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Year 2 RE Drugs > Diabetes Medication > Flashcards

Diabetes Medication Flashcards

1
Q

Metformin is one of the core drugs we need to know. Metformin is able to increase the activity of AMPK, which is a protein kinase that is important for cellular energy homeostasis, largely to activate glucose and fatty acid uptake and oxidation when cellular energy is low. What affect does metformin have on gluconeogenesis via increased activity of AMPK (glucose produced from non-carbohydrate precursors)?

1 - increases gluconeogenesis levels to ensure continues supply of glucose
2 - inhibits gluconeogenesis in the liver, reducing blood glucose
3 - inhibits gluconeogenesis in skeletal muscle
4 - accentuates gluconeogenesis and thus increase blood glucose levels

A

2 - inhibits gluconeogenesis in the liver, reducing blood glucose
- lower levels of gluconeogenesis mean lower glucose released into the blood by the liver

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2
Q

Biguanides, commonly known as metformin are able to have what effect on insulin receptors?

1 - increases number of GLUT-3 receptors on plasma membranes
2 - signals GLUT-4 to desensitise to insulin
3 - signals GLUT-4 in adipose and skeletal muscle to move to plasma membrane
4 - increases insulin receptors in the brain and liver

A

3 - signals GLUT-4 in adipose and skeletal muscle to move to plasma membrane
- GLUT-4 expression increased in muscle and fat allowing glucose to be absorbed and reduce blood glucose

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3
Q

Biguanides, commonly known as metformin has what effect on lipogenic (converting fatty acids and glycerol into TAG) enzymes and fatty acid oxidation?

1 - inhibits lipogenic enzymes and increased fatty acid oxidation
2 - inhibits lipogenic enzymes and fatty acid oxidation
3 - increases lipogenic enzymes and fatty acid oxidation
4 - increases lipogenic enzymes and inhibits fatty acid oxidation

A

1 - inhibits lipogenic enzymes and increased fatty acid oxidation

  • lipogenic enzyme inhibition means FFA are not stored as fat
  • increase fatty acid oxidation means fat is used as an energy source
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4
Q

Biguanides, commonly known as metformin is able to inhibit lipogenic enzymes (storage of FFA and glycerol as TAG) and increase fatty acid oxidation as an energy source. Taking into account this mechanism, what is metformin able to do that other drugs do not do, and part of the reason why metformin is the 1st line drug?

1 - increases beta cell mass
2 - causes weight loss
3 - causes beta cell hypertrophy
4 - reduces glucagon secretion

A

2 - causes weight loss

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5
Q

What are the main side effects of metformin?

1 - gastrointestinal, headaches, B12 deficiency, hypoglycaemia
2 - gastrointestinal, headaches, B2 deficiency, hyperglycaemia
3 - gastrointestinal, weight loss, B12 deficiency, hypoglycaemia
4 - gastrointestinal, weight loss, B12 deficiency, hyperglycaemia

A

1 - gastrointestinal, headaches, B12 deficiency, hypoglycaemia

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6
Q

What are the 3 most common contradictions for metformin prescription?

1 - taking insulin, eGFR <30ml/min/1.73m2, CVD
2 - CVD, eGFR <30ml/min/1.73m2, liver dysfunction due to lactic acidosis
3 - acute metabolic acidosis, eGFR <30ml/min/1.73m2, liver dysfunction due to lactic acidosis
4 - acute metabolic acidosis, eGFR <30ml/min/1.73m2, CVD

A

3 - acute metabolic acidosis, eGFR <30ml/min/1.73m2, liver dysfunction due to lactic acidosis

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7
Q

How can metformin cause lactic acidosis?

1 - increases lactate production in muscles
2 - alters pH of blood leading to lactic acidosis
3 - reduces gluconeogenesis which uses lactic acid
4 - increases enzymes responsible for lactate production

A

3 - reduces gluconeogenesis which uses lactic acid

  • lactate can be recycled in liver during gluconeogenesis to make energy
  • metformin inhibits gluconeogenesis meaning lactate remains in the blood
  • kidneys can remove lactate, but patient with diabetes have impaired eGFR meaning lactate cannot be effectively removed
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8
Q

When glucose is present in the blood, GLUT-2 (glucose transporter) is present on beta cells to detect the blood glucose and allow glucose to enter the beta cell. The glucose undergoes glycolysis (glucose to ATP) and then ATP levels rise causing K+ channels to close and depolarise the cell. What then must occur for insulin to be released by the beta cell?

