12. Cardiac Pathology Flashcards Preview

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Flashcards in 12. Cardiac Pathology Deck (100):

What is ischemic heart disease?

Cardiac ischemia usually secondary to coronary artery disease (CAD).


What is angina pectoris?

Transient cardiac ischemia without cell death resulting in substernal chest pain.


What is a stable angina?

The most common type of angina, caused by coronary artery atherosclerosis with luminal narrowing greater than 75%. Chest pain is brought on by increased cardiac demand (exertional or emotional).


What is Prinzmetal variant angina?

Caused by coronary artery vasospasm, episodic chest pain often occuring at rest.


What is unstable or crecendo angina?

Caused by formation of a nonocclusive thrombus in an area of coronary atherosclerosis. Increasing frequency, intensity and duration of episodes. Occurs at rest. It has a high risk for myocardial infarction.


What is a myocardial infarction (MI)?

Localized area of cardiac muscle necrosis due to ischemia caused by coronary artery atherosclerosis with plaque rupture and superimposed thrombus formation or caused by coronary artery spasm.


Which arteries are the most affected during a myocardial infarction?

I. Left anterior descending (LAD) = 45%. II. Right coronary artery (RCA) = 35%. III. Left circumflex coronary artery (LCA) = 15%.


Which type of infarction is the most common?

Transmural infarction. Caused by ischemic necrosis of >50% of myocardial wall.


What are the clinical symptoms of a myocardial infarction?

Sudden onset of severe "crushing" substernal chest pain, often radiates to the left arm, jaw, and neck. Chest heaviness, tightness and shortness of breath. Diaphoresis, nausea, and vomiting. Jugual venous distension (JVD) could be seen. Anxietey and often have a feeling of impending doom.


In which type of patients do we see atypical presentations of MI with little or no chest pain?

Elderly patients, diabetics, women, and postsurgical patients.


At what time after the myocardial infarction do Q waves representing myocardial necrosis develop?

In 24 to 48 hours.


What can we see in the EKG in transmural ischemia?

ST segment elevation.


What can we see in the EKG in subendocardial ischemia?

ST segment depression.


What gross changes we see in the heart 18-24 hours later after a myocardial infarction?

Vague pallor and softening.


What gross changes we see in the heart 1-7 days later after a myocardial infarction?

Yellow pallor.


What gross changes we see in the heart 7-28 days later after a myocardial infarction?

Central pallor with a red border.


What gross changes we see in the heart months later after a myocardial infarction?

White, firm scar.


When does serum marker CK-MB elevate by, peak, and returns to normal?

Elevated by 4-8 hours, peaks by 18 hours, returns to normal by 2-3 days.


When does serum marker Troponin I and T elevate by, peak, and returns to normal?

Elevated by 3-6 hours, peaks by 16 hours, returns to normal by 7-10 days.


When does serum marker LDH elevate by, peak, and returns to normal?

Elevated by 24 hours, peaks by 3-6 days, returns to normal by 8-14 days.


What do we see microscopically 1-4 hours later following a myocardial infarction?

Wavy myocyte fibers.


What time after a myocardial infarction do we see coagulative necrosis microscopically?

4-24 hours later.


What do we see microscopically 1-4 days later following a myocardial infarction?

Neutrophilic infiltrate.


What time after a myocardial infarction do we see macrophage infilatrion microscopically?

4-7 days later.


What do we see microscopically 7-28 days later following a myocardial infarction?

Granulation tissue.


What time after a myocardial infarction do we see fibrotic scar tissue?

Months later.


What complication is the most common 4-7 days post-MI?

Cardiac rupture.


What happens when we have a ventricular free wall rupture?

Cardiac tamponade.


What happens when we have a interventricular septum rupture?

Left to Right shunt.


What happens when we have a papillary muscle rupture?

Mitral insufficiency.


What is Sudden cardiac death and what causes it?

Death within one hour of the onset of symptoms; caused by fatal cardiac arrhythmia, usually ventricular fibrillation.


What is Dressler syndrome?

It is believed to be an immune system response after damage to heart tissue or to the pericardium, from events such as a heart attack, surgery or traumatic injury. Symptoms include chest pain, which may be similar to chest pain experienced during a heart attack.


What is congestive heart failure (CHF)?

Insufficient cardiac output to meet the metabolic demand of the body's tissues and organs.


What are four causes of Left heart failure?

