Urology Flashcards
inability to retract the foreskin
phimosis
main cause of pathologic phimosis
early forcible retraction
Sx of patho phimosis
secondary non-retractibility after having fully retractable before; painful erections
irritation/bleeding
dysuria/urinary retention
recurrent infections
Tx for patho phimosis
stretching
topical corticosteroid
circumcision (rarely needed)
Paraphimosis
retractable foreskin that can not be returned to natural position; MEDICAL EMERGENCY
Pathophys of paraphimosis
entrapment –> impaired venous flow –> engorgement –> arterial compromise
Causes of paraphimosis
forcible retraction
infection/inflamation
genitourinary procedure (iatrogenic)
sex, trauma
Sx of paraphimosis
swelling
pain
irritability in a preverbal infant
PE for paraphimosis
edema, tenderness
constricting band
color change if ischemia is present
Tx for paraphimosis
pain control
timely manual reduction in office or ED
surgical intervention by urology
Benefits of circumcision
decrease UTIs penile cancer? inflammation/dermatoses STD benefits greater in those w/ congenital uropathy
risk of circumcision
procedure related complications (inadequate removal, bleeding, infection, urethral complications)
Contraindications for cicumcision
unstable infant, congenital penile anomolies (hypospadias, chordee)
Types of circumcision methods
gomco vs. plastibell
Epispadias
congenital anomaly w/ abnormal dorsal displacement of urethral opening
epispadias may occur w/
bladder exstrophy (exposed bladder, into lower abdomen)
Hypospadias
urethral opening on the ventral side (more common than epispadias) - can be on glans, shaft, scrotum, perineum
may accompany hypospadias
chordee
Chordee
abnormal penile curvature
Considerations w/ hypospadias or chordee
palpate testes: if crytorchidism consider disorder of sexual dev. (DSD)
refer to urology
Tx for hypospadias or chordee
CIRCUMCISION NOT DONE DURING NEWBORN PERIOD
surgery performed ~6 months of age to fix hypo or chordee
cryptorchidism
hidden/absent testis; does not descend by 4 months of age
most common GU congenital abnormality
cryptorchidism
Risks of cryptorchidism
testicular torsion
subfertility (improves if corrected before 1 yo)
testicular cancer
Types of cryptorchidism
absent (agenesis or atrophy) undescended retractile (overactive cremasteric reflex) Ascending ectopic
Presentation of cryptorchidism
usually unilateral
location: suprascrotal
US if not palpable
Most descend spontaneously by 3-4 months
Tx for cryptorchidism
urology referral; surgery as soon after 6 mo as possible (before 1 yo); orchiopexy (brought down and attached to scrotum)
Torsion
twisting of spermatic cord due to poorly anchored testicle; VASCULAR COMPROMISE RISK
Incidence of torsion
neonatal
puberty (12-18)
Presentation of torsion
abrupt onset of severe pain
n/v
PE for torsion
edematous, indurated, erythematous scrotum
swollen, tender, slightly elevated
ABSENT CREMASTERIC REFLEX
NEGATIVE PREHN’S SIGN*
Dx for torsion
hx and PE
doppler US is confirmatory (sees blood flow)
Tx for torsion
immediate urology consult
surgical detorsion and fixation (orchiopexy) of both testes
Prognosis of torsion
4-6 hrs: 100% viable
12 hrs: 20% viable
24 hrs: 0% viable
UTI
cystits vs pyelonephritis (kidneys infected); usually from ascending bacteria (e.coli***, klebsiella, proteus, entercoccus, s. aureus)
Sx of UTI
FUO, vomiting, irritability, poor appetitie
Older children: dysuria, frequency, ab pain, back pain, urinary incontinence
PE fo UTI
vitals, ab exam
suprapubic and CVA exam
examine external genitalia
search other sources of fever
How to collect UA
clean-void specimen if potty trained cath speciment suprapubic aspiration (if cath not feasible)
Dx of UTI
UA and culture
(+) bacteriuria w/ pyuria, leukocyte esterase, nitrate (produced by gram neg rods)
C&S: to direct tx
Tx of UTI
Duration of tx 3-10 days Abx depends on C&S: - cephalosporin (cephalexin and cefdinir) - amoxicillin - augmentin - bactrim
F/u for UTI
no f/u needed if C&S
renal bladder US (RBUS) voiding cystourethrogram (VCUG) Renal scintigraphy
when to f/u for UTI
RBUS when:
- <2 yo w/ first febrile UTI
children w/ recurrent
children w/ UTI and FH of renal or urological disease, poor growth or HTN
children who do not respond to abx therapy
Voiding cystourethrogram (VCUG)
invasive, radiation, catheter
test of choice to detect vesicouretral reflux (VUR)
children of any age >2 febrile UTIs
children of any age w/ 1st febrile UTI AND any anomaly on RBUS or temp >102.2 and pathogen other than E.coli, or poor growth or HTN
Vesicoureteral reflux (VUR)
retrograde flow of urine from bladder into upper urinary tract, usually due to closure of ureterovesicular junction (UVJ)
Presentation of vesicoureteral reflux
hydronephrosis (prenatal)
post natal febrile UTI
Dx of VUR
VCUG
VCUG
catheter placed and contrast injected; under fluoroscopy, movement of contrast and anatomy watched while pt voids; graded I (mild) to V severe
Risks in patients w/ VUR
recurrent infections
scarring and damage to kidney
Management of VUR
many cases spontaneously resolve
watchful waiting/surveillance?
