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STEP Pharm II > Drugs for Restrictive Lung Diseases and Pulmonary Artery Hypertension > Flashcards

Drugs for Restrictive Lung Diseases and Pulmonary Artery Hypertension Flashcards

1
Q

Silicosis is a disease typically seen in what patient population?

A

sand blasters, rock miners, and stone cutters

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2
Q

Berylliosis is a disease typically seen in what patient population?

A

workers of aerospace, nuclear weapon, and electronic industries

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3
Q

Silicosis places a patient at increased risk of what?

A

TB

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4
Q

Coal worker’s pneumoconiosis places a patient at increased risk of what?

A

-right sided heart failure

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5
Q

Asbestosis places a patient at increased risk of what?

A

-malignant mesothelioma-carcinoma

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6
Q

Excessive doses of what drugs have been known to precipitate ARDS?

A

-aspirin-cocaine-tricyclic antidepressants

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7
Q

What other thing increases the risk of ARDS?

A

alcohol abuse (only increases risk of trauma and sepsis, doesn’t actually cause it)

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8
Q

What are some potential durgs for the treatment of ARDS?

A

-B2 agonist-NO-PGI2 Inhaled-Corticosteroids-Dietary oil supplements

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9
Q

How is neonatal respiratory distress syndrome treated?

A

-antenatal corticosteroids (increase release of surfactant)-exogenous surfactant

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10
Q

When is exogenous surfactant administered in patients at risk of NRDS?

A

pre-30 weeks

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11
Q

What products are naturally rich in surfactant proteins B and C and DPPC?

A

-Poractant alfa-Calfactant-Beractant

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12
Q

What is the hallmark of sarcoidosis?

A

young black female with non-caseating granulomas involving MULTIPLE organs

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13
Q

Treatment for sarcoidosis?

A

-glucocorticoids-methotrexate

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14
Q

How doe glucocorticoids work?

A

they act principally by binding to glucocorticoidreceptors and modulatingtranscriptional regulation in the nucleus and thus inhibiting pro-inflammatory cytokine production

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15
Q

What cytokines do glucocorticoids inhibit?

A

-IL-1B-TNF

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16
Q

What cytokines do glucocorticoids PROMOTE?

A

IL-10 by macrophages and dendritic cells

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17
Q

What are some AEs of chronic glucocorticoid use?

A

osteoporosis,pancreatitis, steroid-induced diabetes mellitus, cataracts, glaucoma, psychosis, immunosuppression, weight gain, and skinatrophy.

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18
Q

What infections are particularly common in those chronically taking glucocorticoids?

A

candidiasis

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19
Q

How does Methotrexate work?

A

DHFR (dihydrofolate reductase) inhibitionand increases adenosine-mediated immunosuppression

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20
Q

How does Methotrexate increase adenosine-mediated immunosuppression?

A

inhibits conversion of GAR to FGAR and AICAR to FAICAR (stronger)

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21
Q

What does accumulated AICAR result in?

A

AMP deaminase and adenosine deaminase (ADA) activity with increased adenosine 5-P and adenosine

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22
Q

What does accumulation of adenosine 5-P and adenosine in the cell cause?

A

more EXTRAcellular adenosine 5-P and adenosine which binds to A2 receptors yielding an increase cAMP

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23
Q

What does increase in cAMP cause?

A

this is the DIRECT cause of immunosuppression

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24
Q

T or F. Methotrexate is NOT front-line therapy for its anti-inflammatoryeffects.

A

T.

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25
Q

AEs of methotrexate?

A

-dermatologic rxns-birth defects-malignant lymphoma -pulmonary fibrosis

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26
Q

Is idiopathic pulmonary fibrosis a chronic inflammatory disease?

A

No (even the most potent anti-inflammatory agents don’t help)

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27
Q

What happens in IPF?

A

The altered mesenchymal cell phenotype and blockade of apoptosis give rise to an altered stromal cell population and the activated epithelium release a series of profibrogenic factors, TGF-b and PDGF. This creates a new microenvironment in patchy areas (Other areas remain normal instructure and environment.)

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28
Q

Why is pulmonary HTN (greater than 25 mmHg) seen in IPF?

A

remodeling of vessels can occur

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29
Q

Drugs for IPF?

A

pirfenidone [Esbriet] and Nintedanib [Ofev].

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30
Q

What does Nintedanib do?

A

a TKI of VEGF, fibroblast growth factor receptor and PDGF receptormore effective of the two at reducing exacerbations

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31
Q

MOA of Piferidone?

A

Unknown

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32
Q

What is Goodpasture’s syndrome?

A

type II hypersensitivity against the a3 chain of type IV collagen in the BM of lungs and kidney

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33
Q

How is GP treated?

A

plasmapheresis

34
Q

What is Wegener’s Granulomatosis?

A

This is an ANCA-positive autoimmune vasculitis (small-medium vessels), primarily of theupper respiratory tract, lungs and kidney.

35
Q

Treatment of Wegener’s Granulomatosis?

A

-Rituximab -Azathioprine-Cyclophosphamide-Steroids

36
Q

How does Rituximab work?

A

a monoclonal antibody that binds the CD20 cell surface antigen on B-cell precursors and mature B-lymphocytes.

37
Q

How does Rituximab promote cell death?

A

1) AB-dependent recruitment of NK and macrophages2) Complement activation3) Apoptosis induction

38
Q

AEs of Rituximab?

A

-HTN-pruritis/urticaria-asthenia and arthralgia

39
Q

How does Azathioprine work?

A

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

40
Q

AEs of Azathioprine?

