Pharmacology Etc. Flashcards
How do Nitrates relieve variant angina?
Nitrates must be converted to NO via thiol.
NO -> SM relaxation -> coronary a. dilation -> coronary spasm relief
How do Nitrates relieve classic angina?
Nitrates must be converted to NO via thiol.
NO -> SM relaxation -> venous dilation -> reduced pre-load -> reduced oxygen demand
How do CCBs relieve classic angina?
Dilate peripheral arterioles -> decreased PVR and afterload -> decreased contractility and HR.
How do CCBs relieve variant angina?
Increase blood supply by dilation of coronary aa.
How do beta-blockers relieve angina?
Decrease myocardial oxygen demand -> decreased HR -> better myocardial perfusion and oxygen demand at rest and w/ exercise. Leads to decreased contractility , BP and afterload.
What ions flux in Class 1a anti-arrhythmic drugs?
What is the effect on ECG?
Na+ and K+ channels are inhibited.
Increased QT and QRS interval.
Increased AP length and ERP length.
What ions flux in Class 1b anti-arrhythmic drugs?
What is the effect on ECG?
Na+ channels inhibited.
Decrease length of QT interval.
Decreased length of AP. This is due to the fast kinetics.
What ions flux in Class 1c anti-arrhythmic drugs?
What is the effect on ECG?
Na+ inhibited, some K+.
Prolong QRS interval. No change in QT or AP length.
Class 2 anti-arrhythmic drugs’ MOA
What is its effect on its AP graph? SA/AV nodes?
Inhibits If and T- and L-type Ca++ channels.
Decreases slope of phase 4 (If and T-type) and increase threshold (L-type).
@ SA node: decrease HR
@ AV node: decreased AV conductance -> increased PR interval
Class 3 anti-arrhythmic drugs ion flux
What is its effect on ECG, AP time, ERP?
Inhibit K+ channels.
Increase QT interval, AP time, ERP.
Class 4 anti-arrhythmic drugs’ MOA
What is the effect on AP graph?
Blocks L-type Ca++ channels (active and inactive channels). Targets slow response cells.
Decrease slop of phase 0 (depolarization).
Increased threshold (L-type)
Increase ERP.
Bradycardia.
Adenosine MOA
Activates K+ channels and inhibit Ca++ channels and funny currents. This causes marked hyperpolarization and suppression of APs in slow cells.
Inhibits AV conduction and increases nodal refractory period.
Complex MOA of Niacin
Inhibit HSL -> decrease [FFA] -> decreased VLDL synthesis.
Decrease Apo A1 clearance -> increased HDL.
Complex MOA of Fibrates
Activate PPAR-a
- Activate expression of Apo A1 and A2 -> increase HDL.
- Activate lipoprotein lipase -> increased clearance of TGs at endothelium and FFA oxidation at liver.
Complex MOA of Statins
- Inhibit HMG-CoA reductase -> decreased cholesterol.
- Low IC [cholesterol] -> increased LDL R synthesis.
- Increased LDL reuptake from blood.
- Decreased IC [cholesterol] -> decreased secretion of VLDL.
