Community Medicine
1 questionsWhich of the following is the National Deworming Day?
FMGE 2025 - Community Medicine FMGE Practice Questions and MCQs
Question 101: Which of the following is the National Deworming Day?
- A. 11th January
- B. 10th February (Correct Answer)
- C. 10th August
- D. 10th March
Explanation: ***10th February*** - The **National Deworming Day (NDD)** is observed annually on **February 10th** across India as the primary national observance to combat **Soil-Transmitted Helminths (STH)** infections - This day involves mass administration of **Albendazole** to children and adolescents (typically 1-19 years) through schools and Anganwadi centres - This is the officially recognized date for the **first annual round** of the national campaign *10th August* - While this date is used for deworming, it serves as the designated date for the **second round** or **follow-up dose** in states using a biannual strategy - This is not the primary National Deworming Day; **February 10th** remains the nationally recognized date for the official observance *10th March* - This date is incorrect and not officially associated with the **National Deworming Day** in India - The official campaign date is fixed to ensure standardized, synchronized provision of **Albendazole** nationwide *11th January* - **January 11th** is not the recognized date for either the first or second round of the **National Deworming Day** campaign - The program's schedule is intentionally set in February and August to maximize coverage and minimize disruption to academic schedules
Dermatology
1 questionsA child presents with a vesiculobullous, pustular rash around the mouth and on the extremities, along with alopecia and diarrhea. What is the most likely nutritional deficiency?
FMGE 2025 - Dermatology FMGE Practice Questions and MCQs
Question 101: A child presents with a vesiculobullous, pustular rash around the mouth and on the extremities, along with alopecia and diarrhea. What is the most likely nutritional deficiency?
- A. Vitamin C Deficiency
- B. Zinc Deficiency (Correct Answer)
- C. Vitamin D Deficiency
- D. Copper Deficiency
Explanation: ***Zinc Deficiency*** - This clinical presentation represents a classic case of **acrodermatitis enteropathica**, a condition caused by zinc deficiency, characterized by a vesiculobullous, pustular, and eczematous rash in a **periorificial** (around the mouth) and **acral** distribution. - Other key features of zinc deficiency include **alopecia** (hair loss), chronic **diarrhea**, **impaired growth**, and **immunodeficiency**, leading to recurrent infections. *Vitamin C Deficiency* - Known as **scurvy**, this deficiency leads to impaired collagen synthesis, resulting in manifestations like **petechiae**, **ecchymoses**, perifollicular hemorrhage, **bleeding gums**, and **corkscrew hairs**. - In infants, it can present with **subperiosteal hemorrhages**, causing severe pain and reluctance to move (**pseudoparalysis**), but not the periorificial rash seen here. *Vitamin D Deficiency* - This deficiency primarily affects bone mineralization, leading to **rickets** in children and **osteomalacia** in adults. Clinical signs include **bowed legs** (genu varum), **rachitic rosary** (beading of the ribs), and **craniotabes** (soft skull). - Cutaneous manifestations are not a feature of vitamin D deficiency; its role is primarily in **calcium homeostasis** and bone health. *Copper Deficiency* - Copper deficiency primarily manifests with hematological abnormalities like **microcytic anemia** (refractory to iron treatment) and neurological symptoms such as **myelopathy** and peripheral neuropathy. - Cutaneous signs are rare but can include **hypopigmentation** of the skin and kinky, brittle hair (**pili torti**), which are features of the genetic disorder **Menkes disease**.
ENT
2 questionsIdentify the treatment option with the image given below:
A patient presented to the OPD with complaints of greenish black matter in the nose with foul-smelling discharge. What is the diagnosis?
FMGE 2025 - ENT FMGE Practice Questions and MCQs
Question 101: Identify the treatment option with the image given below:
- A. Type 3 tympanoplasty (Correct Answer)
- B. Type 2 tympanoplasty
- C. Type 4 tympanoplasty
- D. Type 1 tympanoplasty
Explanation: ***Type 3 tympanoplasty*** - This procedure, also known as **myringostapediopexy**, involves placing a graft directly onto the head of the stapes, as depicted in the image. - It is indicated when both the **malleus** and **incus** are eroded or absent, but the stapes is intact and mobile, allowing for sound transmission directly to the stapes. *Type 1 Tympanoplasty* - This is a simple repair of a tympanic membrane perforation, also called **myringoplasty**, where the graft is placed to close the hole. - This procedure is only suitable when the **ossicular chain** is completely intact and mobile, which is not the case shown. *Type 2 tympanoplasty* - This is performed when the **malleus** is eroded, and the graft is placed onto the **incus** or the remaining part of the malleus. - The image shows that the incus is also absent, as the graft is placed directly on the stapes, making this option incorrect. *Type 4 tympanoplasty* - This procedure is indicated when only the **stapes footplate** remains and is mobile; the graft is placed directly on the footplate. - This creates a very shallow middle ear space, essentially shielding only the round window and Eustachian tube opening, a more extensive reconstruction than shown.
