Endocrinology Flashcards

(49 cards)

1
Q

Physiological causes of negative energy balance

A

Decreased intake
Increased requirements

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2
Q

Pathological causes of negative energy balance

A

Sepsis
Azotaemia (pre-renal)

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3
Q

Diagnosis of hyperlipaemia in the horse

A

Elevated triglycerides (1.5-5mmol/L = hyperlipidaemia, >5mmol/L = hyperlipaemia)
Blood serum discoloured
Liver enzymes may be elevated (GGT, ALP, SDH, bile acids)
Hyperglycaemia due to insulin resistance

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4
Q

Treatment of hyperlipaemia

A

Provide calories (enteral: hand feeding/any feed or parenteral: glucose infusion even if hyperglycaemic)
Treatment of primary condition (pain relief)

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5
Q

Enteral feeding options in hyperlipaemia if costs are limited

A

Nasogastric tubing soaked pelleted feed
Nasogastric tubing powdered glucose/galactose
Syringe feeding into mouth (dextrose powder/treacle/apple sauce)

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6
Q

What is hyperlipidaemia?

A

Precursor to hyperlipaemia, must be proactive
Triglycerides 1.5-5mmol/L

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7
Q

Mechanism of PPID

A

Neurodegenerative disease
1) Lack of inhibitory dopamine from hypothalamus
2) Hyperplasia and adenoma formation (benign neoplasia)
3) Overproduction of POM-c
4) Over production of ACTH/MCH

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8
Q

What is cushings disease referring to in the horse?

A

PPID/pituitary pars intermedia dysfunction

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9
Q

Difference between cushings in the dog and cushings in the horse

A

ACTH increase in the horse, but no cortisol increase

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10
Q

Signalment for PPID

A

18-25 years old
Ponies and Morgans predisposed

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11
Q

Pathophysiology of sedated/quiet attitude in PPID

A

B-endorphin has opioid activity

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12
Q

Pathophysiology of abnormal adipose deposition in PPID

A

alpha-MSH

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13
Q

Early signs of PPID

A

Muscly atrophy (loss postural muscles = pot belly appearance)
Hair abnormalities
Dull, lack of energy, poor performance
Regional adiposity

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14
Q

Pathophysiology of hair abnormalities in PPID

A

More hair in anagen phase

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15
Q

Where do horses retain long hair when they have PPID?

A

Jugular furrow
Submandibular furrow
Pastern area

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16
Q

What is pathognomic for PPID

A

Hair coat abnormalities

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17
Q

Metabolic changes in advanced PPID (2)

A

Hyperglycaemia
Hyperinsulinaemia

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18
Q

What disease would you be suspicious about in an older horse with an infection that is unusually difficult to treat (dental disease/skin infection/surprisingly high parasite burden/foot abscess etc.)?

A

PPID

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19
Q

Pathophysiolgy of hyperhidrosis in PPID

A

Catecholamine release
Long hair coat

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20
Q

Pathophysiology of pseudolactation in PPID

A

Prolactin is controlled by dopamine, there is loss of dopamine control in PPID

21
Q

Some uncommon signs of PPID

A

PUPD (compression of pars nervosa –> decreased ADH release)
Hyperhidrosis
Pseudolactation
Suspensory ligament breakdown (collagen II)
Central blindness (adenoma compression)
Narcolepsy
Low fertility/irregular cycling

22
Q

If a horse with PPID is obese, what should be measured?

A

Insulin levels (looking for hyperinsulinaemia which predisposes to laminitis)

23
Q

Options when testing for PPID

A

Resting ACTH
TRH stimulation test

24
Q

Benefits of resting ACTH test in PPID

A

One blood sample
Quick
Cheap
Well established reference ranges year round

25
Problems with resting ACTH test for PPID
Less sensitive in early stages Affected by stress/excitement/severe pain/after sedation)
26
Important consideration when taking blood tests for PPID and choice of blood tube
Blood must be chilled, should be done on last visit of the say EDTA
27
Benefit of TRH stim test in PPID
Very sensitive in early stages (use if ACTH negative with high suspicion)
28
Problems with TRH stim test
More expensive Doesn't work year round (no reference ranges established for Autumn/early winter)
29
Treatment for PPID
Pergolide
30
Action of pergolide
Dopamine agonist
31
Next steps if initial PPID treatment isn't effective
ACTH test Assess for concurrent disease Increase pergolide dose May consider slow release injectable form (Cabergoline)
32
Major predisposing factor for insulin dysregulation?
Obesity
33
Insulin dysregulation increases the risk of which disease?
Laminitis
34
EMS phenotype (3 things)
Regional adiposity or obesity Insulin resistance Clinical or subclinical laminitis in absence of recognised cause
35
Functions of adipose tissue
Leptin decreases appetite Adiponectin sensitises tissues to insulin and downregulates inflammatory reactions Production of cytokines (pro-inflammatory)
36
Problem with excess adipose tissue
Leptin released in excess --> leptin resistance --> overstimulation of appetite Pro-inflammatory state
37
Problem with 'thrifty' gene in certain horse breeds
Predisposed to insulin dysregulation if maintained on high starch diet even if not obese (adapted to harsh diet)
38
Is insulin dysregulation in horses usually compensated or uncompensated?
Compensated
39
Problems associated with obesity and EMS
Insulin dysregulation Poorer prognosis for laminitis recovery Pedunculated mesenteric lipomas can cause strangulating small intestinal lesions Hyperlipaemia Abnormal thermoregulation Altered oestrus cycle and reduced fertility Foals born for obese mares have higher risk of OCD Pro-inflammatory state affects other disorders
40
Three stages of insulin resistance
Compensated (normal glucose, hyperinsulinaemia) Uncompensated (hyperglycaemia and hyperinsulinaemia) Type II diabetes mellitus (end stage, persistent hyperglycaemia, beta cell exhaustion/inadequate insulin output)
41
Tests for diagnosing EMS
Basal glucose/insulin Oral sugar test (OST) Combined glucose-insulin test (CGIT)
42
Main problem with all tests for EMS
False negative common
43
Is EMS testing important in management of obese horses?
No, can expect insulin resistance to develop in all obese horses so should aim for weight loss regardless of EMS testing
44
Principles in management of EMS
Weight loss (diet and exercise) Management of laminitis (good farrier) Drugs can enhance weight loss in short term Treat PPID if present (pergolide)
45
Drugs that can be used for weight loss in EMS (3)
Metformin Levo-Tyroxin Ertuglifozin? (Only preliminary studies into safety and efficacy)
46
Action and use of Metformin in EMS treatment
Decreases enteric glucose absorption to reduce post-prandial increase in blood glucose and insulin Given 30-60 mins before feeding For horses that are insulin dysregulated while management changes are put in place (Licensed for use in humans)
47
Levo-tyroxin action
Increases metabolic rate to accelerate weight loss
48
Ertuglifloxin action
Sodium-glucose co-transporter Targets receptors in proximal tubule of kidney to increase glucose loss in urine
49
Metformin licensing
Licensed for use in humans