NEET-PG 2015 Practice Questions

Q: Level of which of the following is not elevated in heart disease

5-nucleotidase. ***5-nucleotidase*** - While other enzymes like LDH, SGOT, and ALP can be elevated in various conditions including heart disease (especially in the context of tissue damage), 5-nucleotidase is **not typically elevated in heart disease**. - Its elevation is more commonly associated with **biliary obstruction** or certain liver pathologies. *LDH* - **Lactate dehydrogenase (LDH)** is a marker of **cellular damage** and can be elevated in myocardial infarction, though it is less specific than troponins. - LDH levels rise later than CK-MB and remain elevated longer, indicating persistent tissue injury. *SGOT* - **Serum glutamic oxaloacetic transaminase (SGOT)**, also known as **aspartate aminotransferase (AST)**, is elevated in acute **myocardial infarction** due to cardiac muscle damage. - While it's a marker for cardiac injury, it's not specific as it's also highly concentrated in the liver. *ALP* - **Alkaline phosphatase (ALP)** can be mildly elevated in heart failure due to **hepatic congestion** caused by reduced cardiac output. - While its primary diagnostic significance is in bone and liver disease, its elevation in advanced heart disease is usually a secondary consequence.

Q: Lines of Zahn are LEAST likely to be seen in -

Lung. ***Lung*** - **Lines of Zahn are LEAST likely in the lungs** because most pulmonary thrombi are actually **emboli that formed elsewhere** (typically in deep leg veins) and then **lodged in pulmonary vessels**. - These pre-formed thrombi developed in **low-flow venous environments** and therefore **lack the characteristic layered appearance** of Lines of Zahn. - Even when thrombi form in situ in pulmonary vessels, the vascular bed characteristics make Lines of Zahn formation less common compared to other sites. *Heart* - **Mural thrombi** in heart chambers (especially post-MI in left ventricle or in atrial fibrillation) commonly show **Lines of Zahn**. - The **high-flow, turbulent environment** with continuous cardiac contractions creates ideal conditions for alternating platelet-fibrin and RBC layer deposition. - These are classic examples of antemortem thrombi with visible Lines of Zahn. *Liver* - **Portal vein thrombosis** and **hepatic vein thrombosis** (Budd-Chiari syndrome) can exhibit **Lines of Zahn**. - Despite being venous, these vessels have **sufficient flow velocity and turbulence** to allow layered thrombus formation. - Lines of Zahn indicate the thrombus formed during life with flowing blood. *Kidney* - **Renal artery thrombosis** and **renal vein thrombosis** frequently show **Lines of Zahn**. - Both arterial and venous renal circulation have adequate flow dynamics for layered thrombus formation. - These represent antemortem thrombi formed in vessels with active blood flow.

Q: Which of the following is a type of small vessel vasculitis?

Granulomatosis with polyangiitis (GPA). ***Granulomatosis with polyangiitis (GPA)*** - GPA is a prototypic **ANCA-associated small vessel vasculitis** characterized by necrotizing granulomas and vasculitis [1], [2]. - It commonly involves the **upper and lower respiratory tracts** and the **kidneys** with necrotizing granulomatous inflammation [1], [2]. - Classified as small vessel vasculitis according to the **Chapel Hill Consensus Conference** classification. *Classical PAN* - This refers to **Polyarteritis Nodosa (PAN)**, which is a **medium-sized vessel vasculitis**. - PAN is characterized by multifocal inflammatory and necrotizing lesions of medium-sized muscular arteries, **not small vessels**. *Giant cell arteritis* - **Giant cell arteritis (GCA)** is a **large vessel vasculitis** that primarily affects the aorta and its major branches, particularly the temporal artery [3]. - Symptoms include headache, jaw claudication, and visual disturbances, reflecting the involvement of larger blood vessels [3]. *None of the options* - This option is incorrect because Granulomatosis with polyangiitis (GPA) is a clear example of a small vessel vasculitis. - There is a correct answer among the provided choices. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 519-520. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 536-537. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 515-516.

Q: Which type of white blood cell plays a primary role in cardiac remodeling and chronic inflammation in heart failure?

