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Pediatrics > Urinary System > Flashcards

Urinary System Flashcards

1
Q

Common pathogens in UTI

A
  • bacterial: E.coli, Kebsiella, Enterobacter, Staphylococcus aureus…
  • viral and fungi less common
  • Viral Utis are limited to the lower urinary tract
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2
Q

Classification of UTI according to site

A

CYSTITIS (lower urinary tract)
- urinary bladder mucosa with symtpoms like dysuria, stranguria, frequency, urgency, malodorous urine, incontincence, hematuria and suprapubic pain

PYELONEPHRITIS (upper urinary tract)

  • diffuse pyogenic infection of the renal pelvis with symtpoms like fever (>38)
  • infants and children may have non-specific signs like poor appetite, failure to thrive, lethargy, irritability, vomiting, diarrhea
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3
Q

Classification of UTI according to episode

A
  1. First infection
  2. Recurrent infection can be
    - unresolevd
    - persistent
    - reinfection
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4
Q

Classification of UTI according to symtpoms

A

ASYMPTOMATIC BACTERIRUIA (ABU)

  • pathogens that are incapable of activating symtpomatic response
  • in significant ABU, luekocyturia can be present without any symptoms

SYMPTOMATIC UTI
- irritative voiding symtpoms, suprapubic pain, fever, malaise

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5
Q

Classification of UTI according to complicating factors

A

UNCOMPLICATED UTI
- infection with morhpological and functional upper and lower urinary tract, normal renal function and competent immune system

COMPLICATED UTI
- in newborns, most patients with clinical evidence of pyelonephritis, children with mechanical or functional obstructions or problems of the upper urinary tract

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6
Q

For acute treatment of UTI, what factors are most important

A

Site and severity

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7
Q

Atypical UTI criteria

A
  • seriously ill
  • poor urine flow
  • abdominal or bladder mass
  • raised creatinine
  • septicemia
  • failure to response to treatment within 48 h
  • ifection with non e. coli organisms
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8
Q

Recurrent UTI

A
  • 2 or more episodes of acute pyelonephritis/ upper urianry tract ifection

or

  • 1 episode of acute pyelonephritis + > 1 episode of cystitis

or

  • > 3 episodes pf cystitis / lower urinary tract infections
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9
Q

Pathogenesis of UTI

A
  • result of ascending infection
  • colonization of the reiurethral area by uropathogenic enteric pathogens
  • in E. coli: pili on the cell surface aid in attaching
  • in kidney, bacterial pathogen generated intense inflammatory resposne that can lead to renal scarring
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10
Q

Risk factors for UTI

A
  • weak anti-bacterial features of the mucous membrane and urine
  • girls
  • incomplete bladder emptying
  • neurogenic bladder
  • white children
  • family history
  • urinary obstruction
  • VUR
  • infrequent voiding
  • vulvitis, balantitis
  • hurried micturition
  • constipation
  • sexual activity
  • bladder catheterization
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11
Q

Bacterial factors that predispose to UTI infection

A
  • infecting organisms are more likely to be associated with structural obnormalities in renal tract
  • in newborn, UTI is more often hematogenous
  • most common infection: e. cloli
  • Proteus infection more common in boys because of its presence under foreskin and predisposes to stone formation
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12
Q

Vesicoureteral reflux

A
  • is the retrograde passage of ruine from the bladder into the upper urinary tract
  • the most common urologic anomaly in children
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13
Q

Pathogenesis of VUR

A

PRIMARY VUR

  • most common form
  • due to incompetent or inadequate closure of the ureterovesical junction

SECONDARY VUR

  • result of abnormally high pressure in the bladder that results in the failure of closure of the UVJ during bladder contraction
  • often associated with anatomic or functional bladder destruction
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14
Q

Grading of VUR

A
  • Grade I: reflux only fills the ureter without dilation
  • Grade II: refluc fills the ureter and the collecting system without dilation
  • Grade III: reflux fills and mildly dilates the ureter and the collecting system with mild blunting of the calyces
  • Grade IV: reflux fills and grossly dilates the ureter and the collecting system with blunting of the calyces
  • Graade V: massive reflux grossly dilated the cpllecting system; all the calyces are blunted with a loss of papillary impression and intrarenal reflux may be presnet; ureteral dilation and tortuosity
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15
Q

Risk factors for renal scarring

A
  • recurrent febrile UTI
  • delay in treatment of acute infection
  • dysfunctional elimination, constipation
  • obstructive malformations
  • VUR
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16
Q

