Resp lecture 2 Flashcards

1
Q

What are type I pneumocytes

A

extremely thin squamous (flattened) cells that line 95% of the total
alveolar surface. They are specialized for GAS EXCHANGE and are INCAPABLE OF CELL DIVISION

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2
Q

What are type II pneumocytes

A

are cuboidal cells interspersed among type I cells. They are as numerous as type I, but cover only 5% of the alveolar air surface. they secrete SURFACTANT and are PROGENITOR CELLS FOR TYPE I PNEUMOCYTES

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3
Q

what two things are important about type I pneumocytes

A

gas exchange and can’t divide

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4
Q

what two things are important about type II pneumocytes

A

secrete surfactant and are progenitor cells for type I pneumocytes

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5
Q

what does type II pneumocyte hyperplasia indicate

A

alveolar injury in the lungs

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6
Q

What are the 6 things that compose the blood-air barrier?

A
  1. Alveolar surfactant
  2. Type I pneumocytes
  3. Basal lamina of type I pneumocytes (the “stuff” the cells sit on)
  4. Interstitial connective tissue*
  5. Basal lamina of capillary endothelial cell
  6. Capillary endothelial cell
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7
Q

The blood-brain barrier consists of:

A
  1. Type I pneumocytes cytoplasm
  2. A dual basal lamina – formed by the fusion of the basement membranes of both the endothelial cell and the type 1 pneumocyte.
  3. Cytoplasm of endothelial cell
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8
Q

what are club cells

A

Club cells are found in bronchioles. BE CAREFUL! Do not confuse club cells with
Type 2 pneumocytes, which are found in the alveoli. Club cells are involved in detoxification of xenobiotics (foreign material) via
mixed function oxidases. Club cells produce protective secretions against oxidative stress and
inflammation. Club cells also produce surfactant.

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9
Q

Atelectasis

A

incomplete distension (or inflation or expansion) of alveoli. Atelectatic portions of the lung are sunken and darker in color. (Think solid, jersey mild chocolate bar instead of aero bar)

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10
Q

What is congenital atelectasis

A

Congenital or neonatal atelectasis occurs because the lungs are not inflated with air at birth. This can occur because of aspiration of amniotic fluid, meconium and/or squamous
epithelial cells which can cause obstruction of small bronchi and bronchioles at the time
of birth. In some cases (for example premature births), there may be a surfactant problem (either
not enough produced, or poor quality), which means alveolar septa stick together and
can’t stay open.

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11
Q

What is acquired atelectasis

A

collapse of the lung after inflation has already taken place. Two types: Compressive or obstructive

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12
Q

what is compressive atelectasis

A

the lungs are compressed by something outside the lungs but within the thoracic cavity

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13
Q

what is obstructive atelectasis

A

something has blocked an airway (within the lung itslef) preventing airflow and causing alveolar collapse

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14
Q

What are some examples of causes of compressive atelectasis

A

space occupying thoracic masses (tumors, abscesses) or transferred pressures (pneumo/hydro/chylo/hemo thorax)

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15
Q

What are some causes of obstructive airways

A

lumen narrowed (mucosal edema or inflamation) or lumen blocked (mucus, exudate, lungworms, aspirated material)

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16
Q

what is emphysema

A

over distension and rupture of alveolar wars forming air bubbles in the lung tissue

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17
Q

what type (primary or secondary) emphysema occurs in animals

A

secondary

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18
Q

what is secondary emphysema

A

distension and rupture of alveolar walls forming air bubbles in lung parenchyma which develops as a consequence of some predisposing condition or disease

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19
Q

what are the two causes of secondary emphysema that are often seen in animals

A
  1. obstruction of outflow of air (as in bronchopneumonia)
  2. agonal at slaughter (from gasping against closed airways)
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20
Q

why does obstruction of air outflow lead to secondary emphysema

A

Air can squeeze past the obstruction on inspiration, however, on expiration (exhalation),
the lung contracts a bit, narrowing the airway slightly, and blocking escape of the air. Eventually there is overinflation and rupture of the alveoli (think of blowing up a balloon
too much and then… POP!).

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21
Q

how to differentiate secondary emphysema from obstruction vs agonal at death

A

agonal at death tends to only occur at the distal edges of the lungs

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22
Q

what is pulmonary congestion

A

accumulation of blood and fluid in the lungs. It is a PASSIVE process

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23
Q

what are heart failure cells

A

alveolar macrophages filled with chewed up red blood cells

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24
Q

what are the two main categories of pulmonary edema

A

cardiogenic and permeability

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25
Q

what is cardiogenic pulmonary edema

A

there is either increased hydrostatic pressure (like in CHF) or an increased volume of blood (like in pulmonary congestion), or hypoproteinemia, or lymphatic obstruction.

These are just your Starling forces.

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26
Q

what is permeability pulmonary edema

A

AKA inflammatory pulmonary edema. Usually develops due to generalized inflammation of the lung or if there is damage to the pneumocytes that line the alveoli (both of these increase vascular permeability)

27
Q

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

A

Froth in the trachea

28
Q

T/F: even a small amount of froth in the lungs is enough to incriminate pulmonary edema as the cause of death in an animal at necropsy

A

FALSE. you need EXTENSIVE froth to kill an animal, plus mild lung edema often develops at the time of death regardless of the actual cause of death

29
Q

in addition to froth, what are three other lesions that indicate pulmonary edema?

