix which may engulf or obliterate the mesangial cell
|
diffuse glomerulosclerosis
|
|
pts with diffuse glomerulosclerosis will eventually develop what
|
nephrotic syndrome
|
|
what type of diabetic related kidney condition is also known as kimmelstiel wilson lesion, and takes the form of ovoid or spherical often laminated hyalin mass situated at the periphery of the glomerulus
|
nodular glomerulosclerosis
|
|
what lesion is pathognomonic for diabetes
|
nodular glomerulosclerosis
|
|
what are the kidney complications associated with diabetes
|
diffuse glomerulosclerosis, nodular glomerulosclerosis, atherosclerosis, pyelonephritis, and glycogen accumulation
|
|
diabetic ocular lesions consist of what
|
proliferative and non-proliferative, retinopathy, cataracts, microaneurysms, and glaucoma
|
|
what type of diabetics do no usually suffer from acute metabolic syndrome but frequently develop the chronic vascular syndrome
|
type 2
|
|
what are the enviormental influences for essential hypertension
|
dietary sodium, stress, smoking, and obesity and oral contraceptives
|
|
what are the 4 mechanisms of pathogeneisis realted to essential hypertension
|
disturbance in the normal negative feedback control of blood pressure on renin release from the kidneys, central nervous system and ans abnormalities, an intrinsiv inability of the kidneys to respond to arterial pressure diuresis, and increased sensitivity of the vascular smooth muscle to hormonal and sympathetic influences
|
|
what type of hypertension is characterized by a rapidly mounting blood pressure, usually to diastolic levels over 120 mmhg with systolic levels over 200 mmhg, and usually results in renal failure unless treated
|
malignant hypertension
|
|
what is the most prominent morphologic finding with malignant hypertension
|
fibrinoid necrosis of the arterioles and hyperplastic arteriolosclerosis
|
|
what type of hypertension is associated with a variety of renal, endocrine, neurologic, and vascular disorders and acounts for only about 5% of the cases of hypertension
|
secondary hypertension
|
|
what renal disorders can cause secondary hypertension
|
acute GN, chronic GN, pyelonephritis, renal artery stenosis and vasculitis
|
|
what initiates the intrinsic coagulation cascade
|
endothelial injury and platelet receptor adheres to the exposed collagen via the von willebrands factor 8
|
|
platelets adhere to collagen and release what in the coagulation cascade
|
ADP
|
|
ADP released from platelets uon binding to collagen does what
|
activates phospholipase A2 in circulating platelets, and this in turn activates the prostaglandin system.
|
|
after activation of the prostaglandin (cyclooxygenase) system what occurs
|
thromboxane A2 is then produced and enters the dense tubular system of the platelets. TXA2 then chelates the Ca and transports it into the platelet cytoplasm.
|
|
TXA2 binding is blocked by what
|
aspirin and ibuprofen
|
|
what is the role of ca after it is transported into the platelet cytosol
|
reacts with calmodulin to phosphorylate, activate, and assemble the contractile components myosin and actomyosin
|
|
what is released from damaged endothelial cells to initiate the extrinsic coagulation cascade
|
tissue factor
|
|
what is normal bleeding time
|
2-9 minutes
|
|
what is a normal platelet count
|
150k/cu.mm - 300k/cu.mm
|
|
what is clot retraction
|
failure of serum seperation denotes a platelet function defect and/or thrombocytopenia
|
|
what is decreased with excessive fibrinolysis or congenital fibrinogen deficiency
|
fibrinogen level
|
|
prothrombin time is prolonged with what deficiency
|
in any extrinsic and common pathway factors (5,7,10, prothrombin and fibrinogen)
|
|
prolonged activated partial thromboplastin time indicates what
|
deficiency in any intrinsic or common pathway factors (5,8,9,10,11,12, prothrombin 2 and fibrinogen 1)
|
|
what does ADP platelet aggregation include
|
measures the platelet release reaction
|
|
platelet factor 3 measures what
|
antiplatelet antibody in the serum, indicates an immune-mediated thrombocytopenia
|
|
clotting time will be prolonged in bleeding disorders for all factors excet for what
|
7 deficiency
|
|
what organisms damage the endothelial lining, exposing underlying collagen in hemorrhagic diatheses related to vessel wall abnormalities
|
measles, rickettsial and bacterial infections
|
|
what is the collagen defect that results in impaired support of the vessel walls related to hemorrhagic diathesis related to vessel wall abnormalities
|
scurvy
|
|
what does ehlers-danlos syndrome cause
|
defective collagen synthesis
|
|
what does cushings syndrome cause
|
protein wasting with loss of perivascular supporting tissue
|
|
what are the lesions of hemorrhagic diseases related to vessel wall abnormalities like
|
petechial and purpuric hemorrhages in the skin or mucous membranes, especially gingival. occasionally joint, muscle, and subperiosteal hemorrhage
|
|
what tests are used to confirm hemorrhagic diathesis related to vessel wall abnormalities
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platelet count, bleeding time, and coagulation tests such as pt and aptt are usually normal. platelet count may be decreased due to platelet plugging of the damaged endothelium
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reduced platelet numbers are known as what
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thrombocytopenia
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what are the causes of hemorrhagic diathesis related to reduced platelet numbers
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generalized diseases of the bone marrow, increased destruction of platelets, and massive transfusions
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what generalized diseases of the bone marrow cause decreased production of platelets and megakaryocytes
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aplastic anemia, leukemia, uremia, myelophthisic disorders and cytotoxic drugs
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what might cause an increase in destruction of platelets
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drugs (haptens), HIV, autoimmune and isoimmune reactions, hypersplenism, and prosthetic devices
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massive transfusions cause what related to platelet numbers
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produces dilutional thrombocytopenia
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what are the lesions associated with hemorrhagic diathesis related to reduced platelet numbers
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multiple skin petechiae and possibly intracranial and GI bleeding, bruising, nosebleeds, bleeging gums, and extensive hemorrhages into soft tissues from only minor trauma
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what are platelet numbers in hemorrhagic diathesis related to reduced platelet numbers
