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| verasian Total Posts: 63 | Posted: Fri Jan 18, 2008 06:46 pm i hope many answers are wrong in the rank projector... let all share every controversies in this thread.. more than 30 keys are wrong.. members let use the oppurtunity given by net medicos to the best.. thank you vasanth |
| verasian Total Posts: 63 | Posted: Fri Jan 18, 2008 06:48 pm i am sure that thrombophlebitis is seen except question the ans is prostrate .. need help from others |
| verasian Total Posts: 63 | Posted: Fri Jan 18, 2008 06:52 pm Flaring of anterior ends of rib is seen in? rickets |
| verasian Total Posts: 63 | Posted: Fri Jan 18, 2008 06:54 pm which of d foll is not a mode of suffocation ? i think the answer is throttling |
| verasian Total Posts: 63 | Posted: Fri Jan 18, 2008 06:55 pm okazaki fragments are seen in double stranded dna replication |
| verasian Total Posts: 63 | Posted: Fri Jan 18, 2008 06:57 pm in g6pd hemolysis seen wit all except-- pyrimethamine will be answer.. as chloroquine also causes hemolysis |
| verasian Total Posts: 63 | Posted: Fri Jan 18, 2008 06:58 pm poorest prognosis in AML.. it is monosomy 7 |
| keya2603 Total Posts: 2 | Posted: Fri Jan 18, 2008 07:51 pm i think most common drug used in pregnancy is methyl dopa |
| verasian Total Posts: 63 | Posted: Fri Jan 18, 2008 08:06 pm keya the question is drug used for hypertensive emergency in pregnancy.. it is labetolol only |
| verasian Total Posts: 63 | Posted: Fri Jan 18, 2008 08:08 pm regarding tubercular osteomyelits i think the ans is periosteal reaction..please others help |
| verasian Total Posts: 63 | Posted: Fri Jan 18, 2008 08:11 pm chorionic villous sampling is not essential for neural tube defects, it is the answer |
| kkrish Total Posts: 274 | Posted: Sat Jan 19, 2008 12:35 am G6 PD DEF.. qunine is not C/I.. ref lippincot biochem 3rd edition page 161.. clearly written..ANTIMALARIARLS INCLUDING PRIMAQUINE N NOT QUININE... |
| kkrish Total Posts: 274 | Posted: Sat Jan 19, 2008 12:57 am Q 184... MC type of occ a... SKIN... Q 180... AML..promylocytic transretinoic acid.. Q 176.. best urine sample.. SUPRA PUBIC... Q.. 169.. enteric fever.. amikacin is not used... q 138... cells not found in ca lung.. kulchitsky r found in small cell ca... though i too cant recall wat i had marked.. |
| litfiba Total Posts: 38 | Posted: Sat Jan 19, 2008 01:22 am agree with everythin except: doc in g6pd in chlorquine.. pyrimeth causes hemolysis just google it and doc in hypertension in preecclempsia in methyl dopa .. as it also reduces renal resistance.. katzung / google i do agree some of the answers and even some questions arent framed properly... there is one about imperforate anus but i clearly remember the child also had meconuria.. so we have to do perineal exploration which was the forth option also the treatment of the CAH and pregnancy wuetion is start steroids at the begining of pregnancy .. googled this |
| litfiba Total Posts: 38 | Posted: Sat Jan 19, 2008 01:30 am However if you are the parent of a child with CAH you no doubt want to be sure that if the unborn baby has inherited CAH then it is treated before birth. This is done by testing the unborn baby for CAH by taking a sample of tissue from the neck of the womb (chorionic villous sampling) or amniotic fluid early on in the pregnancy. This is then genetically tested to see if the unborn baby has CAH and also to determine its sex. Of course the doctors do not know the answer till nearly 14 weeks of the pregnancy so it is likely that they will ask you to take dexamethasone until the answer is known. If the unborn baby does not have CAH or is a carrier but is unaffected then the dexamethasone will be stopped and all will be well. However if the unborn baby has CAH and is a girl then the dexamethasone will be continued till baby is born. This is essential in unborn girls to prevent a build up of androgen turning their genitalia into that resembling boys. If the unborn baby is a boy then the specialist may advise stopping the mother’s dexamethasone as excessive male production in the unborn boy causes no problem. Of course affected babies will need treatment after birth. |
