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122 Cards in this Set
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What is the difference between primary and secondary pericarditis? Which is more common?
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Primary pericarditis is rare and usually viral in origin, it is directly caused by an agent (Coxackie A, B) - associated with myocarditis.
Secondary pericarditis is more common, occurs secondary to acute MI, uremia, or cardiac surgery/irritation. |
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What are the sequelae of pericarditis?
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Hemodynamic Disorders
Complete resolution Progression to fibrosis |
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What is acute pericarditis? What are the four major morphologies?
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Acute pericarditis has a rapid onset, usually involving an infectious agent or direct injury.
1) Serous 2) Fibrinous and serofibrinous 3) Purulent, suppurative 4) Hemorrhagic |
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Describe serous pericarditis - morphology, cause, is it acute/chronic?
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Morphology: noninfectious inflammation, serous fluid
One cause includes Systemic Lupus Erythematosus (SLE) Acute |
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Describe fibirnous and serofibrinous pericarditis - morphology, cause, is it acute/chronic?
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This is the most frequent type - it involves serous fluid mixed with fibrinous exudate.
Typically occurs following an acute MI or cardiac surgery Acute |
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Describe purulent, suppurative pericarditis - morphology, cause, is it acute/chronic?
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Purulent, suppurative (pus) pericarditis is usually bacterial in origin - from invasion of pericardial sac by microbes.
Usually an extension from a neighboring empyema of the pleural cavity Acute |
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Describe hemorrhagic pericarditis - morphology, cause, is it acute/chronic?
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The morphology includes blood mixed with fibrinous exudate.
Usually caused by spread of malignant tumors Acute |
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What is adhesive pericarditis?
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Sometimes, following acute pericarditis, there is organization of the fibrinous exudate - producing thin delicate adhesions.
There is no cardiac impairment of function |
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What is chronic restrictive pericarditis?
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If acute pericarditis becomes very extensive, chronic fibrosis occurs, leading to thick scars obliterating the pericardial cavity.
This results in reduced cardiac output and right sided heart failure (side with most venous return) |
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What are some clinical correlates of acute pericarditis? (pain, disorders, etc.)
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Atypical chest pain - friction rub is most striking characteristic (fibrinous pericarditis)
Hemodynamic disorders: Shock, Cardiac Tamponade |
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What are the clinical correlates of chronic pericarditis?
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Right-sided heart failure
Decreased cardiac output |
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How much pericardial fluid is normal in the pericardial sac?
How does slow effusion manifest? Rapid effusion? |
30-50 mL typical amount of pericardial fluid
Slow effusion - no clinical symptoms Rapid effusion - cardiac tamponade |
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What are the causes of serous pericardial effusion?
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CHF, hypoalbuminemia, renal disease, liver disease
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What are the causes of serosanguinous pericardial effusion?
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Trauma, malignancy
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What is the cause of chylous pericardial effusion?
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Ruptured lymphatic obstruction
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What is endocarditis? What are the two forms?
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Endocarditis: Inflammation of the endocardial lining of the mural wall of the heart or valves.
Types: Infective and Non-infective *Always think VALVES with endocarditis!* |
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What are the most common causes of infective endocarditis?
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*Bacterial Infection*
Vegetations - from masses of dead cells, clots, organisms |
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What are some predisposing factors of infective endocarditis?
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Bacteremia (major factor)
Valvular lesion: Mitral prolapse, Bicuspid aortic valve, Calcified aortic valve, Prosthetic valve Host factors - diabetes, IV drug abuse |
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What are some clinical features of infective endocarditis?
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Fever
Splenomegaly Positive blood culture (many false negatives, due to previous ABx treatment, or deeply embedded organism) |
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What are two complications of infective endocarditis?
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Glomerulonephritis
Arrhythmia |
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Compare acute endocarditis and sub-acute endocarditis. What is the most marked difference? How do survival rates differ?
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Acute: Extensive lesions, previously normal valves, highly virulent bacteria (S. aureus), death within days or a weeks in 50% of patients
Subacute: less valvular destruction, previously abnormal heart valve, low virulent organism (S. viridans), protracted course of treatment (ABx) usually results in patient recovery |
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Describe the morphology of endocarditis.
