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Therapeutics II > Pulmonary Hypertension > Flashcards

Pulmonary Hypertension Flashcards

1
Q

What is pulmonary hypertension?

A

-Pulmonary hypertension is higher than normal blood pressure in the arteries that carry blood away from the heart into the lungs

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2
Q

What is the mean pulmonary artery pressure?

A

20 mmHg at rest

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3
Q

What is pulmonary arterial hypertension?

A

Progressive disease involving endothelial function that leads to elevated pulmonary arterial pressure and pulmonary vascular resistance

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4
Q

Causes of pulmonary arterial hypertension

A

-Genetic
-Drug and toxin exposure
-Disease associated with PAH: CHD, HIV, connective tissue disorders

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5
Q

Treatment for pulmonary arterial hypertension

A

-Medications specifically for treatment of PAH
-CCB in responders
-Lung transplantation

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6
Q

What is pulmonary arterial wedge pressure?

A

-Estimates left atrial pressure
-Normal = 4-12 mmHg
-Elevated numbers signal LV failure or mitral stenosis

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7
Q

How is pulmonary vascular resistance calculated?

A

-Using a formula based on mPAP and PAWP

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8
Q

Negative predictors of pulmonary arterial hypertension

A

-Advanced functional class
-Poor exercise capacity
-High right atrial pressure
-Right ventricular dysfunction
-Low cardiac output.

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9
Q

Signs and symptoms of pulmonary hypertension

A

-Shortness of breath
-Fatigue
-Chest pain
-Edema
-Fainting or light-headedness
-Palpitations

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10
Q

What can be used to diagnose pulmonary hypertension?

A

-Echocardiogram
-Right heart catheterization
-Exercise testing
-Biomarkers

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11
Q

What are the effects of PAH?

A

-The right side of the heart has difficulty pumping against high pulmonary pressures
-Leads to right ventricular failure

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12
Q

WHO functional class 1

A

-Symptom-free when physically active or resting

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13
Q

WHO functional class 2

A

-Slight limitation of physical activity - ordinary activity may cause symptoms
-Comfortable at rest

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14
Q

WHO functional class 3

A

-Marked limitation in physical activity - less than ordinary activity causes symptoms
-Comfortable at rest

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15
Q

WHO functional class 4

A

-Significant symptoms with activity
-Symptoms at rest

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16
Q

Goals of therapy for PAH

A

-Alleviate symptoms
-Improve quality of life
-Prevent or delay disease progression
-Reduce hospitalization
-Improve survival

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17
Q

Pharmacotherapy options for the treatment of PAH

A

-Calcium channel blockers
-Direct pulmonary vasodilator
-Phosphodiesterase 5 inhibitors
-Endothelin receptor antagonists
-Prostacyclins
-Soluble guanylate cyclase stimulator

18
Q

When should an oral CCB be used to treat PAH?

A

After a positive test of acute vasoreactivity

19
Q

How do you treat PAH patients who are treatment naive with FC 2?

A

-Combination therapy with tadalafil and ambrisentan
-Monotherapy with either bosentan, macitentan, ambrisentan, riociguat, sildenafil, or tadalafil

20
Q

How do you treat PAH patients with FC 3 without evidence of rapid disease progression?

A

-Combination therapy with tadalafil and ambrisentan
-Monotherapy with either bosentan, macitentan, ambrisentan, riociguat, sildenafil, or tadalafil

21
Q

How do you treat PAH patients with FC 3 with evidence of rapid disease progression?

A

-Continuous IV epoprostenol, IV treprostinil, or SC treprostinil
-If unable to manage parenteral treatment then give inhaled or oral prostanoid

22
Q

How do you treat PAH patients with FC 4?

A

-Continuous IV epoprostenol, IV treprostinil, or SC treprostinil
-If unable to manage parenteral treatment then give inhaled prostanoid in combination with an oral PDE-5 inhibitor and an oral endothelin receptor antagonist

23
Q

How do you treat PAH patients with FC 3 and 4 with inadequate response to maximal pharmacotherapy?

A

-Lung transplant
-If not a candidate for lung transplant then put on palliative care

24
Q

Which drugs target the nitric oxide pathway?

A

-PDE-5 inhibitors: sildenafil, tadalafil
-Soluble guanylate cyclase stimulator: riociguat

25
Q

Which drugs target the endothelin pathway?

A

Endothelin receptor antagonists: bosentan, ambrisentan, macitentan

26
Q

Which drugs target the prostacyclin pathway?

A

-Prostacyclins: epoprostenol (IV), iloprost (inh), treprostanil (IV, SQ, inh, oral)
-IP prostacyclin receptor agonist: selexipag

27
Q

What is the mechanism of action of PDE-5 inhibitors?

A

-Decreases conversion of cGMP to GMP
-Increased levels of cGMP leads to pulmonary vasodilation

28
Q

What is the mechanism of action of endothelin receptor antagonists?

A

-Overexpression of ET-1 in PH patients, correlates with remodeling
-Blocking ET leads to vasodilation

29
Q

What does the ETA receptor do?

A

-Located on pulmonary smooth muscle walls
-Promotes vasoconstriction, proliferation, and inflammation

30
Q

What does the ETB receptor do?

A

-Receptors on endothelium: promotes vasodilation, stimulates nitric oxide and prostacyclin production
-Receptors on muscle cells of vascular walls: cause vasoconstriction and cell proliferation

31
Q

Required monitoring for endothelin receptor antagonists

A

-Pregnancy test
-LFTs
-Hemoglobin

32
Q

What do we want to see improvement in when treating someone who has pulmonary hypertension?

A

-Exercise capacity
-Functional capacity
-Hemodynamic parameters
-Time to clinical worsening
-WHO FC

33
Q

Why can’t riociguat be used in combination with a PDE 5 inhibitor?

A

Increases risk of hypotension

34
Q

Results of the AMBITION trial

A

-In the combination group, peripheral edema, headache, nasal congestion, dizziness, and anemia were more common than in either monotherapy group
-Rates of hypotension were similar
-Rate of discontinuation and serious ADRs were similar across all groups

35
Q

Mechanism of action of prostacyclins

A

Induce vasodilation in all vascular beds, inhibits platelet aggregation, cytoprotective and antiproliferative effect

36
Q

Adverse reactions to prostacyclins

A

-Headache
-Jaw pain
-Limb pain
-flushing/skin rash
-Diarrhea
-Nausea/vomiting
-thrombocytopenia
-hypotension

37
Q

Is SC or IV preferred for prostacyclins

A

SC is preferred to avoid risks of central lines

38
Q

Clinical pearls for epoprostenol

A

-Start in hospital, titrate to effect
-Requires permanent, stable IV access
-Incompatible with everything
-Inadvertent bolus can lead to CV collapse and death
-Used less often than treprostinil

39
Q

Clinical pearls for treprostinil

A

-start in hospital and titrate up
-IV infusion requires stable access
-SQ/IV dosing is the same

40
Q

Key information for PGI2 analogs

A

-Prostacyclin therapy requires significant education before initiation
-Expensive
-Patients should have their own pumps and supplies
-May need to call a specialty pharmacy

41
Q

Pregnancy considerations for patients with PAH

A

Avoid pregnancy

Therapeutics II (33 decks)

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