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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
Lack of surfactant in NRDS causes:
Increased surface tension, V/Q mismatch, shunt
26
2 tx options for NRDS
Corticosteroids given to mom suspected of birth <30 weeks
27
How do corticosteroids given antenatally treat NRDS?
Promote maturation of baby's lung architecture and biochem to increase surfactant synthesis and release
28
3 available exogenous surfactants
Poractant alpha Calfactant Beractant
29
Exogenous surfactants contain:
Surfactant proteins B&C Neutral lipids Surface-active PLs, like DPPC
30
Hallmark of sarcoidosis
Non-caseating granulomas involving multiple organs | AAF with skin, eye, lung problems
31
Two tx options for sarcoidosis
GC, methotrexate
32
Most potent class of anti-inflammatory Rx
GC
33
3 basic MOA of GCs
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
34
Adverse effects of GC caused by:
Suppression of HPA axis from chronic supraphysiological doses of GC
35
10 AE associated with GC:
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
36
MOA methotrexate for sarcoidosis
Inhibit DHFR --> accumulation of AICAR --> inhibition of ADA and AMP deaminase --> accumulation of adenosine --> stimulation of A2a and A2b receptors --> increase cAMP --> immunosuppresion
37
(T/F): Methotrexate is only used after other tx fails
True - not a first-line tx
38
6 AE of methotrexate:
1. Severe skin rxn 2. Malignant lymphoma 3. Acute or chronic interstitial pneumonitis 4. Pulmonary fibrosis 5. Birth defects 6. Immunosuppression
39
Methotrexate is category ____
X = TERATOGEN!!!!
40
Short-term v. long-term pathophys of idiopathic pulmonary fibrosis
``` Short-term = inflammation leading to remodeling of blood vessel walls Long-term = NOT inflammatory ```
41
Why use corticosteroids for IPF if not a chronic inflammatory process?
Response or non-response can serve as a differential for other lung inflammatory fibrotic diseases
42
Profibrogenic cytokines
TGFbeta, PDGF
43
Remodeling of blood vessel walls in IPF often causes:
Pulmonary artery HTN
44
Rx used in IPF tx?
None have been shown to be beneficial | pt with PAH due to IPF don't have as great of an improvement from PAH Rx
45
Goodpasture's cause
Autoantibodies to non-collagenous domain of type 4 collagen
46
Goodpasture's is type ____ hypersensitivity
II | antibody to antigen on tissues
47
How to tx Goodpasture's
Plasmapheresis to reduce antibody load
48
Size of vessels affected in GPA
Small-medium
49
Tx options for GPA
Rituximab (only Rx labeled for use in GPA) Azathioprine Cyclophosphamide GCs
50
MOA rituximab
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
51
6 AE of rituximab
``` HTN Asthenia Arthralgia Urticaria Pruritis Rhinitis ```
52
How long do effects of rituximab last?
6-9 months after one treatment which is 3 doses
53
MOA azathioprine
Purine analog; disrupts DNA/RNA synthesis; T cells have no salvage pathway --> apoptosis
54
5 AE azathioprine
``` Mutagenic Neoplastic Thrombocytopenic Leukopenic Increase risk of infection ```
55
Active drug of azathioprine
Mercaptopurine (AZA is prodrug)
56
MOA cyclophosphamide
Alkylating agent = B&T cell leukopenia, selective suppression of B cell activity, reduced IG secretion
57
MAJOR AE OF CYCLOPHOSPHAMIDE AND HOW TO PREVENT
Hemorrhagic cystitis --> MESNA
58
5 AE cyclophosphamide
``` Neutropenia Thrombocytopenia Myeloproliferative malignancy Lymphoproliferative malignancy Bladder CA/hemorrhagic cystitis ```
59
Only drug class used in systemic and pulmonary HTN
Ca2+ channel blockers
60
4 causes of PAH
1. Imbalance between vasoconstriction and vasodilation 2. SMC and endothelial cell proliferation, propagation, and hypertrophy 3. Thrombosis 4. Fibrosis
61
Causes of imbalance between vasoconstriction and vasodilation in PAH
Decreased prostacyclin/PGI2 and NO (vasodilators) and increased endothelin-1 (vasoconstrictor)
62
All actions of prostacyclin/PGI2 related to PAH
Vasodilation Anti-proliferation on SMC Inhibition of platelet activation
63
All actions of NO related to PAH
Vasodilation Inhibits SMC activity Inhibition of platelet activation
64
All actions of endothelin-1 related to PAH
Vasoconstrictor | Proliferation of SMC
65
Why is TXA2 elevated in PAH?
Decreased prostacyclin/PGI2 means increased platelet activation, which releases TXA2
66
Characteristic lesion of PAH
Plexiform lesions = thickened arterioles as a result of shear stress
67
How do plexiform lesions contribute to the development of PAH?
