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Endocrine > Hormone-Cell Interaction > Flashcards

Hormone-Cell Interaction Flashcards

1
Q

Endocrine definition

A

chemical messenger produced by 1 cell type that acts on distant cells

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2
Q

Autocrine definition

A

chemical messenger produced by 1 cell type that acts on the same cell

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3
Q

Paracrine definition

A

chemical messenger produced by 1 cell type that acts on a neighboring cell

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4
Q

Hormone

A

produced in 1 tissue, released in blood, and carried to target; or more simply a chemical with autocrine, paracrine, or endocrine function

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5
Q

Endocrine Hormone

A

released by glands into the circulation, affecting distant target cells

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6
Q

Neurohormones

A

secreted by neurons into the circulation, influencing distant target cells

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7
Q

Paracrines

A

secreted by cells into the ECF affecting neighboring cells of different type

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8
Q

Autocrines

A

secreted by cells into the ECF affecting its own function

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9
Q

Cytokines

A

peptides secreted by cells into the ECF that can have autocrine, paracrine, or endocrine function

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10
Q

3 main classes of hormones

A

peptide, steroid, amino acid derivative

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11
Q

Peptide hormone (hydrophilic or polar)

A

synthesized as pre-hormone, stored in vesicle, released by Ca-dependent exocytosis, circulate unbound in blood, short half-life, interact with cell membrane, require 2nd messenger system

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12
Q

Steroids (hydrophobic or nonpolar)

A

released upon synthesis, require plasmatic protein transporters, interact with intracellular receptors in target cells –> protein synthesis

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13
Q

Amino Acid Derivatives (tyrosine)

A

Thyroid Hormones and Catecholamines

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14
Q

Thyroid Hormones

A

stored extracellularly in follicle of thyroid as part of thyroglobulin, crosses cell membrane, blood transport bound to protein, have intracellular receptors

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15
Q

Catecholamines

A

stored in vesicles, do not cross membrane readily, transported in blood free or loosely associated w/ proteins

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16
Q

What 2 glands secrete hormones almost entirely due to neural stimuli

A

adrenal medulla and pituitary

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17
Q

Nervous system and endocrine system work together to maintain homeostasis, this is done by

A

nervous system short term and endocrine for long term

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18
Q

Hormone receptors

A

required by cell for response, can be on membrane, in cytoplasm, or in nucleus

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19
Q

Receptor-Hormone Interaction - Threshold

A

minimum concentration of hormone to elicit a response

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20
Q

Receptor-Hormone Interaction - Saturation

A

response plateaus when all receptors are occupied, regardless of excess increase in hormone concentration

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21
Q

Receptor-Hormone Interaction - Sensitivity

A

Concentration of hormone required to elicit 50% of maximal response

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22
Q

Receptor-Hormone Interaction - Competition

A

Substance that may also bind receptor (endogenous and exogenous)

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23
Q

Receptor-Hormone Interaction - Agonists

A

Chemical agent that binds receptor and elicits the same response

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24
Q

Receptor-Hormone Interaction - Antagonist

A

Chemical agent that occupies the receptor but does not elicit a response

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25
Q

Receptor-Hormone Interaction - Responsiveness

A

determined by the maximal response and dependent on number of receptors

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26
Q

A reduction in the number of receptors will result in a reduction in

A

maximum responsiveness

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27
Q

Sensitivity reflects the receptors

A

affinity for the hormone and the receptors availability

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28
Q

A competitive inhibitor would have what effect on sensitivity and responsiveness?

A

It would require a higher concentration of hormone to produce the same result (decreasing the sensitivity), but the maximal response does not change

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29
Q

An antagonist __________ potency/sensitivity and _______ efficacy

A

reduces; does not effect

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30
Q

The magnitude of the response is dependent on ________________

A

the hormone-receptor complex

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31
Q

the hormone-receptor complex is non covalent and follows

A

1st order kinetics

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32
Q

Kinetics affinity constant of the receptor for the hormone

(K) =

A

[HR] / ([H] x [R]) (% receptors bound)

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33
Q

The hormone concentration in blood [H]

A

refers to the concentration of FREE hormone (unbound to transport proteins)

