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Respiratory > Midterm - Function > Flashcards

Midterm - Function Flashcards

2
Q

asthma results in ____ exhaled NO from airways

A

INCREASED

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3
Q

pathogenesis of asthma

A

periodic airway hyperreactivity/bronchoconstriction & mucus chronic plugging/inflammation

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4
Q

describe the death rate from asthma

A

varies WIDELY and we do not understand why

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5
Q

PFT diagnosis of asthma shows these 5 results:

A
  1. obstructive ventilatory defect, 2. auto-PEEP (increased end-exp pressure), 3. high DLCO, 4. hyperresponsiveness to methacholine challenge, 5. reversible airflow obstruction with bronchodilator
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6
Q

bronchodilator responsiveness in asthma vs COPD

A

reversibility in both, but there is much greater and more consistent reversibility in asthma

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7
Q

methacholine challenge tests?

A

bronchial hyperreactivity

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8
Q

repeated challenge tests in asthma are different in that?

A

they do NOT plateau with time, instead the slope goes straight up (can kill them)

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9
Q

beta agonists prevent ____ hyperreactivity, whereas steroids prevent ______ response

A

initial; late stage

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10
Q

allergic inflammation in asthma is caused by abnormal levels of what helper T cell?

A

Th2, leading to increased mast cells and eosinophils

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11
Q

sputum of an asthmatic may show what four pathologic findings?

A

charcot-leyden crystals (from eosinophils), mucus casts (curschmann’s spirals), creola bodies (ciliated columnar cells), and eosinophils

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12
Q

what is extrinsic asthma?

A

atopic version, presents at young age, family hx of allergies, specific allergic triggers

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13
Q

what is intrinsic asthma?

A

usually adult-onset following severe resp illness, perennial sx refractory to tx, not well understood

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14
Q

lecturer’s clear favorite tx for asthma

A

LABA + ICS

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15
Q

what is samter’s triad?

A

NSAID sensitivity, late-onset asthma, rhinitis and nasal polyps

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16
Q

salicylate sensitivity can cause?

A

asthma

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17
Q

what is COPD?

A

progressive, not fully-reversible airflow limitation usually due to noxious particles

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18
Q

COPD mortality is rising/declining, especially in men/women?

A

rising, especially in women

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19
Q

what percent of COPD occurs in smokers?

A

80-90%

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20
Q

what percent of smokers develop COPD?

A

15-20%

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21
Q

what are three causes of chronic obstruction, and what are their corresponding diseases? Hint: 2/3 are the same disease

A

small airway remodeling (chronic bronchitis), alveolar wall destruction (emphysema), mucus hypersecretion (chronic bronchitis)

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22
Q

what proteases contribute to COPD pathology?

A

elastase, matrix metalloproteases

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23
Q

what counteracts the effects of these proteases, and is missing is genetic COPD?

A

alpha-1 antitrypsin

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24
Q

what are two sources of increase elastolytic activity in COPD?

A

impaired mucociliary clearance –> bacterial colonization –> increased elastase from bacteria, as well as increased inflammation which produces elastlate

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25
Q

what are the consequences of loss of elastic recoil in emphysema?

A
  1. lower driving pressure for expiration, 2. loss of radial traction leading to airway collapse, 3. chest wall expansion
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26
Q

symptoms of COPD

A

SOB, cough (may not be productive), wheezing, fatigue and weakness from working hard to breath, LATE = morning headaches from high CO2, edema

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27
Q

diagnosis of COPD

A

requires spirometry; specifically a low FEV1, increased TLC and RV, decreased IC

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28
Q

classification of COPD is based on?

A

degree of obstruction, as defined by FEV1

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29
Q

why should helium dilution not be used to measure lung volumes in COPD? What should be used instead?

A

helium underestimates degree of abnormality in COPD; whole-body plethysmograph is better

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30
Q

chest radiograph changes of COPD occur ____ and include?

