Equine endocrinopathies 2 Flashcards
Endocrinopathic laminitis, hyperlipaemia, hyperglycaemia, obesity (96 cards)
1
Q
What types of conditions are risk factors for laminitis?
A
- Pro-inflammatory conditions
- Intestinal conditions
- Endrocrinopathic conditions (glucocorticoid or insulin resistance associated)
2
Q
What are the main molecular triggers for laminitis?
A
Insulin and endotoxins
3
Q
What are the predisposing factors for lamintis?
A
- Obestiy
- Breed
- Insulin dysregulation
- PPID
4
Q
Outline the relationship between glucocorticoids and lamiinitis
A
- Exogenous and endogenous
- Induce insulin resistance
- Insulin resistance leads to increased insulin and consequent laminitis
5
Q
Give examples of iatrogenic causes of laminitis and how these may occur
A
- Triamcinolone (glucocorticoid) can lead to hyperglycaemia 3-4 days after 1 dose
- Dexamethasone can increase basal insulin and induce IR over prolonged period
- May have prolonged effects
6
Q
Outline how PPID may predispose to laminitis
A
- Hyperadrenocorticism, increased cortisol leading to IR
- High insulin more likely to develop laminitis
7
Q
Outline how EMS may predispose to laminitis
A
- Obesity, leads to insulin resistance
- Predisposed to laminitis
- Can be seasonal and pasture associated (seasonal obesity, lush grass spring/summer)
8
Q
What factors may exacerbate the development of laminitis?
A
- Progression of obesity
- Diet rich in starches/sugars
- Progression of PPID
- Work on hard floors
9
Q
Explain hyperinsulinaemia induced vasodilation as a trigger factor for laminitis
A
- Increases perfusion to the lamellar tissue
- Increases glucose delivery to hoof tissues (glucotoxicity)
- Advanced glycation end products - role in human diabetic angiopathy, may play role in laminitis
10
Q
What are the effects of insulin on blood vessels?
A
- Balance of constriction and dilation (slight predilection for vasodilation)
- Vasodilation via nitric oxide
- Vasoconstriction via endothelin-1 (ET-1)
11
Q
What are the effects of insulin resistance and corticosteroids on blood vessels?
A
- Reduced vasodilation
- Significant vasoconstriction
12
Q
What are the vascular consequences of hyperinsulinaemia?
A
Vasodilation leading to glucotoxicity and angiopathy
13
Q
What molecules are raised in EMS?
A
FFas, TNFa, interleukins and leptin
14
Q
What molecule is lowered in EMS?
A
Adiponectin
15
Q
What is the physiological role of adiponectin?
A
Regulates glucose metabolism and fatty acid oxidation
16
Q
What is the effect of insulin resistance on adiponectin?
A
IR leads to decreased adiponectin activity
17
Q
What environmental factor may predispose a horse to becoming insulin resistant?
A
Moving from bare pasture to lush spring pasture (high sugar, high calories, eat more), become obese, persistently hyperinsulinaemic so become IR
18
Q
What nutritional changes may lead to a hyperinsulinaemic crisis in a horse?
A
- Increase in grain feeding
- Moving to a new pasture
- Rapid growth of pasture grass
19
Q
Other than nutritional, what other factors may lead to a hyperinsulinaemic crisis in a horse and why?
A
- Any increase in stress and/or inflammation
- Stimulates HPA axis, release of cortisol
- Change in housing, winter, disease
20
Q
Explain the intestinal carbohydrate overload theory of laminitis
A
- Sudden exposure to lush pasture or carb rich feeding
- Exceed digestive capacity of small intestine (bypass)
- Carb overload in hindgut
- Alteration in bacterial flora = lower pH
- Increased intestinal permeability
- Bacterial by-products = systemic inflammation
21
Q
What is the main bacterial by-product that leads to laminitis?
A
Matrix metalloproteinases
22
Q
In what conditions is MMP activity increased leading to laminitis?
