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3152 Immune and Endocrine System > IC10 Pharmacology of Endocrine Disease Drugs > Flashcards

IC10 Pharmacology of Endocrine Disease Drugs Flashcards

1
Q

What is the MOA of metformin? How is it used in practise (monotherapy or combi)?

A
  1. Inhibit Gluconeogenesis
    - stimulate AMP-mediated protein kinase
    - reduce glucose production
  2. Increase cells sensitivity to insulin
    - increase glucose uptake
    - Weight loss
    - Improve hyperlipidemia
    - Does not lead to hyperinsulinemia and hypoglycemia

Can be monotherapy

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2
Q

What is the PK of metformin?

A

A: oral
D: highly rapidly distributed, minimal plasma protein binding
M: -
E: urine (unchanged)

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3
Q

What is the ADR of metformin?

A
  1. Diarrhea, vomiting, indigestion (weight loss)
  2. Anorexia
  3. Increase risk of vit B12 malabsorption –> Vit B12 deficiency
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4
Q

What are the special considerations for Metformin?

A

Use with caution:

  1. in patients with renal problems
  2. and lactic acidosis (hepatic diseases and cardiovascular problem)

Administration:

  1. Take with or after meal (due to GI ADR)
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5
Q

What is the MOA of glipizide? How is it used in practise (monotherapy or combi)?

A

Sulfonylurea
Stimulate functioning beta-cells to produce insulin

  • Targets ATP-dependent K channels
  • Prevents K+ efflux
  • Cause Ca2+ inflow
  • Increase insulin granules exocytosis

Can be monotherapy (when metformin can’t be used)

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6
Q

What is the PK of glipizide?

A

A: oral

  • Avoid taking with food

D: highly plasma protein bound
M: liver (hydroxylation)
E: urine and feces (mainly metabolites, excretion prolonged with renal disease)

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7
Q

What are the ADRs of glipizide?

A
  1. Hypoglycemia (esp. in elderly, but less than other SU)
  2. Weight gain
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8
Q

What are the special considerations for Glipizide?

A

FDI (avoid taking with food)

DDI:
1. CYP450 interactions
2. Hepatic and renal adjustment

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9
Q

What is the MOA of sitagliptin? How is it used in practice?

A

DPP-4 inhibitor

  • DPP-4 enzymatically degrades GLP-1 (glucagon like peptide 1 hormone released after eating)
  • GLP-1 increase insulin release from beta cells, decrease glucagon release [and slows gastric emptying] (in a glucose dependent manner)
  • Inhibit DPP-4 –> accumulates GLP-1
    –> stimulate beta-cells –> more insulin, less glucagon, less hepatic glucose production –> more glucose absorbed and reduce glycogenolysis –> reduce blood glucose levels

Can be monotherapy (when metformin can’t be used)

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10
Q

What is the PK of sitagliptin?

A

A: oral
D: -, long t1/2
M: LOW liver metabolism
E: urine

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11
Q

What are the ADRs of sitagliptin?

A
  1. GI disturbances
  2. Flu-like symptoms (headache, running nose, sore throat)
  3. Skin reactions
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12
Q

What are the special considerations of Sitagliptin?

A

Use with caution in
1. pancreatitis patients
2. renal insufficiency

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13
Q

What is the MOA of liraglutide? How is it used in practise?

A

GLP-1 receptor agonist (long-acting peptide)

  • Activate GLP-1 receptor on beta-cells
    –> increase adenylate cyclase & cAMP –> increase PKA
    –> 1) increase insulin release and 2) reduce glucagon release –> increase glucose absorption and reduce glycogenolysis
    –> insulin secretion subsides when blood glucose level decreases and reaches euglycemia
    –> 3) delay gastric emptying
  • 4) Reduce appetite –> Weight loss
  • Reduce risk of cardiovascular death, non-fatal MI, heart failure among T2DM patients

Adjunct therapy with oral anti-hyperglycemic agents

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14
Q

What is the PK of liraglutide?

A

A: SC
D: -, highly plasma protein bound (due to C16 fatty acid chain), long t1/2
M: non-specific proteolysis (becos it’s a large molecule)
E: different organs

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15
Q

What is the ADR and disadvantage of liraglutide?

A
  1. Injection site reaction
  2. Expensive
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16
Q

What is the MOA of empagliflozin? How is it used in practice?

