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Pulmonary > PHARM: Restrictive Lung Disease > Flashcards

PHARM: Restrictive Lung Disease Flashcards

1
Q

What are the 3 categories of interstitial restrictive lung disease?

A

Pneumoconiosis
ARDS/NRDS
Idiopathic

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2
Q

What are the 4 most common pneumoconioses?

A

Silicosis
CWP
Asbestosis
Berylliosis

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3
Q

How do you treat someone for deposited material (pneumoconiosis)?

A

NO curative treatment for the deposited material (patients should just avoid further exposure)

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4
Q

True or False: alcohol abuse causes ARDS.

A

FALSE: it increases the risk of ARDS due to other causes (like sepsis or trauma)

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5
Q

What treatment may help patients with ARDS?

A

intubation and mechanical ventilation

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6
Q

List the drugs that demonstrate a consistent and unequivocal benefit for ARDS patients.

A

Trick Question–there are none

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7
Q

List the drugs that are used on ARDS patients (despite the fact they don’t work great).

A 
Beta-2 agonist
Inhaled NO
Inhaled PGI2
Corticosteroids
Dietary oil supplements

Pulmonary vessel vasodilators and anti-inflammatory drugs

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8
Q

What is the most common cause of respiratory failure in newborns?

A

NRDS

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9
Q

What is NRDS?

A

Neonatal respiratory distress syndrome arises from surfactant deficiency in immature lungs, leading to increased surface tension, V/Q mismatch, and shunting

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10
Q

What is antenatal corticosteroids?

A

they are steroids given to mothers at risk of delivery <34 weeks

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11
Q

How do antenatal corticosteroids work?

A

enhance maturational changes in fetal lung architecture and biochemistry to increase synthesis and release of surfactant (improving neonatal lung function)

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12
Q

What is another treatment (other than antenatal corticosteroids) for NRDS?

A

exogenous surfactant

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13
Q

Who gets exogenous surfactant?

A

preterm (<30 week) neonates

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14
Q

List the exogenous surfactant products that are used for NRDS.

A

Poractant alfa
Calfactant
Beractant

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15
Q

What are the major ingredients in the exogenous surfactants?

A

DPPC (dipalmitoylphosphatidyl-chlorine)

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16
Q

What are the treatment options available for sarcoidosis?

A

Glucocorticoids

Methotrexate (off label)

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17
Q

True or false: glucocorticoids are the MOST potent anti-inflammatory drug class.

A

TRUE

18
Q

How do glucocorticoids work?

A

bind to receptors and subsequently modulate transcriptional regulation in the nucleus

19
Q

What specific genes are increased/decreased by glucocorticoids?

A

Inhibition of IL-1 and TNF

Promote production of IL-10 and other anti-inflammatory cytokines

20
Q

True or false: glucocorticoids can promote apoptosis of macrophages, dendritic cells and T cells.

A

TRUE! This leads to inhibition of the immune response

21
Q

What is the major side effect of chronic glucocorticoid use?

A

suppression of the hypothalamic-pituitary-adrenal axis

22
Q

What is the MOA of methotrexate?

A

DFR inhibition

23
Q

How does methotrexate lead to immunosuppression?

A

Inhibition of AICAR–> FAICAR leads to AICAR accumulation which inhibits AMP deaminase and ADA. This causes an increase in AMP and Adenosine . Adenosine binds to cell receptors and increases levels of cAMP (which cause immunosuppression)

24
Q

Why is methotrexate not front-line therapy for sarcoidosis?

A

it has severe side effects

25
Q

What are some side effects of methotrexate?

A

dermatologic reactions
birth defects
malignant lymphoma
fatal pulmonary effects

26
Q

True or false: IPF is treated with potent antiinflammatory drugs.

A

FALSE: it is not a chronic inflammatory disease so anti-inflammatory drugs yield little to no therapeutic effect!

27
Q

How can IPF lead to PAH?

A

activated epithelium due to initial short-lived inflammatory process releases profibrogenic factors that may give rise to the remodeling of blood vessel walls (and can lead to PAH)

28
Q

True or flase: patients with IPF do not receive as great a benefit from the drugs used for other forms of PAH.

A

TRUE

29
Q

What is the gold standard treatment for IPF?

A

Trick question- there is none!

30
Q

What is Goodpasture syndrome?

A

autoimmune disease arising from type II hypersensitivity against the alpha3-chain of type IV collagen in the basement membrane of lungs and kidney

31
Q

How do you treat Goodpasture syndrome?

A

plasmapheresis (to reduce the load of auto-antibodies)

32
Q

What is Wegener’s granulomatosis?

A

ANCA-positive autoimmune vasculitis primarily in the upper respiratory tract, lungs, and kidneys

33
Q

What drug is approved to treat Wegener’s granulomatosis?

A

Rituximab

34
Q

What is rituximab?

A

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

35
Q

How does rituximab kill B-cells?

A

1) ADCC (recruiting of macrophages and natural killer cells by binding to their Fc-gamma receptors)
2) Complement mediated cytotoxicity (MAC formation)
3) Induction of apoptosis

36
Q

What are some adverse effects of rituximab?

A

HTN
asthenia (weakness)
pruritis (itching)

37
Q

What drugs are used (off-label) for Wegener’s?

A

Azathioprine
Cyclophosphamide
Corticosteroids

38
Q

What is the MOA of azathioprine?

A

DNA and RNA synthesis inhibitor that may cause immunosuppression via facilitation apoptosis of T cells

39
Q

What are some AEs of azathioprine?

A

Neoplasms
Leukopenia
Thrombocytopenis

40
Q

What is the MOA of cyclophosphamide?

A

alkylating agent that produces B and T cell lymphopenia, selective B-cell suppression, and reduced Ig secretion

41
Q

What are the AEs of cyclophosphamide?

A

bladder cancer
malignancy
neutropenia
thrombocytopenia

Pulmonary (34 decks)

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