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FHB - Endocrine & Reproductive > Lecture 5 (72): HPA Axis and Adrenal Gland > Flashcards

Lecture 5 (72): HPA Axis and Adrenal Gland Flashcards

1
Q

What parts of the adrenal gland are regulated by the HPA axis?

Which are not regulated by HPA axis?

A
  1. Adaptive response to stress
    a) Catecholamines, epinephrine, norepinephrine)
    b) Glucocorticoids – cortisol
  2. Immune function
    a) Anti-inflammatory – glucocorticoids

NOT REGULATED:

1.Maintenance of water, sodium, potassium balance and blood
pressure
2.Mineralocorticoids – aldosterone

  1. Site of “weak” androgen production
    - DHEA/DHEAS
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2
Q

What is the HPA axis for ACTH?

A
  1. Hypothalamus –> CRH/CRF
  2. Pituitary –> ACTH
  3. Adrenal
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3
Q

What is the short feedback of the Adrenal Gland?

Long?

A
  1. ACTh

2. Cortisol

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4
Q

_____ is Central regulator of ACTH HPA axis - 41 amino acids

Produced in parvocellular neurons of _____.

Stimulates _____

A
  1. CRH
  2. PVN
  3. anterior pituitary (POMC/ACTH)
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5
Q

CRH release is _____ (pulsatile/slow).

What is the result?

Half life?

A
  1. PULSATILE
  2. Episodic release of ACTH
  3. Half life - 5 min
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6
Q

CRH uses what type of receptors?

CRH R1/R2 binds with highest affinity to CRH?

What doe R2 bind?

A

G protein-coupled receptors

– CRH R1 and CRH R2. Binds with highest affinity to CRH R1 in anterior pituitary.

CRH R2 binds with higher affinity to Urocortin.

Evidence for multiple intracellular signaling pathways – CRH can activate at least 5 different G proteins

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7
Q

What is CRH synergistic with?

A

AVP

-ACTH release is amplified in the presence of AVP

  • AVP
  • IMPORTANT MODULATOR OF THE STRESS RESPONSE because of the synergistic affect
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8
Q

ACTH:

Produced in the _____pituitary

Regulated by _____ (2) from hypothalamus

What is the precursor?

A
  1. anterior ((corticotroph)
  2. CRH and AVP
  3. Precursor = POMC (pro-opiomelanocortin)
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9
Q

ACTH:

Binds with high affinity to what receptor?

Binds with low affinity what other receptor?

High levels of ACTH lead to ______

A
  1. melanocortin 2 receptor (MC2R)
  2. to MC1R (skin)
  3. hyperpigmentation
    - Melanocye t 1 in skin - can get binding with increased ACTH = HYPERPIGMENTATION
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10
Q

What are some important effects of MC2R (ACTH receptor)?

A

Immediate Effects  stimulate the 1st step of steroid/hormone biosynthesis/ STAR important to transport cholesterol from outer to inner mitochondrial membrane
Subsequent effects
Long – Term consequences of overproduction of ACTH

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11
Q

The 1st step of steroid hormone synthesis requires ACTH why?

A

increases cAMP to increase cholesterol esterase and increase STAR to transport cholesterol from outer to inner mitochondrial membrane

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12
Q

What are the 2 divisions of the Adrenal Gland?

A

FUNCTIONALLY 2 GLANDS

1 Cortex = steroid hormones

  1. Medulla = catecholaines

Cortex derives from mesoderm

Medulla derives from neural crest: modified “sympathetic postganglionic neurons”.

Sympathetic innervation synapses on medullary cells.
in ADRENAL Gland (acting like neural tissue)

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13
Q

What are the 3 layers of the adrenal gland?

A
  1. Zona glomerulosa (mineralcorticoids)
  2. Zona fasciculata (GLUCOCORTICOIDS)
  3. Zona Reticularis - weak androgens (DHEAS)
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14
Q

What hormones do the following layers of the Adrenal Gland make?

  1. Zona glomerulosa
  2. Zona fasciculata
  3. Zona Reticularis
A
  1. Zona glomerulosa (mineralcorticoids)
  2. Zona fasciculata (GLUCOCORTICOIDS)
  3. Zona Reticularis - weak androgens (DHEAS)
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15
Q

What cells make cholesterol within the Adrenal Gland?

A

SPONGIOCYTES

- giant lipid droplets containing cholesterol

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16
Q

What is the blood supply to the ADRENAL gland?

  1. Cortex
  2. Medulla
A

Cortex: Suprarenal arteries break into subcapsular plexus of capillaries (fenestrated).

Medulla: Dual blood supply

Bathes the medullary cells with blood carrying corticosteriods from the cortex – important for conversion of NE to E.

Arterioles break into fenestrated (with diaphragm) capillaries.

All blood drains into central vein

17
Q

Cortisol:

  1. Released in response to_____.
  2. Binds with high affinity to _____. (2 receptors)
  3. Cortisone (inactive) converted to Cortisol by what?
A
  1. acute/chronic stress (physical – starvation, illness; psychological)
  2. glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) in cytoplasm
  3. by 11β-HSD1
18
Q

Corticosteroid Binding Globulin (CBG)/TRanscortin

  1. Made where?
  2. Most found bound to what?
  3. What increases CBG –> increases FREE cortisol?
  4. What decreases CBG?
A
  1. 383 AA glycoprotein made in the liver
  2. 90% circulating cortisol bound to CBG; 7% bound to albumin
    - 4% “free” cortisol
  • 30-fold higher affinity for cortisol than aldosterone
    3. Estrogen decreases CBG – results in increased free cortisol
  1. Shock/severe infection decreases CBG
    - want free cortisol for anti-inflammatory affects
19
Q

What hormone causes more free cortisol?

