Professional Documents
Culture Documents
NURSING
REVIEW OF THE
GENITOURINARY SYSTEM
THE URINARY SYSTEM
The urinary system consists of the kidneys,
ureters, urinary bladder and urethra.
The urinary system eliminates wastes,
controls blood volume regulates blood ion
concentration and pH, and regulates blood
cell production.
THE KIDNEYS
Each kidney is behind the peritoneum, and
surrounded by a renal capsule and a renal
fat pad.
The ureter expands to form the renal pelvis
within the renal sinus, and the renal pelvis
has flower-like extensions called renal
calyces.
The kidney is divided into an outer cortex
and an inner medulla. Each renal pyramid
in the medulla has a base that extends into
the cortex. The apex of each renal
pyramid projects to a calyx.
The Kidneys and the Nephron
THE NEPHRON
The functional unit of the kidney is the
nephron.
The parts of the nephron are the renal
corpuscle, the proximal convoluted tubule,
the loop of Henle, and the distal convoluted
tubule.
The filtration membrane is formed by the
glomerular capillaries, the basement
membrane and the podocytes of Bowman’s
capsule.
The Kidneys and the Nephron
Ureters, Urinary Bladder and
Urethra
Ureters carry urine from the renal pelvis to
the urinary bladder.
The urethra carries urine from the urinary
bladder to the outside of the body.
The ureters and the urinary bladder are
lined with transitional epithelium and have
smooth muscle in their walls.
The internal and external urinary sphincter
muscles regulate the flow of urine through
the urethra.
Ureters, Urinary Bladder and
Urethra
Regulation: Hormonal
Antidiuretic hormone (ADH), otherwise
known as vasopressin, is secreted when
the osmolality of blood increases or when
blood pressure decreases. It increases the
permeability to water of the distal
convoluted tubule and collecting duct and
increases water reabsorption by the
kidney.
Aldosterone increases the rate of sodium
chloride reabsorption, potassium secretion,
and hydrogen ion secretion.
Regulation: Hormonal
Atrial natriuretic factor, secreted from the
right atrium in response to increases in
blood pressure, acts on the kidney to
increase sodium and water loss in the
urine.
Regulation: Neural
Increased sympathetic activity decreases
blood flow to the kidney, decreases
filtration pressure, and decreases filtrate
and urine formation.
Increased volume in the urinary bladder
stretches its wall and activates the
micturition reflex.
Regulation: Neural
Parasympathetic impulses cause
contraction of the urinary bladder and
relaxation of the internal and external
urinary sphincters.
Higher brain centers control the micturition
reflex.
Body Fluid Compartments
Water and the electrolytes are distributed
in two major compartments. Sixty percent
of the total body weight is due to water.
Of the sixty percent, roughly 60% is found
in the intracellular compartment, while 40%
is found in the extracellular compartment.
In the extracellular compartment, 1/3 is
found in plasma.
The main intracellular ions are potassium,
phosphate, magnesium, and sulfate ions,
and there are more protein molecules
intracellularly than extracellularly.
Body Fluid Compartments
Extracellular fluid contains more sodium,
chloride, and bicarbonate ions than in the
intracellular fluid.
Water moves between compartments
continually in response to pressure
differences and osmotic differences
between the compartments.
Sodium Regulation
Increased ADH secretion, Decreased
urine volume and increased plasma DECREASED
INCREASED
volume SODIUM
SODIUM
NORMAL Na+
NORMAL K+
INCREASED DECREASED
CALCIUM Decreased parathyroid hormone CALCIUM
secretion with decreased bone
resorption, decreased intestinal
calcium absorption, and decreased
kidney calcium reabsorption
NORMAL Ca++
DECREASED INCREASED
CALCIUM Increased parathyroid hormone CALCIUM
secretion with increased bone
resorption, increased intestinal
calcium absorption, and increased
renal calcium reabsorption
Acid-Base Balance
The respiratory system functions to
regulate pH. It responds rapidly.
An increased respiratory rate raises the pH
because the rate of carbon dioxide
elimination is increased, and a reduced
respiratory rate reduces the pH because
the rate of carbon dioxide elimination is
reduced.
The kidneys excrete hydrogen ions in
response to a decreasing blood pH, and
they reabsorb hydrogen ions in response
to an increasing blood pH.
Acid-Base Balance
Acidosis is a decrease in pH below the
normal level, and alkalosis is an increase in
pH above the normal level.
