Flashcards in Heart Deck (43):
Where does the ostium primum anomaly occur?
Adjacent to the AV valves and is usally associated with a cleft anterior mitral leaflet
What rae the complicATIONS of ASD's?
Cyanoisis, Atrial Arrhythmias, RVH, Right HF, Bacterial endocarditis, and Paradoxical Emboli
What are VSDs characterized by?
left to right shunt
left ventricular dilation
What anatomical finding is often associated with coarctation of the aorta? clinical finding?
Reduced of Absent femoral pulses
HTN in UE
Which arteries are combined in Truncus ARteriosis?
Aorta, Pulmonary Artery, and Coronary ARteries
In Tetralogy of Fallot, where does the aorta receive blood from?
It overrides the VSD and receives blood from both ventricles
What characterizes Endocardial Fibroelastosis?
- Fibroelastotic thickening of the endocardium of LV (can affect valves)
- Gray-white patches of thickening accompanied by degeneration of subendocardial myocytes
What is the pathological cardiologic outcome of Hyperthyroidsim? What's the main pathophysiologic cause?
High output heart failure
This occurs because peripheral resistnace decreases which requires increased cardiac output.
Over what pathologic processes do mural thrombi often form?
On the endocardium, over the infarction
Over ventricular aneurysms- found at the healed, transmural myocardial infarct
When do subendocardial circumferential infarcts generally occur?
Post hypoperfusion of the heart secondary to poor coronary blood flow, often in the setting of hypotension.
Coronary artery narrowing is common (total occlusion rare and most associated with transmral myocardial infarction)
What is Dressler Syndrome?
Post (2-10 wks) MI syndrome delayed pericarditis. Pain develops and can be confused with postinfarction or recurrent angina.
What occurs for 1/2 deaths after acute MI?
actue infarction is often associated with Premature Vnetricular beats, VTach, complete Heart Block, and VFib- acute ischemia may promote conductiondisturbances and myocardial irritability.
What complications could be seen a between days 3 -7 post MI?
Postmyocardial infarction syndrome??
(1. anterior rupture leads to, Cardiac Tamponade
2. Septal Perforation+ Interventricular septum rupture, throombosis in LAD is MCC
3. Papillary muscle rupture associated with inferior AMIs due toRCA thromboisis and leads to MV REGURG)
What causes cardiac tamponade?
A ruptured myocardial wall
What clinical finding is associated with cardiac tamponade?
Pulsus paradoxus (>10mmHg fall in aerterial blood pressure with inspiration)
when can myocardial rupture and hemorrhage into the pericardial sac occur? Why this time?
Any time during the first 3 weeks but most commonly between the 1st and 4th days.
Because, during this interval the infarcted wall is weak, being composed of soft necrotic tissue.
What degrades the extracellular matrix with the infarct?
Proteases released by inflammatory cells
What complication typically occurs 1-3 days post MI (pathoma) or 2-10 weeks after a transmural MI (Rubin's)?
What defines Cor Pulmonale?
Right Ventricular Hypertrophy
Dilationsecondary to Pulmonary HTN
What's th emost common cause of Cor PUlmonale?
Chronic Obstructive Pulmonary Disease (usually as a result of smoking)
What are common causes of death in Hypertensive patients/?
CHF, Intracerebral hemoorrhage, Coronary atherosclerosis and MI, Dissecting aneurysm of the aorta, ruptured berrky aneurysm of the cerebral ciculation Renal failure (when nephrosclerosis becomes severe)
In Libman-Sacks endocarditis, where are the vegetations normally found?
On the undersurface of the mitral valve close to the origin of the leaflets form the valve ring
What is the likely causes and complication of marantic endocarditis?
Causes: Increased blood coagulability and Immune-complex deposition
Complication: embolization to distant organs
What are three main causes of calcific aortic stenosis?
1. Rheumatic Disease
2. Senile Calcific Stenosis
3. Congenital Bicuspid Aortic Stenosis
In general, it is related to the cumulative effect of years of trauma due to turbulent blood flow around the valve.
Inflammatory lesions distinctively within the heart that consist of foci of eosinophilic material surrounded by T lymphocytes, occasional plasma cells, and plump macrophages called "Anitschkow cells".
Describe Anitschkow cells
Reactive Histiocytes seen with abundant cytoplasm
central round to ovoid nuclei in which the chromatin is disposed in a central, slender, wavy ribbon )caterpillar cells).
What cardiac lesions develop from acute rheumatic fever?
Endocarditis, myocarditis and /or pericarditis
What diseases are the most common causes of Heart Failure in order of most common?
1. Chronic Rheumatic Disease 2. Valvular Stenosis or Insufficiency
What clinical manifestations are seen in bacterial endocarditis?
Infracts and abscesses (brain, kidneys, spleen, intestines, extremities) , neurological dysfunction, mycotic aneurysns of cerebral vessels, intracerebral bleeding
How do hypertrophic myocardial cells appear?
increased diameter wit enlarged , hyperchromatic, rectangular nuclei (boxcar nuclei)
When is the max hypertrophy? how is it observed?
when the supply of oxygen to the myofiber will be deficient
Observed: the distance between the interstitium and the center of each myofiber is increased
IS fibrosis causes left ventricular stiffness
What is diagnostic of Carcinoid Syndrome?
Elevated levels of HIAAA, a metabollite of seratonin
what symptoms are seen with Carcinoid Syndrome?
Release of activ tumor products
Diahrrhea, Flushing, Bronchospasm, and Skin Lesions
Carcinoid heart disease usually affects the right heart, causing changes in the pulmonary and tricuspid valves (plaque like dense fibrous tissue on the valves). It leads to Tricuspid Regurgitation and Pulmonary Stenosis.
It's associated with intestinal carcinoids that have metastasized to the liver.
What charactrizes Chronic Vascular Rejection?
Microscopically, the disorder is characterized by concentric intimal proliferation, leading to occlusion and MI . This complication is painless because the transplanted heart is denervated
What mutations are see in in HCM? What are you most at risk for?
Hyptertophic Cardiomyopathy is associated with mutations of contractile proteins. (it's an AD trait)
At risk of sudden death, particularly during vigrous exercise.
What's the most notable histologic characteristic of this Hypertrophic cardiomyopathy?
Myofiber disarray, which is most extensive in the interventricular septum
What's the most common identifiable cause of dilated cardiomyopathy in the US and Europe?
Alcoholic Cardiomypathy. The degree of myocardial damage is correlated with the lifetime dose of ethanol. Abstinence ameliorates or even reverses the early stages of alcholic cardiomyopathy (not late-stage disease)
Dilated cardiomyopathy is the most commmon type of cardiomyopathy
How does cardiac amyloidosis present?
As a Restrictive cardiomyopathy, characterized by reduced diastolic filling and right sided heart failure.
Amyloid appears amorphous, glassy, and eosinophilic. Congo-stain of course- red green birefringence under polarized light.
Which virus is the most common pathogen associated with myocarditis?
Coxsackievirus Type B in US
How does a cardiac myxoma appear microscopically?
It has a loose myxoid stroma, containing abundant proteoglycans
It is often seen in the L. Atrium
What causes Constrictive Pericarditis?
Exuberant Healing response following acute pericardial injury in which the pericardial space becomes obliterated and the visceral ad pariteal layers are fused in a dens mass of fibrous tissue
Pathologic Process Causes: Bacteria, viruses, or fungi, Active TB,
Previous Radiation therapy to the mediastinum and cardiac surgery
What accumulates in the valves affected by mitral valve prolapse? What complications are patients at risk for?
Myxomatous connective tissue