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SA Disease Yr2 > Exam Revision.. > Flashcards

Exam Revision.. Flashcards

1
Q

Identify 5 causes of Dermatological disease

A
  1. Parasites
  2. Infection
  3. Allergy
  4. Neoplasia
  5. Hormonal imbalance
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2
Q

What is the Aetiology for Atopic Dermatitis?

A
  • Genetic disposition to become sensitive to allergens
  • Have abnormal skin barrier function
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3
Q

What is the Pathophysiology for Atopic Dermatitis?

A
  1. Allergens are proteins that when inhaled or absorbed through skin, resp or GI tract
  2. Causes allergen-specific IgE production
  3. IgE molecules affix to tissue mast cells or basophils
  4. When primed cells encounter specific allergen again
  5. Mast cell degranulation occurs
  6. Resulting in the release of proteolytic enzymes, histamines, bradykins + other vasoactive amines
  7. Leading to inflammation (erythema, oedema + pruritits)
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4
Q

What are the 7 Clinical signs for Atopic Dermatitis?

A
  1. Puritis +++
  2. Inflammation
  3. Lesions
  4. Alopecia
  5. Lichenification
  6. Erythema
  7. Papules
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5
Q

What is Lichenification?

A
  • Thickened + leathery apperance of skin
  • Looks elevated + like elephant skin
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6
Q

What is this?

A

Lichenification

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7
Q

What are the 10 Diagnosis for Atopic Dermatitis?

A
  1. Hx
  2. Clinical signs
  3. Exclusion of other causes (Parasites + Infections)
  4. Examination
  5. Microscopy (Tape, Skin scrape)
  6. Bacterial culture
  7. Fungal culture
  8. Biopsy
  9. Exclusion diet
  10. Intradermal testing
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8
Q

What are the breed dispositions for Atopic Dermatitis?

A
  1. Shar-Pei
  2. Fox Terrier
  3. Golden Retriever
  4. Labrador Retriever
  5. Dalmation
  6. Boxer
  7. Boston Terrier
  8. Lhasa Apso
  9. Scottish Terrier
  10. Shih Tzu
  11. WHWT
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9
Q

At what age are dogs most suspectible to get Atopic Dermatitis?

A

Between 6 months + 3 years old

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10
Q

What 6 areas of the body does Atopic Dermatitis affect?

A
  1. Feet
  2. Face
  3. Ears
  4. Flexural surfaces of front legs
  5. Axillae
  6. Abdomen
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11
Q

What Dermatological disease uses the Favrot’s Criteria?

A

Atopic Dermatitis

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12
Q

What is the Favrot’s criteria?
+
How many are there?

A
  • Critera which a px has to have in order to be diagnosed with AD
  • There is 8 criteria + they are:
    1. Affected ear pinnae (not margins)
    2. Affected front paws
    3. Age of onsent of < 3 years
    4. Chronic or recurrent Yeast infections
    5. Corticosteriod-responsive pruritis
    6. Mostly indoor lifestyle
    7. Non-affected dorsolumbar area
    8. Pruritis w/o skin lesion at onset
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13
Q

What are the treatment options for Atopic Dermatitis?

A
  1. Treat cause
  2. Systemic or topical tx
  3. Antibiotics
  4. Steroids
  5. Antifungals
  6. Antihistamines
  7. Parasiticides

Other:
1. Hormone treatment
2. Exclusion diet
3. Allergen removal
4. Vaccination
5. Immunosupressants
6. Monoclonal antibody therapy

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14
Q

What is Syncope?

A

Fainting

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15
Q

What is Paresis?

A

General limb weakness

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16
Q

True or False.

A seizure is a symptom not a disease.

A

True

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17
Q

What is a Seizure or Convulsion?

A

Violent irregular motion of the limbs, caused by Involuntary contraction of the muscles

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18
Q

What are the 2 Aetiology’s of seizures?

(What can they be split into)

A
  1. Intracranial
  2. Extracranial
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19
Q

What are potential 9 Intracranial causes of Seizures?

A
  1. Hydrocephalus
  2. Encephalitis
  3. Tumours
  4. Idiopathic epilepsy
  5. Head trauma
  6. RTA
  7. Infections
  8. Heatstroke
  9. Cerebral abscesses
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20
Q

What are potential Extracranial causes of Seizures?

A
  1. Liver disease
  2. Portosystemic shunts
  3. Clots
  4. Hypoxia
  5. Allergens
  6. Medications
  7. Metabolic imbalances :
    * Hypocalcaemia
    * Hypoglycaemia
    * Hypokalaemia
    * Hepatic + Renal failure
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21
Q

What is the Aetiology of Epilepsy?

A
  1. Neurological condition
  2. Arises from disruption of Forebrain function
  3. Often Idiopathic (most common)
  4. Suspected genetic link in a no. of breeds (Border collies etc)
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22
Q

What 3 breeds of dog are suspected to have a genetic link to Epilepsy?

A
  1. Border Collies
  2. Hungarian Vislas*
  3. Labradors*

* = Over-represented

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23
Q

What is the Pathophysiology of Epilepsy?

A
  1. Disordered electrical activity of the brain cells
  2. Imbalance in excitatory + inhibitory signals
  3. Can be partial (Cats) or generalised (Dogs)
  4. Has 3 phases:
    * Pre-ictal
    * Ictal
    * Post-ictal
  5. Prolonged seizures = Status Epliepticus (more than 5 mins)
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24
Q

What species is more susceptable to Partial Epilepsy?

A

Cats

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25
Q

What species is more susceptable to Generalised Epilepsy?

A

Dogs

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26
Q

What is a generalised seizure?

A
  • Full blow seizure phase
  • Equivalent of Grand Mal in humans
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27
Q

What are the 3 stages of Epileptic seizures?

A
  1. Pre-ictal
  2. Ictal
  3. Post-ictal
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28
Q

What are seizures called that last longer than 5 minutes + potentially lethal?

A

Status Epliepticus

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29
Q

True or False.

Px with Status Epilepticus can come out of these types of seizures by themselves with no veterinary intervention.

A

False.

They require immediate emergency veterinary care.

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30
Q

What common clinical sign can Status Epilepticus cause?

A

Hyperthermia

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31
Q

Why does Status Epilepticus cause Hyperthermia?

A

Because the seizuring activity of rapid muscle contractions causes the body to heat up

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32
Q

How does Status Epilepticus cause brain damage in px?

