Renal and Urinary Tract Disorders

Transcription

1 Renal and Urinary Tract Disorders Objectives: Congenital Kidney Disorders, Obstructive Kidney Disorders and Kidney cancer. Glomerular and Tubulointerstitial Disorders Acute Kidney Injury and Chronic Kidney Disease Disorders of the Urinary Bladder and Urinary Tract Part 1: Congenital Disorders, Obstructive Kidney Disorders and Kidney Cancers. 1

2 Congenital Kidney Disorders: Development of the kidney occurs between weeks 5-8. Usually congenital kidney problems involve abnormalities with anatomy and positioning of the kidneys. Polycystic Kidney Disease: Autosomal dominant (most common) Characterized by cysts that form from the tubular portions of the nephrons Renal damage occurs a combination of the the pressure of expanding cysts on normal kidney function as well as apoptosis and inflammation of renal tubular cells. Polycystic Kidney Disease: Manifestations: Pain Hematuria Frequent kidney and urinary tract infections Kidney stones Hypertension 2

3 Polycystic Kidney Disease: Treatment: There is no cure, so treatment aims at slowing the progress of the disease and reducing symptoms such as controlling hypertension, pain and infections. Keeping hydrated is important. Eventually, dialysis and kidney transplant is necessary. Obstructive Kidney Disease: The main problem with urinary obstruction is the blockage of urine flow through the urinary tract. The back pressure causes urine to accumulate in the kidney (hydronephrosis). Urine stasis causes infection, damage (pressure necrosis) and scaring to the kidneys depending on the severity. Complete bilateral obstruction with anuria can cause death. Obstruction can be partial or complete. 3

4 Urinary Calculi: (Kidney Stones) an example of obstruction The process of nephrolithiasis involves the formation of insoluble stones (calculi) in the urinary tract. Kidney stones usually form in a single kidney. Stones can stay in the kidney or travel from the kidney to the ureter or urinary bladder. Sometimes kidney stones obstruct urine flow. Urinary Calculi: Stone formation is associated with increased urine concentration of ions and changes in urinary acidity. Stone formation may be due to disturbances in the metabolism of certain ions, impaired renal filtration and reabsorption. Risk factors: previous kidney stone events, genetics, dehydration, obesity, high sodium diet, digestive diseases and surgery, smoking, 3x more likely in females, frequent urinary tract infections, and gout. Urinary Calculi: Stones: Stones can vary in size, shape and number. Calcium oxalate, calcium phosphate, uric acid and struvite. Staghorn calculus 4

5 Urinary Calculi: Manifestations: Pain (from obstruction) Nausea and vomiting, abdominal distention Fever and chills Hematuria Dysuria Urinary Calculi: Treatment: Antibiotics, analgesics, diuretics Ultra sound lithotripsy Surgical removal Preventative measures: diet, increase fluid intake 5

6 Kidney Cancer: Renal Cell Carcinoma: Primarily arises from proximal convoluted tubular cells Risk factors: smoking, obesity, heavy metal and asbestos exposure, cystic kidney disease Manifestations: largely asymptomatic during early stages, with advanced disease: hematuria, flank pain and palpable mass. Kidney Cancer: Wilm s Tumor (nephroblastoma): Kidney tumor in young children which can occur in a single kidney or both kidneys Wilm s tumor often accompanies other urinary tract congenital anomalies The tumor is usually large, but well encapsulated so has a very good survival rate after surgery and chemotherapy. 6

7 Part 2: Glomerular and Tubulointerstitial Disorders Glomerular Disorders: Any disease process that alters or distorts the glomeruli and affects glomerular filtration. 7

8 Glomerular Disorders: Types: Acute Nephritic Syndrome Rapidly Progressive Glomerulonephritis Nephrotic Syndrome Chronic Glomerulonephritis Secondary Glomerular Disease Acute Nephritic Syndrome: Inflammation and proliferation of the glomeruli leading to damage of the glomerular capillary walls Sudden onset of hematuria and proteinuria Decreased GFR and oligouria Edema and hypertension Acute Nephritic Syndrome: Ex. Acute Postinfectious Glomerulonephritis: Occurs after an infection of group A streptoccocal infection. Immune complexes precipitate along the glomeruli The glomeruli enlarge and there is excessive cellular proliferation. Affects more children than adults and usually resolves with antibiotic treatment without complications. 8

