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PHGY210 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Two major systems for physiological activities

A

Endocrine and CNS

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2
Q

ENDOCRINE SIGNALING involves hormone secretion into the blood by an

A

endocrine gland

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3
Q

The hormone is transported to a distant target site by

A

the blood stream

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4
Q

Synthesis and release of the hormone is done by

A

endocrine cells (or neurons)

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5
Q

Detection of the hormone or neurohormone by a

A

specific

receptor protein on the target cells

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6
Q

A change in cellular metabolism triggered by

A

the hormonereceptor interactions

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7
Q

Removal of the hormone results in

A

cellular

response

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8
Q

“Classical”
Endocrine
Organs

A 
Hypothalamus
Anterior and posterior pitutary
Thyroid and parathyroid glands
Atrial natruretic peptides
Adreal Glands (coretex and medulla)
Pancreas (Islets of Langerhans)
Ovaries (females)
Testis (Male)
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9
Q

Hypothalamic - Pituitary Signaling occurs by the

A

blood vessels of the pituitary stalk

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10
Q

Hypothalamic-Hypophyseal Portal system is from the

A

the hypothalamus to the anterior pituitary.

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11
Q

releasing factors

A

releasing hormones

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12
Q

inhibiting factors

A

inhibiting

hormones

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13
Q

-hypothalamic neurohormones

A 
activate or inhibit activity of
one of the six types of hormone
-
producing cellsin the anterior
pituitary
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14
Q

GLYCOPROTEINS Examples

A

FSH, LH, TSH

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15
Q

POLYPEPTIDES Examples

A

ACTH, GH, Insulin, Glucagon, IGFs, oxytocin, calcitonin

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16
Q

STEROIDS Examples

A

aldosterone, cortisol, estradiol, progesterone, testosterone, vitamin D

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17
Q

AMINES Examples

A

T4, T3

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18
Q

SYNTHESIS OF PROTEIN HORMONES: Ribosome

A

Preprohormones

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19
Q

SYNTHESIS OF PROTEIN HORMONES: Rough ER

A

Preprohormones to prohormones

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20
Q

SYNTHESIS OF PROTEIN HORMONES: Golgi Apparatus

A

prehormones packaged into secretory vesicles

prehormone to hormone and other peptide

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21
Q

SYNTHESIS OF PROTEIN HORMONES: Vesicles

A

Storage of hormone

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22
Q

PROPERTIES OF HORMONE RECEPTORS

A

SPECIFICITY: Recognition of single hormone or hormone family
AFFINITY: Binding hormone at its physiological concentration
SATURABILITY: A finite number of receptors
MEASUREABLE BIOLOGICAL EFFECT: A measurable biological response due to interaction of hormone with its receptor

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23
Q

RECEPTOR REGULATION (2)

A

(A) RECEPTORS CAN BE UPREGULATED EITHER BY INCREASING THEIR ACTIVITY
IN RESPONSE TO HORMONE OR THEIR SYNTHESIS.
(B) RECEPTORS CAN BE DOWNREGULATED EITHER BY DECREASING THEIR
ACTIVITY OR THEIR SYNTHESIS

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24
Q

3 mechanisms by which a hormone

can exert effects on target cells:

A

(1) Direct effects on function at the cell membrane.
(2) Intracellular effects mediated by second messenger systems.
(3) Intracellular effects mediated by genomic or nuclear action.

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25
Q

Hormone secretion is precisely regulated by

A

feedback mechanisms

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26
Q

An excess of hormone, or excess hormonal activity, leads to a

A

diminution of

hormone secretion

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27
Q

a deficiency of hormone leads to an

A

increase in hormone

secretion

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28
Q

PITUITARY GLAND Tissues

A

anterior pituitary, posterior pituitary

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29
Q

the anterior pituitary is _______ tissue.

A

endocrine

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30
Q

The posterior pituitary

is ______ tissue

A

neural

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31
Q

Which hormone structure is unlike the others? why

A

Dopamine; it is Short

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32
Q

Hormone Structure

A

Long peptide chain

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33
Q

Neurohypophysis

A

Posterior Pituitary Gland

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34
Q

Posterior Pituitary Gland

  • outgrowth of
  • connected
A
  • hypothalamus

- by the pituitary stalk

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35
Q

Location that secretes oxytocin and vasopressin

A

Posterior Pituitary Gland

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36
Q

vasopressin also known as

A

antidiuretic hormone -ADH

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37
Q

supraoptic nucleus synthesizes

A

vasopressin or ADH

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38
Q

paraventricular nucleus synthesizes

A

Oxytocin

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39
Q

supraoptic nucleus and

paraventricular nucleus axons run

A

down the pituitary stalk and
terminate in the posterior pituitary
close to capillary blood vessels

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40
Q

Prohormones processed in

A

secretory

granules during axonal transport

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41
Q

neurophysins

A
  • carrier molecules that transport the hormones oxytocin and vasopressin
  • Mature hormones liberated from
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42
Q

Neurophysins half lives

A

1-3 minutes

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43
Q

What is the uterus sensistivr to during Parturition? When is paturation?

A

uterus extremely sensitive to oxytocin at end of pregnancy

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44
Q

dilation of uterine cervix by fetal head causes

A

release of oxytocin →

uterine contraction, which assists the expulsion of fetus and then placenta

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45
Q

uterine contraction assists

A

the expulsion of fetus and then placenta

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46
Q

Milk ejection

A

response to the stimulus of suckling, in lactating mother

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47
Q

What hormone causes milk filled ducts to contract and squeeze milk out

A

Oxytocin

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48
Q

Behavioural effects of oxytocin in females

A

Local oxytocin release in the brain reduces anxiety

and enhances bonding and pro-social behaviour

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49
Q

Ejaculation

A

Oxytocin surge during sexual activity assists epididymal

passage of sperm and ejaculation

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50
Q

Behavioural effects of oxytocin in males

A

Local oxytocin release in the brain reduces anxiety

and enhances bonding and pro-social behaviour.

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51
Q

Size of Thyroid Gland and how it varies

A

15 to 20g, varies size with sex, age, diet, reproductive state, etc.

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52
Q

Which sex is Thyroid Gland larger in?

A

Larger in females than males

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53
Q

Amount of healthy thyroid needed to maintain euthyroid state

A

only 39g

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54
Q

major component of the colloid

A

thyroglobulin

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55
Q

thyroglobulin

A

a large protein of 700,000Da

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56
Q

thyroglobulin converts

A

T4 to T3

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57
Q

thyroglobulin contains

A

thyroid hormones thyroxine (T4) and triiodothyronine (T3).

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58
Q

Where do T4 and T3 split off?

A

thyroglobulin

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59
Q

Where do T4 and T3 enter and bind to after being split off?

A

blood where

they bind to special plasma proteins

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60
Q

synthesis of thyroglobulin is under the control of… where

A

TSH of pituitary gland

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61
Q

What does thyroglobulin provide?

A

a type of

storage for T4 and T3 prior to release

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62
Q

What element do Thyroid hormones contain

A

Thyroid hormones contain iodine

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63
Q

What is the availability of iodine to terrestrial vertebrates?

