Nephrology Flashcards

1
Q

What are some signs and sx of UTI in babies?

A
  • Fever
  • Lethargy
  • Irritability
  • Vom
  • Poor feeding
  • Urinary freq
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2
Q

What are the signs and sx of UTI in older infants and children?

A

Fever
Abdo pain - suprapubic
Vom
Dysuria
Urinary freq
Incontinence

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3
Q

How is acute pyelonephritis diagnosed?

A

Temp >38 degrees
Loin pain or tenderness

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4
Q

What are signs of UTI on dip?

A

Nitrites (better indicator) and leukocytes
Also need to send a MSU for MC+S

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5
Q

What is the management of UTI in children?

A
  • All children <3 m w fever = IV abx and have a full septic screen (ideally before abx)
  • Oral abx in children >3m if otherwise well - cefalexin, nitrofurantoin
  • Sepsis or pyelonephritis = inpt IV abx
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6
Q

How do you ix recurrent UTIs?

A

<6 m = abdo US w/i 6 week of first UTI
Recurrent UTIs - abdo USS w/i 6 weeks
Atypical UTIs - abdo US

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7
Q

What is a DMSA scan?

A

Used 4-6 months after a UTI to assess for damage from recurrent or atypical UTIs
Inject DMSA and use gamma camera to assess how well material taken up by the kidneys - patches = scarring

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8
Q

What is vesico ureteric reflux?

A

Urine flows from the bladder back into the ureters = predisposition to developing UTIs and renal scarring.

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9
Q

How do you trest vesico ureteric reflux?

A
  • Avoid constipation
  • Avoid excessively full bladder
  • Prophylactic abx
  • Surgical input
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10
Q

What is a MCUG?

A

Micturating cystourethrogram - ix recurrent UTIs in children <6 months
XR w contrast

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11
Q

What are RF of vulvovaginitis?

A

Wet nappies
Chemical or soaps to clean area
Tight clothing
Poor toilet hygiene
Constipation
Threadworms
Pressure on the area
Heavily chlorinated pools

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12
Q

What are the CF of vulvovaginitis?

A
  • Soreness and itching
  • Erythema around the labia
  • Vaginal discharge
  • Dysuria
  • Constipation
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13
Q

What is the management of vulvovaginitis?

A

Advice:
- Avoid washing w soap or perfumed products
- Good toilet hygiene
- Keep area dry
- Emollients
- Loos cotton clothing
- Treat constipation

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14
Q

What is the triad of nephrotic syndrome?

A

Low serum albumin <35 g/L
High urine protein content >3+ on dip
Oedema

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15
Q

What are the other features in nephrotic syndrome?

A

Frothy urine
Pallor
Derranged lipids (hypercholesterolaemia)
High BP
Hyper coag
Higher risk of infection

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16
Q

What are the causes of nephrotic syndrome in children?

A
  • Minimal change disease is the most common cause in children
  • Intrinsic kidney disease - focal segmental glomerulosclerosis, glomerulonephritis
  • Systemic illness - Henoch schonlein purpura, diabetes, infection
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17
Q

What is the ix into minimal change disease?

A
  • Renal biopsy can’t detect any changes
  • Urinalysis - hyaline cysts and small proteins
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18
Q

How do you manage minimal change disease?

A

Prednisolone - most make a full recovery but can reoccur

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19
Q

What is the management of nephrotic syndrome?

A
  • High dose steroids for 4 weeks and then weaned over next 8w - pred but doesn’t work for all
  • Low salt diet
  • Diuretics for oedema
  • Albumin infusions maybe
  • Abx prophylaxis
  • ACEi/ARBs reduce proteinuria
  • Statins if hypercholesterolaemia?
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20
Q

What is the alt treatment of nephrotic syndrome for steroid resistant children?

A

ACE inhibitors and immunosuppressants eg. cyclosporine, tacrolimus, rituximab

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21
Q

What are some complications of nephrotic syndrome?

