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PHARMACOLOGY - Pulmonary > Drugs for Restrictive Lung Diseases, Cystic Fibrosis, and Pulmonary Artery HTN > Flashcards

Drugs for Restrictive Lung Diseases, Cystic Fibrosis, and Pulmonary Artery HTN Flashcards

1
Q 
Portactant
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
Surfactant Agent

MOA
Purified animal-derived products rich in surfactant proteins B and C, neutral lipids, surface active phospholipids, and dipalmitoylphosphatidyl-choline (DPPC)

Administration
Preterm infants born at less than 30 wks.

Adverse Effects
Contraindications
Other

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2
Q 
Calfactant
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
Surfactant Agent

MOA
Purified animal-derived products rich in surfactant proteins B and C, neutral lipids, surface active phospholipids, and dipalmitoylphosphatidyl-choline (DPPC)

Administration
Preterm infants born at less than 30 wks.

Adverse Effects
Contraindications
Other

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3
Q 
Beractant 
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
Surfactant Agent

MOA
Purified animal-derived products rich in surfactant proteins B and C, neutral lipids, surface active phospholipids, and dipalmitoylphosphatidyl-choline (DPPC)

Administration
Preterm infants born at less than 30 wks.

Adverse Effects
Contraindications
Other

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4
Q 
Methotrexate (pulm) 
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
Immunosuppressive

MOA

  1. DHFR inhibitor preventing pyrimidine synthesis
  2. Increased Adenosine Related Immunosuppression - AICAR builds builds up and inhibits AMP deaminase and ADA (adenosine) deaminase. AMP and adenosine move outside the cell to simulate A2a/b GPCR that increases cAMP and causes Immunosuppression

Administration
Given to Sarcoidosis patients

Adverse Effects
Dermatologic Reactions, Birth Defects, Maliganant Lymphoma, INTERSITIAL PNEUMONITIS and PULMONARY FIBROSIS

Contraindications
Other

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5
Q 
Rituximab (pulm)
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
mAb - immunosuppressive

MOA
Binds CD20 to prevent B-lymphocyte maturation via 3 mechanisms 1) Macrophages and NK cells are recruited to bind Rituximab Fc receptors 2) Rituximab activates completment 3) induction of apoptosis

Metabolism
Slowly metabolized (6-9 month depletion with a single 3-dose drug course)

Administration
Given to patients with Wegner’s

Adverse Effects
Hypertension, asthenia, Pruitis, urticarial, rhinitis, arthralgia

Contraindications
Other

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6
Q 
Azathioprine (pulm) 
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
DNA and RNA synthesis inhibitor

MOA
DNA and RNA synthesis inhibitor that produces immunosuppression possibly by facilitating apoptosis of T cell populations

Administration
Given to Patients with Wegner’s

Adverse Effects
Neoplastic, mutagenic, Leukopenic an THROMBOCYTOPENIC toxicity, and increased risk of infection

Contraindications
Other

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7
Q 
Ivacaftor
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
CFTR potentiator

MOA
Treats CF patients with G551D mutation

Metabolism
Extensive Hepatic Metabolism (CYP3A4 and P-gp inhibition)

Adverse Effects
Upper respiratory symptoms, Pain, GI symptoms, and nasal congestion

Contraindications
INEFFECTIVE in patients homozygous for ∆F508
Other

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8
Q 
Cyclophosphamide (pulm) 
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
Alkylating agent

MOA
Alkylates rapidly growing cells to produce B and T cell lymphopenia with selectivity toward suppression of B-lymphocyte activity

Administration
Used in the treatment of Wegner’s Granulomatosis

Adverse Effects
Associated with neutro- and thrombocytopenia, bladder cancer, myeloproliferative, or lymphoproliferative malignancies

Contraindications
Other

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9
Q 
Corticosteriods
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
Steroid

MOA
Inhibition or inflammatory cytokine synthesis via preventing inhibitor of kB (IkB) from unbining NfkB which woul lead to the production of cytokines like IL-1ß and TNF

Administration
Given to patients with Wegner’s Granulomatosis

Adverse Effects
Contraindications
Other

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10
Q 
Epoprostenol (pulm)
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
Prostanoid

MOA
Used in Pulmonary Artery HTN to mimic the effects of PGI2 (prostacyclin) which is to inhibit platelet agreggation, Induce vasodilation, and retard smooth muscle growth
Used in Pulmonary Artery HTN

Metabolism
Half-life of only 3-5 minutes

Administration
**Continuous IV infusion (RISK OF INFECTION)

Adverse Effects
Dose limiting Hypotension, flushing, muscle pain, bleeding risk

Contraindications
Other

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11
Q 
Iloprost
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
Prostanoid

MOA
Used in Pulmonary Artery HTN to mimic the effects of PGI2 (prostacyclin) which is to inhibit platelet agreggation, Induce vasodilation, and retard smooth muscle growth
Used in Pulmonary Artery HTN