9 Rapidly Progressive Glomerulonephritis: Idiopathic cause, inflammation occurs within a few months Characterized by focal and segmental proliferation of glomeruli cells (leading to a crescent shape that obstructs the glomerular capsule) Example: Goodpasture Syndrome 9

10 Nephrotic Syndrome: Etiologies: idiopathic, immune complex deposition or secondary disease processes (diabetes, hypertension, autoimmunity) Leads to increased glomerular permeability Excessive proteinuria and hypoalbuminemia Edema Hyperlipidemia 10

11 Chronic Glomerulonephritis: Etiologies: some forms of acute glomerulonephritis can lead to the chronic form and sometimes it presents without an acute form previously Glomeruli become sclerosed, kidneys decrease in size Slowly progresses to chronic kidney disease over a number of years Secondary Glomerular Disease: Systemic Lupus Erythematosus Glomerulonephritis: Immune complexes lead to glomerular injury. Diabetic Glomerulosclerosis: Thickening and lesions occur among the glomeruli including a proliferation of mesangial cells. Hypertensive Glomerular Disease: sclerosis occurs in the renal arterioles and arteries (benign nephrosclerosis), kidneys become smaller and develop fibrosis in the glomeruli and other structures Tubulointerstitial Disorders: Disorders that affect the renal tubular structures (PCT, nephron loop, DCT, collecting duct as well as interstitial environments around the tubules) 11

12 Tubulointerstitial Disorders: Types: Renal Tubular Acidosis Pyelonephritis Drug-related nephropathies (acute tubulonephritis or acute tubular necrosis) Renal Tubular Acidosis: Tubular defects in reabsorption of bicarbonate ions or excretion of hydrogen ions resulting in metabolic acidosis. Types: Defects of the PCT (defect of bicarbonate reabsorption), DCT (defect of secretion of acids) and aldosterone issues that impair the reabsorption of Na+ with decreased secretion of H+ and K+. Renal acidosis also occurs with kidney failure. Complications: metabolic bone disease, kidney stones and growth failure in children. Pyelonephritis: Kidney infection, inflammation and infection that affects the interstitial area, the calyces, pelvis and tubules which is usually caused by bacteria Urinary tract infections (UTI) usually result from ascending infections that begin in the urethra and spread to the urinary bladder and then to the kidney. Kidney infections can also occur with hematologic spread (septicemia, endocarditis). Risk factors: female, age, diabetes, neurogenic bladder conditions, pregnancy, catheterization and anything that increases urinary stasis will increase the risk. 12

13 Pyelonephritis: Manifestations: Urinary urgency, frequency, burning, nocturia Hematuria Cloudy urine with ammonia-like or fish odor. Fever, chills, fatigue Flank pain Nausea, vomiting, anorexia Complications: sepsis/septic shock, development of chronic pyelonephritis (kidneys become scarred and leads to chronic kidney disease) Treatment: Antibiotics Drug-Related Nephropathies: Damage and inflammation of tubular structures (and glomeruli) due to therapeutic drugs, exogenous toxins or other nephrotoxic substances. Drugs and toxins can reduce renal blood flow or produce hypersensitivity reactions. Accounts for 75% of acute kidney injury cases. 13

14 Part 3: Acute Kidney Injury and Chronic Kidney Disease Acute Kidney Injury (AKI): A rapid, usually reversible decline in renal function that develops within hours. The kidney is unable to maintain fluid/electrolyte balance and cannot effectively excrete nitrogen wastes. Etiologies: Renal ischemia (hypovolemia, shock, heart failure) Acute tubular necrosis (nephrotoxins, immune) Obstructions Acute renal disease (acute glomerulonephritis, acute pyelonephritis) 14

15 Acute Kidney Injury (AKI): A rapid, usually reversible decline in renal function that develops within hours. The kidney is unable to maintain fluid/electrolyte balance and cannot effectively excrete nitrogen wastes. Etiologies: Renal ischemia (hypovolemia, shock, heart failure) Acute tubular necrosis (nephrotoxins, immune) Obstructions Acute renal disease (acute glomerulonephritis, acute pyelonephritis) Phases of Acute Renal Injury Phase 1: Initiating Phase: the time period in which kidney injury occurs (hours to days) Phase 2: Oligouric Phase 1-5 weeks Kidneys can t perform filtration, reabsorption or secretion. Oligouria Retention of electrolytes, fluids and nitrogen-based compounds (urea, creatinine) 15

