Aiims may 2011: THOROUGH REVIEW

Discussion in 'AIIMS Nov 2013' started by upen, Jun 14, 2011.

  1. upen

    upen Guest

    1. Octreotide is not useful in?
    Insulinoma
    Glucaganoma
    Carcinoid tumor
    Glioma

    Answer: Glioma
    Reference: Goodman and Gillman’s Pharmacology, 11th edition
    Octreotide is available for treatment of carcinoid tumors, glucagonomas, VIPomas, and acromegaly. Octreotide or lanreotide successfully controls excess secretion of growth hormone in most patients, and both have been reported to reduce the size of pituitary tumors in about one-third of cases. Octreotide also has been used to reduce the disabling form of diarrhea that occasionally occurs in diabetic autonomic neuropathy. Since octreotide also can decrease blood flow to the gastrointestinal tract, it has been used to treat bleeding esophageal varices, peptic ulcers, and postprandial orthostatic hypotension.[/b]
  2. upen

    upen Guest

    2. For atherosclerosis which one is true?
    intake of PUFA is associated with decreased risk
    thoracic more severe than abdominal
    extent of lesion in veins same as arteries
    hypercholesterolemia does not increase the risk of atherosclerosis

    Answer: Intake of PUFA is associated with decreased risk
    Reference: Braunwald’s Heart Disease, 8th edition
    Substitution of carbohydrates and/or unsaturated fatty acids for saturated and trans fatty acids reduces LDL cholesterol. Many studies have assessed the quantitative effects of these dietary changes on LDL and other lipids and lipoproteins, as recently summarized and reviewed. When substituted for carbohydrates, the greatest increases in LDL cholesterol result from C12:0 (lauric), C14:0 (myristic), and C16:0 (palmitic) fatty acids found in dairy fat, meat, and tropical oils, with equivalent changes induced by trans monounsaturated fatty acids found in baked goods, stick margarine, and fried “fast foods” such as French fries. In contrast, 18:0 fatty acid (stearic), which is found in many of the same foods, generally does not raise LDL cholesterol levels. No increases in LDL cholesterol follow intake of monounsaturated fatty acids, principally 18:1 (oleic), a major component of olive and canola oils. Polyunsaturated fatty acids of the omega-6 series, principally 18:2 (linoleic), found in vegetable and seed oils such as corn, safflower, and sunflower oils lower plasma total and LDL cholesterol via enhanced receptor-dependent clearance of LDL and decreased LDL production. Availability of linoleic acid modulates the cholesterolemic potential of other fatty acids, such that saturated and trans fats exert a more exaggerated effect on LDL cholesterol when linoleic acid concentrations fall below a threshold value (<3 percent of energy).
  3. upen

    upen Guest

    3. Spleen enters which of the following spaces
    a. Greater sac
    b. Left Paracolic gutter
    c. Infra-colic compartment
    d. Left sub hepatic space

    Gray’s Anatomy, 38th edition, p 1740
    Spleen projects into the Greater Sac
  4. upen

    upen Guest

    4. A male child with Fanconi anemia with hypercalciuria variant of Dents disease: all are true except
    Hypercalciuria
    His father must be affected
    Proteinuria
    Rickets

    Answer: His father must be affected

    Since Dent’s Disease is X-linked disorder, it cannot by transmitted by father to his son. So it is unlikely that the patient’s father is affected.
    Dent's disease and X-linked recessive nephrolithiasis are unusual forms of Fanconi syndrome due to X-linked recessive mutations of the gene encoding CLCN5, a channel belonging to a family of voltage-gated chloride channels. The disorders are characterized by childhood onset of low-molecular-weight proteinuria, hypercalciuria, nephrocalcinosis and nephrolithiasis. Hypophosphatemic Rickets or osteomalacia occurs in 30% of patients, and progressive renal failure from interstitial fibrosis, tubular atrophy, and glomerulosclerosis commonly develops in adulthood. CLCN5 serves to maintain the electrical gradient and acid environment established in proximal tubular cell endosomes by proton-ATPase, which is necessary for the degradation of low-molecular-weight proteins normally filtered by the glomerulus. Defects in CLCN5 appear to disrupt this process and lead to tubular cell dysfunction.
  5. upen

    upen Guest

    5. A 38 years old female underwent laparoscopic cholecystectomy. Histopathology report shows stage 1A carcinoma. What is the further management?
    a. Follow up with imaging
    b. Radical cholecystectomy along with removal of associated lymph nodes
    c. Port site excision
    d. Chemo and radiotherapy

