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PBL SEM 4 > diabetes review > Flashcards

diabetes review Flashcards

1
Q

what is the gold standard test for diagnosing diabetes ?

A

oral glucose tolerance test

  • patient has to fast for at least 8 hours before test
  • then given 150g of glucose and glucose levels measured 2 hours later
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2
Q

what are normal fasting venous plasma glucose levels?

A

fasting < 6.1 mmol/L

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3
Q

what are fasting glucose levels in someone with impaired fasting glycaemia?

A

6.1-6.9 mmol/L

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4
Q

what are fasting glucose levels in someone with diabetes?

A

> _ 7mmol/L

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5
Q

what are glucose levels of someone with impaired glucose tolerance 2 hours post prandial?

A

> _7.8-11mmol/L

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6
Q

what are glucose levels of someone with diabetes 2 hours post prandial?

A

> 11mmol/L

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7
Q

what is HbA1c?

A

glycated haemoglobin

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8
Q

an HbA1c level above what reconfirms a T2D diagnosis?

A

> 48 mmol/mol

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9
Q

what do pancreatic B-cells express, which permit rapid glucose uptake regardless of the extracellular sugar concentration?

A

GLUT2

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10
Q

what cells produce insulin?

A

beta cells of Islets of Langerhans

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11
Q

when is insulin released?

A

in the presence of excess glucose

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12
Q

what are the Ca++ and K+ channels normally like in beta cells?

A
  • Ca++ channels normally closed — keeps Ca++ out
  • K+ channels normally open — -ve potential intracellularly
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13
Q

what happens when glucose enters the beta cell through GLUT2?

A
  • glucokinase breaks down the glucose
  • ADP —> ATP using the energy from the breakdown of glucose
  • ATP locks on to the K+ channels — closing them
  • K+ accumulates in cell
  • -ve potential inside the cell becomes +ve
  • Ca++ channels open
  • Ca++ enters
  • degranulation
  • insulin release
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14
Q

what happens in type I diabetes?

A

beta cells get destroyed —> no or very little insulin produced

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15
Q

what are the effects of insulin on the liver?

A

increased glucose uptake and glycogen synthesis

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16
Q

what are the effects of insulin on the muscle?

A

increase glucose uptake and glycogen synthesis

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17
Q

what are the effects of insulin on adipose?

A
  • increased glucose uptake and storage as fat
  • decreased breakdown to fatty acids (reserve energy)
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18
Q

what are the effects of insulin on blood?

A

glucose levels fall

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19
Q

what are the effects of a lack of insulin on the liver?

A
  • decreased glucose uptake
  • increased glycgoen breakdown and gluconeogenesis
  • conversion of fatty acids to ketone bodies
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20
Q

what are the effects of a lack of insulin on muscle?

A

decreased glucose uptake

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21
Q

what are the effects of a lack of insulin on adipose?

A
  • decreased glucose uptake and storage of fat
  • increased breakdown of fat and release of fatty acids
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22
Q

what are the effects of a lack of insulin on blood?

A

glucose levels rise

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23
Q

what enzyme is used in the breakdown of fat and release of fatty acids?

A

lipoprotein lipase

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24
Q

what happens when ketone bodies build up due to a lack of insulin?

A

H+ generated — there are initially buffered by as buffers are used up —> ACIDOSIS

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25
Q

how does low utilisation of glucose and increased endogenous production of glucose by the liver lead to dehydration and polypdipsia (increased thirst)?

A
  • low utilisation of glucose and increased endogenous production of glucose by the liver
  • hyperglycaemia
  • loss of glucose in urine : osmotic drag of glucose on water, water and glucose lost in urine, electrolytes lost along with water
  • increased urination (polyuria, nocturia)
  • dehydration and polypdipsia
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26
Q

80% of people with T1D at diagnosis have what antibodies?

A

GAD65

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27
Q

69-90% of people with T1D at diagnosis have what antibodies?

A

islet cell antibodies

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28
Q

what are specific tests to help diagnose T1D?

A
  • GAD65 antibodies
  • Islet Cell antibodies
  • ZnT8 antibodies
  • insulin antibodies (IAA)
  • C-peptide/insulin/glucose levels
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29
Q

as T1D progresses, what happens to C-peptide levels? what does this indicate?

