FMGE 2017 Practice Questions

Q: Cutaneous supply over the parotid gland is by:

Greater auricular nerve. ***Greater auricular nerve*** - The **greater auricular nerve**, a branch of the cervical plexus (C2-C3), is the **primary cutaneous nerve** supplying sensation to the skin over the parotid gland and the angle of the mandible. - It ascends from behind the sternocleidomastoid muscle and provides the main sensory innervation to the parotid region, making it the most important nerve for this area. *Auriculotemporal nerve* - The **auriculotemporal nerve** (branch of mandibular division of trigeminal nerve) supplies sensory innervation to the skin of the temporal region, the external auditory meatus, and the tympanic membrane. - While it provides some cutaneous supply to the upper/posterior part of the parotid region, the **greater auricular nerve is the primary cutaneous nerve** over the parotid gland proper. - It also carries postganglionic parasympathetic fibers (from otic ganglion) to the parotid gland for secretomotor function. *Greater occipital nerve* - The **greater occipital nerve** is responsible for cutaneous sensation to the posterior scalp, up to the vertex of the head. - It arises from the dorsal ramus of C2 and has no role in the cutaneous supply over the parotid gland. *Facial nerve* - The **facial nerve (CN VII)** is primarily a motor nerve that controls the muscles of facial expression. - While it passes through the parotid gland and divides within it, it does not provide cutaneous sensory innervation to the skin overlying the gland.

Q: 21st tooth erupts at:-

8 years. ***8 years*** - The **permanent mandibular central incisors** (teeth #24 and #25) and maxillary central incisors (teeth #8 and #9) typically erupt around **6-8 years of age**. - As the question refers to the "21st tooth" (lower left first molar), referring to the typical numbering system in dentistry for permanent teeth, it would correspond to the lower left first premolar (tooth #21), which typically erupts between **10-12 years of age**. However, if assuming a more general interpretation of a "middle tooth" erupting later, 8 years is within the range for central incisors before lateral incisors or premolars. Given the provided correct answer, it likely refers to central incisors which erupt around this age, making 8 years the closest general option if specific tooth numbering is not strictly intended for primary teeth. *10 years* - This age is typically associated with the eruption of **premolars** and **canines**, rather than the earlier erupting central incisors. - While some permanent teeth do erupt around 10 years, it's not the primary eruption time for the permanent central incisors, which are among the earliest to erupt. *6 years* - The first permanent teeth to erupt are generally the **first molars** and the **mandibular central incisors**, typically around 6 years of age. - However, for the "21st tooth" as per the universal numbering system (lower left first premolar), 6 years is too early an age for its eruption. *12 years* - This age is associated with the eruption of **second molars** and sometimes the last of the premolars/canines. - It is too late for the eruption of central incisors, which are among the first permanent teeth to erupt.

Q: Which of the following conditions is characterized by the presence of hyaline deposits in alveolar walls?

Hyaline membrane disease. ***Hyaline membrane disease*** - This condition is pathologically characterized by the presence of **eosinophilic (hyaline) membranes** lining the distal airspaces, which are composed of fibrin, cellular debris, and necrotic cells [1]. - These **hyaline deposits obstruct gas exchange** and are a hallmark of **acute lung injury** in neonates due to surfactant deficiency [2]. *Asthma* - Characterized by **bronchoconstriction**, **mucus plugging**, and **airway inflammation**, but not hyaline deposits in alveolar walls. - Pathologically, there is hyperplasia of goblet cells, hypertrophy of bronchial smooth muscle, and eosinophilic infiltration. *Chronic bronchitis* - Defined by **chronic productive cough** due to hypertrophy of mucous glands and increased mucus production in the bronchi, not alveolar hyaline deposits. - It primarily affects the **large airways** and is associated with chronic inflammation and airway obstruction. *Interstitial lung disease* - Involves inflammation and fibrosis of the **interstitium of the lung**, leading to impaired gas exchange. - While it causes architectural distortion, **hyaline deposits** in the alveolar walls are not a defining pathological feature. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 679-681. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, p. 466.

