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small animals - 614 > 614 - Small Animal Practice T1 > Flashcards

614 - Small Animal Practice T1 Flashcards

1
Q

What are some precautions that need to be taken when giving infectious vaccines?

A

Dont give them to pregnant queens or bitches
They may revert to virulence once injected (though it is uncommon)
Need to be careful about aerosolisation of vaccine especially cat flu vaccine

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2
Q

What is a non-infectious vaccine?

A

An inactivated but antigenically intact virus or organism combined with an adjuvant.
They provide less robust immunity than live, and generally have a shorter DOI than infectious vaccines.
It won’t rever to virulence and usually required multiple doses to induce protection.

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3
Q

Give some examples of adverse vaccine reactions.

A

Pain on injection
Swelling at the injection site
Persistent lump at injection site
Granuloma development + possible progression to feline injection site sarcoma (FISS) in cats
Generalised malaise, fever, inappetence
May have localised or generalised anaphylaxis.
IMHA (in dogs), ITP (in cats)

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4
Q

Which vaccines are most commonly implicated in the formation of FISS?

A

Rabies, FeLV, FIV

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5
Q

What are the fundamental concepts of the WSAVA guidelines?

A

Aim to vaccinate every animal with core vaccines to provide herd immunity
Non-core vaccines should be given no more frequently than is deemed necessary

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6
Q

Name the core vaccines for dogs.

A

Canine distemper virus (CDV)
Canine adenovirus (CAV)
Canine parvovirus type 2 (CPV-2)
+ Rabies if in an endemic area

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7
Q

Name the core vaccines for cats.

A

Feline enteritis/feline parvovirus (FPV)/feline panleukopenia
Feline calicivirus (FCV)
Feline herpesvirus-1 (FHV-1)
+ Rabies if in an endemic area

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8
Q

Name the NON-CORE vaccines for dogs.

A

Bordetella bronchiseptica + canine parainfluenza virus
Leptospirosis
Borrelia/Lyme disease

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9
Q

Name the NON-CORE vaccines for cats.

A

Feline leukaemia
Chlamydopila felis
FIV

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10
Q

Why is the FIP vaccine not recommended?

A

It will only protect cats which are coronavirus antibody negative - which is unlikely after 16 weeks of age because of how common and widespread coronavirus is.

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11
Q

What is the standard puppy vaccination regime for a C3 and why do we vaccinate at these intervals?

A

6-8 weeks old - doesn’t actually do that much for immunity unless the puppy has low MDA
10-12 weeks old - MDA are starting to wane + have less intereference on core vaccine efficacy
14-16 weeks old - MDA will be at almost negligible levels by this stage

Core vaccines should be boosted at 6 months (instead of 12-15) to capture non-responders.

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12
Q

How, why and in what circumstances is titre testing useful?

A

Titre testing tests for seroconversion so will tell us if there is vaccine failure (in which case we can try a different brand) or if there is a need for a booster vaccine when trying to minimise how many vaccinations we are giving (i.e. trienniels, extended duration of immunity of CORE vaccines). There are only titre tests available for CPV, CDV + canine adenovirus via UK.
We can also titre test animals with adverse vaccine reaction history to decide if we need to vaccinate them again or if they are sufficiently covered and we don’t have to risk more adverse reactions - however, most adverse reactions are from kennel cough vaccine and there isn’t a titre test for that currently.

We don’t titre test in cats.

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13
Q

What are the causes of vaccine failure?

A

Presence of MDA
Improper vaccine handling and administration
Vaccine is poorly immunogenic
Host factors lead to poor response
Insufficient time to develop immunity prior to exposure

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14
Q

Discuss the routes of administration of canine kennel cough vaccine and what they cover.

A

Infectious vaccine - intranasal or intraoral
Non-infectious vaccine - parenteral/SC
Intranasal - Bordetella and canine parainfluenza virus
Intraoral - Bordetella, if giving in this route you need to also give parenteral parainfluenza coverage.

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15
Q

Discuss a regime for extended DOI in cats.

A

Year 1: Tricat - to cover herpesvirus, calicivirus (both annual) + panleukopaenia (triennial)
Year 2: Ducat - covers herpes + calicivirus
Year 3: Ducat
Year 4: back to Tricat

NEED TO GET INFORMED CONSENT because this is off-label use.

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16
Q

Which populations of cats might we want to give the FIV vaccine? How about the vaccine for Chlamydophila felis?

A

FIV - cats that are out and able to fight with other cats, especially ferals
Chlamydophila felis - catteries prior to introduction of a new cat

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17
Q

How do we deal with live vaccine spillage on a cat?

A

Clean it off with isopropyl alcohol - it inactivates live virus and won’t damage the cats mouth when they inevitably groom themselves later

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18
Q

Describe the pathogenesis of cat bite abscesses.

A

Injection of oral bacteria under the skin by biting or scratching –> neutrophil + phagocyte infiltration –> pus formation –> body walls off the infection = abscess
May burst spontaneously if pressure necrosis of the dermis occurs

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19
Q

What is the clinical presentation of a cat bite abscess?

A

Grumpy cat, possibly lame and painful
Pyrexic (esp. in first 12 hours)
May not have an overt mass, may have cellulitis
Regional lymphadenopathy
Discharging area with necrotic skin

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20
Q

Discuss treatment and management of a cat bite abscess.

A

If new bite wound or cellulitis - 1 wk course of Ab (generally amoxyclav or doxycycline) + pain relief (meloxicam)
If cellulitis but no abscess - as above.
If abscess - surgical drainage, GA + debride necrotic skin, flush dead space with saline or dilute betadine, close wound but not SC layer +/- drain; then 1 wk Ab + meloxicam, remove sutures 7-10d post-op

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21
Q

Which 2 bacteria are most likely to be transmitted to humans from a cat bite?

A

Pasteurella, Porphyromonas

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22
Q

Name the common sites for grass seeds to implant themselves.

A

Ear canal, nasal cavity, eye under conjunctiva, interdigital, skin of ventral abdomen or thorax, ventral mandible, prepuce, vulva

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23
Q

How do we treat grass seed foreign bodies?

A

Remove them! - find the tract and gently probe
Debride necrotic tissue and flush with saline if possible
Closure for abscess but may not be necessary
Antibiotics if soil microbes involved - Amoxil, amoxyclav

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24
Q

What is atresia ani?

A

Rare congenital abnormality, born without an anus, poor prognosis –> euthanasia.

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25
Q

What are the clinical signs of common anal sac conditions?

A

Impaction - full anal sacs, pain, discomfort, scooting
Sacculitis/inflammation - sac enlargement, perianal redness, swelling, pain, +/- pyrexia + tenesmus
Abscess - pyrexia, swelling, pain, discharge, blood and/or purulent material, +/- discharging sinus + tenesmus

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26
Q

What are the 3 main DDx for scooting?

A

Perineal pruritis, tapeworm infection, full anal glands

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27
Q

How do we treat anal sacculitis?

A

GA, insert a 23g catheter into the duct + gently flush with saline til contents are clear
Instil AB/steroid cream into the sac till its full

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28
Q

How do we treat anal sac abscessation?

A

GA, insert 23g catheter into the duct + gently flush with saline until contents are clear, treat the abscess surgically
AB (cephalexin, clindamycin, amoxyclav) for 10-14d

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29
Q

Define heart failure.

A

Any condition whereby cardiac output is insufficient to deliver adequate blood to meet metabolic demand at normal cardiac filling pressures.

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30
Q

List the presenting complaints associated with cardiac dysfunction.

A

Dyspnoea, tachypnoea, pulmonary oedema, pleural effusion
Syncope
Exercise intolerance
Cough
“Paralysis”
Ascites
Cyanosis
Poor perfusion/prolonged CRT
Poor growth or weight loss
Blindness
Heart murmur

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31
Q

What are the signs of heart DISEASE?

A

Any sign that indicates an abnormality within the heart - it does not imply that failure is present.

Murmur
Arrhythmia
Diagnostic imaging change

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32
Q

What are signs of heart FAILURE?

