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Phase 3a Jemima > Paediatrics - endocrine, renal and urology > Flashcards

Paediatrics - endocrine, renal and urology Flashcards

1
Q

what causes T1DM

A

when the pancreas stops to produce insulin, resulting in the body not being able to uptake glucose into cells

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2
Q

what cells in the pancreas produces insulin

A

beta cells in the islets of langerhans

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3
Q

what is glucagon

A

it is a hormone that increases blood sugar levels. Is is released in response to low blood sugar and stress, and increases blood glucose levels

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4
Q

when does ketogenesis occur

A

when there is an insufficient supply of glucose and glycogen stores are exhausted the liver converts fatty acids to ketones

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5
Q

how does type 1 DM present

A

classical triad:
polydipsia
polyuria
weight loss
less typical presentations are secondary enuresis and recurrent infections

about 25-50 % of children present in diabetic ketoacidosis

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6
Q

how is a new diagnosis of T1DM established

A

Bloods - FBC, renal profile, glucose monitoring
blood cultures
HbA1C
thyroid function tests and TPO antibodies
anti- TTG
insulin antibodies, anti-GAD and islet cell antibodies

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7
Q

what is the general long term management of T1DM

A

subcut insulin regimes
monitoring dietary carbohydrate intake
monitoring blood sugar levels on waking, at each meal and before bed
monitoring for and managing complications

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8
Q

what insulin regimes are normally given in T1DM

A

background long acting and short acting insulin (injected 30mins pre meal) - basal bolus regime

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9
Q

what can injecting insulin into the same spot cause

A

lipodystrophy where the sub cut fat hardens and prevents normal absorption of insulin when further doses are injected into this area

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10
Q

what are two types of insulin pump

A

tethered pump
patch pump

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11
Q

what is an insulin pump

A

it is a small device that continually infuses insulin at different rates to control blood sugar levels.
the pump pushes insulin through a cannula which is replaced every 2-3 days

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12
Q

how old must a child be in order to qualify for an insulin pump

A

over 12

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13
Q

what are the advantages of using an insulin pump

A

better blood sugar control
more flexibility with eating
less injections

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14
Q

what are disadvantages of using an insulin pump

A

difficulties learning how to use a pump
having it attached at all times
blockages in the infusion set
small risk of infection

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15
Q

what is a tethered pump

A

these are devices with replaceable infusion sets and insulin
they usually attach to patients belt or round waist which connects to the cannula
the controls for the infusion are on the pump

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16
Q

what is a patch pump

A

this sits directly on the skin without any visible tubes
when they run out of insulin the whole patch is disposed of and new pump is attaches
normally controlled by separate remote

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17
Q

what are short term complications of T1DM

A

Hypoglycaemia
hyperglycaemia and DKA

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18
Q

what are treatment options for severe hypoglycaemia

A

IV dextrose and IM glucagon

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19
Q

what are the macrovascular complications of T1DM

A

coronary artery disease
peripheral ischaemia - diabetic foot
stroke
hypertension

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20
Q

what are the microvascular complications of T1DM

A

peripheral neuropathy
retinopathy
kidney disease - glomerulosclerosis

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21
Q

what monitoring is done in those with T1DM

A

HbA1c - glycated haemoglobin measured every 3-6 months
capillary blood glucose
flash glucose monitoring - sensor on the skin that measures glucose in the interstitial fluid

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22
Q

what is the pathophysiology of diabetic ketoacidosis

A

when cells in the body have no fuel (glucose) they initiate the process of ketogenesis.
over time ketone acids use up bicarbonate (produced by kidneys) and the blood becomes acidic

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23
Q

why do patients in DKA get dehydrated

A

hyperglycaemia overwhelms the kidneys and glucose starts being filtered into the urine
the glucose in the urine draws water out with it
this causes the patient to urinate a lot
this stimulates excessive drinking

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24
Q

why does DKA cause potassium imbalance

A

insulin normally drives potassium into the cells
without insulin serum potassium can be high/normal due to compensation by the kidneys where as the total body potassium is low as no potassium is stored in cells
when treatment with insulin starts the patient may develop a severe hypokalaemia

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25
Q

what can children in DKA develop

A

cerebral oedema

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26
Q

what causes cerebral oedema in DKA

A

dehydration and high blood sugar concentration cause water to move from the intracellular to extracellular space in the brain
this causes brain cells to shrink and become dehydrated
rapid correction of dehydration and hyperglycemia with fluids and insulin causes a rapid shift in water in the brain and can cause the brain to swell and become oedematous

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27
Q

what are signs of cerebral oedema in those with DKA

A

headaches
altered behaviour
bradycardia
changes to consciousness

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28
Q

what is the treatment for cerebral oedema in DKA

A

slowing IV fluids
IV mannitol
IV hypertonic saline

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29
Q

how does DKA present

A

polyuria
polydipsia
nausea and vomiting
weight loss
acetone smell to their breath
dehydration and hypotension
antlered consciousness
symptoms of underlying trigger

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30
Q

how is DKA diagnosed

A

hyperglycaemia - blood glucose >11mmol/l
ketosis- blood ketones > 3mmol/l
acidosis - pH <7.3

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31
Q

what is the principles of DKA management in children

A
  1. correct dehydration evenly over 48 hours
  2. give a fixed rate insulin infusion

need to prevent hypoglycaemia by adding IV
dextrose once glucose falls below 14mmol/l
add potassium to IV fluids and monitor serum potassium closely

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32
Q

what is adrenal insufficiency

A

it is where the adrenal glands do not produce enough steroid hormones particularly cortisol and aldosterone

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33
Q

what is addisons disease

A

primary adrenal insufficiency
this is when the adrenal glands have been damaged resulting in reduced secretion of cortisol and aldosterone

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34
Q

what causes secondary adrenal insufficiency

A

inadequate ACTH stimulating the adrenal glands resulting in low cortisol being released
- loss or damage to the pituitary gland

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35
Q

what causes tertiary adrenal insufficiency

A

result of inadequate CRH by the hypothalamus

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36
Q

what is a common cause of tertiary adrenal insufficiency

A

long term oral steroids (more than three weeks) causing suppression of the hypothalamus

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37
Q

what are features of adrenal insufficiency in babies

A

lethargy
vomiting
poor feeding
hypoglycaemia
jaundice
failure to thrive

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38
Q

what are features of adrenal insufficiency in older children

A

nausea and vomiting
poor weight gain or weight loss
reduced appetite
abdominal pain
muscle weakness or cramps
developmental delay or poor academic performance
bronze hyperpigmentation to skin in addisons caused by high ACTH levels

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39
Q

what investigations are done in a child with suspected adrenal insufficiency

A

bloods - U+E, blood glucose, FBC
cortisol, ACTH, aldosterone and renin levels
Short synacthen test

