Diabetes Flashcards

1
Q

What percentage of diabetic children are type 1 diabetics?

A

98%

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2
Q

What can contribute to the development of type 1 diabetes?

A
  • FH
  • Enteroviral infections
  • Cow’s milk protein allergy
  • Overnutrition
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3
Q

What is the pathophysiology of type 1 diabetes?

A

This occurs due to a Type IV hypersensitivity autoimmune reaction which destroys ß-cells, which leads to inability to produce insulin.

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4
Q

How does type I diabetes present?

A
  • Early
    • Triad - polyuria, polydipsia, weight loss
    • Enuresis (secondary nocturnal)
    • Candida infection
  • Late
    • Diabetic ketoacidosis
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5
Q

Why does weight loss occur in diabetes type I?

A

As glucose cannot enter the cell, cells become starved for energy. This leads to lipolysis and protein breakdown to get energy for cellular metabolism, leading to weight loss. Polyphagia occurs as a result of this.

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6
Q

Why does polyuria occur in diabetes?

A

The amount of glucose in the blood exceeds the capacity of glucose transporters in the proximal tubule, meaning that glucose is then excreted in the urine. As glucose acts as an osmotic molecule, water is pulled into the urine, thus increaseing the volume of urine produced.

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7
Q

Why does polydipsia occur in diabetes?

A

This is due a by product of polyuria, as vast amounts of water are being lost in the urine

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8
Q

What are the signs and symtpoms of diabetic ketoacidosis?

A
  • Acetone breath
  • Flushed cheeks - ketones
  • Vomiting
  • Dehydration
  • Abdominal pain
  • Kusmmaul breathing
  • Hypovolaemic shock
  • Drowsiness/altered mental state
  • Coma
  • Death
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9
Q

What is pathogenesis of diabetic ketoacidosis?

A

Occurs in a state of uncontrolled catabolism. Rapid lipolysis occurs, leading to elevated circulating FFA’s. These are broken down into fatty acyl-CoA, which in turn is broken down into ketone bodies within the mitochondria. As the ketone bodies are acidic (due to carboxylic acid group).

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10
Q

What are the steps of ketone formation?

A

FFA -> Fatty acyl carnitine -> Acetyl CoA - Acetoacetate.

Acetoacetate is converted either to acetone or ß-hydroxybutyrate

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11
Q

Which ketone body does blood ketone levels look at?

A

ß-hydroxybutyrate

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12
Q

Why does kussmaul’s breathing occur in diabetic ketoacidosis?

A

As the blood becomes majorly acidic due to the accumulation of ketone bodies, the respiratory system responds by hyperventilating in an attempt to blow of CO2 and return the pH to normal

https://www.youtube.com/watch?v=TG0vpKae3Js

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13
Q

Why does abdominal pain and vomiting occur in diabetic ketoacidosis?

A

This is caused by intestinal ileus caused by acidic ketones.

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14
Q

What else contributes to the acidosis seen in diabetic ketoacidosis?

A

Lactic acidosis caused by dehydration and poor tissue perfusion

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15
Q

Why does hyperkalaemia occur in diabetic acidosis?

A

Protons in acidic blood are exchanged for intracellular K+, which increases extracellular K+ levels. As there is a lack of insulin, movement of potassium back into the cell via ATPase is significantly reduced, therefore K+ concentration increases in the blood, which is exacerbated by dehydration and renal failure. K+ is excreted in the urine, and over time this leads to intracellular depletion of K+

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16
Q

What causes dehydration in DKA?

A

Fluid loss from hyperglycaemia

Vomiting caused by DKA

17
Q

What problem does dehydration cause in the context of developing DKA?

A

Dehydration imparis renal function, thus leading to impaired excretion of protons and ketones, thus exacerbating the acidosis

18
Q

What investigations would you do if you suspected DKA?

A
  • Blood Glucose
  • Blood ketones
  • Blood gas
  • U+E’s
  • ECG
  • Blood/Urine cultures
19
Q

What biochemical results would indicate DKA?

A
  • Hyperglycaemia - > 11 mmol/L
  • Ketonaemia/Ketonuria - > 3 mmol/L
  • Metabolic acidosis
    • pH - <7.3
    • HCO3 <15 mmol/L
  • Hyper/hypokalaemia - depending on presentation stage - later, more hypo
  • Anion gap > 10
20
Q

How would you manage a child with DKA?

