AIIMS MAY 2008 Q & A With Explanations

Discussion in 'AIIMS Nov 2013' started by Meena., May 15, 2008.

  1. Meena.

    Meena. Guest

    what is glue sniffing and why is it clinically important?


    Causes

    The commonly held notion that solvent inhalation is innocuous undoubtedly contributes to solvent-inhalant abuse. The wide availability of organic solvents in commonly used household products makes them readily accessible.

    * Commonly abused products
    *
    o Liquids
    + Model Glue
    + Gasoline
    + Contact cement (rubber cement)
    + Lacquers
    + Nail-polish remover
    + Dry-cleaning fluids
    o Aerosols
    + Spray paints
    + Butane fuel, lighter fluid
    + Cooking sprays
    + Cosmetics, hairspray
    + Toiletries, deodorants
    * Chemicals found in abused inhalants
    o Propane
    o Butane
    o n-Hexane
    o Trichloroethylene
    o Freon
    o Benzene
    o Toluene
    o Xylene
    o Acetone
    o Methyl isobutyl ketone

    Background

    Inhalation injury due to hydrocarbons can occur as a result of either accidental or intentional exposure. Inhalant use, the deliberate inhalation of hydrocarbons as a form of recreational drug use, has become a significant health issue affecting children today. Recent epidemiologic data demonstrate that among adolescents, inhalants are the second most widely used class of illicit drugs, and more than 2 million children aged 12 to 17 years report using inhalants at least once in their lifetime. Death from intentional inhalation of hydrocarbon fumes is not uncommon and is usually due to sudden cardiac events or central nervous system depression. The recognition and treatment of inhalant abuse remain challenges for pediatricians and emergency physicians.

    Deliberate inhalation of volatile hydrocarbons for their mood-altering effects is popular among adolescents. Their low cost, ready availability, and ease of use contribute to this problem. Volatile hydrocarbons are contained in glues, solvents, lighter fluid, gasoline, and paints. Most inhalants are composed of several compounds, and almost all pressurized aerosol products can be abused because the propellants are volatile hydrocarbons.
    Pathophysiology

    Most recreational abuse of hydrocarbons by inhalation is accomplished in 3 ways: sniffing, huffing, and bagging.

    * Sniffing, the least potent delivery method, is the inhalation of the volatile substance through the nostrils (ie, sniffing glue).
    * Huffing is the placing of a rag soaked with an inhalant such as gasoline or lighter fluid over the nose and mouth.
    * Bagging involves repeated deep inhalations from a plastic or paper bag filled with a particular hydrocarbon such as spray paint or another propellant.

    Chronic abusers generally inhale 3-4 times daily for 10-15 minutes each time, although prolonged sessions of inhaling 6-7 hours a day as a group activity have been described. Tolerance and physical dependence can occur, although withdrawal symptoms are only infrequently reported.

    Two primary organ systems are affected by inhalation hydrocarbon toxicity: the CNS and the cardiopulmonary system. Volatile hydrocarbons are highly lipid soluble and readily cross the blood-brain barrier. Rapid absorption occurs across the large surface area of the pulmonary vascular bed, and peak blood levels are noted approximately 15-30 minutes after inhalation. Confusion, disorientation, disinhibition, and euphoria are exhibited early. Speech becomes slurred, and motor function becomes impaired, with gait becoming staggered. Hallucinations are frequently described, followed by CNS depression, drowsiness, and sleep. Coma can occur with prolonged or repeated exposures; however, this is unusual because the intentional exposure ceases as the user becomes drowsy.

    Sudden sniffing death syndrome was first described by Bass in 1970. Death occurs after the user is startled during or soon after inhalation. Hydrocarbons can sensitize the myocardium to endogenous and exogenous catecholamines, which can precipitate ventricular dysrhythmias and sudden death. In addition, some limited data have shown toxic effects of hydrocarbons directly on the myocardium, and excess catecholamine concentrations may cause an increase in oxygen demand, coronary artery spasm, platelet aggregation, and thrombus formation. A number of case reports also detail acute myocardial infarction as a complication following hydrocarbon inhalation.

    With acute intoxication, deaths due to asphyxiation from a plastic bag over the head or aspiration of stomach contents are not unusual. Also, trauma-related injury and motor vehicle accidents have been reported, resulting from disinhibition and disorientation following inhalation. Other reported complications include renal tubular acidosis with subsequent hypokalemia and hyperchloremia; frostbite with facial injury and burns to the trachea, mainstem bronchi, esophagus, and oral cavity from intentional inhalation of fluorinated hydrocarbon; bone marrow damage, aplastic anemia, and leukemia due to benzene exposure; and toxic hepatitis from toluene. In contrast to pulmonary injury from aspiration of liquid hydrocarbons, direct pulmonary injury from acute inhalation exposure has not been described.

    Many solvents, particularly toluene, are lipophilic and readily cross the placenta, resulting in characteristic fetal anomalies that include microcephaly, narrow bifrontal diameter, short palpebral fissures, hypoplastic mid face, wide nasal bridge, abnormal palmar creases, and blunt fingertips. The syndrome of toluene embryopathy closely resembles the phenotypic features found in fetal alcohol syndrome.

    With long-term hydrocarbon inhalation, CNS damage occurs, including loss of cognitive functions, gait disturbances, and loss of coordination. Radiographic tests have demonstrated loss of brain mass and white-matter degeneration. Additionally, certain chemicals have been shown to have associations with specific CNS injuries, including peripheral neuropathy, deafness, and optic neuropathy. Other, less common complications of long-term hydrocarbon inhalation include restrictive pulmonary disease, pulmonary hypertension, and reduced diffusion capacity.

    Of note, pulmonary toxicity can occur as a result of hydrocarbon aspiration. This injury differs from hydrocarbon inhalation injury. The most common clinical scenario of hydrocarbon aspiration is that of a young child unintentionally ingesting a hydrocarbon-containing compound such as lamp oil or a cleaning solvent. Hydrocarbons cause direct injury to the respiratory epithelium, producing inflammation and bronchospasm. Direct contact with alveolar membranes can lead to hemorrhage, hyperemia, edema, surfactant inactivation, leukocyte infiltration, and vascular thrombosis. The result is poor oxygen exchange, atelectasis, and pneumonitis. For more information, see Toxicity, Hydrocarbons.
    Frequency
    United States

    National surveys of adolescents in the United States have revealed that, after marijuana, inhalants are the most commonly used class of illicit drugs for 8th and 10th graders; inhalants are the third most widely used illicit drugs for 12th graders. The low cost, ease of use, and ready availability of organic solvents perpetuate their abuse. Recent epidemiologic data suggest a decrease in the prevalence of inhalant abuse, but the overall abuse rates remain high. Inhalant abuse by adolescents in the United States is common: in 2000, more than 2 million adolescents aged 12-17 years reported using inhalants at least once in their lifetime. Since 1975, the National Institute on Drug Abuse annual survey of high-school seniors has documented a lifetime incidence of inhalant abuse of 15-20%, with the highest prevalence of use being in 8th graders.

    Although the trend of lifetime use decreases between the 8th and 12th grades, these data may underestimate the true lifetime use of older adolescents, because many students have dropped out of school by the 12th grade and thus are no longer included in the survey.

    The typical inhalant abuser is a young male of lower socioeconomic class. Overall, males are twice as likely to abuse inhalants as females are; however, between the 8th and 12th grades, the difference is less pronounced. Immigrants from Latin America and American Indians have a higher prevalence of use, and African Americans have a low prevalence of inhalant abuse. Although inhalant abuse is typically thought of as being most common among adolescents, use among adults is also well described, and use in children as young as age 4-6 years has been reported.
    International

    The United Kingdom is the only major country in the Western world that tracks inhalant-abuse fatalities, where an incidence of 2 deaths per week has been documented. In Canada , the patterns of inhalant use are similar to those associated with other illicit substances for experimenters, intermittent users, and long-term abusers. Long-term use tends to be endemic in both the inner-city areas and remote communities, and data show an association between chronic use, lower socioeconomic class, and family dysfunction.
    Mortality/Morbidity

    Although hydrocarbon inhalation was previously thought to be a benign fad, permanent and significant pulmonary and neurologic sequelae clearly may persist even after abuse has discontinued. Recreational solvent inhalation may account for as much as 2% of all deaths among adolescent males. In the United Kingdom, 15% of deaths caused by inhalants occur as a result of suffocation, 15% by accidental trauma, and 15% by aspiration, whereas the remaining 55% are a result of sudden sniffing death syndrome. Of significant concern is that 22% of victims of sudden sniffing death syndrome had no history of inhalant abuse, demonstrating that death can result from any episode of inhalant abuse.

    In the United States, inhalant abuse was responsible for 12.2% of the deaths reported to poison control centers in the group aged 13-19 years. Given that many inhalant-related deaths are never reported to poison control centers, this statistic grossly underestimates the true mortality due to inhalant abuse.

    Ongoing inhalant use has been associated with significant psychosocial Pathology , including failure in school (a high correlation exists between poor academic performance and inhalant abuse) and delinquency. In patients with neurologic symptoms who abused toluene as an inhalant, nearly one third showed deficits in orientation, attention, learning, arithmetic calculation, abstraction, construction, and recall.

