Dogs and cats 25 Flashcards

1
Q

brainstem syndrome which side are signs and the main structures and therefore functions affected - EXAM

A

IPSILATERAL SIGNS
Main structures and functions affected - IMPORTANT
- Mainly white matter similar to the spinal cord
- Proprioceptive tracts (13) - proprioception
- Motor tracts (15) - voluntary motor function
- Ascending reticular activating system (16) - arousal (KEEPS YOU AWAKE)
- Nuclei of the cranial nerves (6, 7, 8, 9) - cranial nerves
- Cardiorespiratory centres - life

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2
Q

Neurological examination what seen with brainstem syndrome

A
  • Observation - from all functions
    ○ Decreased mental status - reticular activating system
    ○ Four limb ataxia/paresis
    ○ Vestibular ataxia
  • Palpation - normal
  • Postural reactions - decreased (proprioception decreased)
  • Spinal reflexes an tone - normal
  • Cranial nerves - affected (expect cranial nerve 2)
  • Sensory systems - normal
    ○ UNLESS COMA
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3
Q

Where is the lesion?

1) If head tilt to left AND proprioception decreased on LEFT
2) If head tilt to the right AND proprioception decreased on LEFT

A

1) left brainstem

2) right forebrain

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4
Q

What are the 2 main things that result from brainstem and forebrain syndrome and the clinical signs

A
  • Cushing reflex
    a. brain lesion -> increase intracranial pressure
    b. Increase systemic blood pressure (BP) to increase cerebral blood flow
    c. Decrease heart rate if baroreflex works
  • Cushing triad
    ○ Brain signs (shallow breathing) - IMPORTANT
    ○ High BP
    ○ Low HR
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5
Q

cerebellar syndrome what side are the signs and the main function

A

IPSILATERAL SIGNS
Functions of the cerebellum
- “Coordination of movements so they are fluid in nature” Sean

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6
Q

Neurological examination what seen with cerebellar syndrome

A
  • Observation
    ○ Cerebellar ataxia
    § Wide based stance
    § Hypermetria - exaggerated movements (lifting the legs higher than needed)
    ○ Intention tremors - worse when intending to do something
  • Palpation - normal
  • Postural reactions - normal
  • Spinal reflexes and tone - normal
  • Cranial nerves
    ○ Normal or decreased
    § No menace response if severe - ipsilateral
    □ Response as involves the forebrain (conscious)
    □ relay in the cerebellum - SAME SIDE AS STIMULATED
    § Anisocoria - rare
    □ Ipsilateral mydriasis
    □ Slowly responsive to light
    □ Fastigial and/or interpositus nuclei
  • Sensory systems – normal
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7
Q

Encephalpathies what are the 7 main ones

A

1) cerebellar abiotrophy
2) hydrocephalus
3) brain tumours
4) thiamine deficiency
5) Meningoencephalitides of unknown origin (MUO)
6) Steroid-responsive-tremor-syndrome
7) Cerebro-vascular accidents (stroke)

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8
Q

Cerebellar abiotrophy what is it, cause and clinical signs

A
  • Degeneration of normal neurons after birth
  • Cause
    ○ Unknown
    ○ Some reclassified: storage disease
    § Am. Staffordshire terrier
  • Genetic
    ○ Aus. Kelpie, Border Colley, Brittany spaniel…
  • Clinical signs = cerebellar
    ○ Progressive (slow or quick)
    ○ Adult (but early or late)
    ○ Plateaus
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9
Q

Cerebellar abiotrphy diagnosis, treatment and prognosis

A
- Diagnosis
○ Strong clinical suspicion
○ MRI when advanced
○ Genetic tests (breed specific)
- No treatment
- Prognosis - can still be alive at 12-13 years of age, other may deteriorate
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10
Q

Hydrocephalus cause, breeds, cliical signs

A
- Congenital - almost always 
○ Likely obstructive
○ No cause on presentation
- Small breed dogs - pugs, Pekinese 
- Clinical signs 
○ First sight…
§ Dome shaped head, open fontanelles, “sunset eyes” - bulging out
○ Neurological
§ Forebrain - variable
§ Slow to train, central blindness (compress occipital lobe), obtundation, pacing
§ Seizures <20%
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11
Q

Hydrocephalus diagnosis and treatment

A
  • Diagnosis
    ○ U/S, CT-scan, MRI
  • Treatment
    ○ When? - no real indications - some plateau and some get worse
    ○ Help reduce CSF formation and increase drainage
    ○ Medical - corticosteroids (increase drainage)
    ○ Surgical; Ventriculo-peritoneal shunt
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12
Q

Brain tumours what are most common in dog and cat, primary or secondary and clinical signs

A
- Dog 
○ Primary -> meningioma, astrocytoma, oligoendrogiloma, glioblastoma, lymphoma 
○ Secondary -> haemangiosarcoma, pituitary adenoma/carcinoma, lymphoma, nasal tumours 
- Cats 
○ Meningioma, gliomas, ependymoma, other primary, lymphoma 
- Primary > secondary
- Older individuals
- Clinical signs
○ Depends on location
§ Forebrain > …
§ Seizures in <25% cats
○ Acute to slowly progressive
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13
Q

Brain tumours diagnosis

A

○ MRI
§ Sensitive, accurate
§ Often characteristic…
□ Meningiomas (grow from the meninges, strong uptake on contrast on tumour and peri-tumoral oedema around the tumour)
□ Gliomas (within the parenchmya - harder to remove surgically)
□ choroid plexus tumours - highly vascular and produce the CSF
§ …but not always - Lymphomas
○ CT-scan
§ Approx. 20% less sensitive and harder to describe the tumours
○ Skull radiographs
○ CSF - non specific
○ Brain biopsy - not common

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14
Q

Brain tumours staging how common metastasis and which hard to treat with chemotherpy

