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renal > miscellaneous > Flashcards

miscellaneous Flashcards

1
Q

composition of renal stones in children

A

a. Calcium oxalate = 60-90%
b. Calcium phosphate = 10%
c. Struvite = 1-14%
d. Uric acid = 5-10%
e. Cystine = 1-5%

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2
Q

most common metabolic abnormality associated with paed renal stones, and other common abnormalities

A

a. Hypercalciuria = most common
b. Hyperoxaluria
c. Cysteinuria
d. Disorders of purine metabolism

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3
Q

what kind of infections commonly cause struvite stones?

A

Often urease producing organisms (eg proteus, klebsiella, E coli, pseudomonas) (PKEP)

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4
Q

what kind of stones are radio-opaque?

A

struvite

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5
Q

what are some urine and blood tests to do when a child has a renal stone?

A

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

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6
Q

what are some genetic conditions that cause reduced Ca absoprtion?

A

Dent
Bartter
Wilson
GSD type 1

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7
Q

what is the main metabolic abnormality associated with CF and renal stones?

A

hyperoxaluria

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8
Q

what measures can we implement to prevent stones for each metabolic abnormality:

– hyperCa:
– hyperox:
– hyperuric:
– hypercysteine:

A
  • 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)

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9
Q

name some conditions that can predispose to uric acid stones

A

• Lesch-Nyhan syndrome
• Myeloproliferative disorder
• Post chemo
• IBD

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10
Q

pathogenesis of struvite stones

A

b. Urinary alkalinsation  excessive production of ammonia  leads to precipitation of Mg ammonium phosphate + calcium phosphate

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10
Q

name some drugs causing calcium stones

A

topiramate, frusemide, steroids

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11
Q

etiology of oxalate stones - causes of primary vs secondary

A

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

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12
Q

rhabdo classic triad

A
  1. muscle pain and weakness
  2. raised CK
  3. myoglobinuria
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13
Q

aetiology of rhabdo

A

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

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14
Q

CK in rhabdo - when does it peak?

A

CK rises 2-12hrs, peaks within 24-72hrs

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15
Q

Cx of rhabdo

A
  • AKI
  • electrolytes + fluid balance
  • compartment syndrome with fluid resus
  • DIC
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16
Q

monosymptomatic vs non-monosymptomatic enuresis

A

monosymptomatic = enuresis without LUTS
non-monosymptomatic = enuresis with LUTS inc. bladder dysfunction

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17
Q

primary vs secondary enuresis

A

primary = never dry
secondary = enuresis after at least 6 months dry

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18
Q

when is daytime vs night time urinary incontinence usually achieved?

A

Day time continence usually achieved by 4 years, night time at 5-7 years

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19
Q

how common is wetting the bed at 4yo vs 6yo?

A

At 4 years of age, nearly 1 in 3 children wets the bed, but this falls to about 1 in 10 by age 6

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20
Q

when do we usually start treatment for bed wetting and why?

A

not before 6yo, because usually spontaneously resolves before then`

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21
Q

two most common bladder dysfunction disorders

A
  1. nocturnal enuresis
  2. OAB
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22
Q

OAB
- definition
- major symptom
- urodynamic study

A
  • definition: abnormal bladder contraction during the filling phase
  • major symptom: urgency
  • urodynamic study: increased detrusor activity
23
Q

abx course duration for cystitis vs pyelo

A

3–7 day course for children with cystitis
7–10 day course for children with pyelonephritis

24
Q

which pt should have iv abx for uti?

A

unwell, or <3mo

25
Q

what kind of counts suggest true UTI?

A

> 108 CFU/L = suggests infection
106-8 CFU/L from catheter or SPA urine suggests infection

26
Q

who needs renal USS with UTI?

A

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

27
Q

features of an atypical UTI

A

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

28
Q

giggle incontinence
- what?
- proposed pathogenesis
- Rx

A
  • urinary incontinence only when laughing in GIRLS only
  • similar to cataplexy, emotional event causing hypotonia
  • anti-cholinergics e.g. oxybutynin purported to work
29
Q

voiding postponement / underactive bladder - what is it?