A

Poor cardiac output - tachycardia, inc. force of contraction, loss of sinus arrhythmia with dec. vagal tone, vasoconstriction (poor peripheral perfusion, cold exremities, pale MM), blood volume expansion + prolonged CRT

Left sided congestion - pulmonary oedema (crackles), pleural effusion in cats (dull ventral lung sounds +/- paradoxical breathing), cyanosis, tachypnoea, restrictive breathing pattern (rapid + shallow), cough

Right sided congestion - jugular pulses, ascites, hepatomegaly, pleural effusion in dogs (dull ventral lung sounds, tachypnoea, cyanosis, restrictive breathing pattern +/- paradoxical breathing), hepatojugular reflux, cachexia

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33
Q

Discuss what should be included in the description of heart auscultation findings.

A
  1. RATE
  2. RHYTHM
  3. AREA
  4. AUDIBILITY
  5. ADVENTITIOUS SOUNDS
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34
Q

How are murmurs classified?

A
  1. LOUDNESS - grades 1 to 6
  2. TIMING - systolic, diastolic, continuous
  3. LOCATION - left or right, base or apex
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35
Q

What is your main differential for a left apical systolic murmur?

A

Mitral regurgitation

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36
Q

What is your main differential for a left basal diastolic murmur?

A

Pulmonic or aortic regurgitation

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37
Q

What is your main differential for a right apical diastolic murmur?

A

Tricuspid stenosis (TS)

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38
Q

What is your main differental for a left basal continuous murmur?

A

Patent ductus arteriosus (PDA)

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39
Q

What is your main differential for a left basal systolic murmur?

A

Pulmonic stenosis (PS), subaortic stenosis (SAS), atrial septal defect (ASD)

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40
Q

What is your main differential for a right basal systolic murmur?

A

Subaortic stenosis (SAS)

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41
Q

What is your main differential for a right apical systolic murmur?

A

Tricuspid regurgitation, ventricular septal defect (VSD)

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42
Q

What is your main differential for a left apical diastolic murmur?

A

Mitral stenosis

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43
Q

Which cardiac biomarkers are available for animals and what are they increased with?

A

Cardiac Troponin I - inc. with myocyte injury and myocarditis
NT-proBNP/Brain Natriuretic Peptide - inc. with myocyte stretch + heart failure

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44
Q

What is the best ancilliary test for heart disease and failure?

A

Echocardiography (ECHO)

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45
Q

What ancilliary testing can we do for heart disease and failure?

A

Echocardiography
ECG + Holter recording
Thoracic US
Thoracic radiography
Blood pressure measurement
General CBC and biochem for pre-existing renal or electrolyte abnormalities
Cardiac biomarkers - cardiac troponin I and NT-proBNP
Angiography

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46
Q

In terms of murmur location - where might you hear dysfunction of each major heart valve?

A

Left base - aortic and pulmonic valves
Left apex - mitral valve
Right apex - tricuspid valve

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47
Q

What is the most common cause of heart failure in dogs?

A

Chronic valvular heart disease/myxomatous mitral valve disease/mitral valve disease/mitral valve degeneration/endocardiosis

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48
Q

What are the clinical signs of disease with chronic valvular heart disease?

A

Left sided apical systolic heart murmur
Cough due to LA enlargement and tracheobronchomalacia
Arrhythmia

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49
Q

List the potential sequelae of chronic valvular heart disease.

A

Chordae tendineae rupture (acute deterioration)
Arrhythmia - usually atrial fibrillation
Cardiac cachexia
Pulmonary hypertension (may see exercise intolerance)
Haemopericardium in severe cases when the LA ruptures
Progression to non-responsive heart failure

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50
Q

If you were suspicious of heart failure and wanting to do thoracic radiography, what view do you NOT want to do?

A

VD

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51
Q

What changes do you expect to see on acilliary testing and imagery in a dog with chronic valvular heart disease?

A

Thoracic rads - LA enlargement with LA wedge (may have other chamber enlargement too), pulmonary oedema, signs of mainstem bronchus compression, pulmonary venous distension
Thoracic US - in LSCHF –> perihilar B lines + more diffuse B lines; in RSCHF –> pleural effusion
Echo - +/- valve flail, LA enlargement, valvular regurgitation + pulmonary hypertension on Dopplet
ECG - sinus tachycardia in failure, wide P waves from LA enlargement, tall wide QRS from LV enlargement, intermittent supraventricular tachyarrhythmias, atrial fibrillation

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52
Q

Briefly describe the different stages of CVHD.

A

Stage A - predisposed but no identifiable structural abnormalities
Stage B1 - structural heart disease present but clinical signs of heart failure have never developed and there is no imaging evidence of remodelling
Stage B2 - structural disease present but clinical signs of heart failure never developed, imaging evidence of remodelling
Stage C - past or current evidece of heart failure present
Stage D - clinical signs of heart failure refractory to standard therapy

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53
Q

At what stage of CVHD do we start the dog on treatment and what is it?

A

Stage B2 - pimobendan and mild sodium restriction, maintain optimal BW/condition

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54
Q

What are the treatments for Stage C CVHD?

A

Furosemide +/- monitor renal values and electrolytes after a few days
Could also use spironolactone
Oxygen
Cage rest
Pimobendan +/- ACE inhibitors
Drain effusions if compromising respiration
Judicious sedation + anxiolysis
Vasodilators
Dobutamine
Treat arrhythmias
Dietary modification - modest sodium restriction, optimise caloric intake to prevent cardiac cachexia
+/- Cough suppresants (if the cough is impacting their quality of life)
Monitor BW, appetite, RR + HR

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55
Q

Discuss the clinical signs of pulmonary hypertension, how to diagnose it, and what drug we can use to treat it (other than treating the underlying cause).

A

Cx - syncope, dyspnoea, RSCHF signs, +/- RS tricuspid murmur, split S2 sound

Dx - ECHO

Tx - sildenafil

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56
Q

What additional therapies can we consider to try and give a dog in Stage D CVDH some relief?

A

Higher doses of furosemide or change to torsemide (which is stronger)
Pimobendan x3/day
Additional diuresis
Vasodilators
Cough suppressants
Anti-arrhythmics
Sildenafil (for pulmonary hypertension)
Short term mechanical ventilation

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57
Q

What 2 valves are commonly affected in infective endocarditis?

A

Aortic and mitral valves

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58
Q

Describe the clinical signs of infective endocarditis.

A

New/sudden onset murmur - usually diastolic (aortic regurgitation)
Pyrexia
Other areas of infection present
Bounding pulse

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59
Q

What are the 6 criteria of diagnosis for infective endocarditis. Differentiate which 3 are major vs minor criteria.

A

MAJOR:
1. Positive ECHO findings - vegetative lesions, destructive lesions, thickened aortic valve leaflets
2. Positive blood cultures or sepsis - 3 positive blood cultures of common skin contaminants, 2 positive cultures of other organisms
3. Recent onset of a diastolic heart murmur

MINOR:
4. Pyrexia
5. Large dog, over 15kg
6. New or worsening systolic heart murmur

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60
Q

Discuss the treatment and prognosis for dogs with infective endocarditis.

A

Tx - initial parenteral ABs, oral ABs for 4-6 weeks (choice based upon C&S results), empirical ABs (amoxyclav AND fluoroquinolones OR gentamicin), treat CHF as necessary (furosemide + pimobendan)

Prognosis - poor, death is usually from CHF, embolisation or sepsis

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61
Q

Which breeds are predisposed to idiopathic dilated cardiomyopathy (IDCM) in dogs?

A

Boxers, Great Danes, Newfoundlands, Saint Bernard, Irish Wolfhound, Dobermann, American Cocker Spanial

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62
Q

Contrast the clinical signs associated with occult disease and clinical failure in dogs with IDCM.

A

Occult disease - arrhythmia (commonly tachyarrhytmias, ventricular tachycardia in Dobermann and Boxers, A Fib in giant breeds and late stage dx), murmur (left apical systolic), ECHO screening
Clinical failure - structural or electrical changes, left or right sided CHF signs, decreased cardiac output signs (syncope is super common)

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63
Q

What echocardiographic findings are associated with idiopathic dilated cardiomyopathy (IDCM) in dogs?

