GLOMERULONEPHRTIS ACUTE AND CHRONIC.pptx

RENAL DISEASE

1. GLOMERULONEPHRITIS

2. GLOMERULONEPHRITIS Glomerulus N ‘ calyces Major calyces Renal pelvis Ureter kidney Cortex 6- ma capsule Glomerulonephritis Inflammation of the gtomeruti and of the small blood vessels fibrous capsule

3. 6n#ot9elial cell Basement membrane Fenestroteg engot#elium Reg blood cell Foot processes ipi| ego cess 3ubepilgelial immune complexes (“Pumps“) PMN Ieutoc/Ie Increased num ero Narrowed capillary lumen Fusion of foot processes Red oo cell

4. Com ,Pa0< Ó2O67 N ursing Educafion Consul7anŁs, Irc. AnSigan- Antibody Complex. F om Recent Stire lfifection Headache Facial / PeriorbiTa\ Edema — Letharąic — Low Graóe Fever — Weighc Gain (Edema) Protein oria Hemacuria Olią uria

5. Review of Anatomy & Physiology of Nephron The nephron is the anatomical and functional unit of kidney. There are about 1 million nephron’s in each kidney. The nephron consists of a tubule closed at one end & other end opening into a connecting tubule. The closed end indented to from a cup shaped glomerular capsule (Bowman’s capsule

6. It is almost encloses a network of arterial capillaries, the glomerulas continuing from the glomerular capsule the remainder of the nephron is about 3cm long. And it has 3 parts : - Proximal convoluted tubule - Loop of Henle’s -Distal convoluted tubule

7. The glomerulas has 3 types of membrane : The Endothelial. Basement Membrane. Epithelial Membrane.

8. These are the filtering membranes of the glomerulas. The nerve supply of the kidney consists of sympathetic & parasympathetic nerves. The presence of both autonomic nervous system controls the renal blood flow pressure.

9. FILTRATION: Filtration takes place through the membranes of the glomerulas. Water & other large number of molecules passes through, although some of reabsorbs later. Blood cells, plasma proteins & other large molecules are unable to filtrates through & remain in the capillaries.

10. The volume of filtrates formed by both kidneys is called glomerular filtration rate. The normal GFR is 125ml/min or 180lit/day. Most of the filtrate is reabsorbed about 1-1.5ml of fluid is excreted per minute as urine.

11. Types of glomerulonephritis Acute glomerulonephriti5 begin5 Suddenly OChronic glomerulonephriti5 - develop5 gradually over Several year5.

12. DEFINATION- Acute glomerular nephritis: It is the inflammation of the glomeruli of both kidneys caused by antigen- antibody reaction with respect to streptococci, which produces damage to the glomeruli, the filtrating bed of the kidney characterized by decrease in the GFR rate accumulation of organic salts, water & other nitrogenous wastes into the body.

13. CAUSES: There is initially URTI or skin infection, usually 1-3 weeks before the onset of symptoms. The most frequent & commonest causative organism is Group A beta hemolytic streptococci.

14. PATHOPHYSIOLOGY: The streptococcal infection from throat or elsewhere from body Attacks the immune system, the immune system produces antibodies against streptococcal antigen. Antigen- Antibody reaction takes place, with complex formation.

15. It gets trapped in the basement membrane of glomerulas the complexes combines with complement.(leucosomal enzyme) ● Destruction of cell occurs.

16. Inflammatory changes occurs in glomerulas. Decreased in the GFR & increased permeability of glomerular walls. Edema, proteinuria & microscopic Hematuria

17. ● CLINICAL MANIFESTATION: ● ● ● ● ● Fever & chills Weakness Generalized Edema Weight gain. headache - - - - G.I. disturbances Nausea/ vomiting. Anorexia Ascites Abdominal pain

18. Cardiac disturbances: - - Pulmonary edema CCF Ophthalmic disturbances: - Visual acuity is reduced

19. Renal disturbances: - - - - - Proteinuria Oliguria Hematuria HTN Decreased P H of urine

20. Diagnostic Evaluation: - Physical Assessment: Observation of the child. Observation of edema over face, periorbital area, over feet. Observation for oliguria, anuria & hematuria.

21. Observation of any visual impairment due to retinal edema. Monitor B.P for evidence of HTN. Observation of any respiratory infection.

22. Urine Analysis: It shows 1+ to 2+ protein. There are RBC, WBC cast which indicates inflammation of glomeruli. Blood Analysis: ESR is elevated. There is normocytic anemia due to heamodilution. The blood levels of urea creatinine is elevated. Serum Potassium and sodium is elevated if oliguria contenous.