Question 102: A patient presented to the OPD with complaints of greenish black matter in the nose with foul-smelling discharge. What is the diagnosis?
- A. Rhinitis caseosa
- B. Allergic rhinitis
- C. Atrophic rhinitis (Correct Answer)
- D. Rhinitis sicca
Explanation: ***Atrophic rhinitis***- This condition is characterized by progressive atrophy of the nasal mucosa and underlying turbinate bones, leading to excessively wide nasal cavities.- The presence of large, dry, **greenish-black crusts** that produce a very offensive, sickening smell (**ozena**) is the classic defining feature, matching the patient's presentation.*Allergic rhinitis*- This condition presents with symptoms like watery rhinorrhea, sneezing, nasal itching, and **conjunctivitis**, often triggered by specific allergens.- It is an inflammatory condition and does not result in the mucosal atrophy or the formation of large, fetid, **greenish-black crusts** (ozena).*Rhinitis caseosa*- This rare form is characterized by the accumulation of a firm, malodorous, **cheese-like** (caseous) material that acts as a foreign body within the nasal cavity, differentiating it from the general crusting of atrophic rhinitis.- While it causes a very foul smell, the material retrieved is typically described as caseous or putty-like, not the widespread greenish-black crusts typical of ozena.*Rhinitis sicca*- This condition involves localized **dryness** and minor crusting, often restricted to the anterior nasal septum, typically seen in dry climates or specific occupations.- It is characterized by persistent dryness and discomfort but generally lacks the severe **mucosal atrophy** or the intense, offensive odor (**ozena**) associated with generalized greenish-black crusts found in atrophic rhinitis.
Obstetrics and Gynecology
3 questionsWhich is the primary chemotherapeutic agent used for cervical cancer?
A woman with forceps delivery 24 hours ago presents with pain in the perineum. Her BP is 80/60 and on examination, there is a swelling with bluish discolouration. Which of the following steps are advised not to do?
Fetal anaemia is monitored by?
FMGE 2025 - Obstetrics and Gynecology FMGE Practice Questions and MCQs
Question 101: Which is the primary chemotherapeutic agent used for cervical cancer?
- A. Platinum-based therapy (Correct Answer)
- B. Immunotherapy
- C. Hormonal therapy
- D. Targeted therapy
Explanation: ***Platinum-based therapy*** - **Cisplatin** is the foundational chemotherapeutic agent utilized, often combined with radiation (**chemoradiation**) for locally advanced disease. - For metastatic or recurrent cervical cancer, combinations using platinum agents (**Cisplatin** or **Carboplatin**) along with **Paclitaxel** are standard first-line systemic treatments. *Immunotherapy* - **Immunotherapy**, specifically checkpoint inhibitors like **Pembrolizumab**, is approved for recurrent or metastatic cervical cancer that progresses after first-line chemotherapy. - It is not the initial or primary systemic treatment modality, which is founded upon platinum agents. *Hormonal therapy* - **Hormonal therapy** is primarily used for hormone-responsive cancers such as **breast cancer** (estrogen/progesterone receptors positive) or **prostate cancer**. - Cervical cancer is typically driven by **HPV infection** and carcinogenesis, making it largely unresponsive to sex hormones. *Targeted therapy* - **Targeted therapy**, such as the **anti-VEGF** agent **Bevacizumab**, is often utilized, but only *in addition to* platinum-based chemotherapy for advanced or recurrent disease. - It is used as an adjunct to systemic chemotherapy, which remains centered on platinum compounds.
Question 102: A woman with forceps delivery 24 hours ago presents with pain in the perineum. Her BP is 80/60 and on examination, there is a swelling with bluish discolouration. Which of the following steps are advised not to do?
