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Molecular Endocrinology > Final Exam > Flashcards

Final Exam Flashcards

1
Q

What are the four types of steroid receptors and their main functions?

A

Glucocorticoids - blood glucose/stress
Mineralocorticoids - sodium/potassium
Androgens - male sex (binds testosterone)
Progesterone - support pregnancy/embryogenesis

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2
Q

What are the key thyroid receptors and their main functions?

A

Thyroid hormone - development/metabolism/heart rate
Estrogen - female sex
Vitamin D - calcium/phosphorus/development/apoptosis

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3
Q

What two families of receptors are nuclear receptors and where are they located?

A

Steroid - cytoplasm
Thyroid - nucleus

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4
Q

What nuclear hormone type is known to be transported across the membrane instead of diffusing across the membrane?

A

Thyroid hormone

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5
Q

What are the hormones for nuclear receptors?

A

Small lipophilic/hydrophobic hormones that can diffuse across the membrane

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6
Q

What are hormone response elements (HRE)?

A

A short DNA sequence within the promoter region of a gene that is capable of binding to specific hormone receptor complexes and regulate transcription.

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7
Q

What is bound to a steroid hormone before the hormone binds?

A

heat shock proteins (HSP)

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8
Q

What happens when heat shock proteins are released from the steroid receptor?

A

The nuclear localization signal (NLS) is exposed, allowing the hormone to bind.

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9
Q

What happens to the hormone-receptor complex in steroid receptor signaling?

A

It is transported into the nucleus and binds to HRE to activate transcription

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10
Q

What are the three domains of a nuclear receptor?

A
  1. Amino terminal domain
  2. DNA binding domain
  3. Ligand binding domain
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11
Q

What is the importance of Zinc in the DNA binding region?

A

Important for dimerization and binding to different regions of DNA (binds with cysteine)

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12
Q

What form of thyroid hormone has genomic actions?

A

T3

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13
Q

What form of thyroid hormone signaling uses signal transduction?

A

Nongenomic

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14
Q

Timing of genomic vs non-genomic actions of thyroid hormones?

A

Genomic - slow enough for transcription
Non-genomic - rapid (seconds to an hour - unless there is cross-talk)

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15
Q

How are non-genomic effects of the thyroid hormone different from genomic effects?

A

Non-genomic effects have nothing to do with the nuclear thyroid hormone receptor and transcription because it is too rapid. Instead, it involves membrane receptors and/or modulation of intracellular pathways.
What is happening at the plasma membrane.

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16
Q

What are integrins?

A

Receptors that mediate attachment between a cell and other cells or the extracellular matrix.

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17
Q

What are examples of non-genomic rapid intracellular effects?

A
  1. Ion flux - sodium and calcium
  2. Mitochondria activity
  3. Glucose and amino acid uptake
  4. Actin polymerization - remodeling, neuronal connections, cell movement, intracellular trafficking, muscle contraction, pseudopod formation)
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18
Q

How are target genes vs ion channels regulated by thyroid hormone?

A

Target genes - genomically/nuclear effects
Ion channels - nongenomically/nonnuclear effects

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19
Q

Where does crosstalk occur?

A

Between thyroid hormone genomic and nongenomic paths - between the receptor and the plasma membrane

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20
Q

How can thyroid hormone affect thyroid receptors in the nucleus (through cross-talk)?

A

Through phosphorylation cascades - when thyroid receptors are phosphorylated, they are activated and co-repressor proteins dissociate.

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21
Q

Give an example of crosstalk.

A

T4 binds integrins at cell surface and stimulates MAPK pathway to phosphorylate thyroid receptors (nongenomic) that then causes dissociation of co-repressors promoting activation of transcription by TR/T3 (genomic).

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22
Q

What is Cretinism?

A

Hypothyroidism in developing children leading to physical and mental disabilities

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23
Q

What are possible causes of Cretinism?

A

Anti-TSH receptor antibodies from mother, severe iodine deficiency or defect in baby’s thyroid axis.

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24
Q

What is HRE specific for?

A

Whatever steroid binds (ARE, ERE, TRE)

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25
Q

What is unique about estrogen receptor classification?

A

It is in the thyroid receptor family based on homology, but it is a steroid (signals like a steroid hormone)

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26
Q

What are thyroid hormones composed of?

A

Two linked iodinated tyrosine molecules derived from iodine (cleaved prohormone thyroglobulin)

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27
Q

What are the two main forms of thyroid hormones?

A

Thyroxine (T4) - most abundant
Triiodothyronine (T3) - most active

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28
Q

What are the effects of hyperthyroidism vs hypothyroidism?

A

Hyper = weight loss (even though eating a lot)
Hypo = weight gain (Hashimoto’s disease)

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29
Q

What are the main functions of thyroid hormones?

A
  1. increase oxygen consumption
  2. increase basal metabolic rate
  3. increase energy expenditure
  4. regulate glucose metabolism
  5. promote fetal growth
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30
Q

What is the importance of iodine in thyroid hormones?

A

Regulates TH production and is an important structural element in TH (T4 has more more iodine than T3)

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31
Q

What do thyroid hormones require to travel in circulation?

A

Blood binding proteins

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32
Q

What is the function of deiodinase?

A

Enzyme-catalyzed removal of iodine and can be either activating or deactivating depending on what iodine is removed

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33
Q

What is the differences between T3 and reversal T3?

A

T3 - deiodination of outer ring of T4 (in peripheral tissue)
rT3 - deiodination of inner ring of T4 (inactive/no genomic effects)

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34
Q

What is the thyroid gland made up of?

A

Small globular sacs (follicles) that are filled with a fluid called colloid

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35
Q

What is the function of follicular cells?

A

Line the follicles, synthesize thyroglobulin and actively take up iodine

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36
Q

What happens at the apical-colloid interface?

A

Iodine is oxidized so that thyroglobulin can be iodinated

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37
Q

Where is iodinated thyroglobulin stored until it is needed?

A

In the colloid (fluid in the follicles)

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38
Q

What happens when TSH stimulates the need for TH?

A

Colloid contents (iodinated thyroglobulin) are engulfed by the same or neighboring follicle cells where cleavage produces T4 and T3 that gets released into circulation.

