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Physiology 2 > Intro To Endocrine > Flashcards

Intro To Endocrine Flashcards

1
Q

Regarding chronotropic control of hormones, which is true?

  1. Negative feedback mechanisms inhibit chronograph frequency
  2. Results in an efficient response to stimuli in real time
  3. The pituitary receives neural stimuli to set a rhythm
  4. Continuous hormone frequency typically results in greater receptor sensitivity
A
  1. Results in an efficient response to stimuli in real time
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2
Q

How can cytokines and neurotransmitters fit the definition of hormone?

A

A hormone is a chemical messenger produced by a synthesizing cell and acting on a target cell which is exactly what cytokines and neurotransmitters do

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3
Q

Insulin is a hormone produced by the pancreas. Describe the region of the pancreas that produces insulin and how it supports the definition of a hormone synthesizing gland.

A

A hormone synthesizing gland is ductless. Insulin is produced by the islets of langerhans which are ductless regions of the pancreas but the pancreas also has acinus/ductal cells that are associated with digestive enzymes. The pancreas is therefore both an exocrine and endocrine gland

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4
Q

Describe why thyroxine is an amine derived hormone while thyrotropin releasing hormone
is a protein hormone.

A

Thyroxine (fat soluble) is derived from the addition of iodine to tyrosine (an amino acid) and then the condensation of 2 tyrosines that were harvested from a protein.
thyrotropin releasing hormone (water soluble) is a protein that is translated in the RER, modified in the golgi and packaged in secretory vesicles.

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5
Q

Insulin, hypothalamic hormones, anterior pituitary hormones are all examples of what hormone class?

A

Protein derived

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6
Q

Sex hormones, adrenal hormones are examples of what hormone class?

A

Steroid derived

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7
Q

How are protein derived hormones produced?

A

mRNA-ribosome- preprohormone- prohormone-active hormone Translation followed by proteolytic cleavage and chemical modification

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8
Q

How are steroid hormones produced?

A

Chemical modification of cholesterol side chains

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9
Q

How are amine derived proteins produced?

A

Chemical modification of amino acids

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10
Q

Tyrosine can be modified by hydroxylations into what water soluble hormones?

A

Catecholamines (dopamine, epinephrine, norepinephrine)

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11
Q

Tyrosine can be modified by condensation (loss of OH group) of two molecules into what lipid soluble hormones?

A

Thyroxine (thyroid hormones)

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12
Q

Tryptophan can be chemically modified to form what hormones?

A

Melatonin and serotonin

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13
Q

Glutamic acid can be chemically modified to form what hormone?

A

Histamine

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14
Q

What is the solubility of peptide/protein derived hormones?

A

Water soluble

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15
Q

What is the solubility of steroid derived hormones?

A

Lipid soluble

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16
Q

What is the solubility of amine derived hormones?

A

Water or lipid, depending on chemical modification

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17
Q

How are protein derived hormones stored?

A

In vesicles in the blood, ECF, synthesizing cell or target cell

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18
Q

How are steroid derived hormones stored?

A

In the ECF bound to albumin or other specific transport protein/globulin, however storage is limited, therefore they are made on demand

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19
Q

Thyroid hormone, catecholamine, melatonin, histamine are examples of what class of proteins?

A

Amine derived

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20
Q

In what form are protein derived hormones stored?

A

Typically in their active form, however they can be proteolytically cleaved after release into the ECF to their active form.

Example: angiotensinogen is stored in vesicles and released to ECF where it is cleaved by renin into angiotensin 1 and further cleaved by ACE into angiotensin 2

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21
Q

What is the rate limiting step of synthesizing steroid hormones?

A

Transport of cholesterol from the cytosol to the mitochondrial matrix for modification

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22
Q

What is the solubility of stercosteroid derived hormones?

A

Lipid soluble

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23
Q

What is the solubility of eicosanoids?

A

Lipid soluble

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24
Q

How are secosteroids produced?

A

Breaking a ring and other modifications of cholesterol

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25
Q

Where are secosteroids stored?

A

Skin, liver, kidneys

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26
Q

What is a classic examples of a secosteroid?

A

Vitamin D

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27
Q

What creates oxysterols (associated with pathology) from cholesterol?

A

ROS

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28
Q

How are ecosanoids produced?

A

Modification of arachadonic acid of a phospholipid

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29
Q

How are eicosanoids stored?