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Vegetations are located on the surface of valves
Commonly affected valves: aortic, mitral, tricuspid Underlying myocardium may be affected Systemic emboli from vegetations may occur and cause septic infarcts |
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What are two major causes of non-infective endocarditis?
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Non-bacterial thrombotic endocarditis
Endocarditis of SLE |
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Describe NBTE
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Non-bacterial thrombotic endocarditis (aka Marantic endocarditis) involves the deposition of small sterile thrombi on the leaflets of cardiac valves
Single or multiple along the lines of closure of the valves |
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Describe the vegetations in NBTE
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Bland and sterile
Loosely attached to the underlying endothelium No inflammatory reactions or invasion of underlying myocardium May give rise to emboli in the heart/brain |
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What conditions/diseases are associated with non-infective endocarditis?
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Cancer
Sepsis Systemic hypercoagulable states: DVT, PE, thrombotic phlebitis with mucinous adenocarcinoma |
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Describe the vegetative lesions seen in RHD
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Rheumatic heart disease is marked by a row of small, warty verrucae along the lines of closure of the valve leaflets.
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Describe the vegetative lesions seen in infective endocarditis
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Infective endocarditis (IE) typically shows large, irregular, and destructive masses that can extend onto the chordae
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Describe the vegetative lesions seen in NBTE
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Nonbacterial thrombotic endocarditis (NBTE) typically shows small, bland vegetations, usually attached at the line of closure. One or many may be present.
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Describe the vegetative lesions seen in Libman-Sacks endocarditis.
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Libman-Sacks endocarditis (LSE) has small or medium-sized vegetations on either or both sides of the valve leaflets, or elsewhere on the endocardial surface.
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What is myocarditis? How is it different from other kinds of heart inflammation?
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Myocarditis is inflammation resulting from initial cell injury that damages the myocardium.
Other heart inflammation, such as that from a myocardial infarction, is not considered myocarditis. |
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What are the major causes of myocarditis?
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Viral infection - Coxsackie A, B; Enteroviruses
Other Infectious organisms - Trypanosomiasis (Chaga's), Trichinosis, Diphtheria, Lyme Disease Hypersensitivity Drugs Rheumatic Fever SLE |
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What is the morphology of myocarditis (gross, microscopic)?
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Gross: Dilated heart, wall is thin, surface is patchy and red
Microscopic: Interstitial inflammation, necrosis |
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What is seen microscopically in hypersensitivity myocarditis?
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Hypersensitivity myocarditis is characterized by interstitial inflammatory infiltrate composed largely of eosinophils and mononuclear inflammatory cells, predominantly localized to perivascular and large interstitial spaces
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How would lymphatic myocarditis appear microscophically?
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mononuclear inflammatory cell infiltrate and associated myocyte injury
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With what kind of sensitivity is hypersensitivity myocarditis associated?
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Drug hypersensitivity
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How does giant-cell myocarditis appear microscopically?
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There is mononuclear inflammatory infiltrate containing lymphocytes and macrophages, extensive loss of muscle, and multinucleated giant cells.
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How does myocarditis-associated Chaga's disease appear microscopically?
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Myofibers are distended with trypanosomes (arrow). There is a surrounding inflammatory reaction and individual myofiber necrosis.
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Rheumatic fever and rheumatic heart disease
Acute or chronic? How is it mediated? Isolated or multisystemic? Associated with any infectious agents? What age range? |
Acute
Immune mediated Multisystem disease Follows Group A Streptococcal pharyngitis (1-5 weeks) |
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What is the pathogenesis of rheumatic fever and rheumatic heart diseases? What type of hypersensitivity is this?
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Antibodies develop against Group A Streptococcal M protein - these antibodies cross-react against cardiac myocyte muscles and result in type II hypersensitivity.
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How is acute rheumatic heart disease related to rheumatic fever?
In what parts of the heart does this type of inflammation present? |
Acute rheumatic heart disease is the cardiac manifestation of rheumatic fever
Endocardium, Valves Myocardium Pericardium |
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What are the three forms of carditis?
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Pericarditis, Myocarditis, Endocarditis
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Describe pericarditis and myocarditis in rheumatic heart disease.