A

limited

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64
Q

thyroid follicular cells are able to

A

trap iodide and transport it across the cell against a chemical gradient
(active transport)

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65
Q

Iodine (I2) used for

A

iodination of tyrosine residues of

thyroglobulin (TGB)

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66
Q

iodination
of tyrosine residues of
thyroglobulin (TGB) is used to form

A

monoiodotyrosine (MIT) and

diiodotyrosine (DIT)

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67
Q

Oxidative coupling of two DIT forms

A

thyroxine (T4)

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68
Q

oxidative coupling of one MIT with one DIT forms

A

triiodothyronine (T3)

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69
Q

T4 and T3 are stored linked to

A

thyroglobulin

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70
Q

rate of all steps of T4 and T3

the formation is increased by

A

TSH

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71
Q

thyroid activity without TSH

A

Without TSH, thyroid has very low

turnover of thyroid hormones

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72
Q

Synthesis and release of TSH controlled by

A

hypothalamic thyrotropin releasing hormone (TRH)

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73
Q

-When T4 and T3 in blood increase they

A

exert a negative feedback at both hypothalamic and pituitary levels

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74
Q

a negative feedback at both hypothalamic and pituitary levels results to

A

decrease release of TRH and TSH

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75
Q

What does TSH lead to?

A

increased production of T4 and T3

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76
Q

What does TSH do to increase the production of T4 and T3?

A

interacts with specific receptors

located on follicular cells of the thyroid gland

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77
Q

How does iodine deficiency affect thyroid hormones?

A

When the supply of iodide is deficient, synthesis of thyroid hormones
decreases andT4 andT3 in circulation decrease.

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78
Q

Iodine deficiency affects on TSH release?

A

Release of TSH increases and the thyroid follicular cells are constantly
stimulated

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79
Q

How does Iodine deficiency affect thyriod gland?

A

-Thyroid enlarges

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80
Q

goiter

A

a visible lump when the thyroid enlarges

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81
Q

What results from an enlarged thyroid due to the iodine deficiency?

A

is unable to synthesize biologically active
thyroid hormones, known as non-toxic
goiter

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82
Q

What hormone stimulates calorigenesis in most cells?

A

Thyroid hormones

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83
Q

How does thyroid hormones promote normal growth?

A

Promote neural branching and myelinization of nerves
Promote development and maturation of the nervous system
Stimulate growth hormone (GH) secretion; Promote bone growth; Promote IGF-I production
by the liver

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84
Q

What results from stimulation of calorigenesis in most cells?

A

Increase cardiac output: rate and strength of cardiac contractions
Increase oxygenation of blood
Increase rate of breathing; Increase number of red blood cells in the circulation

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85
Q

How does thyroid hormones affect carbohydrate metabolism?

A

Promote glycogen formation in the liver; Increase glucose uptake into adipose and muscle

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86
Q

How does thyroid hormones affect lipid turnover?

A

Increased lipid synthesis; Increased lipid mobilization; Increased lipid oxidation

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87
Q

How does thyroid hormones affect protein metabolism?

A

Stimulate protein synthesis

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88
Q

What hormone increases Basal Metabolic Rate

A

Thyroid hormones

Both T4 and T3 increase BMR

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89
Q

BMR

A

the rate at which the organism burns up its stores of fuel to produce energy in the form of heat or
calories

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90
Q

T4 and T3 have profound effects on the metabolism of which macromolecules?

A

carbohydrates, lipids and proteins

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91
Q

How does thyroid hormones affect CNS?

A

Required for normal development of the brain

absence decreases neuronal development

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92
Q

Absence of thyroid hormones at early stages of development leads to

A

irreversible mental retardation

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93
Q

What hormone stimulates the synthesis of the nerve growth factor (NGF)?

A

Thyroid hormones

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94
Q

nerve growth factor

(NGF) induces

A

dendritogenesis and regeneration of sympathetic neurons.

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95
Q

What do T3 and T4 bind to when they enter their target cell nucleus?

A

cognate nuclear receptor

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96
Q

What does the binding of T3 and T4 to their cognate nuclear receptor do?

A

Alters the transcription of specific genes, and thus levels of encoded proteins

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97
Q

With the specific receptor for T4 and T3 located in the mitochondrial membrane, what may result?

A

Thyroid hormones may induce some effects by interactions with plasma
membrane & mitochondria.
-Not blocked by inhibitors of protein synthesis: i.e. de novo gene expression and
protein synthesis not necessary

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98
Q

How does the T4/T3 interact with the plasma membrane? What is this effect independent of?

A

T4/T3 act directly at plasma membrane and increase uptake of amino acids.
This
effect is also independent of protein synthesis

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99
Q

hypothyroidism

A

Hypofunction of the thyroid gland characterized by low levels of thyroid hormones.

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100
Q

hyperthyroidism

A

Hyperfunction of the thyroid gland characterized by high levels of thyroid hormones.

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101
Q

(Hyper/Hypo) thyroidism:

T4-T3 levels (elevated/decreased)

A

Hyper –> Elevated

Hypo –> Decreased

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102
Q

(Hyper/Hypo) thyroidism:
BMR
(elevated/decreased)

A

Hyper –> Elevated

Hypo –> Decreased

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103
Q

(Hyper/Hypo) thyroidism:
Pulse
(increased/decreased)

A

Hyper –> increased

Hypo –> Decreased

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104
Q

(Hyper/Hypo) thyroidism:
body temperature
(increased/lowered)

A

Hyper –> increased

Hypo –> lowered

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105
Q

(Hyper/Hypo) thyroidism:
weight
(loss/gain)

A

Hyper –> loss

Hypo –> gain

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106
Q

(Hyper/Hypo) thyroidism:

  • Carotenemia
  • Exophtalmos
A

Hyper –> Exophtalmos

Hypo –> Carotenmia

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107
Q

(Hyper/Hypo) thyroidism:

-Goiter

A

Hyper –> Goiter (primary or secondary origin)

Hypo –> Goiter (may or may not be present)

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108
Q

Primary hypothyroidism

A

Myxedema

At the level of the thyroid; an inability to synthesize active thyroid hormones.

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109
Q

Primary hypothyroidism (Male vs Female; young vs old)

A

-More common in women than in man; appears at about 40-60 years of age

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110
Q

Primary hypothyroidism Causes

A

(1) Atrophy of the thyroid .
(2) Autoimmune Thyroiditis:
(3) Goitrous Hypothyroidism or Non-Toxic Goitre: )

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111
Q

Autoimmune Thyroiditis:

A

Destruction by antibodies against cellular components of thyroid
A.K.A. autoimmune thyroiditis or Hashimoto’s disease. More common in women.

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112
Q

Goitrous Hypothyroidism or Non-Toxic Goitre:

A

blockage in a step ofT4/T3 synthesis.

-thyroid gland increases in size and there is goitre formation (non-toxic goitre).

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113
Q

Secondary hypothyroidism

A

-At level of the pituitary; synthesis of little or no thyroid stimulating hormone (TSH).

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114
Q

Tertiary hypothyroidism

A

At the level of the hypothalamus; synthesis of little or no thyrotropin-releasing hormone (TRH)

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115
Q

Infantile hypothyroidism

A

-Absence of thyroid gland or incomplete development of thyroid gland at birth

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116
Q

T4/T3 levels of Infantile hypothyroidism at birth

A

At birth infant is normal since the fetus uses mother’s T4/T3.

