Questions FMGE -2008(Part-1,11; Set-A)

Discussion in 'FMGE' started by Guest, Oct 4, 2008.

  1. tarjan.

    tarjan. Guest

    66. The following are example of Apootosis Except-

    a) Graft versus host disease
    b) Menstrual cycle
    c) Pathological atrophy following duct obstruction
    d) Tumour necrosis

    Ans: d)





    --------------

    Apoptosis:

    Programmed cell death is called apoptosis.

    Programmed cell death is needed to destroy cells that represent a threat to the integrity of the organism.

    Examples:

    Cells infected with viruses:

    One of the methods by which cytotoxic T lymphocytes (CTLs) kill virus-infected cells is by inducing apoptosis.

    --
    Cells of the immune system:

    As cell-mediated immune responses wane, the effector cells must be removed to prevent them from attacking body constituents. CTLs induce apoptosis in each other and even in themselves. Defects in the apoptotic machinery is associated with autoimmune diseases such as lupus erythematosus and rheumatoid arthritis.


    Cells with DNA damage:

    Damage to its genome can cause a cell
    •to disrupt proper embryonic development leading to birth defects
    •to become cancerous.
    Cells respond to DNA damage by increasing their production of p53. p53 is a potent inducer of apoptosis.


    Cancer cells:
    Radiation and chemicals used in cancer therapy induce apoptosis in some types of cancer cells.


    Menstruation refers to the monthly shedding of the lining of the uterus (the womb), released through the vagina. The menstrual cycle begins the first day a woman bleeds – in other words, the first day of a period.


    Apoptosis is the death of single cells within clusters of other cells.

    Apoptosis seen in: ---->

    I. Physiological conditions like:

    a. Endometrial cell death during Menstuation cycle
    b. Cell death os virus infected or neoplastic cells in a tumor ( T-cell induced)
    c. Removal of cells during embryogenesis,

    II. Pathological conditions like:
    a. Graft - versus host diseases
    b. Atropy of glands following duct obliteration.
  2. tarjan.

    tarjan. Guest

    9)m\c reason for bradycardia in MI.

    a. septal MI
    b. right vent.M I
    c. Lleft ventricular MI

    ANS: C

    What is Myocardial infarction?
    Myocardial infarction is heart attack, it occurs when an area of heart muscle dies or is permanently damaged because of an inadequate supply of oxygen to that area.


    Myocardial infarction (MI) is the rapid development of myocardial necrosis caused by a critical imbalance between oxygen supply and demand of the myocardium. This usually results from plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium.

    Pathophysiology
    The most common cause of MI is narrowing of the epicardial blood vessels due to atheromatous plaques. Plaque rupture with subsequent exposure of the basement membrane results in platelet aggregation, thrombus formation, fibrin accumulation, hemorrhage into the plaque, and varying degrees of vasospasm. This can result in partial or complete occlusion of the vessel and subsequent myocardial ischemia. Total occlusion of the vessel for more than 4-6 hours results in irreversible myocardial necrosis, but reperfusion within this period can salvage the myocardium and reduce morbidity and mortality.

    Nonatherosclerotic causes of MI include coronary vasospasm as seen in variant (Prinzmetal) angina and in patients using cocaine and amphetamines; coronary emboli from sources such as an infected heart valve; occlusion of the coronaries due to vasculitis; or other causes leading to mismatch of oxygen supply and demand, such as acute anemia from GI bleeding.

    MI induced by chest trauma has also been reported, usually following severe chest trauma such as motor vehicle accidents and sports injuries.


    Causes
    The most frequent cause of MI is rupture of an atherosclerotic plaque within a coronary artery with subsequent arterial spasm and thrombus formation.

    Other causes include the following:

    •Coronary artery vasospasm

    •Ventricular hypertrophy (eg, left ventricular hypertrophy [LVH], idiopathic hypertrophic subaortic stenosis [IHSS], underlying valve disease)

    •Hypoxia due to carbon monoxide poisoning or acute pulmonary disorders (Infarcts due to pulmonary disease usually occur when demand on the myocardium dramatically increases relative to the available blood supply.)

    •Coronary artery emboli, secondary to cholesterol, air, or the products of sepsis

    •Cocaine, amphetamines, and ephedrine

    •Arteritis

    •Coronary anomalies, including aneurysms of the coronary arteries

    •Increased afterload or inotropic effects, which increase the demand on the myocardium

    •Aortic dissection, with retrograde involvement of the coronary arteries
  3. tarjan.

    tarjan. Guest

    10) S1 split seen in ---> RBBB

    Heart Sounds -->S1
    A. 2 main components: M1 (mitral valve closure) and T1 (tricuspid valve closure) MV usually closes slightly before TV. TV closure is softer. Splitting best heard at LLSB or at the apex.

    B. Wide splitting of S1:
    ---1. Ebstein’s Anomaly of the TV
    ---2. RBBB

    C. No splitting of S1 heard in LBBB

    D. Single S1 occurs in SVT not associated with aberrant conduction

    E. Split S1 with ventricular arrhythmias

    F. Loud S1: short PR (0.08-0.12 sec),
    --- 1. Premature beats/tachycardia, MS, TS,
    ----2. atrial myxoma, left-to-right shunts,
    ----3. exercise, fever, anemia, hyperthyroid,
    ----4. epinephrine, anxiety, pregnancy, A-V
    ----5. fistula, child (with a thin chest wall)

    G. Soft S1: long PR (> 0.20 secs), MR, TR,
    ---1.severe AI, HTN, shock, CHF, MI,
    ---2.myocarditis, myxedema, beta blocker
    ---3.infusion, thick chest, emphysema,
    ---4.pericardial effusion
  4. tarjan.

    tarjan. Guest

    17)toxin responsibel for TSS in femals

    Toxins implicated: --->TSST-1; enterotoxins B and C

    Staphylococcal TSS -->More common in females.

    Staphylococcal toxic shock syndrome (TSS):

    Staphylococcal toxic shock syndrome (TSS) is frequently seen in women during menstruation. More recently, with the decline in use of hyperabsorbent tampons, recognition of nonmenstrual TSS has been increasing. Various wounds, many appearing relatively benign, may harbor toxin-producing staphylococci. Thus, herniorrhaphy, mammoplasty, arthroscopy, and other surgical wound infections may be complicated by the development of TSS. Manifestations of TSS usually begin 2 days after surgery.

    Staphylococcal TSS associated with menstruation occurs more frequently in communities without a history of prior antibiotic exposure and is caused primarily by TSST-1–producing organisms. By contrast, nonmenstrual staphylococcal TSS is more common in hospitalized patients who have received prior antibiotic therapy. TSST-1 production is noted in only 50% of the patients. Enterotoxin B and C production is associated with the remainder of nonmenstrual staphylococcal TSS cases.
  5. tarjan.

    tarjan. Guest

    18. In stap. aures food poisoning diarrhea occur due 2?

    a. endotoxin
    b.vagus
    c.exotoxin

    STAPHYLOCOCCUS AUREUS:

    ENTEROTOXINS A, B, C1, C2, D: Affects the GI-tract in S. AURES food poisoning.
  6. tarjan.

    tarjan. Guest

    24)ALL R FEATURES OF ATRIAL MYXOMA EXCEPT -FEVER -
    CLUBBING -
    EMBOLI
    *HYPERTENSION

    Atrial Myxoma

    This is a primary tumor of the heart. It is quite rare. It usually begins in the septum between the two heart ventricles, with 80% of the tumors growing into the left atrium.

