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AA Sal Chest Radiology > Diffuse lung disease/Pulm HTN > Flashcards

Diffuse lung disease/Pulm HTN Flashcards

1
Q

Imaging findings of 3 distinct phases.

  1. acute
  2. subacute (classic sign)
  3. Chronic (classic sign)
A

Hypersensitivity pneumonitis - reaction due to inhaled organic antigens like bird proteins, thermophilic actinomycetes.

  1. Acute (rarely seen) - inflammatory exudate filling alvuli - nonspecific GGO
  2. subacute; centrilobular ground glass; mosaic attenuation. Head cheese sign; patchy GGO and areas of lucency due to mosaic attenuation
  3. upper lobe predominant pulm fibrosis. (head cheese sign)
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2
Q

Classic imaging findings

  1. Demographics
  2. Histologic appearance
  3. Prognosis and response to steroids
  4. Associated with what disease?
  5. 2 types
A

NSIP - Ground glass, subpleural sparing. Effects posterior and peripheral lobes, like UIP

  1. Younger patients (40s-50s) compared to IPF
  2. Thickened alveolar septa from chronic inflammation (less fibrotic change compared to IPF)
  3. Better prognosis than IPF, responds to steroids
  4. Scleroderma (Can show dilated esophagus to suggest scleroderma)
  5. Fibrotic NSIP. Cellular NSIP
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3
Q
  1. Classic imaging
  2. Pathologic corresponding name
A

IPF - Most common ILD, bad prognosis

  1. Honeycombing, traction bronchiectasis, basilar predominant (Apical to basal gradient)
  2. Usual interstitial Pneumonia
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4
Q
  1. Definition of Pulmonary ARTERIAL hypertension
  2. Definition of pulmonary VENOUS hypertension
A
  1. >25mmHG Pulm arterial systolic pressure
  2. >18mm Pulm cap wedge pressure (an approximagion of pulm venous pressure)
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5
Q

How are Precapillary and postcapillary causes of pulm hypertension described?

A
  1. Precapillary: primary abnormality is pulm arterial system or pulm parenchyma leading to alveolar hypoxia
  2. Postcapillary causes: abnormality of pulmonary veins or elevation of pulm venous pressure
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6
Q

WHO 5 groups of pulm HTN etiologies

A
  1. Pulm Arterial HTN - PPH (primary pulm HTN), congenital left to right shunts, Pulmonary veno-occlusive disease and pulm capillary hemangiomatosis
  2. Pulm venous HTN - Left sided heart disease
  3. Pum hpertension a/w chronic hypoxemia - COPD, Interstitial lung disease, sleep apnea,
  4. CTEPH
  5. Pulm HTN due to misc disorders
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7
Q

Pulm HTN findings

Describe hilum convergence sign

A

Main PA diameter > 3 cm

Pulm artery calcifications (pathognomonic)

CTEPH - mosaic attenuation

Ground glass centro-lobular nodules (especially in pulm veno-occlusive disease)

Hilum Convergence sign: hilar pulmnoary artery branches converging into an enlarged PA

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8
Q

Describe the 3 WHO group 1 Pulm HTN etiologies

A

Primary Pulmonary Hypertension (PPH), precapillary: Enlargement of main PA w/ tapering of vessels

Cardiac shunts, Precapillary: (ASD, VSD, PAPVR)

Pulm veno-cclusive disease, precapillary: fibrotic obliteration of pulm veins/venules. Imaging features include pulm arterial enlargement, pulm edema, and ground glass/centrilobular nodules.