When to suspect UTI according to NICE guidelines

A
  • present symtpoms and signs of UTI
  • unexplained fever over 24 hours
  • an alternate site of infection, but who remains unwell
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17
Q

Symptoms of UTI in neonates

A
  • jaundice
  • hypothermia or fever
  • failure to thrive
  • poor feeding
  • vomiting
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18
Q

Symptoms of UTI in infants

A
  • poor feeding
  • fever
  • vomiting, diarrhea
  • strong-smelling urine
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19
Q

Symptoms of UTI in preschoolers

A
  • vomiting, diarrhea, abdominal pain
  • fever
  • strong-smelling urine, enuresis, dysuria, urgency, frequency
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20
Q

Symptoms of UTI in school children

A
  • fever
  • vomitign, abdominal pain
  • strong-smellign urine, frequency, urgencya, flank pain or new enuresis
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21
Q

Symptoms of UTI in adolescents

A
  • more likely to have classic adult symptoms

- girls are more likely to have vagintis than UTI

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22
Q

Urine sampling for newborns, non-toilet trained children

A
  • plastic bag attached to the cleaned geitalia –> often contaminated
  • clean catch urine collectioin: sterile bowl catches urine mid-stream
  • Suprapubic bladder aspiration: most sensitive
  • bladder catherization: rates of contamination are higher
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23
Q

Blood test in UTI

A
  • blood white cell counts
  • C-reactive protein
  • serum pro-calcitonin
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24
Q

Imaging procedures in UTI

A
  • ultrasound
  • MCUG (Micturating cysturetherogram)–> for VUR, bladder volumes, …
  • DMSA scintigraphy: for pyelonephritis and renal scarring
  • Radionuclide cystogram: for VUR
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25
Q

When to do an ultrasound in UTI

A
  • girls younger than 3 with first UTI
  • boys of any age with first UTI
  • children with recurrent UTI
  • First UTI in child with family history of renal disease, abnormal voiding pattern, poor grwoth, hypertension
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26
Q

How to distuingish between upper UTI and lower UTI

A

Acute pyelonephritis: bacteriuria and fever of 38 or higher

Bacteriruia but no systemic featuers: cystitis

27
Q

Criteria for UTI in children (in urine specimen)

A

Suprapubic baldder puncture: any number of CFU per ml (at least 10 identical colonies)

Bladder catherization: >1000 - 50.000 CFU/ml

Midstream void: >10 4 CFU/ ml with symtpoms
>10 5 CFU/ml without symptoms

28
Q

MCUG indications

A
  • boys < 6 months

- if there was atypical UTI

29
Q

Acute pyelonephritis dignostic criteria in children

A
  • fever of 38 or higher
  • leukocyturia
  • significant bacteriuria
  • Changes in blood showing a bacterial infection (leukocytosis and CRP > 20 mg/l)
  • general signs of infalmmation (intoxication, abdominal and flank pain)
  • changes in echoscopy

to confirm diagnosis there must be urine abnormality and at least two other criteria

30
Q

Acute cystitis diagnostic criteria in children

A
  • micturition disturbances
  • luekocyturia
  • significant bacteriruia

to confirn diagnosis there must be urinary disturbances and at least one other diagnosis

31
Q

General treatment stretegy in UTI

A
  • dont treat dysuria without urine test
  • start treatment immediatly if UTI is suspected without urine culture result
  • in patients with uncomplicated cystitis, oral treatment should be given for at least 3-4 days
32
Q

Duration of therapy in febrile urinary tract infection

A
  • parenteral treatment should be continued until the child is afebrile, after which oral antibiotics ahould be given or 7-14 days
  • in complicated UTI with pathogens other than E. coli –> parenteral treatment with broad-spectrumm antibitoics is preferred
  • newborn: 14 days (as for sepsis)
  • pyelonephritis: 10-14 days
  • cystitis: 3-7 days
33
Q

Initial pyelonephritis treatment

A
  • Aminoglycosides iv until the child has no fever and an additional 1-2 days, but no longer than 7 days, then other antibacterial drug by antibiogram until 10-14 days

or

  • group 2 cephalosproins iv until the child has no fever and an additional 1-2 days, then PO until 10-14 days

amoxicillin and clavulanic acid?

