Exam 2 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

List the 3 functions of hormones:

A
  1. maintenance of homeostasis
  2. growth and differentiation
  3. reproduction
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5
Q

Endocrine organs can be divided into what two categories?

A
  1. major endocrine glands
  2. organs w/ endocrine cells
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6
Q

Primary function is to make a hormone and release it when the stimuli are present

A

major endocrine organ

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7
Q

organs that happen to have endocrine cells allowing them to release a hormone although their primary fxn is NOT endocrine regulation

A

organs containing endocrine cells

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8
Q

List specialized endocrine glands (major endocrine organs)

A
  1. parathyroid gland
  2. thyroid gland
  3. pituitary gland
  4. adrenal gland
  5. pineal gland
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9
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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10
Q

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

A

tropic hormone

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11
Q

How do we classify hormones?

A

based on their structure

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12
Q

What are the 3 classifications of hormones?

A
  1. proteins or polypeptides
  2. steroids
  3. tyrosine derivatives
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13
Q

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

A

made in advance and stored in vesicles until signal for release

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14
Q

Protein and polypeptide hormones are synthesized first as ____.

A

Preprohormone

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15
Q

The preprohormone will be converted into:

A

prohormone

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16
Q

In protein and polypeptide hormones what is packed into vesicles of the endocrine cell prior secretion?

A

prohormone

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17
Q

After the prohormone gets cleaved, it is now:

A

active hormone

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18
Q

Mnemonic for protein and polypeptide hormones:

A

Protein/Polypeptide/Pre & Pro hormones (Everything with P’s)

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19
Q

in addition to the active hormone, what gets released in when the prohormone gets cleaved?

A

inactive fragment

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20
Q

What is the first thing that gets cleaved from preproinsulin?

A

signal peptide

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21
Q

After the signal peptide is cleaved from preproinsulin, what occurs?

A

protein folding

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22
Q

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

A

Proinsulin

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23
Q

Proinsulin gets stored in:

A

vesicles

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24
Q

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

A

C-peptide

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25
Q

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

A

C-peptide

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26
Q

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

A

c-peptide levels in the blood stream

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27
Q

protein and polypeptide hormones are often made as an:

A

inactive precurser

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28
Q

The inactive precursor of protein and polypeptide hormones:

A

preprohormone

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29
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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30
Q

Where are the receptors located for protein/polypeptide hormones?

A

In the plasma membrane

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31
Q

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

A

Made and released on demand

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32
Q

Where are the receptors located for steroid hormones?

A

Inside the cell

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33
Q

Why are steroid hormone receptors located inside the cell?

A

steroid hormones can cross the plasma membrane and bind to receptors inside target cells

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34
Q

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

A

protein and polypeptide hormones

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35
Q

Hormones from the adrenal cortex, ovaries and testes:

A

steroid

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36
Q

Steroid hormones are synthesized from (derivatives of):

A

cholesterol

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37
Q

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

A

Aldosterone & Cortisol

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38
Q

DHEA, Androstenedione, testosterone, and estradiol are all steroid hormones involved in:

A

reproduction

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39
Q

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

A

compliment of enzymes present

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40
Q

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

A

made early and stored until secreted

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41
Q

Amine hormones are derived from:

A

amino acid tyrosine

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42
Q

Thyroid hormone, Noepinephrine and Epinephrine are all:

A

amine hormones

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43
Q

Epinephrine and norepinephrine are both:

A

adrenal medullary neurohormones

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44
Q

Thyroid hormone binds to the protein:

A

thyroglobulin

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45
Q

Epinephrine and norepinephrine are stored in vesicles and released via:

A

exocytosis

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46
Q

structurally what is the difference between T3 and T4?

A

the # of Iodide atoms attached

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47
Q

What is a precursor to epinephrine and norepinephrine?

A

Dopamine

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48
Q

Hormones released into circulation can either circulate ____ or ____.

A

Freely or with binding proteins

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49
Q

The majority of ____, ____, and _____ hormones circulate in their free form.

A

amines, peptides and proteins

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50
Q

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

A

Thyroid hormones because its double ring structure makes it soluble enough to where it needs help getting through the plasma

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51
Q

Describe the solubility of amines, peptides/protein hormones:

A

water soluble

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52
Q

_____ & _____ circulate bound to specific transport proteins

A

steroid and thyroid hormones

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53
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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54
Q

What is a shuttle bus found in the plasma (plasma protein) that transports a lot of things such as lipid soluble hormones and fatty acids:

A

albumin

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55
Q

Most binding proteins are synthesized in the:

A

liver

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56
Q

Patients with a compromised liver may show signs of:

A

endocrine deficiencies

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57
Q

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

A

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

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58
Q

It is always the ____ version of the hormone that binds to the receptors and affect the target cell.

A

Free version (binding protein stays in blood vessel)

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59
Q

The constitutive level of plasma hormones

A

basal level

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60
Q

The stimulated level of plasma hormones

A

peak levels

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61
Q

The variable patterns of hormone release (oscillation) is determined by the interaction and integration of multiple control mechanisms which include: (4)

A

hormonal, neural, nutritional, and environmental

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62
Q

When a hormone is constantly secreted in small amounts all of the time:

A

tonic release

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63
Q

Hormone fluctuations that happen dependent on the time of day:

A

circadian rhythm

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64
Q

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

A

cortisol

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65
Q

When does cortisol spike?

A

early morning hours

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66
Q

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

A

stimuli

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67
Q

Growth hormone is secreted during sleep following a circadian rhythm release pattern but also displays:

A

pulsatile secretion

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68
Q

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

A

pulsatile secretions

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69
Q

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

A

chemical

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70
Q

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

A

lipophilic/lipophobic

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71
Q

Ligand/receptor binding demonstrates:

A
  1. specificity
  2. affinity
  3. saturation
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72
Q

Which classes of hormones bind to plasma membrane receptors?

A

polypeptide/protein and amine hormones

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73
Q

What amine hormone does not bind to plasma membrane receptors (exception)

A

thyroid hormone

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74
Q

Which class of hormones binds to nuclear receptors?

A

steroids hormones + thyroid hormone

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75
Q

which amine hormones bind to plasma membrane receptors?

A

epinephrine and norepinephrine

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76
Q

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

Glucagon
Angiotensin
GnRH
SS
GHRH
FSH
TSH
ACTH

A

Plasma membrane receptor - they are peptide and protein hormones

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77
Q

In general, many of the receptors that protein/peptide hormones and amine hormones bind to in the PM are:

A

GPCR

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78
Q

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

A

plasma membrane receptors

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79
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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80
Q

Class of hormone receptors involved in making new proteins

A

nuclear receptors

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81
Q

Thyroid hormone and steroid hormones bind to receptors in the:

A

cytoplasm or nucleus

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82
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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83
Q

Following binding of the steroid or thyroid hormone to the receptor and 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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84
Q

Examples of plasma membrane hormone receptors:

A
  1. g-protein coupled receptor
  2. tyrosine kinase
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85
Q

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

A

this provides a way to achieve specific tissue activation

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86
Q

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

A
  1. thyroid hormone receptors
  2. insulin receptors
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87
Q

Why are thyroid hormone receptors and insulin receptors more widely distributed?

A

Because there actions are something that most cells participate in

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88
Q

How do IGF-1 and insulin work?

A

By activating a tyrosine kinase receptor

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89
Q

If it is a plasma membrane receptor, generally it will activate or inhibit _____ to _____.

A

an existing protein to yield a faster response

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90
Q

Where are nuclear hormone receptors located?

