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07. Endocrine > 7.16 Adrenal Gland Function and Dysfunction > Flashcards

7.16 Adrenal Gland Function and Dysfunction Flashcards

1
Q

Where are the adrenal glands located?

A

They are pyramidal shaped glands that sit ontop of the kidneys.

The left is shaped like a semicircle while the right is shaped like a party hat

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2
Q

Describe the structureof the adrenal gland

A

Like the pituitary, the adrenal gland can be thought of as two embryologically and functionally distinct glands that fused during development

There is an adrenal medulla (outer) and an adrenal cortex (inner)

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3
Q

Compare the adrenal medulla to the adrenal cortex in terms of major functions

A

Adrenal medulla:

  • A modified sympathetic ganglion
  • Neurohormones
  • Secretes catacholamines

Adrenal cortex:

  • True endocrine gland
  • Classical hormones
  • Secretes steroid hormones
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4
Q

Describe the major histological parts of the adrenal cortex and what each part is responsible for

A

“G.F.R”

Zona glomerulosa –> Aldosterone secretion

Zona fasciulata –> Glucocorticoids

Zone reticularis –> Sex hormones

(note there is some overlap between the zona glomeruosa and the zona fasciulata)

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5
Q

Describe the Hypothalamic-Pituitary-Adrenal Axis and the main outputs from each component

A
  • The hypothalamus secretes corticotrophin releasing hormone CRH which travels through the hypothalamic hypophyseal portal to the anterior pituitary
  • The anterior pituitary gland (corticotroph cells) secrete adrenocortitotrophic hormone (ACTH) which travels through the blood to the adrenal glands
  • The adrenal cortex cells respond by secreting cortisol
  • Cortisol acts via a long negative feedback loop to the hypothalamus and the pituitary
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6
Q

What are the main sex hormones from the adrenal cortex?

  • What layers produce them?
A

Androgens, oestrogens, dehydroepiandosterone (DHEA)

They are produced primarily in the zona reticularis (but also in the fasciculata)

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7
Q

What regions of the adrenal cortex produce cortisol?

  • What is the trigger for secretion?
A

The primary zone is the zona fasciculata (but also in the zona reticularis)

  • Cortisol production and secretion is trigger by the hypothalamic-pituitary-adrenal axis (HPAA)
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8
Q

Where are the mineralocorticoids produced?

What stimulates it?

A

Only the zona glomerulosa produces the mineralocoriticoids (aldosterone)

  • It is stimulated by the RAAS pathway and increasing levels of plasma K
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9
Q

How is there a difference in what hormone the cells of the adrenal cortex produce?

A

Different zones of the cortex have slightly different cells as they each possess different enzymes that are able to cause the production of the different hormones

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10
Q

What is the major common backbone for steroid hormone synthesis?

A

Cholesterol backbone which is converted to pregnenolone

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11
Q

Draw the (simplified) pathway from cholesterol to the three steroid hormones (include enzymes)

A
  • Purple = Classic female sex hormones
  • Blue = Classic male sex hormones
  • Green = Glucocorticoids
  • Pink = Mineralocorticoid

(Note there a more steps/enzymes in between the ones shown)

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12
Q

What is a major consequence of having a shared synthesis pathway?

A

They are chemically related leading to a possible cross over effect of their actions

Eg. Mineralocorticoid and Glucocorticoid receptor actions (especially if there is an excess amount of one of them)

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13
Q

What are the higher brain centre functions that trigger/impact the tonic release of CRH from the hypothalamus?

A
  • The circadian rhythm
  • Stress
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14
Q

What are the major functions of cortisol in the body?

A
  • Immune system suppression
  • Stimulates gluconeogenesis in the liver
  • Muscle protein catabolism (substrate for gluconeogenesis)
  • Enhances lipolysis of adipose tissue (Fatty acids for energy)
  • Causes a negative calcium balance (decreases absorption, increases excretion and causes bone breakdown)
  • Influences brain function
  • Adaptation to stress
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15
Q

CRH and ACTH have other functions on the body. What are these?

A

They have stress-related functions in the immune system and the nervous system:

  • Inflammation and immune responses
  • Inhibition of appetite (through urocortion, a brain neuropeptide)
  • Signals for the onset of labour
  • Mood disorder effects
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16
Q

What is POMC (pro-opiomelanocortin)?

A

A large protein that exists in the pituitary glands that is the precursor protein to ACTH

Proteolysis yields several bioactive peptides (in addition to ACTH)

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17
Q

What are the main bioactive products coming from the proteolytic cleavage of POMC in the pituitary gland?

A

POMC is broken down to form ACTH and beta endorphin (an endogenous opiod that blocks pain perception) as well as other fragments

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18
Q

Post-translational processing of POMC outside the pituitary creates more active peptides. What are they?

A

Outside the pituitary gland, the ACTH produced is further cleaved to create alpha MSH (melanocyte stimulating hormone) which results in a decrease in food intake (appetite) and increase in skin melanin and may also affect mood.

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19
Q

What are the melanocortins?

A

The family name for the MSH Hormones (and ACTH)

  • They have a wide variety of effects which depend on the melanocortin receptor subtype that is stimulated
20
Q

Can a person survive without cortisol?

A

We can survive for several days only - once a stress is placed upon a person they will not cope.

It is essential for life as it helps the body cope with long-term stress

21
Q

Why is cortisol important for life and survival?

A

Because it helps the body cope with stress (Especially in the long term)

  • It protects against hypoglycemia by stimulating catabolism of energy stores
  • It is permissive (ie. required) for glucagon and catecholamine actions to occur
22
Q

Describe the use of cortisol as a therapeutic drug

A

Glucocorticoids are readily used as an anti-inflammatory drug

  • It suppresses the immune system (transplant rejection prevention)
  • Inhibits the inflammatory response (stings, allergies, asthma)
23
Q

What are the side effects of long term use of glucocorticoids (cortisol) as a therapeutic drug?

A

It results in the inhibition of the Hypothalamic-Pituitary-Adrenal Axis because of the impact of negative feedback.

Introduction of an exogenous cortisol causes negative feedback to the hypothalamus and pituitary to cease production of CRH and ACTH eventually leading to atrophy of cortisol secreting cells

It is important to taper off doses gradually to prevent the individual from going into adrenal crisis

24
Q

Are the steroid hormones stored in the adrenal gland?

A

NO

They are made on demand in response to stress and feedback pathways

25
Q

Fill in the following table for cortisol

A
26
Q

What are the two major causes of hyperaldosteronism? (primary and secondary)

A
  • Primary hyperaldosteronism (Conn’s syndrome - when the adrenal gland is excessively producing them)
  • Secondary hyperaldosteronism (RAAS) - over stimulation of the adrenal glands due to the Renin-Angiotensin-Aldosterone System
27
Q

What are the consequences of hyperaldosteronism?

A
  • Hypernatremia (increased Na retention)
  • Hypokalemia
  • Hypertension (Na and water imbalances)
28
Q

If a person has excess cortisol in their system, what are they said to have?

A

Cushing’s syndrome

29
Q

What are the 4 major causes of Cushing’s syndrome? (Hypercortisolism)

A
  • Primary adrenal cortex tumours automously secreting cortisol
  • Secondary pituitary tumour (CUSHING’S DISEASE) that autonomously secretes ACTH
  • Hyperstimulation by CRH or ACTH by some other means
  • Iatrogenic hypercortisolism by excess cortisol therapy
30
Q

What are the major consequences of hypercortisolism (Cushing’s syndrome)

A
  • Excess glucose
  • Protein shortage
  • Abnormal fat distribution
31
Q

What is the major causes of adrenogenital syndrome?

(Excess androgen and oestrogen)

A

Lack of enzyme in the cortisol steroidogenic pathway (the main cause is lack of 21-hydroxylase shunting more precursor to the sex hormone pathway)

32
Q

What are the consequences of adrenogenital syndrome?

A

Inappropriate masculinisation (except in adult males)

33
Q

What is the major treatment for adrenogenital syndrome?

A

Treat by giving exogenous cortisol/glucocorticoids

This repairs the deficiency in the glucocorticoids and mineralocorticoids as well as providing the negative feedback to inhibit ACTH (reducing steroid secretion and thus reducing adrenogen/oestrogen secretion)

34
Q

What are the main signs and symptoms of Cushing’s Disease?

A
  • Excess gluconeogenesis leading to hyperglycemia thus it mimics diabetes
  • Muscle protein breakdown and lipolysis leads to wasting
  • Paradoxical fat deposits in the neck, trunk and face due to an increase in appetitte
    • Straie
    • Moon Face
  • Excess glucocorticoid has effect on mineralocorticoid receptor activity leading to salt and water retnetion, oedema, weakness and hypertension
  • Bone resorption leads to osteoporosis
  • Mood elevation and then depression, difficulty learning and with memory
  • Poor wound healing and bruisability (ecchymoses)
35
Q

Describe the differences, and draw the pathway for primary and secondary pathologies. What is the main way to differentially diagnose them?

  • Primary hypersecretion due to problem with the adrenal cortex
  • Secondary hypersecretion due to pituitary problem
  • Secondary hypersection due to a hypothalamic problem
A

Main means of differentiation is to look at the relative levels of cortisol, ACTH and CRH

36
Q

Adrenocortical insufficiency results in hyposecretion of the steroid hormones; it is less common than hypersecretion.

What is the main primary adrenal insufficiencies?

A

Addison’s disease

= this is an attack on the whole adrenal cortex leading to hyposecretion of all the steroid hormones

37
Q

What are the major effects seen in Addinson’s disease?

A
  • Autoimmune destruction of the adrenal cortex
  • Decreased aldosterone (hyponaturemia, hyperkalemia- risk of arrhythmia, hypertension)
  • Decreased cortisol (decreased stress response and hypoglycemia)
38
Q

What is a major hereditary cause of hypocoritoslism and hyperaldosteronism?

A

Steroidal enzyme deficits

These cause an increase in the androngens and adrenogenital syndrome

39
Q

What secondary deficits can occur to cause adrenocortical insufficiency (hyposecretion)?

A

Only cortisol is affected by secondary deficits

  • Abnormal hypothalamus or pituitary problems leading to decreased CRH or ACTH.
  • Mineralocorticoids are not affected by this pathway
40
Q

Describe the adrenal medulla in terms of function and secretions

A
  • It is a modified part of the SNS (ie. it is the post-ganglionic cell)
  • It is involved in the flight-or-fight response
  • It releases Catecholamines
    • Adrenaline
    • ​Noradrenaline
    • Dopamine
41
Q

What is the main cell of the adrenal medulla important for the neurohormonal effect?

A

The chromaffin cell

It secretes and stores the neurohormones

42
Q

What is important about adrenaline synthesis in terms of the adrenal medulla

A

The enzyme that converts noradrenaline to adrenaline, Phenlethanolamine-N-methyltransferase PMNT, is only present in the adrenal medulla

43
Q

What are the main actions of the adrenomedullary catecholamines?

A
  • Flight or fight: ↑HR, ↑Contractility, ↑TPR, ↑BP
  • Metabolism: ↑glucose and free-fatty acid release, ↑BMR
  • Central: ↑arousal and ↑alertness
  • Stress responses
44
Q

What are the hyposecretory catecholamine disorders?

A

There are none recognised

45
Q

What are the hypersecretory catecholamine disorders?

A

Pheochromocytoma

(tumour of the adrenal medulla)

  • These are very rare and potentially deadly (hypertension)
  • The only treatment is removal of the tumour
46
Q

What are the 2 broad types of stresses that disrupt homeostasis?

A

07. Endocrine (10 decks)

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