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BRS Year 2 > Type 2 Diabetes > Flashcards

Type 2 Diabetes Flashcards

1
Q

What is type 2 diabetes?

A

A condition in which the combination of insulin resistance and beta-cell failure result in hyperglycaemia

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2
Q

What condition is associated with type 2 diabetes a lot?

A

Obesity

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3
Q

How is type 2 diabetes initially managed?

A

Lifestyle measures: diet changes and weight loss

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4
Q

Who typically presents with T2DM?

A

Usually late adulthood but can present in youth

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5
Q

What type of diabetes are you most likely to see diabetic ketoacidosis in and why?

A

T1DM

In type 2 you still produce a small enough insulin which is enough to suppress formation of ketones through lipolysis

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6
Q

How much does T2DM reduce life expectancy?

A

A lot when you are younger but less as you get older

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7
Q

Where is T2DM most prevalent? Given an example country

A

Ethnic groups that move from rural to urban lifestyle- biggest change seen in India

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8
Q

What is the biggest contributory factor to developing T2DM?

A

Can be insulin resistance mainly, but beta cell failure contributes

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9
Q

What is fasting glucose for a diagnosis of diabetes?

A

> 7 mmol/L

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10
Q

What is HbA1c for a diagnosis of diabetes?

A

> 48 mmol/L

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11
Q

What is OGTT for a diagnosis of diabetes?

A

> 11 mmol/L

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12
Q

What is fasting glucose in the intermediate stage of diabetes development?

A

Greater than 6 but less than 7 mmol/L

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13
Q

What is OGTT in the intermediate stage of diabetes development?

A

Greater than 7.7 but less than 11 mmol/L

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14
Q

What is HbA1c in the intermediate stage of diabetes development?

A

Greater than 42 but less than 48 mmol/L

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15
Q

How does insulin resistance change as someone is developing diabetes?

A

It curves up and plateaus before diabetes has even been diagnosed

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16
Q

What are the 3 ways of diagnosing diabetes?

A

Fasting glucose
OGTT
Random glucose

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17
Q

What level do beta cells function at diagnosis of T2DM?

A

Around 50%

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18
Q

Does diabetic ketoacidosis occur in T2DM? Explain your answer

A

Not usually, there is a small amount of circulating insulin (not enough to overcome resistance), which is enough to suppress the synthesis of ketone bodies from the breakdown of fat- this is relative insulin deficiency

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19
Q

What happens in long duration type 2 diabetes? What feature of diabetes becomes more prominent once this develops?

A

Beta cell failure may progress to complete insulin deficiency (this is where diabetic ketoacidosis may occur)

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20
Q

Does T2DM have a genetic risk?

A

Yes.

It’s influenced by genes, intrauterine environment and adult environment

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21
Q

How can risk of T2DM be increased in utero?

A

Foetal growth retardation

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22
Q

How is beta cell function assessed?

A

Hyperglycaemic clamp

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23
Q

What is hyperglycaemic clamp?

A

Glucose levels are elevated, in normal people insulin will shoot up, fall rapidly and then steadily fall, with T2 diabetics there will be hardly any rise in insulin

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24
Q

When is hyperglycaemic clamp used?

A

To assess beta cell function

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25
Q

What happens to glucose uptake in skeletal muscles in T2DM?

A

Reduced uptake of glucose due to reduced insulin

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26
Q

What happens to hepatic glucose output in T2DM? How?

A

Increased due to reduced insulin action and increased glucagon action

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27
Q

What happens to insulin sensitivity when we put on weight (in normal people)?

A

Insulin becomes less sensitive so more is secreted

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28
Q

What happens in the liver, adipocytes and muscle when theres insulin resistance?

A

Liver: less glycogen synthesis and greater hepatic glucose output
Adipocytes: less glucose uptake, less triglyceride synthesis
Muscle: less glucose uptake

29
Q

What happens to inflammatory adipokines in T2DM?

A

Levels are high

30
Q

Is T2DM monogenic or polygenic?

A

Polygenic- polymorphisms (Small changes to genes) inc. risk of diabetes
You’re not born with polygenic traits

31
Q

Is MODY monogenic or polygenic?

A

Monogenic

32
Q

What type of adiposity increases T2DM risk most?

A

Visceral adiposity increases risk a lot more than central

33
Q

How does T2DM present?

A 
Hyperglycaemia
Overweight
Dyslipidemia (high cholesterol)
Fewer osmotic symptoms
With complications
Insulin resistance
Later insulin deficiency
34
Q

What are risk factors for T2DM?

A 
Age
High BMI
Ethnicity
PCOS
Family history
Inactivity
35
Q

What is the first line test for the diagnosis of type 2 diabetes?

A

HbA1c

36
Q

When will random glucose work as a diagnostic test?

A

If there are symptoms

37
Q

How is HbA1c used as a diagnostic test?

A

If symptomatic 1 test can confirm diagnosis

If asymptomatic, 2 positive tests confirm diagnosis

38
Q

What is hyperosmolar hyperglycaemic state? What does it commonly present with?

A

An acute compication of T2DM
Presents commonly with renal failure.

Insufficient insulin (NOT ABSENT) for prevention of hyperglycemia but sufficient insulin for suppression of lipolysis and ketogenesis.
Glucose is >30 mmol/L
39
Q

How is type 2 managed?

A 
Diet
Oral medication
Structured education
May need insulin later
Remission / reversal
Prevention of complications
40
Q

How does a T2DM consultation go?

A

Glycaemia: HbA1c, glucose monitoring if on insulin, medication review
Weight assessment
Blood pressure
Dyslipidaemia: cholesterol profile
Screening for complications: foot check, retinal screening

41
Q

What dietary changes are recommended in T2DM?

