FMGE 2024 Practice Questions

Q: Which muscle is innervated by the Abducens nerve?

Lateral rectus. ***Lateral rectus***- The **Abducens nerve (CN VI)** specifically innervates only the **lateral rectus muscle** [1].- This muscle is responsible for moving the eyeball **laterally**, a movement known as **abduction** [1].*Medial rectus*- This muscle is innervated by the **Oculomotor nerve (CN III)**, not the Abducens nerve [1].- The primary action of the medial rectus is **adduction** (moving the eye medially) [1].*Superior oblique*- This muscle is innervated by the **Trochlear nerve (CN IV)**, which is unique among cranial nerves.- Its primary functions are **intorsion** (internal rotation) and **depression** of the eye.*Inferior oblique*- This muscle is innervated by the **Oculomotor nerve (CN III)**, along with the other recti (except lateral) and the levator palpebrae superioris.- Its main actions are **extorsion** (external rotation) and **elevation** of the eye [1].

Q: Which substance is involved in the conjugation process in the liver?

Glucuronic Acid. ***Glucuronic Acid***- The conjugation process is a Phase II detoxification reaction in the liver that increases the compound's polarity and water solubility for excretion.- **Glucuronidation**, catalyzed by **UDP-glucuronosyltransferases (UGT)**, is the most common and critical conjugation pathway, where substrates (like **bilirubin** and drugs) are linked to **glucuronic acid** (provided by UDP-glucuronic acid).*Hyaluronic Acid*- This acid is a large, non-sulfated **glycosaminoglycan** and a primary component of the **extracellular matrix** and **synovial fluid**.- It functions mainly in tissue structure, hydration, and lubrication, not as a conjugating molecule in liver metabolism.*Gluconic Acid*- This is an oxidation product of **glucose**, often used in food and pharmaceutical industries (e.g., as a salt like ferrous gluconate).- While structurally related to glucose metabolites, it is **glucuronic acid**, not gluconic acid, that is utilized for Phase II **conjugation**.*Glycolic Acid*- This substance is the smallest **alpha-hydroxy acid (AHA)** and is widely known for its use as a chemical exfoliator in dermatology.- Although it is an endogenous metabolite, it is not involved in the major Phase II conjugation reactions in the liver; these reactions primarily utilize **glucuronic acid**, sulfate, or glutathione.

Q: A 7-year-old child of short stature presents with skin patches and learning difficulties. Diagnostic workup indicates a defect in DNA repair specifically related to double-strand breaks. What is the most likely diagnosis?

Bloom Syndrome. ***Bloom Syndrome***- This condition is caused by a mutation in the **BLM gene**, which encodes a **RecQ helicase** necessary for homologous recombination repair (a mechanism for **double-strand break** repair), consistent with the clinical presentation.- Key clinical features include **short stature**, **telangiectatic erythema** (skin patches, especially on sun exposure), and intellectual disability/learning difficulties. *Xeroderma Pigmentosum*- This disease results from a defect in **Nucleotide Excision Repair (NER)**, crucial for repairing DNA damage caused by UV light (e.g., pyrimidine dimers), not primarily double-strand breaks.- Patients exhibit extreme **photosensitivity** and have a drastically increased risk of developing multiple skin cancers early in life.*Cockayne Syndrome*- Cockayne syndrome results from defects in genes like *ERCC8* or *ERCC6*, impairing **Transcription-Coupled Repair (TCR)**, a specific type of NER.- While it presents with short stature (often described as **cachectic dwarfism**) and neurological defects, the primary DNA defect is not in the repair of double-strand breaks but rather UV adducts in transcribed DNA.*Lynch Syndrome*- Also known as Hereditary Non-Polyposis Colorectal Cancer (HNPCC), this syndrome is caused by defects in **Mismatch Repair (MMR)** genes (e.g., *MLH1*, *MSH2*).- It primarily predisposes individuals to colorectal and endometrial cancers and is not typically associated with the features of short stature and specific DNA double-strand break repair defects seen in this child.

Q: Which of the following deficiencies causes follicular hyperkeratosis?

