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AIIMS MAY 2011DENTAL:

Discussion

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again a repeat paper.mixture of AIPG DENTAL 2009 AND AIIMS RECENT .MEDICAL QUESTIONS ARE ALSO REPEATED FROM AMIT ASHISH 2009 AND 2010 http://www.aippg.net/forum/f23/dental-aiims-may-2011-a-96600/http://rxdentistry.co.in/forum/showthread.php?219-Aiims-may-2011-discussion

Anatomy:-Q.1 C.nerve not carrying psn stimulatn a)4th b)3rd c)7th d)9th c.n. Nerve Not carrying parasympathetic fibres - Trochlear

Q.2 TMJ dev. (AIPG 2009) a)2wk b)10wk @@@c)20wk d)22wk

Q3. area that lies immediately lateral to the ant. Perforating substance is-a.orbital gyrusB.UNCUSC.OPTIC CHIASMAD.LIMEN INSULE@@@Q. Lateral to optic chiasma Limen insulae @@@

Q.4.which organ posterior 2 pancreas a)kidney @@@b)stomach c)colon d)duodenum

11. Bile ducts: 2. Intrahepatic bile ducts, 3. Left and right hepatic ducts, 4. Common hepatic duct, 5. Cystic duct, 6. Common bile duct, 7. Ampulla of Vater, 8. Major duodenal papilla9. Gallbladder, 10-11. Right and left lobes of liver. 12. Spleen.13. Esophagus. 14. Stomach. Small intestine: 15. Duodenum, 16. Jejunum17. Pancreas: 18: Accessory pancreatic duct, 19: Pancreatic duct.20-21: Right and left kidneys (silhouette).The anterior border of the liver is lifted upwards (brown arrow). Gallbladder with Longitudinal section, pancreas and duodenum with frontal one. Intrahepatic ducts and stomach in transparency

Also Refer AIPG 2011 Medical Q.44. Posterior relations of head of pancreas are all except 1) Common Bile Duct 2) duodenum first part @@3) Aorta 4) IVC Answer 2. Duodenum First part Posterior Surface.—The posterior surface is in relation with the inferior vena cava, the common bile duct, the renal veins, the right crus of the diaphragm, and the aorta.

Q.5. all structure pierced buccinater .except a)parotid gland b)molar glands of cheeks c)buccal br of facicl n d)buccal br of mand n. @@@

Physiology:-Q.6 Intrinsic factor of Castle is secreted by (aiims may 2010 , AI 2009 Medical )a) Chief cells

b) Parietal cells@@c) Mucus cellsd) B cellsRef. Ganong 23rd ed pg 573The gross anatomy of the stomach is shown in Figure 26–4. The gastric mucosa contains many deep glands. In the cardia and the pyloric region, the glands secrete mucus. In the body of the stomach, including the fundus, the glands also contain parietal (oxyntic) cells, which secrete hydrochloric acid and intrinsic factor, and chief (zymogen, peptic) cells, which secrete pepsinogens (Figure 26–5) These secretions mix with mucus

secreted by the cells in the necks of the glands. Several of the glands open on a common chamber (gastric pit) that opens in turn on the surface of the mucosa.Mucus is also secreted along with HCO3 – by mucus cells on the surface of the epithelium between glands.

Q.7 A pt diagnosed withincrease in ldl.his father n broalso had same ds. a)l dl recepter mutation @@@b)familial lipoprotein lipese def

Q8. primary func of muscle spindlea)length b)stretch c)metabolism d}propioceptionQ. golgi spindle detect a)muscle length @@@b)m.tension c)motor n. stimulation (AIPG 2009 Dental Explore Q4)

Q.9. cortical representation of body in cerebrum a) vertical @@@b)oblique c)tandem

Q.10. which one associated with increased aging a)increased cross linkages in collagen b)increased superoxides dismutase c)increased accumulation of free radicals / free radical injury @@@

Q.11 main cause of increased blood flow to exercising muscles a)raised blood flow b)vasodilatation due 2 local metabolite c)increased heart rate Q. Vasodilatation - Accumulation of metabolites

Q.12 visual cycle / Visual transduction - a) Depolarization b) Repolarization c) Hyperpolarization d) hyper depolarisation

Q.13 Bezold’s jarrisch reflex which of the following is true. ?a. Tachycardia with hypovolemia b. Bradycardia with hypovolemia@@@c. Hypertension inspite of hypovolumiad. Bradycardia with normovolemiaRef : Neural Blockade in Clinical Anesthesia and Pain By Michael J. Cousins 4th Ed Pg 249 – 250 Bezold-Jarisch ReflexA cardiovascular decompressor reflex involving a marked increase in vagal (parasympathetic) efferent discharge to the heart, elicited by stimulation of chemoreceptors, primarily in the left ventricle. This causes a slowing of the heart beat (bradycardia) and dilatation of the peripheral blood vessels with resulting lowering of the blood pressure. The concept was originated by a German physiologist Albert von Bezold in 1867, later revised by an Austrian dermatologist Adolf Jarisch in 1937

Q.14. hereditry intestinal polyposis gene a)BRCA b)p53 c)APC d) STK11Q. Non hereditary colon ca gene ? Hmlh1>>> APC P53

APC gene - Adenomatous Polyposis Colitis , ref robbins...p53 - Li-Fraumeni syndrome , BRCA - Breast Cancer...Ans. stk11>APc .. refrnce shafers, neviller u sure about the options??? because Hereditary Intestinal Polyposis may include both 1) Puetz-jeghers which has a STK11 gene defect and2)familial adenematous polyposis which has an APC gene defect....

