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Diabetes Mellitus
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What is Diabetes Mellitus?
Diabetes = to pass through
Mellitus = from honey, sweet
A chronic metabolic disease characterized by
high glucose levels in blood
Results from a lack of or reduced effectiveness
of endogenous insulin
This results in high blood glucose levels
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4% of Australians have diabetes and this
proportion is increasing every year
Carries risk of significant cardiovascular
morbidity and mortality
Affects multiple systems:
Neuropathy, retinopathy, vascular disease,
kidney disease, IHD
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Three Main Types of Diabetes
Type 1 DM
Type 2 DM
Gestational Diabetes
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Type 1 DM
Autoimmune destruction of insulin
producing pancreatic B cells in the islet of
Langerhan by T cells
Results in insufficient insulin production
Can occur at any age, but more common
in children, teenager, and young adults
Daily insulin injections are required
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In adults, Type 1 DM can develop as
Latent Autoimmune Diabetes of Adults
Slower disease progression to insulin
dependence
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Type 2 DM
A progressive loss of pancreatic beta cells
with insulin resistance
Usually occurs later in life however it is
becoming more prevalent in the younger
population due to obesity
Due to a combination of genetic and
environmental factors
Up to 60% can be prevented by diet and
exercise
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Type 2 DM Statistics
Accounts for over 90% of all diabetesAs at 30 June 2014 in Australia:
188 new diagnoses of Type 2 DM per day
68% > 60yo 23% 40 - 59yo
3% 20 - 39yo
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Type 2 DM Statistics
3 in 5 people have cardiovascular disease2/3 of people who die of a myocardial
infarction or stroke also have diabetes or
impaired glucose tolerance10% have long term vision loss
0.6% have ESKD
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Type 2 DM
Associated with:
Obesity
Lack of exercise
Excess alcohol intake
Excess calorie intake
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Type 2 DM
metformin
reduces hepatic gluconeogenesis and
hence insulin requirements
Does not cause weight gain
Gastrointestinal SE limit dosing - may be
better tolerated if slowly titrate dose upand taking it with food
Rare SE lactic acidosis
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Type 2 DM
sulfonylureas (eg gliclazide, glipizide,
glibenclamide, glimepiride)
increase insulin secretion
Cheap
Many years experience of use
Weight gain
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Type 2 DM
incretin-based therapies:
dipeptidyl peptidase-4 (DPP-4)
inhibitors (eg linagliptin, saxagliptin,
sitagliptin, vildagliptin)
increase the concentrations of incretin
hormones (GLP-1 and GIP) that are
produced in the gut following ingestion of
food; GLP-1 stimulates insulin release,
and reduces glucagon secretion
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Type 2 DM
thiazolidinediones (eg pioglitazone,
rosiglitazone)
reduce hepatic glucose output and
peripheral insulin resistance and hence
insulin requirements
weight gain and swollen feet are common
adverse effects - assess risk of fluid
retention before increasing dosage
Avoid in heart failure
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Type 2 DM
dipeptidyl peptidase-4 (DPP-4)
inhibitors (eg linagliptin, saxagliptin,
sitagliptin, vildagliptin)
Well tolerated
No weight gain or hypoglycemia
SE: common - headache, musculoskeletalpain
Rare S/E pancreatitis
No long term safety data
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Type 2 DM
dipeptidyl peptidase-4 (DPP-4)inhibitors (eg linagliptin, saxagliptin,
sitagliptin, vildagliptin)
All appear to have similar efficacy
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Type 2 DM
Glucagon-like peptide-1 (GLP-1)
receptor agonists (eg exenatide,
liraglutide)
synthetic analogues of GLP-1; increase
insulin secretion and reduce glucagon
secretion; also cause a small reduction in
appetite
Given S/C
Improves satiety and weight loss
Si nificant nausea that im roves with time
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acarbosealpha-glucosidase inhibitor
reduces the breakdown of complex
carbohydrate in the gut, thereby reducing
absorption of carbohydrate and hence
insulin requirements
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Acarbose has been shown to improve
HbA1c when added to other noninsulin
antihyperglycaemic drugs.
Poorly tolerated - it is taken with food,
begin at a low dose to minimise
gastrointestinal adverse effects such as
flatulence, bloating and diarrhoea.
