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Year 2 - Endocrine > Adrenal gland > Flashcards

Adrenal gland Flashcards

1
Q

Location of adrenal glands + peritonisation

A

Superior pole of kidneys

Retroperitoneal

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2
Q

Outline diagrammatically the structure of the (compound) adrenal gland, indicating its zonation.

A

Capsule

Zona glomerulosa
Zona fasiculata
Zona reticularis

adrenal medulla

Zona reticularis
Zona fasiculata
Zona glomerulosa

Capsule

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3
Q

Adrenal gland is split into 2 parts

A 
Adrenal medulla (25%)
Adrenal cortex (75%)
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4
Q

Which part of the adrenal gland is the true endocrine gland

A

Adrenal cortex

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5
Q

Adrenal medulla (centre part of adrenal gland) isn’t actually a true endocrine gland, what is its tissue derived from

A

Neural crest tissue

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6
Q

The adrenal cortex (75% of adrenal gland) secretes 3 classes of steroid hormones- name them

A

Mineralocorticoids, e.g. aldosterone

Glucocorticoids, e.g. cortisol

Sex steroids

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7
Q

What class of hormones does aldosterone belong to + function

A

mineralocorticoids

regulates Na+ and K+

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8
Q

What class of hormones does cortisol belong to + function

A

Glucocorticoids

Maintains plasma glucose

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9
Q

Adrenal medulla secretes what class of hormones

A

Catecholamines, e.g. epinephrine (adrenaline), noradrenaline, dopamine

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10
Q

The adrenal cortex is arranged in 3 concentric zones/layers, each layer producing a different class of hormone - name the layers and the hormone type secreted by each

A

Zona glomerulosa - aldosterone (mineralocorticoid)

Zona fasiculata - glucocorticoids

Zona reticularis - sex steroids

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11
Q

Which zone of the adrenal cortex is most superficial

Which zone is the thickest

A

Zona glomerulosa - most superficial

Zona fasiculata - thickest

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12
Q

What are all steroid hormones derived from + how are different steroid hormones derived from the same origin

A

All steroid hormones are derived from cholesterol, but different enzymes found in the different adrenal zones result in different end products of cholesterol

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13
Q

Outline the basic pathway that produces
-mineralocorticoids (e.g. aldosterone)

from cholesterol

+ what key enzyme is involved

A

Cholesterol –> intermediate compound –> progesterone, converted by 21-HYDROXYLASE, into another intermediate compound –> aldosterone

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14
Q

What enzyme is not involved in the production of sex steroids from cholesterol but is required in the production of mineralocorticoids and glucocorticoids from cholesterol

A

21-hydroxylase

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15
Q

Andro-stenedione and testosterone can be converted by what enzyme into forms of oestrogen such as oestrone and oestradiol

(naturally occurring forms of estrogen in females are estrone, estradiol and estriol)

A

aromatase

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16
Q

Defects in the enzyme, 21-hydroxylase, is a common cause of what condition + what does this condition result in

A

congenital adrenal hyperplasia
- resulting in deficiency of aldosterone and cortisol so disruption of salt and glucose balance as 21-hydroxylase is required for production of these

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17
Q

Androgens (male sex hormones such as testosterone) are precursors of what

A

Oestrogens

-androgens are produced in both sexes however just more abundant in males

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18
Q

Ambiguous genitalia is a sign of congenital adrenal hyperplasia (CAH) - why is this

A

Since CAH is when you’re deficient in 21-hydroxylase, mineralocorticoid and glucocorticoid production is limited so accumulating steroid precursors are channelled into excessive adrenal androgen production which doesn’t require 21-hydroxylase

19
Q

Points of control in the hypothalamic-pituitary-adrenal pathway of cortisol

A

Cortisol exhibits long loop negative feedback

  • on ACTH in the AP
  • on CRH in the hypothalamus

ACTH also exhibits short loop negative feedback on CRH in hypothalamus

20
Q

Why does a deficit in 21-hydroxylase cause hyperplasia of the adrenal gland, i.e. why does it get bigger (3)

A

Lack of 21-hydroxylase inhibits synthesis of cortisol.

This removes the negative feedback on ACTH and CRH release.

Increased ACTH secretion excessively stimulates adrenal gland –> enlargement of adrenal glands

21
Q

How is cortisol transported in the blood

A

95% is bound to carrier protein, cortisol binding globulin

only unbound hormone can diffuse into target cells

22
Q

How does cortisol stimulate altered gene expression

A

As it’s a steroid hormone, it binds to cytoplasmic receptor

The hormone receptor complex migrates to the nucleus, binding to DNA to alter gene expression, transcription and translation

23
Q

Describe the normal circadian basal rhythm in plasma total cortisol concentration (3)

A

Burst of cortisol release every morning around 7am, preceded (i.e. before) by a burst of ACTH release (highest during morning because of physiological stress)

Plasma cortisol starts decreasing after about 9am then release fluctuates throughout the day depending on the stimuli

Decreases further towards midnight and stays low until the morning burst

24
Q

Why does cortisol persist in the blood longer than ACTH (adrenocorticotropic hormone)

A

Because cortisol is a steroid hormone so has a longer half life than ACTH (a peptide hormone)

25
Q

Justify the view that the adrenal cortex is essential for survival of the individual while the adrenal medulla is not.

