Dogs and Cats 24 Flashcards

1
Q

Discospondylitis what is it, main pathogens and entry

A
- Intervertebral disc infection
○ Vertebral endplates infection 
○ Bacterial
§ Staphylococcus spp, Steptococcus spp, Brucella
○ Fungal
§ German Shepherd dogs
§ Aspergillus
○ Entry
§ Haematogeneous = urinary tract infections…
§ Foreign bodies + grass awn…
§ Iatrogenic = surgery
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2
Q

Discospondylitis signalment, location and symptoms/signs

A
- Epidemiology
○ Older, male, medium-to-large breed dogs
○ Thoraco-lumbar , L7-S1
○ 40.7% multiple sites
- Symptoms and signs
○ Pain - very painful 
○ Pyrexia - distinction from other diseases above 
○ Neurological deficits
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3
Q

Discospondylitis diagnosis

A

○ CBC
○ Radiographs
§ No changes before 2-4 weeks - cannot rule out
○ MRI>CT - better
○ Looking for the microbe, negative in 50%
§ Disk aspirate
§ Blood, urine, prostatic fluid culture
§ Submit fungal culture if GSD! - IMPORTANT
§ Rapid agglutination test for Brucella (zoonosis!)

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4
Q

Discospondylitis treatment

A
○ Antibiotics
§ Cefalexine
§ Culture results
§ IV if paralysed or pyrexic
§ Mean duration = 53.7 weeks
○ Antifungal if required
§ ++ poor prognosis
○ Pain relief
○ Imaging follow-up
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5
Q

Steroid-responsive meningitis-arteritis what type of disease, what occurs and signalment (hallmark)

A
- Auto-immune disease
○ Aseptic suppurative infiltration
§ Monocytic if protracted
○ Targeting arteries
○ Meninges, joints, guts, pericardium
- Young adults
○ Medium-to-large breed dogs
○ Beagle, Boxer, Bernese mountain dogs
○ “Beagle pain syndrome” - beagles with neck pain + pyrexia = HALLMARK
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6
Q

Steroid-responsive meningitis-arteritis signs

A
○ Neurologic
§ (Wax and waning) neck pain
§ CNS signs if protracted
○ Systemic
§ (Wax and waning) pyrexia
○ Other body systems
§ Polyarthritis (neutrophilic), enteritis, pericarditis
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7
Q

Steroid-responsive meningitis-arteritis diagnosis

A

○ CSF tap - generally enough (with neck pain and pyrexia)
§ Demonstrate neutrophilic inflammation
□ Other times this occurs is with bacterial infection of spinal cord - very rare
§ Aseptic suppurative pleocytosis - NON-DEGENERATE NEURTOPHILS
§ Monocytic if protracted
○ Serum/CSF IgA
○ Joint tap? - can do at the same time of CSF tap
○ Brain + neck MRI?

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8
Q

Steroid-responsive meningitis-arteritis treatment and follow up

A
  • Treatment
    ○ Have to treat others die from systemic inflammatory infection
    ○ Steroids (Steroid responsive)
    § First immunosuppressive, then taper down (need to be systematic - use guidelines)
    § Can take months to resolve
    ○ + azathioprine if relapse (need to go back to steroid immunosuppressive)
  • Follow-up
    ○ CSF taps - before taper need to ensure getting better
    ○ C-reactive protein
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9
Q

Fibro-cartilagineous embolism what occurs, signlament - EXAM

A
  • Embolisation in arterial spinal cord supply -> ischaemic area of the spinal cord that the artery supplies
    ○ Fibrocartilage
    ○ From intervertebral dis
  • Adult non-chondrodystophic dogs
    ○ But all sizes and ages described - mainly large breed besides:
    ○ Miniature Schnauzer
    ○Also cats
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10
Q

Fibro-cartilagineous embolism signs - EXAM

A

○ Ataxia and paresis
○ Hyper-acute to acute < 24h -> peck of clinical signs generally within minutes (sometimes under 24hours) then start to recover
○ Sometimes -> Exercise induced
○ Sudden pain when it occurs then non painful
○ Often asymmetric
○ Intumescences often affected - more arteries to these areas -> more likely for embolism to occur in one of these

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11
Q

Fibro-cartilagineous embolism diagnosis and prognosis - EXAM

A
  • Diagnosis
    ○ Myelography and CT
    § Swelling of the cord
    ○ MRI - only one can see the ischemia of the spinal cord (generally geometric (shape) lesion - characteristic of ischemia)
    § + prognosis value
    ○ Lumbar CSF tap
    § Non specific - just spinal cord injury reflects
  • Self-improving condition - Good prognosis - takes a few weeks
    ○ 85-90%
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12
Q

what are some common toxins that cause tremors, diagnosis and when important

A

Toxins that cause tremors
- Snail baits - metaldehyde, carbamate
- Tremogenic mycotoxins - garbage, compost, mouldy food
- Chocolate
- Cane toad poisoning
- Pyrethroids
- Tetanus
Diagnosis
- Generally presentation, history and clinical signs
- Toxic assays generally not reliable as made for humans and animals can metabolise into different molecules
Most of the time won’t know what is causing - just give supportive treatment
BUT TOXINS BELOW NEED SPECIFIC TREATMENT - so need to identify these and treat accordingly

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13
Q

What toxins need specific treatment - list the 5

A

1) cane toad
2) tetanus
3) pyrethroids
4) snake envenomation
5) tick paralysis

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14
Q

Cane toad poisonings what is it, toxins from where and presentation

A
- Rhinella marina 
○ Toxins -> secrete from skin from the parotid salivary gland (how to identify)
- Presentation
○ More common in endemic area
○ Young dogs 
○ Terriers - love to snap and bite at the toads -> hunters 
○ Toads are nocturnal 
○ Summer > winter
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15
Q

Cane toad toxin mechanism of action

A
  • Absorbed through mucous membranes -> doesn’t have to eat the toad
  • Different toxins
    1. Bufotoxins and bufogenins
    ○ digitalis-like - cardiac tachyarrhythmias
    2. Bufotenines
    ○ serotonergic substance -> hallucination, hyperaesthesia, seizures
    3. Catecholamines
    ○ adrenaline -> arrhythmias, hypertension, tachycardia, bronchoconstriction
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16
Q