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Pericarditis - fibrinous, chest pain, friction rub
Myocarditis - MCC of disease in acute disease, characterized by Aschoff bodies (central areas of necrosis), cells are large, elongate, have large nuclei, some are multinucleated |
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Describe endocarditis in rheumatic valvular disease.
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Involves mitral valve, there are sterile verrucoid vegetations, often seen at the line of closure of the valve. May present as functional consquences of mitral regurgitation or stenosis.
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What occurs in chronic rheumatic heart disease? How are the valves affected?
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There is organization of the acute inflammation, scarring
Mitral or tricuspid valve changes: leaflet thickening, fusion of chordae tendinae, fibrous bridging, fish mouth valve |
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What are the consequences of recurrent infection of mitral and aortic valves?
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Stenosis
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What are a few other features of rheumatic fever?
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Migratory polyarthritis
Subcutaneous nodules Erythema marginatum Sydenham Chorea |
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According to the Jones criteria, what are the major manifestations of rheumatic fever?
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Carditis, polyarthritis, sydenham's chorea, erythema marginatum, subcutaneous nodules
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According to the Jones criteria, what are the minor manifestations of rheumatic fever?
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Fever, arthralgia, elevated acute phase reactants, prolonged PR interval
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What is cardiomyopathy?
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The cause is intrinsic to the myocardium (not the result of HTN, or congenital, valvular, coronary, arterial, or pericardial disease). Cell injury is initiated by the heart muscle itself.
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If a patient presents with cardiac failure, how do you proceed?
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1) Determine underlying cause - so you can correct it
2) Determine precipitating cause - to remove the precipitating cause 3) Determine type of heart failure - systolic/diastolic - to prevent deterioration and to control |
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What are the most common causes of heart failure?
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Ischemic heart disease
Hypertension Valvular heart disease |
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At one point will you consider cardiomyopathy?
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After ruling out the more common diagnoses, then you consider cardiomyopathy
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What are primary causes of cardiomyopathy?
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Idiopathic, familial, endomyocardial fibrosis, eosinophilic endomyocardial disease
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What are secondary causes of cardiomyopathy?
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Inflammatory, immunologic, metabolic, genetic, muscular dystrophy
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What are the three classifications of cardiomyopathy based on mechanism?
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Dilated
Hypertrophic Restrictive |
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What is the clinical presentation of dilated cardiomyopathy?
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Usually a younger patient that presents with progressive heart failure.
There is no evidence of HTN or CAD |
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What morphological considerations are there for dilated cardiomyopathy?
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Transverse endomyocardial biopsy
Mostly helpful in determining presence of a secondary cardiomyopathy |
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What does the heart look like in dilated cardiomyopathy?
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Heart is enlarged, flabby, dilatation in all 3 chambers, mural thrombus
This occurs in the absence of primary valve pathology or CAD |
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What are the microscopic characteristics of dilated cardiomyopathy?
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Heart muscles are hypertrophied
May find some interstitial fibrosis - reflects dead myocytes from reduced perfusion and increased *Reduced perfusion NOT from CAD* |
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What are the causes of dilated cardiomyopathy?
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Familial - autosomal dominant
Toxic - alcohol, doxorubicin Viral myocarditis Pregnancy (late) |
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What is the pathophysiology of dilated cardiomyopathy? How does it affect heart function?
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There is impaired contractility
Ineffective contraction affects systolic function Cardiac ejection fraction is <25% |
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To what diseases is myocardial dysfunction of dilated cardiomyopathy similar?
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Ischemic Heart Disease
Valvular Heart Disease Hypertensive Heart Disease Congenital Heart Disease |
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What is the course of dilated cardiomyopathy? Complications?
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Mural embolism and mitral valve regurgitation may occur
Death usually follows within 2 years |
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How does hypertrophic cardiomyopathy present?
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A young patient presenting with dyspnea, syncome, or even sudden death (HCM most common cause of sudden death among athletes)
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What is the morphology of HCM?
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The heart wall is thick and hypertrophied, without ventricular dilation. The lumen of the ventricle is reduced to "banana-like" shape.
