AIIMS MAY 2008 Q & A With Explanations

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    Meena. Guest

    AIIMS 2008 (Questions With Answers)

    1. Diabetes in pregnancy all except:
    a- Glucose challenge test is done between 24-28 week
    b- 50 gm of sugar given as screening test
    c- Insulin resistance improves with pregnancy
    d- Diabetes control before conception is important to prevent malformation
    Ans: c- Insulin resistance improves with pregnancy

    2. Marker for granulosa cell tumor –
    a- CA 19-9
    b- CA 50
    c- Inhibin
    d- Teratoma
    Ans: c- Inhibin

    3. A 35 yr old female, with post coital bleeding, next step –
    a- Clinical examination and pap smear
    b- Visual inspection with acetowhite
    c- Visual inspection with lugol’s iodine
    d- Colposcopy directed biopsy
    Ans: a- Clinical examination and pap smear

    4. Clue cells are seen in:
    a- Bacterial vaginosis
    b- Candidiasis
    c- Trichomoniasis
    d- Gonorrhoea
    Ans: a- Bacterial vaginosis

    5. Topical antifungal in keratomycosis is –
    a- Silver sulfadiazine
    b- Natamycin
    c- Ketoconazole
    d- Flucytosine
    Ans: b- Natamycin

    6. Which of the following does not handle free radical in less?
    a- Vitamin A
    b- Vitamin C
    c- Vitamin E
    d- Catalase
    Ans: a- Vitamin A

    7. Retinitis pigmentosa is associated with all except
    a- Usher syndrome
    b- Kornzweing syndrome
    c- Kearns-Sayre syndrome
    d- Marfan syndrome
    Ans: d- Marfan syndrome

    8. Choroidal neurovacularization is seen in all except –
    a- Trauma
    b- Angiod streak
    c- Myopia
    d- Hypermetropia
    Ans: d- Hypermetropia

    9. Iridocorneal endothelial syndrome is associated with:
    a- Progressive atrophy of iris stroma
    b- Bilateral stromal edema of iris & cornea
    c- Deposition of collagen in Descemet’s membrane
    d- Deposition of Glycosaminoglycan in Descemet’s membrane
    Ans: a- Progressive atrophy of iris stroma

    10. Pterygium is
    a- A vascular anomaly
    b- A connective tissue degeneration
    c- An inflammatory condition
    d- Associated with Vit. A deficiency
    Ans: b- A connective tissue degeneration

    11. Chalazion of lid is –
    a- Caseous necrosis
    b- Chronic nonspecific inflammation
    c- Chronic lipogranulomatous inflammation
    d- Liposarcoma
    Ans: c- Chronic lipogranulomatous inflammation

    12. An orbital tumor has the following characteristics: Retrobulbar location within the muscle cone, well defined capsule, presents with slowly progressive proptosis, easily respectable, occurs most commonly in the 2nd to 4th decade. The diagnosis is:
    a- Hemangiopericytoma
    b- Dermoid
    c- Capillary hemangioma
    d- Cavernous hemangioma
    Ans: d- Cavernous hemangioma

    13. A 12 yr old boy comes into room with left sided head tilt, on correcting that he has right sided hypertropia. The hypertropia increases on left gaze and tilting the head towards right. Which muscle is paralyzed?
    a- Right superior rectus
    b- Left superior rectus
    c- Right superior oblique
    d- Left superior oblique
    Ans: c- Right superior oblique

    14. All of the following take part in the pathogenesis of macular edema in diabetic retinopathy except:
    a- Retinal pigment epithelium dysfunction
    b- Oxidative stress
    c- VEGF
    d- Increased protein kinase-C
    Ans: a- Retinal pigment epithelium dysfunction

    15. Telecanthus is –
    a- Narrow medial epicanthus
    b- Widely separated medial orbital wall
    c- Lateral epicanthal fold thickened
    d- Increase in intercanthal distance with normal interpupillary distance
    Ans: d- Increase in intercanthal distance with normal interpupillary distance

    16. Turner syndrome is maximally associated with:
    a- Horseshoe kidney
    b- Coarctation of aorta
    c- VSD
    d- ASD
    Ans: b- Coarctation of aorta

    17. Only females are affected in?
    a- Scheie’s syndrome
    b- Hunters syndrome
    c- Hurlers syndrome
    d- Gauchers syndrome
    Ans: ??

    18. Most common cause of seizure in newborn is:
    a- Hypoxia induced ischemic encephalopathy
    b- Hypocalcemia
    c- Metabolic abnormality
    d- Sepsis
    Ans: a- Hypoxia induced ischemic encephalopathy

    19. An infant with cleft lip, cleft palate, polydactly, microcephaly with holoprosencephaly, ectodermal scalp defect is suffering from:
    a- Trisomy 21
    b- Trisomy 18
    c- Trisomy 13
    d- Turner
    Ans: c- Trisomy 13

    20. Auxillary orthotopic liver transplant is indicated for:
    a- Metabolic liver disease
    b- As a standby procedure until finding a suitable donor
    c- Drug induced hepatic failure
    d- Acute fulminant liver failure for any cause
    Ans: d- Acute fulminant liver failure for any cause

    21. Internal oblique, external oblique and transverses is retracted laterally in:
    a- Classic renal approach
    b- Laparoscopic approach
    c- Spigelian hernia
    d- …………….
    Ans: ???

    22. In which of the following head and neck cancers, is lymph node metastasis least common:
    a- Tongue
    b- Buccal mucosa
    c- Hard palate
    d- Lower alveolus
    Ans: c- Hard palate

    23. Most common testicular tumor in prepubertal adults is
    a- Yolk sac tumor
    b- Embryonal cell ca
    c- Seminoma
    d- Teratoma
    Ans: a- Yolk sac tumor

    24. Metabolic abnormality seen in gastric outlet obstruction is
    a- Hypochloremic, hypokalemic acidosis
    b- Hypochloremic, hypokalemic alkalosis
    c- Hyperchloremic, hypokalemic acidosis
    d- Hyperchloremic, hypokalemic alkalosis
    Ans: b- Hypochloremic, hypokalemic alkalosis

    25. Metabolic abnormality seen in large colorectal villous adenoma
    a- Hypokalemic metabolic alkalosis
    b- Hypokalemic metabolic acidosis
    c- Chlorine sensitive metabolic acidosis
    d- Chlorine sensitive metabolic alkalosis
    Ans: b- Hypokalemic metabolic acidosis

    26. Abbey estender flap is based on:
    a- Lingual artery
    b- Facial artery
    c- Labial artery
    d- Internal maxillary artery
    Ans: c- Labial artery

    27. Chronic Burrowing ulcer is caused by:
    a- Microaerophilic streptococci
    b- Peptostreptococcus
    c- Streptococcus viridans
    d- Streptococcus pyogenes
    Ans: a- Microaerophilic streptococci

    28. True about denaturation of proteins is all except:
    a- Unfolding occurs
    b- Disruption of secondary structure occurs
    c- Sequence of amino acids remain the same
    d- Biological activity is retained
    Ans: d- Biological activity is retained

    29. False about Gastric lymphoma is:
    a- Stomach is the most common site
    b- Associate with H. pylori infection
    c- Total gastrectomy with adjuvant chemotherapy is the treatment of choice
    d- 5 yr survival rate after treatment is 60%.
    Ans: c- Total gastrectomy with adjuvant chemotherapy is the treatment of choice

    30. A six yr. old female presents with constipation and urinary retention. On examination a presacral mass is noted. Most probable diagnosis is:
    a- Pelvic neuroblastoma
    b- Rectal duplication cyst
    c- Sacrococcygeal teratoma
    d- Anterior sacral meningocele
    Ans: d- Anterior sacral meningocele

    31. True about treatment of early breast carcinoma
    a- Aromatase inhibitors are replacing tamoxifen in premenopausal women
    b- Postmastectomy radiation therapy is given when 4 or more lymph nodes are positive
    c- Tamoxifen is not useful in post-menopausal women
    d- In premenopausal women, multidrug chemotherapy is given in selected patients
    Ans: b- Postmastectomy radiation therapy is given when 4 or more lymph nodes are positive

    32. The reciptocal inhibition of antagonistic muscle upon lateral gaze is explained by:
    a- Sherrington law
    b- Herning law
    c- Laplace law
    d- Hick’s law
    Ans: a- Sherrington law

    33. Which is the correct statement regarding facial nerve palsy in temporal bone fractures?
    a- More common with transverse fractures
    b- More common with longitudinal fractures
    c- Facial palsy is of immediate onset
    d- It is always associated with CSF leakage.
    Ans: a- More common with transverse fractures

    34. Laryngocele arises from
    a- True cords
    b- Subglottis
    c- Saccule of the ventricle
    d- Anterior commissure
    Ans: c- Saccule of the ventricle

    35. An elderly diabetic with excruciating pain in ear, appearance of granulation in meatus, skull base infection with facial paralysis should be treated with
    a- Penicillin
    b- Ciprofloxacin
    c- 2nd generation cephalosporin
    d- Erythromycin
    Ans: a- Penicillin

    36. Direct bronchoscopy can visualize all except:
    a- Trachea
    b- Vocal cords
    c- First segmental subdivision of branch
    d- Subcarinal lymph nodes
    Ans: d- Subcarinal lymph nodes

    37. Auspitz sign is seen in:
    a- Pustular psoriasis
    b- Plaque type psoriasis
    c- Lichen planus
    d- Pityriasis rubra pilaris
    Ans: b- Plaque type psoriasis

    38. Keratoderma blenorrhagicum is seen in:
    a- Psoriasis
    b- Reiter’s syndrome
    c- Syphilis
    d- Disseminated gonococcal infection
    Ans: b- Reiter’s syndrome

    39. Most common cause of plant induced dermatitis in India:
    a- Poison ivy
    b- Parthenium
    c- Ragweed
    d- Cotton fibres
    Ans: b- Parthenium

    40. Shortest acting NDMR:
    a- Succinyl choline
    b- Rapacuronium
    c- Altracurium
    d- Pancuronium
    Ans: b- Rapacuronium

    41. All of the following are used to maintain proper oxygen flow to the patient except:
    a- Placement of nitrogen flowmeter downstream of the oxygen flowmeter
    b- A proportionater between N2 and O2 control valve
    c- Different pin index for nitrogen and oxygen
    d- Calibrated oxygen concentration analyses
    Ans: c- Different pin index for nitrogen and oxygen

    42. Most common cause of postoperative renal failure:
    a- Decreased renal perfusion
    b- Toxicity of anesthetic drugs
    c- Toxicity of antibiotics
    d- ??
    Ans: a- Decreased renal perfusion

    43. Order of sensitivity of nerve fibres to Local anaesesthetic in decreasing order:
    a- Pain (C and A-delta), Preganglionic sympathetic (B), motor
    b- Preganglionic sympathetic (B), Pain (C and A-delta), sensory, motor
    c- Pain (C and A-delta), sensory, motor, Preganglionic sympathetic (B)
    d- Preganglionic sympathetic (B) sensory, motor, Pain (C and A-delta)
    Ans: b- Preganglionic sympathetic (B), Pain (C and A-delta), sensory, motor

    44. An absolute contraindication of MRI is:
    a- Pacemaker
    b- Prosthetic cardiac valves
    c- Insulin pump
    d- Choclear implants
    Ans: d- Choclear implants

    45. Most chemoresistant tumors among the following is:
    a- Synovial sarcoma
    b- Osteosarcoa
    c- Malignant fibrous histiocytoma
    d- Embryonal rhabdomyosarcoma
    Ans: c- Malignant fibrous histiocytoma

    46. PACS in medical imaging stands for:
    a- Planned archiving common system
    b- Planned archiving computerized system
    c- Picture archiving and communication system
    d- Picture archiving or computerized system
    Ans: c- Picture archiving and communication system

    47. Snowman appearance on x-ray is seen in which cardiac pathology –
    a- Fallots tetrology
    b- TAPVC
    c- TGA
    d- Ebstein’s anomaly
    Ans: b- TAPVC

    48. If the right cardiac silhouette is obliterated, it means the pathology involves:
    a- Right middle lobe
    b- Right lower lobe
    c- Right atrium of heart
    d- Right ventricle of heart
    Ans: a- Right middle lobe

    49. Egg on side appearance is seen in
    a- TOF
    b- TAPVC
    c- Uncorrected TGA
    d- Truncus arteriosus
    Ans: c- Uncorrected TGA

    50. Investigation of choice for acoustic neuroma:
    a- CT without contrast
    b- CT with contrast
    c- MR without contrast
    d- MR with contrast
    Ans: d- MR with contrast

    51. Which of these is not a sign of increased ICT?
    a- Erosion of dorsum sella
    b- Sutural diastasis
    c- Ballooning of sella
    d- Copper-beaten appearance
    Ans: c- Ballooning of sella

    52. Hair on end appearance is seen in
    a- Thallassemia
    b- Scurvy
    c- Rickets
    d- Hemochromatosis
    Ans: a- Thallassemia

    53. Atypical antipsychotic are all except:
    a- Olanzepine
    b- Clozapine
    c- Risperidone
    d- Thioridazone
    Ans: d- Thioridazone

    54. A 25 yr old female patient history of 6 months, altered sensorium, involuntary movements, memory deficit, headache convulsions, abnormal movements, forgetfulness, 4 attack during day, 2 attack at night, CT normal:
    a- Epilepsy
    b- Dissociative disorder
    c- Hypochiondriasis
    d- Somatization disorder
    Ans: a- Epilepsy

    55. A girl with normal milestone spend her time seeing her own hand, do not interact with others, what is the diagnosis?
    a- ADHD
    b- Autism
    c- Asperger’s syndrome
    d- Rett’s disorder
    Ans: b- Autism

    56.Increased suicidal tendency is associated with:
    a- Noradrenaline
    b- Serotonin
    c- Dopamine
    d- GABA
    Ans: b- Serotonin

    57. Irresistible sexual desire in male is known as:
    a- Sadism
    b- Tribadism
    c- Satyriasis
    d- Nymphomania
    Ans: c- Satyriasis

    58. In National Water Supply & Sanitation programme a problem village is defined as all except –
    a- Distance of safe water is greater than 1.6 km
    b- Water is exposed to the risk of cholera
    c- Water source has excess iron & heavy metals
    d- Water infested with Guniea worm
    Ans: d- Water infested with Guniea worm

    59. Endemic ascitis is associated with the following –
    a- Pyrrolizidine
    b- Aflatoxin
    c- Sanguinarine
    d- Beta oxalylamino alanine (BOAA)
    Ans: a- Pyrrolizidine

    60. Which of the following is an example of disability limitation/
    a- Reducing occurrence of polio by immunization
    b- Arranging for schooling of child suffering from PRPP
    c- Resting affected limbs in neutral position
    d- Providing calipers for walking
    Ans: c- Resting affected limbs in neutral position

    61. Specificity of a screening test measures –
    a- True positives
    b- False positives
    c- False negatives
    d- True negatives
    Ans: d- True negatives

    62. ‘Vision 2020’ includes all of the following except –
    a- Onchocerciasis
    b- Epidemic conjunctivitis
    c- Cataract
    d- Trachoma
    Ans: b- Epidemic conjunctivitis

    63. Life cycle of filaria is
    a- Cyclodevelopmental
    b- Cyclopropagative
    c- Propagative
    d- Transovarian
    Ans: a- Cyclodevelopmental

    64. All are criteria for normal Indian Reference male except:
    a- 60 kg
    b- 2200 Kcal/day
    c- 8 hrs in bed
    d- 20-39 age
    Ans: b- 2200 Kcal/day

    65. Adjuvant used in DPT vaccine is
    a- Zinc
    b- Aluminium
    c- Copper
    d- Magnesium
    Ans: b- Aluminium

    66. In India, the cause for maximum maternal mortality is:
    a- Anemia
    b- Hemorrhage
    c- Abortion
    d- Sepsis
    Ans: b- Hemorrhage

    67. In which of the following disease, the overall survival is increased by screening procedure
    a- Prostate Ca
    b- Lung cancer
    c- Colon Ca
    d- Ovarian Ca
    Ans: c- Colon Ca

    68. A man with painful opthalmoplegia, cavernous sinus dilation: diagnosis is –
    a- Gradinego syndrome
    b- Tolosa Hunt syndrome
    c- Cavernous sinus thrombosis
    d- Orbital pseudotumour
    Ans: b- Tolosa Hunt syndrome

    69. Which is not a tumor suppressor gene?
    a- WT-1
    b- Rb
    c- p53
    d- RAS
    Ans: d- RAS

    70. Which is the best distribution study the daily admission of head injury patients in a trauma care centre?
    a- Normal distribution
    b- Binominal distribution
    c- Uniform distribution
    d- Poisson distribution
    Ans: d- Poisson distribution

    71. Mean bone density among two groups of 50 people each is compared with each other. The test of significance used would be:
    a- Paired-t-test
    b- Student t-test
    c- Analysis of variance
    d- Chi-Square test
    Ans: b- Student t-test

    72. After applying a statistical test, an investigator gets the ‘p value’ as 0.01. It means that:
    a- The probability of finding a significant difference is 1%
    b- The probability of declaring a significant difference, when there is truly no difference, is 1%
    c- The difference is not significant 1% times and significant 99% times
    d- The power of the test used is 99%
    Ans: c- The difference is not significant 1% times and significant 99% times

    73. If mean is less than the median, than the data is said to be
    a- Positively skewed
    b- Negatively skewed
    c- Equitable distribution
    d- Normal distribution
    Ans: b- Negatively skewed

    74. Study done on a group of patients showed coefficient of variance for BP and serum creatinine to be 20% & 15% respectively. Inference is that:
    a- Variation in BP is more than in serum creatinine
    b- Variation in serum creatinine is more than in BP
    c- Standard deviation of BP is more than of creatinine
    d- Standard deviation of creatinine is more than of BP
    Ans: a- Variation in BP is more than in serum creatinine

    75. In a study in UK, an association was found between sale of antiarrythmic drug and an increase in deaths due to asthma. This is an example of
    a- Ecological study
    b- Cohort study
    c- Case reference study
    d- Experimental study
    Ans: a- Ecological study

    76. Occupational cancer involve following organs except:
    a- Lung
    b- Breast
    c- Bladder
    d- Liver
    Ans: b- Breast

    77. Cross resistance of isoniazid is seen with:
    a- Rifampicin
    b- Ethionamide
    c- Cycloserine
    d- Ethambutol
    Ans: b- Ethionamide

    78. Which drug is not acetylated?
    a- INH
    b- Dapsone
    c- Hydralazine
    d- Metoclopropamide
    Ans: d- Metoclopropamide

    79. Which is not prodrug?
    a- Enalapril
    b- Clonidine
    c- Salmeterol
    d- Acetazolamide
    Ans: a- Enalapril

    80. Free water clearance decreased by?
    a- Vincristine
    b- Vinblastine
    c- Chlorpropamide
    d- Furosemide
    Ans: d- Furosemide

    81. Which of the following antibiotics acts by inhibiting cell wall synthesis?
    a- Cefepine
    b- Aminoglycosides
    c- Erythromycin
    d- Doxycycline
    Ans: a- Cefepine

    82. Which drug would treat both dermatophysis and candidal infection/
    a- Ketoconazole
    b- Griseofulin
    c- Nystatin
    d- Tolnafet
    Ans: a- Ketoconazole

    83. SIADH is caused by all except:
    a- Vincristine
    b- Vinblastine
    c- Actinomycin D
    d- Cyclophosphamide
    Ans: c- Actinomycin D

    84. Which teratogen causes deafness?
    a- Isotretinoin
    b- Chloroquine
    c- Alcohol
    d- Warfarin
    Ans: a- Isotretinoin

    85. Imatinib is used in the treatment of?
    a- Chronic myelomonocytic leukemia
    b- MDS
    c- ALL
    d- GIST
    Ans: a- Chronic myelomonocytic leukemia d- GIST

    86. Sustained neutropenia is seen with?
    a- Vinblastin
    b- Cisplatin
    c- Carmustine
    d- …………..
    Ans: c- Carmustine

    87. NOT used in scabies?
    a- BHC
    b- Permethrin
    c- Ciclopirox oleamine
    d- Crotamiton
    Ans: c- Ciclopirox oleamine

    88. Not used in erectile dysfunction?
    a- PGE-2
    b- Vardalafil
    c- Phenylephrine
    d- Alprostadil
    Ans: c- Phenylephrine

    89. Which is not a 2nd generation antihistaminic?
    a- Loratidine
    b- Acrivastatine
    c- Cyclizine
    d- ……….
    Ans: c- Cyclizine

    90. True about aminoglycoside is all except:
    a- Are bacteriostatic
    b- Distributed only extracellularly
    c- Excreted unchanged in urine
    d- Teratogenic
    Ans: a- Are bacteriostatic

    91. Loading dose depends on:
    a- Volume of distribution
    b- Clearance
    c- Rate of administration
    d- Half life
    Ans: a- Volume of distribution

    92. Drug not used in H. pylori:
    a- Metronidazole
    b- Omeprezole
    c- Mosapride
    d- Amoxicillin
    Ans: c- Mosapride

    93. Long acting beta-2 agonist?
    a- Albuterol
    b- Salmetarol
    c- Pirlbuterol
    d- Orciprenaline
    Ans: b- Salmetarol

    94. Benzodiazepine antagonist ?
    a- Flumazenil
    b- Naloxone
    c- Furazolidone
    d- Naltrexone
    Ans: a- Flumazenil

    95. Which is Cyt. P450 inhibitor ?
    a- Ketoconazole
    b- Rifampicin
    c- Phenytoin
    d- INH
    Ans: a- Ketoconazole

    96. Which statement is true about carbamazepine?
    a- Used in trigeminal neuralgia
    b- Carbamazepine is an enzyme inhibitor
    c- Can cause megaloblastic anemia
    d- It is the drug of choice for status epilepticus
    Ans: a- Used in trigeminal neuralgia

    97. Drug used in uncomplicated alcohol withdrawal?
    a- Diazepam
    b- Clonidine
    c- Propanalol
    d- Methadone
    Ans: a- Diazepam

    98. Buprenorphine is?
    a- Pure agonist
    b- Pure antagonist
    c- Partial agonist
    d- None
    Ans: c- Partial agonist

    99. In cases of coarctation of aorta which of the following is not involved in collateral formation:
    a- Vertebral artery
    b- Posterior intercostals artery
    c- Axillary artery
    d- Subscapular artery
    Ans: a- Vertebral artery

    100. U/L injury to hypoglossal nerve leads to all except
    a- Hemiatrophy of involved side
    b- Deviation of tongue towards the same side
    c- Loss of taste sensation in one half of the tongue
    d- Fasciculation of the tongue
    Ans: c- Loss of taste sensation in one half of the tongue

    101. If median nerve is injured at the wrist then loss of function of all of the following will take place except:
    a- Lumbrical muscles to the Index finger
    b- Lumberical muscles to the middle finger
    c- Muscles of the thenar eminence
    d- Adductor pollicis
    Ans: d- Adductor pollicis

    102. In standing position, Venous return to heart from lower limbs is affected by all of the following except:
    a- Competant valves
    b- Deep fascia
    c- Arterial pressure
    d- Contraction of calf muscles
    Ans: c- Arterial pressure

    103. Movements taking place during abduction of shoulder joint are all except-
    a- Medial rotation of scapula
    b- Axial rotation of humerus at acromioclavicular joint
    c- Elevation of humerus
    d- Movements at clavicular end of sternoclavicular joint
    Ans: a- Medial rotation of scapula

    104. Lhermitte dulcos disease true is –
    a- Thickened cerebeller folli
    b- Atrophic cerebeller folli
    c- Vermian hypoplasia
    d- Septum pelluidumagenesis
    Ans: a- Thickened cerebeller folli

    105. A man with chest pain, ST segment depression in lead v1-v4, after one hour will not be given:
    a- Beta blocker
    b- Thrombolytic
    c- Morphine
    d- Aspirin
    Ans: b- Thrombolytic

    106. The thoracic duct receives tributaries from all of the following except
    a- Bilateral ascending lumber trunk
    b- Bilateral descending thoracic trunk
    c- Left upper intercostals trunk
    d- Right bronchomediastinal lymphatic trunk
    Ans: d- Right bronchomediastinal lymphatic trunk

    107. True valves in portal venous system
    a- Present at the junction of superior mesenteric artery with the splenic artery
    b- Within the portal vein only
    c- The whole system vein only
    d- In the intrahepatic portion of portal vein
    Ans: c- The whole system vein only

    108. All are the contents of deep perineal pouch except:
    a- Bulbourethral glands
    b- Internal urethral sphincter
    c- Dorsal nerve of penis
    d- Bulb of penis
    Ans: d- Bulb of penis

    109. Which is not a branch of cavernous part of internal carotid artery?
    a- Cavernous branch
    b- Inferior hypophyseal
    c- Meningeal artery
    d- Ophthalmic artery
    Ans: d- Ophthalmic artery

    110. Equilibrium potential for an ion is calculated using
    a- Gibbs Donnan equation
    b- Goldman equation
    c- Nernst equation
    d- Henderson Hesselbach equation
    Ans: c- Nernst equation

    111. Why fetal cells continue to divide but terminally differentiated adult do not divide
    a- There are many cyclin inhibitors which prevent cell to enter into S phase in adult
    b- Phosphatase absent in fetal cells
    c- Proteinase is absent in fetus
    d- Absence of CD kinase
    Ans: a- There are many cyclin inhibitors which prevent cell to enter into S phase in adult

    112. Cerebral blood flow is regulated by all except
    a- Blood pressure
    b- Arterial PCO2
    c- Potassium ions
    d- Cerebral Metabolic rate
    Ans: c- Potassium ions

    113. CSF pressure is mainly regulated by
    a- Rate of CSF formation
    b- Rate of CSF absorption
    c- Cerebral blood flow
    d- Venous pressure
    Ans: b- Rate of CSF absorption

    114. Pulmonary circulation differs from systemic circulation
    a- Pulmonary vasodilation in hypoxia
    b- Pulmonary vasoconstriction in hypoxia
    c- Decreased blood volume during systole
    d- Increased basal vasoconstrictor tone
    Ans: b- Pulmonary vasoconstriction in hypoxia

    115. Regarding Golgi tendon organ true is
    a- Senses dynamic length of muscle
    b- Involved in reciprocal innervation
    c- Alpha-motor neuron stimulation
    d- Senses muscle tension
    Ans: d- Senses muscle tension

    116. Increase in threshold level on applying subthreshold, slowly rising stimulus is k/a
    a- Adaptation
    b- Accomodation
    c- Refractoriness
    d- Electrotonus
    Ans: b- Accomodation

    117. Regarding transport of substances through the cell membrane, all are true except:
    a- Glucose is transported via facilitated diffusion
    b- Active transport is an energy driven process
    c- Facilitated diffusion requires energy
    d- Facilitated diffusion requires carrier protein
    Ans: c- Facilitated diffusion requires energy

    118. In a seriously ill patient, addition of amino acids in diet results in a positive nitrogen balance. The mechanism for this is:
    a- Increased Growth hormones secretion
    b- Enhanced rate of gluconegenesis
    c- Increased absorption of amino acids from diet
    d- Increased secretion of Insulin
    Ans: d- Increased secretion of Insulin

    119. Steroid hormone receptors have attachment site for all except:
    a- Steroid hormone
    b- Transcription repressors
    c- Hormone responsive element
    d- Transcription activators
    Ans: b- Transcription repressors

    120. Phosphatidyl choline in a lipid monolayer, at pH of 3.5 leads to:
    a- Decreased surface potential
    b- Increased surface potential
    c- Decreased dipole moment
    d- Zero dipole moment
    Ans: ???

