Lecture 4 Flashcards

1
Q

Nasal disease: clinical findings

A
  1. Sneezing (paroxysmal? sporadic? reverse?)
  2. Nasal discharge (symmetry? character? onset/duration? progression? inciting cause?)
  3. Stertor
  4. Pawing/rubbing face
  5. Masses/facial distortion
  6. Nasal planum ulceration
  7. Seizures, mentation changes
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2
Q

Nasal discharge: unilateral

A

Unitlateral:

  1. Neoplasia
  2. Tooth root abscess
  3. Foreign body
  4. Fungal
  5. Trauma
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3
Q

Nasal discharge: bilateral

A

Bilateral

  1. Inflammatory rhinitis
  2. Systemic disease (hypertension, coagulopathy)
  3. Neoplasia
  4. Fungal
  5. Viral
  6. Trauma

NOTE: if a tumor is close to the choanae, it can cause BILATERAL nasal discharge

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4
Q

Nasal Discharge - Serous/serosanguineous

A

Serous/serosanguineous

  • HOW MAJORITY OF NASAL DISCHARGE STARTS
  • Often associated w/: viral, allergic, or inflammatory rhinitis
  • Sanguineous (bloody) usually indicates:
    1. Progressive
    2. Erosive
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5
Q

Nasal Discharge - Mucopurulent

A

Mucopurulent

  • Usually indicates SECONDARY bacterial infection
    1. Primary nasal bacterial infections = VERY RARE

Note: if you just give antibiotics for mucopurulent nasal discharge, you might not be able to clear infection - it may recur since it’s a secondary infection

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6
Q

Nasal Discharge - Hemorrhagic

A

Hemorrhagic (epistaxis)

  • Severely errosive disease
    1. Neoplasia
    2. Aspergillosis
  • SYSTEMIC disease
    1. Coagulopathy
      - Inherited vs. acquired
      - Rickettsial disease
    2. Hypertension
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7
Q

Physical Exam (really important)

A
  1. Visual exam of mouth/nose
    - Facial symmetry?
  2. Palpate bones/muscle
    - Palate too if able
  3. Ocular retropulsion
    - Does one side retropulse 1/2 as far as other side?
    …space occupying mass?!
  4. Nasal patency
  5. Fundic exam
    - Look esp. for fungus and neoplasia
  6. Lymph node palpation
    - Submandibular LN are most likely the first place a nasal infection will spread
  7. Neurologic exam
    - Cranial nerves
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8
Q

First-tier diagnostic testing

A
  1. CBC (& blood smear -> platelets)
  2. Cytology
    - Nasal discharge
    - LN/masses
  3. Thoracic radiographs
    - Check for metastasis/fungal infection
  4. Coagulation profile (do a BMBT)
    - If epistaxis
    - Don’t just check platelet #’s, check platelet function
  5. Blood pressure
    - If epistaxis
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9
Q

Second - tier diagnostic testing

A
  1. Anesthetized oral exam
    - Periodontal probe
    - Dental rads
  2. Nasal CT (nasal radiographs less useful)
  3. Rhinoscopy w/ biopsy
    - bacterial/fungal cultures
    - Cytology
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10
Q

If you do a blind biopsy of the nasal cavity, where should you measure your instruments to?

A

Measure instruments to MEDIAL CANTHUS of the eye.

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11
Q

Common Nasal Diseases - Dogs

A
  1. Lymphoplasmacytic Rhinitis*
  2. Aspergillosis*
  3. Neoplasia*
  4. Oral Disease
    - Oronasal fistulae
    - Tooth root abscess
  5. Foreign bodies
  6. Coagulopathies
  7. Trauma
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12
Q

Common Nasal Diseases - Cats

A
  1. Viral rhinitis*
    - Commonly secondary bacterial infection
  2. Chronic rhinosinusitis*
    - Cat version of lymphoplasmacytic rhinitis
  3. Nasopharyngeal polyps*
  4. Neoplasia
    - Carcinoma, lymphoma
  5. Cryptococcosis
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13
Q