A

cytoplasm or nucleus

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91
Q

Nuclear hormone receptors typically leads to:

A

formation of new proteins

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92
Q

Nuclear hormone receptors all act to:

A

increase or decrease gene expression

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93
Q

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

A

hormone responsive element; promotor region; gene trasncription

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94
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 and the response will last a bit longer

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95
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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96
Q

The body often releases multiple hormones…

A

at the same time

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97
Q

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

A
  1. antagonism
  2. additive
  3. synergistic
  4. permissiveness
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98
Q

When two hormones change one variable in opposite directions:

A

antagonism

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99
Q

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

A

additive

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100
Q

Ramps of up the systems response when there is a present of more than one hormone- the combined response is greater than each would give individually (2+3=10)

A

synergistic

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101
Q

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

A

permissiveness

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102
Q

Determine which hormone interaction is being described:

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

A

antagonistic

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103
Q

Determine which hormone interaction is being described:

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

A

synergistic

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104
Q

Determine which hormone interaction is being described:

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

A

permissiveness

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105
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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106
Q

When the last hormone in the pathway inhibits the system upstream:

A

long loops negative feedback

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107
Q

When an intermediate hormone in the pathway inhibits the system upstream:

A

short loop negative feedback

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108
Q

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

A

positive feedback

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109
Q

Causes an endocrine gland to secrete a hormone:

A

tropic hormone

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110
Q

Stabilizes the system and prevents oversecretion:

A

negative feedback

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111
Q

Hormones that have other endocrine glands as their targets:

A

tropic hormones

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112
Q

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

A

TRH

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113
Q

TRH comes from

A

Hypothalamus

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114
Q

TRH acts on the:

A

anterior pituitary

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115
Q

TSH (thyroid stimulating hormone) is released from the:

A

anterior pituitary

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116
Q

TSH is release from the anterior and acts on the:

A

thyroid gland

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117
Q

In the regulation of thyroid hormone: A stimulation causes the hypothalamus to secrete _____ which acts on ____.

A

thyrotropin releasing hormone (TRH); anterior pituitary

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118
Q

In the regulation of thyroid hormone: ______ cells in the anterior pituitary release _____.

A

thyrotropic cells; thyroid stimulating hormone (TSH)

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119
Q

In the regulation of thyroid hormone: TSH stimulates _____cells of the thyroid gland to release ______

A

follicular cells; thyroid hormone

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120
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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121
Q

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

A

metabolic activities

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122
Q

In the regulation of thyroid hormone: Increased body temperature is detected by the hypothalamus and the secretion of ____ by the hypothalamus is ____.

A

TRH; inhibited

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123
Q

In the regulation of thyroid hormone: Thyroid hormone also blocks TRH receptors on thyrotropic cell, inhibiting synthesis and release of ____. Both effects indirectly dampen ____ production in the thyroid.

A

TSH; TH

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124
Q

Thyroid hormone working to negatively feedback is an example of:

A

long loop negative feedback

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125
Q

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

A

endocrine disorders/ pathologies

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126
Q

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

A

thyroid goiter

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127
Q

Disease characterized by increased cortisol levels:

A

Cushing’s Disease

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128
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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129
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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130
Q

List the causes of primary hypersecretion:

A

endocrine gland tumor

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131
Q

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

A

secondary endocrine disorder

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132
Q

List the causes of secondary hypersecretion:

A

A lack of sufficient tropic hormone

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133
Q

List the causes of secondary hypersecretion:

A

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

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134
Q

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

A

paraneoplastic endocrine syndrome

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135
Q

When you think of primary endocrine dysfunction, you should think:

A

LAST GLAND IN PATHWAY

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136
Q

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

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

A

stimulation test

supression test

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137
Q

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

A

hyperfunction

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138
Q

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

A
  1. Plasma hormone levels
  2. Autoantibodies
  3. Urine hormone/ hormone metabolite levels
  4. Stimulation tests by admin of topic or stimulating hormone
  5. Suppression when hyperfunction of endocrine organ is suspected
  6. Measurement of hormone receptor presence, number and affinity
  7. Imaging
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139
Q

Stimulation test work by administering a ____ hormone.

A

tropic or stimulating

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140
Q

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

A

estrogen receptors in breast tumors

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141
Q

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

A
  1. Hashimoto thyroiditis
  2. Type I DM
  3. Graves Disease
  4. Addison disease
  5. Autoimmune hypothyroidism
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142
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), Adrenocorticoptropin hormone (ACTH) are all _____ hormones.

When are they made?

A

polypeptide/protein hormone

made in advance & stored

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143
Q

Epinephrine and Norepinephrine are both ____ hormones.

When are they made?

A

amine hormones

made in advance and stored

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144
Q

Thyroid hormone is a ____ hormone.

When is it made?

A

EXCEPTION:

amine hormone

made in advance and stored (does bind to nuclear receptor though)

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145
Q

Aldosterone, Crotisole, Estradiol and testosterone (mineralcorticoids, glucocorticoids and androgens) are all _____ hormones.

When are they made?

A

steroid hormones

made on demand

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146
Q

List things that would cause stimulation of growth hormone release

A

growth hormone releasing hormone, dopamine, catecholamines (in times of stress and exercise), excitatory amino acids, thyroid , fasting (hypoglycemia)

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147
Q

List things that would cause inhibition of growth hormone release

A

Somatostatin (SS), IGF-1 (due to negative feedback), Glucose (at high levels- hyperglycemia), and free fatty acids

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148
Q

GHRH, Dopamine, Catecholamines, Excitatory amino acids, and thyroid hormone would cause _____ of growth hormone release:

A

stimulation

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149
Q

Somatostatin, IGF-1, Glucose, and FFA would cause ____ of growth hormone release:

A

inhibition

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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 axons 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 located 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 (ACTH)
  4. TSH
  5. Prolactin
  6. Growth hormone
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156
Q

List the hormones secreted by the posterior pituitary:

A
  1. antidiuretic hormone/vasopressin (ADH)
  2. oxytocin
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157
Q

The pituitary gland secretes _____ hormones:

A

peptide

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158
Q

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

A

somatotrophs; GH

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159
Q

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

A

30-40%

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160
Q

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

A

Corticotrophs; ACTH

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161
Q

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

A

20%

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162
Q

Aside from corticotrophs and somatotrophs what other types of cells make up the anterior pituitary and what do they secrete?

A

Thyrotrophs-TSH
Gonadotrophs- LH & FSH
Mammotrophs- prolactin

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163
Q

Adenomas involving somatotropic cells can cause ____ if occurring in children before closure of the long bones epiphyseal plates or _____ in adults with musculoskeletal, neurologic, and other medical consequences.

A

gigantism; acromegaly

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164
Q

Benign tumors of epithelial cells that make 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 and secrete _______ hormones that control endocrine cells in the ____.

A

hypothalamic releasing and inhibiting; 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:

A

hypothalamic-hypophyseal portal blood vessels

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171
Q

The hypothalamic-hypophyseal portal blood vessels carry the hypothalamic hormones to the ____ of the anterior pituitary

A

sinuses

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172
Q

Regulation of Anterior Pituitary Secretion

  1. the _____ releases hormones that enter into the blood
  2. the hormones travel through the _____.
  3. the hormones continue down through the capillary bed to the ____ where they can leave the blood and regulate the activity of 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 vessel allows for:

A

communication from hypothalamus to 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 come 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-protein 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 will stimulate or inhibit anterior pituitary hormone secretion?

A

second messengers (examples= cAMP via adenylate cyclase, IP3, and DAG vis 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 hormones would be _____ (BRAKES)

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 hormones acts directly on target tissues and as a tropic hormone to the ____ which releases ____.

A

Liver; IGF-1

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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 in the liver to activate ____, a cell signaling pathway that causes release of _____.

A

JAK-STAT; IGF-1

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187
Q

A cell signaling pathway in the liver activated by growth hormone that responds by release of IGF-1

A

JAK-STAT

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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 are some effects?

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 GH acting on chondrocytes being necessary for linear growth, what is also necessary for linear growth?

A

IGF-1

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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 muscles to increase protein synthesis what is also necessary for protein synthesis?

A

IGF-1

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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 feed back of the 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 the GH secreted at the highest levels?

A

a few hours after sleep

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199
Q

Growth hormone 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 neonatal period:

The secretion of GH during childhood:

The secretion of GH during puberty:

The secretion of GH during adulthood:

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. IGF-1 (due to negative feedback)
  3. High glucose levels
  4. FFA (High levels of free fatty acids)
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203
Q

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

A

IGFs

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204
Q

IGFs can also be called:

A

somatomedins

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205
Q

IGF-1 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 IGF-1 synthesis:

A

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

IGF-1

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209
Q

Osteocytes responding to mechanical sensors can release:

A

IGF-1

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210
Q

Osteocytes responding to ______ can release IGF-1

A

mechanical sensors

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211
Q

After osteocytes release IGF-1 what happens?

