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Veterinary medicine year 2 > Adrenal gland and HAC > Flashcards

Adrenal gland and HAC Flashcards

1
Q

Where is the adrenal gland located?

A

Next to the kidneys in the retroperitoneal space
Craniomedial on kidneys
Elongated and asymmetrical

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2
Q

Zones of the adrenal glands

A

Cortex - Zona reticularis, fasciulata, glomerulosa
Medulla

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3
Q

What do the zones of the adrenal gland secrete?

A

Medulla - catecholamines
Zona reticularis- androgens
Zona fasciulata- Glucocorticoids
Zona glomerulosa - mineralocorticoids

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4
Q

What % of the adrenal gland is made up of cortex and medulla?

A

Cortex = 80-90%
Medulla= 10-20%

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5
Q

What is the adrenal medulla made of and what does it originate from?

A

Made of neuroendocrine tissue
Originates from the autonomic nervous system
Has sympathetic ganglion cells

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6
Q

How are steroid hormones synthesised?

A

Cholesterol-> pregnenolone by P450 side chain cleavage
Pregnenolone converted into diff corticoids based on the zone
Rate limiting step is P450 as it is stimulated by ACTH

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7
Q

What kind of corticoid is cortisol?

A

GLucocorticoid

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8
Q

What corticoids are corticosteroids>

A

gluco and mineralocorticoids

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9
Q

What is ACTH releasing hormone also called?

A

CRH (Cortico tropin releasing hormone)

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10
Q

How is glucocorticoid release controlled?

A

CRH -> hypothalamus to portal capillary system
CRH = corticotrophin cells in AP release ACTH
ACTH in systemic circulation to adrenal glands to stim synthesis or glucocorticoids (mainly cortisol)

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11
Q

What is ACTH synthesised from?

A

Pro opio mealono cortin (POMC)

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12
Q

What action does POMC go through before the formation of polypeptides>

A

POMC undergoes post translation modifications before it is proteolytically cleaved to form polypeptides
First stage occurs in pars distalis releasing ACTH

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13
Q

What is the action of glucocorticoids?

A

Glucocort in blood w 90% bound to plasma protein
Bind to target cell membrane or cytosolic receptors
Receptor steroid complexes are transported to the nucleus
= ALTERED GENE EXPRESSION

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14
Q

Within the cell what is the role of glucocorticoids?

A

Stimulate gluconeogenesis and glycogenolysis
Cause proteolysis and lipolysis

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15
Q

Role of glucocorticoids on different organs

A

Fat - mobilisation from peripheral stores
Muscle catabolism
Liver - gluconeogenesis (oppose insulin)
Kidney- inc GFR block ADH
Skin - follicular atrophy
Bone - reduce Ca+
Brain- thirst and hunger

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16
Q

What is the role of glucocorticoids in the immune system?

A

Release neutrophils from marginated pool
Down regulates immune responses (T cells function and recruitment and B cell activation)

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17
Q

What type of corticoid is aldosterone?

A

Mineralocorticoid
Class of steroid hormone based on effect on salt and water balance

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18
Q

How is the release of mineralocorticoids controlled?

A

Main stim for aldosterone = Low BP
High serum potassium also stimulates release
Role of ACTH is minor

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19
Q

What are the functions of aldosterone?

A

Role in reg of BP
Acts on cells of DCT and collecting duct to inc reabsorption of Na. Ca and H20)
Stimulates the secretion of potassium into tubular lumen

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20
Q

What kind of hormones are androgens?

A

Steroid hormones
Stimulate development and maintenance of male characteristics

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21
Q

What are androgens precursors for?

A

Oestrogens

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22
Q

What are the most important androgens?

A

Testosterone
DHT
DHEA
androstenedione

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23
Q

What is Hyperadrenocorticism?

A

Excessive production of steroid hormones especially glucocorticoids
Clinical signs often relate to abnormal circulating concentrations of steroid hormones

Cushings

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24
Q

What is hypoadrenocorticism?