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40
Q

what is seen on bloods in primary adrenal failure

A

low cortisol
high ACTH
low aldosterone
high renin

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41
Q

what is seen on bloods in secondary adrenal insufficiency

A

low cortisol
low ACHT
normal aldosterone
normal renin

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42
Q

what is the Short Synacthen test

A

used to confirm adrenal insufficiency
- give patient synacthen (synthetic ACTH)
- blood cortisol is measures at baseline, 30 and 60 minutes after administration
- failure of cortisol to rise indicates primary adrenal insufficiency

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43
Q

how is adrenal insufficiency managed

A

replacement of steroids
- hydrocortisone for cortisol
- fludrocortisone for aldosterone
monitor patient closely for: growth and development, blood pressure, U+E, glucose, bone profile and vitamin D

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44
Q

what needs to happen during acute illness if someone is on steroids

A

their dose of steroid needs to be increased and given more regularly until the illness has resolved
blood sugar needs to be monitored closely
with D+V they need an IM injection of steroid at home and likely need IV steroids

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45
Q

what is an addisonian crisis

A

this is an acute presentation of severe addisons where the absence of steroid hormones result in a life threatening condition

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46
Q

how can patients present in addisonian crisis

A

reduced consciousness
hypotension
hypoglycaemia, hyponatraemia, hyperlalaemia

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47
Q

what is the management of an Addisonian crisis

A

intensive monitoring
parenteral steroids - IV hydrocortisone
IV fluid resuscitation
correct hypoglycaemia

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48
Q

what is congenital adrenal hyperplasia

A

it is a condition caused by congenital deficiency of the 21 hydroxylase enzyme causing underproduction of cortisol and aldosterone and an over production of androgens from birth

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49
Q

what is the inheritance pattern of congenital adrenal hyperplasia

A

autosomal recessive

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50
Q

a deficiency in what enzyme causes congenital adrenal hyperplasia

A

21 hydroxylase
- small number of cases caused by deficiency of 11 beta hydroxylase

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51
Q

what is the pathophysiology of congenital adrenal hyperplasia

A

21 hydroxylase in an enzyme required for converting progesterone into aldosterone and cortisol
in CAH there is a defect in the 21 hydroxylase enzyme meaning there is excess progesterone which is converted into testosterone instead

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52
Q

what is the presentation of severe congenital adrenal hyperplasia

A
  • female patients with CAH present with ambiguous genitalia and enlarged clitoris
  • babies with severe CAH can present shortly after birth with hyponatraemia, hyperkalaemia and hypoglycaemia
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53
Q

how do patients with mild congenital adrenal hyperplasia present

A

present during childhood or after puberty
Female patients - tall for age, facial hair, absent periods, deep voice, early puberty
male patients - tall for their age, deep voice, large penis, small testes, early puberty

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54
Q

what is the management for congenital adrenal hyperplasia

A

cortisol replacements - hydrocortisone
aldosterone replacements - fludrocortisone
female patients with ‘virilised’ genitals may require corrective surgery

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55
Q

where is growth hormone produced

A

by the anterior pituitary gland

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56
Q

what is growth hormone responsible for

A

it is responsible for stimulating cell reproduction and the growth of organs, muscles, bones and increase height

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57
Q

what does growth hormone stimulate the release of

A

the release of insulin like growth factor 1 by the liver

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58
Q

what is congenital growth hormone deficiency

A

the disruption to the growth hormone axis at the hypothalamus or the pituitary gland

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59
Q

what can cause congenital growth hormone deficiency

A

genetic mutation - GH1 or GHRHR genes
empty sella syndrome where the pituitary gland is underdeveloped or damaged

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60
Q

what can cause acquired growth hormone deficiency

A

infection
trauma
interventions - surgery

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61
Q

how does growth hormone deficiency present

A

micropenis in males
hypoglycaemia
severe jaundice

in older infants and children it can present as
poor growth, usually stopping/slowing at 2-3
short stature
slow development of movement and strength
delayed puberty

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62
Q

what investigations can be done to diagnose growth hormone deficiency

A

growth hormone stimulation test - give glucagon/insulin/arginine/clonidine which stimulates growth hormone and look at the response
test other hormone deficiencies
MRI brain
genetic testing - turners or prader-willi
X ray or DEXA scan to determine bone age

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63
Q

how is growth hormone deficiency treated

A

referral to paediatric endocrinology
- daily subcutaneous injections of growth hormone (somatropin)
- treatment of other associated hormone deficiencies
- close monitoring of height and development

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64
Q

what is congenital hypothyroidism

A

this is where a child is born with an underactive thyroid gland
can be a result of underdeveloped thyroid gland or a fully developed gland that isnt producing enough hormone

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65
Q

when would you pick up congenital hypothyroidism in a newborn

A

during the newborn blood spot screening test

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66
Q

how might patients with congenital hypothyroidism present

A

prolonged neonatal jaundice
poor feeding
constipation
increased sleeping
reduced activity
slow growth and development

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67
Q

what is acquired hypothyroidism

A

this is where a child/adolescent develops an underactive thyroid when it was previously functioning normally

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68
Q

what is the most common cause of acquired hypothyroidism

A

autoimmune hypothyroidism - Hashimotos due to anti-TPO and antithyroglobulin abs

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69
Q

how might a child with Hashimotos present

A

fatigue and low energy
poor growth
weight gain
poor school performance
constipation
dry skin and hair loss

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70
Q

how is hypothyroidism managed in children

A

referral to a paediatric endocrinologist
- full thyroid function tests and abs
- levothyroxine orally once per day

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71
Q

what is precocious puberty

A

this is a condition where secondary sexual characteristics appear before 8 in girls and 9 in boys

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72
Q

what are risk factors of precocious puberty

A

brain tumours
cranial irradiation
McCune-Albright syndrome
gonadal tumours
congenital adrenal hyperplasia

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73
Q

what is the pathophysiology of precocious puberty

A

centrally mediated: HPG axis is prematurely activated leading to increased serum gonadotropins, the pattern of endocrine change is the same as in normal puberty
Other: secretion of sex steroids is done independent of the hypothalamic GnRH pulse. There is a loss of feedback regulation. Pubertal develop doesnt follow a normal pattern

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74
Q

how is precocious puberty diagnosed

A

detailed history and exam, parental history and social history
compare growth with previous growth charts
Tanners staging
Prader orchidometer
BLOODS!!

