Papers/Short answers Flashcards

1
Q

Diagnostic yield of D-dimers and thromboelastography in diagnosis of canine CVA?

A

Low

Neither D-dimer concentration nor TEG was significantly associated with a CVA (P = .38 and .2, respectively). D-dimer testing was performed in a low-risk population and showed low sensitivity (30.8%; 95% confidence interval [CI], 10%-61%) and high specificity (86.4%; 95% CI, 64%-96%) for CVA diagnosis. Thromboelastography was performed in a high-risk population and showed moderate sensitivity (64.3%; 95% CI, 44%-81%) and specificity (66.7%; 95% CI, 24%-94%) for CVA diagnosis. Abnormal D-dimer concentration or TEG were not helpful in differentiating hemorrhagic from ischemic stroke (P = .43 and .41, respectively).

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2
Q

Most important clinical and MRI findings in dogs with idiopathic oculomotor neuropathy?
Outcome?

A

1) unilateral ophthalmoplegia/ophthalmoparesis (internal, external, or both) with the absence of other neurologic and ophthalmic signs - mostly combined 79%, or internal (mydriasis) 21%

2) MRI findings
restricted to the oculomotor nerve (enlargement + contrast enhancement)

3) good prognosis, most cases improving or not deteriorating without therapy

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3
Q

Which breeds are most commonly affected by idiopathic oculomotor neuropathy?

A

Boxers and border collies

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4
Q

Which CN is affected in this image?

9.5-year-old male entire Staffordshire
Bull Terrier

A

Mydriasis secondary to internal ophthalmoplegia, and upper eyelid ptosis and neuromuscular strabismus (dorsolateral) secondary to external
ophthalmoparesis of the OS

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5
Q

What is the middle cranial fossa (sinus cavernosus) syndrome?

A

a paired depression of the basiphenoid bone, located
between the rostral and caudal cranial fossa at the base
of the skull.

CN III, IV, V, VI travel there and exit the skull through the orbital fissure (oculomotor nerve, trochlear
nerve, abducens nerve, and ophthalmic branch of the
trigeminal nerve),
round foramen (maxillary branch of the
trigeminal nerve), or
oval foramen (mandibular branch of the trigeminal nerve)

The middle cranial fossa syndrome is a well-recognized syndrome in dogs characterized by variable impairment of these nerves (usually due to neoplastic mass lesion of the middle cranial fossa)

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6
Q

Which medication can cause hypo/anosmia

A

Metronidazole (careful in working dogs for explosive detection)

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7
Q

Genetic epilepsy - which breeds and variants?

A

1) Lagotto Romagnolo - benign familial juvenile epilepsy (LGI2)
2) Rhodesian Ridgeback - juvenile myoclonic epilepsy with photosensitivity (DIRAS1)

ADAM23 gene - Belgian shepherd, schipperke, Finnish spitz, and beagle, Australian shepherd, Kromfohrländer, Labrador retriever, whippet, –> proposing ADAM23 as a common risk gene for epilepsy with low penetranc

  • susp: Dutch partridge dogs (CCDC85A)

Where data are sufficient, they usually support an autosomal recessive or polygenic recessive inheritance (De Lahunta)

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8
Q

Describe postictal MRI changes in dogs

A

T1W hypointense, T2W/FLAIR hyperintense with no or minimal contrast enhancement, and no to minimal local mass effect.

Locations: pyriform lobes and cyngulate gyri, hyppocampus, less commonly in the thalamus and frontal/parietal lobes.

Mostly bilateral and symmetric.

*These lesions are usually transient and not visible on repeat imaging (weeks to months later) once seizure control is achieved. On microscopic examination, these lesions consist of edema, vascular proliferation, neuronal loss, reactive astrogliosis, and occasionally neuronal necrosis. Similar findings are reported in humans and are presumed to be related to the excitotoxic effect of accumulated glutamic acid, which leads to cytotoxic edema.

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9
Q

Which horse breed has a presumptive genetic epilepsy?

A

Arabian foals . onset 3-9 MO, seizures may spontaneously cease after a few weeks

Adult horses may have IE related to the estrous cycle when estrogen levels are increased.

On the basis of negative autopsies in adult horses with late-onset epilepsy, this species may have an idiopathic epilepsy that is not apparent until at least 5 years of age.

