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ENI > Hyper/Hypoadrenocorticism > Flashcards

Hyper/Hypoadrenocorticism Flashcards

1
Q

Where are the adrenals located?

A

The adrenal glands are Located at the cranial pole of the kidneys within the retroperitoneal space
Elongated and are often asymmetrical, being moulded around the neighbouring vessels

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2
Q

Will adults or juveniles have larger adrenals?

A

Size varies greatly and generally those of juveniles are larger than adults

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3
Q

How big are a medium sized dogs adrenals?

A

A medium-sized dog’s adrenals will on average measure 2.5 x 1 x 0.5cm

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4
Q

What do the zones of the adrenals produce?

A

Medulla: Catecholamies
Cortex:
Zona glomerulosa- Mineralocorticoids
Zona fasciculata- Glucocorticoids (some adrogens)
Zona reticularis- Androgens (some glucocorticoids)

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5
Q

The medulla is made up of what kind of tissue?

What does it contain?

A

It consists of Neuroendocrine tissue and contains Sympathetic ganglion cells

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6
Q

What are catecholamines?

A

Epinephrine (adrenaline)

Norepinephrine (noradrenaline)

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7
Q

What is the blood supply to the adrenals?

A

Adrenals supplied by superior, middle, and inferior suprarenal arteries which branch before entering adrenal capsule.
Within the capsule, arteries branch to give three patterns of blood distribution:
Capsular capillaries
Cortical fenestrated capillaries
Medullary arterioles

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8
Q

The cortex of the adrenals is supplied by what type of capillaries?

A

Cortical fenestrated capillaries supply cortex and drain into medullary fenestrated capillaries

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9
Q

The medulla of the adrenals is supplied directly by what?

A

Medullary arterioles go directly to medulla

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10
Q

Define glucocorticoids

A

A class of steroids hormones that bind to the glucocorticoid receptor. The name glucocorticoid (glucose + cortex + steroid) derives from its role in the regulation of the metabolism of glucose, its synthesis in the adrenal cortex and its steroidal structure

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11
Q

Define mineralocorticoids

A

Mineralocorticoids (e.g. aldosterone): A class of steroid hormone characterised by their effects on salt and water balance. The name mineralocorticoid derives from early observations that these hormones were involved in the retention of sodium (a mineral)

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12
Q

What controls glucocorticoid release?

A

Within the hypothalamus there are neurones called the “paraventricular nuclei”
These synthesise and release corticotrophin releasing hormone, or CRH
This control is partly diurnal but also highly influenced by a negative feedback pathway, based on circulating cortisol levels.

When required, CRH is transported down axons to the median eminence. Here the neurones terminate in the “portal capillary bed”
The CRH is then released and travels via the pituitary portal blood system to the pars distalis in the anterior pituitary
Once CRH is in the anterior pituitary, it causes cells called corticotrophin cells to make and release ACTH

ACTH is synthesized from pre-pro-opiomelanocortin (pre-POMC).

ACTH then travels through the systemic circulation to the adrenal glands where is stimulates the adrenal cortex to make glucocorticoid steroid hormones, predominantly cortisol

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13
Q

What controls mineralocorticoid release?

A

Main stimulus for aldosterone release is low blood pressure-RAAS
High serum potassium also stimulates release
Role of ACTH only minor

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14
Q

What does over secretion of glucocorticoids cause?

A

hyperadrenocorticism (HAC)

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15
Q

Under secretion of glucocorticoids and mineralocorticoids is called…

A

primary hypoadrenocorticism (Addison’s)

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16
Q

Once released what happens to 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 transported to the nucleus
Here the complex binds to glucocorticoid response elements (GRE)
Resulting in altered gene expression

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17
Q

What are the effects of glucocorticoids on metabolism?

A

Stimulates gluconeogensis
Stimulates glycogenolysis
Causes proteolysis
Promotes lipolysis

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18
Q

What are the effects of glucocorticoids on fat?

