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17. Clinical Pharmacology and Therapeutics > 4. Pharmacology of Oral Hypoglycaemic Agents > Flashcards

4. Pharmacology of Oral Hypoglycaemic Agents Flashcards

1
Q

What causes blood glucose to rise?

A

Inability to produce insulin due to beta cell failure or insulin production adequate but resistance prevents it working effectively.

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2
Q

What is the treatment plan for type 1 diabetes mellitus?

A

Lifestyle changes + insulin.

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3
Q

What is the treatment plan for type 2 diabetes mellitus?

A

Lifestyle changes + non-insulin therapies.

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4
Q

What non-insulin therapies are available to type 2 diabetics?

A

Biguanides, sulphonylureas, thiazolidinediones, DPP4 inhibitors, a-glucosidase inhibitors, SGLT2s, GLP1, analogues and insulin.

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5
Q

What are the challenges for patients with type 2 diabetes considering adherence?

A

Risk/perceived risk of hypoglycaemia and weight gain/fear of weight gain.

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6
Q

What are the NICE targets in type 2 diabetes for HbA1c if: diet and first two treatment steps, risk of severe hypoglycaemia.

A
  1. 6.5%

2. 7.5%

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7
Q

What is the mechanism of action of metformin?

A

Reduces insulin resistance so increased glucose by tissue. Decreases hepatic glucose production.

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8
Q

What are the results of metformin?

A

Limited weight gain, fewer CVS events.

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9
Q

What are some ADRs of metformin?

A

GI symptoms, lactic acidosis (rare), vitamin B12 deficiency (uncommon).

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10
Q

What is the mechanism of action of sulphonylureas?

A

Stimulate beta cells to release more insulin.

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11
Q

What are the results of taking sulphonylureas?

A

Decreased microvascular risk.

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12
Q

What are the ADRs of sulphonylureas?

A

Weight gain, hypoglycaemia.

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13
Q

What is the mechanism of action of acarbose (a-glucosidase inhibitor)?

A

Inhibits breakdown of carbohydrates to glucose by blocking enzyme a-glucosidase.

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14
Q

What are the ADRs of acarbose?

A

Flatulence, loos stools, diarrhoea.

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15
Q

What is the effect of taking acarbose on HbA1c?

A

Modest reduction of about 0.5%.

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16
Q

What is the mechanism of action of glitazones?

A

Increase insulin sensitivity in muscle and adipose tissue and decrease hepatic glucose output. Binds and activates peroxisome proliferator-activated receptors.

17
Q

What is the main concern with glitazones?

A

Cardiovascular risks, so rarely used.

18
Q

What are the concerns with pioglitazone?

A

Weight gain, fluid retention and heart failure, effect on bone metabolism and bladder cancer.

19
Q

What is the mechanism of action of glucagon like peptide 1 therapies?

A

Increase insulin secretion from beta cells and decreases production of glucagon from alpha cells.

20
Q

What are some examples of glucagon like peptide 1 therapy?

A

Exenatide, lireglutide, lixisenatide.

21
Q

What are the physiological effects of glucagon like peptide 1 therapy on the pancreas, liver, brain, stomach, and muscle?

A

Pancreas - increased insulin secretion and biosynthesis, decreased glucagon secretion.
Liver - decreased glucose production.
Brain - decreased food intake through increased satiety.
Stomach - decreased gastric emptying.
Muscle - increased glucose uptake.

22
Q

What are the two branches of incretin-based therapies?

A

DPP-4 inhibitors and GLP-1 receptor agonists.

23
Q

What is the mechanism of action of DPP-4 inhibitors?

A

Protects native GLP-1 from inactivation by DPP-4.

24
Q

What are some DPP-4 inhibitor drugs?

A

Sitagliptin, vildagliptin, saxagliptin, linagliptin.

25
Q

What is the mechanism of action of GLP-1 receptor agonists?

A

Mimics native GLP-1.

26
Q

What are some GLP-1 receptor agonists?

A

Exenatide, liraglutide.

27
Q

What are the ADRs of incretin-based therapies?

A

GI symptoms, possibly pancreatitis, low risk hypoglycaemia.

28
Q

What is the impact on HbA1c of incretin-based therapies?

A

Modest reduction.

29
Q

What are the ADRs of GLP-1 agonists?

A

GI symptoms (nausea, loose stools, diarrhoea), GORD, hypoglycaemia (low risk), painful to inject, possibly pancreatitis and pancreatic carcinoma.

30
Q

What is a contra-indication of GLP-1 agonist use?

A

eGFR < 30ml/min.

31
Q

What is the mechanism of action of sodium-glucose co-transporter 2 inhibitors?

A

Selectively inhibit SGLT2 in renal proximal tubule so glucose can’t leave, causing osmotic diuresis so more glucose leaves in the urine, the glucose renal limit is effectively reduced.

32
Q

What are the ADRs of SGLT2 inhibitors/glifozins?

A

Increased risk of lower UTIs, polyuria, low risk of hypoglycaemia.

33
Q

What are some SGLT2 inhibitors/glifozins?

A

Dapagliflozin, canagliflozin, empagliflozin.

17. Clinical Pharmacology and Therapeutics (25 decks)

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