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Questions and Answers

What is a common complication associated with cardiac valvular insufficiency?

Aortic rupture

Myocardial hypertrophy (correct)

Pulmonary embolism

Coronary artery disease

Which pathologic feature is most commonly associated with acute pericarditis?

Calcification of the pericardium

Fibrous adhesions

Fibrinous exudate (correct)

Thickening of the pericardial sac

What is a common cause of secondary hypertension?

Genetics

Chronic kidney disease (correct)

Sedentary lifestyle

Obesity

Which type of cardiomyopathy is characterized by a decreased ability to fill the heart due to stiff ventricles?

Restrictive cardiomyopathy Signup and view all the answers

Which pathological change occurs in the myocardium due to systemic hypertension?

Concentric left ventricular hypertrophy Signup and view all the answers

What differentiates infective endocarditis from non-infective endocarditis?

Bacterial infection Signup and view all the answers

What is primarily responsible for cardiac hypertrophy without dilatation?

Increased pressure load Signup and view all the answers

Which type of myocarditis is associated with viral infections?

Viral myocarditis Signup and view all the answers

Which condition leads to both cardiac hypertrophy and dilatation?

Increased pressure load and volume load Signup and view all the answers

What morphological feature characterizes concentric hypertrophy?

Lumen of the chamber is smaller than usual Signup and view all the answers

What is a hallmark clinical feature of constrictive pericarditis?

Diastolic heart failure Signup and view all the answers

Which of the following can cause cardiac dilatation?

Valvular incompetence Signup and view all the answers

Which of the following conditions does NOT typically lead to hypertrophy without dilatation?

Mitral insufficiency Signup and view all the answers

Which condition is associated with increased cardiac output that can lead to hypertrophy?

Paget's disease of the bone Signup and view all the answers

Hypertrophy with dilatation can occur as a compensatory mechanism due to which of the following?

Thyrotoxicosis Signup and view all the answers

Which type of hypertrophy is characterized by an increase in the length of myocardial fibers?

Eccentric hypertrophy Signup and view all the answers

What is the minimum thickness of the left ventricular wall that indicates an increase in heart weight?

15 mm Signup and view all the answers

Which of the following is a common cause of forward heart failure?

Dilated Cardiomyopathy Signup and view all the answers

What cardiac symptom is primarily associated with backward heart failure?

Accumulation of fluid in the lungs Signup and view all the answers

Which physical examination finding is indicative of forward heart failure?

Gallop rhythm Signup and view all the answers

What happens in acute left ventricular failure that leads to dyspnoea?

Fluid accumulation Signup and view all the answers

Chronic left-sided cardiac failure causes what characteristic change in the lungs?

Congestion and discoloration Signup and view all the answers

What is a common clinical feature observed during forward heart failure assessment?

Hypothermia Signup and view all the answers

Which of the following is NOT associated with backward heart failure?

Diminished cardiac output Signup and view all the answers

What is a common consequence of left atrial enlargement in hypertension?

Atrial Fibrillation Signup and view all the answers

Which of the following indicates chronic cor pulmonale?

Right ventricular wall thickness over 10 mm Signup and view all the answers

Which factor is most likely to lead to myocardial ischemia?

Coronary artery disease Signup and view all the answers

What pathological change occurs in the right ventricle during acute cor pulmonale?

Dilatation without hypertrophy Signup and view all the answers

What percentage of occlusion typically results in critical stenosis causing exertional angina?

Over 70% Signup and view all the answers

What is the main cause of progressive congestive heart failure associated with hypertension?

Ischaemic heart disease development Signup and view all the answers

Which of the following is NOT a typical cause of myocardial ischaemia?

Increased oxygen demand Signup and view all the answers

What is a potential direct consequence of chronic hypertensive heart disease?

Stroke Signup and view all the answers

What is a potential consequence of a large transmural anteroseptal infarct?

Ventricular aneurysm Signup and view all the answers

Which complication is directly linked to myocardial rupture after an MI?