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75
Q

how is precocious puberty managed

A

GnRH analogues given nasally, subcut or IM in order to suppress secretion of pituitary gonadotropins
- helps to reduce gonadal maturation and reduces skeletal maturation

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76
Q

what is delayed puberty

A

in males > 14 years
in females > 14 with no breast development or absence of menarche >= 16

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77
Q

what age does puberty start in boys and girls

A

boys = 9-15
girls = 8-14

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78
Q

what is hypogonadism

A

this is a lack of sex hormones, oestrogen and testosterone

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79
Q

what are the two causes of hypogonadism

A

hypogonadotropic hypogonadism hypergonadotropic hypogonadism

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80
Q

what is hypogonadotropic hypogonadism

A

it is a deficiency in FDH and LH (gonadotrophins) leading to a deficiency in testosterone and oestrogen

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81
Q

what can cause Hypogonadotropic hypogonadism

A

abnormal functioning of the hypothalamus or pituitary gland
- previous damage: radiotherapy, surgery
- growth hormone deficiency
- hypothyroidism
- hyperprolactinaemia
- serious chronic conditions
- excessive dieting or exercising
- constitutional delay in growth and development
- Kallman syndrome

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82
Q

what is hypergonadotropic hypogonadism

A

this is where the gonads fail to respond to stimulation from the gonadotrophins
no negative feedback means the anterior pituitary produces large amounts of LH and FSH

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83
Q

what are causes of hypergonadotropic hypogonadism

A

previous damage to the gonads - torsion, cancer, infection i.e mumps
congenital absence of testes or ovaries
Kleinfelters syndrome (XXY)
Turners syndrome (XO)

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84
Q

what is the threshold for initiating investigations in delayed puberty

A

when there is no evidence of pubertal changes in a girl aged 13 or a boy aged 14

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85
Q

how is hypogonadism diagnosed

A

history and exam
assess weight, height, stage of pubertal development
Bloods - FBC, ferritin, U+E, anti TTG or EMA
hormonal testing - FSH and LH, TFT, GH, IGF1, prolactin
genetic testing
imaging - X-ray wrists, pelvic USS, MRI brain

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86
Q

what is Kallmann syndrome

A

a type of hypogonadotropic hypogonadism - it is characterised by absent or delayed puberty and a lack or loss of sense of smell

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87
Q

what is the pathophysiology of Kallmann syndrome

A

Genes associated with Kallmann syndrome disrupt the migration of olfactory nerve cells and GnRH producing nerve cells in the developing brain causing an underdevelopment in GnRH production as well as a change in sense of smell

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88
Q

what are the symptoms of Kallmann syndrome

A

Lack of breast development and menstrual periods in females
no development of sex characteristics in males at puberty - enlarged penis, low voice, hair growth
short stature
anosmia
fatigue
weight gain
mood changes
low sex drive
infertility

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89
Q

what other features unrelated to reproductive health may people with Kallmann syndrome have

A

renal agenesis - one kidney doesn’t develop
cleft lip and palate
dental abnormalities
poor balance
scoliosis
eye movement issues

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90
Q

how is Kallman syndrome diagnosed

A

lack of sexual maturity during puberty prompts investigation
- history and examination
- hormone evaluation
- olfactory function testing
- MRI
- genetic testing

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91
Q

How is Kallmann syndrome treated

A

hormone replacement therapy
- testosterone injections
- oestrogen and progesterone pills/patches
- GnRH injections used to induce ovulation in females
- HCG injections can be used to increase sperm count in males and increase fertility in females
unable to treat anosmia

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92
Q

how do babies present with UTI

A

fever
lethargy
irritability
vomiting
poor feeding
urinary frequency

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93
Q

what are symptoms of UTI in older infants and children

A

fever
abdominal pain - suprapubic
vomiting
dysuria
urinary frequency
incontinence

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94
Q

when is a diagnosis of acute pyelonephritis made

A

when there is either:
a temperature >38
loin pain or tenderness

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95
Q

what is the ideal urine sample for diagnosing UTI

A

clean catch - avoiding contamination

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96
Q

what will be present in a urine sample in a patient with UTI

A

Nitrites - suggestive of bacteria
Leukocytes

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97
Q

what is the management of UTI in children

A

all children under 3 months with a fever should start immediate IV antibiotics (ceftriaxone) have a full septic screen and maybe LP
oral antibiotics will be considered in children over 3 months if otherwise well
- trimethoprim
- nitrofurantoin
- cefalexin
- amoxicillin

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98
Q

when does a patient with recurrent UTI require ultrasound scans

A
  1. all children under 6 months with their first UTI should have USS within 6 weeks
  2. children with recurrent UTIs should have UTI within 6 weeks
  3. Children with atypical UTIs should have USS during illness
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99
Q

what investigations should be done in a child having recurrent UTI

A

Ultrasound scans
DMSA scan
Micturating cystourethrogram

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100
Q

what is a DSMA scan

A

where a radioactive material (DSMA) is injected an using a gamma camera you can visualise this being taken up into the kidneys. Areas where the DSMA isnt taken up indicates scarring that may be a result of previous infection

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101
Q

what is Vesivo-uteric reflux

A

this is where urine can flow from the bladder back into the ureters. This predisposes patients to developing upper urinary tract infections and scarring

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102
Q

how is Vesico-uteric reflux diagnosed

A

using micturating cystourethrogram

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103
Q

how is vesico-uteric reflux managed

A

depends on the severity
- avoid constipation
- avoid excessively full bladder
- prophylactic antibiotics
- surgical input

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104
Q

what is a micturating cystourethrogram

A

it involves catheterising the patient and injecting contrast into the bladder and taking a series of X-rays to determine whether the contrast is refluxing into the ureters

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105
Q

what is micturating cystourethrogram used for

A

investigate atypical or recurrent UTIs in children under 6 months
vesico-uteric reflux
dilation of the ureter
poor urinary flow

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106
Q

what is vulvovaginitis

A

it refers to inflammation and irritation of the vulva and vagina
- common between ages 3-10

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107
Q

what causes vulvovaginitis

A

irritation caused by sensitive and thin skin and mucosa
- wet nappies
- use of chemicals or soaps when cleaning
- tight clothing
- poor toilet hygiene
- constipation
- threadworms
- pressure i.e horse-riding
- heavily chlorinated pools

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108
Q

how does vulvovaginitis present

A

soreness
itching
erythema around the labia
vaginal discharge
dysuria
constipation
urine dipstick - leukocytes with no nitrites

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109
Q

how is vulvovaginitis treated

A

generally no medical treatment is required and management focuses on simple measures
- avoid washing with soap/chemicals
- avoid perfumed or antiseptic products
- good toilet hygiene
- keep area dry
- emollients
- loose clothing
- treat constipation and worms if applicable
- avoid activities that exacerbate the issue

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110
Q

what is nephrotic syndrome

A

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

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111
Q

what are the symptoms of nephrotic syndrome

A

frothy urine
generalised oedema
pallor

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112
Q

what are the features of nephrotic syndrome

A

Triad:
low serum albumin
high proteinuria (3+)
oedema
also have deranged lipid profile with high cholesterol, triglycerides and LDLP, high blood pressure and hypercoagulability

