General Pathology Practice Questions

Q: Which of the following statements is true regarding hemophilia inheritance?

Females can be carriers, and males are typically affected.. ***Females can be carriers, and males are typically affected.*** - Hemophilia is an **X-linked recessive disorder**, meaning the gene responsible is located on the X chromosome. - Males have only one X chromosome, so if they inherit the affected gene, they will express the disorder, while females have two X chromosomes, allowing them to be **asymptomatic carriers** if only one X chromosome carries the mutation. - This option accurately describes the **typical inheritance pattern** where carrier females (heterozygous) transmit the condition to their sons who become affected. *Females can be carriers, and some males may be unaffected.* - While this statement is technically true, it is less precise for describing hemophilia inheritance patterns. - The focus on "some males may be unaffected" is less informative than emphasizing that males who inherit the mutation are **typically affected**, which is the key clinical characteristic. - This option doesn't emphasize the primary pattern that makes X-linked recessive inheritance clinically significant. *Males are carriers, and females are typically affected.* - Males cannot be carriers for X-linked recessive disorders; if a male carries the gene on his single X chromosome, **he will be affected**, not a carrier. - **Females are rarely affected** as they would need to inherit the mutated gene from both parents (an affected father and a carrier/affected mother), which is uncommon. - This statement reverses the actual inheritance pattern. *All males are affected, and females cannot be carriers.* - It is incorrect that all males are affected; only males who **inherit the specific defective X chromosome** will be affected. - Females **can and often are carriers**, as they possess two X chromosomes, and one can carry the mutated gene while the other compensates through X-inactivation (lyonization).

Q: Neurofibromatosis shows which of the following mode of inheritance ?

AD. ***AD*** - **Neurofibromatosis type 1 (NF1)** and **Neurofibromatosis type 2 (NF2)** are both classic examples of **autosomal dominant (AD)** inheritance [1]. - This means that only one copy of the altered gene (on a non-sex chromosome) is sufficient to cause the disorder, and there is a **50% chance** of passing the condition to each child [1]. *AR* - **Autosomal recessive (AR)** disorders require two copies of the altered gene (one from each parent) for the condition to manifest [1]. - Examples include **cystic fibrosis** and **sickle cell anemia**, which have a different pattern of inheritance than neurofibromatosis. *X linked dominant* - **X-linked dominant** disorders are caused by a mutation on the X chromosome, where only one copy of the mutated gene is needed for the condition to appear [1]. - These disorders typically affect females more often than males and show a specific inheritance pattern through X chromosome transmission, which is not seen in neurofibromatosis. *X linked recessive* - **X-linked recessive** disorders are also caused by mutations on the X chromosome but typically affect males more severely as they only have one X chromosome [1]. - Females are often carriers, and the inheritance pattern differs significantly from the clinical presentation and genetic transmission of neurofibromatosis. **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. 53-54.

Q: Factor V Leiden thrombophilia is caused by mutation in which of the following factors?

Factor V (Leiden mutation). ***Factor V*** - Leiden thrombophilia is specifically caused by a **mutation in the Factor V gene**, leading to resistance to activated protein C [1]. - This results in an increased risk of **venous thromboembolism** due to uncontrolled coagulation [1]. *Factor X* - Factor X is crucial for the coagulation cascade but is **not implicated in Leiden thrombophilia**; it does not involve a mutation. - Deficiencies or dysfunctions in Factor X lead to different bleeding disorders rather than thrombophilia. *Factor VII* - Factor VII deficiency typically results in **hemorrhagic conditions**, and does not relate to the **thrombotic risks** of Leiden thrombophilia. - It involves **extrinsic pathway coagulation**, which is distinct from the resistance seen in Factor V Leiden. *Factor IX* - Factor IX is associated with **Hemophilia B** and does not play a role in Leiden thrombophilia. - Its mutation results in bleeding tendencies, contrasting with the **thrombotic risk** of Leiden thrombophilia. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 133-134.

Q: Which of the following genes primarily promotes apoptosis (programmed cell death)?

