Exam II material Flashcards

1
Q

The endocrine system provides ______ of many tissues

A

Broadcast regulation

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2
Q

The specificity of the endocrine system is due to:

A

Receptors

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3
Q

Compared to the nervous system, the responses of the endocrine system are:

A

Slower but longer lasting

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4
Q

Where does the endocrine system release hormones into?

A

The blood

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5
Q

List the three functions of hormones:

A
  1. Maintenance of Homeostasis
  2. Growth & Differentiation
  3. Reproduction
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6
Q

Endocrine organs can be divided into what two categories:

A
  1. Major endocrine glands
  2. Organs containing endocrine cells
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7
Q

Primary function is to make a hormone & release it when the stimuli for release are present:

A

Major endocrine gland

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8
Q

Organs that happen to have endocrine cells within them, allowing them to release a hormone although their primary function is NOT endocrine regulation:

A

Organs containing endocrine cells

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9
Q

List the specialized endocrine glands (Major endocrine glands)

A
  1. Parathyroid gland
  2. Thyroid gland
  3. Pituitary gland
  4. Adrenal gland
  5. Pineal gland
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10
Q

List some organs that contain endocrine cells, but their primary function is NOT endocrine regulation:

A
  1. Hypothalamus
  2. Skin
  3. Adipose tissue
  4. Thymus
  5. Heart
  6. Liver
  7. Stomach
  8. Pancreas
  9. Small intestine
  10. Kidneys
  11. Gonads
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11
Q

A hormone that causes secretion of a hormone by an endocrine gland

A

Tropic hormone

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12
Q

How do we classify hormones?

A

Based on their strucutre

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13
Q

What are the three classifications of hormones?

A
  1. Proteins & polypeptides
  2. Steroids
  3. Tyrosine derivatives
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14
Q

Describe the time period in which protein/polypeptide hormones are made and released:

A

Made in advance & stored in vesicles until signaled for release

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15
Q

Protein/polypeptide hormones are synthesized first as:

A

Preprohormones

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16
Q

The preprohormone will be converted into a:

A

Prohormone

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17
Q

In protein/polypeptide hormones, what is packed into vesicles in the endocrine cell prior to secretion?

A

Prohormone

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18
Q

After the prohormone is cleaved, it is now:

A

Active hormone

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19
Q

The pneumonic for protein/polypeptide hormones:

A

Protein/Polypeptide = Pre & Pro hormone (all begin with Ps)

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20
Q

In addition to the active hormone, what is released when the prohormone is cleaved?

A

Inactive fragments

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21
Q

What is the first thing to be cleaved from preproinsulin?

A

Signal peptide

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22
Q

After the signal peptide is cleaved from preproinsulin what occurs?

A

Protein folding

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23
Q

Following cleavage of the signal peptide from preproinsulin & protein folding, what results:

A

Proinsulin

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24
Q

Proinsulin is stored in:

A

Vesicles

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25
Q

Upon receiving a signal for release into the bloodstream, what is cleaved from proinsulin to convert it to active insulin?

A

C-peptide

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26
Q

Along with insulin release into the bloodstream, what is also released?

A

C-peptide

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27
Q

If you wanted to measure someones baseline endogenous production & release of insulin you could measure the:

A

C-peptide levels in the bloodstream

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28
Q

Protein & polypeptide hormones are often made as an:

A

Inactive precursor

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29
Q

The inactive precursor of protein & polypeptide hormones:

A

Preprohormone

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30
Q

What does the signal peptide in insulin serve as?

A

A marker that tells the cell that insulin needs to undergo exocytosis

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31
Q

Where are the receptors located for protein/polypeptide hormones?

A

In the plasma membrane

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32
Q

Describe the time period in which steroid hormones are made & released:

A

Made & released on demand

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33
Q

Where are the receptors located for steroid hormones?

A

Located inside the cell

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34
Q

Why are steroid hormone receptors located inside the cell?

A

Because steroid hormones can cross the plasma membrane & bind to internal receptors on target cells

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35
Q

Hormones from the hypothalamus, anterior pituitary, posterior pituitary & pancreas:

A

Protein/polypeptide

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36
Q

Hormones from the adrenal cortex, ovaries & testes:

A

Steroid hormones

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37
Q

Steroid hormones are synthesized from:
(derivatives of)

A

Cholesterol

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38
Q

What are two hormones that are derived from cholesterol that are STRUCTURALLY very similar?

A

Aldosterone & Cortisol

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39
Q

DHEA, Androstenedione, Testosterone & Estradiol are all steroid hormones involved in:

A

Reproduction

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40
Q

What determines what steroid hormone will be produced from the precursor cholesterol?

A

The complement of enzymes present

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41
Q

Describe the time period present in which amine hormones are made & released:

A

Made early and stored until secreted

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42
Q

Amine hormones are derived from:

A

Amino acid Tyrosine

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43
Q

Thyroid hormone, Epinephrine & Norepinephrine are all:

A

Amine hormones

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44
Q

Epinephrine & Norepinephrine are both:

A

Adrenal medullary neurohormones

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45
Q

Thyroid hormones bind to the protein:

A

Thyroglobulin

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46
Q

Epinephrine & Norepinephrine are stored in vesicles & released via:

A

Exocytosis

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47
Q

Structurally what is the difference between T3 & T4:

A

The number of iodide atoms attached

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48
Q

What is the precursor to Epinephrine & Norepinephrine?

A

Dopine

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49
Q

Hormones released into circulation can either circulate ____ or ________

A

Freely or with binding proteins

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50
Q

The majority of ____, ____ & ____ hormones circulate in their free form:

A

Amines, Peptide/Protein hormone

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51
Q

What is the exception to most amines circulating in their free form & why?

A

Thyroid hormone

Its double ring structure makes it soluble enough to where it needs help getting through the plasma

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52
Q

Describe the solubility of amines and peptide/proteins hormones:

A

Water soluble

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53
Q

_____ & ____ hormones circulate bound to specific transport proteins

A

Steroid & Thyroid

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54
Q

Some binding proteins are specific for a given hormone, but some plasma proteins such as ___ & ____ can bind to many hormones

A

Globulin & Albumin

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55
Q

Prevalent protein in the plasma that functions as transportation for a lot of different things such as lipid soluble hormones & fatty acids

A

Albumin

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56
Q

Most binding proteins are synthesized in the:

A

Liver

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57
Q

Patients with a compromised/dysfunctional liver may show signs of:

A

Endocrine deficiencies

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58
Q

Why might a patient with a compromised liver show endocrine deficiencies?

A

Because most binding proteins are synthesized in the liver & if you can’t make your binding proteins you can’t get enough hormone into the blood

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59
Q

It is always the ______ version of the hormone that binds to receptors & affects the target cell:

A

Free version (binding protein stays in blood vessel)

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60
Q

The constitutive level of plasma hormones

A

Basal level

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61
Q

The stimulated level of plasma hormones

A

Peak levels

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62
Q

The variable pattern of hormone release (peaks & troughs) is determined by the interaction & integration of multiple control mechanisms which include: (4)

A

Hormonal
Neural
Nutritional
Environmental

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63
Q

When a hormone is constantly secreted in small amounts at a time:

A

Tonic release

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64
Q

Hormone fluctuations that happen dependent on the time of day

A

Circadian rhythm

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65
Q

Give an example of a hormone that follows circadian rhythm release:

A

Cortisol

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66
Q

When does cortisol levels spike?

A

In the early morning hours

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67
Q

What can work in addition to circadian rhythm release to regulate the release of hormones:

A

Stimuli

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68
Q

Growth hormone is released during sleep making it following a circadian rhythm release pattern but also displays:

A

Pulsatile secretion

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69
Q

Secreted in pulses (secretes, stops, secretes, stops)

A

Pulsatile secretion

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70
Q

The location of the hormone receptor depends on the ______ properties of the hormone

A

Chemical

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71
Q

The chemical properties of the hormone that determine the location of the hormone receptor can be:

A

Lipophobic & Liphophillic

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72
Q

Ligand/Receptor binding demonstrates:

A
  1. Specificity
  2. Affinity
  3. Saturation
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73
Q

Which classes of hormones bind to plasma membrane receptors?

A

Polypeptide/Protein hormones
Amine hormones*

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74
Q

What amine hormone does not bind to plasma membrane receptors? (except to the rule)

A

Thyroid hormone

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75
Q

Which class of hormones binds to nuclear receptors?

A

Steroid hormones + thyroid hormone

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76
Q

Which amine hormones bind to plasma membrane receptors?

A

Epinephrine & Norepinpehrine

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77
Q

What type of receptors would the following hormones bind to & why?

  • Glucagon
  • Angiotensin
  • GnRH
  • SS
  • GHRH
  • FSH
  • LH
  • TSH
  • ACTH
A

Plasma membrane receptors- they are peptide/protein hormones

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78
Q

In general many of the receptors that proteins/peptide hormones & amine hormone bind to in the plasma membrane are:

A

G-protein coupled receptors (GPCRs)

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79
Q

Involved in turning on or off a protein that is already in the cell:

A

Plasma membrane receptors

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80
Q

What class of hormone receptors are involved in causing a change in gene expression to get a biological response?

A

Nuclear receptors

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81
Q

Class of hormone receptors involved in making new proteins:

A

Nuclear receptors

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82
Q

Thyroid hormone & steroid hormones bind to receptors located in:

A

Either the cytoplasm or the nucleus

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83
Q

Once the steroid hormone or thyroid hormone binds to the receptor located in the nucleus or cytoplasm what occurs next?

A

Transformation of receptor to expose DNA-binding domain

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84
Q

Following binding of the steroid hormone or thyroid hormone to the receptor & transformation of the receptor to expose the DNA-binding domain what next occurs?

A

Binding to enhancer-like element in DNA

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85
Q

Examples of plasma membrane hormone receptors:

A
  1. GPCR
  2. Tyrosin kinase
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86
Q

Why do plasma membrane hormone receptor numbers vary greatly in different target tissues:

A

Provides a way to achieve specific tissues activation

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87
Q

What are two examples of plasma membrane hormone receptors that are more distributed:

A
  1. Thyroid hormone receptors
  2. Insulin receptors
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88
Q

Why are thyroid hormone receptors & insulin receptors more sidled distributed?

A

Because their actions are something that most cells participate in

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89
Q

How do IGF-1 & Insulin work?

A

By activating a tyrosine kinase receptor

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90
Q

If it is plasma membrane receptor generally it will activate or inhibit _____ to ______

A

An existing protein to yield a faster response

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91
Q

Where are nuclear hormone receptors located?

A

Cytoplasm or nucleus

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92
Q

Nuclear hormone receptors typically leads to:

A

Formation of new proteins

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93
Q

Nuclear hormone receptors all act to:

A

Increase or decrease gene expression

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94
Q

In a nuclear hormone receptor, the hormone receptor complex binds to a ______ in the _____ region of the gene which leads to either the activation or repression of ______

A

Hormone responsive element
Promotor region
Gene transcription

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95
Q

Because nuclear hormone receptors binding a hormone leads to the formation of a new protein, describe the timeline involved:

A

It takes a little bit longer to get the response & the response will last a bit longer

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96
Q

Hormones that bind to nuclear receptors (thyroid hormone & steroid hormones) undergo _____ to get through the plasma membrane

A

SImple diffusion

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97
Q

The body often releases multiple hormones:

A

At the same time

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98
Q

What are the effects of combined hormone actions: (4)

A
  1. Antagonism
  2. Additive
  3. Synergistic
  4. Permissiveness
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99
Q

When two hormones change one variable in opposite directions:

A

Antagonsim

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100
Q

When the response of hormone is equal to the two portions that each hormone provide (2+3=5)

A

Additive

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101
Q

When the combined hormone response is greater than the individual responses of each hormone added together (2+3=10)

A

Synergistic

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102
Q

The presence of one hormone is necessary for another hormone’s maximum affect:

A

Permissiveness

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103
Q

Determine which hormone interaction is being described in the following situation:

Parathyroid increases plasma calcium levels; Calcitonin decreases plasma calcium levels:

A

Antagonism

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104
Q

Determine which hormone interaction is being described in the following situation:

Glucagon, cortisol & epinephrin all increase blood glucose more than the sum of their individual effects:

A

Synergism

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105
Q

Determine which hormone interaction is being described in the following situation:

Thyroid hormone causes expression of B adrenergic receptors in bronchiolar smooth muscle:

A

Permissive

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106
Q

What determines whether the negative feedback will be short loop or long loop?