Q: All of the following special histology stains are used to demonstrate H. pylori in gastric biopsies, except:

Fite's stain. ***Fite's stain*** - **Fite's stain** (or Fite-Faraco stain) is a modified acid-fast stain primarily used to detect **mycobacteria**, particularly **Mycobacterium leprae**, in tissue sections [2]. - It is not used for the identification of **Helicobacter pylori**. *Giemsa stain* - **Giemsa stain** is a common special stain used to visualize **Helicobacter pylori** directly in gastric biopsies due to its ability to stain the bacterial cytoplasm a characteristic **blue color**. - It works by staining the cytoplasmic and nuclear components of cells, making bacteria and inflammatory cells easily identifiable. *Modified Steiner's stain* - **Modified Steiner's stain** is a silver impregnation stain used to demonstrate spirochetes and other bacteria, including **Helicobacter pylori**, by staining them **black**. - It involves a silver solution that precipitates onto the bacterial surface, followed by a reducing agent to visualize the organisms. *Warthin-Starry stain* - The **Warthin-Starry stain** is another silver impregnation method widely employed for detecting spirochetes and bacteria like **Helicobacter pylori** in tissue [1]. - It renders the bacteria visible as **black** or dark brown structures against a pale yellow background, providing excellent contrast [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 771. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 385-386.

Q: In a newly diagnosed case of a sick child with type 1 diabetes mellitus (DM), insulin was given. Which of the following will increase:

pH. ***pH*** - In newly diagnosed, uncontrolled **Type 1 DM**, patients often present with **diabetic ketoacidosis (DKA)**, leading to metabolic acidosis and a **critically low pH** (typically <7.3). - Administering insulin corrects the underlying metabolic derangements, reducing **ketoacid production** and allowing the body's **buffer systems** to restore pH towards normal. - **Correction of acidosis** is the **primary therapeutic goal** and the most clinically significant parameter that increases with insulin therapy in DKA. *Breathing rate* - In **DKA**, patients often exhibit **Kussmaul respirations** (deep, rapid breathing) as a compensatory mechanism to blow off CO2 and reduce acidosis. - As insulin therapy corrects the acidosis, the need for this compensatory mechanism decreases, leading to a **reduction**, not an increase, in breathing rate. *Urine osmolality* - In uncontrolled **Type 1 DM** and **DKA**, high blood glucose leads to **osmotic diuresis**, where glucose pulls water into the urine, resulting in polyuria and typically **low urine osmolality** (dilute urine). - While insulin therapy may allow some increase in urine concentration as osmotic diuresis decreases, this is a **secondary effect** and not the primary clinical focus in acute DKA management. - Additionally, initial fluid resuscitation in DKA treatment maintains diuresis, so urine osmolality changes are variable and less predictable. *Glucosuria* - **Glucosuria** (glucose in the urine) is a hallmark of uncontrolled diabetes due to hyperglycemia exceeding the renal threshold for glucose reabsorption. - Insulin treatment lowers blood glucose levels, which in turn **reduces or eliminates glucosuria**, as the kidneys no longer filter excessive amounts of glucose.

Q: Which of these is the best for management of methanol poisoning?

Fomepizole. ***Fomepizole*** - **Fomepizole** is a competitive inhibitor of **alcohol dehydrogenase**, the enzyme responsible for metabolizing methanol into toxic metabolites like formic acid. - By inhibiting this enzyme, it prevents the formation of these toxic metabolites, thereby reducing organ damage and metabolic acidosis in methanol poisoning. *Naltrexone* - **Naltrexone** is an **opioid receptor antagonist** used in the treatment of alcohol and opioid dependence. - It does not have any direct action on the metabolism of methanol or its toxic byproducts. *Disulfiram* - **Disulfiram** inhibits **aldehyde dehydrogenase**, leading to an unpleasant reaction when alcohol is consumed (flushing, nausea, vomiting). - It is used for alcohol cessation and has no role in the management of methanol poisoning. *Acamprosate* - **Acamprosate** is a medication used to reduce alcohol cravings in individuals recovering from alcohol dependence, possibly by modulating **glutamate neurotransmission**. - It does not directly affect the metabolism of methanol or mitigate its toxic effects.

