Transcript Defects of the Genitourinary System

Defects of the
Genitourinary System
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Review of Anatomy and Physiology of the Genitourinary
System
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The urinary system is composed of:
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The kidneys, ureter, bladder and urethra.
The kidneys lie outside the peritoneal cavity in the upper
posterior portion of the abdominal wall, one on each side.
Each kidney is made up of one million functional units, called
Nephrons.
Water and small molecules are filtered and larger molecules
stay in the bloodstream. What results (is left in the kidneys)
is filtrate. Approximately 20% of the filtrate is plasma, (no
RBC’s, WBC’s, platelets or protein) Substances that pass
through are selectively reabsorbed or filtered (Na, Bicarb, K,
glucose, creatinine, urea). Filtrate becomes concentrated in
the distal tubules and becomes the urine that reaches the
renal pelvis
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Review of Anatomy and Physiology of the
Genitourinary System
• Nephrons are the functional units that form
urine, there are about 1 million in each
kidney. Nephrons are comprised of a
glomerulus and a tubule (proximal tubule,
loop of Henle, distal tubule). Plasma is
filtered across the glomerulus, of the
plasma that enters the tubule, only a small
fraction is excreted as urine. The Nephrons
empty into collecting ducts (tubules) that
join to form the pelvis of each kidney. BP
determines how fast and under what
pressure blood passes through the kidneys,
they receive approximately 1 L of
blood/min. Blood is supplied to the kidneys
via the renal arteries, one to each kidney
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Review of Anatomy and Physiology of the
Genitourinary System
• The main function of the
urinary system is to:
 Regulate fluids, electrolytes and maintain
acid base balance.
 Remove metabolic end products (waste)
form blood.
 Regulate blood pressure.
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Urinary Tract Infection (UTI)
Etiology/ Pathphysiology:
 An infection and inflammation anywhere in the
urinary tract (including the kidneys), caused by
the proliferation of a microorganism, most are
bacterial in nature but virus and fungi can also
be the cause. The most common organism is
Escherichia Coli. (80- 90% in the pediatric
population)
 Cystitis: An infection of the bladder (most
common)
 Polynephritis: An infection of the kidney
itself (can be an acute infection or chronic
infection)
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Urinary Tract Infection
(UTI)
 Urinary Tract Infections (UTI) are more
common in girls, ages 7-11, males 2-6
years. Female to male ratio 9:1. The
incidence peaks again (in females)
during adolescence with sexual activity.
 One cause for the increased incidence in
females is due to the shorter urethra in
the female provides a ready path for
organisms and the urethra opening in
the vagina is so close to the anus.
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Urinary Tract Infection (UTI)
 Symptoms of Cystitis include:
Urgency
Increase frequency of urination
Burning on urination
Pain on urination (dysuria)
A sense of urgency to urinate
Nocturia
Pain or spasm in the bladder region, pain
in lower back
 Pyuria (WBC’s in urine)
 Bacteria and RBC’s (found on urinalysis)
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Urinary Tract Infection(UTI)
 Symptoms of Acute
Polynephritis include:
 Fever
 Chills
 Flank pain
 Dysuria
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Clinical manifestations of UTI
The infant with a UTI initially presents with vague
symptoms:
 Colic
 Jaundice
 Poor eating
 Vomiting
 Fever
 Lethargy
 Irritability
 Increased number of wet diapers
 FTT
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Clinical manifestations of UTI
The preschool child presents with:
 Fever (most common sign)
 Weak urinary stream or dribbling of urine
 Hematuria
 Abdominal pain
 Frequency
 Urgency
 Dysuria
 Incontinence in the toilet trained child
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Clinical manifestations of UTI
The school aged child presents with:
 Diarrhea
 Strong smell to urine
 Hematuria
 Dysuria
 Frequency
 Urgency
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Clinical manifestations of UTI
Children of all ages can present with:
 Abdominal distension
 Dehydration
 Flank pain
 Costroverterbal angle (CVA) tenderness
 Chills and Fever
 Constipation
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Diagnostic Evaluation
Urine analysis (UA)
 Done via the clean catch method (mid-stream urine
after the child has wiped perineum with a cleansing
cloth.
 In infant/toddler obtained by “bagging.
 Will be a “dirty” specimen and evaluated for ph,
presence of ketone, glucose, blood (RBC's).
Urine Culture/Urine sensitivity (UC & S)
 A sterile specimen, must be obtained by urinary
catheterization.
