Adult Hyperglycaemia Flashcards

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1
Q

Patients on SGLT2 Inhibitors may present with what?

A
  • Euglycaemic ketoacidosis
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2
Q

What is the suffix for SGLT2 inhibitors

A
  • Flozins
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3
Q

What is mild to moderate hyperglycaemia/Ketosis

A
  • BGL 11 - 27.8 AND/OR Ketones 0.6 - 3mmol/L
    AND
  • Does not meet criteria for severe hyperglycaemia
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4
Q

What needs to be excluded in mild to moderate hyperglycaemia/ketosis

A

Other causes
- ACS
- Infection/sepsis

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5
Q

What is Severe Hyperglycaemia/ketosis?

A
  • BGL >27.8 AND/OR Ketones >3mmol/L
  • Less than adequate perfusion
  • Clinical features of DKA
  • Clinical Features of HHS
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6
Q

What are some clinical features of DKA

A
  • Kussmauls breathing
  • Altered conscious state
  • Ketotic breath
  • Dehydration
  • Profound thirst
  • Nausea/vomiting
  • Abdominal pain
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7
Q

What are some clinical features of HHS

A
  • Altered conscious state
  • Dehydration
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8
Q

What is the Mx for Severe hyperglycaemia/ketosis

A
  • Request MICA support
  • Cardiac monitoring and ECG
  • Normal Saline 1000 - 2000 mL IV
    + Administer over 1hour if BP > 90mmHg
    + Consult clinician if inadequate response
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9
Q

What is cardiac monitoring required in Hyperglycaemic patients

A
  • Hyperosmolarity forces potassium out of cells leading to hyperkalemia
  • High sugar levels can also lead to kidney disfunction leading to reduced filtration of potassium
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10
Q

When should reduced fluid be provided in Hyperglycaemia?

A
  • Hisotry of cardiac failure
  • Chronic renal failure
  • Elderly
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11
Q

What is the pathophysiology of DKA

A
  1. Type 1 diabetics
  2. Insulin deficieny
  3. Stress, infection of insufficient inulin intake
  4. Increase in Counterregulatory Hormones (Glucagon, Cortisol, Catecholamines, Growth hormone)
  5. Increases lipolysis (Instead of glucose being used)
  6. FFA end up in the liver
  7. Converted to Ketones (Acetate)
  8. Increased glycogenolysis leading to increased amounts of sugar in the body
  9. High levels of sugar feed into the kidneys and draw water and electrolytes (Osmotic diuresis
  10. Leads to dehydration
  11. Renal failure
  12. Shock
  13. Coma
  14. Death
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12
Q

What is the pathophysiology of HHS?

A
  • Type 2
  • Insulin still present
  • Insulin not being utilised properly but inhibiting lipolysis
  • Cells not uptaking sugar
  • Increase glycogenolysis to increase sugar levels
  • High BSL
  • leads to osmotic diuresis
  • leads to dehydration and hypovolaemia
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