Scribd Logo
Upload

Welcome to Scribd!

  • 1 views

    Viral Meningitis

    Uploaded by

    victormatsvaire04
    11. A 31 year old man has an extreme thirst and marked polyuna over the duratio weeks. A 24-hour urine collection was recorded at 3.5 litres. His blood results following Haemoglobin 148 g/L (130-180) White cell count 7 * 10 ^ 9 / L 4-11) Platelets 280 * 10 ^ 9 / L 150-400) Sodium 146 mmol/L (135 * 145) Potassium 3.9 mmol/L (3.5 * 5) Creatinine 80 μποί/1 (70-150) eGFR > 90mL / m * in Random glucose 5.9 mmol/L What is the SINGLE most appropriate initial test? A. Urine osmolality B. Fluid de

    Copyright:

    © All Rights Reserved
    Download as DOCX, PDF, TXT or read online from Scribd

    Viral Meningitis

    Uploaded by

    victormatsvaire04
    1 views5 pages
    11. A 31 year old man has an extreme thirst and marked polyuna over the duratio weeks. A 24-hour urine collection was recorded at 3.5 litres. His blood results following Haemoglobin 148 g/L (130-180) White cell count 7 * 10 ^ 9 / L 4-11) Platelets 280 * 10 ^ 9 / L 150-400) Sodium 146 mmol/L (135 * 145) Potassium 3.9 mmol/L (3.5 * 5) Creatinine 80 μποί/1 (70-150) eGFR > 90mL / m * in Random glucose 5.9 mmol/L What is the SINGLE most appropriate initial test? A. Urine osmolality B. Fluid de

    Original Title

    viral meningitis

    Copyright

    © © All Rights Reserved

    Available Formats

    DOCX, PDF, TXT or read online from Scribd

    Did you find this document useful?

    Is this content inappropriate?

    11. A 31 year old man has an extreme thirst and marked polyuna over the duratio weeks. A 24-hour urine collection was recorded at 3.5 litres. His blood results following Haemoglobin 148 g/L (130-180) White cell count 7 * 10 ^ 9 / L 4-11) Platelets 280 * 10 ^ 9 / L 150-400) Sodium 146 mmol/L (135 * 145) Potassium 3.9 mmol/L (3.5 * 5) Creatinine 80 μποί/1 (70-150) eGFR > 90mL / m * in Random glucose 5.9 mmol/L What is the SINGLE most appropriate initial test? A. Urine osmolality B. Fluid de

    Copyright:

    © All Rights Reserved
    Download as DOCX, PDF, TXT or read online from Scribd
    Download as docx, pdf, or txt
    1 views5 pages

    Viral Meningitis

    Uploaded by

    victormatsvaire04
    11. A 31 year old man has an extreme thirst and marked polyuna over the duratio weeks. A 24-hour urine collection was recorded at 3.5 litres. His blood results following Haemoglobin 148 g/L (130-180) White cell count 7 * 10 ^ 9 / L 4-11) Platelets 280 * 10 ^ 9 / L 150-400) Sodium 146 mmol/L (135 * 145) Potassium 3.9 mmol/L (3.5 * 5) Creatinine 80 μποί/1 (70-150) eGFR > 90mL / m * in Random glucose 5.9 mmol/L What is the SINGLE most appropriate initial test? A. Urine osmolality B. Fluid de

    Copyright:

    © All Rights Reserved
    Download as DOCX, PDF, TXT or read online from Scribd
    Download as docx, pdf, or txt
    of 5

    A\\\\\\\\\\\\\\\\\\\`

    Pharmacy department

    Pathophysiology Group Assignment

    Group Members:

    Chabata Tafara B

    Chitabwa Auxillia

    Chiteka Nyasha

    Chiwara Memory

    Dzimwasha Rodney T

    Elias Stephen

    Gasseler Godman R

    Kutseza Rose M

    Lumumba Soneni

    Mageza Deon T
    QUESTION

    Describe the pathogenesis and manifestations of viral meningitis [25]

    SUGGESTED SOLUTION

    What is meningitis?

    Meningitis is an inflammation of the lining around the brain and spinal cord. Most cases
    of meningitis are probably caused by viruses.. Symptoms of viral meningitis include
    headache, dislike of bright lights, neck stiffness, fever and nausea/vomiting. Patients
    suffering from viral meningitis may also develop a rash or have muscle pain. People
    affected normally recover without medical treatment.

