FA med Exam 1

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FA med Exam 1
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2013-01-26 23:49:37
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FA Medicine
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  1. What are some clinical symptoms of cerebral
    cortex disease?
    Change in mentation

    +/- blindness

    circling
  2. What are some clinical symptoms of brain stem disease?
    CN deficits

    Circling

    Head tilt
  3. What are some clinical symptoms of cerebellar disease?
    Intention tremors

    Hypermetria / dysmetria

    Incoordination
  4. What are some clinical symptoms of spinal cord disease?
    Ataxia

    • Spinal reflexes (increased or decreased depending on
    • location)

    Paralysis / paresis
  5. What are some clinical symptoms of peripheral nerve disease?
    Muscle tone

    Muscle atrophy

    Paralysis / paresis

    Absence of spinal reflexes
  6. What are the common brain stem diseases in ruminants?
    Listeriosis

    • Otitis media / interna (M. bovis, P. multocida, H. somni, C
    • pseudotuberculosis, T. pyogenes)

    TEME (H. somni)

    Brain or pituitary abscess

    Meningeal worm (more often spinal cord)
  7. What are the common brainstem diseases in pigs?
    • Otitis media / interna (P. multocida, S. suis, H. suis, T.
    • pyogenes)
  8. What are the common cerebral diseases in ruminants?
    Cerebrocortical necrosis (CCN)

    TEME

    Nervous ketosis

    Nervous coccidosis (Eimeria)

    Pregnancy toxemia

    HypoMg

    BSE

    Scrapie

    Rabies

    VitA deficiency (prolonged storage of green plants
  9. What are the common cerebellar diseases in ruminants?
    Cerebellar hypoplasia (BVDV type 2)
  10. What are the common spinal cord diseases in ruminants?
    Tetanus

    Enzootic ataxia

    Meningeal worm

    Lymphosarcoma

    CAE
  11. What are the common cerebral diseases in pigs?
    Strep meningitis

    Glasser’s (H. parasuis)

    Edema disease (E. coli)

    HyperNa

    Pseudorabies
  12. In which pigs are clinical symptoms of cortical disease
    seen?
    Nursery
  13. What is the mechanism of polioencephalomalacia (CCN)?
    Altered thiamine metabolism
  14. What are some causes of CCN?
    Pb poisoning

    Lactic acidosis (e.g. grain overload)

    HyperNa

    Bracken fern toxicity

    Sulfur intoxication

    Amprolium intoxication
  15. What is the normal pentose phosphate pathway?
    • Glucose is used to make ATP by the rate limiting enzyme
    • VitB1 dependent transketolase

    • The ATP is used to maintain 3Na+/2K+ pumps on the cell
    • membrane

    Most affected are nervous tissue cells and RBCs
  16. Where do ruminants normally get thiamine?
    Rumen microbes
  17. What does a CSF analysis of CCN in ruminants show?
    Increased protein, monocytes (unless it’s a pig with hyperNa
  18. What does a CSF analysis of a pig with hyperNa show?
    Eosinophilia
  19. What does gross pathology of CCN show?
    Diffuse cerebral edema

    Cerebellum pushed back to magnum foramen

    Wood’s Lamp shows fluorescence in gray and white cerebral cortex
  20. Why do ruminants get Pb poisoning?
    Calves are curious, esp after weaning

    May have mineral deficiency
  21. What is the mechanism of Pb poisoning?
    Pb binds sulfhydryl groups esp on RBCs

    Pb inhibits PPP transketolase in RBCs
  22. What are the clinical symptoms of Pb poisoning?
    Cortical signs like bellowing, mania, seizures

    Cortically blind

    CCN

    Mild anemia

    Diarrhea

    Death from respiratory paralysis
  23. How is Pb poisoning dx?
    Heparinized blood sample

    Tissue samples (liver and kidney)
  24. What is the txt for Pb poisoning?
    Give thiamine

    CaEDTA to chelate Pb in tissues, excreted by kidney

    Cathartics e.g. MgSO4

    Diazepam
  25. What does an increase in rumen lactic acid cause, and why?
    Rumenitis

    Metabolic acidosis (if severe)

    Dehydration (water is pulled into the rumen)

    Bloat (CHOs are fermented)

    Endotoxemia (no more g-)

    CCN (no more thiamine)

    Liver abscess (F. necrophorum gains access to the portal v.)

