Diabetes type 2

• Definition. A condition where there is

increase in insulin resistance which leads to
increased insulin secretion in order to
maintain the normal sugar level.
• However in susceptible people the beta
pancreatic cells are unable to sustain the
increased demand for insulin and slowly
insulin deficiency develops and blood glucose
level rises.
Natural history of type 2 diabetes.A In the early stage of the disorder,
the response to progressive insulin resistance is an increase in insulin
secretion by the pancreatic cells, causing hyperinsulinaemia. Eventually,
the β cells are unable to compensate adequately and blood glucose
rises, producing hyperglycaemia. With further β-cell failure, glycaemic
control deteriorates and treatment requirements escalate. B Progressive
pancreatic β-cell failure in patients with type 2 diabetes in the United
Kingdom Prospective Diabetes Study (UKPDS). Beta-cell function was
estimated using the homeostasis model assessment (HOMA) and was
already below 50% at the time of diagnosis. Thereafter, long-term
incremental increases in fasting plasma glucose were accompanied by
progressive β-cell dysfunction. If the slope of this progression is
extrapolated, it appears that pancreatic dysfunction may have been
developing for many years before diagnosis of diabetes.
• In type 2 diabetes excessive production of
glucose from the liver and under utilization of
glucose by the skeletal muscles result from
resistance to the action of insulin.
• A characteristic feature of type 2 DM is its
association with the following disorders;
1. central (visceral) obesity
2.hypertension
3.dyslipidaemia-characterised by;
elevated LDL
elevated triglycerides
low level HDL
The existence of these cluster of conditions
predispose to cardiovascular disease known as
metabolic syndrome
Other factors that contribute to DM type 2
-Progressive reduction of Beta cells in the pancreas.
-Genetic predisposition
-Environmental – overeating and inactivity
-Age – a disease of middle age and above.
-Prevalence increase with age
-Pregnancy
 investigations
• Urine glucose
• When blood glucose rises above 10mmol/l the
renal threshold, glucose is passed in urine and
urine glucose test is positive.
In pregnant women and children one can have
low threshold due to high GFR and urine glucose
may not be significant.
• Urine ketones
simple dipstick can detect ketones in urine.
This can be found in normal people who have
been fasting, exercising for long periods or
vomiting or those who have been taking a diet
with high fat and low carbohydrate.
When there ketones in urine and its associated
with glycosuria its highly likely to be diabetic
ketoacidosis
• Complete blood count
• Urea and electrolytes
• Lipid profile
• Many patients with type 2 dm are
asymptomatic, others present with;
• Classic symptoms; polyuria, polydypsia,
polyphagia and weight loss.
• Blurred vision
• Lower extremity paraesthesias
• Yeast infections e.g recurrent vaginitis,
balanitis etc
 Diagnosis
• FBS ≥ 7 mmol/l
• 2 hour plasma glucose of ≥11.1mmol/l after
ingestion of 75gm glucose in –OGTT
• A random plasma glucose of ≥11.1 with classic
symptoms
• HbA1c ≥ 6.5
 Management
GOALS
1. treatment of immediate complications-dehydration,
hyperglycemia, electrolyte imbalance, acidosis.
2. Microvascular (eye, kidney damage) risk reduction
through control of glycemia and blood pressure
3. Macrovascular (ie coronary. Cerebrovascular, peripheral
vascular) risk reducton through control of lipids and
hypertension, smoking cessation
4. Metabolic and neurologic risk reduction through control
of hyperglycemia
 Current position professional bodies

1.Individualised glycemic targets and glucose

lowering agents by titrating drugs dosage against
blood sugar.
2.Diet, exercise and education
3. Use of metformin as the optimal first line drug
unless contraindicated
4. After metformin, the use of 1or 2 additional
oral or injectable agents with a goal of minimizing
adverse effects if possible
• 6. where possible treatment decisions should
involve the patient with the focus of patient
preferences, needs and values
• 7. a major focus comprehensive cardiovascular
risk reduction
• Patients on intensive insulin therapy
monitoring should involve blood sugar levels
before meals and occasionary after meals
 Prevention of complications
• HbA1c every 3-6 months
• Yearly dilated eye examinations
• Annual micro albumin and uec checks
• Foot examinations for each visit
• Blood pressure ≤ 130l80 mmHg lower in
diabetic nephropathy
• statin therapy to reduce LDL lipoprotein
cholesteral
 Oral hypoglycemics
• Biguanides
• Action –decrease hepatic glucose production
-decrease git glucose absorption
-increase target cell insulin sensitivity
Example ; metformin
C/indication-metabolic acidosis, with or without
coma, abnormal creatinine clearance including
DKA shock, septicemia renal dx, HONK
• Sulfonylurea- increase beta cell insulin
production, decrease hepatic glucose output,
and increase insulin receptor sensitivity at
peripheral target tissues
• Eg glyburide,glipizide,glimepiride, tolazamide
tolbutamide and glibeclamide
Side effects-hypoglycemia
c/I sulfa allergy, type 1 dm, dka
• Thiazolidinediones
• Action –increase insulin receptor sensitivity
and influence the production of gene products
involved in lipid and glucose metabolism; their
action depends on the insulin for activity
• Examples-pioglitazone, rosiglitazone
c/i- hypersensitivity to product or established
heart failure –NYHA –class iii or iv
• Meglitinides
• Alpha glucosidase inhibitors
• Incretin agonist
• DPP4 inhibitors