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ENI > Physiology of the adrenal glands, hyper/hypoadrenocorticism > Flashcards

Physiology of the adrenal glands, hyper/hypoadrenocorticism Flashcards

1
Q

What are the broad areas within the adrenal glands and which hormones do they produce?

A
  • Medulla - catecholamines
  • Cortex
    • Zone glomerulosa - mineralocorticoids
    • Zone fasciculata - glucocorticoids
    • Zone reticularis - androgens
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2
Q

What is the most peripheral zone within the adrenal cortex and which hormones does it produce?

A

Zone glomerulosa - mineralocorticoids

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3
Q

Which hormones does the Zone fasciculata produce?

A

Glucocorticoids

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4
Q

Which hormones does the Zone reticularis produce?

A

Androgens

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5
Q

Which area consists of 80-90% of the adrenal gland?

A

Cortex

Medulla is only 10-20%

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6
Q

The synthesises of steroid hormones always begins with which molecule?

A

Cholesterol

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7
Q

Give an example of a glucocorticoid and explain the origin of the name ‘glucocorticoid’

A

Cortisol

‘Glucocorticoid’ = has a role in regulation glucose

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8
Q

Describe the control of glucocorticoid release within reference to the HPA axis

A
  • Hypothalamic-pituitary axis
  • CRH is transported from hypothalamus down axons to the portal capillary bed
  • CRH causes corticotrophin cells in the anterior pituitary to release ACTH
  • ACTH travels through systemic circulation to the adrenal glands where it stimulates the synthesis of glucocorticoids, predominantly cortisol.
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9
Q

Glucocorticoids are _______-soluble hormones. This means that…

A

Glucocorticoids are lipid-soluble hormones. This means that when transported in the blood, 90% are bound to plasma proteins. They bind to specific cell membrane/cytosolic receptors at their target, and this complex is then transported to the nucleus where it results in altered gene expression.

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10
Q

What are the actions of glucocorticoids in the body?

A

Stress hormone - variety of roles in different areas of the body

  • Stimulate gluconeogenesis
  • Stimulate glycogenolysis
  • Causes proteolysis
  • Promote lipolysis
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11
Q

What effect do glucocorticoids have on fat?

A

They cause fat mobilisation from peripheral stores

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12
Q

What effect do glucocorticoids have on muscle?

A

They cause muscle catabolism

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13
Q

What effect does glucocorticoids have on the liver?

A

Antagonise insulin

Stimulate gluconeogenesis

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14
Q

What effect do glucocorticoids have on the kidney?

A

Increase GFR

Block the action of ADH

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15
Q

What effect do glucocorticoids have on skin?

A

Follicular atrophy

Sebaceous gland atrophy

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16
Q

What effect do glucocorticoids have on bone?

A

Reduce calcium levels

Osteopenia

17
Q

What effect do glucocorticoids have on the brain?

A

increased hunger and thirst

18
Q

What effect do glucocorticoids have on the immune system?

A

Release neutrophils from the marginated pool

Down-regulates the immune response such as T cell function and recruitment, and B cell activation

19
Q

Mineralocorticoid

A

class of steroid hormone characterised by their effects on salt and water balance e.g. aldosterone

20
Q

Describe the control of mineralocorticoid release

A
  • The main stimulus for aldosterone release is low blood pressure (think RAAS!)
  • High serum potassium also stimulates aldosterone release
  • The role of ACTH is only minor
21
Q

Function of aldosterone

A
  • Plays a central role in the regulation of blood pressure
  • Acts on the cells of the distal tubule and collecting duct to increase reabsorption of Na+, Cl-, and hence water
  • Stimulates the secretion of K+ into the tubule lumen so that it is lost into urine
22
Q

Androgens

A

type of steroid hormone that stimulates/controls the development and maintenance of male characteristics by binding to androgen receptors. Females do have some androgens too.

