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Clin Med II > restrictive lung diseases and PH > Flashcards

restrictive lung diseases and PH Flashcards

1
Q

pulmonary function tests

A
  • noninvasive way to measure how well lungs are expanding and contracting
  • measures gas exchange
  • differentiate obstructive vs. restrictive lung diseases
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2
Q

types of PFT

A
  • spirometry- most common and takes into account age, gender, heigh, race
  • spirometry before and after bronchodilator
  • diffuse capacity for carbon monoxide (DLCO)
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3
Q

tidal volume

A
  • amount of air moved in and out during each breath with normal respiration
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4
Q

vital capacity

A
  • max amount of air that can be moved after max inhale and max exhale
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5
Q

residual volume

A
  • volume of air remaining in lungs after max expiration
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6
Q

total lung capacity

A
  • volume of air in lungs after max inspiration

- includes residual volume

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7
Q

FVC

A
  • max amount of air exhaled after max inhale

- if low= restrictive disorder

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8
Q

FEV1

A
  • amount of air exhaled in 1 sec
  • normal > 70%
  • if less than 70%= obstructive disorder
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9
Q

FEV1/FVC ratio

A
  • ID airflow obstruction

- if < 70%= obstructive disorder

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10
Q

steps to interpreting PFTs

A
  • FEV1- FVC ratio: less than 70%= obstructive
  • rate severity of obstruction
  • bronchodilator response
  • TLC- < 80%= restrictive
  • RV/TLC ratio- not commonly used
  • DLCO
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11
Q

what does DLCO measure

A
  • overall function of alveolar capillary membrane
  • used to assess gas exchange
  • good to differentiate eitiology of restrictive lung diseases
  • low DLCO can indicate ILD
  • normal DLCO can indicate extrathroacic restrictions
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12
Q

what is the pulmonary interstitium?

A
  • network of tissue that extends through alveolar epithelium, basement membrane, and pulm capillary endothelium
  • supports alveoli and capillary beds for gas exchange
  • very thin- should not see on xray
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13
Q

restrictive pulmonary diseases

A
  • inability to fill lungs with air
  • reduced lung volume and total lung capacity
  • can be intrinsic, extrinsic, or medication induced
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14
Q

medications that can cause ILD

A
  • amiodarone
  • mtx
  • nitrofurantoin
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15
Q

intrinsic causes of restrictive lung disease

A
  • diseases of lung parenchyma
  • inflammation or scarring of lung tissue
  • idiopathic fibrotic disease
  • pneumoconiosis
  • sarcoidosis
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16
Q

extrinsic causes of restrictive lung disease

A
  • extra-pulm diseases involving chest wall
  • obesity
  • myasthenia gravis
  • ALS
  • kyphoscoliosis
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17
Q

idiopathic fibrosing interstitial pneumonia

A
  • aka idiopathic pulm fibrosis (IPF)
  • most common dx of pts with ILD
  • poor prognosis
  • mean survival- 2-5 years from time of dx
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18
Q

risk factors for IPF

A
  • smoking
  • occupational exposures
  • GERD d/t micro-aspirations
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19
Q

clinical presentation if IPF

A
  • insidious dry cough
  • exertional dyspnea
  • fatigue
  • tachypnea
  • clubbing
  • inspiratory rales/ crackles
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20
Q

diagnosis of IPF

A
  • PFTs- reduced FVC, reduced DLCO
  • CXR- reticular markings
  • CT- patchy fibrosis with pleural based honeycombing
  • lung biopsy if need to r/o other causes
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21
Q

treatment for IPF

A
  • supportive care
  • nitedanib- tyrosine kinase inhibitor
  • pirfenidone (esbriet)- antifibrotic drug
  • lung transplant if < 65, no substance abuse, and BMI 20-29
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22
Q

supportive care for restrictive lung diseases

A
  • home oxygen
  • vaccines- flu and pneumococcal
  • outpatient pulmonary rehab
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23
Q

pneumoconioses

A
  • “occupational lung disease”
  • ILD d/t inhalation and deposition of inorganic particles and mineral dust in lungs
  • coal workers pneumoconiosis, silicosis, asbestosis
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24
Q

coal workers pneumoconiosis

A
  • aka black lung disease

- d/t coal deposition in lungs that cannot be removed

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25
Q

what is the name for mild coal workers pneumoconiosis

A
  • anthracosis
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26
Q

where is coal workers pneumoconiosis prevalent

A
  • wyoming*
  • west virginia
  • pennsylvania
  • illinois
  • kentucky
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27
Q

clinical presentation of coal workers pneuoconiosis

A
  • early- asymptomatic
  • chronic cough
  • fever
  • DOE
  • sx usually dev 10-15 years after exposure
  • irreversible and progressive despite cessation of exposure
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28
Q