    121. Insulin causes lipogenesis by all except:
    a- Increasing acetyl-CoA carboxylase activity
    b- Increases the transport of glucose into the cells
    c- Inhibits pyruvate dehydrogenase
    d- Decreases intracellular cAMP level
    Ans: c- Inhibits pyruvate dehydrogenase

    122. True about G protein coupled receptors is:
    a- G proteins bind to hormones on the cell surface
    b- All the three subunits alpha, beta and gamma should bind each other G protein to act
    c- G proteins act as inhibitory and excitatory because of difference in alpha subunit
    d- G protein is bound to GTP in resting state
    Ans: c- G proteins act as inhibitory and excitatory because of difference in alpha subunit

    123. Poly(A) tail translate into:
    a- Polyproline
    b- Polylysine
    c- Polyalanine
    d- Polyglycine
    Ans: b- Polylysine

    124. Thiamine deficiency causes decreased energy production because
    a- It is required for the process of transamination
    b- It is co-factor in oxidative reduction
    c- It is co-enzyme for transketolase in pentose phosphate pathway
    d- It is co-enzyme for pyruvate dehydrogenase
    Ans: d- It is co-enzyme for pyruvate dehydrogenase

    125. All are true about glutathione except:
    a- It is a tripeptide
    b- It converts hemoglobin to methemoglobin
    c- It conjugates xenobiotics
    d- It scavenges free radicals and superoxide ions
    Ans: b- It converts hemoglobin to methemoglobin

    126. In molecular cloning, Blue-white screening is used for:
    a- To screen for recombinant vectors
    b- To detect gene mutations
    c- To identify desired chromosomal DNA insert in plasmid vectors
    d- To detect host DNA in situ
    Ans: c- To identify desired chromosomal DNA insert in plasmid vectors

    127. Sweating in Not present in
    a- Heat syncope
    b- Heat cramps
    c- Heat stroke
    d- Heat fatigue
    Ans: c- Heat stroke

    128. Finger print bureau was first established in
    a- India
    b- England
    c- USA
    d- France
    Ans: a- India

    129. Corpus delicti means
    a- Essence of crime
    b- Inquest into death
    c- Postmortem examination
    d- Death by asphyxia
    Ans: a- Essence of crime

    130. Lat organ to be dissected during autopsy in asphyxial death is
    a- Neck
    b- Head
    c- Abdomen
    d- Thorax
    Ans: a- Neck

    131. Nocardia is stained by all except:
    a- Acid fast stain
    b- Kiram’s stain
    c- Alcain blue
    d- Mucin stain
    Ans: b- Kiram’s stain

    132. Selective media for vibrio:
    a- TCBS
    b- Stuart
    c- Skirrows
    d- MYPA
    Ans: a- TCBS

    133. Mark true in following:
    a- Hanta virus pulmonary syndrome is used by inhalation of rodent urine and feces
    b- Kyanasur forest disease is caused by bite of wild animal
    c- Lyssa virus is transmitted by ticks
    d- ???
    Ans: a- Hanta virus pulmonary syndrome is used by inhalation of rodent urine and feces

    134. True about mycoplasma are all except:
    a- They are L forms
    b- Sterol enhances growth
    c- Can grow in cell free media
    d- When growth in liquid medium do not produces turbidity
    Ans: a- They are L forms

    135. About HUS all are except:
    a- Not commonly caused by verocytogenic E-coli
    b- Causes mild to severe Coombs positive hemolytic anemia
    c- Recurrences rare
    d- Transient thrombocytopenia
    Ans: a- Not commonly caused by verocytogenic E-coli
    b- Causes mild to severe Coombs positive hemolytic anemia

    136. True about mycobacterium other than tuberculosis:
    a- Causes disseminated infection
    b- Occurs in persons with normal immunity
    c- Causes decreased efficacy of BCG due to cross immunity
    d- Person to person transmission is seen
    Ans: c- Causes decreased efficacy of BCG due to cross immunity

    137. Malta fever is caused by :
    a- Treponema pallidum
    b- Borrelia burgdorferi
    c- Brucella melitensis
    d- Pseudomonas aeruginosa
    Ans: c- Brucella melitensis

    138. Acute Primary Amoebic Meningoencephalitis true is –
    a- Meningitis caused by acanthamoeba species is acute in nature
    b- Diagnosis is by demonstration of trophozite in CSF
    c- Caused by feco oral transmission
    d- More common in tropical climate
    Ans: b- Diagnosis is by demonstration of trophozite in CSF

    139. Parvovirus B19 does not cause:
    a- Roseola infantum
    b- Alplastic anemia in sickle cell disease
    c- Fetal hydrops
    d- …………….
    Ans: a- Roseola infantum

    140. What is true about Histoplasmosis?
    a- In early stages it is indistinguishable from T.B.
    b- Culture is not diagnostic
    c- Hyphal forms are infectious form
    d- Person to person spread occurs by dropal infection
    Ans: a- In early stages it is indistinguishable from T.B.

    141. True about polio:
    a- Paralytic polio is most common
    b- Spastic paralysis
    c- Increased muscular activity leads to increased paralysis
    d- Polio drop given only in <3 year
    Ans: c- IM injections and increased muscular activity leads to increases the risk of paralytic polio

    142. Which is not a part of HACEK ?
    a- Hemophilus Aphrophilus
    b- Acinetobacter Boumani
    c- Cardiobacterium Hominis
    d- Kingella Kingae
    Ans: b- Acinetobacter Boumani

    143. A patient presents with mediastinal mass with sheets of epithelial cells giving arborizing pattern of reactivity alongwith interspersed lympoid cells. The apt diagnosis would be:
    a- Thymoma
    b- Thymic carcinoid
    c- Primary mediatinal lymphoma
    d- Non-Hodgkin lymphoma
    Ans: a- Thymoma

    144. A 30-yrs old female, RBC counts 4.5 million, MCV 55f1, TC 8000, no history of blood transfusion?
    a- Iron deficiency anemia
    b- Thalessemia major
    c- Thalessemia minor
    d- Megaloblastic anemia
    Ans: c- Thalessemia minor

    145. Ulcerative colitis what is seen?
    a- Cryptitis
    b- Crypt loss
    c- Crypt branching
    d- Proliferating mucosa
    Ans: a- Cryptitis

    146. The gene responsible for folic acid transport is situated on which chromosome?
    a- 10
    b- 5
    c- X
    d- 21
    Ans: d- 21

    147. Hematoxylin bodies seen in:
    a- SLE
    b- PAN
    c- Rheumatoid arthritis
    d- Wegeners granulomatosus
    Ans: a- SLE

    148. CD-99 is for:-
    a- Ewing’s sarcoma
    b- SLL
    c- Sermatofibroma protruberans
    d- Malignant histiocytic fibroma
    Ans: a- Ewing’s sarcoma

    149. Loss of hetrozygosity associated with:
    a- Acute myeloid leukemia
    b- ALL
    c- Retinoblastoma
    d- Promyelocitic leukemia
    Ans: c- Retinoblastoma

    150. Most common primary lymphoma of spleen?
    a- Hodgkin’s lymphoma
    b- Small lymphocytic lymphoma
    c- Anaplastic lymphoma
    d- Burkitt’s lymphoma
    Ans: b- Small lymphocytic lymphoma

    151. Rituximab is used in all except
    a- NHL
    b- PNH
    c- RA
    d- SLE
    Ans: b- PNH

    152. Kasabaach Merrit Syndrome is associated with:
    a- Giant hemangioma
    b- Large aneurysm of aorta
    c- Giant Thrombocytes
    d- A-V malformation
    Ans: a- Giant hemangioma

    153. All are causes of increased anion gap except –
    a- DKA
    b- Starvation
    c- Ethylene glycol poisoning
    d- Glue sniffing
    Ans: d- Glue sniffing

    154. Which valve is least affected in Rheumatic fever?
    a- Pulmonary valve
    b- Tricuspid valve
    c- Mitral valve
    d- Aortic valve
    Ans: a- Pulmonary valve

    155. Drug used to perform stress ECHO?
    a- Thallium
    b- Dobutamine
    c- Adrenaline
    d- Adenosine
    Ans: b- Dobutamine

    156. Torsades de pointes causes?
    a- Eide QRS
    b- Short QRS
    c- Wide QT
    d- Short QT
    Ans: c- Wide QT

    157. True about autonomic neuropathy are all except:
    a- Resting tachycardia
    b- Silent MI
    c- Orthostatic hypotension
    d- Bradyardia
    Ans: d- Bradyardia

    158. In Millard Gubler syndrome all are involved except:
    a- 5th cranial nerve
    b- 6th cranial nerve
    c- 7th cranial nerve
    d- Contralateral hemiplegia
    Ans: a- 5th cranial nerve

    159. For differentiating between Insulinoma and Sulfonylurea related hypoglycemia, the test which is useful is?
    a- Antibody to Insulin
    b- Plasma C-peptide level
    c- Plasma Insulin level
    d- Insulin: Glucose ratio
    Ans: is none.

    160. All are used for treating Pulmonary hypertension except:
    a- Endothelin receptor antagonists
    b- Phosphodiesterase inhibitors
    c- Calcium Channel Blockers
    d- Beta blockers
    Ans: d- Beta blockers

    161. Goodpasture’s disease is characterized by all except:
    a- Glomerulonephritis
    b- Leukocytoclastic vasculitis
    c- Diffuse alveolar hemorrhage
    d- Presence of antibodies to BM
    Ans: b- Leukocytoclastic vasculitis

    162. Alzheimer’s disease, which is involved?
    a- Frontal cortex
    b- Cortical atrophy of temporoparietal cortex
    c- Frontal and parietal cortex
    d- Occipital cortex
    Ans: b- Cortical atrophy of temporoparietal cortex

    163. Rasmussen’s aneurysm involves?
    a- Bronchial aneurysm
    b- Pulmonary aneurysm
    c- Vertebral artery
    d- Posterior intercostal artery
    Ans: b- Pulmonary aneurysm

    164. Damage to categorical hemisphere usually leads to:
    a- Normal speech
    b- Increased speech
    c- Decreased speech
    d- Senseless, fluent speech
    Ans: d- Senseless, fluent speech

    165. 1st drug to be used absence seizures:
    a- Phenytoin
    b- BZD
    c- Valproate
    d- Carbamazepine
    Ans: c- Valproate

    166. Most common inherited childhood tumor is;
    a- Leukemia
    b- Neuroblastoma
    c- Retinoblastoma
    d- Wilm’s tumor
    Ans: c- Retinoblastoma

    167. Absent thumb, radial deviation of wrist, bowling of forearm with thrombocytopenia which investigation need not to be done?
    a- Echocardiography
    b- Bone marrow examination
    c- Platelet count
    d- Karyotyping
    Ans: a- Echocardiography

    168. Macrocephaly is seen in which of the following syndromes?
    a- Metachromatic leucodystrophy
    b- Adrenoleukodystrophy
    c- Canavan’s disease
    d- Krabbe’s disease
    Ans: c- Canavan’s disease

    169. Best prognosis after nerve repair:
    a- Radial
    b- Median
    c- Sciatic
    d- Ulnar
    Ans: a- Radial

    170. Not seen in osteopetrosis:
    a- Compression of cranial nerve
    b- Osteomyelitis of mandible
    c- Pancytopenia
    d- Delayed healing of bone
    Ans: none or best option d- Delayed healing of bone

    171. Material used in verterbroplasty is:
    a- Isomethyl methacylate
    b- Isoethyl methacrylate
    c- Polyethyl methacrylate
    d- Polymethyl methacrylate
    Ans: d- Polymethyl methacrylate

    172. The progesterone of choice for emergency contraception is:
    a- Norethisterone
    b- Medroxyprogesteronacetate
    c- Levonorgestral
    d- Desogestral
    Ans: c- Levonorgestral

    173. Pre-conceptional intake of which of the following results in decrease in incidence of neural tube defect?
    a- Vit. A
    b- Folate
    c- Vit. E
    d- Vit. C
    Ans: b- Folate

    174. Which is most commonly implicated in genital (vulval) warts?
    a- HPV 16
    b- HPV 18
    c- HPV 31
    d- HPV 6
    Ans: d- HPV 6

    175. The cause of fetal death in ectopic pregnancy is postulated as:
    a- Vascular accident
    b- Nutritional adequancy
    c- Endocrine insufficiency
    d- Immune response of mother
    Ans: a- Vascular accident

    176. When in labor, a diagnosis of occipito posterior presentation is made. The most appropriate management in this case would be:
    a- Emergency CS
    b- Wait and watch for progress of labour
    c- Early rupture of membranes
    d- Start oxytocin drip
    Ans: b- Wait and watch for progress of labour

    177. Most valuable diagnostic test in a case of suspected ectopic pregnancy:
    a- Serial Beta-hCG levels
    b- Transvaginal USG
    c- Progesterone measurement
    d- Culdocentesis
    Ans: b- Transvaginal USG

    178. Call-Exner bodies are seen in:
    a- Granulosa cell tumor
    b- Yolk Sac tumor
    c- Choriocarcinoma
    d- Dysgerminoma
    Ans: a- Granulosa cell tumor

    179. A lady with CA ovary in follow up with raised CA 125 level, next step –
    a- CT
    b- PET
    c- MRI
    d- Clinical exam and serial follow up of CA125
    Ans: b- PET

    180. Blood in urine in a patient in labour, diagnosis is –
    a- Impending scar rupture
    b- Urethral injury
    c- Obstructed labour
    d- Cystitis
    Ans: c- Obstructed labour

    181. Androgen insensitivity syndrome true is:
    a- Phenotype may be completely female
    b- Predominantly ovarian component in gonads
    c- Always in female
    d- Testes formed abnormality and receptors are normal
    Ans: a- Phenotype may be completely female

    182. 10 year old girl with primary amenorrhoea, absent breasts, malformed uterus. The most likely diagnosis:
    a- MRKH syndrome
    b- Turner’s syndrome
    c- Swyer syndrome
    d- Mixed gonadal dysgenesis
    Ans: b- Turner’s syndrome

    183. Regarding Alpha Fetoprotein true statement is:
    a- Major source of fetal life is yolk sac
    b- Commonly elevated in Wilm’s tumor
    c- Max level at 20th week
    d- Half-life 5-7 days
    Ans: a- Major source of fetal life is yolk sac

    184. AML with gum infiltration, hepatosplenomegaly:
    a- ALL
    b- M3
    c- M2
    d- M4
    Ans: d- M4

    185. The Electron Microscopy is virtually diagnostic in renal biopsy study of:
    a- Goodpasture’s syndrome
    b- Churg-Strauss syndrome
    c- Alport syndrome
    d- Wgner’s granulomatosis
    Ans: c- Alport syndrome

    186. Bone resorption markers are except:
    a- Tartarate resistant alk. phosphatase (TRAP)
    b- Osteocalcin
    c- Cross linked-N-telopeptides
    d- Urine total free deoxypyridinoline
    Ans: b- Osteocalcin

    187. Marker for granulocytic sarcoma:
    a- CD33
    b- CD38
    c- CD117
    d- CD137
    Ans: c- CD117

    188. Which type of FSGS has worst prognosis?
    a- Tip variant
    b- Collapsing
    c- NOS
    d- Perihilar
    Ans: b- Collapsing

    189. Shock lung is characterized by ?
    a- Alveolar proteinosis
    b- Bronchiolitis obliterans
    c- Diffuse pulmonary hemorrhage
    d- Diffuse alveolar damage
    Ans: d- Diffuse alveolar damage

    190. Ultrasound finding in case of paraganglioma?
    a- Deposition of glycogen
    b- Enlarged mitochondria
    c- Shrunken mitochondria
    d- Dense core granules
    Ans: d- Dense core granules

    191. Steroid resistant nephritic syndrome –
    a- Nephrin
    b- Alpha-acthin-4
    c- Podocin
    d- Transient Receptor Potential 6
    Ans: c- Podocin

    192. A patients with HB-6 gm, TLC 12000, PLATELET-60,000, MCV 12FL, what is the diagnosis?
    a- Aplastic anemia
    b- Megaloblastic anemia
    c- PNH
    d- Myelofibrosis
    Ans: b- Megaloblastic anemia

    193. Most common organism associated with reactive arthritis is:
    a- Staphylococcus
    b- Shigella
    c- Chlamydia
    d- Yersinia
    Ans: c- Chlamydia

    194. Nerve compressed by aneurysm of posterior communicating artery is –
    a- Occulomotor nerve
    b- Optic nerve
    c- Hypophysis cerebri
    d- Trochlear nerve
    Ans: a- Occulomotor nerve

    195. Which is a feature of high altitude pulmonary edema?
    a- Associated with low cardiac output
    b- Associated with pulmonary hypertension
    c- Occurs only in unacclamatized persons
    d- Exercise has no effect
    Ans: b- Associated with pulmonary hypertension

    196. Non-noxious stimulus is perceived as pain in:
    a- Allodynia
    b- Hyperalgesia
    c- Paraesthesia
    d- Hyperpathia
    Ans: a- Allodynia

    197. All are seen in cystinosis except:
    a- Photophobia and blond hair
    b- Renal calculi
    c- Presence of cystine within leukocytes
    d- Fanconi syndrome
    Ans: b- Renal calculi

    198. Which of the following is not true?
    a- William syndrome consists of precocious puberty, mental retardation and obesity
    b- In absence of sunlight daily requirement of vitamin D is 400-600 IU
    c- 1 alpha hydroxylation occurs in kidney
    d- 25 alpha hydroxylation occurs in liver
    Ans: a- William syndrome consists of precocious puberty, mental retardation and obesity

    199. Secondary structure of prion proteins in prion disease like Creutz feldt-Jakob disease (CJD) is –
    a- Beta sheets
    b- Beta bend
    c- Beta turus
    d- Alfa helix
    Ans: a- Beta sheets

    200. Post transplant lymphoma is –
    a- T cell
    b- B cell
    c- Null cell
    d- NK cell
    Ans: b- B cell








    AIIMS MAY 2008 Q & A With Explanations

    Q. Marker for granulocytic sarcoma?
    a)CD33
    b)CD38
    c)CD117
    d)CD153

    ans is c)CD117


    A chloroma, or granulocytic sarcoma, or most appropriately, extramedullary myeloid tumor, is a solid tumor composed of immature malignant white blood cells called myeloblasts. A chloroma is an extramedullary manifestion of acute myeloid leukemia; in other words, it is a solid collection of leukemic cells occurring outside of the bone marrow.

    Diagnosis

    Definitive diagnosis of a chloroma usually requires a biopsy of the lesion in question. Historically, even with a tissue biopsy, pathologic misdiagnosis was an important problem, particularly in patients without a clear pre-existing diagnosis of acute myeloid leukemia to guide the pathologist. In one published series on chloroma, the authors stated that 47% of the patients were initially misdiagnosed, most often as having a malignant lymphoma.

    However, with advances in diagnostic techniques, the diagnosis of chloromas can be made more reliable. Traweek et al. described the use of a commercially available panel of monoclonal antibodies, against myeloperoxidase, CD68, CD43, and CD20, to accurately diagnose chloroma via immunohistochemistry and differentiate it from lymphoma. Nowadays, immunohistochemical staining using monoclonal antibodies against CD34 and CD117 would be the mainstay of diagnosis. The increasingly refined use of flow cytometry has also facilitated more accurate diagnosis of these lesions.
  2. Meena.

    Meena. Guest

    Q. Malta fever is caused by?
    a)
    b)borrelia burgdorferi
    c)brucella melitensis
    d)pseudomonas

    ans is c)brucella melitensis

    Brucellosis, also called undulant fever, or Malta fever, in humans is a highly contagious zoonosis (infectious disease transmitted from animals to humans) caused by bacteria of the genus Brucella. Brucella spp. are small, gram-negative, non-motile, non-spore-forming rods. Brucella spp. are facultative intracellular parasites causing chronic disease, which usually persists for life. Brucellosis is a bacterial disease of both humans and animals recognized since the 19th century.

    Brucellosis in humans is usually associated with the consumption of unpasteurized milk and soft cheeses made from the milk of infected animals, primarily goats, infected with Brucella melitensis and with occupational exposure of laboratory workers, veterinarians and slaughterhouse workers. Some vaccines used in livestock, most notably B. abortus strain 19 also cause disease in humans if accidentally injected. Brucellosis induces inconstant fevers, sweating, weakness, anaemia, headaches, depression and muscular and bodily pain.
  3. Meena.

