2019.Iss2.controversiesinEquinemed & sx Flashcards

1
Q

Diagnostic Testing for Equine Endocrine Diseases: Confirmation VS Confusion

What are instances that plasma ACTH concentration increased other than PPID?

A

chronic and acute disease
malnutrition
other stressors

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2
Q

Diagnostic Testing for Equine Endocrine Diseases: Confirmation VS Confusion

Is there a gold standard test for diagnosis of Equine PPID?

A

No

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3
Q

Diagnostic Testing for Equine Endocrine Diseases: Confirmation VS Confusion

What are normal insulin levels in the equine serum?

A

<20micoU/mL

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4
Q

IS Electrical Nerve Stimulation the Answer for Management of Equine Headshaking?

What virus has a predilection for latency in the trigeminal nerve?

A

equine herpesvirus-1s

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5
Q

Treatment Options for melanoma of gray horses

Locoregional control of melanoma masses depends on:

A

surgical removal
and/or
intralesions chemotherapy (poss. with adjunctive hyperthermia or electroporation)

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5
Q

Treatment Options for melanoma of gray horses

What gene mutation do all gray horses have, that unbalances melanocyte behavior to cause graying and propensities to develop vitiligo & melanoma

A

STX17

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6
Q

Treatment Options for melanoma of gray horses

when are melanomas seen in gray horses?

A

typically arise at 4-8 years of age, that increases approximately by 4-8% annually

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7
Q

Treatment Options for melanoma of gray horses

Are melanomas malignant?

A

variable: sessile to aggressively invasive metastic multicentri ctumors

**early melanomas are considered pre-cancerous

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8
Q

Treatment Options for melanoma of gray horses

Do melanomas shorten the average lifepsan of gray hroses

A

no reliable data that quantify the “gray effect” on longevity

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9
Q

The Equine Sarcoid: Why are there so many treatment options

What are the 6 different types of sarcoids?

A
  1. occult
  2. verrucose
  3. nodular
  4. fibroplastic (pedunculated sessile)
  5. Mixed
  6. malignant
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10
Q

The Equine Sarcoid: Why are there so many treatment options

What is the gold standard treatment of sarcoid?

A

radiation
+/- some form of surgery

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11
Q

The Equine Sarcoid: Why are there so many treatment options

What are the treatment options available for sarcoids?

A
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12
Q

The Equine Sarcoid: Why are there so many treatment options

What is the best treatment for sarcoids?

A

No
**there is a lot of treatment & combinations of treatments that are used worldwide

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13
Q

Exercise Induced Pulmonary Hemorrhage: is it important & can it be prevented?

What is considered the most sensitive indicator of EIPH?

A

bronchoalveolar lavage (BAL): 90-100% of horses having evidence of EIPH on BAL fluid cytology

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14
Q

Exercise Induced Pulmonary Hemorrhage: is it important & can it be prevented?

What is the best accepted method/timing for testing for EIPH?

A

tracheobronchoscopy conducted 30 minutes to 120 minutes after exercise
**preferably after racing

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15
Q

Exercise Induced Pulmonary Hemorrhage: is it important & can it be prevented?

When evaluating horses with EIPH that have a high score, does it mean that its negatively affecting their performance?

A

No
**horses should be re-examined to assess the grade prior to drawing conclusions abotu any negative race day performance. Horses with lower grades are more likely to have consistent EPIH grades at subsequent race starts, but this is also not guaranteed

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16
Q

Exercise Induced Pulmonary Hemorrhage: is it important & can it be prevented?

When hemosiderophages are seen on BAL fluid cytology, does this correlate to disease severity?

A

No

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17
Q

Exercise Induced Pulmonary Hemorrhage: is it important & can it be prevented?

Does EIPH affect racing performance?

A

Yes, however variable reports in severity affecting racing performance

18
Q

Exercise Induced Pulmonary Hemorrhage: is it important & can it be prevented?

IS exercise induced pulmonary hemorrhage a progressive disease?

A

EIPH is described as a progressive disease based on histopathologic examination fo lung tissue from racehorses

19
Q

Exercise Induced Pulmonary Hemorrhage: is it important & can it be prevented?

What is the recommended treatment for EIPH?

A

high-quality evidence exists that furosemide decreases the severity and incidence of EIPH

20
Q

Exercise Induced Pulmonary Hemorrhage: is it important & can it be prevented?

What are recommended management factors in treatment of EIPH?

A

-avoidance of cold weather racing and training
-increasing the intervals between races
-altering the racing strategy in horses with a history of mod-severe EIPH

21
Q

Equine Neonatal Encephalopathy: facts, evidence, and opinions

The mechanisms of equine neonatal encephalopathy can be divided into what 3 general categories/mechanisms?

A
  1. adverse peripartum events, d/t ischemia/hypoxia in the prepartum period (placental disease), at partum (dystocia, c-section), or in the postpartum period (umbilical bleeding/compression, etc)
  2. evidence of placenta dz with variable gestation length
  3. no documented maternal disease, gestation length is normal and foaling is uneventful
22
Q

Equine Neonatal Encephalopathy: facts, evidence, and opinions

the pathophysiology of NE can be divided into what two broad categories?

A
  1. ischemic/hypoxic: oxygen/energy deprivation, reperfusion, hemorrhage, edema, & inflammation
  2. non-ischemic (metabolic & endocrine)
23
Q

Equine Neonatal Encephalopathy: facts, evidence, and opinions

The brain requires what percentage of oxygen and glucose?

