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
When to do an ultrasound in UTI
- 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
26
How to distuingish between upper UTI and lower UTI
Acute pyelonephritis: bacteriuria and fever of 38 or higher | Bacteriruia but no systemic featuers: cystitis
27
Criteria for UTI in children (in urine specimen)
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
MCUG indications
- boys < 6 months | - if there was atypical UTI
29
Acute pyelonephritis dignostic criteria in children
- 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
Acute cystitis diagnostic criteria in children
- micturition disturbances - luekocyturia - significant bacteriruia to confirn diagnosis there must be urinary disturbances and at least one other diagnosis
31
General treatment stretegy in UTI
- 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
Duration of therapy in febrile urinary tract infection
- 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
Initial pyelonephritis treatment
- 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
Acute cystitis treatment
- 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
Long-term sequelae of UTI
- 40% have VUR - renal scars in 8% - large majority will have no long term sequelae
36
Classification of GN by course
- acute - chronic - rapidly progressing
37
Classification of Gn by clinical picture
- nephritic syndrome | - nephrotic syndrome
38
Classification of GN by histology
- memnraboproliferative - membranous nephropathy - extracapillary - minimal change - focal segmental glomerulonecrosis
39
Classification of GN by etiology
- primary | - secondary
40
Classification of GN by IHC
- pauci immune - Anti-GBM - immunocomplex
41
Key features of nephritic syndrome
- 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
Causes of nephritic syndrome (primary and secondary renal diseases)
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
Post-infectious glomerulonephritis clinical features
- 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
Therapy in post-infectious GN
supportive - bed rest - fluid and salt intake restriction - diuretics (loop diuretics, furoseminde --> potassium wasting) - anti-hypertensives - correction of hyprekalemia/ acidosis
45
When to do a biopsy in post-infectious GN
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
IgA nehpropathy clinical features
- macroscopic hematuria 1-2 days after URTI - asymptomatic microhematuria +- proteinuria - acute nephritic syndrome - nephrotic syndrome - nephritic-nephrotic syndrome - decreased GFR
47
Histological features of IgA nephropathy and MEST
- 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
Therapy of IgA nephropathy
- 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
Key features of nephrotic syndrome
- 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
Pathophsyiology of nephrotic syndrome
- 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
General causes of nephrotic syndrome
- 0-3 months: congenital (genetic) - 3-12 months: infantile (genetic and idiopathic) - first decade: idiopathic - < 10 years: idiopathic/ secondary
52
Congenital nephrotic syndrome
mutations in genes encoding podocyte and GBM portiens, lead to impairment of glomerular filtration barrier
53
Finnish type congenital syndrome
- most common cause of congenital NS - autosomal recessive - heavy proteinuria and severe hypoalbuminemia - albumin infision dependence --> nephrectomy frequently needed
54
Nephrotic syndrome beyond infancy
- 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
Minimal change nephrotic syndrome
- 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
Definitions of NS - complete remission - partial remission - Steroid dependent nephrotic syndrome - frequently relapsing nephrotic syndrome - steroid resistant nephrotic syndrome
- 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
Focal segmental glomerulosclerosis
- suspected in cases of steroid resistant nephrotic syndrome - can only be proven by biopsy - MCNS can transform to FSGS - some forms are genetic
58
Nephrotic syndrome: supportive measures
- 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
When to do genetic testing in nephrotic syndrome
- 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
Other therapies for nephrotic syndrome
used in cases of SRNS, some cases of DSNS; FRNS, steroid intolerance - cyclophosphamide - levamisole - calcineurin inhibitors - myophenolate mofetil - azathioprine - rituximab
61
Membranoproliferative Glomerulonephritis two mechanisms
- Alternative complement pathway dysregulation | - Immunocomplex mediated injury via classical complement pathway
62
MPGN therapy
- 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
Membranous nephropathy
- 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
Histologica features of membranous nephropathy
- uniform thickening of the capillary wall within the glomerulus secondary to deposition of subepithelial immune aggregates - no inflammation