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Year 2 - T2 Theme 1 > L17 - Acute complications of diabetes > Flashcards

L17 - Acute complications of diabetes Flashcards

1
Q

Insulin levels in diabetic keto-acidosis

A
  • Absolute insulin deficiency
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2
Q

Insulin levels in hyperosmolar hyperglycaemia state

A
  • Relative insulin deficiency
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3
Q

What is hyperosmolar hyperglycaemia state

A

Hyperosmolar hyperglycemic state (HHS) is a complication of diabetes mellitus in which high blood sugar results in high osmolarity without significant ketoacidosis

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4
Q

Symptoms of hyperosmolar hyperglycaemia state

A

Symptoms include signs of dehydration, weakness, legs cramps, vision problems, and an altered level of consciousness.

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5
Q

Insulin levels in hypoglycaemia

A
  • Relative insulin excess
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6
Q

Effects of insulin deficiency

A
  • Glycogenolysis
  • Glucagon, adrenaline(cortisol) release
  • Lipolysis and reduced esterification of fatty acids
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7
Q

How does lipolysis and reduced esterification of fatty acids increase hepatic glucose output and cause hyperglycaemia

A

–> NEFA –> Ketones –> acetone, acetoacetate, hydroxybutyrate

–> glycerol –> gluconeogenesis –> increase in hepatic glucose output and hyperglycaemia

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8
Q

How does proteolysis and reduced uptake of amino acids increase hepatic glucose output and cause hyperglycaemia

A

Proteolysis and reduced uptake of amino acids –> alanine –> gluconeogenesis –> increase in hepatic glucose output and hyperglycaemia

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9
Q

What causes hyperglycaemia in diabetic ketoacidosis

A
  • Unchecked gluconeogenesis
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10
Q

What causes osmotic diuresis in diabetic ketoacidosis

A
  • Dehydration
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11
Q

What causes ketpsis in diabetic ketoacidosis

A
  • Unchecked ketogenesis
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12
Q

What cases anion-gap metabolic acidosis in diabetic ketoacidosis

A
  • Dissociation of ketone bodies into hydrogen ion and anions
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13
Q

How can insulin deficiency lead to CV collapse

A

Insulin deficiency –> hyperglycaemia –> glycosuria –> dehydration –> renal failure –> shock –> CV collapse

Insulin deficiency –> lipolysis –> increase in FFAs –> ketones –> acidosis –> CV collapse

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14
Q

Physiological effects of insulin deficiency in adipose tissue

A

• Increased lipolysis and reduced esterification of fat
• Insulin deficiency
• Glucagon/adrenaline excess
Results in excess FFA and glycerol from breakdown triglycerides
• FFA substrate for hepatic synthesis of ketone bodies
• Acetoacetate/Hydroxybutyrate – strong organic acids
• (Acetone)
• Rate of ketogenesis is linked to rate of gluconeogenesis
• Muscle and brain can utilise ketones as main energy substrate

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15
Q

What causes ketoacidosis

A
  • Ketoacidosis results when ketone body production exceeds rate of utilisation in peripheral tissues (brain and muscle) and renal clearance
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16
Q

How does insulin deficiency give rise to nausea and abdo pain

A

Lipolysis and reduced esterification of fatty acids –> NEFA –> Ketones –> acidosis –> nausea, abdo pain

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17
Q

How does insulin deficiency cause dehydration

A

Increased hepatic glucose output and hyperglycaemia –> osmotic diuresis –> dehydration

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18
Q

How is acidosis in diabetic ketoacidosis managed

A

• Intracellular buffering - H+ / K+ exchange
○ Potassium hydrogen ion pump
• Respiratory compensation – hyperventilation
○ H+ stimulates respiratory centres
○ Breathe off CO2 (H+ + HCO3- H2O + CO2)
• Renal excretion of H+ (slow response)

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19
Q

Electrolyte disturbances in diabetic ketoacidosis

A
  • Potassium depletion - maybe > 250 mmol
  • Sodium depletion
  • Dehydration
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20
Q

Main differences between cation concentrations between ECF and ICF

A
  • Higher Na+ concentration in interstitial fluid

- Higher K+ concentration in ICF(muscle) - this is due to intracellular buffering - H+/K+ exchange

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21
Q

Age most affected by diabetic ketoacidosis

A
  • Mostly young T1DM
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22
Q

Precipitating causes of diabetic ketoacidosis

A
  • Relative or absolute insulin deficiency
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23
Q

Serum sodium levels in DKA

A

Normal or low

24
Q

Blood glucose levels in DKA

A

Usually <40mmol/l

25
Q

Serum bicarbonate/pH - DKA

A

< 14 mmol/l / ph<7.3

26
Q

Diabetic ketoacidosis - specific precipitating factors

A
  • Infections - pneumonia, urinary tract, viral illnesses, gastroenteritis
  • Error/missed insulin administration
  • Myocardial infarction
  • Previously undiagnosed type 1 diabetes
  • Drugs - steroids
27
Q

Symptoms of diabetic ketoacidosis attributed to hyperglycaemia + dehydration

A
  • Thirst and polyuria
  • Weakness and malaise
  • Drowsiness
  • Confusion
28
Q

Symptoms of diabetic ketoacidosis attributed to acidosis

A
  • Nausea and vomiting
  • Abdominal pain
  • Breathlessness
29
Q

Signs of diabetic ketoacidosis attributed to hyperglycaemia + dehydration

A
  • Dry mouth
  • Sunken eyes
  • Postural or supine hypotension
  • Hypothermia and coma
30
Q

