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MAMS > Physio Exam 3 Endocrine > Flashcards

Physio Exam 3 Endocrine Flashcards

1
Q

5 main groups of hormones

A 
Derivatives of amino acids 
Small peptides
Proteins 
Glycoproteins 
Steroids
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2
Q

Ka=

A

[HR]/[H] [R]

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3
Q

Kd=

A

1/KA= [H] [R]/[HR]

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4
Q

what does Kd calculate?

A

receptor occupancy for any given [H]

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5
Q

what activates adenylate cyclase?

A

alpha subunit bound to GTP

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6
Q

what does the amount of active adenylate cyclase depend on?

A

rate of exchange of GTP for GDP and rate of hydrolysis of bound GTP

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7
Q

what does cAMP do?

A

activates PKA

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8
Q

what does activation of Gqa do?

A

activates PLC

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9
Q

what does PLC do?

A

cleaves PIP2 into diacylglycerol and IP3

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10
Q

what does IP3 do?

A

mobilizes Ca from vesicular storage sites

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11
Q

what does diacylglycerol do?

A

activates PKC

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12
Q

what does Gia do?

A

inhibits adenylate cyclase

activates K channels

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13
Q

what does transducin/Gta do?

A

stimulates cGMP phophodiesterase in photoR

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14
Q

what do serine/threonine kinases activate?

A

Smads

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15
Q

what do Smads do?

A

move to the nucleus and participate with other gene regulatory proteins in influencing transcription

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16
Q

what is the guanylate cyclase a receptor for?

A

ANP

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17
Q

how do guanylate cyclase receptors work?

A

increase cGMP which activates PKG

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18
Q

what do cytokine receptors activate?

A

JAKs

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19
Q

what do JAKs do?

A

phosphorylate STATs

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20
Q

what do STATs do?

A

move to nucleus and regulate transcription

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21
Q

coated pits

A

where hormone-receptor complexes cluster in regions of the membrane

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22
Q

coated vesicles

A

Coated pits invaginate and pinch off from the membrane

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23
Q

what coats coated pits?

A

clathrin

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24
Q

adaptins

A

found in the coat and recognize cytoplasmic domains of receptors to trap them in the pit

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25
Q

HRE

A

hormone response elements

where steroid hormones interact with DNA

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26
Q

what kind of sequence do HREs have?

A

Palindromic sequences or direct repeats

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27
Q

3 structural domains of intracellular hormone receptors

A

c-term binding region
central DNA binding region
variable N-term

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28
Q

what is the sequence of the Central, highly conserved DNA binding domain of intracellular hormone R?

A

Rich in cysteine residues

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29
Q

role of Variable N-terminal domain of intracellular hormone R

A

Participates in recruitment of transcription factors

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30
Q

what do increases and decreases in carrier protein concentration cause?

A

reciprocal changes of free hormone levels

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31
Q

negative cooperativity

A

Increasing receptor occupancy decreases the affinity of remaining receptors for hormone

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32
Q

down regulation

A

Exposure of responsive cells to high concentrations of hormone can lead to a decrease the # of receptors

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33
Q

why are cells down regulated?

A

Protects cell from intense stimulation of chronically elevated hormone levels

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34
Q

Phosphorylation of cytoplasmic domains of the receptor decreases ___

A

affinity for G protein

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35
Q

what mediates uncoupling of receptors from G proteins

A

beta-ARK

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36
Q

beta arrestin

A

binds to the phosphorylated receptor and blocks the interaction with the G-protein

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37
Q

how are peptide hormones inactivated?

A

proteases on the cell membrane

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38
Q

how are steroid hormones inactivated?

A

enzymes in the liver

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39
Q

what does a hormone radioassay measure?

A

nanogram quantities of a hormone

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40
Q

Scatchard analysis

A

Determine binding constants of hormone-receptor interactions and the concentration of receptors in a preparation of cells or membrane fractions

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41
Q

what is the slope a the Scatchard analysis?

A

-Kd^-1

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42
Q

what is the x-intercept of the Scatchard analysis?

A

[Rt]- conc of total binding sites

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43
Q

sella turcica

A

pocket of bone at the base of the brain

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44
Q

neurohypophysis

A

posterior lobe of pituitary

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45
Q

what does the neurohypophysis secrete?

A

oxytocin

ADH

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46
Q

adenohypophysis

A

anterior lobe of pituitary

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47
Q

what does the neurohypophysis develop from?

A

floor of brain

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48
Q

what does the adenohypophysis develop from?

A

roof of mouth

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49
Q

what artery supplies the posterior pituitary?

A

inferior hypophyseal artery

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50
Q

where are hormones from the anterior pituitary stored?

A

near median eminence, near cap plexus of superior hypophyseal artery

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51
Q

primary role of ADH

A

conserve body water and regulate the tonicity of body fluids

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52
Q

target cells of ADH

A

renal cells responsible for reabsorbing water

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53
Q

what stimulates ADH?

A

water deprivation

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54
Q

what does lack of ADH lead to?

A

diabetes insipidus

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55
Q

primary role of oxytocin

A

eject milk from lactating mammary glands

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56
Q

major stimulus of oxytocin

A

suckling by infant

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57
Q

effects of oxytocin

A

contraction of myoepithelial cells mammary gland and ejection of milk

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58
Q

stimulus of oxytocin during labor

A

dilation of cervix

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59
Q

effect of oxytocin during labor

A

positive feedback

enhances muscle contraction

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60
Q

what is the most abundant pituitary hormone?

A

GH

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61
Q

what is prolactin secretion under the control of?

A

dopamine

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62
Q

what does prolactin do?

A

Induces synthesis of casein and lactalbumin in mammary glands
Stimulates breast development

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63
Q

what does excess prolactin cause?

A

galactorrhea

inhibition of GnRH and menstruation

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64
Q

what does deficient prolactin cause?

A

failure to lactate

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65
Q

what is apart of POMC?

