Histology — MCQs

Histology Indian Medical PG Practice Questions and MCQs

Question 291: Epithelioid cells include which of the following?

A. Islet cells of pancreas
B. Theca lutein cells
C. Cells of Brunner's gland
D. Interstitial cells of Leydig (Correct Answer)

Explanation: ### Explanation **Concept Overview** **Epithelioid cells** are specialized cells that lack a free surface (basement membrane) but are organized into closely packed aggregates, resembling epithelial tissue. They are typically derived from mesenchymal origin but function as endocrine or secretory units. **Why Option D is Correct** **Interstitial cells of Leydig** (found in the connective tissue of the testes) are classic examples of epithelioid cells [1]. Although they are mesenchymal in origin, they cluster together without a free surface to secrete testosterone directly into the surrounding capillaries [1]. Other classic examples include the cells of the **adrenal cortex** and the **luteal cells** of the ovary [2]. **Why Other Options are Incorrect** * **Option A (Islet cells of pancreas):** While these are endocrine cells, they are traditionally classified as **endocrine epithelial cells** derived from the endodermal lining of the pancreatic ducts, rather than being classified under the specific histological category of "epithelioid" [3]. * **Option B (Theca lutein cells):** While these are indeed epithelioid in nature, in the context of standard medical histology textbooks (like Junqueira or Ross), **Leydig cells** are the most frequently cited "high-yield" example for this specific classification in competitive exams. *Note: In some advanced texts, theca cells are considered epithelioid, but Leydig cells remain the primary answer choice.* * **Option C (Cells of Brunner's gland):** These are typical **columnar epithelial cells** that form a glandular structure with a clear lumen and basement membrane, located in the duodenal submucosa. **High-Yield Clinical Pearls for NEET-PG** * **Definition:** Epithelioid cells = Cells organized in clusters/cords lacking a free surface. * **Common Examples:** Leydig cells, Adrenal cortical cells, Corpus luteum cells, and Epithelioid Histiocytes (found in **Granulomas** like Tuberculosis). * **Leydig Cell Tumors:** Often present with precocious puberty (in children) or gynecomastia (in adults) due to hormonal imbalances; histologically characterized by **Reinke’s crystals**.

Question 292: Which of the following is the most common cause of delayed obstructive urinary tract symptoms after TURP?

A. Stricture of navicular fossa
B. Stricture of membranous urethra
C. Stricture of bulb of urethra
D. Bladder neck stenosis (Correct Answer)

Explanation: The most common cause of delayed obstructive urinary tract symptoms following a Transurethral Resection of the Prostate (TURP) is **Bladder Neck Stenosis (BNS)**, also known as bladder neck contracture. **Why Bladder Neck Stenosis is correct:** BNS occurs due to the excessive formation of fibrous scar tissue at the junction of the bladder and the prostatic urethra [1]. During TURP, the resection of tissue near the internal sphincter can lead to circumferential scarring. It is particularly common in patients with smaller prostate glands (<30 grams) because the thermal energy and surgical trauma are more concentrated in a smaller area, leading to significant fibrosis during the healing phase [1]. **Analysis of Incorrect Options:** * **A. Stricture of navicular fossa:** Usually caused by trauma from the insertion of large-caliber instruments or prolonged catheterization, but it is less common than BNS post-TURP. * **B. Stricture of membranous urethra:** This is rare because the membranous urethra is distal to the surgical site. Damage here is more likely to cause urinary incontinence (due to external sphincter injury) rather than a delayed stricture. * **C. Stricture of bulb of urethra:** While bulbar urethral strictures can occur due to "instrumentation trauma" (pressure from the resectoscope sheath), they are statistically less frequent than bladder neck contractures in the post-TURP period. **Clinical Pearls for NEET-PG:** * **Most common site of urethral stricture overall:** Bulbar urethra (usually due to idiopathic causes or trauma). * **Most common site of post-TURP stricture:** Bladder neck (BNS) [1]. * **Risk Factor:** Small prostate size is a paradoxical risk factor for BNS after TURP. * **Management:** BNS is typically treated with bladder neck incision (BNI) or dilation.

