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Clin Med I - Comprehensive > Pulmonology > Flashcards

Pulmonology Flashcards

1
Q

What is an Occupational/ Env’al Lung Disease? (Define)

A

Respiratory system dysfunction CAUSED BY or EXACERBATED BY contact with antigens or irritants that are inhales, resulting in acute or chronic illness

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2
Q

What factors determine the pathological result of a toxic inhalation

A
  • Size: smaller travels further
  • Solubility: more soluble travels less
  • Concentration: potency
  • Duration of exposure: also kind of potency
  • Host factors: age, genetics, smoker?, co-morbid conditions, use of protective gear?
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3
Q

What sizes of particles travel where, what fraction do they qualified as,and what type disease do they cause?

A

<100µm : “Inhalable fraction” : enters throatIrritation<10µm : “thoracic fraction” : past the bronchusAcute disease<4µm : “Respirable fraction” : AlveoliChronic disease

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4
Q

Common Occupational/ Env’al Diseases 5 categories

A
  • Airway diseases: Asthma, Reactive Airway Dysfunction Syndrome (RADS), Bronchiolitis Obliterans (BO), Bronchiolitis Obliterans Organizing Pneumonia (BOOP)
  • Pneumoconiosis: Silicosis, Coal Workers Pneumoconiosis (PWC), asbestosis
  • Hypersensitivity pneumonitis
  • Cancer
  • Burn
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5
Q

Upper airway exposure characteristicsWhat’s affected, how, and what to do

A
  • Lg, very water solubledamaging nasopharynx and larynx (edema to epithelial ulceration and frank hemorrhage)
  • Symptoms are short, burning, cough, sputum, sneezing, SOB, bronchospasm (reflex) and hemorrhage
  • remove pt from exposure, irrigation, supplemental al O2, secure airway, give steroid if appropriate, racemic epi
  • example would be ammonia, chlorine gas,
    slide 9 shows burns from anhydous ammonia exposure from gas tank on truck
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6
Q

What can you do for BO, what causes it

A

no, not deodorant, I’m talking about bronchiolitis obliterans:can’t do anything, but systemic steroids may helpsulfur dioxide, Nitrogen oxide gas exposure

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7
Q

What does BO look like?Signs and symptoms

A

dyspnea on exertion,early inspiratory crackle on exam (OR NORMAL)CXR may be normalPFTs may be obstructive pattern (rarely also restrictive)Diagnose via lung biopsy(also History will tell about exposure)

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8
Q

What’s an example of Lower Airway Disease, and how does it present?

A

BOOP

  • fever, dry cough, dyspnea on exertion (like pnemonia)
  • late inspiratory crackle on exam CXR with bilateral patchy infiltrate(BO has none)
  • PFTs typical with restrictive pattern and low DLCO (diffusion of Lung for CO2)
  • Diagnosis is via lung biopsy
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9
Q

What can cause BOOP?How do you treat?

A

Chronic sequel of irritant gas exposureSystemic steroid is usually very helpful for 6-7 months

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10
Q

What does RADS stand for, and what does it look like?(natural history of RADS)

A

Reactive Airway Dysfunction SyndromeLooks like asthma, but not immune mediated,Burn-like damage to airway epithelium

  • short-term exposure with high intensityto respiratory irritant. with onset in hrs-a day
  • cough, wheeze, SOB
  • symptoms last for months, but may remain permanently, in which case the diagnosis changes to asthma.
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11
Q

Tx for RADS

A

Bronchodilators may help

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12
Q

Occupational Asthma is the same as __________ _______ AsthmaWhat percentage of adult asthma is this?Cause?