    As solvent abuse becomes chronic, damage to the CNS becomes irreversible, with changes occurring in the cerebellar and cerebral white matter, including demyelination and gliosis. Psychiatric disorders, spasticity, cognitive changes, and secondary Parkinson disease have been reported. Attention deficit as well as decreased memory retrieval may also occur.
    Race

    Previous data suggested the highest inhalant abuse to be among Latin American immigrants, but in adolescents aged 12-17 years, inhalant users were more likely to be American Indian or Alaskan Native (13.2%), followed by multiracial (11.2%) and white (9.5%). Lowest reported rates were among blacks (5.3%) and Asians (6.5%).
    Sex

    According to data from Wu et al in 2004, the lifetime prevalence rates of inhalant abuse were not significantly different for males and females aged 12-17 years.
    Age

    Peak age of inhalant abuse is 14-15 years, with onset of abuse occurring from ages 6-8 years. Use typically declines by the late teenage years; however, some users will continue to abuse inhalants into adulthood.

    CLINICAL
    Section 3 of 10 Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic �

    * Authors and Editors
    * Introduction
    * Clinical
    * Differentials
    * Workup
    * Treatment
    * Medication
    * Follow-up
    * Miscellaneous
    * References


    History

    A high index of suspicion is required because exposure to most volatile substances is not detectible on physical examination and because people who intentionally abuse inhalants initially deny hydrocarbon inhalation. Presentation of a patient with a characteristic odor of gasoline or kerosene likely suggests exposure; however, patients who present with altered mental status or intoxication should be scrutinized for the possibility of inhalation abuse in addition to abuse of other common drugs.

    Populations at higher risk should be questioned more carefully; higher-risk populations include children and adolescents from families of low socioeconomic status, where unemployment and poverty rates are high, as well as those lacking adult supervision.

    * Common symptoms between episodes of abuse include poor social functioning, underachievement at work or school, apathy, chest pain, and thirst.
    * Carefully investigate the possibility of illicit solvent inhalation in all patients presenting with the following unexplained symptoms or factors:
    o Altered mental status, cerebellar dysfunction, peripheral neuropathy
    o Behavioral changes, deteriorating school performance
    o Pulmonary hypertension with or without cor pulmonale
    o Acute rhabdomyolysis
    o Renal tubular acidosis with severe hypokalemia and hypophosphatemia
    o Gastrointestinal symptoms, such as abdominal pain, hematemesis, nausea, and vomiting
    o Mothers of infants with toluene embryopathy
    * Evaluate for solvent abuse all patients who present after autoerotic asphyxiation, because such chemicals may be used to relax inhibitions.
    * When inhalant abuse is identified, make efforts to specifically identify the toxins involved, recognizing that abusers often ingest a variety of solvent-inhalants and frequently misidentify the substances involved. Hydrocarbons are not often part of a routine toxicology screen; therefore, if clinical suspicion of such an exposure exists, the laboratory must be alerted and specific identifying tests must be ordered.

    Physical

    Patients who have acute decompensation from solvent-inhalant abuse are frequently found near the offending agent; however, many patients who present to medical care have no obvious physical findings to suggest hydrocarbon exposure or inhalant abuse. Some patients may present with subtle signs of abuse such as paint staining around the mouth or nose. A characteristic odor may be detectable on presentation because a significant proportion of the absorbed chemical exits the body via the lungs. Also, the product may have been spilled onto clothing during use.

    Evidence of chronic inhalant abuse may be more subtle. Patients presenting with unexplained peripheral neuropathy and weakness, diffuse gastrointestinal symptoms, or neuropsychiatric symptoms should raise suspicion of chronic solvent-inhalant abuse. Electrolyte abnormalities, including hypokalemia, hypophosphatemia, and acidosis, should further raise suspicion. The nature of these symptoms, however, is not diagnostic of solvent-inhalant abuse; therefore, a very broad differential diagnosis is required. Signs and symptoms are as follows:

    * A single, loud S2 may be evident as a result of pulmonary hypertension.
    * Ventricular arrhythmias or bradycardia
    * Discolored urine may be evident from rhabdomyolysis.
    * Adolescents presenting with unexplained obtundation or seizures should be examined carefully for evidence of recent solvent-inhalant exposure.
    * Physical findings of recent solvent-inhalant abuse include flecks of paint around the nose and mouth and staining of the fingers, nails, and clothing.
    * A solvent aroma may be present on the breath.
    * Rhinitis, nasal mucosal erosions, epistaxis, hoarse voice, and conjunctivitis may result from local exposure.
    * The acute neurologic effects of inhaled solvents generally wear off within minutes to a few hours, but the effects of more chronic use may persist.
    * Muscle weakness, diffuse gastrointestinal symptoms, and neuropsychiatric symptoms make up 3 major symptom patterns of chronic abuse.

    Causes

    The commonly held notion that solvent inhalation is innocuous undoubtedly contributes to solvent-inhalant abuse. The wide availability of organic solvents in commonly used household products makes them readily accessible.

    * Commonly abused products
    *
    o Liquids
    + Model Glue
    + Gasoline
    + Contact cement (rubber cement)
    + Lacquers
    + Nail-polish remover
    + Dry-cleaning fluids
    o Aerosols
    + Spray paints
    + Butane fuel, lighter fluid
    + Cooking sprays
    + Cosmetics, hairspray
    + Toiletries, deodorants
    * Chemicals found in abused inhalants
    o Propane
    o Butane
    o n-Hexane
    o Trichloroethylene
    o Freon
    o Benzene
    o Toluene
    o Xylene
    o Acetone
    o Methyl isobutyl ketone


    DIFFERENTIALS
    Section 4 of 10 Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic �

    * Authors and Editors
    * Introduction
    * Clinical
    * Differentials
    * Workup
    * Treatment
    * Medication
    * Follow-up
    * Miscellaneous
    * References


    Acidosis, Metabolic
    Inhalation Injury
    Status Epilepticus
    Toxicity, Carbon Monoxide
    Toxicity, Ethanol
    Toxicity, Tricyclic Antidepressant
    Ventricular Fibrillation

    Other Problems to be Considered

    Other causes for altered mental status:

    * Intracranial Pathology
    * Electrolyte abnormality
    * Hepatic encephalopathy
    * Encephalitis

    Comorbidities:

    * Multidrug ingestion
    * Other illicit drugs of abuse
    * Sexually transmitted diseases


    WORKUP
    Section 5 of 10 Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic �

    * Authors and Editors
    * Introduction
    * Clinical
    * Differentials
    * Workup
    * Treatment
    * Medication
    * Follow-up
    * Miscellaneous
    * References


    Lab Studies

    * When solvent-inhalant abuse is suspected, specific solvent identification should be requested from the laboratory because solvent inhalants are infrequently included in routine toxicologic screening tests.
    *
    o A complete toxicology screen should be performed because patients who abuse one drug can be simultaneously abusing others.
    o Obtain serologic investigation of renal and hepatic dysfunction, as well as blood and urine testing for rhabdomyolysis.
    o Obtain serum electrolyte levels to diagnose hypokalemia, hypophosphatemia, hypercalcemia, and acidosis from distal renal tubular acidosis caused by chronic hydrocarbon abuse.
    o If indicated from the history and physical examination, laboratory tests should be performed for sexually transmitted disease and, possibly, pregnancy, because of disinhibition and poor judgment.
    o Pregnancy testing should be done for all solvent-abusing females of reproductive age because of the risk of toluene embryopathy.

    Other Tests

    * ECG and echocardiography
    *
    o Identify pulmonary hypertension
    o Evaluate for cardiomyopathy
    o Identify and document dysrhythmias
    * Pulmonary function testing to look for evidence of restrictive disease
    * Neurophysiologic and neuropsychiatric tests for patients with evidence of chronic inhalant use
    * Neuromotor testing in patients with symptoms of peripheral neuropathy


    TREATMENT
    Section 6 of 10 Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic �

    * Authors and Editors
    * Introduction
    * Clinical
    * Differentials
    * Workup
    * Treatment
    * Medication
    * Follow-up
    * Miscellaneous
    * References


    Medical Care

    The care of patients with inhalation abuse is mainly supportive. Because many potential complications involving the pulmonary, cardiovascular, and neurologic systems may be present, careful assessment and stabilization of the "ABCs" should be paramount in the initial management. In addition to acute medical treatment, patients suspected of chronic solvent-inhalant use should be carefully evaluated by a team trained in the treatment of childhood substance abuse.

    * Acute inhalant abuse
    *
    o Medical care of patients following acute decompensation from hydrocarbon inhalation is primarily supportive. Those with significant neurologic impairment who are unable to protect their airway should undergo endotracheal intubation and mechanical ventilation to prevent aspiration and respiratory deterioration. Hypoxic injury to other organ systems, particularly the heart, should be sought and treated accordingly.
    o Because of the sensitization of the myocardium to catecholamines, inotropic agents and bronchodilators should be avoided. Some authors suggest the use of amiodarone to treat ventricular arrhythmias if used early in treatment. Epinephrine administration during resuscitation may be harmful and can lead to recurrence of ventricular fibrillation.
    o Electrolyte abnormalities should be corrected.
    * Chronic inhalant abuse
    *
    o Management of chronic solvent-inhalant abuse should be directed at preventing further abuse.
    o Therapy for commonly involved organs, including the central and peripheral nervous systems, kidneys, liver, lungs, heart, and bone marrow, is primarily supportive.
    o In patients with significant electrolyte abnormalities, typically from distal renal tubular acidosis, parenteral fluid and electrolyte repletion may be necessary. Correction of potassium and phosphorus deficiency may result in rapid improvement in muscle strength. Hypocalcemia is frequently encountered during fluid and electrolyte repletion.