| litfiba Total Posts: 38 | Posted: Sat Jan 19, 2008 02:09 am 2 more corr: the q on mcc of rt aortic arch.. ans is tof.. refer braunwald cardio under tof... 25 % of tof pts have rt aortic arch.. incredible! secondly the q on increased chylomicrons : ans is typ 1 ... referred first aid for usmle step 1 .. which gives all types of lipidemias in a table.. chylomicrons are specifically for typ 1 though in type 3 they may be raised slightly.. really stupid q though and btw.. yaws in not an std.. it is transmitte through skin contact.. wikipedia |
| Admin Total Posts: 890 | Posted: Sat Jan 19, 2008 02:53 pm Dear Users, We have updated most of the corrections in Rank Projector. With regards, Netmedicos |
| verasian Total Posts: 63 | Posted: Sat Jan 19, 2008 03:50 pm friends robbins tel it pyrimethamine... with which shall we go |
| litfiba Total Posts: 38 | Posted: Sat Jan 19, 2008 06:47 pm q 8 ans is steroids .. thalidomide is only for resistant enl.. harr 971 q 28 .. ans is ascending aortic calcif... harr pg 1485 Destruction of collagen and elastic tissues leads to dilation of the aorta, scar formation, and calcification. These changes account for the characteristic radiographic appearance of a calcified ascending aortic aneurysm q 49 .. q was intractable glaucoma.. and the ans is Diffuse melanomas |
| litfiba Total Posts: 38 | Posted: Sat Jan 19, 2008 07:03 pm q 52.. ans is ATP repeat q q 71... je is ans aids is a zoonoses q 80 Although incision and drainage is a relatively quick and easy procedure that provides almost immediate relief to the patient, this approach should be discouraged because there is a tendency for the cyst or abscess to recur.1,5,16 One investigator17 reported a 13 percent failure rate for the procedure. Furthermore, incision and drainage may make later Word catheter placement or marsupialization difficult.1,16 Definitive drainage involves Word catheter placement for Bartholin's duct cysts and gland abscesses, and marsupialization for duct cysts https://www.aafp.org/afp/20030701/135.html Cysts may also be opened permanently, a method called marsupialization, in which an opening to the gland is formed with stitches which hold the secretion channel open. wikipeda q 81.. uterine massage is not invlolved in active man .. and early clamping is obviously imp |
| kkrish Total Posts: 274 | Posted: Sat Jan 19, 2008 07:27 pm jst regarding that q on meconuria.. while going trough baily i found two types of fistulas r der.. high n low ass wid imporforated anus.. meconuria is high fistula.. n treatment for it includes jst removing the fistula n colostomy.. fistula stump can b jst buried in the perinium.. this was imm after the exam.. i might b wrong also.. plz correct me..THEY SAY NA, UR EYES READ WAT UR MIND WANTS TO...  |
| litfiba Total Posts: 38 | Posted: Wed Jan 23, 2008 02:29 am q 52 ans is atp .. repeat q q71 JE needs a vector + HIV in humans originated from cross-species infections by simian viruses in rural Africa, probably due to direct human contact with infected primate blood. Current evidence is that the primate counterparts of HIV-1 and HIV-2 were transmitted to humans on multiple (at least seven) different occasions.. jawetz micro q 159 However if you are the parent of a child with CAH you no doubt want to be sure that if the unborn baby has inherited CAH then it is treated before birth. This is done by testing the unborn baby for CAH by taking a sample of tissue from the neck of the womb (chorionic villous sampling) or amniotic fluid early on in the pregnancy. This is then genetically tested to see if the unborn baby has CAH and also to determine its sex. Of course the doctors do not know the answer till nearly 14 weeks of the pregnancy so it is