A
  • Hypovolaemia
  • Thrombosis
  • Infection
  • Acute or chronic renal fail
  • Relapse
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22
Q

What is HUS?

A

Haemolytic uraemic syndrome - thrombosis in small blood vessels. Usually triggered by shiga toxin (commonly produced by E.coli =
1. Haemolytic anaemia
2. AKI
3. Thrombocytopenia

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23
Q

What is the presentation of HUS?

A

E.coli = gastroenteritis = blood diarrhoea, HUS sx ~5 days after onset of diarrhoea:
- Reduced urine output
- Haematuria or dark brown urine
- Abdo pain
- Lethargy and irritabilty
- Confusion
- Oedema
- HTN
- Bruising

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24
Q

What is the management of HUS?

A

Medical emergency and has 10% mortality:
- Self limiting and supportive treatment mainly
- Renal dialysis may be needed
- Anti HTN if needed
- Maintain fluid balance
- May need blood transfusion

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25
Q

What is enuresis and what are the different types?

A

Enuresis - involuntary urination
Nocturnal enuresis = bed wetting -> can be primary of secondary
Diurnal enuresis = inability to control bladder func during day

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26
Q

When do children normally achieve bladder control?

A

Daytime = 2 years
Nighttime = 3-4 years

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27
Q

What are some causes of primary nocturnal enuresis?

A
  • Overactive bladder
  • Fluid intake prior to bedtime
  • Failure to wake when need wee
  • Psych distress eg. low self esteem, probs at home
  • Chronic constipation, UTI, ID, cerebral palsy
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28
Q

What is the management of primary nocturnal enuresis?

A
  • Toileting and fluid intake and bedwetting diary
  • Reassurance if <5
  • Lifestyle changes - reduce fluid at night, pass urine before bed, close to toilet
  • Encouragement and positive reinforcement, no shame or punishment
  • Treat underlying cause if is one
29
Q

What are some secondary causes of secondary nocturnal enuresis?

A

Child wetting bed after prev dry for >6 m:
- UTI
- Constipation
- T1DM
- New psychosocial prob
- Maltreatment - abuse and safeguarding prob
Treat underlying cause

30
Q

What are some causes of diurnal enuresis?

A

Daytime incontinence but dry at nice:
1. Urge incontinence - overactive bladder
2. Stress incontinence - leakage of urine
+ recurrent UTI, psych probs, constipation

31
Q

What is an enuresis alarm?

A

Makes noise at the first sign of bed wetting - wakes child to stop them from urinating. Not v popular and need lots of dedication

32
Q

What pharm treatment can be used for enuresis?

A
  • Desmopressin - ADH, reduces vol of urine produced by kidneys
  • Oxybutinin for overactive bladder
  • Imipramine - tricyclic AD, not sure how works
33
Q

What is nephritic syndrome?

A

Inflam of the kidney:
- Reduced kidney func
- Haematuria (gross or microscopic)
- Proteinuria (but less than nephrotic syndrome)
- HTN

34
Q

What are the causes of nephritic syndrome in children?

A
  1. Post streptococcal glomerulonephritis
  2. IgA nephropathy
35
Q

What are the CF of post strep glomerulonephritis?

A

1-3 weeks after haemolytic streptococcus infection eg. tonsillitis.
Streptococcal antigens, Ab and complement proteins cause inflam in the glomeruli = AKI.

36
Q

What is the management of post strep glomerulonephritis?

A
  • Supportive mainly, 80% pt make full recovery
  • Other 20% develop CKD
  • If HTN = antihypertensive meds
  • If oedema = diuretics
  • If AKI so bad may need temp renal replacement therapy
37
Q

What are the CF of IgA nephropathy?

A

1-4 days post mild URTI, normally in teenagers or young adults.
IgA deposits in nephrons cause nephritis.
Renal biopsy = IgA deposits and glomerular mesangial proliferation

38
Q

What is the treatment of IgA nephropathy?

