Revision - DKA, HHS & Hypoglycaemia Flashcards

1
Q

What electrolyte abnormality is typically seen in DKA?

A

Hypokalaemia

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2
Q

Triggers for DKA?

A
  • 1st presentation
  • missed insulin doses
  • MI
  • pancreatitis
  • stress
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3
Q

What bicarb level is seen in DKA?

A

<15

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4
Q

Rate of insulin infusion given in DKA?

A

0.1 units/kg/hour

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5
Q

Mx of DKA?

A

1) IV saline infusion

2) Fixed insulin infusion 0.1 units/jg/hr

3) Add 10% dextrose to infusion once blood glucose <14

4) Correct electrolyte abnormalities

5) Stop short acting insulin, continue long acting

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6
Q

How does insulin affect potassium?

A

Causes potassium to be quickly taken up by cells, resulting in hypokalaemia.

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7
Q

What rate of potassium infusion requires cardiac monitoring?

A

if the rate of potassium infusion is greater than 20 mmol/hour

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8
Q

What blood ketone level defines DKA resolution?

A

<0.6

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9
Q

If the criteria for the resolution of DKA has been met, what else is required for the patient to be switched to SC insulin?

A

The patient is eating and drinking.

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10
Q

Who should the patient be reviewed by prior to discharge following DKA?

A

diabetes specialist nurse

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11
Q

Investigation of suspected cerebral oedema in DKA treatment?

A

CT head and urgent senior review

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12
Q

Clinical manifestations of cererbal oedema?

A

Headache, altered mental status, seizures, and focal neurological deficits

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13
Q

Define hypoglycaemia

A

Hypoglycaemia occurs when glucose concentration falls below the normal fasting glucose level.

Typically below 3.3 mmol/L.

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14
Q

What blood sugar level typically defines hypoglycaemia?

A

<3.3 mmol/L

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15
Q

What are the 2 main causes of hypoglycaemia in diabetes?

A

1) High insulin levels:
- patient has taken too much insulin
- has used the same amount of insulin whilst not eating enough or skipping a meal or snack.

2) Sulfonylureas (e.g. gliclazide): a common adverse effect, especially when starting this medication or increasing dose.

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16
Q

What diabetes drug typically causes hypoglycaemia?

A

Sulfonylureas e.g. gliclazide (as well as insulin)

17
Q

What is the action of sulfonylureas?

A

Increase insulin secretion from beta cells of pancreas

18
Q

How can hypopituitarism lead to hypoglycaemia?

A

There is a reduced secretion of GH from the pituitary (GH normally increases glucose production).

19
Q

How can Addison’s disease lead to hypoglycaemia?

A

There is reduced adrenaline and cortisol from the adrenals (these hormones increase glucose levels).

20
Q

Some normal physiological responses to hypoglycaemia:

A

1) Increased glucagon production by pancreas, reduced insulin production

2) Stimulates secretion of adrenaline from adrenal medulla

3) Stimulates secretion of GH from pituitary

4) Stimulate secretion of ACTH from the pituitary which stimulates cortisol secretion from the adrenal cortex.

21
Q

What is Whipple’s triad?

A

Whipple’s triad aids the diagnosis of hypoglycaemia.

1) symptoms or signs of hypoglycaemia

2) low blood glucose

3) resolution of symptoms with the correction of blood glucose

22
Q

What is an insulinoma?

A

a neuroendocrine tumour of the pancreas which causes unregulated secretion of insulin.

23
Q

What further tests may be useful in diagnosing the cause of hypoglycaemia?

A

1) Serum insulin: elevated in insulinoma

2) Serum C-peptide: elevated in insulinoma or sulfonylurea use

3) Serum cortisol: reduced in adrenal insufficiency or hypopituitarism

4) TSH, U&E, LFTs: abnormalities help identify secondary causes of hypoglycaemia such as hypothyroidism, chronic liver disease or kidney disease.

24
Q

What is pseudohypoglycaemia (idiopathic postprandial syndrome)?

A

A rare condition that presents with symptoms of hypoglycaemia after ingesting a meal, with a normal blood glucose level.

25
Q

Mx of hypoglycaemia in hospital if patient is unconscious?

A

1) IV glucose (e.g. 150-160 ml of 10% glucose).

2) If the patient then regains consciousness, switch to using oral glucose.

3) If IV access is not able to be established rapidly, administer glucagon 1mg via the IM or SC route.

26
Q

Mechanism of glucagon?

A

Glucagon stimulates the conversion of stored glycogen within the liver into glucose.

27
Q

Is hypoglycaemia unawareness more commonin type I or II diabetes?

A

Type II

28
Q

Is HHS more commonin type I or II diabetes?

A

Type II

29
Q

Pathophysiology in HHS:

A

1) Hyperglycaemia results in osmotic diuresis with associated loss of sodium and potassium

2) Severe volume depletion results in a significant raised serum osmolarity (typically > than 320 mosmol/kg), resulting in hyperviscosity of blood.

30
Q

If serum osmolarity is not declining despite treatment with 0.9% saline in HHS, what is the next step?

A

The fluid should be switched to 0.45% sodium chloride solution which is more hypotonic relative to the HHS patients serum osmolarity

31
Q

How is HHS managed?

A

Vigorous treatment with 0.9% saline SHOULD normalise blood glucose, bring down serum osmolarity & replace fluid losses.

32
Q

How will a reduction of serum osmolarity affect sodium?

A

A reduction of serum osmolarity will cause a shift of water into the intracellular space.

This will cause a RISE in serum sodium.

33
Q

Calculation for serum osmolality?

A

(2 x Na+) + (glucose) + (BUN)

34
Q

Cause of impaired hypoglycaemia awareness?

A

Due to neuropathy of parts of the autonomous nervous system

35
Q

Rate of dextrose infusion in DKA?

A

125 mls/hr in addition to the saline regime

36
Q
A