A

Work Related Asthma (WRA)15-20%Over 450 agents known and growingProdromal symptoms of UA irritation for some

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13
Q

With OA/ WRA, name two pathways to get it

A

With latency: immunologic bases:High molecular weight >5000 KD, low molecular weight <5000 KDWith out latency: irritant asthma/RADSfaster development than allergen

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14
Q

Symptoms/Risks for OA with latencyRisk factors, and how to make it better

A
  • After chronic daily exposure:
    UA irritation, rhinorrhea, eye itching,Cough mostly while at work/ after workday, wheezing, SOB
  • improves when away from work (weekends)
  • Risk factors include allergies in family (“Atopy”), smoking, genetics
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15
Q

Pathophysiology of OA with LatencyTwo types of agents

A

High molecular weight agents: animal producs, plants, insects, gum, latex, detergentsIgE dependent classic immediate hypersensitivity reactionsIgE attacks inhaled Lg molecule (usually protein)Low molecular weight agents: diisocyanates (foam, pneumonic for occupational exposure), anhydrides, fluxes, wood dust, pharmaceuticalsIgE against LMW + protein (needs protein to respond cuz otherwise it’s too small)

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16
Q

Legal Dx of OA/WRA

A
  • Physician diagnosis of asthma
  • Onset OR WORSENING of asthma after entering workplace
  • Association between symptoms of asthma and work
  • Need 1-3 plus One of the following
  • workplace exposure to agent known to cause occupational asthma
  • work related changes (wrc) in FEV1, or PEF
  • or wrcin bronchial responsiveness
  • Positive response to specific inhalation challenge test
  • Onset of asthma with a clear association with a symptomatic exposure to an inhaled irritant agent in the workplace
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17
Q

Tx for OA/ WRA

A

avoid exposure (change job, living place)protective devices (masks, respirators)usual asthma meds NOT SO HELPFULContinuous exposure may cuase progressive damage

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18
Q

Byssinosis

A

“Monday morning fever and chest tightness”From cotton processing (around the Mississippi river/ Nile river), also yarn, flax, and hempmay become chronic symptoms of cough, tightness of chest, and SOB

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19
Q

Monday morning fever is called that because…What causes it?

A

Byssinosis= Brown lung= Monday morning feversymptoms improve upon repeated exposuresfrom exposure to endotoxins produced by microbial agents contaminating cotton plant

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20
Q

Coal Workers Pneumoconiosis (CWP)

A

aka black lung relatively high exposure from a long exposure 20-30 years

Parenchymal lung disease due to inhalation of coal dust
* cilia try to get it out, but eventually get overwhelmed excess dust precipitate in µ0 and release cytokines–> fibroblasts accumulate aroundµ0 and make reticulin, ultimately collagen formation :coal macule
Cole macule–> coal nodule
More common with Anthracite, than Bituminous

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21
Q

3 types of CWP

A

Simple: asymptomatic, but with small spots (<1cm) on CXR usually in upper part of lungComplicated: coalesces of small nodules to form spots >1cmProgressive Massive Fibrosis :progresses toend-stage lung diseaseCaplan syndrome: formation of nodules in upper lobe and rheumatoid arthritis… rare

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22
Q

Sign/ Symptom of CWP

A

accumulation of carbon dust usually no symptoms withAnthracosisSimple CWP : no symptomsComplicated CWP:progressive dyspnea, cough, sputum, melanoptysis, crackles, and finger clubbing, pulmonary fibrosis–> chronic respiratory failureDecline in FEV1, FVC though years, Decline in DLCO, and hypoxia is obviously present in advanced disease

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23
Q

Dx of CWP

A

In context with exposure, radiographic findings, no need for more testsBiopsy may be needed for atypical cases or when high probability for cancer (usually with PMF– lots of coal workers are old, and are smokers)nodule may bleed during biopsy, as they are so vascular

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24
Q

Tx of black lung

A

none…prevention, early recognition, tx of complicationsbaseline within first 30 days of working, at least every 5 years sinceavoide exposurevaccinationmanaging COPD/ smoking

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25
Q

Describe Silicosis

A

fibrosing disease of lungs from inhalation, retention, and pulmonary reaction to crystalline silica.

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26
Q

who gets silicosis?

A

worse disease for miners, those who work in quarries, drilling, sandblasters,(silica is freshly fractured = higher risk)but also cementers/concrete production, highway repair, potters, foundries, and dental labs.

