Chapter 25: The Pathology of Sudden Death – Practice Flashcards

A comprehensive set of 150 English flashcards in Question-and-Answer style covering multiple-choice, short-answer and long-answer material from Chapter 25 of Knight’s Forensic Pathology.

1. What is the most common natural cause of sudden death in adults?

Coronary artery disease

2. A ruptured heart following myocardial infarction typically occurs:

Between 3–7 days after infarction

3. Which coronary artery is most commonly involved in sudden cardiac death?

Left anterior descending artery

4. In early myocardial infarction (<6 h), which test is most useful at autopsy?

Triphenyltetrazolium chloride (TTC) staining

5. A “saddle embolus” refers to a clot found:

Straddling the pulmonary trunk bifurcation

6. Which cardiomyopathy is most associated with sudden death in young athletes?

Hypertrophic cardiomyopathy

7. SUDEP stands for:

Sudden Unexpected Death from Epilepsy

8. The key microscopic feature of hypertrophic cardiomyopathy is:

Myocyte disarray

9. Which condition does NOT typically cause upper-airway obstruction leading to sudden death?

Bronchiectasis

10. The classic gross feature of asthma seen at autopsy is:

Mucous plugging of bronchi

11. Subendocardial infarction typically affects:

The innermost layer adjacent to the endocardium

12. Which finding is most suggestive of a ruptured berry aneurysm?

Subarachnoid haemorrhage

13. Dissecting aneurysms most commonly affect the:

Ascending thoracic aorta

14. Massive GI bleeding from oesophageal varices is most commonly associated with:

Portal hypertension

15. Which is a classic microscopic finding in fatal asthma cases?

Charcot–Leyden crystals

16. Most common microscopic change in myocardium 2–3 days after infarction:

Coagulative necrosis with neutrophilic infiltration

17. Sudden death due to pulmonary embolism often involves thrombus originating from:

Pelvic or femoral veins

18. Pink teeth are typically associated with:

Drowning and refrigeration

19. Which is NOT a recognised complication of myocardial infarction?

Cardiac myxoma

20. Histochemical TTC staining is used at autopsy to:

Detect myocardial enzyme activity

21. Recognised trigger of sudden cardiac death in coronary atherosclerosis:

Physical stress

22. What colour does viable myocardium stain in TTC staining?

Brick red

23. Intraplaque haemorrhage is associated with:

Rapid plaque expansion and occlusion

24. Which valve disease is most often associated with sudden death?

Aortic stenosis

25. Common complication of myocardial rupture:

Hemopericardium

26. In Dressler’s syndrome, which structure is inflamed?

Pericardium

27. Restrictive cardiomyopathy is associated with:

Diastolic dysfunction

28. Gross indicator of senile myocardium:

Lipofuscin accumulation

29. Typical microscopic finding in myocarditis:

Lymphocytic infiltrate with myocyte necrosis

30. A syphilitic aneurysm most often affects the:

Ascending aorta

31. Marfan syndrome is a risk factor for:

Dissecting aortic aneurysm

32. Enzyme commonly detected by immunohistochemistry in MI:

Troponin I

33. Histological hallmark of late-stage infarction:

Dense collagenous scar

34. Commonest location of atherosclerotic aneurysms:

Infrarenal abdominal aorta

35. In sudden asthma death, which finding supports the diagnosis?

Curschmann spirals

36. Which condition may mimic a café coronary at autopsy?

Epiglottitis

37. Bronchiectasis is a cause of:

Massive haemoptysis

38. A ruptured ectopic pregnancy typically results in:

Haemoperitoneum

39. Which vascular lesion is most often congenital?

Berry aneurysm

40. Main forensic importance of investigating sudden death:

To differentiate natural from unnatural causes

41. Microscopic finding characteristically seen in myocarditis:

Interstitial lymphocytic infiltrate

42. Key macroscopic finding in a dissecting aneurysm:

Intimal tear with formation of a false lumen

43. A common source of thrombus in pulmonary embolism is the:

Deep femoral vein

44. Myocardial rupture occurs when the myocardium is:

Necrotic and weakened

45. Common feature of restrictive cardiomyopathy:

Rigid ventricular walls

46. Myocardial fibrosis predisposes to:

Arrhythmias

47. Known precipitant of coronary artery spasm:

Cocaine use

48. Sudden collapse during intercourse may be linked to:

Aneurysmal rupture

49. A mural thrombus is formed:

On infarcted endocardium

50. Feature characteristic of fulminant myocarditis:

Widespread myocardial necrosis

51. Café coronary is caused by:

Food bolus obstruction of the larynx

52. Aneurysms of which vessel can cause intraperitoneal bleeding?

Splenic artery

53. In any sudden death, what must always be performed?

Full autopsy with histology

54. What causes hyperinflated lungs in asthma?

Air trapping due to bronchospasm

55. Immediate cause of sudden death in epilepsy:

Post-ictal arrhythmia

56. Structure primarily affected in coronary atherosclerosis:

Intima of the coronary artery

57. Which cellular phase follows neutrophil infiltration in MI?

Macrophage infiltration

58. TTC-negative zones in myocardium imply:

Infarcted tissue

59. Pigment often seen in myocardium of elderly individuals:

Lipofuscin

60. Technique that detects mitochondrial damage early in MI:

Enzyme histochemistry

61. Define sudden death and mention its key diagnostic challenge.

Sudden death is an unexpected fatal event occurring within 1–24 hours of symptom onset; the main challenge is the minimal or absent macroscopic findings, requiring thorough autopsy, histology, toxicology and clinical correlation to rule out unnatural causes.

62. List three major natural causes of sudden death.

Coronary artery disease; Hypertrophic or other cardiomyopathies; Pulmonary embolism

63. Describe the gross findings in hypertrophic cardiomyopathy.

Asymmetrical septal hypertrophy; thickened interventricular septum; small stiff ventricular cavity; heart weight often >500 g; possible concentric LV hypertrophy.

64. What is the mechanism of death in massive pulmonary embolism?

Large embolus blocks pulmonary arteries, causing acute right-ventricular failure, sudden circulatory collapse and severe hypoxia leading to death within minutes.

65. Outline how TTC staining is used in early myocardial infarction diagnosis.

TTC detects dehydrogenase activity: viable myocardium stains brick red whereas infarcted tissue remains pale/yellow, allowing identification of infarction within 6 hours when no gross changes are visible.

66. Name five complications of myocardial infarction visible at autopsy.

Cardiac rupture; Mural thrombosis; Pericarditis; Ventricular aneurysm; Myocardial fibrosis.

67. What causes death in dissecting aortic aneurysm?

Blood enters the arterial wall through an intimal tear, dissects the media, may rupture into the pericardial sac causing tamponade; often linked to hypertension or Marfan syndrome.

68. List typical autopsy findings in fatal asthma.

Over-distended (ballooned) lungs; tenacious mucus plugs in bronchi; eosinophil-rich bronchial inflammation; Curschmann spirals; Charcot–Leyden crystals.

69. State three causes of subarachnoid haemorrhage.

Ruptured berry aneurysm; Arteriovenous malformation; Traumatic rupture of cerebral vessels.

70. What findings support a diagnosis of SUDEP at autopsy?

Structurally normal heart and brain, bitten tongue or lip, frothy airway secretions, pulmonary oedema with petechiae, and supportive clinical history.

71. Explain the cause and findings in myocardial rupture.

Occurs 3–7 days post-MI when necrotic myocardium is weakest; tear leads to hemopericardium and tamponade, usually in the anterior wall, causing rapid death.

72. What is mural thrombosis and why is it significant?

Thrombus forming on infarcted endocardium; may embolise to brain, kidneys or gut, commonly complicates transmural MI and ventricular aneurysm, posing risk of sudden systemic infarction.

73. Differentiate between transmural and subendocardial infarction.

Transmural: full-thickness necrosis due to total occlusion, prone to rupture; Subendocardial: inner one-third to half of wall affected by partial occlusion or hypotension, more chronic, harder to see grossly.

74. Describe Dressler’s syndrome.

Autoimmune pericarditis occurring weeks after MI, characterised by fibrinous or haemorrhagic pericardial effusion, fever and chest pain due to immune response to necrotic myocardium.

75. What is the microscopic hallmark of hypertrophic cardiomyopathy?

Myocyte disarray with interstitial fibrosis and enlarged, disorganised cardiac muscle cells.

76. List four risk factors for pulmonary thromboembolism.

Recent surgery; Major trauma; Prolonged immobility/bed rest; Oral contraceptive use; Malignancy.

77. Describe the gross findings in a senile myocardium.

Increased heart weight, diffuse lipofuscin pigmentation, patchy fibrosis, calcified valves and degeneration of the conduction system.

