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SAM > Diseases of the lung in dogs and cats > Flashcards

Diseases of the lung in dogs and cats Flashcards

1
Q

Diseases of the small airways

A
  • Canine chronic bronchitis
  • Bronchiectasis
  • Feline lower airway disease/feline asthma vs. chronic bronchitis
  • Airway foreign bodies
  • Bronchial neoplasia
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2
Q

Types of Bronchitis

A
  • different causes and anatommical localisations (tracheobronchitis, bronchitis, bronchopneumonia)
  • Infectious:
  • Canine infectious respiratory disease complex (CIRDC):
    • CDV, CaHV-1, CRCoV, CIV
    • Kennel cough: CAdV-2, CPIV, Bordetella br., Mycoplasma spp.
  • FHV in cats
  • Parasites
  • fungal
  • Non-infectious:
  • Aspiration
  • Canine chronic bronchitis
  • Feline asthma
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3
Q

Canine chronic bronchitis (CCB)

  • clinical signs and history
A

–> idiopathic form of bronchitis

  • Middle-aged to older dogs; small breeds > large breeds
  • Daily cough for more than 2 months (productive/non productive), exercise intolerance
  • doog condition/overweight, tracheal sensitivity, inspiratory crackles, expiratory wheezes
  • prolonged expiration and expiratory push (expiratory type dyspnea)
  • increased vagal tone –> sinus arrytmia
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4
Q

Canine chronic bronchitis (CCB)

  • Diagnosis
A
  • Blood examination: uslually negative
  • Radiography: we can recognize the alveolar pattern
  • doughnut sign
  • right-sided cariomegaly
  • cor pulmonale or negative
  • Bronchoscopy: we can recognize the inflammation, the sickened bronchial mucosa
  • Hyperemic mucosa
  • mucoid or purulent secretions
  • fibrous nodules on the mucosa
  • BAL, TTL: for microbiology and cytology
  • bacteria +/-
  • nondegenerate neutrophils
  • eosinophils
  • mucous
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5
Q

Differential diagnosis of CCB

A
  • Infection: kennel cough, parasites, fungi, D.immits
  • Aspiration: Accidental, pharyngeal dysphagia, esophageal disease, gastrooesophageal reflux, laryngeal dysfunction
  • Eosinophilic bronchopneumopathy
  • endocardosis (congestive heart failure)
  • pulmonary fibrosis
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6
Q

Treatment of CCB

A
  • Can be controlled but never cured. Goals: control inflammation, prevent worsening of airway disease

- Short acting glucocorticoids:

  • 0.5-1.0 mg/kg prednisolone BID, decreased by half every 5-10 days

- Bronchodilators:

  • Theophylline (GI, tachycardia, excitability)
  • terbutaline (1-2-4 mg/dog PO BID)
  • Albuterol (50ug/kg PO TID)

- Antitussives:

  • if inflammation has beed effectively treated!
  • otherwise mucos can trap in the bronchi and worsen clinical signs
  • Antibiotics: if BAL cytology and microbiology is postive
  • Ancillary therapy:
  • weight reduction,
  • harness instead of collar
  • cool, clean area (smoke, dust, heat)
  • nebulization
  • Inadequately treated: pulmonary hypertension, bronchiectasis, vasular remodelling
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7
Q

What is Bronchiectasis?

A
  • Irreversible dilatation of large airways (bronchi), with accumulation of pulmonary secretions.
  • common in Cocker spaniels
  • Histopathologic response due to long-standing inflammation/irritation (CCB, primary dyskinesia, foreign body, smoke, dust)
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8
Q

Bronchiectasis

  • history, symptoms and diagnosis
A
  • History:
  • chronic productive cough, frequent bouts of pneumonia (initially respond to antibiotics/relapse)
  • Symptoms:
  • loud bronchial sounds,
  • nasal discharge +/- (pneumonia),
  • hemoptysis
  • Diagnosis: Radiography, broncoscopy, CT
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9
Q

Bronchiectasis

  • Treatment
A
  • drugs can not cure the damaged bronchi, only prevent the problem with corect treatment of the underlying disease
  • Lobar bronchiectasis –> lobectomy, antibiotics (based on culture), bronchodilators
  • Cough suppresents must be avoided!
  • Limitation of therapy:
  • if the bronchiectasis affects several lung lobes then the only chance is repeated AB-therapy –> multiresistance
  • if only one lung lobe is affected, then surgical removal of he affected lung lobe can solve the problem
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10
Q

