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Phase 2 3. Endocrinology > Metabolic complications of diabetes > Flashcards

Metabolic complications of diabetes Flashcards

1
Q

What is the incidence of diabeteic ketoacidosis in patients with diabetes?

A

4.6-8 per 1000

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2
Q

What are the common reasons in which DKA occurs?

A

> Presenting episode of T1DM
Poor compliance
Intercurrent infection

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3
Q

What is the mortality rate of DKA?

A

< 2%

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4
Q

What are the key elements of DKA?

A
  • metabolic acidoses (pH < 7.3, bicarbonate <15mmol/l)
  • Hyperglycaemia (>13.9mmol/l)
  • Ketosis

NB: can have normoglyacemic ketoacidosis but this is very unusual

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5
Q

What is the definition of DKA?

A

State of cellular starvation in the midst of plenty

- hyperglycaemia but access to substrate for fuel is denied due to a lack of insulin

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6
Q

What are the characteristics of DKA?

A

Uncontrolled catabolism as cells seek an alternative fuel source, causing:
> Hyperglycaemia
> Dehydration
> Ketoacidosis

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7
Q

What is the normal response to hyperglycaemia?

A

Pancreatic beta cells increase insulin secretion and more glucose is taken up into tissues

Reduced glucagon production by alpha cells

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8
Q

What is the response to hyperglycaemia in absolute insulin deficiency?

A

Unopposed action of glucagon

Osmotic diuresis -> dehydration/ volume depletion -> alsodesterone increases (compensation) -> causes increase K+ excretion -> total body K+ depletion

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9
Q

What effect does DKA have on the kidney?

A

> Osmotic diuresis

> Potassium loss

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10
Q

How does osmotic diuresis occur in DKA?

A
  • Glucose and ketones are freely filtered at glomerulus
  • As blood glucose rises, the maximal reabsorption threshold of glucose is exceeded
  • This means that there is an elevation of solute content in tubules
  • Increased solute conc. in tubular lumen generates an osmotic gradient
  • Results in increased water loss in urine
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11
Q

How does potassium loss occur in DKA?

A
  • Intravascular depletion due to osmotic diuresis causes compensatory hyperaldosteronism
  • Hyperaldosteronism exacerbates renal potassium loss
  • Lack of insulin prevents potassium from moving into cells

NB: Plasma potassium levels may be elevated but total body potassium is depleted

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12
Q

What are the consequences of uncontrolled catabolism?

A

Insulin deficiency promotes LIPOLYSIS and PROTEOLYSIS
These further exacerbate hyperglycaemia as increased aa and TAG feed into gluconeogenesis pathway

Production of ketone bodies as an alternative fuel substance -> perturb the acid-base balance

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13
Q

Explain how metabolic acidosis occurs in DKA?

A
  • Increased production of acidic ketone bodies reduces plasma pH
  • This shifts the buffering system (increased renal excretion of H+ occurs initially, compensatory loss of HCO3-)
  • Increased respiratory rate (later kussmal breathing)
  • Kidney’s ability to compensate becomes compromised due to worsening acidosis and osmotic diuresis
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14
Q

What is the metabolic acidosis profile?

A 
H+ = high
HCO3 = low
pH = low
CO2 = low
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15
Q

What are the counter-regulatory hormones produced in DKA?

A

> adrenaline
cortisol
GH

All increased to promote pathways to produce alternative fuel sources
These exacerbate hyperglycaemia

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16
Q

What is the treatment of DKA?

A

Hypovolaemia = intravenous fluid
Insulin deficiency = intravenous insulin
Hypokalaemia = intravenous potassium

Supportive treatment:

  • NG tube
  • Antiemetics
  • Treatment of precipitating causes
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17
Q

Why is insulin used to treat DKA?

A

> Essential for switching off ketogenesis and uncontrolled catabolism (fluid replacement will not solve DKA)
Blood sugar may return to normal quickly
Resolution of acidosis requires ongoing insulin administration, even after glucose levels return to normal range

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18
Q

What is the normal regime of IV insulin treatment?

A

6U/Hr until BM < 14

ADD 10% dextrose and continue insulin (reduced rate)_

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19
Q

Why is potassium used to treat DKA

A

Total body potassium will require supplementation
Insulin therapy causes intracellular shift of potassium -> will result in hypokalaemia if not supplemented

Cardiac monitoring required

20
Q

What is Hyperosmolar hyperglycaemic state (HHS)?

A

Complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis

21
Q

Which patients develop HHS?

A

Occurs in people with T2DM who experience v. high blood glucose levels (often >40mmol/l)

22
Q

What are the symptoms of HHS?

A 
Urination
Thirst
Nausea
Dry skin
Disorientation, drowsiness and gradual loss of consciousness in later stages
23
Q

What are contributing factors to HHS?

A

Can develop over a course of weeks through a combination of illness and dehydration

Stopping DM medication during illness (e.g. vomiting) can contribute, but blood glucose often rises despite medication due to other hormones the body produces during illness

24
Q

What are the risks associated with large fluid shifts?

A

Central pontine mylinolysis - changes in white matter

Cerebral oedema

25
Q

What is the normal response to hyperglycaemia?

A

High glucose levels -> beta cells secrete insulin -> uptake of glucose by fat and muscle

High glucose levels -> beta cells secrete insulin -> inhibition of glucagon release from alpha cells -> inhibition of glycogenolysis and gluconeogenesis

26
Q

How does HHS occur?

