Module 5 processes Flashcards

1
Q

What is the process of water-soluble hormone cAMP second messenger signalling?

A
  1. hormone (1st messenger) binds receptor
  2. receptor activates G protein
  3. G protein activates adenylate cyclase
  4. adenylate cyclase converts ATP to cAMP (2nd messenger)
  5. cAMP activates protein kinases
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2
Q

How do lipid soluble hormones act and what’s the process?

A

intracellular receptors
1. steroid hormone diffuses through plasma membrane and binds an intracellular receptor
2. receptor-hormone complex enters nucleus
3. receptor-hormone complex binds a specific DNA region
4. binding initiates transcription of gene to mRNA
5. mRNA directs protein synthesis
6. protein translation results in enzymes that promote various metabolic activities OR synthesis of structural proteins OR proteins to be released from target cell
Physiological effect triggered

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3
Q

Define the humoral stimulus

A
  1. endocrine glands sensitive to levels of various substances in blood or extracellular fluid (ions, nutrients)
  2. when concentration outside normal range, it triggers specific endocrine glands to release hormones
  3. released hormones act on target organs to bring about changes that restore concentration of substance to normal range
  4. process usually regulated by feedback mechanism, where effect of hormone reduces its own secretion, maintaining homeostasis
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4
Q

Define the neural stimulus

A
  1. involve nerve fibers that directly innervate glands - endocrine cells receive signals from nervous system
  2. when stimulated by neural input, glands secrete hormones - quick response and can be triggered by external stimuli
  3. hormones released act of specific target organs or tissues, causing rapid changes to meet bodies needs
  4. feedback can be hormonal & neural, depending on pathway and hormones involved
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5
Q

Define the hormonal stimulus

A
  1. release of hormones in response to other hormones produced by endocrine glands, creating cascade of hormonal interactions
  2. when a gland detects presence of another hormone, it may respond by secreting its own hormone
  3. hormones released act on other glands to stimulate or suppress production of further hormones
  4. hormonal stimulus often involves complex feedback loops that regulate levels of various hormones in body - levels of downstream hormones can inhibit secretion of upstream hormones, maintaining balance in system
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6
Q

Describe the hypothalamus and the posterior pituitary connection

A
  1. PVN synthesizes oxytocin (OXT) & SOP synthesizes antidiuretic hormone (ADH)
  2. OXT & ADH travel down hypothalamic-hypophyseal tract
  3. OXT & ADH stored in axon terminals in posterior pituitary
  4. OXT & ADH are released into blood stream at following action potential stimulus
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7
Q

Describe the hypothalamus and anterior pituitary connection

A
  1. hypothalamic neurons make releasing & inhibiting neurohormones
  2. neurohormones travel down special blood vessels to “release” or “inhibit” anterior pituitary hormones
  3. anterior pituitary hormones released into blood stream
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8
Q

Describe the role of the anterior pituitary gland with ACTH

A
  1. corticotropin releasing hormone (CRH) released from hypothalamus triggered by fever/hypoglycemia/stressors
  2. stimulates adrenocorticotropin hormone (ACTH) from anterior pituitary gland
  3. triggers adrenal glands to release corticosteroids
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9
Q

Describe the role of the anterior pituitary gland with GH

A
  1. hypothalamus releases growth hormone releasing hormone (GHRH) triggered by low GH, fatty acids and glucose/high amino acids/exercise/sleep
    OR growth hormone inhibiting hormone (GHIH) triggered by high GH, IGFs, fatty acids, glucose/obesity
  2. stimulates growth hormone (GH) from anterior pituitary gland
  3. triggers direct and indirect effects across body
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10
Q

Describe the role of the anterior pituitary gland with FSH/LH

A
  1. gonadotropin releasing hormones (GnRH) released from hypothalamus
  2. stimulates follicle stimulating hormones (FSH) and luteinizing hormone (LH) from anterior pituitary gland
  3. triggers gonads (ovaries and testes)
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11
Q

Describe the role of the anterior pituitary gland with TSH

A
  1. thyroid releasing hormone (TRH) released from hypothalamus
  2. stimulates thyroid stimulating hormone (STH) from anterior pituitary gland
  3. triggers thyroid gland to release thyroxine - regulates weight/energy levels/internal temp/metabolism…
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12
Q

Describe the role of the anterior pituitary gland with PRL

A
  1. eating, mating, estrogen, ovulation and nursing
  2. stimulates prolactin (PRL) from anterior pituitary gland
  3. triggers lactation
  4. inhibited by prolactin inhibiting peptides
    Regulated by: PIH (dopamine)/estrogens/infant suckling breast
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13
Q

How are thyroid hormone levels regulated?

A
  1. low blood levels of T3 and T4 or low metabolic rate stimulates release of TRH
  2. TRH, carried by hypophyseal portal veins to anterior pituitary, stimulates release of TSH by thyrotrophs
  3. TSH released into blood stimulates thyroid follicular cells
  4. T3 & T4 released into blood by follicular cells
  5. elevated T3 inhibits release of TRH & TSH (negative feedback)
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14
Q

What happens when thyroid hormone levels are low?