    Consultations

    Patients who are suspected of solvent-inhalant abuse should be carefully evaluated by experts who are trained in the treatment of childhood substance abuse. Consultation with specialists, including cardiologists and neurologists, depending on the individual needs of the patient, may also be warranted. Any patient who has unstable hemodynamics or cardiac arrhythmias or who has significantly altered mental status should be admitted to and observed in the pediatric intensive care unit.
    Diet

    Patients should remain on nothing by mouth (NPO) until muscle weakness clearly will not necessitate institution of mechanical ventilation. Also, because of the risk of hypocalcemic seizures, patients should remain NPO during initial fluid and electrolyte repletion.
  2. Meena.

    Meena. Guest

    finger printing was first used in

    a)india
    b)poland
    c)france
    d)US


    ans:india


    Sir William Hershel - 1856

    The English first began using fingerprints in July of 1858, when Sir William Herschel, Chief Magistrate of the Hooghly district in Jungipoor, India, first used fingerprints on native contracts. On a whim, and with no thought toward personal identification, Herschel had Rajyadhar Konai, a local businessman, impress his hand print on the back of a contract.

    The idea was merely ". . . to frighten [him] out of all thought of repudiating his signature." The native was suitably impressed, and Herschel made a habit of requiring palm prints--and later, simply the prints of the right Index and Middle fingers--on every contract made with the locals. Personal contact with the document, they believed, made the contract more binding than if they simply signed it. Thus, the first wide-scale, modern-day use of fingerprints was predicated, not upon scientific evidence, but upon superstitious beliefs.

    As his fingerprint collection grew, however, Herschel began to note that the inked impressions could, indeed, prove or disprove identity. While his experience with fingerprinting was admittedly limited, Sir Herschel's private conviction that all fingerprints were unique to the individual, as well as permanent throughout that individual's life, inspired him to expand their use.

    Dr. Henry Faulds - 1880

    During the 1870's, Dr. Henry Faulds, the British Surgeon-Superintendent of Tsukiji Hospital in Tokyo, Japan, took up the study of "skin-furrows" after noticing finger marks on specimens of "prehistoric" pottery. A learned and industrious man, Dr. Faulds not only recognized the importance of fingerprints as a means of identification, but devised a method of classification as well.

    In 1880, Faulds forwarded an explanation of his classification system and a sample of the forms he had designed for recording inked impressions, to Sir Charles Darwin. Darwin, in advanced age and ill health, informed Dr. Faulds that he could be of no assistance to him, but promised to pass the materials on to his cousin, Francis Galton.

    Also in 1880, Dr. Faulds published an article in the Scientific Journal, "Nautre" (nature). He discussed fingerprints as a means of personal identification, and the use of printers ink as a method for obtaining such fingerprints. He is also credited with the first fingerprint identification of a greasy fingerprint left on an alcohol bottle.

    Gilbert Thompson - 1882

    In 1882, Gilbert Thompson of the U.S. Geological Survey in New Mexico, used his own fingerprints on a document to prevent forgery. This is the first known use of fingerprints in the United States.

    Mark Twain (Samuel L. Clemens) - 1883

    In Mark Twain's book, "Life on the Mississippi", a murderer was identified by the use of fingerprint identification. In a later book by Mark Twain, "Pudd'n Head Wilson", there was a dramatic court trial on fingerprint identification. A more recent movie was made from this book.

    Sir Francis Galton - 1888

    Sir Francis Galton, a British anthropologist and a cousin of Charles Darwin, began his observations of fingerprints as a means of identification in the 1880's. In 1892, he published his book, "Fingerprints", establishing the individuality and permanence of fingerprints. The book included the first classification system for fingerprints.

    Galton's primary interest in fingerprints was as an aid in determining heredity and racial background. While he soon discovered that fingerprints offered no firm clues to an individual's intelligence or genetic history, he was able to scientifically prove what Herschel and Faulds already suspected: that fingerprints do not change over the course of an individual's lifetime, and that no two fingerprints are exactly the same. According to his calculations, the odds of two individual fingerprints being the same were 1 in 64 billion.

    Galton identified the characteristics by which fingerprints can be identified. These same characteristics (minutia) are basically still in use today, and are often referred to as Galton's Details.
  3. Meena.

    Meena. Guest

    Mass in mediastinum with arborizing keratin pattern is-

    a- Thymoma
    b- Anaplastic thyroid cancer
    c- lynphoma
    d- ??

    options pls help

    ans: Thymoma probably

    Thymoma, by definition, is a tumor of thymic epithelial cell origin. It is actually the most common neoplasm in the entire mediastinum. It usually occurs in adults older than 40 years of age and affects males and females equally. Most arise in the anterosuperior mediastinum; however, ectopic sites have been described, including neck, thyroid, lung parenchyma, pleura, etc.. About 30-50% of thymomas are associated with myasthenia gravis. Clinical symptoms include cough, chest pain, dyspnea, weight loss, fever, dysphagia and hoarseness.

    In most instances, the presence of thymoma is revealed by plain chest roentgenograms. CT scan can confirm the location and may reveal some characteristics of the tumor such as cystic changes or involvement of surrounding structures. Grossly, 70-80% of thymomas are encapsulated. Cut surface is usually grey-tan with bulging and lobulated appearance. Occasionally, cystic necrosis and calcification can be seen. Microscopically, the tumor typically consists of jigsaw puzzle-type lobules that are separated by fibrous bands. There is an admixture of neoplastic epithelial cells and non-neoplastic lymphocytes in varying proportions. The polygonal epithelial cells usually have bland vesicular nuclei with inconspicuous nucleoli. Another histologic feature seen in two thirds of thymomas is the presence of perivascular spaces, which are formed and bordered by palisading epithelial cells. In these spaces, there is a suspension of erythrocytes, lymphocytes, plasma cells, mast cells and plasma fluid. Immunostain of cytokeratin is characteristic and features an arborizing network of interconnecting epithelial cell processes. The immature lymphocytes in thymomas can be identified by their positivity for terminal deoxynucleotide transferase (TdT) and OKT6 (CD1a). Electron microscopy reveals elongated cytoplasmic processes, a large number of desmosomes and bundles of tonofilaments in the cytoplasm.

    Four histologic types have been described for thymomas: lymphocyte-predominant, epithelial-predominant, mixed lymphoepithelial and spindle-cell types. Among them, the spindle-cell type is usually encapsulated with minimal invasion and correlates to excellent prognosis. The epithelial-predominant type and mixed type are associated with poor prognosis.

    The main differential diagnoses of thymoma include: (1) Malignant lymphoma---lymphocyte-predominant thymomas can be mistaken for lymphomas. However, the lobular configuration and the biphasic cell composition should establish the diagnosis of thymoma. The demonstration of keratin positivity in the epithelial component is particularly useful. (2) Small cell carcinoma and atypical carcinoid tumor---these tumors do not show lobulation or two-cell population. They are positive for neuroendocrine markers such as neuron-specific enolase (NSE), synaptophysin and chromogranin. (3) Lymphoepithelioma-tumor cells in lymphoepithelioma grow in syncytial pattern with ill-defined borders. Sheets or islands of cells are surrounded by dense mature lymphoplasmacytic infiltrates, negative for TdT or OKT6. For our case, we also need to consider malignant mesothelioma as a differential, because of the gross appearance of this tumor (extensively involving the pleura and encasing the entire lung). In typical mesothelioma, the tumor cells exhibit some areas of tubular and/or papillary growth. The cells have more abundant eosinophilic cytoplasm with sharp borders, and the lymphoid component is absent or inconspicuous. Calretinin is positive in 40-50% of mesotheliomas.

    Although rare, there have been scattered reports about ectopic thymomas, including intrapulmonary and pleural thymomas. Ectopic thymomas are usually considered to result from aberrant descent of the thymic tissue from the third pharyngeal pouch during early development. Before diagnosing ectopic thymoma, one needs to be certain that there is no primary mediastinal thymoma present. In this case, the absence of mediastinal involvement is shown by the negative radiologic and gross autopsy findings in the anterosuperior mediastinum. However, it is not absolutely clear whether this tumor is intrapulmonary or pleural in origin, since both lung and pleura are massively involved.

    Finally, a surprising finding is revealed on sections of left and right ventricles, which is eventually the immediate cause of death for this patient. The etiology of the presence of abundant eosinophils and scattered multinucleated giant cells is not clear. It is unlikely that the heart is directly invaded by the tumor, for cytokeratin stain is negative on these sections. There have been a couple of reports about giant cell myocarditis in patients with malignant thymomas. Autoimmune processes have been suggested in these cases. It is possible that in our patient, the activated T cells produce some kinds of cytokines that eventually trigger an intense reaction in the myocardium
  4. Meena.

    Meena. Guest

    for mediastinal nmass options where.

    1.thymoma
    2.thymic carcinoid
    3.peripheral b cell tumor
    4.hodgkins lymphoma
  5. Meena.

    Meena. Guest

    arya dude..also question on mi had st segment depression in leads v1 to v4...options where...1.lmw heparin

    2.thrombolytic therapy
    3.aspirin
    4.morphine
  6. Meena.

    Meena. Guest

    Regarding G proteins which is true

    a)
    b)alfa,beta,gamma -all units necessary for hormone action
    c)
    d)G protein is specific for hormones

    ans:?


