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Pulm > Pharm - Restrictive Lung Disease and Pulmonary Hypertension > Flashcards

Pharm - Restrictive Lung Disease and Pulmonary Hypertension Flashcards

1
Q

Two divisions of restrictive lung dz

A

Extrapulmonary v. interstitial

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2
Q

Three divisions of interstitial lung disease

A

Pneumoconiosis
ARDS/NRDS
Idiopathic

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3
Q

Idiopathic ILDs

A 
Idiopathic pulmonary fibrosis
GPA
Goodpasture's
Sarcoidosis
Chronic eosinophilic pneumonia
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4
Q

4 pneumoconioses

A
  1. Silicosis
  2. Coal worker’s pneumoconiosis
  3. Asbestos
  4. Berylliosis
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5
Q

Silica dust found in:

A

Quartz, sand

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6
Q

Silicosis often seen in:

A

Sand blasters, rock miners, stone cutters, quarry workers

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7
Q

Silicosis can predispose to:

A

TB

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8
Q

Coal dust contains:

A

Carbon and silica

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9
Q

Coal worker’s pneumoconiosis progresses from:

A

Acanthrosis = mild asymptomatic buildup of carbon in city dwellers and smokers

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10
Q

Coal worker’s pneumoconiosis predisposes to:

A

Pulmonary artery HTN and right-sided HF

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11
Q

Asbestosis seen in:

A

Shipyard workers, construction workers, insulation and mechanics workers

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12
Q

Asbestosis predisposes to:

A

Carcinoma and mesothelioma

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13
Q

Berylliosis seen in:

A

Aerospace, electronics, and nuclear weapons workers

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14
Q

Berylliosis predisposes to:

A

Multi-organ granulomas; mimics sarcoidosis (non-caseating)

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15
Q

Pneumoconiosis tx

A

No curative tx; avoid further exposure

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16
Q

Causative agents of ARDS

A 
ASA
Cocaine
Opioids
Phenothiazines
TCAs
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17
Q

Idiopathic agents causing ARDS

A

Some chemo Rx

Radiological contrast dye

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18
Q

___ increases risk for ARDS but does not directly cause it

A

Alcohol abuse

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19
Q

Caveat of drugs treating ARDS

A

None have been uniformly beneficial

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20
Q

5 Rx used for ARDS

A 
Albuterol
NO
PGI2/prostacyclin
Corticosteroids
Dietary oil supplementation
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21
Q

MOA in ARDS: albuterol and NO

A

Preferential vasodilation of pulmonary vessels supplying functioning alveoli

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22
Q

MOA PGI2/prostacyclin in ARDS:

A

Vasodilation

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23
Q

MOA dietary oil supplementation in ARDS:

A

Antiinflammatory through modulation of arachidonic acid metabolism

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24
Q

Most common cause of respiratory failure in newborns

A

NRDS - newborn respiratory distres syndrome - no surfactant

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25
Q

Lack of surfactant in NRDS causes:

A

Increased surface tension, V/Q mismatch, shunt

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26
Q

2 tx options for NRDS

A

Corticosteroids given to mom suspected of birth <30 weeks

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27
Q

How do corticosteroids given antenatally treat NRDS?

A

Promote maturation of baby’s lung architecture and biochem to increase surfactant synthesis and release

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28
Q

3 available exogenous surfactants

A

Poractant alpha
Calfactant
Beractant

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29
Q

Exogenous surfactants contain:

A

Surfactant proteins B&C
Neutral lipids
Surface-active PLs, like DPPC

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30
Q

Hallmark of sarcoidosis

A

Non-caseating granulomas involving multiple organs

AAF with skin, eye, lung problems

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31
Q

Two tx options for sarcoidosis

A

GC, methotrexate

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32
Q

Most potent class of anti-inflammatory Rx

A

GC

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33
Q

3 basic MOA of GCs

A
  1. Decrease transcription of pro-inflammatory cytokines (IL-1beta, TNF)
  2. Increase transcription of anti-inflammatory cytokines (IL-10)
  3. Promote apoptosis of macrophages, dendritic cells, T cells
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34
Q

Adverse effects of GC caused by:

A

Suppression of HPA axis from chronic supraphysiological doses of GC

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35
Q

10 AE associated with GC:

A
  1. Osteoporosis
  2. Pancreatitis
  3. Oral candidiasis/opportunistic infx
  4. Immunosuppression
  5. Cataracts
  6. Glaucoma
  7. Psychosis
  8. Weight gain
  9. Skin atrophy
  10. Steroid-induced DM
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36
Q

MOA methotrexate for sarcoidosis

A

Inhibit DHFR –> accumulation of AICAR –> inhibition of ADA and AMP deaminase –> accumulation of adenosine –> stimulation of A2a and A2b receptors –> increase cAMP –> immunosuppresion

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37
Q

(T/F): Methotrexate is only used after other tx fails

A

True - not a first-line tx

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38
Q

6 AE of methotrexate:

A
  1. Severe skin rxn
  2. Malignant lymphoma
  3. Acute or chronic interstitial pneumonitis
  4. Pulmonary fibrosis
  5. Birth defects
  6. Immunosuppression
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39
Q

Methotrexate is category ____

A

X = TERATOGEN!!!!

