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My Phase 3a Revision > PAEDS - RENAL > Flashcards

PAEDS - RENAL Flashcards

1
Q

PROTEINURIA
What are some causes of proteinuria?

A
  • Transient (febrile illness, after exercise = no investigation)
  • Nephrotic syndrome
  • HTN
  • Tubular proteinuria
  • Increased glomerular perfusion pressure
  • Reduced renal mass
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2
Q

PROTEINURIA
What is proteinuria?

A
  • Persistent proteinuria is significant + should be quantified by measuring the urine protein/creatinine ratio in an early morning sample
  • Protein should not exceed <20mg/mmol of creatinine
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3
Q

NEPHROTIC SYNDROME
What is nephrotic syndrome?
Who is it most common in?

A
  • Basement membrane in the glomerulus becomes highly permeable to protein, allowing proteins to leak from blood into the urine
  • 2–5y
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4
Q

NEPHROTIC SYNDROME
What are the signs needed in order to make a diagnosis of nephrotic syndrome?

A
  • Heavy proteinuria (>1g/m^2/24h)
  • Hypoalbuminaemia (<25g/L)
  • hypercholesterolaemia
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5
Q

NEPHROTIC SYNDROME
What is the pathophysiology of nephrotic syndrome?

A
  1. Inflammation – from immune cells (Ab’s, Ig’s - IgG), complement proteins, HTN, atherosclerosis, medications/immunisations, infection
  2. Damage to podocytes – protein leakage (albumin, Ab’s)
  3. Increased liver activity – to increase albumin, - Consequential increase in cholesterol + coagulation factors
  4. Reduced oncotic pressure – oedema - Consequential blood volume decrease, RAAS stimulation, exacerbation
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6
Q

NEPHROTIC SYNDROME
What are the 3 main types of nephrotic syndrome?

A
  • minimal change disease
  • membranous glomerulonephritis
  • focal segmental glomerulosclerosis
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7
Q

NEPHROTIC SYNDROME
What is minimal change disease?

A
  • Most common cause in children with no underlying pathology
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8
Q

NEPHROTIC SYNDROME
what is the main symptom of nephrotic syndrome?

A

Pitting oedema - periorbital, ascites, peripheral

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9
Q

NEPHROTIC SYNDROME
what can cause minimal change disease?

A
  • NSAIDs,
  • Hodgkin’s lymphoma,
  • infectious mononucleosis
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10
Q

NEPHROTIC SYNDROME
Who does minimal change disease present in?

A
  • M>F,
  • commoner in Asian children than Caucasians,
  • do not progress to renal failure
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11
Q

NEPHROTIC SYNDROME
What are the features of minimal change disease?

A
  • 1–10y
  • No macroscopic haematuria
  • Normal BP, complement levels, renal function
  • Often precipitated by resp infections
  • 1/3 resolve, 1/3 infrequent relapses, 1/3 frequent relapses
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12
Q

NEPHROTIC SYNDROME
what is the epidemiology of congenital nephrotic syndrome?

A
  • First 3m of life, rare, high mortality
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13
Q

NEPHROTIC SYNDROME
what is the inheritance pattern of congenital nephrotic syndrome?

A

Recessive inheritance with increased incidence in Finnish (UK = consanguinity)

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14
Q

NEPHROTIC SYNDROME
what are the clinical features of congenital nephrotic syndrome?

A

Albuminuria so severe may need unilateral nephrectomy then dialysis for renal failure until renal transplant

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15
Q

NEPHROTIC SYNDROME
What is the clinical presentation of nephrotic syndrome?

A
  • Frothy urine (significant proteinuria)
  • Generalised oedema (pitting + gravitational), can be periorbital (esp on waking)
  • May have scrotal, vulval, leg + ankle oedema too
  • Pallor, breathlessness (pleural effusions) + abdo distension (ascites)
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16
Q

NEPHROTIC SYNDROME
What are some investigations for nephrotic syndrome?

A
  • Urinalysis (proteinuria + microscopic haematuria)
  • Urine MC&S (infection)
  • Renal function (U+Es, creatinine, albumin, urinary Na+ concentration)
  • Lipid profile
  • Systemic disease screen
  • Antistreptolysin O or anti-DNAse B titres + throat swab
  • Renal biopsy for histology if no steroid response
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17
Q

NEPHROTIC SYNDROME
In nephrotic syndrome, what are you looking for with the lipid profile?

A

Deranged (hyperlipidaemia, hypercholesterolaemia)

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18
Q

NEPHROTIC SYNDROME
In nephrotic syndrome, what are you looking for with the systemic disease screen?

A

FBC, CRP/ESR, complement (C3/4) levels, autoimmune screen, hep B/C screen, malaria if abroad

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19
Q

NEPHROTIC SYNDROME
In minimal change disease, what are you looking for with the renal biopsy?

A

Minimal change disease shows normal glomeruli on light microscopy but fusion of podocytes + effacement of foot processes on electron

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20
Q

NEPHROTIC SYNDROME
What are some complications of nephrotic syndrome?

A
  • Hypovolaemia as fluid leaks from intravascular to interstitial space
  • Thrombosis due to loss of antithrombin III
  • Infection due to leakage of immunoglobulins, weakening the immune system + exacerbated by Tx with steroids
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21
Q

NEPHROTIC SYNDROME
What is the general management of nephrotic syndrome?

A
  • Strict fluid balance with restriction, no added salt
  • Tx hypovolaemia if present but albumin infusion is not routine
  • Diuretics if very oedematous + no evidence of hypovolaemia
  • Prophylactic PO penicillin V until oedema-free
  • PCV vaccine
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22
Q

NEPHRITIC SYNDROME
What is nephritic syndrome?

A
  • Acute nephritis is inflammation within the nephrons of the kidneys
  • This leads to reduction in kidney function, macroscopic haematuria + proteinuria
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23
Q

NEPHRITIC SYNDROME
What are some causes of nephritic syndrome?

A
  • Post-streptococcal glomerulonephritis
  • IgA nephropathy (Berger’s disease)
  • Vasculitis (HSP, SLE, Wegener’s, polyarteritis nodosa)
  • Goodpasture’s syndrome
  • Familial nephritis (Alport’s syndrome)
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24
Q

NEPHRITIC SYNDROME
What is post-streptococcal glomerulonephritis?

A
  • Nephritis after group A beta-haemolytic strep pyogenes illness (tonsillitis)
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25
Q

NEPHRITIC SYNDROME
What is the pathophysiology of post-streptococcal glomerulonephritis?

A

Immune complexes made up of streptococcal antigens, antibodies + complement proteins get stuck in glomeruli > inflammation

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26
Q

NEPHRITIC SYNDROME
How does familial nephritis (Alport’s syndrome) present?

A
  • X-linked recessive
  • ESRF by early adult
  • Associated with nerve deafness + ocular defects
  • Mother may have haematuria
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27
Q

NEPHRITIC SYNDROME
What is the clinical presentation of nephritic syndrome?

A
  • Haematuria (often macroscopic) + proteinuria of varying degree
  • Impaired GFR (rising creatinine), decreased urine output + volume overload
  • Salt + water retention > HTN (?seizures) + oedema (eyes)
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28
Q

NEPHRITIC SYNDROME
What are some investigations for nephritic syndrome?

A
  • Urinalysis = haematuria, raised protein, (PCR, RBC casts on microscopy)
  • FBC, U+Es = raised urea) raised creatinine + hyperkalaemic acidosis
  • C3/4 may be low (post-strep, SLE)
  • Antistreptolysin O titre (may be raised), throat/skin swabs for strep
  • Renal biopsy
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29
Q

NEPHRITIC SYNDROME
What is the general management of nephritic syndrome?

A
  • Fluid + electrolyte balance, monitor UO + creatinine
  • Treat HTN + oedema with antihypertensives ±diuretics (ACEi/ARB, furosemide or prednisolone)
  • Nephritis usually settles alone, may need steroids
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30
Q

NEPHRITIC SYNDROME
What is the management of post-strep glomerulonephritis?

A

Supportive, mostly full recovery (some have worsening renal function), penicillin if active infection

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31
Q

HSP
What is Henoch-Schönlein purpura (HSP)?

A
  • IgA mediated small vessel vasculitis leading to inflammation affecting the skin, joints, GI tract + kidneys
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32
Q

HSP
What is the epidemiology of Henoch-Schönlein purpura (HSP)?

A

3-10y, M>F + peaks during winter, preceded by URTI or gastroenteritis

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33
Q

HSP
What is the clinical presentation of HSP?