    Meena. Guest

    Q. Drug used to perform stress ECHO?

    a)thallium
    b)dobutamine
    c)dopamine
    d)adenosine

    ans is b)dobutamine

    Pharmacologic Stress Test
    Aka: Stress Imaging with Pharmacologic Provocation

    Indications
    Cardiac Screening in patients unable to Exercise 5 Mets
    Intermediate pretest risk of CAD


    Tests

    Dobutamine Echocardiogram No Beta Blockers for 24 hours before test
    Avoid if very large body habitus (poor echo window)
    Optison contrast can be used to increase accuracy

    Myocardial Perfusion Imaging with Adenosine
    Avoid in severe COPD, Asthma, Carotid Stenosis
    No nitrates on day of test
    No methylxanthines (e.g. caffeine) for 24 hours prior


    Myocardial Perfusion Imaging with Dipyridamole
    Uses Dipyridamole (Persantine) instead of Adenosine
    Determine Cardiac Risk pre-major non-cardiac surgery
    May also help with prognosis after major surgery


    Dobutamine Stress Echo Test
    What is a dobutamine stress echo test?
    The dobutamine stress echo test involves taking a medication called dobutamine while you are closely monitored. The medication stimulates your heart and makes it "think" it is exercising. The test is used to evaluate your heart and valve function when you are unable to exercise on a treadmill or stationary cycle.

    The test is also used to:

    Determine how well your heart tolerates activity;
    Determine your likelihood of having coronary artery disease (blocked arteries); and
    Evaluate the effectiveness of your cardiac treatment plan.

    Contraindications
    Concurrent Beta-Blocker use
    Body habitus interferes with echocardiogram windows
    Optison contrast can be used to increase accuracy

    Advantages
    Beta adrenergic agonist increases coronary flow 3x
  4. Meena.

    Meena. Guest

    Q. KERATODERMA BLENORRHAGICUM IS ASSOSIATED WITH?

    ANS IS REITER SYNDROME



    REITER'S SYNDROME
    Reiter's syndrome is a clinical tetrad of unknown cause consisting of urethritis, conjunctivitis (or, less commonly, uveitis), mucocutaneous lesions, and arthritis. It occurs most commonly in young men. It may follow (within days or weeks) infection with Chlamydia, Campy lohacter. Salmonella, or Yersinia and is usually accompanied by a systemic reaction, including fever. The arthritis is most commonly asymmetric and frequently involves the large weight-bearing joints (chiefly the knee and ankle); sacroiliitis or ankylosing spondylitis is observed in at least 20% of patients, especially after frequent recurrences. The mucocutaneous lesions may include balanitis, stomatitis, and keratoderma blenorrhagicum, resembling pustular psoriasis with involvement of the skin and nails. Carditis and aortic regurgitation may occur. While most signs of the disease disappear within days or weeks, the arthritis may persist for several months or even years. The test for HLA-B27 is positive in 80% of white patients, but these percentages are 20-30% lower in blacks. (See p 505 for further discussion of HLA-B27.) Characteristically, the initial attack is self-limited and terminates spontaneously.

    Recurrences involving any combination of the clinical manifestations are common and are sometimes followed by permanent sequelae, especially in the joints. 'X-ray signs of permanent or progressive joint disease may be seen in the sacroiliac as well as the peripheral joints.

    Reiter's syndrome must be distinguished from gonococcal arthritis, especially when conjunctivitis has been mild or overlooked. Rheumatoid arthritis, idiopathic ankylosing spondylitis, and psoriatic arthritis must also be considered.

    Treatment is symptomatic. Antibiotics are ineffective. As in psoriatic arthritis, the most useful agents are the nonsteroidal anti-inflammatory agents.
  5. Rider.

    Rider. Guest

    Q.ABBEY ESTENDER FLAP IS BASED ON?

    A.LINGUAL ARTEY
    B.LABIAL ARTEY
    C.FACIAL ARTERY
    D.INTERNAL MAXILLARY ARTERY

    Ans is B.LABIAL ARTEY

    Abbe lip switch
    If the defect is between 1/3 and 2/3 the length of the lip it can be closed by an Abbe flap. The flap was developed by the American plastic surgeon Robert Abbe. It is based on a main artery of the orbicularis oris, the labial artery. A portion of the uninvolved lip (either upper or lower) is rotated across the mouth and into the defect of the involved lip while maintaining the blood supply from the labial artery. After 10-14 days, the blood supply of the flap has been established to the point where the artery can be divided. The Abbe flap has an excellent cosmetic result when it is used to replace the entire philtrum of the upper lip. The technique can also be used when the defect involves the commissure. This is called an Abbe-Estlander flap. This repair takes two surgeries and requires good planning to assure continuity of the vermillion border.

    For defects greater than half the central lip, an Abbe flap will give the best result, however, the remainder of the central lip should be excised.

    The Abbe flap is based on the labial artery and harvested from the central lower lip. For central upper defects, it is elevated to the labiomental fold. For lateral defects, it continues through the chin pad. It is inset above the columella base with extensions to the nasal sill. The flap is divided and inset at two weeks
  6. Rider.

    Rider. Guest

    Q. PACS in medical imaging stands for ?

    1.Portal archiving common system
    2.planning archiving communication scheme
    3.picture archiving communication system.
    4.Photo archiving computerised system.

    ANS IS 3.picture archiving communication system.

    In medical imaging, picture archiving and communication systems (PACS) are computers or networks dedicated to the storage, retrieval, distribution and presentation of images. The medical images are stored in an independent format. The most common format for image storage is DICOM (Digital Imaging and Communications in Medicine).

    Types of images
    Most PACSs handle images from various medical imaging instruments, including ultrasound, magnetic resonance, PET, computed tomography, endoscopy, mammograms, etc

    Uses
    PACS replaces hard-copy based means of managing medical images, such as film archives. It expands on the possibilities of such conventional systems by providing capabilities of off-site viewing and reporting (distance education, telediagnosis). Additionally, it enables practitioners at various physical locations to access the same information simultaneously, (teleradiology). With the decreasing price of digital storage, PACSs provide a growing cost and space advantage over film archives.
    A PACS allows to store volumic exams and to reconstruct 3D images

    PACS is offered by virtually all the major medical imaging equipment manufacturers, medical IT companies and many independent software companies.
    The most difficult area for PACS is interpreting the DICOM image format. DICOM has enough latitude to allow various vendors of medical imaging equipment to create DICOM compliant and uncompliant files that differ in the internal tags used to label the data and the metadata. A feature common to most PACS is to read the metadata from all the images into a central database. This allows the PACS user to retrieve all images with a common feature no matter the originating instrument. The differences between vendors' DICOM implementations make this a difficult task.
  7. Rider.

    Rider. Guest

    Q. Irresistable sexual desire in a male is otherwise known as?

    A.Nymphomania
    B.Tribadism
    C.Satyriasis
    D.Sadism

    Ans is C.Satyriasis

    Hypersexuality is desire to engage in human sexual behavior at a level high enough to be considered clinically significant. Hypersexuality is characterized by a debilitating need for frequent genital stimulation which, once achieved, may fail to result in the expected long-term sexual—or emotional—satisfaction. This dissatisfaction is what is believed to encourage the heightened frequency of sexual stimulation, as well as additional physiological and neurological symptoms.
    The concept of hypersexuality replaces the older concepts of nymphomania (or furor uterinus) and satyriasis. Nymphomania was believed to be a female psychological disorder characterized by an overactive libido and an obsession with sex. In males the disorder was called satyriasis (for etymology of the words, see nymph and satyr). "Nymphomania" and "satyriasis" are no longer listed as specific disorders in the DSM-IV, though they remain a part of ICD-10.
  8. Rider.

    Rider. Guest

    Q.siadh is caused by a/E?

    a)vincristine
    b)vinblastine
    c)actinomycin d
    d)cclophophamide

    ans is c)actinomycin d
    SIADH

    Definition: AVP excess associated with hyponatremia without edema or hypovolemia. The AVP excess is inappropriate in the face of hypoosmolality.

    Ectopic secretion of AVP has been documented from neoplasms and pulmonary tissue. Intracranial lesions likely stimulate AVP release from the neurohypophysis, as do some drugs (e.g. chlorpropamide, vincristine, carbamazepine). Other medications (e.g. chlorpropamide, NSAIDS) potentiate the antidiuretic action of secreted AVP. Hypothalamic SIADH likely involves the baro (volume) receptor system, with a lesion of this system in the chest or CNS resulting in decreased tonic inhibition of magnocellular neuron AVP release.


    CAUSES of SIADH BY PROBABLE MAJOR MECHANISM OF ACTION
    Increased hypothalmic production of ADH
    A. Neuropsychiatric disorders*
    1. Infections: meningitis (tuberculous or bacterial), encephalitis, abscess, Herpes zoster
    2. Vascular: thrombosis, subarachnoid or subdural hemorrhage, temporal arteritis, cavernous sinus thrombosis, cerebrovascular accident
    3. Neoplasm: primary or metastatic
    4. Skull fracture, head injury
    5. Psychosis, delirium tremens
    6. Other: Guillain-Barré syndrome, acute intermittent porphyria, autonomic neuropathy, hypothalamic sarcoidosis, postpituitary surgery, multiple sclerosis, epilepsy, hydrocephalus, lupus erythematosus, Shy-Drager syndrome, peripheral neuropathy, spinal cord lesions


    B. Drugs
    1. Intravenous cyclophosphamide* (increased sensitivity may also contribute)
    2. Carbamazepine (though increased sensitivity is probably important). Hyponatremia is more common with oxcarbazepine.
    3. Vincristine or vinblastine
    4. Thiothixene
    5. Thioridazine, other phenothiazines
    6. Haloperidol
    7. Amitriptyline, other tricyclic antidepressants or serotonin-reuptake inhibitors
    8. Monoamine oxidase inhibitors
    9. Bromocriptine
    10. Lorcainide
    11. Clofibrate
    12. General anesthesia
    13. Narcotics, opiate derivatives
    14. Nicotine

    C. Pulmonary disease
    1. Pneumonia*: viral, bacterial, fungal
    2. Tuberculosis
    3. Lung abscess, empyema
    4. Acute respiratory failure
    5. Positive pressure ventilation (via inhibition of low-pressure cardiopulmonary baroreceptors)
    6. Other: asthma, COPD, atelactasis, pneumothorax, cystic fibrosis

    D. Postoperative patient*
    E. Severe nausea
    F. Pain
    G. Infection with HIV
    H. Idiopathic
    Ectopic (nonhypothalamic) production of ADH
    A. Carcinoma: Small cell carcinoma of lung* (2/3 of patients with small cell have impaired water excretion), bronchogenic, duodenum, pancreas, thymus, olfactory neuroblastoma, bladder, prostate, uterus
    B. Lymphosarcoma, reticulum cell sarcoma, mesothelioma, Ewing sarcoma
    C. Hodgkin's disease, leukemia
    D. Pulmonary tuberculosis (?)
    Potentiation of ADH effect
    A. Chlorpropamide*
    B. Carbamazepine
    C. Psychosis
    D. Intravenous cyclophosphamide
    E. Tolbutamide
    F. Prostaglandin-synthesis inhibitors (salicylates, NSAIDS)
    Exogenous administration of ADH
    A. Vasopressin, desmopressin
    B. Oxytocin
    Possible production of another antidiuretic compound (or increased sensitivity to very low levels of ADH)
    A. Prolactinoma
    B. Waldenstrom's macroglobulinemia
  9. Rider.

    Rider. Guest

    Q. True about telecanthus is ?

    a. increase in intercanthal distance with normal inter papillary distance
    b. widely separated medial wall of orbits
    c.
    ?
    d.?

    ans is a. increase in intercanthal distance with normal inter papillary distance

    help needed to complete othr options

    telecanthus :Abnormally increased distance between the medial canthi of the eyelids.

    option B iS CALLED HYPERTELORISAM
    Hypertelorism is an abnormally increased distance between two organs or bodily parts, usually referring to an increased distance between the eyes (orbital hypertelorism=separated medial wall of orbits), seen in a variety of syndromes, including Basal Cell Nevus syndrome, DiGeorge syndrome and Loeys-Dietz syndrome.
    Hypertelorism can also be seen in Waardenburg syndrome, LEOPARD Syndrome and Cri du chat syndrome. Along with Piebaldism, prominent inner third of the eyebrows, irides of different colour and deafness.
  10. Rider.

    Rider. Guest

    1. A DNA vector comprising a linearized double stranded DNA molecule with a single unpaired nucleotide overhang at at least one 3' end thereof, the single overhanging nucleotide being selected from the group consisting of a uracil residue and an inosine residue.

    2. A vector as claimed in claim 1 wherein the single overhanging nucleotide is a uracil residue.

    3. A vector as claimed in claim 1 wherein the single overhanging nucleotide is an inosine residue.

    4. A vector as claimed in claim 1 wherein there is a single overhanging nucleotide at each end of the DNA molecule.

    5. A kit for the direct cloning of PCR products comprising

    an aliquot of a DNA vector comprising a linearized double stranded DNA molecule with a single unpaired nucleotide overhang at each 3' end thereof, the single overhanging nucleotide being selected from the group consisting of a uracil residue and an inosine residue; and

    an aliquot of a DNA ligase which catalyzes ligation between the DNA vector and PCR products.


    6. A kit as claimed in claim 5 wherein there is a single overhanging nucleotide at each end of the DNA vector.

    7. A kit for the direct cloning of PCR products comprising

    an aliquot of a DNA vector comprising a linearized double stranded DNA molecule with a single unpaired nucleotide overhang at at least one 3' end thereof, the single overhanging nucleotide being selected from the group consisting of a uracil residue and an inosine residue; and

    an aliquot of competent cells which hosts the vector for replication once a PCR product has been ligated into the vector.


    8. A kit as claimed in claim 7 wherein there is a single overhanging nucleotide at each end of the DNA vector.

    9. A method of direct cloning of PCR products for a target DNA sequence comprising the steps of

    performing a polymerase chain reaction procedure to amplify copies of a target DNA sequence producing a plurality of PCR products with single nucleotide overhangs at each end thereof;

    forming a ligation mixture including the PCR products and a linear DNA vector having a single unpaired nucleotide overhang at at least one 3' end thereof, the single overhanging nucleotide being selected from the group consisting of a uracil residue and an inosine residue, the ligation mixture being under conditions favoring ligation of the PCR products not the DNA vector; and

    transforming the ligated vector into a competent host.


    10. The method of claim 9 wherein the single nucleotide overhang is a uracil nucleotide.

    11. The method of claim 9 wherein the single nucleotide overhang is an inosine nucleotide.

    12. The method of claim 9 wherein there is a single nucleotide overhanging at each end of the DNA vector.

    Description:

    BACKGROUND OF THE INVENTION

    There has been much technical development in recent years on methods for manipulating and copying DNA molecules for use in modern techniques of molecular biology and genetic engineering. A reaction known as the polymerase chain reaction, or PCR, described in U.S. Pat. Nos. 4,683,195 and 4,683,202, has become a standard laboratory method for reproducing, or amplifying, copies of a DNA molecule either from an in vitro product or from a native DNA sequence isolated from a living organism. A variety of methods have been developed for cloning the products of PCR amplification into a plasmid vector for the purposes of making large quantities of DNA analysis, or to express DNA as RNA or protein products by other in vitro and in vivo methods.

    One common method for the cloning of the products of PCR reactions involves the use of circular plasmids which can be cut to produce DNA fragments with ends having single 3' dTMP overhangs. A single dAMP overhang present on the DNA insert can be conveniently ligated into a vector having complementary single dTMP overhangs. These so-called "T-vectors" are formed from two closely spaced sequences that are recognized by a specific restriction enzyme that cleaves the plasmid DNA to leave a single 3' dTMP overhang on each end of the linearized vector following cleavage. The use and construction of such a vector is described in U.S. Pat. No. 5,487,993. The T-vector is intended to take advantage of a phenomenon associated with some of the DNA polymerases that are used in the PCR process. For example, a popularly used DNA polymerase, Taq DNA polymerase, often leaves a single unpaired dAMP residue at each end of the DNA molecules which are the product of the PCR reaction. However, the propensity of Taq DNA polymerase to add single 3' dAMP extensions varies with the composition of the 3' ends of the PCR products, the PCR conditions, and the conditions under which the completed reactions are stored (Hu, DNA Cell Biol. 12, 763 (1993); Magnuson et al., BioTechniques 21, 700, (1996)). For example, the presence of a dAMP residue at the 3' end of a duplex is inhibitory to dAMP addition (presumably leaving a blunt end), and other bases such as dCMP, dGMP or dTMP can be preferentially added to ends having specific sequences. Therefore, under many conditions the fraction of PCR products that possess single 3' dAMP extensions on both ends can be relatively low. Therefore, vectors which have only a single 3' dTMP overhang cannot efficiently ligate with these other fragments. Also, while the theoretical cloning efficiency of a single T overhang and a single A overhang is high, practical cloning efficiencies are sometimes lower, and there can be high numbers of false positives arising from vector religation, due to damage of the DNA ends caused by exonuclease contamination of the restriction enzyme, or religation of the small vector fragment produced by restriction enzyme cleavage instead of the PCR product.

    There are other methods for preparing T vectors including the addition of single dideoxy TMP residues at each end of a blunt and linearized plasmid using terminal transferase Holton & Graham, Nucleic Acids Res. 19:1156 (1991), or the addition of linkers containing a single unpaired dTMP residue to a linearized plasmid. However, no method has been described for the preparation of vectors having bases other than dTMP as the single 3' overhang.

    Technology generally desires cloning vectors which optimize or improve efficiency over other vectors then currently available.

    BRIEF SUMMARY OF THE INVENTION

    The present invention is summarized in that a vector for use in the direct cloning of DNA fragments contains at at least one end thereof an overhang of a single nucleotide, the nucleotide being a nucleotide which does not normally occur in DNA, such as a uracil or an inosine residue. The resulting single overhang vector can conveniently be used for the direct cloning of the products of PCR reactions in a convenient and useful manner.

    It is another object of the present invention to describe a method for cloning the direct products of PCR reaction using linearized vectors having a single overhang of non-natively occurring nucleotides, including uracil and inosine.

    It is another object of the present invention to allow the construction of vectors having one or two single nucleotide overhangs in order to selectively clone particular PCR products.

    It is a feature of the present invention that the cloning vectors created with single overhangs, including non-naturally occurring DNA nucleotides, have the inherent characteristic of binding to a wider range of PCR reaction products single nucleotide overhangs than previously available vectors having only a single T overhang.

    Other objects, advantages and features of the present invention will become apparent from the following specification.

    DETAILED DESCRIPTION OF THE INVENTION

    In accordance with the present invention a cloning vector is described in which there is a single nucleotide overhang at the 3' end of each end of the vector. The single nucleotide overhang is of a nucleotide which does not occur normally in DNA, the preferable nucleotides being uracil (U) and inosine (I). Uracil and inosine are both naturally occurring nucleotides, uracil being incorporated in both mRNA and tRNA and inosine also being present in tRNA. Uracil forms hydrogen bonds with adenine (A) while inosine preferentially binds to cytosine (C). This cloning plasmid can be readily used for the direct cloning of the products of polymerase chain reaction (PCR) protocols which normally contain a complementary single nucleotide overhang on those products. The vectors described in this patent application are intended to be an extension of, and an improvement upon, the vectors having a single T overhang as described in U.S. Pat. No. 5,487,993, the specification of which is hereby incorporated by reference.

    The vectors of the present invention extend the capability of in vitro methods of cloning PCR reaction products, and vector preparation, to incorporate nucleotide residues that do not naturally occur in native DNA. These vectors improve the cloning of DNA fragments tailed with single dAMP overhangs. The use of dUMP in place of dTMP as the single end overhang at each end of the vector allows for the potential of more efficient cloning of dTMP-containing inserts since at least for RNA to DNA interactions, the hydrogen bond formed between the nucleotides A and U is stronger than that between the nucleotides T and A. More importantly the use of single nucleotide overhanging additions other than dTMP, such as dIMP, provides the ability to clone fragments containing extensions other than dAMP on the reaction products of the PCR protocol. dIMP can in theory base pair with multiple residues, but practical experience to date suggests dIMP has a practical preference for annealing with dCMP. Virtually any nucleotide that can be synthesized and incorporated into a DNA chain can serve as the 3' extended base allowing for improvements in cloning efficiency and versatility as other nucleotide modifications are developed. It thus becomes possible to clone a variety of species found in a PCR reaction product mix with greater efficiency and selectability than it was heretofore possible.

    In general, the cloning vectors of the present invention will be created by making a blunt ended cloning vector and then adding to each end of the blunt end a single 3' nucleotide overhang. Circular DNA vectors are commonly blunt-ended by digestion with restriction enzymes which have a cutting site leaving a blunt end, such as EcoRV or SmaI. The blunt ended vector can be incubated in a reaction mixture with only the nucleotide sought to be added (e.g., dUTP or dITP), in the presence of an enzyme, such as Taq or Tth DNA polymerases, each of which will add a single nucleotide overhang to a blunt ended double stranded DNA segment.

    An alternative strategy for the products of some PCR reactions is to construct a vector having one blunt end and a single U or I overhang at the other end. A vector of this variation is particularly useful for cloning of PCR products which have a single A overhang only at one of their ends. Since the addition of the dAMP overhang to a PCR product by Taq DNA polymerase, for instance, is dependent to some degree on the DNA sequence of the PCR product, it is not uncommon for a significant fraction of such products to have an overhang only at one end. To make such a single end single overhang vector, one could begin with a vector which is linearized with a restriction enzyme, such as ECORV, which produces blunt ends. Then the single uracil or inosine residue can be added to both ends of the linear vector. Following that, digestion with another blunt-ending endonuclease, such as SmaI, could cleave the vector closely adjacent to only one end to leave one blunt end and one single overhand end. This variation has the advantage of directionality, i.e., the PCR product will ligate into the vector in only one orientation. For this reason, it may be desirable to design PCR primers so as to encourage the production of PCR products which have a single A overhang only at one end, while the other end is blunt. This can be conveniently done by designing the PCR primers so that one primer includes a sequence which discourages the addition of a dAMP (e.g. 5'-TCAGGG . . . ) while the other primer includes a sequence favoring dAMP addition (e.g. 5'-GTTTCTT . . . ). Thus direct directional cloning of PCR products becomes practical.

    The cloning vector constructed in accordance with the present invention may also have any of the many other components commonly carried on cloning and expression vectors. Such components may include a selectible marker such as for antibiotic resistance. The vector should also have an origin of replication to permit high copy number replication in commonly used host cells. Such cloning vectors also usually include a plurality of restriction sites forming a polylinker or multiple cloning site, located adjacent to each side of the single nucleotide overhang to allow easy subcloning of the fragments into other vectors or for the addition of promoters for expression. The vector may also include a bacteriophage origin of replication to allow production of single stranded copies of the recombinant vector for use in, among other things, sequencing procedures. The vector may also include a gene spanning the cloning site which creates an easily detectible phenotype to allow for selection of inserts, such as for example the LacZα gene which is used to span a cloning site to allow for convenient blue-white color screening for recombinant vectors which include an insert at the site within the LacZα gene. Another feature which can be included in such a vector is a positive selection sequence which permits survival of recombinants which disrupt a lethal gene.

    The vector in accordance with the present invention can be sold separately or as part of a cloning kit. The vector would typically be a linearized piece of DNA with the single U or I nucleotide overhang at each 3' end thereof. The vector can be sold with competent host cells with a suitable genotype and which are competent for transformation. The vector may also be sold with an aliquot of a DNA ligase enzyme and buffers which may be conveniently used to ligate PCR amplification products into the vector. A kit including the vector might also include nuclease free water or control inserts with mononucleotide overhangs to check procedures for using the vector. Lastly, the kit may also include a supercoiled plasmid used as a transformation control.

    EXAMPLE

    A Comparison of U and I-Vectors with T-Vectors

    To test the utility of the invention for cloning DNA fragments, vectors were prepared which contained either single 3' dUMP (U-Vector) or dIMP (I-Vector) residues. These vectors were tested by ligating synthetic DNA molecules containing eac of the four naturally occurring nucleotides as single 3' extensions (i.e. dAMP, dTMP, dCMP or dGMP) and transforming the ligation mixtures into competent E. coli cells. The resulting colonies were screened for the presence of inserts.