A

IGF-1 binds to receptors on osteoblasts to enhance bone formation

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212
Q

Mechanisms of action of GH and IGF-1:

Growth in nearly all tissues of the body, mainly IGF-1 occurs through what mechanisms?

A
  1. increased cell size
  2. mitosis
  3. differentiation of bone and muscle cells
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213
Q

Mechanisms of action of GH and IGF-1:

What is the overall outcome of the effects of GH and IGF-1 causing growth in nearly all tissues of the body?

A
  1. increased organ size
  2. increased organ function
  3. increased linear growth
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214
Q

Mechanisms of action of GH and IGF-1:

The effect of amino acid uptake protein synthesis in most cells results in:

A

increased lean body mass

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215
Q

Mechanisms of action of GH and IGF-1:

How does this effect glucose?

A

reduced glucose utilization

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216
Q

Mechanisms of action of GH and IGF-1:

Reduced glucose utilization is due to:

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

Mechanisms of action of GH and IGF-1:

The reduced glucose utilization can lead to:

A

insulin resistance ; diabetogenic

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218
Q

Mechanisms of action of GH and IGF-1:

Describe the effects on fatty acids:

A

mobilization of fatty acids from adipose tissue (lipolysis)

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219
Q

Mobilization of fatty acids from adipose tissues:

A

lipolysis

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220
Q

Mechanisms of action of GH and IGF-1:

Lipolysis results in:

A

increases FFA in blood and use of FFA for energy

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221
Q

Before fusion of the epiphyseal plates, GH and IGF-1 stimulate:

A

chondrogenesis and widening of the epiphyseal plates

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222
Q

Following GH and and IGF-1 stimulating chorndrogenesis and widening of the epiphyseal plates, what occurs?

A

Bone matrix deposition stimulating linear growth

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223
Q

In adults, GH and IGF-1 play a role in regulating the normal physiology of:

A

bone formation

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224
Q

In adult, how do GH and IGF-1 play a role in regulating the normal physiology of bone formation?

A

by increasing bone turnover

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225
Q

How do GH and IGF-1 stimulate the increase in bone turnover (there by regulating bone formation)

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

Kids: GH and IGF-1 =

Adults: GH and IGF-1=

A

chondrogenesis

increased bone turnover

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227
Q

Osteoblasts are of what origin?

A

mesenchymal precursers

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228
Q

What is responsible for the formation of active osteoblasts from the osteoblast precursor?

A

IGF-1

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229
Q

Gigantism occurs in _____; while 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 with pituitary tumors that give rise to gigantism?

A

sella and cavernous sinus

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232
Q

Tumor causing excessive growth hormone release:

A

somatotropic adenoma of the pituitary

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233
Q

Describe the facial features 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, large fleshy nose, frontal bossing, and jaw malocclusion are collectively referred to as:

A

acromegalic faces

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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 affects on the heart and what conditions may occur as a result due to gigantism/acromegaly:

A

cardiomegaly; hypertension and coronary heart disease

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237
Q

Describe the chest and spine in individuals affected by acromegaly/gigantism:

A

barrel chest and kyphosis and hyperostosis

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238
Q

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

A

diabetes mellitus

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239
Q

Growth hormone shifts the body from utilizing ______ to _____ for metabolisms:

A

carbs to fats

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240
Q

Describe the reproductive consequences of gigantism/acromegaly:

A

male sexual dysfunction and menstrual disorders

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241
Q

Describe what can occur due to the thickened skin and hypertrophy of sebaceous and sweat glands in gigantism and acromegaly:

A

Hyperhidrosis and oily skin

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242
Q

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

A

thickened skin (hypertrophy of sebaceous and 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 microadenoma?

A

adenectomy via transphenoid approach followed by medications

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246
Q

Oral manifestations of GH excess: (7)

A
  1. thick rubbery skin, enlarged nose and thick lips
  2. macrocephaly
  3. macrognathia
  4. disproportionate mandibular growth
  5. anterior open bite and malocclusion
  6. macroglossia, dyspnea, dysphagia, dysphonia, sialorrhea,
  7. Hypertrophy of pharyngeal and 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 caused by excess growth hormone includes:

A

mandibular prognathism- jaw jets forward
generalized diastemata- separation of teeth

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249
Q

The anterior open bite and malocclusion in caused by excess GH is due to:

A

combo of macrognathia and tooth migration

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250
Q
  1. Macroglossia:
  2. Dyspnea:
  3. Dysphagia:
  4. Dysphonia:
  5. Sialorrhea:
A
  1. enlarged tongue
  2. difficulty breathing
  3. difficulty swallowing
  4. difficulty speaking
  5. slobbering
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251
Q

The hypertrophy of the pharyngeal and laryngeal tissues in individuals with excess GH can cause_____ and how?

A

sleep apnea - because of the increased growth of the pharyngeal and 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, IGF-1 receptor

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255
Q

A decrease in GHRH or an increase in GHIH could lead to:

A

growth hormone deficiency

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256
Q

What depends on the time of onset and severity of hormone deficiency? (talking about GH)

A

clinical manifestations

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257
Q

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

A
  1. slow linear growth rates (shorter stature)
  2. normal skeletal proportions
  3. pudgy, youthful appearance (decreased lipolysis)
  4. In setting of cortisol deficiency –> hypoglycemia
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258
Q

most common form of dwarfism, autosomal dominant condition, resulting from a mutation in the FGF-3 receptor in the cartilage and brain.

A

achondroplasia

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259
Q

The FGF-3 receptor mutation in achondroplasia makes the receptor overly active and it inhibits cartilage growth at growth plates so:

A

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

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260
Q

mutated receptor in achondroplasia:

A

FGF-3

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261
Q

Oral manifestations of GH deficiency include:

  1. disproportionate delayed growth of the ____ and ____ = ____ facial appearance
  2. ____ and ___ of the ___ regions of the jaws are abnormal and may be disproportionately smaller than adjacent anatomic structures.
  3. solitary ______.
  4. eruption of primary and secondary dentition and shedding of deciduous teeth are _____.
A
  1. skull and facial skeleton; small
  2. tooth formation and 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 and skeletal malocclusion

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263
Q

Incisor defects in a child with growth hormone deficiency occurs in both:

A

primary and permanent dentition

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264
Q

In oral manifestation of GH deficiency:

The tooth formation and growth of the alveolar regions of the jaws are abnormal and may be disproprotionately smaller than adjacent anatomic structures, this can cause:

A
  1. tooth crowding and malocclusion
  2. plaque accumulation
  3. poor oral hygiene
  4. gingivitis and 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 haev axons that go through the infundibulum with their synaptics terminals located in the posterior pituitary gland

A

paraventricular nucleus and 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 the names for the abreviation 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 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 and Oxytocin:

A

VERY Similar structure

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274
Q

What are the 2 primary functions of ADH:

A
  1. vasocronstriction (smooth muscle and blood vessels)
  2. antidiuretic (holds on to water)
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275
Q

ADH/AVP mechanism of action:

  1. Contaction 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

increase in BP

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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:

ADH functions in the renal tubules via:

A

V2 receptors

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280
Q

Where are the V2 receptors (for ADH) located?

A

Late distal tubule and collecting duct

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281
Q

What results when ADH binds to V2 in the late distal tubule and collecting duct?

A

AQP2 proteins are inserted into the apical membrane of tubular epithelial cells

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282
Q

Where is APQ2 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 tubule, and AQP2 being inserted into the apical membrane of tubular epithelial cells, what results?

A

This allows for water resabsorption (in accordance with AQP3 and AQP4) on the basolateral membrane)

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284
Q

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

A

AQP3 and AQP4 in the basolateral membrane

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285
Q

The V2 receptors in the late distal tubule and collecting duct and _____ 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, and _______ are always on the basolateral membrane and allow for the continuation of the water.

A

Aquaporin 2; Aquaporin 3&4

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288
Q

Stimuli for ADH secretion:

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

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

A

Isotonic

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290
Q

In regard to ADH secretion, increased osmolarity is considered:

A

Isovolemic

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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 BP is too low, ADH will function to _______ in order to raise it.