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40
Q

Short-term v. long-term pathophys of idiopathic pulmonary fibrosis

A 
Short-term = inflammation leading to remodeling of blood vessel walls
Long-term = NOT inflammatory
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41
Q

Why use corticosteroids for IPF if not a chronic inflammatory process?

A

Response or non-response can serve as a differential for other lung inflammatory fibrotic diseases

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42
Q

Profibrogenic cytokines

A

TGFbeta, PDGF

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43
Q

Remodeling of blood vessel walls in IPF often causes:

A

Pulmonary artery HTN

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44
Q

Rx used in IPF tx?

A

None have been shown to be beneficial

pt with PAH due to IPF don’t have as great of an improvement from PAH Rx

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45
Q

Goodpasture’s cause

A

Autoantibodies to non-collagenous domain of type 4 collagen

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46
Q

Goodpasture’s is type ____ hypersensitivity

A

II

antibody to antigen on tissues

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47
Q

How to tx Goodpasture’s

A

Plasmapheresis to reduce antibody load

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48
Q

Size of vessels affected in GPA

A

Small-medium

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49
Q

Tx options for GPA

A

Rituximab (only Rx labeled for use in GPA)
Azathioprine
Cyclophosphamide
GCs

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50
Q

MOA rituximab

A

CD20 mab:

  1. ADCC via binding FCyR on CD20 B cells
  2. Complement-mediated cytotoxicity via complement activation leading to membrane attack complex formation
  3. Promotes apoptosis of CD20 B cells
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51
Q

6 AE of rituximab

A 
HTN
Asthenia
Arthralgia
Urticaria
Pruritis
Rhinitis
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52
Q

How long do effects of rituximab last?

A

6-9 months after one treatment which is 3 doses

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53
Q

MOA azathioprine

A

Purine analog; disrupts DNA/RNA synthesis; T cells have no salvage pathway –> apoptosis

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54
Q

5 AE azathioprine

A 
Mutagenic
Neoplastic
Thrombocytopenic
Leukopenic
Increase risk of infection
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55
Q

Active drug of azathioprine

A

Mercaptopurine (AZA is prodrug)

56
Q

MOA cyclophosphamide

A

Alkylating agent = B&T cell leukopenia, selective suppression of B cell activity, reduced IG secretion

57
Q

MAJOR AE OF CYCLOPHOSPHAMIDE AND HOW TO PREVENT

A

Hemorrhagic cystitis –> MESNA

58
Q

5 AE cyclophosphamide

A 
Neutropenia
Thrombocytopenia
Myeloproliferative malignancy
Lymphoproliferative malignancy
Bladder CA/hemorrhagic cystitis
59
Q

Only drug class used in systemic and pulmonary HTN

A

Ca2+ channel blockers

60
Q

4 causes of PAH

A
  1. Imbalance between vasoconstriction and vasodilation
  2. SMC and endothelial cell proliferation, propagation, and hypertrophy
  3. Thrombosis
  4. Fibrosis
61
Q

Causes of imbalance between vasoconstriction and vasodilation in PAH

A

Decreased prostacyclin/PGI2 and NO (vasodilators) and increased endothelin-1 (vasoconstrictor)

62
Q

All actions of prostacyclin/PGI2 related to PAH

A

Vasodilation
Anti-proliferation on SMC
Inhibition of platelet activation

63
Q

All actions of NO related to PAH

A

Vasodilation
Inhibits SMC activity
Inhibition of platelet activation

64
Q

All actions of endothelin-1 related to PAH

A

Vasoconstrictor

Proliferation of SMC

65
Q

Why is TXA2 elevated in PAH?

A

Decreased prostacyclin/PGI2 means increased platelet activation, which releases TXA2

66
Q

Characteristic lesion of PAH

A

Plexiform lesions = thickened arterioles as a result of shear stress

67
Q

How do plexiform lesions contribute to the development of PAH?

A

Causes proliferation of monoclonal endothelial and SM cells and an accumulation of macrophages and progenitor cells = obstruction of blood flow

68
Q

Trigger for initiation of events resulting in PAH

A

Pulmonary artery endothelial cell damage

69
Q

MOA prostanoids

A
  1. PA vasodilation
  2. Retard smooth muscle growth
  3. Inhibit platelet aggregation
70
Q

3 prostanoids

A

Epoprostanol
Iloprost
Treprostinil

71
Q

Prostanoid with longest T1/2? Shortest?