34
Q

Acute cystitis treatment

A
  • nitrofurantoinum, furanginum
  • trimethoprimum

or

  • trimethoprimum/ sulfamethoxazolum

treatment duration 3-5 days or until recepit of microbiologuc findings, then treatment can be adjusted according to patient’s condition and antibiogram

35
Q

Long-term sequelae of UTI

A
  • 40% have VUR
  • renal scars in 8%
  • large majority will have no long term sequelae
36
Q

Classification of GN by course

A
  • acute
  • chronic
  • rapidly progressing
37
Q

Classification of Gn by clinical picture

A
  • nephritic syndrome

- nephrotic syndrome

38
Q

Classification of GN by histology

A
  • memnraboproliferative
  • membranous nephropathy
  • extracapillary
  • minimal change
  • focal segmental glomerulonecrosis
39
Q

Classification of GN by etiology

A
  • primary

- secondary

40
Q

Classification of GN by IHC

A
  • pauci immune
  • Anti-GBM
  • immunocomplex
41
Q

Key features of nephritic syndrome

A
  • hematuria
  • proteinuria (non-nephrotic range)
  • Hypertension (BP>95th percentile)
  • Oliguria (<0.5ml/kg/hr)
  • Renal failure (decrease in GFR < 90ml/min/1.73m2)
  • Edema (less severe, periorbital)
42
Q

Causes of nephritic syndrome (primary and secondary renal diseases)

A

PRIMARY RENAL DISEASE

  • IgA nephropathy
  • membranoproliferative GN
  • Anti-GBM
  • idiopathic crescentic GN

SECONDARY RENAL DISEASE

  • post-infectious GN
  • Henoch-Schönlein purpura nephritis
  • SLE
  • Wegener’s granulomatosus
  • Microscopic polyangiitis
43
Q

Post-infectious glomerulonephritis clinical features

A
  • most commonly post-streptococcal
  • 1-2 weeks after strep throat infection and up to 6 weeks after strep skin infection
  • acute nephritic syndrome
  • decreased C3, increased ASO
  • decreased GFR
  • resolves in 2-3weeks
  • C3 normalization in 6-8 weeks
  • isolated microscopic hematuria up to 2 years
44
Q

Therapy in post-infectious GN

A

supportive

  • bed rest
  • fluid and salt intake restriction
  • diuretics (loop diuretics, furoseminde –> potassium wasting)
  • anti-hypertensives
  • correction of hyprekalemia/ acidosis
45
Q

When to do a biopsy in post-infectious GN

A

usually not needed

INDICATIONS

  • low C3 over 3 months
  • abnormal serum creatinine at 6 weeks
  • proteinuria > 6 months
  • rapidly progressing course

–> shows diffuse endocapillary porliferative GN with subepithelial humps

46
Q

IgA nehpropathy clinical features

A
  • macroscopic hematuria 1-2 days after URTI
  • asymptomatic microhematuria +- proteinuria
  • acute nephritic syndrome
  • nephrotic syndrome
  • nephritic-nephrotic syndrome
  • decreased GFR
47
Q

Histological features of IgA nephropathy and MEST

A
  • IgA deposition in mesangium
  • C3 and IgG and IgM may be present in up to 50%

M: Mesangial hypercellularity
E: endocapillary hypercellularity
S: Segmental gloermulosclerosis
T: Tubular atrophy/ interstitial fibrosis

48
Q

Therapy of IgA nephropathy

A
  • microscopic hematuria –> no therpay required
  • proteinuria over 1g/l –> long-term renoprotection with ACEi/ ARBs
  • blood pressure control (stricter case in proteinuria > 1g/l)
  • if supportive therapy fails: steroids or immunosuppressants (MFF, cyclophosphamide)
  • omega 3 fatty acid supplementation in case of proteinuria > 1g/l
49
Q

Key features of nephrotic syndrome

A
  • heavy proteinuria (> 3 g/l in dipstick or >40 mg/m2/hr or urine protein to creatinine ratio >200mg/mmol, >2.0 mg/mg)
  • hypoalbuminemia (<25g/l)
  • edema (moderate/severe, generalized)
  • hypercholesterolemia
50
Q

Pathophsyiology of nephrotic syndrome

A
  • glomerular filtration barrier consists of fenestrated endothelial cells, GBM and Podocytes
  • loss of negative charge og GBM
  • foot process effacement –> increased protein permeability, loss of protein to urine, hypoalbuminemai
51
Q

