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Endocrine > Diabetic Drugs > Flashcards

Diabetic Drugs Flashcards

1
Q

Name the 6 classes of drugs commonly used in treatment of T2DM. Provide an example of each.

A

Biguanide - Metformin
Sulphonylureas - (gliclaz)ide
Thiazolidinediones - (Pio)glitazone
SGLT2i - (Dapa)gliflazon
DPP4i - (Sita)gliptin
GLP-1RA - (Sema)glutide

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2
Q

Metformin MOA

A

Inhibits complex 1 in respiratory chain =>
Decrease in cellular ATP =>
Increased AMP:ATP ratio =>
Activation of AMP kinase =>
Decreased gluconeogenesis in the liver &
Increased gut glucose utilisation & metabolism

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3
Q

Metformin target organs

A

Kidneys, LIVER, intestine

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4
Q

Metformin class drug

A

Biguanide

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5
Q

Metformin non-glucose benefit

A

Cardiovascular benefit

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6
Q

Metformin effect on weight

A

Weight neutral

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7
Q

Metformin contraindications

A

Heart failure
Renal failure (does should be lowered in renal impairment)
Liver failure

… as Metformin increases lactate production & the liver & kidneys are responsible for clearing Metformin, meaning if they are impaired, lactic acidosis risk is increased

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8
Q

If a patient develops renal impairment, what should happen to their Metformin

A

Dose should be lowered

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9
Q

Metformin side effects

A

GI - anorexia, nausea, pain, bloating, dyspepsia, diarrhoea
Risk of lactic acidosis

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10
Q

Sulphonylureas MOA

A

Binds to sulphonylurea receptor (SUR1) =>
Closure of Kate channels =>
Rise in membrane potential =>
Ca influx =>
Insulin exocytosis

I.e. Glucose independent insulin secretion

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11
Q

Sulphonylurea medication example

A

Gliclazide

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12
Q

Sulphonylurea target organ/cell

A

Pancreatic beta cells

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13
Q

Sulphonylureas benefits

A

Cheap
Potent glucose lowering

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14
Q

Sulphonylureas side effects

A

Weight gain
Hypoglycaemia

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15
Q

Why does Sulphonylureas cause weight gain

A

They increase insulin
Insulin is anabolic & increases fat, glucose & protein uptake
Insulin also stimulates appetite

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16
Q

Why do Sulphonylureas cause hypoglycaemia

A

They cause glucose-independent insulin release

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17
Q

What increases an individuals risk of hypoglycaemia due to Sulphonylureas

A

Increased age
Long time since diabetes diagnosis
Impaired renal function
Lower HbA1c

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18
Q

Sulphonylureas contraindications/cautions

A

Use with care in people with liver or RENAL disease

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19
Q

TZDs MOA

A

Binds to PPAR-𝛾 - nuclear receptor =>
Increases pre-adipocyte to adipocyte conversion =>
Increases fat mass =>
‘Lipid steal’ & reduced fat in liver & muscles =>
Decreased lipotoxicity =>
Increased adipocetin =>
Increased liver insulin sensitivity

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20
Q

TZDs example

A

Pioglitazone

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21
Q

TZDs benefits

A

Cheap
True insulin sensitiser

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22
Q

TZDs contraindications

A

Avoid in HF & in elderly (>65yrs) due to risk fluid retention

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23
Q

TZDs side effects

A

Weight gain
Fluid retention
Increased fracture risk
Mild anaemia

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24
Q

SGLT2i MOA

A

Sodium-glucose transporter 2 inhibitor =>
Reduced renal afferent dilatation & filtration pressure => Increased urinary glucose excretion =>

25
Q

SGLT2i drug example

A

empagliflozin, Dapagliflozin, canagliflozin

26
Q

SGLT2i benefits

A

Weight loss
Mild diuretic & so benefit to HF
Increased urate excretion & so benefit to gout & CVD
Renal protection
Increased FFA & ketones (cardiac fuel) & so cardiac benefit

27
Q

Why are SGLT2i’s beneficial in patients with episodes of gout

A

It increases urate excretion

28
Q

Why are SGLT2i’s beneficial in HF

A

It also reduces Na reabsorption & so is a mild diuretic

29
Q

Why are SGLT2i’s beneficial in CVD

A

Glucose reduction → decreased insulin and increased glucagon → increase in lipolysis → increase in FFA which also increases ketone body production → FFA & ketones are a fuel to cardiac myocytes → cardiac benefit

30
Q

SGLT2i contraindications

A

Reduced eGFR (as causes afferent renal vasoconstriction)
Diuretics (as mild diuretic)
Prolonged fasting/acute illness (as increases urinary glucose excretion regardless of blood glucose levels)