A

keep water

295
Q

ADH working to keep water in the body will resolve what 3 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 problem in elderly but is also associated with lesions in the hypothalamus (thirst center), head trauma, occult hydrocephalus or subsrachnoid hemmorhage

A

hypodipsia

299
Q

List causes of hypodipsia: (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 caused by:

A

ADH inbalance

301
Q

What are the two types of DI?

A

neurogenic (central)

nephrogenic (peripheral)

302
Q

What do DI and DM have in common?

A

Large urine output

303
Q

If you have an increased osmolarity, your would feel:

A

thirsty (under normal conditions)

304
Q

Disease caused by inability to produce and 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 the ADH (give them ADH)

307
Q

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

What might this result in if they are unable to produce ADH.

A

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 respond inappropriotely:

A

Nephrogenic/peripheral DI

311
Q

Describe the levels of ADH in someone with nephrogenic/peripheral DI; why?

A

High levels, because they can produce ADH and the stimulus causing the ADH secretion does NOT get corrected (causing the hypothalamus to secrete more and more)

312
Q

Uncharacteristically really high levels of ADH secretion and not because it is needed (oversecretion of ADH)

A

Syndrome of innappropriate ADH (SIADH)

313
Q

A patient with DI may present with:

A

polyuria

314
Q

Excretion of large volumes of urine:

A

polyuria

315
Q

Describe the urine in a patient with DI:

A

hypotonic and tasteless (Insipid)

316
Q

Other causes of polyuria may include: (Not DI)

A
  1. primary ingestion of excess fluid
  2. Increased 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 and 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 and stress

321
Q

Why do pregnant women pee more?

A

during pregnancy, ADH metabolism (breakdown of ADH) is increased, so more water is released

322
Q

What hormone causes milk ejection from the breasts in lactation?

A

Oxytocin

323
Q

What hormone stimulates contraction of the uterus toward 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 and prolactin:

A

permissive

327
Q

Where is prolactin released from?

A

anterior pituitary

328
Q

What does prolactin cause?

A

milk production

329
Q

What causes the milk ejection in the breast? (mechanism)

A

myoepithelial cell contraction

330
Q

What causes uterine contraction? (mechanism)

A

stretch of cervix at end of pregnancy

331
Q

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

A

sign

332
Q

Enlarged hands, polyuria, and tachycardia are all examples of:

A

signs

333
Q

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

A

symptoms

334
Q

Headache and numbness are both examples of:

A

a symptom

335
Q

Plasma Membrane Hormone Receptors:

List the 4 plasma membrane hormone receptors:

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

Plasma Membrane Hormone Receptors:

What are our two types of G-protein coupled receptors?

A

Gs and Gq

337
Q

Plasma Membrane Hormone Receptors:

Elaborate on the type of Gs coupled receptors:

What second messenger(s) do they produce?

A
  1. B-adrenergic
  2. Calcitonin
  3. ACTH
  4. Glucagon
  5. TSH
  6. Vasopressin

The produce the second messenger cAMP

338
Q

Plasma Membrane Hormone Receptors:

Elaborate on the types of Gq coupled receptors:

What second messenger(s) do they produce?

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

They produce the second messengers IP3, DAG and 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 we want a lot of cells to respond too

343
Q

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

A

T4

344
Q

About 7 % of the active hormones 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 hormones 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 the follicle?

A

Thyroglobuline

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 thryoid follicle=

A

colloid

353
Q

Where is thyroid hormone made and 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 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 follicular cells contain 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
  6. Once inside the colloid, the Iodide gets converted into ____.
A
  1. Iodine
  2. Iodide
  3. Na+/I- symporter (NIS)
  4. Concentrate the Iodide
  5. Pendrin; chloride; iodide
  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 access the ___ where the initial steps of thyroid hormone synthesis occur.

A

thyrocyte; apical membrane; colloid

360
Q

What enzymes works in the iodination and 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- in and Cl- out

363
Q

Pendrin is ALWAYS:

A

moving two negatively charged substances in opposite directions

364
Q

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

A

Thyroglobulin

365
Q

The enzyme involved in all of the production steps in the formation of thyroid hormone (tyrosine, monoiodotyrosine, diiodotyrosine, T3, RT3, and T4)

A

peroxidase

366
Q

Thyroglobulin is made of:

A

a bunch of tyrosine amino acids

367
Q

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

A

pendrin THEN peroxidase

368
Q

T3 and T4 secretion into the blood:

  1. _____ is internalized by endocytosis
  2. The vesicles fuse with ____ in the cell
  3. _____ cleaves T3 and T4 from ____.
  4. T3 and T4 diffuse out of the cell and into ____.
A
  1. colloid
  2. lysosomes
  3. protease; TG
  4. capillaries
369
Q

Colloid is a _____ of thyroid hormones

A

reservoir

370
Q

Majority if not all of T3 and T4 bind with _____ for transport

A

plasma proteins

371
Q

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

A

Thyroxine binding globulin (TBG)

Transthryretin (TTR)

Albumin

372
Q

What causes the long half life of T4?

A

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

T3 and T4 secretion into the blood:

Colloid is taken into the follicular cell via:

A

pinocytosis

375
Q

T3 and T4 secretion into the blood:

T3 and 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 3 different deoiodinases?

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 the enzymatic activity.

A

selenium; sulfur

381
Q

What are carious conditions that inhibit deiodinase activity?

A
  1. selenium deficiency
  2. burns
  3. trauma
  4. advanced cancer
  5. cirrhosis
  6. chronic kidney 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 action occurs ____ compared to T4

A

sooner

384
Q

When does the maximum activity of T3 hormone occur?

A

~2-3 days

385
Q

Compare the activity of T4 to T3

A

T4 has a slower onset but long 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 and synthesis of new proteins

387
Q

The synthesis of new proteins due to the action of T3 and T4 can lead to what 5 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 and T4 synthesizing new proteins that affect metabolism?

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 HR
  4. Increased heart strength
  5. Increased respiration
391
Q

The cardiovascular effects of thyroid hormone are caused by an increased in ______ which is a _____ effect.

A

beta receptors; permissive effect

392
Q

Negative feedback of the thyroid hormone is mainly at the level of ____ but can also occur at ____.

A

anterior pituitary; hypothalamus

393
Q

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

A

anterior pituitary and hypothalamus

TSH and TRH

394
Q

What actually causes the feedback inhibition of thyroid hormone?

A

The anterior pituitary and hypothalamus increasing their expression of deiodinase activity so when T4 levels in these tissues increase, they readily convert it (via deiodinase) to T3 which causes the inhibition

395
Q

Describe the secretion of TSH:

A

pulsatile with increases in evening hours and peak ~ midnight

396
Q

Describe the secretion of Thyroid hormone:

A

Thyroid secretion mirrors TSH secretion (pulsatile with increases in evening hours and peak around midnight) but also is tonically secreted (small amounts)

397
Q

Thyroid hormones stimulates _____ by most metabolically active tissues

A

oxygen consumption

398
Q

How does thyroid hormone effect BMR?

A

increases it

399
Q

Thyroid hormone stimulates ______ metabolism

A

carbohydrate

400
Q

Thyroid hormone stimulates carbohydrate metabolism by:

A
  1. uptake of glucose by cells
  2. enhances glycolysis and gluconeogensis
  3. increases CHO absorption from GI tract
401
Q

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

A

stimulates protein catabolism and synthesis but more catabolism (breakdown)

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 and 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 —> vitamin A

405
Q

Vitamin A is important in:

A

wound healing

406
Q

Thyroid hormone is responsible for decreasing circulating _____ levels.

A person with hypothyroid may have _____ due to this.

A

cholesterol levels

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 devleopment

409
Q

Thyroid hormone impacts _____ so someone with hypothyroidism may have prolonged ___.

A

reflex time; prolonged reflex time

410
Q

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

A

muscle tremors

411
Q

If someone feels tires, but has difficulty sleeping and anxiety, worry and paranoia they may have: (relating to thyroid hormone)

A

hyperthyroidism

412
Q

hyperthyroidism effected on cardiovascular system include:

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

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

A

Thyroid hormone increases the 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 needed to maintain ____ levels.

