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2.2 T1: The endocrine system > T1 L14: Drug treatment for T2 diabetes > Flashcards

T1 L14: Drug treatment for T2 diabetes Flashcards

1
Q

What is the effects of insulin on hepatic cells?

A

Decrease gluconeogenesis, glycogenolysis and ketogenesis (increases glycogen synthesis)

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2
Q

What is the effect of insulin on muscle cells?

A
  • Increases GLUT-4 translocation to the membrane and hence increases glucose uptake, glucose oxidation, glycogen synthesis, amino acid uptake and protein synthesis
  • Decreases glycogenolysis and amino acid release
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3
Q

What effect does insulin have on adipocytes?

A
  • Increases glucose uptake and triglyceride synthesis

- Decreases FFA and Glycerol release

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4
Q

What is the net effect of insulin?

A

To cause hypoglycaemia and increase fuel storage in muscle, fat and liver cells

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5
Q

Gliclazide, Glipizide, and Glimepiride are example of which drug type?

A

Sulfonylureas

They are all orally active and all bound to plasma proteins so they have a long half life

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6
Q

How do Sulfonylureas work?

A

They bind to the ATP site of K+ transporter proteins to close the channel to cause a build up of Ca2+ inside the cell which will make the cell positive.

This process makes the cells release more insulin because Ca2+ is needed to release insulin

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7
Q

What are some secondary mechanisms of action of Sulfaonylureas?

A
  • Sensitize B-cells to glucose
  • Decrease lipolysis
  • Decrease clearance of insulin by the liver
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8
Q

Why are Sulfonlyureases only used for T2 diabetes mellitus not T1?

A

Because the drugs target beta-cells to release more insulin but T1 diabetics don’t have sufficient beta-cells for this to be effective

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9
Q

What are some drug interactions of Sulfonylureases?

A

They potentiate Allopurinol, Aspirin, and alcohol

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10
Q

What is the gold standard for treating T2 diabtes?

A

Metformin - a biguanide

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11
Q

How do Biguanides work?

A

They target insulin resistance by increasing glucose uptake in muscle and decrease glucose production by the liver

They don’t stimulate insulin release or cause hypoglycaemia

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12
Q

What is the mechanism of action of Metformin?

A

Mechanism of action in unknown but involves primarily supressing hepatic glucose production through gluconeogenesis by lowering the levels of PEPCK and glucoe-6-phosphatase

It increases insulin sensitivity, enhances peripheral glucose uptake, increases fatty-acid oxidation, and decreases glucose absorption from the GI tract

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13
Q

How is Metformin excreted?

A

Through urine

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14
Q

Why doesn’t it matter that Metformin isn’t bound to plasma proteins?

A

Because it has it’s effects are in the liver so the hepatic first pass pass effect doesn’t affected it in a negative way

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15
Q

What are some adverse effects of Metformin?

A
  • Rarely produces lactic academia mostly in patients with renal impairment
  • Nausea
  • Abdominal discomfort
  • Diarrhoea
  • Metallic taste
  • Vitamin B12 and folate absorption decreased with chronic use
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16
Q

What are some contraindications of Metformin?

A
  • Hepatic disease
  • Past history of lactic acidosis
  • Chronic hypoxic lung disease because it causes metabolic acidosis
17
Q

What do Glitazones do?

A

They mimic insulin

  • Decrease gluconeogenesis, glucose output, and triglyceride production in the liver
  • Increase glucose uptake
  • Cause differentiation of adipocytes
18
Q

How is the drug Pioglitazone metabolised and excreted?

A

Metabolised in the liver and excreted in faeces (2/3) and in urine (1/3)

19
Q

What are some adverse effects of using Glitazones?

A
  • Fluid retention causing oedema
  • Dose related weight gain because they increase the number of adipocytes

Don’t cause lactic acidosis. Liver damage patients need to be monitored

20
Q

How do Glucagon-like peptide 1 (GLP-1) hormones work?

A
  • Increase insulin secretion
  • Decrease glucagon secretion and hepatic glucose output
  • Decrease food intake
  • Decrease plasma glucose levels
21
Q

Give 2 examples of Glucagon-like peptide-1 analogs

A

Exenatide and Semaglutide

22
Q

How do Dipeptidyl peptidase-4 (DPP-4) inhibitors work?

A

They increase the levels of incretins GLP-1 and GIP

23
Q

What does GLP-1 do?

A

Works to:

  • Stimulate glucose-dependent insulin release
  • Supress hepatic glucose output by inhibiting hepatic glucagon secretion
  • Inhibits gastric emptying
  • Enhances B-cell proliferation
24
Q

Where is Glucagon-like peptide-1 (GLP-1) produced?

A

In L cells of the ilium and colon

25
Q

What does Glucose-dependent immunotropic polypeptide (GIP) do?

A
  • Stimulates glucose-dependent insulin release

- Stimulates glucagon secretion

26
Q

Where is GIP produced?

A

In K cells of the proximal gut

27
Q

Is the drug Vildagliptin reversible?

A

Yes

28
Q

Is the drug Sitagliptin reversible?

A

Yes

29
Q

Is the drug Saxagliptin reversible?

A

No

30
Q

Where are SGLT1 found?

A

In the small intestine and proximal straight tubule of the nephron

31
Q

Where are SGLT2 found?

A

In the proximal convoluted tubule of the nephron

32
Q

Give examples of 2 SGLT2 inhibitors

A

Dapagliflozin and Canagliflozin

33
Q

What effects do SGLT2 inhibitor drugs have all around the body?

A
  • They increase insulin sensitivity in muscles (increase GLUT4 translocation and insulin signalling)
  • Increase insulin sensitivity in the liver (by decreasing glucose-6-phosphate)
  • Decrease gluconeogenesis
  • They improve beta-cell function
34
Q

How do SGLT2 inhibitors reverse glucotoxicity?

A

They inhibit SGLT2 transporters and therefore reverse hyperglycaemia and this reverses the build up of glucose within the body

35
Q

What are some adverse side effects of SGLT2 inhibitor drugs?

A
  • Rapid weight loss
  • Tiredness
  • Osmotic diuretic dehydration
  • Can worsen urinary tract infections and thrush

2.2 T1: The endocrine system (23 decks)

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