Ch 18 - Kidney & Urinary tract disorders Flashcards

1
Q

Renal Agenesis (absence of both kidneys): features (1 syndrome - 5 features)

A

So lack of kidneys > no urine > oligohydramnios (because most of amniotic fluid is made up of fetal urine)
F - Oligohydramnios results in Potter Syndrome (fatal) - fetal compression, low set ears, beaked nose, prominent epicanthic folds, pulmonary hypoplasia causing resp failure, limb deformities > infants may be still born/ die soon after due to resp failure

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2
Q

Multicystic dysplastic kidney: cause, features (1), management (1)

A

Cause - failure of union of ureteric bud (forms ureter, pelvis, calyces, collecting duct) with nephrogenic mesenchyme - so get a non-functioning structure with large fluid-filled cysts and no renal tissue or connection with bladder.
M - half involute by 2 yr so no treatment required, nephrectomy is done only if still very large/ or causing HTN

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3
Q

Polycystic kidney disease: autosomal dominant features (5), autosomal recessive PKD feature (1)

A

ADPKD - discrete cysts of varying size within normal renal parenchyma, HTN, haematuria, enlarged kidneys, extra renal - e.g. hepatic cysts
ARPKD - diffuse bilateral enlargement of both kidneys

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4
Q

What is horseshoe kidney?

A

Fusion of both kidneys at lower poles; predisposes to infection/ obstruction

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5
Q

Duplex anomalies: cause (1) 2 examples

A

Premature ureteric bud division
Duplex ureters - abnormal drainage: ureter from lower pole refluxes, upper pole drains ectopically into urethra/vagina/ may prolapse into bladder, may obstruct urine flow
Duplex pelvis

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6
Q

What is bladder extrophy?

A

When there is failure of fusion of infraumbilical structures - basically the bladder mucosa is exposed (kinda like gastroschisis)

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7
Q

Absence musculature syndrome: what is it?

A

Absence/ def in anterior abdo wall muscles > megacystic megaureters + crytorchidism (undescended testicle)

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8
Q

Urine flow obstruction: can be unilateral (2) or bilateral (2) Give 2 places for each where the obstruction would be
Consequences (2)

A

Obstruction to urine flow leads to dilatation of urinary tract proximal to obstruction.
Unilateral can be at: pelvicoureteric junction (PUJ) or Vesicoureteric junction (VUJ)
Bilateral can be at: Bladder neck or urethra (this will cause hydroureters & hydro nephrosis)
Consequences - Dysplastic kidneys (small + poor function) & if v. severe Potter syndrome

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9
Q

Dysuria alone: differentials 2 Male & 2 Female

A

M - cystitis/balanitis (uncircumsized)

F - Cystitiis/ vulvitis

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10
Q

UTI predisposition: infecting organisms (4)

A

UTIs are usually result of bowel flora entering UT via urethra - except in newborn where its most likely haematogenous.
E. Coli - commonest organism, Klebsiella, Pseudomonas, Proteus, E. Faecalis

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11
Q

UTI predisposition: Antenatally diagnosed renal or urinary tract abnormality

A

increases risk of infection

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12
Q

UTI predisposition: incomplete bladder emptying (4)

A
Contributing factors in some children are:
infrequent voiding > bladder enlargement
Vulvitis
Incomplete micturition
Obstruction from loaded rectum
Neuropathic bladder
vesicoureteric reflux
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13
Q

UTI predisposition: VUR - definition, complications (4)

A

VUJ developmental abnormality (the ureters are displaced laterally and enter directly into bladder rahter than at an angle) > tends to resolve with age
C - Mild reflux into ureters, reflux during bladder filling, intrarenal reflux (into collecting ducts - high risk of scarring), predisposition to UTI/ hydronephrosis

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14
Q

UTI suscpicioun: investigations (2)

A

USS
MCUG - micturating cystourethrogram
DMSA - to check for renal scarring 3 months post UTI

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15
Q

UTI suscpicion/ confirmed management:

1) infant 3 months and children with acute pyelonephritis/ upper UTI - features (3), management (1)
3) Cystitis/lower UTI - feature (1), management (1)

