Diabetes (metabolic complications) Flashcards

1
Q

What are the two major hyperglycaemic complications of diabetes?

A

Diabetic Ketoacidosis

  • metabolic emergency in which hyperglycaemia is associated with metabolic acidosis due to greatly raised ketone levels
  • It is associated with type I DM but can rarely occur in type 2 DM

Hyperosmolar Hyperglycaemic State

  • Characteristic of type 2 DM, a severe hyperglycaemia causes a hyperosmolar state in absence of severe ketosis
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2
Q

Outine the metabolic pathway that underlie diabetic ketoacidosis (DKA)

(pathogenesis)

A
  • Absolute insulin deficiency leads to uncontrolled catabolism
  • In the absence of insulin, hepatic glucose production is increased, and peripheral uptake of glucose is reduced
  • Rising glucose levels leads to an osmotic diuresis, leading to severe dehyrdation
  • Rapid lipolysis occurs in glucose-starved tissues, leading to elevated free fatty acids, which are converted to fatty acetyl-CoA in liver cells
  • Fatty acetyl-CoA can be converted to ketone bodies in mitochondria to generate energy
  • Accumulation of ketone bodies causes a metabolic acidosis (can be detected on breath)
  • Respiratory compensation leads to hyperventilation
  • Acidosis causes vomiting, and further fluid/electrolyte loss
  • Renal perfusion falls, leading to impaired excretion of the raised H+ and ketones
    • There is increased excretion of sodium and potassium
    • Despite a significant total body deficit of K+, initial serum K+ is typically normal, or even elevated (pseudo-hyperkalaemia)
    • This is due to extracellular migration of K+ in response to acidosis & insulin deprivation
    • Serum K+ levels will then usually fall during treatment as the exogenous insulin drive K+ into cells
    • If serum K+ is not monitored and replaced as needed, life-threatening hypokalaemia may develop
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3
Q

What are common resons for the development of DKA?

A
  • Previously undiagnosed diabetes
  • Interruption of insulin therapy
  • The stress of intercurrent illness/surgery
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4
Q

What is hyperglycaemic hyperosmolar syndrome (HHS)?

Who does it occur in?

What are precipitating factors?

A
  • Severe hyperglycaemia causes a hyperosmolar state in the absence of severe ketosis
  • Typically occurs in the elderly, often with undiagnosed T2DM
  • Precipitating factors:
    • Consumption of glucose-rich fluids
    • Medications: thiazide diuretics, steroids, B-blockers
    • Intercurrent illness: infection/MI
  • These patients may be more severely dehyrdated than DKA patients, but there will be no raised ketones (can be lactic acidosis but is generally mild)
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5
Q

What are the clinical presentations of DKA?

A
  • Prostration (collapse - complete physical or mental exhaustion)
  • Kussmaul respiaration: air hunger
  • Nausea & vomiting
  • Abdominal pain
  • Confusion/stupor

On examination there may be evidence of marked dehydration, with the smell of ketones of breath. There is often a history of marked polyuria (litres)

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6
Q

What are the clinical features of Hyperosmolar hyperglycaemic state (HSS)?

A
  • Dehydration
  • Stupor/coma/seizures
  • Evidence of an underlying illness
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7
Q

Describe the clinical symptoms of hypoglycaemia.

How are they grouped?

A

Hypoglycaemia is defined as plasma glucose <3mmol/L, but individual thresholds for symptoms are variable. Symptoms are autonomic or neuroglycopenic:

Autonomic:

  • Sweating
  • Anxiety
  • Hunger
  • Tremor
  • Palpitations

Neuroglycopenic:

  • Confusion
  • Drowsiness/coma
  • Seizures
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8
Q

What are the major counter-regulatory hormone responses to hypoglycaemia?

What does it do?

A

In episodes of hypoglycaemia, the aplha cells of the pancreas will release glucagon, which works to:

  • Increase glycogenolysis
  • Increase gluconeogenesis
  • Inhibit glycogen synthesis

The adrenaline response may be absent in patients with a long history of diabetes (associated with a loss of warning symptoms).

Growth hormone and cortisol may be released over a longer period of time to give a small increase in blood glucose levels

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9
Q

Why might a patient develop hypoglycaemia?

A

In type I DM, the alpha cells (of pancreas) become insensitive to falls in glucose, thus becoming increasingly vulnerable to hypoglycaemia

Aetiology of hypoglycaemia:

  • Excess insulin
    • Inhibits hepatic gluconeogenesis and glycogenolysis
    • Either exogenous or insulinoma
  • Depletion of hepatic glycogen
    • Malnutrition, fasting, exercise or alcohol
    • Liver failure can also cause this

Pituitary insufficiency, adrenal insufficiency and non-pancreatic neoplasms can also cause hypoglycaemia

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10
Q

What is the treatment of hypoglycaemia?

if able to swallow

A
  • Prompt consume 10-20g of fast-acting form of carbohydrate, preferably in liquid form (lucozade)
  • Recheck blood glucose levels after 10-15 minutes
    • Hypoglycaemia should be reversed in about 10 minutes
    • Improvements in signs and symptoms may lag behind improvement in blood glucose
  • If inadequate response, repeat as above and recheck again
  • When symptoms improve, the patient should eat some long-acting carbohydrate
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11
Q

What is the treatment of hypoglycaemia?

if unconscious/ unable to swallow (severe hypoglycaemia)

A
  • Administer IM glucagon immediately
    • If <8 years old: 500 micrograms
    • If >8 years old: 1mg
  • If glucagon not available, the patient has consumed alcohol (glucagon not effective if alcholol drunk), or the person does not respond to glucagon within 10 minutes, call 999 for emergency hospital transfer - IV treatment
  • If the patient responds to glucagon, advise intake of long-acting carbohydrates when able
  • Vomiting is common during recovery, which can precipitate further episodes of hypoglycaemia
  • Within hospital, 100ml of 20% glucose can be used as an alternative to glucagon, and this can be repeated 3 times

Following recovery, never omit insulin in patients with T1DM

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12
Q

Interpret blood gases showing a metabolic acidosis due to DKA

A

Metabolic acidosis will show a low pH, negative base excess and compensatory low pCO2.

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