Endocrine Diseases Flashcards

1
Q

What horses are most affected by pituitary pars intermedia dysfunction (PPID)? What 2 complications are associated?

A

1/5 of horses >15 y/o, with prevalence increasing with each year of age

  1. laminitis (Founder) - 3rd phalanx, lameness, increased heat and pulsations
  2. recurrent infections - abscesses
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2
Q

What is the normal anatomy of the equine pituitary gland?

A

one, layered gland (as apposed to anterior and posterior)

  • pars distalis
  • pars intermedia
  • pars nervosa
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3
Q

What cells are present in the pars distalis and what do they secrete?

A
  • somatotropes: GH
  • gonadotropes: LH, FSH
  • lactotropes: prolactin
  • thyrotropes: TSH
  • corticotropes - POMC
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4
Q

What type of cell is present in the pars nervosa and what do they secrete?

A

magnocellular neurons - oxytocin and ADH

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5
Q

What type of cell is present int he pars intermedia and what do they secrete?

A

melanotropes - POMC

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6
Q

How does the pituitary produce hormones in healthy patients? How does this change in PPID horses?

A

periventricular neurons produce dopamine, which inhibits POMC release from melanotropes = minor ACTH, variable endproducts

periventricular cell bodies and nerve endings degenerate, causing a decrease in dopamine and increase in POMC secretion from melanotropes and the pars intermedia becomes enlarged = increased ACTH and byproducts

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7
Q

What is the normal seasonal cycle of ACTH concentration in horses?

A

tends to remain steady in the beginning of the year, and reaches a peak between mid-July to mid-November

  • horses with PPID will have an exacerbated increase in ACTH during this time of the year
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8
Q

What unique clinical sign is seen in horses with PPID?

A

changes in hair coat = wooly, curly winter coat remains

  • generalized/localized hypertrichosis
  • abnormal shedding
  • hair color changes
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9
Q

What general signs are associated with PPID?

A
  • decreased performance with exercise intolerance
  • changed attitude, docile and lethargic
  • loss of top line and muscle
  • pendulous abdomen, regional fat
  • weight loss
  • abnormal sweating (increased, inadequate)
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10
Q

What 5 complications are associated with PPID in horses?

A
  1. laminitis - increased digital pulses, heat, hoof rings
  2. desmitis/tendinitis
  3. suspensory ligament breakdown
  4. infections - chronic abscesses
  5. parasitism - increased burden and shedding
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11
Q

What are 4 additional clinical signs associated with PPID in horses?

A
  1. loss of reproductive cycle
  2. blindness
  3. seizures
  4. PU/PD
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12
Q

What is the most common way of diagnosing horses with PIPD? What can make this difficult?

A

history and clinical signs - shedding, coat appearance, attitude, infections, parasites, BCS

  • debilitated and aging horses may look like PPID
  • concurrent disease affects clinical signs
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13
Q

What 3 laboratory tests are used to diagnose PPID?

A
  1. resting ACTH levels*
  2. TRH stimulation test
  3. insulin status

(old gold standard = dex suppression test)

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14
Q

What 5 laboratory findings are seen in horses with PPID?

A
  1. hyperglycemia
  2. hyperinsulinemia
  3. hypertriglyceridemia
  4. high fecal egg counts (increased shedding)
  5. relative neutrophilia and lymphopenia
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15
Q

How is it decided which laboratory tests are done to diagnosed PPID? What should be done if tests come back normal?

A

OBVIOUS SIGNS = resting ACTH level; if normal, perform a TRH stimulation test (11/15-7/15); if that is also norma, retest in 3-6 months

SUBTLE SIGNS = TRH stimulation test (11/15-7/15); if normal, retest in 3-6 months

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16
Q

How is the resting ACTH level performed in horses to diagnose PPID?

A
  • baseline sample is taken and placed in a EDTA tube
  • in 4 hours, the sample is centrifuged
  • plasma is separated and put in another EDTA tube
  • plasma sits overnight and the ACTH levels are observed
17
Q

How is TRH stimulation test performed in horses to diagnosed PPID? What is important to note about this test?

A
  • baseline sample is taken in horses that have not been fed grain for 12 hours
  • a follow-up sample is taken 10 minutes after the horse was given 1 mg of TRH IV
  • in 4 hours, the samples are centrifuged
  • plasma is separated and put in another tube
  • plasma sits overnight and the ACTH levels are observed

NOT PERFORMED mid-July to December —> ACTH will naturally be higher and labs do not have a reference interval for this

18
Q

What are 2 other potentially supportive tests used for PPID diagnosis?

A
  1. overnight dexamethasone suppression
  2. MRI specific for PPI enlargement
19
Q

In what ways can horses with PPID be managed to alleviate clinical signs?

A
  • quality nutrition
  • keep optimal BCS
  • dentistry: float older horses 2x a year
  • parasite control
  • water supply
  • hoof care
20
Q

What medical treatment is recommended for horses with PPID?

A

life-long, oral pergolide (Prascend) every day

  • dopamine agonist that replaces the deficit of dopamine to decrease melanotrope formation of POMC
21
Q

What side effects are associated for pergolide (Prascend) treatment of PPID? How is treatment altered when this occurs?

A
  • inappetence
  • weight loss
  • lethargy

stop treatment until appetite returns and re-introduce pergolide at 1/2 dose BID for 4 days

22
Q

What are the initial and long-term responses expected with pergolide treatment in horses with PPID?

A

INITIAL = better attitude, increased activity, resolved PU/PD and hypoerglycemia

LONG-TERM = improved hair coat, muscle mass, and shape, and less likely to develop infections and laminitis

23
Q

When is repeat testing recommended when first starting pergolide treatment?

A

in 30-60 days

24
Q

What is the role of insulin?

A

produced by the pancreas following increased blood glucose resulting in mediated glucose absorption in the liver, adipose tissue, and muscle

25
Q

How is insulin production affected by PPID?

A

INSULIN RESISTANCE!

  • decreased tissue response or uptake of insulin
  • pancreas secretes more insulin to compensate
  • this results in high insulin levels, which deprives tissues of glucose (hoof = laminitis)