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4th Year Endocrinology > Type 1 Diabetes Mellitus + DKA > Flashcards

Type 1 Diabetes Mellitus + DKA Flashcards

1
Q

Pathophysiology of type 1 diabetes mellitus

A

Absolute insulin deficiency due to autoimmune destruction of pancreatic beta cells.

Islets of Langerhaan are responsible for endocrine function of the pancreas. Beta islet cells prouduce insulin which is released into the bloodstream.

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2
Q

What is the role of insulin?

A
  • Stimulates uptake of glucose by the liver, muscle and adipose tissue
  • Stimulates glycogen synthesis
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3
Q

Epidemiology of type 1 diabetes mellitus

A
  • 10-20% of all diabetic patients
  • Most common form of diabetes in <20 years of age
  • Highest incidence at 10-14 years old
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4
Q

Risk factors for type 1 diabetes mellitus

A
  • HLA risk profile: HLA-DR3 and HLA-DR4 (encodes MHC proteins which regulate the immune system)
  • Personal/family history of autoimmune disease eg Hashimoto’s
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5
Q

Clinical features of type 1 DM

A

Symptoms:

  • Polyuria
  • Polydipsia
  • Polyphagia
  • Weight loss
  • Fatigue

Signs:

  • Poor wound healing
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6
Q

Primary investigation for T1DM

A
  • Random blood glucose: ≥ 11mmol/L with clinical features → same day referral
  • Fasting blood glucose: ≥7.0mmol/L is typical
  • Oral glucose tolerance test: ≥11mmol/L two hours after a 75g oral glucose load
  • HbA1c: >48 mmol/L suggests hyperglycaemia over 3 months
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7
Q

Investigations to consider in T1DM

A
  • C-peptide: if atypical features present eg age >50, BMI >25kg/m2
  • Autoantibodies (anti-glutamic acid decarboxylase): if atypical features are present
  • VBG: if concerned about DKA
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8
Q

Management of T1DM

A

Lifestyle:

  • Diet high in fibre and low in fat, sugar and salt
  • Educate regarding carbohydrate counting; allows insulin dose to be matched to intake

Insulin therapy:

  • Basal bolus: first line, long acting insulin regularly (basal) with rapid acting insulin before meals (bolus)
    • Basal: Levemir twice daily or Lantus once daily
    • Bolus: Humalog or Novarapid
  • Mixed insulin regimen: short/rapid acting insulin analogue with intermediate acting insulin - used when unable to tolerate basal-bolus insulin
  • Continuous insulin infusion - if disabling hypoglycaemia or persistent hyperglycaemia (HbA1c >96mmol/mol)
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9
Q

Monitoring in T1DM

A
  • Glucose:
    • ​HbA1c: measured every 3-6 months with a target of ≤48mmol/mol
    • Self monitoring: check blood glucose levels at least 4 times a day. Targets:
      • On waking: 5-7 mmol/L
      • Before meals and other times of the day: 4-7 mmol/L
  • Retinopathy
    • ​Immediate opthalomology referral upon diagnosis and annually thereafter
  • Diabetic foot
    • Should be assessed at least annually; refer urgently to foot protection service if at risk (eg ulceration)
  • Diabetic nephropathy
    • ​Annual measurement of eGFR and urinary albumin:creatinine ratio
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10
Q

Complications of T1DM

A
  • Cardiovascular
    • Ischaemic heart disease
    • Heart failure
    • Peripheral vascular disease
  • Neurological
    • Stroke
    • Carpal tunnel syndrome
    • Neuropathy
  • Endocrine
    • DKA
  • Renal
    • Diabetic nephropathy and CKD
  • Opthalmology
    • Diabetic retinopathy
    • Macular degeneration
    • Open-angle glaucoma
    • Cataracts
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11
Q

What is diabetic ketoacidosis?