    Ligand binding

    GPCRs include receptors for sensory signal mediators (e.g., light and olfactory stimulatory molecules); adenosine, bombesin, bradykinin, endothelin, γ-aminobutyric acid (GABA), hepatocyte growth factor, melanocortins, neuropeptide Y, opioid peptides, opsins, somatostatin, tachykinins, vasoactive intestinal polypeptide family, and vasopressin; biogenic amines (e.g., dopamine, epinephrine, norepinephrine, histamine, glutamate (metabotropic effect), glucagon, acetylcholine (muscarinic effect), and serotonin); chemokines; lipid mediators of inflammation (e.g., prostaglandins, prostanoids, platelet-activating factor, and leukotrienes); and peptide hormones (e.g., calcitonin, C5a anaphylatoxin, follicle-stimulating hormone (FSH), gonadotropic-releasing hormone (GnRH), neurokinin, thyrotropin-releasing hormone (TRH), and oxytocin). GPCRs that act as receptors for stimuli that have yet to be identified are known as orphan receptors.

    Whereas, in other types of receptors that have been studied, ligands bind externally to the membrane, the ligands of GPCRs typically bind within the transmembrane domain.


    G protein can refer to two distinct families of proteins. Heterotrimeric G proteins, sometimes referred to as the "large" G proteins that are activated by G protein-coupled receptors and made up of alpha (α), beta (β), and gamma (γ) subunits.
  7. Meena.

    Meena. 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.
  8. Shishir.

    Shishir. Guest

    which is true about g protein

    a. g protein acts as inhibitory and excietatory as alpha subunit exists in two forms
    b. GTP binds to G protein in resting state
    c. all the three subunits alpha, beta, gamma should bind to eachother for g protein to act
    d. G protien binds to hormone on cell surface

    Ans: a.. G protein acts as inhibitory and excietatory as alpha units exist in two forms.
  9. Shishir.

    Shishir. Guest

    During catabolic phase excess of amino acids lead to increase nitrogen.mechanism?

    a)by repression of catabolism
    b)by increasing anabolism
    c)by repressing catabolism and increasing anabolism
    d)--------
  10. Meena.

    Meena. Guest

    Traits or diagnoses known or suspected to be X-linked (at least in some forms of the diagnosis) are:

    * Adrenoleukodystrophy
    * Alport syndrome
    * Androgen insensitivity syndrome
    * Barth syndrome
    * Becker's muscular dystrophy
    * Centronuclear myopathy
    * Charcot-Marie-Tooth disease
    * Coffin-Lowry syndrome
    * Color blindness
    * Duchenne
    * Fabry disease
    * Fragile X syndrome
    * Glucose-6-phosphate dehydrogenase deficiency
    * Hemophilia A
    * Hemophilia B (Christmas disease)
    * Hunter's Syndrome
    * Hypohidrotic ectodermal dysplasia



    * Incontinentia pigmenti
    * Kabuki syndrome
    * Kennedy disease
    * Lesch-Nyhan syndrome
    * Menkes disease
    * Myotubular myopathy
    * Nonsyndromic deafness and X-linked nonsyndromic deafness
    * Norrie disease
    * Occipital horn syndrome
    * Ornithine transcarbamylase deficiency
    * Rett syndrome
    * Simpson-Golabi-Behmel syndrome
    * Spinal and bulbar muscular atrophy
    * X-linked infantile spinal muscular atrophy (UBE1 gene)
    * Wiskott-Aldrich syndrome
    * X-linked agammaglobulinemia (XLA)
    * X-linked ichthyosis
    * X-linked Severe Combined Immunodeficiency (SCID)
    * X-linked sideroblastic anemia
  11. Meena.

    Meena. Guest

    Q.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.
  12. Shahid.

    Shahid. 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%).
  13. Shahid.

    Shahid. 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)

    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.


    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 can anybdy tell was there any "except " or so in the ques,though i don' think so
  14. Shahid.

    Shahid. Guest

    Some Questions

    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
  15. Shahid.

    Shahid. Guest

    Indan reference man a/e:
    a) 60Kg
    b) spends 8 hrs in bed
    c) 20-39 years
    d) consumes 2200Kcal/day

    Ans: (d) consumes...
    Ref: Park18th (Pg-457)

    1)weighs 60 kg
    2)spends 8hrs in bed, 4-6 hrs sitting & moving around and 2 hrs in walking & in active recreation or household duties
    3)20-39 years
    4)free from disease & physically fit for active work
    on each working day, employed for 8 hrs that involves moderate activity
  16. Shahid.

    Shahid. Guest

    MPS II

    Hunter disease (also referred to as mucopolysaccharidosis type II) is an X-linked recessive metabolic disease. In contrast to Fabry disease, women are very rarely affected. Hunter disease is one of a number of diseases called mucopolysaccharidoses (MPS), which are characterized by a defective degradation of mucopolysaccharides in the lysosomes. Hunter disease is caused by a defective gene, which is located on the X chromosome (Xq27.3-q28) and codes for iduronate-2-sulfatase.


    Fabry disease
    Previously, it was believed that symptoms almost exclusively occur in males due to the hereditary transmission. Since 2001, however, several systematically conducted studies (also here in Mainz) have shown that the condition is also found in females with great variability in clinical manifestations.


    Danon disease

    Danon disease is a subset of the lysosomal storage diseases with an X-linked inheritance and is characterised by a deficiency of the lysosomal protein LAMP-2. The predominant symptom in males is severe cardiomyopathy. Further signs and symptoms are general skeletal muscle weakness with a moderate increase in CK levels as well as mental retardation.

    Danon disease should be considered as the cause of unexplained hypertrophic cardiomyopathy in young males. Females, who pass on the disease-causing gene, can also exhibit symptoms. Symptoms generally emerge later in females than males. The predominant clinical symptom is cardiac arrhythmias. Diagnosing the disease requires the creation of a family tree.
  17. Shahid.

    Shahid. Guest

    All used in Rx of Pul. HTN except:
    a) CCB
    b) PDE inhibitor
    c) Endothelin R antagonist
    d) beta blocker

    Ans:- (d) beta blocker
    Ref:- Harrison 16th (Pg- 1403)

    Treatmant used:-
    1) CCB
    2) Endothelin R antagonist
    3) Sildenafil (PDE inhibitor)
    4) Lung transplantation
  18. Sanny.

    Sanny. Guest

    High anion gap acidosis: The most common causes of a high anion gap metabolic acidosis are ketoacidosis, lactic acidosis (see Acid-Base Regulation and Disorders: Lactic Acidosis), renal failure, and toxic ingestions.

    Ketoacidosis is a common complication of type 1 diabetes mellitus, but it also occurs with chronic alcoholism, malnutrition, and, to a lesser degree, fasting. In these conditions, the body converts from glucose to free fatty acid (FFA) metabolism; FFAs are converted by the liver into ketoacids, acetoacetic acid, and β-hydroxybutyrate (all unmeasured anions). Ketoacidosis is also a rare manifestation of congenital isovaleric and methylmalonic acidemia.

    Renal failure causes anion gap acidosis by decreased acid excretion and decreased HCO3 − reabsorption. Accumulation of sulfates, phosphates, urate, and hippurate accounts for the high anion gap.

    Toxins may have acidic metabolites or trigger lactic acidosis. Rhabdomyolysis is a rare cause of metabolic acidosis thought to be due to release of protons and anions directly from muscle.
  19. Sanny.

    Sanny. Guest

    As compared to embryo adult cell does not divide bcoz?

    a. CDK inhibitors are present in adults which prevents cell from entering in s phase
    b.
    c.

    Ans is CDK inhibitors are present in adults which prevents cell from entering in s phase
  20. Sanny.

    Sanny. Guest

    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 of chloroma

    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.[7]

    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.[8] 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.

    devita p2256
    B. Commonly used markers for flow immunophenotyping in acute leukemia:
    General: CD34, HLA-DR, TdT, CD45
    B-cell markers: CD10, CD19, cCD22, CD20, CD79A, CD24
    T-cell markers: CD1a, CD2, cCD3, CD4, CD8, CD5, CD7
    Myeloid: MPO, CD117, CD13, CD33, CD11c, CD14, CD15
    C. B-lineage acute lymphoblastic leukemia


    Patients with predominant abdominal masses and a diagnosis of carcinoma or sarcoma (particularly leiomyosarcoma) of unknown primary site should have their biopsy specimen stained for c-kit (CD117).
  21. Sanny.

    Sanny. Guest

    Granulocytic sarcoma

    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.
    Contents


    * 1 History
    * 2 Frequency and patterns of presentation
    o 2.1 In acute leukemia
    o 2.2 In myeloproliferative or myelodysplastic syndromes
    o 2.3 Primary chloroma
    * 3 Location and symptoms
    * 4 Diagnosis
    * 5 Prognostic significance
    * 6 Treatment
    * 7 References
    * 8 See also

    History

    The condition now known as chloroma was first described by the British physician A. Burns in 1811[1], although the term chloroma did not appear until 1853.[2] This name is derived from the Greek word chloros (green), as these tumors often have a green tint due to the presence of myeloperoxidase. The link between chloroma and acute leukemia was first recognized in 1902 by Dock and Warthin.[3] However, because up to 30% of these tumors can be white, gray, or brown rather than green, the more correct term granulocytic sarcoma was proposed by Rappaport in 1967[4] and has since become virtually synonymous with the term chloroma.

    Currently, any extramedullary manifestion of acute myeloid leukemia can be termed a granulocytic sarcoma or chloroma. Specific terms which overlap with granulocytic sarcoma include:

    * Leukemia cutis, describing infiltration of the dermis (skin) by leukemic cells, which is also referred to as cutaneous granulocytic sarcoma.
    * Meningeal leukemia, or invasion of the subarachnoid space by leukemic cells, is usually considered distinct from chloroma, although very rarely occurring solid central nervous system tumors composed of leukemic cells can be termed chloromas.