    Though it is a benign tumor, it can become serious when a part of it breaks off and embolizes (moves) into the blood vessels and causes an obstruction of blood flow. If, for example, the tumor embolizes to the brain, it can block off part of the blood supply to the brain and cause a stroke.


    Symptoms:

    Chest pain
    Palpitations
    Shortness of breath
    Edema (swelling of the legs)
    Lightheadedness
    Fainting
    Cough
    Fever
    Loss of energy
    Weight loss
    Clubbed fingers
    Vision loss
    Confusion

    How the Diagnosis Made:

    Examination:
    Ophthalmologic examination may show retinal infarction (death to the retinal tissue) due to emboli.
    Jugular venous distention -- neck veins show increased bulging.
    Heart -- may reveal a middiastolic or presystolic murmur (resembles the murmur of mitral or tricuspid stenosis). The heart rhythm may be irregular.
    Lung exam may show crackles (left sided myxoma only).

    Tests:
    Echocardiogram will show the myxoma and related heart valve problems.
    Other tests that may show the myxoma include Chest X-Ray, CT scan, MRI, and cardiac catheterization.
    EKG may show atrial fibrillation.
    Blood tests: Complete blood count may show anemia. Sedimentation rate is decreased.

    TREATMENT:

    Surgical tumor removal is the only treatment.

    COMPLICATIONS

    Congestive Heart Failure
    Right heart failure
    Peripheral emboli
    Pulmonary Emboli
    Stroke
    Arrythmias (heart irregularities)
  7. tarjan.

    tarjan. Guest

    Q) DOC in Supraventricular Tachycardia (SVT)

    Supraventricular Tachycardia (SVT):

    Supraventricular (originating above the ventricles) tachycardia (SVT) is a series of fast atrial heartbeats that can cause the heart to contract at rates of 250 times per minute or faster.

    SVT can be uncomfortable and frightening. The type of treatment depends on whether the electrical impulses reenter the atria via a bypass tract (Wolff-Parkinson-White syndrome), through the atrioventricular (AV) node, or are caused by a single abnormal group of cells.

    Wolff-Parkinson-White (WPW) Syndrome:

    Wolff-Parkinson-White Syndrome is a common cause of SVT. In WPW there is an abnormal electrical connection between the atria and ventricles. This extra tissue is a short circuit between these chambers. It provides an extra pathway for electrical impulses to be conducted through the tissue that normally blocks electrical impulses between the atria and ventricles. This short circuit is called an accessory pathway, and it allows electrical impulses to travel between the atria and the ventricles without going through the AV node. In WPW, an SVT is usually started when an impulse travels down the AV node to the ventricles and then up through the short circuit tissue to the atria. This impulse can then travel through the atria and down the AV node before the SA node can start the next heartbeat. If the impulse continues to travel in this repeating, circular pattern, it can cause the heart to beat very rapidly.

    AV Nodal Reentrant Tachycardia:

    AV Nodal Reentrant Tachycardia (AVNRT) is another common form of SVT. In AVNRT, there is an extra electrical pathway in or near the AV node. If an electrical impulse is conducted in this pathway, it may direct the impulse through both the AV node and the extra pathway in a repeating, circular pattern. The AV node and the extra pathway are located essentially in the center of the heart. This causes the upper and lower chambers to beat rapidly at the same time instead of in the normal sequence (upper chambers beating first, followed by the lower chambers).

    Rapid AV Nodal Conduction:

    In some SVTs the atria may spontaneously generate multiple rapid impulses. Many of these impulses can travel through the AV node to the ventricles in an erratic manner. As a result, the heart rhythm can become irregular and rapid. If this happens, the heart will not pump blood efficiently.

    Atrial Flutter:

    Atrial flutter is one of the more common SVTs, where the upper chambers of the heart (atria) beat anywhere from 240 to 320 times per minute. This arrhythmia is similar to atrial fibrillation, as it originates entirely within the upper chambers, but it produces a more organized, regular rhythm. It is usually not harmful, but can result in symptoms such as palpitations, shortness of breath, chest tightness, fatigue, and lightheadedness. If left untreated, atrial flutter may eventually lead to conditions associated with other arrhythmias that result in abnormally high heart rates.

    Even though the upper chambers are beating rapidly, the AV node allows only one-half to one-third of the electrical impulses to reach the hearts lower chambers (the ventricles). This prevents the arrhythmia from becoming life-threatening, and keeps the wrist pulse rate at only 100 to 150 beats per minute. This arrhythmia can last for hours or days; therefore, most people with atrial flutter require treatment.

    Normal Rhythm:

    Every normal heart has a normal rhythm. That rhythm varies from person to person. In most healthy people, the heart at rest beats about 60 to 100 times per minute. A small bunch of heart cells called the sinoatrial node keeps time.

    What are the treatment options for supraventricular tachycardia?

    Stopping an episode of SVT
    Many episodes of SVT soon stop on their own, and no treatment is then needed. If an episode of SVT lasts a long time or is severe, you may need to be admitted to hospital to stop it.

    •Medicines which are given by injection into a vein will usually stop an SVT.

    Adenosine is commonly used. It works by blocking electrical impulses in the heart.

    Verapamil is an alternative if adenosine is not advised. For example, some people with asthma cannot have adenosine.
    •Electric shock treatment is sometimes used to stop an episode of SVT.

    Preventing episodes of SVT Options include the following.

    •You can take medication every day to prevent episodes of SVT. Various medicines can interfere with the electrical impulses in your heart.

    They include: digoxin, verapamil, and beta-blockers - but there are others. If one does not work or causes side-effects, another can often be found to suit.

    •Catheter ablation (destruction) treatment may be an option for some types of SVT. A catheter (small wire) is passed via a large vein in your leg into the chambers of your heart. It is guided by special x-ray techniques. The tip of the catheter can destroy a tiny section of heart tissue that is the source or 'trigger' of the abnormal electrical impulses. This is only suitable if the exact site of the trigger can be found by special tests, and be located accurately by the catheter tip. It can be very successful, and after the procedure you do not need to take medication to prevent SVT.

    •Open heart surgery is rarely needed to destroy a 'trigger' of abnormal electrical impulses which is not controlled by the above two options.

    •Not treating is an option if episodes of SVT are infrequent, only last a short time, or cause few symptoms. The treatments above have to be balanced against the possible side-effects and risks. Some people prefer to put up with symptoms if they not too bad and only occur now and then.
  8. malya.

    malya. Guest

    30)A PT ON TPN.WHAT COULD BE THE CAUSE OF MORTALITY IN THAT PT?

    Total parenteral nutrition:

    Total parenteral nutrition (TPN), is the practice of feeding a person intravenously, bypassing the usual process of eating and digestion. The person receives nutritional formulas containing salts, glucose, amino acids, lipids and added vitamins.

    Total parenteral nutrition (TPN), also referred to as Parenteral nutrition (PN), is provided when the gastrointestinal tract is nonfunctional because of an interruption in its continuity or because its absorptive capacity is impaired (Kozier et al, 2004). It has been used for comatose patients, although enteral feeding is usually preferable, and less prone to complications. Short-term TPN may be used if a person's digestive system has shut down (for instance by Peritonitis), and they are at a low enough weight to cause concerns about nutrition during an extended hospital stay. Long-term TPN is occasionally used to treat people suffering the extended consequences of an accident or surgery. Most controversially, TPN has extended the life of a small number of children born with nonexistent or severely deformed guts. The oldest were eight years old in 2003.

    The preferred method of delivering TPN is with a medical infusion pump. A sterile bag of nutrient solution, between 500 mL and 4 L is provided. The pump infuses a small amount (0.1 to 10 mL/hr) continuously in order to keep the vein open. Feeding schedules vary, but one common regimen ramps up the nutrition over a few hours, levels off the rate for a few hours, and then ramps it down over a few more hours, in order to simulate a normal set of meal times.