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9
Q
  1. What is this WHO5 pulm hypertension disease?
  2. Most common causes
A
  1. Who5: fibrosing mediastinitis - progressive proliferation of fibrous tissue w/in the mediastium. May lead to encasement and compression of mediastinal structure
  2. . Histoplasmosis, tb
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10
Q

3 plain film signs of PE

A
  1. Fleischner sign - widening of PA due to clot (picture)
  2. Hampton’s Hump - peripheral wedge shaped opacity - infarct
  3. Westmark sign: focal peripheral hyperlucency secondary to oligaemia in lung distal to PA thrombus
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11
Q
  1. CT findings
  2. Treatment
A

Cryptogenic organizing pneumonia

granulation tissue polyps that fill the distal airways and alveoli

  1. mixed consolidatino and GGO in peripheral and peribornochovascular distribution. Atoll sign (reverse halo)
  2. Tx. Steroids
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12
Q

Respiratory bronchiolitis - Interstitial lung disease (RB-ILD)

Smoking related disease

  1. Describe RB and RB-ILD
  2. CT appearance
  3. Histologic appearance
A
  1. RB: pigmented macrophages are found in respiratory bronchioles (very common in smokers)

RB-ILD is when people have RB + symptoms

  1. Centrilobular nodules and patchy GGO.
  2. Histologically - sheets of macrophages filling the terminal airways.
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13
Q

Desquamative interstitial pneumonia (DIP)

RB-ILD and DIP are a spectrum (both smoking related)

  1. Describe DIP
  2. Imaging features
A
  1. DIP: The macrophages have now made it to the alveoli
  2. Imaging: diffuse-basal predominant, patchy or subpleural GGO. Cysts may also be present.
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14
Q

What is this?

  1. Commonly a/w what?
  2. imaging
  3. histologic landmark?
A

Lymphoid interstitial pneumonia - rare

  1. Sjorden
  2. Diffuse lower lobe predominant GGO. Scattered cysts (due to air trapping). Pneumothorax may occur in advanced disease.
  3. diffuse infiltration of interstitium by lymphocytes
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15
Q

Acute interstitial pneumonia (AIP) - AKA DAD

Acute onset, terrible prognosis.

  1. What is primary cause
  2. What are 2 phases?
A
  1. Primary cause is surfactant destruction
  2. Early exudative phase: hyaline membranes, diffuse alveolar infiltration by immunce cells, noncardiogenic edema

Chronic phase: alveolar wall thickening (1 week after inhalational injury).

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16
Q

Name the interstital lung diseases. Which is the worst? which are smoking related?

A

IPF: (2nd worst. UIP is pathologic name)

NSIP (smoking)

COP

RB-ILD, DIP (both smoking)

LIP

AIP (acute, worst prognosis)

17
Q

Hypersensitivity pneumonitis - Organic antigens

  1. acute phase
  2. Subacute phase? Classic imaging sign?
  3. Chronic
A

Acute: inflammatory exudate filling the alveoli - GGO and centrilobular nodules

subacute: centrilobular ground glass nodules, mosaid attenuation. Head cheese sign

Chronic HSP: upper lobe predominant pulm fibrosis. Superimposed mosaic attenuation, centrilobular nodules, ggo

18
Q

Pneumonoconiosis - INORGANIC dust inhalation

  1. name 2 most common pneumoconioses
  2. Imaging (classic calcs?)
  3. Pneumoconiosis = increased risk of what?
  4. Caplan syndrome
  5. Inhaled disease that effects LOWER Lobes
A
  1. Silicosis, Coal workers pneumoconiosis (CWP)
  2. Uncomplicated disease: multiple upper lobe centrilobular and subpleural nodules

eggshel lymph node calcs (silicosis)

complicated: Progressive massive fibrosis
3. TB
4. RA + CWP or silicosis.
5. Asbestosis (particles are too large to be removed by macrophages/lymphatics)

19
Q

Eosinophilic lung disease

  1. Simple pulmonary eosinophilia - AKA what?

Imaging

  1. Chronic eosinophilic pneumonia - imaging
  2. treatment?
A
  1. Loffler sndrome

Migratory areas of focal consolidation

  1. extensive alveolar filling and interstitial infiltration w/ inflammatory eosinophils.