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39
Q

What cells in the anterior pituitary release thyroid stimulating hormone (TSH)?

A

Thyrotroph cells

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40
Q

What stimulates the production of TSH? What inhibits the production of TSH?

A

Stimulates = TRH
Inhibits = somatostatin and TH negative feedback

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41
Q

What happens to TH production with excess iodine?

A

Negative feedback - inhibits TH production

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42
Q

What are the functions of blood-binding proteins?

A

Make hormones soluble in plasma
Provides a reservoir of hormone that exchanges with free form fraction
Prolonger half-life

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43
Q

What are the two forms hormones take in the plasma?

A

Free form = biologically active
Bound form = blood binding protein (or other molecule)

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44
Q

What are albumins?

A

A family of water-soluble globular proteins (like globulins) that bind to steroids, fatty acids and thyroid hormones

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45
Q

How is TH transported into target cells vs the nucleus of the target cells?

A

TC - by specific carrier/transporter proteins
N - diffusion

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46
Q

What must TH bind to in the cytoplasm in order to move around?

A

Cytoplasmic binding proteins

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47
Q

What is significant about the affinity of thyroid receptors?

A

They have higher affinity for T3 (90%) than T4 (10%), so most of T4 is converted to T3 before binding

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48
Q

What converts T4 into the biologically active form (T3) before binding to thyroid receptors?

A

deiodinase enzymes

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49
Q

Why is the interaction of thyroid receptors (TRs) with retinoid X receptors (RXRs) important gene expression?

A

Forms a heterodimer that interacts with the response element. The interaction between TR and RXR leads to a conformational change leading to the activation or suppression of target genes

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50
Q

What are the effects of cold temperatures on thyroid hormone production?

A

Promotes release of TH and TSH to increase heat production and thermogenesis

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51
Q

Why are thyroid response elements (TREs) considered less specific?

A

Can lead to activation or suppression, not just one specific action/role

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52
Q

What is the difference between the corepressor complex and the coactivator complex?

A

Corepressor - uses histone deacetylases (HDACs) to close chromatin and repressing gene transcription
Coactivator - uses histone acetyltransferases (HATs) to open chromatin for transcription

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53
Q

What are the different substances that have non-genomic effects mediated by changes in levels of T3/T4 in the plasma membrane?

A

Calmodulin
Integrin
PIPs
cAMP
Protein kinase

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54
Q

Why are the levels of PIPs important in nongenomic effects of thyroid hormones?

A

Signal changes in Ca regulation and changes in plasma membrane regulation
Responsive to thyroid hormone levels on the outside of the membrane

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55
Q

What are some examples of second messengers in TH cross-talk?

A

Cyclin dependent kinase (CDK)
Mitogen activated protein kinase (MAPK)
Tyrosine kinase

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56
Q

How does a human fetus acquire TH?

A

Can synthesize TH early on
Substantial transfer of TH across the placenta - contains deiodinases that convert T4 to T3

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57
Q

What is Goiter?

A

Overstimulation of the thyroid gland cause enlargements

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58
Q

How can Goiter arise from both hyperthyroidism and hypothyroidism?

A

Hyper = overstimulation of TRH or TSH
Hypo = thyroid deficiency/lack feedback, so TSH production increases, increasing the size of the thyroid gland

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59
Q

What are possible causes of Goiter?

A

Lack of iodine in diet
Drug blocking
Autoimmune disease

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60
Q

What is Hashimoto’s Thyroiditis (or chronic lymphocytic thyroiditis)?

A

An autoimmune disease where the thyroid gland is attacked by a variety of cell and antibody mediated immune process - common cause of hypothyroidism

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61
Q

How does lymphocyte (WBC) action lead to Hashimoto’s Thyroiditis?

A

Lymphocytes sensitized to thyroidal antigens totally destroy normal thyroidal architecture, decreasing T3 production, increasing TSH (goiter) until gland fails

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62
Q

What is the most common first symptom of Hashimoto’s Thyroiditis?

A

Weight gain despite normal eating habits

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63
Q

What defines Graves Disease?

A

Common form of thyrotoxicosis characterized by hyperthyroidism, goiter and bulging eyeballs.

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64
Q

What are some common characteristics of Graves Disease (other than the main triad)?

A

Change in metabolism
Increased heart rate and blood pressure
Increased ventilation
More anxious state (depression)
Weight loss and sweating
Low levels of carbon dioxide in the blood

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65
Q

What is the difference between autoimmune hypothyroidism and autoimmune hyperthyroidism?

A

Hypo = TSH receptor binds antibodies that block
Hyper = TSH receptor binds antibodies that stimulate

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66
Q

What is another name of vasopressin?

A

Antidiuretic Hormone (ADH)

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67
Q

What hormones does that posterior pituitary release?

A

Oxytocin and vasopressin (or ADH)

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68
Q

What is released from the adrenal medulla?

A

Epinephrine and norepinephrine

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69
Q

What are the three layers of the adrenal cortex and what hormone does each layer secrete?

A
  1. Zona glomerulosa - mineralocorticoids (aldosterone)
  2. Zona fasciculata - glucocorticoids (cortisol)
  3. Zona reticularis - androgens (DHEA)
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70
Q

What is the basis of all hormones produced in the adrenal cortex?

A

Cholesterol - steroid hormones

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71
Q

What does DHEA stand for?

A

Dehydroepiandrosterone

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72
Q

What is the major mineralocorticoid and what is its function?

A

Aldosterone - increases K secretion and sodium and water retention by the kidneys - increasing blood pressure

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73
Q

What is the main regulator of aldosterone?

A

Renin-angiotensin-aldosterone system

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74
Q

What is the Renin-Angiotensin-Aldosterone system activated by?

A

Low blood pressure and high K levels

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75
Q

What is the major glucocorticoid and what is its function?

A

Cortisol - helps the body deal with stress

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76
Q

What tissues does cortisol act on?

A

Liver
Muscles/Smooth muscles
Adipose tissue
Pancreas

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77
Q

What is the main function of mineralocorticoids/glucocorticoids/androgens?

A

Mineralocorticoids - regulation of mineral (K and Na)
Glucocorticoids - regulation of glucose metabolism
Androgens - male hormones

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78
Q

Why is the breakdown of muscle proteins into amino acids important?

