chest Flashcards

1
Q

diagnostic modalities - summary

A
  • in-situ X-ray: P-A, A-P, lying position, Firmann-Dahl method.
  • Fluoroscopy: “motional x-ray” -> movement of the diaphragm/mediastinum (Holczknecht-Jacobson sign), pulsation of the hilum, localisation of casted shades or pathological signs.
    It gives functional information.
  • CT (+ spiral CT, MSCT, HRCT): axial slices, with or without contrast, volume data-sampling, post-processing methods.
  • PET-CT: chest deformities, paralytic thorax (tight apex, acute costovertebral angles), emphysematic thorax (apex is wide, horizontal ribs, wide intercostal spaces)
  • MR: chest wall, mediastinum,, heart, major arteries.
  • radioisotope examination: ventilation, perfusion.
  • ultrasound: pleural fluids.
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2
Q

terminology for describing x-ray of the lungs

A
  1. the typical discrepancies of the hilar caliber, dilated - thick hilar vessels, hypoplastic hilar vessels, centroperipheral caliber discrepancy (cpcd), apicobasal caliber discrepancy (abcd), asymmetry of hila
  2. vascular variances: hyper-, hypo- vascularisation, avascular regions.
  3. parenchymal (interstitial) linear shades, diffuse web-like image, pinstripe and atelectatic streaks
  4. patchy opacities: multiplex small patches (diffuse), irregularly and regularly shaped patchy opacities, blur.
  5. cavernous shades.
  6. transparential shades: less / more transparent.
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3
Q

secondary lobule

A

Anatomical, pathological, physiological unit.
Well visible in case of air trapping or obstruction. Expiration: mosaic pattern - centrilobular GGO, centrilobular emphysema.

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4
Q

pleural fluid

A
  • large amount of pleural fluid will dislocate the midline.
  • we need a Frimann-Dahl snapshot to prove subpulmonal localisation.
  • if pleural adhesions are present, the encapsulated fluid & marked fluid gatherings in the small fissures, may imitate pneumonia on a P-A image.

–> hydrothorax, pneumohydrothorax

  • pleural irregularities on US are called B lines!
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5
Q

atelectasis

A
  • deaeration of the lung tissue and consequential patchy opacities in the air-filled surroundings of the lung.
  • collapse of the lung tissue.
  • DDx: pneumonia.
  • Local atelectasis: think of tumor (esp. if repetitive).
  • empyema thoracis: compression form of atelectasis
  • IRDS: micro- or adhesive atelectasis -> need aerobronchogram!
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6
Q

bronchiectasis

A
  • types: cystic, cylindric.
  • X-ray image: summation of small, ring-like shades.
  • HRCT: “signet-ring” sign -> a small artery-branch next to a wide bronchus.
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7
Q

pulmonary thromboembolism - modalities

A
  • lung scintigraphy -> V/Q scan

- CT angiogaphy

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8
Q

pulmonary abscess on x-ray

A

Every infective, inflammatory, malignant disease can develop an abscess!
- x-ray: a cavern with ragged wall, and an air-filled fluid level inside the patchy opacity. Later the wall will become thinner and smoother.

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9
Q

causes of closure of a bronchus

A
  • foreign body
  • bronchial cc
  • benign intrabronchial tumor
  • mucopurulent plug
  • missed intubation
  • stricture after an infection
  • outer compression by tumor or lymph node
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10
Q

pulmonary mycosis on x-ray

A

pneumonia, small shades, multifocal or extensive, homogenous shadow.

  • aspergilloma: nestles in the cavern of another lung disease (TB, cancer, abscess) OR grows in a bronchiectasial dilation. the lumen of the cavern deforms to the form of a quarter moon (crescent).
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11
Q

lung fibrosis - appearance

A

Irregular, rough/smooth linear-shade network. Covers and deforms the normal structure of the lung. in severe fibrosis, “honeycomb lung” can develop.

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12
Q

bronchial carcinoma

A
  • Histology: squamous cell carcinoma (-central), adenocarcinoma (-peripheral), anaplastic cc, large cell cc, small cell cc.
  • X-ray: the tumor itself and/or symptoms caused by bronchostenosis.
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13
Q

bronchial carcinoma

A
  • central localisation, in the wall of one of the major bronchi, spreading towards the lumen.
  • symptoms: int he beginning -> brnchostenosis, retentive pneumonias, obstructive emphysema, incomplete atelectasis - can be complicated by inflammation. After the extrabronchial breakthrough, unilateral widening of the hilum (the shade becomes homogenous), with irregular outline, spreading towards its environment.
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14
Q

pancoast tumor (bronchial carcinoma)

A
  • in the apex
  • infiltrates the chest wall -> can destroy the posterior arch of the 1st and 2nd ribs & the vertebral bodies.
  • symptoms: pain in the shoulder, Horner-triad, paralytic diaphragm of the affected side.
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15
Q

post-operative monitoring (what to look for)

A
  • localisation of central venous cannula.
  • localisation of endotracheal tube -> the end should be 3-4 cm before the bifurcation.
  • atelectasis: hypoventillation and/or retention of mucus. –> x-ray: homogenous shade of the deflated segment or lobe.
  • aspiration pneumonia (more common in the right side)
  • pulmonary edema
  • pulmonary embolisation
  • pneumonia
  • ARDS (lung in shock) –> RTG image: negative in the beginning, moderate interstitial edema, rapid onset of extensive pulmonary edema.
  • pleural fluid: check with ultrasound
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16
Q

Hodgkin-lymphoma

A
  • Has a pulmonary manifestation in 30-40% of cases.
  • Asymmetric growth of mediastinal shadow - enlarged lymph nodes in the hilus.
  • Can present as patchy opacities with or without cavity, atelectasis, multiplex hilar/subhilar/major disseminated knots, fibrosis, interstitial edema, pleural- , pericardial- fluid, or the combination of these.
  • similar signs in case of leukemias: enlargement of mediastinal lymph nodes, interstitial and alveolar shades (linear and patchy).
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17
Q

definition of interstitial lung diseases

A
  • caused by chronic inflammation of the pulmonary interstitium, resulting in a scarred reconstruction by proliferating connective tissue.
  • Mostly the alveoli and interstitium are affected.
  • the airways and pulmonary vessels are secondarily affected.
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18
Q

clinical signs of interstitial lung diseases

A
  • non-productive cough
  • stress dyspnoea
  • drumstick fingers
  • clubbed nails
  • basal crackling
  • weakness
  • weight loss
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19
Q

diagnostics of interstitial lung diseases

A
  • (ideally) multidisciplinary ILD board: pneumonologists, rheumatologists, radiologists, pathologists
  • laboratory: kidney functions, electrolytes, CRP, differential blood counts, antibodies
  • lung function (restrictive ventilation fault)
  • imaging: x-ray & HRCT
  • bronchoscopy with transbronchial biopsy (TBB) and bronchoalveolar lavage (BAL)
  • open lung biopsy (VATS)
  • biopsy is not necessary in atypical interstitial pneumonia (UIA)
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20
Q

typical patterns of an ILD

A
  • ground glass opacities (milk glass opacity - increased parenchyma decreasement) -> partially filled and/or collapsed alveoli. Eg) active inflammation.
  • consolidation: completely filled and/or collapsed alveoli (accumulation of exudate, transudate, or other tissue in the alveoli).
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21
Q

idiopathic pulmonary fibrosis (heterogenous entity)

A
  • AIP (acute interstitial pneumonitis)
  • UIP (usual interstitial pneumonitis) - 70%
  • DIP (desquamative interstitial pneumonia)
  • RBILD (respiratory bronchiolitis ILD)
  • NSIP (non-specific interstitial pneumonia)
  • BOOP = COP (bronchiolitis obliterans organising pneumonia = cryptogenic organising pneumonia)
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22
Q

interstitial lung diseases on x-ray

A
  • fine-stripping-reticular pattern that is superimposed by a diffuse transparency reduction.
  • increased reticulation with basal dominance.
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23
Q

HRCT in interstitial lung diseases

A
  • central role in detection, diagnosis, and differential diagnosis.
  • acute alveolitis: GGO -> the location of optimal bronchoscopic tissue collection.
  • chronic: nodules, lines and bands, pleural thickening. Final stage: honeycombing
  • pattern of ILD in HRCT:
  • linear reticular pattern
  • nodular pattern
  • structures with density reduction (lesions with “less air”
  • structures with density increase (lesions with “more air”)
24
Q

acute interstitial pneumonia (AIP)

A
  • acute alveolitis: milk opacity (density increase with still recognisable bronchovascular structures).
  • “idiopathic form of ARDS” / ARDS of unclear cause.
  • acute and short prognosis.
  • HRCT image:
    acute -> homogenous GGO (alveolitis), diffuse consolidation.
    chronic -> honeycombing, fibrosis
25
Q

non-specific interstitial pneumonia (NSIP)

A
  • chronic form: manifests in the 4th decade of life.
  • not tobacco-associated.
  • usually occurs as a pulmonary involvement in the context of collagenosis
  • can be treated with systemic glucocorticosteroids -> more favourable prognosis that UIP
  • HRCT image:
  • GGO
  • peripheral, basal, subpleural, symmetrical fine reticular condensation, traction bronchiolectasis
  • NO honeycomb pattern
26
Q

usual interstitial pneumonia (UIP)

A
  • simultaneity of inflammation, proliferation and fibrosis
  • poor prognosis
  • have diaphragm moving disorders -> use ultrasound in M-mode
  • complication: shrinking lung
  • HRCT:
  • very specific -> nearly 100% correct diagnosis
  • GGO (signs of active inflammation and fibroblast proliferation)
  • honeycomb patterns, bronchiectasis –> signs of fibrosis (not present in NSIP) -> subpleural and basally stressed localisation
  • reticular pattern
27
Q

honeycombing “definition”

A

subpleural, multi-rowed, small cystic changes

  • usually appears in the lower lobes, at the end-stage of interstitial lung diseases
    (the upper pole show signs of activity - GGO, alveolitis)
28
Q

ILD: collagenoses & vasculitides

A
  • pulmonary manifestations:
  • rheumatoid arthritis (RA)
  • SLE
  • Sjorgen syndrome
  • systemic sclerosis / scleroderma
  • dermatopolymyositis
  • Wegener granulomatosis
  • x-ray: less sensitive. In pronounced cases -> basal-dominant reticulonodular pattern
  • HRCT: pathological findings in 30%. Pleural thickening. Late stage - fibrosis.
29
Q

occupational lung diseases

A
  • chronic inhalation of inorganic dusts (eg. silicate)
  • long-time exposure
  • alveolar phagocytosis of inhaled particles and interstitial deposition -> interstitial reticulo-granulome formation, sometimes massive fibrosis
  • therapy: stop exposure
  • types: diseases of immunological/unclear etiology & pneumoconiosis (inhaled particles)
  • x-ray:
  • nodular herd often with calcifications
  • hilar / mediastinal lymph nodes with calcifications (“laryngeal calcification”)
  • HRCT:
  • x-ray patterns +
  • micronodular lesions
  • pulmonary fibrosis
30
Q

organising pneumonia (OP)

A
  • occupational -> immunological/unclear etiology
  • idiopathic form: cryptogen-organising pneumonia (COP)
  • non-infectious inflammation that may occur in collagenous diseases, chronic eosinophilic pneumonia, exogenous allergic alveolitis, infections or even as a medication reaction. - symptoms: chronic subfebrile temperatures, dyspnoea, cough.
  • HRCT: band-shaped, subpleural and peribronchial stressed focal consolidations with basal predominance -> migrating consolidations.
  • Atoll sign: ring-like consolidation with a central milk glass.
31
Q

exogen allergic alveolitis, EAA (“farmer lung”, hypersensitivity pneumonitis - HP)

A
  • occupational -> immunological/unclear etiology.
  • immune reaction of the alveoli and bronchioles.
  • inhalation of organic dusts (actinomycetes, aspergilli, excrements, flour), chemotherapeutic agents
  • x-ray: normal in the acute & subacute stage. Fibrosis in the chronic stage.
  • HRCT: acute/subacute stage -> milk glass infiltrates (centrilobular), reticular pattern, bronchial wall thickening
32
Q

silikosis

A
  • occupational / pneumoconiosis
  • inhalation of mineral dusts (eg. SiO2, coal)
  • CT:
  • nodules
  • hilar and mediastinal lymphadenopathy -> Eggshell calcifications
  • complicated pneumoconiosis: fibrosis
33
Q

asbestosis

A
  • occupational / pneumoconiosis
  • inhalation of asbestos fibres
  • manifestation 20-40 years after exposure
  • malignisation: pleural mesothelioma, bronchial carcinoma
  • 5-10% of all asbestosis cases develop with a latency of 20-30 years

*CT:
- interlobular septal thickening
- honeycomb pattern
pleural plaques

34
Q

mesothelioma

A
  • clinical sings: chest pain, dyspnoea, weight loss, fever.
  • infiltration of the thorax wall & ribs come before survival is an average of 18-28 months.
  • x-ray, CT: elongated or glandular pleural thickening - thickness > 10 mm, pleural calcifications.
35
Q

what is the method of choice for characterisation of interstitial changes?

A

HRCT

36
Q

solitary lung nodules: possible causes

A
tuberculoma
bronchial carcinoma
metastasis
hamartoma
abscess
aspergilloma
adenoma
round atelectasis
AV shunt
bronchogenic cyst
sequestration
echinococcal cyst
infarction
37
Q

multiple lung nodules: possible causes

A
  • miliary: TB, sarcoidosis, histiocytosis, silicosis, metastases
  • medium (sub-miliary): bronchogenic TB, metastases, peripheral Kaposi sarcoma
  • large: metastases, Wegener’s disease, lymphoma
38
Q

differential diagnosis of nodules

A

tumor
inflammation
connective tissue disorders & vasculitis
pneumoconioses
vascular diseases
hypersensitivity & idiopathic diseases