A

The location of the hormone that acts as negative feedback in the system

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107
Q

When the last hormone in the pathway inhibits the system upstream

A

Long loop negative feedback

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108
Q

When an intermediate hormone in the pathway inhibits the system upstream

A

Short loop negative feedback

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109
Q

Feedback where the hormonal product or an intermediate hormone enhances the hormone secretion:

A

Positive feedback

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110
Q

Causes an endocrine gland to secrete a hormone

A

Tropic hormone

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111
Q

Stabilizes the system & prevents over-secretion:

A

Negative feedback

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112
Q

Hormones that have other endocrine glands as there targets:

A

Tropic hormones

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113
Q

A tropic hormone from the hypothalamus that acts on the anterior pituitary to release TSH

A

Thyroid releasing hormone (TRH)

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114
Q

Thyroid releasing hormone (TRH) comes from:

A

The hypothalamus

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115
Q

TRH acts on the:

A

Anterior pituitary

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116
Q

TSH (Thyroid stimulating hormone) is released from:

A

The anterior pituitary

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117
Q

TSH is released from the anterior pituitary & acts on:

A

The thyroid gland

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118
Q

In the regulation of thyroid hormone, a stimulus causes the hypothalamus to secrete ____ which acts on the ______

A

TRH
Anterior pituitary

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119
Q

In the regulation of thyroid hormone, _____ cells in the anterior pituitary release _____

A

Thyrotropic cells
Thyroid stimulating hormone

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120
Q

In the regulation of thyroid hormone, TSH stimulates _____ cells of the thyroid gland to release _____

A

Follicular cells
Thyroid hormone (TH)

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121
Q

Thyroid hormone produces effects in the body that include:

A
  1. Increase in metabolic activity
  2. Increase in body temperature
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122
Q

In the regulation of thyroid hormone, thyroid hormone stimulates target cells to increase ____ activities resulting in an increase in basal body temperature

A

Metabolic activities

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123
Q

In the regulation of thyroid hormone, increased body temperature is detected by the hypothalamus & the secretion of _____ by the hypothalamus is ____

A

TRH
Inhibited

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124
Q

In the regulation of thyroid hormone, thyroid hormone also blocks TRH receptors on thyroid cells inhibiting synthesis & release of ____. Both effects indirectly dampen _____ production in the thyroid

A

TSH
TH

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125
Q

Thyroid hormone working to negatively feedback is an example of:

A

Long loop negative feedback

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126
Q

If hormone levels are NOT kept in balance via negative feedback mechanisms what occurs?

A

Endocrine disorders/Pathologies

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127
Q

Enlargement of the thyroid due to increased or decreased thyroid hormone levels:

A

Thyroid goiter

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128
Q

Disease characterized by increased cortisol levels:

A

Cushings disease

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129
Q

Abnormality in the last endocrine organ secreting the hormone leading to either hypo- or hyper-secretion:

A

Primary endocrine disorder

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130
Q

List the causes of primary hyposecretion:

A
  1. Partial destruction of the gland
  2. Dietary deficiency
  3. Enzyme deficiency required for hormone synthesis
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131
Q

List the causes of primary hypersecretion:

A
  1. Endocrine gland tumor
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132
Q

Abnormality in tropic hormone leading to either hypo- or hyper-secretion:

A

Secondary endocrine disorder

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133
Q

List the causes of secondary hyposecretion:

A

A lack of sufficient tropic hormone

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134
Q

List the causes of secondary hypersecretion:

A

A tumor (either in an endocrine gland that secretes tropic hormones or in a non-endocrine tissues that secretes hormones)

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135
Q

When you see an endocrine hormone disturbance as a result of cancer:

A

Paraneoplastic endocrine syndrome

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136
Q

When you think of primary endocrine dysfunction you should think:

A

LAST gland in pathway

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137
Q

Type of diagnostic endocrine function test in which you give something to make hormone levels go up to see if hormone levels actually go up:

Type of diagnostic endocrine function test in which you give something to inhibit the hormone levels in question & look to see if that actual works:

A

Stimulation test

Suppression test

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138
Q

Suppression test would be used to detect what type of endocrine dysfunction:

A

Hyperfunction

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139
Q

List the types of diagnostic test used to examine endocrine function (7):

A
  1. Plasma hormone levels
  2. Autoantibodies
  3. Urine hormone/hormone metabolite levels
  4. Stimulation tests by administration of tropic or stimulating hormone
  5. Suppression tests when hyperfunction of endocrine organ is suspected
  6. Measurement of hormone receptor presence , number & affinity
  7. Imaging
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140
Q

Stimulation tests work by administering a ____ hormone:

A

tropic or stimulating

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141
Q

An example of measuring hormone receptor presence as an endocrine diagnostic function test:

A

Estrogen receptors in breast tumors

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142
Q

What autoantibodies might be tested when doing diagnostic tests of endocrine function:

A
  1. Hashiomoto thyroiditis
  2. Type I DM
  3. Graves disease
  4. Addison disease
  5. Autoimmune hypoparathyroidism
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143
Q

Glucagon, Angiotensin, Gonadotropin releasing hormone (GnRH), Somatostatin (SS), Growth hormone releasing hormone (GHRH), Follicle stimulating hormone (FSH), Lutenizing hormone (LH), Thyroid stimulating hormone (TSH), Adrenocorticotropin hormone (ACTH)

Are all ____ hormones

When are they made?

A

Polypeptide/protein hormones
Made in advance & stored until use

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144
Q

Epinephrine & norepinephrine are ____ hormones

When are they made?

A

Amine hormones

Made in advance and then stored

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145
Q

Thyroid hormone (TH) is a ____ hormone

When is it made?

A

Exception: amine hormone

Made in advance and then stored but does bind to nuclear receptors

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146
Q

Aldosterone, Cortisol, Estradiol, testosterone, also mineralocorticoids, glucocorticoids, and androgens are all _____ hormones

When are they made?

A

Steroid hormones

Made on demand

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147
Q

List things that stimulate growth hormone (GH) release:

A

GHRH
Dopamine
Catecholamines (in times of stress & exercise)
Excitatory amino acids
Thyroid hormone
Fasting (Hypoglycemia)

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148
Q

List things that inhibits growth hormone (GH) release:

A

Somatostatin (SS)
IGF-1 (because of negative feedback)
Glucose (at high levels- hyperglycemia)
Free fatty acids

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149
Q

GHRH, Dopamine, Catecholamines, excitatory amino acids and thyroid hormone would cause ______ of growth hormone release

A

Stimulation

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150
Q

Portion of the pituitary that is truly filled with endocrine cells- a true endocrine gland:

A

Adenohypophysis

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151
Q

Adenohypophysis is referring to what portion of the pituitary gland:

A

Anterior pituitary

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152
Q

Portion of the pituitary that contains axon terminals of hypothalamic neurons:

A

Neurohypophysis

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153
Q

Neurohypophysis is referring to what portion of the pituitary gland:

A

Posterior pituitary

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154
Q

The pituitary gland is locked in the ______ ventral to the ______

A

Sella turcica
Diaphragma sella

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155
Q

List the hormones secreted by the anterior pituitary: (6)

A
  1. FSH
  2. LH
  3. Adrenocorticotropin
  4. Thyroid-stimulating hormone
  5. Prolactin
  6. Growth hormone
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156
Q

List the hormones secreted by the posterior pituitary: (2)

A
  1. ADH/Vasopressin
  2. Oxytocin
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157
Q

The pituitary gland secretes _____ hormones

A

Peptide hormones

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158
Q

What are the most prevalent cells in the anterior pituitary & what do they secrete?

A

Somatotrophs
Growth hormone

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159
Q

What percentage of cells in the anterior pituitary do somatotrophs comprise?

A

30-40%

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160
Q

What is the second most prevalent type of cell in the anterior pituitary & what do they secrete?

A

Corticotrophs
ACTH

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161
Q

What percentage of cells in the anterior pituitary do corticotrophs comprise?

A

20%

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162
Q

Aside from corticotrophs & somatotrophs, what types of cells makeup the anterior pituitary & what do they secrete?

A

Thyrotrophs - TSH
Gonadotrophs- LH & FSH
Mammaotrophs- Prolactin

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163
Q

Adenomas involving somatotropin cells can cause _____ if occurring in children before the closing of long bones (epiphyseal plates) or _____ in adults with musculoskeletal, neurologic, and other medical consequences

A

Gigantism
Acromegaly

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164
Q

Benign tumor of epithelial cells that makes hormones:

A

Adenoma

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165
Q

Endocrine cells are derived from:

A

Epithelial cells

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166
Q

If a benign tumor is involved in somatotropic cells this would cause over secretion of:

A

Growth hormone

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167
Q

Majority of cells in the anterior pituitary are devoted to making _____ & _____

A

GH & ACTH

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168
Q

Neurons in the hypothalamus synthesize & secrete ______ hormones that control endocrine cells in the ______

A

Hypothalamic releasing/inhibiting hormones
Anterior pituitary

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169
Q

The hypothalamic hormones are released into the ______ in the ______ (in the hypothalamus)

A

Primary capillary plexus
Median eminence

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170
Q

Responsible for carrying the hypothalamic hormones to the sinuses of the anterior pituitary gland:

A

Hypothalamic-hypophyseal portal blood vessels

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171
Q

Hypothalamic-hypophyseal portal blood vessels carry the hypothalamic hormones to the ______ of the anterior pituitary gland

A

Sinuses

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172
Q

Regulation of anterior pituitary secretion

  1. ______ releases hormones that enter into the blood
  2. Hormones travel through the ________
  3. Hormones will continue down through the capillary bed to the ______ wire they can leave the blood & regulate activity of the endocrine cells
A
  1. Hypothalamus
  2. primary capillary plexus
  3. Sinus
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173
Q

Two capillary beds in series

A

Portal system

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174
Q

The hypothalamic-hypophyseal portal vessel is comprised of:

A

Primary capillary plexus + sinus

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175
Q

The hypothalamic hypophyseal portal allows for:

A

Communication from the hypothalamus to the anterior pituitary

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176
Q

Where do releasing hormones come from?

A

Hypothalamus

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177
Q

Where do stimulating hormones cone from?

A

Anterior pituitary

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178
Q

The hypothalamic regulatory hormones bind to_____ in the various endocrine cells of the anterior pituitary

A

G-proteins coupled receptors

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179
Q

Following the binding of the hypothalamic hormones to the G-protein coupled receptors in the anterior pituitary, what is responsible for stimulating or inhibiting anterior pituitary hormone secretion?

A

Second messengers (cAMP via Adenylate cyclase, IPs & DAG via Phospholipase C)

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180
Q

Growth hormone inhibiting hormone (GHIH) =

A

Somatostatin

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181
Q

Prolactin inhibiting hormone (PIH) =

A

Dopamine

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182
Q

Growth hormone is secreted by somatotrophs in the anterior pituitary. The releasing hormone (secreted by hypothalamus) would be _____ (gas) while the inhibiting hormone would be ______ (breaks)

A

GHRH
GHIH

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183
Q

GH, a peptide hormone acts _____ on target tissues and as a ______ to the liver

A

Directly
Tropic hormone

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184
Q

GH, a peptide hormone acts directly on target tissues ad as a tropic hormone to the _____ which releases _____

A

Liver
IGF1

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185
Q

In what situation might growth hormone significantly increase and quickly?

A

Prolonged starvation/fasting

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186
Q

Growth hormone acts tropically on the liver to activate _____ a cell signaling pathway that causes the release of _____

A

JAKSTAT
IGF1

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187
Q

A cell signaling pathway in the liver activated by GH that responds by release of IGF1

A

JAKSTAT

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188
Q

What are some target tissues of growth hormone? (6)

A
  1. Liver
  2. Chondrocytes
  3. Muscle cells
  4. Adipose cells
  5. Anterior pituitary (short loop negative feedback)
  6. Hypothalamus (long loop negative feedback)
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189
Q

If GH acts on chondrocytes what results?

