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Therapeutics > Exam 1 Steroid Synthesis > Flashcards

Exam 1 Steroid Synthesis Flashcards

1
Q

How do cells communicate?

A

sender cells make certain chemicals and transmit them → diffuses through the body and receptors receive the chemicals and can decode and respond to them (but other cells don’t have decoders so they don’t understand the message and it means nothing to them)

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2
Q

What are the different modes of cell-cell communication?

A

juxtacrine, endocrine, paracrine, synaptic/neuronal, and autocrine

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3
Q

What is juxtacrine signaling?

A

direct physical contact → example is MHC and T cells

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4
Q

What is endocrine signaling?

A
  1. travels fairly far through the blood to reach target organ expressing receptors
  2. low in concentration, high affinity receptor
  3. minutes to hours
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5
Q

What is paracrine signaling?

A
  1. travels short distance and affects neighboring cells
  2. fairly high local concentration, receptor with low affinity
  3. rapid and localized communication → very fast
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6
Q

What is synaptic/neuronal signaling?

A
  1. involves neurotransmitters, travels a short distance
  2. very high local concentration, dissociate rapidly
  3. very rapid (millisecond) termination
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7
Q

What is autocrine signaling?

A
  1. made and functions in the same cell
  2. similar to paracrine signaling so travels short distance affecting its own cell
  3. high local concentration and low affinity receptor → rapid
  4. cancer cells utilize this method to produce growth factors
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8
Q

What is the difference between intracellular vs cell surface receptors?

A

intracellular → have to cross the membrane so molecules that bind to intracellular receptors are hydrophobic (have no charge)
cell surface receptor → outside of cell so don’t need to cross the membrane, molecules can be charged but the problem is absorption in the blood and crossing to BBB

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9
Q

Steroid hormones have what kind of receptors?

A

they are intracellular so they have no charge

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10
Q

What are steroid hormones?

A
  1. synthesized from cholesterol
  2. planar, rigid, hydrophobic (so can penetrate membrane) that tightly bind to receptors
  3. exist in low concentrations in the body
  4. bound to serum carrier proteins since solubility is not good
  5. share the common mode of action → free hormones diffuse through the cell membrane and bind to specific receptor and regulate transcription of a specific set of genes
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11
Q

What are the 5 major classes of steroid hormones?

A
  1. sex and progestational hormones
    →progesterone (C21) → female menstrual cycle, pregnancy, embryogenesis
    →17beta-estradiol (C18) → estrogen, female hormone
    →testosterone (C19) → androgen, male hormone
  2. adrenocortical hormones
    →glucocorticoids
    →→cortisol (C21) → anti-stress hormone, anti-inflammation
    →mineralocorticoids
    →→aldosterone (C21) → regulator of Na+ uptake in the kidney, raises blood volume and BP
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12
Q

What happens if you don’t have aldosterone?

A

we would lose all of our Na+ in our urine → blood volume decreases → leads to hypotension

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13
Q

What happens if aldosterone levels are too high?

A

we reuptake Na+ and water → blood volume increases and leads to hypertension

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14
Q

Steroid hormones bind to what receptors?

A

to their respective receptors (ex. estrogen receptor, androgen receptor, corticoid steroid receptor, etc)

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15
Q

Steroid receptors belong to what family?

A

nuclear receptor family → example include steroid receptors, thyroid hormone receptors, etc

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16
Q

Steroid receptors contain what?

A

DNA binding domain and a hormone binding domain

17
Q

Where is the steroid receptor normally located?

A

in the cytoplasm

18
Q

What is the classic model of steroid action?

A

hormone enters the cell (with stabilization of heat shock proteins), enter the nucleus and bind to a specific region in DNA to induce transcription (transcription takes time so steroid drugs takes time to see the full effect)

19
Q

DNA binding domains of activated dimers bind to what?

A

bind to specific DNA sequences called hormone response elements (HRE) which is upstream of steroid responsive genes → binding alters the rate of transcription

20
Q

What is the negative feedback loop?

A

hypothalamus releases CRH from stress which activates pituitary glands to release ACTH that activates adrenal glands to release cortisol which can negatively regulate ACTH and CRH to make less if there are high cortisol levels

21
Q

How is cholesterol turned to pregnenolone?

A

extra chain is cleaved by P450scc (CYP11A1)

22
Q

Where do the universal steps of steroid hormone synthesis occur?

A

everywhere in the body (including adrenal glands, ovaries, and testes)

23
Q

What are the 3 major changes in the universal steps?

A
  1. OH to ketone and double bond moves on progesterone from pregnenolone → makes aldosterone (then 17-alpha-hydroxylase can make substrate that will make cortisol then 17,20 lyase can make androstenedione that leads to testosterone and estradiol)
  2. 17-alpha-hydroxylase makes substrate that adds OH on C17 → 17,20-lyase removes 2 extra carbons to make a ketone to make DHEA
24
Q

What is 17-alpha-hydroxylase deficiency?

A
  1. rare form of congenital adrenal hyperplasia (5%)
  2. caused by mutations in CYP17A1 which has both 17-alpha-hydroxylase and 17,20 lyase activities
  3. overproduce mineralocorticoids and deficient in corticosteroids and sex hormones
  4. symptoms: hypocortisolism (enlargement of adrenal glands), ambiguous genitalia, hyperaldosteronism →hypertension
25
Q

What does 21-hydroxylase do?

A

adds an OH group on carbon 21

26
Q

What is 21-hydroxylase deficiency?

A
  1. major form of congenital adrenal hyperplasia (95%)
  2. mutations in CYP21A2 which functions as 21-hydroxylase
  3. symptoms → hypocortisolism (enlargement of adrenal glands), hypoaldosteronism (hyponatremia which can be fatal in infants), premature androgen exposure which leads to ambiguous genitalia in females, hirsutism, early epiphyseal closure (short stature)
27
Q

What is the main takeaway with 17-alpha-hydroxylase deficiency?

A

can still synthesize aldosterone but make more than normal but no sex hormones or corticosteroids

28
Q

What is the main takeaway with 21-hydroxylase deficiency?

A

can’t make cortisol or aldosterone but have too much sex hormones

29
Q

What does aromatase do?

A

makes an aromatic ring structure (turns testosterone to 17-beta-estradiol)

30
Q

How are steroids transported and excreted?

A
  1. transported in plasma by plasma transport proteins
    → corticoid binding globulin (transcortin) → glucocorticoids and progesterone
    → sex hormone binding globulin (SHBG) → testosterone and estradiol
  2. metabolized in the liver to soluble forms by oxidation, sulfation, and glucoronidation that attach more hydrophilic groups to make it more soluble
  3. then excreted in the bile or urine
31
Q

What is excreted in the bile?

A

estrogen → because of its aromatic ring

32
Q

What is excreted in the urine?

A

progesterone, androgens, and glucocorticoids

33
Q

What does aminoglutethimide do?

A
  1. inhibits aromatase and P450scc

2. used to block steroid production in some hormone dependent tumors (breast and prostate)

34
Q

What does ketoconazole do?

A
  1. antifungal at low concentrations (blocks synthesis of ergosterol)
  2. inhibits P450scc, 17-alpha-hydroxylase and 11beta-hydroxylase (is like 21-hydroxylase)
  3. can treat hyperglucocorticoid states (Cushing’s syndrome) → produce too much cortisol
  4. may cause toxic side effects as it blocks synthesis of lots of hormones

Therapeutics (15 decks)

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