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Year 2 RE > Type 2 Diabetes Mellitus > Flashcards

Type 2 Diabetes Mellitus Flashcards

1
Q

What is type 2 diabetes?

A
  • the body produces insulin but the body does not respond
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2
Q

What is the expected number of people that will have T2DM by 2030?

A
  • 5.5 million

- currently 4.9 million

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3
Q

How many patients are predicted to be at risk of T2DM?

A
  • 13.6 million
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4
Q

How much does T2DM cost the NHS each year aprox?

A
  • > £10 billion

- accounts for 10% of the NHS budget

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5
Q

T2DM costs the NHS aprox >£10 billion per year, accounting for 10% of the NHS budget. What is the majority of this money spent on?

A
  • complications of T2DM

- prescriptions

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6
Q

What number of patients that are in hospital have T2DM?

A
  • 20-30%
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7
Q

What is the difference between microvascular and macrovascular?

A
  • microvascular = small blood vessels

- macrovascular = large blood vessels

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8
Q

What are the 3 main microvascular complications that can occur in T2DM?

A
  • retinopathy (disease of blood vessels of the eye)
  • nephropathy (disease and deterioration of kidneys)
  • neuropathy (disease causing nerve damage, mainly peripheries)
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9
Q

What are the 3 main macrovascular complications that can occur in T2DM?

A
  • ischaemic heart disease
  • cardiovascular disease
  • peripheral vascular disease
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10
Q

In order what are the top 3 countries for the incidence of T2DM?

A 
1st = China
2nd = India
3 = USA
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11
Q

Are patients with T2DM have an increased or decreased risk of complications of Covid-19?

A
  • increased risk

- increases the risk of diabetic emergencies

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12
Q

What are the 2 diagnosis of T2DM based on a random glucose measurement?

A

1 - glucose equal to or >11 mmol/L with symptoms

2 - glucose equal to or >11 mmol/L in 2 separate samples

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13
Q

What are the diagnosis of T2DM based on HbA1c?

A
  • > 48 mmol/mol or 6.5%
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14
Q

An oral glucose tolerance test (OGTT) (75grams of glucose) can be used to assess if a patient has or is at risk of T2DM. What are cut offs for the following if the patient is fasted:

  • without diabetes
  • impaired glucose tolerance
  • diabetic
A
  • without diabetes = < 6.0 mmol/L
  • impaired glucose tolerance = 6.0-7.0 mmol/L
  • diabetic = >7.0 mmol/L
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15
Q

An oral glucose tolarence test (OGTT) can be used to assess if a patient has or is at risk of T2DM. What are cut offs for the following 2 hours after the OGTT has been administered?

  • without diabetes
  • impaired glucose tolerance
  • diabetic
A
  • without diabetes = < 7.8 mmol/L
  • impaired glucose tolerance = 7.9-11.0 mmol/L
  • diabetic = > 11.0 mmol/L
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16
Q

In patients with T2DM what are the 4 pathophysiological aspects we need to be aware of that occur in the pancreas?

A
  • increased beta cell apoptosis
  • reduced beta cell mass
  • reduced insulin secretion
  • hyperglucagonemia (excess glucagon secretion as low insulin to inhibits its release)
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17
Q

In patients with T2DM what is the main pathophysiological aspect we need to be aware of in the GIT?

A
  • impaired incretin effect
  • incretin is a factor released by the gut in response to nutrients that facilitates the uptake of glucose by peripheral tissues by stimulating secretion of insulin
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18
Q

In patients with T2DM what are the 2 main pathophysiological aspect we need to be aware of in the liver?

A

1 - insulin resistance

2 - increased hepatic glucose secretion (gluconeogenesis)

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19
Q

In patients with T2DM what is the main pathophysiological aspect we need to be aware of in the muscles?

A
  • insulin resistance
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20
Q

In patients with T2DM what are the 2 main pathophysiological aspect we need to be aware of in adipose tissue?

A

1 - increased circulating fatty acids

2 - hyperlipidaemia

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21
Q

Being over what age increases the risk of T2DM?

A
  • 45 years old

- increases risk 6 fold

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22
Q

Other than age what are the 3 other non-modifiable risk factors for developing T2DM?

A

1 - genetics
2 - ethnicity (south Asia/African Caribbean)
3 - family history

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23
Q

Other than age what are the 3 other modifiable risk factors for developing T2DM?

A

1 - obesity
2 - hyperlipidaemia
3 - hypertension

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24
Q

What are some of the key medications that may increase your risk of developing T2DM?

A
  • glucocorticoids (cortisol causes increased blood glucose through gluconeogenesis)
  • beta blockers (inhibit secretion of insulin)
  • statins
25
Q

What are the 3 stages of T2DM development?

A

1 - normal glucose tolerance
2 - pre-diabetes also known as Impaired glucose tolerance
3 - T2DM

26
Q

What tissue in the body has been linked with releasing something that has been show to increase insulin resistance in skeletal muscle?