A

Can be used to synthesize glucose, fats and generate energy

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79
Q

What is the function of cortisol in the liver?

A

Promotes catabolism of glycogen to glucose

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80
Q

What is the function of cortisol in the muscles?

A

Inhibits glucose uptake and consumption and promotes protein degradation to amino acids

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81
Q

What is the function of cortisol in adipose tissue?

A

Promotes lipid breakdown for additional energy
Lipolysis: triglycerides –> fatty acids and glycerol

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82
Q

What is the function of cortisol in the pancreas?

A

Decreases insulin and increases glucagon secretion = increase blood glucose

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83
Q

How does cortisol maintain higher blood pressure?

A

Increase the sensitivity of vascular smooth muscles to vasoconstrictors and inhibiting the release of vasodilators

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84
Q

What is the mechanism of glucocorticoid drugs?

A

Increase cortisol to reduce inflammation and suppress the immune system

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85
Q

What controls the release of cortisol?

A

Hypothalamic-pituitary-adrenal (HPA) axis

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86
Q

How does the Hypothalamic-pituitary-adrenal (HPA) axis promotes the release of cortisol?

A
  1. Hypothalamus releases CRH in response to stressor
  2. Anterior pituitary release ACTH
  3. Adrenal gland releases cortisol
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87
Q

How does the cortisol negative feedback loop work?

A

Production of cortisol from adrenal gland feedback to the hypothalamus (CRH) and anterior pituitary (ACTH)

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88
Q

When are cortisol levels high vs low?

A

High = morning
Low = night

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89
Q

What is DHEA produced in response to?

A

ACTH from the anterior pituitary

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90
Q

What is DHEA converted into?

A

testosterone or estrogen

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91
Q

What is unique about ADRENAL androgens in males?

A

Only make up a small proportion of androgens in males, most produced by testes.

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92
Q

What is unique about ADRENAL androgens in females?

A

Major source of androgens in females (especially after menopause)

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93
Q

What system is the adrenal medulla apart of?

A

The sympathetic nervous system - “fight or flight” response to short-term stress

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94
Q

What is the adrenal medulla composed of?

A

Modified postganglionic neurons - chromaffin cells

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95
Q

What is the function of sympathetic preganglionic fibers?

A

Stimulate chromaffin cells to produce epinephrine and norepinephrine

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96
Q

What are the functions of epinephrine and norepinephrine in the sympathetic system?

A

Increase cardiac output, accelerate respiratory rate and release stored energy

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97
Q

Where does epinephrine and norepinephrine cause vasoconstriction/vasodilation in the sympathetic system?

A

Cause vasoconstriction in most organs but vasodilation in the heart and skeletal muscles

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98
Q

What are some characteristics of the zona fasciculata?

A

Rich in mitochondria, lipid droplets and SER

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99
Q

Which adrenal cortex layer has no 17alpha-hydroxylase activity?

A

Glomerulosa

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100
Q

Which adrenal cortex layer has no P450aldo activity?

A

Fasciculata

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101
Q

What receptor does cortisol bind to?

A

Glucocorticoid receptors - nuclear receptor

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102
Q

What other receptors can glucocorticoids bind to?

A

Mineralocorticoid receptors

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103
Q

What is the function of corticosteroid-binding globulin (CBG)?

A

A blood binding protein needed to transport cortisol in circulation

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104
Q

Where does mobilization of amino acids occur for glucocorticoids?

A

Muscle, Lymphoid tissue and connective tissue

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105
Q

Where is excess glucose stored (that isn’t used for energy)?

A

Liver and adipose tissue in the form of glycogen and fats

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106
Q

What happens to glycogen stored in the liver during a fasted state?

A

Converted back into glucose to keep supplying the body with energy

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107
Q

What happens once the glycogen store in the liver is used up in a fasted state?

A

The body taps into energy stores in adipose tissues

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108
Q

How does the fasted state result in fat burning?

A

Fat from adipose tissue is broken down into free fatty acids and converted into metabolic fuel

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109
Q

What is cholesterol a precursor for?

A

Bile, steroid hormones and vitamin D

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110
Q

How is cholesterol transported in blood plasma?

A

In lipoproteins

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111
Q

How are lipoproteins classified?

A

Based on their density (VLDL, LDL, HDL) - particles that contain more lipids are larger but have lower density (proteins increase density)

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112
Q

What is the function of the proteins that sit on the surface of the lipoproteins?

A

Serve as “address tags” determining the destination and function of the lipoprotein

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113
Q

What is the function of low-density lipoproteins (LDLs)?

A

Carry cholesterol from the liver to other tissues - has the highest cholesterol content and is the major cholesterol carrier in the blood

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114
Q

What is the function of high-density lipoproteins (HDLs)?

A

Return excess cholesterol to the liver (reverse cholesterol transport)

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115
Q

What happens with high levels of LDL in the blood?

A

Associated with cholesterol plaque build-up and cardiovascular diseases (known as “bad” cholesterol)

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116
Q

Why is HDL known as “good” cholesterol?

A

It removes excess cholesterol from tissues and the blood stream

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117
Q

Where does cholesterol go after being absorbed by the intestines?

A

Carried through the blood stream to the liver

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118
Q

What are cholesterol pools and where are they stored?

A

Combination of endogenous and dietary cholesterols and triglycerides stored in very low density lipoproteins (VLDL)

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119
Q

What happens when muscles and adipose tissue extract triglycerides from the VLDLs?

A

VLDLs get tuned into LDL

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120
Q

What happens with the excess cholesterol that is returned back to the liver vis HDL?

A

Turned into bile that goes to the intestines where it breaks down fat

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121
Q

What is Apolipoprotein B100?

A

A form of LDL - helps move cholesterol around in the body

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122
Q

What happens with high levels of Apolipoprotein B100?

A

Higher risk of cardiovascular disease (because it is a LDL)

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123
Q

Through what process are lipoproteins taken up by cells?

A

Endocytosis after binding to lipoprotein receptors (receptor mediated endocytosis)

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124
Q

Why is cytochrome P450 important in cholesterol degradation?

A

It is the rate limiting step of steroid synthesis by enzymatically removing the cholesterol side chain to make pregnenolone

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125
Q

What are the steps of steroid biosynthesis?

A
  1. Cholesterol
  2. Pregnenolone
  3. Progesterone

Cortisol, corticosterone (aldosterone) and testosterone (estradiol)

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126
Q

Where is 17alpha hydroxylase produced?

A

Thecal cells

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127
Q

Where is 17alpha hydroxylase expressed in the adrenal cortex and why is this important?

A

Layer 2/3 (fasciculata and reticularis) - cortisol and androgens are only expressed in these layers

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128
Q

Where is P450aldo expressed in the adrenal cortex and why is this important?

A

Layer 1 (glomerulosa) - aldosterone only expressed in layer 1

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129
Q

What does StAR stand for and what does it do?

A

Steroidogenic acute regulatory protein - transports cholesterol to the inner mitochondria membrane

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130
Q

What converts cholesteryl esters into cholesterol?

A

Cholesteryl ester hydroxylase (CEH)

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131
Q

What are the three main ways cortisol is regulated?

A

Circadian rhythm, stress and feedback (ACTH and cortisol)

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132
Q

What are the three regulatory feedback mechanisms for cortisol?

A
  1. Short - ACTH from pituitary to CRH in hypothalamus
  2. Long (fast) - ACTH from pituitary to adrenal gland to make cortisol, cortisol to ACTH in pituitary
  3. Long (slow) - ACTH from pituitary to adrenal gland to make cortisol, cortisol to CRH in hypothalamus
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133
Q

What are parvocellular cells?

A

Cells in the lateral geniculate nucleus that release CRH in a circadian dependent pulsatile fashion

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134
Q

What is erythropoietin (EPO)?

A

Made naturally out of oxygen in the kidneys (at higher amplitudes)

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135
Q

What is the precursor for melatonin?

A

Serotonin (5HT) - tryptophan

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136
Q

What is the importance of peripheral oscillators in circadian rhythm?

A

Feedback loops that are entrained by neural pathways, hormones and feeding rhythms

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137
Q

What are examples of external cues that entrain the circadian rhythm?

A

Feeding schedules, light, activity and heat/temperature (thyroid hormone)

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138
Q

What system is responsible for the circadian rhythm response to light cues?

A

Retinohypothalamic tract (retina to SCN)

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139
Q

What is the circadian response to photic input?

A

Induction of various genes and chromatin remodeling within the SCN neurons

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140
Q

What is needed for photoreceptors to produce serotonin?

A

Blue light

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141
Q

What are some stress stimulators of ACTH release?

A

Physical exercise/work
Emotion
Pain
Trauma
Hypoxia - not enough O
Hypoglycemia - low blood sugar
Extreme temperature changes
Surgery
Depression
Infection

142
Q

What is released with CRH during stress?

A

Vasopressin

143
Q

What is Cushing Syndrome?

A

Constant high levels of circulating cortisol due to overproduction by the adrenal gland

144
Q

How does cortisol help the body deal with stress?

A

Mobilizing energy resources, increasing blood glucose and makes it more available in the brain

145
Q

How can high levels of corticosteroids be beneficial?

A

Suppress inflammation and antibody production by B-cells

146
Q

What are some reasons for the high cortisol levels with Cushing Syndrome?

A
  1. Tumor on adrenal gland
  2. High ACTH due to tumor in pituitary gland

Or administration of glucocorticoids for therapeutic purposes

147
Q

What are the key symptoms of Cushing Syndrome?

A
  1. Obesity
  2. More fat development on face and torso (water retention)
  3. High blood pressure
  4. Muscle/bone weakness
148
Q

What is an indicator of Cushing Syndrome?

A

High cortisol levels at night

149
Q

What is another name for Cushing Syndrome?

A

Hyperadrenocorticism

150
Q

What are the benefits of a longer exhalation?

A

Increased CO2 – retention of carbon dioxide in lungs

Vasorelaxation – lower blood pressure (decrease heart rate)

Increased H2O – retaining more water (nasal breathing)

Heat – warmer with longer exhalation

Increased nitric oxide (NO)

151
Q

What is Cushing’s disease?

A

Specific type of Cushing syndrome due to excessive ACTH from a pituitary tumor

152
Q

What is Addison’s disease?

A

Insufficient production of cortisol (often accompanied by an aldosterone deficient)

153
Q

What is another name for Addison’s disease?

A

Hypoadrenocorticism

154
Q

What are the main causes of Addison’s disease?

A

Infectious disease or autoimmune destruction of the adrenal cortex

155
Q

What is hypogycemia?

A

Low levels of glucose in blood

156
Q

Why is there an increase in ACTH production is Addison’s disease?

A

Underproduction of cortisol decreases negative feedback on the pituitary

157
Q

What happens if too much aldosterone is produced?

A

Lose osmotic balance in the kidney lumen

158
Q

What is the main function of aldosterone in the lumen of the kidney tubules?

A

Na+ pumped across cells into extracellular fluid (conserved) while K+ and H+ pumped into lumen (to be lost in urine)

159
Q

What is the major target of mineralocorticoids?

A

Kidney distal tubules (Na/K exchange)

160
Q

How does reabsorption of water occur in response to mineralocorticoids?

A

Passively - osmotic effect directly related to increased resorption of sodium

161
Q

What are the two main regulators of aldosterone secretion?

A
  1. Concentration of K in the extracellular fluid
  2. Angiotensin II (decrease bp = decrease aldosterone, increase bp = increase aldosterone)
162
Q

What is released if blood flow is too high?

A

Atrial natriuretic peptide (ANP)

163
Q

How does ANP regulate blood pressure and salt-water balance?

A

By promoting renal sodium and water excretion

164
Q

How is renin produced?

A

Juxtaglomerular cells in the kidney produce prorenin that is converted into renin in response to a drop in blood pressure

165
Q

What are the main functions of Angiotensin II?

A
  1. Systemic vasoconstriction (arterioles)
  2. Sodium/water retention (kidneys) by…
    - aldosterone release from adrenal
    - ADH release from pituitary
  3. Stimulate thirst (hypothalamus)
166
Q

What is the main function of the Renin-Angiotensin-Aldosterone system (RAAS)?

A

Increased blood volume and blood pressure

167
Q

What is the function of the macula densa cells in the kidneys?

