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Respiratory Diseases > Overview of respiratory pathologies > Flashcards

Overview of respiratory pathologies Flashcards

1
Q

How is the respiratory system divided?

A
  • Divided structurallay and functionally into conducting and respiratory airways.
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2
Q

What is the conducting airways comprised of ?

A
  • The nose, pharynx,larynx,trachea, bronchi and bronhcioles
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3
Q

What are the respiratory airways comprised of?

A

-Respiratory bronchioles, aleveolar sacs, ducts and alveoli

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4
Q

What is the histology of the respiratory wall?

A
  • Innermost layer = epithelium
  • varies in structure depending on location
  • In conducting airways epithelium made of pseudostratified columnar ciliated epithelial cells
  • Have cilia which help move the mucus and trap the particles in the respiratory tract.
  • As the respiratory passages get smaller the epithelial cells transition from pesudo stratified columnar cells to simple columnar epithelium- ideal for facillitation of gas exchange.
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5
Q

Describe the divisions of the bronchial tree.

A
  • Starts at the trachea
  • T = 12 cm long . Have hyaline cartilage which provide structural support to prevent trachea from collapsing during inhalation etc.
  • Bifurcates into the right and left bronchus
  • Right bronchus is usually shorter and wider compared to Left main bronchus
  • Right main bronchus bifurcates into secondary bronchi
  • Left main bronchus - bifurcates into secondary bronchi TO tertiary or segmental bronchi which gives rise to bronchioles.
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6
Q

Describe the histology of the respiratory bronchioles

A
  • Bronchioles are lined with simple columnar epithelial cells
  • These transition to simple cuboidal epithelium in the smaller bronchioles and terminal bronchioles
  • The number of cillia will decrease
  • Cartilage plates in the bronchus are replaced by smooth muscle
  • ## Abscence of the cartilage allows them to be more collapsible and responsive to changes in the smooth muscle tone
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7
Q

What is the respiratory bronchiole?

A
  • A branch from terminal bronchioles
  • Each respiratory bronchiole branches into 2-11 alveolar ducts that retain a cuboidal epithelium
  • Along the walls of the alveolar = single alveoli and numerous alveolar sacs that comprise 2-4 alveoli
  • The space at the entrance from the alveolar duct to an alveolar sac = the atrium
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8
Q

Describe the histology of alveoli

A
  • Alevolar duct branches off into several alveoli
  • The walls of the alveoli are made up of a single layer of squamous epithelial cells = type I pneumocytes - very thin = rapid gas diffusion
  • Type II pneumocytes- connect two alveolar junctions. Cuboidal epithelial cells. Secrete pulmonary surfactant (Helps prevent surface tension and prevents alveolar collapse).
  • Alveolar macrophages - clean and sterilise alveolar spaces
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9
Q

What are some host defence mechanisms ?

A

Uper airways :
- Nasopharynx = nasal hair , mucocilliary apparatus, IgA secretion
- Oropharynx - Saliva. Sloughing of epithelial cells

Conducting airways :
Trachea, bronchi = cough, epiglotic reflexes
sharp- angled branching of airways . Immunoglobulin production (IgG, IgM, IgA)

Lower respiratory tract - surfactant, alevolar macrophages

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10
Q

What are obstructive dieseases?

A
  • Limit airflow due to obstruction. Causes increased airway resistance
  • Airway narrowing (asthma), loss of elsaticity (emphysema) or increased secretions (bronchitis/asthma)
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11
Q

What are restrictive diseases?

A
  • Restrict normal lung movement during respiration
  • Reduced expansion of lung parenchyma
  • Decreased total lung capacity
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12
Q

What is COPD?

