Pathology of Pericardial Disease, Cardiac Tumors, and Congestive Heart Failure Flashcards

1
Q

What are the two major types of pericardial sac accumulations?

A
  1. Pericardial effusion - due to transudate or exudate

2. Hemopericardium - due to trauma or rupture

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2
Q

What is the most likely clinical complication of pericardial fluid accumulation and why?

A

Cardiac tamponade - due to compression of cardiac chambers and impaired diastolic filling of the heart

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3
Q

What are the five types of acute pericarditis (fluid accumulation in pericardial sac with associated inflammation)? Include fluid characteristics

A
  1. Serous - least extra cells in fluid
  2. Fibrinous - Extra fibrin + inflammatory cells
  3. Purulent / suppurative - worst, with acute inflammatory infiltrate
  4. Hemorrhagic - fibrinous + RBCs
  5. Caseous - caseous necrosis within pericardium
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4
Q

What are the usual etiologies of serous pericarditis?

A

Uremia (as in chronic kidney disease), autoimmune disorders like SLE, viral infection

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5
Q

What are the microscopic features of serous pericarditis?

A

Spare number of WBCs in a relateively clear fluid

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6
Q

What is the most common type of pericarditis and what are some common causes?

A

Fibrinous pericarditis

Causes:
Same as serous - 
Uremia, autoimmune disorders
Things which will cause clotting -
s/p myocardial infarction
s/p cardiac surgery
s/p radiation exposure
early bacterial infection
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7
Q

How does fibrinous pericarditis appear grossly?

A

Rough, opaqua visceral / parietal pericardial surfaces with interconnecting stringy fibrous adhesions and varying amounts of cloudly fluid

Stringy adhesions are akin to butter holding two pieces of toast together

“bread and butter” pericarditis = fibrinous

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8
Q

How does fibrinous pericarditis appear microscopically, and what characteristic clinical physical exam finding is associated?

A

Microscopically - moderate number of acute inflammatory cells, with an eosinophilic, fibrous exudate

Clinical finding - pericardial friction rub

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9
Q

What causes purulent / suppurative pericarditis and how does it appear grossly / microscopically?

A

Cause - bacteria infection, maybe from adjacent site or hematogenous / lymphatic spread

Grossly - Creamy / white/ pus fluid in pericardial sac associated w/HYPEREMIA

Microscopically - neutrophils / macrophages of acute inflammatory exudate

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10
Q

What is hemorrhagic pericarditis and how does it look?

A

Fibrinous pericarditis + RBCs -> blood-like fluid in pericardium

Will like a collection of pericardial blood fluid, differing microscopically depending on etiology

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11
Q

What are the causes of hemorrhagic pericarditis?

A
  1. Metastatic malignancy (due to angiogenesis)
  2. Infections i.e. TB, early on which are destructive
  3. Coagulopathies
  4. s/p cardiac surgery
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12
Q

What causes caseous pericarditis?

A

Usually TB

Spreads via local spread from lungs next door, or via mediastinal lymph nodes to pericardial sac

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13
Q

What is the gross and microscopic appearance of caseous pericarditis?

A

Gross: crumbly-white material within pericardial surfaces

Microscopically: Granulomatous inflammation -> with necrotic centers

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14
Q

What is the most common type of chronic pericarditis, and what does it result from? What is it?

A

Adhesive pericarditis -> follows serous or fibrinous pericarditis

It is residual strands of fibrous connective tissue extending between the pericardial surfaces (like the bread and butter)

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15
Q

What are soldier’s plaques?

A

A type of chronic pericarditis characterized by focal, firm, collagenous pericardial thickening which may become calcified

-> when soldiers are marching, they stop abruptly and their RV slams against their chest wall

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16
Q

What is the most frequent chronic pericarditis which results from purulent or caseous pericarditis? Describe.

A

Constrictive pericarditis

-> replacement of pericardial space with a dense collagen or calcified collagen (dense shell)

17
Q

What are the clinical results of constrictive pericarditis?

A

Dense shell causes impaired cardiac diastolic filling and a reduction in cardiac output

18
Q

What is adhesive mediastinopericarditis and what does it follow?

A

Fibrous attachment of parietal pericardium to surrounding mediastinal structures, forcing an incresaed cardiac workload, causing cardiac hypertrophy / dilatation

Most often follows mediastinal radiation / surgery, but can follow purulent / caseous pericarditis

19
Q

What is the most frequent cardiac neoplasm of adults, and and is it benign or malignant?

A

Myxoma - benign

20
Q

Where are myxomas found, and what do they look like grossly and microscopically?

A

Location - atrium, most commonly left atrium, grossly hanging off the wall as a single, polyploid, gelatinous mass

Microscopically - Scattered, spindle-shaped / stellate cells like fibroblasts which are living in a prominent myxoid matrix (secreting extracellular proteoglycans)

21
Q

What are the possible complications of myxoma?

A
  1. Valvular obstruction / injury - seems like mitral stenosis, can injure like a wrecking ball
  2. Tumor embolization -
  3. Cytokine-mediated symptoms - inflammation caused by immune response
22
Q

What is the most common cardiac tumor in children? Describe it. What disease is associated?

A

Rhabdomyoma - bulging, intramyocardial hamartoma (derived from cardiac myocytes)

-Tuberous sclerosis is the common association

23
Q

What are the potential complications of rhabdomyoma and when are they most severe?

A

Valvular or cardiac outflow obstruction because they can be very large relative to the heart, can also cause arrhythmias since they are in the walls

Most severe early on as they are congenital, but as heart grows they do not -> become less problematic overtime

24
Q

Name the cardiac tumor which is an aggregate of myxoid, fibrillary processes located on the upstream valvular surface (i.e. atrium in an AV valve). What is its main complication?

A

Papillary fibroelastoma

Complication - embolization

25
Q

What types of tumors can metastasize to the heart? and where do they typically spread?

A

Carcinomas nearby (i.e. lung / breast)
Melanoma (can go anywhere)
WBC malignancies like leukemias / lymphomas

26
Q

When tumors metastasize to the heart, where do they most commonly spread to and what are the complications of this?

A

Typically the pericardial surfaces

Complications -> cardiac constriction, or hemorrhagic pericardial effusion due to formation of new blood vessels

27
Q

How can mediastinal malignancies interfere with heart function even without metastasis?

A

Block the emptying of SVC -> congestion / edema of head, neck, and arms

28
Q

How do hepatocellular and renal cell carcinoma interfere with heart function?

A

Venous extension can crawl like a snake up the vessels and obstruct the IV

29
Q

How can pulmonary tumor emboli cause heart problems?

A

Metastasis to lungs increased pulmonary pressures -> RV failure

30
Q

What types of cancers commonly cause nonbacterial thrombotic endocarditis (NBTE)?

A

Mucinous adenocarcinomas, especially pancreatic

31
Q

How can lymphomas / leukemias cause heart problems via tumor mediators?

A

Amyloidosis -> overproduction of lambda light chain -> deposition in heart

32
Q

What are the three primary etiologies of congestive heart failure (in a broad sense)?

A
  1. Decreased myocardial contractility - i.e. ischemic heart disease, drug toxicities like doxorubicin
  2. Increased resistance to ventricular filling / ejection - cardiac tamponade, severe HTN, aortic stenosis, coarctation
  3. Systemic diseases - hyperthyroidism, severe anemia
33
Q

What is the end result of how the heart looks in all forms of congestive heart failure?

A

May be initial hypertrophy depending on etiology, but ultimately -> chamber dilatation

34
Q

What physical exam finding is auscultated in the lungs with severe left-sided heart failure?

A

Rales -> due to intra-alveolar transudative edema due to pulmonary congestion and backup of fluid

35
Q

What are heart failure cells?

A

Hemosiderin-laden macrophages caused by phagocytosis of micro-hemorrhages in chronic lung congestion

36
Q

How do the kidneys worsen left-sided heart failure?

A

Decreased renal perfusion leads to activation of RAA system, leading to further fluid retention and worsening pulmonary edema

37
Q

What happens to the brain in left-sided heart failure?

A

Hypoxic encephalopathy -> often manifests as confusion

38
Q

Right-sided heart failure is most common caused by left-sided failure first. What is it called when right-sided failure is caused by significant pulmonary disease?

A

Cor pulmonale

39
Q

Identify the manifestions of heart right-sided heart failure in each of the following locations:

  1. Liver
  2. Spleen
  3. Subcutaneous soft tissue
  4. Pleura, pericardium, &/or peritoneum
A
  1. Liver - nutmeg liver -> centrilobular passive congestion
  2. Spleen - increased portal pressure -> splenic congestion -> splenomegaly
  3. Subcutaneous soft tissue - dependent edema
  4. Pleura, pericardium, &/or peritoneum - transudative effusions (fluid buildup)