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INTERNAL DECK 1 Flashcards

1
Q

Diseases of the nasal cavity and pharynx in dogs and cats overview?

A
  • Viral Rhinitis: Feline Herpesvirus, Calicicvirus, Canine Distemper.
  • Bacterial Rhinitis: Bordetella Bronchiseptica mainly
  • Mycotic Rhinitis: Aspergillosis, Cryptococcus
  • Foreign Bodies
  • Tumours
  • Diseases of the Pharynx: Retropharyngeal abscess, Nasopharyngeal stenosis.
  • Soft Palate abnormalities: elongated soft palate..
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2
Q

History and Clinical signs of nasal cavity?

A

History of: discharge, sneezing, bleeding, pain, stridor, reverse sneezing.
–>Systemic disease: discharge (distemper, viral rhinotracheitis) epistaxis (bleeding disorder).

Physical examination: shape, nasal stridor, closing of mouth, uni-/bilateral discharge, mouth/teeth inspection, depigmentation.

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3
Q

Diagnostic Procedures of the nasal cavity?

A
  • Radiograph: sedation required, limited value. Localizing sites for Biopsy within the nasal cavity and differential diagnosis. Nasal radiographs are evaluated for increased fluid density, loss of turbinates, lysis of facial bones.
  • Rhinoscopy: general anesthesia required, tracheal intubation, sphinx-like posture, visualization and biopsy. Visualize and remove foreign bodies.
  • CT, MRI
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4
Q

FHV-1 and FCV?

A
  • Feline Herpesvirus and Calicivirus.
  • Clinical signs: paroxysmal sneezing, serous ocular and nasal discharge..
  • FHV: can also cause severe conjunctivitis and corneal ulceration, abortion. Can cause Chronic sneezing with irreversible damage to mucosa and turbinates.
  • FCV: can have mild ocular signs, oral ulcers and gingivitis, lameness.
  • Chronic carriers: no signs of sneezing, mild nasal discharge, gingival ulceration
  • Clinical signs: uni-/bilateral mucopurulent nasal discharge, +/- chronic
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5
Q

Bacterial Rhinitis?

A
  • Usually secondary to viral infections, foreign bodies or tumors (disruption of mucosal integrity).
  • Bacterial Rhinitis caused by Bordetella bronchiseptica occurs occassionally in cats and rarely in dogs.
  • Bacteria: Pasteurella, Streptococcus, Staphylococcus, Mycoplasma, Bordetella, Chlamydia.
  • Chlamydophila felis (cats) -> prim. Resp. tract. Inf.
  • Mycoplasma, Chlamydophila -> conjunctivitis
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6
Q

Mycotic Rhinitis?

A
  • More common in dogs
  • Aspergillus spp. > Cryptococcus

.

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7
Q

Mycotic Rhinitis( Aspergillus spp.)?

A

ASPERGILLOSIS (A. FUMIGATUS)
–>canine disease in young dogs with long nose. Fungal plates/mats that invade the mucosal cavity.
Animal with it may have another nasal condition such as neoplasia, prior trauma, immune deficient.
–>Sensitive to palpation and depigmentation or ulceration of external nares.
Systemic can’t occur from Fumigatus usually caused by Asperillus terreus especially in german sheperds.

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8
Q

CRYPTOCOCCUS (C. NEOFORMANS)?

A

Typically a feline disease.
C. var gatti → neurological signs. Usually infects the nasal cavity and CNS in cats and mainly just CNS in dogs. Lungs are infected in both species.
- Clinical signs: nasal discharge, depigmentation, pain, epistaxis
- Diagnosis:
–>Rhinoscopy: see scoping (fungal plaques), bone resorption, conchae atrophy
–>Serology (fungal antibody titres), biopsy, cytology, culture
- Treatment:
Topical → Enilconazole
Systemic → Ketoconazole, Itraconazole,

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9
Q

Polyps?

