Respiratory System Flashcards
Pathogenesis of Cystic Fibrosis
Defect in gene for protein that allows chloride to pass through epithelial cell membranes. Sodium (and thus water) absorption is increased.
- Less water on epithelial surface –> thick, sticky and viscous mucus.
- Elevation of sweat electrolytes
- Pancreatic enzyme insufficiency
CF: pancreas
80-90% of people with CF have pancreatic issues
Thick secretions block pancreatic ducts.
Impaired digestion, failure to thrive, bulky, smelly, frothy stool.
CF: GI tract
10-15% of neonates with CF have meconium ileus.
Rectal prolapse, obstructed intestine.
CI: pulmonary
80-90% of people with CF
Chronic cough, purulent sputum, hypoxia, barrel chest, pectus carinatum.
Chronic pulmonary infection
Kyphosis, clubbing of fingers
CF: fertility
Infertility universal in men, common in women.
Bronchogenic Cyst
Rare. Congenital.
Formation of extrapulmonary, fluid filled cyst in the middle of the chest. Usually middle mediastinum.
Lined by respiratory epithelium; limited by musculo-cartilaginous wall.
May cause respiratory distress in newborns, or secondary infection in older people. Mostly asymptomatic.
Extralobal sequestration
Congenital.
Mass of lung tissue not connected to bronchial tree. Located outside visceral pleura. Usually fed by abnormal artery
Usually manifests in newborns as dyspnea and cyanosis. Older kids, recurrent bronchopulmonary infection
Intralobar sequestration.
Probably acquired
Mass of lung tissue within visceral pleura. Isolated from tracheobronchial tree, supplied by systemic artery
Usually lower lobe, unilateral. Often shows signs of chronic recurrent pneumonia
The Common Cold
Acute, afbrile, self-limiting upper respiratory infection.
Viral.
Most common during fall and spring
Viruses involved with the common cold
Rhinovirus (50%) Coronavirus Adenovirus Parainfluenza virus Other
Influenza
Viral respiratory infection
Fever. Headache.
Also coryza, cough, malaise
Nausea. GI distress.
More common during fall and winter.
Complications include: pneumonia, encephalitis, myocarditis, renal disease.
Cystic Fibrosis
Autosomal recessive (chromosome 7) condition affecting ion (chloride and sodium) transport in the exocrine system.
Median survival: 37 years
Systemic; affects digestive, respiratory and male reproductive systems.
Sinusitis
Inflammation of paranasal sinuses
Bacterial, viral or fungal; or from recurrent allergies
Variable manifestation. Can include: Puerile the rhinorrhea Pressure and pain Headache and toothache Cough Tearing
Acute Bronchitis
Lower respiratory infection (trachea and bronchi)
Short duration, self-limiting
Irritation from smoke, fumes etc. or secondary to flu, measles, chickenpox, pertussis or bacterial infection.
Dry cough (may also develop productive cough)
Wheezing
Sore throat
Fever etc.
Pneumonia
Inflammation of the lungs
Due to infection, inhalation, aspiration
Primary or secondary; one or both lung
50% viral (not so bad)
Altered consciousness, neurological conditions, dysphagia are all risk factors for:
Pneumonia
Lung abscess
Streptococcus pneumonia
Bacterial.
Involved in community acquired pneumonia
Haemophilis influenza
Bacterial.
Not the flu.
Involved with community acquired pneumonia.
Hib vaccine given in infancy
Staphylococcus aureus
Bacteria
Involved in hospital acquired pneumonia
MRSA
Methicillin resistant staphylococcus aureus
Pathogens involved in pneumonia
- Upper respiratory flora
(Streptococcus, staphylococcus, haemophilia) - Enteric saprophytes
(Normal GI anaerobic bacteria) - Extraneous pathogens
(Ex. Mycobacterium tuberculosis,
Viruses)
Subtypes of pneumonia, by area affected
- Aveolar (focal or diffuse, bacterial)
- Interstitial (septa, diffuse and bilateral, mycoplasma or virus)
- Bronchopneumonia (segmental bronchi)
- Lobar: widespread or diffuse
Pneumonia: routes of infection
Inhalation of pathogen
Aspiration of infected secretion from URT
Aspiration of infected particles from GI
Hematogenous spread (from sepsis; usually secondary to UTI and GI infections; IV drug use)
Pathology of pneumonia
Invading microorganisms –>
Inflammatory response does not eliminate pathogens –>
Pathogens release damaging toxins –>
Inflammatory immune response damages tissue –>
Scarring and loss of function
Empyema
AKA pyothorax.
Pleural effusion in which pus enters pleural cavity.
