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Year 2 Endo > Type 2 diabetes > Flashcards

Type 2 diabetes Flashcards

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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?

Study These Flashcards
A

Excess hepatic glucose production

Decreased uptake of glucose by skeletal muscle

25
Why do beta cells stop functioning?
Beta cells become exhausted from overproduction of insulin Creates toxic environment in pancreas Beta cell apoptosis
26
Is inflammation involved in the pathophysiology of T2DM?
Adipokines have a huge variety of effects
27
What does polygenic mean?
Polymorphisms increasing risk of diabetes | ‘Not born with it but high risk and may develop later depending on other factors’
28
What are the main features of monogenic diabetes?
Single gene mutation ==> Diabetes (MODY) | ‘Born with it, always going to develop diabetes’
29
What is the spectrum of genetic/environment interactions?
Low genetic risk + strong environmental High genetic risk + weak environmental High genetic risk + strong environmental Low genetic risk + weak environmental
30
What can you find from GWA studies?
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
What is the role of obesity in T2DM?
``` Major risk factor for T2DM Fatty acids and adipocytokines important Central vs visceral obesity 80% T2DM are obese Weight reduction useful treatment ```
32
How does T2DM present?
``` Hyperglycaemia Overweight Dyslipidaemia Fewer osmotic symptoms With complications Insulin resistance Later insulin deficiency ```
33
What are the risk factors for T2DM?
Age PCOS Increased BMI Family Hx Ethnicity Inactivity
34
How do you diagnose T2DM?
HbA1c most commonly Osmotic symptoms Infections Screening test: incidental finding at presentation of complication Acute; hyperosmolar hyperglycaemic state, Chronic; ischaemic heart disease, retinopathy
35
What are the criteria for diagnosis of T2DM?
1x HbA1c >=48mmol/L with symptoms Or 2x HbA1c >=48 mmol/mol if aysymptomatic
36
What are the main features of hyperosmolar hyperglycaemic state?
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
How do you manage T2DM?
``` Diet Oral medication Structured education May need insulin later Remission / reversal ```
38
What are the categories of diabetes related complications?
Retinopathy Neuropathy Nephropathy Cardiovascular
39
What are the principles of a T2DM consultation?
Glycaemia: HbA1c, glucose monitoring if on insulin, medication review Weight assessment Blood pressure Dyslipidaemia: cholesterol profile Screening for complications: foot check, retinal screening
40
What are the dietary recommendations made for T2DM?
``` Total calories control Reduce calories as fat Reduce calories as refined carbohydrate Increase calories as complex carbohydrate Increase soluble fibre Decrease sodium ```
41
How do you manage excess hepatic glucose production?
Metfomin
42
How do you improve insulin sensitivity?
Metformin | Thiozolidinediones
43
How do you boost insulin secretion?
Sulphonylureas DPP4-inhibitors GLP-1 Agonists
44
How do you Inhibit carbohydrate gut absorption and | Inhibit renal glucose resorption?
Alpha glucosidase inhibitor | SGLT-2 inhibitor
45
What are the main features of metformin?
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
What are the main features of Sulphonylureas?
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
What are the main features of Pioglitazone?
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
What is GLP-1?
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
How do GLP-2 agonists work?
``` Liraglutide, Semaglutide Injectable –daily, weekly Decrease [glucagon] Decrease [glucose] Weight loss ```
50
How do Gliptins (DPPG-4 inhibitor) work?
``` Increase half life of exogenous GLP-1 Increase [GLP-1] Decrease [glucagon] Decrease [glucose] Neutral on weight ```
51
How do SGLT-2 inhibitors work?
Inhibits Na-Glu transporter, increases glycosuria Empagliflozin, dapagliflozin, canagliflozin HbA1c lower 32% lower all cause mortality 35% lower risk heart failure Improve CKD
52
What can cause remission of T2DM?
Gastric bypass surgery Low-calorie diet (800 kcal/day) for 3-6 months
53
What are other aspects of management?
Blood pressure Lipid management, insulin normally inhibits lipolysis - Atorvarstatin 20mg if q-risk > 10% - Atorvarstatin 80mg if IHD/CVD/PVD
54
What skin conditions is seen in T2DM?
Acanthosis nigracans | Darkening of armpits
55
When can you not use HbA1c?
Pregnancy | Sickle cell
56
What is the
Step 1: Metformin Step 2: Another drug e.g. DPP-4 inhibitor, pioglitazone, SU, SGLT-2i Step 3: Further drug or insulin
57
What is the difference between HTN in diabetics?
Type II | Everyone gets ACEi or ARBs not CCB
58
What can cause hypoglycaemia?
``` Missed meals Alcohol Exercise Inapprop insulin Some drugs e.g SU or SGLT-2i ```
59
What is the treatment for a hypo?
Conscious: Oral glucose and complex CHO Impaired conscious: Parenteral: 1mg Glucagon IM 10% IV Dextrose

Year 2 Endo (15 decks)

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