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27
Q

Pathophysiology of Silicosis

A

Macrophages trap the silica, and release cytokines.Fibroblasts migrate and release reticulin, and formulate hyalinzed collagen fibers to form a silicotic nodule.

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28
Q

What is a silicotic nodule?

A

concentric whorled hyalinized collagen fibers with no cells in the middle.Surrounded by cellular connective tissue with reticulin fibers. Birefringent particles are seen in the periphery of the silicotic nodule when examined under polarized light.

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29
Q

Symptoms of Silicosis

A
  • Dyspnea on exertion
  • cough sputum
  • hemoptysis
  • weightloss (usually with TB and/or cancer)
  • Chronic hypoxic respiration failutre with PMF
  • Increases risk of lung cancer (class 2 carcinogen)
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30
Q

3 Types of silicosis presentation?

A

3 Typical presentations: chronic, accelerated, and acuteChronic:Small round nodular densities in upper lobes (ceiling cosis) after a 10-20 yrs exposure. Slow progression with PMF formation >1cmAccelerated: 5-10 years of exposure to relatively higher concentrations. Rapid progression of symptoms. Associated with autoimmune (RA, SLE, scleroderma)Acute:few mths-1 year (up to 5 yrs)aftermassive inhalationof silica, experience acute dyspnea with diffuse lung involvement (lower lung fields). Rapid progression to respiratory failure/death

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31
Q

What is silicosis commonly associated with

A

silico TB (more common with accelerated and acute formHappens because killing off macrophages so more likely to get TB, because can’t fight off mycobacteriumConsider as a differential if fever, weightloss, and productive cough.

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32
Q

Signs of Silicosis

A

Abnormal PFTs before radiographic changesRestrictive and obstructive mixed patternDecrease in DLCOLow PaO2 on ABGNo correlation between PFTs and CRX findings, so do both, and get good H&P

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33
Q

Dx of Silicosis includes

A

Known exposure and radiographic findings is enought, but may also get biopsy to rule out atypical cases, or when high probability for cancer. (esp. if hemoptysis, weight loss)

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34
Q

Tx of Silicosis

A

Prevention: decrease expsure, regular exams with PFTs and CXRs, and remove workers with earlierst signs of silicosis on CXR.Tx complicationsTB: 8 mths,Cancer, pneumothorax.Acute silicosis: whole lung lavage while waiting for a heart/ lung transplant

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35
Q

Asbestos is found in

A

mining, milling, ship building, pipe fitters, boilers, breakes and clutch linings, fire smothering blankets, safety garments.Also those with bystander exposure (painters, electritians, and “women washing husband’s clothes”)In the US, replaced in 1975 with synthetic fibers

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36
Q

What makes a fiber a fiber

A

size. they have a 3:1 ratio of length to width. or 5:1 or more.They move through lungs like a sword moving with gravity when air is slow, and turbulent flow can knock them into the sides of bronchus-bronchioles, especially at birfurcationslike the carina, but can also get all the way to the alveoli

37
Q

Asbestos Diseases include the following 5 conditions

A

Asbestosis: chronic fibrosing disease of the lung
Benign asbestos related pleural effusion=BAPE: younger pts, 10-15 after exposure.Follow for 3 yrs and if tumor free it’s BAPE.
Pleural plaque and pleural calcification:MOST COMMON

Round atelectaisis
Mesothelioma

38
Q

cardinal sign of asbestos exposure

A

Asbestos body:yellow-brown structure seen with light microscopyit’s a asbestos fiber encased in melange of iron/calcium salt/ protein

39
Q

Signs and Symptoms of Asbestosis

A

Dyspnea on exertioncough/ sputumchest tightnesswheezingCXR: reticulonodular pattern predominantly in the basis (base) of the lungPFT: Restrictive pattern sith low DLCO, may also be obstructive pattern too

40
Q

Dx for asbestosis

A

Confirmed exposure, appropriate duration of exposure, CRX findings classic for asbestosis.In unusual cases, biopsy may be needed (evidence of fibrosis, presence of asbestos fibers)

41
Q

Tx of asbestosis

A

no tx for this…usually ends up in respiratory failuresurvey for malignancy (lung cancer/ mesothelioma)Demo of old buildings (built before 1975) is MC exposure.

42
Q

Describe BAPE

A

Benign asbestos related pleural effusion=BAPE: younger pts, 10-15 after exposure. bloody exudate, chest pain, tightness, cough, fever, 50% with no symptoms, symptoms can clear and reoccur in other side. thorocentesis and pleural biopsy needed for dx. Follow for 3 yrs and if tumor free it’s BAPE. risk for pleural thickening.

43
Q

Pleural Plaque description

A

MC type of asbestosis exposure.focal, irregular, raised white lesions, found on parietal and visceral pleura. (seen on PA chest radiograph)A reaction of mesothelial cells to asbestos fibers.SLOW growing plaquesRARE to turn to malignant lesionPFT show slow decline in FVCNo Tx, only surveillance.

44
Q

Describe Round Atelectasis

A

Swelling/ inflammation of pleura traps a portion of the lung and causes the atelectasis. Fluid in the pleural space pushes the pleura and makes fissures that wraps around aportion of the lung. ie a circle of the lung calapses in that areaMore common in menSurgery if significant deterioration/ suspicion of cancer

45
Q

Mesothelioma and highest risk of dangerous form

A

Asbestos exposure, most dangerous form is Crocidolite fiber. M>F 3-4:1rises from parietal or visceral pleura, or on peritoneumassociated with pleural effusion

46
Q

Symptoms, Tx, and Prognosis for Mesothelioma

A

Chest pain, dyspnea, sometimes cough/feverPleural effusion is not uncommonmay invade lungs or chest wallbiopsy open lung needed for dx (using just a needle can spread the cells on the way out)surgery not helpfulnew chemo under investigationmedian survival 8-12 monthsbeing male/ old on dx= poor prognosis

47
Q

Name 4 types of plant inhalants not yet covered (think similar to brown lung), and 2 metal inhalant diseasesand some symptoms after exposure

A

Grain dust: can cause COPD like symptoms with productive cough, and obstructive defects on PFTs, smoking exasturbatesSilo filler’s Disease:exposure to oxides of N particularly NO2. redish brown gas, heavier than air, smells like bleach. Mild exposure: airway irritaion, cough, chest tightness, dyspnea, fatigue. Heacy/ long term exposure: pulmonary edema, asphyxiation, ARDS (Sept-October)Polymer Fume:Teflon makes fluoropolymers which are volatized upon heating. Causes fever, chills, malaise, and sometimes mild wheezing.Metal Fume Fever:acute exposure to fumes/smoke with zinc oxide: causes flu-like symptoms, (welding galvanized steel, symtomswithin hours of exposure, resolve in 24 hrs, recur with exposure)

48
Q

What is Berylliosis

A

Berylliosis Was fluorescent lamp manufacturing, but now Computer/ electronics industryacute relatively large exposure leads to tracheo bronchitisChronic exposureleads to granulomatous parenchymal lung diseasejust likesarcoidosisCRX with miliary pattern (mottled) & lymphedenopathyConfirm Dx with espourehx, lymphocyte proliferation and beryllium in lung

49
Q

Hard Metal Lung Disease :​

A

interstitial lung disease from exposure to powdered tungsten carbide, cobalt. from cutting tools, drill bits. shows up as bronchiolitis, granulomatous, or fibrotic disease. Avoid exposure, steroids can help. also occupational asthma.

50
Q

Hypersentisitvity Pneumonitis (HP)

A

Inflammation disorder from alveolar walls and terminal airways induced by repeated inhallation of organic agents. Farmer’s lung, bird fancier’s disease, and chemical workers. Frequency of HP varies with env’al exposure, and specific antigen.Finnish farmers showed 44:10,000 incidence rate.

51
Q

Pathogenesis & symptoms of HP

A

HP:repeated antigen exposure: immune sensitization of host inflammatory infiltrate in lung (TH1 cells) leading to chronic cellular immune response with granuloma formation. Cell mediated responserepeated exposure to offending agent is sub acute(6mths) then chronic form of disease is progressive to irreversible interstitial fibrosis.

