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BIOM 3200 > Endocrine System > Flashcards

Endocrine System Flashcards

1
Q

What is considered the conceptual framework for the study/understanding of physiology?

A

Homeostasis

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2
Q

Who suggested the concept of homeostasis?

A
  • Claude Bernard

- ‘The Father of modern physiology’

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3
Q

What did Claude Bernard state?

A
  • Our internal environment remains remarkably consistent despite changes in the external milieu
  • Provides stable conditions for body cells to perform functions
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4
Q

How did Walter Cannon contribute to the study of physiology?

A
  • Coined the term ‘homeostasis’ to describe the relative stability of the internal environment
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5
Q

Describe the homeostatic mechanism.

A

Sensory -> Integrating Center -> Effector

  • Can be many or one of each
  • Negative feedback response
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6
Q

Describe negative feedback loops.

A
  • Forever changing/dynamic

- Constant by staying within normal range

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7
Q

Describe the home furnace system homeostatic mechanism if house temperature falls.

A

House temperature falls -> Sensory system (thermostat) -> Response system (furnace) switched on -> Heat is produced -> House temperature rises -> Thermostat -> Furnace switched off

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8
Q

Describe the blood pressure negative feedback loop when standing up.

A

Lying down -> standing up

  1. Blood pressure falls (stimulus)
  2. Blood pressure receptors respond (sensor)
    - > integrating centre
  3. Heart rate increases (effector)
  4. Rise in blood pressure (negative feedback)
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9
Q

Homeostatic control relies on ____?

A

Sensor - constant monitoring
Integrating centre - coordinates b/n sensor and effector
Effector - adjustment

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10
Q

Which two systems maintain homeostasis in large part?

A

Nervous and Endocrine systems

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11
Q

Which factors must be regulated in order to maintain homeostasis? (5)

A
  • Water and electrolytes
  • pH
  • Oxygen and carbon dioxide
  • Temperature
  • Energy sources
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12
Q

Which two things does homeostasis allow for?

A
  • Maintenance of ‘normal’ metabolic function

- Reproductive potential

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13
Q

Why do we care about the endocrine system?

A
  • Many people are affected by endocrine disorders/diseases (ex. Type 2 diabetes)
  • Understanding how homeostasis in the endocrine system works helps us to understand/treat them
  • Diabetes Mellitus is the 6th leading cause of death in Canada
  • Thyroid disorders affect about 5% of population
  • Endocrine ovarian disorders affect about 6% of female population and are most common cause for infertility
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14
Q

How has the prevalence of diagnosed diabetes changed over time?

A
  • Increased

- Not a stand alone disease

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15
Q

What does hyper-function mean?

A
  • Too much hormone
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16
Q

What does hypo-function mean?

A
  • Too little hormone
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17
Q

What does resistance mean?

A
  • Too little effect

- Body doesn’t respond to it

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18
Q

What is endocrinology?

A
  • The study of hormones and the actions of hormones

- The study of how endocrine glands regulate the physiology and behaviour of animals

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19
Q

Where does the term ‘hormone’ come from?

A
  • Greek

- ‘to excite or arouse’

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20
Q

What is the definition of an endocrine gland?

A

A tissue which releases/secretes a substance into the bloodstream; this substance then travels via the blood to influence a target cell
- Ex. Pancreas secretes insulin to travel to liver, muscle, and adipose tissue

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21
Q

What is the classic Minkowski experiment?

A

Discovery of insulin

  1. Surgically remove pancreas - dog develops symptoms of diabetes (wasn’t able to clear glucose from blood)
  2. Implant pieces of pancreas under skin - prevents symptoms of diabetes
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22
Q

What is the Banting and Best experiment?

A

Discover of insulin

  1. Identified anti-diabetic substance in pancreatic extracts
  2. Injected extract prevents symptoms of diabetes (elevated blood glucose)
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23
Q

What is insulin? What does it do?

A
  • Peptide hormone produced by beta cell of pancreas

- Promotes absorption of glucose from blood to skeletal muscle and fat tissue

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24
Q

What does the inactive form of insulin look like?

A
  • Stored form
  • Hexamer
  • Zinc ion and histidine residues holding subunits together
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25
Q

What are the chemical classifications of hormones (3)?

A
  • Amines: derived from tyrosine and tryptophan
  • Proteins/polypeptides (including glycoproteins)
  • Steroids: derived from cholesterol
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26
Q

What are the three levels of effect for hormones?

A 
Autocrine
- SC = TC
Paracrine
- SC affects TC of same tissue
Endocrine
- SC sends hormone through blood stream to TC
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27
Q

Describe protein/peptide hormones.

A 
Synthesis: in advance
Storage: secretory vesicles
Release: exocytosis
Transport: dissolved in plasma
Half life: short
Ex. insulin
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28
Q

Describe steroid hormones.

A 
Synthesis: on demand
Release: diffusion
Transport: bound to carrier proteins
Half life: long
Ex. estrogen/androgen
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29
Q

Describe catecholamine hormones.

A 
Synthesis: in advance
Storage: secretory vesicles
Release: exocytosis
Transport: dissolved in plasma
Half life: short
Ex. epinephrine/norepinephrine
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30
Q

Describe thyroid hormones.

