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Clinical Pharmacology > 6.1.2 Diabetes Type II > Flashcards

6.1.2 Diabetes Type II Flashcards

1
Q

How does insulin resistance develop?

A

Initially overcome by increased pancreatic insulin secretion

Insulin receptors then begin to decline
Decreased GLP-1 secretion in response to oral glucose
Reduced response at B cells, eventually insulin production reduced

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2
Q

How is T2DM managed?

A

Lifestyle
Weight loss

Initially non-insulin therapies such as Metformin

Treat comorbidities

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3
Q

What is the difficulty with medical management of T2DM?

A

Some therapeutics can cause weight gain which can decrease adherence

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4
Q

What are the different classes of T2DM drugs?

A

Biguanides
Sulphonylureas
Thiazolidinediones
Sodium glucose contransporter inhibitors (SGLT2)
Dipeptidyl peptidase 4 inhibitors
Glucagon like peptide 1(GLP-1) receptor agonists

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5
Q

What is an example of a biguanide?

A

Metformin

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6
Q

How do biguanides work?

Metformin

A

Decreased hepatic glucose production by inhibiting gluconeogenesis

Supresses appetite stops you getting biguanide

First line

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7
Q

What are the adverse effects of biguanides?

Metformin

A

GI upset
Nausea
Vomiting
Diarrhoea

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8
Q

When should you not take biguanides?

Metformin

A

Excreted unchanged by kidney
stop if eGFR < 30mL/min
Alcohol intoxication

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9
Q

What are the drug to drug interactions with biguanides?

Metformin

A

ACEi
Diuretics
NSAIDs
(drugs that impair renal function)

Loop and thiazide diuretics as they increase glucose thus reducing metformin action

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10
Q

What is an example of a sulphonylurea? (SU)

A

Gliclazide

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11
Q

How do sulphonylureas work?

(Gliclazide)

A

Stimulate B-cell pancreatic insulin secretion by blocking K+/ATP channels

K+ unable to leave, this depolarises the cell causing voltage-gated Ca2+ channels to open

Rise in Ca2+ causes fusion of insulin with the cell membrane, increased secretion of insulin

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12
Q

How do Beta pancreatic cells usually secrete insulin?

A

Glucose enters the cell via GLUT2 causing an increase in ATP

ATP phosphorylates the K+/ATP channel blocking it, this causes an increase in intracellular potassium leading to cell depolarisation

Voltage-gated Ca2+ channels open

Rise in Ca2+ causes fusion of insulin with the cell membrane, causing secretion of insulin

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13
Q

What are 3 issues with sulfonylureas?

(Gliclazide)

A

Need residual pancreatic function to work

Weight gain through anabolic effects of insulin

May lead to hypoglycaemia

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14
Q

What are the adverse effects of sulfonylureas?

(Gliclazide)

A

Nausea
Vomiting
Diarrhoea
Hypoglycaemia- leads to insulin release at low glucose levels

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15
Q

When should you not use sulfonylureas?

(Gliclazide)

A

Hepatic and renal disease
Caution those at risk of hypoglycaemia

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16
Q

What are the important drug to drug interactions with sulfonylureas?

(Gliclazide)

A

Other hypoglycaemic agents

Loop and thiazide diruectics as these increase glucose

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17
Q

Give examples of thiazolidinediones (glitazones)

A

Pioglitazone
Rosiglitazone

-glitazone suffix

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18
Q

How do thiazolidinediones (glitazones) work?

Pioglitazone Rosiglitazone

A

Increase insulin sensitivity in muscle and adipose

Decreases hepatic glucose output by activating PPAR-gamma in adipose cells

Increased gene transcription

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19
Q

What are some problems with thiazolidinediones (glitazones)?

Pioglitazone Rosiglitazone

A

Half-life not related to duration of action, it takes 6-8 weeks for benefit

Weight gain due to fat cell differentiation

20
Q

What are the adverse effects of thiazolidinediones (glitazones)?

Pioglitazone Rosiglitazone

A

GI upset
Fluid retention
Fracture risk
Bladder cancer

Due to bladder cancer risk, used less frequently

21
Q

When should glitazones not be used?

Pioglitazone Rosiglitazone

A

Heart failure due to fluid retention

22
Q

What are the important drug to drug reactions with glitazones?

Pioglitazone Rosiglitazone

A

Other hypogylcaemic agents

23
Q

What are some examples of sodium-glucose co-transporter inhibitors? (gliflozins)

A

Dapagliflozin
Canagliflozin

-gliflozin suffix

CD as in loop of henle

24
Q

How do SGLT-2 inhibitors (gliflozins work)?

Dapagliflozin Canagliflozin

A

Competitive reversible inhibition of SGLT2 in PCT

Decreases glucose absorption from tubular filtrate, increases urinary glucose excretion

25
Q

What is good about SGLT2 inhibitors (gliflozins)?

Dapagliflozin Canagliflozin

A

Weight loss
Low hypogylcaemic risk

26
Q

When are SGLT2 inhibitors (gliflozins) used?

Dapagliflozin Canagliflozin

A

Add on therapy
Sometimes used as a monotherapy

HFrEF
CVD risk patients with metformin

27
Q

What are the adverse effects of SGLT2 inhibitors (gliflozins)?

Dapagliflozin Canagliflozin

A

UTI
Genital infection
Thirst and polyuria
(Pancreatitis?)

28
Q

Warnings/contraindications of SGLT2 inhibitors (gliflozins)

Dapagliflozin Canagliflozin

A

Hypovolaemia- possible hypotension

29
Q

What are some important drug to drug interactions with SGLT2 inhibitors (gliflozins)?

Dapagliflozin Canagliflozin

A

Antihypertensives
Other hypergylcaemic agents

30
Q

What are the physiological effects of GLP-1 (glucagon like peptide) on different organs?

A

Pancreas
Increased insulin synthesis and secretion (glucose dependent)
Decreased glucagon secretion

Brain
Decreased food intake through increased satiety

Liver (indirect)
Decreased glucose production

Stomach
Decreased gastric emptying

Muscle (indirect)
Increased glucose uptake

31
Q

Give examples of Dipeptidyl peptidase-4 inhibitors (gliptins)

A

Sitagliptin
Saxagliptin

-gliptin suffix

32
Q

How do dipeptidyl peptidase-4 inhibitors (gliptins) work?

Sitagliptin Saxagliptin

A

Prevent incretin degradation, so plasma incretin levels increase

Suppresses appetite- weight neutral

33
Q

Why do dipeptidyl peptidase-4 inhibiors (gliptins) have low hypoglycaemic risk?

Sitagliptin Saxagliptin

A

Glucose dependent, so no stimulation of insulin secretion at normal blood glucose

34
Q

What are the adverse effects of dipeptidyl peptidase-4 inhibitors (gliptins)?

Sitagliptin Saxagliptin

A

GI upset
Small pancreatitis risk

35
Q

When should you not give dipeptidyl peptidase-4 inhibitors (gliptins)?

Sitagliptin Saxagliptin

A

Pregnancy
Pancreatitis history

36
Q

What are the important drug to drug interactions of dipeptidyl peptidase-4 inhibitors (gliptins)?

Sitagliptin Saxagliptin

A

Other hypoglycaemic agents

Thiazide like and loop diuretics as they increase glucose concentration

37
Q

Give some examples of Glucagon-like peptide-1 (GLP-1) receptor agonists (incretin mimetics)

A

Exenatide
Liraglutide
Semaglutide

-tide suffix

38
Q

How do glucagon-like peptide-1 receptor agonists work?

Exenatide Liraglutide Semaglutide

A

Increases glucose dependent synthesis of insulin secretion from beta cells

Activates glucagon-like peptide-1 receptor- resistant to degradation by dipeptidyl peptidase-4

39
Q

How are glucagon-like peptidase-1 receptor agonists given?

Exenatide Liraglutide Semaglutide

A

Subcutaneous injection

40
Q

What is good about glucagon-like peptide-1 receptor agonists?

Exenatide Liraglutide Semaglutide

A

Promotes satiety, can lead to weight loss

41
Q

When are glucagon-like peptide-1 receptor agonists used?

Exenatide Liraglutide Semaglutide

A

If triple therapy is ineffective

42
Q

What are the adverse effects of glucagon-like peptide-1 receptor agonist?

Exenatide Liraglutide Semaglutide

A

GI upset
Decreased appetite with weight loss

43
Q

When should glucagon-like peptide-1 receptor agonists not be used?

Exenatide Liraglutide Semaglutide

A

Renal impairment

44
Q

What are the important drug to drug reactions of glucagon-like peptide-1 receptor agonists?

Exenatide Liraglutide Semaglutide

A

Other hypoglycaemic agents

45
Q

How can we reduce GI upset of drugs treating diabetes?

A

Modified release preparations

Results in fewer GI effects, less frequent dosing and imrpoved adherence

46
Q

Why must you swallow extended-release tablets whole?

A

Coating makes the tablet extended release

Without the coating the tablet will not be slow releasing

Clinical Pharmacology (45 decks)

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