Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y4 Paediatrics > Nephrology > Flashcards

Nephrology Flashcards

1
Q

What might cause AKI in children? *commonly

A

pre-renal - gastroenteritis, blood loss, insensible losses, burns, sepsis, DKA, anaphylaxis *most common in children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what features may be present in the history to suggest AKI as a cause?

A
  • D+V, fluid or blood loss may suggest pre-renal
  • acute gastroenteritis with dehydration and shock
  • oedema
  • blood in urine
  • generally unwell
  • fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are some key signs noticed to support AKI?

A
  • oedema
  • haematuria
  • hypertension
  • signs of sepsis
  • hyperkalaemia signs
  • hyperventilating to balance metabolic acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how might you investigate AKI?

A
  • urine dipstick - blood
  • U&E - sodium and potassium
  • renal USS
  • urinalysis
  • CT-KUB is stone suspected
  • blood gas for acidosis state
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how might you manage an AKI?

A
  • fluid therapy - monitor, don’t give potassium containing fluids
  • optimise medication
  • hyperkalaemia treatment - calcium gluconate
  • metabolic acidosis treated with sodium bicarbonate
  • manage hypertension
  • dialysis considered in those with multi organ failure and haemofiltration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

when might you consider dialysis?

A
  • failure of conservative management
  • hyperkalaemia
  • severe hyponatraemia or hypernatraemia
  • pulmonary oedema or severe hypertension due to volume overload
  • severe metabolic acidosis
  • multisystem failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what might cause CKD in a child?

A

congenital anomalies of kidney and urinary tract, then glomerular disease, familial, systemic diseases affecting kidneys, tubulointerstitial diseases etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how might CKD present?

A
  • abnormal antenatal scan
  • anorexia
  • lethargy
  • polydipsia, polyuria
  • faltering growth

*Many children with chronic kidney disease have had their renal disease detected before birth by antenatal ultrasound or have previously identified renal disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how might you investigate CKD?

A
  • urinalysis - protein
  • U&E
  • FBC
  • USS
  • biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how might you manage CKD?

A
  • nutrition: calorie supplements, NG, restrict protein
  • prevent renal osteodystrophy
  • control salt and water balance
  • human recombinant erythropoietin
  • growth hormone
  • bicarbonate supplements
  • transplant or dialysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what causes UTI in child? what are some RF?

A
  • bacterial from GI tract - E.coli (85%), Klebsiella and staphylococcus saprophyticus
  • RF: under 1, female (under 3m boys), previous UTI, sexual abuse, constipation, immunosuppression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how might UTI present?

A

fever
babies: lethargy, irritable, vomiting, poor feed, increased frequency
abdo pain and loin tenderness
temp, HR, RR, CRT, pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how might you investigate UTI?

A
  • infants microscopy and cultures within 24h if temp over 38c
  • clean catch urine sample, urine collection pads
  • urine dipstick - in leukocyte esterase and nitrites positive send for cultures
    • nitrites better than leukocytes
  • imaging - USS, micturating cystography gold standard for reflux
  • recurrent UTI - investigate for underlying cause with USS, DMSA, VUR, MCUG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how are UTI managed in children?

A
  • all under 3 with fever - IV abx ceftriaxone, full septic screen, blood cultures, bloods and lactate and lumbar puncture
  • oral Abx if over 3m - trimethoprim, nitrofurantoin
  • pyelonephritis - IV Abx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how are UTI prevented in children?

A
  • use the potty more often
  • time child’s potty sessions - as in not to hold pee, empty bladder every 2-3h
  • empty bladder completely
  • proper wiping - front to back
  • stay hydrated
  • avoid constipation
  • choice of clothing - cotton underpants, avoid nylon or tight fitted
  • no bubble baths
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what could cause haematuria?

A
  • UTI
  • irritation to meatus or perineum
  • wilms
  • nephrolithiasis
  • GN
  • IgA nephropathy
  • FSGS
  • alport
  • trauma
  • sickle cell
  • exercise
  • HUS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are some red flags for haematuria?

A
  • Abnormal renal function
  • Proteinuria 2+ or more on the dipstick, please send a urine protein/creatinine ratio
  • Signs of fluid overload: peripheral oedema, ascites, elevated JVP, pulmonary oedema
  • Hypertension
  • Persistent frank/macroscopic haematuria with no cause identified after baseline investigations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the physiology of controlling urination? what age?

A
  • daytime urination by 2 years
  • night time urination by 3-4 years
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what causes primary nocturnal enuresis?

A
  • development variation esp if <5
  • overactive bladder
  • fluids before bed
  • failure to wake up
  • psych distress

*chronic constipations, UTI, LD, CP

20
Q

how would you manage primary nocturnal enuresis?

A
  • reassure parents of children <5 years
  • lifestyle changes
    • reduce fluid intake in evenings
    • pass urine before bed
    • ensure easy access to toilet
  • encouragement and positive reinforcement
  • treat underlying causes e.g. constipation
  • enuresis alarms
  • pharmacological treatment
21
Q

what could cause secondary nocturnal enuresis?

A
  • urinary tract infection
  • constipation
  • type 1 diabetes
  • new psychosocial problems
    • e.g. stress in family or school life
  • maltreatment
22
Q

when would you suspect abuse regarding enuresis?

