General Pathology Practice Questions

Q: Which of the following is NOT a feature of Marfan's syndrome?

Reduced joint mobility. Explanation: Marfan’s syndrome is an **autosomal dominant** connective tissue disorder caused by a mutation in the **FBN1 gene** on chromosome 15, which encodes **Fibrillin-1** [1]. Fibrillin-1 is essential for the structural integrity of the extracellular matrix and for regulating TGF-β signaling [1]. 1. **Why "Reduced joint mobility" is correct:** Patients with Marfan’s syndrome typically exhibit **joint hypermobility** (laxity) rather than reduced mobility [1]. This occurs because the defective fibrillin leads to weakened ligaments and connective tissue. In contrast, reduced joint mobility (contractures) is a hallmark of *Congenital Contractural Arachnodactyly* (Beals Syndrome), caused by FBN2 mutations. 2. **Analysis of incorrect options:** * **Arachnodactyly:** This refers to "spider-like," abnormally long and slender fingers. It is a classic skeletal feature of Marfan’s, often assessed via the Steinberg (thumb) and Walker-Murdoch (wrist) signs [1]. * **Dislocation of the lens (Ectopia lentis):** This occurs in ~60% of patients. Characteristically, the dislocation is **upward and outward** (superior-temporal) due to weakness in the ciliary zonules. * **Aortic dissection:** This is the most serious complication. Cystic medial necrosis leads to dilation of the aortic root, predisposed to Type A dissection and aortic regurgitation [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of death:** Aortic dissection/rupture [1]. * **Cardiovascular:** Mitral Valve Prolapse (MVP) is also frequently seen [1]. * **Differentiation:** To distinguish from Homocystinuria (which also has Marfanoid habitus), remember that Homocystinuria has **downward** lens dislocation, intellectual disability, and increased risk of thrombosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 153-154.

Q: Edema is caused by all of the following mechanisms, EXCEPT?

Increased plasma proteins. This question tests your understanding of **Starling’s Forces**, which govern fluid movement between the intravascular and interstitial compartments. Edema occurs when there is an imbalance in these forces, leading to excess fluid accumulation in the tissues. ### **Explanation of the Correct Answer** **D. Increased plasma proteins:** This is the correct answer because increased plasma proteins (specifically albumin) would **increase plasma oncotic pressure**. According to Starling’s law, plasma oncotic pressure acts as a "magnet" that pulls fluid from the interstitium back into the capillaries. Therefore, an increase in plasma proteins would actually **prevent** edema. Conversely, *decreased* plasma proteins (hypoalbuminemia), seen in Nephrotic syndrome or liver cirrhosis, is a classic cause of edema. ### **Analysis of Incorrect Options** * **A. Increased vascular permeability:** Inflammation or toxins cause endothelial gaps, allowing fluid and proteins to leak into the interstitium (Exudate). This is a hallmark of acute inflammation. * **B. Obstruction to lymphatic flow:** Lymphatics normally drain the small amount of fluid that escapes capillaries. Obstruction (e.g., Filariasis, post-mastectomy) leads to **Lymphedema**. * **C. Sodium retention:** Excess sodium leads to water retention, increasing the **capillary hydrostatic pressure**, which pushes fluid into the tissues. This is seen in Heart Failure and Renal Failure. ### **High-Yield Clinical Pearls for NEET-PG** * **Starling’s Equation:** $Net\ Fluid\ Movement = K_f [(P_c - P_i) - \sigma(\pi_c - \pi_i)]$. * **Pitting Edema:** Usually caused by low oncotic pressure or high hydrostatic pressure (e.g., Cardiac failure). * **Non-pitting Edema:** Characteristic of **Lymphedema** and **Myxedema** (Hypothyroidism due to deposition of mucopolysaccharides). * **First sign of Edema:** Weight gain usually precedes visible clinical edema.

Q: What is the important function of cytosolic cytochrome C?

Apoptosis. ### Explanation **Correct Answer: A. Apoptosis** Cytochrome C is a peripheral membrane protein typically located in the inner mitochondrial membrane. Its presence in the **cytosol** is a hallmark of the **intrinsic (mitochondrial) pathway of apoptosis**. When a cell undergoes stress (DNA damage, oxidative stress, or withdrawal of growth factors), the pro-apoptotic proteins **BAX and BAK** create pores in the mitochondrial outer membrane. This leads to the leakage of Cytochrome C into the cytosol. Once in the cytosol, Cytochrome C binds to **Apaf-1** (Apoptotic protease activating factor-1) and ATP to form a wheel-like complex called the **Apoptosome**. This complex activates **Caspase-9**, triggering a proteolytic cascade that leads to programmed cell death. **Why other options are incorrect:** * **B. Cell Necrosis:** Necrosis is an uncontrolled, accidental cell death characterized by cell swelling and membrane rupture. It is not mediated by the specific Cytochrome C/Caspase pathway. * **C. Electron Transport Chain (ETC):** While Cytochrome C is vital for the ETC (shuttling electrons between Complex III and IV), this function occurs strictly **within the mitochondria**, not the cytosol. The question specifically asks for the *cytosolic* function. * **D. Cell Division:** Cytochrome C has no direct regulatory role in mitosis or the cell cycle. **High-Yield Clinical Pearls for NEET-PG:** * **The "Point of No Return":** The release of Cytochrome C into the cytosol is considered the irreversible step in the intrinsic pathway of apoptosis. * **Bcl-2 Family:** Remember that **Bcl-2 and Bcl-xL** are anti-apoptotic (they prevent Cytochrome C release), while **BAX and BAK** are pro-apoptotic. * **Caspase Cascade:** Intrinsic pathway = Caspase **9**; Extrinsic (Death Receptor) pathway = Caspase **8**. Both converge on executioner Caspases **3 and 6**.

Q: All of the following are intermediate filaments except?

Cadherin. **Explanation:** The cytoskeleton of a cell consists of three main components: microfilaments (actin), microtubules (tubulin), and **intermediate filaments (IFs)**. Intermediate filaments (10 nm) provide structural stability to cells and are tissue-specific markers. **Why Cadherin is the correct answer:** **Cadherins** are not cytoskeletal filaments; they are **transmembrane cell adhesion molecules** (CAMs) [1]. They play a critical role in cell-cell adhesion by forming "adherens junctions" and "desmosomes." They are calcium-dependent proteins that link the internal cytoskeleton of one cell to another, but they do not function as intermediate filaments themselves [1]. **Why the other options are incorrect:** * **Lamin (Option A):** These are type V intermediate filaments found in the **nucleus** (nuclear lamina) of all nucleated cells. They provide structural support to the nuclear envelope. * **Vimentin (Option C):** This is the most common type III intermediate filament. It is the characteristic marker for cells of **mesenchymal origin** (e.g., fibroblasts, endothelium, and most sarcomas). * **Desmin (Option D):** Also a type III intermediate filament, desmin is specific to **muscle cells** (skeletal, cardiac, and smooth muscle). It links myofibrils together. **High-Yield Clinical Pearls for NEET-PG:** * **Cytokeratin:** IF marker for **Epithelial** cells (used to diagnose Carcinomas). * **GFAP (Glial Fibrillary Acidic Protein):** IF marker for **Astrocytes** and ependymal cells (used to diagnose Gliomas). * **Neurofilaments:** IF marker for **Neurons** (used to diagnose Pheochromocytoma or Neuroblastoma). * **Mallory Hyaline bodies** (seen in alcoholic liver disease) are composed of tangled **cytokeratin** intermediate filaments. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 23-24.

Q: In which type of necrosis is tissue architecture preserved?

Coagulative necrosis. **Explanation:** **Coagulative necrosis** is the correct answer because it is characterized by the **preservation of basic tissue architecture** for at least several days [1]. The underlying mechanism involves the denaturation of not only structural proteins but also enzymatic proteins. This denaturation blocks the proteolysis (digestion) of the dead cells; as a result, firm, opaque, "ghost-like" cell outlines persist without nuclei until phagocytes eventually clear the debris [1]. **Why other options are incorrect:** * **Liquefaction necrosis:** In contrast to coagulative necrosis, the tissue is completely digested by hydrolytic enzymes, transforming it into a liquid viscous mass (pus). The architecture is entirely lost. This is typically seen in focal bacterial infections or brain infarcts. * **Fat necrosis:** This refers to focal areas of fat destruction, typically resulting from the release of activated pancreatic lipases [1]. It results in the formation of "chalky white" calcium deposits (saponification), which destroys the original cellular structure [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common Type:** Coagulative necrosis is the most common pattern of necrosis. * **Etiology:** It is characteristic of **hypoxic/ischemic death** in all solid organs **except the brain**. * **Microscopic Hallmark:** "Ghost cells" (cells with preserved outlines but loss of nuclei/organelles) [1]. * **Macroscopic Hallmark:** The affected area is typically firm and pale (infarct) [1]. * **Key Exception:** Ischemia in the **Central Nervous System (CNS)** results in liquefaction necrosis, not coagulative necrosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 53-55.

Question 1

Which of the following is NOT a feature of Marfan's syndrome?

Accepted Answer

Reduced joint mobility

Answer

Arachnodactyly

Answer

Dislocation of the lens

Answer

Aortic dissection

Question 2

Aging is most probably due to:

Accepted Answer

Accumulated free radical injury in tissues

Answer

Non-random mutation in somatic cells

Answer

Decrease in collagen cross-linking

Answer

Increase in superoxide dismutase

Question 3

Edema is caused by all of the following mechanisms, EXCEPT?

Accepted Answer

Increased plasma proteins

Answer

Increased vascular permeability

Answer

Obstruction to lymphatic flow

Answer

Sodium retention

Question 4

SMAC/DIABLO is a:

Accepted Answer

Pro-apoptotic protein

Answer

Anti-apoptotic protein

Answer

Induces necrosis

Answer

Acts both as anti- and pro-apoptotic protein

Question 5

Cystic fibrosis is inherited as an autosomal recessive condition. A normal couple has one daughter affected with the disease. They are now planning to have another child. What is the chance of her sibling being affected by the disease?

Accepted Answer

1/4

Answer

0

Answer

1/2

Answer

3/4

Question 6

A 28-year-old female presents with recurrent abortions and pain in the calves. She is most likely suffering from a deficiency of which of the following?

Accepted Answer

Protein C

Answer

Thrombin

Answer

Factor XIII

Answer

Plasmin

Question 7

What is the important function of cytosolic cytochrome C?

Accepted Answer

Apoptosis

Answer

Cell necrosis

Answer

Electron transport chain

Answer

Cell division

Question 8

All of the following are intermediate filaments except?

Accepted Answer

Cadherin

Answer

Lamin

Answer

Vimentin

Answer

Desmin

Question 9

In which type of necrosis is tissue architecture preserved?

Accepted Answer

Coagulative necrosis

Answer

Liquefaction necrosis

Answer

Fat necrosis

Answer

All of the above

Question 10

Which of the following is an example of a non-dividing/permanent cell?

Accepted Answer

Neuron

Answer

Hepatocyte

Answer

Lymphocyte

Answer

Respiratory epithelium

General Pathology — MCQs

General Pathology — MCQs

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