Chapter 11 - Endocrine Flashcards

1
Q

What is the definition of a hormone (H)?

A

A Hormone is biology active compound release from on tissue into the blood, which carries it to its target tissue. Virtually every tissue produces hormones. (Notes) (pg 306)

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2
Q

What is a “target tissue” (TT)?

A

Target Tissues are a group of cells, which contain specific receptor proteins for the hormones and which therefore, can respond in a specific fashion. (306)

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3
Q

What does the TT do that makes it a TT for a hormone?

A

The TT allows the hormone to respond in a specific fashion according to the receptor protein. (306)
The hormone must bind to the receptor protein to have an action (notes)

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4
Q

“Exocrine gland”

A

“Exocrine gland”: (exo = Outside Greek) secrete chemicals through a duct that leads to the outside of the membrane and thus to the outside of a body surface. (pg 13)

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5
Q

“Endocrine gland”

A

“Endocrine gland”: (endon = Within Greek) secrete chemicals called hormones into the blood. (pg. 13 & 306)

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6
Q

What are some of the “classic” endocrine glands? (Fig 11.1)

A

Classic endocrine glands include: Pituitary Gland, Pineal gland, Hypothalamus, thyroid gland, adrenal gland, pancreas, ovary, test(ies)

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7
Q

Today we know that most tissues produce _____________s.

A

Hormones

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8
Q

What are “neurohormones”?

A

Neurohormones are specialized neurons, particularly in the hypothalamus, which secrete chemical messengers into the blood rather than into a narrow synaptic cleft. (pg. 306)

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9
Q

Hormones affect the _________ of their TT:

A

Receptor Proteins.

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10
Q

We can “classify” hormones (H) in 2 ways:

A

by their chemical structure and function

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11
Q

Chemical Categories:

A

Steroids – lipids derived from cholesterol. (testosterone, estradiol, progesterone, cortisol). Only secreted by the adrenal cortex (corticosteroids) and the gonads (sex steroids).

Amines – lipids derived from the amino acids tyrosine and tryptophan (hormones secreted by the adrenal medulla, thyroid, and pineal glands)

Polypeptides & Proteins – Polypeps contain less than 100 amino acids (generally, ex ADH). Proteins are polypeps with mot than 100 amino acids (ex GH). Insulin contains both.

Glycoproteins: Consist of long polypeps bound to one or more CHO group. Ex. Follicle Stimulating hormone (FSH) and luteinizing hormone (LH).

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12
Q

Polar Hormones:

A

Polypeps/proteins, glycoproteins and catecholamines (secreted by the adrenal medulla, epinephrine, and norepinephrines Derived from Tyrosine) (pg. 308-09)

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13
Q

Non-Polar Hormones:

A

Steroids and Thyroid hormones. These are known as lypophilic hormones, because they are non-polar.

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14
Q

What are the 2 types of “lipid soluble” Hormones? What glands produce them? (pg 307-08)

A

Lipid Soluble hormones are: Steroids and Amines (thyroid hormones). They are known as lypophilic hormones, because they are non-polar.

Steroids: Only secreted by the adrenal cortex (corticosteroids) and the gonads (sex steroids).

Aminies: Thyroid (Triodothyonine (T3) and Tyroxine/Tetraiodothyronine (T4)

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15
Q

When looking at Fig. 11.2, understand why different tissues release different steroids even though the metabolic pathway could go all the way from cholesterol to estradiol-17B.

A

The tissues release differing steroids because each steroids serves a specific purpose in the reproductive/sex system (e.g. ovulation, ejaculation, estrogen, testosterone)

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16
Q

Be able to discuss the structure of thyroxine and what its parent molecule is.

A

Thyroxin, T4, always converted into T3 cannot entire the nucleus.

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17
Q

When we use the terms “Pro-“ or “Pre-hormone” what is meant?

A

In the Inactive form of the hormone (per notes, not important)

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18
Q

Why are only some tissues the TT for a particular hormone?

A

???????

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19
Q

What do the terms “synergistic”, “permissive” and “antagonistic” mean with respect to H interactions? (pg 310)

A

Synergistic: When two or more hormones work together to produce a particular results. These effects may be additive or complementary.

