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General pathology (pathophysiology) > Special pathology - respiratory system > Flashcards

Special pathology - respiratory system Flashcards

1
Q

Respiration can be divided into

A
  1. internal resp.
  2. external resp.
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2
Q

what is internal respiration

A

gas exchange in the metabolizing tissues
oxygen diffuses out of the blood
carbon dioxide diffuses out of the cells

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3
Q

what is external respiration

A

gas exchange in the lungs
oxygen diffuses into the blood
carbon dioxide diffuses into the alveolar air

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4
Q

where is the resp. center located?
and is responsible for?

A

in the medulla oblongata (+pons)

  • automatic respiratory movements
  • homeostatic response to physiological changes: regulates the rate and depth of breathing
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5
Q

respiratory center receives input from (3)

A

chemoreceptors (Co2 )
cerebral cortex
hypothalamus

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6
Q

the conductive system is lined by

A

lined by pseudostratified, ciliated columnar cells + variable proportion of secretory goblet (mucous) and serous cells

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7
Q

what are club cells?

A

Club cells (formerly known as Clara cells) are nonciliated epithelial cells found mainly in bronchioles as well as basal cells found in large airways.

contain numerous biosynthetic organelles
-active role in detoxification of xenobiotics
-critical stem cells in the repair and remodeling
-contribute to the innate immunity

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8
Q

mosst important portion of conductive system?

A

the bronchioles are the most important structures here

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9
Q

what were club cells formerly called?

A

formerly Clara cells

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10
Q

the respiratory exchange system is formed by?

A

formed by alveolar ducts and millions of alveoli
epithelial cells

type I (membranous) pneumonocytes
type II (granular) pneumonocytes

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11
Q

name the 2 types of pneumonocytes

A

type I (membranous) pneumonocytes
type II (granular) pneumonocytes

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12
Q

describe type I (membranous) pneumonocytes

A

are remarkably thin and cover most of the alveolar wall.

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13
Q

describe type II (granular) pneumonocytes

A

appear as large cuboidal cells with lamellar bodies (surfactant) in the cytoplasm.

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14
Q

Hypoxemia

A

abnormally low level of oxygen in the (aterial) blood

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15
Q

Hypoxia

A

condition in which the body or a region of the body is deprived of adequate oxygen supply at the tissue level

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16
Q

Normal Flora of the Respiratory System in cattle

A

Mannheimia haemolytica (formerly Pasteurella haemolytica) - cattle
Pasteurella multocida - cats, cattle, and pigs

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17
Q

Normal Flora of the Respiratory System in cats, cattle, and pigs

A

Pasteurella multocida - cats, cattle, and pigs

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18
Q

Normal Flora of the Respiratory System in dogs and pigs

A

Bordetella bronchiseptica- dogs and pigs

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19
Q

Which portions of the resp. system are considered to be essentially sterile

A

The thoracic portions of the trachea, bronchi, and lungs are considered to be essentially sterile.

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20
Q

Mannheimia (Pasteurella) haemolytica is part of the bovine nasal flora, yet this bacterium causes

A

a devastating disease in cattle—pneumonic mannheimiosis (shipping fever).

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21
Q

name 4 microbial agents

A

viruses
bacteria
fungi
protozoa

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22
Q

name 4 animal products that act as potential agents of resp. pathology

A

dander
feathers
mites
insect chitin

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23
Q

Portals of Entry into the Respiratory System (3)

A

Aerogenous
Hematogenous
Direct (Extension)

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24
Q

3 mechanisms of clearance

A

deposited particles are destroyed, neutralized, or removed from the mucosal surfaces

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25
Q

resp. system Protective mechanisms (4)

A

Sneezing
Coughing
Mucociliary transport
Phagocytosis

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26
Q

defense mechanisms of the conducting system/upper airways and bronchi (4)

A

antibodies
lysozyme
mucociliary clearance
mucus

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27
Q

defense mechanisms of the transitional system/ bronchioles (4)

A

antibodies
antioxidants
club cells
lysozyme

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28
Q

defense mechanisms of the exchange system/alveoli (4)

A

alveolar macrophages
intravascular macrophages
antioxidants
opsonizing antibodies
surfactant

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29
Q

what is the underlying pathogenetic mechanism in many pulmonary diseases

A

Abnormal retention of particles resulting from increased deposition, decreased clearance, or a combination of both is the underlying pathogenetic mechanism in many pulmonary diseases.

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30
Q

why do Very young and older animals have an increased risk of developing respiratory disease

A

At birth, the respiratory and immune systems are not fully developed; this makes it easier for pathogenic organisms to enter and spread within the lungs.