Bax. ***Bax*** - **Bax** is a **pro-apoptotic gene** that actively promotes programmed cell death by forming channels in the mitochondrial outer membrane, leading to cytochrome c release and activation of caspases [1]. - It is a key member of the Bcl-2 family and plays a critical role in the **intrinsic apoptotic pathway** [2]. - Unlike the other options, Bax **promotes** rather than inhibits apoptosis [1]. *Bclx* - **Bcl-xL** is an **anti-apoptotic** gene that **inhibits** cell death by preventing the activation of pro-apoptotic proteins like Bax [1]. - It maintains mitochondrial membrane integrity, thereby **blocking** apoptosis [1]. *Mcl* - **Mcl-1** (Myeloid cell leukemia sequence 1) is an **anti-apoptotic** gene belonging to the Bcl-2 family [1]. - Its primary role is to **inhibit** apoptosis and promote cell survival by sequestering pro-apoptotic proteins [1]. *Bcl2* - **Bcl-2** (B-cell lymphoma 2) is the prototype **anti-apoptotic** gene that **prevents** programmed cell death [3]. - It functions by binding to and inhibiting pro-apoptotic members of the Bcl-2 family, thus maintaining cell viability and **opposing** apoptosis [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 310. [2] 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. 64-67. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 310-311.

Q: Hyaline degeneration is found in -

Alcoholic liver disease. ***Alcoholic liver disease*** - **Mallory bodies**, a form of hyaline degeneration, are characteristic histologic findings in hepatocytes in alcoholic liver disease. - They represent aggregates of **intermediate filaments** and other proteins, indicating severe hepatocellular damage. *Acute myocardial infarction* - Characterized by **coagulative necrosis** of cardiac myocytes due to ischemia, not hyaline degeneration. - Inflammation and subsequent repair with **fibrosis** are key features. *Alzheimer's disease* - Defined by the presence of **senile plaques** (amyloid-beta deposits) and **neurofibrillary tangles** (hyperphosphorylated tau protein). - These are specific protein aggregates, distinct from hyaline degeneration of cellular components. *Acute appendicitis* - Involves acute inflammation of the appendix, leading to **neutrophilic infiltration** and often **fibrinopurulent exudate**. - There is no characteristic hyaline degeneration associated with this inflammatory process.

Q: Lines of Zahn are LEAST likely to be seen in -

Lung. ***Lung*** - **Lines of Zahn are LEAST likely in the lungs** because most pulmonary thrombi are actually **emboli that formed elsewhere** (typically in deep leg veins) and then **lodged in pulmonary vessels**. - These pre-formed thrombi developed in **low-flow venous environments** and therefore **lack the characteristic layered appearance** of Lines of Zahn. - Even when thrombi form in situ in pulmonary vessels, the vascular bed characteristics make Lines of Zahn formation less common compared to other sites. *Heart* - **Mural thrombi** in heart chambers (especially post-MI in left ventricle or in atrial fibrillation) commonly show **Lines of Zahn**. - The **high-flow, turbulent environment** with continuous cardiac contractions creates ideal conditions for alternating platelet-fibrin and RBC layer deposition. - These are classic examples of antemortem thrombi with visible Lines of Zahn. *Liver* - **Portal vein thrombosis** and **hepatic vein thrombosis** (Budd-Chiari syndrome) can exhibit **Lines of Zahn**. - Despite being venous, these vessels have **sufficient flow velocity and turbulence** to allow layered thrombus formation. - Lines of Zahn indicate the thrombus formed during life with flowing blood. *Kidney* - **Renal artery thrombosis** and **renal vein thrombosis** frequently show **Lines of Zahn**. - Both arterial and venous renal circulation have adequate flow dynamics for layered thrombus formation. - These represent antemortem thrombi formed in vessels with active blood flow.

Q: What does Prussian blue staining specifically detect in histology?

Ferric iron. ***Ferric iron*** - The **Prussian blue reaction**, also known as Perls' stain, specifically identifies **ferric iron (Fe3+)** in tissue sections. - This stain is crucial for diagnosing conditions involving **iron overload**, such as hemochromatosis or hemosiderosis, by highlighting iron deposits as blue. *Ferrous iron* - The Prussian blue stain does **not react with ferrous iron (Fe2+)**; it specifically targets the ferric (oxidized) state of iron. - While ferrous iron is present in the body, it is not detected by this particular staining method for routine histological assessment of iron stores. *Glycogen* - **Glycogen** is a polysaccharide storage molecule and is typically stained using the **Periodic Acid-Schiff (PAS) stain**, which produces a magenta color. - Prussian blue staining is entirely unrelated to the detection of glycogen and would not highlight these molecules in tissue. *Lipids* - **Lipids** are fats and are typically stained with lipid-soluble dyes like **Oil Red O** or **Sudan Black**, especially in frozen sections to preserve their structure. - Prussian blue stain has no affinity for lipids and therefore cannot be used to detect them in histological samples.