Ventricular septum rupture Signup and view all the answers

In patients with ischemic cardiomyopathy, which morphological characteristic is commonly observed?

Cardiomegaly with left ventricular hypertrophy Signup and view all the answers

What is the risk associated with a mural thrombus after an AMI?

Thromboembolism Signup and view all the answers

What does reperfusion injury impact after an MI?

Infarct size and function of salvaged myocardium Signup and view all the answers

Which complication occurs 2-3 days after a transmural acute MI?

Fibrino-haemorrhagic pericarditis Signup and view all the answers

Which of the following is characterized by decreased cardiac output and increased oxygen demand?

Ventricular remodelling Signup and view all the answers

Which arrhythmia-related risk is highest after myocardial infarction?

During initial hours post-MI Signup and view all the answers

What type of inflammation is associated with the presence of Aschoff bodies in the myocardium?

Mixed mononuclear inflammatory cells Signup and view all the answers

What is the most common age group for the occurrence of rheumatic fever?

Children aged 5–15 years Signup and view all the answers

Which of the following is a characteristic feature observed in rheumatic valvulitis?

Fish mouth or button hole stenosis Signup and view all the answers

What term describes the characteristic exudate seen in rheumatic pericarditis?

Fibrinous/serofibrinous exudate Signup and view all the answers

Which organ is primarily affected in rheumatic heart disease?

Heart Signup and view all the answers

Which type of arthritis is commonly associated with rheumatic fever?

Migratory polyarthritis Signup and view all the answers

What kind of cells are referred to as Anitschkow myocytes or caterpillar cells?

Activated macrophages Signup and view all the answers

What causes the progressive fibrosis in rheumatic heart disease?

Repeated attacks of rheumatic fever Signup and view all the answers

Study Notes

Integrated Microbiology And Pathology (YIHS300)

Course offered by the Nelson Mandela University Faculty of Health Sciences Medical School in 2024
Focuses on Cardiovascular diseases and Systemic pathology

Topic Overview

Cardiac pathology is a leading cause of morbidity and mortality.
The lecture series delves into diseases of the heart, categorized by the heart layer (endocardium, myocardium, or pericardium).
The disease progression often leads to cardiac failure.
Congenital heart disorders and cardiac neoplasms are also briefly reviewed.

Learning Outcomes (Heart Failure)

Understand right heart failure regarding pathogenesis, clinical features, pathologic features, and short/long-term consequences.
Discuss left heart failure in the same manner as right heart failure.
Compare and contrast left and right heart failure in terms of pathogenesis, clinical features, pathologic features, and short/long-term consequences.

Learning Outcomes (Ischemic Heart Disease)

Explain the progression of ischemic heart disease without symptoms for years.
Compare and contrast stable and unstable angina in clinical, physiologic, and morphologic terms.
Compare and contrast the features and pathophysiology of acute myocardial infarction.
Describe the spectrum of myocardial infarction changes over time.
Identify short-term and long-term complications of myocardial infarction.

Learning Outcomes (Congenital Heart Disease)

Identify and describe common forms of congenital heart disease, including clinical presentation, natural history, and long/short-term complications.
Describe genetic disorders associated with congenital heart disease.
Define left-to-right shunts, right-to-left shunts, shunt reversal, and their correlation with clinical presentation.

Learning Outcomes (Cardiac Inflammatory Conditions)

Describe major cardiac and extracardiac manifestations of rheumatic fever, encompassing its effects on the endocardium, myocardium, and pericardium.
Compare and contrast rheumatic fever and bacterial endocarditis' effects on the heart.
Describe the two major patterns of infective endocarditis and the pathologic changes seen in cardiac valves.
Discuss noninfective endocarditis's pathologic features on cardiac valves.
Describe myocarditis's clinicopathologic features and common causes along with their consequences.
Summarize pericarditis's common causes and resultant clinicopathologic features.

