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Chest Imaging > Pulmonary vascular disease > Flashcards

Pulmonary vascular disease Flashcards

1
Q

Under normal conditions, interstitial spaces of the lung is kept dry by

A

Pulmonary lymphatics located within the axial and peripheral interstitium of the lung

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2
Q

Because there are no lymphatic structures immediately within the alveolar walls (parenchymal interstitium), filtered interstitial fluid is drawn to lymphatics by a

A

Pressure gradient from alveolar interstitium to the axial and peripheral interstitium

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3
Q

When the rate of fluid accumulation in the interstitium exceeds the lymphatic drainage capabilities of the lung, fluid accumulates first within the

A

Interstitial spaces

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4
Q

Most common mechanism of pulmonary edema

A

Change in the normal starling forces that govern fluid movement in the lung

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5
Q

Imbalance of starling forces in pulmonary edema is most commonly the result of

A

Increase capillary hydrostatic pressure, and less commonly diminished plasma oncotic or interstitial hydrostatic pressure

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6
Q

Another mechanism in pulmonary edema aside from imbalance in starling forces

A

Obstruction or abscess of normal pulmonary lymphatics, injury in the epithelium of capillaries and alveoli, causinh increase in capillary permeability that allows protein rich fluid to escape from capillaries into pulmonary interstitium

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7
Q

Thickening of axial interstitium results in what imaging findings

A

Loss of definition of intrapulmonary shadows and thickening of peribronchovascular interstitium causinh peribronchial cuffing and tram tracking

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8
Q

Involvement of peripheral and subpleural interstitial structures in pulmonary edema produces

A

Kerley lines and subpleural edema

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9
Q

Represents thickening of central connective tissue septa and peripheral interlobular septa, respectively

A

Kerley A and B lines

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10
Q

It is the accumulation of fluid within the innermost (interstitial) layer of the visceral pleura

A

subpleural edema

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11
Q

subpleural edema are is best seen in ____ and appears as smooth thickening of the interlobular fissures

A

lateral radiographs

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12
Q

Develops when fluid in the interstitial spaces extends into the alveoli

A

Airspace pulmonary edema

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13
Q

Most common form of pulmonary edema

A

Hydrostatic pulmonary edema

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14
Q

Hydrostatic pulmonary edema is usually caused by elevation in pulmonary venous pressure (pulmonary venous hypertension)

A

elevation in pulmonary venous pressure (pulmonary venous hypertension)

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15
Q

Causes of pulmonary venous hypertension may be divided into four major categories

A

obstruction to left ventricular inflow, left ventricular systolic dysfunction (LV failure), mitral valve regurgiation and systemic or pulmonary volume overload

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16
Q

classic cause of obstruction to left ventricular inflow is

A

mitral stenosis

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17
Q

more common causes of LV inflow obstruction

A

poor left ventricular compliance (diastolic dysfunction), such as caused by hypertrophy or chronic ischemic subendocardial fibrosis

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18
Q

Common causes of LV failure include

A

ischemic heart disease, aortic valve stenosis and regurgitation, and nonischemic cardiomyopathy

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19
Q

Normal pcwp

A

8-12 mmHg

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20
Q

Pcwp level that leads to findings of interstitial pulmonary edema such as loss of vascular definition, peribronchial cuffing and Kerley lines

A

19-25 mmHg

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21
Q

Pcwp level that produces alveolar filling with radiographic findings of bilateral airspace opacities in the perihilar and lower lung zones

A

More than 25 mmHg

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22
Q

classic radiographic findings of Pulmonary Venous Hypertension

A

enlargement of pulmonary veins and redistribution of pulmonary blood flow to the nondependent lung zones

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23
Q

True or false: with PVH in the upright patient with normal lung parenchyma, the upper zone vessels are frequently as large as or larger in diameter than the lower zone vessels

A

true

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24
Q

alveolar pulmonary edema localized to the right upper lung may be seen in patients with

A

severe mitral regurgitation

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25
Q

When respiratory failure develops as a result of this condition, and is associated with increased lung stiffness (noncompliance) it is termed

A

acute lung injury or when severe, ARDS

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26
Q

most common causes of increased permeability edema

A

shock, severe trauma, burns, sepsis, narcotic overdose and pancreatitis

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27
Q

key factors in the development of capillary endothelial damage

A

recruitment and activation of neutrophils in the lung, with release of enzymes and oxygen radicals

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28
Q

Stage of ARDS: happens within 12-24 hours following initial insult, damage to capillary endothelium produces engorged capillaries and proteinaceous interstitial edema

A

Stage 1: exudative

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29
Q

Stage of ARDS: within the first week, injury to type 1 pneumocytes leads to flooding of alveoli with edema fluid and proteinaceous and cellular debris, which form hyaline membranes lining the distal airways and alveoli

