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Pulmonology > 08.26 - Path of Neonatal, Developmental, and Pulmonary Vascular (Nichols) - Questions > Flashcards

08.26 - Path of Neonatal, Developmental, and Pulmonary Vascular (Nichols) - Questions Flashcards

1
Q

Cause of “death rattle”

A

Frothy white pulmonary edema fluid.

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2
Q

Character of edema in cardiogenic vs non-cardiogenic

A

Protein-poor if cardiogenic; Protein-rich if non-cardiogenic (pneumonia, ARDS, etc)

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3
Q

Physical exam sign to tell if pulmonary edema is cardiogenic or not?

A

JVD

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4
Q

Histologic apperance that corresponds to white frothy fluid

A

Pink eosinophilic fluid

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5
Q

Importance of IL-5

A

Eosinophil activation (Asthma)

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6
Q

ARDS is the clinical picture of

A

Acute Lung Injury

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7
Q

In ALI, single alveolar unit acts as

A

Shunt

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8
Q

Surfactant in ALI

A

Inactivated

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9
Q

ARDS is associated with intense

A

Inflammation

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10
Q

ARDS: profound ___-philia, even in the ____

A

Neutrophilia, even in the periphery

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11
Q

ARDS: Severe hypoxemia due to

A

Shunting

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12
Q

Compliance in ARDS

A

Acute decrease in compliance

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13
Q

4 phases of Acute Lung Injury

A

Exudative (edema), Transition (transition), Proliferative (inflammation), Fibrotic (fibroblasts)

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14
Q

Why not treat with maximal FiO2 in ARDS

A

Free radicals

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15
Q

How does PEEP improve oxygenation in ARDS

A

Recruits atelectatic alveoli and increases FRC

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16
Q

Patients with ARDS die due to

A

Multi-organ failure

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17
Q

ARDS survivors have reduction in

A

DLCO

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18
Q

Fat Embolism occurs in

A

long bone fractures in older individuals; sickle cell crisis; orthopedic surgery

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19
Q

What tumor is especially prone to throw emboli

A

Lung Primary

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20
Q

Air embolism is caused by

A

Vascular Catheter, Chest Wall Injury, Brain surg in sitting position, back surg in prone position

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21
Q

Most fat emobli are clinically ___

A

silent

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22
Q

Signs and Symptoms of Pneumothorax

A

Sudden onset dyspnea, chest pain, decreased breath sounds on one side

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23
Q

Primary vs Secondary Pneumothorax

A

Seconday has predisposing factor in lung

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24
Q

Tension Pneumothorax means

A

pressure in pleural cavity above atmospheric

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25
Q

Most common type of TE Fistula

A

Dead-end esophagus with lower esophagus inlet in trachea

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26
Q

Presenation of TE Fistula

A

Pneumonia or Regurgitation of attempted feeding shortly after birth

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27
Q

Bronchogenic Cysts

A

Arise from abnormal detachments of primitive foregut

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28
Q

Pulmonary Sequestration

A

Discrete area of lung tissue that lacks connection to airway system and has abnormal blood supply from aorta

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29
Q

Discrete area of lung tissue that lacks connection to airway system and has abnormal blood supply from aorta

A

Pulmonary Sequestration

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30
Q

Arise from abnormal detachments of primitive foregut

A

Bronchogenic Cysts

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31
Q

Resorption Atelectasis

A

Endobronchial Mass

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32
Q

Plexiform lesion always only occurs in

A

Advanced severe stages of pulmonary HTN

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33
Q

What is common between Group 1 causes of Pulmonary HTN

A

Plexiform lesions

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34
Q

Lungs in Granulomatosis w/ Polyangiitis

A

Hemorrhagic consoldiated lungs with cavitating nodules

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35
Q

Hemorrhagic consoldiated lungs with cavitating nodules

A

Lungs in Granulomatosis w/ Polyangiitis

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36
Q

ELKS

A

Wegener’s: Eyes, Lungs, Kidneys, Skin

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37
Q

Pulmonary edema from ALI is commonly due to __ and less commonly to __

A

Shock, less commonly pulmonary infection

38
Q

Microhemorrhages are microscopically manifested by

A

Accumulation of hemosiderin-laden macrophages in alveoli (heart-failure cells)

39
Q

What causes heart-failure cells

A

Microhemorrhages cleaned up to creat hemosiderin-laden macrophages

40
Q

Most common cause of pulmonary edema

A

Left Sided Heart Failure

41
Q

Normal pulmonary capillary pressure

42
Q

At what pulmonary capillary pressure does fluid leak into interstitium? Alveoli?

