Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

VET 433a - Small Animal Stream 1 > Neuro pt.2 > Flashcards

Neuro pt.2 Flashcards

spinal cord

1
Q

How do we classify myelopathies

A
  1. across the diameter of the spinal cord (partial or transverse)
  2. along the length of neuroaxis (focal, multifocal, diffuse)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

General rules of spinal disease

A
  1. Neuro signs are similar regardless of underlying causes

2. severity of signs variable w/in a region of localization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

6 parts of the neuro exam

A
  1. mentation
  2. cranial nerves
  3. gait
  4. postural rxns
  5. segmental reflexes
  6. 3 P’s (palpation, painfulness, pain perception)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

T/F: mentation and cranial nerves should be normal with a myelopathy

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Intervertebral Disk Disease

A
  • the most common spinal cord disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Function of a normal intervertebral disk

A
  • compression resistance for the vertebrae

- maintaining disk space between vertebrae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Anatomy of a normal IVD (3 parts)

A
  • annulus fibrosis –> annular, fibrous ring that surrounds the pulp and serves to keep the pulp in place. comprised of lamelae to provide strength
  • nucleus pulposus –> distributes biomechanical load.. the jelly filling
  • cartilagenous endplates –> supplies nutrients to the annulus and nucleus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Two types of IVDD

A
  1. Type 1 = Chondroid degeneration –> extrusion

2. Type 2 = Fibroid degeneration –> protrusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Type 1 IVDD (signalment)

A
  • small breeds 1-6 yrs old
  • large breeds any age (less common)
  • cats (rare)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Type 1 IVDD

A
  • acute onset
  • can be progressive or not
  • usually painful
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Type 1 IVDD (clinical signs)

A
  • pain
  • paresis
  • ataxia
  • hyperesthesia
  • incontinece
  • loss of pain sensation
  • lameness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Type 1 IVDD (imaging)

A
  • narrow disc spaces
  • in situ calcification
  • calcification in foramen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Type 1 IVDD (Diagnosis)

A
  • imaging via MRI (loss of disc hydration, deviation of spinal cord, loss of CSF/ epidural fat)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Type 1 IVDD (medical management) (indications, treatment, prongosis)

A

Indications: pain only, ambulatory, non-amb. but good motor fxn
Treatment: rest/ confinement, analgesia, NSAIDs
Prognosis: ok in not severe; recurrence common

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Type 1 IVDD (Surgical management) (indications, benefits, goals, techniques)

A

Indications: any severe grade, rapid progression, failed medical management, severe pain
Benefits: great outcome, low recurrence rates, faster resolution of pain
Goals: decompression, control hemorrhage, disc fenestration
Techniques: hemilaminectomy, ventral slot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Type 1 IVDD ( post-op management)

A
  • nursing care

- rehabilitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

When to refer a Type 1 IVDD

A
  • when it’s grade 0-3 always
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Type 1 IVDD (lookout for this)

A
  • dogs w/out deep pain perception might be having a peracute decline associated w/ myelomalacia (~10-15%) which is 100% fatal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Progressive Hemorrhagic Myelomalacia

A
  • myelomalacia = necrotic spinal cord
  • Ascending/ descending form caused by severe, acute SCI w/ infarctio, ischemia, and hem. necrosis
  • 100% fatal d/t resp. paralysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Progressive Hemorrhagic Myelomalacia (Diagnosis)

A
  • fever, inappetance, pain
  • diffuse, progressing, myelopathy
  • LMN signs develop above/ below
  • Imaging sometimes helps
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Type 2 IVDD

A
  • fibrocartilage degeneration + torsional biomechanical stress
  • separation of annular fibers
  • bulging/ protrusion of annulus –> SC compression and meningeal irritation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Type 2 IVDD (Signalment)

A
  • older, larger breed dogs (most common)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Type 2 IVDD (History)

A
  • chronic (> 2 weeks)
  • reluctance to do strenuous activity
  • myelopathy (variable progression)
  • +/- lameness, incontinence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Type 2 IVDD ( Clinical Signs)

A
  • paraparesis or tetraparesis
  • ataxia
  • pain w/ palpation
  • +/- lameness, incontinence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Type 2 IVDD (diagnosis)

A
  • radiography (narrow disc space, end-plate sclerosis, osteophyte production, spondylosis)
  • CT
  • MRI (gold standard)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Type 2 IVDD (Medical treatment)