A

○ Malignant and brain tumours
§ Metastasis, cytology, local behaviour
○ 23% of dogs have a tumour somewhere else that is unrelated! - due to the age as likely to have other tumours NOT that the brain tumours metastasise (don’t do this that commonly)
§ Important to know this before surgery
○ Lymphoma - hard to treat with chemotherapy
§ FeLV, thorax-abdomen, bone marrow

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15
Q

Brain tumours treatment which treat, which has best prognosis and options

A

○ Primary > secondary (no as metastases - worse prognosis)
○ Meningioma (best prognosis and generally more accessible) > others
○ Palliative
§ Steroids +/- anticonvulsants
§ MST ≈ 2 months
○ Chemotherapy
○ Surgery - brain surgery - WILL GROW BACK
§ MST ≈ 18 months
○ Radiation therapy (megavoltage)
§ MST ≈ 10 to 100 weeks

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16
Q

Thiamine deficiency how does it lead to an encephalopathy and clinical signs

A
○ Thiamine = vitamin B1 – CoE
§ Energy (Krebs cycle)
§ Production of acetylcholine and GABA
Deficiency -> Polioencephalomalacia 
= Lack of grey matter (has high metabolic requirement, highly sensitive) 
- Clinical signs 
○ Central vestibular syndrome
§ Bilateral vestibular syndrome 
§ Neck ventroflexion
§ Facial paralysis
§ Abnormal PLRs
§ Ataxia
○ Forebrain
§ Decreased mental status
§ Seizures
§ Central blindness
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17
Q

Thiamine deficiency diagnosis, treatment and prognosis

A
- Diagnosis
○ MRI – pathognomonic images - symmetry of the lesions in the grey matter 
○ Complicated otherwise
§ [Thiamine] food, erythrocytes
- Treatment
○ Thiamine supplementation
- Good prognosis - Might take a while
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18
Q

Meningoencephalitides of unknown origin (MUO) define, what are the types and cause

A
  • Definitions
    ○ Inflammatory non-infectious (MUCH MORE COMMON)&raquo_space;> infectious (rare)
    ○ Various histo types
    § GME = Granulomatous Meningo-Encephalitis - most common
    § NME = Necrotizing Meningo-Encephalitis
    § NLE = Necrotizing Leuko-Encephalitis
    → Meningo-encephalitis of Unknown Origin (MUO)
  • Aetiology? - unsure but some genetics as breed specific
    ○ Same breeds, young adults
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19
Q

Meningoencephalitides of unknown origin (MUO) clinical signs and diagnosis

A
Clinical signs
○ Depending on location
○ Multifocal!
○ Optic neuritis → acute blindness
○ Spinal forms, neck pain
Diagnosis
a. MRI >> CT - ensure there is something in the brain 
b. CSF tap – meningitis
§ Non-specific mononuclear pleyocytosis
c. Rule out infectious diseases - as using immunosuppressive drugs 
§ PCR on CSF
§ Serology
N. caninum, C. neoformans, distemper
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20
Q

Meningoencephalitides of unknown origin (MUO) treatment and prognosis

A
- Treatment
○ Prednisolone (immunosuppressive)
§ Then tapered down
○ + cyclosporine, azathioprine, cytarabine
○ Follow up crucial
§ Clinical
§ Repeat MRI, CSF?
- Prognosis
○ MST ≈ 300 to 1500 days
○ Importance of short term survival
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21
Q

Cerebro-vascular accidents (stroke) types, cause and clinical signs - EXAM

A
  • Types -> Ischaemic (Artery blockage)&raquo_space;> haemorrhagic (Artery leaking)
  • Causes
    ○ Unknown > 50%
    ○ Hypertension, hypothyroidism, hyperadrenocorticism…
  • Abrupt clinical signs - neuromuscular defects -> head tilt, turn
    ○ Sometimes progression over 48h (oedema)
    ○ Raised ICP if haemorrhagic
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22
Q

Cerebro-vascular accidents (stroke) diagnosis, what should look for and prognosis

A
- MRI diagnosis - helps you to find where the accident is: 
○ Diffusion Weighted Images (DWI)
○ Gradient Echo (T2*)
- Underlying cause
○ Not found in 50% of cases
§ Coagulopathies
§ Hypertension
§ Endocrine diseases
§ Cardiac diseases/hypertension
- Good prognosis - usually recover within 2-3 weeks
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23
Q

Vestibular systems structures and other structures associated with

A
  • Receptors / internal ear - near facial nerve
  • Vestibular nerve / petrous bone
  • Vestibular nuclei / brainstem
    ○ Spinal cord
    § Vestibulospinal tract -> maintain balance of the body
    ○ Brain stem
    § Medial longitudinal formation (MLF) - coordination of eye movements when moving
    § Reticular formation -> arousal -> when going to fall over you wake up
    § Vomiting centre
    § Thalamus - conscious integration
    § Cerebellum - movement coordination
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24
Q

What is the normal functioning of vestibular system and what occurs when things go wrong

A
  • Body balance in response to gravity using Head and eyeballs
    ○ NORMAL - If going to fall to the left the vestibular system stimulation of ipsilateral extensor muscles (left) and inhibition of contralateral extensor muscles -> then correct positioning back into neutral position
    ○ ABNORMAL (lesion on left) - losing stimulation of ipsilateral extensor muscles on the left -> so falls over towards the left
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25
Q

