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Finals > Paediatrics renal > Flashcards

Paediatrics renal Flashcards

1
Q

How will babies present with a UTI?

A

Very non specific !

  • Fever
  • Lethargy
  • Irritability
  • Vomiting
  • Poor feeding
  • Urinary frequency
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2
Q

How will a UTI present in older infants and children ?

A
  • Fever
  • Abdominal pain, particularly suprapubic pain
  • Vomiting
  • Dysuria
  • Urinary frequency
  • Incontinence
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3
Q

What 2 symptoms are suggestive of acute pyelonephritis ?

A
  • Temperature greater than 38°C
  • Loin pain or tenderness
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4
Q

How is a UTI investigated ?

A
  • CLEAN catch urine dipstick
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5
Q

How are children <3mnths old with a UTI managed ?

A
  • Immediate referral to paediatrician
  • Will be treated with IV Abx (e.g. ceftriaxone)
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6
Q

How are children >3mnths with a UTI treated

A
  • Oral Abx as per local guidelines
  • Usually trimethoprim, nitrofuratoin, cefalexin, amoxicillin
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7
Q

Which children should receive an USS following a UTI and when ?

A
  • All children <6 months with their first UTI within 6 weeks, or during the illness if there are recurrent UTIs or atypical bacteria
  • Children with recurrent UTIs within 6 weeks
  • Children with atypical UTIs during the illness
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8
Q

When should a DMSA scan be done in children with UTIs and when ?

A
  • 4-6 mnths after illness and done to assess for damage to the kidneys following recurrent or atypical UTIs
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9
Q

What is a common cause of recurrent UTIs in children?

A

Vesico-Uteric Reflux : abnormal backflow of urine from the bladder into the ureter and kidney.

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10
Q

Explain the pathophysiology of VUR

A
  • Ureters are displaced laterally, entering the bladder in a more perpendicular fashion than at an angle
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11
Q

How is VUR diagnosed ?

A
  • Micturating cystourethrogram (MCUG)
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12
Q

Explain the 5 grades of VUR

A
  • I : Reflux into the ureter only, no dilatation
  • II : Reflux into the renal pelvis on micturition, no dilatation
  • III : Mild/moderate dilatation of the ureter, renal pelvis and calyces
  • IV : Dilation of the renal pelvis and calyces with moderate ureteral tortuosity
  • V : Gross dilatation of the ureter, pelvis and calyces with ureteral tortuosity
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13
Q

What is the classic triad of nephrotic syndrome and why does it occur ?

A
  • Low serum albumin
  • High urine protein content (>3+ protein on urine dipstick)
  • Oedema

Damage to the basement membrane in the glomerulus makes it highly permeable to protein.

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14
Q

what 3 other features can occur in nephrotic syndrome

A
  • Deranged lipid profile, with high levels of cholesterol, triglycerides and low density lipoproteins
  • High BP
  • Hyper-coagulability, with an increased tendency to form blood clots
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15
Q

What is the most common cause of nephrotic syndrome in children ?

A
  • Minimal change disease
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16
Q

Give 5 secondary causes of nephrotic syndrome in children

A
  • Intrinsic kidney disease : focal segmental glomerulosclerosis, membranoproliferative glomerulonephritis
  • Systemic illness : HSP, DM, infection
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17
Q

How does nephrotic syndrome present ?

A
  • Ages 2-5
  • Frothy urine
  • Pallor
  • Generalised oedema
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18
Q

What is seen on urinalysis in minmal change disease

A
  • Small molecular weight proteins
  • Hyaline casts
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19
Q

How is nephrotic syndrome managed ?

A
  • High dose steroids (e.g. prednislone)
  • Given for 4 weeks and then weaned over the next 8 weeks
20
Q

Give 5 complications of nephrotic syndrome

A
  • Hypovolaemia
  • Thrombosis
  • Infection.
  • Acute or chronic renal failure
  • Relapse
21
Q

What is nephritis and give its 3 presenting features

A
  • Inflammation within the nephrons
  • Reduction in kidney function
  • Haematuria
  • Proteinuria (less than in nephrotic)
22
Q

Give the 2 most common causes of nephritis in children

A
  • Post-streptococcal glomerulonephritis
  • IgA nephropathy
23
Q

What is post-streptococcal glomerulonephritis

A
  • Nephritis occuring 1-3 weeks after a B-haemolytic streptococcus infection (e.g. tonsilitis caused by strep pyogenes)
24
Q

what are the features of post-streptococcal glomerulonephritis

A
  • URTI 1-3 wks prior
  • Haematuria
  • Proteinuria causing oedema
  • Bloods : raised anti-streptolysin O titre and low C3.
25
Q

What causes IgA nephropathy and what tare the common features

A
  • Deposition of IgA immune complexes in the kidney
  • Young male with recurrent episodes of macroscopic haematuria
  • Develops 1-2 DAYS after URTI
26
Q

What is strongly associated with IgA nephropathy ?

