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Endocrine > Adrenal Hormones Biochemistry > Flashcards

Adrenal Hormones Biochemistry Flashcards

1
Q

Steroid hormone overview

A

3 parts:

1) adrenal cortex (corticosteroids)
- secretes aldosterone: stimulates renal reabsorption of Na+ and excretion fo K+
- secretes cortisol: increases gluconeogenesis, anti-inflammatory action and protein catabolism

2) ovaries (sex hormone)
- secretes estrogen: controls menstrual cycle, promotes development of secondary female sex characteristics
- secretes progesterone: secretory phase of the uterus and mammary glands. Also promotes implantation and maturation of the fertilized ovum

3) testies (sex hormone)
- secretes testosterone: stimulates spermatogenesis, promotes development of secondary male sex characteristics, promotes anabolism in muscles

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2
Q

Two primary layers of the adrenal gland and what is secreted

A

Adrenal cortex:

  • cortisol (glucocorticoid) and aldosterone (Mineralcorticoid)
  • several androgenic steroids

Adrenal medulla:
- Epinephrine and Norepinephrine

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3
Q

What is the primary substrate used in making steroid hormones in the adrenal gland

A

Cholesterol

Comes from either de novo synthesis or LDL binding to LDL receptors

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4
Q

What are the 4 steps of cortisol production

A

1) cholesterol -> pregnenolone conversion
- this done inside the mitochondrial matrix

2) pregnenolone -> progesterone conversion
3) progesterone -> 11-deoxycortisol

4) 11-deoxycortisol -> cortisol
- conducted in mitochondria

Steps 2-3 are done in the endoplasmic reticulum

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5
Q

What are the two main ways steroid hormones act on their receptor targets

A

1) “Classical”
- steroids bind to cytoplasmic intracellular receptors which form a steroid hormone-receptor complex
- this complex then binds to HRE enhancer regions on DNA which causes easier binding of DNA poly to DNA segments causing transcription of whatever the steroid hormone is suppose to upregulate

2) “Nonclassical”
- steroid hormone receptors after binding to the steroid molecule, regulates cellular functions outside of their actions as transcription factors. This occurs via interacting with proteins at cell membranes and changes the scaffolded protein arrangement to influence signaling networks
- makes it easier to bind to certain things vs other things depending on the cell
- also upregulates certain accessory proteins dependent on the steroid

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6
Q

Nonclassical steroid hormone accessory protein

A

Testosterone/androgens
- ERK1/2 protiens and Src surface

17B-Estradiol/estrogens
- cAMP and AC

Cortisol/glucocorticoids
- eNOS, PI3 kinase, and NMDA receptor

Progesterone/progestins
- PKC and NMDA receptor

Aldosterone/Mineralcorticoids
- NA/H+ exchangers

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7
Q

What differs a steroid vs a sterol?

A

Sterols are a subgroup of steroid.with a hydroxyl group at position 3 on the A-ring

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8
Q

What is the “steroid nucleus”

A

The ABCD ring system that all steroids have

- excludes the hydrocarbon tail

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9
Q

What is the rate limiting step for all steroid hormone synthesis

A

The production of pregnenolone from cholesterol via CYP2A proteins
- this is the parental compound for all steroid hormones and is produced in all tissues that make steroid compounds
(Adrenal cortex/testes/ovaries/placenta)

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10
Q

3 general structures of all hormones

A

1) modified amino acids
- readily cross plasma membrane and can either signal at plasma membrane or intracellularly via receptor binding
- includes TH, adrenaline and NE

2) peptides/protiens/glycoproteins
- cant enter the cell and only signal via receptor binding
- includes GH, insulin and TSH

3) steroids
- signal only via intracellular receptors after passive diffusion across the plasma membrane
- includes cortisol, aldosterone, testosterone, estradiol

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11
Q

What cells inside the adrenal medulla generates catecholamines?

A

Chromaffin cells

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12
Q

What enzymes degrade catecholamines?

A

Monoamine oxidase enzymes (MAOs)

  • breaks down epinephrine/NE into dihydroxymandelic acid
  • can also break down metanephirne and normetanephrine into vanillylmandelic acid (which is urinated out)

COMT

  • breaks down epinephrine and NE to metanephrine or normetanephrine respectively
  • also breaks down dihydroxymandelic acid to vanillylmandelic acid (which is urinated out)
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13
Q

What is the enzyme that converts norepinephrine -> epinephrine?

A

Phenylethanolamine N-methyltransferase (PNMT)

- catalyzes the transfer of a methyl group for SAM -> NE to generate epinephrine

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14
Q

what are high yield hydroxylase and dehydrogenase in the generation of aldosterone and cortisol

A

Hydroxylase:
- CYP21A2

Dehydrogenase:
- HSD17B/B1

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15
Q

Aldosterone signaling

A

Binds to globulin carrier glycoproteins in the blood and then binds to Mineralcorticoid receptors

Two target cell pathways

1) nuclear receptor translocation (genomic)
2) Kinase activation (non-genomic)

both pathways effect gene expression and ion concentration

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16
Q

Aldosterone production regulation

A

Requires angiotensin 2 to bind to its receptors on adrenal-cortical cells and upregulates intracellular calcium

Intracellular calcium increases turns on cyp11B2 to induce aldosterone production

  • in no Ang2 presence or high levels of aldosterone in blood/ high VP/high sodium, hyperpolarizes adrenal-cortical cells and this prevents Cyp11B2 protein production which turns off aldosterone
  • MicroRNAs are responsible for this also
17
Q

Cortisol signaling

A

Binds to a glucocorticoid receptor (GR) which generates genomic and non-genomic actions

  • genomic: upregulations trans activation of DNA and proteins
  • nongenomic: very broad and integrative. Are much faster and have extensive cellular effects
18
Q

Cortisol regulation

A

Expression is induced via stressors
- stress directly causes CRH release in the hypothalamus. This results in ACTH release in the anterior pituitary which then results in cortisol production.

Circadian rhythm occurs with this hormone also

  • AM = high
  • PM = low

negative feedback with cortisol levels in blood

19
Q

What is the first step in producing sex hormones (and is technically the rate limiting steps for sex hormones)

A

Conversion of pregnenolone -> DHEA via CYP17 enzymes

This step locks pregnenolone into becoming a sex hormone

20
Q

What are the three carrier proteins for steroids? Also where are steroids degredated the most?

A

Carriers:

  • Sex hormone-binding globulin (SHBG)
  • Corticosteroid-binding globulin (CBG)
  • albumin

Most is degraded in the liver

21
Q

Pheochromocytoma

A

A rare form of hypertension caused by a neoplasm in the adrenal medulla that secretes excess Catecholamines

Symptoms (all acute, severe and come and go)

  • increased BP
  • heart palpitations
  • throbbing headache
  • diaphoresis

leads to impaired glucose tolerance and causes diabetes mellitus

22
Q

Addison disease

A

Under-active adrenal glands And underproduction of adrenal hormones

Causes: autoimmune reactions, cancer, infections or removal of too much adrenal glands

Symptoms:

  • fatigue
  • orthostatic hypotension
  • hyperpigmentation
  • hyponatremia and Hyperkalemia

Treatment = give corticosteroid administration

23
Q

Cushing disease

A

Hyperaldosteronism and cortisol caused usually by tumors in either the adrenal gland, pituitary gland or hypothalamus or excessive ACTH hormone

  • if in pituitary ACTH will be high, if in adrenal gland ACTH is low
  • if the tumor is in the adrenal gland itself = conn syndrome

Symptoms:

  • fatigue
  • strain on abdomen and moon facies
  • buffalo hump
  • excessive bruising
  • atrophied limb muscles
  • poor DTRs
  • flushing of skin
  • high BP and hypokalemia
  • periods of paralysis

Treatment = tumor removal

24
Q

Congenital adrenal hyperplasia (CAH)

A

Group of autosomal recessive disorders that result in impaired cortisol biosynthesis
- most common = 21-hydroxylase defects**

Symptoms:

  • infertility
  • perturbed sexual development
  • HTN
  • chronic infections

Treatment = provide synthetic deficient enzyme or hormone product

25
Q

3-B-hydroxysteroid dehydrogenase deficiency

A

A subset of CAH

Results in virtually no glucocorticoids, mineralcorticoids, active androgens and estrogens
- this is because no 3-B-hydroxysteroid dehydrogenase results in to conversion of pregnenolone -> progesterone AND no pregnenolone -> DHEA

*Unique symptom = excessive sodium in urine and fluid loss and males present with female-like genitalia

26
Q

17-a-hydroxylase deficiency

A

Results in no conversion of pregneleone -> DEHA and Progesterone -> 17-hydroxyprogesterone

Results in no sex hormones at all and cortisol
- HOWEVER aldosterone is still produced at very excessive levels in the blood (since progesterone builds up and has no other pathway to go down

*Unique = shows HTN and fluid retention on top of female-like genitalia

27
Q

21-a hydroxylase Deficency

A

MOST common form of CAH (90%)

Results in no production of cortisol and aldosterone since progesterone cant be converted into aldosterone and instead all is converted to 17-a-hydroxyprogesterone
- however, 17-a-hydroxyprogesterone cant be converted to 11-deoxycortisol and instead is shuttled to androstenedione

This results in massive amounts of estrone, estradiol, testosterone.

Unique: salt wasting with overproduction of masculinization of genitalia or virilization in males

28
Q

11-B1 hydroxylase deficiency

A

Prevents cortisol and aldosterone from being developed however it does develop a lot of deoxycorticosterone intermediate

Results in similar to 21-a-hydroxylase deficiency except the excess deocycorticosterone leads to suppression of the RAAS system and no aldosterone.

  • However 11-Deoxycorticosterone is still produced in large amounts and acts as 80% aldosterone
  • this results in unique hypertension with low renin**

Also shows overproduction of androgens which causes masculinization and virilization of the external genitalia

29
Q

3-B-hydroxysteroid dehydrogenase enzyme

A

Results in no cortisol or aldosterone

Endocrine (46 decks)

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