Page 365 - First Aid for the USMLE Step 1 2020, Thirtieth edition [MedicalBooksVN.com]_Neat

CARDIOvASCuLAR ``CARdIOvASCulAR—PHARMACOlOGY CARDIOvASCuLAR ``CARdIOvASCulAR—PHARMACOlOGY SECTION III 321

Lipid-lowering agents (continued)

Liver Blood Enterocyte Intestinal lumen
Acetyl-CoA
CHOLESTEROL
HMG-CoA ApoE Lymphatics ABSORPTION
receptor CHY CHY
HMG-CoA CHY
reductase rem Ezetimibe
Mevalonate Triacylglyceride LPL
HDL FFA
pool
Cholesterol Cholesterol
Cholesterol VLDL VLDL FFA FFA
Bile acids Bile acids
MEVALONATE
SYNTHESIS
Niacin BILE ACID
LPL
Statins HDL LPL- REABSORPTION
Lovastatin receptor FFA UPREGULATION
Pravastatin
Simvastatin HDL HDL Bile acid resins
Atorvastatin Lipolysis Fibrates Cholestyramine
Rosuvastatin FFA Gemfibrozil Colestipol
Adipose tissue Bezafibrate Colesevelam
LDL Fenofibrate
LDL
LDL
receptor
ADIPOSE LIPOLYSIS

LDL-RECEPTOR
PCSK9 Niacin
DEGRADATION
PCSK9 inhibitors
Alirocumab
Evolocumab

Cardiac glycosides Digoxin.
+
+
MECHANISM Direct inhibition of Na /K ATPase + 2+ + + Digoxin
Na /Ca
Na /K
Ž indirect inhibition of Na /Ca exchanger. exchanger ATPase
+
2+
2+
 [Ca ] i Ž positive inotropy. Stimulates vagus
nerve Ž  HR.
Ca 2+
Na + K +
2+
↑TnC Ca ↑ cardiac
2+
SR ↑↑Ca binding contraction
ClINICAl uSE HF ( contractility); atrial fibrillation ( conduction at AV node and depression of SA node).
AdvERSE EFFECTS Cholinergic effects (nausea, vomiting, diarrhea), blurry yellow vision (think van Glow),
arrhythmias, AV block.
Can lead to hyperkalemia, which indicates poor prognosis.
Factors predisposing to toxicity: renal failure ( excretion), hypokalemia (permissive for digoxin
binding at K -binding site on Na /K ATPase), drugs that displace digoxin from tissue-binding
+
+
+
sites, and  clearance (eg, verapamil, amiodarone, quinidine).
2+
+
ANTIdOTE Slowly normalize K , cardiac pacer, anti-digoxin Fab fragments, Mg .

FAS1_2019_07-Cardio.indd 321 11/7/19 4:24 PM