General Pathology Practice Questions

Q: Which of the following is an anti-apoptotic gene?

Bcl-2. ***Bcl-2*** - **Bcl-2** (B-cell lymphoma 2) is a proto-oncogene that plays a critical role in regulating **apoptosis** by inhibiting programmed cell death. - It prevents the release of pro-apoptotic factors from the mitochondria, thereby promoting **cell survival**. *c-myc* - **c-myc** is a proto-oncogene involved in cell proliferation, growth, and **apoptosis**; it is not primarily an anti-apoptotic gene. - Upregulation of c-myc can, in fact, sensitize cells to **apoptosis** if survival signals are absent. *p53* - **p53** is a tumor suppressor gene that induces cell cycle arrest or **apoptosis** in response to DNA damage or other cellular stresses. - It is a **pro-apoptotic** gene that actively promotes programmed cell death, rather than preventing it. *Bax* - **Bax** (Bcl-2-associated X protein) is a prominent **pro-apoptotic** protein. - It promotes **apoptosis** by forming pores in the mitochondrial outer membrane, leading to the release of cytochrome c and activation of caspases.

Q: Which of the following is most susceptible to ionizing radiation?

Small lymphocytes. ***Small lymphocytes*** - **Lymphocytes** are highly sensitive to **ionizing radiation** due to their rapid proliferation and vulnerability during DNA synthesis [1]. - Exposure to radiation can lead to rapid **apoptosis** (programmed cell death) of lymphocytes, causing **lymphocytopenia** [1]. *Nerve cells* - **Nerve cells** are generally considered **radioresistant** because they are terminally differentiated and do not undergo cell division. - Their primary function is transmission of electrical impulses, which is not immediately disrupted by typical radiation doses. *Epithelial cells* - **Epithelial cells** (e.g., skin, gut lining) are moderately sensitive to radiation, primarily due to their **high turnover rate** [1]. - However, they are generally less sensitive than lymphocytes, and their damage often requires higher doses or prolonged exposure [1]. *Mature bone* - **Mature bone** is highly resistant to radiation because its cells (osteocytes) are largely quiescent and the extracellular matrix is inert [1]. - Significant damage to bone typically occurs at very high doses, affecting the more sensitive **bone marrow** stem cells within it rather than the mature bone itself [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 111-114.

Q: Type of necrosis seen in case of burn:

Coagulative necrosis.. ***Coagulative necrosis.*** [1] - Burn injuries cause **protein denaturation** due to heat, leading to **cell death** where the cellular architecture is preserved for some time [1]. - This is the **primary and characteristic** type of necrosis directly resulting from thermal injury [1]. - The coagulation of intracellular proteins results in an **infarcted area** that appears firm and opaque [1]. *Both coagulative and liquefactive.* - While coagulative necrosis is the primary type, liquefactive necrosis may occur **secondarily** if there is superimposed infection or tissue breakdown. - However, the question asks for the type of necrosis **seen in case of burn**, which refers to the **primary pathological process** caused by thermal injury itself. - The characteristic and predominant pattern is **coagulative**, not both simultaneously. *Liquefactive necrosis.* - **Liquefactive necrosis** is characterized by the dissolution of dead cells into a viscous liquid mass due to enzymatic digestion. - Typically seen in **bacterial abscesses**, **brain infarcts**, and **hypoxic death of CNS tissue**. - This is not the primary type of necrosis directly caused by thermal injury of a burn. *Caseous necrosis.* - **Caseous necrosis** is a distinct form of cell death associated with specific granulomatous diseases, most notably **tuberculosis**. - Results in cheese-like, friable dead tissue with loss of cellular architecture. - Not characteristic of burn injuries. **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. 51-55.

Q: Crumpled paper appearance of cells is a feature of-

Gaucher disease. ***Gaucher disease*** - The **crumpled paper** or **wrinkled tissue paper** appearance is characteristic of **Gaucher cells**, which are macrophages engorged with **glucocerebroside** [1]. - This accumulation results from a deficiency in the enzyme **glucocerebrosidase**, a hallmark of Gaucher disease [1]. *Asbestosis* - Characterized by the presence of **asbestos bodies** (ferruginous bodies), which are asbestos fibers coated with an iron-protein complex, not cells with crumpled appearance [2]. - This condition involves **pulmonary fibrosis** due to asbestos exposure [2]. *GVHD (Graft-versus-host disease)* - Histologically, GVHD is characterized by **lymphocytic infiltration** and damage to target organs like skin, liver, and GI tract, not by storage cells with a crumpled appearance. - It is an immunological reaction occurring after **allogeneic hematopoietic stem cell transplantation**. *Wilson's disease* - Involves excessive accumulation of **copper** in various tissues, particularly the liver, brain, and cornea. - Diagnosed by markers like low **ceruloplasmin** and high urinary copper, and does not involve cells with a storage-related crumpled appearance. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 162-163. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 698-699.