A

Indications: mild disease, slowly progressing, non-painful, continent
Treatments: anti-inflammatories, physical rehab, supportive care
Prognosis: variable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Type 2 IVDD (Surgical Treatment)

A

Indications: mod-severe myelopathy, short hx or acute onset, deterioration of signs , painful
Prognosis: good if short hx, focal lesion, pain in main finding and not at risk for degenerative myelopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Acute Non-compressive Nucleus Pulposus Extrusion (ANNPE)

A
  • tear in annulus fibrosis (from high impact forces) causing extrusion of normal nucleus pulposus
  • typically peracute injury (high impact injury)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

ANNPE (clinical signs + diagnosis)

A

Clinical signs: paresis/ paralysis, ataxia, +/- LMN signs, +/- hyperesthesia

Diagnosis: MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

ANNPE (Treatment)

A
  • medical – crate rest, time, physical therapy

- if compressive, consider surgery (ventral slot or hemilaminectomy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

ANNPE (prognosis)

A
  • intact nociception = good
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

T/F: all animals w/ CSM (Cervical Spondylomyelopathy) have some degree of stenosis.

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Disc-Associated CSM

A
  • 1* affecting C5-7
  • mostly ventral compression (can be assymetric)
  • Risk Factor: vertebral canal stenosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Disc-Associated CSM (Treatment)

A 
Medical: 
- milder cases, cost restraint
- crate rest, analgesics, NSAIDs, physical rehab
- guarded prognosis
Surgical:
- severe pain, focal lesion
- decompressive surgery
- good prognosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Osseous-Associated CSM

A
  • growth malformation of vertebrae (enlarged articular facets, bony proliferation)
  • primarily the caudal cervical vertebrae
  • typically dorso-lateral compression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

OA-CSM (typical exam findings)

A
  • cervical pain, ataxia, tetraparesis, +/- hypermetria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

OA-CSM (progression)

A
  • pelvic limbs hit first

- often acute decline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

OA-CSM (Imaging)

A

MRI:

– evaluate spinal cord parenchyma = increased intensity w/in spinal cord indicates chronicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

T/F: the treatment for OA-CSM is the same as DA-CSM

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Atlanto-axial Instability (AAI)

A

instability of C1-2 joint leading to injury of the cranial cervical spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

AAI (pathogenesis)

A
  • malformation of C1-2
  • malformation of dens
  • ligamentous abnormalities
  • trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

AAI (Signalment)

A
  • toy/ mini breeds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

AAI (Clinical Signs)

A
  • cervical pain
  • tetraparesis or palegia
  • brainstem signs
  • seizure-like episodes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

AAI (Treatment)

A

Medical:

  • Indications: immature bones, v small patient, resolving mild signs, cost. concerns
  • Tx: splinting/ bandaging, medication, crate rest

Surgery:

  • Indications: mod-severe neuro defects, recurrent cervical pain, unresponsive to medical tx
  • Tx: Dorsal or ventral approach
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

GME (Progression, Diagnosis)

A

Progression: acute, progressive, may wax and wane, most commonly encephalitis, can cause myelitis
Diagnosis: MRI, CSF (pleocytosis, rule out infection), histopath

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

GME (Treatment, Prognosis)

A

Treatment: immune suppression (steroids, pred, dex)
Prognosis:
short term - good/ fair
long term - guarded

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

SRMA (Steroid Responsive Meningitis Arteritis)

A
  • young, large breed dogs
  • progression: acute/ progressive, mainly cervical pain
  • Clinical sings: no neuro deficits, cervical pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

SRMA (diagnosis)

A
  • rule out other dz via CBC/ Chem/ Rads/ US/ w/ n MRI

- CSF analysis - neutrophilic pleocytosis, high protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

SRMA (treatment)

A
  • immune suppression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Meningitis/ Myelitis (clinical signs and diagnosis)

A

Clinical Signs: acute onset pain/ hyerpesthesia, +/- myelopathy or CN signs

Diagnosis: MRI, CSF, culture (blood, urine, CSF, tissue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Meningitis/ Myelitis (CSF analysis findings)

A
  • neutrophilic pleocytosis
  • high protein, low glucose
  • +/- xanthochromia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Meningitis/ Myelitis (treatment)

A
  • Antibiotics
  • meticulous monitoring
  • short course corticosteroids for inflammation control
53
Q

When is it safe/ ok to assume that meningitis is inflammatory and not infectious?

