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Michaelmas 5th year > Adrenal gland > Flashcards

Adrenal gland Flashcards

1
Q

What causes release of glucocorticoids

A

Paraventicular nuclei neurons within hypothalamus synthesise CRH and release it via pituitary portal blood system

CRH travels to pars distalis of anterior pituitary and stimulates corticotrophin cells to make ACTH

ACTH acts on adrenal cortex to cause glucocorticoid production

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2
Q

Layers of the adrenal cortex

A

Outer part = zona glomerulosa
Middle 60% = zona fasciculate
Inner part = zona reticularis

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3
Q

What are the types of hyperadrenocorticism

A

Spontaneous; including pituitary dependent and adrenal dependent

Iatrogenic

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4
Q

Characteristics of pituitary dependent hyperadrenocorticism

A

Excess ACTH secretion from the pituitary due to micro or macroadrenomas cause bilateral adrenal hyperplasia
Therefore get excess production of steroid hormones from adrenal cortex especially glucocorticoids

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5
Q

What are micro vs macroadenomas and which account for more PDH cases

A

Microadenomas are less than 10mm diameter; most cases
Macroadenomas are >10mm

Most arise from pars distalis; 1/3 from pars intermedia

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6
Q

What is the cause of adrenal dependent hyperadrenocorticism

A

even split between adenomas and carcinomas of one adrenal gland
- So see one enlarged gland with tumour; other is atrophied due to negative feedbacl

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7
Q

Signalment of PDH vs ADH

A

PDH mostly in middle aged dogs esp small breeds; poodles, terriers
ADH generally in older, larger breed dogs

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8
Q

Clinical signs of HAC

A

PU/PD
abdominal enlargement
Polyphagia
Hepatomegaly
Muscle wasting/weakness
Dermatological changes

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9
Q

Biochemistry changes with HAC

A

Main one = marked elevation in ALP
Some increase in ALT, cholesterol, bile acid
Reduction in urea

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10
Q

Haematological changes resulting from HAC

A

Stress leukogram
i.e neutrophilia, lymphopenia, eosionpaenia, monocytosis, erythrocytosis

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11
Q

Urinalysis with hyperadrenocorticism

A

Specific gravity usually <1.015
50% of dogs with this show UP:UC of >1 due to protein losing nephropathy

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12
Q

Screening tests for HAC and whether they are good for ruling out or in disease

A

Urinary cortisol:creatinine ration = good to rule out disease (high sensitivity, low specificity)
Low dose dexamathesone suppression test is good for ruling out disease; high sensitivity, low specificity

ACTH stim test; good for ruling in disease (gold standard); good specificity and medium sensitivity

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13
Q

How can we use urinary cortisol:creatinine ration to test for HAC

A

Collect urine in home environment
High ratio means they may have HAC
Low ratio means very unlikely to have hAC

= good to rule out disease if lower suspicion

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14
Q

How does ACTH stimulation test work

A

Measure blood cortisol levels before and after injecting ACTH
- With Cushing’s get increase in cortisol much higher than expected

(unless it is iatrogenic cushings)

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15
Q

How does the low dose dexamethasone suppression test work

A

Take resting blood sampe for cortisol, inject dexamethasone and then measure
In cushings patient don’t get suppression of cortisol production that you would if healthy

Very sensitivity esp for PDH but lower specificity

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16
Q

What should we monitor for having diagnosed pituitary macroadenoma

A

Neurological signs

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17
Q

How can we differentiate ADH and PDH

A

Best way = abdominal ultrasound to look at the dimensions of the adrenal gland
- In ADH only one enlarged, in PDH both enlarged

Can measure endogenous ACTH concentration

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18
Q

Difference in prognosis between ADH and PDH

A

ADH dogs more resistant to medical management so worse prognosis

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19
Q

What are untreated dogs with HAC at risk of

A

UTI, glomerulonephropathies, hypertension, thromboembolic disease, diabetes mellitus, skin infection

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20
Q

What do we use to medically manage hyperadrenocorticism

A

Trilostane
= acts to competitively inhibit 3-beta hydroxysteroid dehydrogenase to reversible reduce steroid production

21
Q

What is the role of aldosterone

A

Regulation of blood pressure; increases reabsorption of Na+, Cl- so get more water reabsorbed and increase in BP
Stimulates secretion of K+

Acid base regulation

22
Q

2What are some causes of primary hypoadrenocorticism

A

Idiopathic atrophy likely via immune-mediated destruction

Can get iatrogenic hypoadrenocorticism e.g from drugs or surgery

23
Q

What is a key difference between primary and secondary hypoadrenocorticism

A

Primary = issue at level of adrenal glands; get deficiency in cortisol and aldosterone

