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Year 2 - Endocrinology > Metabolic Complications Of Diabetes > Flashcards

Metabolic Complications Of Diabetes Flashcards

1
Q

Name the three main metabolic complications of diabetes.

A 
Diabetic ketoacidosis 
Hyperosmolar hyperglycaemic (non-ketonic) state - HHS
Hypoglycaemia
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2
Q

When does DKA commonly arise?

A

Presenting episode of T1DM
Compliance problems
Intercurrent infection

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3
Q

What are the blood results for DKA?

A 
Metabolic acidosis (pH13.9mmol/l)
Ketosis (++)
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4
Q

What are the three main signs of DKA?

A

Hyperglycaemia
Dehydration
Ketoacidosis

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5
Q

Describe osmotic diuresis (occurs in DKA)

A

Glucose and ketones are freely filtered at the glomerulus
When there is too much glucose in the blood/urine, the tubules reach maximum reabsorbance capacity
Glucose is lost in the urine
Increase in these solutes in the urine creates an osmotic gradient, so that more water is lost in the urine

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6
Q

Describe what happens to potassium levels in DKA.

A

Hyperaldosteronism exacerbates renal potassium loss
The lack of insulin prevents potassium from moving into cells
This means that although plasma potassium levels may be elevated, total body potassium is depleted

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7
Q

Briefly describe how insulin deficiency can lead to ketone production.

A

Insulin deficiency allows inhibited lipolysis.
This leads to increased fatty acid levels
Fatty acids enter the mitochondria of cells and are converted to acetyl-CoA
Acetyl-CoA is converted to acetoacetate which in turn is broken down into acetone and beta-hydroxybutyrate
- beta-hydroxybutyrate and acetoacetate are ketones

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8
Q

Why does the body create ketones?

A

Ketones can be converted back into acetyl-CoA by most tissues in the body - so can generate ATP
Used only when there is a deficiency of glucose

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9
Q

Describe metabolic acidosis in relation to DKA.

A

Increased production of acidic ketone bodies reduces the plasma pH
Initially the body compensates by increasing hydrogen ion removal by the kidneys
There is also a loss of bicarbonate ions
Increased breathing happens to get rid of the excess CO2
The renal compensation becomes impaired, the acidosis worsens and the kidney is hypoperfusing

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10
Q

What happens to blood levels of H+, HCO3 and pCO2 during metabolic acidosis?

A

H+ increase
HCO3 decreases
PCO2 decreases

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11
Q

During DKA there is an increase in the counter regulatory hormones of insulin, what are they, and what metabolic process do they promote?

A

Adrenaline - glycogenesis, gluconeogenesis and lipolysis
Cortisol - Gluconeogenesis, lipolysis and inhibition of peripheral glucose uptake
Growth hormone - gluconeogenesis, lipolysis and inhibition of peripheral glucose uptake

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12
Q

How do you treat DKA?

A 
Hypovolaemia - IV fluid
Insulin deficiency - IV insulin 
Hypokalaemia - IV potassium
Supportive treatment 
- NG tube
- antiemetics
- treat precipitating cause
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13
Q

Why is IV insulin so essential in DKA treatment?

A

It switches of ketogenesis and uncontrolled catabolism
Blood sugar returns quickly to normal
Resolves acidosis

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14
Q

What are the guideline for giving IV insulin?

A

6 units/hour until BM

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15
Q

What must you be aware of when giving IV potassium for DKA?

A

Insulin therapy causes intracellularly shift of potassium
Potassium requires regular and close monitoring
Cardiac monitoring is required

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16
Q

What are the risks most greatly associated with HHS?

A

Central pontine mylinosis

Cerebral oedema - due to large fluid shifts

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17
Q

What is the pathogenesis of HHS?

A

Relative (not absolute) insulin deficiency - hyperglycaemia
Hyperglycaemia leads to hyperosmolarity
- osmotic shift to the intravascular space
- intracellularly dehydration
No signs of ketones - suppressed lipolysis by present insulin

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18
Q

Describe osmotic diuresis in HHS.

A

Chronic renal impairment is common, leading to a rescued capacity to excrete glucose
Has a longer, more insidious onset - more profound Hypovolaemia
Impaired thirst leads to lack of water replacement

19
Q

What is the treatment for HHS?

