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Year 2 Endocrinology > T2DM > Flashcards

T2DM Flashcards

1
Q

Define diabetes

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

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2
Q

What is the difference between T1DM and T2DM

A

T2DM is not ketosis prone
T2DM is not mild
T2DM often involves weight, lipids and blood pressure

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3
Q

What is the prevalence of T2DM

A

It varies enormously but is increasing and greatest in ethnic groups that move from rural to urban lifestyles

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4
Q

What gives useful metabolic insights into T2DM

A

MODY relatively uncommon but gives useful metabolic insights

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5
Q

What defects, environments and genes can cause or increase chances of T2DM

A
  • Genes and intrauterine environment (intrauterine growth restriction increases chances of developing T2DM) and adult environment.
    Insulin resistance and insulin secretion defects
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6
Q

What is important in the pathogenesis and complications of T2DM

A

Fatty acids important in pathogenesis and complications

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7
Q

What is MODY

A

Maturity onset diabetes of the young, an autosomal dominant condition with several hereditary forms (1-8) with a positive family history and obesity

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8
Q

What is MODY due to?

A

Ineffective pancreatic B cell insulin production due to mutations of transcription factor genes, glucokinase gene.

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9
Q

What have twin studies shown about diabetes

A

T2DM follows an almost autosomal dominant pattern whereas T1DM has less genetic input.

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10
Q

What is the presentation of T2DM

A

Obese, hyperglucaemic, dyslipidaemia, acute and chronic complications

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11
Q

What is the metabolic problems that cause T2DM

A

There is insulin resistance and insulin secretion deficits

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12
Q

What are the effects of fatty acids and how are they different in obesity and T2DM

A 
In Obesity and T2DM they are elevated
↑ IR Whole body muscle and liver 
↓ B cell function
↑ Liver TG secretion
↑ Organ fat, oxidative stress
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13
Q

What does TNF alpha and IL 6 do?

A

↑ IR Whole body and muscle

↓ adiponectin expression

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14
Q

What is the effects of leptin and what are the changes in it during obesity?

A

Elevated in obesity
↑ IR Whole body muscle and liver
↓ appetite
↑ metabolic rate

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15
Q

What are the effects of glucocorticoids

A

↑ 11β HSD-1 in fat
↑ fat cell size and IR
↑ glucose BP Lipids

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16
Q

What are the effects of endocannabinoids?

A

Insulin inhibits expression in fat

Fat IR > ↑ circulating EC

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17
Q

What are the effects of adiponectin?

A

↓ insulin resistance

Predictive of diabetes

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18
Q

What are the effects of visfactin and where is it found?

A

Visceral fat

↓ IR Whole body

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19
Q

What are the effects of apelin?

A

Insulin stimulates expression in fat
Elevated in hyper Insulin
CV effects

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20
Q

What are the effects of resistin and how are they different in obesity and T2DM

A

Elevated in obesity and T2DM
↑ IR Whole body and liver
↑ Liver TG secretion

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21
Q

What is the link between obesity and T2DM

A
  • More than a precipitant
  • Fatty acids and adipocytokines important
  • Central or omental obesity
  • 80% T2DM are obese
  • Weight reduction useful treatment
22
Q

What is the presentation of T2D

A
  • Osmotic symptoms
  • Infections
  • Screening test
    at presentation of complication
  • Acute; hyperosmolar coma,
  • Chronic; ischaemic heart disease, retinopathy
23
Q

What are microvascular complications of T2DM

A

Retinopathy
Nephropathy
Neuropathy

24
Q

What are metabolic complications of T2DM

A

Lactic acidosis

Hyperosmolar

25
Q

What are macrovascular complications of T2DM

A

Ischaemic heart disease
Cerebrovascular
Renal artery stenosis
PVD

26
Q

What are complications of T2DM that can be due to treatment?

A

Hypoglycaemia

27
Q

What is the basic management of T2DM

A

Education
Diet
Pharmacological treatment
Complication screening

28
Q

Why do you treat T2DM

A

Symptoms
Reduce chance of acute metabolic complications (unlikely in T2DM)
Reduce chance of long term complications; good evidence base (UK prospective diabetes study or UKPDS)

29
Q

What should patients with T2DM eat?