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113
Q

what are causes of nephrotic syndrome

A

minimal change disease - most common
focal segmental glomerulosclerosis
membranoproliferative glomerulonephritis
Henoch schonlein purpura
diabetes
infection - HIV, hepatitis, malaria

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114
Q

what is minimal change disease

A

common cause of nephrotic syndrome where on renal biopsy and microscopy there is minimal/no abnormalities seen

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115
Q

what does urinalysis in minimal change disease show

A

small molecular weight proteins and hyaline casts

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116
Q

what is the management of minimal change disease

A

corticosteroids - prednisolone

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117
Q

how is nephrotic syndrome managed

A

High dose steroids given for 4 weeks and then gradually weaned
low salt diet
diuretics to treat oedema
albumin infusions in severe hypalbuminaemia
antibiotic prophylaxis

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118
Q

what are the different steroid responses in nephrotic syndrome

A
  1. steroid sensitive - response to steroids (80%)
  2. steroid dependent - struggle to wean of steroids due to relapse
  3. steroid resistant - dont respond
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119
Q

what are steroid resistant children given to treat nephrotic syndrome

A

ACE inhibitors
immunosuppressants - cyclosporin, rituximab

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120
Q

what are complications of nephrotic syndrome

A

hypovolaemia as fluid leaks into interstitial space
thrombosis
infection as kidneys leak immunoglobulins
acute or chronic renal failure
relapse

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121
Q

what is nephritis

A

inflammation within the nephrons of the kidneys causing reduced kidney function, haematuria and proteinuria

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122
Q

what are the two most common causes of nephritis in children

A

Post streptococcal glomerulonephritis and IgA nephropathy

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123
Q

what is post streptococcal glomerulonephritis

A

occurs 1-3 weeks after beta-haemolytic streptococcus, where immune complexes get stuck in the glomeruli and cause inflammation leading to AKI

124
Q

what are the symptoms of post streptococcal glomerulonephritis

A

can be asymptomatic
- history of tonsillitis
- malaise
- headache
- vague loin discomfort
- dyspnoea
- smoky urine
- oedema
- anaemia
- raised BP

125
Q

what investigations are done for post streptococcal glomerulonephritis

A

urine sample - blood and protein on dipstick
bloods
imaging
ECG

126
Q

what is the management of post streptococcal glomerulonephritis

A

supportive management - weighing, vitals, strict monitoring of fluid input and output
diet high in carbs
antihypertensives and diuretics may be given
daily urinalysis

127
Q

What causes IgA nephropathy

A

IgA deposits in the nephrons of the kidneys causing inflammation

128
Q

what does a renal biopsy show in IgA nephropathy

A

IgA deposits and glomerular mesangial proliferation

129
Q

what disease is IgA nephropathy also associated with

A

Henoch-schonlein purpura

130
Q

what are signs/symptoms of IgA nephropathy

A

may not have any especially in early disease
- haematuria
- proteinuria
- urinating less often or small amounts
- oedema in legs/feet/eyes

131
Q

what are complications of IgA nephropathy

A

hypertension
rapidly progressive glomerulonephritis
acute kidney injury

132
Q

how is IgA glomerulonephritis diagnosed

A
  • urine sample
  • bloods
  • USS
  • renal biopsy
133
Q

how is IgA nephropathy treated

A

supportive treatment of the renal failure and immunosuppressant medications i.e steroids and cyclophosphamide to slow progression

134
Q

when does IgA nephropathy normally present

A

in teenagers or young adults

135
Q

what is acute glomerulonephritis

A

glomerular injury usually involving inflammatory changes in the glomerular capillaries and glomerular basement membrane

136
Q

what can cause acute glomerulonephritis

A

leukocyte infiltration, antibody deposition and complement activation
- infections
- systemic inflammatory conditions
- drugs
- metabolic disorders
- malignancy
- hereditary disorders
- deposition diseases

137
Q

what are most nephritic syndromes triggered by

A

immune mediated injury

138
Q

what are features of acute glomerulonephritis

A

haematuria with red cell casts
proteinuria
hypertension

139
Q

what are complicated presentations of acute glomerulonephritis

A

hypertensive encephalopathy: restless, drowsy, severe HA, fits, decreased vision, vomiting
AKI: acidosis, hyperkalaemia, seziure, stupor
Fluid overload: pulmonary oedema, cardiac failure
Mixed nephritic-nephrotic

140
Q

how do you diagnose acute glomerulonephritis

A

urinalysis
bloods
throat swabs
chest X ray
renal biopsy

141
Q

how do you treat acute glomerulonephritis

A

supportive
treat underlying infection or cause
monitor fluid balance - restrict/diuretics
beck BP often and salt
if encephalopathy give sodium nitroprusside
haemodialysis if severe renal failure

142
Q

what can cause nephritic syndrome

A

Post strep glomerulonephritis
bacterial endocarditis
viral kidney infections
HIV
lupus
Goodpasture’s syndrome
IgA nephropathy
polyarteritis
granulomatosis with polyangiitis
high blood pressure
diabetic nephropathy
focal segmental glomerulosclerosis

143
Q

what is Goodpastures syndrome

A

anti-glomerular basement membrane disease
anti-GBM antibodies attach the glomerulus and pulmonary basement membranes

144
Q

what antibodies are present in
a. microscopic Polyangiitis
b. granulomatosis with polyangiitis

A

a. P-ANCA
b. C-ANCA

145
Q

what is haemolytic uraemic syndrome

A

thrombosis in small blood vessels throughout the body

146
Q

what normally causes haemolytic uraemic syndrome

A

shiga toxins from wither E.coli 0157 or shigella

147
Q

what is the ‘classic triad’ of Haemolytic uraemic syndrome

A

microangiopathic haemolytic anaemia
acute kidney injury
thrombocytopenia

148
Q

what is microangiopathic haemolytic anaemia

A

destruction of red blood cells due to pathology in the small vessels
- tiny blood clots partially obstruct the small blood vessels and churn the red cells as they pass through causing them to rupture

149
Q

how does haemolytic uraemic syndrome present

A

may initially have a gastroenteritis sx
- fever
- abdominal pain
- lethargy
- pallor
- reduced urine output
- haematuria
- hypertension
- bruising
- jaundice
- confusion

150
Q

what is the management of haemolytic uraemic syndrome

A

medical emergency and requires hospital admission
- IV fluids
- blood transfusions
- haemodialysis
- control high blood pressure
- stool culture to establish causative organism

151
Q

what is enuresis

A

involuntary urination

152
Q

what is nocturnal enuresis

A

bed wetting

153
Q

what is primary nocturnal enuresis

A

it is where a child has never managed to be consistently dry at night

154
Q

what are causes of primary nocturnal enuresis

A

most commonly a variation on normal development
overactive bladder
fluid intake prior to bed - fizzy drinks, juice
failure to wake - deep sleep
psychological distress
secondary causes - chronic constipation, UTI, learning difficulties or cerebral palsy