    Caval syndrome (F. necrophorum causes lung abscesses and death)
  26. How does lactic acidosis occur in a ruminant?
    Ingestion of high CHO

    The microflora shift to be more g+

    Strep/ bovis proliferates

    VFAs increase

    Rumen pH decreases

    G- bacteria and protozoa die

    Lactobacillus proliferates

    Lactic acid increases in the rumen
  27. How is lactic acidosis dx?
    Rumen pH <5.5
  28. How is lactic acidosis tx?
    Give thiamine

    Transfaunate rumen

    IVF of NaHCO3 + KCl or glucose

    Systemic abx

    NSAIDs (if kidneys ok)
  29. Why do you need to give KCl to a ruminant with lactic
    acidosis?
    • HyperK likely, but increasing K will move H+ out of cells
    • and out of tubules(?)
  30. How can lactic acidosis be prevented?
    Adapt animals to a high CHO diet

    Put ionophores and NaHCO3 in feed
  31. What are the clinical symptoms of hyperNa?
    Change in mentation, central blindness, circling

    Aggressive, excitable

    Seizures

    Dog sitting position (pigs)
  32. How is hyperNa dx?
    Serum increase in Na, hemoconcentration, pre renal azotemia, metabolic acidosis (anaerobic glycolysis)

    CSF increase in protein, Na and monocytes (ruminants) or eosinophils (pigs)
  33. What neurological conditions cause pigs to dog sit?
    Rabies, hyperNa
  34. What causes the CS of hyperNa?
    • Increased electrolyte [], followed by heavy water drinking
    • -> water drawn into ventricles
  35. How is hyperNa tx?
    Give IVF with higher [Na] than serum

    Check every hour, adjust IVF accordingly
  36. How is hyperNa related to CCN?
    • The cells are dying, so they’re not performing PPP, so
    • there’s less ATP available
  37. How does amprolium cause CCN?
    Incorrect mixing means [thiamine analogue] competes with thiamine on transketolase
  38. How can amprolium toxicity be dx?
    Hx

    RBC transketolase activity
  39. How is amprolium toxicity tx?
    Give thiamine
  40. How does bracken fern ingestion cause CCN?
    Presence of thiaminases in plant

    Also has oxidizing agents resulting in hemolysis and hematuria
  41. How can bracken fern ingestion be dx?
    Hematuria, bladder TCC
  42. What causes bladder TCC?
    Bovine papilloma virus, bracken fern ingestion
  43. How does sulfur intoxication cause CCN?
    Direct thiamine destruction

    Sulfates converted to sulfide in the rumen (normally hydrogen sulfide)

    Hydrogen sulfide inhibits cytochrome oxidase (electron transport chain) and transketolase enzyme
  44. How is sulfur intoxication dx?
    [Sulfur] in water or feed

    Hx (smell)
  45. How is sulfur toxicity tx?
    Give thiamine, but unlikely to be successful

    Supportive, IVF, transfaunation

    Dexamethasone (reduce cerebral edema)

    Mannitol (reduce cerebral edema)
  46. What is the prognosis of CCN diseases?
    Good except sulfur intoxication
  47. Which pigs are affected by edema disease?
    Weaned piglets
  48. What is the mechanism for edema disease?
    • E. coli adheres to gut via fimbria F18ab, producing a toxin
    • that damages the vascular endothelium
  49. What are the CS of edema disease?
    Lesions include edema of the stomach, colon and eyelids

    Cortical signs (edema and necrosis of cortex)
  50. Which pigs are affected by Strep meningitis?
    Weaned piglets
  51. What are the CS of Strep meningitis?
    Pneumonia

    Polyserositis

    Septicemia (signs on infection more common than neurological signs)

    Incoordination

    Stupor

    Seizures
  52. How is Strep meningitis tx?
    Vaccination and antibiotics, but variably effective
  53. How can Strep meningitis be prevented?
    Vaccines (variably effective, zoonotic)

    Not SEW
  54. Which pigs are affected by Glasser’s disease?
    Weaned piglets
  55. What causes edema disease?
    E. coli
  56. What causes Strep meningitis?
    Strep suis type II
  57. What causes Glasser’s disease?
    Haemophilus parasuis
  58. What are the CS of Glasser’s disease?
    Pneumonia

