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126 Cards in this Set
- Front
- Back
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What are the normal weights of a female and male heart?
What are the normal wall thicknesses of the right and left ventricle? |
Female: 250-300 g
Male: 300-350 g Right ventricle: 0.3-0.5 cm Left ventricle: 1.3-1.5 cm |
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What is it called when marked dilatation of the heart leads to markedly decreased contractility, resulting in fulminant CHF?
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Cardiac decompensation
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What are 5 general mechanisms of cardiovascular dysfunction?
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Pump failure (MC cause)
Obstruction to flow Regurgitant flow (backward flow) (volume overload) Disorders of the conduction system Disruption of the continuity of the circulatory system (knife wound to heart, MVA laceration to aorta, etc.) |
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What is the leading discharge dx in patients >65?
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CHF
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The Frank-Starling Mechanism refers to which of the following?
a) Improved contractility due to dilatation b) Improved contractility due to hypertrophy c) Improved contractility due to increased sympathetic activity d) Improved cardiac output due to increased heart rate e) Improved cardiac output due to increased blood volume |
A
This is one of the adaptive responses to CHF. Others are: *Activation of neurohormonal systems: 1) release of norepinephrine by sympathetic cardiac nerves -> inc heart rate & contractility 2) activation of the renin-angiotensin system 3) release of atrial natriuretic peptide(to counteract RA) *Myocardial hypertrophy All of these help maintain the cardiac output! |
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During cardiac hypertrophy, how does the heart appear to TRY to undergo hyperplasia?
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By induction of immediate-early genes and re-expression of fetal forms of contractile and other proteins.
Altered pattern of protein synthesis may ultimately result in impaired myocyte function (fetal forms may not work as well as adult) |
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Why is there a loss of myocytes with cardiac hypertrophy (several causes)?
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Ischemia (d/t inc metabolic requirements and inc intercapillary distance)
Apoptosis Loss of myocytes leads to: Systolic dysfunction Inc fibrous tissue and therefore impaired diastolic filling |
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Concentric hypertrophy of the LV is typical of what?
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Pressure-overloaded LV (systemic HTN or aortic stenosis)
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Hypertrophy with dilation of the LV is typical of what?
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Volume-overloaded LV (mitral or aortic insufficiency)
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What are some possible causes of LEFT-sided heart failure?
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IHD, hypertension, aortic and mitral valvular disease, cardiomyopathy
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What are some clinical manifestations of LEFT-sided (LV) heart failure?
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*Pulmonary congestion & edema (d/t backward failure)
*Siderophages (hemosiderin, "heart failure cells") *Dyspnea *Orthopnea *PND (paroxysmal nocturnal dyspnea, exaggerated form of orthopnea w/ severe SOB, like choking) Atrial fibrillation & mural thrombi (chronic dilation of LA predisposes to fib and mural thrombi adherent to the wall; mural thrombi can go out aorta into carotids -> stroke) Reduction of renal perfusion: (forward failure) Activation of renin-angiotensin system Prerenal azotemia (inc in BUN & creatinine d/t poor renal perfusion & dec GFR) Hypoxic encephalopathy |
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What are some possible causes of RIGHT-sided heart failure?
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Usually LV failure
Primary & secondary pulmonary HTN |
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What are some clinical manifestations of RIGHT-sided heart failure?
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Most are d/t backward failure!
Congestive hepatomegaly (very common) Peripheral edema Pleural and pericardial effusions Renal congestion Hypoxic encephalopathy Congestive splenomegaly Edema of the bowel wall, Ascites |
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Which of the following is seen with (isolated) left-sided heart failure?
a) Pleural effusions b) Congestive hepatomegaly c) Pulmonary edema d) Pedal edema e) Pericardial effusions |
C!
Dr. Tomlinson says we need to know the difference between pure isolated right and left failure! |
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Acute coronary syndromes (such as sudden cardiac death, MI, unstable angina) are usually caused by what?
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Plaque disruption
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What are the 2 types of MIs?
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Transmural - MC type
Subendocardial - inner 1/3rd to 1/2 wall |
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What is the sequence of events for an MI, beginning with plaque disruption?
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Plaque disruption -> platelet adhesion and aggregation -> release of platelet mediators...
then: -> Vasospasm AND -> activation of coagulation -> thrombus Other mechanisms for MI: Vasospasm Emboli Disease of Intramural vessels (vasculitis, amyloidosis) Hemoglobinopathies |
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In order for a plaque to cause angina, it has to narrow the lumen by at least ___%.
