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FHB Block 4 > L5- HPA Axis and Adrenal Gland > Flashcards

L5- HPA Axis and Adrenal Gland Flashcards

1
Q

What are the three components of the HPA axis?

A

Hypothalamus, pituitary, adrenal gland

Hypothalamus release corticotropin-releasing hormone (CRH)/CRF which stimulates the release of ACTH from the pituitary. ACTH stimulates the release of multiple hormones from the adrenal gland

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2
Q

The adrenal gland is regulated by which axis?

A

HPA

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3
Q

What hormones does the adrenal gland release in response to stress?

A

Epinephrine and norepinephrine and Cortisol

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4
Q

How does the adrenal gland play a role in the immune system?

A

Glucocorticoids (cortisol) are anti-inflammatory

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5
Q

Which adrenal hormone is not regulated by the HPA axis?

A

Mineralocorticoids- aldosterone

–> Maintenance of water, sodium and potassium balance/blood pressure is not regulated by the HPA axis

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6
Q

Is the production of weak androgens such as DHEA/DHEAS regulated by the HPA axis?

A

No

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7
Q

Where in the hypothalamus is corticotropin-releasing hormone synthesized? Where is it released?

A

Corticotropin-releasing hormone is made in the parvocellular neurons of PVN and released at the median eminence and stimulates POMC gene expression and ACTH release from corticotropes in the anterior pituitary

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8
Q

How is the HPA axis regulated?

A

Classical negative feedback pathways:

Cortisol inhibits both ACTH and CRH release.

ACTh inhibits CRH release

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9
Q

What is POMC?

A

POMC is a gene in the anterior pituitary responsible for the synthesis of ACTH

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10
Q

What is the expression pattern (timing) or CRH?

A

Pulsatile

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11
Q

What sorts of stimuli lead to increased CRH production?

A

Stress of all sorts- physical, emotional, chemical

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12
Q

Differentiate CRH R1 from CRH R2

A

CRH has two receptors: CRH R1 and CRH R2 - both G protein-coupled receptors

R1: Found in the anterior pituitary,binds CRH with the highest affinity

R2: Found in the brain- binds with higher affinity to urocoritn

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13
Q

Discuss the relationship between AVP and CRH in response to stress.

A

AVP release acts synergistically with CRH for stimulation of ACTH in response to stress

AVP+CRH leads to higher levels of ACTH than CRH alone

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14
Q

How does the release of cortisol affect the release of AVP and CRH?

A

Cortisol binds to GR in the hypothalamus and pituitary and inhibits the release of AVP and CRH

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15
Q

The release of ACTH is regulated by what two corticotropes from the hypothalamus?

A

AVP and CRH

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16
Q

What is the precursor for ACTH?

A

POMC (pro-opiomelanocortin)

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17
Q

ACTH released from the anterior pituitary binds to what receptor in the adrenal cortex?

A

ACTH binds with high affinity to the melanocortin 2 receptor in the adrenal cortex which leads to the synthesis and release of cortisol

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18
Q

Cortisol release has what two main effects?

A

Increase blood glucose

Decrease inflammatory response

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19
Q

At very high levels, ACTH will bind to what other receptor (with low affinity)? What is the outcome?

A

With sufficiently high levels of plasma ACTH, ACTH will begin to bind to the low affinity melanocortin 1 receptor located in the melanocytes of the skin. This leads to hyperpigmentation.

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20
Q

The adrenal cortex is derived from what germ layer?

A

The mesoderm. The adrenal cortex is glandular

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21
Q

The adrenal medulla is derived from which germ layer?

A

Neural crest- it is essentially a giant sympathetic postganglionic neuron. Sympathetic innervation synapses on medullary cells

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22
Q

What are the three functional layers of the adrenal cortex?

A

Capsule –> zona glomerulosa –> zona fasciculata –> zona reticularis

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23
Q

Generally, what are the immediate effects of ACTH binding to the MC2R in the adrenal cortex?

A

Breakdown of stored cholesterol (cholesterol synthesis) and activation of the STAR protein for synthesis of cholesterol-derived hormones

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24
Q

What are the secondary responses to ACTH binding to the MC2R of the adrenal cortex?

A

Mostly increased gene transcription of the enzymes responsible for generation of conversion to steroid hormones

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25
Q

What are the long-term responses to ACTH binding to MC2R of the adrenal cortex?

A

Hyperplasia of the adrenal gland

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26
Q

How does ACTH regulated the synthesis of aldosterone from the zona glomerulosa?

A

ACTH does NOT regulate aldosterone in the zona glomerulosa, but does regulate the biosynthesis of aldosterone precursors

27
Q

What does ACTH stimulate in the zona fasciculata and reticularis?

A

ACTH stimulates cellular hypertrophy, biosynthesis of cortisol and biosynthesis of DHEA

28
Q

What is produced in the zona glomerulosa?

A

Mineralocorticoids

29
Q

What is produced in the zona fasciculata?

A

Glucocorticoids

30
Q

What is produced in the zona reticularis?

A

weak androgens (DHEA/DHEAS)

31
Q

What is produced in the adrenal medulla?

A

Catecholamines (Epinephrine and norepinephrine)

32
Q

What is the blood supply to the adrenal cortex?

A

Blood from the capsular artery flows from the outer cortex to the adrenal core through a series of capillary beds. The direction of blood flow controls access of steroid hormones to the general circulation

33
Q

What is the blood supply to the adrenal medulla?

