Respiratory Diseases Flashcards

1
Q

Air exchange in the lungs

A

• Pulmonary arteries brings venous blood
• Oxygenated blood leaves the pulmonary veins
• Bronchial arteries bring oxygen and nutrients to lungs
• Originate in the thoracic aorta

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2
Q

Pleural membranes

A

Envelope the lungs
Visceral (inner) and parietal (outer)
Intrapleural space contains pleural fluid: reduced friction when the lungs move upon inhalation and exhalation

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3
Q

Functions of the respiratory system

A

• Primary function gas exchange
• Larynx produces the voice
• Mucosa protects against infections: Mucosa-associated lymphoid tissue (MALT), Tonsils in nasopharynx and pharynx, Lymphoid follicles in the wall of the bronchi
• Alveolar macrophages – defense system: Expectorated from the lungs, seen in sputum
• Maintains acid-base function

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4
Q

Contributing factors to respiratory pathologies

A

The respiratory system is:
1. In direct contact with the environment
2. Exposed to allergens inhaled in the air
3. Inhaled air contains pollutants, airborne particles, and gases that may cause disease
4. Inhaled air contained many potential exogenous carcinogens
5. The heart and lungs form a functional unit

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5
Q

Infectious diseases of the respiratory tract

A

Two groups based on location:
1. The nose and upper respiratory
2. Lower respiratory
Middle respiratory syndrome mostly childhood diseases involving the trachea and bronchi
• Respiratory tract infections = 75% of all infections
• <5% involve the lung

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6
Q

Upper respiratory infections

A

• Mostly caused by viruses (colds, flu)
• Rhinovirus (spring and fall), influenza (winter), parainfluenza
• Acute inflammation of the nose, paranasal sinuses, throat, or larynx (or all of them)
• Short lived, heal spontaneously, no benefit of antibiotic treatment
• Can extend into trachea and bronchi
• May be complicated by pneumonia
• Most common location of infection

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7
Q

Upper respiratory infection etiology and pathogenesis

A

• Mucosa of nose, upper respiratory tract are congested, edematous, infiltrated with inflammatory cells
• Viral: lymphocytes, macrophages and plasma cells
• Bacterial: polymorphonuclear neutrophils (PMNs), yellow pus like exudate
May be complicated by a bacterial superinfection
• Spread into adjacent anatomical structures
• Ex. Bacterial sinusiti

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8
Q

Upper respiratory infection clinical features

A

Classical “flu like” symptoms
• Nasal congestion, inflammation, rhinorrhea
• Throat pain or discomfort
• Hacking cough
• General malaise
• Fever, headaches, muscle pain

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9
Q

Middle respiratory syndromes

A

• Infection of the larynx, trachea, major extrapulmonary
bronchi
• Prevalent in children
1. Croup (laryngitis)
2. Acute epiglottitis
3. Viral tracheobronchitis

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10
Q

Croup (an acutely infection of the larynx)

A

• Children <3 years
• Typically caused by parainfluenza virus
• Acute, potentially life-threatening
• Inflammation of the entire larynx
• Laryngeal swelling and laryngospasm
• Inspiratory stridor (barking or brass cough)
• No specific treatmen

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11
Q

Acute epiglottitis

A

• School aged children and adolescents
• Inflammation, edema to the epiglottis
• Narrowing of the air passage
• Sudden loss of voice, hoarseness, pain
• Haemophilus influenza
• Prevented with immunization

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12
Q

Bronchiolitis

A

• Viral infection
• >80% due to respiratory syncytial virus
• Invades epithelial cells of bronchi and bronchioles
• Death and desquamation of cells
• Inflammatory infiltrate (lymphocytes, plasma cells, macrophages)
• Edema of small airways = obstruction of bronchi and bronchioles

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13
Q

Types of Pneumonia (a lower respiratory syndrome)

A
  1. Alveolar pneumonia
    • Intra-alveolar inflammation
    • Etiology = bacterial infection
    • Bronchopneumonia (focal)
    • Lobar pneumonia (diffuse)
  2. Interstitial pneumonia
    • Involves alveolar septa
    • Etiology = viral infections
    • Diffuse and bilatera
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14
Q