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75%
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Severe fixed coronary obstruction (chronic ischemic heart dz) occurs with >___% obstruction. How can you die suddenly from this?
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90%
die suddenly from Ventricular Arrhythmia |
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Plaque disruption leading to a mural thrombus w/ variable obstruction/?emboli can cause what events?
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Unstable angina
Acute subendocardial MI Sudden death |
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Plaque disruption leading to an occlusive thrombus can cause what events?
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Acute transmural MI
Sudden death |
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In a patient with unstable angina, the involved coronary artery would most likely exhibit:
a) Disrupted plaque with an occlusive thrombus b) Stable plaque with a 75% occlusion c) Stable plaque with a 95% occlusion d) Disrupted plaque with a partially occlusive thrombus |
D
A would be transmural MI or sudden death B&C would be stable angina |
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For each of the following, answer the degree of stenosis, whether or not there is plaque disruption, and what type of thrombus (if any).
a) Stable angina b) Unstable angina c) Transmural MI d) Subendocardial MI e) Sudden death |
a) >75%; none; none
b) Variable (often 50-75); frequent; partially occlusive c) Variable (often 50-75); frequent, occlusive d) Variable; frequent; partially occlusive OR occlusive w/ lysis e) often >90% (high-grade stenoses); frequent; occlusive or partially occlusive w/ thromboemboli (occludes smaller coronary vessel) |
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How much time does it take for each of the following to occur?
a) Onset of ATP depletion b) Loss of contractility c) ATP level reduced to 50% d) to 10% e) Sarcolemmal defects f) Irreversible cell injury g) Microvascular injury |
a) seconds
b) < 2 min c) 10 min d) 40 min e) 20-40 min f) 20-40 min g) >1 hr |
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By ____ hours, most of the "area at risk" of developing MI has undergone necrosis!
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24 hrs
It's important to limit the size of the infarct! |
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Approximately how much at-risk myocardium is still salvageable 2 hours after an occlusion of a coronary artery? What about 4 hrs after?
a) 10% b) 30% c) 50% d) 70% e) 90% |
2 hours - C (50%)
4 hours - B (30%) At 12 hours, there is very little! (<10%) |
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An occlusion of the left circumflex coronary artery will result in an infarct involving where?
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the lateral wall of the left ventricle
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An occlusion of the LAD will result in an infarct involving where?
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the anterior wall of the left ventricle
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An occlusion of the right coronary artery will result in infarction of where?
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The posterior wall of the left ventricle.
In approximately 15 – 30% of patients with occlusion of the RCA, the infarct will extend across the ventricular septum and also involve the posterior wall of the right ventricle. |
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Frequency of
occlusion leading to MI: LAD? RCA? LCX? |
LAD - 40-50%
RCA - 30-40% LCX - 15-20% |
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What stain in a heart makes an MI stand out more?
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triphenyltetrazolium chloride (TTC) stain
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Histology of an infarct shows edema with early coagulative necrosis (pyknotic nuclei & hypereosinophilia) and beginning infiltration by neutrophils. How old is the infarct?
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1 day
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Histology of an infarct shows coagulative necrosis with loss of nuclei and cross striations. There is heavy infiltration by neutrophils. How old is the infarct?
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3-4 days
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Histology of an infarct shows infiltration by macrophages which have phagocytized much of the necrotic cellular debris. How old is the infarct?
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7-10 days
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Histology of an infarct stained with Trichome stain (stains collagen blue) shows granulation tissue with prominent blood vessels. The wavy blue fibers represent early collagen deposition. How old is the infarct?
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3 weeks
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Histology of infarct stained with Trichome stain (stains collagen blue) shows that the infarcted myocardium is completely replaced by dense collagenous fibroconnective tissue (i.e. scar tissue). How old is the infarct?
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6-8 weeks, >8 weeks is a well healed myocardial infarct (MI)
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What are currently the most sensitive & specific biomarkers for confirming a diagnosis of acute MI?