A

late; expanded chest, retrosternal air space, low and flat diaphragm, increased CVA, decrease in peripheral vascularity

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31
Q

exercise causes ____ in pts with COPD

A

dynamic hyperinflation, leading to dyspnea

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32
Q

what effect does COPD have on DLCO?

A

DLCO is decreased because diffusion decreases as a result of alveolar destruction

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33
Q

blood gas analysis in COPD shows?

A

high CO2, relatively normal pH due to chronic state of high CO2 and compensation

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34
Q

when should oxygen therapy be given in lung dz?

A

O2 sat <55% (only drug that can decrease mortality from COPD)

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35
Q

chronic hypoxemia in COPD leads to?

A

RHF, cor pulmonale

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36
Q

best tx for COPD

A

smoking cessation

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37
Q

when should pulmonary rehabilitation therapy be included in a COPD tx regimen?

A

State II: Moderate Disease

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38
Q

who is a good candidate for surgery to treat COPD?

A

has stopped smoking for at least 4 mo, is able to undergo pulm rehab, has potentially removeable areas of lung that are poorly fnc

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39
Q

what 3 things can reduce mortality in COPD?

A
  1. stop smoking, 2. oxygen tx, 3. lung volume reduction surgery in the right patient
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40
Q

one in how many caucasians are a carrier for the CFTR gene?

A

1 in 29 (so affects 1 in 3,300 births)

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41
Q

common problems in patients with CF

A

recurrent infection, allergic rhinitis/sinusitis (nasal polyps), pancreatic insufficiency (most on enzymes), bleeding duodenal ulcers, liver disease and cirrhosis

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42
Q

long-term side effects of CF

A

osteopenia, malnutrition, diabetes mellitis, respiratory failure and need for transplant

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43
Q

median survival age for CF is now?

A

late 30s!

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44
Q

what is locus heterogeneity?

A

ONE GENE with multiple different mutations that can cause a disease; see this in CF

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45
Q

what is the most common genotype of CF?

A

deltaF508

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46
Q

which gender has a survival disadvantage?

A

females

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47
Q

in addition to genetics, what factors contribute to CF phenotype/survival?

A

socioeconomic status, tobacco, nutrition, access to care, adherence

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48
Q

why do CF patients have chronic infection of the airways?

A

thick mucus + high cellular metabolism = great niche for anaerobic organisms like pseudomonas to form biofilms

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49
Q

how does chronic infection lead to lung damage?

A

neutrophils come to clear the infection, which doesn’t work but damages the epithelium anyway (from release of elastase, etc.)

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50
Q

which organisms preferentially inhabit young vs older CF patients?

A

young = haemophilus influenzae; old = pseudomonas aeruginosa

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51
Q

diagnostic criteria for cystic fibrosis

A

1+ typical phenotypic features (sinopulm dz, GI sx, or fam hx) and evidence of CFTR malfunction (sweat test, gene test)

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52
Q

when are the majority of CF patients diagnosed?

A

first year of life

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53
Q

major complications of CF

A

hemoptysis, pneumothorax, resp failure, diabetes, arthritis/vasculitis, gallbladder/kidney stones, infertility in males especially, peri-osteal bone formation (HPOA) (risk increases with age, so does frequency of acute exacerbations)

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54
Q

“acute” therapy for CF includes?

A

IV antibiotics, airway clearance (hypertonic saline, special vests)

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55
Q

“maintenance” therapy for CF includes?

A

inhaled/oral abx, airway clearance (mucolytics, saline, rhDNase)

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56
Q

how expensive is it to treat CF?

A

HUGE BURDEN OF TX

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57
Q

lung transplant survival for CF

A

on high end of survival curve, but still only 25% survival rate 15 years post-transplant

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58
Q

key clinical feature of bronchiectasis

A

copious amounts of purulent sputum

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59
Q

pathologic definition of bronchiectasis

A

pathologic dilatation of airways with or without obstruction; same as CF but without a known cause

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60
Q

other pathologic features of bronchiectasis

A

floppy and inflamed with mucus impaction and complete loss of tapering; INFLAMMATION; br wall may be destroyed while arteries may be hypertrophied; squamous metaplasia; plasma cells, eosinophils; ulceration leading to hemoptysis

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61
Q

what is the most common cause of bronchiectasis?

