Anatomy
1 questionsIdentify the structure labeled in the histology image shown.
INI-CET 2025 - Anatomy INI-CET Practice Questions and MCQs
Question 161: Identify the structure labeled in the histology image shown.
- A. Alveolar duct
- B. Respiratory bronchiole (Correct Answer)
- C. Bronchus
- D. Terminal bronchiole
Explanation: ***Respiratory bronchiole*** - The key identifying feature is the presence of **alveoli** opening directly from its lumen, which is characteristic of the respiratory zone where gas exchange begins. - It represents the transition from the conducting to the respiratory portion of the airway, lined by a simple **cuboidal epithelium** with scattered cilia and club cells. *Terminal bronchiole* - A terminal bronchiole is the most distal part of the **conducting zone** and has a continuous wall without any associated alveoli. - It is lined by simple cuboidal epithelium, which includes **club cells** (formerly Clara cells), but no gas exchange occurs here. *Alveolar duct* - An alveolar duct is a tube whose walls are almost entirely composed of the openings of alveoli and alveolar sacs. - It lacks the more continuous epithelial wall seen in a respiratory bronchiole and is primarily just a passageway lined by alveolar openings. *Bronchus* - A bronchus is a larger airway characterized by the presence of **cartilage plates** or rings and **submucosal glands** in its wall, both of which are absent in the image. - It is lined by **pseudostratified ciliated columnar epithelium** containing goblet cells, which is different from the simple epithelium seen here.
Biochemistry
1 questionsA deficiency of Glucose-6-Phosphatase is associated with which of the following bilirubin patterns?
INI-CET 2025 - Biochemistry INI-CET Practice Questions and MCQs
Question 161: A deficiency of Glucose-6-Phosphatase is associated with which of the following bilirubin patterns?
- A. Direct bilirubin normal, indirect bilirubin increased, and urobilinogen normal (Correct Answer)
- B. Indirect bilirubin increased, direct bilirubin normal, and raised urine urobilinogen
- C. Direct bilirubin increased, indirect bilirubin decreased, and urine urobilinogen/urobilin increased
- D. Raised direct bilirubin, normal indirect bilirubin, and absent urine bilirubin
Explanation: ***Direct bilirubin normal, indirect bilirubin increased, and urobilinogen normal*** - Glucose-6-Phosphatase (G6Pase) deficiency causes **Glycogen Storage Disease Type I (von Gierke disease)**, which is primarily characterized by severe **hypoglycemia**, hepatomegaly, lactic acidosis, and hyperuricemia. - While jaundice is NOT a classical feature of von Gierke disease, some patients may show mild elevation of **unconjugated (indirect) bilirubin**. - The proposed mechanism involves accumulation of **glucuronic acid** (a metabolic byproduct that cannot be converted to glucose due to G6Pase deficiency), which may competitively inhibit **UDP-glucuronyltransferase (UGT1A1)**, the enzyme responsible for bilirubin conjugation. - This results in increased **indirect (unconjugated) bilirubin** with normal direct bilirubin and normal urobilinogen, similar to the pattern seen in Gilbert syndrome. *Indirect bilirubin increased, direct bilirubin normal, and raised urine urobilinogen* - This pattern with raised urobilinogen is more characteristic of **hemolytic conditions** where excessive red blood cell breakdown overwhelms the liver's conjugation capacity. - The increased urobilinogen suggests increased enterohepatic circulation of bilirubin metabolites, which is not a typical feature of G6Pase deficiency. - While indirect bilirubin may be elevated in von Gierke disease, the raised urobilinogen makes this pattern less specific. *Direct bilirubin increased, indirect bilirubin decreased, and urine urobilinogen/urobilin increased* - This pattern is **internally contradictory** and does not match any known pathophysiological mechanism in G6Pase deficiency. - If G6Pase deficiency affects bilirubin metabolism, it would impair conjugation (leading to **increased** indirect bilirubin), not decrease it. - Additionally, decreased indirect bilirubin with increased direct bilirubin would require enhanced conjugation, which is opposite to the proposed mechanism of UGT1A1 inhibition. *Raised direct bilirubin, normal indirect bilirubin, and absent urine bilirubin* - This pattern represents **conjugated hyperbilirubinemia** with defective biliary excretion, characteristic of **Dubin-Johnson syndrome** or **Rotor syndrome**. - These conditions involve defects in hepatocyte transport proteins (MRP2 in Dubin-Johnson), not impaired conjugation. - This pattern is inconsistent with the proposed mechanism in G6Pase deficiency, where impaired conjugation would increase **unconjugated** bilirubin.
Internal Medicine
3 questionsWhy does not every Helicobacter pylori infection lead to ulcers?
