Hypoadrenocorticism Flashcards

1
Q

What are the physiological effects of glucocorticoids?

A
  • Increase gluconeogenesis and glycogenolysis
  • Stimulate proteolysis and lipolysis
  • Fight or flight/stress
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2
Q

Describe the control of aldosterone release

A
  • RAAS
  • Renin release stimulated by baroreceptors in wall of afferent arteriole, macula densa cells stimulated by reduction of Cl delivery and cardiac and arterial baroreceptors
  • Drop in BP stimulates renin secretion
  • Renin released, converts angiotensinogen to angiotensin I and then to angiotensin II
  • Angiotensin II potent vasoconstrictor and stimualtes release of aldosterone from adrenal cortex
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3
Q

Where is aldosterone released from?

A

Zona glomerularis of adrenal cortex

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4
Q

Describe aldosterone function

A
  • Central role in BP regulation
  • Increases reabsorption of Na, Cl and hence water and distal tubule and collecting duct
  • Stimulates secretion of K+ into tubular lumen
  • Stimulates secretion of H+ in exchange for K+ in collecting tubules (acid base balance)
  • Some vasoconstrictor properties
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5
Q

What is the name given to primary hypoadrenocorticism?

A

Addison’s disease

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6
Q

Describe primary hypoadrenocorticism

A
  • Deficiency of glucocorticoids and mineralocorticoids
  • Loss of 85-90% of adrenal cortex
  • May be immune mediated destruction of adrenal gland, likely autoimmune
  • Destruction of glomerulosa and fasciculata, may spare reticularis
  • Aggressive management as corticosteroids are essential for life
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7
Q

Give causes of primary hypoadrenocorticism in dogs

A
  • Idiopathic: probably immune mediated destruction

- Iatrogenic: drugs (drugs used to manage Cushing’s) or surgery (bilateral adrenalectomy)

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8
Q

Describe secondary hypoadrenocorticism

A
  • Deficiency of ACTH
  • Only cortisol deficient (electrolytes normal)
  • Rare
  • Pituitary (sometimes hypothalamic lesion) leading to reduced/absent ACTH
  • Only affects glucocorticoid production
  • mineralocorticoid function preserved
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9
Q

What can be an effect of aldosterone deficiency?

A

Electrolyte imbalances

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10
Q

Outline iatrogenic hypoadrenocorticism

A
  • Exogenous steroids leading to adrenal atrophy (neg feedback, loss of stimulation, sudden removal means unable to produce enoguh quickly)
  • Cortisol deficiency only
  • May have signs of Cushing’s syndrome
  • Can be life threatening
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11
Q

Describe the signalment of canine hypoadrenocorticism

A
  • Younger females (4-6 years, 70% females)
  • Some breed predispositions: standard poodles, bearded collies, Portugese water dog, Leonberge, great Dane, Rottweiler, WHWT, soft coated wheaten terrier
  • Extremely rare in cats
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12
Q

Describe the signs of aldosterone deficiency

A
  • Loss of Na, Cl, H2O
  • Retention of K+, H+
  • Pre-renal renal failure
  • Failure to retain water
  • Electrolyte imbalances, dehydration, hypovolaemia
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13
Q

Describe the signs of glucocorticoid deficiency

A
  • Decreased stress tolerance (no stress response of immune cells)
  • Gastrointestinal signs
  • Weakness
  • Appetite loss
  • Anaemia
  • Impaired gluconeogenesis
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14
Q

Describe the clincal signs of chronic hypoadrenocorticism

A
  • Waxing waning with non-specific signs
  • Worsened by stress
  • Anorexia, vomiting, diarrhoea, PUPD, weakness, lethargy, depression
  • Often appear normal between bouts, esp after fluid therapy or steroids
  • GI signs common
  • Cannot cope with additional stress e.g. long walk,concurren disease, increased acitivty that day
  • Chronically losing sodium so unable to concentrate tubular fluid
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15
Q

Describe the clinical signs of acute hypoadrenocorticism

A
  • Crisis, marked hypovolaemia and azotaemia
  • Collapsed, close to death, extremely weak
  • Recent history of vomiting/diarrhoea, may be fresh or digested bloof present
  • Hypovolaemic shock
  • Paradox bradycardia
  • Abdominal pain
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16
Q

Why does paradox bradycardia occur in acute hypoadrenocorticism?

A
  • Hyperkalaemia

- Has effect on action potential in heart

17
Q

What would be seen on a complete blood count in cases of hypoadrenocorticism?

A
  • Lack of stress leucogram (no neutrophilia or lymphopaenia)

- Anaemia (decreased erythrocytosis due to lack of cortisol and GI loss of blood)

18
Q

What would be seen on blood biochemistry in cases of hypoadrenocorticism?

A
  • Hyperkalaemia, hyponatraemia, hypochloridaemia
  • Hypercalcaemia
  • Hypoglycaemia (cortisol deficiency)
  • Azotaemia
19
Q

What would be seen on biochemistry and urinalysis in cases of hypoadrenocorticism?

A
  • Azotaemia
  • Decreased USG
  • BUN and creatinine increased
20
Q

What would be seen on ECG in cases of hypoadrenocorticism?

A
  • Bradycardia
  • Peaked T waves
  • Widened QRS complexes
  • Descreased P wave amplitude
  • Disappearance of P waves
  • Ventricular asystole (failure to contract)
21
Q

What is the specific diagnostic test used for the definitive diagnosis of hypoadrenocorticism?

A

ACTH stimulation test

22
Q

Describe the results of ACTH stimulation test in the diagnosis of hypoadrenocorticism

A
  • Measure cortisol
  • Flat line stimulation
  • No response to ACTH injection i.e. cortisol stays at same level
23
Q

Outline the management of hypoadrenocorticism

A
  • Fluids
  • Glucocorticoid hormone
  • Mineralocorticoid
  • May address high blood potassium
24
Q

Explain how steroid withdrawal crises occur

A
  • Exogenous steroids have a negative feedback effect on hypothalamus and pituitary
  • Reduced stimulation of adrenal glands
  • Atrophy over time
  • When steroid removed, adrenals unable to produce own corticosteroids
  • Crisis occurs
25
Q

What is a phaechromocytoma?

A

Rare, catecholamine secreting tumour of the adrenal medulla

26
Q

What is meant by a functional tumour?

A

Is able to produce hormones (and thus may have large effect even if small)

27
Q

What type of receptor are adrenoceptors?

A

G-protein coupled

28
Q

What is the action of alpha-2 receptors?

A
  • Inhibit catecholamine release
  • Situated on pre-synaptic emmrbane
  • Catecholamines released into synapse, bind to alpha-1 receptors on post-synaptic membrane and pre-synaptic alpha-2 receptos
  • Binding to the alpha-2 acts as negative feedback to stop secretion
29
Q

What intracellular signalling pathway do alpha1 adrenoreceptors activate?

A
  • Phospholipase C (via Gg)

- Increase activity of protein kinase C (PKC)

30
Q

What intracellular signalling pathway do alpha2 adrenoreceptors activate?

A
  • Adenylate cyclase via Gi

- Descrease activity of protein kinase A (PKA)

31
Q

What intracellular signalling pathway do beta adrenoreceptors inhibit?

A
  • Adneylate cyclase via Gs

- increase activity of protein kinase A (PKA)