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Urinary system Urinary System Consist of: Kidneys Ureters Bladder Urethra General Function: Specific Function: Excretory Regulatory Secretory Urine formation Excretion of waste products Regulation of electrolyte excretion Regulation of acid excretion Regulation of water excretion Auto regulation of blood pressure Regulation of red blood cell production Renal clearance Vitamin D synthesis Secretions of prostaglandins Urine storage Bladder emptying Location and External Anatomy of Kidneys Located retroperitoneally Lateral to T12–L3 vertebrae Average kidney 12 cm tall, 6 cm wide, 3 cm thick -Bean-shaped, brownish-red structures.right lower than left Hilus On concave surface Vessels and nerves enter and exit Renal capsule surrounds the kidney Regions A. 1. Renal parenchyma a. Cortex • Glomeruli, proximal and distal convoluted tubules, cortical collecting ducts, and adjacent peritubular capillaries. b. Medulla • Pyramids 8- 18 pyramids/ kidney 2. Renal Pelvis - it is the concave portion of the kidney through which the renal artery enters and the renal vein exits - composed of afferent arteriole and efferent arteriole Nephrons B. - Functional units of kidney: a) b) c) d) e) f) Glomerulus Bowman’s capsule Proximal tubule Distal tubule Loop of Henle Collecting ducts Calyx C. • • Minor calyx- 4-13 minor calices Major calyx- 2-3 major calices Glomerulus 3 filtering layers: D. 1. 2. 3. Capillary endothelium Basement membrane Epithelium Ureters Fibromuscular tube that connect each kidney to the bladder Narrow, muscular tubes, 24-30 cm long 3 narrowed areas: Ureteropelvic junction Ureteral segment Ureterovesical junction - prevents reflux of urine Urinary Bladder Muscular, hollow- sac located just behind the pubic bone 300- 600 ml of urine 4 layers of the urinary bladder: 1. 2. 3. 4. Adventitia- outermost layer Detrusor- beneath the adventitia Lamina Propria- interface between detrusor and urethelium. Urothelium- innermost layer Urethra Small tube leading from the floor of urinary bladder 1.5 inch in length in females & 8 inch in male Function: passageway for urine & semen Acid- Base Regulation Acid Base Balance Homeostasis of the body fluids at a normal arterial blood pH ranging between 7.35- 7.45 Body fluids are slightly alkaline, metabolic processes of the body generally produced excess acid. Maintained partially through the reabsorption of bicarbonate (HCO3-) in the proximal tubule Acids release hydrogen ions (H+) in solutions Ex. Hydrochloric acid (HCl)- strong acid Carbonic acid (H2CO3)- weak acid Bases or alkalis • decrease hydrogen ion (H+) concentration accept H+ in solutions Ex: Sodium Hydroxide (NaOH) – strong base Bicarbonate (HCO3) – weak base Regulation System 1. Buffer Regulation System - chemicals which neutralizes excess acids and bases a. bicarbonate buffer system - controls the pH in ECF of the body b. phosphate buffer system - important ICF buffer system c. protein buffer system - largest buffer system of the body; includes Hgb in RBC, histone proteins and nucleic acids inside the cells. 2. Respiratory Regulation System - excretes or retains CO2 in the lungs 3. Renal Regulation System - excretion or retention of Hydrogen ions (H+) and bicarbonate ions (HCO3) Acid Base Imbalances 1. Metabolic Acidosis (Base Bicarbonate Deficit) A. Definition - results because of high acid content of the blood, which also causes loss of sodium bicarbonate - characterized by low pH and low plasma bicarbonate concentration - 2 forms: 1. high anion gap acidosis 2. normal anion gap acidosis B. Compensatory Mechanism - increased ventilation and renal retention of bicarbonate - lungs “blow off” CO2 to raise pH and conserve HCO3- Laboratory Findings (ABG) - low plasma pH (below 7.35) or a normal pH (if compensated) - normal PCO2 or low if compensated in an attempt by the lungs to blow off more acid - low plasma bicarbonate: -below 21 mEq/L in adults -below 20 mEq/L in children - low urine pH (below 6) D. Causes -DKA or Diabetic Ketoacidosis with starvation -Salicylate overdose -Lactic Acidosis 2o hypoperfusion -Methanol and ethylene Glycol toxicity -uremia E. F. Manifestations A. Acute - headache - nausea and vomiting - increased RR and depth - peripheral vasodilation - cold and clammy skin B. Chronic -asymptomatic - drowsiness - confusion - shock - dysrhythmia - decreased BP Medical and Nursing Management 1. Correct metabolic defect 2. If resulted from excessive intake of Chloride, eliminate the source of Chloride. 