Bronchiectasis

  • Prognosis and prevention
A
  • Prognosis:
  • chronic recurrent infection
  • resistance to AB treatment
  • pulmonary hypertension, cor pulmonale
  • Prevention:
  • appropriate AB therapy in infectious disease
  • promp removal of foreign bodies
  • appropriate managment of CCB
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11
Q

Feline lower airway disease / feline bronchitis

asthma vs chronic bronchitis

  • history and symptoms
A
  • main key of feline asthma –> bronchoconstriction!
  • increased airway resistance (smooth muscle hypertrophy, bronchial wall edema, glandular hyperplasia) -> cough and respiratory distress
  • Symptoms:
  • paroxysmal-, dry- “hacking” cough, open mouth (loud) brething, prolonged exhalation. expiratory type dyspnea
  • auscultation: harsh lung sounds, crackles, expiratory wheezes or normal
  • percussion: increased resonance
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12
Q

Diagnostic evaluation of feline asthma

A
  • blood test: eosinophilia in 30%, negative heartworm antibody test
  • fecal examination: exclusion of Aelurostrongylus, paragonimus spp, capillaria infection
  • Radiopgraphy:
  • interstitial-, bronchial-, alveolar pattern or normal, hallmark: peribronchial cuffing
  • infiltrated medial lung lobe
  • pulmonary emphysema
  • Bronchoscopy:
  • BAL cytology: sthma eosinophilia vs. neutrophilia in chronic bronchitis, culture
  • Specific test for asthma:
  • whole body plethysmography (increased airway reactivity to nonspecific aerosol stimulant)
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13
Q

Diff diagnosis of feline asthma

A
  • infection:
  • pulmonary parasites, toxoplasmosis, D. immitis, mycoplasmosis, bacterial, fungal, viral infection)
  • Aspiration: accidental, esophageal disease -> reflux
  • idiopathic pulmonary fibrosis
  • neoplasia (carcinoma)
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14
Q

Treatment of feline asthma

A

-Acute therapy: emergency situation

  • cyanosis, open mouth breathing
  • oxygen cage; terbutaline, glucocorticoids + bronchodilatoros
  • chronic managment
  • glucocorticcosteroids
  • prednisolone
  • inhaled fluticasone
  • methyl-perdisolone acetate
  • bronchodilators (terbutaline)
  • anitbiotics
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15
Q

Prevention and prognosis of Feline asthma

A
  • Prevention:
  • Beta-blockers should be avoided! (propranolol, atenolol)
  • cigarette smoke, aerosol spray, upper respiratory viruses
  • Prognosis:
  • anti-inflammatories and bronchodilators alleviates acute clinical signs
  • recurrance of signs
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16
Q

Brochial neoplasia

  • clinical signs, diagnosis, treatment
A
  • Cough, obstructive breathing pattern (loud respirations), hemoptysis
  • Ausculatation: harsh wheezing noises
  • Radiography: soliter mass lesion
  • Treatment: same as pulmonary neoplasia
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17
Q

Pulmonary parenchymal diseases

A
  • Pneumonia
  • infectious diseases
  • aspiration pneumonia
  • eosinophil bronchopneumopathy
  • pulmonary edema
  • pulmonary contusions
  • smoke inhalation
  • ARDS
  • Pulmonary fibrosis
  • Lung lobe torsion
  • pulmonary thromboembolism
  • pulmonary neoplasia
18
Q

Pneumonia classification

A
  • Anatomy:
  • Bronchopneumonia: can be parenchyma and bronchi affected together. e.g in viral infections like Distemper
  • pneumonia
  • interstitial pneumonia: if only the interalveolar space in the level of alveoli is inflammed
  • Lobular or diffuse
  • Origin:
  • Infectious: bacterial, viral, fungal, parasitic
  • Non- infectious: aspiration, idiopathic
  • Duration:
  • acute, subacute, chronic
19
Q

Bacterial pneumonia

  • common complications and protection mechanisms
A
  • Common complications:
  • laryngeal dysfunction, viral pneumoni, aspiration, GI disease, encephalopathy
  • protection mechanism of lower airways:
  • laryngeal function, coughing reflex, mucociliary clearance, epithelial barrier, IgA, alveolar macrophages, IgG
20
Q

