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
When does ketogenesis normally happen?
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
What is characteristic of ketosis?
Acetone smell on their breath
27
Who does ketoacidosis happen in?
Type 1 diabetes
28
how does hyperglycemia cause dehydration?
Glucose begins to be filtered into urine causing osmotic diuresis leading to polydipsia
29
How does potassium imbalance occur in diabetic ketoacidosis?
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
What is the priority treatment in diabetic ketoacidosis?
fluid resuscitation followed by insulin infusion
31
What are children with DKA at high risk of?
cerebral oedema
32
How does cerebral oedema occur in DKA in children?
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
When should you be concerned about cerebral oedema in a patient being treated for DKA?
headaches, altered beahviour, bradycardia or changes in consciousness
34
What is the management for cerebral oedema in DKA?
slow IV fluids, IV mannitol and IV hypertonic saline
35
What is the presentation of DKA?
Polyuria Polydipsia Nausea and vomiting Weight loss Acetone smell to their breath Dehydration and subsequent hypotension Altered consciousness Symptoms of an underlying trigger
36
How is DKA diagnosed?
Hyperglycemia (blood glucose > 11 mmol/L) Ketosis (blood ketones > 3 mmol/L) Acidosis (pH < 7.3)
37
What are the main principles of DKA management in children?
Correct dehydration evenly over 48 hours Give a fixed rate insulin infusion
38
What is adrenal insufficiency?
Where adrenal glands do not produce enough steroid hormones particularly cortisol and aldosterone
39
What is addison's disease?
Adrenal glands are damaged so there is reduction in secretion of cortisol and aldosterone, this is usually autoimmune. Also called primary adrenal insufficiency
40
What is secondary adrenal insufficiency caused by?
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
What is tertiary adrenal insufficiency the result of?
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
What are the features of adrenal insufficiency in babies?
Lethargy Vomiting Poor feeding Hypoglycemia jaundice failure to thrive
43
What are the features of adrenal insufficiency in older children?
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
What is a skin feature of Addisons?
Bronze hyperpigmentation to skin in Addison's caused by high ACTH levels. ACTH stimulates melanocytes
45
What are the investigations for adrenal insufficiency?
U & Es (hyponatremia and hyperkalameia) and blood glucose (hypoglycemia). Cortisol, ACTH, aldosterone and renin levels
46
What are the blood results in addisons? (primary adrenal failiure)
Low cortisol High ACTH Low aldosterone High renin
47
What are the blood resulst in secondary adrenal insufficiency?
Low cortisol Low ACTH Normal aldosterone Normal renin
48
What test can be used to confirm adrenal insufficiency?
Short synacthen test
49
How does the the short synacthen test procedure go?
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
What is the management for replacing cortisol?
Hydrocortisone (glucocorticoid)
51
What is the management for replacing aldosterone?
Fludrocortisone (mineralocorticoid)
52