155
Q

what is the initial step in managing primary nocturnal enuresis

A

establish underlying cause - 2 week diary of toileting, fluid intake and bedwetting episodes

156
Q

what is the management of primary nocturnal enuresis

A

reassure parents of children under 5 that it is likely to resolve without treatment
lifestyle changes: reduced fluid intake in the evenings, pass urine before bed
encouragement and positive reinforcement
treat any underlying causes of exacerbating factors
enuresis alarms
pharmacological treatment

157
Q

what is secondary nocturnal enuresis

A

bed wetting when they have been previously dry for at least 6 months

158
Q

what are causes of secondary nocturnal enuresis

A

UTI
constipation
type 1 diabetes
new psychological problems
maltreatment
think abuse and safeguarding

159
Q

what is diurnal enuresis

A

daytime incontinence

160
Q

what causes diurnal enuresis

A

urge incontinence
stress incontinence
recurrent UTI
psychosocial issues
constipation

161
Q

what is an enuresis alarm

A

this is a device that makes a noise at the first sign of bed wetting, waking the child and stopping them from urinating
- requires a high level of training and commitment and needs to be used consistently for at least 3 months

162
Q

what pharmacological treatment can be used to help with nocturnal enuresis

A

desmopressin - reduced the volume of urine produced by the kidneys
oxybutynin - anticholinergic and reduces contractility of the bladder
imipramine - TCA

163
Q

what are the two types of polycystic kidney disease

A

autosomal recessive PKD
autosomal dominant PKD

164
Q

when does autosomal recessive polycystic kidney disease present

A

in neonates - usually picked up on antenatal ultrasound scans

165
Q

what causes autosomal recessive polycystic kidney disease

A

mutation in the polycystic kidney and hepatic disease 1 (PKHD1) gene on chromosome 6
- gene codes for fibrocystin/productin protein complex responsible for the creation of tubules and maintenance of healthy epithelial tissue

166
Q

what are features of autosomal recessive polycystic kidney disease

A

cystic enlargement of the renal collecting ducts
oligohydramnios (too little amniotic fluid), pulmonary hypoplasia and Potter syndrome (lack of amniotic fluid and kidney failure in unborn infant)
congenital liver fibroids

167
Q

what are the characteristics of Potter syndrome

A

dysmorphic features - underdeveloped ear cartilage, low set ears, flat nasal bridge, abnormalities in skeleton

168
Q

what issues might people with polycystic kidney disease have throughout life

A

liver failure due to fibrosis
portal hypertension
progressive renal failure
hypertension
chronic lung disease

169
Q

what is multicystic dysplastic kidney

A

where the babies kidneys is made up of many cysts while the other kidney is normal (separate to polycystic kidney disease)

170
Q

how is multicystic dysplastic kidney diagnosed

A

antenatal ultrasound scans

171
Q

what is the outcome of multicystic dyspastic kidney

A

usually the healthy kidney is sufficient to lead a normal life - often the cystic kidney will atrophy and disappear before the age of 5

172
Q

what is Wilms tumour

A

it is a specific type of tumour affecting the kidneys in children, typically under the age of 5

173
Q

how does Wilms tumour present

A

mass in the abdomen
abdominal pain
haematuria
lethargy
fever
hypertension
weight loss

174
Q

how is Wilms tumour diagnosed

A

ultrasound of abdomen to look at kidneys
CT or MRI to stage tumour
biopsy for definitive diagnosis

175
Q

how is Wilms tumour managed

A

surgical excision of the tumour along with the affected kidney
adjuvant treatment - chemotherapy and radiotherapy

176
Q

what is the prognosis for Wilms tumour

A

early stage tumours with good histology hold up to 90% cure rate
metastatic disease has a poorer prognosis

177
Q

what is a posterior urethral valve

A

it is an issue where there is tissue at the proximal end of the urethra (closest to bladder) what causes an obstruction of urine output

178
Q

does posterior urethral valve occur in newborn girls or boys

A

boys

179
Q

what does posterior urethral valve cause

A

it causes obstruction to the outflow of urine creating a back pressure into the bladder, ureters and up to the kidneys causing hydronephrosis
a restriction in the urine outflow prevents the bladder emptying fully increasing the risk of UTI

180
Q

how does posterior urethral valve present

A

mild cases may be asymptomatic
difficulty urinating
weak urinary stream
chronic urinary retention
palpable bladder
recurrent urinary tract infections
impaired kidney unction

181
Q

what investigations are done for proximal urethral valve

A

severe cases may be picked up on antenatal scans as oligohydramnios and hydronephrosis
abdominal UUS
micturating cystourethrogram
cystoscopy and ablation

182
Q

how is proximal urethral valve managed

A

mild cases - observed and monitored
catheter temporarily
ablation is definitive management or removal of the extra urethral tissue

183
Q

where do the testes develop in a fetus

A

in the abdomen

184
Q

what are undescended tests

A

where the testes have not migrated down into the scrotum

185
Q

what do undescended testes carry a risk of

A

in older children or after puberty it carries a higher risk of testicular torsion, infertility and testicular cancer

186
Q

what are risk factors for undescended testes

A

family history of undescended testes
low birth weight
small for gestational age
prematurity
maternal smoking during pregnancy

187
Q

what is the management for undescended testes

A

watching and waiting is appropriate in newborns - most cases will descend in 3-6 months
if they have not descended by 6 months they should be seen by a paediatric urologist
orchidopexy (surgery) should be carried out between 6 -12 months of age

188
Q

what are retractile testicles

A

in boys that have not reached puberty their testes can move in and out of the scrotum and into the inguinal canal when cold or the cremasteric reflex is activated
this usually resolves as they go through puberty and the testes settle in the scrotum

189
Q

what is hypospadias

A

it is a condition affecting males where the urethral meatus (opening) is abnormally displaced to the ventral side (underside) of the penis towards the scrotum or further

190
Q

what is epispadias

A

this is where the meatus is displaced to the dorsal side (top side) of the penis

191
Q

how is hypospadias diagnosed

A

it is a congenital condition affecting babies from birth so it is usually diagnosed on the examination of the newborn

192
Q

what is the management of hypospadias

A

paediatric specialist urologist referral
not to circumcise infant until urologist says its okay
mild cases may not require treatment
surgery is usually performed after 3-4 months of age
surgery aims to correct the position of the meatus and straighten the penis

193
Q

what are the complications of hypospadias

A

difficulty directing urination
cosmetic and psychological concerns
sexual dysfunction

194
Q

what is hydrocele

A

a collection of fluid within the tunica vaginalis that surrounds the testes

195
Q

what is a simple hydrocele

A

it is when fluid is trapped in the tunica vaginalis which then gets reabsorbed over time

196
Q

what is a communicating hydrocele

A

it is where the tunica vaginalis around the testicle is connected with the peritoneal cavity via a pathway called the processus vaginalis, this allows fluid to travel rom the peritoneal cavity into the hydrocele, allowing the hydrocele to fluctuate in size

197
Q

how is a hydrocele identified on examination

A

causes a soft, smooth, non tender swelling around one of the testes.
swelling will be in front and below the testicle
they will transilluminate with light

198
Q

what are differential diagnosis for hydrocele

A

partially undescended testes
inguinal hernia
testicular torsion
haemotoma
tumours (rare)

199
Q

what is the management of hydrocele

A

ultrasound to confirm diagnosis
simple hydroceles will resolve within 2 years, just require regular follow up. May require surgery if associates with other issues
communicating hydrocele can be treated with a surgical operation to remove or ligate the connection between the peritoneal cavity and the hydrocele

200
Q

what is Phimosis

A

condition of the penis where the foreskin cant be retracted (very tight)

201
Q

what are the two types of phimosis

A

physiologic - often in children and resolves and they get older
pathologic - infection, inflammation or scarring (lichen sclerosis) causes pathologic phimosis

202
Q

how common is phimosis

A

nearly al babies assigned male at birth have physiological phimosis and as they grow the foreskin changes and gradually pulls back

203
Q

what are symptoms of phimosis

A

cant pull foreskin back from head of penis
discoloration
swelling
soreness or pain
pain while urinating
weak pee stream
blood in urine
smegma
pain on erection or sexual intercourse
ballooning during micturition
paraphimosis (engorgement) - emergency

204
Q

what is the main cause of pathological phimosis

A

pathologic phimosis is most commonly caused by infection including STI, or scarring,
skin conditions - eczema, psoriasis, lichen sclerosus
Penile adhesions or scar tissue
injuries

205
Q

what are the complications of phimosis

A

foreskin inflammation, glans inflammation or foreskin and glans inflammation
UTI
foreskin tears
foreskin gets stuck of trapped behind the glans and you cant pull it down
poor hygiene
long standing - penile cancer

206
Q

how is phimosis diagnosed

A

physical exam
history
urinalysis
urethral discharge culture

207
Q

how is phimosis managed

A

physiologic phimosis usually doesnt need treatment
- corticosteroid cream or gel
- antibiotics
- phimosis surgery involving circumcision

208
Q

what are complications of circumcision

A

bleeding
infection
foreskin is too short or long
pain

209
Q

How do you treat phimosis

A

manipulation with ice packs
compression
osmotic agent
puncture technique
surgical reduction and circumcision

210
Q

what is horseshoe kidney

A

this is a fusion defect of the kidneys with abnormal position, rotation and vascular supply of the kidneys

211
Q

what are the features of horseshoe kidney

A

usually asymptomatic and identified incidentally
may present with abdominal pain and UTI infection

212
Q

how is horseshoe kidney diagnosed

A

USS or CT/MRI
CT urogram may help identify stones, blockages and uteropelvic junction blocks

213
Q

what are renal malformations that may be present in a child

A

complete absence of one or both kidneys
kidneys that are fused together
obstructive renal pelvis defect (partial or complete blockage of kidney drainage)
structural issues

214
Q

what are signs of paediatric renal malformation

A

may be seen on ultrasound during pregnancy
- distended bladder
failure to thrive
frequent urination
frequent UTI
incontinence
nighttime bedwetting
pain when urinating
issues with starting urine flow
weak urinary stream

215
Q

what is Pica

A

it is when people eat non edible items - rather common in children

216
Q

at what age is pica not diagnosed

A

below two as children this age explore objects by mouthing

217
Q

what are reasons why a child might develop pica

A

negative conditions - more common in children living in low socioeconomic situations
nutritional deficiencies - iron, calcium and zinc deficiencies
more common in those with learning disabilities or children with autism
sensory issues
emotional regulation

218
Q

what needs to be established when taking a history from a child with pica

A

what was ingested - is there a risk of poisoning

219
Q

what are the complications of pica

A

poisoning/clinical manifestations - neurological and gastrointestinal side effects
infection/infestation
gastrointestinal - constipation, ulceration, perforation, obstruction
dental - tooth abrasion and tooth surface loss

220
Q

how is pica diagnosed

A

using the DSM-V diagnostic criteria

221
Q

what investigations should be done for a child with pica

A

bloods - FBC, U+E, iron studies, LFT, calcium, phosphate, magnesium, trace elements

222
Q

what is the management for children with pica

A

MDT approach - physicians, social work, dieticians, psychologists, dentists
positive reinforcement
physical interventions
discrimination training between edible and inedible substances
visual screening, with covering eyes for short period of time if pica is attempted

223
Q

what is androgen insensitivity syndrome

A

condition that affects sexual development before birth and during puberty where someone is genetically male however tissues arent able to respond to testosterone and as a result they have external sexual characteristics of a female

224
Q

what are the three forms of androgen insensitivity syndrome

A

complete
partial
mild

225
Q

what is complete androgen insensitivity syndrome

A

this is when the body doesnt respond to androgens at all.
people with this form have external sex characteristics that are typical of a female but do not have a uterus they have male internal sex organs

226
Q

what is partial androgen insensitivity syndrome

A

it is when the bodies tissue is partially sensitive to androgens.
people with this can have genitalia that looks typical for females, genitalia that have both male and female characteristics or typical male genitalia

227
Q

are symptoms of mild androgen insensitivity syndrome

A

people with this are born with male typical sex characteristics but they are often infertile and tend to experience breast enlargement at puberty

228
Q

what are the causes of androgen insensitivity syndrome

A

mutations in the AR gene which codes for a protein called androgen receptor

229
Q

how is androgen insensitivity syndrome inherited

A

X linked recessive syndrome

230
Q

what are the symptoms of complete androgen insensitivity syndrome

A

person with CAIS appears female with no uterus, fallopian tubes or ovaries
very little armpit or pubic hair
at puberty female sex characteristics develop however the person does no menstruate or become fertile

231
Q

how is androgen insensitivity syndrome diagnosed

A

in CAIS its rarely discovered in childhood where as PAIS can be due to the person possibly presenting with both male and female characteristics
Bloods - testosterone, LH, FSH
genetic testing
sperm count
testicular biopsy
pelvic ultrasound

232
Q

what is the treatment for androgen insensitivity syndrome

A

CAIS - testicles removed once the child goes through puberty. Oestrogen replacement prescribed after puberty. may do vaginal dilation
PIAS - gender evaluation, surgery once child is older, receive androgens if wanting to present male or oestrogen if wanting to present female

child and parents need to receive care and support from MDT team specialising in gender medicine

233
Q

what are possible complications of androgen insensitivity syndrome

A

infertility
psychological and social issues
testicular cancer

234
Q

what is testicular torsion

A

it is the twisting of the spermatic cord with rotation of the testicle and is a urological emergency !