Bacterial pneumonia

  • symptoms
A
  • lethargy, fever, dyspnea, coughing (dog >> cat) acute/chronic, exercise intolerance, nasal discharge, hemoptysis and severe dyspnea
  • underlying disease (dysphagia, regurgitation, vomiting, muscular weakness)
  • increased lung sounds and crackles or wheezes + inflammatory fluid
21
Q

Bacterial pneumonia

  • diagnosis and treatment
A
  • Diagnostic evaluation:
  • hematology: WBC increased
  • Radiography:
    • focal or diffuse alveolar pattern (aspiration: cranioventral lung regions)
    • brochiectasis, megaesophagus, mass
  • TTL, Bronchoscopy:
    • BAL (culture, cytology), mass, foreign body, bronchooesophageal fistule, lobular pneumonia (aspiration)
  • Treatment:
  • AB, bronchodilator, lobectomy (focal pneumonia, abscess),
  • saline nebulization, underlying disease (foreign body, neopplasia, GI disease)
  • Organisms: E.coli, Bordetella, Klebsiella, Pasterurella, Pseudomonas, Mycoplasma spp.
22
Q

Viral bronchipneumonia

A
  • Distemper, Morbillivirus (paramyxoviridae family)
  • Exposure (inhalation, po infected secretions) –> replication in macrophages, tonsils –> viremia (2-4 daus: initial fever) –> several tissues (lung, bowel, skin, CNS) –> bronchopneumonia, enteritis, encephalitis
  • Mucopurulent oculonasal discharge, fever, PCR (blood, urine), lethargy, neurologic symptoms (50%), radiography (interstitial, alveolar pattern)
  • treatment: largely supportive (AB, bronchodilators, fluid), seizure control (diaxepam, KBr, phenobarbital), antobody
23
Q

Fungal pneumonia

A
  • Histoplasma capsulatum, Blastomyces dermatitidis, coccidioides immitis, cryptococcus neoformans, aspergillus fumigatus, pneumocystis carinii
  • Diagnosis:
  • BAL/fine needle aspiration of lung; cytology, microbiology, PCR; blood: serology
  • Therapy:
  • itraconazole
  • pneumocystis: trimethoprim + sulfamethoxazole
24
Q

Aspiration pneumonia

  • findings
A
  • aspiration of fluid, food, gastric contents results in pulmonary inflammation
  • megaesophagus
  • laryngeal and pharyngeal dysfunction
  • neuromuscular disease
  • anesthesia, encephalopathy
  • brachycephalic airway conformation
  • forced feeding (contrast radiography)
  • severity of lung injury:
  • volume, pH, toxicity –> obstruction, pulmonary hemorrhage, edema, inflammation, necrosis, bronchoconstriction, infection
25
Q

Aspiration pneumonia

  • clincal signs, diagnosis
A
  • clinical signs:
  • cough, tachypnea, acute onset of rspiratory distress, fever, lethargy, shock
  • cats: wheezes (bronchospasm)
  • diagnostic evaulation:
  • history of vomiting, regurgitation
  • radiography: quite different (interstitial/alveolar, focal/diffuse), but interstitio-alveolar pattern in cranioventral and middle lung lobes
  • megaesophagus
  • complete blood count: leukocytosis
  • bronchoscopy: BAL for culture, cytology
26
Q

Treatment of aspiration pneumonia

A
  • respiratory distress:
  • oxygen
  • fluid therapy (but increased capillary permeability can lead to oedema)
  • Bronchoscopy: removal of the content
  • Antibiotics:
  • culture or empirical; after fever/X-ray lesions + 2-3 weeks
  • Saline inhalation, coupage; +/- bronchodilators
  • corticosteroids: NOT allowed!!
  • prognisis: severity of lung injury/underlying cause
27
Q

Eosinophilic bronchopneumopathy

  • history, clinical signs
A
  • inflammatory disease, unknown etiology
  • hypersensitivity to an environmental or endogenous antigen
  • all breeds, huskies
  • history:
  • coughing, gagging, difficulty breathing, nasal discharge (mucopurulent or serous), ethargy and anorexia
  • physical examination:
  • nasal dicharge, crackles, increased lung sounds (or normal auscultation)
28
Q

