CVS – 2019

Lipoproteins are essential for transporting lipids (fats) in the bloodstream. They are classified based on their density, which depends on the relative proportion of lipids (lower density) and proteins (higher density). The general rule is:

• More lipid → Lower density
• More protein → Higher density

The correct order of lipoproteins from lowest to highest density is:

1. Chylomicrons – Lowest density (highest lipid content, mainly triglycerides)
2. VLDL (Very-Low-Density Lipoproteins) – Higher density than chylomicrons but still lipid-rich
3. IDL (Intermediate-Density Lipoproteins) – Formed from VLDL remnants
4. LDL (Low-Density Lipoproteins) – Higher protein content, “bad cholesterol”
5. HDL (High-Density Lipoproteins) – Highest density (rich in proteins), “good cholesterol”

Correct Answer:

✅ Chylomicrons → VLDL → IDL → LDL ❌ (Correct statement)

Why the Other Options Are Incorrect:

1. “IDL, VLDL, LDL, HDL” ❌ (Incorrect)

   • IDL is denser than VLDL, so IDL cannot come before VLDL.
   • Correct order should be: Chylomicrons → VLDL → IDL → LDL → HDL

2. “HDL, Chylomicrons, LDL, VLDL” ❌ (Incorrect)

   • HDL is the most dense, so it cannot be first.
   • Chylomicrons have the lowest density, but this order places them after HDL, which is incorrect.

3. “VLDL, IDL, LDL, Chylomicrons” ❌ (Incorrect)

   • Chylomicrons should be first as they are the least dense.
   • This option incorrectly places chylomicrons after LDL, which is incorrect.

4. “LDL, HDL, Chylomicrons, VLDL” ❌ (Incorrect)

   • HDL should be last as it has the highest density.
   • Chylomicrons should be first, not after LDL.

End-Diastolic Volume (EDV) refers to the total volume of blood in the ventricles at the end of diastole (ventricular filling) and just before systole (ventricular contraction) begins. This is the maximum amount of blood in the ventricles before ejection occurs.

• EDV is measured at the beginning of the isovolumetric contraction phase, just after the AV valves close and before the semilunar valves open.
• At this point, the ventricles are fully filled, but the volume remains constant because all valves are closed.

Cardiac Cycle Breakdown:

1. Isovolumetric Contraction (EDV Present) ✅

   • Ventricles contract with no volume change because the AV valves are closed and the aortic & pulmonary valves have not opened yet.
   • EDV is measured here.

2. Period of Ejection ❌

   • Why Incorrect? Ventricular volume decreases as blood is ejected into the aorta and pulmonary artery. EDV is no longer present.

3. Isovolumetric Relaxation ❌

   • Why Incorrect? At this stage, the ventricles have already ejected blood, and the volume is now End-Systolic Volume (ESV), not EDV.

4. Period of Filling ❌

   • Why Incorrect? Ventricles are refilling with blood from the atria, but EDV has not been reached yet—it happens only at the end of diastole.

5. None of These ❌

   • Why Incorrect? EDV is clearly present during isovolumetric contraction, making this option incorrect.

The ductus arteriosus is a fetal blood vessel that connects the pulmonary artery to the descending aorta, allowing blood to bypass the non-functioning fetal lungs. It is derived from the sixth pharyngeal arch.

Developmental Origins of the Aortic Arch Derivatives:

Each pharyngeal (branchial) arch contributes to specific vascular structures:

• 1st Arch → Maxillary artery
• 2nd Arch → Stapedial and hyoid arteries
• 3rd Arch → Common carotid artery, internal carotid artery
• 4th Arch → Aortic arch (left), right subclavian artery (right)
• 5th Arch → Rudimentary or absent in humans
• 6th Arch → Ductus arteriosus (left side), Pulmonary arteries

Since the ductus arteriosus arises from the left sixth pharyngeal arch, the correct answer is “Sixth.”

Why the Other Options Are Incorrect:

1. Seventh (Incorrect)

   • The seventh intersegmental artery contributes to the development of the subclavian arteries, not the ductus arteriosus.

2. Fifth (Incorrect)

   • The fifth arch is either absent or rudimentary in humans and does not form major structures.

3. Fourth (Incorrect)

   • The fourth arch contributes to the aortic arch (left) and right subclavian artery (right), not the ductus arteriosus.

4. Second (Incorrect)

   • The second arch contributes to the stapedial and hyoid arteries, which are unrelated to the ductus arteriosus.

Lipoproteins are responsible for transporting lipids in the bloodstream. Very Low-Density Lipoprotein (VLDL) is produced by the liver and primarily carries triacylglycerols (TAGs) to tissues for energy storage or usage.

As VLDL travels through the bloodstream, lipoprotein lipase (LPL) hydrolyzes and removes triacylglycerols, converting VLDL into Intermediate-Density Lipoprotein (IDL). IDL can either be further metabolized into Low-Density Lipoprotein (LDL) or taken up by the liver.

Thus, IDL is formed when triacylglycerol is removed from VLDL.

Why the Other Options Are Incorrect:

1. Fatty Acid (Incorrect)

   • Although triacylglycerols are broken down into glycerol and free fatty acids, IDL formation is specifically due to the removal of triacylglycerol, not just individual fatty acids.

2. Cholesterol (Incorrect)

   • Cholesterol is not removed to form IDL; in fact, as VLDL loses triacylglycerols, its relative cholesterol content increases, making IDL and eventually LDL more cholesterol-rich.

3. Protein (Incorrect)

   • The protein components of lipoproteins (apolipoproteins) do not get removed during this transition. Instead, apolipoprotein composition may change, but the defining factor is triacylglycerol loss.

4. None of These (Incorrect)

   • Since triacylglycerol is the correct answer, dismissing all options would be incorrect.

Prinzmetal variant angina is a rare form of episodic chest pain caused by coronary artery vasospasm. It’s different from other types of angina because it’s:

• Not related to physical activity — can occur at rest, often at night or early morning.
• Caused by transient, sudden narrowing (spasm) of the coronary arteries, reducing blood flow to the heart muscle.
• Relieved by vasodilators like nitroglycerin and calcium channel blockers, which relax the smooth muscle of the artery walls.

On ECG during an episode, you’ll see ST-segment elevation, indicating transient transmural ischemia — but no permanent damage typically occurs unless the spasm is prolonged.

Why the Other Options Are Incorrect:

• “Its anginal attacks are related to physical activity”:
  Unlike stable angina, Prinzmetal angina is not triggered by exertion — it happens spontaneously, often at rest.

• “It is usually relieved by rest”:
  Rest doesn’t necessarily relieve Prinzmetal angina; it’s relieved by vasodilators like nitroglycerin or calcium channel blockers.

• “It is one of the common forms of episodic myocardial ischemia”:
  Prinzmetal angina is relatively rare compared to stable and unstable angina.

• “It is caused by disruption of atherosclerotic plaque”:
  This describes unstable angina or myocardial infarction (MI), where plaque rupture and thrombosis reduce blood flow — not the cause of Prinzmetal angina.

Aschoff bodies are a hallmark histological finding in rheumatic fever, particularly in the myocardium. They are granulomatous lesions that develop as part of the inflammatory response to Streptococcus pyogenes (Group A Streptococcus) infection.

• They consist of activated macrophages, called Anitschkow cells (caterpillar cells), along with lymphocytes and occasional plasma cells.
• Over time, these macrophages can fuse to form multinucleated Aschoff giant cells.
• These lesions are found primarily in the heart’s interstitial tissue, especially in the myocardium, leading to rheumatic myocarditis.

Why the Other Options Are Incorrect:

1. Basophils (Incorrect)

   • Basophils are involved in allergic reactions and do not play a role in Aschoff bodies.
   • They release histamine but are not characteristic of rheumatic fever pathology.

2. B lymphocytes (Incorrect)

   • B lymphocytes produce antibodies, but they are not the main inflammatory cells within Aschoff bodies.
   • Rheumatic fever is primarily T-cell and macrophage-mediated.

3. T lymphocytes (Incorrect)

   • Although T lymphocytes are part of the immune response in rheumatic fever, they are not the defining feature of Aschoff bodies.
   • They play a role in stimulating macrophages, but macrophages (Anitschkow cells) dominate the lesion.

4. Neutrophils (Incorrect)

   • Neutrophils are acute inflammatory cells, primarily seen in bacterial infections or early inflammatory responses.
   • Rheumatic fever is not a bacterial infection but an immune-mediated reaction, and neutrophils do not form Aschoff bodies.

The most common congenital cardiac defect is the ventricular septal defect (VSD). This condition occurs when there is an abnormal opening in the interventricular septum, allowing blood to shunt from the left ventricle to the right ventricle due to higher left-sided pressure.

Why is VSD the most common?

• VSDs account for about 25-30% of all congenital heart defects.
• They can occur alone or as part of more complex heart defects.
• Small VSDs may close spontaneously, but larger ones can cause heart failure, pulmonary hypertension, and failure to thrive if untreated.

Thus, the correct answer is:

✅ Ventricular septal defect (VSD)

Breakdown of Answer Choices:

✅ Correct Option:

• Ventricular septal defect (VSD)
  • The most common congenital heart defect.
  • Causes a left-to-right shunt, leading to increased pulmonary blood flow and potential complications like pulmonary hypertension.

🚫 Incorrect Options:

1. Patent ductus arteriosus (PDA)

   • PDA occurs when the ductus arteriosus (a fetal vessel connecting the aorta and pulmonary artery) fails to close after birth.
   • While common, it is not the most common defect—VSDs occur more frequently.
   • PDA can lead to a continuous “machine-like” murmur and left-to-right shunting.

2. Atrial septal defect (ASD)

   • ASD is a hole in the interatrial septum, leading to left-to-right shunting.
   • It is common but less frequent than VSD.
   • If left untreated, it can cause paradoxical embolism and atrial arrhythmias.

3. Tetralogy of Fallot (TOF)

   • A cyanotic congenital heart defect consisting of four abnormalities:
     1. Pulmonary stenosis
     2. Right ventricular hypertrophy
     3. Overriding aorta
     4. Ventricular septal defect
   • While it is the most common cyanotic congenital heart disease, it is not the most common overall defect.

4. Transposition of the great vessels

   • A severe congenital heart defect where the aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle.
   • This results in two separate circulations, which is incompatible with life unless another defect (e.g., VSD, ASD, or PDA) allows mixing of oxygenated and deoxygenated blood.
   • While critical, it is rarer than VSD.

Trabeculae carneae are anastomosing ridges found in the ventricles of the heart. These are irregular muscular ridges and columns on the inner surface of the right and left ventricles.

Functions of Trabeculae Carneae:

1. Prevent Suction: Their irregular surface reduces suction effects during ventricular contraction, ensuring efficient blood flow.
2. Assist in Contraction: They contribute to ventricular contraction by enhancing force distribution.
3. Conduct Electrical Impulses: Some trabeculae (like the moderator band) play a role in carrying electrical impulses from the conduction system to ventricular walls.

Why the Other Options Are Incorrect?

1. Oblique Sinus ❌

   • Why Incorrect? The oblique sinus is a pericardial space located posterior to the heart, not a muscular ridge inside the ventricles.

2. Papillary Muscles ❌

   • Why Incorrect? Papillary muscles are specialized muscles in the ventricles that attach to chordae tendineae and prevent valve prolapse during systole. They are not ridges.

3. Pectinate Muscles ❌

   • Why Incorrect? Pectinate muscles are muscular ridges found in the atria, especially the right atrium and auricles, not in the ventricles.

4. Chordae Tendineae ❌

   • Why Incorrect? Chordae tendineae are fibrous cords that connect papillary muscles to the atrioventricular (AV) valves (mitral and tricuspid valves), preventing valve prolapse. They are not ridges.

