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CRRAB II Part 2 Respiratory > Path 2nd half - W3 > Flashcards

Path 2nd half - W3 Flashcards

1
Q

How does idiopathic pulmonary fibrosis present?

A
  • slowly progressive pulmonary fiborsis w/gradually worsening dypnea and non-productive cough
  • older than 40
  • males
  • smokers
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2
Q

What does CT of IPF show?

A

diffuse interstitial opacities

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3
Q

Presents with old and young areas of fiborisis, honeycomb changes, and pathcy interstitial fibrosis

A

IPF (idiopathic pulmonary fibrosis)

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4
Q

What is the likely cause of IPF?

A
  • abnormal alvolear healing response to miscellaenous toxic/inurious stimuli (smoking)
  • may be related to TBF-beta
  • reduced telomerase activity –> more epithelial injury w/release of TGF-beta
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5
Q

What is the clinical course of IPF?

A

relentlessy progressive (death within 5 years)

hypoxemia, cyanosis, digitial clubbing

cor pulmonale

heart failure (cause of death in 1/3 patients)

NO KNOWN EFFECTIVE THERAPY

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6
Q

What is non-specific interstitial pneumonitis?

Histologically?

Common in?

A
  • temporally uniform - cellular infiltrate of lymphocytes that progresses on to fibrosis
  • BETTER PROGNOSIS
  • occurs in patient’s w/autoimmune diseases
  • more often in women and at younger age.
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7
Q

How does NSIP present?

A
  • more subacute/febrile illness
  • same fibrotic distribution as IPF but no honeycomb changes
  • responds to steroids - good prognosis.
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8
Q

What is cryptogenic organizing pneumonia? Path? Symtpoms?

Tx?

A
  • mimics community acquired pneumonia
  • flu-like illness
    • cough, malaise, fever, dyspnea on exertion
  • PATH
    • fibroblastic/granulation tissue plugs small airways and alveoli
  • Treatment
    • corticosteroids
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9
Q

What is interstital lung disease associted with/what can it complicate?

A
  1. Rheumatoid arthriits
  2. Scleroderma
  3. polymyositis
  4. systemic lupus
  5. mixed connective tissue
  6. Sjogren’s syndrome
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10
Q

What is ILD associated with from the environment?

A
  • Inhaled inorganic dusts/particles
    • silicates (silicosis, asbestosis, berylliosis)
    • Carbon dust (coal miners pneumoconiosis)
    • Metals (tins, aluminum, hard metals)
  • Inhaled organic dusts
    • hypersensitivity pneumonitis due to thermophili actinomyctes (famer’s get from hay)
    • bacteria, true fungi (aspergillus), animal proteins (bird fancier’s lung)
  • Miscellaneous
    • synthetic
    • vinyl chlorides
    • gases
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11
Q

What causes silicosis? how does it present?

A
  • inhalation of silica (silicon dioxide) - most abundant mineral on earth
  • presents as chronic lung injury from long standing exposure (mining and sand blasting)
  • progressive respiratory insuff. with multiple small fibrotic nodules in UPPER LUNG FILEDS.
  • can cause massive fibrosis
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12
Q

What does silicosis have increased risk for?

A

TB

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13
Q

Can silicosis present acutely?

A

yes, if you have mssiave inhalation expsoure - get respiratory distress.

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14
Q

What does silicosis histology show?

A

fibrocellular parenchymal nodules

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15
Q

What is shown?

A

Silicosis

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16
Q

What causes asbestos related lung disease? types?

A
  • inhalation of natrually occurin mineral fibers (magnesium silicates)
  • classically was in shipyard workers
  • Types
    • serpentine (less toxic)
    • Amphibole (more toxic)
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17
Q

How does asbestosis differ from silicosis?

A
  • starts in LOWER LOBES
  • may see asbestos bodies (get coated w/iron) – called ferruginous body.
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18
Q

What are asbestosis patients at risk for?

A
  1. benign pleural disease - calified plaques, pleural effusions, visceral pleural fibrosis.
  2. malignant mesothelioma - delayed decades after expsoure - often always associated with asbestos.
  3. lung cancer risk - especially if smoker
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19
Q

What is shown?