Acidosis occurs when the pH of blood falls
below 7.35. The two major types are
respiratory acidosis and metabolic
acidosis.
Alkalosis occurs when the pH of blood
increases above 7.45. The two major
types are respiratory alkalosis and
metabolic alkalosis.
Acid-Base Regulation
Decreased respiratory rate with
increased hydrogen generated by
carbon dioxide retention DECREASED
INCREASED
BLOOD pH
BLOOD pH
Decreased rate of carbon dioxide
elimination with increased carbon
dioxide in extracellular fluid
NORMAL BLOOD pH
DYSFUNCTIONAL VOIDING
PATTERNS
ADULT VOIDING
DYSFUNCTION
Both neurogenic and non-neurogenic
disorders
The micturition process involves several
highly coordinated neurologic responses that
mediate bladder function.
A functional urinary system allows for
appropriate bladder filling and complete
bladder emptying.
Usually involves the lower urinary system in
adults, but may progress to involve the upper
urinary system if not treated promptly.
URINARY INCONTINENCE
Risk factors:
Pregnancy: vaginal delivery, episiotomy
Menopause
Genitourinary surgery
Pelvic muscle weakness
Incompetent urethra due to trauma
Immobility
High-impact exercise
Diabetes mellitus
Stroke
URINARY INCONTINENCE
Risk factors:
Age-related changes in the urinary tract
Morbid obesity
Cognitive disturbances: dementia, Parkinson’s
disease
Medications: diuretics, sedatives, hypnotics,
opioids
Caregiver or toilet unavailable
URINARY INCONTINENCE:
Clinical Types
Stress incontinence
Urge incontinence
Reflex incontinence
Overflow incontinence
URINARY INCONTINENCE:
Assessment and Diagnosis
Detailed description of the problem and a
history of medication use
Voiding history and diary of fluid intake and
output
Urodynamic tests (cystometrogram)
Urinalysis and urine culture
URINARY INCONTINENCE:
Medical Management
Depends on the underlying cause
Behavioral therapy are always the first choice
to decrease or eliminate incontinence
Timed voiding
Prompted voiding
Habit retraining
Bladder retraining or “bladder drill”
Pelvic muscle exercises or Kegel exercises
Vaginal cone retention exercises
URINARY INCONTINENCE:
Medical Management
Pharmacologic therapy
Anticholinergics (oxybutynin, dicyclomine)
Tricyclic antidepressants (imipramine, doxepin)
Pseudoephedrine (Sudafed)
Estrogen
URINARY INCONTINENCE:
Surgical Management
Indicated in patients who have not achieved
continence using behavioral and
pharmacologic therapy.
Options vary according to the underlying
anatomic and physiologic problem
URINARY INCONTINENCE:
Nursing Management
Based on the premise that incontinence is not
inevitable with illness or aging and that it is
often reversible and treatable.
Provide support and encouragement during
behavioral therapy
Explain purpose of pharmacologic therapy
Patient education
URINARY RETENTION
Inability to empty the bladder completely
during attempts to void.
Chronic urine retention often leads to
overflow incontinence.
Residual urine is urine that remains in the
bladder after voiding (Normal: complete
bladder emptying in healthy adults younger
than 60; if > 60: 50 to 100 ml).
URINARY RETENTION
Can occur postoperatively in any patient
particularly if the surgery affected the perineal
or anal regions.
General anesthesia reduces bladder muscle
innervation and suppresses the urge to void,
impeding bladder emptying.
URINARY RETENTION:
Pathophysiology
Urinary retention may result from diabetes,
prostatic enlargement, urethral pathology,
trauma, pregnancy, or neurologic disorders
such as cerebrovascular accident, spinal cord
injury, multiple sclerosis, or Parkinson’s
disease.