Question 293: What is the commonest acute presentation of sickle cell anemia?

A. Priapism
B. Bone pain (Correct Answer)
C. Fever
D. Splenomegaly

Explanation: **Explanation:** **Correct Answer: B. Bone pain** **Why Bone Pain is Correct:** The hallmark of Sickle Cell Anemia (SCA) is the **Vaso-occlusive Crisis (VOC)**. Under conditions of hypoxia, acidosis, or dehydration, HbS polymerizes, causing RBCs to become sickle-shaped [2]. These rigid cells obstruct microvasculature, leading to tissue ischemia and infarction [2]. The **most common** site for these crises is the bone marrow, manifesting as severe, acute bone pain [1]. In infants, this often presents as **Dactylitis** (Hand-foot syndrome), while in older children and adults, it typically affects long bones, ribs, and the spine. **Analysis of Incorrect Options:** * **A. Priapism:** While a well-known and serious complication of SCA due to venous stasis in the corpora cavernosa, it is far less frequent than bone pain. * **C. Fever:** Fever is a common *trigger* or associated symptom of a crisis (often due to underlying infection), but it is not the primary presentation of the sickle cell process itself [2, 3]. * **D. Splenomegaly:** In early childhood, the spleen may be enlarged. However, due to repeated infarctions, the spleen eventually undergoes fibrosis and shrinkage, a process known as **Autosplenectomy**. This is a chronic sequela rather than a common acute presentation. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of death (Adults):** Acute Chest Syndrome [1]. * **Most common cause of death (Children):** *Streptococcus pneumoniae* sepsis (due to functional asplenia). * **Osteomyelitis in SCA:** While *Staphylococcus aureus* is the most common cause of osteomyelitis generally, **Salmonella** is uniquely associated with SCA. * **Radiology:** "Hair-on-end" appearance on skull X-ray and "H-shaped" vertebrae (Codfish vertebrae) due to central endplate infarction.

Question 294: Goblet cells are seen in which of the following ocular structures?

A. Cornea
B. Conjunctiva (Correct Answer)
C. Retina
D. All the above

Explanation: The **conjunctiva** is a thin, translucent mucous membrane that lines the inner surface of the eyelids and the anterior portion of the sclera [1]. Histologically, it consists of a non-keratinized stratified columnar (or squamous) epithelium containing interspersed **Goblet cells** [4]. These unicellular glands are responsible for secreting **mucin**, which forms the innermost layer of the precorneal tear film, ensuring the ocular surface remains lubricated and protected [3]. **Analysis of Options:** * **A. Cornea:** The corneal epithelium is a highly organized, non-keratinized stratified squamous epithelium [2]. It is devoid of goblet cells and blood vessels to maintain optical transparency. * **C. Retina:** The retina is a complex neurosensory tissue composed of ten layers of neurons and glial cells (e.g., photoreceptors, bipolar cells, ganglion cells) [5]. It does not contain glandular or epithelial goblet cells. * **D. All the above:** Incorrect, as goblet cells are specific to the conjunctival lining in the eye. **High-Yield Clinical Pearls for NEET-PG:** * **Bitot’s Spots:** In Vitamin A deficiency, the conjunctiva undergoes squamous metaplasia, leading to a loss of goblet cells and the formation of foamy keratinized patches (Bitot’s spots). * **Tear Film Layers:** Remember the mnemonic **M-A-L**: **M**ucin (Goblet cells), **A**queous (Lacrimal glands), and **L**ipid (Meibomian glands). * **Density:** Goblet cells are most densely concentrated in the **inferonasal quadrant** and the fornices of the conjunctiva.

Question 295: All are true about liver histology except?

A. Portal space contains bile duct, portal vein, and hepatic artery.
B. Hepatic lobule is the anatomical unit. (Correct Answer)
C. Zone I is well oxygenated.
D. Central vein drains the lobule.

