Exam 2 Elsaid Worksheet: Anti-Coag + Dyslipidemia

Anticoagulants: UFH, Enoxaparin, Dabigatran, Argatroban, Warfarin, Rivaroxaban, and Fondaparinux

KNOW

_____

• Site of Action: Blood

• MOA: INDIRECT-acting, Activates ATIII, and Inhibits Factor Xa and IIa (thrombin) equally

• Route: IV and SC

• Antidote: Protamine (complete reversal)

UFH

_____

• Site of Action: Blood

• MOA: Indirect-acting, Activates ATIII, and preferentially Inhibits Factor Xa (compared to IIa)

• Route: SC

• Antidote: Protamine (partial reversal)

Enoxaparin

_____

• Site of Action: Blood

• MOA: Direct Thrombin Inhibitor (DTI)

• Route: Oral

• Antidote: Idarucizumab (Praxbind)

Dabigatran

_____

• Site of Action: Blood

• MOA: Direct Thrombin Inhibitor (DTI)

• Route: IV

• Antidote: None

Argatroban

_____

• Site of Action: Liver

• MOA: Vit. K reductase inhibitor (VKOR) resulting in inhibition of synthesis of factors II, VII, IX, X, Protein S&C

• Route: Oral

• Antidote: 

  • Vitamin K (Oral or I.V.) for asymptomatic elevation in INR and non-life threatening situations

  • Kcentra (Prothrombin Complex Concentrate) for major bleeding and life-threatening situations.

Warfarin

_____

• Site of Action: Blood

• MOA: Direct Factor Xa Inhibitor

• Route: Oral

• Antidote: None

Rivaroxaban

_____

• Site of Action: Blood

• MOA: INDIRECT-acting, Activated ATIII, and Inhibits Factor Xa only

• Route: SC

• Antidote: None

Fondaparinux

Dyslipidemia: Atorvastatin, Ezetimibe, Alirocumab, Bempedoic Acid, Cholestyramine, Fenofibrate, Niacin, and EPA/DHA

KNOW

_____

• Site of Action: Liver

• MOA: HMG CoA Reductase inhibitor → significant reduction in cholesterol synthesis in the liver

• Effect on LDL-C, HDL-C, and TG: Lower LDL-C; high-intensity reduce HDL-C, while increasing HDL-C (reverse cholesterol transport)

Atorvastatin

_____

• Site of Action: Intestine

• MOA: Inhibit cholesterol absorption from intestine

• Effect on LDL-C, HDL-C, and TG: Small reduction in LDL-C with NO effect on HDL-C or TGs

Ezetimibe

_____

• Site of Action: Liver

• MOA: Inhibit PCSK9 → recycling of LDL-receptor to surface of hepatocytes

• Effect on LDL-C, HDL-C, and TG: Significant reduction in LDL-C with minor if any effect on HDL-C or TGs

Alirocumab

_____

• Site of Action: Liver

• MOA: Inhibits ACL enzyme and thus cholesterol synthesis in the liver

• Effect on LDL-C, HDL-C, and TG: Good reduction in LDL-C (less than high-intensity statins or PCSK9 inhibitors)

Bempedoic Acid

_____

• Site of Action: Intestine

• MOA: Inhibits bile acid reabsorption → cholesterol being used for bile acid synthesis → lowering LDL-C

• Effect on LDL-C, HDL-C, and TG: Modest effect on LDL-C reduction. May increase circulating levels of TGs (contraindicated in pancreatitis).

Cholestyramine

_____

• Site of Action: Endothelium of Blood Vessels

• MOA: PPAR agonist → upregulation of LPL synthesis → more TG hydrolysis

• Effect on LDL-C, HDL-C, and TG: Reduction in TGs

Fenofibrate

_____

• Site of Action: Adipose Tissue and Liver

• MOA: Inhibits FFA release from adipose tissues while reducing VLDL release from liver

• Effect on LDL-C, HDL-C, and TG: Lowers total cholesterol, TGs while increasing HDL-C

Niacin

_____

• Site of Action: Liver and Endothelium of Blood Vessels

• MOA: Inhibits TG synthesis, VLDL synthesis + release, and promotes LDL expressions

• Effect on LDL-C, HDL-C, and TG: reduces TGs

EPA/DHA