A
  • Because the seizuring activity causes Hyperthermia, leading to overheating the brain
  • Resulting in brain damage
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33
Q

If an Epilpetic seizure is caused by an Infection, what can potentially trigger it?

A

Loud noises

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34
Q

List the possible 8 clinical signs of Pre-ictal?

A
  1. Anxious
  2. Restless
  3. Altered behaviour
  4. Px feels uneasy
  5. Not aware of surroundings
  6. Head pressing
  7. Standing in corner of the room
  8. Disoriented

Some aren’t classed as clinical signs.. more signs associated

Period prior to seizure

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35
Q

List the possible 9 clinical signs of Ictal?

A
  1. Active episodes of fitting
  2. Collapse
  3. Unconciousness
  4. Jaw spasms
  5. Vocalisation
  6. Incontinence
  7. Clonic paddling spasms
  8. Tonic spasms
  9. Panting

Note - actions vary from animal to animal

Episode of fitting

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36
Q

What’s the difference between Clonic + Tonic spasms?

A

Clonic spasms =
* Involuntary rapid + rhythmic jerking or muscle contractions

Tonic spasms =
* Muscle contraction or stiffening that can last seconds > minutes

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37
Q

Despite Tonic + Clonic spasms, name 3 others

A
  1. Tonic-Clonic
  2. Myoclonic
  3. Atonic
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38
Q

If Clonic spasms are Involuntary rapid + rhythmic jerking or muscle contractions
+
Tonic spasms are muscle contraction or stiffening that can last seconds > minutes…

What is the difference between Tonic-Clonic, Myoclonic + Atonic seizures?

A

Tonic-Clonic
* Tonic phase immediately followed with Clonic phase

Myoclonic
* Sporadic jerks or movements typically on both sides of body

Atonic
* Drop attacks + non-convulsive seizures
* Sudden loss of muscle tone w/multiple or extended seizures

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39
Q

List the possible 5 clinical signs of Post-Ictal?

A
  1. Extreme tiredness
  2. Dazed
  3. Ataxia
  4. Hunger
  5. Unresponsive to owner

Recovery period

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40
Q

Why should you not bring a patient straight into the VP if the patient is in Post-ictal?

A

Because:
* They’re in the recovery period
* More stress will can trigger another seizure

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41
Q

What is the exception to bringing in a patient while they’re in Post-ictal?

A

If they are in Status Epilepticus

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42
Q

What are the 8 possible Diagnosis for Epilepsy?

A
  1. Hx
  2. Clinical signs
  3. Physical exam
  4. Neurological exam
  5. Bloods - Biochemistry + Haematology (Infection, toxicity, glucose + uraemia)
  6. MRI (look for tumours)
  7. CT
  8. CSF Tap (Check for meningitis)
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43
Q

Why 2 reasons may you perform a MRI or CT for a patient with Epilepsy?

A

To check for:
1. Tumours
1. Brain abnormalities

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44
Q

Why may you perform a CSF Tap for a patient with Epilepsy?

A

To rule out Meningitis

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45
Q

What are the 9 possible treatment options for Epilepsy?

A
  1. Tx started only when seizures are severe + occur more than 2x a year
  2. Identify + treat cause (if not idiopathic)
  3. Life-long tx
  4. Phenobarbitone
  5. Imepitoin
  6. Postassium Bromide (dogs only)
  7. Levetriacetam
  8. Monitor Liver function
  9. If severe + life-long = Euthansia

Trialed tx is most common

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46
Q

What 4 drugs are in the controlled drugs cabinet, used for the treatment of Epilepsy?

A
  1. Phenobarbitone
  2. Imepitoin
  3. Postassium Bromide (dogs only)
  4. Levetriacetam
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47
Q

What drug can you only give to dogs for the treatment of Epilepsy?
+
What side effects does this drug have?

A
  1. Postassium Bromide
  2. Clinical signs:
    * Sedation
    * Ataxia
    * PU/PD
    * Pancreatitis
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48
Q

How often should you take bloods for Epileptic patients?

A

Q3 - 6 months

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49
Q

How should you treat a patient who is Status Epilepticus?

A
  1. IV or rectal Diazepam
  2. Propofol
  3. Cool px
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50
Q

True or False.

Treatment for patients with Epilepsy does not address the Primary concern, but manages the symptoms

A

True

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51
Q

True or False.

Idiopathic Epilepsy is not a life-long condition

A

False, it is life-long

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52
Q

What are the 6 criteria for when you should you start treatment for Epilepsy?

A
  1. If severe
  2. Occurs more than 2x a year
  3. 1x seizure Q6 m/o
  4. Bad seizures + bad Post-ictal Csigns
  5. < 6 m/o at onset
  6. Owner finds them distressing
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53
Q

Whata are 2 considerations for clients when treating Epilepsy?

A
  1. Expensive, as therapeutic mointoring is required (MRI, Drugs, Regular liver function tests etc)
  2. QOL of pet
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54
Q

When should you stop treatment for Epilepsy?

A

Never!

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55
Q

13 …

What advice should you give to clients during seizures?

A
  1. Low lighting
  2. Keep children + other pets away
  3. Record: time, gaps + frequency of seizures
  4. Reduce noise
  5. Clear all areas
  6. Call VP + VS
  7. Don’t pull tongue out (bite)
  8. Don’t call name
  9. Pillow under head
  10. Stay with them
  11. Stay calm!
  12. Reassure owner pet isn’t in pain
  13. If over 5 minutes long - home vist or come into VP
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56
Q

What parameter can drop if seizuring for long periods of time?

A

Blood sugar

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57
Q

What is the most common treatment for Status Epilepticus?

A

Euthansia

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58
Q

What type of seizure is:

  • Really alarming
  • Dangerous
  • Lasts more than 2 minutes
    or
  • 2 seizures without a break
  • Can be given with IV propofol
A

Status Epliepticus

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59
Q

What rate infusion should Propofol be given to a patient in Status Epilepticus?

A

Constant rate infusion

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60
Q

What seizure starts again as soon as the previous one starts to wear off?

A

Status Epilepticus

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61
Q

What is a Cluster seizure?

A
  • More than 1 seizure close together
  • Px gains consciousness between seizures
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62
Q

What are the 10 possible Aetiologies of Chronic Renal Failure?

A
  1. Common in cats
  2. Kidneys no longer able to compensate
  3. Idiopathic deterioration in geriatric cats (most common)
    1.Hx of Acute Renal Damage (Injury, toxins)
  4. Neoplasia
  5. Polycystic Kidney Disease (Persians)
  6. Chronic infection
  7. Pyelonephritis
  8. Golmerulonephritis
  9. DM
  10. Hypertension
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63
Q

What species is CKD/F most common in?