A

Increased LV diameter
Rounging of LV lumen
Increased LA size
Increased E point to septal separation (EPSS)
Decreased fractional shortening
Wall thinning apparent in advanced disease

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64
Q

What thoracic radiographic findings are associated with IDCM in dogs?

A

Generalised enlargement of cardiac silhouette - Dobermann and Boxers may have minimal cardiomegaly
Pulmonary oedema, pulmonary vein distension if LSCHF
Pleural effusion if RSCHF

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65
Q

Discuss the treatment of dogs with IDCM.

A

ACUTE CHF:
Furosemide
Oxygen
Cage rest
Pimobendan +/- ACE inhibitors
Drain effusions if compromising respiration - thoracocentesis
Judicious sedation (butorphanol will dec. oxygen demands)/anxiolysis
Vasodilators
Dobutamine (to stabilise in acute stage)
+ treat arrhythmia if necessary

CHRONIC CHF:
Pimobendan +/- ACE inhibitors
Furosemide +/- spironolactone +/- thiazide
Salt restricted, high energy diet
Exercise restriction until their condition is under control
Carnitine and taurine in selected breeds

VENTRICULAR ARRHYTHMIAS:
Acute - lidocaine
Chronic - mexilitine, sotalol

ATRIAL FIBRILLATION:
Digoxin +/- Ca channel blocker

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66
Q

What drug class can be used as an antiarrhythmic but should NOT be used in heart failure.

A

Beta blockers

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67
Q

What breeds commonly get pericardial effusion?

A

Golden retriever
GSD

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68
Q

Describe the typical history, clinical signs and physical exam findings of pericardial effusion.

A

History and Cx - if chronic then lethargy, anorexia, weakness, collapse, tachypnoea, muscle wastage/weight loss, RSCHF signs, exercise intolerance; if acute onset then collapse, cardiogenic shock + death

Physical Exam - muffled heart sounds, ascites, pleural effusion, dull ventral lung sounds, jugular venous distension, tachycardia, weak pulses, pulsus paradoxus (weaker pulse during inspiration)

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69
Q

Describe which ancilliary tests are going to be useful in diagnosing pericardial effusion and the findings you would expect.

A

ECHO - diastolic collapse of RA and/or RV confirms cardiac tamponade, try to identify neoplasia

Thoracic radiography - mild to severe enlargement of cardiac silhouette, rounded or globoid cardiac silhouette, sharp edges, +/- pleural effusion

ECG - sinus tachycardia, low voltage QRS complexes

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70
Q

Describe appropriate treatment for a dog with pericardial effusion.

A

Pericardiocentesis
IV fluid therapy until performed if clinically necessary

NO diuretics

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71
Q

Name 2 neoplasias that cause pericardial effusion.

A

Haemangiosarcoma of the right atrium
Chemodectoma

Other less common ones - mesothelioma, ectopic thyroid carcinoma, metastatic neoplasia

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72
Q

What are the 6 phenotypes of feline cardiomyopathies?

A
  1. Hypertrophic
  2. Dilated
  3. Restrictive
  4. ARVC
  5. Non-specific
  6. Idiopathic (primary) or secondary
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73
Q

Describe the possible presentation of feline heart disease.

A

Severe dyspnoea - pleural effusion or pulmonary oedema
Sudden death
Acute hind limb paralysis
Murmur or gallop rhythm detected at routine vaccination

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74
Q

What are potential causes of progression of feline heart disease from stage B2 to C?

A

Stress
Intravenous fluid therapy (IVFT)
Glucocorticoids
General anaesthesia
Often none identified

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75
Q

Which breeds of cat are predisposed to HCM?

A

Maine Coon
American Shorthair

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76
Q

Discuess the pathophysiology of hypertrophic cardiomyopathy in cats.

A

Its typically a symmetric hypertrophy of the left ventricular free wall and interventricular septum, although asymmetric hypertrophy can occur.

Hypertrophy causes diastolic dysfunction including decreased cardiac output (tachycardia, poor pulses, cold extremities), and left sided congestion (LA enlargement, pulmonary oedema, pleural effusion).

Systolic anterior motion of the mitral valve is common.

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77
Q

Describe the expected physical examination findings of hypertrophic cardiomyopathy.

A

+/- murmur - parasternal usually, not consistently present
+/- gallop rhythm
LSCHF - tachypnoea, laboured breathing, pulmonary oedema (crackles), pleural effusion (dull lung sounds ventrally, paradoxical breathing pattern)
Dec. CO signs - tachycardia, cold extremities, weak pulses, hypothermia
Arrhythmias
Aortic thromboembolism

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78
Q

Discuss which ancilliary testing we should do for idiopathic HCM in cats and the expected findings.

A

ECHO - increased wall thickness either generalised and focal, LA enlargement, assess LV outflow tract

Exclude secondary HCM - hypertension (measure SBP) and hyperthyroidism (total T4 concentration)

Thoracic radiography - cardiomegaly, Valentine heart shape (enlarged LA and left auricle cause bulge, apex shift to midline), CHF signs (pleural effusion, pulmonary oedema)

ECG - supraventricular or ventricular ectopic complexes

NT-proBNP cardiac biomarker - will be present

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79
Q

Explain the treatment of hypertrophic cardiomyopathy (HCM) in cats with severe, acute CHF.

A

Do minimal examination and allow them to calm and settle in a quiet room with no dogs, provide oxygen if its not going to stress them out more, can give butorphanol to help calm them.

If in stage B1 - no treatment

If in stage B2 - clopidogrel to try and minimise the risk of ATE (could also use aspirin or low MW heparin), treat arrhythmias if necessary

If in stage C - rest in stress-free environment, oxygen supplementation, furosemide, free access to water + monitor electrolytes, thoracocentesis if due to pleural effusion, sedation with butorphanol, pimobendan +/- dobutamine

To go home - lowest possible dose of furosemide, clopidogrel, pimobendan, can prescribe beta blockers but not if heart failure is present

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80
Q

Discuss the clinical signs, diagnosis, and treatment of dilated cardiomyopathy in cats.

A

Cx - congestive heart failure signs, retinal degeneration if because of taurine deficiency

Dx - ECHO, dietary history, plasma taurine

Tx - give taurine if deficient, pimobendan, heart failure treatment as normal

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81
Q

Explain the expected echocardiography findings for a cat with restrictive cardiomyopathy.

A

Diastolic dysfunction
Absence of hypertrophy of myocardium
Moderate to marked LA or bilateral dilation
Hyperechoic wall segments may indicate fibrosis

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82
Q

What are the risk factors for developing aortic thromboembolism (ATE)?

A

Any feline cardiomyopathies
Enlarged left atrium is a risk factor
May identify sluggish blood flow in the left atrium
May identify thrombus within the left atrium

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83
Q

What are the differentials for sudden onset hind limb paralysis in cats?

A

Aortic thromboembolism (ATE)
Snake envenomation
Trauma
IV disc disease
Spinal lymphoma
Fibrocartilagenous emboli

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84
Q

What is the most common site of thromboembolism in ATE?

A

Aortic trifurcation/iliac arteries (90%)

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85
Q

List the clinical signs of a cat with aortic thromboembolism (ATE).

A

Depends on the site of thromboembolism

Pain
Cardiac disease signs
Hypothermia
Cold extremities
Absent pulses
Cyanosis of pads and nail beds
Muscles may be painful, firm + swollen
Decreased cutaneous sensation and limb reflexes
Loss of motor function

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86
Q

How do we diagnose aortic thromboembolism in a cat?

A

Consistent clinical signs

Blood biochemistry - inc. AST and CK, stress hyperglycaemia, metabolic acidosis, azotaemia, hyperkalaemia

Peripheral vs central blood glucose - low glucose in affected limb

ECHO + colour flow Doppler of the aorta may be used to identify thrombus

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87
Q

Discuss the treatment of aortic thromboembolism in cats.

