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Maddy - CPR II - some pharm > Drugs for Pulmonary HTN > Flashcards

Drugs for Pulmonary HTN Flashcards

1
Q

list 4 prostanoids

A
  • epoprostenol
  • treprostinil
  • iloprost
  • selexipag
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2
Q

list 3 endothelin antagonists

A
  • bosentan
  • ambrisentan
  • macicentan
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3
Q

list the 2 PDE 5 Inhibitors

A
  • sildenafil

- tadalafil

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4
Q

list the guanylate cyclase sensitizer

A

riociguat

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5
Q

describe WHO functional class I

A
  • pts with pulm HTN but w/o resulting limitation of physical activity
  • ordinary activity does not cause dyspnea or fatigue, CP, or near syncope
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6
Q

describe WHO functional class II

A
  • pts with pulm HTN w/ slight limitation of physical activity
  • comfortable at rest
  • ordinary physical activity causes undue dyspnea or fatigue, CP, or near syncope
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7
Q

describe WHO functional class III

A
  • pts w/ pulm HTN w/ marked limitation of physical activity
  • comfortable at rest
  • less than ordinary activity causes undue dyspnea or fatigue, CP, or near syncope
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8
Q

describe WHO functional class IV

A
  • pts w/ pulm HTN w/ inability to carry out any physical activity w/o sx
  • manifest signs of right HF
  • dyspnea and fatigue may be present at rest
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9
Q

MOA epoprostenol

A

prostanoid
- mimic actions of endogenous prostacyclin –> promotes vascular relaxation, suppresses growth of vascular smooth m. cells, inhibits platelet aggregation

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10
Q

effects epoprostenol

A
  • lower pulm art. pressure
  • decreases pulmonary arterial resistance
  • increases exercise tolerance
  • improves short term survival
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11
Q

half life and administration of epoprostenol

A
  • short have life (6 mins)

- continuous IV infusion w/ pump that keeps it cold

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12
Q

toxicities of epoprostenol

A
  • sepsis due to chronic catheter
  • nausea/vomiting
  • HA
  • flushing
  • jaw pain
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13
Q

MOA treprostinil

A

prostanoid
- mimic actions of endogenous prostacyclin –> promotes vascular relaxation, suppresses growth of vascular smooth m. cells, inhibits platelet aggregation

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14
Q

effects treprostinil

A
  • lower pulm art. pressure
  • decreases pulmonary arterial resistance
  • increases exercise tolerance
  • improves short term survival
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15
Q

half life and administration treprostinil

A
  • longer half life than epoprostenol at 4 hrs

- diluted and administered with pump IV, doesn’t require refrigeration

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16
Q

toxicities treprostinil

A
  • sepsis due to chronic catheter
  • jaw pain
  • diarrhea
  • edema
  • nausea
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17
Q

MOA iloprost

A

prostanoid
- mimic actions of endogenous prostacyclin –> promotes vascular relaxation, suppresses growth of vascular smooth m. cells, inhibits platelet aggregation

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18
Q

effects iloprost

A
  • lower pulm art. pressure
  • decreases pulmonary arterial resistance
  • increases exercise tolerance
  • improves short term survival
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19
Q

administration of iloprost

A

inhalation 6-9 times per day

20
Q

toxicities iloprost

A
  • fainting due to hypotension
  • cough
  • HA
  • flushing
  • jaw pain
21
Q

MOA selexipag

A

prostanoid
- mimic actions of endogenous prostacyclin –> promotes vascular relaxation, suppresses growth of vascular smooth m. cells, inhibits platelet aggregation

22
Q

effects selexipag

A
  • lower pulm art. pressure
  • decreases pulmonary arterial resistance
  • increases exercise tolerance
  • improves short term survival
23
Q

administration of selexipag

A

orally BID

24
Q

toxicities selexipag

A
  • HA
  • flushing
  • diarrhea/nausea/vom
  • jaw, limb, muscle pain
  • skin rash
25
Q

MOA bosentan

A

endothelin antagonist

- nonspecifically blocks ETA and ETB endothelin receptors

26
Q

effects bosentan

A

improves exercise tolerance and slows sx progression

27
Q

administration and metabolism of bosentan

A

oral drug

metabolized by liver, highly protein bound

28
Q

toxicities bosentan

A
  • hepatotoxicity
  • teratogenesis
  • HA, flushing, peripheral edema, nasal congestion, anemia
29
Q

drug interactions bosentan

A

accelerate metabolism of warfarin and oral contraceptives

30
Q

MOA ambrisentan

A

endothelin antagonist

- selectively blocks ETA receptors (that normally cause vasoconstriction and promote cell proliferation)

31
Q

effects ambrisentan

A

improves exercise tolerance and slows sx progression

32
Q

administration ambrisentan

A

oral

33
Q

toxicities ambrisentan

A
  • teratogenesis
  • NO hepatotoxicity
  • peripheral edema, nasal congestion, anemia
34
Q

drug interactions ambrisentan

A

does NOT accelerate metabolism of warfarin and oral contraceptives

35
Q

MOA macitentan

A

endothelin antagonist

- nonselective agent

36
Q

administration and half life macitentan

A

18hr half life

once a day dosing

37
Q

toxicities of ambrisentan

A

CYP450 effects similar to bosentan

38
Q

MOA sildenafil

A

blocks phosphodiesterase type V that breaks down cGMP

39
Q

effects sildenafil

A

improves exercise tolerance and slows sx progression

40
Q

administration and half life sildenafil

A

oral

half life 4 hours

41
Q

toxicities of sildenafil

A

well tolerated

  • flushing
  • HA
  • dyspepsia
  • can cause visual disturbances
42
Q

MOA riociguat

A

guanylate cyclase sensitizer

  • sensitizes soluble guanylate cyclase to endogenous NO by stabilizing the NO-sGC binding
  • directly stimulates sGC indepdendent of NO
  • increased generation of cGMP –> increased vasodilation
43
Q

effects riociguat

A

improves exercise tolerance and slows sx progression

44
Q

administration and half life of riociguat

A

oral drug

12 hour half life

45
Q

toxicities of tiociguat

A
  • hypotension, HA, dizziness, dyspepsia

- may cause fetal harm

Maddy - CPR II - some pharm (18 decks)

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