A
  1. increased amino acid uptake
  2. Increased protein synthesis
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190
Q

GH acting on chondrocytes to increase amino acid uptake as well as protein synthesis is ultimately necessary for:

A

Linear growth

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191
Q

In addition to growth hormone acting on chrondocytes being necessary for linear growth what is also necessary for linear growth:

A

IGF1

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192
Q

GH can act on muscles to:

A

Increase protein synthesis

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193
Q

In addition to growth hormone acting on muscle to increase protein synthesis what is also necessary for protein synthesis:

A

IGF1

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194
Q

In excess how does growth hormone affect adipose tissue?

A

Anti-insulin action

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195
Q

What are two locations of negative feedback of growth hormone:

A
  1. Directly feeding back to anterior pituitary (short loop)
  2. Feeding back to hypothalamus (long loop)
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196
Q

If negative feedback via growth hormone occurs on the hypothalamus what hormone may be released:

A

Somatostatin

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197
Q

Describe the secretion of growth hormone:

A

Pulsatile secretion; lower concentration during day with highest levels a few hours after sleep

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198
Q

When is growth hormone secreted at the highest levels:

A

A few hours following sleep

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199
Q

GH secretion can be stimulated by: (5)

A
  1. Starvation (protein deficiency)
  2. Fasting (hypoglycemia)
  3. Acute stress
  4. Exercise
  5. Excitement
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200
Q

The secretion of GH during the neonatal period can be described as:

The secretion of GH during childhood can be described as:

The secretion of GH during puberty can be described as:

The secretion of GH during adulthood can be described as:

A
  1. High secretion
  2. Decreased secretion
  3. Peak levels of secretion
  4. Decreased secretion with age
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201
Q

Stimulation of GH release: (5)

A
  1. GHRH
  2. Dopamine
  3. Catecholamines
  4. Excitatory amino acids
  5. Thyroid hormone
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202
Q

Inhibition of GH release: (4)

A
  1. Somatostatin
  2. IGF1 (due to negative feedback)
  3. High levels of glucose
  4. High levels of free fatty acids
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203
Q

Many of the growth & metabolic effects of GH are mainly produced by:

A

IGFs

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204
Q

IGFs may also be called:

A

Somatomedins

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205
Q

IGF1 is produced in most tissues and acts on neighboring cells in a ____ manner

A

Paracrine

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206
Q

The major site of IGF1 synthesis:

A

The liver

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207
Q

How many IGF binding proteins are there?

A

6

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208
Q

_____ in adults is one of the main growth promoting insulin-like growth factors:

A

IGF1

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209
Q

Osteocytes responding to mechanical sensors can release:

A

IGF1

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210
Q

Osteocytes responding to _____ can release IGF1:

A

Mechanical sensors

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211
Q

After osteocytes release IGF1 what happens?

A

IGF1 binds to receptors on osteoblasts to enhance bone formation

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212
Q

Mechanisms of actions of GH & IGF1:

Growth in nearly all tissues of the body, mainly IGF1 occurs through what mechanisms:

A
  1. increased cell size
  2. mitosis
  3. Differentiation of bone & muscle cells
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213
Q

Mechanisms of actions of GH & IGF1:

What are the overall outcomes of the affects of GH & IGF1 causing growth in nearly all tissues in the body:

A
  1. increased organ size
  2. increased organ function
  3. increased linear growth
  4. increased lean body mass
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214
Q

Mechanisms of actions of GH & IGF1:

Effect of increased amino acid uptake and protein synthesis result in:

A

Increased lean body mass

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215
Q

Mechanisms of actions of GH & IGF1:

How does this effect glucose?

A

Reduced glucose utilization

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216
Q

Mechanisms of actions of GH & IGF1:

Reduced glucose utilization is due to:

A
  1. decreased cellular uptake
  2. increased hepatic glucose production
  3. increased insulin secretion
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217
Q

Mechanisms of actions of GH & IGF1:

The reduced glucose utilization can lead to:

A

Insulin resistance; diabetogenic

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218
Q

Mechanisms of actions of GH & IGF1:

Describe the effects on fatty acids:

A

Mobilization of fatty acids from adipose tissue (lipolysis)

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219
Q

The mobilization of fatty acids from adipose tissue:

A

lipolysis

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220
Q

Mechanisms of actions of GH & IGF1:

Lipolysis results in:

A

Increased FFA in blood and use of FFA for energy

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221
Q

Before fusion of the epiphyseal plates, GH & IGF1 stimulate:

A
  1. Chondrogenesis
  2. Widening of the epiphyseal plates
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222
Q

Following GH and IGF1 stimulating chondrogenesis & widening of the epiphyseal plates, what occurs:

A

Bone matrix deposition stimulating linear growth

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223
Q

In adults, GH and IGF1 play a role in regulating the normal physiology of:

A

Bone formation

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224
Q

In adults, how do GH & IGF1 play a role in regulating normal physiology of bone formation?

A

By increasing bone turnover

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225
Q

How do GH and IGF1 stimulate the increase in bone turnover (thereby regulating bone formation):

A
  1. activation of osteoblasts (mainly)
  2. Increase bone resorption via osteoclasts (lesser extent)
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226
Q

Kids: GH & IGF1 =

Adults: GH & IGF1 =

A

Chondrogenesis

Increased bone turnover

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227
Q

Osteoblast are of what origin?

A

Mesenchymal precursor cells

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228
Q

What is responsible for the formation of active osteoblasts from the osteoblasts precursors?

A

IGF1

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229
Q

Gigantism occurs in ____

Acromegaly occurs in _____

A

Children

Adults

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230
Q

Excess growth hormone in children leading to gigantism is typically caused by:

A

Pituitary tumor (90%)

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231
Q

What areas are commonly involved in pituitary tumors that give rise to gigantism?

A

Sella & cavernous sinus

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232
Q

Tumor causing excessive growth hormone release:

A

Somatotropin adenoma of pituitary

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233
Q

Describe the facial features that may be associated with gigantism/acromegaly: (4)

A

Coarse facial features
Large fleshy nose
Frontal bossing
Jaw malocclusion

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234
Q

Coarse facial features including a large fleshy nose, frontal bossing & jaw malocclusion are collectively reffered to as:

A

Acromegalic facies

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235
Q

What issue with the thyroid may occur with gigantism/acromegaly?

A

Goiter

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236
Q

Describe the potential effects on the heart & what conditions may result due to gigantism/acromegaly

A

Cardiomegaly
Hypertension
Coronary heart disease

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237
Q

Describe the chest & spine in individuals effected by acromegaly/gigantistm:

A

Barrel chest
Kyphosis & hyperostosis

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238
Q

The abnormal glucose tolerance & secondary insulin resistance in an acromegaly/gigantism effected individual may result in:

A

Diabetes Mellitus

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239
Q

Growth hormone shifts the body from using ___ to ____ for metabolism

A

Carbs to fats

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240
Q

Describe the reproductive consequences on individuals with acromegaly/gigantism:

A

Male sexual dysfunction & menstrual disorders

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241
Q

Describe what can occur due to the thicken skin & hypertrophy of sebaceous & sweat glands in gigantism/acromegaly:

A

Hyperhidrosis & oily skin

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242
Q

Hyperhidrosis & oily skin in acromegaly/gigantism can occur due to:

A

Thickened skin (hypertrophy of sebaceous & sweat glands)

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243
Q

What can occur in the joints of individuals with gigantism/acromegaly:

A

Degenerative arthritis

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244
Q

Describe the neuronal effects caused by gigantism/acromegaly:

A

Parathesias due to peripheral neuropathy

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245
Q

What is a potential treatment for pituitary micro adenoma:

A

Adenectomy via transphenoidal approach followed by medication

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246
Q

Oral manifestations of GH excess: (7)

A
  1. Thick rubbery skin, enlarged nose, thick lips
  2. Macrocephaly
  3. Macrognathia
  4. Disproportionate mandibular growth
  5. Anterior bite & malocclusion
  6. Macroglossia, Dyspnea, Dysphagia, Dysphonia, Sialorrhea
  7. Hypertrophy of pharyngeal & laryngeal tissues
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247
Q

Enlarged head=
Enlarged jaw=

A

Macrocephaly
Macrognathia

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248
Q

The disproportionate mandibular growth cause by excess GH includes:

A

Mandibular prognathism- jaw gets forward
Generalized diastemata- teeth separation

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249
Q

The anterior open bites & malocclusion caused by excess GH is due to:

A

Combination of macrognathia & tooth migration

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250
Q

Define each:

Macroglossia
Dyspnea
Dysphagia
Dysphonia
Sialorrhea

A

Enlarged tongue
Difficulty breathing
Difficulty swallowing
Difficulty speaking
Slobbering/droolinh

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251
Q

The hypertrophy of the pharyngeal & laryngeal tissues due to excess GH can lead to ________ & how?

A

Sleep apnea due to the increased growth of pharyngeal & laryngeal tissues obstructing the airway

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252
Q

What are the causes of growth hormone deficiency: (5)

A
  1. Hypothalamic disorders
  2. Mutations
  3. Combined pituitary deficiencies
  4. Radiation
  5. Psychosocial deprivation
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253
Q

Combined pituitary hormone deficiencies:

A

Panhypopituitarism

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254
Q

What type of mutations may lead to GH deficiency:

A

GHRH receptor
GH gene
GH receptor
IGF1 receptor

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255
Q

A decrease in GHRH or an increased in GHIH can lead to

A

Growth hormone deficiency

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256
Q

What depends on the time of onset & severity of hormone deficiency:

(talking about growth hormone)

A

Clinical manifestations

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257
Q

The clinical manifestations caused by complete growth deficiency include: (4)

A
  1. Slow linear growth rates (shorter stature)
  2. Normal skeletal proportions
  3. Pudgy, youthful appearance (decreased lipolysis)
  4. In the setting of cortisol deficiency hypoglycemia
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258
Q

The most common form of dwarfism that is caused by an autosomal dominant conditions that results from a mutation in the FGF-3 receptor in cartilage & brain:

A

Achondroplasia

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259
Q

Mutation in the FGF-3 receptor in the cartilage & brain makes the receptor overly active and it inhibits cartilage growth at growth plates so:

A

Limb growth is reduced (growth of trunk is not impacted)

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260
Q

Mutated receptor involved in achondroplasia:

A

FGF-3

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261
Q

Oral manifestations of GH deficiency include:

  1. Disproportionate delayed growth of the _____ & ____ = ____ facial appearance
  2. _____ & ____ of the ___ regions of the jaws are abnormal & may be disproportionately smaller than adjacent structures
  3. Solitary _____
  4. Eruption of primary & secondary dentition & shedding of deciduous teeth are ______
A
  1. Skull & facial skeleton; small
  2. Tooth formation & growth; alveolar
  3. Median maxillary central incisor
  4. Delayed
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262
Q

How are the oral manifestations of GH deficiency managed:

A

Correction of dental & skeletal malocclusions

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263
Q

Incisor defects in a child with GH deficiency occurs in both:

A

Primary & permanent dentition

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264
Q

Oral manifestations of GH deficiency includes tooth formation & growth of alveolar regions of the jaw are abnormal & may be disproportionately smaller than adjacent anatomic structures this can cause:

A
  1. Tooth crowding & malocclusion
  2. Plaque accumulation
  3. Poor oral hygiene
  4. Gingivitis & perio disease
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265
Q

The posterior pituitary contains ~100,000 _________ whose cell bodies are in the_______

A

Unmyelinated axons of neurons
hypothalamus

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266
Q

Areas of concentrated neuronal cell bodies in the hypothalamus that have axons that go through the infundibulum with their synaptic terminals located in the posterior pituitary gland

A

Paraventricular nucleus & Supraoptic nucleus

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267
Q

The paraventricular nucleus produces ______

A

Oxytocin

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268
Q

The supraoptic nucleus produces _____

A

ADH

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269
Q

List all at the names for the abbreviation ADH:

A
  1. Antidiuretic hormone
  2. Arginine Vasopressin (AVP)
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270
Q

Both ADH and Oxytocin are classified as:

A

Neurohormones

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271
Q

Both ADH and oxytocin are neurohormones made of:

A

Polypeptides of nine amino acids

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272
Q

While the paraventricular nucleus secretes Oxytocin, and the supraoptic nucleus secretes ADH, they both have the ability to:

A

Secrete some of the other neurohormone

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273
Q

Describe the similarities between ADH & oxytocin

A

VERY SIMILAR STRUCTURE & both amine hormones

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274
Q

What are the two primary functions of ADH

A
  1. Vasoconstriction (smooth muscle & blood vessels)
  2. Antidiuretic (holds on to water)
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275
Q

ADH/AVP mechanism of action:

  1. Contraction of vascular smooth muscle via _____
A

V1 Receptors

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276
Q

When ADH causes contraction of vascular smooth muscle through V1 receptors what results?