Microbiology:-Q.15 . all r diamorphic except a/ea)blastomyces dermatidis b)histoplasma c)penicillium marneffi d)phialospora @@@The term Dimorphic fungus has been employed to potential pathogens that grow as mycelial form when incubated at room temperature under laboratory conditions and yeast phase, yeast like cells or spherule form when grown in human tissue or incubated at 37ºC on synthetic laboratory media. Fungi which can exist in two forms-1-as filamentous form or2- as yeast depending on conditions of growth.In host tissue or culture at 37 00 c they occur as yeast while in soil and in cultures at 22 0 c appear as mould.Most fungi causing systemic infection are dimorphic fungi. Example- 1. Histoplasma capsulatum (histoplasmosis)2. Blastomyces dermatitidis(Blastomycosis)3. Coccidiodes immitis (coccoidiomycosis)4. Paracoccidiodes brasiliensis (paracoccoidimycoosis)5. Sporothrix schenekii sporotrichosis)6. Penicillium marneffei7. Malasezia furfur,but cryptococcoosis is not a dimorphic fungusmnemonics-mala sinha bombay primary health center par rahti hai. Highly virulent dimorphic fungi are: Histoplasma capsulatum var.

capsulatum, Histoplasma capsulatum var.

duboisii, Blastomyces dermatitidis, Paracoccidioides brasiliensis, Sporothrix schenckii, Penicillium marneffei and Coccidioides immitis.

Dimorphic fungi cause systemic mycosis often termed as

histoplasmosis, blastomycosis, paracoccidioidomycosis, sporotrichosis, penicilliosis marneffei and

coccidioidomycosis.

Q.16. culture media 4 leptospirosis.. a)korthoff @@@@ b)perkin c)baker

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d)tinsdale

Some examples of selective media include: eosin-methylene blue agar (EMB)

that contains methylene blue – toxic to Gram-positive bacteria, allowing only the growth of Gram negative bacteria

YM (yeast and mold) which has a low pH, deterring bacterial growth

blood agar (used in strep tests), which contains bovine heart blood that becomes transparent in the presence of hemolytic Streptococcus

MacConkey agar for Gram-negative bacteria

Hektoen enteric agar (HE) which is selective for Gram-negative bacteria

mannitol salt agar (MSA) which is selective for Gram-positive bacteria and differential for mannitol

Terrific Broth (TB) is used with glycerol in cultivating recombinant strains of Escherichia coli.

xylose lysine desoxyscholate (XLD), which is selective for Gram-negative bacteria

buffered charcoal yeast extract agar, which is selective for certain gram-negative bacteria, especially Legionella pneumophila

Examples of differential media include: eosin methylene blue (EMB), which

is differential for lactose and sucrose fermentation

MacConkey (MCK), which is differential for lactose fermentation

mannitol salt agar (MSA), which is differential for mannitol fermentation

X-gal plates, which are differential for lac operon mutants

Examples of transport media include: Thioglycolate broth for strict

anaerobes. Stuart transport medium - a non-

nutrient soft agar gel containing a reducing agent to prevent oxidation, and charcoal to neutralise

Certain bacterial inhibitors- for gonococci, and buffered glycerol saline for enteric bacilli.

Venkat-Ramakrishnan(VR) medium for v. cholerae.

Q.17 microaerophilic a)campylobacter @@@b)vibrio c)bacteriods d) pseudomonas Microphillic bacteria. Examples include:

Borrelia burgdorferi , a species of spirochaete bacteria that causes Lyme disease in humans.

Helicobacter pylori , a species of proteobacteria that has been linked to peptic ulcers and some types of gastritis. Some don't consider it a true obligate microaerophile.[1]

Campylobacter has been described as microaerophilic.[2]

Streptococcus intermedius has also been described as microaerophilic.

Streptococcus pyogenes , a well known microaerophile that causes streptococcal pharyngitis.

Q.18 autoinfection seen in

a)giardia b) gnathosp Autoinfection is the infection of a primary host with a parasite, particularly a helminth, in such a way that the complete life cycle of the parasite happens in a single organism, without the involvement of another host. Therefore, the primary host is at the same time the secondary host of the parasite. Some of the organisms where autoinfection occurs are : - Strong Tea Entertains Nana'(mnemonic)

Strongyloides stercoralis,

Teania solium

Enterobius vermicularis,

Hymenolepis nana

Q.19 gas gangrene all except a) cl.histolyticum b)cl.septicum c)cl.sporogens@@@@ d)cl.novyi

General Medicine:-Q.20In which area gall stones pain not percieved a)epigastrium b)rt.hypochondrium c)rt.iliac d)shoulder @@@

Q.21 all r feature of systemic inflammatory disorder SIRS except :a)oral temp>38 c b)leucocytosis c)thrombocytopenia @@@??

