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Pulmonology > Sweatman Restrictive Lung Dz and PAH > Flashcards

Sweatman Restrictive Lung Dz and PAH Flashcards

1
Q

name the surfactant agents

A
  1. Poractant
  2. calfactant
  3. beractant
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2
Q

name the PDE-5inhibitors

A
  1. sildenafil (revatio)

2. tadalafil (adcirca)

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3
Q

Name the immunosupressants for PAH and RLD

A

rituximab, azathioprine, cyclphosphamide and corticosteroids, methotrexate

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4
Q

Name the long chain fatty acid-derived eicosanoids

A

iloprost, triprostinil, epoprostenol

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5
Q

name the ET-1 antagonists

A

bosentan and ambrisentan

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6
Q

Name the CCB’s

A

Diltiazem (NONDHP), Nefdipine (DHP), Amlodipine (DHP)

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7
Q

prostacyclin analog

A

treprostinil, iloprost, epoprostenol

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8
Q

name the three diagnostic categories of restrictive lung disease

A
  1. pneumoconisis
  2. ARDs, NRDS
  3. Idiopathic
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9
Q

name the 4 types of pneumoconiosis

A
  1. silicosis
  2. beryllosis
  3. CWP
  4. asbestosis
    * review what the inhalant is that cuases the disease in each
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10
Q

silicosis predisposes to

A

TB

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11
Q

CWP predisposes to

A

Pulmonary HTN/ right sided heart failure

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12
Q

mesothelioma predisposes to

A

primary carcinoma of the lung and melignant mesothelioma

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13
Q

beryllosis predisposes to

A

multi-organ granuloma formation mimicking sarcoidosis

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14
Q

Drugs that can cause ARDS

A

aspirin, opiates, cocaine, phenothiazines, tricyclic antidresessants
*also idiosyncratic reactions with contrast dye and chemotherapeutic agents

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15
Q

alcohol and ARDS

A

does not directly cause ARD but increases the chanes of ARDS from other causes (sepsis and trauma)

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16
Q

most common cause of ARDS

A

Sepsis, Pneumonia, Aspiration, Trauma–> in that order

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17
Q

current tx of ARDS (terrible data nothing proven to work)

A

> Beta2 agonists (albuterol), NO–> vasodil. increase perfusion of functioning alveoli
corticosteroids–> antinflamm
prostacycline (PGI2)
Dietary oil supplementation –> antiinflamm..modulate arachadonic acid metabolism

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18
Q

tx of NRDS in at risk mothers < 34 weeks

A

antenatal corticosteroids–> increases surfactant production and release in the fetus pre-birth, increasing lung function

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19
Q

Aditional tx of NRDS after birth

A

exogenous surfactant to preterm neonates to reduce pulmonary surface tension and improve lung function

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20
Q

name the exoenous sufactants

A

poractant alfa
calfactant
beractant
*purified animal derivatives rich in surfactant B and C and neutral lipids as well as surface active PL’s (dipalmitoylphosphatidylcholine DPPC)

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21
Q

surface active agent that lowers surface tension

A

dipalmitoyldiphoshatidylcholine DPPC or Lecithin

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22
Q

multi organ inflammatory dz characterized by non-aseating granulomas in an unspecified foreign body reaciton and peri-hilar bilateral infiltrates

A

sarcoidsosis

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23
Q

tx of sarcoidsosis

A

glucocorticoids to control inflamm.

methotrexate (OFF-LABEL USE)

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24
Q

SIDE EFFECTS OF CHRONIC CORTICOSTEROIDS USE

A

inhibition of hypothalamic-pituitary axis, oseoporosis, pancreatitis, steroid-induced DM, cataracts, glaucoma, pyschosis, oral candidiasis, immunosupression, weight gain, skin atrophy

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25
Q

Immune effect of chronic steroids

A

IMMUNE SUPPRESSION-> promote apoptosis of dedritic cells, t cells and macrophages (diminished CMI)

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26
Q

methotrexat MOE

A

DHFRinhibitor-> increase in adenosine mediated immunosupression

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27
Q

MTX and adenosine

A

MTX increases adenosine and causes immunosupresion via adenosine receptors

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28
Q

mechanism of MTX and adenosine immunosupression

A

inhibits AICAR–>FAICAR…AICAR accumulates and inhibits AMP deaminase and Adenosine deaminase–> icnreases adenosine 5’-P and adenosine–> this results in an increase in these products in the extracellular millieu, extracellular adenosine acting via the A2 pathway activated Adnylate cylase, resulting in increased cAMP production in the cell and thus IMMUNOSUPRESSION