General causes of nephrotic syndrome

A
  • 0-3 months: congenital (genetic)
  • 3-12 months: infantile (genetic and idiopathic)
  • first decade: idiopathic
  • < 10 years: idiopathic/ secondary
52
Q

Congenital nephrotic syndrome

A

mutations in genes encoding podocyte and GBM portiens, lead to impairment of glomerular filtration barrier

53
Q

Finnish type congenital syndrome

A
  • most common cause of congenital NS
  • autosomal recessive
  • heavy proteinuria and severe hypoalbuminemia
  • albumin infision dependence –> nephrectomy frequently needed
54
Q

Nephrotic syndrome beyond infancy

A
  • most commonly idiopathic
  • -> minimal change (80%)
  • -> FSGS
  • -> other (mesangial proliferative GN, membranoproliferative GN, membranous nephropathy)
  • genetic
  • secondary (rare, in second decade of life)
  • -> infections (HBV, HCV, malaria, schistosomiasis, HIV)
  • -> systemic disease (HSP, SLE, DM)
  • -> metabolic diseases (Fabry disease, glycogen-storage diseases)
  • -> oncohematological disorders, drugs…
55
Q

Minimal change nephrotic syndrome

A
  • most common form of chilhood NS
  • no changes on light microscopy
  • EM: podocyte feet effacement
  • typically suspected in a non-infant with NS
  • typically non familial
  • frequent triggers: viral, allergies
  • initial therapy with steroids
56
Q

Definitions of NS

  • complete remission
  • partial remission
  • Steroid dependent nephrotic syndrome
  • frequently relapsing nephrotic syndrome
  • steroid resistant nephrotic syndrome
A
  • complete remission: uPCR 200mg or 1+ protein on urine dipstick for 3 consecutive days
  • partial remission: proteinuria reduction of 50% or greater from the presenting value and absolute uPCR between 200 and 2000 mg/g
  • Steroid dependent nephrotic syndrome: two consecutive relapses during corticosteroid therapy, or within 14 days of ceasing therapy
  • frequently relapsing nephrotic syndrome: two or more relapsing within 6 months of initial response, or four or more relapses in any 12 month period
  • steroid resistant nephrotic syndrome: failure to achieve complete remission after 8 weeks of ccs therapy
57
Q

Focal segmental glomerulosclerosis

A
  • suspected in cases of steroid resistant nephrotic syndrome
  • can only be proven by biopsy
  • MCNS can transform to FSGS
  • some forms are genetic
58
Q

Nephrotic syndrome: supportive measures

A
  • edema correction
  • -> diuretics (furoseminde)
  • -> Albumin + furoseminde infusion in case of diuretic resistance and severe hypoalbuminemia)
  • -> moderate slat and fluid restriction
  • blood pressure control
  • complication prevention
  • -> hypercoagubility states (anticoagulation)
  • -> severe hyperlipidemia (statins)
  • -> risk of infections (vaccinations)
59
Q

When to do genetic testing in nephrotic syndrome

A
  • congenital or infantile nephrotic syndrome
  • patients with familiar history of NS of chronic kidney disease
  • multiple associated extrarenal manifestations
  • persistent non-responsiveness to heavy immunosuppression
60
Q

Other therapies for nephrotic syndrome

A

used in cases of SRNS, some cases of DSNS; FRNS, steroid intolerance

  • cyclophosphamide
  • levamisole
  • calcineurin inhibitors
  • myophenolate mofetil
  • azathioprine
  • rituximab
61
Q

Membranoproliferative Glomerulonephritis two mechanisms

A
  • Alternative complement pathway dysregulation

- Immunocomplex mediated injury via classical complement pathway

62
Q

MPGN therapy

A
  • blood pressure control (ACEi/ ARBs)
  • Moderate disease (proteinuria > 0.5g/24h, risk of CKD) –> predinsone or MMF
  • severe disease (proteinuria > 2g/24 h and despite CKD despite immunosuppression)
  • -> Methylpredisolone pulstherapy, other immunisuppressants
63
Q

Membranous nephropathy

A
  • up to 43% of cases secondary to infections (HBV, malaria), systemic disease (SLE, DM, IBD), drug (NSAIDS), malignancies
  • nephrotic syndrome, asymtpomatic proteinuria, macroscopic or microscopic hematuria, hypertension, CKD
64
Q

Histologica features of membranous nephropathy

A
  • uniform thickening of the capillary wall within the glomerulus secondary to deposition of subepithelial immune aggregates
  • no inflammation

Pediatrics (11 decks)

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