A

Dual blood supply- the blood bathes the medullary cells carrying corticosteroids from the cortex, which is necessary for for conversion of NE to E

The other blood supply is clean and not chock full of newly-synthesized hormones from the cortex

34
Q

Which is the active/inactive forms of the major glucocorticoid?

A

Cortisol: active
Cortisone: inactive

35
Q

How does cortisol travel through the blood?

A

Bound to transport proteins- CBG- must dissociate in order to be active.

36
Q

Discuss the timing of the release of glucocorticoids

A

Circadian- peaks around 8am

37
Q

Cortisol binds with high affinity to what two receptors?

A

GR and MR

38
Q

What enzyme is responsible for the conversion of cortisone to cortisol?

A

11 beta-HSD1

39
Q

What enzyme is responsible for the inactivation of cortisol to cortisone?

A

11 beta HSD-2

40
Q

What is the role of corticosteroid binding globulin?

A

CBG is responsible for the transport of 90% of cortisol in the blood

41
Q

How is CBG affected by estrogen? What is the result?

A

Estrogen decreases CBG, which results in free cortisol in the blood

42
Q

How do other stress responses (response to shock/severe infection etc) affect CBG?

A

Stress leads to the decrease of CBG which leads to an increase in free cortisol in the blood/increased bioavailability= greater cortisol effect on the body

43
Q

Where is GR expressed?

A

Ubiquitously in most tissues- which means cortisol can act in nearly all tissues

44
Q

What type of receptor is GR?

A

GR is a transcription factor

45
Q

What does it mean that “cortisol is a pleiotropic hormone”?

A

Cortisol has many different tissue-specific effects:

Decreases connective tissue, inhibits inflammatory immune responses, maintains cardiac output, increases GFR and free water clearance etc…

46
Q

How does cortisol affect metabolism?

A

Cortisol is a potent counter-regulatory hormone to insulin. It mobilizes energy stores to increase plasma glucose levels (hence the name “glucocorticoid”)

47
Q

How does cortisol affect Ca2+ absorption in the kidneys?

A

Cortisol inhibits intestinal calcium absorption

48
Q

How does cortisol affect tyrosine aminotransferase, PEP carboxykinase and glucose-6-phosphatase?

A

Increases –> important for increasing plasma glucose levels via gluconeogenesis

49
Q

How does cortisol affect GLUT4 insertion in the membrane of muscle cells?

A

Decrease: this decreases glucose uptake into muscle cells to preserve plasma glucose levels for the brain and heart during times of stress

50
Q

How does cortisol affect the muscle?

A

Cortisol stimulates proteolysis in the muscle- it simultaneously inhibits amino acid uptake and AKT-phosphorylation resulting in decreased protein synthesis

This is accomplished through transcription of E3 ubiquitin ligase

51
Q

How does cortisol affect adipose tissue?

A

Increase lipolysis

Cortisol redistributes fat stores- results in abdominal obesity, depletion of subcutaneous fat (thinning of limbs)

52
Q

How does cortisol affect the immune system via NF kappa B?

A

Cortisol both binds NF kappa B and increases the transcription of I kappa B thereby inhibiting NF kappa B from translocating into the nucleus and upregulating the transcription of pro-inflammatory cytokines

53
Q

How does the cortisol affect neutrophils, platelets and RBCs?

A

Although cortisol activates neutrophil production such that they increase in number, the neutrophils are inhibited in their function

54
Q

How does cortisol affect bone?

A

Inhibits calcium absorption (via blocking active transport) and inhibits bone formation by decreasing IGF-1 receptors.

Cortisol also increases bone resorption via activation of osteoclasts.

55
Q

How does cortisol affect the cardiovascular system?

A

Stimulation of RBC production and maintains responsiveness to catecholamine

56
Q

How does a glucocorticoid deficiency affect blood pressure?

A

Glucocorticoid deficiencies lead to hypotension

57
Q

How does cortisol affect the CNS?

A

Cortisol mediates psychological response to stress (depression, anxiety, nervousness, panic, etc), and has a negative feedback on the release of CRH and ACTH

58
Q

Differentiate Cushing Disease from Cushing Syndrome

A

Disease: excessive cortisol secretion due to a pituitary adenoma (lots of ACTH produced)

Syndrome: all other problems that lead to increased cortisol

59
Q

Discuss the effects of cushings on a body

A

Changes in fat distribution, osteoporosis, hypertension, glucose intolerance, and purple straie

60
Q

Why must someone be weaned off cortisol/glucocorticoid therapy?

A

Exogenous cortisol leads to a downregulation of ACTH such that ACTH/cortisol is not synthesized normally by the body and leads to zona fasciculata atrophy. Stopping glucocorticoid treatment abruptly can result in shock or death

61
Q

What is adrenal insufficiency?

A

Failure of adrenal glands to secrete glucocorticoids, mineralocorticoids or both.

62
Q

What is addison’s disease?

A

Addisons’ is primary adrenal insufficiency. It is the failure of the adrenal gland to produce hormones, caused by an autoimmune destruction of the adrenals

63
Q

What is a secondary adrenal insufficiency?

A

Failure to secrete CRH or ACTH, most commonly caused by sudden cessation of glucocorticoid therapy.

FHB Block 4 (15 decks)

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