Type 1 diabetes Flashcards

1
Q

Presentation of T1DM

A

DKA picture - features below plus N+V, dehydration, reduced consciousness, symptoms of underlying trigger e.g. sepsis

Hyperglycaemia causing:

  • Polyuria
  • Polydipsia
  • Weight loss

May also present as secondary enuresis (bedwetting in a previously dry child) and recurrent infections

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2
Q

Investigations to do if suspect DKA or T1DM

A

Bloods

  • FBC (any infective trigger)
  • U&Es (dehydrated)
  • CRP
  • Blood ketones
  • Blood glucose and HbA1c, - VBG (for lactate and pH),
  • Blood cultures (if septic picture or infection suspected)
  • LFTs (baseline)

Other bloods to do (-but probably not needed in acute scenario):

  • TFTs - to test for associated autoimmune thyroid disease
  • anti-TTG for associated coeliac disease

Urine dip - to test for ketones, glucose and protein in the urine

ECG if low potassium

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3
Q

Diagnosing DKA (criteria)

A

Hyperglycaemia (glucose>11)
Ketosis (blood ketones >3)
Acidosis (pH <7.3)

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4
Q

Treatment of DKA

A
  • Correct dehydration over next 48h (correcting faster increases the risk of cerebral oedema) - use normal saline plus potassium
  • Fixed rate insulin infusion
  • Monitor potassium closely
  • Treat any underlying trigger e.g. sepsis
  • Monitor for signs of cerebral oedema - monitor GCS
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5
Q

How does DKA relate to hypokalaemia?

A

Insulin normally drives K into cells

Without insulin serum K can be high or normal in DKA but 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, which can lead to fatal arrhythmias

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6
Q

Possible complications of DKA and its treatment

A

Cerebral oedema - 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.

Death - due to dehydration, potassium imbalance and acidosis

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7
Q

Long term management of T1DM

A

Insulin - via a basal bolus regime or an insulin pump

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8
Q

Treatment of hypoglycaemia in T1DM

A

Mild - mixture of rapid acting glucose e.g. glucose tablets or lucozade and slower acting carbohydrate e.g. biscuits

Where there is impaired consciousness:
- IV 10% dextrose (or IM glucagon)

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9
Q

Long term complications

A

Macrovascular:

  • Coronary artery disease
  • Peripheral ischaemia/diabetic foot
  • Stroke

Microvascular:

  • Peripheral neuropathy
  • Retinopathy
  • Kidney disease

Infections increased risk e.g. UTIs, fungal infections (esp. oral and vaginal candidiasis)

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