A

Henoch-schonlein purpura

27
Q

What does HUS lead to traid of ?

A

Young children with a triad of :

AKI
Thrombocytopenia
Microangiopathic haemolytic anaemia

28
Q

what is HUS and why does it lead to thrombocytopenia, AKI and MAHA

A
  • Thrombosis in small blood vessels
  • Formation of clots uses up plts = thrombocytopenia
  • The thrombi and damaged RBCs affects blood flow through kidney = AKI
  • The blood clots obstruct the small blood vessels and destroy the RBC as they pass through = MAHA
29
Q

what most commonly causes HUS

A

Shiga toxin-producing E.coli or shigella

30
Q

How does HUS present ?

A
  • Initial gastroenteritis (causing diarrhoea with turns bloody witin 3 days).
  • 1 wk later - > features of HUS
  • Fever and abdo pain
  • Pallor = normocytic anaemia
  • Bruising = thrombocytopenia
  • Reduced urine output and haematuria
  • Hypertension = renal failure
  • Confusion = uraemia
31
Q

what is seen on investigations in HUS ?

A
  • FBC : anaemia, thrombocytopenia, fragmented blood film: schistocytes and helmet cells
  • U&E: acute kidney injury
  • Stool culture : looking for evidence of STEC infection, PCR for Shiga toxins
32
Q

How is HUS managed ?

A

SUPPORTIVE

  • Fluids
  • Blood transfusion for anaemia
  • Haemodialysis of severe renal failure
33
Q

what can increase the risk of HUS

A
  • Antibiotics and anti-motility medication (e.g. loperamide) used to treat gastroenteritis caused by E.coli or shigella
34
Q

what kind of polycystic kidney disease presents in neonates

A
  • Autosommal recessive polycystic kidney disease (ARPKD)
35
Q

what is ARPKD a result of and when is it picked up ?

A
  • Mutation in the polycystic kidney and hepatic disease 1 (PKHD1) gene on chromosome 6.
  • This gene codes for the fibrocystin/polyductin protein complex (FPC), responsible for the creation of tubules and the maintenance of healthy epithelial tissue in the kidneys
36
Q

Give the 3 main features of ARPKD

A
  • Cystic enlargment of the renal collecting ducts
  • Oligohydramnios, pulmonary hyperplasia and potter syndrome
  • Congenital liver fibrosis
37
Q

Explain the pathophysiology behind the features of ARPKD

A
  • Oligohydramnios is picked up antinatally
  • The lack of amniotic fluid causes Potter syndrome (dysmorphic features) and underdeveloped fetal lungs causing resp failure after birth
  • Cystic kidneys take up space in the abodem and make it hard for the neonate to breathe
38
Q

what is the most common childhood malignancy and when does it usually present

A
  • Wilm’s tumour (nephroblastoma)
  • <5 years
39
Q

How does a Wilm’s tumour present ?

A
  • UNEXPLAINED ENLARGED ABDO MASS (paeds review within 48hrs)
  • Painless haematuria
  • Flank pain
  • Lethargy
  • Fever
  • Weight loss
40
Q

How is a Wilm’s tumour managed

A
  • Nephrectomy with adjuvant chemo or radiotherapy
41
Q

Young girl
Unwell with diarrhoea for 5 days
Now lethargic and pake
Not passed urine in 14 hrs
Became unwell after earting chicken burger
Multiple petechiae on torso and limbs
Oedematous feet

Most likely underlying cause

A

HUS due to E.coli

42
Q
  • Young girl
  • Recent respiratory tract infection
  • Recurrent macroscopic haematuria
  • Mesangial deposition of IgA immune complexes on biopsy
A

IgA nephropathy

43
Q

Differentiating IgA nephropathy from post-streptococcal glomerulonephritis

A

-> IgA = short word = occurs a few days after infection = only causes haematuria

-> Post-streptococcal glomerulonephritis = long word = few weeks following febrile illness = haematuria AND proteinuria (+HTN and oliguria)

44
Q

Presentation of minimal change disease

A
  • Pure nephrotic syndrome with normotension
  • Proteinuria +++++++
45
Q
A

Finals (92 decks)

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