A

SGLT2i (sodium-glucose co-transporter 2)

  • Reduce reabsorption of glucose back into blood circulation
  • Increase urinary glucose excretion (glucosuria)
  • Benefits those with cardiovascular disease (atherosclerosis) + those with renal diseases

dual therapy w metformin / glipizide
OR triple therapy w metformin & glipizide
OR dual therapy with insulin (with or w/o metformin)

17
Q

What is the PK of empagliflozin?

A

A: oral
D: -, highly plasma protein bound, long t1/2
M: liver (glucuronidation)
E: urine and feces

18
Q

What are the ADRs of Empagliflozin?

A

Think of glucose in urine

  1. UTI
  2. Increase urination
  3. Female genital mycotic fungal infection
  4. Diabetic ketoacidosis
19
Q

What are the special considerations of Liraglutide?

A

NIL

20
Q

What is the MOA of carbimazole? What needs to be monitored?

A

Prevent thyroid (T3 and T4) synthesis

  • Converted to active methimazole (after absorption in the serum) –> Inhibit thyroid peroxidase –> reduce iodination of tyrosyl residues in thyroglobulin –> reduce S&S of thyrotoxicosis

Monitor:
Serum TSH levels and thyroid size

21
Q

What is the PK of carbimazole?

A

A: oral, carbimazole converts to methimazole after absorption
D: accumulates in thyroid, NOT plasma protein bound
M: liver, CYP450 and FMO enzyme
E: mainly urine, some feces

22
Q

What are the ADRs of carbimazole?

A
  1. Rashes
  2. Joint pain
  3. Nausea
  4. Jaundice
  5. Agranulocytosis
  6. Hypothyroidism (due to overtreatment, need to monitor and reduce dose when prostate size is decreased and stable TSH normal levels)
23
Q

What are the special considerations of Carbimazole?

A

Takes a while for it to work (3-6 weeks):

  1. Thyroid has long t1/2
  2. need to wait for the thyroid stores to be depleted (even though the onset of action is very fast within 12 hrs)

Thus, continue taking carbimazole even when you don’t see results

24
Q

What is the MOA of levothyroxine? What needs to be monitored and when?

A

Thyroid analogue (T4)

  • Acts like the thyroid hormone
  • De-iodinated from T4 to T3 in the liver (& kidneys, peripheral tissues)
  • Myxoedema coma, severe form of hypothyroidism –> reduced blood flow –> affects guts absorption of levothyroxine (thus can’t use oral) –> use IV liothyronine (synthetic T3) / IV levothyroxine

Monitor:

  • Serum TSH levels
  • 6-8 weeks after starting treatment/ changing levels
  • If persistent high TSH levels, look at –> inadequate dosing, poor compliance, malabsorption, DDI / FDI
25
Q

What is the PK of levothyroxine?

A

A: oral
D: -, highly plasma protein bound, very very long t1/2
M: liver (Phase II: glucuronidation and sulphation)
E: bile, feces and urine

26
Q

What are the ADRs of levothyroxine?

A
  1. Reduced appetite
  2. Anxiety
  3. Diarrhea
  4. Difficulty sleeping
  5. Hair loss

Rare:

  1. Heart issues (arrhythmias, high BP, pain, failure)
  2. Seizures
27
Q

What are the special considerations for levothyroxine?

A
  1. Take 30 mins before meals with water
  2. FDI: grapefruit, pomelo (intestinal CYP3A4 inhibitor), dietary fiber (GI motility)
  3. DDI: drugs that affect gastric pH e.g. PPI, H2RA, antacids

Contraindications:

  1. Heart problems
  2. Epilepsy
  3. Hyperthyroidism
28
Q

What is the ROA for all 7 drugs?

A

Oral Oral Oral SC Oral Oral Oral

29
Q

What is the extent of plasma protein binding and t1/2 for all 7 drugs?

A
  1. rapid, No PPB
  2. High PPB
  3. -, long t1/2
  4. high PPB, long t1/2
  5. High PPB, long t1/2
  6. No PPB
  7. High PPB, longest t1/2
30
Q

What are all 7 drugs metabolized?

A
  2. Liver (I)
  3. Low liver m
  4. Proteolysis
  5. Liver (II) glucuronidation
  6. Liver (I) CYP450 and FMO enzymes
  7. Liver (II) glucuronidation & sulphation
31
Q

How are all 7 drugs excreted?

A
  1. Urine (unchanged)
  2. Urine, feces (metabolites)
  3. urine
  4. diff organs
  5. Urine, feces
  6. Mainly Urine (& feces)
  7. Bile, feces, urine

3152 Immune and Endocrine System (11 decks)

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