Permissive: An H is said to have a permissive effect on the action of a second hormone when it enhances the responsiveness of a target organ to the second hormone or when it increases the activity of the second hormone. The second H won’t work w/o the other. (Notes)

Antagonistic: Hormones not working together. (e.g. Insulin lowers blood sugar, gluc. Raises blood sugar)

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20
Q

When we say a H has a ½ life of 3 days, what do we mean?

A

Half-Life: the time required for the plasma concentration of a given amount of the hormone to be reduced to half of its reference levels. How long does it take for ½ of it to disappear. (Notes)

A ½ life of 3 days is equal to a total of 6 days before the H is fully used.

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21
Q

In what ways did I tell you H are removed from the blood?

A

H’s are removed from the blood by (CANT FIND IN NOTES)

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22
Q

What is the “Priming Effect” (upregulation)?

A

Upregulation increases the # of receptor proteins. (Notes, pg 311)

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23
Q

What is “desensitization” or “downregulation”?

A

Prolonged exposure to high concentrations of polypeps hormones desensitize the T. Cells, which produces less of a response. This causes a decreased # of receptor proteins, which is call downregulation. (e.g. drug addicts).

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24
Q

Read the “Fitness” box concerning “Anabolic Steroids”. (pg 311)

A

Synthetic androgens (male Hs), causes men to develop gynecomastia (an abnormal growth of femalelike mammary tissue.) Female users display masculinization and antisocial behaviors. Inhibits the secretion of FSH and LH from the pituitary.

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25
Q

Mechanics of H action: The 2 mechanisms of “Non-polar” (lipophilic) H. (pg 312-314)

A

Two domains: ligand binding domains, and DNA binding Domains.

Steroid: Some Steroids bind to a cytoplasmic receptor, which then translocates to the nucleus Other Steroid hormones enter the nucleus and then bind to their receptor. In both cases, the steroid-receptor complex can then bind to a specific area of DNA and activate specific genes.

Thyroid: T4 is 1st converted into T3 within the cytoplasm of the target cell. T3 then enters the nucleus and binds to its nuclear receptor. The hormone-receptor complex can then bind to a specific area of DNA and activate specific genes.

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26
Q

Why do steroids and thyroxine need a carrier protein in the plasma?

A

Because they are lipophilic and do not travel dissolved in the aqueous portion of the plasma. After which they mush disassociation from their carrier proteins in the blood in order to pass through the lipid component of the plasma membrane and enter the T. Cell.

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27
Q

Be able to understand and describe what is shown in figures: 11.4, 11.5, 11.6, & 11.

A
  1. 4 & 11.5 pgs. 312 & 313

11. 6 & 11.7 pgs. 314 & 315

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28
Q

Where are the receptor proteins for steroids located? For Thyroxine?

A

Steroids: RP is located in the cytoplasm. (Notes) Two domains: ligand binding domains, and DNA.

Thyroxine: RP is only found in the nucleus.

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29
Q

What does “dimerization” mean?

A

The Process of two receptor units coming together. Both RP’s coming bind to the DNA. Two types Hetero (mixed) & Homo (similar)

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30
Q

What are “2nd messengers”? i.e. What do they do? Where are they formed?

A

Adenylate Cyclase-Cyclic AMP – 1st 2nd Mess to be discovered. When H binds to RP, causes dissociation of subunit from G- Proteins. The subunit moves through the membrane until it reaches the enzyme Adenylate Cyclaes, then binds to and activates this enzyme. ATP → cAMP + PPi cAMP activates the previously inactive enzyme in the cytoplasm called protein kinase. Fig 11.8 (1) The hormone binds to its receptor in the plasma membrane of the target cell. (2) This causes the dissociation of G-proteins, allowing the free α (alpha) subunit to activate adenylate cyclase. (3) This enzyme catalyzes the production of cAMP (cyclic AMP), which (4) removes the regulatory subunit from protein kinase. (5) Active protein kinase phosphorylates other enzyme proteins, activating or inactivating specific enzymes and thereby producing the hormonal effects on the target cell. (pg 315-16)

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31
Q

Phospholipase C–Ca2+

A

Fig. 11.9. Must bind to a Adrenergic receptor, causes constriction of smooth muscles, splits phospholipids into two units (insoitol triphosphate IP3) and (Diacylglycerol DAG). Binds to a protein called calmodulin. See also Tab. 11.5
Fig. 11.9 (1) The hormone binds to its receptor in the plasma membrane of its target cell, (2) causing the dissociation of G-proteins. (3) A G-protein subunit travels through the plasma membrane and activates phospholipase C, which catalyzes the breakdown of a particular membrane phospholipids into diacylglycerol and IP3 (inositol triphosphate). (4) IP3 enters the cytoplasm and binds to receptors in the endoplasmic reticulum, causing the release of stored Ca2+. The Ca2+ then diffuses into the cytoplasm, where it acts as a second messenger to promote the hormonal effects in the target cell.