A

ACTH and β-lipotropin

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66
Q

β-lipotropin role

A

Induces pigmentation and affects adrenal steroid secretion

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67
Q

__ stimulates ACTH synthesis and secretion

A

CRH

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68
Q

half life of FSH, LH, TSH

A

30 min- 2 hrs

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69
Q

pituitary is under the influence of the ___

A

CNS

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70
Q

how does the hypothalamus influence the pituitary?

A

blood-borne factors called hypothalamic releasing hormones

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71
Q

where is GnRH concentrated?

A

medial basal hypothalamic nuclei

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72
Q

what does GnRH do?

A

Stimulates pituitary synthesis and secretion of LH and FSH

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73
Q

what modulates the response to GnRH?

A

sex steroid

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74
Q

high levels of GnRH ___

A

block steroidogenesis

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75
Q

what does GHRH do?

A

Stimulates GH synthesis and release from pituitary directly

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76
Q

what does somatostatin do?

A

inhibits release of GH

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77
Q

what does TRH do?

A

Stimulates pituitary synthesis and secretion of TSH and prolactin

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78
Q

TRH mechanism of action

A

Binds to specific receptors on thyrotropes and activates PLC

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79
Q

where is the highest conc of TRH?

A

hypothalamus

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80
Q

what does PIF do?

A

Tonically inhibits the secretion of prolactin

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81
Q

what does CRH do?

A

Stimulates pituitary ACTH synthesis and release

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82
Q

3 categories of endocrine disorders

A

hyposecretion
hypersecretion
hyporesponsiveness

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83
Q

primary hyposecretion

A

Endocrine target gland secretes too little hormone because its not functioning normally

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84
Q

secondary hyposecretion

A

Endocrine target gland is fine

Tropic hormone produced by pituitary is too low

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85
Q

primary hypersecretion

A

Dysfunctional gland secretes too much hormone

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86
Q

secondary hypersecretion

A

Excessive stimulation by tropic hormone

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87
Q

hyporesponsiveness

A

Target cells don’t respond to the 3rd hormone

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88
Q

3 major causes of hyporesponsiveness

A

Lack or deficiency in receptors for the hormone
Post-receptor defect in target cell
Lack of metabolic activation of a hormone

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89
Q

how does GH act?

A

stimulates mitosis of many target tissues

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90
Q

what chemical messengers does GH mediate?

A

IGF-I, -II

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91
Q

what does plasma conc of IGF-I reflect?

A

availability of GH and/or the rate of growth

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92
Q

what kind of receptor is the IGF R?

A

tyrosine kinase

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93
Q

how does IGF-I act?

A

autocrine or paracrine

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94
Q

what is the main source of IGF-I?

A

liver

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95
Q

how is GH secreted?

A

episodic bursts

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96
Q

what is the primary drive for GH synthesis?

A

GHRH

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97
Q

what is the growth promoting hormone during fetal growth?

A

insulin

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98
Q

how do excess glucocorticoids effect GH secretion?

A

decrease

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99
Q

mid parental height

A

dad’s height+mom’s/2

+2.5 for boys

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100
Q

excess of GH before puberty causes __

A

gigantism

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101
Q

excess of GH after puberty causes __

A

acromegaly

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102
Q

acromegaly symptoms

A 
Disfiguring bone thickening
enlargement of hands and feet
protrusion of lower jaw
increased body hair
glucose intolerance
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103
Q

acromegaly treatment

A

somatostatin analogs

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104
Q

deficiency of GH symptoms

A

failure to grow
short stature
mild obesity
delayed puberty

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105
Q

what does the outer cortex of the adrenal gland produce?

A

steroid hormones

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106
Q

what does the inner medulla of the adrenal gland produce?

A

epi

NE

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107
Q

layers of adrenal cortex

A

Zona glomerulosa
Zona fasciculata
Zona reticularis

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108
Q

Zona glomerulosa produces

A

aldosterone

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109
Q

Zona fasciculata produces

A

cortisol

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110
Q

Zona reticularis produces

A

cortisol

androgens

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111
Q

main mineralocorticoid

A

aldosterone

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112
Q

main glucocortiocoid

A

cortisol

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113
Q

what does the medulla arise from embryonically?

A

neuroectoderm

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114
Q

what are all adrenal cortical hormones derived from?

A

cholesterol

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115
Q

rate limiting step of adrenal hormone synthesis

A

cholesterol to pregnenolone

first step

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116
Q

StAR role

A

stimulates transport of cholesterol from cytosol to mitochondria

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117
Q

are glucocorticoids or aldosterone favored to bind to albumin?

A

glucocorticoids

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118
Q

which receptors do mineralocorticoids bind to?

A

type I in cytoplasm

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119
Q

which receptors do glucocorticoids bind to?

A

type II

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120
Q

what is the controlling factor of cortisol and androgen synthesis?

A

ACTH

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121
Q

Stimulation of ACTH leads to a rise in steroid hormone secretion within __ minutes

A

1-2

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122
Q

when does ACTH secretion peak?

A

early morning

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123
Q

high levels of cortisol cause

A 
increased blood glucose
promotes catabolism
decreased glc use
decreased pro synth
altered fat metab
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124
Q

how does cortisol promote catabolism?

A

Facilitates breakdown of protein from muscle and CT to increase AA used in gluconeogenesis
Stimulates production of gluconeogenic enzymes in the liver

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125
Q

how does cortisol decrease glc use?

A

Inhibits glucose transport into cells except for brain

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126
Q

how does cortisol alter fat metabolism?

A

Increases rates of peripheral fat breakdown → liberate FA and glycerol for gluconeogenesis
Increases central fat deposition

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127
Q

CNS effects of cortisol

A

Feedback inhibition of CRH and ACTH
Affects perception
Initial euphoria followed by depression

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128
Q

CVS effects of cortisol

A

Maintains sensitivity to epinephrine and norepinephrine in vasculature

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129
Q

developmental effects of cortisol

A

Permissive role in maturation of fetal organ systems, intestinal enzymes, surfactant

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130
Q

renal effects of cortisol

A

Cortisol exerts feedback inhibition on secretion of CRH and ADH

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131
Q

bone effects of cortisol

A

Promotes bone breakdown by increasing osteoclast activity

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132
Q

immune function of cortisol

A

suppresses body’s inflammatory response

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133
Q

what does prolonged administration of glucocorticoids cause?

