A. ACUTE AND SECONDARY COMPLICATIONS OF DIABETES Flashcards
what are the 3 acute complications of diabetes
- hypoglycaemia (hypo) - T1DM and T2DM
- diabetic ketoacidosis (DKA) - T1DM
- hyperosmolar hyperglycaemia state (HHS) - T2DM
at what blood glucose level does hypoglycaemia occur
<4 mmol/L
(symptoms present at 3 mmol/L)
how might a type 1 diabetic get hypoglycaemia
- insulin overdose
- excessive exercise
- inadequate CHO intake
how might a type 2 diabetic get hypoglycaemia
- sulphonylureas as they stimulate insulin release (elderly)
- hepatic or renal disease (don’t reabsorb glucose well)
- some drugs (beta-blockers, diuretics and steroids)
side effects of hypoglycaemia
palpitations
tremors
sweating
anxiety
dizziness
hunger
irritability
headache
tingly lips
how does the body act to hypoglycaemia
counter-regulatory activity of SNS in order to increase glucose levels
what is neuroglycopenia/neuroglucopenia
glucose deficiency in brain
symptoms of neuroglycopenia
loss of concentration
slurred speech
behaviour mood changes
seizures
loss of consciousness
treatment of hypoglycaemia if conscious
- sugary drink/food which is absorbed quickly
- Glucogel: ie 40% dextrose (D-glucose) gel
- 10-15 minutes for recovery then a snack (biscuit/bread) for sustained carbohydrates
treatment of hypoglycaemia if unconscious
- IV glucose
- IV/IM/SC glucagon but not after alcohol as works on liver
what is diabetic ketoacidosis (DKA)
- diabetic coma
- more likely in poorly-cotrolled T1DM
- medical emergency
- 10-20% mortality rate
what induces diabetic ketoacidosis (DKA)
- hyperglycaemia and metabolic acidosis (ketosis) due to lots of ketones
what is DKA caused by
- omission or reduction in insulin dose (inhibits ketogenesis and lowers blood glucose)
- illness/infection
- emotional upset
- menstruation/pregnancy ketosis
- rare syndromes of insulin resistance
*stress uses insulin more quickly
consequences of loss of insulin action
Liver:
- gluconeogenesis
- glycogen breakdown
Muscle:
- protein breakdown to amino acids
Adipose tissues:
- lipolysis to fatty acids and glycerol
what happens with the breakdown products: fatty acids, glycerol, amino acids
intermediates for gluconeogenesis
- lots of glucose produced
- lots of ketones produced
consequences of the increase in glucose
osmotic diuresis
- frequent passing of urine
- dehydration
- thirst as:
plasma glucose leads to filtered load (water taken with it) > renal absorption for glucose so get glycosuria
consequences of the ketone bodies
metabolic acidosis
- nausea, vomiting (due to change in pH)
- breathlessness (ventilation to change acid-base balance)
- abdominal pain
severe consequences of metabolic acidosis
- CNS depression
- diabetic coma
- death
severe consequences of dehydration (low blood volume)
- decreased peripheral circulatory volume:
- renal failure
- low cerebral blood flow
- death
treatment of DKA
- hospital
- replacement of fluids, electrolytes (NaCl saline, KCl, glucose 10%)
- IV infusion of insulin (suppress ketogenesis, reduce blood glucose, correct electrolyte imbalance)
- treat cause
what is HHS
- severe hyperglycaemia without ketosis (>40mmol/L)
- managed as DKA but less insulin patients can still make insulin
how to monitor blood glucose in primary care
- HbA1c measurements every 3 months
how to self-monitor blood glucose
- capillary blood glucose testing (glucose meter and test strips)
- continuous glucose monitoring:
a) real time - all the Time
b) flash - measures glucose in interstitial fluid
there is a time lag compared to direct blood glucose monitoring due to I.F being measured
long term (chronic) microvascular complications of DM
- retinopathy
- nephropathy
- neuropathy
specific to DM
