309-313. Metabolic complications of diabetes Flashcards
What 3 features define diabetic ketoacidosis?
- Metabolic acidosis (pH <7.3, bicarbonate <15mmol/l)
- Hyperglycaemia (>13.9mmol/l)
- Ketosis (++)
What are the three acute metabolic complications of diabetes?
Ketoacidosis
Hyperglycaemia
Dehydration
Outline why osmotic diuresis occurs in T1DM (4) which subsequently caused ketoacidosis
Glucose (and ketones) freely filtered by the glomerulus
Maximal reabsorption threshold of glucose exceeded
Increased solute concentration in tubular lumen causes osmotic gradient
Increased water loss in urine
Describe the changes of potassium levels as a result of diabetic ketoacidosis (3)
Hyperaldosteronism exacerbates renal K+ loss
Lack of insulin prevents K+ from moving into cells
Plasma K+ levels may be elevated but total body K+ depleted
How would you treat the following complications of diabetes acutely?
a) Hypovolaemia
b) Insulin deficiency
c) Hypokalaemia
d) Supportive treatment
a) IV fluid
b) IV insulin
c) IV potassium
d) NG tube, antiemetics, precipitating causes
Describe the importance of insulin in the treatment of diabetic ketoacidosis
Insulin is essential for switching off ketogenesis and uncontrolled catabolism
Blood sugar may return to normal quickly after IV insulin administration but should remain continuous to resolve acidosis
As levels lower, add 10% dextrose and continue insulin (reduced rate) to resolve acidosis
Discuss how potassium administration can be used to treat diabetic ketoacidosis
Admission potassium may be high, normal or low
Total body K+ will require supplementation
Insulin therapy causes intracellular shift of K+
K+ requires regular and close monitoring
Cardiac monitoring is required
What does HHS stand for?
Hyperosmolar hyperglycaemic state
Why are ketones not present in T2DM?
Insulin deficiency is RELATIVE so there is enough insulin in the body to prevent ketone formation (as lipolysis can be reduced)
Describe how osmotic diuresis affects patients with T2DM
Chronic renal impairment is common in patients, so there is reduced capacity to excrete glucose
Longer, more insidious onset, more profound hypovolaemia
Impaired thirst leads to lack of water replacement due to cognitive impairment in many patients
Describe the treatment of HHS
Same as for ketoacidosis in T1DM (IV fluid, IV insulin, IV potassium and supportive treatment)
However, needs to be administered with much more caution due to any co-morbidities patients may have
Slower and steadier return to fluid osmolality
Outline how IV insulin is used in the treatment of HHS
Plasma glucose will fall with fluid alone
Insulin start when plasma glucose stable
Target blood glucose 10-15mmol/l acceptable
Fixed rate insulin infusion
What considerations should be made when administering potassium to treat HHS
Potassium shifts are less pronounced than in DKA
If there is chronic renal impairment, may be less able to excrete potassium
Less aggressive replacement required
What is the normal response to hypoglycaemia with relation to insulin and counter regulatory hormones?
Insulin decrease
Increase glucagon Increase adrenaline Increase noradrenaline Increase acetylcholine Increase cortisol Increase growth hormone
What are the autonomic (initial) symptoms of hypoglycaemia?
Sweating Tremor Palpitations Hunger Anxiety
