Antibiotics (but no prophylactic abx) – NO macrobid prophylaxis NEED To see how frequent UTI in kids to ID underlying problem Acetaminophen or Ibuprofen Avoid Pyridium – numbs bladder & takes away pain Don’t want to mas sx of UTI, not good historians Don’t know if they’re getting better or worse Consider possibility of anatomical defects – esp if frequent Avoid foleys Avoid bubble baths and harsh soaps Drying & lead to cracking & irritation of perineum UTIs Urinanalysis (UA) o Can obtain with or without culture Pinpoint Abx that will work Without Culture: Which of the following symptoms are more common in children with UTIs than adults with UTIs? Fever and abdominal pain Dysuria and urgency Hematuria and burning on urination Abdominal pain and HA
UTI: Determining if there is a bigger problem Voiding Cystourethrogram (VCUG) Use of fluoroscopy (real time/video x-rays) to visualize flow of contrast/urine through the urinary tract Into blader, up ureters, up to kidneys & will flow back out – watch flow & rate Looking for structural defects that might inhibit the flow of urine (vesicoureteral reflux) Vesicoureteral Reflux (VUR) Backflow of urine from the bladder into the ureters/kidneys Unilateral or bilateral Caused by a structural defect somewhere in the urinary tract Leads to frequent UTIs and hydronephrosis Hydronephrosis : distention and dilation of the kidney o Change shape of renal penvis nooks & crannies pools urine & stasis Treatment for VUR varies depending on severity: o Mild case: Prophylactic abx o Severe: Surgical management Renal System: Review Functions: o Remove waste products from the body Filters blood & waste comes out as urine o Balance fluid levels Dehydrated – retain more fluid Over = pee a lot o Release hormones that regulate BP (reinin) Abnormal BP as result of renin disturbance o Produce the active form of vitamin D o Stimulate RBC production (erythropoietin) Nephrotic Syndrome
Clinical state characterized by massive proteinuria , hypoalbuminemia, edema, hyperlipidemia, and altered immunity Can be due to primary or secondary cause Primary: “ Minimal Change Nephrotic Syndrome ”, Congenital Defects to the glomeruli o Min change – look at kidney – glomerulus looks MINIMALLY different surface o In depth look with electron microscope -minimal changes at glomerular level Secondary: Lupus, Diabetes, CHF, idiopathic, autoimmune, etc. Patho: o Loss of protein through the kidneys ( proteinuria ) Filters aren’t as good, protein gets through into filtrate – massive proteinuria o Decreased protein in the blood ( hypoalbuminemia ) o Disruption in the oncotic pressure o Water drawn into interstitial space ( edema ) Nephrotic Syndrome: Hyperlipidemia ?
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- Spring '17