Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pulmonary Week 3 > 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Berylliosis is a disease typically seen in what patient population?

A

workers of aerospace, nuclear weapon, and electronic industries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Silicosis places a patient at increased risk of what?

A

TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

-right sided heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Asbestosis places a patient at increased risk of what?

A
  • malignant mesothelioma

- carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A
  • aspirin
  • cocaine
  • tricyclic antidepressants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are some potential durgs for the treatment of ARDS?

A
  • B2 agonist
  • NO
  • PGI2 Inhaled
  • Corticosteroids
  • Dietary oil supplements
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How is neonatal respiratory distress syndrome treated?

A
  • antenatal corticosteroids (increase release of surfactant)

- exogenous surfactant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

pre-30 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A
  • Poractant alfa
  • Calfactant
  • Beractant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the hallmark of sarcoidosis?

A

young black female with non-caseating granulomas involving MULTIPLE organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Treatment for sarcoidosis?

A
  • glucocorticoids

- methotrexate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How doe glucocorticoids work?

A

they act principally by binding to glucocorticoid
receptors and modulating
transcriptional regulation in the nucleus and thus inhibiting pro-inflammatory cytokine production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What cytokines do glucocorticoids inhibit?

A
  • IL-1B

- TNF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What cytokines do glucocorticoids PROMOTE?

A

IL-10 by macrophages and dendritic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are some AEs of chronic glucocorticoid use?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What infections are particularly common in those chronically taking glucocorticoids?

A

candidiasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does Methotrexate work?

A

DHFR (dihydrofolate reductase) inhibition

and increases adenosine-mediated immunosuppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does Methotrexate increase adenosine-mediated immunosuppression?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does accumulated AICAR result in?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does increase in cAMP cause?

A

this is the DIRECT cause of immunosuppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

