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PAH Flashcards

1
Q

What is PAH?

A

Increased BP in pulmonary vasculature
1’ elevation of pulmonary arterial system not 2’

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2
Q

PAH can lead to?

A

Right heart failure- it is a progressive disease

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3
Q

What the clinical markers of PAH?

A

MPAP: >25 mmhg @ rest with PCWP < /= 15 mmHG and PVR >3

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4
Q

What are the initial symptoms?

A

Exertional dyspnea, fatigue, exercise intolerance

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5
Q

What are the progressive symptoms?

A

Dyspnea @ rest, chest pain, syncope, peripheral edema, ascites, pleural effusions, right heart failure

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6
Q

Pah diagnosing risk factors?

A

Female, younger <65 years old, no significant heart/ lung disease
Stimulant use, HIV, cirrhosis, connective tissue disease, heart defects, appetite suppressants

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7
Q

What should you assess for diagnosis?

A

Right ventricular systolic pressure, and residual volume to rule out left heart disease
Pulmonary disease and sleep disorders
Chronic thromboembolic disease

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8
Q

What tests should be done?

A

HIV, LFTs, ANA, TSH, drug screen
ECG, PFT, PSG, RHC

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9
Q

What is the gold standard?

A

Right heart catheterization
Required for insurance approval

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10
Q

How do you manage group 1:

A

PAH- highly specialized and specific meds

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11
Q

How do you manage group 2:

A

Left Heart(venous HTN): treat HFpEF, HFrEF

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12
Q

How do you manage group 3:

A

Lung disease- treat COPD, sleep apnea

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13
Q

How do you manage group 4:

A

Chronic thrombolic embolic PH: surgical care

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14
Q

If it’s precapillary (right), what are the clinical markers?

A

MPAP > 25
PAWP<15

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15
Q

If it’s post capillary (left), what are the clinical markers?

A

MPAP>25
PAWP >15

Regular PH due to LHD

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16
Q

Class 1?

A

Without limitation of physical activity

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17
Q

Class 2?

A

Slight limitation of physical activity but comfortable at rest
Ordinary physical activity causes dyspnea and fatigue and chest pain

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18
Q

Class 3?

A

Marked limitation of physical activity but comfortable at rest, less than ordinary activity causes dyspnea and fatigue and chest pain

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19
Q

Class 4?

A

limitation of ANY physical activity without symptoms- dyspnea and fatigue at rest

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20
Q

If patient is in group 2 or 3 due to left heart disease or hypoxemic, what do you do?

A

Do NOT treat with vasoactive agents
No benefit- worsening fluid
Group 3- no therapies but inhaled treprostinil some improvement of 6MWD and interstial lung disease

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21
Q

1’ PAH

A

Idiopathic, heritable-BMPR2 mutation

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22
Q

2’ PAH

A

Drug and toxin induced, HIV, heart disease, connective tissue, lupus

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23
Q

What drugs are risk factors for PAH?

A

SSRI, amphetamines, methaphetamines, cocaine and St. John’s wort

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24
Q

What is the patho of PAH?

A

Vasoconstriction and cell proliferation
Inflammation
Thrombosis
Decreased PGI2, NO, VIP
Increased ET-1, TxA2, 5-HT

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25
Q

Low risk?

A

Classes 1 and 2
6MWD>440
CI> 2
O2> 65%

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26
Q

Intermediate risk?

A

Class 3

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27
Q

High risk? >10%

A

Class 4
6MWD<165
CI<2
O2<60%
RHF, repeated syncope, pericardial effusion

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28
Q

What are some supportive therapies?

A

Exercise, diuretics, anticoagulation, oxygen, vaccinations, avoidance of pregnancy

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29
Q

Should we use anticoagulants?

A

No- trials indicate no benefit and no assessment of risks vs benefit

30
Q

Should you use CCB?

A

No- low number of patients have a positive vasoreactivity response
Would have to use higher than standard dose

31
Q

What are the prostacyclins?

A

Epoprosterol, illprost, tetroprostinil, selexipag

32
Q

What do prostacyclins do?

A

Increase CaMP= vasodilation and anti proliferation- inhibits platelet aggregation

33
Q

What are the endothelins?

A

Ambrisentan: bosentan + macitentan

34
Q

What do endothelins do?

A

Vasoconstriction and proliferation

35
Q

Which are the NO?

A

Tadalafil, sildenafil, riociguat

36
Q

What does NO do?