A

Hypovolaemia - IV fluid
Insulin deficiency - IV insulin
Hypokalaemia - IV potassium
Supportive treatment

20
Q

Why must you be careful replacing fluid in HHS?

A

There is a slow return to normal osmolality
Fall in plasma sodium must occur at no more than 10mmol/24hrs
Use normal (0.9% saline)
50% fluid loss takes 12 hours
- limited because of cardiac and renal impairment

21
Q

When must IV insulin be administered in HHS?

A

Because glucose levels will decrease as fluid levels do, insulin is administered after plasma glucose levels are stable
5mmol/HR maximum rate of reduction
Rate of insulin infusion
- 0.05units/kg/HR

22
Q

What’s the difference between IV potassium replacement in HHS to DKA?

A

In DKA, the potassium shifts are more pronounced
Because of the chronic renal impairment in HHS - less potassium can be excreted
- less aggressive replacement is required

23
Q

What are the supportive treatments for someone with HHS?

A

Hypercoagulable - venous thrombosis is common
HHS commonly secondary to other pathologies - treat those
Foot ulceration is common - treat this

24
Q

What’s the difference in the age of patients with DKA or HHS?

A

DKA - younger patients

HHS- older patients

25
Q

Which type of diabetes are HHS and DKA mostly associated with?

A

DKA -Type 1

HHS - Type2

26
Q

What is there difference in insulin levels between HHS and DKA?

A

DKA - absolute insulin deficiency

HHS - relative insulin deficiency

27
Q

Out of HHS and DKA, which are lipolysis and ketogenesis more likely to occur in?

A

DKA

28
Q

Which out of DKA and HHS will you lose the most water?

A

HHS (8-10l water deficit) compared to 3-6 litres in DKA

29
Q

What are the levels of plasma sodium likely to be in DKA and HHS?

A

DKA - normal

HHS - high

30
Q

What are the symptoms of HHS?

A 
Increased urination
Thirst
Nausea
Dry skin
Disorientation - and in later stages, drowsiness and gradual loss of consciousness
31
Q

What is the onset time for HHS?

A

Slow onset - over a couple of weeks

32
Q

What is the main feature of HHS?

A

The osmotic diuresis

- a prexisiting renal impairment is common - reducing glucose excretion

33
Q

What is the normal response of the body when faced with hypoglycaemia, in terms of hormones?

A 
Decreased insulin 
Increased glucagon
Increased adrenaline/noradrenaline 
Increase in ACh 
Increase in cortisol
Increase in growth hormone
34
Q

Why do acetylcholine and noradrenaline levels increase in normal hypoglycaemia?

A

The brain detects low blood sugar and increases sympathoadrenal flow

  • sympathetic post ganglionic neurons secrete the hormones
  • the hormones make you hungry
35
Q

Why do adrenaline levels increase in normal hypoglycaemia?

A

The increases sympathoadrenal outflow activates the adrenal medulla - which releases adrenaline
Adrenaline activates tremor sweating

36
Q

What are the early symptoms (autonomic) of hypoglycaemia?

A 
Sweating
Tremor
Palpitations 
Hunger 
Anxiety
37
Q

What are the late (neuroglycopaenic) symptoms of hypoglycaemia?

A

Confusion

Impaired consciousness level

38
Q

Why is hypoglycaemia a problem in diabetics?

A

Lack of endogenous insulin means the insulin levels in the blood can’t be reduced when they are too high
- plasma glucose can’t be increased

39
Q

How is hypoglycaemic unawareness caused?

A

Intensive treatment of T1DM leads to the activation of counter-regulatory hormones at a much lower level

40
Q

What is associated with frequent episodes of hypoglycaemia?

A

Autonomic dysfunction

Altered sensing of hypoglycaemia in the CNS

41
Q

What does hypoglycaemia unawareness cause?

A

Frequent episodes of hypoglycaemia
Nocturnal hypoglycaemia
Significant mobility and mortality
Driving restrictions

42
Q

How is hypoglycaemia treated?

A 
Glucose administration 
Mild hypoglycaemia  (BM
43
Q

How do you treat a person who has hypoglycaemia and a reduced consciousness level?

A 
IM glucose (10-15 mins)
IV dextrose (if IV access)

Year 2 - Endocrinology (14 decks)

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