A
  • Supportive treatment of renal fail - about 15-40% pt = CKD
  • ACEi/ARBs reduce proteinuria and protect renal func
  • Immunosuppressants eg. steroids (helps to reduce proteinuria), cyclophosphamide
39
Q

What are the differentials for nephritic syndrome?

A

SHARP AIM
SLE
Henoch Schonlein purpura
Goodpasture’s disease
Rapidly progressive GN
Post strep GN

Alport’s syndrome
IgA nephropathy
Membranoproliferative GN

40
Q

What are the ix into nephritic syndrome?

A
  • Urine dip = blood +/- protein
  • MC+S = RBC, WBC and casts
  • Biopsy = immunofluorescence = IgA deposition in IgA nephropathy
41
Q

What are some differentials for haematuria?

A
  • Nephritic syndrome - post strep GN or IgA nephropathy
  • UTI
  • Polycystic kidney disease
  • Alport’s syndrome
  • Sickle cell disease
  • Hypercalciuria
  • Henoch Schonlein purpura
  • Wilm’s tumour
42
Q

What are the ix into haematuria?

A
  • Urine dip
  • MC+S
  • BP check
  • Bloods - U+E, lFT, ANA and ANCA
  • Throat swab
  • Urine protein:creatinine ratio
  • Renal tract USS and CT KUB if suspect structural cause
43
Q

What are the different types of PKD?

A

Autosomal recessive - presents in children
Autosomal dominant - presents in adults

44
Q

What are the CF of ARPKD?

A
  • Presents in neonates, usually found on antenatal USS
  • Cystic enlargement of renal collecting ducts
  • Oligohydramnios (reduced urine production)
  • Pulm hypoplasia - resp failure shortly after birth
  • Potter syndrome
  • Congenital liver fibrosis
45
Q

What is Potter syndrome?

A
  • Underdeveloped ear cartilage
  • Low set ears
  • Flat nasal bridge
  • Abnormalities of skeleton
    Due to lack of amniotic fluid
46
Q

What are the consequences of ARPKD?

A

Liver failure due to fibrosis
Portal HTN leading to oesophageal varices
Progressive renal failure
HTN due to renal failure
Chronic lung disease
30% die in neonatal period, 30% survive to adulthood - extensive interventions to survive

47
Q

What is multicystic dysplastic kidney?

A

Only one of the kidneys is cystic, the other is normal - this is normally enough to lead a healthy life. Cystic kidney will often atophy and disappear before the age of 5.
Can be bilat = death in infancy, normally diagnosed on antenatal USS

48
Q

What are the complications of having a single kidney?

A
  • Risk of UTIs - often prophylactic abx
  • HTN
  • CKD in later life
49
Q

What are the CF of autosomal dominant PKD?

A

Renal - flank pain and haematuria in cyst rupture, flank pain and fever in cyst infection, HTN, slow progression to CKD
Extra renal - cysts elsewhere, berry aneurysms in the head circulation, valvular heart disease, diverticular disease

50
Q

What is the management of ARPKD?

A

Fluid overload - diuretics and RRT
HTN - ACEi
UTI - Abx
CKD - Fe and EPO for anaemia, Ca supplement, phosphate etc for metabolic bone disease, GH
End stage kidney disease - transplant or dialysis

51
Q

What is screening of polycystic kidney disease?

A

USS - don’t screen asymptomatic children at the moment
15-39 >3 renal cysts = ADPKD
Different criteria for older pt

52
Q

What are the CF of Wilms tumour?

A

<5 presenting w mass in abdo, doesn’t cross midline, normally non tender !!!, and haematuria
- Haematuria
- Lethargy
- Fever
- HTN
- Weight loss
- Abdo distension
- Normally asymptomatic unless large tumour causes sx

53
Q

What are the ix into Wilm’s tumour?

A
  • USS
  • CT chest, AP to stage
  • Renal biopsy for definitive diagnosis = small round blue cells can be seen but no exclusive to nephroblastoma
54
Q

What is the management of Wilm’s tumour?