A

feedback inhibition of ACTH production, atrophy of adrenal cells, reduced ability to produce cortisol

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134
Q

how is cortisol eliminated by the body?

A

Filtered by glomerulus and appears in the urine

Enzymatically reduced in the liver

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135
Q

when are adrenal androgens critical?

A

fetal development

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136
Q

primary function of aldosterone

A

increase sodium reabsorption in the distal nephron

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137
Q

what is the production of aldosterone under control of?

A

AII
plasma K
ACTH

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138
Q

what is the consequence of increased aldosterone during pregnancy?

A

expanded ECF

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139
Q

what are the cells of the adrenal medulla?

A

chromaffin

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140
Q

ratio of catecholamines in chromaffin cells

A

5 epi:1 NE

1ATP:4 catecholamines

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141
Q

what are catecholamines made from?

A

tyrosine

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142
Q

what enzyme catalyzes the conversion from epi to NE?

A

PMNT

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143
Q

what stimulates release of chromaffin granules?

A

sympathetic cholinergic stimulation

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144
Q

half life of catecholamines

A

10-15 seconds

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145
Q

B cell of pancreas role

A

produces insulin

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146
Q

A cell of pancreas role

A

releases glucagon

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147
Q

D cell of pancreas role

A

releases somatostatin

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148
Q

PP cell of pancreas role

A

releases pancreatic polypeptide

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149
Q

pancreatic polypeptide role

A

Inhibition of gallbladder contraction

pancreatic enzyme secretion

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150
Q

how does blood flow in the pancreatic islet?

A

center outwards

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151
Q

what do Sulfonylureas do?

A

stimulate insulin secretion

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152
Q

how does glucose enter the beta cell?

A

GLUT2

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153
Q

how does increased glc cause insulin release from the beta cell?

A

Increased glucose metabolism → increased ATP/ADP ratio → close ATP sensitive membrane K channel → membrane depolarization → opens voltage sensitive Ca channel → Ca enters cell → exocytosis of secretory granules

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154
Q

2 functions of insulin R

A

Recognize and bind insulin with high affinity and specificity
Generate the signals that modulate insulin’s effector function

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155
Q

insulin R structure

A

glycoprotein with 2 alpha and 2 beta subunits linked by disulfide bridges

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156
Q

alpha subunit of insulin R

A

externally oriented and contains the insulin binding site

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157
Q

beta subunit of insulin R

A

transmembrane protein that plays a role in signal transduction

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158
Q

how does insulin regulate glc homeostasis?

A

controlling hepatic glucose production and utilization of glucose by muscle and adipose tissue

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159
Q

what tissues have GLUT4?

A

muscle

adipose

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160
Q

how does insulin increase K into cells?

A

increase of activity of Na-K ATPase

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161
Q

major stimuli for glucagon secretion

A

falling blood glucose
elevated AA in plasma
sympathetic stimulation

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162
Q

what inhibits glucagon secretion?

A

elevated blood glucose
somatostatin
insulin

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163
Q

where does glucagon have most of its effects

A

liver

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164
Q

how does glucagon act?

A

via receptors with Gs proteins → increases cAMP

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165
Q

actions of glucagon

A

Promotes glycogenolysis and gluconeogenesis → increase glucose release
Increases beta oxidation

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166
Q

what drives satiation?

A

release of appetite-inhibitory peptides from GI tract

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167
Q

how do satiety peptides slow the return of hunger?

A

decrease rate of gastric emptying

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168
Q

incretin

A

peptide hormone that stimulates insulin secretion and improves glucose tolerance during a meal

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169
Q

what is the only peptide that increases appetite?

A

ghrelin

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170
Q

where does ghrelin bind?

A

appetite stimulatory neurons in the hypothalamus

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171
Q

actions of ghrelin

A

Increases food intake
body weight
Decreases fat breakdown

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172
Q

adiposity hormone

A

Basal hormone levels parallel the amount of adipose tissue

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173
Q

where does leptin bind

A

receptors on hypothalamic neurons

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174
Q

which hormone inhibits appetite

A

leptin

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175
Q

__ levels fall with long term exercise programs

A

leptin

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176
Q

orexigenic

A

appetite stimulating

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177
Q

anorexigenic

A

appetite inhibiting

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178
Q

2 peptides in orexigenic pathway

A

NPY

AgRP

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179
Q

what inhibits orexigenic ARC neurons?

A

leptin

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180
Q

2 peptides in anorexigenic pathway

A

CART

POMC

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181
Q

what does AgRP inhibit?

A

melanocortin R in anorexigenic circuit

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182
Q

1,25[OH]2D3 main effects

A

Increases calcium absorption from intestine

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183
Q

PTH main effects

A

Mobilizes calcium from bone

Increases phosphate excretion

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184
Q

calcitonin main effects

A

Ca lowering

inhibits bone resorption

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185
Q

consequence of low Ca conc

A

increases excitability of nerve and muscle cells → hypocalcemic tetany

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186
Q

consequence of high Ca conc

A

cardiac arrhythmia

depresses neuromuscular activity

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187
Q

how much Ca is in the rapidly exchangeable pool?

A

500mM

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188
Q

what 2 homeostatic systems affect the Ca in bone?

A

plasma Ca

bone remodeling

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189
Q

what regulates Ca in the GI tract?

A

1,25[OH]2D3 through negative feedback mechanisms

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190
Q

osteoblasts

A

bone forming cells
Secrete collagen and form a calcified matrix
Derived from fibroblast precursor cells

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191
Q

osteocytes

A

differentiated osteoblasts surrounded by bone matrix

Send processes throughout the bone

192
Q

osteoclasts

A

multinuclear cells that digest and resorb bone
Derived from monocytic precursors
Secrete acids and proteases

193
Q

how is vitamin D3 produced?

