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Equine Final > Nutritional Related Diseases > Flashcards

Nutritional Related Diseases Flashcards

1
Q

What is developmental orthopaedic disease (DOD) the general term for?

A

growth disturbances resulting from any alteration in normal bone formation

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2
Q

What predisposes a horse to DOD?

A
  1. genetics - rapidly growing breeds (thoroughbreds)
  2. exercise
  3. nutrition
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3
Q

Symptoms of DOD include?

A
  • phystitis (growth plates don’t close properly –> inflammation)
  • wobblers syndrome
  • angular leg deformities (bones muscles, ligaments, tendons must grow in tandem AND they don’t..); very little muscle in horses legs to control joints and they’re carrying a lot of weight
  • joint cartilage damage
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4
Q

What are 2 clinical symptoms of DOD?

A
  • epiphystitis

- joint effusion

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5
Q

What are the nutritional causes of DOD?

A
  1. rapid growth
    - excessive protein - delivers different kinds of energy, supports lean body mass but can result in rapid muscle growth that doesn’t match bone, tend, ligament
    - excessive energy - growing animals should be lean, never overweight
  2. mineral imbalances
    - often inadequate amounts in high energy diets
    - need to support rate of growth with adequate P, Ca, Zn, Cu levels
    - Silicon has been shown to be beneficial - increases bone efficiency and decreases lameness
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6
Q

Nutritional solutions for DOD

A

Calcium:Phosphorus

  • adequate amounts in diet (at the right ratio)
  • help with absorption & metabolism

Copper:Zinc

  • Cu stabilizes bone collagen and elastin synthesis
  • Zn excess interferes with Ca absorption
  • not a good idea to add individual nutrients
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7
Q

Nutritional recommendations for DOD

A
  • provide high quality roughage free choice
  • foals can be introduced slowly when they are 1-2 months of age
  • monitor weight gain closely
  • if necessary, supplement with properly balanced grain concentrate
  • feed separately from mare
  • try to avoid rapid growth
  • concentrates = 14-18% protein and have added Ca, P, Cu, Zn (specifically designed for growing horses) –> maintenance + deposition
  • start feeding 1% foals BW/day (have small stomach so divide meals into 2-3 feedings)
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8
Q

Recommendations regarding DOD?

A
  • turnout as long as possible

- no strenuous forced exercise early in life

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9
Q

Weanling nutrition

A
  • should be fed same type of concentrate as when they were nursing and at the same rate
  • maintain steady growth and good body condition
  • plain white or trace mineral say and a good clean source of water should be available free choice
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10
Q

What is exertional rhabdomyolysis?

A

Dissolution of striated muscle with exercise

  • inability to contract muscles
  • unable for muscle to be controlled in a rhythmic manor
  • tying up, monday morning sickness
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11
Q

Symptoms of exertion rhabdomyolysis include?

A
  • muscle stiffness
  • lameness
  • sweating
  • poor performance
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12
Q

Causes of exertion rhabdomyolysis

A
  • overexertion
  • heat exhaustion
  • dietary imbalance (high non-structural CHOs, inadequate vitamin E/Se, electrolyte imbalance)
  • recurrent –> once it happens once, horse is more prone (risk factors, genetics)
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13
Q

What is equine polysaccharide storage myopathy (EPSM)

A

common to draft breeds

Symptoms include:

  • lack or loss of muscle mass or conditioning (especially in the shoulder/hind quarters)
  • string halts, shivers, tying up
  • poor performance
  • diet modifications can help
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14
Q

What does EPSM stand for?

A

equine polysaccharide storage myopathy

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15
Q

What puts a horse at higher risk of colic compared to other herbivores?

A

Limited bacteria in stomach, so can’t handle toxic compounds and are very sensitive to change

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16
Q

Describe positional colic

A

partially attributed to diet - sudden changes cause an increase in gas production –> part of colon becomes lighter –> motility within that section changes –> torsions, displacements, nephrosplenic entrapments
- may or may not require surgery

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17
Q

Colic: malfunction of motility

A

Cause: feed consistency and content, dehydration, antibiotic use –> death of microflora –> no VFA –> fermentation, biomass, pH problem

= impacts where there is a buildup of digest in usually the pelvic flexure or large colon, transverse colon and cecum
- ~40:1 are stalled:pasture = activity gets the gut moving & in the right spot!

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18
Q

Dietary considerations for motility problems

A
  • large concentrate meals and starch content can influence development of colic due to reduced rates of ingest
  • colic can also be due to consumption of sand –> heavy part in Dt –> impaction
  • lower pH due to bacterial production of lactic acid and propionic acid –> bacteria shift –> bacterial have a lower ability to ferment fiber –> horse starts eating hay again but doesn’t have bacteria to ferment it
19
Q

Recommendations for colic regarding motility

A
  • increase meal frequency
  • increase access to hay/pasture
  • hay with high NDF (especially lignin) –> increase flow (insoluble fiber)
  • told growth in hay may also increase relative lignin content as other fibres are degraded by fungas
20
Q

Colic: abnormal absorption

A

cause: generally quick switch in feed or overfeeding in a single meal –> rapid fermentation of starch in hindgut –> bacterial disruptions –> dead bacteria undergo lysis –> release endotoxins –> damage colonic mucosa –> decrease water absorption of water in particular –> colic and diarrhea

21
Q

Treatment for abnormal absorption colic?