A

(-) culture
(-) organism
no systemic infection/ signs
minimal contrast enhancing on MRI

54
Q

Epidural Empyema

A
  • spinal abscess

- occurs following: discospondylitis, foxtail, CNS infection, paraspinal abscess

55
Q

Epidural Empyema (Clinical Signs, Diagnosis, Tx)

A

Clinical Signs - very painful, fever, lethargy , progressive signs
Diagnosis, clinical signs, inflammatory leukogram, imaging
Treatment: abx, surgical drainage if necessary

56
Q

Discospondylitis

A
  • infection of the intervertebral disc and adjacent endplates
  • one of the few causes of disc space widening
57
Q

Discospondylitis (pathogenesis)

A
  • primary disease
  • hematogenous
  • foreign body
  • extension of dz
  • penetrating wound
  • immunosuppresion
58
Q

Discospondylitis (common organisms)

A
  • staph aureus
  • Strep
  • E. coli
  • Brucella
59
Q

Discospondylitis (signalment)

A
  • large/ giant breeds
  • young to middle aged
  • males > females
60
Q

Discospondylitis (Hx)

A
  • chronic, progressive pain
61
Q

Discospondylitis (clinical signs)

A
  • spinal pain, kyphoses, panting, lethargy
62
Q

Discospondylitis (Diagnosis)

A
  • imaging
  • culture (lesion, disc, surgical site)
  • cytology
  • serology
63
Q

Discospondylitis (treatment)

A
  • abx
  • exercise restriction
  • analgesics
64
Q

Fibrocartilage embolism

A
  • infarction of the spinal cord

- obstruction of the arterial supply by fibrocartilage

65
Q

FCE (signalment)

A
  • young to middle aged
  • large breed (especially active dogs during exercise)
  • peracute/ acute onset
66
Q

Are dogs with an FCE painful?

A

not usually

67
Q

FCE (Diagnosis)

A
  • signalment, hx, neuro exam
  • MRI and CSF
  • rule out other causes
  • histopath ( gold standard)
68
Q

FCE (treatment and prognosis)

A

Treatment - supportive care, physical therapy

Prognosis - depends on location and severity; UMN lesions usually are good prognosis while LMN are guarded

69
Q

Degenerative Myelopathy

A
  • slowly progressive degeneration of specific spinal cord tracts and nerve roots in T3-L3
  • hits the pelvic limbs “hard and fast” (sturgers)
70
Q

Degenerative Myelopathy (Signalment and Hx)

A

Signalment: middle - older age, 3 breeds over-represented (GSD, Boxer, Corgi)

Hx - chronic myelopathy, slowly progressive, non-painful

71
Q

Degenerative Myelopathy (Clinical Signs)

A
  • paraparesis
  • non-painful
  • symmetrical
  • retain continence
  • may affect L4-6
72
Q

Degenerative Myelopathy (Treatment, Prognosis)

A

Tx: no known treatment
Prognosis: poor to grave longterm

73
Q

A dog is genetically tested for Degenerative Myelopathy and comes back as AA (affected). What does this tell you?

A
  • the animal is AT RISK for developing this disease

- it does not tell you that they will develop this disease or that they currently have it

74
Q

Spinal Cord Neoplasias (signalment0

A
  • usually older animals

- younger animals have certain predispositions

75
Q

Acute Spinal Cord Injury (ASCI)

A
  • traumatic vertebral fracture luxation
  • acute hemorrhage
  • acute IVD extrusion
  • FCE
  • Congenital vertebral instability
  • acute inflammation
76
Q

Acute Spinal Cord Injury ( When to refer)

A
  • rapid change in neuro status
  • onset of paralysis
  • ventilation problems
  • it’s all about deep pain sensation
77
Q

What is important about prognosis with all neuro dz

A
  • it’s all about the neuro exam and not what you find/ don’t find on imaging
78
Q

Acute Spinal Cord Injury ( primary concern)

A
  • don’t make things worse
79
Q

Is it possible to differentiate pathology affecting the Cauda Equina and LMN pelvic lesions?

