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YR2 LCRS Endocrinology > 16. Type II diabetes mellitus > Flashcards

16. Type II diabetes mellitus Flashcards

1
Q

which specific-tissues does DM cause long-term damage to?

A
  • retina
  • kidneys
  • nerves
  • arteries
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2
Q

what is macrovascular disease?

A

ischaemic heart disease and cerebrovascular disease (stroke)

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3
Q

what only occurs in diabetes?

A

microvascular disease

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4
Q

what is not seen in T2DM that is seen in T1DM?

A

ketosis

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5
Q

what should a normal 2-hour glucose be in an oral glucose tolerance test?

A

less than 7.8mmol/l

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6
Q

at what glucose values does a patient have DM?

A
  • fasting glucose is over 7mmol/l

- 2hr glucose is over 11mmol/l

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7
Q

outline the epidemiology of T2DM

A
  • 10% of 60 year olds suffer from diabetes (and most suffer from T2DM)
  • seen with increasing age
  • prevalence varies depending on ethnicity and environment
  • T2DM is occurring and being diagnosed younger
  • greatest in ethnic groups that have moved from rural to urban lifestyles
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8
Q

what is the pathophysiology of T2DM?

A
  • genes, intrauterine environment and adult environment have a role
  • most T2DM patients are insulin resistant
  • most patients have an insulin secretion defect
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9
Q

how many hereditary forms of Maturity Onset Diabetes of the Young (MODY) are there?

A

8 forms

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10
Q

what is MODY?

A
  • a genetic disease (autosomal dominant)
  • all patients have a positive family history and no obesity
  • ineffective pancreatic B cell insulin production
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11
Q

what are adipocytokines?

A

hormones made by fat cells that are a mechanism of T2DM

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12
Q

what is dyslipidaemia and what is associated with it? what does it lead to?

A

dyslipidaemia involves abnormal handling of cholesterol

it is associated with insulin resistance

it leads to macrovascular disease

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13
Q

why is light birth associated with diabetes in adulthood?

A

there are genes that are susceptible to epigenetic manipulation in-utero

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14
Q

what does T2DM present with?

A
  • obesity
  • insulin resistance and insulin secretion deficit
  • hyperglycaemia and dyslipidaemia
  • acute and chronic complications (though less than T1DM) e.g. hyperosmolar coma (acute), ischaemic heart disease and retinopathy (chronic)
  • osmotic symptoms
  • infections (yeast and microorganisms thrive in high glucose environments)
  • screening test
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15
Q

what causes diabetic dyslipidaemia?

A

very low density lipoprotein triglycerides

these are produced from triglycerides in adipocytes that break down and release glycerol and non-esterified fatty acids. the fatty acids go to the liver where they contribute to low density lipoprotein triglyceride production

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16
Q

what is a common side effect of diabetes treatment? treatment with what gives the exception?

A

weight gain

metformin is the only drug associated with weight maintenance/loss

17
Q

what two things alter and express defects or differences that can result in diabetes?

A
  • maternal microbiota

- adipocytokines

18
Q

what are the complications of T2DM?

A
  • microvascular: retinopathy, nephropathy, neuropathy
  • macrovascular: ischaemic heart disease, stroke, renal artery stenosis
  • metabolic: lactic acidosis, hyperosmolar complications
19
Q

how is T2DM managed?

A
  • education
  • diet
  • pharmacological treatment
  • complication screening
20
Q

why should T2DM be treated?

A
  • symptoms can be alleviated
  • chances of acute metabolic complications can be reduced
  • chances of long term complications can be reduced
21
Q

how should the diet of patients with T2DM change?

A
  • controlled calories
  • increased exercise
  • reduce refined carbohydrate
  • increase complex carbohydrate
  • reduce fat
  • increase unsaturated fat
  • increase soluble fibre
  • monitor salt intake
22
Q

what needs to be treated and monitored in T2DM?

A
  • weight (using an orlistat or surgery)
  • glycaemia
  • blood pressure
  • dyslipidaemia
23
Q

how is glycaemia treated?

A
  • metformin and insulin
  • sulphonylureas and metaglinides
  • a-glucosidase inhibitors
  • thiazolidinediones (act on central adiposity)
  • GLP-1 and DPP4 inhibitors
  • SGLT2 inhibitors
24
Q

what can improve diabetes control?

A

gastric bypass

25
Q

why is metformin used to treat T2DM?

A
  • acts as an insulin sensitiser
  • reduces insulin resistance
  • given when diet alone has not succeeded
  • safe (except some GI side effects)
26
Q

why are sulphonylureas used to treat T2DM?

A

sulphonylureas block ATP sensitive K+ channels even when there is little glucose, to induce insulin release (normally uptake of glucose leads to channel blockage)

if the patient has functional b-cells this will allow insulin secretion

27
Q

why is acarbose (alpha glucosidase inhibitor) used to treat T2DM?

A
  • prolongs oligosaccharide absorption in the gut

- allows insulin secretion to cope

28
Q

why are thiazolidinediones used to treat T2DM?

A
  • act as an insulin sensitiser, mainly peripheral effects

- improves glycaemia and lipids

29
Q

what are the side effects of sulphonyurea, acarbose and thiazolidinediones?

A

sulphonyurea - hypoglycaemia, weight gain

acarbose - flatus

thiazolidinediones - peripheral weight gain, hepatitis, heart failure

30
Q

what is the incretin effect?

A

food stimulates more insulin secretion if given orally rather than intravenously

31
Q

what roles does GLP-1 have in the body?

A
  • stimulates insulin and suppresses glucagon
  • restores b-cell glucose sensitivity
  • increases satiety
32
Q

how can the effects of GLP-1 be clinically manipulated?

A

GLP-1 agonists

  • injectable
  • decrease glucagon concentration and glucose concentration
  • result in weight loss

Gliptins (DPPG-4 inhibitors - DPPG-4 degenerates GLP-1)

  • increases half life of GLP-1
  • increases GLP-1 concentration
  • decreases glucagon concentration and glucose concentration
  • neutral on weight
33
Q

why are SGLT-2 inhibitors used to treat T2DM?

A
  • reduce glucose reabsorption
  • increase polyuria and polydipsia to control glucose
  • inhibits the Na-glucose transporter to increase glycosuria
  • causes HBA1C to be lower
34
Q

what are the other aspects of diabetic control?

A
  • anti-hypertensive treatment to control BP

- increasing HDL and reducing cholesterolaemia to treat diabetic dyslipidaemia

35
Q

how is diabetes screened?

A

look at glucose, fasting glucose and stimulated glucose in high risk individuals

YR2 LCRS Endocrinology (18 decks)

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