A

Stage 2: proliferative

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30
Q

Stage of ARDS: occurring 10 to 14 days following the initial insult, type 2 pneumocytes proliferate in an attempt to reline the denuded alveolar surfaces and fibroblastic tissue proliferates within the interspaces

A

Stage 3: fibrotic

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31
Q

Radiographic pattern of ARDS

A

patchy peripheral airspace opacities by 12-24 hours, with minimal or absent interlobular septal thickening, coalesce over the next dats to produce confluent bilateral airspace opacities with air bronchograms, after a week becomes coarse reticulonodular, if unchanged, honeycombing

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32
Q

in pulmonary edema associated with chronic cardiac failure, the vascular pedicle, which represents the mediastinal width at the level of SVC and left subclavian artery measures

A

> 53 mm on PA radiograph

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33
Q

90% of all primary tracheal tumors in adults are malignant or benign?

A

Malignant

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34
Q

Most common histologic type of primary tracheal malignancy

A

Squamous cell carcinoma

35
Q

Majority of tracheal malignancy arise in what area

A

Distal trachea, within 3-4 cm of tracheal carina

36
Q

Second next common site in tracheal neoplasms

A

Cervical trachea

37
Q

Malignant neoplasm that arises from the tracheal salivary glands and accounts for 40% of primary tracheal malignancies. Tends to involve the posterolateral wall of the distal 2/3 of trachea or main or lobar bronchi

A

Adenoid cystic carcinoma

38
Q

Arises from tracheal cartilage and is identified by the presence of calcified chondroid matrix within the tumor

A

Chondrosarcoma

39
Q

Most common type of thyroid malignancy to invade the trachea

A

Papillary and follicular

40
Q

Extrathoracic primary tumors that are most often associated with hematogeneous endotracheal metastases are carcinomas of

A

Breast, kidney and colon and melanoma

41
Q

capillary permeability edema can sometimes be distinguished from hydrostatic edema by the following:

A

a non-dependent or peripheral distribution of edema, absence of other signs of hydrostatic edema such as interlobular septal thickening and subpleural edema, and a lack of short term change

42
Q

true or false: in neurogenic pulmonary edema, both hydrostatic and increased permeability mechanisms are involved

A

true

43
Q

high altitude pulmonary edema happens in individuals who had rapid ascent of altitudes above

A

3500 m

44
Q

Pathophysiology of high altitude pulmonary edema

A

edema typically develops within 48-72 hours of ascent and appears to reflect a varied individual response to hypoxemia, in which scattered areas of pulmonary arterial spasm result in transient pulmonary arterial hypertension—> causes damage to capillary endothelium and increase permeability edema, typically with a patchy distribution

45
Q

more susceptible to reexpansion pulmonary edema

A

rapid evacuation of large pneumothorax or PE present for more than 48 hours and young age

46
Q

Pulmonary edema may also happen after immediate treatment of acute upper airway obstruction due to

A

creation of markedly negative intrathoracic pressure by attempts to inspire against an extrathoracic airway obstruction, producing decreased interstitial hydrostatic pressure, thereby promoting transudation of fluid into lungs

47
Q

severe and often fatal form of pulmonary edema tha may develop in a pregnant woman when amniotic fluid gains access to the systemic circulation during labor

A

amniotic fluid embolism

48
Q

fetal distress and demise may happen in amniotic fluid embolism because of ___ which play a key role in the pathogenesis of this disorder

A

mucin within fetal meconium

49
Q

contributes to vascular collapse leasding to sudden PAH, cor pulmonale with decreased CO and pulmonary edema in amniotic fluid embolism

A

anaphylactoid reaction and DIC

50
Q

There may be enlargement of central pulmonary arteries and right heart as manifestation of

A

cor pulmonale

51
Q

common complication occurring 24 to 72 hours after the fracture of a long bone such as the femur

A

fat embolism

52
Q

mechanism of pulmonary edema in fat embolism

A

fat is hydrolyzed to its component fatty acidsm causing increased pulmonary capillary permeability and hemorrhagic pulmonary edema

53
Q

systemic findings of fat embolism

A

petechial rash, CNS depression and pulmonary changes

54
Q

Autoimmune diseases associated with pulmonary hemorrhage

A

Goodpasture syndrome, idiopathic pulmonary hemorrhage, granulomatosis with polyangiitis, sytemic lupus erythematosus, RA and polyarteritis nodosa

55
Q

autoimmune disease characterized by damage to the alveolar and renal glomerular basement membranes by a cytotoxic antibody. the antibody is directed primarily against renal glomerular basement membrane and cross reacts with alveolar basement membrane to produce renal injury and pulmonary hemorrhage characteristics of this disorder

