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Transcript of Glomerulonephritis_2
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3/26/2015
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Glomerulonephritis & NephroticsyndromeNinuk DK
What is glomerulonephristis? Glomerulonephritis is
is a kidney conditionthat involves damage/inflammation to theglomeruli.
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Types of glomerulonephritis
Acute glomerulonephritis- begins suddenly
Chronic glomerulonephritis-develops gradually overseveral years.
Glomeruli Glomeruli The filters of the kidneys whichfilter the blood and make urine.
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EtiologyCauses of glomerulonephritis include: Streptococcal infection of the throat ( strep throat) or
skin ( impetigo) Hereditary diseases Immune diseases, such as lupus diabetes High blood pressure Vasculitis (inflammation of the blood vessels) Viruses ( HIV, hepatitis B virus, and hepatitis C virus) Endocarditis (infection of the valves of the heart)
Streptococcal infection of the throat( strep throat) or skin ( impetigo)
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Lupus
PATHOLOGY glomerulonephritis are triggered by immune-
mediated injury. The cellular immune response contributes to the
infiltration of glomeruli by circulating mononuclearinflammatory cells (lymphocytes and macrophages)and crescent formation in the absence of antibodydeposition.
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PATHOLOGY The humoral immune response leads to immune
deposit formation and complement activation inglomeruli.
Antibodies can be deposited within the glomeruluswhen circulating antibodies react with intrinsic orwith extrinsic antigens that have been trapped withinthe glomerulus.
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PATHOLOGY Injury usually occurs as a consequence of the
activation and release of a variety of inflammatorymediators.
Haemodynamic, and toxic stresses can also induceglomerular injury.
A few glomerular diseases are due to hereditarydefects resulting in deformity of the glomerularbasement membrane.
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Pathophisiology Acute Glomerulonephritis
Sign and symptoms
Kidney pain normally happens in the flankregion, which is just below the bottom of ribcage.
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Signs/Symptoms Most common symptoms: Hematuria (dark, brown, orrusty colored,) Foamy urine due toProteinuria Swelling of the face, eyes,ankle, feet, legs, abdomen High blood pressure(hypertension) Fatigue/SOB from anemia orkidney failure.
Signs/Symptoms Symptoms which may alsoappear include: Abdominal pain Cough Diarrhea Fever Joint aches Muscle aches Loss of appetite Shortness of breath
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Risk Factors History of cancer Blood or lymphatic disorders Exposure to hydrocarbon solvents Diabetes Infections
Strep infections Heart infections Viruses
Diagnosis Because symptoms develop gradually, thedisorder may be discovered when there is anabnormal urinalysis during a routine physicalor examination for unrelated disorders.
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Tests and Clinical Procedures Imaging tests:
Abdominal CT scan Abdominal ultrasound Chest x-ray Intravenous Pyelogram (IVP)
Urinalysis and other urine tests: Creatinine clearance Urine concentration test Urine specific gravity Total protein
Glomerulonephritis Nursing Care
Assessment: riwayat infeksi saluran nafasdan kulit, pembedahan, prosedur invasif,penyakit sistemik (SLE)
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Assessment
Kidney pain normally happens in the flankregion, which is just below the bottom of ribcage.
Assessment Most common symptoms: Hematuria (dark, brown, orrusty colored,) Foamy urine due toProteinuria Swelling of the face, eyes,ankle, feet, legs, abdomen High blood pressure(hypertension) Fatigue/SOB from anemia orkidney failure.
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Assessment Symptoms which may alsoappear include: Abdominal pain Cough Diarrhea Fever Joint aches Muscle aches Loss of appetite Shortness of breath
Physical assessment: Dispnea Ceackles/gallop Neck vein distention Elevated blood pressure
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Diagnosing, Planning, & Implementing Excess Fluid Volume Fatigue Risk for Infection Ineffective Role Performance
Intervention Managing infection Preventing complication Appropriate patients education
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Management of infection Anti biotic Stress personal hygiene
Prevent complications Fluid overload: diuretic, sodium + waterrestriction
Antihipertensive drugs Potassium and protein intake restriction Conserve energy: maintain restfullenvironment
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Pts edu Drugs Diet & fluid restriction Measure weight and BP daily Peritoneal dialysis: teach how to preventinfection and how to do it at home
Lifestyle Changes Restrict salt and water intake. Restrict intake of potassium,phosphorous, and magnesium.
Cut down on protein in the diet. Maintain a healthy weight through dietand exercise.
Take calcium supplements.
Patients education:
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Treatments Treatment varies depending the type andseverity of symptoms. High blood pressure may be difficult to control,and it is generally the most important aspect oftreatment. Medicines that may be prescribed include:
Blood pressure medications are often needed tocontrol high blood pressure. Medications that suppress the immune system mayalso be prescribed, depending on the cause of thecondition.
