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Y2 Endocrine > Pharmacology and testing for adrenal disease > Flashcards

Pharmacology and testing for adrenal disease Flashcards

1
Q

The adrenal cortex secretes hormones derived from which molecule?

A

Cholesterol

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2
Q

What are the three regions of the adrenal cortex and what is produced at each?

A 
Zona glomerulosa (outer) - Mineralocorticoids
Zone fasciculata (middle) - Glucocorticoids
Zona reticularis (inner) - Androgens
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3
Q

Which two hormones are produced by the adrenal medulla?

A

Adrenaline and Noradrenaline

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4
Q

What are the functions of glucocorticoids?

A
  • promotes gluconeogenesis in the liver
  • increases lipolysis
  • increases catabolism of proteins
  • inhibits growth
  • inhibits immune response
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5
Q

What are the clinical signs of hyperadrenocorticism/Cushings syndrome?

A
  • Hyperglycaemia (not above renal threshold)
  • Tissue wasting
  • Muscle weakness
  • Pot belly
  • Hair loss
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6
Q

What happens as a result of hypoadrenocorticism/Addisons disease?

A
  • Dogs cannot produce enough glucocorticoids or mineralocorticoids
  • Deficiency can result in an acute medical emergency = Addisons crisis
  • Hyperkalaemia
  • Hyponatremia (low sodium in blood)
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7
Q

Specific blood tests look at which 3 hormones when testing for disorders of the adrenal cortex?

A

Cortisol
Aldosterone
ACTH (Adrenocorticotropic hormone)

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8
Q

Non-specific blood tests look at which 4 molecules when testing for disorders of the adrenal cortex?

A
  • Electrolytes
  • Glucose
  • Lipids
  • Haemotology
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9
Q

Glucocorticoids are regulated by what?

A

The HPA axis

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10
Q

What are the 2 major causes of hyperadrenocorticism?

A
  • Functional adrenal tumour

- Functional anterior pituitary tumour

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11
Q

How does a functional adrenal tumour cause hyperadrenocorticism?

A
  • Causes increased cortisol
  • ACTH is decreased due to negative feedback
  • Unaffected side shrinks due to decreased ACTH
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12
Q

How does a functional anterior pituitary tumour cause hyperadrenocorticism?

A
  • ACTH is increased as tumour stimulates production of cortisol from both adrenals
  • Doesn’t respond to negative feedback
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13
Q

What are the two types of hyperadrenocorticism?

A

Spontaneous: pituitary dependent and adrenal dependent
Iatrogenic: overuse of medicine

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14
Q

Which two tests can be used to test for hyperadrenocorticism?

A

ACTH stimulation test
Dexamethozone suppression test
- both measure basal blood cortisol

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15
Q

What are the 3 treatment methods for hyperadrenocorticism?

A
  • Adrenal steroid synthesis inhibitors
  • Dopamine receptor agonists (horses)
  • Mineralocorticoid receptor antagonist
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16
Q

How does adrenal steroid synthesis inhibitors work in treating hyperadrenocorticism?

A

Trilostane

  • It is a competitive inhibitor of 3-β hydroxysteroid dehydrogenase so inhibits corticosteroid synthesis
  • Very lipid soluble
17
Q

What are the 3 types of hypoadrenocorticism (Addisons)?

A
  • Primary
  • Secondary
  • Latrogenic: sudden withdrawal of high prolonged dose of glucocorticoids
18
Q

How is hypoadrenocorticism treated?

A

Replacement therapy of glucocorticoids and/or mineralocorticoids

19
Q

Which hormone is a glucocorticoid receptor agonist and how does it act to treat hypoadrenocorticism?

A

Cortisol

  • Immune system: function suppressed
  • Liver: gluconeogenesis
  • Muscle: protein catabolism
  • Adipose tissue: lipolysis
20
Q

Describe the pharmokinetics (absorption, distribution and elimination) of glucocorticoids

A

Absorption: by the GI tract, mucus membranes and skin
Distribution: transported bound to plasma proteins
Elimination: duration of action varies from 1/2 to 72 hours

21
Q

What are the adverse effects of corticosteriods?

A
  • Toxic effects following long-term use at high doses
  • Latrogenic hypoadrenocorticism: following withdrawal of long term use of high doses that suppress ACTH secretion
  • Suppression of the response to infection or injury
  • Wound healing is impaired
  • Cushings syndrome
  • Abortion in late pregnancy
  • Laminitis
22
Q

Rising concentrations of glucocorticoids in the blood inhibit what?

A 
Corticotropin-releasing factor (CRF) 
Adrenocorticotropic hormone (ACTH)
23
Q

CRF release and activation of the HPA axis is stimulated by what?

A

Stressors such as physiological factors, excessive heat or cold, injury, infection

24
Q

What is the rate limiting step in the process of glucocorticoid production?

A

The initial step of cholesterol being converted to pregnenolone
- regulated by ATCH

25
Q

How do glucocorticoids affect calcium? What effect does this have on the body?

A

Produce a negative calcium balance by decreasing calcium ion absorption in the GI tract and increasing its absorption by the kidney.
They also cause increased breakdown of bone matrix which may lead to osteoporosis

26
Q

What are the 2 major regulators of aldosterone release?

A

High plasma potassium ion concentration which affect the zona glomerulosa cells of the adrenal directly
Angiotensin (depletion of body sodium ions activates the RAAS)

27
Q

Describe the mechanism of action for glucocorticoid receptor agonists

A

Small lipophilic molecules that enter target cells by simple diffusion.

28
Q

How are glucocorticoid receptor agonists administered?

A

They have been optimised for administration via a range of different routes.
- orally, systemically, intra-articular, eye drops, ointments

29
Q

What are contra-indicators to use glucocorticoid receptor agonists?

A
  • Diabetes
  • Infections
  • Corneal ulceration
  • Cardiac disease
  • Laminitis
  • Pregnancy
  • do not use counter-currently with NSAIDs
30
Q

What is the name of the only licenced veterinary mineralocorticoid receptor agonist?

A

Deoxycorticosterone pivalate (DOCP) via injection

31
Q

What is the target of adrenal steroid synthesis inhibitors?

A

The biosynthesis pathway of steroid hormone synthesis from cholesterol

32
Q

What is the current licenced adrenal steroid synthesis inhibitor drug?

A

Trilostane

- given orally

33
Q

How would you treat Cushings disease in horses?

A

Dopamine receptor agonist - given orally

- Pergolide

Y2 Endocrine (4 decks)

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