Week 1 - Parenchymal and interstitial disease Flashcards

1
Q

Out of the following, which one presents with the worse clinical signs?

  1. URT obstruction
  2. Loss of thoracic capacity
  3. Disease of airway, parenchyma, interstitial
  4. Non CRS conditions
A
  1. URT obstruction

Higher up the obstruction = worse clinical signs

e.g
Blockage of on bronchi = one lung still working
Blockage of trachea = obstruction to the whole lung = bigger decrease in gas exchange = cyanotic

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2
Q

What are the main clinical signs of lung disease (parenchyma and interstitial)?
- Inspiratory/expiratory efforts?
- Cough??
- Cyanosis?
- Respiratory depression?
- Noise?

A
  • Increased inspiratory and expiratory effort (but inspiratory effort predominates)
  • Cough may/may not be present
  • Cyanosis less common
  • Minimal respiratory depression (only in severe cases)

Noise:
- Crackles or wheezes
- Increased/decreased bronchovesicular sounds

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3
Q

Patients with lung disease (parenchyma and interstitial) are fragile, what often needs to be done ASAP?

A

Oxygenate

Emergency ultrasound
- Determine whether the pleural space is involved

Pleural space = decreased lung sound

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4
Q

What are the 6 most common lung diseases in small animals?

A

Aspiration pneumonia
Pulmonary oedema
Drowning
Canine/feline inflammatory airway disease
Eosinophilic lung disease
IPF (idiopathic pulmonary fibrosis)

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5
Q

What is aspiration pneumonia and what is the outcome based on?

A

Inhalation of material into the lower airway.
Material = stomach contents - Acidic and causes damage to stomach.

Outcome:
- pH
- Bacterial contents
- Volume
- Particle size

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6
Q

What are the signs of aspiration pneumonia and how is it diagnosed?

A

Signs:
- Cough
- Harsh/reduced lung sounds
- Tachypneoa
- Pyrexia

Diagnosis:
- Radiograph (alveolar filtrate patchy/focal, lung lobes: right middle, right cranial, left cranial)
- BAL CONFIRMS

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7
Q

What is the treatment for aspiration pneumonia?

A

Supportive
- Oxygen
- Antibiotics

Treat underlying cause

Anti-acid medication if frequent reoccurrence

Metoclopramide to improve motility and increase lower oesophageal sphincter tone.

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8
Q

What lung pattern is seen with aspiration pneumonia?

A

Alveolar
- Bronchograms visible
- Alveoli have soft tissue opacity as fluid present

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9
Q

What is pulmonary oedema?

A

Fluid accumulation in the intersitium and subsequently the alveoli at a rare that exceeds removal.

Leads to respiratory compromise are termed acute lung
injury (ALI) or acute respiratory distress syndrome (ARDS)

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10
Q

What causes pulmonary oedema?

A

Consequence of various conditions
▪ Increased hydrostatic pressure
▪ Reduced oncotic pressure
▪ Increased vascular permeability
▪ Impaired lymphatic drainage

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11
Q

Pulmonary oedema can be cardiogenic or non cardiogenic, what are the mechanisms behind them?

A

CARDIOGENIC
- Increased hydrostatic pressure = forces fluid out of the capillaries and into the surrounding lung tissue
- Causes low protein as vascular permeability remains unchanged= low oncotinc pressure less force pulling fluid back into the blood vessels, making it easier for fluid to leak out into the lung tissue.
- More responsive to treatment as can dress the hydrostatic pressure

NON-CARDIOGENIC
- Driven by lung damage
- Lung damage increases vascular permeability.
- High-protein fluid enters lung tissue.
- Raised pressure disrupts blood flow and ventilation.
- Fluid causes stiff lungs, airway compression, and higher resistance.
- Fluid is cleared by sodium/chloride transport.
- Damaged epithelium prevents fluid removal.
- Harder to treat than cardiogenic oedema as cannot address epithelial damage

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12
Q

What is the most common cause of pulmonary oedema?

A

Pulmonary epithelial injury
(Non cardiogenic, damage to the lung)

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13
Q

What are the signs of pulmonary oedema and how is it diagnosed?

A

Signs:
- Delayed onset (damage -> signs 72hrs later)
- Moist cough (produce froth)
- Orthnopnea
- Cyanosis
- Harsh bronchovascualr lung sounds
- Crackles

Diagnosis:
- Radiograph = unstructured interstitial pattern ‘mist’ that can progress to alveolar (bronchograms and soft tissue opacity).