A

Increases blood pressure

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277
Q

V1 stands for:

A

Vasopressin-1 receptor

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278
Q

When ADH acts on V1 receptors what occurs?

A

Contraction of vascular smooth muscle (blood vessels) leading to increase in BP

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279
Q

ADH/AVP mechanism of action:

Functions in the renal renal tubules via:

A

V2 Receptors

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280
Q

Where are the V2 receptors (for ADH) located?

A

Late distal tubule & collecting duct

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281
Q

What results when ADH binds to V2 in the last distal tubule & collecting duct?

A

AQP-2 proteins are inserted into the apical membrane of tubular epithelial cells

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282
Q

Where is aquaporin-2 inserted following ADH binding to V2 receptors?

A

The apical membrane of tubular epithelial cells

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283
Q

Following ADH binding to V2 receptors in the renal tubules and AQP-2 being inserted into the apical membrane of tubular epithelial cells what results?

A

This allows for water reabsorption (in accordance with AQP3 & AQP4 on the basolateral membrane

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284
Q

For water reabsorption to occur through AQP2 what also has to be present?

A

AQP3 & APQ4 on the basolateral membrane

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285
Q

V2 receptors in the late distal tubule and collecting duct are _____ receptors

A

GPCR

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286
Q

Although water can go through the apical membrane via simple diffusion, the aquaporins allow for:

A

Water channels so a lot more reabsorption can occur

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287
Q

_____ allows for water to enter the apical membrane

_____ are always on the basolateral membrane and allow for the continuation of the water

A

AQP-2

AQP-3 & AQP-4

288
Q

Stimuli for ADH secretion (3)

A
  1. Decreased blood volume
  2. Increased osmolarity
  3. Decreased BP
289
Q

In regard to ADH secretion, decreased blood volume is considered:

A

Isotonic

290
Q

In regard to ADH secretion, increased osmolarity is considered:

A

Isovolemic

291
Q

The most potent stimulator for ADH release is:

A

Increased osmolarity (linear on a graph)

292
Q

If blood volume goes down, ADH will function to _______ to resolve the issue

A

Keep water

293
Q

If the osmolarity of plasma is too high, ADH will function to ____ in order to ______

A

Keep water
Dilute it

294
Q

If your blood pressure is too low, ADH will function to _____ in order to ____-

A

Keep water
Raise it

295
Q

ADH working to keep water in the body will resolve what three issues:

A
  1. High osmolarity
  2. Low BP
  3. Decreased blood volume
296
Q

Decreased or absent feeling of thirst:

A

Hypodipsia

297
Q

Hypodipsia may result in ______ which can cause ______

A

Reduced intake of water
Hypernatremia

298
Q

A common problems in elderly people, but is also associated with lesions in the thirst center of the hypothalamus, head trauma, occult hydrocephalus or subarachnoid hemorrhage

A

Hypodipsia

299
Q

List causes of hypodypsia: (5)

A
  1. Eldery people
  2. Lesions in hypothalamus (thirst center)
  3. Head trauma
  4. Occult hydrocephalus
  5. Subarachnoid hemorrhage
300
Q

Diabetes insipidus is a caused by caused by:

A

ADH imbalance

301
Q

What are the two types of diabetes insipidus:

A

Neurogenic (Central)
Nephrogenic (Peripheral)

302
Q

What do DI and DM have in common?

A

Large urine output

303
Q

If you have increased osmolarity you would feel:

A

Thirst (normal conditions)

304
Q

Disease caused by inability to produce & secrete ADH:

A

Neurogenic/Central Diabetes Insipidus

305
Q

Describe the ADH levels in an individual with Neurogenic/Central DI:

A

Low levels of ADH (they are unable to produce/secrete it)

306
Q

Treatment for a patient with neurogenic/central DI would be:

A

To supplement ADH (likely in the form of medication)

307
Q

Person with a tumor near the posterior pituitary gland has surgical removal of the tumor, causing damage to supraoptic nucleus in the posterior pituitary.

What are they unable to to produce, what disease would this result in?

A

ADH
Neurogenic/Central DI

308
Q

Lacking a response to ADH (like a resistance)

A

Nephrogenic/Peripheral DI

309
Q

Nephrogenic/Peripheral DI occurs in the:

A

Kidneys

310
Q

When ADH is present but the kidneys either do not respond at all, or response inappropriately to the hormone:

A

Nephrogenic/Peripheral DI

311
Q

Describe the levels of ADH an individuals with nephrogenic/peripheral DI would have and why:

A

High levels off ADH because they can produce ADH but the stimulus causing secretion is never satisfied

312
Q

Uncharacteristically, really high levels of ADH secretion & NOT becaue it is needed (Oversecretion of ADH)

A

Syndrome of inappropriate ADH (SIADH)

313
Q

A patient with diabetes insipidus may present with:

A

Polyuria

314
Q

Excretion of large volumes of urine

A

Polyuria

315
Q

Describe the urine in a patient with Diabetes Insipidus:

A

Hypotonic/tasteless (insipid)

316
Q

Other causes of polyuria (not DI) may include: (2)

A
  1. Primary ingestion of excess fluid
  2. Inreased metabolism of ADH (pregnancy)
317
Q

Primary ingestion of excess fluid:

A

Primary polydipsia

318
Q

Increased and uncontrolled secretion of ADH that causes volume expansion & hyponatremia:

A

Syndrome of Inappropriate ADH (SIADH)

319
Q

In the case of a patient with SIADH what would the increased secretion of ADH cause: (2)

A
  1. Volume expansion
  2. Hyponatremia
320
Q

Relative to a dentist, what can cause excessive ADH release?

A

Surgery, pain, stress

321
Q

Why do pregnant women have to pee more?

A

During pregnancy, ADH metabolism is increased so less water is reabsorbed causing her to pee more

322
Q

What hormone causes milk ejection from the breast in lactation?

A

Oxytocin

323
Q

What hormone stimulates the contraction of the uterus towards the end of gestation:

A

Oxytocin

324
Q

Where is oxytocin released from?

A

Posterior pituitary

325
Q

Describe the feedback of oxytocin release:

A

Positive feedback

326
Q

Describe the relationship between Oxytocin & Prolactin:

A

Permissive

327
Q

Where is prolactin released from?

A

Anterior pituitary

328
Q

What does prolactin cause?

A

Milk production in breasts

329
Q

What causes milk secretion in the breast (mechanism)

A

Myoepithelial cell contraction

330
Q

What causes uterine contraction (mechanism)

A

Stretch of cervix at the end of pregnancy

331
Q

Objective evidence of a disease that can be seen or measured:

A

Sign

332
Q

Enlarged hands, polyuria & tachycardia are all examples of:

A

A sign

333
Q

Cannot be measured (they are subjective) but are reported by person:

A

A symptom

334
Q

Headache & numbness are both examples of:

A

A symptom

335
Q

Plasma Membrane Hormone receptors:

List the four plasma membrane hormone receptors:

A
  1. G-protein coupled
  2. Tyrosine-Kinase
  3. Serine Kinase
  4. Cytokine
336
Q

Plasma Membrane Hormone receptors:

What are our two types of GPCRs?

A

Gs & Gq

337
Q

Plasma Membrane Hormone receptors:

Elaborate on the types of Gs coupled receptors: (6)

What second messenger do they produce?

A
  1. Beta-Adrenergic
  2. Calcitonin
  3. ACTH
  4. Glucagon
  5. TSH
  6. Vasopressin

They produce the second messenger cAMP

338
Q

Plasma Membrane Hormone receptors:

Elaborate on the types of Gq coupled receptors: (3)

What second messenger do they produce?

A
  1. Alpha-adrenergic
  2. Angiotensin-II
  3. TRH

They produced the second messengers IP3, DAG, Ca2+

339
Q

What type of plasma membrane hormone receptor would insulin and IGF-1 bind to?

A

Tyrosine-kinase

340
Q

What type of plasma membrane hormone receptor would growth factor bind to?

A

Tyrosine-kinase

341
Q

After cytokine binds to its plasma membrane hormone receptor (leptin) what second messenger does it activate?

A

JAK/STAT

342
Q

Why would some receptors such as the receptors for insulin and thyroid hormone be more widely distributed?

A

Because the effects of these hormones is something that we want a lot of cells to respond to

343
Q

About 93% of the active hormones secreted by the thyroid gland is:

A

T4

344
Q

About 7% of the active hormone secreted by the thyroid gland is:

A

T3

345
Q

T4=
T3=

A

Thyroxine
Triiodothyronine

346
Q

What thyroid hormone is more potent?

A

T3

347
Q

Thyroid hormone impact _____ & _____ and also have a _____ action on ______

A

Metabolism & growth/development
Permissive
Catecholamines

348
Q

What thyroid cells are involved in making thyroid hormone?

A

T thyrocyte cells

349
Q

What is stored in the colloid of a follicle?

A

Thyroglobulin

350
Q

Parafollicular cells secrete:

A

Calcitonin

351
Q

What is the action of calcitonin?

A

Tone down plasma calcium (decrease)

352
Q

In the middle of the thyroid follicle=

A

Colloid

353
Q

Where is thyroid hormone made & stored until it is time to be released?

A

Colloid

354
Q

What is required for thyroid hormone synthesis?

A

Iodine (I2)

355
Q

Thyroid hormone requires iodine (I2) because this is needed for:

A

Thyroid follicular cells to actively transport Iodide (I-) obtained from the diet

356
Q

Iodine synthesis steps:

  1. Thyroid hormone synthesis requires _____
  2. ____ comes from the diet
  3. Thyroid cells have a transporter called:
  4. The follicular cells will:
  5. The iodide gets into the cell and a second transporter called ___ removes ___ and brings ____ into the colloid of the follicular cell
  6. Once inside the colloid Iodide gets concentrated into ______
A
  1. Iodine (I2)
  2. Iodide (I-)
  3. NA+/I- symporter (NIS)
  4. Concentrate the iodide
  5. Pendrin; chloride; iodide (I-)
  6. Iodine
357
Q

The Na+/I- transporter is a ____

A

Symporter

358
Q

The Na+/I- symporter is a _____ transporter

A

Secondary active

359
Q

Iodide must exit the _____ across the ____ to accesse the _____ where the initial steps of thyroid hormones synthesis occur:

A

thyrocyte
apical membrane
colloid

360
Q

What enzyme works in the iodination & coupling process:

A

Peroxidase

361
Q

What is a general term we give for anion exchangers?

A

Pendrin

362
Q

Pendrin is a ______ that exchanges ____ for ____ bringing ____ in and ____ out in the process of thyroid hormone synthesis

A

Anion exchanger
Cl-/I-
I-
Cl-

363
Q

Pendrin is ALWAYS moving:

A

Two negatively charged substances in opposite directions

364
Q

T3 & T4 are produced in the colloid & complexed with:

A

Thyroglobulin (TG)

365
Q

The enzyme involved in all of the production steps in the formation of thyroid hormone:

(Tyrosine, Monoiodotyrosine, Diiodotyrosine, T3, RT3, T4)

A

Peroxidase

366
Q

Thyroglobulin is made of:

A

A bunch of tyrosine amino acids

367
Q

Which works first in making T3 & T4 (pendrin or peroxidase???)

A

Pendrin then peroxidase

368
Q

T3 & T4 secretion into the blood:

  1. ____ is internalized by endocytosis
  2. The vesicles fuse with ____ in the cell
  3. ____ cleaves T3 & T4 from ____
  4. T3 & T4 diffuse out of the cell & into the ___
A
  1. Colloid
  2. Lysosomes
  3. Protease; thyroglobulin
  4. Capillaries
369
Q

Colloid is a ____ of thyroid hormones

A

Reservoir

370
Q

Majority if not all of T3 & T4 bind with ____ for transport:

A

Plasma proteins

371
Q

What are the plasma proteins that T3 & T4 bind to?

