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GIGU Exam 2 > Steroid Biosynthesis (Staudinger) > Flashcards

Steroid Biosynthesis (Staudinger) Flashcards

1
Q

How are all steroid hormones synthesized

A

From cholesterol in the adrenal cortex

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2
Q

What enzyme converts cholesterol into pregnenolone?

A

Desmolase (cytochrome P450scc or CYP11A1)

Catalizes the 1st and rate limiting step

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3
Q

What regulates desmolase activity?

A

Adrenocorticotropic hormone (ACTH)

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4
Q

What is pregnenolone a precuros to?

A

Progesterone –>

Aldosterone & Cortisol (corticosteroids)

Testosterone & Estradiol (sex hormones)

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5
Q

What role does progesterone play in pregnancy?

Lecture: Steroid biosynthesis Correlation box p.247

A
  • Supports gestation (pregnancy) & embryogenesis
  • Is involved in the maintenance of the menstrual cycle.
  • Regulates the voltage gated calcium channels on spermatozoa
  • Prepares the uterus for implantation
  • Causes smooth muscle relaxation
  • Decreases maternal immune response

A decrease in progesterone precedes menstruation, labor & lactation

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6
Q

What is the correlation between glucocorticoids and infant respiratory distress syndrome (IRDS)

Lecture: Steroid biosynthesis Correlation box p.247

A

During delivery, a burst of glucocorticoids alters the lung structure in infants by stimulating the production of surfacants, which allows the air spaces to expand. In preterm neonates this process is defective, leading to IRDS. It can be prevented by giving glucocorticoids to expectant mothers.

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7
Q

How do tissues that have receptors with equal affinity for both mineralo- and glucocorticoids avoid Na+/H2O retention induced by the much higher ciruclating levels of gluocorticoids

Lecture: Steroid biosynthesis Correlation box p.247

A

They metabolze cortisol to cortisone since cortisone has a much lower affinity for the mineralcorticoid receptors

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8
Q

How can licorice cause hypertension

Lecture: Steroid biosynthesis Correlation box p.247

A

Natural licorice roots contain isoflavones which are inhibitors of 11B-dehydrogeanse. This can cause hypertension due to salt retention.

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9
Q

What potentiates testosterone’s affinity for the androgen receptor and what can inhibit the potentiation?

Lecture: Steroid biosynthesis Correlation box p.247

A

Potentiator: conversion to DHT by enzyme-5alpha-reductase

Inhibitor: Finasterode inhibits enzyme-5alpha-reductase

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10
Q

What has Finasteride been used for?

Lecture: Steroid biosynthesis Correlation box p.247

A
  • Treat benign prostatic hyperplasia
  • Male pattern baldness (caused by accumulation of DHT in the scalp)
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11
Q

What drugs bind and activate Mineralcorticoid Receptors (MR)

A
  1. Aldosterone (highest efficacy)
  2. 11-deocycorticosterone (very high efficacy)
  3. Testosterone
  4. Hydroctortisone (cortisol)
  5. Cortisone
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12
Q

What do the drugs that bind to mineralocorticoid receptors (MR) have in common?

A

They increase Na+ retension which can lead to hypertension

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13
Q

What is Primary Aldosteronism/Conn Syndrome

Lecture: Steroid Biosynthesis

A

Adrenal glands produces excessive levels of aldosterone which causes a loss of potassium and retention of sodium leading to hypertension:

  • Body holds on to too much water
  • Increases blood volume
  • Increases blood pressure
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14
Q

What is adrenal hyperplasia?

Lecture: Steroid Biosynthesis

A

Caused by deficiencies in the adrenal enzymes that are used to synthesize glucocorticoids which leads to the increased production of cortisol precurors and androgens from the adrenal gland

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15
Q

What are some symptoms of mild adrenal hyperplasia

A
  • Life threatening sinus infections
  • Life threatening pulmonary infections
  • Orthostatic syncope
  • Shortened stature
  • Severe acne
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16
Q

How can women present with adrenal hyperplasia?

Lecture: Steroid Biosynthesis

A
  • Hirsutism (excess body hair)
  • General oligomenorrhea (infrequent or light periods)
  • Infertility
17
Q

How is adrenal hyperplasia diagnosed?

A

Can be diagnosed when the child is in the womb through:

  • Use of human leukocyte antigen (HLA) haplotype
  • Excess cortisol precursors in amniotic fluid
18
Q

How is adrenal hyperplasia treated?

A

Hormone replacement therapy

19
Q

What enzymes can be mutated to cause adrenal hyperplasia

A

21-hydroxylase & 11-beta-hydroxylase

20
Q

What happens if there is a 21-hydroxylase deficiency?

A

There will be a build up of progesterone and 17-hydroxy progesterone but no aldosterone production

21
Q

What happens if there is a 11-β-hydroxylase deficiency?

A

Accumulation of Deoxycorticosteribe & 11-deoxycortisol but decreased aldosterone synthesis

22
Q

How can hypertension still occur when there is a 11-β-hydroxylase deficiency

A

An 11-β-hydroxylase deficiency causes there to be an accumulation of 11-deoxcysorticosterone. 11-deoxcysorticosterone has a relatively high affinity/efficacy for mineralocorticoid receptor (MR) which can cause hypertension

23
Q

What transports a majority of steroid hormones?

A
  1. Corticosteroid-binding globulin (CBG)
  2. Sex steroid hormone binding globulin (SHBG)
  3. Albumin
24
Q

Describe the HPA axis

A

Hypothalamus (CRH) –> Anterior pituitary (ACTH) –> Adrenal cortex (Cortisol)

25
Q

What is the action of ACTH

A

Binds to GPCR in the zona fasciculata of the adrenal cortex to induce secretion of glucocorticoid steroid hormones (cortisol)

26
Q

Why is the the CYP17A1 gene important?

A

Has both 17alpha-hydroxylase and 17,20-lyase enzymatic activities to produce:

Progestins

Mineralocorticoids

Gluocorticoids

Androgens

Estrogen

27
Q

What happens when there’s a mutation in CYP17A1

A

There will be an accumulation of steroid precurosors with the inability to produce the downstream sex hormones. The accumulated steroid precursors then contribute to the formation of corticosterone, which leads to congenital adrenal hyperplasia

28
Q

How does cortisol suppress immune system?

A
  1. Induce production of I-κBα inhibitory protein which prevents secretion of NF-κB (stimulates cytokine production). Absence of cytokines like IL-2 lead to an inhibition of clonal expansion of B lympocytes
  2. Cortisol promotes T cell apoptosis
29
Q

How is Vitamin D3 (cholecalciferol) obtained?

A
  1. Diet - Ingested as D2 and converted to D3 in the intestine
  2. Skin - Converted from 7-dehydrocholesterol via UV radiation
    * 7-dehydrocholesterol is an intermediate of cholesterol found at high levels in the skin*
30
Q

What is the role of tissues in Vitamin D (calcitriol) Production

A

Vitamin D is initially inert in the form of D2 or D3. To convert it to it’s active form the following must take place:

  1. In the liver, Vitamin D3 is converted to 25-hydroxy vitamin D by 25-hydroxylase
  2. 25-hydroxy vitamin D is transported to the kidney and converted to 1,25-dihyroxy vitamin D (calcitriol - active form) by 1-alpha-hydroxylase which is controlled by parathyroid hormone (PTH) levels.
31
Q

What are some disorders associated with vitamin D

A

Insufficient Vitamin D

  1. Brittle bones (rickets) in children
  2. Osteomalacia in adults
  3. Hypocalcemic tetany (involuntary muscle contraction)

Excess Vitamin D

  1. Elevated calcium in blood and urine
  2. Appear dazed
  3. Loss of apetite
  4. Sarcoidosis

GIGU Exam 2 (8 decks)

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