Oral Surgery:Q22 based on tension and compression trajectories fracture of condyle is best treated by / acc to rule of tensiona and compressional forces acting along the condylar border best way to stabilise a condylar frac against these forces wud require?a) One plate on anterior & one plate on posterior border @@??b) One anterior only c) One laterally only d) One posterior only OR. 1. one plate at the ant border and one plate at the post @@@2. a plate at the anterior border3. a plate at the posterior border4. a plate at the lateral borderiin neeraj wadhwan the answer given is 1…. and the answer is 4. ???

Q23. In a condylar fracture and bone plate synthesis to counteract the dynamic tension &

compression zones the most acceptable place for plating isa. A plate fixed laterally in the neck of the condyle.@@@b. Plate on posterior border of the condyle only.... c. Plate on the anterior border of the condyle only.d. Plate on the anterior & posterior border of the condyle. Ans. A (A plate fixed laterally in the neck of the condyle) Ref: Oral and Maxillofacial Trauma, Raymond J. Fonseca, Robert V. Walker, 3rded, volume 1/552Condylar neck fractures are usually treated by closed reduction."The mandible is exposed, via a submandibular incision, which allows access to the inferior border and entire ramus. A groove is drilled in the lateral ramus to with in the several centimeters with in the fracture line"“Rigid fixation of a right condylar neck fracture uses a miniplate and monocortical screws’

Q24. treatment of communicated fracture (AIPG 2009 Q175 Dental Explore)a) Reconstruction plates 2.5 mm @??b) Dynamic screws / dynamic compression plates with eccentric screwsc) Single Miniplate 1.5mm d) Multiple miniplates

Q25. A condylar fracture with fragment overlap of >5mm and angle >37 degree needs what treatment? (AIPG 2009 Q. 168 Dental Explore)a) closed reduction and IMFb) ORIF @@@@c)soft diet onlyd) no t/t

Q26.fracture of symphsis canot be treated by (Refer Aiims may 2009 Ques)a) 1.5mm One single miniplate b) 2.5mm mono cortical plate c) Lag screws d) 2mm compression plates Q. a/e in symphysis # - single plate Q. A transverse fracture of symphysis is treated by all of the following except a. Two Compression plates. (2mm) b. Two lag screws 3.single Miniplate fixation (1.5mm) @@4.2.4 mm reconstruction plate. single mini plate fixation cannot support the dynamics of fracture at symphysis regionSymphyseal fractures had negative

bending moments only that caused compression at the alveolar side and tension at the lower border of the mandible and relatively high torsion moments. Compressive strain develops along the buccal aspect, whereas tensile strain develops along the lingual aspect. This produces a fracture that begins in the lingual region and spreads toward the buccal aspect. The anterior mandible undergoes shearing and torsional (twisting)forces during functional activities. Application of fixation devices must therefore take these factors into consideration. This is why most surgeons advocate two points of fixation in the symphysis: either two bone plates, two lag screws, or possibly one plate or lag screw combined with an arch bar. Depending on the size of the plate and whether or not an arch bar will also be usedto provide another point of fixation, the fixation could be rigid or functionally stableFixation schemes for mandibular symphyseal fracture.A large compression plate in combination with an arch bar for a symphysis fracture (two-point fixation). Two lag screws inserted across a symphysis fracture (two-point fixation). Two bone plates for a symphysis fracture (two-point fixation). These may or may not be compression plates. Typically the larger one at the inferior border is a compression plate and the one located more superiorly may or may not.Symphysis fracture with either two 2.0 mm miniplates, or a stronger bone plate at the inferior border, as well as using the arch bar as another point of fixation

Q27. most difficult fracture to treat a) Body of mandible b) Condylar c) Angle d) Symphyseal fracture Which of the following are most complicated fractures. (AIIMS may 2009)a. Symphysis@@@???b) Body c) Condyle????d) AngleCondylar fractures are the most complicated fractures because they can effect growth of the fcial structures and because of their close approximity to

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brain structures. Overview of Mandibular Fractures:-Location of mandibular fractures - Fridrich and associates showed that most fractures occur in the body (29%), condyle (26%), and angle (25%) of the mandible. The symphyses account for 17% of mandibular fractures, whereas fractures of the ramus (4%) and coronoid process (1%) have lower occurrence rates. In automobile accidents, the condylar region was the most common fractured site. In motorcycle accidents, the symphysis was fractured most often. When assault was the cause, the angle demonstrated the highest incidence of fracture.[29] Associated injuries with mandibular fractures - Fridrich and associates reported that in patients with mandible fractures, 43% of the patients had an associated injury. Of these patients, head injuries occurred in 39% of patients, head and neck lacerations in 30%, midface fractures in 28%, ocular injuries in 16%, nasal fractures in 12%, and cervical spine fractures in 11%. Other injuries present in this group were extremity trauma in 51%, thoracic trauma in 29%, and abdominal trauma in 14%. Of the 1067 patients studied, 12 (2.6%) died of their associated injuries before the mandible fracture could be treated.[29] Number of fractures per mandible - In patients with mandible fractures, 53% of patients had unilateral fractures, 37% of the patients had 2 fractures, and 9% had 3 or more fractures