3. Administer bicarbonate if pH < 7.1 and bicarbonate level < 10. 4. Closely monitor serum potassium level 5. Correct hypokalemia 6. Give alkalizing agents, if serum bicarbonate level < 12meq/L 7. Hemodialysis 8. Peritoneal dialysis 2. Metabolic Alkalosis (Base Bicarbonate Excess) A. Definition - marked by the heavy loss of acid from the body or by increased level of bicarbonate - characterized by increased pH and increased plasma bicarbonate. B. Compensatory Mechanism - decreased ventilation to conserve CO2 and increase the PaCO2 - lung retains CO2 to lower pH - kidney conserves H+ to excrete HCO3 C. Laboratory Findings (ABG) - high plasma pH (above 7.45) - normal or high PCO2 (above 45 mmHg) as a compensatory elevation - high plasma bicarbonate: - above 28 mEq/L in adults - above 25 mEq/L in children - high urine pH (above 7) D. Causes - overzealous administration of sodium bicarbonate - excessive or prolonged vomiting - excessive diuresis - gastric suction with loss of hydrogen and chloride ions - pyloric stenosis -excessive diarrhea -hyperaldosteronism - Cushing’s syndrome - villous adenoma - cystic fibrosis - hypokalemia E. Manifestations a. Acute - tingling of fingers and toes - slow, shallow respiration (compensatory) - hypertonic muscles - tetany - mental dullness - dizziness - respiratory depression - atrial tachycardia may occur - ventricular disturbances - decreased motility and paralytic ileus b. Chronic - same with acute metabolic alkalosis - PVC (premature ventricular contractions or Uwaves seen in ECG) Medical and Nursing Management: 1. Sufficient chloride must be supplied. 2. Restore normal fluid volume by administering sodium chloride fluids. 3. In patient with hypokalemia, administer potassium as KCl. 4. Administer H2-receptor antagonist such as Cimetidine (Tagamet) to reduce the production of gastric HCl, thereby decreasing the metabolic alkalosis associated with gastric suction. 5. Carbonic anhydrase inhibitors are useful in patients who cannot tolerate rapid volume expansion. 6. Monitor fluid intake and output. 7. Correct the underlying acid-base disorder. Respiratory Acidosis (Carbonic Acid Excess) A. Definition - marked by an increased arterial CO2 concentration (PaCO2), increased carbonic acid, and increased hydrogen ion concentration (low pH) - may be acute or chronic - due to inadequate excretion of CO2 with inadequate ventilation B. Compensatory Mechanism - excess hydrogen is excreted in the urine in exchange for bicarbonate ions - kidney eliminate hydrogen ion and retain HCO3 - kidney will retain increased amounts of HCO3 to increase pH C. Laboratory Findings (ABG) - low plasma pH (below 7.35) or a normal pH (if compensated) - increased PCO2 (above 45 mmHg) - normal or high plasma bicarbonate (HCO3) if compensated - above 28 mEq/L in adults - above 25 mEq/L in children D. Causes - narcotic coma - respiratory depression (drugs, CNS, trauma) - pulmonary diseases (COPD, asthma, pneumonia) - hypoventilation - cardiac arrest/respiratory arrest - head and spinal cord injury - acute pulmonary edema - aspiration of a foreign object - atelectasis - ventricular fibrillation (in anesthesized person) - increased ICP - papilledema - dilated conjunctival blood vessels - hyperkalemia E. Manifestations a. Acute - increased RR, PR and BP - mental cloudiness - feeling of fullness in head - hypoventilation, shallow respiration - poor exhalation - mental alertness and disorientation - cerebrovascular vasodilation - increased cerebral blood flow Chronic - cerebral vasodilation will increase