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PHGY 210 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

(neuro)endocrine signalling

A

hormone secretion by endocrine glands (nerve cells in neuroendocrine signalling)

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2
Q

steps of (neuro)hormones communicate

A
  • synthesis
  • release
  • transport: to target via blood stream
  • detection: via specific receptors on target cell
  • change in cellular metabolism: due to hormone-receptor interactions
  • removal: terminates cellular response
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3
Q

hypothalamic-pituitary signalling

A
  • hypothalamus –> anterior pituitary
  • activate/inhibit hormone-producing cells
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4
Q

classes of hormones

A
  • glycoproteins
  • polypeptides
  • steroids
  • amines
  • ionic calcium (no hormonal signalling)
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5
Q

hormone synthesis

A
  • preprohormones synthesis on ribosomes
  • preprohormones –> prohormones at rough ER
  • prohormones –> hormone + peptides in Glogi
  • hormone storage in vesicles
  • hormone release via exocytosis
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6
Q

thyroid hormones

A
  • Tx: x=number of iodines
  • T3 and T4
  • reverse T3 (rT3) is not a thyroid hormone because cannot bind to thyroid hormone receptor
  • synthesis: I2 from TGB –> MIT and DIT; 1 MIT+ 1 DIT –> T3; 1 MIT + 2 DIT –> T4
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7
Q

hormone receptor characteristics

A
  • specificity
  • affinity
  • saturability
  • measurable
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8
Q

hormone receptors regulation

A
  • up-regulation: increase activity in response to hormone/increase synthesis
  • down-regulation: decrease activity in response to hormone/decrease synthesis
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9
Q

mechanisms by which hormone can exert effect on target cells

A
  • direct
  • intracellular via second messenger
  • intracellular via genomic/nuclear action: receptors within the nucleus, hormones (steroid hormones) enters the nucleus before binding to receptor
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10
Q

hormone secretion feedback control

A
  • low plasma Ca2+ –> stimulation of parathyroid gland –> increase synthesis and release of parathyroid hormone –> increased parathyroid hormone (PTH) secretion –> action on bone, kidney and gut –> increase plasm Ca2+ –> inhibit stimulation of parathyroid gland
  • stress and other stimulus from the brain –> increased CRH secretion –> increased ACTH secretion –> increased cortisol secretion –> inhibit CRH and ACTH secretion
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11
Q

pituitary gland

A
  • anterior/adenohypophysis/pars distalis: endocrine tissue
  • posterior/neurohypophysis/pars nervosa
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12
Q

posterior pituitary gland

A
  • neural tissue
  • secrets oxytocin and vasopressin
  • prohormones processed in secretory granules during axonal transport
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13
Q

effects of oxytocin

A

females:
- parturition
- milk ejection
- behavioural effect: enhances bonding
males:
- ejaculation
- behavioural effect: enhances bonding

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14
Q

thyroid gland

A
  • contains T3 and T4 hormones
  • synthesis of thyroglobulin under TSH regulation –> provides T3 and T4 storage prior to release
  • increased cAMP and/or adneylyl cyclase –> increased T3 and T4 concentration –> inhibition of TRH and TSH –> inhibit T3 and T4 synthesis
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15
Q

effects of thyroid hormones

A
  • stimulation of calorigenessis
  • carbohydrate metabolism
  • lipid turnover
  • protein metabolism
  • promote normal growth
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16
Q

hypothyroidism

A
  • hypofunction of the thyroid gland
  • primary: at level of thyroid, inability to synthesize active thyroid hormones due to atrophy of thyroid, autoimmune thyroiditis or non-toxic goitre
  • secondary: at level of pituitary, little or no synthesis of TSH
  • tertiary: at level of hypothalamus, little or no synthesis or TRH
  • infantile: absent of incomplete thyroid gland development at brith
  • treatment: administration of thyroid hormones
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17
Q

hypertyroidism

A
  • hyperfunction of the thyroid gland
  • primary: at level of thyroid gland, toxic goiter (Graves disease), thyroid adenoma or thyroid cance
  • secondary: at level of anterior pituitary gland, no negative feedback from increasing T3/T4 level
  • tertiary: at level of hypothalamus, no negative feedback from high T3/T4 level, hypothalamic tumor
  • treatment: surgery+replacement therapy, administration of radioactive iodine, administration of antithyroid drugs
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18
Q

