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NYCC Visceral Pathology > Lab 1+2 Cardiac > Flashcards

Lab 1+2 Cardiac Flashcards

1
Q

Describe the normal morphology and attributes of the chambers of the heart

A
  • RV = crescent shaped; <0.5cm thick
  • LV = concentric; 1.3-1.5cm thick
  • M = 280-340g / F = 230-280g
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2
Q

The ____ side of the heart ‘drives’ the ____. Why is this so?

A
  • Right; Left
  • Right side pre-loads the left side
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3
Q

Where does blood originate from in the right atrium?

A

from the body

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4
Q

Where does blood originate from in the left atrium?

A

from the lungs

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5
Q

With concentric hypertrophy, chamber thickness is ____, and chamber volume is ____

A

increased; decreased
(sarcomeres added in parallel)

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6
Q

Concentric hypertrophy occurs due to a ____ overload

A

pressure

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7
Q

Name 3 examples of conditions that predispose one to having concentric hypertrophy?

A
  • chronic hypertension
  • valvular stenosis
  • congenital anomalies (eg. coartcation of aorta)
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8
Q

What term describes the enlarged, hyperchromatic, and rectangular nuclei of thickened hypertrophic myocardial cells?

A

boxcar nuclei

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9
Q

Describe the histological appearance of boxcar nuclei

A
  • cytoplasmic hypertrophy
  • enlarged, hyperchromatic, rectangular nucleus
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10
Q

With eccentric hypertrophy, chamber volume____, chamber size ____, and chamber wall thickness ____.

A

increases; increases; increases
(sarcomeres added in series)

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11
Q

Eccentric hypertrophy is due to a ____ overload

A

volume

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12
Q

Name 3 examples of eccentric hypertrophy

A
  • “athlete’s heart” (vol overload during exercise)
  • increased blood vol during pregnancy
  • dilated cardiomyopathy
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13
Q

How does concentric hypertrophy affect perfusion of heart muscle by coronary arteries?

A

arteries have further to travel and run out of O2, leading to ischemia

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14
Q

What is the most common cause of left sided heart failure?

A

ischemic heart disease

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15
Q

What is pulmonary edema?

A

accumulation of exudate or transudate within alveoli of the lungs

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16
Q

Pulmonary edema often accompanies ____

A

left ventricular failure

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17
Q

Where are heart failure cells found?

A

in the lungs
(hemosiderin-laden macrophages)

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18
Q

What are the clinical features of left-sided heart failure?

A
  • dyspnea
  • orthopnea (difficulty breathing lying down)
  • paroxysmal nocturnal dyspnea (when sleeping for hrs)
  • cough (thin, watery)
  • hemoptysis (cough up blood)
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19
Q

Dilated jugular veins is termed ____

A

neck vein distension

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20
Q

Neck vein distension is a result of ____

A

right-sided heart failure (decreased systemic venous return)

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21
Q

What other signs and symptoms would accompany neck vein distension?

A
  • dependent pitting edema
  • chronic passive congestion of liver (nutmeg liver)
  • ascites
  • hepato/splenomegaly
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22
Q

With right-sided heart failure, where is pitting edema found?

A

bilateral lower extremity

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23
Q

How is pitting edema severity assessed?

A
  • depth
  • time of resorption of pit
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24
Q

What is the most common cause of right-sided heart failure?

A

LSHF

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25
Q

What is the most common congenital anomaly of the heart?

A

ventricular septal defect (VSD)

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26
Q

What are the possible consequences of VSD?

A
  • heart failure (vol overload)
  • endocarditis (murmur = prone)
  • emboli
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27
Q

What are the clinical features of VSD?

A
  • hollow systolic murmur
  • appear blue when shunt changes from L->R to R->L (cyanose tardive)
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28
Q

What is the Eisenmenger complex? What is the mechanism?

A
  • shunt initially left to right, later becomes right to left
  • progressive increases in pulmonary vascular resistance cause RV pressure to increase, eventually exceeding the LV pressure
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29
Q

What is the most common type of atrial septal defect (ASD)?

A

ostium secundum

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30
Q

What is Lutembacher syndrome?

A

combines mitral valve stenosis and ostium secundum septal defect

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31
Q

Patients with Lutembacher syndrome have a much greater risk for ____

A

RSHF (^^vol overload)

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32
Q

What abnormal communication occurs with a patent ductus arteriosus?

A

pulmonary trunk communicates with aorta

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33
Q

What are the consequences of patent ductus arteriosus?