A

1) Refer to hospital! IV Cefotaxime until temp settles > oral AB
2) F - bacteriuria + fever/ loin pain, M - PO co-amoxiclav 7-10 days or IV Cefotaxime for 3 days then oral AB for a week
3) Dysuria only, M - 3 day course of Nitrofurantoin/ tripethoprim/ ceftriaxone/ amoxicillin

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16
Q

Prevention of UTIs (4)

A

Aim is to washout organisms that ascend into bladder from the perineum
High fluid intake
Regular voiding
Ensure complete voiding - double micturition (encourage child to try a second time to empty bladder)
Lactobacillus acidophillus; probiotic colonizes the gut & reduces the number of pathogenic organisms (that may invade)

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17
Q

Primary nocturnal enuresis: definition, causes (3)

A

D - involuntary voiding of urine at least 3/7 in child

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18
Q

Secondary (onset) nocturnal enuresis: definition (1), causes (3), Ix (3)

A

D - child had previously achieved night time dryness
C - Emotional upset (most common), > , constipation, Diabetes
Ix - Urine dipstick, early morning urine osm/ water deprivation test, USS

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19
Q

Management of nocturnal enuresis (3)

A

1st line: Reward systems - star charts: give for agreed behaviour rather than dry nights e.g. if they go to toilet before bed
2nd line: enuresis alarm 7 yrs old

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20
Q

Daytime enuresis: causes (4), Ix (3), management (4)

A

Causes:
detrusor instability (sudden urgent urge to void induced by sudden bladder contractions)
Bladder neck weakness
Neuropathic bladder - enlarged and fails to empty properly, associated with spinda bifida
UTI
Constipation
Ectopic ureter - causes constant dribbling and always damp child
Ix - urine sample microscopy, culture, USS, urodynamic studies
M - Bladder training, pelvic floor exercises, Oxybutynin (anti-cholinergic)

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21
Q

Proteinuria: causes (4)

A

Orthostatic - common postural proteinuria
Minimal change disease
GN
HTN

22
Q

Nephrotic syndrome: triad, causes (3)

A

Proteinuria (hypoalbuminaemia)+ hyperlipidaemia + oedema

Causes - unknown, but some cases secondary to HSP, SLE, minimal change disease

23
Q

Nephrotic syndrome features (3), Ix (3)

A

F - periorbital oedema, ascites, dyspnoea

Ix - dipstick, U & C, albumin, complement levels

24
Q

Steroid sensitive nephrotic syndrome: Features (3), management (1), Complications (2)

A

F - proteinuria resolves with steroids, does not progress to renal failure, precipitated by resp infection
M - oral steroids
C - hypovolaemia, infection, hypercholesterolaemia

25
Q

Management of steroid resistent Nephrotic syndrome: (3)

A

Refer to nephrologist Diuretics, Salt restriction, ACEI

26
Q

Congenital nephrotic syndrome: feature (1), Complication (1), Managment (1)

A

F - presents in 1st 3 months of life
C - hypoalbuminaemia
M - unilateral nephrectomy + dialysis

27
Q

Haematuria: characteristics if glomerular (3), if lower UT (3)

A

Glomerular - Brown, deformed RBCs, casts, proteinuria

UT - red, no proteinuria, unusual in kids

28
Q

Haematuria causes: non glomerular (3), glomerular (3)

A

Non glomerular: infection (by far most common), trauma, stones, bleeding disorders
Glomerular: GN, IgA nephropathy, familial nephritis e.g. Alport syndrome

29
Q

4 causes of acute nephritis

A

Post infectious/strep GN
HSP or other vasculitides
IgA nephropathy
Anti-GBM (v. rare)

30
Q

Post-infectious/strep GN: definition, Ix (2)

A

D - causes a diffuse proliferative GN following a strep sore throat/ skin infection
Ix - Raised ASO + low C3 levels

31
Q

HSP features (3)

A

Preceded by URTI (peak in winter months) palpable rash on buttocks, arthralgia, joint swelling, abdo pain

32
Q

Alport syndrome features (2)

A

Most common familial nephritis (X-linked)

Nerve deafness + ocular defects

33
Q

Vasculitides that affect the kidney: (3)

A

HSP most common, but aslo polyarteritis nodosa, Wegner granulomatosis

34
Q

HTN causes (6)

A

Renal disease: renal parenchymal disease, PKD, RAS

Hyperthyroidism, Phaeo, Cushing, CAH

35
Q

HTN features in kids (4)