235
Q

what is testicular torsion often triggered by

A

activity such as playing sports

236
Q

how does testicular torsion present

A

acute rapid onset unilateral testicular pain
may be associated with abdo pain and vomiting

237
Q

what are the examination findings in testicular torsion

A

firm swollen testicle
elevated testicle
absent cremasteric reflex
abnormal lie
rotation - epididymis not in normal position

238
Q

what is a bell clapper deformity

A

it is one of the causes of testicular torsion. it is where the fixation between the testicle and the tunica vaginalis is absent and the testicle hangs in a horizontal position rather than more vertical, and can twist within the tunica vaginalis

239
Q

what is the management of testicular torsion

A

emergency !
nil by mouth in preparation for surgery
analgesia where required
urgent senior urology assessment
surgical exploration of the scrotum
orchiopexy - corrective and fixing
orchidectomy if testicle necrosed

240
Q

what will testicular torsion look like on ultrasound

A

there will be the whirlpool sign - spiral appearance to spermatic cord and blood vessels

241
Q

what is pyelonephritis

A

it is inflammation of the kidney resulting from a bacterial infection

242
Q

what are risk factors for pyelonephritis

A

female sex
structural urological abnormalities
vesico-uteric reflux (usually in children)
diabetes

243
Q

what are causes of pyelonephritis

A

E. coli - mc
klebsiella pneumoniae
enterococcus
pseudomonas aeruginosa
staphylococcus saprophyticus
candida albicans (fungal)

244
Q

how does pyelonephritis present

A

lower UTI symptoms
fever
loin or back pain
nausea and vomiting
patients may also have systemic illness, LOA, haematuria and renal angle tenderness

245
Q

what investigations are done or pyelonephritis

A

urine dipstick - +++ leukocytes and nitrites
MSU for MCS
bloods
ultrasound or CT scan

246
Q

what is the management of pyelonephritis

A

in the community: 7-10 days of cefalexin, co-amox/trimethoprim (if culture results avaiable), ciprofloxacin
in hospital: IV antibiotics and IV fluids (think sepsis 6)

247
Q

what is chronic pyelonephritis

A

recurrent episodes of kidney infection which can lead to scarring and chronic kidney disease.
DMSA scans can be used to look at the damage to kidneys post infection

248
Q

what are causes of kidney disease in children

A

birth defects
hereditary diseases
infection
nephrotic syndrome
systemic diseases
trauma
urine blockage or reflux

249
Q

what birth defects can cause kidney disease

A

renal agenesis - where a baby is born with one or both kidneys missing
kidney dysplasia - parts of one or both of kidneys dont develop normally
renal hypoplasia - when a baby is born with one or both kidneys are smaller and have fewer nephrons

250
Q

what hereditary diseases can cause kidney disease

A

polycystic kidney disease
alport syndrome - affects the outer lining of the cells in the kidneys

251
Q

what infections can cause kidney disease

A

haemolytic uraemic syndrome
post streptococcal/post infectious glomerulonephritis

252
Q

what systemic diseases can cause kidney disease

A

lupus

253
Q

what trauma can cause kidney disease

A

burns
dehydration
bleeding
injury
surgery
- anything that causes low blood flow pressure to the kidney

254
Q

how is kidney disease diagnosed in children

A

urine testing
bloods - look at GFR
imaging - USS, CT
biopsy
genetics

255
Q

what medications may be prescribed for a child with kidney disease

A

Depending on the underlying cause:
ACE inhibitors/ARBs to lower bp
diuretics
corticosteroids
phosphate binders
growth hormone therapy
sodium bicarbonate
antibiotics

256
Q

what dietary changes may be suggested in a child with kidney disease

A

monitor protein, sodium, potassium and liquid
limiting phosphorus
taking vitamin/mineral supplementation

257
Q

how is kidney failure treated in children

A

kidney transplant
hemodialysis
peritoneal dialysis

258
Q

what are causes of pre renal AKI

A

hypovolaemia
nephrotic syndrome
peripheral vasodilation
impaired cardiac output
drugs

259
Q

what are causes of renal AKI

A

acute tubular necrosis (following pre-renal)
interstitial nephritis
glomerulonephritis
haemolytic-uraemic syndrome
cortical necrosis
bilateral pyelonephritis
nephrotoxic drugs
myoglobinuria/haemoglobinuria
tubular lysis syndrome
renal artery/vein thrombosis

260
Q

what are causes of post renal AKI

A

obstruction
post urethral valves
neurogenic bladder
calculi
tumours

261
Q

what investigations should be done in a child with possible AKI

A

urine - urinalysis with microscopy and culture, protein: creatinine ratio, myoglobin
Bloods - U+E, creatinine, albumin, glucose, bicarb, FBC, blood cultures, auto-anitbodies, clotting
cultures - stool and throat swab
Imaging - USS and CXR

262
Q

how is a child with AKI treated

A

observations
fluid management
electrolyte monitoring - K+, PO4
BP management
medications
potentially dialysis if child is very unwell

263
Q

what are indications for dialysis in AKI

A

severe hyperkalaemia
symptomatic uraemia with vomiting/encephalopathy
rapidly rising urea and creatinine
symptomatic fluid overload
uncontrollable hypertension
encephalopathy or seizures
symptomatic electrolyte problems or acidosis
prolonged oliguria
to remove toxins

264
Q

when should CKD be suspected in paediatric patients

A

failure to thrive
polyuria and polydipsia
lethargy, lack of energy, poor school concentration
other abnormalities such as rickets

265
Q

at what CKD stage do children become symptomatic

A

most children are asymptomatic until approaching chronic renal disease stage 4

266
Q

how do you calculate the estimated GFR

A

40 X height (cm) / creatinine (umol/L)

267
Q

what are congenital causes of chronic kidney disease

A

renal dysplasia
obstructive uropathies
vesicoureteric reflux nephropathy

268
Q

what are hereditary causes of chronic kidney disease

A

Polycystic kidney disease
nephronophtisis
hereditary nephritis
cystinosis
oxalosis

269
Q

what glomerulopathies can cause chronic kidney disease

A

focal segmental glomerulonephritis

270
Q

what multisystem disorders can cause chronic kidney disease

A

systemic lupus erythematosus
Henoch-schonlein purpura
haemoytic uraemic syndrome

271
Q

what investigations should be done in a child with suspected CKD

A

urinalysis
bloods - FBC, iron studies, electrolytes, pH, PTH, U+E
renal tract USS
left hand and wrist X ray for bone age
ECG/ECHO