likely that they will ask you to take dexamethasone until the answer is known. If the unborn baby does not have CAH or is a carrier but is unaffected then the dexamethasone will be stopped and all will be well. However if the unborn baby has CAH and is a girl then the dexamethasone will be continued till baby is born. This is essential in unborn girls to prevent a build up of androgen turning their genitalia into that resembling boys. If the unborn baby is a boy then the specialist may advise stopping the mother’s dexamethasone as excessive male production in the unborn boy causes no problem. Of course affected babies will need treatment after birth. |
| litfiba Total Posts: 38 | Posted: Wed Jan 23, 2008 02:37 am https://www.dundee.ac.uk/medther/tayendoweb/congenital_adrenal_hyperplasia.htm q 80.. ans is marsupialisation .. refeered dutta and shaw Of note, attempts at incision and evacuation are therapeutic only when the lesion has become fluctuant.. johns hopkins manual |
| litfiba Total Posts: 38 | Posted: Wed Jan 23, 2008 02:41 am 86.. mcc of visual morbidity is cataract 115.. flumazenil - benzo antagonist 152.. the boy had GROSS hematuria .. IgA nephropathy is ans.. googled it |
| litfiba Total Posts: 38 | Posted: Wed Jan 23, 2008 02:47 am 167.. 4th option was decreased in valvular incompetence There are three groups of primary lymphoedema in which the functional abnormality and its cause are known; namely (a) large vessel abnormalities such as congenital aplasia of the thoracic duct or cysterna chyli, (b) congenital lymphatic valvular incompetence or congenital aplasia and (c) lymph node fibrosis. The remainder are characterised by a reduced number of lymphatics on lymphography. Such patients can be described as having obliterated lymphatics. If they present within a few years of birth they were probably born with too few lymphatics. However, those who present later in life may have acquired obliterative disease, the cause of which is still obscure.(ABSTRACT TRUNCATED AT 400 WORDS) PMID: 3884629 [PubMed - indexed for MEDLINE |
| litfiba Total Posts: 38 | Posted: Wed Jan 23, 2008 02:53 am 168. cmdt says Doxycycline is effective against chloroquine-sensitive and chloroquine-resistant P falciparum, P vivax, and (apparently) against P ovale and P malariae. It is used prophylactically against chloroquine-resistant and mefloquine-resistant falciparum malaria in Thailand and adjacent countries and elsewhere for patients who cannot tolerate mefloquine or Malarone (Table 35–2). Doxycycline is also used as an adjunct drug with quinine for the treatment of resistant falciparum malaria |
| litfiba Total Posts: 38 | Posted: Wed Jan 23, 2008 02:58 am q 176. ans is suprapubic .. repeat q 180.. apml |
| litfiba Total Posts: 38 | Posted: Wed Jan 23, 2008 03:08 am q 184.. ans is skin q 202.. inv of choice in opd setting for erectile dysfunction is usg duplex scan intracavernous inj is secondary to usg |
| litfiba Total Posts: 38 | Posted: Wed Jan 23, 2008 03:12 am q 230 harrison says on pg 617 PANCYTOPENIA WITH CELLULAR BONE MARROW Primary bone marrow diseases Myelodysplasia syndromes Paroxysmal nocturnal hemoglobinuria Myelofibrosis Some aleukemic leukemia Myelophthisis Bone marrow lymphoma Hairy cell leukemia Secondary to systemic diseases Systemic lupus erythematosus Hypersplenism B12, folate deficiency Overwhelming infection Alcohol Brucellosis Sarcoidosis Tuberculosis Leishmaniasis |
| litfiba Total Posts: 38 | Posted: Wed Jan 23, 2008 03:18 am q 234.. q was use of usg in ca prostate.. ans is surely to take a biopsy.. just google it too many references! |
| litfiba Total Posts: 38 | Posted: Wed Jan 23, 2008 03:29 am with respect to the q on hemolysis i have looked up harrison / cmdt / katzung.. and i cant find a hemat related side effect for chloroquinebut harri says pyrimeth causes megaloblastic and aplastic anemia |
