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Respiratory Medicine Midterm > The Lung Part 2 > Flashcards

The Lung Part 2 Flashcards

1
Q

Acute Lung Injury (ALI)

A
  • Also called non-cardiogenic pulmonary edema
  • abrupt onset of significant hypoxemia and bilateral pulmonary infiltrates in the absence of cardiac failure
  • Acute respiratory distress syndrome (ARDS) is a manifestation of severe ALI
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2
Q

Both ARDS and ALI are associated with

A
  • inflammation-associated increases in pulmonary vascular permeability, edema and epithelial cell death
  • histologic manifestation of these diseases is diffuse alveolar damage (DAD)
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3
Q

ALI is a complication of

A
  • direct injuries to the lungs and systemic disorders
  • Combo of predisposing conditions responsible (shock, oxygen therapy, and sepsis)
  • Nonpulmonary organ dysfunction may also be present in severe cases
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4
Q

Pathogenesis of ALI/ARDS–order of events

A
  • initiated by injury to pneumocytes and pulmonary endothelium
  • Endothelial activation
  • Adhesion and extravasation of neutrophils
  • Accumulation of idntraalveolar fluid and formation of hyaline membranes
  • Resolution of injury
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5
Q

ALI/ARDS–Endothelial activation

A
  • early event
  • sometimes secondary to pneumocyte injury (sensed by resident alveolar macrophages)
  • macrophages secrete TNF that act on neighboring endothelium
  • OR circulating inflammatory mediators may activate pulmonary endothelium directly in setting of severe tissue injury or sepsis
  • Some mediators injury endothelial cells while others (cytokines) activate endothelial cells to express increased adhesion molecules, procoagulant proteins and chemokines
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6
Q

ALI/ARDS Adhesion and extravasation of neutrophils

A
  • Neutrophils adhere to activated endothelium and migrate into interstitium and alveoli where they degranulate and release inflammatory mediators–proteases, ROS, and cytokines
  • Macrophage migration inhibitory factor (MIF) released locally also helps sustain inflammatory response
  • Results in increased recruitment and adhesion of leukocytes, causing more endothelial injury and local thrombosis
  • cycle of inflammation and endothelial damage characteristic of ALI/ARDS
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7
Q

ALI/ARDS–Accumulation of idntraalveolar fluid and formation of hyaline membranes

A
  • Endothelial activation and injury make pulmonary capillaries leaky, allowing interstitial and itraalveolar edema fluid to form
  • Damage and necrosis of type II pneumocytes leads to surfactant abnormalities, further compromising alveolar gas exchange
  • Ultimately, the protein rich edema fluid/debris from dead alveolar epithelial cells organize into hyaline membranes–characteristic feature of ALI/ARDS
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8
Q

ALI/ARDS–Resolution of injury

A
  • impeded due to epithelial necrosis and inflammatory damage that impairs ability of remaining cells to assist with edema resorption
  • Eventually, if inflammatory stimulus decreases, macrophages remove idntraalveolar debris and release fibrogenic cytokines like TGF-B and platelet derived growth factor (PDGF)
  • TGFB and PDGF stimulate fibroblast growth and collagen deposition leading to fibrosis of alveolar walls
  • Bronchiolar stem cells proliferate to replace pneumocytes
  • Endothelial restoration occurs through proliferation of uninjured capillary endothelium
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9
Q

Conditions associated with Development of ARDS

A
  • Infection
  • Physical/injury
  • Inhaled irritants
  • Chemical injury
  • Hematologic conditions
  • Pancreatitis
  • Uremia
  • Cardiopulmonary Bypass
  • Hypersensitivity reactions
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10
Q

Conditions associated with Development of ARDS–Infection

A
  • Sepsis

- Diffuse pulmonary infections (viral, mycoplasma and pneumocystis pneumonia; military TB)

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11
Q

Conditions associated with Development of ARDS–Physical/injury

A
  • Mechanical trauma, including head injuries
  • Pulmonary contusions
  • Near-drowning
  • Fractures with fat embolism
  • Burns
  • Ionizing radiation
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12
Q

Conditions associated with Development of ARDS–inhaled irritants

A
  • Oxygen toxicity
  • Smoke
  • Irritant gases and chemicals
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13
Q

Conditions associated with Development of ARDS–chemical injury

A
  • Heroin or methadone overdose
  • Acetylsalicylic acid
  • Barbiturate overdose
  • Paraquat
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14
Q

Conditions associated with Development of ARDS–hematologic conditions

A
  • Transfusion associated lung injury (TRALI)

- Disseminated intravascular coagulation

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15
Q

Conditions associated with Development of ARDS–hypersensitivity reactions

A
  • Organic solvents

- Drugs

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16
Q

ALI/ARDS is more common and associated with a worse prognosis in

A
  • Chronic alcoholics and smokers

- ARDS is also associated with genes linked to inflammation and coagulation

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17
Q

ALI/ARDS Morphology–Acute stage

A
  • acute stage=lungs are heavy, firm, red and boggy; congested, interstitial and intra-alveolar edema, inflammation, fibrin deposition and DIFFUSE ALVEOLAR DAMAGE
  • Alveolar walls become lined with WAXY HYALINE MEMBRANES (similar to hyaline membrane disease in neonates)
  • Alveolar hyaline membranes consist of fibrin-rich edema fluid mixed with cytoplasmic and lipid remnants of necrotic epithelial cells
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18
Q

ALI/ARDS Morphology–organizing stage

A
  • In the organizing stage type II pneumocytes proliferate and granulation tissue forms in alveolar walls and spaces; the granulation tissue resolves leaving minimal functional impairment
  • Sometimes alveolar septa ensues; fatal cases have superimposed bronchopneumonia
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19
Q

Clinical course of ARDS/ALI

A
  • profound DYSPNEA and TACHYPNEA followed by increasing CYANOSIS and HYPOXEMIA, RESP FAILURE and the appearance of DIFFUSE BILATERAL INFILTRATES on radiographic exam
  • hypoxia may be refractory to oxygen therapy due to ventilation perfusion mismatching and respiratory acidosis can develop
  • Early on, lungs become stiff from loss of surfactant
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20
Q

Functional abnormalities in ALI

A
  • Not evenly distributed throughout the lungs
  • Some lung areas are infiltrated, consolidated, or collapsed (poorly aerated and poorly compliant) and regions that have nearly normal levels of compliance and ventilation
  • Poorly aerated regions continue to be perfused producing ventilation-perfusion mismatch and hypoxemia
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21
Q

Treatments for ALI/ARDS

A
  • no specific treatment
  • due to improvements in therapy for sepsis, mechanical ventilation and supportive care, the mortality rate has decreased with most deaths attributable to sepsis or multi organ failure and sometimes direct lung injury
  • survivors recover pulmonary function but many have persistent impairment in physical and cognitive functions
  • In minority of patients, exudate and diffuse tissue destruction can lead to scarring, interstitial fibrosis, and chronic pulmonary disease
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22
Q

Acute interstitial pneumonia

A
  • widespread ALI of unknown etiology associated with rapidly progressive clinical course
  • aka idiopathic ALI-DAD
  • uncommon
  • mean age 59, equal in M and F
  • Present with acute respiratory failure following illness of less than 3 weeks duration that resemble URI
  • Path features similar to organizing stage of ALI
  • Most deaths occur within 1-2 months
  • In survivors, see recurrences and chronic interstitial disease
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23
Q

Obstructive lung disease (or airway disease)

A

-Increase in resistance to airglow due to partial or complete obstruction at any level from the trachea and larger bronchi to terminal and respiratory bronchioles

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24
Q

Restrictive lung disease

A

-reduced expansion of lung parenchyma and decreased total lung capacity

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25
Q

In diffuse obstructive disorders, pulmonary function tests show

A
  • decreased maximal airflow rates during forced expiration

- LOW FEV1/FVC ratio (less than 0.7)

26
Q

Restrictive disease–pulmonary function tests

A

-proportionate decreases in both total lung capacity and FEV1 leading to normal (or increased) FEV1/FVC ratio

27
Q

Restrictive defects occur in two broad kind of conditions:

A
  • Chest wall disorders (severe obesity, pleural diseases, kyphoscoliosis, and neuromuscular diseases like poliomyelitis)
  • chronic interstitial and infiltrative diseases like pneumoconioses and interstitial fibrosis
28
Q

Common obstructive lung diseases include

A
  • emphysema
  • chronic bronchitis
  • asthma
  • bronchiectasis
29
Q

COPD (chronic obstructive pulmonary disease) is a combination of what two diseases?

A

-Emphysema and chronic bronchitis are clinically grouped together and referred to as COPD since majority of patients have features of both, because they are both triggered by smoking

30
Q

Chronic bronchitis–anatomic site, major pathologic changes, etiology, signs/symptoms

A
  • Bronchus
  • Mucus gland hyperplasia, hyper secretion
  • Etiology: tobacco smoke, air pollutants
  • S/S: Cough, sputum production
31
Q

Bronchiectasis–anatomic site, major pathologic changes, etiology, signs/symptoms

A
  • Bronchys
  • Airway dilation and scarring
  • Etiology: Persistent or severe infections
  • S/S: cough, PURULENT sputum, fever
32
Q

Asthma–anatomic site, major pathologic changes, etiology, signs/symptoms

A
  • Bronchus
  • Smooth muscle hyperplasia, excess mucus, inflammation
  • immunologic or undefined causes
  • Episodic wheezing, cough, dyspnea
33
Q

Emphysema–anatomic site, major pathologic changes, etiology, signs/symptoms

A
  • Acinus!!
  • Airspace enlargement, wall destruction
  • Tobacco smoke
  • Dyspnea
34
Q

Small-airway disease, bronchiolitis–anatomic site, major pathologic changes, etiology, signs/symptoms

A
  • Bronchiole
  • Inflammatory scarring/obliteration
  • Tobacco smoke, air pollutants, miscellaneous
  • cough, dyspnea
35
Q

What other lung disease contributes to obstruction in both emphysema and chronic bronchitis?

