242 Diseases of the Pulmonary Parenchyma Flashcards
1
Q
What is commonly associated with inspiratory, expiratory, or mixed effort?
A
- resp distress caused by pulmonary parenchymal disease results in mixed inspiratory and expiratory effort
- predominantly inspiratory effort observed with upper airway obstruction or pleural space disease
- expiratory effort observed in lower airway/bronchial disorders
2
Q
What are common physical exam findings of animals with pulmonary disease?
A
- unremarkable, or marked systemic or thoracic disease
- weight loss, fever, lymphadenomegaly, and distal limb swelling from hypertrophic osteopathy
- RR & effort, cyanosis, increased or decreased bronchovesicular lung sound, +/- adventitial sounds on auscultation are suggestvie of airway, thoracic space, or pulmonary disease.
3
Q
What are the benefits and drawbacks of evaluating oxygenation?
A
- useful for evaluating animals with suspected pulmonary parenchymal disease, but nonparenchymal disease can cause hypoxemia.
- cyanosis confirms hypoxemia, but is insensitive, subjective, and not useful in anemic animals.
- better tests of oxygenation include pulse oximetry and arterial blood gas analysis.
- blood gas analysis is useful for making decisions on supplemental oxygen or mechanical ventilation and to monitor response to therapy
- also calculating PaCO2 and alveolar-arterial gradients is used to determine mechanisms for hypoxemia.
4
Q
What are the mechanisms of hypoxemia?
A
- hypoventilation
- ventilation: perfusion (V:Q) mismatch
- Right-to-left shunting (intrapulmonary or cardiac)
- Diffusion impairment
- reduced inspired oxygen partial pressure
5
Q
What are examples of hypoventilation? how can it be recognised on blood gases?
A
- Drug induced respiratory depression
- CNS or peripheral nerve disorders
- Upper airway obstruction
Recognised:
- Increased PaCO2
- Normal (A-a) gradient
- Absent radiographic pulmonary infiltrates
6
Q
What are examples of Ventilation:perfusion (V:Q) mismatch? how can it be recognised on blood gases?
A
- bacterial pneumonia
- pulmonary oedema
- pulmonary thromboembolism
Recognised:
- increased A-a gradient
- mildly increased PaCO2
- Improves with O2 supplementation (not TEM)
- pulmonary radiographic changes variable but common
7
Q
What are examples of ‘Right - to -left shunting (intrapulmonary or cardiac)’? how can it be recognised on blood gases?
A
- right-to-left patent ductus arteriosus (cardiac)
- Pulmonary arteriovenous fistulae with marked pulmonary hypertension
- Atelectatic lung (pulmonary)
- Pulmonary thromboembolism
Recognised:
- increased (A-a) gradient
- fails to improve with O2 supplementation
- cardiac or pulmonary radiographic changes common
8
Q
What are examples of ‘Diffusion impairment’? how can it be recognised on blood gases?
A
- asbestos
- idiopathic pulmonary fibrosis
Recognised:
- marked interstitial radiographic infiltrates common
- improves with O2 supplementation
9
Q
What are examples of ‘reduced inspired O2 partial pressure’? How can it be recognised on blood gases?
A
- high altitude
- Anaesthetic accident
- suffocation
Recognised:
- resolves with O2 supplementation
10
Q
What are the implications of the following on CBC in pets with pulmonary disease?
- neutrophilia
- neutropenia
- Eosinophilia
- monocytosis
- thrombocytopenia
- Erythrocytosis
A
- neutrophilia = infectious pneumonia and inflammatory lung disease, including ARDS
- neutropenia = sepsis, ARDS
- Eosinophilia = hypersensitivity disorders, eosinophilic pneumonia, or parasitic disease
- Monocytosis = consider mycotic lung disease, histiocytic disease
- Thrombocytopenia= consider sepsis, pulmonary thromboembolism, vasculitis, pulmonry hemorrhage
- Erythrocytosis: chronic hypoxemia
11
Q
What are the implications of the following on biochem in pets with pulmonary disease?