A
  • deliberate bedwetting
  • punishment for bedwetting (despite parental education)
  • unexplained secondary nocturnal enuresis
23
Q

what are some risk factors for enuresis?

A
  • family history
  • male gender
  • developmental delay (physical or intellectual\0
  • constipation, faecal incontinence
  • ADHD, ASD, anxiety, depression, conduct disorders
  • sleep apnoea
24
Q

what is an enuresis alarm?

A
  • makes a noise at the first sign of bed wetting
  • this wakes up the child and stops them from urinating
25
Q

what are some limitations of an enuresis alarm?

A
  • equires a high level of training and commitment
  • needs to be used consistently for a prolonged period e.g. at least 3 months
  • may add to burden and frustration
26
Q

what are some pharmacological tx for enuresis?

A
  • desmopressin to reduce volume produced by kidneys
  • oxybutynin to reduce contractility of bladder
  • impramine to relax bladder
27
Q

what is the pathophysiology of nephrotic syndrome?

A

basement membrane in the glomerulus becomes highly permeable to protein, allowing proteins to leak from the blood into the urine

podocytes become flattened and allow leakage

28
Q

how is nephrotic syndrome managed?

A
  • high dose steroids
  • low salt diet
  • diuretics
  • albumin infusion
  • abx prophylaxis
29
Q

what is nephritic syndrome?

A
  • Nephritisrefers toinflammationwithin thenephronsof the kidneys
  • and nephritic syndrome is a consequence of glomerulonephritis
30
Q

how is nephritic syndrome managed?

A
  • monitoring of electrolytes, consider intensive care
  • antihypertensives
  • fluid restriction, consider dialysis
  • IgA nephropathy, HSP mx
31
Q

what is HUS?

A

thrombosis in small blood vessels throughout the body, usually triggered by shiga toxins from E. coli O157 or shigella

32
Q

what is the triad of HUS?

A
  • microangiopathic haemolytic anaemia
  • acute kidney injury
  • thrombocytopenia (low platelets)
33
Q

what is the pathophysiology of HUS?

A
  • formation of blood clots consumes platelets, leading to thrombocytopenia
    • blood flow through the kidney is affected by thrombi and damaged RBCs causing AKI
  • MAHA involves haemolysis due to pathology in small vessels (microangiopathy)
    • tiny thrombi partially obstruct the small blood vessels and churn the RBCs as they pass through, causing them to rupture
34
Q

how is HUS investigated?

A

stool culture
FBC
blood smear
U&E
clotting
PCR for shiga
LDH
biopsy

35
Q

how is HUS managed?

A
  • self limiting with supportive
    hypovolaemia, hypertension mx
    red cell transfusion
    short term dialysis or transplant
    plasma exchange
36
Q

what does the underlying pathology of PKD case?

A

mutation in thepolycystic kidney and hepatic disease 1(PKHD1)gene onchromosome 6

  1. Cystic enlargementof therenalcollecting ducts
  2. Oligohydramnios,pulmonary hypoplasiaandPotter syndrome
  3. Congenital liver fibrosis
37
Q

how does PKD present?

A
  • ARPKD usually presents in the antenatal period with the following seen on antenatal scans.
    1. oligohydramniosand
    2. polycystic kidneys
38
Q

how is PKD managed?

A
  • Patients may requirerenal dialysiswithin the first few days of life.
  • Most patients developend stage renal failurebefore reaching adulthood
39
Q

what is Wilms tumour?

A

tumour affecting the kidney in children, typically <5 years old

40
Q

when would you suspect Wilms?

A

should be considered in any child <5 years with a mass in the abdomen

  • abdominal pain
  • haematuria
  • lethargy
  • fever
  • hypertension
  • weight loss
41
Q

how would you investigate Wilms?

A
  • abdominal USS, CT, MRI
  • FBC, U&E, urinalysis
  • CXR
  • LFT
  • bone profile
42
Q

how is WIlms managed?

A
  • surgical excision of tumour and nephrectomy
  • adjuvant treatment depending on stage and metastasis:
    • adjuvant chemotherapy
    • adjuvant radiotherapy
43
Q

what is the pathophysiology of a posterior urethral valve?

A

tissue at the proximal end of the urethra causes obstruction of urine output

obstruction causes back pressure into the bladders and ureter causing hydronephrosis

restriction of outflow of urine means the bladder cannot fully empty, increasing the risk of UTIs

44
Q

how might a posterior urethral valve present?

A
  • asymptomatic
  • difficulty urinating
  • weak urinary stream
  • chronic urinary retention
  • palpable bladder
  • recurrent UTIs
  • impaired kidney function
45
Q

how is a posterior urethral valve investigated?

A
  • antenatal with oligohydramnios and hydronephrosis
  • abdo USS
  • micturating cystourethrogram: shows location of the extra urethral tissue and reflux of urine back into the bladder
  • cystoscopy
46
Q

how is a posterior urethral valve managed?

A
  • simple cases can be observed and monitored
  • temporary management
    • temporary urinary catheter
      • bypasses the valve
  • definitive management
    • ablation or removal of extra tissue
      • usually during cystoscopy

Y4 Paediatrics (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions