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Phys 1412 > Topic 7: Endocrine System > Flashcards

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
Q

FSH

A
  • stimulates 1° to become 2° follicle

- inhibited by ⇑ progesterone (P) (∴ FSH ⇑ when P ⇓)

26
Q

LH

A
  • 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
Q

Estrogen

A
  • required for ovulation
  • development of of 2° sex characteristics
  • stim. growth of + maintains endometrium
  • ⇑ bone growth, closure of epiphyses
28
Q

Progesterone (P)

A
  • from corpus luteum

- prepares uterus for pregnancy

29
Q

Ovarian/Uterine Cycle (~28 days)

A
  • Days 1-14
  • Day 14: Ovulation
  • Days 15-28
  • If fertilization occurs
  • If NO fertilization
30
Q

Days 1-14

A
  • Ovary: Follicular (preovulatory) phase

- Uterus: (at same time as follicular phase)

31
Q

Ovary: Follicular (preovulatory) phase

A
  • 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
Q

Uterus: (at same time as follicular phase)

A 
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
Q

Day 14: Ovulation

A
  • due to LH surge
  • LH triggers:
    • completion of meiosis I ⇒ 2° oocyte
    • rupture of vesicular follicle with release of 2° oocyte
34
Q

Days 15-28

A

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
Q

If fertilization occurs

A
  • 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
Q

If NO fertilization

A

corpus luteum ⇒ corpus albicans (no hCG, low LH)
∴ ⇓ P and E ∴:
-no longer inhibit LH, FSH ⇒ LH, FSH ⇑
-no longer maintain endometrium ⇒ menstruation

37
Q

Contraceptives

A
  • Oral Contraceptives
  • Implants
  • Morning After Pill
38
Q

Oral Contraceptives

A

high E + P ⇒ inhibit GnRH secretion ∴ low FSH, LH (mimics luteal phase) - no follicle maturation, no ovulation

39
Q

Implants

A

e.g. progestin – similar mechanism to oral contraceptives

40
Q

Morning After Pill

A
  • high E and progestin or progestin only

- prevents implantation, ovulation or fertilization

41
Q

Placenta

A

-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
Q

exchange site

A
  • gases, nutrients/wastes, hormones, antibodies (passive immunity)
  • drugs e.g. alcohol, morphine, nicotine
  • viruses e.g. measles polio
43
Q

secretes hormones (placenta)

A

Estrogen + Progesterone
hCG
-maintains corpus luteum for ~6 weeks post-fertilization
-detected by pregnancy tests
-stimulates testosterone secretion by fetal testes

Phys 1412 (12 decks)

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