    Answer: a (Follow up with imaging)

    Maingot’s Abdominal Operations, 11th edition, Chapter 35
    Devita, Hellman and Rosenberg’s Cancer Principles and Practice of Oncology, 8th edition
    For Tis (carcinoma in situ) and T1 (stage IA, cancer invasion that does not extend beyond the gallbladder muscularis) lesions, the available retrospective data suggest that simple cholecystectomy is sufficient in most cases. These lesions are detected most frequently on pathologic examination of gallbladders removed for presumed benign disease. Patients diagnosed with gallbladder cancer in this manner should undergo formal imaging-based staging, and the cholecystectomy specimen should be examined carefully to ensure that all margins are negative for cancer. Patients with imaging studies that reveal no evidence of residual or metastatic gallbladder cancer who are found to have a cystic duct margin that is positive for cancer should undergo reexploration with excision of the common bile duct, regional lymphadenectomy, and hepaticojejunostomy. In contrast, patients with negative margins and negative imaging studies who undergo no additional treatment for their gallbladder cancer have excellent outcomes that are unlikely to be improved by radical surgery.
  6. upen

    upen Guest

    Lambda phage: true is
    causes Mad Cow Disease
    lytic & lysogenic inter-conversion cannot occur.
    lytic form incorporated within host DNA and multiply causing rupture of cell membrane
    lysogenic form incorporated within host DNA and remains dormant

    Answer: lysogenic form incorporated within host DNA and remains dormant

    Bovine spongiform encephalopathy (Mad Cow Disease) is a Prion disease

    Phages can be distinguished on the basis of their mode of propagation. Lytic phages produce many copies of themselves as they kill their host cell. The most thoroughly studied lytic phages, the T-even (eg, T2, T4) phages of Escherichia coli, have demonstrated the need for precisely timed expression of viral genes in order to coordinate events associated with phage formation. Temperate phages are able to enter a non-lytic prophage state in which replication of their nucleic acid is linked to replication of host cell DNA. Bacteria carrying prophages are termed lysogenic because a physiologic signal can trigger a lytic cycle resulting in death of the host cell and liberation of many copies of the phage. The best characterized temperate phage is the E coli phage (lambda).

    Bacteriophages exhibit considerable diversity in the nature of their nucleic acid, and this diversity is reflected in different modes of replication. Fundamentally different propagation strategies are exhibited by lytic and temperate phages. Lytic phages produce many copies of themselves in a single burst of growth. Temperate phages establish themselves as prophages either by becoming part of an established replicon or by forming an independent replicon.
    The double-stranded DNA of many lytic phages is linear, and the first stage in their replication is the formation of circular DNA. This process depends upon cohesive ends, complementary single-stranded tails of DNA that hybridize. Ligation, formation of a phosphodiester bond between the tails, gives rise to covalently bonded circular DNA that may undergo replication in a manner similar to that used for other replicons. Cleavage of the circles produces linear DNA that is packaged inside protein coats to form daughter phages.
    Some temperate bacteriophages can be established in the prophage state as plasmids. The double-stranded DNA of other temperate bacteriophages is established as prophage by its insertion into the host chromosome. Prophages contain genes required for lytic replication (also called vegetative replication), and expression of these genes is repressed during maintenance of the prophage state. A manifestation of repression is that established prophage frequently confers cellular immunity against lytic infection by similar phage. A cascade of molecular interactions triggers derepression (release from repression), so that a prophage undergoes vegetative replication, leading to formation of a burst of infectious particles. Artificial stimuli such as ultraviolet light may cause depression of prophage. The switch between lysogeny—propagation of the phage genome with the host—and vegetative phage growth at the expense of the cell may be determined in part by the cell's physiologic state. A non-growing cell will not support vegetative growth of phage, whereas a vigorously growing cell contains sufficient energy and building blocks to support rapid phage replication.
  7. upen

