Endocrinology 16 - Type 2 Diabetes Mellitus Flashcards
1
Q
Define diabetes mellitus
A
Diabetes mellitus can be defined as a state of chronic hyperglycaemia sufficient to cause long-term damage to specific tissues, notably the retina, kidney, nerves, and arteries
2
Q
List the main characteristics of T2DM
A
- Not ketosis prone
- Not mild
- Often involves weight, lipids and blood pressure
3
Q
Describe the epidemiology of T2DM
A
- Diabetes 10% at 60 years (4-7% T2DM)
- Increasing age, but now seen in children
- Varies enormously, but is increasing
- Occurring and being diagnosed younger
- Greatest in ethnic groups that move from rural to urban lifestyle
4
Q
Describe pathophysiology of T2DM
A
- MODY (uncommon but useful insights)
- Genes and intrauterine environment, as well as adult environment
- Insulin resistance and secretion defects
- Fatty acids important in pathogenesis and complications
5
Q
What is maturity onset diabetes of the young?
A
- Several hereditary forms
- Autosomal dominant
- Ineffective pancreatic B cell insulin production
- Mutations of transcription factor genes, glucokinase gene
- Positive FH, no obesity
- Specific treatment for type
6
Q
Describe the onset and progression of T2DM
A
- Genes (more insulin needs to be produced their whole life, low insulin in the fetus, obesity in the adult)
- Dyslipidaemia caused by insulin resistance adipocytokines
- Insulin resistance and eventual B cell failure and insulin secretion deficit
- Increased hyperglycaemia and dyslipidaemia due to B cell failure
- Acute and chronic complications. May eventually need insulin
7
Q
How important is obesity in T2DM?
A
- More than a precipitant
- Fatty acids and adipocytokines important
- Central or omental particularly (drain directly to the liver)
- 80% T2DM obese at diagnosis
- Weight reduction is useful to adress in treatment
8
Q
How do gut bacteria relate to T2DM?
A
- Fatty acids released by the biome could enter the circulation and alter liver metabolism. Local fermentation of fatty acids
- More important in obesity association than diabetes
- Alter our signalling
- Alter inflammation and metabolic pathways
(correlative not causative at the moment)
9
Q
How does T2DM present?
A
- Heterogenous
- Obesity
- Insulin resistance and secretion deficit
- Hyperglycaemia and dyslipidaemia
- Osmotic symptoms
- Screening test
Acute and chronic complications
- Infections (due to high sugar)
- Hyperosmolar coma (acute complications)
- Ischaemic heart disease or retinopathy (chronic complications)
10
Q
List the complications of T2DM
A
Microvascular
- Retinopathy
- Nephropathy
- Neuropathy
Metabolic
- Lactic acidosis
- Hyperosmolar
Macrovascular
- Ischaemic heart disease
- Cerebrovascular
- Renal artery stenosis
- PVD
- Hypoglycaemia
11
Q
How is T2DM managed?
A
- Education
- Diet
- Pharmacological treatment
- Complication screening
12
Q
Why does T2DM need to be treated?
A
- Symptoms
- Reduce chance of acute metabolic complications
- Reduce change of long term contributions
13
Q
How do patients with T2DM need to eat?
A
- Control calories and increase exercise
- Reduce refined carbohydrate
- Increase complex carbohydrate
- Reduce fat as a proportion of calories
- Increase unsaturated fat as a proportion of fat
- Increase soluble fibre
- Address salt
14
Q
How is T2DM treated and monitored?
A
- Weight
- Glycaemia
- Blood pressure
- Dyslipidaemia
- Gasric bypass
- Metformin
- Acarbose
- Thiazolidinediones
- GLP-1
- Empaglifoxin
15
Q
What are the effects of metformin?
A
- Insulin sensitiser
- Used in overweight patients where diet has not succeeded
- Reduces insulin resistance
- GI side effects
- DO NOT USE if liver, cardiac or mild renal failure
