Urinary System Disorders
Chapter 21 Pgs 420-444
Overview
• Incontinence and Retention • Diagnostic Tests
– Urinalysis – Blood tests – Other tests
• Urinary Tract Obstructions
– Urolithiasis – Tumors
• Renal Failure
– Acute – Chronic
• Diuretic Drugs • Dialysis • Disorders of the Urinary System
– Urinary Tract Infections – Inflammatory Disorders
• Glomerulonephritis
Incontinence and Retention
• Loss of voluntary control of bladder • Stress incontinence
– Increase in intra-abdominal pressure
• Forces urine through sphincter
– Laughing – Coughing – Females weakened
• Inability to empty bladder • May accomp overflow incontinence • Spinal cord injury • Inability to control managed by pads, briefs • Catheter
– Tube inserted in urethra – Drains urine from bladder to collecting bag – Common source of UTI
• Spinal cord injuries, brain damage
Catheter
Diagnostic Tests—Urinalysis
• Constituents, characteristics of urine vary w/ dietary intake, drugs, care of specimen • Normally clear, straw-colored; pH 4.5-8.0 • Appearance
– Cloudy
• Presence of lg amts protein, blood cells, bacteria, pus
– Dark color
• Hematuria (blood), excessive bilirubin, high concentration of urine
– Unpleasant, unusual odor
• infection
Diagnostic Tests—Urinalysis
• Abnormal constituents (high in numbers)
– Blood (hematuria)
• Small, microscopic amts
– Infection, inflammation, tumors of UT
• Lg # RBC
– Increased glomerular permeability or hemorrhage in tract
– Protein (Proteinuria)
• Leakage of albumin into filtrate
– Inflammation, increased glomerular permeability
– Bacteria (Bacteriuria) and Pus (Pyuria)
• Indicates UTI
– Urinary casts
• Microscopic mold of tubules
– Consists of one or more cells, bacteria, protein
• Inflammation of tubules
– Specific gravity
• Ability of tubules to concentrate urine • Low is related to renal failure
RBC Cast
Diagnostic Tests—Blood Tests
• High serum urea and creatinine
– Indicate failure to excrete N wastes
• Due to low GFR
• • • •
•
Metabolic acidosis
– Indicates low GFR, failure of tubules to control acid/base balance
Anemia
– Indicates low erythropoietin secretion and/or bone marrow depression
• Due to accumulating wastes
Electrolytes Antibody level
– Antistreptolysin O (ASO) or antistreptokinase (ASK)
Renin levels
– Indicate cause of hypertension
Diagnostic Tests—Other Tests
• • • Culture and sensitivity tests
– Urine specimens
• ID organism and select drug treatment
Clearance tests
– Creatinine, insulin clearance – Used to asses GFR
Radiologic tests
– – – – – Intravenous pyelography (IVP) Angiography Ultrasound CT, MRI Used to visualize structures and abnormalities
•
Cytoscopy
– Visualize lower UT – Can be used to perform biopsy or remove kidney stones
•
Biopsy
– Acquire tissue specimen for microscopic analysis
IVP (Intravenous Pyelography)
Angiography, Ultrasound
CT
CT, MRI
Diuretic Drugs
• Removes excess Na ion and water from body
– Increase excretion of water thru kidneys and urinary vol
• Take in morning • Prescribed for many disorders
– Renal disease, hypertension, edema, CHF, pulmonary edema
• Most commonly used drug group inhibits NaCl reabsorption • Major side effect is excess loss of electrolytes
– Many cause excessive loss of potassium – Cause muscle weakness or cardiac arrhythmias
Dialysis
• Provides ―artificial kidney‖
– Sustains life after kidney fails
• Acute renal failure or end-stage renal failure (those waiting for a transplant)
• 2 forms
– Hemodialysis – Peritoneal dialysis
Hemodialysis
• Hospital, dialysis center • Pt’s blood moves from implanted shunt in arm artery tube machine exchange of wastes, fluids, electrolytes
– Semipermeable membrane separates pts blood from dialysis fluid
• Constituents move between the 2 compartments
– Ex: wastes in blood dialysate bicarbonate in dialysate blood Blood cells, proteins remain in blood Movement by ultrafiltration, diffusion, osmosis Blood to pt vein
Hemodialysis
• Heparin (anticoagulant) • Required 3Xs/week for 3-4 hrs • Potential complications
– Shunt becomes infected – Blood clot forms – Blood vessels become damaged
• Must move to new site
– Increased risk of hepatitis, HIV
Peritoneal Dialysis
• • Administered in unit or at home At night or continuously
– CAPD (continuous ambulatory peritoneal dialysis)
• • •
Peritoneal membrane serves as semipermeable membrane Catheter w/ entry and exit points implanted Dialyzing fluid instilled in catheter into cavity
– Remains there – Allows exchange of wastes and electrolytes to occur – Dialysate drained from by gravity from cavity into container
• • •
Requires more time than hemo b/c continuous exchange, prevents sudden changes in fluid and electrolyte levels Complications
– Infection in peritoneal cavity
Peritoneal Dialysis