Pathogenesis of pneumonia

A

Pathogens reach the lungs by:
1. Inhaled air droplets
2. Aspiration of infected secretions upper respiratory tract
3. Aspiration of regurgitated gastric contents
4. Hematogenous spread

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15
Q

Complications of pneumonia

A
  1. Pleuritis
    • Extension of inflammation to pleural surface → pleural
    effusion
    • Pyrothorax (pus filled pleural cavity)
    • Empyema (fibrotic encasement of pus)
    • Slow to heal
    • Results in pleural fibrosis
    • Restrictive lung disease
  2. Abscess:
    • Associated with virulent bacteria
    • Destruction of lung parenchyma
    • Suppuration (pus forming)
  3. Chronic lung disease
    • Unresponsive to treatment
    • Bronchiectasis: bronchial wall loss
    • Destruction of lung parenchyma & fibrosis results in “honey comb lun
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16
Q

Clinical features of pneumonia

A

• Systemic signs of infection: fever, chills, prostration
• Local signs of irritation: cough
• Airway obstruction: shortness of breath (dyspnea), rapid
breathing (tachypnea)
• Inflammation and tissue destruction: expectoration of rusty
sputum, hemoptysis (discharge/coughing of blood

17
Q

Pulmonary tuberculosis

A

• Chronic bacterial infectious disease
• Bacteria lack attraction of PMN and therefore no purulent
inflammation
• Bacteria elicit formation of granulomas
• Granulomas composed of lymphocytes and macrophages,
multinucleated giant cells
• Central core = necrosis → caseous necrosis

Primary infection (1st exposure):
• Localized inflammation = Ghon’s complex
• Enlarged lymph nodes
• Heals spontaneously
• Calcification
• Can be reactivated
• Secondary Tuberculosis

18
Q

Dissemination of tuberculosis

A

Spread through airways, the lymphatic system, or blood (hematogenous)
Complications:
Miliary Tuberculosis
• Widespread seeding of bacteria in lungs and other organs
• Formation of granulomas that resemble millet seeds
Tuberculosis pneumonia
• Spread through air spaces
• Massive lobular or lobar pneumonia
• Same lung of contralateral lung
Pleuritis
• Formation of granulomas on visceral and parietal pleur

19
Q

Chronic bronchitis (COPD)

A

• 90% of cases due to smoking
• Air pollution, toxic fumes, respiratory infections
• Thick bronchi and bronchiole walls
• Mucosa infiltrated with lymphocytes, macrophages and plasma cells
• Submucosa shows mucous gland hyperplasia, chronic inflammation
and fibrosis
• Excess production of tracheobronchial mucus
• Cough and expectoration for at least 3 months during 2 consecutive years

20
Q

Bronchiectasis (COPD)

A

• Permanent dilation of bronchi
• Persistent inflammation in airways
• Filled with mucopurulent material which stagnates and cannot be cleared with coughing
• Spreads: intraparenchymal, hematogenous
• Fever, malaise, fatigue

21
Q

Emphysema (COPD)

A

• Enlargement of air spaces in bronchioles
• Destruction of alveolar walls
1. Centrilobular
• Air space in center of lobule/bronchiole
• Smokers
• Leukocytes, proteolytic enzymes, elastic fibers
2. Panacinar
• Air space distal to terminal bronchioles
• Loss of elastic fibers in alveolar walls
• anti-trypsin deficiency ( 1-AT)

22
Q

Bronchitis vs emphysema

A

Bronchitis “Blue Bloaters”
• Prolonged coughing, expectorate, dyspnea, hypoxia → cyanosis
• Bronchial fibrosis → pulmonary hypertension
• Right heart failure → peripheral venous stagnation → cyanosis
• Enlarged heart

Emphysema “Pink Puffers”
• Reduced respiratory surface → compensatory tachypnea
• Hyperventilate to oxygenate blood
• Chest overexpanded (“barrel-
chest”)
• Small heart

