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Endocrinology > Lect. 5 - Adrenal glands > Flashcards

Lect. 5 - Adrenal glands Flashcards

1
Q

Describe the Anatomy of the adrenal glands

A

An adrenal gland is actually two glands,
cortex and medulla that sit upon each
kidney.

The blood supply enters the cortex in
the subcapsular region and flows
through anastomotic capillary beds while
coursing through first the cortex and
then the medulla.

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2
Q

The adrenal cortex comprises three
layers that surround the medulla:

A

zona

  • Glomerulosa
  • Fasciculata
  • Reticularis
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3
Q

The adrenal medulla contains?
Is derived from?

A

chromaffin cells.

of neuroectodermal origin

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4
Q

The adrenal cortex is derived from?

A

mesoderm

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5
Q

The hormone groups produced by the adrenal cortex (3):

A

glucocorticoids
mineralcorticoids
androgens

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6
Q

Glucocorticoids are defined on the basis of

A

the actions they exert on gluconeogensis but are known to exert numerous other effects too.

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7
Q

Name 2 glucocorticoids.

A
  • cortisol (hydrocortisone as drug), controls the body’s use of fats, proteins, and carbohydrates.
  • corticosterone - together with cortisol (hydrocortisone), suppresses inflammatory
    reactions in the body and also affects the immune system.
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8
Q

Cortisol (hydrocortisone as drug), controls

A

the body’s use of fats, proteins, and
carbohydrates.

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9
Q

Corticosterone - together with cortisol (hydrocortisone), suppresses

A

inflammatory reactions in the body and also affects the immune system.

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10
Q

Name the classic mineralcorticoid and its function.

A

electrolyte metabolism e.g. aldosterone.

Inhibits the level of sodium excreted into the urine, maintaining blood volume and blood pressure.

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11
Q

What is Androstenedione?

A

Androstenedione is a precursor of testosterone and other androgens, as well as of estrogens like estrone, in the body. Is producedin teh adrenal cortex.

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12
Q

What is DHEA?

A

Dehydroepiandrosterone is an endogenous steroid hormone precursor produced in the adrenal cortex.

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13
Q

Adrenocortical hormones are classified as either

A

mineralcorticoid or glucocorticoid in their activity, but there is an overlap in their activity.

For example, whereas cortisol is the dominant glucocorticoid hormone, it also has mineralocorticoid effects, although at reduced potency.

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14
Q

The synthesis of all steroid hormones utilizes (2)

A

cholesterol and pregnenolone in the synthetic pathway.

Conversion of pregnenolone to
particular steroid hormones
depends on which steroidogenic
enzymes are present within a given
cell.

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15
Q

If the synthesis of cortisol is prevented by any one of several dysfunctional enzymes, what might occur?

A

other steroid products might be produced in excess.

For example, a block in 21α-hydroxylase will iminish
production of both cortisol and aldosterone and
increase production of the sex steroids.

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16
Q

Are steroid hormones stored or released?

A

Being lipid molecules, steroids are not stored within the cells once synthesized. All steroid hormones synthesized in response to a particular stimulus are released into the circulation by diffusion.

This is in marked contrast to peptide/protein hormones which are packaged within secretory granules during synthesis and are released via exocytosis.

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17
Q

Describe steroid hormone transport

A

Being lipid molecules, Steroid hormones depend on binding plasma proteins for transport in blood .

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18
Q

Clearence half-life of
cortisol?
aldosterone?

A
  • cortisol: 60 min
  • Aldosterone: 20 min

The differences are attributable to protein binding in plasma.

Metabolized in liver.

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19
Q

CRH

A

Corticotropin-releasing hormone

Its main function is the stimulation of the pituitary synthesis of adrenocorticotropic hormone (ACTH), as part of the hypothalamic–pituitary–adrenal axis (HPA axis).

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20
Q

HPA axis

A

Hypothalamic-pituitary-adrenocortical axis.

hypothalamus produces Corticotropin-releasing hormone (CRH) which stimulates the adenohypophysis to synthesize and release adrenocorticotropic hormone (ACTH) which in turn stimulates production and release of cortisol and androgens by the cortex and medulla of the adrenal gland, respectively.

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21
Q

Cortisol exerts negative feedback at the level of

A

both the pituitary and hypothalamus.

In addition, ACTH produced by the corticotrophs negatively feeds back on the hypothalamic neurons in a “short loop.”

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22
Q

Although classified as a glucocorticoid, cortisol affects

A

more than the principal glucose-regulatory
tissues, namely, the liver, fat, and muscle.

Most body tissues, including bone,
skin, other viscera, hematopoietic
and lymphoid tissue, and the central
nervous system (CNS), are target sites
for glucocorticoid action.