A

action of UV light on 7-dehydrocholesterol in the skin

194
Q

how is vitamin D3 transported?

A

through vitamin D binding protein in the plasma

195
Q

what happens to vitamin D3 in the liver?

A

hydroxylated at the 25 position

196
Q

where does vitamin D3 become bio active?

A

kidney

hydroxylated at 1 position

197
Q

what stimulates kidney production of 1,25[OH]2D3

A

PTH
hypocalcemia
hypophosphatemia

198
Q

how does PTH increase production of 1,25[OH]2D3 in kidney

A

decreases intracellular phosphorus concentration in the kidney by enhancing phosphate diuresis

199
Q

main action of 1,25[OH]2D3

A

provide Ca and phosphate to ECF for bone mineralization

200
Q

deficiency of 1,25[OH]2D3 in children causes?

A

rickets

201
Q

deficiency of 1,25[OH]2D3 in adults causes?

A

osteomalacia

202
Q

VDR

A

Transcription factor which regulates gene expression

Produces mRNAs that code for various Ca-binding proteins and Ca and phosphate transporters

203
Q

1,25[OH]2D3 inhibits proliferation of cells with __

A

VDR

204
Q

main action of 1,25[OH]2D3 in GI

A

increase Ca pumping out of basolateral membranes

205
Q

how does 1,25[OH]2D3 increase Ca pumping out of basolateral membranes

A

Promotes phosphate and Ca uptake
Ca entry is enhanced by increases in epithelial Ca channels and intracellular Ca binding protein
Upregulates Ca/Na exchange mechanisms

206
Q

main action of 1,25[OH]2D3 in bones

A

Mobilizes Ca and phosphate by increasing pumping through osteoblasts

207
Q

main action of 1,25[OH]2D3 in kidney

A

Facilitates Ca reabsorption in proximal and distal nephron

208
Q

main action of 1,25[OH]2D3 in distal tubule

A

Induces formation of ECaC and calbindin → enhances Ca uptake

209
Q

main action of 1,25[OH]2D3 in proximal tubule

A

Increases expression of Na-dependent phosphate transporter → enhances phosphate reuptake

210
Q

how is 1,25[OH]2D3 regulated

A

Negative feedback from plasma Ca and phosphate
Negative feedback from 1,25[OH]2D3 overproduction on 1-alpha hydroxylase
Positive feedback from 1,25[OH]2D3 stimulation of renal 24-hydroxylase and production of 24,25[OH]2D3 → degradation

211
Q

half life of PTH

A

20 min

212
Q

where is the Ca sensor?

A

parathyroid gland

213
Q

5 main actions of PTH

A

Increases bone resorption and mobilizes
Decreases plasma phosphate
Increases Ca reabsorption in distal tubules
Increases formation of 1,25[OH]2D3 → increases Ca absorption in intestines
Increases formation of osteoclasts and osteoblasts

214
Q

how does PTH increase bone resorption

A

Increases permeability of Ca in bone fluid of osteoclasts and osteoblasts

215
Q

how does PTH decrease plasma phosphate

A

Increases urine phosphate excretion

216
Q

what expresses RANKL

A

osteoblasts

217
Q

what expresses RANK

A

Precursor monocytic osteoblasts

218
Q

what is OPG?

A

decoy that blocks RANKL and RANK interactions

219
Q

what enhances OPG production

A

estrogens

220
Q

what inhibits OPG

A

cortisol

221
Q

short term effect of PTH

A

increase osteoblastic activity

222
Q

prolonged effect of PTH

A

apoptosis of osteoblasts

223
Q

what does pulsatile PTH cause?

A

bone formation

avoids apoptosis effect

224
Q

actions of PTH in the kidney

A

PTH increases Ca reabsorption in the distal nephron

Inhibits reabsorption of phosphate in the proximal tubule

225
Q

how does PTH work in the kidney

A

PTH activates AC in the basolateral membrane → cAMP

Inactivates Na/phosphate cotransporter in the luminal membrane

226
Q

high amounts of FGF-23 cause

A

decrease number of Na/phosphate cotransporters → reduces phosphate reabsorption
Decreases conversion of 25OHD3 to 1,25[OH]2D3

227
Q

what produces FGF-23

A

osteoblasts

228
Q

what causes production of FGF-23?

A

elevated 1,25[OH]2D3

229
Q

Mg deficiency causes?

A

decreased skeletal response to PTH

decrease release of Ca into blood

230
Q

high levels of Mg cause?

A

inhibit PTH production

231
Q

Mg deficiency CVS effects

A

impaired Na/K ATPase → increased movement of K to ECF → alters intracellular/extracellular ratio

232
Q

high Ca effect on PT gland

A

inhibited PTH secretion → Ca deposited in bone

233
Q

low Ca effect on PT gland

A

increased PTH secretion → Ca mobilized from bones

234
Q

1,25[OH]2D3 effect on PT gland

A

decreasing production of pre-pro-PTH

235
Q

Trousseau’s sign

A

muscle spasm that causes flexion of wrist and thumb with finger extension

236
Q

PT gland tumor effects

A 
Hypercalcemia → cardiac arrhythmia
Hypophosphatemia 
Demineralization of bones
Hypercalciuria 
Ca stones
237
Q

PTH-related peptide actions

A

same as PTH

leads to decreased PTH levels and hypercalcemia

238
Q

what secretes calcitonin

A

C cells of thyroid

239
Q

when is calcitonin secreted?

A

when thyroid gland is perfused with high Ca

240
Q

half life of calcitonin

A

10 minutes

241
Q

actions of calcitonin

A

Decreases plasma Ca and phosphate by decreasing bone resorption
Increases Ca excretion in urine

242
Q

how does calcitonin decrease plasma Ca

A

Acts via receptors on osteoclasts
Inhibits resorption
Decreases Ca permeability in osteoclasts and osteoblasts

243
Q

how do excessive levels of glucocorticoids effect Ca

A

Decrease absorption of Ca by intestine
Increase excretion by kidney
Bone resorption
negative balance

244
Q

GH effects on Ca

A

increases intestinal absorption

245
Q

T3 and T4 effects on Ca

A

Increase Ca by increasing bone resorption

246
Q

GnRH

A

gonadotropin releasing hormone

AK luteinizing releasing hormone

247
Q

1/2 life of GnRH

A

4 min

248
Q

how is GnRH released?

A

pulsatile

249
Q

what does GnRH act on?

A

gonadotropes of anterior pituitary

250
Q

what does GnRH induce?

A

FSH and LH via phospholipase C signaling

251
Q

consequences of constant GnRH levels

A

low FSH and LH due to down regulation of GnRH receptors

252
Q

1/2 life of LH

A

20-30 min

253
Q

what does LH act on?

A

interstitial steroidogenic cells → Leydig cells of the tesis and theca cells of the ovaries

254
Q

FSH 1/2 life

A

2-3 hours

255
Q

what does FSH act on?

A

follicular cells → sertoli cells of the testis and granulosa cells of the ovary

256
Q

LH and FSH have a common alpha subunit with __ and __

A

TSH

hCG

257
Q

how do LH and FSH act on cells?

A

AC/cAMP/PKA

258
Q

what produces T?

A

leydig cells of testis

259
Q

T affect on Hypothalamic-Pituitary-Gonadal Axis

A

Inhibits LH release by anterior pituitary and decreases GnRH release by the hypothalamus

260
Q

how is T converted to DHT?

A

5alpha reductase 1 and 2 in target tissues

261
Q

E1

A

estrone

262
Q

E2

A

estradiol

263
Q

E3

A

estriol

264
Q

which estrogen is a fetal adrenal and liver placental product?

A

E3

265
Q

what cells make androgen precursors female

A

theca cells

266
Q

where and how are androgens converted in females

A

granulosa cells

FSH induced aromatase

267
Q

Moderate, steady levels of estrogen inhibit ____ early in the menstrual cycle

A

LH release

268
Q

Rising levels of estrogen increase LH release before ___

A

ovulation

269
Q

what produces progesterone

A

corpus luteum after ovulation

270
Q

progesterone inhibits?

A

GnRH release

271
Q

__% of sex steroids are bound in plasma

A

98

272
Q

⅔ of T is carried by ____

A

gonadal steroid binding globulin

273
Q

1/2 of T is carried by ___

A

albumin

274
Q

inhibins

A

Glycoproteins with and alpha chain and 1 of 2 beta chains

275
Q

what produces inhibins?

A

FSH stimulated sertoli or granulosa cells

276
Q

where do inihbins act and what is their action?

A

Acts on the anterior pituitary to decrease FSH release

277
Q

what kind of system are inhibins?

A

negative feedback

278
Q

inhibin B

A

produced during follicular phase and in males

279
Q

inhibin A

A

produced during luteal phase

280
Q

what determined gonadal sex?

A

internal genitalia

281
Q

what induces testis development?

A

SRY

282
Q

turner syndrome karyotype

A

XO

283
Q

turner syndrome symptoms

A 
Streak gonad
Amenorrhea
Short stature 
Webbed neck 
Lacking secondary sex characteristics 
1/5000 births
284
Q

Jacobs syndrome karyotype

A

XYY

285
Q

jacobs syndrome symptoms

A

Seemingly normal male
Excess acne
Taller than normal
More aggressive

286
Q

Klinefelter’s syndrome karyotype

A

XXY

287
Q

Klinefelter’s syndrome symptoms

A 
Male genitalia
Increased FSH, LH, E2
Decreased T
Sterility
Feminization 
Retardation 
Common
288
Q

what syndrome is an example of hypergonadotropic hypogonadism

A

Klinefelter’s syndrome

289
Q

what defines phenotypic sex?

A

genital ducts and external genitalia and by secondary sex characteristics

290
Q

what produces mullerian inhibiting hormone

A

sertoli cells

291
Q

what supports differentiation of wolffian ducts?

A

T produced by leydig cells

292
Q

when does the prostate, urethra, penis, and scrotum develop?

A

after T is converted to DHT

293
Q

why do mullerian ducts form in females?

A

lack of MIH and T

294
Q

what supports fetal steroidogenesis?

A

hCG

295
Q

when do T levels reach their max?

A

mid-late 20s

296
Q

thelarche

A

breast development

297
Q

pubarche

A

pubic hair development

298
Q

menarche

A

1st period

299
Q

why are postmenopausal LH and FSH high?

A

low E

lack of inhibin

300
Q

Long bone growth augmented by ___

A

sex steroids

301
Q

adrenarche

A

increased secretion of androgens without changes in cortisol or ACTH levels

302
Q

testicular feminization

A

XY genotype with female external genitalia

303
Q

cause of testicular feminization

A

no functional androgen R

304
Q

5 alpha reductase deficiency syndrome

A

XY genotype
Begins life with female phenotype, later reverts to male phenotype
testes and internal male ducts but no prostate, penis, or scrotum because there is no DHT

305
Q

5 alpha reductase deficiency syndrome cause

A

one of the 2 5 alpha reductase genes in nonfunctional

306
Q

female CAH symptoms

A

Masculinization
Enlargement of clitoris and fusion of labia
Increased muscular development and facial hair → hirsutism
Irregular menses

307
Q

male CAH symptoms

A

Precocious puberty or supermasculinization

308
Q

CAH cause

A

hypersecretion of androgens due to defect in steroid biosynthesis

309
Q

Spermatogonia

A

germ cells, sperm producing stem cell line

310
Q

leydig cells

A

interstitial cells, stimulated by LH, synthesize and secrete T

311
Q

sertoli cells

A

follicular cells, stimulated by FSH, nurse developing sperm

312
Q

what connects sertoli cells?