    1. Method of U-Vector and I-Vector Preparation

    Both the U and I-Vectors were prepared from pT7Blue (Novagen) using the procedures contained in the manufacturer's documentation, using a modification of the Taq DNA polymerase method described by Marchuk et al. (Nucleic Acids Res. 19, 1154 (1991)) for T-vectors.

    2. I-Vector, U-Vector Versus T-Vector Comparison

    A current lot of Novagen's pT7Blue T-Vector was compared with the U and I-Vectors. The vectors were ligated in separate reactions to four synthetic 50 base pair inserts (annealed HPLC purified oligos) which possessed either single 3'-A, 3'-T, 3'-G or 3'-C overhangs respectively at each end. A 212 bp PCR product containing single 3' A overhangs was also tested for cloning in the case of the U-vector. The ligation reaction was transformed into NovaBlue competent cells (Novagen) and the resulting colonies screened by the blue/white method on X-gal/IPTG plates as described in Novagen's published T-Vector protocol. Note that 5 μl of the final transformation reaction were plated for the 50 bp inserts and 10 μl plated for the 212 bp PCR insert. Selected blue or white colonies were then subjected to colony PCR analysis (Gussow & Clackson. Nucleic Acids Res. 17, 4000 (1989)) and/or sequenced to detect the presence of inserts. The results are summarized below.
  11. Sanjay.

    Sanjay. Guest

    long acting b2 adrenoreceptor agonist-salmeterol


    Long acting beta-adrenoceptor agonist
    From Wikipedia, the free encyclopedia
    • Find out more about navigating Wikipedia and finding information •
    Jump to: navigation, search

    Long acting beta-adrenoceptor agonists are usually prescribed for moderate to severe persistent asthma patients or patients with COPD. They are designed to replace the shorter acting B2-agonists such as salbutamol, as they have a duration of action of approximately 12 hours in comparison with the 4-6 hour duration of salbutamol, making them ideal candidates for twice-daily administration.

    Some currently available long acting beta-adrenoceptor agonists are:

    * Salmeterol
    * Formoterol
    * Bambuterol

    Studies are currently underway into ultra long acting beta-adrenoceptor agonists which would have duratoin of action of 24 hours allowing for once daily dosing:[1]

    * Indacaterol

    [edit] Footnotes

    1. ^ Cazzola M, Matera MG, Lötvall J (July 2005). "Ultra long-acting beta 2-agonists in development for asthma and chronic obstructive pulmonary disease". Expert Opin Investig Drugs 14 (7): 775–83. doi:10.1517/13543784.14.7.775. PMID 16022567.

    Tablets This Pharmacology -related article is a stub. You can help Wikipedia by expanding it.
    [hide]
    v • d • e
    Drugs for obstructive airway diseases: asthma/COPD (R03)
    Adrenergics, inhalants
    Short acting β2-agonists: Salbutamol/Levosalbutamol • Fenoterol • Terbutaline • Pirbuterol • Procaterol • Bitolterol • Rimiterol • Carbuterol • Tulobuterol • Reproterol
    Long acting β2-agonists (LABA): Arformoterol • Bambuterol • Clenbuterol • Formoterol • Salmeterol Ultra LABA: Indacaterol
    other: Epinephrine • Isoprenaline (Isoproterenol) • Orciprenaline (Metaproterenol)
    Glucocorticoids
    Beclometasone • Budesonide • Ciclesonide • Fluticasone • Mometasone
    Anticholinergics
    Ipratropium • Tiotropium
    Mast cell stabilizers
    Cromoglicate • Nedocromil
    Xanthines
    Aminophylline • Theobromine • Theophylline
    Leukotriene antagonists
    Montelukast • Pranlukast • Zafirlukast
    Lipoxygenase inhibitor
    Zileuton
  12. Sanjay.

    Sanjay. Guest

    Q. CELL wall synthesis is inhibited by

    a)lomefloxacin
    b)cephalosporin
    c)tetracycline


    ans-b


    How Antibiotics Work--the Mechanism of Action

    Aminoglycosides: Inhibit protein synthesis by binding to a portion of the bacterial ribosome. Most of them are bacteriocidal (i.e., cause bacterial cell death).

    Bacitracin: Inhibits cell wall production by blocking the step in the process (recycling of the membrane lipid carrier) which is needed to add on new cell wall subunits.

    Beta-lactam antibiotics: A name for the group of antibiotics which contain a specific chemical structure (i.e., a beta-lactam ring). This includes penicillins, cephalosporins, carbapenems and monobactams.

    Cephalosporins: Similar to penicillins in their mode of action but they treat a broader range of bacterial infections. They have structural similarities to penicillins and many people with allergies to penicillins also have allergic reactions to cephalosporins.

    Chloramphenicol: Inhibits protein synthesis by binding to a subunit of bacterial ribosomes (50S).

    Glycopeptides (e.g., vancomycin): Interferes with cell wall development by blocking the attachment of new cell wall subunits (muramyl pentapeptides).

    Macrolides (e.g., erythromycin) and Lincosamides (e.g., clindamycin): Inhibit protein synthesis by binding to a subunit of the bacterial ribosome (50S).

    Penicillins: Inhibits formation of the bacterial cell wall by blocking cross-linking of the cell wall structure. The cell wall is a needed protective casing for the bacterial cell.

    Quinolones: Blocks DNA synthesis by inhibiting one of the enzymes (DNA gyrase) needed in this process.

    Rifampin: Inhibits RNA synthesis by inhibiting one of the enzymes (DNA-dependent RNA polymerase) needed in this process. RNA is needed to make proteins.

    Tetracyclines: Inhibit protein synthesis by binding to the subunit of the bacterial ribosome (30S subunit).

    Trimethoprim and Sulfonamides: Blocks cell metabolism by inhibiting enzymes which are needed in the biosynthesis of folic acid which is a necessary cell compound.
  13. Sanjay.

    Sanjay. Guest

    Q. LHERMITTE DUCLOS DISEASE TRUE IS

    1.Thickened cerebeller follia. (ANS)
    2.Atrophic cerebeller folli.
    3.Vermian hypoplasia.
    4.peri--- septum agenesis


    The clinical course in our cases is in accordance with other published cases of LDD (2, 3). LDD is classified as WHO grade I (4), but has the propensity to progress or to recur after surgery. Although rare associations between LDD and other brain tumors have been reported (5, 6), until now, an association between LDD in CS with PNH as found in case 1 has never been described. PNH represents either clusters of neurons demonstrating an arrested migration, or a failure of genetically determined cell death in collections of neuroblasts within the periventricular germinal matrix (7). In the migratory disorder of tuberous sclerosis, PNH is a prominent component, but may also occur as an isolated defect in otherwise normal brains (8). CS, with its several neurologic and cutaneous symptoms, shares features with other phakomatoses, eg, tuberous sclerosis. Sequencing of exon 9 revealed a base exchange A-G in the highly conserved position 2 of the splice acceptor site, a new kind of mutation that has been never described before in CS (1).
    Conventional MR findings and the possible differential diagnoses in our cases are in accordance with other published cases of LDD (2, 3). A non-enhancing mass in the posterior fossa with unilateral hemispheric expansion, hypointense on T1-weighted images and hyperintense on T2-weighted images, with parallel linear striations on the surface of the lesion, should be considered specific for LDD in a middle-aged adult. The morphologic features of the LDD could be demonstrated most clearly with the TIR sequence and the turbo inversion-recovery magnitude (TIRM) sequence. Areas of calcifications, as found in case 1, could be equally well depicted on T2*-weighted images; therefore, a CT scan is not necessary.
    Owing to the T2 effect, the abnormally thickened folia in the LDD were characterized by slightly higher signal intensities on diffusion-weighted images with low b factors than with high b factors, whereas ADC mapping showed no disturbance of water diffusion. The signal on diffusion-weighted images and ADC maps depends on cell density, low extracellular water content, and enhancement of the tumor (9). Profusion of dysplastic cortical neurons in LDD, a thickening of the molecular layer, the loss of Purkinje cells, and thinning of medullary white matter may be responsible for findings on diffusion-weighted images. Comparable to the TIRM sequence, diffusion-weighted imaging, especially ADC mapping, is helpful in postoperative control because it delineates tumor from surgical resection margins, whereas on T2-weighted images, differentiation between both components seems to be more difficult (see case 1).
    Contrast enhancement is not a typical sign of LDD (10). If contrast enhancement is present, other diagnoses, such as (capillary) hemangioblastoma, might be suggested. Hemangioblastomas commonly have enlarged vessels, solid and cystic components, and no striations. There was no contrast enhancement in our cases on MR images, whereas perfusion-weighted imaging in case 1 and xenon CT in case 2 showed increased rCBV and rCBF within the lesion. Siegal et al (11) used relative CBV mapping for routine evaluation of patients with different brain tumors and assumed that regional CBV mapping correlates with active tumor components. We assume that hyperperfusion without enhancement correlates closely to the histopathologic observation of numerous dilated thin-walled blood vessels (9) and generalized proliferation of blood vessels within LDD (4) (Fig 1C). Proliferation of blood vessels per se is not a sign of malignancy. These histologic findings are comparable to some pilozytic astrocytomas or vascularized meningiomas that are WHO grade I (4), but these tumors show contrast enhancement.
    In the examination of intracranial tumors, 201-Tl SPECT may help to differentiate between malignant (high uptake) and benign gliomas (low uptake) (13). Tl-201 is a potassium analogue, and its uptake by tumors is thought to reflect regional blood flow, a defective blood-brain barrier, and cellular uptake via Na+-K+adenosine triphosphatase (ATPase) on the cell membrane. High uptake of 201-Tl also occurs in hypervascular benign tumors, such as meningiomas. In our cases, LDD showed significant uptake of 201-Tl on SPECT scans in relation to histopathologic findings and to perfusion measurements owing to regional increased blood flow rather than dysfunction of ATPase in the diffuse, cortical, accumulated, abnormally large, dysplastic granular cells. Therefore, our findings of high uptake on 201-Tl SPECT scans are in accordance with findings in other low-grade vascularized tumors of the brain (13).
    High FDG uptake, usually indicating malignancy, is misleading in the presented cases. Whether the increased 18-FDG accumulation within the lesion is due to increased overall cell metabolism or reflects an isolated upregulation in enzyme activity of hexokinase remains unclear. In light of histopathologic findings in LDD, characterizing the lesions as hamartomatous overgrowth with double-layered structures comprising a layer with increased density of dysplastic granular cells, the increased 18-FDG uptake may simply reflect the focally increased cell density and/or a different glucose metabolism of these dysplastic cells.
    LDD has some characteristics of tumors, such as decreased NAA and increased lactate, but not increased levels of lipids. On the other hand, decreased Cho/Cr (and myo-inositol/Cr) ratios are in strict contrast to observations in cerebral tumors, where increases of Cho (and myo-inositol) levels are associated with enhanced membrane turnover and demyelination. Verheggen et al (14) showed a decreased Cho/Cr ratio in one case of a bilateral LDD (Fig 3) and concluded that this finding was in strict contrast to observations in cerebral tumors. Lactate, normally undetectable in brain, accumulates in cysts, necrotic tissue, or within active tumors because of the high rate of glycolysis (glucose to lactate) within tumors of all types, including aerobic tumors. Together with the hypermetabolism found in FDG-PET, we assume that the elevated lactate level is due to an abnormal high glucose metabolism (glycolysis) within the LDD, rather than representing high lactate levels in cystic or necrotic components of LDD. Furthermore, in one case of LDD, we found an elevated level of alanine, an alternative reduced partner of pyruvate derived from glycolysis. The normal level of lipids and the histopathologic findings of no necrotic areas within the LDD support our thesis that elevated lactate levels do not represent cell death. Therefore, our results of MRS in LDD are, in part, in contrast to those reported by Verheggen et al (14), which showed no changes in lactate levels (Fig 3).
  14. Sanjay.

    Sanjay. Guest

    Q. All are tumor supressor genes except

    a- WT1
    b- NF2
    C-PTEn
    d- RAS

    ans : RAS

    Examples
    The first tumor suppressor protein discovered was the pRb protein in human retinoblastoma; however, recent evidence has also implicated pRb as a tumor survival factor.

    Another important tumor suppressor is the p53 tumor suppressor protein produced by the TP53 gene. Homozygous loss of p53 is found in 70% of colon cancers, 30 -50% of breast cancers & 50% of lung cancers. Also mutation of p53 have been found in leukemias, lymphomas, sarcomas and neurogenic tumors.It is clear that p53 is just one component of a network of events that lead to tumor formation. Abnormalities of the p53 gene are sometimes inherited, such as in the Li-Fraumeni syndrome (LFS). People with LFS have a higher risk for developing a number of cancers, including soft-tissue and bone sarcomas, brain tumors, breast cancer, adrenal gland cancer, and leukemia.

    PTEN acts by opposing the action of PI3K, which is essential for anti-apoptotic, pro-tumorogenic Akt activation.

    Other examples of Tumour Suppressors include APC and CD95.
  15. Sanjay.

    Sanjay. Guest

    Q. Most common cause of neonatal seizures:

    ans: HIE

    Neonatal seizures are abnormal electrical discharges in the CNS of neonates usually manifesting as stereotyped muscular activity or autonomic changes. Diagnosis is confirmed by EEG; testing for causative conditions is indicated. Treatment depends on cause.

    Seizures occur in up to 1.4% of term infants and 20% of premature infants. Seizures may be a serious neonatal problem and require immediate evaluation. Most neonatal seizures are focal, probably because in neonates generalization of the electrical activity is impeded by lack of myelination and incomplete formation of dendrites and synapses in the brain. Some neonates undergoing EEG for assessment of symptoms of encephalopathy (eg, hypoactivity, decreased responsiveness) are found to have clinically silent seizures (epileptiform electrical activity during an EEG but without any visible seizure activity). Occasionally, clinically silent electrical activity is continuous and persists for > 20 min; at that point, it is defined as electrical status epilepticus.

    Etiology

    The abnormal CNS electrical discharge may be caused by a primary intracranial process (eg, meningitis, ischemic stroke, encephalitis, intracranial hemorrhage, tumor) or may be secondary to a systemic problem (eg, hypoxia-ischemia, hypoglycemia, hypocalcemia, hyponatremia). Seizures resulting from an intracranial process usually cannot be differentiated from seizures resulting from a systemic problem by their clinical features (eg, focal vs generalized).

    Hypoxia-ischemia, the most common cause of neonatal seizures, may occur before, during, or after delivery. Such seizures may be severe and difficult to treat, but they tend to abate after about 3 to 4 days.
  16. Sanjay.

    Sanjay. Guest

    Q. Retinitis pigmentosa is NOT associated with?

    A.Usher syndrome
    B.kornzewig syndrome(Abetalipoprotinemia)
    C.Kearns-Sayre syndrome
    D.Marfan syndrome


    Ans is D.Marfan syndrome


    REF:parson/19th ed./p.344, http://en.wikipedia.org/wiki/Retinitis_pigmentosa

    Retinitis pigmentosa, or RP, is a group of genetic eye conditions. In the progression of symptoms for RP, night blindness generally precedes tunnel vision by years or even decades. Many people with RP do not become legally blind until their 40s or 50s and retain some sight all their life. Others go completely blind from RP, in some cases as early as childhood. Progression of RP is different in each case.
    RP is a group of inherited disorders in which abnormalities of the photoreceptors (rods and cones) or the retinal pigment epithelium (RPE) of the retina lead to progressive visual loss. Affected individuals first experience defective dark adaptation or nyctalopia (night blindness), followed by constriction of the peripheral visual field and, eventually, loss of central vision late in the course of the disease.

    Signs
    Mottling of the retinal pigment epithelium with bone-spicule pigmentation is typically pathognomonic for retinitis pigmentosa. Other ocular features include waxy pallor of the optic nerve head, attenuated retinal vessels, cellophane maculopathy, cystic macular edema, and posterior subcapsular cataract

    A few causes for RP are:• Fahr disease
    • Bardet-Biedl syndrome
    • Lowe syndrome
    • Usher's syndrome • Subacute necrotising encephalomyelopathy
    • Pyruvate carboxylase deficiency
    • MELAS
    • Hereditary sensory-motor neuropathy type 7
    • Rud's syndrome
    • Refsum's disease
    • Kearns-Sayre syndrome
    • Carbohydrate deficient glycoprotein syndrome type 1a
    • Loken Senior syndrome
    • Hallervorden-Spatz disease
    • Abetalipoproteinaemia
    • Homocarnosinase deficiency
    • Mirhosseini-Holmes-Walton syndrome
    • Shwachman-Diamond syndrome
    • HARP syndrome
    • Alström syndrome
    • Medullary cystic renal disease
    • Stargardt's disease
    • Sjogren-Larsson syndrome
    • Tapetochoroidal dystrophy


    EXTRA INFORMATION About other options
    A.Usher syndrome
    A leading cause of deaf-blindness, Usher syndrome (sometimes referred to as "Usher's syndrome") is a relatively rare genetic disorder that is associated with a mutation in any one of 10 genes. Other names for Usher syndrome include Hallgren syndrome, Usher-Hallgren syndrome, rp-dysacusis syndrome and dystrophia retinae dysacusis syndrome.[1] Usher syndrome is incurable at present; however, using gene therapy to replace the missing gene, researchers have succeeded in reversing one form of the disease in knockout mice.[2]

    This syndrome is characterized by deafness and a gradual vision loss. The hearing loss is associated with a defective inner ear, whereas the vision loss is associated with retinitis pigmentosa (rp), a degeneration of the retinal cells. Usually, the rod cells of the retina are affected first, leading to early night blindness and the gradual loss of peripheral vision. In other cases, there is early degeneration of the cone cells in the macula, leading to a loss of central acuity. In some cases, the foveal vision is spared, leading to "doughnut vision"; central and peripheral vision are intact, but there is an annulus around the central region in which vision is impaired.


    OPTION C.Kearns-Sayre syndrome
    Kearns-Sayre syndrome (abbreviated KSS) or oculocraniosomatic syndrome is a disease caused by a 5,000 base deletion in the mitochondrial DNA. As such, it is a rare genetic disease in that it can be heteroplasmic, that is, more than one genome can be in a cell at any given time. Unlike most mitochondrial diseases, it is not maternally inherited. Rather, it occurs sporadically.

    Kearnes-Sayre syndrome starts before the age of 20.
    Presentation
    Its expression is systemic, but many of the most common expressions are in the eyes, with ophthalmoplegia and retinal degeneration, specifically retinitis pigmentosa, as common features.

    Other characteristic features of KSS are dysphagia, proximal weakness, hearing loss, cerebellar ataxia and cardiac conduction defects.

    White matter lesions are usually seen


    OPTION D.Marfan syndrome
    Marfan syndrome is an autosomal dominant genetic disorder of the connective tissue characterized by disproportionately long limbs, long thin fingers, a typically tall stature, and a predisposition to cardiovascular abnormalities, specifically those affecting the heart valves and aorta. The disorder may also affect numerous other structures and organs — including the lungs, eyes, dural sac surrounding the spinal cord, and hard palate.
  17. Hitech.

    Hitech. Guest

    Q. Post ductal co arctation of aorta- all participate in collaterals except:

    a- axillary artery
    b- post intercostal artery
    c- suprascapular artery
    d-vertebral artery

    In the anterior system, the internal mammary arteries and the epigastric arteries join to form collaterals which supply the abdominal wall and the lower extremities.
    In the posterior system, the parascapular arteries connect with the intercostal arteries to form collaterals which supply the distal aortic compartment and primarily the abdominal viscera.
    The left subclavian may form collaterals through linkage to the IMA's and intercostals to give blood supply distally. The right subclavian will join with the vertebral, spinal, cervical, and scapular branches, and will eventually provide blood supply to the intercostal circuit.


    ans: ??? suprascapular?
  18. Hitech.

    Hitech. Guest

    Q. Sweating is absent in

    a- heat syncope
    b- heat exhaustion
    c- heat stroke
    d- heat ?

    ans : heat stroke

    What are heat stroke symptoms?

    Symptoms of heat stroke can sometimes mimic those of heart attack or other conditions. Sometimes a person experiences symptoms of heat exhaustion before progressing to heat strokes. Symptoms of heat exhaustion may include nausea, vomiting, fatigue, weakness, headache, muscle cramps and aches, and dizziness. However some individuals can develop symptoms of heat stroke suddenly and rapidly without warning.

    Different people may have different symptoms and signs of heat stroke. But common symptoms and signs of heat stroke include:

    high body temperature
    the absence of sweating, with hot red or flushed dry skin
    rapid pulse
    difficulty breathing
    strange behavior
    hallucinations
    confusion
    agitation
    disorientation
    seizure
    coma
  19. Hitech.

    Hitech. Guest

    Q. all are branches of cavernous segment of internal carotid artery except

    ans : ophthalmic artery

    The cavernous segment, or C4, of the internal carotid artery begins at the petrolingual ligament and extends to the proximal dural ring, which is formed by the medial and inferior periosteum of the anterior clinoid process. The cavernous segment is surrounded by the cavernous sinus.

    In this part of its course, the artery is situated between the layers of the dura mater forming the cavernous sinus, but covered by the lining membrane of the sinus. It at first ascends toward the posterior clinoid process, then passes forward by the side of the body of the sphenoid bone, and again curves upward on the medial side of the anterior clinoid process, and perforates the dura mater forming the roof of the sinus. This portion of the artery is surrounded by filaments of the sympathetic trunk, and on its lateral side is the abducent nerve, or cranial nerve VI.

    The named branches of the cavernous segment are:

    the meningohypophyseal artery
    the inferolateral trunk
    The cavernous segment also gives rise to small capsular arteries that supply the wall of the cavernous sinus.

    The ophthalmic segment, or C6, extends from the distal dural ring, which is continuous with the falciform ligament, and extends distally to the origin of the posterior communicating artery. The ophthalmic segment courses roughly horizontally, parallel to the optic nerve which runs superomedially to the carotid at this point.

    The named branches of the ophthalmic segment are:

    the ophthalmic artery
    the superior hypophyseal artery
  20. Hitech.

    Hitech. Guest

    Q. Acoustic neuroma gold standard for diagnosis

    ans : MRI

    Magnetic resonance imaging (MRI) is the preferred diagnostic test for identifying acoustic neuromas.

    Other tests used to diagnose acoustic neuroma and to differentiate it from other causes of dizziness or vertigo include:

    Computed tomography (CT) scan of the head
    Audiology (a test for hearing)
    Caloric stimulation (a test for vertigo)
    Electronystagmography (a test of equilibrium and balance)
    Brain stem auditory evoked response (BAER, a test of hearing and brain stem function)
  21. Hitech.

    Hitech. Guest

    Q. bronchoscpy is used to visualise all the following EXCEPT

    a)carinal node
    b)bronchi
    c)larynx
    d)----

    ans-????

    What is bronchoscopy?

    Bronchoscopy is a procedure during which an examiner uses a viewing tube to evaluate a patient's lung and airways including the voice box and vocal cord, trachea, and many branches of bronchi. Bronchoscopy is usually performed by a pulmonologist or a thoracic surgeon. Although a bronchoscope does not allow for direct viewing and inspection of the lung tissue itself, samples of the lung tissue can be biopsied through the bronchoscope for examination in the laboratory.

    There are two types of bronchoscopes - a flexible fiberoptic bronchoscope and a rigid bronchoscope. Since the 1960s, the fiberoptic bronchoscope has progressively supplanted the rigid bronchoscope because of overall ease of use. In some patients, flexible fiberoptic bronchoscopy can be performed without anesthesia, but in most cases, conscious sedation "twilight sleep") is utilized. However, rigid bronchoscopy requires general anesthesia and the services of an anesthesiologist. During the bronchoscopy, the examiner can see the tissues of the airways either directly by looking through the instrument or by viewing on a TV monitor.

    Depending on the indication the examiner will choose between the flexible fiber optic bronchoscope or the rigid bronchoscope. For example, if a patient were coughing up large amounts of blood, a rigid bronchoscope is used since it has a large suction channel and allows for the use of instruments that can better control bleeding. The vast majority of bronchoscopies are performed using the flexible fiberoptic scope because of the improved patient comfort and reduced use of anesthesia.
  22. Hitech.

    Hitech. Guest

    Q. A question on a lady married for a year with various complaints, 2 episodes at nite and 4 in the morning?

    ans: somatisation disorder??