Q28. In fracture of atrophic mandible treatment modality is a) Bone grafting & load bearing ??b) Bone grafting & load sharing c) Open reduction d) Semi rigid Q. Mand with bone loss - Reconstruction plates @@Refer Q. AIIMS May 2009 , Target AIIMS V Q. In fracture through mental foramen in mandible with less than 10mm of bone loss treatment would be, a..Champy’s plate. b..Lag screw c..Non rigid fixation d..Reconstruction plates@@@In the above question there is bone loss of 10mm and the fracture line is passing through mental foramen. To prevent damage to nerve instead of two plates a load bearing reconstruction plate is given. The most simplistic way to discuss fixation schemes for fractures are to divide them into Load-Bearing versus which bear the original load Load-Sharing Fixation that share the loads with the bone on each side of the fracture Load-bearing fixation is a device that is of sufficient strength and rigidity that it can bear theentire load applied to the mandible during functional activities. Injuries that requireload-bearing fixation are comminuted

fractures of the mandible, those fractureswhere there is very little bony interface because of atrophy, or those injuries thathave resulted in a loss of a portion of the mandible (defect fractures). Load bearingfixation is sometimes called bridging fixation because it bridges areas of comminution or bone loss. 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, reconstructionbone plates can provide temporary stability to the bone fragments.Load-sharing fixation is any form of internal fixation that is of insufficient stability to bear all of the functional loads applied across the fracture by the masticatory system. Such a fixation device(s) 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 the variety of 2.0 mm miniplating systems, Lag screw techniques etc..,. However Simple linear fractures can also be treated by load-bearing fixation but reverse is not true.. For the majority of fractures in the dentulous mandibular body and symphysis there is sufficient height of bone to place one load-sharing plate along the inferior and one along the superior aspect of the lateral cortex. Because fixation devices are applied to the lateral surface of the mandible, the ability to use two-point fixation requires that there be sufficient height of bone so that the fixation devices can be placed far apart from one another. For instance, an atrophic mandibular fracture, where there is a vertical height of only 15 mm, would not gain much mechanicaladvantage from placing two bone plates on the lateral surface . In such instances Use of a single strong bone plate (reconstruction plate) is recommended when the vertical height of the mandible is small .Q.29. Alveolar bone grafting in a cleft palate patient is done: (AIPG 2009 Dental Explore)a)after maxillary expansion, cross bite correction, before canine eruption @@@b)before maxillary expansion cross bite correction after canine eruption c)after maxillary expansion cross bite correction after canine eruption d)before maxillary expansion cross bite correction before canine eruption

Q.30. most common impaction (AIPG 2009)a)mesio angular @@b)vertical c)distoangular d)horizontal

Q.31 Route not used in children (AIPG 2009)a)I/M b)subdermal @@@c)sub mucosal d)I/V

Q.32. nitrous oxide N2O acts by (AIPG 2009)a) non specific CNS depression @@@

b)gasserian ganglion blockadec) blocking peripheral pain pathways

Q.33. when a minimal injury as a glancing blow is struck 2 what variable its related (AIPG 2009 Q. 174 Dental Explore)a) angulation @@@b)position c)location d)area of strike

Q.59. while reducing # lingual splaying of segments noted. which will cause increase in (AIPG 2009 Q. 167 Dental Explore)a)intercanthal distance b)interangular distance @c)go-gn distance

CONSERVATIVE Q34 lubricating gel used while rubber dam placement all except (AIPG 2009)a) Soapy water b) Vaseline @@@c) Shaving cream d) Scrub gel

Q35 while placement of ruber dam following technique is NOT used (AIPG 2009)a) Place clamp on tooth and insert the dam b) Place dam on tooth then place clamp over it c) Place dam & frame outside the oral cavity & then on tooth using forcep OVER the dam @@@@d) Place dam & frame outside the oral cavity & then on tooth using forcep UNDER the dam

Q36. to restore ACID eroded non carious lesion which is used (AIPG 2009)a) GIC b) RMGIC @@@@c) Compomer d) composite

Q.37. bonding of GIC to tooth structure is by (AIPG 2009) a)metal ions b)OH IONS c)COO- ions / Carboxlic groups@@d)micromechanical bonding

Q38. fluoride released from GIC restoration is replaced by a) Hydoxl ion @@@b) Aluminium ion c) Silicate ion d) Carboxylate ion

Q.39. In caries,which structure becomes more prominent (AIPG 2009) a)stiae of retzius @@@b) pickerill c)hunter shreger lines d)stie of wickhem

Q40. amalgam poloshing the outersurface arranged in layer known as a) beelby layer @@@b) weelby layer c) sealby layer

Q41 In a class V cavity preparation M-D walls depends on a. Direction of enamel rods@@@b. Contours of gingivac. Size of carious lesiond. Location of contact area Ans. A (Direction of enamel rods) Ref. Sturdevant, 4th ed. pg 755/ 5th ed. pg 797, 798, 799, 801- The Outline form Of Class V amalgam tooth preparation is primarily determined by the location and size of caries or - External shape is related to the contour of marginal gingival- The direction of mesial & distal wall follows the direction of the enamel rods

Proper outline from for Class V amalgam tooth preparations results in extending the cavosurface margins to sound tooth structure, while maintaining a limited axial depth of 0.5 mm inside the DEJ and 0.75 mm inside the cementum (when on the root surface).Presently, a more conservative philosophy is used (resulting in smaller restorations with outline forms that are dictated primarily by the size of the defect