I. Ischemic heart disease. II. Hypertension. III. Myocardial disease. IV. Aortic or mitral valve disease.


What are the symptoms of Left heart failure?

Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, rales, and S3 gallop.


What are heart-failure cells?

Intra-alveolar hemosiderin-laden macrophages.


What are the complications of Left heart failure?

I. Passive pulmonary congestion and edema. II. Activation of renin-angiotensin-aldosterone system leading to secondary hyperaldosteronism. III. Cardiac Shock.


What are the causes of Right heart failure?

I. Most commonly caused by left-sided heart failure. II. Pulmonary or tricuspid valve disease. III. Cor pulmonale.


What is cor pulmonale?

Right-sided heart failure caused by pulmonary hypertension from intrinsic lung disease.


What are the symptoms of Right heart failure?

Jugular venous distention (JVD), hepatospleenomegaly, dependent edema, ascites, weight gain, and pleural and pericardial effusions.


What are the complications of right heart failure?

I. Chronic passive congestion of the liver. II. Cardiac cirrhosis (only with long-standing congestion).


Which type of valvular heart disease is the most common?

Degenerative calcific aortic valve stenosis.


What is degenerative calcific aortic valve stenosis?

Age-related dystrophic calcification, degeneation, and stenosis of the aortic valve.


What type of microscopic changes do we see in mitral valve prolapse?

Myxomatous degeneration.


What is rheumatic valvular disease/acute rheumatic fever?

Rheumatic fever is a systemic inflammatory disease, triggered by a pharyngeal infection with group A beta-hemolytic streptococci. In genetically susceptible individuals, the infection results in production of antibodies that cross-react with cardiac antigens.


What are the five major criteria of Jones criteria?

I. Migratory polyarthritis. II. Pancarditis. III. Subcutaneous nodules. IV. Skin rash (erythema marginatum). V. Sydenham chorea.


What are the three minor criteria of Jones criteria?

I. Fever. II. Arthralgia. III. Elevated acute phase reactants.


How many positive criteria are needed in Jones criteria for diagnosis to be positive?

Required two major or one major plus two minor criteria to be positive.


What are Aschoff bodies?

Fibrinoid necrosis surrounded by macrophages (Anitschkow cells), lymphocytes and plasma cells seen in acute rheumatic heart disease.


What are MacCallum plaques?

Left arterial endocardial thickening seen in acute rheumatic fever.


What characterizes infectious bacterial endocarditis?

Vegetations on the valve leaflets.


What does endocarditis involving the right side of the heart suggest?

Intravenous drug abuse.


Which organism is a high virulence that can cause acute endocarditis?

Staphylococcus aureus.


Which organism is a low virulence that can cause subacute endocarditis?

Streptococcus group viridans. Usually colonizes a previously damaged valve.


What are Roth spots?

Retinal hemorrhages with white or pale centers seen in bacterial endocarditits by immune complex deposition.


What are Osler nodes?

Painful, red subcutaneous nodules on the fingers and toes caused by immune complex deposition. Seen in infective endocarditis.


What are Janeway lesions?

Painless, red lesions on the palms and soles caused by septic emboli seen in infective endocarditis.


What is Marantic endocarditis?

AKA nonbacerial thrombotic endocarditis (NBTE): Small, sterile vegetations along the valve leaflet line of closure in patients with a debilitating disease.


What is coarction of the aorta?

Segmental narrowing of the aorta.


Describe infantile-type coarction of the aorta.

AKA Preductal coarctation, it is severe narrowing of aorta proximal to the ductus arteriosis. Usually associated with a patent ductus arteriosis (PDA), which supplies blood to aorta distal to the narrowing. Also associated with Turner syndrome.


What are the symptoms of infantile-type coarction of the aorta?

Infant with CHF and weak pulses and cyanosis in the lower extremities.


Describe adult-type coarction of the aorta.

Narrowing of the aorta distal to the ductus arteriosis, with collateral circulation via the internal mammary and intercostal arteries. On chest x-ray: notching of the ribs.


What are the symptoms of adult-type coarction of the aorta?

Child or adult with hypertension in the upper extremities and hypotension and weak pulses in the lower extremities.


What does right to left shunt cause and why?

Early cyanosis (blue babies) due to blood shunted past the lungs.


What does left to right shunt cause and why?

Late cyanosis (blue kids) due to pulmonary hypertension that leads to reversal of the shunt.


What are the four diseases that cause right to left shunt?