A
- Endotoxaemia
- Hypoperfusion
- Leukocyte activation/margination in laminar blood vessels
23
Q
Describe the effects of MMPs on the laminae
A
- Degradation of extracellular matrix
- Matrix cannot maintain shape or tensile strength
- Laminae stretch and tear, causing separation at dermal/epidermal junction
24
Q
Outline the vascular theory of laminitis
A
- Ischaemia of laminae may be primary lesion of laminitis in carb overload model
- Ischaemia followed by reperfusion injury, free radical formation, further tissue damage, oedema and necrosis
- Angiopathy precedes disruption to dermal epidermal tissue
25
Outline the basic diagnostic plan for laminitis
1: History - carbohydrate overload?
2: Physical exam - PPID, EMS?
3: Orthopaedic exam and radiography - OBEL grading, degree of rotation
4: Endocrine testing - PPID, IR
26
When should endocrine testing for in a laminitis work up be avoided?
During acute painful laminitis episodes as ACTH will be high due to stress/pain
27
What management steps can be taken to address the risk factors for laminitis?
- Predisposing factors: manage/treat obesity, insulin resistance, PPID, and consistent farrier care
- Prevent exacerbation: regulate starch/sugar intake and total calories, monitor for PPID
- Avoid triggers: avoid sudden changes in feeding practices, gradual introduction to new pastures, treat endotoxaemia and systemic inflammation
28
What management would be beneficial during an acute laminitis episode?
- Treat underlying condition if poss
- Absolute box rest until sound and beyond (1ft deep, soft sawdust bedding)
- NSAIDs to treat inflammation and pain (flunixin, phenylbutazone)
- Cryotherapy
- Remedial farriery
29
Outline the use of limiting pasture grazing in the management of laminitis
- Goal is to manage obesity and stop sugars exacerbating hyperinsulinaemia
- Strategies: short turnout <1hr, grazing muzzles, strip grazing
30
Describe the key points in the use of cryptherapy for the management of laminitis
- Maintain limb temperature 4degreesC for 72hr distally from carpus
- Start ASAP, ideally before endotaoxaemia
- Acute laminitis only
31
What is the physiological basis of cryotherapy in the treatment of laminitis?
Reduce metabolic rate of tissue allowing tissue to be more resistant to hypoxia which occurs with vasoconstriction, as well as decreasing cytokine production and reducing MMP activity
32
Describe the soaking of hay in the management of laminitis
- Min 45min
- Reduces amount of hydrosoluble carbohydrates in feed
- Need to add balancer to make up for vits/mins flushed by soaking
33
In what circumstances may a laminitic horse need to stay off pasture indefinitely?
- If are still hyperinsulinaemic after appropriate management
- if hyperglycaemic and normal insulin (pancreatic exhaustion)
- If repeated laminitis episodes
34
When would hepatic lipidosis occur in the horse and why?
- RARE
- Better synthesis of TAGs and export of VLDL vs ruminants
- Only if FA mobilisation and synthesis exceed oxidation and VLDl excretion
35
What are the potential consequences of lipidosis and how does this impact on the clinical investigation?
- Can affect hepatic function (hepatic failure, hepatic rupture)
- CARE with biopsy
36
How is hepatic lipidosis diagnosed?
- Increased serum TAG concentration
- Biochemical evidence of hepatic dysfunction
- US/histopathological evidence of fatty infiltration of liver (size/echogenicity)
37
What is the relationship between obesity and hepatic lipaemia in the horse?
- Obese animal has more fat that can be converted to VLDLs
- Obese animals also likely to be IR
- IR = no inhibition of lipolysis, higher prod. of VLDLs, lower availability of LPL to clear
38
Outline the role of insulin in lipid metabolism
- Inhibits lipolysis and proteolysis
- Decreases liver glycogenolysis, gluconeogenesis and ketogenesis
- Stimulates lipoprotein lipase (LPL)
39
Outline the role of stress in lipid metabolism
- Releae glucocorticoids, catecholamines, progesterone
- Counteract effects of insulin on lipid metabosim
- Contribute to insulin resistance
40
In what cases must hyperlipaemia always be a top differential?
