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Systemic Pathology 500 > Respiratory System > Flashcards

Respiratory System Flashcards

1
Q

Pathogenesis of Cystic Fibrosis

A

Defect in gene for protein that allows chloride to pass through epithelial cell membranes. Sodium (and thus water) absorption is increased.

  1. Less water on epithelial surface –> thick, sticky and viscous mucus.
  2. Elevation of sweat electrolytes
  3. Pancreatic enzyme insufficiency
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2
Q

CF: pancreas

A

80-90% of people with CF have pancreatic issues

Thick secretions block pancreatic ducts.

Impaired digestion, failure to thrive, bulky, smelly, frothy stool.

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3
Q

CF: GI tract

A

10-15% of neonates with CF have meconium ileus.

Rectal prolapse, obstructed intestine.

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4
Q

CI: pulmonary

A

80-90% of people with CF

Chronic cough, purulent sputum, hypoxia, barrel chest, pectus carinatum.

Chronic pulmonary infection

Kyphosis, clubbing of fingers

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5
Q

CF: fertility

A

Infertility universal in men, common in women.

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6
Q

Bronchogenic Cyst

A

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.

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7
Q

Extralobal sequestration

A

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

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8
Q

Intralobar sequestration.

A

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

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9
Q

The Common Cold

A

Acute, afbrile, self-limiting upper respiratory infection.

Viral.

Most common during fall and spring

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10
Q

Viruses involved with the common cold

A 
Rhinovirus (50%)
Coronavirus
Adenovirus
Parainfluenza virus
Other
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11
Q

Influenza

A

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.

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12
Q

Cystic Fibrosis

A

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.

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13
Q

Sinusitis

A

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
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14
Q

Acute Bronchitis

A

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.

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15
Q

Pneumonia

A

Inflammation of the lungs
Due to infection, inhalation, aspiration

Primary or secondary; one or both lung
50% viral (not so bad)

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16
Q

Altered consciousness, neurological conditions, dysphagia are all risk factors for:

A

Pneumonia

Lung abscess

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17
Q

Streptococcus pneumonia

A

Bacterial.

Involved in community acquired pneumonia

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18
Q

Haemophilis influenza

A

Bacterial.
Not the flu.
Involved with community acquired pneumonia.

Hib vaccine given in infancy

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19
Q

Staphylococcus aureus

A

Bacteria

Involved in hospital acquired pneumonia

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20
Q

MRSA

A

Methicillin resistant staphylococcus aureus

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21
Q

Pathogens involved in pneumonia

A
  1. Upper respiratory flora
    (Streptococcus, staphylococcus, haemophilia)
  2. Enteric saprophytes
    (Normal GI anaerobic bacteria)
  3. Extraneous pathogens
    (Ex. Mycobacterium tuberculosis,
    Viruses)
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22
Q

Subtypes of pneumonia, by area affected

A
  1. Aveolar (focal or diffuse, bacterial)
  2. Interstitial (septa, diffuse and bilateral, mycoplasma or virus)
  3. Bronchopneumonia (segmental bronchi)
  4. Lobar: widespread or diffuse
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23
Q

Pneumonia: routes of infection

A

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)

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24
Q

Pathology of pneumonia

A

Invading microorganisms –>
Inflammatory response does not eliminate pathogens –>
Pathogens release damaging toxins –>
Inflammatory immune response damages tissue –>
Scarring and loss of function

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25
Q

Empyema

A

AKA pyothorax.

Pleural effusion in which pus enters pleural cavity.

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26
Q

Pyothorax/empyema

A

AKA purelent pleuritis

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27
Q

Honeycomb lungs

A

Destruction of lung parenchyma, with fibrosis

Can be a complication of chronic lung disease, especially pneumonia

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28
Q

Honeycomb lung

A

Destruction of lung parenchyma, fibrosis

Can result from stubborn pneumonia or other chronic lung disease

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29
Q

Legionnaire’s Disease

A

Special pneumonia
Caused by Legionella pneumophila

Massive consolidation and necrosis of lung parenchyma, with fever, chills, nausea etc.

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30
Q

Bacteria associated with Legionnaire’s

A

Legionella pneumophila

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31
Q

Pulmonary consolidation

A

Lung fills with fluid; gas exchange cannot occur in that area

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32
Q

Primary TB infection

A

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

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33
Q

Primary TB

A

Usually asymptomatic, or manifests with mild pulmonary symptoms.
M. tuberculosis lodges in lower lung
Epitheliod cell granulomas (with caseous necrotic centres) form around infection.