| litfiba Total Posts: 38 | Posted: Thu Jan 24, 2008 04:50 am the q on which drug is nephrotoxic.. did not have streptomycin.. instead i am sure it had ciprofloxacin which should be the answer as harrison gives TABLE 266-1 Principal Causes of Tubulointerstitial Disease of the Kidney ACUTE INTERSTITIAL NEPHRITIS Drugsa Antibiotics (-lactams, sulfonamides, quinolones, vancomycin, erythromycin, minocycline, rifampin, ethambutol, acyclovir) Nonsteroidal anti-inflammatory drugs Diuretics (thiazides, furosemide, triamterene) Anticonvulsants (phenytoin, phenobarbital, carbamazepine, valproic acid) Miscellaneous (captopril, H2 receptor blockers, omeprazole, mesalazine, indinavir, allopurinol) Infection Bacteria (Streptococcus, Staphylococcus, Legionella, Salmonella, Brucella, Yersinia, Corynebacterium diphtheriae) Viruses (Epstein-Barr virus, cytomegalovirus, Hantavirus, HIV) Miscellaneous (Leptospira, Rickettsia, Mycoplasma) Idiopathic Tubulointerstitial nephritis–uveitis syndrome Anti-tubule basement membrane disease Sarcoidosis |
| litfiba Total Posts: 38 | Posted: Thu Jan 24, 2008 04:51 am the q on which drug is nephrotoxic.. did not have streptomycin.. instead i am sure it had ciprofloxacin which should be the answer as harrison gives TABLE 266-1 Principal Causes of Tubulointerstitial Disease of the Kidney ACUTE INTERSTITIAL NEPHRITIS Drugsa Antibiotics (-lactams, sulfonamides, quinolones, vancomycin, erythromycin, minocycline, rifampin, ethambutol, acyclovir) Nonsteroidal anti-inflammatory drugs Diuretics (thiazides, furosemide, triamterene) Anticonvulsants (phenytoin, phenobarbital, carbamazepine, valproic acid) Miscellaneous (captopril, H2 receptor blockers, omeprazole, mesalazine, indinavir, allopurinol) Infection Bacteria (Streptococcus, Staphylococcus, Legionella, Salmonella, Brucella, Yersinia, Corynebacterium diphtheriae) Viruses (Epstein-Barr virus, cytomegalovirus, Hantavirus, HIV) Miscellaneous (Leptospira, Rickettsia, Mycoplasma) Idiopathic Tubulointerstitial nephritis–uveitis syndrome Anti-tubule basement membrane disease Sarcoidosis |
| litfiba Total Posts: 38 | Posted: Thu Jan 24, 2008 04:51 am the q on which drug is nephrotoxic.. did not have streptomycin.. instead i am sure it had ciprofloxacin which should be the answer as harrison gives TABLE 266-1 Principal Causes of Tubulointerstitial Disease of the Kidney ACUTE INTERSTITIAL NEPHRITIS Drugsa Antibiotics (-lactams, sulfonamides, quinolones, vancomycin, erythromycin, minocycline, rifampin, ethambutol, acyclovir) Nonsteroidal anti-inflammatory drugs Diuretics (thiazides, furosemide, triamterene) Anticonvulsants (phenytoin, phenobarbital, carbamazepine, valproic acid) Miscellaneous (captopril, H2 receptor blockers, omeprazole, mesalazine, indinavir, allopurinol) Infection Bacteria (Streptococcus, Staphylococcus, Legionella, Salmonella, Brucella, Yersinia, Corynebacterium diphtheriae) Viruses (Epstein-Barr virus, cytomegalovirus, Hantavirus, HIV) Miscellaneous (Leptospira, Rickettsia, Mycoplasma) Idiopathic Tubulointerstitial nephritis–uveitis syndrome Anti-tubule basement membrane disease Sarcoidosis |
| litfiba Total Posts: 38 | Posted: Thu Jan 24, 2008 05:12 am sorry for the above triplets! there was some problem anyway here are a few more q to ponder over! Paclitaxel moa-- increase microtubule polymerisation Diffuse axonal injury- white matter lesions all over cns Nasociliary tube insertion - c/o diaghragmatic hernia was described Soil borne a/e - brucella Isolation most useful in- pneumonic plague Gfr measurement- dtpa Meningitis in elderly caused by a/e- herpes Non communicable ds- dont remember options Chaperones- protein folding standard deviation Not a cancer- askin tumor delayed prolonged bleeding by - new vessel formation suture non absorbable .. ?? |
