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PM3B > DIABETIC DRUG THERAPY > Flashcards

DIABETIC DRUG THERAPY Flashcards

1
Q

MoA of gliclazide

A

Promotes insulin secretion from pancreatic beta cells by binding to sulfonylurea receptor SUR1 which then blocks KATP channels - so reduced efflux of potassium which results in depolarisation of beta cells - stimulates calmodulin to release insulin containing secretory granules

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2
Q

What are sulfonylureas?

A

Insulin secretagogues that stimulate insulin release from pancreas to restore early phase insulin release - can get short acting e.g. gliclazide / tolbutamide or long acting e.g. glibenlamide

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3
Q

Side effects of sulfonylureas

A

weight gain - not in overweight pts

risk of hypoglycaemia

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4
Q

How much do sulfonylureas reduce HbA1c by?

A

1.5-2%

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5
Q

when are meglitanides used i.e licensing?

A

Only licensed for use with metformin

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6
Q

MoA of meglitanides e.g. repaglinide and netaglinide?

A

Increase insulin release (early phase response) by binding to a different . but closely related receptor recognised by sulfonylurea - mechanism same - closes k ATP channels

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7
Q

Are the side effects less marked in meglitanides?

A

Yes - less weight gain compared to other short acting ones, reduced risk of hypoglycaemia due to action being dependent . on the presence of glucose

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8
Q

What are short acting sulfonylureas?

A

Gliclazide

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9
Q

What drug classes come under the umbrella term insulin secretagogues?

A

Sulfonylureas e.g gliclazide

meglitanides e.g repaglinide and nateglinide

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10
Q

what drugs work on the . liver?

A

Biguanides and thiazolidinediones - reduce glucose production

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11
Q

What drugs work on the pancreas?

A
  • insulin secretagogues . - sulfonylureas and meglitinides

- GLP-1 incretins improve response to glucose level

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12
Q

What drugs work on skeletal muscle / adipose tissue?

A

thiazolidinediones and biguanides also work on here to reduce insulin resistance

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13
Q

What drugs work on small intestine?

A

Alpha- glucosidase inhibitors e.g. ascarbose to slow absorption of sucrose and starch

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14
Q

what are insulin sensitisers?

A

Require some residual beta cell capacity - enhance the effect of endogenous circulating insulin to reduce insulin resistance and decrease hepatic glucose production
e.g biguanides and thiazo

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15
Q

1st line drug in type 2 diabetes?

A

Metformin - a biguanide

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16
Q

Why is metformin particularly good? / used in overweight too?

A
  • suppresses appetite . so weight loss i.e doesnt get as much weight gain as others
  • reduced risk of hypo
  • cardioprotective
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17
Q

What are the s/e of metformin and how can they be overcome?

A

GI side effect - but can be overcome by gradually . increasing the dose to therapeutic levels or using modified release forms
- also risk of lactic acidosis

18
Q

when is metformin contra-indicated?

A

renal, cardiac, liver . impairment due to inhibition of pyruvate metabolism leading to increased lactic acid build up - if renally impaired for example - cannot excrete the LA

19
Q

MoA of metformin?

A

Reduce glucose production in liver, increases glucose utilisation and uptake in periphery, decreases glucose absorption - via activation of AMPK in liver and skeletal muscle

20
Q

Example of a thiazolidinedione?

A

Pioglitazone

21
Q

MoA of pioglitazone?

A

Reduces peripheral insulin resistance and hepatic . glucose production by stimulating PPAR-gamma (peroxisome proliferator activated receptor gamma) - this modulates the expression of insulin-sensitive genes which control glucose production /transport/utilisation in adipose/muscle/liver

22
Q

What are . the risks of pioglitazone?

A

Can increase risk of heart failure (fluid retention) thus C/I in at risk pts
also small increased risk of bladder cancer so caution in elderly and at risk pts .

23
Q

How long does pioglitazone take to work and why?

A

up to 3 months . due to indirect effect on blood glucose

24
Q

Side effects of pioglitazone

A
  • fluid retention
  • weight gain but note . that it is a less . risk of distiribution (hips and thighs)
  • anaemia . and . GI effects
25
Q

Positive point about pioglitazone?

A

can improve . diabetic dyslipidaemia

26
Q

What is an example of a class and . drug that has inhibiting effects on GI glucose . absorption?

A

Alpha glucosidase inhibitors such as ascarbose

27
Q

MoA of ascarbose

A

Binds to alpha glucosidase with . higher affinity than dietary starch/sucrose - so breakdown of carbs inhibited/ Slows digestion and absorption of carbs post meals - reduces post prandial peak in blood glucose . so stabilises levels.
Not as good at reducing hba1c than metformin and still has GI disturbances e.g. flatulence/diarrhoea

28
Q

what therapies are based on glucagon like peptide?

A
  • dipeptidyl peptidase 4 inhibitors (DPP4)

- GLP-1 analogues

29
Q

What are DPP-4 inhibitors?

A

Gliptins –> They inhibit the enzyme DPP4 which usually breaks down GLP-1 - this means that GLP is free to act (not degraded)and stimulate insulin secretion, and decrease glucagon secretion. Also decreases appetite so good for weight loss

30
Q

Licensing for DPP4 inhibitors and guidance?

A

In combination with either metformin / sulfonylurea / pioglitazone (or sitagliptin also monotherapy with insulin)

Also NICE –> only continue after 6 months if hbA1c reduced by at least 0.5%

31
Q

what drugs are GLP-1 analogues?

A

Exenatide and liraglutide - subcutaenous admin

32
Q

What are GLP-1 analogues?

A

DPP-4 resistant analgoues of GLp1 that bind to and activate GLP-1 receptor so then get the actions of GLP-1, stimulating insulin secretion, reducing glucagon secretion, reducing gastric emptying so weight loss (suppress appetite). Used in combo again

33
Q

What is the guidance on GLP-analogues e.g exenatide or liraglutide?

A

Only continue after 6 months if hba1c reduction of 1% and weight loss of 3%

34
Q

When are sodium-glucose co transporter inhibitors (gliflozins) used?
canagliflozin etc

A

used as monotherapy if diet fails and metformin is inappropriate/contraindicated
Also as an add on therapy with other medicines

35
Q

MoA of sodium-glucose co transpoter inhibitors?

A

Independent of insulin mediated glucose control pathways - actually act on nephron in tubules to block reabsorption of glucose in kidney and promote urinary excretion of it

36
Q

treatment of hypoglycaemia episodes?

A

oral glucose 10-20 g if conscious / swallow
IM/SC glucagon or IV glucose if unconscious or cannot swallow
Once episode is over - give longer acting carbs because glucagon mobilises the glycogen stores and must replenish these using the carbs

37
Q

Common complication in type 1 diabetics?

A

Diabetic ketoacidosis - chronic uncontrolled hyperglycaemia and ketones are due to a build up of free fatty acids due to mobilisation of the other stores. treat with IV rehydration 0.9% saline, insulin infusion and . careful correction of electrolyte . balance

38
Q

What is a common issue with diabetics when they are ill?

A

They . stop taking . insulin . if they feel . unwell and lose their . appetite as . they think it will cause hyperglycaemia. But . in fact - infections increase insulin . requirements

39
Q

Common complication in type 2 diabetics?

A

Hyperglycaemic hyperosmolar state
Medical emergency, very high blood glucose >30mmol/L and hyperosmolality >320 mOsm/L. Due to illness and severe dehydration .

40
Q

Treatment for HHS

A

IV fluids
Normalise blood glucose with low dose IV insulin
LMWH prophylaxis
Prevention of foot ulcers

PM3B (13 decks)

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