    Somatisation is when physical symptoms develop through stress or emotional problems.
    Anxiety and depression can cause physical symptoms like chest pain, dizziness, diarrhoea or
    fatigue. To ‘somatise’ is very common; most people have
    experienced headaches or nausea as a result of worry or a stressful situation. These
    symptoms really exist, they are genuine and by no means could be considered imagined.

    What is Somatisation Disorder?
    Somatisation disorder (formerly known as hysteria or Briquet’s syndrome) is diagnosed when
    a person has experienced multiple physical complaints and symptoms over a long period of
    time. These symptoms cannot be identified or explained through medical examinations or
    tests. People with this disorder have a history of physical problems occurring in different
    areas of their body. They have usually approach a variety of medical practitioners in an
    attempt to find answers to the pain and distress they are experiencing. They have often
    undergone unnecessary medical procedures and tried an array of medications to no avail.
    Somatisation disorder is a very real and debilitating condition that can cause great anguish to
    the affected individual. It is often accompanied by extremes of frustration for the patient and
    doctor alike as medical understanding and procedures fail to recognise the cause and
    existence of the undeniable physical complaints under investigation.
    Somatisation disorder is classed as a somatoform disorder. The somatoform disorders listed
    in the Diagnostic and Statistical manual of Mental Disorders, Fourth Edition (DSM IV) are
    somatisation disorder, undifferentiated somatoform disorder, conversion disorder, pain
    disorder, hypochondriasis, body dysmorphic disorder and somatoform disorder not otherwise
    specified (NOS). The common feature of the somatoform disorders is unexplained physical
    symptoms that can cause the individual immense difficulties in social, occupational, or other
    areas of life.

    Some of the numerous symptoms that can occur with somatisation disorder include:
    Vomiting Pain during urination Vision changes
    Abdominal pain Headaches Paralysis or muscle weakness
    Nausea Shortness of breath Sexual apathy
    Bloating Palpitations Pain during intercourse
    Diarrhoea Chest pain Impotence
    Pain in the legs or arms Dizziness Painful menstruation
    Back pain Amnesia Irregular menstruation
    Joint pain Difficulty swallowing Excessive menstrual bleeding
  23. Deepak.

    Deepak. Guest

    Q. a 25 year old female pt., history of 6 month, loss of conc. , convulsions, abnormal movements , forgetfulness, 4 attack during day , 2 attack at night, ct normal ?

    a.epilepsy
    b.disssociative disorder
    c.somatoform
    d.somatization

    Ref:Ahuja/5th ed/p.107

    Ans c.somatoform(most probably)???????
    This patient didn't fulfill all criteria require for somatization disorder,so it can't be the ans

    Somatoform Disorders are characterized by repeted presentation with physical symptom wchich do not hv adequate physical basis & are not explained by presence of other psychatric disorders,Somatization Disorder is a type of somatoform disorder. Patients with Somatization Disorder will typically visit many doctors trying to get the treatment they think they need


    Somatoform Disorders Types
    • Somatization Disorder
    • Undifferentiated Somatoform Disorder
    • Pain disorder – appears largely to come from the patients psychological factors, it is more commonly in the older age and the ration is nearly equal 2:1,
    • Conversion disorder – is where the patient’s senses of mobility are impaired with no cause only stress being the main factor.
    • Hypochondriasis – is mostly related to the stresses that one faces in life, it is marked by fear and lack of assurance. It is now in all age groups it is no long a disorder for the grown adults nut also the adolescents and children,
    • Body dysmorphic disorder – is a disorder that affects the features on the face or head that are exaggerated.
    • Somatoform Disorder not Otherwise Specified ( NOS )

    Somatization disorder (also Briquet's disorder or, in antiquity, hysteria) is a psychiatric diagnosis applied to patients who chronically and persistently complain of varied physical symptoms that have no identifiable physical origin. One common general etiological explanation is that internal psychological conflicts are unconsciously expressed as physical signs.

    Somatization disorder is a somatoform disorder.[1] The DSM-IV establishes the following five criteria for the diagnosis of this disorder: [2]
    • a history of somatic symptoms prior to the age of 30
    • pain in at least four different sites on the body
    • two gastrointestinal problems other than pain such as vomiting or diarrhea
    • one sexual symptom such as lack of interest or erectile dysfunction
    • one pseudoneurological symptom similar to those seen in Conversion disorder such as fainting or blindness.
    Such symptoms cannot be related to any medical condition. The symptoms do not all have to be occurring at the same time, but may occur over the course of the disorder. If a medical condition is present, then the symptoms must be excessive enough to warrant a separate diagnosis. Two symptoms can not be counted for the same thing e.g.if pain during intercourse is counted as a sexual symptom it can not be counted as a pain symptom. Finally, the symptoms cannot be being feigned out of an effort to gain attention or anything else by being sick, and they can not be deliberately induced symptoms
  24. Deepak.

    Deepak. Guest

    Q. stroid receptors bind to all except?

    a-steroid recptor
    b- transcription promoters
    c- transcription repressors
    d- steroid response elements

    ans??

    Steroid hormone receptors are proteins that have a binding site for a particular steroid molecule. Their response elements are DNA sequences that are bound by the complex of the steroid bound to its receptor.

    The response element is part of the promoter of a gene. Binding by the receptor activates or represses, as the case may be, the gene controlled by that promoter.

    It is through this mechanism that steroid hormones turn genes on (or off).

    For a steroid hormone to turn gene transcription on, its receptor must:
    bind to the hormone
    bind to a second copy of itself to form a homodimer
    be in the nucleus, moving from the cytosol if necessary
    bind to its response element
    activate other transcription factors to start transcription
  25. Deepak.

    Deepak. Guest

    Q. ABOUT HUS ALL IS TRUE EXCEPT?

    A.NOT COMMONLY CAUSED BY VEROCYTOGENIC E COLI
    B.CAUSES MILD TO SEVERE COOMBS POSITIVE HEMOLYTIC ANEMIA
    C.RECUREENCES RARE
    D.TRANSIENT THROMBOCYTOPENIA

    ANS is A.NOT COMMONLY CAUSED BY VEROCYTOGENIC E COLI

    hemolytic-uremic syndrome (or haemolytic-uraemic syndrome, abbreviated HUS) is a disease characterized by microangiopathic hemolytic anemia, acute renal failure and a low platelet count (thrombocytopenia)

    Signs and symptoms
    The classic childhood case of HUS occurs after bloody diarrhea caused by E. coli O157:H7, a strain of E. coli that expresses verotoxin (also called Shiga toxin). The toxin enters the bloodstream, attaches to renal endothelium and initiates an inflammatory reaction leading to acute renal failure (ARF) and disseminated intravascular coagulation (DIC). The fibrin mesh destroys red blood cells and captures thrombocytes, leading to a decrease of both on complete blood count. The usual age of onset is between 2 and adolescence.
    HUS occurs after 2-7% of all E. coli O157:H7 infections.
    Adult HUS has similar symptoms and Pathology but is an uncommon outcome of the following: HIV; antiphospholipid syndrome (associated with Lupus erythematosus and generalized hypercoagulability); post partum renal failure; malignant hypertension; scleroderma; and cancer chemotherapy (mitomycin, cyclosporine, cisplatin and bleomycin).
    A third category is referred to as familial HUS. It represents 5-10% of HUS cases and is largely due to mutations in the complement proteins factor H, membrane cofactor protein and factor I leading to uncontrolled complement system activation. Recurrent thromboses result in a high mortality rate.
  26. Deepak.

    Deepak. Guest

    Q. A patient with chest pain ,ST depression in ....,which is not given?

    a)thrombolytic therapy
    b)aspirin
    c)Ca channel blocker
    d)beta blocker


    ans-

    During an attack of angina pectoris, 50% of patients with normal findings after resting ECG show abnormalities. A 1-mm or greater depression of the ST segment below the baseline, measured 80 milliseconds from the J point, is the most characteristic change. Reversible ST-segment elevation occurs with Prinzmetal angina. Some patients with coronary artery disease may show pseudonormalization of the resting ECG ST-T–wave abnormalities during episodes of chest pain.
  27. Deepak.

    Deepak. Guest

    Q. loading dose of drug depends on

    a)t1/2 of drug
    b)Vd of drug
    c)
    d)


    ans-volume of distribution


    Loading dose
    From Wikipedia, the free encyclopedia
    • Ten things you may not know about images on Wikipedia •
    Jump to: navigation, search

    In pharmacokinetics, a loading dose refers to an initial higher dose of a drug that may be given at the beginning of a course of treatment before dropping down to a lower maintenance dose. A loading dose is most useful for drugs that are eliminated from the body relatively slowly. Such drugs need only a low maintenance dose in order to keep the amount of the drug in the body at the appropriate level, but this also means that, without an initial higher dose, it would take a long time for the amount of the drug in the body to reach that level.

    For an example, one might consider the hypothetical drug foosporin. Suppose it has a long lifetime in the body, and only ten percent of it is cleared from the blood each day by the liver and kidneys. Suppose also that the drug works best when the total amount in the body is exactly one gram. So, the maintenance dose of foosporin is 100 milligrams (100 mg) per day—just enough to offset the amount cleared.

    Suppose a patient just started taking 100 mg of foosporin every day. On the first day, they'd have 100 mg in their system; their body would clear 10 mg, leaving 90 mg. On the second day, the patient would have 190 mg in total; their body would clear 19 mg, leaving 171 mg. On the third day, they'd be up to 271 mg total; their body would clear 27 mg, leaving 244 mg. As one can see, it would take many days for the total amount of drug within the body to come close to 1 gram (1000 mg) and achieve its full therapeutic effect.

    For a drug such as this, a doctor might prescribe a loading dose of one gram to be taken on the first day. That immediately gets the drug's concentration in the body up to the therapeutically-useful level. First day: 1000 mg; the body clears 100 mg, leaving 900 mg. On the second day, the patient takes 100 mg, bringing the level back to 1000 mg; the body clears 100 mg overnight, still leaving 900 mg, and so forth.

    Drugs which may be started with an initial loading dose include digoxin, teicoplanin, voriconazole and procainamide. Phenytoin for acute status epilepticus should also be given with an initial loading dose, co-administered with a benzodiazepine, to immediately stabilize neuronal membranes and electrical activity during a seizure.

    [edit] Calculating the loading dose

    Four variables are used to calculate the loading dose:

    Cp = desired peak concentration of drug
    Vd = volume of distribution of drug in body
    F = bioavailability
    S = salt fraction

    The required loading dose may then be calculated as

    \mbox{Loading dose} = \frac{C_p V_d}{F S}

    For an intravenously administered drug, the bioavailability F will equal 1, since the drug is directly introduced to the bloodstream. If the patient requires an oral dose, bioavailability will be less than 1 (depending upon absorption, etc.), requiring a larger loading dose.
  28. Deepak.

    Deepak. Guest

    Q. An anesthetic machinehas following mechanism to prevent hypoxic mixture except-

    a- nitrous oxide valve is below that of oxygen something
    b- pin index system
    c- oxygen concentration analyser
    d- ??

    Components of a typical machine
    A modern machine typically includes the following components:

    connections to piped hospital oxygen, medical air, and nitrous oxide. Pipeline pressure from the hospital medical gas system (wall outlet) should be around 400 kPa (60 psi; 4 atmospheres).
    reserve gas cylinders of oxygen, air, and nitrous oxide attached via a specific yoke with a Bodok seal. Older machines may have cylinder yokes and flow meters for carbon dioxide and cyclopropane. Many newer machines only have oxygen reserve cylinders. The regulators for the cylinders are set at 300 kPa (45 psi; 3 atmospheres). If the cylinders are left on and the machine is plugged into the wall outlet, gas from the wall supply will be used preferentially, since it is at a higher pressure. In situations where pipeline gases are not available, machines may safely be used from cylinders alone, provided fresh cylinders are available.
    a high-flow oxygen flush which provides pure oxygen at 30 litres/minute
    pressure gauges and regulators to protect the machine components and patient from high-pressure gases
    flow meters (rotameters) for oxygen, air, and nitrous oxide, which are used by the anaesthetist to provide accurate mixtures of medical gases to the patient. Flow meters are typically pneumatic, but increasingly electromagnetic digital flow meters are being used.
    one or more anaesthetic vaporisers to accurately add volatile anaesthetics to the fresh gas flow
    a ventilator
    physiological monitors to monitor the patient's heart rate, ECG, blood pressure and oxygen saturation (additional monitors are generally available to monitor temperature, arterial blood pressure central venous pressure, etc.). In addition, the composition of the gases delivered to the patient (and breathed out) is monitored continuously.
    breathing circuits, most commonly a circle attachment ..breathing hoses connected to a Anaesthesia face mask
    a heat and moisture exchanger (HME)
    scavenging system to remove expired anaesthetic gases from the operating room. Scavenged gases are usually vented to the atmosphere.
    suction apparatus
    There is generally a small work bench built into the machine where airway management equipment is kept within ready reach of the anaesthetist

    Safety features of modern machines

    Based on experience gained from analysis of mishaps, the modern anaesthetic machine incorporates several safety devices, including:

    an oxygen failure alarm. In older machines this was a pneumatic device called a Ritchie whistle. Newer machines have an electronic sensor.
    hypoxic-mixture alarms to prevent gas mixtures which contain less than 21% oxygen being delivered to the patient. In modern machines it is impossible to deliver 100% nitrous oxide (or any hypoxic mixture) to the patient to breathe. Oxygen is automatically added to the fresh gas flow even if the anaesthetist should attempt to deliver 100% nitrous oxide.
    ventilator alarms, which warn of disconnection or high airway pressures
    interlocks between the vaporisers preventing inadvertent administration of more than one volatile agent concurrently
    alarms on all the above physiological monitors
    the Pin Index Safety System prevents cylinders being accidentally connected to the wrong yoke
    the NIST (Non-Interchangeable Screw Thread) system for pipeline gases, which prevents piped gases from the wall being accidentally connected to the wrong inlet on the machine
    pipeline gas hoses have non-interchangeable Schrader valve connectors, which prevents hoses being accidentally plugged into the wrong wall socket
  29. Deepak.

    Deepak. Guest

    Q. Gold standard for acoustic neuroma is
    a) contrast CT
    b) contrast MRI
    c) evoked potential


    Q. Laryngocele arises from

    a) true cords
    b) anterior commissure
    c) saccule of the vestibule


    Q. corpus delicti

    a)essence of crime
    b)conduct of post mortem


    Q. most common cause of reactive arthritis
    a)n.gonorrhea
    b)s.aureus
    c)m.tuberculosis
    d).....


    Q. hair on presentation on skull
    a)thalessemia
    b)sickle cell anemia


    Q. all the following are true about alfa-fetoprotein EXCEPT

    a)half life....
    b)always increased in wilsons ds


    Q. the end codons of t-rna codes for
    a)polyalanine
    b)polycystine


    Q. splenic lymphoma

    a)hodgkin lymphoma
    b)subcortical lymphoma
    c)burkitt lymphoma
    d)????????


    Q. which of the following is true about diagnosis of ectopic pregnancy?
    a)HCG
    b) transvaginal sonography is accurate


    Q. The species of HPV associated with vulval warts
    a. HPV 16
    b. HPV 31
    c. HPV 6


    Q. PAT WITH ST depression in v1 2 v4..pain since 1 hr not give
    1 aspirin
    2 thrombolytic therapy (ANS)
    3 morphine


    Q posterior communicating artery aneurysm causing para lysis of which nucleus
    A.IIIRD
    B.IST
    C.ABDUSCENS
    D.Hyphophysis cerebri
  30. Deepak.

    Deepak. Guest

    Q. best prognosis after repair
    1.radial
    2.median
    3.sciatic
    4.common nerve


    Q. last organ to be opened in case of asphyxial death
    a)thorax
    b)abdomen
    c)head
    d)neck


    Q. CSF pressure depends on
    a)rate of production of CSF
    b)rate of absoption of CSF


    Q. drug which decreases free water clearance
    a)vincristine
    b)chlorpropamide
    c)vinblastin
    d)furosemide


    Q. drug which decreases free water clearance?
    a)vincristine
    b)chlorpropamide
    c)vinblastin
    d)furosemide

    ans???


    Q. which of the foll. is a contraindiacation for MRI?

    a) prosthetic heart valve
    b) pacemaker
    c) --------
    d) --------

    ANS is b) pacemaker ( NOTE that pacemaker in a patient is an ABSOLUTE contraindication for MRI, some other options may also fit in but none is an absolute contr. hence pacemaker is the best choice)


    Q. diabetes in pregnancy all EXCEPT

    a)50 gm of sugar given after post-meal as screening test
    b)diabetes controll before conception is imp to prevent malformation
    c)???


    Q. during rotation of the shoulder joint all of the following takes place EXCEPT
    a)rotation at sternoclavicular joint
    b)raising of humerus
    c)scapular....
    d)...............
  31. Deepak.

    Deepak. Guest

    Q. in hypoglossal nerve damage all EXCEPT
    a)tongue is atrophied
    b)taste sensation is lost


    Q. which is a short acting NDMR
    1.rapacuronium
    2.alcuronium
    3.pipecuronium
    4.sch


    Q. pulmonary edema
    a)associated with pum HT
    b)decrese with exercise
    c)associated only with acclimatization


    Q. which of the following is not true about vitamin D
    a)1 hydroxylation occur in kidney
    b)24 hydroxylation occur in liver
    c)in absence of sunlight 200-400 IU of vitamin....reqd


    Q. all increase free water clearance EXCEPT
    1)VINCRISTINE
    2) CHLORPROPAMIDE
    3) some statin/ hypolipedemic drug
    4) FURESEMIDE


    Q. drugs undergoing acetylation.
    3.in RHD the least commonly involved valve is:a)pulmonary ans
    b)mitral
    c)tricuspid
    d)aortic


    Q. thoracic duct receives tributaries from all except?
    1)bilateral ascending lumbar
    2)bilateral descending thoracic
    3)left upper intercostal
    4)right thoracic duct


    Q. WHITE/BLUE COLOR SCREENING USED IN DNA CLONING IS FOR
    a)scrreening for recombinant vectors(unsure abt option)
    b)---------
    c)-----------
    d)--------

    ans-a
  32. Deepak.

    Deepak. Guest

    Q. The vector may also include a gene spanning the cloning site which creates an easily detectible phenotype to allow for selection of inserts, such as for example the LacZα gene which is used to span a cloning site to allow for convenient blue-white color screening for recombinant vectors which include an insert at the site within the LacZα gene.

    choroidal neovascular membrane is seen in all except

    a- angiod streak
    b- trauma
    c-myopia-
    d- hypermetropia


    Q. A study showed that the coefficient of variation for a group of patients with high blood pressure and high serum creatinine are 20 and 15 respectively
    thus

    ans : the SD of pts with hpertension is more than that of pts with high serum creatinine

    expln:
    CV=SD/mean *100
    therefore if SD increaes so does the CV


    Q. The blue-white screen is a molecular technique that allows for the detection of successful ligations in vector-based gene cloning. DNA of interest is ligated into a vector. The vector is then transformed into competent cell (bacteria). The competent cells are grown in the presence of X-gal. If the ligation was successful, the bacterial colony will be white; if not, the colony will be blue. This technique allows for the quick and easy detection of successful ligation, without the need to individually test each colony.

    ans: to find out the cloned fragment of gene in the vector/bacteria??


    Q. If Wernicke’s area is damaged in the non-dominant hemisphere, the syndrome resulting will be sensory dysprosody - the lack of ability to perceive the pitch, rhythm, and emotional tone of speech.

    Speech is preserved, but language content is incorrect. This may vary from the insertion of a few incorrect or nonexistent words to a profuse outpouring of jargon. Grammar, syntax, rate, intonation and stress are normal. Substitutions of one word for another (paraphasias, e.g. “telephone” for “television”) are common. Comprehension and repetition are poor

    ans: speech is irrelevant and rapid


    Q. Rituximab is used alone or with other medications to treat certain types of cancer (e.g., non-Hodgkin's lymphoma). It is a type of medication called a monoclonal antibody. It works by attaching to certain blood cells from your immune system (B cells) and killing them. It is also used with other monoclonal antibodies and radioactive drugs to treat certain cancers.

    Rituximab is also used with methotrexate to treat moderate-to-severe forms of rheumatoid arthritis. It is usually used for arthritis only after other medications have not worked. It can decrease joint pain and swelling.

    Rituximab is used in all except
    ans : PNH probably


    Q. which condition is not associated with human parvo virus B19
    A.sickle cell crisis
    b.fifth disease
    c.roseola infantum
    d..........

    ANS-ROSEOLA INFANTUM

    ROSEOLA INFANTUM IS ALSO CALLED AS SIXTH DISEASE CAUSED BY A VIRUS OF THE HERPES FAMILY.
  33. Deepak.

    Deepak. Guest

    Q. post ductal co arctation of aorta- all participate in DISTAL collateral formation except:
    a- axillary artery
    b- post intercostal artery
    c- suprascapular artery
    d-vertebral artery


    Q. a pt with cellulitis of external ear with pseudomonal infection ,the drug of choice
    a)ciprofloxacin
    b)cephalosporin
    c)erythromycin


    Q. cystinosis has all the following EXCEPT
    a)cysteine stones in urine common
    b)Corneal crystals
    c)Fanconi syndrome
    d)---------


    Q. the infection caused by eating aquatic foods

    a)anaerobic infections

    b)gram negative infections

    c)gram positive infections
  34. Adityapawar

    Adityapawar Guest

    villlous adenoma is assctd with:

    1.chloride responsive metabolic alkalosis
    2.chloride resistant metabolic alkalosis
    3.metabolic acidosis
    4.??(kindly help,'m sure about other 3)

    [/b] Villous adenomas of the colon usually produce a hyperchlo-
    remic metabolic acidosis because of the loss of large volumes
    of colonic fluid, rich in potassium and bicarbonate. However,
    10 to 20% of these tumors will secrete chloride rather than
    bicarbonate with potassium, and thus result in metabolic alka-
    losis (9).
    ref:http://www.pdfdownload.org/pdf2html...rnals.org/cgi/reprint/11/2/369.pdf&images=yes

    so ans is metabolic acidosis as it is most common

    also as scretory diarhea is assctd with met acidosis(rem the anion gap table also as in VIpoma),as there are few cases with met alkalosis as well .
  35. Adityapawar

    Adityapawar Guest

    1.35yr old lady with post coital bleed ..next management..
    a.pap smear
    b.inspection with acetic acid
    c. inspection with lugol's iodine
    d.hpv testing

    2.csf pressure is mainly due to
    a.rate of formation
    b.rate of absorption
    c.cerebral blood flow
    d.

    3.best investigation for ectopic pregnancy
    a.tvus
    b.serial hcg
    c.mri
    d.

    4.differentiating feature between hypoglycemia due to insulinoma and due to sulfonylurea
    a.insulin/glucose ratio
    b.c-peptide levels
    c.
    d.

    5.a child presents with absent thumb,radius defects,lateral bowing of both forearms, investigation not to be done is
    a.platelet count
    b.BM examn.
    c.karyotyping
    d.echocardiography

    6.child 6yrs. old presenting with urinary retention and constipation diagnosis is
    a.ant. meningomyelocele
    b.rectal duplication cyst
    c.pelvic neuroblastoma
    d.sacral teratoma

    7.approach where ext. oblique , int. oblique, transversus are only retracted and not cut
    a.lumbotomy approach for renal access
    b. classical approach for renal access
    c.spigelian hernia
    d.

    8.choroidal neovascular membranes are seen in all except
    a.hypermetropia
    b. myopia
    c.DM
    d.angioid streak

    9.diabetic macular edema is due to all except
    a.incresed protein kinase c
    b.incresed VEGF
    c. oxidative stress
    d.retinal pigment epithelial dysfunction

    10.presentation with primary amenorrhea, absent breasts, hypoplastic uterus
    a. turner's syndrome
    b.gonadal dysgenesis
    c.klinefelter's
    d.androgeninsensitivity syndrome

    11.electron microscopy is diagnostic in
    a. alport's
    b. good pasture's
    c.wegener's
    d.churg strauss

    12.DNA- blue white screen is used for

    13.venous return does not depend on
    a. arterial BP
    b. calf muscle pump
    c.perforator competency
    d.deep fascia

    14.lady with epithelial ovarian ca. follow up shows rising ca-125 levels.....next mangement
    a.mri
    b.ct
    c.pet
    d.clinical examn. and serial estimation

    15.regarding managament of early breast ca.which is true
    a.radiotherapy given after surgery for atleast 4 nodes positive
    b.trastusumab is not effective now a days
    c.aromatase inhibitors are better than tamoxifen in terms of toxicity
    d. something about combination therapy

    16.most common inherited tumour
    a. retinoblastoma
    b. transient myeloproliferative disorder
    c. leukemia
    d.