In aged animals, a decrease in the animal’s ability to filter out particles and fight off infection may render the lungs more vulnerable to airborne pathogenic organisms and toxic particles.

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31
Q

Epistaxis

A

blood flow from the nose, from the nasal mucosa or from deep in the lungs

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32
Q

Hemoptysis

A

blood in sputum or saliva (coughing or spitting blood)

result of pneumonia
lung abscesses
ulcerative bronchitis
pulmonary thromboembolisms or hemorrhage
pulmonary neoplasia

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33
Q

Rhinitis

A

Inflammation of the nasal mucosa

Innocuous bacteria present normally protect the host through a process called competitive exclusion, whereby potential pathogens are kept at a harmless level.
Disruption of this protective mechanism can result in rhinitis.

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34
Q

the organism that causes strangles

A

Streptococcus equi subspecies equi
or
Streptococcus equi equi

grows in the upper respiratory tract and is capable of causing infection without predisposing factors such as a previous viral disease.

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35
Q

an organism that causes disease of the lower respiratory tract of foals less than 5 months of age, which is slowly progressive and difficult to detect until the foal is quite sick.

A

Rhodococcus equi

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36
Q

viral disease that manifests as a mild respiratory disease in weanling foals and young racehorses

A

Equine Viral Rhinopneumonitis

may occur as a result of infection by either of two closely related herpesviruses, equid herpesvirus-1 and -4 (EHV-1 and EHV-4).

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37
Q

Infectious Bovine Rhinotracheitis caused by?
and common in?
results in?

A

bovine herpesvirus 1 (BoHV-1)

intensive management feedlot systems

results in inspiratory dyspnea

38
Q

sequela to IBR?

A

IBR = Infectious Bovine Rhinotracheitis (bo herpes virus 1)

sequela to IBR would be bronchopneumonia

39
Q

Atrophic Rhinitis is

A

A common worldwide disease of pigs, inflammation and atrophy of nasal conchae (turbinates).

etiopathogenesis is complex

combined infection by specific strains of Bordetella bronchiseptica producing dermonecrotic toxin + toxigenic strains of Pasteurella multocida

40
Q

Pathogens historically associated with atrophic rhinitis include (4)

A

Bordetella bronchiseptica,
Pasteurella multocida,
Haemophilus parasuis, and
viral infections such as porcine cytomegalovirus
(inclusion body rhinitis).

41
Q

CIRD stands for?
and includes what? (4)

A

The canine infectious respiratory disease (CIRD) group.

canine distemper virus
canine adenovirus V-1 and -2
canine parainfluenza virus
canine herpesvirus

The viral lesions in the respiratory tract are generally transient.

42
Q

possible sequelae of respiratory viral infections (3)

A

secondary bacterial rhinitis, sinusitis, and pneumonia are possible sequelae of respiratory viral infections

43
Q

the most common isolates in dogs with bacterial rhinitis (3)

A

Bordetella bronchiseptica
Escherichia coli
Pasteurella multocida

44
Q

name 2 types of exophytic nasal masses

A

Nasal Polyps and Nasal Cysts (Resembling Neoplasms)

Horses-ethmoidal region
Cats- nasopharynx and Eustachian tubes

The pathogenesis –uncertain
follow chronic rhinitis or sinusitis

45
Q

A Cough is

A

Expulsive reflex initiated by irritation of the mucous membrane of the respiratory tract.

46
Q

Cough is common with: (3)

A

inflammation of the respiratory tract
pulmonary emphysema
edema

47
Q

Persistent coughing may cause

A

alveolar dilation and pulmonary emphysema.

In case of emphysema spontaneous pneumothorax can occur with coughing.

48
Q

name some Noninfectious tracheal diseases (7)

A

tracheal dorsal membrane flaccidity/tracheal collapse

tracheal injury/laceration
posttraumatic stenosis

foreign body
intratracheal tumor

smoke inhalation
tracheal avulsion (cats)

49
Q

disorders affecting the trachea that result from extratracheal diseases:

A

-extreme cardiac enlargement

-mediastinal enlargement (lymph node tumor or thymoma, or megaesophagus

50
Q

tracheitis

A

inflammation of the epithelial lining of the trachea

inflammatory response can be infectious or noninfectious

51
Q

Tracheal Collapse and Tracheal Stenosis

A

reduction in tracheal patency. Commonly the
defect extends the entire length of the trachea
rarely affects the cervical portion alone.

