GDM - EPIDEMIOLOGY, DEF , TYPES OF DIABETES AND Pathophysiology

Pathophysiology - GDM

• decrease in insulin (beta cell’s insufficient response) sensitivity & insufficient insulin selection by beta cells is key for mechanism of GDM (results in increase blood glucose)

  • Because of insulin resistance, the Beta cells compensate by releasing insulin

• Increase blood glucose causes inflammation

• GDM disappears AFTER birth of placenta as NO more placenta hormones = insulin sensitivity & BG Levels restored to normal

  • IF ABLE to compensate - will NOT have GDM

Pathophysiology of GDM 2

• Fetoplacental hormones ( glt, cortisol, prolactin, HPL) leads to —>

  • INCREASED insulin resistance

• Compensatory increase in insulin selection if not —>

  • (Compensatory) If not ? GDM

  • (insulin Secretion) Normal in pregnancy

• HPL - Human placental lactogen - increases as measuring ( pregnancy ) progresses

  • creates resistance of insulin for growth baby → maximise fetal growth

    • LGA

    • SGA

Role insulin

• Facilitates glucose uptake —> uptake from blood into cells (liver, skeletal & muscle)

• Stimulates formation & storage of lipids & glycogen

• Decrease in BG levels =

  • increase glucose transport by target cell

  • Accelerating glucose utilisation (target cells) & enhanced ATP production

  • Stimulating glycogen synthesis

  • Decrease in glycogenesis

Role of glucagon

• Mobilises energy reserves & promotes glucose

• Synthesis & glycogen breakdown

• Elevates BG concentrations = stimulating breakdown of glycogen in Skeletal, muscle & liver cells

  • Stimulating breakdown of inglyceridxen in adipose tissues → production of glucose in liver

HbA1c

(50g) Polycose → oral glucose test → no risk factors ( > 7.8mmol)

• oral glucose tolerance (75g) → 24 - 28 weeks

PATHOPHYSIOLOGY - Carbohydrate Metabolism:

Food broken down to provide glucose - essential to all cells of body

• GLUCOSE metabolism controlled by insulin

Insulin secreted by pancreatic (response to increase in glucose) beta cells - insulin unlocks body cells to all uptake of glucose

• THEREFORE Insulin promoTes glucose metabolism in body tissues.

• As blood glucose uptaken - blood glucose decreases

* INSULIN RESISTANCE = When cell stops responding to insulin resulting in increase of blood glucose

GDM1

• (Beta cell insufficient response) Decrease insulin sensitivity & insufficient insulin secretion by beta cells is key for mechanism of GDM (results in increase blood glucose)

• Increase in BG causes inflammation

• GDM disappears after birth of placenta as no more placental hormones = insulin sensitivity & BGL restored to normal

GDM2

• Bc of insulin resistance, the beta cells compensate by releasing insulin - IF ABLE TO COMPENSATE, WILL NOT HAVE GDM

Pathophysiology GDM

Fetoplacental hormones (GH,CORTISOL PROLACTIN,HPL- HUMAN PLACENTALLACTOGen - increases as pregnancy progresses - creates resistance of insulin for growth of baby -maximize Fetal growth- lga & saga)

Then - results in increased muslin

Then - Compensatory 9in not GDM ) increase in insulin (normal in pregnancy )secretion

Role of insulin

• facilitates glucose uptake - uptake from blood into cells (liver , skeletal and muscle)

• Stimulates formation & storage of lipids & glycogen

• Decrease BGL = increase glucose transport by target cells, accelerating glucose utilisation (target cells & enhanced ATP production, stimulating glycogen synthesis, decrease in glycogenesis

Role of glucagon

• mobilises energy reserves& promotes glucose

• Synthesis & glycogen breakdown

• Elevates BG concentrations = stimulating breakdown of glycogen in skeletal muscle & liver cells.stimulating breakdown of inglycerides in adipose tissues → production of glucose in liver

HbA1c

(50mg) poly one - oral glucose test - no risk factors (7.8mmol)

(75g) Oral Glucose tolerance → 24-28 weeks - at risk of GDM (5.5mmol)

Fasting > 5.5mmol/2hr > 9.0mmol)

Oral glucose tolerance test (OGTT)

• done if hba1c & polycose result high

• Diagnostic

• Empty stomach in the AM

• Bloods taken on arrival (fasting 5.5mmol)

• 2hr after sugary drink - blood taken (9.0mml) -one abnormal results required fo diagnostic

Polycose test (50g)

Does not require fasting

Can be done anytime 24-28wks

Only done if hba1c low & no risk factors

1hr after sugary drink,bloods done

Risk factors GdM

• ama >= to 35y/o for Māori, indo Asian & pasifika - 45y/o for other ethnic groups

