Diabetes in the perinatal period Flashcards
what is diabetes
clinical syndrome characterised by hyperglycaemia due to deficiency or diminished effectiveness of insulin. affects normal metabolism of carbs, fat and proteins
pregestational
type 1 - 0.4%
type 2 - 1%
gestational
diagnosed of glucose intolerance of variable degree with onset or first recognition during pregnancy - 5%
carb metabolism in pregnancy
fetus receives glucose via the placenta by facilitated diffusion
Resistance to insulin also an issue caused by human placental lactogen, oestrogen, progesterone and cortisol
3rd trimester maternal use of fat for energy causes an increase in free fatty acids and glycerol, increase risk of ketosis
fetal metabolism
fetus produces insulin from 9 weeks
increased maternal blood glucose levels lead to hyperinsulinemia and macrosomia
type 1 management
team approach - endo, OB, midwives, diabetes educator, dietician
insulin therapy
education
type 1 is
cellular mediated autoimmune destruction of the islet cells
pancreas stops making insulin because of beta cell destruction
without insulin, the body’s cells cant turn glucose into energy
body uses its own fat to substitute for glucose
Due to the destruction of β-cells, patients with T1DM require insulin replacement to achieve euglycaemia
ketoacidosis
chemical substances accumulate in the blood because of utilising fat for energy when treated with exogenous insulin
monitoring diabetes
maintain BGL
reduce long term complications
HbA1c
long term glucose control is measured by a blood test to measure glycosylated haemoglobin
measures % of Hb that is glycoslyated - reflecrs avg. BG during preceding 1-2 months
higher result reflects poorer BGL control should be <7%
insulin requirements during pregnancy
in 1st tri = often need reduction of insulin due to transfer of glucose to fetus and reduction in dietary intake
2nd half = increase in diabetogenic effects of hormones causes an increase in insulin requirements
ketogenesis is risk
last 3-4 weeks = insulin needs plateau or decrease = this increases risk of hypoglycaemia and stillbirth
complications
ketoacidosis
hypoglycaemia
microvascular (neuropathy, nephropathy, retinopathy)
macrovascular
atherosclerotic heart and vascular changes
urinary and vaginal infections
maternal complications
miscarriage
pre-eclampsia
polyhydramnios
infection
pre-term labour
c-section
perinatal and neonatal outcomes
intrauterine death
neonatal mortality
congenital abnormalities
RDS
LGA or IUGR
hypoglycaemia
Hyperbilirubinaemia
type 2
insulin resistance at the tissue level
makes too little insulin or unable to use insulin made
pregnant women with type 2 diabetes risk giving birth to stillborn or major birth defects
A relative lack of endogenous insulin plus pancreatic β-cell dysfunction reduces glucose uptake by cells, resulting in hyperglycaemia. Hyperglycaemia is caused by a lack of endogenous insulin. Insulin deficiency usually occurs because of resistance to the actions of insulin in muscle, fat and the liver, and an inadequate response by the pancreatic β-cells.