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Hyperadrenocorticism Flashcards

1
Q

Where is CRH synthesised and released?

A

Paraventricular nuclei in the hypothalamus

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2
Q

Exlain how ACTH stimulates glucocorticoid production and release

A
  • Transported in blood via transport proteins to adrenal cortex
  • Stimulates cholesterol uptake by adrenal gland
  • Upregulation of enzymes
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3
Q

What is the effect of cortisol onthe HPA axis?

A

Negative feedback

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4
Q

What are the causes of hyperadrenocorticism?

A
  • Spontaneous or iatrogenic

- Spontaneous can be either pituitary or adrenal dependent

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5
Q

Compare the incidence of pituitary vs adrenal dependent hyperadrenocorticism

A
  • 80-90% pituitary

- 10-20% adrenal

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6
Q

Describe pituitary dependent HAC

A
  • Often pituitary tumour
  • Bilateral hyperplasia of glands
  • Microadenomas in 80% of cases, macroadenomas also potential
  • Can arise from pars distalis (70%) or pars intemedia (30%)
  • Lots of stimulation, more cortisol, but will not respond to negative feedback as tumour is autonomous
  • Decrease in CRH as negative feedback via long loop
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7
Q

Describe adrenal dependent HAC

A
  • Adrenal tumout
  • Unilateral enlargement (atrophy of contralateral gland)
  • Negative feedback, reduced ACTH so atrophy of opposite but tumour side is autonomous
  • Independent of pituitary control
  • ACTH concentration very low or undetectable
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8
Q

How can pituitary and adrenal HAC be distinguished?

A
  • Hormone levels

- Imaging

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9
Q

What are the physiological changes that occur in HAC?

A
  • Increased cortisol
  • Protein and fat mobilisation
  • Stimulates gluconeogenesis
  • Stimualtes glycogenolysis
  • Stabilises lysosomes
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10
Q

Describe the signalment for adrenal dependent HAC in dogs

A
  • Older dogs (11-12 years)
  • Larger breeds (>20kg)
  • Females more at risk
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11
Q

Describe the signalment for pituitary dependent HAC in dogs

A
  • Middle aged dogs (7-9 years)
  • Poodles, dachshunds and small terriers predisposed
  • No sex predisposition
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12
Q

Give the clinical signs of canine HAC

A
  • PU/PD
  • Abdominal enlargement (pot belly)
  • Polyphagic
  • Muscle wastage/weakness
  • Thin skin
  • Hair loss
  • Hepatomegaly
  • Lethargy/exercise intolerance/panting
  • Skin cahnges
  • Reproductive changes
  • Calinosis cutis
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13
Q

Outline the physiological basis of PU/PD in canine HAC

A
  • Antogonism of ADH, increased glomerular filtration rate, inhibition of ADH release
  • However is still unclear
  • PD secondary to PU
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14
Q

Outline the physiological basis of pot belly in canine HAC

A
  • Redistribution of fat into abdomen
  • Hepatic enlargement
  • Wasting and weakness of abdominal muscles
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15
Q

Outline the physiological bases of polyphagia in canine HAC

A
  • Assumed to be direct effect of glucocorticoids

- Making up for use of stores through action of cortisol and stimulated hunger by cortisol

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16
Q

Outline muscle wasting/weakness in canine HAC

A
  • Usually gradually, incorrectly considered normal ageing
  • Protein catabolism
  • Decreased muscle mass over limbs, spine and temporal region
  • Excessive panting
  • Myotonia seen occasionally
  • Affected limbs are rigid and extend rapidly after passive flexion
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17
Q

Describe some of the skin changes that occur with canine HAC

A
  • Thinning and reduced elasticity
  • Prominent abdominal veins
  • Due to protein catabolism (atrophic collagen) and loss of subcut fat
  • Excessive scale and comedones
  • Change in hair coat colour
  • Easily bruised
  • Wound healing slow
  • Alopecia (normally symmetrical)
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18
Q

Why is wound healing slow in canine HAC?

A

Cortisol inhibits fibroblast proliferation and collagen synthesis

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19
Q

Describe what is meant by calcinosis cutis and how it occurs

A
  • Less obvious clinically, more on biopsy
  • Firm, slightly elevated plaques surrounded by erythema, secondary infection common
  • Neck, axilla, ventral abdomen and inguinal areas
  • Due to increased calcium uptak efrom gut, alteration in liver metabolism of calcium
  • Deposition in skin and other organd
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20
Q

What are some complications with canine HAC?

