Type 2 Duabetes Flashcards

1
Q

what is type II DM?

A

combination of insulin resistance + beta cell failure → hyperglycaemia

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2
Q

what kind of insulin deficiency is this

A

relative insulin deficiency

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3
Q

what are some predisposing factors?

A

genetic susceptibility, obesity

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4
Q

what ages does type II DM typically affect?

A

usually older/adults but youth and children can also be affected

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5
Q

Normal levels for fasting glucose,2 hour glucose and HbA1C

A
  • fasting glucose?less than 6 mmol/L
  • 2-hr glucose (oral glucose tolerance test)?less than 7.7 mmol/L
  • HbA1c?less than 42 mmol/L
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6
Q

levels indicative of type II DM for:

A
  • fasting glucose?above 7 mmol/L
  • OGTT?above 11 mmol/L
  • HbA1c?above 48 mmol/L
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7
Q

what do values in between these benchmarks sugges

A

intermediate state between normal and type II DM

  • intermediate stage
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8
Q

when in the progression towards type II DM is insulin production highest?

A

Intermediate stage
As it rises to combat increasing insulin resistance
Drops eventually following beta cells can be failure

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9
Q

what test in combination with what else can diagnose type II DM?

A

random glucose within DM range + symptoms of diabetes = diagnosis

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10
Q

can type II DM cause diabetic ketoacidosis?

A

yes but not under usual circumstances (due to relative insulin deficiency)

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11
Q

important consideration for long term type II DM?

A

late in disease course → can progress to complete insulin deficiency bc beta cell failure

important not to stop insulin treatment bc risk of ketoacidosis

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12
Q

what does the insulin response to glucose look like in type II DM?

A

First phase insulin release is lost

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13
Q

what are the consequences of reduced insulin action?

A

less uptake of glucose into muscles

more glucagon action

more hepatic production of glucose

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14
Q

consequences of insulin resistance in adipocytes?

A

less triglyceride formation and storage → more non-esterified fatty acids

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15
Q

An example of mono genic diabetes

A

MODY

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16
Q

What is polygenic diabetes

A

not born with certainty of developing diabetes → high risk contributed to by multiple polymorphisms + other factors

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17
Q

type II DM – associated conditions?

A

obesity (major), perturbations in gut microbiota due to bacterial lipopolysaccharides ferment to short chain FA, intrauterine growth retardation

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18
Q

how might patients with type II DM present?

A

overweight, hyperglycaemia, dyslipidemia

fewer osmotic symptoms

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19
Q

first line diagnostic tool for type II DM?

20
Q

how does this work in detail?

A

1x HbA1c above 48 mmol/L + symptoms

or

2x HbA1c above 48 mmol/L if asymptomatic

Also check for osmotic symptoms,infections. If acute then hyperosmolar hyperglycemia if chronic then ischaemic heart disease and retinopathy present

21
Q

how does a hyperosmolar hyperglycaemic state commonly present?

A

Renal failure

22
Q

Conditions for hyperosmolar hyperglycemia

A

insufficient insulin (not absent) for hyperglycaemia prevention

sufficient insulin for lipolysis and ketoacidosis suppression

Presents commonly with renal failure

23
Q

type II DM management?

A

diet and lifestyle adjustment, oral medication, education, possibly insulin later

24
Q

what specifically should diet adjustments aim to achieve?

A

total calorie control, less calories as simple carbs and fat and more as complex carbs

sodium down, soluble fibre up

25
Q

what can metformin help with

A

decreasing hepatic glucose production, improving insulin sensitivity,increases peripheral glucose disposal
Is biguanjde insulin sensitiser

26
Q

what medications can boost insulin secretion?

A

sulphonylureas, DPP4-inhibitors, GLP-1 agonists

27
Q

what medications can inhibit glucose reabsorption in kidneys and absorption in gut?

A

alpha glucosidase inhibitor, SGLT-2 inhibitor
Targets circulating glycogen

28
Q

metformin contraindications and side effects?

A

GI side effects

severe liver/cardiac or moderate renal failure = contraindicated

-

29
Q

how do sulphonylureas help?

A

bind to and close ATP sensitive K+-channels regardless of glucose and ATP conc → required for insulin release

30
Q

what is pioglitazone?

A

peripheral insulin sensitiser

31
Q

what kind of drug is plioglitazine

A

PPAR agonist

improvement in glycaemia and lipids, weight gain - peripheral not central

32
Q

side effect of some glucose lowering therapies?

A

Weight gain

33
Q

what is GLP-1?

A

gut hormone glucagon like peptide 1

34
Q

When is GLP1 secreted

A

In response to nutrients in the gut

35
Q

What cells is GLP1 secreted from and fcuntion

A

L cells
Stimulates insulin and suppresses glucagon,increases satiety

36
Q

what is the gastrointestinal incretin effect?

A

More insulin response to oral glucose than IV

37
Q

what do GLP-1 agonists do?

A

Decrease glucagon and glucose causes weight loss
Injectable daily/weekly
Liraglutide and semaglutide

38
Q

what do DPPG-4 inhibitors do?

A

Lengthen GLP1 half life
Decrease glucagon and glucose but neutral on weight

39
Q

SGLT2

A

empagliflozin, dapagliflozin
Inhibit sodium glucose transporter so more glycosuria
HbA1c lower,lower mortality,lower heart failure risk and improve CKD

40
Q

What has the potential to induce remission if type 2 diabetes

A

gastric bypass surgery, potentially low-cal diets

41
Q

other aspects of DM management?

A

hypertension, lipids (higher cholesterol (total and HDL), triglycerides raised)

42
Q

Pathophysiology type 2

A

Genes and intrauterine environment and adult environment
Insulin resistance and secretion defects

43
Q

Type 2 consultation

A

Glycaemia HbA1c,glucose,med review
Weight assessment
Blood pressure
Dylipidaemia-cholesterol profile
Screen fir complications eg foot check and retinal screen

44
Q

How else do we get glucose

A

Impaired glucose disposal and increased hepatic glucose increases rhe fasting glucose l else
Thus means that there is decreased storage of glucose thus decreased clearance of glucose which is converted to lactate
Lactate is then converted to glucose via rhe cori cori cycle which increases glucose levels again. The early increase in fasting glucose therefore is a result from the previous nights meal

As well as that impaired glucose levels cause increased glucagon secretion causing production of glucose

45
Q

SNP affect

A

Individual SNP have a mild affect
Cumulative have buggee affects

46
Q

Intra uterine growth retardation

A

Weight at age 1 less than 8.16kg 22% had type 2 diabetes

If weight was >12.25 then 6% had type 2