- hypoalbuminemia
- hypercholesterolemia
- hyperglobulinemia
- hypercalcemia
- increased ALT
A
- hypoalbuminemia = pulmonary thromboembolism resulting from PLN/PLE, systemic inflamm, and infectious disease with pulmonary manifestation
- hypercholesterolemia= pulmonary thromboembolism resulting from PLN
- hyperglobulinemia = infectious and inflamm disease
- hypercalcemia = neoplasia and granulomatous fungal disease
- increased ALT = supports hypoxemia
12
Q
What are the implications of the following on urinalysis in pets with pulmonary disease?
- proteinuria
- bacteruria
A
proteinuria = pulmonary thromboembolism resulting from PLN, systemic inflamm disease
Bacteruria = consider sepsis
13
Q
What are the differential diagnosis associated with alveolar infiltrate?
A
- pneumonia
- oedema (cardiogenic or noncardiogenic)
- hemorrhage/contusion
- primary lung neoplasia
- metastatic neoplasia
- atelectasis
- pulmonary thromboembolism
- drowning
- smoke inhalation
14
Q
What are the differential diagnosis associated with Bronchiolar infiltrate?
A
- feline asthma
- chronic bronchitis
- eosinophilic bronchitis
- peribronchiolar cuffing (e.g. oedemma, inflammation)
- bronchial calcification
15
Q
What are the differential diagnosis associated with interstitial patterns?
A
- Aging change (U)
- Pulmonary fibrosis (U)
- Lymphoma (U)
- Primary lung neoplasia (S>U)
- Pulmonary metastasis (S>U)
- Fungal pneumonia/granuloma (S>U)
- Eosinophilic pneumonia (S>U)
- Foreign body reaction (S>U)
- Hematoma (E)
- Abscess (S)
- Cyst (S)
e= either S= structured U = unstructured
16
Q
What are the differential diagnosis associated with vascular patterns?
A
- Heartworm
- Thromboembolic disease
- Pulmonary hypertension
- Congestive heart failure
17
Q
What are the pulmonary parasites? How are they treated?
A
- lungworm
- Ancylostoma (hookworms) & Toxocara (roundworms) undergo pulmonary migration before adult worm reaches intestine. Only cause verminous pneumonia if massive larval migration. Pyrantel pamoate 5mg/kg PO administered at least twice, 2 weeks apart. Glucocorticoid can amerliorate severe cough but not before ruling other causes of infectious pneumonia
- Lungworms reside primarily in pulmonary parenchyma in airways or both. Fenbendazole (50mg/kg PO q 24h for 10-14 d) or ivermectin. Use in caution with collies and othe rbreeds with MDR-1 (ABCB1).
18
Q
What are the differentials for parasitic lung disease?
A
- bronchopneumonia, eosinophilic pneumonia, asthma, pulmonary granulomatosis, or pulmonary neoplasia.
- intermittent faecal shedding of parasite ova or larvae after expectoration means that faecal exam is an insensitive diagnostic method
19
Q
What are the two pulmonary parenchymal parasites?
A
- Paragonimus kellicotti is in US, and spreads after pets eat crayfish, and migrates through intestine, into peritoneum, across the diaphragm, and into pleural space. Fenbendazole, praziquantel (25mg/kg PO q8h for 3 days) used for treatment
- Filaroides spp. uncommon pulmonary parasites
20
Q
What are the airway parasites
A
- Aelurostrongylus asbtrusus
- Crenosoma vulpis
- oslerus Osleri
- Eucoleus aerophilus
- troclostronylus spp.
21
Q
What is different about the dirofilaria ‘host-parasite interaction’ between in dogs and cats ?
A
Dogs:
- natural host
- mostly mature worms for 5-7 yrs
- mature infection accompanied by microfilaremia
- prevalence varies with geographic region.
