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Notes overviewing various pediatric conditions in the GU system
Typology: Study notes
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PEDS Unit 5 GU Genitourinary Dysfunction in the Pediatric Population Anatomy and Physiology The pediatric genitourinary (GU) system includes the kidneys, renal arteries, renal veins, ureters, bladder, urethra, and internal and external genitalia. Kidney development begins around 3 weeks after conception and continues until about 36 weeks of gestation. Urine production starts around week 10 of gestation. Kidneys are fully functional at birth but not very efficient. Glomerular filtration rate (GFR) typically reaches adult levels by age two. Kidney Function Kidneys play a vital role in maintaining fluid and electrolyte balance. They regulate blood pressure and hormone levels. They filter wastes from the bloodstream. Nephrons are the functional units responsible for the filtration process. Filtration occurs in the glomerulus within the Bowman's capsule. This process allows waste, electrolytes, and water to filter out while retaining proteins and blood cells. During tubular reabsorption , essential electrolytes and water are reabsorbed into the bloodstream. Tubular secretion involves removing excess water, electrolytes, creatinine, and urea into the collecting vessels. Urine travels through the urinary tract and is secreted from the body. Issues can occur at different locations: Pre-renal, Intra-renal, Post- renal. Awareness of the location can influence presentation and symptoms. Assessing the Kidneys Methods include physical examination , history taking , observation of symptoms , and labs, radiology, or other evaluation methods. Infection and Inflammation
PEDS Unit 5 GU Urinary Tract Infection (UTI) : Infections of either the upper or lower urinary tract. o Common in children and can affect any part of the urinary tract. o Bacteria is often the culprit, most commonly E. coli from feces. o Bacteria enters the urinary stream via the urethra. o Urinary stasis (urine remaining in the bladder after voiding) is the single most important post-factor influencing UTI occurrence. o Structural or behavioral issues can lead to urine retention, increasing infection risk. o Untreated cystitis can ascend to the kidneys, becoming pyelonephritis , potentially leading to urosepsis and kidney damage. Bacteriuria : Presence of bacteria in the urine; clinically significant and requires treatment when symptoms are present. Types of UTIs: o Acute : A single episode. o Recurrent : Multiple episodes, may prompt investigation for anatomical anomalies. o Persistent : Bacteriuria that does not resolve with antibiotic therapy. Pyelonephritis : Kidney infection resulting from bacteria ascending from the bladder. Cystitis : Inflammation of the bladder. Urethritis : Inflammation of the urethra. Risk Factors for UTI : Age, bladder and bowel dysfunction, congenital alterations of the urinary tract, recent GU surgery, frequent catheterizations, status of circumcision in males (uncircumcised males have higher risk). Recurrence risk is increased within the first 6-12 months of an initial UTI. Clinical presentation varies by age and can be vague in infants. Common symptoms include fever, lower back pain, abdominal pain, cloudy or discolored urine, pain with urination, frequency, and sometimes vomiting. Recurring UTIs can be associated with inadequate fluid intake, constipation, infrequent urination, or functional voiding. Missed or untreated UTIs can lead to renal scarring, reduced kidney function, and systemic infection. Prevention of recurrent UTI is crucial. Diagnostic Evaluation of UTIs
PEDS Unit 5 GU Results in water and sodium retention, reduced urine output, and edema. Etiology is often unknown. An acute GN may be primary or a manifestation of a systemic disorder. Commonly associated with post-infectious complications , particularly from Group A Strep, pneumococcal, or viral infections. A history of strep bacterial skin or throat infection is the primary risk factor. Pediatric GN is rare but a significant cause of chronic kidney disease in children. More common in school-age children (around 6-7 years) and twice as likely in males. Usually self-limiting, with recovery typically within one to two weeks. Clinical Presentation : Oliguria , hematuria , dark-colored urine, hypertension , pallor, facial edema. Proteinuria is common. Loss of appetite is frequent. Lab Testing : o Urinalysis : Typically shows hematuria and proteinuria. May include a 24-hour urine collection to assess protein excretion. o Blood tests : CBC (often normal), CMP (decreased GFR, elevated BUN and creatinine), lipid panel (typically normal unless nephrotic syndrome is present), sometimes antibody titers. Diagnostic Studies/Imaging : Kidney biopsy, kidney ultrasound, other imaging may be considered for etiology if no response to initial treatment. Imaging is generally deferred otherwise. Treatment : Supportive care focuses on normalizing fluid and electrolyte balance and preventing complications. o Reduction of sodium intake and sometimes fluid restriction. o Close monitoring of I/O and daily weights. o Diuretics and antihypertensives for fluid/electrolyte imbalances. o Antibiotics (like penicillin) if an active strep infection is present. o Medications. Nephrotic Syndrome (NS) A type of glomerular disease characterized by increased protein permeability in the glomerular basement membranes. Key features: Proteinuria (massive urinary protein loss), Hypoalbuminemia (low serum albumin), Hyperlipidemia , and Edema. Pathophysiology :
PEDS Unit 5 GU o Normally, the glomerular membrane is impermeable to large proteins. o In NS, it becomes permeable to proteins, especially albumin. o Albumin is lost in the urine (leading to hyperalbuminuria on urinalysis, but low serum albumin). o Decreased serum albumin causes fluid to shift from plasma to interstitial spaces, leading to edema and ascites. o Hypoalbuminemia activates the Renin-Angiotensin-Aldosterone System (RAAS), increasing ADH and aldosterone secretion, enhancing tubular reabsorption of water and sodium. No routine screening. Most cases are idiopathic. Commonly affects children ages 2-6, more prevalent in males. Relapse is common in pediatric patients. Risk factors include family history or vesicoureteral reflux. Clinical Presentation : Fatigue, frothy/foamy urine (due to protein), hematuria. Significant edema (face, eyes, abdomen) is a hallmark. Anorexia or weight gain due to fluid retention. Labs for NS : o Urinalysis : Proteinuria (+2 on dipstick). Hyaline casts, oval fat bodies, few red blood cells. Typically shows massive proteinuria, hematuria, glucosuria, lipiduria, and fatty acids. o 24-hour urine collection : Measures urine protein and protein to creatinine ratio. o Blood tests : Low serum protein, low albumin. Hematocrit normal or elevated (due to hemoconcentration). Platelet counts may be elevated. Serum sodium concentration may be low. CMP usually reveals normal GFR but increased BUN and creatinine. Serum lipids are elevated. Patient can potentially have hypoglycemia. Diagnostic Studies : Renal ultrasound, CT scan, or MRI may be ordered if no response to initial treatment. A renal biopsy may be indicated only if NS is unresponsive to steroid therapy, to find other causes than idiopathic. Biopsies show damage to epithelial cells. Complications : If untreated, can result in serious complications like infection, blood clots, and kidney failure. Therapeutic Management Objectives :
PEDS Unit 5 GU Labs/Diagnostics : o Blood work. o Imaging studies (PET scans). o Definitive diagnosis : Biopsy, but delayed in Wilms' tumor to prevent tumor rupture and spread. o Anemia is usually secondary to hemorrhage within the tumor. o Hypertension can be caused by secretion of excess renin by the tumor (connecting to the RAAS system). Staging : Two main systems: Children's Oncology Group (COG) and European Group (SIOP). COG (stages 1-5) is primarily used. Staging determined by imaging and pathology findings post-nephrectomy. Prognosis : Depends on tumor histology, stage, molecular features, and age. Five-year survival rate is about 90%. Tumor rupture during surgery affects prognosis. Treatment : Typically involves nephrectomy (surgical removal of the kidney) followed by chemotherapy and radiation. Staging occurs post-nephrectomy. Vesicoureteral Reflux (VUR) Retrograde flow of urine from the bladder into the upper urinary tract.
lower UTI occurs. Classified by degree of reflux, graded I to V , with higher grades associated with increased renal abnormalities and damage. Primary VUR : Congenital, due to abnormal insertion of ureters into the bladder. Secondary VUR : Acquired condition. If a child with reflux develops pyelonephritis, they become very symptomatic (fever, vomiting, chills) quickly. Urine cultures are not typically recommended routinely for patients with reflux but should be obtained if the child becomes symptomatic. Management: o Conservative measures : Wait and see if the child grows out of it. o Surgical interventions : May be done by age 6 for children who don't grow out of it or are at higher risk for renal scarring. Surgery aims to correct the anatomy. Prognosis : Can lead to renal scarring.