| litfiba Total Posts: 38 | Posted: Thu Jan 24, 2008 05:23 pm harrison says TYPE 2 Treatment of ENL must be individualized. If ENL is mild (i.e., without fever or other organ involvement, with occasional crops of only a few skin papules), it may be treated with antipyretics alone. However, in cases with many skin lesions, fever, malaise, and other tissue involvement, brief courses (1 to 2 weeks) of glucocorticoids (initially 40 to 60 mg/d) are often effective. With or without therapy, individual inflamed papules last for 1 week. Successful therapy is defined by the cessation of skin lesion development and the disappearance of other systemic signs and symptoms. If, despite two courses of glucocorticoid therapy, ENL appears to be recurring and persisting, treatment with thalidomide (100 to 300 mg nightly) should be initiated, with the dose depending on the initial severity of the reaction. so steroids are the doc and the ans |
| drvijay Total Posts: 65 | Posted: Fri Jan 25, 2008 12:17 am question 249 is same reprinted in q255 q on integrated management of childhood illness.... |
| drvijay Total Posts: 65 | Posted: Fri Jan 25, 2008 12:28 am q208 option d perlecan is ans.which is not muscle pro |
| drvijay Total Posts: 65 | Posted: Fri Jan 25, 2008 12:41 am q.56 ans is abdominal imaging |
| drvijay Total Posts: 65 | Posted: Fri Jan 25, 2008 12:49 am q. train of four is ans. neuromuscular muscle relaxant |
| litfiba Total Posts: 38 | Posted: Fri Jan 25, 2008 03:13 am Segment* Couinaud segments Caudate 1 Lateral 2, 3 Medial 4a, 4b Right 5, 6, 7, 8 or lobe in the Caudate's case. ref wikipedia / bartleby ans is segments 2, 3 which are lateral to falciform lig |
| litfiba Total Posts: 38 | Posted: Fri Jan 25, 2008 03:30 am train of 4 is used by anesthetists during depoolarisation.(option c ) reference https://www.health.adelaide.edu.au/paed-anaes/talks/Nerve/Nerve.html Train of four To help overcome the problem of forgetting the control height the 'Train of 4' was developed. Four twitches are given at 1/2 second intervals. The first twitch in the train can be used as a control. Each successive twitch becomes lower as the Acetyl choline in the nerve terminal is depleted. After a pause of 30 seconds the Acetyl choline in the nerve terminal will have built up again so the test can be repeated. As well as estimating the 'fade' of twitches in the 'Train of 4' it is also useful to simply count the twitches. Fewer stimuli make it across the neuromuscular junction as the block becomes deeper. For most general surgery a block down to 2 twitches is adequate. When only one twitch is visible the patient may still be able to move slightly. If you give relaxant until no twitches are visible you no longer whether you are giving a little bit to much or a lot too much. 3. Post Tetanic Count The post tetanic count was developed to allow the control of deep blockade. After a period of rapid stimulation (tetany) the nerve cells 'gear up' for action. After a brief pause the twitch height will be increased above baseline for that degree of block. This example shows the train of 4 at the same depth of block before and after tetany. Notice that not only is the height of the twitches increased but also the number of twitches. This is the way post tetanic count is used. Relaxant is gradually given until no twitches at all are visible. Then a burst of tetany is given, a pause, then one twitch every second for 10 seconds. The anaesthetist simply counts how many twitches are visible. When only 1 or 2 twitches are visible the block is deep enough for virtually any surgery. |
| litfiba Total Posts: 38 | Posted: Fri Jan 25, 2008 03:42 am this is a little tricky harrison is a little ambiguous on this this is what is given :Spheroidicity may be quantitatively assessed by measurement of the osmotic fragility of the RBC on exposure to hyposmotic solutions causing a net influx of water (Fig. 93-2). On microscopic examination, spherocytes are usually detected as small cells without central pallor. pgs 608 - 609 but harri also says : The diagnosis of immune spherocytosis is usually readily established by a positive direct Coombs test now it depends on the question .. if inv of choice was asked then osmotic fragility is the ans but if best inv was asked ans would be coombs. as far as i recollect the q said '' woman with spherocytes on ps had anemia and jaundice.. what would u do next? ans.. osmotic fr ..if one goes with our friend harrison really irritating q though |