Cats:
- atypical host
- parasite burden 1-3 worms
- mature worms 2-3 yrs
- mature infection rarely accompanied by microfilaremia
- larval forms eliminated by immune response
- prevalence mature infection = 10% dogs in geographic region
22
Q
What is different about the dirofilaria ‘diagnosis’ between in dogs and cats ?
A
Dogs:
- Diagnosis of mature infection straightforward: knott test, filtration test, Ag ELISA
- heat treatment increases Se Ag test
- Thoracic rads are suggestive when pulmonary artery segments, arterial torrtuosity and pruning, and sometimes right ventricular enlargement.
- Echocardiography - right sided cardiomegaly
Cats:
- Difficult to diagnose infection as microfilaria not often present
- Se ELISA Ag is low due to low worm burden, absent antigenically detectable female worms or immature worms
- Heat treatment will increase Ag sensitivity
- Feline specific HW Ab tests are moderately sensitive and confirm infection is mature or active
- Rad changes inconsistent, but caudal lobar arterial enlargement and parenchymal changes identified.
- Echo detect mature infection but Se & Sp are operator dependent.
23
Q
What is the difference in the clinical signs between in dogs and cats infected with dirofilaria?
A
Dogs:
- well for a while
- CS= cough & exercise intolerance
- RSCHF
- HW caval syndrome -> tricuspid regurgitant murmur, hemolysis with hemoglobinuria, RSCHF, DIC
- Ag-Ab complex deposition causing glomerulonephritis
- Aberrant migration -> eyes, brain, spinal cord, skin, liver
Cat:
- well during infection
- CS resemble asthma
- mature worm burdens can cause GI signs, hypersalivation and V+ or respiratory signs including cough or tachypnea
- sudden death or present with acute dyspnea +/- CNS signs
- RSCHF is rare
- Rare to have organ migration
24
Q
What is different about the dirofilaria ‘diagnosis’ between in dogs and cats ?
A
Dogs:
- Diagnosis of mature infection straightforward: knott test, filtration test, Ag ELISA
- heat treatment increases Se Ag test
- Thoracic rads are suggestive when pulmonary artery segments, arterial torrtuosity and pruning, and sometimes right ventricular enlargement.
- Echocardiography - right sided cardiomegaly
Cats:
- Difficult to diagnose infection as microfilaria not often present
- Se ELISA Ag is low due to low worm burden, absent antigenically detectable female worms or immature worms
- Heat treatment will increase Ag sensitivity
- Feline specific HW Ab tests are moderately sensitive and confirm infection is mature or active
- Rad changes inconsistent, but caudal lobar arterial enlargement and parenchymal changes identified.
25
What is the difference in the clinical signs between in dogs and cats infected with dirofilaria?
Dogs:
- well for a while
- CS= cough & exercise intolerance
- RSCHF
- HW caval syndrome -> tricuspid regurgitant murmur, hemolysis with hemoglobinuria, RSCHF, DIC
- Ag-Ab complex deposition causing glomerulonephritis
- Aberrant migration -> eyes, brain, spinal cord, skin, liver
Cat:
- well during infection
- CS resemble asthma
- mature worm burdens can cause GI signs, hypersalivation and V+ or respiratory signs including cough or tachypnea
- sudden death or present with acute dyspnea +/- CNS signs
- RSCHF is rare
- Rare to have organ migration
26
What is the lifecycle of Angiostrongylus vasorum (french heartworm)?
- indirect lifecycle. L1 is shed in faeces of definitive host and mature into infective L3 stage in snails and slugs. Canids are infected by ingestion-> L3 larva penetrate gut wall and travel to mesenteric lymph nodes where they develop into L5 larva. L5 larva travels to R. ventricle and pulmonary arteries via hepatic veins, portal veins, caudal VC , and mesenteric lymphatics. Adults live and mate in pulmonary artery and right ventricle.