    Polyserositis

    Septicemia

    …looks like Strep meningitis
  59. How can Glasser’s disease be prevented?
    Good vaccine
  60. How is Glasser’s disease tx?
    Abx
  61. How can edema disease, Glasser’s and Strep meningitis be
    differentiated on necropsy?
    Edema disease has edema of stomach and eyelid

    Fibrin on serosal surfaces if Step or Glasser’s
  62. How can CNS diseases in nursery pigs be dx (e.g. Glasser’s,
    edema disease, Strep meningitis, hyperNa)?
    Culture (meninges for Step or Glasser’s, intestine for E. coli)

    Histopathology (purulent meningitis for Strep or Glasser’s, eosinophils for hyperNa)

    Serum analysis (eosinophils and hyperNa)
  63. How does cerebellar hypoplasia occur?
    Inherited or acquired (more common)
  64. In which breeds is cerebellar hypoplasia inherited?
    Hereford, Shorthorn, Angus, Holstein, Guernsey, Ayrshire
  65. How is cerebellar hypoplasia acquired in cattle?
    BVD in-utero infection

    Blue tongue
  66. How is cerebellar hypoplasia acquired in sheep?
    Border disease

    Blue tongue
  67. What are the CS of cerebellar hypoplasia?
    Spasticity

    Dysmetria

    Seizures maybe

    Intention tremors

    Incoordination

    Normal intelligence

    Viable
  68. What diseases cause drooling in ruminants?
    Rabies

    CN VII dysfunction

    Listeria
  69. What can cause spinal cord disease in ruminants and pigs?
    Clostridium tetani
  70. Where is C. tetani found?
    Soil and intestinal tract
  71. How does an animal get infected with C. tetani?
    • Wound is contaminated by soil spores, which vegetate and
    • produce toxins

    • Associated with parturition, retained fetal membranes,
    • vaginal bruising, teeth eruption, castration, tail docking and shearing
  72. What toxins are produced by C. tetani?
    Tetanospasmin (binds inhibitory neurons in spinal cord)

    Tetanolysin (causes tissue damage)
  73. What are the CS of C. tetani infection?
    Uninhibited muscle contractions

    Sawhose stance, pump handle tail lock jaw

    3rd eyelid prolapse

    Bloat

    Exaggerated response to sound

    Sardonic grin

    Death when diaphragm muscles are paralyzed 
  74. How can C. tetani infection be dx?
    Can’t – the toxin is in the nerves, not the blood
  75. How is tetanus tx?
    PPG, neuromuscular relaxants like diazepam or MgSO4

    Tetanus anti-toxin

    Minimize neural input
  76. How is tetanus prevented?
    Vaccine with C. tetani + C. perfringens C and D
  77. What are the characteristics of C. tetani?
    G+ anaerobe
  78. What is enzootic swayback?
    Lambs born to chronically Cu deficient does have progressive posterior ataxia and weakness
  79. What is the mechanism of enzootic swayback disease?
    Cu required for myelin formation in the spinal cord

    Hind limb -> front limb demyelination
  80. What are the CS of enzootic swayback disease?
    Observed progressive ataxia in lambs 0-6 months old

    Maintenance of spinal reflexes
  81. How is enzootic swayback disease tx?
    Can’t reverse any of the neuro signs

    PO Cu if mild
  82. How is enzootic swayback disease prevented?
    Cu supplementation of does
  83. Which lymphosarcoma is BLV-associated?
    Enzootic
  84. What are the juvenile forms of lymphosarcoma?
    Multicentric, thymic, cutaneous, enzootic
  85. How is BLV spread?
    Vertically (8%)

    Colostrum or milk (8%)

    Horizontal (majority)

    Events: dehorning, ear tagging, tattooing, injections, vaccinations, rectal palpation, biting flies
  86. How many animal are infected with BLV, and how many will
    develop enzootic BLV lymphosarcoma?
    >80% infected, <5% get lymphosarcoma
  87. What kind of virus is BLV?
    Retro (exposure = infected)
  88. What organs are commonly affected by lymphosarcoma?
    LNs, retrobulbar, uterus, spinal cord, abomasum
  89. How is lymphosarcoma dx?
    • Persistent lymphocytosis (2 samples 2 weeks apart, 20% sensitive)
    • LN biopsy (best)
    • BLV PCR / AGID / ELISA (only tells you exposure)
  90. How is lymphosarcoma tx?
    n/a – poor px
  91. In which animals are vertebral or epidural abscesses seen?
    Calves

