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425 - Systemic Pathology > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What are the 3 parts of the respiratory tract?

A
  1. Conducting system
  2. Transitional system
  3. Exchange system
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2
Q

What structures are part of the conducting system?

A
  • Nasal cavity
  • Sinuses
  • Larynx
  • Trachea
  • Bronchi

The mucosa of the conducting system is lined primarily by ciliated epithelium and goblet cells that produce mucus.

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3
Q

What structures are part of the transitional system?

A

Bronchioles

Lined by specialized mucosa containing several types of ciliated and secretory cells, such as club cells. Unlike the conducting system, the normal bronchiolar mucosa does not contain goblet cells.

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4
Q

What structures are part of the exchange system?

A

Alveoli

Lined with epithelial cells called pneumocytes. The type 1 (membranous) pneumocytes are thin cells that together with the capillary endothelium and basement membrane, constitute the blood-air barrier. Type 2 pneumocytes are cuboidal and produce surfactant.

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5
Q

What is the function of type 1 and type 2 pneumocytes?

A

1 = Thin cells that constitute blood-air barrier.
2 = Cuboidal cells that produce surfactant.

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6
Q

The nasal cavity is divided by curled shelves of bone covered by a mucous membrane called…

A

turbinates or conchae.

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7
Q

Air from the nasal cavity can enter the pharynx through openings called the…

A

choanae

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8
Q

What are some important functions of the upper respiratory tract?

A
  • Air conduction
  • Air conditioning
  • Air filtration and immune defense
  • Smell
  • Vocalization
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9
Q

What structures are important for air conditioning?

A

Turbinates and nasal sinuses are important for this, they increase the surface area that the incoming and outgoing air is exposed to, allowing the exchange of both heat and moisture.

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10
Q

Where does smell happen?

A

Smell happens at the level of the ethmoid turbinates where there is specialized olfactory epithelium.

Epithelial cells in this area also contain a lot of the p450 enzyme which can help detoxify substances in the air you breathe.

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11
Q

What are the congenital components of brachycephalic airway syndrome (3)?

A
  1. Stenotic nares
  2. Elongated soft palate (extends past epiglottis into the larynx)
  3. Tracheal/laryngeal hypoplasia
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12
Q

What are the secondary malformations of brachycephalic airway syndrome? What causes these to occur?

A

These are acquired through prolonged increased respiratory effort.

  • Everted laryngeal saccules
  • Everted tonsils
  • Hypertrophied and folded laryngeal mucosa
  • Laryngeal edema and collapse
  • Tracheal collapse
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12
Q

What is the difference between laryngeal paralysis in dogs vs in horses?

A

Horses:
- Predominantly affects the left side of the larynx.

Dogs:
- Often bilateral.
- More likely to be caused by a generalized neuromuscular disorder than horses.

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13
Q

Why is laryngeal paralysis usually unilateral in horses?

A

The left side supposedly more commonly affected than the right because the axons of the left recurrent laryngeal nerve are much longer and therefore more susceptible to damage/degeneration.

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14
Q

What are the types of inflammation in the upper respiratory tract?

A
  • Serous rhinitis (red, runny nose that produces clear, watery fluid)
  • Catarrhal (similar to serous but with increased serous and mucus secretion)
  • Purulent/suppurative (boston cream donut type exudate, usually bacterial)
  • Fibrinous (runny scrambled eggs)
  • Granulomatous (cottage cheese or stiff cream cheese type consistency exudate)
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15
Q

What are the clinical signs of feline calicivirus?

How is it different from feline herpesvirus?

A
  • Ocular and nasal discharge.
  • Oral ulcers (characteristic lesion of feline calicivirus, NOT common with feline herpesvirus infection).
  • Conjunctivitis.
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16
Q

What is a potential viral cause for this lesion?

A

Feline calicivirus.

Note: Feline herpesvirus does NOT cause oral ulcers.

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17
Q

What are the two forms of atrophic rhinitis in pigs?