In terms of neurological examination what found on observation and why

A

1) Vestibular ataxia
1. Circling/falling - to the side of the lesion
□ Ipsilateral increase flexion (due to decreased extension)
□ Contralateral increase extension
2. Head tilt
□ Same reason as circling (ipsilateral increase flexion)
□ Scoliosis with neck/trunk turned to the side of the lesion
3. Nystagmus - involuntary, rhythmic oscillation of the eyes
□ Same reasons as above
□ Generally involved both eyes
□ Sudden attempt to re-adjust the axis of the eyeball
® Quick phase opposite to the lesion
□ ALSO
® Horizontal vs rotatory vs vertical
® Positional nystagmus
◊ Absent/abnormal oculo-vestibular reflex (aka oculocephalic or physiological nystagmus)
2) Strabismus
§ Misalignment of the eyes - not as common
§ “Vestibular strabismus”
□ As moving head up Eye on the side of the lesion may struggle to move up and remain in ventro-lateral position

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26
Q

Vestibular disease neurological exam findings all besides observation

A
  • Palpation - normal
  • Postural reactions - normal to abnormal
  • Spinal reflexes and tone - normal
  • Cranial nerves - abnormal
    ○ Absent oculo-vestibular reflex
    ○ Resting (pathological nystagmus)
    ○ Positional nystagmus - vertical nystagmus indicates central vestibular syndrome
    ○ Positional strabismus
  • Sensory systems - normal
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27
Q

What are the 2 main types of vestibular syndromes and what associated with

A
  • Peripheral - lesion in the ear (facial nerve is associated with the ear)
  • Central - lesion in the brain stem (have proprioception tracts within, motor pathways and reticular foramen)
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28
Q

What are the 3 main causes of peripheral vestibular syndrome

A

1) Infectious otitis media-interna - MOST COMMON CAUSE
2) Idiopathic/geriatric vestibular syndrome - second more common
3) Primary secretory otitis media-interna (PSOM)

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29
Q

What is the most common cause of peripheral vestibular disease, pathophysiology, clinical signs and diagnosis

A
Infectious otitis media-interna 
- Physiopathology
○ Often otitis externa
§ Staphylococcus spp. Streptococcus spp.
○ Underlying causes
§ Atopy, foreign bodies…
- Clinical signs 
○ Peripheral vestibular syndrome
○ +/- facial paralysis
○ +/- Horner syndrome
○ Deafness?
- Diagnosis
○ Otoscopic examination
§ Cytological examination
○ Imaging
§ Radiographs
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30
Q

Infectious otitis media-interna treatment and prognosis

A
- Treatment and prognosis
○ Topical treatment
○ Systemic antibiotics - recommended 
§ Based on culture and sensitivity
§ Cephalexin, Amoxicillin
○ Myringotomy, bulla osteotomy - need to drain the puss out 
○ Addressing underlying condition-atopy
- Guarded to fair prognosis
○ Depending if brain extension
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31
Q

Idiopathic/geriatric vestibular syndrome pathophysiology, clinical signs, diagnosis, treatment and prognosis

A
- Physiopathology
○ Unknown – thickening of endolymph?
○ Older dogs – adult cats
- Clinical signs 
○ Peripheral vestibular syndrome
○ Hyperacute, marked (struggle to work and very imbalanced) 
- Diagnosis
○ Exclusion
- Treatment and prognosis
○ No treatment just time 
○ Diazepam 0.5mg/kg TID – motion sickness
- Good prognosis – 2 weeks
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32
Q

Primary secretory otitis media-interna (PSOM) what a cause of, what is involved, main breed, clinical signs, treatment and prognosis

A
peripheral vestibular disease
- Viscous mucus plug
○ Abnormal Eustachian tube
○ Non-infectious at first 
- Cavalier KCS
- Clinical signs
○ Head and neck discomfort
○ Peripheral vestibular signs
§ +/- Horner and facial paresis
- Myringotomy, flush
- Good prognosis
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33
Q

Define a seizure

A

○ brain disorder expressed as a paroxysmal transitory disturbance of brain function that has:
§ a sudden onset,
§ ceases spontaneously,
§ has a tendency to recur,
originates in the prosencephalon (Delahunta)

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34
Q

Seizure what is the main characteristic, clinical signs and what are the 4 phases

A
○ Main characteristics
§ Loss of control
§ Episodic (paroxysmal) - back to normal straight after episode 
§ Repetitive clinical pattern
○ Clinical signs
§ Consciousness
§ Motor	
§ Sensory - hard to detect 
§ Autonomic
§ Psychic - hard to detect
Phases
a. Pre-ictal = prodromes
b. Aura (short)
c. Ictus - seizure itself (burst of motor activity) 
d. Post-ictal
§ Cerebral exhaustion
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35
Q

How does a seizure occur and the 2 main types

A

○ Every neuron has a seizure threshold
○ Imbalance: Excitatory-inhibitory impulses altered:
§ Synapses (dendrites) - brain lesions
§ Cell membrane - brain lesions
□ Genetics (lipoproteins, channels…)
§ Neurotransmitters - idiopathic/familial
□ Inhibitory: GABA
□ Excitatory: glutamate
§ Environment - metabolic
□ Glucose, electrolytes
Types
1) generalised - origin from both forebrain hemispheres
2) partial - one focus lesion in the forebrain

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36
Q

Generalised seizure origin and presentation

A
origin from both forebrain hemispheres
§ Primary generalised 
§ Presentation 
□ Motor signs = convulsion
® Tonic-clonic (tonic - rigid, clonic - uncontrolled extension/jerking) 
□ + loss of consciousness
□ +/- autonomic, psychic, sensory
® Autonomic = salivation, change in pupils size, urination, defecation…
□ Psychic and sensory: hard to tell…
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37
Q

Partial seizure origin, presentation and types within

A
origin from both forebrain hemispheres
§ Primary generalised 
§ Presentation 
□ Motor signs = convulsion
® Tonic-clonic (tonic - rigid, clonic - uncontrolled extension/jerking) 
□ + loss of consciousness
□ +/- autonomic, psychic, sensory
® Autonomic = salivation, change in pupils size, urination, defecation…
□ Psychic and sensory: hard to tell…
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38
Q