A

Benign Growths that occur most often in kittens and young adult cats.
They can extend into the external ear canal, middle ear, pharynx and nasal cavity.
Grossly they are pink, polypoid growths arising from a stalk. Mistaken for neoplasia.
More common in cats.
Canine Nasal Polyps are rare, can result in chronic nasal discharge. Locally destructive to turbinates.

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10
Q

Pharynx Diagnosis?

A
  • Pharyngoscopy if upper respiratory obstruction is indicated, video fluoroscopy, retrograde rhinoscopy, CT (middle ear), US.
  • Fluoroscopy allows you to view inside of the body while it’s in motion.
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11
Q

Diseases of the Pharynx?

A
  1. Retropharyngeal abscess / nasopharyngeal polyps
    - Due to: Migrating foreign body
    - Clinical signs: salivation, fever, dysphagia, painful neck, increase WBC, diagnosis difficult
  2. Nasopharyngeal stenosis
    - Young cats, but rare
    - Clinical signs: open-mouth breathing
    - Diagnsosis and treatment: endoscopy, surgery, balloon dilation
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12
Q

Soft Palate abnormailites?

A
  1. Elongated soft palate
    - Brachycephalic dogs
    - Clinical signs: stertorous breathing, exercise intolerance, collapse, gagging
  2. Cleft palate
    - Neonate patients
    - Causes milk in the nares and aspiration (→ pneumonia) fix with surgery
  3. Soft palate hypoplasia
    - Brachycephalic dogs
    - Clinical signs: chronic rhinitis, gagging, reverse sneezing
    - Prolonged upper airway obstruction resulting in an increased inspiratory effort.
    - Concurrent GI signs are common in Brachycephalic dogs.
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13
Q

Tracheal Diseases History and Physical Examination?

A
  • Common Diseases are Canine Infectious Tracheobronchitis, Canine Chronic Bronchitis, Feline Bronchitis, collapsing trachea and allergic bronchitis.
    Coughing, noisy inspiratory sounds, wheezing expiratory sounds, “goose honk” cough
  • Neck palpation: emphysema, collapse, mass (thyroid gl., hematoma, abscess) → can elicit cough
  • Auscultation: over the larynx, trachea, lungs (sounds usually most intense near origin site)
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14
Q

NON-INFECTIOUS TRACHEITIS:

A

Causes: prolonged barking, tracheal collapse, chronic cardiac disease, allergic lower airway disease
Tests: firm palpation of thoracic inlet → typical tracheal cough; tonsils; +/- cardiac murmur,
+/- lung sounds.

Treatment:
  • Antitussives → codeine, butorphanol, dextromethorphan
  • Broncho-dilating drugs: theophylline/aminophylline,terbutalin.
  • Anti-inflammatory (gcc) → Prednisone
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15
Q

INFECTIOUS TRACHEOBRONCHITIS?

A
  • Canine Infectious Tracheobronchititis, Canine Infectious respiratory disease complex (CIRDC) or Kennel cough is a highly contagious acute disease.
  • Canine Influenza most often causes tracheobronchitis and rhinitis.
  • Causes: Kennel cough complex (CAV-2, CPI, Bordetella bronchoseptica), distemper, others (reo,CVH, mycopl.)
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16
Q

Infectious Tracheobronchitis Clinical signs?

A

Clinical signs: Acute onset of dry, hacking, paroxysmal cough, often followed by retching and gagging, often productive.
Cough can be provoked/stimulated by pinching the trachea.

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17
Q

Tracheal Collapse?

A
  • An open lumen maintained during all phases of respiration by the cartilaginous rings which are connected by fibro-elestic annular ligaments to maintain flexibility. Cartilaginous rings are incomplete dorsally, Dorsal tracheal membrane along with the tracheal muscle completes the rings.
  • The Tracheal collapse refer’s to the narrowing of the lumen resulting from weakened cartilaginous rings , redundancy of the dorsal tracheal membrane or both.
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18
Q

Tracheal Collapse Clinical Signs?

