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AIIMS MAY 2009 (Questions)

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ANATOMY, EMBRYOLOGY & HISTOLOGY

1.

All of the following is true about occulomotor nerve except? a. It carries preganglionic parasympathetic fibres b. It causes constriction of pupil c. It supplies inferior oblique muscle d. It passes through inferior orbital fissure

BIOCHEMISTRY

2.

Within the RBC, hypoxia stimulates glycolysis by which of the following regulatory pathways a. Hypoxia stimulates pyruvate dehydrogenase by increased 2,3-DPG b. Hypoxia inhibits hexokinase c. Hypoxia stimulates release of all glycolytic enzymes from Band -3 on RBC membrane d. Activation of the regulatory enzymes by high PH

PHYSIOLOGY

3.

Skeletal muscle excitation contraction coupling is mediated by a. When calcium is taken up by sarcoplasmic reticulum b. Contracts when actin and myosin filaments shorten c. Contraction is initiated by calcium binding to troponin d. Contraction is initiated by calcium binding to tropomyosin

ORAL MEDICINE AND RADIOLOGY 4. Investigation of choice for a lesion of the temporal bone is a. X-ray b. USG c. CT d. MRI

ORAL SURGERY

5.

In fracture of atrophied mandible with bone loss, what is the best treatment modality a. Bone grafting and load bearing b. Bone grafting and load sharing c. Semi-rigid fixation d. IMF with open reduction

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AIIMS MAY 2009 (Answers & Explanations)

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Ans 1: Option D (It passes through inferior orbital fissure) (GrayAnatomy 39th edition, page 698) The two divisions of occulomotor nerve enter the orbit through the middle part of the superior orbital fissure. In the fissure nasociliary nerve lies in between two divisions while the abducent nerve lies inferolateral to them (BD Chaurasia 4th edition, page 28)

Structures passing through Inferior and Superior orbital fissure Lateral part Lacrimal nerve Frontal nerve Trochlear nerve Lacrimal and middle meningeal artery Middle part Occulomotor nerve Superior Orbital Nasocilliary nerve Fissure Abducent nerve Medial part Inferior ophthalmic vein Sympathetic plexus around internal carotid artery Inferior Orbital Fissure Maxillary nerve Zygomatic nerve Orbital branches of pterygo-palatine ganglion Infraorbital nerve and vessel Communication between inferior ophthalmic vein and the pterygoid plexus of veins

About other options: Option A: Because the Oculomotor nerve carries preganglionic parasympathetic fibers from the Edinger Westphal nuclei, which control the sphincter papillae of the iris and cilliary muscles, severance of this nerve would result in loss of the papillary light and accommodation reflexs (Anatomy by Kurt E. Jhonson, page 217)

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Option B: The Oculomotor, trochlear, and abducens nerves (III, IV, VI) mediate eye movements. The Oculomotor nerve also controls elevation of the eyelid and papillary constriction. Asymmetric pupils are commonly due to cataract extractions, eye drops, or old trauma, but may reflect Horners syndr ome or compression of Oculomotor nerve (Neuropsychology by Gerald Gldstein, page 467) Option C: "The Oculomotor nerve supplies the following extrinsic muscles of the eye: the levator palpebrae superioris, superior rectus, medial rectus, inferior rectus and inferior oblique. It also supplies, through its branch to the ciliary ganglion and the short ciliary nerves, parasympathetic nerve fibers to the following intrinsic muscles: the constrictor papillae of the iris, and ciliary muscles (Snells Clinical Neuroanatomy by Richard Snell, page 340) OCULOMOTOR NERVE: The Oculomotor nerve is entirely motor in function Oculomtor Nerve Nuclei: Has two motor nuclei: i) Main motor nucleus ii) Accessory parasympathetic nucleus Main motor nucleus: o Situated in anterior part of the gray matter that surrounds cerebral aqueduct of the midbrain o Lies at the level of superior colliculus Accessory parasympathetic nucleus (Edinger Westphal nucleus) o Situated posterior to the main Oculomotor nucleus o Preganglionic axons, accompany the other oculomtor fibers to the orbit. Here, they synapse in the ciliary ganglion, and postganglionic fibers pass through the short ciliary nerves to the constrictor papillae of the iris and the ciliary muscles.