What are some common presentations (pheonotypes) of partial seizures

A

§ Facial twitching (simple motor)
§ Other localised motor
□ tonic of one leg +/- trunk +/- neck (simple motor)
§ Hypersyalosis + oral involvement (simple autonomic)
§ Fly biting (simple sensory) - form of hallucination
NOT head bobbing

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39
Q

What are the 3 differential type of seizures in terms of duration and frequency and what is epilepsy

A
1) Isolated
§ One seizure or less / day
2) Cluster
§ Two seizures or more / day
3) Status epilepticus
§ Two seizures within 30 minutes without recovery
§ One seizure > 5 minutes duration
Epilepsy
- Greek epilepsia = to be taken
- Recurrent seizures = 2 or more in the life 
Regardless of the origin! - 
- DOESN'T INDENTIFY THE CAUSE
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40
Q

What are the 3 main types of seizures that help narrow down differentials

A

1) extra-cranial
2) intra-cranial
3) idiopathic (familial)

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41
Q

Extra-cranial seizure disorder diagnosis and main causes and what important to remember

A

○ Abnormal blood contents -> increased neuronal depolarisation
○ Causes mainly metabolic, nutritional, toxic (NEED TO ASK ABOUT EXPOSURE WHEN COME INTO EMERGENCY SEIZURING)
§ Hypoglycaemia
□ Insulinoma, insulin therapy, paraneoplastic, toy puppies, puppy stress, hunting dogs…
§ Hypocalcaemia
□ Post-partum (less due to good nutritional education), hypoparathyroidism (generally primary)
§ Liver insufficiency
□ Congenital vascular anomalies
® Porto-systemic shunt, microvascular dysplasia
§ Terminal acquired hepatopathy
○ Careful: not all clinically significant!
§ They may trigger seizures but not always - likelihood changes

42
Q

Extra-cranial seizure what are the typical clinical presentations

A
§ Seizure phenotype
□ Generalised > partial
□ Possible status epilepticus (toxics, hypoglycaemia)
§ Other clinical signs
□ Depending on the cause
® Kidney diseases (CKD…)
® Liver diseases (congenital PSS…)
43
Q

Intra-cranial seizure common cause, other causes and clinical presentation (differentiating feature)

A

○ E.g. brain tumour
○ Causes mainly - neoplastic and inflammation/infectious
○ Clinical presentation
§ Seizure phenotype
□ Any but partial seizures suggest intracranial disease
§ Interictal neurological signs - IMPORTANT - THIS IS WHAT DIFFERENTIAL INTRACRANIAL FROM OTHERS
□ Forebrain signs… not normal between the seizures
® Mental status
® Central blindness
® Mild ataxia
□ …or more if multifocal

44
Q

Idiopathic (familial) seizures what is the disease, caused by and 3 subgroups

A
○ Idiopathic epilepsy (primary)
§ Idiopathic = disease in its own right
§ Today 3 subgroups
□ Genetic
® Gene identified (Lagotto Romagnolo and Belgian Shepherd)
® Inherited only if pedigree analysis only
® Any breed can get it 
□ Suspected genetic
® High prevalence in the breed (>2%)
□ True idiopathic
® No underlying cause detected
45
Q

Idiopathic epilepsy (primary) clinical presentation and common onset

A
§ Clinical presentation 
□ Seizure phenotype
® Mostly generalised
® But…any really - not set in stone
◊ Large breed dogs / severe, clusters
◊ Small breeds / focal
◊ Cats /focal → generalised
® Rhythmic - can occur every Wednesday etc. 
® Infrequent initially
□ Onset: 6 month to 6 years, but… younger maybe infectious, older generally tumours 
® Juvenile epilepsy
® 35% of older dogs have idiopathic epilepsy
46
Q

Status epileptius how common and causes

A
§ First manifestation of seizures in 60% of epileptic dogs
• 45% intracranial disease
• 30% toxics
• 25% idiopathic
§ Not discriminant
47
Q

Investigation for seizure cause how to rule in or out extra-cranial disease

A

But what is relevant?
○ Glu - IMPORTANT
○ Ca2+, Na2+ - IMPORTANT
○ Alb, TP
○ ALT, ALP
○ Urea, Creat
○ Bile acids tolerance test? - if other biochem results suggest liver dysfunction then maybe
○ Cholesterol and tryglycerides
§ Miniature Schnauzers - in these breeds check above
- What do I get from my CBC? - UNCOMMON CAUSES - lead intoxication

48
Q

Investigation for seziure cause how to rule in or out intracrnail disease

A
- Advanced imaging
○ Gold standard = MRI
§ Soft tissue resolution
○ Tomodensitometry (CT-scan) acceptable
§ Head trauma
- Cerebro-spinal fluid (CSF) tap
○ Cisternal = closer to the brain
49
Q

Therefore what investigation is needed for seizures to find cause

A
  • History + blood work - rule out extracranial
  • Brain imaging + CSF - rule out intracranial
  • IF RULE OUT BOTH -> idiopathic epilepsy
    ○ 12 months history of seizures without interictal signs -> idiopathic most likely as well
    § If other causes wouldn’t be alive or would have other clinical signs
50
Q

Steps in seizure management

A

1) stop the seizure
2) treat underlying cause if necessary
3) long terms management including important consult

51
Q

Steps in stopping a seizure and what if no IV access

A
  1. Place IV catheter
  2. IV diazepam/midazolam
    ○ Few minutes between injections
    ○ No more than 3 injections
  3. IV propofol - prepare to intubate (rare)
  4. IV thiopental / pentobarbital (if propofol doesn’t work) - SLOW INJECTION
  5. General anaesthesia (if all else fails - rare - mainly just toxin causes) - BEWARE OF CARDIAC ARREST
    IF NO ACCESS TO IV -> Intrarectal diazepam
    ○ Few minutes between injections
    ○ No more than 3 injections
    ○ Use Cannule
52
Q