A

Under secretion of glucocorticoids and mineralocorticoids
Addisions

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25
Q

What are the 2 forms of hyperadrenocorticism?

A

iatrogenic
Spontaneous
- pit dependent and adrenal dependent

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26
Q

What is pituitary dependent HyperAC?

A

Most common 80-90% of cases
Excess ACTH secretion = bilateral adrenal hyperplasia

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27
Q

What is adrenal dependent HyperAC

A

10-20% of cases
Independent of pituitary control
Low ACTH

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28
Q

What pathology is seen with PD hyperAC?

A

Microadenomas <10mm in pars distalis or intermedia
Normal negative feedback mechanisms fail
Microadenomas are slow growing and cause neuro signs

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29
Q

What pathology is seen in AD hyperAC?

A

Unilateral adrenal enlargment cause atrophy on contralaterla side
Independent of ACTH( low or undetectable)
50% partly calcified regardless of tumour type

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30
Q

What is the signalment for AD and PD hyperAC?

A

AD = older dogs (females - larger dog breeds)
PD = middle aged dogs(poodle daschunds, terriers no sex predis)

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31
Q

Outline the development of hyperadrenocorticism

A

Onset usually insidious
Initially intermittent
Develops rapidly
Affects lots of organs (pretty much every system)

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32
Q

What are the clinical signs of hyper AC?

A

PU/PD
Pot belly
polyphagia
skin change
hepatomegaly
muscle wastage and weakness
lethargy
repro changes
panting

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33
Q

What causes the pot belly with hyper AC?

A

redistribution of fat into the abdomen
hepatomegaly
wasting and weakness of muscles

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34
Q

Why does PUPD occur with hyperAC?

A

Antagonism of ADH, inc GFR and inhibition of ADH

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35
Q

Why does polyphagia occur with hyperA?

A

direct effect of glucocorticoids

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36
Q

Why does muscle wastage occur with hyperAC?

A

Protein catabolism
decreased muscle mass esp over limbs, spine and temporal regions
Excessive panting and poor exercise toleranxe

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37
Q

Why does skin change with hyperAC?

A

Bilaterally symmetrical alopecia
Thin skin - reduced elasticity
Scale and comedones
Slow wound healing - inhibition of fibroblast proliferation and collagen

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38
Q

What are the treatments fore hyperAC?

A

Trilostane - hydroxysteroid dehydrogenase inhibitor
Mitotane- chemical ablation of adrenal cortex but medulla spared

Adrenalectomy or hypophysectomy (replacement therapy req)

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39
Q

What is the signalment and clinical signs for cats with hyperAC?

A

uncommon as cats are most resistant to effects of glucocorticoids
middle aged <
Approx 75-80% AD
Clinical signs
PUPD
skin fragility
Pendulous abdomen
UTI

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40
Q

Why is is difficult to diagnose hyper adrenocorticism?

A

AD and PD both inc cortisol levels in the same way as stress and chronic illness
PD affects pit gland AD affects adrenal

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41
Q

What tests would present a high suspicion index for hyperadrenocorticism?

A

Blood test - biochem and CBC
Urinalysis
Imaging
Specific diagnostic tests

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42
Q

What are the parameters that should change on blood test for hyperAC?

A

Elevated
- ALP
-ALT
- Cholesterol
- Bile acids
- fasting glucose
Reduced
- Urea (BUN)

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43
Q

Which CBC parameters would suggest hyperAC?

A

Neutrophilia - high
Lymphopenia - low

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44
Q

What should urinalysis show with hyperAC?

A

Low USG- hyposthenuric
UTI evidence

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45
Q

What are the radiogrphic findings with hyperAC?

A

Hepatomegaly
calcinosis cutis
distended bladder
adrenal enlargement/ calcified
Tracheal and bronchial wall mineralisation
Pulmonary metastasis
Osteoporosis

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46
Q

Osteoporosis

A

cause weak and brittle bones

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47
Q

What is the LDDS test?