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Troponin I & T (first detected at 2-4 hrs, peaks at 48 hrs, returns to normal at 7-10 days)
Unchanged levels of CK-MB and troponins over a period of 2 days essentially excludes the diagnosis of acute MI. |
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Systemic Hypertensive Heart Disease!
a) What are the minimal criteria for dx? b) What are some complications? c) What is the morphology (wall thickness, heart weight, histo)? |
a) LVH in the absence of other cardiovascular path
Hx or other evidence of hypertension (EKG & echocardiography are useful to Dx LVH) b) CHF, sudden death, coronary atherosclerosis, atrial fibrillation c) LVH, left ventricular wall may be > 2 cm heart wt. may be > 500 g enlarged myocytes, interstitial fibrosis, big nuclei |
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Pulm Hypertensive Heart Disease! aka Cor Pulmonale
a) What does this include? b) Acute cor pulmonale is secondary to what? c) Chronic cor pulmonale is secondary to what? d) Marked dilatation can cause.... |
a) RVH, dilation & failure secondary to pulm HTN caused by disorders affecting the lungs or pulm vasculature (NOT RVH & dilatation secondary to congenital heart disease & diseases of the left side of the heart)
b) massive PE c) prolonged pressure overload d) tricuspid regurgitation |
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What are the MC valve abnormalities (and are they acquired or congenital)?
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MC are acquired stenoses of the mitral & aortic valves
MC IS AORTIC STENOSIS |
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What is a major cause of acquired mitral stenosis?
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Postinflammatory scarring
(rheumatic heart disease) |
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What are some major causes of acquired mitral regurg?
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Abnormalities of leaflets & commissures (postinflammatory scarring, iInfective endocarditis, mitral valve prolapse during systole)
Tensor Apparatus Abnormalities (rupture of papillary muscle , papillary muscle dysfunction, rupture of chordae tendineae) Abnormalities of LV cavity and/or annulus ( LV enlargement , calcification of mitral annulus) |
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What are some major causes of acquired aortic stenosis?
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Senile calcific aortic stenosis
Postinflammatory scarring Calcification of congenitally deformed valve (bicuspid valve) |
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What are some major causes of aortic regurgitation?
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Intrinsic valvular disease ( postinflammatory scarring, infective endocarditis )
Aortic disease (degenerative aortic dilation, syphilitic aortitis , ankylosing spondylitis , rheumatoid arthritis, marfan syndrome) |
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T/F
Postinflammatory scarring can be a cause for any acquired disease of aortic or mitral valves. |
True!
mitral regurg or stenosis or aortic regurg or stenosis |
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T/F
There are many more causes for stenosis than for regurg. |
False!!
There are more for regurg than for stenosis! |
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A consequence of wear & tear of normal aortic valves in aged patients, or of congenitally bicuspid valves, is what?
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Calcific Aortic Stenosis
usually older than 70, unless bicuspid valve... then in 40s or 50s |
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An 80 yo patient presents to ER after wife said he fainted. He complains of chest pain. He has a history of CHF, and chest xray shows LVH. Further evaluation shows calcified nodules on the aortic valve involving the base and lower half of cusps, but the commissures are not fused.
What do you suspect? How can you confirm your diagnosis? |
Calcific Aortic Stenosis
Dx: echocardiography Clinical: LVH, angina, sudden death, syncope (perf pressure in carotids insufficient), CHF If symptomatic, > 50% mortality rate in 3 yrs if untreated!! Need aortic valve replacement surgery |
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What disorder of the mitral valve is MC in women > 60, patients with myxomatous mitral valve & increased left ventricular pressure?
What are the possible complications of this disorder? |
Mitral Annular Calcification, which is stony hard calcified nodules in the valve ring
Usually without clinical significance! But... May interfere with the function of the valve ring (regurgitation) May impair opening of the mitral leaflets (stenosis) Occasional thrombi formation on ulcerated calcified nodules (emboli) |
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Myxomatous degeneration of the Mitral Valve is the pathologic term for what clinical term?
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Mitral Valve Prolapse
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What is the MC form of valvular heart disease in the industrialized world?
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Myxomatous degeneration of the mitral valve
aka Mitral valve prolapse Deposition of proteoglycans (myxomatous degeneration) |
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In mitral valve prolapse, valve leaflets are deformed & prolapse into the ____ during ______.
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LA; systole
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A patient presents for their yearly check-up, and you hear a systolic click upon auscultation of the heart. The patient says that they have never experienced any cardiac symptoms. What might you suspect?