A

Cats

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64
Q

What is the Pathophysiology of Chronic Renal Failure?

A
  1. Uraemia (Kidney unable to filter nitrogenous waste from blood, Urea)
  2. pH + Electrolyte imbalance (Potassium + Phosphate, due to renal function)
  3. Reduced Erythropoietin production (reduced erythrocyte formation in bone marrow)
  4. Only when 75% of nephrons damaged/lost
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65
Q

What type of anaemia is caused by CRD/F?

A

Non-regenerative anaemia

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66
Q

8 dx tests..

How would you diagnose Non-regenerative anaemia in cats with CRD/F?

A
  1. Physical exam
  2. Haematology bloods
  3. CBC
  4. PCV
  5. Kidney palpatation (see if symmetrical)
  6. Bone marrow biopsy
  7. CT
  8. Ultrasound
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67
Q

What are the 16 possible Clinical signs of CRD/F?

A
  1. PU
  2. PD
  3. V+
  4. Dehydration
  5. Weight loss
  6. Inappetance
  7. Anorexia
  8. Depression
  9. Oral ulcers
  10. Hallitosis
  11. Seizures
  12. Non-regenerative anaemia
  13. Azotaemia
  14. Uraemia
  15. Hypokalaemia
  16. Anuric (End-stage)
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68
Q

What are the 10 possible Diagnosis for CRD/F?

A
  1. Hx
  2. Clinical signs
  3. Physical exam
  4. Urinalysis
  5. USG
  6. Bloods - Haematology + Biochemistry (BUN, Creatinine, SDMA + Electrolytes)
  7. BP
  8. Radiography
  9. Ultrasound
  10. Determine cause + extent of azotaemia

  1. Elevated levels of Urea
  2. Elevated levels of Creatinine
  3. SDMA testing - sensitive to early changes, used alongside Creatinine in IRIS staging
  4. Electrolyte levels - Phosphate for prognosis, to detect Hypokalaemia
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69
Q

What blood chemistry parameters are measured to asses kidney function?

A
  1. BUN
  2. Urea
  3. Creatinine
  4. Symmetrical Dimethylarginine (SDMA)
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70
Q

Why is SDMA testing performed for patients with CRF?

A

Sensitive to early changes, used alongside Creatinine in IRIS staging

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71
Q

What level may rise before the other?

Urea or Creatinine?

A

Creatinine

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72
Q

What USG what potentially indicate CRF in Cats?

A

< 1.035

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73
Q

What is the normal USG for Cats?

A

1.035 - 1.060

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74
Q

Whats the normal USG for Dogs?

A

1.015 - 1.045

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75
Q

What does a declining USG + increasing urine protein levels in the blood raise suspicion of?

A

CRD/F

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76
Q

What 2 things should be ruled out when diagnosing CRF?

A
  1. Presence of blood
  2. Infection
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77
Q

Why would blood + urea testing diagnose renal disease?

A

Because impaired kidney functions leads to a build up of nitrogenous waste in the blood, so this will be indicative upon testing

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78
Q

4 reasons..

Why would you image the kidney for CRD?

A

Because it will show any:
1. Acromegaly
1. Abnormalities
1. Lack of symmetry
1. Stage the disease

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79
Q

What are the treatment options avaliable for CRF?

A
  1. IVFT
  2. Protein + Phosphorus restricted diet
  3. Kidney prescripion diet
  4. Antibiotics
  5. Phosphate binders
  6. Potassium supplements
  7. Hypertension
  8. Amlodipine
  9. Treat anaemia (Nandralone, Erythropoietin)
  10. Monitor urine infections
  11. Mangage anorexia + V+
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80
Q

What are the 2 possible Aeitologies for Diabetes Mellitus?

A
  1. Type 1
  2. Type 2
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81
Q

What is the Aeitology for Type 1 Diabetes Mellitus?

A
  1. B-cells are destroyed
  2. Can no longer synthesise Insulin adequately
  3. Immune-mediated
  4. Breed dispositions
    * WHWT
    * Jack Russel Terriers
  5. Pancreas damage (Inability to synthesise Insulin)
  6. Known as ‘Insulin dependent’

B-cells = gamma

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82
Q

What is Type 1 DM known as?

A
  • Insulin dependent
  • Absloute Insulin deficiency
  • Cannot produce enough Insulin
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83
Q

What is Type 2 DM?

A
  • Reduced ability to respond to Insulin
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84
Q

What is the Aeitology for Type 2 Diabetes Mellitus?

A
  1. Reduced ability to respond to Insulin
  2. Obesity (little fat dogs)
  3. Oestrus
  4. Cushing’s disease
  5. Steroids
  6. Acromeagaly (cats)
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85
Q

What is the Pathophysiology for Diabetes Mellitus?

A
  1. Absloute (Type 1) or relative ( Type 2)
  2. Reduced tissue utilisation of glucose
  3. Leads to hyperglycaemia in bloodstream
  4. Low glucose levels in cells (Due to ^)
  5. Renal threshold for glucose exceeded > Glycosuria
  6. Eventually fats break down as can’t access glucose
  7. Leads to Ketosis > Ketoacidosis
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86
Q

What type of DM is most common in veterinary px?
+
What is it?

A
  1. Type 2
  2. Reduced ability to respond to Insulin
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87
Q

What is the Pathophysiology of Ketoacidosis?

A
  • Acid state in body caused by accumulation of Ketones
  • Gluconeogenesis
    2. Utilises fat + proteins as energy
    3. Because glucose is unavaliable
    4. By product of that is = Acidic Ketone bodies
    5. Results in:
  • Anorexia
  • V+
  • Dehydration
88
Q

What is Ketoacidosis?

A
  • Acid state in body
  • Caused by build up of Ketones
  • Often symptom of DM
  • Fatal
89
Q

What are the potential clinical signs of DM?

A
  1. Polyphagia
  2. PD
  3. PU
  4. Glycosuria

Later:
1. Weight loss
2. Ketosis signs - V+, Depression + Dehydration
3. Development of cataracts (Dogs)

90
Q

Why do dog’s present with Cataracts with DM?

A
  1. Lens doesn’t recieve direct blood supply + relies eye fluids for nutrients
  2. Normally lens absorbs glucose from eye fluids + converts remaining into Sorbitol
  3. If excess glucose in eye fluids + sorbitol production >
    * Sorbitol will:
  4. Pulls water into lens >
  5. Disrupts lens clarity >
  6. Causes cataract formation
91
Q

What are the later clincial signs that may present with DM?

A
  1. Weight loss
  2. Ketosis signs - V+, Depression + Dehydration
  3. Development of cataracts (Dogs)
92
Q

How is DM diagnosed?

A
  1. Hx
  2. Clinical signs
  3. Blood tests (biochemistry + haematology):
    * Blood glucose + curve
    * Fructosamine
    * Glycoslated haemoglobin
  4. Urine testing:
    * Ketodiastix test
    * Multistix
93
Q

What blood tests can you perform for the diagnosis of DM?

A
  • Blood glucose
  • Glucose curve
  • Fructosamine
  • Glycoslated haemoglobin
94
Q

How is a blood glucose test for DM?

A
  • Single test
  • Uses glucometer
    or
  • Biochemistry anaylser
  • Must use fasted sample
  • Cephalic or ear prick
95
Q

What are the 3 benefits of blood glucose tests?

A
  1. Quick
  2. Cheap
  3. Effective
96
Q

What is a Glucose Curve?

A
  • Series of blood glucose samples
  • Taken at regular intervals
  • Over 12 - 24hrs
  • Marked on a graph to produce a trend
97
Q

What is a Fructosamine test for diagnosing DM?

A
  • Serum protein
  • Produced in response to blood glucose
  • 3-week lifespan
98
Q

What is a less common type of testing blood for DM, that is for longer-term monitoring?

A

Glycosylated haemoglobin

99
Q

What 2 things does a Ketodiastix test use to detect in DM?

A
  1. Glucose
  2. Ketones
100
Q

What does a Multistix test use to detect in DM?

101
Q

What are the 2 benefits of the Multistix test to detect in DM?

A
  1. Simple
  2. Quick
102
Q

What are the 4 key principles of treatment for DM?

A
  1. Stabilisation
  2. Management
  3. Monitoring
  4. Emergency presentations
103
Q

How is 4 methods of stabilsation in px w/ DM achieved during treatment?

A
  1. Start on Insulin injections
  2. Monitor blood glucose levels
  3. Adjust insulin level + timing to bring level within acceptable range
  4. Establish daily routine w/owner - timing feed + injections
104
Q

3 things..

How is DM managed?

A
  1. Daily s/c injections of Insulin (BID)
  2. Strict dietary management
  3. Controlled exercise
105
Q

What is this used to deliver?

106
Q
  1. What is this?
  2. What is it used to treat?
  3. What species it for?
A
  1. Oral Hypoglycaemic (velagliflozin)
  2. To tx DM
  3. Cats
107
Q

What do Hypoglycaemics do?

A
  • Inhibit glucose reabsorption
  • Promote excretion of glucose in urine
108
Q

What is the difference between Diabetic Hypoglycaemia + Diabetic Ketoacidosis?

A

Diabetic Hypoglycaemia
* Low blood sugar
* Excess insulin

Diabetic Ketoacidosis
* High blood sugar
* Absloute or relative insulin deficiency

109
Q

What are the possible negative implications for owners with pets who have DM?

A
  1. Expensive
  2. Life-long (dogs > cataracts)
  3. 70% of DM dogs are blind within 1 year
  4. Cataract sx (£2,500)
  5. Needles can be an issue
  6. Euthanasia - question QOL (common, eventually)
110
Q

What % of DM dogs are blind within 1 year?

111
Q

What is the 6 possible Aetiologies of Dilated Cardiomyopathy? (DCM)

A
  1. Idiopathic
  2. Possible genetic biochemical affects
  3. Breed disposition - Large/giant (overrepresentive)
  4. Rare in dogs < 15kg
  5. Can be nutritional (grain-free, peas, lentils, legume seeds, potatoes)
  6. Some cats can be affected - idiopathic or taurine deficiency
112
Q

What cardiovascular disease is rare in dogs < 15kg?

113
Q

What can Mitral Valve Disease lead to?

A

Congestive Heart Failure
(CHF)

114
Q

What cardiovascular disease has a long-silent pre-clinical phase?

115
Q

What disease does this show?

116
Q

What is the Pathophysiology of DCM?

A
  1. Progressive thinning of the myocardium which impairs the efficiency of contraction
  2. Atria become enlarged
  3. The heart wall stretches becoming ‘ballooned’
  4. Eventually, the AV valves stretch leading to regurgitation of blood and atrial enlargement
  5. At this stage, there may be abnormalities in HR and rhythm
  6. Eventually falling CO leads to signs of CHF. (End stage)
117
Q

What are the 9 Clinical Signs of DCM?

A
  1. Lethargy
  2. Depression
  3. Anorexia
  4. Exercise intolerance
  5. Cough
  6. Dyspnoea
  7. Syncope
  8. Murmur
  9. Sudden death
118
Q

9 ..

How is DCM diagnosed?

A
  1. Hx
  2. Clinical signs
  3. Thoracic auscultation
  4. Chest radiography (shows enlarged heart)
  5. ECG
  6. BP measurements
  7. Cardiography
  8. Haematology
  9. Biochemistry
119
Q

What is the Aetiology of Exocrine Pancreatic Insufficiency?
(EPI)

A
  1. Atrophy of exocrine pancreatic cells
  2. Caused by spontaneous atrophy
    or
  3. Secondary to pancreatitis
  4. Secondary to trauma
  5. May be inherited
120
Q

What is the Pathophysiology of EPI?

A
  1. Inadequate production of digestive enzymes
  2. Due to atrophy of pancreatic exocrine cells
  3. Unable to digest foodstuffs fully
  4. L:eading to high-volume faeces
  5. Containing undigested material
  6. Malabsorption leads to:
    * Weight loss
    * Polyphagia
121
Q

What are the 8 Clinical signs of EPI?

A
  1. Polyphagia
  2. Weight loss
  3. Large faecal volume
  4. Steatorrhoea
  5. Undigested material
  6. Flatulence
  7. Poor coat
  8. Muscle wastage

Steatorrhoea = Fat in stools

122
Q

How is EPI diagnosed?

A
  1. Hx
  2. Clinical signs
  3. Faecal examination
  4. Biochemistry - Serum-Tripsin-
    like immunoreactivity     (looking for low levels to confirm disease)
123
Q

What is the Aetiology of the Feline Leukaemia Virus (FeV)?

A
  1. Retrovirus
  2. From Oncornavirus group
124
Q

What is the Pathophysiology of the Feline Leukaemia Virus (FeV)?

A
  1. Replicates in the lymphoid tissue
  2. Enters lymphocytes + monocytes >
  3. Transported around the body >
  4. Enters bone marrow
125
Q

What are the 6 Clinical signs of FeLV?

A
  1. Immunosuppression
  2. Recurrent infections
  3. Anaemia
  4. Tumour development
  5. Lethargy
  6. D+
126
Q

How is FeLV diagnosed?

A
  1. ELISA serum test (for antigen, patient side test with rapid response)
  2. PCR (Isolates viral genetic material)
  3. Viral isolation.
127
Q

What is the Aetiology of Feline Upper Respiratory Disease?
(FURD)

A
  1. Feline herpesvirus type 1 (FHV-1)
  2. Feline calicivirus (FHV)
  3. Bordetella bronchiseptica
  4. Chlamydophila felis
128
Q

What is the Pathophysiology of Feline Upper Respiratory Disease?
(FURD)

A
  1. Replicates in tissue of upper resp tract + ocular systems
  2. Leads to Epithelial necrosis
  3. Irritation of pharynx, larynx + trachea
  4. Rare to see repro and dermatological signs
  5. > Secondary bacterial infections common
  6. **>80% become carriers **
  7. Stress triggers flare ups
129
Q

What are the 10 clinical signs of FURD?

A
  1. Anorexia
  2. Pyrexia
  3. Depression
  4. Sneezing
  5. Conjunctivitis
  6. Hypersalivation
  7. Ocular + nasal discharge
  8. Keratitis
  9. Corneal ulceration
  10. Dyspnoea
130
Q

How is FURD diagnosed?

A
  1. Hx
  2. Clinical signs
  3. Viral transport swab of oropharyngeal region for
    FHV-1 and FCV
131
Q

What is the Aetiology of Gastric Dilation + Volvus?

A
  1. Idiopathic
  2. Large breed dogs
  3. Deep chested dogs commonly effected
132
Q

What is the Pathophysiology of GDV?

A
  1. Stomach dilates + rotates into a twisted position
  2. Gas cannot escape
  3. Distention of the stomach fills the abdominal cavity
  4. Puts pressure on the Caudal Vena Cava
  5. Disrupts venous return to the heart
  6. Pressure on diaphragm compromises breathing
  7. Leading to poor ventilation + damage to
    body tissues
  8. Necrosis of gastric wall + splenic tissue can occur
  9. Due to disruption of blood supply
133
Q

What are the 7 clinical signs for GDV?

A
  1. Restlessness
  2. Retching
  3. Anterior abdominal swelling
  4. Dyspnoea
  5. Collapse
  6. Shock
  7. Death
134
Q

What are the potential methods of diagnosing GDV?

A
  1. Hx
  2. Clinical signs
  3. Tympany of abdomen
  4. Radiography
  5. Emergency sx
135
Q

What is the Aetiology of Hyperthyroidism?

A
  1. Functional thyroid tumour
  2. Usually benign adenomatous hyperplasia of
    the thyroid gland
  3. May affect one or both lobes
  4. Indicating cause theorised but unknown
136
Q

What is the Pathophysiology of Hyperthyroidism?

A
  1. Affected gland overproduces thyroxine
  2. Leads to hypermetabolic state
  3. Thyroxine affects a number of body tissues
  4. So wider range of clinical signs
  5. 2 complications can be:
    * Hypertension
    * Hypertrophic cardiomyopathy
137
Q

What are the 10 Clinical signs of Hyperthyroidism?

A
  1. Polyphagia
  2. Weight loss
  3. Hyperactive
  4. Aggressive
  5. Restless
  6. Tachycardia
  7. V+
  8. D+
  9. Poor coat
  10. PD
138
Q

How do you diagnose Hyperthyroidism?

A
  1. Hx
  2. Clinical signs
  3. T4 levels
  4. Biochemistry
  5. Scintigraphy
  6. Evaluation of cardiac function
  7. Measurement of BP (advisable)
139
Q

What are the 2 common Aetiologies of Hyperadrenocorticism?

A
  1. Pituitary tumour
  2. Adrenal tumour
    * Both lead to serum cortisol
140
Q

What is the Pathophysiology of Hyperadrenocorticism?

A
  1. Overactive tissue in the pituitary or adrenal gland
  2. Leads to inc production of cortisol
  3. High levels of cortisol
  4. > hyperglycaemia + inhibit ADH
  5. Leading to PUPD
  6. High cortisol also causes protein catabolism
  7. Leads > muscle wastage + poor wound healing
  8. Cortisol affects hair growth + fat distribution
141
Q

What are the 9 clinical signs of Hyperadrenocorticisim?

A
  1. PU
  2. PD
  3. Weight loss
  4. Alopecia
  5. Pot-bellied
  6. Hepatomegaly
  7. Muscle weakness
  8. Panting
  9. Thinning of skin
142
Q

What are the 4 reasons to why dogs become Pot-bellied with Hyperadrenocorticisim?

A
  1. Enlarged liver
  2. Abdominal wall stretches as organs get heavier > to accomodate
  3. Muscle atrophy/ catabolism due to excess cortisol + shrink in size
  4. Fat redistribution into abdo cavity
143
Q

What is the other name given to Hyperadrenocorticism?

A

Cushing’s disease

144
Q

What endocrine disease does this dog have?

A

Hyperadrenocorticism

145
Q

How is Hyperadrenocorticism diagnosed?

A
  1. Hx
  2. Clinical signs
  3. ACTH stimulation test
  4. Low dose dexamethasone suppression test
  5. Urinalysis
  6. Endogenous ACTH
  7. Imaging
146
Q

What is the Aetiology of
Hypertrophic Cardiomyopathy?

A
  1. Idiopathic
  2. Genetic link
147
Q

What is the Pathophysiology of Hypertrophic Cardiomyopathy?

A
  1. Progressive thickening of the ventricular muscle > Enlarged heart
  2. Thickened walls
  3. Narrower chambers
  4. Reduced cardiac output
  5. Backpressure
  6. Atrial enlargement
148
Q

What are the 6 Clinical signs of Hypertrophic Cardiomyopathy?

A
  1. Lethargy
  2. Depression
  3. Anorexia
  4. Heart failure
  5. Dyspnoea
  6. Tachypnoea
149
Q

How is Hypertrophic Cardiomyopathy diagnosed?

