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    Acute Glomerulonephritis: By: Jhaziel E. Bermejo

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    Jhaziel Bermejo
    Acute glomerulonephritis is inflammation of the glomeruli in the kidneys that is typically caused by a streptococcal infection. It can cause nausea, vomiting, fatigue, headaches, and edema. Diagnosis involves urinalysis, blood tests, and a renal biopsy. Treatment consists of antibiotics, blood pressure medications, bed rest, and fluid intake. Patients require follow-up care including monitoring of urine and blood tests.

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    Acute Glomerulonephritis: By: Jhaziel E. Bermejo

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    Jhaziel Bermejo
    271 views20 pages
    Acute glomerulonephritis is inflammation of the glomeruli in the kidneys that is typically caused by a streptococcal infection. It can cause nausea, vomiting, fatigue, headaches, and edema. Diagnosis involves urinalysis, blood tests, and a renal biopsy. Treatment consists of antibiotics, blood pressure medications, bed rest, and fluid intake. Patients require follow-up care including monitoring of urine and blood tests.

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    Acute Glomerulonephritis

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    Acute glomerulonephritis is inflammation of the glomeruli in the kidneys that is typically caused by a streptococcal infection. It can cause nausea, vomiting, fatigue, headaches, and edema. Diagnosis involves urinalysis, blood tests, and a renal biopsy. Treatment consists of antibiotics, blood pressure medications, bed rest, and fluid intake. Patients require follow-up care including monitoring of urine and blood tests.

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    Attribution Non-Commercial (BY-NC)
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    271 views20 pages

    Acute Glomerulonephritis: By: Jhaziel E. Bermejo

    Uploaded by

    Jhaziel Bermejo
    Acute glomerulonephritis is inflammation of the glomeruli in the kidneys that is typically caused by a streptococcal infection. It can cause nausea, vomiting, fatigue, headaches, and edema. Diagnosis involves urinalysis, blood tests, and a renal biopsy. Treatment consists of antibiotics, blood pressure medications, bed rest, and fluid intake. Patients require follow-up care including monitoring of urine and blood tests.

    Copyright:

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    Download as PPT, PDF, TXT or read online from Scribd
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    of 20

    ACUTE

    GLOMERULONEPHRITIS
    By: Jhaziel E. Bermejo
    INTRODUCTION
    •DEFINITION
    •CAUSES

    •LABORATORY

    •MANIFESTATIONS
    DEFINITION
     Aka glomerular nephritis, (GN)
     is a renal disease characterized by inflammation of
    the glomeruli, or small blood vessels in the
    kidneys.
     refers to a specific set of renal diseases in which an
    immunologic mechanism triggers inflammation
    and proliferation of glomerular tissue that can
    result in damage to the basement membrane,
    mesangium, or capillary endothelium.
    CAUSES
    Post infectious etiologies
     Streptococcus species
     (i.e., group A, beta-hemolytic).
    Systemic causes

     Vasculitis (ie, Wegener granulomatosis causes


    glomerulonephritis that combines upper and lower
    granulomatous nephritides).
     Collagen vascular diseases (ie, systemic lupus
    erythematosus causes glomerulonephritis through
    renal deposition of immune complexes).
     Cryoglobulinemia causes abnormal quantities of
    cryoglobulin in plasma that result in repeated
    episodes of widespread purpura and cutaneous
    ulcerations upon crystallization.
     Polyarteritis nodosa causes nephritis from a
    vasculitis involving the renal arteries.
     Henoch-Schönlein purpura causes a generalized
    vasculitis resulting in glomerulonephritis.
     Goodpasture syndrome causes circulating
    antibodies to type IV collagen and often results in
    a rapidly progressive oliguric renal failure (weeks
    to months).
     Drug-induced (ie, gold, penicillamine)
    Renal diseases

     Idiopathic rapidly progressive glomerulonephritis


    is a form of glomerulonephritis characterized by
    the presence of glomerular crescents. Three types
    have been distinguished.
     Type I is an antiglomerular basement membrane
    disease,
     type II is mediated by immune complexes, and
     type III is identified by antineutrophil cytoplasmic
    antibody.
    Laboratory tests
     Antistreptolysin-O (ASO) Titer.
     Urinalysis.