ICP - cyanosis and tachypnea will develop - pneumothorax - overdose of sedatives - sleep apnea syndrome - ARDS - muscular dystrophy - myasthenia gravis - Guillain-Barre Syndrome F. Medical and Nursing Management 1. Improve ventilation 2. Bronchodilators 3. Antibiotics 4. Thrombolytics 5. Pulmonary hygiene measures 6. Adequate hydration 7. Supplemental oxygen PRN 8. Mechanical ventilation, use appropriately 9. Semi-Fowler’s position 4. Respiratory Alkalosis (Carbonic Acid Deficit) A. Definition - marked by decreased PaCO2 and increased pH - clinical condition in which the arterial pH is greater than 7.45 and the PaCO2 is less than 38 mmHg - acute and chronic condition may occur B. Compensatory Mechanism - renal excretion of bicarbonate increase, and hydrogen ion is retained - kidneys will excrete increased amounts of HCO3 to lower pH - kidneys conserve H+ and excrete HCO3 C. Laboratory Findings (ABG) - high plasma pH (above 7.45) - decreased PCO2 (below 35 mmHg) - decreased plasma bicarbonate as a compensatory measure - below 21 mEq/L in adults - below 20 mEq/L in children - high urine pH (above 7) Causes - extreme anxiety - “panic” attack - hypoxemia - early phase of salicylate intoxication - gram-negative bacteremia - inappropriate ventilator setting - chronic respiratory alkalosis results from chronic hypercapnia - low serum bicarbonate level Manifestations a. Acute - lightheadedness - inability to concentrate - numbness and tingling from decreased calcium ionization - tinnitus - loss of consciousness at times - tachycardia - ventricular and atrial dysrhythmias - deep or rapid breathing - paresthesias - mental restlessness and agitation progressing to hysteria Medical and Nursing Management 1. Instruct patient to breathe more slowly to allow CO2 to accumulate or breathe into a close system (such as a paper bag) 2. Sedative may be required 3. Correct underlying problems HYDRONEPHROSIS Is distention of the renal pelvis and calices caused by an obstruction of normal urine flow. Etiology congenital or acquired stricture from ulceration of the ureter, or may be due to a calculus. thickening of the bladder walls from cystitis enlarged prostate urethral stricture Pressure from a pregnant or displaced uterus ovarian tumors PRESENCE OF CALCULUS, TUMORS, SCAR TISSUE, CONGENITAL DEFECTS, KINK IN THE URETER URINE FLOW OBSTRUCTION URINE ACCUMULATION & STASIS PRESSURE IN THE KIDNEY WALLS IRREVERSIBLE NEPHRON DESTRUCTION DISTENTION OF THE KIDNEYS SUSTAINED/INTERMITTENT INCREASE PRESSURE Assessment Acute Renal colic Severe back pain Chronic Dull, aching discomfort in the flank on the affected side Painful hydronephrosis that occurs intermittently General Vague intestinal symptoms such as: nausea vomiting abdominal pain Pain in the sides Abdominal mass Nausea and vomiting Very high Fever Dysuria (Painful urination) Increased urinary frequency Hematuria (blood in the urine) High number of white blood cells in the urine Feel fatigued Appear pale Diarrhea Respiratory distress Foam in the toilet water, which may be caused by excess protein in your urine Weight gain due to excess fluid retention High blood pressure Thromboembolism • severe pain and swelling in arm or leg • changes in color or temperature of arm or leg Diagnostics: Ultrasonography Intravenous pyelogram (IVP) Abdominal magnetic resonance imaging (MRI) Urine tests Blood Test Endoscopy Kidney (Renal) Scan Bladder catheterization (insertion of a hollow, flexible tube through the urethra Complications kidney infection (pyelonephritis) urinary tract infection Nursing Diagnosis Excess Fluid Volume related to Sodium Retention Impaired Urinary Elimination related to Inflammation Risk for Infection Pain related to infection Deficient Knowledge related to Factors of Development of the Disease INTERVENTION MEDICAL Pain relief Analgesics Antispasmodic Antibiotics administration SURGICAL Pyeloplasty Pre operative ensure optimal renal function encourage to recognize and express feelings of anxiety Post operative VS permit oral fluids after passage