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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
What happens to glucose uptake in skeletal muscles in T2DM?
Reduced uptake of glucose due to reduced insulin
26
What happens to hepatic glucose output in T2DM? How?
Increased due to reduced insulin action and increased glucagon action
27
What happens to insulin sensitivity when we put on weight (in normal people)?
Insulin becomes less sensitive so more is secreted
28
What happens in the liver, adipocytes and muscle when theres insulin resistance?
Liver: less glycogen synthesis and greater hepatic glucose output Adipocytes: less glucose uptake, less triglyceride synthesis Muscle: less glucose uptake
29
What happens to inflammatory adipokines in T2DM?
Levels are high
30
Is T2DM monogenic or polygenic?
Polygenic- polymorphisms (Small changes to genes) inc. risk of diabetes You're not born with polygenic traits
31
Is MODY monogenic or polygenic?
Monogenic
32
What type of adiposity increases T2DM risk most?
Visceral adiposity increases risk a lot more than central
33
How does T2DM present?
``` Hyperglycaemia Overweight Dyslipidemia (high cholesterol) Fewer osmotic symptoms With complications Insulin resistance Later insulin deficiency ```
34
What are risk factors for T2DM?
``` Age High BMI Ethnicity PCOS Family history Inactivity ```
35
What is the first line test for the diagnosis of type 2 diabetes?
HbA1c
36
When will random glucose work as a diagnostic test?
If there are symptoms
37
How is HbA1c used as a diagnostic test?
If symptomatic 1 test can confirm diagnosis | If asymptomatic, 2 positive tests confirm diagnosis
38
What is hyperosmolar hyperglycaemic state? What does it commonly present with?
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
How is type 2 managed?
``` Diet Oral medication Structured education May need insulin later Remission / reversal Prevention of complications ```
40
How does a T2DM consultation go?
Glycaemia: HbA1c, glucose monitoring if on insulin, medication review Weight assessment Blood pressure Dyslipidaemia: cholesterol profile Screening for complications: foot check, retinal screening
41
What dietary changes are recommended in T2DM?
``` Total calories control Reduce calories as fat Reduce calories as refined carbohydrate Increase calories as complex carbohydrate Increase soluble fibre Decrease sodium ```
42
If lifestyle changes don't work for a diabetic patient, what do we give them?
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
What drug is given to improve insulin sensitivity?
Metformin | Thiozolidinediones
44
What drug is given to boost insulin secretion?
Sulphonylureas DPP4-inhibitors GLP-1 Agonists
45
What drug is given to inhibit carb absorption in gut and inhibit renal glucose absorption?
Alpha glucosidase inhibitor | SGLT-2 inhibitor (renal)
46
What is the first line drug is lifestayle changes have no effect?
Metformin
47
How do sulphonyureas work?
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
What is pioglitazone? | S/Es?
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
How does metformin effect weight?
Lowers it
50
What is GLP-1?
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
What is the incretin effect?
Oral glucose increases insulin almost double as much as intravenous glucose
52
How do DPP-4 inhibitors work?
Inhibits DPP-4 enzyme which metabolises GLP-1
53
How do SGLT-2 inhibitors work? Examples?
Inhibit Na-Glu transporter so encourages glycosuria Lower HBA1C e.g. dapagliflozin, empagliflozin, canagliflozin
54
Do drugs work for diabetes?
Yes but eventually insulin will be needed and beta cell function will always decline
55
What surgery can remit diabetes? (not cure)
Gastric bypass surgery
56
What lifestyle change can remit diabetes?
Very low calorie diet (800-900 cals a day) for 3-6 months
57
How does diabetic ketoacidosis compare to hyperosmolar hyperglycaemic syndrome?
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
What are the different inflammatory adipokines?
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
How do genetic risks and environmental risks vary for the development of T2DM?
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
What is the imact of SNPs on diabetes?
Each individual SNP only has a small effect of risk but cumulative SNPs have a big risk of developing T2DM
61
Apart from obesity, what else can influence diabetes risk?
Stability of gut microbiota. Instability caused by: Obesity and IR Bacterial lipopolysaccharide fermentation to short hain FA Inflammation
62
What are side effects and contraindications of metformin?
GI side effects | Contraindicated in severe liver, cardiac or moderate renal failure
63
What is the effect of GLP-1 agonists and give examples
Decrease glucagon con and glucose conc Injected daily Lead to weight loss E.g. Liraglutide, semaglutide
64
What is the effect of DPPG-4 inhibitors?
Aka. Gliptins Inc. half life of exogenous GLP-1 Increase conc. of GLP-1 Dec. glucagon and glucose conc. No weight change
65
What are pros of SGLT-2 inhibitors?
Improve CKD Lower HbA1C Lower mortality Lower risk of hrt failure
66
What is the most effective medication in increasing beta cell function?
Sulfonylureas | Then metformin, the diet
67
What other aspects of management do we have to consider with T2DM?
Blood pressure management (maybe give ACEi) | Lipid management: Cholesterol, triglycerides, HDLs
68
What are examples of empowering language for a diabetic patient?
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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