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23
Q

Although cortisol is the primary glucocorticoid in humans, in other species (e.g., the rat), what
is the major glucocorticoid?

A

corticosterone is the major glucocorticoid in some other species.

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24
Q

Main Function of Glucocorticoids

A

glucose metabolism modulation

stimulation of hepatic gluconeogenesis, which
involves the conversion of amino acids to carbohydrates.

The net result is an increase in hepatic glycogen and a tendency toward increased blood glucose levels; = insulin resistance (effect is opposite to insulin).

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25
Q

Explain the anti insulin effect of glucocorticoids.

A

Glucocorticoids and insulin have similar effects on liver glycogen metabolism (stimulate gluconeogenesis), but their effects on peripherial use of glucose are different.

Glucocorticoids inhibit glucose uptake by cells and glucose metabolism in peripherial tissues,
particularly in muscle and adipose cells. This is the anti insulin effect.

The chronic administration of glucocorticoids can lead to development of a syndrome called “steroid diabetes” because of the hyperglycemic effect
produced at the level of the liver; use of glucose decreases in the peripheral tissues because of insulin antagonism.

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26
Q

Metabolic Effects of Glucocorticoids on fat metabolism

A

the direct effect on adipose tissue is to increase the rate of lipolysis and to distribute fat into the liver and abdomen (“potbellied” appearance).

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27
Q

Metabolic Effects of Glucocorticoids on protein metabolism

A

protein synthesis is inhibited; protein catabolism is enhanced with an accompanying release of amino acids leading to muscular atrophy.

Two tissues; cardiac and brain, are spared from
the effects of glucocorticoids on protein catabolism.

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28
Q

Metabolic Effects of Glucocorticoids on Calcium metabolism (3)

A

negative Ca2+ balance,
inhibition of ossification,
osteoporosis

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29
Q

Metabolic Effects of Glucocorticoids on Longitudinal growth

A

slowdown of longitudinal growth

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30
Q

Metabolic Effects of Glucocorticoids on Water diuresis

A

whereas glucocorticoids inhibit vasopressin activity
in the distal tubule, the most important effect is to decrease GFR.

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31
Q

Metabolic Effects of Glucocorticoids on the Cardiovascular system

A

increases the sensitivity of arterial vessels to catecholamines

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32
Q

Metabolic Effects of Glucocorticoids on the Immune system

A

suppresses immune system
(macrophages, lymphocytes)

Blocks inflammatory response

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33
Q

One of the most important clinical uses of
glucocorticoids is

A

the suppression of the inflammatory response

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34
Q

glucocorticoids suppress the inflammatory response by

A

inhibiting the synthesis of inflammatory mediators, such as prostaglandins,
thromboxanes, and leukotrienes, that rise as a result of arachidonic acid metabolism.

35
Q

Spontaneously occurring hyperadrenocorticism may be associated with (2)

A
  • inappropriate secretion of ACTH by the pituitary (pituitary-dependent hyperadrenocorticism)
  • or associated with a primary adrenal disorder (adrenal-dependent hyperadrenocorticism)
36
Q

pituitary-dependent hyperadrenocorticism refers to

A

inappropriate secretion of ACTH by the pituitary causing hypersecretion of cortisol/Cushing’s disease

37
Q

adrenal-dependent hyperadrenocorticism rfers to

A

associated with a primary adrenal gland disorder; atrophy, destruction, neoplasm etc.

38
Q

Which cell layer of the adrenal cortex synthesizes aldosterone?

A

The glomerulosa cells of the adrenal cortex synthesize aldosterone from cholesterol via
progesterone.

As with cortisol, no storage pool of presynthesized aldosterone is available in the glomerulosa cell for rapid secretion. Thus, secretion of aldosterone by the adrenal is limited by the rate at which the glomerulosa cells can synthesize the hormone.

39
Q

define secretagogue

A

a substance which promotes secretion.

40
Q

Name 2 physiologically more important secretagogues than ACTH for the stimulation of aldosterone production.

A

Although ACTH also stimulates the production of aldosterone in the glomerulosa cell, increases in extracellular [K+] and the peptide
hormone ANG II are physiologically more important secretagogues.

These secretagogues enhance secretion by increasing the activity of enzymes acting at rate-limiting steps in aldosterone synthesis.

41
Q

Once secreted, what % of circulating aldosterone remains free in plasma?

A

Once secreted, ~37% of circulating aldosterone remains free in plasma. The rest weakly binds to corticosteroid-binding globulin (CBG) (~21%) or albumin (~42%).

42
Q

CBG

A

Transcortin, also known as corticosteroid-binding globulin (CBG).