| litfiba Total Posts: 38 | Posted: Fri Jan 25, 2008 03:56 am Hereditary Spherocytosis Essentials of Diagnosis ● Positive family history. ● Splenomegaly. ● Spherocytes and increased reticulocytes on peripheral blood smear. ● Microcytic, hyperchromic indices. General Considerations Hereditary spherocytosis is a disorder of the red blood cell membrane, leading to chronic hemolytic anemia. Normally, the red blood cell is a biconcave disk with a diameter of 7–8 mcm. The red blood cells must be both strong and deformable—strong to withstand the stress of circulating for 120 days and deformable so as to pass through capillaries 3 mcm in diameter and splenic fenestrations in the cords of the red pulp of approximately 2 mcm. The red blood cell skeleton, made up primarily of the proteins spectrin and actin, gives the red cells these characteristics of strength and deformability. The membrane defect in hereditary spherocytosis is an abnormality in spectrin, the protein providing most of the scaffolding for the red blood cell membranes. The result is a decrease in surface-to-volume ratio that results in a spherical shape of the cell. These spherical cells are less deformable and unable to pass through 2-mcm fenestrations in the splenic red pulp. Hemolysis takes place because of trapping of red blood cells within the spleen. Clinical Findings Symptoms and Signs Hereditary spherocytosis is an autosomal dominant disease of variable severity. It is often diagnosed during childhood, but milder cases may be discovered incidentally late in adult life. Anemia may or may not be present, since the bone marrow may be able to compensate for shortened red cell survival. Severe anemia (aplastic crisis) may occur in folic acid deficiency or when bone marrow compensation is temporarily impaired by infection. Chronic hemolysis causes jaundice and pigment (calcium bilirubinate) gallstones, leading to attacks of cholecystitis. Examination may reveal icterus and a palpable spleen. Laboratory Findings The anemia is of variable severity, and the hematocrit may be normal. Reticulocytosis is always present. The peripheral blood smear shows the presence of spherocytes, small cells that have lost their central pallor. Spherocytes usually make up only a small percentage of red blood cells on the peripheral smear. Hereditary spherocytosis is the only important disorder associated with microcytosis and an increased mean corpuscular hemoglobin concentration (MCHC), often greater than 36 g/dL. As with other hemolytic disorders, there may be an increase in indirect bilirubin. The Coombs test is negative. Because spherocytes are red cells that have lost some membrane surface, they are abnormally vulnerable to swelling induced by hypotonic media. Increased osmotic fragility merely reflects the presence of spherocytes and does not distinguish hereditary spherocytosis from other spherocytic hemolytic disorders such as autoimmune hemolytic anemia. In some laboratories, the osmotic fragility test has been supplanted by ektacytometry, which has the advantage of better reliability and the ability to distinguish spherocytes from other red blood cell so its clear osmotic fragility is the way to go |