A
  • Chronic bronchitis and emphysema often co-exist
  • A chronic inflammatory lung disease that causes obstructed airflow from the lungs, distal respiratory tree
  • 4th leading cause of death in the UK
  • Due to smoking and urban pollution
  • Irreversible disease
  • Defined clinically rather than morphologically (persistant cough for 3 consecutive moths in at least 2 consecutive years)
  • Mucus hyper-secretion in large airways or small airways
  • Inflammed bronchus
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13
Q

What is the pathogenesis of chronic bronchitis 3Hs?

A

3 HS:
- Hypertrophy, Hyperplasia, Hypersecretion
- Hypertrophy and hyperplasia of mucous glands
- Hypersecretion of mucus- increase in goblet cells in the epithelium
- Inflammation - T cells, neutrophils and macrophages (no eosinophils in contrast to asthma)

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14
Q

What is the pathology of chronic bronchitis?

A
  • Goblet cell metaplasia
  • Mucus plugs bronchiolar lumen
  • Inflammation
  • Bronchiolar wall fibrosis
  • Luminal narrowing and airway obstruction
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15
Q

What is emphysema?

A
  • chronic condition where air sacs may be destroyed or narrowed
  • Located distal to the terminal bronchioles
  • Manifested by:
  • Permanent dilation of respiratory bronchioles and alveoli
  • Destruction of elastic wall tissue without significant fibrosis
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16
Q

What are the different types of emphysema?

A

-Centri-acinar ot centrillobular
- Panacinar (PA)/ pan lobular
- Para-septal (distal acinar emphysema or peripheral emphysema)

17
Q

What is panlobular (acinaar) emphysema?

A
  • Dilated alveoli
  • More common in lower lobes
  • Hereditary (presents earlier)
  • Para-septal (Distal acinar emphysema or peripheral emphysema)
18
Q

What is the pathology of emphysema?

A
  • Destruction of alveolar walls without fibrosis
  • Enlarged air spaces
  • Number of alveolar capillaries diminishes
  • Deformed terminal and respiratory bronchiles and loss of septa
19
Q

What is the difference between emphysema with and without bronchitis?

A

-Without bronchitis :
- Shortness of breath (dysponoea), prolonged expiration
- Barrel chest due to use of accessory muscle
- Prolonged onset> 40 years
- Pink puffer - pursed lips breathing

With bronchitis :
- Shortness of breath less prominent
- Patient retains CO2 - Hypoxic and cyanotic
- Blue bloater -cyanotic and tend to be obese

20
Q

What is asthma?

A
  • chronic inflammation of the airways which results in hyper-responsive airways
  • Characterised by a triad of:
  • intermittent and reversible airway obstruction
  • Chronic bronchial inflammation with eosinophils
  • Bronchial smooth muscle hypertrophy and hyper-reactivity
21
Q

How is asthma characterised ?

A

By triggers :
1.) Atopic/extrinsic such as seasonal allergens
2.Non-atopic/ intrinsic such as infection,exercise , drugs
Clinical manifestation = shortness of breath, wheeze, chest tightness and cough as a result of reversible airway

22
Q

What are early and late reactions of asthma?

A

Early:
- Bronchoconstriction
- Hypersection of mucus leading to plugging of airways

Late reaction:
- Inflammation - activation of leucocytes
- Mucosal oedema and miscle hypertrophy- narrow the lumen
- Epithelial cells produce chemokines to attract more TH2 cells and eosinopjils
- Repeated inflammatipn leads to airway remodelling

23
Q

What are morphological changes relating to asthma?

A
  • Excess mucus production by gobley cell and glandular hypertrophy
  • Bronchial wall oedema due to inflammatory exudate : eosinophil and mast cell accumulation
  • Smooth muscle hypertrophy and fibrosis
24
Q

What is bronchiectasis?

A
  • Permanent dilation of main bronchi and bronchioles
  • From pulmonary inflammation and scarring due to infection, bronchial obstruction or lung fibrosis
  • Airways then dilate, as surrounding scar tissue (fibrosis) contracts
  • Secondary inflammatory changes lead to further destruction of airways
  • Symptoms are a chronic cough with dysponea and production of copious amounts of foul-smelling septum
25
Q

What are the causes of bronchiectasis?

