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Physiology 210 > Endocrine Physiology > Flashcards

Endocrine Physiology Flashcards

1
Q

What is the endocrine function?

A 
Mood
Reproduction
Digestion/excretion
Intermediary metabolism
Growth
Puberty
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2
Q

What are the symptoms of endocrine dysfunction?

A

Growth/retardation
Weight gain/loss
Skin pigmentation/dryness/acne/swelling
Sexual characterisitics

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3
Q

How is the nervous system homeostatically regulated?

A

Precise, rapid, finely adjusted, short-term regulation

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4
Q

How is the endocrine system homeostatically regulated?

A

Slower, more sustained control over long-term processes

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5
Q

What are exocrine glands?

A

Empty their secretions into body cavities or onto body surfaces by tubular ducts

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6
Q

What are endocrine glands?

A

Ductless glands that release their secretions internally into the bloodstream

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7
Q

What are the characteristics of endocrine glands?

A 
Paired or unpaired
Organs or scattered cells 
One or more cell-types 
Cells may secrete one or more hormones
Cells in clumps, cords, or scattered
Cells may have smooth ER or rough ER
Cell may/may not have secretory vesicles
Cells may/may not have lipid droplets
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8
Q

What are the glands of the endocrine system?

A 
Hypothalamus/pituitary 
Pineal gland
Thyroid
Parathyroids 
Thymus 
Adrenals 
Pancreas
Ovaries 
Testes
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9
Q

What doe endocrine glands secrete and where?

A

Chemical messengers into the circulatory system

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10
Q

What is paracrine signalling?

A

Target cells in close proximity to the site of release of paracrine substances

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11
Q

What is autocrine signalling?

A

Acts on same cell that secreted the substance

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12
Q

What is endocrine signalling?

A

Target cells in one or more distant places in the body and released into the bloodstream

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13
Q

What is nervous signalling?

A

A neurotransmitter is released into a synapse close to the target site which is either another neuron or an effector cell

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14
Q

What is neuroendocrine signalling?

A

Release messenger molecules into the blood

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15
Q

What are the characteristics of hormones?

A

Chemical messengers that regulate homeostasis
Have high potency
Act at specific receptors
Act with a latency of response (actions are not immediate)
Have limited storage
Are secreted irregularly
Mostly carried in plasma by binding proteins
Are not an energy source
Are not incorporated into other molecules

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16
Q

What are the two main groups of hormones?

A

Steroid

Protein

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17
Q

What are steroid hormones?

A

Derived from cholesterol

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18
Q

How are steroid hormones made?

A

Cholesterol enters the cell bound to LDL
It moves to the mitochondria where is undergoes the first step in steroid biogenesis
Released by diffusion

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19
Q

How are protein hormones made?

A

Made from the translation of messenger RNA
mRNA to pre-hormone to pro-hormone to hormone
Packaged into secretory vesicles and released

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20
Q

What are the functions of secretory vesicles?

A

Protect hormones from proteolytic degradation
provide a reservoir in sites of synthesis
Provides a transport mechanism to the site of release
Provides a release mechanism through which the vesicle membrane is incorporated into the plasma membrane
Provide a release mechanism (exocytosis)
Provides for quantal release of consistent hormone amounts

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21
Q

What are the two types of hormones in the plasma?

A

Bound and free

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22
Q

What are free hormones?

A

Biologically active

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23
Q

What are bound hormones?

A

Inactive when bound to a binding protein

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24
Q

What are the roles of protein binding of plasma hormones?

A

Increases solubility and concentration, providing a reservoir for target sites
Increases size, protecting hormones from clearance and degradation by the liver and kidney and degradation by plasma enzymes
Inactivates free hormones, providing a buffer against large and sudden changes in hormone concentrations
Dynamically regulated with rate of secretion, rate of degradation, and binding to receptors on target cells

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25
Q

How is hormone secretion regulated?

A

Dynamic regulation occurs in response to feedback from target sites
Negative feedback is common, and inhibits secretion when circulating levels are high and increases secretion when circulating levels are low
Positive feedback is rare, but allows discrete events to be rapidly attained

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26
Q

What is the negative feedback pathway?

A

Endocrine gland releases the hormone, hormone travels in the blood to act at its target site, causes release of a product into the bloodstream, product will cause suppression of the gland, decrease in secretion of the hormone from the gland

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27
Q

What is the positive feedback pathway?

A

Endocrine gland releases hormones, acts on the target cell or tissue, produces a product, product will then feedback on the endocrine gland from which the first hormone was released to stimulate it

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28
Q

What is hormone action?

A

Feedback results from hormone action at target sites
The first requisite for hormonal action is the binding of the hormone to a specific receptor
Only those cells that have receptors respond to particular hormones

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29
Q

What is signal amplification?

A

Signal transduction mechanisms allow for amplification of the response following binding of a hormone to its receptor

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30
Q

What are the two types of hormone receptors?

A

Nuclear

Cytoplasmic

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31
Q

What are nuclear receptors?

A

Steroid and thyroid hormones
Located in the nucleus of the cell
Genomically mediated through protein synthesis

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32
Q

What are cytoplasmic receptors?

A

Involved in intracellular transport for cytosol-insoluble steroids
Reservoir storage and organelle actions for thyroid hormones

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33
Q

What is downregulation?

A

(less receptors)
At high hormone concentrations to prevent over-activity
Decreased receptor synthesis/increased degradation
Internalized membrane receptors
Dislocation of receptor and signal transduction system

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34
Q

What is desensitization?

A

At high hormone concentrations to prevent over-activity

Conformational change in lock structure

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35
Q

What is up-regulation?

A

At low hormone concentration to increase activity

Increased receptor synthesis/decreased degradation

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36
Q

What is sensitization?

A

At low hormone concentrations to increase activity

Conformational change in lock structure

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37
Q

What is down-regulation by coated pits?

A

Allows protein hormones to enter the cell

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38
Q

What are the primary ways that endocrine dysfunction occurs?

A

Primary defect in synthesis = problems endocrine gland
Defect in regulation = problem in hormone action
Defect in hormone action = problem with target tissue

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39
Q

What is the hypophysis?

A

The pituitary gland

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40
Q

Where is the pituitary gland?

A

Ventral part of brain

Below the hypothalamus

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41
Q

What are the parts of the pituitary gland?

A

The anterior and posterior pituitary

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42
Q

What is the posterior pituitary?

A

Down-growth from the brain

Neural tissue

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43
Q

What is the anterior pituitary?

A

Derived from non-neural tissue (Rathke’s pouch)

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44
Q

What is the intermediate lobe?

A

Found between the anterior and posterior pituitary

Lost before birth

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45
Q

What are the neural connections between the posterior pituitary and the hypothalamus?

A

Hormones are produced in the hypothalamus nuclei (paraventricular nuclei and supraoptic nuclei)
The hormones are synthesized in the cell bodies of the nuclei and their long axons pass down the infundibulum and end in the posterior pituitary gland where they are stored

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46
Q

What hormones does the posterior pituitary secrete?

A

ADH/vasopressin

Oxytocin

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47
Q

What nuclei makes ADH?

A

Supraoptic nuclei

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48
Q

What nuclei make oxytocin?

A

Paraventricular nuclei

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49
Q

How are protein hormones synthesized in the nerves?

A

Hormone is produced in the cell body of the neuron, packaged into the golgi, transported along the axont to nerve terminals, stored in nerve terminals until appropriate stimulus comes, hormone moves into blood

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50
Q

What is the vasoconstriction action of ADH/Vasopressin?

A

Contraction of blood vessel smooth muscle
Increases blood pressure
Only occurs at high concentrations

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51
Q

What is the anti-diuretic action of ADH/Vasopressin?

A

Increases permeability of the renal collecting duct bu increasing the number of water channels
Vasoconstriction reduces glomerular filtration rate
Contraction reduces the size of the glomerulosa cells, reducing the surface area for filtration

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52
Q

What is the mechanism of action of ADH?

A

Travels to the kidneys
ADH binds to its receptor on the collecting cells
Binding of ADH to its receptor induces synthesis of a second messenger
Cyclic AMP causes the up-regulation of the aquaporin 2 protein via gene transcription

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53
Q

What are factors affecting the secretion of ADH/vasopressin?

A

Plasma volume

Plasma osmolarity

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54
Q

What cells are osmoreceptors?

A

The cells in the hypothalamus
Respond to changes in osmolarity
Ex: Supraoptic nucleus (SON) and paraventricular (PVN)

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55
Q

What receptors sense changes in blood pressure caused by alterations in blood volume?

A

Baroreceptors

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56
Q

What is the main stimuli for ADH release?

A

Decrease in blood volume or an increase in blood osmolarity

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57
Q

What is the effect of dehydration on ADH secretion?

A

Decreased extracellular fluid volume, decreased blood pressure, decreased stretch of blood vessel walls, baroreceptors decrease rate of firing, increased release of ADH, increased water reabsorption or retention from urine, water excretion decreases, water movement back into the plasma increases blood volume levels

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58
Q

What is the effect of water intake on ADH secretion?

A

Increase the extracellular fluid volume, increase in blood volume, increases blood pressure, stimulates stretch receptors or baroreceptors, baroreceptors cause a decrease in ADH release, permeability of the collecting ducts to water decreases, decreased water reabsorption, increased water excretion

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59
Q

What is the relationship between plasma ADH and plasma osmolarity?

A

Osmolarity of the blood increases with dehydration and decreases with over-hydration
Increase in plasma osmolarity = increase in plasma ADH

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60
Q

What is the relationship between plasma ADH and mean arteriole pressure?

A

Decline in MAP results in ADH release

ADH also causes vasoconstriction to increase blood pressure

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61
Q

What else is ADH secretion increased by?

A

Stress/emotion
Heat
Nicotine
Caffeine

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62
Q

What else is ADH decreased by?

A

Cold

Alcohol

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63
Q

Summary of ADH action

A

Synthesis: SON

Secretion: Posterior pituitary

Actions: Increased water retention and vasoconstriction

Stimuli: Increased osmolarity and decreased blood volume

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64
Q

What is a disease caused by low ADH?

A

Diabetes insipidus

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65
Q

What is a disease caused by excess ADH?

A

Syndrome of inappropriate ADH

Problem with ADH production, feedback failure

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66
Q

What is hypothalamic diabetes insipidus?

A

Problem with ADH production

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67
Q

What is nephrogenic diabetes insipidus?

A

Problem with ADH action

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68
Q

What is polyuria?

A

Production of large amounts of dilute urine

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69
Q

What is polydipsia?

A

Excessive thirst and fluid intake

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70
Q

Why is diabetes insipidus bad?

A

Cannot decrease urine flow even when water deprived

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71
Q

What is the treatment for diabetes insipidus?

A

ADH or other anti-diuretics

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72
Q

What is SIADH?

A

Increased ADH levels and decreased aldosterone levels result in hyponatremia or low blood sodium levels

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73
Q

What are the actions of oxytocin?

A 
Uterine myometrium 
-parturition 
-clamping ruptured blood vessels 
-restoration of uterine size 
-sperm movement 
-cervix movement 
Mammary myometrium 
-milk let-down
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74
Q

What is the effect of oxytocin on parturition?

A

Positive feedback loop
Weak uterine contractions push pressure of the fetus against the cervix which will strengthen uterine contractions and cause oxytocin secretion from the posterior pituitary

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75
Q

What is the effect of oxytocin on milk let-down?

A

Positive feedback loop
Suckling further increases the release of oxytocin
Also a conditioned response as visual and auditory stimuli from the infant can stimulate milk let-down

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76
Q

What are the other functions of oxytocin?

A

Released during sexual intercourse and stimulates orgasm

Social bonding

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77
Q

How is oxytocin secretion regulated?

A

Tactile stimuli from the nipples or the genital tract increase secretion
Stress decreases secretion

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78
Q

Summary of Oxytocin

A

Synthesis: PVN

Secretion: Posterior pituitary

Actions: increased lactation and uterine motility

Stimuli: genital/uterine/breast stimulation

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79
Q

What is the consequence of a deficiency of oxytocin?

A

Impaired delivery
Impaired lactation
No problems associated with high levels (excess) of oxytocin

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80
Q

What is the anterior pituitary?

A

Produces hormones essential for growth and reproduction

Controlled by the hypothalamus through the blood supply

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81
Q

How is the anterior pituitary supplied with blood?

A

Median eminence-capillary bed receives axons from nuclei in the hypothalamus and gives rise to the hypothalamo-hyposphyseal portal vessels which run into the anterior pituitary
Secretions from the hypothalamus are released into the capillary beds

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82
Q

What are the nuclei of the hypothalamus that control the anterior pituitary?

A

Parvocellular neurons

Magnocellular neurons

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83
Q

What are the parvocellular neurons?

A

Neurons with small cell bodies and short axons that end in the median eminence
Produce neural secretions that are released into the blood vessels

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84
Q

What are magnocellular neurons?

A

Neuroendocrine cells located in the hypothalamus

Synthesize the hormones ADH/vasopressin (PVN and SON)

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85
Q

What are anterior pituitary gland hormones?

A

Secretion regulated by hormones produced by the hypothalamus

Gonadotropins 
Growth Hormone 
Thyroid stimulating hormone 
Prolactin 
Adrenocorticotropin
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86
Q

What are hypothalamic-releasing hormones?

A

Neural secretions from the hypothalamus

Gonadotropin releasing hormone 
Growth hormone releasing hormone 
Thyrotropin releasing hormone 
Prolactin-releasing factors 
Corticotrophin-releasing hormone 
Somatotropin release inhibitory factor 
Prolactin inhibitory factors
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87
Q

How does the anterior pituitary control secretions with negative feedback?

A

Hormones released from target endocrine gland will provide negative feedback at the level of the anterior pituitary and at the level of the hypothalamus
Autoregulatory loop
Retrograde flow along the blood vessels

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88
Q

What are the effects of growth hormone on muscle?

A

Increased protein synthesis and decreased glucose uptake

Increased muscle mass

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89
Q

What is the effects of growth hormone on the liver?

A

Increased protein synthesis, gluconeogenesis, and somatomedin production

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90
Q

What are the effects of growth hormone on adipose?

A

Decreased glucose uptake and increase lipolysis

Decreased adiposity

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91
Q

What does somatomedin IGF-1 do?

A

Affects the chondrocytes of bone
Increases collagen synthesis, protein synthesis and cell proliferation
Increased linear growth

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92
Q

What does somatomedin IGF-II do?

A

Affects tissues and organs
Increased protein synthesis, RNA synthesis, DNA synthesis, and cell size and number
Increased tissue growth, increased organ size

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93
Q

What are 2 factors regulating growth hormone secretion?

A

Growth hormone inhibiting hormone and growth hormone releasing hormone

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94
Q

What is growth hormone release increased by?

A

Deep sleep, exercise, stress or reduced blood glucose levels, increased blood amino acids, and decreased blood fatty acids

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95
Q

What are the actions of GH on target sites that provide negative feedback?

A

Somatomedins from the liver inhibit GH release
GH inhibits its own release
GH release is inhibited by the products of lipolysis, glucose

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96
Q

What is the 24 hour plasma growth hormone profile of GH?

A

Diurnal pattern of GH release

Number and amplitude of GH is increased in the dark and increased during sleep

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97
Q

How does GH release change in response to blood nutrient levels?

A

Fasting increased GH release episodes
Frequent meals high in glucose or fatty acids suppress hormone release
Frequent meals high in amino acids increase growth hormone release

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98
Q

Summary of Growth Hormone

A

Synthesis: Somatotrophs

Secretion: Episodic, more during stress/sleep, less during aging, GHRH/SRIF balance

Action: Skeletal/soft tissue growth, hyperglycemia/hyperlipidemia, IGF-1 induction

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99
Q

What can a deficiency of growth hormone cause?

A

Dwarfism in juveniles

Somatopause in adults

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100
Q

What is an isolated GH deficiency?

A

Type 1 dwarfism

Defect in GH production

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101
Q

What is Laron-type dwarfism?

A

Defect in GH action

GH is not deficient, IGF-1 levels are deficient

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102
Q

What is the difference between a GH dwarf and a thyroid dwarf?

A

A GH hormone dwarf has normal body proportions but just shorter in height
Thyroid dwarfs have body proportions younger than their age

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103
Q

What is somatopause?

A

GH deficiency in adults
Increased fat and decreased lean mass
Metabolic disturbances
Impaired immune function (thyroid atrophy)

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104
Q

What is acromegaly?

A

Excess growth hormone production in an adult

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105
Q

What are the features of agromegaly?

A

Prognathism (bulging of jaw)
Hirsutism (unwanted male hair growth in females)
Large acral regions (hands and feet)
Enlarged male breast tissue (gynecomastia)

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106
Q

What are the actions of prolactin?

A

Gonadal modulation
-pro-gonadal when gonadal activity is low
-anti-gonadal when gonadal activity is high
Mammary gland development
Lactation
-milk production

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107
Q

What controls prolactin secretion?

A

Prolactin-releasing factors
Gonadal steroids
Mammary stimulation

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108
Q

What are some prolactin-releasing factors?

A

Thyrotropin-releasing hormone

Oxytocin

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109
Q

What are gonadal steroids causing prolactin secretion??

A

Estrogen/testosterone increase

Progesterone decrease

110
Q

What is mammary stimulation?

111
Q

What is hyperprolactinemia?

A

Excess prolactin

112
Q

What are the symptoms of hyperprolactinemia?

A

Gonadal dysfunction
Amenorrhea
Reduced libido

113
Q

What is the treatment for hyperprolactinemia?

A

Dopamine agonist treatment

114
Q

What is hypoprolactinemia?

A

Deficiency of prolactin

115
Q

What are the symptoms of hypoprolactinemia?

A

Gonadal dysfunction

Impaired lactation

116
Q

What is pituitary diabetes?

A

Excess of all anterior pituitary hormones

Hyperglycemia

117
Q

What is hypopituitarism?

A

Deficiency in pituitary hormone production

118
Q

What is panhypopituitarism?

A

Affects all pituitary hormones

119
Q

What is the hypothalamic-pituitary-thyroid axis?

A

Thyrotropin-releasing hormone is secreted from the hypothalamus which will stimulate the secretion of thyrotropin-stimulating hormone from the anterior pituitary.
This stimulates the release of thyroid hormone from the thyroid gland and it goes to target cells

120
Q

What is thyroid-stimulating hormone?

A

Peptide produced by thyrotrophs
Stimulates thyroid growth
Stimulates thyroid hormone biosynthesis?

121
Q

What is a trophic hormone?

A

Affects the growth, nutrition, and function of its target tissue

122
Q

What is a glycoprotein hormone?

A

Contain sugar residues
Alpha and beta subunits in which the biological activity resides in the beta subunit
Sugars are essential for biological activity

123
Q

What is the thyroid gland?

A

Has good blood supply
The follicle is the basic unit of the thyroid gland
When the gland is active, the follicular cells enlarge and the colloid shrinks in size

124
Q

What is thyroglobulin?

A

Precursor to thyroid hormone biosynthesis
Is a glycoprotein that is synthesized is the rough ER of follicular cells and secreted into colloid
Contains tyrosine residues
Not a binding protein

125
Q

What are the two thyroid hormones?

A

Thyroxine (T4)

Triiodothyronine (T3)

126
Q

What is T4?

A

A precursor, large percentage of it is converted to T3

127
Q

What is the biologically active thyroid hormone?

A

T3 (3-5x more active than T4)

128
Q

How is thyroid hormone synthesized?

A

Iodide is co-transported with sodium into the follicular cell
The iodide ions diffuse across the apical membrane of the follicular cells and are transported into the colloid by an anion transporter
Iodide is then oxidized and attached to rings of tyrosine in thyroglobulin
The iodinated ring of one MIT or DIT is added to a DIT at another spot
Endocytosis of thyroglobulin containing T3 and T4 molecules
Secretion of T4 and T3

129
Q

What makes T3?

A

DIT on TG + MIT

130
Q

What makes T4?

A

DIT on TG + DIT

131
Q

Summary of thyroid hormone synthesis

A

Assembly of raw material

  • tyrosine
  • iodine

Iodination of tyrosine (thyroid peroxidase)

  • Tyr + 1 iodine = MIT
  • MIT + 1 iodine = DIT

Coupling of iodotyrosines
-MIT + DIT = T3
-DIT + DIT + T4
Coupling is due to the action of an enzyme thyroid peroxidase

132
Q

What are thyroid hormone-binding proteins?

A

Thyroid hormone-binding proteins
-only a small amount of T3 and T4 is found in plasma free

Thyroid-binding globulin (T3, T4, most important)

Thyroid-binding albumin (T3, T4)

Thyroid-binding pre-albumin (T4)

133
Q

What does thyroid hormone do?

A

No specific target sites
Latent, long-lasting responses
Increases oxygen and glucose uptake by most tissues and increased BMR (calorigenesis)

134
Q

What is the effect of thyroid hormone on metabolic rate and heat production? (main effects)

A

Increases metabolic rate
Increases O2 and glucose uptake and mitochondrial enzymes
Has a calorigenic effect

135
Q

What is the effect of thyroid hormone on neural activity?

A

Increased irritability, mentation, and beta-receptors

Decreased reflex times

136
Q

What is the effect of thyroid hormone on intermediary metabolism?

A

Carb absorption

Decreased plasma cholesterol

137
Q

What is the effect of thyroid hormone on growth and development?

A

Psychogenic/physical

Growth hormone synergy

138
Q

What are the three types of thyroid hormone receptors?

A

Membrane bound
Cytoplasmic
Nuclear

139
Q

What are membrane-bound thyroid hormone receptors?

A

Linked to channels which allow glucose and oxygen to be taken up into the cell

140
Q

What are cytoplasmic thyroid hormone receptors?

A

Roles in intracellular storage of thyroid hormone or production of ATP in mitochondria

141
Q

What are nuclear thyroid hormone receptors?

A

Effects on protein synthesis gene transcription

142
Q

What are the unique features of the thyroid hormone?

A

Synthesized and stored extracellularly in colloid
Contain iodine molecules
Hydrophobic or lipid soluble even though it is derived from amino acids
Secreted by diffusion and carried in plasma by binding proteins
Mechanism of action: membrane, cytoplasmic, and nuclear receptors

143
Q

What happens when there is excess thyroid hormone?