A
  • Are common!
  • Urinary tract infections (decreased immune function)
  • Glomerulonephropathies (increased GFR)
  • Hypercoagulability
  • Hypertension
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21
Q

Describe feline HAC

A
  • Uncommon
  • Skin fragile and rips
  • middle aged to older cats
  • Most PDH, 20-25% ADH
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22
Q

Describe the symptoms of feline HAC

A
  • PU/PD
  • Polyphagia
  • Weight loss
  • Extreme skin fragility
  • Pot belly
  • UTIs
  • Diabetes mellitus
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23
Q

What cell type is found in the pars intermedia?

A

Melanotrophs

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24
Q

What hormones are produced by the pars intermedia

A
  • POMC as precursor
  • ACTH (ony 2% of total normal production of ACTH!)
  • alpha-MSH
  • CLIP
  • beta-endorphin
  • beta-MSH
  • beta-LPH
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25
Q

What is the role of MSH?

A

Regulation of appetite, sexual behaviour and melanin production

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26
Q

What is the role of CLIP?

A
  • Corticotropin-like intermediate lobe peptide

- Modulation of pancreaitic enzyme function

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27
Q

What is the role of beta-endorphin?

A

Behaviour (docility)

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28
Q

What is the role of beta-lipotrophin?

A
  • Melanin production

- Steroidogenesis and lipolysis

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29
Q

Outline the control of POMC production

A
  • Dopamine has negative feedback on POMC production Removal of negative feedback then have constant stimulation of production
  • CRH and ADH have stimulatory effect
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30
Q

How is ACTH produced from POMC?

A

Cleavage by prohormone convertase 1

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31
Q

What is the effect of excess ACTH

A

Increased stimulation of adrenal glands to produce excess cortisol secretion

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32
Q

What is the name given to hyperadrenocorticism in the horse?

A
  • Pituitary pars intermedia dysfunction

- aka Equine Cushing’s disease

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33
Q

What is the cause of PPID?

A
  • Pars intermedia leads to excessive production of POMCs and so the derived peptides
  • Leads to hyperadrenocorticism
  • Lack of inhibitory control on pars intermedia cell function is what permits development of adenomas
  • Neurodegeneration of paraventricular neurones due to oxidative stress (impaired negative feedback)
  • Decreased peripheal cleavage of POMC peptides which remain active
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34
Q

Explain how hypothalamic dopamine has inhibitory control on the pars intermedia cell function

A
  • Binds to D2 receptors

- Control of POMC mRNA expression and POMC release

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35
Q

Give the clinical signs of PPID (top 3 first)

A
  • Hirsutism
  • Weight loss/wastage
  • PU/PD
  • Laminitis
  • Recurring infections
  • Poor performance
  • Regional adiposity (pot belly)
  • Fat pads on eye socket
  • Docility/lethargy
  • Neurologic signs (blindness, narcolepsy)
  • Infertility
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36
Q

Describe the physiological basis of hirsutism in PPID

A
  • Do not shed coat
  • Poorly understood
  • Chronic elevation fo MSH
  • Pituitary compression of hypothalamic thermoregulatory centre
  • Increased production of androgens
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37
Q

How does PPID lead to laminitis?

A
  • High glucocorticoid concentration

- Persistent hyperinsulinaemia and persistent hyperglycaemia

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38
Q

How does PPID lead to PU/PD

A
  • Poorly understood
  • Pituitary compression inducing reduced secretion of ADH
  • ACTH/cortisol inhibiting ADH action
  • Hyperglycaemia/glycosuria leading to osmoti diuresis
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39
Q

How does PPID lead to weight loss/fat mobilisation?

A
  • Pot bellied appearnce, swayback, abnormal fat deposits

- Glucocorticoids have catabolic effect on skeletal muscle

40
Q

How does PPID lead to lethargy/increased docility?

A
  • beta-endorphin increase

- Doping effect on brain

41
Q

How does PPID lead to neurologic impairment?

A
  • Blindness due to compression of optic haism
  • Narcoplespy (cause unknown, may be due to lack of dopaminergic control and hus decreased orexin that regulates sleep-wake cycles)
42
Q

How does PPID lead to immunesuppression and give examples of common conditions

A
  • Increased concentration of immunosuppressive hormones (cortisol, alpha-MSH, beta-endorphin)
  • Typically skin infections, sinusitis, cellulitis
43
Q

Describe the epidemiology of PPID

A
  • Older horses (15-30% of horses >15 years)
  • Minimum 7 years of age
  • Ponies predisposed
  • No gender prevalence
  • Often pituitary microadrenomas and adenomas found at post mortem in horses with no clincal signs
44
Q

What is included when diagnosing PPID?