A
  • Palpable purpuric rash affecting extensor surfaces of lower limbs + buttocks
  • Joint pain (knees + ankles, may be swollen + painful, reduced ROM)
  • Colicky abdo pain (GI haemorrhage > haematemesis + melaena, intussusception)
  • Renal involvement (IgA nephritis > haematuria + proteinuria)
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34
Q

HSP
What are some investigations for HSP?

A
  • Exclude DDx of non-blanching rash
    – FBC + blood film (thrombocytopenia, sepsis + leukaemia), CRP, cultures, HSP = afebrile
  • Urinalysis for proteinuria + haematuria
  • PCR to quantify proteinuria
  • Renal biopsy if severe renal issues to determine if Tx
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35
Q

HSP
What might happen if proteinuria becomes severe in HSP?
What would you monitor?

A
  • Nephrotic syndrome
  • BP + serum albumin
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36
Q

HSP
What is the management of HSP?

A
  • Supportive = analgesia for arthralgia, inconsistent evidence for steroid use
  • Often good prognosis, self-limiting but 1/3 recur
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37
Q

HAEMOLYTIC URAEMIC SYNDROME
What is haemolytic uraemic syndrome (HUS)?

A
  • Thrombosis within small blood vessels throughout the body, usually triggered by a bacterial toxin (shiga)
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38
Q

HAEMOLYTIC URAEMIC SYNDROME
What is the classic HUS triad?

A
  • Microangiopathic haemolytic anaemia (due to RBC destruction)
  • AKI (kidneys fail to excrete waste products like urea)
  • Thrombocytopenia
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39
Q

HAEMOLYTIC URAEMIC SYNDROME
What are some causes of HUS?

A
  • Mostly E. Coli 0157 producing Shiga toxin, can be Shigella (?Petting zoo)
  • Use of Abx + antimotility agents to treat gastroenteritis caused by these pathogens can increase risk of HUS
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40
Q

HAEMOLYTIC URAEMIC SYNDROME
What is the clinical presentation of HUS?

A
  • Prodrome of bloody diarrhoea
  • Urine > reduced output, haematuria or dark brown
  • Abdo pain, lethargy
  • Oedema, HTN, bruising
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41
Q

HAEMOLYTIC URAEMIC SYNDROME
What are some investigations for HUS?

A
  • FBC (anaemia, thrombocytopenia), fragmented blood film
  • U+Es reveal AKI
  • Stool culture
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42
Q

HAEMOLYTIC URAEMIC SYNDROME
What is the management of HUS?

A
  • ABCDE as emergency
  • Often self-limiting so supportive > refer to paeds renal unit for ?dialysis
  • Anti-hypertensives, careful fluid balance, blood transfusions
  • Plasma exchange if severe + not associated with diarrhoea
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43
Q

HAEMATURIA
How can you differentiate the source of haematuria based on its presentation?

A
  • Glomerular = brown urine, deformed red cells, presence of casts, often with proteinuria
  • Lower urinary tract = red urine, occurs at beginning or end of stream, not accompanied by proteinuria
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44
Q

HAEMATURIA
What is the most common cause of haematuria?
What are the other 2 broad causes?

A
  • UTI
  • Glomerular or non-glomerular
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45
Q

HAEMATURIA
What are some glomerular causes of haematuria?

A
  • Acute/chronic glomerulonephritis,
  • IgA nephropathy,
  • familial nephritis,
  • post-strep glomerulonephritis,
  • HSP,
  • goodpasture’s
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46
Q

HAEMATURIA
What are some non-glomerular causes of haematuria?

A
  • Wilm’s tumour,
  • trauma,
  • stones (esp if FHx),
  • sickle cell disease
  • other bleeding disorders
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47
Q

HAEMATURIA
What investigations for haematuria should all patients get?

A
  • Urinalysis + urine MC&S
  • FBC, platelets, clotting + sickle cell screen
  • U+Es, creatinine, albumin, Ca2+, phosphate
  • USS kidneys + urinary tract
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48
Q

HAEMATURIA
What investigations would you do if you suspected glomerular haematuria?

