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Module 17 > Equine Obesity & Related Disorders > Flashcards

Equine Obesity & Related Disorders Flashcards

1
Q

what are the clinical signs related to obesity

A

rarely present directly for obesity

dyspnea/exercise intolerance/poor performance

recurrent laminitis

may present with PUPD

abnormal fat deposits vs uniform obesity

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2
Q

what can the cresty neck score indicate

A

independent indicator of insulin resistance

more predictive of insulin dysregulation than BCS

relates to omental fat, insulin response and adipokine production

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3
Q

what is the signalment of obesity

A

certain breeds may be predisposed

any equid can develop obesity

ponies/natives/donkeys/miniature breeds increased

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4
Q

how would you manage obesity through feeding management (4)

A
  1. remove concentrates
  2. low calorie roughage
  3. roughage soaked to remove soluble sugars
  4. limit roughage intake (BUT not excessively)
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5
Q

what % of non-soluble carbohydrates is recommended in a diet roughage

A

<10% content

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6
Q

how long should you soak roughage to reduce soluble sugars

A

12 hr

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7
Q

what % of water soluble carbohydrates can soaking roughage remove

A

24-43% removed through soaking

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8
Q

how do you limit roughage intake

A

grazing muzzles can reduce DMI to 77-83% grazing without muzzle

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9
Q

how much % of roughage is needed in the diet

A

~1.25-1.5% of BM as DMI

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10
Q

is it better to graze in evening or morning for obese horses

A

graze at night

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11
Q

what else needs to be considered when feeding an obese horse

A

supplement with protein and water soluble vitamins to meet RDA

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12
Q

what can obesity lead to (4)

A
  1. impaired insulin sensitivity
  2. uncontrolled breakdown of body fat
  3. joint/bone problems
  4. infertility
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13
Q

what medical investigations are indicated in ponies/horses presenting with laminitis

A

chief ddx = hyperinsulinemia and peripheral insulin resistance = equine metabolic syndrome

equine cushing’s disease (PPID) must also be considered

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14
Q

what are the clinical pathology changes seen in equine metabolic syndrome (3)

A
  1. increased blood triglycerides
  2. resting hyperinsulinemia or increased post prandial insulin response
  3. may be decreased insulin clearance
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15
Q

how does insulin dysregulation occur (7)

A
  1. High levels of adipokines (excess fat stores) counteract the insulin receptors —> insulin resistance
  2. When have a starch rich meal they will have impaired glucose uptake, reduced suppression of gluconeogenesis & impaired insulin signalling which will stimulate lipogenesis —> both of which lead to hyperglycemia
  3. Hyperglycemia stimulates the B cells of the pancreas to secrete more insulin which isn’t effective so the negative feedback mechanisms doesn’t work —> hyperinsulinemia
  4. Insulin resistance also leads to reduced suppression of lipolysis and hepatic VLDL synthesis —> leads to hypertriglyceridemia
  5. Cells are not able to uptake of glucose and will allow ongoing breakdown of fat —> hypertriglyceridemia which counters insulin sensitivity
  6. Hypertriglyceridemia leads to compensatory pancreatic secretion and reduced hepatic insulin clearance —> hyperinsulinemia
  7. Adiponectin is produced to improve insulin sensitivity —> EMS horses will have lower levels of this
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16
Q

what does equine metabolic syndrome cause (5)

A
  1. insulin insensitivity
  2. glucose intolerance
  3. dyslipidemia
  4. hypertension
  5. insidious laminitis
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17
Q

why does insulin resistance lead to laminitis

A

vascular compromise, hypercoagulable state

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18
Q

how does EMS lead to insulin resistance

A

Adipose tissue produces cytokines: TNF-alpha, IL-1, IL-6 –> may cause direct laminar inflammation

11B-hydroxysteroid dehydrogenase

  • Increased in omental fat
  • Promotes production of active cortisol
  • Counters the action of insulin in peripheral receptors
  • Increased insulin resistance
  • Adipose tissue functions as endocrine organ
  • Omental fat store is correlated to neck crest size

Intestinal acretin production may be increased and stimulate further pancreatic insulin

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19
Q

how does EMS/insulin resistance cause vascular changes

A

Sustained hyperinsulinemia causes vascular dysfunction

Change in vascular form and function

Microagglutination

Reduces perfusion and cause further inflammation

Multiple subclinical episodes of laminitis occur

Reduction in effective perfusion

Progressive inflammatory response

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20
Q

how do vascular changes due to EMS/insulin resistance lead to changes in the hoof

A

Eventual disruption of laminar attachments and pedal bone rotation or sinking

Elongation and altered keratinization of laminae

Acute signs of laminitis with loss of hoof capsule stability

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21
Q

how is EMS diagnosed with a combined insulin-glucose tolerance test

A

12 hour fast

Take baseline blood glucose

Give 0.3ml/kg 50% glucose IV and 0.1 iu/kg soluble insulin IV

Take further blood samples for glucose @ 1m, 5m, 10m then q10 mins up to 1 h, then q 30 mins up to 2 and half hours

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22
Q

how are combined insulin-glucose tolerance results interpreted

A

Normal response:

Should see the serum glucose level decrease below baseline at 30minutes

EMS:

Slower response and glucose levels do not fall below baseline —> resistance

Measurement at 45 mins —> will measure endogenous insulin production

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23
Q

how is EMS diagnosed with oral glucose test

A

Protocol:

Fast overnight

Measure basal insulin and glucose concentration

Give small chaff meal containing 1g/kg glucose

Remeasure blood insulin and glucose concentration at 2h

24
Q

how are the results of oral glucose test for EMS interpreted

A

Interpretation:

Significant hyperinsulinemic response at 2h if insulin resistant (if EMS)

