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BRS YEAR 2 > Type 2 Duabetes > Flashcards

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

19
Q

first line diagnostic tool for type II DM?

A

HbA1c

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

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

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

BRS YEAR 2 (42 decks)

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