Q: Many drugs are used as rescue therapy for preventing the adverse effects of anticancer drugs. Folinic acid is used in:-

Methotrexate toxicity. ***Methotrexate toxicity*** - **Folinic acid (leucovorin)** is a reduced folate that bypasses the metabolic block caused by **methotrexate** on dihydrofolate reductase. - It replenishes the body's **folate stores** and protects healthy cells from methotrexate's cytotoxic effects, particularly in the bone marrow and gastrointestinal tract. *Cyclophosphamide toxicity* - **Cyclophosphamide** toxicity, primarily hemorrhagic cystitis, is prevented by **mesna** (2-mercaptoethane sulfonate). - Mesna inactivates the urotoxic metabolite **acrolein** in the urine, preventing bladder damage. *Doxorubicin toxicity* - **Doxorubicin** causes cardiotoxicity, which can be mitigated by the iron-chelating agent **dexrazoxane**. - Dexrazoxane reduces the formation of **free radicals** that contribute to doxorubicin-induced myocardial damage. *Cisplatin toxicity* - **Cisplatin** toxicity, especially nephrotoxicity, is largely prevented by **aggressive hydration** and administration of **diuretics**. - **Amifostine** is another agent that can reduce cisplatin-induced nephrotoxicity, neurotoxicity, and ototoxicity by acting as a cytoprotectant.

Q: Ritodrine is a:-

β2 agonist. ***β2 agonist*** - Ritodrine is a **selective beta-2 adrenergic receptor agonist** primarily used as a **tocolytic agent** to relax the uterus and stop premature labor. - Its action involves stimulating **beta-2 receptors** in the myometrium, leading to decreased intracellular calcium and uterine smooth muscle relaxation. *α1 antagonist* - Alpha-1 antagonists block **alpha-1 adrenergic receptors**, causing vasodilation and are used to treat conditions like **hypertension** or **benign prostatic hyperplasia**. - Ritodrine's mechanism is distinct, as it targets beta-2 receptors, not alpha-1. *β antagonist* - Beta antagonists (beta-blockers) block **beta adrenergic receptors** (beta-1, beta-2, or both) and are used for conditions like **hypertension**, **angina**, or **arrhythmias**. - Ritodrine is an agonist, meaning it activates receptors, rather than blocking them. *α agonist* - Alpha agonists stimulate **alpha adrenergic receptors**, causing vasoconstriction and increased blood pressure, as seen with agents like **phenylephrine**. - Ritodrine specifically targets beta-2 receptors, leading to opposite effects like smooth muscle relaxation in the uterus and bronchi.

Q: Mechanism of action of Pemetrexed is:-

Thymidylate synthase inhibitor. ***Thymidylate synthase inhibitor*** - **Pemetrexed** is a **multi-targeted antifolate agent** that primarily inhibits **thymidylate synthase (TS)**, the key enzyme responsible for synthesizing thymidine monophosphate, an essential building block for DNA synthesis. - While pemetrexed also inhibits **dihydrofolate reductase (DHFR)** and **glycinamide ribonucleotide formyltransferase (GARFT)**, its **primary and most clinically significant mechanism** is TS inhibition, making it particularly effective in mesothelioma and non-small cell lung cancer. - This multi-targeted action enhances its cytotoxic effects compared to single-target antifolates. *Dihydrofolate reductase inhibitor* - While pemetrexed does inhibit **DHFR** as part of its multi-targeted mechanism, this is a **secondary action**, not its primary mechanism. - Classical DHFR inhibitors include **methotrexate** and **trimethoprim**, which specifically target this enzyme. - In exam contexts, pemetrexed is best classified by its **primary target: thymidylate synthase**. *Topoisomerase inhibitor* - **Topoisomerase inhibitors** target enzymes that control DNA topology during replication and transcription. - Examples include **irinotecan** and **topotecan** (topoisomerase I inhibitors) and **etoposide** (topoisomerase II inhibitor). - This is not the mechanism of action for pemetrexed. *Dopamine agonist* - **Dopamine agonists** activate dopamine receptors and are used in neurological conditions like Parkinson's disease (e.g., **pramipexole**, **ropinirole**). - This mechanism is completely unrelated to anticancer agents and folate metabolism.