Cane toad toxin clinical signs and diagnosis

A
Clinical signs 
- Hyperaemic mucous membranes and salivation - first ones to see - GENERALLY PRESENT WITH 
- Hyperaesthesia seizures, ataxia, tremors, depressed or altered mental state 
- Tachycardia and cardiac arrhythmias 
- Vomiting 
- Respiratory distress 
○ Can have aspiration pneumonia 
Diagnosis 
- History 
- Access to toads
- Clinical signs
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17
Q

Can toad toxin treatment with 4 options and prognosis

A

Treatment
1. Manage life threatening problems
○ IV catheter -> give diazepam
§ Tremors/seizures
§ Respiratory compromise
§ Arrhythmias
2. Decontaminate
○ Wash gums thoroughly - rinse and wipe until salivation has stopped (5-20mins)
○ Decontamination of the stomach if required
§ If toad swallowed (unlikely) need to get out of the stomach - endoscopy with sedation
3. Cyproheptadine - cannot induce vomiting when seizures or tremors
4. Supportive care
Prognosis
- Prognosis is good if veterinary treatment is sought early
- About 90% survival

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18
Q

Tetanus what toxin from, how common, what occurs and what does the toxin do, susceptibility of species

A

Clostridium tetani
○ Ubiquitous
○ Spores enter a wound and develop if conditions are anaerobic
§ Young dogs during teething is common - breaking of epithelial barrier
○ Exotoxin = tetanospasm
§ Tetanospasm spreads via the blood and is taken up by nerves (CNS)
§ Prevents CNS inhibitory neurotransmitter release - signs of hyperexcitability
□ Glycine and gamma-amminobutyric acid (GABA)
§ Bound toxin is irreversible
○ Susceptibility: horse and humans > dogs > cats

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19
Q

Tetanus onset of clinical signs, and examples of clinical signs

A
  • Onset of clinical signs may take up to 3 weeks -> so may not find the wound (always look but not always there)
    ○ Signs are progressive
    § Earlier the
    ○ Loss of inhibition of motor neurons -> sustained spasm
  • May be generalised or localised (esp. cats) - can localise in one limb (looks like aorta thromboembolism (BUT will have pulse, be warm and have blood flow in the leg)
  • Examples
    ○ Stiff gait - trouble getting up, moving around
    ○ Saw-horse stance
    ○ Ears drawn together
    ○ Muscle spasm in response to stimuli
    ○ TEL protrusion
    ○ Salivation
    ○ Regurgitation
    ○ Opisthotonus
    ○ Respiratory difficulty
    ○ Trismus
    ○ Recumbency
  • Generally gets worse before it gets better
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20
Q

Tetanus diagnosis and treatment

A

Diagnosis
- History - wound, parturition, teething, surgery
- Clinical signs are very specific but can be subtle
○ WHEN WE WANT TO TREAT
- If don’t know JUST TREAT AS IF IT IS ANYWAY -> because consequences if you don’t is very severe
Treatment
- SUPPORTIVE CARE
○ Sedation, muscle relaxants
○ Analgesia
○ Minimise external stimuli
- Metronidazole (or clindamycin)
- Debride the wound
- Anti-toxin (mop up any free toxin - DOESN’T STOP THE ONE ALREADY BOUND)

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21
Q

Tetanus complications and prognosis

A
Complications 
- Hypertension 
- Tachycardia
- Spasticity of respiratory muscles 
- Aspiration pneumonia 
- Lack of nutrition 
- Urinary and faecal retention 
Prognosis 
- GUARDED 
- Most patients will deteriorate further before they improve 
- Recovery can be prolonged (7-14 days) - EXPENSIVE 
- Survival rate in dogs 50-92% with adequate support
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22
Q

Pyretrhoids what toxic to, found in, absorption, mechanism of actin and metabolism

A
  • Toxic to cats
  • Flea products
    ○ Dog spot on is the main culprit
    ○ Often get multiple cats from the same household
  • Rapid absorption
  • Slows down activation and inactivation of sodium channels
    ○ -> repetitive firing of action potentials
  • Metabolised by liver via glucuronidation
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23
Q

Pyrethroid clinical signs and diagnosis

A
Clinical signs 
- Salivation 
- Vomiting
- Hyper-excitability 
- Hyperaesthesia 	
- Tremors 
- Seizures 
- Respiratory difficulty
- Weakness 
Diagnosis 
- History 
○ Signs are noticed about 3 hours after a spot on product has been applied 
○ Occasionally an owner will be reluctant to confess 
- Clinical signs 
○ Look for an oily substance on fur with characteristic smell
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24
Q

Pyrethroid treatment and prognosis

A
Treatment 
- Decontaminate by washing copiously with lukewarm water (too warm vasodilate will absorb more) and dish water detergent 
- Anti-seizure medication 
- Muscle relaxants 
- Supportive care 
- Lipid therapy?
Prognosis
- Recovery usually takes 24-48 hours 
- Good prognosis if prompt and adequate care
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25
Q

List 10 toxins that decrease activity of the nervous system

A
  1. Snake envenomation
  2. Tick paralysis
  3. Ethylene glycol
  4. Barbiturate - scavenging the euthanasia carcass
    ○ Present as in under general anaesthesia -> supportive care will generally get better
  5. Intermediate or delayed presentation of organophosphate and carbamate
  6. Baclofen
  7. Monensin
  8. Alpha-latrotoxin
  9. Tetrodotoxin
  10. Botulism
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26
Q

Snake envenomation what are the 6 main toxins and snakes wtihin, which most common and why

A
  • Peduonaja (brown snakes)
  • Botechis (tiger snakes)
  • Pseudechis (black snakes)
  • Austelaps (copperheads)
  • Oxyuranus (taipans)
  • Acanthophis (death adders)
    Top 3 most common as more common in areas where humans are around
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27
Q

What are the 5 main toxins found in snake venom and how classified

A
- Classified according to their site of action 
○ Neurotoxins -
○ Myotoxins
○ Procoagulants
○ Anticoagulants 
○ Cytotoxins
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28
Q

Neurotoxins in snake venom what snakes found within,mechanism of action, clinical signs