Signs of diabetic ketoacidosis attributed to acidosis

A
  • Facial flush
  • Hyperventilation
  • Smell of ketones on breath and ketonuria
31
Q

Diabetic ketoacidosis - management

A
  • Confirm diagnosis and check for precipitating causes
  • Rehydrate and monitor fluid balance (IV fluids - saline with added potassium, consider urinary catheter)
  • Lower glucose (intravenous insulin - fixed rate 0.1 unit/kg/hr
  • Monitor electrolytes - potassium(and sodium)
  • Prevent clots - prophylactic low molecular weight heparin
32
Q

DKA - other management factors

A
  • Is the patient conscious?
    Assess GCS
    If concern, call ITU
  • At risk of aspiration
    Consider NG tube
  • Monitor recovery
    Glucose, ketones, pH, potassium - hourly
33
Q

DKA - recovery

A
  • pH normal, ketones <2+ (urine), vomiting settled
  • Resume normal diet
  • Switch from intravenous to normal subcutaneous insulin
34
Q

Hyperosmolar hyperglycaemic state - normal age

A

Usually > 40 years

35
Q

Precipitating causes of hyperosmolar hyperglycaemic state

A
  • Previously undiagnosed
  • Steroids
  • Diuretics
  • Sugar
36
Q

HHS - Serum sodium levels

A
  • Usually high
37
Q

HHS - blood glucose levels

A
  • Often > 40mmol/l
38
Q

HHS - Serum bicarbonate/pH

A
  • Normal / pH 7.4
39
Q

HHS - Serum ketones

40
Q

HHS - mortality

A

30% (thromboses)

41
Q

HHS subsequent course

A

Diet/tablet controlled

42
Q

DKA - mortality

A

5% depending on age

43
Q

DKA - subsequent course

A

Insulin dependent

44
Q

HHS - management

A

• Correct the profound dehydration

  • Confirm diagnosis and check for precipitating causes
  • Rehydrate & monitor fluid balance
    • Iv fluids - saline with added potassium
    • Consider urinary catheter
  • Lower glucose (once glucose not improving with fluids)
    • Intravenous insulin – fixed rate 0.05Unit/kg/hr
  • Monitor electrolytes
    • Potassium (and sodium)
  • Prevent clots
    • Treatment low molecular weight heparin
45
Q

What is hypoglycaemia

A
  • Hypoglycaemia is a biochemical term and exists when blood sugar <4mmol/l but is often used to describe a clinical state
46
Q

Classification of hypoglycaemia

A
  • Asymptomatic - awake vs sleeping
  • Mild symptomatic (patient can treat himself)
  • Severe symptomatic (help needed by third party)
  • Coma and convulsions
47
Q

Symptoms of hypoglycaemia - autonomic - sympathomedullary activation

A
  • Sweating, feeling hot
  • Trembling or shakiness
  • Anxiety
  • Palpitations
48
Q

Neuroglycopenic symptoms of hypoglycaemia

A
  • Dizziness, light-headedness
  • Tiredness
  • Hunger, nausea
  • Headache
  • Inability to concentrate, confusion, difficulty speaking, poor coordination, behavioural change, automatism
  • Coma and convulsions, hemiplegia
49
Q

Causes of hypoglycaemia

A
  • Insulin
    Inappropriately excessive doses
    Not eating, or insufficient carbs
  • Sulfonylureas
50
Q

Hypoglycaemia - counter-regulation

A
  • Glucagon, adrenaline, cortisol and GH all have ‘anti-insulin effects’
  • Glucagon stimulates glycogenolysis and gluconeogenesis and is probably primary response
  • Adrenaline increases glycogenolysis
  • GH and cortisol limit glucose disposal in peripheral tissues, but this effect takes several hours so of little benefit acutely
  • Sympathetic nerves may also directly activate hepatic glycogenolysis and stimulate glucagon secretion
51
Q

Treatment of minor episodes of hypoglycaemia

A
  • 2-g carbohydrate as sugary drink, fruit juice, glucose tablets, glucose gels followed by something ‘starchy’ to eat
  • Glucose gels
52
Q

Treatment of hypoglycaemic coma

A
  • IM or IV glucagon 1mg

- IV dextrose 25g (150ml 10% glucose)

53
Q

How many times can glucagon be given per day

A
  • Glucagon can only be given once daily

- It will not reverse hypoglycaemia in patients with recurrent hypos, anorexia or severe liver disease

54
Q

Treatment pathway - Mild/moderate hypoglycaemia

A

Patient conscious, orientated and able to swallow –> give 5 level teaspoons glucose powder in water or 120 mls lucozade or 5 glucose tablets

  • Test blood glucose after 15 mins, if <4 mmol/l repeat up to 3 times
  • If this has been repeated 3 times, consider 10% glucose IV 100ml/hr or 1 mg glucagon IM

Give long acting carbs (eg 2 biscuits or a slice of bread or next meal if due)

  • DO NOT omit subsequent doses of insulin
55
Q

Treatment pathway - Severe hypoglycaemia

A
  • Patient unconscious/fitting/very aggressive or nil by mouth (NBM) –> Check ABC, stop any IV insulin. If patient suitable for IM glucagon give 1 mg. If not give 10% IV glucose 150ml. Repeat up to 3 times –> Recheck glucose level after 15 mins it should now be above 4mmol/L Give long acting carbs

Year 2 - T2 Theme 1 (20 decks)

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