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

A

T.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
AEs of methotrexate?
- dermatologic rxns - birth defects - malignant lymphoma - pulmonary fibrosis
26
Is idiopathic pulmonary fibrosis a chronic inflammatory disease?
No (even the most potent anti-inflammatory agents don't help)
27
What happens in IPF?
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 in structure and environment.)**
28
Why is pulmonary HTN (greater than 25 mmHg) seen in IPF?
remodeling of vessels can occur
29
Drugs for IPF?
pirfenidone [Esbriet] and Nintedanib [Ofev].
30
What does Nintedanib do?
a TKI of VEGF, fibroblast growth factor receptor and PDGF receptor more effective of the two at reducing exacerbations
31
MOA of Piferidone?
Unknown
32
What is Goodpasture's syndrome?
type II hypersensitivity against the a3 chain of type IV collagen in the BM of lungs and kidney
33
How is GP treated?
plasmapheresis
34
What is Wegener's Granulomatosis?
This is an ANCA-positive autoimmune vasculitis (small-medium vessels), primarily of the upper respiratory tract, lungs and kidney.
35
Treatment of Wegener's Granulomatosis?
- Rituximab - Azathioprine - Cyclophosphamide - Steroids
36
How does Rituximab work?
a monoclonal antibody that binds the CD20 cell surface antigen on B-cell precursors and mature B-lymphocytes.
37
How does Rituximab promote cell death?
1) AB-dependent recruitment of NK and macrophages 2) Complement activation 3) Apoptosis induction
38
AEs of Rituximab?
- HTN - pruritis/urticaria - asthenia and arthralgia
39
How does Azathioprine work?
DNA and RNA synthesis inhibitor that also produces immunosuppression, possibly by facilitating apoptosis of T cell populations.
40
AEs of Azathioprine?
- leukopenia/thrombocytopenia | - neoplasms
41
How does Cyclophosphamide work?
an alkylating agent that also produces (B & T cell) lymphopenia, selective suppression of B-lymphocyte activity and decreased immunoglobulin secretion.
42
AEs of Cyclophosphamide?
- bladder cancer - myeloproliferative malignancy - neutropenia
43
Pulmonary HTN can occur from what four min mechanisms?
1) an imbalance between vasoconstriction and vasodilation (due to a relative decrease in prostacyclin and NO production, as well as an increased production of endothelin-1 and a more pronounced presence of thromboxane A2); 2) smooth muscle and endothelial cell proliferation, propagation, and hypertrophy (due to the production of growth inhibitors and mitogenic factors); 3) thrombosis; and 4) fibrosis.
44
What are Plexiform | lesions?
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, smooth muscle cells, and an accumulation of circulating cells (e.g., macrophages and progenitor cells) and lead to significant obstruction of blood flow.
45
The approach to pulmonary HTN therapy is based on what?
severity of disease
46
What are some drug options for pulmonary HTN?
- Prostanoids - Endothelin-1 receptor antagonists - Phosphodiesterase Type 5 Inhibitors - CCBs
47
What are some prostanoids?
- Epoprostenol - Iloprost - Treprostinil
48
How do Prostanoids work?
Induce pulmonary artery vasodilation, retard smooth muscle growth and disrupt platelet aggregation
49
How is Epoprostenol given?
continuous IV (T1/2= 3-5 min)
50
AEs of Epoprostenol?
- hypotension | - risk of catheter infection
51
How is Iloprost given?
6-9 inhaled doses/day (T1/2= 25 min)
52
AEs of Iloprost?
- hemoptysis | - cough, flushing, and headaches
53
How is Treprostinil given?
continuous SC or IV infusion (T1/2=4 hrs)
54
AEs of Treprostinil?
- injection site rxn - jaw pain - diarrhea
55
DD interactions of Treprostinil?
CYP2C8 drugs (gemfibrozil and rifampin)
56
What is something to always monitor when giving prostanoids?
bleeding risk
57
T or F. Endothelin-1 Receptors antagonists are available PO
T. Advantage over Prostanoids
58
What are the Endothelin-1 Receptors antagonists?
- Bosentan | - Ambrisentan
59
How is Bosentan given?
PO BID
60
AEs of Bosentan?
- liver damage - anemia - CYP inducer - nasopharyngitis
61
How is Ambrisentan given?
PO QD
62
AEs of Ambrisentan?
- peripheral edema - headache - CYP2C9, 3A4 metabolism
63
Which Endothelin-1 Receptor antagonist is tetraogenic?
Both
64
How do Phosphodiesterase Type 5 Inhibitors work?
perpetuate endogenously generated cGMP leading to vasodilation and reduce cellular proliferation.
65
Phosphodiesterase Type 5 Inhibitors should never been taken in which patients?
those taking organic nitrates
66
What are the Phosphodiesterase Type 5 Inhibitors?
- Sildenafil | - Tadalafil
67
AEs of Sildenafil?
- headache - nosebleed - dizziness with sudden hearing loss - CYP
68
AEs of Tadalafil?
- headache - change in color vision - CYP - back pain
69
How do CCBs work?
preventing access of Ca2+ into cells during | membrane depolarization, thus blocking the key mediator of smooth muscle contraction
70
Are CCBs effective in pulmonary HTN?
some, but not all patients will benefit (some may undergo a vasodilator challenge before use)
71
What are some drugs used for vasodilatory challenge of pulmonary circulation?
- IV epoprostenol - adenosine - inhaled NO
72
How does a vasodilatory challenge work?
Patients receive a carefully escalated dosing rate and pulmonary arterial pressure (PAP) and cardiac output (CO) are monitored for 2-3 hr. A patient who responds positively to a vasodilator challenge (i.e., lower PAP without lower CO) may then be prescribed certain CCBs
73
Why even worry about doing a vasodilatory challenge?
limit risk of potentially fatal hemodynamic decompensation with CCBs
74
What are some CCBs?
- Diltiazem - Nifedipine - Amlodipine
75
How are CCBs given?
PO
76
AEs of Diltiazem?
- bradycardia, hypotension | - edema
77
AEs of Nifedipine?
- flushing, edema | - heartburn
78
AEs of Amlodipine?
- edema - fatigue - hypotension
79
Something to always consider with CCBs?
CYP substrate
80
Why is Verapamil avoided with PAH treatment?
Because of its strong negative inotropic properties, which | makes it more likely to induce symptomatic bradycardia than the others.
81
What is the goal of CCB treatment?
Is for the patient to achieve NYHA-FC I or II | after 3–4 months. If this is not achieved, alternative therapy needs to be considered.
82
Define NYHA-FC I or II
I) No limitations or symptoms associated with normal physical activity II) Mild symptoms and/or slight limitation during normal physical activity

Pulmonary Week 3 (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions