Dogs and cats 25 Flashcards
brainstem syndrome which side are signs and the main structures and therefore functions affected - EXAM
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
Neurological examination what seen with brainstem syndrome
- 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
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
1) left brainstem
2) right forebrain
What are the 2 main things that result from brainstem and forebrain syndrome and the clinical signs
- 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
cerebellar syndrome what side are the signs and the main function
IPSILATERAL SIGNS
Functions of the cerebellum
- “Coordination of movements so they are fluid in nature” Sean
Neurological examination what seen with cerebellar syndrome
- 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
Encephalpathies what are the 7 main ones
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)
Cerebellar abiotrophy what is it, cause and clinical signs
- 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
Cerebellar abiotrphy diagnosis, treatment and prognosis
- 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
Hydrocephalus cause, breeds, cliical signs
- 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%
Hydrocephalus diagnosis and treatment
- 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
Brain tumours what are most common in dog and cat, primary or secondary and clinical signs
- 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
Brain tumours diagnosis
○ 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
Brain tumours staging how common metastasis and which hard to treat with chemotherpy
○ 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
Brain tumours treatment which treat, which has best prognosis and options
○ 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
Thiamine deficiency how does it lead to an encephalopathy and clinical signs
○ 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
Thiamine deficiency diagnosis, treatment and prognosis
- 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
Meningoencephalitides of unknown origin (MUO) define, what are the types and cause
- Definitions
○ Inflammatory non-infectious (MUCH MORE COMMON)»_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
Meningoencephalitides of unknown origin (MUO) clinical signs and diagnosis
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
Meningoencephalitides of unknown origin (MUO) treatment and prognosis
- 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
Cerebro-vascular accidents (stroke) types, cause and clinical signs - EXAM
- Types -> Ischaemic (Artery blockage)»_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
Cerebro-vascular accidents (stroke) diagnosis, what should look for and prognosis
- 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
Vestibular systems structures and other structures associated with
- 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
What is the normal functioning of vestibular system and what occurs when things go wrong
- 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
In terms of neurological examination what found on observation and why
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
Vestibular disease neurological exam findings all besides observation
- 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
What are the 2 main types of vestibular syndromes and what associated with
- 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)
What are the 3 main causes of peripheral vestibular syndrome
1) Infectious otitis media-interna - MOST COMMON CAUSE
2) Idiopathic/geriatric vestibular syndrome - second more common
3) Primary secretory otitis media-interna (PSOM)
What is the most common cause of peripheral vestibular disease, pathophysiology, clinical signs and diagnosis
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
Infectious otitis media-interna treatment and prognosis
- 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
Idiopathic/geriatric vestibular syndrome pathophysiology, clinical signs, diagnosis, treatment and prognosis
- 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
Primary secretory otitis media-interna (PSOM) what a cause of, what is involved, main breed, clinical signs, treatment and prognosis
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
Define a seizure
○ 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)
Seizure what is the main characteristic, clinical signs and what are the 4 phases
○ 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
How does a seizure occur and the 2 main types
○ 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
Generalised seizure origin and presentation
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…
Partial seizure origin, presentation and types within
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…
What are some common presentations (pheonotypes) of partial seizures
§ 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
What are the 3 differential type of seizures in terms of duration and frequency and what is epilepsy
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
What are the 3 main types of seizures that help narrow down differentials
1) extra-cranial
2) intra-cranial
3) idiopathic (familial)
Extra-cranial seizure disorder diagnosis and main causes and what important to remember
○ 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
Extra-cranial seizure what are the typical clinical presentations
§ Seizure phenotype □ Generalised > partial □ Possible status epilepticus (toxics, hypoglycaemia) § Other clinical signs □ Depending on the cause ® Kidney diseases (CKD…) ® Liver diseases (congenital PSS…)
Intra-cranial seizure common cause, other causes and clinical presentation (differentiating feature)
○ 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
Idiopathic (familial) seizures what is the disease, caused by and 3 subgroups
○ 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
Idiopathic epilepsy (primary) clinical presentation and common onset
§ 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
Status epileptius how common and causes
§ First manifestation of seizures in 60% of epileptic dogs • 45% intracranial disease • 30% toxics • 25% idiopathic § Not discriminant
Investigation for seizure cause how to rule in or out extra-cranial disease
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
Investigation for seziure cause how to rule in or out intracrnail disease
- Advanced imaging ○ Gold standard = MRI § Soft tissue resolution ○ Tomodensitometry (CT-scan) acceptable § Head trauma - Cerebro-spinal fluid (CSF) tap ○ Cisternal = closer to the brain
Therefore what investigation is needed for seizures to find cause
- 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
Steps in seizure management
1) stop the seizure
2) treat underlying cause if necessary
3) long terms management including important consult
Steps in stopping a seizure and what if no IV access
- Place IV catheter
- IV diazepam/midazolam
○ Few minutes between injections
○ No more than 3 injections - IV propofol - prepare to intubate (rare)
- IV thiopental / pentobarbital (if propofol doesn’t work) - SLOW INJECTION
- 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
Facts about seizures: how common in sudden death, how common lead to euthanasia
- 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)
In terms of seizures why is there a high morbidiy
→ 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
What are some possible therapeutic options for idiopathic seizures
- 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
Treating the underlying cause in seizure management what is involved
- Intracranial ○ Tumour reduction = ↓ seizure frequency (humans) ○ MUOs ○ Hydrocephalus - Extracranial ○ Clear the toxic ○ PSS management - ± anticonvulsant medication
What are 4 main things need to talk about in initial consultation when diagnose idiopathic epilepsy
- 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
When do you need to start a treatment plan for seizures
- 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
Therapeutic objectives to talk about in inital consultation for idiopathic epilepsy what need to discuess
- 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
First line treatments for seizure control what are the 3 main ones, what do and which recommended
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
phenobarbital what used for, what is it and pros and cons
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
Potassium bromide and imepitoin what used for and pros and cons
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
Follow-up after treatment of seizure, how done and when
- 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
What if have too many seizures vs therapeutic objectives?
