Tricuspid and Pulmonary Valve Diseases

Podcast

Play an AI-generated podcast conversation about this lesson

Questions and Answers

What is one effect of tricuspid stenosis or incompetence?

Increased central venous pressure (correct)

Decreased pressure in the right atrium

Cardiac depression

Left ventricular hypertrophy

Which of the following is a common cause of pulmonary stenosis?

Heart murmur

Atrial septal defect

Coronary artery disease

Rheumatic valvulitis (correct)

Which condition is associated with dilated right ventricles due to pulmonary incompetence?

Congenital heart disease

Myocardial infarction

Infective endocarditis

Mitral stenosis (correct)

Which factor is NOT commonly blamed for congenital heart diseases?

Genetic factors Signup and view all the answers

What is the primary period during which congenital heart diseases can arise due to abnormal embryogenesis?

Weeks 3 through 8 of gestation Signup and view all the answers

Which condition results in blood shunted from the left atrium to the right atrium?

Atrial septal defect Signup and view all the answers

What is a common consequence of a significant ventricular septal defect (VSD)?

Hypertrophy of the right ventricle Signup and view all the answers

Which type of congenital heart defect is characterized by a persistent opening between the pulmonary artery and aorta?

Patent ductus arteriosus Signup and view all the answers

Which sequence correctly identifies the prevalence of types of ventricular septal defects?

90% are large defects below the aortic valve Signup and view all the answers

What pathological change can occur in the right ventricle due to atrial septal defect (ASD)?

Hypertrophy and dilatation Signup and view all the answers

What major long-term risk is associated with untreated ventricular septal defect (VSD)?

Infective endocarditis Signup and view all the answers

Which of the following is a key characteristic of Fallot's tetralogy?

Right-to-left shunt Signup and view all the answers

In patent ductus arteriosus (PDA), the abnormal blood flow is primarily between which two structures?

Pulmonary artery and aorta Signup and view all the answers

What is the consequence of the ductus arteriosus failing to close after birth?

Heart failure Signup and view all the answers

Which of the following is NOT a part of the tetralogy of Fallot?

Aortic stenosis Signup and view all the answers

What is a significant consequence of right-to-left shunting in tetralogy of Fallot?

Cyanosis Signup and view all the answers

What does atherosclerosis primarily affect in the circulatory system?

Medium-sized and large arteries Signup and view all the answers

Which risk factor is commonly associated with the development of atherosclerosis?

High cholesterol levels Signup and view all the answers

What characterizes the morphological changes in atheroma development?

Patchy deposits of fatty materials Signup and view all the answers

Which of the following complications is associated with atheroma?

Decreased blood flow Signup and view all the answers

What is a potential consequence of prolonged hypoxia due to cyanosis in patients with tetralogy of Fallot?

Polycythemia Signup and view all the answers

What primarily causes the thickening and hardening of muscular arteries in atherosclerosis?

Fibrofatty plaques or atheromas in the tunica intima Signup and view all the answers

Which of the following is a non-modifiable risk factor for atherosclerosis?

Genetic abnormalities Signup and view all the answers

In the pathogenesis of atherosclerosis, which substance is primarily accumulated in the vessel wall?

Low-density lipoprotein (LDL) Signup and view all the answers

What does the term 'sclerosis' in atherosclerosis refer to?

The scarring tissue in the plaques Signup and view all the answers

What is the consequence of endothelial injury in the process of atherosclerosis?

Increased vascular permeability and leukocyte adhesion Signup and view all the answers

Which of the following describes the gross appearance of atherosclerotic lesions?

Yellow raised streaks and necrotic ulcers with rough edges Signup and view all the answers

What happens to monocytes during the progression of atherosclerosis?

They adhere to the endothelium and become macrophages Signup and view all the answers

Which of the following conditions is characterized by localized fibrofatty plaques in arteries?

Atherosclerosis Signup and view all the answers

Which components are found in atherosclerotic plaques?

Smooth muscle cells, macrophages, and T cells Signup and view all the answers

What is a significant effect of uncomplicated atheroma in large arteries?

No clinical effects Signup and view all the answers

What is a characteristic microscopic feature of cholesterol in atherosclerotic lesions?

Needle-shaped or rhombic-shaped empty spaces Signup and view all the answers

What occurs due to fragmentation of the internal elastic lamina in atherosclerosis?

Atrophy of the media opposite the atheroma Signup and view all the answers

What is the most dangerous clinical effect of atheroma?

Coronary artery thrombosis Signup and view all the answers

Which statement accurately describes the appearance of foam cells in atherosclerotic plaques?

They contain cholesterol-rich lipid cores. Signup and view all the answers

What may form as a result of advanced atheroma in the arterial wall?

Formation of an aneurysm Signup and view all the answers

What process may occur due to severe ischemia caused by atheromatous plaques?