A
  • adipose tissue

- through the release of free fatty acids

27
Q

In addition to releasing free fatty acids, adipose tissue has been show to trigger the release of other molecules which have been show to increase insulin resistance in skeletal muscle. What are these molecules?

A
  • adipokines (class of cytokines)

- these tigger inflammation at the muscle level

28
Q

In addition to releasing free fatty acids, adipose tissue has been show to trigger the release of other molecules which have been show to increase insulin resistance in skeletal muscle. What are these molecules?

A
  • adipokines (class of cytokines)

- these tigger inflammation at the muscle level

29
Q

Adipose tissue is able to release free fatty acids and induce inflammation as adipokines (a class of cytokines), which have been shown to increase insulin resistance in skeletal muscle. This then causes an impairment in the function of something in the mitochondria, what is this?

A
  • beta oxidation (fatty acid breakdown to produce energy) is reduced
30
Q

In addition to adipokines causing inflammation, and a reduction in beta oxidation due to fatty acid build up, there are 3 other things that can trigger which ultimately cause defects in translation pathways and reduced protein quality from the skeletal muscle cells?

A
  • impaired protein synthesis and quality
  • lipotoxicity (due to lipid derivate accumulation)
  • insulin resistance
31
Q

What is ectopic fat?

A
  • excess adipose tissue in locations not classically associated with adipose tissue storage
32
Q

Ectopic fat is excess adipose tissue in locations not classically associated with adipose tissue storage. Why is determining the amount of ectopic fat, which can come in the form of visceral or subcutaneous, a patient has important in a patient with or suspected of having T2DM?

A
  • increased adipose tissue is a risk factor for developing T2DM
  • due to fatty acids, beta oxidation and inflammation all increasing insulin resistance
33
Q

Increased levels of ectopic fat (excess adipose tissue in locations not classically associated with adipose tissue storage, which can come in the form of visceral or subcutaneous) causes increased circulating levels of fatty acids. What are 4 key things that these circulating fatty acids can then go on to cause in T2DM patients?

A

1 - adipocyte hypertrophy
2 - reduction in adipogenic genes (adipocyte proliferation)
3 - reduced lipogenic genes (lipolysis, inability to store fat)
4 - increase inflammation

34
Q

Increased levels of ectopic fat (excess adipose tissue in locations not classically associated with adipose tissue storage, which can come in the form of visceral or subcutaneous) causes increased circulating levels of fatty acids. This has been shown to reduce in adipogenic and lipogenic genes. Why is a reduction in adipogenic genes a bad thing in T2DM?

A
  • adipogenic genes ensure sequestration of lipids into adipocytes
  • adipogenic genes are also important to ensure hyperplasia rather than hypertrophy
  • without effective adipogenicity lipids can result in ectopic fat and lipotoxicity, inflammation and insulin resistance
35
Q

What is lipogenesis?

A
  • the conversion of fatty acids and glycerol into fats, or a metabolic process through which acetyl-CoA is converted to triglyceride for storage in fat
  • important for removing fat from the circulation and reducing ectopic fat
36
Q

Increased levels of ectopic fat (excess adipose tissue in locations not classically associated with adipose tissue storage, which can come in the form of visceral or subcutaneous) causes increased circulating levels of fatty acids. This has been shown to reduce in adipogenic and lipogenic genes. Lipogenesis is the conversion of fatty acids and glycerol into fats, or a metabolic process through which acetyl-CoA is converted to triglyceride for storage in fat. Why is this important in T2DM?

A
  • lipogenic genes ensure fat is absorbed into adipocytes and stored as triglycerides
  • triglycerides are less harmful to the body
  • without effective lipogenicity lipids can result in ectopic fat and lipotoxicity, inflammation and insulin resistance
37
Q

Increased levels of ectopic fat (excess adipose tissue in locations not classically associated with adipose tissue storage, which can come in the form of visceral or subcutaneous) causes increased circulating levels of fatty acids. This has been shown to cause adipocyte hypertrophy, rather than hyperplasia. Why is adipocyte hypertrophy a bad thing in T2DM?

A
  • adipocyte hypertrophy = adipocyte dysfunction, cell death, immune cell recruitment and inflammation
  • macrophages and monocytes trigger inflammation
  • inflammation leads to insulin resistance
38
Q

In normal muscle sensitivity to insulin, insulin is able to bind with the insulin receptor GLUT-4. How does this then cause an increase in glucose uptake from the blood and lower blood glucose?

1 - GLUT-4 receptors increase in size and can bind more insulin
2 - GLUT-4 receptors have increased sensitivity and can bind more insulin
3 - more GLUT-4 receptors open once one binds insulin
4 - GLUT-4 contained within vesicles is released

A

4 - GLUT-4 contained within vesicles is released

- GLUT-4 receptors make their way to the membrane and absorb glucose from the blood

39
Q

What is metabolic syndrome?

A
  • a cluster of conditions that occur together, increasing your risk of heart disease, stroke and type 2 diabetes
40
Q

Metabolic syndrome is a cluster of conditions that occur together, increasing your risk of heart disease, stroke and type 2 diabetes. The diagnosis criteria we need to be aware to diagnosis someone with metabolic syndrome is central obesity and what?