Causes proliferation of monoclonal endothelial and SM cells and an accumulation of macrophages and progenitor cells = obstruction of blood flow
68
Trigger for initiation of events resulting in PAH
Pulmonary artery endothelial cell damage
69
MOA prostanoids
1. PA vasodilation 2. Retard smooth muscle growth 3. Inhibit platelet aggregation
70
3 prostanoids
Epoprostanol Iloprost Treprostinil
71
Prostanoid with longest T1/2? Shortest?
Treprostinil | Epoprostanol
72
ROA each prostanoid
Epoprostanol - IV Iloprost - inhalation Treprostinil - subQ or IV
73
AE of all prostanoids
Bleeding (inhibit platelet aggregation) Hypotension (vasodilation) HA
74
AE epoprostanol
Flushing Muscle pain Risk for catheter infection
75
AE iloprost
``` **HEMOPTYSIS Cough Flushing Muscle cramps Tongue/back pain ```
76
AE treprostinil
``` Erythema/pain/rash at injection site (subQ one!) Diarrhea Nausea Jaw pain CYP2C8 INTERACTIONS ```
77
Drugs to avoid with treprostinil
Gemfibrozil (inhibits CYP2C8 so reduces treprostinil clearnace) Rifampin (induces CYP2C8 so enhances treprostinil clearance)
78
Problems with prostanoids
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
2 endothelin antagonists
Bosentan | Ambrisentan
80
MOA endothelin antagonists
Reduce SMC proliferation and inhibit vasoconstriction through ETA and ETB receptors
81
Inhibition of ETA receptors responsible for:
Inhibition of SMC proliferation | ETAR on SMCs
82
Inhibition of ETB receptors responsible for:
Inhibition of vasoconstriction | ETBR on endothelial cells
83
AE of both endothelin antagonists
Category X!! (like methotrexate) Headache CYP2C9 and 3A4 inducers
84
AE of bosentan
Elevated LFTs Anemia Nasopharyngitis
85
AE of ambrisentan
Peripheral edema | Also induces OATP and P-glycoprotein
86
2 PDE5 inhibitors
Sildenafil | Tadalafil
87
MOA PDE5 inhibitors
Prevent breakdown of cGMP in NO pathway --> SM relaxation/vasodilation + reduce cellular proliferation
88
ROA of each PDE5 inhibitor
Sildenafil - PO or IV | Tadalafil - PO
89
AE of both PDE5 inhibitors
Dyspepsia | CYP3A4 substrates
90
AE sildenafil
``` HA Epistaxis Flushing Insomnia Dizziness with sudden hearing loss ```
91
AE tadalafil
Back pain | Change in color vision (NAION)
92
What must be done before prescribing a CCB to a pt with PAH and why?
Vasodilator challenge - not all patients with PAH respond to CCBs and some can have potentially fatal hemodynamic decompensation
93
Explain the vasodilatory challenge
Epoprostanol, adenosine, or NO given in progressively higher dosing rate ---> if PAP and CO drop, can be prescribed a CCB for PAH
94
3 CCBs used for PAH
Nifedipine Amlodipine Diltiazem
95
AE of all CCBs
CYP3A4 substrate | Hypotension
96
AE of dilt
Bradycardia Edema HA
97
AE nifedipine
Heartburn Flushing Edema
98
AE amlodipine
Fatigue | Edema
99
Why is verapamil not used in PAH?
Strong negative inotropic (decreased contraction) effects more likely to cause bradycardia than others
100
Goal of CCB tx for PAH
Get to NHYA I or II within 3-4 months | If not, change to another class
101
___% of pt respond to vasodilator challenge, and of those only ___% respond to CCB
15% | 50%
102
Pancreatitis
GCs
103
Malignant lymphoma
MTX
104
Cataracts
Gcs
105
Plasmapheresis
Goodpasture's
106
Duration of action 6-9 months
Rituximab
107
Asthenia
Rituximab
108
Thrombocytopenia
Cyclophosphamide, AZA
109
Bleeding risk
Prostanoids
110
Tongue pain
Iloprost
111
Jaw pain
Treprostinil
112
CYP3A4 substrates
PDE5 inhibitors and CCBs
113
CYP2C9 substrate
Ambrisentan
114
CYP2C8 substrate
Treprostinil
115
Pulmonary fibrosis
MTX
116
Hemoptysis
Iloprost
117
Limited availability
Endothelin antagonists
118
Elevated PFTs
Bosentan
119
Edema
Ambrisentan | CCBs
120
Epistaxis
Sildenafil
121
Change in color vision
Tadalafil
122
Bradycardia
Dilt
123
Heartburn
Nifedipine
124
Hemorrhagic cystitis
Cyclophosphamide
125
Dizziness w/ hearing loss
Sildenafil
126
Category X
MTX | Endothelin antagonists
127
Skin atrophy
GCs
128
Severe derm rxns
MTX
129
HTN
Rituximab
130
Psychosis
GCs
131
Acute or chronic interstitial pneumonitis
MTX
132
Prodrug
AZA
133
Nausea and diarrhea
Treprostinil
134
Nasopharyngitis
Bosentan
135
OATP and P-glc substrate
Ambrisentan
136
Dyspepsia
PDE5 inhibitors

Pulm (33 decks)

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