    Bacteremic animals (omphalophlebitis, endocarditis, liver abscess, pneumonia)

    Working ruminants like bucking bulls
  92. What agent usually causes vertebral or epidural abscesses?
    T. pyogenes
  93. What are the CS of vertebral or epidural abscesses?
    Gradual onset of paresis and paralysis

    Sudden vertebral fracture and paralysis
  94. How can vertebral or epidural abscesses be dx?
    CSF has neutrophils and macrophages, high protein

    Radiographs very helpful
  95. How are spinal cord diseases managed?
    Dx to know the px

    Treat the underlying disease

    Pain management

    Physiotherapy

    Sling

    Float tank

    Beach balls
  96. What are the 4 “m’s” of downer cows?
    Musculoskeletal

    Metabolic (hypoCa, hypoK)

    Mastitis

    Metritis
  97. What does the radial n. supply?
    Extends the elbow, carpus and digits of thoracic limb

    Cutaneous sensation to lateral part of the leg
  98. How does radial n. paralysis occur?
    Prolonged recumbency
  99. What is the txt for radial n. paralysis?
    Bandage, splint, or cast the fetlock to avoid abrasion

    Use deep soft bedding

    Dexamethasone to stabilize the cell membrane and prevent inflammation
  100. What happens when a cell membrane is damaged?
    PLA2 breaks phospholipids down to arachidonic acid

    • Arachidonic acid is broken down to thromboxanes,
    • prostaglandins and prostacyclins (COX1, COX2) or leukotrienes (lipoxygenase)
  101. Where do steroids inhibit inflammation?
    Inhibits PLA2
  102. Where do NSAIDs inhibit inflammation?
    COX1 or COX2
  103. What does the obturator n. supply?
    Muscles that adduct the hip
  104. When is obturator n. damage seen?
    Dystocia from feto-pelvic disproportion pressure ischemia
  105. How is obturator n. damage tx?
    Put in stall with good footing

    Hobble

    Float tank

    Corticosteroids and NSAIDs
  106. What is the most common nerve injury in dairy cattle?
    Sciatic n. damage
  107. What causes sciatic n. damage?
    Injecting the gluteal muscles

    Pelvic fracture

    Dystocia
  108. What are the CS of sciatic n. damage?
    • Dropped stifle, hip and hock
    • Flexion of fetlock
  109. What does the peroneal n. supply?
    Flexor muscles of the hock

    Extensor muscles of the digit
  110. How is the peroneal n. damaged?
    Exposed superficially distal to the stifle

    Prolonged recumbence
  111. What are the CS of peroneal n. damage?
    Hyper-extension of the hock (looks super straight)

    Flexion of the fetlock
  112. What does the tibial n. supply?
    Extensor muscles of the hock

    Flexors of the digits
  113. What causes tibial n. damage?
    Irritating injections in the caudal leg (near stifle)

    Dog or coyote bite
  114. What are the CS of tibial n. damage?
    Over-flexed hock

    Extended fetlock and pastern
  115. What nerve paralysis is seen in calves?
    Femoral n. if pulled during dystocia from a posterior position

    Secondary to injection site abscess
  116. What does the femoral n. supply?
    Quadriceps, so flexes hip
  117. What are the CS of femoral n. damage?
    Non weight bearing if severe

    Muscle atrophy

    Absence of patella reflex
  118. How is peripheral n. damage tx?
    NSAIDs

    Corticosteroids

    Good footing

    Bandage the limb to prevent pressure sores

    Float tank

    Time (<14 days)
  119. What does the sciatic n. supply?
    Extensor muscles of the hip

    Flexor muscles of the stifle and distal limb
  120. What does the sciatic n. divide into?
    Tibial and peroneal n.
  121. What is botulism caused by?
    Clostridium botulinum B, C, D
  122. How do animals get botulism?
    Ingest a pre-formed toxin from carcasses or rotting vegetation