Disorders of the Urinary System: Urinary Tract Infections (UTI)
• Very common • Urine is excellent medium for microorganismal growth
– Escherichia coli
• Most are ascending
– Perineal cavity mucosa bladder ureters kidneys
UTI—Etiology
• Females more anatomically vulnerable
– Short urethra – Proximity to anus – Frequent irritation to tissues
• Tampons, bubble bath, sexual activity
• Older males with prostatic hypertrophy and retention of urine prone to UTI
UTI—Etiology
• • • • • Incontinence Bladder retention of urine Obstruction of urine flow Congenital abnormality Pregnancy, scar tissue, kidney stones, vesicourethral reflex
– Urine does not flow freely
• Decreased host resistance (immunosuppression) • Impaired blood supply to bladder (aging) • Diabetes mellitus
UTI: Cystitis—Pathophysiology
• Bladder wall and urethra inflamed, red, swollen
– Decreased bladder capacity
UTI: Cystitis—Signs and Symptoms
• Pain in lower abdomen • Dysuria, frequency, urgency
– Inflammation of bladder wall irritated by urine
• Systemic signs of infection • Cloudy urine with unusual odor • Urinalysis indicates bacteria (+100,000/mL), pyuria, microscopic hematuria
UTI: Pyelonephritis— Pathophysiology
• 1 or both kidneys involved • Infection from ureter renal pelvis medullary tissue (tubules and interstitial) • Purulent exudate fills kidney pelvis and calyces • Abscess and necrosis seen in medulla
– May extend thru cortex to capsule – Severe may compress renal artery and vein and obstruct urine flow to ureter
• Bilateral obstruction results in acute renal failure
• Recurrent chronic infection
– Can lead to fibrous tissue over calyx
• Loss of tubule function
UTI: Pyelonephritis—Signs and Symptoms
• Signs of cystitis • Pain
– Dull aching in lower back – Results from renal capsule stretching
• Urinalysis
– Similar to cystitis – Except urinary cast
• Leukocytes or renal epithelial cells present
– Involvement of renal tubules
UTI—Treatment
• Antibiotics (Bactrim) • Increase fluid intake
– Especially cranberry juice
• Tannin decreases ability of E. coli to adhere to bladder mucosa
• Infection reoccurs unless predisposing factors removed
Disorders of the Urinary System: Inflammatory Disorders
• Glomerulonephritis
– Many forms
• Acute Poststreptococcal Glomerulonephritis (APSGN)
– Follows streptococcal infection » Originates as upper resp infection, middle ear infection, strep throat – Primarily affects kids 3-7 (especially boys)
– develops 2 weeks after previous infection
• Antistreptococcal antibodies create antigen-antibody complex
– Type III hypersensitivity rxn – Lodge in glomerular capillaries
• Cause inflammation in both kidneys
– Increase cap perm and cell proliferation » Leakage of proteins and erythrocytes into filtrate
Inflammatory Diseases: Glomerulonephritis— Pathophysiology
• Severe inflammation
– Congestion and proliferation interfere w/ filtration in kidney
• Decrease GFR and retention of fluid and wastes
– If blood flow impaired, acute renal failure
• Low blood flow increase renin increase bp and edema
– Scar tissue on kidney
Glomerulonephritis—Signs and Symptoms
• Back pain
– Stretching renal capsule
• Dark, cloudy urine • Oliguria • Facial edema, then generalized
– Low osmotic pressure of blood – Salt, water retention
• Generalized signs of inflammation • Increased bp
Glomerulonephritis—Diagnostic Tests
• Blood tests
– High serum urea and creatinine and decreasing GFR – Streptococcal antibodies, ASO, ASK – Metabolic acidosis
• Low serum bicarbonate, low pH
• Urinalysis
– Confirms presence of proteinuria, erythrocyte casts
Glomerulonephritis—Treatment
• • • • Sodium restriction Glucocorticoids Antibiotics Recovery w/ minimal damage
– Imp to prevent further exposure to streptococcal infection and recurrent inflam – Adults more difficult
• Acute renal failure in 2% • Chronic glomerulonephritis in 10%
– Gradually destroys kidneys
• Postrecovery testing should be done
Urinary Tract Obstructions: Urolithiasis
• Also called:
– Calculi – Kidney stones
• Frequently reoccur if not treated
Calculi—Pathophysiology
• Can develop anywhere in UT; lg or small • Once any solid material or debris forms • Tend to form when:
– excessive amts of relatively insoluble salts are in filtrate – Insufficient fluid intake creates highly concentrated filtrate
• 75% composed of calcium salts
– Remainder: uric acid, struvite, oxalate
• Usually cause manifestations only when obstruct flow of urine
– Infection if stasis of urine
Kidney Stones—Pathophysiology: Types of Stones
• Calcium stones
– Form when calcium levels high in urine
• Hypercalcemia
• Mixed inorganic salts
– Infection
• Debris from infection begin deposition of crystals
– Urine pH alkaline
• Uric acid stones