A
  1. Non-progressive atrophic rhinitis (NPAR)
  2. Progressive atrophic rhinitis (PAR)

PAR is more important.

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18
Q

What are the causes of NPAR and PAR in pigs?

A

Non-progressive atrophic rhinitis (NPAR) = bordetella bronchiseptica

Progressive atrophic rhinitis (PAR) = pasteurella multocida

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19
Q

Which strains of Pasteurella multocida are more often associated with atrophic rhinitis?

A

Type D are more often associated with AR than type A

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20
Q

What is the result of Pasteurella multocida infection that causes atrophic rhinitis?

A

The strains of Pasteurella multocida causing atrophic rhinitis produce potent cytotoxins that inhibit bone formation and promote bone resorption – leading to the deformation of the turbinates and the snout.

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21
Q

How does Pasteurella multocida colonize the nasal mucosa?

A

Not very well, unless the mucosal surface has been breached/ulcerated by another pathogen. This is most commonly done by toxin- producing strains of Bordetella bronchiseptica.

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22
Q

How can PAR be diagnosed?

A

Both Pasteurella and Bordetella can be cultured from a nasal swab, however, diagnosis of PAR requires toxin detection through PCR or ELISA.

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23
Q

How can you distinguish between PAR and NPAR?

A

Because both PAR and NPAR can be identical grossly and clinically, it is essential that culture be used to distinguish between them.

However, to prove PAR, culture alone is not adequate because there are strains of P. multocida that do not produce the cytotoxin, so you must isolate the associated toxin using PCR or ELISA.

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24
Q

Where can pseudostratified, ciliated respiratory epithelium with goblet cells be found?

A

In the conducting system and some of the transitional system?

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25
Q

Describe the appearance of bronchi on histology.

A

The bronchi (singular bronchus), are surrounded by decreasing amounts of cartilage and smooth muscle – the amount of cartilage and smooth muscle decreases as the diameter of the airway gets smaller.

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26
Q

Describe the appearance of bronchioles on histology.

A

Bronchioles have no cartilage, little smooth muscle, no glands or mucus cells (so no mucociliary apparatus in bronchioles) and the epithelial lining has fewer ciliated cells.

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27
Q

What are the differences between a respiratory bronchus and a respiratory bronchiole?

A

Respiratory bronchus:
- Lined by cartilage
- Have mucociliary clearance abilities (glands and goblet cells present, many ciliated cells present)

Respiratory bronchiole:
- NO cartilage
- NO glands or mucus cells (no mucociliary apparatus)
- Club cells present

Bronchioles have fewer defense mechanisms (no mucociliary apparatus, no goblet cells and few ciliated cells), and less structural support (no cartilage) which makes bronchioles more susceptible to collapse and infection.

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28
Q

How much of the alveolar surface area is covered by type I pneumocytes?

A

95%

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29
Q

How do pneumocytes replicate?

A

Type I pneumocytes are incapable of cell division. Type II pneumocytes are progenitor cells for type I pneumocytes.

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30
Q

How much of the alveolar surface area is covered by type II pneumocytes?

A

5%

They are equal in number to type I pneumocytes but cover less surface area since they are not flattened.

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31
Q

What are the components of the blood-air barrier?

A
  1. Alveolar surfactant
  2. Type I pneumocytes
  3. Basal lamina of type I pneumocytes
  4. Interstitial connective tissue
  5. Basal lamina of capillary endothelial cell
  6. Capillary endothelial cell
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32
Q

What causes the respiratory system to be vulnerable to airborne injury?

A
  1. The extensive surface area of the alveoli, which are the interface between the blood in alveolar capillaries and inspired air.
  2. The large volume of air passing continuously into the lungs.
  3. The high concentration of noxious elements that can be present in the air.
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33
Q

Where are club cells found?

A

Bronchioles

34
Q

What is the function of club cells (3)?

A
  • Detoxification of xenobiotics (foreign material) via mixed function oxidases.
  • Produce protective secretions against oxidative stress and inflammation.
  • Also produce surfactant
35
Q

What are the main defense mechanisms of the conducting system?

