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Endocrinology > Type 2 Diabetes > Flashcards

Type 2 Diabetes Flashcards

1
Q

What age range do T2DM patients present?

A

Middle age +

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2
Q

What is the BMI range in T2DM patients?

A

Normal-high (25+)

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3
Q

What history of autoimmune disease do T2DM patients have?

A

No history usually

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4
Q

Is there family history link with T2DM?

A

Yes, often have FHx

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5
Q

What will ketones appear as on T2DM urinalysis?

A

0 to +

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6
Q

Is HbA1c helpful at presentation?

A

No

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7
Q

What are the glucose levels at presentation?

A

10-25

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8
Q

How does T2DM present acutely?

A

Hyperglycaemic Hyperosmolar Syndrome

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9
Q

What are the C-peptide levels at presentation?

A

normal-raised

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10
Q

Are C-peptides present at 5 years post diagnosis?

A

Yes

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11
Q

Do T2DM patients present with complications? If so, how many?

A

Yes, 30%

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12
Q

What is the definition of T2DM?

A

Insulin resistance with relative insulin deficiency

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13
Q

How can obesity cause insulin resistance?

A

Obesity + lack of activity
Adiposity (inc FFAs, inc Adipokines)
Insulin resistance

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14
Q

How can obesity lead to relative insulin deficiency?

A

Obesisty + lack of activity
Adiposity (inc FFAs, inc Adipokines)
Lipotoxicity
Vulnerable beta cells (genetics) can’t respond and produce more insulin

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15
Q

How do normal beta cells respond to obesity?

A

Compensatory increase in insulin production

Euglycaemia

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16
Q

Why is T2DM a progressive disease?

A

Beta cells deteriorate

No change in insulin sensitivity

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17
Q

What symptoms do T2DM patients present with?

A 
Polyuria
Polydipsia
Blurred vision
Tiredness
Recurrent UTIs
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18
Q

What is the typical underlying cause of HHS?

A

undiagnosed T2DM

T2DM treated with diet only

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19
Q

What can trigger HHS?

A 
CVS event (MI/Stroke)
Steroid therapy
Sepsis
Diuretics
High refined sugar intake
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20
Q

What is the aetiology in HHS?

A

Older patient
T2DM
If young then non white

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21
Q

What can precipitate HHS and why?

A

Frequent infection
Stress hormone release
(eg glucagon -> inc blood sugar)

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22
Q

What is the median glucose in HHS?

A

60

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23
Q

What will renal function be in HHS?

A

significant impairment

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24
Q

How is Na+ affected in HHS?

A

Often raised

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25
Q

How is osmolality affected in HHS? To what value? Why?

A

Often raised
Around 400
Hyperglycaemia/Hypernatraemia (ie concentrated blood)

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26
Q

What are the biochemical differences in HHS and DKA?

A

HHS is less ketonaemic/acidotic

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27
Q

How do you treat HHS compared to DKA? Why?

A

Fluids: more slowly in HHS(risk cerebral oedema)
Insulin: more slowly in HHS (more sensitive)
Na+: avoid rapid fluctuations (0.45%saline maybe)
LMWH for all unless contraindicated

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28
Q

What conditions are associated with insulin resistance syndrome?

A

Hypertension
Hyperlipidaemia
Hyperglycaemia

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29
Q

How is metabolic syndrome defined?

A 
Insulin resistance syndrome OR T2DM
With 2+ :
Microalbuminuria
BMI >30
Dislipidaemia (TG>1.7, HDL<1.0)
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30
Q

What are the aims of treatment in diabetes?

A 
Manage hyperglycaemia symptoms
Improve glycaemic control
Minimise weight gain
Help with weight loss
Reduce Micro/Macro complications
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31
Q

What is the first line treatment of T2DM?

A

Metformin

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32
Q

What of drug is metformin?

A

biguinide

insulin sensitizer

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33
Q

What is the action of metformin?

A

Reduces hepatic gluconeogenesis by stimulating AMPK
Increasing glucose uptake and utilization in skeletal muscle
Insulin signalling increased
Reduces CHO absorption
Increased fatty acid oxidation

34
Q

What effect does metformin have on:

a) HbA1c
b) Weight
c) micro/macro complications
d) Lipid profile

A

a) lowers HbA1c by lowering insulin resistance
b) reduces weight
c) prevents Micro/Macro complications
d) reduces TG and LDL

35
Q

Why is metformin used in pregnancy?

A

Safe in gestational diabetes

36
Q

What effect does metformin have on hyper/hypoglycaemia?

A

reduces hyerglycaemia

NO hypos

37
Q

What are the adverse effects of metformin?

A 
GI symptoms: nausea, vomiting, abdo pain, diarrhoea, taste disturbance.
Lactic acidosis
Liver failure 
Rash 
Anaemia (rare)
38
Q

How do you try and prevent GI effects with metformin?

A

Start low, go slow

39
Q

What are the risk factors for lactic acidosis when using metformin?

A

high pre-existing risk

MI, HF etc

40
Q

Why do you have to measure eGFR with metformin?

A

Risk of renal toxicity

41
Q

What changes in metformin dose have to be made with a) eGFR 30-45
b) eGFR < 30?

