Renal/Urology Flashcards
UTI
i) what should be given to all children under 3m with a fever? name two others things that should be done?
ii) what should be considered in children >3m if otherwise well? name three drugs that may be given
iii) what should all children under 6m with their first UTI have? what should children with recurent UTIs have? what should children with atypical UTIs have?
iv) what can a DMSA scan be used for? what does it involve?
i) IV abx eg ceftriaxone
do a full septic screen and consider an LP
ii) >3m - consider oral abx eg trimethoprim, nitro, cefalexin, amox
iii) all <6m first UTI should have an abdo US within 6 weeks
recurrent UTI - US abdo within 6 weeks
atypical UTI - abdo US during the illness
iv) use 4-6m after illness to assess for damage from recurrent/atypical UTIs
inject radioactive DMSA and use a gamma camera to assess how well it is taken up by the kidneys (patches of reduced uptake = infection)
VESICO-URETERIC REFLUX
i) what is it? what does it predispose to?
ii) how is it diagnosed? name three instances this test may be done (RFs)
iii) name three ways it can be managed
i) urine flowing from the bladder back into the ureters > predis to upper UTIs and renal scarring
ii) dx using micturating cystourethrogram (MCUG) - catetherise and inject contrast and see if contras refluxes
do MCUG if there is a FH of VUR, dilatation of ureter on US or poor urinary flow
iii) mx by avoiding constipation, avoiding a very full bladder, prophylactic abx, surgical input
NEPHROTIC SYNDROME
i) what happens? what ages is it most common between? name three key presenting features
ii) what is the classic triad seen?
iii) name three other features seen (lipids, BP, blood)
iv) what is the most common cause in children? name three secondary causes?
i) occurs when the basement membrane in the glom becomes highly permeable to protein > proteins leaak from blood to urine
common between 2-5yrs
px with frothy urine, general oedema and pallor
iii) triad - low serum albumin, high urine prot content (>3+ prot on dipstick) and oedema
iv) also see deranged lipids - high chol/trigly and LDL
high BP, hypercoaguability
iv) most common cause is minimal change disease
secondary - focal segmental glomsclerosis, membranoprolif glomneph, or second to systemic illness eg HSP, diabetes, infection
MINIMAL CHANGE DISEASE
i) what is it the most common cause it? is it clear why it occurs?
ii) what is seen on renal biopsy/microscopy? what will be seen on urinalysis? (2)
iii) how is it managed? is it likely to recur?
i) most common cause of nephrotic syndrome
not clear why it occurs - dev without RFs etc
ii) nothing is seen on biopsy/micro
urine - small molecular weight proteins and hyaline casts
iii) mx with corticosteroids eg pred
most recover but also likely to recur
MX AND COMPLICATIONS OF NEPHROTIC SYNDROME
i) which drugs are used to manage it? what type of diet may be advised?
ii) what can be given for oedema? what protein may need to be infused
iii) if initial tx doesnt work - what can be given? (2)
iv) name three complications
v) why may patients get thrombosis
i) high dose steroids eg pred for 4 weeks then wean over 8 weeks
low salt diet
ii) diuretics for oedem
albumin infusion for severe hypoalb
iii) if steroid resistant can give ACEi and immsupp like cyclosporin/tacrolimus
iv) hypovolaemia, infection due to leaking Igs/immsupp tx, acute/chronic renal fail, relapse
v) thrombosis - clotting prots lost and liver responds to low alb by making clotting proteins
NEPHRITIS
i) what is it? name three things it causes
ii) what are the two most common causes?
iii) when does post strep glomneph occur? what happens? what type of kidney injury happens? how are most pts managed?
iv) what happens in IgA nephropathy? what will renal biopsy show? when does it usually px? how is it managed? (2)
i) inflammation within nephrons
causes reduced kidney function, haematuria, proteinuria (less than in nephrotic)
ii) post strep glomneph and IgA nephropathy
iii) PSGN occ 1-3 weeks post betaa haemolytic strep diseasae eg tonsilitis caused by strep pyog
immune complexes get stuck in glom and cause inflammation > AKI
manage is supportive
iv) IgA deposits in nephrons > inflam
renal biopsy shows IgA deposits and glom mesangial proliferation
usually px in young adults/teenagers
supportive tx of renal faul and immsupp eg steroids
HAEMOLYTIC URAEMIC SYNDROME
i) when does it occur? what bacterial toxin is it usually triggered by? what bacteria makes this? name another bacteria that makes it
ii) what are the classic triad of symptoms? (HAT) use of which type of medications can increase the risk? (2)
iii) what illness is usually seen first? whaat happens 5 days later? name four symptoms of HUS
iv) how quickly should it be managed? what is tx mainstay?
v) what may a patient be referred for? name a medication that may be given? which other two things can be given
i) occ when there is thrombosis in small blood vessels throughout body
triggered by shiga toxin - made by ecoli 0157 and shigella
ii) triad - haemolytic anaemia, AKI and thrombomytopenia HAT
giving abx/anti motlility meds eg loperamide can inc risk
iii) see gastroenteriris with blood diarrhoea then HUS symp start 5d later
symp - low urine output, haematuria/dark urine, abdo pain, lethargy, confusion, oedema, HTN
iv) medical emergency but mainstay is supportive
v) refer for renal dialysis may be required
give anti hypertensives
fluid balance and blood transfusions
POLYCYSTIC KIDNEY DISEASE
i) which type most commonly presents in children? when is it usually picked up? which mutation is seen?
