AIPGMEE 2012 - Discussion: Questions and answers with ref.

Discussion in 'NEET 2013 All india Exam' started by radhe, Jan 12, 2012.

  1. radhe

    radhe Guest

    Q. 1. Lymphoma least commonly associated with?
    a. Ataxia-telangiectasia syndrome
    b. Common variable immunodeficiency disease
    c. Sjögren's syndrome
    d. Lynch 2
    ans, Lynch 2

    ref
    Table 110–5 Diseases or Exposures Associated with Increased Risk of Development of Malignant Lymphoma



    Inherited immunodeficiency disease

    Klinefelter's syndrome

    Chédiak-Higashi syndrome

    Ataxia-telangiectasia syndrome

    Wiskott-Aldrich syndrome

    Common variable

    immunodeficiency disease

    Acquired immunodeficiency diseases

    Iatrogenic immunosuppression

    HIV-1 infection

    Acquired hypogammaglobulinemia
    Autoimmune disease

    Sjögren's syndrome

    Celiac sprue

    Rheumatoid arthritis and systemic lupus erythematosus

    Chemical or drug exposures

    Phenytoin

    Dioxin, Phenoxy herbicides

    Radiation

    Prior chemotherapy and radiation therapy


    this table is from harri. 18th
  2. radhe

    radhe Guest

    Q 2. myasthenia gravis
    a. type 1
    b. type 2
    c. type3
    d. type 4 hypersensitive reaction,

    ans. b. type 2

    ref. robbins
    Type II hypersensitivity is mediated by antibodies directed toward antigens present on cell surfaces or extracellular matrix. The antigenic determinants may be intrinsic to the cell
    membrane or matrix, or they may take the form of an exogenous antigen, such as a drug metabolite, that is adsorbed on a cell surface or matrix. In either case, the hypersensitivity reaction
    results from the binding of antibodies to normal or altered cell-surface antigens. Three different antibody-dependent mechanisms involved in this type of reaction are depicted in Figure 6-
    14 and described next. Most of these reactions involve the effector mechanisms that are used by antibodies, namely the complement system and phagocytes.
    Opsonization and Complement- and Fc Receptor-Mediated Phagocytosis
    The depletion of cells targeted by antibodies is, to a large extent, because the cells are coated (opsonized) with molecules that make them attractive for phagocytes. When antibodies are
    deposited on the surfaces of cells, they may activate the complement system (if the antibodies are of the IgM or IgG class). Complement activation generates byproducts, mainly C3b and
    C4b, which are deposited on the surfaces of the cells and recognized by phagocytes that express receptors for these proteins. In addition, cells opsonized by IgG antibodies are recognized
    by phagocyte Fc receptors, which are specific for the Fc portions of some IgG subclasses. The net result is the phagocytosis of the opsonized cells and their destruction ( Fig. 6-14A ).
    Complement activation on cells also leads to the formation of the membrane attack complex, which disrupts membrane integrity by "drilling holes" through the lipid bilayer, thereby
    causing osmotic lysis of the cells.
    Antibody-mediated destruction of cells may occur by another process called antibody-dependent cellular cytotoxicity (ADCC). This form of antibody-mediated cell injury does not involve
    fixation of complement but instead requires the cooperation of leukocytes. Cells that are coated with low concentrations of IgG antibody are killed by a variety of effector cells, which bind
    to the target by their receptors for the Fc fragment of IgG, and cell lysis proceeds without phagocytosis. ADCC may be mediated by monocytes, neutrophils, eosinophils, and NK cells.
    Although, in most instances, IgG antibodies are involved in ADCC, in certain cases (e.g., eosinophil-mediated cytotoxicity against parasites), IgE antibodies are used. The role of ADCC in
    hypersensitivity diseases is uncertain.
    Clinically, antibody-mediated cell destruction and phagocytosis occur in the following situations: (1) transfusion reactions, in which cells from an incompatible donor react with and are
    opsonized by preformed antibody in the host; (2) erythroblastosis fetalis, in which there is an antigenic difference between the mother and the fetus, and antibodies (of the IgG class) from
    the mother cross the placenta and cause destruction of fetal red cells; (3) autoimmune hemolytic anemia, agranulocytosis, and thrombocytopenia, in which individuals produce antibodies to
    their own blood cells, which are then destroyed; and (4) certain drug reactions, in which antibodies are produced that react with the drug, which may be attached to the surface of
    erythrocytes or other cells.
    Complement- and Fc Receptor-Mediated Inflammation
    When antibodies deposit in extracellular tissues, such as basement membranes and matrix, the resultant injury is because of inflammation and not because of phagocytosis or lysis of cells.
    The deposited antibodies activate complement, generating byproducts, such as C5a (and to a lesser extent C4a and C3a), that recruit neutrophils and monocytes. The same cells also bind to
    the deposited antibodies via their Fc receptors. The leukocytes are activated, they release injurious substances, such as enzymes and reactive oxygen intermediates, and the result is damage
    to the tissues ( Fig. 6-14B ). It was once thought that complement was the major mediator of antibody-induced inflammation, but knockout mice lacking Fc receptors also show striking
    reduction in these reactions. It is now believed that inflammation in antibody-mediated (and immune complex-mediated) diseases is because of both complement and Fc receptordependent
    reactions.[29]
    Antibody-mediated inflammation is the mechanism responsible for tissue injury in some forms of glomerulonephritis, vascular rejection in organ grafts, and other diseases ( Table 6-4 ).
    As we shall discuss in more detail below, the same reaction is involved in immune complex-mediated diseases.
    Antibody-Mediated Cellular Dysfunction
    In some cases, antibodies directed against cell-surface receptors impair or dysregulate function without causing cell injury or inflammation. For example, in myasthenia gravis, antibodies
    reactive with acetylcholine receptors in the motor end-plates of skeletal muscles impair neuromuscular transmission and therefore cause muscle weakness ( Fig. 6-14C ). In pemphigus
    vulgaris, antibodies against desmosomes disrupt intercellular junctions in epidermis, leading to the formation of skin vesicles. The converse (i.e., antibody-mediated stimulation of cell
    function) is noted in Graves disease. In this disorder, antibodies against the thyroid-stimulating hormone receptor on thyroid epithelial cells stimulate the cells, resulting in hyperthyroidism.
  3. radhe