43
Q

The two primary mechanisms controlling
aldosterone release are the

A
  • renin-angiotensin system (RAS)
  • extracellular potassium K+
44
Q

RAS keeps the circulatory blood volume
constant by promoting aldosterone-induced
what exactly?

A

sodium retention during periods of
hypovolemia and by decreasing aldosterone-dependent sodium retention during
hypervolemia.

45
Q

independently of the RAS, what directly regulates aldosterone secretion

A

Plasma potassium ions

46
Q

In addition to RAS & K+, aldosterone secretion is
influenced by several other factors such as: (3)

A

ACTH,
natriuretic peptides,
and a variety of neurotransmitters.

47
Q

AVP

A

arginine vasopressin which is the same this as ADH

48
Q

Renin is secreted by

A

juxtaglomerular cells of kidney

49
Q

Renin is secreted in response to (2)

A

A decrease in arterial blood pressure.
A decrease in sodium load delivered to the distal tubule.

50
Q

What detects a decrease in arterial blood pressure in order to secrete renin?

A

vascular receptors in the afferent arteriole stimulate renin secretion in response to reduced renal perfusion pressure

51
Q

What detects a decrease in sodium load in order to secrete renin?

A

Na+ concentration of blood delivered to the distal tubule is measured by the macula densa cells of the juxtaglomerular apparatus.

52
Q

angiotensinogenase is also called

A

renin

is a proteolytic enzyme which splits a leucine-valine bond of angiotensinogen which Yields decapeptide angiotensin I (biologically inactive).

53
Q

What converts angiotensin I to angiotensin II and where?

A

Angiotensin converting enzyme (ACE) in the lung

54
Q

Angiotensin II binds to AT1 receptors on zona granulosa cells and stimulates aldosterone biosynthesis.

But it is also a very potent..?

A

vasoconstrictor and thus raises blood pressure via more than 1 mechanism

55
Q

Angiotensin II has a short half life of

A

~ 2 min

56
Q

name 3 effects of angiotensin II

A

effect on the hypothalamus to increase thirst

effect on blood vessels, vasoconstriction

effect on the adrenal cortex to produce aldosterone which increases Na+ and water retention

= all increase blood pressure

57
Q

Potassium ions directly regulate

A

aldosterone secretion from the zona glomerulosa, independently of the renin-angiotensin system

58
Q

Name aldosterone’s 3 effects on the kidney.

A
  • Stimulates Na+ reabsorption (lowers Na+ excretion)
  • Lowers H2O excretion
  • Stimulates K+ excretion
59
Q

ACTH stimulates the secretion of the adrenocortical androgens, called?

A

dehydroepiandrosterone (DHEA) and androstenedione

The adrenal androgens are weak hormones.

60
Q

Adrenal androgens are metabolically converted to

A

testosterone, and further into dihydrotestosterone

61
Q

what is the most abundant
steroid hormone in the circulation.

A

dehydroepiandrosterone/DHEA, with its sulphate conjugate (DHEAS), is the most abundant steroid hormone in the circulation.

The concentration of DHEA and androstenedione follows a diurnal
rhythm similar to that of cortisol.

62
Q

chromaffin cells may also be called

A

pheochromocytes (cells of the adrenal medulla)

can be regarded as modified postganglionic
sympathetic neurons lacking axons.

63
Q

Adrenal catecholamines

A

Produced by adrenal medulla
* epinephrine (also called adrenaline)
* norepinephrine (also called noradrenaline)

64
Q

main effects of epinephrine (also called adrenaline)

A

this hormone increases the heart rate and force of heart contractions,

facilitates blood flow to the muscles and brain, causes relaxation of smooth muscles,

helps with conversion of glycogen to glucose in the liver, and other activities.

65
Q

main effects of norepinephrine (also called noradrenaline)

A

this hormone has little effect on smooth muscle, metabolic processes, and cardiac output, but has strong vasoconstrictive effects, thus increasing blood pressure.

66
Q

the major catecholamine secreted by the adrenal medulla of most mammals

A

epinephrine

In whales and chicken norepinephrine dominates over epinephrine.

67
Q

Synthesis of catecholamines begins with what amino acid

A

Synthesis of catecholamines begins with the amino acid tyrosine which is taken up by chromaffin cells in the medulla and converted to norepinephrine and epinephrine.

68
Q

Secretion of norepinephrine and epinephrine is stimulated by

A

acetylcholine releasefrom preganglionic sympathetic fibers innervating the medulla.

Manytypes of “stresses” stimulate such secretion, including exercise, hypoglycemia and trauma.

