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HPA axis and adrenal gland (L5) Flashcards

1
Q

Catecholamines

A

Epinephrine, norepinephrine

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2
Q

Glucocorticoids

A

Cortisol

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3
Q

Two things regulated by the HPA axis

A

Adaptive response to stress and anti-inflammatory immune function

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4
Q

Things NOT regulated by the HPA axis in which the adrenal gland is involved

A

Maintainance of blood pressure, sodium, and potassium mediated by mineralocorticoids
“Weak” androgen production

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5
Q

Where is corticotropin releasing hormone made?

A

In the paraventricular nucleus

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6
Q

CRH stimulates what gene?

A

POMC

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7
Q

How is CRH linked to the adrenal gland?

A

Stimulates release of ACTH in the anterior pituitary, which then stimulates the adrenal gland to produce and release cortisol

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8
Q

How is the HPA axis regulated?

A

By classical feedback mechanisms

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9
Q

What are some of the stimuli for CRH release?

A

Physical/emotional stress, hypoglycemia, others

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10
Q

How long is CRH?

A

41 amino acids

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11
Q

Where is CRH made?

A

Parvocellular cells in the paraventricular nucleus

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12
Q

How is CRH released?

A

In pulses

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13
Q

Half life of CRH

A

~5 minutes

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14
Q

CRH receptors

A

There are two.
CRH binds with higher affinity to CRHR1 in the anterior pituitary
CRHR2 binds with more affinity to urocortin

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15
Q

Second messengers of CRH binding

A

At least five different ones are activated; PKA release is the most important for ACTH release

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16
Q

CRH acts synergystically with what other hormone?

A

AVP

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17
Q

What does the synergystic action of AVP and CRH do?

A

Increases the amplitude of ACTH release

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18
Q

Negative feedback mechanism

A

Cortisol binds to nuclear steroid glucocorticoid receptors in the nucleus and inhibits synthesis and release of CRH and ACTH

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19
Q

What is the precursor to ACTH?

A

POMC (pro-opiomelanocortin)

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20
Q

What else can the POMC gene encode?

A

Beta-lipotropin
Beta-endorphin
Melanocortin stimulating hormone
Enkephalin

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21
Q

Important hormones from POMC gene during pregnancy and development

A

Beta-MSH
Beta-endorphin
Enkephalin
(Made in the intermediate lobe)

