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PATHPROS > HEART PATHOLOGY -1 > Flashcards

HEART PATHOLOGY -1 Flashcards

Covers Heart Failure, Congenital Heart Disease and Ischemic Heart Disease

1
Q

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

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

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2
Q
  1. What is the late complication of MI characterized by a paradoxical bulge during systole?
  2. What are the effects of this complication?

Deborah Dalmeida MD

A
  1. Ventricular Aneurysm
  2. mural thrombus , Arrhythmias, heart failure

Deborah Dalmeida MD

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3
Q
  1. List 2 causes for Systolic dysfunction due to impaired ventricular contractility
  2. List 2 causes for Systolic dysfunction due to increased afterload

Deborah Dalmeida MD

A
  1. Myocardial infarction, MR,AR, Dilated cardiomyopathy
  2. AS, SEVERE HYPERTENSION

Deborah Dalmeida MD

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4
Q

Common AV canal / Endocardial cushion defect is assoc with which genetic abnormality

Deborah Dalmeida MD

A

Down Syndrome (Trisomy 21)

Deborah Dalmeida MD

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5
Q
  1. List 4 causes for diastolic dysfunction

Deborah Dalmeida MD

A

a. LVH
b. Restrictive cardiomyopathy
c. Myocardial fibrosis
d. Pericardial constriction/Tamponade
e. Amyloid deposition

Deborah Dalmeida MD

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6
Q
  1. Embryologic basis of Tetralogy of Fallot
  2. Components of TOF

Deborah Dalmeida MD

A
  1. anterosuperior displacement of the infundibular septum.
  2. VSD

obstruction of the right ventricular outflow tract (subpulmonary stenosis)

Over riding aorta

right ventricular hypertrophy

Deborah Dalmeida MD

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7
Q
  1. State one clinically significant complication of patent foramen ovale.
  2. When does it occur?

Deborah Dalmeida MD

A
  1. Risk of paradoxical embolism.
  2. Occurs if the right atrial pressure becomes elevated.

Deborah Dalmeida MD

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8
Q

Morphologic change in the following organs in RHF:

Heart

Liver

Spleen

Deborah Dalmeida MD

A
  • 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

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9
Q

Pressure Volume loops in systolic and diastolic dysfunction are important

Deborah Dalmeida MD

A

Revise Slides 7 and 9 of my ppt on Heart Failure

Deborah Dalmeida MD

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10
Q
  1. Irreversible injury of ischemic myocytes occurs first in which zone?
  2. Why ?

Deborah Dalmeida MD

A
  1. Subendocardial zone
  2. 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

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11
Q

Mechanism of reperfusion injury in ischemic myocardium

Deborah Dalmeida MD

A

Free radical mediated (oxidative stress)

calcium overload

inflammatory cells

Deborah Dalmeida MD

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12
Q

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

A
  1. Eccentric hypertrophy
  2. Volume overload (Eg:Chronic MR or AR)

Deborah Dalmeida MD

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13
Q

episodic myocardial ischemia; caused by coronary artery spasm

Deborah Dalmeida MD

A

Prinzmetal variant angina

Deborah Dalmeida MD

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14
Q

MI -Temporal changes

When would you be likely to see gray white scar on gross appearance?

Deborah Dalmeida MD

A

2-4 weeks

Deborah Dalmeida MD

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15
Q

List the Right-to-left shunts

Deborah Dalmeida MD

A
  • Tetralogy of Fallot
  • Transposition of the great arteries
  • Tricuspid atresia
  • Total anomalous pulmonary venous connection
  • Persistent truncus arteriosus

Deborah Dalmeida MD

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16
Q

3 patterns of myocardial rupture following an MI

Deborah Dalmeida MD

A
  • Ventricular free wall rupture
  • Rupture of the ventricular septum
  • Papillary muscle rupture

Deborah Dalmeida MD

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17
Q

MI -Temporal changes

What change would you be likely to see on light microscopy at 4-12 hours?

Deborah Dalmeida MD

A

Early coagulation necrosis

Deborah Dalmeida MD

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18
Q

Microscopic findings in left heart failure

Deborah Dalmeida MD

A
  • progressive edematous widening of alveolar septa
  • accumulation of edema fluid in the alveolar spaces
  • hemosiderin-laden macrophages- ‘heart failure cells’

Deborah Dalmeida MD

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19
Q

The earliest detectable feature of myocyte necrosis

Deborah Dalmeida MD

A

disruption of the integrity of the sarcolemmal membrane

Deborah Dalmeida MD

20
Q

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

A

Fibrinous pericarditis

Deborah Dalmeida MD

21
Q
  1. Congenital heart disease assoc with poorly controlled DM during pregnancy
  2. What is the embryologic defect here?

Deborah Dalmeida MD

A
  1. Transposition of the great vessels
  2. abnormal formation of the truncal and aortopulmonary septa

Deborah Dalmeida MD

22
Q
  1. List the possible complications proximal to the coarctation of aorta
  2. List the possible complications distal to the coarctation of aorta

Deborah Dalmeida MD

A
  1. ↑Upper extremity SBP, dilation of the Aortic root, berry aneurysms
  2. decrease in the SBP and pulse amplitude in the lower extremity , leg claudication , hypertension, development of collateral circulations

Deborah Dalmeida MD

23
Q

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

Deborah Dalmeida MD

A

Unstable angina

Deborah Dalmeida MD

24
Q

triad of fever, pericarditis and pericardial effusion post MI

Caused by autoantibodies directed against antigens within the damaged pericardial tissue (type II hypersensitivity reaction )

Deborah Dalmeida MD

A

Dressler Syndrome

Deborah Dalmeida MD

25
Q

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

A
  1. Coarctation of aorta
  2. distal to the takeoff of the left subclavian artery

(Refer Slide 33, 35 of my ppt on Congenital Heart Diseases)

Deborah Dalmeida MD

26
Q

MI -Temporal changes

a. 0.5- 4 hours

Deborah Dalmeida MD

A

a. Waviness of fibers

Deborah Dalmeida MD

27
Q

List 3 causes for high output heart failure

Deborah Dalmeida MD

A

Severe anemia

Hyperthyroidism

Thiamine deficiency

Deborah Dalmeida MD

28
Q

What is the Clinical consequence of this lesion shown in the image, that has occured following an MI?

Deborah Dalmeida MD

A

The lesion shown is ventricular free wall rupture. It leads to Cardiac tamponade .

Deborah Dalmeida MD

29
Q

The type of arrhythmia largely responsible for sudden cardiac death during the course of acute MI

A

Ventricular fibrillation

30
Q

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

A

Patent ductus arteriosus

31
Q

Identify the condition using the clues provided

  1. Mutation of SCN5A gene that normally functions as a Sodium channel
  2. prolongation of the QT segment in ECGs
  3. susceptibility to malignant ventricular arrhythmias.
A

Long QT syndrome

32
Q

Clinical features of TOF

A
  • 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
33
Q

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?

A
  1. Di George Syndrome
  2. Truncus arteriosus, TOF - Congenital abnormalities of the cardiac outflow tracts
34
Q

MI -Temporal changes

When would you be likely to see well established granulation tissue ?

A

10-14 days

35
Q

Congenital cardiac defects assoc with Turner Syndrome

A

bicsuspid aortic valve

coarctaion of aorta

36
Q

What murmur develops as a result of this lesion that follows a MI?

A

The lesion shown is papillary muscle rupture.

The murmur is acute mitral regurgitation.

37
Q

List the Left to right shunts

A
  • ASD
  • VSD
  • Patent ductus arteriosus
38
Q

What is the cause for the radiologic finding in this condition?

Dyspnea

Orthopnea

Paroxysmal nocturnal dyspnea

S3 gallop

A

Pulmonary edema (Clinical features indicate left heart failure)

(The blue arrows indicate air bronchograms)

39
Q

Congenital heart disease assoc with maternal Rubella infection

A

Patent ductus arteriosus

40
Q

90% of all ASDs are what type?

A

Secundum type

41
Q

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.

A

VSD

42
Q

List 4 changes associated with aging of the heart

A

Decreased left ventricular cavity size

Sigmoid -shaped ventricular septum

Lambl excrescences; Calcific deposits

Brown atrophy, lipofuscin deposition

43
Q

a. Time period during which the mycoardium is most susceptible to rupture following infarction
b. Why?

A

a. 3-7 days
b. Beginning of phagocytic activity

44
Q

MI -Temporal changes

What change would you be likely to see at 12-24 hours?

A

Contraction band necrosis

45
Q

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

A

Total Anomalous Pulmonary Venous Return

46
Q

Identify the CHD based on the clues provided
Congenital absence of tricuspid valve
Poorly developed right ventricle and pulmonary artery

A

Tricuspid atresia

47
Q

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

A

Ebstein anomaly

PATHPROS (36 decks)

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