low dose prophylactic antibiotics
surgical correction
aggressive screening (UA) in febrile/symptomatic pts
Renal scintigraphy
nuclear medicine scan using radioisotope dimercaptosuccinic acid (DMSA) to detect acute pyelonephritis and renal scarring;
decreased uptake of DMSA indicates scarring or inflammation; not recommended in evaluation of kids w/ first UTI
Indications for referral in kids with UTI
severe VUR (grade III-V) or obstruction renal abnormalities impaired kidney function elevated BP bowel or bladder dysfunction refractory to primary care measures
Horseshoe kidney
most common type of renal fusion; caused by abnormal migration in 5th-9th week gestation
S/sx of horseshoe kidney
usually asymptomatic
may have pain, hematuria
most have associated uro problem (VUR, hypospadias, undescended testes) or may be associated w/ other genetic disorders;
Risk with horseshoe kidney
small risk of Wilms Tumor (most common renal malignancy in kids)
Dx of horseshoe kidney
US, VCUG (if UTI), serum creatinine
normal Cr and no hydronephrosis: no further eval
Cr elevated or hydronephrosis: renal scan
Management of horseshoe kidney
excellent prognosis w/o intervention
w/ VUR: consider prophylactic abx
Nocturnal enuresis (NE)
incontinence in kids >5 yo; common
Etiology of NE
genetic
bladder maturation
organic cause
Tx for NE
1st line: most spontaneously resolve – education (motivation, urination, fluid intake)
2nd line: pharm >6yo:
Pharmacologic tx for NE
DDAVP/Desmopressin (synthetic ADH) – effective short term but high relapse rate
Ddx for hematuria
UTI, kidney stone, malignancy trauma post-infectious glomerulonephritis neoch-schonlein purpura hemolytic uremic syndrome alport syndrome
Labs for microscopic hematuria (>3 RBCs)
- if asymptomatic, repeat UA dip and microscopy in 2-3 weeks (if resolved, follow up prn); consider urine cx if UTI suspected, RBUS, referral
Gross hematuria labs
UA w/ microscopy/urine cx
serum Cr
Serum complement (low level in SLE, glomerular etiology)
Consider antistreptolysin Ab (ASO), ANA
Imaging: RBUS/CT w/o contrast
If persistent- refer
Post infectious glomerulonephritis sx
7-14 days after GAS (pharyngitis or impetigo)
throat
bloat- edema peri-orbital or peripheral due to kidneys not removing waste and fluid
coke- colored urine
elevated BP
Labs for post-infectious glomerulonephritis
gross hematuria (dark cola urine) - RBC Casts** (diagnositc of GN)
increased serum Cr
+ASO (antistreptolysin Ab) titer
low complement (C3, C4)
Tx for GN
supportive
Immunoglobulin A vasculitis henoch-schonlein purpura (HSP)
IgA vasculitis: immune mediated, cause unknown
Sx of HSP
Tetrad:
- Abdominal pain
- typical maculopapular purpuric rash (usually on LE)
- arthralgias (knees/ankles)
- renal involvement
Tx for HSP
supportive; spontaneously resolution of symptoms
HUS cause
shiga toxin producing E.coli
Sx of HUS
prodrome w/ abd pain, vomiting, diarrhea (usually bloody)
Followed by triad:
- hemolytic anemia
- thrombocytopenia
- AKI
Labs for HUS
CBC, peripheral smear, renal function, UA
Tx for HUS
supportive, possible dialysis
no abx
Alport syndrome aka
hereditary nephritis
cause of alport syndrome?
genetic mutations that affect collagen proteins in kidneys, eyes and ears
Sx of alport syndrome
\+FH of end stage renal failure Syndrome includes: - glomerular disease (microhematuria) - deafness - visual distruabnce
Proteinuria
foamy urine, excessive proteins in urine
Ddx for proteinuria
Benign/transient (fever, hypovolemia, exercise) SLE DM GN Nephrotic syndrome*
Nephrotic syndrome
renal disease (intrinsic or post infectious) causing massive renal protein loss in urine
Sx of Nephrotic syndrome
O's: PrOteinuria O shaped face (edema due to water retention) HypOalbuminemia Hyperlipidemia
Why do Nephrotic syndrome have HLD
body compensates for protein loss by increasing the synthesis of albumin, as well as other molecules including LDL and VLDL
Evaluation of proteinuria
BP UA w/ microscopy first AM void UA to check for proteinuria prior to meal/activity protein/Cr ratio CMP Hx refer to nephrology