- A. Repair the wound in the ward (Correct Answer)
- B. Inform senior about her
- C. Shift patient to OT
- D. Give Blood Transfusion
Explanation: ***Repair the wound in the ward*** - This patient has a **perineal hematoma** with hemodynamic instability (BP 80/60 mmHg indicating hypovolemic shock) - Surgical evacuation of hematoma requires **proper anesthesia, adequate lighting, sterile conditions, and availability of resuscitation equipment** - all available in OT, not in ward - Ward-based repair would be inadequate and dangerous in an unstable patient - **Standard protocol:** Hemodynamically unstable obstetric emergencies require OT management *Inform senior about her* - This SHOULD be done immediately - Perineal hematoma with shock is a **medical emergency requiring senior consultation** - Essential for proper decision-making and management *Shift patient to OT* - This SHOULD be done as part of proper management - **Surgical evacuation of hematoma** under anesthesia is required - OT provides controlled environment for managing complications *Give Blood Transfusion* - This SHOULD be done urgently - BP 80/60 indicates **hypovolemic shock** from concealed bleeding in hematoma - **Resuscitation with blood products** is essential before and during surgical management - Cross-matched blood should be arranged immediately
Question 103: Fetal anaemia is monitored by?
- A. Amniocentesis
- B. MCA-PSV (Correct Answer)
- C. Maternal blood
- D. Fetal blood
Explanation: ***MCA-PSV*** - **Middle Cerebral Artery-Peak Systolic Velocity (MCA-PSV)** is a non-invasive Doppler ultrasound method to assess for fetal anemia. It measures the peak velocity of blood flow in the fetal middle cerebral artery. - In anemic fetuses, blood viscosity decreases, leading to increased cardiac output and higher cerebral blood flow velocity. A value greater than **1.5 Multiples of the Median (MoM)** for gestational age is highly predictive of moderate to severe fetal anemia. *Maternal blood* - Maternal blood testing, such as the **Indirect Coombs Test (ICT)**, is used to detect maternal antibodies against fetal red blood cells, indicating maternal sensitization and risk of fetal hemolysis. - While a rising titer suggests an increased risk, it does not directly quantify the severity of anemia in the fetus itself; it serves as a screening tool to identify pregnancies needing closer surveillance. *Fetal blood* - Fetal blood sampling, performed via **cordocentesis**, is the gold standard for diagnosing and quantifying the degree of fetal anemia by directly measuring fetal hemoglobin. - However, it is an invasive procedure with significant risks (e.g., fetal loss, hemorrhage) and is reserved for confirming severe anemia indicated by non-invasive tests like MCA-PSV, or for therapeutic intervention like intrauterine transfusion. *Amniocentesis* - Historically, amniocentesis was used to measure the level of bilirubin in the amniotic fluid (spectrophotometry at ΔOD450) as an indirect marker of hemolysis. - This invasive method has been largely replaced by the non-invasive, safer, and more accurate MCA-PSV Doppler assessment for monitoring fetal anemia.
Pathology
3 questionsWhat is the earliest time after myocardial infarction when triphenyl tetrazolium chloride (TTC) staining can detect infarcted tissue?
Which of the following is a change seen in irreversible cell injury?
Histopathological examination showed follicular cells with abundant pink eosinophilic cytoplasm WITHOUT nuclear grooves or ground-glass nuclei. This is most characteristic of?
FMGE 2025 - Pathology FMGE Practice Questions and MCQs
Question 101: What is the earliest time after myocardial infarction when triphenyl tetrazolium chloride (TTC) staining can detect infarcted tissue?
- A. 3 hours (Correct Answer)
- B. 1 hour
- C. 30 minutes
- D. Immediately
Explanation: ***3 hours***- **TTC (Triphenyl Tetrazolium Chloride)** staining detects viable myocardium by reacting with **lactate dehydrogenase** (LDH) and other mitochondrial dehydrogenases, resulting in a **brick-red color** [1].- Necrotic myocardium loses these enzymes, preventing the color change and leaving the infarcted tissue **pale yellow**; this process usually takes at least **3 hours** post-occlusion to be grossly detectable [1].*1 hour*- The time interval is too short for the complete depletion of **dehydrogenases** from the infarcted cells necessary to prevent the TTC reaction and produce a visually distinct **pale area**.- Reliable gross detection by TTC requires cellular necrosis advanced enough to cause enzyme leakage, which typically requires more time than 1 hour [1].*30 minutes*- At 30 minutes post-MI, myocardial damage is often still in the stage of **reversible injury**, and the cell membranes and internal enzyme systems are still largely intact [2].- This limited timeframe does not allow for sufficient enzyme leakage or inactivation required to produce a clear negative (unstained) reaction with the **tetrazolium salt** [1].*Immediately*- Immediate staining will show uniformly red tissue because sufficient time has not passed for the irreversible cell injury (**necrosis**) and subsequent loss of intrinsic **enzymatic activity**.- Myocardium must undergo several hours of severe ischemia and necrosis before the gross chemical findings detected by **TTC** become apparent [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 552-554. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 552.