Gangrene starting at the toes Signup and view all the answers

Study Notes

Tricuspid Valve Disease

Tricuspid stenosis, incompetence, or a combination of both have similar effects.
Pressure rises in the right atrium, causing dilation.
Central venous pressure increases, leading to systemic venous congestion and "cardiac edema".
When combined with mitral stenosis or left ventricular failure, tricuspid lesions decrease pulmonary venous congestion and pulmonary hypertension by limiting blood flow to the lungs and left side of the heart.

Pulmonary Valve Disease

Pulmonary Stenosis

Causes: Congenital, Rheumatic valvulitis, Infective endocarditis.
Effects: Right ventricular hypertrophy, Right-sided heart failure.

Pulmonary Incompetence

Causes: Functional (mitral stenosis), Congenital, Infective endocarditis.
More commonly caused by pulmonary hypertension, leading to dilation of the pulmonary artery and valve ring.
Effects: Right ventricular hypertrophy and dilation, Right-sided heart failure.

Congenital Heart Diseases

Definition: Abnormalities of the heart present at birth.
Most common among all congenital birth defects, arising from abnormal embryogenesis during gestational weeks 3 through 8.
Clinical Presentation: Ranges from severe anomalies (incompatible with life) to mild lesions causing minimal symptoms.

Etiology

The exact cause is unknown.
Potential contributing factors:
- Viral infections in the mother during the first trimester (rubella, Coxsackie virus).
- Medications or drugs (thalidomide, cortisone).
- Alcohol and/or tobacco use during pregnancy.
- Nutritional and vitamin deficiencies in pregnancy.
- Maternal diabetes
- Down syndrome, Turner syndrome, and Marfan syndrome.
- Syphilis.

Classification

Three main categories:
- Malformations with left-to-right shunt (non-cyanotic)
  - Atrial septal defect (ASD)
  - Ventricular septal defect (VSD)
  - Patent ductus arteriosus (PDA)
- Malformations with right-to-left shunt (cyanotic)
  - Fallot’s tetralogy
  - Transposition of great vessels
- Malformations that interfere with blood flow (non-cyanotic with no shunt)
  - Coarctation of the aorta
  - Aortic stenosis & incompetence
  - Mitral stenosis & incompetence
  - Pulmonary stenosis

Atrial Septal Defect (ASD)

Definition: Defect in the interatrial septum.
Even with large defects, it may have minimal impact on circulation.
Blood is oxygenated when leaving the heart.
Effects:
- Blood flows from the left to the right atrium.
- Right atrial hypertrophy and dilation.
- Right ventricular hypertrophy and dilation, leading to pulmonary congestion and pulmonary hypertension.
- Chronic pressure overload can damage the cardiac endothelium, increasing the risk of infective endocarditis.

Ventricular Septal Defect (VSD)

Definition: Defect in the interventricular septum.
Most common congenital heart anomaly (about 30% of all congenital heart diseases).
Often part of other congenital anomalies like Fallot’s tetralogy.
Types:
- Small Defect: Rare, occurs in the muscular part of the septum (10%). Cardiac hypertrophy does not occur.
- Big Defect: More common (90%), occurs in the membranous septum just below the aortic valve.
Effects:
- Blood shunts from the left ventricle to the right ventricle and pulmonary artery, causing slight enlargement.
- Right ventricular hypertrophy.
- Pulmonary artery dilation, lung congestion, and pulmonary hypertension.
- Progressive pulmonary hypertension can reverse the shunt, leading to blood flow from right to left, causing cyanosis.

Patent Ductus Arteriosus (PDA)

Definition: Persistent open duct between the pulmonary artery and aorta.
Blood flows from the aorta to the pulmonary artery.
The ductus arteriosus arises from the left pulmonary artery and joins the aorta just distal to the origin of the left subclavian artery.
During fetal life, it allows blood flow from the pulmonary artery to the aorta.
Shortly after birth, the ductus constricts and closes within 1 to 2 days, becoming a fibrous ligament (ligamentum arteriosum).
Effects:
- Blood flow from the aorta to the pulmonary artery.
- Left ventricular hypertrophy and dilation to compensate for shunted blood.
- Right ventricular hypertrophy and dilation due to increased strain.
- Lung congestion and pulmonary hypertension in chronic cases.
- Failure to close the ductus leads to heart failure.

Fallot’s Tetralogy

The most common cyanotic heart anomaly.
Components:
- Ventricular septal defect.
- Displacement of the aorta to override the VSD.
- Pulmonary stenosis (obstruction).
- Right ventricular hypertrophy.
Effects:
- Right-to-left blood shunting.
- Decreased pulmonary blood flow.
- Increased aortic blood volume.
- The aorta receives mixed oxygenated and deoxygenated blood, resulting in cyanosis.
- Cyanosis leads to polycythemia (due to hypoxia) with blood hyperviscosity and susceptibility to thrombosis.
- Clinical severity depends on the degree of pulmonary stenosis.
- Increased risk of infective endocarditis and systemic embolization.