A
  • central obesity AND any 2 of the following 4:
  • raised triglycerides (≥ 150 mg/dL (1.7 mmol/L)
  • reduced HDL cholesterol (Males < 40 mg/dL (1.03 mmol/L and Females < 50 mg/dL (1.29 mmol/L)
  • raised blood pressure (BP ≥ 130 or diastolic BP ≥ 85 mm Hg)
  • raised fasting plasma glucose ( ≥ 5.6 mmol/L)
41
Q

When assessing patients waist circumference as a measure of central obesity, which can tell if a patient has metabolic syndrome or not, what non-modifiable risk factor must be taken into account?

A
  • account for ethnicity

- different ethnicities have different distribution of adipose tissue

42
Q

How does exercise affect glucagon and insulin secretion from the pancreas?

A
  • glucagon = increased release (stimulates glycogen release from muscles and fat)
  • insulin = decreased release as this would inhibit glucose for energy and try to store it as glycogen)
43
Q

How does exercise affect insulin sensitivity?

A
  • exercise stimulates GLUT-4 sensitivity and number

- more GLUT-4 = increased blood glucose absorption

44
Q

What 3 main effects does exercise have on the liver?

A

1 - increase gluconeogenesis (non-carb substrates (such as lactate, amino acids, and glycerol) into glucose
2 - increased fat oxidation (metabolise fat for energy)
3 - increased glycogenolysis (glycogen into glucose)

45
Q

What effects does exercise have on the lipolysis?

A
  • increased lipolysis (breakdown to triglycerides)

- essentially using fat as an energy source

46
Q

What effects does exercise have on the blood vessels and heart?

A
  • increased cardiac output

- increased vasodilation

47
Q

Exercise increases blood flow and muscle permeability. What 3 things increase in the muscle?

A

1 -increased glucose uptake
2- increased glycolysis (conversion of glucose into energy)
3 - increased fat oxidation (breakdown of fat for energy)

48
Q

T2DM has now been shown that we can revere T2DM. What is the diagnosis of remission of T2DM?

A
  • HbA1c < 48mmol/mol (6.5%)

- sustained for at least six months

49
Q

What is the most common cause of death amongst patients with T2DM?

A
  • ischaemic heart disease (also called coronary heart disease)
  • essentially narrowing of the arteries of the heart due to atherosclerotic plaque formation
50
Q

What are the 5 key treatment strategies used in T2DM?

A 
1 - diet
2 - exercise
3 - weight loss
4 - medication
5 - complication prevention (statins, anti-hypertensive and/or anti-platelet therapy)
51
Q

What are the 3 key macronutrient recommendations for patients with T2DM?

A

1 - low carbohydrate source
2 - reduce saturated and trans fats
3 - increase fibre intake

52
Q

What weight loss should patients with T2DM aim for?

A
  • 5-10% of body weight
53
Q

When would a patient with T2DM be considered for bariatric surgery?

A
  • BMI >35kg/m2 with recent diagnosis of T2DM and undergoing tier 3 (multidisciplinary team)
  • asians with BMI 30-34kg/m2 may be considered
54
Q

Hypertension is a risk factor in T2DM. How often should hypertension be monitored in a patient with T2DM, and what is the diagnosis of hypertension in a patient with T2DM?

A
  • at least annually

- BP >140/90 mmHg

55
Q

Hypertension in a T2DM patient is a BP >140/90 mmHg and should be monitored at least annually. What medication should be considered for patients with T2DM and hypertension?

A
  • ACE inhibitors (inhibit angiotensin II formation)

- Angiotensin receptor blockers (ARBs) (block the effects of angiotensin II)

56
Q

If a patient with T2DM has a Q-risk (a scoring system to determine the risk of having cardiovascular event in the next 10 years) >10%, what medication should they be started on to help manage their lipid profile?

A
  • atorvastatin at 20mg (if lifestyle intervention has failed)
  • Atorvastatin inhibits HMG-CoA reductase, rate limiting step in cholesterol synthesis
57
Q

If a patient with T2DM has a Q-risk (a scoring system to determine the risk of having cardiovascular event in the next 10 years) >10% they should be started on atorvastatin at 20mg (if lifestyle intervention has failed) which is able to inhibit HMG-CoA reductase, rate limiting step in cholesterol synthesis. If 20mg is insufficient, what is the maximum dose permitted?

A
  • 80mg taken once a day orally
58
Q

Although patients with T2DM do not have routine glucose monitoring, what are the 3 exceptions to this rule?

A

1 - patient is on insulin
2 - evidence of hyperglycaemia
3 - patient on oral medication to may increase hyperglycaemia
4 - if patient is pregnant or planning pregnancy

59
Q

What is the emergency presentation of a patient with T2DM?

A
  • Hyperosmolar Hyperglycaemic State (HHS)
  • very concentrated blood glucose levels
  • often >40mmol/L

Year 2 RE (53 decks)

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