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Reproduction, Development and Aging > Endocrine System > Flashcards

Endocrine System Flashcards

1
Q

4 types of endocrine signalling

A

Classical
Neuroendocrine
Paracrine
Autocrine

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2
Q

Classical endocrine signalling

A

Endocrine cell releases hormone, which is transported in the blood to the target cell, initiating a response

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3
Q

Neuroendocrine signalling

A

Neuroendocrine cell releases neurohormone, which is transported in the blood to the target cell, initiating a response

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4
Q

Autocrine signalling

A

Endocrine cell releases hormone, which diffuses through interstitial fluid and acts on the releasing cell, initiating a response

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5
Q

Paracrine signalling

A

Endocrine cell releases hormone, which diffuses through interstitial fluid and acts on a nearby cell, initiating a response

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6
Q

What does the forebrain develop into?

A

The telencephalon which becomes the cerebrum

The diencephalon which becomes the thalamus and hypothalamus

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7
Q

What does the midbrain develop into?

A

The mesencephalon, which becomes the midbrain of the brainstem

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8
Q

What does the hindbrain develop into?

A

The metencephalon which becomes the pons and the cerebellum

The myelencephalon which becomes the medulla

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9
Q

Describe the development of the pituitary gland

A

At week 3 of development, the embryo contains neuroectoderm and oral ectoderm. The neuroectoderm develops into the neurohypophyseal bud and the oral ectoderm develops into the hypophyseal pouch. During the fetal period, these pinch off, becoming the posterior pituitary and the anterior pituitary, respectively.

Neuroectoderm —> neurohypophyseal bud —> PP
Oral ectoderm —> hypophyseal pouch —> AP

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10
Q

Hormonal feedback control of the hypothalamus and anterior pituitary

A

Stimulus excites hypothalamus which releases GnRH
GnRH excites AP to release LH and FSH
LH and FSH act on the gonads to release estradiol and the hypothalamus to prevent further GnRH release
Estradiol acts on a) the target tissue, b) the AP to prevent further LH/FSH release and c) the hypothalamus to prevent further GnRH release

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11
Q

Anterior boundary of the hypothalamus

A

Anterior commissure and lamina terminalis

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12
Q

Posterior boundary of the hypothalamus

A

Mamillary bodies and midbrain

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13
Q

Superior boundary of the hypothalamus

A

Thalamus

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14
Q

Hormones released from the AP

A 
ACTH
FSH
LH
TSH
Prolactin
Growth hormone
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15
Q

Hormones released from the PP

A

ADH

Oxytocin

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16
Q

Hormones released from the hypothalamus

A 
TRH
GnRH
CRH
Dopamine
GHRH
Somatostatin
PRF

Also Oxytocin + ADH, which are then stored in the PP for later release

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17
Q

Median eminence

A

Highly vascular part of the brain that hormones are released into

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18
Q

Hypophyseal portal system

A

Large vessels that spiral around the infundibulum of the pituitary to reach the AP (allows carrying of hormones from hypothalamus to AP)

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19
Q

Histological differentiation between AP and PP

A

PP contains mainly non-myelinated axonal processes (also some capillaries) which don’t pick up H&E stain very well, so it appears light pink. AP contains many hormone release cells which do pick up stain, so it appears dark pink.

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20
Q

Acidophil

A

Chromophil in the AP (stains pink with H&E)

Releases GH and mammotrophs

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21
Q

Basophil

A

Chromophil in the AP (stains purple with H&E)

Releases ACTH, TSH, LH and FSH

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22
Q

Name a somatotroph

A

GH

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23
Q

Name a thyrotroph

A

TSH

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24
Q

Name a gonadotroph

A

LH or FSH

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25
Q

Name a corticotroph

A

ACTH

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26
Q

Name a lactotroph

A

Prolactin

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27
Q

Where are the cell bodies of the neurosecretory PP cells located?

A

In the hypothalamus

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28
Q

ACTH release and action

A

CRH from hypothalamus travels through hypophyseal portal system to AP where ACTH is released. Acts on adrenal cortex of adrenal glands to produce glucocorticoids.

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29
Q

TSH release and action

A

TRH from hypothalamus travels through hypophyseal portal system to AP where TSH is released. Acts on thyroid gland to release thyroid hormones.

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30
Q

GH release and action

A

GHRH from hypothalamus travels through hypophyseal portal system to AP where GH is released. Acts on liver to produce somatomedins which act on bone, muscle and other tissues.

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31
Q

Prolactin release and action

A

PRF from hypothalamus travels through hypophyseal portal system to AP where prolactin is released. Acts on mammary glands.