CXR findings for coal workers pneumoconiosis

A
  • small rounded nodular opacities at first

- eventually dev larger opacities with progressive fibrosis

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29
Q

treatment for coal workers pneumoconiosis

A
  • supportive care

- minimize exposure

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30
Q

silicosis

A
  • d/t inhalation of crystalline silica

- silica found in glass, optical fibers, porcelain, sand casting

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31
Q

occupations at risk for silicosis

A
  • mining
  • masonry
  • glass manufacturing
  • foundry work
  • sandblasting
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32
Q

clinical presentation of silicosis

A
  • cough
  • dyspnea
  • sometimes fever or pleuritic chest pain
33
Q

dx of silicosis

A
  • decreased FEV1, decreased DLCO, normal FEV1/FVC ratio
  • CXR- bilateral diffuse ground glass opacities early, small innumerable rounded densities later
  • dx of exclusion
  • get Tb test
34
Q

treatment for silicosis

A
  • supportive care
  • avoid further exposure
  • steroid therapy to minimize sequelae
  • lung transplant
35
Q

complications of silicosis

A
  • Tb*
  • aspergillosis
  • lung cancer
  • CKD
36
Q

asbestosis

A
  • pneumoconiosis d/t asbestos inhalation

- asbestos found in construction and inhalation

37
Q

occupations at risk for asbestosis

A
  • plumbers, pipefitters
  • steamfitters
  • biolermakers
  • electricians
  • insulation workers
  • carpenters
  • laborers
  • welders
  • janitors
38
Q

clinical presentation of asbestosis

A
  • usually asymptomatic for 20-30 years after exposure
  • DOE
  • cough
  • weight loss
  • clubbing
39
Q

diagnosis of asbestosis

A
  • inspiratory crackles
  • reduced vital capacity, total lung capacity, and low DLCO
  • CXR- thickened pleura or calcific plaques
  • CCT- coarse honeycombing, hazy ground glass of peripheral pleura
  • need to r/o other causes
40
Q

treatment of asbestosis

A
  • supportive care
  • avoid further exposure
  • steroid therapy- limited
  • smoking cessation
41
Q

complications of asbestosis

A
  • malignant mesothelioma
42
Q

sacroidosis

A
  • multisystem granulomatosis disorder
  • affects lungs in 90% of pts
  • can also affect LN, eyes, skin, liver, spleen, heart, NS
  • non-caeseating granulomas*
43
Q

who is sarcoidosis common in

A
  • young black women

- northern european whites

44
Q

clinical presentation of sarcoidosis

A
  • cough- dry and hacking
  • progressive dyspnea
  • atypical chest pain
  • fever/ night sweats
  • weighht loss
45
Q

diagnosis of sarcoidosis

A
  • CXR- bilat hilar adenopathy
  • CT- right paratracheal lymphadenopathy with diffuse reticular infiltrates, galaxy sign
  • dx often includes biopsy
46
Q

treatment of sarcoidosis

A
  • close observation if asymptomatic

- 90% of pts respond to PO steroids X 4-6 weeks

47
Q

pulmonary hypertension (PH)

A
  • pulmonary arterial pressure > 25 mmHg
  • generally is a feature of advanced disease and need to det underlying cause
  • most common cause= lung disease
48
Q

causes of PH

A
  • increased pulm vasc resistance (in pulm arteries)- most common
  • elevated LA pressure
  • increased pulmonary BF- limited significance
49
Q

diagnosis of PH

A
  • TTE good screening but not definitive

- gold std= R heart catheterization

50
Q

TTE findings for PH

A
  • if PH > 50 and tricuspid valve regurg velocity > 3.4 m/sec suggests PH
  • if PH < 36 and tricuspid regurg < 2.8 m/sec likely NOT PH
51
Q

what is the pulmonary capillary wedge pressure (PCWP)