69
Q

The plasma half-life of catecholamines is

A

very short (1–3 min)

70
Q

adrenergic b-receptors (in particular b2-receptors) have a much higher affinity for

A

epinephrine than norepinephrine

(whilst adrenergic a-receptors have about the same affinity for both)

71
Q

The effects of catecholamines depend on the

A

density of the different subtypes of receptors on specific organs and on the relative
concentrations of epinephrine and norepinephrine.

These effects are modulated by reflex mechanisms, e.g., as the blood pressure increases the heart rate is slowed and cardiac output tends to decrease.

72
Q

What is a Pheochromocytoma?

A

are catecholamine-producing neuroendocrine
tumors arising from either chromaffin cells of the adrenal medulla or extra-adrenal paraganglia. The latter are referred to as extra-adrenal pheochromocytoma or paragangliomas.

Pheochromocytoma is considered to be rare in dogs and even less frequent in cats.

73
Q

Adrenocortical insufficiency two major forms are:

A
  • (1) primary adrenocortical insufficiency due to lesions or disease processes in the adrenal cortices
  • (2) secondary adrenocortical insufficiency due to insufficient ACTH release by the pituitary.

In addition to these conditions of absolute hormone deficits, there can be relative adrenocortical insufficiency.

74
Q

primary adrenocortical insufficiency is due to

A

lesions or disease processes in the adrenal cortices.

results from progressive destruction of the adrenal cortices, which must involve 90% or more of the adrenocortical tissue before it causes symptoms and signs.

The immune-mediated destruction typically
terminates in absolute deficiencies of glucocorticoids and mineralocorticoids,
together with high plasma levels of ACTH due to
pronounced negative feedback to the hypothalamus and pituitary.

75
Q

secondary adrenocortical insufficiency is due to

A

insufficient ACTH release by the pituitary.

76
Q

Addison’s disease is

A

Primary adrenocortical insufficiency, The atrophy of the renal cortex is probably the end result of immune-mediated destruction.

The immune-mediated destruction typically
terminates in absolute deficiencies of glucocorticoids and mineralocorticoids,
together with high plasma levels of ACTH due to
pronounced negative feedback to the hypothalamus and pituitary.

Thomas Addison in 1855 first described the syndrome in man, which at that time was usually the result of tuberculosis.

77
Q

Feedback loop: elevated cortisol inhibits

A

release of corticotropin (ACTH) by the corticotrophs in the adenohypophysis.

it also inhibits release of corticotropin releasing-hormone by hypothalamic neurosecretory cells.

78
Q

Cortical adrenal tissue destruction may also be confined to the middle and inner zones
of the adrenal cortex, resulting in what is known as

A

atypical primary hypoadrenocorticism.

mineralocorticoid activity is retained which makes this condition easier to overlook.

the symptoms and signs of typical or classic primary hypoadrenocorticism are absent.

79
Q

Primary hypoadrenocorticism may be part of a polyglandular deficiency syndrome. Concurrent endocrine gland failure may include (3)

A

primary hypothyroidism,
type I diabetes mellitus,
and primary hypoparathyroidism.

80
Q

Other possible causes of primary
adrenocortical insufficiency, besides immune mediated tissue destruction (5)

A
  • adrenocortical hemorrhage
  • fungal infection
  • metastatic disease
  • iatrogenic hypoadrenocorticism
  • Treatment of hypercortisolism with o,p’-DDD or trilostane may deliberately or
    unintentionally destroy the adrenal cortices.
81
Q

Clinical manifestations of Primary
hypoadrenocorticism (dogs)

A
  • primarily young to middle-aged dogs (mean
    four years) with a predilection for females.
  • There is breed disposition; Portuguese water dogs, poodles, and Nova Scotia duck
    tolling retrievers. It is an inherited disorder in some breeds.
  • Weakness
  • Fatigue
  • Anorexia
  • Vomiting
  • hypotonic dehydration
82
Q

Clinical manifestations of Primary
hypoadrenocorticism (cats)

A
  • VERY RARE
  • A disease of young to middle-aged animals
  • There have been two reported cases of primary hypoadrenocorticism
    in cats due to infiltration of the adrenals by malignant lymphoma.
  • Weakness
  • Fatigue
  • Anorexia
  • Vomiting
  • hypotonic dehydration
83
Q

Primary hypoadrenocorticism Patients presenting with acute collapse/addisonian crisis usually have evidence of

A
  • Severe depression,
  • Weakness
  • hypotonic dehydration
  • generalized, marked hypovolaemia with hypotension
  • Vomiting
  • Diarrhoea
  • abdominal pain
  • hypothermia

The clinical manifestations are primarily due to mineralcorticoid deifciency.

Endocrinology (16 decks)

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