A

glucose; insulin; blood glucose

415
Q

Thyroid hormone effects on the endocrine system:

The 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:

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 increased _____ and _____ intake.

A

appetite and food

418
Q

Thyroid hormone effects on the GI system:

Thyroid hormone causes increased rate of ______ and _____ of GI tract.

Individuals with hyperthyroidism may have _____ due to this, while individuals with hypothyroidism may have ____ due to this.

A

secretion and motility

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 and euthyroidism

422
Q

Goiter can be caused excessive amounts of _____ secretion.

A

TSH

423
Q

High TSH stimulates thyroid to stimulate larges amounts of _____ into ______ resulting in gland enlargement/ goiter

A

Thyroglobin colloid into follicles

424
Q

The most common form of hyperthyroidism

A

Grave’s disease

425
Q

Although Grave’s disease is the most common form of hyperthyroidism, hypothyroidism can also occur due to:

A

thyroid adenoma

426
Q

Grave’s disease is a _____ disease.

Explain this:

A

autoimmune disease.

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 and T4)

427
Q

Describe the category of disorder that Grave’s disease is, and who the hypothalamus and anterior pituitary are affected:

A

Primary endocrine disorder- bc issue is at level of thyroid gland

strong negative feedback causes TSH and TRH levels to be reduced

428
Q

Grave’s disease is more common in:

A

The gals

429
Q

List the signs and symptoms of Grave’s dizzzeeeez

A
  1. sweating/heat intolerance
  2. increased metabolism
  3. increased appetite
  4. weight loss
  5. fine hair/ protein synthesis
  6. increase NS response (emo instability, insomnia, nervy, resletessness)
    7.fine tremor
  7. goiter
  8. exophthalmos (bug eyed)
  9. pre-tibial myxedema
430
Q

Treatment for the gravy:

A

radioactive iodine to ablate the thyroid followed by L thyroxine (T4) to prevent hypothyroidism, surgery rarely indicated

antithyroid drugs

beta-blockers to block permissive effect of thyroid hormone

431
Q

Oral symptoms of hyperthyroidism may include:

A
  • burning mouth syndrome
  • gum disease
  • excessive salivation
  • weakening of mandible
  • increased caries risk
432
Q

Elevated thyroid hormone with stressful events or serious illness causing fever, tachycardia, elevated BP, nausea, vomiting, diarrhea and breathing problems:

A

thyroid storm (thyrotoxicosis)

433
Q

What can bring on a thyroid storm?

A

-trauma
-surgery
-infection
-DKA
-MI

434
Q

Overall a thyroid storm can be described as:

A

exaggerated sympathetic response

435
Q

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

A

administration of epinephrine is CONTRAINDICATED and elective dental care should be deferred

436
Q

autoimmune reaction against the thyroid gland that destroys it rather than stimulates it

A

hashimotos thyroiditis

437
Q

What is the most common cause of hypthyroidism?

A

Hashimoto’s thyroiditis

438
Q

Prior to diagnosis of hashimoto’s thyroiditis, most patients first exhibit:

A

autoimmine thyroiditis

439
Q

In hashimoto’s thyroiditis, inflammation leads to ___ of the thyroid resulting in _____.

A

fibrosis; decreased section of thyroid hormone

440
Q

What is the target of the antibodies in hashimotos thryoiditis?

A

peroxidase

441
Q

What class of disorder is Hashimoto’s characterized by?

A

primary endocrine disorder

442
Q

Another form of hypothyroidism (not hashimoto’s) is due to:

A

low iodine

443
Q

Hypothyroidism due to low iodine is classified as:

A

primary endocrine disorder

444
Q

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

A

T3 and T4 low; and TRH and TSH high

445
Q

In hypothyroid states, goiter is due to _____, while no goiter is due to _____.

A

iodine deficiency; TSH deficiency

446
Q

Hypothyroidism due to iodine deficiency = ______ = _____ deficiency

Hypothyroidism due to TSH deficiency = _______ = ______ deficiency

A

goiter; primary

no goiter; secondary

447
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. hair loss
  9. loss of lateral eyebrows
  10. slow pulse (bc decreased # of beta receptors)
  11. enlarged heart
  12. facial edema
  13. peripheral edema
448
Q

Unique symptom seen in severe hypothyroid cases:

A

myxedema

449
Q

In hyperthyroidism patients, where does the myxedema occur?

In hypothyroidism patients, where does the myxedema occur?

A

hyper= pretibial myxedema

hypo= face

450
Q

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

A

hyaluronic acid and chondroitin sulfate

451
Q

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

A

myxedema; L-thyroxine (T4)

452
Q

Required for post-natal brain maturation

A

Thyroid hormones

453
Q

Results from congenital absence of thyroid gland:

A

congenital cretinism

454
Q

Results from iodine deficient diet; most common cause world wide:

A

endemic cretinism

455
Q

Cretinism can cause ______ of neonates.

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

A

physical and mental retardation

Obese, stocky and short with large protruding tongue

456
Q

Cretinism can cause lack of development of ____.

A

nervous system

457
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
458
Q

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

A

decreased activity of fibroblasts

459
Q

Patients with hypothyroidism are sensitive to:

A

central nervous system depressants and barbiturates

460
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

461
Q

Only 0.1% of the body’s calcium is found in the:

1% of the body’s calcium is found in the:

The rest of the body’s calcium is stored in the:

A

ECF
Cells and organelles
bones

462
Q

When levels of calcium are too low:

A

neuronal hyper-excitability (tetany due to extra Na+ influx)

463
Q

When levels of calcium are too high:

A

neuronal depression (blocks Na+ influx)

464
Q

Carpal spasms can be due to:

A

HYPOcalcemia

465
Q

Control points for calcium and phosphate include:

A
  1. absorption- via intestines
  2. excretion- via urine (calcium and phosphate) and feces (calcium only)
  3. temporary storage- via bones (hydroxyapatite)
466
Q

Ca(10)PO4(6)OH(2)

A

hydroxyapatite

467
Q

What the hormones that regulate plasma calcium?

A

PTH, Calcitriol, and Calcitonin

468
Q

How does PTH regulate plasma calcium and phosphate?

A

Increases plasma calcium
Decreases plasma phosphate

469
Q

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

A
  1. mobilizes calcium from bone
  2. Enhances renal reabsorption of calcium
  3. Increases intestinal absorption of calcium (INDIRECTLY)
470
Q

How does calcitriol regulate plasma calcium and phosphate?

A

Increases plasma calcium
Increases plasma phosphate

471
Q

How does calcitriol work to raise plasma calcium and phosphate?

A

Calcitriol is the primary hormones that enhances intestinal absorption of calcium and it also causes absorption of phosphate

472
Q

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

A

Calcitriol

473
Q

What are the other names for calcitriol?

A

1,25-dihydroxycholecalciferol

Vitamin D3

474
Q

Calcitriol acts on the intestines ______ to enhance absorption of calcium and also phosphate. While PTH acts on the intestines _____ to enhance absorption.

A

Directly; Indirecty

475
Q

Calcitonin comes from:

A

parafollicular cells of the thyroid gland

476
Q

How does calcitonin regulate plasma calcium and phosphate?

A

Decreases plasma calcium and phosphate

477
Q

How does calcitonin work to lower plasma calcium and phosphate?

A

It stimulates bone formation

478
Q

What hormones stimulate bone formation?

A
  1. calcitonin
  2. insulin
  3. growth hormone
  4. IGF-1
  5. estrogen
  6. testosterone
479
Q

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

A

Calcitriol and PTH

480
Q

Calcitriol and parathryoid hormone stimulate bone matrix _______ .

How does this effect plasma calcium?

A

resorption; increases plasma calcium

481
Q

Bone resorption:

  1. Osteoblasts release ______.
  2. ____ binds to the _____ on preosteoclasts and this leads to activation of _____.
A

1.RANK ligand
2. RANK-L binds to the RANK receptors; osteoclasts

482
Q

What is the goal of bone resorption?

A

Increase plasma calcium levels

483
Q

What type of cell is activated during bone resorption? What activates this type of cell?

A

Osteoclasts; Rank Ligand

484
Q

Factors that stimulate bone matrix resoprtion:

A
  1. PTH
  2. Excessive levels of calcitriol
  3. Prolactin
  4. Corticosteroids
485
Q

What is the goal of bone deposition?