Q: Radiation mediates its effect by

Ionization of the molecules. ***Ionization of the molecules*** - Radiation, particularly **ionizing radiation**, interacts with biological molecules by ejecting electrons, leading to the formation of highly reactive **ions and free radicals** [1]. - This **ionization** process is the primary mechanism by which radiation damages cellular components, including **DNA** [2]. *Protein coagulation* - While radiation can cause protein damage, **coagulation** is not its primary or direct mechanism, especially at clinically relevant doses. - Protein coagulation is more typically associated with **heat** or certain strong chemical agents. *Osmolysis of cells* - **Osmolysis** refers to the rupture of cells due to excessive water influx, often caused by changes in osmotic pressure. - Radiation does not directly induce **osmotic imbalances** leading to cell lysis. *Denaturation of DNA* - While radiation ultimately leads to **DNA damage**, denaturation (unfolding) is a specific type of damage, often caused by heat or extreme pH. - The direct effect of radiation is **ionization**, which then indirectly causes various forms of DNA damage including breaks, cross-links, and base modifications, but not solely "denaturation" [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 101-102. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Central Nervous System Synapse, pp. 436-437.

Q: Following pathogenetic mechanisms operate in septic shock except -

Increased peripheral vascular resistance. Following pathogenetic mechanisms operate in septic shock except - ***Increased peripheral vascular resistance*** - Septic shock is characterized by profound **vasodilation** and a subsequent **decrease in systemic vascular resistance (SVR)**, leading to hypoperfusion. - The body's compensatory mechanisms attempt to increase cardiac output rather than constrict peripheral vessels, making increased PVR an unlikely finding in established septic shock. [1] *Direct toxic endothelial injury* - **Bacterial products** (e.g., endotoxins from Gram-negative bacteria) and inflammatory mediators directly damage the **endothelium**, leading to capillary leak and microvascular dysfunction. - This endothelial damage contributes significantly to the widespread organ damage seen in sepsis. *Veno constriction* - While initial compensatory mechanisms might involve elements of vasoconstriction to maintain blood pressure, the hallmark of septic shock is widespread **vasodilation**, which includes both arterial and venous beds. - Early, fleeting venoconstriction is overshadowed by the profound venodilation and loss of venous tone that ultimately contributes to reduced preload and distributive shock. *Activation of complement* - The innate immune response in sepsis triggers the **complement cascade**, leading to the generation of potent inflammatory mediators. - Complement activation contributes to endothelial damage, leukocyte recruitment, and further amplification of the systemic inflammatory response.

Question 1

Which of the following is an anti-apoptotic gene?

Accepted Answer

Bcl-2

Answer

c-myc

Answer

p53

Answer

Bax

Question 2

Which of the following is most susceptible to ionizing radiation?

Accepted Answer

Small lymphocytes

Answer

Nerve cells

Answer

Epithelial cells

Answer

Mature bone

Question 3

The following pattern of aberration occurs, when irradiation is done at which of the following phase of cell cycle?​

Accepted Answer

Both 1 and 2

Answer

Early S phase

Answer

G1 Phase

Answer

G2 phase

Question 4

Type of necrosis seen in case of burn:

Accepted Answer

Coagulative necrosis.

Answer

Liquefactive necrosis.

Answer

Caseous necrosis.

Answer

Both coagulative and liquefactive.

Question 5

Crumpled paper appearance of cells is a feature of-

Accepted Answer

Gaucher disease

Answer

Asbestosis

Answer

GVHD

Answer

Wilson's disease

Question 6

Stain used in electron microscopy

Accepted Answer

Phosphotungstic acid

Answer

Coomassie blue

Answer

2.5% FAM

Answer

Saffranin

Question 7

Endotoxin shock is initiated by:

Accepted Answer

Cytokine action

Answer

Endothelial injury

Answer

Peripheral vasodilation

Answer

Increased vascular permeability

Question 8

A 28-year-old woman is pinned by falling debris during a hurricane. An X-ray film of the leg reveals a compound fracture of the right tibia. The leg is immobilized in a cast for 6 weeks. When the cast is removed, the patient notices that her right leg is weak and visibly smaller in circumference than the left leg. Which of the following terms best describes this change in the patient's leg muscle?

Accepted Answer

Atrophy

Answer

Hyperplasia

Answer

Metaplasia

Answer

Ischemic necrosis

Question 9

Radiation mediates its effect by

Accepted Answer

Ionization of the molecules

Answer

Protein coagulation

Answer

Osmolysis of cells

Answer

Denaturation of DNA

Question 10

Following pathogenetic mechanisms operate in septic shock except -

Accepted Answer

Increased peripheral vascular resistance

Answer

Direct toxic endothelial injury

Answer

Veno constriction

Answer

Activation of complement

General Pathology — MCQs

General Pathology — MCQs

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