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Physiology Exam 4 > Steroid Hormone Receptors > Flashcards

Steroid Hormone Receptors Flashcards

1
Q

Cell signaling allows?

A

Communication among cells to coordinate their behavior for the benefit of the whole organism

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2
Q

“Cell signaling allows communication among cells to coordinate their behavior for the benefit of the whole organism.” Behavior refers to?

A
  1. Control of gene expression
  2. Control of protein function
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3
Q

Steroid hormone receptors are _____ receptors

A

Intracellular

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4
Q

Signaling molecules can also be called?

A
  1. Ligands
  2. Agonists
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5
Q

Signaling via steroid hormone receptors involves?

A
  1. Common structure
  2. Common signaling mechanism
  3. Multiple rounds of transcription
  4. Location of receptors
  5. Specificity and speed
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6
Q

Aldosterone binds to what receptor?

A

Mineralcorticoid

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7
Q

Thyroid hormone binds to what receptor?

A

Thyroid hormone receptor

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8
Q

Steroids are _____ derivatives

A

Cholesterol

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9
Q

Steroid hormone receptors include?

A
  1. Cortisol receptor
  2. Estrogen receptor
  3. Testosterone receptor
  4. Vitamin D3 receptor
  5. Retinoic acid receptor
  6. Thyroid hormone receptor
  7. Mineralocorticoid receptor
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10
Q

Are all signaling molecules which act via steroid hormone receptors steroids?

A

No.

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11
Q

Examples of non-steroid ligands which act on steroid hormone receptors

A
  1. Thyroxine
  2. Retinoic acid
  3. Vitamin D3
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12
Q

All cholesterol derivatives have what type of backbone?

A

4 aromatic rings

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13
Q

Most important carrier protein for cortisol

A

Transcortin

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14
Q

Most important carrier protein for thyroid hormone

A

Thryoxine-binding-globulin

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15
Q

Steroid hormone receptor have a common structure. They all contain?

A
  1. Transcription-activating domain
  2. DNA binding domain
  3. Hormone-binding domain
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16
Q

Why are ligands in the bloodstream bound to carrier proteins?

A

Prevent excretion in the kidney

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17
Q

How long do ligands remain in the bloodstream before excretion?

A

Hours → long time / slow process

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18
Q

How do ligands enter cells?

A

Diffusion across lipid membrane

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19
Q

How are ligands able to diffuse across the lipid membrane?

A

They’re lipid soluble of course!

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20
Q

What happens when ligands bind to intracellular receptors?

A

Activate receptor

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21
Q

What does the activated hormone-receptor complex do?

A
  1. Enters nucleus
  2. Dimerizes
  3. Binds to specific sequence on DNA
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22
Q

When activated hormone-receptor complex binds to DNA, what happens?

A

Transcription is initiated → if appropriate transcription factors are present

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23
Q

Where are intracellular receptors located?

A

Cytosol or nucleus

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24
Q

Intracellular receptors in the nucleus reside as?

A

Inactive receptors on DNA

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25
Q

2 examples of receptors located in cytosol

A
  1. Glucocorticoid receptor
  2. Aldosterone receptor
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26
Q

2 examples of receptors located in nucleus

A
  1. Thyroid hormone receptor
  2. Vitamin D3 receptor
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27
Q

Steroid hormone receptors are specific. What are the 2 things necessary for them to work?

A
  1. Cell must contain receptor
  2. Regulatory proteins must be present → some of these are cell-specific
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28
Q

General speed of signaling via intracellular receptors

A

Slow

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29
Q

Why is signalling via intracelular receptors slow?

A
  1. Long diffusion path for ligand
  2. Effect requires transcription and translation
  3. Termination requires excretion of hormone
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30
Q

Reservoir for ligands

A

Carrier proteins

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31
Q

How is hormone excreted?

A

Bile after conjugation in liver

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32
Q

Aldosterone is produced in response to?

A

Decrease in blood pressure (Renin-Angiotensin-Aldosteron system)

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33
Q

Aldosterone originates rom?

A

Adrenal cortex → no storage

34
Q

Aldosterone carrier proteins

A
  1. Transcortin
  2. Albumin
35
Q

How does aldosterone increase blood pressure?

A

Increases Na+ and water retention, K+ excretion

36
Q

Renin is released by?

A

Kidney in response to drop in blood pressure

37
Q

Where does renin go after it’s released by the kidney?

A

Into blood strem

38
Q

Renin catalyzes what reaction?