In secondary = issue is at the level of ACTH release so specifically get deficiency in cortisol (normal aldosterone)

24
Q

What is addison’s disease

A

Primary hypoadrenocorticism

25
Q

What s the pathophysiology of addison’s disease

A

Lack of aldosterone causes loss of Na+/Cl-/H2O, retention of K+/H+, pre-renal renal failure

Also glucocorticoid deficiency: low stress tolerance, GI signs, weakness, anaemia

26
Q

Signalment of Addison’s disease

A

Young-middle aged dogs, mostly female, standard poodles and other breeds predisposed

27
Q

Chronic vs acute Addison’s presentation

A

Chronic: non-specific signs; anorexia, vomiting, weight loss, weakness, shivering, PU/PD

Acute = in shock; hypovolaemic and azotaemic

28
Q

WHy might a dog in an addisonian crisis have bradycardia despite being in shock

A

Due to hyperkalaemia

29
Q

Biochemistry findings in addison’s disease

A

Increase potassium
Decreased Na+ and Cl-
(DECREASED Na:K MAY BE MORE SENSITIVE)

Azotaemia

30
Q

Haematology changes with addison’s disease

A

Lack of stress leukogram where it might be expected or reverse
Half have anaemia; decreased erythrocytosis due to lack of cortisol

31
Q

Difference in biochemistry profile between acutely presenting and chronic waxing/waning addisons

A

ONly see typical electrolyte changes (high K+, low Na+, low Cl-) with acute presentation
With chronic one don’t because aldosterone secreting tissue has high reserve capacity

32
Q

What Na:K do we expect in dog with Addison’s

A

<23 (this is low)

33
Q

What is a screening test for Addison’s disease

A

Measure basal cortisol
Very sensitive but not specific
If >55nmol/L then not addison’s

34
Q

Gold standard way to diagnose addison’s disease

A

ACTH stim test
Inject synthetic ACTH and measure change in cortisol levels; if the dog has addison’s expect none or small rise in plasma cortisol because zona fasiculata is destroyed

35
Q

Key steps in managing acute addisonian disease

A

Aggressive fluid therapy
Glucocorticoids

Important to reduce K+; fluid restoration helps kidneys to excrete it, can use sodium bicarbonate to help reverse it

36
Q

Long term management of addison’s disease

A

Monthyl injection of desoxycortone pivalate
= just mineralocorticoids replacement so need prenisolone supplementatino

37
Q

Histopathological changes in pituitary dependent hyperadrenocorticism

A

Pituitary dependent hyperplasia of the cortex; zona glomerulosa shows hypertrophy and hyperplasia too as part of poorly understood compensatory mechanism in response to Na/K balance etc

38
Q

Histopath of cortex in canine addison’s disease

A

Very cellular; mainly T lymphocytes
Diffuse and severe cortical atrophy with all layers reduced in thickness

39
Q

What do most functaional canine adrenocortical neoplasms secrete

A

Cortisol

40
Q

In which species do we commonly get functional neoplasms from oestrogen secreting cells of zona reticularis

A

Ferrets

41
Q

In which speces do we get functional neoplasms from aldosterone secreting cells of zona glomerulosa

A

cat

42
Q

What are phaeochromocytomas and what do they secrete

A

Adrenal medulla neoplasms
Mainly produce norepinephrine despite adrenaline being the main catecholamine of the normal adrenal medulla

43
Q

What complication can occur with malignant phaeochromocytomas

A

Can grow and invade vena cava

44
Q

What causes proliferative adrenal lesions in ferrets

A

After neutering don’t have sex steroids do no downregulation of GnRH production from hypothalamus
–> So get more LH release –> chronic stimulation of zona reticularis which makes sex steroids –> increase in sex steroids

45
Q

Pathology of adrenal lesions in ferrets

A

Hyperplasia; 45%l tends to be bilateral
Adrenocortical carcinoma - 45%
Adrenocortical adenoma

46
Q

Clinical signs of hyperadrenocorticism in ferrets

A

Hiar loss
Lethargy
Loss of appetite
Thin skin
Sexual aggression in neutered males
Males may show difficulty urinating due to enlarged prostate
Swollen vulva in spayed females
PU/PD
Pot bellied apperance due to fall in muscle mass

47
Q

Calcinosis cutis is specific to what disease

A

hyperadrenocorticism

48
Q

Myxoedema is specific to what disease

A

Hypothyroidism

49
Q

What type of renal fialure do we see in Addison’s disease and what is the urine concentratino like

A

= pre-renal renal failure due to hypovolaemia

BUT get dilute urine (unusual for pre-renal failure) because of severely low Na+ causing medullary washout

Unable to concentrate urine despite being dehydrated!

Michaelmas 5th year (41 decks)

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