A

form bone, take calcium out of blood and put into bone

486
Q

_____ stimulates bone matrix deposition and inhibits osteoclasts.

A

calcitonin

487
Q

Calcitonin stimulates bone matrix deposition and inhibits osteoclasts which ultimate does _____ to plasma calcium.

A

decreases

488
Q

If calcium levels in the blood are sufficient, we don’t need to:

A

break down bone

489
Q

Anabolic or anti-resorptive factors (for bone)=

A
  1. estrogens
  2. calcitonin
  3. testosterone
  4. calcium
  5. BMP
490
Q

In order to avoid RANK-L further activating osteoclasts, ____ will bind to RANK-L to prevent it from binding to the RANK-L receptor

A

OPG

491
Q

OPG binding to RANK-L ultimately leads to:

A

apoptotic osteoclasts

492
Q

Osteoclasts that do NOT function to break down bone:

A

Apoptotic osteoclasts

493
Q

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

A

Osteoporosis

494
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
495
Q

Describe why Vitamin D deficiency can lead to osteoporosis:

A

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

496
Q

Describe why inadequate calcium intake can lead to osteoporosis:

A

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

497
Q

Describe why glucocorticoid medications can lead to osteoporosis:

A

They supress the immune response leading to risk of weak and brittle bones

498
Q

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

A

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

499
Q

Treatments for osteoporosis include:

A
  1. exercise
  2. PT
  3. Estrogen replacement
  4. Calcium
  5. Vitamin D
  6. Bisphosphonates
500
Q

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

A

PTH

501
Q

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

A

Parathyroid glands

502
Q

Parathyroid hormone (PTH) is secreted by:

A

chief cells

503
Q

What are the effect of PTH? How?

A

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

504
Q

How does PTH decrease plasma phosphate?

A

Increasing renal excretion

505
Q

Describe the renal excretion effects on calcium and phosphate by PTH:

A

Increases renal excretion for phosphate

Decreases renal excretion for calcium

506
Q

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

A

It causes more synthesis of vitamin D, which in turn causes more intestinal absorption of calcium.

507
Q

When PTH is secreted to to decreased ECF calcium, this leads to:

A

Hypertrophy of parathyroid gland

508
Q

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

A

Increase

509
Q

What conditions would lead to hypertrophy of the parathyroid gland:

A

Chronic cases - pregnancy, rickets, and lactation

510
Q

Chronically, if you hypertrophy the parathyroid gland, it becomes:

A

even better at secreting PTH

511
Q

Increased ECF concentration of calcium leads to ______ of the parathyroid gland.

A

decreased activity

512
Q

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

A

decrease

513
Q

What conditions can cause a decrease in activity and 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
514
Q

Describe the effect on plasma calcium:

Bone resorption:

A

increases plasma calcium

515
Q

Describe the effect on plasma calcium:

Resabsorption of calcium by renal tubules

A

increases plasma calcium

516
Q

Describe the effect on plasma calcium:

Conversion of 25-hydroxycholecalciferol to 1-25dihydroxycholecalciferol

A

increases plasma calcium

517
Q

Describe the effect on plasma phosphate:

Decreased reabsorption by renal tubules:

A

decreases plasma phosphate

518
Q

Where do we get cholecalciferol (vitamin D3) from:

A

skin (from sun)

519
Q

In the process of calcitriol synthesis, cholecalciferol is converted to ______ ; by what organ?

A

25-hydroxycholecalciferol ; liver

520
Q

In the process of calcitriol synthesis, 25-hydroxycholecalciferol is converted to _____; by what organ?

A

1-25 dihydroxycholecalciferol (Calcitriol); kidney

521
Q

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

A

parathyroid hormone

522
Q

Where is the main effect of calcitriol?

A

Intestines - absorption of calcium and phosphate from diet

523
Q

Where can calciferol act although not the main effect?

A

Kidneys (reduced excretion of calcium and phosphate); Bones (indirectly causes bone deposition)

524
Q

Vitamin D3 can be stored in the liver for:

A

several months

525
Q

Describe the regulation of calcitriol levels:

A

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

526
Q

Someone with a compromised liver or kidney function may exhibit:

A

Vitamin D deficiency

527
Q

peptide hormone secreted by parafollicular cells

A

calcitonin

528
Q

Parafollicular cells reside in the _____ and may also be called _____.

A

thryoid gland; C-cells

529
Q

Calcitonin is released in response to:

A

elevated free plasma calcium

530
Q

Calcitonin lowers the level of plasma calcium by decreasing the activity of ____, thus decreasing _____.

A

decreases the activity of osteoclasts thus decreasing bone resorption

531
Q

Not a major controller of calcium in humans:

A

calcitonin

532
Q

What two systems does calcitonin act on?

A

bone and kidneys

533
Q

Excess PTH secretion due to a parathryroid gland tumor:

A

primary hyperparathyroidism

534
Q

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

A

osteoclastic activity; cystic bone disease; osteitis fibrosa cystica

535
Q

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

A

cystic bone disease (osteoitis fibrosa cystica)- primary hyperparathryoidism

536
Q

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

A

polyuria and calciuria

537
Q

What happens to phosphate levels and why in patients with primary hyperparathyroidism:

A

low phosphate due to increased renal excretion

538
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)

539
Q

Primary hyperparathyroidism signs and symptoms include:

A

Stones, Bones, abdominal groans, and psychic moans

540
Q

Describe the stone component to primary hyperparathyroidism:

A
  1. renal stones
  2. nephrocalcinosis
  3. polyuria
  4. polydipsia
  5. uremia
541
Q

Describe the bones component to primary hyperparathyroidism:

A
  1. cystic bone disease
  2. osteomalacia/rickets
  3. arthritis
542
Q

Describe the abdominal groans component of primary hyperparathyroidism:

A
  1. constipation
  2. indigestions
  3. nausea
  4. vomiting
  5. peptic ulcers
  6. pancreatitis
543
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, suport, coma
544
Q

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

A
  1. proximal muscle weakness
  2. Keratitis
  3. conjunctivitis
  4. Hypertension
  5. itching
545
Q

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

A

secondary hyperparathyroidism

546
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
547
Q

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

A

osteoporosis

548
Q

Disease that would result from accidental surgical parathyroid gland removal, not common

A

primary hypoparathyroidism

549
Q

What increases membrane Na+ permeability leading to neuromuscular excitability and muscle spasms

A

hypocalcemia

550
Q

What the condition name for the wonky ass hand:

A

carpal spasm

551
Q

How many adrenal glands and where are they located?

A

2 adrenal glands, located on top of each kidney

552
Q

describe the structure of a adrenal gland?

A

outer cortex + inner medulla

553
Q

What portion of the adrenal gland is essential for life?

A

Adrenal cortex

554
Q

The adrenal cortex secretes:

A
  1. corticosteroids
  2. mineralcorticoids
  3. sex hormones
555
Q

Is the adrenal medulla essential for life?

A

no

556
Q

The adrenal _____ is a true endocrine organ

A

cortex

557
Q

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

A

Secreting epinephrine and norepinephrine in resonse to sympathetic nervous system stimulation

558
Q

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

A

emergencies

559
Q

The adrenal cortex secretes several hormones that are made from:

A

cholesterol

560
Q

What are the 3 layers of the adrenal cortex?

A

Zona glomerulosa
Zona fasiculata
Zona reticularis

561
Q

The largest zone of the adrenal cortex

A

fasculata

562
Q

The zona glomerulosa secretes ______ and is regulated by ______.

A

mineralcorticoids; RAAS

563
Q

RAAS stands for:

A

Renin-angiotensin-aldosterone system

564
Q

The zona fasciulata secretes _____ and is regulated by _____.

A

glucocorticoids; HPA (CRH and ACTH)

565
Q

HPA stands for:

A

hypothalamic-pituitary -adrenal axis

566
Q

The zona reticularis secretes ____ and is regulated by ____.

A

androgens; HPA

567
Q

The adrenal medulla is related to the ____ and secretes _____.

A

Sympathetic Nervous System; Catecholamines

568
Q

What type of cells secrete catecholamines?

