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RENAL FAILURE

RENAL FAILURE. DR / ABD ELGHANY HEFNAWY. Maintainance of blood and fluids electrolytes haemostasis. Clearing of metabolites and nitrogenous wast products. -Na, K & Cl -Ca, Ph & Mg -Bicarbonate. -Urea -Creatinine -Uric acid -Ammonia. Erythropiotine. α -Hydroxylase.

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RENAL FAILURE

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  1. RENAL FAILURE DR / ABD ELGHANY HEFNAWY

  2. Maintainance of blood and fluids electrolytes haemostasis Clearing of metabolites and nitrogenous wast products -Na, K & Cl -Ca, Ph & Mg -Bicarbonate -Urea -Creatinine -Uric acid -Ammonia Erythropiotine α-Hydroxylase Renine 5 type I deiodinase 1.25 (DHCC) T4 T3 Regulates secretion of aldesterone Erythropiosis Physiological roles of the kidney Hormones & enzymes

  3. Nephron

  4. Glucose -Bicarbonate -Na Blood Blood -Na & K -Cl Glomerular filteration Ca, Ph, & Mg Na & K

  5. Functions of the Kidneys A. Homeostatic Functions 1. Waste excretion (urine formation) a. Nitrogenous end products: urea, creatinine, uric acid, etc. b. Metabolic degradation of peptide hormones: glucagon, insulin, PTH, growth hormone, FSH, and gastrin. 2. Fluid/electrolyte balance (Na+, K+, water) 3. Acid/base regulation: • kidneys generate and reclaim filtered bicarbonate, as well as secrete excess acid to maintain balance. 4. Balance of other electrolytes (Ca++, Mg++, Phosphate PO4 3-)

  6. B. Non-excretory functions • Renin-angiotensin mechanism to control BP(Blood Pressure • Kidney senses decreased BP • Secretes renin (enzyme), which converts Angiotensin I to angiotensin II • Angiotensin II is a vasoconstrictor  increased BP • Angiotensin II also stimulates aldosterone secretion • Aldosterone increases Na+ and H2O reabsorption, increased plasma volume, and increased BP (aldosterone also stimulates potassium secretion into tubules)

  7. Rennin-Angiotensin-Aldosterone System Fall in NaCl, extracellular fluid volume, arterial blood pressure Angiotension III Helps Correct Adrenal Cortex Juxtaglomerular Apparatus Angiotensinase A Lungs Liver Renin + Converting Enzyme Angiotensinogen Angiotensin I Angiotensin II Aldosterone Increased Sodium Reabsorption

  8. 2. Produces erythropoietin • Stimulates erythropoiesis in bone marrow b. The anemia of CRF is primarily caused by impaired erythropoiesis c.  RBC formation is mainly due to  erythropoietin production in the diseased kidneys, although other compounds that accumulate in renal failure may also suppress erythropoiesis.

  9. 3. Maintains Calcium-Phosphorus bone homeostasis • Activates Vitamin D (Hydroxylation of 25-OH-D3 to 1,25-OH-D3) in kidney disease, can supplement calcitriol, but very expensive Low vit. D  less Ca++ absorbed b. Inverse relationship between Ca++ and P, so when P is retained by diseased kidney, Ca++ levels decline (less calcium reabsorbed by the kidney). c. Low serum calcium  parathyroid gland releases PTH: Parathyroid Hormone: works to elevate serum Ca++ by pulling it from the bones  fragility, muscular weakness, decreased muscular tone, and general neuromuscular hypoexcitability.

  10. Vitamin D from UV exposure Active Vit D3

  11. خلاصــــة Functions of the Nephron Secretion Reabsorption Excretion Filtration Secretion =transferring solutes from the blood into the tubule lumen. Most important secretory products are K+, NH4+, and H+.

  12. High levels of urea and creatinine Azotemia Anaemia Definition Sudden inability of kidney for clearing of the metabolites, nitrogenous wast products or maintanance of blood and fluids electrolytes haemostasis.

  13. Etiology

  14. Post-renal Renal Damage of kidney Azotemia Pre-renal • -Nephritis • -Glomerulonephritis • -Pyelonephritis -Nephrosis • -Nephrotoxin • (Aminoglycosides,Hb, • Myoglobine & heavy metals) • Trauma - Cancer • -Coryn.,Leptospirosis • & Streptococus -Dehydration -Hyperthermia -Heart and circulatory diseases -Renal ischemia -Hypovalemic chock -Haemolytic anemia _Haemorrhage -Obstruction of collecting system -Urolithiasis -Uretheral obstructoin -Rupture of UB -Obstruction of ureters -Paralytic bladder

  15. Pathogenesis

  16. Etiology and predisposing factors Damage of the functional and structural unite of the kidney ( nephron) Pathological and biochemical alterations Clinical signs of kidney damage or RF Inability of the kidney for performing their physiological roles

  17. Myoglobinuria Myoglobin Nephrotoxine Renal azotemia Anorexia Triglyceride Damage of nephron Gluconeogenesis Hyperlipemia Renal Failure

  18. Clinical signs ( Non-specific)

  19. 1- Intermittente fever ( if infectious causes are suspected). 2-Polyuria in case of renal azotemia. 3-Oliguria in case pre-renal azotemia. 4-Anuria or dysuria in case of pos-trenal azotemia. 5- Anorexia and weakness.

  20. 6-Decreased performance. 7-Odema due to proteinuria. 8-Abdominal palpation show painful enlarged kidney. 9- Specific signs according to the etiolgical factors.

  21. Abdominal pain Thirst Dehydration Stomatitis with tongue ulcer

  22. Gastrointestinal disturbances in CRFOral lesions • Foul odor • Stomatitis • Erosions and ulcers • Tongue tip necrosis (fibrinoid necrosis and focal ischemia)

  23. VD (Vitamin-D), VDR (Vitamin-D Receptors), CaR (Calcium Receptors)

  24. Serum Urine Blood -Hyponatremia (Na) -Hypokalemia (K) -Hypochloremia (Cl) -Hypocalcemia ( Ca) -Hypoproteinemia -Hypoglycemia -Hyperlipemia -Increased urea and creatinine levels -Hypophosphatemia -Low specific gravity -Hematuria -Pyoueria -Haemoglobinuria -Presence of crystals -Acidosis -Anaemia -Haemoconcentration -Increased PCV Laboratory finidings

  25. Diagnosis 1- History and clinical signs 2- Laboratory findings 3- X-rays 4- Ultrasonography

  26. Treatment

  27. -Correction of electrolytes and fluid balance. -Identification and treatment of underlying diseases. -Supportive treatment. -Treatment of complications

  28. -Fluid therapy -Dextrose 5% ( IV) -Sodium Bicarbonate 5% (IV) -Oral fluids by nasogastric tube -Saline ( NaCl 0.9%) IV

  29. -Antimicrobial drugs. -Diuretic for flushing the kidney ( furosemide as Lasix). -Flunixine meglumine (0.25 mg/ kg).

  30. Treatment of secodnary complcations As:- -Stomatitis -Urine scalding -Hyperlipemia

  31. Thanks alot for your patience

  32. وسائل التواصل Email: abdelghani72@yahoo.com Abdelghany.hefnawy@bu.edu.eg Facebookabdelghanyhefnawy د.عبد الغني حفناوي Web site to download lectures www.bu.edu.eg/staff/abdelghanyhefnawy (Courses) Tel 01011676482

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