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Phase 3a > Paeds RENAL > Flashcards

Paeds RENAL Flashcards

1
Q

causes of UTI?

A 
E.coli
enterobacter 
klebsiella 
Proteus (phosphate stones)
pseudomonas (indicates structural defect)
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2
Q

symptoms of UTI in infants

A

poor feeding, vomiting, irritability, failure to thrive, diarrhoea

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3
Q

symptoms of UTI in children

A

abdominal pain, fever, dysuria, increased frequency, haematuria

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4
Q

lower UTI symptoms

A 
urgency 
frequency 
nocturne
dysuria
suprapubic pain 
fever
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5
Q

upper UTU symptoms

A

abdominal pain
nausea and vomiting
rigors

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6
Q

UTI investigations

A

urine collection
bloods - cultures, FBC, U&E, ESR, CRP
urine dip MC and S
USS - check for abnormalities

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7
Q

management of UTI

A

General: fluid, analgesics, antiemetics
<3 months –> refer to specialist
>3 months
upper UTI - cephalosporin or co-amoxiclav 7-10 days
lower UTI - trimethoprim, nitrofurantoin, cephalosporin or co-amoxiclav for 3 days

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8
Q

what are the clinical features of pyelonephritis?

A

fever
loin pain
vomiting
white cells in urine

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9
Q

what is enuresis?

A

involuntary discharge of urine by day or night or both in children aged 5 years or older in the absence of congenital or acquired defects of the nervous system or urinary tract.

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10
Q

what is primary nocturnal enuresis?

A

the child had never achieved continence

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11
Q

what is nocturnal secondary enuresis?

A

the child has been dry for at least 6 months before

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12
Q

what is the management of nocturnal enuresis?

A

look for possible underlying causes/triggers (constipation, DM, UTI)
advise of fluid intake, diet and toilet behaviour
rewards systems

first line treatment for children under the age of 7 is an enuresis alarm

first line treatment for children over the age of 7 - desmopressin.

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13
Q

what can cause daytime enuresis?

A 
lack of attention to the bladder sensation 
detrusor insability
bladder neck weakness 
UTI, constipations 
neuropathic bladder

secondary - may be due to emotional upset, UTI, polyuria from DM

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14
Q

what are the classifications of acute kidney injury?

A

pre-renal - most common in children
renal - there is salt water retention
post renal - urinary obstruction

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15
Q

management of acute kidney injury?

A

metabolic acidosis –> sodium bicarbonate
hyerkalaemia –> calcium gluconate if ECG changes, salbutamol, calcium change resin, glucose and insulin, dietary restriction

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16
Q

how would you treat pre-renal AKI?

A

suggested by hypovolaemia - needs to be corrected with fluid replacement

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17
Q

how would you treat renal AKI?

A

if fluid overload - restrict fluids, emergency management of metabolic abnormalities

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18
Q

how would your treat post-renal AKI?

A

relief of obstruction with nephrostomy or catheterisation

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19
Q

what is acute kidney injury

A

oliguria - less than 0.5 ml/kg per hour

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20
Q

what are pre-renal causes of AKI

A
  • most common cause in children - hypovolaemia (burns, sepsis, gastroenteritis, haemorrhage, nephrotic syndrome), circulatory failure
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21
Q

what are renal causes of AKI

A

vascular (haemolytic uraemia syndrome (HUS), vasculitis, embolus, renal vein thrombosis)
Tubular (acute tubular necrosis, ischaemic, toil, obstructive)
glomerular - glomerulpnephritis
interstitial - interstitial nephritis, pyelonephritis

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22
Q

what are post renal causes of AKI?

A

obstruction

congenital or acquired

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23
Q

what is the presentation if chronic kidney disease?

A 
anorexia 
lethary 
polydipsia 
polyuria 
failure to thrive 
body deformities 
hypertension 
acute on chronic renal failure 
unexplained normochromic normocytic anaemia
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24
Q

management of chronic kidney disease

A

Reduce CV risk - Control BP, statin
Potassium control - Dietary restriction
Prevention osteodystrophy - Calcium carbonate, vit D
Treat anaemia - Subcut EPO
Treat acidosis - Sodium bicarbonate
Prophylaxis - Influenza and pneumococcal vaccinations

Calorie supplements
NG feeding
Fluid correction
Hormonal abnormalities

Dialysis and transplant

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25
Q

what causes chronic kidney disease?

A 
hypertension 
diabetes
glomerular sclerosis 
lupus 
RA
HIV
NSAIDS 
toxins - tobacco
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26
Q

what can uraemia cause?

A 
nausea 
loss of appetite
encephalopathy (tremor)
pericarditis 
increase bleeding 
ureic most - crystals in skin
27
Q

what happens to potassium levels in CKD?

A

less potassium is excreted which leads to mild up in blood

hyperkalemia - can cause arrhythmias

28
Q

what happens to calcium levels in CKD?

A

low - hypocalcemia

kidneys activate vitamin D which aids the absorption of calcium

29
Q

what happens when calcium levels are low?

A

parathyroid hormone is released which causes the bones to lose calcium
this leads to bone being brittle which is called renal osteodystrophy

30
Q

how is CKD diagnosed ?

A

changes in GFR
less than 15ml/kg/1.73m2

kidney biopsy to look for changes such as glomerular sclerosis.

31
Q

what are the three manifestations of nephrotic syndrome?