A
  • compromised gas exchange
  • pulmonic area murmur on auscultation (Machine-like hum)
  • cardiomegaly
    (under normal conditions should obliterate into ligamentum arteriosum)
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34
Q

Describe the caliber of the aortic valve seen with a congenital bicuspid aortic valve

A

smaller than normal lumen

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35
Q

What are the consequences of a congenital bicuspid aortic valve?

A
  • LV works harder to overcome smaller lumen -> pressure overload
  • LV hypertrophy & calcification
  • may lead to endocarditis or sudden death; ^LSHF
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36
Q

What is the classic triad of symptoms seen with congenital bicuspid aortic valve?

A
  • exertional dyspnea
  • angina pectoris
  • syncope
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37
Q

What cluster of abnormalities encompasses Tetrology of Fallot?

A
  • pulmonary valve stenosis
  • RV hypertrophy
  • VSD
  • over-riding aorta (dextroposition of aorta)
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38
Q

How does a patient with Tetrology of Fallot present at birth? What direction of shunt does this condition produce?

A
  • cyanotic at birth
  • right to left shunt
39
Q

What is the characteristic term given to Tetrology of Fallot visualized on a radiograph?

A

Boot-shaped heart
(right-sided heart shadow, apex rotated up)

40
Q

What congenital heart disease is most predictive of clubbing of the fingers?

A

Tetrology of Fallot

41
Q

How do patients with left-to-right shunting diseases present at birth?

A

normal at birth (cyanose tardive)

42
Q

What congenital disease is characterized by localized narrowing of the lumen of the aorta?

A

coarctation of aorta

43
Q

What are the outward signs of an individual with coarctation of the aorta?

A
  • upper limb hypertension (headache, nosebleeds)
  • lower limb hypotension (pale, weak, vascular claudication)
44
Q

What radiographic features would you expect in an individual with coarctation of the aorta?

A

rib-notching (dilated intercostal aa before/above narrowing)

45
Q

What are the areas of pale appearance in a heart with acute myocardial infarction?

A

ischemia/hypoperfusion

46
Q

What are the darker areas surrounding the pale areas in a heart with acute myocardial infarction?

A

hyperemia indicating inflammatory response

47
Q

A histological view of heart tissue after acute myocardial infarction would show ____ necrosis of the heart muscle as evidenced by ____

A

coagulative
eosinophilia

48
Q

Within 24 hours post-myocardial infarction, what type of cells would be found in the region?

A

neutrophils

49
Q

In healed tissue after myocardial infarct, what is the pale grey material that the necrotic area is replaced by?

A

collagen-rich connective tissue

50
Q

What is found at 1 day post-myocardial infarct?

A

deeply eosinophilic cells (PMNs) with characteristic changes of coagulative necrosis

51
Q

What is found at 1 week post-myocardial infarct?

A
  • PMNs replaced by macrophages
  • ^granulation tissue (pre-scar formation)
52
Q

What is found at 1 month post-myocardial infarct?

A

progressive collagenization -> dense fibrous tissue present

53
Q

Why is each time period in the healing of myocardial infarct important?

A

each has its own potential complication

54
Q

In a biopsy of heart tissue taken after an MI, describe the appearance of the myocardium

A

coagulative necrosis:
- eosinophilic due to lack of nuclei in muscle cells
- neutrophils occupy spaces between dead myocytes

55
Q

In a biopsy of heart tissue, how long after an MI would there be a distinct lack of nuclei in the myocytes?

A

1 day (coagulative necrosis)

56
Q

What is the term given to the apparent colour change in a micrograph of heart tissue 1 day post-MI?

A

eosinophilic (pink)

57
Q

At 1 week post-MI, what is a potentially serious complication?

A

increased risk of myocardial rupture (granulation tissue)

58
Q

Describe the appearance of healed MI tissue

A
  • ample CT = relatively acellular
  • resident fibroblasts within dense scar tissue
59
Q

What is the causative organism of rheumatic heart disease?

A

Untreated streptococcal infection

60
Q

What layers of the heart are affected acutely by rheumatic heart disease?

A

all layers (pancarditis)

61
Q

What are Aschoff bodies?

A

granulomas within the heart during acute rheumatic heart disease

62
Q

How do Aschoff bodies present?

A

matrix of chronic inflammatory cells, necrotic debris, and giant cells

63
Q

What are Anitchkow cells?

A

Giant cells with caterpillar-shaped nuclei within Aschoff bodies

64
Q

What valves of the heart are most commonly affected by chronic rheumatic fever?

A
  1. mitral valve
  2. aortic valve
65
Q

What are the complications of chronic rheumatic fever?