A
  • Metabolic state as a complication of T1DM (predominantly)
  • Medical emergency: due to dehydration and electrolyte imbalances
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12
Q

Triad of DKA

A
  • Hyperglycaemia
  • Acidosis
  • Ketonaemia
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13
Q

Pathophysiology of DKA

A
  • Net reduction in insulin
  • Reduced glucose entry into cells
  • Metabolism of lipids as an alternative energy source
  • Fatty acids converted to ketone bodies (acetoacetic acid + beta-hydroxybutyric acid) by liver
  • Ketones increase acidity of blood resulting in ketoacidosis and produce acetone (which produces pear drop breath)

Also:

  • Increase in counter regulatory hormones (eg cortisol)
  • ↑ gluconeogenesis, ↑glycogenolysis
  • Hyperglycaemia
  • Osmotic diuretics
  • Dehydration and electrolyte abnormalities
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14
Q

Why does acidosis result in hyperkalaemia?

Why do we replace potassium in DKA?

A

H+ ions in blood move into cells, K+ moves out of cells.

Also insulin required for sodium potassium ATPase.

There is total body potasium loss as potassium is excreted in urine and there is reduced potassium within cells.

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15
Q

Symptoms of DKA

A
  • Abdominal pain
  • Nausea and vommiting
  • Polyuria and polydipsia
  • Weight loss
  • Inability to tolerate oral fluids
  • Lethargy and confusion
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16
Q

Signs of DKA

A
  • Fruity ‘pear drop’ smell of acetone on the breath
  • Dehydration
    • Mild: only just detectable
    • Moderate: dry skin and mucous membranes, reduced skin turgor
    • Shock: tachycardia, hypotensive (late), drowsiness, reduced urine output
  • Kussmal respiration: deep, laboured breathing
17
Q

Investigations for DKA

A
  • Bedside
    • Urine dip: glycosuria and ketonuria
    • Bedside ketone and capillary glucose
  • Bloods
    • ABG/VBG: quickest way to ascertain pH and HCO3 levels
    • U&Es: electrolyte derangement and acute kidney injury due to dehydration
    • FBC and CRP: raised inflammatory markers may suggest underlying infection as a precipitant
    • Infection screen: if an infection is the suspected trigger
18
Q

Diagnostic criteria for DKA

A
  • Glucose >11 mmol/L or known DM
  • HCO3 <15 mmol/L and/or venous pH <7.30
  • Ketonaemia (≥3 mmol/L) or 2+ ketonuria
19
Q

Management of DKA

A
  • IV fluid
    • SBP < 90mmHg
      • 1 litre 0.9% NaCl over 15 minutes
    • SBP > 90mmHg: typical regimen
      • 1 litre 0.9% NaCl over 1 hour
      • 1 litre 0.9% NaCl with KCL over next 2 hours
      • 1 litre 0.9% NaCl with KCL over next 2 hours
      • 1 litre 0.9% NaCl with KCL over next 4 hours
      • 1 litre 0.9% NaCl with KCL over next 4 hours
      • 1 litre 0.9% NaCl with KCL over next 6 hours
  • Insulin
    • Fixed-rate insulin infusion
      • Commence at 0.1 U/kg/h
      • Add in 10% glucose once glucose levels drop below 14.0 mmol/L
      • Do not stop long acting insulin
  • Anticoagulation: patients are at increased risk of VTE
20
Q

What potassium concentration is given to patients with DKA?

A
  • Serum potassium concentration > 5.5 = none
  • Serum potassium concentration 3.5-5.5 = 40 mmol/L
  • Serum potassium concentration < 3.5 consider HDU/ITU for replacement via central line
21
Q

Complications of DKA

A
  • Hypokalaemia and hyperkalaemia
    • Potentially life threatening
    • Hyperkalaemia: extracellular shift of K+ due to acidosis
    • Hypokalaemia: due to correction of acidosis
  • Hypoglycaemia
    • Due to rapid correction of ketoacidosis
    • May result in rebound ketosis
  • Cerebral oedema
    • More common in children (70-80% of diabetes related deaths)
    • Likely to be iatrogenic

4th Year Endocrinology (7 decks)

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