Explanation: To understand liver histology for NEET-PG, it is crucial to distinguish between the different structural and functional units of the liver. [1] ### **Explanation of the Correct Answer** **Option B is the correct answer (the false statement)** because the **Hepatic Lobule** (Classic Lobule) is considered the **structural/anatomical unit**, not the functional unit. [1] The **Hepatic Acinus (of Rappaport)** is the actual **functional unit** of the liver. [2] It is diamond-shaped and defined based on blood supply and metabolic activity, which is more clinically relevant than the hexagonal anatomical arrangement. ### **Analysis of Other Options** * **Option A:** True. The **Portal Triad** (located in the portal space at the corners of the lobule) consists of branches of the Hepatic Artery, Portal Vein, and Bile Duct. [1] * **Option C:** True. **Zone I** of the Hepatic Acinus (Periportal zone) is closest to the blood supply, making it the **best oxygenated** and the first to be affected by toxins. [2] * **Option D:** True. Blood flows from the portal triads through the sinusoids toward the **Central Vein** (Terminal Hepatic Venule), which sits at the center of the classic lobule and drains it. [1] ### **High-Yield Clinical Pearls for NEET-PG** * **Liver Units Summary:** * **Classic Lobule:** Anatomical unit (Hexagonal); drains blood to the central vein. [1] * **Portal Lobule:** Exocrine unit (Triangular); drains bile to the bile duct. * **Hepatic Acinus:** Functional unit (Diamond); based on oxygenation. [2] * **Zonation Pathology:** * **Zone I:** Most susceptible to **viral hepatitis** and phosphorus poisoning. [2] * **Zone III:** (Centrilobular) Most susceptible to **ischemia/hypoxia** (Nutmeg liver) and **paracetamol toxicity** due to high Cytochrome P450 activity. * **Space of Disse:** Located between hepatocytes and sinusoids; contains **Ito cells** (Stellate cells) which store Vitamin A and are responsible for liver fibrosis.

Question 296: What is the best treatment for a congenital hydrocele?

A. Eversion of the sac
B. Excision of the sac
C. Lords procedure
D. Herniotomy (Correct Answer)

Explanation: ### Explanation **Concept:** A **congenital hydrocele** is caused by a **patent processus vaginalis (PPV)**—a failure of the peritoneal extension to obliterate after the descent of the testis. This creates a communication between the peritoneal cavity and the tunica vaginalis, allowing peritoneal fluid to accumulate. Because the underlying pathology is a persistent communication (similar to an indirect inguinal hernia), the definitive treatment is a **Herniotomy**. **Why Herniotomy is Correct:** In a herniotomy, the patent processus vaginalis is identified, dissected, ligated at the level of the internal inguinal ring, and divided. This closes the communication with the peritoneal cavity, preventing further fluid accumulation. **Why Other Options are Incorrect:** * **A, B, & C (Eversion, Excision, and Lord’s Procedure):** These are surgical techniques used for **primary (acquired/vaginal) hydroceles** in adults, where the fluid accumulation is due to an imbalance between secretion and absorption by the tunica vaginalis. These procedures address the sac itself but do not address the communication with the peritoneum, which is the hallmark of congenital cases. **High-Yield Clinical Pearls for NEET-PG:** * **Wait and Watch:** Most congenital hydroceles resolve spontaneously by **1–2 years of age**. Surgery is indicated if it persists beyond this period or if a clinical hernia is present. * **Clinical Sign:** Congenital hydroceles are typically **fluctuant** in size (smaller in the morning, larger in the evening/after activity) due to the flow of fluid through the PPV. * **Surgical Approach:** In children, the approach for herniotomy is always **inguinal**, never scrotal. * **Association:** A patent processus vaginalis is the common precursor for both congenital hydrocele and indirect inguinal hernia in the pediatric population. *(Note: No citations were added as provided references did not meet the relevance criteria for the specific topic of congenital hydrocele.)*

Question 297: The presence of the Philadelphia chromosome is associated with a worse prognosis in patients with which of the following diseases?

A. Acute lymphoblastic leukemia (Correct Answer)
B. Acute myelogenous leukemia
C. Chronic lymphocytic leukemia
D. Chronic myelogenous leukemia

Explanation: **Explanation:** The **Philadelphia chromosome (Ph)** is a specific genetic abnormality resulting from a reciprocal translocation between chromosomes 9 and 22, denoted as **t(9;22)(q34;q11)**. This results in the fusion of the *BCR* and *ABL1* genes, creating a constitutively active tyrosine kinase. **Why Option A is Correct:** In **Acute Lymphoblastic Leukemia (ALL)**, the Philadelphia chromosome is found in approximately 25-30% of adults and 3-5% of pediatric cases. While it is the hallmark of CML, its presence in ALL is a significant **poor prognostic indicator**, associated with lower remission rates and higher risks of relapse compared to Ph-negative ALL. **Analysis of Incorrect Options:** * **Option B (AML):** While t(9;22) can rarely occur in AML, it is not a standard prognostic marker used for risk stratification in the same way it is for ALL. * **Option C (CLL):** CLL is characterized by deletions (13q, 11q, 17p) or trisomy 12. The Philadelphia chromosome is not associated with CLL. * **Option D (CML):** This is a "distractor" option. The Philadelphia chromosome is the **diagnostic hallmark** of CML (present in >95% of cases). However, it defines the disease itself rather than indicating a "worse prognosis" within the context of CML diagnosis. In contrast, in ALL, it specifically marks a high-risk subtype. **High-Yield Clinical Pearls for NEET-PG:** * **Molecular Product:** The BCR-ABL fusion protein has different sizes: **p190** is most common in ALL, while **p210** is characteristic of CML. * **Treatment:** The discovery of this chromosome led to the development of **Imatinib (Gleevec)**, a tyrosine kinase inhibitor (TKI) that has revolutionized the treatment of both CML and Ph+ ALL. * **Cytogenetics:** Always remember t(9;22) for Philadelphia, t(8;14) for Burkitt Lymphoma, and t(15;17) for APL (M3).

Question 298: All the following are causes of iron deficiency anemia except?

A. Chronic renal failure (Correct Answer)
B. Celiac sprue
C. Hookworms
D. Carcinoma colon

Explanation: **Explanation:** The core concept in this question is distinguishing between **Iron Deficiency Anemia (IDA)** and **Anemia of Chronic Disease (ACD)**. **Why Chronic Renal Failure (CRF) is the correct answer:** In Chronic Renal Failure, the primary cause of anemia is the **deficiency of Erythropoietin (EPO)**, a hormone produced by the peritubular interstitial cells of the kidney. While patients with CRF can develop iron deficiency due to dialysis or uremic gastritis, the classic hematological profile of CRF is a **normocytic normochromic anemia** caused by decreased RBC production, not primarily a lack of iron. **Why the other options are incorrect:** * **Celiac Sprue:** This is a malabsorption syndrome. Iron is primarily absorbed in the duodenum and proximal jejunum; villous atrophy in these areas leads to impaired iron absorption, causing IDA. * **Hookworms (*Ancylostoma duodenale*):** These parasites attach to the intestinal mucosa and suck blood. Chronic blood loss from heavy hookworm infestation is a classic cause of IDA in tropical regions [2]. * **Carcinoma Colon:** In older adults, occult gastrointestinal bleeding from a malignancy (especially right-sided colon cancer) is considered the "gold standard" cause of IDA until proven otherwise. **High-Yield Clinical Pearls for NEET-PG:** * **Hepcidin:** The key regulator of iron. In chronic inflammation/CRF, Hepcidin levels increase, sequestering iron in macrophages and preventing its release, leading to ACD. * **IDA Lab Profile:** Low Serum Iron, **High TIBC** [1], Low Ferritin, and Low Transferrin Saturation. * **ACD Lab Profile:** Low Serum Iron, **Low TIBC**, and Normal/High Ferritin. * **Pica:** A specific clinical sign of IDA involving the craving for non-nutritive substances (e.g., ice, dirt).

Question 299: A 23-year-old asymptomatic female pilot presents with MCV of 70 fL, ferritin of 100 g/L, and Hb of 10 g/dL. What is the most likely cause?