1 - depolarisation opens Ca2+ channels, Ca2+ signals exocytosis of insulin in vesicles
2 - re-polarisation opens Ca2+ channels, Ca2+ signals exocytosis of insulin in vesicles
3 - depolarisation opens Na+ channels, Na+ signals exocytosis of insulin in vesicles
4 - depolarisation opens K+ channels, Ca2+ signals exocytosis of insulin in vesicles

A

1 - depolarisation opens Ca2+ channels, Ca2+ signals exocytosis of insulin in vesicles

  • Ca2+ entry into the cell signals exocytosis of vesicles containing insulin
  • insulin is released into the blood
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9
Q

What is the mechanism of action of the drug group sulphonylureas, with the drug we need to know Gliclazide?

1 - blocks Na+ channels closing on beta cell causing cellular depolarisation
2 - blocks K+ channels closing on beta cell causing cellular re-polarisation
3 - blocks K+ channels closing on alpha cell causing cellular depolarisation
4 - blocks K+ channels so they cannot open on beta cell causing cellular depolarisation

A

4 - blocks K+ channels so they cannot open on beta cell causing cellular depolarisation

  • K+ ATP sensitive channel not as sensitive in T2DM so doesn’t open as much
  • binds and blocks K+ channels from opening
  • K+ cannot leave the beta cell and the cell depolarises, Ca2+ channels open and insulin is released
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10
Q

What are the 3 main side effects of sulphonylureas, with the drug we need to know Gliclazide?

1 - hypoglycaemia, weight gain, secondary failure of beta cells due to excessive stress
2 - hyperglycaemia, weight loss, secondary failure of beta cells due to excessive stress
3 - hypoglycaemia, weight gain, hypertrophy of beta cells due to excessive stress
4 - hypoglycaemia, weight loss, secondary failure of alpha cells due to excessive stress

A

1 - hypoglycaemia, weight gain, secondary failure of beta cells due to excessive stress

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11
Q

What are the 2 main contraindications of sulphonylureas, with the drug we need to know Gliclazide?

1 - lactic acidosis, chronic porphyuria, G6PD deficiency
2 - ketoacidosis, acute porphyuria, G6PD deficiency
3 - lactic acidosis, acute porphyuria, G6PD deficiency
4 - ketoacidosis, acute porphyuria, age

A

1 - lactic acidosis, chronic porphyuria, G6PD deficiency

  • G6PD deficiency leads to RBC destruction
  • cautions: age, obesity (as drug can cause weight gain)
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12
Q

In a normal healthy person glucose passes through the glomerulus, into the filtrate and then through the collecting tubules. 100% of the glucose is then reabsorbed along with Na+, mainly in the convoluted proximal tubule by sodium-dependent glucose co-transporters (SGLT-2) (except if glucose is above 10mmol/L). What is the mechanism of action of (SGLT-2) inhibitors?

1 - inhibit SGLT-2, K+ and glucose are not reabsorbed
2 - inhibit SGLT-2, Na+ and glucose are not reabsorbed
3 - activate SGLT-2, Na+ and glucose are not reabsorbed
4 - activate SGLT-2, Na+ and glucose are reabsorbed

A

2 - inhibit SGLT-2, Na+ and glucose are not reabsorbed

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13
Q

In a normal healthy person glucose passes through the glomerulus, into the filtrate and then through the collecting tubules. 100% of the glucose is then reabsorbed along with Na+, mainly in the convoluted proximal tubule by sodium-dependent glucose co-transporters (SGLT-2) (except if glucose is above 10mmol/L). SGLT-2) inhibitors are able to inhibit SGLT-2 so Na+ and glucose are not reabsorbed. Does this group of drugs have any affect on insulin secretion?