A

a) half dose

b) stop meds

42
Q

What is the second line treatment in T2DM?

A

Sulphonylureas

43
Q

What kind of drugs are SUs?

A

Insulin secretagogues

44
Q

Give an example of 1st generation SUs

A

Tolbutamide

45
Q

Give examples of 2nd generation SUs

A

Glicazide

Glibemclamide (aka Glyburide)

46
Q

Why are 2nd generation SUs used more frequently?

A

more potent

47
Q

When are sulphonylureas used?

A

intolerant to metformin

add on to metformin

48
Q

What is the action of SUs?

A

Bind to SUR1 sub unit
close kATP channel
beta cell depolarisation
insulin released

49
Q

Why is it important that SUs act independently of plasma glucose?

A

can cause insulin to be released even with normal-low glucose levels
causes hypo

50
Q

What effect do sulphonylureas have on:

a) HbA1c
b) micro/macro complications
c) weight

A

a) reduces HbA1c by inc insulin secretion
b) reduces MICRO complications only
c) weight gain

51
Q

What are the adverse effects of SUs?

A 
Can cause hypos
Weight gain
Does not prevent MACRO complications
Hypersensitivity (rare)
Blood dyscrasias (rare) 
Liver dysfunction (rare)
52
Q

When would SUs be 1st line?

A

Underweight T2DM patients

53
Q

What groups of patients should care be taken with SUs?

A

Elderly
HGV drivers
(risk hypos)

54
Q

What is the aim of Thiazolodinediones in T2DM?

A

Increase action of insulin at target sites

55
Q

What is the action of mechanism in TZDs?

A

PPARy agonist
Allows transcription of GLUT4, lipoprotein lipase and fatty acid transport protein
Increased fatty acid storage
Reduced hepatic gluconeogenesis

56
Q

How does PPARy act?

A

binds with RXR

PPARy-RXR = transcription factor

57
Q

How do TZDs effect:

a) HbA1c
b) Hyper/hypoglycaemia

A

a) reduces HbA1c by inc insulin sensitivity

b) Reduces hyper/ no hypos

58
Q

What are the adverse effects of TZDs?

A

Weight gain
Fluid retention
Does not prevent micro/macro complications
Increased bone fractures

59
Q

Why do you get weight gain with TZDs?

A

Subcutaneous fat and fluid retention

60
Q

Why do you get fluid retention with TZDs?

A

Na+ reabsorption in the kidney

61
Q

What patients should you be aware of when perscribing TZDs?

A

HF patients

Fluid retention could worsen HF

62
Q

What contraindications are there for TZDs?

A

patients over 65

63
Q

Give examples of TZDs

A

Pioglitazone
Rosiglitazone
Troglitazone

64
Q

Why is pioglitazone the only licensed TZD?

A

Rosiglitazone causes MI

Troglitazone causes liver failure

65
Q

What are incretins derived from?

A

intestinal secretion of insulin

66
Q

What is GLP-1 and where is it secreted?

A

Glucagon like peptide

secreted from L cells in ileum and colon

67
Q

What is GIP and where is it secreted from?

A

Glucose dependent Insulinotropic peptide

K cells in jejunum/duodenum

68
Q

What action do GIP and GLP-1 carry out on pancreas and what is the effect?

A

increase insulin production
increase glucose uptake in skeletal muscle
Decrease blood glucose

69
Q

What action do GLP-1 have on alpha cells?

A

Decreases glucagon release
reduces glucose release
decreased blood glucose

70
Q

What enzyme terminates action of GLP-1 dnd GIP?

A

Dipeptidyl peptidase 4 (DPP4)

71
Q

What are incretin analogues?

A

GLP-1 agonists

72
Q

What are the effects of incretin analogues?

A 
Promote insulin secretion
Reduces HbA1c
Suppresses glucagon
Increases weight loss
Reduces appetite
73
Q

What are the adverse effects of incretin analogues?

A

nausea (resolves in 6-8weeks)
injections
pancreatitis?

74
Q

What are examples of incretin analogues? What are their modes of administration? what are their half lives?

A

Exenatide-BD-subcut injection-60-90mins
Exendin LAR-once weekly
Liraglutide-OD-subcut injection-10-14hrs (DPP4 resistant)
Lixisenatide-OD- subcut injection

75
Q

What is the action of DPP4 inhibitors?

A

inhibit action of DPP4

prolongs action of GLP1 and GIP

76
Q

What are examples of DPP4 inhibitors?

A

Sitagliptin

Vildagliptin

77
Q

What are the effects of DPP4 inhibitors?

A

Weight neutral
No hypos
Suppress glucagon
Promotes insulin secretion (reduces HbA1c)

78
Q

What are the adverse effects of DPP4 inhibitors?

A

Not very potent
No weight loss
Pancreatits?

79
Q

What is the action of SGLT2 inhibitors?

A

prevent glucose re-absorption in proximal tubule
Glucosuria
Reduce blood glucose
reduces calories

80
Q

What are the effects of SGLT2 inhibitors?

A

Reduce HbA1c

Weight loss

81
Q

What are the adverse effects of SGLT2 inhibitors?

A

Thrush
UTIs
(sugary urine=breeding ground for bacteria)

Endocrinology (17 decks)

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