    Chronic TPN is performed through a central intravenous catheter, usually in the subclavian or jugular vein. Another common practice is to use a PICC line, which originates in the arm, and extends to one of the central veins, such as the subclavian. In infants, sometimes the umbilical vein is used.

    Battery-powered ambulatory infusion pumps can be used with chronic TPN patients. Usually the pump and a small (100 ml) bag of nutrient (to keep the vein open) are carried in a small bag around the waist or on the shoulder. Outpatient TPN practices are still being refined.

    Aside from their dependence on a pump, chronic TPN patients live quite normal lives


    Complications
    The most common complication of TPN use is bacterial infection, usually due to the increased infection risk from having an indwelling central venous catheter. In patients with frequent bacterial infections, fungal infections can also occur. Liver failure, often related to Fatty liver, may sometimes occur. This condition is due to the difficulty in processing food taken in directly into the bloodstream.

    Two related complications of TPN are venous thrombosis and rarely priapism. Fat infusion during TPN is assumed to contribute to both.

    Other complications of TPN are related to the difficulties the body has processing TPN. One complication is non-anion gap metabolic acidosis.

    Total parenteral nutrition increases the risk of acute cholecystitis due to complete unusage of gastrointestinal tract, which may result in bile stasis in the gallbladder. The risk of acute cholecystitis is increased accordingly.

    A recent small-scale study at Children's Hospital Boston on the cause of liver failure suggests it may be due to a large difference in omega-6 to omega-3 ratio. When treated with Omegaven, a different fatty acid infusion (which is approved for limited use in the U.S.), two patients were able to recover from their condition.

    In critical and/or perioperative care:

    Parenteral nutrition is indicated to prevent the adverse effects of malnutrition in patients who are unable to obtain adequate nutrients by oral or enteral routes. Other indications are short gut syndrome, high-output fistula, prolonged ileus, or bowel obstruction. However, the decision to initiate TPN needs to be made on an individual patient basis, as different patients will have differing abilities to tolerate starvation.

    The nutrient solution consists of water and electrolytes; glucose, amino acids, and lipids; essential vitamins, minerals and trace elements are added or given separately. Previously lipid emulsions were given separately but is becoming more common for a "three-in-one" solution of glucose, proteins, and lipids to be administered.

    Complications are either related to Catheter insertion, or Metabolic (including the Refeeding Syndrome). Catheter complications include pneumothorax, accidental arterial puncture, and catheter-related sepsis. The complication rate at the time of insertion should be less than 5% . Catheter-related infections may be minimised by appropriate choice of catheter and insertion technique. Metabolic complications include the Refeeding Syndrome characterised by hypophosphataemia and other electrolyte abnormalities. Hyperglycemia is common at the start of therapy, and hypoglycaemia is likely to occur with abrupt cessation of TPN. Liver dysfunction can be limited to a reversible cholestatic jaundice and to fatty infiltration (demonstrated by elevated transaminases). Severe hepatic dysfunction is a rare complication.

    Overall, patients receiving TPN have a higher rate of infectious complications. This is related to hyperglycemia
  9. Suman.

    Suman. Guest

    32)A Q ON ARDS--DIAGNOSTIC CRITERIA


    Definition Criteria for ALI and ARDS:
    Acute respiratory distress syndrome (ARDS) is a life-threatening lung condition that prevents enough oxygen from getting into the blood.


    Clinical Conditions Associated with Development of Acute Respiratory:

    Distress Syndrome
    Direct lung injury Indirect lung injury
    Pneumonia Sepsis
    Aspiration of gastric contents Severe trauma
    Inhalation injury Acute pancreatitis
    Near drowning Cardiopulmonary bypass
    Pulmonary contusion Massive transfusions
    Fat embolism Drug overdose
    Reperfusion pulmonary edema post lung
    transplantation or pulmonary embolectomy




    Criteria for ALI 9acute lung injury)--Acute in onset

    Oxygenation: A partial pressure of arterial oxygen to fractional inspired oxygen concentration ratio < 300 mm per Hg (regardless of PEEP)
    Bilateral pulmonary infiltrates on chest radiograph Pulmonary artery wedge pressure < 18 mm per Hg or no clinical evidence of left atrial hypertension.

    ALI = acute lung injury; ARDS = acute respiratory distress syndrome; PEEP = positive end-expiratory pressure.



    Criteria for ARDS - Acute in onset

    Oxygenation: A partial pressure of arterial oxygen to fractional inspired oxygen concentration ratio < 200 mm per Hg (regardless of PEEP) ilateral pulmonary infiltrates on chest radiograph Pulmonary artery wedge pressure < 18 mm per Hg or no clinical evidence of left atrial hypertension.

    -
    Tests used to diagnose ARDS include:

    Arterial blood gas
    Bronchoscopy
    CBC and blood chemistries
    Chest x-ray
    Sputum cultures and analysis
    Tests for possible infections

    -

    Treatment

    Typically persons with ARDS need to be in an intensive care unit (ICU).

    The goal of treatment is to provide breathing support and treat the underlying cause of ARDS. This may involve medications to treat infections, reduce inflammation, and remove fluid from the lungs.

    A breathing machine is used to deliver high doses of oxygen and a continuous level of pressure called PEEP (positive end-expiratory pressure) to the damaged lungs. Patients often need to be deeply sedated with medications when using this equipment.
  10. suman.

    suman. Guest

    Diagnostic Criteria for Adult Respiratory Distress Syndrome (ARDS)

    Acute Respiratory Distress Syndrome (ARDS) is a syndrome of inflammation and increased permeability associated with a constellation of clinical, radiologic, and physiologic abnormalities unexplained by elevations in left atrial or pulmonary capillary pressure.

    All definitions of this syndrome include patients who meet the following criteria:

    Identifiable associated condition

    Acute onset

    Pulmonary artery wedge pressure </=18 mm Hg or absence of clinical evidence of left atrial hypertension

    Bilateral infiltrates on chest radiography

    Acute lung injury (ALI) is present if Pao2/Fio2 ratio is </= 300

    Acute respiratory distress syndrome is present if Pao2/Fio2 ratio </= 200

    ARDS = acute respiratory distress syndrome; Pao2 = partial pressure of arterial oxygen; Fio2 = percentage of inspired oxygen.

    Clinical Conditions Associated with Development of Acute Respiratory Distress Syndrome

    Direct lung injury

    Pneumonia

    Aspiration of gastric contents

    Inhalation injury

    Near drowning

    Pulmonary contusion

    Fat embolism

    Reperfusion pulmonary edema post lung transplantation or pulmonary embolectomy

    Indirect lung injury

    Sepsis

    Severe trauma

    Acute pancreatitis

    Cardiopulmonary bypass

    Massive transfusions

    Drug overdose
  11. tarjan.

    tarjan. Guest

    37)MC TYPE OF PEMPHIGUS IN INDIA?

    ANS: Pemphigus vulgaris (PV). (Most Common Type of PEMPHIGUS in India)


    Definition

    Pemphigus is a group of rare skin disorders that cause blisters of your skin or mucous membranes, such as in your mouth or on your genitals.

    Pemphigus can occur at any age, but often strikes people in middle age or older. Although it affects all races and cultures, pemphigus tends to be more common in people of Middle Eastern or Jewish descent.

    Usually a chronic condition, pemphigus is best controlled by early diagnosis and treatment, which may include medications or treatments similar to those used for severe burns. The less widespread your pemphigus is, the easier it may be to control.

