Topic 7: Endocrine System Flashcards

1
Q

Endocrine System: Overview

A
  • regulates growth, reproduction, metabolism (long-term events)
  • glands and tissues secrete hormones which travel in blood to target cells (= cells with specific receptors for that hormone)
  • bind to receptors and change cell activity
  • receptors (proteins) found:
    • on the cell membrane
    • intracellular (nuclear)
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2
Q

Hormone Types

A
  • Water soluble

- Lipid soluble

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3
Q

Water Soluble Hormones

A
  • peptides, proteins, catecholamines (= 1st messenger)
  • steps:
    • hormone binds to cell membrane receptors (do not enter the cell for their actions)
    • hormone-receptor complex activates membrane proteins e.g. G-proteins
    • G-proteins then activate 2nd messenger systems
      e. g. cAMP, Ca2+
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4
Q

example using cAMP (cyclic adenosine monophosphate) as second messenger

A
  • hormone binds to cell-surface receptor and activates a G-protein
  • G-protein activates adenylate cyclase (membrane protein)
  • adenylate cyclase converts ATP to cAMP (=second messenger) ∴ ⇑ [cAMP]
  • cAMP activates protein kinases (in cytosol)
  • protein kinase acts on other proteins (phosphorylates) to alter their activity ∴ changes cell activity
    e. g. epinephrine on liver cells (activates cAMP) ⇒ causes breakdown of glycogen to glucose ⇒ released to blood
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5
Q

Why use 2nd messenger systems?

A
  • hormone can’t enter cell (water soluble)
    b) rapid acting (enzymes already present - just activate)
  • 1 hormone molecule ⇒ many enzyme molecules activated ⇒ multiplies signal
  • limited - messenger broken down or removed
    e. g. cAMP broken down by phosphodiesterase in the cell
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6
Q

Lipid Soluble Hormones

A
  • steroids (e.g. cortisol) and thyroid hormones
  • trigger protein synthesis
    • takes time ∴ slow, but long lasting response
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7
Q

Lipid Soluble Hormones steps for action

A
  • enter target cell and bind to intracellular (nuclear) receptors in cytosol or nucleus
  • hormone-receptor complex binds to a specific region on DNA (activates genes) ⇒ starts gene transcription – produces messenger RNA (mRNA)
  • mRNA attaches to ribosomes to produce proteins (translation)
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8
Q

Regulation of Hormone Secretion into Blood

A

stimuli acting on an endocrine gland may be:

  • Humoral Stimulus
  • Neural Stimulus
  • Hormonal Stimulus
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9
Q

Humoral Stimulus

A

stimulus = ions/nutrients

e. g.1: ↑blood glucose (after eating carbs)
- pancreatic β-cells (of Islets of Langerhans) detect glucose and release insulin ⇒ ↓blood glucose
e. g.2: ↓Blood Ca2+
- parathyroid gland detects ↓Ca2+ and releases parathyroid hormone (PTH) ⇒ ↑bone resorption (breakdown) by - ↓osteoblast activity and ↑osteoclast activity ⇒ ⇑ blood Ca2+

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10
Q

Neural Stimulus and Hormonal

A

-see notes for diagram

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11
Q

Stress

A
  • any extreme external or internal stimulus e.g. surgery, infections, strong emotions, exams
  • triggers a set of body changes called General Adaptation Syndrome
  • all co-ordinated directly or indirectly by the hypothalamus
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12
Q

Stress Phases

A
  • Phase 1: Alarm Reaction (Fight or Flight Response)
  • Phase 2: Resistance Reaction
  • Phase 3: Exhaustion
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13
Q

Phase 1: Alarm Reaction (Fight or Flight Response)

A

immediate = NS
effects of SNS + endocrine:
-⇑ blood glucose (glucose)
-SNS inhibits insulin release
-Epi, NE trigger conversion of glycogen to glucose in the liver
-⇑ HR, force of contraction
-⇑ respiration rate
-⇓ blood flow to skin + abdominal viscera
-∴ more available to skel. and card. m., and brain (O2 and glucose to working organs)
-⇓ digestion, urine production

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14
Q

Phase 2: Resistance Reaction

A
  • long term ⇒ endocrine
  • permits recovery from the effects of 1) (tissue repair, etc) or response to longer term stress (e.g. starvation)
  • hypothalamic hormones initiate phase 2)
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15
Q

Phase 2: Resistance Reaction-hypothalamic hormones initiate phase 2)

A
  • GH

- Cortisol

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16
Q

-GH

A

stimulates growth (protein production), cell reproduction

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17
Q

-Cortisol

A
  • released within 30 sec of the stress but the response not for hours – steroid hormone - acts at nuclear receptors
  • inhibits insulin release
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18
Q

Phase 2: Resistance Reaction-Release of hormones cause

A
  • ⇑ blood glucose:
  • inhibition of: immune system, bone formation, formation of CT (delayed healing)
  • release of aldosterone and antidiuretic hormone (ADH)
19
Q