A

No

80
Q

T/F: all sacral and caudal nerve roots pass over the L7-S1 disc space before exiting out the foramen

A

T

81
Q

Cauda Equina Syndrome (clinical signs)

A 
Motor:
- Tail
- Anus
- Pelvic Limb
- Bladder
Sensory Abnormalities
- (-) conscious proprioception 
- change to body sensation (parasthesia, anesthesia, etc)
Psuedoexaggeration fo patellar reflex
\+/- Apparent Pain
82
Q

What is psuedoexaggeration of the patellar reflex?

A

loss of antagonism of muscles innervated by the femoral nerve by muscles related to sciatic nerve

83
Q

Cauda Equine Syndrome (Diagnosis)

A
  • rule out other myelopathies

- Hx, PE, NE, CT, MRI, CSF, Myelogram, Dynamic radiographs

84
Q

Lumbosacral Vertebral Canal Stenosis (cause)

A 
Acquired in large breed dogs
Stenosis is 2* to all or one of the following:
- type 2 disc protrusion
- hypertrophy/ plasia of ligaments
- thickening of vertebral arch/ facets
- +/- instability
85
Q

Lumbosacral Vertebral Canal Stenosis ( signalment, Hx)

A

Signalment:
- male, large breed dogs (GSD)
Hx:
- slowly progressive, trouble rising

86
Q

Lumbosacral Vertebral Canal Stenosis (Diagnosis, Prognosis)

A

Diagnosis:
- orthopedic exam, spinal radiographs, CT, MRI
Prognosis:
- mild signs = good

87
Q

Lumbosacral Vertebral Canal Stenosis (Treatment)

A

Medically – only if minor signs

Surgical – dorsal laminectomy +/- internal stabilization

88
Q

Discospondylitis

A
  • bacterial or fungal infection of the intervertebral disc and adjacent vertebral body
89
Q

Discospondylitis (Physical Exam and Neuro Exam)

A
  • fever
  • marked spinal pain
  • no neuro deficits
90
Q

Discospondylitis (Imaging)

A
  • neoplasia will not cross disc space

- end-plate destruction, collapse of IV disc

91
Q

Discospondylitis (prognosis)

A
  • good for bacterial
92
Q

Type 1 myofibers

A
  • postural muscles
  • “slow” twitch, oxidative metabolism
  • appears dark on pH4.3 stain
93
Q

Type 2 myofibers

A
  • movement muscles
  • “fast twitch”, glycolytic metabolism
  • appears light on pH4.3 stain
94
Q

T/F: myofiber type is determined by the type of innervation of the motor neuron

A

T

95
Q

T/F: a de-nervation, re-nervation event can cause signficiant portions of a muscle to change myofiber type

A

T

96
Q

3 ways to classify neuromuscular disease.

A
  1. neuropathies
  2. “junction”-opathies
  3. myopathies
97
Q

Clinical Signs of Neuromuscular Disease

A

Focal or generalized weakness
Functional: gait abnormalities, paresis/ paralysis, exercise-induced weakness
Physical: muscle atrophy/ hypotrophy/ hypertrophy
Cervical Ventroflexion: classical sign in cats
Megaesophagus

98
Q

Diagnostic approach to NM disease

A

Hx
PE, NE, minimum database
Functional Testing: Electromyography
Biopsy: muscle, nerve

99
Q

Electromyography (decreased insertional activity)

A

decreased muscle mass

100
Q

Electromyography (increased insertional activity)

A

hyperexcitable muscle

101
Q

Electromyography (fibrillation potentials and positive sharp waves)

A
  • popping

- rain on tin roof

102
Q

Electromyography (complex repetitive discharge)

A
  • motorcycle idling
103
Q

Electromyography ( myotonic potentials)

A
  • pathognomonic for myotonia congenita

- sounds like an air horn/ dive bomber

104
Q

Nerve and Muscle Biopsy

A
  • be smart about how you do this (would like a functional nerve post-biopsy, etc.)
  • Fixed - formalin kills tissue
  • Frozen - permits assessment of enzymatic fxn
105
Q

Categories of Neuropathies

A
  • Mononeuropathies
  • Multiple Mononeuropathies
  • Polyneuropathies
106
Q

Neuropathies: Histopath

A
  • angular atrophy of myofibers (whatever that means)
  • denervation atrophy = both type 1 and 2
  • end-stage denervation = pyknotic nuclear clumps
  • myofiber type grouping = chronic denervation, renervation
107
Q

Tetanus

A
  • C. tetani infection, anaerobic conditions
  • toxin enters nerve and ascends to cord
  • destruction of inhibitory interneuron (renshaw cell) synapse to LMN
108
Q

