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CEP > Drug Management of Diabetes > Flashcards

Drug Management of Diabetes Flashcards

1
Q

2 major cell types of pancreatic islets

A
  • Alpha cells (glucagon)
  • Beta cells (insulin)
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2
Q

What type of agent is glucagon?

A

Potent hyperglycaemic agent

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3
Q

What is the major target of glucagon and what does it promote?

A
  • Target = liver
  • Glycogenolysis
  • Gluconeogenesis
  • Release of glucose into blood
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4
Q

What type of agent is insulin?

A

Potent hypoglycaemic agent

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5
Q

What does insulin binding trigger?

A
  • Oxidation of glucose for ATP production
  • Polymerisation of glucose to glycogen
  • Conversion of glucose to fat
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6
Q

How does glucose regulate insulin?

A
  • Glucose enters beta cells
  • ATP concentration increases
  • ATP-sensitive K+ channel activity decreases
  • K+ efflux decreases, cell depolarised
  • Voltage-gated Ca2+ channels open
  • Ca2+ causes secretion of insulin (exocytosis)
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7
Q

What tissues contain insulin receptors?

A
  • Liver
  • Muscle
  • Fat
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8
Q

What subunits make up the insulin receptor (and what bit do they form)?

A
  • 2 alpha subunits (extracellular binding site)
  • 2 beta subunits (transmembrane tyrosine kinase)
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9
Q

What does the insulin receptor do upon binding?

A
  • Phosphorylates insulin receptor substrate (IRS) proteins
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10
Q

What does phosphorylation of IRS proteins cause (and what is subsequently caused)?

A
  • Enzyme activation and gene expression
    > Causes expression of Glut-4 transporter so increased glucose uptake
    > Causes increased glycogen synthesis
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11
Q

What are the injected drugs given?

A
  • Insulin
  • Incretin mimetics
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12
Q

What are the oral drugs given (for type 2)?

A
  • Biguanides
  • Sulfonylureas
  • Thiazolidinediones
  • Gliptins
  • Glucose transport inhibitors
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13
Q

2 types of insulin

A
  • Short acting
  • Long acting
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14
Q

Onset and peak of the 2 types of insulin

A
  • SA = 30min onset, 2-4h peak
  • LA = onset 1-2h, peak 4-12h
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15
Q

Different dose regimes of insulin

A
  • SA 3x before meals, LA 1-2x
  • Pre-mixed SA + LA 1-2x
  • Continuous infusion
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16
Q

Primary management methods for type 2

A
  • Diet/exercise/lifestyle modifications
  • Intermittent fasting
  • VLCD
17
Q

What happens if primary management fails?

A
  • Drugs
  • Insulin (1/3 people)
18
Q

Where do biguanides produce their effects?

A
  • Liver
  • Muscle
19
Q

What do biguanides do?

A
  • Decrease gluconeogenesis (liver)
  • Increase fatty acid oxidation
  • Decrease carb absorption (intestine)
  • Increase glucose uptake by skeletal muscle
20
Q

Side effects of biguanides

A
  • Lactic acidosis
  • GI disturbances
21
Q

When and with what are biguanides combined (and what does that do)

A
  • For obese patients
  • Combined with acarbose (decreases carb absorption)
22
Q

Mechanism of sulfonylurea action

A
  • Drug binds part of ATP-sensitive K+ channel
  • Channel closes
  • Beta cell depolarises
  • Ca2+ enters and increases insulin secretion
  • Increases tissue sensitivity to insulin
23
Q

Different durations of action of sulfonylureas

A
  • Long –> t1/2 = 10h
  • Short –> t1/2 = 4h
24
Q

Side effects of sulfonylureas

A
  • Hypoglycaemia
  • Diuretic actions
25
Q

How are other sulphonylurea receptor modulators similar to sulphonylureas?

A

Decrease ATP-sensitive K+ channel activity by binding SUR

26
Q

How do other sulphonylurea receptor modulators differ from sulphonylureas?

A
  • Shorter duration of action
  • More selective for ATP-sensitive K+ channels in beta cells
27
Q

Side effects of other sulphonylurea receptor modulators

A
  • Hypoglycaemia
  • Stimulate appetite
  • Contraindicated in pregnancy/breastfeeding
28
Q

What receptor do thiazolidinediones bind to and what is the effect?

A

Binds nuclear receptor PPARγ - affects gene expression

29
Q

Primary action of thiazolidinediones

A
  • Increase fatty acid uptake in adipose tissue
  • Increase lipogenesis in adipose tissue
30
Q

Secondary effect of decreased plasma fatty acids from thiazolidinediones

A
  • Increased glucose uptake
  • Decreased gluconeogenesis
31
Q

What are thiazolidinediones used with?

A

Sulfonylureas or metformin

32
Q

Side effects of thiazolidinediones

A
  • Weight gain
  • Liver toxicity
  • Heart failure
33
Q

What are incretins?

A

GI hormones that cause insulin secretion

34
Q

What do GLP-1 agonists do?

A
  • Increase insulin production in the pancreas
  • Slow gastric emptying
  • Lower blood glucose after a meal
  • Induce satiety
35
Q

How are GLP-1 agonists administered?

A

Injection

36
Q

What is the function of gliptins?

A

Inhibit dipeptidyl peptidase-4 (DPP-4)

37
Q

What does DPP-4 do?

A

Metabolises incretins

38
Q

Mechanism of glucose transport inhibitors

A
  • Increase glucose and Na+ loss in proximal convoluted tube of kidney
  • Promotes osmotic diuresis
39
Q

Side effects of glucose transport inhibitors

A
  • Peripheral vascular disease
  • Hypotension
  • Dehydration
  • Ketoacidosis
  • UTIs

CEP (14 decks)

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