Insulin <87 mU/l at 2h if ‘healthy’ horse following 1g/kg glucose

25
how is the oral corn syrup test done to diagnose EMS
Protocol: Overnight fast Measure basal glucose and insulin 0.45 ml/kg BW corn syrup Remeasure glucose and insulin at 60 mins \> 110 uIU/ml measured by RIA
26
what are the advantages of the oral corn syrup test to diagnose EMS
Higher sensitivity for ID Mimics response to feed Insulin at 60 min differentiated 5 previously laminitis ponies from 3 ponies with no history of laminitis Simple to perform
27
what are the treatment options for EMS (6)
1. progressive weight loss 2. anti hyperglycemic agents (metformin) 3. address laminitis when present 4. thyroxine supplementation to increase basal metabolic rate 5. exercise once laminitis resolved 6. change of function
28
how can metformin be used to treat EMS (3)
1. improved hepatic sensitivity to insulin 2. reduced fasting hepatic glucose output 3. improved peripheral uptake of glucose short lived response in horses
29
how do you address underlying laminitis in EMS (4)
1. NSAIDs 2. additional analgesia 3. remedial trimming/farrier 4. box rest
30
what are the changes seen in chronic laminitis in EMS
rotation of pedal bone in LF and RF remodelling of the tip of P3 in both feet and reduced sole thickness long toe evidence of previous sinking of the pedal bone --\> increased founder distance parallel lines
31
what is PPID
Pituitary Pars Intermedia Dysfunction
32
what causes PPID
endogenous ACTH increased
33
how is PPID diagnosed
dexamethasone suppression test TRH stimulation test combined TRH/dexamethasone test glucose & insulin: secondary insulin resistance in PPID
34
how is hypothyroidism diagnosed
cannot diagnose on T3/T4 values alone --\> free versus total T3/T4 TSH concentration function testing more reliable --\> TRH/TSH concurrent meds can confound results
35
what is hyperlipemia
particularly seen in obese animals which develop negative energy balance glycogen stores depleted --\> fatty acids to provide energy --\> excessive mobilization of fatty acids --\> hepatic lipidosis --\> insulin resistance
36
at what level of plasma triglyceride concentration does hepatic dysfunction occur and what would this indicate
\> 5mmol/l = hyperlipemia
37
what are instrinsic factors of hyperlipemia (5)
1. breed 2. sex 3. reproductive activity (pregnancy, lactation) 4. genetics 5. age
38
what are the extrinsic factors of hyperlipemia (6)
1. inappetence 2. feed restriction 3. underlying disease 4. obesity 5. stress 6. inactivity
39
what are the clinical signs of hyperlipemia (7)
1. non-specific malaise in early stages 2. variable appetite progressing to anorexia 3. suspect in any poorly obese ponly 4. very high index of suspicion if periparturient 5. metabolic acidosis; hepatic/renal dysfunction 6. signs of primary/underlying disease often present 7. abortion
40
what is the pathophysiology (5)
1. negative energy balance 2. concurrent disease 3. hormonal influences (ex. ACTH concentrations increased in PPID) 4. increased risk toward end of pregnancy 5. increased likelihood in both PPID and EMS
41
what occurs in normal fat metabolism
In normal triglyceride metabolism it is stored, when energy is required hormone sensitive lipase breakdowns down TGs into glycerol and FFAs
42
what hormones are hormone sensitive lipase stimulated by
Hormone sensitive lipase is stimulated by the stress hormones ## Footnote **Cortisol** **ACTH** **Glucagon** **Catecholamines** **Thyroid hormones** **GH**
43
what is insulin's role in fat metabolism
Insulin will inhibit the breakdown of TGs and will simulate the esterification of glycerol + FFAs into TGs
44
what occurs once glycerol and free fatty acids are released from adipose tissue
Glycerol and FFAs released by adipose tissue will be processed by the liver FFAs undergo beta-oxidation to release energy + ketones Glycerol is redistributed around the body and will be released from the liver in the form of LDL and VLDL
45
what occurs if there is a negative energy balance in fat metabolism
More lipid will be broken down and liver is not able to process glycerol + FFAs which will end up being stored in the liver VLDL instead of being taken up by the tissues, will be stored in the liver Blood will have milky appearance
46
how is hyperlipemia diagnosed
Plasma: opaque TGs \> 5 mmol/l Cholesterol increased Liver enzymes increased Liver function tests: check bile acid concentration Hypoglycemia, azotemia, metabolic acidosis, electrolyte disturbances
47
what are the initial clinical signs of hyperlipemia (6)
1. signs of depression and lethargy 2. inappetence 3. adipsia 4. weakness 5. reduced GIT motility and fecal output 6. mucus-coated inspissated feces
48
what are the mild/progressive clinical signs of hyperlipemia
1. reluctance to move 2. muscle fasciculations 3. intermittent abdominal pain 4. diarrhea 5. CNS dysfunction; ataxia, sham drinking, dysphagia, head-pressing, circling
49
what are the late cinical signs of hyperlipemia (6)
1. recumbency 2. convulsions 3. champing 4. nystagmus 5. mania 6. abortion
50
what are the triglyceride, glucose, electrolyte changes expected to see in hyperlipemia
increased TGs glucose decreased/N/increased electrolytes decreased/N/increased
51
what would the pH, HCO3, PCO2 changes you would expect to see in hyperlipemia
pH decreased HCO3 decreased PCO2 increased
52
what hepatic damage/function changes would you expect to see in hyperlipemia
sorbitol dehydrogenase increased AST increased ALP increased GGT increased ammonia increased total bilirubin increased
53
what would you expect to happen to urea/creatinine in hyperlipemia
both increased
54
how do you treat hyperlipemia (6)
1. nutritional support 2. ID and treat underlying disease 3. correct fluid and electrolyte deficits 4. diurese to reduce metabolic acidosis 5. decreased lipolysis & increased clearance of lipids (exogenous insulin, exogenous heparin) 6. monitoring clinical and labs
55
how do you provide nutritional support in hyperlipemia
most critical component of treatment reverses negative energy balance increases blood [glucose] --\> increased insulin --\> decrease lipolysis appetite usually reduced --\> enteral or parenteral nutrition required
56
what are the options to provide nutritional support (3)
1. highly palatable feedstuffs 2. enteral feeding (homemade gruels, commercial preps) 3. parenteral feeding ($$, potential complications)
57
how do you prevent hyperlipemia (6)
1. energy balance 2. body condition 3. minimize stres 4. exercise 5. close monitoring of at risk animals 6. early intervention

Module 17 (31 decks)

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