A

20% oxygen
20% glucose

24
Q

Equine Neonatal Encephalopathy: facts, evidence, and opinions

What is considered important in the delayed lesion severity and disease progression of NE?

A

reperfusion injury & blood redistrubtion in response to ischemia

25
Q

Equine Neonatal Encephalopathy: facts, evidence, and opinions

Describe the pathogenesis of inflammation in NE.

A

microglial cells release inflammatory mediators & promote cerebral infiltration by peripheral luekocytes

26
Q

Equine Neonatal Encephalopathy: facts, evidence, and opinions

describe the phases of cerebral injury after an ischemic-hypoxic event.

A

phase 1: neurons deprived of energy & oxygen, shifting to anaerobic metabolism, release of inflammatory mediators, cell swelling, cell death, etc.

phase 2: secondary energy failure; 6 hours to day
glutamate release, continuation of reperfusion injury, cell necrosis, apoptosis

phase 3: tertiary brain injury; weeks to years:
ongoing brain injury: astrogliosis, delayed cell death, remodeling, tissue repair

27
Q

Equine Neonatal Encephalopathy: facts, evidence, and opinions

What is the primary main excitatory neurotransmitter, with prolonged exposure leads to neuronal injury & death.

28
Q

Equine Neonatal Encephalopathy: facts, evidence, and opinions

When is glutamate released?

A

-continuously released from neurons & removed by astrocytes in an equilibrium that can be disrupted & reduced ATP supply

29
Q

Equine Neonatal Encephalopathy: facts, evidence, and opinions

What is the proposed mechanism for magnesium sulfate administration in NE foals?

A

glutamade excitotoxicity can be blocked by NDMA and AMPA receptors

30
Q

Equine Neonatal Encephalopathy: facts, evidence, and opinions

Why is astrocyte dysfunction in NE foals detrimental to continued neuronal damage?

A

astrocytes provide a steady source of energy for neurons

31
Q

Equine Neonatal Encephalopathy: facts, evidence, and opinions

What are the risk factors for equine NE/NMS?

A

maternal: any condition resulting in systemic inflamm or ischemia/hypoxia can impair perfusion

placental: placentitis, placental separation

fetal: congenital anomalies, twins, prematurity/dysmaturity, sepsis, umbilical cord compression, dystocia

32
Q

Are there shared mechanisms in the pathophysiology of different clinical forms of laminitis and what are the implications for prevention & treatment

What are the 3 types of laminitis?

A
  1. endocrinopathic laminitis: assoc with insulin dysregulation, which may be primary (EMS), assoc with PPID or iatrogenic (secondary to corticosteroid admin)
  2. Sepsis related laminitis: systemic illness characterized by systemic inflammation, particularly in response to endotoxemia (eg, colitis, metritis, pneumonia)
  3. Support Limb laminitis: develops in horses with painful limb conditions such as fractures or synovial sepsis, this form primarily affects the limb contralateral to the primary injury, but often multiple limbs affected
33
Q

Are there shared mechanisms in the pathophysiology of different clinical forms of laminitis and what are the implications for prevention & treatment

What are the major forms of laminitis & their corresponding experimental models?

34
Q

Are there shared mechanisms in the pathophysiology of different clinical forms of laminitis and what are the implications for prevention & treatment

Glucose consumption by the lamellae is performed by what?

A

GLUT-1 transporter
**uptake is non-insulin dependent

35
Q

Are there shared mechanisms in the pathophysiology of different clinical forms of laminitis and what are the implications for prevention & treatment

What are preventative & early therapeutic efforts should be aimed at for laminitis?

A
  1. perfusion enhancement sin horses at risk of SLL
  2. Control of local & systemic inflammation for SRL
  3. early diagnosis & careful management of ID for endocrinopathic laminitis
36
Q

Are there shared mechanisms in the pathophysiology of different clinical forms of laminitis and what are the implications for prevention & treatment

What therapeutic has a marked antiinflammatory effect in experimental models in sepsis related laminitis?

A

continuous digital hypothermia (cryotherapy)

37
Q

Are there shared mechanisms in the pathophysiology of different clinical forms of laminitis and what are the implications for prevention & treatment

What are strategies to minimize ongoing lamellar damage:

A

-anti-inflammatory therapy
-confinement and restriction of locomotor activity
-mechanical foot support
-digital hypothermia

38
Q

What do we know about hepatitis viruses in horses?

List causes of hepatitis in horses

39
Q

What do we know about hepatitis viruses in horses?

what is known about equine parvovirus?

40
Q

What do we know about hepatitis viruses in horses?

What is known about equine hapcivirus?

41
Q

Fetal membrane removal in the mare: proactive vs reactive approaches

what factors are associated with a higher occurrence of retained fetal membranes?

A

mare age
previous RFM
breed
peripartum complications: abortion, dystocia, placentitis, prolonged gestation, hydropic conditions

42
Q

Fetal membrane removal in the mare: proactive vs reactive approaches

What are the potential risks of controlled fetal membrane removal:

A

-increased risk of hemorrhage when separating the microvilli from the endometrium
-tearing membranes during removal, thus causing RFM
-retained microvilli, which can provide a nidus for infection
-uterine horne eversion/intussusception or prolapse