A

tight junctions that form a blood testis barrier

313
Q

Seminiferous tubules

A

sperm production

314
Q

rete testis

A

collects sperm from multiple seminiferous tubules

315
Q

Efferent ductules

A

conducts sperm to epididymis

316
Q

Epididymis

A

passage where sperm undergo maturation

317
Q

Vas Deferens

A

exit for sperm to seminal vesicles

318
Q

seminal vesicle

A

drains into vas deferens above the prostate

Form ejaculatory duct

319
Q

what does the seminal vesicle produce?

A

fructose

prostaglandins

320
Q

Prostate gland

A

joins ejaculatory duct with urethra

321
Q

what does the prostate produce?

A

buffered secretions to aid sperm in motility and fertilization

322
Q

Bulbourethral (Cowper’s) gland

A

drains into urethra

Produces lubricating mucus

323
Q

Urethra

A

common urogenital passage through penis

324
Q

Scrotum

A

external pouch that suspends testes away from body

325
Q

Cryptorchidism

A

testes remain in abdomen

Infertile, but virile

326
Q

sperm pathway

A 
Seminiferous tubules 
rete testis 
efferent ductules 
epididymis 
vas deferens
ejaculatory ducts 
prostate 
urethra
327
Q

spermatogenesis

A 
Spermatogonium 
continual mitosis 
primary spermatocyte (2n/2DNA) 
1st mitotic division 
2 secondary spermatocytes (1n/2DNA) 
2nd mitotic division 
4 spermatids (1n/1DNA) 
loss of cytoplasm 
4 sperm
328
Q

how long to form primary spermatocyte?

A

2 months

329
Q

how long to pass through epididymis?

A

12 days for full maturation

330
Q

fetal T effects

A

induces Wolffian derived duct system directly

Induces prostate, urethra, penis, scrotum through DHT

331
Q

puberty T effects

A

induces facial, pubic, axillary hair, sebaceous glands, sperm production, larynx development, fat and muscle distribution, promotion of bone growth and cessation of bone growth

332
Q

adult T effects

A

sex drive, muscle growth and maintenance, erythropoiesis, male pattern baldness, cholesterol

333
Q

Oligospermia

A

<20 million sperm/ml

334
Q

Oligospermia causes

A

decreased GnRH, poor nutrition, environmental factors

335
Q

viagra effects

A

inhibits phosphodiesterase-5 → hydrolyzes the cGMP involved in Ca channel closure

336
Q

Oogonia

A

germ cells

337
Q

theca cells

A

interstitial cells

338
Q

theca cells are stimulated by ___ to produce androstenedione

A

LH

339
Q

granulosa cells

A

follicular cells

340
Q

female counterpart of leydig cells

A

theca cells

341
Q

female counterpart of sertoli cells

A

granulosa cells

342
Q

granulosa cells are stimulated by __ to produce aromatase

A

FSH

343
Q

role of aromatase in females

A

Converts androstenedione → estrogen

344
Q

Fimbriae

A

ciliated, finger-like structures on the ampulla of the oviduct

345
Q

Oviduct

A

uterine tube/Fallopian tube

346
Q

Fimbriae role

A

Receives ovum from ovary

347
Q

oviduct role

A

Transports ovum from ovary to the uterus

Provides appropriate environment for fertilization

348
Q

oogenesis

A

Oogonia → continual mitosis until birth → fixed # of primary oocytes (2n/2DNA)
Reduced 10x through atresia by puberty
Primary oocyte → 1st mitotic division → 2ndary oocyte (1n/2DNA) plus polar body
→ 2nd mitotic division → egg (1n/1DNA) plus polar body

349
Q

early follicular stage hormones

A

LH and FSH rise as inhibitors fall

350
Q

what hormone stage does menstruation take place in?

A

early follicular

351
Q

what stimulates new cohorts of follicles?

A

rising FSH

352
Q

what do proliferating granulosa cells secrete during the early follicular phase?

A

inhibin B

353
Q

mid follicular stage hormones

A

rising inhibin B suppresses FSH release

354
Q

what does the FSH decrease cause in the mid follicular stage?

A

stimulates dominant follicle, atresia of others

355
Q

why do E levels increase in the mid follicular stage?

A

LH-stimulated theca cell production of androgens and conversion by aromatase into estrogen in granulosa cells

356
Q

what does E cause in the mid follicular stage?

A

growth of granulosa and theca cells through paracrine signalling

357
Q

late follicular stage

A

estrogen induced growth of follicle → rising estrogen levels → follicular growth

358
Q

what does the increased E cause in the late follicular stage?

A

anterior pituitary increased sensitivity to GnRH by increased GnRH R on gonadotropes
Positive feedback

increased LH R on theca cells

359
Q

what happens to LH during the late follicular stage?

A

increases

360
Q

why does ovulation occur?

A

due to increase in LH action on granulosa cells

Releases lytic enzymes and prostaglandins to expel oocyte

361
Q

early luteal stage

A

remaining luteal cells produce less estrogen and inhibin B and more progesterone and inhibin A

362
Q

mid luteal stage

A

corpus luteum grows

Increase progesterone, estrogen, inhibin A

363
Q

what does Increase progesterone, estrogen, inhibin A cause in the mid luteal phase?

A

Inhibits GnRH and LH

Inhibin A inhibits FSH

364
Q

what is produced if implantation occurs?

A

hCG

365
Q

late luteal phase

A

corpus luteum degenerates

Progesterone, estrogen, inhibin A decrease

366
Q

what happens at the end of the hormonal cycle?