I. Teratology of Fallot. II. Transposition of the great vessels. III. Tricuspid atresia. IV. Truncus arteriosis. [4Ts to the Right]


What are the three diseases that cause left to right shunt?

I. Ventricular septal defect. II. Atrial spetal defect (ASD). III.PDA [Left is a HOLE]


What are the classic tetrad of tetralogy of Fallot?

I. Pulmonary outflow obstruction/stenosis. II. Right ventricular hypertrophy. III. VSD. IV. Overriding aorta.


What are the clinical symptoms of tetralogy of Fallot?

Cinical cyanosis, shortness of breath (SOB), digital clubbing, and polycythemia.


What is the Transposition of the great arteries?

Abnormal development of the truncoconal septum results in inversion of the aorta and pulmonary arteries with respect to the ventricles.


What is truncus arteriosis?

Failure to develop a dividing septum between the aorta and pulmonary artery, resulting in a common trunk. Causes massive blood flow to the lungs which cause pulmonary hypertension.


What is Tricuspid atresia?

Absence of a communication between the right atrium and ventricle due to developmental failure to form the tricuspid valve. Assocaited with right ventricle hypoplasia and an ASD.


What is the most common cause of cyanotic heart disease?

Tetralogy of fallot.


What is the most common congenital heart defect?

Ventricular septal defect.


What is Eisenmenger syndrome?

Reversal of shunt: Originally Left to Right but converts to Right to Left.


What is Eisenmenger complex?

A large ventricular septal defect that leads to pulmonary hypertension and later to shunt reversal and cyanosis.


What do we hear in auscultation of a ventricular septal defect?

Systolic murmur.


Which disease that causes left to right shunt is associated with paradoxical emboli?

Atrial septal defect.


Which type of atrial septal defect is the most common?

Ostium secundum.


What are Patent ductus arteriosus (PDA)?

Direct communication between the aorta and pulmonary artery due to the continued patency of the ductus arteriosis after birth.


Which disease is associated with patent ductus arteriousus (PDA)?

Congenital rubella infections and prematurity.


What do we hear in auscultation of a PDA?

Machinery murmur.


What substance can close the PDA?



What substance can keep PDA open?

Prostaglandin E2.


What is dilated cardiomyopathy?

Cardiac enlargement with dilation of all four chambers resulting in progressive congestive heart failure.


Which drugs can cause dilated cardiomyopathy?

Adriamycin (doxorubicin) and cocaine.


Which viruses can cause dilated cardiomyopathy?

Coxsackievirus B and enteroviruses.


What do we see in echocardiogram in dilated cardiomyopathy?

Decreased ejection fraction.


What is the most common cause of sudden cardiac death in young athletes?

Hypertrophic cardiomyopathy.


What is restrictive cardiomyopathy?

Uncommon form of cardiomyopathy caused by disease that produce restriction of cardiac filling during diastole.


What are four things that cause restrictive cardiomyopathy?

I. Amyloidosis. II. Sarcoidosis. III. Endomyocardial fibroelastosis. IV. Loeffler endomyocarditis.


What is carcinoid hear disease?

Right-sided endocardial and valvular fibrosis secondary to exposure ot serotonin in patients with carcinoid tumors which have metastasized to the liver. There is plaque-like thickening of the endocardium and valves of the right side of the heart.


What are the five major symptoms of carcoid syndrome?

I. Skin flushing. II. Diarrhea. III. Cramping. IV. Bronchospasms and wheezing. V. Telangiectasias. [SD-CB-T for Carcinoid]


How is carcinoid syndrome diagnosed?

Urinary 5-hydroxyindoleacetic acid (5-HIAA).


Which cardiac tumor is associated in caused the "ball-valve" obstruction of the valves?

Cardiac myxoma.


What are cardiac myxoma?

Benign tumor usually arising within the left atrium near the fossa ovalis. Micro: Stellate-shaped cells within a myxoid background.


Which cardiac tumor is associated with tuberous sclerosis?

Cardiac rhabdomyoma.


Which cardiac tumor affects primarily on pediatric patients?

Cardiac rhabdomyoma.


What is cardiac rhabdomyoma?

Benign tumor usually arising withing the myocardium.


What is tuberous sclerosis?

An autosomal dominant disease characterized by multiple hamartomas, cortical tubers, renal angiomyolipomas, cardiac rhabdomyomas, pulmonary hamartomas.