defect of insulin secretion and/or insulin action

→ chronic hypergylcemia w/ disturbances in fat, carbohy, prot metabolism

→ microvascular → retinopathy, nephropathy, neuropathy

→ macrovascular → CV, cerebrovascular, PAD

<110 mg/dl

<140 mg/dl

Basal: > 126 mg/dl

2h OGTT > 200 mg/dl

Random > 200 mg/dl

Fasing plasma gluc < 126 mg/dl

AND

OGTT between 140 - 200 mg/dl

📷

Fasting plasma gluc 110-125 mg/dl

OGTT <140 mg/dl

>6,5% → diabetes

6-6,5% → prediabetes - increased risk,prevention important!

• DM yes/no
• What Type
• Micro and macrovascular complications
• comorbidities
• CV risk

• 4-P→ Polydypsia, Polyuria, Polyphagia, poundloss
• weight loss
• weakness
• irritability
• ketoacidosis → nausea+vomiting

• dehydration
• fruity breath - Kussmaul
• nausea, vomiting, abdominal pain
• altered neurological state, coma

explanation later

• C-peptide
• Auto-ABs
• plasma glucose levels (fasting, postprandial, noctural)
• HbA1c

Additionally:

• Crea + Albuminuria/ Proteinuria
• Lipidprofile
• Full blood count
• thyroid hormones
• other autoimmune disease marker!

inflammatory! (adipokines)

• C Reactive Protein
• Fibrinogen level
• Liver enzymes: aminotransferases, gamma-GT
• Uric acid

• prior meal + snack
• prior to exercise
• when low Gluc is suspected + after treating low Gluc
• prior to critical task (driving etc.)

⇒ 📷

Type 1:

After initial presentation, honeymoon period often occurs where glycemic control can be achieved with little or no insulin treatment (residual cells still able to produce insulin). Once these cells destroyed→ complete insulin deficiency

Type 2:

Early on, glucose tolerance remains normal despite insulin resistance (B cells compensate with increased insulin production) with time: Insulin resistance and compensatory hyperinsulinism continue ⇒ cells are unable to maintain the hyperinsulinemic state which results in glucose intolerance and DM

Type 1:

Insulin

Type 2:

• Lifestyle modification
• Non-insulin anti-hyperglycemic agents → metformin should be the initial antihyperglycemic agent of choice. Additional agents to be selected on the basis of clinically relevant issues, such as glucose lowering effectiveness, risk of hypoglycemia, and effect on body weight
• Insulin therapy

Type 1: DKA if severe

Type 2: HHS, DKA if severe

• increased risk for spontaneous abortion and congenital malformations
• Macrosomia (big boiii 👶🏼)

• overweight/obese
• mother >35y
• multiparity (also prior signs of GD → macrosomia, fetal mortality)
• history of IFG or IGT
• excessive weight gain (during first 6month of pregnancy)
• PCOS

high risk before week 24 → negative → repeat week 24-28

moderate risk → week 24-28

• DM in pregnancy
• Gestational DM

Random Gluc >200 → check FPG or A1C → if FPG>126 or A1C>6.5% = diabetes mellitus in pregnancy

ONE of:

fasting >92

1h plasma gluc > 180

2h plasma gluc > 153

during pregnancy weeks 24-28