 To evaluate the presence of WBC’s, bacteria
 Sensitivity will indicate which antibiotic organism is
sensitive to.
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Diagnostic Evaluation
Intravenous pyelogram (IVP)
 A radiological procedure done by injecting dye
(IV) to visualize the structure of the urinary
tract. (kidneys and bladder)
Voiding Cystourethrogram (VCUG)
 To establish the presence of urinary reflux and
other UT abnormalities. Done by placing a Foley
and injecting dye into the UT and with a type of
x ray used to watch the progression of the
urinary flow through the UT.
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Causes of UTI in pediatric patient
 Anatomical differences in girls
 Urinary stasis - holding urine in allows for over growth
of bacteria. The bladder is a nice warm place in which
bacteria will thrive if left there to long
 Contamination from incorrect toileting/cleaning
 Irritation from caustic agents (girls-bubble baths)
 Structural defects
 Reflux
 Incomplete voiding (holding) of urine, children tend to
leave some behind as they are to busy to stay in the
bathroom, encourage double voiding.
 Tight fitting clothing or diapers. Diapers are a nice
warm breading ground for bacteria.
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Treatment of UTI
Bacterial UTI is treated with a 7-10 course of
PO or IV antibiotics.
The most commonly used antibiotics are:
Bactrim/Septra, nitrofurantoin, amoxicillin,
sulfasoxazole, Cefaclor and ampicillin.
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Nursing considerations
 Obtain UA & UC & S before starting
antibiotics.
 Monitor child's response to antibiotics.
 Encourage liberal intake of fluids
 Repeat UA 48-72 hours after antibiotics
have started and 1 week after therapy has
ended.
 Instruct parents on the importance of
completing the complete course of
antibiotics.
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Nursing considerations
 Teach child (age appropriate) to void
frequently.
 Instruct child and parent about proper
cleaning after voiding/stooling (Front-back)
 Instruct about the avoidance of bubble
baths (esp. in girls)
 Encourage the use of cotton underwear
(esp. in girls)
 Teach the child that they should void the
first time the “urge” to void presents, not
wait.
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Vesicouretral Reflux
Urinary reflux is the abnormal retrograde flow of
urine into the ureter (urine goes back up ureter
towards the kidneys).
Reflux itself does not cause UTI but it is associated
with a higher risk of Polynephritis.
With the presence of reflux , infected urine (a
simple UTI or just overgrowth of bacteria) has
direct access to the kidneys, the result is usually
Polynephritis.
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Vesicouretral Reflux
Reflux and recurrent febrile UTI (Polynephritis) can cause
renal scarring.
It is treated in one of two ways:
 Surgery to correct any anatomical defect that might
be causing the reflux
 Low dose prophylaxis with antibiotics, frequent UC &
S (every 2-3 months) and every time the child is
febrile. A yearly VCUG to assess.
Most children will outgrow the reflux within a few years.
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Hypospadias
A congenital defect in which the urethral
opening (urinary meatus) is located
on the underside of the penis. It can
be located at anywhere on the
underside of the penis. Can be
associated with chordee, a band of
tissue that will pull the penis
downward into a curvature.
Occurs in 1:300 boys
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Hypospadias
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Treatment and Nursing considerationsHypospadias.
 Child can not be circumcised at birth as the
foreskin may be used during surgical repair.
Surgery may be done as young as 3 months or
as late as 2 years. Will be done in the infant if
a chordee is present.
 Depending on the severity and exact location
of meatus the surgical procedure can be done
as an outpatient.
 Surgery is successful when the child voids
through the newly constructed urethra.
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Acute Glomerulonephritis
Etiology: an acute inflammation of the
glomerulus. It is not an infection of the kidney,
but the direct result of an antigen-antibody
response to a preceding GABHS infection. It is
commonly preceded by a strep
pharyngitis/tonsillitis 1-2 weeks prior to the
onset of nephritis. (80% of cases) Most
common in the 2-6 year age. But can occur in
any age group. Can be acute or chronic.
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Acute Glomerulonephritis
Pathology: exact mechanism of action is
unknown, it is believed to be an
antibody-antigen type reaction that
stimulates IgG (an antibody ,the major
immunoglobulin found in serum). This
antibody –antigen response creates a
membrane type substance that lodges in
the glomerulus.
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Acute Glomerulonephritis
The glomerulus become edematous and infiltrated
with leucocytes which in turn occlude the
capillary lumen, decreasing the plasma
filtration rate leading to an excessive
accumulation of H2O and retention of Na that
expands interstitial fluid volume and plasma
volume, causing circulatory congestion and
edema. Hypertension is associated with
Glomerulonephritis.