Facts about seizures: how common in sudden death, how common lead to euthanasia

A
  • Sudden death in epilepsy (SUDEP)
    ○ From multi-organ failure
    § Extremely high body temperatures
    ○ Extremely rare - DON’T DIE DURING SEIZURE IN DOG
    § Toxic > idiopathic
  • But status epilepticus leads to euthanasia
    ○ Morbidity → owner’s perception
    ○ 2/3 of idiopathic epileptic euthanized
    § Increase Seizure frequency
    § Status epilepticus and clusters (bad phenotypes)
53
Q

In terms of seizures why is there a high morbidiy

A
→ the real problem: associated morbidity
- Post-ictal changes
○ Confusion / restlessness
○ Exhaustion / sleepiness
○ Thirst / hunger
○ Ataxia
○ Central blindness
○ Aggression 
Seizures and social impact
- Not as bad as humans -> don't need to worry about driving or meeting etc
- But anxiety and behaviour
○ Abnormal perception
○ Demented behaviours
54
Q

What are some possible therapeutic options for idiopathic seizures

A
  • Evidence -> drugs
    ○ Possible surgery (corpus callostomy) and vagal stimulation (eyeball compression, devices (surgically implanted vs external)
  • Low to absent evidence - diet and acupuncture
    ○ Diet - ketogenic diet, fatty acid supplementation, medium chain triglycerides - NO SCIENCE
55
Q

Treating the underlying cause in seizure management what is involved

A
- Intracranial
○ Tumour reduction = ↓ seizure frequency (humans)
○ MUOs
○ Hydrocephalus
- Extracranial
○ Clear the toxic
○ PSS management
- ± anticonvulsant medication
56
Q

What are 4 main things need to talk about in initial consultation when diagnose idiopathic epilepsy

A
  • The facts:
    ○ Seizures rarely kill
    ○ No social impact - not conscious during generalised seizures (suffer possible pain afterwards - exhausted muscles)
    ○ Anticonvulsants = only option according to science
  • Freedom of seizure (almost) never achievable
    ○ Lifelong treatment
    ○ Need for therapeutic objectives
    § One seizure a month or a few?
    □ Need a balance between seizure side effects and medications side effects -> QUALITY OF LIFE
  • Side effects from treatments
  • Quality of life (QoL) is central - MAIN OBJECTIVE
57
Q

When do you need to start a treatment plan for seizures

A
  • After one isolated seizure?
    ○ NO! - MAY NEVER HAVE ANOTHER SEIZURE (not epileptic yet)
  • 2015 ACVIM consensus when to treat:
    ○ Identified structural lesion (brain tumour - know will seizure again)
    ○ Status epilepticus or clusters
    ○ 2 or more seizures within 6 months
    ○ Prolonger, severe or unusual post-ictal changes
58
Q

Therapeutic objectives to talk about in inital consultation for idiopathic epilepsy what need to discuess

A
  • Primary: 0 seizures? - PRETTY MUCH NEVER ACHIEVE
  • Secondary: set number?
    ○ Reasonable therapeutic objective -> 50% decrease
    ○ Starting point but may have to tailor over time
  • Tertiary: - improve the quality of life
    ○ Improve phenotype
    § Generalised → partial
    ○ ↓ duration of seizure
    ○ ↓ duration/phenotype of post-ictal phase
  • IMPORTANT - seizure dairy to ensure get the therapeutic objective
59
Q

First line treatments for seizure control what are the 3 main ones, what do and which recommended

A

1) Phenobarbital
○ Barbiturate: GABA receptor - increase the neural potential
2) Potassium Bromide (KBr) (bromide hyperpolarise the membrane)
○ Negatively charged ion: Br -
3) Imepitoin (PexionTM) - doesn’t work??
○ GABA receptor

60
Q

phenobarbital what used for, what is it and pros and cons

A

used for first line treatment of seizures
- Barbiturate: GABA receptor - increase the neural potential
Pros - Efficacy - IS GOOD, safe (if monitor) and long half-life, cheap
Therapeutic essay - can measure the amount in the blood
- Can check the therapeutic range (too much can lead to liver failure (way beyond for A LONG PERIOD)
Side effects - PU/PD, increased appetite, sedation, ALP increased (not liver toxicity - microsomal hepatic enzyme induction)
- If don’t give more food THEN WONT BE FAT

61
Q

Potassium bromide and imepitoin what used for and pros and cons

A

first line treatment for seizures
1) potassium bromide
Pros - VERY SAFE, therapeutic essay as well
Cons -> long half-life - stead state takes 3-4 months
CONTRA-INDICATED IN CATS
2) imepitoin
Pros - no side effects - VERY SAFE
CONS - does it even work?, VERY EXPENSIVE

62
Q

Follow-up after treatment of seizure, how done and when

A
  • Phenobarbitone assay
    ○ Therapeutic range: 60-180 μmol/L
    § Above risk of toxicity, below possibly decreased seizure control (some dogs will still respond to the low levels)
    ○ Biochemistry for liver
    ○ Check seizure diary - ask questions about side effects and quality of life
  • When
    ○ 2-4 weeks after initiation (steady state)
    ○ Every 6 to 12 months - once happy with number of seizures
    ○ When contemplating increase in dose
    ○ Suspicion of toxicity
63
Q

What if have too many seizures vs therapeutic objectives?

