Hyperglycemia Insulin resistance |
Biguanides |
Increases liver and muscle insulin sensitivity; decreases hepatic glucose production |
|
Sulphonylureas |
Insulin secretogogues |
|
Alpha-glucosidase inhibitors |
Delay the absorption of polysaccharides and also act to attenuate postprandial glucose excursions |
|
Sulphonylurea-like agents |
Insulin secretogogues |
|
Thiazolidinediones |
Insulin sensitizers that improve glucose uptake in adipose tissues and skeletal muscles |
|
Insulin |
Reduces hepatic glucose output and increases peripheral glucose utilization |
Hypertension |
ACE inhibitors |
Block the formation of AT-II, increase bradykinin level. As a result reduce vasoconstriction, reduce sodium and water retension, and increase vasodilation (through bradykinin). |
|
Angiotensin receptor blockers Losartan and valsartan |
Competitive inhibition of AT-II receptor (Type 1). Effect more specific on AT-II action, less or none on bradykinin production or metabolism. |
|
Beta blockers |
Inhibit renin release and AT-II and aldosterone production and lower peripheral resistance; may decrease adrenergic outflow from the CNS. |
|
Calcium channel blockers |
Dilate peripheral arterioles and thereby reduce BP by inhibiting calcium influx into arterial SM cells. |
|
Diuretics |
Lower BP by depleting body sodium stores resulting in reduction of total blood volume and cardiac output; initially peripheral vascular resistance increases but declines when CO returns to normal level (6-8 weeks) |
Dyslipidemia |
Statins |
Increase lipid profile and decrease atherogenic tendency. Lower LDL-C, improve TC:HDL-C, lower apo B. |
|
Fibric acid derivatives |
Increase lipid profile and decrease atherogenic tendency. Lower TGs, raise HDL-C, lower TC:HDL-C and shift LDL from smaller to larger particles. |
Platelet activation and |
Aspirin |
Antiplatelet effect |
aggregation |
Clopidogrel |
Irreversible blockade of the adenosine diphosphate (ADP) receptor on platelet cell membranes |
|
Ticlopidine |
Interferes with platelet membrane function |