    Frequency and patterns of presentation

    In acute leukemia

    Chloromas are rare; exact estimates of their incidence are lacking, but they are uncommonly seen even by physicians specializing in the treatment of leukemia. Chloromas may be somewhat more common in patients with the following disease features:[5]

    * French-American-British (FAB) classification class M4 or M5
    * those with specific cytogenetic abnormalities (e.g. t(8;21) or inv(16))
    * those whose myeloblasts express T-cell surface markers, CD13, or CD14
    * those with high peripheral white blood cell counts

    However, even in patients with the above risk factors, chloroma remains an uncommon complication of acute myeloid leukemia.

    Rarely, a chloroma can develop as the sole manifestation of relapse after apparently successful treatment of acute myeloid leukemia. In keeping with the general behavior of chloromas, such an event must be regarded as an early herald of a systemic relapse, rather than as a localized process. In one review of 24 patients who developed isolated chloromas after treatment for acute myeloid leukemia, the mean interval until bone marrow relapse was 7 months (range, 1 to 19 months).[6]

    In myeloproliferative or myelodysplastic syndromes

    Chloromas may occur in patients with a diagnosis of myelodysplastic syndrome (MDS) or myeloproliferative syndromes (MPS) (e.g. chronic myelogenous leukemia (CML), polycythemia vera, essential thrombocytosis, or myelofibrosis). The detection of a chloroma is considered de facto evidence that these pre-malignant conditions have transformed into an acute leukemia requiring appropriate treatment. For example, presence of a chloroma is sufficient to indicate that chronic myelogenous leukemia has entered its blast crisis phase.

    Primary chloroma

    Very rarely, chloroma can occur without a known pre-existing or concomitant diagnosis of acute leukemia, acute promyleocytic leukemia or MDS/MPS; this is known as primary chloroma. Diagnosis is particularly challenging in this situation (see below). In almost all reported cases of primary chloroma, acute leukemia has developed shortly afterward (median time to development of acute leukemia 7 months, range 1-25 months).[5] Therefore, primary chloroma could be considered an initial manifestation of acute leukemia, rather than a localized process, and could be treated as such. Where disease development or markers indicate progresses to acute promyleocytic leukemia (AML3) treatment should be tailored to this form of disease.

    Location and symptoms

    Chloromas may occur in virtually any organ or tissue. The most common areas of involvement are the skin (also known as leukemia cutis) and the gums. Skin involvement typically appears as violaceous, raised, nontender plaques or nodules, which on biopsy are found to be infiltrated with myeloblasts. Note that leukemia cutis differs from Sweet's syndrome, in which the skin is infiltrated by mature neutrophils in a paraneoplastic process. Gum involvement (gingival hypertrophy) leads to swollen, sometimes painful gums which bleed easily with tooth brushing and other minor trauma.

    Other tissues which can be involved include lymph nodes, the small intestine, the mediastinum, epidural sites, the uterus, and the ovaries. Symptoms of chloroma at these sites are related to their anatomic location; chloromas may also be asymptomatic and be discovered incidentally in the course of evaluation of a person with acute myeloid leukemia.

    Central nervous system involvement, as described above, most often takes the form of meningeal leukemia, or invasion of the subarachnoid space by leukemic cells. This condition is usually considered separately from chloroma, as it requires different treatment modalities. True chloromas (i.e. solid leukemic tumors) of the central nervous system are exceedingly rare, but has been described.

    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.[7]

    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.[8] 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.

    Prognostic significance

    There is conflicting evidence on the prognostic significance of chloromas in patients with acute myeloid leukemia. In general, they are felt to augur a poorer prognosis, with a poorer response to treatment and worse survival[9]; however, others have reported that chloromas associate, as a biologic marker, with other poor prognostic factors, and therefore do not have independent prognostic significance.[10]

    Treatment

    As described above, chloromas should always be considered manifestations of systemic disease, rather than isolated local phenomena, and treated as such. In the patient with newly diagnosed leukemia and an associated chloroma, systemic chemotherapy against the leukemia is typically utilized as the first-line treatment, unless there is an emergent indication for local treatment of the chloroma (e.g. compromise of the spinal cord). Chloromas are typically quite sensitive to standard anti-leukemic chemotherapy.

    If the chloroma is persistent after completion of induction chemotherapy, local treatment such as surgery or radiation therapy is often considered.

    Patients presenting with a primary chloroma typically receive systemic chemotherapy, as development of acute leukemia is nearly universal in the short term after detection of the chloroma.

    Patients treated for acute leukemia who relapse with an isolated chloroma are typically treated with systemic therapy for relapsed leukemia. However, as with any relapsed leukemia, outcomes are unfortunately poor.

    Patients with "pre-leukemic" conditions such as myelodysplastic syndromes or myeloproliferative syndromes who develop a chloroma are often treated as if they have transformed to acute leukemia.
  22. Meena.

    Meena. Guest

    which of the following is true about diagnosis of ectopic pregnancy

    a) TVS
    b) cudocentesis
    c) serial hcg

    ans TVS
  23. Meena.

    Meena. Guest

    Q. What is true about Histoplasmosis?

    a)in early stages it is indistinguishable from TB
    b)Blood culture is not diagnostic
    c)Hyphal forms are infectious form
    d)antibody detection is useful in early stages

    ans is a)in early stages it is indistinguishable from TB

    REF: Robbins/7th ed/page no.754

    As this Q was a direct pick from robbins.I am quoting exact lines from robbins:


    Histoplasma capsulatum infection is acquired by inhalation of dust particles from soil contaminated with bird or bat droppings that contain small spores(microconidia),the infectious form of the fungus(NOT HYPHAL FORM,OPTION C).
    The clinical presentation & morphologic lesions of histoplasmosis strikingly resembles those of TB(OPTION A).



    The diagnosis of histoplasmosis is firmly established by culture of the fungus(OPTION B)
    Antigen detection in body fluids is most useful in early stages because antibodies are formed 2-6 wk after infection(OPTION D)
  24. Meena.

    Meena. Guest

    Q. All the following are seen in increased ICT in X ray ( I m kind of quite sure it was X ray and not CT ) are all except...

    1. Balloning of sella
    2. Separation of sutural lines.
    3. Increased convolutions of the brain.
    4. ?? Enlarged ventricles??
  25. Meena.

    Meena. Guest

    Q. IN POST DUCTAL COARCTATION OF AORTA, WHICH OF THE FOLLOWING DISTAL ANASTOMOTIC ARTERY IS Not involved .

    a. vertebral arteries
    b. axillary arteries
    c. subscapular artery
    d. posterior intercostal artery
  26. Shahid.

    Shahid. Guest

    Q.In case of Post-ductal Coarctation distal anastomotic artery which is NOT involved?

    A. Subscapular artery
    B. Posterior intercostal artery
    C. Vertebral arteries
    D. Axillary arteries

    Ans is C. Vertebral arteries

    Ref:Grey’s Anatomy 39th
    ed,chapter on angiology,
    Snell’s clinical Anatomy /6th ed/p.132
    ,BDC/3rd ed./vol.1/p.234

    Clinicall the cardinal sign of aortic coarctation is absent or diminished pulses in the femoral arteries of both lower limb.To compensate for the diminished volume of blood reaching the lower part of the body,an enormous collateral circulation develops with dilatation of the internal thoracic,subclavian,& post.intercoastal arteries.

    THIS are the lines from Grey’s Anatomy:

    In postductal coarctation of aorta,In the anterior thoracic wall,the thoraco-acromial,lateral thoracic & the subscapular arteries from the axillary,the suprascapular from the subclavian & the first & second post.intercoastal arteries from the coastocervical trunck anastamose with the third,& lower post.intercoastal arteries.

    High Yield Point -
    Mnemonic For Branches of axillary artery

    She Tastes Like Sweet Apple Pie
    S: superior thoracic
    T: thoracoacromial
    L: lateral thoracic
    S: subscapular
    A: ant. circumflex humoral
    P: post. circumflex humoral
  27. Shahid.

    Shahid. Guest

    Q. the exact question was "which of the following drugs is a vestibular nerve teratogen?"

    -chloroquine
    -alcohol
    -warfarin
    -cephalosporin
  28. Shahid.

    Shahid. Guest

    Q. A lady with CA ovary with follow up with raised CA 125 level ,NEXT STEP?

    a.CT
    b. PET
    c.MRI
    d) clinical exam n serial follow up of CA125
  29. Simran.

