502 Flashcards
normal characteristics of urine
pH 5-9
specific gravity 1.001 - 1.035
protein < 20 mg/dL
urobilinogen up to 1 mg/dL
newborn renal fxn
produces dilute urine
2 mL/kg/hr
unable to reabsorb
glomerular filtration matures around 1-2 yrs
children renal fxn
shorter urethras
prone to UIT
complete bladder control at 4-5 yrs
ability to regain full renal fxn after ARF
aging renal fxn
(+)muscle thickness/(-)capacity/(+)frequency
(-)contractility and tone/(+)retention
(-)sphincter control (x2 for women)
(-)urethral length (affected by w/d of estrogen)
(+)prostate enlargement/(+)retention
hypospadias
opening on dorsal side (top)
more common
surgical correction 6-12 mos
should not be circumcised
epispadias
opening on ventral side (bottom)
VUR
vesicoureteral reflux
bladder extrophy
extrusion of bladder through defect in lower abdominal wall
may be associated with genital anomalies or anus defects
risk for kidney damage due to VUR s/p corrective surgery
MSRE
modern staged repair of extrophy
- bladder closure
- epispadias repair
- BNR (bladder neck reconstruction at 5 yrs
CPRE
complete primary repair of extrophy
bladder closure, epispadias repair, and BNR done simultaneously
primary VUR vs secondary VUR
congenital abnormality vs. acquired condition (UTI or obstruction)
graded I - V by how distended ureter is/how deep into nephrons
VUR management (stage I-II)
80% probability of spontaneous resolution
VUR management (less severe)
inject bulking agent (Deflux)
VUR management (stage IV-V)
surgical correction
ureter reimplantation
renal US to R/O obstruction
UTI
-bacteria ascending through urethra: E. coli (most common) streptococci S. saprophyticus occasionally fungal or parasitic -obstruction or void dysfunction -reflux -should be R/O in any presenting child with malaise or changed urinary habits
UTI (upper) involves:
renal parenchyma, pelvis, and ureters
>pyelonephritis
VUR
glomerulonephritis
UTI (lower) involves:
urinary tract
absent clinical manifestations
cystitis
urethritis
febrile UTI indicates:
pyelonephritis
kidney scarring from childhood UTIs cause concern regarding:
renal HTN and impaired fxn in adulthood
glomerulonephritis manifestations:
hematuria, proteinuria acute edema of eyelids/ankles (worse in AM) pulmonary edema proteinuria HTN renal insufficiency fever fatigue
nephrotic syndrome (kinds)
primary (MCNS): minimal change
secondary: systemic disease (SLE, poisoning)
congenital
process of nephrotic syndrome:
glomerular membrane becomes permeable to albumin > hyperalbuminuria > hypoalbuminemia > fluid shift from plasma to interstitial spaces > hypovolemia/ascites
nephrotic syndrome s/s:
proteinuria (frothy) hypoalbuminemia/hyperalbuminuria dependent edema (worsens through day) hypovolemia/normotensive pallor/fatigue \++cholesterol/triglycerides
management of nephrotic syndrome:
reduce relapse:
high-dose prednisone, cytoxan, cyclosporine
manage fluid balance:
diuretics, albumin infusion
infection prevention:
PCN prophylaxis, pneumococcal vax, no live virus
enuresis
inability to control voiding:
most master by 5 yrs
females often before males
controlled by CNS; can be r/t delayed maturation
enuresis medications:
antidiuretics
anticholinergics
antidepressants/temporal therapy
osgood-schlatter disease:
most frequent cause of knee pain in kids
usu ages 9-16
overuse associated w/running, twisting, jumping
irritation of patellar ligament at its attachment to the tibial tuberosity
RICE interventions:
Rest
Ice
Compression
Elevation
traction
pull/force exerted on one part of body in presence of counterforce
focus of traction on:
spine
pelvis