Androgens are precursors for all oestrogens.

e.g. testosterone, dihydrotestosterone (DHT), dehydroepiandrosterone (DHEA), androstenedione

23
Q

Hyperadrenocorticism

A

a condition characterised by excessive production of steroid hormones esp. glucocorticoids from the adrenal cortex.

a.k.a. Cushing’s

24
Q

Causes of canine HAC

A
  • Can be spontaneous or iatrogenic
  • Iatrogenic: dog on excessive steroid therapy
  • Spontaneous: may be pituitary-dependent or adrenal-dependent.
25
Q

Differentiate between adrenal- and pituitary-dependent HAC

A
  • Pituitary-dependent (PDH): 80-90% cases. Excess ACTH secretion results in bilateral adrenal hyperplasia.
  • Adrenal-dependent (ADH): 10-20% cases. Adenomas or carcinomas. These are independent of pituitary control so there is low circulating ACTH.
26
Q

Which is usually harder to control - PDH or ADH?

A

ADH

27
Q

Of canine PDH, where do the majority of tumours arise from?

A
  • 70% pars distalis
  • 30% pars intermedia
28
Q

Which type of canine HAC does this diagram depict?

A

Pituitary-dependent HAC
In this type of HAC, normal negative feedback mechanisms fail

29
Q

Which type of canine HAC does this diagram depict?

A

Adrenal-dependent HAC

Unilateral adrenal enlargement which causes atrophy of the contralateral side. This is independent of ACTH control (ACTH is low or undetectable because the pituitary gland is normal and responds to negative feedback).

30
Q

Signalment for canine PDH

A
  • Generally seen in middle-aged dogs (7-9 years)
  • Poodles, dachshunds and small dogs more predisposed to PDH
  • No sex predispositions
31
Q

Signalment for canine ADH

A
  • Generally seen in older dogs (11-12 years)
  • Larger breed dogs appear more at risk
  • Females slightly more at risk
32
Q

Describe the classic canine HAC presentation

A
  • Small, terrier-type dog with pot-bellied appearance and hairloss
  • Signs develop over time and may be dismissed as “just ageing”
  • Signs may be intermittent and may take a while for client to notice
33
Q

Clinical signs of canine HAC

A
  • PUPD
  • Polyphagia
  • Abdominal enlargement
  • Hepatomegaly
  • Skin changes
  • Muscle wasting/weakness
  • Lethargy/exercise intolerance/panting
  • Repro changes if entire
34
Q

Give the thresholds for PUPD in canine HAC and explain with PUPD is seen with this disease

A

Polydipsia (PD) >100ml/kg/day

Polyuria (PU) >50ml/kg/day

Polydipsia occurs secondary to polyuria. Polyuria mechanism not fully known but likely due to antagonism of ADH and increased GFR stimulated by cortisol.

35
Q

Why does abdominal enlargement occur in a dog with HAC?

A
  • Redistribution of fat into the abdomen + hepatic enlargement + wasting/weakness of abdominal muscles
36
Q

Why does polyphagia occur in a dog with HAC?

A
  • Assumed to be a direct effect of the glucocorticoids
  • May progress to scavenging → dog often treated for worms prior to diagnosis
37
Q

Describe the skin changes seen with canine HAC and why they occur

A
  • Bilaterally symmetrical alopecia → caused by inhibitory effect of steroids on anlagen phase
  • Thin skin and reduced elasticity with prominent abdominal veins → caused by protein catabolism (e.g. of collagen) and loss of subcutaneous fat
  • Excessive scale and comedomes
  • Slow wound healing → caused by inhibition of fibroblast proliferation and collagen synthesis
  • Secondary pyoderma common → immune system is largely suppressed so infections are more common
  • May see calcinonsis cutis (calcification of soft tissue inc. skin; evident on biopsy)
38
Q

What are the treatment options for canine HAC?

A
  • Surgery: adrenalectomy or hypophysectomy. Cannot survive with adrenals so will need replacement therapy.
  • Drugs:
    • Trilostane (licensed): reversal enzyme inhibitor that blocks cortisol production
    • Mitotane: causes chemical ablation of adrenal cortex but spares medulla
39
Q

Describe the characteristics of feline HAC

A
  • Rare: cats are resistant to the effects of most glucocorticoids
  • Signalment: middle-aged to older cats
  • 75-80% cases PDH, 20-25% ADH
  • Clinical signs: PUPD, polyphagia, pendulous abdomen, weight loss, extreme skin fragility, UTIs.

ENI (11 decks)

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