A
  • ESR, C3/4 + anti-DNA antibodies
  • Throat swab + antistreptolysin O/anti-DNAse B titres
  • Hepatitis B/C screen
  • Renal biopsy if recurrent haematuria, abnormal renal function/complement levels or significant persistent proteinuria
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49
Q

HYPOSPADIAS
What is hypospadias?

A
  • Urethral meatus is abnormally displaced posteriorly on the penis
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50
Q

HYPOSPADIAS
What is epispadias?

A

Meatus displayed anteriorly on top of the penis

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51
Q

HYPOSPADIAS
What is the clinical presentation of hypospadias?

A
  • Ventral urethral meatus
  • Hooded prepuce
  • Chordee (ventral or downwards curvature of the penis in more severe forms)
  • Usually identified during NIPE
52
Q

HYPOSPADIAS
What is the management of hypospadias?

A
  • Do NOT circumcise as foreskin often needed for later reconstructive surgery
  • Refer to paediatric specialist urologist
  • Mild cases may not require any treatment
  • Surgery done <2y to correct position of meatus + straighten penis
53
Q

UTI
What is a urinary tract infection (UTI)?

A
  • Growth of bacteria within the urinary tract (>10^5 single organism/ml)
54
Q

UTI
How can UTIs be differentiated anatomically?

A
  • Upper tract infection involves the kidneys (pyelonephritis) + associated with fever, loin pain/tenderness
  • Lower tract infection involves bladder (cystitis) + low-grade fever with urinary Sx
55
Q

UTI
When is a UTI classified as atypical?

A
  • Septicaemia
  • Poor urine flow
  • Non-E. Coli
  • Failure to respond
56
Q

UTI
What are some causes of UTI?

A
  • # 1 = E. coli, often from bowel contamination
  • Proteus (M>F, predisposes to formation of phosphate stones in urine)
  • Pseudomonas (may indicates structural abnormality)
57
Q

UTI
What is a complication of E. Coli which might make it difficult to treat?

A
  • Can become resistant to penicillin by producing beta-lactamase (ESBL E. Coli) which breakdown the beta lactam part of Abx making it ineffective
58
Q

UTI
What are some risk factors for UTI?

A
  • Incomplete bladder emptying
  • Vesico-ureteric reflux
  • Structural abnormality (horseshoe kidney, ureteric strictures)
  • Inadequate toilet hygiene
59
Q

UTI
What is the clinical presentation of UTI in infants?

A

Non-specific =
- fever,
- irritable,
- D+V,
- prolonged neonatal jaundice,
- failure to thrive,
- septicaemia,
- febrile convulsions (>6m)

60
Q

UTI
What is the clinical presentation of UTI in children?

A
  • Loin/abdo (suprapubic) pain,
  • fever (± rigors),
  • febrile convulsions,
  • increased frequency,
  • dysuria,
  • haematuria,
  • recurrent enuresis,
  • offensive urine
61
Q

UTI
What are some investigations for UTI?

A
  • Urinalysis for nitrites, leukocytes esterase
  • Urine sample MC&S = collection pads (babies), MSU clean catch, suprapubic aspiration from bladder under USS worse case
62
Q

UTI
In terms of performing ultrasounds scans in UTI, what are the guidelines?

A
  • USS within 6w if 1st UTI + <6m but responds well to Tx within 48h or during illness if recurrent or atypical bacteria
63
Q

UTI
What are some complications of UTI?

A
  • Recurrent kidney infections can cause renal scarring predisposing to HTN, chronic renal failure + even pregnancy complications later in life
64
Q

UTI
What is the supportive management of UTI?

A
  • Good fluid intake, analgesia
  • Wipe front>back
  • Regular voiding + ensure complete bladder emptying
65
Q

UTI
Admission criteria for UTI?

A
  • Admission if <3m, systemically unwell or significant risk factors
66
Q

UTI
What is the management of children under 3m in UTI?

A

ALL children <3m + fever get immediate IV cefuroxime + full septic screen (blood cultures, FBC, CRP lactate, LP etc)

67
Q

UTI
What is the management of UTI for >3m with upper UTI?

A

?Admission for IV, if not PO co-amoxiclav for 7–10d

68
Q

UTI
What is the management of UTI for >3m with lower UTI?

A

3d PO trimethoprim, nitrofurantoin, amoxicillin or cephalosporin with follow-up if still unwell after 24-48h

69
Q

UTI
What is the management of UTI for ESBL E. Coli?