of flatus maintain sterility of nephrostomy tube ensure unobstruction in the nephrostomy tube or catheter never clamp nephrostomy tube MIO In case of ureteral stent Monitor for bleeding MIO Assess for signs of UTI monitor colicky pain & decrease urine output (stent displacement) NEPHROTIC SYNDROME Is a set of clinical manifestations caused by protein wasting secondary to diffuse glomerular damage. ETIOLOGY Nephrotic syndrome is a protein wasting disease Caused by: glomerulonephritis diabetes mellitus Lupus erythematosus Amylodidosis Carcinoma Membranous glomerulonephritis Glomerular basement membrane damage Glomerular permeability to plasma protein proteinuria Albumin depletion in the blood hypoalbuminemia Alteration in osmotic pressure in the vessels Fluid moves to interstitial spaces Increase synthesis of LDL, HDL in the liver with decrease lipid catabolism Decreased plasma volume edema Hyperlipidemia Stimulates aldosterone secretion lipiduria Sodium & water retention Decreased glomerular filtration rate edema Assessment Proteinuria Hypoalbuminemia (low level of albumin in the blood) Edema (swelling) Hypercholesterolemia (high level of cholesterol in the blood) High blood pressure Susceptibility to infections Oliguria Hematuria Diagnostics: Complete medical history and physical examination Urinalysis Blood analysis Kidney biopsy Complications kidney infection (pyelonephritis) urinary tract infection Blood clots High blood cholesterol and elevated blood triglycerides Poor nutrition High blood pressure Acute kidney failure Chronic kidney failure Nursing Diagnosis Altered Nutrition: Less Than Body Requirements related to Increased Metabolic Demands Fluid Volume Excess related to Reduced Urine Output Potential Impairment of Skin Integrity related to Edema Fatigue related to Increased Metabolic Demands Risk for Infection Related to Altered Immune Response Secondary to Treatment URINARY TRACT INFECTION Inflammation of the bladder or the urethra caused by gram-negative bacteria, with Escherichia coli causing most cases. Etiology Caused by gram-negative bacteria • • Escherichia coli Kleibshiella Proteus Pseudomonas Obstruction of the urine flow Benign Prostatic Hyperplasia Assessment Lower Urinary Tract Infection (Cystitis) - pain on urination - Frequent urination - Nocturia - Incontenence - Suprapubic pain - Hematuria ` - dysuria - foul-smelling urine - increased WBC, pus and bacteria in urine Upper Urinary Tract Infection (Pyelonephritis) - Fever - Chills - Flank or Low Back Pain - Nausea and Vomiting - Headache - Malaise - Painful Urination Diagnostics: Antibiogram Urinalysis Urine culture and Sensitivity Nitrate testing Intravenous pyelography Computed tomography (CT Scan) Ultrasonography (Ultrasound) Retrograde Urethrogram (Infants) X-ray and Intravenous Urography (X-rays of the urological system following intravenous injection of iodinated contrast material) Complications Damage and scarring of the urinary tract lining Pyelonephritis Chronic Renal Failure due to extensive kidney damage Sepsis Nursing Diagnosis Acute Pain related to Inflammation and Infection of Urethra, Bladder and Other Urinary Tract Structures Altered Urinary Elimination related to Irritation and Inflammation of the Bladder Mucosa Altered Health Maintenance related to Prevention of Recurrent Infections Deficient Knowledge related to Factors Predisposing the Patient to Infection and Recurrence, Detection and Prevention of Recurrence and Pharmacologic Therapy Risk for Fluid Volume deficit related to Fever, Nausea, Vomiting and Possible Diarrhea NURSING INTERVENTION Promotive Preventive Do not delay urination. Empty bladder regularly. Clean the urethral meatus after intercourse. Increase fluid intake. Careful sexual practice. Intake of grape juice. Curative Eat well-balanced diet. Good hygiene practice. Medications given: cholinergics to relieve urinary retention anti-cholinergics to decrease bladder muscle spasm antibiotics: Ciprofloxacin phenazopyridine for pain Revision of abnormalities in urinary