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105 Cards in this Set
- Front
- Back
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What are characteristics of stable angina?
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pain that is precipitated by exertion and is relieved by rest or vasodilators. Results from narrowing of coronary vessels by atherosclerotic plaque
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What are characteristics of unstable angina?
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prolonged or recurrent pain at rest. often is indicative of imminent MI
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What is Prinzmetal angina?
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intermittent chest pain at rest. It is generally caused by vasospasm
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What are the cells involved in the evolution of a myocardial infarct?
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neutrophils, macrophages, and fibroblasts
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What is a transmural infarction?
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myocardial necrosis that traverses the entire ventricular wall from the endocardium to the epicardium
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What is a subendodermal infarction?
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myocardial necrosis that is limited to the interior one third of the wall of the left ventricle
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What are the complications of an MI?
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Arrhythmia, Myocardial (pump) failure, myocardial rupture, ruptured papillary muscle, mural thrombosis, ventricular aneurysm
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what is the most common cause of death in the first several hours after an MI?
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arrhythmia
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what can myocardial pump failure result in?
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congestive heart failure and/or shock
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what is a myocardial rupture?
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occurs w/in the first 4-7 days and may result in death from cardiac tamponade.
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what is cardiac tamponade?
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compression of the heart by hemorrhage into the pericardial space
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At what time do neutrophils appear in viable tissue adjacent to a MI?
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after 12 hours
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Post-MI, the lesion has slight swelling and change of color. the histologic section shows a loss of striations of muscle fibers, a loss of nuclei and infiltration of the lesion by neutrophils. How long after the MI has this occurred?
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12-24 hours
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gross changes of an infarct show pale or reddish brown infarct with surrounding hyperemia. how long is it post-MI?
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24 hours
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gross changes of an infarct show increasingly yellow color. histologic section shows macrophages and neutrophils. how long is it post MI?
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3 days
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gross section of a heart shows a yellow lesion surrounded by a congested red border. histologic section shows mostly macrophages, some neutrophils and some young fibroblasts. how long is this patient post-MI?
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7 days
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gross section of a heart shows a lesion of yellow necrotic tissue that is being replaced by red, newly formed vascular tissue. histology shows increasing numbers of fibroblasts, with fewer macrophages and neutrophils. how long post-MI?
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10 days
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What test would you run to diagnose Rheumatic Fever?
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ASO antibody - evidence of recent streptococcal infection
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what is the etiology of rheumatic fever?
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immunologic response to streptococcal antigens that also respond to self-antigens
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What is the classic lesion of rheumatic fever and what is it composed of?
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Aschoff Body is an area of focal interstitial myocardial inflammation characterized by fragmented collagen and fibrinoid material, large Anitschkow myocytes and multinucleated giant cells
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What are the general anatomic changes in rheumatic fever?
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pericarditis, myocarditis, endocarditis
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where does rheumatic endocarditis usually occur?
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points of high stress (e.g. points of valve closure and posterior wall of left atrium)
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what is the early appearance of the valves affected by rheumatic endocarditis?
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valve leaflets are red and swollen and tiny, warty, bead-like rubbery vegetations form along the lines of closure. not a source of emboli
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what are the long-term characteristics of valvular rheumatic endocarditis?
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fibrotic healing and thickening of the valve leaflets. may cause fusion of valve cusps as well as thickening of cordae tenineae.
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what are characteristics of the mitral valve after long-standing Rheumatic Heart Disease?
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fish-mouth buttonhole deformity, insufficiency, or combination. mitral stenosis marked by diastolic pressure higher in left atrium than in left ventricle
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what is the classic presentation of acute rheumatic fever?
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fever, malaise, increased ESR; migratory polyarthritis, subcutaneous nodules over bony prominences and erythema marginatum.
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what CNS complications are possible with rheumatic fever?
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emotional lability and Sydenham chorea
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what are complications of infectious endocarditis?
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ulceration and perforation of the valve cusps or rupture of a chordae tendineae, distal embolization causing septic infarcts,
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what is the cause of most acute infectious endocarditis cases?
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staph aureus, secondary to IV drug users (involves tricuspid valve)
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what is the most common cause of subacute bacterial endocarditis? what is the classic patient profile?
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strep viridans. patients with congenital heart disease or preexisting valvular heart disease
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small vegetations on either or both surfaces of the valve leaflets is characteristic of what disease?
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SLE (Libman-Sacks endocarditis)
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what is marantic endocarditis?
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small, sterile fibrin deposits randomly arranged along the line of closure of the valve leaflets. may cause sterile emboli. associated with metastatic cancer and wasting conditions
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autopsy of a patient shows thickened endocardial plaques involving the mural endocardium or valvular cusps of the right side of the heart. What is the underlying cause?
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secretory products of carcinoid tumors --> serotonin most common. must be from metastatic disease in the lung
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what does a midsystolic click on cardiac auscultation signify?