Ans 2: Option C (Hypoxia stimulates release of all Glycolytic enzymes from Band 3 on RBC membranes) Journal based question: References on which answer is based are provided at the end of explanation Hypoxia causes Deoxygenation of Hemaglobin and Increases band 3 Tyrosine Phosphorylation. This stimulates the releasing of all Glycolytic enzymes from band 3 on the RBC membrane thereby stimulating Glycolysis Glycolytic Enzymes and Band 3 on RBC membrane: Band 3 is a multifunctional RBC membrane protein that plays several important roles in RBC metabolism and morphology Band 3 membrane abundance and its organization within the RBC is important for normal anion exchange activity, cytoskeletal structure, cell shape and glycolytic activity Glycolytic enzymes are organized into a complex on the human RBC membrane (Band 3) The assembly and disassembly of the glycolytic enzymes from the band 3 complex is regulated by physiologically relevant stimuli. Phosphorylation of band 3 or Deoxygenation of Hb can lead to release of all Glycolytic enzymes from the membrane, even though only a single site on band 3 is modified. Thus Red cell deoxygenation and Band 3 tyrosine phosphorylation have been reported to accelerate glycolysis Hypoxia causes deoxygenation of Hemaglobin and increases band 3 tyrosine phosphorylation and thereby stimulates glycolysis by releasing Glycolytic enzymes from Band 3 on the RBC membrane Based mainly on in vitro studies, it is believed that band -3 function is regulated by its phosphorylation status. Increased band-3 tyrosine phosphorylation has been shown to stimulate glycolysis. Studies have indicated that hypoxia increases band-3 tyrosine phosphorylation in vitro Journal Reference: Journal articles Assembly and regulation of a glycolytic enzyme complex on the human erythrocytic membrane (http://www.pass.org/cgi/abstract/full/102/7/2402)

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Ans 3: Option C (Contraction is initiated by calcium binding to troponin) Troponin: These are actually complexes of three loosely bound protein subunits, each of which plays a specific role in controlling muscle contraction. One of the subunits (troponin I) has a strong affinity for actin, another (troponin T) for tropomyosin, and a third (troponin C) for calcium ions. This complex is believed to attach the tropomyosin to the actin. The strong affinity of the tropnin for calcium is believed to initiate the contraction process (Gyutons Medical Physiology, 11th edition, page 76)

Ans 4: Option C (CT): Refer Text below Bony architecture is best visualized by a CT scan The single best investigation of choice for assessing a lesion of the temporal bone is a CT scan MRI is now regarded the investigation of choice for all space occupying lesions of the brain whether in the anterior, middle or posterior cranial fossa (Most useful for infratemporal posterior fossa lesions) but it is not the investigation of choice for assessing a lesion of the temporal bone. Thus an intra cranial space occupying lesion within the temporal lobe may be better assessed by an MRI scan, but a lesion of the temporal bone such as fracture of the temporal bone is better investigated with a CT scan. USG & X-ray can give limited information and cannot be regarded as investigation of choice Remember: Investigation of choice for multiple Bone Metastasis: Bone scan Investigation of choice for Spine Metastasis: MRI (Also visualizes spinal cord involvement) Investigation of choice for Acute Head injury: CT scan

Ans 5: Option A (Bone grafting and load bearing) Load-bearing fixation is a device that is of sufficient strength and rigidity that it can bear the entire load applied to the mandible during functional activities. Injuries that require load-bearing fixation are comminuted fracture of the mandible, those fractures where there is very little bony interface because of atrophy, or those injuries that have resulted in a loss of portion of mandible (defect fractures) (Petersons Principles of Oral and Maxillofacial Surgery, 2nd edition, page 375) LOAD BEARING: Injuries that require load-bearing fixation are comminuted fractures of mandible, those fractures where there is little bony interface because of atrophy, or those injuries that have resulted in a loss of portion of the mandible (defect fractures)

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In such cases the fixation device must bridge the area of communition, minimal bone contact, or bone loss, and bear all of the forces transmitted across injured area that are generated by masticatory system. Load bearing fixation is sometimes called bridging fixation because it bridges areas of communication or bone loss. The most commonly used load-bearing device is a mandibular reconstruction bone plate Such plates are relatively large, thick, and stiff. They use screws that are generally greater than 2.0 mm in diameter (most commonly 2.3 mm, 2.4 mm, or 2.7 mm) When secured to the fragments on each side of the injured area by a minimum of three bone screws, reconstruction bone plates can provide temporary stability to the bone fragments. The bone plates are not prosthetic devices and will usually fail in time (several months to years later) by either loosening of the screws or fracture of the plate, but can provide stability until the comminuted fragments have consolidated and/or the missing bone has been replaced with grafts.

LOAD-SHARING: Is any form of internal fixation that is of insufficient stability to bear all of the functional loads applied across the fracture of the masticatory system. Such a fixation device requires solid bony fragments on each side of the fracture that can bear some of the functional loads. Fractures that can be stabilized adequately with load-sharing fixation devices are simple linear fractures, and constitute the majority of mandibular fractures. Fixation devices that are considered load-sharing include variety of 2.0 mm miniplating systems that are available from a number of manufacturers. Lag-screw techniques are also load-sharing in that the bone that is compressed is sharing the functional loads with the screws.

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Simple linear fractures can also be treated by load-bearing fixation. Comminuted or defect fractures or those where a minimum of bone contact is present, cannot be treated by load-sharing fixation because there is insufficient bone stock adjacent to the fracture to resist displacement by functional forces.

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