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ENI 2 > the structure and function of the adrenal glands and pathophysiology of HAC > Flashcards

the structure and function of the adrenal glands and pathophysiology of HAC Flashcards

1
Q

where is the adrenal gland located ad decribe their appearance

A
  • next to the kidneys within the retroperitoneal space
  • cranial aspect of the kidneys
  • elongated and are often asymmetrical being moulded around the neighbouring vessels
  • size varies (juveniles are larger than adults)
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2
Q

describe the anatomy of the adrenal cortex

A
  • constitues 80-90% of gland
  • 3 zones: outisde to inside: zona glomerulosa, fasciculate and reticularis
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3
Q

what do the 3 zones of the adrenal cortex produces respectively

A

inside to outside:
1. zona glomerulosa = mineralcorticoids
2. zona fasciculate = glucocorticoids
3. zona reticularis = androgens

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4
Q

describe the adrenal medulla

A
  • only 10-20% of gland
  • neuroendocrine tissue
  • has sympathetic ganglion cells
  • secretes catecholamines
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5
Q

what does the adrenal medulla secrete

A

catecholamines
- adrenaline
- noradrenaline

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6
Q

discuss the synthesis of steroid hormones

A
  • synthesis of all steroid hormones begins with cholesterol
  • cholesterol is converted into pregnenolone by P-450 side chain cleavage enzyme (rate limiting step is activated by ACTH)
  • pregnenolone is converted into different corticoids according to the zone: glomerulosa = aldosterone, fasciculata = glucocorticoids, reticularis = androgens
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7
Q

what are glucocorticoids and give an example

A

example: cortisol
- metabolises glucose
- synthesized in the adrenal cortex
- steroidal structure

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8
Q

how is the release of glucocorticoids controlled

A
  • CRH is transported from the hypothalamus down axons to the portal capillary bed
  • CRH causes corticotropom cells in the anterior pituitary to make and release ACTH
  • ACTH travels through the systemic circulation to the adrenal glands where it stimulates synthesis of glucocorticoids (predominanatly cortisol)
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9
Q

discuss the importance of POMC in relation to ACTH

A
  • ACTCH is synthesized from pro-opiomelanocortin (POMC)
  • POMC undergoes a series of post translation modifications before it is proteolytically cleaved to yield various polypeptides with varying physiological actions
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10
Q

discuss the physiology of glucocorticoids

A
  • once released, glucocorticoids are transported in the blood, 90% bound to plasma proteins
  • they bind to specific cell membrane or cytosolic receptors at their target
  • these receptor-steroid complex is then trasnported to the nucleus
  • resulting in altered gene expression
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11
Q

how do glucocorticoids act

A
  • they are stress hormones
  • stimulate gluconeogenesis
  • stimulate glycogenolysis
  • causes proteolysis
  • promotes lipolysis
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12
Q

what are the actions of glucocorticoids on fat

A

mobilisation from peripheral stores

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13
Q

what are the actions of glucocorticoids on muscle

A

catabolism

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14
Q

what are the actions of glucocorticoids on the liver

A
  • gluconeogenesis
  • antagonise insulin
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15
Q

what are the actions of glucocorticoids on the kidneys

A
  • increased GFR
  • blocks ADH action
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16
Q

what are the actions of glucocorticoids on skin

A
  • follicular atrophy
  • sebaceous gland atrophy
17
Q

what are the actions of glucocorticoids on bone

A
  • reduces calcium levels
  • osteopaenia
18
Q

what are the actions of glucocorticoids on the brain

A
  • hunger
  • thirst
19
Q

what are the actions of glucocorticoids on the immune system

A
  • release neutrophils from marginated pool
  • down regulates immune response (T cell function and recruitment/B cell activation
20
Q

what are mineralcorticoids and give an example

A

example: aldosterone
- a class of steroid hormone characterised by their effects on salt and water balance. the name derives from their involvement in retention of sodium and mineral