long bones of UE/LE
purpose of traction:
provide rest/immobilize
prevent/improve contractures
correct deformity
treat dislocation
casts: plaster v. fiberglass
plaster: inexpensive, molds easy, but heavy, long drying time, and can’t get wet
fiberglass: quick-drying and water resistant, but more costly and not ideal for young children or sever breaks (don’t mold easy)
treatment of compartment syndrome:
don’t elevate above the heart (slows arterial perfusion, increases venous pressure)
no ice (causes vasoconstriction)
bivalve cast, loosen under layer
loosen surgical dressings
fasciotomy (surgical): removal of fascia decreases pressure and allows perfusion
compartment syndrome s/s:
myoglobinuria (protein from damaged muscle)
precipitates like gel/blocks renal tubules
dark reddish brown urine
types of traction:
manual (applied to body part by hand, usu during cast application)
skin (applied to surface, indirectly to skeletal structures, like dunlop/humeral or buck/hip)
skeletal (directly to skeletal via pin, wire, tongs)
scoliosis is:
lateral curvature of spine with vertebral rotation
types of scoliosis
adolescent idiopathic (occurs during growth spurt)
congenital
infantile/juvenile
neuromuscular
scoliosis s/s:
prominent scapula/hip
uneven shoulders/scapulae
spinous process misaligned
uneven fit/hem of clothing
osteomyelitis is:
bacterial infection of bone that involves cortex or marrow cavity
etiology/epidemiology of osteomyelitis:
S. aureus most common organism exogenous (from penetrating wound) or hematogenous (preexisting infection) boys/girls 2:1 commonly at 5-14 yrs
osteomyelitis s/s:
hx of trauma at affected area leukocytosis \++ESR irritability elevated temp local tenderness/swelling/pain \+bone culture
osteomyelitis treatment:
immobilization (prevents spread of infection)
antibiotics (3-4 weeks usu, up to 6)
surgical intervention if necessary
juvenile arthritis is:
autoimmune disease, cause unknown peak ages of onset 1-3 yrs and 8-10 yrs occurs before age 16 girls/boys 2:1 30% of children suffer long term limitations
types of juvenile arthritis:
50% pauciarticular (onset of fewer joints)
40% polyarticular (onset of 5+ joints)
10% systemic (variable arthritis/systemic)
juvenile arthritis s/s:
swelling/stiff/loss of fxn in affected joint
warm/erythematous
leukocytosis during flares
synovial thickening
systemic: maculopapular rash, fever, hepatosplenomegaly, pericarditis, lymphadenopathy
pharmacological management of JA:
corticosteroids
NSAIDS
cytotoxic drugs
DM1: age at onset: inheritance: nutritional status: insulin: sulfonylurea therapy: symptoms: onset:
insulin-dependent DM any age, usu before 30 yrs recessive usually nonobese dependent none polyuria/polydipsia/polyphagia, weight loss, fatigue and irritability abrupt
DM2: age at onset: inheritance: nutritional status: insulin: sulfonylurea therapy: symptoms: onset:
non insulin-dependent DM usu starts in 40s/peaks in 50s, but increasing incidence in childhood and adolescences dominant 60-80% patients obese insulin required in 20-30% of cases sulfonylurea therapy effective none, OR DM1 similar (thirst/fatigue), OR vascular/neural/visual complications, frequent infections (esp skin, gums, bladder), slow healing cuts/bruises, tingling/numbness in hands or feet gradual onset
gestational diabetes:
develops during pregnancy
detected at weeks 24-28
Bg usually returns to normal 6 weeks postpartum
increased risk for C-section, prenatal complications
increased risk for development of DM2
treatment: nutrition, insulin
secondary diabetes:
