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LCRS Endocrinology > 16. Type 2 Diabetes Mellitus > Flashcards

16. Type 2 Diabetes Mellitus Flashcards

1
Q

Definition of Diabetes

A

A state of chronic hyperglycaemia sufficient to cause long-term damage to specific tissues, notably retina, kidneys, nerves and arteries

  • NOT ketosis prone
  • NOT mild
  • Often involves weight, lipids and blood pressure
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2
Q

Fasting blood glucose levels in T2DM

A

> 7mmol/L

In between defining markers for the mean and for diabetes:

  • Impaired fasting glucose 6-7mmol/L (fasting BG)
  • Impaired glucose tolerence 7.8-11.1mmol/L (glucose tolerence test)
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3
Q

Clinical significence of MODY (maturity onset diabetes of the young)

A

Gives metabolic insights into the pathophysiology of diabetes

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4
Q

Factors that influence the pathophysiology of T2DM

A
  • Genetics
  • Intrauterine environment- epigenetic changes that influence the functioning of genes over the rest of life
  • Adult environment

Fatty acid prevalence is also significant

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5
Q

MODY causes

A
  • Several hereditary forms
  • Autosomal dominant
  • Mutations of transcription factor genes + glukokinase gene
  • Ineffective pancreatic Beta cell insulin production
  • No obesity in patients with a positive family history

Treatment is dependant on type

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6
Q

Role of adipocytokines in T2DM

A

Inflammatory factors secreted by adipose tissue (IL6-TNFa) can contibute to insulin resistence

Secretion is increased in obesity

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7
Q

Initial problems of insulin resistence (before hyperglycaemia)

A
  • Metabolic dyslipidaemia
  • Stimulates the mitogenic pathway which causes smooth muscle hypertrophy and increased BP
  • Dyslipidaemia and hypertension increase the risk of macrovascular disease (e.g progressive atheroma in arteries)

This can all happen while the blood sugar is normal- 50% of patients present with complications of diabetes

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8
Q

Low birth weight link to diabetes

A

Low birth weight increases the risk of impaired glucose tolerence and diabetes

This is believed to be due to an epigenetic effect

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9
Q

Relationship between insulin secretion and resistence in old age

A
  • As we grow older we produce less and less insulin
  • We also become more and more insulin resistent

At some point, resistence and secretion will intersect meaning we dont produce enough insulin- around 110 years in caucasions

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10
Q

Phases of insulin secretion

A

Following intake of glucose, a normal individual will have TWO phases of insulin secretion

  1. 1st Phase- stored insulin that is ready to be released
  2. 2nd Phase- Over a period of time, more insulin is produced and released

Patients with T2DM will have no insulin response

People with IGT (impaired glucose tolerence) will still have some insulin production but will loose their first phase response- takes longer to produce a response. Can get around this with complex carbohydrates

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11
Q

Cause of increased blood gluocse in T2DM

A

Insulin lowers blood glucose by reducing Hepatic Glucose Output and increasing glucose disposal:

  • When we have not eaten HGO maintains BG at 4mmol/L
  • Afer we have eaten insulin reduces HGO
  • It also drives any excess glucose into muscle and adipose tissue

FPG= fasting plasma glucose

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12
Q

Relationship between insulin sensitivity and insulin secretion

A

There isnt a single correct amount of insulin that we should produce- this is dependant upon how insulin resistant we are:

  • As we get older our sensitivity decreases so our secretion should increase to maintain normal PG
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13
Q

Effects of insulin resistence

A

Adipocytes contain triglycerides which can be broken down into glycerol and Non-esterified fatty acids (NEFA)

  • Insulin would prevent this breakdown (no need for gluconeogenesis)

Breakdwon is particularly marked for omental adipocytes (why waist circumference is a good predictor for ischaemic heart disease)

Glycerol and NEFA travel to the liver

In the liver: glycerol is used to make glucose- gluconeogenesis and glucose is then released- glycogenolysis

  • Insulin would decrease HGO

NEFA cannot be used to produce glucose, but is instead used to produce VLDLs which are ATHEROGENIC- why insulin resistence contributes to atherogenic profile

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14
Q

Link between obesity and T2DM

A

80% of T2DM patients are obese- weight reduction is a useful treatment

  • Obesity is part of the mechanism for diabetes- Adipocytokines modulate insulin resistence
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15
Q

Gut microbiota link to T2DM

A
  • The gut microbiome appears to be assoicated with obesity, insulin resistence and T2DM
  • Various lipopolysaccharides are fermented by the gut bacteria into short chain fatty acids
  • These short chain FAs can then enter the circulation and modulate bile acids
  • This is a trigger for inflammation and the adipocytokine pathway
  • Microbiota transplants are being investigated as a treatment method
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16
Q