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mitral valve prolapse
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what is the most frequent valvular lesion and in what segment of the population does it most frequently occur?
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mitral valve prolapse in young women
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what inherited disorder is mitral valve prolapse associated with?
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marfan syndrome
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what can cause mitral valve insufficiency?
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rheumatic heart disease, mitral valve prolapse, infective endocarditis, damage to a papillary muscle from MI.
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what are common causes of aortic valve stenosis?
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calcification from normal age-related degeneration, congenital bicuspid aortic valve, rheumatic heart disease
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what causes aortic insufficiency?
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nondissecting aortic aneurysm, rheumatic heart disease, syphilitic aortitis
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pulmonary valvular complications are most commonly associated with what?
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congenital defects (ie tetralogy of Fallot)
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what cardiac anomaly is associated with Turner syndrome?
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coarctation of the aorta
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what cardiac anomalies are frequently associated with down syndrome?
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endocardial cushion defects
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there is an increased incidence of patent ductus arteriosus in which patients?
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those living at high altitudes
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adult patient has pulmonary hypertension and slow onset of cyanosis. what is the cause?
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atrial septal defect, ventricular septal defect, patent ductus arteriosus
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Ventricular septal defect results in what?
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small defects may close spontaneously, but lager defects may lead to pulmonary hypertension, right-sided heart failure and late cyanosis
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What is tetralogy of Fallot?
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pulmonary infundibular or valvular stenosis, VSD, overriding aorta, right ventricular hypertrophy
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kid has cyanosis from birth, is easily fatigued, and symptoms are relieved by squatting. what is the diagnosis?
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tetralogy of Fallot
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patent ductus arteriosis is closed by the administration of what?
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indomethacin
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what keeps the ductus arteriosis patent in fetal life?
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PGE2 and low oxygen tension
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patient has hypertension in upper extremities and cerebral vessels only. there is notching of the ribs on x-ray. what is the diagnosis?
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coarctation of the aorta
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what is necessary for survival in a child born with transposition of the great vessels?
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compensatory anomaly, such as patent ductus arteriosus
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What are findings in congenital rubella syndrome?
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cardiovascular defects, microcephaly with mental retardation , deafness, cataracts, and growth retardation
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what does anti-rubella IgM Abs signify?
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recent infection
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what does anti-rubella IgG Abs signify?
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recent primary infection, past infection or reinfection
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What are the cyanotic diseases?
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1. transposition of the great vessels
2. tetralogy of Fallot 3. other right-to-left shunts 4. left-to-right shunts may present later in life |
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what are three main causes of dilated cardiomyopathy?
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alcoholism, thiamine deficiency, prior myocarditis
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what is the most common cause of restrictive cardiomyopathy?
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amyloidosis
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inherited hypertrophic cardiomyopathy is characterized by what?
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asymmetric septal hypertrophy; disoriented, tangled, and hypertrophied myocardial fibers on microscopy; AD inheritance, left ventricular outflow obstruction
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what is an often cause of unexpected death in young athletes?
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hypertrophic cardiomyopathy
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what is the most common cause of biventricular heart failure in young patients with no other history of heart disease?
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coxsackievirus
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serous pericarditis is associated with what conditions?
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SLE, rheumatic fever, viral infections
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what are characteristics of serous pericarditis?
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clear, straw-colored, protein-rich exudate containing small numbers of inflammatory cells
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what can cause fibrinous or serofibrinous pericarditis?
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uremia, MI, acute rheumatic fever
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characteristics and causes of hemorrhagic pericarditis?
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tumor invasion of pericardium, or tuberculosis or other bacterial infection. characterized by bloody inflammatory exudate
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what are characteristics of chronic constrictive pericarditis?
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thickening and scarring of pericardium with loss of elasticity. may mimick signs and symptoms of right-sided heart failure. marked by proliferation of fibrous tissue
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what is the most frequently occurring primary cardiac tumor?
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myxoma...most often found in adults
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rhabdomyoma is seen in which patients?
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infants and young children (associated with tuberous sclerosis)
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what are the causes of left-sided heart failure?
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ischemic heart disease, hypertension, aortic and mitral valvular disease, myocardial diseases
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what are the clinical manifestations of left-sided heart failure?
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dyspnea and orthopnea, pleural effusion with hydrothorax, reduction in renal perfusion (activation of Renin-angiotensin --> retention of salt and water), cerebral anoxia
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what is the most common cause of right-sided heart failure?
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left-sided heart failure
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what are clinical manifestations of right-sided heart failure?
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renal hypoxia (leading to greater fluid retention and peripheral edema), enlarged and congested liver and spleen (nutmeg liver), distention of the neck veins
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What is Cor Pulmonale?
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RV hypertrophy and/or dilation secondary to lung disease or primary disease of the pulmonary vasculature, such as primary pulmonary hypertension
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patient older than 50 has ring-like calcifications in the media of the radial and ulnar arteries that does not obstruct blood flow. What is the diagnosis?