A

Exogenous glucocorticoid administration should = reduced ACTH
Expected findings normal= cortisol release from adrenal
Spontanous HAC= reduced or absent response

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48
Q

What % of PDHAC and ADHAC should a highly sensitive LDDS test detect?

A

90-95%
positive result with low dose dexamethasone test = cortisol greater than 50nmol/l at 8 hours
Limited use at differentiating PD and AD HAC

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49
Q

Why is there a need to determine between PD and AD hyperAC?

A

AD more resistant to medical management
PD prognosis is better
AD - adrenalectomy = only option

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50
Q

What test differentiates between AD and PD hyperAC?

A

HDDS
Endogenous ACTH
Adrenal imaging
Pituitary imaging

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51
Q

What is the role of the HDDS test?

A

inc dose fo dex inhibits cortisol in some cases of PDH
in PD high dose inhibits pit ACTH secretion through neg feedback suppressing cortisol
Adrenocortical tumours are autonomous so cortisol is not suppressed as ACTH is already suppressed

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52
Q

Why is HDDS not used anymore?

A

25-30% of cases fail to suppress with HDDS

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53
Q

Why can endogenous ACTH be used to diagnose AD hyper AC? UNSURE

A

PDH falls within the normal range

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54
Q

What is the expected outcome for ADH and PDH with adrenal imaging?

A

PDH- symmetrically enlarged and normal conformation
ADH- will have one enlarged gland and one atrophied gland (may see invasion of malignant tumour)

55
Q

Why is pituitary imaging not used?

A

Needs CT or MRI but are both expensive
Size difference is not clearly defined
Useful if neruo signs are present as can look for large pituitary tumour

56
Q

What tests are required for PPID?

A

History and physical exam
Biochemistry - hyperglycaemia, hyperinsulinaemia, hypertriglyceridemia
CBC- neutrophilia and lymphopenia
Resting ACTH
TRH stim
DST
Combined DST-TRH test
Insulin
POMC

57
Q

What is the role of RAAS in the control of mineralocorticoid release?

A

Renin carried out angiotensinogen-> angiotensin I
ACE carries out Angiotensin I-> II
Angiotensin II= vasoconstrictor \
Angiotensin II= stimulates aldosterone release from adrenal cortex

58
Q

How is a decrease in BP detected?

A

Renin release stimulated by
1. baroreceptors in afferent arteriole
2. cells of macula densa in distal tubule
3. Cardiac and arterial baroreceptors

59
Q

What stimulates macula densa cells in DCT?

A

Stimulated by a reduction in NaCl delivery

60
Q

What is the function of aldosterone?

A

Regulates BP acting on distal tubules and collecting ducts
- Inc reabsorption of ions and water - conserving Na
Secretes potassium
Increase in water retention increases BV so BP

61
Q

What are the classifications for hypoadrenocorticism?

A

Primary - loss of adrenal cortex (addisons)
Secondary - deficiency of ACTH
Iatrogenic - exogenous steroids

62
Q

What occurs in primary HypoAC?

A

deficiency of glucocorticoids (cortisol) and a deficiency of mineralocorticoids (aldosterone)
Loss of 85-90% of the adrenal cortex

63
Q

What are the different causes of Addison’s disease in dogs?

A

Idiopathic atrophy, probably immune mediated destruction
Iatrogenic - Mitotane, trilostane, bilateral adrenalectomy

64
Q

How is iatrogenic hypoadrnocorticism characterised?

A

Exogenous steroids cause adrenal atrophy
Cortisol deficiency only
Patient may show signs of cushings
Patient may develop signs of addisons disease if steroids are abruptly discontinued
Can be life threatening

65
Q

WHat is the signalment for addisons disease?

A

Young to middle aged dogs
70% females
Any breed but breed dispositions
rare in cats

66
Q

Which breeds of dogs are predisposed to addisons?

A

Collies
bearded collies
Portuguese water dog
Leonberger
Great dane
Rottweiler
WHTH
soft coated wheaten terrier

67
Q

Outline the pathophysiology of hypoadrenocorticism?