Pyothorax/empyema
AKA purelent pleuritis
Honeycomb lungs
Destruction of lung parenchyma, with fibrosis
Can be a complication of chronic lung disease, especially pneumonia
Honeycomb lung
Destruction of lung parenchyma, fibrosis
Can result from stubborn pneumonia or other chronic lung disease
Legionnaire’s Disease
Special pneumonia
Caused by Legionella pneumophila
Massive consolidation and necrosis of lung parenchyma, with fever, chills, nausea etc.
Bacteria associated with Legionnaire’s
Legionella pneumophila
Pulmonary consolidation
Lung fills with fluid; gas exchange cannot occur in that area
Primary TB infection
Asymptomatic
Characterized by Type 4 Hypersensitivity
Lymphocytes release cytokines
Macrophages become epitheloid cells
Some epitheloid cells fuse into Mutinucleated giant cells
Epitheloid cells, giant cells, lymphocytes create granulomas wall off infection:
Caseous necrosis centre
Primary TB
Usually asymptomatic, or manifests with mild pulmonary symptoms.
M. tuberculosis lodges in lower lung
Epitheliod cell granulomas (with caseous necrotic centres) form around infection.
Ghon’s Complex
Localized lung lesion found at site of initial TB infection.
Macrophages and lymphocytes respond to TB infection
Lymphocytes release cytokines
Some macrophages become epitheloid cells
Some epitheloid cells fuse to become multinucleated giant cells
Granulomas (consisting of epitheloid, lymphocyte and giant cells) form around central caseous necrosis
Most common extrapulmonary manifestation of TB
Lymphadenopathy
But meningitis most deadly
Most common and most feared extrapulmonary manifestations of TB
Most common: lymphadenophathy
Most feared: meningitis
Lung Abscess
Localized accumulation of pus in lung
Usually develops as complication of pneumonia
Aspiration of pathogen-containing oral secretions
Inflammation –> necrosis and abscess formation –> rupture with “putrid malodourous expectorations” –> air/fluid filled cavity
Pathogens associated with lung abscesses
Mostly anaerobic
Most common aerobic pathogens: staph and strep
Immunocompromised patients may have mycobacteria or fungi (more severe and stubborn)
Areas involved in pneumonia
- alveolar (focal or diffuse, bacterial)
- interstitial (septa; diffuse and bilateral,; mycoplasma or virus)
- bronchopneumonia (segmental bronchi)
- lobar (widespread or diffuse)
Pneumonia: routes of infection
Inhalation of pathogen
Aspiration of infected secretion from URT
Aspiration of infected particles from GI
Hematogenous spread (from sepsis; usually secondary to UTI and GI infections; IV drug use)
Pathology of pneumonia
Invading microorganisms –>
Inflammatory response does not eliminate pathogens –>
Pathogens release damaging toxins –>
Inflammatory immune response damages tissue –>
Scarring and loss of function
Pleuritis
Inflammation of pleura
Possible complication of pneumonia
Leads to pleural effusion, possible pyothorax and/or empyema
Obliterates pleural cavity –> lungs cannot expand –> restrictive lung disease
Pyothorax/empyema
AKA purelent pleuritis
Bronchectasis
Pathological dilation of bronchi
Honeycomb lung
Destruction of lung parenchyma, fibrosis
Can result from stubborn pneumonia or other chronic lung disease
Pneumocystis Carinii Pneumonia
PCP
Special form of progressive, often fatal, pneumonia
Idiopathic, but opportunistic.
Seen mostly in immunocompromised
Legionnaires Disease
Special form of pneumonia
Caused by legionella pneumophila
Causes massive consolidation and necrosis of lung parenchyma, as well as fever, headache, and GI issues
Pulmonary consolidation
Lung fills with fluid; gas exchange cannot occur in that area
Pulmonary Tuberculosis
Infectious, inflammatory systemic disease of the lungs
Type 4 hypersensitivity reaction
May involve lymph nodes and/or other organs
Caused by Myobacterium tuberculosis
Primary TB
Usually asymptomatic.
M. tuberculosis lodges in lower lung
Epitheliod cell granulomas (with caseous necrotic centres) form around infection.
Ghon’s Complex
Localized lung lesion found at site of initial TB infection.
Macrophages and lymphocytes respond to TB infection
Lymphocytes release cytokines
Some macrophages become epitheloid cells
Some epitheloid cells fuse to become multinucleated giant cells
Granulomas (consisting of epitheloid, lymphocyte and giant cells) form around central caseous necrosis
Secondary TB
When resistance is low, TB may reactivate.
Dry cough, hemoptysis, fever, anorexia, night sweats
May scar lungs
Most common and most feared extrapulmonary manifestations of TB
Most common: lymphadenophathy
Most feared: meningitis
Lung Abscess
Localized accumulation of pus in lung
Usually develops as complication of pneumonia
Aspiration of pathogen-containing oral secretions
Pathogens associated with lung abscesses
Mostly anaerobic
Most common aerobic pathogens: staph and strep
Immunocompromised patients may have mycobacteria or fungi (more severe and stubborn)
Chronic Obstructive Pulmonary Disease
Chronic airflow limitation that is not fully reversible.
