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Year 2 Endocrinology > T2DM > Flashcards

T2DM Flashcards

(50 cards)

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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

Study These Flashcards
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

Study These Flashcards
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

Study These Flashcards
A

Retinopathy
Nephropathy
Neuropathy

24
Q

What are metabolic complications of T2DM

Study These Flashcards
A

Lactic acidosis

Hyperosmolar

25
What are macrovascular complications of T2DM
Ischaemic heart disease Cerebrovascular Renal artery stenosis PVD
26
What are complications of T2DM that can be due to treatment?
Hypoglycaemia
27
What is the basic management of T2DM
Education Diet Pharmacological treatment Complication screening
28
Why do you treat T2DM
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
What should patients with T2DM eat?
- 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
What should you monitor in T2DM
Weight Glycaemia Blood pressure Dyslidiaemia
31
What is a new exciting study of a new treatment for diabetes
Gastric bypass - improved diabetes control. Adverse events and nutritional deficiency increased therefore larger and longer trials needed
32
What is metaformin?
A biguanide, insulin sensitiser that reduces insulin resistance
33
How does metaformin work
It reduces insulin resistance by a reduced hepatic glucose output and an increased peripheral glucose disposal
34
When is metaformin used
In an overweight patient w/ T2DM where diet alone has not succeeded
35
When should metaformin not be used?
If severe liver, severe cardiac or mild renal failure
36
What is acarbose?
An alpha glucosidase inhibitor that prolongs the absorption of oligosaccharides therefore allowing insulin secretion to cope, following defective first phase insulin
37
What is the side effect of acarbose
Flatus
38
What are thiazolidinedones
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
What is an example of a thiazolidinedone
Pioglitazone
40
What are side effects of thiazolidinedones
Hepatitis, heart failure
41
What does GLP1 do?
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
What are treatment options for T2DM
``` Metaformin Acarbose Thiazolidinedone GLP1 agonists DPPG4 inhibitors (gliptins) Empaglifozin ```
43
What are GLP1 based treatment options?
GLP1 agonist or Gliptins (DPPG4 inhibitor)
44
What do GLP1 agonists do? What are examples of them
``` Exenatide, liraglutide (Injectable) Long acting GLP-1 agonist Decrease [glucagon] Decrease [glucose] Weight loss ```
45
What do gliptins do (DPPG4 inhibitors)
Increase half life of exogenous GLP-1 Increase [GLP-1] Decrease [glucagon] Decrease [glucose]
46
What does empaglifozin do?
Inhibits Na-Glu transporter, increases glycosuria | leading to lower HbA1c
47
What are other aspects of the body that should be controlled in T2DM
``` - Blood pressure Possibly 90% T2DM Clear benefits to treatment - Diabetic dyslipidaemia Cholesterol ↑ Triglyceride ↑ HDL-Cholesterol ↓ Clear benefits to treatment ```
48
What is the problem with screening for diabetes
The mortality, morbidity and cost. The specifics of screening programmes are unclear and which tests should be done and how often in who
49
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
lecure t2dm
50
How can insulin resistance lead to macrovascular disease
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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