| litfiba Total Posts: 38 | Posted: Fri Jan 25, 2008 03:56 am and cmdt says on pgs 1906- 08 Hereditary Spherocytosis Essentials of Diagnosis ● Positive family history. ● Splenomegaly. ● Spherocytes and increased reticulocytes on peripheral blood smear. ● Microcytic, hyperchromic indices. General Considerations Hereditary spherocytosis is a disorder of the red blood cell membrane, leading to chronic hemolytic anemia. Normally, the red blood cell is a biconcave disk with a diameter of 7–8 mcm. The red blood cells must be both strong and deformable—strong to withstand the stress of circulating for 120 days and deformable so as to pass through capillaries 3 mcm in diameter and splenic fenestrations in the cords of the red pulp of approximately 2 mcm. The red blood cell skeleton, made up primarily of the proteins spectrin and actin, gives the red cells these characteristics of strength and deformability. The membrane defect in hereditary spherocytosis is an abnormality in spectrin, the protein providing most of the scaffolding for the red blood cell membranes. The result is a decrease in surface-to-volume ratio that results in a spherical shape of the cell. These spherical cells are less deformable and unable to pass through 2-mcm fenestrations in the splenic red pulp. Hemolysis takes place because of trapping of red blood cells within the spleen. Clinical Findings Symptoms and Signs Hereditary spherocytosis is an autosomal dominant disease of variable severity. It is often diagnosed during childhood, but milder cases may be discovered incidentally late in adult life. Anemia may or may not be present, since the bone marrow may be able to compensate for shortened red cell survival. Severe anemia (aplastic crisis) may occur in folic acid deficiency or when bone marrow compensation is temporarily impaired by infection. Chronic hemolysis causes jaundice and pigment (calcium bilirubinate) gallstones, leading to attacks of cholecystitis. Examination may reveal icterus and a palpable spleen. Laboratory Findings The anemia is of variable severity, and the hematocrit may be normal. Reticulocytosis is always present. The peripheral blood smear shows the presence of spherocytes, small cells that have lost their central pallor. Spherocytes usually make up only a small percentage of red blood cells on the peripheral smear. Hereditary spherocytosis is the only important disorder associated with microcytosis and an increased mean corpuscular hemoglobin concentration (MCHC), often greater than 36 g/dL. As with other hemolytic disorders, there may be an increase in indirect bilirubin. The Coombs test is negative. Because spherocytes are red cells that have lost some membrane surface, they are abnormally vulnerable to swelling induced by hypotonic media. Increased osmotic fragility merely reflects the presence of spherocytes and does not distinguish hereditary spherocytosis from other spherocytic hemolytic disorders such as autoimmune hemolytic anemia. In some laboratories, the osmotic fragility test has been supplanted by ektacytometry, which has the advantage of better reliability and the ability to distinguish spherocytes from other red blood cell so its clear osmotic fragility is the way to go |
| litfiba Total Posts: 38 | Posted: Fri Jan 25, 2008 04:13 am with regards to the pain d/t ureteric calculus this is what i found in guyton pg 604 : Spasm of a Hollow Viscus. Spasm of a portion of the gut,the gallbladder, a bile duct, a ureter, or any other hollowviscus can cause pain, possibly by mechanical stimulationof the pain nerve endings. Or the spasm might cause diminished blood flow to the muscle, combined with the muscle’s increased metabolic need for nutrients, thus causing severe pain. Often pain from a spastic viscus occurs in the form of cramps, with the pain increasing to a high degree of severity and then subsiding. This process continues intermittently, once every few minutes.The intermittent cycles result from periods of contraction of smooth muscle. For instance, each time a peristaltic wave travelsalong an overly excitable spastic gut, a cramp occurs. The cramping type of pain frequently occurs in appendicitis,gastroenteritis, constipation, menstruation, parturition,gallbladder disease, or ureteral obstruction. confused? hehe.. the first part says pain is d/t irritation of the nerves in the intramural ureter ( one option ) and the next para says its d/ t contractions d/t peristalisis the other option!! i guess this one is upto the machine checking our sheets! |