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14
Q

How is pulmonary oedema treated?

A

Address underlying cause, treat ARDS/ALI
Oxygen supplementation
+/- Sedation
Support – keep affected lung dependent

Diuretics less effective for non-cardiogenic oedema but still indicated

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15
Q

What causes physical lung injury, how is it diagnosed and treated?

A

CAUSE:
Thoracic trauma
- Chest wall damage and pain
- Increased reps rate (animal count be in RTA with a broken leg, make sure increase resp is not thoracic damage and not just pain).

DIAGNOSIS
Thoracic radiograph
- Lag phase between clinical findings and radiograph changes

TREATMENT
- Supportive care - oxygen
- Stabilisation of thoracic wall

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16
Q

What is drowning and how is it different to aspiration pneumonia?

A

Aspiration of pneumonia is aspiration of stomach contents

Drowning is aspiration of a liquid e..g river water

17
Q

How does drowning affect the lungs and what are common causes?

A

Alveoli fill with fluid – dilutes surfactant and leads to alveolar
collapse and intrapulmonary vascular shunting leading to ventilation-perfusion
mismatching

Reduced compliance and inflammation leads to ARDS
worsening hypoxaemia

Causes:
- Unable to exit water
- Seizure while swimming
- More common in dogs

18
Q

What are the clinical signs of drowning and how is it diagnosed?

A

SIGNS
- Respiratory distress
- Arrest
- Coughing
- Unconscious
- Increased or decreased lung sounds
- No crackles as lungs are flooded!

Diagnosis:
- Radiograph (lung pattern varied from interstitial to alveolar)
- Sand bronchograms (alveolar have radio-opaque lookO) = negative prognostic indicator
- Unable to maintain saturation on oxygen therapy
- No evidence of antibiotics or corticosteroid

19
Q

What is chronic inflammatory lung disease?

A

Unknown but thought to be caused by triggers (infections, allergies, inhaled irritants).

Persistent inflammation = chronic changes to mucosa and mucus production, respiratory smooth muscles, reduce ciliary movement and scarring.

Variable oedema

A persistent cough becomes an ongoing cough.

Airflow is reduced

Increases risk of secondary infection and dynamic airway disease

20
Q

What are clinical signs of canine chronic bronchitis?

A

8 yrs old +
Toy and small breed dogs

  • Persistent, productive or nonproductive cough
  • Exercise intolerance,
  • Increased expiratory effort
  • Prolonged expiratory phase
  • Wheezing
  • Acute exacerbation of disease can occur during excitement, stress, or when a secondary, complicating factor (e.g. pneumonia) occurs
  • Acute respiratory distress
21
Q

What is the main difference between feline asthma and feline chronic bronchitis?

Is treatment the same for them?

A

Asthma = eosinophilic airway inflammation, coughing, dyspnea, respiratory distress.

Bronchitis = Neutrophillic airway inflammation, less wheezing, more coughing.

Treatment is the same!

22
Q

How can chronic inflammatory airway disease be investigated?

A

MDB (minimum database = shows co-morbidities)
Pulse oximetry
Radiographs – lateral recumb. or standing
CT
BAL (TTW?) – culture and PCRs? Bronchoscopy

23
Q

How can chronic inflammatory airway disease be treated?

A

Anti-inflammatories
Bronchodilators (asthma)
Anitbiotics
Supportive therapy
Regular assessment

24
Q

Eosinophilic lung disease
- common in dogs or cats?
- clinical signs
- diagnostic
- treatment

A

Dogs = eosinophilic bronchopneumopathy

Cats = reactive eosinophilic airway disease (asthma)

Signs
- Acute or chronic
- Coughing
- Weight loss

Diagnosis
- Radiograph = bronchointersitial pattern and alveolar
- Bloods - circulating eosinophils

Treatment
- Prednisalone
- Prognosis good unless other organs are involved

25
Q

Which dogs are prone to interstitial/idiopathic pulmonary fibrosis (IPF)?

A

West Highland Terrier’s
Middle aged to older dogs

26
Q

What are the clinical signs of IPF?

A
  • Insidious (slow) onset
  • Chronic breathlessness which is slowly progressive
  • Coughing
  • Exercise intolerance
  • Owner may notice cyanosis
  • Crackles
  • Prolonged expiratory phase with expiratory effort.
27
Q

How is IPF diagnosed?

