4. Pharmacology of Oral Hypoglycaemic Agents Flashcards

(33 cards)

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
What is the mechanism of action of GLP-1 receptor agonists?
Mimics native GLP-1.
26
What are some GLP-1 receptor agonists?
Exenatide, liraglutide.
27
What are the ADRs of incretin-based therapies?
GI symptoms, possibly pancreatitis, low risk hypoglycaemia.
28
What is the impact on HbA1c of incretin-based therapies?
Modest reduction.
29
What are the ADRs of GLP-1 agonists?
GI symptoms (nausea, loose stools, diarrhoea), GORD, hypoglycaemia (low risk), painful to inject, possibly pancreatitis and pancreatic carcinoma.
30
What is a contra-indication of GLP-1 agonist use?
eGFR < 30ml/min.
31
What is the mechanism of action of sodium-glucose co-transporter 2 inhibitors?
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
What are the ADRs of SGLT2 inhibitors/glifozins?
Increased risk of lower UTIs, polyuria, low risk of hypoglycaemia.
33
What are some SGLT2 inhibitors/glifozins?
Dapagliflozin, canagliflozin, empagliflozin.