Macrophages. ***Macrophages*** - **Macrophages** are increasingly recognized for their critical role in the pathogenesis and progression of **heart failure**, contributing to **cardiac remodeling**, chronic inflammation, and fibrosis - They infiltrate failing myocardium and play dual roles: promoting both **inflammation** and **tissue repair** - Their activation state (M1 vs M2 phenotypes) can significantly influence cardiac function and prognosis in heart failure patients - They secrete **cytokines**, **growth factors**, and **matrix metalloproteinases** that contribute to ventricular remodeling *Eosinophils* - **Eosinophils** are primarily involved in **allergic reactions** and defense against **parasitic infections** - While they can contribute to inflammation in specific cardiac conditions (e.g., **eosinophilic myocarditis**, **Loeffler endocarditis**), they are not primarily associated with the general pathophysiology of chronic heart failure *T cells* - **T cells** are central to **adaptive immunity**, including cell-mediated responses and modulation of immune reactions - Though T cells play a role in inflammatory processes in certain forms of heart disease, particularly **viral myocarditis**, they are not the predominant immune cell driving chronic cardiac remodeling in heart failure *B cells* - **B cells** are responsible for producing **antibodies** and are key players in humoral immunity - While B cells can contribute to autoimmune forms of heart disease and certain inflammatory processes, they are not typically the primary immune cell associated with the progression of chronic heart failure

Q: Heart failure cells are seen in -

Pulmonary edema. ***Pulmonary edema*** - Heart failure cells, or **hemosiderin-laden macrophages**, are typically found in the lungs during pulmonary edema due to left-sided heart failure [1]. - This condition leads to **increased pulmonary capillary pressure**, causing leakage of red blood cells into the alveoli, which macrophages then phagocytose [1]. *Pulmonary abscess* - Characterized by a **localized collection of pus** within the lung, typically due to infection, rather than heart failure. - Does not typically involve **hemosiderin-laden macrophages** indicative of chronic pulmonary congestion. *Pulmonary infarction* - Causes **tissue death** due to obstruction of blood flow, leading to necrosis rather than heart failure cells. - Typically presents with **infarcted lung tissue**, showing a different pathological process than seen in heart failure. *PulmonaryTB* - Primarily caused by **Mycobacterium tuberculosis**, leading to cavitary lesions and granulomatous inflammation, not heart failure cells. - The presence of **caseating granulomas** is characterized but does not indicate chronic pulmonary congestion. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 536-538.

Q: Obliterative endarteritis in vasa vasorum is seen in -

Tertiary Syphilis. ***Tertiary Syphilis*** - **Obliterative endarteritis** of the **vasa vasorum** is a hallmark pathological finding in tertiary syphilis, particularly affecting the **aorta**. - This inflammation and occlusion of the small blood vessels supplying the aorta lead to **ischemic injury** of the aortic wall, causing **aneurysms** and **aortic regurgitation**. *Essential Hypertension* - While hypertension can lead to vascular changes like **arteriolosclerosis** and **hyperplastic arteriolosclerosis**, it does not typically involve obliterative endarteritis of the vasa vasorum. - The vascular damage in essential hypertension is more generalized to smaller arteries and arterioles, not specifically the vasa vasorum. *Systemic Lupus Erythematosus* - SLE is an **autoimmune disease** that can cause **vasculitis**, but the specific pattern of obliterative endarteritis of the vasa vasorum is not characteristic. - Vascular involvement in SLE is diverse, ranging from small vessel vasculitis to accelerated atherosclerosis, but distinct from syphilitic changes. *Pulmonary Tuberculosis* - Tuberculosis is primarily an **infectious granulomatous disease** affecting the lungs and other organs; it does not typically cause obliterative endarteritis of the vasa vasorum. - Although it can cause vascular complications like **aneurysms** (e.g., Rasmussen's aneurysm) due to erosion, the underlying mechanism is not the same as syphilitic changes.

Q: Which type of artery is most commonly involved in PAN?

Muscular. ***Muscular*** - **Polyarteritis nodosa (PAN)** predominantly affects **medium to small-sized muscular arteries**, leading to inflammation, necrosis, and microaneurysms [1]. - This involvement often causes **organ ischemia** and symptoms related to the affected organs, such as the kidneys, gastrointestinal tract, and skin [1]. *Elastic* - **Elastic arteries**, such as the aorta and its major branches, are typically spared in PAN due to their larger size and distinct histological structure. - Diseases like **Takayasu arteritis** or **Giant cell arteritis** are more commonly associated with vasculitis affecting large elastic arteries. *Arterioles* - While arterioles can be affected in various forms of vasculitis, they are not the primary target in classic PAN. - Involvement of arterioles is more characteristic of **microscopic polyangiitis** or **Churg-Strauss syndrome** [2]. *Capillaries* - **Capillaries** are the smallest blood vessels, and their involvement is rare in PAN. - Conditions like **Henoch-Schönlein purpura** or some drug-induced vasculitides more typically affect capillaries, often resulting in palpable purpura [2].