A

-small airway disease–chronic bronchiolitis

36
Q

Asthma is distinguished from chronic bronchiolitis and emphysema by the presence of

A
  • REVERSIBLE bronchospasm
  • some patients can develop an irreversible component
  • some patients with otherwise typical COPD have a reversible component–said to have COPD/asthma
37
Q

COPD risk factors

A
  • Clear association bw SMOKING and emphysema
  • women and african americans more susceptible than other groups
  • Also associated with env. and occupational pollutants, airway hyper responsiveness and genetic polymorphisms
38
Q

Emphysema

A
  • characterized by irreversible enlargement of airspaces distal to terminal bronchiole, accompanied by destruction of their walls without obvious fibrosis
  • small airway fibrosis present in emphysema
39
Q

Fout types of emphysema

A
  • Centriacinar
  • panacinar
  • paraseptal
  • irregular
  • *only centroacinar and panacinar cause clinically significant airflow obstruction!!
40
Q

Most common form of emphysema

A

-centroacinar emphysema

41
Q

Centriacinar (centrilobular) emphysema

A
  • central or proximal parts of acini formed by respiratory bronchioles are affected whereas distal alveoli are spared
  • so both emphysematous and normal airspaces exist within same acinus and lobule
  • lesions more common and severe in UPPER LOBES, especially in APICAL segments
  • Inflammation around bronchi and bronchioles is common
  • In severe centriacinar emphysema, the distal acinus may be involved
42
Q

Centriacinar emphysema occurs predominantly in

A

-heavy smokers, often in association with chronic bronchitis (COPD)

43
Q

Panacinar (pan lobular) emphysema

A
  • Acini are uniformly enlarged from level of respiratory bronchiole to terminal blind alveoli
  • Pan=entire acinus, NOT entire lung!
  • occurs in LOWER zones and in ANTERIOR margins of lung and most severe at BASES
  • associated with A1-ANTITRYPSIN DEFICIENCY!
44
Q

Distal acing (paraseptal) emphysema

A
  • Proximal acinus is normal
  • DISTAL PART mostly involved
  • more striking near the PLEURA along the lobular connective tissue septa and at margins of lobules
  • occurs near areas of fibrosis, scarring or atelectasis and more severe in UPPER half lungs
  • multiple, continuous, enlarged airspaces from less than 0.5 cm to more than 2 cm in diameter, sometimes forming cyst like structures
  • associated with SPONTANEOUS PNEUMOTHORAX in young adults!!
45
Q

Pathogenesis of emphysema

A
  • Inhaled cigarette smoke or other toxic particles cause lung damage and inflammation
  • results in parenchymal destruction (emphysema) and airway disease (bronchiolitis and chronic bronchitis)
46
Q

Emphysema pathogenesis–Inflammatory mediators and leukocytes

A

-increased LTB4, IL8, TNF released by resident epithelial cells and macrophages and attract inflammatory cells from circulation (chemotactic factors), amplify inflammatory process (pro inflammatory cytokines) and induce structural changes (growth factors)

47
Q

Emphysema pathogenesis–Protease-antiprotease imbalance

A
  • proteases released from inflammatory cells and epithelial cells that break down connective tissue
  • emphysema patients have deficiency of protective anti-proteases
48
Q

Emphysema pathogenesis–oxidative stress

A
  • substances in tobacco smoke, alveolar damage, and inflammatory cells produce oxidants, which may lead to more tissue damage and inflammation
  • Mouse models exp support role of oxidants–NRF2 gene inactivated; NRF2 encodes TF that serves as sensor for oxidants in alveolar epithelial cells and other cell types
  • Intracellular oxidants activate NRF2 which up regulates expression of multiple genes that protect cells from oxidant damage
  • Mice w/o NRF2 significantly more sensitive to tobacco smoke than normal mice
  • Genetic variants in NRF2, NRF2 regulators and NRF2 target genes associated with smoking-related lung disease in humans
49
Q

Emphysema pathogenesis–infection

A

-no role in initiation of tissue destruction but bacterial and/or viral infections exacerbate associated inflammation and chronic bronchitis