A

Sense the amount of sodium, potassium and chloride in the ascending tubules of the kidneys and inform the juxtaglomerular cells if renin is needed

168
Q

What are the effects of excess aldosterone on renin secretion?

A

Inhibits renin secretion

169
Q

What happens with too much aldosterone vs not enough aldosterone?

A

Too much aldosterone:
- High blood pressure – water retention
- Lose too much potassium – cardiac problem
- Too much ACTH

Not enough aldosterone (not enough adrenal function):
- Low blood pressure
- Glucocorticoid deficiency – go hand in hand
- Retain too much potassium – had for heart

170
Q

What competes with cortisol for mineralocorticoid receptors?

A

Aldosterone (but cortisol concentrations are 100x greater)

171
Q

What blocks cortisol from binding to mineralocorticoid receptors? How does it do this?

A

Cortisone

172
Q

Where are steroids synthesized?

A

Smooth ER and mitochondria

173
Q

What is chronic licorice intoxication?

A

Water and sodium retention coupled with low plasma K causing hypertension and low renin activity

174
Q

What converts cortisol to cortisone (inactive form)?

A

11-beta hydroxysteroid dehydrogenase (HSD)

175
Q

What does licorice inhibit?

A

11-beta hydroxysteroid dehydrogenase (HSD) - not inactivation of cortisol (to cortisone)

176
Q

Where is CRH found?

A

In the hypothalamic paraventricular nucleus (PVN)

177
Q

Where is the circadian rhythm of cortisol secretion derived from?

A

Connections between the PVN and SCN

178
Q

What projections from the SCN regulate sleep-wake cycles?

A

Projections to the dorsomedial and posterior hypothalamic areas

179
Q

What is the function of the seminiferous tubules in the testes?

A

Produce spermatozoa and contain Sertoli cells

180
Q

What are Leydig/interstitial cells?

A

Major endocrine cells of the testes that produce sex steroid hormones (testosterone mostly, DHT and estradiol) and activins

181
Q

What is the function of Sertoli cells?

A

Produce inhibins and factors (ex. androgen-binding proteins)
Nurse cells for spermatozoa
Limit the amount of cytotoxins that can reach the spermatozoa

182
Q

What does DHT stand for?

A

Dihydrotestosterone

183
Q

In the mitochondria, what cleavage enzyme coverts cholesterol to pregnenolone?

A

Cytochrome P450 side chain (P450SCC)

184
Q

Where does pregnenolone translocate to for conversion to testosterone?

A

Smooth ER

185
Q

What two routes can pregnenolone take to be converted to testosterone?

A
  1. Progesterone
  2. Dehydroepiandrosterone (DHEA)
186
Q

What is the difference between testosterone and dihydrotestosterone?

A

Testosterone is the predominant androgen and dihydrotestosterone is the more potent androgen

187
Q

How is testosterone converted to the more potent androgen DHT?

A

5alpha reductase

188
Q

Testosterone and DHT bind to the same androgen receptor, which one has higher affinity?

A

DHT

189
Q

What is estradiol?

A

The predominant from of estrogen

190
Q

What are the two different estrogen receptors?

A

ER-alpha and ER-beta

191
Q

What happens after estrogen binds to its receptor?

A

HSP dissociates
Homodimer or heterodimer formed with another estrogen-receptor complex

192
Q

What does GnRH release?

A

LH and FSH

193
Q

What is the function of LH in testosterone?

A

Stimulates Leydig cells to produce and secrete testosterone

194
Q

What is the function of FSH in testosterone?

A

Stimulates testicular growth and acts on Sertoli cells to enhance production of androgen-binding protein (ABP)

195
Q

What is the function of inhibins?

A

Inhibit FSH release

196
Q

What is the function of activins?

A

Augment GnRH-mediated release of FSH

197
Q

Where are inhibins produced in males vs females?

A

Males - Sertoli cells
Females - Granulosa cells and corpus luteum

198
Q

Where are activins produced in males vs females?

A

Males - Leydig cells
Females - Granulosa cells and corpus luteum

199
Q

What three cells are ovarian follicles comprised of?

A
  1. Oocytes
  2. Granulosa cells
  3. Theca cells
200
Q

What is the function of granulosa cells?

A

Only have FSH receptors and produce estradiol

201
Q

What is the function of theca cells?

A

Only have LH receptors and produce androgens (androstenedione) that are precursors for granulosa cells to convert to estradiol

202
Q

What is the function of the corpus luteum?

A

Produces progesterone in response to LH

203
Q

What is follicular atresia?

A

The depletion of the pool of oocytes during childhood/adulthood

204
Q

What happens with proliferation of granulosa cells?

A

Begin expressing FSH, estrogen and androgen receptors

205
Q

What happens with maturation of follicles?

A

Production of more estradiol leading to an increase in the LH and FSH receptor density

206
Q

What cells express 17alpha-hydroxylase and lack aromatase?

A

Theca cells

207
Q

What cells lack 17alpha-hydroxylase but have aromatase?

A

Granulosa cells

208
Q

What ovarian follicle cells are more exposed to the circulatory system? Why is this important?

A

Theca cells - to take up cholesterol from circulation and synthesize androgen precursors

209
Q

What is the function of aromatase?

A

Convert androgens into estrogens

210
Q

What happens when estrogen levels continually rise?

A

Uterine lining (endometrium) thickens and LH surge promotes ovulation

211
Q

Why is the LH surge required?

A

For maturation of the oocyte

212
Q

How does LH promote the formation of the corpus luteum?

A

Promotes the granulosa cells and theca cells that remain in the ovulated follicle to differentiate into granulosa lutein cells and theca lutein cells

213
Q

What does LH stimulate the corpus luteum to produce?

A

Progesterone

214
Q

What is estradiol production stimulated by?

A

FSH

215
Q

What is considered a dominant follicle?

A

Follicle with the most granulosa cells (most FSH receptors)

216
Q

When do granulosa cells start to express LH receptors for the production of progesterone?

A

In the luteal phase with formation of the corpus luteum

217
Q

What are the main functions of FSH in ovulation?

A

Stimulates maturation of the ovarian follicles (prevents follicular atresia)
Promotes estradiol production by granulosa cells and the corpus luteum

218
Q

What are the main functions of LH in ovulation?

A

Triggers ovulation and the development of the corpus luteum
Stimulates production of androgens by theca cells
Stimulate progesterone production by corpus luteum

219
Q

What happens with rising levels of estradiol?

A

Negative feedback on LH and FSH

220
Q

What do female hormonal contraceptives tend to be made of?

A

Two synthetic sex hormones - ethinyl estradiol and progestin

221
Q

How doe female hormonal contraceptives prevent ovulation?

A

Mimicking the negative feedback effects of estradiol and progesterone - lowering FSH and LH and suppressing ovarian production of estradiol and progesterone

222
Q

What does the endometrium consist of?

A

Glands, stromal fibroblasts and extracellular matrix

223
Q

What are the effects of estrogen vs progesterone on the endometrium?

A

Estrogen - promotes growth
Progesterone - inhibits growth

224
Q

What is endometriosis?

A

Chronic inflammatory disease involving growth of endometrial tissue outside of the uterine cavity

225
Q

What are the three possible ways endometriomas are formed?

A
  1. Retrograde menstruation theory - backward flow of endometrial tissue through the fallopian tubes
  2. Coelomic metaplasia theory - extrauterine cells abnormally differentiate into endometrial cells
  3. Lymphatic and circulatory spread - endometrial cells enter the blood stream and implant on distance tissues
226
Q

What are the effects of DNA methylation?

A

Gene repression

227
Q

What is the function of GATA-binding factor 6 in endometriotic cells?

A

Converting progesterone to androstenedione

228
Q

What is the function of Steroidogenic Factor-1 (SF-1) in endometriotic cells?

A

In combination with GATA6 - plays a role in the conversion of cholesterol to estradiol in endometriotic cells

229
Q

What is the function of ESR2s in endometriotic cells?

A

Encodes the estrogen receptor beta (ErBeta)

230
Q

What is the cumulative effects of GATA6, SF1 and ESR2 in endometriotic cells?

A

Hypomethylation - increasing gene expression leading to elevated estrogen signaling and reduced progesterone signaling

231
Q

What does the increased estradiol signaling by GATA6, SF1 and ESR2 stimulate?

A

COX-2 and ESR2

232
Q

What happens with the stimulated production of COX-2 and ESR2?

A

High local concentration of estradiol and prostaglandins, which allows cell survival and promotes pain and inflammation

233
Q

What does the decreased progesterone signaling by GATA6, SF1 and ESR2 stimulate?

A

Prevent formation of weaker estrone

234
Q

What are clinical management options for endometriosis?

A
  1. Progestins (decrease LH and FSH)
  2. GnRH agonists (down regulates GnRH receptors - decrease LH and FSH)
  3. GnRH antagonists (decrease LH and FSH)
  4. Oral contraceptives (stop GnRH production)
235
Q

What are some biological mechanisms that allow endometriotic cells to survive outside the uterus?

A
  1. Reduced apoptosis
  2. Defective differentiation
  3. Inflammation
  4. Angiogenesis
  5. Genomic alterations
  6. Epigenomic alterations
236
Q

How is FSH regulated?

A

Primarily regulated at level of gene expression

237
Q

How is LH regulated?

A

Some gene expression, but LH surge mostly regulated at level of secretion

238
Q

What causes the differential production and release of FSH vs LH?

A
  1. GnRH pulse frequency
  2. Levels/signaling of ovarian hormones - activins, inhibins, estradiol, progesterone, testosterone (GPCRs)
239
Q

What frequency of pulsatile release from the GnRH favors FSH vs LH?

A

Low-frequency = FSH secretion
High-frequency = LH secretion

240
Q

Is LH or FSH stored in vesicles?

A

LH - pre-synthesized and stored in storage granules for LH surge

241
Q

What is the function of kisspeptins in pulsatile release of GnRH?

A

Regulate GnRH secretion and the hypothalamic-pituitary gonadal (HPG) axis

242
Q

What stimulates the LH surge?

A

When estradiol levels reach a certain (high) threshold

243
Q

How does positive feedback of the hypothalamic-pituitary-ovary axis lead to the LH surge?

A

High estradiol triggers a massive release of GnRH, increasing GnRH pulse frequency.
Pituitary sensitivity to GnRH increases inducing expression of GnRH receptors
Stimulate LH secretion

244
Q

What hormones have negative feedback effects on estradiol release?

A

Ovarian hormones = estradiol, progesterone, testosterone and inhibins

245
Q

What happens in puberty?

A

Increased FSH and LH production, therefore increased gonadal sex steroid production

246
Q

What is the earliest even of puberty in males and females?

A

Onset of pulsatile release of GnRH during REM sleep

247
Q

What is thought to be the puberty “on switch” and why?

A

Kisspeptin signaling - important role in GnRH pulses/secretion

248
Q

How does estradiol/testosterone stimulate growth spurts?

A

Estradiol - Stimulates IGF-1 and GH
Testosterone - Enhance GH effects to increase IGF-1

249
Q

What are some signs of declining female fertility with age?

A

Aging oocytes and loss of ovarian follicles (impaired folliculogenesis)

250
Q

What happens to LH/FSH levels during menopause?

A

Very high levels of LH/FSH

251
Q

What causes the high levels of LH/FSH during menopause?

A
  1. Decrease inhibins, increase activins
  2. Increase GnRH pulse frequency
  3. Decreased negative feedback due to low progesterone
252
Q

What happens to estradiol levels in menopause?

A

Fluctuate greatly in perimenopause and fall drastically in menopause

253
Q

What happens to circulating androgens in menopause?

A

Decrease (but less that estradiol)

254
Q

Where are post-menopausal estrogens derived?

A

Peripheral tissues converting/aromatizing androgens (ex. adrenal glands producing androstenedione)

255
Q

What is the predominant estrogen in postmenopausal women?

A

Estrone (1/3 potency of estradiol)

256
Q

What are some key features of estrogen?

A

Adipose tissue metabolism
Cardio protection
Neuroprotection
Maintenance of bone density
Growth and proliferation of breast tissues
Enhancement of insulin sensitivity and glucose tolerance

257
Q

What receptors does E/NE bind to?