A

–> “goose-honk” cough
–> Cough elicited by palpation, eating, drinking, excitement
+/- cyanosis
- Inspiratory noises heard by auscultation
- Tracheobronchomalacia can be primary or secondary and can affect the trachea or bronchi.
- Collapse may occur extrathoracic/cervical OR intrathoracic/bronchial. Dogs with extrathoracic present signs with upper airway obstruction.
- More pronounced respiratory distress pronounced on inspiration for extrathoracic and more pronounced on expiration for intrathoracic( loud wheezing cough).
Tracheal collapse is rare in cats.

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19
Q

Tracheal Dysplasia?

A
  • ->Affects: congenital problem in young dogs.
  • ->Bulldogs, Boston Terriers
  • ->Clinical signs: Dyspnea, productive coughing, fever if bronchopneumonia.
  • ->Diagnostic tests: Auscultation, sensitive trachea, radiography (trachea, thoracic inlet), leukocytosis
  • ->OBS! Tracheal edema in tracheitis may mimic hypoplasia on the radiographs → x-ray in asymptomatic patients.
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20
Q

Tracheal Parasites?

A
  • Caused by: Oslerus Osleri (Filaroides Osleri) = lungworm
  • Clinical signs: chronic dyspnea, dry cough, inspiratory wheezing sounds. Indistinguishable from Canine Infectious Tracheobronchitis
  • The hosts of lung parasites generally cough up an swallow the eggs or larvae.
  • Adults worms live at the carina and mainstem bronchi and cause a local, nodular inflammation with fibrosis.
  • Treatment: Ivermectin( Cannot be admin. To collies or associated breeds Fenbendazole used instead.)
21
Q

Canine Chronic Bronchtitis?

A
  • ->Cough that occurs on most days for 2 or more consecutive months.
  • ->Histological changes include long term inflammation, fibrosis and hyperplasia.
  • ->Mucus Hypersecretion is a component of the disease but the cough may sound productive or non-productive.
  • ->Good condition/overweight, tracheal sensitivity, inspiratory crackles, expiratory wheezes
22
Q

Canine Chronic Bronchitis Diagnosis?

A 
Radiography
-->A Bronchial pattern with increased interstitial markings is seen. Changes are mild and difficult to distinguish. Most useful for ruling out other diseases.
Bronchoscopy
-->Hyperemic mucous membranes
-->Mucoid or purulent secretions
-->Fibrous nodules on the mucosa
BAL:
\+/- Bacteria, cytology and sensitivity
PCR for mycoplasma
Non-degenerate neutrophils, eosinophils
Increased mucus
23
Q

CCB Treatment?

A

Controlled, but never cured → goal: control inflammation, prevent worsening of airways. Managed Symptommatically.
Short-acting anti-inflammatories → Prednisolone
Bronchodilators → Theophylline: used for years to treat it, Terbutaline,
Antitussives → if inflammation is effectively treated. If not, mucus trapped in bronchi
Antibiotics → if BAL cytology and microbiology is +. Doxycycline for Mycoplasma

24
Q

Bronchiectasis?

A
  • Irreversible dilation of the large airways (bronchi), with accumulation of pulmonary secretions
  • Bronchiectasis can be cylindrical(tubular) or saccular(cystic).
  • Saccular Bronchiectasis is characterized by unifrom dilation of the airways.
History:
Chronic productive cough
Frequent bouts of pneumonia
Symptoms:
Loud bronchial sounds
\+/- Nasal discharge (pneumonia)
Hemoptysis (= coughing up blood)
TREATMENT: 
Not cough suppressants!!
Bronchodilators, Lobectomy.
25
Q

Feline Bronchial Disease?

A

Inflammation of the conducting airways (bronchi and bronchioles).
A spectrum of inflammatory small airway disease characterized by signs.
Cats airways are much more prone to brocnhoconstriction than dogs.

26
Q

Feline Bronchial disease Patho?

A

PATHO: Increased airway resistance (smooth muscle hypertrophy, bronchial wall edema, glandular hyperplasia) → cough and respiratory distress.