    Simran. Guest

    Q. Androgen insensitivity syndrome true is?

    A) Phenotype may be completely female
    B) Predominantly ovarian component in gonads
    C) Always in female
    D) Testes formed abnormally and receptors are normal

    Ans is A) Phenotype may be completely female

    REF:William’s obstetrics/21st ed/page no.160
    http://www.nlm.nih.gov/medlineplus/ency/article/001180.htm

    Androgen insensitivity syndrome (AIS)(Testicular feminization) is when a person who is genetically male (has one X and one Y chromosome) is resistant to male hormones called androgens. As a result, the person has some or all of the physical characteristics of a woman, despite having the genetic makeup of a man.
    The syndrome is divided into two main categories: complete and incomplete. Complete AIS results in someone who looks female. In the incomplete AIS syndrome, the degree of sexual ambiguity varies widely from individual to individual.
    Causes
    The syndrome is caused by various genetic mutations on the X chromosome. The mutations make a developing male baby unable to respond to androgens. (Androgens are responsible for male physical characteristics.)
    If the androgen insensitivity is complete, this prevents the development of the penis and other male body parts. The child is born appearing to be a girl. The complete form of the syndrome occurs in as many as 1 in 20,000 live births.
    Different degrees of androgen resistance can result in a wide variety of outward symptoms. Incomplete AIS can include other disorders, such as Reifenstein's syndrome (also known as Gilbert-Dreyfus syndrome or Lubs syndrome), which is associated with hypospadias (where the opening of the urethra is on the underside, rather than at the tip, of the penis), gynecomastia (breast development in men), and cryptorchidism (when one or both testes fail to descend into the scrotum after birth).
    Also included in the broad category of incomplete AIS is infertile male syndrome, which is sometimes due to an androgen receptor disorder.
    Symptoms(option d ruled out)
    In its classic form (complete androgen resistance), the person appears to be female but has no uterus, and has sparse armpit and pubic hair. At puberty, female secondary sex characteristics (e.g., breasts) develop, but menstruation and fertility do not.
    Complete AIS is rarely discovered during childhood, unless a mass is felt in the abdomen or groin that turns out to be a testicle when it is explored surgically. Most with this condition are not diagnosed until they fail to menstruate or they try to become pregnant and find that they are infertile.
    Incomplete AIS, however, is often discovered during childhood because a person may have both male and female physical characteristics. Many have partial fusion of the outer vaginal lips, an enlarged clitoris, and a short, blind-ending vagina.
    The individual is often diagnosed because of ambiguous genitalia. Sometimes, though, the person has primarily male characteristics and the only symptom is a low sperm count as an adult, perhaps with breast enlargement.
  30. Simran.

    Simran. Guest

    Tumors

    Principal tumors that secrete AFP are endodermal sinus tumor (yolk sac carcinoma), neuroblastoma, hepatoblastoma, and hepatocellular carcinoma.

    With regard to hepatocellular carcinoma, AFP is not useful for screening but is somewhat useful for surveillance after treatment.

    Rare AFP-secreting tumor types include carcinoma in a malignant mixed Müllerian tumor.

    In Wilms tumor AFP is rarely elevated, but when it is elevated it may serve as a marker of disease progression or recurrence.

    There are case reports of elevated AFP associated with teratoma. However, some of these case reports involve infants but do not correct for the normal elevation of AFP in infants, while others ignore the likelihood that teratoma (and other germ cell tumors) may in fact be mixed tumors containing elements of endodermal sinus tumor.

    In patients with AFP-secreting tumors, serum levels of AFP often correlate with tumor size. Resection is usually associated with a fall in serum levels. Serum levels are useful in assessing response to treatment.
  31. dr manju

    dr manju Guest

    musicians nerve

    :?: which is musicians nerve ? a RADIAL NERVE b ULNAR NERVE
  32. Sanjay.

    Sanjay. 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.
  33. Shalini.

    Shalini. Guest

    CONTROVERSIAL QUESTIONS in the paper....

    1.lymphatic metastasis least in ....hard palate? tongue? gingiva ?soft palate?

    2.cavernous sinus enlargement, retrobulbar pain .......tolosa hunt syndrome ?

    3.venous flow depends on a/e......?

    4.iridicorneal endothelial edema......?

    5.female 35 post coital bleeding...Ix...pap smear with clinical examination

    6.ectopic pregnancy termination of events....vascular cause/ immunological?

    7.persistently elevating ca 125....Ix...... CT SCAN/ regular follow up ( somethimg like that/ mri?

    8.villous adenoma.....chlorne sensitive alkalosis

    9.female with multiple disorder........somatisation

    10.pancytopenia WITH REDUCED MCV..... MYELOFIBROSIS

    11..insulinoma v/s sulphonylurea induced hypoglycemia......

    12.dye not used for nocardia......kirim's.

    13.mcv 12.....platelet count 60,000..hb 9 .......iron deficiency

    14.female with urinary retention and constipation....sacrococcygeal teratoma

    15.occipitoposterior presentation in labour....cs?
    16.granulocytic sarcoma.....cd117 / 33?

    17.stomach lymphoma.........false is prognosis of survival 60%

    18.primary splenic lymphoma m.c ....is small cell lymphoma type

    19.bowed radius bilaterally syndrome...investigation not useful-BM/ karyotype?

    20.boy with head deviation to opp. side .... RIGHT superior RECTUS palsy …

    21.prion structure....beta pleated

    22.cystinosis a/e.......blonde hair and...

    23.anasthetic and nerve fibre sensitivity- GOD KNOWS..!!!

    24.g protein....true is.....???

    25.vit d false statement is.... options???

    26.amino acid rich diet....positive nitrogen balance-????

    27.female pregnant with hematuria....impending scar rupture

    28.true abt breast ca.....post op chemo reduces risk of recurrence

    29.absolute c/i of mri....pacemaker

    30.false abt osteopetrosis ......options??

    31.ict maintained by decreased csf absorption
    32.MOTT.......options??

    33.mass in chest with linear stroma of fibrous strands and keratin sheets...... THYMOMA

    34.coefficient of variation.........systolic b.p nad craeatinine ......standard deviation of systolic(20) more than creatinine(15)

    35.disease in females....schies ??????

    36.steroid receptor which does not attach....???

    37.blue white.........plasmid...................for clonal and main chromosomal differentiation
    38.nernst equation????

    39.material used in vertebroplasty.....PMMA

    40.phophatidyl choline in a lipid monolayer when ph is decreased below its pKa
    a)increases surface potential
    b)decreases surface potential
    c)decreases dipole movement
    d)zero dipole movement
  34. Meena.

    Meena. Guest

    AMEGAKARYOCYTIC THROMBOCYTOPENIA WITH ABSENT RADII (TAR)

    The TAR syndrome is an autosomal recessive bleeding disorder that has affected all ethnic groups and often presents as bleeding in the neonatal period. Thrombocytopenia is severe, but other blood elements are normal. Bone marrow megakaryocytes are usually absent. Chromosome breakage studies are normal.

    Patients have absent radii, but the thumbs are normal.


    Deaths can occur from bleeding during the first year, and platelet transfusions may be necessary. However, most survivors have spontaneous improvement of their platelet counts. There are no associated blood disorders. Prenatal diagnosis can be made by fetal ultrasound
  35. Meena.

    Meena. Guest

    differentiation of hypoglycemia due to insulinoma from that due to sulfonylurea overdosage is by insulin:glucose ratio. the reasons being

    1- in both there is normal biohemical mechanism of secretion so C peptide will secreted with every molecule of insulin secreted whether by insulinoma or by sulfonylurea-stimulated pancreas.
    2- though quantitatively secretion of insulin is more in insulinoma more than 70% is secreted as proinsulin and hence levels of plasma insulin (the standard tests only detect plasma insulin and not total insulin which includes plasma insulin and proinsulin) and of C-peptide may be spuriously similar in both the hypoglycemic conditions.
    3- as insulinoma is a slowly developing insidious condition, sympathetic activation maintains normoglycemia despite raised plasma inslin levels and hypoglycemia is seen intermittently whenever the tumor is stimulated to secrete or stored secretions are rleased.
    4- an insulin:glucose ratio >0.3 is virtually diagnostic of hypoglycemia due to insulinoma.
  36. Meena.

    Meena. Guest

    A Pt. with HB-6gm, TLC 1200,PLATELET-60,000, MCV 12FL,what is the DIAGNOSIS??

    A. APLASTIC ANEMIA
    B.MEGALOBLASTIC ANEMIA
    C.PNH
    D. MYELOFIBROSIS
  37. Surbhi.

    Surbhi. Guest

    Treating hypertension after stroke
    Hypertension is the most important potentially reversible risk factor for cerebrovascular disease in all age groups. A continuous relation exists between increasing blood pressure and the likelihood of stroke, such that a 7 mm Hg increment in diastolic blood pressure is associated with a doubling of the relative risk of stroke.1 The preventive role of antihypertensive treatment in reducing morbidity and mortality from stroke is well established: treatment that produces a long term reduction in diastolic blood pressure of 5-6 mm Hg results in a 35-40% fall in the risk of stroke.2,3

    About four fifths of patients with stroke have raised blood pressure on admission to hospital and about one third have a history of hypertension.4 Raised blood pressure usually falls spontaneously within a few days5; 10 days after an ischaemic stroke two thirds of patients are normotensive.6 Doctors are therefore faced with the problem of deciding in whom and when to treat raised blood pressure.

    There is conflicting evidence about the prognostic significance of hypertension immediately after acute stroke. Using multivariate analysis, Carlberg and colleagues found that previous hypertension most strongly predicted raised initial blood pressure in patients admitted to an acute stroke unit.7 Hypertension preceding stroke is, however, not invariably associated with an adverse prognosis in terms of either early fatality or functional recovery.*RF 8-10* Although early studies suggested that hypertension immediately after stroke was associated with increased fatality and poor functional recovery,11,12 more recent work has suggested that raised blood pressure early after cerebral haemorrhage or infarction is related to 30 day fatality only in patients with impaired consciousness,13 which is the single most important adverse prognostic factor for survival after stroke.14 In addition, Levy and colleagues found no association between blood pressure at admission and recovery in a series of patients with acute stroke.8 These results explain the controversy surrounding the early use of hypotensive treatment after acute stroke.15,16

    In health, cerebral circulation is kept constant by autoregulation at a mean systemic arterial pressure (diastolic+ (systolic-diastolic)/3) between 55 and 125 mm Hg. This capacity to regulate cerebral blood flow is reduced in elderly people.17 In patients with chronic hypertension autoregulation begins at a higher systemic pressure, and below this level there is a direct relation between cerebral blood flow and mean arterial pressure.

