General Pathology Practice Questions

Q: What percentage of offspring will be affected by color blindness when a healthy male mates with a heterozygous female?

25%. ***25%*** - Color blindness is **X-linked recessive**. A healthy male (XY) and heterozygous female (XᶜX) produce one affected combination, XᶜY, among four equally likely offspring combinations. - The affected combination is a **son inheriting Xᶜ** from the carrier mother; therefore, 1 of 4 total offspring, or **25%**, is expected to be affected. *100%* - **100% affected** is incorrect because the carrier mother can transmit either her normal X chromosome or Xᶜ, while the healthy father contributes a normal sex chromosome. - This outcome would require a much higher-risk parental combination, such as an **affected father and homozygous affected mother**, not the stated cross. *50%* - **50%** is the expected proportion of sons affected, because half of the mother’s X chromosomes carry Xᶜ; it is not the proportion of all offspring. - Among all offspring, the other half are daughters, and with a healthy father they are not clinically affected in this cross, making the total affected proportion **25%**. *0%* - **0% affected** is incorrect because the carrier mother has a 50% chance of transmitting Xᶜ to each son, producing the affected genotype XᶜY. - The healthy father does not eliminate the risk because sons inherit their **single X chromosome from the mother**; one of the four possible combinations is affected.

Q: All of the following are features of wet gangrene except?

Line of demarcation. ***Line of demarcation*** - A **line of demarcation** is a clear inflammatory boundary separating necrotic tissue from viable tissue, classically seen in dry gangrene. - Wet gangrene spreads rapidly because of bacterial infection, edema, and tissue destruction, so it usually lacks an organized **demarcation line**; therefore, this is the exception. *Arterial and venous block* - Wet gangrene is associated with **arterial insufficiency and venous obstruction**, causing ischemia, congestion, and edema that support bacterial growth. - This is not the exception because combined **arterial and venous block** is a recognized setting for wet gangrene, unlike the predominantly arterial occlusion of dry gangrene. *Not localized* - Wet gangrene is poorly localized because infection and necrosis extend rapidly through edematous tissue, often without a clear **inflammatory boundary**. - The absence of a line of demarcation allows **rapid extension** and may promote systemic toxemia or sepsis, making this a feature of wet gangrene. *Spreads faster* - Bacterial superinfection in wet gangrene produces **toxins and enzymes** that accelerate tissue destruction and allow the necrosis to spread rapidly. - Unlike dry gangrene, which progresses relatively slowly after arterial occlusion, wet gangrene characteristically **spreads faster** and is more likely to cause systemic infection.

Q: Laminated concretions of calcium and proteins are:

Schaumann's bodies. ***Schaumann's bodies*** - **Schaumann’s bodies** are laminated, concentric concretions composed of calcium and proteins, typically located within multinucleated giant cells in non-caseating sarcoid granulomas. - Their association with **sarcoidosis** and their appearance as intracellular laminated concretions directly match the description. *Asteroid bodies* - **Asteroid bodies** are stellate, eosinophilic inclusions within sarcoid giant cells, formed from compressed cytoskeletal elements rather than laminated calcium-protein material. - Although associated with **sarcoidosis**, their characteristic star-shaped appearance distinguishes them from the concentric laminated concretions described here. *Gamna-Gandy bodies* - **Gamna-Gandy bodies** are siderofibrotic nodules in the spleen, classically associated with portal hypertension and containing hemosiderin, fibrous tissue, and calcium. - Their **splenic location** and iron-rich composition distinguish them from the characteristic laminated calcium-protein concretions of Schaumann’s bodies. *Ferruginous bodies* - **Ferruginous bodies** are asbestos fibers coated with iron-containing proteinaceous material, producing characteristic beaded or dumbbell-shaped golden-brown rods. - Their **asbestos association** and coated-fiber morphology do not represent laminated intracellular calcium-protein concretions.

Q: All of the following are viral inclusion bodies, EXCEPT:

Psammoma bodies. ***Psammoma bodies*** - **Psammoma bodies** are concentric, laminated deposits of **dystrophic calcium** resembling grains of sand, rather than inclusions produced by viruses. - They occur characteristically in certain tumors, including **papillary thyroid carcinoma**, serous ovarian tumors, meningioma, and mesothelioma, so this is the exception. *Negri bodies* - **Negri bodies** are eosinophilic intracytoplasmic inclusions found in hippocampal pyramidal neurons and cerebellar Purkinje cells during **rabies** infection. - This option does not fit the exception because Negri bodies are a recognized **viral inclusion** associated with a specific viral disease. *Molluscum* - **Molluscum bodies**, also called Henderson-Patterson bodies, are large eosinophilic intracytoplasmic inclusions caused by **molluscum contagiosum** virus. - This option does not fit the exception because these inclusions are characteristic of a **poxvirus** infection in molluscum contagiosum lesions. *Bollinger bodies* - **Bollinger bodies** are large granular intracytoplasmic inclusions associated with **fowlpox** infection; smaller Borrel bodies may occur within them. - This option does not fit the exception because Bollinger bodies represent recognized **viral inclusions** in infected avian cells.

