Diabetes in the perinatal period Flashcards

1
Q

what is diabetes

A

clinical syndrome characterised by hyperglycaemia due to deficiency or diminished effectiveness of insulin. affects normal metabolism of carbs, fat and proteins

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2
Q

pregestational

A

type 1 - 0.4%
type 2 - 1%

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3
Q

gestational

A

diagnosed of glucose intolerance of variable degree with onset or first recognition during pregnancy - 5%

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4
Q

carb metabolism in pregnancy

A

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

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5
Q

fetal metabolism

A

fetus produces insulin from 9 weeks
increased maternal blood glucose levels lead to hyperinsulinemia and macrosomia

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6
Q

type 1 management

A

team approach - endo, OB, midwives, diabetes educator, dietician
insulin therapy
education

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7
Q

type 1 is

A

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

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8
Q

ketoacidosis

A

chemical substances accumulate in the blood because of utilising fat for energy when treated with exogenous insulin

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9
Q

monitoring diabetes

A

maintain BGL
reduce long term complications

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10
Q

HbA1c

A

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%

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11
Q

insulin requirements during pregnancy

A

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

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12
Q

complications

A

ketoacidosis
hypoglycaemia
microvascular (neuropathy, nephropathy, retinopathy)
macrovascular
atherosclerotic heart and vascular changes
urinary and vaginal infections

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13
Q

maternal complications

A

miscarriage
pre-eclampsia
polyhydramnios
infection
pre-term labour
c-section

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14
Q

perinatal and neonatal outcomes

A

intrauterine death
neonatal mortality
congenital abnormalities
RDS
LGA or IUGR
hypoglycaemia
Hyperbilirubinaemia

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15
Q

type 2

A

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.

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16
Q

GDM

A

carb intolerance of variable severity with onset at first recognition during the present pregnancy
24-28 weeks
the body is unable to produce enough insulin for its own needs, because of either impaired insulin secretion, impaired insulin action, or both.

17
Q

GDM pathophysiology

A

Beta cell production of insulin is limited. If the body is unable to produce enough insulin, gestational diabetes develops.
Generally normal blood glucose level in first half of pregnancy

18
Q

risk factors GDM

A

obesity
previous macrosomic baby weighing >4.5kg
previous GM, fam history
maternal age >25
ATSI, maori, middle eastern, asian
poor obstetric history

19
Q

GDM diagnosis

A

fasting = plasma glucose of >5.1mmol/L
1 hr = >10mmol/L
2 hrs = 8.5mmol/L

diet management and control
insulin therapy
self monitoring
short acting (actrapid, novarapid, lispro)
long acting protophane
oral (metformin, gilbenclamide)
diet
exercise
prevention of infection

20
Q

diabetes management in labour and birth

A

BGLs hourly
dextrose infusion commenced to maintain BGL between 4-7mmol/L and CTG
macrosomic fetus = informed of risks and benefits of vaginal birth, IOL and LSCS

21
Q

postnatal care

A

Insulin requirements fall rapidly after birth, so BGLs done frequently.
Insulin doses are reduced if type 1, or ceased if GDM.
Breastfeeding encouraged.
Family planning discussion and that oral contraceptives may affect carbohydrate metabolism and therefore insulin requirements.
A follow up glucose tolerance test (GTT) is recommended at 6-8 weeks and/or HbA1c at 3 months. If impaired glucose tolerance, arrange endocrinologist review.
Other women should be advised about a healthy lifestyle and to have a GTT every 2 years.

22
Q

management to prevent hypoglycaemia

A

BGLs fall to 2.6 post birth
commence feeding around 1 hr and assess BGL 2 hr post birth
feed at least 3rd hourly to maintain BGL
checked 4-6 hrs for the first 24-48 hrs

23
Q

signs of neonatal hypoglycaemia

A
  • Hypothermia
  • High pitched cry
  • Poor temperature control
  • Sweating
  • Poor suck or refusal to feed
  • Tremors
  • Exaggerated Moro reflex
  • Irritability
  • Lethargy
  • Hypotonia (decreased muscle tone)
  • Seizures
  • Cyanosis
  • Pallor (pale)
  • Tachypnoea/apnoea
  • Tachycardia
  • Congestive heart failure
  • Respiratory distress
24
Q

management neonatal hypogylcaemia

A

*Clinical definition varies according to the age and hours old an infant is, however a safe definition of a low BGL is below 2.6mmol/L, whether the neonate is symptomatic or not.
 If asymptomatic feed immediately.
 Repeat BGL in 1 hour
 If >2.6 mmol/L feed as usual
 If <2.6mmol/L repeat feed
*If symptomatic, or if the BGL remains below 2.6mmol/L after second feed, or is below hospital policy threshold for oral feeds then the neonate is given IV dextrose 10% 10mL as a bolus dose
*Bolus dose followed with 10% dextrose infusion in a nursery

25
Q

role of insulin

A

facilitates the uptake of glucose by facilitating its movement from the blood into target cells (liver, skeletal and muscle)
* stimulates formation and storage of lipids and glycogen
* lowers circulating blood glucose.

It does this by:
* increasing glucose transport by target cells
* accelerating glucose utilisation (target cells) and enhanced ATP production
* stimulating glycogen synthesis (skeletal, muscle and liver cells)
* decreasing glucogenesis.