Page 25 of 34

PA26.{8,10} | Pericardial Disease & Cardiac Tumours — SDL Guide

Learning Objectives

Classify the etiology of pericarditis into infective, immune-mediated, and neoplastic categories
Describe the gross and microscopic features of the six morphological types of pericarditis
Explain the pathophysiology of cardiac tamponade and identify Beck's triad
Distinguish constrictive pericarditis from cardiac tamponade in terms of mechanism and etiology
Compare the features of pericardial effusion types — serous, serosanguineous, and chylous
Describe the pathological features, clinical presentation, and complications of cardiac myxoma
List the primary benign and malignant cardiac tumours, noting relative frequency
Classify vascular tumours and identify distinguishing features of haemangioma, Kaposi sarcoma, angiosarcoma, and glomus tumour

INSTRUCTIONS

Diseases of the pericardium are tested disproportionately because they generate dramatic, exam-ready clinical pictures — the scratch of a friction rub, a heart silhouetted like a water bottle, a patient whose blood pressure falls with each breath. This module ties the morphology you will see on glass slides directly to those bedside signs, and then pivots to cardiac and vascular tumours, where pattern recognition (myxoma vs metastasis, Kaposi vs angiosarcoma) determines both diagnosis and management. Work through each block before moving ahead.

References

Robbins & Cotran Pathologic Basis of Disease, 10th ed., Ch 12 (textbook)
Harsh Mohan Textbook of Pathology, 8th ed., Ch 16 (textbook)

Version 2.0 | NMC CBUC 2024

CLINICAL SCENARIO

A 28-year-old man presents two weeks after a 'flu-like illness' with sharp chest pain that worsens when he leans back and eases when he sits forward. Auscultation reveals a scratchy, to-and-fro sound at the left sternal border. ECG shows diffuse saddle-shaped ST elevation. Three days later the pain abates — but his neck veins are distended, his heart sounds are muffled, and his systolic blood pressure drops 15 mmHg on inspiration. What has changed morphologically, and why is he now in danger?

WHY THIS MATTERS

Pericardial disease bridges internal medicine, cardiothoracic surgery, and the autopsy table. TB remains the leading cause of constrictive pericarditis in India. Cardiac tamponade is a reversible cause of obstructive shock — missed only when the pathophysiology is not understood. Atrial myxoma mimics mitral stenosis clinically, yet is cured by surgery if caught. For the NMC CBUC examination PA26.8 and PA26.10 appear as long-answer questions requiring etiology + morphology + complications in a structured answer.

RECALL

Before you begin, revisit these concepts from Year 1:

Pericardium — visceral (epicardium) + parietal layers; normal fluid 15–50 mL (ultrafiltrate)
Inflammation sequence — exudate, organisation, fibrosis (from General Pathology)
Granulomatous inflammation — Langhans giant cells, central caseation (TB) [PA Block 1]
Heart anatomy — left atrial position relative to mitral valve [PY cardiovascular]
Obstructive shock — mechanism differs from distributive/cardiogenic shock [PY]

If any of these feel shaky, spend five minutes reviewing before continuing.

Pericarditis — Etiology

A medical infographic showing inflamed pericardium around the heart with infective, immune-mediated, neoplastic, and other causes leading to pericarditis. — **Panel A:** Anterior cutaway of heart showing visceral pericardium, parietal pericardium, inflamed pericardial layers, pericardial cavity, and pericardial effusion.. **Panel B:** Infective causes: viral pericarditis with Coxsackievirus B, echovirus, influenza; tuberculous pericarditis with Mycobacterium tuberculosis and hematogenous spread from lung; pyogenic bacterial pericarditis with Staphylococcus, Streptococcus, Gram-negative bacteria, and frank pus.. **Panel C:** Immune-mediated sterile causes: rheumatic fever pancarditis with fibrinous exudate, SLE immune-complex deposition with serosanguineous effusion, Dressler syndrome 2–10 weeks post-myocardial infarction with anti-myocardial antibodies, and uraemic pericarditis in chronic kidney disease.. **Panel D:** Neoplastic and other causes: metastatic tumours from lung, breast, and lymphoma causing hemorrhagic effusion; post-irradiation, trauma, and hypothyroidism causing transudative effusion..

Pericarditis is inflammation of the pericardium. Causes are grouped into three broad categories:

1. Infective
• Viral — Coxsackievirus B, echovirus, influenza (commonest in young adults; often self-limiting)
• Tuberculous — Mycobacterium tuberculosis; haematogenous spread from pulmonary focus; important in India; tends to progress to constrictive disease
• Pyogenic/bacterial — Staphylococcus, Streptococcus, Gram-negatives; secondary to pneumonia, septicaemia, or mediastinitis; produces frank pus

2. Immune-mediated (sterile)
• Rheumatic fever — part of pancarditis; fibrinous exudate
• Systemic lupus erythematosus (SLE) — immune-complex deposition; serosanguineous effusion
• Dressler syndrome — autoimmune pericarditis 2–10 weeks post-myocardial infarction; anti-myocardial antibodies
• Uraemic pericarditis — in chronic kidney disease; "metabolic" sterile exudate; unique because it occurs without infective trigger

3. Neoplastic / other
• Metastatic tumours (lung, breast, lymphoma) — haemorrhagic effusion
• Post-irradiation, trauma, hypothyroidism (transudative effusion)

Morphological Types of Pericarditis

The exudate type determines the gross and microscopic appearance. Six patterns must be known:

1. Serous pericarditis
Clear, straw-coloured fluid (mostly protein-poor). Seen in viral, rheumatic, SLE, uraemic early. Visceral surface looks normal or mildly injected. Minimal fibrin. Usually resolves without sequelae.

2. Fibrinous ("bread-and-butter") pericarditis
The classic. Exudate rich in fibrin forms shaggy, rough, irregular tags on both pericardial surfaces. When the surfaces are pulled apart at autopsy it looks exactly like two pieces of buttered bread being separated — hence the eponym. Seen in: MI (early), rheumatic fever, uraemia, viral. Friction rub on auscultation. May resolve or organise to adhesions.

Three-panel medical illustration showing fibrinous pericarditis with shaggy fibrin tags on the epicardial surface, a magnified tissue detail, and a normal-versus-pathological comparison. — **Panel A:** Gross anterior heart specimen with reflected pericardium, shaggy fibrin tags, epicardial surface, and underlying myocardium.. **Panel B:** Magnified epicardial surface showing fibrinous exudate over visceral pericardium with myocardium beneath.. **Panel C:** Comparison of normal smooth pericardial surfaces with fibrin-coated surfaces producing the bread-and-butter appearance..

3. Serofibrinous pericarditis
Mixture: serous transudate plus fibrinous deposits. Most common overall type. Same causes as fibrinous.

4. Purulent (suppurative) pericarditis
Thick, creamy pus fills the pericardial sac. Neutrophil-rich exudate on histology. Caused by pyogenic bacteria. Risk of organisation → fibrous obliteration. High mortality if untreated.

5. Haemorrhagic pericarditis
Blood-stained fluid ± fibrin. Key causes: TB (also caseous — see below), malignancy (metastatic or primary cardiac), anticoagulant therapy, ruptured aortic aneurysm. Distinguish from haemopericardium (pure blood, e.g., trauma, aortic dissection).

6. Caseous pericarditis
Specific to TB. Central caseation with epithelioid granulomas and Langhans giant cells on histology. Strong tendency to organise and calcify → constrictive pericarditis. AFB (acid-fast bacilli) demonstrable by Ziehl-Neelsen stain.

Three-panel medical illustration showing 10x histology of caseous pericarditis with central caseous necrosis, epithelioid macrophages, a Langhans-type giant cell, and pericardial involvement. — **Panel A:** Central caseous necrosis, epithelioid macrophages, peripheral lymphocytes, fibrous pericardium. **Panel B:** Langhans-type giant cell, peripheral horseshoe nuclei, epithelioid macrophages. **Panel C:** Heart surface, pericardium, granulomatous inflammation, caseous focus.

SELF-CHECK

A 35-year-old presents with fever, chest pain, and a pericardial friction rub. At autopsy the pericardial surfaces show shaggy fibrin strands that separate like buttered bread. This morphological type is most characteristically associated with which condition?

A. Pyogenic bacterial infection

B. Acute myocardial infarction

C. Metastatic carcinoma

D. Chylothorax

Reveal Answer

Answer: B. Acute myocardial infarction

Fibrinous ('bread-and-butter') pericarditis is classically seen in acute MI, rheumatic fever, and uraemia. The shaggy fibrin exudate without frank pus or haemorrhage is the hallmark. Pyogenic infection produces purulent (suppurative) pericarditis; metastases cause haemorrhagic effusion; chylothorax is a pleural, not pericardial, finding.

Pericardial Effusion

Diagram showing excess fluid in the pericardial cavity, fluid-type classification, and why rapid accumulation can cause cardiac tamponade at lower volumes than chronic effusion. — **Panel A:** Heart, fibrous pericardium, parietal serous pericardium, pericardial cavity, pericardial effusion fluid, visceral serous pericardium/epicardium, >50 mL threshold. **Panel B:** Serous transudate, clear pale yellow fluid, hypoalbuminaemia, nephrotic syndrome, cardiac failure, hypothyroidism, serosanguineous fluid, TB, malignancy, trauma, anticoagulants, post-cardiac surgery, chylous fluid, lymphatic obstruction, mediastinal tumour, thoracic duct trauma. **Panel C:** Slow chronic effusion, distensible pericardium, 1-2 L accommodation, minimal haemodynamic effect, rapid effusion, non-distensible pericardium, cardiac compression, tamponade risk, 150-200 mL threshold, rate of accumulation.

A pericardial effusion is excess fluid in the pericardial cavity (>50 mL). Classification by fluid type:

Type	Appearance	Mechanism / Causes
Serous (transudate)	Clear, pale yellow	Low oncotic pressure (hypoalbuminaemia, nephrotic), high hydrostatic pressure (cardiac failure), hypothyroidism
Serosanguineous	Blood-tinged	TB, malignancy, trauma, anticoagulants, post-cardiac surgery
Chylous	Milky white	Lymphatic obstruction (mediastinal tumour, thoracic duct trauma)

Rate of accumulation matters more than volume. The pericardium can accommodate 1–2 L if it distends slowly (chronic effusion) with minimal haemodynamic effect. Rapid accumulation of as little as 150–200 mL can cause tamponade because the pericardium cannot stretch fast enough.