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Pulmonary > PATH: Neonatal, Developmental and Vascular Diseases > Flashcards

PATH: Neonatal, Developmental and Vascular Diseases Flashcards

1
Q

What are the 2 broad causes of pulmonary edema?

A

Hemotynamic Forces

microvascular Injury

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2
Q

What are some hemodynamic forces that can lead to pulmonary edema?

A 
increased hydrostatic pressure (common)
 decreased oncotic pressure (less common)
lymphatic obstruction (rare)
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3
Q

What are some examples of microvascular injury that can lead to pulmonary edema?

A 
shock (common)
pulmonary infection (less common)
inhaled toxins (much less common)
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4
Q

What is the MOST COMMON cause of pulmonary edema?

A

left sided heart failure

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5
Q

Why do “heart failure cells”= hemosiderin-laden macrophages collect in the alveoli in some cases of pulmonary edema?

A

Extremely high hydrostatic pressure can burst capillaries leading to microhemorrhages that are “cleaned up” by these macrophages

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6
Q

Where does fluid first accumulate in the lung after leaking out of capillaries?

A

septal capillaries–> interstitium–> airspaces

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7
Q

At what hydrostatic pressure does fluid leak from the capillaries and into the interstitium?

A

20 mmHg

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8
Q

At what pressure does fluid transudate out into the alveoli to cause pulmonary edema?

A

25 mmHg

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9
Q

What clinical sign of pulmonary edema will be seen before a patient develops pulmonary crackles?

A

dyspnea due to increased pulmonary venous pressure

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10
Q

What is the appearance of pulmonary edema fluid?

A

thin, white and frothy

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11
Q

What is the microscopic appearance of lung with pulmonary edema?

A

alveoli with thin, pale pink, finely granular material and the small blood vessels are congested

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12
Q

What is acute lung injury?

A

abrupt onset of hypoxemia and bilateral (radiographic) pulmonary infiltrates in the absence of heart failure

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13
Q

What value divides ARDS into its 3 different severities?

A

ratio of arterial oxygen pressure divided by fraction of inspired oxygen
(PaO2/FiO2)

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14
Q

What is a normal PaO2/FiO2?

A

476

100 mm Hg/ 0.21

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15
Q

What is the 4 most common causes of ARDS?

A

sepsis
diffuse pneumonia
gastric aspiration
trauma

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16
Q

What are the molecular mediators of early ARDS? What releases them?

A

TNF and IL-1 released by alveolar macrophages

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17
Q

What do TNF and IL-1 do in the alveoli?

A

activate endothelial cells making them put up adhesion molecules for neutrophils

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18
Q

What do neutrophils do in the alveoli?

A

they degranulate and release injurious proteases and ROSs

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19
Q

What is “Diffuse alveolar damage”?

A

histopathologic counterpart of ARDS

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20
Q

What occurs in the first 12-24 hours of diffuse alveolar damage?

A

congestion, interstitial and alveolar edema, and neutrophils (initially in capillaries, then interstitium and finally airspaces)

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21
Q

What occurs in the 24-72 hours following onset of diffuse alveolar damage?

A

loose granular pink edema fluid in the alveoli gradually condenses into dense, darker pink, smooth “hyaline membranes”

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22
Q

Why might you misdiagnose diffuse alveolar damage as cancer around the 2nd day of injury in diffuse alveolar damage?

A

type 2 pneumocytes start proliferating to replace dead type 1 cells (and look like cancer cells)

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23
Q

What happens to the hyaline membrane in diffuse alveolar damage?

A

it is gradually resolved over 3 weeks if the patient lives

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24
Q

What occurs around 72 hours following onset of diffuse alveolar damage?

A

lymphocytes, macrophages, and fibroblasts infiltrate the interstitium

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25
Q

What occurs in the organizing phase of diffuse alveolar damage?

A

granulation tissue forms in alveolar walls that may resolve or (if more severe) lead to scarring

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26
Q

What is the presentation of a patient with diffuse alveolar damage?

A

dyspnea, cyanosis and diffuse pulmonary crackles within 6-72 hours and worsen rapidly

27
Q

How do you treat ARDS?

A

mechanical ventilation

28
Q

What is a pulmonary thromboembolism?

A

thrombi in the lungs that have traveled there from elsewhere in the body.

29
Q

What is Virchow’s triad?

A

endothelial injury
abnormal blood flow
hypercoagulability

30
Q

Where do most venous thromboemboli come from?

A

DVT in thigh

31
Q

What is the gross pathology of thromboemboli?

A

firm, variegated, sometimes with alternating light and dark layers (lines of Zahn), tubular, branched and crammed into pulmonary arteries like coiled snakes

32
Q

Describe the gross pathology of a pulmonary infarct?