     Renal Biopsy. Is the most confirmatory

    diagnostic procedure.
     Electrolytes, including BUN and creatinine (to

    estimate the glomerular filtration rate


    [GFR]): The BUN and creatinine levels
    will exhibit a degree of renal compromise.
     Complete blood cell count
     Streptozyme test
     Erythrocyte sedimentation ratio (ESR) usually is
    increased.
     Urine or plasma creatinine level greater than 40;
    decreased renin level is noted.
     Cultures of throat and skin lesions to rule out
    Streptococcus species may be obtained.
     Blood cultures
     Imaging Studies
     Radiography
     Echocardiography
     renal ultrasonography
     CT scan
    MANIFESTATIONS
     Nausea and vomiting  Hematuria
     fatigue and tiring  Hypertension
    easily,  Generalized edema
     headaches,  Proteinuria
     twitchy movements  Oliguria
     mental confusion and  Anorexia
    disorientation.
    PATHOPHYSIOLOGY
    Diagram presentation
    MANAGEMENT
    •Antibiotic and antihypertensive drugs
    •Follow up care

    •Patient teachings
    MANAGEMENT
     Antibiotics.
     Antihypertensive.
     Bed rest.
     Increase oral fluid intake.
    Antibiotic and antihypertensive drugs

    Antibiotics
     The Penicillin is the DOC in treating acute
    glomerulonephritis of a poststreptococcal group A
    beta-hemolytic etiology.
     
     Penicillin V (Veetids)
     Inhibits enzymes and cell wall receptors, resulting in
    cell wall synthesis inhibition. Other autolytics enzymes
    are also activated, degrading the bacterial cell wall.
     Nonselective beta-blocker with cardioselective
    alpha1 blocker
     Labetalol is used for hypertensive encephalopathy and
    malignant hypertension.
     
     Labetalol (Normodyne)
     Has nonselective beta-antagonist and cardioselective
    alpha1-antagonist effects. Beta-blocking effects
    predominate, particularly when used IV. Low lipid
    solubility means bioavailability is reduced by first pass
    metabolism and enhanced by coadministration of food.
    Drug is not removed by hemodialysis.
     Loop diuretics
     Loop diuretics are used for hypertensive encephalopathy
    with CNS signs and circulatory congestion or pulmonary
    edema. Furosemide is DOC for this indication.
     
     Furosemide (Lasix)
     Inhibits absorption of sodium and water in ascending limb
    of loop of Henle by interfering with Na+/K+/Cl- channel. An
    antihypercalcemic effect is mediated by an increased
    excretion of calcium.
     Corticosteroids
     Methylprednisolone is used for nonstreptococcal
    etiologies of acute glomerulonephritis, particularly in
    lupus nephritis and in idiopathic progressive
    glomerulonephritis.
     
     Methylprednisolone (Medrol)
     Has anti-inflammatory effect and is
    immunosuppressive. Metabolized by hepatic
    transformation and renal excretion.
    Follow-up
    Further Outpatient Care
     Urinalysis at 2, 4, and 6 weeks and at 4, 6, and 12

    months
     Cessation of follow-up care when urinalysis is

    normal
     Blood pressure monitoring during each visit

     Serum creatinine level monitoring at 2, 6, and 12

    months
     Serum complement usually normal by 6 weeks
    Patient Education
     Upon discharge from the ED, patient education should
    emphasize the importance of close follow-up care.
     Indicate that strenuous exercise should be avoided
    because exercise can induce proteinuria, hematuria,
    and cylindruria (renal cylinders or casts in the urine) in
    healthy individuals.
     Limit the patient to a diet with no added salt until
    edema, hypertension, and azotemia clear.
     Restrict fluids in patients with significant edema.
     Restrict protein in the presence of azotemia and
    metabolic acidosis (ie, approximately 0.5 g/kg/d).
     The patient should avoid high-potassium foods.

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