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Pulmonary Review > Diffuse Parenchymal Lung Disease > Flashcards

Diffuse Parenchymal Lung Disease Flashcards

1
Q

This is the pulmonary alveolar and capillary endothelium and the spaces between the perivascular and perilymphatic tissues. Centrally, it involves the peribronchiolar and peribronchial tissues.

A

Parenchyma

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2
Q

Which of the following are “major” idiopathic intersititial pneumonias?

IPF, LIP, NSIP, RBILD, PPFE, DIP, COP, AIP

A 
IPF
NSIP
RBILD
DIP
COP
AIP
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3
Q

What is the gold standard imaging for DPLD?

A

HRCT

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4
Q

True/False: bronchoscopy is indicated for all establishment of diagnosis for DPLD.

A

FALSE

It’s useful to exlude other infection, DAH, and eosinophilia

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5
Q

What WBC cell line is increased on BAL in NSIP?

A

BAL usually shows >20% lymphocytes

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6
Q

There is usually a mixed pattern of WBCs on BAL in COP, but what happens to the CD4/CD8 ratio?

A

Usually decreased

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7
Q

BAL showing >5% CD1a-positive cells is diagnostic of what DPLD on BAL?

A

Pulmonary Langerhans cell histiocytosis

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8
Q

BAL showing eosinophilia (>20-25%) is seen in what DPLD?

A

Acute and chronic eosinophilic pneumonia

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9
Q

What is the gold standard for diagnosing most IIP?

A

VATS surgical lung biopsy

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10
Q

True/False: UIP is seen only on pathology in patients with IPF

A

False

Can be seen in connective tissue diseases, asbestosis, drug-induced lung disease, and environmental and occupational exposure

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11
Q

Median survival of IPF after diagnosis?

A

3-5 years

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12
Q

Where is the fibrosis on CT in IPF?

A

Basilar and peripheral fibrosis, microscopic subpleural and paraseptal fibrosis

Also see some honeycoming

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13
Q

True/False: this patient needs a surgical lung biopsy for the diagnosis of IPF.

65 y/o presents with dyspnea. CT shows fibrosis in subpleural site, basilar predominancy, reticular abnormalities, and honeycoming

A

FALSE

This pattern is classic for IPF, therefore no Bx needed

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14
Q

True/False:

There are associations between IPF and history of smoking, GERD, and occupational/environmental exposures

A

TRUE

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15
Q

FVC and DLCO cutoffs for lung transplant listing in IPF?

A

FVC < 60% predicted

DLCO < 40% predicted

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16
Q

Which one is typically steroid responsive - NSIP or IPF?

A

NSIP

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17
Q

This form of NSIP shows mild to moderate intersitial chronic inflammation, type II pneumocyte hyperplasia in areas of inflammation

A

Cellular NSIP

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18
Q

This form of NSIP has dense or loose interstitial fibrosis with uniform appearance, lung architexture is frequently preserved, and there are absence of fibroblastic foci

A

Fibrotic NSIP

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19
Q

Which is more steroid responsive and has a better prognosis, fibrotic or cellular NSIP?

A

Cellular NSIP

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20
Q

What are the known
genetic associations with
pulmonary fibrosis?

A 
Mutations in hTERT and
hTR are risk factors for
pulmonary fibrosis
underlying the inheritance
in 8–15% of familial cases.
In these families, IPF is
inherited as an autosomal
dominant trait with agedependent
penetrance.
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21
Q

What is seen on CT for NSIP?

A

Diffuse GGO’s
Reticular opacities
Traction bronchiectasis
NO honeycoming

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22
Q

This medication used in the treatment of NSIP has the following side effects:

Hyperglycemia, HTN, insomnia

A

Glucocorticoids

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23
Q

This medication used in the treatment of NSIP has the following side effects:

GI upset, abnormal LFTs

A

Azathioprine

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24
Q

This medication used in the treatment of NSIP has the following side effects:

GI upset, abnormal LFTs, leukopenia

A

Mycophenolate mofetil

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25
Q

This medication used in the treatment of NSIP has the following side effects:

Bladder cancer, neutropenia

A

Cyclophosphamide

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26
Q

This form of DPLD is believed to follow an inciting injury that causes chronic lung inflammation, buds of intra-alveolar granulation tissue, this causes alveolar epithelial injury with cell death and denudation of basal laminae. Fibroblasts then deposit matrix in layers creating appearance intra-alveolar buds.

A

COP/BOOP

BOOP is a way better name. Why did they change that.

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27
Q

So what is seen on histopathology in COP?

A

Intra-alveolar buds of granulation tissue made of myofibroblasts, fibroblasts, and loose connective tissue in similar age

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28
Q

What is seen on CT scans in COP?

A

Multiple migratory patchy alveolar infiltrates (GGO’s or consolidation that are preipheral/basilar, can also see air bronchograms

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29
Q

True/False: most patients need a surgical lung biopsy for the diagnosis of COP

A

TRUE

Have to r/o other conditions, and TBBx are less reliable because of the patchy nature of the disease

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30
Q

Mainstay of treatment for COP?

A

Steroids, usually need long course (6-12 months)

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31
Q

This form of DPLD is rapidly progressive, can have viral prodrome, similar to ARDS but without a specific cause

A

AIP (Hamman Rich Syndrome)

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32
Q

What is seen on biopsy of AIP?

A

Diffuse alveolar damage

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33
Q

What are the 2 stages of AIP?

A

Initially there is edema, hyaline membranes, and microbascular thrombi –> loose organizing fibrosis with alveolar septa and type II pneumocytes

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34
Q

What is done to confirm the diagnosis of AIP?

A

Sugical lung biopsy - shows DAD

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35
Q

Treatment of AIP?

A

Thoughts and prayers

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36
Q

This DPLD is characterized by interstitial process in smokers and lung biopsy shows bronchiolitis

A

RBILD

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37
Q

Which of the following characteristic(s) is seen on lung biopsy of RBILD:

  • Fibrosis
  • Pigmented alveolar macrophages in and around the respiratory bronchioles and surrounding alveoli
  • Interstitial inflammation
  • Germinal centers
A

Pigmented alveolar macrophages in and around the respiratory bronchioles and surrounding alveoli

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38
Q

What is seen on CT for RBILD?

A

Bronchial wall thickening
Fine centrilobular nodules
Bilateral patchy GGO in upper and lower lung zones
Possible emphysema (these are smokers afterall)

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39
Q

Treatment of RBILD?