The hypertrophy is ASYMMETRIC, DISPROPORTIONATE. Different from aortic stenosis and HTN. Septum is very thick relative to the free left ventricular wall. |
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How do plaques form in the heart in HCM? What is the effect?
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Plaques form because the hypertrophy results in internal friction in the heart, chafing areas and causing fibrous tissue, scarring, "sticky" spots. Often present at the left ventricular outflow tract near the junction with the anterior mitral leaflet.
Results in functional left ventricular outflow obstruction |
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How does HCM appear microscopically?
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Bizarre, disorganized structure of myocytes
FIbrosis |
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What is the pathophysiology of HCM?
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Diastolic dysfunction
Impairment of compliance Reduced EDV (preload) and increased left ventricular contractility Outflow is narrowed, creating increasing afterload |
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What two diseases have similar pathophysiology to HCM?
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Aortic Stenosis
Hypertensive heart disease |
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What kinds of fibrosis are present in restrictive cardiomyopathy? Is there hypertrophy? Infiltration?
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There is myocardial and endocardial fibrosis (including Loefller endomyocarditis, Endomyocardial fibrosis)
Hypertrophy is present Infiltration occurs via amyloid, hemochromatosis, glycogen deposition |
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What is the pathophysiology of restrictive cardiomyopathy?
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Impairment of compliance
Diastolic dysfunction Ventricles do not fill adequately Cardiac output decreases Systemic venous pressure is persistently elevated |
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What are two heart conditions with similar pathophysiology to restrictive cardiomyopathy?
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Constrictive pericarditis, hypertrophic cardiomyopathy
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Which two cardiomyopathies cause diastolic dysfunction? Which causes systolic dysfunction?
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Diastolic dysfunction: HCM and Restrictive Cardiomyopathy
Systolic dysfunction: Dilated Cardiomyopathy |
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Which cardiomyopathy shows myofiber disarray?
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HCM
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Which cardiomyopathies show myocyte hypertrophy? Which don't?
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Myocyte hypertrophy: Dilated cardiomyopathy, HCM
NO Myocyte hypertrophy: Restrictive cardiomyopathy |
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Which cardiomyopathy may show sarcoid granuloma formation, amyloid, Fe, glycogen?
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Restrictive cardiomyopathy
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What cardiomyopathy is associated with...
...Asymmetrical thickening and hypertrophy of wall, narrow chambers? ...Enlarged heart, floppy, dilated chambers with thin walls? ...Normal size (may be enlarged), non-dilated chambers? |
HCM
Dilated cardiomyopathy Restrictive cardiomyopathy |
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What cardiomyopathy may be genetic in origin, or caused by Friedrich ataxia?
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HCM
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What cardiomyopathy may be caused by genetic factors, alcohol, drugs, viral myocarditis, or pregnancy?
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Dilated cardiomyopathy
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What cardiomyopathy may be caused by amyloid, hemochromatosis, sarcoidosis, fibrosis: radiation, Loeffler, endomyocardial?
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Restrictive cardiomyopathy
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What is a CABG? What is a Cardiac Valve Surgery?
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CABG - Coronary Artery Bypass Graft - myocardial revascularization
Cardiac Valve Surgery - replacement or repair |
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When is CABG indicated?
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Most cases of left main coronary artery stenosis
Need for heart (valve, LV aneurysm) or other major surgery. Osteal or heavily calcified lesions. Major complications in cath. lab eg. perforation with bleeding, occlusion of coronary, trapped catheter or guide wire. Severe and diffuse disease especially in diabetes/renal disease/poor ventricular function. Failure of stenting |
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Compare beating heart CABG with cardiac arrest CABG
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Cardiac arrest – allows accurate suture placement, easy access to coronaries, but there is full heparinization, more bleeding.
Beating heart – lesser accessibility, technically demanding, some emphasize quicker recovery and fewer neurological deficits. |
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What are the benefits to using the Internal Mammary Artery (IMA) over a Saphenous Venous Gaft (SVG) in a CABG?