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Type 2 DM
Sodium-glucose co-transporter 2
inhibitors (eg dapagliflozin)
reduce glucose reabsorption in the kidney
Causes an osmotic diuresis
Their short-term efficacy is modest, and
long-term efficacy and safety are unknown
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Type 2 DM
Insulin
Most people with type 2 diabetes
eventually require insulin treatment due to
the natural history of progressive beta cell
failure
SE: weight gain, hypoglycemia
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Type 2DM
Drug
Metformin
Sulfonylurea
Thiazolidinedione
DPP4-I
Acarbose
SGLT2 inhibitors
GLP1 agonist
Insulin
Effect on weight
Nil (decrease)
Increase
Increase
Nil
Nil
Decrease
Decrease
Increase
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Type 2 DM Management
Pathway1.Diet and exercise
2.Add metformin
3.Add either:Sulfonylurea
DPP4 inhibitor/GLP-1 agonist
Insulin
4.Add insulin +/- remove oral
antihypoglycemics (or triple therapy)
5.More complex insulin dosing required
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Type 2 DM
Addition of basal insulin (vs multiple
doses) to oral anti hypoglycemics causes
less weight gain and hypoglycemia
Basal insulin also gives better glycaemic
control, especially if given in the evening
long-acting insulin is usually given once
daily in the morning or evening. Start with
low dose (eg 10 units SC before evening
meal); increase dose in 24 unit
increments at intervals of 24 days.
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Type 2 DM
Management options should consider:
life-expectancy
glycaemic control risk of hypoglycaemia
comorbidities
preference (consider tolerability,complexity of the regimen, occupation,
and cost barriers for non-subsidised
options)
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Type 2 DM - Hypoglycemia
Symptoms: sweating, hunger, faintness,
palpitations, tremor, headache, visual
disturbance and altered mood
Insulin and sulfonylureas have a high risk
of hypoglycemia
Other drugs are less likely to cause
hypoglycemia alone
Combination of other drugs with insulin or
sulfonylureas can potentiate severe
hypoglycemia
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Type 2 DM
Generally, treatment targets are:
fasting blood glucose, 48 mmol/L
postprandial blood glucose, 6
10 mmol/L glycated haemoglobin concentration
(HbA1c), 53 mmol/mol (7%)
HbA1c(mmol/mol) = 10.93 x HbA1c(%)
23.5
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Type 2 DM
Also consider lowering cardiovascular risk:
Smoking cessation, hypertension, weight
management, hyperlipidaemia
low-dose aspirin in patients with
cardiovascular disease
an ACE inhibitor (or, if intolerant, a sartan)
to delay progression of renal disease in
patients with microalbuminuria or
proteinuria (including normotensive
patients)
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Gestational Diabetes Mellitus
(GDM) High blood glucose levels in a pregnant
woman without preexisting diabetes
Affects 1 in 20 pregnancies
Increased risk of: Miscarriage Preeclampsia
Congenital malformations
Macrosomia 3x need for Caesarean section delivery
4x risk of baby needing ICU care
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Gestational Diabetes
Dysregulation of blood glucose levels are
due to human placental lactogen and
progesterone
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Gestational Diabetes
Pregnant women are screened for GDM at 24-
28 weeks with an Oral Glucose Challenge Test,
if positive, confirm with an Oral Glucose
Tolerance Test Perform the test earlier if the woman has risk
factors e.g. previous GDM, obesity
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Gestational Diabetes
After the baby is delivered, blood glucose levels
usually improve or return to normal
Blood glucose should be tested again six weeks
after delivery If the woman becomes pregnant again, there is
a high chance of having GDM again
There is a 20-50% chance of the womandeveloping T2DM later in life
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Gestational Diabetes
Treatment of GDM is with diet control and s/c
insulin if needed
Frequent small meals with complex carbohydrates
Insulin is safe and efficacious Oral hypoglycaemic agents are contraindicated
due to risks to the baby
Metformin and glyburide have been trialed and shown
to be effective with no fetal adverse effects (no longterm data though)
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Summary
Diabetes is increasing in incidence
Carries risk of significant cardiovascular
risk as well as damage to other organs
Insulin is becoming used earlier in
treatment - better glycemic control and
preserves beta cell population
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References
Therapeutic Guidelines
AIHW
Diabetes Australia Australian Medicines Handbook
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