Atherosclerosis

Definition: A common degenerative disease characterized by patchy fatty material deposits in the walls of medium-sized and large arteries, followed by fibrosis, reducing blood flow.
Thickening and hardening of large and medium-sized muscular arteries, primarily affecting the tunica intima, marked by fibrofatty plaques (atheromas).
Fatty substances, cholesterol, cellular waste products, and calcium build up in the inner lining of an artery, forming plaque.

Major Risk Factors

Non-modifiable:
- Genetic abnormalities
- Family history
- Increasing age
- Male gender
Modifiable:
- Hyperlipidemia
- Hypertension
- Cigarette smoking
- Diabetes
- Inflammation

Pathogenesis

Response to Injury Theory: Atherosclerosis is a response to endothelial injury.
Injury can be:
- Gross: Physical or chemical trauma.
- Subtle: Hypertension, diabetes, hyperlipidemia, cigarette smoking.
Steps:
1. Endothelial injury and dysfunction, leading to increased vascular permeability, leukocyte adhesion, and thrombosis.
2. Accumulation of lipoproteins (mainly LDL and oxidized forms) in the vessel wall.
3. Monocyte adhesion to the endothelium, followed by migration into the intima and transformation into macrophages and foam cells.
4. Platelet adhesion.
5. Factor release from activated platelets, macrophages, and vascular wall cells, recruiting smooth muscle cells from the media or circulating precursors.
6. Smooth muscle cell proliferation, extracellular matrix production, and recruitment of T cells.
7. Lipid accumulation both extracellularly and inside cells (macrophages and smooth muscle cells).

Gross Picture:

Yellow streaks and patches: Deposition of cholesterol in the subintimal connective tissue.
Raised white plaques or nodules: Fibrosis around deposited lipids.
Superficial atheromatous ulcers: Necrosis of the endothelium covering the lesions, having irregular outlines, sharp edges, and rough floors.
Calcification: Chalky white appearance of atheromatous nodules and ulcers due to calcium deposits.
Thrombi: Over ulcers and rough surfaces.
Media atrophy: The media opposite the lesion is thin and atrophic.
Components:
1. Smooth muscle cells, macrophages, and T cells.
2. Extracellular matrix: collagen, elastic fibers, and proteoglycans.
3. Intracellular and extracellular lipids.

Microscopic Picture:

Cholesterol deposition: Free or inside smooth muscle cells, macrophages (foam cells).
Empty spaces: Cholesterol crystals appear as needle-shaped or rhombic-shaped empty spaces in paraffin sections (dissolved).
Fibrosis and hyalinosis: Of the subintimal connective tissue around the deposited lipids.
Calcium granules: Dark blue stained calcium granules in old lesions.
Internal elastic lamina fragmentation: With media atrophy opposite the atheroma.
Stages:
- Appearance of fat in the subintimal layer, both free and inside macrophages.
- Hypertrophy and upward migration of smooth muscle fibers to the intima.
- Central fat necrosis.
- Surface fibrous cap formation.
- Process spread to the underlying media.
- Surface ulceration with thrombus formation.
- Cholesterol deposits in the central lesion.
Foam cells: Within the lipid-rich core of the atheromatous plaque.

The Fibrous Plaque

Atherosclerosis is a chronic, progressive disease that starts with the formation of fatty streaks.
Fatty streaks are early lesions that are characterized by the accumulation of lipids within the intima of the artery.
As the disease progresses, the fatty streaks develop into fibrous plaques.
These plaques are made up of a core of lipid material that is covered by a fibrous cap.

The Complicated Plaque

Fibrous plaques can become unstable over time.
This instability is due to several factors, including the accumulation of inflammatory cells and the thinning of the fibrous cap.
When a complicated plaque ruptures, it can expose the underlying lipid material to the bloodstream.
This can trigger the formation of a thrombus, which can block the artery and lead to a heart attack or stroke.

Clinical Effects

Uncomplicated atheroma of large arteries: Usually asymptomatic, minimal lumen reduction.
Advanced atheroma: Aneurysm formation can occur.
Emboli: Fragments of thrombi and atheromatous debris from ulcerated plaques can form emboli, lodging in arteries of the legs and abdominal organs.
Narrowing and occlusion of smaller arteries: Chronic ischemia or sudden occlusion due to thrombosis, leading to infarction.
Coronary artery thrombosis: A dangerous effect leading to heart attacks.
Gangrene: Severe ischemia causing gangrene starting in the toes and spreading proximally.

References:

This text is from a medical lecture, so no specific reference need to be provided. It is important to consult medical textbooks and scholarly articles for a more comprehensive understanding of the topics discussed.

Studying That Suits You

Use AI to generate personalized quizzes and flashcards to suit your learning preferences.

Description

Explore the complexities of tricuspid and pulmonary valve diseases, including stenosis and incompetence. Understand their causes, effects on heart function, and the relationship with congenital heart diseases. This quiz covers vital information that is essential for comprehending cardiac conditions and their implications.