Learning Outcomes (Valvular Dysfunction)

Discuss the causes, clinicopathologic features, and complications associated with cardiac valvular stenosis.
Describe the etiologies, clinicopathologic features, and complications of cardiac valvular insufficiency.
Compare and contrast valvular stenosis and insufficiency.
Outline cardiac disorders that lead to valvular stenosis and insufficiency.

Learning Outcomes (Hypertension)

Describe the pathogenesis and the gross and microscopic adaptive changes in the myocardium resulting from pulmonary hypertension
Discuss the pathogenesis and the gross and microscopic adaptive changes in the myocardium resulting from systemic hypertension.
Describe mechanisms + epidemiology of primary hypertension, and discuss causes of secondary hypertension.
Compare and contrasting the pathogenesis and clinicopathologic features of primary and secondary cardiac tumors.

Learning Outcomes (Pericardial Disease)

Classify pericarditis: acute, chronic, and constrictive
Compare and contrast the clinical features of haemopericardium(acute effusion) and constrictive pericarditis.
Discuss the pathology of chronic pericarditis associated with infections like rheumatic fever and TB.
Discuss aetiopathogenesis and clinical presentations of haemopericardium (cardiac tamponade).
Describe clinicopathological features and common causes of myocarditis, and their consequences.
Compare and contrast the clinicopathologic features of dilated, restrictive, and hypertrophic cardiomyopathies.

Cardiac Failure

Heart failure arises when adaptive mechanisms fail to meet peripheral tissue demands, leading to decreased cardiac output and tissue perfusion.
Systolic heart failure manifests as reduced ejection fraction (normal 45-65%). Causes include ischemia, pressure/volume overload from hypertension or valvular disease.
Diastolic heart failure (HFPEF) occurs when the heart chambers cannot fully relax/expand and fill during diastole. This can be caused by conditions like hypertension.

Cardiac Compensation

Heart rate and dilatation (overstretching) are compensatory mechanisms that fail to compensate for high rates and overstretching.
The inability to compensate leads to heart failure.
Hypertrophy (muscle mass increase) also fails to compensate.

Compensatory Mechanisms

Compensatory enlargement in the form of cardiac hypertrophy, cardiac dilatation, or both.
Tachycardia (increased heart rate) due to activation of neurohumoral system (releasing norepinephrine, atrial natriuretic peptide, activating renin-angiotensin-aldosterone mechanism).

Aetiology of Cardiac Hypertrophy

Right ventricular hypertrophy: Pulmonary stenosis and insufficiency, Tricuspid insufficiency, Mitral stenosis and/or insufficiency, and chronic lung diseases.
Left ventricular hypertrophy: Systemic hypertension, Aortic stenosis and insufficiency, Mitral insufficiency, Coarctation of the aorta, Left ventricular hypertrophy and failure, congenital anomalies (septic defects and patent ductus arteriosus), and conditions with increased cardiac output. (thyrotoxicosis, anemia, arteriovenous fistulae.)

Causes of Cardiac Failure

Pulmonary Circulation: A low pressure system (systolic arterial pressure = 24 mmHg, pressure gradient artery/vein = 8 mmHg). Right ventricular mass and coronary blood supply.
Systemic Circulation: A high pressure system (systolic arterial pressure = 120 mmHg, pressure gradient artery/vein = 90 mmHg). Left ventricular mass and coronary blood supply.
Main causes of right ventricular failure: Conditions elsewhere in the body causing obstruction to pulmonary blood flow (e.g. lung disease, mitral, stenosis).
Main causes of left ventricular failure: Ischemic heart disease, systemic hypertension. Additional, less common causes include aortic valve disease, mitral valve incompetence, and congenital heart disease.

Pathophysiology of Symptoms and Signs

Low output to the lungs is not usually significant unless right ventricular failure is a result of left ventricular failure.
There is overfilling of the right atrium, systemic veins, and capillaries.
Chronic venous congestion and oedema also result in cyanosis.
Increased pulmonary artery pressure and congestion of pulmonary veins and capillaries cause dyspnea.
Low cardiac output leads to systemic anoxia.