Which of the following malignancies is unrelated to obesity?
A 32-year-old woman presents with easy bruising and petechiae. Her platelet count is 18,000 / mm³. Hemoglobin and total leukocyte count are normal. She recently recovered from a mild upper respiratory tract infection. Peripheral smear shows no abnormal cells. What is the most appropriate next step in management?
INI-CET 2025 - Internal Medicine INI-CET Practice Questions and MCQs
Question 161: Why does not every Helicobacter pylori infection lead to ulcers?
- A. H. pylori infects the antrum even in asymptomatic individuals
- B. Disease associated with host factors and environmental influences
- C. Increased risk of peptic ulcer disease when H. pylori is present with NSAIDs
- D. Majority of H. pylori infections are asymptomatic (Correct Answer)
Explanation: The vast majority of H. pylori infections are asymptomatic or cause only mild gastritis, meaning the organism's presence alone is not sufficient to cause pathology [1]. Only a small percentage (around 10-20%) of individuals infected with Helicobacter pylori will develop a peptic ulcer or gastric malignancy [1]. The organism generally colonizes the gastric antrum, leading to chronic gastritis and potentially ulcers through increased gastrin and acid secretion; however, in most people, this subsequent hypergastrinaemia has no clinical consequences [1]. Host factors and environmental influences determine who develops ulcers, but the baseline state is generally non-ulcerative gastritis. While increased risk of peptic ulcer disease occurs when H. pylori is present with NSAIDs, these are cofactors that damage the mucosal barrier and do not explain the high rate of asymptomatic carriage in the general population.
Question 162: Which of the following malignancies is unrelated to obesity?
- A. Pancreas
- B. Stomach
- C. Meningioma
- D. Multiple myeloma (Correct Answer)
Explanation: ***Multiple myeloma*** - While obesity is a risk factor for several cancers, there is limited or conflicting evidence directly linking **multiple myeloma** to high BMI, making it the most unrelated option among the choices provided. - The primary established risk factors for multiple myeloma include age (over 65), African descent, male sex, and a history of monoclonal gammopathy of undetermined significance (**MGUS**). [1] ***Stomach*** - Obesity, particularly abdominal obesity, increases the risk of developing **gastric cardia adenocarcinoma** due to increased prevalence of **gastroesophageal reflux disease (GERD)** and subsequent Barrett's esophagus. - Chronic inflammation and hormonal changes associated with high body fat contribute to the oncogenesis of stomach cancer. ***Pancreas*** - Obesity is a well-established risk factor for **pancreatic cancer**, increasing the risk by approximately 20-50% compared to healthy-weight individuals. [2] - The mechanism involves chronic low-grade inflammation, **insulin resistance**, and altered levels of adipokines (like leptin) and insulin-like growth factors. ***Meningioma*** - **Meningioma**, the most common primary central nervous system tumor, has a clear association with obesity. - High BMI contributes to increased risk, possibly mediated by elevated levels of **leptin** and **estrogen** (especially in postmenopausal women) which can act as growth factors.
Question 163: A 32-year-old woman presents with easy bruising and petechiae. Her platelet count is 18,000 / mm³. Hemoglobin and total leukocyte count are normal. She recently recovered from a mild upper respiratory tract infection. Peripheral smear shows no abnormal cells. What is the most appropriate next step in management?
- A. Platelet transfusion
- B. Splenectomy
- C. Oral corticosteroids (Correct Answer)
- D. Bone marrow biopsy
Explanation: ***Oral corticosteroids*** - This is the **first-line treatment** for newly diagnosed Immune Thrombocytopenic Purpura (ITP), especially when the platelet count is severely low (typically <30,000/mm³) and the patient exhibits bleeding symptoms like **petechiae** and easy bruising [1]. - Corticosteroids reduce the clearance of antibody-coated platelets by the **reticuloendothelial system** (primarily splenic macrophages) and suppress autoantibody production. ***Platelet transfusion*** - Platelet transfusions are generally **contraindicated** in ITP because the transfused platelets are rapidly destroyed by the same autoantibodies that target the patient's native platelets [1]. - They are reserved only for **life-threatening hemorrhage** (e.g., intracranial bleeding) or for pre-operative stabilization, usually given concurrently with high-dose IVIG or corticosteroids. ***Bone marrow biopsy*** - A **bone marrow biopsy** is usually not required for a young patient with classic ITP presentation (isolated thrombocytopenia, normal Hb/TLC, recent infection, and normal peripheral smear). - It is typically mandatory only if the patient is older (e.g., >60), has unexplained cytopenias in other lineages, or is **refractory** to first-line treatment. ***Splenectomy*** - Splenectomy is a **second-line treatment** option, typically reserved for patients with chronic ITP who fail to respond adequately to medical therapy (corticosteroids and IVIG) after 6 to 12 months [2]. - Although the spleen is the primary site of autoantibody production and platelet destruction, it is not the **most appropriate immediate next step** in initial management [2].
