Genitourinary Flashcards
signs of renal disease in utero
- oligohyramnios
- polyhydramnios
- intrauterine growth retardation
oligohydramnios
reduced urine production
polyhydramnios
reduced swallowing of amniotic fluid /w
increased urine production
signs of renal disease in children
- abnormal growth (small stature)
- hypertension
- dehydration
- edema
physical features w/ potential
underlying renal defects
- fetal alcohol syndrome
- down syndrome
- pre-auricular skin tags or pits
- external ear deformities
- eye abnormalities (cataracts, coloboma, aniridia)
name the condition
coloboma
(“leaking pupil”)
name the condition
aniridia
(absence of iris)
control of kidney filtration
glomeruar filtration
- rate of blood flow through glomerulus controlled by arteriolar tone
- renin
- hormone prod. in juxtaglomerlar apparatus
- responds to glomerular flow and perfusion
- sensitive to low blood flow and low serum sodium
- renin-angiotensin-aldosterone axis
products absorbed and produced
by proximal tube
- reabsorbs
- 2/3 of filtered volume
- Na+ and Cl-
- glucose
- amino acids, K+, PO4 almost completely reabsorbed
- NaHCO3 reabsorption set by bicarb threshold
- produces
- calcitriol (Vit D analog)
Role of Loop of Henle
determines urine concentration
components absorbed by distal tubule and collecting ducts
- impermeable to water except if ADH present
- active reabsorption of NaCl into bloodstream
- collecting ducts are primary site of ADH production and aldosterone
urinary anion gap
causes of low and elevated gap
measured gap between serum anions and cations
- low
- increased renal acid secretion
- increased NH4 production
- elevated
- caused by metabolic acidosis
causes of increased anion-gap
metabolic acidosis
MUDPILES
- Methanol
- Uremia
- Diabetic ketoacidosis
- Iron, Inhalents (CO, cyanide, toluene), Isoniazid, Ibuprofen
- Lactic acidosis
- Ethylene glycol, ethanol ketoacidosis
- Salicylates, starvation ketoacidosis, sympathomimetics
maturation of renal function
(urine concentration, GFR, tubular reabsorption)
- max. urine concentration - infants cannot concentrate urine (produce same amount even if dehydrated)
- GFR - reaches adult levels by 1-2 years old
- tubular reabsorption - adult levels by 1-2 y-o
urinalysis
what dipstick checks for
pH, protein, glucose, ketones, blood leukocytes
urinalysis
what microscope checks for
pyuria, hematuria, casts, crystals
urinalysis
what spot calcium/creatinine checks for
renal stones, hematuria
renal imaging
what US used for
most utilized in peds
kidney size, dilation, assess cortex vs. medulla
used to evaluate bladder filling/function
position of ureters/urethra
reflux into kidneys/ureters
voiding cystourethrogram (VCUG)
what is nephrotic syndrome
heavy and persistent proteinuria
with protein losses (albumin)
signs of nephrotic syndrome
- pitting edema and/or ascites
- anorexia, malaise, abdominal pain
- increased BP (25%)
- shock d/t sudden albumin decline and fluid loss
- NO gross hematuria or renal insufficiency
2 sources of proteinuria
- tubular
- glomerular
tubular proteinuria
types of proteins seen
low molecular weight
tubular proteinuria
conditions
- acute tubular necrosis
- pyelonephritis
- polycystic kidney
tubular proteinuria
causes
tubular toxins:
antibiotics
chemotherapy
glomerular proteinuria
type of protein seen
large and small
glomerular proteinuria
evidence of disease
- hematuria
- casts
- HTN
MC but least severe nephrotic syndrome
minimal change disease
least common but most severe nephrotic syndrome
IgA nephropathy
primary nephrotic syndrome
minimal change disease characteristics
- MCC nephrotic syndrome in children (80% in children < age 7)
- MC in males
- most respond to steroids within 4 weeks
- treat with oral steroids x12 weeks
primary nephrotic syndrome
focal segment glomerulosclerosis characteristics
- 10-20% of kids w/ NS
- no specific tx - less steroid responsive
- may need nephrectomy, dialysis, transplant
primary nephrotic syndrome
membranoproliferative glomerulonephritis characteristics
- 5-10% of kids w/ NS
- caused by hypocomplementemia (immune complex deposits)
- tx is to stop deposition of immune complexes
what is secondary nephrotic syndrome
protein losses from kidney occur secondary to other diseases
- vasculitis
- chronic infections (hepatitis, malaria, HIV)
- diabetes
- renal vein thrombosis
- amyloidosis
- heart disease
- malignancies
- drug reactions
when/what to check for proteinuria
- first morning urine - r/o orthostatic or transient proteinuria which are not significant
- presence of 1+ or higher protein on dipstick 2 or more times
nephrotic syndrome treatment
- steroids
- loop diuretics for edema
- B-blockers or Ca+ channel blockers for HTN
complications of nephrotic syndrome
- peritonitis and bacteremia
- side effects of high dose steroids
- hypovolemia from diuretics or diahhrea
- loss of coagulation factors -
- hypercoagulable state
- DVT
general presentation of glomerulonephritis
gross hematuria
acute vs. chronic glomerlonephritis
- acute
- post streptococcal (PSGN) MC
- chronic
- IgA neuropathy MC
presentation of acute glomerulonephritis
- ages 2-12
- MC in boys
- HTN most serious problem
- 10 days after strep infection (PSGN)
- OR-
- 4-6 weeks after impetigo (undiagnosed)
S/s of glomerulonephritis
- variable presentation
- asymptomatic microscopic hematuria
- or more acute
- often assoc. w/ concurrent URI
- rapidly progressing
- can quickly progress to renal disease
- observe emergently until no blood
- glomerular blood brownish
- casts and dymorphic RBCs
x-lined disorder of collagen defect in glomerular basement membrane
(name, s/s)
Alport syndrome
- hearing and vision problems
(can’t see, can’t hear)
- renal failure in males
non-glomerular causes of hematuria
- painless gross hematuria
- sickle cell
- Wilms tumor
- strenuous exercise
- kidney trauma
- urolithaisis
- hypercalcemia
Tx of gomerulonephritis
- sick or not sick
- observation if not sick
- recheck urine and BP weekly
- refer to nephrology if becoming chronic or BP elevated
- Na+ restrictions, diuretics, antihypertensives for BP
- treat underlying cause
- ACE inhibitors reduce glomerular HTN
- post-step usually self limited and benign
- others w/ higher risk of chronic disease
hemolytic uremic syndrome (HUS)
triad/cause
- microangiopathic hemolythic anemia
- thrombocytopenia
- renal injury secondary to syndrome
- assoc. w/ shigatoxin and diarrheal illnesses
- E. coli - verotoxin (VT)
- important cuase of kidney injury in children
- typically < 5 y/o
- non-diarrheal more severe
- HIV, complement defects, medications, malignancy, pregnancy
hemolytic uremic syndrome (HUS)
S/s
- verotoxin causes hemorrhagic enterocolitis
- bloody stools
- 7-10 days after stools - lethargy, oliguria
- irratability, pallor, petechiae
- HTN from volume overload and renal injury
- seizures (25%)
- rare: pancreatitis, dysfunction, colonic perf.