27
Q

Feline Bronchial Disease Clinical Signs?

A

Cats with idiopathic Bronchitis have some degree of airway eosinophilia. Major clinical feature is cough.
Signs are slow and progressive weight loss, anorexia, depression.
Common signs of Bronchitis: cough, wheezing, respiratory distress.
Cough: chronic, more than 2 months. Paroxysmal, dry, “hacking” cough, open mouth, (loud) breathing, prolonged expiration
Respiratory distress: mild to severe, usually obstructive expiratory dyspnea. Wheezing
Auscultation: harsh lung sounds, crackles, expiratory wheezes or normal
Percussion: increased resonance

28
Q

Feline Bronchial Disease Treatment?

A

Acute stabilization for emergency (cyanosis, open mouth breathing)–>Oxygen chamber
Sedation → Butorphanol (anxiol. + antitu.),
Anti-inflammatory → glucocorticoids
Bronchodilator → Terbutaline

Long term treatment:
Rule out parasitism as cause of eosinophilic bronchoalveolar lavage by treating prophylactically with fenbendazole

Glucocorticoids → Prednisolone, inhaled Fluticasone. GC relieve clinical signs and may protect the airways from long term affects of chronic Bronchitis
Bronchodilators → Terbutaline (inh), Salbutamol, Theophylline.
Antibiotics → doxycycline (culture or PCR for mycoplasma before start)

AVOID BETA BLOCKERS FOR FELINE ASTHMA!!

29
Q

Bacterial Pneumonia?

A
  • Primary bacterial bronchopneumonia is rare, and more commonly secondary to: Laryngeal dysfunction, viral pneumonia, aspiration,GI diseases, encephalopathy

Clinical signs:

  • Cough which is productive. Cough less common in cats.
  • Lethargy, fever, dyspnea, acute/chronic coughing (dog&raquo_space; cat), exercise intolerance
  • Mucopurulent nasal discharge, hemolysis.
  • Underlaying disease (dysphagia, regurgitation, vomiting, muscular weakness)
  • Increased lung sounds and crackles or wheezes.
30
Q

Viral Pneumonia?

A

Pathogen: distemper, Morbillivirus (Paramyxoviridae family)
Pathogenesis: exposure (inhalation, po. Infected secretions) → replication in macrophages, tonsils
→ viremia (2-4 days: initial fever) → several tissues (lung, bowel, skin, CNS) → bronchopneumonia, enteritis, encephalitis.

31
Q

Aspiration Pneumonia?

A

= Aspiration of fluid, food, or gastric content resulting in pulmonary inflammation.

Causes:

  • Megaesophagus
  • Laryngeal and pharyngeal dysfunction
  • Neuromuscular disease, anesthesia, encephalopathy
  • Brachycephalic airway conformation
  • Forced feeding (contrast radiography)
32
Q

Eosinophilic Bronchopneumonia?

A
  • Inflammatory disease of unknown etiology (hypersensitivity to an environmental/endogenous AG)
  • Can be in the airways or interstitium.
  • Allergic Bronchitis and Idiopathic Bronchitis are the most common diseases seen in cats.
  • Because it’s a hypersensitivity response, considerations include Heartworm, pulmonary parasites, drugs and allergens.
33
Q

Pulmonary Edema?

A

= Fluid accumulation in the intersititum and alveoli.

Causes: - Most Pulonary Edema is resulting from increased vacular permeability. ↑ Vascular hydrostatic pressure: left-sided CHF, excessive fluid adm (anuric renal failure) ↑ Vascular permeability: vasculitis, ARDS ↓ Plasma oncotic pressure: hypoalbuminemia ↓ Transpulmonary pressure: upper airway obstruction Impaired lymphatic drainage: left-sided CHF, neoplastic processes
34
Q

Acute Respiratory Distress Syndrome? (ARDS)

A
  • Acute hypoxemic respiratory failure due to lung injury and increased pulmonary capillary permeability
  • Usually secondary to: sepsis, pancreatitis, aspiration, shock, microbial pneumonia.
  • Early phase: proteinaceous fluid (increased capillary permeability)
  • Late phase:↑ inflammatory cells, hyaline membrane formation, fibrosis → Pulmonary hypertension.

