General Pathology Practice Questions

Q: What is the characteristic finding of sweat chloride levels in patients with cystic fibrosis?

Increased. **Explanation:** The correct answer is **B (Increased)**. **Pathophysiology:** Cystic Fibrosis (CF) is caused by a mutation in the **CFTR (Cystic Fibrosis Transmembrane Conductance Regulator)** gene. The CFTR protein functions differently depending on the tissue. In the **sweat glands**, its primary role is the **reabsorption** of chloride ions from the primary secretion back into the ductal cells [1]. Sodium follows chloride to maintain electrical neutrality. In CF patients, the defective CFTR channel cannot reabsorb chloride; consequently, chloride remains in the sweat, leading to an abnormally high concentration of salt (NaCl) on the skin surface [1]. **Analysis of Incorrect Options:** * **Option A (Decreased):** This is incorrect because the defect lies in the inability to *reabsorb* chloride from the lumen. Decreased levels are not seen in CF [1]. * **Option C & D (No change / May increase or decrease):** Sweat chloride levels are consistently elevated in classic CF, making these options clinically inaccurately. **High-Yield NEET-PG Pearls:** * **Gold Standard Diagnosis:** The **Pilocarpine Iontophoresis Sweat Test** is the diagnostic test of choice. A chloride concentration **>60 mmol/L** is diagnostic of CF. * **Tissue Paradox:** Remember the "CFTR Paradox"—in the **respiratory and GI tracts**, CFTR failure leads to decreased chloride *secretion* (causing thick, dehydrated mucus), whereas in **sweat glands**, it leads to decreased chloride *reabsorption* [1]. * **Genetics:** Most common mutation is **ΔF508** (Class II defect: protein misfolding and degradation). * **Clinical Sign:** Mothers often report that the infant "tastes salty" when kissed. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Lumen Of Sweat Duct, pp. 475-476.

Q: Mutation in Marfan's syndrome is associated with which gene?

Fibrillin I. **Explanation:** **Marfan’s Syndrome** is an autosomal dominant disorder of connective tissue caused by a mutation in the **FBN1 gene** located on chromosome **15q21**. This gene encodes **Fibrillin-1**, a glycoprotein that serves as a major structural component of extracellular microfibrils. These microfibrils form a scaffold for the deposition of elastin and are essential for maintaining the structural integrity of tissues such as the aortic wall, skeletal system, and the suspensory ligaments of the lens. **Analysis of Options:** * **Fibrillin-1 (Correct):** Mutations lead to mechanical weakness of connective tissues and excessive activation of **TGF-β**, which contributes to the clinical manifestations (e.g., aortic root dilation) [1]. * **Collagen I:** Mutations here are associated with **Osteogenesis Imperfecta** (brittle bone disease) and certain types of Ehlers-Danlos Syndrome. * **Collagen IV:** This is a key component of the basement membrane; mutations are associated with **Alport Syndrome**. * **Fibrillin-2:** Mutations in the FBN2 gene (chromosome 5) cause **Congenital Contractural Arachnodactyly** (Beals Syndrome), which mimics Marfan’s but lacks the cardiac and ocular complications. **Clinical Pearls for NEET-PG:** 1. **Skeletal:** Dolichostenomelia (long limbs), arachnodactyly (long fingers), and pectus excavatum [1]. 2. **Ocular:** **Ectopia lentis** (dislocation of the lens), typically **upward and outward** (superior-temporal). 3. **Cardiovascular:** The most life-threatening complication is **Aortic Dissection** preceded by cystic medial necrosis. Mitral Valve Prolapse (MVP) is also common [1]. 4. **Diagnostic Sign:** Steinberg sign (thumb sign) and Walker-Murdoch sign (wrist sign). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 153-154.

Q: What is the initiating mechanism in endotoxic shock?