52
Q

Symptoms/ Signs of HP(acute, subacute, chronic)

A

Acute HP:4-12 hours after exposure: abrupt viral-like respiratory symptoms: cough, dyspnea, chest tightness, fevers, chills, malaise with crackles, tachycardia, tachypnea, feverSubacute:dyspnea, cough, sputum, fatigue, malaise, chest tightness, weight loss. crackles, occasional wheezes, hypoxiaChronic HP:Dyspnea, cough, symptoms of heart failure, cyanosis, clubbing, crackles, peripheral edema.

53
Q

Diagnosis and Tx of HP

A

Confirmed by biopsy of transbronchial, VATS see loose non-caseating granulomas.On CT see ill-defined nodularities, haziness on CXRDx: chronological order of symptoms and exposure, presence of repeated exposure hx and symptoms. presence of precipitating IgG antibody against the offending agent (although this is not Sn or Sp)Tx: removal of offending agent, avoidance. Steroid is tx for all three forms.

54
Q

Differential Dx for HP

A

Acute HP: Asthma, URI, Viral Phenmonia, Inhalation feverSubacute/ Chronic: sarcoidosis, interstitial lung disease, lymphoma

55
Q

Etiology of asthma

A

Conductive airways disease of chronic inflammation

56
Q

What is the negative pressure in the chest?How is it created?

A

-4 because in the chest cavity it is 756,and the lungs are 760, so the interpleural space creates a negative 4 with the visceral pleura sticking to the lungs, and the parietal pleura sticking to the expanded chest cavity from the diaphragm contraction (expansion down)

57
Q

How does the resistance change in the “pipes”How does it happen in asthma?

A

Resistance is higher on the walls, thus slower, but it is overcomable if the pressure is increasedThe higher the resistance, the lower the flow.But you can increase the force by pushing out air faster to keep the flow the same… this is why asthmatics have to work harder to push the air out, and that extra energy expense can make them more tired, in addition to the increased mucous that blocks oxygen exchange.

58
Q

The greater the resistance… what does flow do?

A

Flow “slows” which means lower FEV1

59
Q

A wheeze is what kind of flow

A

Turbulent More resistance than laminar

60
Q

Describe the resistance in pipes. Adding up series and parellel, which has more. Use these numbers to tell me why…3 In series of pipes with each resistance =2Vs.3 pipes in parallel each with resistance of 2

A

Parallel has less resistance because to add them, you do the reverse so… In series: 2+2+2=6resistanceIn parallel: 1/2+1/2+1/2= 1.5 resistance

61
Q

1 trachea, how many small airways

A

Several thousand less than 2mm diameter

62
Q

Trachea have higher or lower resistance than bronchioles?

A

Higher resistance, because it is not in parallel, but bronchioles are

63
Q

Air way resistance _________(rises or falls) when the lung is reaching capacity.

A

Falls because we are pulling the airway open to a larger volume

64
Q

Because even diseased airways are stretched open to a wider size, and that means it is earlier to get air in, or out?

A

Easier in because when they are expanded, they have less surface area to volume, so resistance on the way in is less

65
Q

Why do people with COPD and asthma purse their lips when they exhale?

A

They’re trying to keep the pressure up in their airways to make exhale easier since that will make the airway stay expanded so they get less resistance.

66
Q

What can the body do to change the distribution of air flow if a certain area is compromised, say by being filled with blood after a car accident?

A

It can bronchoconstrict with the vagal (parasymp) innervation, using ACh/ methacholine, Also can use histamine, and it will constrict if it detects a decrease in PACO2.It can bronchodilate with beta2 adrenergic receptors.Matching blood flow to perfusion

67
Q

Asthma is worse during the day!True or falseExplain the mechanism why

A

False. Less Catecholemines (NE,Epi, DA) at night and early morning hours… the catecholomines are sympathetic, and so they are less active at night so we can rest, but they also bronchidilate… less dilation= more asthma, waking asthmatics up to cough

68
Q

Why are allergies related to asthma?