Q42. on a radiograph an RCT treated tooth 2 years back a radiolucent cyst enlarged even after sugery what is the reason a) Leaking from unobturated main canal @@@b) Unobturated accessory canal c) Apex was not resected d) Actinomyces infection

Q.43. lateral incisor with periapical abcess n sinus tract. treatment of sinus tract - a) no treatment @@@@

Q.44 If histologic slide n contents of canal space could b obtained most common finding in radioluency region is (AIPG 2009)a)normal pulp b)osteoclastic activity @@@c)A.I. d)decrease in cellularity

Q45. Acid etching is done to a) Dec. micro leakage @@@b) Dec. polymerization shrinkage c) Dec. coefficient of thermal expansion d) Dec. porosity in restorative material

Orthodontics:-Q.46. normal mandibular plane angle a)17-30 @@@b)115-130 c)25-40 Ref : Textbook Of Oral And Maxillofacial Surgery By Neelima Malik 2nd ED Pg 274 – 276 Normal mandibular plane angle value is :• 22o in Down’s analysis, • 32o in Steiner’s analysis • 25o in tweed analysis

Q. 47. If interincisal distance is 131 degree, it implicates.a. Maxillary incisors are retroclinedb. Incisors are proclined@@@@c. Incisors are crowdedd. Incisors are retroclined.

Q48. Abt y axiswhat is true - obtained by joining sella gnathion to F H plane

Community Dentistry:-Q.49. true about simple random sampling a)every element has an equal probability of being included b)based on similar characteristics c)suitable 4 large hetrogenous population

Q.50. guidelines accordingto baby friendly hospital initiative includes all except a) mother n infant 2 b together 4 24 hr. b)initiate breast feeding in 4 hr of normal delivery c)giving no food or drink other than breast milk d)encourage breast feeding on demand e. Mother to feed baby 4 hrs @@@

Q.51. which one is true about normal distribution (AIPG 2009)a)meam median mode coincide at 1 pt / Mean = Mode = Median @@@b) values distributed in normal range

Q.52. all except are approaches 2 health education a/ea)provision of incentives @@@b)service approach

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c)education .... d)health approach

Q.53. increase in false positives cases in community a)cefepime b)cefoperazone c)cefotaxime Is this the Questn or is it : Q. Which cephalo do nt require dose redn - Cefoperazone Q. inf false positive - low prevalence Similar Questn from AIIMS May 2010 Medical47. A test has high false positive rate in a community. True isa) High prevalenceb) Low prevalence@@@c) High sensitivityd) High specificity

Q.54. All of the following measures are used for nutrition assessment to indicate inadequate nutrition except.a. Increased 1-4yr mortality rateb. Birth weight < 2500gmc. Hb< 11.5 g/dl during 3rd trimester of pregnancy.@@@@d. Decrease weight for heightans. C (Hb < 11.5 g/dl during 3rd trimester of pregnancy) Ref : CMDT 2008/677; Park 19th / 515-518; Ghai 6th/101; Nelson's 18th7228Anemia in pregnancy is defined as Hemoglobin measurement below lOg/dl and not 11.5 g/dL Hemoglobin levels less than lOg/dl during pregnancy may be used to indicate inadequate nutrition (nutritional anemia) and not a Hemoglobin level of less than ll.Sg/dl. This is therefore the single best answer of exclusion.Increased 1-4 year mortality rate indicates un undernutrition / malnutrition in a community (Park l9th/517)'Mortality in the age group of 1 to 4 years is particularly related to malnutrition' - Park 19th/517Vital & Health Statistics (Mortality & Morbidity data): Indicators of Malnutrition in Community• 1 to 4 year mortality rate• Infant mortality rate• Second year mortality rate• Rate of low birth weight babies• Life expectancy

Q.55. pt on acarbose n insulin has got hypoglycemic attack..treatment ???a) maltose b)glucose @@@c) galactose d)sucrose

Q56. Which does NOT cause hypoglycemia (AIIMS May 2011 Medical)A. Insulin B. GlimipirideC. NateglinideD. Acarbose@@Acarbose is an anti-diabetic drug used to treat type 2 diabetes mellitus· Acarbose inhibits enzymes (glycoside hydrolases) needed to digest carbohydrates, to be specific, alpha-glucosidase enzymes in the brush border of the small intestines and pancreatic alpha amylase. Pancreatic alpha-amylase hydrolyzes complex starches to oligosaccharides in the lumen of the small intestine, whereas the membrane-bound intestinal alpha-glucosidases hydrolyze oligosaccharides, and disaccharides to glucose and other monosaccharides in the small intestine. Inhibition of these enzyme systems reduces the rate of digestion of complex carbohydrates. Less glucose is absorbed because the carbohydrates are not broken down into glucose molecules. In diabetic patients, the short-term effect of these drugs therapies is to decrease current