A

Thyroxine-binding globulin (TBG)
Transthyretin (TTR)
Albumin

372
Q

What causes the long half-life of T4?

A

The strength of its binding to the transport protein

373
Q

Because T3 doesn’t bind as tightly to the transport protein its half life is:

A

2-3 days

374
Q

For T3 & T4 to be secreted into the blood:

Colloid is taken into the follicular cell via:

A

Pinocytosis

375
Q

For T3 & T4 to be secreted into the blood:

T3 & T4 undergo ____ to be secreted into the blood

A

Simple diffusion

376
Q

Target cells make active T3 by using enzymes called ____ that remove an Iodine from T4

A

Deiodinases/Iodinases

377
Q

Individual target cells can alter their exposure to T3 by regulating:

A

Their tissue Deiodinase synthesis

378
Q

What are the three different Deiodinases?

A

D1, D2, D3

379
Q

All three of the deiodinases contain a rare amino acid called:

A

Selenocysteine

380
Q

In selenocysteine there is a ___ molecule in the place of _____ which is essential for their enzymatic activity

A

Selenium in the place of sulfur

381
Q

What are various conditions that inhibit deiodinase activity?

A
  1. Selenium deficiency
  2. Burns
  3. Trauma
  4. Advanced cancer
  5. Cirrhosis
  6. Chronic kidneys disease
  7. MI
  8. Febrile states
  9. Fasting
  10. Stress
382
Q

If someone has a condition that inhibits deiodinase activity they could show signs of:

Why?

A

Hypothyroidism

Because they are not able to convert T4 to T3

383
Q

T3 actions occur ____ compared to T4

A

Sooner

384
Q

When does the maximum activity of T3 hormone occur?

A

Around 2-3 days

385
Q

Compare the activity of T4 to T3:

A

T4 has a slower onset but a longer duration of action (can last until about 40 days)

386
Q

A variety of genes have the thyroid hormone response element which can lead to:

A

Gene transcription & synthesis of new proteins

387
Q

The synthesis of new proteins due to the action of T3 & T4 can lead to what five main responses?

A
  1. Metabolism
  2. Cardiovascular response
  3. CNS development
  4. Growth
  5. Many other system responses
388
Q

A big effect of the thyroid hormone is on metabolism, what effects can be seen due to T3 & T4 synthesizing new proteins that effect metabolism: (9)

A
  1. Increased BMR
  2. Increased glucose absorption
  3. Increased gluconeogenesis
  4. Increased glycogenolysis
  5. Increased lipolysis
  6. Increased protein synthesis
  7. Increased O2 consumption
  8. Increased mitochondria
  9. Increased Na+/K+ ATPase activity
389
Q

Background amount of oxygen utilized by cells; a basic indicator of metabolism

A

BMR

390
Q

A big effect of the thyroid hormone is on the cardiovascular system, what are some effects relating to this?

A
  1. Increased cardiac output
  2. Increased tissue blood flow
  3. Increased heart rate
  4. Increased heart strength
  5. Increased respiration
391
Q

The cardiovascular effects of thyroid hormone are caused by an increase in ____ which is a ____ effect

A

Beta-receptors; permissive effect

392
Q

The negative feedback of the thyroid hormone is mainly at the level of ____ but can also occur _____

A

Anterior pituitary
Hypothalamus

393
Q

It is T4 that is the circulating form of thyroid hormone that is able to caused the feedback inhibition, but it gets converted into T3 in the _____ & ___ so its actually the T3 that inhibits the secretion of ____ & ____

A

Anterior pituitary & hypothalamus
TSH & TRH

394
Q

What actually causes the feedback inhibition of thyroid hormone:

A

The anterior pituitary and hypothalamus express deiodinase so when T4 levels in the tissues increases they readily convert it (via deiodinase) to T3 which actually causes the inhibition

395
Q

Describe the secretion of TSH:

A

Pulsatile with increases in evening hours & peak around midnight

396
Q

Describe the secretion of thyroid hormone:

A

Thyroid hormone secretion mirrors TSH (pulsatile with increase in evening hours & peak around midnight) but also tonically secreted (small amounts)

397
Q

Thyroid hormone stimulates _____ by most metabolically active tissues:

A

Oxygen consumption

398
Q

How does thyroid hormone effect the BMR?

A

Increases it

399
Q

Thyroid hormone stimulates ____ metabolism:

A

Carbohydrate

400
Q

Thyroid hormone stimulate carbohydrate metabolism by:

A
  1. Uptake of glucose by cells
  2. Enhances glycolysis & gluconeogenesis
  3. Increases CHO absorption from GI tract
401
Q

Describe the effects of thyroid hormone on metabolism relating to proteins:

A

Stimulate proteins catabolism & synthesis (but mostly catabolism)

402
Q

Describe the effects of thyroid hormone relating to fat:

A

Stimulates fat metabolism

403
Q

Thyroid hormone stimulates fat metabolism by:

A

Increasing lipid mobilization & oxidation of fatty acids

404
Q

Thyroid hormone is required to convert _____ to_____, which is why hypothyroid patients may exhibit yellow skin

A

Beta carotene to vitamin A

405
Q

Vitamin is important in:

A

Wound healing

406
Q

Thyroid hormone is responsible for decreasing circulating ____ levels.

A person with hyperthyroidism may have ______ due to this

A

Cholesterol
Hyperlipidemia

407
Q

With no thyroid hormone at all, what would the BMR look like?

A

BMR levels would be around 45-50% of normal rate

408
Q

Thyroid hormone is needed for _____ regarding the nervous system:

A

Needed for normal development

409
Q

Thyroid hormone impacts ____, so someone with hypothyroidism may have have prolonged _____

A

Reflex time
Prolonged reflex time

410
Q

In someone with hyperthyroidism, due to the increased reactivity of neuronal synapses they may experience:

A

Muscle tremors

411
Q

If someone feels tired but has difficulty sleeping, and anxiety, worry & paranoia they may have:

(relating to thyroid hormone effect on NS)

A

Hyperthyroidism

412
Q

Hyperthyroidism effects on cardiovascular system include:

A
  1. increased expression of beta-adrenergic receptors
  2. increased blood flow, HR and heart contractility
413
Q

Describe the permissive effect of thyroid hormone on the cardiovascular system. What might this cause?

A

Thyroid hormone increases expression of beta-adrenergic receptors and this would lead to an increased SNS response

414
Q

Thyroid hormone effects on the endocrine system:

Increased ___ consumption that results in increased secretion of ____ needed to maintain ____ levels

A

Glucose
Insulin
Blood glucose

415
Q

Thyroid hormone effects on the endocrine system:

Thyroid hormone causes activation of bone formation so this causes a need for increased:

A

PTH secretion

416
Q

Thyroid hormone effects on the endocrine system:

Thyroid hormone causes increased inactivation of ___ which leads to more ____ release by the _____

A

Glucocorticoids; ACTH; anterior pituitary

417
Q

Thyroid hormone effects on the GI system:

Thyroid hormone causes in increase _____ & ____ intake

A

Appetite
Food

418
Q

Thyroid hormone effects on the GI system:

Thyroid hormone causes increased rate of ____ & _____ of GI tract

Individuals with hyperthyroidism may have ____ due to this

Individuals with hypothyroidism may have ____ to this

A

Secretion & motility of GI tract

Diarrhea

Constipation

419
Q

Enlarged thyroid gland=

A

Goiter

420
Q

Goiter is an enlarged thyroid gland that:

A

DOES NOT indicate functional status

421
Q

Goiter can be seen in:

A

Hypothyroidism, Hyperthyroidism & Euthyroidism

422
Q

Normal levels of thyroid hormones

A

Euthyrodism

423
Q

Goiter can be caused by:

A

Excessive amounts of TSH secretion

424
Q

High TSH stimulate thyroid to secrete large amounts of _____ into ____ resulting in gland enlargement /goiter

A

Thyroglobin colloid
Follicles

425
Q

The most common of hyperthyroidism

A

Graves disease

426
Q

Although graves disease is the most common form of hyperthyroidism, hyperthyroidism can also occur due to:

A

Thyroid adenoma

427
Q

Graves disease is an ____ disease

Explain how:

A

Autoimmune

Antibodies to the TSH receptor called thyroid stimulating immunoglobulins are produced and they stimulate the thyroid gland directly to produce too much thyroid hormone (T3 & T4)

428
Q

Describe the category of disorder that Graves Disease is, and how the hypothalamus & anterior pituitary are effected:

A

Primary Endocrine disorder- because issue is at level of thyroid gland

Strong negative feedback causes TSH & TRH levels to be reduced

429
Q

Graves disease is more common in:

A

The girlies

430
Q

List the signs & symptoms of Graves Disease:

(10)

A
  1. Sweating/heat intolerance
  2. Increased metabolism
  3. Increased appetite
  4. Weight lose
  5. Fine hair/proteins synthesis
  6. Increased NS response (Emo instability, insomnia, nervy, restlessness)
  7. Fine tremor
  8. Goiter
  9. Exophthalmus (bug eyes)
  10. Pretibial myxedema
431
Q

Treatment of thyroid disease:

A

Radioactive iodine to ablate thyroid gland followed by L-thyroxine (T4) to prevent hypothyroidism

Antithyroid drugs

Beta-blockers to block permissive effect of thyroid hormone

(Surgery rarely indicated)

432
Q

Oral symptoms of hyperthyroidism may include:

A
  • Burning mouth syndrome
  • Gum disease
  • Excessove salivation
  • Weakening of mandible
  • Increased caries risk
433
Q

Elevated thyroid hormone with stressful event or serious illness causing fever, tachycardia, elevated BP, nausea, vomitting, diarrhea, breathing problems:

A

Thyroid storm (thyrotoxicosis)

434
Q

What can bring on a thyroid storm/thyrotoxicosis?

A

Trauma, surgery, infection, DKA or MI

435
Q

Overall a thyroid storm can be described as:

A

Exaggerated sympathetic response

436
Q

In patients with hyperthyroidism or those that exhibit signs/symptoms of it what is extremely important?

A

Administration of epinephrine is CONTRAINDICATED & elective dental care should be deferred

437
Q

Autoimmune reaction against the thy gland that destroys it rather than stimulating it:

A

Hashimoto’s thyroiditis

438
Q

What is the most common cause of hypothyroidisim:

A

Hashimoto’s thyroiditis

439
Q

Prior to diagnosis of Hashimoto’s thyroiditis, most patient first exhibit:

A

Autoimmune thyroiditis

440
Q

In Hashimoto’s thyroiditis, inflammation leads to ____ of the thyroid resulting in ____

A

Fibrosis
Decreased secretion of thyroid hormone

441
Q

What is the target of the antibodies in Hashimoto’s thyroiditis?

A

Peroxidase

442
Q

What class of disorder is Hashimoto’s characterized by?

A

Primary endocrine disorder

443
Q

Another form of hypothyroidism (not Hashimoto’s) can be due to:

A

Low iodine

444
Q

Hypothyroidism due to low iodine is classified as:

A

Primary endocrine disorder

445
Q

In the absence of iodine describe the levels of T3, T4, TSH, & TRH:

A

Low T3 & T4
Elevated TRH & TSH

446
Q

In hypothyroid state, goiter is due to _____ while no goiter is due to _____

A

Iodine deficiency
TSH deficiency

447
Q

Hypothyroidism due to iodine deficiency= _____ = _____ deficiency

Hypothyroidism due to TSH deficiency= _____ = _____ deficiency

A

Goiter, Primary

No goiter, Secondary

448
Q

Symptoms of hypothyroidism may include:

A
  1. Weight gain
  2. Constipation
  3. Cold/diminished perspiration
  4. Lethargy
  5. Impaired memory
  6. Lack of NS stimulation
  7. Coarse, dry brittle hair
  8. Hairloss
  9. Loss of lateral eyebrows
  10. Slow pulse (bc decreased number of beta receptors)
  11. Enlarged heart
  12. Facial edema
  13. Periperhal edema (hands & feet)
449
Q

Unique symptom seen in sever cases of hypothyroidism:

A

Myxedema

450
Q

In hyperthyroidism patients where does the myxedema occur?

In hypothyroidism patients where does the myxedema occur?