A
  1. Increase dose (based on drug assay)
    ○ 15-30% depending on the serum concentration
    ○ General rule -> once know the serum concentration with the dose you are at - if you increase the dose by 25% will increase the serum concentration by 25%
    § So can know that when you add if you will be over the therapeutic range
  2. Add another medication (only once exhausted one medication)
    ○ Potassium Bromide - NOT IN CATS (so in cats need to go below)
    ○ Levetiracetam (Keppra TM)
    ○ Zonisamide (Zonegran TM)
    ○ Gabapentin (Neurontin TM
64
Q

what are 6 differential diagnosis for acute lesion in T1-L3 area in dachshund grade 3 with back pain, which most likely and why aren’t others

A
  1. Degenerative disk disease - DISC EXTRUSION DUE TO SIGNALMENT MOST LIKELY
  2. Congenital vertebral malformations - more chronic (may acutely present as deteriorate)
  3. Extradural tumour - generally more chronic (exceptions)
  4. Discospondylitis - fever, extra-neural signs - less likely
  5. Traumatic - vertebral fracture, luxation - generally grade 4 or grade 5 (not in this case)
  6. Fibro-cartilagineous embolism (FCE) - back pain so less likely, also symmetrical in this case
65
Q

If have lesions localisation of Left hand side- L4-S3 and Right hand side- T3-L3 what disease thinking and why

A
  • Effect white and grey material of the spinal cord
  • Fibro-cartilagineous embolism - IMPORTANT IN LECTURE
    ○ Hyperacute
    ○ Exercise induced, sudden pain when occurs then non painful
    ○ Intumescences often affected
66
Q

Anorexia how common, associated with, define and issues

A
  • Common
  • Associated with multiple diseases
  • Diagnostic and therapeutic challenge
  • Definitions : Anorexia, Hyporexia
  • Lack of appetite vs. inability to eat
  • Numerous complications of anorexia
    ○ Cat -> can lead to hepatic lipidosis
67
Q

What is the diagnostic approach to anorexia

A
- History 
○ Drug
§ Digoxin, chemotherapy, antibiotics, opioids 
○ Environment
§ Competition, change in diet, change in contact with people 
- Physical examination
○ Digital rectal exam
- If required
○ Neurological exam 
○ Clinical pathology - urinalysis, faecal 
○ Imaging 
○ Pathology
68
Q

What are the treatment options for anorexia (principles)

A
- Treat underlying cause
○ Definitive therapy if possible
- Dietary appetite stimulation
○ Treat nausea and pain first - maropitant 
- Appetite stimulants
○ Small benefit
- Assisted feeding - nasooesophageal tube, oesophageal, gastric tubes (oesophageal issues)  
○ If ↓ RER ≥ 3 days
- No disease benefits from starvation
- Use the gut and use it early
69
Q

Dysphagia what is it, the 5 main types, what occurs and clinical signs and what is the main issue

A
  • Difficult or painful swallowing
    1) Oral dysphagia - results from oral disease - difficultly prehension and breaking down
    ○ Might only chew on one side of the mouth
    2) Pharyngeal dysphagia - impaired irritation to back of the mouth
    ○ Repeated swallowing attempts with flexing of head
    3) Cricopharyngeal dysphagia - impaired relaxation of cricopharyngeal muscles
    ○ Regurgitation, coughing, repeated swallowing
    4) Oesophageal dysphagia - impairment of movement of bolus through oesophagus
    ○ Regurgitation - WILL SAY VOMITING
    5) Gastroesophageal dysphagia - difficult passage through caudal oesophageal sphincter
    ○ Regurgitation - differentiate with swallowing studies
  • ANY CAN CAUSE ASPIRATION PNEUMONIA - image the chest
70
Q

General history presentation for dysphagia

A
  • Young : congenital
    ○ Time of weaning, hypothyroidism
  • Young / middle aged : FB, caustic substances
    ○ Westies -> oesophageal FB most common -> treatment of choice endoscopy
  • Geriatric / chronic disease : systemic illness
  • Acute onset
    ○ Obstruction, mass, inflammation
    • other neurological disease
      Neuropathies, NMJ disorders, myopathies
71
Q

Dysphagia diagnostic approach

A
  • Complete physical exam
  • Observe eating
  • Oral exam - +/- radiographs of mouth
  • Neurological exam (care Rabies!)
  • Survey head / neck / thorax radiographs
  • CBC, biochemistry, urinalysis
  • Advanced
    ○ Contrast video fluorography motion studies
  • Endoscopy
72
Q

Dysphagia treatment principles

A
  • Treat underlying cause
  • Empirical
    ○ Alter food consistency, frequency, position (bailey chair)
    ○ Feeding tube
  • Rx aspiration pneumonia / pneumonitis
73
Q

Orbital disease how common, anatomy and what occurs

A
  • Common
  • Anatomy
    ○ Frontal, lacrimal, zygomatic, presphenoid, basiphenoid and palantine bones
    ○ Globe, CN II – VII, blood vessels, TEL / lacrimal / zygomatic gland, extra ocular / masticatory muscles, fat, periorbita
    ○ Lots of superimposition -> radiographs not great often need ultrasound, CT or MRI
  • Compression or invasion of
    ○ Sinuses, teeth, ramis
74
Q

Diagnostic approach to orbital disease

A
- History
○ Onset, duration, behavioural changes - invasion to forebrain, ask about vision 
- Physical examination
○ Can you retropulse the eye, painful, opening and closing mouth, oral exam, neurological exam 
- Primary signs - presentation 
○ Exophthalmos, enophthalmos, strabismus
- Secondary signs
○ Altered vision, eye not moving properly, facial paralysis, droopy eyes, corneal oedema, unable to blink 
- CBC
○ Infectious or inflammatory causes?
- Biochemistry
- FNA cytology - OFTEN NEEDED need to be careful of other structures 
- Radiographs
- Ocular ultrasound 
- CT - generally what start with 
- MRI - if brain involvement 
- Surgery - imaging first
75
Q

