Pharm--Restrictive/PAH Flashcards
Some drugs that commonly cause ARDS?
Aspirin, cocaine, antidepressants
NRDS treatment options
Beractant
Beractant MOA/components
Proteins B, C, lipids
**DPCC - main component of surfactant
Sarcoidosis treatment options?
Glucocorticoids
MTX (immunosuppression)
Name some pro-inflammatory cytokines that glucocorticoids downregulate
IL-1
TNF
What about anti-inflammatory cytokines that steroids upregulate?
IL-10
MTX has additional actions that lead to immunosupression via this mediator
Adenosine
MTX AEs
Cat X
Malignant lymphoma
Infection risk
Dermatologic reactions-severe
IPF drugs
None really help; some use corticosteroids to dx - if there is response, it is probs not IPF
Wegener’s granulomatosis drugs
Rituximab, azathioprine, cyclophosphamide, steroids
Rituximab MOA Wegener’s
Binds CD20 and depletes B cells
Azathioprine MOA Wegener’s
DNA/RNA synthesis inhibitor that also causes immunosupperssion of T cells (apoptosis)
Azathioprine AEs
Thrombocytopenia, 2ndary maligs
Cyclophosphamide MOA Wegener’s
Alkylating agent - B and T depletion - also selective B suppression
What systemic HTN drugs are also used for PAH? Why not others?
Ca2+ channel blockers; different mechanism
The four causes of PAH
1) Imbalance between constriction/dilation
2) Smooth muscle/endothelial proliferation
3) Thrombosis
4) Fibrosis
Role of prostacyclin in PAH
Prostacyclin inhibits platelet activation and smooth muscle growth
Role of endothelin in PAH
Induces smooth muscle proliferation
Epoprostenol MOA
prostanoid that induces:
vasodilation
smooth muscle growth retardation
Platelet de-aggregation
Iloprost
prostanoid that induces:
vasodilation
smooth muscle growth retardation
Platelet de-aggregation
Treprostinil
prostanoid that induces:
vasodilation
smooth muscle growth retardation
Platelet de-aggregation
Compare the half lives of the prostanoids
Iloprost 25 min!
Epoprostenol 3-5 min!
Treprostinil 4 hrs
Epoprostenol AEs
Dose-limiting hypotension Myalgia HA Flushing Monitor for bleeding
Iloprost AEs
Hemoptysis
Cough, flushing, HA
Treprostinil AEs
Jaw pain, N/V
Monitor for bleeding
CYP2C8 interactions
Clearance issues with gemfib and rifampin
Endothelin receptor antagonists advantage over prostanoids
Can be taken orally
Bosentan MOA
endothelin receptor antag; blocks smooth muscle proliferation and pulmonary vasoconstriction
Ambrisentan MOA
endothelin receptor antag; blocks smooth muscle proliferation and pulmonary vasoconstriction
Ambristentan AEs
Edema, better for liver than Bosentan, teratogenic
Bosentan MOA
Teratogenic, LIVER, anemia
PDE type 5 inhibitors MOA
Keep cGMP around leading to vasodilation
Tadalafil AEs
C/I nitrates
Back pain, dyspepsia
Change in color vision
What is vasodilator challenge?
Some pts on CCBs get fatal hemodynamic collapse, so it is important to give a carefully escalated dosing rate and monitor effects. If they do ok then can use CCB
Diltiazem MOA
CCB
Amlodipine MOA
CCB
Diltiazem AE
bradycardia, hypotension
Amlodipine AE
Edema, hypotension, fatigue
Verapamil and PAH
Avoided because of strong negative ionotropism (risk for bradycardia)
Goal of CCB therapy for PAH?
Class I or II NYHA by 3-4 months