A

myo & pericarditis heal w/out complications;
endocarditis may lead to chronic complications:
- bacterial endocarditis
- mural thrombi (cardiac vegetations) in atrial or ventricular chambers
- congestive heart failure
- stenosis of valves -> stiff, non-compliant

66
Q

What is the term for the characteristic appearance of thickened orifice of mitral valve leaflets? What is this a long-term consequence of?

A
  • fish-mouth resemblance
  • chronic rheumatic heart disease (endocarditis)
67
Q

Mitral valve leaflets which protrude superiorly into the atria is termed ____

A

mitral valve prolapse

68
Q

What predisposes an individual to mitral valve prolapse?

A
  • familial distribution
  • inherited collagen diseases (Marfan syn, Ehlers-Danlos syn, osteogenisis imperfecta)
69
Q

Auscultation of mitral valve prolapse reveals a characteristic ____

A

midsystolic click

70
Q

Why does mitral valve prolapse predispose the patient to endocarditis?

A
  • murmur = turbulence
  • damage & inflammation of endocardium in area of turbulence
71
Q

How does MVP predispose valves to vegetations?

A
  • endocarditis -> damage to valves (Virchow’s triad)
  • generate adhesion molecules -> thrombi
72
Q

What are septic emboli?

A

thrombo-emboli + bacteria

73
Q

Where might septic emboli deposit if originating in the LV/mitral valve/aortic valve?

A
  • soles/palms/distal extremities (Janeway lesion/Osler’s node)
    -nail beds
    -retina (Roth’s spots)
  • cerebral bleeds?
74
Q

What are Roth’s spots?

A

retinal hemorrhages associated with septic emboli originating in the left side of the heart

75
Q

What are Janeway lesions?

A

septic emboli to the skin of distal extremities without pain

76
Q

What are Osler’s nodes?

A

septic emboli to the skin of distal extremities with pain

77
Q

Name the 3 types of cardiomyopathy

A
  • dilated (MC)
  • hypertrophic
  • restrictive
78
Q

Describe the appearance of dilated cardiomyopathy

A

enlargement of all chambers, with both ventricles more severely affected (eccentric hypertrophy)
-flabby, pale myocardium

79
Q

What are the predisposing factors to dilated cardiomyopathy?

A
  • alcohol use
  • family predisposition
  • CAD, MI, HTN
80
Q

Describe the organization of myocardial fibers of hypertrophic cardiomyopathy?

A

myocardial fiber disarray

81
Q

What are the consequences of myocardial fiber disarray?

A
  • myocardium undergoes significant hypertrophy to compensate
  • leads to subaortic stenosis
  • compressed branches of coronary aa due to surrounding hypertrophic tissue
82
Q

What occurs to heart tissue with restrictive cardiomyopathy?

A
  • CT or other protein (amyloid) deposited between cardiac myocytes
  • decreased compliance -> resistance to passive filling of heart -> decreased SV and Q
83
Q

What conditions predispose an individual to restrictive cardiomyopathy?

A
  • amyloidosis, metastatic carcinoma, sarcoid granulomas
  • endomyocardial disease
  • genetic & storage disease (eg. hemochromatosis)
84
Q

What is the most common neoplasm of the heart, characterized as a “gelatinous mass?”

A

cardiac myxoma

85
Q

What is the age of onset of a cardiac myxoma?

A

adulthood

86
Q

What is the cell of origin of a cardiac myxoma?

A

loose, myxoid stroma (CT eg. fibroblast)

87
Q

What is the preferential location of a cardiac myxoma?

A

left atrium

88
Q

What is the most common pediatric tumor of the heart?

A

rhabdomyoma

89
Q

What is the age of onset of a rhabdomyoma?

A

childhood (pediatric)

90
Q

What is the cell of origin of a rhabdomyoma?

A

cardiac myocytes

91
Q

What is the preferential location of a rhabdomyoma?

A

ventricles (MC: LV)

92
Q

Name a proposed mechanism of a “water bottle” appearance (enlarged cardiac shadow) on a radiograph?

A

Cardiac tamponade:
rapid accumulation of large fluid volume in pericardial cavity due to ruptured MI, dissection, or hemopericardium (blood/exudate filled pericardial sac)

93
Q

How does a “water bottle” appearance differ from a “boot-shaped” heart?

A
  • boot-shaped: apex angulated upward
  • water bottle: enlarged, globular, pericardium ‘sags’
94
Q

How is cardiomegaly assessed?

A

Cardiothoracic ratio >0.5
(lat diameter of <3 shadow / lat diameter of thoracic cage)

NYCC Visceral Pathology (40 decks)

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