16 Manifestations of Phase 2: Edema Acidosis Complications of Phase 2: (if oligouria continues, or AKI remains untreated) Hypertension Uremia: significant accumulation of nitrogen based compounds in the blood Seizures, coma Treatment for Phase 2: Treat underlying disorder Hemodialysis High calorie diet low in sodium, potassium and protein. IV therapy (Sodium bicarbonate IV), careful monitoring of electrolytes Diuretics, fluid restriction Drug treatment for hyperkalemia Phase 3: Diuretic Phase Kidney begins to secrete, but still cannot reabsorb or filter normally yet. Kidney tissue is in repair or recovery Increased urine output, but BUN, creatinine, electrolytes remain high in the blood 16

17 Treatment during Phase 3: Continue dialysis, IV therapy, careful diet Give fluids Gradually discontinue treatment as kidney function recovers Phase 4: Recovery Phase Kidney function normalizes gradually so BUN, creatinine levels begin to normalize Sometimes if damage is significant AKI could lead to Chronic Kidney Disease. Chronic Kidney Disease (CKD) Takes months or years to develop Characterized by the destruction of tissue with irreversible sclerosis and progressive loss of kidney function 17

18 Stage 1 and 2: Glomerular Filtration Rate (GFR) normal in Stage 1 and mildly decreased in stage 2 (60-89ml/min/1.73m2) Not normally diagnosed except accidentally Stage 3: Renal Insufficiency (the transition phase) Diagnosed according to kidney damage or moderate reduction in GFR (30-59) Kidney filters and secretes, but reabsorption is affected. Urine is dilute, polyuria, nocturia Stage 4: Severe reduction in GFR Preparations are being made for kidney replacement therapy (dialysis) Kidney gradually losses ability filter, reabsorb and secrete. Uremia (BUN high): significant accumulation of nitrogen-based compounds in blood 18

19 Stage 5: Classified as renal failure, GFR less than 15 Patients are treated with dialysis (possibly kidney transplant) Oligouria leading to anuria if not treated Chronic Renal Failure Phosphate Nat/H 2O Stage I, II, III K+ Nitrogen Wastes EPO Production & RBC Destruction Acid/Base Balance Calcium Vitamin D Synthesis Diminished Hyponatremia Loss of H 2O Stage III - V Hypernatremia Stage I, II, III Hypokalemia Due to electrolyte imbalance Stage III - V Stage I, II, III Azotemia Stage III - V Uremia By Stage III Anemia Loss of Bicarbonate Base Hypocalcemia Excretion Diminished Increased Reabsorbtion Edema Hyperkalemia Impaired Immune function Acidosis Altered mental Blood Volume HTN and Edema Lungs/Systemic GI Tract Issues Neurological /Nervous System problems Sexual dysfunction Uremic frost Blood Disturbances Hypercalcemia Secondary Hyperparathyroidsim Hyperphosphotemia Pericardial Effusion Demineralization of bone Heart Failure Increase in fractures/bone pain Itchy skin (phosphate) Manifestations of CKD: Fluid and electrolyte imbalance that involves water retention which can lead to edema and hypertension. Excessive potassium retention and calcium (loss and excess) lead to cardiac arrhythmias and muscle weakness). Toxic effect from drugs/hormones not eliminated properly. Anemia (hematuria, hemolysis, bone marrow suppression by uremia, impaired EPO) affects heart. 19

20 Uremia Manifestations: Loss of weight due to anorexia, vomiting, diarrhea (due to uremic toxins). Toxins affect nervous system: confusion, apathy, convulsions, coma. Increased infections. Blood Clotting difficulties (petechiae), decreased platelet function. Multiple organs are affected. Uremic Frost: deposition of uremic toxins on skin (dry, itching skin). Calcium and Phosphate Impaired phosphate elimination leads to increased phosphate levels in blood causing calcium levels to fall. Hypocalcemia causes release of PTH causing release of calcium phosphate from bone. Impaired activation of Vit. D3 to calcitriol impairs absorption of calcium from small intestine. PTH continues to increase (secondary hyperparthyroidism). Bone Pain, Bone fractures can occur. Metabolic Acidosis. Treatment for CKD: Prevent UTI s and infections Control hypertension Control diabetes Diet: protein, sodium/water, potassium restriction dependent on stage Administer recombinant EPO Replace activated Vit. D3 Hemodialysis or Peritoneal Dialysis, Kidney transplant 20