A
  • Mucociliary clearance
  • Antibodies
  • Lysozyme
  • Mucus
  • Coughing
  • Sneezing
36
Q

What are the main defense mechanisms of the transitional system?

A
  • Club cells
  • Antioxidants
  • Lysozyme
  • Antibodies
37
Q

What are the main defense mechanisms of the exchange system?

A
  • Alveolar machophages (inhaled pathogens)
  • Intravascular pathogens
  • Opsonizing antibodies
  • Surfactant
  • Antioxidants
38
Q

What are the three portals of entry into the respiratory system?

A
  1. Aerogenous (inhalation)
  2. Hematogenous (blood-borne)
  3. Direct extension (wounds that penetrate chest, migrating FB, perforation of esophagus or diaphragm)
39
Q

What is atelectasis?

A

Incomplete distension (or inflation or expansion) of alveoli

40
Q

What is the term for incomplete distension of alveoli?

A

Atelectasis

41
Q

Describe the appearance of atelectasis.

A

Ateletatic areas of the lungs are sunken and darker in colour.

42
Q

What are the two forms of atelectasis?

A
  1. Congenital
  2. Acquired
43
Q

What are the two types of acquired atelectasis?

A
  1. Compressive atelectasis: The lungs are compressed by something outside the lungs but within the thoracic cavity
  2. Obstructive atelectasis: Something has blocked an airway (within the lung itself), preventing airflow and causing alveolar collapse.
44
Q

What is emphysema?

A

Distension and rupture of alveolar walls forming air bubbles in lung parenchyma.

45
Q

Which type of emphysema occurs in animals?

A

Secondary emphysema does occur in animals, primary does not. As a secondary condition, this type of emphysema develops as a consequence of some predisposing condition or disease.

Usually caused by an airway obstruction in animals.

46
Q

What condition is this?

A

Emphysema

47
Q

What is the term for the areas pointed to by the black areas?

A

Atelectasis

More specifically, compressive acquired atelectasis.

48
Q

What are the two main categories of causes of pulmonary edema?

A
  1. Cardiogenic (hydrostatic) edema
  2. Permeability (inflammation related) edema
49
Q

What is a lesion that you might see on post-mortem examination of an animal that might indicate that pulmonary edema was the cause of death?

A

Froth in the trachea

It is necessary to see extensive froth in airways to incriminate pulmonary edema as the actual cause of death.

50
Q

Finding this on necropsy might indicate…

A

that pulmonary edema was the cause of death.

51
Q

What are three lesions on the lungs that might indicate pulmonary edema?

A
  1. Lungs that fail to collapse when the chest cavity is opened. You may see rib-impressions on the surface of the lungs.
  2. Edematous lungs will have prominent interlobular septa.
  3. Lungs are often darker than normal, wet, and heavier than normal.
52
Q

What are the 4 main types of pneumonia?

A
  1. Bronchopneumonia
  2. Interstitial pneumonia
  3. Granulomatous pneumonia
  4. Embolic pneumonia

The “BIG E”

53
Q

What is the lesion distribution in bronchopneumonia?

A

Cranioventral consolidation.

54
Q

What is the lesion distribution in interstitial pneumonia?

A

Diffuse

55
Q

What is the lesion distribution in granulomatous pneumonia?

A

Multifocal

56
Q

What is the lesion distribution in embolic pneumonia?

A

Multifocal

57
Q

Where is the inflammation centered in bronchopneumonia?

A

The inflammation is centred on airways, which often contain exudate.

58
Q

What is the cause of bronchopneumonia?

A

Bronchopneumonia is most often caused by inhalation or aspiration of:
- Bacteria
- Stomach contents (called aspiration pneumonia).
- Stomach tubing contents

59
Q

What are 3 common sequelae of suppurative bronchopneumonia?