The correct answer is “Transposition of the Great Vessels (TGA).” This is a congenital heart defect in which the two major arteries leaving the heart—the pulmonary artery and the aorta—are swapped (transposed). Normally, the pulmonary artery arises from the right ventricle and the aorta arises from the left ventricle, ensuring proper oxygenation of blood. However, in TGA, these arteries are incorrectly connected, causing a serious circulation problem.

Why “Transposition of the Great Vessels” is Correct:

In TGA:

• The pulmonary artery arises from the left ventricle instead of the right.
• The aorta arises from the right ventricle instead of the left.

This means that deoxygenated blood returning from the body is pumped back to the body without getting oxygenated, while oxygenated blood from the lungs keeps recirculating to the lungs instead of reaching the body. Without an additional defect like an atrial septal defect (ASD), ventricular septal defect (VSD), or a patent ductus arteriosus (PDA) to allow mixing of oxygenated and deoxygenated blood, this condition is incompatible with life.

Why the Other Options Are Incorrect:

1. Patent Ductus Arteriosus (PDA):

   • PDA is a condition where the ductus arteriosus, a fetal blood vessel that normally closes after birth, remains open (patent).
   • This causes abnormal mixing of blood between the pulmonary artery and aorta but does not involve their transposition.
   • It does not explain the complete switch in origin of the great vessels.

2. Tetralogy of Fallot (TOF):

   • TOF is a different congenital heart defect with four components:
     1. Pulmonary stenosis (narrowing of the pulmonary outflow tract)
     2. Right ventricular hypertrophy
     3. Overriding aorta
     4. Ventricular septal defect (VSD)
   • Unlike TGA, TOF does not involve the swapping of the great vessels. Instead, it leads to cyanotic spells due to mixing of oxygenated and deoxygenated blood.

3. Coarctation of the Aorta:

   • Coarctation means narrowing of the aorta, usually near the ductus arteriosus.
   • It causes high blood pressure before the constriction and low blood pressure after it, but it does not involve the transposition of the pulmonary artery and aorta.
   • Patients with coarctation have obstructed blood flow, not an abnormal connection between the heart and great vessels.

4. None of These:

   • Since TGA is the correct condition, choosing “None of These” would be incorrect.

The infundibulum (also called the conus arteriosus) is a funnel-shaped region of the right ventricle that leads to the pulmonary valve. It is the outflow tract of the right ventricle and directs blood from the right ventricle into the pulmonary artery and then to the lungs for oxygenation.

Why the Other Options Are Incorrect:

1. Aortic valve
   The aortic valve is located at the outflow tract of the left ventricle, not the right ventricle. The left ventricular outflow tract is not referred to as the infundibulum.
2. None of these
   This option is incorrect because the infundibulum is indeed associated with the pulmonary valve.
3. Right atrioventricular valve
   The right atrioventricular valve (also called the tricuspid valve) is located between the right atrium and the right ventricle. It is not associated with the infundibulum, which is part of the right ventricular outflow tract.
4. Left atrioventricular valve
   The left atrioventricular valve (also called the mitral valve or bicuspid valve) is located between the left atrium and the left ventricle. It is not associated with the infundibulum.

A maturational crisis occurs during key developmental transitions in life when individuals face new challenges that require adaptation. These crises are normal and expected but can cause stress as individuals adjust to new roles and responsibilities.

Why “Maturational crisis” is the Correct Answer:

• It occurs at predictable life stages, such as adolescence, parenthood, retirement, or aging.
• It results from internal struggles related to identity, independence, or major life changes.
• Example: A teenager struggling with identity formation or an adult adjusting to retirement.

Why the Other Options Are Incorrect:

1. Developmental crises (Incorrect)

   • While similar, this term is less commonly used than “maturational crisis” in psychology and counseling.

2. Emergency crises (Incorrect)

   • Emergency crises are immediate, life-threatening situations (e.g., natural disasters, accidents), not predictable life transitions.

3. Situational crises (Incorrect)

   • Situational crises result from unexpected external events (e.g., job loss, divorce), while maturational crises are linked to life stage transitions.

4. None of these (Incorrect)

   • One of the given options is correct, making this answer incorrect.

Autosomal Dominant Hypercholesterolemia (ADH) is a genetic disorder characterized by high levels of low-density lipoprotein (LDL) cholesterol in the blood, leading to an increased risk of premature atherosclerosis and cardiovascular disease.

The most common genetic defects associated with autosomal dominant hypercholesterolemia involve mutations in:

1. LDL receptor (LDLR) gene → Most common cause (~85-90%)
2. Apolipoprotein B-100 (ApoB-100) gene → Defective LDL binding (~5-10%)
3. PCSK9 gene mutations (less common, ~1-3%) → Leads to reduced LDL receptor degradation

Since ApoB-100 is responsible for binding LDL to its receptor, defective ApoB-100 results in poor LDL clearance, leading to hypercholesterolemia.

Correct Answer:

✅ Apo B-100 ❌ (Correct statement)

Why the Other Options Are Incorrect:

1. “Lipoprotein lipase” ❌ (Incorrect)

   • Lipoprotein lipase (LPL) deficiency leads to hypertriglyceridemia, not hypercholesterolemia.
   • LPL deficiency is associated with Familial Chylomicronemia Syndrome (Type I Hyperlipoproteinemia, autosomal recessive).

2. “Apo B-48” ❌ (Incorrect)

   • ApoB-48 is involved in chylomicron assembly and transport and does not play a role in LDL metabolism.

3. “Apo C-2” ❌ (Incorrect)

   • ApoC-2 activates lipoprotein lipase (LPL), which is required for triglyceride breakdown.
   • ApoC-2 deficiency leads to Type I Hyperlipoproteinemia (chylomicronemia syndrome), not hypercholesterolemia.

4. “Apo E-2” ❌ (Incorrect)

   • ApoE-2 mutations are associated with Type III Hyperlipoproteinemia (Familial Dysbetalipoproteinemia).
   • This leads to increased chylomicron remnants and IDL, but not primarily LDL-related hypercholesterolemia.

The second heart sound (S₂) is produced by the sudden closure of the semilunar valves (aortic and pulmonary valves) at the end of systole. This closure prevents the backflow of blood from the aorta and pulmonary artery into the ventricles as the heart transitions from systole (contraction) to diastole (relaxation).

The correct answer is:

✅ Semilunar valve at the end of systole

Breakdown of Answer Choices:

✅ Correct Option:

• Semilunar valve at the end of systole
  • The second heart sound (S₂) occurs at the end of ventricular systole when the aortic and pulmonary valves close.
  • This marks the beginning of diastole, preventing the backflow of blood into the ventricles.
  • S₂ has two components:
    • Aortic valve closure (A₂) – occurs slightly earlier
    • Pulmonary valve closure (P₂) – occurs slightly later

🚫 Incorrect Options:

1. Pulmonary valve at the beginning of sinoatrial node action potential

   • Incorrect because the SA node initiates the electrical impulse but does not directly cause heart sounds.
   • The pulmonary valve closes at the end of systole, not during SA node activation.

2. Pulmonary valve in the middle of systole

   • Incorrect because the pulmonary valve remains open in mid-systole to allow blood ejection into the pulmonary artery.

3. Aortic valve in the middle of systole

   • Incorrect because the aortic valve is open in mid-systole to allow blood ejection into the aorta.

4. Semilunar valve at the beginning of systole

   • Incorrect because at the beginning of systole, the semilunar valves are opening, not closing.
   • The first heart sound (S₁) occurs at the beginning of systole due to AV valve closure (mitral and tricuspid valves).

Elastic arteries, such as the aorta and pulmonary arteries, are specialized for withstanding high-pressure blood flow. Their structure includes three primary layers:

1. Tunica intima – The innermost layer, consisting of an endothelium (simple squamous epithelium), a subendothelial layer, and an internal elastic lamina (IEL).
2. Tunica media – The thickest layer, composed of fenestrated elastic membranes (elastin sheets), smooth muscle cells, and collagen. This elastic structure allows the artery to stretch and recoil with each heartbeat.
3. Tunica adventitia – The outermost layer, containing connective tissue, vasa vasorum (small blood vessels that supply large arteries), and nerves.

Correct Answer: Presence of pericytes in tunica media

Pericytes are contractile cells that are typically found in capillaries and post-capillary venules, where they provide structural support and regulate permeability. They are not found in the tunica media of elastic arteries, which instead consists of smooth muscle cells and fenestrated elastic membranes.

Why the Other Options Are Correct Components of an Elastic Artery?

1. Presence of fenestrated elastic membrane in tunica media ✅

   • Elastic arteries have multiple fenestrated elastic membranes in their tunica media. These allow for the diffusion of nutrients and oxygen to smooth muscle cells deep within the wall.

2. Presence of an internal elastic lamina ✅

   • The internal elastic lamina (IEL) is a distinct, wavy layer of elastin that separates the tunica intima from the tunica media. It is present in all arteries but is more prominent in muscular arteries.

3. Presence of tunica intima ✅

   • Like all blood vessels, elastic arteries have a tunica intima, which includes an endothelial layer that lines the lumen.

4. Presence of connective tissue ✅

   • The tunica adventitia contains connective tissue (mostly collagen and elastic fibers), which provides structural support and elasticity to the artery.

Apolipoproteins (Apo) are proteins that serve as structural components of lipoproteins and play a crucial role in lipid transport and metabolism.

Apolipoprotein B-100 (ApoB-100) is a key structural and functional protein found on certain lipoproteins. It plays a significant role in:

• Lipid transport in the blood
• Recognition by LDL receptors (for cholesterol uptake into cells)
• Metabolism of lipoproteins

Lipoproteins Containing ApoB-100:

1. Very-Low-Density Lipoproteins (VLDL) – Transport triglycerides from the liver to peripheral tissues.
2. Intermediate-Density Lipoproteins (IDL) – Transient particles derived from VLDL.
3. Low-Density Lipoproteins (LDL) – “Bad cholesterol,” delivers cholesterol to tissues.

Since ApoB-100 is found on both LDL and VLDL, the correct answer is:

Correct Answer:

✅ Low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) ❌ (Correct statement)

Why the Other Options Are Incorrect:

1. “High-density lipoprotein (HDL)” ❌ (Incorrect)

   • HDL contains ApoA-I, ApoA-II, and ApoC, not ApoB-100.

2. “Chylomicrons” ❌ (Incorrect)

   • Chylomicrons contain ApoB-48, not ApoB-100.
   • ApoB-48 is essential for intestinal lipid transport.

3. “Low-density lipoprotein (LDL)” ❌ (Partially Correct)

   • LDL does contain ApoB-100, but this answer is incomplete because VLDL also contains ApoB-100.

4. “Fatty acids” ❌ (Incorrect)

   • Free fatty acids are not lipoproteins and do not have apolipoproteins.

Stable angina, also called typical angina pectoris, is the most common type of angina and occurs when the myocardial oxygen demand exceeds supply due to fixed atherosclerotic narrowing of the coronary arteries.

• Symptoms: Chest pain or discomfort, often described as pressure or tightness, that arises with exertion or stress and is relieved by rest or nitroglycerin.
• Pathophysiology: Caused by fixed coronary artery stenosis, leading to transient myocardial ischemia.
• EKG findings: ST-segment depression during episodes of chest pain (indicating subendocardial ischemia).

Why the Other Options Are Incorrect:

• Unstable angina: This is a more severe and unpredictable form of angina, occurring at rest or with minimal exertion and not relieved by rest. It’s part of the acute coronary syndrome (ACS) spectrum.
• Crescendo angina: A worsening pattern of angina where the frequency, duration, and severity of attacks increase — often a feature of unstable angina.
• Prinzmetal angina (Variant angina): This is caused by coronary artery vasospasm rather than atherosclerosis and often occurs at rest. ST-segment elevation is seen during episodes.
• Variant angina: Another term for Prinzmetal angina, characterized by transient coronary vasospasm leading to chest pain at rest.

The fibrous pericardium is the outermost layer of the pericardium, which encloses the heart. It is a tough, inelastic connective tissue layer that serves to protect the heart and anchor it in place within the thoracic cavity.