A
headache
vomiting
convulsions
facial palsy
FTT
HF
36
Q

Renal masses causes: unilateral (3) bilateral (3)

A
Wilm's tumour
Multicystic kidney
obstructed hydronephrosis
Bilat:
ARPKD
ADPKD
tuberous sclerosis
37
Q

Predisposing causes of Renal calculi in children (3)

A

Uncommon in childhood so when they occur need to figure out the predisposing factor:
UTI
structural anomalies of UT
Metabolic abnormalities

38
Q

Renal calculi are either phosphate or Calcium containing, give examples of what would cause these types of stones (1, 2)

A

Phosphate - most common; occur with infection - commonly Proteus
Calcium containing - idiopathic hypercalciuria, distal renal tubular acidosis,

39
Q

Features of renal calculi (3), management (4)

A

F - haematuria, loin pain, UTI, structural anomaly

M - spontaneous passing, high fluid intake, surgery, correction of anomaly, lithotripsy

40
Q

Renal tubular disorders: Fanconi syndrome - general description, features (4)

A

Abnormalities of renal tubular function may occur at any point along nephron. Fanconi is generalized proximal tubular dysfunction - excessive loss of AAs, glucose, phosphate, Bicarb, sodium, calcium, urate.
F - polydispia + polyuria; salt depletion & dehydration; hyperchloraemic metabolic acidosis; rickets; FTT

41
Q

Refer to Lissaeurs pg 342 for image of specific transport defects, but basically there can be a defect at any point & depending on that the substance that should have been reabsorbed/secreted will not. Give some examples (4)

A

Glycosuria
Cystinuria - renal calculi
Pseudohypoparathyroidism - due to increased phosphate reabsorption; obesity, depressed nasal bridge & short fing
RTA II - due to reduced bicarb reabsorption; metabolic acidosis + alkaline urine + growth failure
Bartter syndrome: due to reduced chloride reabsorption; hypokalaemia + hyponatremia + hypochloraemia + metabolic alkalosis

42
Q

AKI causes: pre-renal (2) causes

A

Hypovolaemia - gastroenteritis, burns sepsis, haemorrhage
Circulatory failure
(pre renal causes most common)

43
Q

Renal causes of AKI: vascular (2), tubular (2), glomerular (1), interstitial (2)

A

Vascular: vasculitides, HUS, renal vein thrombosis
Tubular: ATN, ischaemic, obstructive
glomerular: GN
Interstitial: pyelonephritis, interstitial nephritis

44
Q

Post renal causes of AKI (2)

A

Obstruction:
Congenital - post urethral valves
acquired - blocked urinary catheter

45
Q

Management of pre-renal failure(1) renal failure: if metabolic acidosis (1), hyperphosphataemia (2), hyperkalaemia (3)

A

Pre-renal - fluid replacement
Renal failure - 2 most common causes are HUS & ATN
metabolic acidosis - Sodium bicarb
Hyperphosphataemia - CaCO3 + dietary restriction
Hyperkalaemia - calcium gluconate if see ECG changes, glucose + insulin

46
Q

Management of post-renal failure (2)

A

Nephrostomy after correction of electrolyte abnormalities

47
Q

Indications for dialysis in renal failure: (4)

A
If conservative management fails
severe hypo/hypernatremia
HTN
pulmonary oedem
severe acidosis
48
Q

HUS: cause (1), features (3), Management (1)

A

C - secondary to E. Coli O157 due to uncooked beef
F - Triad of renal failure + MAHA + TTP
M - dialysis

49
Q

CKD causes (3)

A

Very uncommon in children
Most commonly caused by structural malformations
GN
Systemic disease

50
Q

CKD features (5)

A
anorexia
FTT
polyuria/polydipsia
incidential finding of proteinuria
HTN
unexplained normocytic normochromic anaemia
51
Q

Management of CKD: diet (2), prevention of renal osteodystrophy (2), control acidosis and fluid balance (2), hormonal abnormalities (1)

A

Diet - cal supplements, NGT
Prevention of renal osteodystrophy - 2dary HPT develops > osteitis fibrosa cystica + osteomalacia > phosphate restriction via diet, CaCO3,
Acidosis - salt supplements + HCO3 + fluid
Hormonal abnormalities - get GH resistance - give recombinant HGH