A
  • Nephrectomy - tumour and affected kidney removed
  • Chemo RT adjuvant after surgery, deps on stage of disease and spread
  • > 90% 5 year survival : )
55
Q

What are the stages of CKD?

A

Stage 1. >90 ml/min
2. 60-89 ml/min
3. 30-59 ml/min
4. 15-29 ml/min
5. <15 ml/min = ESRF

56
Q

What are signs and sx of CKD?

A
  • Anaemia
  • Anorexia, N+V
  • Osteodystrophy = bony deformities
  • Hyperkalaemia, met acidosis
  • HTN
  • Fluid overload
  • Polydipsia and polyuria
57
Q

What are the main causes of CKD in children?

A
  • Obstructive uropathy
  • Hypoplastic or dysplastic kidneys (under developed)
  • Reflux nephropathy
  • Focal segmental glomerulosclerosis
  • AD or AR PKD

Congenital probs = <12, glomerulonephritis >12

58
Q

What is the general management of CKD?

A

Nutrition - cal supplements, gastrotomy or NGT, restrict food w K and phosphate
Congenital structural probs - salt supplements and free access to water
Nephrotic syndrome - fluid and salt restriction to prevent fluid overload
Bicarb supplements prevent acidosis

Anaemia - EPO subcut

59
Q

What is renal osteodystophy?

A

Phosphate retention and hypocalcaemia due to reduced activation of vit d = secondary hyperparathyroidism = osteomalacia. Is a form of metabolic bone disease.
Treat - phosphate restriction, activated vit D supplements

60
Q

What are the options of RRT in CKD?

A

Renal replacement therapy:
- Transplantation, need to be 10kg min weight, living related donors highest success
- Immunosuppression - tacrolimus, prednisolone, mycophenolate mofetil to prevent rejection
- May need dialysis if can’t receive a transplant in time - haemodialysis, peritoneal dialysis

61
Q

What are the causes of AKI in children?

A

Pre renal (most common in children) - hypovolaemia eg. burns, sepsis, haemorrhage, HF
Renal - HUS, vasculitis, GN, VTE, pyelonephritis
Post renal - congenital obstruction

62
Q

What suggests acute on chronic renal failure?

A

Faltering growth, anaemia, metabolic bone disease

63
Q

What are the CF of AKI in children?

A

Oliguria
Raised creatinine >1/5x preference reference range

64
Q

What children are at risk of AKI?

A
  • Nephro urological, cardiac, liver disease
  • Malignancy or bone marrow transplant
  • Dep on others for access to fluids
  • Nephrotoxic meds - ACEi, ARBs, NSAIDs, tacrolimus, contrast
  • Major surgery
  • Septic
65
Q

What are the ix in AKI?

A
  • Bloods - FBC, U+E, cr, bone profile, albumin
  • Urine dip and MC+S
  • Urinary tract USS
  • Can also do immunoglobulins, ANCA, CK, LDH, antiDNAase
66
Q

What is the management of AKI?

A

Fluid balance monitoring
Remove nephrotoxic meds
Manage underlying cause
RRT if conservative management fails, hyperkalaemia, severe hyponatraemia or hypernatraemia, pulm oedema, severe met acidosis

67
Q

What is posterior urethral valve?

A

Tissue at the proximal end of the urethra that causes obstruction, in newborn boys. Causes hydronephrosis and increases risk of UTIs.

68
Q

What are the CF of post urethral valve?

A
  • Can be asymptomatic
  • Dysuria
  • Chronic urinary retention
  • Palpable bladder
  • Recurrent UTIs
  • Reduced eGFR
  • Severe - oligohydramnios and bilat hydronephrosis in fetus = pulm hypoplasia
69
Q

What are the ix into post urethral valve after birth?

A

Abdo USS = enlarged, thickened bladder and bilat hydronephrosis
MCUG = location of the tissue and reflux into bladder
Cystoscopy can be used to ablate or remove extra tissue