Common Mechanisms of action!

Question 1

Sulfonylureas

eg: Gliclazide

Answer 1

augmenting insulin secretion and consequently are effective only when some residual pancreatic beta-cell activity is present

*stimulating insulin exocytosis

Question 2

Tamoxifen

Answer 2

anti-oestrogen which induces gonadotrophin release by occupying oestrogen receptors in the hypothalamus, thereby interfering with feedback mechanisms

*may act as oestrogen in endometrium

Question 3

Warfarin

Answer 3

inhibiting vitamin K dependent clotting factors (II, VII, IX, X) in addition to the anticoagulant proteins C and S

Question 4

Methotrexate

Answer 4

inhibits the enzyme dihydrofolate reductase, essential for the synthesis of purines and pyrimidines affecting inflammatory response

Question 5

ACEi

eg: ramipril

Answer 5

Limit conversion of Angiotensin-1 to angiotensin-2 (which leads to vasoconstriction etc)

relaxes efferent vessels and decreases renal hydraulic pressure, protecting vascular network of kidney but costing eGFR

Question 6

Prednisolone

Answer 6

Prednisolone exerts predominantly glucocorticoid effects with minimal mineralocorticoid effects

reduces inflammation and suppresses the immune system

Question 7

DIGOXIN

Answer 7

competes with potassium at myocyte Na+/K+/ ATPase, limiting Na+ influx

Ca2+ outflow depends on Na+ so accumulates in cell

lengthens action potential and slows HR

*important as K+ levels can affect digoxin action, low K+ augments effect and high K+ limits

Question 8

NSAID

Answer 8

inhibit prostaglandin synthesis

*prostaglandins dilate afferent renal vessels promoting flow into the kidney and maintaining perfusion which NSAIDS affect -> AKI bad