    There are several types of pemphigus including:

    1. Pemphigus vulgaris (PV). (Most Common Type of PEMPHIGUS in India)
    2. Pemphigus vegetans.
    3. Pemphigus foliaceus.
    4. Pemphigus erythematosus.
    5. Paraneoplastic pemphigus.



    Symptoms

    Pemphigus is characterized by blisters on your skin and mucous membranes. The blisters rupture easily, leaving open sores, which may ooze and become infected. The signs and symptoms of the three main types of pemphigus differ depending on the type:

    Pemphigus vulgaris. The most common form, pemphigus vulgaris usually begins with blisters in your mouth, which then erupt on your skin. Blisters can also break out on the mucous membranes of your genitals. The blisters typically are painful, but don't itch.
    Pemphigus foliaceus. This type doesn't usually affect mucous membranes. The blisters, which usually begin on your face and scalp and later erupt on your chest and back, usually aren't painful. They tend to be crusty and itchy.
    Paraneoplastic pemphigus. This form, which may be associated with a malignancy, causes painful sores on your mouth and lips and in your esophagus, as well as skin lesions. This form of pemphigus can also cause lesions in your lungs, resulting in progressive lung disease and making it difficult for you to breathe (dyspnea).

    Causes

    Exactly what triggers pemphigus is unknown, but it's an autoimmune disorder.

    Normally, your immune system attacks foreign invaders, such as harmful viruses and bacteria. But in pemphigus, your immune system mistakenly produces antibodies that attack healthy cells in your skin and mucous membranes, and more specifically proteins called desmogleins in the majority of cases. Desmogleins bind skin cells to each other. The antibodies binding to the skin cause separation of the cells of the top layer of your skin (epidermis). This separation reaction is known as acantholysis.

    Sometimes, pemphigus develops as a side effect from certain medications, such as blood pressure drugs or chelating agents. This type of pemphigus usually disappears when the medicine is stopped.

    Paraneoplastic pemphigus is caused by additional antibodies to those seen in other forms of the disorder. It develops in people who have cancer, usually lymphoma or leukemia. In cases in which the cancer hasn't yet been discovered, the appearance of pemphigus blisters may alert doctors to look for a malignancy.

    Risk factors

    Pemphigus isn't contagious, and there's no way to predict who'll get it. However, your risk increases if:

    You're middle-aged or older.
    You're of Mediterranean or Jewish descent.
    You have another autoimmune condition, particularly myasthenia gravis, a chronic disorder characterized by muscle weakness and fatigue, or thymoma, a tumor of the thymus. The thymus is an organ that produces white blood cells known as lymphocytes, an important part of your immune system.

    When to seek medical advice

    See your doctor if you develop blisters inside your mouth or on your skin. If you've been treated for pemphigus, see your doctor if you develop any of the following:

    New blisters or sores
    A rapid spread in the number of sores
    Fever
    Chills
    Achy muscles or joints
    A general sense of feeling ill (malaise)

    Tests and diagnosis

    Because it's uncommon, pemphigus can be difficult to diagnose. Blisters are common to a number of conditions, so besides taking a medical history and examining your skin and mouth, your doctor may lightly rub unblistered skin with a cotton swab or finger. With pemphigus, the top layers of your skin are likely to separate easily from the lower layers (positive for Nikolsky sign). Other tests may include:

    Skin biopsy. In this test, a piece of tissue from a blister is removed and examined under a microscope. Examination of the biopsy tissue may also involve a process called direct immunofluorescence (DIF). DIF entails staining the tissue with fluorescent dye to make the antibodies "light up" under a special microscope so that they can be identified.
    Blood tests. The purpose of these tests is to detect and identify antibodies (anti-desmogleins) in your blood.

    Complications

    Possible complications of pemphigus are infection of your skin and spread of infection through your bloodstream (sepsis). Systemic infection can be fatal.

    Complications of paraneoplastic pemphigus include respiratory problems. The mortality rate for this type of pemphigus is estimated to be 90 percent, independent of the underlying cancer.

    Other complications are the possible side effects of the medications used to treat pemphigus, particularly corticosteroids.

    Treatments and drugs

    Treatment, which aims at reducing signs and symptoms and preventing complications, is most effective when it begins as early as possible. The less widespread pemphigus is, the easier it may be to control. Specific treatment methods depend on the severity of the disease.

    Mild pemphigus
    If your pemphigus isn't too widespread, you may be able to remain at home for treatment. The mainstay of treatment is usually corticosteroids, such as prednisone. However, using corticosteroids over an extended time or in high doses may cause serious side effects, including:

    Weight gain
    Mood swings
    Elevated blood sugar (diabetes)
    Osteoporosis
    Redistribution of body fat, leading to a round face (moon face)
    Increased chance of infection because of suppression of the immune system

    Corticosteroids may be combined with other medications, including:

    Immunosuppressants. These medications, such as azathioprine (Imuran) or methotrexate (Rheumatrex), help keep your immune system from attacking healthy tissue. These drugs have serious side effects, including increased risk of infection.
    Antibiotics and antifungal medications. These may be prescribed to control or prevent infections.

    Additionally, other medications, such as dapsone, intravenous immunoglobulin and rituximab (Rituxan), also may be prescribed. These medications have had some success in treating pemphigus in small clinical trials.

    Severe pemphigus
    Widespread pemphigus may require you to stay in the hospital, where you may receive treatment similar to treatment for severe burns. The open sores make you highly vulnerable to infection, which, if it spreads to your bloodstream, may be fatal. Along with the medications listed above, you may also be given:

    Fluids. Because you may have lost bodily fluids due to oozing of the sores, you may receive fluids through a vein (intravenously), as well as electrolytes — minerals such as sodium, potassium and calcium that maintain the balance of fluids in your body — and proteins.
    Intravenous feeding. This may be necessary if mouth sores make it too painful for you to eat.
    Anesthetic mouth lozenges. These can help control pain of mild to moderate mouth sores.
    Therapeutic plasmapheresis. In this process, the fluid part of your blood, called plasma, is removed from blood cells by a device known as a cell separator. The purpose is to get rid of the antibodies that are attacking your skin. The plasma is replaced with donated plasma or intravenous fluids.
  12. tarjan.

    tarjan. Guest

    43) WHICH ANTIBODY HAS BEST4 CELIAC DISEASE (SENSITIVE &SPECIFIC)?

    *ANTI ENDOMYSIAL AB


    Tissue Transglutaminase antibodies (to the endomysial antigen) are a new alternative test to compliment the Endomysial antibody test.

    Coeliac Disease (CD):

    Coeliac Disease (CD) is a chronic life-long inflammatory disease of the small bowel intestinal lining and may even affect as much as 1% of the UK child population according to the British Medical Journal. It is triggered by a delayed allergic reaction to a protein called gluten in the normal diet. Gluten is a protein found mainly in Wheat and to a lesser extent in Rye and Barley. Hence the alternative name for the condition of Gluten-sensitive Enteropathy. People with stable Coeliac Disease will tolerate Oats in the diet.

    Coeliac Disease (CD) is an inherited disease of the intestinal immune system and affects both men and women. It is highly prevalent in the United Kingdom, affecting 1 in 300 or more people but can be quite difficult to reliably detect. Most CD is finally diagnosed in adulthood usually in the 30-45 year age group. As a result, many cases go undiscovered and are often falsely diagnosed as Irritable Bowel Syndrome (IBS). In fact only about one third of cases are ever diagnosed as CD and appropriately treated with a gluten-free diet. Untreated CD is associated with long-term health risks such as osteoporosis, anaemia and gastrointestinal malignancy.