A
  • History
  • Physical examination
  • Biochemistry
  • Hormone testing
  • Diagnostic imaging
45
Q

What would you expect to find in the history of a horse with PPID?

A
  • Respiratory infection, sinusitis
  • Old
  • pottery when walking
  • Lost weight
  • Changes in demeanour, PU/PD
46
Q

What would you expect to find on biochemistry of a horse with PPID?

A
  • Hyperglycaemia/hyperinsulinaemia
  • Hypertriglyceridemia
  • Neutrophilia and relative lymphopaenia
47
Q

What tests can be done to diagnose PPID?

A
  • Resting ACTH
  • TRH stimulation test
  • Dexamethasone suppression test (DST, less common)
  • Combined DST-TRH
  • Insulin resistance tests
  • Test for POMC
48
Q

Describe resting ACTH in PPID diagnosis

A
  • Seasonal variation in normal levels (higher August to October) so cannot compare across seasons and need to know ref range
  • Collect sample and separate plasma ASAP
  • Submit chilled as is very sensitive to temperature
49
Q

What may cause false negatives in resting ACTH testing for PPID?

A
  • Incorrect storage
  • Early PPID
  • Not accounting for season
50
Q

What may cause false positive in resting ACTH testing for PPID?

A
  • Stress/pain (laminitis)

- Not accounting for season

51
Q

Describe the TRH mediated ACTH response test (now known as TRH stimulation test) in PPID testing

A
  • Relies on aberrant response of pit adenomas to TRH with subsequent further release of ACTH
  • Mechanism poorly understood
  • Sample baseline, measure ACTH, administer TRH IV, sample 30 mins later
  • In PPID, ACTH will be >100pg/mL after TRH
  • Not suitable July to November
  • Used where have normal ACTH but still suspect
52
Q

Describe the dexamethasone suppression test

A
  • OBSOLETE
  • Standard and overnight
  • In both would normally have suppression of plasma cortisol, no change if PPID
  • Avoid July to October
53
Q

Describe the old TRH stimulation test

A
  • Same as new, but measured cortisol concentration rather than ACTH
  • No longer recommended (unless in combination with DST)
54
Q

Describe the DST-TRH test for PPID

A
  • Indicated for subtle cases without obvious clinical signs
  • Baseline sample
  • Dex administered, sample 3 hours after dec (T2)
  • Sample 3 hours after TRH (T3)
  • sample 24 hours after dex (T4) i.e. 4 samples in total
  • Positive if cortisol >1ug/dL at 24 hours and cortisol at T2 >66% cortisol at T3
55
Q

Describe resting insulin testing for PPID

A
  • Evaluation of insulin resistnace
  • Reasonably sensitive, low specificity (EMS, stress, pain)
  • ## Negative prognostic value (higher risk of laminitis with IR)
56
Q

Discuss imaging in PPID diagnosis

A
  • CT, MRI may identify pituitary enlargement
  • CT: difficult positioning
  • MRI: hardly avaialble
  • Require GA, costly, poor sensitivity
57
Q

Explain why the ACTH stimulation test is not useful in PPID diagnosis

A
  • Will not stiulate cortisol production from maximally stimulated adrenal glands
  • Equine Cushing’s disease is central and not peripheral in origin
  • Horses do not get adreanl dependent Cushing’s
58
Q

What is the main treatment for PPID?

A
  • Administration of D2-agonists (pergolide, bromocriptine)
  • Ameliorates clinical signs of PPID
  • Decreases ACTH concentration in most cases
59
Q

Define polydipsia and give values for the dog and cat

A
  • Excessive water intake
  • Dog: >90-100ml/kg/day
  • Cat: >45ml/kg/day
60
Q

Define polyuria and give an approximate value

A
  • Excessive urine output

- >50ml/kg/day

61
Q

List factors external to an animal that would influence their water intake

A
  • Temperature
  • Activity level
  • Stress
  • Hunger
  • Humidity
  • Water content of diet
  • Drugs
  • Other diseases
  • Access to water
62
Q

Give the cause of primary nephrogenic diabetes insipidus

A

Congenital/familial lack of ADH receptors

63
Q

Give the potential causes of secondary nephrogenic diabetes insipidus

A
  • Acquired condition

- Several diseases/toxicities that interfere with binding of ADH to its receptors and/or its action in the kidney

64
Q

Give causes of central diabetes insipidus

A
  • Tumour or degeneration of hypothalamus/neurohypophysis preventing or reducing release of ADH
  • Idiopathic
  • Trauma
65
Q

List endocrinopathies that can cause secondary nephrogenic diabetes indipidus

A
  • Hyperadrenocorticisim
  • Hypoadrenocorticism
  • Hyperthyroidism
  • Hypercalcaemia
66
Q