A

They are not. Instead they are made on demand

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30
Q

Prostaglandin, thromboxane, leukotriene are examples of what class of hormone?

A

Eicosanoids

31
Q

What inhibit COX-mediated production of eicosanoids?

A

Glucocorticoids and NSAIDs

32
Q

What is the precursor for creating all steroid derived hormones?

A

Prenenolone

33
Q

HOw is cholesterol acquired for steroid production?

A

Mostly through diet via LDLs

Adrenal cortex and gonads contain enzymes to create cholesterol from acetyl CoA is levels are insufficient in the serum

34
Q

How does a secosteroid differ from a steroid derived hormone?

A

A secosteroid (vitamin D) is a cholesterol with a broken ring at carbons 9,10.

35
Q

What do eicosanoids regulate?

A

inflammation, vasodilation, mucus secretion

36
Q

Type 1 diabetes is characterized by low serum insulin. Describe the receptor expression on the target cell.

A

High levels of insulin receptor on target tissue

37
Q

Type 2 diabetes is characterized by high serum insulin. Describe the receptor expression on the target cell.

A

Low levels of insulin receptor on target tissue

38
Q

What is the importance of hormone and receptor concentration in normal physiology?

A

Precise control over both hormone and receptor expression concentrations is important to avoid hyperinsulinemia and receptor desensitization

39
Q

What is the hormonal control of parathyroid hormone?

A

Parathyroid is under humoral control, such that when calcium is low, parathyroid hormone will be released

40
Q

What is the hormonal control of the thyroid hormone?

A

It is under neuronal control, such that when a sensory neuron detects a disturbance in homeostasis, the hypothalamus releases thyroid releasing hormone, which stimulates the pituitary to release thyroid stimulating hormone and then the thyroid gland releases thyroxine

41
Q

How would serum cortisol levels be affected in a patient with hypertension and cirrhosis of the liver or renal failure?

A

Hypertension would cause cortisol to be delivered to target tissue faster than normal blood pressure so the cell receptors would be desensitized and hormone action more pronounced. Both cirrhosis and renal failure will cause cortisol to not be excreted, therefore hormone will be in excess.

42
Q

A new drug prevents melatonin production. Could this drug cause a change in growth hormone or cortisol production?

A

Yes, because both GH and cortisol follow circadian rhythm, which can be set by daylight. Melatonin is a hormone whose production is inhibited in light (specifically blue).

43
Q

If hypothalamic hormones are controlled by chronotropic control, does negative feedback apply to hypothalamic hormones?

A

Yes. The frequency of hypothalamic release does not change, however, the amplitude (concentration at the period of release) can be modified by negative feedback. Chronotropic control superimposed on negative feedback is important for the ability to control systems in real time.

44
Q

What is the direct intracellular target/change of an enzyme linked receptor?

A

Autophosphorylation on the intracellular portion of the receptor. A soluble (cytosolic) kinase is the next target

45
Q

Most enzyme-linked receptors are ________.

A

Tyrosine kinases which means that the autophosphorylation occurs at an intercellular tyrosine

46
Q

The autophosphorylation of tyrosine in an enzyme- linked receptor can lead to what?

A
  • soluble protein kinase activity
  • induce transcription
  • activate adenylcyclase
47
Q

What is the direct intracellular target/change of an G protein coupled receptor?

A

A conformational change of transmembrane receptor due to binding of hormone, will activate the G-protein complex. The alpha subunit of the G-protein has GTPase activity

48
Q

Activated G-protein can result in the following:

A
  • activate protein kinase
  • activate adenylcyclase
  • activate phospholipase C
  • regulate ion channels
  • or be inhibitory
49
Q

What is the direct intracellular target/change of the secondary messenger adenylcyclase?

A

It is an enzyme that produces cAMP which can activate a variety of protein kinases and amplify the signal

50
Q

What is the direct intracellular target/change of the secondary messenger phospholipase C?

A

It is an enzyme that produces IP3 and DAG from inositol phosphate in the cell membrane

51
Q

What is the direct intracellular target/change of the secondary messenger IP3?

A

Release of calcium from the SER

52
Q

What is the direct intracellular target/change of the secondary messenger DAG?

A

Protein kinase activity and prostaglandin production

53
Q

What is the direct intracellular target/change of the secondary messenger calcium:calmodulin?

A

Calmodulin is a protein kinase activator that requires calcium binding. Calcium is released from SER by IP3 or via ion channels.

54
Q

What is the direct intracellular target/change of a lipid soluble hormone receptor?

A

Receptor is a transcription factor in the cytoplasm or the nucleus

Receptor:hormone complex bind response elements, regions of DNA to induce/suppress transcription.

55
Q

List 4 ways a hormone receptor can change in the presence of excess hormone.

A
  1. Ligand binding site can acquire a lower affinity
  2. If hormone binds the receptor, the intracellular signaling can be inhibited
  3. The receptor can be sequestered in a cytoplasmic vesicle
  4. The receptor can be degraded
56
Q

A tyrosine to alanine mutation has occurred on the intracellular portion of an enzyme-linked
receptor. What will happen?

A

The OH of tyrosine is needed for autophosphorylation of the enzyme-linked receptor. Alanine does not have an OH, therefore the receptor would not be able to produce an intracellular signal pathway.

57
Q

A serine to threonine mutation has occurred on the intracellular portion of an enzyme-linked
receptor. What will happen?

A

Both serine and threonine have an OH group that are capable of autophosphorylation, so this mutation would have no effect on the receptors ability to conduct an intracellular signal

58
Q

What would happen if the Ga:GTP subunit were soluble in the cytoplasm?

A

The Ga:GTP subunit binds adenyl cyclase and phospholipase C. AC and PLC are membrane-bound enzymes. A soluble Ga:GTP would not bind these enzymes and thus no cAMP, IP3, or DAG would form.

59
Q

What would happen if the vitamin D receptor could not form a dimer?

A

Because vitamin D is lipid soluble, its receptor is intracellular and a transcription factor. Vitamin D must bind the receptor before entering the nucleus and activating transcription. If the receptor is unable to form a dimer, not vitamin D:receptor complex will form and it will be unable to enter the nucleus.

60
Q

What kind of hormone (or its analog) binds to a receptor to elicit a hormone response?

A

Agonist ligand

Example pharmaceutical analogs: prednisone and glucocorticoids

Example hormones: all major hormones

61
Q

What kind of hormone (or its analog) binds to a receptor to inhibit a hormone response?

A

Antagonist ligand

Blocks binding of agonist

62
Q

What are partial agonists/antagonists?

A

Hormones (or their analogs) that bind to receptor to elicit/inhibit hormone response that is less potent than the full agonist/antagonist

Pharmaceutical that need to slow but not stop a signal will be of the category

63
Q

What are mixed agonist/antagonist hormones (or their analogs)?

A

compounds that act in different ways through the same receptor, but action is dependent on the target cell

Ex: tamoxifen is an estrogen antagonist in breast but an agonist in bone in menopausal women by inhibiting osteoclasts at bone

64
Q

Destructive process occurring at an endocrine gland will result in what?

A

Deficiency in the hormone it produces

Example: autoimmune, infection, infarction, compression (tumor)

65
Q

Other than destructive processes, what other mechanism of disease can cause endocrine hormone deficiency.

A

Genetic defects in the hormone production or hormone receptor

66
Q

What are mechanisms of endocrine disease that could lead to excess hormone?

A

overproduction by the gland that normally

secretes it, or the hormone could be made by a non-endocrine tissue in tumorogenesis.

67
Q

In what capacity could a tumor influence endocrine function?

A
  1. Cause deficiency by overcrowding an endocrine gland
  2. Tumor can produce excess hormone in addition to natural gland
  3. Tumor of endocrine gland causes excess
68
Q

How can the immune system cause endocrine disorders?

A
  1. Autoimmunity toward endocrine gland causes deficiency
  2. Autoimmunity in which the antibody is agonist causes excess
  3. Autoimmunity in which the antibody is antagonist causes deficiency
69
Q

What organs secrete protein derived hormones?

A

Pituitary, parathyroid pancreas, hypothalamus

70
Q

What organs secrete amine derived hormones?

A

Thyroid, adrenal medulla and pineal gland

71
Q

What organs secrete steroid derived hormones?

A

Adrenals, ovaries, testes, placenta

72
Q

Which has a more direct way of activating the second messenger pathway, GPCRs or Enzyme-linked receptors?

A

GPCRs are more direct

73
Q

Do GPCRs autophosphorylate?

A

No, never

Physiology 2 (2 decks)

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