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IMA has better long term patency
There are fewer subsequent procedures Conduits have limited availability Bilateral IMA increases risk of wound infection slightly (esp. with diabetes) IMA surgery is technically more demanding |
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Compare Tissue and Mechanical Prosthetic heart valves
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Tissue: mostly porcine, usually do not need anticoagulation, silent, fail in 8-15 years
Mechanical: durable (25-35 years), requires anticoagulation, careful lab monitoring, noisy |
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What is the most common congenital cardiovascular defect? What are the other ones in decreasing order of incidence?
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3 million with bicuspid aortic valve
VSD > ASD > PDA > valvular pulmonary stenosis, coarctation of aorta > tetralogy of fallot > valvular aortic stenosis > AV septal defect > Transposition of great arteries > hypoplastic right heart syndrome. |
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When would one insert just an annulus into a valve and not just replace the whole valve
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When the leaflets are intact and it is simply an overdilated valve (so failure of the leaflets to close) then an annulus/ring can be inserted to keep the diameter at the right side for the valves to be effective.
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Who should have a coronary angiogram?
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Any patient where significant CAD is suspected (symptoms, risk factors, positive stress test, MI)
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Describe how an angiogram is performed
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An arterial puncture (femoral) is made, and a guidewire inserted. The needle is removed and a sheath introducer (like a large IV, has a dilator and a hemostasis valve) is inserted.
It is then guided up to the aorta, or the target location to be visualized with contrast. |
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What are some of the shapes of diagnostic catheters?
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Judkins right, Judkins left, Pigtail
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What are some treatments beyond TLC and medications for CAD?
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PTCA (balloon), PTCA + stent, CABG
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When should a patient have a PTCA without a stent?
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Patients with lesions in small vessels, patients who need heart surgery soon, patients in dangerous occupations/accident-prone, patients who may have difficulty with medical compliance
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What is an inflation device (as it pertains to angioplasty)?
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It is used to obtain controlled inflation of the balloon catheter.
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What is a balloon catheter?
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A small diameter hollow tube with a second smaller tube attached to a material at the base of the catheter. Balloon inflated via the smaller tube once it is placed across the lesion
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What is a PTCA?
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PTCA: Percutaneous transluminal coronary angioplasty
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What is a coronary stent?
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A metal tube or coil/mesh formed as a cylinder which is designed to keep the dilated artery open.
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What are the two kinds of stents? Compare the two.
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Bare metal stent (BMS) - stimulates intimal hypertension in first year - restenosis/occlusion. 20% have problems.
Drug eluting stent (DES) - may tend to thrombose after a few years (earlier if no double antiplatelet therapy. 5% have problems. |
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With PCI (percutaneous coronary intervention) and CABG, which has better survival rates? Fewer repeat procedures?
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PCI and CABG survival rates about the same - however CABG has better survival in higher risk cases.
Within a year 26% of those with PCI need replacement techniques, compared with 4% Within five years. 40% of those wtih PCI need repeat procedures, compared to 10%. |
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Which reduces pain from angina more - PCI or CABG?
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CABG
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What are the approximate costs for...
...Chest X-Ray? ...CT (reformatted)? ...MRI? ...Cardiac ultrasound? ...Nuclear medicine (stress imaging, cardiac functional imaging, MI imaging) ...Angiography? |
Chest X-Ray: $100
CT (reformatted) - $2,000 MRI - $3,000 Cardiac ultrasound - $1,000 Nuclear medicine - $2,000 Angiography - $5,000-15,000 |
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How would Pulmonary Edema appear in X-Rays?
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Lower lobe vessels - fuzzy borders
Equalize upper and lower vein size Septal lines from interstitial edema (Kerley B Lines) Pleural effusion - unilateral or bilateral |
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How would cardiomegaly appear in chest X-rays?
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If the cardiac silhouette is > half of the greatest diameter of the thoracic cavity on PA exposures it indicates cardiomegaly
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What are some things one can see about the lungs in a chest X-ray?
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Pulmonary vascular congestion
Cephalization Interstitial Edema Pleural effusion |
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What can an chest X-ray show about the heart?
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size/configuration, post-operative
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What can echocardiography reveal about the heart?
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Ultrasound of the heart, to visualize chambers, valves, vessels, pericardium, functional movement, walls.
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What nuclear medicine modalities are there?
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Functional and anatomical information
Stress myocardial perfusion imaging Acute myocardial infarct imaging MUGA (multigated acquisition) |
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What agents are used for stress myocardial imaging? How much stenosis must there be before it will be visualized?
