adrenocorticoids Flashcards

1
Q

what medulla adrenal gland produce?

A

catecholamines eg: adrenaline

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2
Q

the outer zona glomerulosa (cortex of adrenal) produce

A

aldosterone

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3
Q

the middle zona fascicula (cortex of adrenal) produce

A

cortisol

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4
Q

the inner zona reticularis (cortex of adrenal) produce

A

sex hormone

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5
Q

function of cortisol

A
  • restore homeostasis following stress
  • cortisol is controlled by negative feedback to CRH (cortisol releasing hormone in hypothalamus)
  • inhibit prostaglandin production (repress the trc of COX-2)
  • blockade of transcription activity of NF-kB
  • activation of endothelial nitric oxide synthase
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6
Q

explain hydrocortisone (cortisol)

A
  • major glucocorticoids
  • produced in zona fasciculata
  • ~20mg/day secreted
  • short half life 60-180 mins
  • water soluble
  • 95% globulin binding
  • secreted in circadian rhythm
  • readily diffuse through cell membrane
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7
Q

explain aldosterone

A
  • major mineralocorticoids
  • produced in zona glomerulosa but main production is in renin-angiotensin pathway
  • 50% bound with low affinity to albumin
  • salt-retaining activity
  • for electrolytes and water balance
  • efflux of K+ and H+
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8
Q

effects of too much aldosterone production

A
  • hypernatremia
  • hypokalemia
  • alkalosis
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9
Q

cortisol function

A
  1. effect on metabolism
    - carbohydrates- prevent utilise glucose, anti-insulin effect, promote glucose synthesis
    - proteins- catabolic hormone
    - lipids- excessive lipid moonface, ‘buffalo hump’, lipid in the trunk
  2. as anti-inflammatory function
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10
Q

what glucocorticoid do in direct genomic action?

A

increase transcription of ANTI-inflammatory genes

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11
Q

what glucocorticoid do in indirect genomic action?

A

dampen the transcription of PRO-inflammatory genes

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12
Q

what causes glucocorticoid resistance?

A
  • familial glucocorticoid resistance
  • glucocorticoid receptor modification
    eg: phosphorylation, nitrosylation, ubiquitination
  • increased pro-inflammatory trc factors
  • defective histone acetylation
  • increased P-Gp (efflux of steroids)
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13
Q

clinical uses for glucocorticoids

A
  • opthalmic diseases
  • endocrine disorders
  • rheumatic disorders
  • collagen disorders
  • allergic eg: asthma
  • dermatological diseases
  • respiratory diseases
  • neoplastic disease
  • haematological disorders
  • UC, TB, meningitis
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14
Q

clinical uses for mineralocorticoids

A
  • as replacement therapy for Addison’s disease

- treatment of salt-losing adrenogenital syndrome

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15
Q

drug for asthma inhalation

A

beclomethasone

  • have to rinse mouth
  • might cause fungal infection
  • immunosupressive drug
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16
Q

drug for asthma orally

A

prednisolone (glucocorticoids)

17
Q

drug for asthma IV

A

hydrocortisone

18
Q

effects of toxicity of glucocorticoids

A
  • hypothalamic-pituitary-adrenal supression
  • euphoria to depression in withdrawal of drug
  • hyperglycemia
  • loss of muscle bulk (increase proteolysis, decrease protein synthesis)
  • redistribution of body fat
  • growth retardation in children
  • immunosuppression
  • cause osteoporosis
  • decrease Ca absorption in GIT
  • decrease gonadotrophin secretion, hypogonadism
  • congenital malformations
  • dyslipidemia
  • hypertension
  • thrombosis
  • vasculitis
  • cataracts
  • glaucoma
  • increase Na+ retention and K+ excretion
19
Q

commonly used anti-inflammatory STEROIDS

A
  • cortisol
  • fludrocortisone
  • prednisone
  • prednisolone
  • dexamethasone
20
Q

causes of cushing’s disease

A
  • adrenal hyper-activity by eg: adrenal tumour

- excessive exposure to glucocorticoids

21
Q

treatment for cushing’s disease

A

reduce glucocorticoids dosage and surgery

22
Q

what is Addison’s disease

A
  • adrenal insufficient
  • auto-immune disorders
  • both CORTISOL and ALDOSTERONE lacking
23
Q

clinical sign and symptoms of Addison’s disease

A
  • fatigue
  • wasting
  • dizziness
  • pigmentation
  • nausea
  • diarrhoea
  • low bp
24
Q

treatment for Addison’s disease

A

cortisol with fludrocortisone

25
Q

what is conn’s syndrome?

A
  • hyper production of aldosterone
  • aldosterone producing adenoma
  • aldosterone secreting carcinoma
  • inability of adrenal cortex to carry out 17a-hydroxylation
26
Q

clinical signs and symptoms of conn’s syndrome

A
  • muscle weakness
  • hypertension
  • hypokalemia
  • cardiac arrhythmia
27
Q

treatment of conn’s syndrome

A
  • surgery removal of adenoma

- spironolactone (aldosterone receptor agonist)