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Pulmonary Pathology > ARDS and Pathology of ARDS > Flashcards

ARDS and Pathology of ARDS Flashcards

1
Q

Components of ARDS

A

Low PaO2 (hypoxemia), bilateral infiltrates, low lung compliance. NO left atrial hypertension (problem is ALL pulmonary).

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2
Q

Definition of ARDS

A

PaO2/FIO2 re getting 100% fio2.

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3
Q

Definition of ALI

A

PaO2/FIO2 <300.

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4
Q

Causes of ARDS

A

Sepsis, pneumonia, aspiration, pancreatitis, burns, trauma, transfusions and toxic inhalation.

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5
Q

Pathologic state of ARDS and ALI

A

Diffuse alveolar damage. This is a failure of the alveolar capillary membrane which causes the flooding of alveolar airspaces with proteinaceous material.

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6
Q

Makeup of fluid in the alveolar spaces during ARDS

A

Proteinaceous

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7
Q

What happens when there is diffuse alveolar damage?

A

Proinflammatory cells release proinflammatory cytokines TNF, IL1, IL8. This also causes the production of oxygen derived free radicals.

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8
Q

What is the difference between fluid produced in ARDS and left heart failure?

A

Left heart failure = clean, not proinflammatory like ARDS

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9
Q

What happens during ARDS

A

Depletion of surfactant, disturbance of microcirculation, and fibroblast proliferation in the late stage.

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10
Q

What is the consequence of surfactant depletion?

A

Atalectasis, gas exchange disturbance and decreased pulmonary compliance

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11
Q

What is the consequence of microvascular disturbance?

A

Altered response to NO, cytokine induced activation of the coagulation cascade. This is enhanced by hypoxemia, so theres a high degree of vasoconstriction occurring.

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12
Q

Fibroblast proliferation in the late phase

A

After day 7, fibroblasts enter to help heal and lay down scartissue.

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13
Q

VILI

A

Ventilator induced lung injury. Positive airway pressure delivered to lung can cause barotrauma and volutrauma. This exacerbates the cytokine release and damages the good area of the lung.

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14
Q

Distribution of DAD in the lung?

A

Diffuse!!! Patchy!

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15
Q

Phases of ARDS and timing

A

Exudative phase to start off: Edema from 0-3d. Hyaline membranes from 1-14d. Proliferative phase begins at day 7 with interstitial inflammation and fibrosis.

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16
Q

When do type 2 pneumocytes become hypeprlastic

A

During the proliferative phase.

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17
Q

Imaging of ARDS

A

Bilateral infiltrates and hypoxemia, but normal left heart function. Imaging tells us nothing about the cause. The xray looks whited out. CT scan reveals the patchy nature of ARDS.

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18
Q

Management of ARDS

A

Treat underlying cause first. ARDS is a syndrome, not a disease. Then engage in lung protective strategy of mechanical ventilation with low tidal volume. Also supportive care like pain management and prevention of DVT

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19
Q

What happened to other interventions?

A

Steroids, prone positioning, inhaled NO. DIdn’t work

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20
Q

Outcomes of ARDS

A

about 40% mortality.

21
Q

What determines the degree of mortality from ARDS

A

Underlying cause

22
Q

Predictors of mortality in ARDS

A

Advanced age, sepsis, degree of organ dysfunctions

23
Q

After recovering from ARDS what is the problem

A

Impaired lung function (restrictive) due to fibrosis.

24
Q

Non-pulmonary sequellae of ARDS

A

Muscle wasting, polyneuropathy, neurocognitive impairment, depression, anxiety. PTSD

25
Q

Neonatal respiratory distress syndrome

A

Also called hyaline membrane disease. Occurs from premature birth and lack of surfactant. Symptoms occur within minites of birth and include rapid shallow breathing, nostril flairing, retraction breathing, grunting and cyanosis.

26
Q

CXR for neonatal respiratory distress syndrome?

A

Ground glass appearance

27
Q

Blood gas for neonatal RDS?

A

Hypoxemia, hypercapnea

28
Q

Risk factors for NRDS?

A

Maternal diabetes.

29
Q

How to prevent NRDS

A

Maternal steroids to induce surfactant production.

30
Q

What is idiopathic DAD known as

A

Acute Interstitial Pneumonia (AIP)

31
Q

What is DAD?

A

Diffuse alveolar damage – caused by diffuse alveolar capillary/epithelial damage. Rapid onset of severe life-threatening respiratory insufficiency, cyanosis, and severe arterial hypoxemia.

REFRACTORY to oxygen therapy

32
Q

Pathogenesis of DAD

A

Not well understood, but potential role of PMNs, endotoxins, complement,

33
Q

What does injury to vascular endothelium cause?

A

Excess vascular fluid and protein leaking out into the alveoli, eventually cellular necrosis, inflammation and fibrosis

34
Q

Key feature of DAD (SUPER IMPORTANT)

A

Hyaline Membranes, caused by the exudation of protein rich fluid into the alveoli.

35
Q

What does the recovery of DAD look like histologically?

A

Hyperplasia of type II pneumocytes and fibrosis.

36
Q

Three histologic stages of DAD

A

Early/acute exudative stage – characterized by edema and hyaline membranes. Days 1-7

Proliferative/Organizing Stage. Days 7-21

Fibrotic Stage. Day 21+

37
Q

Gross features of early ARDS

A

Boggy/wet lung. Heavy. Due to exudates.

38
Q

What do hyaline membranes look like?

A

Pink membrane. Lots of fibrin in the alveolar spaces.

39
Q

Histology of the proliferative phase?

A

Hyaline membranes disappear then blue fibroblasts proliferate. Type II pneumocyte hyperplasia.

40
Q

Eosinophilic Pneumonia

A

Usually due to a parasite like ascaris or filiariasis. Most of these are self limited and include simple eosinophilic pneumonia, tropical eosinophilic pneumonia, chronic eosinophilic pneumonia, acute eosinophilic pneumonia.

All of these hav eperipheral eosinophilia except for the acute version

41
Q

How is acute eosinophilic pneumonia different from the others?

A

No peripheral blood eosinophilia

42
Q

How to treat eosinophilic pneumonia?

A

Steroids

43
Q

Histology of Eosinophilic pneumonia?

A

LOTS of eosinophils in the alveolar spaces. Looks like regular pneumonia but has eos instead of neutrophils

44
Q

DAD with eosinophilia?

A

Acute eosinophilic pneumonia. Has hyaline membranes

45
Q

Organizing Pneumonia

A

Loose connective tissue in alveoli seen as a manifestation of lung injury from a variety of insults. Formally known as bronchiolitis obliterans organizing pneumonia.

46
Q

Clinical features of organizing pneumonia

A

Subacute cough and SOB.

47
Q

Histology of organizing pneumonia

A

Fibroblastic plugs in small airways. Intervening lung is more or less normal. NO other findings like granulomas.

Usually need to take a wedge biopsy to confirm this.

48
Q

Why does OP happen?

A

Many etiologies (lupus, drug reaction, others)

49
Q

What is idiopathic organizing pneumonia called?

A

Cryptogenic organizing pneumonia

Pulmonary Pathology (11 decks)

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