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117
Q

Physical affects of Infantile hypothyroidism after a few months

A 
exhibits decreased physical growth & mental development
growth retardation (dwarfism) and the mental retardation associated with cretinism.
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118
Q

Treatment for hypothyroidism

A

administration of thyroid hormones

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119
Q

Primary hyperthyroidism

A

at the level of the thyroid gland

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120
Q

Toxic Diffuse Goiter (Graves Disease):

A

Autoimmune disease characterized by presence of substance produced by lymphocytes
called Long Acting Thyroid Stimulator (LATS)

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121
Q

Long Acting Thyroid Stimulator (LATS)

A

an antibody that mimics the action of TSH and

stimulating release of T3 and T4

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122
Q

toxic goitre

A

Formation of goitre

synthesizes biologically active T4/T3 from constant stimulation by LATS increases mass of thyroid leading to the

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123
Q

Thyroid adenoma or thyroid cancer

A

-synthesize of thyroid hormones independent ofTSH stimulation

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124
Q

Secondary hyperthyroidism

A 
level of anterior pituitary gland
no negative feedback from increased levels of T3/T4 and synthesize autonomously thyroid
stimulating hormone (TSH). Often due to the presence of a pituitary tumor
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125
Q

Tertiary Hyperthyroidism:

A

at level of the hypothalamus
No negative feedback of high T3/T4 to decrease synthesis of thyrotropin releasing hormone
(TRH) Often it is due to the presence of a hypothalamic tumor.

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126
Q

Treatment for Hyperthyroidism

A
  1. Surgery plus replacement therapy (administration of thyroid
    hormones) .
  2. Administration of radioactive Iodide (131I) about 5 mCi.
  3. Administration of antithyroid drugs such as propylthiouracil
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127
Q

What do antithyroid drugs (propylthiouracil) do?

A

blocks addition of iodine to thyroglobulin

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128
Q

Specific care requirements for the administration of antithyroid drugs

A

Care must be taken not to inhibit the synthesis of thyroid hormones to a great extent and cause
hypothyroidism.

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129
Q

What does radioactive Iodide (131I) do?

A

The radioactive iodide concentrates in the cells of the thyroid follicles and destroys them. Replacement therapy may be administered as needed.

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130
Q

What are calcium ions essential for?

A
  • essential structural component of the skeleton.
  • important in normal blood clotting.
  • with Na+ and K+ helps maintain transmembrane potential of cells.
  • important in excitability of nervous tissue
  • important in contraction of muscles
  • important in release of hormones and neurotransmitters.
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131
Q

Concentration of calcium in cellular and extracellular fluid

A

~10mg/100ml.

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132
Q

Where does the calcium ions exist in circulation

A

50% free, 50% bound to albumin

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133
Q

Where is about 99 % of the body’s calcium?

A

Bone

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134
Q

What does bone serve as for calcium?

A

Bone thus serves as a calcium reservoir

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135
Q

Maintenance of plasma calcium is achieved mainly by

A

exchange between bone and plasma

under influence of hormones

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136
Q

How do hormones affect the intestines and kidneys?

A

Hormones affect intestinal absorption of calcium and excretion of by kidneys

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137
Q

Where is Parathyroid hormone (PTH) produced?

A

protein and is produced by parathyroid glands

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138
Q

What does Parathyroid hormone (PTH) do?

A

increases circulating levels of Ca++

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139
Q

What does Calcitonin do?

A

-lowers the circulating levels of Ca++

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140
Q

What does Vitamin D do? (calcium)

A

-Increases the circulating levels of Ca++

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141
Q

Where is Calcitonin (PTH) produced?

A

protein and is produced by the parafollicular or “C” cells of the thyroid gland

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142
Q

Where is calcium obtained?

A

obtained in the diet; milk, cheese, eggs, butter etc.

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143
Q

Where is calcium absorbed?

A

-absorbed from the digestive tract primarily in the duodenum and upper jejunum.

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144
Q

What increases the absorption of calcium?

A

Its absorption is increased by vitamin D and PTH

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145
Q

From the plasma, where does the calcium go?

A
  • some of the calcium will be deposited in bone or cells of other tissues
  • some will go through the kidney and into the urine
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146
Q

What hormone increases calcium deposition

in bone?

A

calcitonin

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147
Q

What hormone increases calcium loss through kidneys into urine?

A

calcitonin

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148
Q

What occurs when calcium plasma concentration is below 10mg/100ml?

A

PTH will stimulate reabsorption

of calcium from the kidney and removal of calcium from the bone (bone resorption)

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149
Q

Stable concentrations of calcium in blood is achieved mainly by exchange between

A

calcium between

bone and plasma under hormonal influence

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150
Q

Where is the parathyroid hormone secreted?

A

from parathyroid chief cells

embedded in surface of thyroid

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151
Q

Where are parathyroid glands located?

A

back side of the thyroid gland

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152
Q

What results from the Removal of parathyroids

A

severe drop
in plasma calcium levels causing
tetanic convulsions and death

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153
Q

PTH amino acid structure

A

84 amino acid polypeptide - only Nterminal 34 amino acids important for
full activity.

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154
Q

What is PTH synthesized as part of?

A

a larger

protein, preproparathyroid hormone,

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155
Q

How does preproparathyroid produce PTH?

A

undergoes proteolytic cleavage

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156
Q

Half-life of PTH

A

-Very short half-life – 3-18 minutes

depending on individual

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157
Q

FUNCTIONS OF PTH (3)

A
  1. Increase the concentration of plasma calcium :
  2. Control of PTH release
  3. Mechanism of PTH activity
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158
Q

What is the release of PTH controlled by?

A

controlled directly by the circulating concentration of calcium

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159
Q

What mechanism of PTH controls the activity?

A

binding to cognate receptor on target cells exerts

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160
Q

PTH impact on bone resorption

A

increases bone demineralization -increases Ca++in body

fluids

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161
Q

PTH impact on kidney

A

increase the reabsorption of Ca++ in proximal convoluted tubule

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162
Q

PTH impact on Vitamin D synthesis

A

stimulates the conversion of 25-hydroxyvitamin D3 to
1,25-dihydroxyvitamin D3 (1,25D3; biologically active form of vitamin D)
primarily in kidney

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163
Q

PTH impact on gut

A

PTH and 1,25D3, facilitate the absorption of Ca++ from the gut

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164
Q

hypoparathyroidism

A

low levels of PTH in circulation

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165
Q

Symptoms of hypoparathyroidism

A

-low plasma calcium
-production of biological active vitamin D is decreased
Tetany, convulsions more serious clinical problems of hypoparathyroidism

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166
Q

hypocalcemia

A

low plasma calcium

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167
Q

convulsions

A

Spasms of laryngeal muscles may lead to death by asphyxiation.

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168
Q

Tetany

A

Ca++ <7mg/100ml -increased neural overexcitability - muscle spasms

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169
Q

hyperparathyroidism

A

high levels of PTH in circulation

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170
Q

hyperparathyroidism is often caused by

A

parathyroid adenoma of parathyroid producing too much PTH

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171
Q

hyperparathyroidism 1,25D3 levels

A

-high production of 1,25D3.