tract. Rehabilitative Education about importance of completing medication cycle. Evaluation and instruction about voiding patterns, sexual practices, and hygiene practices. ACUTE GLOMERULONEPHRITIS A specific set of renal diseases in which an immunologic mechanism triggers inflammation and proliferation of glomerular tissue that can result in damage to the basement membrane, mesangium, or capillary endothelium Etiology Beta-hemolytic Streptococcal infection Viral or parasitic infection Assessment Hematuria Oliguria Edema (peripheral or periorbital) Headache flank pain Shortness of breath or Dyspnea Hypertension Skin rashes Arthritis Pharyngitis Impetigo Respiratory infection Pulmonary hemorrhage Heart murmur may indicate endocarditis Scarlet fever Weight gain Abdominal pain Anorexia Skin pallor Palpable purpura in patients with HenochSchönlein purpura Oral ulcers Diagnostics: Complete blood cell count Electrolytes, including BUN and creatinine (to estimate the glomerular filtration rate [GFR]): The BUN and creatinine levels will exhibit a degree of renal compromise. Urinalysis Streptozyme test: This test includes many streptococcal antigens that are sensitive for screening but are not quantitative. Antistreptolysin O (ASO) Erythrocyte sedimentation ratio (ESR) usually is increased. Urine or plasma creatinine level greater than 40; decreased renin level is noted. Blood cultures Ultrasonography Abdominal radiographic imaging (ie, computed tomography) Renal biopsy Complications Sclerosis progressing toward renal failure Other complications can develop in patients who present with severe hypertension, encephalopathy, and pulmonary edema. It includes the following: Hypertensive retinopathy Hypertensive encephalopathy Rapidly progressive glomerulonephritis Chronic renal failure Nephrotic syndrome Nursing Diagnosis Alteration in Nutrition due to Compromised Renal Function Fluid Volume Excess due to Reduced Urine Output Activity Intolerance due to Need to Rest the Kidney Potential Impairment of Skin Integrity due to Edema Potential for Infection due to Reduction in Natural Defense Mechanisms Nursing Interventions Promotive Preventive prompt treatment of URTI or sore throat culture and sensitivity test; antibiotics as indicated Curative eat balanced diet teach client to live healthfully bed rest dietary sodium restrictions low protein diet sufficient carbohydrate to prevent muscle wasting and nitrogen imbalance antibiotic: Penicillin anti-hypertensive drugs diuretic therapy Rehabilitative maintain follow-up healthcare report any exacerbation in signs and symptoms CHRONIC GLOMERULONEPHRITIS Is the advanced stage of a group of kidney disorders, resulting in inflammation and slowly worsening destruction of glomeruli. Etiology Acute glomerulonephritis Immunologic reactions in the body Assessment Signs: Hypertension Edema Nocturia Weight loss Hematuria Proteinuria Casts and blood in the urine Symptoms: Headache Dyspnea Blurring of vision Lassitude Weakness or fatigue DIAGNOSTICS: Serum chemistry CBC Urinalysis Renal ultrasonogram Biopsy Kidney Complications • • • • • • • • Metabolic acidosis Pulmonary edema Pericarditis Uremic encephalopathy Uremic gastrointestinal bleeding Uremic neuropathy Severe anemia and hypocalcemia Hyperkalemia Nursing Diagnosis Altered Nutrition: Less Than Body Requirements related to Increased Metabolic Demands Fluid Volume Excess related to Reduced Urine Output Fatigue related to Increased Metabolic Demands Risk for Impaired Skin Integrity Risk for Infection related to Altered Immune Response Secondary to Treatment Nursing Interventions Promotive Preventive avoid infections, especially respiratory and urinary tract infection Curative eat balanced diet teach client to live healthfully high calorie, low protein, sodium restricted diet provide/assist in hygiene monitor signs of pulmonary edema and congestive heart failure rest is essential take prescribed medications appropriately Rehabilitative maintain follow-up healthcare report any exacerbation in signs and symptoms