A

-leukopenia/thrombocytopenia-neoplasms

41
Q

How does Cyclophosphamide work?

A

an alkylating agent that also produces (B & T cell) lymphopenia, selective suppression of B-lymphocyte activity and decreased immunoglobulin secretion.

42
Q

AEs of Cyclophosphamide?

A

-bladder cancer-myeloproliferative malignancy-neutropenia

43
Q

Pulmonary HTN can occur from what four min mechanisms?

A

1) an imbalance betweenvasoconstriction and vasodilation (due to a relative decrease in prostacyclin and NOproduction, as well as an increased production of endothelin-1 and a more pronounced presence ofthromboxane A2); 2) smooth muscle and endothelial cell proliferation, propagation, and hypertrophy (dueto the production of growth inhibitors and mitogenic factors); 3) thrombosis; and 4) fibrosis.

44
Q

What are Plexiformlesions?

A

Thickened arterioles as a result of shear stress- are the histologic hallmark of patients with IPAH or heritable PAH. These lesions result in proliferation of monoclonal endothelial cells, smoothmuscle cells, and an accumulation of circulating cells (e.g., macrophages and progenitor cells) andlead to significant obstruction of blood flow.

45
Q

The approach to pulmonary HTN therapy is based on what?

A

severity of disease

46
Q

What are some drug options for pulmonary HTN?

A

-Prostanoids-Endothelin-1 receptor antagonists -Phosphodiesterase Type 5 Inhibitors -CCBs

47
Q

What are some prostanoids?

A

-Epoprostenol-Iloprost-Treprostinil

48
Q

How do Prostanoids work?

A

Induce pulmonary artery vasodilation, retard smooth muscle growth and disrupt platelet aggregation

49
Q

How is Epoprostenol given?

A

continuous IV (T1/2= 3-5 min)

50
Q

AEs of Epoprostenol?

A

-hypotension-risk of catheter infection

51
Q

How is Iloprost given?

A

6-9 inhaled doses/day (T1/2= 25 min)

52
Q

AEs of Iloprost?

A

-hemoptysis -cough, flushing, and headaches

53
Q

How is Treprostinil given?

A

continuous SC or IV infusion (T1/2=4 hrs)

54
Q

AEs of Treprostinil?

A

-injection site rxn-jaw pain-diarrhea

55
Q

DD interactions of Treprostinil?

A

CYP2C8 drugs (gemfibrozil and rifampin)

56
Q

What is something to always monitor when giving prostanoids?

A

bleeding risk

57
Q

T or F. Endothelin-1 Receptors antagonists are available PO

A

T. Advantage over Prostanoids

58
Q

What are the Endothelin-1 Receptors antagonists?

A

-Bosentan-Ambrisentan

59
Q

How is Bosentan given?

60
Q

AEs of Bosentan?

A

-liver damage-anemia-CYP inducer -nasopharyngitis

61
Q

How is Ambrisentan given?

62
Q

AEs of Ambrisentan?

A

-peripheral edema -headache-CYP2C9, 3A4 metabolism

63
Q

Which Endothelin-1 Receptor antagonist is tetraogenic?

64
Q

How do Phosphodiesterase Type 5 Inhibitors work?

A

perpetuate endogenously generated cGMP leading to vasodilation and reduce cellular proliferation.

65
Q

Phosphodiesterase Type 5 Inhibitors should never been taken in which patients?

A

those taking organic nitrates

66
Q

What are the Phosphodiesterase Type 5 Inhibitors?

A

-Sildenafil-Tadalafil

67
Q

AEs of Sildenafil?

A

-headache-nosebleed-dizziness with sudden hearing loss -CYP

68
Q

AEs of Tadalafil?

A

-headache-change in color vision-CYP -back pain

69
Q

How do CCBs work?

A

preventing access of Ca2+ into cells duringmembrane depolarization, thus blocking the key mediator of smooth muscle contraction

70
Q

Are CCBs effective in pulmonary HTN?

A

some, but not all patients will benefit (some may undergo a vasodilator challenge before use)

71
Q

What are some drugs used for vasodilatory challenge of pulmonary circulation?

A

-IV epoprostenol-adenosine-inhaled NO

72
Q

How does a vasodilatory challenge work?

A

Patients receive a carefully escalated dosing rate and pulmonary arterial pressure (PAP) and cardiac output (CO) are monitored for 2-3 hr. Apatient who responds positively to a vasodilator challenge (i.e., lower PAP without lower CO) maythen be prescribed certain CCBs

73
Q

Why even worry about doing a vasodilatory challenge?

A

limit risk of potentially fatal hemodynamic decompensation with CCBs

74
Q

What are some CCBs?

A

-Diltiazem-Nifedipine-Amlodipine

75
Q

How are CCBs given?

76
Q

AEs of Diltiazem?

A

-bradycardia, hypotension-edema

77
Q

AEs of Nifedipine?

A

-flushing, edema-heartburn

78
Q

AEs of Amlodipine?

A

-edema-fatigue-hypotension

79
Q

Something to always consider with CCBs?

A

CYP substrate

80
Q

Why is Verapamil avoided with PAH treatment?

A

Because of its strong negative inotropic properties, whichmakes it more likely to induce symptomatic bradycardia than the others.

81
Q

What is the goal of CCB treatment?

A

Is for the patient to achieve NYHA-FC I or IIafter 3–4 months. If this is not achieved, alternative therapy needs to be considered.

82
Q

Define NYHA-FC I or II

A

I) No limitations or symptoms associatedwith normal physical activityII) Mild symptoms and/or slight limitationduring normal physical activity

STEP Pharm II (42 decks)

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