    Samuel Gee first described the condition in 1888. The classical symptoms are malabsorption of food and chronic diarrhoea associated with anaemia, rickets, failure to grow, abdominal bloating, offensive bulky stools, a blistering rash on the buttocks and mouth ulcers. Small children usually become symptomatic when they are weaned off milk onto solids. They present with weight loss, refusal to feed, irritability, abdominal swelling and diarrhoea. However in adults, the disease often presents in an atypical form and may be missed – especially with non-specific symptoms such as fatigue, mouth ulcers, skin rashes, vague abdominal pains, intermittent diarrhoea and chronic anaemia.

    A rash called Dermatitis Herpetiformis may occur rarely in Coeliac Disease. It is an intensely itchy rash with symmetrical fine blisters which typically appear on the back, elbows or scalp, almost all people with Dermatitis Herpetiformis have Coeliac Disease.

    Certain groups of people are at greater risk for developing Coeliac Disease. It is commoner in individuals from families that already have the condition (being linked to the HLA DQ3 gene). Coeliac Disease is more likely to occur in people with Diabetes on Insulin, Downs Syndrome, Sarcoidosis, Infertility, IgA antibody deficiency and certain autoimmune diseases such as Thyroid disease, Rheumatoid Arthritis, Chronic active Hepatitis, Addisons disease and Sjorgens syndrome of dry eyes and mouth.

    How is Coeliac Disease diagnosed?

    A recently developed blood test has revolutionised the diagnosis of Coeliac Disease. Up until this point, CD could only be detected after years of severe symptoms and an intestinal biopsy. This resulted in milder cases of Coeliac Disease remaining undiagnosed or being misdiagnosed. The Coeliac Screening blood test measures antibodies in the blood to Gluten or Gliaden in the diet and the damaged Endomysial muscle of the bowel. The Anti-Gliaden (AGA) Antibodies disappear on a Gluten-free diet and are a good indicator of Gluten avoidance and disease resolution. The Endomysial (EMA) Antibodies persist in all people with untreated and treated Coeliac Disease and this is an excellent screening test. These tests are however not 100% accurate in diagnosing CD. 2% of sufferers with IgA deficiency will have a negative EMA test while some people with a positive EMA test may have no CD symptoms at all. Tissue Transglutaminase antibodies (to the endomysial antigen) are a new alternative test to compliment the Endomysial antibody test.

    We do therefore recommend that people with a positive EMA screening test still have an intestinal biopsy to confirm the presence of CD before embarking on a lifelong diet of wheat and gluten avoidance. The intestinal biopsy can now readily be done at the time of oesophago-gastrointestinal endoscopy (OGD). The small intestinal biopsy must be done after a wheat-based diet for accurate diagnosis. A biopsy specimen taken on a wheat-free diet might show a completely normal intestinal lining. Anti-Reticulin (ARA) Antibodies may also be measured in CD but most UK Pathology laboratories tend to test for the Anti-Gliaden IgA and the Anti-Endomysial (EMA) antibodies.

    Complications of Coeliac Disease

    Coeliac sufferers absorb fewer nutrients from their diet and so may develop nutritional deficiencies. 50% will develop osteoporosis or fractures from calcium deficiency. There is a two-fold increased risk of cancers of the mouth, throat and gullet as well as intestinal lymphomas and carcinomas. They develop chronic anaemia due to not absorbing iron and folic acid from the damaged bowel. There is a strong link with insulin dependant Diabetes through the HLA DR3 gene. People with Downs Syndrome have a 43 times greater chance of developing Coeliac Disease but will often develop a milder form of the disease.

    Treatment of Coeliac Disease

    The only effective treatment of CD is strict lifelong complete avoidance of Gluten found in cereals such as Wheat, Rye and Barley (many tolerate Oats). It is completely safe to eat Maize, Corn or Rice. The Coeliac Society of Great Britain is a wonderful support-organisation that provides extensive information on gluten-free diets and foods. Gluten-free flour may be prescribed on the NHS. Unfortunately, CD patients are not entitled to free prescriptions. With the increased potential for developing osteoporosis, sufferers should be closely monitored and all menopausal women and men over 55 years of age who suffer with CD should have bone density (DEXA) scanning.

    Final Comment

    Coeliac Disease is significantly under-diagnosed in the UK and most cases are detected later in their 40’s due to the ill-defined symptoms that occur. The EMA screening test is an important development and all patients with vague intestinal symptomatology. Particularly patients with unexplained diarrhoea, anaemia, mouth ulcers, rashes and chronic fatigue should be tested as well as those with associated diabetes, thyroid disease, Downs syndrome and osteoporosis.
  13. tarjan.

    tarjan. Guest

    Zollinger-Ellison Syndrome

    45)A Q ON ZES--WHICH IS NOT TRUE ONE OF THE OPTION READ--REDUCED BAO:MAO WHICH S D ANS.

    Zollinger-Ellison Syndrome:

    BAO/MAO ratio >0.6 is highly suggestive of ZES, but a ratio <0.6 does not exclude the diagnosis.

    Zollinger-Ellison syndrome (ZES) is caused by a non–beta islet cell, gastrinsecreting tumor of the pancreas that stimulates the acid-secreting cells of the stomach to maximal activity, with consequent gastrointestinal mucosal ulceration.

    ZES may occur sporadically or as part of an autosomal dominant familial syndrome called multiple endocrine neoplasia type 1 (MEN 1). The primary tumor is usually located in the duodenum, the pancreas, and abdominal lymph nodes,
    but ectopic locations have also been described (eg, heart, ovary, gall bladder, liver, kidney).

    Pathophysiology:

    The symptoms of ZES are secondary to hypergastrinemia, which causes hypertrophy of the gastric mucosa, leading to increased numbers of parietal cells and increased maximal acid output. Gastrin by itself also stimulates acid secretion, resulting in increased basal acid secretion. The large quantity of acid produced leads to gastrointestinal mucosal ulceration. It also leads to diarrhea and malabsorption. Malabsorption in ZES usually is multifactorial, being caused by direct mucosal damage by acid, inactivation of pancreatic enzymes, and precipitation of bile salts. ZES is sporadic in 75% of patients, while in the other 25% it is associated with MEN 1, an autosomal dominant condition characterized by hyperparathyroidism, pancreatic endocrine tumors, and pituitary tumors.

    CLINICAL History:

    • Abdominal pain is the most common symptom, present in 75% of patients. Typically, it is located in the upper abdomen and mimics that of peptic
    ulcer disease. This symptom is reported more frequently by men and patients with the sporadic form of ZES.

    • Of patients with ZES, 73% have diarrhea, and this is the most common symptom in patients who have MEN 1/ZES and in female patients.

    • The combination of diarrhea and abdominal pain is present in more than half the patients.
    • Heartburn is the third most common symptom, and this symptom mimics gastroesophageal reflux disease (GERD).

    • Other symptoms include nausea, vomiting, gastrointestinal bleeding, and weight loss. Gastrointestinal bleeding frequently is due to ulceration in the duodenum and is the presenting symptom in 25% of patients.

    • In patients in whom MEN 1/ZES is suspected, a history indicative of nephrolithiasis, hypercalcemia, and pituitary disorders should be sought. A family history of nephrolithiasis, hyperparathyroidism, and gastrinoma also may be present.


    Causes

    • ZES is caused by a non–beta islet cell, gastrin-secreting tumor of the pancreas that stimulates the acid-secreting cells of the stomach to maximal activity, with consequent gastrointestinal mucosal ulceration.
    • ZES may occur sporadically or as part of MEN 1.