PEDS Unit 5 GU Enuresis (Bedwetting) Inappropriate urination, usually at night, but can be during the day. Definition: Occurs at least twice a week for at least 3 consecutive months. May involve regression during times of stress. Evaluate in children of chronological/developmental age at least 5 years to rule out other medical conditions. Primary Enuresis : Child has never been free of bedwetting for any extended period. Secondary Enuresis : Child develops bedwetting after having urinary control. Risk Factors : Family history, twin siblings, bladder dysfunction disorders, being male (more common), emotional events (new sibling, divorce, abuse), behavioral disorders. Nursing Care : o Teach child/parents to urinate prior to bedtime. o Restrict fluids about two hours before bed. o Avoid caffeine in the afternoon/evening (caffeine is a diuretic). o Use positive reinforcement instead of punishing. o Encourage keeping a calendar of wet/dry days. o Child can assist with linen/clothing changes. o Wake child at scheduled intervals during the night to void. o Avoid constipation. o Take medications as prescribed. Medications : o Antidiuretic (like desmopressin acetate or vasopressin): Reduces urine volume. Usually given as a nasal spray at bedtime. Treatment typically 4-6 months with tapering. Teach to avoid sun exposure and monitor for increased suicidal ideations (this seems like important safety information from source, though the suicidal ideation link is unexpected for this medication type based on outside knowledge; relying strictly on source info here). o Anticholinergics (like oxybutynin): Reduce bladder contractions. Side effects include dry mouth and constipation. Alterations in the GU Tract (Congenital Anomalies - CAKUT)
PEDS Unit 5 GU Acute Kidney Injury (AKI) Rapid onset. Potentially reversible damage. Rare in general pediatrics but more common in hospitalized children. Sudden decreased urine output is a key symptom. Can disrupt acid-base balance, electrolyte/fluid excretion or retention, affecting all body systems. Nephron damage may be reversible or lead to irreplaceable cell death. Often precipitated by an acute event. Causes: o Pre-renal : Decreased blood flow to the kidneys (dehydration, shock, sepsis). o Intra-renal : Direct kidney trauma, hydronephrosis, infections, inflammatory processes, toxic medications. o Post-renal : Obstructive disorders, bladder dysfunction. Treatment: Aims to address the underlying cause and manage complications. Focus on fluid/electrolyte balance. May require ICU management to avoid fluid overload. Diuretics used cautiously. Monitor blood pressure frequently, use antihypertensives as indicated. Hyperkalemia treated with dietary restriction of potassium-rich foods, insulin, and resins. Poses immediate life-threatening risks. Chronic Kidney Disease (CKD) Progressive , non-reversible loss of kidney function. Can follow previous AKI. Often linked to congenital conditions (CAKUT). Gradual onset. Risk factors: Congenital anomalies, inherited conditions, recurrent infections (like UTIs), nephrotic syndrome, glomerulonephritis. Symptoms: Develop slower than AKI. Swelling (edema), decreased urinary output, protein/blood in urine, decreased appetite, fatigue, hypertension, vomiting, shortness of breath, delayed growth, anemia, bone pain, itchy skin. Treatment: Varies based on kidney function levels. Aims to delay further disease progression. Support growth and development. o Medications: ACE inhibitors, vitamin D. o Dietary therapy: Monitoring protein, sodium, potassium, and fluid intakes.
PEDS Unit 5 GU o Advanced CKD may require dialysis or kidney transplant. Leads to long-term developmental challenges. AKI vs CKD Summary Onset : AKI is rapid, CKD is gradual. Reversibility : AKI potentially reversible, CKD non-reversible. Prevalence : AKI rare in general peds but more common in hospitalized, CKD linked to congenital conditions. Risk : AKI has immediate life-threatening risks, CKD leads to long-term developmental challenges. Renal Function Studies Labs : Essential for assessing renal function. Include CBC, CMP, UA, Creatinine, GFR, BUN, Urine Culture & Sensitivity. o High creatinine levels indicate reduced kidney function. o GFR measures filtration efficiency. o Urine protein to creatinine ratio assesses protein excretion. Imaging : Abdominal Xray, Renal Ultrasound, Nuclear Medicine Studies evaluate potential urinary tract blockages. Treatment based on findings: AKI treatment addresses the underlying cause. CKD treatment varies based on function level. Nursing Considerations for AKI/CKD Both AKI and CKD have profound effects on growth, development, and family dynamics.