Q: Which of the following is NOT an endogenous chemoattractant?

Integrins. ***Integrins*** - **Integrins** are leukocyte **adhesion molecules** that bind endothelial ligands such as ICAM-1 and VCAM-1, producing firm adhesion during extravasation. - Unlike chemoattractants, integrins do not establish a **chemical gradient** directing leukocyte migration, making them the correct choice. *IL 8* - **IL-8** is an endogenous **CXC chemokine** secreted by macrophages and endothelial cells that primarily recruits neutrophils toward sites of inflammation. - Because IL-8 directly promotes **neutrophil chemotaxis**, it is an endogenous chemoattractant and therefore does not fit the “NOT” category. *LTB4* - **LTB4** is generated through the **5-lipoxygenase pathway** of arachidonic acid metabolism and is a potent endogenous chemoattractant for neutrophils. - Its ability to recruit and activate **neutrophils** identifies LTB4 as an endogenous chemoattractant rather than the exception. *C5a* - **C5a** is a potent endogenous mediator produced during **complement activation** through the classical and alternative pathways. - C5a promotes **neutrophil recruitment** and activates inflammatory pathways, so it is an endogenous chemoattractant and not the correct answer.

Q: Which of the following is NOT responsible for the generation of Reactive Oxygen Species during Ischemia-Reperfusion Injury?

Activation of the complement system. ***Activation of the complement system*** - **Complement activation** mediates inflammation during reperfusion but does not directly generate reactive oxygen species through its biochemical cascade. - Although complement-derived **C3a and C5a** recruit neutrophils that can produce ROS, complement itself is not a direct ROS source, making this the exception. *Infiltrating leukocytes* - **Infiltrating neutrophils** generate ROS through NADPH oxidase during the respiratory burst after reperfusion. - This option fits because leukocyte-derived **superoxide** contributes directly to oxidative tissue injury during the inflammatory response. *Incomplete redox reactions by damaged mitochondria* - **Damaged mitochondria** contain disrupted electron transport chains that incompletely reduce oxygen when oxygen returns during reperfusion. - Formation of **superoxide radicals** from leaky mitochondrial electron transport is a recognized direct mechanism of ROS generation in ischemia-reperfusion injury. *Compromised cellular antioxidant defense mechanisms* - Ischemia depletes **glutathione and superoxide dismutase**, weakening cellular antioxidant defenses before reperfusion. - Compromised **antioxidant capacity** allows newly generated ROS to accumulate because the cell cannot adequately neutralize them.

Q: A 52-year-old woman loses her right kidney following an automobile accident. A CT scan of the abdomen 2 years later shows marked enlargement of the left kidney. The renal enlargement is an example of which of the following adaptations?

Hypertrophy. ***Hypertrophy*** - The remaining kidney undergoes **compensatory hypertrophy**, with enlargement of existing renal cells to increase filtration after loss of the contralateral kidney. - Adult nephrons are essentially **permanent cells**; increased workload stimulates protein and organelle synthesis, particularly enlargement of proximal convoluted tubule cells. *Dysplasia* - **Dysplasia** is disordered cellular growth and maturation, usually involving epithelium and potentially representing a preneoplastic change. - The uniform enlargement of the remaining kidney after unilateral loss reflects a **compensatory adaptation**, not abnormal epithelial organization. *Hyperplasia* - **Hyperplasia** means an increase in cell number, whereas the predominant adult renal response is enlargement of existing cells after nephron loss. - Although limited **hyperplasia** may occur in collecting ducts, adult kidneys cannot generate enough new nephrons to account for this compensatory enlargement. *Atrophy* - **Atrophy** is a reduction in cell size and often organ size, which is opposite to the marked enlargement observed in the remaining kidney. - The increased functional demand produces **compensatory growth**, rather than the shrinkage associated with reduced workload, ischemia, denervation, or other causes of atrophy.

Q: Which protein does Cytochrome C interact with to initiate apoptosis?

Apaf-1. ***Apaf-1*** - Cytochrome C binds **Apaf-1** in the cytosol, with ATP or dATP, to assemble the wheel-like apoptosome complex. - The apoptosome recruits and activates **caspase-9**, initiating the executioner caspase cascade of the intrinsic mitochondrial pathway. *IL-10* - **IL-10** is an anti-inflammatory cytokine that suppresses macrophage activation and is not a component of the mitochondrial apoptosis pathway. - Cytochrome C instead binds **Apaf-1** in the cytosol, leading to apoptosome formation and activation of caspase-9. *Bcl-2* - **Bcl-2** is an anti-apoptotic mitochondrial membrane protein that prevents Cytochrome C release rather than binding it after release. - In the intrinsic pathway, released Cytochrome C interacts with **Apaf-1**, not with the Bcl-2 protein family. *FADD* - **FADD** is an adapter in the extrinsic, death-receptor pathway and does not participate in Cytochrome C-mediated apoptosome formation. - FADD links Fas to **caspase-8**, whereas Cytochrome C activates the intrinsic pathway through Apaf-1 and caspase-9.