DeLahunta

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10
Q

Toxins able to cause seizures (most important ones)

A

Lead: paint, linoleum, tar paper, wallboard, and roofing materials.
Metaldehyde - snail bait,

Hexachlorophene soap, ethylene glycol antifreeze, chlorinated hydrocarbon and organophosphate insecticides, fluoroacetate (1080), rodenticide (particularly bromethalin), fungicides with mercury, arsenicals in insecticides, and phenol and cresol germicides, and 5-fluorouracil.

De Lahunta

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11
Q

CBC changes with lead poisoning (in a dog with seizures)

A

Nucleated red blood cells, basophilic stippling, and a low packed cell volume (PCV) (may be present)

De Lahunta

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12
Q

How can the bromide serum levels be decreased more quickly then by simply discontinuing the drug?

A

NaCl IV infusion

De Lahunta

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13
Q

Which ASM has the potential to cause megaoesophagus?

A

KBr

  • develops in the first few months of initiating therapy. It resolves rapidly with discontinuation of potassium bromide.

De Lahunta

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14
Q

Two phases of sleep

A

1 slow-wave
2 REM (or paradoxical)

During slow-wave sleep, normal resting muscle tone exists. In paradoxical sleep, complete atonia of all skeletal muscles occurs, except those necessary for respiration. This state causes a flaccid paralysis. Sporadically, the extraocular muscles breakthrough this lower motor neuron (LMN) inhibition and contract, causing eye movements, which is the basis for also naming paradoxical sleep rapid eye movement sleep. This portion of the sleep cycle is when dreaming occurs. Occasionally, other muscle groups break through this inhibition and contract. This breaking through is what is observed in small animals when, during their sleep, they exhibit facial muscle twitches or sporadic movements of their digits.
During slow-wave sleep, a decrease occurs in the heart and respiratory rates. In paradoxical sleep, respirations are shallow, more rapid, and irregular. Normally in small animals, slow-wave sleep occurs in 10- to 15-minute intervals, with approximately 5 minutes of paradoxical sleep.

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15
Q

Four components of Narcolepsy in humans

A

1) excessive daytime sleepines
2) cataplexy - collapse due to complete atonia of skeletal muscles - the most common sign we observe in animals

3) hypnagogic hallucinations
4) sleep paralysis
-these 2 can only be appreciated in humans

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16
Q

Which breeds have an inherited basis for narcolepsy and which gene is involved?

A

CANARC gene - chromosome 12
- autosomal recessive

doberman pinschers, Labrador retrievers, and dachshunds

(the gene codes for a hypocretine receptor found on neurons of the locus coeruleus and dorsal raphe nucleus)

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17
Q

Two forms of narcolepsy

A

1) genetic (CANARC gene) - defect in the hypocretin receptors in dorsal raphe nucleus and locus coeruleus neurons

2) acquired - low hypocretin levels in CSF (immune mediated destruction of the neurons of ventrolateral hypothalamic nucleus?)

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18
Q

Which drugs facilitate and which inhibit paradoxical sleep?

A

1) Physostigmine and arecoline facilitate
2) atropine, scopolamine, norepinephrine, serotonin inhibit it.

De Lahunta

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19
Q

Breeds of horses with an inherited form of narcolepsy

A

Shetland ponies, the American miniature horse, and probably the Suffolk draft horse

De Lahunta

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20
Q

DDs for cataplexy?

A

Syncope - rapid onset and recovery, same as cataplexy

Seizure - uncontrolled muscle movements (and cataplexy is atonic)
Neuromuscular disorders - not so abrupt and recovery not so quick

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21
Q

Which drug can be used to provoke a cataplectic episode?

A

physostigmine at 0.05 to 0.1 mg/kg of body weight should not induce cataplexy in a normal dog but may provoke an episode in the patient at risk for such an episode

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22
Q

Which drugs can be used to stop a cataplectic episode?

A

1) imipramine (Tofranil) IV at 0.5– 1.0 mg/kg of body weight, - antidepressant that inhibits the reuptake of norepinephrine and has anticholinergic actions.
2) IV atropine sulfate at 0.02–0.04 mg/kg of body weight may also interrupt the episodes.

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23
Q

Drugs to treat narcolepsy

A

1) acquired narcolepsy (hypocretin deficiency) -
- Imipramine - norepinephrine reuptake inhibitor - has anticholinergic effects 0.5 mg/kg TID
- Selegeline - MAO inhibitor . increases the conc. of norepinehrine in CNS 0.5-1 mg/kg SID
- Methylphenidate (Ritalin) - stimulant only for excessive sleepiness
- Yohimbine - alpha-2 adrenergic antagnist - increases the release of norepinephrine
- Modafinil and Oxzbate in humans

24
Q

Which gene variant is associated with congenital myotonia?