Microbiology
1 questionsNeutrophilic granulomatous mastitis is caused by which of the following organisms?
INI-CET 2025 - Microbiology INI-CET Practice Questions and MCQs
Question 161: Neutrophilic granulomatous mastitis is caused by which of the following organisms?
- A. Corynebacterium minutissimum
- B. Staphylococcus aureus
- C. Corynebacterium kroppenstedtii (Correct Answer)
- D. Mycobacterium tuberculosis
Explanation: ***Corynebacterium kroppenstedtii*** - This organism is the most commonly identified cause of **idiopathic granulomatous mastitis (IGM)**, specifically the subtype characterized by **neutrophilic microabscesses** adjacent to **non-caseating granulomas**. - It is a **lipophilic diphtheroid** often isolated from breast aspirates or biopsies of patients with **chronic, relapsing breast inflammation**. *Corynebacterium minutissimum* - This bacterium is primarily associated with **erythrasma**, a superficial skin infection presenting as reddish-brown patches, especially in intertriginous areas. - It is generally not involved in causing deep-seated, chronic granulomatous inflammation or abscess formation within the breast parenchyma. *Mycobacterium tuberculosis* - *M. tuberculosis* causes **tuberculous mastitis**, which is histologically defined by the presence of **caseating granulomas** and large areas of necrosis. - This differs from neutrophilic granulomatous mastitis, which features predominantly **non-caseating granulomas** mixed with neutrophils and microabscesses. *Staphylococcus aureus* - *S. aureus* is the leading cause of **acute mastitis** and **breast abscesses**, characterized by rapid onset, pain, fever, and abundant acute inflammatory cells (pus). - It is typically associated with acute suppurative changes, not the chronic, indolent, granulomatous tissue reaction found in neutrophilic granulomatous mastitis.
Pathology
3 questionsTransplant rejection does not occur in which of the following conditions?
In renal transplant biopsy, which of the following stains is not used to identify organisms?
Histopathological features of granulosa cell tumor include all except:
INI-CET 2025 - Pathology INI-CET Practice Questions and MCQs
Question 161: Transplant rejection does not occur in which of the following conditions?
- A. Bare lymphocyte syndrome
- B. Severe Combined Immunodeficiency (SCID) (Correct Answer)
- C. Chronic granulomatous disease
- D. DiGeorge syndrome
Explanation: The condition of Severe Combined Immunodeficiency (SCID) is characterized by a profound failure of adaptive immunity due to defects in the creation or function of both T-lymphocytes and B-lymphocytes [1]. Transplant rejection is a primarily cell-mediated process dependent on functional T-cells; since SCID recipients lack these critical immune cells, they cannot recognize or attack the donor graft, thus rejection does not occur [1]. Bare lymphocyte syndrome (BLS) is characterized by defective expression of MHC class I or MHC class II molecules, leading to severe immunodeficiency but typically not the complete and absolute absence of T-cell function like SCID. While severely immunocompromised, the mechanisms required for adaptive immunity are present, albeit impaired, and rejection risk is complex, making SCID the more definitive answer. Chronic granulomatous disease (CGD) involves an inherited deficiency of NADPH oxidase in phagocytes, impairing their ability to kill internalized microbes using oxidative burst [2]. CGD affects the innate immune system; the adaptive immune system (T-cells responsible for recognizing the graft) remains fully functional, meaning rejection will occur. DiGeorge syndrome causes variable degrees of T-cell deficiency due to the hypoplasia or aplasia of the thymus resulting from impaired development of the third and fourth pharyngeal pouches [2]. Though T-cell function is impaired, many patients retain residual or partial T-cell immunity, meaning a delayed or mild form of transplant rejection can still occur [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 246-248. [2] 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. 167-168.
Question 162: In renal transplant biopsy, which of the following stains is not used to identify organisms?