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172
Q

high PTH affect on bone and kidneys

A

high PTH stimulates bone resorption and calcium reabsorption from kidney.

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173
Q

1,25D3 affect on intestines

A

-1,25D3 increases calcium absorption from the intestines.

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174
Q

hyperparathyroidism calcium levesls

A

-elevated calcium in circulation.

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175
Q

formation of kidney stones is a common symptom of

A

hyperparathyroidism

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176
Q

Severe cases of hyperparathyroidism can result in

A

cardiac arrhythmias, depressed neuromuscular excitability,

calcium deposition on walls of blood vessels and cartilaginous regions of bones

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177
Q

Treatment of hyperparathyroidism

A 
removal of (affected) parathyroids and replacement therapy of 1,25D3
and Ca++
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178
Q

Treatment of hypoparathyroidism

A

removal of (affected) parathyroids and replacement therapy of 1,25D3 and Ca++

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179
Q

Where do we get VITAMIN D from?

A
  • available from limited dietary sources (cod liver oil, fatty fish).
  • can be synthesized from a cholesterol metabolite,
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180
Q

VITAMIN D is synthesized by

A
  1. UVB light + 7-dehydrocholesterol in skin.
  2. 25-hydroxylation in liver followed by…
  3. 1-hydroxylation in kidney and several peripheral tissues-> 1,25-dihydroxyvitamin D3.
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181
Q

PHYSIOLOGICAL FUNCTIONS of VITAMIN D: (3)

A
  1. primary function: increase calcium absorption from the intestine.
  2. regulates the immune system -> protects against infection, anti-inflammatory
  3. anticancer properties
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182
Q

REGULATION OF VITAMIN D SYNTHESIS IN KIDNEY IN conditions of low calcium

A
  • increased in conditions of low calcium, when PTH is also increased
  • depressed by high calcium
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183
Q

Vitamin D affect in northern countries

A

In northern countries, absence ofUVB may lead to vitamin D deficiency and deficient bone mineralization

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184
Q

Rickets in growing individuals

A

deficient bone mineralization

baldness

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185
Q

Skin colour affect on vitamin D

A

vitamin D deficiency is more severe in dark-skinned people.

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186
Q

Low vitamin D in adults leads to

A

osteomalacia (soft bone).

187
Q

Hereditary vitamin D

-resistant Rickets is due to

A

– due to inactivating
mutation in the vitamin D
receptor

188
Q

CALCITONIN peptide structure

A

32 amino-acid calcium-lowering peptide hormone

189
Q

Where is calcitonin manufactured?

A

-manufactured in parafollicular or “C” cells of the thyroid gland

190
Q

How does calcitonin lower the plasma calcium?

A

by promoting transfer of Ca++ from blood to bone,

and increasing urinary excretion of Ca

191
Q

Impact of increase in plasma calcium to calcitonin?

A

-rise in plasma Ca++ increases release of calcitonin.
-decrease in plasma calcium concentration decreases the release of
calcitonin

192
Q

Absence of calcitonin impact on calcium homeostasis?

A

Absence of calcitonin does not compromise calcium homeostasis in man,
suggesting that its biological importance is limited.

193
Q

Location of Adrenal Glands

A

-located adjacent to upper surface of kidneys

194
Q

Adrenal Glands size in male vs female

A

-heavier in the male than in the female

195
Q

two distinct types of tissue in adrenal glands

A

cortex and medulla

196
Q

Histologic appearance of Cortex

A

large-lipid containing epithelial cells

197
Q

Histologic appearance of Medulla

A

chromaffin cells-fine brown granules when fixed with potassium
bichromate

198
Q

Origin of Cortex

A

derived from mesoderm

199
Q

Origin of Medulla

A

derived from neural crest

200
Q

Function of Cortex

A

Produces steroid hormones; glucocorticoids (major one being
cortisol in human) and mineralocorticoids (e.g.
aldosterone), and progestins

201
Q

Function of Medulla

A

Produces catecholamines epinephrine and norepinephrine
& some peptide hormones (enkephalins, dynorphins and atrial natriuretic
peptides)

202
Q

Adrenal Cortex layers

A
  • zona glomerulosa
  • zona fasciculata
  • zona reticularis
203
Q

zona glomerulosa produces

A

mostly mineralocorticoids (aldosterone).

204
Q

zona fasciculata produces

A

produces mainly glucocorticoids (cortisol).

205
Q

zona reticularis produces

A

glucocorticoids, progestins, androgens & estrogens

206
Q

Synthesis of adrenal steroids controlled by

A

pituitary hormone adrenocorticotropin (ACTH).

207
Q

18-hydroxylase is synthesized of

A

mineralocorticoid

aldosterone

208
Q

18-hydroxylase is only present in

A

zona glomerulosa

209
Q

17a-hydroxylase is absent in

A

zona glomerulosa

210
Q

Does the zona glomerulosa produce glucocorticoids

A

zona glomerulosa does not produce

glucocorticoids.

211
Q

Function of steroid

hormones

A

to regulate (increase or
decrease) the transcription of
hormone/receptor-specific target
genes

212
Q

Physiological role of Aldosterone

A 
Sodium metabolism 
- increases the
reabsorption of Na+ by the kidney
- Also affects the plasma concentration of K+ and H+
- loss of K+ and H+
in urine balance
reabsorption of Na+.
213
Q

Main Glucocorticoids in humans

A

Cortisol

214
Q

Glucocorticoids affect on salt retention

A

Some activity but less effective than aldosterone. Can be important under pathological
conditions when plasma cortisol remains elevated

215
Q

Glucocorticoids effects on protein and carbohydrate metabolism

A
  • Stimulate the synthesis of a number of gluconeogenic enzymes in hepatocytes, and several enzymes that breakdown proteins in muscle and other tissues
  • released amino acids enter liver and are converted to glucose and glycogen (gluconeogenesis).
  • Decrease glucose uptake by muscle and adipose tissue and decrease glycolysis (glucose oxidation) to conserve glucose for other tissues.
  • leads to increased blood glucose levels -> increased insulin secretion *
216
Q

adrenal diabetes

A

Increased blood glucose due to excess of glucocorticoid activity
– if prolonged, may lead to destruction of beta-cells of pancreas and true diabetes mellitus.

217
Q

Glucocorticoids on Lipid metabolism

A

maintain or increase the levels of lipolytic enzymes in the adipose tissue cells and augments lipolytic action of other hormones, e.g. epinephrine

218
Q

Excess of what can lead to hyperlipidemia and hypercholesterolemia

A

excess of glucocorticoids

219
Q

Anti-inflammatory and immunosuppressive actions of glucocorticoids:

A

-Reduce inflammatory responses: e.g. at sites of injury.
-Cause atrophy of the lymphatic system (lymph nodes, thymus, spleen)
-decreased levels of circulating lymphocytes and reduced antibody formation. Therefore
glucocorticoids used in organ transplantation
-decrease histamine formation and thus decrease allergic reactions.