A

Supportive - analgesia, treat underlying heart condition, cage rest, IVFT, monitor electrolytes, monitor azotaemia

Thrombolytic therapy - streptokinase, tissue plasminogen activator

Prevent further clot formation - clopidogrel, low MW heparin, aspirin, oral factor Xa inhibitors (rivaroxaban)

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88
Q

Describe the typical innocent murmur.

A

Systolic, low grade (1-2/6)
Audibility varies with HR, body position, exercise, stress
Usually audible at the left sternal border, basal
Does not radiate
Confined to early or mid systole
Usually disappears by the age of 4-6 months old

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89
Q

What are the red flags in juvenile murmurs?

A

Late systolic, pansystolic, holosystolic, diastolic or continuous
Loud murmur (>3/6)
Apical or right sided murmur
Murmur radiates
Persistence of the murmur beyond 6 months of age
Additional signs of cardiovascular dysfunction - cyanosis, poor pulse quality, dyspnoea

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90
Q

Name the 3 most common congenital cardiac defects in dogs.

A

Patent ductus arteriosus
Pulmonic stenosis
Aortic stenosis

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91
Q

Name the 2 most common congenital cardiac defects in cats.

A

AV dysplasia
Ventricular septal defects

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92
Q

List the expected physical examination findings of a dog with PDA.

A

If LEFT to RIGHT shunt - continuous or machinery murmur left base, widened pulse pressure, precordial thrill common left heart base, LSCHF may occur

If RIGHT to LEFT shunt (rare) - cyanosis of caudal part of the body, erythrocytosis, loss of murmur

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93
Q

How do we diagnose congenital heart diseases?

A

Echocardiogram
Thoracic radiography

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94
Q

List the expected clinical signs of a ventricular septal defect (VSD).

A

Murmur on right parasternal edge, loud with small to moderate sized defects, soft with large defects
LSCHF common though right sided can occur
Cyanosis

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95
Q

What types of stenosis are there and what breeds are predisposed?

A

Pulmonic stenosis - valvular, subvalvular, supravalvular: English bulldog, Boxers, Beagles

Aortic/subaortic stenosis: Newfoundlands, Golen retrievers, Boxers

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96
Q

List the clinical signs of pulmonic stenosis.

A

Ejection murmur left heart base
Exertional fatigue
Weakness
Syncope
Pulse strength often fair
RSCHF signs - ascites

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97
Q

What is the treatment for pulmonic stenosis?

A

Balloon dilation/valvuloplasty
Surgery

98
Q

List the clinical signs and physical exam findings associated with subaortic stenosis.

A

Murmur - harsh systolic ejection murmur at left heart base
May be precordial thrill LH base
Weak pulses, low sysolic blood pressure
Exertional syncope + sudden death - reduced cardiac output, peripheral vasodilation, arrhythmias

99
Q

How do we treat subaortic stenosis?

A

Exercise restriction and beta blockers
Surgery/balloon dilation
Increased risk of endocarditis, antibiotics if anticipate bacteraemia

100
Q

Describe the expected echocardiographic changes associated with mitral valve dysplasia.

A

Valve leaflets focally or diffuselt thickened
Valve leaflets may be absent
Chordae tendineae may be short or absent
Valve leaflets may be displaced from normal position

101
Q

Why do arrhythmias develop?

A
  1. Abnormal impulse formation - enhanced normal automaticity, depressed normal automaticity, abnormal automaticity
  2. Abnormal impulse propagation - conduction delays or blocks, extrafunctional or anatomical circuits
102
Q

Why do arrhythmias develop?

A

Hypoxaemia
Ischaemia
High catecholamine concentrations
Electrolyte imbalances

103
Q

Discuss the clinical consequences of arrhythmias.

A

May reduce cardiac output
Exercise intolerance/weakness
Syncope
Death

104
Q

Describe how to differentiate between a supraventricular premature complex and ventricular premature complex.

A

SVPC - abnormal P wave direction, normal QRS complexes
VPC - no P wave, wide and bizarre QRS complexes

105
Q

What is an ECG rhythm called if it is not sinus?

A

Ectopic

106
Q

What are the 4 types of sinus rhythms?

A

Normal sinus rhythm
Sinus bradycardia
Sinus tachycardia
Sinus arrhythmia

107
Q

Describe the approach to cardiac arrhythmias.

A
  1. Identify the arrhythmia
  2. Is it indicative of a serious underlying cardiac disease?
  3. Is it indicative of a serious underlying systemic disease?
  4. Is the arrhythmia a premonitory sign of a worse, more life threatening rhythm disturbance?
  5. Is the arrhythmia compromising cardiovascular function?
  6. Do we need to treat the arrhythmia?
108
Q

What is the normal rate of depolarisation from the SA node in a dog?

A

60-80 depolarisations per minute

109
Q

List 3 cardiac causes of supraventricular arrhythmias.

A

Mitral valve/tricuspid valve endocardiosis
Dilated cardiomyopathy
Cardiac neoplasia
Congenital malformation
High SNS tone
Digoxin administration

110
Q

List 3 cardiac causes of ventricular arrhythmias.

A

Dilated cardiomyopathy
Myocarditis
Pericarditis
Myocardial fibrosis
Myocardial ischaemia
Myocardial trauma
Cardiac neoplasia
Heartworm/Dirofilariasis
Congenital disease
Mechanical stimulation

111
Q

List 3 extra-cardiac causes of supraventricular arrhythmias.

A

Catecholamines
Electrolyte abnormalities
Acidosis/alkalosis
Hypoxia
Thyrotoxicosis
Severe anaemia
Thoracic surgery
Electrocution

112
Q

List 3 extra-cardiac causes of ventricular arrhythmias.

A

Hypoxia
Electrolyte abnormalities
Acidosis/alkalosis
Thyrotoxicosis
Hypothermia
Fever, sepsis, toxaemia
Trauma
GDV
Splenic disease
Pulmonary disease
Uraemia
Pancreatitis
Pheochromocytoma
CNS disease

113
Q

What are the steps in interpreting an ECG?

A
  1. Are P and QRS complexes identifiable?
  2. Determine the rate and rhythm
  3. Is there a P for every QRS? - if yes then its a sinus rhythm, if no then its ectopic

IF SINUS - is there a QRS for every P wave? - if no then it’s heart block

IF ECTOPIC - is intermittent or sustained?
If intermittent - is it premature or escape? Supraventricular or ventricular?
If sustained - is it supra ventricular or ventricular? Escape or tachycardia?

114
Q

What is the main differential for supraventricular tachyarrhythmias? What are the causes?

A

Main DDX: sinus tachycardia
Causes - anaemia, hypovolaemia, CHF, pain, stress

115
Q

Where do supraventricular tachyarrhythmias arise?

A

Atrial or junctional (AV node) - they arise above the bundle of His

116
Q

When and how do we treat supraventricular tachycardia?

A

Treat when its overly fast (>220bpm), persistent and appears to be contributing to clinical signs

Treat with vagal manoeuvres to ensure its not sinus, and then go for drugs (digoxin + beta blockers (not in a pt with heart failure), or calcium channel blockers)

117
Q

Explain what a vagal manoeuvre is and how its used.

A

Either carotid vessel massage or pressure on the eyes should increase parasympathic nervous system tone and slow the heart rate down if its sinus.
We can use it to tell if an arrhythmia is sinus or not.

117
Q

What am I? (ARRHYTHMIA EDITION)
ECG - irregularly irregular RR interval, no P waves, variable R wave height but normal QRS
Auscultation - like a tennis ball in a clothes dryer, very chaotic

A

Atrial fibrillation

118
Q

Describe the treatment for atrial fibrillation.

A

Slow the heart rate
Drugs - digozin, beta blockers, diltiazem
Concurrently treat the underlying heart failure if present

119
Q

Why do you need to be careful about using beta blockers and diltiazem to treat supraventricular tachycardia in animals with heart failure?

A

As they are negative chronotropes and inotropes they decrease the rate and force of contraction of the heart - if the animal is in heart failure you can cause decompensation and death unless you are certain the arrhythmia is what’s causing the heart failure.

