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Year 2 Endo > Type 2 diabetes > Flashcards

Type 2 diabetes Flashcards

1
Q

What is type 2 diabetes?

A

The combination of insulin resistance and beta-cell failure result in hyperglycaemia

Associated with obesity but not always

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2
Q

How can type 2 diabetes be managed?

A

The resultant chronic hyperglycaemia may initially be managed by changes to diet / weight loss and may even be reversible

With time glucose lowering therapy e.g. insulin, is needed

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3
Q

What insulin deficiency do you get in T2DM?

A

Relative insulin deficiency as opposed to absolute

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4
Q

Why is diagnosing T2DM more difficult now?

A

T2DM may present in youth / young adults

Diabetic ketoacidosis can be a feature of T2DM

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5
Q

If you are diagnosed early what does this mean for prognosis?

A

On average die earlier a patient is diagnosed with T2DM

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6
Q

What are some epidemiological facts of T2DM?

A

Prevalence of T2DM varies enormously

Increasing prevalence

Occurring and being diagnosed younger

Greatest in ethnic groups that move from rural to urban lifestyle

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7
Q

What ethnic groups are more susceptible to T2DM?

A

Asian
Pacific Islanders
Afro-Caribbean’s

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8
Q

What are the stages of development of type 2 diabetes?

A

Normal
Intermediate state
T2DM

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9
Q

What glucose levels can define intermediate state via fasting glucose levels?

A

<6mmol/L (normal)
Impaired fasting glycaemia
>7 mmol/L (T2DM)

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10
Q

What glucose levels can define intermediate state via 2hr glucose (OGTT)?

A

<7.7 mmol/L
Impaired glucose tolerance
>11 mmol/L

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11
Q

What glucose levels can define intermediate state via HbA1c?

A

<42 mmol/L
Pre-diabetes or non-diabetic hyperglycaemia
>48 mmol/L

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12
Q

What is the relationship between insulin resistance and stage of development of T2DM?

A

Insulin resistance increases
Non-linear relationship
Curve that plateaus

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13
Q

So, if insulin resistance plateaus why does T2DM develop from the intermediate state?

A

Insulin production decreases

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14
Q

What are the 4 ways of diagnosing T2DM?

A

Fasting glucose
2-hour glucose tolerance test
HbA1c
Random blood glucose (only with symptoms)

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15
Q

What is beta-cell function at diagnosis of T2DM?

A

By the time someone presents with T2DM they have already lost some beta-cell function already

In order to present with hyperglycaemia

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16
Q

What are the main features of relative insulin deficiency?

A

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

Relative deficiency of insulin

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17
Q

Why is the fact that the insulin deficiency is relative important?

A

This is important to understand as it explains why the hyperglycaemia encountered does not cause ketosis under ‘usual’ circumstances

Enough insulin to suppress the beta-oxidation forming ketones

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18
Q

What happens when T2DM is longterm?

A

beta-cell failure may progress to complete insulin deficiency
Usually on insulin at this point in any case, but important not to stop as at risk of ketoacidosis

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19
Q

What factors are associated with an increased risk of T2DM?

A 
Genes
Intrauterine environment (early foetal programming that modifies risk)
Adult environment 
Insulin resistance
Insulin secretion defects
Fatty acids
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20
Q

What is a misconception of T2DM?

A

HETEROGENOUS

People develop T2DM at variable BMI, ages and progress differently

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21
Q

What does reduced insulin action cause?

A

less uptake of glucose into skeletal muscle

hepatic glucose production is also increased due to both a reduction in insulin action and increase in glucagon action

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22
Q

What is the relationship between insulin resistance and secretion?

A

Non-linear

Downward curve

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23
Q

What happens to the relationship between resistance and secretion in T2DM?

A

People developing type 2 diabetes have ‘fallen off the curve’
And for a given degree of insulin sensitivity secrete less insulin

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24
Q

What are the consequences of insulin resistance?

A

Excess hepatic glucose production

Decreased uptake of glucose by skeletal muscle

25
Q

Why do beta cells stop functioning?

A

Beta cells become exhausted from overproduction of insulin
Creates toxic environment in pancreas
Beta cell apoptosis

26
Q

Is inflammation involved in the pathophysiology of T2DM?

A

Adipokines have a huge variety of effects

27
Q

What does polygenic mean?

A

Polymorphisms increasing risk of diabetes

‘Not born with it but high risk and may develop later depending on other factors’

28
Q

What are the main features of monogenic diabetes?

A

Single gene mutation ==> Diabetes (MODY)

‘Born with it, always going to develop diabetes’

29
Q

What is the spectrum of genetic/environment interactions?

A

Low genetic risk + strong environmental

High genetic risk + weak environmental

High genetic risk + strong environmental

Low genetic risk + weak environmental

30
Q

What can you find from GWA studies?

A

400 SNPs have been found to increase risk of T2DM

TCF7L2 has the strongest effect (1.4%)

Summation of multiple SNPs can contribute majorly

31
Q

What is the role of obesity in T2DM?

A 
Major risk factor for T2DM
Fatty acids and adipocytokines important
Central vs visceral obesity
80% T2DM are obese
Weight reduction useful treatment
32
Q

How does T2DM present?

A 
Hyperglycaemia
Overweight
Dyslipidaemia
Fewer osmotic symptoms
With complications
Insulin resistance
Later insulin deficiency
33
Q

What are the risk factors for T2DM?