50
Q

A1-antitrypsin and emphysema

A
  • patients with deficiency of antiprotenase a1-antitrypsin have increased tendency to develop pulmonary emphysema which is compounded by smoking
  • a1 antitrypsin normally present in serum, tissue fluids and macrophages is major inhibitor of proteases (esp elastase) secreted by neutrophils during inflammation
  • encoded by proteinase inhibitor (Pi) locus on chromosome 14
  • Pi locus is polymorphic; Z allele associated with decreased levels of a1-antitrypsin–develop panacinar emphysema at earlier age and more severe if pt smokes
  • injury (like from smoking) increases activation and influx of neutrophils leads to release of proteases which in absence of a1 antitrypsin activity results in excessive digestion of elastic tissue and emphysema
51
Q

Other genetic variants linked to emphysema

A
  • nicotinic acetylcholine receptor–influences addictiveness of tobacco smoke and behavior of smokers
  • same variants associated with lung cancer risk
52
Q

Factors contributing to airway obstruction in emphysema

A
  • loss of elastic tissue in walls of alveoli that surround respiratory bronchioles reduces radial traction and causes respiratory bronchioles to collapse during expiration leading to functional airway obstruction despite normal mechanics
  • Goblet cell hyperplasia with mucus plugging of lumen
  • inflammatory infiltrates in bronchial walls consisting of neutrophils, macrophages, B cells (sometimes forming follicles), and T cells
  • Thickening of bronchiolar wall due to smooth muscle hypertrophy and peribronchial fibrosis
  • all these changes narrow bronchiolar lumen and cause obstruction
53
Q

Emphysema gross morphology

A
  • advanced emphysema=voluminous lungs overlapping the heart and hiding it when the anterior chest wall is removed
  • upper 2/3 of lungs more affected
  • Large apical blebs or bullae more characteristic of irregular emphysema secondary to scarring and of distal acinar emphysema
  • Large alveoli easily seen on cut surface of fixed lungs
54
Q

Emphysema microscopic morphology

A
  • abnormally large alveoli separated by thin septa with only focal centriacinar fibrosis
  • loss of attachments of alveoli to outer wall of small airways
  • LARGE pores of Kohn making septa appear as if they were floating or protrude into alveolar spaces with a club shaped end
  • Prolonged vasoconstriction leads to pulmonary arterial HTN
  • As alveolar walls are destroyed, there is decrease in capillary bed area
  • With advanced disease there are even larger abnormal airspaces and possibly blebs or bull, which deform and compress respiratory bronchioles and vasculature of lung
55
Q

Clinical course of emphysema

A
  • no symptoms until 1/3 of pulm parenchyma damaged
  • Dyspnea occurs first and is progressive
  • cough and wheezing is usually chief complaint (confused with asthma)
  • Cough/ expectoration variable-dependent on extent of bronchitis
  • weight loss is common and severe (can look like cancer)
  • Barrel chested and dyspneic with prolonged expiration, sits forward in hunched over position and breathes through pursed lips
  • Impaired expiratory airflow measured by spirometry is key to diagnosis!
56
Q

Severe emphysema symptoms

A
  • cough is slight!!
  • severe overdistension, low diffusion capacity and normal blood gas volumes are rest; patients may over ventilate and remain well oxygenated–called “pink puffers”
  • can develop cor pulmonale and CHF related to secondary pulm HTN–poor prognosis!!
57
Q

Death in most patients with emphysema is due to

A

1) coronary artery disease
2) respiratory failure
3) right sided heart failure
4) massive collapse of lungs secondary to pneumothorax

58
Q

Treatment of emphysema

A
  • smoking cessation
  • oxygen therapy
  • long-acting bronchodilators with inhaled corticosteroids
  • physical therapy
  • bullectomy
  • lung volume reduction surgery and lung transplantation in selected patients
  • a1-AT replacement tx in progress/being evaluated
59
Q

Predominant bronchitis–age of onset, dyspnea, cough, infections, respiratory insufficiency, cor pulmonale, airway resistance, elastic recoil, chest radiograph, appearance

A
  • age: 40-45
  • Dyspnea: Mild, late
  • Cough: Early; copious sputum
  • Infections: Common
  • Respiratory insufficiency: Repeated
  • Cor pulmonale: Common
  • Airway resistance: Increased
  • Elastic recoil: Normal
  • Chest radiograph: Prominent vessels; large heart
  • Appearance: Blue bloater
60
Q

Predominant emphysema–age of onset, dyspnea, cough, infections, respiratory insufficiency, cor pulmonale, airway resistance, elastic recoil, chest radiograph, appearance

A
  • age: 50-75
  • Dyspnea: severe, early
  • Cough: Late; scanty sputum
  • Infections: Occasional
  • Respiratory insufficiency: Occasional
  • Cor pulmonale: Rare; terminal
  • Airway resistance: Normal or slightly increased
  • Elastic recoil: Low
  • Chest radiograph: Hyperinflation; small heart
  • Appearance: Pink puffer

Respiratory Medicine Midterm (17 decks)

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