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Endocrinology 2 > Type 2 Diabetes Mellitus > Flashcards

Type 2 Diabetes Mellitus Flashcards

1
Q

what is the pathophysiology of type 2 diabetes?

A

combination of insulin resistance and beta-cell failure, resulting in hyperglycemia and associated with obesity

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2
Q

what is the initial treatment for someone with type 2 diabetes?

A

lifestyle changes and weight loss

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3
Q

can type 2 diabetes be reversible?

A

yes

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4
Q

what level of fasting glucose is normal?

A

less than or equal to 6mmol/L

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5
Q

what level of fasting glucose classes as impaired fasting glycaemia (intermediate state) ?

A

from 6 to 6.9 mmol/L

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6
Q

what level of fasting glucose classes as type 2 diabetes?

A

greater than or equal to 7 mmol/L

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7
Q

2 hour glucose in the OGTT at which values is considered normal?

A

<7.7mmol/L

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8
Q

2 hour glucose in the OGTT at which values is considered impaired glucose tolerance (an intermediate state) ?

A

7.7-10.9mmol/L

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9
Q

2 hour glucose in the OGTT at which values is considered diabetic?

A

greater than or equal to 11

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10
Q

hbA1c at which values is considered

  1. normal
  2. pre-diabetes (intermediate state)
  3. diabetes
A
  1. <42mmol/mol
  2. 42-47.9mmol/mol
  3. greater than or equal to 48mmol/mol
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11
Q

how do insulin resistance and insulin production change going from normal to intermediate state to diabetic state?

A

Normal -> intermediate: insulin resistance increases and insulin production increases to compensate

Intermediate -> diabetic: insulin production decreases and insulin resistance plateaus.

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12
Q

when can we use random glucose to diagnose diabetes type 2?

A

when someone also has symptoms of diabetes

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13
Q

why do people with type 2 diabetes not tend to get ketosis?

A

enough insulin is present in circulation to inhibit/suppress lipolysis and fatty acid beta-oxidation

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14
Q

why do people with long-duration type 2 diabetes sometimes get ketoacidosis?

A

because all their beta cell function has been lost

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15
Q

In healthy people, what is the relationship between insulin secretion and insulin sensitivity?

A

as insulin sensitivity decreases, insulin production increases

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16
Q

In type 2 diabetes, what happens in the liver, adipocytes and muscle?

A

Liver: produces excess glucose (insulin usually causes glucose to convert to glycogen whereas lack of insulin converts glycogen to glucose)

Muscle: no uptake of glucose from blood by GLUT transporter

Adipocytes: No uptake of glucose into adipocytes and number of triglycerides in the blood rising (because insulin encourages the conversion of triglycerides to NEFA)

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17
Q

adipocytes produce adipokines, what are these?

A

inflammatory chemicals which contribute to development of type 2 diabetes

18
Q

MODY stands for what and what is it caused by?

A

Maturity Onset Diabetes in the Young and it is caused by a single gene mutation

19
Q

Diabetes mellitus types 1 and 2 have what type of genetic inheritability?

A

polygenic

20
Q

where is the part of the body that poses the highest risk for type 2 diabetes when it has more body fat?

A

visceral obesity > subcutaneous obesity

21
Q

what is the presentation of type 2 diabetes mellitus?

A 
hyperglycaemia
overweight
dyslipidaemia
fewer osmotic symptoms
complications
insulin resistance
later insulin deficiency
22
Q

What are the risk factors for T2DM?

A 
age
BMI
ethnicity
PCOS
family history
inactivity
23
Q

first line test for diagnosis of type 2 diabetes mellitus?

A

HbA1c

24
Q

what is the key management for hyperosmolar hyperglycaemic state in people with type 2 diabetes?

A

rehydration with IV fluids

25
Q

what is the management of type 2 diabetes?

A 
diet/lifestyle changes
oral medication
structured education
may need insulin later
remission/reversal
26
Q

what monitoring do people with type 2 diabetes need?

A 
HbA1c, glucose monitoring if on insulin
Medication review
weight assessment
blood pressure
dyslipidemia: cholesterol profile
screening for complications eg. foot check and retinal screening
27
Q

What are the four main goals for drug treatments for T2DM?

A
  • Reduce hepatic glucose production
  • Improve insulin sensitivity
  • Boost insulin secretion
  • Inhibit carbohydrate gut absorption and inhibit renal glucose absorption
28
Q

what does metformin do?

A

reduce hepatic glucose output and improves insulin sensitivity

29
Q

Thiazolidinediones have what effect? Give an example.

A

Improve insulin sensitivity

Pioglitazone

30
Q

sulphonylureas, DPP4-inhibitors, GLP-1 agonists all do what? What do we do if these stop working?

A

boots insulin secretion

move onto insulin

31
Q

what do alpha-glucosidase inhibitor and SGLT-2 inhibitor do?

A

inhibit carbohydrate gut absorption and inhibit renal glucose reabsorption

32
Q

what is the first line drug for T2DM?

A

metformin

33
Q

what are the side effects / cautions of metformin?

A

GI side effects

Contra-indicated in severe liver, severe cardiac or moderate renal failure

34
Q

normal insulin release requires closure of which channel? What do sulphonylureas do to this channel?

A

ATP-sensitive potassium channel

They close the channel independent of glucose, boosting insulin production

35
Q

Pioglitazone has what side effect?

A

peripheral weight gain

36
Q

Pioglitazone is an agonist at which receptor?

A

PPAR-gamma

37
Q

What does GLP-1 do?

A
  • incretin/gut hormone, secreted in response to nutrients in the gut. Transcription product of pro-glucagon gene, mostly from L-cell.
  • stimulates insulin, suppresses glucagon, increases satiety
38
Q

Give 2 examples of GLP-1 agonists?

A

Liraglutide, semaglutide

39
Q

what does DPPG-4 enzyme do? What happens if you inhibit it?

A

Metabolises GLP-1

Longer half-life of GLP-1

40
Q

GLP-1 agonists cause:

1.weight loss
2, weight gain
3. weight neutral

A

1

41
Q

What do SGLT-2 inhibitors do?

A

inhibit Na-Glu transporter, increasing glycosuria (makes you pee out more glucose)

Endocrinology 2 (17 decks)

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