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22
Q

Main actions of ACTH in the adrenal gland

A

Stimulates steroid biosynthesis

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23
Q

ACTH in the zona reticularis and fasciculata

A

Cellular hypertropy
DHEA production
Cortisol production

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24
Q

ACTH in the adrenal medulla

A

Stimulates conversion of dopamine to norepinephrine

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25
ACTH in the zona glomerulosa
Does not directly affect aldosterone production, but does mediate the synthesis of aldosterone precursors
26
What is the main receptor for ACTH?
MC2R (melanocortin 2) - high affinity
27
What is the secondary receptor for ACTH?
MC1R in the skin (high ACTH levels can lead to hyperpigmentation)
28
Where does the adrenal cortex come from embryologically?
The mesoderm
29
Where does the medulla come from embryologically?
The neural crest; the medulla is a "modified sympathetic postganglionic neuron"
30
Order of adrenal layers from superficial to deep with percentage surface area
``` Zona glomerulosa (15%) Zona fasciculata (65-80%) Zona reticularis ( ```
31
What feature is most striking in the ultrastructure of a steroidogenic cell?
The presence of large lipid droplets
32
Capsular artery
Gives rise to arterioles that perfuse the adrenal cortex all the way through the medulla
33
What is made in each of the layers of the adrenal cortex?
ZG: mineralocortocoids ZF: glucocortocoids ZR: androgens M: catecholamines
34
To what is cortisol bound in the blood, and how much of it is free?
Bound to corticosteroid binding globulin,
35
When does cortisol peak?
Around 8AM
36
To what family does CBG belong?
The serpin family of protease inhibitors, but it is NOT one
37
How long is CBG and where is it made?
383 amino acid glycoprotein made in the liver
38
CBG's relative affinity for cortisol vs. aldosterone
30x greater for cortisol
39
Estrogen and CBG
Estrogen decreases the amount of available CBG, increasing the amount of free cortisol
40
What external factor decreases CBG?
Shock/severe infection
41
Glucocorticoid receptors - location and abundance
Nuclear receptor that is ubiquitously expressed in most tissues
42
Mechanism of GRs
Cortisol binds to the receptors in the cytoplasm, dissociates its associated proteins, and then translocates to the nucleus and acts as a transcription factor
43
General metabolic actions of cortisol
Increases the amount of glucose in the blood; potent counter-regulatory hormone to insulin
44
Cortisol's effect on metabolic enzymes
Increases activity of tyrosine aminotransferase, PEPCK, and G6Pase.
45
Cortisol's effect on glucose transporters
Decreases the amount of GLUT4 on muscle cells
46
Positive effects of cortisol on skeletal muscle
Increases MuRF and E3 ubiquitin ligase, stimulating protein degradation
47
Negative effects of cortisol on skeletal muscle
Downregulates AKT phosphorylation and amino acid uptake, decreasing protein synthesis
48
MgII gene
Upregulated by cortisol, which encodes for monacylglycerol lipase
49
Lipe gene
Encodes hormone sensitive lipase, which is upregulated by cortisol
50
Angpt gene
Upregulated by cortisol; increases cellular cAMP and activates hormone sensitive lipase
51
Redistribution of fat
Induced by cortisol; results in abdominal obesity and thinning of limbs
52
Immune system and cortisol
Proinflammatory response disrupted by binding directly to activated NFkB and inhibiting its transcription factor activity in the nucleus AND by increasing transcription of IkB that also helps keep NFkB sequestered in the cytoplasm
53
Four effects of cortisol on the immune system
1. Stimulates anti-inflammatory cytokines 2. Inhibits prostaglandins 3. Supresses antibody production 4. Increases neutrophils, platelets, and RBCs
54
Negative effects of cortisol on bone
Inhibits bone formation by decreasing IGF-1 Rs | Inhibits intestinal calcium absorption
55
Positive effects of cortisol on bone
Increases bone resorption by activating osteoclasts
56
CV maintenance by cortisol
Maintains catecholamine pressor effects | Maintains vascular integrity and reactivity
57
CNS effects of cortisol
Emotional response and perceptivity (Depression, rage, anxiety, panic, nervousness) Inhibits CRH and ACTH
58
Cushing disease
Excess cortisol release due to pituitary adenoma
59
Cushing syndrome
Excess cortisol NOT caued by pituitary adenoma
60
Symptoms of cushing disease (5)
``` Change in body fat distribution Osteoporosis Hypertension (excess GCs activate MRs) Glucose intolerance (due to antagonistic effects on insulin) Purple striae ```
61
What happens with prolonged glucocorticoid therapy?
Constant negative feedback on the pituitary and hypothalamus to release CRH and ACTH causes atrophy of these neurons, resulting in dependence on exogenous GCs
62
When is acute GC treatment used?
In the case of medical emergencies such as asthma attacks, autoimmune flares, or septic shock
63
When is chronic GC treatment used?
For immunosuppressive therapy, autoimmune diseases, adrenal insufficiency, and as treatment to help pre-term infants
64
Define adrenal insufficiency.
The inability to produce glucocorticoids, mineralocorticoids, or both
65
Primary adrenal insufficiency
Failure of the adrenal gland itself; usually manifested as Addison's disease (70%). Autoimmune destruction
66
Secondary adrenal insufficiency
Lack of CRH or ACTH; usually caused by sudden cessation of glucocorticoid therapy

Endocrine (11 decks)

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