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medial calcific sclerosis (Monckeberg arteriosclerosis)
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what are characteristics of arteriolosclerosis?
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hyaline thickening or proliferative changes of small arteries and arterioles, especially in the kidneys.
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what is hyperplastic arteriolosclerosis?
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concentric, laminated, onionskin thickening of the arteriolar walls. accompanied by necrotizing arteriolitis. called malignant nephrosclerosis in the kidneys (associated with malignant hypertension)
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describe the plaques of atherosclerosis
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central core of cholesterol and cholesterol esters; lipid-laden macrophages, or foam cells; calcium; and necrotic debris. Core is covered by subendothelial fibrous cap
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What are complications of atherosclerotic plaques?
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1. Ulceration, hemorrhage into the plaque, or calcification of the plaque
2. thrombus formation --> produces obstructive disease 3. Embolization of an overlying thrombus or of plaque material itself |
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What mitogenic factors are important in the formation of atherosclerosis?
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PDGF, FGF, epidermal growth factor, TGF-alpha
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what mediates the conversion of monocytes to lipid-laden foam cells?
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Beta-VLDL receptor and the scavenger receptor, which recognizes modified LDL
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where do most atherosclerotic aneurysms occur?
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descending abdominal aorta
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What causes aneurysms?
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cystic medial necrosis
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where do berry aneurysms most often occur and why?
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congenital weakness of the media at bifurcations of cerebral arteries
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Berry aneurysms are associated with what genetic disease?
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Adult polycystic kidney disease
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what is the most frequent cause of subarachnoid hemorrhage?
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berry aneurysm
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in what disease do you find a "tree-bark" appearance of the aorta?
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syphilitic aortitis --> can lead to a luetic aneurysm. involves ascending aorta --> can lead to aortic valve insufficiency
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what is the most common tumor of infancy?
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hemangioma --> responsible for port-wine stain birthmarks
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toxic exposure to what causes hemangiosarcoma?
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arsenic, thorium dioxide (a radioactive diagnostic agent). Polyvinyl chloride is associated with angiosarcoma of the liver
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mediterranean patients, ashkenazie jews, AIDS patients, young african children
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kaposi's sarcoma
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what is polyarteritis nodosa?
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necrotizing immune complex inflammation of small- and medium-sized arteries. marked by destruction of arterial media and internal elastic lamella, resulting in aneurysmal nodules.
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what infection is associated with polyarteritis nodosa?
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HBV
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what serum antibodies are seen in polyarteritis nodosa?
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P-ANCA
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where is polyarteritis nodosa found?
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1. kidneys (vasculitis in arterioles and glomeruli)
2. coronary arteries 3. musculoskeletal system (myalgia, arthralgia, arthritis) 4. GI tract 5. CNS (eye or skin) |
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how does leukocytoplastic vasculitis present?
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palpable purpura
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describe Henoch-Schonlein purpura
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hemorrhagic urticaria of the extensor surfaces of the arms, legs, buttocks; associated with antecedent URIs
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Describe Wegener granulomatosis
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necrotizing granulomatous vasculitis of small and medium sized vessels of the respiratory tract kidneys and other organs
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what are the major clinical manifestations of wegener's granulomatosis?
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dominated by respiratory tract signs and symptoms, especially of the paranasal sinuses and lungs, and necrotizing glomerulonephritis. manifest by fibrinoid necrosis of small arteries and veins, early infiltration by neutrophils...granulma formation
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what lab tests are seen in wegener's granulomatosis?
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C-ANCAs
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how does temporal arteritis present?
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headache, tenderness with palpable nodules along the course of the involved artery, visual impairment, polymyalgia rheumatica
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absent pulses in carotid, radial, or ulnar arteries; fever, night sweats, malaise, myalgia, arthritis and arthralgia...what's the diagnosis?
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takayasu arteritis (aka aortic arch syndrome)
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what is Kawasaki disease?
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acute self-limited illness of infants and young children characterized by acute necrotizing vasculitis of small- and medium-sized vessels
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very young child presents with fever, hemorrhagic edema of conjunctivae, lips, and oral mucosa and cervical lymphadenopathy. also has coronary artery vasculitis what is the diagnosis?
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Kawasaki disease
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What is Buerger disease?
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acute inflammation involving small- to medium-sized arteries of the extremities, extending to adjacent veins and nerves. results in painful ischemic disease, often leading to gangrene.
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who suffers from buerger disease?
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young men who are heavy smokers
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marked increase in diastolic blood pressure, focal retinal hemorrhages and papilledema, LV hypertrophy and LV failure what is diagnosis and prognosis?
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malignant hypertension; early death
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what are the renal manifestations of malignant hypertension?
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nephrosclerosis and rupture of glomerular capillaries and arterioles resulting in flea-bitten kidneys.
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