A
  • Obstruction: tumours/foreign bodies/impaction of mucus
  • Infection: Necrotising pneumonia, esp.with virulent organisms (TB mixed flora on culture)
  • Congenital/ hereditary:
  • Cystic fibrosis : production of abnormally viscoid mucus causes obstructionand predisposes to infection
  • Immunodeficiency : immunoglobulin deficiencies - predispose to infection
  • Kartagener syndrome (immotile cilia syndrome) - impaired mucociliary clearance-stagnation of secretions
26
Q

What is the pathogenesis of bronchiectasis ?

A
  • Predisposed by two main factors:
  • Interference with drainage of bronchial secretions :
  • Obstruction of proximal airway, e.g. tumour, foreign body
  • Abnormality in the viscocity of bronchial mucus , e.g. cystic fibrosis
  • Immotile cilia syndrome, in which cilia are abnormal
  • Recurrent and persistent infection weakening bronchial walls
  • Predisoosed to reterntion of secretions
  • Immunodeficiency states, particularly hypogammaglobulinemia
  • In many cases in adults, no cause can be found (idiopathic bronchiestasis)
27
Q

What is acute respiratory distress syndrome?

A
  • Caused by diffuse alveolar damage as a result :
  • Direct (pneumonia/aspiration of gastric contents)
  • Indirect (sepsis/severe trauma) lung injury
  • Acute inflammation of alveoli, heavily involving neutrophils, rapidly damages capillaries and epithelium
  • Imbalance of pro and anti-inflammatory mediators: uncontrolled inflammatuon
  • Acute onset of dyspnea and hypoxemia due to vascular leakiness and loss of surfactant affecting gaseous exchange
  • High mortality rate (60%)
28
Q

What is the pathogenesis of acute respiratory distress?

A
  • Damaging stimulus to lung
  • damage to alveolar lining cells
  • Damafe to capillary endothelium
  • Interstitial edema . High protein exudation into alveoli (hyaline membranes)
  • Death in acute phase
  • regeneration of Type II alveolar lining cells
  • Inflammation of interstitium
  • Organisation leading to interstitial fibrosis
  • Mild local fibrosis : recovery eith minimal residual respiratory dysfunction (0%)
  • Marked interstirial fibrosis (honeycomb lung)
  • Death due to chronic severe respiratory impairement (20%)
29
Q
A
30
Q

What is IPF morphology?

A
  • Stimulated fibroblasts deposit collagen and ECM excessively for an extended time
  • Patchy innterstitial fibrosis that worsens with time
  • Fibroblastic foci- become more collagenous and less cellular
  • Causes collapse of alveolar walls and formation of cystic spaces - honeycomb fibrosis/honeycomb lung
31
Q

What is pneumoconiosis?

A
  • Group of fibrosing diseases resulting from exposure (often occupational) to toxix inhaled particulates:
  • Asbestos (asbestpsos), silica (sillicosis), coal dust (coal workers pneumoconios)
  • 5-10 um particles don’t distal airways
  • Immune response stimulated by particles/macrophages travelling in lymphatics
  • Lesions consist of pigmented/pale nodules of particle laden macrophages and dense collagen
32
Q

What are the types of pneumoconiosis ?

A
  • Develops over a long time (Devades) even after exposure is stopped
  • Sillicosis and asbestosis associated with increased risk of cancer
  • Asbestos workers + smoking often with increased risk of cancer
  • Asbestos workers + smoking often leads to carcinoma possible due tp adsorption of carcinogens onto fibers trapped deep in the lung
33
Q

Acinus

A
  • functional respiratory unit that consists of the resp bronchioles, alveolar ducts, sacs and the alveoli
    • contains all parts of resp airways

Respiratory Diseases (17 decks)

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