- L1 offspring penetrate bronchial and alveolar walls and are coughed up and ingested then passed in the faeces.
27
What is the difference in the treatment in dogs and cats infected with dirofilaria?
Dogs:
- adulticide treatment should be preceded by identifying comorbid conitions and severity of disease & doxycycline treatment to eradicate Wolbachia
- melarsomine is only approved adulticide
- caval syndroma managed with physical removal of worms
Cats:
- Adulticide is not recommended due to toxicity, lack of efficact, and fatalities due to thromboembolism
- chemoprophylaxis is done when adult infection identified
- bronchopulmonary disease benefit from corticosteroid therapy
- bronchodilator and oxygen may be useful in cats with resp distress
- surgical removal of mature worms
28
What is the lifecycle of Angiostrongylus vasorum (french heartworm)?
- indirect lifecycle. L1 is shed in faeces of definitive host and mature into infective L3 stage in snails and slugs. Canids are infected by ingestion-> L3 larva penetrate gut wall and travel to mesenteric lymph nodes where they develop into L5 larva. L5 larva travels to R. ventricle and pulmonary arteries via hepatic veins, portal veins, caudal VC , and mesenteric lymphatics. Adults live and mate in pulmonary artery and right ventricle.
L1 offspring penetrate bronchial and alveolar walls and are coughed up and ingested then passed in the faeces.
29
What are the clinical signs of angiostrongylus vasorum?
CS range:
- resp disease related to inflamm response to the parasite and syndrome of bleeding diathesis
- the cause of bleeding is not understood, but related to consumptive coagulopathy
- Neurologic signs occur if CNS hemorrhage
- Pulmonary hypertension with cor pulmonale and syncope, and spontaneous pneumothorax.
-
30
What is the cause of bacterial pneumonia?
- bacteria inhaled or aspirated into lung, through pleural space or intrathoracic structures, or through lung hematogenosly.
- Most bacteria are secondary pathogens and cause disease opportunistically (immune suppression, aspiration).
- mixed flora, and obligate anaerobes:
E. coli, klebsiella, pasteurella, coagulase-positive staphylococci, streptococci, myoplasma, and BB.
31
What is the medication of choice for A. vasorum?
- fenbendazole 25-50 mg/kg PO q 24h for 10-20 days
- Prophylaxis: spinosad and milbemycin oxime
- post treatment reactions include dyspnea, ascites, and sudden death
32
What is the cause of bacterial pneumonia?
- bacteria inhaled or aspirated into lung, through pleural space or intrathoracic structures, or through lung hematogenosly.
- Most bacteria are secondary pathogens and cause disease opportunistically (immune suppression, aspiration).
- mixed flora, and obligate anaerobes:
E. coli, klebsiella, pasteurella, coagulase-postive staphylococci, streptococci, myoplasma, and BB.
33
What are the diagnostic tests for suspected bacterial pneumonia?
- T-Rads: alveolar pulmonary pattern with ventral distribution. Sometimes only single lung lobe involved (e.g. FB or aspiration). Dorsocaudal involvement may predominate after hematogenous bacterial exposure, and all lung fields in cases of severe pneumonia. Occasionaly abscessation, pleural effusion, or pneumothorax identified.
CBC: neutrophilia +/- left shift, lymphopenia, and mild anemia are inconcsistent and common findings
Arterial blood gas or pulse oximetry measurement: hypoxemia
- lavage airways (transtracheal or transoral) wash can be safe and inexpensive
- BAL can be used for obtaining samples for cytology and culture
- If severe bacterial pneumonia, FB, aspiration, or when pulmonary consolidation is present, anaerobic culture should be requested in addition to routine aerobic culture
- Mycoplasma PCR might be considered as well.
- Noninfectious respiratory disease can be associated with secondary bacterial infection
34
Lit the factors that predispose development of bacterial pneumonia....
