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Clin Med II > restrictive lung diseases and PH > Flashcards

restrictive lung diseases and PH Flashcards

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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
what is the name for mild coal workers pneumoconiosis
- anthracosis
26
where is coal workers pneumoconiosis prevalent
- wyoming* - west virginia - pennsylvania - illinois - kentucky
27
clinical presentation of coal workers pneuoconiosis
- early- asymptomatic - chronic cough - fever - DOE - sx usually dev 10-15 years after exposure - irreversible and progressive despite cessation of exposure
28
CXR findings for coal workers pneumoconiosis
- small rounded nodular opacities at first | - eventually dev larger opacities with progressive fibrosis
29
treatment for coal workers pneumoconiosis
- supportive care | - minimize exposure
30
silicosis
- d/t inhalation of crystalline silica | - silica found in glass, optical fibers, porcelain, sand casting
31
occupations at risk for silicosis
- mining - masonry - glass manufacturing - foundry work - sandblasting
32
clinical presentation of silicosis
- cough - dyspnea - sometimes fever or pleuritic chest pain
33
dx of silicosis
- 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
treatment for silicosis
- supportive care - avoid further exposure - steroid therapy to minimize sequelae - lung transplant
35
complications of silicosis
- Tb* - aspergillosis - lung cancer - CKD
36
asbestosis
- pneumoconiosis d/t asbestos inhalation | - asbestos found in construction and inhalation
37
occupations at risk for asbestosis
- plumbers, pipefitters - steamfitters - biolermakers - electricians - insulation workers - carpenters - laborers - welders - janitors
38
clinical presentation of asbestosis
- usually asymptomatic for 20-30 years after exposure - DOE - cough - weight loss - clubbing
39
diagnosis of asbestosis
- 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
treatment of asbestosis
- supportive care - avoid further exposure - steroid therapy- limited - smoking cessation
41
complications of asbestosis
- malignant mesothelioma
42
sacroidosis
- multisystem granulomatosis disorder - affects lungs in 90% of pts - can also affect LN, eyes, skin, liver, spleen, heart, NS - non-caeseating granulomas*
43
who is sarcoidosis common in
- young black women | - northern european whites
44
clinical presentation of sarcoidosis
- cough- dry and hacking - progressive dyspnea - atypical chest pain - fever/ night sweats - weighht loss
45
diagnosis of sarcoidosis
- CXR- bilat hilar adenopathy - CT- right paratracheal lymphadenopathy with diffuse reticular infiltrates, galaxy sign - dx often includes biopsy
46
treatment of sarcoidosis
- close observation if asymptomatic | - 90% of pts respond to PO steroids X 4-6 weeks
47
pulmonary hypertension (PH)
- pulmonary arterial pressure > 25 mmHg - generally is a feature of advanced disease and need to det underlying cause - most common cause= lung disease
48
causes of PH
- increased pulm vasc resistance (in pulm arteries)- most common - elevated LA pressure - increased pulmonary BF- limited significance
49
diagnosis of PH
- TTE good screening but not definitive | - gold std= R heart catheterization
50
TTE findings for PH
- 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
what is the pulmonary capillary wedge pressure (PCWP)
- indirect measure of L heart pressure by inflating balloon in pulmonary artery
52
WHO functional classifications for PH
- 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
cor pulmonale
- 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
what is the most common cause of death in cor pulmonale
- circulatory collapse
55
what is the worst prognosis for cor pulmonale
- pulmonary artery hypetension
56
si/sx of PH
- initially asymptomatic - DOE - dyspnea at rest in advanced disease - fatigue - often goes undiagnosed or misdiagnosed - sx of RHF
57
physical exam findings for PH
- initially increased intensity of S2 split - widened S2 split - R ventricular S3 - tricuspid regurg - elevated JVP - hepatomegaly - peripheral edema/ ascites
58
diagnostic tests for PH
- CXR- usually normal but may see cardiomegaly - EKG - echo - need to ID cause
59
EKG findings for PH
- R axis deviation - poor r wave progression - RV hypertrophy
60
V/Q scan
- sensitive for multiple small PE
61
group 1 PH
- intrinsic issue with arteries - impacts all 3 layers of vessel wall - dx of exclusion
62
possible causes of group 1 PH
- idiopathic - hereditary - drugs or toxins - CT disorders - HIV - portal HTN - congenital heart diseases- VSD or ASD
63
treatment for group 1 PH
- no effective primary tx | - requires advanced therapy
64
group 2 PH
- L heart disease | - LA HTN -> increased pulmonary pressure
65
treatment for group 2 PH
- HF treatment | - advanced therapy can be harmful
66
group 3 PH
- generally d/t severe lung disease and hypoxemia - most common type - COPD, ILD, obstructive sleep apnea
67
treatment for group 3 PH
- O2- only modality to improve mortality - digoxin may improve RVEF and control HR - advanced therapy is generally not recommended
68
group 4 PH
- chronic thromboemblic disease | - multiple small PE that accumulate over time
69
treatment for group 4 PH
- anticoagulation | - advanced therapy consideration
70
group 5 PH
- unclear mechanism | - may be hematologic, systemic disorders, metabolic disorders
71
treatment for group 5 PH
- target specific cause | - advanced therapy does have favorable response esp if d/t sarcoidosis
72
primary therapy for PH
- address underlying cause
73
advanced therapy for PH
- address PH itself - CCB - endothelin receptor blockers - PDE-5 inhibitors - lung transplant - used in class II, III and IV despite adequate primary therapy
74
vasoreactive tests
- 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
vasoreactive agents used in testing
- enepoprostenol - adenosine - inhaled NO
76
prostanoid formulations
- 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
endothelin receptor antagonists
- improve exs capacity, dyspnea, and hemodynamics | - drugs end in "-entan"
78
PDE-5 inhibitors
- prolong vasodilatory effect of NO - improves pulm hemodynamics and exs capacity - end in "-fil"
79
guanylate cyclase stimulants
- 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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