A

Hyperthyroidism
Increased BMR
Primary thyroid dysfunction by thyroid
Secondary thyroid dysfunction caused by pituitary gland
Tertiary thyroid dysfunction caused by hypothalamus
Grave’s diesase

144
Q

What is primary thyroid dysfunction?

A

Produce excess thyroid hormone (T3, T4)

Toxic goiter

145
Q

What is secondary thyroid dysfunction?

A

Increased thyrotropin-stimulating hormone

Goiter

146
Q

What is tertiary thyroid dysfunction?

A

Increased thyrotropin-releasing hormoning

Goiter

147
Q

What is Grave’s disease?

A

Autoimmune disease in which antibodies develop against TSH receptors

148
Q

What are the characteristics of Grave’s disease?

A

Large swelling or goiter in the neck
Overstimulation of the growth and activity of the thyroid gland
Exopthalamos (bulging of the eyes)
Increased BMR
Tachycardia
Increased signs of sympathetic nervous system activation

149
Q

What happens when there is a thyroid hormone deficiency?

A

Hypothyroidism

Decreased BMR

150
Q

What are some causes of hypothyroidism?

A

Endemic goitre
Primary thyroid dysfunction
Hashimoto’s thyroiditis
Secondary or tertiary thyroid dysfunction

151
Q

What is an endemic goitre?

A

Dietary Iodine deficiency

Too much TSH

152
Q

What is Hashimoto’s thyrodiditis?

A

An autoimmune disease where antibodies are developed against T3 and T4 or against thyroglobulin
Causes a goitre

153
Q

What is cretinism?

A

Caused by hypothyroidism in utero
Severely stunted mental and physical development
Irreversible

154
Q

What is myxedema?

A

Caused by hypothyroidism in adults

Accumulation of hyaluronic acid and mucus edema under the skin

155
Q

What are hypothyroid characteristics?

A 
Dull blank expression
Slow mentation
Slow speech
Lethargic (gain weight)
Decreased BMR
Bradycardia ( slower normal heart rate)
156
Q

What are the adrenal glands?

A

Overlie each kidney

Two endocrine glands: adrenal cortex and adrenal medulla

157
Q

What are steroid hormones of the adrenal cortex?

A

Cortisol
Corticosteroids
Androstenedione
DHEA

158
Q

Which of the adrenal cortex hormones provide feedback?

A

Cortisol at the hypothalamus and anterior pituitary

159
Q

What is adrenocorticotropin?

A

Peptide hormone
Produced by cells called pituitary corticotrophs
Stimulates adrenal blood flow, adrenal growth, and adrenal steroidgenesis

160
Q

How is ACTH released?

A

Hypothalamus releases corticotrophin-releasing hormone which stimulates the anterior pituitary to product adrenocoritcotropic hormone which stimulates steroidogenesis in all zones of the adrenal cortex and in the presence of ADH ACTH is released

161
Q

What does POMC do?

A

Produces adrenocorticotropin (ACTH) and beta-lipotropic hormone
ACTH produces alpha-MSH for skin pigmentation
B-LPH produces beta-MSH for skin pigmentation
ACTH is part of the stress response

162
Q

What are the zones of the adrenal cortex?

A

Glomerular zone
Fascicular zone
Reticular zone

163
Q

What is the glomerular zone?

A 
Outer zone
Produces aldosterone
No metabolism (salt/water retention)
164
Q

What is the fascicular zone?

A

Middle zone
Produces cortisol
Intermediate metabolism (sugar)

165
Q

What is the reticular zone?

A

Inner zone
Produces androgens
Sex characteristics

166
Q

How is steroidogenesis done in the glomerular zone?

A

Cholesterol to pregnenolone to progesterone to corticosterone to aldosterone

167
Q

What is the molecular mechanism of aldosterone action?

A

Steroid hormone
Main function is for sodium retention
Synthesize proteins that move sodium into the collecting duct cells
Acts on kidney tubules to stimulate sodium reabsorption
Acts on receptors in the nucleus or the cytoplasm

168
Q

How is aldosterone secretion regulated?

A

Low plasma volume/low sodium concentrations causes kidneys to release renin, renin converts angiotensiogen to angiotensin 1 and angiotensin 1 is converted to angiotensin 2 by angiotensin converting enzyme (ace). Angiotensin 2 acts on adrenal cortex to promote aldosterone production, aldosterone stimulates sodium retention and potassium excretion

169
Q

What are the aldosterone site of synthesis and actions?

A

Glomerulosa zone
Water and electrolyte balance
Angiotensin 2 will stimulate the release of aldosterone in response to a decrease in extracellular fluid volume or a decrease in the concentration of Na+ in the blood

170
Q

What is Conn’s syndrome?

A

Excess aldosterone causes increased sodium retention and decreased potassium uptake in the renal tubule which causes hypertension

Decreased K+ uptake in the renal tubule also caused increased urinary loss of K+ which causes alkalosis which causes tetany, muscular weakness, and dysrhythmia

171
Q

What is steroidogenesis in the fascicular zone?

A

Cholesterol to pregnenolone to cortisol

172
Q

What are the actions of cortisol?

A

Intermediary metabolism
Increases blood glucose through anabolic effects on the liver and catabolic effects on other tissues
-stimulates gluconeogenesis in the liver (Anabolic effect)
-stimulation of triglyceride breakdown in adipose tissue, with release of glycerol and fatty acids into the blood (Catabolic effect)
Stimulation of the breakdown of skin, connective tissue, and muscle which releases amino acids (Catabolic effect)

173
Q

What are the actions of glucocorticoid (glucose + cortex + steroid)?

A 
Mobilizes glucose for brain/heart use 
Increased substrate availability 
Increased substrate uptake by the liver 
Increased gluconeogenesic enzymes 
Increased glycogenolysis (breakdown of glycogen to glucose)
174
Q

What are the functions of cortisol in stress?

A 
Prevents inflammation 
Prevents autoimmunity 
Mobilizes glucose (glucocorticoid action)
175
Q

How is the secretion of cortisol controlled?

A

Stress/diurnal rhythm stimulates the hypothalamus to release CRH which acts on the pituitary to release ACTH which acts on the adrenal cortex to make cortisol
Increased plasma levels on cortisol provide feedback inhibition at the level of the anterior pituitary and the hypothalamus

176
Q

What is the diurnal rhythm of cortisol?

A

Diurnal rhythm: rhythm of release is synchronized with day/night cycle
Levels of cortisol are low at the end of the day but rise during sleep
High first thing in the morning and fall throughout the day

177
Q

What is primary adrenal insufficiency?

A

Addison’s disease
Defect in the adrenal cortex, cortisol is not made and there is no feedback inhibition
Levels of ACTH are high
increased POMC activity = increased skin pigmentation

178
Q

What is secondary adrenal insufficiency?

A

Defect at the level of the pituitary
Pituitary does not produce ACTH and the adrenal cortex is not stimulated to produce cortisol
No POMC levels and no increased skin pigmentation

179
Q

What is Addison’s disease?

A

Primary adrenal insufficiency
Reduced cortisol secretion which causes reduced gluconeogenesis which causes hypoglycemia
All zones in the adrenal cortex may be affected by primary insufficiency
-could be reduced aldosterone secretion which will cause hyponatremia, hypovolemia, and hyperkalemia = hypotension
Hypotension is the classical sign

180
Q

What is Cushing’s syndrome?

A

When there is prolonged exposure to cortisol

181
Q

What causes Cushing’s syndrome?

A

Pituitary tumor, adrenal tumor, ectopic tumor

182
Q

What would a pituitary tumor cause?

A

High production of ACTH which stimulates the adrenal cortex to produce too much cortisol
Most common form of Cushing syndrome

183
Q

What would an adrenal gland tumor cause?

A

High levels of cortisol which inhibits the production of ACTH from the pituitary through feedback regulation

184
Q

What would an ectopic tumor cause?

A

Can produce ACTH which stimulates cortisol production from the adrenal cortex; high levels of cortisol inhibit ACTH production from the pituitary; tumor is not inhibited from producing ACTH and cortisol levels remain high

185
Q

What are the features of Cushing’s disease?

A

Moon face
Buffalo hump
Hirsutism (male facial hair growth in women)

186
Q

What is steroidogenesis in the reticular zone?

A

Cholesterol to pregnenolone to 17-OH-pregnenolone to dehydroepiandrosterone (DHEA)

187
Q

What are adrenal androgens?

A

DHEA (weak androgen, 20% testosterone potency) is synthesized in the zona reticularis
Converted to testosterone/estrogens in other tissues
Involved in secondary sex characteristics, libido in women, and a source of estrogen in postmenopausal women

188
Q

How is DHEA released?

A

The hypothalamus releases CRH which stimulates the anterior pituitary to release ACTH which stimulates the adrenal cortex to synthesize DHEA

189
Q

What is the steroidogenesis of DHEA?

A

When pathways that make aldosterone or cortisol are blocked, large amounts of DHEA are produced which can be converted to testosterone

190
Q

What is adrenogenital syndrome?

A

Pathways that make aldosterone and cortisol are deficient and instead all of the precursors enter the pathway to make DHEA
Results when excess androgens are produced in the adrenal cortex

191
Q

What are the symptoms of adrenogenital syndrome in females?

A 
Masculinization of genitals 
Hirsutism 
Male-type balding 
Heavy arms and legs 
Involution of breasts
192
Q

What are the symptoms of adrenogenital syndrome in males?

A

Pseudo puberty

193
Q

What is calcium involved in?

A 
Neurotransmission
Muscular contraction
Blood clotting 
Cell cytoskeleton 
Cell metabolism 
Skeletal support
194
Q

What is phosphate involved in?

A

Glycolysis
Energy transfer
Cofactor for many enzymes and skeletal support

195
Q

What are 2 hypercalcemic hormones?

A

Act to increase calcium levels in blood

Parathyroid hormone 
Vitamin D3 (VD)
196
Q

What is the hypocalcemic hormone?

A

Act to decrease blood calcium levels

Calcitonin (CT)

197
Q

What are the effects of the parathyroid hormone on plasma ion concentrations?

A

Increase plasma calcium

Decrease plasma phosphate

198
Q

What are the effects of parathyroid hormone on the kidney?

A

Increased calcium reabsorption
Decreased phosphate reabsorption
Increased vitamin D activation

199
Q

What are the effects of parathyroid hormone on the bones?

A

Increased bone resorption

200
Q

What are the effects of parathyroid hormone on the GIT?

A

Indirect effect by increased vitamin D formation

201
Q

How is parathyroid hormone secreted?

A

Calcium: Hypercalcemia inhibits, hypocalcemia stimulates

Vitamin D3: 1,25(OH)2D3 inhibits

202
Q

Parathyroid hormone summary

A

Source: parathyroid gland (chief cells)

Action: Increased calcium and decreased phosphate

Stimulus: decreased calcium (hypocalcemia)

203
Q

What is hyperparathyroidism?

A 
Increased PTH, calcium, and  1,25(OH)2D3
Decreased phosphate
Soft tissue calcification (kidney stones) 
Weak bones, fractures 
GIT dysfunction
204
Q

What is primary hyperparathyroidism?

A 
Problem with the parathyroid gland itself 
Increased PTH, calcium, and  1,25(OH)2D3
Decreased phosphate
Soft tissue calcification, death
Calcification of blood vessels, aneurysm
205
Q

What is secondary hyperparathyroidism?