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34
Q

Plasmatic protein is determined by

A

secretion, metabolism, and binding to plasma proteins

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35
Q

Most hormones are released

A

in short bursts or in oscillations (circadian)

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36
Q

Metabolic Clearance Rate (MCR)

A

volume of blood cleared of hormone per unit of time

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37
Q

A high MCR means

A

the hormone in quickly cleared from the blood and that hormone has a SHORT HALF-LIFE

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38
Q

Metabolic clearance is performed by

A

Liver, kidney, or metabolized after uptake by target cell

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39
Q

Half life of a hormone is __________ proportional to the MCR

A

inversely

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40
Q

Half-life for a catecholamine is

A

2-3 min generally

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41
Q

Half-life for a thyroid hormone is

A

6.5 days generally

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42
Q

Which has a shorter half-life and why, steroid or peptide hormone?

A

peptide, it is unbound

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43
Q

Affinity

A

liklihood that the receptor will bind the hormone with a given [H]

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44
Q

Affinity can be determined by

A

ka (association constant) / kd (dissociation constant) = [HR] / [H] x [R] = K

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45
Q

equilibrium dissociation constant

A

the concentration of hormone (at equilibrium) that is required for binding to 50% of the receptor sites

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46
Q

The lower the dissociation constant Kd

A

the HIGHER the affinity (a smaller amount of H is required to elicit a response)

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47
Q

Concentration of receptors:

A

receptors are constantly synthesized and degraded; regulation of this allows the cell to alter its physiological response to a hormone

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48
Q

Up regulation

A

means to synthesize more receptors or slow the degradation; in response to LOW [H] levels

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49
Q

Down regulation

A

means to synthesize less receptors or speed degradation; in response to HIGH [H] levels

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50
Q

Homologous regulation

A

modulation of number of receptors by the hormone itself (NE can increase NE receptors at low [NE])

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51
Q

Heterologous regulation

A

modulation of number of receptors by non-primary hormones (Estrogen can increase Progesterone receptors)

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52
Q

The Kd concentration is normally equivalent to

A

the number of receptors occupied.

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53
Q

ED50

A

concentration of hormone required to elicit 50% of maximal response

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54
Q

Kd is normally equivalent to

A

ED50

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55
Q

If Kd does not equal ED50 then

A

this means that the 100% response occurs even when 100% of receptors are NOT occupied

56
Q

Spare receptors

A

at maximal response, there are some spare receptors; allows for rapid response and termination of response, or obtaining a response with a low [H] with relatively low affinity

57
Q

5 components of a feedback loop

A

Stimulus, sensor, setpoint, integrating center, and effector

58
Q

The stimulus of a feedback loop

A

the hormone, or variable related to the hormones action (ions) - controlled variable

59
Q

Setpoint of the feedback loop

A

the required concentration of the stimulus

60
Q

Integrating Center of the feedback loop

A

where comparison occurs between the setpoint and the actual concentration and an “error” message develops

61
Q

Effector of the feedback loop

A

mechanism that returns the level of stimulus back to the setpoint

62
Q

Effector causes opposite action

A

if stimulus concentration is LESS than set point, effector causes an increase to stabilize the stimulus

63
Q

All hormones use ___________ feedback mechanisms

A

Negative

64
Q

Positive feedback

A

a deviation from setpoint causes effector to increase the deviation (non-regulatory and Unstable)

65
Q

Positive feedback occurs by

A

further increasing the [H] or increasing the # of receptors

66
Q

Example of positive feedback

A

Labor and oxytocin levels; as the baby presses down on pressure receptors in the cervix oxytocin levels rise and cause more forceful contractions until the pressure is relieved

67
Q

Permissiveness

A

The presence of a hormone is required for another hormone to have its FULL EFFECT

68
Q

Example of permissiveness

A

presence of thyroid hormone is permissive for the effect of epinephrine on lipolysis (thyroid hormone has a small effect on lipolysis alone)

69
Q

Counter regulatory hormones

A

hormones that have opposing effects on the same variable

70
Q

Example of counter regulatory hormones

A

Glucagon is counter regulatory to insulin

71
Q

Trophic hormones

A

hormone that stimulate the secretion of another hormone and/or the growth of that endocrine gland