Tetanus (diagnosis and tx)

A

Diagnosis: clinical signs ( tetany, risus sardonicus), Hx

Treatment: antitoxin ( can only give once), debridement, abx w/ anaerobic spectrum

109
Q

Mononeuropathies

A
  • radial neuropathy, facial paralysis, etc

- common causes: trauma, iatrogenic, idiopathic, neoplasia, inflammatory

110
Q

Brachial Plexus Avulsion

A

musculocutaneous (C6-8) (biceps, withdrawal)
radial (C7-T1) (triceps, weight bearing)
median/ ulnar (C8-T2)

111
Q

Lumbosacral Plexus Avulsion

A

Femoral (L4-6) (patellar reflex, weight bearing)
Sciatic (L6-S1) (gastroc reflex, withdrawal and flexion)
Pudendal (S1-3)

112
Q

Acute Polyradiculoneuritis

A
  • rapid onset flaccid tetraparesis/ plegia
  • LMN signs in all 4 limbs
  • often history of bite or other antigen. stimulus w/in past 2 weeks
  • causes an immune mediated attack of ventral nerve root (primarily motor fxn loss) and demyelination
113
Q

T/F: an animal suffering from acute polyradiculoneuritis will have intact sensory fxn but little motor abilities to react appropriately

A

True

114
Q

Polyradiculoneuritis (Treatment, Recovery)

A

Tx: supportive care
Recovery: time for remyelination and axonal regrowth is weeks to months

115
Q

Polyradiculoneuritis (EMG, CN)

A

EMG: spontaneous activity > 4-5 days
CN: rarely affected

116
Q

Chronic Polyneuropathies

A
  • often pelvic limb more affected
  • generalized weakness/ LMN signs
  • plantigrade/ palmigrade stance
117
Q

What’s 2+2?

A

IDK, but maureen’s a big loserface lmao

118
Q

Junctionopathies - histopath

A
  • usually absent or non-specific

- diagnosis based on other assays

119
Q

Pre-synaptic Junctionopathies ( two categories)

A
  1. decreased ACh release: inability to activate AChR (hypocalcemia, high Mg, botulism, tick paralysis, aminoglycosides)
  2. elevated ACh release: weakness caused by continued depolarization of post-synaptic membrane and depletion of pre-synaptic vesicles (low Mg, envenomation)
120
Q

Tick Paralysis

A
  • dermacentor, Ixodes (australia)
  • salivary neurotoxin secreted by tick causes reversible interference of Ca mediated ACh release –> rapidly ascending UMN paralysis
  • Diagnosis: find the tick
  • Treatment: tick hunt and removal, supportive
121
Q

Botulism

A
  • ingestion of type C neurotoxin from C. botulinum
  • irreversible inhibition of ACh release from cholinergic nerve terminals
    CS: acute onset LMN signs, fatal tetraplegia and areflexia, mild weakness, megaesophagus/ aspiration pneumonia
    Diagnosis: organism detection
    Treatment: supportive care, C. botulinum antitoxin
122
Q

Synaptic Cleft Disorders

A
  • Cholinesterase Inhibitors
  • inhibit breakdown of ACh prolong active at receptor
  • organophosphates and carbamates **
123
Q

Myasthenia Gravis (Acquired or Congenital)

A

Acquired: autoimmune attack against AChR resulting in depletion of receptors (dogs)

Congenital: deficiency or functional disorder of AChR (nicotinic)

124
Q

Acquired MG (age range)

A

2-4 years, 9-13 years old

125
Q

Acquired MG (History and CS)

A

Focal – esophageal, pharyngeal, facial weakness
Generalized – generalized weakness +/- the areas above

  • exercise intolerance
  • regurgittaion/ megaesophagus
  • mediastinal mass (thymoma)
  • acute tetraplegia
126
Q

Acquired Maureen’s G-stupid (Diagnosis)

A
  • immunological testing: gold standard, AChR antibodies
  • pharmacological testing: short acting AChE inhibitor
  • Electrodiagnostics: decremental response
127
Q

Acquired MG (treatment)

A
  • cholinesterase inhibitors (pyridostigmine)
128
Q

Congenital MG

A
  • onset at 6-12 weeks
  • generalized weakness
  • breed disposition - labs
  • diagnosis - no immune testing
  • treatment - variable

VET 433a - Small Animal Stream 1 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions