INI-CET 2024 Practice Questions

Q: Which of the following is the PRIMARY action of the superior oblique muscle?

Intorsion. ***Intorsion*** - The **primary action** of the **superior oblique muscle** is **intorsion** (internal rotation), which means rotating the top of the eyeball medially (towards the nose). - This action helps to counteract the **extorsion** caused by the inferior oblique muscle and stabilize the visual field during head tilt. *Depression* - While the superior oblique muscle does contribute to **depression** (moving the eye downwards), this is a **secondary action**, particularly when the eye is in **abduction** [1]. - The **inferior rectus muscle** is the primary depressor of the eye [1]. *Abduction* - The superior oblique has a minor **tertiary action** of **abduction** (moving the eye away from the midline) [1]. - However, the **lateral rectus muscle** is the primary abductor of the eye [1]. *Adduction* - **Adduction** (moving the eye towards the midline) is primarily performed by the **medial rectus muscle** [1]. - The superior oblique muscle does **NOT** contribute to adduction; this is not one of its actions [1].

Q: Substantia nigra is connected to which part of the basal ganglia?

Striatum. ***Striatum*** - The **substantia nigra pars compacta (SNc)** provides **dopaminergic input** to the striatum via the **nigrostriatal pathway**, which is crucial for motor control [1]. - This connection establishes the direct and indirect pathways of the basal ganglia, modulating **movement initiation** and **inhibition** [1]. *Thalamus* - The thalamus acts as a **relay station** for information leaving the basal ganglia, but it is not directly connected to the substantia nigra as a primary input or output structure within the basal ganglia circuitry [1]. - The basal ganglia influence the thalamus, which then projects to the **motor cortex**, but the direct connection from substantia nigra is to the striatum. *Pallidum* - The **pallidum (globus pallidus)** receives input from the striatum and projects to the thalamus, but it is not directly connected to the substantia nigra as the **primary recipient** of nigral efferents [1]. - While it's part of the basal ganglia, the substantia nigra's main direct projection is to the **striatum**. *Subthalamic nucleus* - The **subthalamic nucleus (STN)** is an excitatory component of the basal ganglia that receives input from the cortex and projects to the globus pallidus. - While there are some indirect connections, the STN is not the primary target of the **nigrostriatal dopaminergic projections** from the substantia nigra [1].

Q: Congenital lactic acidosis is due to the defect of:

Pyruvate dehydrogenase. ***Pyruvate dehydrogenase*** - A defect in **pyruvate dehydrogenase (PDH)** is the most common cause of **congenital lactic acidosis** - PDH is a crucial enzyme complex that converts **pyruvate to acetyl-CoA**, linking glycolysis to the citric acid cycle - When PDH is deficient, **pyruvate accumulates** and is shunted to **lactate** via lactate dehydrogenase, causing persistent elevation of blood lactate levels - Clinical features include **neurological dysfunction, developmental delay, and metabolic acidosis** from birth or early infancy *Transaldolase* - **Transaldolase** is an enzyme in the **pentose phosphate pathway** - Its deficiency primarily affects **NADPH production and ribose-5-phosphate synthesis**, not lactate metabolism - Transaldolase deficiency causes hepatosplenomegaly and liver dysfunction, but is **not a direct cause of congenital lactic acidosis** *Alpha-ketoglutarate dehydrogenase* - **Alpha-ketoglutarate dehydrogenase** is part of the **citric acid cycle (TCA cycle)** - Its deficiency would impair energy production and lead to accumulation of **alpha-ketoglutarate**, not lactate - Defects cause **neurological dysfunction** but do not primarily present with **lactic acidosis** *Branched chain alpha-ketoacid dehydrogenase* - **Branched chain alpha-ketoacid dehydrogenase (BCKDH)** metabolizes **branched-chain amino acids** (leucine, isoleucine, valine) - Deficiency causes **maple syrup urine disease (MSUD)**, characterized by accumulation of **branched-chain keto acids** and their corresponding amino acids - Presents with characteristic maple syrup odor in urine, neurological symptoms, but **not lactic acidosis**

Q: Which gene defect causes familial hypercholesterolemia?

LDL Receptor. ***LDL Receptor*** - Familial hypercholesterolemia (FH) is primarily caused by mutations in the **LDL receptor (LDLR) gene**, which leads to impaired clearance of **low-density lipoprotein (LDL)** from the blood. - This defect results in significantly elevated levels of **LDL cholesterol** and an increased risk of premature cardiovascular disease. *Apo E* - Mutations in the **Apo E gene** are associated with **Type III hyperlipoproteinemia (dysbetalipoproteinemia)**, characterized by elevated **chylomicron remnants** and **VLDL remnants**. - This condition presents with xanthomas and premature atherosclerosis, but is distinct from the primary defect in FH. *Apo CII* - **Apo CII** is a cofactor for **lipoprotein lipase (LPL)**, an enzyme essential for the breakdown of **triglycerides** in chylomicrons and VLDL. - Deficiency in Apo CII or LPL causes **Type I hyperlipoproteinemia (familial chylomicronemia syndrome)**, leading to marked **hypertriglyceridemia**, not hypercholesterolemia. *Apo B48* - **Apo B48** is a structural component of **chylomicrons**, which are responsible for transporting dietary fats from the intestines. - It is not directly involved in the primary defect of **LDL clearing** that characterizes familial hypercholesterolemia.

Q: Which of the following is typically not associated with upper motor neuron (UMN) lesions?

Atrophy. ***Atrophy*** - **Severe atrophy** (significant muscle wasting) is a hallmark of **lower motor neuron (LMN) lesions**, where the direct innervation to the muscle is interrupted, leading to denervation and subsequent muscle mass loss [1]. - While some disuse atrophy can occur with UMN lesions due to **immobility**, it is typically not as pronounced or rapid as that seen with LMN lesions [1]. *DTR increased* - **Increased deep tendon reflexes (DTRs)**, also known as hyperreflexia, are a classic sign of **upper motor neuron (UMN) lesions** due to the loss of inhibitory control from higher centers on spinal reflex arcs [1]. - The stretch reflex arc becomes more excitable without descending modulation, leading to exaggerated responses. *Spasticity* - **Spasticity** is characterized by a **velocity-dependent increase in muscle tone** with increased resistance to passive stretch, often accompanied by hyperreflexia [1]. - This is a cardinal sign of **upper motor neuron (UMN) lesions**, resulting from the disinhibition of spinal reflex mechanisms. *Rigidity* - **Rigidity** is a form of hypertonia characterized by a **constant resistance to passive movement** throughout the entire range of motion, independent of the speed of movement [2]. - While it can be seen in some UMN conditions involving the basal ganglia (such as Parkinson's disease), it is **not a typical or direct consequence of UMN tract lesions** in the way spasticity is [2],[3].

Q: A 40-year-old male experiences flashes of light. Which of the following can likely be the reason?

Retinal detachment. ***Retinal detachment*** - Flashes of light, or **photopsia**, are a classic symptom of **retinal detachment**, often caused by the retina pulling away from the underlying choroid. - This sensation occurs as the detached retina is mechanically stimulated, sending abnormal signals to the brain that are interpreted as light flashes. *CRAO* - **Central Retinal Artery Occlusion (CRAO)** typically presents with **sudden, painless, severe vision loss** in one eye, not flashes of light. - The primary pathology is a blockage of blood flow to the retina, leading to **ischemia** and vision impairment. *SAH* - **Subarachnoid Hemorrhage (SAH)** is a neurological emergency characterized by **sudden, severe headache** (thunderclap headache), stiff neck, and altered mental status. - While it can cause visual disturbances, these are usually **diplopia** or **visual field defects** due to cranial nerve involvement, not flashes of light related to retinal pathology. *Branch retinal artery occlusion* - **Branch Retinal Artery Occlusion** causes **sudden, painless vision loss** in a specific part of the visual field corresponding to the occluded branch. - Like CRAO, it is an ischemic event and does not typically present with flashes of light; instead, it results in a **scotoma** or partial vision loss.

Q: Which of the following is not a polysaccharide vaccine?

Hepatitis B vaccine. ***Hepatitis B vaccine (recombinant protein vaccine)*** - This is a **recombinant protein vaccine** which contains **HBsAg** (Hepatitis B surface antigen) produced in yeast. - As it uses a protein antigen, it is not a polysaccharide vaccine. *Pneumococcal vaccine (includes polysaccharide forms)* - There are two types: **Pneumococcal Polysaccharide Vaccine (PPSV23)** which is a pure polysaccharide vaccine, and **Pneumococcal Conjugate Vaccine (PCV13, PCV15, PCV20)** which contains polysaccharides conjugated to a protein carrier. - Both types utilize **polysaccharide antigens** from *Streptococcus pneumoniae* to elicit an immune response. *Meningococcal vaccine (includes polysaccharide forms)* - Similar to pneumococcal vaccines, there are **meningococcal polysaccharide vaccines (MPSV4)** and **meningococcal conjugate vaccines (MCV4)**. - These vaccines use **polysaccharides** from the capsule of *Neisseria meningitidis* as their immunogenic component, either alone or conjugated. *H. Influenza B vaccine (conjugate vaccine derived from polysaccharides)* - This is a **conjugate vaccine** that uses a **polysaccharide capsule antigen** from *Haemophilus influenzae type B* (Hib) chemically linked to a protein carrier. - Conjugation improves immunogenicity, especially in infants, by converting the T-independent polysaccharide antigen into a T-dependent one.

Q: Spinal sensory nucleus of the trigeminal has 2nd order neurons to carry which sensation?

Pain. ***Pain*** - The **spinal trigeminal nucleus** receives nociceptive (pain) and thermal sensations from the face - Its **second-order neurons** relay these signals to higher centers for pain perception - This is the primary function of the spinal (descending) trigeminal nucleus *Proprioception* - **Proprioception** from the face and masticatory muscles is primarily processed by the **mesencephalic trigeminal nucleus** - This nucleus contains the **first-order neurons** for proprioception, which is unique among sensory nuclei *Touch* - **Discriminative touch** and pressure sensations from the face are primarily processed by the **principal (chief) sensory trigeminal nucleus** - This nucleus is distinct from the spinal trigeminal nucleus *Vibration* - **Vibration** sense is a type of mechanoreception, falling under the broader category of discriminative touch - Like other fine touch sensations, it is primarily processed by the **principal sensory trigeminal nucleus**

Question 1

Which of the following is the PRIMARY action of the superior oblique muscle?

Accepted Answer

Intorsion

Answer

Adduction

Answer

Abduction

Answer

Depression

Question 2

Substantia nigra is connected to which part of the basal ganglia?

Accepted Answer

Striatum

Answer

Thalamus

Answer

Pallidum

Answer

Subthalamic nucleus

Question 3

Congenital lactic acidosis is due to the defect of:

Accepted Answer

Pyruvate dehydrogenase

Answer

Transaldolase

Answer

Alpha-ketoglutarate dehydrogenase

Answer

Branched chain alpha-ketoacid dehydrogenase

Question 4

Which gene defect causes familial hypercholesterolemia?

Accepted Answer

LDL Receptor

Answer

Apo E

Answer

Apo CII

Answer

Apo B48

Question 5

Which of the following is typically not associated with upper motor neuron (UMN) lesions?

Accepted Answer

Atrophy

Answer

DTR increased

Answer

Spasticity

Answer

Rigidity

Question 6

A 40-year-old male experiences flashes of light. Which of the following can likely be the reason?

Accepted Answer

Retinal detachment

Answer

CRAO

Answer

SAH

Answer

Branch retinal artery occlusion

Question 7

A 75-year-old man presents with a fracture of the intracapsular neck of the femur. What is the most common management option for this patient?

Accepted Answer

Hemiarthroplasty

Answer

Total Hip Replacement

Answer

Dynamic Hip Screw

Answer

Conservative Management

Question 8

A 26-year-old male presented with proximal 1/3rd fracture shaft of the femur. What is the treatment of choice in this patient?

Accepted Answer

Interlocking Nail

Answer

Hip Spica

Answer

Above knee Cast

Answer

Above knee Slab

Question 9

Which of the following is not a polysaccharide vaccine?

Accepted Answer

Hepatitis B vaccine

Answer

Pneumococcal vaccine

Answer

Meningococcal vaccine

Answer

H. Influenzae B vaccine

Question 10

Spinal sensory nucleus of the trigeminal has 2nd order neurons to carry which sensation?

Accepted Answer

Pain

Answer

Proprioception

Answer

Touch

Answer

Vibration

INI-CET 2024

Anatomy

Biochemistry

Internal Medicine

Ophthalmology

Orthopaedics

Pharmacology

Physiology