Paediatric Endocrinology Flashcards

1
Q

What is T1DM?

A

A disease where the pancreas stops being able to produce insulin

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2
Q

What viruses can trigger T1DM?

A

Coxsackie B virus and enterovirus

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3
Q

What is the body’s ideal blood glucose concentration?

A

between 4.4 and 6.1 mmol/L

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4
Q

Where is insulin produced?

A

beta cells in the islets of langerhans

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5
Q

Where is glucagon produced?

A

alpha cells in the islets of langerhans in the pancreas

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6
Q

How do 25-50% of young patients present with new type 1 diabetes?

A

with diabetic ketoacidosis

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7
Q

What are the classic triad of symptoms of hyperglycaemia?

A

polyuria
polydipsia
weight loss

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8
Q

what are less typical symptoms of diabetes in young children?

A

secondary enuresis
recurrent infections

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9
Q

What tests should occur in a child with a new diagnosis of diabetes?

A

baseline fbc, renal profile and lab glucose
Blood cultures in patients with suspected infection
HbA1c
Thyroid function tests and thyroid peroxidase antibodies to test for associated autoimmune thyroid disease
Tissue transglutaminase for associated coeliac disease
Insulin antibodies, anti-GAD antibodies and islet cell antibodies to test for antibodies associated with destruction of the pancreas

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10
Q

What is the long-term management for diabetes?

A

Subcutaneous insulin
Monitoring dietary carbs, blood sugars and complications

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11
Q

What can insulin injected into the same spot repeatedly cause?

A

lipodystrophy which prevents normal absorption of insulin

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12
Q

What does basal bolus insulin refer to?

A

long acting insulin and then short acting insulin

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13
Q

What are the advantages and disadvantages of an insulin pump?

A

better blood sugar control, more flexibility with eating and less injections.
learning to use the pump, having it attached at all times, blockages and small risk of infections

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14
Q

What are the two types of insulin pump?

A

Tethered pump
Patch pump

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15
Q

What are the short term complications of diabetes?

A

hypoglycemia
hyperglycemia

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16
Q

What are the typical symptoms of hypoglycemia?

A

hunger, tremor, sweating, irritability, dizziness and pallor

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17
Q

How can hypoglycemia be treated?

A

rapid actin glucose such as lucozade and slower acting carbohydrates such as biscuits

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18
Q

How can severe hypoglycemia be treated?

A

IV dextrose and intramuscular glucagon

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19
Q

What are other causes of hypoglycemia than diabetes?

A

Hypothyroidism, glycogen storage disorders, growth hormone deficiency, liver cirrhosis, alcohol and fatty acid oxidation defects

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20
Q

What is a common complication of hypoglycemia?

A

Nocturnal hypoglycemia

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21
Q

What are the long term macrovascular complications of diabetes?

A

Coronary artery disease
Peripheral ischaemia
Stroke
Hypertension

22
Q

What are the microvascular complications of diabetes?

A

Peripheral neuropathy
Retinopathy
Kidney disease, particularly glomerulosclerosis

23
Q

What are infection related complications related with diabetes?

A

UTI
Pneumonia
Skin adn soft tissue infections, particularly in the feet
Fungal infections

24
Q

What is monitored in children with diabetes?

A

HbA1c every 3 to 6 months
Capillary blood glucose
Flash glucose monitoring

25
Q

When does ketogenesis normally happen?

A

when there is an insufficient supply of glucose and glycogens. The liver takes fatty acids and turns them into ketones which are water soluble and can cross the blood brain barrier

26
Q

What is characteristic of ketosis?

A

Acetone smell on their breath

27
Q

Who does ketoacidosis happen in?

A

Type 1 diabetes

28
Q

how does hyperglycemia cause dehydration?

A

Glucose begins to be filtered into urine causing osmotic diuresis leading to polydipsia

29
Q

How does potassium imbalance occur in diabetic ketoacidosis?

A

Insulin normally drives potassium into cells. Serum potassium may be normal or high in diabetic ketoacidosis because kidneys balance it however total body potassium is low becuase no potassium is stored in cells. When treatment with insulin starts, patients can develop severe hypokalaemia (low serum potassium) very quickly, and this can lead to fatal arrhythmias

30
Q

What is the priority treatment in diabetic ketoacidosis?