A

Consequence of low blood calcium
Decreased calcium and increased PTH
Happens in rickets (juveniles) and osteomalacia (adults) when there is impaired uptake of calcium in the GIT
In renal failure when there is impaired calcium reabsorption in the kidney

206
Q

What is primary hypothyroidism?

A

Decreased PTH, calcium, and 1,25(OH)2D3
Increased phosphate
Increase neuromuscular activity
Causes tetany, asphyxia-death

207
Q

What is Trousseau’s sign?

A

Hypoparathyroidism

Involuntary contraction of the carpal muscles (hand) due to hypocalcemia and tetany

208
Q

What is Chvostek’s sign?

A

Hypocalcemia

Tap the trigemial nerve which runs along your check for tetany and a snarl

209
Q

What is pseudohypoparathyroidism?

A

Increased PTH, decreased calcium, increase phosphate, decreased 1,25(OH)2D3
Tissue insensitivity to PTH action - the receptors don’t work

210
Q

What is hypoparathyroidism?

A

Levels of calcium are low leading to poor teeth health

211
Q

What is calcitonin?

A

Peptide hormone
Opposes the action of PTH
Parafollicular cells produce it

212
Q

What are the effects of calcitonin on the plasma ion concentration?

A

Calcium and phosphate decrease

213
Q

What are the effects of calcitonin on the kidneys?

A

Decreased calcium reabsorption, phosphate reabsorption, and vitamin D activation

214
Q

What are the effects of calcitonin on the bone?

A

Decreased bone resorption

215
Q

What are the effects of calcitonin on the GIT?

A

Decreased calcium absorption

216
Q

What is the clinical use of calcitonin?

A

No excess/deficiency syndromes
Treatment of postmenopausal osteoporosis (brittle bone disease, absence of estrogen, PTH action on bone is not antagonized)
Treatment of Padget’s disease (characterized by excessive osteoclast(break down brown) activity)

217
Q

Summary of calcitonin

A

Source: parafollicular (C) cells of the thyroid
Thyroid hormone but does not contain iodine

Action: decreased calcium and phosphate

Stimulus: increased calcium

218
Q

What is vitamin D?

A

Steroid hormone that regulates plasma calcium and phosphate levels
Main synthesis in the skin

219
Q

How is vitamin D synthesized?

A

Vitamin D is formed by 7-dehydrocholesterol
More than 90% of calcium in made from a process in the skin
Small percent it taken through the diet
Very weak until converted in the liver to its very active form

220
Q

What is the synthesis and metabolism of vitamin D?

A

7-dehydrocholesterol is converted into vitamin D in the skin (inactive) which enters circulation and travels to the liver where it is converted by 25-hydroxylase to 25-OH-Vitamin D, then converted again in the kidney by 1-alpha hydroxylase to active 1,25 Vitamin D (active moiety) or by 24-hydroxylase to inactive 24,25 Vitamin D (inactive moiety)
Enzymatic conversion in the liver and kidney is required for activation

221
Q

What are the effects of Vitamin 1,25 D on plasma ion concentrations?

A

Increased calcium and phosphate

222
Q

What are the effects of Vitamin 1,25 D on the kidneys?

A

Increased calcium and phosphate reabsorption

223
Q

What are the effects of Vitamin 1,25 D on the bones?

A

Promote PTH action

224
Q

What are the effects of Vitamin 1,25 D on the GIT?

A

Increased absorption of calcium and phosphate

Main site of vitamin D action

225
Q

What are the GIT actions of Vitamin D?

A

Increase the absorption of calcium from the GIT

Vitamin D diffuses across cell membranes which binds to receptors in the nucleus of the intestinal cell which exerts its effects through gene transcription and the synthesis of proteins (calcium channels, calcium binding proteins, calcium ATPase

226
Q

Vitamin D Summary

A

Source: liver precursor photoisomerized in the skin to cholecalciferol; 25 hydroxylated in the liver and 1alpha-hydroxylated in the kidney

Action: increased calcium and phosphate

Stimulus: Increased PTH and low calcium

227
Q

What are unique features of vitamin D?

A

Calcium is a homeostatic regulator
Made from a cholesterol derivative
Secreted internally into the bloodstream
Not water soluble and is protein-bound in the plasma (transcalciferin)
Acts at distant target sites
Acts through nuclear receptors

228
Q

What happens when there is a vitamin D deficiency?

A

Rickets in juveniles

Osteomalacia in adults

229
Q

What happens when there is an excess of vitamin D3?

A

Vitamin D toxicity

230
Q

What is rickets?

A

Decreased vitamin and calcium cause poor bone formation

Decreased vitamin D, calcium, and increased PTH cause increased bone resorption

231
Q

What is vitamin D toxicity?

A

Causes hypercalcemia

Soft tissue calcification

232
Q

What does the endocrine gland of the pancreas do?

A

Regulates blood sugar

233
Q

Where is the endocrine gland of the pancreas found?

A

With the organ called the Islet of Langerhans

234
Q

What are the cell types of the pancreatic islets?

A

Alpha cells
Delta cells
Beta cells

235
Q

What do alpha cells do?

A

Secrete glucagon

236
Q

What do beta cells do?

A

Secrete insulin

Comprise the bulk of the endocrine gland of the pancreas

237
Q

What do delta cells do?

A

Somatostatin

238
Q

What are the paracrine interactions in the pancreatic islets?

A

Delta cells release somatostatin which inhibits alpha and beta cells
Beta cells release insulin which inhibits alpha cells
Alpha cells release glucagon which stimulates beta cells and delta cells

239
Q

What is neural innervation of the pancreatic islets (sympathetic)

A

Increased glucagon and decreased insulin

Splanchnic nerve

240
Q

What is neural innervation of the pancreatic islets (parasympathetic)?