A

Hyper= Pretibial myxedema

Hypo= face

451
Q

Myxedema occurs due to increased quantities of ____ & ____ bound with protein plus water that accumulates in the skin

A

Hyaluronic acid & Chondroitin sulfate

452
Q

Dull expressionless facies with puffiness of eyelids, swollen, cool waxy dry, coarse & pale skin, with lots of creases describes a patient effected with ______ and the treatment would be _____

A

Myxedema
L-thyroxine (T4)

453
Q

Required for postnatal brain maturation

A

Thyroid hormones

454
Q

Results from congenital absence of thyroid gland:

A

Congenital cretinism

455
Q

Results from iodine deficient diet; most common cause worldwide:

A

Endemic cretinism

456
Q

Cretinism can cause ____ of neonates.

Skeletal growth is more inhibited than soft tissue growth resulting in:

A

Physical & mental retardation

Obese, stocky & short with large protruding tongue

457
Q

Cretinism can cause a lack of development of the:

A

Nervous system

458
Q

List the hypothyroidism oral manifestations: (6)

A
  1. Macroglossia
  2. Dysgeusia
  3. Delayed tooth eruption
  4. Poor wound healing
  5. Increased periodontal disease
  6. Salivary gland enlargement
459
Q

The poor wound healing and increased risk of infection in a hypothyroidism patient is due to:

A

Decreased activity of fibroblasts

460
Q

Patients with hypothyroidism are sensitive to:

A

Central nervous system depressants or barbituates

461
Q

85% of the body’s phosphate is stored in the ___

14-15% of the body’s phosphate is stored in the ___

Less than 1% of the body’s phosphate is stored in the ___

A

Bones

Cells

ECF

462
Q

Only 0.1% of the bodies calcium is found in the _____

1% of the bodies calcium is found in the _____

The rest of the bodies calcium is stored in the ____

A

ECF

Cells & organelle

Bones

463
Q

When levels of calcium are too low:

A

Neuronal hyper-excitability (tetany due to extra NA+ influx)

464
Q

When levels of calcium are too high:

A

Neuronal depression (Blocks Na+ influx)

465
Q

Carpal spasms can be due to:

A

HYPOcalcemia

466
Q

Control points for calcium & phosphate include:

A
  1. Absorption- via intestines
  2. Excretion- via urine (calcium & phosphate) & feces (calcium only)
  3. Temporary storage- via bone (hydroxyapatite)
467
Q

Ca10(PO4)6(OH)2

A

Hydroxyapatite

468
Q

What are the hormones that regulate plasma calcium?

A

PTH, Calcitriol, Calcitonin

469
Q

How does PTH regulate plasma calcium & phosphate?

A

Increases plasma calcium
Decreases plasma phosphate

470
Q

How does PTH work to raise plasma calcium & lower plasma phosphate?

A
  1. Mobilizes calcium from bone
  2. Enhances renal reabsorption of calcium
  3. Increases intestinal absorption of calcium (indirectly)
471
Q

How does calcitriol regulate plasma calcium & phosphate?

A

Increases plasma calcium
Increases plasma phosphate

472
Q

How calcitriol work to raise plasma calcium & phosphate?

A

Calcitriol is the primary hormone that enhances intestinal absorption of calcium & it also causes absorption of phosphate

473
Q

The primary hormone that enhances intestinal absorption of calcium and also causes absorption of phosphate

A

Calcitriol

474
Q

What are the other names for calcitriol?

A

1,25-dihydroxyxholecaliferol
Vitamin D3

475
Q

Calcitriol acts on the intestines ____ to enhance absorption of calcium & also phosphate, while PTH acts on the intestines _____ to enhance absorption of calcium

A

Directly
Indirectly

476
Q

Calcitonin comes from:

A

Parafollicular cells of the thyroid gland

477
Q

How does calcitonin regulate plasma calcium & phosphate?

A

Decreases plasma calcium
Decreases plasma phosphate

478
Q

How does calcitonin work to decrease plasma calcium & phosphate?

A

By simulating bone formation

479
Q

What hormones stimulate bone formation?

A
  1. Calcitonin
  2. Insulin
  3. Growth hormone
  4. IGF-1
  5. Estrogen
  6. Testosterone
480
Q

______ & _____ stimulate bone matrix resorption which functions to increase plasma calcium

A

Calcitriol
PTH

481
Q

Calcitriol & PTH stimulate bone matrix ___

How does this effect plasma calcium?

A

Resorption

Increases plasma calcium

482
Q

Bone resorption:

  1. Osteoblasts release _____
  2. _____ binds to the ____ on preosteoclasts and this leads to the activation of ______
A
  1. RANKL
  2. RANKL; Rank receptors; osteclasts
483
Q

What is the goal of bone resorption?

A

To increase plasma calcium levels

484
Q

What type of cell is activated during bone resorption?

What activates this type of cell?

A

Osteoclasts

RANKL binding to its receptor on preosteoclasts

485
Q

Factors that stimulate bone matrix resorption:
(4)

A
  1. PTH
  2. Excessive levels of calcitriol
  3. Prolactin
  4. Corticosteroids
486
Q

What is the goal of bone deposition?

A

To form bone- put calcium into bone from the blood

487
Q

_____ stimulates bone matrix deposition and inhbits osteoclasts

A

Calcitonin

488
Q

Calcitonin stimulates bone matrix deposition and inhibits osteoclasts which ultimately does what to plasma calcium?

A

Decreases

489
Q

If calcium levels in the blood are sufficient we dont need to:

A

Breakdown bone

490
Q

Anabolic or anti-resorptive factors (for bone)=

A
  1. Estrogens
  2. Calcitonin
  3. Testostserone
  4. Calcium
  5. BMP
491
Q

In order to avoid RANKL further activating osteoclasts ____ will bind to it so it cannot bind to its receptor

A

OPG

492
Q

OPG binding to RANKL ultimately leads to:

A

Apoptotic osteoclasts

493
Q

Osteoclast that do NOT function to break down bone:

A

Apoptotic osteoclasts

494
Q

Affects almost 10 million individuals in the US, though only a small proportion are diagnosed & treated. Occurs when there is an imbalance in bone resorption & bone formation

A

Osteoporosis

495
Q

Risk factors for osteoporosis: (superficial)

A
  1. Vitamin D deficiency
  2. Inadequate calcium intake
  3. Glucocorticoid medications
  4. Reduced physical activity
  5. Estrogen deficiency
  6. Cigarette smoking
  7. Alcohol
496
Q

Describe why vitamin D deficiency can lead to osteoporosis:

A

Because this can lead to really high PTH levels (secondary hyperparathyroidism) which leads to excessive bone breakdown

497
Q

Describe why inadequate calcium intake can lead to osteoporosis:

A

Because this can lead to really high levels of PTH (secondary hyperparathyroidism) which leads to excessive bone breakdown

498
Q

Describe why glucocorticoid medications can lead to osteoporosis:

A

They suppress the immune response leading to the risk of weak & brittle bones

499
Q

Describe why post-menopausal estrogen deficiency can lead to osteoporosis:

A

Estrogen stimulates the process of bone matrix deposition so the lack of estrogen would throw the balance off

500
Q

Treatments for osteoporosis include:

A
  1. Excerise
  2. PT
  3. Estrogen replacement
  4. Calcium
  5. Vitamin D
  6. Bisphosphonates
501
Q

When giving vitamin D to an osteoporosis patient you must make sure ____ levels do not get too high

A

PTH

502
Q

Four pea-sized glands on the posterior surface of the thyroid glands:

A

Parathyroid glands

503
Q

PTH is secreted by:

A

Chief cells

504
Q

What are the effect of PTH & how?

A

Increased plasma calcium by: indirectly increasing intestinal absorption, decreasing renal excretion & increasing bone resorption

505
Q

How does PTH decrease plasma phsophate?

A

By increasing renal excretion

506
Q

Describe the renal effects of calcium & phosphate by PTH:

A

Increases renal excretion for phosphate
Decreases renal excretion for calcium

507
Q

Why is PTH’s effect on the intestinal absorption of calcium considered indirect?

A

Because it causes more synthesis of vitamin D which in turn causes increased intestinal absorption of calcium

508
Q

When PTF is secreted due to decreased ECF calcium this leads to:

A

Hypertrophy of Parathyroid gland

509
Q

How would a decrease in ECF calcium concentration effect the rate of PTH secretion?

A

Increase

510
Q

What conditions would lead to hypertrophy of the parathyroid gland?

A

Chronic cases- pregnancy, rickets, lactation

511
Q

Chronically if you hypertrophy the parathyroid gland, it becomes:

A

Even better at secreting PTH

512
Q

An increased ECF concentration of calcium leads to ___ of the parathyroid gland

A

Decreased activity

513
Q

If the parathyroid gland has a decrease in activity, it will have a ____ in size

A

Decrease

514
Q

What conditions can cause a decrease in activity & size of the parathyroid gland?

A
  1. Increased vitamin D intake at excessive levels
  2. Excess quantities of calcium in diet
  3. Bone resorption caused by factors other than PTH
515
Q

Describe the effect on plasma calcium:

Bone resorption

A

Increases

516
Q

Describe the effect on plasma calcium:

Reabsorption of calcium by renal tubules:

A

Increases plasma calcium

517
Q

Describe the effect on plasma calcium:

Conversion of 25-hydroxycholecalciferol to 1, 25-dihydroxycholecalciferol:

A

Increases plasma calcium

518
Q

Describe the effect on plasma phosphate:

Decreased reabsorption by renal tubules:

A

Decreases plasma phosphate

519
Q

Where do we get Cholecalciferol (vitamin D3) from?

A

Skin from sun

520
Q

In the process of calcitriol synthesis:

Cholecalciferol is converted to ____ by what organ?

A

25-Hydroxycholecalcierfol
Liver

521
Q

In the process of calcitriol synthesis:

25-Hydroxycalciferol is coverted to _____ by what organ?

A

1,25-dihydroxycholecalciferol (calcitriol)
Kidney

522
Q

In the process of calcitriol synthesis:

What tells the kidney to do the conversion of 25-dihydroxycholecalciferol to the active form?

A

Parathyroid hormone

523
Q

Where is the main effect of Calcitriol?

A

Intestine- absorption of Ca & Phosphate from diet

524
Q

Where can calciferol act although not the main effect?

A

Kidneys- reduced excretion of Ca & Phosphate
Bones- bone deposition (indirectly)

525
Q

Vitamin D3 can be stored in the liver for:

A

Several months

526
Q

Describe the regulation of calcitriol levels:

A

Tightly regulated- if someone takes excess vitamin D3 the liver will still only convert so much into the 25-hydroxycholecalciferol

527
Q

Someone with compromised liver and kidney function may exhibit:

A

Vitamin D deficiency

528
Q

Peptide hormone secreted by parafollicular cells:

A

Calcitonin

529
Q

Parafollicilar cells reside in the ____ and may also be called ____

A

Thyroid gland
C cells

530
Q

Calcitonin is released in response to:

A

Elevated free plasma calcium

531
Q

Calcitonin decreases the levels of plasma calcium by decreasing the activity of ___ thus decreasing ____

A

Osteoclasts
Bone resporption

532
Q

Not a major controlled of calcium in humans:

A

Calcitonin

533
Q

What two systems does calcitonin act on?

A

Bone & kidneys

534
Q

Excess PTH secretion due to a parathyroid gland tumor would be classified as:

A

Primary hyperparathyroidism

535
Q

Primary hyperparathyroidism can lead to extreme ____ activity in bones causing _____, more specifically _____

A

Osteoclastic activity
Cystic bone disease
Osteitis fibrosa cystica

536
Q

Such excessive bone breakdown that we see scar tissue & fibrosis in bones:

A

Cystic bone disease (Osteitis fibrosa cystica) (caused by primary hyperparathyroidism)

537
Q

Primary hyperparathyroidism can cause hypercalcemia leading to: (in relation to urine)

A

Polyuria & Calciuria

538
Q

What phosphate levels and why in patients with primary hyperparathyroidsim?