A
  • All major venomous genera
  • Pre-synaptic and post-synaptic toxicity
    ○ Depresses the ACh release (irreversible damage)
    ○ Prevents ACh receptor interaction (reversible)
    ○ Post-synaptic -> generally reversible with anti-toxins
    § Black adders -> mainly post so will see more rapid recovery with anti-toxin
  • Takes some time to get clinical signs but takes days to recover from
    ○ Weakness, ataxia, flaccid paralysis
    § Can be from mild - severe -> can get full paralysis within 1 hour
    □ Severe need to put on ventilator
    ○ Tongue protruding - mainly in cats
    ○ Dilated non-responsive pupils
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29
Q

Myotoxins in snake venom which snakes within, what do they cause, general presentation within cats and dogs and how does myopathy form

A
  • NOT in brown snakes, mainly an issue in tiger snake
  • Delayed myotoxicity generally -> next day afterwards generally present
  • Causes progressive rhabdomyolysis -> marked increase in CK levels
    ○ Not high within 12 hours, more of an increase the next 12 hours
  • General presentation with cats
    ○ Don’t notice the cat out hunting and gets bitten
    ○ That night doesn’t eat meal, next day still within the same spot
    ○ Return from work still hasn’t moved -> take to the vet - TYPICAL CAT SNAKE BITE
    § May have full paralysis by this point
  • Presentation in dogs
    ○ Generally don’t see the dog getting bitten but see near the snake or after killed the snake
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30
Q

Myotoxins in snake venom what occurs with myopathy and secondary complications

A
  • Myopathy
    ○ Slow onset of weakness
    ○ Myoglobinura (dark red urine)
    ○ Generalised pain - cannot do pain scores - JUST
    ○ Hyperkalaemia and renal failure are possible secondary complications - NEED TO FLUSH OUT THE PIGMENT FROM KIDNEYS
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31
Q

Procoagulants in snake venom what snake common in, what does it cause, when return to normal and clinical signs before paralysis

A
  • Most common in brown snakes
  • Causes coagulopathy by depleting clotting factors - can occur within 15 mins
    ○ Can see just bleeding into organs - can get brain haemorrhage
  • Markedly prolonged clotting times
    ○ Indicates significant envenomation
  • Clotting returns to normal after 24-36 hours
  • DON’T DO FOR THE JUGULAR FOR BLOOD
    ○ Peripheral veins if possible as can put pressure bandage on
  • Pre-paralytic signs
    ○ Vomiting, urination, defecation, sudden collapse and apparent recovery
    ○ -> INDICATES significant envenomation - NEED ANTI-VENOM
    ○ Generally vomiting, collapse and recover
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32
Q

What snakes are the following toxins found within 1. haemolysins 2. cytotoxins 3. anticoagulants

A

Haemolysins - black snakes, copperheads, tigers
Cytotoxins - black snakes -> swelling
Anticoagulants - black snakes -> inhibit blood clotting, reversible

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33
Q

Snake bite diagnosis

A
  • History
  • Clinical signs
  • Clotting times - aPTT (or ACT) if acute
  • Snake venom detection kit - if acute
    ○ Can only pick up free venom -> within the first 12 hours most will be bound
    § Cannot detect venom bound to receptors sites
    § Cannot detect venom bound with anti-venom
    ○ Detects immuno-type, there is cross reaction
    ○ Detects very low levels of venom
    ○ Specific - able to tell you the type of snake and therefore type of anti-venom
    ○ But not sensitive
  • CK - if delayed (only if myolysins are present)
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34
Q

snake bite treatment what treat with, how and how much to give

A
- Antivenom 
○ Most effective in first 12 maybe 24 hours 
○ Use if systemic signs are apparent 
○ Dilute in saline 1:10 or to 10ml/kg which ever is less
○ Give over 20-30mins 
○ Give the appropriate immunotype 
How much antivenom 
§ Non clinical bites 
□ If not showing systemic signs -> observe
§ Dose per bite NOT PER KG 
□ Mild envenomation
□ Moderate envenomation 
□ Severe envenomation
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35
Q

snake bite treatment how to choose an antivenom and how to know which snake

A

○ Choosing antivenom
§ Tiger-brown combination - tiger, brown, copperhead and most black snakes - MOST COMMON
§ Mulga (king brown) snakes - black snake av not as common now
§ Taipans - taipan av (NORTHERN AUSTRALIA)
§ Death adders - death adder av
§ Polyvalent antivenom treats all venous aussie snakes - very expensive
○ Which snake
§ Local knowledge
§ Appearance (unreliable)
§ Clinical signs (unreliable)
§ Morphological identification (scale counting)
□ Required the head and tail of the snake to be intact
§ SVDK
§ If still unsure consider polyvalent antivenom

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36
Q

monitoring a dog with a snake bite how long for and what monitoring

A
○ Even without clinical signs monitor for 24 hours because if will see signs generally then 
○ Monitoring for:
§ Hypoxaemia/hypoxia
§ Ventilatory failure
§ Hyperkalaemia
§ Renal function
§ Anaemia
§ Coagulopathy - generally gets better with time so generally don't need to use blood products (only if SEVERE anaemia or bleeding into lungs)
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37
Q

Tick paralysis what is the main tick, where found, how much needed to kill and distinct morphological features

A
- Ixodes holocyclus 
○ East coast of australia
○ One female to kill 
○ Many nymphs need to kill 
○ Hundreds of larvae need to kill 
morphological
- Forelimbs and hindlimbs are dark
- Middle legs are more light
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38
Q

Tick paralysis mechanism of action

A
  • Holocyclotoxin - from the salivary glands of the tick when she feeds
  • Neurological effect
    ○ Decreased ACh release at NMJ
  • Cardiac effect
    ○ Diastolic heart failure
    ○ Arrhythmias - can lead to sudden death
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39
Q

Clinical signs of tick paralysis

A
  • Signs develop about 5-7 days after tick attachment
  • Change in voice - one of the most common early signs
  • Coughing/hacking/retching
  • Expiratory grunt
  • Salivation
  • Regurgitation
  • Stumbling/weakness
  • Progressive paralysis leading to complete collapse
  • Respiratory difficulty - multifactorial issues (therefore management needs to be multifactorial) - PUT ON VENTILATOR
    ○ Respiratory muscle paralysis
    ○ Respiratory fatigue
    ○ Laryngeal paralysis
    ○ Pooling of saliva
    ○ Regurgitation - due to megaoesophagus
    ○ Aspiration pneumonia
    ○ Pulmonary oedema
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40
Q

Tick paralysis diagnosis

A
  • History of visitation to an endemic tick area
  • Clinical signs
  • Finding an ixodes holocyclus tick (tick search)
  • Finding a “tick crater” - once leaves, leaves inflammation behind
    ○ SHAVE TO VISULIASE AND REMOVE ANY TICKS (just because found one doesn’t mean there isn’t another)
    § Need to look in ears, around mouth and anus
    ○ Pyrethrin wash as well
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41
Q

Tick paralysis treatment

A
  • Remove tick asap (tell owners to bring it in for identification)
  • Ensure minimal stress, give acetylpromazine (ace) if necessary
  • Tick anti-venom- slow - over 30 minutes
    ○ 5 to 20mL per animal
    ○ IV or IP
  • Tick search (clip long hair if not too stressful)
  • Acaricide treatment - fipronil spay or pyrethroid bath (dogs only)
  • Supportive care
42
Q

Care for paralysed patients in general what provide and prognosis

A
- Supportive 
○ IV fluids
§ Treat shock is present
§ Maintain urine output 
○ Pain relief (opioids)
○ Oxygen supplementation 
§ May need tracheostomy 
§ Endotracheal intubation
§ Mechanical ventilation 
- Anxiolytics 
- Manage gastrointestinal complications 
- Lubricate eyes - cannot blink 
- use a blind, tap eyes shut as cannot themselves for sleeping 
- Clean mouth, lubricate tongue 
- Monitor 
○ SpO2 and PCO2
○ Fatigue, monitor RR
- Keep in sternal recumbency 
In most cases - PROGNOSIS IS GOOD
43
Q

what are the 7 steps in cardiac arrest what is the most important in terms of survival and which best chance

A
  1. Warning signals of impending cardiac arrest
  2. Cardiac arrest
  3. Basic life support
  4. Advanced life support
  5. Return of spontaneous circulation
  6. Time of recovery
  7. Discharge from hospital with acceptable quality of life
    ○ ALSO POST CPR RECOVERY THAT IS IMPORTANT
    - Ones under anaesthesia have best chance to survive to discharge
44
Q

Prevention of cardiac arrest why best and how done and 2 main things needed

A
  • Best cure as prognosis is BAD
  • Respiratory distress
    ○ Oxygen cage, intubation of the patient, emergency tracheostomy (NEED TO BE PREPARED - have equipment and aseptic technique but may not need to be done (only done if cannot intubate), mechanical ventilation
    1) preparedness
    2) early recognition
45
Q

Preparedness for cardiac arrest what is needed

A
  • May not always be able to prevent cardiac pulmonary arrest
  • CPR training is needed
    ○ Need both knowledge of how to do didactic training - cognitive skills
    ○ Also need stimulation technologies that provide immediate feedback to teach psychomotor skills
  • Environment that is inducive of successful CPR
    ○ Cognitive aids -> CPR algorithm (know the steps), dosage charts
    ○ Crash cart -> defibrillator, monitoring, tracheooesophageal tubes, drugs, needles
    ○ Issues that can compromise CPR attempt
    § Broken or missing equipment
    § Incomplete stocking of crash cart
    § Expired drugs, missing syringes
    ○ Multiple studies demonstrate outcome effects
46
Q

Early recognition for CPR how done and why

A
  • Clinical diagnosis
    ○ Cardiac arrest -> unconscious and not breathing
    § If anaesthesia harder to determine, respiratory depression and unconscious is normal
    □ Need other monitoring equipment like ECG, blood pressure, blood gases etc.
    § Should I palpate a pulse? - HARD TO DO SO NO
  • Want to get compressions started as soon as possible
47
Q

What are the 5 main steps in CPR and things within

A
  • Top -> unresponsive, apnoeic patient
    CPR initiate immediately - TEAM IMPROVES OUTCOME -> YELL FOR HELP
    ○ CPR
    1) Basic life support
    a) Start with chest compressions - MOST IMPORTANT ASPECT
    b) ventilation - as soon as possible
    2) advanced life support - run once got basic life support going
    a) monitoring - ECG, End tidal CO2
    b) drugs - reversal agents
    3) evaluate patient - check ECG - only for <5 seconds
    4) depending on result either defibrillation or back to basic life support
    5) Hopefully at some point animal gets return of spontaneous circulation
    □ Post cardiac arrest care
    ® Is very important and takes highly intensive monitoring -> referral is the best option
48
Q

Basic life support chest compression with CPR what are the 5 important aspects

A

1) Posture important to maintain uninterrupted chest compressions -> need to be dorsal
1. identify chest compression spot
2 - shoulders vertical to compression point
3 - elbows locked
4 - core muscles - driving force
- Doesn’t matter if in left or right lateral recumbency
2) Compression rate -> 100-120 cpm - Staying alive -> oh oh oh oh staying alive, staying alive
3) Minimise pause
- It is recommended that CPR be performed 2 minutes cycles WIHTOUT interruption, and duration of pauses between cycles minimized
4) Compression depth
- PUSH HARD - 1/3 to 1/2 of width of chest
5) Decompression -> need to allow the chest to re-extend every compression to allow for blood flow

49
Q

in terms of chest compression during CPR where on round vs deep chested dogs

A

Round chested - Heart far away from ribs - hard to get directly, reduce chest as much as possible to increase intra-thoracic pressure, compression highest point of the chest
Keel-chested dogs - ventricles under chest wall, ribs relatively flat -> can squeeze ventricles themselves - MORE EFFECTIVE

50
Q

Basic life support ventilation when done, what with, how and other ventilation can do

A
  • Intubate and ventilate AS SOON AS POSSIBLE
    i) Ventilation in intubated animal
    } What – Ambu bag and anaesthesia machine
    } How – Normal chest rise
    – 10 breaths per minute, 1 second inspiratory time
  • w One breath every 6 seconds
    – No coordination with chest compression required
    ii) Mouth to snout ventilation - if by yourself may need to do
    } Hold mouth closed tightly
    } 2 ventilations every 30 compressions
    } Need to Interrupt compressions to deliver breaths - so not ideal
51
Q