A
  1. Physical exam
  2. Auscultation for murmur
  3. Radiography
  4. Ultrasound
  5. Echocardiogram
  6. ECG
  7. Lab tests
  8. BP measurement
150
Q

What is the 6 possible Aetiologies for Immune-mediated Haemolytic Anaemia?
(IMHA)

A
  1. Toxaemia
  2. Some drugs
  3. Incompatible blood transfusion
  4. Mycoplasma hemofelis
  5. Babesia canis
  6. Some recent vaccinations
151
Q

What is the Pathophysiology for IMHA?

A
  1. Destruction of RBCs by the animal’s immune system
  2. Or due to parasites + toxins
  3. Eventually leading to reduced circulating RBC volume
  4. Bone marrow releases immature RBCs to compensate (Non-regenerative anaemia)
  5. Spherocytes (partially phagocytosed RBCs) can be seen in the circulation
  6. Haemolysis may occur + lead to
  7. Increased bilirubin in blood
  8. > jaundice
152
Q

What are 11clinical signs of IMHA?

A
  1. Pale mm
  2. Weakness
  3. Exercise intolerance
  4. Murmur
  5. Tachycardia
  6. Dyspnoea
  7. Collapse
  8. Inappetent
  9. Petechiation
  10. Haemorrhage
  11. Jaundice
153
Q

How do you diagnose IMHA?

A
  1. PCV
  2. Reticulocyte count
  3. MCV (Mean Corpuscular Volume) - size of RBCs
  4. MCHC (Mean Corpuscular Hemoglobin Concentration) - haema concentration, part of CBC
  5. Blood smear:
    * RBC morophology
    * Heinz bodies
    * Toxins
    * HB level

1.Coombs test
1. Agglutination
1.Faecal occult blood

154
Q

What is the 5 possible Aetiologies of Keratoconjuncitivtis sicca?

A
  1. Reduced or absence of ability to form tears
  2. Immune-mediated
  3. Breed predispositions (protruberant eye breeds)
  4. Secondary to some endocrine conditions
  5. Drug toxicity
155
Q

What is the What is the common name given to Keratoconjuncitivtis sicca?

156
Q

What is the Pathophysiology of Keratoconjuncitivtis sicca?

A
  1. Reduced activity in the lacrimal glands
  2. > to inadequate formation of the aqueous tear film
  3. As adequate tear film is essential for corneal health
  4. Absence or reduced tear film
  5. Leads to corneal drying + inflammation
157
Q

What are the 4 clinical signs of Keratoconjuncitivtis sicca?

A
  1. Mucoid/mucopurulent conjunctivitis
  2. Dogs w/ sticky discharge in medial canthus
  3. Neovascularisation of cornea
  4. Couding or dull/dry cornea
158
Q

How is Keratoconjuncitivtis sicca diagnosed?

A
  1. Hx
  2. Clinical signs
  3. Schirmer tear test (definitive)
  4. Fluorescein (to rule out ulceration)
159
Q

What are the 2 Aetiologies of Laryngeal Paralysis?

A
  1. Idiopathic
  2. Polyneuropathy (Nervous system dysfunction)
160
Q

What is the Pathophysiology of Laryngeal Paralysis?

A
  1. Damage to the recurrent laryngeal nerves that:
    * Supply the muscle of larynx
    * Moves the vocal cords
  2. Leads to the functional failure of the vocal folds
  3. Unable to open vc fully during inspiration
  4. Inspiration is difficult as stay closed position
  5. Leading to dyspnoea
161
Q

What are the 7 Clinical signs of Laryngeal Paralysis?

A
  1. Cough
  2. Increased inspiratory noise
  3. Exercise intolerance
  4. Voice change
  5. Difficulty swallowing food + water
  6. Acute collapse
  7. Resp disease
162
Q

How is Laryngeal Paralysis diagnosed?

A
  1. Hx
  2. Clinical sign
  3. Examination of the layrnx
    * Under sedation
    * Using a laryngoscope or endoscope
    * To visualise the vocal folds
    * During inspiration
163
Q

What is the Aetiology of Mast Cell Tumour?

A
  1. Neoplasia affecting the histiocytes (mast cells)
  2. Breeds predisposed
  3. Different grades of tumour:
    * Benign > highly malignant
    * Around 20% of skin tumours in dogs
164
Q

What is the Pathophysiology of Mast Cell Tumour?
(MCT)

A
  1. Cells undergo malignant transformation
  2. Behaviour varies between grades
  3. Degranulation of mast cells in tumour
  4. Leads to systematic signs
  5. Often skin tumours
  6. Occasionally found in:
    * GI Tract
    * Spleen
    * Bone marrow
  7. Graded from I-III
  8. According to how well differentiated the cells are
  9. Grade III = poorest prognosis
165
Q

What are the 6 Clinical signs of Mast Cell Tumours?

A
  1. Appearance very varied
  2. Usually found on the skin surface
  3. Benign or low grade:
    * Small
    * Slow-growing masses
  4. Higher grade:
    * Masses
  5. Histamine release - associated with:
    * Swelling
    * Inflammation
    * Ulceration
  6. Some occur in the s/c layer
166
Q

How is Mast Cell Tumour diagnosed?

A
  1. FNA:
    * Confirms diagnosis
  2. Biopsy:
    * Assesses grade
    * Incisional or excisional
  3. Evaluation of local lymph nodes:
    * Assist with grading
  4. Imaging: detection of mets by:
    * Radiography
    * CT
    * MRI
167
Q

What is the Aetiology of Mitral Valve Disease?
(MVD)

A
  1. Idiopathic
  2. Breed dispositions:
    * Commonly Smaller breeds, but can be in larger breeds too
    * CKCS
    * Dachshunds
    * Chihuahuas
    * Terriers
    * Schnauzers
    * Bichons
    * Poodles
    * Spainels
    * Luchers
    * Labrador retrievers
  3. Age-related changes to heart valves
  4. Ruptured Chordae tendinae (Heart valve can’t open)
  5. Occurs in 10% of dogs
168
Q

What is the Pathophysiology of Mitral Valve Disease?

A

Mitral valve:
* Left side
* Between Atrium + Ventricle
1. Age-related degeneration
2. Valve becomes:
* Irregular
* Floppy
* Thick
* Lumpy
2. Results in imperfect seal
3. > Leaky valve
4. Mitral Valve Regurgitation (Blood leaks wrong way)
6. Heard as heart murmur

169
Q

What is Mitral Valve Disease also called?

A
  • Mitral Valve Insufficiency
  • Mitral regurgitation
170
Q

What is this cardiovascular disease?

A

Mitral Valve Disease

171
Q

What are the 2 main basic stages of Mitral Valve Disease?

A
  1. Asymptomatic or Preclinical
  2. Congestive Heart Failure
172
Q

What are the 4 stages of Mitral Valve Disease?

A
  1. A:
    * Breed prone + no murmur
  2. B1:
    * Murmur + no symptoms or change on ultrasound/x-rays
  3. B2:
    * Heart shape changes on ultrasound + x-rays
  4. C:
    * Symptoms of Congestive Heart Failure
    * Death
173
Q

What are the 2 Clincical Signs of Asymptomatic stage of MVD?

A
  1. Asymptomatic!
  2. Very mild murmur
174
Q

What are the 11 Clincical Signs of Congestive Heart Failure phase of MVD?

A
  1. Tachypnoea
  2. Dyspnoea
  3. Lethargy
  4. Coughing
  5. Syncope
  6. Collapse
  7. Weight loss
  8. Inappetent
  9. Distended abdomen
  10. Exercise intolerance
  11. Murmur
175
Q

What is the prognosis for a px w/CHF?

A

Several months > Years until HF

176
Q

What are the treatment options for Mitral Valve Disease?

A
  1. Hx
  2. Clinical signs
  3. Physical exam - RR, HR, BP measurements
  4. Ausculation of heart + lungs
  5. Radiography (Chest)
  6. Ultrasound - Echocardiogram (size + shape of heart + valves)
  7. ECG
  8. Biochemsitry + Haematology
  9. Urinalysis
  10. Liver + kidney tests
  11. Monitoring
  12. Medications:
    * Indodilators (Pimobendan) - increase heaart function
    * Diuretics (Furosemide or Spirinolactone) - to remove fluid from the lungs
    * ACE inhibitors (Angiotensin Converting Enzymes, Benazepril)
    * Cardiac glycosides (Digoxin - rhythm balance)
  13. Lifestyle:
    * Weight management
    * Controlled exercise
    * Low salt diet
177
Q

What is the Aetiology of Osteoarthiritis?
(OA)

A
  1. Also known as DJD:
    * Degenerative Joint Disease
    * Primary disease of joint cartilage
    * But can be secondary to abnormal stresses on joints
  2. Develops as a result of underlying:
    * Deformity (Cruciate - ligament - rupture)
    * Trauma (Fracture)
  3. Affects 1 in 5 dogs
  4. Most common cause of lameness
    * Can be caused by:
  5. Osteochondritis Dissecans
    * Abnormality of articulate cartilage, leads to abnormal wear on joint surfaces
178
Q

What is this skeletal disease?

A

DJD or Osteoarthritis

179
Q

What is the Pathophysiology of OA?

A
  1. Characterised by degeneration of articular cartilage
  2. Articular cartilage = essential cushioning of end of bones + joints - should be smooth
  3. Degeneration of articular cartilage = bones rub together + cause new bone formation
  4. Often associated with formation of new bone + joint surface
  5. Progressive onset but can be acute
180
Q

What are the 12 Clinical signs of OA?

A
  1. Stiffness
  2. Lameness - worse after rest
  3. Reluctance to jump
  4. Swelling
  5. Inflammation
  6. Crepitus
  7. Pain
  8. Gait alteration (Due to pain)
  9. Muscle atrophy of affected limb(s)
  10. Potential inapetence
  11. Personality behaviour
  12. Reduced ROM

Less common in Cats

181
Q

What is the diagnosis for OA?

A
  1. Hx - ex intolerance, stiff joints, reduced ROM
  2. Clinical signs
  3. Physical exam
  4. Evidence of crepitus
  5. Radiography
  6. Arthroscopy - into joint to visualise articulate cartilage + lesions
  7. CT
  8. MRI
  9. Synovial Fluid Analysis (Fluid from joint space)
    Looks for:
    * Infectious cells
    * Immune cells
    * Neoplastic cells
182
Q

What the treatment options for OA?

A

Often combo of med + sx management
1. Controlled exercise routine
2. NSAIDs
3. Analgesics + Opioids - Tramadol, Gabapentin
4. Corticosteroids (severe)
5. Pentosanpolysuphate injection (Librela for dogs)
6. Weight management(Obese, to maintain muscle tone)
7. Nutraceuticals (Cod liver oil, Fish oil, High in EFAs)
8. Sx:
* Arthroscopy
* Joint replacement

183
Q

What is the 5 Aetiologies of Otitis Externa?

A
  1. Infection
  2. Parasites
  3. Trauma
  4. Allergy
  5. Neoplasia
184
Q

What is the Pathophysiology of Otitis Externa?

A
  1. Irritation or self-trauma
  2. Leads to:
    * Tissue hyperplasia
    * Inflammation
    * Excess production of wax
  3. Any obstruction of canal
  4. Leads > accumulation of cerumen discharge
  5. Leave predisposed to infection
185
Q

What are the 10 Clinical Signs of Otitis Externa?

A
  1. Head shaking
  2. Head tilt
  3. Ear scratching
  4. Self-trauma
  5. Pain
  6. Inflammation
  7. Thick, waxy or purulent discharge
  8. Foul smelling ears/wax
  9. Yeasty smell
  10. Thickening of ear lining
186
Q

How is Otitis Externa diagnosed?

A
  1. Hx
  2. Clinical signs
  3. Visualisation + Aural exam
  4. Otoscope exam
  5. Ear swabs taken for culture + sensitivity
187
Q

What is the Aetiology of Osteosarcoma?

A
  1. Primary malignant neoplasm of bone tissue
  2. Common in large breeds
188
Q

What is the Pathophysiology of Osteosarcoma?

A
  1. Undergo **malignant transformation **> to formation of:
    * Swelling
    * Boney growth
    * Destruction of bone architecture
  2. Damage to bone tissue
  3. Leads to weakening of bone + pathological fracture
  4. Common - Metastatic spread to lungs
  5. Usually found in metaphysis of long bones

Pathological fracture = Spontaenous fractures from trauma or weakening of bone

189
Q

What is a pathological fracture?

A

Spontaenous fractures from trauma or weakening of bone

190
Q

What are the 4 Clinical signs of Osteosarcoma?

A
  1. Lameness
  2. Swelling of site
  3. Pathological fracture
  4. Coughing
191
Q

How is Osteosarcoma diagnosed?

A
  1. Radiography
  2. CT
  3. MRI
  4. Biopsy
192
Q

What is the Aetiology of Pancreatitis?

A
  1. Idiopathic
  2. Linked to high-fat diet
  3. Some drugs
  4. Secondary to trauma
193
Q

What is the Pathophysiology of Pancreatitis?

A
  1. Pancreatic enzymes activated prematurely within the pancreas or
  2. Unable to exit into duodenum
  3. Presence enzymes in pancreatic tissue results in
  4. Auto-digestion of the pancreatic tissue
  5. Process causes inflammation + necrosis of pancreas
194
Q

What are the 8 Clinical signs of Pancreatitis?

A
  1. Anterior abdominal pain (praying position)
  2. V+
  3. Depression
  4. Anorexia
  5. Shock
  6. Pyrexia
  7. Dehydration
  8. Chronic - vague + variable
195
Q

How is Pancreatitis diagnosed?

A
  1. Hx
  2. Clinical signs
  3. Physical exam
  4. Blood tests - measure Pancreatic Lipase **
    * Spec cPL (Dogs)
    * Spec fPL (    Cats**)
196
Q

What is the Aetiology of Parvovirus?

A

CPV-2
(Most common strain)

197
Q

What is the Pathophysiology of Parvovirus?

A
  1. Rapidly dividing cells in:
    * Gut wall
    * Lymph tissue
    * Bone marrow
  2. Destroys the gut lining
  3. Leads to:
    * Inability to absorb nutrients
    * Bacteria enters blood
  4. Affects on bone marrow + Lymph tissue
  5. Suppresses immune response > leukopenia
198
Q

What are the 8 Clinical Signs of Parvovirus?

A
  1. Depression
  2. Anorexia
  3. Severe V+
  4. Haemorrhagic D+
  5. Pyrexia
  6. Severe weight loss
  7. Severe dehydration
  8. Shock
199
Q

How is Parvovirus diagnosed?

A
  1. Hx
  2. Clinical signs
  3. Faecal testing (ELISA detects CPV2 antigen)
  4. Faecal PCR (CPV2 DNA detected in faeces)
  5. Serum antibody
200
Q

What is the Aetiology of Pyometra?

A
  1. Secondary bacterial Infection of uterus
  2. Often E coli
  3. Common in unspayed older bitches that have had several seasons
  4. Can be seen in younger animals
201
Q

What is the Pathophysiology of Pyometra?

A
  1. Cystic changes in the uterus
  2. Bacterial infection during oestrus
  3. Open cervix allows entry of bac into uterus
  4. Large accumulation of pus due to immune response of phagocytosis
  5. Is Open or closed
  6. Bacterial toxins enter the bloodstream
  7. Leads to Septicaemia/toxaemia
202
Q

What are the 12 Clinical signs of Pyometra?

A
  1. Vaginal discharge (open)
  2. Lethargy
  3. Inappetence
  4. PU
  5. PD
  6. V+
  7. Distended abdomen
  8. Painful abdomen
  9. Pyrexia
  10. Pale MM
  11. Weakness
  12. Collapse
203
Q

How is Pyometra diagnosed?

A
  1. Hx
  2. Clinical signs
  3. 6/8 weeks since last season
  4. Radiography of abdomen
  5. Ultrasound
  6. Bloods - Leukocyte counts may indicate infection
204
Q

What is the Aetiology for Tracheal Collapse?

A
  1. Idiopathic
  2. Potential combo of:
    * Genetic
    * Nutritional
    * Allergic triggers
205
Q

What is the Pathophysiology of Tracheal Collapse?

A
  1. Incomplete formation or weakening of c-shaped tracheal cartilages
  2. Leads > inability to maintain patency of the trachea
  3. During inspiration:
    * Cervical portion of trachea collapses
  4. Leads > airway obstruction
  5. During expiration:
    * Thoracic portion of the trachea collapses
206
Q

What are the 3 Clinical signs of Tracheal Collapse?

A
  1. Exercise intolerance
  2. Goose honk
  3. Progressive signs of resp disease (may be paroxysmal)

Paroxysmal = occurs suddenly/sudden onset of abnormal movements

207
Q

How is Tracheal Collapse diagnosed?

A
  1. Fluoroscopy video X-ray (For real time diagnosis)
  2. Chest radiography
208
Q

What is the Aetiology of Urolithasis or Feline Lower Urinary Tract Disease? (FLUTD)

A
  1. Infection (rare)
  2. Calculi/Crystals
  3. Usually idiopathic cystitis
209
Q

What is the Pathophysiology of Urolithasis or Feline Lower Urinary Tract Disease? (FLUTD)

A
  1. Irritation + inflammation of the bladder wall +/or urethra
  2. May cause recurrent bouts of cystitis
  3. Uroliths cause urinary obstruction
  4. Trauma/iatrogenic damage may result in
  5. Bladder wall dysfunction or Urinary tract rupture
  6. Inability to void urine leads to >
  7. Azotaemia + Csigns associated w/ARF
210
Q

What are the 11 Clinical Signs of Urolithasis or Feline Lower Urinary Tract Disease? (FLUTD)

A
  1. Cystitis
  2. Oliguria
  3. Anuria
  4. Incontinence
  5. Varying frequency/volume of urine
  6. Abnormal micturition
  7. Licking external genitalia
  8. Depression
  9. V+
  10. Anorexia
  11. Dehydration
211
Q

How is Urolithasis/Feline Lower Urinary Tract Disease diagnosed?

A
  1. Hx
  2. Clinical signs
  3. Physical exam
  4. Observation of micturition
  5. Neurological exam
  6. Urinalysis
  7. Radiography
  8. Ultrasound
212
Q

What is the Aetiology of Wobbler’s?

A
  1. Complex
  2. Multifactorial
  3. Progressive
  4. Breed dispositions:
    * Great Danes
    * Dobermanns
  5. Primarily genetic
  6. Nutritional:
    * Protein
    * Calcium
    * Phosphorus
213
Q

What is the Pathophysiology of Wobbler’s?

A
  1. Narrowing of the cervical vertebral canal
  2. Due to developmental abnormalities of cervical vertebrae in young dogs (Great Danes) = OA-CSM
  3. Degenerative changes occur in older dogs (Dobermanns) = DA-CSM
  4. Narrowed canal impinges on spinal cord
  5. Causing compression + results in neurological deficits
214
Q

What are the 9 Clinical Signs of Wobbler’s syndrome?

A
  1. Weakness in 4-pelvic limbs
  2. More pronounced in hind limbs
  3. Scuffing nails
  4. Inco-ordinated gate
  5. Ataxia
  6. Wobbly gait
  7. Neck pain
  8. Paralysis
  9. 2-engine gate

SA Disease Yr2 (26 decks)

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