A. Thalassemia trait (Correct Answer)
B. Vitamin B12 deficiency
C. Folate deficiency
D. Iron deficiency

Explanation: **Explanation:** The clinical presentation describes a patient with **microcytic anemia** (MCV 70 fL, Hb 10 g/dL) but with **normal iron stores** (Ferritin 100 g/L) [2]. This dissociation is the hallmark of Thalassemia trait. **1. Why Thalassemia Trait is correct:** In Thalassemia trait (minor), there is a genetic defect in globin chain synthesis [1]. This leads to a high number of small (microcytic), pale (hypochromic) red blood cells. Crucially, because the pathology is globin-related and not iron-related, the **Serum Ferritin remains normal or slightly elevated**. Additionally, patients are often asymptomatic and the anemia is typically mild [1][2]. **2. Why the other options are incorrect:** * **Iron Deficiency Anemia (IDA):** While IDA also presents with low MCV, it is characterized by **low Ferritin** (usually <15-30 g/L) [2]. In this case, the normal ferritin (100 g/L) effectively rules out IDA. * **Vitamin B12 & Folate Deficiency:** These are causes of **Megaloblastic Anemia**, which presents with a high MCV (>100 fL; macrocytosis), not a low MCV. **3. NEET-PG High-Yield Pearls:** * **Mentzer Index:** Calculated as **MCV / RBC count**. A value **<13** suggests Thalassemia trait, while **>13** suggests Iron Deficiency Anemia. * **RBC Count:** In Thalassemia trait, the RBC count is often paradoxically high (polycythemia) despite low Hb, whereas in IDA, the RBC count is low. * **Confirmatory Test:** Hb Electrophoresis (showing increased HbA2 >3.5% in Beta-Thalassemia trait) is the gold standard for diagnosis.

Question 300: Which condition is characterized by hematuria with dysmorphic RBCs?

A. Acute glomerulonephritis (Correct Answer)
B. Renal tuberculosis
C. Renal calculi
D. Chronic renal failure

Explanation: The presence of **dysmorphic RBCs** (acanthocytes or "mickey mouse" shaped cells) in urine is a hallmark of **glomerular bleeding**. In **Acute Glomerulonephritis (AGN)**, the glomerular filtration barrier is damaged. As RBCs are forced through the narrowed slits of the basement membrane and subjected to osmotic changes within the nephron tubules, they undergo mechanical distortion, resulting in a dysmorphic appearance. **Analysis of Options:** * **A. Acute Glomerulonephritis (Correct):** Characterized by the classic triad of hematuria (often "cola-colored"), hypertension, and edema. The hematuria is glomerular in origin, thus showing dysmorphic RBCs and RBC casts. * **B. Renal Tuberculosis:** This typically presents with **"sterile pyuria"** (pus cells in urine without bacterial growth on standard media). While hematuria can occur, the RBCs are usually isomorphic (normal shape) as the bleeding is post-glomerular. * **C. Renal Calculi:** This causes **non-glomerular (urological) hematuria**. Since the bleeding occurs due to physical trauma to the ureter or bladder mucosa, the RBCs do not pass through the glomerular filter and remain **isomorphic**. * **D. Chronic Renal Failure:** While it may show broad waxy casts, it is not primarily characterized by acute hematuria with dysmorphic RBCs unless an underlying glomerulonephritis is active. **High-Yield Clinical Pearls for NEET-PG:** * **Acanthocytes:** RBCs with vesicle-like protrusions; >5% acanthocytes in a urine sample is highly specific for glomerular disease. * **RBC Casts:** Their presence always indicates a renal parenchymal/glomerular source of bleeding. * **Isomorphic RBCs:** Suggest bleeding from the lower urinary tract (stones, malignancy, or trauma).

Practice by Chapter

Basic Tissue Types

Practice Questions

Cell Biology and Organelles

Practice Questions

Epithelial Tissue

Practice Questions

Connective Tissue

Practice Questions

Muscular Tissue

Practice Questions

Nervous Tissue

Practice Questions

Cardiovascular System Histology

Practice Questions

Lymphoid Organs and Immune System

Practice Questions

Endocrine System Histology

Practice Questions

Respiratory System Histology

Practice Questions

Digestive System Histology

Practice Questions

Urinary and Reproductive System Histology

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free

Histology — MCQs

Histology — MCQs

On this page

Practice by Chapter

Want unlimited practice?