Advanced life support monitoring which useful and which not during CPR

A

Useful
1) ECG - arrest rhythm guides drug therapy
2) end tidial CO2 (ETCO2) – efficacy of CPR, early indicator of ROSC
Not useful
– pulseOx - need a pulse
– Indirect blood pressure - need a pulse

52
Q

In terms of monitoring with ETCO2 during CPR and are increase associated with, used to, which level unlikely to survive and therefore need to evaluate and what is increases suddenly

A
  • Increase EtCO2 values are associated with
  • > Increase CO, increase coronary perfusion, increase ROSC/survival in people and animals
  • Use EtCO2 to:
  • > Identify poor BLS (basic life support) quality
  • > Identify ROSC
  • If EtCO2 <15mmHg - unlikely to survive
  • > Evaluate compression quality - Rate, depth, recoil/leaning
  • > Confirm correct ventilation - RR - 10/min ( 6 seconds between breaths) - Tidal volume is not too large
  • If EtCO2 increases suddenly
  • > Evaluate for ROSC (return of spontaneous circulation)
53
Q

Advanced life support during CPR drugs what method of administration and what drugs should use

A

◊ Methods of drug administration -> intravenous, intraosseous, intratracheal
◊ Reversal agents
} Reverse any sedative agents
– Flumazenil: benzodiazepines
– Naloxone: opioids
– Atipamezole: alpha-2 agonists
} Can be helpful even long after drug administered
◊ Intravenous fluids
} During CPR in euvolaemic or hypervolaemic dogs and cats, routine administration of IV fluids IS NOT RECOMMENDED

54
Q

Evaluating the patient during CPR, with what, how and 4 main situations that may then occur

A

check ECG
® Only stopping compressions for Short (<5 seconds) period
® Evaluate - Pulse, heartbeat, ECG
® ECG
◊ NEED TO STOP THE COMPRESSIONS to evaluate
1) Asystole
2) pulseless electrical acitivity (PEA)
3) ventricular fibrillation
4) pulseless ventricular tachycardia (pVT)

55
Q

Asystole on evaluation during CPR what does that mean and treatment

A
  • No mechanical or electrical activity
  • Common arrest rhythm
  • Treatment - don’t learn dosages (All on dosing chart)
    – Basic life support to maintain blood flow to tissues
    – Vasopressors
    -> Redistributing blood flow to heart and brain
    -> The use of low dose (0.01mg/kg) ADRENALINE administered every 3-5 minutes early in CPR is recommended
    -> The use of high dose (0.1mg/kg) adrenaline may be considered after prolonged CPR
    -> The use of vasopressin (0.8U/kg) as a substitute or in combination with epinephrine every 3-5 minutes may be considered
    – +/- anticholinergics
    -> Increase vagal tone with some aetiologies of CPA
    -> In dogs and cats with asystole or PEA potentially associated with increased vagal tone, use of atropine is reasonable
    -> In dogs and cats routine use of atropine during CPR may be considered
56
Q

Pulse electrical activity on evaluation of CPR what need to do, how common, what means and treatment

A

} If see this have to determine is it normal or PEA -> PEA WILL NOT HAVE A PUSLE
} Common arrest rhythm (40%)
} Electrical activity in the conduction system +/- myocardium
} No effective mechanical activity
} EtCO2 remains low
} Treatment - same as Asystole above

57
Q

Ventricular fibrillation on evaluation of CPR what is it, treatment and if refractory

A

} Uncoordinated depolarisation of ventricular myocytes
} Treatment: electrical defibrillation
– Current simultaneously depolarizes all myocytes
– All myocytes simultaneous in refractory period
– Normal pacemaker re-established
- CONTINUE COMPRESSION WHILE CHARGING THE MACHINE
w Administer single shock (AFTER YELLING CLEAR) then immediately resume compressions for 1 cycle
w Check ECG at the end of the cycle to see if worked
} If refractory ventricular fibrillation
– Can increase dose (J) by 50% once
– Consider anti-arrhythmics
w Amiodarone improves outcomes
w Class III anti-arrhythmic
w Expensive
w Can cause anaphylaxis in dogs
If amiodarone is not available, consider lignocaine

58
Q

Pulseless ventricular tachycardia on evaluation of CPR how to determine and treatment

A

} IS there a pulse? -> if not than THIS
} Treatment
- Defibrillation - same as ventricular fibrillation

59
Q

If go back to basic life support after evaluation what need to do

A

® Change compressor, perform 1 full cycle = 2 mins
® Evaluate the patient AGAIN - check the ECG
◊ Repeat above steps depending on situation

60
Q

Define neuro-muscular weakness, what a lesion of and generally what not involved

A

○ Weakness = dominant sign
○ Lesion of the motor unit - JUST MOTOR ISSUES
§ Motor neuron -> lower motor neuron + axons + neuro-muscular junction + muscle fibres (innervated by the one motor neuron)
□ Issue with any of these components -> weakness
® Main function - generate strength! -> if damage - WEAKNESS
○ Strictly , sensory not covered
§ But well generally get ataxia from sensory nerves being damaged

61
Q

Neuromuscular defects what seen on observation/gait

A

○ Weakness - too weak to lift body and walk properly
○ Lameness
○ Stilted gait - short stepped gait
○ Paresis - weakness from lack of motor function -> two ways can occur
§ Problem with motor unit -> STRICT DEFINITION – LMN -> flaccid
§ Destroy spinal cord (severe spinal cord damage) - UMN -> rigid
○ Paralysis (rare)

62
Q

Neuromuscular defects proprioceptive ataxia and palpation

A
  • Proprioceptive ataxia?
    ○ YES in some neuropathies (motor and sensory nerves - once sensory nerves involved then yes)
    ○ NOT for NMJ and muscle diseases!
    § Generally will get hopping reflex abnormal - NOT DUE TO PROPRIOCEPTION but due to weakness
  • Palpation
    ○ Muscle atrophy
    § Neuro- and myo-pathies
    § Neurogenic atrophy more common (4-8 days) > disuse atrophy (4-8 weeks)
    § Selective vs diffuse
    □ When know which muscles are innervated by which nerves can help
    § NOT for NMJ diseases - need loss of AXONS
63
Q