How can you make a dx of this? |
Mitral valve prolapse
Dx: systolic click in asymptomatic patients (valve leaflets "slap" wall) systolic murmur (d/t mitral regurg) echocardiography |
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What is believed to be the cause of mitral valve prolapse?
What are some rare complications a/w it? |
Many cases appear to be inherited as an AD trait
Believed to be due to a defect in connective tissue Commonly seen in Marfan syndrome Complications in 3%: mitral regurgitation, endocarditis, arrhythmias & stroke |
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How does the morphology of the heart differ between RF and RHD?
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RF: pancarditis, Aschoff bodies (well-circumscribed inflam nodules), Anitschkow cells (diagnostic of RF!), vegetations (verrucae composed of fibrin)
RHD: fibrosis with thickening of the leaflets (#1 mitral #2 aortic), commissural fusion (via bands of fibrous tissue, causing severe stenosis!) shortening, thickening & fusion of the cords (shortening and fusion can cause regurg) |
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An acute, immune-mediated multi-system disease occurring a few weeks after an episode of group A streptococcal pharyngitis, MC in children 5-15 yo, is what?
Manifestations? |
Rheumatic Fever (RF)
Manifestations of RF: carditis, migratory polyarthritis, subcutaneous nodules, erythema marginatum, Sydenham’s chorea |
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RF can eventually lead to a disorder that manifests with murmurs, hypertrophy and dilatation, CHF, atrial fib, thromboemboli, and increased risk of infective endocarditis. What is this disease?
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Rheumatic Heart Disease (RHD): a deforming fibrotic valvular disease
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In RHD, there is a hypersensitivity reaction induced by a)_____________. Ab’s directed against b)________ cross-react with c)_____________. Genetic factors regulate susceptibility.
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a) Group A Strep
b) M proteins c) tissue glycoproteins |
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Plump activated macrophages with very prominent chromocenters are pathognomonic for what?
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rheumatic fever
These are called Anitschkow cells |
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Plump activated macrophages with very prominent chromocenters are pathognomonic for what?
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rheumatic fever
These are called Anitschkow cells |
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Commissural fusion is a characteristic feature of what?
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RHD! and is usually not present in other forms of valvular disease. Called "fish mouth" stenosis
The mitral valve is almost always involved in RHD and RHD is the cause of mitral stenosis in ~ 99% of cases. |
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Commissural fusion is a characteristic feature of what?
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RHD! and is usually not present in other forms of valvular disease. Called "fish mouth" stenosis
The mitral valve is almost always involved in RHD and RHD is the cause of mitral stenosis in ~ 99% of cases. |
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_____________ is a destructive infection typically involving a previously normal valve, caused by a HIGHLY virulent organism, fatal in > 50% of patients within days to weeks.
____________ is less destructive & involves a deformed valve, caused by an organism of LOW virulence, more protracted course, most patients recover. |
Acute endocarditis
Subacute endocarditis |
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What are some predisposing factors to infective endocarditis?
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abnormal valve or a prosthetic valve
neutropenia, immunosuppression, diabetes IV drug abuse, dental or surgical procedures |
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What is the MC causative organism of endocarditis of a NORMAL valve?
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Staph aureus
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What is the MC causative organism of endocarditis of an ABNORMAL valve?
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Strep viridans
can be prevented w/ prophylactic use of antibiotics |
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What is the MC causative organism of endocarditis of a PROSTHETIC valve?
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Staph epidermidis
can be prevented w/ prophylactic use of antibiotics |
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What valves are most commonly involved with vegetations in bacterial endocarditis?
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Aortic and mitral
tricuspid in IV drug users! |
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What are some symptoms of bacterial endocarditis?
How can you confirm the diagnosis? |
symptoms: fever, murmurs, petechiae, Roth spots
Dx: blood cultures, echocardiography |
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What are some possible complications of bacterial endocarditis?
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regurgitation or stenosis
CHF ring abscess prosthetic valves – dehiscence w/ leak septic emboli glomerulonephritis |
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What are some possible complications of bacterial endocarditis?
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regurgitation or stenosis
CHF ring abscess prosthetic valves – dehiscence w/ leak septic emboli glomerulonephritis |
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Which of the following is considered pathognomonic for Rheumatic Fever?
a) Vegetations (verrucae) b) Anitschkow cells c) Pancarditis d) Commissural fusion e) Fusion of chordae tendineae |
B
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What condition consists of small masses or platelets and fibrin on the leaflets of valves (only loosely attached, usually along the lines of closure), often encountered in debilitated patients (such as those w/ cancer or sepsis w/ DIC) who have a hypercoagulable state?