70
Q

UTI
What is a recurrent UTI?

A
  • ≥2 UTIs with ≥1 with systemic Sx (or ≥3 without)
71
Q

UTI
What are the investigations for recurrent + atypical UTIs?

A
  • USS within 6w in all children with recurrent UTIs
  • DMSA (dimercaptosuccinic acid) scan (renal scarring 4-6m)
  • Micturating cystourethrogram (<6m) if FHx of vesico-ureteric reflux, dilatation of ureter on USS, poor urinary flow (catheterise + inject contrast into bladder)
72
Q

UT ABNORMALITIES
Name 6 urinary tract abnormalities

A
  • Renal agenesis
  • Multicystic dysplastic kidney
  • Polycystic kidney disease
  • Pelvic/horseshoe kidney
  • Posterior urethral valves
  • Prune-belly syndrome
73
Q

UT ABNORMALITIES
What is renal agenesis?

A
  • Absence of both kidneys
74
Q

UT ABNORMALITIES
What is a serious complication of renal agenesis and how does that present?

A
  • Absence of both kidneys causes severe oligohydramnios + hence foetal compression from reduced foetal urine excretion - this can cause Potter syndrome (fatal)
    • Low-set ears, beaked nose, prominent epicanthic folds + downward slant to eyes
75
Q

UT ABNORMALITIES
What are some other consequences of oligohydramnios in renal agenesis?

A
  • Pulmonary hypoplasia > respiratory failure
  • Limb deformities such as severe talipes
76
Q

UT ABNORMALITIES
What is multicystic dysplastic kidney?

A
  • Non-functioning structure with large fluid-filled cysts with no renal tissue or connection with bladder
77
Q

UT ABNORMALITIES
What causes multicystic dysplastic kidney?

A

Failure of union of ureteric bud with nephrogenic mesenchyme

78
Q

UT ABNORMALITIES
What is the management of multicystic dysplastic kidney?
What is a complication?

A
  • Half involuted by 2y + nephrectomy only indicated if very large or HTN
  • No urine production so if bilateral > Potter syndrome
79
Q

UT ABNORMALITIES
How does polycystic kidney disease differ from MDK?

A
  • Some renal function remained in polycystic kidney disease
80
Q

UT ABNORMALITIES
What are the two types of polycystic kidney disease?

A
  • AD = HTN, haematuria in childhood with renal failure in adulthood
  • AR = defect on chromosome 6 that encodes fibrocystin, protein for normal renal tubule development
81
Q

UT ABNORMALITIES
How might autosomal recessive polycystic kidney disease present?

A
  • Antenatal USS or with abdo masses or renal failure
  • Neonates may develop Potter syndrome secondary to oligohydramnios
82
Q

UT ABNORMALITIES
What are some complications of autosomal recessive polycystic kidney disease?

A

Often liver involvement with portal + interlobular fibrosis

83
Q

UT ABNORMALITIES
What is pelvic/horseshoe kidney?

A
  • Abnormal caudal migration when the lower poles are fused in the midline
84
Q

UT ABNORMALITIES
What is a complication of pelvic/horseshoe kidney?

A

Abnormal position can predispose to infection or obstruction to urinary outflow

85
Q

UT ABNORMALITIES
What is posterior urethral valves?
What is a consequence?

A
  • Tissue at proximal end of urethra causes obstruction to urinary outflow, M>F
  • Back pressure into bladder, ureters + up to kidneys > hydronephrosis
  • Also prevents complete bladder emptying > risk of UTI
86
Q

UT ABNORMALITIES
How can posterior urethral valves present in utero?
What is a complication of posterior urethral valves?

A
  • Oligohydramnios + potentially pulmonary hypoplasia
  • Risk of dysplastic kidneys, at its worse if bilateral could lead to potter syndrome
87
Q

UT ABNORMALITIES
What is Prune-belly syndrome?

A
  • Absent musculature leading to large bladder + Dilated ureters (megacystis-megaureters) + cryptorchidism
88
Q

UT ABNORMALITIES
What are the 2 first steps in management of urinary tract abnormalities?
How is the management split after that?