Therapeutic management Corticosteroids (prednisone) Dietary management Restriction of fluid intake Prevention of infections Monitoring for complications: infections,severe GI upset, ascites, or respiratory distress
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Physiotherapy treatment Patient education Endurance ExerciseWalking test walking, swimming, bicycling, aerobic dancingCirculatory exercise
Exerciseprogram duringdialysis
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Prognosis Glomerulonephritis may be a temporary andreversible condition, or it may get worse.Progressive glomerulonephritis may lead tochronic kidney failure and end-stage kidneydisease.
AGNTreatment and nursing care: Bed rest may be recommended during theacute phase of the disease
A record of daily weight is the most usefulmeans for assessing fluid balance
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Nursing care specific to the child with AGN Allow activities that do not expend energy Diet should not have any added salt Fluid restriction, if prescribed Monitor weights Education of the parents
Nursing diagnosis for the child withglomerulonephritis
Fluid volume excess r/t to decreased plasmafiltration
Activity intolerance r/t fatigue Altered patterns of urinary elimination r/tfluid retention and impaired filtration
Altered family process r/t child with chronicdisease, hospitalizations
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A case study Jung-Lin Chang is a 23-year-old graduatestudent in biology. He presents at theuniversity health center, brown and foamyurine. The physician there admits him to theinfirmary and orders a throat culture,ASOtiter,CBC,BUN, serum creatinine, andurinalysis.
Assessment Connie King, the nurse admitting Mr. Chang, notes that his history is essentiallynegative for past kidney or urinary problems. He relates having had a pretty badsore throat a couple of weeks before admission. However, it was during midterms,so he took a few antibiotics he had from a previous bout of strep throat, increasedhis fluids, and did not see a doctor. The sore throat resolved, and he felt well untilnoticing the change in his urine. He admits that his eyes seemed a little puffy, buthe thought this was due to lack of sleep and fatigue. He has eaten little the past 2days, but was not alarmed because his food intake is irregular most of the time.Physical assessment findings include: T 98.8 F (37.1 C) PO, P 98, R 18, and BP136/90. Weight 165 pounds (75 kg), up from his normal of 160 (72.5 kg). Moderateperiorbital edema and edema of hands and fingers noted. Throat culture isnegative, but the ASO titer is high. CBC essentially normal. BUN 42 mg/dL, serumcreatinine 2.1 mg/dL. Urinalysis reveals the presence of protein, red blood cells,and RBC casts.A subsequent 24-hour urine protein analysis shows 1025 mg ofprotein (normal 30 to 150 mg/24 hours). The physician diagnoses acutepoststreptococcal glomerulonephritis and places Mr. Chang on bed rest withbathroom privileges. He orders fluid restriction (1200 mL/day) and a restrictedsodium and protein diet.
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DIAGNOSISMs. King develops the following nursing diagnosesfor Mr. Chang: Excess fluid volume related to plasma proteindeficit and sodium and water retention Risk for imbalanced nutrition: Less than bodyrequirements related to anorexia Anxiety related to prescribed activity restriction Risk for ineffective therapeutic regimenmanagement related to lack of information aboutglomerulonephritis and treatment
EXPECTED OUTCOMES The expected outcomes are that Mr. Chang will: Maintain blood pressure within normal limits. Return to usual weight with no evidence of edema. Consume adequate calories following prescribed
dietary limitations. Verbalize reduced anxiety regarding ability to continue
studies. Demonstrate an understanding of acute
glomerulonephritis and prescribed treatment regimen.
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PLANNING AND IMPLEMENTATION Ms. King plans the following nursing interventions for Mr. Chang. Vital signs every 4 hours; notify physician of significant changes. Weigh daily; intake and output every 8 hours. Schedule fluids allowing 650 mL on day shift, 450 mL on evening shift, and100 mL on night shift. Arrange dietary consultation to plan a diet that includes preferred foods asallowed. Provide small meals with high-carbohydrate between-meal snacks. Encourage Mr. Chang to talk about his condition and its potential effects. Assist with problem solving and exploring options for maintaining studies. Enlist friends and family to listen and provide support. Teach Mr. Chang and his family about acute glomerulonephritis andprescribed treatment. Instruct in appropriate antibiotic use
EVALUATION Mr.Chang is released from the infirmary after 4days.He decides to return to his parentshome forthe 6 to 12 weeks of convalescence prescribed byhis doctor. Mr. Changs renal function graduallyreturns to normal with no further azotemia andminimal proteinuria after 4 months. He verbalizesunderstanding of the relationship between thestrep throat, his inappropriate use of antibiotics,and the glomerulonephritis. He says,I may notalways remember to take every pill on time in thefuture, but I sure wont save them for the nexttime again!
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Critical Thinking in the Nursing Process1. How did Mr. Changs use of a few previouslyprescribed antibiotics to treat his sore throataffect his risk for developing poststreptococcalglomerulonephritis?2. What additional risk factors did Mr. Chang havefor developing glomerulonephritis?3. The initial manifestations of acutepoststreptococcal glomerulonephritis andrapidly progressive glomerulonephritis are verysimilar. What diagnostic test would the physicianuse to make the differential diagnosis?
Nephrotic SyndromeChronic renal disorder in which the basement
membrane surfaces of the glomeruli areaffected, cause loss of protein in the urine.
