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PHGY 210 > Endocrynologie > Flashcards

Endocrynologie Flashcards

1
Q

What is endocrinology?

A
  1. Coordination of physiological processes
    ex: coorodinating mvt, respiration, circulation, digestion, excretion, metabolism all at once
    endocrine system + CNS = major coordinating factors
  2. Long distance communication
    communicating between cells through chemical substances secreted by releasing cells and interact with specific receptors → specific physiological effects
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2
Q

What are the 2 type of signalling ?

A

Paracrine Signaling:
Very local, could be direct contact with target cell

Autocrine Signaling:
Cell releasing a hormone and has specific receptor on its surface (subcategory of paracrine but cell comunicates with itself)

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3
Q

What are the steps of hormone communication?

A
  1. Synthesis (of hormone by endocrine cell (or neutron in case of neurohormone)
  2. Release (of hormone …)
  3. Transport of hormone/neurhormone to target site by blood stream
  4. Detection of hormone/neurhormone by specific receptor protein on target cell
  5. Change in metabolism triggered by hormone
  6. Removal of the hormone (terminates the cellular response)

*Each step = potential source of signalling/response

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4
Q

How does the Hypothalamic-Pituitary signaling work?

A

Hypothalamic neurohormones released from hypothalamus (?) and inhibit/activates activity of 6 types of hormones-producing cells in the anterior pituitary
neurohormones are called releasing hormones/factors or inhibiting hormones/factor

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5
Q

What are the different classes of hormones and what are they base one?

A

Based on their structure

Glycoproteins (encoded by genes)
Polypeptides (encoded by genes)
Steroids (small molecules)
Amines (small molecules)
Ion Calcium (considered hormone bc calcium sensing receptors

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6
Q

How are hormones produced?

A

First produced as pre-hormones (synthesis on ribosomes)
prehormones → prohormones (Rough endoplasmic reticulum)
Hormones stored into vesicles with other peptides and are released from the cell

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7
Q

What are 4 important steroid hormones?

A

Cortisol
Aldosterone
Testosterone
Estradiol (Estrogene)

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8
Q

What is a unique feature of the Thyroid hormones?

A

They have Iodine in their structure

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9
Q

What are the properties of hormone receptors?

A
  1. Specificity: recognition of 1 single hormone/hormone family
  2. Affinity: Bonding hormone at its physiological concentration
  3. Should show saturability: finit # receptors
  4. Measureable biological effect: effect = response du to interaction of hormone with its receptor
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10
Q

What can be the issues in regulation of the receptors?

A

Upregulated → either by increasing their activity in response to hormone or their synthesis

Downregulated → either by decreasing their activity of their synthesis

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11
Q

What are the 3 mechanisms by which a hormone can exert effetc on a target cell?

A
  1. Direct effects on function at cell membrane
    ex: insuline receptor activates glucose membrane carrier (to bring glucose into the cell)
  2. intracellular effects mediated by second messenger systems
    *First messenger = the hormone that binds to the receptor → ATP converted to cAMP
  3. intracellular effects mediated by genomic of nuclear action
    *Signaling by nuclear receptors including receptors for steroid hormones → steroid hormones have receptors inside the cytoplasm (not on cell surface), not at the surface and go into the nucleus to act on protein synthesis and alter functional response
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12
Q

By what mechanism is hormone secretion regulated?

A

Feedback mechanisms (negative most of the time, an excess of hormone leads to diminution of its sercretion)

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13
Q

How does the plasma Ca2+ regulation negative feeback loop work?
What organs are concerned by Ca2+?

A

Low plasma → ↑ stimulation of parathyroid gland → ↑ Synthesis/release of parathyroid hormone → ↑ PTH → Action on bond, kidney, gut → ↑ plasma Ca2+

Bond, kidney, gut!

*Negative feedback loop when Ca2+ plasma increases, decreases stimulation of parathyroid glands

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14
Q

What are the complete names of these acronymes ?
CRH
ACTH

A

CRH = corticotopin releasing hormone (secretion in hypothalamus)

ACTH = adrenocorticotopic hormone (secretion in anterior pituiraty gland)

cortisol (glucocorticoid) (secretion in adrenal cortex)

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15
Q

How does the regulation mechanism of stress work?

A

Stress or other inputs from other brain areas → INCREASE in CRH secretion (in Hypothalamus) → increase in plasma CRH → INCREASE in ACTH secretion (in anterior pituitary gland) → increase in plasma ACTH → INCREASE cortisol secretion (in adrenal cortex) → increase cortisol in plasma → target cell (of cortisol) responds to increase in cortisol

Résumé: CRH → ACTH → cortisol
Hypothalamus → anterior pituitary gland → adrenal cortex → target cell

*Negative feedback mechanism acts on hypothalamus secretion of CRH and anterior pituitary gland secretion of ACTH

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16
Q

What are the 2 parts of the pituitary gland?

A

Anterior pituitary gland → endocrine tissue

Posterior pituitary gland → neural tissue

17
Q

Which important hormone is not encoded by genes?

A

Prolactin-inhibiting hormone
PIH, Dopamine

*but component necessary for dopamine synthesis are encoded by genes

18
Q

What is the pathway of Oxytocin and Vasopressin?

A

Posterior Pituitary Gland does Neurohypohysis !!

Outgrowth of hypothalamus (connected to pituitary stalk)

Secretion of Oxytocin and Vasopressin (antidiuretic hormone - ADH)

Oxytocin and vasopressin synthesized in 2 hypothalamic nuclei (supra topic nucleus and paraventricular nucleus) *axons run down the pituitary stalk and terminate in posterior pituitary close to capillary blood vessels

*In axons, during transport, prohormones are processed in secretory granules (secretory granule travels the axon)

Mature hormone liberated from the Neurophysins I (for Oxytocin) and II (for vasopressin aka ADH)
Neurophysins = carrier molecules

ADH → Kidneys
Oxytocin → Uterus and Lactating mammary gland

*Circulating half-life of 1-3mins

19
Q

What is the circulating half-time of oxytocin and vasopressin?
Why?

A

1-3 min to allow tight control

20
Q

What are the roles of oxytocin ?

A

Females:
Parturition → uterus very sensitve to oxytocin at end of pregnancy, dilaiton uterine cervix causes oxytocin → uterine contraction
Milk ejection → response to stimulus of suckling, Causes milk filled ducts to contract and squeeze milk out
Behavioural effects → anxiety, enhances bonding, pro-social behaviour

Males:
Ejaculation → Oxytocin surge during sexual activity → epididimial passage of sperm and ejaculation
Behavioural effects → anxiety, enhances bonding, pro-social behaviour

21
Q

What are characteristics of Colloid? Thyroglobulin? Thyroid Gland?

A

Colloid: major component = thyroglobulin, a large protein of 700,000 Da, Follicles in thyroid filled with colloid
Colloid contains thyroid hormone thyroxine (T4) and triiodothyronine (T3)

Thyroglobulin = protein your thyroid gland makes
Thyrglobulin = type of storage for T3, T4 before release
T3 and T4 are split off of it and enter blood where they bind to special plasma proteins

Synthesis of thyroglobulin under control of TSH of pituitary gland

Thyroid gland:
15 to 20 g (varies w/ diet, sex, etc.)
Larger in females than males
Only 3g of healthy thyroid needed to maintain euthyroid state (normal functional state)

22
Q

What are the complete words for T3 and T4?

A

Thyroid hormone thyroxine
Triiodothyronine

23
Q

What are the Tyroid hormones containing iodine (and their %?
What about the presence of iodine in the Thyroid hormones?

A

T4 = 90%
T3 = 9%
reverse T3 = 0.9%

-Availability of iodine limited in diet, etc.
- Cellular mechanisms developped for concentration, utilization of iodine in thyroid gland

  • Thyroid follicular gland able to trap iodide and transport across the cell againsat chemical gradient (active transport)
24
Q

How are the thyroid hormones synthesised?

A
  1. I- from plasma carried into thyroid follicular gland
  2. I- oxidized to Iodine (I2)
  3. I2 used of iodination of tyrosine residues of thyroglobulin (TGB) → forms monoiodotyrosine (MIT) + diiodotyrosine (DIT)
    so I2 + TGB → MIT + DIT
  4. Oxidative coupling of 2 DIT → Thyroxine (T4)
    oxidative coupling of 1 MIT + 1 DIT → triiodothyronine (T3)
  5. Hormones stored linked to thyroglobulin until go to plasma

*Rate of synthesis (all steps) ↑ by TSH

25
Q

How is thyroid activity controlled?

A

TSH = thryoid stimulating hormone
interacts with specific receptors in follicular cells → increase production of T4 and T3

Without TSH, very low turnover of thyroid hormones
Synthesis + release of TSH controlled by hypothalamic TRH
TRH → TSH → specific receptors → increase in cAMP and Adenylyl cyclase → Thyroid hormones T3, T4

Negative feedback loop when T4 and T3 in blood increase at hypothalamic (TRH) and anterior pituitary (TSH) level

26
Q

What are the complete names of TSH and TRH?
role in control of thyroid hormone release

A

TSH =Thyroid stimulating hormone
TRH = thyrotropin releasing hormone

27
Q

What happens when there is iodine deficiency

A

Synthesis of thyroid hormones ↓ and T4 and T3 in circulation ↓

Release of TSH ↑ so thyroid folicular cells constantly stimulated
Thyroid enlarges (possibly → goiter)

Non-toxic goiter: bc enlarged, thyroid enable to synthesize biological active thyroid hormones due to the iodine deficiency,

28
Q

What are the effects of Thyroid hormones?

A

Metabolism → increase CO, oxygenation of blood, rate of breathing, #RBC in circulation + carbs, lipids, proteins turnover

Growth → normal growth, stimulates growth hormone (GH) secretion

Neural development → neural branching, myelinization

29
Q

What is the MOLECULAR mechanism of action of thyroid hormone? (on their target cells)

A
  1. Analogous to mechanism of action of steroid hormones: T3, T4 enter target cell nucleus → bind to their cognate nuclear receptor → alters transcription of specific genes → levels of encoded proteins
  2. Thyroid hormones may induce some effects by interactions with plasma membrane and mitochondria → specificT3/T4 receptor in mitochondiral membrane
  3. T3/T4 act directly at plasma membrane → increase uptake of amino acid (independent of protein synthesis) → linked with growth
30
Q

What are the abnormalities of thyroid function?

A

Hypothyroidism → hypofunction of thyroid gland, low levels of thyroid hormones → weight gain, low metabolism

Hyperthyroidism → hyperfunction of thyroid gland, high levels of thyroid hormones → weight loss, higher body temp/heart rate, heat intolerance

*present at birth or occurs later in life

31
Q

What is primary hypothyroidism? (Myxedema)

A
  • At level of the thyroid
  • inhability to synthesize active thyroid hormones
  • More common in women than in man
  • appears at about 40-60 years old

Causes:
1. Atrophy of thyroid (idiopathic atrophy = we don’t rlly know)
2. Autoimmune thyroiditis = Hashimoto’s disease = destruction by antibodies of cellular componenents of thyroid (more common in women) ( Hashimoto → genes recognize some part of thyroid as antigen)
3. Goitrous Hypothyroidism/Non-toxic Goitre = blockage in T3/T4 synthesis → Thyroid gland increases in size → goitre formation

32
Q

What causes secondary hypothyroidism?

A

At the level of the pituitary
Synthesis of little/no TSH (Thyroid stimulating hormone)

33
Q

What causes tertiary hypothyroidism?

A

At level of hypothalamus
Synthesis of little/no TRH (thyrotropin releasing hormone)

34
Q

What causes infantile hypothyroidism?

A
  • Absence of thyroid gland/ incomplete dev. (of thyroid gland) at birth
    *fetus uses mother’s T3/T4, few months old, decrease in physical growth and mental dev.
    Need early treatment bc can become irreversible
35
Q

What is treatment for all types of Hypothyroidism?

A

Administration of thyroid hormones

36
Q

What is primary hyperthyroidism?

A

At level of the thyroid gland
2 types:

  1. Toxic Diffuse Goiter (Graves Disease):
    - Autoimmune disease characterized by presence of Long Acting Thyroid Stimulator (LATS) produced by Lymphocytes → it is an antibody that mimics TSH
    - Constant stimulation by LATS increases mass of Thyroid → Toxic Goitre → bc synthesising biologically ACTIVE T4/T3
  2. Thyroid adenoma/thyroid cancer
    - Synthesis of thyroid hormones independant of TSH
37
Q

What causes secondary hyerthyroidism?

A
  • level of anterior pituitary gland
  • No negative feeback from increased levels of T3/T4 on the TSH
  • Often due to PITUITARY TUMOR
38
Q

What causes Tertiary Hyperthyroidism?

A
  • At level of hypothalamus
  • No negative feedback of high T3/T4 on synthesis of TRH
  • often due to presence of HYPOTHALAMIC TUMOR
39
Q

What are possible treatments for hyperthyroidism?

A
  1. Surgery + replacement therapy (administration of thyroid hormones)
  2. Administration of radioactive iodide (131I, 5mCi) → radioactive iodide concentrates in thyroid follicles → destroy them + replacement therapy if needed
  3. Administration of antithyroid drugs → propylthiouracil → blocks addition of iodine to thyroglobulin → careful not too much and cause hypothyroidism

PHGY 210 (7 decks)

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