A 
Synthesis: in advance
Storage: secretory vesicles
Release: diffusion
Transport: bound to carrier proteins
Half life: long
Ex. thyroxine
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31
Q

Describe the specificity of receptors?

A

Receptors are highly specific for a particular hormone, but non-specific binding does occur (e.g. hormone ‘overspill’)

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32
Q

How is continued/future signalling allowed?

A

Continuous turn-over of receptor-hormone complex (hormone may be released)

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33
Q

Receptors for most hormones are found where?

A

In the plasma membrane of target cells (transmembrane receptors)

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34
Q

Where are receptors for steroid and thyroid hormones found?

A

Inside target cells
Steroid - Cytoplasm
Thyroid - Nucleus

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35
Q

Describe transmembrane receptor binding.

A
  • Hormone binds extracellular domain of receptor and activates one or more cytoplasmic signaling pathways
  • Many involve phosphorylation and enzyme activation
  • Some lead to DNA/mRNA/protein response
  • Others just have local effect in target cell
  • Ex. adenylate cyclase pathway and phospholipase C pathways
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36
Q

What are the steps in adenylate cyclase pathways?

A

1 - Hormone binds receptor, G-proteins dissociate
2 - Alpha-subunit activates adenylate cyclase
3 - AC catalyzes production of cAMP from ATP
4 - cAMP removes regulatory unit from protein kinase
5 - PK activates other molecules (hormonal response)

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37
Q

What is an example of the adenylate cyclase pathway?

A
  • Epinephrine binds to beta-adrenergic receptors (resulting in activation)
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38
Q

What did Robert Lefkowitz and Brian Kobilka focus on? Why is it important?

A
  • G protein-coupled receptors

- Crucial to unravelling complex network of signalling b/n cells

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39
Q

Describe the Phospholipase C - Ca2+ pathway?

A

1 - Hormone binds receptor
2 - G-proteins dissociate
3 - Alpha-subunit activates PLC
4 - PLC causes breakdown of membrane phospholipid to IP3
5 - IP3 binds endoplasmic reticulum
6 - Release of stored Ca2+ into the cytoplasm
7 - Ca2+ activates other molecules (hormonal response)

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40
Q

What is an example of the phospholipase C - Ca2+ pathway?

A

Epinephrine binds to alpha-adrenergic receptors

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41
Q

Which G alpha subunit subtypes correspond to which enzymes?

A

G(s)alpha => adenylate cyclase

G(q)alpha => Phospholipase C

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42
Q

Describe the hypothalamus-anterior pituitary gland - peripheral target axes?

A

Hypothalamus (blood vessel) -H1-> Anterior pituitary cells (main circulation) -H2-> [Peripheral endocrine gland -H3-> main circulation -> tissue response] OR [Non-endocrine tissue -> tissue response]

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43
Q

What are 7 hypothalamic hormones involved in the control of the anterior pituitary gland?

A
  • Prolactin-inhibiting hormone/dopamine
  • Prolactin-releasing hormone
  • Thyrotropin-releasing hormone
  • Corticotropin-releasing hormone
  • Growth hormone-inhibiting hormone/somatostatin
  • Growth hormone-releasing hormone
  • Gonadotropin-releasing hormone
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44
Q

Describe the hypothalamus - anterior pituitary gland - adrenal cortex axis?

A

(Hypothalamus) CRH -> (Anterior pituitary) ACTH -> (Adrenal cortex) Cortisol -> Many tissues

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45
Q

Describe the central stimulatory control of Corticotropin-releasing hormone?

A
  • In hypothalamic paraventricular nucleus
  • Noradrenergic
  • Stimulates pre-proCRH gene and protein expression
  • Processed to CRH
  • Stimulates pulsatile release of CRH
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46
Q

What are inhibitory influences on CRH synthesis/release?

A
  • Physiological levels of cortisol inhibit release of CRH
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47
Q

What are the steps of CRH synthesis/release?

A

1 - CRH produced by parvocellular neurosecretory cells within hypothalamic PVN
2 - CRH is released at median eminence from neurosecretory nerve terminals into blood vessels in hypothalamo-pituitary portal system
3 - CRH travels through blood vessels to anterior pituitary, where it stimulates corticotropes to secrete ACTH

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48
Q

What is ACTH derived from?

A

Pro-opiomelanocortin (or POMC)

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49
Q

What are convertases?

A
  • Enzymes that cleave POMC

- Different convertases give rise to different products

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50
Q

What type of hormones does the adrenal cortex release?

A 
- Steroids
Specifically...
- Glucocorticoids
- Mineralocorticoids
- Sex steroids
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51
Q

Which category of hormones does the adrenal medulla release?

A
  • Catecholamines

- It is known as a modified sympathetic ganglia

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52
Q

What is cholesterol converted into in the zona fasciculata?

A

Cholesterol -> pregnenolone -> 17OH-pregnenolone -> 17OH-progesterone -> 11-deoxycortisol -> cortisol

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53
Q

What is the dominant glucocorticoid in humans? In rodents?

A

Humans - Cortisol

Rodents - Corticosterone

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54
Q

Describe the binding at steroid hormone receptors?