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Nephrotic syndrome is a condition where thereis a change in renal function, which ischaracterized by: hypoproteinemia edema hyperlipidemia proteinuri ascites decrease in urine output
Etiology Primary renal parenchymal disease Acute post-streptococcal glomerulonephritis Idiopathic Glomerular Systemic Diseases DM, renal abnormalities that are characteristic of diabetes isdiabetic nephropathy Amyloidosis / associated with chronic diseases such astuberculosis, chronic osteomiliti, lung abscess, ulcerative colitisand neoplasms. SLE is known as lupus nephritis. SN is a clinical manifestation ofSLE Mechanical circulatory disorders Renal vein thrombosis The increase in renal venous pressure can lead to increasing thebasal membrane permeability resulting in leakage of plasma Right heart syndrome Proteinurin to congestive heart disease.
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Pathophysiology In nephrotic syndrome, type III hypersensitivity reaction occurs in which the immune
complex precipitated in the tissue. Activation of the complement system also stimulates vaksoaktive amines (including
histamine) and this substance causes retraction of endothelial cells thus increasingvascular permeability.
Changes in membrane glomerolus, causing increased permeability, allowing theproteins (especially albumin) out through the urine (proteinurine).
Decreased oncotic pressure causing albumin moves from intra vascular space intointerstitiel.
Transfer of proteins to the interstitial cavity causing lipoproteinemia. It stimulates the liver to compensate by increasing the production of lipoproteins and
increased concentrations of blood fats (hyperlipidemia). When the liver is not able to compensate for damage in fat and protein metabolism. Transfer of protein exit the vascular system, causing fluid to move into the space plasma
interstitisel resulting edema and hypovolemia. Decrease in vascular volume stimulates renin angiotensin system, which allows the
secretion of aldosterone and antidiuretic hormone (ADH). Aldosterone stimulates increased reabsorsi distal tubules of the sodium and water,
leading to increased edema.
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Contrast of normal gloumerular activity withchanges seen in Nephrotic Syndrome
Pathogenesis of Proteinuria:- Increase glomerular permeability for proteins due to loss of negative
charged glycoprotein
Degree of protineuria:- Mild less than 0.5g/m2/day Moderate 0.5 2g/m2/day Sever more than 2g/m2/day
Type of proteinuria:- A-Selective proteinuria: where proteins of low molecular weight .such as
albumin, are excreted more readily than protein of HMW B-Non selective : LMW+HMW are lost in urine
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pathogenesis of hypoalbuminemia
*Due to hyperproteinuria----- Loss of plasmaprotein in urine mainly the albumin.
*Increased catabolism of protein during acutephase.
pathogenesis of hyperlipidemia:-*Response to Hypoalbuminemia reex to liver -- synthesis of
generalize protein ( including lipoprotein ) and lipid in theliver ,the lipoprotein high molecular weight no loss in urine hyperlipidemia
*Diminished catabolism of lipoprotein
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pathogenesis of edema:- *Reduction plasma colloid osmotic
pressure secondary tohypoalbuminemia Edema and hypovolemia
*Intravascular volume antidiuretichormone (ADH ) and aldosterone(ALD) water and sodium retention Edema
*Intravascular volume glomerularfiltration rate
(GFR)water and sodium retentionEdema
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How many pathological typescauses nephrotic syndrome?
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Clinical Manifestation weight increased anorexia edema anasarca abdominal pain swelling of the face, especially around the eyes voleme urine decreased, sometimes colored thick andfoamy pale skin the child becomes irritable, tiredness / lethargy celulitis, pneumonia, peritonitis or sepsis azotemia blood pressure is usually normal / up slightly
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AssessmentFour most common characteristics:1. Massive proteinuria2. Hypoalbuminemia (K+ normal, BP normal)3. Edema usually starts in periorbital area and
dependent areas of the body and progresses togeneralized, massive edema. Pitting edema of 4+.Caused by hypo albumin which causes shift of fluidsto extracellular space. *There is an insidious weightgain- shoes don't fit, etc
4. Hyperlipidemia* Of note is that there is no
hematuria or hypertension
Focus Assessment Urinary System (oliguric, urine retention,proteinurin and urine discoloration).
Fluid and electrolyte balance (excess fluid,edema, ascites, weight gain, dehydration)
Circulation (increased blood pressure) Neurology (decreased level of consciousness dueto dehydration)
Breathing (shortness of breath, tachypnea) Mobility (redness, malaise)
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Other signs and symptomsFatigue
Anorexia
Weight gain
Abdominal pain from large amount of fluid in abdominal
Treatment of nephrotic syndrome Varies with degree of severity Treatment of the underlying cause Prognosis depends on the cause Children usually have the minimal changesyndrome which responds well to treatment
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Nursing Diagnosis Impaired Urinary Elimination related to Naand water retention.
Excess Fluid Volume related to edema Imbalanced Nutrition Less Than BodyRequirements related to damage proteinmetabolism
Ineffective Breathing Pattern related tosuppression of the diaphragm due to ascites