Orbital disease causes, general and more specific causes

A
- Inflammatory
○ Orbital &amp; retrobulbar abscess
§ FB tracking up - bones 
○ Eosinophilic myositis
§ Inflammatory, pain on mouth, swollen extra-ocular muscles, atrophy (muscle wastge) 
○ Extra ocular polymyositis
§ Immune mediated response 
○ Orbital emphysema
§ Significant trauma 
○ Retrobulbar haemorrhage
§ Trauma, coagulopathy, neoplasia 
○ Granuloma 
- Neoplastic : Primary, metastatic, local invasion
- Cystic : Zygomatic mucocele
- Congenital
76
Q

Orbital treatment and prognosis

A

Treatment
- Treat cause
○ If infectious may need culture and sensitivity
- Medical – Rx infections, drainage, lavage, managing cornea ulceration
- Surgery (histopathology / culture)
- Dentistry – remove diseased teeth
- Myositis – Immunosuppressives
Prognosis
- Inflammatory : Favourable
- Neoplastic : usually malignant - guarded prognosis

77
Q

Oral tumours how common, incidence how increase, typical signs, how look and diagnosis and character

A
  • Common in dogs and cats
  • Incidence increases with age
  • Typical signs
    ○ Lose teeth, facial deformity, oral anorexia, bleeding, lymph node enlargement (less likely)
  • All look grossly same (except black melanomas - still need biopsy to confirm)
  • Require detailed oral exam
    ○ Best with sedation / GA
  • Can be locally invasive
78
Q

Staging oral tumours what are important parts and prognostic factors - EXAM

A
  • Document - take pictures, measurements
  • FNA (mass), LN - dangerous -> often come back inflammatory or necrotic - COULD STILL BE NEOPLASIA
    ○ LN - important to see if spread
  • CBC / Biochemistry
  • Cats : FeLV / FIV test
  • 3 view chest radiographs (CT) - when malignant - nose, mouth, neck, chest
  • +/- Abdominal ultrasound (e.g. older patient) - RARE - more for melanoma (tends to go to abdomen)
  • Skull / dental radiographs - not as preferred
  • CT / MRI - best for planning or determining if CNS involvement
  • Biopsy (incision vs. excisional) - usually image first then biopsy
  • Prognostic factors
    ○ Further forward, less than 2cm, without lymph node involvement or bone lysis - BEST
79
Q

Oral tumours symptomatic care what is involved

A
  • Secondary infection & inflammation common
    ○ Antibiotics - systemic stomatitis is common
    ○ Anti-inflammatories - NSAID or corticosteroids
  • Analgesia
  • Oral rinses - keep moist mouth, prevent salivation build up
  • Feeding tube - important post-surgery
80
Q

Types of oral tumours and which is most common

A
  • Melanoma (30-40%)
  • Squamous cell carcinoma (20-30%)
  • Fibrosarcoma (10-20%)
  • Odontogenic tumours
  • Papilloma
  • Others : Multilobular tumours, plasma cell, mast cell, granular cell, transmissible venerable tumours, osteosarcoma, sarcoma, lymphoma
81
Q

Feline oral tumours what percentage of tumours, character, what age, most common and treatment

A
  • 10% of feline tumours
  • Usually detected late, most > 90% malignant
  • Older cats > 10 years
  • Most squamous cell carcinoma - increased risk for smoking households, flea collars
    ○ Sublingually and on mandible most common
  • Rx: (Surgery) > Radiation therapy
82
Q

Idiopathic trigeminal neuritis presnetation, differential, clinical signs, treatment and recovery

A
  • Acute onset dropped jaw
  • DDx: Infectious, Inflammatory, neoplastic
  • ↓ Motor function, variable ↓ sensory function
  • Rx: Supportive feeding
  • Usually recover 3 weeks
83
Q

Masticatory muscle myositis what is it, breeds, acute and chronic clinical signs

A
  • Focal autoimmune myositis
    ○ Type II M myofibers of mastication - only found in temporal and masseter muscle
    § Other muscles groups in the body - NOT AFFECTED
  • Young large breed dogs
  • Acute:
    ○ Swelling, pain, limited opening, ↑ [CK]
  • Chronic:
    ○ Atrophy, limited opening
84
Q

Masticatory muscle myositis diagnosis, treatment and prognosis

A
  • Dx : Antibodies against type II M myofibers - blood test
    ○ CT, MRI, EMG, Histopathology - can have changes within those muscle groups
  • Rx : Immunsupressives: Prednisolone (Azathioprine)
  • Good prognosis but atrophy usually persists
    ○ Usually aiming for function - open mouth and eat
    § Measure the distance between incisors -> are they increasing in their ability to open the mouth
    ○ Cosmetic will remain the same
85
Q

oral tumours in dogs list 7 and their character

A

1) oral malignant melanoma - invasive, distant metastasis
2) oral squamous cell carcinoma - erosive/proliferative mass, locally aggressive but good prognosis
3) oral fibrosarcoma - histologically low grade, but biologically high grade, cure unlikely
4) odontogenic origin - acanthomatous ameolobastoma
5) oral lymphoma - poor prognosis, chemotherapy cannot cure
6) ronillar tumours - rare - cannot cure
7) salivary gland tumour - rare, invasive - not possible to cure

86
Q

What is considered weight loss, why occurs, main issue and how to recognize

A
  • Loss than more than 10% of body weight
  • Energy use or loss > energy intake
  • Long DDx list
    ○ Investigate other problems first (if present)
  • Determine appetite when the weight loss began
    Recognition of weight loss
  • Body condition scoring
87
Q

Approach to weight loss

A
- History
○ Diet, clinical signs - diarrhoea, vomiting, appetite, activity 
- Physical examination
○ GI, cardiovascular, neurological 
- Haemogram, biochemistry, urinalysis
○ Cats: FIV, FeLV, TT4
- Faecal flotation
- Thoracic radiographs
- Abdominal ultrasound >abdominal radiographs
- Repeat PE
- Organ function testing (BATT, ACTH stim, TLI, B12)
- GI endoscopy Vs. Laparotomy
- CNS
88
Q