A

Not an absolute insulin deficiency, but RELATIVE
> Affects action of insulin, but glucagon action not entirely unopposed
> Some ongoing insulin action - enough to suppress ketone production
- low level of insulin action cannot suppress persistent hyperglycaemia and osmotic diuresis
> Osmotic diuresis - chronic renal impairment is common -> reduced capacity to excrete glucose
- illness longer, insidious onset, more profound hypovolaemia
- cognitive impairment common -> impaired thirst response leads to lack of water replacement

27
Q

What is the treatment of HHS?

A

Cautious administration due to co-morbidities and potential for over-rapid replacement

Hypovolaemia - fluid replacement
Insulin deficiency - IV insulin
Hypokalaemia - IV potassium

Supportive treatment

28
Q

What are the key points of fluid treatment in HHS

A

Normal (0.9%) saline used

29
Q

What are the key points of IV insulin treatment in HHS?

A

Plasma glucose will fall with fluid alone
Only start insulin treatment once plasma glucose is stable

5mmol/hr = maximum rate of reduction
Target blood glucose 10-15mmol/l acceptable

Fixed rate insulin infusion

  • 0.05 units/kg/hr
  • 4 units/hr in 80kg
30
Q

What are the key points of potassium treatment in HHS?

A

Potassium shifts are less pronounced than in DKA
Chronic renal impairment may make the patient less able to excrete potassium
> less aggressive potassium replacement therapy is therefore required

31
Q

What are supportive treatment measures used in HHS?

A

Coagulation monitoring - patients are hypercoagulable - venous thrombosis common due to severe dehydration

Foot ulceration common

32
Q

What are the key features of DKA compared with HHS

A
  • Absolute insulin deficiency
  • Generally lower BMs
  • Lipolysis and ketogenesis
  • 3-6 L water deficit
  • Plasma sodium usually normal
  • Younger patients
  • Short history
  • Usually T1DM
  • Acidosis
33
Q

What are the key features of HHS compared with DKA

A
  • Relative insulin deficiency
  • BMs often very high
  • Often absent lipolysis and ketogenesis
  • 8-10 L water deficit
  • Older patients
  • Insidious history
  • Usually T2DM
  • Hypernatraemia
  • No acidosis

HHS often has more CNS manifestations

34
Q

What is the normal response to hypoglycaemia?

A

Reduction in insulin release
Increased glucagon release

Inhibition of glucose uptake by fat and muscle
Increased glycogenolysis and gluconeogenesis

35
Q

What is the response to hypoglycaemia with exogenous insulin (in diabetes)?

A

No capacity to switch off insulin production
Dependent on counter-regulatory hormones to avoid a precipitous drop in blood glucose levels
- Increased sympathetic adrenal outflow -> increases substance for gluconeogenesis
- Causes symptoms of hypoglycaemia

36
Q

What are the symptoms of hypoglycaemia?

A 
Initial symptoms: Autonomic
> Sweating
> Tremor
> Palpitations
> Hunger
> Anxiety

Later symptoms: Neuroglycopaenic (impaired substrate delivery to the brain)
> Confusion
> Impaired conscious level

37
Q

What are the counter-regulatory mechanisms

A 
Increase of:
> glucagon
> adrenaline
> noradrenaline
> acetylcholine
> cortisol
> growth hormone
38
Q

What is the response to hypoglycaemia in T1DM?

A

No capacity to switch off insulin
Very dependent on CNS response
(NB: there is no increase of counter-regulatory hormones until after there is a significant increase in blood sugar)

Hunger/drive to eat is the only mechanisms by which these patients can correct hypoglycaemia
- don’t have the same reserve capacity to compensate via by regulating insulin secretion

39
Q

How is mild hypoglycaemia treated?

A 
Can be self-corrected
15-20g fast acting carbohydrate
> 150ml non-diet soda
> 3 or more glucose tablets
> 5 sweets
> A small glass of fruit juice
> glucose gel

Retest BM after 15-20 mins

Give a long-acting carbohydrate after administration of the short-acting to prevent further drop in blood sugar

40
Q

How is severe hypoglycaemia treated?

A

Requires help from another person

15-20g fast acting carbohydrate
> 150ml non-diet soda
> 3 or more glucose tablets
> 5 sweets
> A small glass of fruit juice
> glucose gel

Retest BM after 15-20 mins

Give a long-acting carbohydrate after administration of the short-acting to prevent further drop in blood sugar

41
Q

How is hypoglycaemia treated in reduced conscious level?

A 
IM glucose if not in hospital
IV dextrose (if IV access)
42
Q

What are the measures needed to be taken with hypoglycaemia and driving?

A

Wait 45 mins after normalisation of blood sugar before driving
Make it clear that you are no longer in charge of the car by leaving the driving seat, removing the ignition key

If hypoglycaemia unawareness -> DVLA informed

43
Q

What is hypoglycaemia unawareness?

A

Altered sensing of hypoglycaemia in CNS - autonomic dysfunction, mechanism not clear

44
Q

What causes hypoglycaemia unawareness?

A

Autonomic nervous system becomes blunted due to frequent exposure to low blood sugars
Symptoms only present once there is onset of neuroglycopaenia
May be due to frequent unnoticed episodes of nocturnal hypoglycaemia

45
Q

What is the difference in counter-regulatory effects in normal patients vs. T1DM patients?

A

T1DM on intensive therapy will have counter-regulatory mechanisms come into effect at lower glucose levels due to treatment with insulin suppressing mechanism

Phase 2 3. Endocrinology (25 decks)

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