Inflammatory response to injury is altered => structural changes to airway ==> more inflammation
Almost always caused by environmental factors (most commonly smoking, but also chronic respiratory infections, periodontal disease, cooking fumes, etc)
Includes chronic bronchitis and/or emphysema
Chronic Bronchitis
Productive cough lasting for at least 3 months, for two consecutive years
Pathogenesis of Chronic Bronchitis
Irritants –> mucous hypersecretion and hypertrophy of mucous glands; also epithelial atrophy and smooth muscle hypertrophy –> airway obstruction
Also, cilia damage increases susceptibility to infection
Chronic Bronchitis: Why “blue bloaters”?
Cyanosis from insufficient arterial oxygenation
Peripheral edema from right ventricular failure
(may lead to cor pulmonale)
Increased residual lung volume
Chronic Bronchitis: Clinical manifestions
Persistent productive cough Gnarly sputum SOB with prolonged exhalation Fever Malaise Recurrent infection
Emphysema
Destruction of lung parenchyma and pathological accumulation of air.
Enlargement of airspaces beyond the terminal bronchiole.
Loss of elasticity, airway collapse, and gas trapping.
Emphysema: pathogenesis
Inhaled particles –> destruction of elastic protein in lungs –> permanent enlargement of alveoli
Loss of elasticity –> narrowing or collapse of bronchioles
Emphysema: Why “pink puffers”?
Hyperventilation compensates
Muscle wasting due to increased TNF alpha production, which can further impair lung function
Blebs and bullae
In emphysema.
Pockets of air formed between the alveoli (blebs) and within the parenchyma (bullae)
Emphysema: Clinical manifestations
Exertional dyspnea Dyspnea at rest Thin, wasted appearance Tachypnea Hypertrophy of accessory respiratory muscles Barrel chest Anxiety
Bronchiectasis
Progressive form of obstructive lung disease characterized by irreversible destruction and dilation of airways
Associated with chronic bacterial infection
Obstruction: Chronic bronchitis vs emphysema
Chronic bronchitis: obstruction caused by mucous and narrowing of lumen
Emphysema: obstruction caused by change in lung tissue –loss of elasticity, destruction of septa, partial airway collape
Bronchiectasis: pathophysiology
Any condition that narrows the lumen (TB, viral infections, pneumonia, CF) –> inability to clear secretions –> chronic recurrent infections
- -> inflammation, mucous, fibrosis –> destruction of interstitium and alveoli
- -> bronchial walls thicken, become flabby and scarred
- -> may cause emphysema
Bronchiectasis: symptoms
Productive cough Clubbing Dyspnea Fatigue Weight loss Hemoptysis Gnarly sputum
Allergic Rhinitis
AKA hay fever, seasonal allergies
Hypersensitivity Type 1
Mostly affecting nose and eyes
Allergic Rhinitis: pathogenesis
Acute vasomotor response mediated by histamine and related vasoactive substances released locally in the nose from mast cells coated with IgE
Asthma
Reversible COPD
Increased responsiveness of bronchial tree to stimuli
Hypersensitivity Type 1
Biochemical, autonomic, immunologic, infectious, endocrine and psychological factors
Three forms of Asthma
- Extrinsic (atopic or allergic asthma)
- - hypersensitivity, mostly in the young - Intrinsic (nonallergic)
- - idiopathic, adult onset
- - possible viral exposure? - Occupational
- - narrowing of airways caused by workplace exposure
Status asthmaticus
Acute attack that cannot be altered with routne care
Medical emergency
Asthma: pathogenesis
Inflammatory response causes thick mucous, increased vascular permeability and congestion, thickening of airway walls and increased contractile response of smooth muscle
–> trapping of distal air –> hypoxemia, obstructed airway, increased WOB
–> coughing, wheezing, SOB
Pneumoconioses
Lung diseases caused by inhalation of mineral dusts, fumes, or particulate matter.
Mostly occupational.
Most common pneumoconioses
- Coal workers’
- Silicosis
- Asbestosis
Extent of damage in pneumoconioses depends on:
- Duration of exposure
- Concentration of particles (air quality index)
- Size, shape and solubility (small and regular worst).
- Biochemistry of particulates
- - inert (like coal) less reactive –> long exposure
- - more reactive (asbestos)more damage faster
- - asbestos insoluble and remain in lungs forever.
Coal Miners’ pneumoconioses
Carbon particles inhaled, ingested by alveolar macrophages, somewhat expectorated.
Black lung
Silicosis
Pneumoconiosis
Destroys macrophage cell membrane; dead macrophages release silica, which is ingested by more macrophages.