In other words the glomerulus became clogged
and normal plasma filtration cannot occur and
massive edema occurs as fluid is pushed into
the intestinal tissue.
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Clinical Manifestations of
Glomerulonephritis
 Child is in their usual state of good health
until strep infection.
 Has an average 10 day “incubation” period
from the time of the initial strep infection to
the onset of symptoms.
 Initial signs are edema of face, periorbital
edema, anorexia and dark urine.
 Facial edema is more prominent upon
awakening (dependant edema), it then
spreads to the abdomen and extremities
during the day.
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Clinical Manifestations of
Glomerulonephritis
UO is decreased
Urine is cloudy, having the color or tea or cola.
Child is pale, irritable and lethargic
moderate – severe hypertension may be
present.
 The younger child will look ill but seldom have
complaints
 The older child will c/o headache, abdominal
pain
 In all ages groups: vomiting, dysuria, anorexia,
cough and dyspnea due to pulmonary
congestion from fluid retention.
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Laboratory findings
 UA & UC & S
 Proteinuria will be present (1+ - 4+)
 Hematuria
 Presence of RBC’s
 Blood tests
 Elevated BUN
 Creatinine
 Alterations in electrolytes
 Metabolic acidosis
 Decreased Na & Ca
 Increased K+, Ph, albumin
 CBC
 Mild anemia with drop in Hct
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Potential complications
 Deteriorating renal function
 Significant t hypertension
 Significant anemia (most common in
the chronic version)
 Cardiac failure (due to increased
blood volume secondary to retention
of Na & H20 which will cause
pulmonary congestion).
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Treatment
There is no specific treatment for
Glomerulonephritis, treatment is
symptomatic.
 Correction of hypertension, with
diuretics and or Antihypertensives.
 Correction of any electrolyte
imbalances
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Nursing Care of the child with
Acute Glomerulonephritis
 Child can be treated at home if BP and UO is
normal
 The child with significant hypertension, edema,
gross hematuria and oliguria need to be
hospitalized.
 Bed rest is required during the acute phase
 Monitoring for fluid & electrolyte imbalances
 Antihypertensives and diuretic as ordered
 Diet restrictions depend on severity: Na & fluid
intake may be restricted to some extent.
Foods high in K+ are restricted during periods
of oliguria to prevent hyperkalemia. Other wise
child can have a normal diet.
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Nursing Care of the child with
Acute Glomerulonephritis
Strict I & O
Daily weights
Vital signs with BP q4h
Antibiotic therapy in children that show
persistent strep
 Skin care of edematous areas to prevent skin
breakdown.
Almost all children recover quickly, and
reoccurrence is rare. The child will need follow
up visits weekly x 1 month, then monthly for 6
months for routine UA: microscopic hematuria
may persist for months.
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Nephrotic Syndrome (Nephritis)
Etiology:
Idiopathic, increased glomerular membrane
permeability to plasma protein resulting in:
 Proteinuria
 Hypoalbuminemia
 Hyperlipidemia
 Edema
Normally the glomeruli are impermeable to
albumins and other proteins (esp. albumin
which is 60% of the body's protein)
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Nephrotic Syndrome (Nephritis)
Pathphysiology:
Characterized by increased glomerular permeability to plasma
protein, resulting in massive urinary protein loss, this
increased permeability allows albumin to pass into the urine
Tubular reabsorption of Na & H2O is increased, expanding the
intravascular volume. Protein deficiency leads to increased
osmotic pressure allowing fluids to escape into tissue, massive
edema results. Hyperlipidemia is caused by the liver producing
more albumin to compensate for losses by synthesing more
proteins and lipids.
The loss of protein leads to decreased immunoglobulins and
increases susceptibility to infection.
Incidence is slightly higher in girls than boys. It primarily affects
school age children.
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Clinical manifestations in the child with
Nephrotic syndrome
 Previously well child shows increasing
weight gain over a period of days or weeks
 Fluid retention with generalized severe
edema occurs in face, abdomen, genital
area, and extremities (onset of edema can
be gradual or rapid)
 Child becomes anorexic, irritable and
lethargic.
 Child c/o abdominal pain due to abdominal
distension
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Clinical manifestations in the child
with Nephrotic syndrome
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Pallor
Fatigue and activity intolerance
BP is usually normal or lower than normal.
Urine:
 Oliguria
 Dark & frothy
 Contains RBC’s (but no gross hematuria is
present).