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32
Q

Tyrosine Kinase:

A

See Fig 11.11, pg 318-319. - Activated when phosphorlated. Growth factors (EGF epidermal growth factors, PDGF platelet-derived growth factor, and IGFs insulin-like growth factors).
Fig. 11.11 - The insulin receptor consists of two parts, each containing a beta polypeptide chain that spans the membrane, and an alpha chain that contains the insulin-binding site. (a) When two insulin molecules bind to the receptor, the two parts of the receptor phosphorylate each other. (b) This greatly increases the tyrosine kinase activity of the receptor. (c) The activated receptor tyrosine kinase then phosphorylates a variety of “signal molecules” that produce a cascade of effects in the target cell.

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33
Q

What are the 1st messengers?

A

The first messengers are_______

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34
Q

Re-study the “adenylate cyclase –cAMP system, especially as shown in Fig 11.8 This system is the same as the ____________ receptor system

A

Norepinephrine (fig. 7.31, pg 189)

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35
Q

What is phosphodiesterase?

A

Phosphodiesterase is the enzyme, which is activated via a G-protein, when Epinephrien binds to its alpha-adrenergic receptor.

36
Q

Learn the “Phospholipase C-Ca++” system, especially as shown in Fig. 11.9. This is also known as the ____ ____________ receptor system.
pg 317

A

Alpha-Adgernic. Fig 11.9 - Some hormones when the bind to their membrane receptors activate phospholipase C (PLC). This enzyme catalyzes the formation of inositol triphosphate (IP3), which causes Ca++ channels to open in the endoplasmic reticulum. Ca++ is thus released and acts like a second messenger in the action of the hormone.

This is also known as the 2nd Messenger ??

37
Q

The membrane phospholipids are split into _______ & ________

A

The membrane phospholipids split into two units (insoitol triphosphate IP3) and (Diacylglycerol DAG). Both are second messengers, but IP3 is understood better.

38
Q

Study Fig 11.10

A

Epinephrine can act through two second-messenger systems. The stimulation of Beta-adrenergic receptors invokes the camp second-messenger system, and the stimulation of the Alpha-adrenergic receptors invoke the Ca++ second messenger system.

39
Q

What Hormone binds to the “Tyrosine Kinase” receptor?

pg 318 to 319

A

???

40
Q

What are the responses of tissues to insulin? i.e. what does insulin cause to happen?

A

???

41
Q

What is “autophosphorylation”?

A

Autophosphorylation is when the insulin binding and dimerization occurs, the enzymatic site is active in each unit of the receptor, and on unit phosphorylates the other.

42
Q

Study Fig 11.11 and Fig.11.12 (not in 9th ed.)

A

Fig. 11.11 see above
Fig. 11.12: Insulin stimulates glucose update by means of GLUT4 carriers. Insulin stimulates intracellular vesicles that contain the GLUT4 carries proteins to fuse with the plasma membrane of skeletal muscle and liver cells, as in exocytosis. The increased number of GLUT4 carries in the plasma membrane allows these organs to take glucose out of the blood plasma by facilitated diffusion.

43
Q

The Pituitary gland Is also called the ____________

A

The Master Gland

44
Q

It has 2 parts the 1st is ____________ or ______________ and the 2nd is _________ or __________

A

1st: The Anterior or pars distalis
2nd: The Posterior or pars tuberalis

45
Q

What is MSH? What does it do?

A

MSH, melanocyte-stimulating hormone, is causes the darkening of skin.

46
Q

What is “Pituitary Dwarfism”? Gigantism? What is the cause of both?

A

“Pituitary Dwarfism” is caused by inadquate GH secretion during childhood.
“Pituitary Gigantism” is cause by excessive GH secretion .

47
Q

What are the 2 H from the Post. Pit.? Where are they produced? What causes their release?