A

Aldosterone deficiency = Loss of Na, Cl and H2O, retention of K+ and H+, Pre renal failure
Glucocorticoid deficiency= decreased stress tolerance , GI signs, weakness, appetite loss and impaired gluconeogenesis

68
Q

Compare chronic and acute hypoAC?

A

Chronic = waxing waning with non specific signs
Acute= addisonian crisis form with marked hypovolaemia and azotaemia

69
Q

What clinical signs are expected with chronic hypoAC?

A

Anorexia
Vomiting
Diarrhoea
PUPD
weakness
Lethargy
Depression

Appear normal between bouts esp after fluid therapy/ steroids

70
Q

What clinical signs are expected with acute hypoAC?

A

signs caused by hypovolaemic shock
Collapsed
Paradox of relative brachycardia caused by hypokalaemia
abdo pain caused by pancreatitis

71
Q

What clinical pathology is expected with hypoAC?

A

Lack of stress leucogram - no neutrophilia or lymphopenia
Anaemia
Lower erythrocytosis - lack of cortisol
GI blood loss

72
Q

What are the clinical findings for hypoAC on biochemistry?

A

hyperkalaemia
hyponatraemia
hypochloridaemia
Na:K ration <23

all due to aldosterone deficiency - dec renal tubular resorption of Na and Cl and dec excretion of K+

73
Q

What clinical pathology is expected with hypoAC and urinalysis?

A

Azotaemia ( inc renal parameters)
Hypoglycaemia - 27%
dec USG ( inappropriately low in dehydrated animal)

74
Q

What changes are seen on ECG with hypoAC?

A

Changes related to hyperkalaemia
- bradycardia
peaked T waves
Widened QRS
Decrease in P wave or disappearance
Ventricular asystole

75
Q

How is a hypoAC diagnosis made?

A

High index of suspicion
ACTH stimulation test
- Measure cortisol in flat line stimulation
Dex can be used prior to test as therapy

76
Q

How is hypoAC treated?

A

Mineralocorticoids
GLucocorticoids - in acute crisis or times of stress

77
Q

What is the embryological origin of the adrenal gland?

A

Neuroectoderm

78
Q

Phaeochromocytoma

A

Tumour that starts in the inner medulla of the adrenal gland

79
Q

What is meant by a functional tumour of the adrenal gland?

A

Produces hormones

80
Q

What structures may be invaded by an adrenal tumour?

A

Vena cava
Aorta
Kidney
Renal vessels

81
Q

Which receptors do epinephrine and nor epinephrine bind to?

A

Alpha and beta
2 types of alpha and 3 types of beta

82
Q

What do alpha 1 receptors activate?

A

Activate phospholipase which increases the activity of protein kinase 2

83
Q

What happens at alpha 2 receptors?

A

inhibition of catecholamine release, Inhibit adenylate cyclase which decreases the activity of protein kinase A

84
Q

What do Beta receptors activate?

A

Adenyl cyclase increasing the activity of protein kinase A

85
Q

What affect does catecholamine have on energy substrates?

A

Mobilise substrates of remediate energy - glycogenolysis, gluconeogenesis, lipolysis

86
Q

Which arm of the ANS is the adrenal gland associated?

A

Sympathetic

87
Q

What drug is appropriate for bronchodilation?

A

Clenbuterol

88
Q

What drug is appropriate for vasodilation?

A

Prazosin

89
Q

What drug is appropriate for sedation?

A

detomidine

90
Q

What clinical signs are associated with phaeochromocytoma?

A

Tachycardia
hypertension
Panting
Diarrhoea
Constibation
PUPD
Weight loss
Restlessness
High blood glucose - insulin resistance

91
Q

What are the 4 potentials used to differentiate between PDH and ADH?

A

Endogenous ACTH
LDDS
HDDS
Imaging adrenals
Imaging pituitary

92
Q

What separates the pituitary from the brain?

A

Diaphragma sell ( part of the dura mata)

93
Q

What do the cells of the pars distalis secrete?

