Pulmonary Pathology Flashcards
1
Q
Describe basic respiratory system anatomy
A
- Trachea, right / left principal bronchus, lobar bronchi (secondary), segmental bronchi (tertiary), terminal bronchioles, respiratory bronchioles, alveolar ducts / sacs, alveoli
- From conducting to respiratory areas we see a loss of cartilage, mucous secreting cells, goblet cells, cilia and cells become progressively flattened
2
Q
What are characteristics of the trachea
A
- Pseudo-stratified columnar ciliated epithelium
- Goblet cells
- C-shaped cartilage
- Smooth muscle at opening of C-shaped hyaline cartilage
- Serous / mucous glands
- Conducting
- Connects upper respiratory tract to lungs via bronchial tree, posterior wall is fibrous tissue
3
Q
What are characteristics of the bronchi
A
- Pseudo stratified columnar ciliated
- Goblet cells
- Pieces of hyaline cartilage
- Smooth muscle encircles lumen
- Serous / mucous glands
- Conducting
4
Q
What are characteristics of the bronchioles (terminal and respiratory)
A
- Bronchioles / Terminal: Simple columnar ciliated, exocrine / club cells, supported by smooth muscle and elastic fibres, conducting
- Respiratory: Simple cuboidal, some ciliated, exocrine cells, smooth muscle, respiratory
5
Q
What are characteristics of the alveolar ducts / alveoli
A
- Alveolar Duct: Mostly simple squamous, respiratory
- Alveoli: Simple squamous, type I (pneumocytes, squamous epithelium 95%) and type II (pneumocytes, cuboidal epithelium, surfactant producing), respiratory
6
Q
What are obstructive lung diseases
A
- Increase in resistance to airflow due to partial / complete obstruction of the airways
- Obstruction is worse with expiration, more force required
- Decreased expiratory flow rate
- FEV1 sec to FVC (deepest breath) ratio is decreased
- FEV1/FVC is ≤ 70% in adults and < 85% in children
- Types: Chronic bronchitis, emphysema, asthma, ARDS
7
Q
What is chronic bronchitis (OLD)
A
- Cough with sputum production ≥ 3 months in 2 consecutive years
- Aetiology (smoking)
- Hypertrophy of submucosal mucus glands, hyperplasia of goblet, hyper secretion of mucous
- Simple: Productive cough (no airflow obstruction)
- Asthmatic: Cough, intermittent bronchospasm and wheezing
- Obstructive: Cough and outflow obstruction
8
Q
What is emphysema (OLD)
A
- Damaged / enlarged alveoli
- Aetiology (smoking or a1-antitrypsin deficiency)
- Dyspnea, lungs enlarged
- Permanent dilation of air spaces distal to terminal bronchioles
- Destruction of alveolar walls (loss of elastic recoil)
- Asymptomatic until 1/3 of parenchyma is destroyed
- Reactive oxygen species / free radicals attract neutrophils
- Increased neutrophil elastase, pro-inflammatory cytokines, neutrophils and macrophage elastase
9
Q
What is asthma (OLD)
A
- Chronic inflammation of airways (hyper-reactive)
- Recurrent episodes of wheezing, breathlessness, chest tightness and cough caused by reversible bronchospasm
- Status Asthmaticus: Severe, prolonged / continuous, rare, can be fatal
- Extrinsic: Type I HS (IgE)
- Intrinsic: Non-immunological, aspirin, viral infections, cold, exercise and stress
10
Q
What are restrictive lung diseases
A
- Intrinsic lung diseases, limited potential of lung to expand), reduced lung compliance and reduced TLC, FVC and FEV1, progressive breathlessness and cough
- Diffuse and chronic involvement of pulmonary connective tissue (alveolar interstitium)
- Types: Acute interstitial disease (ARDS), chronic interstitial diseases (idiopathic pulmonary fibrosis, pneumoconiosis, sarcoidosis, hypersensitivity pneumonitis)
11
Q
What is ARDS (RLD)
A
- Acute respiratory distress syndrome
- Caused by infection, burns, gas inhalation, protein-rich edema (hypoxemia)
- Can be fatal within a few days (lung damage / fibrosis)
- Diffuse alveolar capillary and epithelial damage
- Leakage of proteins and fibrin into alveoli and hyaline membrane, severe fluid buildup
- Bright eosinophilic hyaline membrane, regenerative hyperplasia of type II cells, collapsed alveoli and proteinaceous debris present
- Lungs are large and dusky red, firm and airless by palpation
12
Q
What are the types of ARDS
A