    radhe Guest

    Q. 3.All are true about third stage labour except
    a contolled cord traction,
    b methergine.
    c syntosinon.
    d massage of uterus
    Ans. B. methargin
  4. radhe

    radhe Guest

    WHAT?
    Active management of the third stage of labor (AMTSL) includes three steps:
    1. Administration of a uterotonic drug (oxytocin, 10 IU injection, is the drug of choice)
    2. Controlled cord traction
    3. Uterine massage after delivery of placenta WHY?

    Every year, there are 14 million cases of postpartum hemorrhage (PPH), or excessive bleeding that occurs after childbirth. PPH accounts for approximately 25% of maternal deaths worldwide 1 and for up to 60% of
    deaths in some countries. 2 PPH also causes significant long-term morbidity. 3 Research has validated AMSTL as a best practice that reduces:
    • The incidence of PPH from uterine atony (i.e., the failure of the uterus to contract after delivery) by up to 60%4
    • The need for blood transfusion (with medical risks, hospital stay, and attendant costs)5
    • Ultimately, death and ill health from PPH3 Active management of the third stage of labor is:
    • A safe, cost-effective, and sustainable intervention
    • More humane and ethical than having to deal with the complications of PPH, especially for women who already may be anemic or malnourished2
    • A practice that can save facilities money, according to studies conducted in Guatemala, Vietnam, and Zambia6,7
    • A way to increase the effectiveness and economic impact of maternal and child health programs
    • A practice that has been adopted by many types of providers, after relatively short training sessions that include practical experience
    WHEN?
    AMTSL should be offered to every woman, at every birth, by every provider, because:
    • The vast majority of cases of PPH cannot be predicted in advance,2 but they can be prevented with AMTSL.
    • The health status of many women is compromised by anemia at the time of delivery, making even a small amount of blood loss dangerous, so reducing blood loss at birth could be life-saving.
    WHAT can be done to increase the use of active management of the third stage of labor?
    Advocacy:
    • Create policy support for the routine use of AMTSL as one of the most effective interventions to prevent PPH—the major killer of women in childbirth—and save women’s lives.
    • Introduce international research findings and guidelines into national policy dialogue and development—e.g., the International
    Confederation of Midwives (ICM)/ International Federation of Gynecology and Obstetrics (FIGO) joint statement on AMTSL8 and the World Health Organization (WHO) guideline.
    • Promote community- and facility-based commitment for routine availability and use of AMTSL for all women during childbirth.
    • Partner with regional task forces, civil society, and professional associations to promote local commitment.
    • Collaborate with the U.S. Agency for International Development (USAID), WHO, United Nations Children’s Fund (UNICEF), United Nations Population Fund (UNFPA), and other donors and cooperating agencies to
    gain support for including AMTSL at all levels and integrating it into service-delivery guidelines.
    Active Management of the Third Stage of Labor for Prevention of Postpartum Hemorrhage:
    A Fact Sheet for Policy Makers and Program Managers FAC T S H E E T Training:
    • Include AMTSL in appropriate preservice and in-service curricula and trainings.
    • Provide support for training (e.g., through audiovisuals, anatomic models, reference materials, job aids, and training supplies).
    • Carry out training follow-up, monitoring, and supervision.
    • Confirm authorization and legal authority of provider cadres who can deliver AMTSL and related services, including injections.
    (Consider facility and community level.)
    • Integrate AMTSL into comprehensive safe motherhood training programs. (Skills training in AMTSL alone is possible when a comprehensive training is not possible or was recently completed.)
    Service delivery:
    • Ensure adequate infrastructure, labor/delivery space, and utilities (e.g., running water, toilets, and electrical power), if possible.
    • Support training using job aids, supervision, and monitoring.
    • Make available logistics system support (e.g., cold or cool chain with light protection for drug commodities and appropriate packaging and dosage for prophylaxis and treatment, including oxytocin and/or
    ergometrine or syntometrine, on the Essential Drugs List).
    • Support cross-cutting issues (e.g., quality improvement, infection prevention, and access to skilled assistance at delivery).
    • Provide supplies (e.g., oxytocin, needles, and syringes).
  5. radhe

    radhe Guest

    Q. 4. Drug used in irritable bowel syndrome?
    a. Lubiprostone
    b.
    c.
    d.

    ans. lubiprostone
  6. radhe

    radhe Guest

    Chloride Channel Activators

    Lubiprostone is a bicyclic fatty acid that stimulates chloride channels in the apical membrane of intestinal epithelial cells. Chloride secretion induces passive movement of sodium and water into the bowel lumen and improves bowel function. Oral lubiprostone was effective in the treatment of patients with constipation-predominant IBS in large phase II and phase III randomized double-blinded placebo-controlled multicenter trials. Responses were significantly greater in patients receiving lubiprostone 8 g twice daily for 3 months than in those receiving placebo. In general, the drug was quite well tolerated. The major side effects are nausea and diarrhea. Lubiprostone is a new class of compounds for treatment of chronic constipation with or without IBS.
    harri 18th

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