Metabolism
Half-life of 25 minutes

Administration
requires 6-9 doses/day each lasting 10 minutes

Adverse Effects
HEMOPTYSIS, cough, flushing, muscle cramps, tongue/back pain

Contraindications
Other

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12
Q 
Treprostinil
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
Prostanoid

MOA
Used in Pulmonary Artery HTN to mimic the effects of PGI2 (prostacyclin) which is to inhibit platelet agreggation, Induce vasodilation, and retard smooth muscle growth
Used in Pulmonary Artery HTN

Metabolism
Half-life of 4 hours

Administration
Continuous subcutaneous IV infusion=> more stable in solution

Adverse Effects
CYP2C8 drug-drug interactions possible (Gemfibrozil decreases clearance, Rifampin increases clearance) Jaw pain, Injection site irritation, bleeing risk

Contraindications
Other

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13
Q 
Bosentan
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
Endothelin-1 antagonist

MOA
Given to people with PAH to block smooth muscle proliferation and pulmonary arterial vasoconstriction by binding endothelin-1 type A (smooth muscle) and type B (endothelial) receptors
Used in Pulmonary Artery HTN

Metabolism
5-8 hours; Extensive Hepatic metabolism by CYP2C9 and 3A4. (cyp inducers like Rifampin could cause drug-drug interactions

Administration
Oral Administration

Adverse Effects
Teratogenic effects, and LIVER (elevated LFTs) and BLOOD (anemia) toxicities, nasopharyngitis

Contraindications
Other
**Major advantage of prostacyclins is oral activity.

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14
Q 
Lumacaftor/Ivacaftor
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
CFTR potentiator

MOA
Lumacafor added a conformational stabilizer to the drug action of Ivacaftor. This improves CFTR protein delivery to the cell surface

Metabolism
Lumacaftor is a strong CYP INDUCER meaning Ivacaftor stays in the system 3x as long (9-27 hours)

Adverse Effects
Upper respiratory symptoms, Pain, GI symptoms, and nasal congestion

Contraindications
Other

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15
Q 
Ambrisentan
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
Endothelin-1 antagonist

MOA
Given to people with PAH to block smooth muscle proliferation and pulmonary arterial vasoconstriction by binding endothelin-1 type A (smooth muscle) and type B (endothelial) receptors
Used in Pulmonary Artery HTN

Metabolism
Half-life 15 hours; extensive CYP2C9, 3A4, OATP, and P-gp substrate

Administration
Oral Administration

Adverse Effects
Teratogenic effects (note lack of liver (LFTs normal) and blood toxicities as seen with bosentan), PERIPHERAL EDEMA

Contraindications
Other
**Major advantage of prostacyclins is oral activity.

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16
Q 
Sildenafil
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
Phosphodiesterase Type 5 Inhibitors

MOA
Perpetuate Endogenously generated cGMP (produced from NO pathway) leading to vasodilation and reduced cellular proliferation
Used in Pulmonary Artery HTN

Metabolism
3-4 hours, PO, IVP TID, CYP3A4 > 2C9 substrate (cyp3A4 inhibitors/inducers/ substrates may interfere)

Administration
Oral, IVP, TID

Adverse Effects
DIZZINESS with SUDDEN HEARING LOSS, Epistaxis, Insomnia, Dyspepsia

Contraindications
*DO NOT USE IN PATIENTS TAKING ORGANIC NITRATES

Other

17
Q 
Tadalafil
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
Phosphodiesterase Type 5 Inhibitors

MOA
Perpetuate Endogenously generated cGMP (produced from NO pathway) leading to vasodilation and reduced cellular proliferation
Used in Pulmonary Artery HTN

Metabolism
Half-life 17 hours; CYP3A4 substrate (interactions with inducers/substrates/inhibitors)

Administration
Oral, QD

Adverse Effects
CHANGE IN COLOR VISION (non-arteritic anterior ischemic optic neuropathy), backpain

Contraindications
*DO NOT USE IN PATIENTS TAKING ORGANIC NITRATES

Other

18
Q 
Diltiazem
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
Calcium Channel Blocker (CCB)

MOA
Preventing access of calcium into cells during membrane during membrane depolarization. Ca2+ is the key mediator in smooth muscle contraction.

Metabolism
Half life 3-6 hours; CYP3A4 substrate

Administration
PO TID

Adverse Effects
Bradycardia, Hypotension, edema, headache

Contraindications
Other

19
Q 
Nifedipine
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
Calcium Channel Blocker (CCB)

MOA
Preventing access of calcium into cells during membrane during membrane depolarization. Ca2+ is the key mediator in smooth muscle contraction.

Metabolism
Half life 2-5 hours; CYP3A4 substrate

Administration
PO QD

Adverse Effects
Heartburn, Flushing, edema, hypotension

Contraindications
Other

20
Q 
Amlodipine
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
Calcium Channel Blocker (CCB)

MOA
Preventing access of calcium into cells during membrane during membrane depolarization. Ca2+ is the key mediator in smooth muscle contraction.

Metabolism
Half life 35-50 hours; CYP3A4 substrate

Administration
PO QD

Adverse Effects
Edema, fatigue, hypotension

Contraindications
Other

21
Q

What are some drugs known to precipitate ARDS in susceptible individuals?

