NEET-PG 2015 - Internal Medicine Practice Questions

Q: Hutchinson's Triad is specifically associated with which type of syphilis?

Congenital Syphilis. ***Congenital Syphilis*** - **Hutchinson's Triad** is a classic constellation of symptoms specific to **congenital syphilis**, reflecting the long-term effects of *in utero* infection [1]. - The triad includes **Hutchinson's teeth** (notched incisors), **interstitial keratitis** (corneal inflammation), and **sensorineural hearing loss**. *Tertiary syphilis* - This stage is characterized by **gummas**, **cardiovascular syphilis** (e.g., aortitis), and **neurosyphilis**, but not Hutchinson's triad [1]. - These manifestations develop years after initial infection in adults. *Primary syphilis* - The primary stage is marked by the appearance of a **painless chancre** at the site of infection [1]. - It does not involve the systemic, long-term complications seen in congenital syphilis. *Secondary Syphilis* - This stage typically presents with a **diffuse maculopapular rash**, **lymphadenopathy**, and sometimes **condylomata lata** [1]. - These are acute systemic symptoms, distinct from the developmental abnormalities of Hutchinson's triad.

Q: Which of the following is NOT part of the classic triad of normal pressure hydrocephalus?

Headache. ***Headache*** - Headache is **not a typical symptom** of normal pressure hydrocephalus (NPH) and is generally absent, differentiating NPH from other forms of hydrocephalus. - While headaches can occur in other brain conditions, they are **not part of the classic diagnostic triad** for NPH. *Dementia* - **Cognitive impairment**, often manifesting as **subcortical dementia** with executive dysfunction and memory problems, is a core feature of NPH [1]. - This symptom typically progresses and can be a significant cause of disability in affected individuals. *Gait disturbance* - An **ataxic gait** or "magnetic gait" (difficulty lifting feet off the floor) is often the **earliest and most prominent symptom** in NPH. - It significantly impacts mobility and balance, contributing to falls. *Urinary incontinence* - **Urinary urgency and incontinence**, often appearing later than gait disturbance but earlier than dementia, is the third component of the classic triad [1]. - This symptom results from the pressure effects on the **sacral micturition centers** [1].

Q: A 45 year old lawyer presents with pain in the abdomen more so in the epigastric region that worsens with eating spicy food and is relieved by bending forward. Complications of the above mentioned condition could be all except:

Splenic Vein Thrombosis. ***Splenic Vein Thrombosis*** - The patient's symptoms (epigastric pain worsening with spicy food, relieved by bending forward) are highly suggestive of **pancreatitis**, not peptic ulcer disease [1]. **Splenic vein thrombosis** is a known complication of chronic pancreatitis due to inflammation and compression of the splenic vein [2]. - While pancreatitis can cause significant morbidity, **splenic vein thrombosis** is a specific vascular complication associated with prolonged inflammation of the pancreas, leading to localized portal hypertension and potentially isolated gastric varices. *Perforation* - **Perforation** (specifically of a peptic ulcer or potentially surrounding bowel in severe pancreatitis) is a severe complication that can occur in conditions causing abdominal pain, but it is not the *exception* among the given options for the likely underlying condition indicated by the patient's symptoms (pancreatitis) [3]. - This complication typically leads to **peritonitis**, a medical emergency requiring immediate surgical intervention [3]. *Bleeding* - **Bleeding** (e.g., from a pancreatic pseudocyst rupturing into the gastrointestinal tract or from localized varices secondary to portal hypertension in pancreatitis) is a recognized complication of the patient's likely underlying condition [1]. - Gastrointestinal bleeding can also result from **gastric erosions** or ulcers exacerbated by ongoing inflammation. *Gastric Outlet Obstruction* - **Gastric outlet obstruction** can occur as a complication of severe or chronic pancreatitis, often due to **inflammation**, **fibrosis**, or **pseudocyst formation** compressing the duodenum [1]. - This typically presents with **postprandial vomiting** and early satiety, which can arise in the context of chronic pancreatic inflammation.

Q: In cobalamin deficiency which is not seen

Microcytic anemia. Microcytic anemia - Cobalamin deficiency typically leads to macrocytic anemia due to impaired DNA synthesis, not microcytic anemia [1]. - Microcytic anemia is usually associated with iron deficiency, thalassemia, or anemia of chronic disease [1]. Long tract signs - Long tract signs are common in cobalamin deficiency due to posterior column and corticospinal tract involvement leading to symptoms like spasticity. - They indicate involvement of pathways that are affected by vitamin B12 deficiency. Loss of proprioception - Loss of proprioception can occur in cobalamin deficiency due to damage to the dorsal columns of the spinal cord. - It is a common clinical finding indicating the involvement of sensory pathways. Rhomberg sign - A positive Rhomberg sign indicates impaired proprioception, which can happen in cobalamin deficiency. - It reflects difficulty maintaining balance, emphasizing sensory dysfunction associated with the deficiency.

Q: Which of the following is the most common type of multiple sclerosis?

Relapsing remitting type. ***Relapsing remitting type*** - **Relapsing-remitting multiple sclerosis (RRMS)** is characterized by clearly defined attacks of worsening neurological function (relapses) followed by periods of partial or complete recovery (remissions). - Approximately **85%** of people with MS are initially diagnosed with RRMS, making it the most common form [1]. *Progressive relapsing multiple sclerosis* - This is a rare form of MS characterized by a **steady neurological decline** from the onset, with superimposed acute relapses. - Unlike RRMS, there are **no periods of remission** in PRMS. *Primary progressive multiple sclerosis* - **Primary progressive multiple sclerosis (PPMS)** is characterized by slowly worsening neurological function from the onset, without early relapses or remissions [1]. - It accounts for roughly **15%** of all MS cases, making it less common than RRMS [1]. *Secondary progressive multiple sclerosis* - **Secondary progressive multiple sclerosis (SPMS)** typically develops in individuals who initially had RRMS, where the disease begins to progress steadily, with or without occasional relapses. - It is a **later stage** of MS and not the most common initial presentation.

Q: What does a motor score of 4 on the Glasgow Coma Scale indicate?

Withdrawal or flexion to pain. A motor score of 4 on the **Glasgow Coma Scale (GCS)** signifies that the patient **withdraws or flexes their limb** away from a painful stimulus. - This response indicates a degree of purposeful movement but is not considered localization to the pain. *Decerebrate posturing* - This represents a GCS motor score of **2**, characterized by **extension and internal rotation of the arms** and extension of the legs in response to pain [1]. - It suggests severe damage to the **brainstem**, specifically below the red nucleus [1]. *Decorticate posturing* - This corresponds to a GCS motor score of **3**, where the patient exhibits **flexion and adduction of the arms** with extension of the legs to painful stimuli [1]. - It often indicates damage to the **corticospinal tracts** above the red nucleus [1]. *Localizes to pain* - This is a GCS motor score of **5**, where the patient **moves their hand beyond the chin** attempting to remove the painful stimulus. - It indicates a higher level of conscious response and purposeful movement compared to withdrawal.

Q: Increased ICP is shown by

Reduction in GCS. ***Reduction in GCS*** - A **decrease in Glasgow Coma Scale (GCS)** score is a primary indicator of increased intracranial pressure (ICP) due to compromised brain function [1], [2]. - Increased ICP can lead to **cerebral ischemia** and neuronal damage, manifesting as altered consciousness and lower GCS scores [1]. *Pupil constriction (Miosis)* - **Miosis**, or pupil constriction, is typically associated with **pontine lesions** or **opioid use**, and rarely directly with increased ICP unless it specifically involves brainstem compression at the pontine level. - Increased ICP more commonly causes **pupil dilation (mydriasis)**, especially unilateral, due to compression of the oculomotor nerve (CN III) [1]. *Systemic hypotension* - **Systemic hypotension** is generally *not* a direct sign of increased ICP; rather, increased ICP often results in **systemic hypertension** as part of Cushing's triad. - Hypotension in the context of brain injury might indicate **spinal shock** or other systemic issues, but generally not directly elevated ICP. *Tachycardia* - **Tachycardia** is also *not* typically associated with increased ICP; instead, **bradycardia** (slow heart rate) is a hallmark sign, forming part of Cushing's triad. - Tachycardia might suggest **hypovolemia**, **pain**, or other systemic stressors, but not directly increased ICP.

Q: Which of the following sites is responsible for the amnestic defect in Wernicke's Korsakoff syndrome:

Thalamus. ***Thalamus*** - Damage to the **medial dorsal nucleus of the thalamus** is a key pathological finding in Wernicke's Korsakoff syndrome, directly contributing to the severe **anterograde and retrograde amnesia** [1]. - The thalamus plays a crucial role in memory consolidation and retrieval, acting as a relay station for information processing between cortical and subcortical structures. *Mammillary body* - While **mammillary body damage** is characteristic of Wernicke-Korsakoff syndrome, it is primarily associated with the **acute Wernicke encephalopathy phase** and contributes to the overall amnesia through its connections with the thalamus and hippocampus, rather than being the sole site for the amnestic defect [1]. - The mammillary bodies are part of the **Papez circuit**, which is important for episodic memory, but their lesion alone doesn't fully explain the complete amnestic syndrome. *Hippocampus* - The **hippocampus** is critical for the formation of new memories, and its damage typically causes **anterograde amnesia**, as seen in conditions like temporal lobe epilepsy or anoxia. - While memory is affected, direct **hippocampal lesions are not the primary pathology** in Wernicke-Korsakoff syndrome; the memory impairment arises from damage to structures *connected* to the hippocampus, such as the thalamus and mammillary bodies. *Periventricular Grey matter* - The **periventricular grey matter** is involved in various autonomic functions and pain modulation, not directly in memory formation or retrieval. - While lesions in this area can occur in Wernicke-Korsakoff syndrome, they are not considered the primary cause of the **amnestic defect**.

Q: Which of the following is the most common initial presenting feature of multiple sclerosis:

Optic Neuritis. ***Optic Neuritis*** - **Optic neuritis** is a very common initial symptom of multiple sclerosis, occurring in 20-25% of patients. - It presents with **unilateral vision loss** (often painful), blurred vision, and a central scotoma, reflecting inflammation and demyelination of the optic nerve [1]. *Cerebellar Ataxia* - While **cerebellar ataxia** (impaired coordination, balance, speech) can occur in MS, it is less common as an initial presenting symptom. - It often develops later in the disease course due to demyelination in the **cerebellum** or its connections [1]. *Internuclear ophthalmoplegia* - **Internuclear ophthalmoplegia (INO)** is a specific eye movement disorder common in MS but rarely the very first symptom [1]. - It results from a lesion in the **medial longitudinal fasciculus (MLF)**, causing impaired adduction of one eye during conjugate gaze with nystagmus in the abducting eye. *Diplopia* - **Diplopia** (double vision) can be an early symptom of MS, but it is less frequent as the very first presentation compared to optic neuritis [1]. - It typically arises from lesions affecting the **cranial nerves** controlling eye movements (III, IV, VI) or their brainstem nuclei.

Q: What are the expected neurological manifestations in a patient with complete absence of the corpus callosum?

Severe developmental delays. ***Severe developmental delays*** - Complete agenesis of the corpus callosum often results in **significant neurological impairments** due to the disruption of interhemispheric communication essential for coordinated brain function. - This typically manifests as **intellectual disability**, **developmental delays** in motor and speech skills, and difficulties with complex cognitive tasks. *Mild cognitive impairment* - While some individuals with partial agenesis or isolated cases might present with mild cognitive issues, **complete absence** usually leads to more profound deficits. - Mild impairment would not fully capture the extensive neurological challenges associated with a total lack of such a critical brain structure. *Seizures* - Seizures can occur in patients with corpus callosum agenesis, but they are not the **most encompassing** or universally expected neurological manifestation. - Seizures are often part of a broader syndrome of developmental abnormalities rather than the primary expected outcome of the agenesis itself. *No significant neurological deficits* - The corpus callosum is vital for **integrating information** between the cerebral hemispheres, affecting a wide range of sensory, motor, and cognitive functions. - Therefore, its complete absence almost invariably leads to notable neurological deficits, making a lack of significant issues highly unlikely.

Question 1

Hutchinson's Triad is specifically associated with which type of syphilis?

Accepted Answer

Congenital Syphilis

Answer

Tertiary syphilis

Answer

Primary syphilis

Answer

Secondary Syphilis

Question 2

Which of the following is NOT part of the classic triad of normal pressure hydrocephalus?

Accepted Answer

Headache

Answer

Dementia

Answer

Gait disturbance

Answer

Urinary incontinence

Question 3

A 45 year old lawyer presents with pain in the abdomen more so in the epigastric region that worsens with eating spicy food and is relieved by bending forward. Complications of the above mentioned condition could be all except:

Accepted Answer

Splenic Vein Thrombosis

Answer

Bleeding

Answer

Gastric Outlet Obstruction

Answer

Perforation

Question 4

In cobalamin deficiency which is not seen

Accepted Answer

Microcytic anemia

Answer

Loss of proprioception

Answer

Rhomberg sign

Answer

Long tract signs

Question 5

Which of the following is the most common type of multiple sclerosis?

Accepted Answer

Relapsing remitting type

Answer

Progressive relapsing multiple sclerosis

Answer

Primary progressive multiple sclerosis

Answer

Secondary progressive multiple sclerosis

Question 6

What does a motor score of 4 on the Glasgow Coma Scale indicate?

Accepted Answer

Withdrawal or flexion to pain

Answer

Decorticate posturing

Answer

Decerebrate posturing

Answer

Localizes to pain

Question 7

Increased ICP is shown by

Accepted Answer

Reduction in GCS

Answer

Pupil constriction (Miosis)

Answer

Systemic hypotension

Answer

Tachycardia

Question 8

Which of the following sites is responsible for the amnestic defect in Wernicke's Korsakoff syndrome:

Accepted Answer

Thalamus

Answer

Hippocampus

Answer

Mammillary body

Answer

Periventricular Grey matter

Question 9

Which of the following is the most common initial presenting feature of multiple sclerosis:

Accepted Answer

Optic Neuritis

Answer

Cerebellar Ataxia

Answer

Internuclear ophthalmoplegia

Answer

Diplopia

Question 10

What are the expected neurological manifestations in a patient with complete absence of the corpus callosum?

Accepted Answer

Severe developmental delays

Answer

Mild cognitive impairment

Answer

Seizures

Answer

No significant neurological deficits

NEET-PG 2015 — Internal Medicine