- Acute (1-6 d): Sloughing of bronchial and alveolar epithelium, neutrophils present, air space filled with protein rich edema fluid, lung injury (neutrophil / platelet dependent), delayed resolution
- Sub-Acute (7-14 d): Some edema reabsorbed, attempted repair, proliferation of alveolar epithelial type II cells, fibroblast infiltration and collagen deposition
- Chronic (14 d): Resolution of acute neutrophilic infiltrate, increased mononuclear cells and alveolar macrophages, increased fibrosis and repair of alveoli epithelium
13
Q
What is interstitial lung disease (RLD)
A
- Many different lung conditions
- Forms of interstitial lung disease cause thickening of the interstitium due to inflammation (alveolitis)
- Scarring (fibrosis, honeycomb lung), edema
14
Q
What is pulmonary fibrosis (RLD)
A
- Lung tissue is damaged and undergoes fibrosis
- Difficulty expanding and increased restriction / air volume in the lungs
- Idiopathic PF (unknown causes)
15
Q
What is atelectasis (RLD)
A
- Incomplete expansion / collapse of lung
- Caused by obstruction, restriction or preterm
- Results in reduced gas exchange, rapid shallow breathing, coughing, hypotension, tachycardia, fever, cough, pain
16
Q
What is pneumoconiosis (RLD)
A
- Inhalation of dusts / fumes
- Range from asymptomatic anthracosis to fibrotic lungs with compromised function / hypertension
- Accumulation of macrophages in lung parenchyma
17
Q
Summarise the different between restrictive vs obstructive lung diseases
A
- Restrictive: FVC is reduced, airways not obstructed, able to expel air reasonably fast
- Obstructive: Airway obstruction, slow exhalation, reduced FVC
- FEV1/FVC ratio is lower in persons with obstructive (> 69%) than with restrictive (88-90%)
18
Q
What is pneumonia
A
- Caused by bacteria, virus, mycoplasma and fungus
- Presents as acute or chronic
- Fibrin-purulent alveolar exudate in (acute bacterial)
- Mononuclear interstitial infiltrates (viral)
- Granulomas and cavitation (chronic)
19
Q
What is acute pneumonia
A
- Community acquired
- Streptococcus pneumoniae
- Follows upper respiratory tract viral infection
- Lung parenchyma filled with inflammatory exudate leading to fibrin-supportive consolidation
- Onset abrupt, high fever, shaking chills, chest pain, productive mucopurulent cough
20
Q
What is lobar pneumonia
A
- Acute exudative inflammation of an entire pulmonary lobe
- Lobe enlargement, loss of spongy appearance
- Red / grey hepatisation
Stages:
1. Alveolar lumen contains serous exudate of rare leucocytes / bacteria
2. Exudate rich fibrin with bacteria, leucocytes, erythrocytes
3. Alveolar lumens filled with leukocytic exudate, neutrophils / macrophages
4. Resolution, exudate within alveolar spaces drained
21
Q
What is broncho pneumonia
A
- Affects one or more lobes
- Suppurative peri-bronchiolar inflammation
- Small yellow-tan patches
- Multiple small foci of inflammation / condensation
- Extensive congestion and dilation of BV and areas of poorly circumscribed consolidation
22
Q
What is tuberculosis
A
- Chronic pneumonia caused by mycobacterium tuberculosis
- Granulomatous inflammation
- Tubercular granulomas undergo caseous necrosis
- Primary (previously unexposed, asymptomatic )
- Secondary (reactivation of primary lesions, fever / night sweats, malaise, anorexia)
- Ghon complex (lesion after primary, ghon focus, lymphadenopathy, nearby lymph node)
23
Q
What is miliary tuberculosis
A
- 5% of progressive primary TB
- Mycobacterium tuberculosis enter blood stream and infect other organs
- Cell-mediated immune response activated
- Macrophages infiltrate and form granuloma
24
Q
List vascular lung diseases
A
- Pulmonary Embolism
- Pulmonary Hypertension
25
Q
What are neoplastic lung diseases
A
- Risk Factors: Smoking, radiation exposure, asbestos exposure, air pollution, genetic predisposition
- Lung Carcinoma: Large (10-15%), small (20-25%), squamous (25-40%) or adenocarcinoma (25-40%)
26
Q
What is red vs grey hepatisation in lobar pneumonia
A
- Red Hepatisation: Early exudate is full of bacteria, RBC, neutrophils, fibrin, day 3-4, firm, red appearance, liver-like consistency, cut surface is dry and rough
- Grey Hepatisation: Later exudate contains macrophages, broken down RBC, debris, day 5-7, cut surface wet, greyish purulent liquid drains