31
Q

SGLT2i side effects

A
  • Genital candiasis - secondary to glycosuria
  • Fournier gangrene - rare but severe
  • Hypovolaemia, hypotension & dehydration - diuretic effect
  • DKA
  • Slight increase in LDL and HDL cholesterol
32
Q

Why do SGLT2i’s increase the risk of DKA

A

Glucose reduction → decreased insulin and increased glucagon → increase in lipolysis → increase in FFA which also increases ketone body production → ketocosis → increased ketoacidosis risk

33
Q

What medication increases the risk of Fournier gangrene

A

SGLT2i’s

34
Q

TZDs target cell/ receptor

A

Adipocytes (PPAR-𝛾 - nuclear receptor)

35
Q

SGLT2i target cell/ receptor

A

sodium glucose transporter 2 in the proximal convoluted tubules in the kidneys

36
Q

Describe the incretin effect

A

Intestine releases GLP1 & GIP in response to nutrients
These hormones bind to receptors on pancreatic beta cells
& amplify insulin release upon presence of glucose

GLP-1 has a very short half life and is broken down by the enzyme DPP4

37
Q

GLP-1RA MOA

A

GLP-1 receptor agonist that avoids breakdown by DPP4
This promotes insulin secretion & lowers glucose
It also reduces appetite (hypothalamus)
It also reduces gastric emptying (intestine)

38
Q

GLP-1RA drug example

A

Semaglutide

39
Q

GLP-1RA benefits

A

Weight loss (by reducing appetite)
Lowers blood pressure & so CV benefit
Avoids hypoglycaemia (as insulin only enhanced in presence of glucose)

40
Q

GLP-1RA side effects

A

N&V, bloating from gastroperesis (delayed gastric emptying)
Gallstones

41
Q

Why does GLP-1RA benefit the kidneys

A

It reduces new onset macroalbuminuria
(But no impact on eGFR)

42
Q

GLP-1RA contraindications

A

Acute pancreatitis

43
Q

GLP-1RA formulation

A

SC injections

44
Q

DPP4 inhibitors

A

Inhibit DPP4 enzyme =>
Inhibit GLP & GIP breakdown =>
Increased insulin & decreased glucagon & lower bp

45
Q

DPP4i benefits

A

Weight neutral
Lowers blood pressure
Avoids hypoglycaemia (as insulin only enhanced in presence of glucose)

46
Q

DPP4i side effects

A

N&V
Increased risk of pancreatitis
May increase HF risk

47
Q

DPP4i formulation

A

Oral

48
Q

DPP4i & GLP-1RA target organ/cell

A

Intestine

49
Q

What is first line T2DM treatment

A

Metformin

50
Q

What extra medication would you add in patients with atherosclerotic disease (e.g. previous MI) & T2DM

A

GLP-1RA
(Or SLGT2i if eGFR okay & GLP-1RA not tolerated)

51
Q

What extra medication would you add in patients with heart failure or chronic kidney disease & T2DM

A

SLGT2i
(Or GLP-1RA if eGFR not okay)

52
Q

What medication would you avoid if you want to reduce the risk of hypoglycaemia in a patient with T2DM

A

Sulphonylureas

53
Q

What medication would you add in patients with T2DM who need to lose weight

A

SGLT2i or GLP-1RA

54
Q

What medication would you add in patients with T2DM where cost is a problem

A

Sulphonylureas or TZDs

55
Q

What insulin regime are most T1DM patients on & why

A

Basal-bolus regime
- Long-acting 1-2/day & rapid-acting insulin before each meal
- mimics normal physiological insulin secretion

56
Q

Name 3 rapid acting insulins (bolus insulin analogues)

A
  • Insulin aspart (NovoRapid),
  • lispro (Humalog),
  • glulisine (Apidra)
57
Q

Name 2 long acting insulins (basal insulin analogues)

A
  • lantus (glargine),
  • levemir (dertermir)
58
Q

Summarise the different insulins available

A

Rapid acting (analogue)
- preferred bolus insulin
- Humalog, NovoRapid, Apidra
- 60-90mins peak

Short acting (soluble)
- Humulin S (human insulin), Actrapid, Insuman Rapid
- 2-4hr peak

Intermediate acting (isophane)
- Insulatard, Humulin I (human isophane), insuman basal
- 4-6hr peak

Long acting (analogue)
- preferred basal insulin
- Lantus (glargine), levemir (dertermir)
- less peak activity

59
Q

Insulin injection site should be rotated to prevent…

A

Lipohypertrophy

Endocrine (22 decks)

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