A

Clinical signs
- diffuse crackles, dyspnoea, coughing

Radiograph
- Unstructured interstitial lung pattern
- +/- right sided cardiomegaly
- +/- pulmonary hypertension

CT
- Diffuse increase in opacity
- Loss appearance of blood vessels

Bronchosocpy
- Rule out other inflammatory conditions

LUNG BIOPSY IS ONLY DEFINITIVE BUT RARELY USED

28
Q

What can be seen on an IPF radiograph?

A

Severe interstitial/alveolar
pattern
Generalised cardiomegaly
Right sided emphasis
Abdominal distension Hepatomegaly

29
Q

What is the success of IPF treatment dependent on?

A

Whether active inflammation is present.

There are two types:

  1. Large cellular inflammatory reaction with less fibrosis = easier to treat.
  2. Mixed inflammatory and fibrotic pattern -> fibrosis harder to treat
30
Q

How is IPD treated?

A

Symptomatic treatment
- Avoid collars (trauma), harness only, avoid smoke inhalation

Inhaled therapy
- Bronchodilator, corticosteroids

Oral therapy
- Bronchodilators - especially if concurrent airway collapse
- Corticosteroids

Antibiotic as necessary

Management of pulmonary hypertension

31
Q

What is the prognosis for IPF?

A

Guarded

Long term palliation of clinical signs is needed.

Median survival time = 15.5 months (reported up to 4 years)
- Depends on the extent of fibrosis on diagnosis

32
Q

Why are the clinical signs for A.vasorum so diverse?

A

Because all stages cause problems!

Adult antigens
- Cause Type III hypersensitivity (immune complex deposition) - Complement activation ▪
- Immune infiltrate in lungs and other tissues

▪ Egg deposition/L1
- Pulmonary inflammation/granuloma formation
- Pulmonary arteriolar vasoconstriction
- End arteritis and fibrosis of vessels

33
Q

What are the two main side effects of an A.varsorum infection?

A

Coagulopathies
- Anemia
- Haemorrhages
- Prolonged bleeding from wounds or after surgery
- Thrombocytopenia

Neurological dysfunction (migrate around CNS)
- Paresis, depression, spinal pain, behavioural changes, ataxia

34
Q

How is A.varsorum I diagnosed?

A

SNAP test

PCR (on BAL or pharynx swabs)

Faecal - intermittently shed so would need 3 consecutive negatives to rule out (more time consuming than SNAP or PCR)

35
Q

How is A.vasorum treated (licenses and unlicensed)?

A

Licensed:
- Imidacloprid and Moxidectin
- Milbemycin oxide and praziquantel

Unliscened
- Fenbendazole (most vets go to!)

Supportive treatment
- Bronchodilators
- Corticosteroids
- Phosphodiesterase inhibitors (for pulmonary hypertension)
- Cage rest
- Oxygen therapy

The thrombocytopenia often resolves once the worms have been treated.

Note: animals can get worse with treatment and may be need to be hospitalised.

36
Q

How can A.vasorum be prevented?

A
  • Regular worming (every 3 months with moxidectin and imidacloprid)
  • Reduce time dogs could be in contact with slugs and snails
37
Q

What are the clinical signs for animals with pulmonary thromboembolism

A

Acute onset dyspnoea
Few radiographic signs Hypercoagulable states (underlying problem -> trauma, sepsis, exogenous corticosteroids, IMHA)
Pulmonary hypertension

38
Q

What is the a ventilation perfusion missmatch?

A

For effective gas exchange to occur, alveoli must be ventilated and perfused. Ventilation (V) refers to the flow of air into and out of the alveoli, while perfusion (Q) refers to the flow of blood to alveolar capillaries.

V/Q mismatch can be caused by various factors, such as lung conditions like pulmonary embolism, asthma, COPD, and interstitial lung diseases

39
Q

What are some clinical sighs for physiological/metabilic causes of interstitial disease, and give some examples.

A

Open-mouthed/panting/shallow breathing

  • Hyperthermia/heat stroke/fever
  • Obesity
  • Excitement/fear/stress/pain/shock

Caused by:
- Parturition/false pregnancy/eclampsia
- Anaemia/abnormal haemoglobin
- Acidosis
- CNS disease
- Endocrine dz, e.g. HAC & steroid tx, hypert4
- Neuromuscular disease