A
  • Control total calories/increase exercise (weight)
  • reduce refined carbohydrate (less sugar)
  • increase complex carbohydrate (more rice etc)
  • reduce fat as proportion of calories (less IR)
  • increase unsaturated fat as proportion of fat (IHD)
  • increase soluble fibre (longer to absorb CHO)
  • Address salt (BP risk)
30
Q

What should you monitor in T2DM

A

Weight
Glycaemia
Blood pressure
Dyslidiaemia

31
Q

What is a new exciting study of a new treatment for diabetes

A

Gastric bypass - improved diabetes control. Adverse events and nutritional deficiency increased therefore larger and longer trials needed

32
Q

What is metaformin?

A

A biguanide, insulin sensitiser that reduces insulin resistance

33
Q

How does metaformin work

A

It reduces insulin resistance by a reduced hepatic glucose output and an increased peripheral glucose disposal

34
Q

When is metaformin used

A

In an overweight patient w/ T2DM where diet alone has not succeeded

35
Q

When should metaformin not be used?

A

If severe liver, severe cardiac or mild renal failure

36
Q

What is acarbose?

A

An alpha glucosidase inhibitor that prolongs the absorption of oligosaccharides therefore allowing insulin secretion to cope, following defective first phase insulin

37
Q

What is the side effect of acarbose

A

Flatus

38
Q

What are thiazolidinedones

A

Peroxisome proliferator-actived receptor agonists PPAR-γ that are insulin sensitizers, mainly peripheral. Adipocyte differentiation modified, weight gain but peripheral not central. Improvement in glycaemia and lipids according to evidence based on vascular outcomes

39
Q

What is an example of a thiazolidinedone

A

Pioglitazone

40
Q

What are side effects of thiazolidinedones

A

Hepatitis, heart failure

41
Q

What does GLP1 do?

A

Transcription product of proglucagon gene, mostly from L cell and secreted in response to nutrients in the gut
-> Stimulates insulin, suppresses glucagon SO Increases satiety and restores B cell glucose sensitivity

42
Q

What are treatment options for T2DM

A 
Metaformin
Acarbose
Thiazolidinedone
GLP1 agonists
DPPG4 inhibitors (gliptins)
Empaglifozin
43
Q

What are GLP1 based treatment options?

A

GLP1 agonist or Gliptins (DPPG4 inhibitor)

44
Q

What do GLP1 agonists do? What are examples of them

A 
Exenatide, liraglutide
(Injectable)
Long acting GLP-1 agonist
Decrease [glucagon]
Decrease [glucose]
Weight loss
45
Q

What do gliptins do (DPPG4 inhibitors)

A

Increase half life of exogenous GLP-1
Increase [GLP-1]
Decrease [glucagon]
Decrease [glucose]

46
Q

What does empaglifozin do?

A

Inhibits Na-Glu transporter, increases glycosuria

leading to lower HbA1c

47
Q

What are other aspects of the body that should be controlled in T2DM

A 
- Blood pressure
Possibly 90% T2DM
Clear benefits to treatment
- Diabetic dyslipidaemia
Cholesterol ↑
Triglyceride ↑
HDL-Cholesterol ↓
Clear benefits to treatment
48
Q

What is the problem with screening for diabetes

A

The mortality, morbidity and cost. The specifics of screening programmes are unclear and which tests should be done and how often in who

49
Q

Can you draw a table comparing prevalence, typical age, onset, habitus, family history, geography, weight loss, ketosis prone, serum insulin, HLA association, Islet B cells and islet abs between t1 and t2 DM

A

lecure t2dm

50
Q

How can insulin resistance lead to macrovascular disease

A

Insulin resistance leads to dyslipidaemia leading to increased mitogenic pathway leading to hypertrophy and increased BP leading to macrovascular disease

Year 2 Endocrinology (21 decks)

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