- 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 - 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
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
- Degenerative disk disease - DISC EXTRUSION DUE TO SIGNALMENT MOST LIKELY
- Congenital vertebral malformations - more chronic (may acutely present as deteriorate)
- Extradural tumour - generally more chronic (exceptions)
- Discospondylitis - fever, extra-neural signs - less likely
- Traumatic - vertebral fracture, luxation - generally grade 4 or grade 5 (not in this case)
- Fibro-cartilagineous embolism (FCE) - back pain so less likely, also symmetrical in this case
If have lesions localisation of Left hand side- L4-S3 and Right hand side- T3-L3 what disease thinking and why
- 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
Anorexia how common, associated with, define and issues
- 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
What is the diagnostic approach to anorexia
- 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
What are the treatment options for anorexia (principles)
- 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
Dysphagia what is it, the 5 main types, what occurs and clinical signs and what is the main issue
- 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
General history presentation for dysphagia
- 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
- other neurological disease
Dysphagia diagnostic approach
- 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
Dysphagia treatment principles
- Treat underlying cause
- Empirical
○ Alter food consistency, frequency, position (bailey chair)
○ Feeding tube - Rx aspiration pneumonia / pneumonitis
Orbital disease how common, anatomy and what occurs
- 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
Diagnostic approach to orbital disease
- 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
Orbital disease causes, general and more specific causes
- Inflammatory ○ Orbital & 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
Orbital treatment and prognosis
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
Oral tumours how common, incidence how increase, typical signs, how look and diagnosis and character
- 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
Staging oral tumours what are important parts and prognostic factors - EXAM
- 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
Oral tumours symptomatic care what is involved
- 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
Types of oral tumours and which is most common
- 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
Feline oral tumours what percentage of tumours, character, what age, most common and treatment
- 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
Idiopathic trigeminal neuritis presnetation, differential, clinical signs, treatment and recovery
- Acute onset dropped jaw
- DDx: Infectious, Inflammatory, neoplastic
- ↓ Motor function, variable ↓ sensory function
- Rx: Supportive feeding
- Usually recover 3 weeks
Masticatory muscle myositis what is it, breeds, acute and chronic clinical signs
- 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
Masticatory muscle myositis diagnosis, treatment and prognosis
- 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
oral tumours in dogs list 7 and their character
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
What is considered weight loss, why occurs, main issue and how to recognize
- 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
Approach to weight loss
- 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
If still not sure about weight loss what to do next and what are some challenging cases
- ? 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
Feline hyperthyroidism what age, how common, caused by (3 types)
- 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
Feline Hyperthryoidism history
- 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)
Feline hyperthryoidism physical exam findings
- 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
Feline hyperthryoidism clinical pathology findings
- 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
Feline hyperthyroid concurrent problems what are the 3 main ones
1) chronic kidney disease
2) throtoxic cardiomyopathy
3) hypertension (always measure BP)
chronic kidney disease as a concurrent feline hyperthryoid issue what age, how occurs, what is important and what need to monitor
○ 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
Thyrotoxic cardiomyopathy as a concurrent feline hyperthryoid issue how occurs, clinical signs, how many sizes, what seen, treatment
§ 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
Feline hyperthyroidism diagnosis and some additional tests, are they usually done
- 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
Feline hyperthryoid what are the 4 treatment options - EXAM
- Radioactive iodine - most common now
- Medical management
- Thyroidectomy
- Dietary
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
- 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
Radioactive iodine therapy for feline hyperthryoidism positives, how given and negatives
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
Radioactive iodine what care at home is required afterwards
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