A 
Total calories control
Reduce calories as fat 
Reduce calories as refined carbohydrate
Increase calories as complex carbohydrate
Increase soluble fibre
Decrease sodium
42
Q

If lifestyle changes don’t work for a diabetic patient, what do we give them?

A

Metformin
Aka. Biguanide
It’s first line if lifestyle changes aren’t working
Reduces insulin resistance through reduced HGO and inc. peripheral glucose disposal

43
Q

What drug is given to improve insulin sensitivity?

A

Metformin

Thiozolidinediones

44
Q

What drug is given to boost insulin secretion?

A

Sulphonylureas
DPP4-inhibitors
GLP-1 Agonists

45
Q

What drug is given to inhibit carb absorption in gut and inhibit renal glucose absorption?

A

Alpha glucosidase inhibitor

SGLT-2 inhibitor (renal)

46
Q

What is the first line drug is lifestayle changes have no effect?

A

Metformin

47
Q

How do sulphonyureas work?

A

Bind to ATP sensitive K+ channel and close it independant to glucose so insulin production is boosted

Normal insulin release requires closure of ATP sensitive K+ channel

48
Q

What is pioglitazone?

S/Es?

A

It’s a peroxisome proliferator-activated receptor agonist PPAR-y
Insulin sensitizers, mainly peripheral
Adipocyte differentiation modified so you can get weight gain- peripheral however, not central
Side effects (of older types): hepatitis, heart failure

49
Q

How does metformin effect weight?

A

Lowers it

50
Q

What is GLP-1?

A

Gut hormone which stimulates insulin and suppresses glucagon
Increases satiety
Secreted in response to nutrients in gut from L cells
Transcripted from pro-glucagon gene

51
Q

What is the incretin effect?

A

Oral glucose increases insulin almost double as much as intravenous glucose

52
Q

How do DPP-4 inhibitors work?

A

Inhibits DPP-4 enzyme which metabolises GLP-1

53
Q

How do SGLT-2 inhibitors work? Examples?

A

Inhibit Na-Glu transporter so encourages glycosuria
Lower HBA1C

e.g. dapagliflozin, empagliflozin, canagliflozin

54
Q

Do drugs work for diabetes?

A

Yes but eventually insulin will be needed and beta cell function will always decline

55
Q

What surgery can remit diabetes? (not cure)

A

Gastric bypass surgery

56
Q

What lifestyle change can remit diabetes?

A

Very low calorie diet (800-900 cals a day) for 3-6 months

57
Q

How does diabetic ketoacidosis compare to hyperosmolar hyperglycaemic syndrome?

A

Volume: In DK you’re dehydrated wheras is HHS you’re hypovolemic

Glucose: In DK, >11mmol/L. In HHS, >30mmol/L

Capillary blood ketones: DK, >3mmol/L. HSS <3mmol/L

Osmolarity: DK its variable. HHS >320mmol/l

Treatment: IV fluids for both immediately. In DK insulin given immediately at rate infusion of 0.1 units/kg/h. In HHS insulin only given immediately if capillary ketones >1mmol/L (urine >2), otherwise hold insulin until fluid resuscitation

58
Q

What are the different inflammatory adipokines?

A

TNF-a & IL-6: stimulate lipolysis and VLDL secretion- inc. insulin resistance, dec. adiponectin expression
Endocannabinoids: As fat IR inc. circulation EC inc.
Glucocorticoids: Inc. 11B HSD-1 in fat. Inc. IR. Inc. glucose, BP and lipids
Adiponectin: dec. insulin sensitivity. Predictive of diabetes
Leptin: Elevated in obesity. Inc. IR, dec. appetite, inc. metabolic rate
Fatty acids: Elevated in obesity and T2DM. Inc. IR, Dec b cell function, increased liver TG secretion, inc. organ fat
Visfatin: Visceral fat. Dec IR
Resistin: Inc. in obesity and T2DM. Inc. IR, Inc. liver TG secretion
Apelin: Insulin stimulated its expression in fat. Elevated in hyperinsulin. CV affects

59
Q

How do genetic risks and environmental risks vary for the development of T2DM?

A

If you have a low genetic risk, you’ll need a strong environmental risk
If you have a high genetic risk you will need a weak environmental risk

60
Q

What is the imact of SNPs on diabetes?

A

Each individual SNP only has a small effect of risk but cumulative SNPs have a big risk of developing T2DM

61
Q

Apart from obesity, what else can influence diabetes risk?

A

Stability of gut microbiota. Instability caused by:
Obesity and IR
Bacterial lipopolysaccharide fermentation to short hain FA
Inflammation

62
Q

What are side effects and contraindications of metformin?

A

GI side effects

Contraindicated in severe liver, cardiac or moderate renal failure

63
Q

What is the effect of GLP-1 agonists and give examples

A

Decrease glucagon con and glucose conc

Injected daily
Lead to weight loss

E.g. Liraglutide, semaglutide

64
Q

What is the effect of DPPG-4 inhibitors?

A

Aka. Gliptins

Inc. half life of exogenous GLP-1
Increase conc. of GLP-1
Dec. glucagon and glucose conc.

No weight change

65
Q

What are pros of SGLT-2 inhibitors?

A

Improve CKD
Lower HbA1C
Lower mortality
Lower risk of hrt failure

66
Q

What is the most effective medication in increasing beta cell function?

A

Sulfonylureas

Then metformin, the diet

67
Q

What other aspects of management do we have to consider with T2DM?

A

Blood pressure management (maybe give ACEi)

Lipid management: Cholesterol, triglycerides, HDLs

68
Q

What are examples of empowering language for a diabetic patient?

A

Person living with diabetes
What are your thoughts on your glucose levels?
Lets talk through options and see what suits you?

BRS Year 2 (110 decks)

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