A

Stop that whacko tobacco

The roids dont work.

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40
Q

This form of DPLD on histopathology shows pigment-laden macrophages in alveolar spaces in a homogenous pattern with preserved alveolar architecture and minimal fibrosis or honeycoming

A

DIP

The pigment in the macrophages from the smoke

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41
Q

What is seen on HRCT in DIP?

A

peripheral GGOs in lower lung zones, no honeycombing, possible small lung cysts and emphysematous changes

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42
Q

What is required to establish the diagnosis of DIP?

A

Surgical lung Bx

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43
Q

Treatment of DIP?

A

STOP SMOKING

Roids are controversial

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44
Q

What connective tissue disease is associated with LIP?

A

Sjogrens syndrome

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45
Q

What % of patients die within the first 5 years after the diagnosis of LIP?

A

50%

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46
Q

What is seen on pathology in LIP?

A

Interstitial and bronchovascular infiltrate of small lymphocytes and plasma cells

Poorly formed nonnecrotizing granulomas with multinucleated giant cells are sometimes seen

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47
Q

What is seen on HRCT in LIP?

A

Bilateral GGOs, centrilobular nodules, patchy bronchovascular thickening, interlobular septal thickening, and thin-walled cysts

lol like everything

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48
Q

What’s required for diagnosis of LIP?

A

Surgical lung Bx

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49
Q

Mainstay of treatment for LIP?

A

Steroids

Response is variable

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50
Q

Name 3 smoking-related ILDs

A

DIP
RBILD
Langerhans cell histiocytosis

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51
Q

Give me the connective tissue disorder (CTD) associated with the following antibody:

dsDNA

A

SLE

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52
Q

Give me the connective tissue disorder (CTD) associated with the following antibody:

SSA

A

SLE, SS, myositis

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53
Q

Give me the connective tissue disorder (CTD) associated with the following antibody:

SSB

A

Sjogrens syndrome

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54
Q

Give me the connective tissue disorder (CTD) associated with the following antibody:

Scl-70 (topoisomerase I)

A

Systemic sclerosis

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55
Q

Give me the connective tissue disorder (CTD) associated with the following antibody:

CCP

A

RA

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56
Q

Give me the connective tissue disorder (CTD) associated with the following antibody:

RNP

A

MCTD

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57
Q

Give me the connective tissue disorder (CTD) associated with the following antibody:

Jo-1, EJ, PL7

A

Dermatomyositis/polymyositis/antisynthetase syndrome

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58
Q

This type of CTD can cause ILD, obstructive airway disease, lung nodules, or pleural involvement.

A

Rheumatoid arthritis (RA)

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59
Q

What 5 histological patterns can be seen on biopsy on RA associated ILD?

A 
UIP (most common)
COP
Follicular bronchiolitis
LIP
DAD
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60
Q

As HRCT for RA associated ILD can show GGO, reticulation, bronchiectasis, and/or micronodules, what “patterns” can be seen as well?

A

UIP
NSIP
Bronchiolitis
COP

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61
Q

Treatment for RA associated ILD?

A

Steroids
Cytotoxic drugs (azathioprine, mycophenolate, cyclosporine, cyclophosphamide)
Biologics (TNFa inhibitors)
Lung transplant

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62
Q

This form of CTD can present with symptoms such as skin thickening, telangiectasias, digital nail pitting, GERD, esophageal dysmotility, and dysfunction

A

Systemic sclerosis (scleroderma)

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63
Q

What complication can occur in >15% of patients with scleroderma, which can be isolated or secondary to ILD?

A

Pulmonary arterial hypertension.

Elevated levels of endothelin-1 vasoconstriction, vascular endothelail cell proliferation, smooth muscle hypertrophy, and irreversible vascular remodeling in the lungs

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64
Q

Most common CT finding for scleroderma related ILD?

A

NSIP

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65
Q

Treatment for scleroderma related ILD?

A

Steroids (low dose only as high dose can cause renal crisis)

Cytotoxic drugs (cyclophophamide most common)

Lung transplant

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66
Q

Signs and symptoms of inflammatory myopathies (polymyositits, deermatomyositits, anti-synthetase syndrome)?

A

myalgias
muscle weakness
fatigue

Gottrons papules
Heliptrope rash
Mechanics hands

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67
Q

Most common CT findings on inflammatory myopathy associated ILD?

A

NSIP

Can also see UIP, COP, DAD

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68
Q

Inflammatory myopathy associated ILD is usually treated with steroids despite their lack of evidence. What is the most common cytotoxic medication used in this condition?

A

Azathioprine

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69
Q

What cytotoxic agent is used in inflammatory myopathy associated ILD in severe, life threatening disease?

A

Cyclophosphamide

Also, you can use mycophenolate, cyclosporine, methotrexate, IVIG, and rituxan

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70
Q

This form of CTD can present like cough, dyspnea, wheezing, chest pain, and sicca symptoms

A

Sjogren syndrome

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71
Q

What 4 patterns can be found on HRCT in Sjogren syndrome associated ILD?

A

NSIP
LIP
COP
UIP

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72
Q

Treatment for Sjogren associated ILD?

A

Steroids

Azathioprine

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73
Q

This manifestation of lupus presents with acute onset of fever, cough, dyspnea, and hypoxia that can lead to respiratory failure. After infection is ruled out, it’s treated with high doses of steroids.

A

Acute lupus pneumonitis

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74
Q

This manifestation of SLE is characterized by progressive hemorrhage on BAL fliuid with hemosiderine-laden macrophages.

A

DAH

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75
Q

Treatment for DAH related to SLE?

3 things

A

High dose steroids
Cyclophosphamide
Plasmapharesis

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76
Q

This manifestation of SLE associated ILD presents with dyspnea, pleuritic chest pain, small lung volume, and diaphragmatic elevation. Treated with steroids.

A

Shrinking lung syndrome

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77
Q

This manifestation of SLE associated ILD is seen in older men with insidious onset of cough and dyspnea. Treated with steroids and steroid-sparing agents (azathioprine, MMF). Cyclophosphamide reserved foir refractory cases

A

Chronic ILD

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78
Q

This form of CTD occurs in white younger smokers, presents with cough and dyspnea, secondary PTX (10-15%), fevers, weight loss, malaise, anorexia, pulmonary HTN.

