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endo y3s1 > IC11 PK of drugs for DM > Flashcards

IC11 PK of drugs for DM Flashcards

1
Q

Metformin MOA

A

Increase glucose uptake into tissues
* Reduces gluconeogenesis in liver → increase AMP-activated protein kinase
* May enhance tissue sensitivity to insulin

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2
Q

Metformin PK
absorption

BA, duration of action

A

Oral; F ~40-60%
Duration of action: 8-12 hours

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3
Q

Metformin PK
distribution

Vd, t1/2

A

Rapidly distributed to all parts of the body

Minimal plasma protein binding
Large Vd (>5-8L)

t1/2: 3h

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4
Q

Metformin PK
excretion + precaution

A

Unchanged in urine

To avoid in patients with renal insufficiency → retains metformin in body; higher t1/2
Important to monitor kidney function

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5
Q

Metformin
clinical uses & benefits

A
  1. T2DM → alone or with other oral hypoglycemic agents (combination therapy)
    Does not result in hyperinsulinemia/ hypoglycemia
  2. Useful in obese patients
    Reduces appetite; helps regulate body weight
    Improves lipids levels
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6
Q

Metformin Adverse effects

A, GI, V, R, LA

A
  1. Anorexia
  2. GI disturbances: to take with or after meal
    Diarrhoea & vomiting → weight loss
    Indigestion
  3. Increase risk of Vit B12 malabsorption → Vit B12 deficiency
  4. Use with caution in patients with renal problems/ lactic acidosis
    Gluconeogenesis: glucose generated from lactate
    Metformin reduces amount of lactate to be broken down ⇒ lactic acidosis
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7
Q

glipizide MOA

A

Lowers blood glucose by increasing release of insulin from pancreas

Main target: pancreatic β-cell ATP-sensitive (KATP) channel
controls β-cell membrane potential

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8
Q

glipizide requirements

A

functioning β-cells in pancreas islets

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9
Q

glipizide effects in b-cells

A
  1. glipizide bind to SU receptor proteins
  2. Inhibition of KATP channel mediated K+ efflux (membrane depolarisation)
  3. Ca2+ channel opens → Ca2+ enters cell
  4. Formation of vesicles containing insulin granules
  5. Triggers Ca-dependent exocytosis of vesicles with insulin granules
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10
Q

glipizide PK
absorption

F, onset, duration of action

A

Oral; F>95% (delayed with food intake)
Onset of action: 30 mins
Duration of action: 12-24 hours

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11
Q

glipizide PK
distribution

Binding & t1/2

A

Binds extensively (~99%) to plasma proteins [primary albumin]
t1/2 = 4h

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12
Q

glipizide PK
metabolism

A

By liver (90%); hydroxylation
10% remain as parent drug (unchanged)

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13
Q

glipizide PK
excretion

problem?

A

<10% unchanged & metabolites excreted in urine & faeces

Actions prolonged with patients with renal disease
Reduction in excretion of parent compound ⇒ overdose; over lowering of blood glucose

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14
Q

glipizide (compared to other SU)

A

Lower risks of hypoglycemia

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15
Q

glipizide AE

A

Hypoglycemia (more common in elderly)
Possibly due to DDI/ lower kidney function (lesser clearance of drug)

Weight gain ⇒ not ideal for obese patients

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16
Q

Sitagliptin (DPP-4i)
role of incretins

A

Group of metabolic hormones released after eating
Augment secretion of insulinin glucose-dependent manner
* presence of hyperglycemia = triggers secretion of insulin

16
Q

Sitagliptin (DPP-4i)
requirements for incretins to work

A

Requires pancreas to be working → inflamed pancreas will have decreased effects on insulin production

17
Q

Sitagliptin (DPP-4i)
how incretin works

A
  1. Hormones passes through circulation & enters pancreas ⇒ stimulates insulin production
    Results in lower glucose levels due to increased uptake by cells & decreasing gluconeogenesis
  2. Inhibition of glycogenesis by GLP-1 ⇒ reduction in hepatic glucose production
  3. Gastric emptying delayed ==> feel more full
18
Q