A

FSH and LH rise and stimulate a new cohort

367
Q

menstrual phase days ___

A

1-5

368
Q

events during menstrual phase

A

Initiation to completion of bleeding

endometrium sloughs off

369
Q

Proliferative phase → days ___

A

5-14

370
Q

proliferative phase events

A

Under the influence of estrogen, endometrium regenerates, thickens, and forms glandular structures
Progesterone R appear on endometrial cells due to estrogen
Myometrium thickens and acquires progesterone R

371
Q

Secretory phase → days __

A

14-28

372
Q

secretory phase events

A

Increasing progesterone → mucus and fluid secretion, glycogen synthesis, vascularization
Inhibits myometrial contraction
Preparing for implantation

373
Q

effects of estrogen and progesterone at the end of the menstrual cycle

A

Decrease estrogen and progesterone → deprive endometrium of support → constriction of blood vessels, reduced blood flow, prostaglandin secretion, death of tissue

374
Q

what do estrogens stimulate

A 
growth and maintenance of the reproductive tract
female body configuration
bone growth
epiphyseal plate closure
pubic hair growth
cervical mucus secretion
breast development
prolactin secretion
myometrial contraction
375
Q

what do estrogens inhibit

A

GnRH release
milk producing effects of prolactin
atherosclerosis

376
Q

what does progesterone stimulate

A

breast glandular growth
uterine secretion
cervical mucus secretion
increased body temp

377
Q

what does progesterone inhibit

A

GnRH release
myometrial contractions
milk producing effects of prolactin

378
Q

why is there an increase in temp after ovulation that persists thru the luteal phase?

A

Thermogenic effect of progesterone

379
Q

Clomiphene

A

E2 agonist

Increases GnRH → increased FSH

380
Q

Phased protocols for assisted ovulation

A

Administration of FSH while blocking normal cycle with GnRH antagonist
Terminate with a pulse of hCG to trigger ovulation

381
Q

how do progestin only BC work?

A

decrease LH, FSH, E2

Suppresses ovulation and produces thick cervical mucus and a thin atrophic endometrium

382
Q

Capacitation

A

epididymis derived proteins are stripped off sperm
Transmembrane proteins rearranged
Metabolism and motility increase

383
Q

Hyperactivation

A

R-mediated Ca influx converts slow wave-like beating to rapid whip-like beating

384
Q

what triggeres hyperactivation of sperm

A

paracrine signal from egg

385
Q

Acrosome reaction

A

sperm head binding to zona pellucida → exocytosis of a trypsin-like proteolytic enzyme (acrosin) from the acrosome

386
Q

what produces hCG

A

trophoblasts after invasion into endometrium

387
Q

role of hCG

A

Maintains corpus luteum for 2 months
Stimulates P and E production
Prevents further ovulation

388
Q

functional progesterone withdrawal

A

Efficacy of inhibition decreases as childbirth approaches

Ratio and distribution of P R isoforms change

389
Q

RU486

A

Competitive inhibitor of progesterone

Causes endometrial degradation and myometrial contraction

390
Q

what are the cooperative products of fetal adrenal synthesis of DHEAS from placental pregnenolone

A

Estradiol/estriol

391
Q

Placental Lactogen role

A

Facilitates breast development
Maintains positive protein balance
Mobilizes fat for energy
Promotes high glucose levels required for nourishing fetus

392
Q

how are uterine muscles coupled?

A

E-induced gap junctions

393
Q

what stimulates uterine muscles?

A

stretch

394
Q

what induces oxytocin R

A

estrogen

395
Q

what cooperatively stimulates breast development

A

E and P, placental lactogen, and prolactin

396
Q

what makes prolactin

A

lactotrophs in anterior pituitary

397
Q

half life prolactin

A

20 min

398
Q

prolactin functions

A

Mammogenesis
Lactogenesis
Galactopoiesis

399
Q

Mammogenesis

A

growth and development of mammary gland

400
Q

Lactogenesis

A

initiation of lactation

401
Q

Galactopoiesis

A

maintenance of milk production

402
Q

what inhibits prolactin release

A

dopamine

403
Q

what stimulates prolactin

A

estrogen

404
Q

milk ejection reflex

A

Suckling → neural input to the hypothalamus → inhibits dopamine release, stimulates PRF release

405
Q

how to stimulate milk synthesis

A

Decrease dopamine → anterior pituitary releases prolactin → stimulates milk synthesis

406
Q

what does oxytocin stiulate

A

myoepithelial cells of the breast to contract

407
Q

most basic role of thyroid hormone

A

gain control → amplification or diminution of physio processes

408
Q

what is the chemical structure of thyroid hormone based on?

A

thyronine

409
Q

thyroxine

A

T4

fully iodinated thyronine

410
Q

most physio active form of thyroid hormone

A

T3

3’,3,5-triiodothyronine

411
Q

Thyroid hormonogenesis

A

Thyroid hormonogenesis → iodination and coupling of tyrosine rings to make thyronine

412
Q

what kind of NZs are important for thyroid hormone metab

A

selenium containing

413
Q

TRH

A

Thyrotropin releasing hormone

stimulates TSH in anterior pituitary

414
Q

what syntesizes and secretes TRH

A

cells in the median eminence and arcuate nucleus

415
Q

what stimulates TRH

A

neurogenic input
Alpha-adrenergic catecholamines
vasopressin

416
Q

most important regulator of TRH

A

long loop neg feedback from plasma T3 and T4

417
Q

how is TRH inactivated?

A

TRH-degrading ectoenzyme

418
Q

what synthesizes and secrete TSH?

A

Thyrotropes in the anterior pituitary

419
Q

physio role of TSH

A

stimulate thyroid follicular cells

420
Q

what controls synthesis of TSH

A

plasma levels of free thyroid hormones

421
Q

where does most T3 in the thyrotrope come from?

A

intra-pituitary conversion of T4 → T3

Acheived by deiodinases

422
Q

Binding of T3 to nuclear R ___

A

inhibits production of TSH

423
Q

TRH ___ negative control of TSH

A

antagonizes

promotes synthesis

424
Q

what kind of secretion does TSH have?

A

pulsatile with a circadian rhythm

Levels are higher at night

425
Q

what inhibits TSH secretion?

A

dopamine

somatostain

426
Q

__ inhibits the thyroid axis

A

glucocorticoids

427
Q

how do glucocorticoids inhibit the thyroid?