220
Q

Effects of glucocorticoids on bone

A

-decrease the protein matrix of the bone through their protein catabolic effect. As a result,
increased loss of Ca++ from the bone leading to osteoporosis

221
Q

osteoporosis

A

weakens bones to the point where they break easily

222
Q

Control of glucocorticoid secretion is done by

A

pituitary adrenocorticotropin

ACTH

223
Q 
pituitary adrenocorticotropin
(ACTH) structure
A

39 amino acid polypeptide

224
Q

What is 39 ACTH synthesized as part of

A

larger protein known as

proopiomelanocortin (POMC)

225
Q

feedback control of cortisol secretion is via

A

hypothalamus and anterior pituitary

226
Q

In cases of enzyme deficiencies (lack of 11bhydroxylase) where cortisol is not produced; how is ACTH secretion impacted

A

ACTH secretion is unchecked

227
Q

Enzyme deficiencies where cortisol is not produced can result from

A

congenital adrenal hyperplasia

228
Q

treatment for congenital adrenal hyperplasia

A

administration of cortisol, which (a)
corrects the deficiency and (b) normalizes the
ACTH secretion

229
Q

What/where does ACTH bind to?

A

binds to specific ACTH receptor

on membranes of zona fasciculata and zona reticularis cells

230
Q

ACTH stimulation of adenylyl cyclase leading to

increased production of

A

cyclic AMP

231
Q

Daily rhythm of plasma cortisol and ACTH levels at night /morning

A
  • diurnal rhythm of ACTH and cortisol secretion
  • minimum at midnight and
    maximum in the morning.
232
Q

the daily rhythm of plasma cortisol and ACTH compared to sleep

A

-rhythm may be independent of sleep and

abolished by stress and Cushing’s disease.

233
Q

activation steroidogenic enzymes leads to

A

increased synthesis and release of steroid

hormones

234
Q

What activates steroidogenic enzymes

A

ACTH

235
Q

How does stress, affect syntheisis and release of CRH, ACTH, and cortisol

A

increase

236
Q

Common types of physiological stresses

A

pain, fear, exercise, hunger, cold, hemorrhage

237
Q

Release of cortisol during stress advantageous impacts

A
  • provides energy and

amino acids through the breakdown of tissue proteins, especially under conditions where normal feeding not feasible

238
Q

Release of cortisol during stress disadvantageous impacts

A

cortisol inhibits wound healing.

239
Q

Prolonged stress would maintain constantly high levels of

A

glucocorticoids

240
Q

constantly high levels of glucocorticoids can lead to

A 
increased blood glucose (true diabetes mellitus), decreased
immune responses (individual will become susceptible to infections), loss of
bone etc
241
Q

Addison’s Disease

A

hypofunction of adrenal cortex

242
Q

What is Addison’s disease characterized by ?

A

characterized by failure of the adrenal

cortex to produce adrenocortical hormones

243
Q

What effect may the gland have with addison’s disease

A

involve total destruction of the gland

244
Q

What does Addison’s disease mostly results from?

A

autoimmune attack on the
adrenal glands, but can also be caused by
tuberculosis.

245
Q

Cushing’s Disease

A

hyperfunction of adrenal cortex

246
Q

What is Cushing’s Disease characterized by ?

A

by hyperplasia of the
adrenal cortex due to increased circulating
levels of ACTH.

247
Q

In Cushing’s Disease, how are the productions of glucocorticoids and mineralocorticoids impacted?

A

excessive production of glucocorticoids
as well as increased production of
mineralocorticoids.

248
Q

Location of the pancreas

A

located behind the stomach

249
Q

Percentage of pancreas that is exocrine

A

99 % of pancreas is exocrine and secretes the digestive enzymes

250
Q

Islets of Langerhans

A

scattered within the exocrine pancreas are small endocrine structures, compact mass of cells with good vascularization

251
Q

beta-cells

A

synthesize insulin

About 60 % of the cells of the islets of Langerhans

252
Q

alpha-cells

A

synthesize glucagon

About 25 % of the cells of the islets

253
Q

Insulin and glucagon

A

small protein hormones and both control of glucose

concentration in blood

254
Q

Why is insulin very important?

A

insulin is more important than glucagon and insulin deficiency or absence compromises
significantly the well-being of the individual and if not treated may lead to death

255
Q

Only hormone that acts primarily to

decrease blood glucose

A

-Insulin

256
Q

Where is glucose always present?

A

In the blood

- 80 mg/100 mL

257
Q

Where is there little free glucose ?

A

in tissues

258
Q

How must glucose enter cells

A

Where is glucose always present?

259
Q

What is glucose converted into in the liver and muscle cells

A

glycogen

260
Q

What is glucose converted into in the adipose tissue cells?

A

to fat and stored for later use

261
Q

What happens to glucose in many cells of the body cells?

A

oxidized to produce

energy

262
Q

Insulin receptor

A

Membrane receptor, stimulates
insertion of glucose transport proteins stored in
cytoplasm into plasma membrane

263
Q

How does the insertion of glucose transport proteins into plasma membrane affect glucose uptake

A

increases glucose uptake

264
Q

Results when the b-cells are destroyed

A

Insulin deficiency

265
Q

Insulin deficiency

A

Results when the b-cells are destroyed

266
Q

What can Insulin deficiency lead to

A

Diabetes Mellitus

267
Q

Diabetes Mellitus

A

most tissues cannot take
up glucose efficiently, glucose accumulates in
circulation.

268
Q

Can Insulin deficiency occur if there is no glucose in diet

A

Occurs even if no glucose in diet because of
increased gluconeogenesis (e.g. protein
breakdown to amino acids and synthesis of
glucose)

269
Q

During Insulin deficiency what is the principal source of energy?

A

free fatty acids (FFA) - increased lipolysis

270
Q

What occurs when fat is inefficiently used

A

incomplete
oxidation of FFA and increased circulating
acetoacetic acid and b-hydroxybutyric acid
(metabolic acidosis) and acetone (ketosis -
acetone smell in breath of untreated diabetics).

271
Q

How does increased lipolysis affect blood pH

A

leads to decreased blood pH, and death unless treatment is provided

272
Q

pH affect from diabetic coma

A

decreased blood pH

273
Q

glycosurea

A

presence of reducing sugars in the urine

274
Q

At >180mg% what happens to glucose

A

glucose spills over into urine

275
Q

How does diabetes mellitus effect the water in urine

A

-leads to loss of water in urine, causing polyurea

276
Q

polyurea

A
  • dehydration and increased thirst
277
Q

polydipsia

A

increased thirst

278
Q

What leads to ketosis, and metabolic

acidosis?

A

untreated diabetes

279
Q

Treatment of diabetes Mellitus

A

-administration of insulin is needed to restore individual back to normal.

280
Q

in diabetic comas, what must be corrected in addition to insulin administration?

A

acidosis and associated electrolyte imbalance

281
Q

diabetes insipidus

A

persons suffering from

antidiuretic hormone deficiency

282
Q

Two types of diabetes

A

type 1 insulin-dependent or type 2 insulin independent

283
Q

type 1 diabetes

A

deficiency of insulin

284
Q

type 2 diabetes

A

hyporesponsiveness to insulin

285
Q

what happens to b-cells during type 1 diabetes?