Clinical signs:

  • Extreme anxiety, tachycardia, discolouration of MM.
  • Cyanosis, crackles (end-inspiration, expiration), wheezes, underlaying disease

Diagnosis:

  • Non-cardiogenic lung edema
  • Blood Gas analysis
35
Q

Pulmonary Fibrosis?

A

Interstitial lung disease–>Fibrotic Infiltration primarily alveolar septa.
Affects: West highland white terrier, Staffordshire bull terriers, cats
Pathology: alveolar septal fibrosis, interstitial fibrosis, epithelial hyperplasia, focal calcification

Chronic and progressive pulmonary signs:
-dyspnea, exercise intolerance, +/- cough, cyanosis, crackles.

Diagnosis:

  • radiography: diffuse, interstitial pattern
  • echocardiography: moderate to severe pulmonary hypertension
  • A definite diagnosis requires a lung biopsy
36
Q

Pulmonary Thromboembolism?

A
  • Abnormal gas exchange, pulmonary infarction

-Usually secondary to: Heartworm disease, immune-mediated hemolytic anemia (IMHA), neoplasia, DIC,
Hyperadrenocorticism (Cushing’s), PLE, PL-nephropathy.

Clinical signs:
Sudden onset of respiratory distress, Cardiovascular shock, Tachypnea.
Cyanosis, Haemorrhage, edema and bronchoconstriction is addition to decreased blood flow.
Vasoconstriction results in Pulmonary Hypertension.

Diagnosis:

  • Standard: pulmonary angiography
  • Antithrombin III: not conclusive may indicate a clot though
  • Arterial Blood-gas
37
Q

Pleural Effusion?

A

THE BUILD-UP OF EXCESS FLUID BETWEEN THE LAYERS OF THE PLEURA.
Clinical Signs: inspiratory dyspnea with delayed exp., ext. neck, tachypnea, open mouth breathing, cyanosis
Percussion: horizontal dullness, Diernhofer-triangle (= air-containing triangle).
Auscultation: bronchial sounds above fluid, zero sounds beneath fluid.

38
Q

Types of fluid?

A

Transudate: Low protein content and low nucleated cells. Primary cells are Mononuclear.

Modified transudates: have slightly higher protein concentration. Primary cells are neutrophils and mononuclear cells.
Transudate and Modified Transudate are formed as a result of increased Hydrostatic Pressure, decreased plasma oncotic pressure(result of Hypoalbunaemia) or lymphatic obstruction.

Exudates have a high protein concentration compared to transudates.

39
Q

Hydrothorax?

A

Hypoalbuminemia
CHF: mainly in cats
Diaphragmatic hernia
Portal hypertension

40
Q

Pyothorax = septic exudate?

A

Causes: obligate anaerobic bacteria (Actinomyces, Nocardia): dogs + cats via port of entry (skin injuries), exudate is reddish-brown, turbulent.

FIP: cats. Honey-like, viscous exudate (++ fibrinogen and globulin), in both cavities.

Clinical Signs: are similar to that of pleural effusion and abscess formation. Tachypnea, decreased lung sounds, systemic inflammatory response.

41
Q

Chylothorax = lymph in thorax?

A
  • Accumulation of chyle within the thoracic cavity.
  • Fibrosing Pleuritis and Pericarditis can be associated with chylothorax.
  • Due to: ↓ lymphatic drainage due to rupture or obstruction of lymphatic flow.
42
Q

Pneumothorax?