All ponies, miniatures, or donkeys that are inappetant for even short periods of time
41
Explain the physiology behind inappetance leading to hyperlipaemia
- Shift into NEB
- Use fat stores
- Too efficient and produce too many VLDLs
- Leads to hyperlipaemia
42
What are some clinical signs for hyperlipaemia?
- Generally simply quite/dull demeanour
| - More variable include icterus, anorexia, weakness, ataxia, diarrhoea, colic, fever, pendent oedema
43
What other conditions may commonly mask hyperlipaemia?
- infections/parasitism
- Primary colic
- PPID
- Laminitis
44
Explain why primary colic and PPID may be risk factors for hyperlipaemia
- Colic: fast patient until identify cause
| - PPID: excess glucocorticoids inhibiting insulin
45
In what physiological states is hyperlipaemia a greater risk?
- Higher energy demand states e.g. pregnancy (late gestation) and lactation
46
Explain the breed predisposition for hyperlipaemia
- Minis/ponies/donkeys have relative insulin insensitivity to favour lipolysis
- Horses more likely to develop hypertriglyceridaemia
47
Explain why stress/pain is a risk factor for hyperlipaemia
- Catabolic neuroendocrine response
- ACTH, ADH, GH, catecholamines, glucocorticoids and glucagon released
- Insulin suppression and increased lipolysis
48
List some risk factors for hyperlipaemia
- Obesity
- Breed
- Female
- Stress/pain/disease
- Anything that affects appetite and shifts into NEB: anorexia, intestinal parasitism, Enteritis/colic, gastrci/large colon impactions, dysphagia, peritonitis, metritis, laminitis, dental disease, hospitalisation
49
Explain the physiology of VLDL production
- Increased energy demand => lipolysis in adipose tissue => FFAs, non-EFAs, and glycerol
- FFAs enter tricarboxylic acid cycle, gluconeogenesis or become TAGs
- TAGs stored in liver or become VLDLs in blood
- VLDLs take into tissues through LPL action, available for mobilisation where needed
50
Outline the pathophysiology of equine hyperlipaemia
- In hyperlipaemia, efficient synthesis of TAGs from FFAs and quick release into blood as VLDLs
- VLDL contain greater TAG concentration in hyperlipaemia
- LPL induces uptake of VLDLs by peripheral tissue (incl. adipose)
- Cause of hyperlipaemia is not overproduction of VLDLs, but decreased clearance by LPL
51
How does the activity of LPL change with equine hyperlipaemia?
Increases 2-fold with hyperlipaemia
52
Explain the role of endotoxaemia in hyperlipaemia
- Increases hepatic synthesis and secretions of VLDL from liver
- Inhibits LPL activity at high endotoxin concentrations
- Endotoxaemia often leads to hypovolaemia which will lead to azotaemia
53
Explain the role of azotaemia in hyperlipaemia
Interferes with LPL action
54
Why are obese animals more at risk of equine hyperlipaemia?
- Excessive store for NEFA and FFAs
- Release of larger VLDL concentration
- LPL cannot keep up = hyper lipaemia
55
Outline a diagnostic plan for equine hyperlipaemia
- History (signalment, behaviour)
| - Plasma triglyceride concentration
56
At what concentration, does plasma triglyceride concentration indicate hyperlipidaemia in ponies/minis/donkeys and what is the importance of this?
(Horses?)
- >1.5-5mmol/L (130-500mg/dL)
- Rarely results in clinical recognisable disease but high risk of hyperlipaemia
- Can reverse and prevent hyperlipaemia at this stage
- (horses >5mmol/L but no gross lipaemia)
57
At what concentration does plasma triglyceride concentration indicate hyperlipaemia?
.5mmol/L (500mg/dL)
58
What common abnormalities may be be found haematology/biochem in cases of equine hyperlipaemia?
- Iindicators of liver disease e.g. GGT, ALP, SDH, bile acids, glucose
- Falsely high creatinine
59
Why can hyperlipaemia affect creatinine results on biochemistry?
Turbidity from hyperlipaemia iterferes with light/colour analysis of creatinine concentration
60
What are the main goals in the treatment of equine hyperlipaemia?