A

post-infection (some recall bias), but 50% is idiopathic

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62
Q

clinical sx of bronchiectasis

A

cough, mucopurulent sputum, dyspnea, wheeze, chest pain, fatigue, anorexia, weight loss, hemoptysis, exacerbations, finger clubbing, cyanosis/cor pulmonale end stage

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63
Q

clinical sx of PCD

A

neonatal resp problems, recurrent otitis media, sinus inversus, infertility

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64
Q

gold standard investigation for bronchiectasis

A

sputum microbiology

65
Q

bacterial colonization in bronchiectasis

A

mycobacteria, same as CF, no organisms at least 20% of the time

66
Q

if a HRCT scan is positive for bronchiectasis, what should you do?

A

follow up diagnostic tests to confirm CF, CVID, A1AT, PCD (nasal NO), CTD, ABPA

67
Q

how do you diagnose PCD?

A

nasal NO measures significantly low

68
Q

treatment for bronchiectasis

A

abx, airway clearance, bronchodilators, anti-inflammatory agents, surgery if local, transplant if severe, oxygen tx prolongs life

69
Q

what constitutes a sufficiently severe FEV1 to consider transplant in pt with bronchiectasis?

A

FEV1 <30% predicted

70
Q

which airway clearance tx used in CF should NOT be used in pts with other forms of bronchiectasis?

A

rhDNase (pulmozyme)

71
Q

full time tx with this antibiotic can be used for its anti-inflammatory abilities in patients with bronchiectasis; shown to decrease exacerbations

A

macrolides (only if confident no mycobacteria infection)

72
Q

there have been several recent studies considering ______ antibiotics for improved QOL and decreased exacerbation in patients with bronchiectasis

A

inhaled

73
Q

when to use IV abx?

A

during exacerbation, refractory to oral, hemoptysis, resistant gram neg, previous hx

74
Q

what medicines should be given before/during a lung transplant?

A

tacrolimus, mycophenolate, and steroids

75
Q

what are the 3 requirements for normal inspiration?

A
  1. compliant chest wall, 2. normal muscle strength, 3. compliant lungs
76
Q

obstructive lung disease causes impaired ______, while restrictive lung disease causes impaired ______

A

expiration; inspiration

77
Q

major abnormalities causing decreases compliance of the chest wall

A
  1. fibrothorax, 2. kyphoscoliosis, 3. morbid obesity
78
Q

weakness of respiratory muscles occurs in?

A
  1. myasthenia gravis, 2. ALS
79
Q

abnormalities of the lung parenchyma that cause decreased lung compliance

A

sarcoidosis, idiopathic pulm fibrosis (UIP)

80
Q

interstitial lung disease would better be called?

A

diffuse parenchymal lung disease (expansion extends beyond the interstitium)

81
Q

DPLD/ILD mimics these two common diseases

A

CHF, pulmonary infection (pneumonia)

82
Q

DPLD leads to diffusion impairment due to?

A

decreased lung compliance and pulm HTN?

83
Q

lung volumes in IDL

A

low TLC, FRC, and RV

84
Q

lung volumes in pts with muscle weakness

A

low TLC, high RV

85
Q

lung volumes in pts with obesity

A

low FRC

86
Q

most severe side effect of ILD

A

pulmonary HTN –> RVH –> cor pulmonale/RHF

87
Q

the majority of DPLD is caused by?

A

unknown etiology

88
Q

known etiologies of DPLD include?

A

inhaled organic dusts (hypersens pneumonia), pneumoconiosis, iatrogenic (radiation, drugs)

89
Q

DPLDs with unknown etiology

A

sarcoidosis, idiopathic pulm fibrosis (UIP), BOOP/COP, eosinophilic pneumonia, CTD-related ILD

90
Q

sarcoidosis is most common in?

