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67 Cards in this Set

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What is the precursor of all steroid hormones?
How is cholesterol transported from the liver to the adrenal gland (and gonads and placenta)?
Name the 3 zones of the adrenal cortex (from capsule to medulla).
1) Glomerulosa
2) Fasciculata
3) Reticularis
Which steroid hormone is produced in the zona glomerulosa?
Aldosterone (mineralocorticoids).
Which steroid hormone is produced in the zona fasciculata?
Cortisol (glucocorticoids).
Which steroid hormones are produced in the zona reticularis?
Androgens (DHEA, Testosterone, Estrogen, Androstenedione, Progesterone).
What is the function of cortisol (glucocorticoids)?
Increase plasma blood glucose by activating gluconeogenesis, and inhibiting insulin.
What is the function of aldosterone (mineralocorticoids)?
Increase Na+ retention and therefore water retention and blood pressure.
What is the function of androgens?
Development of secondary sexual characteristics, etc.
To which cell layer does ACTH bind to in the adrenal cortex, and what is the ensuing product?
Plasma membrane of cells in the zona fasciculata, producing cortisol.
To what cell layer of the adrenal cortex will Angiotensin-II bind, and what steroid hormone will be produced?
Zone glomerulosa, producing aldosterone.
What is the rate-limiting step of cortisol, aldosterone, and DHEA biosynthesis, where does it occur, and by what enzyme?

What stimulates this conversion?
Cholesterol --> pregnenolone.
Mitochondrial membrane.

Which family of enzymes are critical in the formation of all steroid hormone biosynthesis?
CypP450 enzymes, which hydroxylate intermediates.
Steroid hormone products of the adrenal cortex are synthesized and secreted _________, not ________.
on demand; stored.
Which hormone secreted by the female ovaries, is only a transient intermediate in the adrenal cortex?
Pregnenolone branches into what 2 products?
1) Progesterone (transient)
2) DHEA - reticularis
Progesterone branches into what 2 products?

What enzymes motivate this conversion?
1) Aldosterone - glomerulosa
2) Cortisol - fasciculata

Cyp450 (c21 and c11 respectively)
What effect does an increase in cortisol have on the hypothalamus/pituitary hormone pairs?
Negative feedback control on the hypothalamus, decreasing CRH/ACTH release - and vice versa.
What substrate is critical in the functioning of cortisol?

What enzyme facilitates this?
11-OH group is critical for physiological activity.

What is the effect of cortisone?
Anti-inflammatory steroid.
In aldosterone, what substrate-specific reaction occurs that is important for kidney action?
Tying up the 11-OH group to form a hemiacetal.
What is Congenital Adrenal Hyperplasia (CAH)?
Deficient Cyp450(c21)
Block aldosterone and cortisol pathways
Back up the reticularis pathway
Increase androgen output (male sex hormones)
What is the cause of Congenital Adrenal Hyperplasia (CAH)? What test is used to diagnose it?
Deficient Cyp450(c21). Inject ACTH and observe a rise in 17-OH-Progesterone, which gets backed up when Cyp450(c21) is deficient.
What are the clear clinical characteristics of CAH and in whom are they most clearly observed?
Ambiguous genitalia and hirsutism seen clearly in female infants.
Where are weak androgens converted to strong androgens?
Liver, muscle, adipose tissue.
What function do strong androgens play in the female?
Major source of testosterone in females, maintain secondary sexual characteristics, are the sole estrogen precursors.
Describe how cortisol is secreted by the adrenal cortex (in an unstressed individual)?
Pulsatile bursts.
What is significant about Pro-opiomelanocortin (POMC)?
It derives into ACTH; ACTH production will also result in MSH and opioid formation.
How does cortisol respond to different levels of stress?
Major stress - cortisol rises steeply.
Minor stress - cortisol rises, but not as much.
What stimulation test is used to confirm hypopituitarism with respect to the secretion of cortisol?
Insulin injection will cause neither ACTH nor cortisol to rise in response to increased plasma glucose levels.
How is cortisol transported in plasma?
80% is bound to CBG (Cortisol Binding Globulin), 15% bound to albumin, and 5% is free and active.
How is aldosterone transported in plasma?
60% is bound to albumin (no globulin transporter), and the rest is free since it is more water soluble than cortisol.
Between cortisol and aldosterone, which has a faster turnover rate?
Where are cortisol and aldosterone catabolized?
In the liver.
What structures of aldosterone and cortisol are preserved during catabolism?
Steroid nucleus. Side groups are conjugated and inactivated for secretion.
What molecule can be measured as an indicator of cortisol secretion?
True/False: Cortisol is required for survival.
What processes does cortisol stimulate?
1) Liver gluconeogenesis
2) Fat lipolysis
What hormone does cortisol block?
What counterintuitive process occurs during cortisol secretion?
Glycogen synthesis. Cortisol causes some glucose to be released into the circulation, and some to store as glycogen.
*Increased insulin will suppress gluconeogenesis and glycogenolysis. How will cortisol affect these processes?
More insulin is required in the presence of cortisol for insulin to have the same effect.
Increased insulin will increase glucose uptake from the circulation. How will cortisol affect this process?
It will require more insulin to take up the same amount of glucose. Sometimes cortisol results in hyperglycemia.
*How does cortisol affect host defense mechanisms?
1) Supresses inflammation (cortisone), usually in response to long-term stress, by blocking phospholipase A2, which blocks the formation of leukotrienes and prostaglandins.
2) Suppresses immune response (block cytokine release, block fever cytokines, block T and B cell proliferation)
True/False: Aldosterone is necessary for survival.
How will the kidney respond to a low circulating blood volume and pressure?
RAA pathway: Renin is released converting AT --> AT-I and ACE is released to convert AT-I --> AT-II.
What are the main functions of AT-II?
1) Regulation of aldosterone synthesis
2) Vasoconstriction