Lymphoplasmacytic Rhinitis

A
  1. Doliocephalics (Dachshunds and Whippets)
  2. Clinical signs:
    • Chronic nasal discharge (often bilateral; may or may not be blood)
    • Nasal congestion (stertor)
    • Sneezing
  3. Nasal inflammation of unknown etiology (multifactorial?)
  4. ~ 1/3 of K9 disease referrals
  5. DIAGNOSIS OF EXCLUSION
    • Definitive: nasal biopsy, rule out infectious causes of inflammation w/ bacterial and fungal cultures
  6. Difficult to manage
    • NOT GOING TO CURE
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14
Q

Lymphoplasmacytic Rhinitis: treatment

A
  1. Anti-inflammatories
    • Glucocorticoids (systemic or inhaled) - minimal improvement anecdotally
    • Immunomodulatory antibiotic and NSAID (doxycycline + piroxicam)
  2. Anti-histamines
  3. Itraconazole (anecdotal improvements in some humans)
  4. Treat secondary infections (controversial)
  5. Environmental modification
    • Cigarette smoke
    • Perfume/cleaners/air fresheners
    • Litters
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15
Q

Fungal Rhinitis

A

Cryptococcus neoformans

  • Cats
    • Nasal, cutaneous (get skin cytology if you see any skin issues), CNS
    • Typically causes a mutated nose!
  • Dogs
    • Disseminated disease more common (ie. skin, bone, CNS signs)
    • Nasal disease frequently subclinical

NOTE: if there are skin issues, it is easier to diagnose a fungal infection thro skin issues than it is thro nasal sampling!

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16
Q

Cryptococcus

A
  1. Diagnosis
    • Organism ID (visual)
      • Cytology, histopath culture
    • Antigen assay (not definitive as it may pick up other fungal Ag; can be used to monitor response to treatment)
  2. Treatment (depends on where disease is localized)
    • Fluconazole
    • Amphotericin B
17
Q

Fungal Rhinitis - Aspergillus

A

Aspergillus fumigatus

  1. Common fungal organism affecting K9
  2. Sino-nasal disease
  3. GS and other dolicocephalic breeds predisposed
  4. Clinical signs:
    • Nasal discharge*: serous ==> mucopurulent +/- epistaxis
    • NASAL PLANUM DEPIGMENTATION* (non-specific, but classic w/ Aspergillus)
    • Sneezing*
    • Nasal pain, systemic signs (lethargy, hyporexia), rarely neurologic signs (it can infiltrate thro cribiform plate)
18
Q

Nasal Aspergillus

A
  1. Diagnosis
    • CT* (really important since the best treatment is topical)
    • Rhinoscopy + cytology/histopathology
  2. Treatment
    • TOPICAL CLOTRIMAZOLE*
    • Topical enilconazole
    • Relapse is common, systemic therapy isn’t really effective

NOTE: Aspergillus may not invade locally, but it can secrete pro-inflammatory molecules that lead to turbinate atrophy!

19
Q

Cats and Aspergillosis?

A
  1. Cats get sino-nasal disease like dogs
  2. Also affected by sino-orbital aspergillosis (SOA)
    • can be an extension of sino-nasal disease
    • prognsosis for SOA is POOR
20
Q

Feline Upper Respiratory Disease Complex

A

Feline URDC - usually multifactorial

  1. Herpesvirus** (majority of cases)
    • FHV - up to 38% of URI
  2. Calicivirus* (#2 cause)
    • FCV - up to 36%
  3. Chylamidia felis, Mycoplasms, Bordetella bronchiseptica
  4. Coinfections are common, especially in crowded conditions
21
Q

Feline Viral Rhinotracheitis

A

Feline Herpes virus 1

  1. Shed intermittently = “latency”
    • they almost all become chronic carriers and may relapse w/ clinical signs during times of stress
  2. Labile outside host
  3. Eyes and Nose primarily affected*!
    • Keratitis, sneezing, corneal ulceration
22
Q

Feline Calicivirus

A
  1. Shed CONTINUOUSLY (always)
    • can persist in environment for weeks
  2. Clinical signs mostly seen orally
    • Often see erosions/ulcers
23
Q

Feline Viral Rhinitis

A
  1. Young or multi-cat households
  2. Vaccination reduces severity and incidence
    • Modified-live FVRCP
  3. Severity of signs highly variable
    • May develp PERMANENT nasal discharge (turbinate remodeling)
24
Q