Backward and Forward Heart Failure

Backward heart failure occurs when a ventricle fails to eject blood normally, increasing end-diastolic volume and pressure in the atria, which then increases pressure in the veins.
Forward heart failure is caused by diminished cardiac output resulting from impaired myocardial function(reduced systolic function), leading to cardiogenic shock. It results in diminished renal perfusion and activation of the renin-angiotensin-aldosterone system.

Dyspnea in Cardiac Failure

Acute pulmonary oedema results from fluid accumulation in the lungs, leading to dyspnea and hypoxia.
Chronic venous congestion of the lungs leads to the lungs becoming bulky, congested, and brownish in colour.

Left Sided Cardiac Failure

Clinical manifestations arise from decreased left ventricular output, resulting in fluid accumulation in the lungs.
This includes symptoms like cough, dyspnea, orthopnea, and paroxysmal nocturnal dyspnea.
Blood stasis in the left heart chambers; secondary left atrial dilation usually accompanies mitral regurg.

Congested Cardiac Failure

Congestion in the systemic venous circulation arises from right heart failure.
Reduced left ventricular output, mitral valve incompetence, and increased pulmonary vascular resistance contribute to chronic pulmonary venous congestion.
Fluid retention results in pleural effusion and ascites.

Right Sided Cardiac Failure

Right-sided heart failure is affected by upstream of right heart (due to caval and portal venous congestion/reduced cardiac output).
Blood stasis in right heart chambers, followed by engorgement of portal venous system, systemic venous system, and pleural, pericardial, and peri-toneal effusions and ascites.
Peripheral edema can affect dependent areas, worsening fluid retention, and leading to a severe, generalised form of edema (anasarca). Renal and brain complications may also arise due to decreased blood flow.

Systemic (Left-Sided) Hypertensive Heart Disease

Left ventricular hypertrophy without other cardiovascular pathology.
Hypertension in other organs like the kidney may accompany this condition.
The major feature is thickening (15mm to 20mm) in the LV wall of the heart which is symmetrical with an increase in heart mass.

Pulmonary (Right-Sided) Hypertensive Heart Disease (Cor Pulmonale)

Right-side heart disease caused by pulmonary disorders, characterized by right ventricle dilation, or hypertrophy. Occurs acutely from severe pulmonary embolism or chronically - caused by chronic lung diseases and pulmonary vessel diseases.

Myocardial Ischemia

An imbalance between myocardial supply (perfusion) and cardiac metabolic demands.
Causes of myocardial ischaemia - Reduced blood flow due to atherosclerosis, coronary artery disease, coronary emboli, myocardial vasculitis, vascular spasm, and conditions - such as anaemia - causing reduced oxygen availability in blood.
Chronic vascular occlusion, or complete blockage in one or more coronary arteries or branches, occurs in approximately >90% of patients with IHD.
Acute plaque change is a sudden alteration of a stable plaque of atherosclerosis leading to critical stenosis, through a rupture, erosion, ulceration, or deep haemorrhage and manifest as acute coronary syndromes (unstable angina, acute myocardial infarction, sudden death).

Four Common Clinical Presentations of Myocardial Ischemia

Angina Pectoris: Episodes of chest discomfort caused by transient myocardial ischaemia.
Acute Myocardial Infarction (AMI): Myocardial necrosis from prolonged ischaemia (involving anatomic regions as LAD).

Evolution of Acute Myocardial Infarction

Time sequence of onset and progression of myocardial ischemia, including onset of ATP deletion, loss of contractility, and progression of ischemia necrosis.
Progression of ischemic necrosis includes Subendocardial zone, Wavefront region, Completed infarct.

