DIABETES MELLITUS

DEFINING DIABETES
• Diabetes Mellitus Type 1 : Autoimmune disorder causing
destruction insulin-producing beta cells of the islets of Langerhans

• Diabetes Mellitus: Relative deficiency of insulin due to an excess of

adipose tissue. 
HOW DO THEY PRESENT?
Type 1 DM- tend to be younger Type 2 DM
YOUNG PATIENTS MIDDLE AGED OR OLDER
• Weight loss  • Incidental finding on routine blood
• Polydipsia tests
• Polyuria  • Polydipsia
• May present with DKA • Polyuria
Þ Nausea and vomiting
Þ Abdominal pain
Þ Reduced consciousness level
Investigations: 4 main ways to check Blood Glucose
1. Finger-prick bedside glucose monitor
2. One-off blood glucose: fasting or non-fasting
3. HbA1c: Measures the amount of glycosylated haemoglobin and represents
the average blood glucose over the past 2-3 months
4. Glucose tolerance test.
Þ a fasting blood glucose is taken
Þ Then a 75g glucose load is taken
Þ After 2 hours a second blood glucose reading is then taken
TEST NORMAL IMPAIRED GLUCOSE TOLERANCE DIABETES
75g OGTT <7.8 mmol/L >= 7.8 – 11 mmol/L >11 mmol/L
Drug class Mechanism of action Route Main side-effects Contraindication
Insulin Direct replacement SC Hypoglycaemia
Weight gain
Lipodystrophy

Metformin Increases insulin Oral Gastrointestinal upset Low BMI

sensitivity& Lactic acidosis Renal failure
suppresses Weight loss
gluconeogenesis

Sulfonylurea Increase beta cells Oral Hypoglycaemia  Patients at risk of

Gliclazide insulin secretion Weight gain hypoglycaemia
Severe hepatic/renal
impairment
Thiazolidinedione Increases fat/muscle glucose Oral Weight gain Heart failure
Pioglitazone uptake Fluid retention
Fractures
DPP-4 inhibitors Increases incretin levels Oral Pancreatitis
(-Gliptins) (hormone released by gut to
e.g. Sitaglipitin increase insulin after food)

SGLT-2 inhibitors Increases urinary glucose Oral UTIs Renal failure

(-Gliflozins) excretion Ketoacidosis
e.g. Dapagliflozin
GLP-1 agonists Incretin (GLP-1) mimetic SC GI upset (n&v) Renal failure
(-tides) Pancreatitis PMH
e.g. Exanetide Weight losss Pancreatitis
Severe GI
disease
INSULIN REGIMENS – TYPE 1 DM
COMPLICTAIONS OF DIABETES
• Cardiovascular disease: Increased risk of Ischaemic Heart disease
• Increased risk for peripheral vascular disease: claudication
• Diabetic neuropathy: polyneuropathy, mono-neuropathy (carpal
tunnel syndrome)
• Nephropathy: kidney damage
• Retinopathy: vision loss
• Poor healing + neuropathy -> Ulcers
DIABETES IN
PREGNANCY
Pregnant patients may have:

1. Pre-existing diabetes: Individuals who have had a

diagnosis of DM prior to pregnancy

2. Gestational diabetes: Those in which diabetes

appears during pregnancy and disappears after
delivery
Risk factors for Gestational diabetes
• BMI > 30
• Previous macroscopic baby
• Previous gestational diabetes
• 1st degree relative with diabetes
• Ethnic groups: south Asian, middle eastern etc.
DIAGNOSTIC THRESHOLDS FOR
GESTATIONAL DIABETES

• Fasting glucose ≥ 5.6 mmol/l

• 2- hour glucose ≥ 7.8 mmol/l
Management of Gestational Diabetes
• Monitoring
 Followed up in a joint diabetes and Antenatal clinic weekly
 Taught self-monitoring
Fasting target 5.3 mmol/L
1 hr after meals 7.8mmol/L)
• Conservative: Advice on diet and exercise
• Medical:
Þ Metformin
Þ Insulin
• Fasting plasma Glucose <7 mmol/l (126 mg/dl)
 Trial of diet and exercise
If glucose targets are not met within 1-2 weeks -> initiate
metformin
If targets are still not met insulin is initiated

• Fasting Plasma Glucose >7 mmol/l (126 mg/dl) at the time of

diagnosis -> insulin should be initiated
USA CLASSIFCATION
PRE-EXISTING DIABETES MANAGEMENT
• Monitoring
Þ Detailed anomaly scan at 20 weeks gestation
Þ Tight glycaemic control to reduce complications
Þ Screen for retinopathy as can worsen during pregnancy
• Conservative
Þ Weight loss if BMI >27
Þ Diet and exercise advice
• Medical
Þ Folic acid 5mg/day form pre-conception to 12 weeks gestation
Þ Stop oral hypoglycaemic apart from metformin
Þ Initiate insulin
Complication of Diabetes in Pregnancy
MATERNAL NEONATAL
Polyhydramnios (foetal polyuria) Macrosomia
Pre-term labour (polyhydramnios) Shoulder dystocia
Small for gestational age
Respiratory distress syndrome
(surfactant)
polycythaemia: neonatal jaundice
 CARDIOTOCOGRAPH
Define Risk Low or high
Contractions Record number of contractions in 10 minutes)
Duration
Intensity (felt via examination)

Baseline Rate Average rate in 10 minutes

Normal 110- 150 bpm
Bradycardia, Tachycardia
Variability Normal (at rest 10 – 25bpm)
1. Reassuring >= 5 bpm
2. Non-reassuring <5bpm between 40 -90 minutes
3. Abnormal < 5 bpm > 90 minutes
Accelerations Abrupt increase in baseline heart rate of >15 bpm for >15 seconds
2 accelerations every 15 minutes
Present/Absent
Decelerations Abrupt decrease in baseline heart rate of >15 bpm for >15 seconds.
Overall impression Reassuring, Non-reassuring normal
OTHER RISK FACTORS OBSTETRIC COMPLICATIONS
• Lack of Pre-natal care • Multiple gestation
• Smoking • Postdate gestation
• Drug abuse • Previous caesarean section
• Intrauterine growth restriction
MATERNAL MEDICAL ILLNESS • Premature rupture of membranes
• Gestational diabetes • Congenital malformations
• Hypertension • Induction of labour
• Asthma • Pre-eclampsia
Foetal Tachycardia > 160 bpm
• Foetal hypoxia
• Chorioamnionitis: Maternal fever
• Hyperthyroidism
• Foetal or maternal anaemia
Foetal Bradycardia <120 bpm
Mild 100- 120 bpm
• Postdate gestation
Severe <80 bpm >3 mins
1. Prolonged cord compression
2. Cord prolapse
3. Epidural
4. Maternal seizure
5. Rapid foetal decent
DELIVER IMMEDIATELY IF CAUSE
NOT IDENTIFIED AND CORRECTED
Reduced Variability
• Foetal sleeping
• Foetal hypoxia
• Foetal tachycardia
• Prematurity <28 weeks gestation
Early decelerations
• Normal – physiological
• Start when uterine contraction begins and recover when uterine
contraction ends
 LATE DECELERATIONS
 BEGIN AT PEAK OF UTERINE CONTRACTIONS
 RECOVER AFTER CONTRACTION ENDS

PROLONGED DECELERATION
 DECELERATION > 2 MINS
 IF > 3 MINS ABNORMAL

BOTH REQUIER FOETAL BLOOD SAMPLING =IF ACIDOTIC = EMERGENCY C SECTION