A

Destruction of the b-cells in the pancreas

286
Q

Destruction of the b-cells of pancreas causes

A

Type 1 diabetes where synthesis of insulin does not occur

287
Q

Treatment for Destruction of the b-cells of pancreas

A

administration of insulin is needed associated with proper diet

288
Q

Defective insulin release causes

A

Type 1 diabetes where insulin is not released

289
Q

Defective insulin release treatment

A

Drugs stimulating insulin release could be

administered again associated with proper diet and exercise.

290
Q

Affect on brain when blood glucose reaches 20-30mg/100ml?

A

the availability
of glucose for the brain is not sufficient and the individual may fall into a coma known as insulin shock or hypoglycemic coma

291
Q

insulin shock or hypoglycemic coma

A

To little glucose in brain

292
Q

insulin shock or hypoglycemic coma treatment

A

treated with
immediate administration of glucose, otherwise death or permanent brain
damage may occur

293
Q

Insulin levels in TYPE 2 DIABETES

A

Insulin levels normal or abnormally high

294
Q

problem in type 2 diabetes

A

hyporesponsiveness of target cells to insulin

295
Q

insulin resistance often

due to

A

decreased number of insulin receptors on target cells

296
Q

What type of diabetes is associated with obsiety?

A

Type 2

297
Q

overeating affect on insulin/ insulin receptor levels?

A 
prolonged high insulin levels decrease
number receptors (downregulation)
298
Q

treatment for type 2 diabetes

A
  • proper diet and exercise

- decreased caloric intake, decreased insulin, upregulation of receptors

299
Q

how do insulin receptors change in response to endurance?

A

insulin receptors increased in response to frequent endurance exercise,
independent to changes in body weight

300
Q

JUVENILE DIABETES MELLITUS

A

Juvenile diabetes mellitus appears in childhood and is insulin dependent

301
Q

B cells in JUVENILE DIABETES MELLITUS

A

The b-cells

of pancreas do not produce insulin

302
Q

Treatment of JUVENILE DIABETES MELLITUS

A

Treatment requires administration of insulin

303
Q

Glucose tolerance test

A

Blood Glucose Concentration compared Time

304
Q

How is glucose tolerance changed in diabetes?

A

Glucose tolerance is decreased in diabetes
(low or absence of insulin) and is increased in
hyperinsulinism

305
Q

How did blood glucose change in normal vs diabetic individuals?

A

increase in blood glucose is

greater and returns to normal more slowly

306
Q

Purpose of insulin section feedbacks?

A

control of insulin release to avoid hypoglycemia.

307
Q

beta cells responding to levels of blood glucose is a

A

negative feedback mechanims

308
Q

beta cells affect on insulin section

A

secreting little or no

insulin when blood glucose low, secreting much more when the blood glucose is high

309
Q

The release of what (2) induce insulin release

A

release of gastrin and vagal impulses to the beta-cells induce insulin release, as
a result insulin starts to leave the pancreas even before the blood glucose begins to
rise during meals

310
Q

What peptide hormone is synthesized and released by alpha cells of pancreas.

A

Glucagon

311
Q

-Metabolic functions of glucogon compared to insulin

A

opposite

312
Q

metabolic function of glucogon

A

Raises blood sugar

313
Q

How does glucagon raise blood sugar in the liver?

A

by promoting glycogenolysis (breakdown of glycogen) and

gluconeogenesis (synthesis of glucose) in the liver.

314
Q

How does glucagon raise blood sugar in adipose tissue?

A

glucagon increases rate of lipolysis leading to increased

concentration of free fatty acids in circulation

315
Q

What is glucagon release controlled by?

A

concentration of glucose in circulation

316
Q

What does low blood glucose stimulate in pancreatic alpha cells?

A

to increase synthesis and release of glucagon

317
Q

What does high blood glucose stimulate in pancreatic alpha cells?

A

high blood glucose content decreases release and synthesis

318
Q

Is more glucagon super important for increased blood glucose content?

A

Glucagon not as important as insulin, other hormones increase blood glucose content such as cortisol (glucocorticoids) as well as epinephrine, nor-epinephrine etc

319
Q

Where is growth hormone produced?

A

anterior lobe of the pituitary

320
Q

What is growth hormone responsible for?

A

growth

321
Q

Somatotropin is also known as

A

growth hormone

322
Q

What is growth hormone do? (2)

A

-Increases protein synthesis in many tissues such as bone, muscle, kidney, liver by
enhancing amino acid uptake by cells and by accelerating the transcription and
translation of mRNA

  • increases the rate of lipolysis and utilization of free fatty acids as a source of energy
323
Q

What direct affect of growth hormone is not mediated by somatomedins?

A

increases the rate of lipolysis and utilization of free fatty acids as a source of
energy

324
Q

Where are somatomedins produced?

A

liver

325
Q

What condition are somatomedins produced?

A

under stimulation of GH

326
Q

How do somatomedins compare to insulin?

A

structurally similar to insulin

327
Q

Another name for somatomedins

A

insulin-like growth factors I and II (IGFI and IGF-II)

328
Q

IGFI and IGF-II

A

bind to insulin receptors and insulin at high

concentrations may bind to somatomedin receptors)

329
Q

What do somatomedins do?

A

increase protein synthesis and stimulate growth

330
Q

The GH released is controlled by

A

mediated

by two hypothalamic neurohormones

331
Q

What two hypothalamic neurohormones control GH release

A
  • growth hormone releasing hormone
  • somatostatin (growth hormone
    inhibiting hormone
332
Q

somatoliberin

A

growth hormone releasing hormone
(GRH) also known as somatoliberin,
which stimulates growth hormone
release

333
Q

somatostatin

A

(growth hormone inhibiting hormone), which inhibits

growth hormone release

334
Q

How are GRH and somatostatin regulated?

A

tightly regulated by
an integrated system of neural, metabolic,
and hormonal factors

335
Q

GH Deficiency in young leads to ?

A

In the young, absence of growth hormone leads to decreased physical growth

336
Q

Excess GH in young leads to ?

A

In young individual leads to gigantism.

337
Q

Excess GH in later in life (adult) leads to what condition?

A

condition of acromegaly

338
Q

acromegaly

A

many bones get longer and heavier

particularly at the cartilaginous regions of the bones

339
Q

primary reproductive organs

A

the gonads, testes in the male, ovaries in the female

340
Q

Two functions of the gonads

A

Gametogenesis

Secretion of sex hormones (specific steroids)

341
Q

Gametogenesis

A

the production of reproductive cells known as gametes;
the spermatozoa in the male
ova in the female

342
Q

Name of male reproductive cells (gametes)?

A

spermatozoa

343
Q

Name of female reproductive cells (gametes)?

A

ova

344
Q

Male sex hormone

A

testosterone (androgen) in the male

345
Q

Female sex hormone

A

estrogen and progesterone in the female

346
Q

Are the differences in reproductive endocrinology in males and females, quantitative or
qualitative

A

is quantitative and not

qualitative

347
Q

Are androgens unique to males?

A

No

348
Q

Are estrogens unique to females?