A

Mobilisation from peripheral stores

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19
Q

What are the effects of glucocorticoids on muscle?

A

catabolism of muscle

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20
Q

What are the effects of glucocorticoids on the liver?

A

Gluconeogenesis

Antagonise insulin

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21
Q

What are the effects of glucocorticoids on the kidney?

A

Increased GFR

Block ADH action

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22
Q

What are the effects of glucocorticoids on the skin?

A

Follicular atrophy

Sebaceous gland atrophy

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23
Q

What are the effects of glucocorticoids on bone?

A

Reduce calcium levels

Osteopaenia (loss of protein and mineral)

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24
Q

What are the effects of glucocorticoids on the brain?

A

Causes hunger and thirst

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25
Q

What are the effects of glucocorticoids on the immune system?

A

Release neutrophils from marginated pool

Down regulates immune response

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26
Q

What are the effects 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 secretion of H+ in exchange for K+ in the collecting tubules, so regulating acid/base

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27
Q

What are androgens?

A

Androgens are also steroid hormones
Androgens are precursors for all oestrogens
Stimulate or control the development and maintenance of male characteristics by binding to androgen receptors

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28
Q

What are the most important androgens?

A

Testosterone
Dihydrotestosterone (DHT)
Dehydroepiandrosterone (DHEA)
Androstenedione

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29
Q

Androgens can be given as anabolic steroids to increase appetite and body weight as they cause…

A

Protein synthesis from amino acids
Increase muscle fiber size
Increase bone growth and remodeling

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30
Q

Hyperadrenocorticism is aka…

A

Cushing’s disease

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31
Q

In dogs Hyperadrenocorticism (HAC) has two forms…

A

Pituitary-dependent (PDH) 80-90% cases

Adrenal-dependent (ADH) 10-20% cases

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32
Q

What does Pituitary-dependent HAC cause?

A

Excess ACTH secretion and bilateral adrenal hyperplasia

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33
Q

In adrenal dependant HAC, ACTH levels are ………………., why?

A

ACTH concentration low or undetectable as these are Independent of pituitary control so cortisol production is independent of ACTH

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34
Q

What is the signalment for adrenal dependent HAC?

A

Generally seen in older dogs (median 11-12 years)
Larger breed dogs appear more at risk
Females slightly more at risk

35
Q

What is the signalment for pituitary dependent HAC?

A

PDH seen in middle-aged dogs (median 7-9 years)
Poodles, Dachshunds and small Terriers predisposed to PDH
No sex predisposition for PDH

36
Q

What are the clinical signs of HAC?

A 
PU/PD (most cases)
Abdominal enlargement (pot belly) 
Polyphagic
Hepatomegaly
Muscle wasting/weakness
Lethargy/exercise intolerance / panting
Skin changes (alopecia)
Reproductive changes
Calcinosis cutis
37
Q

What causes the pot belly in HAC

A

Re-distribution of fat into the abdomen
Hepatic enlargement
Wasting and weakness of abdominal muscles

38
Q

What causes the muscle wasting in HAC?

A

Caused by protein catabolism

Decreased muscle mass apparent over limbs, spine and temporal region

39
Q

What causes changes to the skin in HAC?

A

Thinning and reduced elasticity causes prominent abdominal veins
Due to protein catabolism (atrophic collagen) and loss of subcutaneous fat

The animal also has Excessive scale and comedones and is Easily bruised

40
Q

What is calcinosis cutis?

A

Firm, slightly elevated plaques surrounded by erythema
Secondary infection common
Neck, axilla, ventral abdomen and inguinal areas

41
Q

What is the signalment for feline HAC?

A

Rare
middle aged to older cats
Approx 75-80% due to PDH and 20-25% due to ADH

42
Q

Pituitary Hyperadrenocorticism (HAC) in horses is also known as…

A

Pituitary Pars Intermedia Dysfunction (PPID)

43
Q

What hormones have a positive and negative effect on POMC breakdown?