In response to low blood pressure/volume.
What plasma ion concentration is critical in aldosterone regulation?
How is essential hypertension and edema typically treated?
ACE inhibitors to lower the synthesis of aldosterone.
How do steroid hormones act on the nucleus?
Hormones bind to their receptors, which will transform into transcription factors and enter into the nucleus.
*What types of dimers are formed by steroid hormone receptors as they act as transcription factors? How will they act on DNA?
Homomeric dimers.

Induce transcription by recruiting RNA polymerase, but sometimes suppress it.
Steroid hormone receptors may interact with transcription factors in 3 ways. Describe them.
1) Homomeric dimer can bind to a positive HRE, inducing transcription.
2) Homomeric dimer can bind to a negative HRE, suppressing transcription.
3) Homomeric dimer can bind directly to the positive transcription factor itself, suppressing transcription.
Describe how cortisol induces anti-inflammatory effects.
Cortisol binding will induce the transcription of anti-inflammatory protein Lipocortin-1, which inhibits phospholipase A2, which blocks formation of leukotrienes and prostaglandins. An IL-1 antagonist will also form.
The pro-inflammatory TF NF-κβ is also inhibited.
*What is the bodyguard protein (11β-HSD)?
Due to the high structural similarity between cortisol and aldosterone, the bodyguard protein prevents cortisol from binding to aldosterone receptors, which would cause hypertension.
What molecule will inhibit the bodyguard protein (11β-HSD)?
Glycyrrhetinic Acid, GA, (found in licorice), and will induce hypertension.
What is primary Cushing's Syndrome? What is its distinctive feature?
An adrenal cortex adenoma or carcinoma resulting in hypersecretion of cortisol. The distinctive feature is a DROP in ACTH levels.
What is secondary Cushing's Syndrome?
Also known as Cushing's DISEASE, this is a hypersecretion of Cortisol due to moderately excessive pituitary output of ACTH.
What is Ectopic ACTH Syndrome?
Hypersecretion of cortisol due to increased ACTH from sources other than adrenal cortex or pituitary (lung cancer).
What are the symptoms for Cushing's?
Moon-shaped face, muscle wasting, increased facial hair, blood vessel thinning, thin skin.
How would you differentiate a hypersecreting cortisol disorder?
High Cortisol, Low ACTH - Primary Cushing's (adenoma)

If High Cortisol AND High ACTH:
High dose of DEX resulting in suppression of ACTH - Secondary Cushing's.
High dose of DEX resulting in NO suppression of ACTH - Ectopic ACTH Syndrome.
Low dose of DEX resulting in suppression rules out Cushing's.
What is primary Addison's Syndrome?
Also known as Addison's DISEASE, adrenal cortex (target organ) failure results in low levels of cortisol.
What is secondary Addison's Syndrome?
Deficiency in the pituitary gland, resulting in low cortisol levels.
What is tertiary Addison's Syndrome?
Deficiency in the hypothalamus, resulting in low cortisol levels.
What are the symptoms for Addison's?
High levels of ACTH and MSH (hyperpigmentation) in Primary Addison's.
Low levels of ACTH (pale skin and inability to tan) in Secondary and Tertiary Addison's.
How do you test for Addison's?
If plasma cortisol is low, administer ACTH to the adrenal cortex. No cortisol production - Primary Addison's.
Cortisol produced - Secondary or Tertiary Addison's.
When do you measure cortisol?
8 AM, when the level is highest.
What hormone pair does an injection of insulin affect?
CRH/ACTH will increase in a normal individual.
What effect does cortisol have on the bone and connective tissue?
Decrease bone formation and increase bone resorption; decrease connective tissue - typical in osteoporosis.