Non-transmural (Subendocardial) Infarcts

Non-transmural infarctions occur when a coronary thrombus resolves before transmural necrosis occurs, involving longer duration of severe hypotension or prolonged ischemic conditions.
The condition shows fewer chest pain signs, fewer complications, lower fatality compared to transmural infarcts.

Complications (Myocardial Infarction)

Papillary Muscle Dysfunction, Myocardial Rupture, Arrhythmias, Pericarditis, Dressler Syndrome, Mural Thrombus, Ventricular Aneurysm, Ventricular Remodelling .

Morphological Changes In Myocardial Infarction

Time sequence of macroscopic and microscopic changes during myocardial infarction.
Gross changes include various colors of the lesion and gradual transition from initial inflammation to scar tissue
Microscopic changes show necrosis, inflammatory response, and scar formation

Restoration of Tissue Perfusion

Reperfusion injury can occur after treatment. Delays in the return of function may sometimes occur due to the reperfusion process.

Chronic IHD with Heart Failure: Ischemic Cardiomyopathy

Progressive congestive heart failure (due to myocardial damage)
May show scars (healed infarcts) and mural thrombi.

Sudden Cardiac Death

Unexpected death from cardiac causes, within 1 to 24 hours.
Etiologies include arrhythmia caused by ischaemic injury, or due to dilation and alteration in heart chamber conduction systems.

Endocardial Disorders

Valvular diseases affecting left side of the heart (mitral or aortic valve, rarely combined).
Stenosis: failure of a valve to open completely during diastole, obstructing blood flow.
Insufficiency/incompetence: failure of a valve to close completely during systole, resulting in backward blood flow.
Diseases causing valve deformities - Rheumatic heart disease (RHD), Endocarditis (and complications), Myxomatous degeneration (floppy valve syndrome), and Carcinoid heart disease.

Acute Rheumatic Fever

Inflammation and Aschoff bodies in all three heart layers, causing pancarditis.
Valvular vegetations sometimes present

Rheumatic Heart Disease

Autoimmune disorder that usually follows group A beta-hemolytic streptococcal infections (e.g. tonsillitis / pharyngitis) occurring within 2-3 weeks.
Resulting inflammatory damage leads to progressive fibrosis of the endocardium and valves, largely causing chronic scarring. The heart is the primary target organ

• Cardiac Manifestations of Right Heart Disease: Pancarditis (affecting all layers of the heart). Rheumatic Endocarditis: Thickening, loss of translucency, valve leaflet cusps involvement. Rheumatic Myocarditis: Tiny pale foci of Aschoff bodies throughout the myocardium, often seen in interventricular septum, left ventricle, and left atrium. Rheumatic Pericarditis: Fibrous/serofibrinous exudate (bread and butter) appearance of the pericardium. • Extracardiac Lesions: –Migratory polyarthritis: Systemic joint pain and swelling that moves from one joint to another. –Subcutaneous nodules: Small, painless nodules on joints, tendons, ligaments, or vertebrae. –Erythema marginatum: Non-pruritic macular rash on trunk and limbs. –Sydenham chorea: Neurological disorder characterized by involuntary, purposeless movements. • Diagnostic Criteria: Presence of two or more major criteria OR one major criterion and two minor criteria.

Chronic Constrictive Pericarditis

Rare condition characterized by fibrous or fibrocalcific pericardial thickening.
Results in mechanical interference with heart function, leading to decreased cardiac output.
Often caused by longstanding conditions such as tuberculous pericarditis or purulent/haemopericarditis.

Chronic / Healed Pericarditis

Organisation of pericardial inflammation resulting in small fibrous plaques or delicate adhesions.
Usually does not affect cardiac function but can involve adhesions, obliteration of the pericardial sac and adherence with other parietal layers (mediastinal pericarditis), affecting systolic contractility + workload increment.

Cardiac Neoplasms

Primary tumours are very rare, with myxoma being the most common benign tumour.
Metastatic tumours are more common and result from haematogenous or lymphatic spread, possibly from disseminated cancers.