    TREATMENT
    Medical Care
    • The goals of treatment are medical control of gastric acid hypersecretion
    and surgical resection of the tumor.
    •
    If the patient is acutely ill, immediate control of gastric acid ypersecretion can be achieved with intravenous proton pump inhibitors. Previously, this was accomplished with histamine 2 (H2) receptor blockers. Intravenous pantoprazole was approved recently by the US Food and Drug Administration. Proton pump inhibitors are superior to H2 blockers for the control of gastric acid hypersecretion.

    o Patients who are candidates for surgical resection should be referred for resection of the tumor.
    o For patients with metastatic disease, chemotherapy, interferon, and octreotide may be helpful. The response to these agents in most studies has been low. Liver transplantation for hepatic metastasis also has been reported. For patients with a single confined liver metastatic lesion, surgical resection may be attempted.

    Surgical Care:

    • All patients with sporadic ZES without hepatic metastases or medical
    contraindications to surgery are advised to undergo surgical resection of the tumor because this decreases the risk of developing liver metastases,
    which can decrease the survival of these patients.

    • The role and timing of surgical resection in patients with MEN 1 is less clear. An attempt at surgical resection has been recommended if the tumor is larger than 2.5 cm. Cure is rarely achieved by surgical resection
    in patients with MEN 1; however, it may reduce the risk of subsequent metastatic disease.

    • Because this is a rare tumor, surgical resection should be attempted only


    -MEDICATION:

    Drugs:
    Omeprazole (Prilosec)
    Lansoprazole (Prevacid)
    Pantoprazole (Protonix)
    Esomeprazole magnesium (Nexium)
  14. quit.

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    49)DRUG USED4TREMORS IN HYPERTHYROIDISM?

    --PROPRANOLOL

    Tremor Overview:

    Tremors are a type of involuntary shaking movement. Involuntary means you shake without trying to do so.

    See also:

    1. Drug-induced tremor
    2. Essential tremor
    3. Familial tremor
    4. Hand tremor

    Causes:

    Tremors are caused by problems with the nerves supplying certain muscles. They may affect the whole body or just certain areas, as with hand tremor.

    Types of tremors include:

    Drug-induced tremor (tremors caused by certain drugs)

    Essential tremor (no known cause)

    Familial tremor (runs in families)


    Other causes of tremors may include:

    Alcohol withdrawal
    Cigarette smoking
    Hyperthyroidism
    Parkinson's disease
    Pheochromocytoma
    Too much caffeine
    Use of certain medications
    Wilson's disease

    All people have some tremor when they move their hands. Stress, fatigue, anger, fear, caffeine, and cigarettes may temporarily worsen this type of tremor.

    Symptoms;

    Tremors may affect the hands, arms, head, eyelids, voice box, or other muscles. They rarely affect the legs or feet.

    The shaking usually involves small, rapid movements -- more than 5 times a second.

    The tremors may:

    Occur when you move (action-related tremor), and may be less noticeable with rest Come and go, but generally get worse as you age Disappear with sleep Get worse with stress, caffeine, and certain medications Not affect both sides of the body the same way Head nodding may be a symptom of a tremor.

    If the tremor affects the voice box, you may have a shaking or quivering sound to your voice.

    Exams and Tests:

    Your doctor can make the diagnosis by performing a physical exam and asking questions about your medical and personal history.

    A physical exam will show shaking with movement. There are usually no other problems with coordination or changes in thinking or brain function.

    The quality of the tremor is often the most helpful thing in determining the cause.
    What parts of the body are affected?
    Does it happen at rest, when moving or both?
    How fast, and how obvious is it?

    Further tests may be needed to rule out other reasons for the tremors. Blood tests and imaging studies (such as a CT scan of the head, brain MRI, and x-rays) are usually normal.

    Treatment:

    Treament may not be necessary unless the tremors interfere with your daily activities or cause embarrassment.

    Treatment depends on the cause. Tremors caused by an medical condition such as hyperthyroidism will likely get better when the condition is treated.

    If the tremors are caused by certain medicine, stopping the drug usually helps them go away. Never stop taking any medicine without first talking to your doctor. See: Drug-induced tremor

    Medicines may help relieve symptoms. How well medicines work depend on the individual patient.

    Two medications used to treat tremors include:

    Propranolol, a drug that blocks the action of stimulating substances called neurotransmitters, particularly those related to adrenaline
    Primidone, an antiseizure drug that also control the function of some neurotransmitters
    The drugs can have significant side effects.

    Side effects of propranolol include:

    Fatigue
    Nose stuffiness
    Shortness of breath (people with asthma should not use this drug)
    Slow heart beat
    Side effects of primidone include:

    Drowsiness
    Difficulty concentrating
    Nausea
    Problems with walking, balance, and coordination
    Other medications that may reduce tremors include:

    Antiseizure drugs such as gabapentin and topiramate

    Mild tranquilizers such as alprazolam or clonazepam.

    Blood pressure drugs called calcium-channel blockers such as flunarizine and nimodipine.
    Botox injections, given in the hand, have been used to reduce tremors by weakening local muscles.

    In severe cases, surgery to implant a stimulating device in the brain may be an option.

    Possible Complications:

    Severe tremors can interfere with daily activities, especially fine motor skills (such as writing). If the tremor affects the voice box, speech problems can occur.


    Prevention:

    Stress and caffeine can make tremors worse. Avoid caffeinated drinks such as coffee, tea, and soda, and other stimulants. Exercise and counseling to reduce emotional stress may also help.

    Alcoholic beverages in small quantities may decrease tremors but can lead to alcohol dependence and alcohol abuse, especially if you have a family history of such problems. How alcohol helps relieve tremors is unknown.
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    50)AN EASY Q--WHICH CAUSES HYPOCALCEMIA? ANS WAS CALCITONIN.


    Hypocalcemia: -->Synonyms and related keywords: hypocalcemia, low calcium, low ionized calcium

    Hypocalcemia is defined as a total serum calcium concentration of:

    1. less than 2.1 mmol/L (8.5 mg/dL) in children,
    2. less than 2 mmol/L (8 mg/dL) in term neonates, and
    3. less than 1.75 mmol/L (7 mg/dL) in preterm neonates.

    Although total serum calcium levels are often measured and reported, ionized calcium is the active and physiologically important component.

    Total calcium level includes both the ionized fraction and the bound fraction. The ionized calcium level is affected by the albumin level, blood pH, serum phosphate, serum magnesium, and serum bicarbonate, and it may be reduced by exogenous factors that may bind calcium, such as citrate from transfused blood or free fatty acids from total parenteral nutrition (TPN). At a physiologic pH of 7.4, 40% of total calcium is bound to albumin; 10% is complexed with bicarbonate, phosphate, or citrate; and the remaining 50% is free ionized calcium. The normal range for ionized calcium is 1-1.25 mmol/L (4-5 mg/dL).


    The concentration of calcium in the serum is critical to many important biologic functions, including the following:

    • Calcium messenger system by which extracellular messengers regulate cell function

    • Activation of several cellular enzyme cascades

    • Smooth muscle and myocardial contraction

    • Nerve impulse conduction

    • Secretory activity of exocrine glands


    Causes:

    Overall, one of the most common causes of hypocalcemia is renal failure, which results in hypocalcemia because of inadequate 1-hydroxylation of 25-hydroxyvitamin D and hyperphosphatemia due to diminished glomerular filtration.

    Although hypocalcemia is most commonly observed among neonates, it is frequently reported in older children and adolescents, especially in PICU settings.