A

Vasodilation and anti proliferation

37
Q

What happens to prostacyclin levels in PAH?

A

It goes down - so need to give

38
Q

What is clinical marker of just pulmonary hypertension?

A

MPAP>25 at rest

39
Q

What is the response of vasoreactivity testing?

A

Defined as MPAP decrease by >10 to <40 AND maintain/ improve cardiac output

40
Q

What SE are possible with prostacyclin?

A

Flushing, headache, nausea, vomiting, anxiety, hypotension and chest pain
Later- muscoskeletal pain and neuropathic pain Long term

41
Q

How do you deal with SE of prostacyclins?

A

Titrate drug to se and keep titrating till patient develops then stop and start again once feels better

42
Q

Epoprostenol is the only prostacyclin to show a ——

A

Decrease in mortality

43
Q

What happens if you abruptly DC prostacyclins?

A

Rebound pulmonary HTN

44
Q

Epoprostenol has a ——- half life so,

A

Short, the moment you stop you’ll get side effects within minutes

45
Q

What is the prostacyclin dosing?

A

Ng/ kg/ min
1 mg= 1,000,000ng
Dosing weight should never change without consulting provider

46
Q

When giving prostacyclins what should you know?

A

Back up pump and tubing need to be available
Dedicated central line - do not flush other meds through line
Home pump not good
Do not draw labs from the line

47
Q

Epoprostenol comes in 2 forms:

A

Veletri- more stable
Flolan

48
Q

Which are the inhaler prostacyclins?

A

Iloprost and treprostinil
Too many dosing, 6-9 in a day

49
Q

What are the oral prostacyclins?

A

Treprostinil and selexipag

50
Q

Treprostinil

A

Less invasive and simpler
Monotherapy for class 2-3

51
Q

Selexipag

A

More subjective improvements of symptoms

52
Q

In pah endothelins is ——-

A

High- we don’t want so we antagonize to prevent vasoconstriction and cell proliferation

53
Q

Endothelin patho,

A

Causes vasoconstriction and mitogenic effects by binding to A/B receptors found in pulmonary smooth muscle and endothelial cells

54
Q

What drugs are the endothelins antagonist?

A

Bosentan, ambrisentan, macitentan

55
Q

What are the se of endothelins Antagon.?

A

Hepatotoxicity, REMs pregnancy-need 2 forms of BC, edema

56
Q

Which of the endothelin drugs have more hepatotoxicity?

A

Bosentan , so do baseline LFT

57
Q

Endothelins are metabolized by?

A

2C19 -PPI metabolized by this
and 3A4

58
Q

If bosentan is a 3a4 inducer then

A

Concentration of sildenafil, warfarin, plavix, and protease inhibitors will go down.

59
Q

Macitentan benefit?

A

Enhanced tissue penetration and receptor binding- reason for less liver issues
Minimal drug interactions

60
Q

Patho of phosphodiesters?

A

Break down camp so no vasodilation- so need to inhibit

61
Q

Phosphodiesterase inhibitors do what?

A

Vasodilator and increase gmp to Camp and more NO

62
Q

Which are the phosphodiesterase I?

A

Sildenafil -20mg tid
Tadalafil- 40 mg
Guanylate Cyclase stimulator
Riociguat

63
Q

Major se of pde5I?

A

Flushing, headaches, syncope, visual changes, diarrhea
Do not use with riociguat and nitrates-increased HTN
Do not use with Bocentan-3A4 inducer

64
Q

Pde5I get metabolized how?

A

By 3A4- inhibitors will increase drug concentrations

65
Q

Riociguat contraindicated and se?

A

Syncope
Do not use with nitrates and pde5I or crcl <15
Smokers decrease concentration since works as inducer

66
Q

Treatment for class 1?

A

No theory recommended
Monitor for development of symptoms

67
Q

Treatment for class 2?

A

Monotherapy or combo- ambrisentan and tadalafil

68
Q

Treatment for class 3?

A

Monotherapy or combo- ambrisentan and tadalafil
Can use Epoprostenol or treprostinil if rapid disease progression

69
Q

Treatment for class 4?

A

Epoprostenol

70
Q

Combo therapy: ambrisentan and tadalafil- benefits and negs?

A

Significant improvement in functional outcomes but more adverse effects- peripheral edema, nasal congestion and headache

71
Q

How do you use sequential combinations?

A

Upfront combo- start with one then add another (2-3 drugs)
Never remove drugs

Isbp (4 decks)

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