A

black females 20-40 years old

91
Q

best theory on cause of sarcoidosis

A

Th1 mediated immune response from something inhaled interacting with T cells and APCs; greatest genetic linkage in MHC-related genes

92
Q

putative antigens in sarcoid

A

mycobacteria, propionibacteria

93
Q

Lofgren’s syndrome (seen in sarcoid)

A

fever, adenopathy, erythema nodosum, symmetrical ankle arthritis

94
Q

cutaneous involvement occurs in ____% of sarcoid

A

25

95
Q

stage I sarcoidosis

A

intrathoracic LN only (spont remission in 2/3)

96
Q

stage II sarcoidosis

A

parenchymal involvement + adenopathy

97
Q

stage III sarcoidosis

A

parenchymal involvement, NO adenopathy

98
Q

stage IV sarcoidosis

A

upper lobe fibrosis with hilar retraction, honeycomb changes, large bullae and cysts (lungs clear on exam)

99
Q

lupus pernio

A

indurated plaques and discoloration on the face, indicates prolonged course of sarcoid, can biopsy and find non-caseating granulomas

100
Q

diagnostic test for sarcoid

A

bronchoscopy to exclude infection and take a biopsy

101
Q

diagnostic criteria for sarcoid

A

1) granulomas, 2) no other cause of granuloma (TB, fungus, cancer-lymphoma or epithelioid)

102
Q

treatment of sarcoid

A

often don?t need tx, start with corticosteroids, then chemotx, anti-TNF

103
Q

who gets IPF/UIP?

A

older adults

104
Q

why is it important to diagnose UIP?

A

it has a much poorer prognosis and decreased survival time relative to other IIPs

105
Q

what is important to rule out in a case that resembles UIP?

A

connective tissue diseases, autoimmune diseases

106
Q

what is the pathogenesis of IPF?

A

defective injury repair: injury to alveoli epithelium –> tissue damage and death –> damage to BM and release of cytokines –> stimulation of fibroblasts –> collagen deposition (impeding normal recovery)

107
Q

risk factors for IPF

A

family hx, smoking, environmental dust exposure, chronic aspiration from GERD, infectious agents

108
Q

clinical presentation of IPF

A

age >50, gradual onset, progressive dyspnea on exertion, nonproductive paroxysmal cough, bibasilar crackles like velcro (80%), digital clubbing (25-50%)

109
Q

late stage IPF may present with?

A

sleep apnea, cyanosis, cor pulmonale, peripheral edema

110
Q

pulmonary function in IPF

A

reduced FVC and FEV1, high FEV1/FVC, reduced lung volumes across the board, decreased diffusion capacity (low DLCO), decreased PaO2 and increased A-a gradient, desaturation on exercise

111
Q

IPF on x-ray

A

subpleural and basilar distribution of infiltrate; usually bilateral but not necessarily symmetrical

112
Q

High res CT can be diagnostic for IPF. What 4 things should you find?

A
  1. subpleural honeycomb, 2. basilar distribution, 3. traction bronchiectasis, 4. minimal ground glass opacity
113
Q

when clinical and radiological assessment is inconclusive for ruling out UIP/IPF, you should do a?

A

video-assisted thoracoscopic (VATS) biopsy

114
Q

histopathology of IPF

A

temporal heterogeneity!!

115
Q

treatment of IPF

A

oxygen tx (to prevent/delay RHF), lung transplant

116
Q

cancer deaths from lung cancer are greater than the next ____ cancers combined

A

5!

117
Q

lung cancer is most common in and kills more ___ than any other demographic

A

african american men

118
Q

risk factors for lung cancer (6)

A

smoking, second hand smoke, family hx BIG, previous tobacco-related cancer, occupational exposure, COPD

119
Q

women are more likely to get this type of lung cancer

A

adenocarcinomas, non-smoking related lung cancer

120
Q

evidence suggests that the biological difference seen in women with lung cancer is, in part, due to?