Eosinophilic bronchopneumopathy

  • diagnosis and treatment
A
  • Radiography:
  • diffuse interstitial, alveolar, bronchial or combination
  • nodules or mass-like lesions (eosinophilic granulomatosis)
  • Blood test:
  • peripheral eosinophilia
  • Bronchoscopy:
  • green, green-yellow mucos, mucosal thickening
  • BAL, mucosal brushing (large number of eosinophils)
  • Diagnosis:
  • rule out other causes!
    • migrating parasites, bacterial or fungal infections, heartwor or neoplasia, allergy testing
  • Treatment:
  • glucocorticoids at immunosuppresove dosages lasting weeks to months; hyposensitization?
  • prognosis: generally good
29
Q

Pulmonary oedema

  • physiological processes
A
  • Fluid accumulation in the interstitium and alveoli
  1. vascular hydrostatic pressure increases: left-sided congestive hearth failure (CHF), excessive fluid administration (anuric renal failure)
  2. plasma oncotic pressure decreases: hypoalbuminemia
  3. vascular permability increases: vasculitis, ARDS
    • Protein rich fluid will enter the interstitium, and this protein will bind water. fureosemide will not be so effective in this case.
  4. impared lymphatic drainage: left-sided CHF, neoplastic process
  5. decreased transpulmonary pressure: upper airway obstruction
  • Noncardiogenic oedema: ARDS, acute upper airway obstruction, neurogenic oedema (seizures, head trauma)
  • Cardiogenic pulmonary oedema: CHF
30
Q

Pulmonary oedema

  • symptoms, diagnosis and treatment
A
  • Symptoms
  • restricted type dyspnea. It is superficial, rapid respiration without coughing.
  • panting + cyanosis
  • Coughing: in severe cases bloody expectoration of blood-tinged fluid
  • Auscultation:
  • Lung: crackles hear on inspiration and end-expiration (in dorso-caudal lung fields). In severe edeme quiet lung sounds in cats!
  • Heart: murmur +/- (but mitral endocardiosis, cardiomyopathy), arrhytmia, tachycardia
    • Heart murur without sinus tachycardia: pulmonary disease > cardiogenic edema
  • Radiography:
  • Cardiogenic edema: interstitial pattern in the hilar and caudo-dorsal lung regions, cardiomegaly, pulmonary veous enlargement
  • Noncardiogenic: absence of cardiac and pulmonary venous changes
  • Treatment:
  • Furosemide (2-4 mg/kg IV every 4-12 hr)
  • oxygen therapy (intubation, positive pressure ventilation)
  • sedatives: acepromazine in dog and cat. Morphine sulfate in dog
  • prognosis: variable
  • severity of edema, treatment and underlying disease
31
Q

Smoke inhalation

  • history and etiology
A
  • direct injury: heat, particulate matter, toxic gases
  • etiology:
  • acute phase (0-36 hr) tissue injury –> capillary permability increases –> oedema, tissue hypoxia
    • shock, pain
    • CO gas inhibits oxygen binding to Hb –> tissue hypoxia
  • Later phase (2-4 days): edema decrease, mucosal secretion increase, decreased mucociliary clearance, secondary bacterial colonization –> tracheobronchtis, pneumonia
32
Q

Smoke inhalation

  • clinica signs, diagnosis
A
  • Clinical signs:
  • skin injury, smell of smoke, loss of consciousness, upper airway stridor (laryngeal edema), ocular and nasal discharge, cyanosis
  • some patients have minima signs but 24-36 hr later then can occur! (ARDS, infection, laryngeal edema).
  • Diagnostic evaluation:
  • history, clinical signs, radiography (oedema, pneumonia), BAL, culture
  • Carboxyhemoglobin is not distinguished from oxyhemoglobi with blood gas analysis or pulse oxymetry!
33
Q

Smoke inhalation

  • treatment
A
  • observation for at least 24-48hr
  • tracheostomy: severe laryngeal oedema, obstruction
  • oxygen cage: half-life of CO in room air is 4hr, in 100% O2 30 min
  • bronchodilators, antibiotics (culture)
  • fluid therapy (but edema!)
  • analgesic
  • Corticosteroids: laryngeal edema/acute cardiovascular shock!
  • prognosis: wrong if severe respiratory distress, infectious pneumonia, neurological signs and cutaneous burns
34
Q

ARDS

  • history, pathogenesis
A

= Acute Respiratory Distress Syndrome

  • acute hypoxemic respiratory failure caused by lung injury and pulmonary capillary permeability increase
  • Sepcial form of pulmonary edema caused by damaged capillary network, caued by cytochrome storm
  • the cytochrome storm will increase capillary permability. protein rich fluid can enter the pulmonary interstitium, leading to intersitial pattern o X-ray and interstitial hypoxia
  • Secondary to: sepsis, pancreatitis, aspiration, shock, microbal pneumonia, SIRS, babesiosis
  • Pathogenesis: pporly understood
  • early phase: proteinaceous fluid (capillary perm increase)
  • Later: inflammtory cells increase, hyaline membrane formation, fibrosis –> pulmonary hypertension
  • irreversible
35
Q

ARDS

  • clinical signs, diagnosis, treatment
A
  • Clinical signs:
  • extreme anxiety, tachycardia, cyanosis, crackles (end-inspiration, expiration), wheezes, underlying disease
  • Diagnosis:
  • noncardiogenic lung oedema: auscultation, radiography, echocardiography
  • protein (edema)/protein(plasma): 80-90%, in cardiogenic edema 50%
  • Treatment:
  • oxygen therapy (intubation, PEEP)
  • fluid therapy (low-normal circulatory volume)
  • furosemide (early phase)
  • glucocorticoids?
  • blood gas analysis (control)
  • prognosis: generally poor
36
Q

Pulmonary fibrosis

A
  • Idiopathic interstitial lung disease (pneumonia): WHW, staffordshire bill terriers, (cats)
  • pathologically: alveolar septic fibrosis, interstitial fibrosis, epithelial hyperplasia, focal calcification
  • dyspnea, exercise intolerance, cough +/-, cyanosis, crackles
    • Ca: chronic and progressive pulmonary signs
    • Fe: rare, faster course of the disease. Acute!
  • radiography: diffuse interstitial pattern
  • echocardiography: moderate to severe pulmonary hypertension
  • biopsy, poor prognosis: die of hypoxaemia
  • dog: 1-3 years
  • cat: few weeks
  • there is no effective treatment!
  • cough suppressants, PHT: syldenafil, glucocorticoids?, bronchodilators?
37
Q

Lung lobe torsion

A
  • Large, deep-chested dogs (greyhounds)
  • idiopathic, pleural effusion, surgery, trauma= acute disease
  • lung lobe torsion –> venous congestion –> exudation (bloody pleural effusion), necrosis, anemia
  • clinical signs:
  • respiratory distress, tachypnea, cough, hypotension, dyspnea, fever, lethargy
  • diagnosis:
  • deep chested dogs, pleural effusion,
  • radiography: rounding of the lung lobe edges
  • bronschospy, CT
  • surgical exploration
  • treatment:
  • removal of pleural flud, oxygen, fluid/shock therapy, surgery
38
Q

Pulmonary thromboembolism (PTE)

A
  • secondary to:
  • heartworm disease, IMHA, neoplasia, DIC, hyperadrenocorticism, PLE, PL-nephropathy etc.
  • PTE: abnormal gas exchange, pulmonary infarction
  • Clinical signs:
  • middle-aged to older, acute respiratory distress, tachypnea, cyanosis
  • acute, lethat disease
  • Diagnosis:
  • difficult to diagnose
  • D-dimer, antitrombin III, blood gas, radiography, echocardiography (logated in the pulmonary artery)
  • pulmonary agniogram is the gold standard
  • treatment:
  • Thrombolytic therapy (surgical, catheter, drugs: tissue plasminogen activator etc.)
    • underlying disease
39
Q

Pulmonary edema

  • clinical sigs, diagnois
A
  • Metastatic > primary (carcinoma, osteosarcoma)
  • chronic cough, exercise intolerance, respiratory distress, dyspnea, weight loss, anorexia
  • physcal examination:
  • origin of metastasis: abdominal mass, effusion, lameness
  • auscultation, percussion
  • radiography:
  • is the key tool in the diagnostic approach!
  • LL x2, VD/DV
  • false negative: size, obscured by the heart or liver; periosteal proliferation (hypertrophic osteopathy)
  • false positive: eosinophlic bronchopneumopaty
  • CT: more sensitive to tumors
  • Definitive diagnosis: biopsy ,(thoracoscopy) or FNA
  • Treatment:
  • primary pulmonary neoplasia: lobectomy
40
Q
A

SAM (6 decks)

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