Neuromuscular defects spinal reflexes and cranial nerves results

A
  • Spinal reflexes - tone
    ○ Decreased to absent
    ○ Variable in NMJ diseases
    ○ Variable in myopathies
  • Cranial nerves
    ○ No menace, no blink - facial nerve
    ○ Impaired mastication - trigeminal nerve
    § Masticatory muscle atrophy
    § “Dropped jaw”
    ○ External ophtlamoplegia (eyeballs to not move at all) - 3,4,6
    ○ Vestibular syndromes - cranial nerve 8 (vestibular nerve)
    ○ Laryngeal/pharyngeal innervation - cranial nerve 10 (vagus)
    § Change in voice = dysphonia
    § Inspiratory stridor
    § Regurgitation - aspiration pneumonia
    ○ Oesophageal innervation
    § Dogs > Cats
    § Megaoesophagus - consequences -> aspiration pneumonia
64
Q

Neuromuscular defects what effects on the sensory system and what if affected

A

○ Usually WNL
○ From hyper- to an-aesthesia
§ Hyperaesthesia in specific neuropathies
§ Hypo to an-aesthesia in traumatic nerve injuries (branchial plexus issue - will lead to sensory destruction - no sensation to arm
§ Hypo to an-aesthesia in sensory polyneuropathies
○ Have to be euthanasia - no way can fix the sensory nerves

65
Q

Autonomic disorders what seen with parasympathetic and sympathetic disorders

A
  • Parasympathetic
    ○ Mydriasis, dry eyes/nose, megaoesophagus, tachycardia, urine retention…
  • Sympathetic
    ○ Myosis and Horner’s syndrome, bradycardia/hypotension, urine dribbling…
66
Q

What are the 4 main diagnostic tests for neuromuscular defects

A

1) creatinine kinase
2) electrolytes
3) chest radiographs
4) electrophysiology

67
Q

Creatine kinases in testing for neuromuscular defects how helps, what is a significant change and what gives false positives

A

○ = CPK (creatine phospho kinase)
○ In muscles
○ Reflection of injury - when damaged release CK into blood
§ Normal range: 50-400 IU/L
§ Usually significant increase - 2,000-3,000 significant
○ Kinetics: ½ life = 6h
○ Can help monitor for improvement
○ False positive
§ Renal failure
§ Decubitus - if not moving will get a false positive

68
Q

Electrolytes and chest radiographs how used to test for neuromuscular defects

A
  1. Electrolytes - should check as soon as have weak patient
    ○ Hypokalaemia - weakness in all four limbs (ventral flexion of the legs) - generally the cats
    ○ Hypercalcaemia
  2. Chest radiographs
    ○ Megaoesophagus = common presentation when weak oesophageal muscles or damage to vagus nerve
    ○ Aspiration pneumoniae
69
Q

Electrophysiology what are the 3 main ones can use for neuromuscular defects

A

1) electromyography (EMG)
2) electroneuography - not on exam
3) electroneurography

70
Q

Electromyography (EMG) what used for, in normal patient what see and what see abnormaly, how sensitive

A

neuromuscular defects testing
§ In normal patient should have a flat-line (anaesthesia - no innervation)
§ Denervation hypersensitivity - detect in abnormal patients (Myopathy or neuropathy)
□ When cut off axon supply the neuromuscular junction because unstable and hypersensitive to low Ach levels -> resulting in depolarisation and motor activity at levels that shouldn’t be occurring
□ Takes 4 to 8 days
§ Very Sensitive - > 5% axonal loss!

71
Q

Neuropathies what are the 6 main ones

A

1) Laryngeal paralysis-polyneuropathy complex
2) Idiopathic facial nerve paralysis
3) Diabetic polyneuropathy
4) Hypothyroid-polyneuropathy? - CONTROVERSIAL -
5) Peripheral Nerves Sheath Tumours (PNSTs) - important
6) Idiopathic polyradiculoneuritis - important

72
Q

Laryngeal paralysis-polyneuropathy complex what also called, what occurs and the breeds found in

A

Dying back disease”
○ Axonal loss from the extremities…
§ + myelin loss in Leonbergers
○ Long nerves: 2 sciatic and recurrent laryngeal - longest nerves
- Several forms
○ Inherited - Leonbergers
○ Breed related, congenital?
§ Dalmatians, Rottweilers, Pyrenean Mountain dogs
○ Older large breed dogs, acquired?
§ Retrievers, St Bernard,…cross breed dogs…

73
Q

Laryngeal paralysis-polyneuropathy complex clinical signs, diagnosis, treatment and prognosis

A
  • Clinical signs
    ○ Sciatic nerve
    § Able to walk - but not able to flex stifle or hock as well (hock keeps dropping)
    § Some ataxia - sensory nerves involved
    § Cranial tibial muscle commonly atrophy (sciatic nerve)
    § Reflexes -> no tone in muscle, poor or no flexion over hock and reflexes
    ○ Recurrent laryngeal nerve
    § Laryngeal paralysis -> inspiratory stridor
  • No specific diagnosis
    ○ Electrophysiology, nerve biopsy…
  • No specific treatment
    ○ Arythenoid lateralization, cricoid implant
  • Poor prognosis
    ○ But slow deterioration in older dogs…
74
Q

Idiopathic facial nerve paralysis pathogensis, breeds, presentation, treatment and outcome

A
- Pathogenesis? 
○ Bell’s palsy? Herpesvirus?
○ No inflammation described in dogs but in people yes
- Middle aged dogs
○ Cocker spaniel
- Loss of blink, dropped cheek
○ Parasympathetic involvement (dry eye)?
- No treatment
○ Artificial tears - if don't recover within 1-2 weeks then may not recover so need for life 
○ Corticosteroids? Acyclovir? - no research confirming but has been found in humans -> steroids 
- Outcome - 50% recover - guarded 
○ Dogs don't die but recovery
75
Q

Diabetic polyneuropathy physiology, clinical signs and prognosis

A
- Physiopathology - not sure 
○ Axonal + myelin disease - sometimes damaging these
§ Vascular hypothesis?
§ Metabolic hypothesis?
§ Immune hypothesis? 
- Clinical signs
○ Cat: pelvic limbs pantigrady
○ Dog: tetraparesis - short choppy gait
○ Will also get ataxia - sensory fibres also involved
○ Muscle atrophy and weakness 
- Guarded prognosis
○ even with Diabetus mellitus control may be permanent
76
Q

Hypothyroid-polyneuropathy importance? pathophysiology, clinical signs, diagnosis, treatment and prognosis

A

CONTROVERSIAL - keep in differential list but at the bottom of the list - rule out everything else
- Pathophysiology
○ ↓ mitochondrial ATPase activity?
○ ↑ acid mucopolysaccharides?
- Clinical signs
○ Cranial nerves V, VII, VIII, X weakness
§ Could be idiopathic facial nerve or vestibular syndrome effecting the different nerves
○ LMN tetraparesis
- Diagnosis
○ T4 + TSH - hypothyroid
- Treatment
○ Thyroxine - may help? - generally do better
- Good prognosis

77
Q

Peripheral Nerves Sheath Tumours (PNSTs) pathology in dogs and clinical signs - EXAM

A
  • Pathology
    ○ Dog: all locally invasive - all tumours called PNST as all will move into all parts of spinal cord
    § 75% intervertebral foramen or within the vertebral canal
    § More common in brachial plexus
  • Clinical signs
    ○ Very painful
    ○ Insidious lameness - generally in one leg
    § Thoracic > pelvic limbs
    ○ Hemi-/tetraparesis
    ○ Cranial nerves V, VII, VIII - can be exclusively effected
    § Clinical signs based on the function of cranial nerve
    § Trigeminal nerve PNST - atrophy of temporalis muscle ONLY ON ONE SIDE (without dropped jaw)
    □ Other conditions for trigeminal nerve - trigeminal neuritis (dropped jaw and both sides) - differentiate
78
Q

Peripheral Nerves Sheath Tumours (PNSTs) diagnosis, treatment and outcome - EXAM

A
  • Diagnosis
    ○ Electrophysiology
    ○ MRI > CT - to find where the tumour is
  • Treatment
    ○ Surgery
    § Amputation - if in brachial plexus -> amputation of the leg especially front leg can lead to poor outcomes
    § +/- hemi-/dorsal laminectomy - remove the functions of the nerve that you remove - BAD
    § As soon as tumour has reached the foramen of the spinal cord -> WILL RECURR -> surgery not indicated
    ○ Radiation therapy - can help
  • Poor outcome
79
Q

Idiopathic polyradiculoneuritis how common, what is it and trigger - EXAM

A
  • Common in Australia - can look like tick paralysis (need to shave to do tick search)
  • Auto-immune disease
    ○ Inflammation localised at Ventral root (motor)
  • Trigger unknown
    ○ Campylobacter jejuni (from raw chicken meat) - what we think, respiratory infections, vaccine -> trigger in people??
    ○ Giving dog raw chicken meat increase chance of getting this by 73%
80
Q

Idiopathic polyradiculoneuritis clinical picture - EXAM

A

○ Generally little fluffy dog given chicken meat
○ Dysphonia - difficulty barking
○ Ascending, progressive (5 to 10d) tetraparesis - start at hindlimb then go to forelimb
§ Sometimes descending
§ Reflex is decreased, weakness, but sensory is present (will feel everything)
§ But keep wagging tail!
§ No urinary incontinence
○ Facial paralysis - rare
○ Spinal Hyperesthesia - probably due to spinal cord inflammation - NOT SEEN IN AUSTRALIA

81
Q

Idiopathic polyradiculoneuritis treatment and prognosis

A
  • Treatment
    ○ No treatment… NO CORTICOSTEROIDS - inflammation is gone at this point, just axonal death
    § Will trigger more muscle atrophy and increase risk or urinary tract infection
    ○ …other than supportive cares…
    ○ Human IV Ig (immunoglobins)
  • Good prognosis
    ○ 2w to 6m for recovery - depends on where the insult occurs and the length that need to recover
    § If smaller dog can be quicker recovery as not as long nerves
    ○ Sometimes respiratory muscles paralysis
    ○ Coohound paralysis: worse if reccurs
82
Q

Junctionopathies what are the 3 main ones

A

1) Myasthenia gravis - IMPORTANT
2) botulism
3) tick paralysis

83
Q

Myasthenia gravis what are the 2 main forms, causes and associated with

A
- Congenital form
○ Lack of AChR
○ Young JR and Fox terriers, miniature Dachshund
- Acquired form - more common 
○ IgG bound on α-subunit of AChR - preventing ACh from binding 
○ In association with…
§ Thymic masses- MOST COMMON
§ Hypothyroidism 
§ Other autoimmune disorders
§ Tumors
§ Methimazole therapy in cats
84
Q

Myasthenia gravis what are the 3 main clinical forms and clinical signs

A
  1. Generalized form
    ○ Appendicular muscles exercise induced weakness -> exercises then stops as cannot keep going, improves with rest and can exercise again
    ○ + neck ventroflexion in cats, plantigrade, struggles to keep walking
    ○ Muscle tremors and weakness = pure motor no sensory
    ○ Facial, pharyngeal-laryngeal and oesophageal muscles
    ○ Regurgitation, secondary aspiration pneumoniae
  2. Focal form
    ○ Facial, pharyngeal-laryngeal and oesophagus muscles
    ○ 36% of dog, 15% of cats
  3. Fulminating
    ○ Consistent generalized weakness - not just exercise induced
    ○ Intercostal muscles, diaphragm - death from respiratory paralysis (1-2days)
85
Q

Myasthenia gravis diagnosis

A
  • Chest radiographs - determine if megaoesophagus or not
  • Edrophonium (Tensilon®) test
    ○ Acetylcholine esterase inhibition
    ○ Pre-atropination
    ○ Alternative: neostigmine - what we have in australia
    § Wait till dog is exhausted and then give this IV and should be able to work again (inhibits the ACh esterase that breaks down ACh so increase the amount of ACh in the synpase)
  • Electrodiagnosis
    ○ Repetitive nerve stimulation
    § ± edrophonium test
    ○ Single fibber EMG
  • Anti-AchR antibody concentration (lab done in California)
    ○ May be seronegative even when have it
86
Q