A
  • Presence of air in the pleural space. More air in pleural space, parenchyma becomes more dense and incomplete expansion of the lung.
  • Open pneumothorax = communication with the outside, usually due to trauma
  • Closed pneumothorax = no communication with the outside, air leaking from airways/parenchyma .
  • Traumatic closed pneumothorax: due to trauma, but closed. Due to airway obstruction, pulmonary hemothorax, hypovolemic shock.
  • Spontaneous closed pneumothorax: not due to trauma Idiopathic: large, deep-chested dogs (huskies).
43
Q

Concentric vs Eccentric?

A
  • Ventricular systolic pressure load induces concentric hypertrophyMyocardial fibres and ventricular walls thicken. Hypertrophized Heart. Common causes of Concentric Hypertrophy are Aortic Stenosis( LV hypertrophy), Pulmonic stenosis( RV hypertrophy).
  • With severe Hypotrophy, chronic myocardial hypoxia stimulates further fibrosis.
  • Chronic volume loading increases diastolic wall stress and leads to eccentric hypertrophy. Dilated Heart. Common causes are Mitral Dysplasia(LS), Tricuspid Dysplasia(RS), Ventricular Septal Defect( L+R).
44
Q

Heart Failure Compensation?

A

. Sympathetic nervous system activated to increase cardiac output.
. Another way is to increase Preload through ADH which increases the filling volume= Increases Stroke volume.
. If this system keeps getting activated, heart cells working harder and die off.
. Causes Cardiac Hypertrophy as the cells expand and contrect harder.
.- Excessive activation of neurohormonal compensatory mechanisms can lead to clinical syndrome of Congestive Heart Failure(CHF). These mechanisms support circulation when there is acute hypertension and hypovolaemia however chronic activation can cause the heart to deteriorate.

45
Q

Systolic vs Diastolic Heart Failure?

A

Systolic: can’t contract sufficiently
e.g. mitral valve regurgitation, DCM

Diastolic: can’t distend sufficiently
e.g. myocardial fibrosis, hypertrophic & restrictive cardiomyopathy, pericard. d

46
Q

Left Sided Heart Failure?

A
  • Instead of the heart pumping of the left ventricle pushing into the circulation system, some blood leaks through mitral valves back into left atrium and back up into lungs.
  • Tachypnea, dyspnea, mixed type
  • Worsening cough
  • Cerebral hypoxia → Adam-stokes syndrome = syncope (temporarily fainting)
  • Mild prerenal azotemia
  • Cold extremities
  • Pleural fluids (cats only)
  • Pulmonary edema (harsh lung sounds, crackles)
  • Increased left atrial pressure → increased pressure in the pulmonary veins + capillaries → transudate/fluid leakage from capillaries → pulmonary edema → tachypnea → dyspnea.
47
Q

Right Sided Heart Failure?

A
  • Causes poor venous blood return to the heart. When the heart contracts, instead of the right ventricle pushing the blood through the lungs of oxygenation, some blood leaks through the tricuspid valves back into the right atrium.
    Congested V. jugularis → distension, positive hepatojugular reflux
    Congestion in the abdominal organs (liver) → hepatomegaly
  • Ascites
  • Pleural fluid/effusion
  • Subcutaneous edema/fluid leaks into the limbs causing peripheral edema
48
Q

Treatment of Congestive HF?

A
  • Decrease preload: decrease congestion & burden of heart → diuretics, venodilators
  • Decrease afterload and cardiac burden → arterial dilators (OBS! Hypotension)
  • Increase contractility: Calcium sensitizer
  • Treat neurohormonal overcompensation (usually lead to increased venous pressure)–>ACE Inhibitors, Aldosterone blocker.
49
Q

Diuretics?

A
  • Decrease Preload
  • Loop Diuretic: Furosemide–> activates RAAS. Lowers BP.
  • TO INCREASE CONTRACTILITY = CALCIUM SENSITIZERS (INOTROPIC AGENTS). Pimobendan enhances Ca+= contractability.
  • ACE inhibitors: Enalapril, Benazepril indicated for chronic heart failure. Blocks angiotensin allowing vasodilatory effects
  • Aldosterone Blocker: Spironolactone

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