A
  • Antenatal Dx + start prophylactic Abx to prevent UTI
  • Bilateral hydronephrosis and/or dilated lower urinary tract in a male
  • Unilateral hydronephrosis in male or any anomaly in female
89
Q

UT ABNORMALITIES
What is the management of bilateral hydronephrosis and/or dilated lower urinary tract in a male?

A
  • Bilateral seen in bladder neck obstruction or posterior urethral valves
  • USS within 48h of birth to exclude posterior urethral valves
    – Abnormal = MCUG + surgery if required (ablation during cystoscopy)
    – Normal = stop Abx, repeat USS after 2-3m
90
Q

UT ABNORMALITIES
What is the management of unilateral hydronephrosis in male or any anomaly in female?

A
  • Unilateral seen in pelviureteric or vesicoureteric junction obstruction
  • Abnormal = further investigations
  • Normal = stop Abx, repeat USS after 2-3m
91
Q

ACUTE KIDNEY INJURY
What is acute kidney injury (AKI)?
What is it characterised by?

A
  • Spectrum of potentially reversible, reduction in renal function
  • Rapid rise in creatinine + development of oliguria (<0.5ml/kg/h)
92
Q

ACUTE KIDNEY INJURY
What are the 3 broad causes of AKI?

A
  • Pre-renal (most common cause in children)
  • Renal
  • Post-renal
93
Q

ACUTE KIDNEY INJURY
What are some pre-renal causes of AKI?

A
  • Hypovolaemia = nephrotic syndrome, haemorrhage, sepsis, burns
  • Circulatory failure
94
Q

ACUTE KIDNEY INJURY
What are some renal causes of AKI?

A
  • Vascular = HUS, vasculitis, embolus)
  • Glomerular = glomerulonephritis
  • Interstitial = interstitial nephritis, pyelonephritis
  • Tubular = acute tubular necrosis
95
Q

ACUTE KIDNEY INJURY
What are some post-renal causes of AKI?

A
  • Obstruction = congenital like posterior urethral valve or acquired like blocked urinary catheter
96
Q

ACUTE KIDNEY INJURY
What are some investigations for AKI?

A
  • FBC, U+Es (high urea), high creatinine, USS to identify if obstruction
  • Can have hyperkalaemia, hyperphosphataemia + metabolic acidosis
97
Q

ACUTE KIDNEY INJURY
What is the management of AKI?

A
  • Maintain strict fluid balance (IV fluids if hypovolaemic, restrict if overload)
  • If failure of conservative Mx, severe electrolyte disturbances or acidosis then ?dialysis
98
Q

CHRONIC KIDNEY DISEASE
What are some causes of chronic kidney disease (CKD)?

A
  • Structural malformations (congenital dysplastic kidney)
  • Glomerulonephritis
  • Hereditary nephropathies
  • Systemic diseases
99
Q

CHRONIC KIDNEY DISEASE
What is the clinical presentation of CKD?

A
  • Failure to thrive, anorexia + vomiting
  • HTN, acute-on-chronic renal failure, anaemia
  • Bony deformities from renal osteodystrophy
  • Incidental proteinuria, polydipsia + polyuria
100
Q

CHRONIC KIDNEY DISEASE
What are some investigations for CKD?

A
  • Monitor growth
  • FBC = anaemia due to reduced EPO
  • U+Es + electrolytes (Ca2+ low, phosphate high)
101
Q

CHRONIC KIDNEY DISEASE
What is the management of CKD?

A
  • Diet + NG or gastrostomy feeding may be needed for normal growth
  • Phosphate restriction + activated vitamin D to prevent renal osteodystrophy
  • May need recombinant growth hormone
  • Recombinant erythropoietin to prevent anaemia
  • Dialysis + transplantation if in ESRF (GFR <15ml/min/1.73m^2)
102
Q

VESICOURETERIC REFLUX
what is it?

A

retrograde flow of urine from the bladder into the upper urinary tract
it is usually congenital

103
Q

VESICOURETERIC REFLUX
how is it graded?

A

graded using International Reflux Study grading system

104
Q

VESICOURETERIC REFLUX
how is it diagnosed?

A
  • micturating cystourethrogram: radiocontrast medium introduced to catheterised bladder, reflux is detected on voiding
  • indirect cystogram
105
Q

VESICOURETERIC REFLUX
what is the management?

A

aim is to prevent renal scarring

  • antibiotic prophylaxis
  • surgery - not commonly recommended
106
Q

PYELONEPHRITIS
what are the risk factors?