Key Points About the Fibrous Pericardium:

• It is NOT attached to the heart itself but instead surrounds it.
• It is firmly attached to surrounding structures for support:
  • Inferiorly: Anchored to the central tendon of the diaphragm, helping stabilize the heart during respiration.
  • Superiorly: Continuous with the adventitia of the great vessels (aorta, pulmonary trunk, superior vena cava).
  • Anteriorly: Attached to the posterior surface of the sternum via sternopericardial ligaments.

Since the fibrous pericardium does not directly attach to any chamber of the heart, the correct answer is:
✅ “Is not attached to any part of the heart.”

Why the Other Options Are Incorrect:

1. Left Atrium (Incorrect)

   • The left atrium is in direct contact with the serous pericardium but not the fibrous pericardium.
   • The posterior part of the left atrium is related to the esophagus, not the fibrous pericardium.

2. Left Ventricle (Incorrect)

   • The left ventricle is enclosed within the pericardium but is not directly attached to the fibrous pericardium.

3. Right Ventricle (Incorrect)

   • The anterior surface of the right ventricle lies closest to the fibrous pericardium, but it is not structurally attached to it.

4. Right Atrium (Incorrect)

   • The right atrium is also enclosed within the pericardial sac but does not have a direct attachment to the fibrous pericardium.

Aspartate transaminase (AST) and alanine transaminase (ALT) are key liver enzymes that play a crucial role in amino acid metabolism. They are released into the bloodstream when liver cells are damaged, making them important biomarkers for liver disease.

• ALT (Alanine transaminase) is more specific to liver damage, as it is predominantly found in hepatocytes.
• AST (Aspartate transaminase) is also present in the liver but can be found in other tissues such as the heart and muscles.
• AST/ALT ratio can help differentiate liver conditions:
  • ALT > AST → Suggests viral hepatitis or fatty liver disease (NAFLD).
  • AST > ALT (typically AST:ALT > 2:1) → Suggests alcoholic liver disease.
  • Very high levels (>1000 U/L) → Suggest acute liver failure, ischemic hepatitis, or severe toxic liver injury.

Since both AST and ALT levels rise significantly in liver disease, this is the most appropriate answer.

Why the Other Options Are Incorrect:

❌ Infection

• While some viral infections (e.g., hepatitis A, B, C, D, E) can elevate AST and ALT, infection alone (e.g., bacterial or non-hepatic viral infections) does not typically cause transaminase elevation.

❌ Myocardial infarction (MI)

• AST can be elevated in MI because it is found in cardiac muscle, but ALT is not significantly increased in MI.
• For cardiac injury, troponins (cTnI, cTnT) and creatine kinase-MB (CK-MB) are more specific markers than AST.

❌ Inflammation

• General inflammation (such as in infections or autoimmune conditions) does not necessarily raise AST and ALT unless the liver is involved.
• Specific liver inflammation (hepatitis) can cause enzyme elevation, but the term “inflammation” alone is too broad.

❌ Trauma

• Severe trauma (especially to muscle) can elevate AST because AST is found in skeletal muscle, but ALT is primarily a liver enzyme.
• Trauma without liver injury does not usually cause significant ALT elevation.

During embryonic development, the cardinal venous system plays a crucial role in forming the major veins of the body.

Development of the Venous System:

• The anterior cardinal veins are responsible for draining blood from the head, neck, and upper limbs.
• The right and left anterior cardinal veins initially run separately but later connect via an anastomosis.
• This anastomosis between the right and left anterior cardinal veins ultimately forms the brachiocephalic vein.

Formation of Major Veins:

• The right brachiocephalic vein is derived from the right anterior cardinal vein.
• The left brachiocephalic vein forms from the anastomosis between the right and left anterior cardinal veins.
• The superior vena cava (SVC) is later formed by the merging of the right brachiocephalic vein and the right common cardinal vein.

Thus, the correct answer is the brachiocephalic vein because it originates from the anastomosis of the right and left anterior cardinal veins.

Why the Other Options Are Incorrect:

1. External iliac vein (Incorrect)

   • The external iliac vein is part of the lower limb venous system and develops from the posterior cardinal veins, not the anterior cardinal veins.

2. All of these (Incorrect)

   • Only the brachiocephalic vein is formed from the anastomosis of the anterior cardinal veins.
   • The other veins listed have different embryological origins.

3. Popliteal vein (Incorrect)

   • The popliteal vein is found in the lower limb and forms from the posterior cardinal veins, not the anterior cardinal veins.

4. Digital palmar veins (Incorrect)

   • The digital palmar veins are small veins in the hand, which develop from the venous plexuses of the limb buds, not from the anterior cardinal veins.

The internal elastic lamina is a fenestrated sheet of elastic material that separates the tunica intima from the tunica media in blood vessels. It is most clearly seen in muscular arteries (also called distributing arteries), such as the radial or femoral arteries. Muscular arteries have a well-defined internal elastic lamina because they need to withstand and regulate high pressure and blood flow.

Why the Other Options Are Incorrect:

1. Aorta
   The aorta is an elastic artery and has multiple elastic laminae throughout its tunica media, but the internal elastic lamina is less distinct compared to muscular arteries.
2. Inferior vena cava
   The inferior vena cava is a large vein and does not have a prominent internal elastic lamina. Veins generally have thinner walls and less elastic tissue compared to arteries.
3. Arterioles
   Arterioles have a very thin internal elastic lamina, which may be absent in smaller arterioles. Their walls are primarily composed of smooth muscle.
4. Medium-sized vein
   Medium-sized veins, like other veins, lack a prominent internal elastic lamina. Their walls are thinner and contain less elastic tissue compared to arteries.

Atherosclerosis is a chronic, progressive disease that primarily affects the intima of blood vessels. It leads to plaque formation, vascular remodeling, and reduced elasticity of the arteries. The changes in the vessel wall include intimal thickening, smooth muscle proliferation, and inflammation, but the adventitia does not disappear.

The correct answer is:

✅ Disappearance of adventitia (This is NOT true)

Breakdown of Answer Choices:

🚫 Incorrect Options (True Statements):

1. Focal thickening of intima ✅ (True)

   • One of the hallmarks of atherosclerosis is intimal thickening due to the accumulation of lipids, inflammatory cells, and fibrous tissue.
   • Over time, this contributes to plaque formation and vascular narrowing.

2. Increase in concentric smooth muscles of media ✅ (True)

   • Smooth muscle cells proliferate in the media due to the release of growth factors such as platelet-derived growth factor (PDGF).
   • This leads to arterial stiffness and loss of compliance.

🚫 Incorrect Options:

3. None of these ❌ (Incorrect)

   • Since one of the statements is false (disappearance of adventitia), this option is incorrect.

4. All of these ❌ (Incorrect)

   • Since not all statements are true, this option is incorrect.

✅ Correct Option (NOT True Statement):

• Disappearance of adventitia ❌ (False)
  • The adventitia does not disappear in chronic atherosclerosis.
  • Instead, it may undergo fibrosis and inflammation, contributing to vessel remodeling.

Cor pulmonale is right-sided heart failure that occurs secondary to lung disease. It results from increased pressure in the pulmonary arteries (pulmonary hypertension), which overloads the right ventricle, leading to hypertrophy and eventual failure.

• Pulmonary hypertension: A direct cause of cor pulmonale, as it increases the afterload on the right ventricle.
• Chronic altitude sickness: At high altitudes, hypoxia-induced vasoconstriction raises pulmonary artery pressure, contributing to right ventricular strain.
• Chronic obstructive pulmonary disease (COPD): One of the most common causes of cor pulmonale due to chronic hypoxia and destruction of pulmonary capillary beds, leading to pulmonary hypertension.
• Kyphoscoliosis: A chest wall deformity that restricts lung expansion, leading to chronic hypoxemia and increased pulmonary vascular resistance, eventually resulting in cor pulmonale.

Why “Metabolic alkalosis” is incorrect:

• Metabolic alkalosis is a systemic acid-base disturbance caused by loss of acid (like vomiting) or bicarbonate retention.
• It does not affect the pulmonary vasculature directly and therefore does not lead to cor pulmonale.

Cardiac output (CO) is the amount of blood the heart pumps per minute, calculated using the formula:

CO=Heart Rate (HR)×Stroke Volume (SV)CO = \text{Heart Rate (HR)} \times \text{Stroke Volume (SV)}CO=Heart Rate (HR)×Stroke Volume (SV)

An increase in certain factors can negatively impact this equation, leading to decreased cardiac output.

The correct answer is:

✅ Heart rate (when excessively high)

Breakdown of Answer Choices:

✅ Correct Option:

• Heart rate
  • If heart rate increases too much (severe tachycardia, >180 bpm), the heart does not have enough time to fill properly between beats.
  • This leads to a decrease in stroke volume, which in turn reduces cardiac output despite the higher heart rate.

🚫 Incorrect Options:

1. Blood pressure

   • High blood pressure (hypertension) increases afterload, making the heart work harder, but it does not necessarily decrease cardiac output unless it leads to heart failure.

2. None of these

   • Incorrect because an excessively high heart rate can reduce cardiac output.

3. Blood volume

   • Increased blood volume usually raises venous return, which increases stroke volume and cardiac output unless the heart is failing.

4. Stroke volume

   • If stroke volume increases, cardiac output also increases, so this answer is incorrect.

During embryonic development, the venous system of the embryo undergoes significant remodeling to form the major veins of the adult circulatory system.

• The right anterior cardinal vein and the right common cardinal vein merge to form the right-sided venous drainage system.
• These two veins ultimately contribute to the formation of the superior vena cava (SVC), which is responsible for draining deoxygenated blood from the upper body into the right atrium of the heart.

Thus, the superior vena cava is primarily derived from the right anterior cardinal vein and the right common cardinal vein.

Why the Other Options Are Incorrect:

❌ Sinus venosus

• The sinus venosus is a primitive venous structure in the embryonic heart that receives blood from the cardinal, umbilical, and vitelline veins.
• It later contributes to the development of the right atrium, SA node, and part of the vena cava, but it is not directly formed by the right anterior and right common cardinal veins.

❌ Right brachiocephalic vein

• The right brachiocephalic vein forms from the right anterior cardinal vein, but it does not involve the right common cardinal vein.
• Instead, it is a part of the venous drainage system that leads into the superior vena cava.

❌ Left brachiocephalic vein

• The left brachiocephalic vein forms from the anastomosis of the left and right anterior cardinal veins.
• It is not derived from the right common cardinal vein, so this option is incorrect.

❌ Ductus venosus

• The ductus venosus is a fetal circulatory structure that shunts oxygenated blood from the umbilical vein directly to the inferior vena cava (IVC), bypassing the liver.
• It is not related to the formation of the superior vena cava and is derived from a different embryological pathway.

The P wave in an electrocardiogram (ECG) represents atrial depolarization, which occurs before atrial contraction. This is the correct answer because depolarization is the electrical event that triggers muscle contraction. In the heart, electrical impulses originate from the sinoatrial (SA) node, spreading through the atria and causing them to depolarize. This depolarization generates the P wave and is immediately followed by atrial contraction, which helps push blood into the ventricles.

Breakdown of Answer Choices:

✅ Correct Option:

• Atrial depolarization before atrial contraction begins
  • Depolarization refers to the change in electrical charge that prepares the heart muscle for contraction.
  • The P wave represents the depolarization of the atria.
  • This occurs just before the mechanical contraction of the atria, which helps in ventricular filling.

🚫 Incorrect Options:

1. Ventricular repolarization before ventricular relaxation

   • Ventricular repolarization corresponds to the T wave in the ECG, not the P wave.
   • Repolarization is the process by which the heart muscle cells reset their electrical charge to prepare for the next beat.
   • This occurs after contraction, not before it.