A
  1. lungs fail to collapse when cavity is opened
  2. edematous lungs will have prominent interlobular septa
  3. lungs are often darker than normal, wet, and heavier than normal
30
Q

At necropsy, lung tissue oozes red-tinged fluid and you can see foamy fluid in the bronchi. What does this indicate

A

Pulmonary edema

31
Q

What are the four main types of pneumonia

A
  1. Bronchopneumonia
  2. interstitial pneumonia
  3. granulomatous pneumonia
  4. Embolic pneumonia

ACRONYM: BIG E

32
Q

what is pneumonia

A

Any inflammatory lesion in the lung

33
Q

what is the difference between pneumonia and pneumonitis

A

there isn’t any. They’re the same thing.

34
Q

what is the most common form of pneumonia

A

bronchopneumonia

35
Q

Bronchopneumonia: important details

A
  • centered on airways, often contain exudate
  • cranioventral consolidation
  • caused by inhalation or aspiration of bacteria, stomach contents, or stomach tubing contents.
36
Q

What are the two types of bronchopneumonia

A

Suppurative (lobular)

Fibrinous (lobar)

37
Q

the cranioventral portion of a lung is dark red to purple and feels firm. What is your diagnosis

A

bronchopneumonia

38
Q

if there is dark grey to black areas of lung tissue due to aspiration of stomach acid in the cranioventral portion, what should your diagnosis be

A

necrotizing bronchopneumonia

39
Q

what are the 3 common sequelae of suppurative bronchopneumonia

A
  1. pleural adhesions (fibrous, tough adhesions between the visceral and parietal pleura)
  2. lung abscesses (pockets of purulent material in the lung)
  3. bronchiectasis (rupture of the bronchial wall)
40
Q

Which (fibrous vs fibrinous) adhesions are permanent

A

fibrous

41
Q

What do fibrous adhesions on the lungs indicate

A

only indicate that the animal had a previous pneumonia, not necessarily that is currently had pneumonia at the point of death

42
Q

What indicates chronic bronchopneumonia?

A

fibrous adhesions AND abscesses

43
Q

what is bronchiectasis

A

the rupture and dilation of a bronchial wall due to the effects of enzymes
(produced and secreted by neutrophils and macrophages) during inflammation. The enzymes degrade the bronchiole, therefore this is a IRREVERSIBLE lesion. It is also COLLATERAL DAMAGE to the airway due to the inflammatory process

44
Q

What is the only way 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 airway (bronchial cartilage) surrounding the purulent center

45
Q

difference between fibrinous and fibrous adhesions

A

fibrinous - yellow, easy to pull off

fibrous - white, shiny, hard to pull off (think of tape on cardboard).

Has to do with the chronology of the lesion - fibrin indicates active (acute or subacute) process. Fibrous indicates scarring, and therefore chronic processes.

46
Q

Important details on interstitial pneumonia

A

inflammation is centered on alveolar interstitium.

There are many different etiologies (viruses, toxic gases, Ag-Ab complex deposition, endothelial damage…)

lungs are diffusely rubbery or meaty, frequently have rib imprints, and fail to collapse.

47
Q

Rib impressions on the UP side is important to diagnose

A

interstitial pneumonia

48
Q

what causes the rubbery texture of the lungs in interstitial pneumonia

A

hypercellularity and edema of the interstitium.

49
Q

T/F: interstitial pneumonia is caused by inhaled bacteria and is centered on airways

A

FALSE. This refers to bronchopneumonia. Bacteria doesn’t cause interstitial pneumonia, and inflammation is centered on the connective tissue, not the airways

50
Q

what are three clues that indicate interstitial pneumonia

A
  • all lung loves are affected (diffuse distribution)
  • faint rib impressions on the caudal lung surface
  • lungs fail to collapse
51
Q

T/f you can diagnose bronchointerstitial pneumonia based on gross examination of lung

A

FALSE. this requires histology

52
Q

Granulomatous pneumonia: important details

A
  • granulomas distributed throughout lung.
  • caused by:
    1. phagocytosis-resistant bacteria
    2.systemic fungal disease
    3. parasites or FBs
    4.systemic infection
  • route of entry is either AEROGENOUS (inhaled), or BLOOD BORNE (hematogenous)
53
Q

Embolic pneumonia: important details

A

inflammation is centered in pulmonary blood arterioles and capillaries

hematogenous.

begins with hyperemic or hemorrhagic foci which progress into abscesses.

Diffuse, random distribution

54
Q

T/F phagocytosis-resistant bacteria like Mycobacteria or Rhodococcus cause embolic pneumonia

A

FALSE. These cause granulomatous pneumonia

55
Q

What is required to differentiate granulomatous pneumonia from embolic pneumonia

A

histology

56
Q

What is hydrothorax

A

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

57
Q

what is hemothorax

A

accumulation of blood in the chest cavity (should see blood
clots!)

58
Q

what is chylothorax

A

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

59
Q

what is pyothorax

A

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

60
Q

what is pneumothorax

A

accumulation of air in the thorax.

61
Q

T/F chyle adheres to the outer surface of the lungs or pericardium

A

false. this occurs with fibrinous purulent exudates in the thorax, but not with chyle.

62
Q

on necropsy, you notice a dull, tan to grey exudate that sticks to the pleural surface and the surface of the pericardium. What is you diagnosis

A

pyothorax. (NOT chylothorax, which may look the same but doesn’t stick)

63
Q

T/F pleuritis may make it hard for an animal to breathe, but it is not painful in itself.

A

FALSE!!!! its super super painful

64
Q
A