21
Q

how is the release of mineralcorticoid controlled

A
  • main stimulus for aldosterone release is low blood pressure (RAAS)
  • high serum potassium also stimulates release
  • role of ACTH only minor
22
Q

what is the function of aldosterone

A
  • plays a central role in the regulation of BP
  • acts on cells of distal tubule and collecting duct to increase reabsorption of Na, Cl and hence water
  • stimulates the secretion of K+ into the tubular lumen
23
Q

what are androgens

A
  • steroid hormones
  • stimulate or control the development and maintenance of male characteristics by binding to androgen receptors
  • androgens are precursors for all oestrogens
  • most important androgens are: testosterone, dihydrotestosterone, dehydroepiandrosterone and androstenedione
24
Q

what is hyperadrenocoricism

A
  • a condition that can develop in all domestic species and is characterised by the excessive production of steroid hormones, especiall glucocorticoids, from the adrenal cortex
  • clinical signs therefore relate to abnormal circulating concentrations of steroid hormones
  • often called cushings disease
25
Q

discuss canine HAC and its prevalence

A
  • can be either spontaneous or iatrogenic (caused by tx)
  • spontaneous has 2 forms: pituitary dependent and drenal depedent
  • pituitary dependent = 80-90% of cases
  • in PDH, excess ACTH secretion results in bilateral adrenal hyperplasia
  • adrenal dependent = 10-20% of cases (either adenoma or carcinoma)
  • independent of pituitary control
26
Q

discuss PD HAC pathology

A
  • most arise from pars distalis, less from pars intermedia
  • normal negative feedback mechanism fails (tumour ignores feedback and keeps stimulating ACTH production)
27
Q

Discuss AD HAC pathology

A
  • unilateral adrenal enlargement which causes atrophy of contralateral side
  • independent of ACTH control
  • ACTH concentration low or undetectable (because high levels of cortisol circ so pituiatary doesnt need to produce)
  • approx 50% will be calcified regardless of tumour type (due to interaction btwn calcium and cortisol)
28
Q

discuss the common signalment of a dog with HAC

A
  • ADH in older dogs (11-12) PDH in middle aged (7-9)
  • poodles, dachshunds and small terriers predisposed to PDH
  • larger breeds appear more at risk for ADH
  • no sex predisposition for PDH, females slightly more at risk for ADH
29
Q

describe the clinical signs of HAC and when they are most commonly seen

A
  • more common in small breed dogs
  • onset usually insidious and disguised as “aging”
  • may be initially intermittent
  • can occasionally develop rapidly
  • affects multiple organs (liver, muscle, bone, kidneys, immune system, repro, etc)

Clinical signs:
- PU/PD
- Abdominal enlargement
- polyphagic
- skin changes
- hepatomegaly
- muscle wasting/weakness
- lethargy/exercise intolerance/panting
- repro changes

30
Q

list reasons for PU/PD in cushinoid dogs and relate them to the physiology

A
  • PD secondary to PU
  • antagonism of ADH, increased GFR and inhibition of ADH release
31
Q

list reasons for abdominal enlargement in cushingoid dogs and relate them to physiology

A
  • pot belly appearnace
  • re distribution of fat into the abdomen due to breakdown of fat caused by increased cortisol
  • hepatic enlargement
  • wasting and weakness of abdominal muscles (protein breakdown)
  • makes palpation of abdo easier
32
Q

list reasons for cuchingoid dogs having skin changes and relate them to the physiology

A
  • bilaterally symmetrical alopecia due to inhibitory effects of steroids on anagen phase of hair growth
  • thin skin and reduced elasticity with prominent abdominal veins due to protein catabolism and loss of SQ fat
  • excessive scale and comedones
  • slow wound healing due to inhibition of fibroblast proliferation and collagen synthesis
33
Q

what response woul you expect in a healthy dog if you injected them with ACTH

A

increase cortisol

34
Q

what would you expect to happen in a healthy dog if you injected them with glucocorticoids

A

decreased cortisol and ACTH production

35
Q

how is HAC treated

A
  • vetoryl (trilostane)
  • adrenalectomy or hypophysectomy (requires hormone replacement
36
Q

d

discuss feline HAC

A
  • uncommon
  • cats are more resistant to the effects of glucocorticoids
  • signalment = middle aged to older cats
  • most due to PDH
  • clinical signs same as in dogs

ENI 2 (81 decks)

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