Test 3: 43 non infectious pulmonary disease Flashcards

1
Q

5 common small animal lung diseases that are not pneumonia

A
  • Pulmonary contusions
  • Allergic airway diseas
  • Non-cardiogenic pulmonary edema
  • Pulmonary thromboembolism
  • Pulmonary interstitial fibrosis
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2
Q

common causes of pulmonary contusions

A

Compression-decompression injury → HBC, High rise syndrome, kicks, abuse, shock waves

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3
Q

clinical signs of pulmonary contusion

A
  • Acute/severe respiratory distress/tachypnea OR may develop progressively over 24-48 hours
  • Other signs of trauma- thoracic limb fractures, abrasions, pneumothorax, rib fractures, pleural effusion, diaphragm rupture, arrhythmias, pericardial effusion
  • Auscultation: normal or increased breath sounds; crackles and/or wheezes: May worsen over a 24-hour period, Can be asymmetric/unilateral or generalized, Can be difficult to interpret around other thoracic pathology
  • Hemoptysis is uncommon in small animals (compared to humans)
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4
Q

diagnosis of pulmonary contusion

A

B lines on ultrasound

Thoracic radiographs: patchy/diffuse interstitial or alveolar lung infiltrates; localized or generalized

CT

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5
Q

treatment of pulmonary contusion

A

O2
intubation if severe
pain meds

antibiotics not used unless pneumonia devleops

prognosis: usually resolves in 10-14 days

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6
Q

DDX for allergic airway disease

A

Parasitic allergic airway disease
Eosinophilic bronchopneumopathy
Feline asthma

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7
Q

clinical signs of allergic airway disease

A

Range from asymptomatic, chronic disease (>2 months) or acute crisis
* Cough, crackles, wheeze, respiratory distress
* Expect lung hyperinflation thickened bronchi/bronchioles
* Lower airway inflammation– mucosal edema, airway smooth muscle hypertrophy, airway constriction, excessive production of airway secretions

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8
Q

what are some parasites that can cause allergic airway disease

A

Migrating parasites:
§ Toxocara canis (roundworms)
§ Ancylostoma caninum (hookworms)
§ Strongyloides stercoralis (pinworms)

Primary lung parasites:
§ Paragonimus kellicotti (lung fluke)
§ Aelurosrongylus abstrus (cat lungworm)
§ Capillaria aerophile
§ Filaroides hirthi (dog lungworm)

Dirofilaria immitis: antimicrofilarial antibodies trap microfilaria in pulmonary
capillaries

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9
Q

diagnosis of parasitic allergic airway disease

A

Fecal testing + Baermann
heartworm testing
CBC (↑eosin)
Xray: interstitial infiltrates, bronchial thickening, alveolar consolidation

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10
Q

treatment of parasitic allergic airway disease

A

Anthelminthic medications +/- corticosteroids

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11
Q

EBP allergic airway disease is more common in

A

younger well conditioned Siberian Huskies, Alaskan Malamutes with yellow green nasal discharge

Hypersensitivity with eosinophilic infiltration of lung/mucosa

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12
Q

diagnosis of EBP allergic airway disease

A

CBC- peripheral eosinophils seen in 60% of cases
Thoracic radiographs: diffuse bronchointerstitial pattern
Often alveolar infiltrates from secondary pneumonia
Bronchoscopy: yellow-green mucous, thick airways
Cytology- >50% eosinophils in 87% of cases

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13
Q

treatment of EBP allergic airway disease

A

Glucocorticoids – often lifelong

Perform culture and sensitivity – treat for infectious pneumonia if present!!

“Eosinophilic pneumonia of undetermined origin”
Hypersensitivity with eosinophilic infiltration of lung/mucosa in younger well conditioned dogs with yellow- green nasal discharge

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14
Q

feline asthma is a type — hypersensitivity reaction to aeroallergens

A

1

leads to reversible bronchoconstriction →inflammation/bronchitis with thick airways and mucous production

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15
Q

feline asthma usually occurs in —

A

young adult/middle aged, well conditioned cat with a chronic cough

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16
Q

clinical signs of feline asthma

A

Episodic bronchoconstriction leads to increased end-expiratory volume/air trapping, increased work of breathing, and respiratory fatigue