A

fluid replacement

22
Q

Dietary considerations for abnormal absorption

A

change feed gradually

  • allows hindgut bacteria to adapt
  • reduces excess gas production
  • ultimately helps avoid blockage

adequate exercise
- moderate exercise stimulates blood flow and intestinal motility, minimizes gas production and/or accumulation and bloating

23
Q

Overall considerations for colic prevention

A

maintain gut microflora by:

  • consistent feeding management
  • do not forget about hydration (especially when transporting)
  • think about proper turnout management
  • consider a pro- or prep ionic after antibiotic use
  • proper training management
24
Q

Complications associated with colic-

A

Laminitis: any inflammation of the laminae that interdigitate between the hood wall and phalange 3

  • cause: endotoxemia = toxins secreted by bacteria or toxaemia; redirection of blood flow
  • really bad at handling any type of toxin
  • changes in cardiovascular function –> decreased or increased blood flow
  • Arg is a precursor for NO = bad
25
Q

Laminitis treatment

A

fluid therapy, NSAIDs, drugs to increase blood flow or decrease blood viscosity

26
Q

Colic considerations

A
  • parasites infect lining of cecum and colon –> inflammation and changes intestinal motility (e.g. gastric emptying, SI motility, rate of passage)
  • tapeworms can cause blockages
  • NOT what your horse eats but what interacts with the food your horse eats –> colic
27
Q

dietary considerations for heaves

A
  • reduce exposure to environmental contaminants (use pasture instead of hay)
  • later in season –> dampness –> horses are in more –> dust/mold/less ventilation

feed pellets and wet feed/hay
- include fiber sources in pellets = beet pulp –> improve microflora –> improve gut immune function

28
Q

What part of the stomach is most commonly affected by ulcers?

A

proximal portions

- they are’t protected by mucus

29
Q

What is the cause of ulcers?

A

Horses stomachs constantly secrete bile –> epithelial tissue become damaged

  • can be related to physical form of feed (horses like long stem forages)
  • intestinal parasites
  • fermentation in the stomach –> VFA –> trigger ulcerations (adds HCl)
30
Q

What are some recommendations to control acid production?

A
  • keep constant movement of feed through gut
  • constant HCl –> want a constant supply of food
  • increase particle size (increased SA –> more content to different pH, enzymes, bacteria)
31
Q

2 causes and their type of ulcer?

A
  1. stress/high grain feeding –> more acid production
    - should increase energy through fat = ulceration of non-glandular part of stomach due to increased acid production –> functional problems with glandular part of HCl secretion
  2. the use of NSAIDs –> compromises mucosal synthesis –> ulceration of the glandular part of stomach due to compromised mucosal barrier
32
Q

Symptoms of ulcers

A
  • colic signs
  • unthriftiness
  • decreased athletic performance
  • decreased athletic performance
  • increased heart rate, respiratory rate
33
Q

Treatment of ulcers

A

Sucralfate and H2 inhibitors

Is therapeutic treatment the right solution?

  • long term implications in healthy model
  • drugs used to treat things - we don’t have data about the use of therapeutic drugs in a prophylactic chronic approach
  • race horses: is HCl down regulated so much that when they’re done racing they won’t have enough?
34
Q

What are the pros to stabling?

A
  • protection
  • avoidance of parasites
  • individual attention
  • reduction in damage caused by other horses
35
Q

What are the pros to paddock?

A
  • no restriction of movement
  • social contact = herd animals
  • ability to express natural behaviour = flight
36
Q

Management considerations

A
  1. body weight management
    - rapid growth and weight gain - highly processed feeds/early weaning –> problems
    - DOD
  2. Feeding management
    - feed on the floor? feed higher? what about sand paddocks?
    - may have to change level of feeding depending on age
    - feeding on sand = reason you’d want the hay off the ground
  3. Genetic management
  4. dental management
    - oral health and bacteria is in relation to the bacteria in the rest of the body
    - dental manament for oral health
  5. parasite and disease management
37
Q

What is Cushing’s Disease

A

PPID = disease of the pars pituitary intermedia dysfunction

  • more in old
  • chronic and progressive neuroendocrine disease
38
Q

Consequences of Cushing’s

A
  • insulin resistance (polydipsia = drink a lot; polyuria = pee a lot)
  • laminitis
  • curly coat
  • metabolic –> trouble maintaining BT
39
Q

What is metabolic syndrome: insulin resistance?

A
  • increases co-morbitidities = hyperlipidemia, laminitis, PPID –> more glucose –> liver –> more lipids from excess glucose –> laminitis –> PPID
40
Q

What is the cause of insulin resistance?

A

Long term consumption of high glycemic feels and dependent on lean to fat ratio, physical activity and diet

  • highly processed grains in discrete meals (a lot of starch all at once)
  • differences in lean:fat = high proportion of adipose –> inflammation –> insulin resistance
  • physical activity –> promotes glucose uptake from tissues (especially muscle) –> increases sensitivity

More insulin to facilitate uptake of glucose from peripheral circulation –> keeps compounding –> hyper-insulin insensitive –> increase in glucose

41
Q

What is hyperlipidemia?

A

Excessive concentrations of lipid (TG)

  • 100-500 mg/dL normal vs. 1700
  • usually from mobilization of adipose, but also hyperglycaemia
  • exceeds body’s capacity to oxidize lipids
42
Q

Why is feed intake reduced in hyperlipidemia?

A

Blood high in fat/glucose/insulin = fed state hormone = body things it’s in a fed state

43
Q

Treating hypelipidemia

A
  • high fat/high fibre diet

- increases aerobic exercise

Equine Final (13 decks)

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