Pathology Flashcards

1
Q

What are the 4 primary defense mechanisms of the respiratory tract?

A
  1. Particle deposition (air turbulence,warm, humid nasal turbinate air)
  2. Mucociliary escalator
  3. alveolar mø
  4. inflammation and pulmonary immune response
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2
Q

What is the number one cause of congestion/edema?

A

Increased capillary hydrostatic pressure

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3
Q

What is the main reason why horses get sick?

A

Because of transportation and stress

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4
Q

What is Hypostatic Congestion?

A

NO SIGNIFICANCE! Dead animal in prolonged lat recumbency -> gravity causes blood to go into side closest to ground -> post-mortem change

know its normal b/c lungs are still soft

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5
Q

What are other causes of edema?

A
  1. increased permeability
  2. injury of epithelial cells (toxic gases, 100% O2, virus infection)
  3. injury of endothelial cells (Virchow’s triad)
  4. decreased plasma oncotic pressure (chronic nephritis, cirrhosis)
  5. lymphatic obstruction (e.g., metastatic malignant melanoma in lung)
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6
Q

What is an embolus and embolism?

A

Embolus: Any foreign body circulating in the blood or lymphatic

Embolism: an embolus gets stuck in a smaller caliber vessel

embolism more common than thrombosis

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7
Q

What causes thrombus to form?

A

Parsites (e.g., heartworms), hypercoag. disorders, endothelial damage

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8
Q

Why are renal infarcts much more common than lung infarcts?

A

One renal artery versus a dual artery system in the lungs

need ~60% of pulmonary vasculature to be affected to have clinical signs (there are millions of vessels in the lungs!)

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9
Q

What is a consequence of pulmonary thrombi or emboli?

A

Pulmonary infarct (super rare)

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10
Q

What are two abnnormalities of inflation in the lungs?

A

Atelectasis and Emphysema

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11
Q

What is the defintion and causes of Atelectasis?

A

Atelectasis: too little air in the lung/incomplete expansion of the lung
- Congenital: fetal
- Acquired: Obstructive v. Compressive

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12
Q

What are cases of Congenital-caused Atelectasis?

A

Fetal: stillborne
Neonatal and dystocia: aspirate colostrum, hypoxic conditions

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13
Q

What is collateral ventilation and what species lack it?

A

Ventilation of alveoli via pathways that bypass normal airways; beneficial in disease states of obstructed or restricted airways as it serves as a back-up system. Bovine, swine and marine mammals lack this.

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14
Q

What is Obstructive - Acquired Atelectasis?

A

Inflammatory exudates obstructing bronchioles (or parasites, neoplasia)

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15
Q

What is Compressive - Acquired Atelectasis?

A

blood, pus or air in the lungs that causes the pleural cavity to lose its negative pressure -> lungs collapse

hemothorax, chylothorax, pneumothorax

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16
Q

Interstitial Emphysema

A
  • Most common type in ruminants
  • forced expiration (pneumonia, agonal breaths) causes bronchiolar collapse -> alveolar rupture -> air leaks into interlobular septa
  • Remember: bovines have NO collateral ventilation! The trapped air in the distal alveoli is what causes the alveoli to rupture
Causes of forced expiration: pneumonia, agonal breathing

Emphysema: tissue expansion by air or gas

17
Q

Where do most primary lung tumors orginate from?

A

From the alveolar and bronchiloar epithelium, and are frequently located in the pulmonary hilum

18
Q

What is Feline lung-digit syndrome?

A

where lung cancer selectively spreads or metastasizes to the nailbeds and toes, usually occurring before signs of respiratory distress/pulmonary disease

The observation of lameness or progressive, lytic lesions of the digits should prompt veterinarians to work up for a primary lung mass, especially in high-risk cats. Up to 88% of carcinoma in the feline digit may be metastatic from a pulmonary lesion.

19
Q

What is the general rule of tumor malignancy potential in dogs and cats?

A

Dogs: tumors > 3cm in diameter
Cats: tumors >1cm in diameter
= potentially malignant

most malignant tumors originate from benign proliferations!

20
Q
A
21
Q
A

fibrin = damage to vasculature = damage to coag cascade

22
Q
A
23
Q
A

Common sequela = pulmonary abscess

24
Q
A

Granuloma: a focal cluster of macrophages/inflammatory cells that form in response to infection.

NO PUS!

25
Q

What is bronchlectasis

A

Rupture and dilation of bronchial wall due to enzymatic effect of neutrophils and macrophages; is an irreversible lesion!

occurs in cows with mycoplasma bovis infection

26
Q

Etiology of suppurative vs fibrinous bronchopneumonia

A

Suppurative bronchopneumonia: mycoplasma spp.

Fibrinous bronchopneumonia: highly pathogenic bacteria (Mannheimia, Actinobacillus)

27
Q

Pathogenesis of fibrinous inflammation in bronchopneumonia

A

severe lung injury -> fibrinogen leaks out of vessels & is converted into fibrin via thrombin (clotting enzyme) -> fibrin deposits in the pulmonary tissue

28
Q

Distributiom of aspiration pneumonia

A

cranioventral unilateral!

29
Q

texture of interstitial pneumonia

A

elastic- alveolar walls become inflammed/thickened

30
Q
A

embolism pneumonia

abscesses all over the lung = origin is not the lungs

"embolic showers"
31
Q

Sequel to embolic pneumonia

A

Pulmonary abscesses

32
Q
A

Granulomatous pneumonia in foal with Rhodococcus equi

Rhodococcus equi is a bacterium that lives in the soil and can cause pneumonia in young (1 to 6 months old) foals.

Infection progresses slowly and foals often do not begin to show clinical signs until the disease has become severe.

R. equi can infect immunocompromised humans and cause lung infections.

Many foals infected with R. equi recover, but those that are severely affected may not survive.

Good foal management, regular screening, and early detection are the best approaches to prevent R. equi infection.

33
Q
A

Verminous pneumonia (small ruminants) – by parasites // lung worms

Protostrongylus, Neostrongylus