A

CRH and ADH have a positive effect on this, a dopamine has a negative effect

44
Q

So in horses how does PPID cause Hyperadrenocorticism?

A

In PPID there is a pars intermedia adenoma which causes excessive production of POMC’s derived peptides eg. ACTH and from that arises Hyperadrenocorticism

45
Q

How does dopamine control POMC?

A

D2 dopamine receptors cause Inhibition of expression of POMC mRNA expression and POMC hormone release from the pars intermedia

46
Q

What are the symptoms of PPID?

A 
Hirsutism 
Weight Loss/wastage 
PU/PD
Laminitis
Recuuring infections
Pot belly
Lethargy
Neorlogical signs eg narcolepsy and blindness
Infertility
47
Q

What causes Hirsutism in PPID?

A

Chronic elevation of MSH

48
Q

What causes PU/PD in PPID?

A

Pituitary compression induces decreased secretion of ADH
ACTH/cortisol inhibit ADH action
Hyperglycaemia/glucosuria osmotic diuresis

49
Q

What causes laminitis in PPID?

A 
High glucocorticoid concentration
Persistent hyperinsulinaemia (high levels of insulin) and persistent hyperglycaemia
50
Q

What causes the recurring infections in horses with PPID?

A

Increased concentration of immunosuppressive hormones: Cortisol / α-MSH / β-endorphins

51
Q

What causes the lack of muscle and pot belly in horses with PPID?

A

Glucocorticoids have catabolic effect of skeletal muscle

52
Q

What causes the lethargy in horses with PPID?

A

Increased β-endorphin

53
Q

What causes the narcolepsy and blindness in horses with PPID?

A

Blindness: ± compression of optic chiasm
Narcolepsy: unknown but could be Lack of dopaminergic control

54
Q

In horses the pars intermedia is more active in …………………. so we should avoid using the resting ACTH test then

A

Aug-oct

55
Q

When testing for PPID and using the resting ACTH what can give us false negatives and positives?

A

False negatives: Sample not stored properly (chilled and separated ASAP), not accounting for season, early PPID

False positives: Stress and pain

56
Q

Why do we not use base cortisol levels in diagnosing PPID?

A

Often normal with PPID, large variation throughout the day

57
Q

How to we do a TRH mediated ACTH response when testing for PPID?

A

Baseline blood sample, Administer 1mg TRH, o Blood sample 10/30 minutes later, Measure ACTH concentration.

With PPID ACTH concentration is >100pg/mL after TRH
NOT SUITABLE JULY TO NOVEMBER

58
Q

What tests do we do for PPID?

A

Resting ACTH
TRH mediated ACTH response
Combined DST-TRH test
Resting insulin

59
Q

How do we do a combined DST-TRH test when diagnosing PPID?

A

Take a baseline blood sample, IV dexamethasone, sample 3 hours later and give IV TRH, blood sample 30 mins later and then 24h after dex

60
Q

To use resting insulin for PPID testing what must we rule out?

A

Need to rule-out Equine Metabolic Syndrome

61
Q

In a biochemistry profile for a HAC dog, what will be elevated and what will be reduced?

A 
ALP- alkaline phosphatase (usually marked) in > 90% cases as its induced by steroids.
ALT (mild-moderate)
Cholesterol
Bile acids (mild-moderate)
Fasting glucose
Parameters reduced
Urea (BUN)
62
Q

In urinalysis of a dog with HAC what is the protein: creatine ratio?

A

> 1 in half of dogs

63
Q

What tests can we use to screen (does this animal have HAC?) small animals?

A
  1. Urinary cortisol:creatinine ratio
  2. ACTH stimulation test
  3. Low dose dexamethasone suppression (LDDS) test
  4. 17 alpha-OH progesterone
64
Q

Is urine cortisol:creatinine good for snout or spin?