A

Pulmonary Langerhans Cell Histiocytosis

AKA histiocytosis X, pulmonary Langerhans granulomatosis, or pulmonary eosinophilic granuloma

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79
Q

Staining for which 2 antigens and protein is seen in the pathology for Langerhans?

A

CD1a antigen

S-100 protein

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80
Q

What are the names of the intracellular inclusions seen on electron microscopy in Langerhans?

A

Birbeck granules

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81
Q

CT findings for Langerhans?

A

Nodules and thin-walled cysts, mainly in the upper lung zones

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82
Q

Other than obviously to stop smoking, which things are used in severe/refractory Langerhans?

A

Steroids

Lung transplant

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83
Q

This form of ILD affects premenopausal women, characterized by hamartomatous proliferation of atypical smooth muscles along lymphatics in the lung, thorax, abdomen, and pelvis

A

LAM

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84
Q

What genetic condition is associated with LAM?

Hint: multisystem genetic disorder caused by mutation of the TSC1 or TSC2 gene

A

Tuberous sclerosis

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85
Q

True/False: recurrent pneumothorax is common in LAM

A

TRUE

Can affect 50-80% of patients

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86
Q

LAM cells come in 2 flavors: myofibroblast-like spindle-shaped cells and epithelioid-like polygonal cells. What 2 melanola-associated proteins do both cells express?

A

HMB-45

CD63

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87
Q

Which cells are pathognomic of pulmonary Langerhans cell histiocytosis on bronchoalveolar lavage?

A

BAL showing > 5% CD1a- positive cells is virtually diagnostic of pulmonary Langerhans cell histiocytosis.

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88
Q

HRCT findings for LAM?

A

Multiple thin-walled cysts with no specific region.

NO NODULES ARE SEEN (unlike Langerhans)

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89
Q

Which patients do not need a surgical lung biopsy for the diagnosis of LAM?

A

If they have characteristic features, as in ANY of the following:

Renal angiomyolipoma
Chronic chylous ascites with abdominal lymphadenopathy
Characteristic histopathologic findings on lymph node biopsy

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90
Q

As estrogen is involved in the pathogenesis for LAM, recommendation is to avoid pregnancy or exogenous estrogen. However, what medication is used in LAM?

A

Sirolimus (mTOR inhibitor)

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91
Q

TRUE/FALSE: corticosteroids can be used in the treatment for LAM

A

FALSE

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92
Q

The pathogenesis of this condition is from acute cigarette smoke exposure with other proallergic allergenic exposure leads to the release of inflmmatory cytokines, leading to massice recruitment and activation of eosinophils in lungs

A

Acute eosinophilic pneumonia (AEP)

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93
Q

HRCT findings for AEP?

A

Patchy alveolar GGOs, interlobular thickening, and pleural effusions

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94
Q

What % of eosinophils do you need to have on BAL in AEP in the setting of normal peripheral eosinophils?

A

> 20-25%

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95
Q

Treatment for AEP?

A

Smoking cessation and high doses of corticosteroids improves symptoms in first 24-48 hours

Keep on therapy for 2-4 weeks

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96
Q

This ILD is characterized by affecting middle-aged women, cough, dyspnea, fever, night sweats, asthma, elevated IgE, elevated peripheral eosinophilia.

A

Chronic Eosinophilic Pneumonia (CEP)

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97
Q

CXR findings for CEP?

A

Bilateral diffuse PERIPHERAL infiltrates

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98
Q

Though BAL will show eosinophilia in CEP, what will TBBx show?

A

Eosinophilic microabscesses
Low-grade vasculitis
Interstitial fibrosis

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99
Q

Treatment for CEP?

A

Steroids with a very slow taper

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100
Q

This condition is a chronic, multisystem disease with unknown etiology that is characterized by noncaseating granulomas

A

Sarcoidosis.

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101
Q

This mimicker of sarcoidosis is characterized by the following:

Patient works with circuit boards/electronics, similar findings on CXR, diagnosis made by lymph transfer test on BAL

A

Berylliosis

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102
Q

This mimicker of sarcoidosis is characterized by the following:

Medication used to treat HCV and other conditions that promotes granuloma formation

A

Interferon therapy

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103
Q

Responders to what national terrorist event have a high rate of pulmonary sarcoidosis?

A

World trade center responders

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104
Q

True/False: sarcoidosis is more prevalent in younger (<40 y/o) than older

A

TRUE

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105
Q

True/False: sarcoidosis affects women more than men

A

TRUE

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106
Q

True/False: sarcodiosis has the highest prevalence in Sweden, Denmark, and among African Americans

A

TRUE

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107
Q

True/False: sarcoidosis has no genetic links

A

FALSE

6% heredity in whites
17% in African americans

No specific gene, but histocompatability complex on chromosome 6p most studied

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108
Q

True/False: smoking is protective in sarcoidosis

A

TRUE

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109
Q

True/False: HLA DQB1*0201 is associated with favorable outcomes in sarcoidosis

A

TRUE

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110
Q

Describe stage 1, 2, 3, and 4 on imaging for sarcoidosis

A

1- hilar lymphadeopathy
2- adenopathy with lung disease
3- lung disease only
4- fibrosis and honeycoming

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111
Q

What form of sarcoidosis has the highest rate of spontaneous remission?

A

Nodular sarcoidosis

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112
Q

What are the 3 components to Lofgren syndrome?

A

Erythema nodosum
Hilar LAD
Arthralgias

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113
Q

Outcomes for Lofgren syndrome?

A

Resolves in 2 years in >90% of patients

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114
Q

Which ethnicities does the following extrathoracic forms of sarcoidosis affect:

Chronic uveitis
Lupus pernio
Erythema nodosum
Cardiac and ocular disease

A

Chronic uveitis - african americans

Lupus pernio - puerto ricans

Erythema nodosum- europeans

Cardiac and ocular disease - japanese

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115
Q

PFT findings in sarcoidosis?

A

Obstruction or restriction
Methacholine often positive
FVC and DLCO are most predictive long-term markers of disease

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116
Q

What is the role for ACE levels in sarcoidosis?

A

Not specific for the diagnosis but can be used for disease monitoring

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117
Q

What is the CD4:CD8 in sarcoidosis?

Bonus: sensitivity, specificity, PPV, and NPV

A

> 3.5

Sensitivity 53%, specificity of 94%, PPV 76%, NPV 85%

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118
Q

What is the normal distribution of granulomas in the lung?

