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ADVANCED RENAL ANATOMY AND PHYSIOLOGY •Urinary system parts •How Kidney’s Work •Kidney Failure •Transplantation URINARY SYSTEM PARTS AND FUNCTION Kidneys • Purple brown organs • Remove liquid wastes from the blood • nephrons • Stabilize balance of salts and substances in blood • Produce erythropoietin Ureters • Muscles on ureter walls tighten and relax • Force urine downward • Small amounts of urine emptied into bladder about every 10-15 seconds URINARY SYSTEM PARTS AND FUNCTION Bladder • • • • Hollow organ located in the lower abdomen Held in place by ligaments Bladder walls relax and expand to store urine Can store up to 2 cups urine for 2-5 hours Sphincter muscles • • Keep urine from leaking Nerves alert person that it is time to empty the bladder Urethra URINARY SYSTEM PARTS AND FUNCTION Facts about urine • Adults pass about a quart and ½ each day • Volume formed at night is about ½ that of daytime • Normal urine is sterile • Tissues of bladder are isolated from urine and toxic • • substances by a coating that discourages bacteria growth Normal urine output is 40-60 mL/hr Minimum urinary output in the ICU setting is 30 mL/hr URINARY SYSTEM PARTS AND FUNCTION RENAL FAILURE Generally due to diseases affecting the nephron Most diseases attack both kidneys simultaneously Most common diseases of kidney • Diabetes • HBP DISEASES OF THE KIDNEY Diabetic neuropathy • Body unable to use glucose properly • If glucose stays in the blood, it can be poison • Unused glucose in the blood causes damage to nephron High Blood Pressure • Damages the small vessels in the kidneys • Damaged vessels cannot filter waste DISEASES OF THE KIDNEY (2 of 5) Glomerular disease • Auto-immune disease • Infection related disease • Sclerotic disease DISEASES OF THE KIDNEY Congenital kidney diseases • Polycystic kidney disease (PKD) • • • Cysts replace much of the mass of the kidney Autosomal recessive • Abnormal formation of the nephron Signs of kidney disease • • • HBP Anemia Blood protein in urine http://content.revolutionhealth.com/contentimages/im ages-image_popup-r7_kidneyscompared.jpg DISEASES OF THE KIDNEY Trauma Poisons Acute renal failure • Blood loss • Drugs or poisons • May lead to permanent renal failure DISEASES OF THE KIDNEY Chronic kidney disease • • Gradual loss of kidney function Increased risk of stroke or heart disease End stage renal disease • Requires dialysis or transplant Signs of kidney disease • • • • • • Frequent urination Tired or itchy Nausea or vomiting Swelling of hands or feet Skin may darken Muscle cramps DIAGNOSTICS FOR RENAL DISEASE HBP measurement Microalbumineria/proteinuria • Healthy kidneys remove waste but leave • protein in blood Protein in urine is indicator that kidneys not working adequately DIAGNOSTICS FOR RENAL DISEASE Glomerular filtration rate (GFR) • Calculation of how efficiently kidneys are filtering waste • Measurement of creatninine in the blood • Breakdown of muscle cells during activity (creatine) • Normal blood creatinine level 0.8-1.4 mL/dL • Levels can increase 10 X in kidney failure DIAGNOSTICS FOR RENAL DISEASE (2 of 2) Blood Urea Nitrogen (BUN) • Manufactured in liver-byproduct of amino • • acids and ammonia Healthy kidneys remove urea from blood to urine Normal 26 mEq/L Renal imaging Renal biopsy TREATMENT FOR RENAL DISEASE Blood pressure Diet • • • • Protein Cholesterol Sodium Potassium Stop smoking Treat anemia Dialysis ALDOSTERONE Hormone made by the cortex of the adrenal gland Controls the reabsorption of Na+ and excretion of K+ to control fluid balance, and electrolytes Secreted in response to low salt levels Increases BP HIGHER THAN NORMAL VALUES Primary hyperaldosteronism Secondary hyperaldosteronism from cardiac or renal disease Low sodium diet Pregnancy LOWER THAN NORMAL VALUES High sodium diet Congenital adrenal hyperplasia ROLE IN SECRETION Levels of aldosterone increased by • Decreased serum sodium • Increased serum potassium • Increased angiotensin 2 REGULATION OF ACID BASE BALANCE pH equal to (-) log of H+ Metabolic acidosis Main goal of acid-base homeostasis is to maintain a normal PH • Low pH=acidosis • High pH=alkalosis • Low pH w/o HCO3- compensation METABOLIC ACIDOSIS Symptoms • Chest pain • Palpitations • Altered mental status • Dyspnea • Muscle weakness • Kussmal’s respirations • Neurological/cardiac complications • Seizures METABOLIC ACIDOSIS Diagnosis • ABG • • • • • • • ECG Electrolyte Glucose Renal function CBC Urinalysis Possible toxicology • Low pH/low HCO3- METABOLIC ACIDOSIS Two types: • Accumulation of fixed acids (ex: lactic acid) • Will present with a high anion gap • Hypoxemia can cause lactic acidosis • Excessive loss of HCO3- • Will present with a normal anion gap METABOLIC ACIDOSIS Anion gap calculation • [Sodium + potassium]-[chloride + bicarb]=remaining anions • Normal level 8-16 mEq/L Metabolic acidosis with increased anion gap • • • • Lactic acidosis Ketoacidosis CRF Ingestion of acids (salicylate intoxication) METABOLIC ACIDOSIS With a normal anion gap • Diarrhea (bicarb loss) • Pancreatic fistula • Ingestion of ammonium chloride • Renal failure • Renal tubular acidosis from failure to reabsorb bicarb METABOLIC ACIDOSIS Pathophysiology • • • Compensatory mechanism H+ + HCO3- ↔ H2CO3 ↔ CO2 + H2O Enzyme carbonic anhydrase maintains equilibrium between bicarbonate and H2CO3 • Converted into carbon dioxide and water Intracellular buffering of hydrogen atoms • • • Proteins Phosphates Carbonate in bone • Respiratory compensation • Decreasing H by decreasing CO • Renal compensation + • 2 Physically removes H+ from the body by retaining HCO3+ METABOLIC ACIDOSIS Treatment • Emergency • Intravenous bicarbonate • 50-100 mEq • ABG monitoring • Dialysis ACID BASE BUFFERS Respiratory center stimulation • 3-12 minutes to correct Kidneys excrete acid or alkaline urine • • 24-48 hours to correct With a body PH of 7.40, urine PH = 7.33-7.37 Buffers • • • Bicarbonate buffer system • Carbonic acid (H2CO3) and sodium bicarbonate (NaHCO3) Phosphate buffer system • • H2PO4 and HPO4 High concentrations in tubular fluid Protein buffer system • Amino acids inside cells RESPIRATORY REGULATION Hydrogen ion action on medulla oblongata Affect rate of alveolar ventilation • • Acidic condition can increase alveolar ventilation rate 4-5 times normal Alkalotic condition can decrease alveolar ventilation rate by 50-75% As pH returns to normal alveolar ventilation compensatory stimulus lost • Compensation of hydrogen ion concentration effectiveness 50-75% RENAL REGULATION Kidneys • Physically remove H+ from body • Excrete <100 mEq fixed acid per day • Also control excretion or retention of HCO3– • If blood is acidic, then more H+ are excreted • and all the HCO3– is retained, vice versa While lungs can alter CO2 in seconds, the kidneys require hours to days to change HCO3– and affect pH. RENAL REGULATION Reabsorption of HCO3– • For every H+ secreted, an HCO3– is reabsorbed. • They react in the filtrate, forming H2CO3 which dissociates into H2O and CO2. • CO2 immediately diffuses into cell, is hydrolyzed and H+ is secreted into filtrate, HCO3– diffuses into blood • Thus, HCO3– has effectively been moved from the filtrate to the blood in exchange for H+. • If there is excess HCO3– that does not react with H+, it will be excreted in urine. RENAL REGULATION Steps of bicarbonate reabsortption • Tubules not very permeable to bicarbonate • ion because it is a large ion Reabsorption begins with reaction of H+ secreted in tubule and HCO3- in tubular fluid • Carbonic acid • Carbonic acid dissociates into CO2 and H2O • Water become part of peritubular fluid • CO2 diffuses into epithelial cells or into blood RENAL REGULATION Steps of bicarbonate reabsorption (cont) • CO2 combines with water to form a new • bicarbonate ion If patient is acidotic (excess H+) bicarbonate ion will almost be completely removed from urine and reabsorbed back into the blood. RENAL REGULATION ↑ CO2 ↑ H+ secretion (↑ HCO3reabsorption) ↓ CO2 ↓ H+ secretion (↓ HCO3reabsorption) TITRATION OF BICARBONATE Hydrogen ion secretion =3.5 mmol/min Bicarbonate ion = 3.49 mmol/min • • Ions combine with each other in tubules End products of CO2 and H2O Normal metabolic processes produce slightly more H+ that is not matched up with HCO3- • • Leftover H+ secreted in urine In alkalotic state, leftover HCO3- will be secreted in urine TITRATION OF BICARBONATE Metabolic compensation takes longer (earliest @ 24-48 hours) but compensation is complete vs. respiratory compensation at ~ 75%