    MEDICATION:

    Drugs:

    1. Calcium, intravenous
    2. Calcium glubionate (Neo-Calglucon)
    3. Calcium carbonate (Oystercal, Caltrate, Tums, Os-Cal)
    4. Calcitriol (Rocaltrol)
    5. Dihydrotachysterol (DHT, Hytakerol)


    Prognosis:

    • Most cases of early neonatal hypocalcemia resolve within 48-72 hours without any clinically significant sequelae.
    • Late neonatal hypocalcemia secondary to exogenous phosphate load and magnesium deficiency also responds well to phosphate restriction and magnesium repletion.
    • When caused by hypoparathyroidism, hypocalcemia requires continued therapy with vitamin D metabolites and calcium salts. The period of therapy depends on the nature of the hypoparathyroidism, which can be transient, last several weeks to months, or be permanent.


    --


    Medications and Toxins Causing Hypocalcemia

    There are many drugs associated with hypocalcemia, and one class may inhibit excessive bone resorption. These drugs include mithramycin (plicamycin), bisphosphonates, calcitonin, and oral or parental phosphate preparations.

    Hypocalcemia after administration of a bisphosphonate can be prolonged. Hypocalcemia and osteomalacia have been described with prolonged therapy with anticonvulsants such as diphenolhydantoin (phenytoin) or phenobarbital. Hypocalcemia has also been found in patients undergoing pheresis and plasmapheresis with citrated blood.

    Radiographic contrast dyes may contain the calcium chelator, ethylenediaminetetra-acetic acid (EDTA), resulting in low serum calciums.

    Gadolinium administration for MRI imaging causes a transient hypocalcemia. Fluid overdoses during dialysis, over-fluorinated public water supplies, and ingestion of fluoride-containing cleaning agents have all been associated with low serum calcium levels. In this case, the hypocalcemia is thought to be due to excessive rates of skeletal mineralization secondary to formation of calcium difluoride complex.

    Chemotherapeutic agents such as the combined use of 5-fluorouracil and leucovorin, may result in mild hypocalcemia. The hypomagnesemia caused by cisplatinum can induce hypocalcemia.

    AIDS patients that are treated with the drug phosphocarnate (trisodium phosphonoformate) have been reported to have hypocalcemia. It is unclear whether this is due to chelation or complexing of calcium in the extracellular fluid.

    During surgical procedures, hypocalcemia has been recognized to occur in the absence of citrated blood infusions 18 and was associated with physiologic increases in serum PTH levels. It is thought that surgery-associated hypocalcemia was due to acute hemodilution by physiological saline. Symptoms are variable in this setting. Hypoparathyroidism is also associated with transfusion-dependent patients with beta-thalassemia.
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    12)after injury to one eye other aslo worsen glucoma cat. sym. opthalmia ?

    ANS: SYMPATHETIC OPHTHALMIA

    DESCRIPTION: A rare, bilateral granulomatous uveitis, associated with either a perforating eye injury in the region of the ciliary body or a retained foreign body in the eye. The exact cause is unknown, but it is believed to be related to sensitivity (i.e., a reaction) to uveal pigment.

    It has been known to follow uncomplicated intraocular surgery for cataracts or glaucoma. The injured eye becomes inflamed first, and the other eye follows (i.e., "sympathetically"). Symptoms include photophobia, redness, and blurred vision; in some cases, there are also "floaters" and possibly pain. The history of trauma differentiates this condition from other types of granulomatous uveitis; other differentiating factors include its bilateral, diffuse, and acute nature.


    Sympathetic ophthalmia (SO) is an inflammatory condition that affects both eyes. SO occurs after a penetrating injury to one eye. With rare exceptions, the injury involves a penetrating wound resulting from trauma or surgery. The injured eye is termed the "exciting" eye and the non-injured eye is referred to the "sympathizing" eye.


    History
    Sympathetic ophthalmia was known to Hippocrates over 2000 years ago. The first written reference to sympathetic ophthalmia appeared about 1000 A.D. stating that "[t]he right eye, when diseased, often gives suffering to the left." In the 16th century, Bartisch wrote in his textbook of Ophthalmology that after injury in one eye, "the other good eye is in great danger." The term sympathetic ophthalmia was coined by William MacKenzie in 1840. He presented 6 cases of penetrating wounds in one eye with development of inflammation in the other eye within three weeks to one year. In 1905, Ernest Fuchs described the classical microscopic findings in SO. Since then the disease has became well recognized in Ophthalmology .



    Course of Disease
    SO is manifested by a gradual onset with a progressive course marked by frequent periods of worsening. The time between the injury in the "exciting" eye and the onset of SO ranges from 5 days to 66 years. Approximately two-thirds of SO cases occur within the period of two weeks to two months following injury, with 90% occurring within the first year. Usually patients notice blurry vision and pain in both eyes without other symptoms outside the eyes. Eye examination usually shows red and painful eyes with a swollen middle layer of the eye (uvea).



    Diagnosis and Testing:
    There are no tests that can tell an eye doctor without a doubt that a patient has SO. However, a history of eye injury or surgery combined with the finding of inflammation in both eyes raises SO as a possible diagnosis. The eye doctor will obtain a complete history and perform a careful examination of the eyes, including tests of vision, eye pressure, and inflammation in the eye, using special instruments which magnify the dilated eyes under bright light.

    Special testing such as fluorescein angiograms, indocyanine green angiography, or ultrasound may be performed. The eye doctor will likely obtain blood tests and a chest X-ray to ensure that other diseases which may look similar to SO are not present. Some of these include Vogt-Koyanagi-Harada disease, sarcoidosis, intraocular lymphoma, and the white dot syndromes (please see the separate monographs on these topics).



    Treatment
    The main treatment for SO is aggressive anti-inflammatory administration. Corticosteroids are the most common agent used initially. Prompt and adequate dosage is required to achieve control. Some patients may require admission to the hospital to receive medications through their veins. SO can be a difficult disease to treat and may require additional therapy, including the use of more than one immunosuppressive medication.



    Cause of Condition
    While the cause of SO is not yet completely understood, most scientists believe that the disease is caused by an attack mounted by the patient's own immune system against certain parts of the eye tissue, possibly the uvea and/or retina. Some scientists think that certain germs or microorganisms may play a role in the cause of SO
  17. quit.

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    4-extra capsular cataract surgery-parts of lens which are excised?

    The center (nucleus) of the lens.

    Extracapsular cataract extraction:

    This procedure requires a larger incision, about 2/10 inch (10 mm), where the cornea and sclera meet. Through this incision your surgeon opens the lens capsule, removes the center (nucleus) of the lens in one piece and vacuums out the softer outer lens, leaving the capsule in place.
  18. quit.

    quit. Guest

    5- SAFE strategy for trachoma-S stands for?


    What is the SAFE strategy?

    In its effort to eliminate blinding trachoma, the World Health Organization developed a series of interventions to control trachoma known by the acronym SAFE: Surgery, Antibiotics, Facial cleanliness, and Environmental improvement.

    S – Lid surgery for those at immediate risk of blindness
    A – Antibiotics to treat individual cases and to reduce infection in a community
    F – Facial cleanliness and hygiene promotion to reduce transmission
    E – Environmental improvements such as provision of water and household sanitation


    ---

    S - Surgery

    Surgery reverses the in-turned eyelashes of people with severe trachoma. Lid surgery is a fairly simple procedure that can be offered in the community or at health centers. Offering community-based surgery is the best way to encourage people suffering with trichiasis to seek help. Lid surgery takes away the pain of lashes scraping against the eyes and prevents further damage, but does not restore sight that was already lost.



    A - Antibiotics

    Antibiotics are used to treat active trachoma and reduce infection in a community. Antibiotics may be given on a case-by-case basis or in mass drug administration to the community. The World Health Organization currently recommends mass drug administration if the prevalence of active trachoma among children aged 1 to 9 years exceeds 10 percent. Pfizer Inc. generously donates millions of doses of the antibiotic Zithromax ® for trachoma control.