Leads to inflammation/bronchitis with thick airways and mucous production

Crackles/wheeze on auscultation

17
Q

diagnosis of feline asthma

A
  • CBC: rarely see a circulating eosinophilia
  • Thoracic radiographs: diffuse bronchial or bronchointerstitial pattern; lung lobe collapse can be seen secondary to mucous plugging
  • Cytology- eosinophilia, may be neutrophilia
18
Q

treatment of feline asthma

A

Remove allergens- air fresheners, cigarette smoke, dust exposure

Steroids and bronchodilators →oral or inhaled

19
Q

young- middle age cat with crackles/wheezing

A

Feline asthma

diffuse bronchial or bronchointerstitial pattern (donuts); lung lobe collapse can be seen secondary to mucous plugging

bronchoconstriction →Leads to inflammation/bronchitis with thick airways and mucous production

20
Q

Accumulation of extravascular fluid within pulmonary parenchyma or alveoli with a normal pulmonary capillary wedge
pressure

A

non cardiogenic pulmonary edema

Increased permeability from damaged microvascular barrier and alveolar epithelium

21
Q

DDX for Non-Cardiogenic Pulmonary Edema

A

Neurogenic pulmonary edema
Negative pressure pulmonary edema
ALI/ARDS

22
Q

explain neurogenic pulmonary edema

A

Following acute neurologic event (trauma, seizures), increase in intracranial pressure causes surge in catecholamines, increasing vascular resistance and causes alveolar capillary leakage

Mechanisms are poorly understood but are often acute in onset and resolve within 48 hours.

23
Q

explain Negative pressure pulmonary edema

A

Choking, strangulation, near-drowning causes acute intra-thoracic negative pressure, increasing cardiac afterload and similar catecholamine surge and alveolar capillary leakage

Mechanisms are poorly understood but are often acute in onset and resolve within 48 hours.

24
Q

ALI →ARDS

A

Inflammation leads to vasculitis, increased permeability, and inflammatory cell infiltration/protein rich fluid leakage into lungs

secondary to severe systemic disease such as sepsis or pancreatitis

25
Q

clinical signs of ALI or ARDS

A

Severe dyspnea, bilateral pulmonary infiltrates, crackles, hemoptysis, and ventilatory failure
§ Ventilation is often required
§ Prognosis is guarded

secondary to severe systemic disease (sepsis, trauma)
inflammation leads to vasculitis and leakage of protein rich fluid into the lungs

26
Q

diagnosis of non-cardiogenic pulmonary edema

A

History- strangled, drowning, seizures, trauma

Auscultation- dorsocaudal crackles

Bedside thoracic ultrasound: evidence of “B-lines”

Thoracic radiographs: alveolar pattern- typically dorsocaudal but variable

27
Q

— can cause pulmonary thromboembolism

A

thrombi, fat, septic emoboli,
metastatic neoplasia, or parasites

28
Q

diagnosis of pulmonary thromboembolism

A

difficult!!

Coagulation testing →FDP/D-Dimer may be high
Thoracic radiographs: often normal, rarely evidence of poorly perfused areas
CT Angiogram: gold standard

29
Q

treatment of pulmonary thromboembolism

A

Supportive care: oxygen!
Identify and treat underlying disease
+/- Thrombolytic therapy

30
Q

inflammation and scarring resulting from deranged pulmonary remodeling

A

pulmonary interstitial fibrosis

31
Q

obstruction of pulmonary vasculature by thrombi, fat, septic emoboli,
metastatic neoplasia, or parasites

A

pulmonary thromboembolism

32
Q

clinical signs of pulmonary interstitial fibrosis

A

Common in West Highland White Terriers (also seen in other terriers, cats)

Slow progression of signs- dyspnea, cyanosis, syncope, cough

Loud, coarse, inspiratory crackles

33
Q

diagnosis of pulmonary interstitial fibrosis

A

Thoracic radiographs: often non-specific, diffuse interstitial pattern

CT: may support radiographic findings

Cytology: usually low population of inflammatory cells

Lung biopsy: definitive diagnosis

common in westies

34
Q

treatment of pulmonary interstital fibrosis

A

Glucocorticoids
Bronchodilators

Prognosis is often guarded, with eventual progression to respiratory failure