A

Near or within the connective tissue sheath of bronchioles and subpleural or perilobular spaces (lymphangitis distrubution)

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119
Q

Spontaneous remission in sarcoidosis based on the stage of disease?

A

1 - 55-90%
2 - 40-70%
3 - 10-20%
4 - 0%

120
Q

When do you use chloroquine/hydroxychloroquine in sarcoidosis?

A

When there is skin and CNS disease

121
Q

When to use infliximab in sarcoidosis?

A

Refractory disease and extrapulmonary manifestations

122
Q

This condition is when there is lipoproteinaceous material accumulates in the alveolar tissue due to GM-CSF dysregulation

A

Pulmonary Alveolar Proteinosis (PAP)

123
Q

What is the mutation that causes congenital PAP?

A

Mutations on genes for surfactant B, C, or beta-c chair of the receptor for GM-CSF

124
Q

What exposures can cause secondary PAP?

A 
Silica exposure
PJP pneumonia
Malignancies
Autoimmune disease
Immune deficiencies
Certain drugs
125
Q

Which of the following suggest PAP on lab findings?

Elevated LDH
Elevated CEA
Cytokeratin 19
Mucin KL-6
Surfactant protein-A, B, or D
Serum or BAL showing GM-CSF antibodies
A

ALL OF THEM

126
Q

PFT findings on PAP?

A

Restrictive pattern

Decrease in DLCO out of proportion to restriction

127
Q

HRCT findings for PAP?

A

Patchy GGOs or cosolidation + Thickening of interlobular space = Crazy paving!!!

128
Q

Although you can expect to find BAL fluid for PAP to be a milky effluent that shows granular, acellular, eosinophilic, proteinaceous material with foamy macrophages, what finding of electron microscopy is confirmatory?

A

Lamellar bodies (concentrically laminated phospholipid structures)

129
Q

True/False: PAS+ proteinaceous alveolar deposits in the absence of a cellular infiltrate and normal septa are characteristic of PAP

130
Q

Average duration of effect for whole lung lavage in PAP?

A

~15 months

131
Q

What are the benefits for subQ or inhaled GM-CSG in PAP?

A

Oxygenation benefit

Some have complete response

132
Q

True/False: patients with PAP are at higher risk of infections, such as mycobacteria, aspergillus, and nocardia

133
Q

Most common condition that causes primary pulmonary amyloidosis?

A

Multiple myeloma

134
Q

What 3 areas of the lung are affected in pulmonary amyloidosis?

Also, their symptoms per area?

A

Parenchymal - cough, sputum production, dyspnea, hemoptysis

Tracheobronchial - wheezing, dyspnea, cough, hemoptysis

Upper airway - macroglossia with OSA

135
Q

What is seen on biopsy using polarized microscopy in pulmonary amyloidosis?

A

Apple-green birefringence

136
Q

What is seen on bronchoscopy in pulmonary amyloidosis?

A

Possible focal nodules or skiny pale plaques

137
Q

Other than obviously treating the underlying cause for pulmonary amyloidosis, what immunomodulator can be used to treat pleural effusions in primary systemic amyloidosis?

A

Bevacizumab

138
Q

True/False: median survival is 16 months in nodular-only pulmonary amyloidosis

A

FALSE

Nodular only is typically benign. Otherwise, survival is 16 months.

139
Q

This is an autosomal dominant disease that causes cystic lung disease, fibrofolliculomas, and skin tags

A

Birt-Hogg-Dube (BHD)

140
Q

Which tumor suppressor does the BDH gene encode for on chromosome 17?

A

Folliculin

141
Q

Is tracheobronchopathia osteochondroplastica associated with amyloid disease?

A

No, tracheobronchial amyloid is its own disease entity but can present very similarly. Submucosal involvement (posterior wall) is seen only with tracheobronchial amyloid disease.

142
Q

What tumors are more common in patients with BDH syndrome?

A

Renal tumors (RCC, oncocytic hybrid tumor, clear cell carcinoma)

143
Q

Symptoms of BHD?

A

PTX in 25% of patients, otherwise can cause dyspnea and cough

144
Q

How do you diagnose BHD?

A

Open lung biopsy

Helps exclude other things that can cause thin-walled cysts like LAM, LIP, LHC, and malignancies

145
Q

This condition is when there are lipid-laden macrophages seen on BAL in chronic laxative users (mineral oil)

A

Exogenous lipoid pneumonia

Also can be seen when people use old nasal sprays, aspiration, and bronchography

146
Q

What can cause endogenous lipoid pneumonia?

A

Proximal airway obstruction with resultant cholesterol-filled macrophages distally

Rarely associated with Neimann-Pick disease

147
Q

Chest CT scan findings on lipoid pneumonia?

A

Consolidations with or without GGOs, airspace nodules, and occasional crazy paving when associated with PAP

Negative Hounsfield units is diagnostic

148
Q

What special staining can be done to diagnose lipoid pneumonia?

A

Sudan black and oil red O

They should lipid-filled vacuoles

149
Q

What clinical presentation can the following medications cause (think drug induced lung injury):

ACEi, ARBs

150
Q

What clinical presentation can the following medications cause (think drug induced lung injury):

beta blockers, ASA/NSAIDs, cetuximab

A

Bronchospasm

151
Q

What clinical presentation can the following medications cause (think drug induced lung injury):

Tocolytics, IL-2, ASA, NSAIDS

A

Noncardiogenic pulmonary edema

152
Q

What clinical presentation can the following medications cause (think drug induced lung injury):

Methotrexate, taxanes, PCN, sulfa drugs

A

Hypersensitivity pneumonitis

153
Q

What clinical presentation can the following medications cause (think drug induced lung injury):

bleomycin, taxol, amiodarone, nitrofurnatoin

A

Chronic fibrosis

154
Q

What clinical presentation can the following medications cause (think drug induced lung injury):

Estrogren (and estrogen receptor agonists, especially with factor V Leiden mutation

155
Q

What clinical presentation can the following medications cause (think drug induced lung injury):

Hydralazine, isonizaid, penacillamine, procainamide, quinidine

156
Q

What clinical presentation can the following medications cause (think drug induced lung injury):

imatinib, dasatinib

A

Acute lung injury, pleural effusion

157
Q

What clinical presentation can the following medications cause (think drug induced lung injury):

Dasatinib, methamphetamine

A

pulmonary HTN

158
Q

Name the following drug that is known to cause lung injury based on the following characteristics:

Older patients, pathology shows foamy macrophages with fibrosis and lamellated inclusions, imaging shows fibrosis/COP/mass lesions with or without cavitation

A

Amiodarone

159
Q

Treatment for amiodarone lung toxicity?