*resulting from: cushing syndrome hyperthyroidism pancreatitis parenteral nutrition cystic fibrosis hemochromatosis *results from treatment with: corticosteroids thiazides phenytoin atypical antipsychotics like clozapine *usu resolved w/resolution of above
DM methods of diagnosis:
HbA1c > 6.5%
Fasting Bg > 126
random Bg > 200 + s/s
2hr OGTT > 200 w/glucose load of 75g
rapid-acting insulin (aspart)
onset: 15 min
peak: 60-90 min
duration: 3-4 hr
short-acting insulin (regular, ending in -R)
onset: 30-60min
peak: 2-3 hr
duration: 3-6 hr
intermediate-acting insulin (NPH, ending in -N)
onset: 2-4 hr
peak: 4-10 hr
duration: 10-16 hr
long-acting insulin (glargine)
onset: 1-2 hr
NO PEAK
duration: 24+ hr
somogyi effect
overabundance of insulin overnight > hypoglycemia > rebound hyperglycemia
dawn phenomenon
waning insulin (+growth hormone surge?) > hyperglycemia not rebound, unlike somogyi
sick day rules:
call PCP Bg Q4h test for ketonuria when Bg >240 drink 8-12 sugar free fluids Qh when awake observe for changes in n/v or fever
hypoglycemia:
mild: 40-70
moderate: 20-40
s/s: diaphoresis, tremor, tachycardia, palpitations, moves to tachypnea, cold/clammy skin, pallor, change in mood
tx with CHO, fruit juice/soft drink/hard candy/skim milk/saltines/graham crackers
pelvic floor exercises
kegels (10 reps 3-5xday 4-8 weeks)
vaginal weights/cones
urge control technique
be still, squeeze x5, distract, walk, then bathroom
most common cause of incontinence in women:
fecal impaction
most common cause of incontinence in men:
prostate enlargement
PVR is:
post void residual
tested 10 min post void
50-100cc normal
>200cc abnormal
surgical interventions for urinary retention:
BPH reduction
TURP
bladder sling/suspension
BPH is:
noncancerous enlargement of prostate
50% of men will have BPH by age 50
90% of men will have BPH by age 80
AA men develop at a younger age
BPH s/s:
void hesitancy unsteady stream nocturia frequency vesical tenesmus intermittent starting and stopping
TURP is:
transurethral resection of prostate
correction of BPH
removal of prostate tissue using resectoscope inserted through urethra
AKI: onset: nephrons involved: duration: reversible? mortality: urine status: most common cause:
acute kidney injury sudden 50% 2-4 weeks, < 3 mos yes high oliguria to polyuria ATN
CKD: onset: nephrons involved: duration: reversible? mortality: urine status: most common cause:
chronic kidney disease gradual 80-90% permanent no poor diagnosis w/o HD/transplant polyuria to oliguria diabetic nephropathy
common abnormalities cause by renal failure:
fluid disturbances
electrolyte imbalance
accumulation of nitrogenous waste/toxin
neurologic disorders
prerenal AKI:
55-60% of cases results from decreased perfusion pathology doesn't reach parenchyma caused by hypovolemia, heart failure, hypotension, shock, hepato-renal syndrome, cyclosporin/tacrolimus resolved with resolution of cause
intrarenal AKI:
35-40% of cases
results from damage to glomeruli, interstitium, or tubules
pathology reaches parenchyma
caused by ischemia, immune complexes (lupus), RBC waste (sickle cell), nephrotoxins (aminoglycosides, contrast dye)
postrenal AKI:
<5% of cases results from obstruction to urine flow can move backward into parenchyma cased by obstruction: calculi, stone, tumor, fibrosis, clot, prostate resolved with resolution of cause
clinical manifestations of AKI:
- oliguria ( HF, pulm edema, effusions
- metabolic acidosis (buildup of H+)
- decreased sodium excretion, hyponatremia
- decreased potassium secretion, hyperkalemia
prerenal AKI urine:
SG > 1.015
Na+ < 10-20
Os > 500
intrarenal AKI urine:
SG < 1.010
Na+ > 40
Os < 350
RBC/WBC, casts