A
  • indirect measure of L heart pressure by inflating balloon in pulmonary artery
52
Q

WHO functional classifications for PH

A
  • I- no limit on physical activity
  • II, slightly limited, comfortable at rest
  • III- marked limitation, comfortable at rest
  • IV- inability to do any physical activity without sx, sx at rest
53
Q

cor pulmonale

A
  • right heart disease secondary to PH
  • RV hypertophy d/t pulmonary pressure -> decreased contractility
  • low CO and BP -> decreased perfusion to vital organs and syncope
54
Q

what is the most common cause of death in cor pulmonale

A
  • circulatory collapse
55
Q

what is the worst prognosis for cor pulmonale

A
  • pulmonary artery hypetension
56
Q

si/sx of PH

A
  • initially asymptomatic
  • DOE
  • dyspnea at rest in advanced disease
  • fatigue
  • often goes undiagnosed or misdiagnosed
  • sx of RHF
57
Q

physical exam findings for PH

A
  • initially increased intensity of S2 split
  • widened S2 split
  • R ventricular S3
  • tricuspid regurg
  • elevated JVP
  • hepatomegaly
  • peripheral edema/ ascites
58
Q

diagnostic tests for PH

A
  • CXR- usually normal but may see cardiomegaly
  • EKG
  • echo
  • need to ID cause
59
Q

EKG findings for PH

A
  • R axis deviation
  • poor r wave progression
  • RV hypertrophy
60
Q

V/Q scan

A
  • sensitive for multiple small PE
61
Q

group 1 PH

A
  • intrinsic issue with arteries
  • impacts all 3 layers of vessel wall
  • dx of exclusion
62
Q

possible causes of group 1 PH

A
  • idiopathic
  • hereditary
  • drugs or toxins
  • CT disorders
  • HIV
  • portal HTN
  • congenital heart diseases- VSD or ASD
63
Q

treatment for group 1 PH

A
  • no effective primary tx

- requires advanced therapy

64
Q

group 2 PH

A
  • L heart disease

- LA HTN -> increased pulmonary pressure

65
Q

treatment for group 2 PH

A
  • HF treatment

- advanced therapy can be harmful

66
Q

group 3 PH

A
  • generally d/t severe lung disease and hypoxemia
  • most common type
  • COPD, ILD, obstructive sleep apnea
67
Q

treatment for group 3 PH

A
  • O2- only modality to improve mortality
  • digoxin may improve RVEF and control HR
  • advanced therapy is generally not recommended
68
Q

group 4 PH

A
  • chronic thromboemblic disease

- multiple small PE that accumulate over time

69
Q

treatment for group 4 PH

A
  • anticoagulation

- advanced therapy consideration

70
Q

group 5 PH

A
  • unclear mechanism

- may be hematologic, systemic disorders, metabolic disorders

71
Q

treatment for group 5 PH

A
  • target specific cause

- advanced therapy does have favorable response esp if d/t sarcoidosis

72
Q

primary therapy for PH

A
  • address underlying cause
73
Q

advanced therapy for PH

A
  • address PH itself
  • CCB
  • endothelin receptor blockers
  • PDE-5 inhibitors
  • lung transplant
  • used in class II, III and IV despite adequate primary therapy
74
Q

vasoreactive tests

A
  • used to det if pt wil benefit from CCB
  • admin short acting vasodil and measure hemodynamic response with R catheterization
  • if pos admin CCB, if neg use other agents
75
Q

vasoreactive agents used in testing

A
  • enepoprostenol
  • adenosine
  • inhaled NO
76
Q

prostanoid formulations

A
  • improve hemodynamics, functional capacity, and survival in IPAH
  • continuous infusion with implantable central venous catheter and portable pump
  • only therapy to prolong survival
  • epoprostenol*, treprostinil, iloprost
77
Q

endothelin receptor antagonists

A
  • improve exs capacity, dyspnea, and hemodynamics

- drugs end in “-entan”

78
Q

PDE-5 inhibitors

A
  • prolong vasodilatory effect of NO
  • improves pulm hemodynamics and exs capacity
  • end in “-fil”
79
Q

guanylate cyclase stimulants

A
  • stimulate NO receptor
  • increase sensitivity of receptor to NO
  • directly stimulates receptor to mimic action of NO
  • Drug- riociguat

Clin Med II (16 decks)

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