blood glucose levels; the long-term effect is a reduction inHbA1c level. · Acarbose can be used alone to treat type II diabetes or can be combined with sulfonylureas such as glyburide or metformin or with insulin.· Since acarbose prevents the digestion of complex carbohydrates, the drug should be taken at the start of main meals (taken with first bite of meal). · Since acarbose prevents the degradation of complex carbohydrates into glucose, some carbohydrate will remain in the intestine and be delivered to the colon. In the colon, bacteria digest the complex carbohydrates, causing gastrointestinal side-effects such as abdominal pain, flatulence and diarrhea. Acarbose therapy is not advised in the presence of certain medical conditions such as inflammatory bowel disease or intestinal obstruction and chronic intestinal diseases that interfere with digestion or absorption as there is risk of complications.· Since Acarbose is not acting by release of insulin from pancreas, its monotherapy does not produce hypoglycemia. Adding insulin or a sulfonylurea and meglinitide, which act by releasing insulin from pancreas( by blocking potassium channel on beta cells of pancreas), to acarbose therapy may lower blood glucose more than acarbose alone. If a patient using acarbose suffers from a bout of hypoglycemia, the patient must eat something containing monosaccharides, such as fruit juice or glucose tablets. Since acarbose will prevent the digestion of complex carbohydrates, starchy foods will not effectively reverse a hypoglycemic episode in a patient taking acarbose.· Hepatitis has been reported with acarbose use. Therefore, liver enzymes should be checked before and during use of this medicine.· Acarbose may interfere with digoxin absorption thereby decreasing digoxin blood levels and its effect. Therefore, the digoxin dose may need to be increased if acarbose is begun

Q.57. most cariogenic sugar a) glucose b)sucrose @@@c)lactose d)fructose

Q. 58) Fructosamine a/e - Screening of diabetes

Q. 60. hybridization of dna homologous but not identical inc with

Pharmacology:-Q. 61 Ifosfamide not true (Aiims May 2011 Medical)A. It is a nitrogen mustardB. Metabolized by CYP3A4 enzyme of liverC. More neurotoxic than cyclophosphamideD. Chloroacetaldehyde is active metabolite @@Ans: D. Chloroacetaldehyde is active metaboliteIfosfamide is an alkylating agent belongs to subclass nitrogen mustard. It is an analog of other nitrogen mustard cyclophosphamide. Both of them are given as prodrug and activated by ring hydroxylation in the liver. Ifosfamide is activated by CYP3A4 and cyclophosphamide is activated by CYP2B. This difference of enzyme activation may account for the somewhat slower activation of ifosfamide in vivo, and the inter patient variability in toxicity of both molecules.The active Iphosphamide metabolites such as 4-hydroxyIphosphamide and its tautomer, aldophosphamide, are carried in the circulation to tumor cells where aldophosphamide cleaves spontaneously, generating stoichiometric amounts of

phosphoramide mustard and acrolein. Phosphoramide mustard is responsible for antitumor effects, while acrolein causes hemorrhagic cystitis often seen during therapy with cyclophosphamide. Cystitis can be reduced in intensity or prevented by the parenteral coadministration of mesnaAn equimolar quantity of chloroacetaldehyde (CA) is formed in each of these reactions and this toxic metabolite has been implicated in the neurotoxicity and nephrotoxicity which may accompany IFO-therapyOxidation of 4-hydroxyifosfamide results in another inactive metabolite which is 4-keto-IFO (KETO).CNS toxicity is manifest in the form of nausea and vomiting, particularly after intravenous administration of ifosfamide. Ifosfamide is the most neurotoxic among all alkylating agents, producing altered mental status, coma, generalized seizures, and cerebellar ataxia. These side effects have been linked to the release of chloroacetaldehyde from the phosphate-linked chloroethyl side chain of ifosfamide.Ifosfamide has virtually the same toxicity profile as cyclophosphamide, although it causes greater platelet suppression, neurotoxicity, nephrotoxicity, and in the absence of mesna, urothelial damage

Q. 62. piogltazone false is ---a) peroxisome proliferative activated

receptors PPAR b) used in DM 1???c) metabolized by liver d) c/I in cardiac dystolic function

AIIMS May 2011 MedicalQ. True about pioglitazone all except?A. Act on PPaR gamma receptor.B. C/ I in cardiac diastolic dysfunctionC. Undergoes hepatic metabolismD. Decreased insulin resistance ???Ans ???????? None or if D option is

Pioglitazone acts on insulin gene and even in absence of insulin helps in metabolism of carbohydrate ( Then Ans will be D)

Pioglitazone is selective agonists for nuclear peroxisome proliferator–activated receptor-gamma (PPAR gamma) and activates insulin-responsive genes that regulate carbohydrate and lipid metabolism. It exerts its principal effects by increasing insulin sensitivity in peripheral tissue.

It can also activate genes that regulate fatty acid metabolism in peripheral tissue. It increases glucose transport into muscle and adipose tissue by enhancing the synthesis and translocation of specific forms of the glucose transporters. Although muscle is insulin-sensitive tissue, PPAR gamma is virtually absent in skeletal muscle. This drug causes activation of adipocyte hormones and/or adipokines, the most promising of which is adiponectin. Adiponectin is associated with increased insulin sensitivity and stimulates glucose transport into muscle and increases fatty acid oxidation

It is metabolized by the liver and may be administered to patients with renal insufficiency but should not be used if there is active hepatic disease or significant elevations of serum liver transaminases.

