Endocrine Flashcards

1
Q

What are the parts of the anterior pituitary gland?

A

Pars distalis and pars tuberalis

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2
Q

Where is the pars intermedia located?

A

Between the anterior and posterior parts

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3
Q

Describe the physiology of the pituitary gland

A

Stress -> hypothalamus releases CRH and vasopressin -> pituitary secretes ACTH -> adrenals secrete cortisol

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4
Q

What type of feedback loop does cortisol have on the pituitary and hypothalamus?

A

Negative feedback loop

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5
Q

What is the main type of cell in the pars intermedia?

A

Melanotropes

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6
Q

What disorder in humans has similar lesions to PPID in horses?

A

Parkinson’s disease

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7
Q

How does dopamine normally influence pituitary hormones?

A

Interacts with melanotropes to inhibit ACTH and alpha-MSH which control cortisol release

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8
Q

How is dopamine different in PPID horses?

A

Oxidative neurodegeneration damages dopaminergic hypothalamic neurons. This leads to the loss of inhibitory tone in pars intermedia (increased ACTH production)

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9
Q

What are clinical signs of PPID?

A

Hypertrichosis, chronic or intermittent lameness, sole abscesses, PU/PD, sweating, muscle wasting, lethargy, recurrent infections, abnormal fat deposits, inappropriate lactation, blindness, seizures

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10
Q

What clinicopathologic changes are associated with PPID?

A

Hyperglycemia, hyperinsulinemia, hypertriglyceridemia, increased liver enzymes, increased ACTH (consistent but not always active). Sometimes anemia, neutrophilia, lymphopenia, high fecal egg count.

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11
Q

How is PPID diagnosed?

A

Clinical signs, age, endogenous ACTH concentration (consider seasonal RR- higher in the fall), response to therapy, necropsy

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12
Q

What is the gold standard for PPID diagnosis?

A

Stimulation test. Grain fasted then administer 1mg TRH IV, draw sample in EDTA tubes 10 min later, submit plasma for ACTH measurement. Recommended to do in the spring.

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13
Q

Would you expect ACTH to be high or low for a horse with PPID?

A

High

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14
Q

How is PPID treated?

A

Pergolide (dopaminergic agonist, can reduce appetite), cyproheptadine (serotonin agonist, can be added on), management (deworming, manage laminitis, hair-trims, adequate nutrition)

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15
Q

What are the 3 main components of equine metabolic syndrome?

A

Obesity, insulin dysregulation, and laminitis

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16
Q

What is the common signalment for equine metabolic syndrome?

A

Likely susceptible from birth, 5-10 years old at presentation, described as “easy keepers”

17
Q

What clinical signs are associated with equine metabolic syndrome?

A

Laminitis, obesity, regional adiposity (cresty neck, around tail head, behind shoulder, prepuce or mammary gland), “easy keeper”

18
Q

How is equine metabolic syndrome diagnosed?

A

Based on signalment, clinical signs, diagnosis of insulin resistance (IV glucose tolerance test or combined glucose insulin tolerance test)

19
Q

Describe the combined glucose insulin test

A

Grain fast overnight, obtain baseline glucose and insulin, administer dextrose IV then insulin IV, then check BG at intervals. If insulin >100uU/mL at 45 min- resistant

20
Q

What insulin concentration measurement is consistent with hyperinsulinemia?

A

> 50uU/mL

21
Q

What result on an insulin tolerance test is consistent with insulin resistance?

A

<50% decrease in BG from baseline 30 mins after insulin administration

22
Q

How is equine metabolic syndrome managed?

A

Restrict/eliminate grazing, don’t feed grain, provide mineral/vitamin/protein ration balancer, add daily exercise (unless laminitis present). Levothyroxine can be used to increase metabolic rate, activity level, and insulin sensitivity. Metformin hydrochloride can be used to increase insulin sensitivity.

23
Q

How does adult hypothyroidism occur in horses?

A

VERY RARE- from exogenous compounds, pituitary disorders, iodine deficiency or excess, or neoplasia

24
Q

What clinical signs are consistent with adult hypothyroidism?

A

Lethargy, poor performance, obesity, laminitis, cresty neck, EMS or PPID

25
Q

What are signs of surgically thyroidectomized horses?

A

Lethargy, poor performance, decreased body temperature, decreased appetite, scaly hair, anemia, low heart rate, respiratory signs

26
Q

How is hypothyroidism diagnosed?

A

Serum levels of T3 and T4 (increased TSH, decreased T3 and T4)

27
Q

How should T3 and T4 react to TSH or TRH administration?

A

T3 should double at 2 hours, T4 should double at 4 hours

28
Q

How is hypothyroidism treated in adult horses?

A

Daily iodine intake 1-5mg, levothyroxine supplementation 20ug/kg

29
Q

Describe congenital goiter

A

Thyroid enlargement causing inadequate or excessive iodine intake by mare. Causes stillbirths, prematurity, hypothermia, weakness, and physeal dysgenesis. Prognosis poor.

30
Q

Describe congenital hypothyroidism and dysmaturity syndrome in foals

A

Causes increased gestational length but dysmature foals, weak at birth, hypothermic, musculoskeletal problems, thyroid glands histologically hyperplastic w/ small follicles and minimal colloid. Baseline thyroid hormones can be low or normal but TSH response is always decreased. Prognosis guarded.