23. ray shows prominent vascular markings due to hypervolemia. Throat swab culture which may show hemolytic streptococci organism. Increased antistreptolysin titre. Biopsy: Kidney biopsy. Serum complement level is decreased

24. Differential Diagnosis Hypersensitivity reaction. Hemolytic uremic syndrome. SLE. Nephrotic syndrome.

25. Complications Chronic glomerular nephritis. Left ventricular failure. Pulmonary edema. Renal failure. Encephalopathy.

26. Medical management Bed rest. Antibiotics. Antihypertensive. Diet. Restriction of fluid. Weight monitoring. Diuretics. Rx of prolonged oliguria.

27. Chronic glomerulonephritis It is an advanced irreversible impartment of renal function with or without symptoms. It may develop as a primary Glomerular disease or may occur secondary in SLE,drug induce nephropathy or polyarteritis.

28. ¥'4inimaI Change G fomerulonephritis Abno rmal Podocyres Seen on Electron f•1icroscopr Treat with Supportive care + Prednisolone Cost respond well ?'dembranous Glomerulonephritis /MGNj Thickened Glomerular Basement Membrane Usual\ idiopathic I/3 have chi onic NGN II8 go into remission I/3 progress to renal failure hocai Segmental Glomerulosclerosis Segments of Glomeruli Develop Sclerosis Present with Nephroric Syndrome Genecic causes identified Steroids often inePeccive 50a Progress o Renal Failure IgA ¥'gephropathy ! losc common type of GN in adults i•1acroscopic haemaruria Appear5 24-48hrs pose URTI/GI infection lgA deposiM seen in che matrix Vasculi¢ic Disorders f'4ernbranoproIiferative Glomerulonephritis *• a r ( i u n e m e diated) S e cond s r t ^ L E H , ep) Usually progresses to End Stage Renal Failure Rapidly Progressive Glomerulonephritis tCresce›\t›cj Po lyarlgi his S malvlessel vasculicis - ANCA •ve Treac with long cerm steroids */- cyocoxic agenLS Gran‹ lomaeo s is v :i culiris Lungs, Kidney A ocher organs ‹- ANCA +v.• Treat w‹th Steroids * Cyclophosphamide Post Infectious Glomerulonephritis Occurs weeks after URTI Usually Strep f‘yogenes Supportive treatmen Resolves over 2- 4 weeks G oodpa s tut'es Syndrome Autoimmune anci- GBi•1 ancibody G1omerulus A Lung aPecced Haemacuria & Haemopcysis Treac wich steroids +l- sceroid sparing agency

29. Etiological factors Repeated attacks of streptococci. SLE Drugs induced Nephropathy. Thickening of basement membrane. Glomerulo- sclerosis. Polyarteritis.

30. PATHOPHYSIOLOGY Due to etiological factors Diffuse thickening of glomerular basement membrane Glomerular sclerosis takes place

31. Deposition of immunoglobulin, complement & fibrin In late stage glomeruli become sclerosis with tubular, interstitial& vascular changes.

32. G o erulonephritis

33. Clinical manifestation The condition remains a symptomatic and may be diagnosed during accidental urine examination. The presenting features includes edema severe hypertension, hematuria, anemia, nocturia, bone pain, bone deformity, failure to thrive.

34. Diagnostic evaluation Urine Analysis: It shows 1+ to 2+ protein. There are RBC, WBC cast which indicates inflammation of glomeruli. Blood Analysis: ESR is elevated. There is normocytic anemia due to heamodilution. The blood levels of urea creatinine is elevated. Serum Potassium and sodium is elevated if oliguria contenous .

35. X- ray shows prominent vascular markings due to hypervolemia. Throat swab culture which may show hemolytic streptococci organism. Increased antistrptolysin titre. Biopsy: Kidney biopsy. Serum complement level is decreased

36. Management No specific treatment. Steroid & other immunosuppessrasive drugs are helpful. Antibiotics. Antihypertensive. Symptomatic & supportive treatment.

37. Nursing management. Providing care during hospitalization. Administration of medicines. Maintaining proper fluid balance & assessing edema.

38. Providing nutritious diet. Preventing infections. Emotional & psychological support. Education to family.

39. NURSING DIAGNOSIS Hematuria R/T dysfunction of glomeruli due to infection. Alteration in body temperature R/T infection. Activity intolerance R/T edema.

40. Fluid volume excess R/T glomerular dysfunction. Disturbed body image R/T physiological changes secondary to edema.

41. Impaired nutritional status less than body requirement. Risk of impaired skin integrity R/T edema.

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