A

Low phosphate due to increased renal excretion

539
Q

Describe why someone with primary hyperparathyroidism would exhibit muscle weakness and easy fatigability:

A

Too much calcium- blocks sodium influx leading to neuronal depression (impedes signaling by neurons)

540
Q

Primary hyperparathyroidism signs and symptoms include:

A

Stones, bones, abdominal groans & psychic moans

541
Q

Describe the stone component of primary hyperparathyroidism:

A
  1. Renal stones
  2. Nephrocalcinosis
  3. Polyuria
  4. Polydipsia
  5. Uremia
542
Q

Describe the bones component of primary hyperparathyroidism:

A
  1. Cystic bone disease
  2. Osteomalacia/rickets
  3. Arthritis
543
Q

Describe the abdominal groans component of primary hyperparathyroidism:

A
  1. Constipation
  2. Indigestion
  3. Nausea
  4. Vomiting
  5. Peptic ulcers
  6. Pancreatitis
544
Q

Describe the psychic moans component of primary hyperparathyroidism:

A
  1. Lethargy/fatigue
  2. Depression
  3. Memory loss
  4. Paranoia
  5. Personality change
  6. Confusion, stupor, coma
545
Q

Other symptoms, not included in stones, bones, moans and groans from primary parahyperthyroidism include:

A
  1. Proximal muscle weakness
  2. Keratitis
  3. Conjunctivitis
  4. Hypertension
  5. Itching
546
Q

High PTH levels that occur as compensation for hypocalcemia & NOT due to an issue with the parathyroid gland:

A

Secondary Hyperparathyroidism

547
Q

What are the two causes of hypocalcemia that lead to secondary hyperparathyroidism?

A
  1. Vitamin D deficiency
  2. Chronic renal disease- cannot synthesize Vit D3
548
Q

What disease are you at risk for with high levels of PTH?

A

Osteoporosis

549
Q

Disease that would results from accidental surgical parathyroid gland removal (not common):

A

Primary Hypoparathyroidism

550
Q

What increases membrane Na+ permeability leading to neuromuscular excitability & muscle spasma

A

Hypocalcemia

551
Q

What is the condition for the wonky ass hand:

A

Carpal spasm

552
Q

How many adrenal glands do we have?

Where are they located?

A

Two adrenal glands

One ontop of each kidney

553
Q

Describe the structure of an adrenal gland:

A

Outer cortex + inner medulla

554
Q

What portion of the adrenal gland is essential for life?

A

Adrenal cortex

555
Q

The adrenal cortex secretes:

A
  1. Corticosteroids
  2. Mineralcorticoids
  3. Sex hormones
556
Q

Is the adrenal medulla essential for life?

A

No

557
Q

The adrenal _____ is a true endocrine organ

A

Cortex

558
Q

Although it is not essential for life, the adrenal medulla is important in:

A

Secreting epinephrine & norepinephrine in response to sympathetic nervous system stimulation

559
Q

The adrenal medulla hormones are NOT essential for life but help an individual deal with:

A

Emergencies

560
Q

The adrenal cortex secretes several hormones that are made from:

A

Cholesterol

561
Q

What are the three layers of the adrenal cortex?

A

Zona Glomerulosa
Zona Fasciculata
Zona Reticularis

562
Q

The largest zone of the of the adrenal cortex:

A

Zona Fasciculata

563
Q

The Zona Glomerulosa secretes _____ and is regulated by ______

A

Mineralcorticoids
RAAS

564
Q

RAAS stands for:

A

Renin-angiotensin-aldosterone system

565
Q

The Zona Fasciculata secretes ____ and is regulated by _____

A

Glucocorticoids
HPA (CRH, ACTH)

566
Q

HPA stands for:

A

Hypothalamic-pituitary-adrenal axis

567
Q

The Zona Reticularis secretes ____ and is regulated by _____

A

Androgens
HPA

568
Q

The adrenal medulla is related to the _______ & secretes ____

A

Sympathetic nervous system; catecholamines

569
Q

What type of cells secrete catecholamines?

A

Chromaffin cells

570
Q

The do the chromaffin cells of the adrenal medulla secrete Epi & NE?

A

Directly into the blood

571
Q

What are the three tissues involved in the HPA?

A

Hypothalamus, pituitary, adrenal gland

572
Q

Why does the zona glomerulosa secrete so much aldosterone?

A

Bc enzymes involved in the formation of aldosterone from cholesterol are highly expressed in the zona glomerulosa

573
Q

What enzyme is responsible for the conversion of cortisol to cortisone?

A

11HSD Beta 2

574
Q

What enzyme is responsible for the conversion of cortisone to cortisol?

A

11HSD Beta 1

575
Q

The reactions that occur for the synthesis of steroid hormones in the adrenal cortex take place in the ______ or the _____

A

Mitochondria
Endoplasmic reticulum

576
Q

Describe the activity of cortisone at cortisol receptors:

A

Reduced activity

577
Q

Can be used to make testosterone & androgens:

A

Androstenedione

578
Q

Aldosterone is classified as a:

A

Mineralcorticoid

579
Q

Aldosterone functions in the kidneys to:

A
  1. Increase renal reabsorption of sodium
  2. Increase renal secretion of Potassium
580
Q

Aldosterone working to increase renal reabsorption of Na+ and increasing renal secretion of K+ results in:

A

Increase in ECF volume and mean arterial pressure

581
Q

What stimulates aldosterone secretion?

A
  1. Angiotensin II
  2. Increased levels of K+
  3. Decreased levels of Na+
582
Q

Aldosterone has effects on:

A
  1. Kidney
  2. Sweat glands
  3. Salivary glands
583
Q

What portion of the adrenal cortex is responsible for aldosterone secretion?

A

Zona Glomerulosa

584
Q

What are the main functions of angiotensin-II

A
  1. Vasoconstriction
  2. Release of aldosterone
585
Q

What function of angiotensin-II is interrelated to the sympathetic nervous system:

A

Release of aldosterone

586
Q

Since aldosterone causes increased tubular reabsorption of sodium, ultimately raising blood sodium levels what happens to water?

A

Water retention occurs because where sodium goes water follows

587
Q

The effects of aldosterone on sweat glands is important to:

A

Conserve body salt in hot environments

588
Q

The effects of aldosterone on the salivary gland is important in:

A

Conservation of sodium during high rates of salivary secretion

589
Q

In addition to hyperkalemia ______ causes secretion of aldosterol

A

Angiotensin II

590
Q

An enzyme release by the cells in the kidneys in response to a variety of stimuli (Example: SNS)

A

Renin

591
Q

Angiotensin converting enzyme (ACE) is produced by the:

A

Endothelium

592
Q

List the steps of the RAAS:

A

Angiotensinogen gets converted to Angiotnesin I by the enzyme Renin

Angiotensin I gets converted to Angiotensin II by the enzyme ACE

593
Q

Angiotensin II ultimately causes the secretion of _____ but also does ____, ____ & _____

A

Ultimately aldosterone secretion but also ADH secretion, thirst stimulation & vasoconstriction

594
Q

What do vasoconstriction, aldosterone secretion, ADH secretion & thirst stimulation all have in common?

A

These all work to raise BP

595
Q

In RAAS, the nonactive precursor made by the liver and found in the plasma:

A

Angiotensinogen

596
Q

Where is large amounts of ACE found?

A

In the lungs

597
Q

Alot of _____ medications target RAAS:

A

HTN

598
Q

How do ACE inhibitors work?

A

If you inhibit ACE you will make less angiotensin II= lower BP

599
Q

Primary hyperaldosteronism may also be called:

A

Conn’s syndrome

600
Q

In primary hyperaldosteronism where is the problem?

A

The adrenal gland

601
Q

What are the causes of primary hyperaldosteronism?

A
  1. Adrenal adenoma (benign)
  2. Adrenal hyperplasia
  3. Adrenal carcinoma (malignant)
602
Q

Describe the levels involved in primary hyperaldosteronism (Conn’s syndrome):

A

Low levels of renin

603
Q

Signs & symptoms of primary hyperaldosteronism (Conn’s syndrome) include:

A

Hypertension
Hypernatremia
Hypokalemia
Headaches
Weakness
Fatigue
Polyuria
HYPOKALEMIC ALKALOSIS
LOW PLASMA RENIN

604
Q

Explain why someone with primary hyperaldosteronism would have low levels of plasma renin?

A

Due to so much aldosterone production we will have strong negative feedback

605
Q

A byproduct of cells trying to regulate the K+ levels in the case of primary hyperaldosteronism (Conn’s)

A

Hypokalemic alkalosis

606
Q

In hypokalemic alkalosis the cells attempt to regulate K+ levels leads to an absence of:

A

H+ in the ECF

607
Q

Treatment options for primary hyperaldosteronism (Conn’s) include:

A

Surgical removal of tumor or most of the adrenal tissue when hyperplasia is present

Mineralcorticoid receptor antagonist

608
Q

Disease caused by decreased blood flow and pressure in the renal artery- in which the kidney thinks BP is low and secretes renin excessively

A

Secondary hyperaldosteronism

609
Q

Describe the levels of renin in secondary hyperaldosteronism:

A

High levels of renin

610
Q

What are causes of secondary hyperaldosteronism?

A
  1. CHF
  2. Renal artery stenosis
611
Q

How might CHF lead to secondary hyperaldosteronism?

A

Pumping function of heart is declined, leading to low BP, and aldosterone levels will rise to compensate

612
Q

How might renal artery stenosis lead to secondary hyperaldosteronism?

A

Renal artery pumps blood to kidney and there can be an atherosclerotic plaque in the vessels resulting in decreased blood flow to kidney. Kidney now thinks BP is low and secretes excessive renin to try to compensate for the “low BP.” Extra renin leads to extra angiotensin II which leads to extra aldosterone secretion

The other kidney is working just fine

613
Q

Signs & symptoms of secondary hyperaldosteronism include:

A
  1. High plasma renin
  2. Hypernatremia w/extracellular volume expansion
  3. Edema
  4. Decreased cardiac output
  5. Similar clinical findings to primary hyperaldosteronism (EXCEPT RENIN LEVEL)
614
Q

Hormone that functions in the mobilization of energy stores & suppresses the immune system:

A

Cortisol

615
Q

What hormone is secreted in response to stress?

A

Cortisol

616
Q

Cortisol is categorized as a _____ and comes from the ______ of the adrenal cortex

A

Glucocorticoid
Zona fasciculata

617
Q

More cells in the adrenal cortex make ____ than any other cells because of the size of the Zona Fasciculata

A

Cortisol

618
Q

What are some examples of stressors that may cause cortisol secretion?

A

Heat
Cold
Hypo/Hyperglycemia
(Not just psychological stress)

619
Q

Cortisol says “there is a stressful situation, let me throw a bunch of nutrients in the blood” but a consequence of cortisol is that:

A

It suppresses the immune system

620
Q

When does cortisol levels spike? What hormone is opposite of this?

A

Early morning hours; Growth hormone

621
Q

Cortisol feeds back and inhibits:

A
  1. ACTH secretion from anterior pituitary
  2. CRH secretoin from hypothalamus
622
Q

Describe what type of feedback is seen through cortisol:

A

Long loop only

623
Q

What are the four main actions of cortisol?

A
  1. Gluconeogenesis
  2. Protein mobilization
  3. Fat mobilization
  4. Stabilizes lysosomes
624
Q

The action of cortisol leads to the suppression of immune function?

A

Stabilizing lysosomes

625
Q

Why are other hormones secreted when ACTH is secreted?

A

Because the gene for ACTH forms a larger protein (a preprohormone)

626
Q

What is the name of the preprohormone that ACTH is derived from?

A

Proopriomelanocortin (POMC)

627
Q

In addition to ACTH being synthesized from POMC what else is secreted?

A
  1. Melanocyte stimulating hormone (MSH)
  2. Beta-endorphin
  3. Beta-lipotrophin
628
Q

A clinical sign of elevated ACTH pathologically is:

A

Increased skin pigmentation from melanocytes)

629
Q

What is a byproduct of ACTH production?

A

MSH

630
Q

Cortisol has a similar affinity for the ____ receptor as _____

A

Mineralcorticoid receptor (MR)
Aldosterone

631
Q

What is found at higher circulating concentrations, aldosterone or cortisol?

A

Cortisol

632
Q

Since cortisol is able to bind to the MR receptor, why doesn’t it cause a mineralcorticoid effect?

