Biochemistry
3 questionsWhich enzyme is required for cutting the DNA strand during synthesis?
DNA microarrays allow detection of gene mutations through which process?
Protein glycosylation occurs in:
NEET-PG 2012 - Biochemistry NEET-PG Practice Questions and MCQs
Question 401: Which enzyme is required for cutting the DNA strand during synthesis?
- A. DNA polymerase
- B. DNA ligase
- C. Topoisomerase (Correct Answer)
- D. Helicase
Explanation: ***Topoisomerase*** - **Topoisomerases** are enzymes essential for DNA replication; they induce temporary **single- or double-strand breaks** in DNA to relieve **supercoiling** ahead of the replication fork. - This cutting and rejoining activity prevents the DNA from becoming excessively tangled and facilitates the unwinding process required for synthesis. *DNA polymerase* - **DNA polymerase** is responsible for **synthesizing new DNA strands** by adding nucleotides, not for cutting the DNA backbone. - It works by moving along the template strand, reading the bases, and then adding complementary nucleotides to the growing DNA strand. *DNA ligase* - **DNA ligase** functions to **join DNA fragments** together by forming phosphodiester bonds, especially in sealing Okazaki fragments during lagging strand synthesis. - Its role is to ligate (join) cut strands, not to initiate cuts in the DNA. *Helicase* - **Helicase** unwinds the DNA double helix into single strands using ATP hydrolysis; it **separates the two strands** but does not cut the phosphodiester backbone. - This enzyme creates the replication fork by disrupting hydrogen bonds between base pairs, making the DNA accessible for replication machinery.
Question 402: DNA microarrays allow detection of gene mutations through which process?
- A. Polymerase Chain Reaction
- B. Cloning
- C. Southern Blotting
- D. Hybridization (Correct Answer)
Explanation: ***Hybridization*** - DNA microarrays detect mutations by **hybridizing labeled patient DNA** to **thousands of oligonucleotide probes** containing known DNA sequences immobilized on a solid surface. - A mismatch between the patient's DNA and the probe results in **reduced or absent hybridization**, indicating a **mutation or genetic variation**. - This principle allows **high-throughput screening** of multiple genes simultaneously. *Polymerase Chain Reaction* - PCR is used to **amplify specific DNA sequences exponentially**, creating millions of copies from minimal starting material. - While PCR may be used to **prepare DNA samples** before microarray analysis, it is **not the detection mechanism** on the chip itself. *Cloning* - Cloning involves creating **identical copies of DNA fragments, cells, or organisms** using vectors and host cells. - It's a method for **producing large quantities** of specific DNA sequences but **not a detection technique** for mutations on microarrays. *Southern Blotting* - Southern blotting detects specific DNA sequences through **gel electrophoresis, membrane transfer, and probe hybridization**. - While it also uses hybridization, it is a **low-throughput technique** analyzing one sample at a time, unlike the **high-throughput parallel analysis** of DNA microarrays.
Question 403: Protein glycosylation occurs in:
- A. Peroxisomes
- B. Endoplasmic reticulum (ER) (Correct Answer)
- C. Mitochondria
- D. Golgi bodies
Explanation: ***ER*** - **N-linked glycosylation**, the most common type of protein glycosylation, initiates in the **endoplasmic reticulum (ER)**, where an oligosaccharide precursor is transferred to asparagine residues of newly synthesized proteins. - The ER environment facilitates protein folding and quality control, ensuring correctly folded glycoproteins are transported further. *Golgi bodies* - While **further modification and processing** of glycosylated proteins occur in the Golgi apparatus, the initial step of N-linked glycosylation begins in the ER. - The Golgi is responsible for trimming and adding different sugar residues to complete the **glycan chains** and for sorting the glycoproteins to their final destinations. *Mitochondria* - Mitochondria are primarily involved in **cellular respiration** and **ATP production**. - They do not play a significant role in protein glycosylation; most mitochondrial proteins are imported from the cytoplasm in an unglycosylated state. *Peroxisomes* - Peroxisomes are involved in various **metabolic processes**, including fatty acid oxidation and detoxification. - They are not known to be sites of protein glycosylation.
Internal Medicine
1 questionsWhich components of cigarette smoke are known to contribute to coronary artery disease?
NEET-PG 2012 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 401: Which components of cigarette smoke are known to contribute to coronary artery disease?