• Prev LGA baby ( > 4000g)

• Family history - first degree relative

• Increased bmi > 27kg/m2 in indo asain, >= 30kg/m2 in other ethnic groups

• Prev GDM

• Prev impaired fasting glucose or impaired glucose tolerance

PCOS

• Cvd or (vd),presistant hypertension (135/80mmhg >=),elevated triglycerides/cholesterol

• Acanthosis nigrican (brown darkening of skin folds)

• Long term use of steroids antipsychotic meds

• Physical inactivity/sedentary (lazy/careless) lifestyle

Screening - Hba1c

• As rBC are made they combine with glucose in blood to form hba1c link - this can cause inflammation and ends __ damage - pet

• hba1c (glycated haemoglobin) - tested on whole body

• Indicates average BGL over prev 6-8wks

• Reliable method of detecting probable diagnosed diabetes in first 20wks gets

• DO NOT OFEER HBA1C AS DIAGNOSTIC TEST FOR GDM AS NOT SENSITIVE ENOUGH.

Why HBA1c

• hba1c screening (threshold >= 34.4mmol) was superior to risk factor screening risk factor screening alone would miss 18% of all subjects and a third of Europeans who had an hba1c >8% (64mmol)

Plan with hba1c results

• wome with GDM have 3mnths pp and then annually

• Levels decline during pregnancy

• If diabetes under control , plan birth at 40wks if not well managed , plan birth at 38-39wks

• hba1c 4=40mmol/mol (NORMAL)

• Receive; dietary advice, lifestyle advice and have a glucose challenge (polycose) or oral GTT at 24-28wks (if polycose > 7.mmo> 11.1ml refer to dip)

• Hba1c 41 - 49mmol receive; dietary advice, and lifestyle advice and OGTT at 24-28wks (pre diabetic)

• hba1c >= 50mmol receive: care from dip an specialist (diabetic NOT GDM)

Further advice - Plan with hba1c results

• eat healthy and balanced diets with 30mins of exercise (moderate) per day

• Women with risks factors should avoid excessive weight gain - healthy diet and lifestyle should continue pp

• To avoid GDM: prior and during pregnancy take into consideration their lifestyles

BMI Chart - average levels

• BMI - underweight < 18.5 - REC weight gain 13-18kgs

• Healthy weight 18.5 - 24.9 → 11-16kg

• Overweight 25-29.9 → 7-11kgs

• Obese >30 → 5-9kgs

• Twins/multiples: different BMI chart (weight gain)

Diabetogenic state: peak @ 24-28gst

• occurs in pregnancy to ensure optimal glucose uptake by fetus

• Due to placental hormones (also increase i adiposity) Causing insulin resistance and compensatory hyperinsulianemia - begins in 2nd tr and right through pregnancy, resembling t2dm levels

• In 2nd and 3rd tri, placental steroids and hormones exacerbate tissue insulin resistance

• If maternal pancreatic insulin response inadequate = 1st maternal then Fetal hyperglycemia

Diabetes overall 1

• absolute or relative deficiency of insulin production by pancrease

• Lacoste cannot be inverted to glycogen or released as energy so = increase in BGL

• Glucose osmotically active = draws water after it resulting in polyurice and thirst

• Due to lack of glucose uptake,body tries to seek glucose through fats and proteins -. Production of ketones by liver -. Ketosis

Diabetes overall 2

T1DM - Beta cels destruction → decrease in insulin products and release

T2DM - Beta cells work but not as efficiently as cells receptors are resistant to insulin - resistance can cause insufficient beta cell function of insulin release

GDM - Pancreatic B cells insufficient insulin secretion , insulin secretion due to placental hormones

Diabetes/GDM Poor management consequences Women

• retinopathy may worsen in pregnancy and should consult ophthalmologist prior to conception and further consultations during pregnancy

• Nephropathy - in combinations with PE and chronic hypertension = pre term birth , pet, miscarriage, increased risk of t2dm, c/s and IOL, polyhydramnos ,UTI

Diabetes/GDM Poor management consequences Fetal

CDV and neural tube defects (13x-20x more common in diabetic pregnancies)

LGA

Stillbirth

Preterm (SROM OR Planned to avoid SB)

Congenital malformation

Birth trauma due to LGA

Hypoglycaemia PN

Diabetes/GDM Poor management consequences - MW Role

• Advise and information sharing preconception and during pregnancy

• Refer to dip

• AN care components: history taking = current and past contraception menstrual history

• Screening fro existing diabetic complications

• Doc and management of situation

• Med review

• High doc 5mg folic acid pre conception and 1st tri

• Smoking/alchol help

• BMI and referral to dietian