The adrenal medulla Flashcards

1
Q

summarise the adrenal medulla

A
  • part of the ANS
  • receives innervation from a long pre-ganglionic neurone
  • Ach as NT
  • involved in catecholamine synthesis
  • main site of ad (ad predominates here)
  • PNMT enzyme contained within chromaffin cells
  • not essential for life unlike cortex
  • Ad released via SNS input, pre-packaged hormones in vesicles released into blood
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2
Q

the primitive neural crest differentiates into …

A
  • sympathetic ganglia
  • chromaffin cells
  • via D and migration processes
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3
Q

the RLS during NAd synthesis Is catalysed by

A
  • tyrosine hydroxylase
  • can be unregulated and downregulated via regulation of this enzyme
  • inhibited by a-methyltyrosine and NAd (negative feedback)
  • during high levels of catecholamines
  • high rate of stimulation from SNS stimulates TH
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4
Q

PNMT converts

A

NAd - Ad

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5
Q

adrenaline secretion can be regulated via

A

stressors- hypoT- SNS activation

  • ACTH/ cortisol (increase Ad secretion)
  • no negative feedback system at play
  • ACTH unregulates PNMT when blood supply passes through the cortex cells
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6
Q

alpha R

beta R

A
  • Adrenaline
  • Noradrenaline
    increased activity from medulla - more beta mediated effects then SNS innervation
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7
Q

metabolic inactivation of Ad/NAd

A
  • occurs in the liver/kidney
  • COMT (Ad- metadrenaline)
  • MAO ( MetA- VMA)
  • excreted via kidney
  • elevated VMA levels indicative of XS levels
  • hypertension/ pheochromocytoma
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8
Q

effects of Ad on the CNS

A
  • increased altertness
  • arousal
  • increased anxiety
  • increased muscle tremor
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9
Q

effects of Ad on the periphery

A
  • increased HR (b1R) , contractility
  • vasodilation of skeletal muscle vessels (cAMP)
  • bronchodilation
  • widespread activation of medulla - Ad dominates - B2R
    direct innervation (Nad from terminals) - a1 R - constriction
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10
Q

effects on metabolism include

A
  • muscle- glycogen breakness
  • hepatic - glycogenolysis / glucneogenesis)
  • adipose - mobilisation of free FA
  • aims to elevate blood glucose levels
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11
Q

why do we need a medulla?

A
  • longer lasting effects than SNS
  • SNS doesn’t innverate whole body whilst hormones release into the bloodstream do
  • different affect than SNS- dominance of Ad over NAd
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12
Q

pheochromocytoma

A
  • XS catecholamines
  • tumour of chromaffin cells
  • chronic over secretion
  • use of VMA levels as diagnostic technique
  • iodinated tracers / scans
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13
Q

symptoms of PC include

A
  • episodes of high BP
  • sudden severe headache
  • palpitations and chest pain
  • pallor of skin and sweating
  • anxiousness

-

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14
Q

treatments of PC include

A
  • ACE Inhibitors (reduces aldosterone production)
  • anti- hypertensive drugs
  • beta blockers
  • surgical removal of just one gland (require atleast one for aldosterone production)
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