Feline Viral Rhinitis - management

A
  1. Stress avoidance
  2. Relative isolation
  3. Long term (controversial)
    • L-lysine (may increase shedding, don’t use in shelter)
    • Famciclovir
  4. Partially anorexic?
    • Smelly or warmed food
    • Clean nose
    • Antibiotics as needed
  5. Systemically ill?
    • Supportive care (NOTE: doxycycline is good vs. Chlamydia, Bordetella and Mycoplasma
25
Q

Nasal neoplasia

A
  1. Older animals
    • ADENOCARCINOMA (most common nasal tumor in K9), sarcomas, LYMPHOMA (most common nasal tumor in cats)
  2. Locally invasive
    • Bone destruction
    • CNS signs (cribiform plate)
  3. RADIATION THERAPY is treatment of choice
    • NSAIDS (piroxicam)
26
Q

Large Airway Disease

A
  1. Infectious tracheobronchitis

2. Tracheal collapse

27
Q

K9 Infectious Tracheobronchitis

“Kennel Cough”

A
  1. Bordetella bronchiseptica*
  2. Canine Parainfluenza virus*
  3. Canine Adenovirus type-2
  4. Younger dogs, history of recent exposure
  5. Paroxysmal, non-productive (unless 2nd infection develops), harsh cough
    • Typically inducible
28
Q

Canine Infectious Tracheobronchitis (kennel cough) Treatment/management

A
  1. Most cases = MILD and SELF-LIMITING
    • 7-10 days of supportive care
  2. Persistent non-productive cough
    • Antitussives +/- anti-inflammatory
  3. Severe or prolonged cases
    • Antibiotics
29
Q

CITB (kennel cough) “Prevention”

A
  1. DHPP vaccination
    • H = infectious hepatitis = Adenovirus 1 (CAV-2 is in vaccine ==> cross protective w/ type 1)
    • P = parainfluenza virus*
30
Q

CITB (kennel cough) vaccination

A
  1. Modified live intranasal
    • B. bronchiseptica (+/- viral pathogens)
    • FASTER immunity (early as 72 hours)
    • Can initiate YOUNGER (3 weeks)
    • Reduces shedding*
  2. SubQ
    • B. bronchiseptica Ag
    • Need booster (immunity 1-2 weeks post 2nd injection)
    • Initiate at 6 weeks
31
Q

Tracheal collapse

A
  1. Progressive degeneration of cartilage rings
    • Dorso-ventral flattening of rings
    • Laxity of dorsal tracheal membrane
  2. Collapse at
    • Cervical trachea* ==> inspiration
    • Thoracic trachea* ===> expiration
    • Mainstem/lobar bronchi
    • Collapse may be through entire trachea and lead to various dyspnic signs in both inspiratory and expiratory
32
Q

Tracheal collapse characteristics

A
  1. Middle to older aged dogs (progressive disease)
  2. Small/toy breed dogs
  3. “Goose-honk” cough
  4. Exercise intolerance
    • exacerbation of cough w/ excitement is common
33
Q

Tracheal Collapse Diagnosis

A
  1. Clinical signs (may also hear stridor, but often don’t since it’s so dynamic)
  2. Physical exam
  3. Radiographs
  4. Fluoroscopy*
  5. Bronchoscopy
    • Gold standard
34
Q

Tracheal collapse: grading

A

Grade 1: <25% closed
Grade 2: 25-50% closed
Grade 3: 50-75% closed
Grade 4: Completely closed

You need a scope down the trachea to grade the collapse

35
Q

Tracheal Collapse Management

A
  1. ANTITUSSIVES (mainstay of therapy)
  2. Anti-inflammatories (you may use a short, tapering dose of predisone to decrease inflammation)
  3. Bronchodilators (work on beta-2 adrenergic receptors - in bronchiolar smooth muscle - so it doesn’t help tracheal collapse directly, but it reduces the total resistance to airflow)
  4. WEIGHT LOSS* (decrease pressure on trachea causing coughing)
  5. SUPPORTIVE (harness, heat avoidance)
  6. End-stage: stenting (a finite treatment..)
36
Q

Tracheal collapse: pathophysiology

A

Collapse causes inflammation and cough ==> coughing causes tracheal inflammation ==> inflammation perpetuates cough

You may need to “break the cycle” of inflammation to relieve the cough