    upen Guest

    Triplex DNA structure is due to
    A)Hoogsteen pairing
    B) increased guanine residues
    C) palindromic sequence
    D) polypyrimidine tracts

    Answer: Hoogsteen pairing

    Nucleotides participating in a Watson-Crick base pair can form a number of additional hydrogen bonds, particularly with functional groups arrayed in the major groove. For example, a cytidine residue (if protonated) can pair with the guanosine residue of a GC nucleotide pair, and a thymidine can pair with the adenosine of an AT pair. The N-7, O6, and N6 of purines, the atoms that participate in the hydrogen bonding of triplex DNA, are often referred to as Hoogsteen positions, and the non-Watson-Crick pairing is called Hoogsteen pairing, after Karst Hoogsteen, who in 1963 first recognized the potential for these unusual pairings. Hoogsteen pairing allows the formation of triplex DNAs. The triplexes shown are most stable at low pH because the CGC triplet requires a protonated cytosine. The triplexes also form most readily within long sequences containing only pyrimidines or only purines in a given strand. Some triplex DNAs contain two pyrimidine strands and one purine strand; others contain two purine strands and one pyrimidine strand.
    Four DNA strands can also pair to form a tetraplex (quadruplex), but this occurs readily only for DNA sequences with a very high proportion of guanosine residues.
    A particularly exotic DNA structure, known as H-DNA, is found in polypyrimidine or polypurine tracts that also incorporate a mirror repeat.
  8. upen

    upen Guest

    What is not true about Antiphospholipid Syndrome?
    recurrent abortion
    thrombosis
    pancytopenia
    lupus anticoagulant

    Answer: Pancytopenia

    Clinical Manifestations of the Antiphospholipid Syndrome
    Venous and arterial thromboembolism
    Pregnancy losses and complications
    Thrombocytopenia
    Stroke
    Cerebral vein thrombosis
    Livedo reticularis, necrotizing skin vasculitis
    Coronary artery disease
    Valvular heart disease
    Kidney disease
    Pulmonary hypertension, acute respiratory distress syndrome
    Atherosclerosis and peripheral artery disease
    Retinal disease
    Adrenal failure, hemorrhagic adrenal infarction
    Gastrointestinal manifestations: Budd-Chiari syndrome, mesenteric and portal vein obstructions, hepatic infarction, esophageal necrosis, gastric and colonic ulceration, gallbladder necrosis
    Sensorineural hearing loss
    Catastrophic antiphospholipid syndrome with microangiopathy
  9. anisa

    anisa Guest

    Which is not a paraneoplastic syndrome of RCC?
    Cushing syndrome
    Malignant hypertension
    Erythrocytosis

    Answer: Cushing syndrome

    Williams Endocrinology
    The tumors that produce the ectopic corticotropin syndrome are primarily of neuroendocrine cell origin. In published series, approximately 45% are SCLC, 15% are thymic carcinoids, 10% are bronchial carcinoids, 10% are islet cell tumors, 5% are other carcinoid tumors, 2% are pheochromocytomas, and 1% are ovarian adenocarcinomas. However, adenocarcinoma and squamous carcinoma are also occasionally associated with the syndrome. It appears that SCLC is greatly underrepresented in these referral series; it probably accounts for well over 50% of unselected cases.

    Paraneoplastic syndromes are common in renal cell carcinoma and are often what suggests the diagnosis, yet they rarely have prognostic significance. These syndromes include hypercalcemia, erythrocytosis, hypertension, fever of unknown origin, anemia, and hepatopathy (Stauffer's syndrome).

