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BRS YR2 > Type 2 Diabetes Mellitus > Flashcards

Type 2 Diabetes Mellitus Flashcards

1
Q

What is type 2 diabetes?

A
  • condition with the combination of insulin resistance and beta cell failure in hyperglycaemia
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2
Q

How does the WHO classify T2DM?

A
  • genetic risk + obesity
  • insulin resistance
  • relative insulin deficiency
  • hyperglycaemia
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3
Q

What is latent autoimmune diabetes in adults(LADA)?

A
  • autoimmune diabetes leading to insulin deficiency present later in life
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4
Q

How can monogenic diabetes present phenotypically?

A
  • T1DM
  • T2DM
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5
Q

When can T2DM present?

A

Can present in all decade of life

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6
Q

When is the prevalence of T2DM greatest?

A

ethnic groups that move from rural > urban lifestyle

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7
Q

What fasting glucose levels indicate T2DM?

A

+7mmol/L

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8
Q

What 2hr glucose tolerance test results indicate T2DM?

A

+11mmol/L

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9
Q

What random glucose levels indicate T2DM?

A

+11.1mmol/L

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10
Q

What can be used to diagnose T2DM?

A
  • random glucose (high)
  • symptoms of diabetes
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11
Q

Why does T2DM not cause ketosis under normal circumstances?

A

due to T2DM being a relative insulin deficiency (insulin is produced but not enough to overcome resistance)

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12
Q

What happens in long-duration T2 diabetes?

A
  • beta-cell failure may progress to complete insulin deficiency
  • usually on insulin, DO NOT STOP (ketoacidosis)
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13
Q

What is the biggest contributory factor to the development of type 2 diabetes?

A

both

  • beta cell failure
  • insulin resistance
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14
Q

What is a normal fasting glucose levels?

A

<=6mmol/L

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15
Q

What does it mean if fasting glucose levels are between 6-7mmol/L?

A

Impaired fasting glycaemia

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16
Q

What 2hr glucose tolerance test results are normal?

A

<7.7mmol/L

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17
Q

What HbA1c levels indicate type 2 diabetes?

A

> =48mmol/mol

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18
Q

What HbA1c levels are normal?

A

<42mmol/mol

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19
Q

What does 2hr glucose tolerance test result between 7.7-11 mmol/L indicate?

A

Impaired glucose tolerance

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20
Q

What does HbA1c levels between 42-48mmol/mol mean?

A

pre-diabetes or non-diabetic hypergylcaemia

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21
Q

What happens to insulin during T2 diabetes?

A
  • maximum insulin resistance
  • reduced insulin production
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22
Q

What happens to insulin during the intermediate stage of developing T2 diabetes

A
  • increasing resistance
  • maximum insulin production
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23
Q

What is a rapid way to diagnose T2 diabetes?

A

random glucose (>11.1), and symptoms

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24
Q

What happens to beta cell mass when developing T2DM?

A

already reduced at time of diagnosis

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25
Q

What does a relative insulin deficiency mean?

A

insulin is produced by pancreatic beta-cells but not enough to overcome insulin resistance

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26
Q

When does ketoacidosis typically form?

A

when there is no insulin

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27
Q

What makes the tissues resistance to the action of insulin?

A

a mix of:

  • adipose cytokines (adipokines)
  • internal adiposity (fatty acids)
  • pro-inflammatory state
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28
Q

Why is diabetes heterogenous?

A

variable:

  • BMI
  • ages
  • progression
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29
Q

What is one of the first signs of developing T2DM?

A

the loss of the first phase insulin release

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30
Q

What is the impact of the loss of first phase insulin release?

A
  • less uptake of glucose into skeletal muscle
  • hepatic glucose production is increased due to a reduction in insulin action and an increase in glucagon action.
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31
Q

What is the impact of high glucose?

A
  • impaired insulin-mediated glucose disposal
  • excessive glucagon-mediated glucose disposal
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32
Q

What is the relationship between insulin secretion and insulin sensitivity in T2DM?

A

Low insulin sensitivity, low insulin secretion

33
Q

What are the consequences of insulin resistance?

A
  • increased hepatic glucose production
  • adipocytes, increased fatty acid uptake, and triglycerides form unhealthy lipids (usually inhibited insulin)
  • less glucose muscle uptake
34
Q

What does monogenic mean?

A

single gene mutation (eg; MODY)
inevitable development

35
Q

What does polygenic mean?

A

polymorphisms increasing the risk of diabetes
factor dependent

36
Q

What types of mutations cause T2DM?

A

polygenic

37
Q

What causes T2DM?

A
  • genetic risk
  • strong environmental factor (precipitant)
38
Q

What is the role of obesity in T2DM?

A
  • major risk factor
  • 80% of T2DM are obese
39
Q

What is central obesity?

A

excess fat in the abdominal area

40
Q

What are other factors implicating developing T2DM?

A
  • pertubations in microbiota
  • intra-uterine growth retardation (little when born)
41
Q

How does T2DM present?

A
  • hyperglycaemia
  • overweight
  • dyslipidaemia
  • fewer osmotic symptoms (blurred vision, polyuria…)
  • complications (eg retinopathy)
  • insulin resistance
  • later insulin deficiency
42
Q

What are the risk factors of T2DM?

A
  • age
  • high BMI
  • ethnicity
  • PCOS
  • family history
  • sedentary
43
Q

What is the first line test for diagnosis?

A

HbA1c
1 x HbA1c >=48mmol with symptoms
or
2 x HbA1c >=48mmol asymptomatic

44
Q

What is an acute metabolic decompensation?

A
  • life threatening state due to hyperglycaemia
  • in T2DM hyperosmolar hyperglycaemic state
45
Q

What is hyperosmolar hyperglycaemic state?

A

unchecked gluconeogenesism and osmotic diuresis

46
Q

How does hyperosmolar hyperglycaemic state present?

A

commonly presents with renal failure

unlikely to present with acidosis

47
Q

Why does a hyperosmolar hyperglycaemic state occur?

A

insufficient insulin for prevention of hyperglycaemia but sufficient insulin for suppression of lipolysis and ketogenesis

48
Q

How do you manage T2DM?

A
  • diet + physical activity
  • oral medication
  • education
  • insulin later
  • remission/reversal
49
Q

What are the complications associated with T2DM?

A
  • retinopathy
  • neuropathy
  • nephropathy
  • cardiovascular problems
50
Q

How do you prevent the complications associated with T2DM?

A
  • good cholesterol
  • good HbA1c
  • good blood pressure
51
Q

What is involved in a T2DM consultation?

A
  • glucose levels
  • weight assessment
  • blood pressure
  • cholesterol profile
  • complications screening
52
Q

How do you check on glucose levels for a consultation?

A
  • HbA1c
  • if on insulin, glucose monitor
53
Q

How do you screen for the complications associated with T2DM?

A
  • foot check
  • retinal screening
  • urine test
54
Q

What are the dietry recommendations for T2DM?

A 
- calorie control 
reduce:
- fat
- refined carbohydrates
- sodium
increase
- complex carbohydrates
- soluble fibre
55
Q

What treats all 4 aspects for T2DM pathophysiology?

A

weight loss

56
Q

What can be used to treat the excess hepatic glucose production in T2DM?

A

metformin

57
Q

What can be used to increase insulin sensitivity in T2DM?

A
  • metformin
  • thiozolidinediones
58
Q

What can be used to boost insulin secretion?

A
  • sulphonylureas
  • DPP4 inhibitors
  • GLP-1 agonists
59
Q

What can be used to inhibit carbohydrate gut abosrption and renal glucose absorption to reduce the excess glucose in circulation?

A
  • alpha glucosidase inhibitor
  • SGLT-2 inhibitor
60
Q

What is Metformin?

A
  • Biguanide
  • insulin sensitiser
61
Q

When is metformin used?

A 
first line 
(if dietry/lifestyles changes have made no difference)
62
Q

What does metformin do?

A
  • reduced hepatic glucose output
  • increases peripheral glucose disposal
63
Q

What are the side effects of metformin?

A

GI side effects

64
Q

When is metformin contraindicated?

A
  • severe liver failure
  • servere cardiac failure
  • moderate renal failure
65
Q

How do sulphonylureas increase insulin release?

A

bind to the ATP sensitive potassium channel causing it to close and causing it to produce insulin (independent of glucose/ATP)

66
Q

What is Pioglitazone?

A 
insulin sensitiser (through peripheral tissues)
Peroxisome proliferator-activated receptor agonists.
67
Q

How does Pioglitazone work?

A
  • modifies adipocyte differentiation, causing production of peripheral fat not central when weight is gained.
  • improvement in glycaemia and lipids
68
Q

What are the side effects of Piogiltazone>

A
  • hepatitis
  • heart failure
69
Q

What is GLP-1?

A
  • a gut hormone that is secreted in response to nutrients
  • transcription production from L cells
70
Q

What does GLP-1 do?

A
  • simulates insulin, suppreses glucagon
  • increased satiety
71
Q

What do GLP-1 agonists do?

A
  • (Liraglutide, Semaglutide)
  • decrease glucagon, decrease glucose
  • weight loss
72
Q

What do SGLT-2 inhibitors do?

A
  • inhibits the Na-Glu transporter, increases glycosuria
  • lowers HbA1c
  • Empagliflozin, dapagliflozin, canagliflozin
  • 32% lower all cause mortality
  • 35% lower risk heart failure
  • Improve CKD
73
Q

What is the effect of treatment on beta cell failure?

A

nothing

74
Q

Why does GLP-1 have a short half-life?

A

rapid degradation from enzyme dipeptidyl peptidase-4 (DPP4 inhibitor)

75
Q

What do Gliptins/DPPG-4 inhibitors do?

A
  • Increase half life of exogenous GLP-1
  • Increase GLP-1
  • Decrease glucagon and glucose
  • Neutral on weight
76
Q

What can lead to the remission of T2DM?

A
  • gastric bypass surgery
  • 800kcal/day diet for 3-6 months
77
Q

What are the other aspects of T2DM management?

A

blood pressure and lipid management

78
Q

How can blood pressure be managed?

A

ACE inhibitors

BRS YR2 (67 decks)

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