120
Q

Describe the QRS complexes of ventricular tachycardia (VT).

A

Wide and bizarre

121
Q

What indicates a need for treatment for ventricular tachycardia or ventricular premature complexes?

A

Evidence of compromised CO
Fast underlying HR - >180bpm in dogs, >240bpm in cats
No identifiable or treatable underlying causes
Multiform foci - more generalised disease of the myocardium
Rhythm disturbance is frequent or sustained
R on T phenomenon is present on ECG

122
Q

Describe the acute and chronic medical treatment of ventricular tachycardia and ventricular premature complexes.

A

ACUTE
Lidocaine
Magnesium - either chloride or sulphate salt
Sotalol - oral, works in 20-30 mins, beta blocker with activity against K channels

CHRONIC
Sotalol +/- mexiletine
Amiodarone

123
Q

What 3 arrhythmias should you NEVER treat and why?

A
  1. Escape complexes/rhythms - supraventricular (junctional) escape rhythm, ventricular escape rhythm: it may be whats keeping the animal alive, so suppressing it is fatal
  2. Accelerated idioventricular rhythm: its due to high vagal tone and there should still be sufficient ventricular filling between beats
124
Q

How do you tell if you are dealing with supraventricular or ventricular tachycardia and not an escape rhythm?

A

The rate of depolarisation.
If from the AV node it will be 40-60/min, whereas if its an escape rhythm its been generated by Purkinje fibres and will be much slower, closer to 20-40/min

125
Q

What treatment do I need?:
On ECG I have no P or T waves or QRS complexes, and there is irregular, chaotic movement of the baseline and all the leads are definitely attached.

A

Defibrillation
Its ventricular fibrillation

126
Q

At what rate is a rhythm considered a bradyarrhythmia in a dog and cat?

A

Dogs - <60bpm
Cats - <90bpm

127
Q

List the common clinical signs of bradyarrhythmia.

A

Lethargy, reduced activity, fatigue, exercise intolerance, episodic weakness or disorientation, collapse or syncope

128
Q

List 3 causes of vagally mediated bradycardia.

A

Chronic respiratory disease
GIT disease
Hypothyroidism
Drug administration - digoxin, medetomidine
Ocular or retrobulbar disease
CNS disease

129
Q

Describe the ECG features of atrial standstill caused by hyperkalaemia, what causes it, and how to treat it.

A

ECG features - bradycardia, absence of P waves, very peaked and tall T waves, “escape” rhythm, changes roughly correlate with severity of hyperkalaemia

Causes - cats with urethral obstruction, dogs with acute hypoadrenocorticism, dogs or cats with acute renal failure

Treatment - treat cause (e.g. mineralocorticoid replacement if addisons), glucose + insulin to drive potassium into cells to reduce hyperkalaemia, calcium gluconate (same sort of thing)

130
Q

Name and differentiate the types of atrioventricular block.

A

1st degree - prolonged PR interval
2nd degree - intermittent AV conduction
3rd degree - complete block + emergence of superimposed ventricular escape rhythm

131
Q

What diagnostic tests can we do for bradyarrhythmias?

A

Atropine response test
Exclusion of hyperkalaemia

132
Q

Explain what sick sinus syndrome is and what breeds are predisposed?

A

Instability of the SA node leading to an unpredictable sinus rhythm - alternating bradycardia and supraventricular tachycardia
Miniature schnauzer, west highland white terriers are predisposed

133
Q

Describe the treatment for sick sinus syndrome.

A

Propantheline or propentofylline
Pacemaker implantation

134
Q

Explain the pathophysiology of parvovirus.

A

Virus is transmitted from the environment, either horizontally or vertically to the host
Virus enters the oronasal cavity, infects lymphoid tissue –> 1-5d of viraemia
Affects the rapidly dividing cells of the GI tract, especially crypt epithelial cells causing villus blunting
–> dec. absorption –> diarrhoea
–> necrosis –> sloughing + blood
–> inflammation
= PROFUSE SMALL INTESTINAL HAEMORRHAGIC DIARRHOEA
Lack of GI integrity can lead to bacteraemia and sepsis

135
Q

Describe the infectivity of parvovirus.

A

Shedding in faeces 3-14d post-infection
Clinical signs develop 5-12d post-infection
There is an asymptomatic period where they still shed virus

136
Q

List the clinical signs of parvovirus.

A

Foul smelling, bloody diarrhoea + vomiting
Leukopaenia + fever
+/- sepsis –> DIC
+/- brain or spinal cord haemorrhage
+/- myocarditis (if its a puppy infected in utero)
+/- intention tremors, ataxia (if its a kitten infected in utero)

137
Q

How do we diagnose parvovirus?

A

Clinical signs
Vaccination history - usually incomplete
ELISA
PCR
Serology

138
Q

Describe the treatment for parvovirus.

A

IVFT - correct the dehydration + monitor electrolytes
Monitor potassium, glucose and albumin - correct if needed, may require plasma for hypoalbuminaemia, and may become anaemic and require blood transfusion
Monitor white cell counts regularly - leukopaenia is going to drastically decrease their chance of beating sepsis
IV aminopenicillins - ampicillin or amoxycillin to treat bacteraemia
Maropitant to lessen abdominal pain and nausea
Place an NG or NO tube - feeding early is important
Palpate for intussusception daily
+/- Passive immune therapy + viral drugs

139
Q

What are the infectious agents of canine infectious tracheobronchitis?

A

Bordetella bronchiseptica, Mycoplasma, canine parainfluenza virus

140
Q

List the clinical signs of canine infectious tracheobronchitis.

A

Paroxysmal cough + terminal retch in an otherwise active, healthy dog
Honking cough exacerbated by exercise of excitement, may or may not be productive
Pyrexia
Anorexia
Lethargy
Submandibular lymphadenopathy
Oropharyngeal erythema
Positive tracheal pinch test
Less common - progression to pneumonia, ocular + nasal discharge, respiratory distress

141
Q

Explain the treatment for an uncomplicated case of canine infectious tracheobronchitis.

A

Rest, isolate from other dogs, soft food diet
Consider doxycycline (7-10d course) but only if clinical signs last 7-10d (persistent cough)

142
Q

What additional treatment is required for a complicated case of canine infectious tracheobronchitis?

A

IV antimicrobials - amoxicillin + enrofloxacin to start but guide with C&S
IVFT
Nebulisation
Supportive care
Thoracic rads - antitussives if the chest is clear
Endo-tracheal wash

143
Q

Name the vector for Ehrlichia canis.

A

Rhipicephalus sanguineus (Brown Dog Tick)

144
Q

List the clinical signs of Ehrlichia canis.

A

Pyrexia, lethargy, thrombocytopaenia, anorexia, myalgia, lymphadenopathy, bleeding diatheses

145
Q

Which diagnostic tests would be appropriate for diagnosing Ehrlichia canis?

A

Platelet count, PCV, buccal mucosal bleeding time
PCR
Antibody serology

146
Q

Describe the treatment for Ehrlichia canis.

A

Doxycycline 5mg/kg PO q12h or 10mg/kg PO q24h for 28 days
Imidocarb diproprionate 5mg/kg SC injection 14 days apart

147
Q

An unvaccinated dog in NSW presents with lethargy, vomiting, diarrhoea, and icterus. After taking a blood and urine sample you find azotaemia, hyperbilirubinaemia and glucosuria. What are you most suspicious of?

A

Leptospirosis

148
Q

Discuss the testing options for heartworm.

A

ANTIGEN TEST - detects proteins from adult females, variable sensitivities and specificities, capable of detecting most occult infections (adult worms present but no circulating mff), firstline test in Aus

MICROFILARIEA DETECTION TEST, MODIFIED KNOTT TEST - detection + identification of circulating mff >6-7 months post infection, some infections might be amicrofilaraemic

PCR - detects mff DNA, not commercially available in WA

149
Q

Explain prophylaxis and testing requirements for heartworm in dogs.