    Amyloidosis has been mentioned in Harrison 17th ed and Devita and Hellman's Oncology 8th ed.

    I could not find Cushing syndrome as a manifestation of RCC in prominent books
  10. anisa

    anisa Guest

    True statement
    if prevalence of goitre is greater than 5%, it is called endemic
    the clinical effects of thyroid storm is due to increased thyroxine levels

    Williams Textbook of Endocrinology, 11th edition
    The prevalence of goiter, diffuse or nodular, differs widely depending on the iodine intake by the population living in a given area. Thus, goiter may occur endemically, due mainly to iodine deficiency, or sporadically, depending whether the goiter prevalence in children is more or less than 5%, respectively.

    Greensban's Basic Endocrinology, 8th edition
    At one time it was thought that thyroid storm was due to sudden release or "dumping" of stored T4 and T3 from the thyrotoxic gland. Careful studies have revealed, however, that the serum levels of T4 and T3 in patients with thyroid storm are not higher than in thyrotoxic patients without this condition. There is no evidence that thyroid storm is due to excessive production of T3. Also, in thyrotoxicosis, the number of adrenergic binding sites for catecholamines increases, so that heart and nerve tissues have increased sensitivity to circulating catecholamines. In addition, there is decreased binding to TBG, with further elevation of free T3 and T4. The present theory is that in this setting, with increased binding sites available for catecholamines, an acute illness, infection, or surgical stress triggers an outpouring of catecholamines which, in association with high levels of free T4 and T3, precipitates the acute problem.

    As it is mentioned in Harrison, 17th edition, that endemic goitre is if prevalence > 5 % in the population, we will go with it is as the true option. But as mentioned in William's Endocrinology, remember that the prevalence is mentioned IN CHILDREN
  11. anisa

    anisa Guest

    Berry aneurysm: defect is in
    internal elastic lamina
    media/muscle cell layer
    mucoid material media
    low grade inflammation of vessel wall

    Answer: Internal elastic lamina

    Adams and Victor’s Neurology, 9th edition
    Saccular aneurysms (berry aneurysms) take the form of small, thin-walled blisters protruding from arteries of the circle of Willis or its major branches. Their rupture causes a flooding of the subarachnoid space with blood under high pressure. As a rule, the aneurysms are located at vessel bifurcations and branchings and are generally presumed to result from developmental defects in the media and elastica of the arteries. An alternate theory holds that the aneurysmal process is initiated by focal destruction of the internal elastic membrane, which is produced by hemodynamic forces at the apices of bifurcations (Ferguson). As a result of the local weakness in the vessel wall, the intima bulges outward, covered only by adventitia; the sac then gradually enlarges and may finally rupture.
  12. upen

    upen Guest

    Thrombosis is seen in all except-
    DIC
    PNH
    ITP
    HIT

    Answer: ITP

    Although thrombotic complications occur in other forms of hemolytic anemia as well, they are particularly prominent and severe in PNH. The reason for the high prevalence of thrombosis is not entirely clear, but it may be related to activation of platelets by complement, the procoagulant activity of red cell membranes, or the intravascular release of ADP from red cells, leading to platelet aggregation. Venous thromboses represent one of the most frequent clinical manifestations of PNH. The Budd-Chiari syndrome, which results from hepatic vein thrombosis, has been observed repeatedly. Pulmonary hypertension has occurred and has been attributed to widespread thromboses in the pulmonary microvasculature. Arterial as well as venous thrombosis has been documented.

    A number of drugs cause thrombocytopenia by inducing antibody formation that ultimately targets the megakaryocyte and/or platelet. The most severe and life-threatening is heparin-induced thrombocytopenia (HIT), an immune-mediated disorder caused by antibodies that recognize a neoepitope in platelet factor 4 exposed when it binds heparin. The result is activation of platelets and the coagulation cascade and, ultimately, thrombosis. HIT affects up to 5 percent of patients exposed to heparin.