A
  • Aspirin
  • Cocaine
  • Opioids
  • Phenothiazines
  • Tricyclic Antidepressants
22
Q

What are women at risk of giving birth at less than 34 weeks administered to ensure neonatal lung health?

A

Corticosteriods to increase synthesis and release of surfactant

23
Q

What treatment methods are available to treat patients with sarcoidosis?
• how do they work?

A

Methotrexate:
Immunosuppressive by inhibiting DHFR

Glucocorticoids:
Inhibit the release of pro-inflammatory cytokines like IL-1ß and TNF and promotes release of anti-inflammatory cytokines such as IL-10.
Also, they promote apoptosis of macrophages, dendritic cells, and T cells.

24
Q

What are some key side effects of chronic corticosteroid use?

A 
Chronic Use May: 
• Suppress hypothalamic-pituitary-adrenal (HPA) axis
• osteroporosis
• Pancreatitis
• Steroid induced diabetes mellitus
• Cataracts
• Glaucoma
• Psychosis
• Oral Candidiasis 
• Weight gain
25
Q

T or F: Idiopathic pulmonary fibrosis is a chronic inflammatory disease, thats why we use anti-inflammatories to treat it.

A

FALSE, we DO NOT use anti-inflammatories to treat because this is NOT an inflammatory condition

**In fact, being unresponsive to corticosteriods may help to diagnose Idiopathic pulmonary fibrosis

26
Q 
Nintedanib 
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
Tyrosine Kinase Inhibitor

MOA
VEGF, FGF (fibroblastic growth factor), PDGF (Platelet Derived Growth Factor) receptor blocker

Metabolism
Esterases, with CYPs playing only a minor role

Administration
Adverse Effects
Contraindications
Other

27
Q 
Pirfenidone
Drug Class
MOA
Metabolism
Administration
Adverse Effects
Contraindications
Other
A

Drug Class
Unknown

MOA
Unknown ability to inhibit pulmonary fibrobast proliferation

Metabolism
Hepatic Metabolism to inactive products

Administration
Adverse Effects
Contraindications
Other

28
Q

Between nintedanib and pirfenidone, which appears to be the best at decreasing exacerbations and mortality from IPF?

A

Nintedanib reduces IPF mortality and exacerbations

29
Q

What is goodpasture’s syndrome?

• what is the most effective way to treat it?

A

Goodpasture’s:
Type II hypersensitivity against the alpha-3 chain of type IV collagen in the basement membrane of the lung and kidney.

Tx:
Plasmapheresis

30
Q

What are the 4 primary causes of pulmonary artery hypertension?

A
  1. Imbalance between vasoconstriction and vasodilation (decreased PGI2 and NO, with increased Endothelin-1)
  2. Smooth muscle and endothelial cell propagation and proliferation as well as hypertrophy
  3. Thrombosis
  4. Fibrosis
31
Q

What is the problem with lacking prostacyclin?
• Lacking NO?
• Too much Endothelin-1?

A
  • A lack of PGI2 (prostacyclin) leads to increased TXA2 allowing for more platelet aggregation. PGI2 also inhibits smooth muscle growth
  • NO is needed to inhibit platelet stimulation and to relex smooth muscle
  • Too much endothelin-1 induces smooth muscle proliferation
32
Q

What is the advantage of both of the endothelin-1 antagonists over the prostacylin mimicking drugs using in PAH?
• Disadvantage?

Name all 5 of these drugs

A

Endothelin-1 Receptors antagonists:
• Orally active

Disadvantage:
• BOTH ARE TERATOGENIC and bosentan is associated with liver and blood

33
Q

What is the most common side effect in both of the Phosphodiesterase Type 5 inhibitors?

A

Headache is the most common side effect for both Sildenafil and Tadalafil

34
Q

Why do calcium channel blockers work in Pulmonary Artery Hypertension?

A

They block Ca2+ from entering the cell, Ca2+ is a key mediator in smooth muscle contraction

35
Q

What are some of the problems with using Calcium channel blockers for Pulmonary Artery HTN?

A

NOT ALL PATIENTS respond to the drugs

• Some develop potentially fatal hemodynamic decompensation

36
Q

What requirements must be met before a patient can be prescribed a calcium channel blocker for Pulmonary Artery Hypertension?

A

They must pass the vasodilator challenge

  • This includes administering IV epoprosteno, IV adenosine, and inhaled nitric oxide.
  • Doses are escalated and and Pulmonary Artererial pressure (PAP) and Cardiac Output are monitored for 2-3 hours
  • Patiens who experience a drop in PAP without a reduction in CO pass => they can get a CCB.
37
Q

Why are drug-drug interactions a real concern when considering a CCB for your patient?

A

They are all CYP3A4 metabolized so you much watch out for Drug-Drug interactions

38
Q

Why should we consider the use of CCB (calcium channel blockers) if they only work for 1/2 or the 15% that are candidates for this therapy?

A

They are way cheaper

PHARMACOLOGY - Pulmonary (30 decks)

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