A

Snout

A low ratio make HAC extremely unlikely

65
Q

Is the ACTH stimulation test good for spin or snout?

A

Spin

So Don’t exclude HAC if negative

66
Q

How do you carry out an ACTH stimulation test for small animals?

A

Starve overnight
Collect heparin sample time 0
Inject synthetic ACTH i.v
Collect second sample 30-60 minutes later into heparin tube again

A positive result is very high cortisol after 30-60 min

67
Q

Is low dose dex good for snout or spin?

A

Snout, detects 90-95% of cases.

68
Q

How do you carry out a low dose dex test?

A

Starve overnight
Collect baseline heparin sample
Inject 0.01mg/kg dexamethasone i.v
Collect heparin samples at 3 and 8 hours

‘Positive result’ = cortisol > 50 nmol/l at 8 hours as negative feedback fails

69
Q

How do we differentaite between adrenal dependant HAC and pituitary dependant HAC?

A 
1. Endogenous ACTH
PDHAC = increased ACTH
ADHAC = decreased ACTH
2. Adrenal imaging
3. Pituitary imaging
70
Q

Hypoadrenocorticism is aka…

A

Addison’s disease

71
Q

Renin release is stimulated by..

A

Baroreceptors in the wall of the afferent arteriole
Cells of the macula densa in the early distal tubule which are stimulated by a reduction in Cl delivery
Cardiac and arterial baroreceptors

72
Q

What does renin do?

A

Renin carries out the conversion of angiotensinogen to angiotensin 1

73
Q

What enzyme converts angiotensin I to angiotensin II?

A

Angiotensin I is converted to angiotensin II by the enzyme ACE from pulmonary and renal endothelium

74
Q

What are the effects of angiotensin II?

A 
Increase sympathetic activity
Increase tubular reabsorbtion of Na/Cl
Increase tubular excretion of K 
Arteriolar vasoconstriction
Aldosterone secretion
ADH secretion
75
Q

What causes Addison’s in dogs?

A

Idiopathic atrophy-
probably immune-mediated destruction

Iatrogenic caused by prolonged use of Exogenous steroids

76
Q

What is the signalment for Canine hypoadrenocorticism?

A

Young-middle aged dogs. Median age 4-6 years

poodles, bearded collies, leonberger, great Dane, WHWT and Rottweiler

77
Q

What does hypoadrenocorticism cause?

A

Aldosterone deficiency

Glucocorticoid deficiency

78
Q

What are the clinical signs of chronic hypoadrenocorticism?

A

Anorexia, vomiting, diarrhoea, PU/PD, weakness, lethargy, depression and weakness

79
Q

What are the clinical signs of acute hypoadrenocorticism?

A

Usually collapsed or extremely weak
May have recent history of V+/D+
Signs caused by hypovolaemic shock
MAY have paradox of relative bradycardia (due to hyperkalaemia)

80
Q

What is the CBC of a dog with hypadrencorticism look like?

A

Lack of stress leucogram (so no neutrophilia or lymphopenia)

Anemia: decreased erythrocytosis due to lack of cortisol

81
Q

What does the biochemistry profile of a dog with hypadrencorticism look like?

A

hyperkalaemia (increased K+)
hyponatraemia (Decreased Na+)
hypochloridaemia (Decreased Cl-)
Na:K ratio <23

Due to aldosterone deficiency:
Decreased renal tubular resorption of Na+ and Cl
Decreased excretion of K+ (and H+)

82
Q

What does the urinalysis of a dog with hypadrencorticism look like?

A

Urinalysis will show a decreased urine specific gravity

83
Q

What does the electrocardiogram of a dog with hypadrencorticism look like?

A

bradycardia, peaked T waves, widened QRS complexes, P wave amplitude or disappearance of P waves, ventricular asystole (failure to contract)

ENI (33 decks)

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