It can also cause anemia, weight gain, edema, and plasma volume expansion. Because of edema, this drug should not be used in patients with New York Heart Association class 3 or 4 heart failure. Obese hypertensive individuals and those with cardiac diastolic dysfunction are at greatest risk for fluid retention.

Q. 63. Exantenide true except? (AIIMS May 2011 Medical Questn , SWT 011)A. It is GLP analogue B. Used for DM-IC. Used in DM - 2C. Given by S/C route

D. Increase glucagen secretion @@Ans : DExenatide is a glucagon-like peptide (GLP-1) receptor agonist. GLP-1 is released from the upper and lower bowel that augment glucose-dependent insulin secretion. This hormones is termed as incretin.GLP-1 significantly augments glucose-dependent insulin secretion. Studies have shown that it increases beta cell mass of pancreas. GLP-1 also reduces glucagon secretion, slows gastric emptying, and decreases appetite by acting on CNS. By slowing gastric emptying, it retards the quantity of food reaching the small intestine and hance reduces, post parandial hyperglycemia. By reducing appetite, it is also helpful in reducing weight of patient in DM 2. It also improves Hb1Ac level in blood. Circulating GLP-1 is rapidly (1 to 2 minutes) inactivated by the dipeptidyl peptidase IV enzyme (DPP-IV) present in body but exenatide is resistant to DPP-IV and has full agonist activity at GLP-1 receptors. It is given as sudcutaneous injections in combination therapy with other agents in subjects with type 2 DM. Exenatide side effects include a self-limiting nausea and it can cause hypoglycemia when used in conjunction with oral insulin secretagogue.Liraglutide is another GLP-1 agonist with long half life.An alternative approach to GLP-1 therapy is to inactivate the DPP-IV protease, thereby increasing endogenous circulating GLP-1 levels. Sitagliptin and vildagliptin is orally effective DPP-IV inhibitors.These agents are well tolerated and appear to result in less nausea than the GLP-1 analogs. However, since DPP-IV can metabolize a wide range of peptides, there is a theoretical concern about the long-term safety of these compounds. DPP-IV inhibitors prolong the action of neuropeptides such as substance P and macrophage-derived chemokines. Prolonging these messengers may produce inflammation (effect on substance P), increase blood pressure (effect on neuropeptide Y), or cause allergic reactions (effect on chemokines).Other events are often mild and include nasopharyngitis, upper respiratory tract infection, headache, and cough.Q.64. not a sign of succesful stellate ganglion block a)nasal stuffiness b)guttman sign c)horner syndrome d)bradycardia @@@??

Q.65. anesthetic drug injected for paravertebral block least likely diffuse 2 a)epidural space b)inter costal space c)sup n inf paravertebral space d) sob arachnoid space @@@?

Q.66. adverse effects of valpoic acid derivative r all except a)alopecia b)liver failure c)wt. gain d)osteomalacia @@@???

Q.67. Which of the following drugs is both anti resoptive and bone formative? (AIIMS may 2010 Medical)a) Strontium ranelate@@@b) Calcitoninc) Ibadronated) TeriperatideRefer Similar Questn AIPG 2011 Medical42. 39. All of the following decrease bone resorption in osteoporosis except? 1.Alendronate 2.Etidronate

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3.Strontium 4.Teriparatide @@@@Drugs for treatment of bone diseases Bisphosphonates : Nitrogenous (Alendronic acid, ibandronic acid, incadronic acid, pamidronic acid, risedronic acid, zoledronic acid)Non-nitrogenous (Etidronic acid, clodronic acid, tiludronic acid) Bone morphogenetic proteins : Dibotermin alfa • Eptotermin alfa Other : Resorption inhibitor (Ipriflavone) • Aluminium chlorohydrate • Dual action bone agent (Strontium ranelate) •RANKL inhibitor (Denosumab) • Cathepsin K inhibitor (Odanacatib)Strontium ranelate, a strontium(II) salt of ranelic acid, is a medication for osteoporosis marketed as Protelos or Protos by Servier. It is unusual in the sense that it both increases deposition of new bone osteoblasts and reduces the resorption of bone by osteoclasts. It is therefore promoted as a "dual action bone agent" (DABA).Alendronate inhibits osteoclast-mediated bone-resorptionWhereas pyrophosphate and the first bisphosphonate, etidronate, are capable of inhibiting both osteoclastic bone resorption as well as the mineralization of the bone newly formed by osteoblasts, alendronate and the other potent N-containing bisphosphonates such as risedronate, ibandronate, and zoledronate specifically inhibit bone resorption without any effect on mineralization at pharmacologically achievable dosesTeriparatide increases both bone formation and bone resorption

Q.68. ideal analgesia..... a)short onset of action, high efficacy,intermediate duraton b)short onset ,high efficacy,short duration c)intermediate onset,?????? Q. Patient controlled analgesia ?