  • centrilobular nodules: bronchial disease, pulmonary edema, vasculitis
  • perilymphatic nodules: sarcoidosis, silicosis, lymphangiosis, cc
  • random: miliary TB, miliary fungal infection, miliary viral infection, metastases
39
Q

perilymphatic nodules: DDx

A
  • silicosis:
  • upper lobe
  • pseudo-plaques
  • calcified hilar lymph nodes
  • sarcoidosis:
  • upper lobe
  • symmetric lymphadenopathy (BHL)
  • peribronchovascuar nodules
  • lymphangitis:
  • irregular nodular thickening of the interlobular septa
  • pleural effusion
40
Q

random distribution of lung nodules : DDx

A
  • inflammatory:
  • TB
  • virus: CMV, flu, chickenpox
  • fungi: blastomycosis, histoplasmosis
  • metastases:
  • thyroid cancer
  • adenocarcinoma
41
Q

solitary pulmonary nodules (< 3 cm)

A

round or oval
surrounded by the lung parenchyma

benign Vs malignant - depends on:

  • density
  • growth rate
  • wind, shape
  • cavitation
  • air
  • calcification
  • size
42
Q

density: the three types of lung nodules (<3 cm)

A
  • solid nodule
  • parsolid (semisolid) nodule
  • clear ground glass (GG) (nonsolid) nodule
43
Q

growth rate of solitary nodule

A
  • volume doubling time (VDT): volume doubling over time = 26% diameter increase
  • solid nodules:
  • VDT: 20-400 days: most likely malignant
  • VDT: <20 or > 400 days: likely benign
  • there is no growth in 2 years: the most reliable sign of benign behaviour
  • subsolid nodules can grow very slowly
44
Q

wind, shape of solitary nodule

A
  • sharp, spherical: 20-30% malignant

- lobulated, spiculated, irregular: 33-100% malignant

45
Q

cavitation of solitary nodules

A
  • especially in squamous cell carcinoma
  • any size
  • often eccentric
  • often thick, irregular wall ( =/> 5mm)
  • air and/or liquefaction
  • often air-fluid level
46
Q

air in the solitary nodule

A
  • air bronchogram
  • cyst-like hypodensities (“soap bubbles”)
  • most commonly: adenocarcinoma
47
Q

calcification in the solitary nodule

A
  • benign patterns: diffuse, central, popcorn, laminated

- malignant pattern: stippled, eccentric

48
Q

node detection

A
  • CAD = computer aided diagnosis: better for hilar than peripheral nodes
  • RAD = diagnosis by a radiologists: better for subpleural than central nodules
49
Q

primary tumors

A
  • benign: hamartoma, chondroma, lipoma -> rare
  • semimalignant: adenoma, hamartoma, carcinoid
  • malignant bronchial carcinoma
  • BAC (bronchoalveolar carcinoma)
50
Q

semimalignant tumors

A
  • adenoma, hamartoma, carcinoid
  • x-ray: round or lobulated node with well demarcated boundary, calcifications
  • CT: small hilar lymphadenopathy, possible metastases
51
Q

malignant bronchial carcinoma

A
  • central: in hilar area, unclear hilar extension
  • peripheral: in the lung parenchyma or along the thoracic wall
  • pancoast tumor: in the lung apex. Grows transpleurally though the chest wall, infiltrating the cervical sympathetic ganglia
52
Q

bronchoalveolar carcinoma (BAC)

A
  • spreads into the alveoli
  • manifested by multinodular, infiltrative condensations in the peripheral pulmonary parenchyma
  • can also appear int he from of round condensations
  • 1-9% of all lung tumors
  • subtype of NSCLC (adenocarcinoma)
  • 50% asymptomatic
  • terminal bronchioles + alveoli are affected
  • slow, non-invasive growth -> the blood and lymph vessels surrounding the lung parenchyma are not affected -> lepidic growth
  • pre-invasive malignant lesions (in situ carcinoma) -> invasive adenocarcinoma
  • non-smoker, women, Asia
53
Q

carcinoid

A
  • central lesion
  • well circumscribed, round or oval
  • 2-5 cm
  • homogenous contrast enhancement
  • calcification (eccentric)
54
Q

metastases

A
  • hematogenous spread: breast, prostate, kidney, thyroid, cervical, testicular, bone, melanoma, gastrointestinal and pancreatic tumors
  • lymphatic spread: breast, bronchial carcinoma
  • lymphangitis carcinomatosa
55
Q

staging of lung cancer

A
  • DDD (detection, delineation, differentiation)
  • nodules: > 8-10 mm –> DO STAGING
  • TNM staging:
  • T: CT, MRI assessment of some cases (resectability)
  • N: PET-CT
  • M: PET-CT or MRI
56
Q

screening for lung cancer

A

CT

  • low dose CT
  • volumetry
  • disadvantages:
  • overdiagnoses
  • false positive cases –> reduced by categorisation of nodules & volumetry for accurate assessment of growth
  • resection through benign disease
  • advantages:
  • fear-induced anxiety –> smoking cessation