miscellaneous Flashcards
composition of renal stones in children
a. Calcium oxalate = 60-90%
b. Calcium phosphate = 10%
c. Struvite = 1-14%
d. Uric acid = 5-10%
e. Cystine = 1-5%
most common metabolic abnormality associated with paed renal stones, and other common abnormalities
a. Hypercalciuria = most common
b. Hyperoxaluria
c. Cysteinuria
d. Disorders of purine metabolism
what kind of infections commonly cause struvite stones?
Often urease producing organisms (eg proteus, klebsiella, E coli, pseudomonas) (PKEP)
what kind of stones are radio-opaque?
struvite
what are some urine and blood tests to do when a child has a renal stone?
Serum - UEC, CMP, uric acid, gas (acid, HCO3), PTH, vitamin D
Urine:
pH, microscopy and culture
metabolites (24h/Cr ratio): Cystine, calcium, oxalate, uric acid, citrate, Mg
what are some genetic conditions that cause reduced Ca absoprtion?
Dent
Bartter
Wilson
GSD type 1
what is the main metabolic abnormality associated with CF and renal stones?
hyperoxaluria
what measures can we implement to prevent stones for each metabolic abnormality:
– hyperCa:
– hyperox:
– hyperuric:
– hypercysteine:
- inc fluid intake AND:
– hyperCa: esp reduced Na, inc protein, inc K //2nd line Kcitrate
– hyperox: reduce oxalate, Kcitrate
– hyperuric: alkalise urine with Kcitrate, allopurinol/uricase
– hypercysteine: alkalise urine with Kcitrate, reduce Na, PENICILLAMINE (makes them more soluble)
name some conditions that can predispose to uric acid stones
• Lesch-Nyhan syndrome
• Myeloproliferative disorder
• Post chemo
• IBD
pathogenesis of struvite stones
b. Urinary alkalinsation excessive production of ammonia leads to precipitation of Mg ammonium phosphate + calcium phosphate
name some drugs causing calcium stones
topiramate, frusemide, steroids
etiology of oxalate stones - causes of primary vs secondary
Primary hyperoxaluria (PH1 most common)
Secondary e.g. malabsorption (IBD/CF):
1) Increased enteric oxalate absorption if not enough Ca binding it in the gut OR
2) Fatty acids usually bind calcium in GIT: less FA > more Ca absorbed
rhabdo classic triad
- muscle pain and weakness
- raised CK
- myoglobinuria
aetiology of rhabdo
a. Hereditary myopathies and inflammatory muscle diseases
b. Traumatic muscle injury
c. Increased voluntary or involuntary muscle activity (seizures, severe asthma, heat stroke)
d. Toxins: alcohol and drugs (neuroleptic malignant syndrome, malignant hyperthermia)
e. infection e.g. influenza
CK in rhabdo - when does it peak?
CK rises 2-12hrs, peaks within 24-72hrs
Cx of rhabdo
- AKI
- electrolytes + fluid balance
- compartment syndrome with fluid resus
- DIC
monosymptomatic vs non-monosymptomatic enuresis
monosymptomatic = enuresis without LUTS
non-monosymptomatic = enuresis with LUTS inc. bladder dysfunction
primary vs secondary enuresis
primary = never dry
secondary = enuresis after at least 6 months dry
when is daytime vs night time urinary incontinence usually achieved?
Day time continence usually achieved by 4 years, night time at 5-7 years
how common is wetting the bed at 4yo vs 6yo?
At 4 years of age, nearly 1 in 3 children wets the bed, but this falls to about 1 in 10 by age 6
when do we usually start treatment for bed wetting and why?
not before 6yo, because usually spontaneously resolves before then`
two most common bladder dysfunction disorders
- nocturnal enuresis
- OAB
OAB
- definition
- major symptom
- urodynamic study
- definition: abnormal bladder contraction during the filling phase
- major symptom: urgency
- urodynamic study: increased detrusor activity
abx course duration for cystitis vs pyelo
3–7 day course for children with cystitis
7–10 day course for children with pyelonephritis
which pt should have iv abx for uti?
unwell, or <3mo
what kind of counts suggest true UTI?
> 108 CFU/L = suggests infection
106-8 CFU/L from catheter or SPA urine suggests infection
who needs renal USS with UTI?
Seriously unwell children, those with renal impairment, and boys <3 months of age should have a renal ultrasound prior to discharge
Other children do not require an ultrasound for a first UTI; a non-urgent renal ultrasound should be arranged for children who have recurrent UTIs
features of an atypical UTI
a. Clinical symptoms = poor stream/ palpable kidneys/ bladder
b. Unusual organism = proteus, enterococcus
c. Bacteremia/ septicaemia
d. Prolonged clinical course
e. Known antenatal abnormalities
f. Raised Cr
g. Failure to respond to treatment within 48 hours
giggle incontinence
- what?