Q: Which of the following statements is true regarding the Duffy Fy(a-b-) blood group?

lacks Fy(b) antigen. ***lacks Fy(b) antigen*** - The **Duffy Fy(a-b-)** phenotype indicates absence of both Fy a and Fy b antigens on red blood cells. - Since the phenotype is **Fy(a-b-)**, it definitively lacks the **Fy b antigen** (indicated by the "b-" notation). - This phenotype is common in people of **African descent** and confers natural **resistance to Plasmodium vivax malaria**, as these antigens serve as receptors for the parasite to enter RBCs. *lacks H- antigen* - The **H antigen** belongs to the **H/h blood group system** and is a precursor to A and B antigens in the ABO system. - The absence of H antigen (Bombay phenotype - Oh) is completely **unrelated to the Duffy blood group system**. - Duffy antigens are on the **DARC (Duffy Antigen Receptor for Chemokines)** protein, distinct from the H antigen. *lacks A-antigen* - The **A antigen** is part of the **ABO blood group system** and defines blood types A and AB. - The Duffy blood group system is **genetically and structurally independent** from the ABO system. - Having Fy(a-b-) phenotype does not affect A antigen expression. *All of the options* - This is incorrect because the Duffy Fy(a-b-) phenotype **specifically refers only to the absence of Duffy antigens** (Fy a and Fy b ). - It has **no relationship** with A, B, or H antigens, which belong to different blood group systems controlled by different genes on different chromosomes.

Q: Amount of blood loss in Stage I of hemorrhagic shock is -

<15%. ***<15%*** - Stage I (Class I) hemorrhagic shock is characterized by **minimal blood loss of up to 15%** of total blood volume (up to 750 mL in a 70 kg adult). - This is the **universally accepted ATLS definition** for Class I hemorrhage. - At this level, compensatory mechanisms maintain normal vital signs with minimal clinical manifestations. - Patients typically show minimal or no symptoms, with possible mild tachycardia only. * 100 bpm), tachypnea, and decreased pulse pressure, but blood pressure remains normal. - This is too broad to specifically define Stage I. * 120 bpm), altered mental status, and decreased urine output. - This is far beyond the compensated Stage I definition.

Question 1

Level of which of the following is not elevated in heart disease

Accepted Answer

5-nucleotidase

Answer

SGOT

Answer

ALP

Answer

LDH

Question 2

Lines of Zahn are LEAST likely to be seen in -

Accepted Answer

Lung

Answer

Liver

Answer

Kidney

Answer

Heart

Question 3

Which of the following is a type of small vessel vasculitis?

Accepted Answer

Granulomatosis with polyangiitis (GPA)

Answer

Classical PAN

Answer

Giant cell arteritis

Answer

None of the options

Question 4

Which type of white blood cell plays a primary role in cardiac remodeling and chronic inflammation in heart failure?

Accepted Answer

Macrophages

Answer

Eosinophils

Answer

T cells

Answer

B cells

Question 5

Heart failure cells are seen in -

Accepted Answer

Pulmonary edema

Answer

Pulmonary infarction

Answer

Pulmonary abscess

Answer

Pulmonary tuberculosis

Question 6

Obliterative endarteritis in vasa vasorum is seen in -

Accepted Answer

Tertiary Syphilis

Answer

Essential Hypertension

Answer

Systemic Lupus Erythematosus

Answer

Pulmonary Tuberculosis

Question 7

Concentric hypertrophy of left ventricle is seen in -

Accepted Answer

Congenital aortic stenosis due to bicuspid aortic valve

Answer

Mitral Stenosis

Answer

Aortic Regurgitation

Answer

Hypertrophic Obstructive Cardiomyopathy

Question 8

Which type of artery is most commonly involved in PAN?

Accepted Answer

Muscular

Answer

Capillaries

Answer

Elastic

Answer

Arterioles

Question 9

Which of the following statements is true regarding the Duffy Fy(a-b-) blood group?

Accepted Answer

lacks Fy(b) antigen

Answer

lacks H- antigen

Answer

lacks A-antigen

Answer

All of the options

Question 10

Amount of blood loss in Stage I of hemorrhagic shock is -

Accepted Answer

<15%

Answer

<10%

Answer

<30%

Answer

<40%

NEET-PG 2015

Biochemistry

Pathology

Surgery