    17.paraganglioma- histological finding is
    a. dense neurosecretory granules
    b.
    c.
    d.

    18.false about NHL of stomach
    a. most common site is stomach
    b. survival rate is 60%
    c.
    d.

    19.lymph node mets. is least common in ca of
    a.tongue
    b.hard palate
    c. floor of the mouth
    d. inferior gingiva

    20.cause of fetal death in ectopic pregnancy
    a. vascular accident
    b.nutritional adequacy
    c.withdrawal of hormones
    d. maternal.......

    21.amoebic meningoencephalitis...true is
    a.acute caused by acanthamoeba
    b.feco oral transmission
    c.diagnosis by trophozoites in csf
    d.

    22.neurotransmitter associated with suicidal tendency
    a. serotonin
    b.dopamine
    c.norepinephrine
    d.

    23.in a crically ill patient, aa substitution for nitrogen retention causes
    a.increase in protein synthesis
    b. decrease in protein synthesis
    c. both
    d. incresed gluconeogenesis

    24.best drug for uncomplicated alcohol withdrawl syndrome
    a, diazepam
    b.propranolol
    c.clonidine
    d.buprenorphine

    26.bronchoscopy - not directly visualised is
    a. sub cranial (must be sub carinal -printing mistake in paper) lymph nodes
    b.vocal cords
    c.tachea
    d.first segmental division of airway

    27. tributaries of thoracic trunk- all except
    a.rt. lymphatic trunk
    b.lt. lymphatic trunk
    c. asc. lumbar trunk
    d. desc. thoracic trunk

    28.auspitz sign seen in
    a. plaque psoriasis
    b.
    c.
    d.

    29.occipitoposterior position diagnosed ... managemnet
    a. wait for progress
    b. LSCS
    c.
    d.

    30.indian refernce male -all true except
    a. 21-39 yrs
    b.60 kg
    c.consuming 2200 k cal
    d.8hrs in bed

    31.increased ICT all are seen except
    a. markings on skull
    b. convolutions......
    c.
    d.

    32.which of these is energy independent
    a. facilitated diffusion
    b. co-transport
    c.active transport
    d.

    33.good pasture's charac. by all except
    a. diffuse alveolar hge.
    b.presence of antibodies to BM
    c.glomerulonephritis
    d.leukocytoclastic vasculitis
  36. Adityapawar

    Adityapawar Guest

    KASABAACH MERRIT SYNDROME is associated with?
    A.Giant Haemangioma
    B.
    C
    D.Giant Thrombocytes

    Ans is A.Giant Haemangioma

    Synonyms and related keywords: Kasabach-Merritt syndrome, KMS, giant hemangioma syndrome, thrombocytopenia, giant hemangioma with consumptive coagulopathy, disseminated intravascular coagulation, DIC, neonatal lesion

    Hemangiomas, the most common tumors of infancy, typically undergo rapid postnatal growth for several months, followed by a prolonged phase of involution. The combination of hemangioma, thrombocytopenia, and coagulopathy is termed Kasabach-Merritt syndrome (KMS). The hemangioma may be an obvious superficial lesion or a lesion within a visceral organ or even within the brain. Thrombocytopenia is often severe (ie, <50,000 platelets/mm3). Thrombocytopenia and consumptive coagulopathy are not complications of all hemangiomas, and size alone does not determine which hemangiomas are associated with thrombocytopenia and coagulopathies. KMS is an infrequent but potentially fatal complication of rapidly growing hemangiomas in infants.
  37. Adityapawar

    Adityapawar Guest

    Gum hyperplasia is seen in:
    (a)ALL
    (b)M2
    (c)M3
    (d)M4(ANS)

    Gingival hyperplasia is secondary to infiltration of the gingival tissue with leukemia cells and is well described in the literature.1-4 In the most extensive review of the topic, gingival hyperplasia was observed in acute myelogenous leukemia (AML) with a frequency of 3% to 5% among 1,076 patients receiving anti-leukemia chemotherapy at a referral centre.5 Gingival hyperplasia is most commonly seen with the AML subtypes acute monocytic leukemia (M5) (66.7%), acute myelomonocytic leukemia (M4) (18.5%), and acute myelocytic leukemia (M1, M2) (3.7%).
  38. Adityapawar

    Adityapawar Guest

    True statement regarding Iridocorneal Endothelial syndrome is

    Deposition of collagen in the Descemet's membrane
  39. Adityapawar

    Adityapawar Guest

    Pterygium is:
    (a) ?
    (b)vascular disorder
    (c)inflammation
    (d)disorder of collagen degeneration(ANS)
  40. Adityapawar

    Adityapawar Guest

    Mediastinal mass with histopathological features of sheets of lymphocytes and keratinising whorls. Diagnosis is :
    (a)Thymic carcinoid
    (b)Thymoma...
  41. Adityapawar

    Adityapawar Guest

    genital warts are caused by
    a)HPV 6
    b)HPV 16
    c)----------
    d)-----------

    Genital warts are the most easily recognized sign of genital HPV infection. They can be caused by strains 6, 11, 30, 42, 43, 44, 45, 51, 52 and 54 of genital HPV; types 6 and 11 are responsible for 90% of genital warts cases
    genital warts (or Condyloma, Condylomata acuminata, or venereal warts) is a highly contagious sexually transmitted infection caused by some sub-types of human papillomavirus (HPV). It is spread through direct skin-to-skin contact during oral, genital, or anal sex with an infected partner. Genital warts are the most easily recognized sign of genital HPV infection. They can be caused by strains 6, 11, 30, 42, 43, 44, 45, 51, 52 and 54 of genital HPV; types 6 and 11 are responsible for 90% of genital warts cases.[1] Most people who acquire those strains never develop warts or any other symptoms. HPV also causes many cases of cervical cancer; types 16 and 18 account for 70% of cases; however, the strains of HPV that cause genital warts are not linked to the strains that cause cancer.

    Genital warts often occur in clusters and can be very tiny or can spread into large masses in the genital or penis area. In women they occur on the outside and inside of the vagina, on the opening (cervix) to the womb (uterus), or around the anus. They are approximately as prevalent in men, but the symptoms may be less obvious. When present, they usually are seen on the tip of the penis. They also may be found on the shaft of the penis, on the scrotum, or around the anus. Rarely, genital warts also can develop in the mouth or throat of a person who has had oral sex with an infected person. The viral particles are able to penetrate the skin and mucosal surfaces through microscopic abrasions in the genital area, which occur during sexual activity. Once cells are invaded by HPV, a latency (quiet) period of months to years may occur. The latency period just means the HPV virus is in an incubation period. Having sex with a partner whose HPV infection is in the incubation period still leaves you vulnerable to becoming infected yourself. In other words, just because one can't see the genital warts, doesn't mean they are not there. HPV virus can last from 3 months to 2 years without a symptom. That causes the increase of HPV infectors and sometimes you cannot track down who was the source of the infection.
    Contents
    [hide]

    * 1 Treatment
    * 2 Misdiagnosis cautions
    * 3 References
    * 4 External links
    o 4.1 Images

    [edit] Treatment

    Genital warts may disappear without treatment, but sometimes eventually develop a fleshy, small raised growth. There is no way to predict whether they will grow or disappear.

    Depending on the size and location of the wart, and other factors, a doctor will offer one of several ways to treat them.

    * Imiquimod (Aldara) a topical immune response cream, applied to the affected area
    * A 20% podophyllin anti-mitotic solution, applied to the affected area and later washed off
    * A 0.5% podofilox solution, applied to the affected area but not to be washed off
    * A 5% 5-fluorouracil (5-FU) cream
    * Trichloroacetic acid (TCA)
    * Pulsed dye laser
    * Liquid nitrogen cryosurgery
    * Electric or laser cauterization

    Podophyllin and podofilox should not be used during pregnancy, as they are absorbed by the skin and may cause birth defects in the fetus. 5-fluorouracil cream should not be used while trying to become pregnant or if there is a possibility of pregnancy.

    Small warts can be removed by freezing (cryosurgery), burning (electrocautery), or laser treatment. Surgery is occasionally used to remove large warts that have not responded to other treatment.

    Some doctors inject the antiviral drug interferon-alpha directly into the warts, to treat warts that have returned after removal by traditional means. The drug is expensive, and does not reduce the rate that the warts return.

    Although treatments can remove the warts, they do not remove the HPV virus, so warts can recur after treatment. Traditional theories postulated that the virus remained in the body for a lifetime. However, new studies using sensitive DNA techniques have shown that through immunological response the virus can either be cleared or suppressed to levels below what PCR tests can measure. [2] According to the Center for Disease Control's report on HPV to Congress in 2004, studies have shown that 70% of new HPV infections clear within one year, and as many as 91% clear within two years. The median duration of new infections is typically eight months. The gradual development of an effective immune response is thought to be the likely mechanism for HPV DNA clearance. The state of the immune system determines the chances of removing the virus entirely and can be affected by factors such as HIV infection, certain medications, stress, or illness.[3] There is even some suggestion that effective treatment of the wart may aid the body's immune response[citation needed].

    [edit] Misdiagnosis cautions

    It is a common misconception among men that hirsuties papillaris genitalis are genital warts. Hirsuties papillaris genitalis is not contagious and no treatment for it is necessary. Some may deem it unsightly and there are various methods of ridding the penis of the condition such as carbon dioxide laser treatment.

    Genital warts (condylomata) should not be confused with Molluscum contagiosum (MC), which is often transmitted sexually, but does not occur internally as do condylomata. MC looks like small warts, which are much smaller than condylomata genital warts. It does not increase the risk of cervical cancer for women. Genital warts should not be confused with Fordyce's spots, which are considered benign.
  42. Adityapawar

    Adityapawar Guest

    All the following are atypical antipsychotics EXCEPT:

    a)thirodazine
    b)Clozapine
    c)Risperidone
    d)Olanzapine

    ans:eek:ption A


    The atypical antipsychotics (also known as second generation antipsychotics) are a class of prescription medications used to treat psychiatric conditions. Some atypical antipsychotics are FDA approved for use in the treatment of schizophrenia. Some carry FDA approved indications for acute mania, bipolar mania, psychotic agitation, bipolar maintenance, and other indications.

    Atypicals are a heterogeneous group of otherwise unrelated drugs united by the fact that they work differently from typical antipsychotics. Most share a common attribute of working on serotonin receptors as well as dopamine receptors. One drug, amisulpride, does not have serotonergic activity, instead it has some partial dopamine agonism. Another drug, aripiprazole, also displays some partial dopamine agonism, 5-HT1A partial agonism and 5-HT2A antagonism.[1]
    Contents
    [hide]

    * 1 History
    * 2 Pharmacology of the atypicals
    * 3 Side effects
    o 3.1 Tardive Dyskinesia
    o 3.2 Metabolic side effects with atypical antipsychotics
    * 4 Atypical antipsychotic medications
    * 5 See also
    * 6 References
    * 7 External links

    [edit] History

    The first atypical anti-psychotic medication, clozapine, was discovered in the 1950s, and introduced in clinical practice in the 1970s. Clozapine fell out of favor due to concerns over drug-induced agranulocytosis. With research indicating its effectiveness in treatment-resistant schizophrenia and the development of an adverse event monitoring system, clozapine reemerged as a viable antipsychotic. Despite the effectiveness of clozapine for treatment-resistant schizophrenia, agents with a more favorable side effect profile were sought after for widespread use. During the 1990s, olanzapine, risperidone, and quetiapine were introduced, with ziprasidone and aripiprazole following in the early 2000s. The newest atypical anti-psychotic, paliperidone, was approved by the FDA in late 2006.

    The atypical anti-psychotics have found favor among clinicians and are now considered to be first line treatments for schizophrenia and are gradually replacing the typical antipsychotics. Most researchers agree that the defining characteristic of an atypical antipsychotic is the decreased propensity of these agents to cause extrapyramidal side effects and an absence of sustained prolactin elevation.

    More recent research is questioning the notion that second generation anti-psychotics are superior to first generation typical anti-psychotics. Using a number of parameters to assess quality of life University of Manchester researchers found that typical anti-psychotics were no worse than atypical anti-psychotics. The research was funded by the National Health Scheme of the UK[2]

    [edit] Pharmacology of the atypicals

    The mechanism of action of these agents is unknown, and differs greatly from drug to drug. The variation in the receptor binding profile is such that the only effect all have in common is an anti-psychotic effect; the side effect profiles vary tremendously. While modulation of the dopamine neurotransmitter system is the most important mechanism by which anti-psychotics exert their benefits, the role of the serotonergic activity of the atypicals is debated. Some researchers believe that D2 receptor antagonism, coupled with 5-HT2A receptor antagonism, is responsible for the "atypicality" of atypical anti-psychotics. Others believe that fast dissociation (a fast Koff) from the D2 receptor, allowing for better transmission of normal physiological dopamine surges, better explains the pharmacological evidence.

    There is extensive evidence that atypical anti-psychotics have less of an affinity for D2 receptors and more of an affinity for the D4 receptors.[citation needed] This is primarily because atypical anti-psychotics are somewhat less likely to cause tardive dyskinesia.[citation needed] The idea is that D2 receptors are dopaminergically ubiquitous and affect the motor system as much as the motivational aspect of the dopamine system. On the other hand, D4 is a more accurate dopamine receptor subtype. Atypical anti-psychotics also affect the norepinephrine, acetylcholine, and histamine receptors of various subtypes. [1] However, studies have shown that D4 selective antagonism has no anti-psychotic effect.[citation needed]

    [edit] Side effects

    The side effects reportedly associated with the various atypical antipsychotics vary and are medication-specific. Generally speaking, atypical antipsychotics are hoped to have a lower likelihood for the development of tardive dyskinesia than the typical antipsychotics. However, tardive dyskinesia typically develops after long term (possibly decades) use of antipsychotics. It is not clear, then, if atypical antipsychotics, having been in use for a relatively short time, produce a lower incidence of tardive dyskinesia.

    Akathisia is more likely to be less intense with these drugs then the typical antipsychotics[citation needed] although many patients would dispute this claim. In 2004, the Committee for the Safety of Medicines (CSM) in the UK issued a warning that olanzapine and risperidone should not be given to elderly patients with dementia, because of an increased risk of stroke. Sometimes atypical antipsychotics can cause abnormal shifts in sleep patterns, and extreme tiredness and weakness.

    In 2006, USA Today published an article about the effects of antipsychotic medication in children. None of the atypicals (Clozaril, Risperdal, Zyprexa, Seroquel, Abilify and Geodon) have been approved for children, and there is little research on their effects on children. From 2000–2004, there were 45 reported deaths in which an atypical antipsychotic was listed as the "primary suspect." There were also 1328 reports of serious, and sometimes life threatening, side effects. These include tardive dyskinesia (involuntary jerking and facial grimacing) and dystonia (involuntary muscle contractions that can interfere with talking and eating).

    [edit] Tardive Dyskinesia

    All the atypical antipsychotics warn about the possibility of tardive dyskinesia in their package inserts and in the PDR. It is not possible to truly know the risks of tardive dyskinesia when taking atypicals, because tardive dyskinesia can take many decades to develop and the atypical antipsychotics are not old enough to have been tested over a long enough period of time to determine all of the long-term risks.

    However, the atypicals may cause serious metabolic disorders to make them equally dangerous as the older anti-psychotic drugs.[citation needed]

    [edit] Metabolic side effects with atypical antipsychotics

    Recently, metabolic concerns have been of grave concern to clinicians, patients and the FDA. In 2003, the Food and Drug Administration (FDA) required all manufacturers of atypical antipsychotics to change their labeling to include a warning about the risks of hyperglycemia and diabetes with atypical antipsychotics. It must also be pointed out that although all atypicals must carry the warning on their labeling, some evidence shows that all atypicals are not equal in their effects of weight and insulin sensitivity.[citation needed] The general consensus is that clozapine and olanzapine are associated with the greatest effects on weight gain and decreased insulin sensitivity, followed by risperidone and quetiapine.[citation needed] Ziprasidone and aripiprazole are thought to have the smallest effects on weight and insulin resistance,[citation needed] but clinical experience with these newer agents is not as developed as that with the older agents.

    [edit] Atypical antipsychotic medications

    * Clozapine (Clozaril) (FDA-approval: 1990) Available in oral tablets and dissolving tablets (FazaClo).
    * Risperidone (Risperdal) (FDA-approval: 1993) Available in oral tablets, dissolving tablets, liquid form, and extended release intramusclar injection.
    * Olanzapine (Zyprexa) (FDA-approval: 1996) Available in oral tablets, dissolving tablets, and intramuscular injection.
    * Quetiapine (Seroquel) (FDA-approval: 1997) Available only in oral tablets.
    * Ziprasidone (Geodon) (FDA-approval: 2001) Available in oral capsules and intramuscular injection.
    * Aripiprazole (Abilify) (FDA)-approval: 2002) Available in oral tablets and dissolving tablets.
    * Paliperidone (Invega) (FDA)-approval: 2006) Available in extended-release oral tablets.
    * Asenapine FDA has accepted NDA as of November 26, 2007. [3]
    * Iloperidone (Zomaril) FDA has accepted NDA as of November 27, 2007. [4]
    * Sertindole (Serlect) (Not approved by the FDA for use in the USA).
    * Zotepine (Not approved by the FDA for use in the USA).
    * Amisulpride (Not approved by the FDA for use in the USA).
    * Bifeprunox (Not approved by the FDA for use in the USA).
    * Melperone Approved in Europe. Currently in clinical trial in the USA.
  43. Adityapawar

    Adityapawar Guest

    Imatinib is used in the treatment of

    a)gastrointestinal stromal tumors
    b)chronic myeloid tumors
    c)---------
    d)-------------


    ans:eek:ption A

    matinib is a drug used to treat certain types of cancer. It is currently marketed by Novartis as Gleevec (USA) or Glivec (Europe/Australia ) as its mesylate salt, imatinib mesilate (INN). It was originally coded during development as CGP57148B or STI-571 (these terms are used in early preclinical publications). It is used in treating chronic myelogenous leukemia (CML), gastrointestinal stromal tumors (GISTs) and a number of other malignancies.

    http://en.wikipedia.org/wiki/Imatinib




    ------------------------------------------------

    Imatinib is a drug used to treat certain types of cancer. It is currently marketed by Novartis as Gleevec (USA) or Glivec (Europe/Australia ) as its mesylate salt, imatinib mesilate (INN). It was originally coded during development as CGP57148B or STI-571 (these terms are used in early preclinical publications). It is used in treating chronic myelogenous leukemia (CML), gastrointestinal stromal tumors (GISTs) and a number of other malignancies.

    It is the first member of a new class of agents that act by inhibiting particular tyrosine kinase enzymes, instead of non-specifically inhibiting rapidly dividing cells.
    Contents
    [hide]

    * 1 Molecular Pharmacology
    * 2 Uses
    * 3 Tolerability and side effects
    * 4 Metabolism
    * 5 History
    * 6 See also
    * 7 References
    * 8 External Links

    [edit] Molecular Pharmacology

    Imatinib is a 2-phenylaminopyrimidine derivative that functions as a specific inhibitor of a number of tyrosine kinase enzymes. It occupies the TK active site, leading to a decrease in activity.

    There are a large number of TK enzymes in the body, including the insulin receptor. Imatinib is specific for the TK domain in abl (the Abelson proto-oncogene), c-kit and PDGF-R (platelet-derived growth factor receptor).

    In chronic myelogenous leukemia, the Philadelphia chromosome leads to a fusion protein of abl with bcr (breakpoint cluster region), termed bcr-abl. As this is now a continuously active tyrosine kinase, imatinib is used to decrease bcr-abl activity.
    Mechanism of action of imatinib


    The active sites of tyrosine kinases each have a binding site for ATP. The enzymatic activity catalyzed by a tyrosine kinase is the transfer of the terminal phosphate from ATP to tyrosine residues on its substrates, a process known as protein tyrosine phosphorylation. Imatinib works by binding to the ATP binding site of bcr-abl and inhibiting the enzyme activity of the protein competitively.

    Imatinib is quite selective for bcr-abl – it does also inhibit other targets mentioned above (c-kit and PDGF-R), but no other known tyrosine kinases. Imatinib also inhibits the abl protein of non-cancer cells but cells normally have additional redundant tyrosine kinases which allow them to continue to function even if abl tyrosine kinase is inhibited. Some tumour cells, however, have a dependence on bcr-abl.[1] Inhibition of the bcr-abl tyrosine kinase also stimulates its entry in to the nucleus, where it is unable to perform any of its normal anti-apoptopic functions.[2]

    [edit] Uses
    Glivec / Gleevec
    Glivec / Gleevec

    Imatinib is used in chronic myelogenous leukemia (CML), gastrointestinal stromal tumors (GISTs) and a number of other malignancies. One study demonstrated that Imatinib mesylate was effective in patients with systemic mastocytosis, including those who had the D816V mutation in c-Kit.[3] Experience has shown, however, that imatinib is much less effective in patients with this mutation, and patients with the mutation comprise nearly 90% of cases of mastocytosis. Early clinical trials also show its potential for treatment of hypereosinophilic syndrome and dermatofibrosarcoma protuberans.

    In laboratory settings, imatinib is being used as an experimental agent to suppress platelet-derived growth factor (PDGF) by inhibiting its receptor (PDGF-Rβ). One of its effects is delaying atherosclerosis in mice with diabetes.[4]

    Recent mouse animal studies at Emory University in Atlanta have suggested that imatinib and related drugs may be useful in treating smallpox, should an outbreak ever occur.[5]

    Gleevec is also being used in the treatment of certain brain tumors to include high grade glioblastoma.

    [edit] Tolerability and side effects
    bcr-abl kinase, which causes CML, inhibited by imatinib (small molecule).
    bcr-abl kinase, which causes CML, inhibited by imatinib (small molecule).

    In the United States, the Food and Drug Administration has approved imatinib as first-line treatment for CML.[1] Imatinib has passed through Phase III trials for CML, and has been shown to be more effective than the previous standard treatment of α-interferon and cytarabine. Although the long-term side effects of imatinib have not yet been ascertained, research suggests that it is generally very well tolerated (eg. liver toxicity was much less than predicted). Broadly, side effects such as edema, nausea, rash and musculoskeletal pain are common but mild.

    Severe congestive cardiac failure is an uncommon but recognised side effect of imatinib and mice treated with large doses of imatinib show toxic damage to their myocardium.[6]

    [edit] Metabolism

    Metabolism of imatinib occurs in the liver and the main metabolite, N-demethylated piperazine derivative, is also active. The major route of elimination is in the bile, only a small portion is excreted in the urine. Most of imatinib is eliminated as metabolites, only 25% is eliminated unchanged. The half-lives of imatinib and its main metabolite are 18 and 40 hours, respectively.

    [edit] History

    Imatinib was identified in the late 1990s by Novartis chemists. Dr Brian J. Druker led many of the key clinical trials confirming the efficacy of imatinib in CML. Its development is the template for rational drug design. Soon after identification of the bcr-abl target, the search for an inhibitor began. Chemists used a high-throughput screen of chemical libraries to identify the molecule 2-phenylaminopyrimidine. This lead compound was then tested and modified by the introduction of methyl and benzamide groups to give it enhanced binding properties, resulting in imatinib.[7]

    Gleevec received FDA approval in May 2001. On the same month it made the cover of TIME magazine as the "magic [bleep]" to cure cancer.