Affected segments with a reduced lumen contain froth and even are covered by a diphtheritic membrane.

tracheobronchial collapse or central airway collapse.
+ horses, cattle

In horses, the so-called scabbard trachea is characterized by lateral flattening so that the tracheal lumen is reduced to a narrow vertical slit

52
Q

Brachycephalic Obstructive Airway Syndrome (BOAS)

A

increased airflow resistance caused by:
stenotic nostrils and nasal meatuses
excessively long soft palate

Brachycephalic canine breeds

53
Q

what is scabbard trachea

A

In horses, the so-called scabbard trachea is characterized by lateral flattening so that the tracheal lumen is reduced to a narrow vertical slit.

A type of tracheal collapse.

54
Q

Secondary changes to Brachycephalic Airway Syndrome (4)

A

nasal and laryngeal edema caused by forceful inspiration

leads to severe upper airway obstruction, respiratory distress, and
exercise intolerance

55
Q

Laryngeal Edema

A

common feature of acute inflammation

swelling of the epiglottis and vocal cords can obstruct the laryngeal orifice and int he worst case scenario lead to asphyxiation

(mucosa of the epiglottis +vocal cords is thickened and swollen often protrudes dorsally onto the epiglottic orifice, a gelatinous appearance )

56
Q

Chronic bronchitis

A

inflammatory changes within the bronchial mucosa with increased mucus production

when chronic:
Bronchial wall thickening which contributes to airflow obstruction and further worsens inflammation which induces cough which sustains inflammation

57
Q

To achieve gaseous exchange, a balanced ratio of

A

the volumes of air to capillary blood must be present in the lungs (ventilation/perfusion ratio), and the air and capillary blood must be in close proximity across the alveolar wall.

58
Q

atelectasis

A

pulmonary tissue collapsed

59
Q

emphysema

A

overinflated/hyperinflation of alveoli leading to alveolar wall damage

60
Q

Compressive atelectasis has two main causes:

A

space-occupying masses in the pleural cavity, such as abscesses and tumors, or

transferred pressures, such as that caused by bloat, hydrothorax, hemothorax, chylothorax, and empyema (=pockets of pus)

61
Q

hypostatic atelectasis

A

when Atelectasis (= pulmonary tissue collapse) occurs when large animals are kept recumbent for prolonged periods, such as during anesthesia

The factors contributing to hypostatic atelectasis are a combination of blood-air imbalance, shallow breathing, airway obstruction because of mucus and fluid that has not been drained from bronchioles and alveoli, and from inadequate local production of surfactant.

Atelectasis can also be a sequel to paralysis of respiratory muscles and prolonged use of mechanical ventilation or general anesthesia in intensive care.

62
Q

Pulmonary Emphysema in animals is a secondary condition resulting from

A

variety of pulmonary lesions.

Lesions are typically secondary to obstruction of outflow of air.

with bronchopneumonia, exudate plugging bronchi and bronchioles causes an airflow imbalance where the volume of air entering exceeds the volume leaving the lung leading to emphysema.

63
Q

in cattle, Interstitial emphysema

A

wide interlobular septa, and lack of collateral ventilation in these species does not permit air to move freely into adjacent pulmonary lobules.

Result- accumulated air penetrates the alveolar and bronchiolar walls and forces its way into the interlobular connective tissue, causing notable distention of the interlobular septa.

64
Q

Pulmonary edema can be physiologically classified:

A

cardiogenic (hydrostatic; hemodynamic)

noncardiogenic (permeability)

65
Q

Hydrostatic (cardiogenic) pulmonary edema develops when

A

elevated rate of fluid transudation

and/or increased hydrostatic pressure in the vascular compartment or decreased osmotic pressure in the blood

66
Q

causes of hydrostatic pulmonary edema (4)
this is also known as hemodynamic pulm. ed.

A

congestive heart failure (increased hydrostatic pressure)

iatrogenic fluid overload

disorders in which blood osmotic pressure is reduced, such as with hypoalbuminemia

+ also occurs when lymph drainage is impaired, secondary to neoplastic invasion of lymphatic vessels

67
Q

Permeability edema (inflammatory) occurs when:
(2)

A

excessive opening of endothelial gaps

or damage to the cells that constitute the blood-air barrier
(endothelial cells or type I pneumonocytes)

68
Q

name 4 inflammatory mediators contributing to permeability edema

A

leukotrienes
platelet-activating factor (PAF)
cytokines,
vasoactive amines

released by neutrophils, macrophages, mast cells, lymphocytes, endothelial cells, and type II pneumonocytes

69
Q

ARDS

A

Acute Respiratory Distress Syndrome

shock lung

70
Q

Acute Respiratory Distress Syndrome characterized by ?

