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Flashcards in Pathology Lab-Cardiac Deck (29)
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How did the plaque shown below cause an MI?

Note the red circumscribed by yellow and white layers. White = fibrous cap. Yellow = lipid. Red = thrombus from a ruptured plaque. Bleeding within the plaque can expand the plaque and cause occlusion.


Where in the image below was the source of an MI that caused sudden death in a patient?



What coronary arteries were likely occluded in the patient's heart seen below? What percentage of people have occlusions in the LCA, RCA and LCX?

LCA = 50%, RCA = 30%, LCX = 20%.


How fresh is this infarct?



What causes the pattern seen below?

These are contraction bands. This happens as a consequence of reperfusion of myocytes that have been irreversibly damaged. This causes them to die in a maximally contracted state.


How are these patients going to present

They are likely at 6 days post-MI and are at maximal softening and at risk of rupture.


What complications arise when a patient is about 7 days after an MI?

CHF, arrhythmias, mural thrombus and fibrinous pericarditis. 


Why was this patient prone to develop this thrombus?

After an MI, collagen deposition where the scar is does not contract with the rest of the heart. This creates an aneurism, stasis in that area and clot formation.     


Which one of the patients seen below will present earlier in life?

The patient with the bicuspid valve. It undergoes more stress because of its abnormal shape and calcifies earlier.


Why are dilated, failed hearts heavier than a normal heart in patients with aortic stenosis?

Initially, CHF with aortic stenosis is preceded by ventricular hypertrophy and weight gain.


How do you determine if someone has aortic stenosis from rheumatic fever?

They will also have stenosis of the mitral valve and will have commissure fusion.


What structures are prone to rupture in a patient that you hear a mid systolic click during chest auscultation?

Chordae tendinae. They are thinned and stretched from mitral valve prolapse.


Where do vegetations tend to accumulate in rheumatic heart disease? Lupus? NBTE? What type of vegetations are these?

These are all sterile vegetations. In rheumatic heart disease they form along the lines of closure in the mitral valve. In lupus they form on both sides (Libman-Sachs).


What conditions promote NBTE?

Hypercoaguable states (cancer) promotes sterile vegetation accumulation in non-bacterial thrombotic endocarditis.


What is your diagnosis?

Note the focal collection of giant, activated macrophages with caterpillar nuclei. This is an Aschoff body with Anitzchow cells that are typical of acute rheumatic heart disease. These bodies disappear in chronic rheumatic fever.


How do you diagnose someone clinically with rheumatic heart disease?

JONES criteria. 


What type of cardiomyopathy has problems with ejection fraction? What types have trouble with diastolic filling?

EF = dilated. Diastolic filling = Restrictive and hypertrophic.


What genetic component causes the condition seen below?

This is hypertrophic cardiomyopathy. An autosomal dominant disorder affecting the proteins in the sarcomere.


What conditions can cause the condition seen below?

Genetic mutation of cytoskeletal proteins (dystrophin). Alcoholism (thiamine deficiency). Pregnancy (most subtle form). Adriamycin (chemotherapy). Coxsackie virus.


You are treating a patient who has confirmed hypertrophic cardiomyopathy. Why is this patient prone to sub-acute infectious endocarditis?

Strep viridans is in our normal flora. It has a lower virulence, makes dextran which can bind to fibrin and can cause sub-acute endocarditis as the mitral valve gets damaged in hypertrophic cardiomyopathy.


Why are patients with HOCM at high risk for stroke?

Increased pressure in the LV causes left atrial dilation. This is a prime environment for stasis and thrombus formation.


Why are patients with this condition at high risk for angina and syncope?

Note the disarrayed and hypertrophic myocardium. This is HOCM. Decreased blood flow in the outflow tract and thus decreased coronary blood supply + increased O2 demand by myocardial hypertrophy.


What are secondary health problems that come with the condition seen below?

This is dilated cardiomyopathy. Note the enlarged myocytes and fibrosis from tissue damage. Thrombus formation, arrhythmias, regurgitation and decreased ejection fraction.


A 45-year-old woman with a history of childhood “heart murmur” complained of fatigue, weight loss and recurrent episodes of fever. The patient had a dental extraction about 6 weeks before onset of symptoms. On physical exam a diastolic murmur was heard at the apex. Subungual splinter hemorrhage was noted. Where do you start in your diagnosis of the patient?

Blood culture and determine if she has a new or changed heart murmur. This is likely sub-acute endocarditis.


Why do more virulent organisms cause larger vegetations in endocarditis? Which is acute and which is subacute?

The top image is acute endocarditis. In addition to the fibrin-platelet clot, bacteria elicit a large inflammatory response and larger vegetations. Note on the bottom image: thickened valve and shortened cordae tendinae, indicative of a more sub-acute endocarditis.


How is this condition caused by endocarditis?

Embolus of vegetation, blocking kidney blood supply and causing ischemia.


A four-month-old female infant presented with a history of tachycardia, tachypnea and slow eating. A loud, blowing left parasternal pansystolic murmur was present, heard best over the lower left sternal border and was accompanied by a thrill. Chest x-ray showed mild cardiomegaly and borderline increased pulmonary vasculature. ECG suggested left ventricular hypertrophy. What is causing the murmur you hear?

Ventricular septal defect


What conditions often present with Turner's syndrome?

Aortic coarctation and bicuspid aortic valve.


This baby presented with clubbing of the fingers and toes along with early cyanosis. Vascular lung markings are diminished. What is your diagnosis in this patient?

Note the hypertrophic ventricular septum and thickened right ventricular wall. Note the stenotic pulmonary artery, overriding aorta and VSD. This patient has tetrology of Fallot.

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