A

chromaffin cells

569
Q

Where do the chromaffin cells of the adrenal medulla secrete Epi and NE?

A

into the blood

570
Q

What are the three tissues involved in the HPA?

A

Hypothalamus, Pituitary, Adrenal gland

571
Q

Why does the zona glomerulosa secrete so much aldosterone?

A

Because enzymes involve din the formation of aldosterone from cholesterol are highly expressed in the zona glomerulosa

572
Q

What enzyme is responsible for the conversion of Cortisol to corisone?

A

11HSD Beta 2

573
Q

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

A

11HSD Beta 1

574
Q

The reactions that occur for the synthesis of steroid hormones in the adrenal cortex take place in the:

A

mitochondria or endoplasmic reticulum

575
Q

Describe the activity of cortisone at cortisol receptors

A

reduced activity

576
Q

Can be used to make testosterone and androgens:

A

Androstenedione

577
Q

Aldosterone is classified as a:

A

mineralcorticoid

578
Q

Aldosterone functions in the kidneys to:

A
  1. increased renal reabsorption of Na+
  2. increase renal secretion of K+
579
Q

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

A

Increase in ECF fluid volume and mean arterial pressure

580
Q

What stimulates aldosterone secretion?

A
  1. angiotensin II
  2. Increased levels of K+
  3. Decreased levels of Na+
581
Q

Aldosterone has effects on:

A
  1. kidney
  2. sweat glands
  3. salivary glands
582
Q

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

A

Zona glomerulosa

583
Q

What are the main functions of angiotensin II?

A
  1. vasoconstriction
  2. release of aldosterone
584
Q

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

A

release of aldosterone

585
Q

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

A

Water retention occurs because where sodium goes water follows

586
Q

The effects of aldosterone on sweat glands is important to:

A

conserve body salt in hot environments

587
Q

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

A

conservation of sodium during high rates of salivary secretion

588
Q

In addition to hyperkalemia, _____ causes secretion of aldosterone

A

angiotensin II

589
Q

Enzyme released by the cells in the kidneys in response to a variety of stimui (example SNS)

A

Renin

590
Q

Angiotensin converting enzyme (ACE) is produced by the:

A

endothelium

591
Q

List the steps of RAAS

A

Angiotensinogen gets converted to angiotensin I by the enzyme Renin

Angiotensin I gets converted to Angiotensin II by the enzyme ACE

592
Q

Angiotensin II ultimately causes secretion of _____ but also does _____, _____, and _____.

A

ultimately aldosterone secretion but also ADH secretion, thirst stimulation, and vasoconstriction

593
Q

What do vasconstriction, aldosterone secretion, ADH secretion and thirst stimulation all have in common?

A

All these work to raise BP

594
Q

In RAAS, the non-active precursor made by the liver and found in the plasma:

A

angiotensinogen

595
Q

Where is large amounts of ACE found?

A

In the lungs- COVA

596
Q

A lot of _____ medications target RAAS

A

HTN

597
Q

How do ACE inhibitors work?

A

If you inhibit ACE you will make less angiotensin II

598
Q

Primary hyperaldosteronism may also be called:

A

Conn’s Syndrome

599
Q

In primary hyperaldosteronism, where is the problem?

A

adrenal gland

600
Q

What are the causes of primary hyperaldosteronism?

A
  1. adrenal adenoma (benign)
  2. adrenal hyperplasia
  3. adrenal carcinoma (malignant)
601
Q

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

A

Low levels of renin

602
Q

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

A
  1. HTN
  2. Hypernatremia
  3. Hypokalemia
  4. Headaches
  5. Weakness
  6. Fatigue
  7. HYPOKALEMIC ALKALOSIS
  8. LOW PLASMA RENIN
603
Q

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

A

Due to so much aldosterone being produced and it strongly negatively feedingback

604
Q

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

A

Hypokalemic alkalosis

605
Q

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

A

H+ levels in the ECF

606
Q

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

A

surgical removal of tumor or most of the adrenal tissue when hyperplasia is present, or a minercorticoid receptor antagonist

607
Q

Caused by decreased bloodflow and pressure in the renal artery, (the kidney thinks BP is low and secretes renin excessively)

A

Secondary hyperaldosteronism

608
Q

Describe the levels of renin in secondary hyperaldosteronism:

A

High levels of renin

609
Q

What are causes of secondary hyperaldosteronism?

A
  1. CHF
  2. Renal artery stenosis
610
Q

How might CHF lead to secondary hyperaldosteronism?

A

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

611
Q

How might renal artery stenosis lead to secondary hyperaldosteroneism?

A

Renal artery pumps blood to kidney and there can be an atherosclerotic plaque in the vessel resulting in decreased bloodflow to kidney. The kidney now thinks BP is low and secretes excessive renin to try and compensate for the “low BP” and then that extra renin causes extra angiotensin II which leads to extra aldosterone

The other kidney is working just fine

612
Q

Signs and symptoms of secondary aldosteronism include:

A
  1. high plasma renin
  2. hypernatremia with extracellular volume expansion
  3. edema
  4. decreased cardiac output
  5. similar clinical findings as primary hyperaldosteronism
613
Q

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

A

Cortisol

614
Q

What hormone is secreted in response to stress?

A

Cortisol

615
Q

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

A

glucocorticoid; zona fasiculata

616
Q

More cells in the adrenal cortex make ____ than any other cells because of the size of the zona fasiculata

A

cortisol

617
Q

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

A
  • heat
  • cold
    -hypo/hyperglycemia
    (not just psychological stress)
618
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

suppresses the immune system

619
Q

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

A

early morning hours; growth hormone

620
Q

Cortisol feedsback and inhibits:

A
  1. ACTH secretion from AP
  2. CRH secretion from hypothalamus
621
Q

Describe what type of feedback is seen through cortisol:

A

Long loop

622
Q

What are the 4 main actions of cortisol?

A
  1. Gluconeogenesis
  2. Protein mobilization
  3. Fat mobilization
  4. Stabilizes lysosomes
623
Q

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

A

Stabilizing lysosomes

624
Q

Why are other hormones secreted when ACTH is secreted?

A

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

625
Q

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

A

Proopiomelanocortin (POMC)

626
Q

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

A
  1. Melanocyte stimulating hormone (MSH)
  2. Beta endorphin
  3. Beta lipotropin
627
Q

A clinical sign of elevated ACTH pathologically is:

A

increased skin pigmentation (from melanocytes)

628
Q

What is a byproduct of ACTH production?

A

MSH

629
Q

Cortisol has a similar affinity for the ____ receptor as ____.

A

mineralcorticoid receptor (MR) as aldosterone

630
Q

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

A

Cortisol

631
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)

632
Q

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

A

cortisone; cortisol

633
Q

A genetic deficiency in the 11B2HSD receptor leads to the syndrome:

A

AME (Apparent Mineralocorticoid excess)

634
Q

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

A

glycerrhetinic acid; 11B2HSD

635
Q

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

A

Increased sodium reabsorption and increased potassium secretion

636
Q

Where would we find 11B2HSD receptors? Where would we find 11B1HSD receptors?

A

kidneys, salivary glands, sweat glands

skin

637
Q

High circulating cortisol levels such as in cushings syndrome can:

A

Overwhelm the 11HSDB2 enzyme

638
Q

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

A

High BP

639
Q

Effects of cortisol on metabolism:

Stimulation of both ___ and _____ in the liver resulting in _____.

A

gluconeogenesis; glycogenolysis; increases blood glucose

640
Q

Effects of cortisol on metabolism:

____ action resulting in decreased glucose uptake in the muscle and fat but not the brain or heart.

A

anti-insulin action

641
Q

Effects of cortisol on metabolism:

Makes ___ worse by increasing ___ levels, ____ level, and ____ formation and ____ secretion.

A

diabetes
glucose levels
lipid levels
ketone body formation
insulin secretion

642
Q

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

A

cortisol and insulin are antagonists

643
Q

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

A

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

644
Q

Effects of cortisol on metabolism:

Inhibits ____ synthesis and increases ____ especially in skeletal muscles.

