peds44 Flashcards
repletion phase for hyponatremic or isonatremic dehydration
replace fluids over 24 hours
repletion phase for hypernatremic dehydration
replace more slowly over 48 hours to minimize risk of cerebral edema
oral rehydration salt salotions
balanced mixtures of glucose and electrolytes (since glu co-transport still works in secretroy diarhhea, whereas other pways of Na absorption are impaired)
when is ORT inapprop
severe life-threatening dehydration, paralytic ileus, or GI obstruction, patients with extremely fast stool losses or repeated severe emesis losses
microscopic hematuria
greater than 6 RBCs per HPF, detected on 3 or more consec samples
urinary dipstick for hamturia
detects hemoglobin or myoglobin in the urine
false neg on urine dipstick for hematuria
vit C ingestion
RBC casts
glomerular bleeding (acute or active glomerulonephritis)
dymorphic RBCs
originating in the glomerulus, ofetn have blebs
RBCs that look normal
originate in the lower urinary tract
large numbers of RBCs (esp in the presence of dysuria)
may indicate acute hemorrhagic cystitis (due to bacterial or viral infection or chemotherapeutic agents like cyclophosphamide)
proteinuria
more than 100 mg/m2/day
how to screen for proteinuria
urine dipstick; it detects albumin
false pos on urine dipstick for protein
if urine is very concentrated (sg>1.025) or alkaline (pH > y) or If patient received certain meds (peniccilin, aspirin, oral hypoglycemic agents)
false neg on urine dipstcik for protein
if the urine is very dilute
most accurate way to detect proteinuria
24 hour protein collection ; normal Is less than 100 mg/m2
random spot urine
protein to creatinine ratio; early morning sample is ideal;
normal urine TP/CR for 6-24 months
<0.5
normal urine TP/CR for > 2 years is <0.2
right
benign transient proteinuria
may be associated with vigorous exercise, fever, dehydration, and CHF
wht if dipstick is pos for blood but no rbcs on microscopic U/A
hemoglobinuria or myoglobinura
RBC casts
glomerulonephritis; if no casts, can be glomerular or lower urinary source
examples of tubular proteinuria
interstitial nephritis, ischemic renal injury (ATN), and tubular damage due to nephrotoxic drugs
marker for tubular proteinuria (as opposed to glomberular)
urinary B2 microglobulin
glucosuria and aminoaciduria
accompany tubular proteinuria
nephritic syndrome
gross hematuria, htn, fluid overload from renal insuff
most common form of acute glomerulonephritis in school aged kids
psotstrep glomerulonephritis; but rare before age 2
when does post strep glomerulonephritis develop relative to infection
8-14 days after infection of skin or pharynx with group A beta hemolytic strep
low serum complement (C3)
transient in post-strep GN
prognosis of post strep GN
usually normalizes in 6-8 weeks; severe renal failure is rare
diagnosis of poststrep GN
ASO titer, ADB titer
bx in post-strep gn?
not typically indicated but if you were to do it, youd see mesangial cell proliferation
does antibiotic tx of strep reduce the risk of post strep GN?
no, but it does reduce the risk of rheumatic fever
bergers diseaes
aka IgA nephopathy
most common type of chronc glomerulonephritis world wide
bergers disease
when does bergers disease usually present?
second or third decade of life
bergers diseae more common in what races?
asia, australian, and in native americans; rare in african american
clinical features of bergers
recurrent bouts of hematuria assoc with resp infections
diagnosis of iga nephropathy (bergers)
renal biopsy shows mesangial prolif and incr mesangial matrix
treatment for iga nephropathy
mainly supportive; meds only recommended for patients with associated pathologic proteinuria or renal insuff
henoch-schonlein purpura nephritis
igA mediated vasculitis with palpable purpura on the butt and thigh, abdominal pain, arthritis and hematuria
prognosis
in majority of patients, the renal featurs of HSP are self-limited with recovery in 3 months; 1 to 5% develop chronic renal failure
membranoproliferative glomerulonephritis
mesangial hypercellularity and thickened glomerular basement membrane
prognosis for membranoproliferative glomerulonephritis
variable, but most patients ultimately develop end stage renal disease
managmeent of membranoproliferative glomerulonephritis
some patients repsond to steroids; ace inhib may slow progression
membraneous nephropahty
more common in young kids; heavy proteinuria and often progresses to renal insuff
most common cause of nephrotic syndrome in the US
membraneous nephopathy
nephrotic syndrome characterisitics
heavy proteinuria (>50 mg/kg/day), hypoalbuminemia, hypercholesterolemia, and edema
when does nephrotic syndrome present?
2/3 present before 5 years
types of nephrotic syndrome
primary (most common), NS that results from other primary glomerular diseases; NS that results from systemic diseases
most common cause of primary NS
minimal change disease
systemic diseases that can cause NS
SLE and HSP