- Debilitation
- Prolonged recumbency
- Systemic immunosuppression: drug-related (C-roids, chemo), inection (FeLV, FIV), Endocrine disorders (HyperA, DM),
- Immunodeficiency stages: age, congenial immunodeficiency (e.g. breed related syndromes, severe combined immunodeficiency disease, phagocytic defects)
- Defective resp defences: Primary ciliary dyskinesia, IgA deficiency
- Damage resp epithelium: smoke inhalation, drowing, infection, neoplasia, ARDS
- Aspiration
- Pleural/mediastinal/airway infection
- Penetrating thoracic injury
- Airway obstruction (functional or structural)
- Bronchiectasis
- Sepsis/bacteremia
35
What are the diagnostic tests for suspected bacterial pneumonia?
- T-Rads: alveolar pulmonary pattern with ventral distribution. Sometimes only single lung lobe involved (e.g. FB or aspiration). Dorsocaudal involvement may predominate after hematogenous bacterial exposure, and all lung fields in cases of severe pneumonia.
CBC: neutrophilia +/- left shift, lymphopenia, and mild anemia are inconcsistent and common findings
Arterial blood gas or pulse oximetry measurement: hypoxemia
-
36
What is the treatment of mild, moderate, and severe bacterial pneumonia?
Mild, stable disease:
Amoxi/clav, FLuoroquinolone, OR TMS
Moderate:
- Monotherapy: Amoxyclav OR TMS
- Combination: beta-lactam AND fluoroquinolone OR Clindamycin AND Fluoroquinolone
Severe unstable:
- Monotherapy: meropenem OR imipenem-cilastatin OR ticarcillin
- Combination: betalactam (ampicillin, amoxy/clav, second or 3rd gen cephalosporin) OR clindamycin AND EITHER Fluoroquinolone (enroflox, marboflox, orbiflox) OR aminoglycoside (e.g. amikacin, gentamicin)
37
When is oxygen therapy indicated with bacterial penumonia?
if PaOx <80mmHg or SpO2 <94% then O2 supplementation should be provided. Placement of intranasal cannula and humidifed oxygen. If persistently hypoxemic, or marked resp effort then mechanical ventilation is required.
38
When are brondhodilators used? What is the problem with using mucolytics?
- bronchodilators are not routinely used. Inhaled albuterol or oral methylxanthine bronchodilator (e.g. theophylline) are considered in animals that remain hypoxic, despite supplemental O2, if there is concurrent bronchoconstriction (especially in cats), or prior to administration of inhalant drug therapy.
- mucolytic N-acetylcysteine (NAC) reduced viscosity by breaking mucin disulfide bonds, but unfortunately nebulisation of NAC causes bronchoconstriction.
- Oral NAC at 125mg -600mg PO q8-12h is good.
39
What is a nebuliser?
| what can nebulisers be used for? What medications can be given via nebulisation?
- nebulisers create small particles 0.5-3 um) that penetrate deeply into resp tract.
- used for resp infections
- simple saline nebulisation improve mucus fluidity and function of the mucociliary escalator
- deliver antimicrobials, bronchodilators, glucocorticoids, or mucolytic agents.
- aminoglycosides are often used instead.
- gentamicin 6-8 mg/kg qs 5-10 mL in saline, via nebulisation for animals with susceptible airway pathogens once daily as adjunct to systemic antimicrobial administration
- bronchodilators and glucocorticods for inhalational are readily available for reasonable price
- nebulisation of mucolytic agents causes bronchoconstriction so is not advocated.
40
What is the problem of using bronchoilators
- bronchodilators are not routinely used. Inhaled albuterol or oral methylxanthine bronchodilator (e.g. theophylline) are considered in animals that remain hypoxic, despite supplemental O2, if there is concurrent bronchoconstriction (especially in cats), or prior to administration of inhalant drug therapy.
- mucolytic N-acetylcysteine (NAC) reduced viscosity by breaking mucin disulfide bonds, but unfortunately nebulisation of NAC causes bronchoconstriction.
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