A

Stop amio

Steroids for >6mo

160
Q

Name the following drug that is known to cause lung injury based on the following characteristics:

F>M, acute HP, COP, cellular NSIP, no zonal predominance, used in UTIs

A

Nitrofurnatoin

161
Q

Name the following drug that is known to cause lung injury based on the following characteristics:

Pneumonitis, fever, +/- rash, pulmonary eosinophilia, COP, NSIP pattern

A

5-ASA/Sulfasalazine

sulfa causes more than 5-ASA

162
Q

Name the following drug that is known to cause lung injury based on the following characteristics:

Acute/subacute/chronic presentation, HP, NSIP, AIP, occasional eosinophilia, rarely associated with NHL

A

methotrexate

163
Q

Name the following drug that is known to cause lung injury based on the following characteristics:

Used in CML therapy, patho shows pneumocyte dysplasia and typical broncial lining cells, imaging shows NSIP pattern, bronch rarely shows PAPq

164
Q

Name the following drug that is known to cause lung injury based on the following characteristics:

Various times of presentation, HP, DAD, NSIP, and UIP all possible, avoid high O2 delivery to avoid pulmonary toxicity

165
Q

Name the following drug that is known to cause lung injury based on the following characteristics:

Acute vs subacute presentation, noncariogenic pulmonary edema or AIP, imaging shows ALI and pleural effusions, pussible pulm HTN

A

Imatinib/dasatinib

166
Q

Name the following drug that is known to cause lung injury based on the following characteristics:

Potentially life-threatening pneumonitis, path shows sarcoidosis/ALI/COP, imaging shows ALI/effusions/COP, needs early discontinuation if suspected

A

Interferon

167
Q

Name the following drug that is known to cause lung injury based on the following characteristics:

Acute and chronic sequelae, forein body granulomatosis, ALI, imaging shows septic emobli/DAH/bullae/edema

168
Q

Name the following drug that is known to cause lung injury based on the following characteristics:

Subacute or chronic, path shows COP or NSIP, imaging shows GGO’s/COP/NSIP in a specific region

A

Radiation therapy

169
Q

Sandblasting, tunneling, drill operation, digging, glass manufacturing, hard rock mining, oven-brick making, stone cutting, masonry, foundry work, natural gas extraction via fracturing, and sandy and dry soil agriculture pose one to what pneumoconiosis?

170
Q

What are the timeframes for the chronic, accelerated, or acute silicosis based on presentation after exposure?

A

Chronic: 10-30yr after exposure

Accelerated: <10yr

Acute: weeks to 4-5yr

171
Q

Presentation of simple silocosis?

A

Mid-upper long zone nodules <1cm

172
Q

Presentation of massive fibrosis in silcosis?

A

Coalescence of lung nodules >1cm (with possible eggshell calcification), upward hilar retraction, lower lobe hyperinflation

173
Q

Presentation of acute silicosis?

A

Mid-lower zone GGOs with consolidation

174
Q

What stage of silicosis is seen on pathology given the following results (early, nodule, or acute)?

Peribronchovascular paraseptal, and subpleural dust-laden macrophages

175
Q

What stage of silicosis is seen on pathology given the following results (early, nodule, or acute)?

Concentric collagen fibers around a hyaline center

A

Silicotic nodule

176
Q

What stage of silicosis is seen on pathology given the following results (early, nodule, or acute)?

Alveolar filling with proteinaceous material, PAS+

177
Q

Most common presentation for coal workers pneumoconiosis?

A

Chronic bronchitis

178
Q

TRUE/FALSE: coal miners pneumoconiosis can present with a simple upper zone nodules or massive fibrosis, similar to silicosis

179
Q

Based on the following description, is this a coal macule or a Caplan nodule?

Focal lesions with necrotic center surrounded by lymphocytes and plasma cells

A

Caplan nodule

A coal macule is a focal collection of coal dust in pigment-laden macrophages

180
Q

Piperfitters, steamfitters, electricians, insulation worders, boilermakers, welders, construction workers and shipbuilders, plastic and rubber manifacturing workers, yarn/thread/fabric millworkers, and those who work with brakelining or cement are subject to which pneumoconiosis?

A

Asbestosis

181
Q

Latency period of asbestosis?

A

10-40 years

182
Q

HRCT findings for asbestosis?

A

Subpleural lines, parenchymal and interlobular septal fibrosis, honeycoming, pleural plauqes

183
Q

Tell me the name of the large asbestos fibers coated with iron from hemosiderin

A

Ferruginous bodies

184
Q

Aerospace, aircraft, and alloy production, automotive, ceramics, defence, dental and prosthetics, electronics, nuclear, recyclinf of electronics, and telecommunications are at risk for which pneumoconiosis?

185
Q

What form of beryllium (acute or chronic) is more rare and is associated with pneumonitis, tracheobronchitis, and nasopharyngitis?

186
Q

What are the clinical symptoms of chronic beryllium pneumoconiosis?

A

~10 yrs from exposure there is dyspnea, cough, fever, night sweats, fatigue, and/or weight loss

187
Q

HRCT findings for beryllium pneumoconiosis?

A

parenchymal nodules, septal thickening, GGOs, hilar and mediastinal LAD

188
Q

Pathology findings for beryllium pneumoconiosis?

A

Noncaseating granulomas

189
Q

Which interstitial lung disease resembles acute silicosis histologically and on imaging?

A

Secondary pulmonary alveolar proteinosis, which causes alveolar filling with proteinaceous material that consists mostly of phospholipids and surfactant, staining with periodic acid–Schiff reagent (silicoproteinosis). Other exposures with similar findings are aluminum, silica, titanium, cement, insulation, sawdust, paint, varnish, chlorine, nitrogen dioxide, and fertilizer.

190
Q

Types of infections that are increased in silocosis?

A

Myocobacterial and fungal

191
Q

True/False: lung cancer is increased in silociosis

192
Q

True/False: connective tissue disease are increased in silociosis

A

TRUE

Scleroderma, RA, and vasculitis

193
Q

Which autoimmune disease is associated with Caplan syndrome?

