Home >> Exams >> MD MS EE >> AIIMS MD MS EE >> AIIMS MD MS EE 2008 NOVEMBER >> ForumTopic: AIIMS MD MS EE 2008 November Mock Test Series is online now
You need to be logged in to post messages.
| Author: | Message |
| Admin Total Posts: 890 | Posted: Mon Sep 15, 2008 01:03 am Dear Users, AIIMS MD MS Entrance Examination 2008 November Mock Test Series is online now and can be accessed here - https://www.netmedicos.com/?aiimsmdmsee2008nov/mocktestseries/dailymock4aiimsmdmsee2008nov/ The old AIIMS mock test series for 2008 May examination is over now. You can access the new series and take one mock test daily to compare your performance with respect to other examinees. With regards, Netmedicos |
| Varunrag Total Posts: 72 | Posted: Wed Oct 01, 2008 02:19 am Most radiosensitive tumor ? Ca pancreas or cervix |
| PAMELA Total Posts: 9 | Posted: Thu Oct 09, 2008 09:54 pm ca cervix..... for sure.. ca pancreas is radio resitant |
| superbdoc Total Posts: 273 | Posted: Fri Oct 17, 2008 03:11 am Instead of creatin new topic I am clubbing some questions from Mock test series that acc to me merit discussion...Others are welcome to add on. Test 947 Question 16: On sectioning of an organ at the time of autopsy, a focal, wedge-shaped firm area is seen accompanied by extensive hemorrhage, with a red appearance. The lesion has a base on the surface of the organ. This finding is typically of ? A) Lung with pulmonary thromboembolism B) Heart with coronary thrombosis C) Liver with hypovolemic shock D) Kidney with septic embolus |
| jemzcal Total Posts: 127 | Posted: Fri Oct 17, 2008 03:30 am lung is the organ with dual blood supply. hence the infarcts there will be red. and the description in the q fits lung infarction |
| superbdoc Total Posts: 273 | Posted: Fri Oct 17, 2008 03:57 am Thanx jemzcal for reply and approach to it.. Next up... Same series...A direct question... Reduced salivary flow following irradiation is dose dependent. At what does does the flow reach essentially zero ? A) 4000 rads B) 5000 rads C) 6000 rads D) 7000 rads Please give the reference too to enable all users get allied questions...  |
| superbdoc Total Posts: 273 | Posted: Fri Oct 17, 2008 05:58 am BAL is useful in treating poisoning due to all except ? A) Lead B) Organic Mercury C) Cadmium D) Arsenic |
| superbdoc Total Posts: 273 | Posted: Fri Oct 17, 2008 06:04 am In Klippel-Feil syndrome, the patient has all of the following clinical features except ? A) Low hair line B) Bilateral Neck webbing C) Bilateral shortness of sterno mastoid muscles D) Gross limitations of neck movements This is an often confusing qn for me....so do clear it.. |
| superbdoc Total Posts: 273 | Posted: Fri Oct 17, 2008 06:06 am Misexpression of which of the following homoeobox genes alters the position of the forelimbs during development ? A) HOXA7 B) HOXB8 C) HOXC9 D) HOXD10 Whats thi HOX and the whole funda....Is it just mug up..?? |
| jemzcal Total Posts: 127 | Posted: Fri Oct 17, 2008 05:17 pm BAL is cintraindicated in Fe and Cd poisoning |
| superbdoc Total Posts: 273 | Posted: Tue Oct 21, 2008 04:54 pm Test :952 Question 11 When does switch-over from fetal to adult hemoglobin synthesis begin ? A) 14 weeks gestation B) 30 weeks gestation C) 36 weeks gestation D) 7 - 10 days postnatal Key Answer: A My Answer: C Please comment/clarify...  |
| superbdoc Total Posts: 273 | Posted: Tue Oct 21, 2008 04:55 pm where is Quiz # 950...?? I cant see that..  |
| superbdoc Total Posts: 273 | Posted: Wed Oct 22, 2008 06:17 pm Qn. 16 in AIIMS mock 909 Autoimmunity can be caused due to all of the following except ? A) The presence of forbidden clones B) Expression of cryptic antigens C) Negative selection of T-cells in the thymus D) Inappropriate expression of the MHC proteins Please solve/tell which years repeat this is...  |
| jemzcal Total Posts: 127 | Posted: Wed Oct 22, 2008 09:49 pm putting it simply,, autoimmunity results when there is a defect in the normal immunoregulatory system. if we look at the options and analyse option c, it is actually a process that occurs normally in the thymus. by negative selection we eliminate antigens that are similar to constituents in our body. so how can a normal process cause autoimmunity!! i cant locate which years paper this was from. |