 Massive proteinuria
 High SG
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Potential complications of Nephrotic
syndrome
 Hypovolemic shock due to decrease intravascular
volume.
 Hypercoagulability (loss of protein result in the loss of
coagulation proteins) can cause thrombi formation.
 Respiratory compromise (due to fluid retention and
abdominal distension.
 Skin breakdown from massive edema
 Infection (cellulitis, peritonitis, pneumonia, sepsis)
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Laboratory evaluation
UA
 Proteinuria
 Hematuria
Blood tests
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Decreased albumin level
Increased cholesterol level
Increased triglyceride level
Increased Hgb & Hct
Increased platelet count (can be as high as
500,000- 1 million)
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Medical Management
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Corticosteroid use: Prednisone or prednisolone to induce
remission. 2mg/kg/d, response is usually within 7-21 days,
dose will be tapered after 4-8 weeks.
Management of electrolyte imbalance
Protein replacement (either dietary or IV 5% albumin) .
Reduction of edema
 Diuretic therapy must be used with caution to
prevent intravascular depletion, thrombus formation
and electrolyte imbalances
 Dietary restriction of Na
 Pain management
 Prophylactic antibiotic therapy to prevent secondary
infections caused by immunosuppression.
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Medical Management
Nephritis can be either acute or chronic. 2/3 of
children will have a relapse. The chronic
disease process is characterized by long
term remissions and exacerbation, about
80% of children will eventually recover
completely.
For those children in who steroids fail to
produce remission, they will be treated with
immunosuppressant therapy, relapses are
treated with high dose steroids
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Nursing Interventions –
Nephrotic Syndrome
 Assess for respiratory distress :pulmonary edema
 Assess for signs of hypokalemia: (arrhythmias, flat T
waves, wide QRS, increased PR interval, decreased HR,
hypotension.
 Assess for signs of decreased cardiac function :
hypotension, hypertension, CHF.
 Assess for signs of hypo/hyponatremia due to diuretic
use:
Hyponatremia:
 CNS: lethargy, weakness, apathy, dizziness,
seizures, encephalopathy.
 CV: hypotension
Hypernatremia:
 CNS: disorientation, muscle twitching.
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Nursing Interventions –
Nephrotic Syndrome
 Assess for signs of infection: fever, cellulitis (from skin
breakdown), peritonitis (red, tender abdomen),
increased WBC
 Assess for pain and comfort level
 Parental and patient support
 Daily weights, strict I & O
 Activity is not restricted unless edema is extensive,
ambulation should be encouraged
 Diet: low salt during period of generalized edema,
fluid restriction if edema is massive.
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Wilm’s Tumor
(Nephroblastoma)
A intrarenal tumor. It is the most common
malignant abdominal tumor of childhood.
The tumor is separated from the kidney by
a membranous capsule. It is a rapidly
developing tumor.
This capsule encloses the tumor, palpation of
the tumor can cause the capsule to rupture
disseminating cancer cells.
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Wilm’s Tumor
Prognosis for long term survival depends on stage at time
of diagnosis, tumor cell markings and presence of
metastasis (lungs, liver, other kidney). Over 75% of
children have a 5 year survival rate.
Most frequently seen between the age of 2-5 years, peak
incidence at 3-4 years, rarely seen after the age of 7.
There is a slightly higher incidence in boys.
A small portion of Wilm’s tumors show a genetic basis.
Almost exclusively unilateral, however can be bilateral :
this is a very poor prognostic indicator.
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Laboratory Tests/ Diagnostic
criteria for Wilm’s tumor
Abdominal x ray
Ultrasound
CT
MRI
IVP
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Clinical manifestation
 Usually asymptomatic in early stages
 Almost exclusively diagnosed after
history from the mother/ guardian
noting a mass while bathing the child
located to one side of the abdomen.
 Pain and hematuria may be present in
some children.
 Hypertension may be present (25%)
due to increase in renin production.
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 Sign over bed “No abdominal
palpation”.
 Allergy alert bracelet & sign on chart,
cardex stating “No abdominal
palpation”.
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Treatment
 Nephrectomy to remove tumor and
kidney, usually is done within 24-48
hours after diagnosis.
 Follow up with chemotherapy for all
children.
 Bone marrow aspiration to rule out
metastasis.
 If bilateral, a partial Nephrectomy
may be done to the least affected
side .
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Renal System
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Abdominal anatomy
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Renal anatomy
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Renal anatomy
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Nephrons
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Urinary tract Obstruction
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