HUS
laboratory findings
- CBC- anemia, thrombocytopenia
- peripheral smear- schistocytes, burr cells, helmet cells
- elevated LDH, AST, reticulocytes, bilirubin
- decreased haptoglobin
“chewed up” RBCs
HUS treatment
- supportive care
- volume repletion
- RBC transfusion
- HTN management
- dialysis
categories of renal failure
- pre-renal
- renal
- post-renal
cause/sign of pre-renal failure
- glomerular hypoperfusion
- MC dehydration
- others:
- cardiac failure
- hemorrhage
- cirrhosis
- shock
- sign: very concentrated urine
causes/sign of renal failure
- usually tubular injury
- hypoxic ischemic tubular injury
- infection (sepsis)
- nephrotoxic agents
- (myoglobin, meds, contrast medium)
- inflammation
- Interstitial nephritis
- sign: mild hematuria/proteinuria, SG < 1.015
causes/sign of post-renal failure
- urinary tract obstructions
- sign: reduced urine volume
MCC chronic kidney disease
greater than/less than 10 y/o
- < 10 y/o
- congenital anomalies:
agenesis, duplication, polycystic, ureteral implantation, kidney parenchyma
- > 10 y/o
- focal glomerulosclerosis
signs of kidney failure / CKD
- growth failure
- fractures and bone deformities
- delayed puberty
- HTN
- renal osteodystrophy
- hormonal abnormalities
- uremia
Tx of CKD
- nutritional supplements / tube feeding
- treat acidosis - NaHCO3, Na+ citrate
- dialysis
- address salt needs based on Na+ excretion
- anemia - supplement erythropoietin and iron
- renal ostedystrophy - PO4 restriction, Vit D
- renal transplant
2 types of pediatric HTN
- essential
- leading cause in children and adults - obesity
- secondary
- typically renal
at what age do you begin
routine measurements of BP
3 y/o
correct cuff size
“2 fingers under the cuff”
effect of too large/small cuff on BP measurement
too large - low BP
too small - high BP
diagnosis of HTN in children
3 measurements over 95 %tile
- UA, electrolytes, Ca+, BUN, Cr tests
- renal US
- cardiac evaluation
Tx of HTN in children
- address underlying cause (esp. renal)
- anti-hypertensives (like adults)
- Ca+ blockers
- ACE inhibitors
- B-blockers
- diet and exercise
backward flow of urine from bladder up ureter
vesicoureteral reflux
causes/risks of vesicoureteral reflux
- junction of ureter and bladder congenitally malformed - can be familial
- incomplete emptying leading to kidney infections and scarring (reflux nephropathy)
- increased pressure of urine in renal pelvis -> decreased renal function and failure
- neurologic bladder in 50% w/ VUR
- significant incontinence and bladder training difficulties
Dx of VUR
- ususally unnoted until UTI
- voiding cystourethrogram (VCUG)
- bladder filled w/ contrast - allows grading
- radionucleotide cystogram
- renal US to ID abnormalities
vesicoureteral reflux Tx
- antibiotics to prevent recurrent UTI
- teach good bladder/bowel habits to minimize urinary retention
- deflux procedure - produce a valve at entry of ureter in to bladder
- surgical reimplantation of ureters into bladder
congenital kidney abnormalities
renal agenesis assoc. w/ this
diabetes during pregnancy
congenital kidney abnormalities
renal hypoplasia/dysplasia assoc. w/ this outcome
eventual kidney failure
congenital kidney abnormalities
polycystic kidney disease assoc. w/ this
genetic defect in structure - possible kidney failure
congenital kidney abnormalities
posterior uretheral valves MC patient
1 DDx when 3 mo male w/ UTI
when childhood urinary incontinence unacceptable
after age 5
potty training characteristics
- age varies by child and parent
- daytime dryness preceeds nighttime
issues preventing daytime dryness
- poor habits
- UTI undiagnosed
- structural problem
issues preventing nighttime dryness
- age
- bladder size
- ADH production (DDAVP)
- behavioral