A

ferruginous body of asbestosis

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20
Q

Is a biospy always done with asbesotis?

A

No, if exposure fits symptoms and chest imaging you don’t need one - see calcified pleural plaques.

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21
Q

How does coal workers pneumoconiosis present?

A
  • blackening of lungs (anthracosis)
    • ​get small nodules in lupper lung fields.
  • 90% benign
  • 10% have massive fibrosis - likely co-existent silica inhalation
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22
Q

What causes hypersensitivity pneumonitis?

A
  • immunologically mediated -mixed interstitila and alvolar
  • antibody rxn to inhaled organ antigen
  • many etiologies
  • MUST REMOVE PATIENT FROM AGENT.
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23
Q

how does hypersensitivity pneumonitis present?

A
  • farmer’s lung
  • pigeon breeder’s lung
  • clinally
    • acute attacks 4-6 hours after exposure
    • fever
    • dyspnea
    • cough
    • leukocytosis
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24
Q

What is seen on CT w/ hypersensitivity pneumonitis?

A

mid/upper zone ground glass or nodular opacities

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25
Q

Treatment for hypersensitivity pneumonitis

A

Avoid exposure.

Course of corticosteroids w/more severe.

REVERSIBLE IF CAUGHT EARLY.

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26
Q

How is hypersensitivity pneumonitis diagnosed?

A
  • CT
  • flow cytometry
    • see more CD8 than CD4 cells (lymphocytosis)
  • inhalation history
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27
Q

What is seen w/eosinophilic pneumonias?

Types>

A
  • pulonary infiltrates and alveolar or blood eosinophilia
  • Acute = febrile illness, life thrreatening hypoxiab
  • Chronic - underlying asthma too.
  • simple pulmonary eosinophilia - minimal symptoms, associated w/drugs, fungal.

Tx with corticosteroids.

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28
Q

Smoking related interstitial lung disease:

A
  1. Idiopathic pulmonary fibrosis - SMOKERS
  2. desquamative interstitial pneumonia and respiratory bronchiolitis-interstiital lung disease.
  3. pulmonary langerhands cell histiocytosis.
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29
Q

What is seen in desquamative interstitial pneumonia and respiratory bronchiolitis-interstiital lung disease

A
  • dyspnea, cough, hypoxemia, pulmonary infiltrates
  • SMOKERS
  • pigmented macrphages in alveolar spaces
  • smoking cessation improves, but if they don’t stop could lead to fibrosis
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30
Q

Presenation of pulmonary langerhans cell histiocytosis

A
  • limited to smokers
  • cough, dyspnea, chest pain, fever
  • pneumothroax
  • diffuse pulmonary nodules in UPPER ZONE CYSTS
  • get proliferation of langerhan’s cells
  • smoking cessation improves in only 1/3 patinets
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31
Q

Sarcoidosis

A
  • granulomatous disease that often invovles lung
  • cough
  • dyspnea
  • chest pain
  • fatigue
  • malaise
  • weight loss
  • other skin, joints, organs
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32
Q

how old are most patinets with Sarcoidosis? Who is it more common in?

A

10-40 years old.

AFrican Americans - 2.4% risk.

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33
Q

What is seen on CXR with Sarcoidosis

A

bilateral hilar adenopathy - may see reticular pulmonary opacities in mid to upper zones.

progression = non caseating granulomas along lymphatics and involves alveoli.

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34
Q

What is the often diagnosis for Sarcoidosis

A

biospy of lymph nodes - see granulomatous lymphadenitis.

Increased CD4/CD8 ratio > 4:1 - predicitive. Helps w/diagnosis.

may have hypercalcemia

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35
Q

What is shown

A

Sarcoidosis - lymph node w/non caseating granulomas

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36
Q

What is pulmonary alveolar proteinosis (PAP)?

A
  • rare disorder - diffuse lung disease w/filling of alveolar spaces by proteinaceous pink material
  • no associated inflammation or architectural issue.
  • surfactant related protein - largely due to inability of pulmonary macrophages to metabolize it.
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37
Q

Clinical features of PAP

A

progresive dyspnea

cough with gelatinous sputum

fatigue

weight loss

fever

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38
Q

3 types of PAP

A
  1. Acquired - adults - have serum autoantibody to granulocyte/monocyte CSF cuasing macrophage dysfunction.
  2. Secondary - high level of DUST, heme maligancies, infection.
  3. Congential - mutation in GM-CSF production.
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39
Q

Treatment for PAP

A

whole lung lavage - tx w/recombinant GM-CSF

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40
Q

What is BAL as a diagnostic tool. Use?

A

Use = cytology for malignant cells. Micro for clean culture.

Good for looking for fungal organisms.

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41
Q

what is seen on BAL with

PAP:

Sarcoid:

Hypersensitivity penumonitis:

A

cloudy milky fluid

CD4/CD8 ratio > 3.5

CD4/CD8 decreased

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42
Q

What can cause a PE?

A

bloot clot

air

fat

amniotic fluid

tumor

43
Q

What are the symptoms of a massive PE?

A

systolic BP < 90

increased CVP - neck distention

Right heart failure –> can lead to death.

44
Q

Predisposing factors for PE:

A

Immobiliziation/post surgical

Pregnancy/contraceptive.

Obesity

Cardiac disease.

Cancer.

Anti phospholipid syndrome

heparin induced thrombocytopenia.

45
Q

What can cause congenital hypercoagulability?

A

Factor V leidin

prothrombin gene mutation

Deficiencies of factor C or S

antithrombin III

46
Q

What are some symptoms of PE?

A

Hypotension

Dyspena

Tachycardia

Pleuritic chest pain

calf/thig pain or swelling

signs of acute RV failure

47
Q

How can you differentiate between pre and post mortem clot?

A

pre has lines of zahn

48
Q

Does serum D-dimer have a high or low PPV for PE?

A

high negative PV - if norml.

normal = high PPV — can rule out then. When you have a clot anywhere you can have d-dimer elevation.

49
Q

What could cause chronic/recurrent small emboli?

A

pulmonary hypertension

cor pulmonale.

50
Q

what do you see on path with pulonary hypertension

A

medial hypertrophy of arterioles and small arteries.

may have vasospastic component.

51
Q

What is the mutation with inherited pulmonary hypertension

A

BMPR2 locus mutation - incomplete penetrance so there are environmental cofactors that trigger it.

52
Q

What can be seen on CXR with pulmonary hypertension

A

normally none, otherwise increasing pulmonary vasculature

53
Q

Clinical features of pulmonary hypertension

A

COPD, ILD underlying diseases

increased pulmonic compnent of 2nd heart sound

exertional dyspnea, lethargy, fatigue

RV hypertrophy w/RV failure/cor pulmonale.

54
Q

what causes pulonary arteriovenous malformations

A
  • hereditary hemorrhagic telangiectasis (osler-weber-rendu)
  • presents in adulthood
55
Q

Symptoms of pulonary arteriovenous malformations

A

dyspnea

hypoxemia

hemotpysis

clubbing due to R to L shunt

56
Q

Common causes of hemoptysis - pulmonary hemorrhage

A

bronchogenic carcioma

Bronchiectasis

Bronchitis

bacterial pneumonia

TB

PE

fungus ball

pulmonary abscess

57
Q

Diffuse alveolar hemorhage (DAH) syndrome

A

medical emergency

presents abrupt/rapdily evolving symtpoms: cough, hemotptysis, fever, dyspena, hypoxemia.

CT: diffuse alveolar opacities.

could casue anemia.

58
Q

What can cause Diffuse alveolar hemorhage (DAH) syndrome

A

Drug/toxic injury - amidodarone.

ARDS/DAD

anticogaulation

mitral stenosis

pulmonay capillaritis

pulmonary infection/bone marrow transplant.

cocaine use

59
Q

Goodpasture syndrome diagnosis

A

anit-GBM antibody - against glomerular and pulmonary alveolar basement membrane.

linear IgG fluorescence

60
Q

What is seen on path with Goodpasture syndrome

A

lungs - focal necrosis of alveolar walls w/alveolar hemorrhage

kidney: crescentic glomerulonephritis

61
Q

pulmonary capillaritis

A

neutrophilic inflammation of alveolar capillaries - commonest cause.

62
Q

Wegeners granulomatosis presentaiton

A

manifests with sinusitis

pulmonary nodules w/alveolar hemorrhage

renal disease - rapidly progressive.

63
Q

How is Wegener’s dx?

Tx?

A

ANCA (c)

treat w/steroids + immunosuppression (cytoxan)

64
Q

SLE diagnosis

Tx.

A
  • Dx = ANA and anti-ds DNA.
  • Tx = corticosteroids + immunsuppression.
  • Sx = diffuse alveolar hemorrahge - 5% have pulmonary capillaritis
65
Q

Who presents with idiopathic pulmonary hemosiderosis/hemorrhage

A

young patients/children

intermittient/recurrent

often iron dficiency anemia - macrophages w/hemosiderin

does respond to steroids

25% get autoimmune disease

66
Q

What is the most common lung tumor?

A

carcinoma- 99%

most common visceral cancer in the world.

67
Q

Risk factors for lung tumors (carcinoma)

A

Cigarette smoking (90%)

Radiation exposure.

Asbestos

Pulmonary fibrosis.

68
Q

non small cell carciomas:

A
  1. Adenocarcinoma - 40-50%
    1. female dominant.
    2. may not be related to smoking (small #)
  2. Squamous carcioma. 20-30%
  3. Large cell undifferentiated carcinoma 5-15%
  4. miscellaenous
69
Q

How is small cell carcinoma different from the others?

A

It’s derived from neuroendocrine portion of the lung.

70
Q

what is typical for sqamous cell on CXR

A

big mass, more central than peripheral.

CT - may show cavitation.

71
Q

What drives treatment for non-small cell carcinoma (adenocarcinoma)

A

Histological class + ancillary molecular and biomarker testing to include EGFR, ALK, ROS and PDL-1

72
Q

Well behaved lung maligancy =

A

carcinoid tumor

well differentiated neuroendocrine carcionoma.

73
Q

What cancers of lung can go to salivary gland?

A

Mucoepidermoid

Adenoid cystic

74
Q

Classic lung cancer presentation?

A

> 40 years

long term smoker

cough

hemoptysis

hoarsness (tumor on laryngeal nerve or laryngeal carcionma)

dyspnea

pleural effusion/pericardial effusion

75
Q

central mass lesion =

peripheral mass lesion =

A
  • central
    • squamous
    • small cell
  • peripheral
    • adenocarcinoma
76
Q

What causes pancoast tumor?

A

chest wall expansion in APEX

leads to Horner’s syndrome - ptosis, constricted pupil, anhidrosis.

elevated diphgram (phrenic nerve paralysis)

77
Q

What should you think with hoarsness in a smoker?

A

mass in medistinum

laryngeal cancer

78
Q

Superior vena cava syndrome

A

could be caused by masses

see redness and swelling of face (especially when waking up in morning) and venous distention.

79
Q

Lepidic pattern of adenocarcinoma

resembles:

fails to respond to:

A

resembles pneumonia.

fails to respond to pneumonia.

80
Q

Where are lung cancers commonly metastases?

A

Liver.

Bone (pathological fracture may be first)

Adrenals.

Brain. (small cell carcinoma commonly) - seizure or focal neurological deficit may be first symptom.

81
Q

What paraneoplastic syndromes can occur w/lung cancer

A
  • tumor associated hormone compounds
  • hypercalcemia due to bone metastases
  • tumor production of PTH related to protein, calcitriol (Vitamin D)
82
Q

Syndromes seen with small cell carcinoma:

A
  • Inappropriate ADH secretion w/hyponatremia
  • cushing’s syndrome due to ACTH prodcution.
  • Neurologic syndromes
    • cerebellar ataxia.
    • lambert eaton.
  • Carcinoid syndrome: diarrhea, flushing, cyanosis
    • see only after hepatic metastases
83
Q

systemic effects of lung cancer;

A
  • Heme - anemia, luekocytosis, hypercoag.
  • MS: clubbing, hypertrophic osteoarthropathy, inflammatory myopathy
    *
84
Q

How is adenocarcionma treated (what drug)

A

EGFR inhibitors.

