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CVSOH 4 > Small Animal and Equine Clinical Nutrition > Flashcards

Small Animal and Equine Clinical Nutrition Flashcards

1
Q

What is RER?

A

Resting energy requirement - energy used at rest in thermoneutral conditions. Very similar to basal metabolic rate

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2
Q

What is the RER for animals 2-30kg?

A

RER = 30(BW in kg) + 70

RER (kcal ME/day) = 70(BW in kg) ^0.75

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3
Q

How is food intake calculated?

A
  • Calculate RER for patient (kcals ME/day)
  • Calculate food intake weight/day – divide evenly between meals
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4
Q

Define maintenance energy requirement.

A

Energy used, in thermoneutral conditions, by a moderately active animal including energy required to obtain and use the food.

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5
Q

How does neuter status affect MER?

A

Entire dogs = 1.8 x RER
Neutered dogs = 1.6 x RER
Entire cats = 1.4 x RER
Neutered cats = 1.2 x RER

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6
Q

How does pregnancy affect MER?

A

Dogs = 3 x RER in last trimester

Cats = 2 x RER, by parturition, gradual increased throughout pregnancy

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7
Q

How does lactation affect MER?

A

Dogs = 4-8 x RER or free choice

Cats = 2-6 x RER or free choice, peak at 6 weeks post parturition

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8
Q

How does working effect RER?

A

Dogs = 2-8 x RER
Cats n/a

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9
Q

How does growth affect MER?

A

Dogs < 4 months = 3 x RER
Dogs 50-80% adult kg = 2.5 x RER
Dogs >80% adult kg = 1.8-2 x RER

Cats = 2.5 x RER

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10
Q

How do you feed dogs and cats for weight loss?

A
  • Not appropriate for growth, pregnancy, lactation
  • Dogs 1.0-1.2 x RER for current weight
  • Cats 0.8- 1.0 x RER for current weight
  • If loss slower than desirable decreases calorie intake by 5-10%
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11
Q

What are the aims of weight loss at regular re-weighs?

A
  • Aim 1-2% BW loss/week in dogs
  • Nearer 0.5-1% BW loss/week in cats – hepatic lipidosis risk when fat is moving around too quickly in the liver can swamp the liver in cats
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12
Q

How does calorie restriction aid weight loss?

A

Weight loss diets have less calories, more nutrients and can help animals feel fuller than just decreased amounts of normal diet. Exercise important too

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13
Q

What is addressed by encouraging oral intake?

A
  • The underlying disease
  • Fluid deficits, electrolyte imbalances
  • Nausea, pain, stress
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14
Q

Why should you never syringe feed?

A

Creates aversions – risk of inhalation pneumonia

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15
Q

What abnormalities may exacerbate anorexia in cats?

A

Many anorexic cats are B12 with/without potassium deficient

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16
Q

How are hospitalised patients fed their RER?

A
  • Hypermetabolic states may be an exception – e.g. sepsis, burns, head trauma
  • Overfeeding is detrimental too
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17
Q

How are ill animals monitored for condition/weight?

A
  • If losses continue; consider 25% increase in offered food
  • Reassess every few days
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18
Q

When is naso-oesophageal feeding used?

A

Suitable for short term (<7days) nutritional assistance

Unsuitable if:
- Regurgitating/vomiting
- Nasal, oral, pharyngeal, oesophageal disease
- Laryngeal incompetence

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19
Q

When are oesophagostomy tubes used?

A

Well tolerated. Require GA for placement – surgical procedure

Indications include:
- Diseases restricting N-O tube use (facial trauma, nasal disease etc.)
- Any disease where medium term hyporexia anticipated

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20
Q

What are the indications and contraindications for gastrostomy tubes?

A

Indications – where bypass of proximal GI tract needed. Particularly oesophageal disease

Contraindications – vomiting, severe gastric disease/surgery or local peritonitis

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21
Q

What are the advantages of naso-oesophageal feeding?

A
  • No GA required
  • Quick to place
  • Easy to remove, no healing required
  • Well tolerated
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22
Q

What are the disadvantages of naso-oesophageal feeding?

A
  • Short term
  • Risk of aspiration, not anchored in GIT
  • Irritating, can inhibit spontaneous eating
  • Can block, narrow lumen
  • Time consuming feeds
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23
Q

What are the advantages of oesophageal feeding?

A
  • Can administer larger volumes more easily
  • Can administer medications more easily
  • Can be managed at home with owner
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24
Q

What are the disadvantages of oesophageal feeding?

