Histopathology - Heart

Question 1

Answer 1

Anemic Myocardial Infarction

 Myocardium

 Infarct = loss of function and necrosis due to ischemia (inadequate blood flow)

o Anemic infarct = pale, white; usually observed in tissues supplied by terminal arteries, and in solid organs (spleen, kidney, liver)

o Hemorrhagic infarct = red, typical in lung because of double blood supply, in loose tissues, and with venous occlusions (e.g. ovarian torsion)

 Eosinophilic, necrotic patch. No nuclei are seen in the cardiomyocytes of the infarcted area.

 Red discoloration is due to RBCs from damaged capillaries, seen at higher power.

 Border of non-infarcted and infarcted area has mild inflammation, e.g. neutrophil

granulocytes.

 Signs of necrosis:

1. Nuclear changes:

o karyolysis = no nucleus
o karyopyknosis = shrinkage o karyorhexis = breaks up

2. Cytoplasm swollen and eosinophilic

 White spaces seen between cardiomyocytes are artifacts from edema

 Eosinophilic “necrotic bands” are present due to hypercontraction of the sarcomeres

 Lipofuscin seen among the healthy myocytes. This is a ‘wear and tear’ pigment that

accumulates in the nuclei with age.

Question 2

Answer 2

Myocardial hypertrophy

 Hypertrophy of myocardium means that the myocytes increase in size to cope with increased burden.

o These cells cannot divide, so there is no hyperplasia

Myocardial hypertrophy

o Caused by systemic hypertension or aortic valve stenosis which require the L.V. to produce higher pressure

 Hypertrophy increases oxygen and energy demands, which may lead ischemia, foci of necrosis

 Big, eosinophilic cells and fibrocytes between them.

o Connective tissue is seen among the myocardial cells because necrosis causes

replacement by connective tissue

 Cross-striation

 Myocytes thickened with irregularity in size and shape of nuclei

 Loose and dense parts surrounded by fatty tissue with vessels

 Lipofuscin

 We can use RBC (7 micrometers) between the myocardial cells as a ruler. Myocardial cells

should not be more than 3 RBC in size.

 Sign of ischemia = contour of nucleus becomes sharp instead of round

 If we do not see end-to-end anastomosis, think hypertrophy (=same amount of cells, but

bigger)

Question 3

Answer 3

Pericarditis Fibrinosa

 N.B. “fibrinous” does not mean the same as “fibrous”. Fibrinous means “rich in fibrin”, and is related to acute inflammation. “Fibrous” is a chronic state.

 5 types of acute inflammation based on exudate

1. Serous: in blisters, burns. Watery, protein-poor fluid from plasma or secretions of mesothelial cells.
2. Fibrinous: consequence of more severe injuries resulting in greater vascular permeability. Contains more proteins, including fibrinogen. Extravascular fibrin appears eosinophilic. This type of exudate is characteristic of inflammation in lining of body cavities, and occurs in infection. Two outcomes for the fibrinous exudate are resolution (exudate is degraded by fibrinolysis and debris is removed by macrophages) and organization (exudate is invaded by fibroblasts and blood vessels, leading to scar tissue)
3. Purulent: Pus consisting of neutrophils, necrotic cells, edematous fluid, bacteria, 4. Hemorrhagic: Exudate contains proteins and RBC, as in influenza
4. Gangrenous: Immune system dysfunctional; tissue necrotic

 Effusion = fluid in serous cavity

o Transudate = low protein content effusion

o Exudate = high protein content effusion
o The border is protein content 3 g/L. Rivalta test: sulphosalicylic acid is added and

precipitation indicates high protein content

 Here, we see cross-section of heart with subepicardial fat.

 Pericardium here is obvious. (Normal mesothelial cells are very thin)

 RBC are seen in dilated blood vessels (active hyperemia) of the pericardium, though they are

not usually

 Amorphous, eosinophilic material at the edge is fibrin

 Lipofuscin is the brown pigment.

 Myocardium appears normal

 Inflammatory cells present: mostly lymphocytes, plasma cells, macrophages

 Macroscopically called “villous heart”/”bread and butter heart”

 Can occur locally, e.g. infarctions, or on entire heart, e.g. virus

Question 4

Answer 4

Myocarditis Rheumatica

 This is a non-infectious granuloma because bacteria are no-longer present (it is a post- streptococal disease from Strep pyogenes).

 Antibodies against the Strep attack our own cells

 Inflammation in all 3 layers of the heart (peri-, myo-, endocardium) = pancarditis

(endocardium not seen here)

 Pericardium should be thin layer of mesothelium, but here there is fibrinous pericardititis

 Stages of myocarditis:

1. Exudative phase – loose, edematous intersitium, fibrinoid necrosis surrounded by neutrophils
2. Proliferative phase – Aschoff bodies,

 Rheumatic granulomas around blood vessels. They are perivascular granulomas known as “Aschoff nodules” in the myocardium, consisting mainly of T cells, scattered plasma cells, and macrophages (=Anitschkow/caterpillar cells with an intracellular ribbon of chromatin)

 Endocardial, i.e. valve, involvement results in fibrinoid necrosis

Question 5

Answer 5

Fibrosis Myocardii

 Just myocardium, no pericardium

 Cardiomyocytes have even extracellular matrix deposition = scar tissue

o MI heals with scar formation
o Could also be caused by chronic ischemia

 Macroscopically appears gray

Question 6

Answer 6

Virusos Myocarditis

 Lymphocytic infiltration

 Chronic inflammation

 Coxsackie virus (Chagas Disease) is common

Question 7

Answer 7

Endocarditis bacterialis

 Endocarditis mostly affects valves
o Exception: Libman-Sachs endocarditis develops on parietal endocardium

 Macroscopically, valve has vegetations

 This section is from a valve

 Note myocardium at bottom of slide

 Vegetations are composed of fibrin and bacterial clouds, which stain blue

 Endocarditis can be infection (caused by microorganisms) or non-infectious (e.g. rheumatic

endocarditis, Libman-Sachs, marantic)

o Infection endocarditis can be acute or subacute