A
  • vesicoureteral reflux (VUR) = most common + most important
  • previous history of UTI
  • siblings with a history of UTI
  • female sex
  • indwelling urinary catheter
  • intact prepuce in boys
  • structural abnormalities of the kidneys and lower urinary tract
107
Q

PYELONEPHRITIS
what is the pathophysiology?

A

pyelonephritis occurs after faecal flora colonize the urethra and ascend into the bladder and kidney

108
Q

PYELONEPHRITIS
what is the most common causative organism?

A

E.coli = 80% of cases

109
Q

PYELONEPHRITIS
what is the clinical presentation?

A
  • 25% have no clinical signs
  • 50% present with only flank pain

toddlers = fever and irritability, poor feeding, lethargy, abdominal pain

older children = fever, vomiting, flank pain, dysuria, urgency, increased frequency

110
Q

PYELONEPHRITIS
What are the investigations?

A
  • urine microscopy and culture
  • CT KUB with contrast
111
Q

PYELONEPHRITIS
what is the management?

A
  • empirical antibiotics then targeted based on cultures
  • severe = hospitalisation and IV antibiotics
112
Q

PYELONEPHRITIS
how can it be prevented?

A

children <2yrs diagnosed with a UTI should have a renal USS

113
Q

PYELONEPHRITIS
what are the complications?

A
  • recurrence
  • renal scarring
  • hypertension
114
Q

NOCTURNAL ENURESIS
what is it?

A

bedwetting during sleep

115
Q

NOCTURNAL ENURESIS
what are the different types?

A
  • Primary nocturnal enuresis = never been consistently dry at night
  • Secondary nocturnal enuresis = previously been dry for >6 months
  • Monosymptomatic = only has symptoms at night
  • Non-monosymptomatic = daytime wetting symptoms as well as night time wetting
116
Q

NOCTURNAL ENURESIS
what are the causes?

A
  • not waking to bladder signals
  • inadequate levels of vasopressin (ADH)
  • overactive bladder
  • constipation
  • UTIs
  • Family history
  • Anxiety/stress
  • poor bedtime routines
117
Q

NOCTURNAL ENURESIS
what is the presentation of inadequate levels of vasopressin?

A
  • large volumes of urine passed at night
  • wet in the early part of the night
  • wet more than once per night
118
Q

NOCTURNAL ENURESIS
what is the presentation of an overactive bladder?

A
  • damp patches that occur at night also occur during the day
  • the volume of urine passed is variable
  • children often wake after wetting at night
119
Q

NOCTURNAL ENURESIS
what are the investigations?

A
  • physical examination (back, genitalia + lower limbs)
  • urinalysis + MS&C
  • bladder scan
  • uroflowmetry
  • ultrasound
120
Q

NOCTURNAL ENURESIS
what supportive care can be given to help?

A
  • motivation, support and patience
  • drinking enough
  • drinking regularly
  • stopping drinks before bed
  • avoid drinks that avoid the bladder
  • regular timed toileting
  • establish a bedtime routine
  • refrain from using nappies
  • avoid lifting child out of bed before they are awake
  • treat and prevent constipation
121
Q

NOCTURNAL ENURESIS
what is the medical management?

A
  • antibiotics for infection
  • laxatives for constipation
  • alarms
  • desmopressin
  • anticholinergic medications (oxybutynin + tolterodine) for detrusor relaxation
122
Q

ALPORT’S SYNDROME
what is it?

A

A genetic disorder which damages glomeruli resulting in gradual loss of kidney function and CKD

123
Q

ALPORT’S SYNDROME
what are the 3 types?

A

X-linked Alport syndrome (XLAS)
Autosomal recessive Alport syndrome (ARAS)
Autosomal dominant Alport syndrome (ADAS)

124
Q

ALPORT SYNDROME
what is the clinical presentation?

A
  • haematuria
  • oedema
  • hypertension
  • loss of kidney function
  • progressive hearing loss
  • proteinuria
  • vision problems
125
Q

ALPORT SYNDROME
what is the management?

A

ACE inhibitors
dialysis
kidney transplant

126
Q

ALPORT SYNDROME
what are the investigations?

A
  • genetic testing
  • tissue biopsy
  • urinalysis
  • hearing tests

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