A

Rheumatoid arthritis. Caplan syndrome is a nodular reaction that occurs in individuals exposed to coal dust who also have rheumatoid arthritis or who will have rheumatoid arthritis within the next 5–10 years. The nodules can vary in diameter (0.5–5.0 cm) and are usually multiple, bilateral, and peripherally located. They contain a necrotic center surrounded by lymphocytes and plasma cells and a very small amount of coal dust.

194
Q

Which pneumoconiosis is associated with melanoptysis?

A

Coal workers’ pneumoconiosis. Melanoptysis is the expectoration of black sputum containing carbonaceous particles. It occurs when a conglomerate of nodules cavitates and ruptures into the airway. Melanoptysis has also been reported with freebase cocaine smoking, malignant melanoma, and aspergilloma caused by Aspergillus niger, as well as in progressive massive fibrosis caused by silicosis.

195
Q

This is the accumulation of coal dust in the lungs, often asymptomatic and can be seen in people living in large urban areas where there is significant air pollution

A

Anthracosis

cough cough I think I’m getting the black lung, pop

196
Q

This type of asbestosis fiber are curly stranded, curved, easily degraded by macrophages, and have a low malignancy risk

A

Serpentine (chrysotile)

197
Q

This type of asbestos fiber is rod-like, straight, insoluble, cannot be degraded by macrophages, and has a high malignancy risk

A

Amphibole

crocidolites, amosite, anthophyllite, tremolite-actinolite

198
Q

TRUE/FALSE: shorter asbestos fibers are more carcinogenic than long ones

A

FALSE

Longer are worse

199
Q

Pathology of benign asbestos pleural effusions?

A 
Exudative
Eosinophilic
Bloody
Can resolve spontaneously
Low malignancy risk
200
Q

TRUE/FALSE: pleural plaques with asbestosis by themselves have an increased malignancy risk

201
Q

TRUE/FALSE: there is a multiplactive risk of cancer in those with history of asbestos exposure and those who smoke

202
Q

This presentation in asbestosis shows diffuse visceral pleural thickening, usually unilateral, concomitnt with asbestosis, considered direct extension of parenchymal fibrosis

A

Pleural fibrosis

203
Q

This presentation in asbestosis is when you see a pleural-based “mass-like” lesion with hilar structure “comet-tail” sign, carries no evidence of malinancy risk

A

Visceroparietal reaction (rounded atelectasis)

204
Q

Timeline for the development of bronchogenic carcinoma after asbestos exposure?

205
Q

CT findings for mesothelioma?

A

Unilateral parietal pleural mass, nodularity, or thickening with pleural effusion, volume loss right>left side

206
Q

This disease results from exposure to hydrated magnesium silicate (working in pharmaceuticals or inhaling baby powder if inhaling illicit drug tablets), CT shows fibrosis/nodules/lower lobe emphysema, path shows multinucleated giant cells

207
Q

Most common metal that can cause hard metal lung disease?

A

Cobalt

Can cause COPD, AIP, or fibrosis

208
Q

What blood or bronchoalveolar lavage test is used to assist in diagnosing chronic beryllium disease?

A

Beryllium lymphocyte proliferation test

209
Q

Type of hypersensitivity reaction(s) for hypersensitivity pneumonitis (HP)?

A

Combined type III and type IV

210
Q

Name the disease of HP associated with the following antigen and exposure:

Antigen - Faenia rectivirgula (bacteria)

Exposure - mold hay, grain, silage

A

Farmers lung

211
Q

Name the disease of HP associated with the following antigen and exposure:

Antigen - Thermoactinomyces vulgaris (bacteria)

Exposure - contaminated forced-air systems, water reservoirs

A

Humidifier lung, air conditioner lung, ventilation pneumonitis

212
Q

Name the disease of HP associated with the following antigen and exposure:

Antigen - T. vulgaris (bacteria)

Exposure - moldy sugar cane

A

Bagassosis

213
Q

Name the disease of HP associated with the following antigen and exposure:

Antigen - Aspergillus clavatus (fungi)

Exposure - moldy barley

A

Malt workers lung

214
Q

Name the disease of HP associated with the following antigen and exposure:

Antigen - Cryptostroma corticale (bacteria)

Exposure - Moldy maple bark

A

Maple bark strippers lung

215
Q

Name the disease of HP associated with the following antigen and exposure:

Antigen - Penicillum casei (bacteria)

Exposure - Moldy cheese

A

Cheese washers lung

Seriously i cant make this stuff up. What am i even writing right now. More to follow.

216
Q

Name the disease of HP associated with the following antigen and exposure:

Antigen - Thermoactinomyces viridus (bacteria)

Exposure - Moldy cork

217
Q

Name the disease of HP associated with the following antigen and exposure:

Antigen - Mucor stolonifer (fungi)

Exposure - Moldy paprika pods

A

Paprika slicers lung

..see!

218
Q

Name the disease of HP associated with the following antigen and exposure:

Antigen - Avian droppings, feathers, serum

Exposure - Parakeets, pigeons, chickens, turkeys

A

Pigeon breeders or fanciers lung

219
Q

Does is this more consistent with acute, subacute, or chronic HP?

Pathology shows poorly formed noncaseating granulomas, peribronchiall mononuclear cell infiltration

220
Q

Does is this more consistent with acute, subacute, or chronic HP?

HRCT shows nodules, GGO’s, and honeycombing

221
Q

Does is this more consistent with acute, subacute, or chronic HP?

Pathology shows loose and poorly formed arranged noncaseating granulomas with mononuclear alverolitis in the presence of fibrosis with thick alveolar septa

222
Q

Does is this more consistent with acute, subacute, or chronic HP?

Pathology shows more well formed, but loose and poorly arranged noncaseating granulomas, bronchioloitis with or without organizing pneumonia

223
Q

What is seen on BAL in HP?

A

Elevated lymphocytes (>50%)

Inversion of CD4:CD8 (proliferation of CD8 cells)

224
Q

True/False:

Although inhalation of gases/antigens/fumes result in hyperacute cytokine release without cosequent lung injury, with or without lung alveolar damage, or subacute parenchymal disease, exposure does NOT result in HP.

225
Q

Exposure to welding and brass work can lead to the inhalation of what toxic agent?

