General Pathology Practice Questions

Q: The MYC gene product functions as which of the following?

Transcription activator. **Explanation:** The **MYC gene** (specifically c-MYC) is a proto-oncogene that encodes a protein belonging to the **transcription factor** family [1]. Once activated by mitogenic signaling pathways (like RAS/MAPK), the MYC protein translocates to the nucleus [2]. It binds to specific DNA sequences (E-box sequences) by forming a heterodimer with the **MAX protein**. This complex acts as a potent **transcription activator**, promoting the expression of genes required for cell cycle progression (e.g., Cyclin D), metabolism, and protein synthesis. **Analysis of Incorrect Options:** * **A & B (Protein kinase/Growth factor inhibitors):** These functions are characteristic of **Tumor Suppressor Genes** (like CDKN2A/p16 or APC). MYC is an oncogene; its overexpression promotes growth rather than inhibiting it. * **C (GTPase):** This is the characteristic function of the **RAS protein**. RAS acts as a molecular switch by cycling between an active GTP-bound state and an inactive GDP-bound state. **NEET-PG High-Yield Pearls:** * **Burkitt Lymphoma:** Classically associated with the **t(8;14)** translocation, which moves the c-MYC gene (Chr 8) to the IgH locus (Chr 14), leading to constitutive MYC expression [3]. * **Amplification:** **N-MYC** is commonly amplified in Neuroblastoma (correlates with poor prognosis), while **L-MYC** is associated with Small Cell Carcinoma of the Lung. * **Function:** MYC is often called a "master regulator" of metabolism (Warburg effect) and cell growth. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 292-293. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 296-297. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 324-325.

Q: A person showing two cell lines derived from one zygote is termed as?

Mosaicism. **Explanation:** **Mosaicism** is defined as the presence of two or more populations of cells with different genotypes in one individual, all of which are derived from a **single zygote** [1]. This occurs due to a post-zygotic mutation or non-disjunction during early embryonic development (mitosis) [1]. A classic clinical example is Mosaic Turner Syndrome (45,X/46,XX) or Mosaic Down Syndrome [1]. **Analysis of Incorrect Options:** * **Chimerism (Option A):** This refers to an individual composed of cells derived from **two or more different zygotes**. This can occur through the fusion of two embryos or via the exchange of hematopoietic stem cells between twins in utero. * **Segregation (Option C):** This is a basic principle of Mendelian genetics (Law of Segregation) stating that allele pairs separate during gamete formation (meiosis) and randomly unite at fertilization. * **Pseudo-dominance (Option D):** This occurs when a recessive trait appears to be inherited in a dominant fashion. This typically happens when a homozygous recessive individual mates with a heterozygous carrier, or due to a deletion of the dominant allele on the homologous chromosome. **High-Yield Clinical Pearls for NEET-PG:** * **Germline Mosaicism:** If a mutation occurs only in the germ cells, an unaffected parent can have multiple children with an autosomal dominant disorder (e.g., Osteogenesis Imperfecta). * **Lyonization:** X-inactivation in females is a form of physiological mosaicism. * **Confined Placental Mosaicism:** A discrepancy where the placenta has a chromosomal abnormality but the fetus is normal; this is a common cause of "false positives" in Chorionic Villus Sampling (CVS). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 168-171.

Q: What is the trinucleotide repeat seen in Fragile X syndrome?

CGG. **Explanation:** **Fragile X Syndrome** is the most common inherited cause of intellectual disability and is characterized by a trinucleotide repeat expansion in the **FMR1 gene** located on the X chromosome [1]. 1. **Correct Option (A) CGG:** The expansion occurs in the 5' untranslated region of the FMR1 gene. Normal individuals have 6–50 repeats. In Fragile X, this expands to a "full mutation" of **>200 CGG repeats**, leading to hypermethylation of the promoter, gene silencing, and a deficiency of the Fragile X Mental Retardation Protein (FMRP) [1]. 2. **Incorrect Option (B) CTG:** This repeat is associated with **Myotonic Dystrophy** (Type 1). 3. **Incorrect Option (C) CAG:** This is the most common repeat in polyglutamine diseases, most notably **Huntington’s Disease** and Spinocerebellar Ataxias [1]. 4. **Incorrect Option (D) GAA:** This repeat is seen in the frataxin gene in **Friedreich’s Ataxia**. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Triad:** Intellectual disability, large everted ears, and **macro-orchidism** (post-pubertal). * **Cytogenetics:** When cells are cultured in folate-deficient medium, the X chromosome shows a "fragile site" (breakage) at the distal long arm (Xq27.3) [2]. * **Anticipation:** The disease shows "anticipation," where the severity increases or age of onset decreases in successive generations due to further expansion of the repeats during oogenesis. * **Premutation (55–200 repeats):** Associated with Fragile X-associated Tremor/Ataxia Syndrome (FXTAS) and Premature Ovarian Failure [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 177-181. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 186-187.

Question 1

A 22-year-old primigravida had a fetal screening ultrasound study at 18 weeks showing a single large cerebral ventricle and fused thalami. On physical examination at birth at 36 weeks' gestation, the infant is small for gestational age and has multiple anomalies, including postaxial polydactyly of hands and feet, cyclopia, microcephaly, cleft lip and palate, and rocker-bottom feet. The infant dies 1 hour after birth. Which of the following CNS abnormalities best explains these findings?

Accepted Answer

Holoprosencephaly

Answer

Anencephaly

Answer

Arnold-Chiari II malformation

Answer

Dandy-Walker malformation

Question 2

In cell death, from which cellular component are myelin bodies derived?

Accepted Answer

Cell Membrane

Answer

Rough Endoplasmic Reticulum

Answer

Cytoplasm

Answer

Lysosome

Question 3

Neurofibromatosis I is inherited in which pattern?

Accepted Answer

Autosomal dominant

Answer

Autosomal recessive

Answer

X-linked recessive

Answer

X-linked dominant

Question 4

The MYC gene product functions as which of the following?

Accepted Answer

Transcription activator

Answer

Protein kinase inhibitor

Answer

Growth factor inhibitor

Answer

GTPase

Question 5

A person showing two cell lines derived from one zygote is termed as?

Accepted Answer

Mosaicism

Answer

Chimerism

Answer

Segregation

Answer

Pseudo-dominance

Question 6

All of the following characteristics are true of liposarcoma EXCEPT:

Accepted Answer

Is commonly found in the retroperitoneum

Answer

Frequently gives rise to embolization in lymphatics

Answer

Is the most common soft tissue sarcoma

Answer

Arises very rarely in subcutaneous tissue

Question 7

A patient with sepsis has a TLC of 15,000 cells/mm³ with the following differential: Neutrophils 40%, Eosinophils 7%, Band cells 15%, Metamyelocytes 5%, and Lymphocytes 35%. What is the immature to total neutrophil ratio (I:T ratio)?

Accepted Answer

20%

Answer

23%

Answer

30%

Answer

33%

Question 8

Hematopoietic stem cells differ from progenitor stem cells in that they can:

Accepted Answer

Long-term reconstitution of bone marrow

Answer

Form terminally differentiated cells

Answer

Produce growth factors

Answer

Have receptors for anchoring proteins

Question 9

What is the trinucleotide repeat seen in Fragile X syndrome?

Accepted Answer

CGG

Answer

CTG

Answer

CAG

Answer

GAA

Question 10

What are the similar features between cerebral abscess and cerebral infarct?

Accepted Answer

Liquefactive necrosis

Answer

Coagulative necrosis

Answer

Heal by collagen formation

Answer

Always develop from emboli from other site

General Pathology — MCQs

General Pathology — MCQs

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