- treatment of underlying concurrent disease
- Elimination of stress
- Improvement of energy intake
- Inhibition of fat mobilisation from adipose tissue
- Increase TAG uptake by peripheral tissues
61
Outline the approach to the treatment of concurrent disease in equine hyperlipaemia
- Provide suitable analgesia to improve appetite while major disease is undergoing treatment
- Control promary disease
- Resolve fluid/electrolyte deficitys
- IV nutrition (rare, expensive)
62
Outline the approach to the removal of stressors in the management of equine hyperlipaemia
- Remove any stress possible
| - prevent herd stress factors
63
What are the approaches to improving energy intake in equine hyperlipaemia?
- Carb rich diet, hand grazing, sweet feeds, leafy hay, anything but avoid fat rich ideally
- If anorexia, 4 options: dextrose, enteral nutrition, partial parenteral nutrition, insulin therapy
- Sooner start with parenteral nutritional = better outcome, proactive
64
Outline the dextrose/glucose approach to the anorexic pony with hyperlipaemia
- 5% dextrose/glucose at maintenance rate
- Unlikely to provide daily caloric req
- suitable in first instance but not long term
- consider risk of hyperglycaemia if IR
65
Outline the enteral nutrition approach to the anorexic pony with hyperlipaemia
- Nasogastric tube
- Ready brek, complan, crush and dissolved stuf cubes via nasogastric tube
- Any high carb, high energy food (ideally low fat)
66
Outline the partial parenteral nutrition approach to the anorexic pony with hyperlipaemia
- If enternal not possible e.g post-op colic surgery
- 5% dextrose + 8.5% amino acid solution
- Monitor glycaemia closely
67
Outline the insulin therapy approach to the anorexic pony with hyperlipaemia
- Hyperglycaemia only!
- Insulin zinc suspension 0.15IU/kg SC BID
- Increase dose by 0.05IU/kg if hyperglycaemia does not improve
- Dubious efficacy with IR
68
What has been suggested that may be used to inhibit fat mobilisation in equine hyperlipaemia?
- Nicotinic acid
| - Efficacy unproven in horses
69
Outline increasing the TAG uptake in treatment of equine hyperlipaemia
- Heparin, 40-25 IU/kg BID
- Stimulates LPL to remove TAGs from blood
- LPL already at ma rate in affected ponies so benefits questionable, need to monitor haemostasis regularly
70
What is the prognosis for equine hyperlipaemia?
Poor, estimated mortality 60-100% of affected ponies
| - If survives, TAGs normal within 3-10 days
71
How can equine hyperlipaemia be prevented?
- Avoid breeding, transporting grossly obese ponies
- Controlled exercise and feed intake
- Avoid drastic weight reduction
72
Describe a treatment plan for partial aprenteral nutrition
- Provide 50% of digestible energy requirement for maintenance as PPN
- Provide 50% of crude protein requirement = amino acids to be provided
73
Calculate components of a parenteral nutrition solution
- Digestible energy requirement = 1.4 + (0.03 x bwt kgs) =Mcal/day
- Add 20% for late pregnancy, and 70% for lactation
- To calculate crude protein provided/day, do Digestible energy x 40 (Mcal) = amino acids
- Subtract amino acid calories from total energy req (4kcal/g of protein) = energy to be provided from 50% dextrose solution (500g/L = 1700kcal/L)
74
Outline a monitoring plan for patients receiving treatment of equine hyperlipaemia
- Check blood glucose q2-4 hours for first 12 hrs of new protocol
- Urine dipstick to check for glucose
- Monitor plasma TAG concentrations
- Consider blood gas analysis or measurement of plasma bicarbonate concentrations to check metabolic acidosis
75
When is enteral feeding recommended over other methods in the treatment of equine hyperlipaemia, and what are the 3 approaches?
- Where finances are limited
- 1: complete pelleted food, calculate cals required, begin with 25% then increase to 50% over 3 days, soak in warm water and pump in via nasogastric tubes 1-4 times daily
- 2: dextrose and galactose powder mixed with water and in via nasogastric tube, use insulin at the same time to prevent hyperglycaemia
- 3: mouth feeding via syringe, can use dextrose powder in water or treacle by heating in pan with water
76
What are potential risks of enteral feeding for the treatment of equine hyperlipaemia?