A

If the puppy is younger than 2 months old - start prophylaxis, don’t need to test
Dogs aged 2-7 months - start prophylaxis but test for antigens and mff 6 months later
Dogs >7 months old - test for Ag and mff before you start prophylaxis, retest 6 months later

For cases of non-compliance - test 6 months after the lapse of prophy

150
Q

Explain the interpretation of a false negative Ag test for heartworm.

A

Low numbers of worms, only male worms are present, female worms are too immature, poor test sensitivity, poor test technique

151
Q

Explain the interpretation of a false positive antigen test for heartworm.

A

Specificity is less than 100% for the test, more likely when local prevalence is low

152
Q

Explain the next step in testing when a heart worm antigen test comes back positive.

A

Repeat the antigen test (possibly a different brand) and perform a Knott’s test

153
Q

What is the next step for an asymptomatic dog with a positive heartworm antigen test and a negative Knott’s test?

A

Start prophylaxis

154
Q

What is the next step for an asymptomatic dog with a negative heartworm antigen test and a positive Knott’s test?

A

Identify microfilaria, they may be Acanthocheilonema instead of Dirofilaria

155
Q

What is the next step for a dog with a positive heartworm antigen test and a positive Knott’s test?

A

Start heartworm treatment

156
Q

What drugs are available for use as heartworm prophylaxis?

A

Milbemycin, ivermectin, moxidectin, selamectin

157
Q

What is the prevalence of heartworm infection in cats compared to dogs?

A

10%

158
Q

List the clinical signs of heartworm disease in cats.

A

Dyspnoea, wheezing, vomiting, neurological signs, sudden death, respiratory signs

159
Q

Which diseases are included in Feline Upper Respiratory Disease?

A

Feline herpesvirus (FHV-1)
Feline calicivirus (FCV)
Chlamydia felis

160
Q

List the clinical signs of feline herpesvirus (FHV-1).

A

Lethargy, fever, sneezing, ocular discharge, nasal discharge
+/- conjunctivitis, oral ulceration, keratitis, corneal ulceration

161
Q

List the clinical signs of feline calicivirus (FCV).

A

Oral ulceration
+/- lethargy, fever, sneezing, conjunctivitis, ocular or nasal discharge, lameness

162
Q

List the clinical signs of Chlamydia felis infection in a cat.

A

Conjunctivitis + chemosis, ocular discharge
+/- nasal discharge, lethargy, fever, sneezing

163
Q

Explain the diagnostic testing for cat flu.

A

PCR testing of a oropharyngeal or conjunctival swab - may be sensitive if they are shedding the virus but is also found in healthy cats, has low predictive value

164
Q

Describe the treatment of a cat with Chlamydia felis.

A

Doxycycline 5-10mg/kg BID 3-4 weeks
Enrofloxacin 5mg/kg SID 3-4 weeks

165
Q

Describe the treatment for a cat with viral rhinitis.

A

Not curative but will lessen Cx
Famiciclovir 125mg PO q8-12h - safe for long-term
Topical cidofovir BID
Lysine 250-500mg PO SID may help for FHV-1
Human alpha2b interferon 50U PO daily or topical interferon (conjunctival) may help
Judicious use of antibiotics if secondary bacterial infection present - amoxycillin, amoxyclav, doxycycline

166
Q

What additional treatment does a very sick cat with viral rhinitis need?

A

Hospitalisation
NO or NG tube to feed
Warm feed up and syringe feed otherwise - soft, aromatic baby foods
Mirtazapine - to stimulate appetite
+/- IVFT
Clean secretions - good nursing
Nebulising with NaCl steam
+/- 0.9% NaCl nasal drops if cat is compliant
Mycolytic drugs may help break up thick nasal secretionsn - bromhezine hydrochloride

167
Q

What is the prevalence of feline leukaemia virus in Australia?

A

1-4%

168
Q

Discuss the 3 possible outcomes for FeLV infection.

A

ABORTIVE INFECTION (tonsils) - virus is eliminated before it spreads, lifelong protection against infection, happens in 30-40% of cases (old more likely), may test +ve in first 1-2 weeks then test negative on POC test

PROGRESSIVE INFECTION (blood) - spread + viraemia, death within a few years due to haematopoetic neoplasia, bone marrow suppression + refractory or opportunistic infections, persistent +ve result on POC test, 30-40% of cats (young more likely)

REGRESSIVE INFECTION (bone marrow) - spread + transient viraemia (2-8 weeks) but persistence of virus in body cells with rare cases of bone marrow suppression –> lymphoma or virus reactivation, test positive for first 2-8 weeks, then may be + or - on POC test and PCR, will have FeLV Abs

169
Q

What is the POC test?

A

= Point of Care test
Used for FeLV diagnosis - tests for p27 antigen
Witness test has the highest NPV and PPV

170
Q

What are the common outcomes for FeLV cases?

A

Poor prognosis for FeLV positive lymphoma cases
Persistent infected cats often have weight loss, pyrexia, anaemia, rhinitis, D+, lymphadenopathy and die in 2-3 years

171
Q

How is feline immunodeficiency virus transmitted?

A

Cat bite and fight wounds most of the time
Highest concentration of viral particles in blood and saliva

172
Q

Describe the phases of FIV infection.

A

PRIMARY (viraemic) - malaise, may have lymphadenopathy, lasts weeks to months

SECONDARY (asymptomatic) - limited viral replication, can last years, some cats never make it to stage 3 + die from other things

TERTIARY (terminal) - viral replication increases, clinical disease, lymphoma, opportunistic infections, gingivostomatitis, occasional immune mediated diseases

173
Q

Describe the pathophysiology of feline infectious peritonitis (FIP).

A

Infection with feline coronavirus (FCoV) by faecal-oral route
In 10% of FCoV infected cats the virus mutates to cause FIP - usually due to stress, breed, genetics + host immune system
Causes an immune mediated reaction –> granulomas (ocular + neuro signs) and/or vasculitis (ascites, pleural or pericardial effusion)

174
Q

How can we diagnose FIP?

A

FCoV antibody test
Clinical suspicion of FIP - Cx (pyrexia)
CBC + biochem - lymphopaenia, hyperglobulinaemia (low A:G ratio), may have inc. liver enzymes, kidney enzymes
Immunocytochemistry or immunofluorescence
Mutation PCR on effusion samples
IHC of organ biopsies (usually PM)

175
Q

Describe the treatment of toxoplasmosis in cats.

A

Clindamycin BID 4 week course

176
Q

How is toxoplasmosis transmitted?

A

Ingestion of sporulated oocysts from faeces or tissue cysts (meat), via placenta or milk, or via contaminated water or food sources
Rodents intermediate host
ZOONOTIC

177
Q

How do we diagnose toxoplasmosis in cats?

A

Serology LCAT - repeat in 4 weeks to assess for rising titres
Presence of Cx

178
Q

What is the typical signalment for laryngeal paralysis in dogs?

A

Older large breed dogs - Labrador

179
Q

What is the typical signalment for collapsing trachea in dogs?

A

Older small breed dogs - Yorkie, Pomeranian

180
Q

What is the typical signalment for idiopathic pulmonary fibrosis in dogs?

A

Older West Highland White Terriers or Staffordshire Bull Terriers

181
Q

What sort of history is important when working up a case with respiratory signs?

A

Precise description of what the animal is doing - try to get the owners to take videos if possible
Any in contact animals
Recent kennelling
Are they kept indoor or outdoor or both?
Vaccination and prophy status
Duration and progression of clinical signs
Any exacerbating factors? - i.e. exercise, excitement

182
Q

Explain the difference between a cough and expiration reflex.

A

A cough is a reflex used to clear material from the lower airways, and requires stimulation of cough receptors, deep inhalation then contraction of respiratory muscles against a closed glottis, then rapid expiration.

An expiration reflex is similar except that there is no inspiratory phase before the cough. This usually occurs when there is laryngeal irritation, as it is counter productive to suck material further down into the airways.

183
Q

Describe postural breathing.

A

Mouth open
Neck extended
Elbows abducted
Reluctance or inability to lie down

184
Q

Explain the difference between stridor and stertor.