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less than 20,000/cu.mm
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what are the test results for hemorrhagic diathesis related to reduced platelet numbers
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prolonged bleeding time, poor clot retraction, throbocytopenia, other coagulation tests are normal
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what type of hemorrhagic disease is produced by von willebrands's disease
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HD related to defective platelets
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what is the defect in von willebrand's disease
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an absence of von willebrand's factor 8 which adheres platelets to endothelium and or collagen
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what do tests show in von willebrand's disease
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prolonged bleeding time, APTT can be either normal or prolonged, ADP platelet aggregation is subnormal, and platelet count, fibrinogen level and PT are normal
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definitive diagnosis of von willebrand's disease involves what test
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ristocetin agglutination test, aggregation of the platelets does not ocur if the factor is missing
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what disease interferes with adhesion of platelets to collagen because of a deficiency of a platelet membrane glycoprotein. transmitted as an autosomal recessive
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bernard-soulier syndrome
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what defect is an absence of the platelet membrane glycoprotein fibrinogen receptor necessary for aggregation
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glanzmann's thrombasthenia
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glanzmann's thrombasthenia is a congenital lifelong bleeding disorder transmitted as whata type of genetic disease
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autosomal recessive and is characterized by failure of platelets to aggregate in response to ADP
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what do tests show with glanzmann's thrombastenia
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easy bleeding and no clot retractin, bleeding time is prolonged, ADP platelet aggregation is subnormal, and all coagulation tests are normal
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what does chediak higashi syndrome involve
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the formation of non-functional platelets
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what is a prostaglandin inhibitor and interferes with both the platelet aggregation and release reactions
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aspirin and NSAIDS
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what type of hemorrhagic diathesis shows bleeding represented by large post traumatic ecchymoses or hematomas or prolonged bleeding after lacerations or surgical procedures
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HD related to abnormalities in clotting factors
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what are the acquired causes of HD related to abnormalities in clotting factors
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vitamin K deficiency, liver disease, malabsorption diseases, warfarin poisoning
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what are the hereditary causes of HD related to abnormalities in clotting factors
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factor 7,8,9,10 deficiency
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hemophilia A is associated with what factor deficiency
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8
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what genetic inheritability is a deficiency of factor 8
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sex linked recessive
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factor 8 is carried and stabilized by what
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von willebrand factor
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what characterizes hemophilia A
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easy bruisability and bleeding accompanied by bleeding into the weight bearing joint and GI and urinary tracts. clots are formed but are not stabilized
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what do tests show in hemophilia A
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bleeding time, platelet count, fibrinogen level, PT and ADP platelet aggregation are normal. the APTT is prolonged and whole blood and plasma cloting is prolonged
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what factor is deficient in christmas disease aka hemophilia B
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factor 9 deficiency
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how is hemophilia B inherited
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x-linked inheritance of males
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factor 7 deficiency is intrinsic/extrinsic
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extrinsic
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factor 7 deficiency is characterized by what
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gingival bleeding, epistaxis, hemarthrosis, and profuse bleeding after surgery. PT is prolonged, and clotting time is not prolonged
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what is a rare condition that is clinically similiar to factor 7 deficiency, with both PT and APTT prolonged
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factor 10 deficiency
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what is an acquired thrombohemorrhagic disorder occurring as a secondary complication in avariety of diseases
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disseminated intravascular coagulation
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what are the causes of DIC
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results from consumption of platelets and coagulation factors due to the introduction of some foreign matter into the bloodstream. this may be caused by viruses, rickettsia, bacteria, and or cell debris such as that from a dead fetus.
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what do tests show in DIC
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all platelet and coag tests can be abnormal, both coagulation cascades are initiated because of release of tissue factor or thromboplastic substances into the circulation and widespread injury to endothelial cells
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