May also be caused by medications
URINARY RETENTION:
Complications
Chronic infections
Calculi
Pyelonephritis and sepsis
Hydronephrosis and obstructive form of
uropathy and chronic renal failure
Urine leakage with perineal skin breakdown
and irritation
URINARY RETENTION:
Nursing Management
Prevent overdistention of the bladder
Treat infection
Correct obstruction
Promote normal urinary elimination
Providing privacy
Ensuring an environment and a position conducive
to voiding
Assisting the patient with the use of the bathroom
or commode
Applying warmth to relax the sphincters
URINARY RETENTION:
Nursing Management
Promote normal urinary elimination
Giving patient hot tea
Offering encouragement and reassurance
Simple trigger techniques (turning on the water
faucet while the patient is trying to void, stroking
the inner thighs or abdomen, tapping above the
pubic area, dipping the patient’s hands in warm
water)
Administering analgesics post-surgery
URINARY RETENTION:
Nursing Management
Promote urinary elimination
Transurethral catheterization
Suprapubic catheterization
Promoting home care
CATHETERIZATION
Relieve urinary retention
Assist with postoperative drainage in urologic
and other surgeries
Provide means to monitor accurate urine
output in critically ill patients
Promote urinary drainage in patients with
neurogenic bladder dysfunction or urine
retention
Prevent urinary leakage in patients with stage
III to IV pressure ulcers
CATHETERIZATION:
Indwelling Devices
A closed drainage system is essential
Has to be changed at least every two weeks
using aseptic techniques
Change drainage bags every three days
using aseptic techniques
CATHETERIZATION:
Nursing Management
Assessing the patient and the system
Minimizing trauma
Use an appropriate-sized catheter.
Lubricate the catheter adequately with a
water-soluble lubricant during insertion.
Insert the catheter far enough into the
bladder to prevent trauma to the urethral
tissues when the retention balloon is
inflated.
Secure catheter properly.
CATHETERIZATION:
Nursing Management
Retraining the bladder.
Preventing complications.
MANAGEMENT OF
PATIENTS WITH GUT
DYSFUNCTION
URINARY DISORDERS
UTI
Caused by pathogenic microorganisms in the
urinary tract and classified as either upper or
lower urinary tract infections
Lower UTI:
Cystitis (inflammation of the urinary bladder)
Prostatitis (inflammation of the prostate gland)
Urethritis (inflammation of the urethra
Upper UTI:
Acute and chronic pyelonephritis (inflammation of
the renal pelvis)
Interstitial nephritis (inflammation of the kidney)
UTI
One of the most common reasons patients
seek health care.
Most cases occur in women, with one of
every five women in the US developing a UTI
sometime during her life (higher incidence in
developing countries).
Urinary tract is also the most common site of
nosocomial infection.
UTI
Risk factors:
Inability or failure to empty the bladder completely
Obstructed urinary flow
Decreased natural host defenses or
immunosuppression
Instrumentation of the urinary tract
Inflammation or abrasion of the urethral mucosa
Contributing conditions:
Diabetes mellitus
Pregnancy
Neurologic disorders
Gout
LOWER UTI
Mechanisms which maintain the sterility of the
bladder:
Physical barrier of the urethra
Urine flow
Ureterovesical junction competence
Various antibacterial enzymes and antibodies
Antiadherent effects mediated by the mucosal
cells of the bladder
LOWER UTI:
Pathophysiology
Bacteria gains access to the bladder, attach
to and colonize the epithelium of the urinary
tract to avoid being washed out during
voiding.
Pathogens evade host defense mechanisms.
Inflammation is initiated.
Most UTIs result from fecal organisms that
ascend from the perineum to the urethra and
the bladder and then adhere to the mucosal
surfaces.
LOWER UTI:
Pathophysiology
Routes of infection:
Ascending infection (up the urethra)
Hematogenous (through the bloodstream)
Direct extension (fistulous tract from the intestines)
LOWER UTI:
Clinical Manifestations
Asymptomatic (50%)
Frequent pain and burning on urination
Frequency, urgency, nocturia, incontinence
Suprapubic or pelvic pain and tenderness
Back pain and hematuria
LOWER UTI: Assessment and
Diagnostic Findings
UTI is diagnosed by bacteria in the urine:
colony count of 105 colony-forming units per
mL of urine on a clean-catch midstream or
catheterized specimen (major criterion).
UTI have subsequent sepsis have occurred
with lower bacterial colony counts, however.
Cellular studies:
Microscopic hematuria (>4 RBCs/hpf)
Pyuria (>4 WBCs/hpf)
LOWER UTI: Assessment and
Diagnostic Findings
Urine cultures remain the gold standard in
documenting a UTI and can identify the
specific organisms present.
The following groups of patients should have
urine cultures obtained when bacteriuria is
present:
All men
All children
Women with a history of compromised immune
function or renal problems
Diabetic patients
LOWER UTI: Assessment and
Diagnostic Findings
The following groups of patients should have
urine cultures obtained when bacteriuria is
present (cont’d):
Patients who have undergone recent
instrumentation (including catheterization) of the
urinary tract
Patients who were hospitalized recently
Patients with prolonged or persistent symptoms
Patients with 3 or more UTIs in the past year
Pregnant women
Postmenopausal women
Sexually-active women or with new partners
LOWER UTI:
Medical Management
Management typically involves pharmacologic
therapy and patient education.
