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A. MLA Map Endocrine and Metabolic > Type 2 Diabetes Mellitus > Flashcards

Type 2 Diabetes Mellitus Flashcards

1
Q

Which of the following are diagnostic of T2DM based on a random glucose measurement?

1 - Glucose >11.1 mmol/l with Symptoms
2 - Glucose = > 11.1 mmol/l on 2 occasions
3 - HbA1c = > 48 mmol/mol ( 6.5% )
4 - all of the above

A

4 - all of the above
2 - glucose equal to or >11 mmol/L in 2 separate samples

Hypoglycaemia is <4mmol/L

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2
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. Match cut off values for the following if the patient is fasted:

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

Hypoglycaemia is <4mmol/L

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3
Q

An oral glucose tolarence test (OGTT) can be used to assess if a patient has or is at risk of T2DM. Match cut off values for the following after an OGTT:

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

Hypoglycaemia is <4mmol/L

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4
Q

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

1 - increased beta cell apoptosis
2 - reduced beta cell mass
3 - reduced insulin secretion
4 - hyperglucagonemia (excess glucagon secretion as low insulin to inhibits its release)
5 - all of the above

A

5 - all of the above

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5
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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6
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)
2 - increased hepatic glucose secretion (gluconeogenesis)

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7
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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8
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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9
Q

Being over what age increases the risk of T2DM?

1 - 16 y/o
2 - 25 y/o
3 - 45 y/o
4 - 65 y/o

A

3 - 45 years old
- increases risk 6 fold

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10
Q

Other than age which of the following are non-modifiable risk factors for developing T2DM?

1 - genetics
2 - ethnicity (south Asia/African Caribbean)
3 - family history
4 - all of the above

A

4 - all of the above

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11
Q

What modifiable risk factors for developing T2DM?

1 - obesity
2 - hyperlipidaemia
3 - hypertension
4 - all of the above

A

4 - all of the above

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12
Q

Which of the following medications may increase the risk of developing T2DM?

1 - glucocorticoids
2 - beta blockers
3 - statins
4 - all of the above

A

4 - all of the above

  • glucocorticoids = cortisol increases blood glucose through gluconeogenesis
  • beta blockers = inhibit secretion of insulin
  • statins
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13
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

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14
Q

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

1 - adipocytes
2 - neuronal cells
3 - hepatocytes
4 - renal cells

A

1 - adipocytes
- adipose tissue
- through the release of free fatty acids

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15
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?

1 - neutrophils
2 - thyroglobulin
3 - adipokines
4 - lymphocytes

A

3 - adipokines (class of cytokines)
- these tigger inflammation at the muscle level

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16
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?

1 - lipolysis
2 - gluconeogenesis
3 - beta oxidation
4 - glycolysis

A

3 - beta oxidation
- fatty acid breakdown to produce energy is reduced

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17
Q

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

1 - impaired protein synthesis and quality
2 - lipotoxicity (due to lipid derivate accumulation)
3 - insulin resistance
4 - all of the above

A

4 - all of the above

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18
Q

What is ectopic fat?

A
  • excess adipose tissue in locations not classically associated with adipose tissue storage
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19
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?

1 - increases risk of T1DM
2 - increases risk of renal failure
3 - increases risk of NAFLD
4 - increases risk of T2DM

A

4 - increases risk of T2DM

  • increased adipose tissue is a risk factor for developing T2DM
  • due to fatty acids, beta oxidation and inflammation all increasing insulin resistance
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20
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. Which of the following can circulating fatty acids then go on to cause in T2DM patients?

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

A

5 - all of the above

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21
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 excess lipids can result in ectopic fat and lipotoxicity, inflammation and insulin resistance
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22
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
23
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, lipotoxicity, inflammation and insulin resistance
24
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
25
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
  • GLUT-4 receptors make their way to the membrane and absorb glucose from the blood
26
Q

What is metabolic syndrome?

A
  • a cluster of conditions that occur together, increasing your risk of heart disease, stroke and type 2 diabetes
27
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 how many of the following?

  • 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)
A
  • central obesity and any 2 or more of the other criteria
28
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?

1 - age
2 - gender
3 - ethnicity

A

3 - account for ethnicity
- different ethnicities have different distribution of adipose tissue

29
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)
30
Q

How does exercise affect insulin sensitivity?

A
  • exercise stimulates GLUT-4 sensitivity and number
  • more GLUT-4 = increased blood glucose absorption
31
Q

Which of the following effects can exercise have on the liver?

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)
4 - all of the above

A

4 - all of the above

32
Q

Does exercise increase or decrease lipolysis?

A
  • increased lipolysis (breakdown to triglycerides)
  • essentially using fat as an energy source
33
Q

Exercise increases blood flow and muscle permeability. Which of the following occur in the muscle?

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

A

4 - all of the above

34
Q

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

1 - HbA1c < 58mmol/mol (6.5%)
2 - HbA1c < 50mmol/mol (6.5%)
3 - HbA1c < 48mmol/mol (6.5%)
4 - HbA1c < 40mmol/mol (6.5%)

A

3 - HbA1c < 48mmol/mol (6.5%)
- sustained for at least six months

35
Q

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

1 - liver failure
2 - renal failure
3 - ischaemic heart disease/coronary heart disease
4 - cerebral hypoxia

A

3 - ischaemic heart disease/coronary heart disease
- essentially narrowing of the arteries of the heart due to atherosclerotic plaque formation

36
Q

Which of the following are key treatment strategies used in T2DM?

