Singh Pathology of Respiratory System #1 Flashcards
What are the basic necessities for fetal lung development?
- Space in the thoracic cavity
- Ability to inhale
- amniotic fluid to inhale and appropriate motion of the chest wall
What makes up normal bronchial histology?
- Ciliated respiratory epithelium
- Smooth muscle and submucosal glands
- Cartilage
What is the predominant histology in lung tissue?
Alveolar parenchyma
What makes up the alveolar structure?
- Capillary endothelium
- Fused basal laminae of alveolar epithelium and capillary endothelium
- Alveolar epithelium
- made of type 1 pneumocytes
- Type 2 pneumocytes
What can cause pulmonary hypoplasia?
- Reduced space in thoracic cavity
- diaphragmatic hernia
- Impaired ability to inhale
- oligohydramnios
- airway malformation
- chest wall motion disorders
What is a duplication/foregut cyst?
- Detached outpouchings of foregut seen along the hilum and mediastinum
- It can be respiratory, esophageal, or gastroenteric
Complications of foregut cysts and treatment?
- Complications could be rupture of the cyst, infection, or compression of the airway
- Excision is curative
What is Congenital Pulmonary Airway Malformation (CPAM/CCAM)?
- 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
What are the characteristics of CPAM?
- Communicates with the tracheobronchial tree
- Detected on fetal US
- Deadly due to hydrops or pulmonary aplasia
- Infected later in life
What is a pulmonary sequestration?
- nonfunctioning lung tissue that forms as an accessory lung bud, usually in lower left lobe
Characteristics of Pulmonary sequestrations?
- lacks connection to the tracheobronchial tree (unlike CPAM)
- Independent arterial supply
- Can be intralobar or extralobar
What is atelectasis?
- Inability to completely expand lung parenchyma
What are the three types of atelectasis?
- 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
What is happening?
- Pulmonary edema
What are the hemodynamic causes of pulmonary edema?
- Hemodynamic dysfunction
- Pushing out
- LHF
- volume overload
- Pulmonary vein obstruction
- Leaking out
- Hypoalbuminemia
- Nephrotic syndrome
- Liver disease
- Pushing out
What are two other causes to pulmonary edema besides hemodynamic dysfunction?
- Injury to alveolar wall
- bacterial pneumonia
- Sepsis
- Smoke inhalation
- aspiration
- Unknown mechanisms
- Neurogenic
- High altitude
What is Acute lung injury? (ALI)
- Acute onset of hypoxemia and bilateral lung infiltrates
- NO evidence of cardiac failure
What is ARDS?
- Abrupt onset of symptoms
- Hypoxemia <200
- ALI is less than 300 PaO2/FiO2
- B/l infiltrates
- Not cardiac
Mechanism behinds ARDS?
- Endothelial activation
- Adhesion and extravasation of neutrophils
- Accumulation of intraalveolar fluid
- Formation of hyaline membranes
- Resolution
In ARDS what creates Hyaline membranes
- Edema + Fibrin + Cell debris
- This is DAD diffuse alveolar damage
What are the stages of ARDS and what characterizes each one?
- Exudative
- edema hyaline membranes and neutrophils
- Proliferative
- fibroblast proliferation organizing pneumonia early fibrosis
- Fibrotic
- extensive fibrosis, loss of normal alveolar architecture
After the proliferative phase of ARDS what are the two possible outcomes?
- Resolution with restoration of normal cell structure and function
- Fibrosis with destruction and distortion of normal cell structure
- Irreversible