A
  • GA required
  • Stoma site can be infected
  • Can dislodge if patient vomits or regurgitates, aspiration risk
  • Can block
  • Time consuming feeds
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25
Q

What are the advantages of PEG tube feeding?

A
  • Large lumen to administer medication
  • Can be in situ for months, managed by owner
26
Q

What are the disadvantages of PEG tube feeding?

A
  • GA required
  • Has to be in situ for 7 days before removal, not good for short term support
  • Cannot use it for 1st 24h
27
Q

What are the complications of feeding tubes?

A
  • Stoma infections
  • Tube dislodgement/migration
  • Tube obstruction
  • ‘Re-feeding syndrome’ – give time of normal metabolism to kick in
  • Insulin release following prolonged fasting/anorexia - causes hypophosphatemia, haemolysis, hypokalaemia
28
Q

What are the general principles for feeding tubes?

A
  • Keep tube sealed to prevent air entry
  • Tube hygiene
  • Record all tube intervention on hospital records
  • Complete, appropriate, liquid diet, room temperature
  • If hyporexic prior to hospitalisation – feed ¼ - 1/3 requirement on day 1. Gradually increase to 100% over 3-4 days
  • Infuse slowly
  • Flush well with water (5-10mls) before/after use
  • Blockages – try carbonated water
  • Feed until voluntary oral intake of >85% requirement
29
Q

How are tubes placed?

A
  1. Apply LA – proxymetacaine a few drops, leave for 1 minute, put in eyes as well as this will be more comfortable due to nasolacrimal duct
  2. Measure distance from the nose to the 7th to 9th ribs and mark the end of the tube
  3. Pre-place tape
  4. Lubricate tube
  5. Insert the tube ventromedially, hold head upwards towards the ceiling so it is easier to pass
  6. Secure tapes to tube
  7. Glue into position
  8. Apply buster collar ASAP
30
Q

What is EMS in horses?

A

Equine metabolic syndrome - obesity or regional adiposity (at the waist), insulin dysregulation/resistance (IR), and subclinical or clinical laminitis

31
Q

Distinguish compensated and uncompensated insulin dysregulation/resistance in horses.

A

Compensated - EMS, PPID. Euglycaemia, may have this at rest or only as a response to feeding

Uncompensated - type 2 DM. Hyperinsulinaemia, hyperglycaemia, glucosuria

32
Q

How is laminitis linked to EMS in horses?

A
  • Histopathologically differs from laminitis secondary to toxin exposure
  • Hyperinsulinaemia is direct cause of laminitis
33
Q

Describe insulin resistance in horses as an adaptation for survival.

A

-Breakdown of glucose and fat stores and stimulates hepatic gluconeogenesis
- Keeps a glucose supply for vital (non-insulin dependent) tissues – CNS
- Ability to mobilise energy stores and prioritise vital tissues = survival benefit if poor diet

34
Q

Which breeds have a predisposition to insulin resistance in horses?

A

Hardy breeds

35
Q

What factors are strongly associated with insulin resistance in horses?

A
  • Obesity
  • No longer subject to seasonal weight loss
  • Lack of exercise – exercise promotes insulin sensitivity
  • Chronic progressive obesity and chronic laminitis ensue
36
Q

What are the clinical signs of insulin resistance in horses?

A
  • BCS 7/9-9/9
  • Regional adiposity - cresty neck, tail head, preputial swelling/mammary gland
  • Laminitis
  • Possible related disease - hyperlipidaemia, lipoma
37
Q

What syndrome are the result of insulin dysregulation in horses?

A

EMS
PPID
Both

38
Q

How can insulin resistance in horses be diagnosed?

A
  • Resting insulin and glucose
  • Oral glucose tolerance test
  • Intravenous glucose tolerance test
  • Euglycaemic hyperinsulinaemic/euinsulinaemic hyperglycaemic clamp
39
Q

How is the best first line to test insulin resistance in horses done?

A
  • Starve overnight
  • Take resting glucose and insulin
  • Feed 1g/kg glucose in horse’s breakfast/syringe in Karolyte syrup
  • Continue starving
  • Insulin and glucose at 2-3 hours
  • With insulin dysregulation usually then have hyperinsulinaemia and normoglycaemia
40
Q

How can diet be used to manage insulin resistance in horses?

A
  • Low carbohydrate
  • No concentrate
  • If thin, oil
  • Multivitamin and mineral supplement
  • No grass, grass muzzle
41
Q

What are the considerations of exercise in management of insulin resistance in horses?

A
  • Major effect on insulin insensitivity
  • But what if laminitic?
42
Q

How can weight loss be achieved in horses with insulin resistance for management?