A

No,

349
Q

What can produce small amounts of estrogen

A

Testes

produce small amounts of estrogen

350
Q

What can androgens be converted into?

A

androgens can be converted into estrogens by

a single enzymatic step in several non gonadal tissues (bone, for example)

351
Q

Where are androgens usually produced in females (amounts too)?

A

produced in small amounts in ovaries and in larger amounts by the adrenals

352
Q

How is estrogen produced in males?

A

locally in tissues by the conversion by aromatase

of testosterone the estrogen estradio

353
Q

Estrogen deficiency in males results in

A

(i) Leads to increased body fat.

(ii) Contributes to sexual desire and erectile function.

354
Q

Gonadotropin releasing hormone (GnRH) is secreted by

A

hypothalamus

355
Q

How does Gonadotropin releasing hormone (GnRH) travel?

A

travels to anterior

pituitary via hypothalmo-pituitary portal vessels

356
Q

What stimuilates the release of pituitary gonadotropins

A

follicle-stimulating hormone

FSH) and luteinizing hormone (LH

357
Q

FSH and LH stimulates

A

development of spermatozoa or ova, and secretion of sex

steroids

358
Q

Where do sex steroids exert effects

A

effects in gonads, in other
parts of the reproductive system, and body
(e.g. estrogen maintains bone density; i.e.
prevention of osteoporosis)

359
Q

where is inhibin protein produced?

A

Gonads

360
Q

What does inhibin protein do?

A

feeds back on the anterior pituitary

361
Q

-The principal function of testes

A

production of mature germ cells

(spermatogenesis) , and steroid hormones
(steroidogenesis) .

362
Q

Females supplyy of ova

A

e females, who at birth has her

whole life’s supply of ova,

363
Q

Males supply of precursor germ cells

A 
the male
continually renews his pool of precursor
germ cells (spermatogonia) so that a
relatively constant supply is available
throughout life
364
Q

The process of spermatogenesis takes

place within the

A

Coiled seminiferous

tubules of the testes

365
Q

The time it takes for maturation from immature spermatogonia to the mature spermatozoon

A

approximately 60

days in humans

366
Q

Two cell types are critical for

maturation of spermatozoa

A

Leydig cells and Sertoli cells

367
Q

Where are Leydig cells located?

A

outside the seminiferous

tubules

368
Q

In response to LH, what do Leydig cells do?

A

synthesize androgens

369
Q

Where are Sertoli cells located?

A

within the seminiferous

tubules

370
Q

What are Sertoli cells intially involved in?

A

sperm maturation process

371
Q

In response to FSH, what do Sertoli cells do?

A

synthesize

Androgen Binding Protein (ABP) and inhibin

372
Q

What is Spermatogenesis dependent on? where? how much?

A 
critically dependent on androgen
concentrations
-within seminiferous tubules,
- 10 times higher
than androgen concentration in circulation
373
Q

What happens if less than 10 times higher concentration in seminiferous tubules than circulation?

A

otherwise spermatogenesis ceases

374
Q

What ensures high androgen concentration

within seminiferous tubules

A

presence of ABP synthesized by Sertoli cells

375
Q

Testicular androgen synthesis regulated by

A

two negative feedback loops:

376
Q

two negative feedback loops for Testicular androgen synthesis

A

Hypothlamic-pituitary-Leydig cell axis

Hypothalamic-pituitary-seminiferous-tubules axis:

377
Q

Hypothlamic-pituitary-Leydig cell axis

A

GnRH stimulates release of LH and FSH -
stimulate Leydig cells and Sertoli cells. Leydig cells produce androgen, which
inhibit the release of GnRH , LH and FSH

378
Q

Hypothalamic-pituitary-seminiferous-tubules axis

A

non steroidal inhibin

secreted by the sertoli cells inhbits FSH release only

379
Q

Principal functions of ovary

A

production of mature

eggs, and steroid hormones

380
Q

What do mature eggs, and steroid hormones do

A

regulate the reproductive tract and influence sexual behavior

381
Q

Where are germs cells at brith

A

At birth ovary contains non-proliferating

pool of germ cells or oocytes

382
Q

Number of ova at birth vs pubery

A

about 2 million), which are its whole life supply of ova.

At puberty only ~400,000 ova left

383
Q

The oocytes are surrounded by a

A

single layer
of granulosa cells and a basement membrane
making up the structures called primordial
follicles -

384
Q

fundamental reproductive units of

the ovary

A

primordial follicles

385
Q

Growth of primordial follicles is controlled by? until?

A

gonadotropins and
steroid hormones until the follicles either
ovulate or degenerate (atresia).

386
Q

Follicular development leads to one of two events

A
  1. Follicular Atresia

2. Ovulation

387
Q

Follicular Atresia

A

Although many follicles initiate growth and development in each
reproductive cycle, in humans usually only one follicle will ovulate in each
reproductive cycle - remaining secondary follicles degenerate in a process
known as atresia

388
Q

atresia

A

process of remaining secondary follicles

389
Q

Ovulation

A

follicular rupture

390
Q

What happens to ruptured follicle?

A

Ruptured follicle transformed into Corpus

Luteum

391
Q

What does Corpus Luteum do

A

secretes progesterone

392
Q

What cell/s cells contribute to

formation of the corpus luteum

A

Both theca and granulosa cells

393
Q

a temporary

endocrine structure within the ovary? what does it synthesize?

A

corpus luteum

progesterone and estrogens

394
Q

Progesterone and estrogens amounts following ovulation? what happens after?

A

Progesterone and estrogens are produced in large
amounts by corpus luteum for few days following
ovulation but then drop off unless implantation of
the fertilized ovum occurs

395
Q

-Upon implantation, corpus luteum transformed

into

A

corpus luteum of pregnancy

396
Q

corpus luteum of pregnancy is responsable for

A

synthesis of progesterone and estrogens and
creation of proper endocrine environment for maintenance of pregnancy until progesterone and
estrogen synthesis by placenta established

397
Q

In absence of implantation what happens to corpus luteum?

A

Luteolysis occurs

life span of corpus luteum limited

398
Q

What induces luteal regression?

A

prostaglandins which decrease LH binding and thus

steroidogenesis

399
Q

What may be trigger for initiation of next

reproductive cycle

A

Decrease of plasma progesterone and

estrogen

400
Q

Prior to day 1 of the menstrual cycle what happens to the endometrium? under the influence of what?

A

-Prior to day one, endometrium thickens under influence of estradiol

401
Q

What induces the appearance of specialized glycogen-secreting glands

A

progesterone

402
Q

What occurs on day 1 of menstrual cycle?

A

first day of detectable vaginal bleeding

deterioration of uterine endometrium

403
Q

When does menses begin?

A

when estradiol and progesterone very low in circulation, when
the blood vessels supplying endometrium constrict reducing the blood supply

404
Q

When the endometrium deteriorates where does it flow?

A

flows through the cervix into the vagina

405
Q

How long does bleeding last? what happens to the ovaries?

A

Bleeding occurs for ~5 days during which, ovaries are endocrinologically rather inactive

406
Q

Low estradiol and progesterone lead to secretion of what hormone and decreases what

A

to increased
pituitary FSH secretion (lack of –ve feedback loop)
decrease in non-steroidal ovarian inhibin

407
Q

What does non-steroidal ovarian inhibin do?

A

selectively inhibits secretion of FSH, may

contribute to elevation in FSH release

408
Q

What happens to ovarian follicles under influence of FSH

A

Under influence of FSH, cohort of ovarian follicles

develop.

409
Q

What does FSH stimulate in menstrual cycle?

A

granulosa cells of follicles to proliferate

410
Q

How does the stimulation of granulosa cells of follicles to proliferate affect estrogen levels? and granulose cells?

A

production of estrogen, which further stimulates granulosa cell proliferation

411
Q

What occurs on day 8 of the menstrual cycle?

A

one follicle becomes dominant and
committed to further development. Remaining
follicles begin to degenerate by atresia

412
Q

What does the dominant follicle produce? effects?

A

produces increasingly more estradiol

increasing estradiol stimulates uterine endometrium proliferation

413
Q

What happens to the endotherium by day 13?

A

the endometrium very thick

414
Q

What induces the production of endometrial progesterone receptors?

A

Estradiol

415
Q

Moderate estradiol concentrations on FSH release

A

negative feedback

416
Q

What does moderate estradoil concentraions stimulate? which in turn stimulates?

A

stimulate synthesis of LH by pituitary and increase sensitivity of pituitary to GnRH

stimulates LH synthesis

417
Q

Under influence of developing follicles at high estradiol concentrations what happens?

A

estrogen concs.

continue to build

418
Q

Elevated estrogen concs. stimulate

A

LH release - LH surge

419
Q

On day 14 what happens to FSH

A

small increase in FSH release also occurs

420
Q

What happens to LH synthesis by day 14.

A

Stimulation of LH synthesis by estradiol and increased sensitivity of the anterior pituitary to GnRH leading to increased LH synthesis by anterior pituitary known as estrogen +ve feedback control mechanism

421
Q

What feedbacks does estrogen exert?

A

-ve feedback - decreased GnRH and LH release
+ve feedback -
increased sensitivity of anterior pituitary cells to GnRH and increased LH synthesis

422
Q

At day 14, what is the size of the follicle and why does it rupture? cause on ovum

A

the follicle has become huge.
The sudden surge of LH causes the
follicle to rupture and the ovum is ejected

423
Q

Oral contraceptives contain

A

estrogen and progesterone

424
Q

What do Oral contraceptives do

A

maintain moderate circulating levels of estrogen and progesterone suppress the release of LH and FSH from the pituitary and prevent ovarian
follicles from maturing and being ovulated

425
Q

Under the influence of LH the follicle becomes

A

corpus luteum

426
Q

Under the influence of LH the follicle produces

A

large amounts of

estradiol and progesterone

427
Q

The production of large amounts of

estradiol and progesterone induces

A

endometrial growth of the uterus

the endometrium becomes glandular

428
Q

The luteal Phase occurs when there is

A

no fertilization

429
Q

What happnes during the luteal Phase? how long does it last?

A
  • egg degenerates, corpus luteum degenerates (luteolysis)

14 days

430
Q

What happens after 14 days in absence of implantation?

  • corpus luteum
  • steriod levels
  • uterune endometrium
  • menstruation
  • FSH secretion
A

After 14 days in absence of implantation corpus luteum degenerates, steroid levels drop,
uterine endometrium degenerates, menstruation begins and pituitary starts to increase its
secretion of FSH,

431
Q

At ovulation where is the unfertilized egg taken? where is it propelled towards?

A

unfertilized egg is taken by the fimbria of the oviduct (or fallopian tube)
Is being propelled towards the lumen of the uterus

432
Q

If sexual intercourse takes place around the ovulation time what happens

A 
fertilization!
some spermatozoa
deposited in the vagina will travel as
far as the oviduct and one of these will
fertilize the egg
433
Q

After fetilization what happens to the egg? where is it transported?

A

Egg starts dividing to the stage of
blastocyst during its transport down
the oviduct into the uterine lumen

434
Q

After implantation, the Blastocyst differentiates into (2)? which becomes the?

A

Blastocyst differentiates into trophoblast (becomes
the placenta) and the inner cell mass (which will form
the embryo)

435
Q

Around time of implantation, trophoblast starts to

synthesize

A

human chorionic gonadotropin (HCG)

436
Q

human chorionic gonadotropin (HCG) has similar properties to

A

LH-like properties

437
Q

WHat does HCG stimiute

A

the corpus

luteum to continue secreting gonadal steroids

438
Q

After about 12th week of pregnancy endocrine function of corpus luteum is taken over by

A

placenta

439
Q

The plcenta with the developing fetus forms the

A

fetoplacental unit

440
Q

HCG appears in what? and what is the levels used for?

A 
HCG quickly appears
in blood and urine
where it forms the
basis for the biological
or immunological
pregnancy test
441
Q

lactation

A

The secretion of milk by the breast

442
Q

What. is required for lactation

A

Normal mammary

development under endocrine control

443
Q

Ductal

A

Mature non-pregnant mammary glands

444
Q

marked

enhancement of duct growth and duct branching in puberty occurs because of

A

increasing levels of estrogens

445
Q

in prescence of estrogen, marked enhancement of duct growth and duct branching
but relatively little development of the

A

alveoli

446
Q

What stimulates the growth of the aveoli

A

Progesterone

447
Q

most breast enlargement due to

A

fat deposition under the glandular tissue

448
Q

What causes both

ductal and alveoli structures to fully develop

A

Under influence of several hormones, including estrogen,

progesterone, prolactin, human placental lactogen

449
Q

Milk production during pregnancy controlled by

A

prolactin

450
Q

What inhibits milk secretion

A

high estrogen levels

451
Q

What induces milk synthesis and the alveoli secrete

milk, filling the ducts

A

Prolactin

452
Q

What causes ducts contract to cause milk ejection.

A

under action of oxytocin

453
Q

What do ferent

fibers (nerves) from nipple stimulate

A

Prolactin from anterior pituitary and oxytocin from posterior pituitary

454
Q

What sustains milk production?

A

Prolactin

455
Q

What causes milk letdown or ejection

A

oxytocin

456
Q

Milk contains

A

water, protein, fat and carbohydrate lactose and antibodies

457
Q

What can be transmitted from mother to infant through breast milk?

A

infectious agents

such as viruses and drugs

458
Q

Lactational amenorrhea

A

Maintained nursing stimulates prolactin production, which inhibits the secretion of FSH
and LH

459
Q

What does Lactational amenorrhea block

A

The resumption of the reproductive cycle

460
Q

Menopause

A

loss of ovarian steroid production

461
Q

Effect on hormones from Depletion of follicles

A

loss of capacity for steroid (estrogen and progesterone)

hormone production by the ovary

462
Q

What induces the following symptoms?:
hot flashes, dry vagina,
restlessness, bone loss (osteoporosis - long term)

A

-Lack of estrogens

463
Q

What eliminates–ve feedback loop and rise in

levels of plasma gonadotropins FSH and LH

A

Cessation of ovarian steroid hormone production

464
Q

The constantly high levels of plasma FSH is

most reliable indicator for

A

onset of menopause

PHGY210 (6 decks)

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