A

20mmHg; 25mmHg

43
Q

Increased pulmonary venous pressure causes __ before it causes transudation of fluid into lungs (crackles)

44
Q

Gross Path of Pulmonary Edema

A

Lungs are red, wet, heavy, and exude white froth

45
Q

When is pulmonary edema fluid pink

A

High hydrostatic pressure –> ruptured capillaries

46
Q

Abrupt onset of hypoxemia and bilateral pulmomary infiltrates in absence of heart failure

47
Q

Common scenario when ALI is first to endothelial cells

A

Septic Shock

48
Q

Common scenario when ALI is first to pneumocytes

A

Gastric Acid Aspiration; Smoke inhalation

49
Q

Cutoffs for mild, moderate, and severe ARDS

A

PaO2 300-200; 200-100; <100

50
Q

Normal PaO2? PaO2/FiO2?

A

100mmHg; 475mmHg

51
Q

ARDS is acute diffuse inflammatory lung injury, leading to

A

Incr vascular permeability and pulmonary edema

52
Q

4 most common causes of ARDS

A

Sepsis, Diffuse Pneumonia, Gastric Aspriation, Trauma

53
Q

2 notable molecular mediators of ARDS

A

TNF and IL-1, secreted by Macrophages

54
Q

Role of Macrophages and Neutrophils in ARDS

A

Mac’s secrete TNF and IL-1 –> Activate endothelium –> Recruit PMN’s –> Release injurious mediators

55
Q

Histopathological counterpart of ARDS

A

Diffuse Alveolar Damage

56
Q

Earliest visible changes in ARDS

A

12-24 hours - Congestion, Interstitial and Alveolar Edema, PMN’s

57
Q

24-72 hours ARDS

A

Hyaline membranes

58
Q

When do hyaline membranes appear in ARDS

A

24-72 hours after injury

59
Q

What starts about 48 hours after injury in ARDS

A

Type 2 Pneumocytes proliferate and look scary

60
Q

When do type 2 pneumocytes begin proliferating in ARDS

A

48 hours after injury

61
Q

What starts about 72 hours after injury in ARDS

A

Lymphs, Macs, and Fibros infiltrate interstitium

62
Q

What occurs in Organizing phase of ARDS

A

Granulation tissue forms in alveolar walls

63
Q

Alveolar Hyaline Membranes is hallmark of

A

Diffuse Alveolar Damage – ARDS

64
Q

Clinical manifestations of ARDS appear how long after injury

A

Within 6-72 hours

65
Q

Mainstay of treatment for ARDS

A

Mechanical ventilation

66
Q

Presenting symptoms of ARDS

A

Dyspnea, Cyanosis, Diffuse Crackles

67
Q

Pulmonary infarcts tend to be ___, wedge-shaped, and hemorrhagic

A

Subpleural

68
Q

Top Sign and Symptom of PTE

A

Dyspnea, Tachypnea (Pleuritic Chest pain, Leg pain)

69
Q

Best test for PTE

A

Spiral CT with IV Contrast

70
Q

Pulmonary HTN is defined as

A

Mean Pulmonary Arterial Pressure >25mmHg at rest (Normal <20mmHg)

71
Q

Pulmonary HTN is most often due to ___ or ___

A

Heart Disease or Intrinsic Lung Disease

72
Q

Germline mutation found in 75% of Primary Pulmonary HTN

73
Q

Haploinsufficiency of BMPR2 leads to dysfunction and ___

A

proliferation of endothelial cells and vascular SM cells

74
Q

Finding common to all forms of pulmonary HTN

A

Hypertrophy and Hyperplasia of SM in Tunica Media of pulmonary muscular and elastic arteris

75
Q

Sign of Pulmonary HTN

A

Incr intensity of pulmonic component of S2

76
Q

Gold standard for dx of Pulmonary HTN

A

Right Heart Catheterization

77
Q

Hemoptysis is most often due to

A

Pulmonary infection

78
Q

Most pulmonary hemorrhagic syndromes are forms of

A

Autoimmune Vasculitis

79
Q

Resorption Atelectasis results from

A

Complete obstruction of an airway

80
Q

Contraction Atlectasis

A

Pulmonary or Pleural fibrosis prevents expansion

81
Q

Histopathology of NRDS and ARDS

A

Essentially the same

82
Q

Giving the mother __ reduces risk of RDS in premature infants

A

Glucocorticoids

83
Q

Aspiration pneumonia is more common in which lung

84
Q

Pulmonary infarcts, because of dual blood supply, are typically ___

A

hemorrhagic

85
Q

Holes between adjacent alveoli

A

Pores of Kohn

86
Q

Typical alveolar bacterial infection spreads throughout a lobule via

A

Pores of Kohn, until it reaches interlobular septa

87
Q

When will bacteria spread across interlobular septa

A

If it necrotizing

88
Q

Oligohydramnios causes what lung problem

A

Hypoplasia

89
Q

There is more blood in the __ of the lungs and more gas in the __

A

Blood = Base; Air = Apices

90
Q

Hematogenous metastases are more numerous and larger in which parts of lungs

A

Bases = Better blood supply

Pulmonology (31 decks)

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