- A. Nicotine, carbon monoxide, and tar (Correct Answer)
- B. Carbon monoxide and tar
- C. Carbon dioxide
- D. Tar and nicotine
Explanation: ***Nicotine, carbon monoxide, and tar*** - **Nicotine** directly affects the cardiovascular system by increasing **heart rate**, **blood pressure**, and causing **vasoconstriction**, as well as promoting atherogenesis [2]. - **Carbon monoxide** binds to hemoglobin with higher affinity than oxygen, forming **carboxyhemoglobin**, which reduces oxygen delivery to tissues, leading to **endothelial damage** and contributing to atherosclerosis [1]. - **Tar** contains various **carcinogens** and toxic chemicals that contribute to inflammation, oxidative stress, and lipid peroxidation, all of which are implicated in the development and progression of **atherosclerosis**. *Carbon monoxide and tar* - While both contribute significantly, this option **omits nicotine**, which is a major contributor to the cardiovascular effects of smoking. - Nicotine's direct impact on **vasoconstriction** and **atherogenesis** is a critical factor in coronary artery disease [2]. *Carbon dioxide* - **Carbon dioxide** is a product of respiration and combustion but is not considered a primary direct contributor to the pathogenesis of **coronary artery disease** from cigarette smoke in the same way as nicotine, carbon monoxide, and tar. - Its presence in smoke primarily relates to its role in **respiratory physiology** rather than direct vascular damage. *Tar and nicotine* - This option correctly identifies **tar** and **nicotine** as contributors but **omits carbon monoxide**, which plays a crucial role in reducing oxygen-carrying capacity and directly damaging the endothelium [1]. - The impact of **carbon monoxide** on cardiac oxygen supply is a significant mechanism in smoking-related cardiovascular disease [1].
Pathology
5 questionsMaximum collagen deposition in wound healing is seen at -
What laboratory findings are associated with common variable hypogammaglobulinemia?
Li–Fraumeni syndrome is associated with mutations in which of the following genes?
All of the following statements about Giant cell arteritis are true except?
What change is seen in the vessels during the initial stage of Raynaud's phenomenon?
NEET-PG 2012 - Pathology NEET-PG Practice Questions and MCQs
Question 401: Maximum collagen deposition in wound healing is seen at -
- A. End of third week (Correct Answer)
- B. End of first week
- C. End of 2 months
- D. End of second week
Explanation: ***End of third week*** - By the end of the **third week**, the proliferative phase of wound healing is well underway, characterized by significant **collagen deposition**. [1] - At this stage, **Type III collagen** is initially laid down, which is later replaced by stronger **Type I collagen**, contributing to increasing wound strength. *End of first week* - The first week primarily involves the **inflammatory phase** and the initial stages of **proliferation**, with minimal new collagen deposition. [2] - While some **fibroblasts** are present, the amount of collagen synthesized is still relatively low. *End of second week* - Collagen synthesis is ongoing during the second week, but the **peak deposition rate** and overall amount of collagen accumulated are typically not as high as at the end of the third week. - The wound is gaining strength, but further increase in collagen content and remodeling is yet to occur. *End of 2 months* - By 2 months, the wound is in the **remodeling phase**, where the total collagen content might be substantial but the *rate of new collagen synthesis* has slowed down. - At this stage, there is a balance between **collagen synthesis** and **degradation**, and the collagen fibers are being reorganized and cross-linked to further improve tensile strength. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-119. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 115.
Question 402: What laboratory findings are associated with common variable hypogammaglobulinemia?
- A. Low serum immunoglobulin levels (Correct Answer)
- B. Decreased B cell count
- C. Increased B cell count
- D. Neutropenia
Explanation: ***Low serum immunoglobulin levels*** - **Common variable hypogammaglobulinemia (CVID)** is characterized by significantly **low levels of IgG, IgA, and/or IgM** due to impaired B cell differentiation into plasma cells. - This deficiency in antibodies is the hallmark of the disorder, explaining the increased susceptibility to infections. *Decreased B cell count* - While CVID involves impaired B cell function, the **B cell counts** in the peripheral blood are typically **normal** or sometimes even elevated [1]. - The problem lies in their inability to differentiate and produce adequate antibodies, not in their numerical presence [1]. *Increased B cell count* - An increased B cell count is not a characteristic finding in CVID; peripheral B cell numbers are usually normal [1]. - If B cell counts are significantly increased, other conditions such as certain **lymphoproliferative disorders** should be considered. *Neutropenia* - **Neutropenia** (low neutrophil count) is not a primary diagnostic feature of CVID, although it can occur in some patients with autoimmune complications. - The defining laboratory finding is the **deficiency of immunoglobulins**, leading to recurrent infections. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 249-250.
Question 403: Li–Fraumeni syndrome is associated with mutations in which of the following genes?
- A. Gene RB1
- B. Gene BRCA1
- C. Gene P21
- D. Gene TP53 (Correct Answer)
Explanation: ***Gene TP53*** - Li-Fraumeni syndrome is a rare, inherited cancer susceptibility syndrome associated with germline mutations in the **TP53 tumor suppressor gene**. - The **TP53 gene** encodes the p53 protein, which plays a critical role in cell cycle arrest, DNA repair, and initiation of apoptosis in response to cellular stress, thus preventing tumor formation. *Gene P21* - The **p21 gene** (CDKN1A) is a cyclin-dependent kinase inhibitor that acts downstream of p53, mediating p53-induced cell cycle arrest. - While p21 is involved in the p53 pathway, mutations in p21 itself are not the primary cause of Li-Fraumeni syndrome. *Gene RB1* - The **RB1 gene** encodes the retinoblastoma protein, a tumor suppressor involved in cell cycle regulation, particularly in controlling passage from G1 to S phase. - Mutations in **RB1** are primarily associated with hereditary retinoblastoma and osteosarcoma, not Li-Fraumeni syndrome. *Gene BRCA1* - The **BRCA1 gene** is a tumor suppressor gene involved in DNA repair, especially homologous recombination. - Germline mutations in **BRCA1** are strongly associated with hereditary breast and ovarian cancer syndrome, not Li-Fraumeni syndrome.
