Pedi GU Flashcards
Kidney damage; result of increased glomerular membrane permeability leads to too much protien (albumin) in urine and decreased albumin in bloodstream leading to decreased osmotic pressure then fluid shifts into interstitial tissues leading to edema. Decreased blood volume in vascular space leads to kidneys conserving Na+ and H20 causing edema. Loss of proteins in bloodstream causes liver to produce more lipoproteins which causes hyperlipidemia.
Congenital (inherited genetic defect), secondary (known cause: disease, meds, toxins), primary (idiopathic, 3 kinds: 85% “minimal change”)
S/s age 2-3 years: generalized edema; irritability, malaise, decreased urine output, resp distress?
Nephrotic Syndrome
Treatment: Reduce edema, decrease proteinuria: Corticosteroids (prednisone); diuretics (Lasix), immunosuppressants, antihypertensives
Interventions: Monitor BP, urine output, lytes, skin; Meds/side effects, supportive care, improve nutrition
Nephrotic Syndrome Treatment and Nursing Interventions
Inflammation and cellular proliferation of the glomeruli not caused by direct infection of kidneys. most common: follows exposure to Group A beta-hemolytic streptococcus. Impaired capillary perfusion, reduced glomerular filtration leads to water and Na+ retention (edema). Children 4-12y; s/s develop 1-2 weeks after pharyngitis.
S/s: gross hematuria, edema, hypertension - can progress to encephalopathy.
No specific treatment, manage hypertension, maintain fluid volume (anti-hypertensives and diuretics)
Nursing: monitor fluid status, lytes (? restrict Na+, K+, protein), skin (bedrest), infection; support
Acute Glomerulonephritis
One of the main causes of Acute Kidney Injury (AKI) in children. Triad: microangiopathic hemolytic anemia, thrombocytopenia, and AKI/acute renal failure (ARF). Typical - diarrhea episode (90%), shiga toxin or veotoxins (vs. atypical). E coli, s pneumoniae, shigella dysenteriae; contaminated food, swimming. Approximately 2-3 in 100,000; peaj 6 mos - 4 years.
S.s Following gastroenteritis: sudden pallor, weak/lethargic; vomiting, abdominal pain, anorexia, ascites
Hemolytic Uremic Syndrome (HUS)
Labs confirm triad- low Hgb and PLTs, high LDH, BUN/Cr; Supportive care - treat htn, anemia (blood); dialysis if anuric/seizures (same as care for ARF)
Hemolytic Uremic Syndrome Nursing Interventions
Kidneys cannot concentrate urine and remove waste; can lead to toxicity/death
Acute- sudden onset (develops over days-weeks), may be reversible
Prerenal AKI- hypovolemia/dehydration/surgical shock/sepsis
Chronic (CKD)- gradual, develops over months-years, permanent and irreversible leads to dialysis or transplant.
S/s: Azotemia (Accumulation of nitrogenous waste in blood), oliguria/anuria (very little (dark) or no urine output), electrolyte abnormalities, low Na+, high K+, low Ca+, high phos.
Treatment: Depends on underlying cause; ICU level care.
Interventions: sz? F+E balance, BP, I & O; dialysis (method?), med dosing, compromised immunity, diet restrictions; missed school/development
Renal Failure
Provoke urine output (chronic: diuretics for hypertension)
Mannitol and Lasix
Calcium gluconate and Na+ Bicarb
Reduce blood K+ levels; alleviate acidosis
Reduce blood K+ levels by moving K+ and glucose into cells
Glucose and Insulin
Labetolol or Nipride and Hydralazine
Drugs that manage hypertension for the GU system:
Treats anemia
Folic acid, RBC’s
Peritoneal, hemo-, Continuous Renal Replacement Therapy (CRRT) or Continuous Veno-Venous Hemofiltration (CVVH)
In center vs at home
fluid shifts, BP, lytes
Dialysis
Administer and manage meds- consider nephrotoxicity Renal dosing- prevent further damage Maintain adequate hydration Maintain normal F and E balance Meet nutritional requirements Prevent infection Promote bladder emptying Promote pain relief/emptying Promote healing/prevent skin breakdown Provide emotional and psychosocial support
GU Nursing Interventions
