GU Flashcards
urinary system
maintains balance
hormonal fxns:
stimulation of production of erythropoietin
production of renin (BP regulation)
metabolism of vitamin D to its active form (calcium metabolism)
excretes waste
functionally immature until puberty
pediatric differences in GU sx
kidney- larger in relation to stomach- prone to injury
urethra- shorter- risk for bacteria into bladder (UTI)
GFR- slower in infant; risk for dehydration
bladder capacity- 30ml in newborn; increases to adult size by 1 yr
reproductive organs- immature at birth until adolescence
review of urinary A&P
glomerular filtration- process of filtering blood as it flows through kidneys
tubular resorption- necessary fluids, electrolytes, proteins & blood cells are retained
tubular secretion- waste products & fluids filtered out
urinary system
for kidneys to function effectively, following conditions need to be present: unimpaired renal blood flow adequate GFR normal tubular function unobstructed urine flow
significant data when assessing PMHX for GU disorders
PMHX- maternal polyhydramnios, oligohydramnios, diabetes, HTN, alcohol/ cocaine ingestion
neonatal hx- presence of single umbilical artery, abdominal mass, chromosome abnormality, congenital malformation
family hx- renal disease/ uropathology, chronic UTIs, renal calculi, hx of parental enuresis
structural defects- misc disorders/ anomalies of GU tract
bladder extrophy- extrusion of bladder outside of body
hydrocele- painless swelling of scrotum d/t collection of fluid
phimosis- inability to retract prepuce @ an age when it should retract (3 yo)
testicular torsion- rotation of testicle that interrupts its blood supply
at risk of losing testicle
bladder extrophy
rare congenital defect
etiology- failure of abdominal wall to close during fetal development- leads to eversion of bladder
treatment- surgical reconstruction in several stages
nursing care- cover w/ wet sterile gauze post-delivery, prepare for surgery
urinary/ renal disorders
structural disorders: hypospadias/ epispadias bladder extrophy obstructive uropathy hydronephrosis vesicoureteral reflux enuresis- continued incontinence of urine past age of toilet training
hypospadias/ epispadias
congenital anomalies involving abnormal location of urethral meatus
result from failure of urethra folds to fuse completely over urethral groove
familial tendency but exact mechanism unknown
hypospadias often in conjunction w/ congenital inguinal hernias, undescended testes, chordee (more common than epispadias)
epispadias often occurs w/ bladder extrophy
hypospadias vs epispadias
hypospadias- urethral meatus may be located anywhere along course of ventral surface of penile shaft
epispadias- meatal opening is located on dorsal surface of penile shaft, & may be at level of bladder neck
hydronephrosis
obstruction of ureteropelvic junction/ other parts of ureter causes dilation of kidney
pelvis & calyces of kidney are dilated
can occur as congenital defect, result of obstructive uropathy/ secondary to VUR
hydronephrosis
accumulation of urine in renal pelvis as result of obstructed outflow, & compromises kidney function
most children w/ hydronephrosis are born w/ condition, but can develop during childhood. it is most common urinary tract anomaly & ranges in severity
in mild hydronephrosis, pelvic dilation is barely noticeable, whereas in severe hydronephrosis swelling occupies much of abdomen
hydronephrosis
mild-moderate cases- may be no s/sx & condition can resolve w/in 1st yr of life
abdominal mass
s/sx similar to UTIs
can be assoc w/ VUR
in more severe cases, when kidney fxn is affected, infant/ child can experience pain, bleeding, & infections
tx= surgery to correct blockage
vesicoureteral reflux
VUR results in backflow or urine from bladder into kidneys
valvelike mechanism @ junction of ureter & bladder prevents urine reflux into ureters; when there is defect of vesicoureteral junction= VUR results
