Drugs for Restrictive Lung Diseases and Pulmonary Artery Hypertension Flashcards Preview

Pulmonary Week 3 > Drugs for Restrictive Lung Diseases and Pulmonary Artery Hypertension > Flashcards

Flashcards in Drugs for Restrictive Lung Diseases and Pulmonary Artery Hypertension Deck (82)
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1

Silicosis is a disease typically seen in what patient population?

sand blasters, rock miners, and stone cutters

2

Berylliosis is a disease typically seen in what patient population?

workers of aerospace, nuclear weapon, and electronic industries

3

Silicosis places a patient at increased risk of what?

TB

4

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

-right sided heart failure

5

Asbestosis places a patient at increased risk of what?

-malignant mesothelioma
-carcinoma

6

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

-aspirin
-cocaine
-tricyclic antidepressants

7

What other thing increases the risk of ARDS?

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

8

What are some potential durgs for the treatment of ARDS?

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

9

How is neonatal respiratory distress syndrome treated?

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

10

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

pre-30 weeks

11

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

-Poractant alfa
-Calfactant
-Beractant

12

What is the hallmark of sarcoidosis?

young black female with non-caseating granulomas involving MULTIPLE organs

13

Treatment for sarcoidosis?

-glucocorticoids
-methotrexate

14

How doe glucocorticoids work?

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

15

What cytokines do glucocorticoids inhibit?

-IL-1B
-TNF

16

What cytokines do glucocorticoids PROMOTE?

IL-10 by macrophages and dendritic cells

17

What are some AEs of chronic glucocorticoid use?

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

18

What infections are particularly common in those chronically taking glucocorticoids?

candidiasis

19

How does Methotrexate work?

DHFR (dihydrofolate reductase) inhibition

and increases adenosine-mediated immunosuppression

20

How does Methotrexate increase adenosine-mediated immunosuppression?

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

21

What does accumulated AICAR result in?

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

22

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

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

23

What does increase in cAMP cause?

this is the DIRECT cause of immunosuppression

24

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

T.

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