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RE > Acute complications of diabetes > Flashcards

Acute complications of diabetes Flashcards

1
Q

What occurs in the autonomic system during hypoglycaemia (<4)?

A

Adrenal glands produce adrenaline and pancreas produces glucagon in an attempt to release liver glucose stores.

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2
Q

What are the first signs of hypoglycaemia?

A

Shaking
Blurred vision
Headache
Hunger
Anxiety
Sweating

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3
Q

At what glucose level would someone experience neuroglycopaenic symptoms?

A

<2.8

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4
Q

What do neuroglycopaenic symptoms indicate?

A

That the brain is getting insufficient supply of glucose.

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5
Q

What are the neuroglycopaenic symptoms?

A

Slurred speech
Slower reactions
Seizures
Dizziness
Confusion
Coma

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6
Q

What causes hypoglycaemic unawareness?

A

Neuroglycopenia occurs before autonomic symptoms.
Reduced sympathetic activation due to cellular adaption from recurrent hypoglycaemia. This leads to hypoglycaemic associated autonomic failure.
Body failures to recognise the need to correct glucose levels.

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7
Q

What is the immediate treatment of hypoglycaemia?

A

20g quick/rapid acting carbs

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8
Q

Once blood glucose is above 4mmol/L, what type of carbs should be given?

A

Slow release carbs 10-20g

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9
Q

How long does a glucagon s/c or IM injection take to increase blood glucose levels?

A

10 minutes

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10
Q

In what conditions would glucagon injections be less effective in?

A

Chronically malnourishes
Depleted glycogen stores
Severe liver disease

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11
Q

What % of dextrose is recommended for hypos?

A

20%

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12
Q

How much IV dextrose is given during a hypo?

A

100mls over 10/15mins.

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13
Q

Why should insulin never be omitted in a T1DM?

A

Increases their risk of DKA

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14
Q

What is the diagnosis criteria for DKA?

A

CBG >11mmol/L
Ketones >3 (Capillary) or >2+ (Urine)
Acidosis - HCO3- <15 or pH <7.3

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15
Q

Why is it important to be aware of the effects of early intervention in DKA?

A

Early intervention to correct glucose levels could show a normal blood glucose levels, but would not correct ketones or acidosis therefore patient may still have DKA.

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16
Q

During insulin deficiency, what happens in the liver?

A

The liver switches to making glucose by increasing gluconeogenesis (synthesise glucose) + glycogenolysis (Glycogen to glucose). The reduces glycogenesis (formation of glycogen).

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17
Q

During insulin deficiency, what happens in fatty tissue?

A

Lipolysis increases to generate fatty acids that can be oxidised in the TCA cycle.
Adipogenesis decreases.

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18
Q

During insulin deficiency, what happens in skeletal muscle?

A

Increase in glycogenolysis (using glycogen reserves).
Increased in lipolysis - to generate fatty acids.
Decrease in glycogenesis and protein synthesis - catabolised into amino acids that can be utilised by the liver in further gluconeogenesis.

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19
Q

Which regulatory hormones are increased in insulin deficiency?

A

Cortisol
GH
Catecholamines
Glucagon

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20
Q

How does insulin deficiency cause shock and CV collapse?

A

Insulin deficiency –> Hyperglycaemia –> Glycosuria –> Dehydration (+Electrolyte loss) –> Renal failure –> Shock –> CV collapse.

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21
Q

How does insulin deficiency cause acidosis and CV collapse?

A

Insulin deficiency –> Lipolysis –> Increase in FFA’s –> Ketones –> Acidosis –> CV collapse

22
Q

What are the common signs of DKA?

A

Polyuria
Polydipsia
Nausea
Abdo pain
Ketone breath
Kussmaul breathing
Lethargy
Confusion
Coma

23
Q

Which ketone body in DKA increases 10 fold?

A

3-beta-hydroxybutyrate

24
Q

Which medications can cause DKA?

A

Seroids

25
Q

How does the body compensate in acidosis?

A

Intracellular buffering - H+/K+ exchange
Respiratory - hyperventilation. H+ stimulates respiratory centres + can breathe off CO2,
Renal excretion of H+

26
Q

Which electrolytes can be affected by renal secretion of H+ during acidosis?

A

K+ + Na+ loss = dehydration

27
Q

At which GCS would ITU be involved in DKA?

A

<12

28
Q

Which levels of pH and Bicarb would indicate a severe acidosis?

A

pH <7.1
Bicarb <5

29
Q

During DKA, when would IV K+ be administered?

A

If K+ <5.5 - 40mmol/L
If K+ <3.5 - may need additional K+

30
Q

How is DKA treated?

A

Fixed rate IV insulin - 0.1unit/kg/hr
50 units of Actrapid in 50ml N/Saline

31
Q

Which is the fluid management for someone in DKA?

A
32
Q

For the treatment of DKA, how quickly should ketones and glucose reduce by?

A

Ketones 0.5mmol/L/hr
Glucose 3mmol/L/hr

33
Q

How quickly should bicarb rise by during the treatment of DKA?

A

3mmol/L/hr

34
Q

Which fluid is given in addition to N/Saline + K+ during DKA treatment?

A

IV Dextrose

35
Q

When should Dextrose be given during DKA treatment and at what percentage?

A

10% dextrose when CBG’s <14mmol/L
125ml per hour

36
Q

During DKA, if a patient is not eating and drinking, what type of insulin replacement would be most appropriate?

A

Variable rate insulin regime (sliding scale)

37
Q

If ketonaemia and acidosis is not resolving with the treatment of DKA, which medication should be increased and by how much?

A

Insulin = by 1unit per hour

38
Q

What are the complications of DKA treatment?

A

Cerebral oedema
Hypo/hyperkalaemia
Hypoglycaemia
Pulmonary oedema

39
Q

What is the diagnostic criteria for HHS?

A

Hypovolaemia
Hyperglycaemia >30mmol/L (Without significant hyperketonaemia)
Osmolarity >320mosmol/kg

40
Q

What are clinical features of HHS?

A

Insidious onset
Polyuria
Polydipsia
Muscle weakness
Blurred vision
Hallucinations
Coma
Clinical signs of dehydration

41
Q

Which are the precipitants of HHS?

A

Infection
MI
High dose steroids
Cocaine

42
Q

How is HHS treated?

A

Replace fluid loss
Correct electrolytes and osmolarity
Reduce glucose
Treat precipitant

43
Q

Which fluid is given in HHS?

A

N/Saline

44
Q

How much N/Saline is given during the treatment of HHS?

A

3-6L +ve balance by 12 hours

45
Q

During the treatment of HHS, Na+ should not exceed a reduction of how much in 24 hours and why?

A

> 10mmol - risk of cerebral oedema

46
Q

During the treatment of HHS, glucose should not exceed a reduction of how much in 24 hours?

A

5mmol/L

47
Q

Is IV Insulin given during the treatment of HHS?

A

No - only if glucose doesn’t reduce or if ketones are present.

48
Q

What are some complications of HHS treatment?

A

Fluid overload
Cerebral oedema
Central pontine myelinosis

49
Q

How is osmolarity calculated?

A

2xNa+ + Urea + glucose

50
Q

What is the normal osmolarity range?

A

275-295mmol/kg

51
Q
A
52
Q

Does HHS or DKA have a higher mortality rate?

A

HHS

RE (18 decks)

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