A
  • no
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14
Q

What are the main side effects of sodium-dependent glucose co-transporters (SGLT-2) inhibitors?

A
  • glucosuria
  • genital and urinary tract infection (lots of sugar increases risk of infection)
  • euglyaemic (normal blood glucose) DKA, can often be missed as blood glucose appears normal
  • polyuria
  • hypotension (due to water loss)
  • reduce bone density
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15
Q

What are the 4 main contraindications for sodium-dependent glucose co-transporters (SGLT-2) inhibitors?

A

1 - risk of diabetic ketoacidosis
2 - chronic kidney disease
3 - age (fluid volume loss)
4 - heart failure (loss of volume)

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16
Q

Incretins are a group of hormones responsible for reducing blood glucose, such as glucagon like peptide-1 (GLP-1). Enteroendocrine cells are specialised cells that are able to release incretins. in the pancreas and small intestines. What effect does GLP-1 agonist have on the pancreas?

1 - inhibit insulin and glucagon release
2 - increase insulin and glucagon release
3 - increase insulin and inhibit glucagon release
4 - inhibit insulin and increase glucagon release

A

3 - increase insulin and inhibit glucagon release

17
Q

Incretins are a group of hormones responsible for reducing blood glucose, such as glucagon like peptide-1 (GLP-1). Enteroendocrine cells are specialised cells that are able to release incretins. in the pancreas and small intestines. GLP-1 agonists are able to increase insulin and inhibit glucagon release from the pancreas. What other 3 effects can they have?

1 - increase hepatic gluconeogenesis and gastric emptying, increase peripheral insulin sensitivity
2 - reduce hepatic gluconeogenesis and gastric emptying, increase peripheral insulin sensitivity
3 - increase hepatic gluconeogenesis and gastric emptying, reduce peripheral insulin sensitivity
4 - reduce hepatic gluconeogenesis, gastric emptying and peripheral insulin sensitivity

A

2 - reduce hepatic gluconeogenesis and gastric emptying, increase peripheral insulin sensitivity
- reduced gastric emptying reduces blood glucose spikes

18
Q

Incretins are a group of hormones responsible for reducing blood glucose, such as glucagon like peptide-1 (GLP-1). Enteroendocrine cells are specialised cells that are able to release incretins. What are the 3 main side effects of GLP-1 agonists?

1 - gastrointestinal, hyposensitivity (immunity), local skin reactions to injection sites
2 - gastrointestinal, hypersensitivity (immunity), systemic skin reactions to injection sites
3 - weight loss, hypersensitivity (immunity), local skin reactions to injection sites
4 - gastrointestinal, hypersensitivity (immunity), local skin reactions to injection sites

A

4 - gastrointestinal, hypersensitivity (immunity), local skin reactions to injection sites

19
Q

If a patient has been diagnosed with T2DM, or is at risk of developing T2DM as per a rise in HbA1c >48mmol/mol (6.5%), what are the first 2 things that must be discussed prior to medications?

1 - diet only
2 - exercise only
3 - metformin
4 - diet and exercise

A

4 - diet and exercise

20
Q

If a patient has been diagnosed with T2DM, or is at risk of developing T2DM as per a rise in HbA1c >48mmol/mol (6.5%), the first 2 things that must be discussed prior to medications are exercise/physical activity and diet. If diet and exercise fail, what is the first line medication treatment for this group of patients that could be prescribed with diet and exercise?

1 - sulphonylureas
2 - insulin
3 - metformin
4 - SGLT-2 inhibitors

A

3 - standard metformin

- if poorly tolerated (GI symptoms) modified metformin should be prescribed (reduces GI effects)

21
Q

If a patient has been diagnosed with T2DM, or is at risk of developing T2DM as per a rise in HbA1c >48mmol/mol (6.5%), the first 2 things that must be discussed prior to medications are exercise/physical activity and diet. If diet, exercise and metformin fail at trying to reduce HbA1c below 48mmol/mol, what is the next treatment option for patients?