A

alpha/beta adrenergic receptors

258
Q

What is the rate limiting step in catecholamine synthesis?

A

Tyrosine hydroxylase

259
Q

What induces the production of phenyl ethanolamine N-methyltransferase (PNMT)?

A

Cortisol

260
Q

What adrenergic receptors activate Gi vs Gq vs Gs?

A

Alpha 1 = Gq (PLC)
Alpha 2 = Gi (AC)
Beta = Gs (AC)

261
Q

What binds to Gq GPCRs?

A

Angiotensin II

262
Q

What is the synthesis pathway for catecholamines?

A

Tyrosine
(Tyrosine Hydroxylase)
DOPA
(DOPA decarboxylase)
Dopamine
(Dopamine-beta hydroxylase)
Norepinephrine
(PNMT)
Epinephrine

263
Q

What are the three interfaces for calcium exchange?

A
  1. Intestines
  2. Bones
  3. Kidney (renal tubules)
264
Q

What are the main regulators of calcium?

A

Vitamin D and PTH (some calcitonin)

265
Q

What is used to keep extracellular Ca 10,000 fold greater than intercellular Ca?

A

ATP-dependent Ca pumps and Na/Ca exchangers

266
Q

What type of calcium had regulatory effects?

A

Ca unbound

267
Q

What signals the release of Ca from the ER and mitochondria into the cell?

A

Inositol triphosphate (IP3) signaling

268
Q

What are the effects of PTH and VD when there is low serum calcium?

A

PTH increases Ca release from bone and decreases Ca loss in urine
VD increases absorption of Ca in intestines and increase reabsorption of Ca in kidneys

269
Q

What is the difference between calcitriol and calcitonin?

A

Calcitriol increases blood calcium levels and calcitonin decreases blood calcium levels

270
Q

What do osteoblasts vs osteoclasts have receptors for?

A

Osteoclasts = calcitonin
Osteoblasts = PTH and VD

271
Q

What is the function of osteoclasts?

A

Bone reabsorption - cell moves to bone surface and secretes acid and enzymes to break down bone

272
Q

What are osteoclasts stimulated/inhibited by?

A

Stimulated = osteoblasts
Inhibited = calcitonin

273
Q

What is the function of osteoblasts?

A

Bone forming - secrete bone matrix

274
Q

What do lymphoid progenitor cells mature into?

A

Lymphocytes (T/B cells) - immunity
Myeloid progenitor cells

275
Q

How does HCl produced by osteoclasts help with bone remodeling?

A

Breakdown of hydroxyapatite into calcium and phosphate for release into the blood stream

276
Q

What is the function of macrophages in bone remodeling?

A

“Mop” up after osteoclast breakdown and apoptosis

277
Q

Where is calcitonin made?

A

Parafollicular cells in thyroid gland (C-cells)

278
Q

What is the function of VD in bone formation?

A

Maintaining normal blood levels of calcium and phosphate

279
Q

What is one of the precursors for VD?

A

7-dehydrocholesterol

280
Q

How is Vitamin D production upregulated?

A

Decreased phosphate, calcium and VD
Increased PTH

281
Q

What form of VD is used to determine VD levels?

A

25OHD3 in the liver

281
Q

Where is VD precursor stored until needed?

A

Liver and fat

282
Q

What is the inactive form of VD and when is it synthesized?

A

24,25(OH)2D3 - synthesized when VD levels are already good

283
Q

What deactivated VD in the liver and kidneys?

A

Hydroxylases

284
Q

What happens to VDR when bound to 1,24(OH)2D (calcitriol)?

A

Forms a heterodimer with retinoic X receptor on VD response element (VDRE)

285
Q

What does binding of VDR and RXR to VDRE stimulate?

A

Transcription and production of proteins - maintaining normal blood levels of calcium and phosphate

286
Q

What promotes the uptake of Ca ions in the intestines?

A

VD by upregulating mRNA

287
Q

What happens to PTH with an increase in Ca ion influx?

A

Inhibition of PTH synthesis and release from granules

288
Q

What is the role of calcitonin in bone remodeling?

A

Inhibits osteoclasts and stimulates osteoblasts

289
Q

How are the effects of calcitonin different from the effects of PTH?

A

Calcitonin - Ca influx increases secretion
PTH - Ca influx decreases secretion

290
Q

What receptor does PTH vs calcitonin use?

A

PTH = GPCR(Gq)
Calcitonin = GPCR (Gs)

291
Q

What kind of receptors is the MT1 melatonin receptor?

A

GPCR (Gi)

292
Q

What are the effects of melatonin of estrogen?

A

Reduces estrogen signaling -suppresses ER-alpha mRNA expression and reduces cAMP levels

293
Q

What are the down-regulatory effects of melatonin?

A

Down-regulates growth factor pathways that support cell proliferation and survival

294
Q

What is the role of VD in breast cancer?

A

Higher levels of VD are associated with a decrease risk of breast cancer
Inhibits ERalpha, aromatase and COX-2

295
Q

What was VD found to activate the transcription of?

A

Tryptophan hydroxylase at VDRE

296
Q

Why is it important that calcitonin acts faster than PTH?

A

Prevent hypercalcemia by inhibiting osteoclast breakdown of bone into Ca and phosphate

296
Q

What are some causes of hypercalcemia?

A

Hyperparathyroidism (ex. tumor)
Increased Ca absorption (gut/bone)
Decreased Ca excretion (kidney)
Overproduction of VD

297
Q

What are some causes of hypocalcemia?

A

Hypoparathyroidism
Decreasing Ca absorption

298
Q

How can corticosteroid medications lead to hypocalcemia?

A

Reduce inflammation/immune system with side effect of decrease Ca absorption

299
Q

What causes Rickets?

A

Lack of VD causing decreased Ca and phosphate

300
Q

What are the results of Rickets?

A

Secondary hyperparathyroidism (PTH too high) and increased bone resorption

301
Q

What is osteomalacia?

A

Mineralization of newly formed bone matrix is defective

302
Q

What causes osteomalacia?

A

Lack of VD, low Ca or low phosphate leading dysfunction of osteoblasts

303
Q

What is the function of cytokine FGF23?