2. Atrial repolarization before sinoatrial node contracts

   • Atrial repolarization happens, but it is not represented clearly on the ECG because it occurs during the QRS complex (ventricular depolarization).
   • The SA node initiates depolarization, so it cannot contract after repolarization.

3. Ventricular depolarization before ventricular contraction

   • Ventricular depolarization is represented by the QRS complex, not the P wave.
   • It triggers ventricular contraction, but this happens later in the cardiac cycle.

4. Atrial repolarization before atrial contraction begins

   • This is incorrect because repolarization occurs after contraction, not before it.
   • Atria must depolarize first (P wave), then contract, and finally repolarize.

Cyanosis is a bluish discoloration of the skin and mucous membranes caused by an increased concentration of deoxygenated hemoglobin (Hb) in the blood. It occurs when the oxygen saturation of hemoglobin drops below normal levels, leading to a darker color of the blood, which gives the skin a blue or purplish hue.

Types of Cyanosis:

There are two primary types of cyanosis:

1. Central Cyanosis – Due to arterial blood desaturation (low oxygen levels in the arterial blood). It occurs in conditions such as:

   • Congenital heart diseases (e.g., Tetralogy of Fallot)
   • Respiratory failure (e.g., COPD, pulmonary edema)
   • High-altitude sickness
   • Severe anemia with extremely low oxygen-carrying capacity

2. Peripheral Cyanosis – Due to impaired blood circulation or excessive oxygen extraction by tissues. It occurs in conditions such as:

   • Cold exposure (vasoconstriction)
   • Shock (reduced perfusion)
   • Severe heart failure (poor systemic circulation)

Correct Answer:

✅ Increased amount of deoxygenated hemoglobin ❌ (Correct statement)

Why the Other Options Are Incorrect:

1. “Decreased amount of hemoglobin” ❌ (Incorrect)

   • A low hemoglobin level (as in anemia) does not directly cause cyanosis because cyanosis depends on the concentration of deoxygenated hemoglobin, not the absolute amount of hemoglobin.
   • In fact, severe anemia can prevent cyanosis from occurring, even in cases of hypoxia, because there isn’t enough hemoglobin to become deoxygenated.

2. “Increased amount of oxygen” ❌ (Incorrect)

   • If there is more oxygen in the blood, this would lead to better oxygenation, reducing the risk of cyanosis rather than causing it.

3. “Increased amount of carbon dioxide” ❌ (Incorrect)

   • High levels of carbon dioxide (CO₂), a condition called hypercapnia, can cause respiratory acidosis and breathing difficulties, but it does not directly cause cyanosis. Cyanosis is linked to oxygenation, not carbon dioxide levels.

4. “None of these” ❌ (Incorrect)

   • The correct cause of cyanosis is increased deoxygenated hemoglobin, so this option is incorrect.

Lactic acid is a key metabolite that functions as a localized vasodilator, particularly in active tissues such as exercising muscles. When metabolic demand increases, the accumulation of lactic acid lowers the pH, leading to vasodilation to improve blood flow and oxygen delivery.

Mechanism of Vasodilation by Lactic Acid:

1. During intense activity, muscles generate ATP anaerobically, producing lactic acid as a byproduct.
2. Lactic acid dissociates into lactate and hydrogen ions (H⁺), lowering pH.
3. Low pH triggers vasodilation by acting on vascular smooth muscle cells, increasing local blood flow.
4. This helps in oxygen delivery and removal of metabolic waste, preventing muscle fatigue.

Clinical Relevance:

• This local metabolic control ensures adequate perfusion in tissues with high oxygen demand, such as exercising skeletal muscle and cardiac muscle.
• Lactic acid buildup in ischemic conditions (e.g., angina, peripheral artery disease) also triggers compensatory vasodilation to increase blood supply.

Why the Other Options Are Incorrect:

❌ None of these

• Incorrect, because lactic acid is a known metabolic vasodilator.

❌ Increased pH

• Incorrect, because an increase in pH (alkalosis) usually causes vasoconstriction, not vasodilation.
• Acidosis (low pH) is associated with vasodilation.

❌ Increased oxygen

• Incorrect, because oxygen causes vasoconstriction in many vascular beds.
• In systemic circulation, low oxygen (hypoxia) leads to vasodilation, while in pulmonary circulation, high oxygen causes vasoconstriction (opposite effect).

❌ Decreased carbon dioxide

• Incorrect, because CO₂ is a potent vasodilator (especially in cerebral circulation).
• Decreased CO₂ (hypocapnia) leads to vasoconstriction, reducing blood flow (e.g., in hyperventilation-induced dizziness).

Cardiac and skeletal muscle share several structural and functional characteristics, but one key similarity is their resting membrane potential.

Resting Membrane Potential in Cardiac and Skeletal Muscle:

• Both cardiac and skeletal muscle cells have a negative resting membrane potential, typically around -85 mV to -90 mV in skeletal muscle and approximately -85 mV in cardiac muscle.
• This potential is maintained by the sodium-potassium (Na⁺/K⁺) pump, which keeps more sodium (Na⁺) outside and more potassium (K⁺) inside the cell.
• A stable resting potential is crucial for both muscle types, allowing them to generate action potentials and contract when stimulated.

Since both cardiac and skeletal muscle maintain a resting membrane potential, this is the correct answer.

Why the Other Options Are Incorrect:

1. Length of Muscle Fibers (Incorrect)

   • Skeletal muscle fibers are much longer (up to several centimeters), while cardiac muscle fibers are shorter and branched.

2. Rhythmicity (Incorrect)

   • Cardiac muscle has intrinsic rhythmicity due to pacemaker cells in the SA node, while skeletal muscle does not contract rhythmically on its own and requires neural stimulation.

3. Plateau (Incorrect)

   • Cardiac muscle has a plateau phase in the action potential (due to slow Ca²⁺ influx), while skeletal muscle action potentials lack a plateau phase.

4. Refractory Period (Incorrect)

   • Cardiac muscle has a longer refractory period to prevent tetanic contractions, whereas skeletal muscle has a shorter refractory period, allowing for summation and tetanus.

The pulmonary veins are not associated with the right atrium. Instead, they are directly connected to the left atrium. Here’s why:

• Function of Pulmonary Veins:
  The pulmonary veins carry oxygenated blood from the lungs to the left atrium. This is a critical part of the systemic circulation, ensuring that oxygen-rich blood is pumped into the left ventricle and then distributed to the rest of the body.
• Right Atrium Anatomy:
  The right atrium receives deoxygenated blood from the body via the superior vena cava and inferior vena cava, as well as from the heart itself via the coronary sinus. The pulmonary veins have no role in the right atrium’s function or anatomy.

Why the Other Options Are Appropriate:

1. Superior vena cava opening:
   The superior vena cava drains deoxygenated blood from the upper half of the body (head, neck, arms, and chest) into the right atrium. This is a correct association with the right atrium.
2. Sinus venorum:
   The sinus venarum is the smooth-walled posterior part of the right atrium. It receives the openings of the superior vena cava, inferior vena cava, and coronary sinus. This is a correct anatomical feature of the right atrium.
3. Coronary sinus opening:
   The coronary sinus collects deoxygenated blood from the heart muscle (myocardium) and drains it into the right atrium. This is a correct association with the right atrium.
4. Inferior vena cava opening:
   The inferior vena cava drains deoxygenated blood from the lower half of the body (abdomen, pelvis, and legs) into the right atrium. This is a correct association with the right atrium.

Paroxysmal tachycardia refers to sudden episodes of rapid heart rate that begin and end abruptly. When the origin of the abnormal rhythm is above the ventricles (i.e., in the atria or the atrioventricular (AV) node), it is called supraventricular tachycardia (SVT).

The term supraventricular literally means “above the ventricles”, meaning it originates in the atria or AV node, but not in the ventricles.

The two main types of SVT are:

1. Atrial Tachycardia (AT) – Originates from an ectopic focus in the atria, leading to rapid atrial depolarization independent of the SA node.
2. Atrioventricular (AV) Nodal Reentrant Tachycardia (AVNRT) – The most common type of SVT, caused by re-entry circuits within or near the AV node.

Since both atrial tachycardia and AV nodal tachycardia are categorized as supraventricular tachycardias, the correct choice is:
✅ Atrial and A-V nodal

Why the Other Options Are Incorrect:

❌ “Atrial”

• Partially correct, as atrial tachycardia is an SVT, but this answer excludes AV nodal tachycardia, which is also a type of SVT.

❌ “A-V nodal”

• Partially correct, as AV nodal reentrant tachycardia (AVNRT) is an SVT, but this answer excludes atrial tachycardia, which is also a type of SVT.

❌ “Ventricular”

• Incorrect, because ventricular tachycardia (VT) originates from the ventricles, not from the atria or AV node, meaning it is not supraventricular.
• Ventricular tachycardia is more dangerous and can lead to ventricular fibrillation.

❌ “Atrial and ventricular”

• Incorrect, because while atrial tachycardia is an SVT, ventricular tachycardia is not.
• SVTs originate above the ventricles, while ventricular tachycardia originates within the ventricular myocardium.

The fossa ovalis is a depression in the interatrial septum of the right atrium. It represents the remnant of the foramen ovale, an opening in the fetal heart that allows blood to bypass the non-functioning fetal lungs. After birth, the foramen ovale normally closes, leaving behind the fossa ovalis.

• The upper border of the fossa ovalis is a raised ridge called the limbus of the fossa ovalis. This structure marks the edge of the foramen ovale in the fetal heart.
• The limbus is formed by a part of the septum secundum, a structure involved in fetal heart development.

Why the Other Options Are Incorrect:

1. Thebesian valves are present (Incorrect)

   • The Thebesian valve is a small fold of tissue guarding the coronary sinus opening, not related to the fossa ovalis.
   • The coronary sinus is responsible for draining venous blood from the heart muscle into the right atrium.

2. Lies anterior to atrium proper (Incorrect)

   • The fossa ovalis is actually located in the interatrial septum, which is a medial structure in the right atrium, not anterior to the atrium proper.

3. Eustachian valve is present (Incorrect)

   • The Eustachian valve is a remnant of a fetal structure that directs blood flow from the inferior vena cava (IVC) toward the foramen ovale in fetal circulation.
   • It is present near the IVC opening in the right atrium, not in relation to the fossa ovalis.

4. None of These (Incorrect)

   • Since the correct answer is the upper border of the fossa is called the limbus of fossa ovalis, dismissing all options would be incorrect.

The venous system of the lower limb is divided into superficial and deep veins. Deep veins accompany arteries and are responsible for returning oxygen-depleted blood to the heart.

The deep veins of the lower limb include:

1. Anterior tibial vein – Drains blood from the anterior compartment of the leg.
2. Popliteal vein – Formed by the union of the anterior and posterior tibial veins, located behind the knee.
3. Femoral vein – Continuation of the popliteal vein, runs through the thigh.
4. External iliac vein – Formed by the continuation of the femoral vein, drains into the common iliac vein.

Since all the options listed are deep veins of the lower limb, the correct answer is “All of these.”

Why the Other Options Are Correct:

1. External iliac vein (Correct – Deep Vein)

   • This is a proximal deep vein that forms when the femoral vein passes under the inguinal ligament.
   • It ultimately drains into the common iliac vein.

2. Popliteal vein (Correct – Deep Vein)

   • It forms from the merging of the tibial veins behind the knee.
   • It continues as the femoral vein as it ascends.

3. Femoral vein (Correct – Deep Vein)

   • This is the main deep vein of the thigh, receiving blood from the popliteal vein and smaller deep veins.
   • It passes into the pelvis to become the external iliac vein.

4. Anterior tibial vein (Correct – Deep Vein)

   • Runs alongside the anterior tibial artery, draining blood from the anterior leg muscles.
   • Joins the posterior tibial vein to form the popliteal vein.

Since all these veins belong to the deep venous system, the correct answer is: “All of these.”