A

Both are inspiratory.
Stertor - nasal passages, disappears when mouth breathing
Stridor - laryngeal, present when mouth breathing

185
Q

Name and describe the different categories of breathing pattern.

A

Normal - 1:1-1:2 inspiratory to expiratory ratio, chest wall + abdominal wall move in unison, 10-30 breaths per min.

Restrictive - shallow rapid respiration without exaggeration of the inspiratory or expiratory component, may be panting.

Insipiratory Obstructive - inc. duration of inspiration, often loud inspiratory noise

Expiratory Obstructive - inc. duration of expiration, associated with effort, occasional externally audible noise, wheeze often audible by stethoscope

Insp + Exp Obstructive - inc. duration of both inspiration + expiration, often with associated effort + noise, fixed obstruction

Paradoxical - movement of the chest or flanks in the opposite direction to what is expected, marked inspiratory effort causes the diaphragm to be pulled up and abdomen pulled in

186
Q

Differentiate between wheezes and crackles.

A

Wheezes - expiratory, air flowing through narrow airways
Crackles - inspiratory, popping open of small ariways and alveoli

187
Q

What is a transtracheal wash and when do we do it?

A

Insert a needle into the proximal trachea + feed a small catheter through it to push saline in to the larger airways.
It can be done awake or sedated and in unstable patients but can be difficult unless its very quiet.

188
Q

What are the advantages of doing a bronchoalveolar lavage over a transtracheal wash?

A

Samples smaller airways and alveoli
Can do blind or endoscope-guided so you can decide where you want to sample from - makes it more likely that you can get useful information from the testing
Less stressful for the dog as is done under GA

189
Q

Explain the difference between hypoxaemia and hypoventilation.

A

Hypoxaemia = dec. arterial partial pressure of oxygen
Hypoventilation = dec. excretion of carbon dioxide –> inc. arterial partial pressure of carbon dioxide

190
Q

What are the 3 causes of hypoxaemia?

A
  1. Decreased inspired oxygen concentration
  2. Decreased ventilation - due to upper airway obstruction, pleural effusion, diaphragmatic hernia, neuromuscular disorders, etc.
  3. Venous admixture - ventilation/perfusion mismatch, anatomic shunts, diffusion defect
191
Q

Describe how we can assess hypoxaemia in a patient.

A

Physical exam - mucous membranes pale to cyanotic, tachycardia
Arterial blood gas analysis on a sample from a peripheral artery - assess PaO2
Haemoglobin saturation - either using pulse oximetry or haemoximeter

192
Q

What are the potential causes of hypoventilation?

A

Neurological
Chest wall muscular disease - including exhaustion
Upper airway obstruction
Compression - i.e. pleural space disease or abdominal distention

193
Q

When should we be giving oxygen?

A

Shock
Decreased oxygen content - PAaO2 <80mmHg, SpO2 <95%, clinical signs of anaemia
Pale or cyanotic mucous membrane colour
Increased respiratory effort/dyspnoea

194
Q

In a respiratory disease context - when should we intubate?

A

When there is low PaO2 despite oxygen supplementation + other appropriate therapies for the individual context
PaO2 <60mmHg
SpO2 <90%
High PaCO2 >60mmHg - will need to ventilate for them
Increased work of breathing + distress due to developing respiratory fatigue
Upper airway obstruction not relieved by cooling + sedation

195
Q

Discuss the risks of intubation in a patient in respiratry distress.

A

Shock, heat stroke, congestive heart failure, hypoxaemia, acidosis
Oxygen toxicity
Ventilation induced lung injury - stretch injury, shear injury, infection, inflammation, micro-aspiration, effects of long GA

196
Q

What history and clinical signs localise to the nasal cavity or nasopharynx?

A

Sneezing and reverse sneezing
Nasal discharge
Stertor
Pain + head shyness
Facial deformity
Neurological signs
Decreased appetite + dysphagia

197
Q

Describe the physical examination findings and tests you would like to do if you suspected disease in the nasal cavity or nasopharynx.

A

Complete physical exam - of course
Check for discharge, pigment changes, patency of nostrils, odour
Examine the mouth and palpate local lymph node

198
Q

Which 4 criteria would make you investigate further if you had a patient come in with clinical signs localising to the nasal cavity or nasopharynx?

A

Systemic cause suspected
Chronic signs
Severe haemorrhage, pain, anaemia
Suspicion of foreign body

199
Q

List 3 systemic differentials of disease localising to the nasal cavity or nasopharynx.

A

Coagulopathy
Hyperviscosity
Hypertension
Systemic vasculitis
Systemic infection

200
Q

Describe the haematological, biochemistry and urinalysis changes you might see in nasal cavity or nasopharyngeal disease, and what they might indicate.

A

Anaemia - if the animal is still bleeding
Neutrophilia +/- toxic changes - severe bacterial infection
Thrombocytopaenia - primary haemostatic disorders, coagulopathy
Hyperviscosity - can be a cause of haemorrhage, so might also be seeing anaemia
Hyperglobulinaemia - plasma cell tumours (multiple myeloma) or Erlichia
Erythrocytosis - could be pathological or due to hypoxia
Haematuria or proteinuria - might suggest other organ involvement, so a systemic disease more likely

201
Q

A dog comes in with epistaxis. What testing would you like to do to investigate?

A

CBC - checking for anaemia, thrombocytopaenia
Blood smear - to check for clumping and confirm thrombocytopaenia
Coagulation testing - buccal mucosal bleeding time (BMBT) for platelet function (bleeding should stop within 5 minutes), PT, PTT, ROTEM, angiostrongylus testing
Could do cryptococcal antigen testing or aspergillus serology
CT (better than rads) - assess cribriform plate, brain, orbit, alveolar bone, locate subtle lesions
Endoscopy - good for foreign bodies and masses, stenosis
Biopsy - pinch biopsy (blind or endoscopic), core biopsy if mass –> histopathology + culture (mainly fungal)

202
Q

List 3 infectious disease causes of nasal cavity or nasopharyngeal disease.

A

Sinonasal aspergillosis
Cryptococcosis
Bacterial rhinitis
Parasitic rhinitis
Paediatric feline upper respiratory tract

203
Q

Describe the clinical signs and how we diagnose sinonasal aspergillosis in dogs.

A

Mucopurulent blood-tinged discharge - unilateral then bilateral
Pain + head shyness
Depigmentation of nares
Potentially nervous signs

Diagnosis by CT, rhinoscopy, biopsy, culture of Aspergillus fumigatus (commonly)

204
Q

How do we treat sinonasal aspergillosis?

A

Rhinoscopic debridement
Local therapy - 1 hour GA, clotrimazole or enilconazole +/- frontal sinus trephination

205
Q

Name the 2 causative agents of cryptococcosis.

A

Cryptococcus neoformans
Cryptococcus gattii

206
Q

Differentiate the clinical signs of cryptococcosis in dogs and cats.

A

Dogs - rhinosinusitis may be subclinical +/- CNS signs +/- GI signs

Cats - upper respiratory signs, local LN enlargement, skin lesions, facial deformity, optic neuritis, chorioretinitis

207
Q

Explain how we diagnose cryptococcosis.

A

Cytology of nasal discharge or FNA
Latex cyptococcal antigen test (LCAT) - done with serum
Histopathology
Fungal culture can differentiate causative species

208
Q

How do we treat cryptococcosis?

A

Long term fluconzaole
Treat until antigen titre is zero

209
Q

Discuss the treatment principles for bacterial rhinitis.

A

Symptomatic treatment of infection
Broad spectrum first line antibiotics
Nursing care
Treat underlying cause

210
Q

A dog presents with acute onset sneezing and serous nasal discharge. What is your major differential diagnosis and how do you want to proceed?

A

DDx - nasal foreign body

Do a physical exam and attempt nasal cavity examination, CT, then endoscope.

211
Q

A middle aged Dachshund presents with sneezing and chronic bilateral mucopurulent nasal discharge. List 3 differentials.