    F - Facial cleanliness

    Dirty faces are associated with active trachoma. Children with dirty faces are more likely to transmit trachoma if they have an active infection or to get trachoma if they are not infected. Discharge from the eyes and nose attracts flies that can bring the infection or carry it to other people. Wiping or rubbing dirty eyes with cloths, bed sheets, or a mother's shawl can contribute to the transmission of trachoma. With support from the Carter Center Trachoma Control Program, communities are educated on the importance of clean faces.



    E - Environmental improvement

    Trachoma persists where people live in poverty with crowded living conditions and without water, sanitation, and proper waste disposal. Transmission of trachoma occurs where these conditions exist and should be expected to return after antibiotic treatment if the conditions are not changed. Improvements like construction of household pit latrines and hand-dug wells will bring about sustainable elimination of trachoma.
  19. farha.

    farha. Guest

    27. The calories required by one year old child?

    ANS: 900 kcal for 1 Year child


    Daily Estimated Calories and Recommended Servings for Grains, Fruits, Vegetables, and Milk/Dairy by Age and Gender

    Years 1 : Calories† 900 kcal

    years 2 - 3: Calories† 1000 kcal

    Years 4 - 8: Calories†:
    Female ---->1200 kcal ----Male ---->1400 kcal

    Years 9 - 13: Calories†:
    Female ----->1600 kcal ----Male --------->1800 kcal

    Years 14 - 18: Calories†:
    Female ----->1800 kcal ----Male ------>2200 kcal
  20. farha.

    farha. Guest

    28. Sunray sign on xray seen in-?
    ANS: osteosarcoma

    Osteosarcoma

    Primary tumour arising from bone and producing bone with variants depending on the appearance of the prominent cell type (may look like a fibrosarcoma, chondrosarcoma or myxosarcoma)


    X-Rays

    Variable with combination of bone destruction and bone formation
    Sun ray spicules and Codmans triangle may be evident
    Cortical breach common
    Adjacent soft tissue mass
    Joint space rarely involved
    25% Lytic
    35% Sclerotic
    40% Mixed
  21. farha.

    farha. Guest

    29. Tardy ulnar palsy seen in-?

    Cubital Tunnel Syndrome

    The most common location: Elbow region

    The ulnar nerve is a branch of the bundle of nerves that start in the neck and come down the arms. It's located on the inside of the elbow. It supplies messages to muscles in the forearm and hand. The ulnar nerve also provides sensation over the fourth and fifth fingers of the hand, palm, and the back of the forearm.

    C8 and T1 nerve roots give rise to the medial cord which in turn, forms the ulnar nerve.


    The ulnar nerve can get trapped inside the soft tissue around it. The most common site of entrapment is in the elbow. The result is a condition called tardy ulnar palsy. This problem was first described in 1878.

    Tardy refers to the fact that the problem is delayed. It doesn't happen until thickening or scarring of the tunnel around the ulnar nerve closes down on the nerve.


    Ulnar nerve is very vulnerable to damage at the level of elbow. While passing through the cubital tunnel it is liable to compression producing an entrapment neuropathy called as Cubital Tunnel Syndrome.

    Thus, there is tardy ulnar nerve palsy when there are variations in the musculo-fascial structures in the cubital tunnel. Ulnar nerve undergoes considerable proximo-distal excursion with the movements at the elbow joint and pressure by fibrous bands at the origin of flexor carpi ulnaris, prolonged flexion of elbow, encroachment of neighbouring muscles in the tunnel; shallow ulnar groove, etc. can produce this condition.

    Fifty upper limbs from 25 cadavers were carefully dissected to study the Anatomy of cubital tunnel. The groove on the posterior surface of medial epicondyle was deep in 90% cases. A broad transverse ligament was found roofing the tunnel in 66%. An arcuate ligament in the origin of flexor carpi ulnaris was found in 18% Epitrochlearis anconeus muscle was present in 16% and the floor of the tunnel was found to be encroached by an extension of medial head of triceps in 6% cases. Ulnar nerve shows a distinct thickening and flattening while it passes through the tunnel and in 30% limbs it is covered by a sleeve of fibrous sheath.


    Tardy ulnar nerve palsy can be tested by following methods :

    (a) Tinel’s Test –There is positive percussion test over the ulnar nerve at the level of medial epicondyle (Dobyns, 1983; Campbell, 1998)

    (b) Positive elbow flexion text : With the elbow fully flexed patient will complain of numbness and tingling in the little and ring fingers within one minute (Dobyns, 1983; Campbell, 1998).

    (c) Buchler and Thayer in 1988 described another method of testing in which the patient sits with both arms and shoulder in anatomical position. Then he is asked to flex fully both the elbow joints with the wrist joints maintained in full extension. The test is positive if any symptoms occur within 3 minutes. The symptoms are resolved by elbow extension
    (Joshi and Kotwal, 1999).

    Complete Anaesthesia in the area of middle and distal phalanges of little finger (Autonomous zone of the ulnar nerve) strongly suggests total division of this nerve (Campbell, 1998).
  22. farha.

    farha. Guest

    30. Rigor mortis is due to-?

    Definition of Rigor mortis

    Rigor mortis: Literally, the stiffness of death. The rigidity of a body after death. Rigor mortis is a good example of a Latin term (one in this case that was coined in the 19th century) remaining intact in contemporary medical usage (and crime writing).

    Rigor mortis is due to a biochemical change in the muscles that occurs several hours after death, though the time of its onset after death depends on the ambient temperature.

    The biochemical basis of rigor mortis is hydrolysis in muscle of ATP, the energy source required for movement. Without ATP, myosin molecules adhere to actin filaments and the muscles become rigid.


    What is rigor mortis?
    Rigor mortis refers to the state of a body after death, in which the muscles become stiff. It commences after around 3 hours, reaching maximum stiffness after 12 hours, and gradually dissipates until approximately 72 hours after death. Rigor mortis occurs due to changes in the Physiology of muscles when aerobic respiration ceases.

    Muscles are made up of two types of fibre. These fibres have connections between them that lock and unlock during muscle contraction and relaxation. These connections are controlled by a biochemical pathway within the cell, which is partially driven by the presence of calcium ions. The concentration of calcium ions is higher in the fluid surrounding muscle cells than it is inside the cells, so calcium tends to diffuse into the cell. High calcium levels inside the cell drive the biochemical pathway in the direction that maintains muscle contraction. To relax, muscle cells must expel the calcium ions from the cell and this requires energy molecules to pump them across the cell membrane.

    After a body has died, the chemical reaction producing these energy molecules is unable to proceed because of a lack of oxygen. The cells no longer have the energy to pump calcium out of the cell and so the calcium concentration rises, forcing the muscles to remain in a contracted state.

    This state of muscle stiffening is known as rigor mortis and it remains until the muscle proteins start to decompose.
  23. titan.

    titan. Guest

    8) punched out lesion in skull
    ewings sarcoma
    m.myeloma
    sec.
    oteosarcoma

    ANS: Multiple Myeloma

    Workup
    The workup of suspected multiple myeloma includes a skeletal survey. This is a series of X-rays of the skull, axial skeleton and proximal long bones.

    Myeloma activity sometimes appear as "lytic lesions" (with local disappearance of normal bone due to resorption), and on the skull X-ray as "punched-out lesions" (pepper pot skull).

    Magnetic resonance imaging (MRI) is more sensitive than simple X-ray in the detection of lytic lesions, and may supersede skeletal survey, especially when vertebral disease is suspected.

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