adrenal gland 2 Flashcards

1
Q

metabolic roles of cortisol

A

↑ Gluconeogenesis to maintain blood glucose levels
↑ Glycogen synthesis to maintain glucose storage
↑ Protein catabolism
↑ Lipolysis
↑ Appetite
↑ Insulin resistance

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2
Q

non-metabolic roles of cortisol

A

Immune system: antiinflammatory and immunosuppressive effects
Wound healing: ↓ wound healing
Blood pressure: mild mineralocorticoid effect, ↑ blood pressure

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3
Q

why does cortisol limit wound healing

A

fibroblast inhibition → ↓ collagen synthesis → ↓ wound healing

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4
Q

why does cortisol increase blood pressure

A

mild mineralocorticoid effect (stimulation of aldosterone receptors in high concentrations) and ↑ potassium excretion → ↑ blood pressure

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5
Q

what promotes secretion of glucocorticoids in the adrenal cortex

A

CRH from the hypothalamus stimulates ACTH in the pituitary gland which stimulates secretion of glucocorticoids from the adrenal cortex

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6
Q

ACTH stands for

A

adrenocorticotropic hormone

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7
Q

what triggers CRH release from the hypothalamus

A

Psychological/physical pain and stress
Pyrogens, epinephrine, histamine
Hypoglycemia
Hypotension

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8
Q

what is the negative feedback mechanism for cortisol

A

Cortisol inhibits the secretion of CRH and ACTH via negative feedback, which, in turn, results in a decrease in cortisol secretion.

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9
Q

what triggers the rhythmic release of CRH

A

impulses by the suprachiasmatic nucleus trigger the rhythmic release of CRH, the SCN also transmits signals directly to the adrenal cortex via neural pathways

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10
Q

what does 5a reductase do

A

coverts testosterone into dihydrotestosterone (DHT)

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11
Q

what do 5a reductase inhibitors do

A

inhibit the conversion of testosterone into dihydrotestosterone (DHT) via 5a-reductase
eg. finasteride

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12
Q

what hormones are created in the adrenal medulla

A

catecholamines
eg. noradrenline, adrenaline, dopamine

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13
Q

where else are catecholamines synthesised

A

Catecholamines (norepinephrine, epinephrine, dopamine) can also be synthesized in specific regions of the CNS eg. substantia nigra and locus coeruleus and postganglionic adrenergic neurons.

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14
Q

which catecholamine has the shortest half life

A

adrenaline

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15
Q

how are catecholamines degraded

A

via catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO)

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16
Q

what do monoamine oxidase inhibitors do

A

elevate catecholamine concentration in the synaptic cleft

17
Q

what activity does adrenaline have

A

both a and b adrenergic agonist activity
causes bronchial smooth muscle relaxation, cardiac stimulation, peripheral vasodilation (small doses) and peripheral vasoconstriction (large doses)

18
Q

what is vanillylmendelic acid (VMA)

A

an end stage metabolite of catecholamines
Urinary excretion is elevated in patients with pheochromocytoma and neuroblastoma.

19
Q

What is a pheochromocytoma?

A

A catecholamine-secreting tumor that develops in the adrenal medulla.

20
Q

What percentage of pheochromocytomas are malignant?

A

Approximately 10%.

21
Q

What are the symptoms of excess sympathetic nervous system stimulation in pheochromocytoma?

A
  • Episodic hypertensive crises
  • Paroxysmal headaches
  • Diaphoresis
  • Heart palpitations, tachycardia
  • Pallor
  • Abdominal pain, nausea
  • Anxiety

other symptoms include: weight loss due to increased basal metabolism, hyperglycaemia, polycythaemia if EPO is secreted, additional features of hereditary disorders

22
Q

Can pheochromocytomas be asymptomatic?

A

Yes, they may also manifest with persistent hypertension.

23
Q

What confirms the diagnosis of pheochromocytoma?

A

Elevated catecholamine metabolites eg. VMA in the plasma or urine.
imaging studies are used to determine the location of the tumor

24
Q

What is the treatment of choice for pheochromocytoma?

A

Surgical resection.
Preoperative alpha-adrenergic blockade (e.g., phenoxybenzamine) is indicated to prevent intraoperative complications such as hypertensive crises.