A

Metal fume fever (Zn oxide)

226
Q

Exposure to contaminated grains, moldy hay, silage, flour, textile materials, and wood chips can lead to the inhalation of what toxic agents?

A

Organic dust toxic syndrome, thermophilic bacteria, and fungal spores

227
Q

True/False: inhalation of metals or organic dust can lead to flu-like symptoms that take 2-3 weeks to resolve.

A

FALSE

Typically resolves in 12-48 hours

228
Q

True/False: inhalation of metals or organic dust typically leads to no radiographic changes

229
Q

The following inorganic low water solubility agents can cause what effects on the lung if inhaled?

Chlorine, chloramine (from cleaning products or swimming pools)
Nitrogen dioxide (silo fillers disease and explosives), ozone (welding), aerosols, phosgene (welding)
Metals (cadmium, mercury, nickel carbonyl) from welding, brazing, flame cutting, electronic recycling

A

Acute irritant lung injury with DAD

230
Q

Symptoms of acute irritant lung injury with DAD from inorganic low solubility agents?

A

HEENT symptoms, acute dyspnea, bronchiolitis, may develop 2-6 wks later

231
Q

Radiographic changes from acute irritant lung injury with DAD from inorganic low solubility agents?

A

Airspace opacities, noncardiogenic edema, GGOs (with metals)

232
Q

The following organic low water solubility agents can cause what effects on the lung if inhaled?

Fire eaters lung (flame blowing performances)
Paraquat (ingestion)
Popcorn workers lung (diacetyl butanedione from flavor industry workers)

A

Acute irritant lung injury with DAD

233
Q

Symptoms of acute irritant lung injury with DAD from organic low solubility agents?

A

Acute dyspnea, respiratory failure, bronchiolitis 2-6 weeks later, GI symptoms (from paraquat)

234
Q

Radiographic changes from acute irritant lung injury with DAD from organic low solubility agents?

A

Airspace opacities, noncardiogenic edema

235
Q

Smoke inhalation (with high water solubility) can cause what effect on the lungs?

A

Acute irritant lung injury and DAD

236
Q

Exposure to nylon (flock workers disease from textile manufacturing) or ardystil (from textile printing sprayers) can cause what effects on the lung?

A

Lung parenchymal disease

237
Q

Symptoms from exposure to nylon or ardystil?

A

Dyspnea progressing to ILD over months to years (usually NSIP or COP)

238
Q

What properties of toxic gases and fumes determine their pattern of lung injury?

A

Water solubility, duration of exposure, and depth of inhalation. For example, more water-soluble gases such as chlorine cause more upper-airway irritation and symptoms than less water-soluble agents such as nitrogen dioxide, which cause more small airways disease and alveolar damage.

239
Q

Based on the following characteristics, is this more consistent with sensitizer-induced asthma or irritant-induced asthma?

Absent latency period

240
Q

Based on the following characteristics, is this more consistent with sensitizer-induced asthma or irritant-induced asthma?

onset within months to years

A

Sensitizer

241
Q

Based on the following characteristics, is this more consistent with sensitizer-induced asthma or irritant-induced asthma?

Usually from fumes, gases, smoke, vapors

242
Q

Based on the following characteristics, is this more consistent with sensitizer-induced asthma or irritant-induced asthma?

From complete antigens (MW > 10kd) or incomplete antigens (haptens, chemicals with MW <10kd)

A

Sensitizer

243
Q

Based on the following characteristics, is this more consistent with sensitizer-induced asthma or irritant-induced asthma?

From animal and plant proteins, enzymes, flour, cereal, isocyanates, anhidrates, metals, drugs, dyes and bleaches, amines, glues and resins, and wood dust

A

Sensitizer

244
Q

Based on the following characteristics, is this more consistent with sensitizer-induced asthma or irritant-induced asthma?

From chlorine gas, aldehydes, alkaline dusts, bleaching agents, cleaning products (ammonia), accidental spills, smoke from fires

245
Q

Based on the following characteristics, is this more consistent with sensitizer-induced asthma or irritant-induced asthma?

Immunologic response

A

Sensitizer

246
Q

Based on the following characteristics, is this more consistent with sensitizer-induced asthma or irritant-induced asthma?

Diagnosis is made by confirming asthma diagnosis (PFTs followed by methacholine)

A

Sensitizer

247
Q

Based on the following characteristics, is this more consistent with sensitizer-induced asthma or irritant-induced asthma?

Diagnosis made by asthma diagnosis, then by establishing occupational relationship, and then possibly by specific inhalation challenge

248
Q

Based on the following characteristics, is this more consistent with sensitizer-induced asthma or irritant-induced asthma?

Pathology shows either epithelial sloughing and hemorrhage (acute) or epithelial cell regeneration with increased basement membrane thickness due to collagen deposition (chronic)

249
Q

Based on the following characteristics, is this more consistent with sensitizer-induced asthma or irritant-induced asthma?

Pathology is similar to asthma

A

Sensitizer

250
Q

Based on the following characteristics, is this more consistent with sensitizer-induced asthma or irritant-induced asthma?

Symptoms present while at work, improvemet on weekends or vacations

A

Sensitizer

251
Q

Tell me what the following organ does to acclimate to high altitude:

Ventilation

A

Hyperventilation, respiratory alkalosis

252
Q

Tell me what the following organ does to acclimate to high altitude:

Brain

A

Hypoxia induced vasodilation
Hypocapnia induced vasoconstriction
Constant cerebral blood flow

253
Q

Tell me what the following organ does to acclimate to high altitude:

Kidneys

A

Increased bicarb excretion, EPO production

254
Q

Tell me what the following organ does to acclimate to high altitude:

Heart

A

Increase blood pressure
Increased CO
Decreased SV (bicarb diuresis and fluid shifts)

255
Q

Tell me what the following organ does to acclimate to high altitude:

Pulmonary vasculature

A

Hypoxia-induced vasoconstriction

256
Q

Tell me what the following organ does to acclimate to high altitude:

Hematologic

A

Increased Hgb synthesis

257
Q

Tell me what the following organ does to acclimate to high altitude:

Oxyhemoglobin curve

A

Left shift due to alkalosis

258
Q

Prevention medications for altitude motion sickness?

A

Acetazolamide, dexamethasone

259
Q

Treatment for mild and moderate altitude motion sickness?

A

Mild - conservative (meds for symptoms)

Moderate/severe - descent, oxygen, hyperbaric therapy, acetazolamide, dexamethasone

260
Q

Mechanism for high-altitude pulmonary edema?