Graves disease

A

autoimmune disease due to presence of LATS (antibody that mimics the actions of TSH and stimulates T3 and T4 release)

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19
Q

calcium homeostasis regulation by

A
  • parathyroid hormone (PTH)
  • calcitonin
  • vitamin D
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20
Q

parathyroid hormone (PTH)

A
  • secreted by parathyroid chief cells
  • 4 parathyroid glands
  • structure: 84 amino acid polypeptide with only the N-terminal 34 amino acids important for full function
  • function: increases plasma calcium concentration via bone resorption, reabsorption in the kidney, vitamin D synthesis and absorption in gut
  • release controlled directly via binding to circulating calcium
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21
Q

hyoparathyrodism

A
  • hypofunction of the parathyroid gland
  • hypocalcemia
  • decreased production of active vitamin D
  • treatment: administration of active vitamin D and calcium supplements
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22
Q

hyperparathyroidism

A
  • hyperfunction of the parathyroid gland
  • often due to parathyroid adenoma producing too much PTH
  • hypercalcemia
  • kidney stone formation due to calcium deposition
  • treatment: removal of affected parathyroids and replacement therapy of active vitamin D and calcium
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23
Q

vitamin D

A
  • D3: from animals
  • D2: from plants
  • function: increases calcium absorption in intestine, regulates immune system and anticancer properties (via inhibition of proliferation)
  • regulated by calcium and PTH level
  • high altitude –> more UVB exposure –> shorter vitamin D winter
  • more circulating vitamin D metabolite in Caucasian Americans compared to African Americans
  • induces secretion of antibacterial activity in antimicrobial proteins
24
Q

Rickets

A
  • vitamin D deficiency –> osteomalacia (soft bones)
  • increased likelihood of infections, autoimmune diseases, allergies and cancer
25
Q

calcitonin

A
  • produced in the thyroid gland
  • function: decrease circulating calcium level by promoting calcium transfer from blood to bon and increase urinary excretion
26
Q

adrenal glands

A
  • adjacent to upper surface of the kidneys
  • cortex
  • medulla:
27
Q

adrenal cortex

A
  • outer layer
  • lipid containing epithelial cells
  • derived from mesoderm
  • function: produce steroid hormones regulated by ACTH
  • 3 layers: zona glomerulosa –> aldosterone, zona fasciculata –> cortisol, and zona reticularis –> progestin, androgen and estrogen
28
Q

adrenal medulla

A
  • inner layer
  • chromaffin cells
  • derived from neural crest
  • function: peptide hormones
29
Q

aldosterone

A
  • sodium metabolism
  • affects plasma potassium and hydrogen ion concentration
30
Q

cortisol

A
  • salt retention
  • protein and carbohydrate metabolism –> increased blood glucose level
  • lipid metabolism
  • anti-inflammatory and immunosuppressive
  • affects glucocorticoids on bone
  • can be stimulated by variety of stress stimuli
31
Q

mechanism of ACTH actions

A

bind to specific ACTH receptors –> stimulates adenylyl cyclase –> cAMP production and release –> activation of steroidogenic enzymes –> increased synthesis and release of steroid hormones

32
Q

Addison’s disease

A
  • hypofunction of the adrenal gland
  • causes: destruction or autoimmune attack of the adrenal gland or tuberculosis
  • decreased cortisol level –> decreased blood sugar level, lipolysis and gluconeogensis –> lack of energy –> treatment: carbohydrate metabolism
  • decreased aldosterone level –> decreased ion and water loss in urine –> decreased ECF, plasma volume and CO –> hyperkalemia and acidosis –> treatment: electrolyte blood level control
33
Q

Cushing’s disease

A
  • hyperfunction of the adrenal gland
  • causes: increased circulating levels of ACTH or adrenal tumor
  • increased production of sex hormones and androgens –> masculinization
  • diagnosis: puffiness of face, masculinizing effect, hypertension, increased blood glucose or steroid metabolites in urine
  • characterized by hyperplasia of adrenal cortex or both
  • increased cortisol level –> increased blood glucose level, insulin secretion, protein breakdown and decreased protein synthesis –> osteoporosis
  • increased aldosterone level –> increased ion and water loss in urine –> increased ECF and plasma volume, hypertension –> hypokalemia and alkalosis
  • treatment: surgery –> subtotal removal of adrenal cortex
34
Q