A

Adrenal cortex produces cortisol

  • loss of cortisol means we can’t deal with physiological stress, particularly in terms of maintaining BG levels.
  • Cortisol is crucial in helping to protect the brain from hypoglycaemia; it has a permissive action on glucagon, which is vital as glucagon alone is inadequate in responding to a hypoglycaemic challenge
26
Q

Physiological stress v psychological stress

A

physiological - maintaining plasma glucose, BP etc

psychological - mental stress

27
Q

Overall function of cortisol (a glucocorticoid)

A

Influences glucose metabolism

28
Q

Cortisol has glucocorticoid AND non-glucocorticoid actions

- describe the non-glucocorticoid actions of cortisol (i.e. those that don’t influence glucose metabolism) (4)

A
  1. Decreases Ca2+ absorption from gut and increases its excretion in urine –> net Ca2+ loss
  2. Impairs mood + cognition - associated with hypercortisolaemia
  3. Permissive with noradrenaline, particularly in vasoconstriction
  4. Suppresses the immune system - cortisol reduces circulating lymphocytes, antibody formation and inhibits inflammation
29
Q

Effect on plasma glucose concentration of administering cortisol to a normal subject; and list the TARGET SITES and processes of cortisol underlying that effect

(i.e. describe the glucocorticoid actions (those that influence glucose metabolism) of cortisol) (4)

A

Increases plasma glucose - by acting on liver, muscle, adipose tissue

  1. Stimulates gluconeogenesis - cortisol acts on LIVER TISSUE and stimulates formation of glucose from amino acids
  2. Stimulates proteolysis - cortisol acts on MUSCLE TISSUE and stimulates breakdown of muscle to provide gluconeogenic substrates
  3. Stimulates lipolysis - cortisol acts on ADIPOSE TISSUE and stimulates adipose tissue breakdown which increases free fatty acids creating an alternative energy source and also a gluconeogenic substrate
  4. Decrease insulin sensitivity
30
Q

Side effects of glucocorticoid therapy (3)

A

Muscle wasting - as cortisol stimulates protein breakdown

Loss of percutaneous fat - as cortisol stimulates lipolysis so get thinking of skin

Increased susceptibility to infection as immune function suppressed

31
Q

Function of aldosterone + effect of increased aldosterone

A

MAINTAINS BP
- increases the reabsorption of Na+ ions (and therefore H2O) and promotes the excretion of K+ ions

increased aldosterone –> increased blood volume and BP

32
Q

Where does aldosterone act on

A

distal tubule of the kidney

33
Q

Hypersecretion of cortisol causes (i.e. hyperfunction of adrenal cortex) (3)

A

Cushing’s syndrome
Cushing’s disease
Iatrogenic - too much cortisol administered

34
Q

Cushing’s syndrome involves hypersecretion of what

Cushing’s syndrome aka

A

of cortisol, commonly due to a tumour in the adrenal cortex

Primary hypercortisolism

35
Q

Cushing’s disease involves hypersecretion of what

Cushing’s disease aka

A

of cortisol, commonly due to a tumour in the pituitary gland

Secondary hypercortisolism - excess ACTH

36
Q

What disease is associated with adrenal hypofunction + describe it

A

Addison’s disease

-hyposecretion of all adrenal steroid hormones (not just cortisol) due to autoimmune destruction of adrenal cortex

37
Q

What’s special about post-ganglionic fibres in the adrenal medulla

A

They have no axons, so just release their neurohormones (adrenaline) into blood

38
Q

What is a pheochromocytoma + where is it found + what effect does it have

A

rare neuroendocrine tumour, found in adrenal medulla which results in excess catecholamines (adrenaline etc)
–> increased HR –> increased CO –> increased BP

Is diabetogenic (i.e. causes DM like symptoms)

39
Q

Tertiary hypercortisolaemia would be due to a pathology where

A

Hypothalamus

40
Q

Why do we need to be careful when withdrawing chronic glucocorticoid treatment

A

Exogenous cortisol enhances negative feedback effects of cortisol on the hypothalamus and pituitary releasing CRH and ACTH respectively

So withdrawing it decreased the negative feedback effects,?

41
Q

Precursor of adrenaline and noradrenaline

A

Dopamine

42
Q

Schematics of a normal hypothalamic-pituitary-adrenal axis + negative feedback

A 
CRH
|
| 
ACTH
|
|
Cortisol

Cortisol production from adrenal gland will exhibit negative feedback on ACTH and CRH

43
Q

Precursors of the sex steroids (2)

A

DHEA (dehydroepiandrosterone)
Andro-stenedione

Ultimately from cholesterol

44
Q

Progesterone is a precursor of… (2)

A

mineralocorticoids (aldosterone)

glucocorticoids (cortisol)

Year 2 - Endocrine (21 decks)

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