Question 102: Which of the following is a change seen in irreversible cell injury?
- A. Amorphous density of mitochondria (Correct Answer)
- B. Cellular Swelling
- C. Bleb formation
- D. Clumping of chromatin
Explanation: ***Amorphous density of mitochondria***- This refers to the formation of large, irregular, dense calcium deposits within the mitochondrial matrix, which is a classic morphological feature indicating irreparable damage to the organelle [1].- The presence of these **amorphous densities** signifies severe mitochondrial dysfunction, including the complete loss of inner membrane potential and irreversible failure of **oxidative phosphorylation**, committing the cell to necrosis [2].*Bleb formation*- Small, transient surface blebs are common manifestations of **reversible** cell injury resulting from alterations in the cytoskeleton due to ATP depletion [1].- While uncontrolled blebbing is a feature preceding plasma membrane rupture in necrosis, its simple occurrence is not exclusively tied to irreversible injury, unlike profound mitochondrial changes [4].*Clumping of chromatin*- This initial condensation of nuclear material is characteristic of **reversible** cell injury, often due to decreased ATP causing a decrease in nuclear components and an acidic intracellular environment.- This reversible change must progress to irreversible nuclear hallmarks like **pyknosis** (irreversible condensation) or karyorrhexis/karyolysis to confirm cell death [4].*Cellular Swelling*- **Cellular swelling** (or hydropic change) is the most common manifestation of **reversible** cell injury [4], resulting from the failure of the ATP-dependent **Na+/K+ pump** [3].- This failure leads to the influx and accumulation of intracellular sodium and water, a condition that can be reversed if oxygenation and ATP synthesis are restored [3]. **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. 53-55. [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. 102-103. [3] 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. 56-57. [4] 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, p. 53.
Question 103: Histopathological examination showed follicular cells with abundant pink eosinophilic cytoplasm WITHOUT nuclear grooves or ground-glass nuclei. This is most characteristic of?
- A. Follicular CA (Correct Answer)
- B. Papillary CA
- C. Medullary CA
- D. Anaplastic CA
Explanation: ***Follicular CA (Hürthle cell variant)*** - The description of **follicular cells with abundant pink eosinophilic cytoplasm** is characteristic of the **Hürthle cell variant** (also known as the oncocytic or oxyphil variant) of follicular thyroid carcinoma. - This **eosinophilic appearance** is due to the presence of numerous abnormal **mitochondria** within the cytoplasm of the tumor cells. - The **absence of nuclear features** (grooves, ground-glass nuclei) helps distinguish this from the Hürthle cell variant of papillary carcinoma [2], [3]. - Diagnosis requires evidence of **capsular or vascular invasion** to differentiate from Hürthle cell adenoma [1], [5]. *Papillary CA* - While papillary carcinoma can also have a **Hürthle cell variant**, it would show characteristic **nuclear changes** including **Orphan Annie eye nuclei** (ground-glass chromatin), **nuclear grooves**, and **intranuclear pseudoinclusions** [3], [4]. - The question specifically excludes these nuclear features, making follicular carcinoma more likely. - The classic variant shows papillary architecture with defining nuclear features [3]. *Medullary CA* - This tumor originates from **parafollicular C-cells** (not follicular cells) and is characterized by the presence of **amyloid deposits** (derived from calcitonin) in the stroma [4], [5]. - The tumor cells are usually spindle or polygonal and lack the described eosinophilic follicular cell morphology. - Positive for **calcitonin** and **CEA** on immunohistochemistry. *Anaplastic CA* - Anaplastic carcinoma is highly undifferentiated and consists of bizarre, **highly pleomorphic cells**, including spindle cells and **multinucleated giant cells** [4]. - It is characterized by extensive necrosis, high mitotic activity, and lacks the structural and cellular uniformity of differentiated follicular tumors. - Shows aggressive invasive behavior with poor prognosis [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1100-1101. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1099-1100. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1099. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 429-430. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 428-429.