CH 1 General Principles Flashcards

1
Q

How is endocrine function controlled?

A

hormones derived from circulation OR hormones produced locally OR neuroendocrine stimulation

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2
Q

Where do Thyroid Hormones bind to its receptor?

A

Receptors are located within the cell. TH is special because it is an amino acid derivative that doesn’t bind on the cell surface. Instead, it is transported into the cell to bind to its receptor.

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3
Q

How are protein/peptide hormones synthesized & released?

A

synthesis (ribosome) –> post-translation modification (ER) –> packaging + more modification (Golgi) –> complete hormone & “pro” fragments remain within a secretory vesicle until Ca++ induces hormone release

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4
Q

What are steroid hormones derived from?

A

cholesterol

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5
Q

Where are steroid hormones synthesized?

A

Adrenal Cortex, Gonads, Placenta

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6
Q

What are AA hormones derived from?

A

Tyrosine

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7
Q

Define endocrine effect.

A

hormone is released into the circulation & travels in blood

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8
Q

Define paracrine effect.

A

hormone released from one cell that produces a biologic effect on a neighboring cell

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9
Q

Define autocrine effect.

A

hormone produces a biologic effect within the same cell that released it

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10
Q

What are the purposes of having a hormone bound to a binding protein?

A

serves as a reservoir for the hormone; prolong hormone’s half life; regulate the activity of hormone (by determining how much hormone is free)

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11
Q

Define dynamic equilibrium between a hormone & its carrier protein

A

Dynamic equilibrium allows adjustments that prevent clinical manifestations of hormone deficiency or excess. Secretion of the hormone is adjusted rapidly following changes in levels of carrier proteins. For example, if more hormone is bound, more will be secreted to prevent hormone deficiency.

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12
Q

How are hormones inactivated in the liver? & what are their possible fates?

A

phase I (proteolysis, oxidation, reduction, hydroxylation, decarboxylation) & phase II (methylation, glucoronidation, sulfation, or reduction with glutathione). Degraded hormones are then excreted by the liver (bile) or kidney (urine)

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13
Q

How is affinity of a hormone determined?

A

by rate of dissociation & association for the hormone-receptor complex (under equilibrium conditions); a reflection of how tight a hormone-receptor interaction is

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14
Q

define Kd

A

dissociation constant – hormone concentration required for binding 50% of receptor sites

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15
Q

Define specificity of a hormone

A

the ability of a hormone receptor to discriminate among hormones with related structures

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16
Q

What are the subunits of a G-protein coupled receptor? What variations are possible?

A

alpha, beta, gamma; can have alpha(s) / alpha(i) / alpha(q)

17
Q

Track the signal of a hormone that activates Protein Kinase A

A

hormone binds to Gprotein –> alpha(s) releases GDP & binds GTP –> Gprotein dissociates –> alpha(s) dissociates from beta/gamma –> alpha(s) activates Adenylate Cyclase to make cAMP –> cAMP activates PKA resulting in a cascade

18
Q

Track the signal of a hormone that activates Protein Kinase C

A

hormone binds to Gprotein –> alpha(q) releases GDP & binds GTP –> Gprotein dissociates –> alpha(q) dissociates from beta/gamma –> alpha(q) activates phospholipase C –> phospholipase C hydrolyzes phosphatidylinositol bisphosphate into diacylglycerol (DAG) & inositol triphosphate (IP3). –> DAG activates PKC resulting in a cascade. IP3 opens calcium channels.

19
Q

what specific enzyme terminates cAMP cascade?

A

phosphodiesterase

20
Q

what classification of enzyme stops a Gprotein cascade?

A

phosphatase

21
Q

Track the signal of a hormone that causes a Calcium cascade

A

hormone binds to Gprotein –> alpha(q) releases GDP & binds GTP –> Gprotein dissociates –> alpha(q) dissociates from beta/gamma –> alpha(q) activates phospholipase C –> phospholipase C hydrolyzes phosphatidylinositol bisphosphate into diacylglyceral (DAG) and inositol triphosphase (IP3). –> IP3 binds to Ca++ channels that release Ca++ –> high [Ca++] binds to calmodulin resulting in a cascade

22
Q

How do Receptor Protein Tyrosine Kinases work?

A

hormone binds –> activated receptor results in intrinsic enzymatic kinase activity that phosphorylates tyrosine residues on the catalytic domain of the receptor itself, increasing its kinase activity by creating a specific binding/docking site for additional proteins –> proteins are recruited and activated, initializing a downstream signaling cascade

23
Q

How does the Thyroid Hormone Receptor work?

A

Thyroid hormone must be transported into cell. The unoccupied receptor is BOUND to DNA & REPRESSES transcription. Binding of hormone allows transcription to take place.

24
Q

How does the Steroid Hormone Receptor work?

A

Steroid hormone receptor is initially bound to inhibiting receptor-associated proteins, unbound to DNA, and inactive. Binding of a steroid hormone causes the receptor to dissociate from inhibiting associated proteins. Hormone-Receptor complex translocates to nucleus to bind to DNA and initiate gene transcription.

25
Q

What are some methods of hormone receptor regulation for desensitization?

A

1) endocytosis & degradation via lysosome induced by hormone binding to cell surface receptor. 2) receptor phosphorylation. 3) change of a protein involved in signal transduction. 4) production of an inhibitor. 5) one hormone can downregulate/decrease expression of receptors for another hormone

26
Q

list the 3 ways hormone release is controlled.

A

neural, hormonal, nutrient/ion

27
Q

which endocrine organs are under neural control?

A

pancreas, adrenal gland

28
Q

Define Tropic Hormone.

A

A tropic hormone is one released from one endocrine organ that stimulates hormone release from another endocrine organ

29
Q

what are the three types of feedback mechanisms?

A

long loop, short loop, & ultra-short loop

30
Q

What is the difference between a decreased hormone response vs a decrease in hormone sensitivity?

A

When there is a decrease in responsiveness, no matter how high the hormone concentration, maximal response isn’t achieved. Decreased hormone sensitivity requires higher hormone concentrations to produces 50% of maximal response.