A
  • Pleural Adhesions – fibrous, tough adhesions between the pleural surface of the lung (visceral pleura) and the pleural surface of the thorax (parietal pleura).
  • Lung Abscesses – “pockets of purulent material” in the lung.
  • Bronchiectasis – rupture of the bronchial wall.
60
Q

Which type of adhesion is permanent?

A

Fibrous is permanent, not fibrinous which can be peeled off.

61
Q

What is needed to determine the difference between a lung abscess and bronchiectasis?

A

Histology

A lung abscess is surrounded by a fibrous tissue capsule.

Bronchiectasis will still have remnants of the airway (bronchial cartilage) surrounding the purulent center.

62
Q

Where is the inflammation centered in interstitial pneumonia?

A

The inflammation is centered on alveolar interstitium.

63
Q

Can interstitial pneumonia be caused by inhaled bacteria?

A

NOOOOO that’s bronchopneumonia

64
Q

What are the features of lungs with interstitial pneumonia?

A
  • All of the lung lobes are affected and the lung tissue feels “rubbery”.
  • Faint rib-impressions on the lung surface.
  • The lungs fail to collapse.
65
Q

What is bronchointerstitial pneumonia and how is it diagnosed?

A

Cases with microscopic lesions that share some histologic features of both bronchopneumonia and interstitial pneumonia.

Diagnosed with histology.

66
Q

What are the most common causes of granulomatous pneumonia?

A
  • Phagocytosis-resistant bacteria, such as species of Mycobacterium or Rhodococcus.
  • Systemic fungal disease, such as infections with Blastomyces, Coccidioides, Histoplasma, or Cryptococcus spp.
  • Less commonly, granulomatous pneumonia can be caused by aberrant migration of parasite larvae or migrating foreign bodies
  • Granulomatous pneumonia may also be found as part of systemic infections, such as with feline infectious peritonitis virus in cats.
67
Q

Granulomatous pneumonia can be caused by which routes of entry?

A

Either via the aerogenous route (ie: inhaled), or pathogenic organisms can seed the lung via a blood-borne (hematogenous) route

68
Q

Where is inflammation centered in embolic pneumonia?

A

Inflammation is centered in pulmonary blood arterioles and capillaries.

69
Q

What is the progression of embolic pneumonia?

A

Embolic pneumonias begin with hyperemic or hemorrhagic foci (early lesions = red spots) -> which can over time progress to form multiple abscesses.

70
Q

What is the term for accumulation of a transudate in the thorax?

A

Hydrothorax

71
Q

What is hydrothorax?

A

Hydrothorax is the accumulation of a transudate (usually clear yellowish to red fluid)

72
Q

What is the term for accumulation of blood in the chest cavity?

A

Hemothorax

73
Q

What is a hemothorax?

A

Accumulation of blood in the chest cavity

74
Q

What is the term for the accumulation of lymph in the thorax?

A

Chylothorax is the accumulation of lymph or chyle. This is usually an opaque, “milky”, white fluid.

75
Q

What is chylothorax?

A

Chylothorax is the accumulation of lymph or chyle. This is usually an opaque, “milky”, white fluid.

76
Q

What is pyothorax?

A

Pyothorax is the accumulation of purulent exudate or “pus” in the thorax. Pus isalso a white fluid, which sticks to the surface of the thoracic organs.

77
Q

What is the term for accumulation of purulent exudate in the thorax?

A

Pyothorax

78
Q

What is pneumothorax?

A

Pneumothorax is the accumulation of air in the thorax.

79
Q

What is the term for the accumulation of air in the thorax?

A

Pneumothorax

80
Q

What is this condition?

A

Hydrothorax (can also see atelectasis)

81
Q

What indicates that the fluid in a chest is actually a hemothorax vs just blood-tinged fluid?

A

The presence of blood clots in the thorax.

82
Q

Name the condition.

A

Chylothorax

83
Q

How can you distinguish chylothorax and pyothorax?

A

Chyle doesn’t adhere to the outer surface of the lungs or pericardium (this occurs with fibrinous or purulent exudates in the thorax – but not with chyle).

425 - Systemic Pathology (6 decks)

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