A
  • Feed 1/3 less than were
  • Not less than 1kg forage per 100kg
  • Soak hay > 1 hour
  • Haynet with small holes
43
Q

What is the purpose of metformin in managing horses with insulin resistance?

A
  • Aids weight loss and reduces glucose spikes by blocking SI carbohydrate absorption
  • So can help return to insulin sensitivity but only by aiding weight loss
44
Q

What is the purpose of levothyroxine in managing horses with insulin resistance?

A

Increase metabolic rate and so enhance weight loss

45
Q

What is the purpose of SGLT2 inhibitors in managing horses with insulin resistance?

A
  • Lower insulin levels in horses
  • Some risks of hyperlipaemia
46
Q

Too high levels of what, directly causes laminitis?

A

Insulin

47
Q

Describe hyperlipaemia in horses.

A
  • Serum triglyceride concentration in excess of 500mg/dl
  • Leads to fatty infiltration of liver
  • Clinical signs liver disease
  • Poor prognosis
48
Q

Describe hyperlipidaemia in horses.

A
  • Increase in serum triglyceride (but less than 500mg/dl)
  • Without grossly lactescent blood
  • Without fatty infiltration of liver and block blood flow to organs
49
Q

What is the pathogenesis of hyperlipaemia in horses?

A
  • Any VLDLs the liver cannot use is put back into the circulation
  • Increased and/or energy demands increased – glycogen stored depleted, energy provided by fatty acid oxidation
  • Fatty acid mobilisation triggered by negative energy balance or stress (causing catecholamine and glucocorticoid release)
  • Endothelial lipoprotein lipase is the rate limiting enzyme. Over production of triglyceride, more than ELL can cope with causes hyperlipaemia and hepatic lipidosis. Disease of acute starvation, as if you suddenly stop eating, you cannot gradually make more ELL to deal with this
50
Q

Which horses are at risk for hyperlipaemia?

A
  • Obesity
  • Ponies – IR genetic predisposition
  • In foal – progesterone makes you more insulin resistance
  • Donkeys
  • Excess stores fatty acid
  • Increased risk insulin resistance – EMS, glucocorticoids, catecholamines, progesterone
51
Q

How is hyperlipaemia in horses diagnosed?

A

Depression
Anorexia
Ataxia
Icterus
Blood triglyceride level
Opalescent blood
Raised serum activity of liver enzymes
Raised bile acids

52
Q

How is hyperlipaemia in horses treated?

A
  • Treat hepatic disease
  • Treat underlying disease
  • Wean foal
  • Tempt to eat
  • Enteral nutrition
  • Glucose infusion
  • Partial parenteral nutrition
  • Monitor blood glucose, hourly at first
  • Insulin – SC or infusion may be required
53
Q

Who is most at risk of hyperlipaemia in horses?

A

Pony on a crash diet

54
Q

You are looking after an overweight pony which stopped eating. You find this is due to a fractured tooth. As well as treating the tooth what must you do?

A
  • Get food/glucose in somehow
  • Take blood for triglycerides
  • If not eating, IV glucose
55
Q

What are the roles of parathyroid hormone?

A
  • Stimulation osteoclastic bone resorption
  • Stimulation Ca reabsorption in renal tubules
  • Inhibition phosphate reabsorption in renal tubules
  • Increases intestinal Ca and P absorption
56
Q

What is the role of vitamin D?

A
  • Active metabolite
  • Stimulates intestinal Ca and P absorption
  • Stimulates renal Ca and P absorption
57
Q

What is the role of calcitonin?

A

Inhibits osteoclast function during hypercalcaemia

58
Q

Explain the clinical signs of hypocalcaemia in horses.

A
  • Increased neuromuscular excitability
  • Ca is a Na channel antagonist – when Ca concentrations are low, Na channels are easily activated
  • Nerve and muscle fibre excitability, muscle fasciculations, tremor, tetany
  • Can have tachycardia, but bradycardia if very severe as reduced cardiac muscle contractility
59
Q

What are some consequences of hypocalcaemia in horses?

A
  • Synchronous diaphragmatic flutter/thumps - diaphragmatic contractions synchronous with heartbeat, after prolonged exercise
  • Hypocalcaemic tetany - lactation (from 2 weeks before foaling to weaning). Anxiety, ataxia, tremors, seizure, dyspnoea
  • Hypocalcaemic seizures - hypocalcaemia and sepsis
  • Ileus
  • Retained placenta
60
Q

What is the consequence of rapid administration of calcium in a hypocalcaemic horse?

A

Cardiovascular complications

CVSOH 4 (25 decks)

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