A

1 - Steroid hormone transported bound to plasma carrier protein
2 - Binds cell cytoplasm receptor
3 - Translocates to nucleus and binds DNA (acts as TF)
4 - Stimulates gene transcription
5 - Protein products
6 - Response

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55
Q

Why is cortisol (stress hormone) essential for life?

A
  • Protects against hypoglycemia by promoting gluconeogenesis (promotes breakdown of skeletal muscle for glucogenic precursors)
  • Natural regulator of immune system (clinical use as anti-inflammatory agents)
  • Affects brain function (mood, memory, learning)
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56
Q

What is Cushing’s Syndrome?

A
  • Result of chronically high levels of glucocorticoids in the blood
  • Can be caused by taking glucocorticoid drugs, or diseases that result in excess cortisol, ACTH, or CRH levels
  • Primary hypercortisolism
  • Could be caused by Cushing’s Disease
  • ACTH levels are lower than CD
  • Causes changes in metabolism which give rise to puffy appearance and CNS disorders
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57
Q

What is Cushing’s Disease?

A
  • A pituitary-dependent cause of Cushing’s Syndrome
  • A tumour in the pituitary gland produces large amounts of ACTH, causing adrenal glands to secrete excess cortisol
  • Secondary hypercortisolism
  • ACTH levels are higher than CS
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58
Q

What happens if Cushing’s Syndrome is not treated?

A
  • Disease worsens
  • Health deteriorates
  • Especially worsening diabetes/high blood pressure
  • Can lead to strokes or myocardial infarction
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59
Q

Describe the medical management/treatment for Cushing’s Syndrome

A
  • Insulin for diabetes
  • Anti-hypertensives for blood pressure
  • Surgery to remove pituitary or adrenal gland
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60
Q

What is Addison’s Disease?

A
  • Caused by inadequate secretion of glucocorticoids
  • Primary hypocortisolism
  • Result of adrenal insufficiency (caused by genetics, autoimmune, or acquired)
  • High dose steroids > 1 week begins to suppress adrenal glands by suppressing CRH and ACTH
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61
Q

Describe adrenal cortisol secretion.

A
  • Continuous
  • Pulsatile (helps to regulate)
  • Circadian rhythm
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62
Q

How does insomnia relate to the HPA axis?

A
  • People with insomnia secrete more cortisol around sleep time
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63
Q

Describe pituitary pars intermedia dysfunction.

A
  • In horses
  • pars intermedia does not form properly
  • Affects older horses
  • Impaired pituitary gland
  • Hyperplasia/hypertrophy of pars intermedia -> increased secretion of cortisol by adrenal glands -> high blood glucose and suppression of immune system
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64
Q

What are some common signs of PPID in horses?

A
  • Hypertrichosis (excessive hair)
  • Abnormal/patchy hair coat
  • Muscle atrophy
  • Excessive sweating
  • Formation of fat pads
  • Pot-bellied
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65
Q

How is PPID diagnosed in horses?

A

Measure fasting, resting basal blood ACTH and insulin levels

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66
Q

What is the treatment of PPID in horses?

A 
Pharmacotherapy
- Pergolide
- Acts on pituitary gland to decrease circulating ACTH
Lifestyle
- Exercise
- Weight loss (if obese)
- Limit starch/sugar in horse's diet
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67
Q

What is melanocyte-stimulating hormone?

A
  • Another POMC derivative
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68
Q

What are the components of the melanocortin system?

A
  • Opioid peptide: beta-endorphin (acts on pituitary to block pain)
  • 4 peptide hormones: alpha/beta/gamma-melanocyte stimulating hormone and adrenocorticotropic hormone
  • 5 melanocortin system receptors (G-protein coupled)
  • 2 melanocortin system antagonists (Agouti and AGRP)
  • 2 melanocortin system regulators (mahogany and syndecan-3)
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69
Q

What is the key to the melanocortin system?

A
  • Cell specificity
  • Post-translational processing of POMC is cell-specific
  • Different MCRs on different cell types
  • Provides latitude for control/regulation of various physiological processes
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70
Q

What are the steps in which alpha-MSH affects pigmentation?

A
  1. alpha-MSH binds MC1R
  2. Activates adenylate cyclase signalling pathway
  3. Activates cAMP response element-binding protein (CREB) - TF: binds CRE and promotes microphthalmia-associated TF (MITF) synthesis
  4. MITF promotes synthesis of melanogenic enzymes (ex. dopachrome tautomerase [DCT])
  5. Melanin produces dark pigment
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71
Q

How does a mutation in alpha-MSH or MC1R affect pigmentation?

A
  • Prevents dark pigmentation
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72
Q

What type of mutations are POMC mutations?

A
  • Autosomal recessive
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73
Q

What are the clinical characteristics of POMC mutations?

A
  • Hyperphagia (lack of alpha-MSH)
  • Severe, early-onset obesity
  • Normal birth weight, but rapid weight gain
  • Red hair and pale skin
  • Adrenal insufficiency (lack of ACTH to promote cortisol secretion from adrenal cortex)
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74
Q

What is the Agouti mouse?

A
  • Result of spontaneous mutation wherein mice overproduce Agouti protein
  • Agouti inhibits MC1R and MC4R signalling
  • In skin, alpha-MSH binding to MC1R produces dark pigmentation
  • In hypothalamus, alpha-MSH binding to MC3R and MC4R helps to regulate appetite and energy balance
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75
Q

What is agouti-related protein?

A
  • Another hypothalamic protein

- Inhibits MC4R

76
Q

What is red hair a result of?

A
  • 2 copies of a recessive mutation in MC1R
77
Q

What makes jaguar black?

A
  • Melanism

- Dominant gene mutation in MC1R

78
Q

Describe the hypothalamus-anterior pituitary gland-thyroid axis?

A

TRH -> TSH -> Thyroid gland -> Thyroid hormones -> Many tissues

79
Q

What is the hypothalamus-anterior pituitary gland-thyroid axis (including structures and hormones)?

A

Hypothalamus -Thyrotropin-releasing hormone-> Anterior pituitary -Thyroid-stimulating hormone-> Thyroid -Thyroxine-> inhibits responsiveness

80
Q

Describe the thyroid gland and its location?

A
  • Just below larynx
  • On either side of trachea
  • 2 lobes
  • Connected by isthmus
  • Largest purely endocrine gland
  • Lateral to the first 3-8 tracheal rings
81
Q

What do follicles do?

A
  • Follicles include follicular cells and colloid

- Take up iodide (I-) from blood

82
Q

What happens in the colloid?

A
  • Colloid is the large circular cells

- Thyroid peroxidase helps attach it to a tyrosine residue in thyroglobulin

83
Q

Where is thyroglobulin made?

A
  • Made by follicle cells
  • It is a long peptide chain with lots of tyrosine residues
  • Transported to colloid
  • Side chain of tyrosine is important in T3/T4 synthesis
84
Q

How is I- brought into cells? What happens to it?

A
  • I- is brought from blood into follicular cells by sodium-iodide transporter, then into colloid by a transporter called pendrin
  • I- is converted to an iodine radical (extremely reactive) by TPO, and added to thyroglobulin
85
Q

How does the iodine radical attach to thyroglobulin?

A
  • Via tyrosine residues
    1 - The attachment of 1 iodine radical on a tyrosine residue produces MIT
    2 - The attachment of 2 iodine radicals on a tyrosine residue produces DIT
86
Q

What does the iodine radicals do to tyrosine residues?

A
  • Iodine radical causes tyrosine residues to cross-link (fold in on itself)
87
Q

What do enzymes in the colloid do to MIT/DIT?

A
  • Modify their structures
  • Make thyroid hormones via condensation:
  • > T3
  • > T4
88
Q

Are T3 or T4 bioactive?

A
  • T3 is bioactive, but T4 is not
89
Q

What happens after T3/T4 are synthesized?

A
  • They are still attached to thyroglobulin
  • Thyroglobulin gets taken back up by follicular cells and cut up so that the T3/T4 are separated
  • T3 and T4 get secreted to bloodstream
90
Q

What is thyroid hormone in blood bound to?

A
  • Thyroxine-binding protein
91
Q

What type of thyroid hormone is biologically active?

A
  • Free thyroid hormone

- Has to dissociate from carrier protein to produce effects in target cells

92
Q

Describe the receptor binding of thyroid hormones?

A
  1. Thyroxine (T4) + carrier protein
  2. T4 -> T3 (triiodothyroine)
  3. T3 uses binding proteins to enter nucleus
  4. Hormone-receptor complex binds DNA (acts as TF)
  5. Stimulates gene transcription
  6. Protein products
  7. Response
93
Q

What is the timing of thyroid hormone secretion?

A
  • Circadian rhythm of thyroid hormones in humans

- Secretion is highest b/n 10-2 to increase basal metabolic rate

94
Q

What are the physiological actions of thyroid hormones?

A
  • Elevates BMR (thyroid hormone production often impairs with age)
  • Needed for normal embryonic/fetal development, particularly for development of CNS
  • Needed for normal gonadal development and function
  • Thyroid hormone deficiency or excess may therefore have serious consequences
95
Q

What does hypothyroidism look like?

A
  • Abnormally low BMR = weight gain
  • Lethargy
  • Intolerance to cold
96
Q

What does hyperthyroidism look like?

A
  • Increased BMR = weight loss
  • Muscular weakness
  • Nervousness
  • Protruding eyes (exophthalmos)
97
Q

What is cretinism?

A
  • Congenital deficiency of thyroid hormones usually due to maternal hypothyroidism
  • Reduced physical growth and severe mental deficiency
98
Q

How do thyroid hormones affect terminal brain differentiation?

A
  • Thyroid hormone-dependent development of brain begins in utero - completed after birth
  • Dendritic and axonal growth, myelin formation and synapsis formation
  • Neuronal migration
  • Maternal thyroid hormones first supply needs of embryo/fetus
99
Q

How can cretinism be treated?

A
  • Treatment with thyroxine (T4) soon after birth (before one month) restores development of intelligence
100
Q

What can cretinism be caused by?

A
  • Innate maternal hypothyroidism

- Dietary iodine deficiency

101
Q

What are some causes of hypothyroidism?

