HEART PATHOLOGY -1 Flashcards
Covers Heart Failure, Congenital Heart Disease and Ischemic Heart Disease
Which vessel is most likely to have been involved in Myocardial infarction involving the following area?
A. anterior wall of left ventricle near the apex; the anterior portion of ventricular septum;
B. inferior/posterior wall of left ventricle; posterior portion of ventricular septum;
c. lateral wall of left ventricle except at the apex
Deborah Dalmeida MD
A. Left anterior descending coronary artery
B.Right coronary artery
C.Left circumflex coronary artery
(Refer Slide 34 of my ppt on Ischemic Heart Disease)
Deborah Dalmeida MD
- What is the late complication of MI characterized by a paradoxical bulge during systole?
- What are the effects of this complication?
Deborah Dalmeida MD

- Ventricular Aneurysm
- mural thrombus , Arrhythmias, heart failure
Deborah Dalmeida MD
- List 2 causes for Systolic dysfunction due to impaired ventricular contractility
- List 2 causes for Systolic dysfunction due to increased afterload
Deborah Dalmeida MD
- Myocardial infarction, MR,AR, Dilated cardiomyopathy
- AS, SEVERE HYPERTENSION
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Common AV canal / Endocardial cushion defect is assoc with which genetic abnormality
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Down Syndrome (Trisomy 21)
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- List 4 causes for diastolic dysfunction
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a. LVH
b. Restrictive cardiomyopathy
c. Myocardial fibrosis
d. Pericardial constriction/Tamponade
e. Amyloid deposition
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- Embryologic basis of Tetralogy of Fallot
- Components of TOF
Deborah Dalmeida MD
- anterosuperior displacement of the infundibular septum.
- VSD
obstruction of the right ventricular outflow tract (subpulmonary stenosis)
Over riding aorta
right ventricular hypertrophy
Deborah Dalmeida MD
- State one clinically significant complication of patent foramen ovale.
- When does it occur?
Deborah Dalmeida MD
- Risk of paradoxical embolism.
- Occurs if the right atrial pressure becomes elevated.
Deborah Dalmeida MD
Morphologic change in the following organs in RHF:
Heart
Liver
Spleen
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- Heart - hypertrophy and dilation of the right atrium and ventricle.
- Liver and Portal - centrilobular regions are grossly red-brown and slightly depressed (because of cell death) and are accentuated against the surrounding zones of uncongested tan liver producing the characteristic “nutmeg liver” appearance,
- Congestive splenomegaly
Deborah Dalmeida MD
Pressure Volume loops in systolic and diastolic dysfunction are important
Deborah Dalmeida MD
Revise Slides 7 and 9 of my ppt on Heart Failure
Deborah Dalmeida MD
- Irreversible injury of ischemic myocytes occurs first in which zone?
- Why ?
Deborah Dalmeida MD
- Subendocardial zone
- a. the myocardial perfusion pattern proceeds from epicardium to endocardium
b. subjected to the highest pressure from the ventricular chamber
c. has few collateral connections
d. perfused by vessels that must pass through layers of contracting myocardium
Deborah Dalmeida MD
Mechanism of reperfusion injury in ischemic myocardium
Deborah Dalmeida MD
Free radical mediated (oxidative stress)
calcium overload
inflammatory cells
Deborah Dalmeida MD
1. Concentric/ Eccentric hypertrophy?
Ventricular dilation in proportion to the increase in wall thickness
Wall thickness may be increased, normal, or less than normal.
New sarcomeres are assembled in series
2. This condition is due to pressure overload/ volume overload?
Deborah Dalmeida MD
- Eccentric hypertrophy
- Volume overload (Eg:Chronic MR or AR)
Deborah Dalmeida MD
episodic myocardial ischemia; caused by coronary artery spasm
Deborah Dalmeida MD
Prinzmetal variant angina
Deborah Dalmeida MD
MI -Temporal changes
When would you be likely to see gray white scar on gross appearance?
Deborah Dalmeida MD

2-4 weeks
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List the Right-to-left shunts
Deborah Dalmeida MD
- Tetralogy of Fallot
- Transposition of the great arteries
- Tricuspid atresia
- Total anomalous pulmonary venous connection
- Persistent truncus arteriosus
Deborah Dalmeida MD
3 patterns of myocardial rupture following an MI
Deborah Dalmeida MD
- Ventricular free wall rupture
- Rupture of the ventricular septum
- Papillary muscle rupture
Deborah Dalmeida MD
MI -Temporal changes
What change would you be likely to see on light microscopy at 4-12 hours?
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Early coagulation necrosis
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Microscopic findings in left heart failure
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- progressive edematous widening of alveolar septa
- accumulation of edema fluid in the alveolar spaces
- hemosiderin-laden macrophages- ‘heart failure cells’
Deborah Dalmeida MD
The earliest detectable feature of myocyte necrosis
Deborah Dalmeida MD
disruption of the integrity of the sarcolemmal membrane
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Identify this complication of an MI
- occurs about the second or third day following a transmural infarct
- Precordial friction rub is present on auscultation
- caused by increased vessel permeability in the pericardium
Deborah Dalmeida MD