    DIC: When procoagulants are produced or introduced into the blood and overcome the anticoagulant mechanisms of coagulation, thrombin is generated, which can lead to disseminated intravascular coagulation. The clinical manifestations of intravascular coagulation include (1) multiorgan dysfunction caused by microthrombi, (2) bleeding caused by consumption of platelets, fibrinogen, factor V, and factor VIII, and (3) secondary fibrinolysis. Exposure of blood to tissue factor is the most common trigger. This event can occur when mononuclear phagocytes and endothelial cells are induced to generate and express tissue factor during the systemic inflammatory response syndrome (e.g., gram-negative and gram-positive infections, fungemia, burns, severe trauma) or when contact is established between blood and tissue factor constitutively present on membranes of cells foreign to blood (e.g., malignant, placental, brain, adventitial cells, or traumatized tissues).

    Symptoms and signs of ITP depend on the platelet count. Approximately one third of patients have platelet counts greater than 30 x 109/liter at diagnosis and no significant bleeding, although bleeding symptoms are generally seen in patients with counts below this level. Purpura (ecchymoses and petechiae), epistaxis, menorrhagia, and gingival bleeding are common. Hematuria, hemoptysis, and gastrointestinal bleeding are less common. Intracerebral hemorrhage is rare and generally occurs in patients with platelet counts less than 10 x 109/liter and usually is associated with trauma or vascular lesions. The incidence of life-threatening complications is highest in patients older than 60 years; however, mortality rates are low in patients with ITP, even in those with severe thrombocytopenia. The purpuric lesions seen in ITP are not palpable, do not blanch with pressure, and often develop on distal regions of the extremities and on skin areas exposed to pressure (e.g., around tight belts and stockings and at tourniquet sites). Hemorrhagic bullae, which may develop in the buccal mucosa, generally reflect acute, severe thrombocytopenia. Bleeding after surgery, trauma, or tooth extraction is common.
  13. upen

    upen Guest

    30 yrs, hypertensive lady, G 2P2, with menorrhagia: Treatment
    Mirena
    Ocps
    Hysterectomy
    transcervical resection of endometrium

    Answer: Mirena

    Danforth's Obstetrics and Gynecology, 10th edition
    • Abnormal uterine bleeding is a significant issue and accounts for 20% of all gynecologic visits.
    • Endometrial assessment to exclude cancer is indicated in any woman older than 35 years who is suspected of having anovulatory uterine bleeding.
    • An absolute definition of postmenopausal bleeding may be difficult, but generally, any bleeding, spotting, or staining after 12 months of amenorrhea should be viewed as endometrial cancer until proven otherwise, and endometrial evaluation becomes mandatory.
    • Curettage or various types of suction aspiration often will be fraught with error, especially in cases in which the abnormality is not global but focal (polyps, focal hyperplasia, or carcinoma involving small areas of the uterine cavity).
    • Fluid instillation into the uterus coupled with transvaginal sonography enhances the diagnostic accuracy especially in perimenopausal patients with dysfunctional abnormal bleeding (no anatomic abnormality) from those with globally thickened endometria or those with focal abnormalities (polyps, myoma).
    • Low-dose combination oral contraceptive pills are considered to be the first-line treatment of abnormal uterine bleeding when it occurs in otherwise healthy, nonsmoking, premenopausal women, regardless of their contraceptive status.
    • Oral contraceptive pills are not recommended for women with a history of deep vein thrombosis; for those over age 35 who smoke; and for those with other cardiovascular risk factors, particularly hypertension.
    • Hysterectomy (total or supracervical) is the only definitive cure for benign abnormal uterine bleeding that has failed to respond to medical treatment.

    The levonorgestrel-releasing intrauterine system (IUS) will result in decreased bleeding over time and is effective in the treatment of menorrhagia. It also provides contraception. Although not specifically FDA approved for treating abnormal uterine bleeding, trials have shown the IUS to be a cost-effective alternative to hysterectomy, although more than 40% of women in the IUS group eventually underwent hysterectomy.