A
  • Insufficient dietary iodine
  • Thyroid gland defect
  • Impaired thyroid hormone pathway
  • Insufficient TSH (anterior pituitary)
  • Insufficient TRH (hypothalamus)
  • Mutant TSH or TRH receptors (genetic)
  • Mutant thyroid hormone transport proteins
  • Autoimmunity
102
Q

What are some causes of hyperthyroidism?

A
  • Thyroid gland defect
  • Impaired thyroid hormone pathway
  • Overproduction of TSH (anterior pituitary)
  • Overproduction of TRH (hypothalamus)
  • Mutant TSH or TRH receptors (genetic)
  • Mutant thyroid hormone transport proteins
  • Autoimmunity
103
Q

What is goitre?

A
  • Hypothyroidism
  • Abnormal growth of thyroid gland
    Low iodine intake (thyroid can’t produce enough thyroid hormones) -> Low plasma T3 and T4 -> High TRH (from hypothalamus) -> High plasma TSH (from anterior pituitary) -> Stimulates excess growth of thyroid to try to make more thyroid hormones
104
Q

What is Grave’s disease?

A
  • Hyperthyroidism
    Autoantibodies bind TSH receptor and activate thyroid gland -> High plasma T3 and T4 -> Low TRH (from hypothalamus) -> Low plasma TSH (from anterior pituitary)
105
Q

What are some treatments of thyroid disorders?

A
  • Pharmacotherapy
  • > Synthroid: Levothyroxine (synthetic T4)
  • > Stimulants: Furosemide (increased T4->T3)
  • > Blockers: Thiouracil derivatives, thiocarbamides (less iodination and T4->T3)
  • Radiation therapy
  • Surgery
  • Diet, electrolyte infusions, etc.
106
Q

Describe the hypothalamus-anterior pituitary gland-somatotropic axis?

A

GHIH -| GH -> Liver -> IGFs -> Many tissues

107
Q

What are all the aspects of the hypothalamus-anterior pituitary gland-somatotropic axis?

A

PVN -GHRH-> Anterior pituitary -GH-> Liver -IGF-> Many tissues

108
Q

Describe GH

A
  • 191 AA polypeptide
  • Synthesized, stored and secreted by somatotropic cells of anterior pituitary gland
  • Most abundant anterior pituitary hormone
  • Short half life: 6-20 mins
  • Plays important role in growth
109
Q

What are the GH secretion patterns like?

A
  • GH secretion occurs as several large pulses or peaks each day, 10-30 mins in duration
  • The largest GH peak occurs about 1 hr after onset of sleep
  • Basal levels highest early in life; greatest during pubertal growth spurt then decline
110
Q

List 6 factors that increase GH secretion.

A
  • Sleep
  • Exercise
  • Hypoglycemia
  • High dietary protein
  • Steroids
  • Ghrelin (hunger hormone)
111
Q

List 3 factors that decrease GH secretion.

A
  • Hyperglycemia
  • Glucocorticoids
  • Endocrine disruptors
112
Q

What are the metabolic effects of GH and IGF?

A
  • GH stimulates synthesis and release of IGF from many tissues
  • IGF-1 (from liver): polypeptide hormone with 40% homology to insulin
  • GH also mobilizes fuel sources in other tissues
  • IGF affects growth in cartilage/bone and muscles/other organs
113
Q

How is bone formed?

A
  • Bone contains calcified extracellular matrix (ECM) formed when calcium phosphate crystals precipitate and attach to lattice (collagen) support
  • Most common form of calcium phosphate crystal is hydroxyapatite (Ca10(PO4)6(OH)2
114
Q

What are the 3 bone cell types?

A

Osteoblasts - bone formation
Osteoclasts - bone resorption/breakdown
Osteocytes - derived from osteoblasts

115
Q

What does the bone look like at 2 months (fetus), 2-3 months (fetus), childhood, and adolescence?

A

First 2 months - just collagen/cartilage
2-3 months - blood vessel and bones begin to develop (grows from cartilage growth plates)
Childhood - more cartilage turns into bone
Adolescence - bone containing osteocytes is present, cartilage growth plates at either end of bone promote growth in young adulthood

116
Q

Describe the processes involved in linear bone growth?

A
  • cartilage growth (epiphyseal) plates contain chondrocytes (collagen-producing cells)
  • Collagen contributes to chondrification (cartilage formation)
  • Osteoblasts invade and lay bone matrix (hydroxyapatite) on top of cartilage base
  • Osteoblasts get stuck in matrix -> osteocytes (paracrine and endocrine function)
  • Bone remodeling requires turnover (osteoblast and osteoclast activity)
117
Q

What hormones stimulate bone growth/turnover?

A
  • GH and IGF-1
118
Q

What is pituitary dwarfism?

A
  • Under production of GH in childhood/adolescence

- 2 types: proportionate and disproportionate

119
Q

What is pituitary gigantism?

A
  • Over production of GH in childhood/adolescence
120
Q

What is Laron-type dwarfism?

A
  • Pygmies

- Decreased responsiveness to GH (GH receptor deficiency) that begins in childhood

121
Q

What is reduced BMD a consequence of?