A

Angiotensinogen → angiotensin I

39
Q

Renin function

A

Initiate angiotensin II release in response to drop in blood pressure

40
Q

What enzyme converts angiotensin I to angiotensin II

A

Angiotensin converting enzyme

41
Q

Angiotensin II stimulates?

A

Aldosterone production and release from adrenal cortex

42
Q

In addition to aldosterone production and release, angiotensin II causes?

A
  1. Vasoconstriction
  2. Na+ and water retention
43
Q

How do angiotensin II and aldosterone increase blood pressure?

A
  1. Increased blood volume
  2. Vasoconstriction
44
Q

T3 full name

A

Tri-iodo-thyronine

45
Q

T3 is released in response to?

A

Cold and stress

46
Q

T3 origin

A
  1. Thyroid gland synthesizes and stores prohormone thyroxine (T4)
  2. 1 iodine removed → T3 generated
47
Q

2 T3 carrier proteins

A
  1. Thyroxine-binding prealbumin
  2. Thyroxine-binding globulin
48
Q

T3 effect

A
  1. Thermogenesis
  2. Mobilization of fat and protein
49
Q

How does T3 cause thermogenesis, mobilization of fat and protein?

A

General increase in metabolism: increased O2 consumption and ventilation

50
Q

TRH stands for?

A

Thyrotropin releasing hormone

51
Q

TRH is released by?

A

Hypothalamus

52
Q

TRH is released from hypothalamus in response to?

A

Cold and stress

53
Q

After being released from the hypothalamus, TRH goes where?

A

Bloodstream → pituitary gland

54
Q

TRH causes relase of?

A

TSH

55
Q

TSH stands for?

And is also called?

A

Thyroid stimulating hormone

Thyrotropin

56
Q

TSH is released from?

A

Pituitary

57
Q

TSH stimulates what gland?

A

Thyroid

58
Q

TSH stimulates the thyroid gland to release?

A

Thyroid hormone

59
Q

Thyroid hormone released from thyroid gland in response to TSH stimulus consists of?

A
  1. T3
  2. T4 (prohormone thyroxin)
60
Q

How is T4 converted to T3?

A

De-iodinases

61
Q

De-iodinases are mainly located where?

A

Kidney and liver

62
Q

T4 feedback?

A

Negative → inhibits TSH release from pituitary gland

63
Q

Feline hyperthyroidism presentation

A
  1. Weight loss (despite good appetite)
  2. Tachycardia
  3. Hyperexcitability
  4. Vomiting/diarrhea
  5. Poor hair coat
64
Q

Feline hyperthyroidism diagnosis

A
  1. Rule out other diseases
  2. Determine plasma levels of T4
65
Q

Feline hyperthyroidism prevalance

A

Most common endocrine disorder in older cats

66
Q

Feline hyperthyroidism environmental causes

A
  1. Longer livespan
  2. Exposure to chemicals
67
Q

Chemical which can cause feline hyperthyroidism

A

Polybrominated diphenyl ethers (PBDEs) → flame retardants

68
Q

Feline hyperthyroidism is most often caused by?

A

Thyroid adenoma

69
Q

Only 2% of cats with hyperthyroidism are diagnosed with?

A

Thyroid adenocarcinoma

70
Q

Feline hyperthyroidism treatment

A
  1. Methimazole (tapazol)
  2. Surgical removal of thyroid gland
  3. Radio-iodine tratement
71
Q

Methimazole (tapazol)

A

Inhibits T3/T4 production

72
Q

Why are phosphate groups used so often?

A

Availability of ATP as phosphate donor

73
Q

3 AAs containing -OH groups, likely to gain phosphate

A
  1. Serine
  2. Threonine
  3. Tyrosine
74
Q

Kinase

A

Phosphorylates

75
Q

Phosphatase

A

Dephosphorylates

76
Q

6 serine/threonine kinases

A
  1. A-kinase
  2. C-kinase
  3. G-kinase
  4. CaM kinase
  5. MAP-kinase
  6. IKB kinase
77
Q

CaM kinase stands for?

A

Calmodulin-activated kinase

78
Q

MAP-kinase stands for?

A

Mitogen-activated protein kinase

79
Q

Examples of tyrosine kinases

A
  1. Insulin receptor
  2. Many growth factor receptors
  3. SRC
  4. JAK
80
Q

How does signaling via steroid hormones lead to more than one round of transcription?

A
  1. Steroid hormone receptor complex activates primary response genes
  2. Primary response proteins are synthesized
  3. Primary response proteins shut off primary response gene
  4. Primary response proteins turn on secondary response genes

Physiology Exam 4 (10 decks)

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