Fibrinous pericarditis
Deborah Dalmeida MD
- Congenital heart disease assoc with poorly controlled DM during pregnancy
- What is the embryologic defect here?
Deborah Dalmeida MD

- Transposition of the great vessels
- abnormal formation of the truncal and aortopulmonary septa
Deborah Dalmeida MD
- List the possible complications proximal to the coarctation of aorta
- List the possible complications distal to the coarctation of aorta
Deborah Dalmeida MD

- ↑Upper extremity SBP, dilation of the Aortic root, berry aneurysms
- decrease in the SBP and pulse amplitude in the lower extremity , leg claudication , hypertension, development of collateral circulations
Deborah Dalmeida MD
Stable/ Unstable/ Prinzmetal Angina?
Pattern of increasingly frequent, prolonged (>20 min), or severe chest discomfort, described as frank pain, precipitated by progressively lower levels of physical activity or even occurring at rest
Caused by the disruption of an atherosclerotic plaque with superimposed partial thrombosis
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Unstable angina
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triad of fever, pericarditis and pericardial effusion post MI
Caused by autoantibodies directed against antigens within the damaged pericardial tissue (type II hypersensitivity reaction )
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Dressler Syndrome
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1. Identify the congenital heart disease
Systolic pressure in the arms is greater than that in the legs
Claudication pain in the lower limbs
Midsystolic ejection murmur
2. What is the site of coarctation here - proximal or distal to the takeoff of the subclavian artery?
Deborah Dalmeida MD

- Coarctation of aorta
- distal to the takeoff of the left subclavian artery
(Refer Slide 33, 35 of my ppt on Congenital Heart Diseases)
Deborah Dalmeida MD
MI -Temporal changes
a. 0.5- 4 hours
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a. Waviness of fibers
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List 3 causes for high output heart failure
Deborah Dalmeida MD
Severe anemia
Hyperthyroidism
Thiamine deficiency
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What is the Clinical consequence of this lesion shown in the image, that has occured following an MI?
Deborah Dalmeida MD

The lesion shown is ventricular free wall rupture. It leads to Cardiac tamponade .
Deborah Dalmeida MD
The type of arrhythmia largely responsible for sudden cardiac death during the course of acute MI
Ventricular fibrillation
Identify the CHD based on the clues provided and the heart sound attached
continuous, machine-like murmur, heard best at the left subclavicular region
assoc with maternal mumps

Patent ductus arteriosus
Identify the condition using the clues provided
- Mutation of SCN5A gene that normally functions as a Sodium channel
- prolongation of the QT segment in ECGs
- susceptibility to malignant ventricular arrhythmias.
Long QT syndrome
Clinical features of TOF

- Children - dyspnea on exertion.
- “Spells” may occur following exertion, feeding, or crying when systemic vasodilatation results in an increased right to- left shunt.
- Manifestations of such spells include irritability, cyanosis, hyperventilation, and occasionally syncope or convulsions.
- Symptoms are alleviated by squatting
1. Identify the condition
thymic hypoplasia
hypocalcaemia
outflow tract defects of the heart
dysmorphic facies.
deletion within chromosome 22q11.
2. Which cardiac defect is associated with this condition?
- Di George Syndrome
- Truncus arteriosus, TOF - Congenital abnormalities of the cardiac outflow tracts
MI -Temporal changes
When would you be likely to see well established granulation tissue ?
10-14 days
Congenital cardiac defects assoc with Turner Syndrome
bicsuspid aortic valve
coarctaion of aorta
What murmur develops as a result of this lesion that follows a MI?

The lesion shown is papillary muscle rupture.
The murmur is acute mitral regurgitation.
List the Left to right shunts
- ASD
- VSD
- Patent ductus arteriosus
What is the cause for the radiologic finding in this condition?
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
S3 gallop

Pulmonary edema (Clinical features indicate left heart failure)
(The blue arrows indicate air bronchograms)
Congenital heart disease assoc with maternal Rubella infection

Patent ductus arteriosus
90% of all ASDs are what type?

Secundum type
Identify the CHD based on the clues provided and the heart sound attached
most common type of CHD
tachypnea, poor feeding, failure to thrive, and frequent lower respiratory tract infections
murmur that is best heard at the left sternal border.

VSD
List 4 changes associated with aging of the heart
Decreased left ventricular cavity size
Sigmoid -shaped ventricular septum
Lambl excrescences; Calcific deposits
Brown atrophy, lipofuscin deposition
a. Time period during which the mycoardium is most susceptible to rupture following infarction
b. Why?
a. 3-7 days
b. Beginning of phagocytic activity
MI -Temporal changes
What change would you be likely to see at 12-24 hours?

Contraction band necrosis
Identify the CHD based on the clues provided
pulmonary veins empty into the right atrium instead of returning blood from the lungs into the left atrium
Total Anomalous Pulmonary Venous Return
Identify the CHD based on the clues provided
Congenital absence of tricuspid valve
Poorly developed right ventricle and pulmonary artery
Tricuspid atresia
Identify the CHD based on the clues provided
downward displacement of an abnormal tricuspid valve into an underdeveloped right ventricle.
Leads to tricuspid regurgitation
Associated with maternal Lithium intake
Ebstein anomaly