Sitagliptin (DPP-4i) MOA

A
  • Binds & inhibits DPP-4 → reduces enzymatic degradation of GLP-1
  • Prolongs action of endogenous incretins, increasing β-cells stimulation
    [Increase glucose-stimulated insulin release]
  • Suppression of 𝝰-cell mediated glucagon release & hepatic glucose production

Overall: Decreased blood glucose level

19
Q

Sitagliptin (DPP-4i) PK

A, D, M, E

A

Absorption
Oral; F ~87%
Distribution
t1/2 = 10-12 hours
Metabolism
Low liver metabolism
Excretion
80% excreted unchanged in urine
Remaining metabolites excreted in faeces

20
Q

Sitagliptin (DPP-4i) AE

GI, F, S

A

GI disturbances
Flu-like symptoms: headache, running nose, sore throat
Skin reactions: rash/ itch

21
Q

Sitagliptin (DPP-4i) caution in patients

A

patients with hx of pancreatitis (inflamed pancreas)

22
Q

Liraglutide (GLP-1 agonist) Effects

A

Initial rapid release of endogenous insulin
Suppression of glucagon release by pancreas
Delay gastric emptying
reduces appetite → weight loss; beneficial for obese patients

23
Q

Liraglutide (GLP-1 agonist) MOA

A

Activates GLP-1 receptor on pancreatic β-cells
↑adenylate cyclase → ↑cAMP → ↑PKA → ↑insulin secretion & ↓glucagon release

24
Q

Liraglutide (GLP-1 agonist) MOA
change in insulin levels

A

Insulin secretion reduces as glucose concentration decreases & approaches euglycemia

25
Q

Liraglutide (GLP-1 agonist)
effect of DDP4 enzyme

A

Long acting peptide: DPP-4-resistant form of GLP-1
Delay in breaking down of drug by peptidases

26
Q

Liraglutide (GLP-1 agonist) PK
absorption

route of administration, dose progession, F

A

SC: upper arm, abdomen, thigh

Once-daily dose
Increase dose weekly: 0.6mg → 1.2mg → 1.8mg → 2.4mg → 3.0mg
Regime helps reduce GI symptoms
3mg maintenance dose

F = 55%

27
Q

Liraglutide (GLP-1 agonist) PK
distribution

t1/2

A

C16 fatty acid binds to plasma proteins (albumin)
t1/2 = 13 hours

28
Q

Liraglutide (GLP-1 agonist) PK
metabolism

A

Endogenously metabolised, similar to polypeptides
No specific organ as major route of elimination

29
Q

Liraglutide (GLP-1 agonist) PK
excretion

A

Little/ none excreted unchanged → all polypeptides broken down to amino acids

30
Q

Liraglutide (GLP-1 agonist) AE

GI, CNS

A

Nausea/vomiting (improves when body adjusts to treatment)
GI: Diarrhoea/constipation
CNS: Headache/tiredness

31
Q

Empagliflozin (SGLT2i) MOA

A

Inhibition of SGLT2
* Reduces reabsorption of filtered glucose back into bloodstream
* Reduces renal threshold for glucose ⇒ increases urinary glucose excretion

32
Q

Empagliflozin (SGLT2i)
normal function of SGLT

A

Normal function of SGLT
Reabsorbs glucose back into bloodstream
90% by SGLT2 ⇒ target of drug
10% by SGLT1

33
Q

Empagliflozin (SGLT2i) PK

A, D, M, E

A

Absorption
Oral; F = 60-80%
Cmax = 1-2 hours
Distribution
Highly plasma protein bound
t1/2 = 12 hour → dose OD
Metabolism
Minimal metabolism in liver via glucuronidation
Excretion
~40% unchanged in faeces; ~27% unchanged in urine
Majority not broken down

34
Q

Empagliflozin (SGLT2i) AE

A

UTI → important to drink more water
Increased urination
Female genital mycotic fungal infection
Diabetic ketoacidosis

endo y3s1 (16 decks)

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