A

Increased insulin and increased glucagon

Vagus nerve

241
Q

What is the action of glucagon?

A

Promotes the breakdown of stored forms of energy to increase blood glucose
Catabolic

242
Q

What is the action of insulin?

A

Converts nutrients into stored forms to lower blood glucose

Anabolic

243
Q

What is the structure of insulin?

A

Proinsulin and C-peptide have weak insulin-like activity but connecting the two make insulin

244
Q

What are the actions of insulin?

A

Functions in intermediary metabolism
Islet beta cells secrete insulin which decreases blood glucose, blood fatty acids, blood amino acids and increase protein synthesis and fuel storage
Overall increases the storage of metabolic fuels

245
Q

What are the factors affecting insulin secretion?

A

Increasing food intake, blood glucose concentration, blood amino acid concentration, and blood fatty acid concentration will stimulate the secretion of insulin
Stress will inhibit the secretion of insulin

246
Q

What is the primary stimulus for insulin secretion?

A

High plasma glucose

247
Q

How does plasma glucose control insulin secretion?

A

An increase in plasma glucose concentration stimulates beta cells to secrete insulin and the increased plasma insulin causes increased uptake of glucose by adipose tissue and muscle for storage, net uptake of glucose by the liver, this will all decrease the glucose in the plasma and insulin can return to normal levels

248
Q

What is glucagon

A

Peptide hormone produced by alpha cells
Acts to raise the concentration of glucose and fat in the bloodstream
Catabolic

249
Q

What are glucagon actions on glucose?

A

Decreased glycogenesis, Increased gluconeogenesis and glycogenolysis

250
Q

What are glucagon actions on lipids?

A

Increased lipolysis

Decreased lipogenesis

251
Q

What are glucagon actions on protein?

A

Minor increase in degradation

252
Q

What are the catabolic actions of glucagon?

A

Hormone of fasting
Glycogen to glucose
Protein to amino acids
Triglycerides to fatty acids and glycerol

253
Q

What are the anabolic actions of insulin?

A

Hormone of feasting
Glucose to glycogen
Amino acids to proteins
Fatty acids and glycerol to triglycerides

254
Q

What are nutritional factors that regulate glucagon secretion?

A

Decreased glucose and increased amino acids

255
Q

What are GIT hormones that regulate glucagon secretion?

A

Increased gastrin and CCK

Decreased secretin

256
Q

What are neural stimuli that regulate glucagon secretion?

A

Increased stress

Increased food

257
Q

What are the effects of plasma glucose levels on glucagon secretion and insulin secretion?

A

Increased plasma glucose concentration causes an increase in insulin secretion (beta cell) and inhibits glucagon secretion (alpha cell) and glucose levels go back to normal

Decreased plasma glucose concentration causes an increase in glucagon secretion (alpha cell) and a decrease in insulin secretion (beta cell) which causes glucose levels to go back to normal

258
Q

What is the neural regulation of glucagon secretion?

A

Sympathetic stimulation = inhibit beta cells to reduce insulin secretion, stimulate alpha cells to increase glucagon secretion

Intake of food will stimulate the parasympathetic system to stimulate the release of insulin and glucagon

259
Q

What is diabetes mellitus?

A

Insulin deficiency and glucagon excess syndrome

260
Q

What happens when there is a deficiency of insulin causing decreased glucose uptake by cells?

A

There is a decreased uptake of glucose by cells causing hyperglycemia, osmotic diuresis, cellular dehydration, and circulatory failure and impaired renal functioning

261
Q

What happens when there is a deficiency of insulin that causes increased free fatty acids?

A

Increased delivery of free fatty acids to the liver which increases ketogenesis which causes high ketone levels that upset the normal pH balance in the blood which leads to acidosis and a diabetic coma, fruity breath

262
Q

What happens when there is a deficiency of insulin that causes increased amino acid release from cells?

A

Increased amino acid release from cells which are utilized by the liver to make more glucose
Causes protein catabolism which results in wasting syndrome (break down of muscle)

263
Q

What are the metabolic consequences of insulin deficiency?

A

Polyuria (production of large amount of urine, urine contains a lot of glucose which is Glucosuria)
Polydipsia (excessive thirst)
Polyphagia (excessive hunger or increased appetite)

264
Q

What is type 1 diabetes?

A

Insulin dependent or juvenile-onset

An autoimmune disease that attacks the beta cells of the pancreatic islets causing a loss of insulin secretion
Treated with insulin
10-20% of diabetes

265
Q

What is type 2 diabetes?

A

Insulin independent or adult-onset

Associated with insulin resistance (no destruction of beta cells)
Target cells have decreased response to insulin
They may have normal or high plasma insulin levels
There is insulin receptor downregulation leading to insulin resistance
Associated with diabetes
80-90% of diabetes
Treated with diet and weight reduction

266
Q

What are complications of diabetes mellitus?

A 
Cardiovascular disease 
-atheroscleosis
-gangrene
-hypertension
Nephropathy
Retinopathy
Dermopathy
Neuropathy
Ulcers/infections
267
Q

What are the causes of insulin excess?

A 
Insulin-secreting tumor 
Insulin overdose 
Reactive hypoglycemia (hypersensitive beta cells)
268
Q

What are the symptoms of insulin excess?

A

Hypoglycemia
Sympathetic activation
Insulin shock

269
Q

What is the treatment of insulin excess?

A

Glucose for diabetics

Low carbohydrates for reactive hypoglycemia

270
Q

What are protein hormones

A

Amines
Peptides
Proteins

271
Q

What is the effect of thyroid hormone on cardiovascular action?

A

via B-receptors (beta)

Physiology 210 (12 decks)

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