A

protein synthesis; proteolysis (provides source of AA for glycoenogenesis)

645
Q

Effects of cortisol on metabolism:
Cortisol excess leads to ___ weakness, pain, ____ skin and abdominal ____ due to the protein catabolic effect.

A

muscle weakness
thin skin
abdominal striae

646
Q

Effects of cortisol on metabolism:

promotes ____; and shifts the energy system from utilization of _____ to _____ in times of stress.

A

lipolysis

glucose to fatty acids

647
Q

Effects of cortisol on metabolism:

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

A

lipid

648
Q

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

A

cortisol

649
Q

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

A

circulatory failure; permissive action; catecholamines

650
Q

Lack of cortisol also prevents mobilization of _____ (glucose and free fatty acids) during stress and can result in ____.

A

energy sources; fatal hypoglycemia

651
Q

Vasoconstriction of blood vessels occurs via:

A

alpha 1 receptor

652
Q

Describe the effect cortisol has on catecholamines (alpha 1 receptor) on blood vessels

A

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

653
Q

Why would blood pressure decrease when cortisol levels are low?

A

The presence of cortisol allows the alpha receptors response to be maximized, so without the maximum response, blood pressure would be lower

654
Q

How does cortisol effect the immune system?

A

suppresses immune system function

655
Q

What are few ways that cortisol suppresses the immune system:

A
  1. stabilizes the lysosomal membrane
  2. opposes inflammation (decrease WBC migration and phagocytosis)
  3. suppresses T-Lymphocytes
656
Q

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

A

Their anti-inflammatory action

657
Q

How can treatment with glucocorticoids cause osteoporosis?

A

because cortisol stimulates bone resorption via an increase in RANK-L expression by osteoblasts

658
Q

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

A

osteoblasts and osteocytes

659
Q

The zona reticularis is responsible for the secretion of:

A

androgens

660
Q

The zona reticularis begins secreting adrenal androgens around the age ____ , peaking around age _____, and then _____ with age.

A

age 8, age 20, decreasing with age

661
Q

Adrenal androgens secreted by the zona reticularis include:

A

DHEA/DHEAS
Andostenodione
Testosterone
Estrogens

662
Q

Describe the effects of adrenal androgens in males vs. females:

A

andrenal androgens have only weak effects in makes but contribute ~50% of active androgens in females

663
Q

Describe the effects of adrenal androgens in females:

A

growth of pubic hair, axillary hair, and libido

664
Q

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

A

precocious pseudopuberty

665
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

666
Q

If boys are affected by precocious psuedopuberty brought on by excessive androgen secretion from the adrenal gland, this can cause:

A

early development of secondary sexual characteristics (under age 8)

667
Q

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

A

21-hydroxylase deficiency

668
Q

21-hydroxylase deficiency leads to an overproduction of:

A

androgens (DHEA, DHEAS, Androstenedione)

669
Q

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

A

virilization and and precocious pseudopuberty in females

670
Q

Precocious psuedopuberty:

A

early puberty not caused by HPA secreting GRH and instead due to adrenal androgens in excess

671
Q

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

A

aldosterone and cortisol

aldosterone and cortisol

androgen precursors (DHEA, DHEAS, Androstenedione)

672
Q

Androstenedione is a precursor to:

A

testosterone, 5-dihydrotestosterone, and estrogens

673
Q

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

A

greatest effect

674
Q

Why does the precursor androstenedione have the greatest affect (compared to DHEA and DHEAS)?

A

because it is more readily converted peripherally to testosterone and estrogens

675
Q

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

A

aldosterone or cortisol

676
Q

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

A

ovarian tumors

677
Q

Virilizing adrenal tumors are ___, and virilization is usually due to _____.

A

rare; hypersecretion of adrenal androgens

678
Q

List some signs and symptoms of virilizations:

A

Male pattern baldness, male musculature, clitoromegaly, increased libido, rapid linear growth with advanced bone age

679
Q

Primary adrenal insufficiency:

A

Addison’s Disease

680
Q

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

A

adrenal cortex

681
Q

In about 80% of Addison’s cases, atrophy occurs due to ______ of all cortical zones

A

autoimmune destruction

682
Q

Describe the level of ACTH in Addison’s dx

A

High ACTH

683
Q

Describe the levels of corticosteroid production in Addisons disease:

A

Low corticosteroids

684
Q

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

A

glucocorticoid, mineralcorticoid and adrogen secretion

685
Q

Secondary adrenal insufficiency is due to low levels of:

A

ACTH

686
Q

IF the pituitary gland is unable to secrete enough ACTH this would result in:

A

low cortisol production (secondary adrenal insufficiency)

687
Q

Often latrogenic due to abrupt cessation of steroid therapy:

A

secondary adrenal insufficiency

688
Q

What is affected in primary adrenal insufficiency that is not affected in secondary adrenal insufficiency?

A

mineralcorticoid secretion

689
Q

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

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

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

A

Both- both have lack of cortisol production

primary only

Both- Addisons has loss of androgens; and then secondary has low ACTH leading to low androgen production

690
Q

Two important symptoms of glucocorticoid deficiency include:

A

hypoglycemia because normally raises blood glucose

Low BP due to the lack of alpha 1 receptor permissive effect

691
Q

Hyperpigmentation in primary adrenal insufficiency is due to excess of:

A

POMC-

692
Q

Cushings Disease is a _____ disorder characterized by ______.

Cushings syndrome is a _____ disorder characterized by _____.

A

secondary- occurs due to brain- High ACTH

primary- occurs due to adrenal cortex- low ACTH

693
Q

Both cushings disease and syndrome is characterized by:

A

high cortisol levels

694
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
695
Q

To distinguish between cushings disease and syndrome, what hormone level would you look at?

A

ACTH

696
Q

Conn’s syndromes is an issue with ______

Cushings syndrome is an issue with ____

Pheochromocytoma is an issue with ____

A

mineralcorticoids

glucocorticoids

catecholamines

697
Q

Sudden release of hormones causing sudden “attack” due to chromaffin cell tumor in the adrenal medulla resulting in excessive secretion of EPI and NE

A

Pheochromocytoma

698
Q

What cells are involved in pheochromocytomas?

A

chromaffin cells

699
Q

Can be characterized by an exaggerated sympathetic response:

A

Pheochromocytoma

700
Q

What hormones are inovled in pheochromocytoma?

A

Epi and NE

701
Q

Entire length of thick filament (some overlapping thin filament)

A

A-band

702
Q

Includes ONLY thin filaments:

A

I-band

703
Q

ONLY thick filaments:

A

H-zone

704
Q

Where thin filaments are anchored:

A

Z-line

705
Q

Links the central regions of thick filaments:

A

M-line

706
Q

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

A

Increases

707
Q

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

A

Decreases

708
Q

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

A

THE A-BAND DOES NOT CHANGE IN LENGTH

709
Q

Why does the A- band not change length?

A

Its the length of the thick filament

710
Q

Functional unit of skeletal muscle:

A

sarcomere

711
Q

The thin filament is composed of what 3 elements?

A

actin, tropomysin and torponin

712
Q

What type of actin molecules make up the active site in which myosin binds?

A

G-actin

713
Q

What all does troponin bind?

A

actin, tropomoysin and calcium

714
Q

Troponin has 3 globular proteins:

A

T, C and I

715
Q

The C globular protein of troponin binds to:

A

calcium

716
Q

The thick filament is composed of:

A

Myosin

717
Q

The myosin filament has multiple cross-bridges where heads can bind to the:

A

G-actin molecule

718
Q

Dark band:

A

A-band

719
Q

Light band:

A

I band

720
Q

In muscle, function as an ATPase enzyme:

A

myosin

721
Q

When myosin binds to ATP, what happens?

A

Hydrolyzes the ATP

722
Q

What regulate when contracton can happen?

A

Troponin and Tropomyosin

723
Q

Protein that connects thin filaments to glycoproteins in the sarcolemma

A

Dystrophin

724
Q

Provides scaffolding for sarcomeres:

A

Dystrophin-glycoprotein complex

725
Q

What is the difference between Duchenne’s and Becker’s muscular dystrophy?

A

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

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

726
Q

List some types of muscular dystrophies:

A

Duchenne, Beckers, Myotronic, Oclulopharyngeal, and limb girdle