insulin

A
  • decreases blood pressure
  • facilitate glucose entering into the cell
  • produced in the beta cells
  • deficiency –> glucose accumulation –> diabetes mellitus: increased lipolysis and free fatty acids, decreased blood pH, and ketosis
35
Q

type I diabetes

A
  • insulin-dependent
  • due to destruction of beta cells of pancreas or defective insulin release
36
Q

type II diabetes

A
  • insulin-independent
  • hyporesponsiveness of target cells to insulin
  • associated with obesity
37
Q

juvenile diabetes

A
  • insulin dependent
  • appears in childhood
  • beta cells of pancreas do not produce insulin
38
Q

glucagon

A
  • opposite metabolic functions as insulin
  • raise blood sugar by promoting glycogenolysis (glycogen breakdown) and gluconeogensis (glucose synthesis)
39
Q

growth hormone (GH)

A
  • increase protein synthesis
  • increases rate of lipolysis
  • e.g. somatotropin (STH): produced by liver under stimulation of GH
  • growth hormone releasing hormone (GRH)
  • growth hormone inhibiting hormone
  • deficiency –> decreased physical growth
  • excess (childhood) –> gigantism
  • excess (adult) –> acromegaly
40
Q

growth hormone releasing hormone (GRH)

A
  • aka. somatoliberin
  • stimulates GH release
41
Q

growth hormone inhibiting hormone

A
  • aka. somatostatin
  • inhibit GH release
42
Q

gonad functions

A
  • gametogenesis
  • sex hormone secretion
43
Q

estrogen deficiency in males

A
  • synthesis via conversion from testosterone by aromatase
  • deficiency: increased body fat and decreased sexual desire and erectile function
44
Q

reproductive function conotrol

A
  • GnRH release in hypothalamus
  • FSH and LH release –> stimulates development of spermatozoa or ova, and secretion of sex steroids
45
Q

function of testes

A
  • spermatogenesis: within the coiled seminiferous tubules, dependent on androgen concentration
  • steroidogenesis
46
Q

maturation of spermatozoa

A
  • ~60 days
  • Leydig cells: located outside the seminiferous tubule, in response to LH –> androgen synthesis
  • sertoli cells: located within the seminiferous tubule, involved in sperm maturation, in response to FSH –> ABP and inhibin synthesis
47
Q

function of ovary

A
  • production of mature egg
  • steroid hormone synthesis
48
Q

follicle development

A

oocyte –> primordial follicles (oocyte surrounded by granulosa) –> primary follicle –> preantral/secondary follicle –> early antral follicle –> mature follicle

49
Q

follicular development lead to

A
  • follicular atriesia: degeneration of secondary follicles
  • or ovulation: 1/cycle
50
Q

luteinization

A
  • after ovulation
  • ruptured follicle –> corpus luteum: synthesize and secretes progesterone and estrogen/estradiol
51
Q

relationship between FSH/LH level with estrogen/progesterone level

A
  • FSH cause cohort of ovarian follicles to develop (proliferation) –> increased production of estrogen
  • LH and FSH level spike at ovulation (larger increase in LH level)
  • progesterone level increases once corpus luteum is formed (post-ovulation)
52
Q

effects of estradiol on brain and pituitory

A
  • moderate level: negative feedback on FSH release, stimulate LH release –> increase sensitivity of pituitary to GnRH –> stimulates LH synthesis
  • positive (increased sensitivity of anterior pituitary cells to GnRH and increased LH synthesis) and negative feedback (decreased GnRH and LH release)
53
Q

luteal phase

A

no fertilization –> egg degenerates

54
Q

fertilization and implantation

A
  • at ovulation, unfertilized egg is taken by the fimbria, and propelled towards the lumen of the uterus
  • egg divide to blastocyst during transport down the oviduct into the uterine lumen
55
Q

lactation

A
  • prolactin: milk production
  • oxytocin: milk ejection
  • lactational amenorrhea: maintained nursing stimulates prolactin inhibition, blocking FSH and LH secretion –> blocks resumption of reproductive cycle
56
Q

after implantation blastocyst differentiate into

A
  • trophoblast: –> placenta, synthesize HCG
  • inner cell mass: –> embryo
57
Q

menopause

A
  • loss of ovarian steorid products due to depletion of follicles –> decreased/depletion of steroid hormone productions

PHGY 210 (5 decks)

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