Vitamin A. ***Vitamin A***- Deficiency in Vitamin A (retinol) impairs the differentiation of **keratinizing epithelia**, leading to **squamous metaplasia**.- This results in **follicular hyperkeratosis** (also known as **phrynoderma** or 'toad skin'), where keratin plugs block the hair follicles, giving the skin a rough, bumpy appearance.*Vitamin C*- Deficiency causes **scurvy**, primarily due to defective collagen synthesis, leading to fragile blood vessels.- The characteristic skin finding is **perifollicular hemorrhage** (petechiae around hair follicles) and **painless gum bleeding**, not hyperkeratosis due to keratin plugging.*Vitamin E*- This deficiency primarily acts as an **antioxidant deficiency**, leading to increased susceptibility of cell membranes to oxidative damage.- Clinical manifestations often include **hemolytic anemia** (due to erythrocyte membrane damage) and **neurological symptoms** (e.g., ataxia, peripheral neuropathy).*Vitamin B6*- Deficiency of pyridoxine is often associated with cutaneous symptoms like a **seborrheic dermatitis-like rash** and **cheilosis** (cracked lips).- It is crucial for coenzyme functions but does not directly cause the severe keratin plugging characterized by widespread follicular hyperkeratosis.

Q: A 45-year-old patient presents with itchy, flat-topped, polygonal, violaceous papules on the inner wrists and flexors surfaces of the forearms. The lesions have a characteristic shiny surface and are arranged in a linear pattern. The patient denies any recent medication changes. What is the treatment?

Topical steroids. ***Topical steroids***- **Lichen planus** is an inflammatory, immune-mediated disorder, and high-potency **topical corticosteroids** are the first-line treatment for localized cutaneous disease on flexural surfaces.- They reduce the inflammation (T-cell-mediated injury to the **basal layer** of the epidermis) and effectively alleviate symptoms like intense **pruritus** (itching).*Antibiotics*- Lichen planus is a **sterile inflammatory process**, not caused by a bacterial infection, making antibiotics ineffective for treating the underlying pathology.- Antibiotics are reserved for infectious conditions like cellulitis or **secondary bacterial infection** of the lesions, which is not indicated here.*Immunosuppressants*- Systemic **immunosuppressants** (e.g., methotrexate, cyclosporine) are reserved for severe, widespread, or treatment-refractory cases, or extensive subtypes like **erosive oral lichen planus**.- For localized cutaneous disease, the risk profile of systemic immunosuppression does not justify its use over topical therapy.*Anti-fungal*- Anti-fungal agents are used to treat infections caused by fungi, such as **Tinea corporis** (ringworm), which presents with scaly, erythematous plaques, not flat-topped violaceous papules.- Lichen planus is an autoimmune/inflammatory dermatosis; therefore, anti-fungals have no role in its primary management.

Q: A 50-year-old male presents with right-sided serous otitis media and a history of cervical lymphadenopathy. The probable diagnosis is?

Nasopharyngeal cancer. ***Nasopharyngeal cancer***- Presents classically with the triad of **nasal obstruction/epistaxis**, **unilateral serous otitis media** (due to **Eustachian tube obstruction** by the tumor), and **cervical lymphadenopathy** (often metastatic).- The patient's presentation (adult age, unilateral SOM, and history of metastatic lymphadenopathy) is highly suggestive of this malignancy. *Angiofibroma*- This is a highly **vascular benign tumor** almost exclusively found in **adolescent males**, which contradicts the patient's age (50).- Primary symptoms are severe, recurrent **epistaxis** and nasal obstruction, rather than chronic serous otitis media as the dominant feature. *Adenoid hypertrophy*- While it commonly causes serous otitis media by blocking the **Eustachian tube opening**, it is a disease of **children** and is extremely rare to present *de novo* in a 50-year-old adult.- It typically causes **bilateral symptoms** (SOM, snoring) and is not associated with regional metastatic **cervical lymphadenopathy** in this age group. *Tonsillar abscess*- Symptoms typically include severe **sore throat**, **trismus** (difficulty opening the mouth), and a **"hot-potato" voice**, indicating an acute infection.- This is an acute condition that does not typically cause chronic unilateral serous otitis media as its primary or only otologic manifestation.

Q: A 22-year-old male with recurrent bleeding, presents with bowing of posterior maxillary wall on CECT. All are false except?