23
Q

Asthma

A

• Increased responsiveness of bronchial tree to a variety of stimuli
• Acute to chronic inflammatory response
• Reversible airway obstruction
• Marked by wheezing, coughing, dyspnea
• ~10% children, 5% adults
• 50% of cases begin in childhood
• 2:1 male to female ratio

24
Q

Two types of asthma

A
  1. Atopic: extrinsic allergen
    • Type I hypersensitivity reaction, IgE
  2. Nonatopic: intrinsic – attacks
    • Physical factors (heat or cold)
    • Exercise
    • Psychological stress
    • Chemical irritants, air pollution
    • Bronchial infection
25
Pathogenesis of asthma
Inhale allergen/antigen Stimulates inflammatory cells Produces mediators resulting in: • Increased blood vessel permeability • Contraction of smooth muscle cells • Mucous secretion Rapid response (histamine) Delayed response (leukotrienes Involves mucus in the lumen, inflammation & basement membrane thickening, enlarged mucous glands, smooth muscle hyperplasia
26
Hypersensitivity pneumonitis
• Extrinsic allergic alveolitis • Immune disorder • Repeated inhalation of foreign antigens • Molds, fungi • Bird droppings, animal fur, wood dust • Acute vs. chronic
27
Hypersensitivity pneumonitis pathogenesis
Acute: Antibodies react with inhaled antigen in alveoli Complement activation Influx of leukocytes Chronic: Cell mediated reaction (T lymphocytes) Granulomas Granulation tissue Fibrosis Honeycomb lung
28
Pneumoconiosis
• Inhalation of mineral dusts, fumes organic or inorganic matter 1. Mineral dust pneumoconiosis 2. Silicosis 3. Asbestosis Lung injury depends on: • Duration of exposure • Concentration of the particle • Size, shape, solubility of particle • Biochemical composition
29
Silicosis vs asbestosis
Silicosis • Inhalation of small silica crystals • Fibronodular lesions in the lung parenchyma Asbestosis • Pulmonary fibrosis • Pleural fibrosis, pleural plaques • Lung cancer • Mesothelioma
30
Pneumoconiosis pathogenesis
• Macrophages take up particles and are stimulated to release various cytokines (TNF, IL-1) • Promotes inflammation • Stimulates proliferation of fibroblasts and collagen • Destruction of tissue, repair, and fibrosis contribute to restructuring of the lung parenchyma • Loss of respiratory surface
31
Acute respiratory distress syndrome (ARDS)
• Clinical term used to describe changes in lungs resulting from an acute lung injury • All of which cause respiratory failure • Shock - trauma, cardiac failure • Pneumonia • Toxic lung injury – fumes, drug
32
Pathogenesis of ARDS
Lung injury, either of the capillary or alveolar epithelium, that eventually results in respiratory failure
33
Atelectasis
• Incomplete expansion or collapse of alveoli • Minor focal atelectasis are common in many pulmonary diseases • Massive atelectasis of the entire lung is less common • Causes: deficient surfactant, compression of the lungs from the outside, resorption of air distal to bronchial obstruction Pneumothorax with the air, hydrothorax with water, tumours can lead to obstruction
34
Carcinoma of the larynx
• <2% of all cancers • Pathologically linked to smoking and alcohol • Vocal cords are most common location • Laryngeal tumours present as nodules or ulcerations of the mucosa • 75% - 5-year survival rate treated by surgery or radiation
35
Lung carcinoma
• Most common malignant tumour of internal organs in Canada • Most related to cigarette smoking • Rare before the age of 40, incidence rises with age • Poor prognosis: 5-year survival rate is 10-15%
36
Clinical features of lung cancer
• Bronchial irritation • Local extension into mediastinum or pleural cavity: pleural effusion • Distant metastases – lungs heavily vascularized • Systems effects of neoplasia • Paraneoplastic syndromes – Cushing's syndrome: small cell carcinoma of the lung secreting ACTH, hyperstimulation of the adrenals
37
Metastatic cancer in lungs
May present as: • Solitary lesion • Multiple lesions (“cannonballs” on x-ray films) • Diffuse involvement of lungs