Flashcards in Drugs for Restrictive Lung Diseases and Pulmonary Artery Hypertension Deck (82)
Silicosis is a disease typically seen in what patient population?
sand blasters, rock miners, and stone cutters
Berylliosis is a disease typically seen in what patient population?
workers of aerospace, nuclear weapon, and electronic industries
Silicosis places a patient at increased risk of what?
Coal worker’s pneumoconiosis places a patient at increased risk of what?
-right sided heart failure
Asbestosis places a patient at increased risk of what?
Excessive doses of what drugs have been known to precipitate ARDS?
What other thing increases the risk of ARDS?
alcohol abuse (only increases risk of trauma and sepsis, doesn't actually cause it)
What are some potential durgs for the treatment of ARDS?
-Dietary oil supplements
How is neonatal respiratory distress syndrome treated?
-antenatal corticosteroids (increase release of surfactant)
When is exogenous surfactant administered in patients at risk of NRDS?
What products are naturally rich in surfactant proteins B and C and DPPC?
What is the hallmark of sarcoidosis?
young black female with non-caseating granulomas involving MULTIPLE organs
Treatment for sarcoidosis?
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
What cytokines do glucocorticoids inhibit?
What cytokines do glucocorticoids PROMOTE?
IL-10 by macrophages and dendritic cells
What are some AEs of chronic glucocorticoid use?
pancreatitis, steroid-induced diabetes mellitus, cataracts, glaucoma, psychosis, immunosuppression, weight gain, and skin
What infections are particularly common in those chronically taking glucocorticoids?
How does Methotrexate work?
DHFR (dihydrofolate reductase) inhibition
and increases adenosine-mediated immunosuppression
How does Methotrexate increase adenosine-mediated immunosuppression?
inhibits conversion of GAR to FGAR and AICAR to FAICAR (stronger)
What does accumulated AICAR result in?
AMP deaminase and adenosine deaminase (ADA) activity with increased adenosine 5-P and adenosine
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
What does increase in cAMP cause?
this is the DIRECT cause of immunosuppression
T or F. Methotrexate is NOT front-line therapy for its anti-inflammatory
AEs of methotrexate?
Is idiopathic pulmonary fibrosis a chronic inflammatory disease?
No (even the most potent anti-inflammatory agents don't help)
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.)**
Why is pulmonary HTN (greater than 25 mmHg) seen in IPF?
remodeling of vessels can occur
Drugs for IPF?
pirfenidone [Esbriet] and Nintedanib [Ofev].