A

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

30
Q

Mx of nocturnal enuresis

A
  1. bed wetting alarm: 8-10 weeks
  2. desmopressin: works quick. restrict fluids 1h pre and 8h post, risk of hyponatraemic seizures
  3. oxybutynin if OAB component
31
Q

what is dysfunctional voiding? what do we name non-neurogenic dysfunctional voiding?

A

habitual contraction of the sphincter during voiding, producing uroflow curves of a staccato type

Hinman-Allen syndrome

32
Q

what time of day is urge incontinence usually the worst?

A

afternoon

33
Q

Mx options for enuresis

A

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

34
Q

most common reason for desmopression ineffectiveness

A

reduced nocturnal bladder capacity

35
Q

how does oxybutynin work?

A

anti-cholinergic: Decrease frequency of detrusor contractions during the filling phase of the bladder

36
Q

leading cause of death post renal transplant

A

cardiac death

37
Q

CKD vs AKI = reduction in nephron what?

A

Reduction in total nephrons = CKD
Reduction in single nephron GFR = AKI

38
Q

pre-renal, renal and post-renal causes of AKI

A

pre-renal: hypovolaemia, sepsis, hypoalbuminaeami
renal: vascular, glomerular, tubular, interstitial
post-renal = obstruction

39
Q

differentiate between pre-renal AKI and ATN

A

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)

40
Q

aetiology of ATN

A

most common intrarenal cause of AKI, either from:
ischaemia (60%) - all causes of pre-renal AKI can cause ischaemic ATN
nephrotoxic (40%) - nsaids, aminoglycosides,

41
Q

ATN vs AIN

A

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.

42
Q

AIN + young female + eyes = what?

A

TINU = tubulointerstitial nephritis with uveitis
autoimmune
adolescent females
uveitis

43
Q

little blood or protein in the urine … think of what kind of renal disease?

A

tubular! e.g. acute tubulointerstitial nephritis

44
Q

pre-renal vs intrarenal BUN:Cr ratio

A

pre-renal ratio > 20 because RAAS activation causes water retention
intra-renal ratio <20 because they kidneys are alllll screwed

45
Q

indications for dialysis mnemonic

A

AEIOU

Refractory:…
acidosis
electrolyte derangement
intoxicants/drugs
overload
uraemia

46
Q

medical management of CKD - memory aid

A

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)

47
Q

haemodialysis vs haemofiltration

A

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

48
Q

empiric PD peritonitis abx

A

Coverage for GP and GN organisms – IV vancomycin + ceftazadime

49
Q

most common organisms causing PD peritonitis

A

CONS > Streptococci > Staphylococcus

50
Q

renal transplant complications: major timeframes, and most common causes of each

A

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

51
Q

most common cause of allograft rejection due to recurrent disease

A

FSGS recurrence!

52
Q

what viruses can cause renal allograft dysfunction?

A

Herpesviruses (CMV, HSV, VZV, EBV)
Polyomavirus nephropathy (BK nephropathy)

53
Q

most common malignancy post renal transplant

A

EBV PTLD

54
Q

most common post-transplant bacterial infections

A

pneumonia and UTI

55
Q

induction immunotherapy in renal transplants

A
  1. T cell antibodies
    - ATGAM, thymoglobulin = polyclonal antibodies against human T-lymphocyte antigens > rapid depletion of T lymphocytes
    - OKT3 = monoclonal antibody against CD3
  2. IL-2 receptor antibodies
  3. Anti-CD25 antibodies = basiliximab: Prevent T cell proliferation but do not cause T cell depletion
  4. Alemtuzumab (Campath) = anti CD52 on T/ B cells/ monocytes and NK cells
56
Q

maintenance immunotherapy in renal transplant

A

Usually calcineurin inhibitor (tacrolimus or cyclosporin) + steroids + anti-proliferative agent (azathioprine, sirolimus or MMF)

renal (6 decks)

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