A

estrogen signaling

121
Q

areas of previous scarring (such as fibrotic lung dz) may be a precurser for this type of cancer

A

adenocarcinomas

122
Q

this type of non-small cell lung cancer is most likely to metastasize

A

adenocarcinomas

123
Q

hypertrophic periosteoarthritis and clubbing are signs of?

A

adenocarcinoma

124
Q

these lungs cancers are usually central

A

squamous cell, small cell

125
Q

this lung cancer is usually peripheral

A

adenocarcinoma

126
Q

BAC is now known as?

A

non-mucinous adenocarcinoma with lepidic features (adenocarcinoma in situ)

127
Q

is ACIS more common in men or women? Smokers or non-smokers?

A

women, non-smokers

128
Q

this is the only primary lung cancer that can present with multiple nodules

A

BAC/ACIS

129
Q

what does ACIS look like on a HRCT?

A

ground glass, infiltrate/consolidation with air bronchograms

130
Q

what lung cancer frequently causes frothy sputum?

A

BAC/ACIS

131
Q

this lung cancer occurs in smokers, causes obstruction of the airway with distal atelectasis, may cavitate, and presents with hypercalcemia and clubbing

A

squamous cell

132
Q

this substance is the cause of hypercalcemia in lung cancer

A

PTH-like substance produced by tumor

133
Q

hypercalcemia is never seen in this type of lung cancer

A

small cell lung cancer

134
Q

bulky central tumor with extensive mediastinal lymph node involvement, grows rapidly and presents with SIADH

A

small cell lung cancer

135
Q

what are the symptoms of SIADH

A

low sodium assoc with mental status changes

136
Q

specific symptoms assoc with lung cancer

A

cough, hemoptysis, dyspnea, hoarseness, SVC syndrome, headache, mental status changes, sx of pneumonia, chest wall or bone pain

137
Q

what are paraneoplastic syndromes?

A

clinical disorders not related to size or metastasis of cancer; may even precede diagnosis

138
Q

paraneoplastic syndromes seen in non-small cell lung cancer

A

hypercalcemia, HPO, clubbing

139
Q

paraneoplastic syndromes seen in small cell lung cancer

A

SIADH, Cushing’s, Lambert-Eaton (muscle weakness), cerebellar degen, periph neuropathy, weight loss

140
Q

best diagnostic test for primary lung cancer

A

endobronchial biopsy

141
Q

what are the downsides to sputum cytology?

A

need more than 3 specimens, negative result does not exclude cancer

142
Q

what should be done to assess whether a pleural effusion is malignant or paramalignant?

A

thoracentesis

143
Q

when and how should transthoracic needle biopsies be performed?

A

to diagnose a peripheral lesion; perform under CT guidance

144
Q

non-small cell lung cancer is usually diagnosed at what stage?

A

stage IV

145
Q

treatment for early stage non-small cell lung cancer

A

surgical resection (plus chemo after sometimes for hilar node, mediastinal node, large tumor)

146
Q

treatment of locally advanced NSCLC

A

chemo + surgery, chemo + radiation (combination tx)

147
Q

treatment of stage IV NSCLC

A

considered incurable, palliative care only; chemotx improves survival, sx control, and QoL; standard of care to differentiate subtype

148
Q

specific mutations seen in NSCLC

A

EGFR, KRAS

149
Q

predominant risk factor for SCLC

A

smoking

150
Q

median survival for SCLC without tx

A

2-4 months

151
Q

what are the stages of SCLC?

A

limited vs extensive

152
Q

limited SCLC

A

confined to hemithorax

153
Q

extensive SCLC

A

tumor beyond radiation port, including malignant pleural effusion

154
Q

treatment of limited SCLC

A

chemo + XRT, prophylactic cranial radiation (1.5 year survival)

155
Q

treatment of extensive SCLC

A

same as limited, but still only 5-10% survival at 2 years (less than 1 year survival)

156
Q

what happens if you screen 55-79 year old smokers with low dose spiral CT?

A

decreased mortality, but LOTS OF FALSE POSITIVES

157
Q

smoking cessation decreases pathology of these diseases

A

COPD, CVD, lung cancer

Respiratory (15 decks)

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