Pathcy peripheral consolidation w/ upper lobe preference

  1. Steroids
20
Q

Pulmonary vasculitis (name 3)

A

Churg-Strauss, microscopic polyangiitis, Wegner

21
Q

Churg-Strauss - small vessel vasculitis

  1. Imaging
  2. Which titer is positive?
A
  1. periphearl consolidation or ground glass
  2. P-Anca
22
Q

microscopic polyangiitis

  1. Describe clinical findings
  2. Imaging
A
  1. Most common cause of pulm hemorrhage w/ renal failure
  2. Diffuse central predominant ground glass
23
Q

Wegner’s granulomatosis - Systemic small vessel vasculitis

  1. Classic clinical triad
  2. Titer?
  3. 3 places it effects
A
  1. Sinusitis, lung involvement, renal insufficiency
  2. C-Anca is positive
  3. Upper airways - nasopharyngeal/eustachian tube obstruction. involvement of larynx/bronchi

Lungs; Multiple cavitary nodules - don’t respond to abx

Kidneys

24
Q

Lung Drug toxicity. What reaction patterns can occur?

A

Pulm Edema, ARDS, organizing pneumonia, eosinophillic pneumonia, bronchiolitis obliterans, pulm hemorrhage, NSIP, UIP.

25
Q

Radiation lung injury

  1. Early radiation pneumonitis
  2. Radiation fibrosis
A
  1. Occurs w/in 1 month - most severe at 3-4 months after treatment. Ground glass cenetered at radiation port
  2. 6-12 months after therapy.

Key finding is distribution of fibrosis and traction bronchiectasis.

26
Q

Sarcoidosis

  1. Stages of fibrosis (0-4)
  2. Most common CT finding of sarcoidosis
  3. Bronchial involvement may cause what lung pattern?
A
  1. Stage 0: normal

Stage 1: Hilar or mediastinal adenopathy only

Stage 2: Adenopathy WITH lung changes

Stage 3: Diffuse lung disease WITHOUT adenopathy

Stage 4: End stage fibrosis

  1. Perilymphatic nodules of variable sizes.
  2. Mosaid attenuation due to air trapping.
27
Q

Pulmonary langerhans cell histiocytosis - smoking related lung disease

  1. Disease is most often isolated to lungs, but where else can it effect?
  2. Progressgion of disease
  3. radiographic findings
  4. treatment
A
  1. Lucent bone lesions, diabetes insipidus, hypophysitis, skin involvement.
  2. Nodules –> Cavitary nodules –> irregular cysts. It can sometimes present as pneumothorax
  3. upper lobe predominant cysts, and irregular peribronchovascular
  4. Responds to steroids and quitting smoking
28
Q

Ddx for disease affecting lungs, and bones?

A

PLCH, malignancy, tb, fungal disease, sarcoidosis, gaucher disease

29
Q

Pulmonary alveolar Proteinosis - idiopathic disease causing filling of the alveoli w/ proteinaceous lipid rich material

  1. Radiographic findings
  2. CT hallmark
  3. Susceptible to superimposed infection, particularly whar?
  4. Treatment?
A
  1. May have perihilar opacification like pulm edema, but heart size is normal and there are no pleural effusions.
  2. Crazy paving.
  3. Nocardia (presents as consolidation)
  4. Bronchioalveolar lavage.
30
Q

Lymphangioleiomatosis - thin regular shaped cysts involveing all 5 lobes

  1. Describe pathogenesis
  2. Epidemiology
  3. Treatment?
  4. Associated with what complications
A
  1. Bronchiolar obstruction and lung destruction due to proliferation of muscle cells in small vessels, lymphatics, and bronchioles
  2. Women w/ child bearing age. 1% of patiets w/ tuberous sclerosis have LAM.
  3. Some cases respond to anti-estrogen therapy
  4. Chylothorax, pneumothorax

AA Sal Chest Radiology (6 decks)

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