A

Somatotrophs- GH
Lactotrophs - prolactin
Corticotrophs- POMC, ACTH, betalipotropin
Gonadotrophs- FSH and LH
Thyrotrophs- TSH

94
Q

What causes equine cushings disease?

A

A pars intermedia adenoma causes excessive production of POMCs-derived peptides

95
Q

What is the pathogenesis of PPID?

A

Lack of inhibitory control of pars intermedia cell function = adenoma
Inhibition mediated by hypothalamuc dopamine on D2
Neurodegeneration of periventricular neurones so impaired -ve feedback

96
Q

What is the role of D2 receptors?

A

inihibition of the expression of POMC mRNA expression and instead POMC hormone release

97
Q

Why do we treat PPID with D2 agonists?

A

PPID = dec peripheral cleavage of POMC peptides which remain active
D2 agonists fixes clinical signs of PPID and decreases ACTH conc in most cases

98
Q

What factors in other species other than horses can regulated melanotrope function?

A

TRH
Serotonin
GABA

99
Q

What are the clinical signs of PPID?

A

Hirutism
Weight loss
PUPD
Laminitis
Recurring infections
Poor performance
Pot belly
Docility
Neuro signs
Infertility

100
Q

What is hirtuism?

A

Coat does not shed
Occurs with PPID as chronic elevation of MSH, pit compression on hypothalamic thermo centre, inc production of androgens

101
Q

Why does laminitis occur with PPID?

A

high glucocorticoid conc
persistent hyperinsulinaemia and persistent hyperglycaemia = laminitis

102
Q

Why does PUPD occur with PPID?

A

Pit compression= decr secretion of ADH
ACTH inhibits ADH action
Hyperglycaemia causes osmotic diuresis

103
Q

Why does weight loss occur with PPID?

A

Glucocorticoids have a catabolic effect on skeletal muscles

104
Q

Why does lethargy occur with PPID?

A

Beta endorphin is increased

105
Q

Why does neuro impairment occur with PPID?

A

Blindness from compr of optic chiasm
Narcolepsy unknown

106
Q

Why is there impaired response to infection with PPID?

A

Inc conc of immunosuppressive hormones such as cortisol, alpha MSH, beta endorphin

107
Q

What predisposes a horse to PPID?

A

> 15 years
No gender prevalence

108
Q

Expectations of biochemistry of horse with PPID?

A

hyperglycaemia, hyperinsulinaemia
Hypertriglyceridaemia
Neutrophilia and lymphopaenia

109
Q

What can we test for with PPID?

A

resting ACTH
TRH stimulation
DST
Combined DST-TRH test
Insulin levels
POMC

110
Q

How is DST carried out for PPID?

A

Standard DST: Baseline at 8,12, 16, 20 ,24
40ug/kg dex IM
Normal horses fall to >30% of baseline cortistol concentration
Overnight DST: baseline 4-6pm
40ug/kg dex IM
Last sample 15-20 hours
Normal horses show suppression of plasma cortisol

111
Q

What is the TRH stim test testing for?

A

Cortisol
Relies on aberrant response of pit adenoma to TRH w subsequent further release of ACTH

112
Q

How is TRH stim test carried out?

A

Baseline blood sample is taken
1mg TRH is given IV
A blood sample is taken 30 mins later
Cortisol conc is then measured for both samples

113
Q

What would be PPID response to TRH stim test?

A

Cortisol concentration should inc by 25-50% in horses w PPID
Only 41 % sensitive 92% specificity

114
Q

What is the gold standard TRH test?

A

ACTH response to TRH
relies on abberant response of pitui adenoma to TRH w subsequent further release of ACTH
1. A blood sample is taken
2. 1mg of TRH is administered IV
3. Another blood sample is taken 10 minutes later
4. The ACTH concentration is measured
Pos = ACTH higher than 110mg/ml at 10 mins

Used for normal resting ACTH but high clinical suspicion
sens 77 spec 82

115
Q

How is the combined DST-TRH test carried out?