- proposed pathogenesis
- Rx
- urinary incontinence only when laughing in GIRLS only
- similar to cataplexy, emotional event causing hypotonia
- anti-cholinergics e.g. oxybutynin purported to work
voiding postponement / underactive bladder - what is it?
habitual holding e.g. school > reduced frequency > inc bladder capacity > underactive bladder > increased abdominal pressure to void and overflow incontinence and UTI risk
females > males
Mx of nocturnal enuresis
- bed wetting alarm: 8-10 weeks
- desmopressin: works quick. restrict fluids 1h pre and 8h post, risk of hyponatraemic seizures
- oxybutynin if OAB component
what is dysfunctional voiding? what do we name non-neurogenic dysfunctional voiding?
habitual contraction of the sphincter during voiding, producing uroflow curves of a staccato type
Hinman-Allen syndrome
what time of day is urge incontinence usually the worst?
afternoon
Mx options for enuresis
non-pharm at least 3-6 months first:
- treat other conditions eg constipation, ADHD
- timed voiding / double voiding
- void diary
- reduce caffeine/sugar in evening
- rewards
Active therapy:
1. alarm
2. desmopressin (oral - IN a/w hypoNa seizures)
3. other e.g. oxybutynin for OAB, tamsulosin
most common reason for desmopression ineffectiveness
reduced nocturnal bladder capacity
how does oxybutynin work?
anti-cholinergic: Decrease frequency of detrusor contractions during the filling phase of the bladder
leading cause of death post renal transplant
cardiac death
CKD vs AKI = reduction in nephron what?
Reduction in total nephrons = CKD
Reduction in single nephron GFR = AKI
pre-renal, renal and post-renal causes of AKI
pre-renal: hypovolaemia, sepsis, hypoalbuminaeami
renal: vascular, glomerular, tubular, interstitial
post-renal = obstruction
differentiate between pre-renal AKI and ATN
Pre-renal = concentrating ability of kidney retained
i. Concentrated urine with LOW urinary sodium
ii. LOW fractional excretion of sodium + excretion
iii. High urinary specific gravity
Intrinsic = will not have kidneys which are capable of concentrating + have things in the kidney which should not be there eg. casts
i. Dilute urine with HIGH urinary sodium
ii. HIGH fractional excretion of sodium + excretion
iii. Low urinary specific gravity (dilute urine)
aetiology of ATN
most common intrarenal cause of AKI, either from:
ischaemia (60%) - all causes of pre-renal AKI can cause ischaemic ATN
nephrotoxic (40%) - nsaids, aminoglycosides,
ATN vs AIN
ATN:
hours to days
ischaemia vs nephrotoxins
muddy brown casts
oliguria
AIN:
weeks-months
drugs (NSAIDS!) vs infection vs systemic disease
non-oliguric, systemic features e.g. rash, vomiting, fever
eosinophilia, hematuria, pyuria
white cell casts, and red blood cells.
AIN + young female + eyes = what?
TINU = tubulointerstitial nephritis with uveitis
autoimmune
adolescent females
uveitis
little blood or protein in the urine … think of what kind of renal disease?
tubular! e.g. acute tubulointerstitial nephritis
pre-renal vs intrarenal BUN:Cr ratio
pre-renal ratio > 20 because RAAS activation causes water retention
intra-renal ratio <20 because they kidneys are alllll screwed
indications for dialysis mnemonic
AEIOU
Refractory:…
acidosis
electrolyte derangement
intoxicants/drugs
overload
uraemia
medical management of CKD - memory aid
in CKD,
bastard = bone i.e. calcium/phosphate/vit D
— can’t activate vit D: low Ca abs, bad phos excretion: Ca supps, PO4 binders, vit D supp
chronic - cardiac/cardiomyopathy
health - HTN (ACE/ARB)
problems - proteinuria (ACEI)
never - nutrition
ever - electrolytes
fucking - fluids
go - growth
away - anaemia (EPO) / acidosis (sodi bic)
haemodialysis vs haemofiltration
Haemodialysis
• Primarily removes solute by DIFFUSION
• Dialysate fluid is used
Haemofiltration
• Uses HYDROSTATIC PRESSURE to induce the filtration of plasma water across the haemofilter membrane
• Solutes are removed by CONVECTION
• Dialysate fluid is NOT used
empiric PD peritonitis abx
Coverage for GP and GN organisms – IV vancomycin + ceftazadime
most common organisms causing PD peritonitis
CONS > Streptococci > Staphylococcus
renal transplant complications: major timeframes, and most common causes of each
immediate = up to 1 week post
- postischemic AKI, vascular thrombosis, urologic complications (ie, urinary leak or obstruction), and rarely, hyperacute rejection.
early = 1-12 weeks
- allograft rejection, calcineurin inhibitor toxicity, urinary obstruction, infection, hypovolemia, and recurrent disease
late acute = >3mo
- same
late chronic = years
- chronic allograft injury, calcineurin toxicity, hypertensive nephrosclerosis, viral infection, recurrent/de novo disease
most common cause of allograft rejection due to recurrent disease
FSGS recurrence!
what viruses can cause renal allograft dysfunction?
Herpesviruses (CMV, HSV, VZV, EBV)
Polyomavirus nephropathy (BK nephropathy)
most common malignancy post renal transplant
EBV PTLD
most common post-transplant bacterial infections
pneumonia and UTI
induction immunotherapy in renal transplants
- T cell antibodies
- ATGAM, thymoglobulin = polyclonal antibodies against human T-lymphocyte antigens > rapid depletion of T lymphocytes
- OKT3 = monoclonal antibody against CD3 - IL-2 receptor antibodies
- Anti-CD25 antibodies = basiliximab: Prevent T cell proliferation but do not cause T cell depletion
- Alemtuzumab (Campath) = anti CD52 on T/ B cells/ monocytes and NK cells
maintenance immunotherapy in renal transplant
Usually calcineurin inhibitor (tacrolimus or cyclosporin) + steroids + anti-proliferative agent (azathioprine, sirolimus or MMF)