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34
Q

Ghon’s Complex

A

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

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35
Q

Most common extrapulmonary manifestation of TB

A

Lymphadenopathy

But meningitis most deadly

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36
Q

Most common and most feared extrapulmonary manifestations of TB

A

Most common: lymphadenophathy

Most feared: meningitis

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37
Q

Lung Abscess

A

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

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38
Q

Pathogens associated with lung abscesses

A

Mostly anaerobic

Most common aerobic pathogens: staph and strep
Immunocompromised patients may have mycobacteria or fungi (more severe and stubborn)

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39
Q

Areas involved in pneumonia

A
  1. alveolar (focal or diffuse, bacterial)
  2. interstitial (septa; diffuse and bilateral,; mycoplasma or virus)
  3. bronchopneumonia (segmental bronchi)
  4. lobar (widespread or diffuse)
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40
Q

Pneumonia: routes of infection

A

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)

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41
Q

Pathology of pneumonia

A

Invading microorganisms –>
Inflammatory response does not eliminate pathogens –>
Pathogens release damaging toxins –>
Inflammatory immune response damages tissue –>
Scarring and loss of function

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42
Q

Pleuritis

A

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

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43
Q

Pyothorax/empyema

A

AKA purelent pleuritis

44
Q

Bronchectasis

A

Pathological dilation of bronchi

45
Q

Honeycomb lung

A

Destruction of lung parenchyma, fibrosis

Can result from stubborn pneumonia or other chronic lung disease

46
Q

Pneumocystis Carinii Pneumonia

A

PCP
Special form of progressive, often fatal, pneumonia

Idiopathic, but opportunistic.
Seen mostly in immunocompromised

47
Q

Legionnaires Disease

A

Special form of pneumonia
Caused by legionella pneumophila

Causes massive consolidation and necrosis of lung parenchyma, as well as fever, headache, and GI issues

48
Q

Pulmonary consolidation

A

Lung fills with fluid; gas exchange cannot occur in that area

49
Q

Pulmonary Tuberculosis

A

Infectious, inflammatory systemic disease of the lungs
Type 4 hypersensitivity reaction
May involve lymph nodes and/or other organs
Caused by Myobacterium tuberculosis

50
Q

Primary TB

A

Usually asymptomatic.
M. tuberculosis lodges in lower lung
Epitheliod cell granulomas (with caseous necrotic centres) form around infection.

51
Q

Ghon’s Complex

A

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

52
Q

Secondary TB

A

When resistance is low, TB may reactivate.
Dry cough, hemoptysis, fever, anorexia, night sweats
May scar lungs

53
Q

Most common and most feared extrapulmonary manifestations of TB

A

Most common: lymphadenophathy

Most feared: meningitis

54
Q

Lung Abscess

A

Localized accumulation of pus in lung
Usually develops as complication of pneumonia

Aspiration of pathogen-containing oral secretions

55
Q

Pathogens associated with lung abscesses

A

Mostly anaerobic

Most common aerobic pathogens: staph and strep
Immunocompromised patients may have mycobacteria or fungi (more severe and stubborn)

56
Q

Chronic Obstructive Pulmonary Disease

A

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

57
Q

Chronic Bronchitis

A

Productive cough lasting for at least 3 months, for two consecutive years

58
Q

Pathogenesis of Chronic Bronchitis

A

Irritants –> mucous hypersecretion and hypertrophy of mucous glands; also epithelial atrophy and smooth muscle hypertrophy –> airway obstruction

Also, cilia damage increases susceptibility to infection

59
Q

Chronic Bronchitis: Why “blue bloaters”?

A

Cyanosis from insufficient arterial oxygenation
Peripheral edema from right ventricular failure
(may lead to cor pulmonale)
Increased residual lung volume

60
Q

Chronic Bronchitis: Clinical manifestions

A 
Persistent productive cough
Gnarly sputum
SOB with prolonged exhalation
Fever 
Malaise
Recurrent infection
61
Q

Emphysema

A

Destruction of lung parenchyma and pathological accumulation of air.

Enlargement of airspaces beyond the terminal bronchiole.
Loss of elasticity, airway collapse, and gas trapping.

62
Q

Emphysema: pathogenesis

A

Inhaled particles –> destruction of elastic protein in lungs –> permanent enlargement of alveoli

Loss of elasticity –> narrowing or collapse of bronchioles

63
Q

Emphysema: Why “pink puffers”?

A

Hyperventilation compensates

Muscle wasting due to increased TNF alpha production, which can further impair lung function

64
Q

Blebs and bullae

A

In emphysema.

Pockets of air formed between the alveoli (blebs) and within the parenchyma (bullae)

65
Q

Emphysema: Clinical manifestations

A 
Exertional dyspnea
Dyspnea at rest
Thin, wasted appearance
Tachypnea
Hypertrophy of accessory respiratory muscles
Barrel chest
Anxiety
66
Q

Bronchiectasis

A

Progressive form of obstructive lung disease characterized by irreversible destruction and dilation of airways

Associated with chronic bacterial infection

67
Q

Obstruction: Chronic bronchitis vs emphysema

A

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

68
Q

Bronchiectasis: pathophysiology

A

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
69
Q

Bronchiectasis: symptoms

A 
Productive cough
Clubbing
Dyspnea
Fatigue
Weight loss
Hemoptysis
Gnarly sputum
70
Q

Allergic Rhinitis

A

AKA hay fever, seasonal allergies
Hypersensitivity Type 1
Mostly affecting nose and eyes

71
Q

Allergic Rhinitis: pathogenesis

A

Acute vasomotor response mediated by histamine and related vasoactive substances released locally in the nose from mast cells coated with IgE