A

levels fall — indicates lack of endogenous insulin production

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30
Q

___ blood glucose and low/absent _____ is very characteristic of T1D

A
  • high
  • C-peptide
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31
Q

describe T2D

A
  • due to insulin resistance
  • less acute onset compared to type 1
  • progressive decline in beta cell function
  • prediabetes : (at risk of diabetes/high risk for diabetes) — non-diabetic hyperglycaemia
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32
Q

in which diabetes is there a progressive decline in beta-cell function?

A

type 2

  • may have up to 50% beta cell loss at time of diagnosis
  • and 4-6% decline per year thereafter
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33
Q

what is the link between beta cell loss and medication?

A

as time goes by, previously effective medication becomes less effective a beta cells are no longer able to produce enough insulin

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34
Q

IGT vs IFT

A

IGT = impaired glucose tolerance
IFT = impaired fasting glucose

35
Q

what are modifiable risk factors for T2D?

A
  • overweight and obesity
  • sedentary lifestyle
  • previously identified glucose into leaven (IGT and/or IFG)
  • metabolic syndrome — hypertension, decreased HDL cholesterol, increased triglycerides)
  • dietary factors
  • intrauterine environment
  • inflammation
36
Q

what are non-modifiable risk factors for T2D?

A
  • ethnicity
  • family history of T2D
  • increasing age
  • history of gestational diabetes (in mother)
  • polycystic ovary syndrome (in mother)
37
Q

what BMI is classified as underweight for white European and asian populations?

A

less than 18.5 kg/m2

38
Q

what BMI is increasing but acceptable risk for ill health and premature death in white european and asian populations?

A
  • white europeans = 18.5-24.9 kg/m2
  • asian populations = 18.5-23 kg/m2
39
Q

what BMI is increased risk for ill health and premature death in white european and asian populations?

A
  • white europeans = 25-29.9 kg/m2
  • asians = 23-27.5 kg/m2
40
Q

what BMI is high risk for ill health and premature death in white european and asian populations?

A
  • white europeans = 30 kg/m2 or higher
  • asians = 27.5 kg/m2 or higher
41
Q

for every 1cm increase in waist, by what % does the risk of developing t2d and risk of IFG increase?

A

risk of t2d = 3.5%
risk of IFG = 3.2%

42
Q

for every 1 kg/m2 increase in BMI, how much does the risk of developing t2d and risk of IFG increase?

A

risk of t2d = 8.4%
risk of IFG = 9.5%

43
Q

on average, a 50 year old individual with diabetes and no history of vascular disease will die how many years earlier compared to someone without diabetes?

A

6

44
Q

what are the effects of decreasing HbA1c by 1%?

A
45
Q

what are the different treatment options for controlling hyperglycaemia in type 2 diabetes?

A
  1. lifestyle intervention = where we start
  2. insulin sensitisation eg. metformin, pioglitazone (thiazolidinedione)
  3. insulin secretion — DPP-4 inhibitors, GLP-1 receptor agonists, meglitinides, SUs
  4. glucose excretion = insulin independent — SGLT2 inhibitors
  5. insulin replacement — injected insulin
46
Q

look at power point for big treatment tables

A

ugh

47
Q

what is 1st line diabetes pharm treatment?

A

metforin

48
Q

metformin dose?

A

start at 500mg once daily, can increase up to 2g (can increase more up to 3g but not acutually very useful)

49
Q

when should metformin be used in caution?

A
  • chronic kidney disease : GFR <45 — decrease dose to 500mg. GFR <30 — stop metformin as it can increase the risk of lactic acidosis when GFR drops
  • illness — may need to stop to prevent lactic acidosis
50
Q

what is 2nd line drug treatment for diabetes?

A

SU = sulphonylurea ….. but can use other drugs

51
Q

how do sulphonylureas work?

A

bind to and close ATP sensitive K+ channels in pancreatic beta cells

52
Q

name a sulphonylurea

A

glicazide

53
Q

what is 3rd line therapy for diabetes?

A

in obese/overweight, if HA1c 64 (8%) eg. SGLT2i/DPP4-inhibitors/GLP1-receptor agonists

if HbA1c > 80 — will likely need insulin

54
Q

when should metformin be avoided?