A

DNA mutation of the gene responsible for chloride channel 1 in the muscle membrane

CLCN1

This voltage-gated chloride channel 1 plays a role in the repolarization of the muscle cell membrane after contraction. When the function of this channel is deficient, muscle cell relaxation is delayed. No light microscopic lesions exist in the affected muscles of animals with inherited nondystrophic myotonia.

25
Q

Breeds of animals with congential myotonia

A

Documented in:
- rats
- goats (pygmy)
- horses
- cats
- dogs
- buffaloes
- pigs

Dog breeds with CLCN1 variant:
Miniature Schnauzer
Jack Russell Terrier (common)
Australian Cattle dog
Labrador Retriever
American Bulldog
In addition to these breeds, has been described clinically in Cocker Spaniels and
Chow Chows (common)

26
Q

Which electrolyte disturbance is connected to myotonia in horses?

A

Inherited hyperkalemic periodic paralysis

27
Q

Most likely diagnosis?

1YO Chow chow with muscle atrophy and stiff gait

A

Myotonia congenita

28
Q

Most likely diagnosis?

8 MO standardbreed with stiff gait

A

Myotonia congenita

29
Q

Causes of pseudomyotonia (complex repetative discharges)?

A

1) dystrophinopathy (retriver)
2) dietary deficiency of vitamin E/selen in farm animals

30
Q

Most common disease associated with acquired myotonia?

A

Hyperadrenocorticism

persistent characteristic gait stiffness associated with significant muscle hypertrophy

31
Q

Difference between true and pseudomyotonic discharges on EMG?

A

On EMG the complex, repetitive discharges observed with pseudomyotonia (acquired myotonia with huperadrenocorticism, or myotonia associated with dystrophinopathy) start and stop abruptly, without the waxing and waning that is seen in “true” myotonia.

32
Q

Patomechanism of tetnospasmin?

A

interferes with the interneuron release of the inhibitory neurotransmitter glycine in the spinal cord ventral gray horn and γ-aminobutyric acid (GABA) in the brainstem motor nuclei.

The toxin gains access to motor neurons at their telodendrons at the neuromuscular junctions and binds to the axonal gangliosides, where it is transported to the spinal cord within a few hours.74 The toxin passes from the general somatic efferent neuronal cell bodies to the adjacent inhibitory neurons at their synaptic sites. There the toxin binds to and enters the interneuron, called a Renshaw cell.69 This toxin is a zinc endopeptidase that cleaves the cell membrane protein necessary for the release of the inhibitory neurotransmitter and therefore blocks the release of the inhibitory neurotransmitter, glycine or GABA. The toxin usually remains bound to the interneuron for 3 or more weeks. In most cases the toxin spreads rapidly within the central nervous system (CNS), or the toxin may circulate through the vascular system to neuromuscular junctions and thereby gain access to other areas of the CNS. Although this tetanospasmin may bind to other neurons, the major site is on the inhibitory interneurons that synapse on the alpha motor neurons that innervate the antigravity extensor muscles.

33
Q

Most likely Dx in this cow?

A

Tetanus
Note the retracted ears, taut lips, extended neck, and elevated tail.

34
Q

Difference between tetanus and tetany?

A

Tetanus - sustained contraction of muscles without relaxation that most commonly affects extensor (antigravity) muscles.

Tetany - sustained contraction of muscles, usually the extensors, which is variably intermittent and is related to varying degrees of relaxation of affected muscles.

35
Q

Causes of tetany

A

1) hypocalcaemia
2) strychnine intox
3) inherited congenital tetany in polled Hereford calves (aka inherited congenital bovine myoclonus) (Glra1 gene variant)
4) familial reflex myoclonus of Labrador retriever puppies
5) lavender Arabian foal syndrome (lethal) (MYO5A gene)

36
Q

Dysfunction of which nerves is seen in bovine spastic paresis (Elso heel)?

A

hyperactivity of the γ-efferent neurons that innervate the intrafusal muscle fibers in the neuromuscular spindles of the gastrocnemius muscle

37
Q

Which drug can help diagnose constant repetitive myoclonus (wrongly termed chorea) with distemper infection?

A

Lidokain IV stops the myoclonus.

Oral procainamide can be used as chronic therapy.

De Lahunta

38
Q

Difference between hypo-, dys-, and demyelination?

A

1) hypomyelination -animals have recognizable clinical signs at birth or when they are able to walk.

2) dysmyelination - animals usually show clinical signs after they are a few weeks or months of age and have exhibited normal neuromuscular activity.

3) demyelination - myelin is formed and maintained normally, and the animal is normal until affected by a disease process that causes the loss of myelin.

39
Q

Name some toxins able to induce a whole body tremor

A

metaldehyde (snail bait), pyrethrins,
lead,
hexachlorophene,
chlorinated hydrocarbons, organophosphates,
and numerous mycotoxins (penitrem A from Penicillium)
Macadamia nuts

40
Q

Common breeds for “head bobbing” (postural repetitive myoclonus)?

A

Doberman pinscher
English bulldog
Boxer

41
Q

Dog breed with susp. inheretad basis for orthostatic tremor (postural repetitive myoclonus)

A

young adult Great Dane

42
Q

Which molecule is degraded by tetanospasmin

A

Synaptobrevin (a vesicle-associated membrane protein) in the Renshaw intrneurons - the result is irreversibly impeded release of GABA (brain) and glycin (SC)

43
Q

How fast does tetanospasmin travel retrogradely in the axons of motor neurons to reach the interneurons?

A

Once bound, the toxin becomes internalized by endocytosis and is carried along the axon in a retro grade fashion at a pace of 75 to 250 mm per day.

44
Q

Clinical signs in horses with tetanus?

A
  • Stiffness (most commonly) - horses are hesitant to lower their neck
  • stilted gait
    -retraction of lips, flaring of nostrils (risus sadonicus)
  • trismus
  • prolapse of nicticating membrane
  • urine retention
  • fecal and gas retention

DDs: rabies, strychnine intoxication,
exertional rhabdomyolysis, and myositis.

45
Q

Which virus probably causes Theilers disease (fatal hepatitis)

A

Equine Parvovirus (EqPV-H)

46
Q

Negative prognostic factors for horses with tetanus?

A

Recumbant
severe/terminal signs
dysphagia

VCNA

47
Q

Which are the most common botulinum neurotoxins?

A

A, B, and C

(There are 8 different BoNTs: A, B, Ca, Cb, D, E, F, and G)

Type C is important for Europe (A,B USA)

48
Q

Three routes by which an equide can acquire botulism?

A

1) wound infection
2) ingestion of preformed toxin (food, soil, carrion)
3) from GIT (shaker foal syndrome)

49
Q

Which proteins are targets for the botulinum toxin

A

Toxin type A and E - SNAP-25 (synaptobrevin associated protein)

Toxin type B,D,F,G - VAMP-2 (synaptobrevin)

Type C - syntaxin 1 and SNAP-25

*only in PNS - it can not cross BBB, prevention of release of acetylcholin

50
Q

Which muscles have high requiements for acetylcholine and are therefore affected early in botulism?

A

tongue, eyelids, tail, and anal sphincter

51
Q

Which cells are most susceptible to damage in hyperammonemia (PSS)?

A

astrocytes

In liver failure, muscle, kidney, and the rumen become important means of detoxifying intestinal ammonia, and astrocytes play a role in uptaking ammonia and forming glutamine, a strong osmolar molecule, to help protect neurons from ammonia toxicity. Astrocytes also play a role in taking up and metabolizing other
proinflammatory and neuromodulating molecules

52
Q

Which protein is central to the pathogenesis of rabies?

A

Glycoprotein G

it forms spikes (peplomers) on the virus lipid bilayer membrane that are required for receptor binding, internalization, invasion, and immune evasion.

53
Q

What are Negri bodies?

A

Rhabdoviruses induce the formation of cytoplasmic inclusions (Negri bodies in lyssavirus) that are minifactories containing all the machinery (N, P, M, G, L) and cellular proteins required for viral replication.

*round, eosinophillic, perikarion, 0.3-20 mcm
* mainly in the Purkinje cells, brainstem nuclei neurons, pyramidal cells of the hippocampus (Ammons horn), and sometimes SC
* only around 50% of animals develop Negri bodies

54
Q

Name the prion disease affecting humans and domestic animals

A

1) sheep and goats (scrapie),
2) cattle (bovine spongiform encephalopathy [BSE]),
3) cervidae (chronic wasting disease),
4) mink (transmissible mink encephalopathy),
5) cats (feline spongiform encephalopathy),
5) human beings (kuru, Creutzfeldt Jakob disease, and others)

55
Q

Which TSE was found to cross species barriers?

A

BSE (bovine spongiform encephalopathy)

56
Q
A