22. The adrenal gland Flashcards

1
Q

What are the three different types of hormones?

A

Amine
Peptide
Steroid

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2
Q

Where can an endocrine hormone have an effect in a cell?

A

At the cell surface
In the cell cytoplasm
In the nucleus of the cell

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3
Q

What are different effects mediated by endocrine hormones?

A

Increased hormone production
Release of stored hormone
Cell multiplication

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4
Q

Where is the adrenal gland located?

A

Superiorly to the kidney at the posterior abdominal wall

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5
Q

What are the divisions of the adrenal gland and what do they produce?

A

Inner medulla

Outer cortex divided into three zones:
Zona glomerulosa - mineralcorticoid hormones e.g. aldosterone
Zona fasciculata - glucocortoid hormones e.g. cortisol
Zona reticulosa - andorgenic steroids e.g. testosterone

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6
Q

What are the forms of stress that the adrenal gland responds to?

A

Physiological states of stress:
Starvation
Infection
Severe volume loss

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7
Q

Where are mineralcorticoids released from?

A

From the zona glomerulosa of the adrenal cortex

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8
Q

How can the adrenal cortex produce so many different hormones?

A

Via the expression of different enzymes and cofactors in the individual cells of the different zones

E.g. cells of the zona glomerulosa will contain aldosterone synthase

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9
Q

What is the main mineralocorticoid and how does this have an effect in the body?

A

Aldosterone

RAAS system - activation of which increases the blood pressure via increased Na+ reabsorption via up-regulation of ENaC channels, H20 reabsorption via increased ADH

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10
Q

How does aldosterone lead to an increased Na+ reabsorotion

A

Aldosterone binds to Na+/K+ ATPase and activates these transporters
This results in the upregulation of ENaC channels

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11
Q

Where is the mineralcorticoid receptor (activated by aldosterone) located?

A

Located in the nucleus

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12
Q

What is Conn’s syndrome?

A

Hyperaldosterone - excess production of aldosterone

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13
Q

What are the effects of hyperaldosterone?

A

Hypertension
Decreased plasma renin activity
Increased aldosterone secretion

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14
Q

Why might someone develop hyperaldosteronism?

A

Aldosterone producing adenoma in the zona glomerulosa

Bilateral adrenal hyperplasia

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15
Q

How can you recognise this for diagnosis?

A

In investigations, should have a high aldosterone level and a low renin level
CT scan of the adrenal gland - is a tumour present? (this can be removed)

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16
Q

How can cortisol lead to hyperaldosteronism?

A

Cortisol (glucocorticoid) also binds to the mineralcorticoid receptor
SO is normally converted to the inactive form cortisone which does not bind to the receptor
Some food types can inactivate the enzyme that converts cortisol to cortisone and so the cortisol binds to the mineralcorticoid receptor and results in a mineralcorticoid excess

17
Q

How is cortisol released?

A

Corticotropin releasing hormone (CRH) is released from the hypothalamus
Causes the release of ACTH from the pituitary gland
Leads to the production of cortisol from the zona reticulosa of the adrenal glnad

18
Q

How is the release of cortisol (glucocorticoids) controlled?

A

Many feedback loops:
Glucocorticoid production will inhibit CRH production from the hypothalamus and can also inhibit ACTH production from the anterior pituitary gland

ACTH production itself can also feedback on the hypothalamus and inhibit CRH release and ACTH can also feedback onto itself and inhibit it’s own release from the anterior pituitary

19
Q

What is the effect of glucocorticoids on the immune system?

A

Inhibits the immune system

20
Q

What are the actions of glucocorticoids (cortisol)?

A

In starvation - tissue breakdown for fuel
In infection - immunosuppression
In hypotension - increased blood pressure

21
Q

What is Cushing’s syndrome?

A

Where there is too much cortisol produced
All the process i.e. tissue breakdown, immunosuppression, increase in BP will be increased - myopathy and osteoporosis will result from an increased breakdown of muscle and of bone

22
Q

How can Cushing’s syndrome occur?

A

Corticotroph adenoma of the pituitary

ACTH secreting tumour

23
Q

What is Addison’s disease?

A

Primary adrenal cortex failure, generally due

SO have problems producing adrenal androgens, glucocorticoids and mineralcorticoids

24
Q

Why is Addison’s disease dangerous?

A

The body is unable to respond to stress due to the lack of cortisol - an addisonian criss can occur:
Low BP
Low blood glucose
Low sodium and high potassium

25
Q

What is adrenal hyperplasia and what are the signs of this?

Comes up in exams

A

Various different forms of this - when various enzymes do not work at birth e.g. 21-hydroxylase deficiency and means that the hormones of the adrenal gland are not produced

Salt-losing
Adrenal insufficiency
Virilisation i.e. female babies born with male genitalia
Adrenal hyperplasia

26
Q

What hormones are produced by the adrenal medulla?

A

Catecholamines - adrenaline and noradrenaline

27
Q

What is the importance of the roles of the catecholamines in the stress response?

A

Noradrenaline - important in the stress response to low blood pressure
Adrenaline - important in the stress response to low blood sugar

28
Q

Which cells secrete adrenaline and noradrenaline?

A

Chromaffin cells

29
Q

What occurs following the activation of the following adrenoreceptors?

Alpha 1
Beta 1
Beta 2

A

Alpha 1 - stimulates smooth muscle contraction i.e. vasoconstriction
Beta 1 - Positive inotropic and chronotropic of the heart, increased renin, lipolysis
Beta 2 - Bronchial, vascular, uterine smooth muscle relaxation, glygogenolysis

30
Q

What are the symptoms of cathetholamine excess?

A
Dyspnea
Fatigue 
Headache
Hypertension 
Palpitation 
Congestive heart failure
Weight loss