Type 2 Duabetes Flashcards

(46 cards)

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
what can metformin help with
decreasing hepatic glucose production, improving insulin sensitivity,increases peripheral glucose disposal Is biguanjde insulin sensitiser
26
what medications can boost insulin secretion?
sulphonylureas, DPP4-inhibitors, GLP-1 agonists
27
what medications can inhibit glucose reabsorption in kidneys and absorption in gut?
alpha glucosidase inhibitor, SGLT-2 inhibitor Targets circulating glycogen
28
metformin contraindications and side effects?
GI side effects severe liver/cardiac or moderate renal failure = contraindicated -
29
how do sulphonylureas help?
bind to and close ATP sensitive K+-channels regardless of glucose and ATP conc → required for insulin release
30
what is pioglitazone?
peripheral insulin sensitiser
31
what kind of drug is plioglitazine
PPAR agonist improvement in glycaemia and lipids, weight gain - peripheral not central
32
side effect of some glucose lowering therapies?
Weight gain
33
what is GLP-1?
gut hormone glucagon like peptide 1
34
When is GLP1 secreted
In response to nutrients in the gut
35
What cells is GLP1 secreted from and fcuntion
L cells Stimulates insulin and suppresses glucagon,increases satiety
36
what is the gastrointestinal incretin effect?
More insulin response to oral glucose than IV
37
what do GLP-1 agonists do?
Decrease glucagon and glucose causes weight loss Injectable daily/weekly Liraglutide and semaglutide
38
what do DPPG-4 inhibitors do?
Lengthen GLP1 half life Decrease glucagon and glucose but neutral on weight
39
SGLT2
empagliflozin, dapagliflozin Inhibit sodium glucose transporter so more glycosuria HbA1c lower,lower mortality,lower heart failure risk and improve CKD
40
What has the potential to induce remission if type 2 diabetes
gastric bypass surgery, potentially low-cal diets
41
other aspects of DM management?
hypertension, lipids (higher cholesterol (total and HDL), triglycerides raised)
42
Pathophysiology type 2
Genes and intrauterine environment and adult environment Insulin resistance and secretion defects
43
Type 2 consultation
Glycaemia HbA1c,glucose,med review Weight assessment Blood pressure Dylipidaemia-cholesterol profile Screen fir complications eg foot check and retinal screen
44
How else do we get glucose
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
SNP affect
Individual SNP have a mild affect Cumulative have buggee affects
46
Intra uterine growth retardation
Weight at age 1 less than 8.16kg 22% had type 2 diabetes If weight was >12.25 then 6% had type 2