| litfiba Total Posts: 38 | Posted: Fri Jan 25, 2008 04:49 am about the q on congenital hemochromatosis : which is not involved: liver skin dm ?? deferoxamine therapy is used or was it arthritis- not sure this is what nelson says pg 1634 Iron Overload Disorders The disorders leading to iron overload are not disorders of hemoglobin. Hereditary hemochromatosis (HH) is a disorder of iron absorption leading to toxicity in the fourth to fifth decades of life. Iron absorption is primarily in the liver, heart, and pancreas leading to hepatic cirrhosis and liver failure.There are three pediatric forms of iron overload. Juvenile hemochromatosis (type 2), atransferrinemia/hypotransferrinemia, and neonatal hemochromatosis. Juvenile hemochromatosis differs from HH in that the iron loading is primarily in the heart and endocrine system with associated morbidity (i.e., cardiac arrhythmias and failure, diabetes mellitus). Without phlebotomy, death occurs in the third decade. There is no genetic determinant. Infants born with atransferrinemia have a disorder similar to HH but also have anemia owing to the lack of transferrin. Neonatal hemochromatosis is a rare disease that presents as hepatic iron overload leading to liver dysfunction and failure in the neonatal period. It is sometimes associated with neonatal giant cell hepatitis in drug index of nelson Deferoxamine mesylate Chelating agent. Desferal. Powder for injection: 500?mg. Caution: Contraindicated in patients with primary hemochromatosis. so from the above the only organs not mentioned are skin and joint disease. anyone has a better reference? |
| litfiba Total Posts: 38 | Posted: Fri Jan 25, 2008 04:57 am q on water soluble vit ans is folate .. wikipedia / biochem books ive seen in some posts retinoic acid is given ... a d e k are fat sol |
| litfiba Total Posts: 38 | Posted: Sat Jan 26, 2008 05:47 am q 81. answer is uterine massage... which is not included in the active management but in treatment of pph. |
| litfiba Total Posts: 38 | Posted: Sat Jan 26, 2008 08:08 pm q 172 ans should be perineal exploration sabiston text of surgery - imperforate anus A posterior sagittal approach as championed by Peña is the procedure most frequently performed.[29] This consists of determination of the location of the central position of the anal sphincter by electrical stimulation of the perineum. An incision is then made in the midline extending from the coccyx to the anterior perineum and through the sphincter and levator musculature until the rectum is identified. The fistula from the rectum to the vagina or urinary tract is divided. The rectum is then mobilized, and the perineal musculature is reconstructed. The third and final stage is closure of the colostomy, which is performed a few months later. Anal dilations are begun 2 weeks after the pull-through procedure and continue for several months after the colostomy closure. and nelson apart from treatment also says More than 90% of the time, the diagnosis can be established by a meticulous perineal inspection |
| litfiba Total Posts: 38 | Posted: Sat Jan 26, 2008 08:16 pm retinoids used in : ans is apml harrison pg 478 Leukemias and certain squamous neoplasms, including those of the skin and cervix, appear to beuniquely responsive in certain cases to retinoids. In particular, tretinoin is part of curative regimens for acute promyelocytic leukemia (APL)and appears to act by causing accelerated degradation of the fusion protein created by the t(15; 17) translocation that fuses the retinoic acid receptor and the promyelocytic leukemia (PML) transcription factor |
| Admin Total Posts: 890 | Posted: Thu Jan 31, 2008 10:18 pm Dear litfiba, Updated - retinoids used in - apml. With regards, Netmedicos |
| Admin Total Posts: 890 | Posted: Thu Jan 31, 2008 10:39 pm Dear Litfiba, Updated - Perineal exploration as answer for Imperforate Anus With regards, Netmedicos |