A

From bone - inhibits VD production and blocks phosphate reabsorption in kidneys

304
Q

What is FGF23 linked with?

A

Increased rickets and osteomalacia
Human chronic kidney disease

305
Q

What is FGF23 secreted in response to?

A

Secreted by osteocytes (osteoblasts) in response to oral phosphate or increased 1,25(OH)2D3

306
Q

What is Lytic Paget’s Disease (Osteitis Deformans)?

A

Rapid bone loss due to a high rate of bone degradation/reabsorption
Increased by FGF23

307
Q

How can Lytic Paget’s Disease (Osteitis Deformans) be treated?

A

Calcitonin

308
Q

How does kidney deterioration lead to secondary hyperparathyroidism?

A

Decreases VD formation and increased phosphate retention leading to decreased serum Ca and increased PTH

309
Q

What is osteoporosis?

A

Disorder of the bones in which the bones become brittle, weak and easily broken - decrease in mineralization and strength of bones over time

310
Q

How does Cushing’s disease lead to an increased chance of osteoporosis?

A

High levels of cortisol

311
Q

What is associated with osteoporosis?

A

Low estrogen and high glucocorticoids
Long-term VD insufficiency

312
Q

What is the main circulatory form of VD?

A

25(OH)D - calcitriol

313
Q

What happens with decreased functionality of steroidogenic factor-1 (SF-1)?

A

Low levels of androgens leading to 46XY females

314
Q

What happens with translocation of sex-determining region Y (SRY) protein (SRY still functional)?

A

Part of the Y chromosome has been translocated to part of the X chromosome = 46XX males

315
Q

What happens with mutation of sex-determining region Y (SRY) protein (SRY not functional)?

A

46XY females

316
Q

What is the function of sex-determining region Y (SRY) protein?

A

Initiates teste development

317
Q

What levels of androgens are needed to develop as a male/female?

A

Male = High levels
Female = Low levels

318
Q

What is the bipotential period?

A

When either Mullerian ducts or Wolffian ducts can form

319
Q

What causes the gonadal differentiation of Mullerian ducts and Wolffian ducts?

A

Mullerian = exposure to estrogens
Wolffian = exposure to androgens (testosterone)

320
Q

What is the fetus highly sensitive to during the bipotential phase?

A

Androgens

321
Q

What is the function of Anti-Mullerian hormone (AMH)?

A

Produce Steroli cells and Leydig cells that control stabilization of Wolffian ducts

322
Q

What is Amenorrhea?

A

Lack of menstrual cycle after age 16

323
Q

What are some causes of amenorrhea?

A
  1. GnRH deficiency (Kallmann’s Syndrome) - GnRH neurons not developing properly
  2. Functional hypothalamic amenorrhea - reduced GnRH pulse frequency
  3. Hyperprolactinemia - DA not inhibiting prolactin release
324
Q

What inhibits GnRH release?

A

Prolactin - inhibited by dopamine

325
Q

What is Klinefelter’s Syndrome (male 47, XXY)?

A

Extra X chromosome that changes the amount of estradiol in circulation - no clear secondary sex characteristics

326
Q

What is Turner’s syndrome (female 45,X)

A

Loss of an X chromosome leading to gonadal dysgenesis - no secondary sex characteristics

327
Q

What is androgen insensitivity syndrome?

A

Testes present but absent Wolffian ducts - female appearing external genitalia

328
Q

What is Intersex 46, DSD?

A

Have testes but genital ducts/external genitalia not fully masculinized

329
Q

How does androgen biosynthetic dysfunction in 46, XY individuals occur?

A
  1. LHR mutation
  2. 17alpha hydroxylase deficiency
  3. 5alpha reductase deficiency
330
Q

How does excess androgen in 46, XX individuals occur?

A
  1. 21alpha hydroxylase deficiency
  2. Aromatase deficiency
  3. Increased androgen exposure
331
Q

What is the function of 21alpha hydroxylase?

A

Production of cortisol and aldosterone

332
Q

What happens with use of testosterone injections?

A

Lower FSH levels, decreasing normal production of androgens

333
Q

What affects both aging and obesity?

A

Caloric intake

334
Q

What are the risks of testosterone therapy?

A

Heart attack, stroke, blood clots and heart-rhythm irregularities

335
Q

What are the effects of ageing on pancreatic functioning?

A

Decrease glucose metabolism by increasing insulin resistance and decreasing insulin secretion

336
Q

What are the effects of ageing on thyroid functioning?

A

Decrease TSH and decrease T3 (due to decreased T4 metabolism)

337
Q

What are the effects of ageing on pituitary functioning?

A

Decrease in GH

338
Q

What are the effects of ageing on liver functioning?

A

Decrease IGF-1

339
Q

What are the effects of ageing on gonadal/adrenal functioning?

A

Decrease E2, T and DHEA

340
Q

What are some examples of autoimmune diseases?

A

Addison’s
Graves
Hashimoto’s
Type 1 Diabetes

341
Q

How do T/B cells have such a diverse recognition capacity?

A

They can rearrange their DNA during development to change the ability of antibodies and receptors to recognize different types of polypeptides

342
Q

What is the function of T/B cells?

A

Immune function
T = T cell receptors
B = antibodies

343
Q

What is a central pathogenic step in the development of autoimmune disease?

A

Breakdown of self-tolerance

344
Q

How are dangerous T and B cells with self reactive receptors eliminated?

A

Negative selection (apoptosis)

345
Q

What are possible disruptors of self-tolerance?

A

Defects in apoptosis-related death receptor molecules
Defects in internal apoptosis mechanisms
Defects in suppression of T cells
Defects in B cell tolerance to self
Hypocortisolism

346
Q

What are the effects of cortisol on the immune system?

A

Suppresses the immune system (T/B cells)

347
Q

What are environmental factors that effect autoimmunity?

A

Infectious agents
Diet
Toxins

348
Q

What is the connection between Type 1 diabetes and Rubella?

A

Antibodies against rubella proteins have a similar molecular structure to the antibodies against proteins in the beta-cells of the pancreas

349
Q

What happens with circadian levels of cortisol?

A

Lower immune function (T-cells)

350
Q

What does Addison’s disease develop antibodies against?

A

21-alpha hydroxylase

Molecular Endocrinology (2 decks)

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