78. What findings suggest asthma-related death at autopsy?

Mucus-plugged bronchi, hyperinflated lungs, eosinophilic inflammation, pulmonary oedema and Charcot–Leyden crystals.

79. State how myocarditis causes sudden death.

Inflammation and necrosis disrupt conduction pathways, triggering fatal arrhythmia; heart may look normal grossly but shows lymphocytic infiltrate microscopically.

80. Name three causes of fatal upper-airway obstruction.

Food bolus (café coronary); Acute epiglottitis; Foreign-body aspiration

81. How can minor trauma cause death in coronary artery disease?

Physical or emotional stress increases myocardial oxygen demand, may trigger plaque rupture, thrombosis or arrhythmia, precipitating fatal MI.

82. Explain intraplaque haemorrhage.

Rupture of microvessels within an atherosclerotic plaque causes sudden expansion, acute lumen narrowing, ischaemia or infarction; usually a microscopic finding.

83. What causes sudden death in aortic stenosis?

Fatal arrhythmia from hypertrophied ventricle, reduced coronary perfusion, or sudden decompensated heart failure, especially in calcific or congenital stenosis with concentric LVH.

84. List histochemical or immunohistochemical methods useful in early MI.

TTC enzyme staining; NADH or LDH enzyme stains; Troponin I immunohistochemistry; Myoglobin immunostaining.

85. Describe the features of berry aneurysm rupture.

Sudden severe headache followed by collapse; subarachnoid haemorrhage at base of brain; congenital saccular aneurysm visible in circle of Willis.

86. Explain the difference between stable and unstable coronary plaques.

Stable plaques have thick fibrous caps, small lipid cores and rarely rupture; unstable plaques have thin caps and large lipid cores, prone to rupture and thrombosis even with moderate stenosis.

87. Significance of mural thrombi in ventricular aneurysms:

Serve as sources of systemic emboli causing stroke or visceral infarction due to stasis within the akinetic aneurysmal segment.

88. What are the mechanisms of death in SUDEP?

Post-ictal cardiac arrhythmia, autonomic dysfunction and central apnoea, usually with no significant structural pathology.

89. Name three microscopic changes seen 5–10 days post-MI.

Dense macrophage infiltration; Granulation tissue formation; Early collagen deposition as necrotic debris is removed.

90. What does a dissecting aortic aneurysm look like at autopsy?

Longitudinal intimal tear with blood dissecting into the media, creating a double-barrel aorta; false lumen often filled with clot and may rupture into the pericardium.

91. How does a ruptured ectopic pregnancy cause sudden death?

Tubal implantation ruptures, producing massive intraperitoneal haemorrhage, hypovolaemic shock and rapid collapse; autopsy shows hemoperitoneum and tubal rupture site.

92. What is meant by “senile myocardium”?

Age-related myocardial degeneration marked by fibrosis, myocyte loss, lipofuscin deposition and valvular calcification, predisposing to arrhythmia.

93. List findings in sudden death from haemoptysis.

Airways filled with blood, congested oedematous lungs, underlying lesions such as tuberculosis cavities, tumours or bronchiectasis; trauma must be excluded.

94. How do you differentiate MI from agonal heart changes?

Use TTC staining and histology: true MI shows coagulative necrosis and enzyme loss, whereas agonal changes are artefactual; correlate with clinical data and serum enzymes (troponin, CK-MB).

95. How does acute pancreatitis cause sudden death?

Enzymatic autodigestion leads to necrosis and haemorrhage, triggers a systemic inflammatory response and hypovolaemic shock; autopsy reveals swollen haemorrhagic pancreas with fat necrosis.

96. What vascular sites of aneurysm commonly cause sudden death?

Abdominal aorta (atheromatous); Ascending aorta (dissecting); Cerebral arteries (berry); Splenic or renal arteries.

97. What causes arrhythmia in myocardial fibrosis?

Scar tissue disrupts conduction pathways, creating electrical instability that can lead to fatal ventricular arrhythmias.

98. Source of embolus in postpartum pulmonary embolism:

Deep vein thrombosis of the leg or pelvic veins formed due to immobility and hypercoagulability.

99. Conditions that must be excluded in sudden death in epilepsy:

Head trauma; Drug overdose; Asphyxia; Underlying cardiac disease—SUDEP is a diagnosis of exclusion.

100. List three findings in a ruptured syphilitic aneurysm.

Destruction of vasa vasorum weakening ascending aortic wall; Aortic regurgitation; Hemopericardium from rupture in tertiary syphilis.