1 - diet, exercise and stronger does of metformin
2 - diet, exercise, metformin and bariatric surgery
3 - diet, exercise, metformin and a sulphonylureas (gliclazide) or SGLT-2
4 - diet, exercise, metformin and a sulphonylureas (gliclazide) and SGLT-2

A

3 - diet, exercise, metformin and a sulphonylureas (gliclazide) or SGLT-2

22
Q

If a patient has been diagnosed with T2DM, or is at risk of developing T2DM as per a rise in HbA1c >48mmol/mol (6.5%), the first 2 things that must be discussed prior to medications are exercise/physical activity and diet. If diet, exercise, metformin and a sulphonylureas (gliclazide) or SGLT-2 fail at trying to reduce HbA1c below 48mmol/mol, what is the next treatment option for patients?

1 - diet, exercise and stronger does of metformin
2 - diet, exercise, metformin and bariatric surgery
3 - diet, exercise, metformin and a sulphonylureas (gliclazide) or SGLT-2
4 - diet, exercise, metformin and a sulphonylureas (gliclazide) and SGLT-2

A

4 - diet, exercise, metformin and a sulphonylureas (gliclazide) and SGLT-2

23
Q

If a patient has been diagnosed with T2DM, or is at risk of developing T2DM as per a rise in HbA1c >48mmol/mol (6.5%), the first 2 things that must be discussed prior to medications are exercise/physical activity and diet. If diet, exercise, metformin, sulphonylureas (gliclazide) and SGLT-2 fail at trying to reduce HbA1c below 48mmol/mol, what is the next treatment option for patients?

1 - diet, exercise, metformin and a sulphonylureas (gliclazide), SGLT-2 and insulin
2 - diet, exercise, metformin and bariatric surgery
3 - diet, exercise, metformin and a sulphonylureas (gliclazide) or SGLT-2
4 - diet, exercise, metformin and a sulphonylureas (gliclazide) and SGLT-2

A

1 - diet, exercise, metformin and a sulphonylureas (gliclazide), SGLT-2 and insulin

24
Q

If a patient has a HbA1c >48mmol/ml (6.5%), they have failed to respond to lifestyle changes, and they are unable to be prescribed metformin, what would be the first line treatment?

1 - sulphonylureas or SGLT-2 inhibitors
2 - insulin or SGLT-2 inhibitors
3 -SGLT-2 inhibitors and bariatric surgery
4 - SGLT-2 inhibitors alone

A

1 - sulphonylureas or SGLT-2 inhibitors

25
Q

Insulin is used to treat T1DM. Insulin duration affects can vary. What is added to the insulin that determines its duration?

1 - protamine
2 - glucose
3 - protease
4 - prolactin

A

1 - protamine

- affects insulins solubility meaning it cannot be absorbed as quickly by cells

26
Q

What is the standard first line 2 stage insulin regime that is recommended clinically?

A

1 - long acting = basal

2 - quick acting to cover meal = bolus

27
Q

What insulin regime is depicted in the image below that is recognised as the gold standard treatment using insulin?

1 - bolus regime
2 - twice daily insulin regime
3 - basal-bolus regimen/multi-daily injection therapy
4 - once daily insulin regime

A

3 - basal-bolus regimen/multi-daily injection therapy

  • GOLD STANDARD for T1DM management
  • accounts for post-prandial hyperglycaemia and continued low does of insulin
  • covers entire 24 hour period
28
Q

What is the insulin to carbohydrate ratio?

1 - 1:1 = 1 unit of insulin:1 gram of carbs
2 - 1:1 = 1 unit of insulin:10 grams of carbs
3 - 1:1 = 1 unit of insulin:20 grams of carbs
4 - 1:1 = 1 unit of insulin:100 grams of carbs

A

2 - 1:1 = 1 unit of insulin:10 grams of carbs

29
Q

When glucose is present in the blood, which glucose transporter is present on beta cells to detect the blood glucose?

1 - GLUT-1
2 - GLUT-2
3 - GLUT-3
4 - GLUT-4

A

2 - GLUT-2

Year 2 RE Drugs (5 decks)

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