85
Q

How do carcinoid tumors commonly present?

Treatment?

A

central/bronchial location w/obstruction, hemoptysis or peripheral nodule.

Usually resectable.

Typical type have good 10 year survival.

86
Q

Most common benign tumor of the lung:

A

Hamartoma - disorganized tumor of the native tissue.

87
Q

What is the most common site of metastatic neoplasia?

A

lUNG

88
Q

how do metasases to lung present commonly?

A

multiple, bilateral lung nodules.

89
Q

What could cause increased fluid production with nonifnlammatory (transudate)?

A
  • increased hydrostatic pressure (CHF)
  • nephrotic syndrome
  • cirrhosis w/ascites
  • peritoneal dialysis
90
Q

Term for decreased lymphatic resorption

A

chylothorax

can occur due to interuptions to thoracic duct.

91
Q

what defines exudate?

A

pleural fluid protein > 2.9 gm

pleural fluid cholesterol >45 mg

pleural fluid LDH

92
Q

most common causes of exudative effusions

A

bacterial pneumonia

malignancy

viral

pulmonary embolism

93
Q

What lab values are associated w/parapneumonic effusion/empyema

A

low pleural fluid glucose <60mg

and pH < 7.3

iMPLIES NEED FOR CHEST TUBE DRAINAGE.

94
Q

HOW SHOULD you treat recurrent pleural effusions

A

pleural space obliteration w/talc pleurodesis

95
Q

What causes 2’ spontaenous pneumo

A

air leak from underlying lung disease:

emphysema, astham, CF, TB, pneumonia, neoplasia

96
Q

How does a pneumothorax present?

A

Dsypnea w/chest pain

physical exam: diminished breath sounds, hyperresonant percussion.

Arterial blood gases - hypoexmia and hypercarbia.

97
Q

How is pneumothorax treated?

A
  • Tube thoracostomy w/water seal device.
  • resportion occurs gradually in most patients.

persistent or recurrent

  • stapling of blebs
  • pleural space obliteration
98
Q

List some primary pleural tumors

A
  1. Solitary fibrous tumor - benign
    1. submesothelial fibrous tissue
    2. large - displace lung.
    3. surgery cures.
  2. Malignant mesothelioma
    1. BIG BAD TUMOR OF PLEURA
    2. 90% to asbestos exposure
    3. latent for up to 45 yrs.
99
Q

Symptoms and imaging of malignant mesothelioma

A

chest pain, dyspnea, bloody pleural effusion

diffuse pleural thickening, effusion + calcified pleural plaques

Histology: epithelio and or sarcomatous w/invasion of chest wall.

100
Q

Most common congenital lung lesion

A

Congenital pulmonary airway malformation

101
Q

List some neonatal lung diseases w/o congnetial malformation - caused by dysfunctional transition from fetal life.

A
  • Transient tachypnea - late term infants - see in first 72 hours.
  • Persistent pulmonary hypertension - term/late term
    • failure to convert to postnatal circulation
  • Respiratory distress syndrome - most common
    • premature infants - more common in 36 weeks or less.
    • hyaline membrane disease
102
Q

What do you see with RDS (possible long term risk)

A

Bronchopulmonary dysplasia - have a lot of fibrosis and diffusion defect issues.

103
Q

What 2 things are used to monitor fetal lung maturity?

A
  1. Lamellar body count
    1. counts small particles - low ocunts are sign of immaturity
    2. want > 50,000 .
  2. Phosphatidyl glycerol
    1. ​if negative = signficant RDS risk
    2. high positive = no risk

CRRAB II Part 2 Respiratory (18 decks)

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