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PAH (exam 3) Flashcards

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1
Q

pulmonary arterial hypertension

A

high blood pressure in the lungs

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2
Q

In PAH, increased pressure in the vessels is caused by

A

obstruction in the small arteries in the lungs

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3
Q

what kind of heart failure does PAH cause?

A

right sided HF

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4
Q

group 1 PAH

A

pulmonary arterial hypertension

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5
Q

group 2 PAH

A

PH due to left heart disease

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6
Q

group 3 PAH

A

PH due to lung disease and/or chronic hypoxia

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7
Q

group 4 PAH

A

PH due to blood clots in the lungs

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8
Q

group 5 PAH

A

PH due to blood and other disorders (sickle cell disease)

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9
Q

____________ use during pregnancy increases the risk of _________ PAH

A

SSRI

newborn

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10
Q

disorders associated with PAH

A

connective tissue diseases (scleroderma)
liver disease
HIV
congenital heart disease

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11
Q

drugs associated with PAH

A

stimulant use drugs (methamphetamine, cocaine, weight loss stimulants)

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12
Q

main symptoms of PAH

A

exertional dyspnea
fatigue that progressively worsens

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13
Q

as the disease progresses, symptoms of ____________ dysfunction and failure are present. these include:

A

right heart

dyspnea at rest, low extremity edema, chest pain, and syncope

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14
Q

what is required for definitive diagnosis of PAH?

A

pulmonary artery catheterization

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15
Q

normal pulmonary arterial pressure

A

25/10 mmHg (mean PAP of 15 mmHg)

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16
Q

In PAH, the PAP increases to around ______________

PAH is diagnosed if mean PAP is

A

4-/20 mmHg

greater than or equal to 25 mmHg

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17
Q

mean PAP =

A

1/3(systolic PAP) + 2/3(diastolic PAP)

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18
Q

PAH arises from changes in the

A

small pulmonary arteries and arterioles (effects PVR)

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19
Q

major cause of mortality of PAH

A

right side HF

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20
Q

In pulmonary HTN, there is an increase in ____________ for the right side of the heart

overtime this increased pressure leads to _____________-

A

afterload

Right ventricles dysfunction and right heart failure

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21
Q

can respiratory failure occur in PAH

A

yes

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22
Q

major pathogenic components in the development of PAH

A

sustained vasoconstriction
pulmonary vascular remodeling
in situ thrombosis
vascular wall stiffening