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Thallium 201 - cellular uptake follows Na/K pump directly related to vascular perfusion.
Sestamibi Tc99m - parallels Thallium, with passive diffusion into myocytes directly related to perfusion. 90% stenosis must be present before lack of activity |
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How do you differentiate normal, ischemia, and infarction with stress myocardial imaging?
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First take a resting image with contrast, then a peak stress image with contrast.
If both images are clear, result is normal If there is no activity under stress, and activity at rest at the same spot, result is ischemia If there is no activity in either image in the same spot, it is an infarction. |
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What is a CT?
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CT, or computed topography, is an imaging modality that uses radiation to take a series of 2D images around a single axis of rotation, which can also used to generate a 3D image.
High dose of radiation |
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What is an MRI?
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MRI, or magnetic resonance imaging, does not use radiation, but rather high powered magnets and radio frequency energy to generate 2D images around a single axis of rotation, which can be used to generate a 3D image.
No radiation, but patients with metallic implants cannot have an MRI unless the implant is removed. |
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What is the Seldinger technique?
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This is the procedure for inserting a catheter into a vessel.
A sharp hollow needle (trocar) is inserted first, then a round-tipped guidewire is inserted through the lumen of the trocar, the trocar is withdrawn, and a "sheath" or blunt cannula can be passed over the guidewire into the vessel. Through the cannula/sheath, one can access parts of the vasculature for various procedures. |
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What are some complications associated with angiography?
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<5% of patients have groin hematoma (from puncture site) - most common problem
Contrast agent may cause renal failure or anaphylaxis Catheter-related complications - vessel dissection, cholesterol and thrombus embolism) < 1% Incidence of death is low < 0.05% Total complications <5% |
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What intravascular contrast agents are used?
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Iodine (ionic older version and may cause burning, non-ionic)
Carbon dioxide (if patient allergic to iodine) Gadolinium |
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If a patient has an iodine allergy, what do you do?
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Treat it as any allergic reaction in the acute phase-dependent type of reaction
If there is a need to use the contrast, don't use iodine, or pretreat with steroids, diphenhydramine, use non-ionic (better tolerated), limit volume of iodine. |
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How does an aortic dissection progress and what are the names of the two lumens it creates?
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An aortic dissection is a process by which the muscular layer of the aortic wall splits in a longitudinal fashion, creating 2 lumens.
False lumen - the new channel created by the splitting of the wall True lumen - the native lumen |
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Is an aortic dissection spontaneous or gradual? Is it associated with trauma? Does it happen in healthy individuals or those at risk?
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Aortic dissection is spontaneous, but not associated with trauma - often occurs in predisposed patients.
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How does an aortic transection occur? What usually causes it? Where is it most commonly located?
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Aortic transections are the result of a traumatic injury - most often deceleration injury involving seat belts.
95% of the transections are at the aortic isthmus - between the subclavian and the ligamentum arteriosum. |
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Trace the path of the aorta from the heart and the three branches from the arch.
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Aorta --> aortic arch:
Brachiocephalic Trunk, Left Common Carotid, Left Subclavian Brachiocephalic Trunk --> produces the Right Common Carotid, Right Subclavian, and Right Vertebral Artery Left Common Carotid --> straight up Left Subclavian --> Left Vertebral Artery branches off |
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Why are CTs and Ultrasounds more accurate than angiograms for assessing vessels?
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CT and Ultrasound are more accurate than angiograms because an angiogram not show the surrounding tissue of the lumen.
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What is an endovascular stent graft?
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A stent that fits into the aorta and forks at the split at the bottom - must be sure not to block the renal arteries.
Purpose: prevents an AAA from bursting |
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What is atherosclerotic occlusive disease? How does it present?
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Must know which artery it is, severity of disease, and superimposed complications (plaque ulceration or subintimal hemorrhage, acute thrombosis, distal embolization).
Often is occlusion of the aortoiliac area, and has sudden change in symptoms - claudication, dimished pulses, tissue loss-ulcers, rest pain, cadaveric extremity, gangrene. Chronic changes - hair loss, skin changes |