prevents complete emptying & creates reservoir for bacterial growth
VUR
most children w/ symptomatic UTIs have VUR
diagnosis:
renal US
VCUG- voiding cystourethorogram- x-ray exam of bladder & lower urinary tract that uses fluoroscopy & contrast material
complications- reflux of infected urine can cause pylonephritis
*similar to GER
disorders affecting urinary elimination
UTIs- most common GU disorder of children
enuresis- inability to control urination
UTI
microbial invasion of kidneys, ureters, bladder, urethra
neonatal period- UTIs occur most commonly in males, possibly bc of higher incidence of congenital abnormalities
by age 4 mos- UTIs are more common in females bc of placement & size of urethra
causes:
incomplete bladder emptying
irritation by bubble baths
poor hygiene
VUR
urinary tract obstruction
pathophysiology:
bacteria enter urethra & ascend urinary tract
e. coli causes 75-90% of UTIs in females
UTI
other s/sx: V/D irritability poor PO intake malodorous urine oliguria constipation *most common clinical presentation in child <2= FEVER complications: risk of renal failure UTI <1 delay in diagnosis anatomic/ neurologic obstruction recurrent episodes of upper UTI clinical findings: abdominal pain enuresis frequency/ urgency pain/ burning w/ urination (dysuria) hematuria lethargy/ irritability poor feeding patterns cloudy, foul-smelling urine \+/- blood, positive nitrites, positive leukocyte esterase
enuresis
repeated involuntary voiding by child who has reached age where bladder control is expected (5-6yo)
nocturnal= more common in boys
diurnal= more common in girls
primary, intermittent, secondary
enuresis
primary- child has never had dry night; attributed to maturational delay & small functional bladder
intermittent- child has occasional nights/ periods of dryness
secondary- child begins bedwetting who has been reliably dry for 6-12 mos; assoc w/ stress, infections, sleep disorders
clinical manifestations for diurnal:
frequency
urgency
constant dribbling
involuntary loss of control after voiding
nocturnal:
bedwetting
enuresis
thorough hx is obtained
clinical therapy:
multitreatment approach
limit drinks before bedtime, void just before bed
1/3 of nocturnal treated w/ meds:
imipramine hydrochloride (tricyclic antidepressant)
desmopressin acetate (DDAVP)- antidiuretic effect
meds not recc for <6 yo
behavioral interventions (more common than meds)- fluid intake programs, bladder alarms, bladder training
enuresis
nursing management:
thorough hx:
what interventions have already been tried, describe voiding/ bowel elimination patterns, whether enuresis is primary/ secondary, whether child is concerned/ any evidence of sexual abuse
evaluated if parent/ child are equally motivated to resolve problem
teaching
urinary/ renal disorders
acquired disorders that result in altered renal fxn:
nephrotic syndrome
acute glomerulonephritis
hemolytic-uremic syndrome
nephrotic syndrome
kidneys lose significant amount of protein in urine, resulting in low blood levels of protein
not specific disease, but clinical state characterized by:
proteinuria
hypoalbuminemia
hyperlipidemia (compensatory mechanism for liver to secrete fats)
edema
nephrotic syndrome
classified as primary/ secondary
MCNS results from disorder w/in glomerulus
if nephrons allow increased protein to escape from blood, leads to edema/ hypoalbuminemia
glomerular injury–> protein leakage into urinary space–> plasma volume down, CO down–> stimulation of RAAS–> sodium & H2O rentention–> expansion of sodium space–> edema
nephrotic syndrome
primary occurs predominantly in preschool children incidence peaks btwn 2-3 yrs syndrom rare after age 8 more common in boys some forms may progress to ESRD characteristic s/sx include: edema/ weight gain excessive clotting factors hyperlipidemia low serum sodium
nephrotic syndrome
clinical manifestations by body system:
renal- oliguria; dark, frothy urine
CV- normotensive; HTN later
vascular- thrombosis
GI- anorexia, abd pain, N/V/D
