Singh Pathology of Respiratory System #1

Question 1

What are the basic necessities for fetal lung development?

Answer 1

• Space in the thoracic cavity
• Ability to inhale
  
  • amniotic fluid to inhale and appropriate motion of the chest wall

Question 2

What makes up normal bronchial histology?

Answer 2

• Ciliated respiratory epithelium
• Smooth muscle and submucosal glands
• Cartilage

Question 3

What is the predominant histology in lung tissue?

Answer 3

Alveolar parenchyma

Question 4

What makes up the alveolar structure?

Answer 4

• Capillary endothelium
• Fused basal laminae of alveolar epithelium and capillary endothelium
• Alveolar epithelium
  
  • made of type 1 pneumocytes
  • Type 2 pneumocytes

Question 5

What can cause pulmonary hypoplasia?

Answer 5

• Reduced space in thoracic cavity
  
  • diaphragmatic hernia
• Impaired ability to inhale
  
  • oligohydramnios
  • airway malformation
  • chest wall motion disorders

Question 6

What is a duplication/foregut cyst?

Answer 6

• Detached outpouchings of foregut seen along the hilum and mediastinum
• It can be respiratory, esophageal, or gastroenteric

Question 7

Complications of foregut cysts and treatment?

Answer 7

• Complications could be rupture of the cyst, infection, or compression of the airway
• Excision is curative

Question 8

What is Congenital Pulmonary Airway Malformation (CPAM/CCAM)?

Answer 8

• arrested development of pulmonary tissue with formation of intrapulmonary cystic masses
  
  • the tissue development stops at a certain stage and just repeats that stage of development over and over

Question 9

What are the characteristics of CPAM?

Answer 9

• Communicates with the tracheobronchial tree
• Detected on fetal US
• Deadly due to hydrops or pulmonary aplasia
• Infected later in life

Question 10

What is a pulmonary sequestration?

Answer 10

• nonfunctioning lung tissue that forms as an accessory lung bud, usually in lower left lobe

Question 11

Characteristics of Pulmonary sequestrations?

Answer 11

• lacks connection to the tracheobronchial tree (unlike CPAM)
• Independent arterial supply
• Can be intralobar or extralobar

Question 12

What is atelectasis?

Answer 12

• Inability to completely expand lung parenchyma

Question 13

What are the three types of atelectasis?

Answer 13

• Resorption (obstructive)
  
  • Airway obstruction with gradual resorption of air decreases lung expansion
• Compression
  
  • accumulation of material in pleural cavity compresses lung parenchyma
• Contraction
  
  • Fibrotic or innate restrictive process in pleura or peripheral lung

Question 14

What is happening?

Answer 14

• Pulmonary edema

Question 15

What are the hemodynamic causes of pulmonary edema?

Answer 15

• Hemodynamic dysfunction
  
  • Pushing out
    
    • LHF
    • volume overload
    • Pulmonary vein obstruction
  • Leaking out
    
    • Hypoalbuminemia
    • Nephrotic syndrome
    • Liver disease

Question 16

What are two other causes to pulmonary edema besides hemodynamic dysfunction?

Answer 16

• Injury to alveolar wall
  
  • bacterial pneumonia
  • Sepsis
  • Smoke inhalation
  • aspiration
• Unknown mechanisms
  
  • Neurogenic
  • High altitude

Question 17

What is Acute lung injury? (ALI)

Answer 17

• Acute onset of hypoxemia and bilateral lung infiltrates
• NO evidence of cardiac failure

Question 18

What is ARDS?

Answer 18

• Abrupt onset of symptoms
• Hypoxemia <200
  
  • ALI is less than 300 PaO2/FiO2
• B/l infiltrates
• Not cardiac

Question 19

Mechanism behinds ARDS?

Answer 19

• Endothelial activation
• Adhesion and extravasation of neutrophils
• Accumulation of intraalveolar fluid
• Formation of hyaline membranes
• Resolution

Question 20

In ARDS what creates Hyaline membranes

Answer 20

• Edema + Fibrin + Cell debris
• This is DAD diffuse alveolar damage

Question 21

What are the stages of ARDS and what characterizes each one?

Answer 21

• Exudative
  
  • edema hyaline membranes and neutrophils
• Proliferative
  
  • fibroblast proliferation organizing pneumonia early fibrosis
• Fibrotic
  
  • extensive fibrosis, loss of normal alveolar architecture

Question 22

After the proliferative phase of ARDS what are the two possible outcomes?

Answer 22

• Resolution with restoration of normal cell structure and function
• Fibrosis with destruction and distortion of normal cell structure
  
  • Irreversible