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CPR Exam 2 > (6.1) Pulmonary Hypertension (Wolff) > Flashcards

(6.1) Pulmonary Hypertension (Wolff) Flashcards

1
Q

What are the (4) prostanoids?

A

-prost

Epoprostenol

Treprostinil

Iloprost

Selexipag

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2
Q

What are the (2) PDE 5 inhibitors?

A

-afil

Sildenafil

Tadalafil

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3
Q

What are the (3) endothelin antagonists?

A

-sentan

Bosentan

Ambrisentan

Macicentan

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4
Q

What is the (1) guanylate cyclase sensitizer?

A

Riociguat

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5
Q

If you get a positive CCB vasopressor test…

What drugs do you use?

A

Nifedipine

Diltiazem

Amlodipine

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6
Q

What is the primary target for the drugs we are learning for this lecture?

A

Pulmonary aterial hypertension (PAH)

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7
Q

What is the definition of PAH?

A

Sustained elevation of mean pulmonary arterial pressure (mPAP) is

greater than or equal to 25mmHg at rest

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8
Q

What is the normal pulmonary pressure?

A

14 plus or minus 3 mmHg

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9
Q

What population is typically affected by pulmonary HTN?

A

Young women

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10
Q

What is pulmonary arterial hypertension (PAH) characterized by?

A

Progressive increase in pulmonary vascular resistance (PVR)

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11
Q

What does PAH eventually lead to (anatomically)?

A

Right ventricular overload –> right ventricular failure = premature death

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12
Q

What are the EARLY symptoms of PAH?

A

Dyspnea upon exertion

Fatigue

Chest pain

Tachycardia

Pain on the upper right side of the abdomen

Anorexia

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13
Q

What are the LATE symptoms of PAH?

A

Syncope

Swelling in legs and ankles

Cyanotic lips and skin

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14
Q

What is a MAJOR genetic correlation to produce PAH?

A

BMPR2

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15
Q

What is a MAJOR drug that can predispose pts to PAH?

A

Fenfluramine/phentermine

“fen/phen” weight loss pill

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16
Q

What are key components (ligands) involved in pulmonary vascular remodeling?

A

5-HT

ET-1

17
Q

What is the gold standard for measuring pulmonary pressure?

A

Right heart catheterization

18
Q

What is the MOA for epoprostenol?

A

Mimics the actions of endogenous prostacyclin

(endogenous prostacyclin is a compound that promotes vascular relaxation)

19
Q

Noteworthy about epoprostenol?

A

VERY SHORT HALF LIFE!!!

(6 min)

Must be given by continuous IV

20
Q

What are the toxicities associated with epoprostenol?

A

Sepsis due to chronic catheter

Life threatening problems if pump lines become clogged

Common side effects = N/V, Headace, flushing jaw pain

21
Q

Since epoprostenol wasn’t great…came out with another drug that has the same MOA, but has a few differences in the pharmacokinetics…

What drugs am I talking about?

A

Treprostinil

22
Q

What is unique about the pharmacokinetics of treprostinil?

A

SubQ infusion with a LOT of pain

Higher half life (4hrs) than epoprostenol

Doesn’t require refrigeration

23
Q

Same MOA as both epoprestenol and treprostinil… slightly different pharmacokinetics and toxicities…

What drug am I talking about?

A

Iloprost

24
Q

What are the unique pharmacokinetics of iloprost?

A

Administered via INHALATION

25
Q

What are the side effects of Iloprost?

A

Fainting due to hypotension

Cough, headache, flushing, jaw pain

26
Q

Since epoprostenol, treprostinil, iloprost all had some bad qualities to them, came out with another drug that is an oral medication used to treat PAH.

What drug am I talking about?

A

Selexipag

27
Q

What is the major downside to using selexipag?

A

SUPER EXPENSIVE

$225 per pill

28
Q

What is the MOA of bosentan?

A

Nonspecifically blocks the ETA and ETB endothelin receptors

29
Q

What are the side effects associated with bosentan?

A

Hepatotoxicity

Teratogenesis

30
Q

What are the noteable drug interactions with bosentan?

A

ORAL CONTRACEPTIVES

Warfarin

31
Q

What is the MOA of ambrisentan?

A

SELECTIVELY blocks the ETA receptors

32
Q

What are the advantages and disadvantages of using ambrisentan?

A

Disadvantage: SUPER expensive, teratogenesis

Advantages: Does not damage liver, does not interfer with warfarin or oral contraceptives

33
Q

MOA of sildenafil?

A

Selectively blocks phosphodiesterase type V

34
Q

What is the MOA of riociguat?

A

Dual mode of action:

1) Sensitizes soluble guanylate cyclase (sGC) to endogenous nitric oxide (NO)
2) Directly stimulates sGC independent of NO

(Together, the increased generation of cGMP leads to increased vasodilation)

35
Q
A

CPR Exam 2 (21 decks)

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