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Paediatrics > Nephrology part 2 > Flashcards

Nephrology part 2 Flashcards

1
Q

What is Acute kidney injury?

A
  • “Abrupt loss of kidney function, resulting in the retention of urea and other nitrogenous waste products and in the dysregulation of extracellular volume and electrolytes”
  • Anuria/ oliguria (<0.5ml/kg/hr)
  • Hypertension with fluid overload
  • Rapid rise in plasma creatinine
    □ Serum creatinine >1.5x age specific reference creatinine (or previous base line if known)
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2
Q

How are AKI warning score interperated?

A
  • AKI 1: measure creatinine >1.5-2x reference creatinine/ ULRI
  • AKI 2: Measure reference creatinine 2-3x reference creatinine/ ULRI
  • AKI 3: Serum creatinine >3x reference creatinine/ ULRI
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3
Q

What are the different causes of AKI in children?

A
  • Pre-renal e.g. heart failure
  • Perfusion problem
  • Intrinsic renal problems
    □ Glomerular disease
    ® Haemolytic Uraemic syndrome (HUS)
    ® Glomerulonephritis
    □ Tubular injury
    ® Acute tubular necrosis (ATN)
    ◊ Consequence of hypoperfusion
    ◊ Drugs
    □ Interstitial nephritis
    ® NSAIDs
    ® Autoimmune
  • Post-renal
    □ Obstructive
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4
Q

How is AKI managed in children?

A
  • Prevention
  • 3 Ms
    □ Monitor
    ® Urine output, PEWs (paediatric early warning score), BP, weight
    □ Maintain
    ® Good hydration
    □ Minimise
    ® Drugs (ibuprofen)
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5
Q

What are the long term concequences of AKI in children?

A
  • Blood pressure
  • Protein monitoring
  • Evolution to CKD
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6
Q

What are the causes of haemolytic uraemic syndrome?

A 
- Typical HUS- post diarrhoea 
□ Entero-Haemorrhagic E. coli (EHEC)
® Ventrotoxin producing E. coli (VTEC)
® Shiga toxin producing E. coli (STEC)
- Other causes
□ Pneumococcal infection
□ Drugs e.g. chemotherapy drugs
- Atypical HUS
□ Defect in alternative compliment pathway
® Autoimmune
® Drugs
® Hereditary
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7
Q

What is the period of risk of HUS?

A

® Up to 14 days after onset of diarrhoea

® 15% develop HUS

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8
Q

What happens about 3 days after ingesting E.coliO157:H7?

A

® Diarrhoea
® Abdominal pain
® Fever
® Vomiting

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9
Q

What happens about 4-6 days after ingesting E.coliO157:H&?

A 
® Diarrhoea become bloody
◊ Bloody diarrhoea= thrombotic 
® Has a normal 
◊ platelet count 
◊ Creatinine concentration
◊ Packed-cell volume
® No red cell fragmentation
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10
Q

What happens about 7 days after ingesting E.coliO157:H&?

A

® Diarrhoea improves
® Spontaneous resolution (~85%)
® HUS (~15%)

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11
Q

How is haemolytic uraemic syndrome managed in children?

A 
□ Monitor (5 kidney functions)
® Fluid balance, electrolytes, acidosis
® Hypertension
® Aware of other organs 
□ Maintain
® IV normal saline and fluid 
® Renal replacement therapy 
□ Minimise
® No antibiotics/ NSAIDS
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12
Q

What are the long term complications of HUS in children?

A
  • Blood pressure
  • Proteinuria monitoring
  • Evolution to CKD
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13
Q

What are the congenital anomalies of the kidney and the urinary tract (CAKUT)?

A
  • Reflux nephropathy
  • Dysplasia
  • Obstructive uropathy (example- posterior urethral valves)
  • Remember: think syndromic (May not be isolated)
    □ Turner
    □ Trisomy 21
    □ Branchio-oto-renal
    □ Prune Belly syndrome
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14
Q

What percentage of paediatric CKD cases are congenital?

A

55%

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15
Q

What percentage of paediatric CKD cases are hereditary?

A

17%

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16
Q

Give examples of hereditory causes of CKD?

A
  • Cystic kidney disease

- Cystinosis

17
Q

What percentage of paediatric CKD cases are caused by glomerulonephropathy??

A

10%

18
Q

What factord affect renal progression in children?

A
  • Late referral
  • Hypertension
  • Proteinuria
  • High intake of protein, phosphate and salt
  • Bone health
    □ PTH
    □ Phosphate
  • Acidosis
  • Recurrent UTIs
19
Q

What is the management of CKD in children?

A

Variable depending which function affected

20
Q

What is the definition of a urinary tract infection?

A
  • Clinical signs PLUS
    □ Bacteria culture from midstream urine
    □ Any growth on suprapubic aspiration or catheter
21
Q

What is the presentation of UTI in neonates?

A

® Fever
® Vomiting
® Lethargy
® Irritability

22
Q

What is the presentation of UTI in pre-verbal children?

A 
□ Common
® Fever
□ Middle
® Abdominal pain
® Abdominal/ loin tenderness 
® Vomiting
® Poor feeding  
□ Least common
® Lethargy 
® Irritability
23
Q

What is the presentation of UTI in verbal children?

A 
□ Common
® Frequency
® Dysuria 
□ Middle
® Abdominal pain or tenderness
□ Least common
® Fever
® Malaise 
® Vomiting
24
Q

How can you obtain a urine sample in children?

A
  • Normal social cleanliness- water
  • Clean catch urine or midstream urine
  • Collection pads, urine bags
  • Sick infants
    □ Catheter samples or suprapubic aspiration (USS)
  • Acutely unwell- do not delay treatment
25
Q

What are the suggestive tests of UTI in children?

A 
□ Dipstix
® Leukocyte esterase activity, nitrates
® Unreliable <2 years
□ Microscopy 
® Pyuria >10 WBC per cubic mm
® Bacteria
□ Culture >10^5 colony forming units 
® E.coli (most common)
26
Q

How is UTI treated in children?

A 
- Lower tract
□ 3 days oral antibiotic
- Upper tract/ pyelonephritis
□ Antibiotics for 7-10 days
® Oral if systemically well
□ No role for prophylaxis 
- Prevention
□ Fluids, hygiene, constipation
□ Voiding dysfunction
27
Q

What are the principles of investive immaging of the renal tract?

A 
- Screening for children at risk of progressive scarring
□ Reflux nephropathy
- Capture those with renal dysplasia
- Urological abnormalities/ unstable bladder
□ Voiding dysfunction
- Guidelines who to investigate
□ Upper tract symptoms 
□ Younger
□ Recurrent
28
Q

What immaging investigations can be done on children with renal tract problems?

A 
- Ultrasound
□ Structure
- DMSA (isotope scan)
□ Scaring/ function
- Micturating cystourethrogram MAG3 scan
□ Dynamic
29
Q

How do kidneys cause metabolic bone disease?

A

○ Kidneys wee out phosphate
- High phosphate results in increased PTH
○ Kidneys activate vitamin D

30
Q

What are the treatment principles of metabolic bone disease?

A
  • Low phosphate diet
  • Phosphate binders (calcium containing)
  • Active vitamin D
  • Growth hormone (if ongoing poor growth)
31
Q

What is the cardiovascular risk in metabolic bone disease?

A

○ Accelerated atherosclerosis

  • Traditional risk factors
  • Anaemia/ metabolic bone disease

Paediatrics (13 decks)

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