List non-endocrine disease that can cause secondary nephrogenic diabetes insipidus

A
  • Chronic renal disease
  • Liver disease
  • Infection (sepsis, pyelonephritis, pyometra)
  • Drugs (diuretics
67
Q

Describe how exogenus ADH can be used to distinguish central from primary nephrogenic diabetes insipidus

A
  • In central: ADH would increase USG as are able to concentrate urine again as have corrected lack of ADH
  • In nephrogenic: no effect on USG as problem lies with nephrons and lack of ADH receptors
68
Q

Describe changes expected in biochemistry with HAC

A
  • High ALP (alkaline phosphatase, steroid induced)
  • Mid to moderate increase in ALT
  • Cholesterol incerase
  • Bile acids increased
  • Fasting glucose increase
  • BUN decreased
69
Q

Describe changes expected in complete blood count (CBC) with HAC

A
  • Stress response: neutophilia and lymphoenia

- Produced in reposne to increased steroids

70
Q

Describe changes expected in urinalysis with HAC

A
  • USG often <1.015 but can be hyposthenuric (<1.008)
  • UP:UC ratio >1
  • Proteinuria
  • Evidence of UTI (inflam cells, but may be reduced due to steroidal effects)
71
Q

Describe common radiographic findings in HAC

A
  • Hepatomegally, pot-bellied, calcinosis cutis, distended bladder (PUPD), adrenal enlargement/calcificationin ADHAC
  • On thoracic sometimes tracheal and bronchial wall mineralisation, pulmonary metastasis, osteoporosis
72
Q

Describe common ultrasonographic findings in HAC

A
  • Normal size woudl be 12-33mmx3-7mm
  • Hyperplastic adrenals large but normal echogenicity
  • Compare size of both glands
  • Thickness >7.5mm for left gland considered sensitive
  • Distinguish between ADHAC and PDHAC (unilateral vs bilateral enlargment)
  • May see evidence of metastatic disease in vena cava
73
Q

What are the features of HAC diagnosis?

A
  • Strong index of suspicion (sgnalment etc)
  • History
  • Thorough clinical examination
  • Blood test investigations (Biochem, CBC)
  • Urinalysis
  • Imaging
  • Specific diagnostic tests
74
Q

What are the 2 types of specific diagnostic tests for HAC?

A
  • Screening

- Differentiating (ADHAC or PDHAC?)

75
Q

What are the HAC screening tests?

A
  • Urinary cortisol:creatinine ratio
  • ACTH stimulation test
  • Low dose dexamethasone suppression (LDDS) test
  • 17-alpha-OH progesterone
76
Q

Describe urinary cortisol:creatine ratio in HAC diagnosis

A
  • Cortisol has diurnal variation
  • But ratio tells us what cortisol has been doing over last few hours
  • Low ratio makes HAC extremely unlikely i.e. high sensitivity
  • High ratio could be HAC but not necessarily i.e. low specificity
  • Good for ruling out but false positives possible
77
Q

Describe the ACTH stimulation test in HAC diagnosis

A
  • High sensitivity
  • Best specificity of screening tests
  • Good for ruling in disease
  • Starve overnight, baseline at any point in day (heparin sample) T0, admin ACTH IV, sample 30-60 min later (heparin tube)
  • Normal: pre-stim <200nmol/, post-stim:<600nmol/l
  • Positive: post-stim >600nmol/l
  • Supraphysiological admin of ACTH should lead to increased cortisol
  • Exaggerated response with Cushings (both forms)
78
Q

Describe the low dose dexamethasone test in HAC diagnosis

A
  • More sentitive, low specificity (more false positive)
  • Few false negatives
  • prolonged hospital stay
  • Starve overnight, collect baseline heparin sample, Admin dex IV, heparin samples 3 and 8 hours later
  • Measure cortisol in each
  • Normal: neg loops stimulated, endogenous cortisol reduced
  • Positive: cortisol not suppressed, >50nmol/l at 8 hours
79
Q

Describe the 17 alpha-OH progesterone test in HAC diagnosis

A
  • Measure intermediate steroid hormones in cortisol production pathway rather than cortisol
  • Assays available
  • Uncommon to be used in practice
80
Q

Explain the importance of differentiation between ADHAC and PDHAC

A
  • Different treatments
  • For ADHAC: adrenalectomy
  • ADHAC usually more resistant to treatment
  • PDHAC has better prognosis
  • With pituitary macroadenomas diagnosed ened to monitor for neurological signs
81
Q

List the HAC differentation tests

A
  • High dose dexamethasone suppression test
  • Endogenous ACTH
  • Adrenal imaging
  • Pituitary imaging
82
Q