Acute pharmacologic therapy:
Uncomplicated in women: single-dose, short-
course (3 to 4 days), or 7- to 10-day therapeutic
courses
Complicated UTI: cephalosporin or
ampicillin/aminoglycoside combination for 7 to 10
days; TMP-SMZ; quinolones
Emphasize completion of regimen even if
symptoms subside
LOWER UTI:
Medical Management
Long-term pharmacologic therapy
Reinfection in women after completion of
antimicrobial therapy: another short course of full-
dose antimicrobial agent may be prescribed; if
there is no recurrence, medication is taken every
other night for 6 to 7 months.
Other options: a dose of antimicrobial agent after
sexual intercourse, a dose at bedtime, or a dose
every other night, or three time per week
Cranberry juice?
UPPER UTI:
Acute Pyelonephritis
Bacterial infection of the renal pelvis, tubules,
and interstitial tissue of one or both kidneys.
Frequently secondary to ureterovesical reflux;
other causes include urinary tract obstruction,
bladder tumors, strictures, BPH, urinary
stones
Kidneys are often enlarged with interstitial
infiltration of inflammatory cells.
Abscesses may be noted on the renal
capsule.
ACUTE PYELONEPHRITIS:
Assessment and Diagnosis
An ultrasound or a CT scan may be
performed to locate any obstruction in the
urinary tract.
IVP is rarely indicated during acute
pyelonephritis (normal findings in 75% of
patients)
Urine culture and sensitivity tests are
performed to determine the causative
organism so that appropriate antimicrobial
agents can be prescribed.
ACUTE PYELONEPHRITIS:
Medical Management
Uncomplicated: treated as outpatients
Other patients, including pregnant women,
may be hospitalized for at least 2 to 3 days of
parenteral therapy. Once afebrile, oral
agents may be substituted.
Pharmacologic therapy:
2-week course of TMP-SMZ, ciprofloxacin,
gentamicin with or without ampicillin, or a third-
generation cephalosporin
Analgesics to relieve pain
Antipyretics to lyse the fever
CHRONIC
PYELONEPHRITIS
Usually results from repeated bouts of acute
pyelonephritis
May cause end-stage renal disease
Usually no symptoms of infection unless an
acute exacerbation occurs
Fatigue, headache, poor appetite, polyuria,
excessive thirst, weight loss
Tests to determine the extent of the disease:
intravenous urogram, measurement of
creatinine clearance, BUN and creatinine
levels.
CHRONIC
PYELONEPHRITIS
Complications:
End-stage renal disease
Hypertension
Nephrolithiasis
Medical management:
Nitrofurantoin or TMP-SMZ to suppress bacterial
growth
Careful monitoring of renal function with proper
adjustment of dosages depending on renal
clearance
CHRONIC
PYELONEPHRITIS
Nursing management:
Monitoring of fluid intake and output
Unless contraindicated, liberal fluid intake up to 3
to 4 li/day
Monitor TPR every 4 hours and administer
antipyretic drugs and antibiotics as prescribed
Patient education on the prevention of UTI:
adequate fluid consumption, regular bladder
emptying and proper perineal hygiene
UPPER URINARY TRACT
INFECTIONS
ACUTE PN CHRONIC PN
ANTIGEN-ANTIBODY PRODUCT
RENAL FAILURE
AGN: Clinical Manifestations
Hematuria (primary presenting feature)
Proteinuria (primarily albumin)
Azotemia (elevated BUN and serum
creatinine levels)
Oliguria/anuria
Anemia
Edema and hypertension (75% of patients)
Headache, malaise, flank pain
CVA tenderness
AGN: Clinical Manifestations
Circulatory overload with dyspnea, engorged
neck veins
Cardiomegaly and pulmonary edema
Confusion, somnolence and seizures (uremic
encephalopathy)
AGN: Assessment and
Diagnostic Findings
Ultrasonography of the kidneys: large,
swollen and congested kidneys
Electron microscopy and immunofluorescent
analysis if kidney biopsy samples:
demonstration of immunoglobulins and typical
glomerular changes
Serologic tests: increased serum complement
levels (within 2 to 8 weeks)
Urinalysis showing RBC casts and other
sediments
AGN: Complications
Hypertensive encephalopathy
Heart failure
Pulmonary edema
Uremia
AGN: Medical Management
Treating symptoms
Preserve kidney function
Treat complications
Pharmacologic therapy:
Penicillin (if with residual streptococcal infection)
Corticosteroids and immunosuppresants
Loop diuretics and antihypertensive medications
GENERALIZED EDEMA
(FLUID MOVES FROM VASCULAR SPACE TO EXTRACELLULAR SPACE
SODIUM RETENTION
EDEMA
NEPHROTIC SYNDROME:
Clinical Manifestations
Edema (major manifestation)
Malaise, headache, irritability and fatigue
Hypertension usually not a manifestation
NEPHROTIC SYNDROME:
Assessment and Diagnosis
Proteinuria exceeding 3 to 3.5 g/day is
sufficient for the diagnosis of nephrotic
syndrome.
