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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
Q

how is the oral corn syrup test done to diagnose EMS

A

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
Q

what are the advantages of the oral corn syrup test to diagnose EMS

A

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
Q

what are the treatment options for EMS (6)

A
  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
Q

how can metformin be used to treat EMS (3)

A
  1. improved hepatic sensitivity to insulin
  2. reduced fasting hepatic glucose output
  3. improved peripheral uptake of glucose

short lived response in horses

29
Q

how do you address underlying laminitis in EMS (4)

A
  1. NSAIDs
  2. additional analgesia
  3. remedial trimming/farrier
  4. box rest
30
Q

what are the changes seen in chronic laminitis in EMS

A

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
Q

what is PPID

A

Pituitary Pars Intermedia Dysfunction

32
Q

what causes PPID

A

endogenous ACTH increased

33
Q

how is PPID diagnosed

A

dexamethasone suppression test

TRH stimulation test

combined TRH/dexamethasone test

glucose & insulin: secondary insulin resistance in PPID

34
Q

how is hypothyroidism diagnosed

A

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
Q

what is hyperlipemia

A

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
Q

at what level of plasma triglyceride concentration does hepatic dysfunction occur and what would this indicate

A

> 5mmol/l

= hyperlipemia

37
Q

what are instrinsic factors of hyperlipemia (5)

A
  1. breed
  2. sex
  3. reproductive activity (pregnancy, lactation)
  4. genetics
  5. age
38
Q

what are the extrinsic factors of hyperlipemia (6)

A
  1. inappetence
  2. feed restriction
  3. underlying disease
  4. obesity
  5. stress
  6. inactivity
39
Q

what are the clinical signs of hyperlipemia (7)

A
  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
Q

what is the pathophysiology (5)

A
  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
Q

what occurs in normal fat metabolism

A

In normal triglyceride metabolism it is stored, when energy is required hormone sensitive lipase breakdowns down TGs into glycerol and FFAs

42
Q

what hormones are hormone sensitive lipase stimulated by

A

Hormone sensitive lipase is stimulated by the stress hormones

Cortisol

ACTH

Glucagon

Catecholamines

Thyroid hormones

GH

43
Q

what is insulin’s role in fat metabolism

A

Insulin will inhibit the breakdown of TGs and will simulate the esterification of glycerol + FFAs into TGs

44
Q

what occurs once glycerol and free fatty acids are released from adipose tissue

A

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
Q

what occurs if there is a negative energy balance in fat metabolism

A

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
Q

how is hyperlipemia diagnosed

A

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
Q

what are the initial clinical signs of hyperlipemia (6)

A
  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
Q

what are the mild/progressive clinical signs of hyperlipemia

A
  1. reluctance to move
  2. muscle fasciculations
  3. intermittent abdominal pain
  4. diarrhea
  5. CNS dysfunction; ataxia, sham drinking, dysphagia, head-pressing, circling
49
Q

what are the late cinical signs of hyperlipemia (6)

A
  1. recumbency
  2. convulsions
  3. champing
  4. nystagmus
  5. mania
  6. abortion
50
Q

what are the triglyceride, glucose, electrolyte changes expected to see in hyperlipemia

A

increased TGs

glucose decreased/N/increased

electrolytes decreased/N/increased

51
Q

what would the pH, HCO3, PCO2 changes you would expect to see in hyperlipemia

A

pH decreased

HCO3 decreased

PCO2 increased

52
Q

what hepatic damage/function changes would you expect to see in hyperlipemia

A

sorbitol dehydrogenase increased

AST increased

ALP increased

GGT increased

ammonia increased

total bilirubin increased

53
Q

what would you expect to happen to urea/creatinine in hyperlipemia

A

both increased

54
Q

how do you treat hyperlipemia (6)

A
  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
Q

how do you provide nutritional support in hyperlipemia

A

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
Q

what are the options to provide nutritional support (3)

A
  1. highly palatable feedstuffs
  2. enteral feeding (homemade gruels, commercial preps)
  3. parenteral feeding ($$, potential complications)
57
Q

how do you prevent hyperlipemia (6)

A
  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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