(There is little sign of inflammation and no microorganisms) |
Nonbacterial Thrombotic Endocarditis (NBTE)
They are sterile, noninflammatory, and nondestructive! Thrombotic vegetations may give rise to emboli |
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Nonbacterial Thrombotic Endocarditis (NBTE) is highly a/w what cancer?
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mucinous adeno-carcinoma
(which probably relates to the procoagulant effect of circulating mucin) |
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Small sterile vegetations, composed principally of fibrin, located on both the upper and undersurfaces of the mitral and tricuspid valves should be highly suspicious for what?
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Endocarditis of SLE (Libman-Sacks Endocarditis)
Foci of fibrinoid necrosis! Subsequent fibrosis & deformity in some cases can resemble RHD |
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In Libman-Sacks Endocarditis, ________ bodies can sometimes be seen.
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Hematoxylin (pathognomonic!)
Hematoxylin bodies are blue staining round to oval bodies, which represent bare nuclei that are coated with antinuclear antibodies (ANAs) |
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Vegetations on a valve that are large, irregular, and destructive are likely which of the following?
a) Rheumatic Fever (RF) b) Infective endocarditis c) Nonbacterial Thrombotic Endocarditis (NBTE) d) Libman-Sacks Endocarditis (LSE) |
B
RF would be small (1-2 mm) and along line of closure of valve NBTE would be relatively small (1-5 mm), along line of closure, and loosely attached LSE would be relatively small (1-4 mm), and usually on both upper and undersurface |
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Carcinoid Syndrome is caused by a carcinoid tumor which secretes __________.
The carcinoid tumor is derived from what type of cells? What are the symptoms? |
serotonin (5-HT)
Neuroendocrine cells flushing, N/V/D, cramps, asthma-like Sx’s (d/t GI stimulation and bronchospasm from serotonin) |
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50% of patients w/ carcinoid syndrome go on to develop what?
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Carcinoid Heart Disease
Plasma level of serotonin correlates with severity of the lesions! |
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Which side do lesions typically occur in Carcinoid Heart Syndrome and why? When might they occur on the opposite side?
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Right-side since serotonin is inactivated in the lungs (by enzyme in endothelial cells)
May develop left-sided lesions w/ congenital shunts or tumor |
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The thickening of the endocardium of right atrium & ventricle, tricuspid & pulmonary valves in carcinoid heart disease is due largely to what?
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Deposition of acid mucopolysaccharides (NOT d/t fibrosis)
may develop right-sided valvular stenosis or insufficiency |
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Secretion of which of the following mediators best correlates with the development of carcinoid heart disease?
a) Histamine b) Bradykinin c) Kallikrein d) Prostaglandins e) Serotonin |
E
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What are some possible causes of myocardial disease (which can then result in a cardiomyopathy)?
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infections
immunologic disorders metabolic disorders toxic substances neuromuscular diseases genetic diseases |
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Progressive hypertrophy, dilatation, and contractile dysfx leading to progressive CHF is typical of what?
The ejection fraction is typically what %? |
Dilated Cardiomyopathy (DCM)
<25% (normal is 50-65%) 50% of patients die w/i 2 years! |
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What are some possible etiologies of DILATED cardiomyopathy?
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viral myocarditis (e.g. coxsackie B)
alcohol abuse cobalt chemotherapeutic drugs (Adriamycin) nutritional deficiency (e.g. thiamine) pregnancy (peripartum cardiomyopathy) genetic (20 - 50% of cases), mutations in: - cytoskeletal genes (e.g. dystrophin) - mitochondrial genes - sarcomere genes - nuclear envelope genes (lamin A & C) Many cases are idiopathic! |
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Describe the morphology of DILATED cardiomyopathy.
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heart is enlarged, globoid & “flabby”
all chambers are dilated, often with mural thrombi histologic changes are nonspecific |
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Impaired diastolic filling & obstruction of the left ventricular outflow tract is indicative of which type of cardiomyopathy?
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Hypertrophic Cardiomyopathy (HCM)
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A patient presents with complaints of chest pain. They have CHF. Further eval shows that they have a fib, a systolic murmor, and infective endocarditis of the mitral valve.
There is also asymmetric septal hypertrophy, with a ratio of 1.5. There is myocyte hypertrophy, disarray, and fibrosis. What is your suspected dx? What causes this condition? |
Hypertrophic Cardiomyopathy
All cases are due to mutations in sarcomere genes! (> 400 mutations have been identified in 9 genes; severity of HCM can vary widely depending upon which mutation the patient has) Clinical Features: angina, arrhythmias, sudden death atrial fibrillation with mural thrombus formation systolic murmur, CHF infective endocarditis of the mitral valve Morphology: asymmetric septal hypertrophy, ratio > 1.3 myocyte hypertrophy, myocyte disarray, fibrosis |
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In restrictive cardiomyopathy, there is impaired diastolic filling.
a) Ventricular walls are ____________ in thickness b) Which chambers of the heart (if any) are dilated? c) What are some possible causes? |
a) Normal or mildly increased
b) Ventricles are not dilated, atria are often dilated c) May be idiopathic or a/w: radiation fibrosis amyloidosis sarcoidosis metastatic tumor storage diseases Endomyocardial fibrosis Loeffler endomyocarditis Endocardial fibroelastosis |
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What are the MC cause of myocarditis?
Some other causes? |
MC - Viral infections (esp. Coxsackie A & B) - Uncertain if viruses injure myocytes directly or initiate an immune response
Infections (chlamydiae, rickettsiae, bacteria, fungi, protozoa, helminths) Immune-mediated Rxns (poststreptococcal, SLE, drug HS, transplant rejection) Unknown (sarcoidosis, giant cell myocarditis) |
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Which type of myocarditis has an unknown cause, occurs in adults 20-50 yo, and has a poor prognosis?
What are 2 other types of myocarditis? |
Giant cell myocarditis
(There are scattered giant cells with extensive loss of cardiac myocytes) Chagas disease (Trypanosoma cruzi) Hypersensitivity myocarditis |
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What are some clinical features of myocarditis?
What can it progress to? |
fever, fatigue, dyspnea, palpitations, precordial pain
heart failure, systolic murmur, arrhythmias Some cases progress to DCM |
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Lymphocytic myocarditis is the pattern usually seen with _________ myocarditis.
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Viral myocarditis
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Numerous eosinophils within the inflammatory infiltrate is the pattern usually seen with __________ myocarditis.
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hypersensitivity (reactions to various drugs, most commonly antibiotics)
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Myocarditis with distended myofibers and trypanosomes is indicative of what?
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Chagas disease
(commonly encountered in South America) |
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(Primary/Secondary) pericarditis is most common.
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Secondary! (d/t heart dz, thoracic or systemic disorders)
Primary is unusual |
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What type of pericarditis is seen with RF, SLE, uremia, and viral infection?
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Serous pericarditis
mild inflammation serous exudate |
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What type of pericarditis is seen with acute MI, postinfarction (Dressler) syndrome, radiation, heart sx, RF, SLE, and uremia?
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Fibrinous pericarditis
inflammation fibrinous exudate (“shaggy” appearing) |
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Which type of pericarditis has a loud pericardial friction rub?
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Fibrinous Pericarditis
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Which type of pericarditis is seen with bacterial infection?
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Suppurative Pericarditis
acute inflammation purulent exudate |
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Organization of which pericarditis often produces constrictive pericarditis?
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Suppurative Pericarditis
(constrictive pericarditis may also have hx of hemorrhagic or caseous pericarditis) |
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What type of pericarditis is seen with malignancy, bacterial infections, bleeding diathesis, TB, and heart sx?
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Hemorrhagic Pericarditis
fibrinous OR suppurative exudate mixed w/ blood |
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Which type of pericarditis resembles a restrictive cardiomyopathy, except the heart is encased by a thick fibrous tissue?
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Constrictive Pericarditis
Rx’ed by pericardiectomy |
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Primary cardiac tumors are....
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Myxoma (MC!)
Fibroma Lipoma Papilloma Fibroelastoma Rhabdomyoma Angiosarcoma |
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Metastatic tumors in the heart can come from where?
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Melanoma, lung, breast, esophagus, lymphoma
Clinically mostly silent May result in restrictive cardiomyopathy |
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About 90% of myxomas are located where?
How can you make the dx? |
in the atria
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Biopsy of the atrium of a heart shows gelatinous polypoid masses, stellate & other cells embedded in a myxoid extracellular matrix, derived from multipotential mesenchymal cells. What is the dx?
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Myxoma!
echocardiography |
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What are some clinical manifestations of myxoma?
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Obstruction of mitral valve orifice
Embolization -> stroke Fever & malaise secondary to secretion of IL-6 ~ 10% have Carney complex |
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An AD condition comprising of myxomas of the heart and skin, hyperpigmentation of the skin (lentiginosis), and endocrine overactivity is called what?
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Carney Complex
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Histologic section of a mass in the left atrium shows loose-appearing myxoid stroma d/t the abundance of mucopolysaccharides. There is also abnormal vascular structure. What is the mass?
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A myxoma
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Most congenital heart defects arise from faulty embryogenesis between __-__ weeks gestation.
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3-8
1% of live births MC type of heart disease in children |
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What is the MC genetic cause of congenital heart disease?
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Trisomy 21
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What type of shunt occurs in Eisenmenger Syndrome?
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Left to right shunt
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What is the MC congenital cardiac malformation?
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Ventricular septal defect (42%)
Atrial septal defect is 10% The rest are even less! Truncus arteriosus, total anomalous pulmonary venous connection, and tricuspid atresia are the least common. |
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Which congenital cardiac malformations are more common in boys?
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Coarctation of Aorta
Aortic stenosis (3:1) Transposition of great arteries |
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Which congenital cardiac malformations are more common in girls?
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Atrial septal defect (ASD)
PDA |
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What is the MC type of ASD?
What are some possible complications of ASD? |
Ostium secundum type (~90%)
Irreversible pulm HTN (<10%), right-sided heart failure, paradoxical embolization. Mortality rate is low! They are usually isolated, resulting in a left to right shunt, often with a systolic murmur. Most do not become symptomatic before adulthood. |
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Most VSD's involve what?
What are some possible complications of VSD? |
Membranous septum (~90%)
Irreversible pulm HTN, late cyanosis, right-sided heart failure. Clinical significance varies widely & is a function of the size. They are often a/w other cardiac defects, resulting in a left to right shunt, often with a systolic murmur. |
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An infant with a continuous harsh murmur may have what congenital cardiac anomaly?
What are some possible complications of this anomaly? |
PDA
Irreversible pulmonary hypertension, late cyanosis, right-sided heart failure. Clinical significance varies widely & is a function of the diameter. They are usually isolated (~90%), resulting in a left to right shunt, with a continuous harsh murmur. They can sometimes be treated medically w/ indomethacin! |
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What is the MC form of cyanotic congenital heart disease?
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Tetralogy of Fallot
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Anterior displacement of the truncoconal (aortico-pulmonary) septum, leading to unequal division of the truncus arteriosus & conus cordis is the cause of what congenital heart defect?
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Tetralogy of Fallot
Patency of the ductus arteriosus is beneficial Most patients do well after surgery |
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What are the 4 features of Tetralogy of Fallot?
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Overriding aorta
VSD Subpulmonary stenosis Right ventricular hypertrophy Clinical features depend primarily on the degree of subpulmonary stenosis. Mild = “pink tetralogy” Marked = “classic tetralogy” |
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What happens if the truncoconal septum does not follow its normal spiral course during embryogenesis?
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Transposition of the Great Arteries
Incompatible with postnatal life unless a shunt is present: - VSD (35%), patent foramen ovale or PDA (65%) - May need to create a shunt (septostomy) - Marked RVH develops - Is a form of cyanotic congenital heart disease - Corrected with an arterial-switch operation |
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How do you distinguish b/w the infantile and adult forms of coarctation of the aorta?
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Infantile - narrowing of aortic arch proximal to a PDA
Adult - narrowing of aortic arch opposite a closed ductus arteriosus |
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Cyanosis in the lower half of the body, with a systolic murmur and continuous murmur, is indicative of coarctation of the aorta (with/without) a PDA.
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WITH
may require surgery during the neonatal period |
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HTN in UE, and dec BP, pallor, claudication, coldness in LE, w/ LVH, notching of ribs on CXR, and systolic murmur is indicative of what?
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Coarctation of aorta without a PDA
May go unrecognized until well into adulthood Surgery yields excellent results |