    Pathogenesis of viral meningitis

    The pathogenesis of each agent or family of viruses that causes viral meningitis varies.
    However, the occurrence of viral meningitis is an uncommon complication of common
    systemic infections. Viruses initially enter the host through the respiratory tract,
    gastrointestinal tract, urogenital tract, or breaks in the skin. Most viruses replicate near
    the entry site (primary replication) and gain access to the CNS by the more common
    haematogenous route or through neural pathways (peripheral nerves). After primary
    replication, the virus spreads to lymphatic tissue, where there may be amplification of the
    virus load, and then into the bloodstream, causing a “primary viremia.” The virus may
    enter the CNS during the primary viremia or, more likely, during a “secondary viremia,”
    after amplification at secondary sites such as muscle, skin, internal organs, and fat. The
    virus then enters the CNS across the choroid plexus or by infection of capillary
    endothelial cells. Some viruses (rabies, herpes simplex virus, varicella zoster virus, and
    poliovirus) can utilize the neural route entering the CNS through axonal transport from
    mucosa, muscle, or neuromuscular junctions. Viruses entering the CNS across the
    choroid plexus are more likely to cause viral meningitis, whereas the other pathways are
    more likely to be utilized by viruses causing encephalitis or myelitis.

    Once the virus reaches the choroid plexus, it usually replicates there, resulting in spread
    throughout the CSF, and allowing the virus to reach meningeal and ependymal cells.
    The virus apparently replicates in these cells, causing cell destruction and inciting
    inflammation. The inflammation consists primarily of mononuclear cells, with focal
    destruction of the ependymal lining, fibrotic basal leptomeninges, and inflammation of
    the choroid plexus. Occasionally, perivascular cuffing in superficial layers of the cortex is
    seen. Inflammation in deeper parts of the brain and neuronal necrosis are not seen. The
    combination of the meningeal and ependymal cell destruction and the subsequent
    inflammatory response apparently is responsible for the clinical manifestations of fever,
    neck stiffness, headache, and photophobia. In most cases (but not all), the immune
    system inflammatory response limits the amount of viral replication and the length of the
    viral meningitic syndrome.

    Clinical manifestations

    In most cases, the onset of the illness is sudden. In some cases, a prodromal "influenza-
    like illness" may occur for several days prior to the onset of CNS disease. The most
    common symptoms of viral meningitis are headache, fever, and neck stiffness, soreness,
    or pain. The headache is usually intense, and is frontal to retro-orbital in location. Less
    common manifestations include photophobia, malaise, myalgias, nausea, vomiting, sore
    throat, chills, and drowsiness.

    On physical examination, the patient does not look ill or toxic, as occurs with bacterial
    meningitis. The temperature ranges from 38°C to 40°C. Nuchal rigidity or neck stiffness
    is present in about 50% of patients at the onset of disease, and in a higher proportion
    during the course. Kernig and Brudzinski signs are found in the minority, and physical
    exam alone is insufficient to rule meningitis in or out. The classic clinical triad of fever,
    headache, and neck stiffness occurs in less than half of cases. Extraneural
    manifestations may provide clues to the underlying causative viral infection. The
    enteroviruses can cause diffuse rashes or more specific syndromes.The group A
    coxsackieviruses often cause hand-foot-and-mouth disease and herpangina, whereas
    the group B coxsackieviruses characteristically cause pleurodynia and myocarditis or
    pericarditis. Both coxsackieviruses and echoviruses can also cause conjunctivitis and
    myopathies. Parotitis occurs in about half of the patients with mumps meningitis.
    However, with viruses that less frequently cause viral meningitis, such as herpes simplex
    type 2 and arboviruses, there are usually no systemic manifestations.

    After the first few days of illness, the course is one of slowly progressive improvement.
    The duration may be several days to several weeks.

    Sharry ZEE………………………………………………………………………………………

    Graves' disease is an autoimmune disease is most frequently diagnosed form of


    hyperthyroidism, a condition characterized by overactivity in the thyroid. In Graves', the
    immune system attacks the thyroid gland,
    1 Reaction immediate, related to IGE production, Asthma
    IGE antibody
    2 Cytotoxic hypersensitivity caused antibody Mysthenia gravis Insulin
    mediated reaction IgG antibodies . killer cells INSULIN resistant diabetes
    rather than mast cells are involved and Pernicious anemia

    complement production increases


    3 Complex hypersensitivity circulating Lupus nephritis . systemic
    autoantibodies that are linked to targeted lupus
    antigens. Antigen and antibodies unite and form
    immune complexes which activate the
    complement system and cause local tissue
    damage. Antigen antibodies coplexed that are
    formed in the circulation may deposit in the blood
    vessels
    Delayed reaction eg delayed rush after Rheumatoid
    inoculation of tuberculin in tuberculosis skin test. T arthritis.Peripheral
    lymphocytes rather than antibodies function. t neuropathy Inflammatory
    lymphocytes produces lyphokines which stimulate bowel disease (Crohn's
    an influx of microphages to perform phargocytosis disease)Contact dermatitis

    You might also like