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Year 4 - Paediatrics > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is diabetes insipidus?

A

Lack of ADH or lack of response to ADH preventing the kidneys from being able to concentrate the urine.
Normally ADH lowers the amount of water the kidneys make into urine to prevent dehydration. In diabetes insipidus, too much water is pulled from the blood by the kidneys causing the body to create dilute urine and thirst.

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2
Q

How does ADH work?

A

Released from the posterior pituitary and stimulates water reabsorption by stimulating the insertion of aquaporins into the membranes of kidney tubules (collecting ducts). These channels transport solute-free water through tubular cells back into the blood, decreasing plasma osmolarity and increasing urine osmolarity.

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3
Q

What are the types of diabetes insipidus in children/mothers?

A

1) Nephrogenic DI
2) Central/cranial DI
3) Dispogenic DI
4) Gestational DI

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4
Q

What happens in nephrogenic DI?

A

Collecting ducts of the kidneys do not respond to ADH.

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5
Q

What can cause nephrogenic DI?

A
  • drugs e.g. lithium
  • mutations in AVPR2 gene on X chromosome that codes for ADH-R
  • intrinsic kidney disease
  • renal failure, sickle cell disease, polycystic kidney disease
  • electrolyte disturbance (hypokalaemia, hypercalcaemia)
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6
Q

What happens in cranial/central DI?

A

The hypothalamus does not produce ADH for the posterior pituitary gland to secrete/

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7
Q

What can cause cranial/central DI?

A
  • can be idiopathic
  • brain tumours
  • head injury
  • brain malformations
  • brain infections e.g. meningitis, encephalitis, TB
  • brain surgery or radiotherapy

(most often due to damage of hypothalamus of pituitary gland)

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8
Q

What happens in dipsogenic DI?

A

Problem with child’s sense of thirst causing them to be abnormally thirsty and drink a lot. Consequently the child produces more urine.

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9
Q

What happens in gestational GI?

A

Occurs only during pregnancy and usually goes away once the baby is born.
It may reoccur in subsequent pregnancies.

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10
Q

What is primary polydipsia?

A

When patient has a normally functioning ADH system but drink excessive quantities of water leading to excessive urine production.

DO NOT have diabetes insipidus.

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11
Q

How does diabetes insipidus present in children?

A
  • polyuria
  • polydipsia
  • dehydration
  • weight loss
  • postural hypotension
  • hypernatraemia
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12
Q

How may diabetes insipidus present in babies?

A
  • irritability
  • poor feeding
  • failure to thrive
  • high fevers
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13
Q

What investigations should be done for diabetes insipidus?

A
  • U&Es (high serum osmolality, hypernatraemia)
  • urine dipstick (low urine osmolality)
  • water deprivation test
  • MRI (pituitary gland)
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14
Q

What is the method of a water deprivation test?

A

1) avoid fluids for 8 hours (fluid deprivation)
2) then measure urine osmolality and administer desmopressin (synthetic ADH)
3) measure urine osmolality 8 hours later

Gives 2 results for urine osmolality:

  • after deprivation
  • after ADH
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15
Q

What results from the water deprivation test would be expected in cranial/central DI?

A

Urine Osmolality
After deprivation: low
After ADH: high

Patient lacks ADH but kidneys are capable of responding to ADH.
Initially urine osmolality remains low as it continues to be diluted by excessive water secretion in the kidneys.
Then when synthetic ADH is given, the kidneys respond by reabsorbing water and concentrating the urine to urine osmolality will be high.

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16
Q

What results from the water deprivation test would be expected in nephrogenic DI?

A

Urine osmolality
After deprivation: low
After ADH: low

Patient is unable to respond to ADH and they are diluting their urine with excessive water secretion by the kidneys. Urine osmolality will be low initially and remain low even after synthetic ADH given.

17
Q

What results from a water deprivation test would be expected in primary polydipsia?

A

Urine osmolality
After deprivation: high
After ADH: high

High urine osmolality after 8 hours of water deprivation indicates no DI.

18
Q

What is the management for diabetes insipidus?

A
  • treat underlying cause where possible
  • treat mild cases conservatively

DESMOPRESSIN (synthetic ADH)

  • replace ADH in cranial DI
  • higher doses under close monitoring in nephrogenic DI
19
Q

What are some complications of untreated DI in children?

A
  • brain damage
  • impaired mental function
  • hyperactivity
  • short attention span
  • poor growth
  • restlessness
20
Q

In what way do children most commonly present with a new diagnosis of T1DM?

A

Diabetic ketoacidosis (DKA)

Life threatening, medical emergency

21
Q

What is the cause of DKA?

A

Occurs in T1DM
Where the patient is not producing adequate insulin themselves and it not injecting adequate insulin to compensate for this.

It occurs when the body does not have enough insulin to use and process glucose.

22
Q

What are the 3 main problems in DKA?

A
  • ketoacidosis
  • dehydration
  • potassium imbalance
23
Q

What is normal ketogenesis?

A

Normally occurs when there is insufficient supply of glucose and glycogen stores are exhausted.

Liver takes fatty acids and converts them to ketones (water soluble FA) which can be used as fuel. They can cross the BBB and be used by the brain.
Ketones/ketone acids are buffered in normal patients so blood does not become acidotic.

24
Q

When does ketogenesis occur in normal healthy patients?

A
  • fasting conditions

- on very low carbohydrate, high fat diet

25
Q

How are ketone levels measured?

A
  • urine dipstick

- blood using ketone meter

26
Q

What characteristic do people with ketosis have?

A

Acetone smell to their breath.

27
Q

What happens in ketosis and underlying pathology?

A

Underlying pathology e.g. T1DM causes extreme hyperglycaemia ketosis resulting in life threatening metabolic acidosis.

28
Q

What is ketoacidosis and what does it cause in DKA?

A

When cells in the body have no fuel and think they are starving, they initiate the process of ketogenesis so have useable fuel.

Over time glucose and ketone levels get higher and higher.

Kidneys initially use bicarbonate to buffer the ketone acids in the blood and maintain a normal pH.

Over time, ketone acids use up the bicarbonate and blood becomes acidic = ketoacidosis.

29
Q

How does dehydration occur in DKA?

A

Hyperglycaemia overwhelms the kidneys and glucose starts being filtered into the urine.
Glucose in the urine draws water out with it (osmotic diuresis) causing polyuria and severe dehydration.

Dehydration stimulates the thirst centre to tell the patient to drink lots` of water = polydipsia.

30
Q

What causes the potassium imbalance in DKA?

A

Normally insulin drives potassium into cells. In DKA and without insulin, potassium is not added to and stored in cells.

Serum potassium can be high/normal in DKA as kidneys continue to balance blood potassium with potassium excreted in urine.

Total body potassium is low as no K+ is stored in cells.

31
Q

What is the risk with potassium when starting treatment for DKA?

A

Treatment is with insulin which will drive K+ into cells. Since total K+ is low in DKA, patients can very quickly develop severe hypokalaemia leading to fatal arrhythmias.

32
Q

What are children with DKA specifically at high risk of developing?

A

Cerebral oedema.

33
Q

Why does cerebral oedema occur in DKA?

A

Dehydration and high blood sugar causes water to move from intracellular space into extracellular space.

Brain cells shrink and become dehydrated.

Rapid correction of dehydration and hyperglycaemia (fluids and insulin) cause a rapid shift in water from extracellular to intracellular space in brain cells.

Causes brain to swell, become oedematous, which can lead to brain cell destruction and death.

34
Q

What should be monitored to look for signs of cerebral oedema in DKA?

A

Hourly neurological observations

35
Q

What signs should you look for to suggest cerebral oedema in DKA?

A
  • headaches
  • altered behaviour
  • bradycardia
  • altered consciousness
36
Q

What is the management for cerebral oedema?

A
  • slowing IV fluids
  • IV mannitol (osmotic diuretic)
  • IV hypertonic saline
  • experienced paediatrician
37
Q

How does DKA present?

A

Symptoms of hyperglycaemia, dehydration, acidosis

  • polyuria
  • polydipsia
  • N&V
  • weight loss
  • acetone smell to breath
  • dehydration & hypotension
  • altered consciousness
  • symptoms of underlying trigger e.g. sepsis
38
Q

What criteria must be met to diagnose DKA?

A
  • Hyperglycaemia (blood glucose >11mmol/L)
  • Ketosis (blood ketones >3mmol/L)
  • Acidosis (pH<7.3)
39
Q

What is the management for DKA in children?

A
  • correct dehydration evenly over 48 hours (reduce risk of cerebral oedema)
  • fixed rate insulin infusion (allows cells to start using glucose again, switches off ketone production)
  • treat underlying triggers (e.g. abx for sepsis)
  • prevent hypoglycaemia with IV dextrose (once blood glucose <14mmol/L)
  • add K+ to IV fluids and monitor serum K+
  • monitor glucose, ketones, pH to assess progress and determine when to switch to SC insulin
  • avoid fluid boluses (minimise cerebral oedema unless need for resus)

Year 4 - Paediatrics (13 decks)

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