A
  1. increase thyrotropin releasing hormone (TRH) released from hypothalamus
    - TRH binds to TRH receptors in anterior pituitary to trigger…
  2. increased thyroid stimulating hormone (TSH) released from anterior pituitary
    - TSH circulates, binds to TSH receptors in thyroid gland
  3. increased T4 & T3 release from follicular cells of thyroid gland
  4. increase circulating T4 & T3 levels
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15
Q

How is calcium homeostasis regulated by PTH

A
  1. high level of Ca2+ in blood stimulates thyroid gland parafollicular cells to release more calcitonin (CT)
  2. CT inhibits osteoclasts, decreasing blood Ca2+ level
  3. low level of Ca2+ in blood stimulates parathyroid gland chief cells to release more parathyroid hormone (PTH)
  4. PTH promotes release of Ca2+ from bone extracellular matrix into blood and slows loss of Ca2+ in urine, increasing blood Ca2+ level
  5. PTH also stimulates the kidneys to release calcitriol
  6. calcitriol stimulates increased absorption of Ca2+ from foods, which increases blood Ca2+ level
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16
Q

Describe the long-term responses to stress

A
  1. stress detected by hypothalamus causes synthesis & release of CRH
  2. CRH activates anterior pituitary gland
  3. anterior pituitary gland releases ACTH into bloodstream
  4. ACTH activates adrenal gland
  5. zona reticularis releases glucocorticoids & zona glomerulosa releases mineralocorticoids
17
Q

Describe how glucocorticoid secretion is controlled

A
  1. STIMULUS (disrupting homeostasis by decreasing)
  2. CONTROLLED CONDITION (glucocorticoid level in blood)
  3. RECEPTORS (neurosecretory cells in hypothalamus)
    - input - increased CRH & decreased cortisol
  4. CONTROL CENTRE (corticotrophs in anterior pituitary)
    - output - increased ACTH
  5. EFFECTORS (cells of zona fasciculata in adrenal cortex)
    - secrete glucocorticoids
  6. RESPONSE (increased glucocorticoid level in blood)
    - return to homeostasis
18
Q

Describe catecholamines and how they’re produced

A

chromaffin cells - post ganglionic cells of SNS
1. action potentials triggered by hypothalamus activate SNS
2. action potentials travel along preganglionic sympathetic axons to adrenal medulla
3. activation of chromaffin cells, multistep synthesis of: epinephrine (adrenaline) 80% & norepinephrine (noradrenaline) 20%
4. secretion of epinephrine & norepinephrine

19
Q

Summarize how glucagon impacts BGL

A
  1. low BGL stimulates alpha cells to secrete GLUCAGON
  2. glucagon acts on liver cells to:
    - convert glycogen into glucose
    - form glucose from lactic acid & certain amino acids
  3. glucose released by liver cells raises blood glucose level to normal
  4. if BGL continues to rise, inhibits release of glucagon
20
Q

Summarize how insulin impacts BGL

A
  1. high BGL stimulates beta cells to secrete INSULIIN
  2. insulin acts on various body cells to:
    - accelerate facilitated diffusion of glucose into cells
    - speed conversion of glucose into glycogen
    - increase uptake of amino acids & increase protein synthesis
    - speed synthesis of fatty acids
  3. BGL fall
  4. if BGL continue to fall, inhibits release of insulin
21
Q

Describe the development of ovarian follicles

A
  1. primordial follicles (ovarian reserve)
  2. primary follicle
  3. secondary follicle
    4a. early antral follicle
    4b. antral follicle
  4. follicle ruptures
  5. corpus luteum (forms from ruptured follicle)
    - 1 egg/oocyte per follicle
    - female gametes not replenished throughout life
22
Q

Describe the basic pattern of interactions along the hypothalamic-pituitary-gonadal (HPG) axis

A
  1. hypothalamus produces gonadotropin releasing hormone (GnRH)
  2. acts on cells within the anterior pituitary to produce gonadotropins - luteinizing hormone (LH) & follicle stimulating hormone (FSH)
  3. act on the gonads (testes or ovaries)
23
Q

Describe the first 4 steps of hormonal regulation of testis by HPG

A
  1. hypothalamus releases GnRH, which reaches anterior pituitary via portal system
  2. GnRH causes anterior pituitary gonadotropic cells to release FSH & LH
  3. FSH indirectly stimulates spermatogenesis by causing Sertoli cells to release androgen binding protein (ABP), keeping local concentration of testosterone high
  4. LH stimulates Leydig cells to secrete testosterone, which is essential for spermatogenesis
24
Q

Describe the last 3 steps of hormonal regulation of testis by HPG (7 overall)

A
  1. testosterone acts at other body sites (e.g. stimulate maturation of sex organs & libido)
  2. negative feedback by testosterone inhibits FSH & LH release from anterior pituitary & GnRH release from hypothalamus
  3. inhibin released from Sertoli cells feeds back on anterior pituitary, decreasing FSH release
25
Q

What are the 6 stages of regulating the Ovarian cycle

A
  1. GnRH Stimulation: Gonadotropin-releasing hormone (GnRH) prompts FSH & LH release from the anterior pituitary.
  2. Follicular Growth: FSH & LH cause follicles to develop and produce steroid hormones.
  3. Negative Feedback: Estrogen inhibits FSH & LH release via the hypothalamus & pituitary.
  4. Dominant Follicle Survival: Only the dominant follicle endures estrogen’s suppressive effects.
  5. Estrogen Surge & LH Surge: High estrogen levels prompt a surge in LH, leading to ovulation.
  6. Negative Feedback supression: Rising plasma progesterone & estrogen, along with inhibin, further inhibit LH & FSH release. Declining LH & FSH levels halt follicle development.