ii) name three features? what can it px with antenatally? what can this lead to?
iii) what may a neonate need in first few days of life? what usually happens before adulthood?
iv) name four problems patients may have throughout life? what is the prognosis?
i) auto recessive PKD (dom px in adults)
usually picked up on antenatal US
mutation in PKHD1 on chr 6 < codes for FPC complex - creates tubules and main healthy ep tissue in kidney/liver/panc
ii) cystic enlargement of renal collecting ddicts, oligohydroamnios/pulm hypoplasia, congenital liver fibrosis
can px with oligohydroamnios (lack of amniotic fluid due to kidneys producing less urine in utero) > leads to under dev lungs (pulm hypoplasia) causing resp failure shortly after birth
iii) may need renal dialysis in firsy few days and may get end stage renal fail before adulthood
iv) through life - liver failure, portaal HTN, renal fail, high BP, CLD
poor prognosis - 1/3 die as neonates and 1/3 make it to adulthood
POSTERIOR URETHRAL VALVE
i) who does it px in? what happens to the urethra? what does this cause? what is there increased risk of?
ii) name four presenting symptoms?
iii) what two things may be picked up on antenatal scans if severe?
iv) name three investigations that can be done when presenting after birth?
v) how may mild cases be mx? what can be done while waiting for definitive mx? what is definitive mx?
i) occurs in newborn boys
there is tissue at prox end of urethra (closest to bladder) that causes obstruction of urine > back pressure to bladder > kidneys > hydronephrosis
inc risk of UTIs
ii) can be asymp or px with difficulty urinating, weak urinary stream, chronic urine retention, palpaable bladder, recurrent UTI
iii) in utero - bilateral hydronephrosis and oligohydroammnios (low am fluid > pulm hypoplasia and resp failure postnatally)
iv) abdo US (enlarged thick bladder with bilat HN)
MCUG - location of extra urethraal tissue
cystoscopy - camera to urethra to visualise tissue and to treat
v) mild - watch and wait
ccan insert temp urinary catheter whilst waiting for definitive mx
definitive is ablation or removal of the tissue usually during cystoscopy
UNDESCENDED TESTES
i) where do testes initially dev? where do they then move to? via which structure?
ii) what is us UT aka? where might the testes be palpable? name three risks of UT in older children?
iii) name four RF for UT?
iv) what mx is done in newborns? how long does it take most UT at birth to descend? when should a patient be referred to a urologist?
v) what sx procedure may be done to correct? between which age?
vi) what are retractile testes? when is this normal? why does it happen?
i) initially dev in abdomen then migrate down through the ing canal and into the scrotum
ii) aka cryptorchidism
may be palp in the ing canal
risks in older children - inc risk of testicular torsion, infertility and testicular cancer
iii) RF are FH of UT, low birth weight, SGA, prematurity, maternal smoking during pregnancy
iv) watch and wait for newborns and most will desc in 3-6m
if not desc by 6m then refer to urology
v) orchidopexy is surgical corection and done 6-12m
vi) retractile - testes may move out of scrotum and into ing canal when its cold or the cremasteric reflex is activated (normal variant)
normal until puberty when it usually resolves
HYPOSPADIAS
i) what is it? what is epispadias? what type of condition is it and when is it dx?
ii) who should the child be referred to? what procedure should not be done?
iii) what may be done for mild cases? between what ages may surgery be performed? what does surgery do?
iv) name three complications
i) urethral meatus is abormally displaced to the ventral side of the penis towards the scrotum
epispadias is meatus displaced to dorsal side (top side of penis)
congenital condition dx on newborn exam
ii) refer to urology for mx
dont circumcise
iii) mild - watch and wait
surgery between 3-4m to correct position of meatus and straighten the penis
iv) hard to urinate, cosmetic/psych concerns, sexual dysfunction
HYDROCELE
i) what is it? which layer of the testes is implicated?
ii) what is a simple hydrocele? does it need treating?
iii) what is a communicating hydrocele? what happens?
iv) how does a hydrocele feel? where will the swelling be? which type remains one side and which type changes volume?
v) what is the key feature when examining a hydrocele?
i) collection of fluid within the tunica vaginalis that surrounds the testes
TV used to be part of peritoneal mem but seperates in development
ii) simple - fluid gets trapped in the tunica vaginalis and fluid usually gts reabs over time and the HC disappears
iii) communicating - TV around the testicle is connected with the peritoneal cavity via the processcus vaginalis > fluid travels from the peritoneal cav to the hydrocele - fluctuates in size
iv) feels soft, smooth, non tender swelling around one teste > swelling infront and below the testicle
simple remains one size and communicating may change size
v) hydrocele will transluminate with light - hold a pen torch flat against the skin and it will light up
HYDROCELE MANAGEMENT
i) name four differential dx for a scrotal/inguinal swelling in a neonate?
ii) which imaging is first line?
iii) how long do simple HC usually take to resolve?
iv) how are communicating HC treated?
i) hydrocele, partially desc testes, ing hernia, testicular torison, haematoma, tumour
ii) ultrasound
iii) simple usually resolves in 2 years
iv) communicating - surgery to remove or ligate the connection bet peritoneal cavity and hydrocele (processus vaginalis)