    After an ischaemic stroke, the normal mechanisms of cerebral circulatory autoregulation are impaired. Perfusion in the ischaemic penumbra, the potentially viable neural tissue surrounding the infarcted area, becomes pressure dependent.18 A rise in systemic arterial pressure may therefore be an adaptive response to maintain the blood flow to this vulnerable area. For this reason, hypotension after stroke should also be sought and treated to avoid further anoxic cerebral damage in parts of the brain with marginal circulation.

    The decision to treat hypertension immediately after ischaemic stroke cannot be taken lightly, especially given the well known hazards of cerebral hypoperfusion from overzealous early blood pressure reduction.19,20 It is important to identify those few patients with hypertensive encephalopathy or aortic dissection whose initial clinical presentation may mimic acute cerebral infarction and who obviously require urgent management of their hypertension. But the more familiar clinical picture is of an elderly patient, often with a history of hypertension, who has substantially raised blood pressure in the first few days after admission to hospital with a stroke. Should such patients receive antihypertensive treatment; which drugs should be used; and how long after the stroke should treatment begin?

    No consensus has emerged regarding treatment of hypertension in the acute phase after stroke. Marked hourly fluctuations in blood pressure have been shown in the first 24 hours,21 and in most patients hypertension will settle gradually without specific treatment.5,6 Furthermore, patients with acute stroke show extreme hypersensitivity to hypotensive treatment4 especially if they are elderly or if the cerebral autoregulatory curve has been shifted as a result of pre-existing longstanding hypertension. No randomised controlled trials looking specifically at antihypertensive treatment in acute stroke have been reported. Hypotension was recognised as a predictable side effect of treatment in studies examining the potential cerebral protective effects of ß blockers and nimodipine in acute ischaemic stroke; these studies showed no beneficial effect on mortality or morbidity for these drugs.*RF 22-24*

    Extreme and persistent hypertension is more likely with intracerebral haemorrhage than with infarction.25 Once again, no randomised trials have been performed that would allow clear clinical guidelines to be drawn up. Nevertheless, very high blood pressures (systolic pressure >200 mm Hg; diastolic pressure >120 mm Hg) associated with intracerebral bleeding (established by computed tomography or magnetic resonance imaging) should be treated early, to limit the development of vasogenic oedema due to disruption of the blood-brain barrier in the ischaemic area around the haemorrhage.20

    Much stroke care occurs in the community, where computed tomography is not available, and a more pragmatic approach is necessary. It may therefore be prudent not to lower the diastolic blood pressure to below 110 mm Hg soon after acute stroke.26 In North America, the treatments advocated for blood pressure reduction soon after stroke tend to be short acting vasodilator drugs such as sodium nitroprusside and labetalol.4,20 Careful monitoring of blood pressure is required with these agents, and they may therefore be difficult to use outside an intensive care unit or designated stroke unit. Current British practice favours the use of short acting oral vasodilators such as nifedipine.27 Such agents may be given sublingually or through a nasogastric tube if swallowing is impaired.

    No consensus exists regarding the optimal timing to initiate long term hypotensive treatment in patients with persistently raised blood pressure a few days after a stroke. But because in most patients blood pressure has stabilised within seven to 10 days, many doctors start treatment at about this time in those remaining hypertensive.6 Antihypertensive treatment that has been initiated in hospital should certainly be reviewed after discharge. In a recent study, two thirds of patients who left hospital after recovering from stroke had significantly raised blood pressures throughout the first year's follow up.28

    Although trials in older adults have shown the efficacy of antihypertensive treatment in reducing morbidity and mortality from first ever stroke,29,30 the long term benefits of secondary stroke prevention by treating hypertension are uncertain and extrapolating from studies of primary prevention may be inappropriate. Few data on the role of blood pressure reduction in decreasing the risk of recurrent stroke are available from clinical trials. In a small randomised study, treatment of hypertension after stroke failed to alter the rates of recurrence.31 Trials of long term secondary stroke prevention by treating hypertension with angiotensin converting enzyme inhibitors or diuretics are currently under way in China and Australasia. Much work remains to be done regarding the behaviour of hypertension after stroke and the effects of its treatment.
  38. Guest

    Guest Guest

    WITH x-ray features of -

    Thumb beaten appearance, prominent vascular markings, sutural diastases, ballooning of sellar, shift of calcified pineal gland

    D/D on CT are

    1. Hydrocephalus
    2. Cerebellar tumour
    3. Basal meningioma
  39. Sanjay.

    Sanjay. Guest

    The exact question was
    Signs of increased ICT A/E
    a) Increased convolutional markings
    b) sellar erosion
    c) ballooning of sella
    d) suture diastasis
  40. Sanjay.

    Sanjay. Guest

    Drug that is a vestibular teratogen?
    a)chloroquine
    b)alcohol
    c)valproinic acid
    d)warfarin

    Among the chemical teratogens, medicinal drugs play a predominant role, a prominent example being thalidomide, which led to a considerably increased frequency of malformations in the early 1960s. Quinine and aminoglycoside antibiotics also give rise to malformations. Cytostatics and medicaments used in the treatment of epilepsy (e.g. diphenylhydantoin, trimethadione, and valproinic acid) may also be responsible. Both excessively high doses of retinoic acid (retinoic acid embryopathy) and vitamin A deficiency (VAD syndrome) during pregnancy can produce ear malformations
  41. Sanjay.

    Sanjay. Guest

    Most common primary splenic tumor
    a) Hodgkins lymphoma
    b) Anaplastic large cell lymphoma
    c) Small lymphocytic lymphoma
    d) Burkitts lymphoma

    Stomach lymphoma false
    a) Stomach is most common site
    b) total gastrectomy with chemotherapy is mainstay of treatment
    c) T cell type
    d) survival rate is 60 %
  42. Sanjay.

    Sanjay. Guest

    The area that we cannot visualise via Bronchoscopy ?
    A.Vocal cord
    B.Sub cranial lymph nodes(I think they meant sub carinal,but they did typing mistake)
    C.Tracheal bifurcation
    D.1st segmental subdivision of bronchi

    Ans is B.Sub cranial lymph nodes
  43. Sanjay.

    Sanjay. Guest

    Nerve compressd by aneurysm of post communicating Artery is?
    a.Occulomolar Nerve
    b.optic N.
    c.Hypopyhsis cerebri
    d.Trochlear N.

    Ans is a)Occulomolar Nerve
  44. Sanjay.

    Sanjay. Guest

    While standing,which does not contribute to increased venous return to lower limbs?
    A. Muscle contraction of soleus
    B. Arterial BP
    C. competence of perforators
    D. Deep Fascia in leg
  45. Sanjay.

    Sanjay. Guest

    Chloroquine is the drug of choice for the prophylaxis and treatment of sensitive malaria species during pregnancy (1,2,3 and 4) . The drug is also indicated for the treatment of extraintestinal invasion by the protozoan parasite, Entamoeba histolytica (5). Chloroquine is generally considered safe for these purposes by most authorities (1,2,3,4,5,6 and 7) . However, the antimalarial is embryotoxic and teratogenic in rats given a 1000-mg/kg dose, causing embryonic death in 27% and producing anophthalmia and microphthalmia in 47% of the surviving fetuses (8).

    Chloroquine crosses the placenta to the fetus with fetal concentrations approximating those in the mother (9). In seven mothers at term in the second stage of labor, chloroquine, 5 mg/kg IM, produced mean levels in maternal blood, cord venous blood, and cord arterial blood of 0.736, 0.703, and 0.663 µg/mL, respectively. The time interval from administration to sampling averaged 5.3 hours (range 2.4–10.5 hours). The calculated cord:maternal serum ratio was 0.93. In the pregnant monkey, an 125I-labeled chloroquine analogue crossed the placenta and concentrated in the fetal adrenal cortex and retina (10). Chloroquine rapidly crosses the placenta in pregnant mice and selectively accumulates in the melanin structures of the fetal eyes (11). The drug was retained in the ocular structures for 5 months after elimination from the rest of the body.

    The risks of complications from malarial infection occurring during pregnancy are increased, especially in women not living in endemic areas (i.e., nonimmune women) (12,13 and 14) . Infection is associated with a number of severe maternal and fetal outcomes: anemia, abortion, stillbirths, prematurity, low birth weight, fetal distress, and congenital malaria (12,13 and 14) . However, it is not yet clear if all of these are related to malarial infection (13). For example, prevention of low birth weight and the resulting risk of infant mortality by antimalarial chemoprophylaxis has not yet been proven (13). Increased maternal morbidity and mortality includes adult respiratory distress syndrome, massive hemolysis, disseminated intravascular coagulation, acute renal failure, and hypoglycemia, with the latter symptom occurring in up to 50% of women in whom quinine is used (14). Severe Plasmodium falciparum malaria in pregnant nonimmune women has a poor prognosis and may be associated with asymptomatic uterine contractions, intrauterine growth retardation, fetal tachycardia, fetal distress, hypoglycemia, and placental insufficiency because of intense parasitization (13). Because of the severity of this disease in pregnancy, chemoprophylaxis is recommended for women of childbearing age who are traveling in areas where malarial is present (12,13 and 14) .