Complications of T2DM

A

Can be split into FOUR seperate catagories

1. MICROVASCULAR

  • Retinopathy
  • neuropathy
  • Nephropathy

2. MACROVASCULAR

  • Ishcaemic heart disease
  • Cerebrovascular
  • Renal artery stenosis

3. METABOLIC (much rarer than in T1DM)

  • Lactic acidosis
  • Hyperosmolar

4. TREATMENT

  • Hypoglycaemia
17
Q

Basic catgories of treatment in T2DM

A
  • Education
  • Diet
  • Pharmacological treatment
  • Complication screening
18
Q

Diet changes required in T2DM

A

Complec carbohydrates speads out the carbohydrate load meaning there is no need for first phase insulin release:

  • Control total calories/ increase exercise (to control weight)
  • Reduce REFINED CARBOHYDRATES
  • Increase COMPLEX CARBOHYDRATES
  • Reduce fat as a proportion of calories
  • Increase soluble fibre (to increase absorbtion time for CHO)
19
Q

What should be monitored in T2DM?

A
  • Weight
  • glycaemia
  • blood pressure
  • Dyslipidaemia
20
Q

Main drugs used in the treatment of T2DM

A
  • Orlistat- pancreatic lipase inhibitor
  • Mataformin- used to treat insulin resistence in teh liver
  • Sulphonylureas- increases insulin secretion
  • Alpha glucosidase inhibitor- delays glucose absorption
  • Thiazolidinediones- act on adipocytes and address peripheral insulin resistence
21
Q

Metaformin effects and side effects

A

Metaformin is an oral antihyperglycaemic drug- a biguanide

  • It is an insulin sensitiser
  • Used in almost all T2DM patients but more ofetn in obese patients
  • Reduces insulin resistence

Side effects:

  • Has adverse GI effects: should not use if patient has severe liver, cardiac or renal failure
22
Q

Beta cells function

A
  • Glucose is transported into the beta cell via GLUT-2 transporters
  • Glucokinase then converts is to G-6-phosphate etc.
  • ATP is used to close a K+ ATP sensitive channel, cuasing hyperpolarisation
  • Ca2+ influx is then triggered via a VG channel, causing insulin exocytosis

SULPHONYLUREAS block the ATP sensitive potassium channel- cuasing insulin secretion

23
Q

Glibenclamide effect and side effects

A

This is a sulphonylurea (insulin SECRETAGOGUE)

  • Used in lean patients with T2DM where diet alone has been ineffective

Side effects:

  • Hypoglycaemia
  • Weight gain
24
Q

Acarbose effects and side effects

A

Acarbose is an alpha glucosidase inhibitor

  • Prolongs the absorption of oligosaccharides
  • Allows insulin secretion to cope with the loss of first phase insulin release
  • AS EFFECTIVE AS METAFORMIN

Side effects:

  • Sugars reach the large intestine where they are fermented so gas is a problem
25
Q

Thiazolidinediones effect and side effects

A

A peroxisome proliferator-activated receptor (PPARy) agonist

E.G Pioglitazone

  • Insulin sensitiser- mainly peripheral
  • Improvement in glycaemia and hyperlipidaemia
  • Good vascular outcomes
  • Adipocyte differentiation is modified

Side effects:

  • Hepatitis
  • Heart failure
26
Q

Glucagon like Peptide-1 release and effects

A

Oral glucose load triggers a bigger insulin release than is seen when the same glucose is given IV- this is the INCRETIN EFFECT

  • GLP-1 is a gut hormone released in response to food in the gut
  • Transcription product of the pro-glucagon gene
  • Released by L cells
  • Stimulates insulin and suppressed glucagon
  • Increases satiety

It has a short half life due to rapid degredation by dipeptidyl peptidase- 4

GLIPTINS inhibit DPP-4 and therefore make GLP-1 last longer

27
Q

Other important monitoring treatments

A

There are separate treatments for the different aspects of diabetes e.g. blood pressure, blood sugar, cholesterol

28
Q

Methods of preventing the progression of diabetes

A

This can be achieved by indentifying individuals likely to develop the disease:

  • Gestational diabetes- a temporary diabetes that is experienced by some pregnant woment- helps to identify high risk women
  • Impaired glucose tolerence- will almost always lead to diabetes in the future
29
Q

T1DM vs T2DM

A

LCRS Endocrinology (18 decks)

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