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ENDOCRINOLOGY 2 > TYPE 2 DIABETES MELLITUS > Flashcards

TYPE 2 DIABETES MELLITUS Flashcards

1
Q

What is type 2 diabetes?

A

Condition where combination of insulin resistance and beta-cell failure result in hyperglycaemia. Not always associated with obesity

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2
Q

Which type of diabetes causes relative insulin deficiency and absolute insulin deficiency?

A

Type 1 - absolute insulin deficiency

Type 2 - relative insulin deficiency because insulin still produced but not enough to overcome insulin resistance

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3
Q

In what age groups does T2DM develop in?

A

T2DM traditionally thought to be condition of late adulthood but now increasing in all age groups especially in early-adulthood

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4
Q

T2DM is most prevalent in which population?

A

Ethnic groups which move from rural to urban lifestyle

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5
Q

What are the targets of glucose levels for those at risk of developing T2DM?

A

Fasting glucose: < 6mmol/L
2-hr glucose (OGTT): < 7.7 mmol/L
HbA1c: < 42 mmol/mol

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6
Q

What are the targets of glucose levels for those with T2DM?

A

Fasting glucose: < 7mmol/L

HbA1c: < 48mmol/mol

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7
Q

Describe the relationship between insulin resistance and production as you go through the 3 stages of T2DM

A

Normal: Insulin resistance begins increasing with insulin production mirroring in order to make up for this

Intermediate: Insulin resistance keeps increasing. Insulin production increases until a certain point where it then decreases due to beta cells being worn out

Type 2 diabetes: Insulin resistance stays at its max level and insulin production continues to fall

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8
Q

What are the tests for diagnosis of T2DM?

A

First line test for diagnosis:
1 x HbA1c >= 48 mmol/L with symptoms
2 x HbA1c >= 48 mmol/L with no symptoms

Random glucose level of > 11.1 with symptoms of diabetes

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9
Q

What is the range of an impaired fasting glycaemia?

A

6-7 mmol/L

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10
Q

What is the range of an impaired glucose tolerance?

A

7.8 - 11.1 mmol/L in a 2 hour glucose test (OGTT)

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11
Q

Why does the hyperglycaemia of T2DM not cause ketosis under normal circumstances?

A

Insulin is still being produced in T2DM (relative deficiency of insulin) which means ketone body synthesis from fatty acids and acyl-coA inhibited

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12
Q

When could ketoacidosis occur in patients with T2DM?

A

Infections or if insulin not taken for those with long duration T2DM

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13
Q

Why do you have to be careful in long duration T2DM?

A

Beta-failure may progress to complete insulin deficiency so need to make sure patient doesn’t stop taking insulin as risk of ketoacidosis

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14
Q

After a glucose load to the body what is lost in T2DM?

A

First phase insulin release is lost causing a blunted amount of plasma insulin compared to the normal peak for those with normal glucose tolerance

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15
Q

Why does hepatic glucose output increase in T2DM?

A

Reduction of insulin action

Increase in glucagon action

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16
Q

What is the relationship between insulin resistance and insulin sensitivity in those with T2DM?

A

For a given degree of insulin sensitivity secrete less insulin

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17
Q

How does insulin resistance of the organs and tissues occur in T2DM?

A

Adipocytes release vast amounts of adipokines e.g. glucocorticoids, TNF alpha, IL-6, leptin… which drive a toxic pro-inflammatory state

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18
Q

What type of diabetes is monogenic?

A

MODY (mature onset of diabetes in young)

19
Q

What types of diabetes are polygenic?

A

Type 1 + 2

Other factors also in play

20
Q

What percentage of those with T2DM are obese?

A

80%

21
Q

What are some associations of T2DM other than obesity?

A

Disturbances to gut microbiota

Intra-uterine growth retardation

22
Q

What are the clinical presentations of T2DM?

A 
Hyperglycaemia
Overweight
Dislipidaemia
Fewer osmotic symptoms
Insulin resistance
Later insulin deficiency
23
Q

List the risk factors of T2DM

A 
Age
Increased BMI
PCOS
Genetics
Inactivity
Ethnicity
24
Q

What is hyperosmolar hyperglycaemic state?

A

A diabetic emergency where patients often present with acute renal failure

No significant ketoacidosis because insulin enough to suppress lipolysis and ketogenesis but not enough to prevent hyperglycaemia

Usually an identifiable precipitating event (infection, MI)

25
Q

Describe the management of T2DM

A
  • Diet
  • Oral medication
  • Structured education
  • May need insulin later

Blood pressure management e.g. ACE inhibitors
- hypertension common

Lipid management

  • cholesterol and triglycerides raised
  • HDL cholesterol reduced
26
Q

What is checked during a T2DM consultation?

A

HbA1c, glucose monitoring if on insulin and medication review for glycaemia

Weight assessment
Blood pressure
Cholesterol profile for dyslipidaemia
Screening for complications e.g. foot check, retinal screening

27
Q

What drug is used to reduce HGO?

A

Metformin

28
Q

Which drugs improve insulin sensitivity?

A

Metformin, thiozolidinediones

29
Q

Which drugs boost insulin secretion?

A

Sulphonyleureas
DPP4 inhibitors
GLP-1 agonists

30
Q

Which drugs inhibit carbohydrate gut absorption and inhibit renal glucose output?

A

Alpha glucosidase inhibitor

SGLT-2 inhibitor

31
Q

Why is weight loss recommended for those who have T2DM?

A

It helps with every pathophysiology of T2DM

32
Q

When should metformin not be used?

A

Severe liver, cardiac or moderate renal failure

33
Q

Which drug should be used as first line if dietary/lifestyle change has made no difference?

A

Metformin

34
Q

What is the mechanism of action of sulphonylureas?

A

Normal insulin release needs ATP sensitive potassium channels to close so that potassium can open the calcium channel

Sulphonylureas bind to the potassium channel and close it, independent of ATP and thus glucose

35
Q

What class of drug does Pioglitazone belong to?

A

Thiozolidinediones

36
Q

What is the mechanism of Pioglitazone?

A

PPAR-gamma agonist causing mainly peripheral insulin sensitisation

37
Q

What is GLP-1?

A

Glucagon like peptide-1

Gut hormone which is secreted in response to nutrients in gut causing insulin increase and glucagon decrease.

It is a transcription product of pro-glucagon gene mostly from L cell

Gives feeling of satiety

Short half life due to rapid degradation from enzyme DPP4

38
Q

What is the incretin effect?

A

There is a greater response in insulin secretion when an oral glucose load is administered rather than IV

39
Q

What are some GLP-1 agonists and there effects on weight?

A

Liraglutide, semaglutide

Weight loss

40
Q

What are some DPP4 inhibitors and what do they do?

What are their effects on weight?

A

Gliptins

Increase half life of exogenous GLP-1

Neutral on weight

41
Q

How do SGLT-2 inhibitors work and what additional effects do they have?

A

Inhibits Na-Glu transporter increasing glycosuria
Lowers HbA1c
Improves chronic kidney disease
Decreases risk of myocardial infarction

42
Q

What is the effect of drug treatment on beta cell function?

A

May slow down beta-cell function loss but cannot stop it

43
Q

How can remission of T2DM occur?

A

Gastric bypass surgery has potential

Very low calorie diet for 3-6 months

ENDOCRINOLOGY 2 (12 decks)

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