Q: All of the following statements about pralidoxime in organophosphate poisoning are true except:-

It should be started after 24 hours of poisoning. ***It should be started after 24 hours of poisoning*** - **Pralidoxime (2-PAM)** is most effective when administered **early** in organophosphate poisoning, ideally within minutes to a few hours of exposure. - Delaying administration beyond **24-48 hours** significantly reduces its efficacy because the bond between the organophosphate and **acetylcholinesterase (AChE)** becomes **irreversible** (a process called "aging"). *It does not cross blood brain barrier* - **Pralidoxime** is a **quaternary ammonium compound**, which makes it highly polar and unable to readily cross the **blood-brain barrier**. - Therefore, it primarily reactivates **acetylcholinesterase** in the **peripheral nervous system** but has limited effect on central nervous system symptoms. *Reactivates the AChE enzyme* - **Pralidoxime** works by **reactivating the acetylcholinesterase enzyme** that has been inhibited by organophosphates. - It does this by binding to the organophosphate molecule, thereby freeing the active site of the **AChE enzyme** to metabolize **acetylcholine** again. *It is given intravenously* - **Pralidoxime** is typically administered via **intravenous (IV) infusion** to achieve rapid and sustained therapeutic concentrations. - Due to its poor oral absorption, oral administration is not a suitable route for treating acute organophosphate poisoning.

Question 1

Cutaneous supply over the parotid gland is by:

Accepted Answer

Greater auricular nerve

Answer

Auriculotemporal nerve

Answer

Greater occipital nerve

Answer

Facial nerve

Question 2

21st tooth erupts at:-

Accepted Answer

8 years

Answer

10 years

Answer

6 years

Answer

12 years

Question 3

Which of the following conditions is characterized by the presence of hyaline deposits in alveolar walls?

Accepted Answer

Hyaline membrane disease

Answer

Asthma

Answer

Chronic bronchitis

Answer

Interstitial lung disease

Question 4

All of the following special histology stains are used to demonstrate H. pylori in gastric biopsies, except:

Accepted Answer

Fite's stain

Answer

Giemsa stain

Answer

Warthin-Starry stain

Answer

Modified Steiner's stain

Question 5

In a newly diagnosed case of a sick child with type 1 diabetes mellitus (DM), insulin was given. Which of the following will increase:

Accepted Answer

pH

Answer

Breathing rate

Answer

Urine osmolality

Answer

Glucosuria

Question 6

Which of these is the best for management of methanol poisoning?

Accepted Answer

Fomepizole

Answer

Naltrexone

Answer

Disulfiram

Answer

Acamprosate

Question 7

Many drugs are used as rescue therapy for preventing the adverse effects of anticancer drugs. Folinic acid is used in:-

Accepted Answer

Methotrexate toxicity

Answer

Cyclophosphamide toxicity

Answer

Doxorubicin toxicity

Answer

Cisplatin toxicity

Question 8

Ritodrine is a:-

Accepted Answer

β2 agonist

Answer

β antagonist

Answer

α agonist

Answer

α1 antagonist

Question 9

Mechanism of action of Pemetrexed is:-

Accepted Answer

Thymidylate synthase inhibitor

Answer

Topoisomerase inhibitor

Answer

Dihydrofolate reductase inhibitor

Answer

Dopamine agonist

Question 10

All of the following statements about pralidoxime in organophosphate poisoning are true except:-

Accepted Answer

It should be started after 24 hours of poisoning

Answer

It does not cross blood brain barrier

Answer

Reactivates the AChE enzyme

Answer

It is given intravenously

FMGE 2017

Anatomy

Dental

Pathology

Pediatrics

Pharmacology