A

Inhibit hypothalamic expression and synthesis of TRH
Decreased responsiveness of thyrotrope to TRH
Decreases plasma T3 levels by inhibiting deiodinase activity in the pituitary and peripheral tissues

428
Q

how does I- get into the follicle cell?

A

MIS

429
Q

where is TG synthesized and glycosylated?

A

within follicular cells

430
Q

where do thyroid hormonogenic processes take place?

A

lumen

431
Q

what catalyzes thyroid hormonogenic processes take place?

A

thyroid peroxidase (TPO)

432
Q

where do Chemical reactions catalyzed by TPO take place?

A

outer apical membrane surface

433
Q

what mediates TPO recations?

A

hydrogen peroxide generated by NADPH oxidase

434
Q

pendrin

A

Cl-I transport protein on the apical membrane

435
Q

organification

A

TPO Covalently attaches iodine atoms to aromatic tyrosine rings in thyroglobulin

436
Q

how to get precursor forms of thyroid hormones

A

Combines 2 iodinated rings while they are still attached to thyroglobulin

437
Q

how much organified TG is stored in colloid?

A

2-3 months

438
Q

how does TG turn into T3 and T4?

A

Thyroglobulin undergoes proteolysis → T3 and T4, constituent AA of thyroglobulin into cytosol

439
Q

how do. T3 and T4 enter the bloodstream

A

specific transporters at the basolateral membrane

440
Q

what is an important regulator of TH production

A

iodine

441
Q

Rate limiting step of TH synthesis

A

iodide transport from bloodstream into follicular cell

442
Q

perchlorate

A

Competitive inhibitors of NIS

443
Q

Wolff-Chaikoff effect

A

autoregulatory mechanism that protects against acute iodine excess

444
Q

how long does the Wolff-Chaikoff effect last

A

26-60 hours

445
Q

how does Wolff-Chaikoff effect end?

A

escape- Effect diminishes as the gland escapes from inhibition by adapting to higher iodine levels and resumes normal hormone synthesis

446
Q

Majority of circulating T4 and T3 are bound to ___

A

plasma proteins
Thyroxine binding globulin (TBG)
Albumin
Transthyretin

447
Q

Physiological thyroid states correlates with ___

A

free hormone levels

448
Q

All of the T4 in the bloodstream comes from ____

A

direct secretion from the thyroid gland

449
Q

20% of the T3 in the bloodstream comes ___

A

directly from the thyroid

450
Q

80% of the T3 in the bloodstream comes ___

A

from peripheral conversion of T4 → T3 by intracellular deiodinase

451
Q

T3 or T4 faster metab rate?

A

T3

452
Q

how do Th exert effects?

A

binding to non-histone protein nuclear receptors in conjunction with thyroid hormone response elements (TREs)
Affects the types and rates of translation of various RNAs in cells for enzymes and other cellular products

453
Q

what tissues have a lot o TH R?

A

myocardial

liver

454
Q

sympathetic adrenergic TH effects

A

increase beta R activity

increase beta R in heart, liver, muscle, adipocytes

455
Q

energy expenditure TH effects

A

↑Na+/K+-ATPase expression
↑thermogenesis, heat dissipation
↑ adaptation to cold climate

456
Q

oxygen consumption TH effects

A

increase number mitochondria in most tissues

457
Q

heart TH effects

A

↑ contractility (positive inotropic effect)
↑ sarcoplasmic Ca2+-ATPase expression
↑ activity and number of β-adrenergic receptors

458
Q

skeletal muscle Th effects

A

↑ protein catabolism and glycogenolysis

Muscle fiber type switch from slow to fast

459
Q

GI tract TH effects

A

maintains normal gut motility

↑ glucose absorption

460
Q

cholesterol TH effects

A

↑ cholesterol synthesis

↑ LDL clearance (by ↑ hepatic LDL receptors)

461
Q

skeletal TH effects

A

promotes bone maturation, advances bone age
promotes bone growth (permissive for IGF-1 and
maintains normal GH gene expression)
↑ bone turnover in adults

462
Q

plasma hormones TH effects

A

maintains normal half-lives of hormones and drugs

463
Q

NS TH effects

A

maintenance of normal mental/emotional function and

normal reflexes, including respiration

464
Q

when does thyroid gland form in fetus

A

1st trimester

465
Q

why does TBG production increase in pregnancy?

A

Allows total thyroid hormone pool to increase during gestation without increasing free hormone levels

466
Q

hyperthyroidism symptoms

A 
Basal metabolic rate is increased
Voracious appetite
Weight loss 
Hyperdefecation 
Nervousness
Tremors
Tachycardia
Larger pulse pressure
Increased SV and CO
Lower systemic vascular resistance
Shortened circulatory times
Thin, smooth skin 
Increased heat production and intolerance
467
Q

hyperthyroidism treatment

A

Aimed at decreasing overproduction with drugs that inhibit synthesis or inhibiting peripheral effects
Surgery or radioactive iodine therapy → destroy gland to create a hypothyroid state that can be treated

468
Q

hypothyroidism symptoms

A 
Slowing of metabolic rate
Can lead to high cholesterol 
Cold intolerance
Lethargy
Fatigue
Dementia
Thick, dry skin 
Constipation 
Bradycardia
469
Q

hypothyroidism treatment

A

Hormone replacement therapy

T4 has a longer half life, used more than T3

470
Q

what life threatening emergency can hypothyroidism cause?

A

myxedema coma

471
Q

what life threatening emergency can hyperthyroidism cause?

A

thyroid storm

472
Q

graves disease cause

A

Caused by autoantibodies against TSH R

Mimics action of TSH

473
Q

hashimoto’s cause

A

Non stimulating autoantibodies against the thyroid

Eventually destroys gland

474
Q

what causes a goiter in hashimotos?

A

inflammation and lymphocytic infiltration

475
Q

thyroiditis

A

Inflammation of thyroid gland

Hyperthyroidism followed by hypothyroidism then euthyroidism

MAMS (8 decks)

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