A

proteinuria
hypoalbuminaemia
oedema

32
Q

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

A

minimal change disease

can also be caused by focal glomerulosclerosis and poost stept nephritis

33
Q

what happens in nephrotic syndrome?

A

there is damage and inflammation to the podocytes which normally help protein loss from the glomerulus which leads to protein loss to the nephron tubule.

34
Q

what is nephrotic syndrome treated?

A

90% of proteinuria resolves with corticosteorid therapy

35
Q

what are the complications of nephrotic syndrome?

A

hypovolaemia
thrombosis
infection
hypercholestoleamia

36
Q

how does minimal change disease present?

A

nearly always presents as nephrotic syndrome

37
Q

What are the causes of minimal change disease?

A

the majority are idiopathic
drugs - NSAIDS, rifampicin
Hodgkin’s lypmhoma, thymoma
infectious mononucleosis

38
Q

what are the features of nephrotic syndrome?

A

nephrotic syndrome
normotension - hypertension is rare
highly selective proteinuria
renal-biopsy: electron microscopy shows fusion of podocytes

39
Q

how is minimal change disease managed?

A

80% of cases are steroid responsive

cyclophoshphamide in the next step for steroid-resistant cases

40
Q

what is congenital nephrotic syndrome?

A

when nephrotic syndrome presents within the first 3 months of life.
it is rare
commonest kind is recessively inherited
associated with high mortality usually due to complications of hypoalbuminaemia

41
Q

what are the causes of acute nephritis?

A

post infectious (including streptococcus)
Vasculitis (HSP, SLE, wegener granulomatosis)
IgA nephropathy and mesangiocapillary glomerulonephritis
anti-glomerular basement membrane disease (good pasture syndrome)

42
Q

what are the clinical features of nephritic syndrome?

A

decreased urine output and volume overload
hypertension which may cause seizures
oedema, characteristically around the eyes
haematuria and proteinuria

43
Q

how is nephritic syndrome. managed?

A

water and electrolyte balance and the use of diuretics when necessary

44
Q

what are the features of henoch-schonlein purpura?

A 
characteristic skin rash on buttocks and extensor surfaces of arms and legs 
arthralgia 
periarticular oedema 
abdominal pain 
glomerulonephritis
45
Q

what is the common factors for HSP to occur?

A 
between 3 and 10 years 
more common in boys
peaks during winter months
often preceded by a response infection 
cause is unknown
46
Q

what is Alport syndrome

A

it is a familial nephritis
usually an X-linked recessive disorder that processes to end-stage renal failure by early adult life in males and is associated with nerve deafness and ocular defects.

47
Q

what is hypospadias?

A

congenital abnormality of the penis which occurs in approx 3/1000 male infants
an abnormal opening below the urethra
can also happen in girls but way way more common in boys

48
Q

what is hypospadias characterised by?

A

a ventral urethral meatus
a hooded prepuce
chord (ventral curvature of the pernis) in more sever form
the urethral meatus may open proximally in the more severe variants

49
Q

is is hypospadias treated?

A

corrective surgery is performed before 2 years of age

50
Q

what are the investigations for nephrotic syndrome

A 
LFT
lipids 
infection 
calcium (low)
renal injury 
urine 
bloods 
CXR
renal USS
51
Q

what are the investigations for HSP?

A

bloods (raised IgA, raised ESP, ASO titre (check for PSG)

urine dip

52
Q

what is the management for HSP?

A

analgesia for MSK pain

prednisolone is severe

53
Q

what is the presentation of post streptococcal glomerulonephritis?

A

URTI or pharyngitis

then two weeks later
haematuria
oliguria
proteinuria

odema
hypertension
signs of CV overload

54
Q

what are the investigations for post streptococcal glomerulonephritis?

A 
bloods 
- FBC - anaemia 
- U&amp;Es - increased urea and creatinine, increased potassium, acidosis
- antistreptolysin O increased 
anti DNAase B titre 
low C3
urinalysis - haematuria, proteinuria
renal biopsy
55
Q

what is the management of post streptococcal glomerulonephritis?

A

penicillin - 10 days
treat hypertension and fluid overload
correct metabolic imbalances

56
Q

what is vesicoureteric reflux?

A

there is abnormal back flow of urine from the bladder to the ureter and kidneys

there is abnormal vesicoureteric junction where the ureters enter the bladder - the ureters are displaced laterally, entering the bladder in a more perpendicular fashion than at an angle therefore shortened ureter, and the junction cannot function adequately

57
Q

what is the grading of vesicoureteric reflux?

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

58
Q

what are the investigations and management for vesicoureteric reflux

A

micturating cystourethrogram for diagnosis

DMSA should also be performed to check for scarring

59
Q

what are the triad of features of haemolytic uraemia syndrome (HUS)?

A

acute renal failure
microangiopathic haemolytic syndrome
thrombocytopenia

60
Q

what is typical HUS

A

secondary HUS

classically caused by shiga toxin producing E.coli (STEC)

61
Q

what is atypical HUS?

A

primary HUS due to complement dysregulation

62
Q

what investigations would you perform for HUS?

A

FBC (anaemia, thrombocytopenia, fragmented blood film)
U&E (acute kidney injury)
stool culture

63
Q

What is the management of HUS?

A

supportive treatment - fluids, blood transfusion and dialysis if required.

Phase 3a (41 decks)

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