Dogs and Cats 24 Flashcards

Question

List 10 toxins that decrease activity of the nervous system

Answer 1

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

Answer 2

- 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

Answer 3

``` - Classified according to their site of action ○ Neurotoxins - ○ Myotoxins ○ Procoagulants ○ Anticoagulants ○ Cytotoxins ```

Answer 4

- 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

Answer 5

- 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

Answer 6

- 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

Answer 7

- 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

Answer 8

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

Answer 9

- 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)

Answer 10

``` - 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 ```

Answer 11

○ 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

Answer 12

``` ○ 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) ```

Answer 13

``` - 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 ```

Answer 14

- 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

Answer 15

- 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

Answer 16

- 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

Answer 17

- 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

Answer 18

``` - 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 ```

Answer 19

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

Answer 20

- 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

Answer 21

- 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

Answer 22

- 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

Answer 23

- 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

Answer 24

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

Answer 25

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

Answer 26

- 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

Answer 27

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

Answer 28

- 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)

Answer 29

◊ 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

Answer 30

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)

Answer 31

- 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

Answer 32

} 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

Answer 33

} 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

Answer 34

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

Answer 35

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

Answer 36

○ 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

Answer 37

○ 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)

Answer 38

- 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

Answer 39

- 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

Answer 40

○ 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

Answer 41

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

Answer 42

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

Answer 43

○ = 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

Answer 44

2. Electrolytes - should check as soon as have weak patient ○ Hypokalaemia - weakness in all four limbs (ventral flexion of the legs) - generally the cats ○ Hypercalcaemia 3. Chest radiographs ○ Megaoesophagus = common presentation when weak oesophageal muscles or damage to vagus nerve ○ Aspiration pneumoniae

Answer 45

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

Answer 46

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!

Answer 47

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

Answer 48

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…

Answer 49

- 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…

Answer 50

``` - 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 ```

Answer 51

``` - 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 ```

Answer 52

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

Answer 53

- 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

Answer 54

- 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

Answer 55

- 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%

Answer 56

○ 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

Answer 57

- 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

Answer 58

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

Answer 59

``` - 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 ```

Answer 60

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)

Answer 61

- 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

Answer 62

- 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

Answer 63

- 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

Answer 64

``` - 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 ```

Answer 65

``` - 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 ```

Answer 66

1) Masticatory muscles myositis - important | 2) Idiopathic polymyositis - important

Answer 67

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)

Answer 68

○ 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

Answer 69

``` - 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 ```

Answer 70

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

Answer 71

○ 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

Answer 72

- 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

Answer 73

``` EVERYTHING IS CONTRALATERAL Main structures: - Cerebral cortex - Basal nuclei - Thalamus - Hypothalamus - Limbic system ```

Answer 74

``` 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 ```

Answer 75

``` - 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 ```

Answer 76

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

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Dogs and Cats 24 Flashcards

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