Q: During cell death, myelin figures are derived from which of the following?

Cell membrane (lipid bilayer). ***Cell membrane (lipid bilayer)*** - **Myelin figures** are whorled phospholipid masses formed during cell injury and death from the breakdown of **cellular membranes**, particularly the plasma membrane and **endoplasmic reticulum**. - These structures represent damaged membrane lipids (phospholipids) that undergo structural rearrangement into concentric lamellar (layered) configurations resembling myelin. - The term "cell membrane" encompasses both the plasma membrane and lipid-rich intracellular membranes, making this the most accurate answer among the options provided. - They are a characteristic morphologic feature of **irreversible cell injury** and can be seen with electron microscopy. *Cytoplasmic components* - While cytoplasmic proteins and organelles do degrade during cell death, they do not form the organized **phospholipid structures** characteristic of myelin figures. - Cytoplasmic breakdown produces different morphologic changes such as cytoplasmic eosinophilia and loss of ribosomes. *Mitochondrial structures* - Mitochondria have their own membranes that are damaged during cell death (leading to release of cytochrome c and other apoptotic factors). - However, mitochondrial membranes are not the primary source of **myelin figures**, which predominantly arise from ER and plasma membranes. *Nuclear membrane* - The nuclear envelope does fragment during cell death, contributing to nuclear changes like **karyopyknosis, karyorrhexis, and karyolysis**. - While technically a membrane structure, the nuclear envelope is not the primary source of myelin figures, which are mainly derived from the more abundant plasma and ER membranes.

Question 1

Which of the following statements is true regarding hemophilia inheritance?

Accepted Answer

Females can be carriers, and males are typically affected.

Answer

Females can be carriers, and some males may be unaffected.

Answer

Males are carriers, and females are typically affected.

Answer

All males are affected, and females cannot be carriers.

Question 2

Neurofibromatosis shows which of the following mode of inheritance ?

Accepted Answer

AD

Answer

AR

Answer

X linked dominant

Answer

X linked recessive

Question 3

Which of the following factors play a major role in the initiation of thrombus formation?

Accepted Answer

Endothelial injury

Answer

Vasoconstriction

Answer

Coagulation cascade activation

Answer

Platelets activation

Question 4

Factor V Leiden thrombophilia is caused by mutation in which of the following factors?

Accepted Answer

Factor V (Leiden mutation)

Answer

Factor X

Answer

Factor VII

Answer

Factor IX

Question 5

Which of the following genes primarily promotes apoptosis (programmed cell death)?

Accepted Answer

Bax

Answer

Bclx

Answer

Mcl

Answer

Bcl2

Question 6

What is the key pathophysiological difference between acid and alkali injuries in terms of tissue necrosis?

Accepted Answer

Alkali injuries cause liquefactive necrosis

Answer

Acid injuries cause coagulative necrosis

Answer

Alkali injuries lead to deeper tissue damage

Answer

Acid injuries are less severe than alkali injuries

Question 7

Hyaline degeneration is found in -

Accepted Answer

Alcoholic liver disease

Answer

Alzheimer's disease

Answer

Acute myocardial infarction

Answer

Acute appendicitis

Question 8

Lines of Zahn are LEAST likely to be seen in -

Accepted Answer

Lung

Answer

Liver

Answer

Kidney

Answer

Heart

Question 9

What does Prussian blue staining specifically detect in histology?

Accepted Answer

Ferric iron

Answer

Ferrous iron

Answer

Glycogen

Answer

Lipids

Question 10

During cell death, myelin figures are derived from which of the following?

Accepted Answer

Cell membrane (lipid bilayer)

Answer

Cytoplasmic components

Answer

Mitochondrial structures

Answer

Nuclear membrane

General Pathology — MCQs

General Pathology — MCQs

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