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PULM > PHARM-restrictive lung disease and pulm. htn > Flashcards

PHARM-restrictive lung disease and pulm. htn Flashcards

1
Q

Amantadine/Rimantadine MOA

A

inhibits the M2 ion channel of Influenza A and and reduces viral replicationand duration of symptoms

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2
Q

Zanamivir/Oseltamivir MOA

A

Influenza A and B Neuraminidase inhibitors, inhibits virus release, limiting the spread of the virus

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3
Q

What 5 categories of drugs would you use to treat ARDS?

A
  1. beta-2 agonist, albuterol IV (vasodilate vessels to functional alveoli)
  2. inhaled NO (vasodilate vessels to functional alveoli
  3. inhaled prostacylcin (vasodilator)
  4. corticosteroids (antiinflamm.)
  5. dietary oil supplementation (anti-inflamm. mod. AA metab.)
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4
Q

what do you give women at risk of delivering before 34 wks?

A

antenatal corticosteroids, increases synth. of surfactant

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5
Q

what do you give a baby born before 34 wks?

A

exogenous surfactant (poractant alfa, calfactant, beractant)

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6
Q

what 2 types of drugs do you give to pts with sarcoidosis?

A
  1. anti-inflamm. glucocorticoids

2. methotrexate

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7
Q

what are the most potent anti-inflamm. agents and how do they work?

A

glucocorticoids:
inhibit proinflamm. cytokines (IL-1beta, TNF)
promote production of anti-inflamm. cytokines (IL-10 by mphage and dendritic cells)
promote apoptosis of immune cells

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8
Q

what are some serious adverse effects of chronic corticosteroid use?

A 
suppression of HPA axis
osteoporosis, pancreatitis
steroid-induced diabetes mellitius
cataracts
glaucoma
psychosis
opportunistic infections
immunosuppression
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9
Q

How does methotrexate treat sarcoidosis?

A

dihydrofolate reductase inhibitor

prevents AICAR from becoming FAICAR, leads to buildup of adenosine (has immunosuppressive effects)

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10
Q

What are some important adverse effects of methotrexate therapy?

A

severe derm. rxns
birth defects and malignant lymphoma
increased risk of infection
pot’l fatal pulm. effects including acute or chronic interstitial pneumonitis and pulmonary fibrosis

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11
Q

How would a doctor use corticosteroid treatment for idiopathic pulmonary fibrosis?

A

IPF doesn’t respond to corticosteroids so that info could be used to adjust a ddx

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12
Q

what are 2 important profibrogenic cytokines that are released by an altered stromal cell pop. and activated epithelium?

A

TGF-beta

PDGF

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13
Q

what drugs are shown to be beneficial in idiopathic pulm. fibrosis?

A

none yet reported

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14
Q

What are 4 drugs that are commonly used to treat Wegener’s?

A
  1. Rituximab (on-label use)
  2. Azathioprine
  3. Cyclophosphamide
  4. Corticosteroids
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15
Q

How does rituximab work?

A

immunosupp. mAb binds to CD20 cell surface on B-cell precursors and mature B cells and are killed 3 ways. ADCC, complement-mediated cytotoxicity, induction of apoptosis

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16
Q

What are some of the important adverse effects of rituximab?

A 
HTN
asthenia
pruritis
urticarial
rhinitis
arthralgia
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17
Q

MOA azathioprine

A

DNA and RNA synth. inhib. that also produces immunosupp. possibly by apoptosis of t cells

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18
Q

MOA cyclophosphamide

A

alkylating agent that also produces B cell and T cell lymphopenia, selective supp. of B-cell activity and decreased Ig secretion

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19
Q

what are some important adverse effects of cyclophosphamide?

A

hemorrhagic cystitis, neutropenia, thrombocytopenia, bladder cancer, myeloproliferative, lymphoproliferative malignancies

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20
Q

what are the 4 causes of pulmonary artery HTN?

A
  1. decreased vasodilators ( PGI2, NO) and increased vasoconstrictors (endothelin-1, TXA2)
  2. smooth muscle and endothelial cell prolif., propagation, hypertrophy
  3. thrombosis
  4. fibrosis
21
Q

what is the characteristic histologic finding in pulmonary artery hypertension?

A

plexiform lesions (thickened arterioles as a result of shear stress)

22
Q

MOA of Prostanoids

A

induce pulmonary artery vasodilation, slow smooth muscle growth and disrupt platelet aggregation

23
Q

Name the 3 prostanoids

A

Epoprostenol
Iloprost
Treprostinil

24
Q

which prostanoid has the shortest half life?

A

epoprostenol (continuous IV infusion)

25
Q

which prostenol has the longest half life?

A

treprostinil

26
Q

what is 1 adverse effect common to all the prostanoids?

A

risk of bleeding, esp. if pt is anticoagulated

also headache

27
Q

what are some adverse effects of epoprostenol?

A

dose limiting hypotension
muscle pains
headaches
flushing

28
Q

what are some adverse effects of iloprost?

A 
cough
flushing
headaches
hypotension
HEMOPTOSIS
29
Q

what are some adverse effects of treprostinil?

A 
rash and pain at injection site
headache
nausea
diarrhea
vasodilation
jawpain
30
Q

what are some important drug interactions with treprostinil?

A

decreased clearance w/ gemfibrozil, increased clearance w/ rifampin

CYP2C8

31
Q

What is a major disadvantage to using prostanoids that aren’t available orally?

A

have to have people who can store and reconstitute the drug

very expensive

32
Q

how do the endothelin-1 receptor antagonists work?

A

block smooth muscle proliferation and pulm. arterial vasoconstriction

33
Q

What are the advantages and disadvantages to endothelin-1 receptor antagonists?

A

advantage: orally active
disadvantage: expensive drugs, Cat. X, bosentan also associated w/ liver and blood toxicities

34
Q

what are the main adverse effects of bosentan?

A

elevated LFT, anemia, extensive hepatic metabolism CYP2C9, 3A4

35
Q

what are the main adverse effects of ambrisentan?

A

peripheral edema and headache (most common)
fewer liver problems
CYP2C9, 3A4, OATP, P-gp substrate

36
Q

How do the phosphodiesterase type 5 inhibitors work?

A

block the destruction of endogenously generated cGMP leading to vasodilation and reduce cellular proliferation

37
Q

what is the one drug you can’t take with PDE type 5 inhibitors?

A

nitrates

38
Q

Name the 2 phosphodiesterase type 5 inhibitors

A

sildenafil

tadalafil

39
Q

what is the most common side-effect of PDE type 5 inhibitors?

A

headache

40
Q

what are the main side-effects of tadalafil?

A

headache
backpain, dyspepsia
Change in color vision
CYP3A4 substrate

41
Q

how do the Calcium channel blockers work?

A

prevent entry of Calcium into smooth muscle cell during depolarization, vasodilation endures

42
Q

what is one important thing to remember about CCBs when considering prescribing them to a pt?

A

it doesn’t work on all pts

43
Q

What is a vasodilator challenge?

A

pts receive a carefully escalated dosing rate and the pulm. arterial pressure and CO are monitored to see if the pts respond to the drug. (decrease PAP, w/o decrease in CO)

44
Q

what are the 3 main CCBs used for pulmonary arterial hypertension?

A

diltiazem
nifedipine
amlodipine

45
Q

what is the goal of giving CCB therapy for pts with pulm. HTN?

A

goal is to achieve NYHA-FC 1 or II after 3-4 months, if not consider alternative therapy

46
Q

which CCB has the longest half-life?

A

amlodipine

47
Q

what is the indication for cyclophosphamide in restrictive lung disease and pulmonary artery HTN

A

used off label for wegener’s granulomatosis

48
Q

what is the dose limiting adverse effect of epoprostenol?

A

hypotension

49
Q

what is the route of therapy for iloprost?

A

6-9 inhaled doses a day major hassle

PULM (14 decks)

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