A

Treprostinil

Epoprostanol

72
Q

ROA each prostanoid

A

Epoprostanol - IV
Iloprost - inhalation
Treprostinil - subQ or IV

73
Q

AE of all prostanoids

A

Bleeding (inhibit platelet aggregation)
Hypotension (vasodilation)
HA

74
Q

AE epoprostanol

A

Flushing
Muscle pain
Risk for catheter infection

75
Q

AE iloprost

A 
**HEMOPTYSIS
Cough
Flushing
Muscle cramps
Tongue/back pain
76
Q

AE treprostinil

A 
Erythema/pain/rash at injection site (subQ one!)
Diarrhea
Nausea
Jaw pain
CYP2C8 INTERACTIONS
77
Q

Drugs to avoid with treprostinil

A

Gemfibrozil (inhibits CYP2C8 so reduces treprostinil clearnace)
Rifampin (induces CYP2C8 so enhances treprostinil clearance)

78
Q

Problems with prostanoids

A

No oral Rx so must be stored and reconstituted; shelf life diminishes each times it’s reconstituted; back up pump necessary; annual cost > $35k

79
Q

2 endothelin antagonists

A

Bosentan

Ambrisentan

80
Q

MOA endothelin antagonists

A

Reduce SMC proliferation and inhibit vasoconstriction through ETA and ETB receptors

81
Q

Inhibition of ETA receptors responsible for:

A

Inhibition of SMC proliferation

ETAR on SMCs

82
Q

Inhibition of ETB receptors responsible for:

A

Inhibition of vasoconstriction

ETBR on endothelial cells

83
Q

AE of both endothelin antagonists

A

Category X!! (like methotrexate)
Headache
CYP2C9 and 3A4 inducers

84
Q

AE of bosentan

A

Elevated LFTs
Anemia
Nasopharyngitis

85
Q

AE of ambrisentan

A

Peripheral edema

Also induces OATP and P-glycoprotein

86
Q

2 PDE5 inhibitors

A

Sildenafil

Tadalafil

87
Q

MOA PDE5 inhibitors

A

Prevent breakdown of cGMP in NO pathway –> SM relaxation/vasodilation + reduce cellular proliferation

88
Q

ROA of each PDE5 inhibitor

A

Sildenafil - PO or IV

Tadalafil - PO

89
Q

AE of both PDE5 inhibitors

A

Dyspepsia

CYP3A4 substrates

90
Q

AE sildenafil

A 
HA
Epistaxis
Flushing
Insomnia
Dizziness with sudden hearing loss
91
Q

AE tadalafil

A

Back pain

Change in color vision (NAION)

92
Q

What must be done before prescribing a CCB to a pt with PAH and why?

A

Vasodilator challenge - not all patients with PAH respond to CCBs and some can have potentially fatal hemodynamic decompensation

93
Q

Explain the vasodilatory challenge

A

Epoprostanol, adenosine, or NO given in progressively higher dosing rate —> if PAP and CO drop, can be prescribed a CCB for PAH

94
Q

3 CCBs used for PAH

A

Nifedipine
Amlodipine
Diltiazem

95
Q

AE of all CCBs

A

CYP3A4 substrate

Hypotension

96
Q

AE of dilt

A

Bradycardia
Edema
HA

97
Q

AE nifedipine

A

Heartburn
Flushing
Edema

98
Q

AE amlodipine

A

Fatigue

Edema

99
Q

Why is verapamil not used in PAH?

A

Strong negative inotropic (decreased contraction) effects more likely to cause bradycardia than others

100
Q

Goal of CCB tx for PAH

A

Get to NHYA I or II within 3-4 months

If not, change to another class

101
Q

___% of pt respond to vasodilator challenge, and of those only ___% respond to CCB

102
Q

Pancreatitis

103
Q

Malignant lymphoma

104
Q

Cataracts

105
Q

Plasmapheresis

A

Goodpasture’s

106
Q

Duration of action 6-9 months

107
Q

Asthenia

108
Q

Thrombocytopenia

A

Cyclophosphamide, AZA

109
Q

Bleeding risk

A

Prostanoids

110
Q

Tongue pain

111
Q

Jaw pain

A

Treprostinil

112
Q

CYP3A4 substrates

A

PDE5 inhibitors and CCBs

113
Q

CYP2C9 substrate

A

Ambrisentan

114
Q

CYP2C8 substrate

A

Treprostinil

115
Q

Pulmonary fibrosis

116
Q

Hemoptysis

117
Q

Limited availability

A

Endothelin antagonists

118
Q

Elevated PFTs

119
Q

Edema

A

Ambrisentan

CCBs

120
Q

Epistaxis

A

Sildenafil

121
Q

Change in color vision

122
Q

Bradycardia

123
Q

Heartburn

A

Nifedipine

124
Q

Hemorrhagic cystitis

A

Cyclophosphamide

125
Q

Dizziness w/ hearing loss

A

Sildenafil

126
Q

Category X

A

MTX

Endothelin antagonists

127
Q

Skin atrophy

128
Q

Severe derm rxns

129
Q

HTN

130
Q

Psychosis

131
Q

Acute or chronic interstitial pneumonitis

132
Q

Prodrug

133
Q

Nausea and diarrhea

A

Treprostinil

134
Q

Nasopharyngitis

135
Q

OATP and P-glc substrate

A

Ambrisentan

136
Q

Dyspepsia

A

PDE5 inhibitors

Pulm (33 decks)

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