A

ADH (Antidiuretic Hormone-promotes water retention) and Oxytocin (stimulates contractoins of uterus during labor and mamary glands). Both of these are produced in the hypothalamus

48
Q

Why is the Pituitary no longer called the “Master Gland” of the body?

A

Because secretion of its hormones is controled by hormones secreted by the hypothalamus.

49
Q

What are the 3 layers of the adrenal cortex?

pg 326

A

??

50
Q

What are the names of the 3 types of H produced by the Ad. Cortex. Know a specific name for each type.

A

??

51
Q

How does Cushing Syndrome differ from Addison’s D?

A

??

52
Q

Who was Hans Selye and what did he discover about stress?

A

??

53
Q

What are the names of the 2 types of cells that make up most of the Thyroid?

A

??

54
Q

The major structures found in the Thyroid are called ______________s.

A

??

55
Q

What is found in the lumen of these structures?

A

??

56
Q

What are the 2 major actions that Thyroxine causes in its TT?

A

??

57
Q

What mineral is important for thyroxine?

A

??

58
Q

What happens if a person has too little of this mineral in their diet? A person who has this condition is said to be _____________

A

??

59
Q

What is Calcitonin? Where does it come from? What does it do?

A

??

60
Q

What is “Graves Disease”? A person who has it is said to be _________

A

??

61
Q

What is a “Toxic” goiter? What are some of its symptoms?

A

??

62
Q

What is “Cretinism”? What causes it?

A

??

63
Q

Where are the Parathyroid Glands located? What do they produce? In response to what?

A

??

64
Q

What action does PTH have in our body?

A

??

65
Q

The pancreas is both a _________gl. And a _____________gl.

A

??

66
Q

The endocrine portion is located in the _________s of ______________

A

??

67
Q

What are the 2 major types of cells found in this portion?

A

??

68
Q

What H does each cell type produce? What is the stimulus for release of each?

A

??

69
Q

What is the TT for Glucagon and what action does it have on its TT?

A

??

70
Q

What are some of the TT for insulin? What is its major action on them?

A

??

71
Q

What are some of the characteristics of D. Mellitus?

A

??

72
Q

Know a little about the Pineal Gl. And the Thymus Gl. Of what importance is each to us?

A

??

73
Q

Study the section on the Gonads and Placenta. Learn the information in the italicized print.

A

??

74
Q

What is hCG? What is important about it (2 things)?

A

??

75
Q

What is an “autocrine”? (Definition). Give the name of a specific one.

A

??

76
Q

What is a “paracrine”? (Definition). Give the name of a specific one.

A

??

77
Q

What are Eicosanoids? What are Prostaglandins? From what molecule are they made?

A

??

78
Q

What are NSAIDS?

A

??

79
Q

What is the abbreviated name for “cyclooxygenase:?

A

??

80
Q

Adrenocorticotropic Hormone (ACTH)

A

TT: Adrenal Cortex
Principal Action: Stimulates secretion of glucocorticoids
Regulation: Stimulated by CRH (corticotropin-releasing hormone); inhibited by glucocortidcoids

81
Q

Thyroid-Stimulating Hormone (TSH)

A

TT: Thyroid Gland
Principal Action: Stimulates secretion of thyroid hormone.
Regulation: Stimulated by TRH (Thyroptropin-releasing hormone); inhibited by thyroid hormone

82
Q

Growth Hormone (GH)

A

TT: Most Tissue
Principal Action: Promotes protein synthesis and growth; lipolysis and increased blood glucose.
Regulation: Inhibited by somatostatin; stimulated by GH-Releasing Hormone.

83
Q

Follicle-Stimulating Hormone (FSH)

A

TT: Gonads
Principal Action: Promotes gamete production and stimulates estrogen production in females.
Regulation: Stimulated by GnRH (gonadotropin-releasing hormone); inhibited by sex steroids and inhibin.

84
Q

Prolactin (PRL)

A

TT: Mammary glands and other sex accessory organs.
Principal Action: Promotes milk production in lactating females; additional actions in other organs.
Regulation: Inhibited by PIH (prolactin-inhibiting Hormone)

85
Q

Luteinzing Hormone

A

TT: Gonads
Principal Action: Stimulates Sex hormone secretion; ovulation and corpus luteum formation in females; stimulates testosterone secretion in males.
Regulation: Stimulated by GnRH (gonadotropin-releasing hormone); inhibited by sex steroids