A

Baseline sample
Dexamethasone
Sample 3 hourse after dex + TRH
Blood sample 30 mins after TRH
Blood sample 24 hours after dex

Positive if cortisol is >1ug /dL

Sens 88 Spec 76

116
Q

What is resting insulin?

A

Evaulation of insulin resistance
Reasonable sensitivity low specificity
Need to rule out EMS

Negative prognostic value

117
Q

How can POMC be measured?

A

Beta-endorphin
Alpha MSG
CLIP
Disproportionately higher than ACTH in horses with PPID
Not validated in horses

118
Q

How can diagnosis of PPID be made via imaging?

A

CT, MRI , might identify pituitary enlargement
CT: difficult positioning
MRI: might be useful but hardly available
Require GA
Costly
Poor sensitivity

119
Q

Why is ACTH stimulation test not used in horses?

A

Iatrogenic ACTH will not stimulate cortisol production from the adrenal glands which are already maximally stimulated
Means that it is useless in horses because Equine cushings disease is central and not peripheral in origin

120
Q

What is the effect of catecholamines binding to alpha receptors?

A

Vasoconstriction
Pupil dilation
Intestinal relaxation
Pilomotor contraction
Bladder sphincter contraction

121
Q

What is the affect of catecholamines binding to Beta 1 receptors?

A

Increased heart rate
Increased contractility

122
Q

What is the affect of catecholamines binding to Beta 2 receptors?

A

Vasodilation
Bronchodilation
Glycogenolysis
Lipolysis

123
Q

What is the signal transduction of catecholamines?

A

Bind to receptors and activate second messengers
Often G protein coupled receptors

124
Q

Give some examples of pathways for signal transduction of catecholamines

A

Adenyl cyclase
Phospholipase C, IP3, DAG
Ion channels

125
Q

What is the function of adenyl cyclase beta receptors?

A
  1. Bind to cell surface receptor
    1. Activates G protein which stimulates adenylyl cyclase
  2. Generates cyclic AMP (cAMP)
  3. Activates protein kinase A
  4. The protein kinase A is phosphorylated
  5. this causes a biological response
126
Q

What are the affects of cAMP?

A

catalytic subunit of protein kinase A enters the nucleus

This binds to the cAMP-response element binding protein and phosphorlyates

CREB binds to CRE and changes gene expression

127
Q

What is the effect of cAMP on the heart?

A

Ca+ ion channel opening time is prolonged which in turn strengthnes the contractions
Increase uptake into SR at the end of contraction= shortens contraction

128
Q

What is the phospholipase C alpha receptor transduction pathway?

A

The hormone binds to the cell surface receptor
The activated phospholipas C via the G protein
Phospholipid PIP2 is broken down to IP and DAG

129
Q

Importances of medullary hormones

A
  • Medullary epinephrine and norepinephrine have the same general effects as the sympathetic nervous system
  • There is a widespread and simultaneous stimulation of tissue via nervous and endocrine systems
  • Medullary hormones result in additional effects on tissues without direct sympathetic innervation
  • For example- metabolic acitions appropriate fight or flight
130
Q

How do catecholamines affect stressed animals?

A

Stress hyperglycaemia can occur due to persistent activation of catecholamines that therefore increase the available blood glucose

131
Q

How does the metabolic effect of catecholamines increase fatty acid levels and why?

A
  1. Hormone-sensitive lipase (HSL) is stimulated by catecholamines
  2. Therefore the triglycerides stored in adipose tissues is hydrolysed to yield glycerol and three fatty acids
    this glycerol can be used for glucose
  3. Higher circulating plasma fatty acid levels are used for energy
132
Q

List the 3 importance of medullary epinephrine

A

Metabolic stimulus
Cardiac effects
Blood vessels within the muscle

133
Q

hat is the overall effect of norepinephrine?

A

Has a more profound effect on the blood vessels

This increases total peripheral resistance

Raises blood pressure

134
Q

What is the overall effect of epinephrine?

A

Has a more profound effect on the heart

Increases heart rate and contractility

This increases cardiac output

Veterinary medicine year 2 (23 decks)

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