Tumor vessels lack contractility. ***Tumor vessels lack contractility*** (CORRECT - Most relevant to bleeding) - **Juvenile Nasopharyngeal Angiofibroma** (JNA) consists of numerous thin-walled vessels that are **deficient in smooth muscle** (muscular coat). - This lack of normal vessel musculature prevents effective **vasoconstriction** and hemostasis after trauma or spontaneous rupture, leading to severe and recurrent **epistaxis**. - This is the **key pathological feature** explaining the recurrent bleeding in this patient. *Outgrown the blood supply* (FALSE) - JNA is highly **vascularized**, with profuse blood supply primarily from branches of the **external carotid artery** (maxillary artery, ascending pharyngeal artery). - The tumor has abundant, not inadequate, blood supply—hence the risk of massive hemorrhage during surgical excision. *Bleeding is from the adjacent invading blood vessels* (FALSE) - Bleeding is **intrinsic** to the tumor, emanating from the tumor's own abnormal, thin-walled sinusoidal vessels embedded within its fibrous stroma. - While JNA is locally invasive, the pathological hemorrhage originates from the **delicate tumor vasculature itself**, not from adjacent normal vessels. *It lacks capsule* (TRUE - But less relevant to bleeding) - JNA is indeed **non-encapsulated**, which contributes to its locally aggressive behavior, invasion of surrounding structures, and tendency to recur after incomplete excision. - However, this feature relates more to **local extension and recurrence** rather than the bleeding tendency, which is specifically due to the **non-contractile vessels**.

Q: A person who was mentally unsound at the time of committing a crime is exempt from liability if they were unaware of the nature of their actions or its consequences. What is this principle called?

McNaughton rule. ***McNaughton rule (M'Naghten rule)*** - This is the **correct answer** as it establishes the legal test for insanity defense based on whether the accused was aware of the **nature and quality of the act** or knew it was **wrong** - Originated from the **1843 case of Daniel M'Naghten** in England and remains the most widely used insanity defense standard - Key principle: A person is not criminally responsible if, at the time of committing the act, they were **laboring under such a defect of reason from disease of the mind** as to not know the nature and quality of the act or that it was wrong - Applied in **India under Section 84 of the Indian Penal Code** *Durham's rule (Product test)* - This rule states that an accused is not criminally responsible if the unlawful act was the **"product of mental disease or defect"** - Much broader than M'Naghten rule - Used briefly in US courts but largely abandoned due to being too broad *Currens rule* - This test focuses on whether the defendant had the **capacity to conform their conduct** to the requirements of law - Emphasizes volitional control rather than cognitive understanding - Less commonly used standard *Irresistible impulse test* - This is a **supplementary test** that asks whether the defendant could **control their actions** even if they knew they were wrong - Addresses volitional incapacity rather than cognitive incapacity - Does not match the question's emphasis on "unaware of nature or consequences"

Q: What nutritional deficiency is commonly associated with a chronic alcoholic presenting with a pruritic, eczematous rash on the neck and dorsum of the hands?

Vit B3. ***Vit B3*** - This presentation is classic for **pellagra**, the syndrome caused by **niacin (Vitamin B3)** deficiency, characterized by the 3 Ds: **Dermatitis**, **Diarrhea**, and **Dementia** [1], [2]. - The described **pruritic, eczematous rash** on sun-exposed areas (neck, hands, often called Casal's necklace if circumferential on the neck) is the typical **photosensitive dermatitis** associated with pellagra [1], [2]. *Vit B1* - Deficiency in **thiamine (B1)** causes **Beriberi** or **Wernicke-Korsakoff syndrome**, which primarily affects the nervous and cardiovascular systems [3], [4]. - Clinical features include **ataxia**, **ophthalmoplegia**, and high-output heart failure, but not this characteristic eczematous rash [3], [4]. *Vit D* - Deficiency leads to defective bone mineralization, causing **Rickets** in children and **Osteomalacia** in adults (resulting in bone pain and fractures). - While common in alcoholics, **Vitamin D** deficiency is not the cause of the specific, widespread, photosensitive eczematous rash described. *Vit C* - **Ascorbic acid (Vitamin C)** deficiency causes **Scurvy**, which presents with symptoms related to impaired collagen synthesis. - Hallmark features include **gingival bleeding**, **perifollicular hemorrhages**, and **impaired wound healing**, without the specific photosensitive dermatitis seen in pellagra.

Q: Acute liver failure is a clinical feature of which of the following?