21 Part 4: Disorders of the Urinary Bladder and Urinary Tract 21

22 Lower Urinary Tract Obstruction and Stasis: Classification: congenital or acquired defects, degree (partial or complete obstruction), acute or chronic, and upper or lower urinary tract. Etiologies: Compression of urethra (enlarged prostate gland), sexually transmitted infections (STIs), tumors, fecal impaction, congenital deformities, prolapse/atrophy of pelvic support structures Lower Urinary Tract Obstruction and Stasis: Manifestations (after a period of time): Urinary difficulties (straining, hesitancy, small/weak urine stream, increased frequency, feeling like bladder isn t emptied, overflow incontinence) Bladder distention Increased frequency of UTIs Lower Urinary Tract Obstruction and Stasis: : Compensations: Hypertrophy and hypersensitivity of bladder Diverticula form on the inner bladder surface Decompensations: Detrusor muscle shortens and becomes ineffective so urine tends to accumulate in the bladder, there is incomplete emptying of the bladder. Increased urinary tract infections. Vesicoureteral reflux (backup and stasis of urine from lower urinary tract into ureters and kidneys). Urinary bladder becomes over-stretched, overflow continence occurs. 22

23 Neurogenic Bladder Disorders: characterized by nervous system problems that lead to detrusor muscle and external urethral sphincter dysfunction. Types: Spastic Bladder Flaccid Bladder 23

24 Spastic Bladder: Failure to store urine due to conditions that cause bladder spasm and a decrease in bladder volume. Damage to the neural regions above the micturition center in sacral spinal cord (ANS and SNS) such as spinal cord injuries, injuries to higher brain centers, brain tumors, stroke, MS, Parkinson Disease lesions in the pons variolli. Flaccid Bladder: Failure to empty urine effectively due to injury of the micturition center in the sacral spinal cord, the cauda equina or the sacral nerves that supply the bladder due to traumas, tumors, congenital defects. In addition, damage to peripheral nerves that supply the bladder can lead to spastic bladder. (diabetes, trauma) The bladder losses muscle tone, overstretches and has weak contraction ability. Along with this, the external urethral sphincter and the perineal musculature is also weakened. Treatment of Neurogenic Bladder Conditions: Catheterization: insertion of tube into the bladder through the urethra (temporary or permanent indwelling catheters). Bladder retraining: Monitoring fluid intake, specific manual massage methods, biofeedback Drugs: anti-muscarinic (spastic bladder) and cholinergic drugs (flaccid bladder) as well as muscle relaxants. Surgical procedures 24

25 Urinary Incontinence: involuntary loss or leakage of urine Types: Stress incontinence Overactive bladder (urge incontinence) Overflow incontinence Functional incontinence Urinary Incontinence: Stress Incontinence Etiologies: anatomic weakness in the pelvic floor muscles surrounding the urethra Stress incontinence will occur with anything that increases pressure on the bladder or increased abdominal pressure: loss of urine during coughing, laughing, sneezing, heaving lifting, jumping/running Increased risk for females, elderly, surgeries of pelvic floor muscles Urinary Incontinence: Overactive Bladder/Urge Incontinence Urge Incontinence: involuntary loss of urine with a urgent need to void. Overactive bladder: also includes increased frequency of urination, difficulty with urination, incomplete bladder emptying and nocturia which can sometimes occur without incontinence. Etiologies: CNS and neural control dysfunction and bladder smooth muscle dysfunction. Associated with stroke, Parkinson disease, MS, aging, diabetes. 25

26 Urinary Incontinence: Overflow Incontinence Loss of urine when there is an excessive retention of urine in the absence of detrusor activity due to nervous system lesions or bladder neck obstruction (enlargement of prostate, fecal impaction). Urinary Incontinence: Functional Incontinence Occurs when there is delayed time between feeling the need to urinate and actually urinating. Elderly, psychological issues, medications Urinary Incontinence: Treatment: Treat underlying disorder if possible. Behavior training: fluid management, timed voiding, pelvic floor exercises (kegel, vaginal weight training), bladder retraining. Drugs: beta-adrenergic agonist drugs, anticholinergic drugs Surgical procedures (anatomical restructure, surgically implanted artificial sphincters) Use of urine collection devices, pads. 26

27 Bladder Cancer: Most commonly occurs in the transitional epithelium lining the bladder. Manifestations: painless hematuria (gross or microscopic) and dysuria. Risk factors: smoking, exposure to industrial toxins, chronic bladder infections, bladder stones. 27

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