A

subpleural, wedge-shaped and hemorrhagic

33
Q

What is in a thromboembolus?

A

variable mixture of all the elements of blood (red cells, platelets, fibrin) with condensation of the fibrin over time

34
Q

What are the major symptoms of pulmonary thromboembolus?

A

dyspnea (73%), pleuritic chest pain (44%), leg pain (44%), leg swelling (41%), cough (34%)

35
Q

What are the major signs of a pulmonary thromboembolus?

A

tachypnea (54%), tachycardia (24%), pulmonary crackles (18%)

36
Q

What lab values may be elevated in a patient with a pulmonary thromboembolism?

A 
erythrocyte sedimentation rate (ESR) 
lactate dehydrogenase (LDH) aspartate aminotransferase (AST)
B-type natriuretic peptide (BNP)
37
Q

What is most likely the “best test” for pulmonary thromboembolism?

A

spiral computed tomography with IV contrast

38
Q

How do you treat a pulmonary thromboembolism?

A

anticoagulation (ex. heparin followed by warfarin) +/- thrombolytic therapy

39
Q

What is the definition of pulmonary HTN?

A

mean pulmonary arterial pressure of ≥25 mmHg at rest.

40
Q

What are the major causes of pulmonary HTN?

A

heart disease

intrinsic lung disease

41
Q

What is primary pulmonary HTN?

A

idiopathic pulonary HTN (not associated with another disease)

42
Q

What mutations have been found in 75% of familial cases of primary pulmonary HTN?

A

Inactivating germline mutations in the bone morphogenetic protein receptor type 2 (BMPR2) gene

needs a second hit

43
Q

What is the consequence of the inactivation of the bone morphogenetic protein receptor type 2 (BMPR2) gene ?

A

dysfunction and proliferation of endothelial cells and vascular smooth muscle cells

44
Q

What pathological finding is universal among all forms of pulmonary HTN?

A

Hypertrophy and hyperplasia of the smooth muscle in the tunica media of the pulmonary muscular and elastic arteries

45
Q

What are the most common symtpoms of pulmonary HTN?

A

none by itself, but exertional dyspnea and fatigue, which often relate to the underlying heart or lung disease causing the pulmonary hypertension

46
Q

What are the signs of pulmonary HTN?

A

Increased S2

Raised JVP

47
Q

What is the gold standard for diagnosing pulmonary HTN?

A

right heart catheterization

48
Q

After treating the underlying cause of pulmonary HTN, what is the treatment?

A

prostanoids, endothelin receptor antagonists, phosphodiesterase 5 inhibitors, and soluble guanylatecyclase stimulant

49
Q

What is the main cause of hemoptysis?

A

pulmonary infection

50
Q

What is the major cause of pulmonary hemorrhagic syndromes?

A

Autoimmune vasculitis: Goodpasture syndrome, Wegener’s

51
Q

What must you do when evaluating hemoptysis?

A

make sure it is not actually hematemesis

52
Q

What is compression atelectasis?

A

when significant volumes of fluid (transudate, exudate or blood), tumor, or air (pneumothorax) accumulate within the pleural cavity and collapse the lung

53
Q

What is contraction atelectasis?

A

when pulmonary or pleural fibrosis prevents lung expansion.

54
Q

What causes resorption atelectasis?

A

complete obstruction of the airway

55
Q

Why do premature babies get neonatal RDS?

A

lack of surfactant production prior to the third trimester of pregnancy. Surfactant reduces alveolar surface tension, facilitating alveolar expansion and preventing alveolar collapse atelectasis.

56
Q

How can you treat neonatal RDS?

A

synthetic surfactant delivered via endotracheal intubation OR giving the mother glucocorticoids

57
Q

What is pulmonary hypoplasia?

A

defective development of the lungs caused by abnormalities that compress the lung or impede normal lung expansion in utero, such as congenital diaphragmatic hernia and oligohydramnios (deficiency of amniotic fluid).

58
Q

How do tracheoesophageal fistulas present?

A

pneumonia or regurgitation of attempted feeding shortly after birth

59
Q

Why is aspiration pneumonia more common in the right lung?

A

right mainstem bronchus is more vertical than the left.

60
Q

Why do emboli in the lungs cause a lower incidence of infarction than in other organs?

A

lungs have a dual blood supply, when they do infarct, they are HEMORRHAGIC

61
Q

True or false: alveoli are closed off.

A

FALSE: they have pores of Kohn between adjacent alveoli that can allow bacteria to spread

62
Q

Why do neonates whose kidneys failed to make urine in fetal life develop pulmonary hypoplasia?

A

because normal lung development requires “breathing” amniotic fluid largely composed of fetal urine.

63
Q

Why are hematogenous metastases more numerous and larger in the basal lower lobes?

A

because there is more blood at the base of the lungs

Pulmonary (34 decks)

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