A

pulmonary hypertension
intravascular aggregation of neutrophils in the lungs

acute lung injury
diffuse alveolar damage

permeability edema

formation of hyaline membranes
(mixture of plasma proteins, fibrin, surfactant, and cellular debris from necrotic pneumonocytes)

71
Q

name 4 major cytokines

A

TNF-α, interleukin (IL)-1, IL-6, IL-8

72
Q

Pulmonary thromboembolism can have 2 origins

A
  1. local thrombus formation
  2. translocation of a thrombus present elsewhere in the venous circulation
73
Q

Lung inflammation is a highly regulated process that involves a complex interaction between: (2)

A
  1. cells imported from the blood

(platelets, neutrophils, eosinophils, mast cells, lymphocytes)

2.pulmonary cells

(type I and II pneumonocytes;
endothelial and Club [Clara] cells;
alveolar and intravascular macrophages;
stromal interstitial cells,
such as mast cells, interstitial macrophages, fibroblasts, and myofibroblasts).

74
Q

name 2 arachidonic acid metabolites

A

(leukotrienes and prostaglandins)

75
Q

what is balt hyperplasia

A

Bronchus-Associated Lymphoid Tissue (BALT)

76
Q

PRRS

A

porcine reproductive and respiratory syndrome

77
Q

what is verminous pneumonia

A

Lungworm infection, also known as verminous bronchitis or verminous pneumonia

78
Q

what 3 factors canpredispose to secondary bacterial pneumonia

A

viral infections
toxic gases
pulmonary edema

79
Q

secondary bacterial pneumonia onset after viral infection

A

5 to 7 days after a viral infection

at this time, the phagocytic function of pulmonary alveolar macrophages is decreased and the mucociliary clearance of particulate are notably impaired

Other mechanisms by which viruses impair defense mechanisms are multiple and remain poorly understood.

80
Q

Pneumothorax

A

presence of air in the thoracic
normally - negative pressure to facilitate inspiration

81
Q

forms of pneumothorax (2)

A
  1. spontaneous (idiopathic) pneumothorax air leaking into the pleural cavity from the lungs occurs without any known underlying disease or trauma
  2. secondary pneumothorax
    movement of air into the pleural cavity results from underlying pulmonary or thoracic wall disease
82
Q

causes of secondary pneumothorax: (6)

A

penetrating wounds to the thoracic wall
perforated esophagus

iatrogenic trauma to the thorax and lung during a transthoracic lung biopsy or thoracoscopy

tracheal rupture from improper intubation
rupture of emphysematous bullae
parasitic pulmonary cysts (Paragonimus spp.)

83
Q

Pleural Effusion

A

accumulation of any fluid in the thoracic cavity

transudate
modified transudate
exudate
blood
lymph
chyle

84
Q

hydrothorac fluid is

A

serous, clear, and odorless and fails to coagulate when exposed to air

85
Q

Causes of hydrothorax are the same as those involved in edema formation in other organs: (4)

A

increased hydrostatic pressure (heart failure), decreased oncotic pressure (hypoproteinemia-in liver disease)

alterations in vascular permeability (inflammation) ,
obstruction of lymph drainage (neoplasia)

86
Q

What occurs if hydrothorac persists?

A

If the fluid persists, it irritates the pleura and causes mesothelial hyperplasia and fibrosis, which thickens the pleura.

87
Q

Excessive fluid in the thorax causes compressive what?

A

atelectasis resulting in respiratory distress

88
Q

Blood in the thoracic cavity is called

A

hemothorax, but the term has been used for exudate with a sanguineous component.

Causes
rupture of major blood vessel as result of trauma
erosion of a vascular wall by malignant cells or inflammation (e.g., aortitis)
ruptured aortic aneurysms
coagulopathies; warfarin toxicity
DIC and thrombocytopenia.

Hemothorax is generally acute and fatal.

89
Q

chylothorax

A

The accumulation of chyle (lymph rich in triglycerides) in the thoracic cavity is a result of the rupture of major lymph vessels, usually the thoracic duct or the right lymphatic duct.

The clinical and pathologic effects of chylothorax are similar to those of the other pleural effusions.

90
Q

causes of chylothorax (6)

A

thoracic neoplasia
Trauma
congenital lymph vessel anomalies

lymphangitis
Dirofilariasis
iatrogenic rupture of thoracic duct during surgery

91
Q

chronic pleuitis will results in?

A

serosal fibrosis and tight adhesions between visceral and parietal pleurae

When extensive, these adhesions can obliterate the pleural space.

General pathology (pathophysiology) (16 decks)

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