72
Q

Asthma

A

Reversible COPD
Increased responsiveness of bronchial tree to stimuli
Hypersensitivity Type 1
Biochemical, autonomic, immunologic, infectious, endocrine and psychological factors

73
Q

Three forms of Asthma

A
  1. Extrinsic (atopic or allergic asthma)
    - - hypersensitivity, mostly in the young
  2. Intrinsic (nonallergic)
    - - idiopathic, adult onset
    - - possible viral exposure?
  3. Occupational
    - - narrowing of airways caused by workplace exposure
74
Q

Status asthmaticus

A

Acute attack that cannot be altered with routne care

Medical emergency

75
Q

Asthma: pathogenesis

A

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

76
Q

Pneumoconioses

A

Lung diseases caused by inhalation of mineral dusts, fumes, or particulate matter.

Mostly occupational.

77
Q

Most common pneumoconioses

A
  1. Coal workers’
  2. Silicosis
  3. Asbestosis
78
Q

Extent of damage in pneumoconioses depends on:

A
  1. Duration of exposure
  2. Concentration of particles (air quality index)
  3. Size, shape and solubility (small and regular worst).
  4. Biochemistry of particulates
    - - inert (like coal) less reactive –> long exposure
    - - more reactive (asbestos)more damage faster
    - - asbestos insoluble and remain in lungs forever.
79
Q

Coal Miners’ pneumoconioses

A

Carbon particles inhaled, ingested by alveolar macrophages, somewhat expectorated.

Black lung

80
Q

Silicosis

A

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.

81
Q

TB is a common complication of what pneumoconiosis?

A

Silicosis

82
Q

Asbestosis

A

Asbestos particles engulfed by macrophages, which release inflammatory mediators.

Risk of cancer (malignant mesothelioma)

83
Q

Pneumothorax

A

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

84
Q

Pathogenesis of pneumothorax

A

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.

85
Q

Types of pneumothorax

A
  1. Spontaneous
  2. Traumatic
  3. Open
  4. Iatrogenic
  5. Tension
86
Q

Spontaneous Pneumothorax

A

Generally occurs due to blebs and bullae but can occur due to TB, lung abscess and other lung disease.

87
Q

Tension pneumothorax

A

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.

88
Q

Clinical manifestation of pneumothorax

A

Dyspnea
Sharp pleuritic chest pain
Fall in blood pressure
Weak and rapid pulse

89
Q

Pleurisy

A

AKA pleuritis

Inflammation of the pleura caused by infection, injury or tumour.

Can be primary or secondary.

90
Q

Two types of pleuritis

A
  1. Dry

2. Wet

91
Q

Dry pleuritis

A

Serous fluid between visceral and parietal layers unchanged

Two layers rub against each other –> pain

92
Q

Wet pleuritis

A

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)

93
Q

Diaphragmatic pleurisy

A

Inflammation reaches diaphragm –> secondary to pneumonia

Pain referring to neck, upper traps, shoulder.

94
Q

Pleural Effusion

A

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.

95
Q

Ventilatory Failure

A

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.
96
Q

Ventilators Failure: problems with neural control of respiration.

A

Brainstem lesions (to areas measuring CO2) can depress spontaneous breathing.

97
Q

Ventilatory Failure resulting from Muscle pathologies.

A

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.

98
Q

Ventilators failure and chest wall lesions

A

Restricts chest expansion

Deformities of chest cavity (kyphoscoliosis), pleural fibrosis, pleural tumours, extreme obesity.

99
Q

Ventilator failure and problems with airways

A

CF (bronchial mucous plugs)

COPD asthma

100
Q

Adult Respiratory Distress Syndrome

A

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

101
Q

Lung cancer

A

Bronchiogenic carcinoma
Malignancy of the epithelium of the respiratory tract

Most fatal cancer; 90% due to smoking.

Structural, functional, toxic and malignant changes

102
Q

Two types of lung cancer

A
  1. Small cell (SCLC)/ oat cell

2. Non-small cell (NSCLC)

103
Q

Small Cell lung cancer

A

20% of all lung cancers
Highly aggressive, almost always in smokers.

60% widespread metastasis at time of
diagnosis.

104
Q

Non Small Cell Lung Cancer

A

80% of all lung cancers

Includes squamous cell carcinoma, adenocarcinoma (most common), large cell carcinoma, and mesothelioma.

40% metastasized at time of diagnosis

105
Q

Where does lung cancer most often metastasize to?

A

Mediastinum, pleural cavity and lymph nodes, then Liver and brains

(Also bones, kidneys, adrenals)

106
Q

Paraneoplastic syndromes

A

Indirect effects of cancer

Ex. Squamous cell CA –> extra
PTH –> hypercalcemia in blood –> brittle bones and heart problems

107
Q

Extension of lung tumour into mediastinum/pleural cavity leads to:

A

Obstruction–>atelectasis –> infection
Pleural effusion
Progressive dyspnea
Pain and paralysis of muscles of diaphragm and vocal cords.

Systemic Pathology 500 (3 decks)

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