A
  • Underproduction/decreased sensitivity to GH in adults
  • BMD = bone mineral density
  • Increased risk of fractures
122
Q

What is alopecia in dogs associated with?

A
  • Under production or decreased sensitivity to GH in adults

- Hair loss, thin skin

123
Q

What hormone inhibits GH synthesis?

A
  • Increased CORTISOL inhibits GH synthesis
124
Q

What is acromegaly?

A
  • Over production of GH in adulthood
  • Thickening of bones/joints and skin
  • Enlargement of internal organs (tongue, liver, spleen)
125
Q

Who is a real-life example of gigantism and acremegaly?

A

Andre the giant

126
Q

How are GH disorders treated? What side effects would there be?

A
  • Recombinant/synthetic human GH for children with short stature
  • Daily injections for about 2 years = 1ft3” increased height
  • $22000/year
  • Side effects = glucose intolerance, pancreatitis, psychological problems
127
Q

What molecules/atoms provide the structural integrity of bone?

A
  • Calcium and phosphate

- In the form of hydroxyapatite

128
Q

What processes are intracellular/extracellular calcium ions essential for?

A
  • Neuromuscular excitation
  • Blood coagulation
  • Hormone signalling
  • Enzyme activity
  • Fertilization
129
Q

How much calcium is in your body? Where is it found?

A
  • 70kg person has about 1.2 kg Ca2+ in their body
  • 99% is in bones as hydroxyapatite
  • Soft tissues: 11g intracellular, and 1g extracellular
130
Q

Describe the regulation of intracellular calcium? Extracellular calcium?

A

Intracellular is tightly regulated
- Associated with membranes in mitochondria, ER, and plasma membrane
Extracellular is VERY tightly regulated
- 50% ionized/free calcium
- 40% protein-bound calcium
- 10% calcium complexed with phosphate/citrate

131
Q

What happens if intra/extracellular levels of Ca2+ drop?

A
  • Bone Ca2+ will be sacrificed
132
Q

How is total body calcium maintained?

A 
Intake = diet
- About 1/3 absorbed in small intestine
- Absorption is hormone-regulated
- About 1000mg/day is recommended
Output = kidneys
- Lost through urine
133
Q

Which 3 hormones regulate the movement of Ca2+ b/n the intestine, bone, and kidney?

A
  • Parathyroid hormone (PTH)
  • Calcitriol (activated form of 1,25-(OH)2 Vitamin D3)
  • Calcitonin (acts opposite to PTH)
134
Q

Where is PTH made?

A
  • Made by chief cells of 4 parathyroid glands
  • Located on back of thyroid gland
  • Parathyroid glands are essential for life (can NOT be removed)
135
Q

Describe PTH and its secretion.

A
  • Peptide hormone
  • Secreted by chief cells of parathyroid glands
  • When plasma Ca2+ begins to fall, PTH acts to raise Ca2+ to normal levels
  • Raises blood Ca2+
136
Q

What are the 3 mechanisms by which PTH raises blood Ca2+?

A
  • Stimulates osteoclasts to resorb (absorb into circulation) bone
  • Stimulates kidneys to reabsorb Ca2+ from filtrate
  • Stimulates kidneys to produce enzyme needed to activate vitamin D (to calcitriol), which in turn promotes better intestinal absorption of dietary Ca2+
137
Q

Describe the process of PTH stimulation of osteoclasts. What is the result?

A
  • Resorption of bone
  • Decrease in blood Ca2+ is sensed by parathyroids
  • PTH is secreted
  • Kidneys and bones then are activated
  • Kidneys induce the reabsportion of Ca2+
  • Dissolution of CaPO4 crystals in bone
  • Leads to increased blood Ca2+
  • Negative feedback
138
Q

What cells are responsible for bone formation? How do they do this?

A
  • Osteoblasts
  • Secrete matrix of collagen protein
  • Becomes hardened by deposits of hydroxyapatite
139
Q

What cells are responsible for bone resorption and how do they go about this?

A
  • Osteoclasts

- Dissolve hydroxyapatite and return bone Ca2+ to blood

140
Q

What does PTH stimulation of the kidneys do?

A
  • Production of enzyme (1 alpha-hydroxylase) needed to activate vitamin D to calcitriol
  • Calcitriol promotes intestinal absorption of dietary Ca2+
  • 7-dehydrocholesterol is converted to vit D3 by sunlight in sebaceous glands of skin
  • Vitamin D3 is bound to Vit D binding protein (DBP) for transport in blood
  • In liver, Vit D3 -> 25-OH-D3 by 25-hydroxylase
  • 25-OH-D3 (inactive) is released to blood bound to DBP
  • Low blood 25-OH-D3 is a sign of Vit D deficiency
141
Q

How does PTH convert vitamin D to calcitriol?

A
  • Promotes 1alpha-hydroxylase activity in kidney
  • Converts inactive 25-OH-D3 to active calcitriol (1,25-(OH)2-DH3)
  • Calcitriol is released to blood bound to DBP
142
Q

Describe calcitriol and its secretion.

A
  • Steroid hormone
  • Secreted by cells of proximal tubule of nephron of kidney in response to PTH
  • Raises blood Ca2+ by 3 mechanisms
143
Q

By what 3 mechanisms does calcitriol raise blood Ca2

+?