A

11B2HSD enzyme converts cortisol to cortisone in aldosterone responsive tissues making sure the aldosterone binds to the MR receptor, not cortisol

633
Q

____ does not bind to GC or MR receptors with as high of an affinity as _____

A

Cortisone; Cortisol

634
Q

A genetic deficieny of 11B2-HSD that leads to the syndrome:

A

AME (apparent mineralocorticoid excess)

635
Q

______ is a compound found in licorice that inhibits the activity of _____

A

Clycerhetininc acid
11B2-HSD

636
Q

What do we expect under normal conditions when the adolsterone binds the mineralocorticoid receptor in the epithelial cells of the kidney:

A

Increased sodium reabsorption
Increased potassium secretion

637
Q

Where would we find 11B2HSD receptors?

Where would we find 11B1HSD receptors?

A

Kidneys, Salivary gland & Sweat glands

Skin

638
Q

High circulating cortisol levels such as in Cushing’s syndrome can:

A

Overwhelm the 11HSDB2 receptor

639
Q

Both AME syndrome & high circulating cortisol levels will ultimately cause:

A

High blood pressure

640
Q

Effects of Cortisol on metabolism:

Stimulation of ____ & _____ in the liver resulting in ______

A

gluconeogenesis & glycogenolysis
Increases plasma glucose

641
Q

Effects of Cortisol on metabolism:

____ action resulting in decreased glucose uptake in the muscle & fat but not the brain & heart

A

Anti-insulin

642
Q

Effects of Cortisol on metabolism:

Makes _____ worse by increasing ____ levels, ____ levels, & ____ formation & ____ secretion

A

Diabetes
Glucose, lipid
Ketone body
Insulin

643
Q

Describe what two hormones are antagonists when dealing with the carbohydrate effect of cortisol on metabolism:

A

Cortisol & insulin are antagonist

644
Q

Describe what can happen with a diabetic that is scared of the dentist due to cortisol:

A

They come in, they get stressed out, their cortisol levels rise and in turn their blood sugar rises (bc cortisol stimulates gluconeogenesis & glycogenolysis)

645
Q

Effects of cortisol on metabolism:

Inhibits ____ synthesis & increases ______ especially in skeletal muscle

A

Protein; proteolysis (provides a source of AA for glycoenogenesis)

646
Q

Effects of cortisol on metabolism:

Cortisol excess leads to ____ weakness, pain, ___ skin and abdominal ___ due to the protein catabolic effect

A

Muscle
Thin
Abdominal striae

647
Q

Effects of cortisol on metabolism:

Promotes ____, and shifts the energy system to utilization of ____ to ____ in times of stress

A

Lipolysis
Glucose to fatty acids

648
Q

Effects of cortisol on metabolism:

Causes ____ deposition in certain areas (abdomen, interscapular “buffalo hump” and a rounded “moon face”

A

Lipid

649
Q

95% of the glucocorticoid activity is due to the secretion of:

A

Cortisol

650
Q

Absence of cortisol contributes to _____ due to the loss of _____ of _____ on blood vessels

A

Circulatory failure
Permissive action
Catecholamines

651
Q

Lack of cortisol prevents mobilization of ______ (glucose & free fatty acids) during stress & can result in _____

A

Energy sources
Fatal hypoglycemia

652
Q

Vasoconstriction of blood vessels occurs via:

A

Alpha 1 receptors

653
Q

Describe the effect cortisol has on catecholamines (Alpha1 receptor) on blood vessels:

A

Permissive effect- the presence of cortisol allows the alpha 1 receptors effect to be maximized

654
Q

Why would BP decrease when cortisol levels are low:

A

The presence of cortisol allows the alpha1 receptors response to be maximized, so without the maximum response BP would be lower

655
Q

How does cortisol effect the immune system?

A

Suppresses immune system

656
Q

What are a few ways that cortisol suppresses the immune system?

A
  1. Stabilizes lysosomal membrane
  2. Opposes inflammation (by decreasing WBC migration & phagocytosis)
  3. Suppresses T lymphocytes
657
Q

What property of glucocorticoids allows them to be used in treatment of patients with diseases/conditions involving exaggerated inflammatory response?

A

Their anti-inflammatory action

658
Q

How can treatment with glucocorticoids cause osteoporosis?

A

Because cortisol stimulates bone resorption via an increase in RANKL expression by osteoblast

659
Q

Treatment with glucocorticoid promotes apoptosis of _____ & ____ which can further lead to osteoporosis

A

Osteoblasts & Osteocytes

660
Q

The zona reticularis is responsible for the secretion of:

A

androgens

661
Q

The zona reticularis begins secreting adrenal androgrens around age _____, peaking around age _____ & ______ with age

A

8; 20; decreasing

662
Q

Adrenal androgens secreted by the zona reticularis include:

A

DHEA/DHEAS
Androstenedione
Testosterone
Estrogens

663
Q

Describe the effects of adrenal androgens in males versus females:

A

Adrenal androgens have only weak effects in males but contribute ~50% of active androgens in females

664
Q

Describe the effects of adrenal androgens in females:

A

Growth of pubic hair, axillary hair & libido

665
Q

A condition resulting from excess androgen production in pre-pubertal boys:

A

Precocious pseudopuberty

666
Q

Normally puberty in boys is stimulated by _____ which leads to the secretion of FSH and LH

But if the adrenal gland is oversecreting androgens it can lead to:

A

Hypothalamus secreting GRH

Early puberty NOT due to the hypothalamic pituitary axis

667
Q

If boys are effected by precocious pseudopuberty brought on by excessive androgen secretion from the adrenal gland this can cause:

A

Early development of secondary sexual characteristics (under age 8)

668
Q

______ deficiency can result in virilization in newborn females & pseudo-hermaphroditism

A

21-hydroxylase deficiency

669
Q

21-Hydroxylase deficiency leads to an overproductionof:

A

Androgens (DHEA, DHEAS, Androstendione)

670
Q

Androgen secreting tumors producing excess androgen result in: (in females)

A

Virilization & precocious pseudopuberty in females

671
Q

Precocius pseudopuberty:

A

Early puberty not caused by HPA secreting GRH, but instead due to adrenal androgens in excess

672
Q

21-hydroxylase is an enzyme critical for making ___ & ____ and in the absence of this enzyme there is buildup of excessive amounts of _____ & _____ precursors resulting in excessive production of ______

A

Aldosterone & cortisol
Aldosterone & cortisol precursors
Androgen precursors (DHEA, DHEAS, Andrestenedione)

673
Q

Androstenedione is a precursor to:

A

Testosterone
5-Dihydrotestosterone
Estrogenes

674
Q

Although androstenedione is not the precursor made in the greatest amounts compared to DHEA & DHEAS, it is the precursor with the:

A

Greatest effect

675
Q

Why does the precursor androstenedione have the greatest effect (compared to DHEA & DHEAS)

A

Because it is more readily convertied peripherally to testosterone & estrogens

676
Q

In adults, hormonally active, benign adrenal adenomas usually secrete _____ or ____

A

Aldosterone or cortisol

677
Q

Virilizing tumors in women are more likely to be caused by:

A

Ovarian tumors

678
Q

Virilizing adrenal tumors are ____ and virilization is usually due to ______

A

Rare; hypersecretion of adrenal androgens

679
Q

List some signs & symptoms of virilization:

A

Male-pattern baldness
Male muscularture
Clitoromegaly
Increased libido
Rapid linear growth with advanced bone age

680
Q

Primary adrenal insufficiency

A

Addison’s

681
Q

Addison’s disease can be caused by primary atrophy or injury to the _____

A

adrenal cortex

682
Q

In about 80% of Addison’s atrophy occurs due to ____ of all cortical zones

A

autoimmune destruction

683
Q

Describe the level of ACTH in addison’s disease:

A

High levels of ACTH

684
Q

Describe the levels of corticosteroid production in addison’s disease:

A

Low corticosteroids

685
Q

Addison’s disease can be characterized by a loss of:

A

Glucocorticoid, mineralcorticoid, & androgen secretion

686
Q

Secondary adrenal insufficiency is due to low levels of:

A

ACTH

687
Q

If the pituitary gland is unable to secrete enough ACTH this would restult in:

A

Low cortisol production (secondary adrenal insufficiency)

688
Q

Often latrogenic due to abrupt cessation of steroid therapy

A

Secondary adrenal insufficiency

689
Q

What is affected in primary adrenal insufficiency that is NOT affected in secondary adrenal insufficiency:

A

Mineralcorticoid secretion

690
Q

Would signs and symptoms of glucocorticoid deficiency be seen in primary or secondary adrenal insufficiency or both?

Would signs and symptoms of mineralcorticoid deficiency be seen in primary or secondary adrenal insufficiency or both?

Would signs and symptoms of androgen deficiency be seen in primary secondary adrenal insufficiency or both?

A

Glucocorticoid deficiency= both- both have lack of cortisol production

Mineralcorticoid deficiency= primary only

Androgen deficiency= Both- In addisons there is a loss of androgen & in secondary there is low ACTH leading to low androgen production (bc ACTH stimulates androgen production)

691
Q

Two important symptoms of glucocorticoid deficiency include:

A

Hypoglycemia- because cortisol normally raises blood glucose

Low BP- due to the lack of alpha1 receptor permissive effect

692
Q

Hyperpigmentation in primary adrenal insufficiency is due to excess of ______

A

POMC

693
Q

Cushing’s disease is a _____ disorder its characterized by _____

Cushing’s sydnrome is a _____ disorder characterized by ____

A

Secondary- occurs due to brain- high ACTH

Primary- occurs due adrenal cortex- low levels of ACTH

694
Q

Both cushings disease/syndrome is characterized by:

A

High cortisol levels

695
Q

Cushings Disease or Syndrome?

  1. Secondary disorder
  2. Primary disorder
  3. Due to adrenal cortex
  4. Due to brain
  5. Oversecretion of ACTH leads to excessive cortisol level
  6. Overproduction of cortisol leads to low levels of ACTH
A
  1. Disease
  2. Syndrome
  3. Syndrome
  4. Disease
  5. Disease
  6. Syndrome
696
Q

To distinguish between Cushing’s disease & syndrome, what hormone levels would you look at?

A

ACTH

697
Q

Conn’s syndrome is an issue with _____

Cushing’s syndrome is an issue with _____

Pheochromoyctomoa is an issue with ______

A

Mineralcorticoids

Glucocorticoids

Catecholamines

698
Q

Sudden release of hormone causing sudden “attack” due to chromaffin cell in the adrenal medulla resulting in excessive secretion of epi & norepi

A

Pheochromocytoma

699
Q

What cells are involved in pheochromocytoma?

A

Chromafin cells

700
Q

Can be characterized by an exaggerated sympathetic response:

A

Pheochromocytoma

701
Q

What hormones are invovled in pheochromocytoma:

A

Epi & Norepi

702
Q

Entire length of thick filament (some overlapping thin filament)

A

A-band

703
Q

Includes ONLY thin filaments

A

I-band

704
Q

Includes only thick filaments

A

H-zone

705
Q

Where thin filaments are anchored

A

Z-line

706
Q

Link the central regions of thick filaments

A

M-line

707
Q

When a sarcomere shortens during contraction, what happens to the zone of overlap

A

Increases

708
Q

When a sarcomere shortens during contraction , what happens to the I-band?

A

Decreases

709
Q

When the sarcomere shortens during contraction, what happens to the A-band?

A

THE A-BAND DOES NOT CHANGE IN LENGTH

710
Q

Dark band:

Light band:

A

A-band

I-band

711
Q

In muscle, functions as an ATPase enzyme:

A

Myosin

712
Q

When myosin binds to ATP what happens?

A

It hydrolyzes the ATP

713
Q

What regulate when contraction can happen?

A

Troponin & tropomyosin

714
Q

Protein that connects thin filaments to glycoproteins in the sarcolemma:

A

Dystrophin

715
Q

Provides scaffolding for sarcomeres:

A

Dystrophin-glycoprotein complex

716
Q

What is the difference between Duchenne & Beckers muscular dystophy?

A

Duchennes= more severe, low levels of dystrophin if any at all

Beckers= makes some dystrophin but not enough, because of this muscle cells weaken and, better prognosis

717
Q

List some types of muscular dystrophy:

A

Duchenne
Beckers
Myotonic
Oculopharyngeal
Limb girdle