| kolsurgeon Total Posts: 13 | Posted: Thu Oct 23, 2008 08:07 am Here is the complete explanation: A) Presence of forbidden clones causes autoimmunity. Normally, there is a random production of T cells due to permutations and combinations leading to formation of different clones of cells each clone being directed against a specific antigen. The thymus processes these T cells so that there is a NEGATIVE SELECTION of T cells which have the receptor directed against the common body antigens. These are known as forbidden clones. When these clones are accidentally present due to thymic malfunction, autoimmunity results. B) Expression of crypic antigens also causes autoimmunity. Cryptic antigens are normally secluded from the knowledge of the thymus so that the thymus cannot delete the particular clone of cells directed against these antigens. A common example is the antigens of the testis (the blood testis barrier prevents testicular antigens to come to the knowledge of the thymus). This process can be reversed during vasectomy when these antigens are expressed into the circulation. C) is the correct answer as has been described. D) In appropriate expression of the MHC proteins also causes autoimmunity. The T cells recognize an antigen presented to them in conjunction with the MHC protein which is specific for a particular individual. If there is mal-expression of the MHC complex then the T cells would mount an action against the cells expressing these abnormal proteins and autoimmunity results.  |
| jemzcal Total Posts: 127 | Posted: Thu Oct 23, 2008 08:56 am wow!!!! |
| kolsurgeon Total Posts: 13 | Posted: Thu Oct 23, 2008 09:05 am Many of you are pretty much confused with the question regarding the HOX genes so I thought I would highlight some important points related to that since it is an extensive topic! A homeobox is a DNA sequence found within genes that are involved in the regulation of patterns of development (morphogenesis) in animals, fungi and plants. Genes that have a homeobox are called homeobox genes and form the homeobox gene family. Hox genes are a subgroup of homeobox genes. In vertebrates these genes are found in gene clusters on the chromosomes. In mammals four such clusters exist, called Hox clusters (Hox A, Hox B, Hox C, Hox D). The gene name "Hox" has been restricted to name Hox cluster genes in vertebrates. Only genes in the HOX cluster should be named Hox genes. So note: homeobox genes are NOT Hox genes, Hox genes are a subset of homeobox genes. Hox genes are of utmost importance because they determine segmental pattern during development. Hox A: Present in chromosome 7. Subsets of Hox A genes of importance include: Hox A5: Methylation of this gene may result in the loss of its expression and, since the encoded protein upregulates the tumor suppressor p53, this protein may play an important role in tumorigenesis. Hox A7: This gene is highly similar to the antennapedia (Antp) gene of Drosophila. Hox A9: A specific translocation event which causes a fusion between this gene and the NUP98 gene has been associated with myeloid leukemogenesis. Hox A10: it may function in fertility, embryo viability, and regulation of hematopoietic lineage commitment. Hox A11: This gene is involved in the regulation of uterine development and is required for female fertility. Mutations in this gene can cause radio-ulnar synostosis with amegakaryocytic thrombocytopenia. Hox A13: Expansion of a polyalanine tract in the encoded protein of this gene can cause hand-foot-uterus syndrome, also known as hand-foot-genital syndrome. Hox B cluster is present in chromosome 17. Important gene subsets include: Hox B2: Increased expression of this gene is associated with pancreatic cancer. Hox B3: Increased expression of this gene is associated with a distinct biologic subset of acute myeloid leukemia (AML). Hox B4: Intracellular or ectopic expression of this protein expands hematopoietic stem and progenitor cells in vivo and in vitro, making it a potential candidate for therapeutic stem cell expansion. Hox B5: Increased expression of this gene is associated with a distinct biologic subset of acute myeloid leukemia (AML) and the occurrence of bronchopulmonary sequestration (BPS) and congenital cystic adenomatoid malformation (CCAM) tissue. Hox B6: involved in development of lung and skin. Altered expression of this gene or a change in the subcellular localization of its protein is associated with some cases of acute myeloid leukemia and colorectal cancer. Hox B7: Increased expression of this gene is associated with some cases of melanoma and ovarian carcinoma. Hox B8: Increased expression of this gene is associated with colorectal cancer and the obsessive-compulsive spectrum disorder trichotillomania. Hox B9: Increased expression of this gene is associated with some cases of leukemia, prostate cancer and lung cancer. Hox B13: This gene has been implicated to play a role in fetal skin development and cutaneous regeneration. Hox C cluster is present in chromosome 12. Important gene subsets include: Hox C8: The product of this gene may play a role in the regulation of cartilage differentiation. It could also be involved in chondrodysplasias or other cartilage disorders. Hox C11: It has a role in early intestinal development. Hox C13: The product of this gene may play a role in the development of hair, nail, and filiform papilla. Hox D cluster is present on chromosome 2. Important gene subsets are: Hox D1: Mutations in this gene have been associated with severe