12 - Endocrinology Flashcards

1
Q

What are the three most common chronic conditions in childhood?

A
  • Asthma
  • Cerebral palsy
  • Type 1 diabetes
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2
Q

What is the pathophysiology and aetiology of Type 1 diabetes?

A

Autoimmune condition where beta cells in the Islets of Langerhan’s are attacked by T-cells so they cannot produce insulin

Genetic component (HLA-DR)

Can be triggered by viruses like Coxisackie and Enterovirus

Peak onset 5-7 years

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3
Q

What is the typical presentation of T1DM in children?

A
  • 50% present in DKA!!!!!
  • Several weeks of polyuria, polydipsia and weight loss
  • Secondary eneurisis
  • Recurrent infections
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4
Q

If a child presents with symptoms of T1DM e.g polyuria, polydipsia, what investigations should you do for a diagnosis?

A

Symptoms plus a random blood glucose >11 is diagnostic

If no symptoms this is when two tests are needed on separate occasions

Always check ketones

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5
Q

If you suspect a child has T1DM in a GP, they should be immediately referred on the same day to a paediatric MDT team. What investigations will this team do?

A
  • Random blood glucose: >11
  • Ketones
  • HbA1c: >6.5
  • Autoantibodies: Insulin antibodies, anti-GAD antibodies and islet cell antibodies
  • Fasting glucose: >7
  • C-Peptide
  • FBC and U+Es
  • Autoantibodies for other autoimmune conditions e.g TFTs and TPO antibodies for hypothyroidism and anti-TTG for coaeliac
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6
Q

What are the autoantibodies in T1DM?

A
  • Islet Cell antibody
  • Anti-GAD antibody
  • IA2 antibody
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7
Q

What are the principles of treatment for children with T1DM?

A

Provided by paediatric MDT with 24 hour access to advice

NEEED WRITTEN CARE PLAN!

  • Insulin regime
  • Diet explained
  • Recognising signs of hypo/hyperglycaemia and DKA and how to manage
  • Sick day rules
  • Blood glucose monitoring on waking, at each meal and before bed
  • Diabetes UK
  • Managing complications e.g foot care
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8
Q

What regime of insulin is usually given in paediatrics?

A

Basal Bolus

  • Long acting insulin once a day
  • Short acting insulin 30 minutes before meals based on amount of carbohydrates in meal

OR Insulin Pump

  • Child needs to be over 12 and struggling with HbA1c control
  • Cannula changed every 2-3 days and rotate sites
  • Allows better control and less injections
  • Tethered or Patch
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9
Q

Why do children need to rotate injection sites with insulin injections?

A
  • Prevent lipodystrophy
  • Ensure good absorption
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10
Q

What is the honeymoon period with T1DM?

A
  • Immediately after diagnosis, insulin requirements may be very low if the pancreas is still able to produce a significant amount of insulin
  • Need to monitor child closely during this because insulin requirements can suddenly increase as the remaining beta cells are destroyed
  • Also, as blood glucose may be normal in this period on very low insulin doses, parents may incorrectly think that the condition has gone away
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11
Q

Hypoglycaemia is a short term complication of T1DM. How can we teach parents to recognise this and how can they manage it if it is mild?

Memorise image

A

Blood glucose below 4

Signs:

Irritable, confused, hunger, sweaty, shaky dizziness, seizures

Management:

  • Mild: 0.3g/kg rapid acting glucose such as glycogen or lucozade
  • Monitor every 15 minutes
  • If not improved repeat first step and monitor in another 10 minutes
  • If improved then give long-acting carbohydrate to maintain e.g toast or biscuits
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12
Q

What are some examples of 10-20g glucose (0.3g/kg) to give to a child orally when they have hypoglycaemia?

A
  • 3–6 glucose tablets
  • 90–180 mL of fizzy drink or squash (not sugar-free)
  • 50–100 mL of Lucozade Energy
  • 2–4 spoonfuls of sugar added to a cup of drink (for example water)
  • Four large jelly babies
  • 1–2 tubes of Dextrogel 10g
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13
Q

If hypogylcaemia is severe (e.g LOC, seizures, coma) then it is not safe to give oral glucose. What can be given instead and at what dose?

A

IV 10% Dextrose: 2mg/kg bolus then 5mg/kg infusion

OR

IM Glucagon: 0.5mg if <25kg, 1mg if >25kg

If response give long acting carbohydrate, if no response after 10 minutes ring 999

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14
Q

How can blood glucose levels be monitored short term?

A

Need to monitor at least 5 times a day in children, 4 times a day in adults

Glucose Meter: Capillary blood glucose taken on waking, two hours after meals, if feeling a hypo and before driving

Continuous Glucose Monitoring Sensor: Monitors the glucose levels in the interstitial fluid of the subcutaneous tissue, 5 minute time lag so if feeling hypo need to do capillary blood glucose. Need a new sensor every 2 weeks and need a reader

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15
Q

What are the long term complications of T1DM for children?

A
  • Growth and pubertal development (delay in puberty and obesity)

Macrovascular Complications

  • Coronary artery disease
  • Peripheral ischaemia causes poor healing, ulcers and “diabetic foot
  • Stroke
  • Hypertension

Microvascular Complications

  • Peripheral neuropathy
  • Retinopathy
  • Kidney disease, particularly glomerulosclerosis

Infection Related Complications

  • Urinary tract infections
  • Pneumonia
  • Skin and soft tissue infections, particularly in the feet
  • Fungal infections, particularly oral and vaginal candidiasis
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16
Q

What accessories are needed for a person on insulin therapy?

A
  • Needles
  • Lancets
  • Glucose meter
  • Ketone meter
  • Test strips
  • Glucagon
  • Sharps bin
  • Insulin passport
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17
Q

Should you rub the site of an insulin injection?

A

NO! Increases rate of absorption

Can apply a bit of pressure to stop leakage

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18
Q

How often should a child with T1DM be followed up?

A

4 clinics a year

  • Screen for retinopathy
  • Check their feet
  • Check blood glucose, HbA1c, microalbuminuria
  • REFER TO DAFNE
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19
Q

What is the biggest cause of death due to DKA in children that is rare for adults?

A

Cerebral Oedema

Hypokalaemia and Aspiration pneumonia are other common causes

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20
Q

What is the pathophysiology of Diabetic Ketoacidosis?

A

Ketoacidosis, dehydration and potassium imbalance

Ketoacidosis

Ketogenesis initiated when no insulin for fuel. Initially kidneys produce bicarbonate to buffer ketone acids in the blood but over time the ketone acids use up the bicarbonate and the blood starts to become acidic. This is called ketoacidosis

Dehydration

Glucose starts being filtered into the urine which draws water out with it in a process called osmotic diuresis. This causes the patient to urinate a lot and have excessive thirst

Potassium Imbalance

Insulin normally drives potassium into cells. Serum potassium can be high or normal in diabetic ketoacidosis, as the kidneys continue to balance blood potassium with the potassium excreted in the urine, however total body potassium is low because no potassium is stored in the cells. When treatment with insulin starts, patients can develop severe hypokalaemia very quickly, and this can lead to fatal arrhythmias

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21
Q

How may DKA present in a child?

A
  • Polyuria
  • Polydipsia
  • Abdominal pain
  • Kussmaul deep breathing
  • Nausea and vomiting
  • Weight loss
  • Acetone smell to their breath
  • Dehydration
  • Drowsy
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22
Q

What is the diagnostic criteria for DKA?

A
  • Hyperglycaemia (i.e. blood glucose > 11 mmol/l)
  • Ketosis (i.e. blood ketones > 3 mmol/l and 3+ in urine)
  • Acidosis (i.e. pH < 7.3) and Bicarbonate <15
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23
Q

What investigations should you do if you suspect DKA?

A

Need to find the source of infection or trauma

  • U+Es - looking for electrolyte abnormalities
  • FBC - looking for raised infective markers
  • Blood cultures
  • Urine MSU
  • Chest x-ray - looking for focus of infection
  • ECG - complications of potassium disturbance
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24
Q

How is the severity of DKA ranked?

A

8% dehydration is 80ml/kg dehydration

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25
Q

How is DKA in children treated?

A
  1. Correct dehydration evenly over 48 hours: give IV 0.9% saline with 20mmol/L KCl to prevent hypoK. Done slowly to prevent cerebral oedema

2. Give a fixed rate insulin infusion: 0.1units/kg/hr, allows cells to use glucose again and switches off ketosis. Only start insulin after 1 hr of fluids

3. Once BM <14mmol/L: Add 5-10% glucose to IV 0.9% saline with 20mmol/L

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26
Q

When can you transition from fixed rate insulin (short acting) to SC (long-acting) insulin?

A
  • Blood ketone levels <1.0mmol/L
  • Patient is able to tolerate food

Give a dose of subcutaneous insulin, feed the patient. Stop infusion 10–60min after subcutaneous insulin injection

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27
Q

What are some important principles to consider when treating DKA in children?

A
  • Avoid fluid boluses to minimise risk of cerebral oedema, unless required for resuscitation.
  • Treat underlying triggers, e.g antibiotics for se
  • Prevent hypoglycaemia with IV dextrose once blood glucose falls below 14mmol/l
  • Add potassium to IV fluids and monitor serum potassium closely
  • Monitor for signs of cerebral oedema
  • Monitor glucose, ketones and pH to assess their progress and determine when to switch to subcutaneous insulin
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28
Q

What monitoring needs to be done whilst managing DKA in paediatric patients?

A
  • Hourly blood glucose,
  • Hourly fluid input & output
  • Neurological status at least hourly to monitor for cerebral oedema
  • U+Es 2 hourly after start of IV therapy then 4 hourly
  • 1-2 hourly blood ketone levels
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29
Q

Why may cerebral oedema occur in paediatric DKA?

A

Dehydration and high blood sugar concentration cause water to move from the intracellular space to extracellular space. Brain cells to shrink and become dehydrated

Rapid correction of dehydration and hyperglycaemia with fluids and insulin causes a rapid shift in water from the extracellular space to the intracellular space in the brain cells. This causes the brain to swell and become oedematous, which can lead to brain cell destruction and death

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30
Q

What are some signs of cerebral oedema occurring in a child with DKA?

A

Neurological Obs are done hourly!!!

  • Headache
  • Altered behaviour
  • Altered consciousness
  • Bradycardia
  • Brisk reflexes
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31
Q

If cerebral oedema is suspected in DKA what is the management?

A
  • Involve seniors
  • Slow IV fluids by ½
  • IV Mannitol
  • Hypertonic saline
  • Hyperventilate to blow off CO2 and decrease blood flow
  • Move to ICU
32
Q

How do you calculate fluid requirement in DKA?

A

Hourly rate = (48h maintenance + deficit (never use more than 10% deficit) – fluid already given) ÷ 48

33
Q

What are some other complications of DKA apart from cerebral oedema and arrhythmias due to hypokalaemia?

A
  • Pre-renal AKI - Secondary to dehydration.
  • Hypoglycaemia - As a consequence of rapid correction of ketosis.
  • Cerebral oedema
  • Pulmonary oedema
  • Rhabdomyolysis
  • Thrombosis
  • Stroke
34
Q

When should you consider type 2 diabetes in a child?

A
  • Strong family history of type 2 diabetes.
  • Obesity
  • Hypertension
  • Hypercholesterolaemia
  • Black or Asian family origin
  • No insulin requirement, or have an insulin requirement of less than 0.5 units/kg body weight/day after the partial remission phase
  • Evidence of insulin resistance (e.g acanthosis nigricans).
35
Q

What information needs to be given to a child with type 2 diabetes?

A
  • HbA1c monitoring and targets of <6.5%
  • Lifestyle advice
  • Monitoring for complications e.g retinopathy, neuropathy
  • Refer to Diabetes UK
36
Q

What medication can be given to children with T2DM?

A
  • Metformin as soon as have diagnosis
  • +/- Insulin
37
Q

What lifestyle advice can you give to children with type 2 diabetes?

A
  • Diet
  • Exercise
  • Alcohol
  • Smoking
38
Q

How should GP screen for and manage complications in children and young people with type 2 diabetes?

A
  • NHS retinopathy yearly screening programme from age 12
  • Foot check once a year aged 12-17. Explain importance of daily foot care if <12
  • Yearly early morning first-void urine sample, for assessment of microalbuminuria by estimation of the albumin:creatinine ratio (ACR). If 3-30 this is microalbuminuria so need to improve blood glucose control
  • Check for HTN at diagnosis and yearly
  • Check for dyslipidaemia (LDL:HDL) at diagnosis and yearly
39
Q

Why may blood glucose control suddenly get worse in paediatric diabetes?

A
  • Endocrine changes leading to increased insulin resistance
  • Erratic meal and exercise patterns
  • Poor adherence to treatment regimens.
  • Eating disorders
  • Hazardous and risk-taking behaviours
40
Q

What information should you give to diabetic teenagers??

A
  • Sex can lead to hypo so keep sweets handy
  • Not to drink alcohol on an empty stomach as risk of hypo
  • To tell their friends about their diabetes and how to treat a hypo just in case
  • To carry diabetes ID with them, because a hypo could be mistaken for drunkenness
  • To alternate drinks with plenty of water to avoid dehydration
  • After a night out, they should eat before bed
41
Q

How can you tell the difference between type 1 and type 2 diabetes in children?

A
42
Q

What are the four types of diabetes insipidus and what are they caused by?

A
  • Central: not enough ADH is made because of damage to the hypothalamus or pituitary gland e.g meningitis/encephalitis, brain tumour, anti epileptics
  • Nephrogenic: kidneys don’t respond to ADH due to medicines or chronic disorders such as sickle cell, PCKD, lithium
  • Dipsogenic: child has an increased thirst so they wee more
  • Gestational: Occurs during pregnancy and goes away after birth
43
Q

What electrolyte imbalance can cause a picture like DI so it is important to rule these out?

A
  • Hypercalcaemia
  • Hypokalaemia
44
Q

What are the symptoms of diabetes insipidus in children and babies?

A
  • Polydipsia
  • Polyuria
  • Weight loss due to preference for water over food
  • Eneurisis and issues toilet training
  • Nocturia

Babies:

  • Irritability
  • Poor feeding
  • Excessively wet nappies
  • Failure to grow
  • High fevers
45
Q

What tests are done to diagnose children with diabetes insipidus and what will these tests show?

(memorise images)

A

ALWAYS EXCLUDE T1 AND T2DM FIRST

  • Water deprivation test: will continue to produce lots of dilute urine with little glucose when should be small amounts of concentrated urine. If lots of glucose consider T1DM
  • Vasopressin test: After water deprivation test given injection of ADH. If this stops excess urine this is cranial DI, if it does not this is nephrogenic DI
  • U+E’s and Ca: check for hypernatraemia, hypokalaemia and hypercalcaemia
  • MRI: look for structural issues with pituitary gland and tumours
  • Renal US: look for PCKD
  • Gene testing
46
Q

What complications can occur if DI is let untreated in children?

A
  • Poor growth
  • Seizures due to hypernatraemia
  • Brain damage
  • Impaired mental function
  • Hyperactivity
  • Short attention span
  • Electrolyte imbalance
  • Restlessness
47
Q

How is the water deprivation test carried out in children?

A
48
Q

How is diabetes insipidus treated in children?

A
  • Providing free access to water: try to avoid ADH in neonates due to risk of hyponatraemia
  • Dietary management: low sodium/salt diet
  • Monitor U+Es: especially sodium
  • CDI: IM or Nasal Spray Desmopressin
  • NDI: NSAIDs and Thiazides to encourage more ADH production
  • Treatment of the underlying cause: e.g remove brain tumour
49
Q

What are some of the causes of hypothyroidism in children?

A

Thyroid hormone needed for brain development so risk of intellectual disability and neurodevelopment issues without it

Congenital (never had functioning thyroid)

  • Athyreosis: absent thyroid gland
  • Dysgenesis: underdeveloped thyroid gland
  • Dyshormonogenesis: developed thyroid gland not producing hormones
  • Maternal antithyroid drugs or autoantibodies

Acquired (had a functioning thyroid that stopped functioning)

  • Prematurity
  • Hashimoto’s: Autoimmune with anti-TPO and anti-thyroglobulin
  • Autoimmune: Associated with T1DM and coeliac’s
  • Trisomy 21
  • Hypopituitarism
50
Q

What is the most common diagnosis for congenital hypothyroidism?

A

Picked up on newborn heel prick blood spot screening test

51
Q

What are some other signs of congenital hypothyroidism before it is picked up on the newborn blood spot screening test?

A
  • Prolonged neonatal jaundice
  • Poor feeding
  • Constipation
  • Increased sleeping
  • Reduced activity
  • Slow growth and development
  • Protruding tongue
  • Hypotonia
  • Umbilical hernia
52
Q

How may acquired hypothyroidism present in children?

A
  • Fatigue and low energy
  • Poor growth/Short stature
  • Weight gain
  • Poor school performance/Low IQ
  • Constipation
  • Dry skin and hair loss
  • Delayed puberty
53
Q

What investigations need to be done for congenital hypothyroidism?

A
  • TFTs (TSH, T3, T4)
  • Thyroid US
  • Thyroid antibodies
54
Q

How is congenital hypothyroidism managed?

A
  • Levothyroxine: adjust to TFTs
  • Monitor growth chart
  • Monitor mental development and milestones
  • Beware of overtreatment: hyperthyroidism
55
Q

What are the causes of childhood obesity?

A
  • Medical: hypothyroidism, Prader-Willi syndrome, GH deficiency, Cushing’s
  • Drugs: Carbamazepine, Sodium Valproate, Steroids
  • Genetics: prematurity, gestational diabetes, obese parents
  • Deprivation: low socioeconomic class has higher risk
  • Sleep deprivation: low leptin levels and high ghrelin levels
  • Diet: fast processed foods high in carbohydrates
  • Exercise: sedentary games e.g TV, Xbox
56
Q

How is childhood obesity diagnosed?

A

UK WHO chart if <4, 1990 BMI chart if >4

Above 91st centile: overweight

Above 98th centile: obese

Above 99.6th centile: severely obese

57
Q

What questions do you need to be asking if a child is overweight?

A
  • Any physical or emotional problems from being overweight? e.g bullying
  • Any contributing factors e.g family life, medical issues, diet, exercise
  • Stress long term complications of obesity
  • Screen for hypertension, diabetes and dyslipidaemia
58
Q

What are the long term consequences of childhood obesity?

A
  • Type 2 diabetes
  • Sleep apnoea
  • Orthopaedic problems
  • Non-alcoholic fatty liver disease
  • PCOS
  • Vitamin D deficiency
  • Atherosclerosis
  • Early-onset cardiovascular disease
  • Breast and bowel cancer
  • Subfertility
  • Hypertension
59
Q

What is a management plan for obesity in childhood?

A
  • What has been tried before? It is important to involve the whole family
  • Dietary modification (refer to dietician) AND exercise (at least 60 minutes a day)
  • The MEND programme (Mind, Exercise, Nutrition…Do it)
60
Q

What are some causes of hypertension in children?

A
61
Q

What is the difference between thyrotoxicosis and hyperthyroidism?

A

Hyperthyroidism: presence of too much thyroid hormone

Thyrotoxicosis: clinical manifestations of too much thyroid hormone

62
Q

How may hyperthyroidism present in a child?

A
  • Goitre/Neck lump
  • Tremors
  • Anxiety
  • Tachycardia
  • Weight loss
  • Loss of periods
63
Q

What investigations should you do for suspected hyperthyroidism?

A
  • TFTs: low TSH, high T4
  • Thyroid US
  • Thyroid autoantibodies
  • Thyroid isotope schintography
64
Q

How is hyperthyroidism in children managed?

A

First line: Drug treatment.

  • Carbimazole 0.75mg/kg/day
  • Block and replace or titration
  • Continue for 36 months
  • Add Propranolol initially if significant autonomic symptoms/signs.

Second line (treatment failure or relapse after 36 months):

  • Radioiodine therapy
  • Surgery requiring referral to regional centre

Eye disease: refer to ophthalmologist.

65
Q

What is Rickets and some risk factors for this?

A

Clinical manifestation of Vitamin D deficiency

  • Prematurity
  • Breast fed babies
  • Northern hemisphere
  • Lack of sunlight e.g playing indoors on video games
  • Hyperpigmented skin
  • Concealed clothing
  • Malabsorption
  • Obesity
  • Renal and Liver disease
  • Anticonvulsants
66
Q

Why is Vitamin D important during pregnancy?

A
  • Improves neonatal bones
  • Improves immune system of child
  • Improves lung development of child so less asthma
  • No Vit D passed on through breast milk
67
Q

What are some clinical features of rickets?

A
  • Aching and swollen wrist joints
  • Craniotabes
  • Bowed femurs
  • Poor growth and development
  • Delayed dentition
  • Weakness
  • Constipation
68
Q

Why are bones ‘soft’ in Rickets?

A
  • Vitamin D is needed for mineralisation of bone
69
Q

What investigations are done for the diagnosis of Rickets?

A
  • Serum Vitamin D
  • X-Ray of long bone: bowed femurs and widened epiphyseal growth plates
  • Bone profile: may be low calcium, low phosphate, and raised alkaline phosphatase
  • PTH
  • TFTs, U+Es, LFTs, Coeliac screen: to rule out underlying causes e.g CKD
70
Q

What are some differentials for Rickets?

A
  • Bone cancer
  • Bone fracture
  • Hyperparathyroidism
  • Hypothyroidism
  • Juvenile idiopathic arthritis
  • Muscular dystrophies
71
Q

How is Rickets managed?

A
  • Fixed loading dose daily for 8–12 weeks, followed by regular maintenance vitamin D3 therapy of 400-600 IU
  • If no symptoms and just Vit D deficiency then no loading dose needed
  • Assess calcium intake and increase in diet or tablets if necessary
  • Encourage lifestyle changes e.g more sunlight
  • Monitor serum VitD levels and bone profile
72
Q

How can Vitamin D deficiency be prevented?

A
  • Daily supplements up to age 4, especially if breast fed or <500ml formula
  • Diet changes e.g salmon, red meat, egg yolks, fortified food like cereal
  • Sun exposure
  • Increase calcium intake e.g milk, yoghurt, spinach
73
Q

What are causes of polydipsia in children?

A
  • T1DM
  • Diabetes insipidus
  • Psychogenic causes
  • Lithium
74
Q

How do you work out how much fluid to give during DKA?

A

If shocked can give 10ml/kg bolus over 15 minutes

Maintenance (for 2 days) + Deficit (%dehydration based off severity) - Any bolus then divide by 48 to work out ml/hr

75
Q

What supportive care should you do for DKA?

A
  • NG tube if drowsy or slow deep breathing as risk of aspiration pneumonia
  • Transfer all to HDU
76
Q

What electrolyte derangement is most common in DKA?

A

HypoK once insulin started