The isovolumetric contraction phase is an essential part of the cardiac cycle that occurs at the beginning of ventricular systole (contraction). During this phase:

• The ventricles contract, increasing pressure inside them.
• The atrioventricular (AV) valves (mitral and tricuspid valves) close to prevent backflow into the atria, producing the first heart sound (S₁).
• The semilunar valves (aortic and pulmonary valves) remain closed because ventricular pressure has not yet exceeded the pressure in the aorta and pulmonary artery.
• Since all four valves are closed, no blood enters or exits the ventricles, making this phase isovolumetric (constant volume).

Thus, the correct answer is:

✅ Ventricles contract but no emptying occurs

Breakdown of Answer Choices:

✅ Correct Option:

• Ventricles contract but no emptying occurs
  • Ventricular contraction begins, but blood is not yet ejected because the pressure inside the ventricles is still lower than the pressure in the aorta and pulmonary artery.
  • Since both the AV and semilunar valves are closed, ventricular volume remains constant.

🚫 Incorrect Options:

1. Atrioventricular valves are open

   • Incorrect because the AV valves close at the start of ventricular systole to prevent blood from flowing back into the atria.
   • The closing of the AV valves produces the first heart sound (S₁).

2. Atrial muscles contract

   • Incorrect because atrial contraction occurs during the late diastolic phase (atrial systole), which happens before isovolumetric contraction.
   • During isovolumetric contraction, the atria are in diastole (relaxation).

3. Ventricles are filling

   • Incorrect because ventricular filling occurs during diastole, not during isovolumetric contraction.
   • During isovolumetric contraction, no blood enters or leaves the ventricles.

4. End diastolic volume increases

   • Incorrect because end-diastolic volume (EDV) refers to the volume of blood in the ventricles at the end of diastole, before contraction begins.
   • During isovolumetric contraction, ventricular volume remains constant; it does not increase.

After muscle contraction, calcium ions (Ca²⁺) must be actively transported back into the sarcoplasmic reticulum (SR) to allow muscle relaxation. This process is carried out by the Ca²⁺-ATPase pump, also known as the SERCA (Sarcoplasmic/Endoplasmic Reticulum Ca²⁺-ATPase) pump.

The Ca²⁺-ATPase pump uses ATP to actively transport calcium ions from the cytoplasm into the sarcoplasmic reticulum, reducing cytoplasmic Ca²⁺ levels and leading to muscle relaxation.

Thus, the correct answer is:

✅ Ca-ATPase pump

Breakdown of Answer Choices:

✅ Correct Option:

• Ca-ATPase pump
  • Also known as the SERCA pump.
  • Uses ATP to pump Ca²⁺ back into the sarcoplasmic reticulum after contraction.
  • Essential for muscle relaxation.

🚫 Incorrect Options:

1. Ca-Na pump

   • There is no direct Ca-Na pump responsible for moving calcium into the sarcoplasmic reticulum.
   • While the Na⁺/Ca²⁺ exchanger (NCX) exists in other cellular processes, it is not responsible for calcium reuptake into the SR.

2. Na-ATPase pump

   • Incorrect because Na⁺-K⁺ ATPase maintains sodium and potassium balance, not calcium transport into the SR.

3. Na pump

   • Incorrect because this is not directly involved in calcium transport within muscle cells.

4. K pump

   • Potassium transport is not related to calcium reuptake in the sarcoplasmic reticulum.

Cardiac muscle acts as a functional syncytium, meaning that the individual cardiac muscle cells (myocytes) work together as one coordinated unit. This happens because:

• Intercalated discs connect adjacent cardiac muscle cells, containing:

  • Gap junctions → Allow rapid electrical impulses to pass between cells.
  • Desmosomes → Provide strong mechanical attachment between cells.

• This electrical coupling enables simultaneous contraction of large groups of cardiac cells, functioning as a single unit (syncytium).

• This ensures efficient pumping of blood from the atria and ventricles.

Why the Other Options Are Incorrect:

• “It is more similar to smooth muscle” → Incorrect

  • Cardiac muscle is more similar to skeletal muscle because both are striated and have actin and myosin filaments.
  • Smooth muscle is non-striated and functions differently.

• “It is not striated” → Incorrect

  • Cardiac muscle is striated, like skeletal muscle, due to the organized arrangement of actin and myosin filaments.

• “It doesn’t have intercalated disks between its cells” → Incorrect

  • Intercalated discs are a hallmark of cardiac muscle and are essential for its syncytial function.
  • They contain gap junctions and desmosomes.

• “It doesn’t have actin or myosin filaments” → Incorrect

  • Cardiac muscle has both actin and myosin filaments, arranged in sarcomeres, which produce its striated appearance and allow contraction.

Vasodilators are substances that relax blood vessels, leading to a decrease in vascular resistance and an increase in blood flow. They typically act by stimulating the production of nitric oxide (NO), prostaglandins, or kinins, which trigger smooth muscle relaxation.

Endothelin, however, is a vasoconstrictor, meaning it narrows blood vessels and increases blood pressure.

Why Endothelin is Not a Vasodilator:

• Endothelin (ET-1, ET-2, ET-3) is a potent vasoconstrictor peptide produced by endothelial cells.
• It acts via endothelin receptors (ETA and ETB) on vascular smooth muscle, leading to calcium influx and strong vasoconstriction.
• Endothelin is involved in hypertension, heart failure, and pulmonary hypertension due to its vasopressor effects.

Thus, Endothelin is not a vasodilator, but rather a vasoconstrictor.

Why the Other Options Are Vasodilators:

1. Kinin (Correct – Vasodilator)

   • Bradykinin and kallidin are kinins that promote vasodilation by stimulating nitric oxide (NO) and prostaglandin release.
   • They also increase vascular permeability, contributing to inflammation and lowering blood pressure.

2. Prostaglandins (Correct – Vasodilator)

   • Prostacyclin (PGI₂) is a strong vasodilator that inhibits platelet aggregation and relaxes vascular smooth muscle.
   • Other prostaglandins, like PGE₂, also contribute to vasodilation.

3. Nitrous Oxide (Nitric Oxide, NO) (Correct – Vasodilator)

   • NO is one of the most important vasodilators in the body.
   • It is produced by endothelial nitric oxide synthase (eNOS) and acts by increasing cGMP, leading to smooth muscle relaxation.

4. None of these (Incorrect)

   • This answer would mean that all the substances listed are vasodilators, which is false because Endothelin is a vasoconstrictor.

Aschoff bodies are pathognomonic (characteristic) of rheumatic fever, a post-streptococcal autoimmune inflammatory disease. They are granulomatous lesions found primarily in the myocardium and consist of:

• Fibrinoid necrosis
• Anitschkow cells (also called caterpillar cells — large macrophages with wavy chromatin)
• Lymphocytes and plasma cells

These bodies reflect the immune response targeting the heart tissue after Group A Streptococcus infection, often leading to rheumatic heart disease.

Why the Other Options Are Incorrect:

• Type-II hyperlipidemia: This condition involves elevated LDL cholesterol and leads to atherosclerosis, not granulomatous inflammation like Aschoff bodies.
• Diabetes mellitus: Chronic hyperglycemia in diabetes can cause vascular damage (like hyaline arteriolosclerosis), but Aschoff bodies are not seen in this disease.
• Hyaline atherosclerosis: This is a vascular condition often seen in hypertension and diabetes, characterized by homogeneous pink hyaline deposits in the vessel walls — completely different from Aschoff bodies.
• None of these: Since rheumatic fever is the correct answer, this option is incorrect.

Omega-3 unsaturated fatty acids are essential fatty acids that promote cardiovascular health due to their protective effects on the heart and blood vessels.

Benefits of Omega-3 fatty acids:

• Reduce inflammation → Helps prevent atherosclerosis (hardening of the arteries).
• Lower triglycerides → Reduces the risk of coronary artery disease.
• Decrease blood pressure → Helps manage hypertension.
• Improve endothelial function → Keeps blood vessels flexible and responsive.
• Prevent arrhythmias → Stabilizes heart rhythms.

Sources:

• Fatty fish: Salmon, mackerel, sardines.
• Flaxseeds and chia seeds.
• Walnuts and plant oils like flaxseed oil.

Why the Other Options Are Incorrect:

• Omega-11 unsaturated fatty acids:

  • Not a recognized essential fatty acid group.
  • Not widely studied for cardiovascular effects.

• Omega-6 unsaturated fatty acids:

  • Found in vegetable oils, nuts, and seeds.
  • In moderation, they’re beneficial, but excessive intake can promote inflammation and increase heart disease risk.

• Saturated fatty acids:

  • Found in animal fats, butter, and processed foods.
  • Excess consumption leads to increased LDL cholesterol and higher risk of atherosclerosis.

• None of these:

  • Incorrect because Omega-3 fatty acids clearly benefit cardiovascular health.

Muscular arteries (distributing arteries) are medium-sized arteries responsible for delivering blood to specific organs and tissues. They are characterized by:

• Tunica media:

  • Contains multiple concentric layers of smooth muscle cells.
  • Allows vasoconstriction and vasodilation, which regulate blood flow and pressure.
  • Less elastic tissue compared to elastic arteries (like the aorta).

• Examples: Radial artery, femoral artery, and brachial artery.

Why the Other Options Are Incorrect:

• Muscular adventitia:

  • The adventitia (outer layer) of muscular arteries contains connective tissue, collagen fibers, fibroblasts, and vasa vasorum (in larger arteries).
  • It is not primarily muscular.

• Concentric elastic in the media:

  • This describes elastic arteries (like the aorta), which have abundant concentric elastic fibers to withstand high pressure from blood ejected by the heart.
  • Muscular arteries have more smooth muscle, less elastic tissue.

• Vasa vasorum in the intima:

  • Vasa vasorum (“vessels of vessels”) supply oxygen and nutrients to larger arteries but are found in the tunica adventitia, not the intima.
  • The intima contains the endothelium, basement membrane, and subendothelial connective tissue.

• None of these:

  • Incorrect because the media’s smooth muscle layers are a key distinguishing feature of muscular arteries.

Anitschkow cells are a type of macrophage found in the inflammatory lesions of rheumatic heart disease. They are characteristic cells seen in Aschoff bodies, which are granulomatous structures present in the myocardium of patients with acute rheumatic fever.

These cells have distinctive “caterpillar-like” nuclei, which result from condensed chromatin forming a wavy or ribbon-like appearance. They play a role in the immune response associated with rheumatic heart disease, which is triggered by an abnormal immune reaction to Group A Streptococcus (Streptococcus pyogenes) infection.

Thus, the correct answer is:

✅ Macrophages

Breakdown of Answer Choices:

✅ Correct Option:

• Macrophages
  • Anitschkow cells are a specialized type of macrophage found in Aschoff bodies.
  • They have a wavy (“caterpillar-like”) nuclear chromatin pattern, a hallmark of rheumatic myocarditis.

🚫 Incorrect Options:

1. None of these

   • Incorrect because Anitschkow cells are macrophages, making this answer incorrect.

2. T cells

   • While T cells play a role in the immune response of rheumatic fever, Anitschkow cells are not T cells—they are macrophages.

3. B cells

   • Incorrect because B cells are involved in antibody production, but Anitschkow cells are not lymphocytes; they are part of the monocyte-macrophage lineage.

4. Neutrophils

   • Incorrect because neutrophils are acute inflammatory cells, whereas Anitschkow cells are macrophages found in chronic inflammatory lesions (Aschoff bodies) of rheumatic fever.

ApoB-100 is a structural protein found on low-density lipoproteins (LDL) and very-low-density lipoproteins (VLDL). It plays a crucial role in lipid metabolism by binding to LDL receptors (LDLR), which mediate the uptake of LDL particles into cells.

Primary Organ with ApoB-100 Receptors:

• The liver is the primary organ that expresses LDL receptors for ApoB-100.
• LDL receptors in the liver regulate blood cholesterol levels by removing LDL from circulation via receptor-mediated endocytosis.
• After internalization, LDL is degraded in lysosomes, and cholesterol is released for cellular use or stored.