Periodontics - Q. 69. Toothbrush abrasions more on - Maxillary left

Q. 70. All inv in periodontitis except - (AIIMS May 2009, AIPG 2009, AIIMS May 2008)Neisseria

Q. 71. All found in healthy perio except - (Refer to Explanation AIIMS May 2009, AIPG 2009, AIIMS May 2008 Dental Explore) Eubacterium

Q. 72. Periodontitis A.A. (AIPG 2009)- Gm negative anaerobes Rods

Q. 73. Role of plaque is obsolete in - Desquamative gingivitis

Q. 74. Chronic gingivitis h/f - Disruption of gingival fib n infiltration of lymphocytes plasma cells

Q. 75. False abt juvenile periodontitis - Bone loss simultaneous Q. Which of the following is untrue of LJP localized juvenile periodontitis? (AIIMs may 2009 )a) more common in femalesb) mirror image type of bone loss is seen bilaterallyc) Amount of bone destruction is proportional to the amount of plaque @@@

d) aggressive periodontal bone destruction compared to normal periodontitisans Camount of bone destruction is far advanced then the inflammatory changes caused by deposition of plaque. The amount of bone destruction far exceeds the amount of plaque deposition

Q. 76. .tfo least affects (repeat ap 2007)(Also Refer Target AIIMS V Q84 pg 52-53)a)periodontium b)enamel c)cementum d)epithelial attachment@@@

Q. 77. wich is not an abrasiv in dentrificea)CaCo3 b)amylose @@@c)silicate

Q. 78. In periodontitis pt.which one used a)tooth paste with max abrasive b)tooth paste with min abrasive @@@c)tooth powder with max abrasive d) no abrasive

Q. 79. brushing technique in pd patientsa)roll b)scrub c)bass d)sulcular@@@

Oral Pathology / Oral MedicineQ. 80. Malignant transformation - Junctional neavus

Q. 81. Self healing carcinoma among the following is .a. Leukoplakiab. Keratoacanthoma@@c. Benign neuromad. MelanomaAns. B (Keratoacanthoma) Ref: Burket’s 10thed/167, Shafer 4thEd/88 & 5thEd/116 & 6th ed Pg 82Keratoacanthoma (self healing carcinoma, molluscum pseudo-carcinomatosum, molluscum sebaceum) is a relatively common low-grade malignancy that originates in the pilosebaceous glands. Trauma, HPV virus, genetic factors and immuno compromised status have been implicated as etiologic factors. It occurs twice commonly in men than women, usuaLly on sun exposed areas. Lips and the vermillion bolder of both the upper and lower lip are affected with equal frequency.The clinical course of the Lesion is one of its unusual aspects. It begins as a small firm nodule that develops to full size over period 4-8 wks and then undergoes spontaneous regression over the next 6-8 wks (self healing carcinoma)If spontaneous regression does not occur, the lesion is usually treated by surgical excision parakeratin or orthokeratin surface layer with central plugging is important histologic feature.Keratoacanthoma is a localized lesion (usually found on sun-exposed skin, including the upper lipQ. 82. CVS manifestation in AIDS / HIV include all except A/E - a)pericardial tamponade(?) b) Aortic aneurysm @@

Q.83. widening of predentin layer n presence of large areas of interglobular demtin n irregular tubular pattern of dentin a) D.I b) dentin dysplasia c) odontodysplasia @@@

Q.84. not associated with natal teeth (Also refer Target AIIMS V Q 64 Pg 36-37)a)van de woude syndrome @@@b)sotos syn c)cleft palate d)ellis van crevold

Q.85. Most common developmental cyst a. Median anterior maxillary cyst@@@@b. Globulomaxillary cystc. Median palatal cystd. Median mandibular cyst Ans. A (Median anterior maxillary cyst) Ref:- Shafer, 4th Ed., Page 70 & 6th Ed Pg 63Median anterior maxillary cyst is also called Nasopalatine cyst. Median Anterior Maxillary Cyst(Nasopaltine Duct Cyst; Incisive Canal Cyst)The anterior maxillary cyst, which lies in or near the most common type of maxillary developmental cyst. It arises from proliferation of epithelial remants of the nasopalatine duct or cord of epithelial cells lying within the incisive canal

Radiology:-Q. 86. RVG sensors are protected from infection / While using the Radio visiography, the best method of infection control for receptors is (Aiims may 2009) a) Autoclave the receptors after each useb) immerse the receptors in disinfectantc) wipe the sensor with 5.25% hypochlorite solutiond) cover with impervious plastic sheath@@@@@Ref : Infection Control & Occupational Safety Recommendations for Oral Health Professionals in India 2007 by anil kohli 1st/124.The digital sensors and receptors are semicritical instruments. The digital receptor is used in the patient's oral cavity needs to be sheathed with a plastic sheath extending at least 5 inches outside the patient's mouth. The sheath needs to be changed between patients and the digital receptor and only needs to be wiped with a disinfectant wipe if contaminatedDo not immerse Digital Receptors (ones with electronic leads) in disinfectant as the leaching of liquidsmay short the circuits in the receptor. Digital Sensors (that do not have leads) may be immersed in a disinfectant per manufacturer's recommendation.

Q. 87. rvg use compared to conventional radiography a) Same b) Half @@@c) 1/5 d) increased

Q.88 which of the following is identified only by radiographs? (AIPG 2009)a) mental foramen @@@b)apical cystc) PA granulomad)chronic periodontitis

Q.89. ceph radiology distance b/w film n source (AIPG 2008) – 5 feet from midsagittal plane

Q. 90. RFLP

Q. 91. Upper 2 R/L Leakage frm main canal