72
Q

Synergy

A

when 2 hormones that have the same biological response, produce a greater response together than the individual responses alone

73
Q

Example of Synergy

A

Thyroid and Growth Hormones have synergistic effects on bone growth

74
Q

Peptide hormone synthesis, storage, and secretion

A

synthesized as a pre-pro-hormone, stored in a secretory vesicle, released via Ca-dependent exocytosis into ECS for RAPID response

75
Q

Peptide hormone transport

A

Hydrophilic and soluble in plasma (except somatomedins and IGF require transport proteins)

76
Q

Post-receptor events

A

Bind integral receptors on plasma membrane of effector cell causing 2nd messenger cascades

77
Q

Hormone receptor/Ion channel

A

Hormone binding opens ion channels that can alter membrane potential or act as a 2nd messenger itself (Ca)

78
Q

Hormone receptor/protein kinase

A

Hormone Binding causes phosphorylation (tyrosine phosphorylation if tyrosine kinase) which generates a biological response

79
Q

Hormone receptor/ JAK

A

hormone binding activates JAK which phosphorylates specific proteins for a biological response

80
Q

Hormone receptor/Gproteins

A

Hormone binding activates a G protein and causes an increase in the 2nd messenger which activates a protein kinase for phosphorylation of specific proteins

81
Q

5 Major 2nd messengers

A

cAMP, cGMP, inositol triphosphate, DAG, Ca, Ca-calmodulin

82
Q

cAMP/G protein (Gs)

A

Hormone binding –> GDP replaced with GTP on G protein –> activation of adenylyl cyclase –> converts Mg-ATP to cAMP (which ends when GTP is hydrolyzed) –> cAMP activates protein kinase

83
Q

How does cholera toxin effect cAMP?

A

inhibits the conversion of GTP to GDP in which adenylyl cyclase would be constitutively on

84
Q

cAMP/G protein (Gi)

A

GTP binding to G protein causes adenylyl cyclase inhibition (rather than activation)

85
Q

Pertussis toxin effects cAMP pathway by

A

interfering with Gi, preventing the inhibition of adenylyl cyclase (constitutively active)

86
Q

cAMP activates protein kinase by

A

binding to the regulatory unit of the kinase and causing a dissociation of the regulatory subunit and the catalytic unit; causing the kinase to be activated

87
Q

Phosphodiesterase

A

metabolizes cAMP to inactive 5’-AMP

88
Q

What if the same hormone binds the same receptor in a different cell?

A

the cell response may be different

89
Q

What is a different hormone binds the receptor in the same cell?

A

It may produce the same effect by increasing cAMP

90
Q

What accounts for different tissues differential response to cAMP increase?

A

cAMP may activate a different type of protein kinase OR the proteins subject to phosphorylation may be different depending on the proteins genetically expressed in that particular cell type

91
Q

Protein hormone metabolism

A

circulate free and are free to excrete and metabolize

92
Q

Major sites for protein hormone degradation

A

liver and kidney

93
Q

The half life of polypeptide hormone is ________ than larger protein hormones

A

shorter

94
Q

Steroid hormones are

A

lipophilic, have cholesterol as a common precursor

95
Q

Steroids hormones differ by

A

functional group, degree of saturation, and length of side chain

96
Q

4 classes of steroids include

A

estrogen, androgen, glucocorticoids, and mineralcorticoids

97
Q

Steroids are produced mainly in the

A

adrenal cortex, testis, ovary, and placenta

98
Q

Cholesterol for steroid hormone synthesis comes from

A

LDL in the liver, the lipid droplet is taken up by endocytosis and store din a non-membrane bound lipid droplet

99
Q

cholesterol esterase

A

stimulated by trophic hormones –> PKA; causes free cholesterol release from the lipid droplet

100
Q

Steroidogenic acute regulatory protein (StAR)

A

transports free cholesterol to the mitochondria

101
Q

Peripheral-type benzodiazepine receptor (PBR)

