Understanding Nephrology: An In-Depth Look at Kidney Functions and Diseases

pwm olly indrajani n.w
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Explore the intricate world of nephrology, delving into the anatomy and functions of the kidneys, common diseases affecting them, and clinical approaches for diagnosis and treatment. Discover the diverse realm of renal pathology and clinical assessments for comprehensive care.

  • Nephrology
  • Kidney Functions
  • Renal Pathology
  • Clinical Approach
  • Diseases

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  1. PWM Olly Indrajani 12-6-2012

  2. Nephrologi Batasan: ilmu yg mempelajari fungsi dan patofisiologi ginjal dan saluran2 penunjangnya serta penyakit2nya. Dasar2 yg perlu: 1. Anatomi & histologi 2. Fisiologi & biokimia 3. Patologi & laborat. 2

  3. Introduction: 150gm: each kidney 1700 liters of blood filtered 180 L of G. filtrate 1.5 L of urine / day. Kidney is a retro-peritoneal organ Blood supply: Renal Artery & Vein One half of kidney is sufficient reserve kidney function: Filtration, Excretion, Secretion, Hormone synthesis.

  4. STRUCTURE OF THE KIDNEYS

  5. Kidney Anatomy:

  6. STRUCTURE OF THE KIDNEYS

  7. Kidney Anatomy:

  8. Introduction Functions of the kidney: excretion of waste products regulation of water/salt maintenance of acid/base balance secretion of hormones Diseases of the kidney glomeruli tubules interstitium vessels

  9. Renal Pathology Outline Glomerular diseases: Glomerulonephritis Tubular diseases: Acute tubular necrosis Interstitial diseases: Pyelonephritis Diseases involving blood vessels: Nephrosclerosis Cystic diseases Tumors

  10. Pendekatan klinis: Anamnesis Pemeriksaan fisik Laboratorium Pem. Penunjang: a. radiologis: - BOF b. biopsi ginjal. 1. 2. 3. 4. - IVP - CT Scan - MRI 11

  11. Anamnesis: 1. Keluhan utama: 2. Penyakit terdahulu 3. Anamnesa keluarga. a. dysuria,polyuri,polakisuri, b. edema c. nyeri d. penurunan fungsi ginjal e. hematuria 12

  12. Pemeriksaan fisik: inspeksi auskultasi perkusi palpasi 13

  13. Pem.laboratorium: 1.Urinalisis: - pH, BJ, warna - albumin - reduksi - bilirubin/urobilin - sedimen: eri,leko, kristal,silinder epitel. 2. Kimia darah: kreatinin plasma klirens kreatinin konsentrasi ureum plasma. 14

  14. Abnormal findings Azotemia: BUN, creatinine Uremia: azotemia + more problems Acute renal failure:oliguria Chronic renal failure:prolonged uremia

  15. Clinical Syndromes: Nephriticsyndrome. Oliguria, Haematuria, Proteinuria, Oedema. Nephroticsyndrome. Gross proteinuria, hyperlipidemia, Acuterenalfailure Oliguria, loss of Kidney function - within weeks Chronicrenalfailure. Over months and years - Uremia

  16. Nephrotic syndrome Nephritic syndrome Massive proteinuria Hypoalbuminemia Edema Hyperlipidemia/-uria Hematuria Oliguria Azotemia Hypertension

  17. What are the possible causes of this appearance of the kidneys?

  18. Glomerulopathy - Proses inflamasi glomerulus - Terjadi akibat berbagai sebab yg berbeda etiologi, patofisiologi ataupun patogenesanya - Dulu dikenal dg istilah glomerulonephritis - Peyebab utama Gagal Ginjal - Manifestasi klinis bisa tanpa gejala sampai gejala yang berat - Terpenting:menghambat progresifitas kerusakan 23

  19. Klasifikasi glomerulopathy Klasifikasi klinis Klasifikasi lesi histopatologi Klasifikasi berdasar etiologi&patogenesis Klasifikasi berdasar proses imunologi 1. 2. 3. 4. 24

  20. Klasifikasi klinis: Kelainan urine tanpa keluhan Sindroma nefrotik Sindroma nefritik akut Sindroma nefritik kronik Sindroma RPGN (Rapid Progressive Glomerulonephritis) 1. 2. 3. 4. 5. 25

  21. Klasifikasi lesi histopatologis Lesi minimal a. b. Lesi glomerulosklerosis fokal segmental c. Lesi mesangioproliferatif (IgM) d. Lesi mesangioproliferatif (IgA) (penyakit Berger) e. Lesi proliferatif akut f. Lesi membranoproliferatif g. Lesi membranosa h. Lesi bulan sabit (crescentic) i. Lesi glomerulosklerosis. 26

  22. Klasif. Etiologi& patogenesa a. Kelainan imunologi b. Kelainan metabolik: - nefropati diabettik - nefropati as. Urat - amiloidosis primer/sekunder c. Kelainan vaskuler d. Disseminated Intravascular Coagulopathy (DIC) e. Kel. Herediter: sindr.Alport, peny.Fabry f. Patogenesis tak diketahui: lipoid nefrosis 27

  23. Klasifikasi. imunologi Peny. Kompleks immun: 1. Circulating immune complex: Nephropathy Berger Henoch-Schonlein Purpura Nefritis Lohlein (endokar.bakteri) 2. Pembentukan komplek imun insitu: Glom. Post Streptococcus infection Glom. Membranosa a. b. Peny.AGBM: sindroma Goodpasteur. 28

  24. Minimal change disease

  25. Minimal change disease Normal glumerular structure

  26. Normal glomerulus Minimal change disease

  27. Focal Segmental Glomerulosclerosis Primary or secondary Some (focal) glomeruli show partial (segmental) hyalinization Unknown pathogenesis Poor prognosis

  28. Focal segmental glomerulosclerosis

  29. Membranous Glomerulonephritis Autoimmune reaction against unknown renal antigen Immune complexes Thickened GBM Subepithelial deposits

  30. Membranous glomerulonephritis

  31. Post-infectious glomerulonephritis

  32. IgA Nephropathy Common! Child with hematuria after (URI) Upper Respiratory Infection IgA in mesangium Variable prognosis

  33. IgA nephropathy

  34. Sindroma nefrotik Batasan: sindroma klinik ok.berbagai penyakit yg ditandai dg meningkatnya perm.membran basal glomerulus thd protein dg.G/ utama proteinuri > 3,5 gram/24 jam. Patofisiologi: - meningkatnya perm.GBM - Bila loss albumin> produksi - Hipoalbumin edema anasarka - Hiperlipidemia : patogenesanya belum jelas - Ggn. Metab.lemak lipiduria: oval Fat Bodies proteinuri hipoalbuminemi 39

  35. Etiologi: Glomerulopati primer Glomerulopati sekunder: a. infeksi: sifilis, malaria, TBC, tifus,virus b. nefrotoksin: diuretik merkuri, bismuth, 1. 2. preparat emas c. allergen: sengatan lebah, gigitan ular, tepung sari. d. peny.kolagen: SLE, PAN,dermatomiositis, peny.Goodpastur, giant cell arteritis. e. peny.lain: Hodgkin, mieloma, leukemi, DM, feokromositoma, miksedema, gagal jantung kongestif, SBE, perikarditis konstriktif, amiloidosis, trombosis vena renalis, obstruksi vena cava inferior. 40

  36. Nephrotic Syndrome Massive proteinuria Hypoalbuminemia Edema Hyperlipidemia Lipiduria

  37. Gejala klinis: - kencing berbuih - Sembab tungkai yg progresif s/d anasarka - Sesak nafas (bila ada cairan pleura) - Sebah dan perut buncit (bila ada asites) 42

  38. Pemeriksaan & diagnosis 1.urinalisis: - proteinuri +3 - torak eritrosit: khas utk SN prim - glukosuri: bila ok DM. 2.ekskresi protein 24 jam (Esbach) 3.kadar albumin serum 4. Elektroforesa protein serum & protein urin 5.kadar lipid plasma 6.tes imunologi 7.pem.radiologi: BOF, IVP, foto thorax 8. Biopsi ginjal. +4, lipiduria 43

  39. Diagnosis banding: Penyakit dg edema dan hipoalbuminemi lain: Penyakit hati kronis Malnutrisi Gagal jantung 1. 2. 3. 44

  40. Penatalaksanaan Diet TKTP rendah garam. Obat: a. diuretik b. antiagregasi platelet: dipiridamol c. infus albumin d. kortikosteroid:prednison 2mg/kg/hr 4 minggu lalu tapering off e. imunosupresif: siklofosfamid 2 mg/ kg/hr atau klorambusil 0,2 mg/kg/hr selama 8 minggu. 1. 2. 3. Koreksi penyakit primernya 45

  41. Komplikasi: Kelainan kardiovaskuler (atherosclerosis) Shock hipovolemi Mudah terserang infeksi Gagal ginjal kronik. 1. 2. 3. 4. 46

  42. Identify the pathophysiology and clinical manifestations of urinary tract infections. UTI (Cystitis): Evaluation: History and physical examination includes queries about risk factors; s/s such as pain, odor, hematuria, vital signs, temperature, U/A, culture. Treatment: Antimicrobial therapy, pain medication.

  43. Identify the pathophysiology and clinical manifestations of urinary tract infections. Pyelonephritis: An infection of the renal pelvis and interstitium. Causes include: kidney stones, reflux, pregnancy, neurogenic bladder, instrumentation, female sexual trauma. Pathophysiology: Can be spread by ascending microorganisms along the ureters or blood borne pathogens. Inflammation affecting the pelvis, calyces, medulla. Signs/Symptoms: Fever, chills, flank or groin pain, frequency, dysuria. Evaluation: Urine culture, U/A, clinical s/s, radiologic evaluation. Treatment: Antibiotic therapy, pain management

  44. Describe glomerulonephritis including etiology, pathophysiology, and clinical manifestations. Glomerulonephritis: Inflammation of the glomerulus Glomerular disease is the most common cause of chronic and end-stage renal failure. Etiology (Varied): Immunological causes (most common), drugs, toxins, vascular disorders, and systemic diseases Types: Acute, rapidly progressive, chronic.

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