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23
Q

PAH functional class I

A

no symptoms/functional limitation

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24
Q

PAH functional class II

A

slight limitation of physical activity

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25
PAH functional class III
marked limitation of physical activity
26
PAH functional class IV
symptoms with any activity or at rest
27
lifestyle modifications for PAH
sodium restricted diet avoidance of high altitude
28
patients at risk for VTE should receive
warfarin
29
patients with fluid overload should receive
a loop diuretic
30
when is oxygen treatment required in PAH?
when oxygen saturation is below 90%
31
commonly used vasodilatory CCBs can be used to treat PAH?
long acting nifedipine sustained release diltiazem amlodipine
32
which vasodilatory CCB should not be used in PAH?
verapamil
33
CCBs are ineffective in PAH when
there is significant stiffening of the pulmonary arteries
34
Targeted therapies for patients who can't take CCBs
Prostacyclin receptor agonists endothelia receptor antagonists PDE5 inhibitors sGC stimulator
35
targeted therapies cause
vasodilation, reduce vascular remodeling and reduce platelet activation
36
Prostacyclin receptor agonists (prostanoids) examples
epoprostenol (Flolan) Treprostinil (Tyvaso) Iloprost (Ventavis) Selexipag (Uptravi)
37
endothelial receptor antagonists
Bosentan (Tracleer) Ambrisentan (Letairis) Macitentan (Opsumit)
38
PDE5 inhibitors examples
sildenafil (Revatio) tadalafil (adcirca)
39
sGC stimulator example
Riociguat (Adempas)
40
PAH class I patients should receive
mono therapy or no therapy
41
PAH class II-III patients should receive
combination therapy
42
PAH class IV patients should receive
combination therapy with a parenteral prostacyclin receptor agonist
43
prostacyclin receptor agonist MOA
activate the IP receptor (Gs coupled) which increases CAMP and reduce calcium leads to vasodilation, reduced platelet activation and reduced vascular remodeling
44
In PAH, there is a reduction in which prostaglandin?
PGI2
45
Prostacyclin (PGI2)
released by vascular endothelial cells maintain homeostasis physiological antagonist of TxA2
46
Epoprostenol
synthetic form of PGI2 given continuous infusion via pump 1/2 life: 3-5 min
47
Treprostinil
given IV/SC infusion, inhaled or oral longer half life that epoprostenol
48
Iloprost
given by inhalation longest half life
49
Selexipag
not structurally related to PGI2 has an active metabolite oral
50
active metabolite of selexipag
ACT-333679
51
ADRs of prostacyclin receptor agonists
pain hypotension GI cough (if given inhalation)
52
treprostinil and selexipag are metabolized by
CYP2C8
53
prostacyclin receptor agonists have to be ____________ due to the chance of _________________ with sudden discontinuation
titrated up rebound PAH
54
which prostacyclin receptor agonist is recommended in stage IV PAH
IV epoprostenol
55
endothelin I primarily bind to the _______ receptor and causes ______________
ETA vasoconstriction
56
In PAH, there is up to a ____________ in plasma endothelin-1 and level of elevation correlates with _________________
10x increase severity of disease
57
MOA of endothelin receptor antagonists
block the ETA receptor (Gq coupled) which reduces IP3, DAG and calcium leads to vasodilation, reduced platelet activation and reduced vascular remodeling
58
ambrisentan
selectively blocks ETA receptor
59
Bonsentan and Macitentan
blocks both ETA and ETB receptors (higher affinity for A)
60
ADRs of endothelin receptor antagonists
hypotension peripheral edema anemia increased liver enzymes
61
how does endothelin receptor antagonists increase liver enzymes?
drug metabolites compete with bile acids for binary excretion causes bile build up
62
bosentan induces
CYP3A4 and 2C9
63
endothelin receptor antagonists are contraindicated in
pregnancy
64
bonsetan has a BBW for
hepatotoxicity
65
endothelin receptor antagonists have to go through the ________ program due to their BBW for ______________
REMS skull and facial abnormalities in fetus and CV malformation
66
In PAH a reduction in synthesis of ___________ occurs leading to a reduction in cGMP
nitric oxide
67
guanylate cyclase converts
GTP to cGMP
68
PDE5
enzyme that breaks down cGMP to inactive GMP
69
example of medications that increase cGMP
PDE5 inhibitors sGC stimulator
70
ADRs of PDE5 inhibitors
hypotension myalgia (tadalafil) dose dependent visual disturbance
71
PDE5 inhibitors are metabolized by
CYP3A4
72
PDE5 inhibitors should not be used in combination with
nitrates or riociguat
73
sGC stimulator MOA
directly stimulates soluble guanylate cyclase and increases binding of nitric oxide to sGC
74
ADRs of sGC stimulator
hypotension GI anemia hemorrhage
75
riociguat is metabolized by
3A4, 1A1, 2C8, 2J2
76
sGC stimulator should not be used in combination with
nitrates or PDE5 inhibitors
77
riociguat is contraindicated in ____________ and has to go through ___________
pregnancy REMS
78
riociguat is approved for treatment in
PAH chronic thromboembolic PH
79
if a woman with PAH becomes pregnant what should be discontinued?
endothelin receptor antagonists riociguat
80
what is the best choice for treatment of a pregnant woman with PAH?
IV epoprostenol
81
pediatric PAH
treated similar to adults bosentan only drug approved 3 and up
82
why should woman avoid getting pregnant if they have PAH?
changes in hemodynamics during pregnancy can lead to mortality

Pharmacology II (18 decks)

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