Question 404: All of the following statements about Giant cell arteritis are true except?
- A. Involves large to small sized arteries (Correct Answer)
- B. Granulomatous inflammation
- C. Segmental nature of the involvement
- D. Can involve the aorta and its major branches
Explanation: ***Involves large to small sized arteries*** - Giant cell arteritis (GCA) predominantly affects **medium to large-sized arteries**, most commonly the branches of the **carotid artery**, such as the temporal arteries [1]. - While it can affect various arteries, it does not typically involve **small-sized arteries**, such as arterioles, directly as a primary site of inflammation. *Granulomatous inflammation* - GCA is characterized histologically by **granulomatous inflammation** within the arterial wall, which includes multinucleated **giant cells** and lymphocytes [2]. - This specific inflammatory pattern is a hallmark feature used in the diagnosis of GCA upon biopsy [2]. *Segmental nature of the involvement* - The arterial inflammation in GCA is often **segmental**, meaning that affected arteries may have inflamed and non-inflamed sections alternating along their length [2]. - This segmental involvement often necessitates **longer biopsies** (e.g., 2-3 cm for temporal artery biopsy) to increase the diagnostic yield. *Can involve the aorta and its major branches* - GCA can indeed affect the **aorta** (aortitis) and its major branches, leading to complications like **aneurysms** or **dissections**. - Involvement of these larger vessels can manifest as symptoms such as **claudication** in the limbs or asymptomatic aneurysms detectable on imaging [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 688-689. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 516-517.
Question 405: What change is seen in the vessels during the initial stage of Raynaud's phenomenon?
- A. No pathological changes (functional vasospasm only) (Correct Answer)
- B. Thrombosis
- C. Fibrinoid necrosis
- D. Hyaline sclerosis
Explanation: ***No pathological changes (functional vasospasm only)*** - Raynaud's phenomenon, particularly **primary Raynaud's** (Raynaud's disease), is characterized by **functional vasospasm** of arterioles, especially in fingers and toes, in response to cold or stress [1]. - In its initial stages, there are no structural changes or pathological alterations within the vessel walls; the vasoconstriction is entirely **functional** [1]. *Thrombosis* - **Thrombosis** involves the formation of a blood clot within a vessel, obstructing blood flow. - While severe Raynaud's can, in rare cases, lead to digital ischemia and microthrombosis, it is **not the primary or initial change** seen in typical Raynaud's phenomenon. *Fibrinoid necrosis* - **Fibrinoid necrosis** is a type of vascular damage associated with severe autoimmune diseases or malignant hypertension, where fibrin and plasma proteins deposit in the vessel wall. - This is a **structural, irreversible change** and is not characteristic of the initial, functional vasospasm seen in Raynaud's phenomenon. *Hyaline sclerosis* - **Hyaline sclerosis** is a change in small arteries and arterioles, often seen in benign essential hypertension or as part of the aging process, where the vessel wall thickens and becomes hyaline (glassy) due to plasma protein leakage and fibrosis. - This represents a **chronic structural change** and is not the acute, intermittent, functional vasoconstriction defining the initial stage of Raynaud's. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 520-522.
Pharmacology
1 questionsWhich of the following is a guanosine analogue?
NEET-PG 2012 - Pharmacology NEET-PG Practice Questions and MCQs
Question 401: Which of the following is a guanosine analogue?
- A. Abacavir (Correct Answer)
- B. Bromodeoxyuridine
- C. Allopurinol
- D. Acyclovir
Explanation: ***Abacavir*** - **Abacavir** is a nucleoside reverse transcriptase inhibitor (NRTI) used in HIV treatment. - It is a **carbocyclic analogue of guanosine** (specifically, a 2'-deoxyguanosine analogue). - Structurally, it contains a modified cyclopentane ring instead of the ribose sugar, but retains the guanine base, making it a guanosine analogue. *Acyclovir* - **Acyclovir** is also a **guanosine analogue** - specifically an acyclic guanosine analogue. - It is an antiviral drug used to treat herpes simplex virus (HSV) and varicella-zoster virus (VZV) infections. - Note: Both Abacavir and Acyclovir are technically guanosine analogues; in this PYQ context, Abacavir is the expected answer. *Bromodeoxyuridine* - **Bromodeoxyuridine** is a **pyrimidine analogue**, specifically a thymidine analogue. - It is incorporated into DNA during replication and is used in research and as a radiosensitizer. *Allopurinol* - **Allopurinol** is a purine analogue (hypoxanthine analogue) that inhibits xanthine oxidase. - It is primarily used to treat **gout** and prevent kidney stones by reducing uric acid production. - While it's a purine derivative, it is not specifically a guanosine analogue.