- A. Masson Fontana
- B. PAS (Periodic acid-Schiff) stain
- C. Congo red (Correct Answer)
- D. Gomori methenamine silver
Explanation: ***Congo red*** - **Congo red** is a special stain primarily used to look for **amyloid deposition**, which appears as an apple-green birefringence under polarized light [1]. - It is a diagnostic stain for **amyloidosis** and has **no role in the identification of infectious organisms** (bacteria, fungi, or parasites) in tissue biopsies [2]. - This is the stain that is **NOT used to identify organisms** in renal transplant biopsies. *Gomori methenamine silver* - This stain, often abbreviated as **GMS**, is excellent for demonstrating the cell walls of **fungi** (e.g., *Pneumocystis*, *Aspergillus*, *Cryptococcus*) which appear as black structures. - It is frequently used in transplant pathology to rule out opportunistic fungal infections. *PAS (Periodic acid-Schiff) stain* - **PAS** stain is used to highlight mucopolysaccharides, basement membranes, and certain cell walls, making it useful for identifying various organisms. - It stains the cell walls of **fungi** and the capsules of some organisms, making it valuable in detecting infections. *Masson Fontana* - **Masson Fontana** stain is primarily used to identify **melanin** pigment in tissues. - While it is not a standard organism identification stain in routine renal transplant pathology, specialized silver-based modifications have been described for detecting certain fungal organisms in research settings. - However, it is not considered a primary stain for organism identification in clinical practice. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 268-269. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 533-534.
Question 163: Histopathological features of granulosa cell tumor include all except:
- A. CA-125 positivity (Correct Answer)
- B. Microfollicular pattern
- C. Coffee bean nuclei
- D. Call-Exner bodies
Explanation: ***CA-125 positivity*** - **CA-125** is a **serum marker** predominantly associated with **epithelial ovarian cancer** (especially serous carcinoma), not a histopathological feature visible on microscopy. - It is not typically expressed by granulosa cell tumors (GCTs), which are sex cord-stromal tumors that produce **Inhibin** as their characteristic serum marker [1]. - **This is NOT a histopathological feature** but rather a laboratory/serological test, making it the correct answer to this "EXCEPT" question. *Incorrect: Microfollicular pattern* - Granulosa cells arrange themselves in **microfollicular or macrofollicular patterns**, creating small cystic spaces that are a key architectural feature [1]. - This pattern of growth is one of the characteristic **histopathological findings** seen on routine microscopy of adult GCTs. *Incorrect: Coffee bean nuclei* - This describes the characteristic appearance of tumor cell nuclei with **longitudinal grooves or infoldings**, giving them a distinct **'coffee bean'** appearance [1]. - This unique **nuclear morphology** is a classic and essential **histopathological feature** observed on H&E staining for diagnosis of GCT [1]. *Incorrect: Call-Exner bodies* - These are **small rosette-like structures** with central cystic spaces filled with eosinophilic material, formed by granulosa cells arranged in a circular pattern [1]. - Their presence is a **pathognomonic microscopic feature** of adult GCTs and represents follicular differentiation seen in these sex cord-stromal tumors [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1036-1037.
Pharmacology
1 questionsIn which condition erythropoietin will be useful for treatment?
INI-CET 2025 - Pharmacology INI-CET Practice Questions and MCQs
Question 161: In which condition erythropoietin will be useful for treatment?
- A. Nutritional anemia
- B. Aplastic anemia
- C. Anemia in chronic kidney disease (Correct Answer)
- D. Anemia in myelodysplastic syndrome
Explanation: ***Anemia in chronic kidney disease*** - **Erythropoietin (EPO)** deficiency is the primary cause of anemia in chronic kidney disease (**CKD**), as the damaged kidneys cannot produce adequate amounts. - Recombinant human EPO (**rHuEPO**) is the standard treatment to stimulate **erythropoiesis** in the bone marrow, correcting the anemia and improving quality of life. ***Anemia in myelodysplastic syndrome*** - While erythropoiesis-stimulating agents (ESAs) like EPO are occasionally used in lower-risk myelodysplastic syndrome (**MDS**) patients, especially those who are transfusion-dependent, the response rates are variable and dependent on underlying cytogenetics and serum EPO levels. - The primary defect in MDS involves abnormal **hematopoietic stem cell function** (a primary bone marrow failure) rather than just EPO deficiency, making treatment difficult. ***Nutritional anemia*** - This category, including **iron deficiency anemia** and **megaloblastic anemia** (Vitamin B12 or folate deficiency), is primarily treated by supplementing the specific deficient nutrient. - Giving EPO would be ineffective unless the underlying nutritional deficit is corrected, as the bone marrow lacks the necessary building blocks for red blood cell production. ***Aplastic anemia*** - Aplastic anemia is a condition of **pancytopenia** caused by bone marrow failure due to the destruction or suppression of hematopoietic stem cells, often immune-mediated. - The primary treatment involves **immunosuppressive therapy** (e.g., antithymocyte globulin) or **hematopoietic stem cell transplantation**, as erythropoietin production is usually adequate, and the bone marrow is simply unable to respond.