    Congenital malaria may occur in up to 10% of infants born to mothers not living in endemic areas (14). In most cases, clinical malaria manifests 3–8 weeks after birth, probably as a result of exchange of infected maternal erythrocytes at birth, and is characterized by fever, hepatosplenomegaly, jaundice, and thrombocytopenia (14). In areas of hyperendemicity, transplacental passage of maternal IgG may protect the newborn against development of clinical malaria (14).

    Congenital defects have been reported in three infants delivered from one mother who was treated during pregnancy with 250–500 mg/day of chloroquine for discoid lupus erythematosus (15). In addition, this woman also had two normal infants, who had not been exposed to chloroquine during gestation, and one normal infant who had been exposed. Anomalies in the three infants were Wilms' tumor at age 4 years, left-sided hemihypertrophy (one infant), and cochleovestibular paresis (two infants).

    A 1985 report summarized the results of 169 infants exposed in utero to 300 mg of chloroquine base once weekly throughout pregnancy (16). The control group consisted of 454 nonexposed infants. Two infants (1.2%) in the study group had anomalies (tetralogy of Fallot and congenital hypothyroidism) compared to four control infants who had defects (0.9%). Based on these data, the authors concluded that chloroquine is not a major teratogen, but a small increase in birth defects could not be excluded (16).

    Breast Feeding Summary

    Chloroquine is excreted into human breast milk (9,17). When chloroquine, 5 mg/kg intramuscular, was administered to six nursing mothers 17 days postpartum, mean milk and serum concentrations 2 hours later were 0.227 µmg/mL (range 0.163–0.319 µmg/mL) and 0.648 µmg/mL (range 0.46–0.95 µmg/mL), respectively. The mean milk:blood ratio was 0.358 (range 0.268–0.462). Based on an average consumption of 500 mL of milk/day, an infant would have received about 114 µmg/day of chloroquine, an amount considered safe by the investigators (9). In an earlier study, three women were given a single dose of 600 mg of chloroquine 2–5 days postpartum (17). Serum and milk samples were collected up to 227 hours after administration. The milk:plasma area under the concentration-time curve ratios for chloroquine and the principal metabolite, desethylchloroquine, ranged from 1.96 to 4.26 and from 0.54 to 3.89, respectively. Based on a daily milk intake of 1000 mL, the nursing infants would have ingested between 2.2%–4.2% of the maternal doses over a 9-day period (17).

    Although the amounts of chloroquine excreted into milk are not considered to be harmful to a nursing infant, they are insufficient to provide adequate protection against malaria (12). The American Academy of Pediatrics considers the drug to be compatible with breast feeding (18).
  46. Sanjay.

    Sanjay. Guest

    drugs considered to be teratogenic in humans

    quinine
    alcohol
    warfarin
    valproic acid
  47. Abbas.

    Abbas. Guest

    Venous return on standing from supine position depends on all except
    a) Arterial blood pressure
    b) Sheath of deep fascia
    c) Competency of valves
    d) Contraction of calf muscles
    Ans: a. Arterial blood pressure

    Ref B.D.C Anatomy Chapter on Venous drainage, lymphatic drainage, Segmental & sympathetic innervation and embryology of lower limb

    Factors helping venous return

    A. Genaral factors
    1. Negative intrathoracic pressure, which is made more negative during inspiration.
    2. Arterial pressure and overflow from capillary bed.
    3. Compression of veins accompanying arteries by arterial pulsation.
    4. The presence of valves in veins which support the column of blood and maintain unidirectional flow.

    B. Local Factors (venous, muscular and fascial)
    1. Veins of lower limb- more muscular, more valves and superficial veins connected to deep veins by perforators.
    2. When the limb is active muscular contraction compresses the deep veins and drives blood upwards.
    3. Tight sleeve of deep fascia makes muscular compression of the veins much more effective by limiting outward bulging of the muscles. (Weakness of this sheath leads to accumulation of venous blood in the superficial veins of leg reducing the venous return).

    Hence as we see, all the four given options aid in venous return. Now the question specifically asks what happens when a person stands from supine position. In this case all the local factors will be effective to aid venous return against gravity.

    About arterial pressure – (ref Ganong 22nd ed pg 630)
    On standing from supine, immediately there is fall in venous return due to gravity which leads to fall in cardiac output and consecutively fall in arterial blood pressure. This is countered by autoregulatory mechanisms (baroreceptors) increasing heart rate to maintain cardiac output. Relatively little venoconstriction occurs in the periphery, but there is a prompt increase in the circulating levels of renin and aldosterone. The arterioles constrict, helping to maintain blood pressure. So it is evident that arterial pressure tends to fall on standing which needs to be maintained by autoregulatory mechanism. Hence in this particular situation arterial pressure, if at all contributory to venous return, is of least importance.

    Note – The role of deep fascia in aiding venous return is not mentioned in many standard text books, so apparently that may seem as the answer. But B.D.C. clearly mentions about it and also ganong pg.630 (22nd ed) indirectly refers to it by saying “These long legged animals (giraffes) do not develop ankle edema despite their very large increment in vascular pressure in legs due to gravity because they have tight skin and fascia in the lower legs – in a sense a built in antigravity suit – and a very effective muscle pump.”
  48. Guest

    Guest Guest

    ans

    drugs considered to be teratogenic in humans

    quinine
    alcohol
    warfarin
    valproic acid


    warfarin is the answer, that's why we use heparin in pregnancy
  49. Sunil.

    Sunil. Guest

    Pathophysiology

    Many studies have demonstrated that chronic hyperglycemia, as well as hyperlipidemia and hypertension, contribute to the pathogenesis of DR (11–14). The exact mechanisms by which elevated glucose initiates the vascular disruption in retinopathy remain poorly defined, and, not surprisingly, several pathways have been implicated. The vascular disruptions of DR/DME are characterized by abnormal vascular flow, disruptions in permeability, and/or closure or nonperfusion of capillaries.

    A hallmark of early DR is the change in the structure and cellular composition of the microvasculature (15–17). Endothelial cells are responsible for maintaining the blood-retinal barrier, and damage to them results in increased vascular permeability. In early stages of DME, breakdown of the inner blood-retinal barrier may occur, resulting in accumulation of extracellular fluid in the macula (7,18).

    Pericytes are essential cellular components in the regulation of retinal capillary perfusion, and damage to these cells in diabetes leads to altered retinal hemodynamics, including abnormal autoregulation of retinal blood flow (19). Loss of retinal pericytes represents another early feature of DR (20–22) and correlates with microaneurysm formation (15,20,23). Another common feature of DR is the thickening of the capillary basement membrane and increased deposition of extracellular matrix components. This feature may contribute to the development of abnormal retinal hemodynamics (24–26), including abnormal autoregulation of retinal blood flow.

    There is evidence that retinal leukostasis may also play an important role in the pathogenesis of DR. Leukocytes possess large cell volume, high cytoplasmic rigidity, a natural tendency to adhere to the vascular endothelium, and a capacity to generate toxic superoxide radicals and proteolytic enzymes (27). In diabetes, there is increased retinal leukostasis, which affects retinal endothelial function, retinal perfusion, angiogenesis, and vascular permeability. In particular, leukocytes in diabetes are less deformable, a higher proportion are activated, and they may be involved in capillary nonperfusion, endothelial cell damage, and vascular leakage in the retinal microcirculation (27). A recent study showed that diabetic vascular leakage and nonperfusion are temporally and spatially associated with retinal leukostasis in streptozotocin-induced diabetic rats (28). There are many capillary occlusions by leukocytes and capillary dropout or degeneration associated with leukocytes in the diabetic retina (27). Serial acridine orange leukocyte fluorography and fluorescein angiography (FA) show trapped leukocytes directly associated with areas of downstream nonperfusion in the diabetic retinal microcirculation (27). Whereas leukostasis probably plays a key role in the pathogenesis of DR, platelets and erythrocytes are also involved in this process.

    As a result of occluded capillaries, retinal ischemia stimulates a pathologic neovascularization mediated by angiogenic factors, such as vascular endothelial growth factor (VEGF), which results in proliferative diabetic retinopathy (PDR) (29,30). This neovascularization is the predominant feature of PDR. Hemorrhaging of new vessels into the vitreous may also lead to tractional retinal detachment (5).

    Understanding the diabetes-induced mechanisms that contribute to pericyte loss, endothelial cell proliferation, neovascularization, and alterations in basement membrane structure is therefore central to the design of pharmacological therapeutic strategies to treat and prevent early diabetes-related microvascular changes.


    The mechanisms that contribute to cellular damage in the retina include increased flux through the polyol pathway leading to sorbitol accumulation, production of advanced glycation end products (AGEs), increased oxidative stress, and activation of the protein kinase C (PKC)-ß pathway
  50. Sunil.

    Sunil. Guest

    most significant in regulating CSF pressure?

    a)absorption of CSF
    b)production of CSF
    c)blood flow

    ans-blood flow

    The volume of blood contained within the venous sinuses is reduced to a minimum as part of the compensatory process. However, should free flow of venous blood be impeded by a number of simple causes (*INFO* Table 1) then this increase in volume of the venous system in a critically swollen brain will lead to a rapid rise in ICP. In practice, it is imperative to ensure that when the patient is in the supine or lateral position that a head up tilt to a maximum of 30° is obtained. This improves venous drainage with minimal effect on arterial pressure [1]. Venous drainage is passive and thus maximised by ensuring there is no pressure on, or kinking, of the neck veins. In addition the higher the head, the greater the effect of gravity on the flow of venous blood. However, as the head is raised, the gravitational effect on the arterial pressure at the brain is also increased. This is a disadvantage as it reduces the pressure of blood perfusing the brain. The best compromise is the position described above of 30°.

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