B. Amanita Phalloides poisoning. Correct Option B: Amanita Phalloides poisoning - This is due to the presence of potent hepatotoxins, primarily **alpha-amanitin**, which severely damages hepatocytes by inhibiting **RNA polymerase II**. - Ingestion often leads to a delayed presentation of **fulminant hepatic failure** (acute liver failure), necessitating aggressive supportive care and often liver transplantation [1]. *Incorrect Option A: OP poisoning* - Organophosphate poisoning primarily causes a **cholinergic crisis** by inhibiting acetylcholinesterase, leading to massive accumulation of acetylcholine (e.g., SLUDGE syndrome) [2]. - While severe hypoxia or shock might secondarily damage the liver, **acute liver failure** is not the characteristic or primary toxicity of organophosphates [2]. *Incorrect Option C: Belladonna poisoning* - Belladonna contains **atropine** and other anticholinergic compounds, causing profound **anticholinergic syndrome** (e.g., delirium, mydriasis, tachycardia, urinary retention). - Hepatic necrosis or **acute liver failure** is not a feature of anticholinergic toxicity. *Incorrect Option D: Morphine poisoning* - Morphine, an opioid, causes toxicity characterized by the classic triad of **respiratory depression**, altered mental status, and **pinpoint pupils** (miosis). - Opioid toxicity is centered on the central nervous system and respiratory system; it does not directly cause primary **acute liver failure**.

Question 1

Which muscle is innervated by the Abducens nerve?

Accepted Answer

Lateral rectus

Answer

Medial rectus

Answer

Inferior oblique

Answer

Superior oblique

Question 2

Which substance is involved in the conjugation process in the liver?

Accepted Answer

Glucuronic Acid

Answer

Gluconic Acid

Answer

Hyaluronic Acid

Answer

Glycolic Acid

Question 3

A 7-year-old child of short stature presents with skin patches and learning difficulties. Diagnostic workup indicates a defect in DNA repair specifically related to double-strand breaks. What is the most likely diagnosis?

Accepted Answer

Bloom Syndrome

Answer

Lynch Syndrome

Answer

Xeroderma Pigmentosum

Answer

Cockayne Syndrome

Question 4

Which of the following deficiencies causes follicular hyperkeratosis?

Accepted Answer

Vitamin A

Answer

Vitamin C

Answer

Vitamin E

Answer

Vitamin B6

Question 5

A 45-year-old patient presents with itchy, flat-topped, polygonal, violaceous papules on the inner wrists and flexors surfaces of the forearms. The lesions have a characteristic shiny surface and are arranged in a linear pattern. The patient denies any recent medication changes. What is the treatment?

Accepted Answer

Topical steroids

Answer

Anti-fungal

Answer

Antibiotics

Answer

Immunosuppressants

Question 6

A 50-year-old male presents with right-sided serous otitis media and a history of cervical lymphadenopathy. The probable diagnosis is?

Accepted Answer

Nasopharyngeal cancer

Answer

Tonsillar abscess

Answer

Angiofibroma

Answer

Adenoid hypertrophy

Question 7

A 22-year-old male with recurrent bleeding, presents with bowing of posterior maxillary wall on CECT. All are false except?

Accepted Answer

Tumor vessels lack contractility

Answer

Outgrown the blood supply

Answer

It lacks capsule

Answer

Bleeding is from the adjacent invading blood vessels

Question 8

A person who was mentally unsound at the time of committing a crime is exempt from liability if they were unaware of the nature of their actions or its consequences. What is this principle called?

Accepted Answer

McNaughton rule

Answer

Durham's rule

Answer

Currens rule

Answer

Irresistible impulse test

Question 9

What nutritional deficiency is commonly associated with a chronic alcoholic presenting with a pruritic, eczematous rash on the neck and dorsum of the hands?

Accepted Answer

Vit B3

Answer

Vit D

Answer

Vit C

Answer

Vit B1

Question 10

Acute liver failure is a clinical feature of which of the following?

Accepted Answer

B. Amanita Phalloides poisoning

Answer

C. Belladonna poisoning

Answer

D. Morphine poisoning

Answer

A. OP poisoning

FMGE 2024

Anatomy

Biochemistry

Dermatology

ENT

Forensic Medicine

General Medicine

Internal Medicine