L9 HPA axis Flashcards

1
Q

Effects of glucocorticoids?

A
maintain homeostasis during stress
eg - anxiety, infection, haemorrhage
anti-inflammatory 
energy balance/metabolism
formation of bone/cartilage
regulation of BP 
cognition
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2
Q

ULTRADIAN RHYTHM

A

Pulsatility’ of hormone release
anultradian rhythmis a recurrent period or cycle repeated throughout a 24-hour day. In contrast, circadianrhythmscomplete one cycle daily

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3
Q

11-Beta-HSD enzymes

A

tissue specificity - gating of GC access to nuclear receptors

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4
Q

Cushings syndrome

A
too much cortisol
weight gain 
central obesity 
hypertension 
insulin resistance
osteoporosis 
the excess cortisol could be caused by pit adenoma ACTH secreting cells 
or adrenal tumour - adenoma 
ectopic ACTH - carcinoid
Iatrogenic - steroid treatment
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5
Q

clinical features of cushings syndrome

A

Central obesity with thin arms & legs
Fat deposition over upper back (‘buffalo hump’)
Rounded ‘moon’ face
Thin skin with easy bruising, pigmented striae
Hirsutism

Hypertension
Diabetes
Psychiatric manifestations
Osteoporosis

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6
Q

what is Addisons disease

A
too little cortisol 
body wastage
gradually ill 
slight pain is referred to stomach
vomiting
skin discolouration - tanned
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7
Q

Pathogenesis of addisons disease

A

primarily adrenal insufficiency

iatrogenic - patients on high dose, long term steroids which is suddenly stopped at a time of stress

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8
Q

clinical features of addisons disease

A

malaise, weak, weight loss, increased skin pigmentation,

hypotension, hypoglycaemia

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9
Q

Type 1 autoimmune polyendocrine syndrome

A

rare
infancy onset
AIRE gene
common phenotype - addisons, hypoparathyroidism, candidiasis

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10
Q

Type 2 autoimmune polyendocrine syndrome

A

commoner but still rare
infancy to adulthood
polygenic
common phenotype - addisons, T1D, autoimmune thyroid disease

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11
Q

How can you assess the HPAA?

A

Basal - blood -timing circadian rhythm (cortisol, ACTH), urine 24 hour collection - area under curve (cortisol) saliva - no timing(cortisol)
dynamic tests -
stimulated - ACTH, CRH
suppressed - dexamethasone

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12
Q

Too much cortisol assessments

A

24 hour urinary free cortisol
measure area under curve
midnight cortisol - blood saliva
9am ACTH with paired cortisol

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13
Q

Too little cortisol

A

9am cortisol
synACTHen test -adrenal response to ACTH
insulin tolerance test - response to hypoglycemic stress
U+E in addisons disease
sodium low pottasium high due to mineralocorticoid deficiency
can measure renin and aldo conc - aldo will be low and renin high
reduced glucose

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14
Q

Imaging HPAA

A

Once you identify a patient has cushings consider
CXR
MRI pituitary
CT adrenals

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15
Q

Management of cushings

A

surgical depending on cause
transphenoidal adenectomy
adrenalectomy
pituitary radiotherapy

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16
Q

Management of addisons disease?

A

steroid hormone replacement therapy - glucocorticoid

Patients with primary adrenal insufficiency also need mineralocorticoid replacement therapy (fludrocortisone).
Patients with secondary adrenal insufficiency will often be taking other hormone replacement therapy (do not need fludrocortisone).