Pulmonary Hypertension (Drugs) Flashcards
Bosentan
Endothelin Receptor Antagonists
- Treats PAH
MOA:
- Blocks Endothelin A receptors on SMC
–> Vasodilation
Epoprostenol
Prostacyclin
- Treats PAH (Largest reductions in pulmonary arterial pressure)
MOA:
- Binds SMC IP Receptors–> Increases cAMP Signaling
–> Vasodilation
Riociguat
sGC Activator - Allosteric Activator
- Treats PAH
MOA:
- Binds to sGC (different binding area than NO)
–> Potentiates effects of NO converting GTP into cGMP
–> Vasodilation
Sildenafil
Phosphodiesterase 5 Inhibitor (PDE5i)
- Treats PAH
MOA:
- Inhibit PDE5i
–> Prevents breakdown of cGMP
–> Increase cGMP Signaling
–> Vasodilation
Tadarafil
Phosphodiesterase 5 Inhibitor (PDE5i)
- Treats PAH
MOA:
- Inhibit PDE5i
–> Prevents breakdown of cGMP
–> Increase cGMP Signaling
–> Vasodilation
Nifedipine
Ca2+ Entry Antagonists
- Treats PAH
MOA:
Reduces Calcium entry into SMC
–> Arterial DIlation
–> Reduces BP
Inhaled NO
Diagnosis of PAH
- Not used for treatment
MOA:
- PAH will cause high resistant state to remain in infant
–> NO forces a shift from high to low resistance
Vasopressin
Treats Shock/Hypotensive State (AKA ADH)
MOA:
- Used with Noradrenaline
–> Increases Water Reabsorption
–> Increase Blood Volume
–> Increase Cardiac Output
–> Increase Arterial Pressure
Adrenaline
Adrenergic Vasopressors:
- Treats Shock/Hypotensive State
MOA:
- Alpha 1 Effect
–> Vasoconstriction
–> Increases Cardiac Output
–> Increases Arterial Pressure
Noradrenaline
Adrenergic Vasopressors:
- Treats Shock/Hypotensive State
MOA:
- Alpha 1 Effect
–> Vasoconstriction
–> Increases Cardiac Output
–> Increases Arterial Pressure
Dobutamine
Adrenergic Vasopressors:
- Treats Shock/Hypotensive State
MOA:
- Beta 1 Effect (Cardiogenic Shock)
–> Vasoconstriction
–> Increase Cardiac Output
–> Increase Arterial Pressure