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MD1 endocrinologie > Introduction et notions de base endocrinologie > Flashcards

Introduction et notions de base endocrinologie Flashcards

1
Q

What is endocrinology?

A

The branch of medicine that studies hormones

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2
Q

What is a hormone?

A

Molecule produced by a cell in response to a precise stimulus which is liberated and then stimulates a specific cell with a specific receptor.

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3
Q

What are the principal endocrine glands?

A
  • hypothalamus-hypophysis
  • parathyroid
  • thyroid
  • adrenal glands
  • pancreas
  • testicles/ovaries

Can also be other things:

  • adipose tissue
  • heart
  • kidneys
  • skin
  • thymus… etc.
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4
Q

What is the endocrine effect?

A

Hormone is released from a cell into the blood. through which it travels to the target cell

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5
Q

What is the paracrine effect?

A

Hormone is released and stimulates neighbouring cell

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6
Q

What is the autocrine effect?

A

Hormone is released and has effect on that same cell (auto-modulation)

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7
Q

Overview of autocrine, endocrine, and paracrine

A
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8
Q

What are the principal hormones released by the hypothalamus and their general effects? (8)

A

Called libérines:

  1. CRH (corticotropin-releasing hormone): stimulates ACTH
  2. GHRH (growth hormone-releasing hormone): stimulates GH
  3. GnRH (or LHRH) –> gonadotropin-releasing hormones: stimulates LH and FSH
  4. TRH (thyrotropin-releasing hormone): stimulates TSH
  5. Somatostatin: inhibits GH
  6. Dopamine: inhibits prolactin
  7. Oxytocin and vasopressin (ADH): go towards neurohypophysis to be secreted
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9
Q

What are the principal hormones released by the pituitary gland? (7)

A

Anterior pituitary:

  1. ACTH (adrenocorticotropic hormone)
  2. GH (growth hormone)
  3. FSH and LH (follicle-stimulating hormone and luteinizing hormone)
  4. TSH (thyroid-stimulating hormone)
  5. PRL (prolactin)

Posterior pituitary (neurohypophysis): synthesized by hypothalamus and released by posterior pituitary

  1. ADH
  2. Oxytocin
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10
Q

What are the principal hormones released by the thyroid? (3)

A
  1. T4 (thyroxine)
  2. T3 (triiodothyronine)
  3. Calcitonin
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11
Q

What are the principal types of hormones released by the adrenal glands? (4)

A
  1. Glucocorticoids (ex: cortisol)
  2. Mineralocorticoids (ex: aldosterone)
  3. Catecholamines
  4. Androgens
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12
Q

What are the hormones released by the pancreas? (2)

A
  1. Insulin
  2. Glucagon
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13
Q

What hormone is released by the testicles?

A

Testosterone

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14
Q

Which hormones are released by the ovaries?

A
  1. Estrogen
  2. Progesterone
  3. Androgens
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15
Q

Which hormone is released by the parathyroid gland?

A

PTH (parathormone) –> phosphocalcic effect

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16
Q

What kinds of hormones are hydrosoluble? (4)

A

Proteins, polypeptides, glycoproteins, and amines

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17
Q

Which hormones are hydrosoluble? (19)

A

Hypothalamus:

  • CRH, GHRH, GnRH, TRH, somatostatin, and dopamine

Pituitary gland:

  • ACTH, GH, FSH, LH, TSH, prolactin, ADH, oxytocin

Parathyroid and thyroid:

  • PTH and calcitonin

Pancreas:

  • Insulin and glucagon

Adrenal glands:

  • Catecholamines
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18
Q

What are the 6 steps of hydrosoluble hormone synthesis?

A
  1. Gene activation
  2. DNA transcription
  3. mRNA formation
  4. mRNA translation –> protein (ribosomes)
  5. Maturation of polypeptide (ER and golgi –> pre-pro/pro)
  6. Exocytosis –> secretion
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19
Q

What is a preprohormone?

A

precursor protein to one or more prohormones

  • pre radical allows the protein to anchor in the membrane of the ER
  • this radical is cleaved to form a prohormone
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20
Q

What is a prohormone?

A

hormone + radical that migrates into the Golgi body which will later be cleaved by endopeptidases in the secretory vesicle to form the active hormone

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21
Q

Overview of prepro, pro, and active hormones:

A
22
Q

What are 2 examples of clinical uses of prohormones?

A
  • peptide C –> sécrétion endogène d’insuline
  • hyperpigmentation (maladie d’Addison)
23
Q

What is peptide C?

A

useful for measuring endogenic insulin production since they’re produced in a 1:1 ratio in the body therefore should be present in similar amounts in the blood

24
Q

How does hyperpigmentation in Addison’s disease work?

A

Addison’s disease = primary adrenal insufficiency which causes a decrease in cortisol production

  • this decrease causes an increase in CRH and ACTH production to try to increase CORT production and since there is no negative feedback from CORT levels
    • gamma-MSH is produced when producing ACTH, therefore when production of one is increased so is the other
      • this leads to increased melanocyte production which causes hyperpigmentation
25
Q

What is the “secretion pattern” of hydrosoluble hormones?

A

Periodic and rhythmic

The rhythm varies and can either be:

  1. pulsatile
  2. circadian
  3. monthly (ex: menstrual cycle/TSH and LH levels)
26
Q

How are hydrosoluble hormones secreted and transported?

A

Secreted:

  1. Stored hormones are first released from granules (FAST)
  2. Causes increased synthesis which takes a bit longer

Transport:

  • Not bound to anything therefore quite short half-life
  • Cannot be taken by mouth because they would be digested by proteases
    • This explains why you can’t take pill versions of these hormones and they must be injected.. ex: insulin
27
Q

How do hydrosoluble hormones work?

A

Stimulate membrane receptors since they cannot enter cells

Two main kinds of receptors:

  1. G-protein coupled receptors
  2. Tyrosine kinase receptors
28
Q

How do G-protein coupled receptors work?

A
  1. Hormone binds to receptor on cell membrane
  2. G-protein is activated
  3. G-protein interacts with effector proteins
    • ex: adenylate cyclase, phospholipase C, and phosphodiesterase
  4. Effector proteins produce second messengers which amplify signal
    1. Adenylate cyclase: inc. cAMP
    2. Phospholipase C: IP3, DAG, and calcium
    3. Phosphodiesterase: dec. cAMP
  5. These second messengers lead to the regulation of 1+ proteins which lead to the biological response
29
Q

Which hormones use G-protein coupled receptors?

A

Adenylate cyclase activation:

  • Epi/norepi (beta receptors)
  • Calcitonin
  • PTH
  • ADH, ACTH, FSH/LH, TSH
  • Glucagon

Phospholipase C:

  • Epi/norepi (alpha-1)
  • Oxytocin
  • Others…

Adenylate cyclase inhibition:

  • Epi/norepi (alpha-2)
30
Q

How do tyrosine kinase receptors work?

A
  1. Hormone binding to receptor leads to creation of dimer/structural change which activates tyrosine kinase
  2. Tyrosine kinase phosphorylates relay proteins which starts intracellular cascade/response

TK can either be:

  • Intrinsic: on receptor itself
  • Extrinsic: within the cytoplasm of the cell (JAK-STAT)
31
Q

Which hormones use tyrosine kinase receptors? (4)

A
  1. Insulin
  2. IGF-1 and IGF-2
  3. Prolactin
  4. GH

1 and 2 –> intrinsic TK

3 and 4 –> cytoplasmic TK

32
Q

What are the two kinds of liposoluble hormones?

A
  1. Stéroïdes
  2. Type stéroïdes
33
Q

What are the three kinds of steroid hormones and the two kinds of “type stéroïde” hormones?

A

Steroid:

  1. Ovarian (estradiol, progesterone)
  2. Testicular (testosterone)
  3. Corticosurrénales (cortisol, aldosterone, DHEAS)

Type stéroïdes:

  1. Thyroid hormones (T4 and T3)
  2. Vitamin D
34
Q

How are steroids synthesized?

A
  1. Cholesterol is stored in lipidic vacuoles
  2. Cholesterol is transported to mitochondria
    • (StAR: steroidogenic acute regulatory peptide)
  3. Intra-mitochondrial synthesis of cholesterol metabolites (enzymes)
  4. Diffusion towards endoplasmic reticulum –> conversion into active hormones
  5. Active hormones diffuse towards the cell membrane towards circulation
35
Q

What does steroid hormone formation depend on?

A

Depends on the location in which the hormone is created, but they’re all from cholesterol

36
Q

What are the five steps of thyroid hormone production?

A
  1. Capture iodine
  2. Thyroglobuline synthesis
  3. Iodine fixation (3 or 4 depending on hormone)
  4. Couplage
  5. Stockage
  6. Sécrétion
37
Q

How are liposoluble hormones secreted and transported?

A

Secreted:

  • Diffusion
  • Secretion controlled by synthesis
  • Not many intracellular reserves
  • Rhythmic/cyclic

Transport:

  • bound to proteins
    • ex: CBG, SHBG, TBG, albumin
38
Q

How is the amount of circulating liposoluble hormones controlled?

A

Fraction libre (0.03%-10%)

39
Q

How do liposoluble hormone receptors work?

A

Cellular response caused by an intracellular receptor

What are the two kinds:

  1. Cytoplasmic (steroids)
  2. Nuclear (type stéroïdes): TR, ER, VDR, RXR
40
Q

How do steroid hormone receptors work?

A
41
Q

What are the three parts of nuclear receptors?

A
  1. Ligand binding domain: on receptor binds to hormone
  2. DNA binding domain: binds to nuclear DNA which activated protein synthesis
  3. N-terminal domain: modulate hormonal activity
42
Q

How do “type stéroïde” receptors work?

A
43
Q

What happens when intracellular receptors are activated?

A
  • Start or stop the activity of specific genes
  • Start or stop the synthesis of specific enzymes
  • Provoque physiological reactions specific to the target call
44
Q

What are the characteristics of peptidic and steroid hormones?

A

Peptidique:

  • Hydrosoluble
  • Non liées
  • Courte demi-vie
  • Récepteurs membranaires (G-protein, tyrosine kinase)

Stéroides:

  • Liposoluble
  • Liées à des protéines de transport
  • Demi-vie + longue
  • Récepteurs intracellulaires (cytoplasmique, nucléaire)
45
Q

What are hormone secretion and action controlled by? (6)

A
  1. SNC
  2. Immune system
  3. Age
  4. Pregnancy
  5. Circadian cycle/rhythm
  6. Negative and positive feedback
46
Q

What do hypo and hyper mean?

A

Hypo: diminution sécrétion hormonale (glande cible)

Hyper: augmentation sécrétion hormonale (glande cible)

47
Q

What are the three main mechanisms that cause endocrinopathies?

A
  1. Déficience hormonale
  2. Excès de sécrétion hormonale
  3. Résistance hormonale
48
Q

How do hormonal deficiencies work?

A

Destruction of glandular tissue:

  • dim. hormonale secretion
  • lower hormonal concentration
  • dim. hormonal action in the tissue –> hypo

Causes:

  • Infection (ex: tuberculosis)
  • Autoimmune (ex: cytotoxicity, blockers)
  • Vascular (ex: Sheehan)
  • Inflammation
  • Tumours (ex: craniopharyngoma)
  • Hereditary (ex: athyeosis)
  • Chx, radiotx, chimiotx
49
Q

How does excessive hormone secretion happen?

A

Causes:

  1. increased hormone secretion
  2. increased plasmatic concentration of homrones
  3. increased action of glandular tissue –> hyper

How?

  • Increased production due to loss of sensibility to retroaction systems
  • Malignant tissue that produces hormones
  • Peripheral transformation of precursors into hormones by other tissues
  • Cellular destruction causes hormones to be released
  • Autoimmunity
  • Iatrogenic
50
Q

Causes of hormonal resistance:

A
  1. Acquired/congenital (mutations)
  2. Heterogenic mutations

These mutations can prevent:

  1. Hormone binding to receptor
  2. Receptor binding to hormone
  3. Hormone working after binding to receptor

Presentation?

  • Normal or increased hormone levels with sx of hormonal deficiency
    • ex: complete androgen insensitivity syndrome and insulin resistance
51
Q

How can endocrine function be evaluated?

A
  1. Hormonal dosage
  2. If you think its hyposecretion –> stimulation tests
  3. If you think its hypersecretion –> suppression tests
  4. Imagery (only done once you know what the problem is)
    • Look at glandular anatomy
    • Look for tumours/nodes
52
Q

What kinds of imagery can be used to evaluate different glands?

A
  1. Echo: thyroid, ovaries, testicles
  2. TDM: selle turcique (pituitary), adrenals, pancreas
  3. MRI: more sensible than TDM but same organs
  4. Nuclear medicine:
    1. Sestamibi/Tech: parathyroid adenoma
    2. Iodine (capture/scintigraphie): functional nodules, hyperthyroidism

MD1 endocrinologie (6 decks)

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