Endothelial injury. The initiating event in endotoxic (septic) shock is **Endothelial injury**. Endotoxic shock is primarily triggered by **Lipopolysaccharide (LPS)**, a component of the cell wall of Gram-negative bacteria [2]. 1. **Why Endothelial Injury is Correct:** When LPS enters the bloodstream, it binds to Lipopolysaccharide-binding protein (LBP) and interacts with **CD14 and TLR-4 receptors** on macrophages and endothelial cells. This triggers a massive release of inflammatory cytokines (TNF-α, IL-1) [3]. These mediators cause direct damage to the vascular endothelium [1]. This injury exposes the subendothelial collagen, activating the coagulation cascade (leading to DIC) and causing the release of nitric oxide (NO), which is the primary driver of the subsequent systemic effects. 2. **Why Other Options are Incorrect:** * **Peripheral vasodilation (A):** This is a *result* of the endothelial injury and the release of potent vasodilators like Nitric Oxide. * **Increased vascular permeability (C):** This occurs *after* endothelial injury and activation [1]. The "leaky" capillaries lead to edema and hypovolemia, but this is a secondary structural consequence. * **Reduced cardiac output (D):** In the early (hyperdynamic) phase of septic shock, cardiac output is actually **increased**. **High-Yield Clinical Pearls for NEET-PG:** * **Key Mediator:** **TNF-α** is the primary cytokine mediator of septic shock [3]. * **Receptor:** **TLR-4** (Toll-like receptor 4) is the specific pattern recognition receptor for LPS. * **Nitric Oxide (NO):** Produced by inducible Nitric Oxide Synthase (iNOS) in response to cytokines, it is responsible for the characteristic hypotension. * **Warm Shock:** Septic shock is initially a "warm shock" due to peripheral vasodilation, unlike hypovolemic or cardiogenic shock.

Question 1

Time taken by tissue to develop frank necrosis is approximately:

Accepted Answer

4 hours

Answer

30 minutes

Answer

1 hour

Answer

2 hours

Question 2

HER-2/NEU receptor gene mutation is seen in which cancer?

Accepted Answer

Breast cancer

Answer

Squamous cell carcinoma

Answer

Glioblastoma

Answer

All of the above

Question 3

What is the characteristic finding of sweat chloride levels in patients with cystic fibrosis?

Accepted Answer

Increased

Answer

Decreased

Answer

No change

Answer

May increase or decrease

Question 4

Myasthenia gravis is caused by dysfunction of -

Accepted Answer

Thymus gland

Answer

Pineal gland

Answer

Pituitary gland

Answer

Parathyroid gland

Question 5

Which of the following statements about amyloidosis is false?

Accepted Answer

It is made of proteins that calcify.

Answer

It can be a complication of chronic infections.

Answer

It is associated with extracellular eosinophilic hyaline material.

Answer

It shows apple-green birefringence under polarized light.

Question 6

A 40-year-old female presented with acute painful swelling of the left leg. Ultrasound of the left leg showed deep venous thrombosis. Which of the following abnormalities is least likely to be involved in this condition?

Accepted Answer

Hypohomocysteinemia

Answer

Factor V Leiden mutation

Answer

Prothrombin gene mutation

Answer

Protein C deficiency

Question 7

Mutation in Marfan's syndrome is associated with which gene?

Accepted Answer

Fibrillin I

Answer

Collagen I

Answer

Collagen IV

Answer

Fibrillin II

Question 8

What is the initiating mechanism in endotoxic shock?

Accepted Answer

Endothelial injury

Answer

Peripheral vasodilation

Answer

Increased vascular permeability

Answer

Reduced cardiac output

Question 9

Senescent cells are deficient in which enzyme?

Accepted Answer

Telomerase

Answer

RNA polymerase

Answer

DNA polymerase

Answer

Helicase

Question 10

A tissue preparation is experimentally subjected to a hypoxic environment. The cells in this tissue begin to swell, and chromatin begins to clump in cell nuclei. ATPases are activated, and ATP production decreases. Which of the following ions accumulating in mitochondria and the cytosol contributes most to these findings and to eventual cell death?

Accepted Answer

Ca2+

Answer

Cl-

Answer

HCO3-

Answer

K+

General Pathology — MCQs

General Pathology — MCQs

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