- Reflux
- Smaller stomach size if have been anorexic for a few days can limit amount that should be administered
- Hyperglycaemia
- Owner compliance/competence
77
Why might haemoconcentration occur in a diabetic horse?
Glucosuria leads to free water loss
78
Outline the medical and husbandry management of a diabetic horse
- Fluids
- Feed soaked hay and low/no concentrates
- Continue exercise and feed intake
- Ensure partial parenteral nutrition
- Administer insulin as CRI or subcut injections
79
Why may hyperlipaemia develop in a diabetic horse?
- Low insulin output if type I
| - Insulin not inhibiting hormone sensitive lipase
80
When assessing a case of laminitis, how should the lameness be assessed?
- Use fingers rather than hoof testers
- Flexion tests are absolutely contraindicated
- This is because feet will be too painful and may cause further damage
81
Describe the commonly features identified in the front and hind limbs of a laminitic pony
- Front: pounding digital pulses, will not lift limb, hoof wall warm, pain at pressure over coronary band
- Hind: warm, but no digital pulses palpable
82
Other than management for the condition itself, what other treatment should be provided for a horse with PPID?
- NSAID, e.g. phenylbutazone to control hoof wall inflammation
- Remedial farriery
83
Outline the welfare issues associated with obesity
- Increases the risk of other diseases (laminitis, derm conditions, chronic musculoskeletal conditions)
- Inflammatory disease
- Fat mares pass on risk of greater adiposity
84
Explain how fat mares increase the risk of adioposity in their offspring
- Epigenetics
- Not born fat, but higher fat cell to muscle cell ratio
- End up overfeeding and fat cells become a risk
85
Give examples of factors that increase the risk of obesity in horses
- Being on a yard with other fat horses as becomes normalised
- The microbiome
- Turning out on grass in the summer (overfed but undernourished, may take on 2x required calories but fewer vitamins and minerals)
86
List the factors that are addressed in the management of an obese horse
- Control calories
- Maintain feed bulk
- Provide optimal nutrition
- Lifestyle change
87
Why is calorie control required in the management of an obese horse?
- Is the only way to reduce fat
- Reduces IR
- Reduces chronic inflammation
- Improves health and welfare of horses
88
What amount of faeces should be produced by a normal horse?
1-3% BW
89
How can grass be restricted in horses and why is this important?
- Having sparse pasture, or restricting time outside
| - Most obese horses fed very little concentrate by owner, so most calories are coming from grass, esp. in summer
90
Why is it important to maintain feed bulk when managing and obese horse?
If reduce fibre, risk stereotypies, gastric ulcers and colic, as well as increased cortisol which can lead to IR
91
How can feed bulk be maintained in horses?
- Soak hay to remove sugar but maintain bulk and fibre
| - Replace grass with low quality forage
92
What is the importance of providing optimal nutrition in the management of obese horses?
- Likely to be deficient in key minerals e.g. Cu, Zn, Na, P, Ca
- Hay deficiency in quality protein, vitamins and minerals, esp. anti-oxidants
- Soaking hay remoes nutrients and minerals
93
How can optimal nutrition be provided when managing an obese horse?
- Balance vitamins and minerals using feed balancers (100g/100kg BWT)
- Give when grazing, winter and restricted grazing, soaking hay, hay, calorie control diet
- Barley or oat straw
- Carrots can also be fed
94
Why is wheat straw an inappropriate feed stuff for horses?
High levels of lignin which increases risk of impaction
95
Describe the general lifestyle changes that need to be implemented in the management of an obese horse
- change diet in conjuntion with exercise to increase metabolic rate
- Protect against insulin resistance
- Encourage winter weight loss in leisure horses
- Pastured horses stay as fit as exercised horses (can turn out with muzzle to prevent overfeeding)
- No rugs in winter, daily turnout, clip underneath and leave hair on top
96
Suggest an exercise regime for the management of an obese horse
- brisk exercise 30mins every day, 7 days a week (HR 80bpm for 30 mins), - this is protective against IR even before fat loss