Myxoma

Most common primary cardiac tumour; found frequently in the left atrium.
Often single, can be multiple; polypoid, pedunculated (stemmed), and spherical, soft and hemorrhagic, resembling an organizing thrombus on the walls of the heart.
Macroscopic: Myxoid or mucoid intercellular stroma. Sparse cellularity with stellate-shaped, spindled, and polyhedral cells. Occasional multinucleate tumour giant cells.

Congenital Cardiac Disease

Anomalies in heart or great vessels, arising from embryogenesis defects between gestational weeks 3-8.
Significant anomalies may cause stillborn infants, whereas others are compatible with life, presenting in infancy or later in life.
Some include septal defects, stenotic lesions in valves and vascular pathways, outflow tract anomalies, and anomalous coronary arteries.

Reading Task

The task is a reading assignment from a specific textbook or website, requiring the student to review various categories of congenital heart diseases.

Specific Types of Infective Endocarditis

Tuberculous endocarditis: Presence of tubercles on valvular and mural endocardium.
Syphilitic endocarditis: Aortic valve incompetence.
Fungal endocarditis: Candida or Aspergillus from IV drug users or those with prosthetic valves.
Other relevant organisms - Staphylococcus aureus, Staphylococcus epidermidis, Staphylococcus viridians, Staphylococcus mutans with predisposing factors including IV drug abusers, prosthetic valves, patients with a previously damaged valve or those who have recently had a dental extraction.

Non-Rheumatic Endocarditis

Non-bacterial forms:
Thrombotic (cachectic or marantic): Sterile thrombotic vegetations on heart valves.
Atypical Verrucous (Libman-Sacks): Fibrin, platelet deposition over thrombi. Etiologies often related to underlying diseases (e.g., systemic lupus erythematosus).

Complications of Endocarditis

Cardiac complications: Valvular insufficiency/stenosis, ring abscess, suppurative pericarditis, and valvular dehiscence.
Embolic complications: Involvement of left or right sided lesions of brain, spleen, kidney (left side) or lung infarct or abscess (right side).
Renal complications: Focal or diffuse glomerulonephritis.

Prosthetic Valves

Complications: Thromboembolism, structural failure, and infective endocarditis.

Myocarditis

Inflammation of the heart muscle that can affect any age group.
Classified as:
- Myocarditis in Connective Tissue Diseases: Rheumatoid Arthritis, Systemic Lupus Erythematosus, Polyarteritis Nodosa, Dermatomyositis, and Scleroderma.
- Idiopathic (Fiedler's) Myocarditis: Often with sudden severe cardiac failure or death with no apparent cause.
- Infective (Viral Myocarditis) - Caused by viral infections such as Influenza, Poliomyelitis, Mononucleosis, Hepatitis, Smallpox, Chickenpox, Measles, Mumps, Rubella, and certain types of Viruses. Suppurative myocarditis: Caused by pyogenic bacteria from septicemia, pyaemia, or from spreading infections

Cardiomyopathy

A group of myocardial diseases of unknown cause, primarily divided into:
Idiopathic Dilated Cardiomyopathy: Dilatation of all 4 heart chambers, leading to progressive cardiac failure.
Idiopathic Restrictive Cardiomyopathy: Restriction in ventricular filling; causes reduction in ventricular volume.
Idiopathic Hypertrophic Cardiomyopathy: Cardiac enlargement with asymmetrical Hypertrophy; more prominent in the septum.

Pericardial Disorders

Pleural effusion and haemopericardium: Fluid build-up causes restricted filling when accumulation is too rapid.
Chronic Pericarditis: Fibrous or fibrocalcific pericardial thickening; results from various causes (tuberculosis, pus, or bleeding), usually from pre-existing processes
Acute Pericarditis: Inflammatory reactions due to infections (viral, bacterial), autoimmune issues, trauma, or post-surgery, accompanied by chest pain. - Serous, Fibrinous/Serofibrinous, Purulent, Hemorrhagic.

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