Pyuria and granular and epithelial casts on
urinalysis
Needle biopsy of the kidney may be
performed for histologic diagnosis of the
etiology
Serum markers (anti-C1q antibodies is the
most reliable for assessing disease activity in
lupus nephritis)
NEPHROTIC SYNDROME:
Complications
Infection (deficient immune response)
Thromboembolism
Pulmonary emboli
Acute renal failure
Accelerated atherosclerosis
NEPHROTIC SYNDROME:
Medical Management
Objective is to preserve renal function
Diuretic agents for severe edema
ACE-inhibitors in combination
Cyclophosphamide and azathioprine
Corticosteroids
Low-sodium, liberal-potassium diet
Protein intake should be about 0.8 g/kg/day
with emphasis on high biologic value proteins
(dairy products, eggs, meats)
Diet should be low in saturated fats
NEPHROTIC SYNDROME:
Nursing Management
Similar to that of acute glomerulonephritis
during the early phase of the disease
As the disease worsens, management is
similar to that of chronic glomerulonephritis
Patient education
Monitoring and regulation of fluid intake and
output
Monitoring for onset of acute infections
Vigilance against possible thromboembolic
phenomena
RENAL FAILURE
Transient or permanent inability of the
kidneys to perform their normal function
of urine formation (filtration, secretion
and reabsorption.
Two types:
Acuterenal failure – reversible, transient
Chronic renal failure – irreversible,
permanent
ACUTE RENAL FAILURE
Stages:
Oliguric/anuricphase – azotemia
Diuretic phase – increased urine output
Recovery phase – full recovery of renal
function
Types:
Pre-renal ARF
Intrinsic renal ARF
Post-renal ARF
CHRONIC RENAL FAILURE
Stages:
Stage I: 80-125 ml/min (normal renal
function)
Stage II: 50-80 ml/min (diminished renal
reserve; chronic renal impairment)
Stage III: 20-50 ml/min (chronic renal
impairment)
Stage IV: 5-20 ml/min (chronic renal
insufficiency
Stage V: < 5 ml/min (ESRD)
MANIFESTATIONS
Azotemia / Uremia
Uremic frost
Uremic fetor
Uremic encephalopathy
Uremic cardiomyopathy / pericarditis
Uremic gastropathy
MANIFESTATIONS
Edema
Multiple electrolyte imbalance
Hypernatremia
Hyperkalemia
Hypermagnesemia
Hyperphosphatemia
Hypocalcemia
MANIFESTATIONS
Metabolic acidosis
Anemia
Hypertension
MANAGEMENT
Aggressive Management
Supportive Management
UROLITHIASIS
Refers to stones (calculi) in the urinary tract.
Formed when urinary concentrations of
calcium oxalate, calcium phosphate and uric
acid increase (supersaturation) and
dependent on the amounts of the substance,
ionic strength, and pH of the urine
UROLITHIASIS:
Pathophysiology
Supersaturation of calcium oxalate, calcium
phosphate, uric acid
Deficiency of substances that normally
prevent crystallization in the urine (citrate,
magnesium, nephrocalcin, uropontin)
Stones often occur in dehydrated patients
They may deposit in many areas of the
urinary tract, including the renal pelvis,
ureters, ureterovesical junction and urinary
bladder.
UROLITHIASIS:
Pathophysiology
Factors that favor the formation of stones:
Infection
Urinary stasis
Immobility
Hypercalcemia
Hyperuricemia