A

Goodpasture syndrome

56
Q

diagnosis of Goodpasture disease

A

immunofluoresent studies of renal or lung tissue

57
Q

development of pulmonary hemorrhage in vasculitides such as granulomatosis with polyangitis, SLE, RA and polyarteritis nodosa are due to

A

small vessel pulmonary arteritis and capillaritis which results in spontaneous hemorrhage

58
Q

main laboratory test in patients with suspected pulmonary embolism

A

plasma D-dimer level

59
Q

It is a degradation product of fibrin and is a very sensitive indicator of the presence of venous thrombosis

A

D-dimer

60
Q

First examination obtained in all patients with suspected PE

A

chest radiograph

61
Q

most common radiographic findings in pulmonary embolism without infarction are

A

peripheral airspace opacities and linear atelectasis

62
Q

Known as the westermark sign which is extremely rare finding in pulmo embolism

A

localized peripheral oligemia with or without distended proximal vessels

63
Q

known as Hampton hump in infarction related to pulmo embolism

A

presence of pleural effusion and the development of a pleura-based wedge-shaped opacity which lacks air bronchogram

64
Q

Hampton hump in pulmo embolism is usually seen in what area

A

posterior or lateral costophrenic sulcus of the lung

65
Q

in embolism without infarction, airspace opacities should resolve completely within how many days

A

7-10 days

66
Q

first imaging study to be done in pregnant women with a normal chest radiograph in the diagnosis of pulmo embolism

A

Ventilation/perfusion lung scintigraphy using IV macroaggregated albumin radiolabeled with technetium (Tc-99m)

67
Q

Recommended study for detection of pulmonary embolism

A

CT angiography of pulmonary arteries

68
Q

CT pulmo angiography is better done in what phase of respiration

A

expiratory

69
Q

chronic emboli should be suggested when

A

filling defect is adherent to the vessel wall rather that in the center of lumen or when a web is present

70
Q

technique selectively used whena definitive diagnosis of pulmo embolism or DVT cannot be achieved by less invasive means. It requires right heart and pulmonary artery catheterization

A

digital subtraction angiography

71
Q

secondary signs of pulmo embolism in pulmonary angiography include

A

prolonged arterial phase, diminished peripheral perfusion and delay in the venous phase

72
Q

causes of nonthrombotic pulmonary embolism

A

air embolism, fat embolism, methylmethacrylate embolization complicating vertebroplasty, radioactive seed implant embolization from prostate brachytherapy

73
Q

pulmonary tumor emboli usually comes from what malignancies

A

renal cell carcinoma, breast cancer, HCC and GI malignancy

74
Q

pulmonary arterial hypertension is defined as a systolic pressure in the pulmonary artery exceeding ___ mmHg either measured directly by right heart catheterization or as estimated by echocardiography

A

30

75
Q

typical radiographic findings of PAH

A

enlarged main and hilar pulmonary arteries that taper rapidly toward the lung periphery

76
Q

useful measurement for enlargement of central pulmonary artery, usually indicating PAH in the absence of a left-to-right shunt is a transverse diameter of proximal interlobar artery on PA radgiograph that exceeds

A

16 mm

77
Q

in patients younger than 50 years, in the diagnosis of PAH, a ratio of diameter of the MPA( measured at the level of the main Right PA) to the transverse diameter of ascending aorta at the same level greater than 1 strongly correlated with a mean PA pressure greater than

A

20 mmHg

78
Q

In patients older than 50 years, a maximum transverse measurement of MRA greater than ___ mmHg correlates better with PAH

A

29

79
Q

Flattening or bowing of the interventricular septum toward the LV indicates

A

RV hypertension

80
Q

Signs of long standing PAH

A

RV hypertrophy, RV dilatation, and right heart failure (cor pulmonale)

81
Q

disease among young women in whom medial hypertrophy and intimal fibrosis obliterate the muscular arteries

A

plexogenic pulmonary arteriopathy

82
Q

a condition related to PVOD which is characterized by the proliferation of capillaries throughout the pulmonary interstitium, resulting in benular obstruction

A

pulmonary capillary hemangiomatosis

83
Q

combination of pulmonary edema with a normal sized heart, absent findings for PVH, normal PCWP and insiduous onset of dyspnea should suggest this diagnosis rather than left heart failure, mitral valve disease or large vessel pulmonary venous occlusion

A

pulmonary capillary hemangiomatosis/PVOD

84
Q

radiographic findings in PCH/PVOD

A

interlobular septal thickening, centrilobular nodular ground-glass opacities, and pleural effusions

Chest Imaging (9 decks)

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