272
Q

how is CKD treated in children

A

referral to paediatric nephrologist, treatment will depend on underlying cause
- dietician input - vitamin supplements and -
- minimum protein
- fluid and electrolyte balance
- oral iron supplements + subcut epo
- control hypertension, reduce proteinuria, statins
- dialysis
- renal transplant

273
Q

what is renal dysplasia

A

small kidneys

274
Q

what is renal agenesis

A

it is where baby is born with only one/no kidneys

275
Q

what are the different types of renal agenesis

A

unilateral
bilateral

276
Q

what are symptoms of renal agenesis

A

a child with no working kidneys and underdeveloped lungs (potter syndrome) will have life threatening issues soon after birth
high blood pressure
proteinuria
vesicoureteral reflux
clubfoot
congenital heart conditions - ASD/VSD
congenital urological abnormalities
imperforate anus or anal atresia

277
Q

how is renal agenesis diagnosed

A

often picked up on antenatal scans due to low levels of amniotic fluid
ultrasound
after birth - abdominal uss, CT, MRI

278
Q

how is renal agenesis treated

A

4/10 fetuses with bilateral renal agenesis die in utero or are premature with most dying from respiratory distress after birth
inject saline into uterus to restore amniotic fluid
after birth dialysis until a kidney transplant is available
unilateral agenesis may require blood pressure medication, frequent examinations, kidney function tests and urine protein tests

279
Q

what is Henoch-schonlein purpura

A

it is an IgA vasculitis which presents with glomerulonephritis, abdominal pain, arthralgia and purpura

280
Q

what are risk factors for Henoch-schonlein purpura

A

most notable is a preceding upper respiratory tract infection
age: 4-6 years
male sex

281
Q

what are symptoms of Henoch-schonlein purpura

A

purpuric and petechial rash commonly on lower back and buttock
abdominal pain associated with nausea and vomiting and less commonly bloody diarrhoea
joint pain in knees and ankles
frothy urine
haematuria
low grade fever
preceding upper respiratory tract infection

282
Q

what will be seen on clinical examination in a child with Henoch-schonlein purpura

A

rash on lower limbs and buttocks
arthralgia most commonly in the hips, knees and ankles with tenderness and swelling
GI symptoms (50%)
haematuira, proteinuria, nephrotic/nephritic syndrome and renal failure

283
Q

what are differential diagnosis for Henoch-schonlein purpura

A

meningococcal septicaemia
idiopathic thrombocytopenic purpura
haemolytic uraemic syndrome
mechanical causes

284
Q

what investigations need to be done in a child with suspected Henoch-schonlein purpura

A

blood pressure
urinalysis
bloods - U+E, FBC, clotting, LFT, anti-streptolysin O antibodies (group A strep)
imaging - abdominal USS
other - renal biopsy

285
Q

what is the diagnostic criteria for Henoch-schonlein purpura

A

palpable purpura and one of the following:
- diffuse abdominal pain
- arthralgia
- renal involvement
- typical histopathology (glomerulonephritis or vasculitis)

286
Q

how is Henoch-schonlein purpura managed

A

most children will have complete spontaneous recovery within weeks to months but may require supportive care
- paracetamol
- prednisolone
- NSAIDS

287
Q

what is the follow up for Henoch-schonlein purpura

A

followed closely to ensure renal involvement doesnt occur
urine dip and BP regularly or 6 months after diagnosis
children with concerning features must be re-reviewed in secondary care
children can be discharged if they have two consecutive normal urine dips and normal BP at 6 months

288
Q

what are complications of Henoch-schonlein purpura

A

relapse - 30-40%
renal failure - 1%

289
Q

what is multicystic dysplastic kidney

A

condition where one or both of a babies kidneys dont develop normally in utero where cysts replace normal kidney tissue

290
Q

what are the different types of multicystic dysplastic kidney

A

unilateral
bilateral

291
Q

what are symptoms of multicystic dysplastic kidney

A

babies with multicystic dysplastic kidney in only one kidney will have no signs, some babies the affected kidney may be large and cause pain
in babies with bilateral multicystic dysplastic kidney they often do not survive after birth

292
Q

how is multicystic dysplastic kidney diagnosed

A

antenatal scans will often pick up multicystic dysplastic kidney
may be found incidentally on scans for other conditions after birth

293
Q

how is multicystic dysplastic kidney managed

A

if no symptoms - regular checks to test for BP, bloods (kidney function tests), urine tests and regular ultrasounds
if the affected kidney doesnt shrink over time, the child may have surgery to remove it
if both kidneys are affected or the healthy kidney is damaged then a kidney transplant, haemodialysis or peritoneal dialysis will be required

294
Q

what is fanconi syndrome

A

condition which affects the proximal tubules of the kidney and their ability to absorb electrolytes and other substances

295
Q

what molecules are unable to be reabsorbed correctly in fanconi syndrome

A

phosphorus
glucose
potassium
bicarbonate
uric acid
amino acids

296
Q

what are symptoms of inherited fanconi syndrome

A

polyuria
dehydration
polydipsia
pain in your bones
muscle weakness
bone weakness
bone fractures
small stature

297
Q

what are symptoms of acquired fanconi syndrome

A

muscle weakness
hypophosphatemia
hypokalemia
hyperaminoaciduria
metabolic acidosis
polyuria
dehydration
polydipsia

298
Q

what are the two kinds of fanconi anaemia

A

inherited
acquired

299
Q

what causes inherited Fanconi syndrome

A

cystinosis - amino acid cystine builds up in body and causes many issues
Lowe syndrome
Wilsons disease
inherited fructose intolerance
Dent disease
glycogenosis
Hereditary tyrosinemia type 1

300
Q

what causes acquired fanconi syndrome

A

certain drugs - antibiotics, antiretrovirals, chemotherapy, anticancer medication
kidney transplant
multiple myeloma
AL amyloidosis
Light chain proximal tubulopathy
lead poisoning
toluene exposure
certain herbal therapies

301
Q

which medications cause fanconi syndrome

A

cisplatin
ifosfamide
tenofovir
valproic acid
aminoglycoside antibiotics - gentamicin
deferasirox

302
Q

how is fanconi syndrome diagnosed

A

history and exam
urinalysis
bloods

303
Q

how is fanconi syndrome treated

A

inherited often has no cure, acquired you may recover
- IV fluids
- sodium bicarb to restore pH
- phosphate supplement plus vitamin D
- in certain conditions need to avoid fructose, glucose or tyrosine
- remove any medications that may be causing it

304
Q

what are complications of childhood obesity

A

type 2 diabetes
high cholesterol and BP
joint pain
breathing issues
NAFLD
social and emotional complications

305
Q
A

Phase 3a Jemima (16 decks)

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