    Wound contamination
  123. Which animals get botulism?
    Animals with pica eating rotting carcasses or vegetation because of a mineral deficiency
  124. What is the botulism toxin mechanism?
    Inhibits release of Ach from pre-synaptic membrane
  125. What are the CS of botulism?
    Flaccid paralysis (progressive caudal to cranial, esp limbs, throat and jaws)

    Normal sensation and mentation

    Occurs in 1-4 days

    Respiratory arrest
  126. What is the px for botulism?
    Few will recover in 3-4 weeks
  127. How is botulism dx?
    Find pre-formed toxin in the feed
  128. How is botulism tx?
    Symptomatic
  129. How is botulism prevented?
    Vaccination
  130. What are the five freedoms according to the Brambell report and the OIE code for animal welfare?
    Freedom from hunger, thirst and malnutrition

    Freedom from physical and thermal discomfort

    Freedom from pain, injury and disease

    Freedom to express normal behavior

    Freedom from fear and distress
  131. What are the four principles of good welfare according to David Fraser?
    Maintain basic health

    Reduce pain and distress

    Accommodate natural behaviors and affective states

    Natural elements in the environment
  132. What are some examples of the principles of Davis Fraser being upheld?
    Maintain basic health: check BCS

    Reduce pain and distress: check for disease and injury, low stress handling

    Accommodate natural behaviors and affective states: watch herd interactions

    Natural elements in the environment: tress, shade, water, salt
  133. What are the two main emphases of standards to assess animal welfare?
    Animal-based measures performance standards or outcome criteria

    Practices that are prohibited
  134. How do animals get sulfur intoxication?
    High sulfate feed or water
  135. What bacteria are commonly isolated from spinal cord abscesses?
    Trueperella pyogenes most commonly isolated

    Streptococcus (especially in pigs), Mycoplasma, Staphylococcus, and Corynebacterium have been reported
  136. How are spinal cord abscesses tx?
    Abx that penetrate BBB (macrolides, tetrayclines)
  137. When do you see CS of botulism?
    3-7 days after ingestion (pre-formed toxin)
  138. What is the definition of a "natural" product?
    • No officially regulated definition
    • -look for USDA verification
    • -minimally processed
    • -no artificial ingredients
    • -no preservatives
    • No specific restriction on management 
    • practices during the life of the animal!
  139. Describe the USDA label for natural beef cattle.
    • No abx
    • No hormone implants
    • Vegetarian diet
    • Maybe ionophores
    • Don't need organic feed
    • Affidavit = certification = "brand"
  140. Describe the USDA label for certified organic beef cattle.
    • No abx, ionophores, hormone implants
    • Vegetarian organic diet only
    • Cows are organically managed last 1/3 in-utero, and rest of lifeOrganic feed for >3 yearsAccess to pasture >120 days / year = 30% DMI
  141. What are the requirements for selling organic milk?
    Cows have been eating organic food for >1 year
  142. What is a violation of organic feed of beef cattle?
    • No drugs (e.g. hormones)
    • No supplements or additives
    • No plastic feed pellets
    • No urea / manure
    • No animal by-products
  143. What are some of the allowed drugs in organic beef cattle?
    • Disinfectants
    • Aspirin
    • Atropine
    • Butorphanol
    • Chlorhex
    • Vaccines
    • IVF
    • Flunixin
    • Iodine
    • Glucose
    • Oxytocin
    • Lidocaine
    • Xylazine
    • Furosemide
    • H2O2
    • Mineral oil
  144. What are the basics of how to run an organic beef program?
    • Prevention is the key!
    • -select appropriate breeds & types
    • -provide balanced nutrition
    • -appropriate housing for the species, clean environment
    • -provide natural behavior, stress reduction & exercise
    • -chose appropriate vaccination program
  145. Which drugs are general accepted in organic beef cattle?
    • natural
    • -if synthetic must be specifically allowed
  146. What is the approach for treating infectious disease without anti-microbials according to Dr. Karreman?
    • -stimulation or modulation of the immune system via biologics
    • -antibacterial phytotherapy
    • -antioxidants
    • -fluid therapy for rehydration need proper  circulation
    • -use of antiseptics for lavage & irrigation as needed
  147. When do you see CS of C. tetani?
    2-3 weeks after wound infection

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