A

In this order:

  1. ABC - Airway, Oxygen 100%, Fluids
    • Fluids - bolus if shocked, then maintenance over 48 hours
  2. Insulin infusion - after fluids have been running for 1 hour
  3. Potassium replacement
  4. ACidosis monitoring - bicarb if child shocked
  5. Re-establish oral fluids, subcut insulin and diet
  6. Identify the underlying cause of DKA - e.g. infection
21
Q

When should fluid bolus be given in DKA, and how much fluid should be given as a bolus in DKA?

A

Only if clinically shocked

One bolus of 0.9% saline at 10ml/kg.

If shock not after this corrected, then call consultant

22
Q

What is important to remember when giving fluids to children who are dehydrated from DKA?

A

Don’t rehydrate too quickly as it will lead to cerebral oedema

23
Q

How would you calculate maintenance fluid for children with DKA?

A

Hourly rate = (Deficit/48hrs) + maintenance per hour

*Was (48hr maintenance + deficiet - bolus given), but in 2015 BSPED guidlines, above is given

  • Things to remember
    • Deficit percentage based on pH
      • Assume 5% if mild - moderate DKA (pH >/=7.1)
      • Assume 10% if severe DKA (pH<7.1)
    • Maintenance per hour
      • <10kg - 2ml/kg/hr
      • 10-40kg - 1ml/kg/hr
      • >40kg - fixed fluid of 40 ml/hr
    • If >20ml/kg bolus given, subtract volume from deficit + maintenance
24
Q

What concentration of insulin would you give to a child with DKA?

A

0.1 U/kg/hr IV

  • Consider 0.05 U/kg/hr in:
    • Young children,
    • Blood glucose <14 mmol/l
    • Blood glucose falling >5 mmol/l/h
25
Q

What monitoring would you perform whilst managing a child in DKA?

A
  • Blood glucose
  • Ketones
  • Electrolytes
  • Gases
  • Basic obs
  • Fluid input/output
  • Neuro obs
  • ECG
  • Weight
26
Q

How does cerebral oedema present in a child with/being treated for DKA?

A

Almost exclusively confined to paediatric DKA

  • Headache +/- vomiting
  • Irritability
  • Reduced conscious level
  • Increased ICP
  • Decreased pulse
  • Increased BP
  • Focal neurology - nerve palsies
27
Q

How would you manage a child with cerebral oedema?

A
  • Exclude hypoglycaemia
  • Call for help - Consider PICU
  • Mannitol 1g/kg - IMMEDIATELY
  • Fluid restriction - cut fluid intake by 1/2
  • Elevate head end of bed
  • CT scan
28
Q

How would you assess a child suspected of having diabetes?

A
  • Random cap glucose test
    • >11mmol/l - Diabetes - lost 80% of beta cells
    • <11mmol/L - other cause
  • Fasting cap glucose test - >7 mmol/L - diabetes - lost 80% of beta cells
  • Glucose, ketones (urine and blood) and ABG - DKA assessment
29
Q

How would you generally manage a child with type I diabetes?

A
  • Insulin therapy
  • Education - injections, diet, monitoring, sick day rules
30
Q

What are the different types of insulin used in the management of type I diabetes?

A
  • Short acting - duration up to 8 hrs, max effect 1-4 hrs
  • Intermediate acting - peak 6-8hrs, works for 10-12 hrs
  • Long acting - cover 24 hrs
  • Mixed - intermediate (70%) + short acting (30%)
31
Q

What can be acute complications of type I diabetes?

A
  • Hypoglycaemia
  • DKA
32
Q

What is a basal bolus regimen?

A
  • Lantus/levemir as the baseline - provides 24 hour cover
  • Novorapid - give before each meal
    • Dose depends on CHO load and blood glucose
33
Q

What is a twice a day regimen?

A

Humulin M3/Novomix 30 - before breakfast and before tea, taken at same time each day

Need to take mid morning, mid afternoon and bedtime snack

34
Q

What is the threee times a day regimen?

A
  • Humulin M3/Novomix 30
  • Novorapid
  • Levemir/Insulatard
35
Q

Where are the most commonly used injection sites for insulin injection?

A
  • Usually buttocks or thigh
  • Abdomen > buttocks > thighs
  • Muscle has faster absorption than subcut
36
Q

If a child being treated for DKA developed a headache, what would you suspect?

A

Cerebral oedema - report immediately

37
Q

What is the following?

A

Acanthosis nigricans - brown to black, poorly defined, velvety hyperpigmentation of the skin. It can indicate that a child amy have type II diabetes