Endocrinology Flashcards

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
Q

Problems with resting ACTH test for PPID

A

Less sensitive in early stages
Affected by stress/excitement/severe pain/after sedation)

26
Q

Important consideration when taking blood tests for PPID and choice of blood tube

A

Blood must be chilled, should be done on last visit of the say
EDTA

27
Q

Benefit of TRH stim test in PPID

A

Very sensitive in early stages (use if ACTH negative with high suspicion)

28
Q

Problems with TRH stim test

A

More expensive
Doesn’t work year round (no reference ranges established for Autumn/early winter)

29
Q

Treatment for PPID

A

Pergolide

30
Q

Action of pergolide

A

Dopamine agonist

31
Q

Next steps if initial PPID treatment isn’t effective

A

ACTH test
Assess for concurrent disease
Increase pergolide dose
May consider slow release injectable form (Cabergoline)

32
Q

Major predisposing factor for insulin dysregulation?

A

Obesity

33
Q

Insulin dysregulation increases the risk of which disease?

A

Laminitis

34
Q

EMS phenotype (3 things)

A

Regional adiposity or obesity
Insulin resistance
Clinical or subclinical laminitis in absence of recognised cause

35
Q

Functions of adipose tissue

A

Leptin decreases appetite
Adiponectin sensitises tissues to insulin and downregulates inflammatory reactions
Production of cytokines (pro-inflammatory)

36
Q

Problem with excess adipose tissue

A

Leptin released in excess –> leptin resistance –> overstimulation of appetite
Pro-inflammatory state

37
Q

Problem with ‘thrifty’ gene in certain horse breeds

A

Predisposed to insulin dysregulation if maintained on high starch diet even if not obese (adapted to harsh diet)

38
Q

Is insulin dysregulation in horses usually compensated or uncompensated?

A

Compensated

39
Q

Problems associated with obesity and EMS

A

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
Q

Three stages of insulin resistance

A

Compensated (normal glucose, hyperinsulinaemia)
Uncompensated (hyperglycaemia and hyperinsulinaemia)
Type II diabetes mellitus (end stage, persistent hyperglycaemia, beta cell exhaustion/inadequate insulin output)

41
Q

Tests for diagnosing EMS

A

Basal glucose/insulin
Oral sugar test (OST)
Combined glucose-insulin test (CGIT)

42
Q

Main problem with all tests for EMS

A

False negative common

43
Q

Is EMS testing important in management of obese horses?

A

No, can expect insulin resistance to develop in all obese horses so should aim for weight loss regardless of EMS testing

44
Q

Principles in management of EMS

A

Weight loss (diet and exercise)
Management of laminitis (good farrier)
Drugs can enhance weight loss in short term
Treat PPID if present (pergolide)

45
Q

Drugs that can be used for weight loss in EMS (3)

A

Metformin
Levo-Tyroxin
Ertuglifozin? (Only preliminary studies into safety and efficacy)

46
Q

Action and use of Metformin in EMS treatment

A

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
Q

Levo-tyroxin action

A

Increases metabolic rate to accelerate weight loss

48
Q

Ertuglifloxin action

A

Sodium-glucose co-transporter
Targets receptors in proximal tubule of kidney to increase glucose loss in urine

49
Q

Metformin licensing

A

Licensed for use in humans