A
  • Maximizes bone resorption by osteoclasts (promotes bone mineralization when blood Ca2+ levels are sufficient)
  • Maximizes Ca2+ reabsorption in kidney
  • Increases dietary Ca2+ and P absorption in small intestine (unique to calcitriol)
144
Q

Describe calcitonin and its secretion.

A
  • Peptide hormone
  • Secreted by parafollicular cells/C-cells of thyroid gland
  • When plasma Ca2+ begins to rise, calcitonin acts to reduce blood Ca2+ by 2 mechanisms
145
Q

By what two mechanisms does calcitonin reduce blood Ca2+?

A
  • Promotes excretion of Ca2+ in the urine

- Inhibits bone resorption by osteoclasts

146
Q

What is hyperparathyroidism? What does it lead to?

A
  • Overactive parathyroid
  • Too much PTH in blood
  • Hypercalcaemia (too much Ca2+ in blood)
  • Increased bone resorption-> poor BMD -> fractures
  • Increased thirst and urination
147
Q

What is hypoparathyroidism and what does it lead to?

A
  • Underactive parathyroid
  • Not enough PTH in blood
  • Hypocalcaemia (not enough Ca2+ in blood)
  • Muscular weakness
  • Ataxia (lack of voluntary muscle control)
  • Cardiac arrhythmias
148
Q

How do bone diseases occur?

A
  • Manifest from changes in ratio of mineral to collagen in bone matrix
149
Q

What is a bone disease associated with a vitamin D deficiency in infants?

A
  • Rickets
  • Bones do not mineralize properly during development and cannot support the body’s weight when learning to walk
  • Permanent
  • Only reversible with surgery
  • Leads to bowed legs
150
Q

What is a bone disease in adolescents/adults that is associated with vitamin D deficiency?

A
  • Osteomalacia
  • Bones become demineralized
  • Bone fractures can occur more easily
  • Can be reversed with supplementation
151
Q

What is a bone disease associated with vitamin D deficiency in middle-aged to elderly?

A
  • Abnormal loss of both mineral and organic (collagen) parts of bone
  • Bone fractures occur more easily and often lead to mortality
  • Difficult to reverse due to erosion of bone
152
Q

What was found to be successful in the treatment of rickets?

A
  • UV treatment

- Cod oil

153
Q

When is peak bone mass achieved?

A

20-30 years of age

154
Q

Do men or women have a higher peak bone mass?

155
Q

Who is at highest risk for osteoporosis? Why?

A
  • Women after menopause

- Lack of estrogen (which protects bones by stimulating osteoblasts)

156
Q

What types of pharmaceuticals can treat osteoporosis?

A
  • Bone-forming therapies
  • Anti-resorptive therapies
  • Calcitonin
  • Hormone replacement therapy (for post-menopausal women)
  • Selective estrogen receptor modulators
157
Q

How can osteoporosis be prevented?

A
  • Avoid malnutrition
  • Achieve dietary vitamin D and calcium needs
  • Perform regular weight-bearing exercise
  • Avoid smoking and excessive alcohol intake (which prevents Ca2+/Vit D absorption)
158
Q

Describe the hypothalamus-anterior pituitary-gonadal axis?

A

Hypothalamus -GnRH-> Anterior pituitary -FSH/LH-> Gonads -> Inhibin/gametes/sex steroids

159
Q

What are the 2 parts of the testes?

A
  • Seminiferous tubules

- Interstitial tissue

160
Q

Describe the cells within the seminiferous tubules?

A
  • Sertoli cells
  • Express FSH receptor
  • Involved in spermatogenesis in response to FSH
  • Secrete inhibin (inhibits anterior pituitary production of FSH)
  • Secrete MIF (role in male reproductive system development)
161
Q

Describe the cells within the interstitial tissue?

A
  • Leydig cells
  • Express LH receptor
  • Produce testosterone in response to LH
162
Q

What happens to testosterone after it is secreted?

A
  • Converted to 5-DHT by 5alpha-reductase in epididymis, seminal vesicles, prostate, skin, hair, liver, and brain
163
Q

What are the actions of testosterone/5-DHT during fetal development?

A
  • Masculinizes reproductive system and external genitalia
164
Q

What are the actions of testosterone/5-DHT during puberty/adulthood?

A
  • Growth, maintenance and maturation of :
    • Male reproductive system
    • Secondary sex characteristics
    • Bone/muscle mass
  • Brain
  • Sex drive
165
Q

What are the 5 steps of sperm transport?

A

1 - Seminiferous tubules drain sperm and other secretions into epididymis (duct on surface of testicular capsule)
2 - Becomes vas deferens, which extends to abdomen
3 - Seminal vesicles add secretions in response to testosterone
4 - Enters prostate, which adds secretions in response to testosterone (semen)
5 - Empties into urethra

166
Q

Describe the 4 steps in the erection of the penis?

A

1 - NO released from parasympathetic axon in penis and acts on VSMC to activate guanylate cyclase (catalyzing GTP->cGMP)
2 - cGMP causes Ca2+ channels in VSMC membrane to close, decreasing cytoplasmic [Ca2+]
3 - VSMC relaxes, causing vasodilation of penis arterioles and enlargement of erectile tissue
4 - Phosphodiesterase degrades cGMP, stopping erection

167
Q

How does viagra work?

A
  • Inhibits PDE, increasing availability of cGMP to promotes sustained erection
168
Q

What does anabolic steroid abuse do?

A
  • Exogenous anabolic steroids induce negative feedback on hypothalamic-pituitary axis, inhibiting FSH and LH secretion
  • Leads to reduced:
  • – Sperm -> infertility
  • – Testosterone and 5-DHT -> diminished secondary sex characteristics
169
Q

Describe the effectiveness of testosterone as male contraception given every 4 or 6 months?

A

4 months: No LH, FSH, or sperm escape

6 months: Sperm escape => ineffective

170
Q

What characterizes female reproductive physiology?

A
  • Complex cycling of endocrine hormones

- 2 about 28 day cycles occur simultaneously (ovarian and menstrual cycles)

171
Q

Describe the ovarian cycle?

A
  • Anterior pituitary hormones (FSH,LH) act on the ovaries

- Ovaries produce ova (eggs) in preparation for fertilization

172
Q

Describe the menstrual cycle?

A
  • Ovaries produce hormones (estrogen, progesterone) that act on the uterus
  • Uterus gets ready for pregnancy, then is stripped of endometrial lining if implantation doesn’t occur
173
Q

What does the menstrual discharge consist of?

A
  • About 80 mL of blood, fluid, cell debris from outer layer of uterine endometrium
174
Q

What is responsible for menstrual bleeding?

A
  • Endometrial spiral arteries

- Animals that lack these arteries do not bleed

175
Q

What happens in stage 0 of 4 of the menstrual/ovarian cycle?

A

HPG-axis
- Increased gonadotropin (FSH/LH) secretion from anterior pituitary

Ovaries
- FSH influences several ovarian follicles to begin maturation

Uterus
- Menstrual bleeding begins = day 1

176
Q

Describe stage 1 of 4 in the menstrual/ovarian cycle?

A

HPG-axis

  • Early: estrogen inhibits GhRH, FSH, LH (-ve feedback)
  • Late: estrogen promotes GnRH and LH (+ve feedback)

Ovaries: Follicular phase

  • Early: FSH decreases
  • Late: Granulosa cells of follicles secrete estrogen; LH increases

Uterus: Menstruation, Proliferative phase
- Estrogen stimulates endometrial growth

177
Q

What happens in stage 2 of 4 of the menstrual/ovarian cycle?

A

OVULATION
HPG-axis
- LH surge

Ovaries

  • Mature follicle ruptures, releasing oocyte into fallopian tube
  • Estrogen decreases
  • Released oocyte is surrounded by zona pellucide (proteins) and corona radiata (granulosa cells)
  • What is left forms corpus luteum
178
Q

Describe stage 3 of 4 of the menstrual/ovarian cycle?

A

HPG-axis
- Progesterone/estrogen inhibit GhRH, FSH, LH (-ve feedback)

Ovaries: Early-mid luteal phase
- Early: Corpus luteum develops, produces progesterone and estrogen

Uterus: Secretory phase
- Progesterone/estrogen promote endometrial thickening in anticipation of pregnancy

179
Q

What happens in stage 4 of 4 of the menstrual/ovarian cycle?

A

HPG-axis
- Negative feedback on HPG-axis removed since progesterone and estrogen decrease

Ovaries: Late luteal phase
- Corpus luteum regresses (lives about 12 days)

Uterus: Menstruation phase
- Endometrium requires progesterone or else vasculature contracts and dies, sloughs off, menstruation starts (14 days post ovulation)

180
Q

Why do women who want to know when they ovulate check their temperature?

A
  • Starting at 1 day after the LH surge, basal body temperature sharply rises
  • Progesterone is responsible for the change
181
Q

How does hormonal female contraception work?

A
  • Synthetic estrogen and progesterone
  • Elevation of these ovarian hormones leads to negative feedback inhibition of HPG-axis so ovulation never occurs
  • Stimulates a false luteal phase
182
Q

What happens at menopause?

A
  • Occurs at 45-55 years
  • Point when ovaries are depleted of follicles, therefore stop secreting estrogen
  • Weak form of estrogen made in adipose tissue
183
Q

How does the amount of adipose tissue in post-menopausal women affect the risk of osteoporosis?

A
  • Post-menopausal women with increased adipose tissue have a decreased risk of osteoporosis
  • However, there is other metabolic consequences
184
Q

What is hormone replacement therapy?

A
  • Synthetic estrogen or estrogen and progesterone

- Research suggests that the risks of long-term HRT use outweigh the benefits for most women

185
Q

What are the benefits of hormone replacement therapy?

A
  • Relieve menopausal symptoms: hot flashes, mood swings, trouble sleeping
  • Reduce risk of osteoporosis and colon cancer
186
Q

What are the risks of long-term hormone replacement therapy?

A
  • Increase risk of breast and ovarian cancer, heart disease, stroke and pulmonary embolism

BIOM 3200 (4 decks)

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