    Gleevec, which costs $32,000 per year for a 400 mg/day dose, is often cited as an example of pharmaceutical industry innovation that justifies the high cost of drugs. Marcia Angell and Arnold S. Relman argue that Gleevec is actually an example of the contribution of taxpayer-supported research and of industry inaction. Drucker tested several, and imatinib was the most potent, and unusually, had almost no effect on normal cells. Novartis had "little corporate enthusiasm," they write, but Drucker persisted[8].

    In 2007, imatinib became a test case through which Novartis challenged India's patent laws. This would make it harder for Indian companies to produce generic versions of drugs still manufactured under patent elsewhere in the world. Organisations such as Médecins Sans Frontières argue that a change in law would make it impossible for Indian companies to produce cheap antiretrovirals (anti-AIDS medication), endangering access to these drugs in Third World countries.[9] On 6 August 2007 The High Court in Chennai, India, dismissed the writ petition filed by Novartis, challenging the constitutionality of Section 3(d)of Indian Patent Act and deferred to the World Trade Organization (WTO) forum to resolve the TRIPS compliance question.
  44. Adityapawar

    Adityapawar Guest

    insulin causing lipogenesis by all except?
    1 causes glucose 2 move inside cell
    2 inhibits pyruvate dehydrogenase
    3 increse camp
    4 increses activity of acetl coa carboxylase


    ans is 3)Increases C-AMP
    REF:Harper/27th ed./p.201-202

    Insulin stimulates lipogenesis by
    *Increasing acetyl co-A carboxylase activity

    *Increasing transport of glucose into cell(Adipose tissue)

    *Converts inactive form of pyruvate dehydrogenase to active form in adipose tissue

    *insulin by its ability to depress the level of intracellular cyclic amp & inhibits lipolysis in adipose tissue decrease the conc. Of plasma FFA & therefore long chain acyl coa, inhibitor of lipogenesis
  45. Shishir.

    Shishir. Guest

    long acting b2 adrenoreceptor agonist-salmeterol


    Long acting beta-adrenoceptor agonist
    From Wikipedia, the free encyclopedia
    • Find out more about navigating Wikipedia and finding information •
    Jump to: navigation, search

    Long acting beta-adrenoceptor agonists are usually prescribed for moderate to severe persistent asthma patients or patients with COPD. They are designed to replace the shorter acting B2-agonists such as salbutamol, as they have a duration of action of approximately 12 hours in comparison with the 4-6 hour duration of salbutamol, making them ideal candidates for twice-daily administration.

    Some currently available long acting beta-adrenoceptor agonists are:

    * Salmeterol
    * Formoterol
    * Bambuterol

    Studies are currently underway into ultra long acting beta-adrenoceptor agonists which would have duratoin of action of 24 hours allowing for once daily dosing:[1]

    * Indacaterol

    [edit] Footnotes

    1. ^ Cazzola M, Matera MG, Lötvall J (July 2005). "Ultra long-acting beta 2-agonists in development for asthma and chronic obstructive pulmonary disease". Expert Opin Investig Drugs 14 (7): 775–83. doi:10.1517/13543784.14.7.775. PMID 16022567.

    Tablets This Pharmacology -related article is a stub. You can help Wikipedia by expanding it.
    [hide]
    v • d • e
    Drugs for obstructive airway diseases: asthma/COPD (R03)
    Adrenergics, inhalants
    Short acting β2-agonists: Salbutamol/Levosalbutamol • Fenoterol • Terbutaline • Pirbuterol • Procaterol • Bitolterol • Rimiterol • Carbuterol • Tulobuterol • Reproterol
    Long acting β2-agonists (LABA): Arformoterol • Bambuterol • Clenbuterol • Formoterol • Salmeterol Ultra LABA: Indacaterol
    other: Epinephrine • Isoprenaline (Isoproterenol) • Orciprenaline (Metaproterenol)
    Glucocorticoids
    Beclometasone • Budesonide • Ciclesonide • Fluticasone • Mometasone
    Anticholinergics
    Ipratropium • Tiotropium
    Mast cell stabilizers
    Cromoglicate • Nedocromil
    Xanthines
    Aminophylline • Theobromine • Theophylline
    Leukotriene antagonists
    Montelukast • Pranlukast • Zafirlukast
    Lipoxygenase inhibitor
    Zileuton
  46. Shishir.

    Shishir. Guest

    Ketoconazole

    Ketoconazole is an azole medication used to treat a broad spectrum of fungi It was originally developed in the late 1970's in the oral form and granted FDA acceptance in 1981. Shortly after the topical formulations were undergoing trials and proven effective.
    The 2% cream and 1% shampoo are now available over the counter. It is effective against yeasts and dermatophytes, both systemically and topically.
    It is now mainly used systemically in treating life-threatening fungal infections
    Trade Name:

    * Nizoral* Janssen

    Dosage Forms:

    * Topical: Cream: Ketoconazole cream 2% Nizoral*
    * Shampoo: Ketoconazole shampoo 1% and 2% Nizoral Shampoo*
    * Oral: Tablets: Ketoconazole tablets 200 mg
    * Suspension: Ketoconazole oral suspension 100mg/5mL Nizoral*

    Uses

    Labeled Indications


    Off-Label Uses

    Topical

    * Tinea corporis, cruris, pedis
    * Pityriasis versicolor
    * Cutaneous candidiasis
    * Seborrehic dermatitis
    * Dandruff

    Systemic Tinea corporis, cruris, pedis, severe and unresponsive to Griseofulvin therapy

    * Chromomycosis
    * Chronic mucoutaneous candidiasis
    * Candidiasis, oropharyngeal

    Other (selection)

    * Paracoccidiomycosis
    * Candidiasis, systemic

    Systemic

    * OnychomycosisParonychia #
    * Leishmaniasis, cutaneous #
    * Candidiasis, vulvo-vaginal #


    # - not included in Canadian product labeling


    Therapeutic Regimen

    Adult


    Pediatric

    Systemic

    * Pityriasis versicolor
    * Ketoconazole 200mg po daily x5-10d

    Other antifungal indications Ketoconazole 200-400mg po daily.

    * Therapy to be continued for 1-2 weeks in candidal infections; for 1- 8 weeks in dermatophytes; and for 6 months or longer in systemic mycoses

    Topical

    * Dandruff
    * Ketoconazole 1% shampoo every 3-4 days for up to 8 weeks

    Seborrehic dermatitis

    * Ketoconazole 2% shampoo or cream twice a week for 2-4 weeks. Apply to the hair and scalp, leave for 5 minutes and wash off

    Pityriasis versicolor

    * Ketoconazole 2% shampoo single application to the affected areas and surrounding skin. Leave for 5 minutes and rinse.

    Tinea corporis, cruris, pedis and cutaneous candidiasis

    * Ketoconazole 2% cream applied to the affected areas, and surrounding skin once a day until clear.

    Systemic

    * Safety and efficacy have not been established for systemic use in children < 2 years of age

    > 2 years of age

    * Ketoconazole 3.3-6.6 mg/kg po daily

    Vulvovaginal candidiasis

    * Ketoconazole 5-10 mg/kg po daily yx5d

    Paronychia

    * Ketoconazole 5-10 mg/kg po daily

    Topical

    * Safety and efficacy have not been established for topical use



    Safety Information

    * Concurrent use with cisapride, aztemizole and terfenadine is contraindicated.
    * Ketoconazole cream contains sulfites to which some patients may be allergic
    * Hepatotoxicity may occur and has led to reported deaths.
    * Ketoconazole may increase serum digoxin concentrations and lead to toxicity.

    Side Effects

    * Local cutaneous effects may include itching, stinging, irritation or contact dermatitis.
    * Cutaneous effects may include hypersensitivity reactions including exfoliative dermatitis and Stevens-Johnson syndrome
    * Gastrointestinal effects may include nausea, abdominal pain, diarrhea, constipation, loss of appetite and rarely, hepatotoxicity.
    * Hematologic effects may include agranulocytosis or thrombocytopenia.
    * Other effects may include headache, dizziness and drowsiness. Azospermia, impotence, decreased libido in menstrual irregularities may occur as a result of corticosteroid and testosterone suppression.

    FDA Pregnancy Category C
    Animal studies have shown teratogenicity and embryonic toxicity when given very high oral doses. Use of ketoconazole is not recommended during pregnancy or lactation.
    Mechanism of Action / Pharmacokinetics

    The azole antifungals interfere with cytochome P450 enzyme activity and inhibit demethylization of 14-alpha-methylsterolsterols to ergosterol. Since ergosterol is essential to the fungal cell membrane, when it is depleted the fungal cells are destroyed.
    Ketoconazole may also interfere with the conversion of lanosterol to cholesterol, affecting steroid hormone synthesis.
    Systemic ketoconazole is well distributed, however it does not penetrate the CSF. Topical application does not result in significant systemic absorption.
  47. Shishir.

    Shishir. Guest

    Vitamin D

    From Wikipedia, the free encyclopedia
    • Interested in contributing to Wikipedia? •
    Jump to: navigation, search
    Cholecalciferol (D3)
    Cholecalciferol (D3)
    Ergocalciferol (D2). Note double bond at top center.
    Ergocalciferol (D2). Note double bond at top center.

    Vitamin D is a group of fat-soluble prohormones, the two major forms of which are vitamin D2 (or ergocalciferol) and vitamin D3 (or cholecalciferol).[1] The term vitamin D also refers to metabolites and other analogues of these substances. Vitamin D3 is produced in skin exposed to sunlight, specifically ultraviolet B radiation.

    Vitamin D plays an important role in the maintenance of organ systems.[2]

    * Vitamin D regulates the calcium and phosphorus levels in the blood by promoting their absorption from food in the intestines, and by promoting re-absorption of calcium in the kidneys.
    * It promotes bone formation and mineralization and is essential in the development of an intact and strong skeleton. However, at very high levels it will promote the resorption of bone.
    * It inhibits parathyroid hormone secretion from the parathyroid gland.
    * Vitamin D affects the immune system by promoting phagocytosis, anti-tumor activity, and immunomodulatory functions.

    Vitamin D deficiency can result from inadequate intake coupled with inadequate sunlight exposure, disorders that limit its absorption, conditions that impair conversion of vitamin D into active metabolites, such as liver or kidney disorders, or, rarely, by a number of hereditary disorders.[2] Deficiency results in impaired bone mineralization, and leads to bone softening diseases, rickets in children and osteomalacia in adults, and possibly contributes to osteoporosis. Research has indicated that vitamin D deficiency is linked to colon cancer; conflicting evidence links vitamin D deficiency to other forms of cancer.
    Contents
    [hide]

    * 1 Forms
    * 2 Biochemistry
    o 2.1 Production in the skin
    + 2.1.1 Synthesis mechanism (form 3)
    o 2.2 Mechanism of action
    * 3 Nutrition
    o 3.1 In food
    * 4 Deficiency
    o 4.1 Diseases caused by deficiency
    o 4.2 Groups at greater risk of deficiency
    * 5 Overdose
    * 6 Role in immunomodulation
    * 7 Role in cancer prevention and recovery
    * 8 Role in coronary disease prevention
    * 9 Notes and References
    * 10 External links

    [edit] Forms

    Several forms (vitamers) of vitamin D have been discovered. The two major forms are vitamin D2 or ergocalciferol, and vitamin D3 or cholecalciferol.

    * Vitamin D1: molecular compound of ergocalciferol with lumisterol, 1:1
    * Vitamin D2: ergocalciferol or calciferol (made from ergosterol)
    * Vitamin D3: cholecalciferol (made from 7-dehydrocholesterol in the skin).
    * Vitamin D4: 22-dihydroergocalciferol
    * Vitamin D5: sitocalciferol (made from 7-dehydrositosterol)

    Chemically, the various forms of vitamin D are secosteroids; i.e., broken-open steroids.[3] The structural difference between vitamin D2 and vitamin D3 is in their side chains. The side chain of D2 contains a double bond between carbons 22 and 23, and a methyl group on carbon 24.

    Vitamin D2 is derived from fungal and plant sources, and is not produced by the human body. Vitamin D3 is derived from animal sources and is made in the skin when 7-dehydrocholesterol reacts with UVB ultraviolet light at wavelengths between 270–300 nm, with peak synthesis occurring between 295-297 nm.[4][5] These wavelengths are present in sunlight at sea level when the sun is more than 45° above the horizon, or when the UV index is greater than 3.[6] At this solar elevation, which occurs daily within the tropics, daily during the spring and summer seasons in temperate regions, and almost never within the arctic circles, adequate amounts of vitamin D3 can be made in the skin only after ten to fifteen minutes of sun exposure at least two times per week to the face, arms, hands, or back without sunscreen. With longer exposure to UVB rays, an equilibrium is achieved in the skin, and the vitamin simply degrades as fast as it is generated.[1]

    In humans, D3 is as effective as D2 at increasing the levels of vitamin D hormone in circulation; [7] However, in some species, such as rats, vitamin D2 is more effective than D3.[8] Both vitamin D2 and D3 are used for human nutritional supplementation, and pharmaceutical forms include calcitriol (1alpha, 25-dihydroxycholecalciferol), doxercalciferol and calcipotriene.[9]

    [edit] Biochemistry

    Vitamin D is a prohormone, meaning that it has no hormone activity itself, but is converted to the active hormone 1,25-D through a tightly regulated synthesis mechanism. Production of vitamin D in nature always appears to require the presence of some UV light; even vitamin D in foodstuffs is ultimately derived from organisms, from mushrooms to animals, which are not able to synthesize it except through the action of sunlight at some point in the synthetic chain. For example, fish contain vitamin D only because they ultimately exist on calories from ocean algae which synthesize vitamin D in shallow waters from the action of solar UV.

    [edit] Production in the skin
    The epidermal strata of the skin. Production is greatest in the stratum basale (colored red in the illustration) and stratum spinosum (colored orange).
    The epidermal strata of the skin. Production is greatest in the stratum basale (colored red in the illustration) and stratum spinosum (colored orange).

    The skin consists of two primary layers: the inner layer called the dermis, composed largely of connective tissue, and the outer thinner epidermis. The epidermis consists of five strata; from outer to inner they are: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale.

    Vitamin D3 is produced photochemically in the skin from 7-dehydrocholesterol. The highest concentrations of 7-dehydrocholesterol are found in the epidermal layer of skin, specifically in the stratum basale and stratum spinosum.[4] The production of pre-vitamin D3 is therefore greatest in these two layers, whereas production in the other layers is reduced.

    Synthesis in the skin involves UVB radiation which effectively penetrates only the epidermal layers of skin. While 7-Dehydrocholesterol absorbs UV light at wavelengths between 270–300 nm, optimal synthesis occurs in a narrow band of UVB spectra between 295-300 nm. Peak isomerization is found at 297 nm. This narrow segment is sometimes referred to as D-UV.[10] The two most important factors that govern the generation of pre-vitamin D3 are the quantity (intensity) and quality (appropriate wavelength) of the UVB irradiation reaching the 7-dehydrocholesterol deep in the stratum basale and stratum spinosum.[4]

    A critical determinant of vitamin D3 production in the skin is the presence and concentration of melanin. Melanin functions as a light filter in the skin, and therefore the concentration of melanin in the skin is related to the ability of UVB light to penetrate the epidermal strata and reach the 7-dehydrocholesterol-containing stratum basale and stratum spinosum. Under normal circumstances, ample quantities of 7-dehydrocholesterol (about 25-50 µg/cm² of skin) are available in the stratum spinosum and stratum basale of human skin to meet the body's vitamin D requirements,[4] and melanin content does not alter the amount of vitamin D that can be produced.[11] Thus, individuals with higher skin melanin content will simply require more time in sunlight to produce the same amount of vitamin D as individuals with lower melanin content. As noted below, the amount of time an individual requires to produce a given amount of Vitamin D may also depend upon the person's distance from the equator and on the season of the year.

    [edit] Synthesis mechanism (form 3)
    1. Vitamin D3 is synthesized from 7-dehydrocholesterol, a derivative of cholesterol, which is then photolyzed by ultraviolet light in 6-electron conrotatory electrocyclic reaction. The product is pre-vitamin D3.
    2. Pre-vitamin D3 then spontaneously isomerizes to Vitamin D3 in a antarafacial hydride [1,7]Sigmatropic shift.
    3. Whether it is made in the skin or ingested, vitamin D3 (cholecalciferol) is then hydroxylated in the liver to 25-hydroxycholecalciferol (25(OH)D3 or calcidiol) by the enzyme 25-hydroxylase produced by hepatocytes, and stored until it is needed.

    25-hydroxycholecalciferol is further hydroxylated in the kidneys by the enzyme 1α-hydroxylase, into two dihydroxylated metabolites, the main biologically active hormone 1,25-dihydroxycholecalciferol (1,25(OH)2D3 or calcitriol) and 24R,25(OH)2D3. This conversion occurs in a tightly regulated fashion.

    Calcitriol is represented below right (hydroxylated Carbon 1 is on the lower ring at right, hydroxylated Carbon 25 is at the upper right end).

    [edit] Mechanism of action

    Once vitamin D is produced in the skin or consumed in food, it is converted in the liver and kidney to form 1,25 dihydroxyvitamin D, (1,25(OH)2D) the physiologically active form of vitamin D (when "D" is used without a subscript it refers to either D2 or D3). Following this conversion, the hormonally active form of vitamin D is released into the circulation, and by binding to a carrier protein in the plasma, vitamin D binding protein (VDBP), it is transported to various target organs.[3]

    The hormonally active form of vitamin D mediates its biological effects by binding to the vitamin D receptor (VDR), which is principally located in the nuclei of target cells.[3] The binding of calcitriol to the VDR allows the VDR to act as a transcription factor that modulates the gene expression of transport proteins (such as TRPV6 and calbindin), which are involved in calcium absorption in the intestine.

    The Vitamin D receptor belongs to the nuclear receptor superfamily of steroid/thyroid hormone receptors, and VDR are expressed by cells in most organs, including the brain, heart, skin, gonads, prostate, and breast. VDR activation in the intestine, bone, kidney, and parathyroid gland cells leads to the maintenance of calcium and phosphorus levels in the blood (with the assistance of parathyroid hormone and calcitonin) and to the maintenance of bone content.[12]

    The VDR is known to be involved in cell proliferation, differentiation. Vitamin D also affects the immune system, and VDR are expressed in several white blood cells including monocytes and activated T and B cells.[9]

    [edit] Nutrition

    Few foods are naturally rich in vitamin D, and most vitamin D intake is in the form of fortified products including milk, soy milk and cereal grains or supplements.[1]

    A blood calcidiol (25-hydroxy-vitamin D) level is the accepted way to determine vitamin D nutritional status. The optimal level of serum 25-hydroxyvitamin D is 35–55 ng/mL; with some debate among medical scientists for the slightly higher value.

    The U.S. Dietary Reference Intake for adequate intake (AI) of vitamin D for infants, children and men and women aged 19–50 is 5 micrograms/day (200 IU/day).[13] Adequate intake increases to 10 micrograms/day (400 IU/day) for men and women aged 51–70 and up to 15 micrograms/day (600 IU/day) past the age of 70. These dose rates will be too low during winter months above 30° latitude. In the absence of sun exposure, 1000 IU of cholecalciferol is required daily for children. 4000 IU of vitamin D may be required for adults absent summer UVB. [1]
    Milk and cereal grains are often fortified with vitamin D.
    Milk and cereal grains are often fortified with vitamin D.

    In light of its apparent health benefits, The Canadian Cancer Society recommends that non-white adults take 1,000 IU daily year-round and whites take that amount in fall and winter. The Canadian Pediatric Society recommends 2,000 IU daily for pregnant and breastfeeding women.[14]

    [edit] In food

    Season, geographic latitude, time of day, cloud cover, smog, and sunscreen affect UV ray exposure and vitamin D synthesis in the skin, and it is important for individuals with limited sun exposure to include good sources of vitamin D in their diet.

    In some countries, foods such as milk, yogurt, margarine, oil spreads, breakfast cereal, pastries, and bread are fortified with vitamin D2 and/or vitamin D3, to minimize the risk of vitamin D deficiency.[15] In the United States and Canada , for example, fortified milk typically provides 100 IU per glass, or one quarter of the estimated adequate intake for adults over the age of 50.[1]
    Fatty fish, such as salmon, are natural sources of vitamin D.
    Fatty fish, such as salmon, are natural sources of vitamin D.

    Fortified foods represent the major dietary sources of vitamin D, as very few foods naturally contain significant amounts of vitamin D.

    Natural sources of vitamin D include:[1]

    * Fish liver oils, such as cod liver oil, 1 Tbs. (15 mL) provides 1,360 IU
    * Fatty fish species, such as:
    o Herring, 3 oz provides 1383 IU
    o Catfish, 3 oz provides 425 IU
    o Salmon, cooked, 3.5 oz provides 360 IU
    o Mackerel, cooked, 3.5 oz, 345 IU
    o Sardines, canned in oil, drained, 1.75 oz, 250 IU
    o Tuna, canned in oil, 3 oz, 200 IU
    o Eel, cooked, 3.5 oz, 200 IU
    * Mushrooms provide over 2700 IU per serving (approx. 3 oz or 1/2 cup) of vitamin D2, if exposed to just 5 minutes of UV light after being harvested;[16] this is one of a few natural food-based sources of vitamin D for vegans.
    * One whole egg, 20 IU

    [edit] Deficiency

    Vitamin D deficiency can result from: inadequate intake coupled with inadequate sunlight exposure, disorders that limit its absorption, conditions that impair conversion of vitamin D into active metabolites, such as liver or kidney disorders, or, rarely, by a number of hereditary disorders.[2] Deficiency results in impaired bone mineralization, and leads to bone softening diseases, rickets in children and osteomalacia in adults, and possibly contributes to osteoporosis.[2]

    [edit] Diseases caused by deficiency
    Calcitriol (1,25-dihydroxycholecalciferol). Active form. Note extra OH groups at upper right and lower right.
    Calcitriol (1,25-dihydroxycholecalciferol). Active form. Note extra OH groups at upper right and lower right.

    The role of diet in the development of rickets was determined by Edward Mellanby between 1918–1920.[17] In 1921 Elmer McCollum identified an anti-rachitic substance found in certain fats could prevent rickets. Because the newly discovered substance was the fourth vitamin identified, it was called vitamin D.[17] The 1928 Nobel Prize in Chemistry was awarded to Adolf Windaus, who discovered the steroid 7-dehydrocholesterol, the precursor of vitamin D.

    Vitamin D deficiency is known to cause several bone diseases[18] including:

    * Rickets, a childhood disease characterized by impeded growth, and deformity, of the long bones. The earliest sign of subclinical vitamin D deficiency is Craniotabes, abnormal softening or thinning of the skull.[19]
    * Osteomalacia, a bone-thinning disorder that occurs exclusively in adults and is characterized by proximal muscle weakness and bone fragility.
    * Osteoporosis, a condition characterized by reduced bone mineral density and increased bone fragility.

    Prior to the fortification of milk products with vitamin D, rickets was a major public health problem. In the United States, milk has been fortified with 10 micrograms (400 IU) of vitamin D per quart since the 1930s, leading to a dramatic decline in the number of rickets cases.[12]

    Vitamin D malnutrition may also be linked to an increased susceptibility to several chronic diseases such as high blood pressure, tuberculosis, cancer, periodontal disease, multiple sclerosis, chronic pain, depression, schizophrenia, seasonal affective disorder, peripheral artery disease[20] and several autoimmune diseases including type 1 diabetes (see role in immunomodulation).[12][21]

    [edit] Groups at greater risk of deficiency

    Vitamin D requirements increase with age, while the ability of skin to convert 7-dehydrocholesterol to pre-vitamin D3 decreases.[22] In addition the ability of the kidneys to convert calcidiol to its active form also decreases with age, prompting the need for increased vitamin D supplementation in elderly individuals. One consensus concluded that for optimal prevention of osteoporotic fracture the blood calcidiol concentration should be higher than 30 ng/mL, which is equal to 75 nmol/L.[23] One billion people in the world are currently Vitamin D deficient, if 75 nmol/L is used as cutoff value for insufficiency.[24][25]

    The American Pediatric Association advises vitamin D supplementation of 200 IU/day (5μg/d) from birth onwards.[1] (1 IU Vitamin D is the biological equivalent of 0.025 μg cholecalciferol/ergocalciferol). The Canadian Paediatric Society recommends that pregnant or breastfeeding women consider taking 2000 IU/day, that all babies who are exclusively breastfed receive a supplement of 400 IU/day, and that babies living above 55 degrees latitude get 800 IU/day from October to April.[26] Health Canada recommends 400IU/day (10μg/d).[27] While infant formula is generally fortified with vitamin D, breast milk does not contain significant levels of vitamin D, and parents are usually advised to avoid exposing babies to prolonged sunlight. Therefore, infants who are exclusively breastfed are likely to require vitamin D supplementation beyond early infancy, especially at northern latitudes.[27] Liquid "drops" of vitamin D, as a single nutrient or combined with other vitamins, are available in water based or oil-based preparations ("Baby Ddrops(R)" in North America, or "Vigantol(R) oil" in Europe). However, babies may be safely exposed to sunlight for short periods; as little as 10 minutes a day without a hat can suffice, depending on location and season. The vitamin D used for in supplements and infant formula is not distinguishable in efficacy from that produced by the body naturally. The risk of overdose is not present with natural exposure to sunlight, because the skin's capacity to produce vitamin D is self-limiting (skin production is thought to reflect the dose of vitamin D to which our evolution optimized human biology). In contrast, care should be given to limit oral intake for infants to no more than 1000 IU (25 mcg) daily, or for adults no more than 10,000 IU (250 mcg) daily.