Substance released that stimulate formation of collagenous nodules –> destroy lung parenchyma and cause massive pulmonary fibrosis.
TB is a common complication of what pneumoconiosis?
Silicosis
Asbestosis
Asbestos particles engulfed by macrophages, which release inflammatory mediators.
Risk of cancer (malignant mesothelioma)
Pneumothorax
Accumulation of gas in pleural cavity
Caused by defect in pleura or chest wall.
Can result in atelectasis on affected side
Secondary typically from COPD, CF or other path
Recurrence likely
Pathogenesis of pneumothorax
Air enters pleural cavity
Lung collapses partially –> separation between visceral and parietal pleura –> lung collapse toward hilum
–> SOB and mediastinal shift towards affected side –> compression of opposite lung.
Types of pneumothorax
- Spontaneous
- Traumatic
- Open
- Iatrogenic
- Tension
Spontaneous Pneumothorax
Generally occurs due to blebs and bullae but can occur due to TB, lung abscess and other lung disease.
Tension pneumothorax
Site of rupture acts as a one-way valve permitting air to enter on inspiration but preventing escape during expiration.
Continually increasing pressure may collapse lung tissue –> displacement of heart and great vessels –> decreased venous return and cardiac output.
Clinical manifestation of pneumothorax
Dyspnea
Sharp pleuritic chest pain
Fall in blood pressure
Weak and rapid pulse
Pleurisy
AKA pleuritis
Inflammation of the pleura caused by infection, injury or tumour.
Can be primary or secondary.
Two types of pleuritis
- Dry
2. Wet
Dry pleuritis
Serous fluid between visceral and parietal layers unchanged
Two layers rub against each other –> pain
Wet pleuritis
Increase in serous fluid between visceral and parietal layers.
“Pleurisy with effusion”
Less chafing –> less pain
Lung compression may interfere with breathing
Can get infected –> purulent pleurisy (empyema)
Diaphragmatic pleurisy
Inflammation reaches diaphragm –> secondary to pneumonia
Pain referring to neck, upper traps, shoulder.
Pleural Effusion
Increase fluid between visceral and parietal pleura
Can be secondary to any lung pathology that causes edema. (Congestive heart failure, liver or kidney disease, trauma, pulmonary embolism, malignancy, etc)
Increased secretion or decreased drainage.
Ventilatory Failure
Reduced ability to bring air into lungs.
Secondary to alveolar hypoventilation.
Occurs in conditions that affect:
- neural control of respiration
- respiratory muscles
- chest wall
- airways.
Ventilators Failure: problems with neural control of respiration.
Brainstem lesions (to areas measuring CO2) can depress spontaneous breathing.
Ventilatory Failure resulting from Muscle pathologies.
Problems with the nerve to the muscle, the NMJ, or the muscle itself.
Poliomyelitis (spinal cord – respiratory paralysis)
SC injury
Tetanus – spasm of respiratory muscles
Myasthenia gravis – affects NMJ
Muscular dystrophy – muscle wasting, respiratory muscle failure.
Ventilators failure and chest wall lesions
Restricts chest expansion
Deformities of chest cavity (kyphoscoliosis), pleural fibrosis, pleural tumours, extreme obesity.
Ventilator failure and problems with airways
CF (bronchial mucous plugs)
COPD asthma
Adult Respiratory Distress Syndrome
Problem with gas exchange
Leads to acute respiratory failure.
Shock, pneumonia, toxic lung injury, aspiration.
Damage to endothelial cells in pulmonary capillaries or to alveolar lining
Lung cancer
Bronchiogenic carcinoma
Malignancy of the epithelium of the respiratory tract
Most fatal cancer; 90% due to smoking.
Structural, functional, toxic and malignant changes
Two types of lung cancer
- Small cell (SCLC)/ oat cell
2. Non-small cell (NSCLC)
Small Cell lung cancer
20% of all lung cancers
Highly aggressive, almost always in smokers.
60% widespread metastasis at time of
diagnosis.
Non Small Cell Lung Cancer
80% of all lung cancers
Includes squamous cell carcinoma, adenocarcinoma (most common), large cell carcinoma, and mesothelioma.
40% metastasized at time of diagnosis
Where does lung cancer most often metastasize to?
Mediastinum, pleural cavity and lymph nodes, then Liver and brains
(Also bones, kidneys, adrenals)
Paraneoplastic syndromes
Indirect effects of cancer
Ex. Squamous cell CA –> extra
PTH –> hypercalcemia in blood –> brittle bones and heart problems
Extension of lung tumour into mediastinum/pleural cavity leads to:
Obstruction–>atelectasis –> infection
Pleural effusion
Progressive dyspnea
Pain and paralysis of muscles of diaphragm and vocal cords.