20
Q
  1. Glucorticoids are made where?
  2. Peaks where?
  3. Bound to what transport proteins in blood? (active/inactive?)
A
  1. Made in the Zona Fasciculata Cortisol
    - Accounts for more than 80% of cortical hormones
  2. Released in circadian manner – peaks around 8:00 AM
  3. Bound to transport proteins in blood (CBG) – must dissociate in order to be active (~ 5% free)
21
Q

Why is cortisol a pleiotropic hormone?

A

CORTISOL:
decrease bone formation OSTEOPOROSIS risk
mood
state of arrousal
maturation of fetus
increase surfactant in blood ( Cortisol given to premature babies to increase surfactant production)
MOBILIZES GLUCOSE - gluconeogenesis

22
Q

What are the metabolic action of cortisol?

What does it counter?

A

Metabolic Actions – potent counter-regulatory hormone to insulin.

Mobilizes energy stores – increase plasma glucose = “glucocorticoid”.

  1. Increase gluconeogenesis and plasma glucose levels
  2. Increase lipolysis
  3. Breaks down muscle protein - proteolysis
  4. Redistributes fat – abdominal obesity, depletion of subcutaneous fat
  5. Antagonizes insulin action
  6. Inhibits intestinal calcium absorption** (will discuss more in Ca2+ regulation lecture)
    = BONE BREAKDOWN (one of the reasons)
23
Q

What are the main functions of cortisol?

WHat 3 enzymes does it need for this?

A
  1. Increase gluconeogenesis an plasma glucose levels
  2. Glucose - 6- Phosphotase
  3. PEPCK
  4. Tyrosin Aminotransferase
24
Q

How does cortisol affect muscle?

A
  1. Inhibit GLUT 4 insertion on membrane
  2. Decrease glucose uptake in muscle cells
  3. Maintains PLASMA GLUCOSE!
  4. PROTEOLYSIS
    - cortisol stimulates protein degradation and decreases protein synthesis

how? stimulate the phosphorylation of FOXO- P

= stimulate E3 ubiquitin ligase to increase protein degradation

25
How does Cortisol affect fat stores?
Increases lipolysis STIMULATE GENE TRANSCRIPTION: (2lipases) Mag Lipase HSTL (lipase)
26
Glucocorticoid Receptor: 1. What do local inflammatory responses cause? 2. GR increases _____ 3. Glucocorticoids prevent ____ translocation to the nucleus.
Local inflammatory responses decreased by GR action on NF-κB (pro-inflammatory cytokines) GR increases IκB transcription Glucocorticoids prevent NF-κB nuclear translocation
27
What are cortisol functions on the immune system?
Immune – 1. Decreases inflammation 2. stimulates anti-inflammatory cytokines 3. inhibits prostaglandins 4. Suppresses antibody production 5. Increases neutrophils, platelets, and RBCs. (Anti-inflammatory effects are primary reason for glucocorticoid therapy)
28
What are the 3 affects of Cortisol on bone? What receptors does it decrease?
Inhibits intestinal calcium absorption – transcellular transport Inhibits bone formation – decrease IGF-I receptors Increases bone resorption – activation of osteoclasts
29
What are the affects of Cortisol on CARDIOVASCULAR?
1. Cardiovascular – during “physical stress” want blood to flow to brain/heart – away from periphery 2. Stimulates red blood cell production 3. Maintains responsiveness to catecholamine pressor effects 4. constrict peripheral vessels via alpha-adrenergic receptors 5. Dilate coronary arteries in heart via beta-adrenergic receptors 6. Glucocorticoid excess = increased blood pressure/hypertension Maintains vascular integrity and reactivity
30
What does cortisol have negative feedback on?
1. CRH and ACTH release
31
What are the actions of cortisol on the CNS?
``` Central Nervous System – Emotional response depression anxiety nervousness panic rage/aggression ```
32
What is cushing disease? Why does it occur? What are the symptoms?
Excessive cortisol secretion due to PITUITARY adenoma Change in body fat distribution – moon face, buffalo hump, abdominal obesity, thin skin, bruising Inhibition of intestinal calcium absorption – osteoporosis Hypertension – excess glucocorticoids activate MR Glucose intolerant – antagonism of insulin action Purple Striae – Fragile thin skin stretches over increased abdominal fat, vessels hemorrhage into striae **Also occurs with long-term glucocorticoid therapy
33
When is glucocorticoid therapy administered?
Medical Emergencies High acute dose to treat septic shock, severe asthma, severe autoimmune disease flare Usually no long-term side effects Chronic Anti-inflammatory Immunosuppressive Adrenal insufficiency Pre-term infants – improved lung function
34
What are the analogs of glucocorticoid?
1. Cortisol 2. Prednisone 3. Methylprednisone 4. Dexamethasone 5. Fludrocortisone
35
What is adrenal insufficiency? Describe: 1. Primary AI 2. Secondary AI Which one is Addison's disease? Which is associated with failure to secrete CRH or ACTH? Which is failure at the adrenal level?
1. Failure of adrenal to secrete glucocorticoids, mineralocorticoids, or both. Primary – failure at adrenal level Addison’s Disease = autoimmune destruction of adrenals 70% of primary AI cases Secondary – failure to secrete CRH or ACTH Most common cause = sudden cessation of glucocorticoid therapy Anticipated if patient takes greater than 30 mg hydrocortisone, 7.5 mg prednisone, 0.75 mg dexamethasone for longer than 3 weeks

FHB - Endocrine & Reproductive (17 decks)

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