skin- pallor, shiny w/ prominent veins, brittle hair, edema, skin breakdown
pulmonary- resp distress & pulmonary congestion
diagnostic tests:
UA- severe proteinuria (primary indicator), hematuria & casts; elevated spec gray bc of proteinuria
renal biopsy- identifies type of nephrotic syndrome child has, & can be used to monitor response to medical management
blood studies show serum creatanine, BUN, cholesterol
nephrotic syndrome
treatment depends on cause of disease, may include:
corticosteroids (PREDNISONE)- reduce swelling/ excretion of protein in urine; take RX x 6 wks, then taper
diuretics- help w/ swelling
ace inhibitors
antithromboltiics- hyperlipidemia
NSAIDs
nephrotic syndrome discharge planning
parents need to monitor protein in urine daily using dipsticks
understand that relapses do occur
no added salt diet
monitor daily weight
no s/sx of disease for 2 yrs= disease free
APSGN (acute poststrep glomerulonephritis)
most often response to GABHS infection of skin/ pharynx
other organisms- staph, pneumococcus, coxsackievirus
abx are for strep infection, not APSGN
body responds to strep bacteria by forming antibodies, which combine w/ bacterial antigens to form antigen-antibody complexes–> these get trapped in glomerulus & cause inflammatory response
APSGN
highest in ages 2-12 more common during winter/ spring months child typically has recent respiratory infection (w/in 1-2 wks)/ strep/ impetigo; recovers, then develops after 8-14 days clinical manifestations: abrupt onset of abdominal pain irritability microscopic hematuria (most all cases) acute HTN nonspecific s/sx: include general malaise, weakness, anorexia
APSGN
clinical manifestations:
dark urine (brown, tea, cola colored)- OFTEN 1ST CLINICAL S/SX
dark urine caused by hemolysis of RBC that have penetrated glomerular basement membrane & passed into tubular system
periorbital edema/ dependent edema- onset of puffiness of face/ eyelids is sudden; usually prominent upon awakening
in some cases- generalized edema & other features of circulatory congestion, such as dyspnea, may be present
edema is result of defect in renal excretion of salt & water, can result in acute HTN- HIGH STROKE RISK
APSGN lab findings
hematuria proteinuria leukocytes decreased serum protein anemia ESR increased serum IgG antibodies against strep + circulatory overload causing EKG changes
APSGN nursing care
VS, especially BP
F&E’s w/ strict I&O’s, specific gravity
daily weights
urine dipstick for +hematuria, + proteinuria
assess edema (periorbital, dependent)
measure abdominal girth
auscultate heart/ lung sounds, not respiratory effort
monitor neurologic signs secondary to HTN (LOC, HA, sz activity, vomiting)
glomerulonephritis vs/ nephrotic syndrome
APSGN:
manifestations- hematuria, edema, school age, HTN
management- supportive, antihypertensives, low Na+ diet
NS:
manifestations- proteinuria, edema (insidious onset, large amount), hypovolemia, normotensive (until later stages), pallor, fatigue, toddler
management- prednisone to initiate remission
diuretics, possible abx, possible albumin, no salt diet
hemolytic uremic syndrome (HUS)
3 features: hemolytic anemia thrombocytopenia ARF features an antecedent diarrheal illness e. coli--> majority of cases 6 mos- 4 yrs
causes of HUS
antecedent diarrheal illness idiopathic inherited drug related assoc w/ malignancies transplantation malignant HTN tx: maintaining acid/ base balance, controlling HTN, & maintaining fluid balance supportive therapy
dialysis
peritoneal dialysis- preferred method for children
abdominal cavity acts as semipermeable membrane for filtration
can be managed at home in some cases
warmed solution enters peritoneal cavity by gravity, remains for time before removal
hemodialysis
requires creation of vascular access & special dialysis equipment
best suited for children who can be brought to facility 3x/ week for 4-6 hrs
achieves rapid correction of fluid & electrolyte abnormalities