    OCPs are contraindicated because the patient is hypertensive. Why not give a trial of MIRENA before hysterectomy?
  14. anisa

    anisa Guest

    A lactating woman has Sputum positive TB. The neonate is 3 months old. What is the recommended chemoprophylaxis
    1. INH 3mg/kg for 3 months
    2. INH 5mg/kg for 3 months
    3. INH 3mg/kg for 6 months
    4. INH 5 mg/kg for 6 months


    answer - 2 .INH 5mg/kg for 3 months


    reference parks psm 20th edition page no 170

    for infants , if mother or any other household members is smear positive , then chemoprophylaxis should be given for 3 months . then do a mantoux test . if mantoux test is negative , stop chemoprophylaxis . and give bcg (if not previously vaccinated ).if the test is positive , continue chemoprophylaxis for a total duration of 6 months .
  15. anisa

    anisa Guest

    GOLD STANDARD TEST for insulinoma
    1. 72 hr fasting test
    2. Plasma insulin levels
    3. C-peptide levels
    4. Low glucose levels < 30 mg/dl

    answer - 1 . 72 hr fasting test


    The diagnosis of insulinoma is based on Whipples triad ie typical symptoms of hypoglycaemia induced by fasting, demonstration of hypoglycaemia (ie plasma glucose # 2.8 mmol/l) at the time of symptoms and prompt reversal of symptoms after glucose administration, in the presence of inappropriately high or normal insulin, proinsulin and C-peptide.
    The supervised 72-hour fast is the gold standard test for the diagnosis of insulinoma. The test is necessary to document hypoglycaemia and its relationship to the patients symptoms, as well as to demonstrate inappropriate insulin concentration in the face of hypoglycaemia. Levels of plasma glucose, insulin, C-peptide and proinsulin are measured simultaneously at baseline and at intervals throughout the fast . The fast should be terminated when patients have symptoms or signs of hypoglycaemia and simultaneously have fasting glucose in the hypoglycaemic range (# 2.8 mmol/L). At the end, the plasma levels of glucose, insulin, C peptide, proinsulin, -hydroxybutyrate and sulphonylurea are measured.
  16. anisa

    anisa Guest

    Not a side effect of naloxone?
    1. Hypertension
    2. Seizures
    3. Pulmonary edema
    4.cardiac arrthymia

    answer : 2 . Seizures


    ref gdman gillman chapter 21 p no 577 e book 11th edition
    Antagonism of opioid effects by
    naloxone often is accompanied by “overshoot” phenomena.
    For example, respiratory rate depressed by opioids transiently
    becomes higher than that before the period of depression.
    Rebound release of catecholamines may cause hypertension,
    tachycardia, and ventricular arrhythmias. Pulmonary edema
    also has been reported after naloxone administration

    Tonic-clonic seizures, occasionally seen as part of the
    toxic syndrome with meperidine and propoxyphene, are
    ameliorated by treatment with naloxone

    acute opiod toxicity - frank convulsions noted occasionaly in infant and children .this not seen with naloxone .
  17. anisa

    anisa Guest

    A 38 years old female underwent laparoscopic cholecystectomy. Histopathology report shows stage 1A carcinoma. What is the further management?
    a. Follow up with imaging
    b. Radical cholecystectomy along with removal of associated lymph nodes
    c. Port site excision
    d. Chemo and radiotherapy

    Answer: a (Follow up with imaging)

    Maingot’s Abdominal Operations, 11th edition, Chapter 35
    Devita, Hellman and Rosenberg’s Cancer Principles and Practice of Oncology, 8th edition
    For Tis (carcinoma in situ) and T1 (stage IA, cancer invasion that does not extend beyond the gallbladder muscularis) lesions, the available retrospective data suggest that simple cholecystectomy is sufficient in most cases. These lesions are detected most frequently on pathologic examination of gallbladders removed for presumed benign disease. Patients diagnosed with gallbladder cancer in this manner should undergo formal imaging-based staging, and the cholecystectomy specimen should be examined carefully to ensure that all margins are negative for cancer. Patients with imaging studies that reveal no evidence of residual or metastatic gallbladder cancer who are found to have a cystic duct margin that is positive for cancer should undergo reexploration with excision of the common bile duct, regional lymphadenectomy, and hepaticojejunostomy. In contrast, patients with negative margins and negative imaging studies who undergo no additional treatment for their gallbladder cancer have excellent outcomes that are unlikely to be improved by radical surgery.


