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OS Pulmonary > Pharm--Restrictive/PAH > Flashcards

Pharm--Restrictive/PAH Flashcards

1
Q

Some drugs that commonly cause ARDS?

A

Aspirin, cocaine, antidepressants

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2
Q

NRDS treatment options

A

Beractant

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3
Q

Beractant MOA/components

A

Proteins B, C, lipids

**DPCC - main component of surfactant

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4
Q

Sarcoidosis treatment options?

A

Glucocorticoids

MTX (immunosuppression)

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5
Q

Name some pro-inflammatory cytokines that glucocorticoids downregulate

A

IL-1

TNF

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6
Q

What about anti-inflammatory cytokines that steroids upregulate?

A

IL-10

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7
Q

MTX has additional actions that lead to immunosupression via this mediator

A

Adenosine

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8
Q

MTX AEs

A

Cat X
Malignant lymphoma
Infection risk
Dermatologic reactions-severe

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9
Q

IPF drugs

A

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

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10
Q

Wegener’s granulomatosis drugs

A

Rituximab, azathioprine, cyclophosphamide, steroids

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11
Q

Rituximab MOA Wegener’s

A

Binds CD20 and depletes B cells

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12
Q

Azathioprine MOA Wegener’s

A

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

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13
Q

Azathioprine AEs

A

Thrombocytopenia, 2ndary maligs

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14
Q

Cyclophosphamide MOA Wegener’s

A

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

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15
Q

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

A

Ca2+ channel blockers; different mechanism

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16
Q

The four causes of PAH

A

1) Imbalance between constriction/dilation
2) Smooth muscle/endothelial proliferation
3) Thrombosis
4) Fibrosis

17
Q

Role of prostacyclin in PAH

A

Prostacyclin inhibits platelet activation and smooth muscle growth

18
Q

Role of endothelin in PAH

A

Induces smooth muscle proliferation

19
Q

Epoprostenol MOA

A

prostanoid that induces:
vasodilation
smooth muscle growth retardation
Platelet de-aggregation

20
Q

Iloprost

A

prostanoid that induces:
vasodilation
smooth muscle growth retardation
Platelet de-aggregation

21
Q

Treprostinil

A

prostanoid that induces:
vasodilation
smooth muscle growth retardation
Platelet de-aggregation

22
Q

Compare the half lives of the prostanoids

A

Iloprost 25 min!
Epoprostenol 3-5 min!
Treprostinil 4 hrs

23
Q

Epoprostenol AEs

A 
Dose-limiting hypotension
Myalgia
HA
Flushing
Monitor for bleeding
24
Q

Iloprost AEs

A

Hemoptysis

Cough, flushing, HA

25
Q

Treprostinil AEs

A

Jaw pain, N/V
Monitor for bleeding
CYP2C8 interactions
Clearance issues with gemfib and rifampin

26
Q

Endothelin receptor antagonists advantage over prostanoids

A

Can be taken orally

27
Q

Bosentan MOA

A

endothelin receptor antag; blocks smooth muscle proliferation and pulmonary vasoconstriction

28
Q

Ambrisentan MOA

A

endothelin receptor antag; blocks smooth muscle proliferation and pulmonary vasoconstriction

29
Q

Ambristentan AEs

A

Edema, better for liver than Bosentan, teratogenic

30
Q

Bosentan MOA

A

Teratogenic, LIVER, anemia

31
Q

PDE type 5 inhibitors MOA

A

Keep cGMP around leading to vasodilation

32
Q

Tadalafil AEs

A

C/I nitrates
Back pain, dyspepsia
Change in color vision

33
Q

What is vasodilator challenge?

A

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

34
Q

Diltiazem MOA

A

CCB

35
Q

Amlodipine MOA

A

CCB

36
Q

Diltiazem AE

A

bradycardia, hypotension

37
Q

Amlodipine AE

A

Edema, hypotension, fatigue

38
Q

Verapamil and PAH

A

Avoided because of strong negative ionotropism (risk for bradycardia)

39
Q

Goal of CCB therapy for PAH?

A

Class I or II NYHA by 3-4 months

OS Pulmonary (13 decks)

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