If still not sure about weight loss what to do next and what are some challenging cases

A
  • ? Occult neoplasia
  • Wait and retest
  • The challenging cases
    ○ Gastric disease without vomiting
    ○ Small intestine disease without diarrhoea
    ○ CNS disease without CN deficits / seizures
    ○ Hepatic disease with normal ALT, ALKP
    ○ Hypoadrenocorticism with normal electrolytes
    ○ Occult inflammatory disease
    ○ Dry FIP
89
Q

Feline hyperthyroidism what age, how common, caused by (3 types)

A
  • Common cats > 8 years of age
  • MOST COMMON ENDOCRINE DISEASE IN CAT
  • No breed or sex predilection
  • Caused by:
    ○ >98% benign adenoma or hyperplasia
    § > 80% bilateral at diagnosis
    ○ < 2% thyroid carcinoma
    ○ Idiopathic
    ? Nutritional, environmental, chemical, goitrogen
90
Q

Feline Hyperthryoidism history

A
  • Weight loss despite normal or ↑ appetite
  • Gradual in onset
  • Vomiting, Diarrhoea, Pu/Pd
  • Poor hair coat - looking scruffy
  • Behavioural changes - some become hyperactive, others more quiet
  • Large bulky stools
  • Heat intolerance
  • Apathetic (10%) : lethargy, weakness, weight loss, anorexia, cardiac changes
  • Asymptomatic (early)
91
Q

Feline hyperthryoidism physical exam findings

A
- Palpable thyroid goitre (90% of cases)
○ Can be preclinical
○ Can be ectopic
- Tachycardia
- Heart murmur / gallop (50% of cases) - Thyrotoxic Cardiomyopathy 
- Dehydration - generally hypotensive 
- Weight loss
- Measure BP for hypertension
92
Q

Feline hyperthryoidism clinical pathology findings

A
  • CBC : significant changes uncommon
    ○ Mild polycythemia, stress leukogram, dehydration
  • Biochemistry
    ○ ↑ ALT, < 600 IU/L (50-75% of cases) usually more increased than ALP
    ○ ↑ BUN & Creatinine (30-40%) - typically concurrent renal disease
    ○ ↑ [P] (20%)
  • Urinalysis
    ○ Moderate concentrated
    ○ Occult UTI - subclinical bacterial infections
93
Q

Feline hyperthyroid concurrent problems what are the 3 main ones

A

1) chronic kidney disease
2) throtoxic cardiomyopathy
3) hypertension (always measure BP)

94
Q

chronic kidney disease as a concurrent feline hyperthryoid issue what age, how occurs, what is important and what need to monitor

A

○ Older patients
○ Hyperthyroidism ↑ GFR & may mask CKD (33% of cases)
§ Yet same survival if unmask underlying CKD with treatment
○ Hyperthyroidism & Hypothyroidism can -> CKD
§ Important to establish euthyroidism
○ Need to monitor renal function with Rx

95
Q

Thyrotoxic cardiomyopathy as a concurrent feline hyperthryoid issue how occurs, clinical signs, how many sizes, what seen, treatment

A

§ Hyperthyroidism -> ↑ Cardiac output, hypertension, ventricular eccentric hypertrophy (rare dilated)
§ Tachycardia, systolic murmur, gallop
§ 20-30% cases have cardiomegaly
§ ECG: Tachycardia, increased R wave
§ (Rare: Ventricular arrhythmias / CHF < 5%)
§ Reversible with treatment
§ Echocardiograph to DDx other cardiomyopathies if clinically required

96
Q

Feline hyperthyroidism diagnosis and some additional tests, are they usually done

A
  • Total T4 - above reference range
    ○ Can get false negatives - repeat test in a few weeks
    ○ Can have other diseases repressing the total T4 - abscess
  • If Equivocal results
    ○ Thyroid Scintigraphy - DONE
    ○ fT4 by equilibrium dialysis - NOT DONE
    ○ T3 suppression test - NOT DONE
    ○ TRH stimulation - NOT DONE
97
Q

Feline hyperthryoid what are the 4 treatment options - EXAM

A
  1. Radioactive iodine - most common now
  2. Medical management
  3. Thyroidectomy
  4. Dietary
98
Q

What are some important considerations for treatment of choice for feline hyperthryoidism and in terms of client perspective what is low and high impact on choice

A
  • Clinical severity
  • Concurrent disease (cardiac / renal)
  • Age
  • GA / surgery risk
  • Access to radio-iodine
  • Surgical skill, post-operative care
  • Owner / cat compliance
  • Cost
  • Prognosis
  • Side effects
  • Low impact on treatment choice
    ○ Cost of treatment
    ○ Travel distance
    ○ Waiting times for treatment
  • High impact on treatment choice*
    ○ Hospitalisation times when long
    ○ Concerns about how pet will cope away from home
99
Q

Radioactive iodine therapy for feline hyperthryoidism positives, how given and negatives

A

PROS
- Simple, safe, effective, definitive, works on ectopic tissue
- Best option most cats, > 90% cure with 1 treatment
- Readily available*
- Longest survivals
- No requirement for GA, surgery, ongoing medications
Given SC or PO (orally - generally done here)
CONS
- Small risk of hypothyroidism, need facilities & stable patient, requires isolation ( 7 days)
○ Some animals if high risk not appropriate as cannot give intensive monitoring
- High initial cost ($1530 at UVET) but most cost effective long term

100
Q

Radioactive iodine what care at home is required afterwards

A

Restrict close contact to few minutes daily in the first 2 weeks
- Special precaution if pregnant, children
○ Change litter with rubber gloves
○ Clean excretions with paper towels, discard
- Recommended recheck with veterinarian at 1 month and 3 months