A

fluid resuscitation followed by insulin infusion

31
Q

What are children with DKA at high risk of?

A

cerebral oedema

32
Q

How does cerebral oedema occur in DKA in children?

A

dehydration and high blood sugar move into extracellular space in the brain causing brain cells to shrink and become dehydrated. Rapid correction of dehydration and hyperglycemia with fluids and insulin causes a rapid shift in water to the intracellular space in the brain cells causing the brain to swell

33
Q

When should you be concerned about cerebral oedema in a patient being treated for DKA?

A

headaches, altered beahviour, bradycardia or changes in consciousness

34
Q

What is the management for cerebral oedema in DKA?

A

slow IV fluids, IV mannitol and IV hypertonic saline

35
Q

What is the presentation of DKA?

A

Polyuria
Polydipsia
Nausea and vomiting
Weight loss
Acetone smell to their breath
Dehydration and subsequent hypotension
Altered consciousness
Symptoms of an underlying trigger

36
Q

How is DKA diagnosed?

A

Hyperglycemia (blood glucose > 11 mmol/L)
Ketosis (blood ketones > 3 mmol/L)
Acidosis (pH < 7.3)

37
Q

What are the main principles of DKA management in children?

A

Correct dehydration evenly over 48 hours
Give a fixed rate insulin infusion

38
Q

What is adrenal insufficiency?

A

Where adrenal glands do not produce enough steroid hormones particularly cortisol and aldosterone

39
Q

What is addison’s disease?

A

Adrenal glands are damaged so there is reduction in secretion of cortisol and aldosterone, this is usually autoimmune. Also called primary adrenal insufficiency

40
Q

What is secondary adrenal insufficiency caused by?

A

Inadequate ACTH stimulating the adrenal glands so low levels of cortisol. This is a result of loss or damage to the pituitary gland. Can be due to congenital underdevelopment (hypoplasia) of the pituitary gland, surgery, infection, loss of blood flow or radiotherapy

41
Q

What is tertiary adrenal insufficiency the result of?

A

Inadequate CRH release by the hypothalamus usually due to long term oral steroids causing suppression of the hypothalamus. When exogenous steroids are suddenly withdrawn the hypothalamus does not wake up fast enough and endogenous steroids are not adequately produced.

42
Q

What are the features of adrenal insufficiency in babies?

A

Lethargy
Vomiting
Poor feeding
Hypoglycemia
jaundice
failure to thrive

43
Q

What are the features of adrenal insufficiency in older children?

A

Nausea and vomiting
poor weight gain or weight loss
Reduced apetite
Abdominal pain
Muscle weakness or cramps
Developmental delay or poor academic performance
Bronze hyperpigmentatoion to skin in Addisons

44
Q

What is a skin feature of Addisons?

A

Bronze hyperpigmentation to skin in Addison’s caused by high ACTH levels. ACTH stimulates melanocytes

45
Q

What are the investigations for adrenal insufficiency?

A

U & Es (hyponatremia and hyperkalameia) and blood glucose (hypoglycemia).

Cortisol, ACTH, aldosterone and renin levels

46
Q

What are the blood results in addisons? (primary adrenal failiure)

A

Low cortisol
High ACTH
Low aldosterone
High renin

47
Q

What are the blood resulst in secondary adrenal insufficiency?

A

Low cortisol
Low ACTH
Normal aldosterone
Normal renin

48
Q

What test can be used to confirm adrenal insufficiency?

A

Short synacthen test

49
Q

How does the the short synacthen test procedure go?

A

usually performed in the morning. Patient given synacthen (synthetic ACTH) and blood cortisol is measured at baseline, 30 and 60 minutes after. Cortisol level should double in response to to synacthen. A failure to rise indicates primary adrenal insufficiency

50
Q

What is the management for replacing cortisol?

A

Hydrocortisone (glucocorticoid)

51
Q

What is the management for replacing aldosterone?

A

Fludrocortisone (mineralocorticoid)

52
Q
A