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Pulmonary > PHARM: PAH > Flashcards

PHARM: PAH Flashcards

1
Q

True or False: most drugs used against systemic HTN work for pulmonary HTN.

A

FALSE: only CCBs have been shown to help pulmonary as well as systemic HTN

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2
Q

What are the 4 main “causes” of PAH?

A

1) Impalance between vasoconstriction and vasodilation
2) SM/Endothelial cell proliferation, propogation, and hypertrophy
3) Thrombosis
4) Fibrosis

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3
Q

What is the “sine qua non” of patient with IPAH or heritable PAH?

A

plexiform lesions (thickened arteroiles as a result of sheer stress)

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4
Q

What does prostacyclin do in pulmonary arteries?

A

inhibits platelet activation and smooth muscle growth

also vasodilates

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5
Q

What does NO do in pulmonary arteries?

A

increases cGMP which leads to inhibition of platelet activation and smooth muscle activity (so vasodilation)

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6
Q

What does TXA2 do in pulmonary capillaries?

A

activates platelets

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7
Q

What does endothelin-1 do in pulmonary vessels?

A

induces smooth muscle growth

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8
Q

What are the 4 classes of drugs used to treat PAH?

A

Prostanoids
Endothelin-1 Receptor Antagonists
Phosphodiesterase Type 5 Inhibitors
CCBs

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9
Q

What is a prostanoid?

A

prostacyclin derivative that induces pulmonary artery vasodilation, retards smooth muscle growth and disrupts platelet aggregation

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10
Q

List the prostanoids used to treat PAH.

A

Epoprostenol
Iloprost
Treprostinil

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11
Q

What are the disadvantages of prostanoids?

A

Very expensive and NONE of them are oral (Epoprostenol is IV, Iloprost is inhaled, Treprostinil is SC or IV)

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12
Q

Why does epoprostenol have to be IV infused?

A

it has a 3-5 minute half-life (very short)

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13
Q

What are the dose limiting toxicities of epoprostenol?

A

Hypotension
Muscle pains
HA
Flushing

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14
Q

What are the AEs of iloprost?

A

Cough
Flushing
Hemoptysis* (rarely)

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15
Q

What are the AEs of treprostinil?

A

Injection site erythema, rash, pain.
Jaw pain
CYP2C8 drug interactions

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16
Q

What is the MOA of endothelin-1 receptor antagonists?

A

block the smooth muscle proliferaiton and pulmonary arterial vasoconstriction produced by endothelin-1 upon binding to its Type A (smooth muscle) and Type B (endothelial cell) receptors

17
Q

What is the advantage of endothelin-1 receptor antagonists over prostacyclins?

A

they are all orally active!

18
Q

What are the disadvantages of endothelin-1 receptor antagonists?

A

Expensive

TERATOGENIC

19
Q

What are the 2 endothelin-1 receptor antagonists used to treat PAH?

A

Bosentan

Ambrisentan

20
Q

What are the AEs of Bosentan?

A

Liver and Blood toxicities

CYP interactions

21
Q

What are the AEs of Ambrisentan?

A

Peripheral Edema
HA

*Less likely to cause liver problems and have CYP interactions

22
Q

What is the MOA of phosphodiesterase Type 5 inhibitors?

A

perpetuate endogenously generated cGMP leading to vasodilation and reduce cellular proliferation

23
Q

Who should NEVER talk a phosphodiesterase Type 5 inhibitor?

A

someone taking organic nitrates

24
Q

List the 2 phosphodiesterase Type 5 inhibitors used to treat PAH.

A

Sildenafil

Tadalafil

25
Q

What are phosphodiesterase Type 5 inhibitors also used for?

A

erectile dysfunction

benign prostatic hyperplasia

26
Q

What are some AEs of Sildenafil?

A

HA
Epistaxis
Dizziness with sudden hearing loss
CYP interactions

27
Q

What are some AEs of tadalafil?

A

headache
back pain
change in color vision (NAION)
CYP interactions

28
Q

What is the MOA of CCBs?

A

prevent access of Ca2+ into cells during membrane depolarization (block the key mediator of SM contraction, permitting a vasodilation to endure)

29
Q

True or false: all patients with PAH respond well to CCBs.

A

FALSE: some can even get worse

30
Q

How do you test to see if patient will respond to CCBs?

A

“vasodilator challenge”

31
Q

What is involved with a vasodilator challenge?

A

IV epoprostenol,IV adenosine, or inhaled NO are received at escalated dosing rates while PAP and CO are monitored for 2-3 hours

32
Q

What is considered to be a positive vasodilator challenge?

A

Decreased pulmonary arterial pressure with NO decrease in CO

33
Q

What CCBs have been used to treat PAH?

A

Diltiazem (immediate release)
Nifedipine (extended release)
Amlodipine

34
Q

What are the AEs of diltiazem?

A 
bradycardia
hypotnesion
HA
edema
cyp interactions
35
Q

What are the AEs of nifedipine?

A 
Flushing
edema
hypotension
heartburn
cyp interactions
36
Q

What are the AEs of amlodipine?

A

edema
fatigue
hypotension
cyp interactions

37
Q

Why is verapamil NOT used in PAH treatment?

A

it has strongly negative inotrophic properties which make it more likely to cause bradycardia

38
Q

What percent of tested patients are positive for the vasodilator challenge?

A

15%

39
Q

What is the goal of CCB therapy for PAH patients?

A

to reach NYHA-FC 1 or II after 3-4 months: meaning mild symptoms and/or slight limitation during normal physical activity or less

Pulmonary (34 decks)

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