A

Foreign body
Nasal cavity neoplasia
Bacterial rhinitis
Idiopathic lymphoplasmacytic rhinitis

212
Q

You undergo diagnostic testing for a Daschund with sneezing and chronic mucopurulent bilateral nasal discharge. Biopsy results confirm idiopathic lymphoplasmacytic rhinitis. How do we treat?

A

Doxycycline + NSAIDs
Avoid irritants

213
Q

A cat presents with mucopurulent nasal discharge, sneezing, stertorous breathing, gagging, and a head tilt. On further examination there is miosis, ptosis, enopthalmos and nictitating membrane prolapse + hyperaemia. What is your main differential?

A

Feline nasopharyngeal polyps

214
Q

What are the main types of nasal neoplasia that dogs and cats get?

A

Dogs - adenocarcinoma, squamous cell carcinoma, sarcoma
Cats - adenocarcinoma, lymphoma, sarcoma

215
Q

Describe the clinical signs and diagnosis of nasal neoplasia.

A

Nasal discharge, epistaxis, stertor, facial pain, facial deformity, ocular discharge, CNS signs

Diagnose by direct nasal investigation, CT, biopsy

216
Q

Which clinical signs localise to the larynx?

A

Stridor
Cough, expiration reflex
Inspiratory obstructive breathing pattern

217
Q

Which clinical signs localise to the trachea?

A

Cough (+/- tracheal pinch)
Obstructive breathing pattern - inspiratory, expiratory or both

218
Q

Which clinical signs localise to the bronchi?

A

Cough
Expiratory obstructive breathing pattern
+/- wheezes - high pitched (sibilant), low pitched (sonorous)

219
Q

A dog comes in and you’re super smart and have localised the problem to the larynx. What diagnostic testing do you want to do?

A

Upper airway examination, direct evaluation
Fluoroscopy
Rads or CT
Endoscopy
Sampling for culture, cytology or histopathology - cytology brush, FNA, biopsy

220
Q

You’ve localised clinical signs to the trachea or bronchi. What diagnostic testing do you want to do?

A

Rads
CT
Fluoroscopy
Endoscopy
Sampling for culture, cytology, and histopathology - transtracheal wash, bronchoalveolar lavage, cytology brush, biopsy

221
Q

What are the characteristics of brachycephalic obstructive airway syndrome (BOAS)?

A

Brachycephalic breed - Bulldog, pug, etc.
Stenotic nares
Elongated soft palate
Tracheal hypoplasia
Eversion of laryngeal saccules
Laryngeal collapse
Enlarged palatine tonsils
+/- Obesity

222
Q

A French Bulldog presents in respiratory distress with an inspiratory obstructive pattern of dyspnoea, stertor, stridor and hyperthermic. What is the acute medical management for this dog?

A

Calm them down to reduce oxygen demands and severity of the collapse, sedate
Avoid heat, can actively cool them
Oxygen - care not to stress them further or impare ability to ventilate
Control their airways - intubate and ventilate if necessary (can otherwise do tracheostomy if oedema is too severe)
Glucocorticoids - give dexamethasone to reduce swelling

223
Q

Discuss the concurrent disorders associated with BOAS.

A

Hiatal hernia
Delayed oesophageal transit
Gastro-oesophageal reflux
Increased risk of aspiration pneumonia
GI inflammation, IBD changes
Aerodigestive disorder

224
Q

How do we diagnose BOAS?

A

History and signalment
Clinical signs
Upper airway examination
Radiography
For other secondary problems - haematology, biochemistry, radiography, fluoroscopy, endoscopy

225
Q

Discuss the chronic management of a dog or cat with BOAS.

A

Surgery - soft palate resection, rhinoplasty, laryngeal sacculectomy
Decrease weight
Restrict exercise to avoid collapse
Treat concurrent disorders

226
Q

Discuss the aetiology of laryngeal paralysis.

A

Older large breed dogs
Labradors
Idiopathic but suspected neuropathy - concurrent proprioceptive deficits or oesophageal dysmotility

227
Q

List the expected clinical signs of a dog with laryngeal paralysis.

A

Change in bark - becomes more hoarse
Exercise intolerance
Stridor
Coughing
Cyanosis
Syncope
+/- gaggping, dysphagia, proprioceptive deficits

228
Q

A dog is presented to you with signs of laryngeal paralysis. How are you going to acutely manage them and later diagnose the condition?

A

Calm, sedate, avoid heat, oxygen, intubate, glucocorticoids

Diagnose by upper airway examination and then additional tests for concurrent or secondary diseases

229
Q

Discuss the aetiology of tracheal collapse.

A

Dorsoventral collapse of tracheal rings due to decreased glycoprotein and glycosaminoglycan in cartilage.
It’s common in older toy breeds, and associated with obesity, inhaled irritants, and concurrent airway disease.

230
Q

List the clinical signs that would make you suspicious of tracheal collapse.

A

Chronic paroxysmal cough - goose honking, harsh but non-productive
Cyanosis
Syncope
Wheezes and rhonchi
Referred sounds
Concurrent heart disease is common

231
Q

You have a toy poodle come in with a chronic paroxysmal goose-honking cough, cyanosis, wheezes, and referred sounds. Discuss what diagnostic testing you would like to do and what your expected diagnosis is.

A

DDx: tracheal collapse

Tracheobronchoscopy
Thoracic rads - inspiratory and expiratory
Fluoroscopy

232
Q

Explain the chronic management of a dog with tracheal collapse.

A

Weight reduction if obesity is a problem
Treatment of heart disease if at stage B2 or above
Control infections
Avoid inhaled irritants
Use a harness instead of a collar to reduce pressure on trachea on walks
Cough suppresents - butorphanol parenteral or diphenoxylate/atropine or codeine PO
Surgical stent implantation - only in an advanced case that is severely obstructive, will make coughing worse
+/- bronchodilators, glucocorticoids

233
Q

List the clinical signs of chronic bronchitis in a dog.

A

Chronic cough >2 month duration - productive or not
Tachypnoea
Sibilant wheezes
+/- crackles
+/- tracheal pinch test positive

234
Q

Discuss the expected radiographical, bronchoscopy, and BAL findings of a dog with chronic bronchitis.

A

Rads - bronchial pattern, right heart enlargement +/- alveolar component

Bronchoscopy - inflammation, mucous +/- tracheobronchomalacia, bronhiectasis

BAL - neutrophilic or mixed inflammation

235
Q

Describe the treatment plan of a dog chronic bronchitis.

A

Anti-inflammatory drugs
Bronchodilators
Antitussives if the cough is non-productive
Antibiotics if indicated
Nebulisation
Coupage

236
Q

What are the 4 components of feline bronchial disease?

A
  1. Airway inflammation
  2. Hyperresponsiveness
  3. Airway remodelling
  4. Chronic bronchitis
237
Q

List the acute and chronic clinical signs of feline bronchial disease.

A

Acute - severe dyspnoea, open-mouth breathing, tachypnoea, expiratory obstructive pattern +/- cyanosis

Chronic - cough

238
Q

Name 3 differentials for dyspnoea in cats and how to differentiate them.

A
  1. Acute bronchial disease
  2. Pleural effusion
  3. Pulmonary parenchymal disease

Differentiate by breathing pattern, lung sounds, T-FAST

239
Q

Discuss the expected radiographical, bronchoscopy, and BAL cytology findings for a cat with feline bronchial disease.

A

Rads - bronchial pattern, air trapping, atelectasis in right middle lobe, may be unremarkeable

Bronchoscopy - inflammation, some increased mucous, not specific though

BAL - eosinophilic or mixed inflammation, rule out parasites

240
Q

Describe the acute and chronic treatment of feline bronchial disease.

A

Acute - no stress, oxygen, terbutaline IV or IM, inhaled salbutamol, glucocorticoids IV or IM

Chronic - glucocorticoids PO, avoid inhaled irritants, inhaled bronchodilators for acute events at home, additional immunosuppressats, antibiotics if infectious +/- oral bronchodilators, cyproheptadine

241
Q
A

small animals - 614 (1 decks)

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