A

Hypoxic vascoconstriction leads to capillary stress fractures, resulting in pulmonary edema

261
Q

Treatment for high-altitude pulmonary edema?

A

Oxygen, descent, hyperbaric therapy, nifedipine, tadalafil, or sildenafil

262
Q

Medications used to prevent high-altitude pulmonary edema?

A

Nifedipine, tadalafil, sildenafil, dexamethasone, salmeterol

263
Q

This condition at altitude can cause headaches, ataxia, confusion, hallucinations, stupor, and coma.

A

High-altitude cerebral edema

264
Q

Medications for the treatment of High-altitude cerebral edema?

A

Acetazolamide, dexamethasone

265
Q

Which transcription factor is responsible for most of the adaptive changes that occur during acclimatization?

A

Hypoxia-inducible factor-1α stimulates vascular endothelial growth factor, which itself stimulates angiogenesis and nitric oxide synthesis. These changes result in greater blood flow and oxygen delivery to tissues.

266
Q

Supplemental oxygen use amount that is a contraindication to air travel?

267
Q

Altitude of air cabin pressure on a plane?

268
Q

How does a high-altitude stimulation test work?

A

A 15.1% oxygen concentration with nitrogen mixture is given via a tight-fitting mask, SpO2 is measured

ABG taken after 20 minutes

If oxygen remains 88% or greater and PaO2 is >55mmHg, then no supplemental oxygen is required.

269
Q

How many days do you have to avoid air travel after radiographic resolution of pneumothorax?

270
Q

How long should you postpone air travel if you dove once per day?

Extra: how long to postpose if you dove multiple time or have had to have decompression stops?

A

Once/day - 12 hours

Multiple times - 48 hours

271
Q

This is when, on ascending from deep water, tissues become loaded with increased quantities of oxygen and nitrogen leading to liberation of these gasses causes vascular obstruction, vessel rupture, or tissue compression –> inflammation and clotting

A

Decompression sickness (the bends)

272
Q

This is when there is increased partial pressure of nitrogen in the nervous system tissue that can result in confusion (100ft) or the loss of consciousness (>300 ft)

A

Nitrogen narcosis

273
Q

In diving medicine, which gas law explains the pathophysiology of most types of barotrauma?

A

Boyle’s law. At a constant temperature, the volume of a gas is inversely proportional with the pressure to which it is subjected.

274
Q

Which gas law explains the pathophysiology behind decompression sickness and nitrogen narcosis?

A

Henry’s law. At a constant temperature, the amount of a gas dissolved in a liquid is directly proportional to the partial pressure of that gas.

275
Q

What 3 conditions can be a complication of barotrauma in diving?

A

Pneumomediastinum

Pneumothorax

Arterial gas embolism

276
Q

How to avoid barotrauma (and resultant clinical conditions) during diving?

A

Avoid breath holding during ascent

277
Q

True/False: barotrauma to the middle ear in diving and eustachian tubes can cause tympanic membrane rupture

278
Q

Symptoms of type 1 decompression sickness?

A

MSK pain, skin pruritis/erythema, lymphatic problems (LAD, peau d’orange)

279
Q

Symptoms of type 2 decompression sickness?

A

Neurologic - parasthesias, weakness, parlysis, memory loss, ataxia

Pulmonary - chest pain, wheezing, dyspnea, pharyngeal irritation, acute RHF

280
Q

Treatment of decompression syndrome?

A

Hydration
100% oxygen
L lateral decubitus position
Hyperbaric oxygen

281
Q

Prevention of decompression sickness?

A

Hydrate
Avoid rapid descent
Avoid alcoholic beverages

282
Q

This therapy increases oxygen delivery by increasing its dissolution in plasma (Henry’s law), reduces volume of gas bubbles (Boyle’s law), replaces nitrogen with oxygen, promotes vasoconstriction, ameliorates ischemia-reperfusion inflmmation, facilitates angiogenesis and fibroblast proliferation, and increases neutrophil bactericidal activity

A

Hyperbaric oxygen therapy

283
Q

What is hyperbaric oxygen therapy used to treat?

A 
CO and CN poisoning
Decompression sickness and air embolism
Acute traumatic or thermal injury
Radiation injury
Nonhealing ulcers, skin grafts, and wounds
Clostridial myositis or myonecrosis
284
Q

Case: patient presents to the ER with malaise, dzziness, and lactic acidosis. EKG shows NSTEMI. Carboxyhemoglobin level 18%. Cause?

A

CO poisoning

285
Q

Indications for hyperbaric oxygen therapy in CO poisoning?

A 
Unconscious
Mental status changes
Neurologic deficit
End-organ ischemia
CO-Hb >25% (20% in pregnancy)
286
Q

This is when there is the conversion of the ferrous (Fe2+) to ferric (Fe3+), for which oxygen cannot bind.

A

Methemoglobinemia

287
Q

Medications that can increase formation of methemoglobinemia?

A 
Dapsone
Topical benzocaine or lidocaine
Inhaled NO
Nitroglycerin
Nitroprusside
Chloroquine
Metoclopramide
Sulfonamides
Aniline derivatives
288
Q

What is the saturation gap in methemoglobinemia?

A

Difference between pulse oximetry and measured oxygen saturation in blood gas

289
Q

Treatment for methemoglobinemia?

A

Methylene blue if methemoglobinemia level >30%

290
Q

Symptoms of thermal lung injury from smoke inhalation?

A

Cough, stridor, wheezing, hoarseness, carbonaceous sputum, blistering, and oropharyngeal edema

291
Q

Exposure to this substance can cause headache, anxiety, confusion, vertigo, coma, seizures, tachycardia, HTN, arrhythmias, and “cherry-red” lip color due to inhibition of OXPHOS by bidning to cytochrome oxidase a3

A

CN poisoning

292
Q

Drug most commonly assoicated with CN poisoning?

A

Nitroprusside

293
Q

Treatment for CN poisoning?

A

Hydroxycobalamin
Induce methemoglobinemia (amyl nitrate, sodium nitrite0
Sodium thiosulfate

294
Q

Bleomycin, amiodarone, nitrofurnatoin, mitomycin, and paraquat can cause the formation of what?

A

Free radicals

295
Q

Treatment for radiation-induced pneumonitis?

A

Corticosteroids

Pulmonary Review (14 decks)

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