1 - diet
2 - exercise
3 - weight loss
4 - medication
5 - complication prevention (statins, anti-hypertensive and/or anti-platelet therapy)
6 - all of the above

A

6 - all of the above

37
Q

Which of the following is NOT a key macronutrient recommendations for patients with T2DM?

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

A

4 - increased protein intake

38
Q

What weight loss should patients with T2DM aim for?

1 - 1-2% body weight
2 - 2-5% body weight
3 - 5-10% body weight
4 - >20% body weight

A

3 - 5-10% body weight

39
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
40
Q

Hypertension is a risk factor in T2DM. How often should hypertension be monitored in a patient with T2DM?

1 - 12 weeks
2 - 6 months
3 - annually
4 - every 2 years or as required

A

3 - annually
- BP >140/90 mmHg

41
Q

Hypertension is a risk factor in T2DM. What is the diagnosis of hypertension in a patient with T2DM?

1 - >130/80 mmHg
2 - >140/90 mmHg
3 - >150/100 mmHg
4 - >180 mmHg

A

2 - >140/90 mmHg

42
Q

Hypertension in a T2DM patient is a BP >140/90 mmHg and should be monitored at least annually. Which of the following medications should be considered as 1st line treatment for a patients with T2DM and hypertension?

1 - ACE-I or ARB-II
2 - statins
3 - metformin
4 - beta blocker

A

1 - ACE-I or ARB-II
- Angiotensin receptor blockers (ARBs) (block the effects of angiotensin II)

43
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?

1 - ACE-I or ARB-II
2 - statins
3 - metformin
4 - beta blocker

A

2 - statins

  • atorvastatin at 20mg (if lifestyle intervention has failed)
  • Atorvastatin inhibits HMG-CoA reductase, rate limiting step in cholesterol synthesis
44
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?

1 - 40mg
2 - 80mg
3 - 120mg
4 - 200mg

A

2 - 80mg
- taken once a day orally

45
Q

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

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
5 - all of the above

A

5 - all of the above

46
Q

What is the emergency presentation of a patient with T2DM?

A
  • Hyperosmolar Hyperglycaemic State (HHS)
  • very concentrated blood glucose levels
  • often >40mmol/L
47
Q

According to the new algorithm, which of the following are now assessed in a patient newly diagnosed with T2DM prior to prescribing?

1 - HbA1c
2 - cardiovascular risk
3 - kidney function risk
4 - all of the above

A

4 - all of the above

48
Q

If able to take, what is the 1st line medication for all patients diagnosed with T2DM?

1 - Dapagliflozin (SGLT-2)
2 - Metformin (Biguanides)
3 - Gliclazide (Sulfonylurea)
4 - Dulaglutide (GLP-1)

A

2 - Metformin (Biguanides)

  • if GI effects are affected we can try modified release (MR) metformin

If Gliclazide is combined with metformin there is a risk of hypoglycaemia

49
Q

If a patient has been diagnosed with T2DM and has a high risk of cardiovascular disease, what additional drug can be prescribed alongside the metformin?

1 - Dapagliflozin (SGLT-2)
2 - Linagliptin (DPP4 inhibitor)
3 - Gliclazide (Sulfonylurea)
4 - Dulaglutide (GLP-1)

A

1 - Dapagliflozin (SGLT-2)

50
Q

What drug should be prescribed in T2DM who cannot be prescribed T2DM?

1 - Dapagliflozin (SGLT-2)
2 - Linagliptin (DPP4 inhibitor)
3 - Gliclazide (Sulfonylurea)
4 - Dulaglutide (GLP-1)

A

1 - Dapagliflozin (SGLT-2)

51
Q

According to the new NICE algorithm In a patient who is symptomatic and is hyperglycaemic, which 2 of the following should be tried to treat the patient?

1 - Dapagliflozin (SGLT-2)
2 - Linagliptin (DPP4 inhibitor)
3 - Gliclazide (Sulfonylurea)
4 - Dulaglutide (GLP-1)
5 - insulin

A

3 - Gliclazide (Sulfonylurea)
5 - insulin

52
Q

If a patient is sick, has abdominal pain, diarrhoea and/or vomiting, the following drugs should be stopped:

  • glucose lowering medication (metformin, SGLT-2 inhibitor and GLP-1 agonist)
  • ACE, ARB, diuretics and mineralcorticoid receptor antagonists
  • statins

These medications should only be restarted when the patient has begun eating and drinking normally for how long?

1 - 12h
2 - 24h
3 - 48h
4 - 72h

A

3 - 48h

53
Q

If a patient is hypoglycaemic (blood glucose is 1.4 mmol/L) which of the following is the most appropriate treatment?

1 - Oral long-acting carbohydrate, eg biscuits, bread, sandwich
2 - Oral 40% Glucogel® x2 tubes
3 - Intramuscular Glucagon 1mg
4 - Intravenous Dextrose 20%, 100 ml over 15 minutes
5 - Intravenous Dextrose 50%, 100 ml over 15 minute

A

4 - Intravenous Dextrose 20%, 100 ml over 15 minutes
- Faster acting than IM glucagon

Once glucose is >4.5mmol/L give patient long acting carbohydrates

DO NOT OMIT INSULIN IF PATIENT TAKING THIS

A. MLA Map Endocrine and Metabolic (10 decks)

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