developmental defects on the anterior-posterior (a-p) limb axis. Hox D3, D4, D8, D11, D12, D13: Deletions that removed the entire HOXD gene cluster or 5' end of this cluster have been associated with severe limb and genital abnormalities. In addition, Hox D4 may play a role in determining positional values in developing limb buds. Hox D8 may also play a role in adult urogenital tract function. Mutations of Hox D13 cause synpolydactyly. Hox D10: The encoded nuclear protein functions as a sequence-specific transcription factor that is expressed in the developing limb buds and is involved in differentiation and limb development. Mutations in this gene have been associated with Wilm's tumor and congenital vertical talus (also known as "rocker-bottom foot" deformity or congenital convex pes valgus) and/or a foot deformity resembling that seen in Charcot-Marie-Tooth disease. Hope this information is useful to you all! I have extensively researched on this topic so you can be dea sure about the information! |
| superbdoc Total Posts: 273 | Posted: Thu Oct 23, 2008 02:28 pm thanx kolsurgeon for that exhaustive report.....I am definitely indebted for your research and help.... |
| superbdoc Total Posts: 273 | Posted: Thu Oct 23, 2008 02:30 pm Has any1 noticed the salivary flow qn and Klippel-Feil qn...?? Please help if u find time... |
| jemzcal Total Posts: 127 | Posted: Thu Oct 23, 2008 03:08 pm we declare you as an asset to this discussion panel. keep up the posts. great job. |
| jemzcal Total Posts: 127 | Posted: Thu Oct 23, 2008 04:54 pm kindly spare your thoughts on this question which type of hyperthyroidism shows raised uptake of I131? a goitrous b euthyroid c hypothalamic d schirmidt's node |
| kolsurgeon Total Posts: 13 | Posted: Thu Oct 23, 2008 06:38 pm Again, many of you are having a problem understanding this syndrome so I thought maybe I should try and explain you the whole syndrome complex so that you don't have to mug it up blindly! Klippel-Feil syndrome The central problem in Klippel Feil syndrome is a congenital fusion or synostosis of 2 or more cervical vertebrae. Now, try to imagine what happens when the cervical spine shortens: it leads to a shortening of the neck and as a result of shortening of the neck there is a low posterior hairline in addition. This fusion of the cervical spine leads to a decreased range of motion (ROM) of the cervical spine. Please note that flexion and extension of the neck are better preserved than lateral motion of the neck because the former occur between the occiput and the atlas. It is important to remember that the changes that occur in the anterior part of the neck are secondary to the spinal abnormality and not congenital. To compensate for this cervical spine shortening, the skin and muscles of the anterior part of the neck take on a webbed appearance, also known as "pterygium colli". Therefore, neck webbing is also present in this syndrome. The sternomastoid muscle is not abnormal by itself but may be contracted in certain individuals (leading to torticollis) and these individuals would have an increased range of motion of the neck following release of the contracted sternomastoid. In any event, the sternomastoid is NOT shortened. Therefore, Klippel-Feil syndrome comprises of: 1. Shorteing of cervical spine. 2. Bilateral neck webbing. 3. Decreased range of motion of neck. 4. occasional contraction of sternomastoid which is essentially normal. It is important to note the associated anomalies in this syndrome: 1. Musculoskeletal: cervical ribs, congenital fusion of ribs, syndactyly, CTEV, sacral agenesis. 2. Urinary tract abnormalities: renal agenesis, horseshoe kidney, double collecting system, renal ectopia. All patients diagnosed with Klippel-Feil syndrome need to have a complete genitourinary evaluation. 3. Cardiovascular anomalies: VSD, PDA, coarctation of aorta, patent foramen ovale. 4. Lung, ovarian and vaginal anomalies. 5. Deafness. 6. Synkinesia or mirror movements. 7. Various types of neurological deficits. I have deliberately included only the most important ones from the purpose of your examinations. Let's hope this clears your doubts!! In the end, I thought that maybe it would be beneficial to highlight a few characteristics of the Klippel-Trenaunay-Weber syndrome: 1. Port-wine stains. 2. Varicose veins. 3. Hemihypertrophy. The important point to remember is that arteriovenous fistulae are RARELY found in this syndrome (which distinguishes this from Parkes-Weber syndrome where hypertrophy occurs as a result of A-V fistulae). |
| superbdoc Total Posts: 273 | Posted: Thu Oct 23, 2008 06:51 pm It is such a wonderful original post...I thank you and netmedicos for providing me a platform for my grievances.. |
| superbdoc Total Posts: 273 | Posted: Wed Dec 24, 2008 08:48 pm Any Hope of renewing the interest of members in this topic..?? Wish kolsurgeon returns soon |