Hyoeradrenocorticism 1 Flashcards

1
Q

Does hyperadrenocorticism have a characteristic clinical picture?

A
  • changes can be subtle early on in dz
  • insidious onset means presentation at variable stages
  • 2* problems frequently -> death
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2
Q

What is hyperadrenocorticism?

A
  • clinical problem d/t subacute over exposure to GCs
    > naturally occouring
  • clinical signs don’t indicate causality
  • can be pituitary dependant (PDH) or adrenal dependent (ADH)
    > iatrogenic
  • chronically administered under dosage
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3
Q

Hx findings with HAC?

A
  • PUPD
  • appetite
  • excercise intolerance
  • anoestrus (intact females)
  • abdominal distension (50%)
  • coat Changes (50%)
  • alopecia and hyperligmentation (30%)
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4
Q

Clinical signs HAC?

A
  • panting
  • muscle weakness and atrophied
  • hepatomegaly and abdominal distension
  • ^ abdo fat deposition
  • testicular atrophy and increased vulva size, gynacomastia
  • dermal changes
  • altered mentation (underwhelmed)
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5
Q

Detail the dermal changes potentially seen with HAC

A
  • non primary
  • symmetrical alopecia (trunk»extremities)
  • non-pruritic
  • hyperpigmentation
  • hyperkeratosis and flaking skin
  • comedons
  • calcinosis cutis (deposition Ca P)
  • infections or infestations (recurrent, esp skin)
  • can see subcut BVs
  • thin, wrinkly, aged skin
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6
Q

Updated clinical picture with HAC in the dog

A
  • PUPD
  • panting excessively (weak muscles, ^ abdo cavity size, ^ risk pulmonary thromboemboli)
  • relatively inactive (usually put down to ‘old for their age’)
  • epaxial muscle wastage
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7
Q

Updated clinical picture of HAC in the cat

A
  • difficult to manage DM (^GC can cause DM in the cat but NOT DOG - cats b cells get damaged/worn out, dogs dont)
  • varying degrees of insulin resistance
  • present for varying periods of time
  • usually no other signs
  • UNCOMMON
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8
Q

Clin path with hyperadrenocorticism

A
  • eosinopeania, lymohopeania
  • ^ ALP, ^ ALT (disproportionate ^ ALP in dog, microenvironment changes ^ ALP and ISOENZYME of ALP stimulated by GC - not in cats )
  • hyoercholesterolaemia
  • ^ thrombocyte count
  • v urine specific gravity (??)
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9
Q

Why do animals most commonly die with hyperadrenoocorticsm

A
  • PTS d/t 2* problems
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10
Q

How does hyperadrenocorticism cause alopecia?

A
  • telogen effluvium type alopecia
  • non pruritic
  • most common over trunk (normal head and limbs)
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11
Q

When else may telogen effluvium be seen?

A

Parturition d/t hormonal changes

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12
Q

Why does abdomenal distenion occour with hyperadrenocorticism?

A
  • muscle pathology (myotonia)

- redistribution subcut fat -> abdo

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13
Q

Why is testicular atrophy seen with HAC?

A
  • ve feedback
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14
Q

What causes the PUPD with HAC?

A

1* PD mostly

- some degree of ADH interference but minimal

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15
Q

Which disease is severe insulin resistance seen?

A

laminitis

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16
Q

How do ALP changes in cats differ to dogs?

A
  • ALP shorter t1/2 cf. dogs
  • increases rarely seen
  • no iso-enzyme induction
17
Q

what are the biomarkers for excess GC activity?

A

NONE

18
Q

What is the exception to 1* PD with adrenocorticism? Ie. when should you not tell the owners to take up water to stop PU overnight etc.

A

Any sign of infectino (pyometra, UTI etc.) -> endotoxins that interfere with concentrating ability

19
Q

Are basal plasma cortisol and urinary corticoid excretion useful measurements for HAC Dx?

A

NO

- often ^ in non-HAC