Q: Which of the following is false regarding reversible cell injury?

Breakdown of plasma membrane. ***Breakdown of plasma membrane*** - **Breakdown of the plasma membrane** indicates loss of membrane integrity, with leakage of intracellular contents and calcium influx that promote **irreversible injury**. - This is the false statement because reversible injury may cause **blebbing** or loss of microvilli, but the plasma membrane remains structurally intact. *Hydropic change* - **Hydropic change** is a classic manifestation of reversible injury caused by failure of the **Na+/K+-ATPase**, leading to intracellular sodium and water accumulation. - This option is not false because **cellular swelling** is often the earliest light-microscopic change and can resolve when the injurious stimulus is removed. *Accumulation of myelin figures in the cytoplasm* - **Myelin figures** are whorled phospholipid masses derived from damaged cellular membranes and may begin appearing with **membrane injury** during the reversible stage. - This option is not false because myelin figures can occur before complete membrane disruption, although they become more prominent with **progressive or irreversible injury**. *Detachment of ribosomes from the endoplasmic reticulum (ER)* - **Ribosomal detachment** from rough ER follows ER swelling and ATP depletion, reducing protein synthesis while remaining potentially **reversible** if the insult is removed. - This option is not false because dissociation of ribosomes is a recognized feature of **reversible cell injury**, unlike plasma membrane breakdown.

Q: Which of the following is a congenital deformity?

Congenital talipes equinovarus (CTEV). ***Congenital talipes equinovarus (CTEV)*** - **Congenital talipes equinovarus (CTEV)** is a classic **deformation**, involving abnormal position or shape caused by mechanical forces acting on a normally developing fetal foot. - Extrinsic **uterine constraint**, such as that associated with oligohydramnios or multiple gestations, can produce this congenital deformity. *Congenital heart disease* - **Congenital heart disease** is generally classified as a **malformation**, arising from an intrinsic developmental error during organogenesis rather than from external mechanical forces. - It therefore does not represent a **deformation**, which results when mechanical forces alter the form or position of an otherwise normally developing structure. *Cleft lip* - **Cleft lip** is a **malformation** caused by failure of the maxillary and medial nasal processes to fuse during facial development. - Because it results from an intrinsic failure of **embryonic fusion**, rather than uterine constraint, it is not classified as a deformation. *Potter sequence* - **Potter sequence** is a **sequence**, in which multiple abnormalities develop secondary to one initiating event, classically renal agenesis causing oligohydramnios. - Its secondary features, including **flattened facies** and pulmonary hypoplasia, do not make it a primary deformation.

Question 1

What percentage of offspring will be affected by color blindness when a healthy male mates with a heterozygous female?

Accepted Answer

25%

Answer

0%

Answer

50%

Answer

100%

Question 2

All of the following are features of wet gangrene except?

Accepted Answer

Line of demarcation

Answer

Spreads faster

Answer

Arterial and venous block

Answer

Not localized

Question 3

Laminated concretions of calcium and proteins are:

Accepted Answer

Schaumann's bodies

Answer

Ferruginous bodies

Answer

Asteroid bodies

Answer

Gamna-Gandy bodies

Question 4

All of the following are viral inclusion bodies, EXCEPT:

Accepted Answer

Psammoma bodies

Answer

Molluscum

Answer

Negri bodies

Answer

Bollinger bodies

Question 5

Which of the following is NOT an endogenous chemoattractant?

Accepted Answer

Integrins

Answer

C5a

Answer

LTB4

Answer

IL 8

Question 6

Which of the following is NOT responsible for the generation of Reactive Oxygen Species during Ischemia-Reperfusion Injury?

Accepted Answer

Activation of the complement system

Answer

Incomplete redox reactions by damaged mitochondria

Answer

Compromised cellular antioxidant defense mechanisms

Answer

Infiltrating leukocytes

Question 7

A 52-year-old woman loses her right kidney following an automobile accident. A CT scan of the abdomen 2 years later shows marked enlargement of the left kidney. The renal enlargement is an example of which of the following adaptations?

Accepted Answer

Hypertrophy

Answer

Atrophy

Answer

Dysplasia

Answer

Hyperplasia

Question 8

Which protein does Cytochrome C interact with to initiate apoptosis?

Accepted Answer

Apaf-1

Answer

IL-10

Answer

Bcl-2

Answer

FADD

Question 9

Which of the following is false regarding reversible cell injury?

Accepted Answer

Breakdown of plasma membrane

Answer

Detachment of ribosomes from the endoplasmic reticulum (ER)

Answer

Hydropic change

Answer

Accumulation of myelin figures in the cytoplasm

Question 10

Which of the following is a congenital deformity?

Accepted Answer

Congenital talipes equinovarus (CTEV)

Answer

Potter sequence

Answer

Congenital heart disease

Answer

Cleft lip

General Pathology — MCQs

General Pathology — MCQs

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