Pharm--Restrictive/PAH Flashcards by Matt McCulloch

Some drugs that commonly cause ARDS?

Aspirin, cocaine, antidepressants

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NRDS treatment options

Beractant

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Beractant MOA/components

Proteins B, C, lipids

**DPCC - main component of surfactant

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Sarcoidosis treatment options?

Glucocorticoids

MTX (immunosuppression)

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Name some pro-inflammatory cytokines that glucocorticoids downregulate

IL-1

TNF

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What about anti-inflammatory cytokines that steroids upregulate?

IL-10

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MTX has additional actions that lead to immunosupression via this mediator

Adenosine

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MTX AEs

Cat X
Malignant lymphoma
Infection risk
Dermatologic reactions-severe

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IPF drugs

None really help; some use corticosteroids to dx - if there is response, it is probs not IPF

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Wegener’s granulomatosis drugs

Rituximab, azathioprine, cyclophosphamide, steroids

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Rituximab MOA Wegener’s

Binds CD20 and depletes B cells

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Azathioprine MOA Wegener’s

DNA/RNA synthesis inhibitor that also causes immunosupperssion of T cells (apoptosis)

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Azathioprine AEs

Thrombocytopenia, 2ndary maligs

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Cyclophosphamide MOA Wegener’s

Alkylating agent - B and T depletion - also selective B suppression

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What systemic HTN drugs are also used for PAH? Why not others?

Ca2+ channel blockers; different mechanism

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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