A
  • eGFR <30
  • severe hepatic impairment
  • stop with intercurrent illness
55
Q

when is metformin MR (modified release) used?

A

if GI intolerance

56
Q

metformin onset?

A

slow onset — if need rapid control consider SU therapy

57
Q

what is a complication of metformin?

A

vitamin B12 deficiency — peripheral neuropathy

58
Q

what does metformin do?

A
  • decreases hepatic glucose production
  • decreases intestinal glucose absorption
  • improves insulin sensitivity in peripheral tissues
59
Q

in metformin there is a very low risk of what?

A

hypoglycaemia - because it works by increasing insulin sensitivity and if glucose levels are low it will not work

60
Q

what benefits can metformin have?

A

reduce CV mortality
mortality and cancer benefit
weight neutral - may even help lose a bit of weight

61
Q

alcohol and metformin?

A

alcohol can be used in moderation but it increases the risk effect of lactic acidosis

62
Q

when can hypoglycaemia occur with metformin?

A

RARE but can occur in:
- starvation
- excessive exercise when fasting
- alcohol intoxication

63
Q

what are the primary physiological actions of insulins (treatment)?

A
  • increases glucose disposal
  • decreases hepatic glucose production
64
Q

disadvantages of treatment with insulin?

A

hypoglycaemia
weight gain
injectable
training requirements

65
Q

what do meglitinides (glinides) do?

A

increase insulin secretion by acting on KATP channels

66
Q

what are the advantages of glinides?

A
  • shorter acting so can be used to decrease postprandial glucose excursions
  • dosing flexibility
  • can be used in those at risk of hypoglycaemia
67
Q

what do alfa-glucosidase inhibitors do?

A

slows intestinal carb digestion/absorption

68
Q

advantages of alfa-glycosidase inhibitors?

A
  • no hypoglycaemia
  • decrease post prandial glucose excursions
  • poss decrease CVD events
69
Q

what do SGLT2 inhibitors do?

A

increase glucose excretion from kidneys by blocking reabsorption

70
Q

advantages of SGLT2 inhibitors?

A

insulin independent mechanism

71
Q

disadvantages of SGLT2 inhibitors?

A

diuretic effect, thrush (due to glucose in urine)

72
Q

describe GLP-1 receptor agonists

A
  • injectable SC therapy and costs ££££
  • generally used as ‘add on’ therapy — 3rd line, earlier if weight loss desirable
  • weight loss, reduction in SBP
  • GI side effects
  • weekly, daily or BD
  • licence with insulin
  • weight loss benefit
  • need to stop if HbA1c <1% and 3% loss of weight not achieved at 6 months
73
Q

what are sympathetic signs of hypos?

A

sweating, tremulousness, palpitations, blurring, hunger, pins and needles

74
Q

what are neuroglycopenic signs of hypos?

A

confusion, incoordination, drowsiness, seizures, coma

75
Q

what is DKA?

A

diabetic ketoacidosis

76
Q

who is DKA seen in?

A

type 1 DM, new diagnosis, long standing type 2 rarely

77
Q

what levels are seen in DKA?

A
  • hyperglycaemia >11mol/L (may be normoglycaemic)
  • ketones >_3mmol/L, urine >2+ ketones
  • acidosis: bicarbonate <15, ph <7.3
78
Q

DKA treatment

A
  • IV fluids
  • K+ replacement
  • insulin replacement
  • replacement of electrolytes
  • LMWH, antibiotics
79
Q

what is HHS?

A

hyperosmolar hyperglycaemic state

80
Q

who is HHS seen in?

A

poorly controlled t2d

81
Q

what are osmolality levels in HHS?

A

> 320

82
Q

HHS treatment

A
  • IV fluids, IV fluids, IV fluids
  • replace electrolytes
  • IV insulin may be needed (only if glucose not dropping despite iv fluids)
  • LMWH (DVT prophylaxis)
83
Q

The progressive decline in beta-cell function during the natural history of type 2 diabetes might be expected to lead to what?

A

a gradual loss of effectiveness for antihyperglycaemic therapies that lower blood glucose levels via the action of endogenous insulin

84
Q

what agents might be expected to be effective at all stages of the natural history of t2d?

A

insulin independent therapies - they are combinable with insulin-dependent therapies

PBL SEM 4 (50 decks)

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