    If Sabiston is to be followed, then port site excision will be the preferred answer. "Recurrent cancer at port sites and peritoneal carcinomatosis have been reported after laparoscopic cholecystectomy, even for patients with in situ disease; therefore, all port sites should be excised if a patient has had a previous laparoscopic cholecystectomy."


    As said in bhatia....
    If there is any controversy in surg qn....
    Final reference book they follow in aiims is sabiston....

    Ans... Is port site excision r in this manner should undergo formal imaging-based staging, and the cholecystectomy specimen should be examined carefully to ensure that all margins are negative for cancer. Patients with imaging studies that reveal no evidence of residual or metastatic gallbladder cancer who are found to have a cystic duct margin that is positive for cancer should undergo reexploration with excision of the common bile duct, regional lymphadenectomy, and hepaticojejunostomy. In contrast, patients with negative margins and negative imaging studies who undergo no additional treatment for their gallbladder cancer have excellent outcomes that are unlikely to be improved by radical surgery.

    If Sabiston is to be followed, then port site excision will be the preferred answer. "Recurrent cancer at port sites and peritoneal carcinomatosis have been reported after laparoscopic cholecystectomy, even for patients with in situ disease; therefore, all port sites should be excised if a patient has had a previous laparoscopic cholecystectomy."
  18. mahak

    mahak Guest

    Berry aneurysm-defect lies in
    a)degeneration of internal elastic media
    b)dep`osition of mucoid material in media
    c)defect inmuscular layer

    ANS=```A

    Under hemodynamic stress augmented by experimental
    treatments, further degenerative changes of the internal elastic lamina and involvement of the medial
    layer are considered to occur and result in aneurysm formation there.
    .
    .
    .
    Although the mechanism of degeneration
    of the internal elastic lamina at the juxta-apical groove
    is not clear, both previous and present studies show that
    the site of degeneration of the endothelial cells correlates
    with the site of degenerative changes of the internal elastic lamina and involvement of the medial
    muscle layer are considered to result in aneurysmal
    development there.
    .
    .
    The site of aneurysmal formation
    was always restricted to the site just distal to the apical
    intimal pad. It was apparent even in arteries without any
    depression that the internal elastic lamina was thinned,
    fragmented, and partly absent at this site. Under this
    degenerated internal elastic lamina, the medial muscle
    layer looked intact. Thus, it can be said that the portion
    with degenerated internal elastic lamina is the site of
    a very early stage of aneurysmal development


    ref:Stroke 1988, 19:507-511
  19. mahak

    mahak Guest

    WHICH OF THE FOLLOWING IS VARIANT OF GIANT CELL TUMOR
    a)chondroblastoma
    b)nonossifying fibroma
    c)osteogenic srcoma

    ans=c>a(op`en for discussion)

    The
    differential diagnosis of GCT of the head and neck includes
    central giant cell reparative granuloma (CGCRG), ‘‘brown
    tumor’’ of hyperparathyroidism, or, more rarely, giant
    cell–rich osteogenic sarcoma. The distinctions between
    these entities may be impossible to make on a biopsy
    without radiographic and clinical correlation


    There has been a great deal written about giant
    cell tumors of bone. Some investigators have been
    quite strict in the classification6 of such lesions,
    excluding all other giant cell lesions as variantsbenign
    chondroblastoma of bone, nonosteogenic
    fibroma, aneurysmal bone cyst, giant cell tumors
    of subperiosteal type
  20. cushing's synd is seen as paraneoplastic synd with RCC (given in Robbins)

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