1013 - Pathophysiology of Diabeetus Flashcards
What is the difference between type I and type II diabetes?
Type I is an autoimmune disease, in which iset beta-cells are destroyed by the immune system - it is a disease of insulin deficiency.
Type II develops in insulin-resistant subjects when beta-cell compensation fails. It is therefore related to defects in both insulin action (resistance) and insulin secretion (compensation fails).
What are the two pathways that lead to diabetic ketoacidosis?
Glucose and Lipids (both due to insulin lack)
Glucose - increased gluconeogenesis and decreased cell up take leads to hyperglycaemia, glycosuria, thus osmotic diuresis and dehydration.
Lipids - Decreased insulin leads to increased lipolysis, and therefore increased ketogenesis via beta-oxidation. This leads to Ketonaemia and ketonuria (therefore more osmotic diuresis and dehydration). Ketonaemia leads to metabolic acidosis, body tries to compensate via tachypnoea. Ketones also lead to vomiting.
What tests would you do with suspected DKA? Why?
Vitals - Low BP (shock/dehydration?) Tachycardia (hypovolaemia), tachypnoea (metabolic acidosis).
Urine - check for glucose and ketones
Blood glucose
UECs - Na, K, and HCO3- will well be out of whack. Creatinine may be high due to dehydration.
FBC (confirm acidosis)
LFT (liver disease as cause?)
What can trigger DKA? What is mortality rate?
Mortality 3-5%
Triggers - infection, MI/Trauma/Stress, New-onset T1DM, or insulin omission/non-compliance.
What happens to sodium in DKA? Why?
Often hyponatraemia - diluted due to osmotic water movement out of cells, and urinated out due to diuresis.
What happens to creatinine in DKA? Why?
Raised (pre-renal) due to dehydration.
What happens to potassium in DKA? Why?
Could go either way, but most commonly SERUM potassium will be hyperkalaemic, despite whole-body K+ deficit.
Hyperkalaemia due to H+/K+ exchanger, and non-effect of insulin promoting co-transport of K+ into cells with glucose.
Whole-body deficit due to urinary and GI losses (diuresis and vomiting/diarrhoea).
How do you treat DKA?
IV infusion of Actrapid to reintroduce insulin
IV Saline to replace fluids
Monitor and correct electrolyte imbalance SLOWLY - particularly K+
Aim is to investigate and treat the underlying cause rather than just the symptoms.
What causes hyperglycaemia in T2DM? (4)
Decreased incretin effect means insulin is not stimulated, and hepatic glucose production increases due to hepatic insulin resistance.
Impaired glucose tolerance in peripheral tissues - they are not taking up the glucose because of insulin resistance.
Impaired beta-cell compensation for insulin resistance (including by reduced beta-cell volume and increased apoptosis) - insulin secretion defect.
Kidney keeps reabsorbing it until maxed out - not excreting.
How can T1DM and T2DM be distinguished if you are unsure?
Measure insulin and islet autoantibodies - presence of insulin suggests T2DM, presence of islet autoantibodies confirms T1DM.
What are the three types of Diabetes Mellitus?
Type 1 - Immune-mediated
Type 2 - Insulin-resistant
Gestational
Briefly outline gestational diabetes
Impaired carb tolerance in mother - hyperglycaemia crosses the placenta, leading to hyperinsulinaemia in foetus and excessive foetal growth.