⇑ blood glucose

A
  • liver stimulated to produce new glucose from fats and later from proteins
  • little insulin (because of inhibition) - glucose not taken up well, especially by skeletal muscle (at rest) and adipose tissue. ∴:
    • glucose spared for use by NS
    • metabolism of non-nervous tissue directed to use fats for energy (control = GH, cortisol) - if stress continues, cortisol inhibits GH release and proteins are then also used
    • Overall: ⇑ blood FA and aa ⇒ energy (except brain)
20
Q

release of aldosterone and antidiuretic hormone (ADH)

A

reduces salt and water loss at kidney to maintain blood volume

21
Q

Phase 2: Resistance Reaction-Long term effects

A

⇓ weight, ⇑ bp, ⇑ HR, immune suppression (cortisol), ⇓ bone density, ⇑ risk of type 2 diabetes (because of ⇑ blood glucose)

22
Q

Phase 3: Exhaustion

A

Results from:

  • depletion of body resources i.e. lipid reserves
  • loss of K+ (aldosterone effect)
  • damage to organs (heart, liver, kidneys)
23
Q

Functions of Testosterone

A
  • development of organs of reprod. tract + 2° sex characteristics
  • stimulates bone growth at epiphyseal plate (converted in bone to estrogen (E) to stop growth = closure of plate)
  • promotes protein anabolism
  • directly stimulates spermatogenesis
24
Q

♀ Reproductive Hormones-Hormone Functions

A
  • FSH
  • LH
  • Estrogen
  • Progesterone (P)
25
FSH
- stimulates 1° to become 2° follicle | - inhibited by ⇑ progesterone (P) (∴ FSH ⇑ when P ⇓)
26
LH
- stimulates Estrogen (E) production from theca + granulosa cells of follicle - surge in LH ⇒ ovulation and then formation of corpus luteum from remnants of follicle - in follicular phase - E from 2° follicle rises for a few days ⇒ stim LH release (via GnRH) ⇒ stim. follicle to ⇑ E secretion etc (+ve feedback) ⇒ leads to LH surge - luteal phase - P inhibits LH release
27
Estrogen
- required for ovulation - development of of 2° sex characteristics - stim. growth of + maintains endometrium - ⇑ bone growth, closure of epiphyses
28
Progesterone (P)
- from corpus luteum | - prepares uterus for pregnancy
29
Ovarian/Uterine Cycle (~28 days)
- Days 1-14 - Day 14: Ovulation - Days 15-28 - If fertilization occurs - If NO fertilization
30
Days 1-14
- Ovary: Follicular (preovulatory) phase | - Uterus: (at same time as follicular phase)
31
Ovary: Follicular (preovulatory) phase
- Early on: P low ∴ LH + FSH secreted - some 1° follicles ⇒ 2° follicles (due to FSH) - follicles secrete E ∴ blood E rises - Later on: one (usually) 2° follicle becomes vesicular follicle
32
Uterus: (at same time as follicular phase)
``` Menstrual phase (days 1-5): -stratum functionalis shed (outer layer of endometrium) and denuded areas bleed -∴ menstrual flow = blood, cells, and secretions Proliferative phase (days 6-14) -E ⇒ repair + proliferation of stratum functionalis (due to mitosis in stratum basalis) ```
33
Day 14: Ovulation
- due to LH surge - LH triggers: - completion of meiosis I ⇒ 2° oocyte - rupture of vesicular follicle with release of 2° oocyte
34
Days 15-28
Ovary: Luteal Phase -High P from corpus luteum inhibits GnRH (∴ LH + FSH) ∴ no follicles develop Uterus: Secretory Phase -Progesterone from corpus luteum: -prepares endometrium for implantation - becomes vascular, thick, and stores glycogen -inhibits uterine contractions
35
If fertilization occurs
- placenta secretes human chorionic gonadotropin (hCG) - hCG maintains corpus luteum (similar structure to LH) - corpus luteum ⇒ P, E for about 6 weeks, then the placenta takes over (secretes P, E) - FSH, LH inhibited by high P (no new follicles develop)
36
If NO fertilization
corpus luteum ⇒ corpus albicans (no hCG, low LH) ∴ ⇓ P and E ∴: -no longer inhibit LH, FSH ⇒ LH, FSH ⇑ -no longer maintain endometrium ⇒ menstruation
37
Contraceptives
- Oral Contraceptives - Implants - Morning After Pill
38
Oral Contraceptives
high E + P ⇒ inhibit GnRH secretion ∴ low FSH, LH (mimics luteal phase) - no follicle maturation, no ovulation
39
Implants
e.g. progestin – similar mechanism to oral contraceptives
40
Morning After Pill
- high E and progestin or progestin only | - prevents implantation, ovulation or fertilization
41
Placenta
-formed from chorion (fetus) and endometrium (maternal) -blood vessels of mother and fetus in close proximity (no blood mixing) functions: -exchange site -secretes hormones
42
exchange site
- gases, nutrients/wastes, hormones, antibodies (passive immunity) - drugs e.g. alcohol, morphine, nicotine - viruses e.g. measles polio
43
secretes hormones (placenta)
Estrogen + Progesterone hCG -maintains corpus luteum for ~6 weeks post-fertilization -detected by pregnancy tests -stimulates testosterone secretion by fetal testes