Myasthenia gravis treatemnt

A
  • Self-resolution?
    1) Supportive treatment
    ○ Aspiration pneumonia
    § Antibiotics
    § Change decubitus
    ○ Nutritional: solid/elevated food (bailey chair)
    2) Tube…
    ○ Neostigmine methylsulfate (Prostigmine®), par-enteral - as above
    § May self-resolve if give for a few months then take off and remains good
    3) Corticoid therapy
    ○ Anti-inflammatory dose - not immunosuppressive
    Cat>Dog
    ○ Other: cyclosporine, mycophenolate mofetil
    4) Surgical management of concurrent tumor - thymoma
    ○ Pros and cons
    § If leave only one cell will still have
87
Q

Myasthenai gravis prognosis dogs vs cat

A
  • Dog mortality = 40 to 60% at 1y
    ○ Main cause is aspiration pneumonia due to megaoesophagus
  • Better in Cat - less striated muscles in oesophagus so less likely to get megaesophagus and therefore aspiration pneumonia
88
Q

Botulism where found, toxin, what does it do and clinical signs

A
- Botulinum toxin
○ Spoiled food, raw meat, carrions…
○ Clostridium botulinum
○ A, B, C1, C2, D, E, F, G
○ pre-synaptic disease -> Cleaving of the exocytosis-proteins -> no ACh released into the synaptic clef 
- Clinical signs (1 to 6d)
○ Tetraparesis
○ Cranial nerves
○ Respiratory muscles
○ Autonomous system
§ Brady-, tachy-cardia, mydriasis, KCS, urine/faeces retention
89
Q

Botulism diagnosis, treatment and prevention

A
- Diagnosis 
○ Generally just clinical suppression 
○ Tests generally not done 
○ Evidence of toxin in
§ Blood
§ Food, vomitus, faeces
Electrophysiology
§ Repetitive nerve stimulation
- Treatment
○ Time, self-resolution
○ Antitoxin
§ When recent exposure
- Prevention
○ Cook the food!
- 100 for 10 mins or 80 for 30mins
90
Q

What are the 2 main myopathies we need to know

A

1) Masticatory muscles myositis - important

2) Idiopathic polymyositis - important

91
Q

Masticatory muscles myositis -what is it, cause, breed and clinical signs - EXAM

A

myopathy
- Auto-immune
- Type IIM myofibers
○ Digastricus, temporalis, masseter - generated from same aortic arch
- Usually large breed dogs
- Clinical signs
○ Acute phase -> MM swelling then atrophy - generally not presented at this point
○ Myalgia - painful muscles
○ Atrophy and fibrosis of the muscles
○ Trismus (locked in semi-closed or semi-open) inability to open jaw - DO NOT FORCE ON THE JAW (break it)

92
Q

Masticatory muscles myositis diagnostic tests

A

○ CK, EMG (electromyography), muscle biopsy
○ Imaging - MRI, CT of the head -> abdominal signals in the muscles
○ Type II fibre antibodies - check concentration
§ Good for monitoring

93
Q

Masticatory muscles myositis treatment and prognosis

A
- Immunosuppressive treatment
○ Prednisone 2mg/kg/d - usually enough by itself 
○ Tapering of doses over 6-8m
§ Monitoring: type IIM fibers antibodies
○ Supportive therapy 
§ Semi-formed food 
- Good prognosis
94
Q

Idiopathic polymyositis what is the cause, breeds and clinical signs

A

myopathy
- Auto-, dys-immune?
○ Muscle infiltration by lymphocytes
○ Pre-lymphoma?
- Large breed dogs- Boxer, Newfoundland
- Clinical signs
○ Focal or diffuse inflammation
○ ±association with masticatory muscles myositis (MMM)
Systemic - pyrexia, weakness, excercise intolerance
muscles - stiff gait, myalgia, muscular atrophy
other - dysphagia, megaoesophagus, change in bark, stridor

95
Q

Idiopathic polymyositis diagnostic tests

A

○ CK, EMG
○ MRI
○ Muscle biopsy, immunostaining -> can see inflammatory cells between the myocytes
○ Ruling out infectious diseases - IMPORTANT AS TREAT IS IMMUNOSUPPRESSIVE
§ Neospora, Leptospira, toxoplasma - ensure seronegative

96
Q

Idiopathic polymyositis treatment, monitoring and prognosis

A
  • Immunosuppressive treatment
    ○ Prednisone 2mg/kg/d
    § Tapering of doses over 6-8m
    ○ Monitoring: recheck every 6 weeks (tapering)
    § Clinical presentation, CK levels (for muscle insult), muscle biopsy? (GA and can be issue with small dog as larger area - generally not done)
  • Good prognosis - most dogs take 6-8months
97
Q

Forebrain structures and what need to remember with syndromes

A
EVERYTHING IS CONTRALATERAL 
Main structures:
	- Cerebral cortex
	- Basal nuclei
	- Thalamus 
	- Hypothalamus
	- Limbic system
98
Q

What are the main functions of the forebrain to and from and superior functions

A
TO the forebrain
○ Proprioception
○ Other sensations
§ Tactile, cold/heat
○ Special senses
§ Audition, vision, smell
○ Arousal -> vestibular system wakes you up 
- FROM the forebrain
○ Voluntary motor function - NOT PARALYSIS OR PARESIS -> role of brainstem
- “Superior” functions
○ Behaviour, Memory
○ Mental status
○ Water consumption, Appetite
○ Carbohydrates metabolism
○ Body temperature, Heart rate
99
Q

Forebrain lesions what clinical signs seen with observation and gait

A
- Observation
○ Seizures - FOREBRAIN ONLY - important 
○ Central blindness
○ Decreased mental status
§ If large lesion
○ (Abnormal behaviour)
- Gait
○ Circling - large circling (small for vestibular) 
§ To the side of the lesion 
§ Right forebrain lesion -> dog blind on left side (left forebrain control right side will be able to see the right side - ignore the left side of the world (will ignore the left side of the food bowel) 
○ Pacing/wandering
○ Head pressing
○ Minimal proprioceptive deficits
100
Q

Neurological examination what seen with forebrain lesions

A
○ Palpation - normal 
○ Postural reactions - decreased 
○ Spinal reflexes and tone - normal 
○ Cranial nerves - decreased 
§ Menace response and facial sensation 
○ Sensory systems 
§ Hypo/an/-aesthesia