section fisher's power point presentation on urinary system

1. The URINARY SYSTEM

2. Acid-Base Regulation Acids release H + ions in a solution Overview: Hydrogen ions determine the relative acidity of body fluids by: Bases accept H + ions in a solution

12. Metabolic Acidosis Definition: -characterized by low pH (<7.35) and low bicarbonate (<22mEq/L) Compensatory Mechanisms: - the respiratory system attempts to return the pH to normal by increasing the rate & depth of respiration. CO 2 elimination increases, and the PaCO 2 falls. Effects on ABG: ↓ pH ↓ HCO 3 - ↓ PaCO 2

16. Metabolic Alkalosis Definition: - is characterized by a high pH (> 7.45) and a high bicarbonate ( > 26 mEq/L). Compensatory Mechanism: - Rate and depth of respirations decrease, retaining CO 2 Effects on ABG: - ↑pH - ↑ HCO 3 - - ↑PaCO 2

20. Respiratory Acidosis Definition: - characterized by a pH of < 7.35 and a PaCO 2 greater that 45 mmHg. It may be acute or chronic . In chronic respiratory acidosis, the bicarbonate is higher than 26 mEq/L as the kidneys compensate by retaining bicarbonate. Compensatory Mechanism: - Kidneys conserve bicarbonate to restore carbonic acid; bicarbonate ratio of 1:20

24. Respiratory Alkalosis Definition: - characterized by a pH > 7.45 and a PaCO 2 of < 35 mmHg. Compensatory Mechanism: Kidneys excrete bicarbonate and conserve H + to restore carbonic acid: bicarbonate ratio. Effects on ABG: - ↑pH - ↓PaCO 2 - ↓HCO 3

33. Normal Abnormal

39. PATHOPHYSIOLOGY Damaged glomerular capillary membrane Loss of plasma proteins(Albumin) Hyperlipidemia Hypoalbuminemia Generalized edema Activation of Renin-Angiotensin system Sodium and water retention EDEMA Stimulates synthesis of lipoproteins Decreased oncotic pressure

43. Lower UTI a.) Urethritis - inflammation of urethra b.) Prostatitis – infection of prostate gland c.) Cystitis – inflammation of urinary bladder Upper UTI a.) Pyelonephritis – inflammation of kidneys

44. Infection gain access to bladder SCHEMATIC DIAGRAM Colonized epithelium Evade host defense mechanism Inflammation Organisms ascends to urethra and bladder ADHERE MUCOSAL SURFACES

54. Increased gromerular permeability Decreased GFR hematuria proteinuria azotemia Activation of renin- angiotensin-aldosterone system hypoalbuminemia Sodium and water retention edema hypertension Initiating event (infection, antigen/antibody formation, systemic disease) Gromerular-capillary membrane inflammation PATHOGENESIS OF GROMERULONEPHRITIS

59. Ineffective Protection The effects of both the gromerular disorder and treatment with anti-inflammatory and cytotoxic drugs can depress the immune system, increasing the risk for infection. 5. Ineffective role performance The manifestation and treatment of gromerular disorders can affect to maintain usual roles and activities. Fatigue and muscle weakness may limit physical and social activities. Bed rest or activity limitations may be ordered to minimize the degree of proteinuria.

63. 6. Monitor closely for bleeding during the first 24 hours after the procedure. a. Check the V/S frequently. Notify the physician of tachycardia, hypotension, and other signs of shock. b. Monitor biopsy site for bleeding c. Check hemoglobin and hematocrit d. Observe for and report complains of back or flank pain, shoulder pain, pallor, lightheadedness e. monitor urine output for quantity and hematuria. 7. Encourage fluids during the initial postprocedure period

69. Slow, progressive destruction of the glomerolus Cortex layer shrinks to 1-2 mm in thickness Bands of scar tissue distort the remaining cortex Surface of the kidney becomes rough & irregular shape Scarring at the glomeruli & tubules Thickenned branches of the renal artery Severe glomerular change End stage renal disease

71. Note: Nusing Care for Chronic Glomerulonephritis is the same as Acute Glomerulonephritis.

72. Thank You...! by: Group 2, BSN 3-Fisher