    Obese individuals may have lower levels of the circulating form of vitamin D, probably because of reduced bioavailability, and are at higher risk of deficiency. To maintain blood levels of calcium, therapeutic vitamin D doses are sometimes administered (up to 100,000 IU or 2.5 mg daily) to patients who have had their parathyroid glands removed (most commonly renal dialysis patients who have had tertiary hyperparathyroidism, but also to patients with primary hyperparathyroidism) or with hypoparathyroidism.[28] Patients with chronic liver disease or intestinal malabsorption disorders may also require larger doses of vitamin D (up to 40,000 IU or 1 mg (1000 micrograms) daily).

    The use of sunscreen with a sun protection factor (SPF) of 8 inhibits more than 95% of vitamin D production in the skin.[12][29] Recent studies showed that, following the successful "Slip-Slop-Slap" health campaign encouraging Australians to cover up when exposed to sunlight to prevent skin cancer, an increased number of Australians and New Zealanders became vitamin D deficient.[15] Ironically, there are indications that vitamin D deficiency may lead to skin cancer.[30] To avoid vitamin D deficiency dermatologists recommend supplementation along with sunscreen use.

    The reduced pigmentation of light-skinned individuals tends to allow more sunlight to be absorbed even at higher latitudes, thereby reducing the risk of vitamin D deficiency.[23] However, at higher latitudes (above 30°) during the winter months, the decreased angle of the sun's rays, reduced daylight hours, protective clothing during cold weather, and fewer hours of outside activity, diminish absorption of sunlight and the production of vitamin D. Because melanin acts like a sun-block, prolonging the time required to generate vitamin D, dark-skinned individuals, in particular, may require extra vitamin D to avoid deficiency at higher latitudes. In June 2007, The Canadian Cancer Society began recommending that all adult Canadians consider taking 1000 IU of vitamin D during the fall and winter months (when typically the country's northern latitude prevents sufficient sun-stimulated production of vitamin D).[31] At latitudes below 30° where sunlight and day-length are more consistent, vitamin D supplementation may not be required.[6] Individuals clad in full body coverings during all their outdoor activity, most notably women wearing burquas in daylight, are at risk of vitamin D deficiency. This poses a lifestyle-related health risk mostly for female residents of conservative Muslim nations in the Middle East, but also for strict adherents in other parts of the world.[32]

    [edit] Overdose

    For more details on this topic, see hypervitaminosis D.

    Vitamin D stored in the human body as calcidiol (25-hydroxy-vitamin D) has a large volume of distribution and a long half-life (about 20 to 29 days).[9] However, the synthesis of bioactive vitamin D hormone is tightly regulated and vitamin D toxicity usually occurs only if excessive doses (prescription forms or rodenticide analogs) are taken.[33] Although normal food and pill vitamin D concentration levels are too low to be toxic in adults, because of the high vitamin A content in codliver oil, it is possible to reach toxic levels of vitamin A (but not vitamin D) via this route, [34] if taken in multiples of the normal dose in an attempt to increase the intake of vitamin D. Most historical cases of vitamin D overdose have occurred due to manufacturing and industrial accidents.[35]

    Exposure to sunlight for extended periods of time does not cause vitamin D toxicity.[35] This is because within about 20 minutes of ultraviolet exposure in light skinned individuals (3–6 times longer for pigmented skin) the concentration of vitamin D precursors produced in the skin reach an equilibrium, and any further vitamin D that is produced is degraded.[36] Maximum endogenous production with full body exposure to sunlight is 250 µg (10,000 IU) per day.[35]

    The exact long-term safe dose of vitamin D is not entirely known, but dosages up to 250 micrograms (10,000 IU) /day in healthy adults are believed to be safe.[9], and all known cases of vitamin D toxicity with hypercalcemia have involved intake of or over 1,000 micrograms (40,000 IU)/day[35]. The U.S. Dietary Reference Intake Tolerable Upper Intake Level (UL) of vitamin D for children and adults is 50 micrograms/day (2,000 IU/day), with evidence that this value is too low by a factor of 5. In adults, sustained intake of 2500 micrograms/day (100,000 IU) can produce toxicity within a few months.[2] For infants (birth to 12 months) the tolerable UL is set at 25 micrograms/day (1000 IU/day), and vitamin D concentrations of 1000 micrograms/day (40,000 IU) in infants has been shown to produce toxicity within 1 to 4 months. In the United States, overdose exposure of vitamin D was reported by 284 individuals in 2004, leading to 1 death.[37] The Nutrition Desk Reference states "The threshold for toxicity is 500 to 600 micrograms [vitamin D] per kilogram body weight per day."[38] The US EPA published an oral LD50 of 619 mg/kg for female rats.[39]

    Serum levels of calcidiol (25-hydroxy-vitamin D) are typically used to diagnose vitamin D overdose. In healthy individuals, calcidiol levels are normally between 32 to 69 ng/mL (82 to 176 nmol/L), but these levels may be as much as 15-fold greater in cases of vitamin D toxicity. Serum levels of bioactive vitamin D hormone (1,25(OH2)D) are usually normal in cases of vitamin D overdose.[2]

    Some symptoms of vitamin D toxicity are a result of hypercalcemia (an elevated level of calcium in the blood) caused by increased intestinal calcium absorption. Vitamin D toxicity is known to be a cause of high blood pressure.[40] Gastrointestinal symptoms of vitamin D toxicity can include anorexia, nausea, and vomiting. These symptoms are often followed by polyuria (excessive production of urine), polydipsia (increased thirst), weakness, nervousness, pruritus (itch), and eventually renal failure. Other signals of kidney disease including elevated protein levels in the urine, urinary casts, and a build up of wastes in the blood stream can also develop.[2] In one study, hypercalciuria and bone loss occurred in four patients with documented vitamin D toxicity.[41] Another study showed elevated risk of ischaemic heart disease when 25D was above 89 ng/mL.[42]

    Vitamin D toxicity is treated by discontinuing vitamin D supplementation, and restricting calcium intake. If the toxicity is severe blood calcium levels can be further reduced with corticosteroids or bisphosphonates. In some cases kidney damage may be irreversible.[2]

    [edit] Role in immunomodulation
    Cholecalciferol (D3)
    Cholecalciferol (D3)

    The hormonally active form of vitamin D mediates immunological effects by binding to nuclear vitamin D receptors (VDR) which are present in most immune cell types including both innate and adaptive immune cells. The VDR is expressed constitutively in monocytes and in activated macrophages, dendritic cells, NK cells, T and B cells. In line with this observation, activation of the VDR has potent anti-proliferative, pro-differentiative, and immunomodulatory functions including both immune-enhancing and immunosuppressive effects.[43]

    Effects of VDR-ligands, such as vitamin D hormone, on T-cells include suppression of T cell activation and induction of regulatory T cells, as well as effects on cytokine secretion patterns.[44] VDR-ligands have also been shown to affect maturation, differentiation, and migration of dendritic cells, and inhibits DC-dependent T cell activation, resulting in an overall state of immunosuppression.[45]

    VDR ligands have also been shown to increase the activity of natural killer cells, and enhance the phagocytic activity of macrophages.[9] Active vitamin D hormone also increases the production of cathelicidin, an antimicrobial peptide that is produced in macrophages triggered by bacteria, viruses, and fungi.[46] Vitamin D deficiency tends to increase the risk of infections, such as influenza[47] and tuberculosis[48][49][50]. In a 1997 study, Ethiopian children with rickets were 13 times more likely to get pneumonia than children without rickets.[51]

    These immunoregulatory properties indicate that ligands with the potential to activate the VDR, including supplementation with calcitriol (as well as a number of synthetic modulators), may have therapeutic clinical applications in the treatment of; inflammatory diseases (rheumatoid arthritis, psoriatic arthritis), dermatological conditions (psoriasis, actinic keratosis), osteoporosis, cancers (prostate, colon, breast, myelodysplasia, leukemia, head and neck squamous cell carcinoma, and basal cell carcinoma), and autoimmune diseases (systemic lupus erythematosus, type I diabetes, multiple sclerosis) and in preventing organ transplant rejection.[43] However the effects of supplementation with vitamin D, as yet, remain unclear, and supplementation may be inadvisable for individuals with sarcoidosis and other diseases involving vitamin D hypersensitivity.[52][35][53][54] [55]

    A 2006 study published in the Journal of the American Medical Association, reported evidence of a link between Vitamin D deficiency and the onset of Multiple Sclerosis; the authors posit that this is due to the immune-response suppression properties of Vitamin D.[56]

    [edit] Role in cancer prevention and recovery

    The vitamin D hormone, calcitriol, has been found to induce death of cancer cells in vitro and in vivo. Although the anti-cancer activity of vitamin D is not fully understood, it is thought that these effects are mediated through vitamin D receptors expressed in cancer cells, and may be related to its immunomodulatory abilities. The anti-cancer activity of vitamin D observed in the laboratory has prompted some to propose that vitamin D supplementation might be beneficial in the treatment or prevention of some types of cancer.[9]

    A search of primary and review medical literature published between 1970 and 2007 found an increasing body of research supporting the hypothesis that the active form of vitamin D has significant, protective effects against the development of cancer. Epidemiological studies show an inverse association between sun exposure, serum levels of 25(OH)D, and intakes of vitamin D and risk of developing and/or surviving cancer. The protective effects of vitamin D result from its role as a nuclear transcription factor that regulates cell growth, differentiation, apoptosis and a wide range of cellular mechanisms central to the development of cancer.[57] In 2005, scientists released a metastudy which demonstrated a beneficial correlation between vitamin D intake and prevention of cancer. Drawing from a meta-analysis of 63 published reports, the authors showed that intake of an additional 1,000 international units (IU) (or 25 micrograms) of vitamin D daily reduced an individual's colon cancer risk by 50%, and breast and ovarian cancer risks by 30%.[58] Research has also shown a beneficial effect of high levels of calcitriol on patients with advanced prostate cancer.[59] A randomized intervention study involving 1,200 women, published in June 2007, reports that vitamin D supplementation (1,100 international units (IU)/day) resulted in a 60% reduction in cancer incidence, during a four-year clinical trial, rising to a 77% reduction for cancers diagnosed after the first year (and therefore excluding those cancers more likely to have originated prior to the vitamin D intervention).[60][61] In 2006, a study at Northwestern University found that taking the U.S. RDA of vitamin D (400 IU per day) cut the risk of pancreatic cancer by 43% in a sample of more than 120,000 people from two long-term health surveys.[62][63]

    A 2006 study using data on over 4 million cancer patients from 13 different countries showed a marked difference in cancer risk between countries classified as sunny and countries classified as less–sunny for a number of different cancers.[64] Research has also suggested that cancer patients who have surgery or treatment in the summer — and therefore make more endogenous vitamin D — have a better chance of surviving their cancer than those who undergo treatment in the winter when they are exposed to less sunlight.[65]

    However, a large scientific review undertaken by the National Cancer Institute found no link between baseline vitamin D status and overall cancer mortality. They did find that vitamin D was beneficial in preventing colorectal cancer, which showed an inverse relationship with blood levels "80 nmol/L or higher associated with a 72% risk reduction".[66]

    [edit] Role in coronary disease prevention

    Research indicates that vitamin D may play a role in preventing or reversing coronary disease.[67] As with cancer incidence, a qualitative inverse correlations was found between coronary disease incidence and serum vitamin D levels of 32.0 versus 35.5 ng/mL.[68] Cholesterol levels were found to be reduced in gardeners in the UK during the summer months.[69] Heart attacks peak in winter and decline in summer in temperate[70] but not tropical latitudes.[71] The issue of vitamin D in heart health has not yet been settled. Exercise may account for some of the benefit attributed to vitamin D, since vitamin D levels are higher in physically active persons.[72] Moreover, there may be an upper limit after which cardiac benefits decline. One study found an elevated risk of ischaemic heart disease in Southern India in individuals whose vitamin D levels were above 89 ng/mL.[73] These sun-living groups results do not generalize to sun-deprived urban dwellers. Among a group with heavy sun exposure, taking supplemental vitamin D may result in blood levels over the ideal range, while urban dwellers not taking supplemental vitamin D may fall under the levels recognized as ideal, and being above or below the preferable levels may cause adverse affects on the health of each group.

    Researchers at the Harvard Medical School in Boston reported in Circulation, the Journal of the American Heart Association, January 2008 that vitamin D deficiency is associated with an increase in high blood pressure and cardiovascular risk. Researchers monitored the vitamin D levels, blood pressure and other cardiovascular risk factors of 1739 people, of an average age of 59 years for 5 years. They found that those people with low levels of vitamin D had a 62% higher risk of a cardiovascular event than those with normal vitamin D levels.[74]
  48. Shishir.

    Shishir. Guest

    List of drugs that causes agranulocytosis or neutropenia sorted as per probability
    (Anti-neoplastic drugs are not included)

    Dipyrone
    Mianserin
    Sulfasalazine
    Co-trimoxazole
    Anti-arrythmic agents
    Procainamide
    Ajmaline
    Tocainide
    Aprindine
    Amiodarone
    Penicillins
    Amoxycillin
    Aziocillin
    Benzylpenicillin
    Phenethicillin
    Cloaxacillin and penicillin
    Thiouracil derivatives
    Methyl thiouracil
    Propyl thiourcil
    Phenylbutazone
    Cimetidine
    Penicillamine
    Diclofenac
    Carbamazepine
    ACE-Inhibitors
    Captopril
    Enalapril
    Hydrochlorothiazide with potassium sparing diuretics
    Indomethacine
    Cephalosporins
    Cephalexin
    Cepahazolin
    Cefuroxime
    Cefitaxime
    Cephradine
    Oxyphenbutazone
    Nitrofurantoin
    Salicylic acid derivatives
    Clozapine
    Carbimazone
    Sulphonylurea derivatives
    Glibenclamide
    Tolbutamide
    Methyldopa
    Thiamazole
    Nucleosides
    Aminoglutethimide
    Ibuprofen
    Pentazocine
    Levamizole
    Promethazine
    Chloramphinicol
    Acetaminophen and combinations
    Perazine
    Mebhydrolin
    Ranitidine
    Imipramine
    Miscellaneous drugs (relatively lower probability)
    Phenytoin
    Chlorthalidone
    Sulphamethizole
    Norfloxacin
    Naproxen
    Clomipramine
    Trazodone
    Omeprazole
    Alimemazine
    Pirenzepine
    Ticlopidine
    Ibopamine
    Hydralazine
    Nifedipine
    Nalidixic acid
    Doxycycline
    Clindamycin
    Gentamycin
    Fusidic acid
    Dapsone
    Azapropazone
    Propyphenazone
    Sulindac
    Piroxicam
    Pirprofen
    Niflumic acid
    Allopurinol
    Glafenine
    Valproate
    Levadopa with carbidopa
    Chlorpramazine
    Haloperidol
    spironolactone
    Zuclopenthixol
    Zopiclone
    Cinnarizine
    Metronidazole
    Pyrimethamine combinations
    Thophylline
  49. Shishir.

    Shishir. Guest

    In Tolosa-Hunt syndrome

    , inflammation of the cavernous sinus (behind the eyes) causes severe eye pain and irritation or damage of the nerves of the face. Males and females are affected equally by Tolosa-Hunt syndrome, which usually affects people more than 20 years old.
    Symptoms
    Tolosa-Hunt syndrome begins with severe pain behind or around one eye that comes on suddenly. The pain can be constant and intense. As the sinus inflammation increases and spreads, nerves in the face can be affected, producing symptoms such as drooping eyelid (ptosis) of the affected eye or numbness and tingling in the forehead. Difficulty controlling eye movements (ophthalmoplegia) and the pupil may cause sensitivity to light and double or blurred vision. If left untreated, vision loss is possible.
    Diagnosis
    The International Headache Society criteria for Tolosa-Hunt syndrome are:
    One-sided eye pain for an average of 8 weeks if left untreated
    Associated irritation or damage to the third, fourth, or sixth cranial nerves
    The pain is relieved within 48 hours of starting to take steroid medication
    Other conditions have been ruled out by testing.
    Often, the last condition is the most important, since many conditions can causes symptoms similar to Tolosa-Hunt syndrome. Magnetic resonance imagaing (MRI), angiography, or computed tomography (CT) can help determine if somthing else, such as a tumor, is causing the eye pain. If Tolosa-Hunt syndrome is present, the sinus inflammation can generally be seen during these tests as well.
    Treatment
    Fortunately, Tolosa-Hunt syndrome is not a fatal disorder, and can be treated with steroid medication such as prednisone. This usually provides pain relief within 24-72 hours of starting to take the medication. The vision problems and forehead numbness may take weeks or months to resolve, and sometimes the symptoms never go away completely.
    As many as 30-40% of individuals may have a relapse (recurrence) of Tolosa-Hunt syndrome, generally on the same side. Because many disorders can have similar symptoms, individuals should report any new symptoms or side effects from treatment to their physicians.
  50. Shishir.

    Shishir. Guest

    Testicular tumors account for 2% of all pediatric tumors, with an incidence of 0.05-2 per 100,000 children. A bimodal age distribution is observed; one peak occurs in the first 2 years of life, and the second occurs in young adulthood.

    Pediatric prepubertal testicular tumors are dramatically different from adult neoplasms. Germ-cell tumors account for only 60-77% of testicular tumors in children but account for 95% of testicular tumors in adults. Adult germ-cell tumors with malignant potential, such as seminoma and embryonal carcinoma, are not present in prepubertal patients. Teratomas, which are uniformly benign in children, are often malignant in adults.

    The most common germ-cell tumors are teratomas and yolk-sac tumors, which account for about 65% of testis tumors. Some series report that teratomas, which most believe are vastly underreported because of their benign nature, may account for almost 50% of prepubertal testicular tumors. However, in tumor registries yolk-sac tumors are more common than teratomas, which may reflect a reporting bias.1, 2 Gonadal stromal tumors are significantly less frequent than germ-cell tumors (ie, tumors of non–germ-cell origin) and primarily include juvenile granulosa-cell tumors, Leydig-cell tumors, and Sertoli-cell tumors.

    The vast majority of yolk-sac tumors in children (85%) present as clinical stage I disease, compared with 35% in adults. Alpha-fetoprotein (AFP) can be used as a reliable marker because levels are increased in more than 90% of yolk-sac tumors and because the yolk sac is extremely sensitive to chemotherapy. Therefore, patients can be safely managed with observation after orchiectomy followed by chemotherapy for recurrent tumors. Retroperitoneal lymph node dissection is limited to those children with persistent retroperitoneal lymphadenopathy or increased serum tumor markers after orchiectomy and chemotherapy.

    Prepubertal teratomas account for 30% of testicular germ-cell tumors in children and are uniformly benign. Although 80-90% of adult teratomas are found to contain carcinoma in situ elsewhere in that testis, this is not true in prepubertal boys with teratoma. Histology is often pure with diploid DNA content containing all 3 embryological germ layers (ectoderm, mesoderm, and endoderm). Testis-sparing surgery with frozen section is a reasonable consideration for this and other benign prepubertal tumors. No follow-up is recommended for prepubertal teratomas, whereas postpubertal patients should be followed as adults.

    Epidermoid cysts are benign tumors of epithelial origin. They are often firm and well-defined, with a central hypoechoic region or mixed internal echogenicity surrounded by an echogenic rim on ultrasonography. These tumors are benign and, following tumor enucleation, do not require follow-up.

    Seminomas and mixed germ-cell tumors are extremely rare in prepubertal children. Most believe that seminomas should be managed as in adults and mixed germ cell tumors should be treated based on the most malignant subtype.

    Sertoli-cell tumors are the most common gonadal stromal tumors in prepubertal children. These tumors tend to appear as painless masses in boys younger than 6 months and produce no endocrinologic effects; however, 14% of patients present with gynecomastia. All reported lesions in children less than 5 years of age have been benign. Therefore, children younger than 5 are adequately treated with orchiectomy and do not require metastatic evaluation. Older children should undergo chest radiography and abdominal CT scanning to rule out metastases. Metastases are treated with a combination of radiotherapy, chemotherapy, and retroperitoneal lymph node dissection. Large-cell calcifying Sertoli-cell tumor is a variant with large amounts of cytoplasm and calcification. One-third of patients with this tumor have associated genetic abnormalities; however, these tumors are universally benign.

    Leydig-cell tumors are the second most common gonadal stromal tumors in children and are also benign. These tumors most often occur in boys aged 5-10 years, and the synthesis of testosterone may produce precocious puberty, gynecomastia, and elevated levels of 17-ketosteroids. Leydig-cell tumors must be differentiated from hyperplastic nodules that develop in boys with poorly controlled congenital adrenal hyperplasia (CAH).

    Juvenile granulosa-cell tumors account for 27% of all neonatal testicular tumors and commonly appear as cystic, painless testicular masses. They almost exclusively appear in the first year of life and most appear by age 6 months. They can be associated with anomalies of the Y chromosome, mosaicism, and ambiguous genitalia. These tumors are hormonally inactive and benign.

    Gonadoblastoma occurs in association with disorders of sexual development (intersex). About 80% of cases involve phenotypic females with intra-abdominal testes or streak gonads. The putative gonadoblastoma gene is on the Y chromosome, and the tumor almost always develops in a child with a Y chromosome. The streak gonads in patients with mixed gonadal dysgenesis often develop gonadoblastomas. The incidence peaks at puberty, and early gonadectomy is recommended in patients at risk for gonadoblastoma. Metastatic spread of a gonadoblastoma occurs in 10% of patients. These tumors may elevate serum levels of beta-human chorionic gonadotropin (beta-HCG).

    Cystic dysplasia of the testis is a benign lesion that is often associated with ipsilateral renal agenesis or dysplasia. This association, along with a characteristic ultrasonographic appearance (ie, hypoechoic lesions), permits preoperative diagnosis and possible treatment with testicular-sparing surgery.

    Leukemia and lymphoma are the most common malignancies to affect the testis secondarily and account for 2-5% of all testis tumors; most present bilaterally. Because the blood-testis barrier may protect the intratesticular cells, the testis may be the site of residual tumor in children after therapy.

    Paratesticular structures can give rise to various benign (lipoma, leiomyoma, hemangioma, or fibroma) and malignant tumors; however, these are extremely rare. Rhabdomyosarcoma is the most common malignant tumor (17%) and may arise from the distal spermatic cord and appear as a scrotal mass or hydrocele. These tumors have a bimodal distribution and occur in boys aged 3-4 months and in teenagers. As many as 70% of patients have involvement of the retroperitoneal lymph nodes at presentation. These tumors are highly aggressive and spread via the blood, lymphatics, or direct extension to the lungs, the cortical bone, or to the bone marrow in 20% of patients at the time of diagnosis. Radical inguinal orchiectomy followed by retroperitoneal lymph node dissection is recommended for all children older than 10 years, and in those younger than 10 years with retroperitoneal disease. Those with positive lymph nodes are treated with multimodal therapy (chemotherapy and radiation).

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