A

Because histamines bronchoconstrict, creating wheezing… turbulent breath …aka asthma with exhalation .

69
Q

Forced vital capacity maneuver is normal if it can be done in…

A

3 seconds… it is really the airway resistance that is normal if they can complete the FVC expiration in 3seconds

70
Q

Most people just look at FEV1, and FEV, and the ratio of FEV1/FEV, but Dr. Delaney thinks we should also look at…

A

The middle section of the breath, especially if FEV1 and the FEV1/FEV ratio is normal.This is the MMEFR: maximum mid-expiration flow rate aka FEF25-75.

71
Q

Why should we also look at MMEFR?

A

Because it is better insight into the small airways, so particularly important for asthma and COPD

72
Q

FEV= ____-_____= ______All those acronyms from the breathing graph made by electronic spirometers

A

FEV = FVC=TLC- RV

73
Q

How do we suspect people have asthma?

A

Compare expected FEV1/FEV to the patient’s, and it will be lower than expected.

74
Q

How does the residual volume in patients with asthma change during an attack/ in general?

A

The residual volume is increased compared to expected for age and height because they are blowing out hard and fast, so there is more air trapped behind.

75
Q

In a flow volume loop, why does the slope decrease in the expiration?

A

Loosing the driving pressure, and the airways are getting smaller, so it’s harder to push the last part of the air out.

76
Q

A peak flow meter can also tell you if they have max effort by…

A

Looking at the initial curve… should go highest at beginning. If not they either didn’t inhale enough, or blew out too slowly. See slide 21 for graphic

77
Q

How do you know if someone has an obstructive ventilate defect?

A

FEV1/FEV is lower than 70%

78
Q

Three mechanisms in asthma/ COPD that make it obstructive, and which does asthma have?

A

1) More secretions than can be cleared2) Inflammation of the wall, swelling and impinging lumen3) breakdown of surrounding tissue, only in COPD

79
Q

What are some common triggers for asthma symptoms

A

Viral infections, cold air, allergens, tobacco smoke, exercise, stress, night/ parasympathetic

80
Q

Our current treatment goals for asthma is to treat symptoms, prevent attacks, and prevent__________

A

Remodeling from scar tissue from long term inflammation. This is done with steroids, and symptomatic treatment is with adrenergics.

81
Q

What wbc is high in asthmatics?

A

Eosinophilia disease. Because… allergiesMaybe also good at attacking parasites. ;)

82
Q

Which th cells are seen in asthma?

A

Th2 are more, but both are present always… the allergic response shifts to a TH2 predominance, and they are producing interlukens, which perpetuate the inflammation cycle and make more eosinophils, which make more interlukens .etc…

83
Q

What muscles let an asthmatic develop higher force of expiration

A

Scalenes, SCM, intercostals( accessory muscles) which work to expand rib cage and clavicles higher to further expand area of lung.

84
Q

Hallmark diagnostic for asthma vs. other obstructive diseases

A

allergy related, night time coughing, FEV1/FVC is under 75%, have exasurbations, and feel breathless, and chest tightness.

85
Q

Why do asthmatics cough at night

A

because their constriction is parasympathetic, which is more active at rest, so their bronchioles are constricting under Acetylcholine. Also from histamines.

86
Q

What other things are asthma patients likely to have

A

can be related to nasal polyps, skin allergies, eczema, familial allergies, environmental exposure, sinusitis, GERD, possibly sleep apnea

87
Q

normally it takes ___ seconds to expel FVC

A

3.

88
Q

Why does FEV1/FVC tell us it might be asthma?

A

Because if it is low ratio that means it has a high resistance to get the air out, and there is air trapping.

89
Q

If FEV1/FVC is normal but you still suspect asthma, what can you look at?

A

the second half of forced expiration. aka FEF25-75. aka MMER. That will tell us what is happening in the distal airway

Clin Med I - Comprehensive (6 decks)

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