Describe the high dose dexamethasone suppression test in HAC differentiation

A
  • Not good at differentiating but is calssed as one!
  • Same protocol as LDDS, but more dex
  • Theory: in PDHAC should inhibit pit ACTH secretion through negative feedback and suppress cortisol
  • Adrenocortical tumours are autonomous and thus cortisol not suppressed
  • But often fails to suppress PDH so no longer recommended
83
Q

Describe endogenous ACTH in HAC differentiation

A
  • ACTH measured
  • PDHAC should be high (pit tumour producing lots of ACTH)
  • ADHAC should be low (-ve feedback dur to high levels of cortisol from adrenal tumour)
  • Difficult sample to handle, needs to remain chilled
84
Q

Describe adrenal imaging in HAC differentiation

A
  • PDHAC: symmetrical enlargement and normal conformation
  • ADHAC: one enlarged gland and one atrophied gland
  • May see invasion of malignant tumour
85
Q

Describe pituitary imaging in HAC differentation

A
  • Uncommon
  • CT or MRI
  • 505 of dogs with PDHAC have detectable pit mass on MRI
  • Normal vs enlarged ot clearly defined
  • Contrast agent used to highlight tumour
86
Q

Describe diagnosis of feline HAC

A
  • Uncommon, diagnosis difficult
  • Urine cortisol:creatinine sensitive screening test
  • ACTH stim (but 50% cats have within reference range results)
  • LDDS test combined with ACTH stim more reliable
  • Usually concurrent diabetes mellitus
87
Q

Expain how PPID can lead to laminitis

A
  • Hyperinsulinaemia
  • Endothelial cell dysfunction (inhibition of NO release by endothelial cells, endothelin-1 synthesis and sympathetic nervous activation enhancing vasoconstriction)
  • Digital vasoconstriction takes place
  • Impaired glucose uptake from epidermal laminal cells
  • Altered epidermal cell function or mitosis
  • Matrix metalloproteinase activation
  • Pro-inflammatory/pro-oxidative state also in lamellar tissue
88
Q

Compare PPID and EMS

A
  • EMS = equine metabolic syndrome
  • Defined by presence of obesity, insulin resistance and predisposition to laminitis, younger animals, pro-inflammatory
  • PPID is loss of regulation of hormonal output from pars intermedia of pituitary gland
89
Q

Outline the diagnosis of EMS

A
  • Aim to confirm IR status combined with clinical signs and rule out PPID
  • Resting insulin and glucose measurement
  • Proxis of insulin sensitivity
  • Dynamic testing e.g. in-feed glucose challenge
  • Blood pressure measurement
  • Adipokine measurement (research)
90
Q

Desribe basal insulin/glucose measurement for EMS

A
  • Simple, cheap
  • High resting insulin highly suggestive of IR
  • Low insulin and high glucose point towards T2 diabetes
  • Little sensitivity and specificity
  • Affected by stress, whether fed or fasted and season (if at pasture)
91
Q

Describe the oral glucose challenge test for EMS diagnosis

A
  • Fast overnight
  • Administer non-glycaemic feed (chaff) with 1g/kg glucose powder orally
  • Measure insulin at 2h
  • Insulin >85IU/ml indicative of IR
92
Q

Describe the combine G-I test (CGIT) for EMS diagnosis

A
  • Fast overnight
  • Obtain basal glucose and insulin
  • Administer glucose
  • Measure glucose 1 min after admin then every 5 mins after for 45 mins, then every 15 mins for 2-3 hours
  • Measure insulin at 45 min
  • Prolonged hypercalcaemia suggests IR
  • High insulin at 45 mins suggests exaggerated insulin response
93
Q

What are the anatomical landmarks used to locate the adrenal glands on ultrasound?

A
  • Kidneys
  • Vena cava
  • Aorta
94
Q

What is the normal size of the adrenal glands in the dog?

A
  • Width upper limit: 7.5-10m

- Length: 20-30mm

95
Q

What is the normal size of the adrenal glands in the cat?

A
  • Width: 3/9-4.3mm

- Lenght: 10.7mm

96
Q

What ultrasonographic and radiographic signs, other than adrenomegaly, support a diagnosis of hyperadrenocorticism?

A
  • Hepatomegaly
  • Enlarged/displaced bladder +/- cystoliths
  • Dystrophic mineralisation of soft tissues e.g. kidney
  • Osteopaenia (thinning bones)
  • Adrenal mass
  • Excellent contrast on radiography due to intra-abdominal fat
  • Calcinosis cutis

Endo (30 decks)

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