– Develop w/ hyperuricemia
• Due to gout, cancer chemo
• Calcium oxalate
– Certain vegetarian diets – High levels of oxalate in urine
Kidney Stones
Calculi—Signs and Symptoms
• Stones in kidney/bladder frequently asymptomatic • Obstruction of ureter causes attack
– ―renal colic‖
• Consists of intense spasms in back and groin • Pain caused by vigorous contractions of ureter
– Effort to pass the stone
Calculi—Treatment
• Small stones eventually passed out • Larger stones
– Extracorporeal shock-wave lithotripsy (ESWL)
• Decreases need for invasive surgery
– Some drugs can partially dissolve
• Need to prevent recurrences
ESWL
Urinary Tract Obstructions: Tumors—Renal Cell Carcinoma
• Primary, silent tumor • Arises from tubule epithelium • Asymptomatic in early stage
– Often metastize to liver, lungs, bones, CNS at time of diagnosis
• Common after 50
– More freq in males and smokers
• Initial sign is painless hematuria • Other manifestations
– Dull aching flank pain, palpable mass, anemia
• Treatment is kidney removal
– 5 yr survival rate 50%
Renal Failure: Acute Renal Failure—Pathophysiology
• • • • • May fail suddenly for different reasons Failure reversible if primary problem successfully treated Dialysis required Develops rapidly Either:
– Directly decreases blood flow to kidney – Inflammation and necrosis of tubules cause obstruction and back pressure
• Greatly decreases GFR and oliguria
• Blood tests show high N (kidneys not removing wastes) • If cause not promptly treated, chronic
Acute Renal Failure—Etiology
• Acute bilateral kidney disease
– Glomerulonephritis
• Low GFR
• Severe prolonged circulatory shock or heart failure
– Results in tissue necrosis – Burns: Hb accum in tubules = obstruction
• Nephrotoxins
– Drugs, chemicals, toxins
• Aspirin, NSAIDs, penicillin
– Cause tubule necrosis and obstruction of blood flow
• Mechanical obstruction
– Calculi, blood clots, tumors – Block urine from leaving kidney
Acute Renal Failure—Treatment
• Important to reverse primary problem quickly • Dialysis • Recovery evidenced by increased urine output
– May take couple months before renal tubules fully recover
Chronic Renal Failure— Pathophysiology
• Gradual, irreversible destruction of kidney nephrons • May result from:
– Chronic kidney disease
• Bilateral pyelonephritis
– Systemic disorders
• Hypertension • Diabetes
– Long term exposure to nephrotoxins
• Asymptomatic until well advanced
– Due to reserve function of nephrons – Can’t be stopped once in advanced
• Scar tissue and loss of functional organization
– Further degenerative changes
Chronic Renal Failure— Pathophysiology: Stages
• Decreased reserve
– 60% nephron loss – Low GFR, high creatinine levels
• Both still in normal range
– Normal urea levels – No apparent clinical signs – Remaining nephrons adapt
• Increase capacity for filtration
Stages
• Renal Insufficiency
– – – – – 75% nephron loss Changes in blood chemistry and manifestations GFR decrease to 20% of normal Significant retention of N wastes in blood Decrease tubule function
• Failure to concentrate urine and control secretion for exchange of acids and electrolytes
– Excretion of lg vol of dilute urine – High bp – Cardiovascular system compensates
Stages
• Uremia (End-stage renal failure)
– +90% nephron loss – negligible GFR – Fluid, electrolytes, wastes retained in body
• All systems affected
– Oliguria or anuria – Regular dialysis or transplant needed to sustain life
Chronic Renal Failure—Signs and Symptoms
• Early signs
– Increase urine output (polyuria) – General signs – Increase wastes and altered blood chemistry
• Bone marrow depression, impaired cell function
– Increase bp
•
Uremic signs
– – – – – – – Oliguria Dry, hyperpigmented skin Peripheral neuropathy (abnorm sensations in lower limbs) Males impotence, decrease libido; females irreg menstrual cycle Encephalopathy (lethargy, memory lapses, seizures, tremors) CHF, arrhythmias Failure of kidneys to activate vitamin D
• Leads to hypocalcemia, osteodystrophy, osteoporosis, tetany
– Uremic frost on skin, urine-like breath – Systemic infection
• pneumonia
Chronic Renal Failure—Diagnostic Tests
• Metabolic acidosis becomes decompensated
– Serum pH below 7.35 – Low GFR – Tubule function lost
• Azotemia
– Presence of N wastes in blood
• Severe anemia • Varying electrolyte levels
– Depends on amt water retained
Chronic Renal Failure
• Affects all body systems • Difficult to maintain control of blood chemistry and body fluid levels • Drugs to treat:
– Hypertension, arrhythmias, heart failure – Dosages adjusted b/c decreased ability to excrete them
• Subject to many complications
– Affect uremia – Infection increases wastes in body; compromises all body systems