A

receptor that allows internalization of free cholesterol by the mitochondria

102
Q

Cytochrome P450

A

modifies cholesterol to pregnenolone

103
Q

Pregnenolone

A

common precursor to all steroid hormones

104
Q

Major steroid hormones:

A

aldosterone, cortisol, estradiol, and testosterone

105
Q

The rate-limiting step of steroid hormone synthesis

A

cholesterol to pregnenolone by P450 in the mitochondria

106
Q

pregnenolone in the testis

A

converts it to testosterone

107
Q

pregnenolone in the adrenal cortex

A

converts it to aldosterone or cortisol

108
Q

Storage of steroid hormones

A

lipophilic and therefore diffuse out of the cell into the ECS, no storage or pre-formed molecules required

109
Q

Transport of steroid hormones

A

some hormone is dissolved in the blood, while most are attached to transport proteins (>50kDa). when free [H] decreases Hormone will release from the transport protein to raise the free concentration

110
Q

Steroid hormone and its specific transport protein

A

high affinity, dissociation is slow, tightly bound to traverse capillaries, large transport protein to avoid glomerular filtration

111
Q

If a hormone is loosely bound to a non-specific transport protein

A

when the complex traverses the capillary bed, the hormone will dissociate and diffuse into tissues

112
Q

Hormones bound to albumin and pre albumin cause ____________ of the free hormone available to the tissues

A

underestimate

113
Q

Example of non-specific transport protein

A

albumin and pre-albumin

114
Q

An increase in transport proteins will increase the amount of bound hormone

A

decreasing the amount of “free” hormone in plasma

115
Q

Control systems use which concentration for regulating plasma [H]?

A

FREE plasma concentration (if more is bound, then the body will secrete more into plasma until the FREE [H] rises to normal)

116
Q

Mechanism of steroid hormones

A

receptor located in the nucleus or cytoplasm, binding to receptor causes activation of the DNA-binding domain which binds to DNA and turns on protein synthesis

117
Q

Why does steroid hormone leave its transport protein and enter cells?

A

It has a greater affinity for the receptor

118
Q

Steroid hormones are ___________ than peptide hormones

A

slower acting; they need to turn on gene transcription

119
Q

Half life of steroid hormones

A

is longer than peptides because they are bound to transport proteins

120
Q

Steroid metabolism

A

occurs mainly in the liver

121
Q

Steroid halflives increase as their

A

affinity for transport proteins increases

122
Q

Amino acid hormones: 2 major types

A

catecholamines (NE and Epi) and thyroid hormones

123
Q

Amino acid hormones are derived from

A

tyrosine

124
Q

Catecholamines act like

A

peptide hormones (soluble and bind plasma membrane receptors)

125
Q

Thyroid hormones act like

A

steroid hormones (transport proteins –>intracellular receptors)

126
Q

Phospholipase A2

A

main enzyme responsible for releasing arachidonic acid

127
Q

Eicosanoids are formed from

A

arachidonic acid

128
Q

Arachidonic acid

A

phospholipid component of the plasma membrane released by phospholipid A2 and C-beta

129
Q

Cortisol inhibit

A

phospholipase A2

130
Q

arachidonic acid can be converted to

A

thromboxanes, prostacyclines, prostaglandins, or leukotrienes

131
Q

eicosanoids act as

A

2nd messengers (intracellular enzymes and ion channels or paracrine effects)

132
Q

Prostaglandins

A

COX enzyme; useful for hemostasis, water excretion, gastric secretion, integrity of stomach lining, vascular reactivity (paracrine or autocrine function)

133
Q

Leukotrienes

A

LOX enzyme; LTB-F4, LTB4 acts during inflammation and LTC-E4 are slow-reacting anaphylaxis

134
Q

Thromboxanes

A

Platelets convert PHG2 to thromboxane A2 which induces platelet aggregation and vasoconstriction

135
Q

Prostcyclines

A

endothelial cells convert PGH2 to PGI2 which inhibits platelet aggregation and causes vasodilation

136
Q

NSAIDS reverse which eicosanoids

A

reverses COX and the productions of prostaglandins, prostacyclines, and thromboxanes

Endocrine (9 decks)

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