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29
Q

POTENTIALLY FATALA DVERSE EFFECTS OF METHOTREXATE

A

ACUTE OR CHRONIC INTERSTITIAL PNEUMONITIS AND PULMONARY FIBROSIS

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30
Q

MTX CONTRAINDIATED IN

A

PT.’S WITH EXISITING IMMUNOSUPRESSION, LUNG DISEASE

CAN CAUSE BIRTH DEFECTS AND MALIGNANT LYMPHOMA

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31
Q

IS IPF A chronic inflammatory disease

A

NO–> EVEN THE MOST POTENT ANTI-INFLAMMATORY DRUGS WILL HAVE LITTLE TO NO EFFECT
*15% of interstitial lung disease to which no other cause can be attributed

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32
Q

HISTOPATH OF IPF

A

TEMPORAL HETEROGENEITY

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33
Q

SATISFACTORY TX FOR IPF

A

NONE AT THE MOMENT COMPARED TO PLACEBO (IN FACT SOME DID WORSE)
*PATIENTS WITH IPF DO NOT GET THE BENEFIT FROM OTHER DRUGS FOR OTHER FORMS PAH

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34
Q

HOW DOES IPF LEAD TO PAH

A

SHORT-LIVED INFLAMMATORY PRIOCESS LEADS TO PROLIFERATION AND MOBILIZATION OF FIBROLYSIS, apoptosis and a return to normal organ function–>
MESNchmye is now altered and leads to altered stromal cell type and activated epithelium– rlease of TGFb and PDGF–> if capillaries remodeled, PAH will ensue

35
Q

good pasture syndrome is caused by

A

type II hypersensitivity against alpha3 chain of type IV collagen (anti-GBM disease) of the glomeruli and alveoli
anti IgG and anti Igm autoantibodies

36
Q

tx of goodpastures

A

plasmaphoresis (IVIg)

37
Q

define wegener’s

A

C-ANCA associated autoimune vasculitis of small-medium sized vessels of the upper respiratory tract, lungs and kidney

38
Q

ANCA in wegner’s

A

C anca–> anti-proteinase-3 Anti-neutrophil cytoplasmic antibody

39
Q

Rituximab

A

minoclonal anti-CD20 antibody

40
Q

MOA for rituximab

A

induces plasma cell apoptosis via

  1. ADCC (recruits macrophages and NK cells by binding to FC receptors of phagocytes and FAB fragement of CD20)
  2. CDCC–> generates MAC’s on plasma cells
  3. INduction of apoptosis directly
41
Q

side effects of rituximab

A

HTN, asthenia, pruritis, urticaria, rhinitis, arthralgia

42
Q

azathioprine MOA

A

DNA and RNA synthesis inhibitor–> induces apoptosis in T cell populations

43
Q

azithioprine side effects

A

neoplastic, mutagenic, leukopenic and thrombocytopenic oxicities, CAN INCREASE RISK OF INFECTION

44
Q

CYCOPHOSPHAMIDE MOA

A

alkylating agent that also produces B and T cell lymphopenia, selective supression of B lymphocytes activity and decreased Ig secretion

45
Q

side effects of cyclophosphamide

A

hemorrhagic cystitis–> MESNA is prophylacitc
neutro thrombocytopenias
bladder cancer
myeloproliferative or lymphoproliferative malignancies

46
Q

Only drug used for systemic HTn that also works partially in PAH

A

CCB’s

47
Q

pathogenesis of PAH

A

decrease in production of PGI2 and NO
increase in production of Endothelin 1 and TXA2 (more pronounced presence)
*leading to smooth muscle and endothelial cell proliferation, propagation and hypertrophy (thanks to growth inhibitors and mitogenic factors–> eventually fibrosis and thrombosis

48
Q

resultant of PAH and sheer stress

A

pexiform lesions (more common in females)

49
Q

PLEXIFORM LESION ETIOLOGY

A

PULMONARY ARTERY ENDOTHELIAL DAMAGE–> proliferation of monoclonal endothelial cells smooth muscles and accumulation of circulating cells (macrophages)–> lead to SIGNIFICANT OUTFLOW OBSTRUCTION

50
Q

PGI2 CAUSES WHAT normally

A

inhibits platelet activation and smooth muscle growth

51
Q

endothelin also causes what normally

A

smooth muscle growth

52
Q

absence of PGI2 has what effect on TXA2

A

now allows TXA2 to act unchecked leading to improper platelet aggregation

53
Q

NO usually has what effect in the lungs

A

inhibits platelet activation and inhibits smooth muscle cell growth

54
Q

PGI2 causes what effect on blood vessels

A

increase cAMP and causes vasodilation

55
Q

NO is made from what precursor and turns into what

A

L-arginine–> cGMP

56
Q

effect of NO on blood vessels

A

turns L-arginine into NO–> increase cGMP–> leading to vasodilaiton and antiproliferaiton

57
Q

endothelin ahs what effect on the pulmonary blood vessels

A

vasoconstriction and muscle cell proliferaiton

58
Q

depletion of B cells by rituximab lasts how long

A

6-9 mos following 3 doses

59
Q

MOA for all prostanoids

A

induce PAvasodilation, retard smooth muscle growth and disrupts platelet aggregation

60
Q

rout of epoprostenol

A

requires constant IV infusion (half life=5 minutes)

61
Q

epoprosternol AE’s

A

hypotension, flushing, headaches, bleeding if anticoagulated, catheter infection

62
Q

Iloprost route

A

6-9 inhaled doses daily (half life 25 minutes) 10 minutes per dose

63
Q

Iloprost AE’s

A

hemoptysis (MUST MONITOR), flushing, cough, headaches-most common
*hypotension, tongue/back pains, minotor for bleeding

64
Q

Treprostinil route

A

continuous SC infusion half life 4 hours or IV infusion (more stable

65
Q

AE associated with treprostinil

A

injection site erythema, rash headache, nasue/ diarrhea, –> MONITOR FOR BLEEDING

  • -> CYP 2C8 D-D INTRXNS
  • ->DEC CLEARANCE WITH GEMFIBROZIL
  • -> INCREASED CLEARANCE WITH RIFAMPIN
66
Q

ET1 ANTAGONISTS MOA

A

block smooth muscle proliferation signal and pulmonary arterial vasocnstriction produced by ET1 binding to ET-1 TYPE A RECEPTORS AND TYPE B RECEPTORS

67
Q

ET1-A RECEPTORS ARE LOCATED WHERE

A

SMOOTH MUSCLE

68
Q

ET1-B RECEPTORS ARE LOCATED WHERE

A

ENDOTHELIAL CELLS (BLOOD VESSELS)

69
Q

ADVANTAGE OF ET1 ANTAGONISTS

A

ORALLY AVAILABLE, EASIER DOSING

70
Q

DISDVANTAGES OF ET1 ANTAGONISTS

A

EXPENSIVE AND CATEGORY X (MAJOR TERATOGENS)

71
Q

BOSENTAN ALSO ASSOCIATED WITH

A

LIVER AND BLOOD TOXICITIES

72
Q

HALF LIVES OF ET1 ANTAGS

A

BOSENTAN –> 5-8HRS BID *HEPATOTOXICITY

AMBRISENTAN–> 15 HOURS QD

73
Q

CYPS INVOLEVED WITH ET1 ANTAGS

A

CYP 3a4 and CYP 2c9

ambrisenten is a substrate and inhibitor if pgp as well as OATP

74
Q

PDE 5 inhibitors–> MOA

A

perpetuate endogenous cGMP leading to vasodilation and reduce deulluar proliferation

75
Q

PDE5 inhibitors should not be taken in pt.’s taking

A

organic nitrates such as NITROGLYCERINE FOR ANGINA

76
Q

name the PDE5 inhibitors

A

sildenafil (3-4 hours), tadalafil (17 hours)

77
Q

major side effects of sildenafil and tadalafil

A

S–> epistaxis, dizziness, hearing loss

T–> change in color vision,back pain dyspepsia,

78
Q

CCB MOA

A

prevent calcium from entering cell and inhibit SM vasoconstrcition–> cause vasorelaxation–> dec blod pressure

79
Q

vasodilation challenge–> ONLY 15% of patient are candiates for CCB therapy due to negative vasodilaiton challeneg

A

IV epoprostenol, IV adenosine, and inhaled NO–> measure CO and PAP for 3 hours…if PAP goes down without a decrease in CO

80
Q

do CCB’s improve mortality

A

yes–> but dont work in everyone and can lead to CV collapse

81
Q

name the ccb’s and their major side effects

A

diltiazem-> bradycard, hypotension
nefedipine–> flushing, edema, hypotension, heartburn
amlodipine–> edema, fatigue, hypotension

82
Q

CCB avoided in PAH

A

verapamil–> negative inotropic effect

83
Q

goal of CCB therapy…

A

get the pt. back to functional class 1 or 2 by 3-4 mos…if not achieved..consider alternative therapy

Pulmonology (10 decks)

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