Other tissues (e.g., adrenal glands and gonads) also have LDL receptors, but the liver is the dominant site of LDL clearance.

Correct Answer:

✅ Liver ❌ (Correct statement)

Why the Other Options Are Incorrect:

1. “Suprarenal glands (Adrenal glands)” ❌ (Incorrect)

   • Adrenal glands do have LDL receptors, but their main function is steroid hormone synthesis, not LDL clearance.
   • The liver remains the primary site for ApoB-100 receptor activity.

2. “Heart” ❌ (Incorrect)

   • The heart relies mainly on fatty acids for energy and does not play a major role in LDL metabolism.

3. “Kidney” ❌ (Incorrect)

   • The kidney is involved in lipid metabolism, but it is not the primary site of LDL receptor expression.

4. “Gonads” ❌ (Incorrect)

   • Gonads utilize cholesterol for steroid hormone synthesis, but they do not primarily regulate LDL metabolism.

Lactic acid acts as a localized vasodilator by relaxing vascular smooth muscle, thereby increasing blood flow to tissues that require more oxygen. This effect is particularly important in:

• Exercising muscles, where anaerobic metabolism produces lactic acid, triggering vasodilation to enhance oxygen and nutrient delivery.
• Ischemic conditions, where tissues experience low oxygen levels and produce lactic acid as a compensatory response.

Lactic acid works by reducing local pH, which stimulates vasodilation and improves blood supply to oxygen-deprived tissues.

Why the Other Options Are Incorrect:

• Increased pH:

  • Higher pH (alkalosis) is associated with vasoconstriction, not vasodilation.
  • Lower pH (acidosis), which occurs due to lactic acid accumulation, promotes vasodilation.

• Increased oxygen:

  • High oxygen levels typically lead to vasoconstriction, especially in the pulmonary circulation, where vessels constrict to divert blood away from well-oxygenated areas.

• Decreased carbon dioxide:

  • Low CO₂ levels (hypocapnia) cause vasoconstriction, particularly in the brain and systemic circulation.
  • High CO₂ (hypercapnia) leads to vasodilation to enhance blood flow and remove excess CO₂.

• None of these:

  • Incorrect, since lactic acid is a well-known vasodilator.

During embryonic heart development, the right auricle (right atrial appendage) arises from the primordial atrium, which is the early embryonic structure that forms both the right and left atria.

• The primordial atrium initially consists of a common atrial chamber, which later divides into right and left atria.
• The trabeculated part of the right atrium, including the right auricle, originates from this primordial atrium.
• The smooth-walled portion of the right atrium comes from the sinus venosus, but the question specifically asks about the right auricle, which is trabeculated and derived from the primordial atrium.

Why the Other Options Are Incorrect:

❌ Sinus venosus

• Incorrect, because the sinus venosus contributes to the smooth-walled portion of the right atrium, not the right auricle.
• The sinus venosus forms the sinus venarum, which is the smooth posterior part of the right atrium where the superior and inferior vena cava drain.

❌ Bulbus cordis

• Incorrect, because the bulbus cordis contributes to the development of the right ventricle and outflow tracts, not the auricle.

❌ None of these

• Incorrect, because the primordial atrium clearly gives rise to the right auricle.

❌ Truncus arteriosus

• Incorrect, because the truncus arteriosus forms the great arteries (ascending aorta and pulmonary trunk), not the atria or auricles.

Wolff-Parkinson-White (WPW) syndrome is caused by the presence of an accessory pathway (bundle of Kent) that bypasses the normal conduction system of the heart. This pathway allows electrical impulses to travel directly from the atria to the ventricles, leading to increased conductivity and the potential for re-entrant tachycardias (e.g., atrioventricular re-entrant tachycardia or AVRT). The hallmark ECG finding in WPW syndrome is a short PR interval and a delta wave (slurred upstroke of the QRS complex).

Why the Other Options Are Incorrect:

1. Increased sympathetic stimulation of heart
   While increased sympathetic stimulation can exacerbate arrhythmias, it is not a defining feature of WPW syndrome. WPW is primarily a structural and electrical abnormality, not a result of autonomic dysfunction.
2. Increased automaticity
   Increased automaticity refers to the ability of cardiac cells to spontaneously generate electrical impulses. WPW syndrome is not caused by increased automaticity but rather by the presence of an accessory conduction pathway.
3. Increased contractility
   Increased contractility refers to the strength of cardiac muscle contraction. WPW syndrome does not directly affect contractility; it is an electrical conduction disorder.
4. None of these
   This option is incorrect because WPW syndrome is indeed characterized by increased conductivity due to the presence of an accessory pathway.

The plateau phase of the action potential in cardiac muscle is a key feature that differentiates it from action potentials in skeletal muscle and neurons. This phase is essential for prolonging contraction and ensuring coordinated heartbeats.

Phases of Cardiac Action Potential (Ventricular Myocytes):

1. Phase 0 (Depolarization) → Rapid Na⁺ influx due to voltage-gated Na⁺ channels opening.
2. Phase 1 (Initial Repolarization) → K⁺ efflux (outflow) due to opening of transient K⁺ channels.
3. Phase 2 (Plateau Phase) → Ca²⁺ influx via L-type calcium channels, balancing the outward movement of K⁺ and maintaining a long plateau.
4. Phase 3 (Repolarization) → Closure of Ca²⁺ channels and continued K⁺ efflux restores resting potential.
5. Phase 4 (Resting Membrane Potential) → Maintained by the Na⁺/K⁺ ATPase and K⁺ leak channels.

The plateau phase (Phase 2) is primarily caused by the inward movement of Ca²⁺ through L-type calcium channels, counteracting K⁺ efflux and delaying repolarization. This prolonged depolarization is crucial for:

• Preventing tetanic contractions in the heart.
• Ensuring proper ventricular filling before the next contraction.

Correct Answer:

✅ Ca²⁺ (Calcium ion) ❌ (Correct statement)

Why the Other Options Are Incorrect:

1. “Cl⁻ (Chloride ion)” ❌ (Incorrect)

   • Cl⁻ plays no major role in the cardiac action potential.

2. “Na⁺ (Sodium ion)” ❌ (Incorrect)

   • Na⁺ is responsible for Phase 0 (Depolarization), but it does not cause the plateau.

3. “K⁺ (Potassium ion)” ❌ (Incorrect)

   • K⁺ is involved in Phase 1 (initial repolarization) and Phase 3 (final repolarization), but it does not sustain the plateau.

4. “HCO₃⁻ (Bicarbonate ion)” ❌ (Incorrect)

   • Bicarbonate is involved in acid-base balance, not cardiac action potentials.

Blood leaves the left ventricle by passing through the aortic valve. The aortic valve is a semilunar valve located between the left ventricle and the aorta. When the left ventricle contracts during systole, the aortic valve opens, allowing oxygenated blood to be pumped into the aorta and distributed to the rest of the body.

Why the Other Options Are Incorrect:

1. Tricuspid valve
   The tricuspid valve is located between the right atrium and the right ventricle. It allows blood to flow from the right atrium into the right ventricle and is not involved in blood leaving the left ventricle.
2. Mitral valve
   The mitral valve (also called the bicuspid valve) is located between the left atrium and the left ventricle. It allows blood to flow from the left atrium into the left ventricle but is not involved in blood leaving the left ventricle.
3. Pulmonary valve
   The pulmonary valve is located between the right ventricle and the pulmonary artery. It allows deoxygenated blood to flow from the right ventricle into the pulmonary artery and is not involved in blood leaving the left ventricle.
4. None of these
   This option is incorrect because the aortic valve is indeed the correct answer.

The pulmonary artery carries deoxygenated blood from the right ventricle to the lungs for gas exchange. Compared to systemic arterial blood (oxygenated blood in the aorta), pulmonary arterial blood has the following characteristics:

1. Higher Carbon Dioxide (CO₂) Content ✅
   • The pulmonary artery carries venous blood, which has returned from the systemic circulation after oxygen has been used by tissues.
   • This blood is rich in carbon dioxide (CO₂), a metabolic waste product from cellular respiration.
   • CO₂ is transported in three main forms:
     • Dissolved CO₂ (~7%)
     • Carbaminohemoglobin (~23%) (bound to hemoglobin)
     • Bicarbonate (HCO₃⁻) (~70%) (formed by carbonic anhydrase reaction in RBCs).
   • Once in the lungs, CO₂ is released into the alveoli and exhaled.

Why the Other Options Are Incorrect?

1. Has higher pH ❌

   • Why Incorrect? Pulmonary artery blood has a lower pH compared to systemic arterial blood.
   • The presence of more CO₂ (which forms carbonic acid) makes it slightly more acidic.
   • Systemic arterial blood has a higher pH (~7.4) than pulmonary artery blood (~7.35).

2. Has greater amount of hemoglobin ❌

   • Why Incorrect? The total hemoglobin concentration does not significantly differ between pulmonary artery and systemic arterial blood.
   • However, oxygen saturation of hemoglobin differs (pulmonary artery hemoglobin is deoxygenated, whereas systemic arterial hemoglobin is oxygenated).

3. Has more oxygen ❌

   • Why Incorrect? Pulmonary artery blood is deoxygenated, meaning it contains less oxygen than systemic arterial blood.
   • Oxygen levels increase after passing through the lungs, where gas exchange occurs.

4. None of these ❌

   • Why Incorrect? Pulmonary artery blood definitely has more carbon dioxide than systemic arterial blood, making this option incorrect.

Lipoproteins are classified based on their density, which depends on their protein-to-lipid ratio. High-density lipoprotein (HDL) has the highest density because it contains more protein and less lipid compared to other lipoproteins.

The correct answer is:

✅ Highest protein and minimal lipid proportion

Breakdown of Answer Choices:

✅ Correct Option:

• Highest protein and minimal lipid proportion
  • Density of lipoproteins is determined by the ratio of protein to lipid.
  • Proteins are denser than lipids, so lipoproteins with higher protein content and lower lipid content have higher density.
  • HDL has the highest protein content (~50%) and lowest lipid content, making it the most dense lipoprotein.
  • This high protein content allows HDL to efficiently transport cholesterol from tissues back to the liver for metabolism (reverse cholesterol transport).

🚫 Incorrect Options:

1. Minimal protein and highest lipid proportion ❌

   • This describes chylomicrons, which are the least dense lipoproteins, not HDL.
   • More lipid and less protein = lower density.

2. None of these ❌

   • Incorrect because HDL’s high protein-to-lipid ratio explains its high density.

3. Minimal protein and minimal lipid proportion ❌

   • A lipoprotein with low protein and low lipid content would not exist in this form.
   • Lipoproteins must contain significant amounts of at least one component.

4. Highest protein and highest lipid proportion ❌

   • If HDL had high lipid content, it would be less dense.
   • Lipids are less dense than proteins, so this statement contradicts HDL’s actual structure.

Ventricular septal defect (VSD) is the most common congenital heart defect (CHD). It occurs when there is a hole in the interventricular septum, the wall between the left and right ventricles. This causes left-to-right shunting of blood, where oxygenated blood from the left ventricle flows into the right ventricle, leading to:

• Increased pulmonary blood flow
• Pulmonary hypertension over time
• Right ventricular hypertrophy in severe cases

Clinical features:

• Harsh holosystolic murmur (heard best at the left lower sternal border)
• Failure to thrive, poor feeding, and recurrent respiratory infections in infants with large VSDs
• Small VSDs may remain asymptomatic and sometimes close spontaneously

Why the Other Options Are Incorrect:

• Tetralogy of Fallot:

  • It’s a cyanotic heart defect and less common than VSD.
  • Involves four abnormalities: VSD, pulmonary stenosis, overriding aorta, and right ventricular hypertrophy.

• Atrial septal defect (ASD):

  • Common, but not as frequent as VSD.
  • Involves an opening in the atrial septum, leading to left-to-right shunting.

• Patent ductus arteriosus (PDA):

  • Failure of the ductus arteriosus closure after birth.
  • Causes continuous “machinery-like” murmur.

• Transposition of great vessels:

  • A cyanotic and serious defect, but it’s rare compared to VSD.
  • Involves switching of the aorta and pulmonary artery, leading to incompatible circulation without early intervention.

Sinusoidal capillaries (sinusoids) are specialized blood vessels found in organs that handle large molecules, cells, and blood filtration. These capillaries have:

• Large, irregular lumens
• Discontinuous or fenestrated endothelial cells
• Incomplete basement membranes
• Wide spaces between cells, allowing free exchange of large proteins, cells, and plasma

These features are crucial for the functions of the following organs:

• Bone marrow: For release and maturation of blood cells into circulation
• Spleen: For filtration of old or damaged red blood cells
• Liver: For exchange of large plasma proteins and metabolic products between the blood and hepatocytes

Why the Other Options Are Incorrect:

• Elastic arteries: Large arteries like the aorta that contain elastin for maintaining blood pressure and accommodating pulse waves — not capillaries.
• Fenestrated capillaries: Found in tissues with high rates of exchange (like endocrine glands, kidneys, intestinal villi), but they have smaller pores and a continuous basement membrane, unlike sinusoidal capillaries.
• Continuous capillaries: The most common type, found in muscles, skin, and the blood-brain barrier — tightly packed endothelial cells allow only small molecule exchange.
• None of these: Incorrect, because sinusoidal capillaries are the right choice.

Both the tricuspid valve and the semilunar valves (aortic and pulmonary valves) share a common structural feature: they all have three cusps (leaflets).

Breakdown of Valve Structures:

• Tricuspid Valve → Located between the right atrium and right ventricle, it has three cusps (hence the name “tricuspid”).
• Semilunar Valves (Aortic & Pulmonary) → Located at the outflow tracts of the heart, both have three cusps as well.

Thus, the correct answer is “Have three cusps.”

Why the Other Options Are Incorrect:

1. Have two cusps (Incorrect)

   • The mitral valve (bicuspid valve) has two cusps, but the tricuspid and semilunar valves both have three.

2. Produce the first heart sound (Incorrect)

   • The first heart sound (S1) is caused by the closure of the tricuspid and mitral valves, but not the semilunar valves.

3. Have tendinous filaments attached (Incorrect)

   • Only atrioventricular (AV) valves (tricuspid and mitral) have chordae tendineae to prevent prolapse.
   • Semilunar valves lack chordae tendineae.

4. Produce the second heart sound (Incorrect)

   • The second heart sound (S2) is due to the closure of semilunar valves (aortic and pulmonary) but not the tricuspid valve.

Sodium nitroprusside is the drug of choice in hypertensive emergencies because:

• Mechanism of action: It’s a direct-acting vasodilator that releases nitric oxide (NO), leading to smooth muscle relaxation in blood vessels.
• Effect: Causes rapid reduction in blood pressure by dilating both arteries and veins, leading to decreased afterload and preload.
• Onset: Immediate, within seconds of IV administration.
• Duration: Short-acting, allowing precise titration of blood pressure.
• Indications: Used in hypertensive crises, aortic dissection, and acute heart failure when rapid BP control is crucial.

Why the Other Options Are Incorrect:

• Captopril:

  • An ACE inhibitor used for long-term management of hypertension, not emergencies.
  • Slower onset of action compared to sodium nitroprusside.

• Propranolol:

  • A non-selective beta-blocker, used for chronic hypertension, angina, and arrhythmias.
  • Not fast-acting enough for hypertensive emergencies.

• Atropine:

  • An anticholinergic drug that increases heart rate by inhibiting the parasympathetic nervous system.
  • Used in bradycardia, not for hypertension.

• None of these:

  • Incorrect because sodium nitroprusside is clearly the most commonly used drug in hypertensive emergencies.

Genetics is a non-modifiable risk factor for coronary heart disease (CHD). Non-modifiable risk factors are those that cannot be changed or controlled by an individual. Here’s why genetics fits this category:

• Inherited Predisposition:
  Genetic factors, such as a family history of CHD, can significantly increase an individual’s risk of developing the disease. For example, mutations in genes related to lipid metabolism (e.g., LDL receptor gene) or other cardiovascular pathways can predispose someone to CHD.
• Fixed Nature:
  Unlike lifestyle factors, genetic makeup is determined at birth and cannot be altered. While lifestyle changes can mitigate some risks, the genetic component remains unchanged.

Why the Other Options Are Modifiable:

1. Obesity:
   Obesity is a modifiable risk factor. It can be addressed through lifestyle changes such as diet, exercise, and weight management. Reducing obesity lowers the risk of CHD.
2. Diabetes:
   Diabetes is a modifiable risk factor. While some individuals may have a genetic predisposition to diabetes, the condition can often be managed or prevented through lifestyle changes, medication, and blood sugar control.
3. Smoking:
   Smoking is a modifiable risk factor. Individuals can quit smoking, which significantly reduces their risk of CHD and other cardiovascular diseases.
4. None of these:
   This option is incorrect because genetics is indeed a non-modifiable risk factor.

As blood flows through body tissues, hemoglobin must release oxygen to meet the metabolic needs of the cells. Several physiological changes occur in the tissues that reduce hemoglobin’s affinity for oxygen, facilitating oxygen unloading.

This is represented by a rightward shift of the oxygen-hemoglobin dissociation curve, known as the Bohr effect.

Factors Leading to a Rightward Shift in Tissues:

1. Increased Carbon Dioxide (CO₂) Levels

   • Actively metabolizing tissues produce more CO₂.
   • CO₂ binds to hemoglobin and lowers blood pH (forms carbonic acid via carbonic anhydrase), promoting oxygen release.

2. Decreased pH (Increased Acidity)

   • A lower pH reduces hemoglobin’s affinity for O₂, allowing more oxygen to be released into the tissues.
   • This is known as the Bohr effect, where low pH enhances oxygen unloading.

3. Increased Temperature

   • Active tissues generate heat, which reduces hemoglobin’s affinity for oxygen and promotes O₂ unloading.

4. Increased 2,3-Bisphosphoglycerate (2,3-BPG)

   • 2,3-BPG is produced by red blood cells in hypoxic conditions and binds to hemoglobin, reducing its affinity for O₂.
   • This helps deliver more oxygen to tissues during conditions like high altitude or chronic hypoxia.

Why the Other Options Are Incorrect?

1. Hemoglobin affinity for oxygen decreases and the curve shifts to the left ❌

   • Why Incorrect? A leftward shift means higher hemoglobin affinity for O₂, making it harder to unload oxygen at tissues—opposite to what happens in body tissues.

2. Hemoglobin affinity for oxygen increases and the curve shifts to the left ❌

   • Why Incorrect? Increased affinity (leftward shift) happens in conditions like alkalosis, low CO₂, low temperature, and fetal hemoglobin (HbF)—which is not the case in body tissues.

3. Hemoglobin affinity for oxygen increases and the curve shifts to the right ❌

   • Why Incorrect? A rightward shift is associated with decreased affinity, not increased.

4. None of these ❌

   • Why Incorrect? The correct physiological response is a decrease in hemoglobin affinity for oxygen with a rightward shift in the dissociation curve.

Antioxidants are molecules that help neutralize free radicals—unstable molecules that can damage cells through oxidative stress. Oxidative stress is implicated in aging, cancer, cardiovascular diseases, and neurodegenerative disorders. Among the given options, the best natural antioxidant is Vitamin E.

Why Vitamin E is the Correct Answer?

Vitamin E is a fat-soluble vitamin that primarily functions as a powerful lipid-soluble antioxidant. It protects cell membranes from oxidative damage by scavenging lipid peroxyl radicals. This is especially important in biological membranes, where oxidative stress can compromise cell integrity and function. Vitamin E works in conjunction with Vitamin C, which helps regenerate oxidized Vitamin E, enhancing its effectiveness.

Why the Other Options Are Incorrect?

1. Vitamin B12 (Cobalamin)

   • Function: Vitamin B12 is essential for DNA synthesis, red blood cell formation, and neurological function.
   • Why Incorrect? While B12 plays a crucial role in metabolic reactions and prevents megaloblastic anemia, it does not function primarily as an antioxidant.

2. Vitamin A (Retinol, Beta-Carotene, Retinoic Acid)

   • Function: Vitamin A is important for vision, immune function, and epithelial cell maintenance.
   • Why Incorrect? Although beta-carotene (a precursor of Vitamin A) has some antioxidant properties, Vitamin A itself is not the most effective natural antioxidant compared to Vitamin E.

3. Vitamin B6 (Pyridoxine)

   • Function: Involved in amino acid metabolism, neurotransmitter synthesis, and hemoglobin production.
   • Why Incorrect? While Vitamin B6 has some role in reducing homocysteine levels, which may contribute to oxidative stress, it does not function as a primary antioxidant.

4. Vitamin C (Ascorbic Acid)

   • Function: A water-soluble vitamin that acts as an antioxidant in the aqueous environment of cells and helps regenerate Vitamin E.
   • Why Incorrect? Vitamin C is a potent antioxidant, but since it primarily acts in aqueous environments (cytoplasm and plasma) rather than in lipid-rich environments like cell membranes, it is not considered the best natural antioxidant compared to Vitamin E.

The epicardium is the outermost layer of the heart wall and is also known as the visceral layer of the serous pericardium. It’s a thin layer of mesothelium and underlying connective tissue. This layer:

• Contains coronary blood vessels, nerves, and lymphatics that supply the heart.
• Provides protection and lubrication as the heart moves within the pericardial sac.
• Often contains adipose tissue, especially near the coronary arteries and major vessels.

Because of this structural and supportive role, the epicardium is the layer where heart nerves are found.

Why the Other Options Are Incorrect:

• Myocardium:
  This is the thick, muscular layer responsible for the contractile function of the heart. While it’s the powerhouse of the heart, it does not contain nerves — those run through the epicardium and innervate the myocardium.

• Sub-endothelial layer:
  A thin layer of connective tissue just beneath the endocardium — it does not house nerves but serves as support for the endothelial lining.

• Sub-epithelial connective tissue:
  Found in various epithelial-lined organs, but in the heart, the sub-endothelial layer takes this role — no nerve presence here.

• Epithelial layer:
  Refers to the endocardium’s endothelial lining, which is smooth and continuous with the vascular endothelium — does not contain nerves.

Let’s carefully break down the anatomy of the right ventricle (RV) and why the mitral valve isn’t found there:

• Mitral valve (bicuspid valve):
  Found exclusively in the left side of the heart, between the left atrium and left ventricle. It has two cusps and prevents backflow of oxygenated blood into the left atrium during ventricular contraction.
  • Since it’s part of the left heart, it’s not present in the right ventricle — making this the correct answer.

Why the Other Options Are Found in the Right Ventricle:

• Conus arteriosus (Infundibulum):
  A smooth outflow tract that leads to the pulmonary valve, directing deoxygenated blood toward the pulmonary arteries. It’s a distinctive feature of the right ventricle.

• Chordae tendineae:
  Fibrous cords that connect the cusps of the tricuspid valve to the papillary muscles in the right ventricle, preventing valve prolapse during systole.

• Supraventricular crest:
  A muscular ridge in the right ventricle that separates the inflow and outflow tracts — a landmark structure of the RV.

• Trabeculae carneae:
  Irregular muscular ridges on the inner walls of the right and left ventricles — common in both but very prominent in the right ventricle.

The atrioventricular (AV) node is responsible for delaying impulse transmission in the heart. This delay is crucial for proper cardiac function, as it allows the atria to complete contraction and empty blood into the ventricles before ventricular systole begins.

The delay occurs due to:

1. Smaller diameter fibers in the AV node, which conduct impulses more slowly.
2. Fewer gap junctions, leading to slower electrical conduction between cells.
3. Higher resistance to impulse propagation, preventing rapid transmission.
4. Complex structure, requiring the impulse to traverse multiple nodal cells before reaching the Bundle of His.

This delay lasts about 0.1 seconds (100 ms) and ensures efficient atrial contraction before ventricular contraction, optimizing cardiac output.

Why the Other Options Are Incorrect?

1. Purkinje fibers ❌

   • Function: Purkinje fibers are responsible for rapid conduction of electrical impulses to the ventricular myocardium, leading to synchronized ventricular contraction.
   • Why Incorrect? These fibers speed up conduction rather than delay it.

2. Bundle branches ❌

   • Function: The right and left bundle branches transmit impulses from the AV node to the Purkinje system.
   • Why Incorrect? They ensure rapid impulse transmission, not delay it.

3. Sinoatrial (SA) node ❌

   • Function: The SA node is the heart’s primary pacemaker, setting the rhythm of electrical impulses.
   • Why Incorrect? The SA node generates impulses but does not delay them.

4. Inter-nodal fibers ❌

   • Function: These fibers conduct impulses from the SA node to the AV node.
   • Why Incorrect? They help transmit impulses without delay.

The right femoral artery is the most commonly accessed site for left heart catheterization. It is located in the groin and provides a direct route to the aorta and coronary arteries. The femoral artery is large and easily accessible, making it a preferred site for catheterization procedures. However, other access sites, such as the radial artery, are also used depending on the patient’s condition and the physician’s preference.

Why the Other Options Are Incorrect:

1. Left external iliac artery
   The left external iliac artery is not typically used for left heart catheterization. It is deeper and less accessible than the femoral artery.
2. Right common iliac artery
   The right common iliac artery is also not typically used for catheterization. It is located deeper in the pelvis and is less accessible than the femoral artery.
3. Left radial artery
   The left radial artery is an alternative access site for left heart catheterization, particularly for patients with peripheral artery disease or other contraindications to femoral access. However, it is not the most commonly used site.
4. Left femoral artery
   While the left femoral artery can be used for catheterization, the right femoral artery is more commonly accessed due to its anatomical convenience and the preference of right-handed operators.

he heart rate (HR) can be calculated from an ECG using the following formula:

Heart Rate=300Number of large boxes between two consecutive QRS complexes\text{Heart Rate} = \frac{300}{\text{Number of large boxes between two consecutive QRS complexes}}Heart Rate=Number of large boxes between two consecutive QRS complexes300​

Each large box (comprising 5 medium boxes or 25 small boxes) on an ECG grid represents 0.2 seconds.

Each medium box contains 5 small boxes, where each small box represents 0.04 seconds.

Step-by-Step Calculation:

1. The QRS complex occurs every 5 medium boxes.

2. Since 1 large box = 5 medium boxes, this means the QRS complexes are 5 medium boxes apart, equivalent to 1 large box.

3. Using the formula:

   Heart Rate=300Number of large boxes between R waves\text{Heart Rate} = \frac{300}{\text{Number of large boxes between R waves}}Heart Rate=Number of large boxes between R waves300​ Heart Rate=3005\text{Heart Rate} = \frac{300}{5}Heart Rate=5300​ Heart Rate=60 beats per minute (bpm)\text{Heart Rate} = 60 \text{ beats per minute (bpm)}Heart Rate=60 beats per minute (bpm)

Correct Answer:

✅ 60 beats/min ❌ (Correct statement)

Why the Other Options Are Incorrect:

1. “65 beats/min” ❌ (Incorrect)

   • If the QRS complex was appearing every ~4.6 large boxes, the heart rate would be around 65 bpm, but here, it is exactly 5 large boxes.

2. “70 beats/min” ❌ (Incorrect)

   • This would occur if the QRS complex appeared every ~4.3 large boxes, which is not the case here.

3. “50 beats/min” ❌ (Incorrect)

   • If the QRS complex was occurring every 6 large boxes, the heart rate would be 50 bpm, but here it is 5 boxes apart.

4. “55 beats/min” ❌ (Incorrect)

   • This would be correct for about 5.5 large boxes, but we have exactly 5 boxes.

The superior vena cava (SVC) is a major vein that returns deoxygenated blood from the upper body to the right atrium of the heart. It is formed by the union of the right and left brachiocephalic veins and extends downward into the right atrium.

Correct Anatomical Features of the SVC:

• Length: Approximately 7 cm, not 10 cm.
• Formation: Created by the right and left brachiocephalic veins, which merge behind the first right costal cartilage.
• Location: It begins behind the first right costal cartilage, not at the first costal cartilage itself.
• Valves: The SVC has no valve separating it from the right atrium, allowing blood to flow freely.
• Receives Azygous Vein: The azygous vein drains into the SVC just before it enters the right atrium.

Since the SVC begins behind the first right costal cartilage, saying it “begins at the first costal cartilage” is incorrect.

Why the Other Options Are Correct:

1. Has 10 cm length (Incorrect Statement – The SVC is around 7 cm, not 10 cm)

   • The SVC is short, about 7 cm in length, not 10 cm.
   • It extends from the junction of the brachiocephalic veins to the right atrium.

2. Formed by right and left brachiocephalic veins (Correct)

   • The SVC forms when the right and left brachiocephalic veins join at the level of the first right costal cartilage.

3. Is not separated from the right atrium via any valves (Correct)

   • Unlike the inferior vena cava, which may have a rudimentary Eustachian valve, the SVC has no valve at its entry into the right atrium.

4. Receives azygous vein (Correct)

   • The azygous vein drains into the posterior side of the SVC, just before it enters the right atrium.
   • The azygous system helps return blood from the thoracic wall and upper lumbar region.

Blood flow can be laminar (smooth) or turbulent (disordered). Turbulence occurs when there are chaotic changes in blood flow, leading to eddies and vortices. One of the main causes of turbulence is increased velocity of blood because:

• According to Reynolds number (Re), which predicts blood flow type:Re=velocity×diameter×densityviscosityRe = \frac{\text{velocity} \times \text{diameter} \times \text{density}}{\text{viscosity}}Re=viscosityvelocity×diameter×density​
• If velocity increases, Reynolds number increases, making blood flow more likely to become turbulent.
• High blood velocity is seen in conditions like arterial stenosis, anemia, and hyperdynamic circulation, all of which increase turbulence.

Thus, increased velocity of blood is the correct answer.

Why the Other Options Are Incorrect:

1. Decreased density of blood (Incorrect)

   • Density is a factor in Reynolds number, but decreasing density actually reduces turbulence, making blood flow more laminar.

2. Increased viscosity of blood (Incorrect)

   • Higher viscosity (e.g., in polycythemia) actually reduces turbulence by increasing resistance to flow, promoting laminar flow instead.

3. Increased length of vessel (Incorrect)

   • The length of a blood vessel affects resistance (Poiseuille’s Law) but does not directly contribute to turbulence.

4. Decreased diameter of vessel (Incorrect)

   • While narrowing a vessel (e.g., in stenosis) can cause localized turbulence, a smaller diameter usually reduces Reynolds number overall, making flow more laminar unless velocity significantly increases.

Type II-a hyperlipidemia, also known as familial hypercholesterolemia, is characterized by elevated levels of low-density lipoprotein (LDL) and total cholesterol in the blood. Here’s why cholesterol is the correct answer:

• Pathophysiology of Type II-a Hyperlipidemia:
  This condition is caused by a defect in the LDL receptor gene, leading to impaired clearance of LDL particles from the bloodstream. As a result, LDL cholesterol accumulates in the blood, contributing to atherosclerosis and increased cardiovascular risk.
• Lipoprotein Profile in Type II-a:
  • LDL cholesterol is significantly elevated.
  • Total cholesterol is increased due to the high LDL levels.
  • Triglycerides are typically normal or only mildly elevated.
• Cholesterol as the Key Marker:
  Since LDL is the primary carrier of cholesterol in the blood, elevated LDL directly leads to increased total cholesterol levels. This is the hallmark of type II-a hyperlipidemia.

Why the Other Options Are Incorrect:

1. Very low-density lipoprotein (VLDL):
   VLDL is primarily responsible for transporting triglycerides, not cholesterol. In type II-a hyperlipidemia, VLDL levels are usually normal or only slightly elevated.
2. High-density lipoprotein (HDL):
   HDL is known as “good cholesterol” because it helps remove excess cholesterol from the bloodstream. In type II-a hyperlipidemia, HDL levels are typically normal or even reduced, not increased.
3. Intermediate-density lipoprotein (IDL):
   IDL is a transient lipoprotein formed during the conversion of VLDL to LDL. It is not a major feature of type II-a hyperlipidemia and is not typically elevated in this condition.
4. Chylomicrons:
   Chylomicrons are responsible for transporting dietary triglycerides from the intestines to other tissues. They are not associated with type II-a hyperlipidemia, which is characterized by cholesterol, not triglyceride, abnormalities.

Tocopherol, commonly known as Vitamin E, is a fat-soluble antioxidant that plays a crucial role in protecting cells from oxidative damage caused by free radicals.

How Tocopherol Acts as an Antioxidant:

• Prevents lipid peroxidation: Tocopherol stabilizes cell membranes by preventing oxidative damage to polyunsaturated fatty acids (PUFAs).
• Protects against chronic diseases: By reducing oxidative stress, Vitamin E helps lower the risk of conditions like cardiovascular disease, neurodegenerative disorders, and aging-related damage.
• Works with other antioxidants: It interacts with Vitamin C and glutathione, which help regenerate its antioxidant capacity.

Since antioxidants are vital for neutralizing free radicals, tocopherol (Vitamin E) is the correct answer.

Why the Other Options Are Incorrect:

1. Niacin (Incorrect)

   • Niacin (Vitamin B3) is not an antioxidant; instead, it plays a role in energy metabolism as part of NAD+ and NADP+ (coenzymes involved in redox reactions).

2. Folate (Incorrect)

   • Folate (Vitamin B9) is essential for DNA synthesis and cell division, particularly during pregnancy, but it does not function as an antioxidant.

3. Thymine (Incorrect)

   • Thymine is a nucleotide (part of DNA structure), not a vitamin or antioxidant.

4. Cholecalciferol (Incorrect)

   • Cholecalciferol (Vitamin D3) helps with calcium absorption and bone health, but it does not have antioxidant properties.

Muscular arteries, also known as distributing arteries, have a distinct smooth muscle layer sandwiched between two elastic laminae in their tunica media. These two elastic layers are:

1. Internal elastic lamina (IEL) – Separates the tunica intima from the tunica media.
2. External elastic lamina (EEL) – Separates the tunica media from the tunica adventitia.

Between these two elastic laminae, the tunica media is composed primarily of smooth muscle fibers that regulate blood flow by vasoconstriction and vasodilation. This structural organization allows muscular arteries to control the distribution of blood to various organs and tissues.

Why the Other Options Are Incorrect:

❌ Elastic artery

• Incorrect. Elastic arteries (e.g., the aorta, common carotid artery) have multiple layers of elastic fibers within their tunica media instead of a clear single internal and external elastic lamina.
• Their primary function is to withstand high-pressure fluctuations and maintain continuous blood flow using elastic recoil.

❌ Medium-sized vein

• Incorrect. Veins have a thinner tunica media compared to arteries and lack well-defined internal and external elastic laminae.
• Their walls are more compliant to accommodate low-pressure blood flow.

❌ Arteriole

• Incorrect. Arterioles have only a single internal elastic lamina and a relatively thin smooth muscle layer.
• They lack an external elastic lamina because their function is to regulate blood pressure and resistance, not to manage large-scale distribution like muscular arteries.

❌ Lymphatic vessels

• Incorrect. Lymphatic vessels have thin walls with very little smooth muscle and lack well-defined elastic laminae.
• Their primary function is draining interstitial fluid back into the bloodstream, and they rely on valves and external muscle contractions to move lymph.