A

Age
PCOS
Increased BMI Family Hx
Ethnicity Inactivity

34
Q

How do you diagnose T2DM?

A

HbA1c most commonly

Osmotic symptoms
Infections
Screening test: incidental finding
at presentation of complication
Acute; hyperosmolar hyperglycaemic state,
Chronic; ischaemic heart disease, retinopathy

35
Q

What are the criteria for diagnosis of T2DM?

A

1x HbA1c >=48mmol/L with symptoms

Or

2x HbA1c >=48 mmol/mol if aysymptomatic

36
Q

What are the main features of hyperosmolar hyperglycaemic state?

A

Presents commonly with renal failure.

Insufficient insulin (NOT ABSENT) for prevention of hyperglycemia but sufficient insulin for suppression of lipolysis and ketogenesis.

Absence of significant acidosis.

Often identifiable precipitating event (infection, MI).

37
Q

How do you manage T2DM?

A 
Diet
Oral medication
Structured education
May need insulin later
Remission / reversal
38
Q

What are the categories of diabetes related complications?

A

Retinopathy
Neuropathy
Nephropathy
Cardiovascular

39
Q

What are the principles of a T2DM consultation?

A

Glycaemia: HbA1c, glucose monitoring if on insulin, medication review

Weight assessment

Blood pressure

Dyslipidaemia: cholesterol profile

Screening for complications: foot check, retinal screening

40
Q

What are the dietary recommendations made for T2DM?

A 
Total calories control
Reduce calories as fat 
Reduce calories as refined carbohydrate
Increase calories as complex carbohydrate
Increase soluble fibre
Decrease sodium
41
Q

How do you manage excess hepatic glucose production?

A

Metfomin

42
Q

How do you improve insulin sensitivity?

A

Metformin

Thiozolidinediones

43
Q

How do you boost insulin secretion?

A

Sulphonylureas
DPP4-inhibitors
GLP-1 Agonists

44
Q

How do you Inhibit carbohydrate gut absorption and

Inhibit renal glucose resorption?

A

Alpha glucosidase inhibitor

SGLT-2 inhibitor

45
Q

What are the main features of metformin?

A

Biguanide, insulin sensitiser

First line if dietary / lifestyle adjustment has made no difference

Reduces insulin resistance

Reduced hepatic glucose output

Increases peripheral glucose disposal

GI side effects

Contraindicated in severe liver, severe cardiac or moderate renal failure

46
Q

What are the main features of Sulphonylureas?

A

Normal insulin release requires closer of the
ATP-sensitive potassium channel

Sulphonylureas eg gliclazide, bind to the ATP-sensitive potassium channel and close it, independent of glucose / ATP

47
Q

What are the main features of Pioglitazone?

A

Peroxisome proliferator-actived receptor agonists PPAR-γ

Insulin sensitizer, mainly peripheral

Adipocyte differentiation modified, weight gain but peripheral not central

Improvement in glycaemia and lipids

Evidence base on vascular outcomes

Side effects of older types hepatitis, heart failure

48
Q

What is GLP-1?

A

Gut hormone

Secreted in response to nutrients in gut

Transcription product of pro-glucagon gene, mostly from L-cell

Stimulates insulin, suppresses glucagon

↑ satiety (feeling of ‘fullness’)

Short half life due to rapid degradation from enzyme dipeptidyl peptidase-4 (DPP4 inhibitor)

Used in treatment of diabetes mellitus

49
Q

How do GLP-2 agonists work?

A 
Liraglutide, Semaglutide
Injectable –daily, weekly
Decrease [glucagon]
Decrease [glucose]
Weight loss
50
Q

How do Gliptins (DPPG-4 inhibitor) work?

A 
Increase half life of exogenous GLP-1
Increase [GLP-1]
Decrease [glucagon]
Decrease [glucose]
Neutral on weight
51
Q

How do SGLT-2 inhibitors work?

A

Inhibits Na-Glu transporter, increases glycosuria
Empagliflozin, dapagliflozin, canagliflozin
HbA1c lower
32% lower all cause mortality
35% lower risk heart failure
Improve CKD

52
Q

What can cause remission of T2DM?

A

Gastric bypass surgery

Low-calorie diet (800 kcal/day) for 3-6 months

53
Q

What are other aspects of management?

A

Blood pressure

Lipid management, insulin normally inhibits lipolysis

  • Atorvarstatin 20mg if q-risk > 10%
  • Atorvarstatin 80mg if IHD/CVD/PVD
54
Q

What skin conditions is seen in T2DM?

A

Acanthosis nigracans

Darkening of armpits

55
Q

When can you not use HbA1c?

A

Pregnancy

Sickle cell

56
Q

What is the

A

Step 1: Metformin
Step 2: Another drug e.g. DPP-4 inhibitor, pioglitazone, SU, SGLT-2i
Step 3: Further drug or insulin

57
Q

What is the difference between HTN in diabetics?

A

Type II

Everyone gets ACEi or ARBs not CCB

58
Q

What can cause hypoglycaemia?

A 
Missed meals 
Alcohol
Exercise
Inapprop insulin
Some drugs e.g SU or SGLT-2i
59
Q

What is the treatment for a hypo?

A

Conscious: Oral glucose and complex CHO

Impaired conscious:
Parenteral: 1mg Glucagon IM
10% IV Dextrose

Year 2 Endo (15 decks)

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