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32
Q

FSH and LH release and action

A

GnRH from hypothalamus travels through hypophyseal portal system to AP where LH and FSH are released. Act on testes to release inhibin and testosterone and ovaries to release estrogen, progesterone and inhibin.

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33
Q

Oxytocin release and action

A

Sensory stimulation causes direct release of oxytocin from PP which acts on uterine smooth muscle and mammary glands in females and smooth muscle in vas deferens and the prostate gland in males.

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34
Q

ADH release and action

A

Osmoreceptor stimulation causes direct release of ADH from PP which act on the kidneys to concentrate urine in the loop of Henle.

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35
Q

Growth hormone feedback

A

GHRH from hypothalamus acts on AP to release GH which acts on epithelia, adipose tissue and the liver. In the liver, somatomedins are released, which stimulates the growth on skeletal muscle, cartilage and other tissues, but also negatively feeds back to inhibit GHRH in the hypothalamus and positively feeds back to stimulate GHIH in the hypothalamus, both of which prevent further GH release from the AP.

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36
Q

Prolactin feedback

A

Non-pregnant state: Prolactin secretion acts on neuroendocrine cells to secrete dopamine, which inhibits prolactin secretion.
Pregnancy and after birth: Placental lactogen, a placental polypeptide hormone produced during pregnancy to supply additional energy to the fetus, bypasses normal prolactin feedback to inhibit dopamine. Prolactin secretion is increased; before birth, this normally feeds back to increase dopamine. After birth, addition of suckling stimulus is thought to cause PRF release from hypothalamus, increasing prolactin secretion.

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37
Q

HPG axis (ovary)

A

GnRH released from hypothalamus which travels through hypophyseal portal system to AP, released LH and FSH. These act on the ovaries to produce estrogen which inhibits suprachiasmic nucleus of the hypothalamus. This inhibits further GnRH release.

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38
Q

GnRH signal transduction

A

Hypothalamus releases GnRH, which travels through hypophyseal portal capillaries to the gonadotroph cell. GnRH binds GPCR, causing PLC release. PLC is cleaved by PIP2 to produce IP3 and DAG. IP3 causes calcium release and DAG causes PKC release. Ca+2 and PKC increases LH and FSH synthesis and secretion from the gonadotroph into the circulation.
In thecal cells or Leydig cells in the gonads, LH binds GPCRs, causing adenylate cyclase to be cleaved into cAMP which activates PKA. The GPCR also activates PLC, which produces DAG and IP3, producing PKC and Ca+2 respectively. PKA + PKC + Ca+2 causes oogenesis, spermatogenesis and steroidogenesis.
In granulosa cells or Sertoli cells in the gonads, FSH binds GPCRs, activating adenylate cyclase, then cAMP, then PKA, contributing to oogenesis, spermatogenesis and steroidogenesis.

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39
Q

Kallmann syndrome

A 
GnRH deficiency leading to:
Delayed puberty
Amenorrhoea
Anosmia/hyposmia
Myopia and other eye problems
Coeliac disease and type II diabetes common comorbidities
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40
Q

Estrogen feedback on GnRH neuronal network

A

LH and FSH act on ovary to induce ovulation. Developing follicles produce estrogen which feeds back on the pituitary and GnRH neurons (positively and negatively). After ovulation, corpus luteum produces progesterone, which negatively feeds back to pituitary and GnRH neurons.

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41
Q

Estrogen signalling in GnRH neurons

A

Estrogen released into synapse, then diffuses through channels on cell membrane, inducing Ca+2. Also converts ERbeta to ERK via CAMKII and PKA signalling. ERK + Ca+2 activate TF CREB.

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42
Q

What is Kisspeptin key for?

A

Puberty initiation

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43
Q

Oogenesis

A

Formation and development of ovum
Oogonium
Mitosis leads to primary oocyte
Meiosis – arrest in prophase I
Primary oocyte
Meiosis I completed leads to first polar body
Meiosis – arrest in metaphase II leads to secondary oocyte
Fertilisation by sperm leads to completion of meiosis II
Second polar body and mature ovum follows

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44
Q

Why do fallopian tubes need to be free?

A

Need to move and pick up oocytes during ovulation

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45
Q

Surrounding support cells of oocyte

A

Granulosa cells

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46
Q

When has a human female developed all her oocytes by?

A

6 months gestational age –about 7 million

This drops to 1 million around birth and 300,000 around puberty

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47
Q

Follicle

A

Oocyte + granulosa cells

Located near the surface of the ovary in the cortex

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48
Q

When does meiosis halt?

A

In fetal development, end of prophase, just prior to metaphase 1
In follicular development, metaphase II, waiting for fertilisation to occur

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49
Q

Follicular wave

A

Multiple follicles recruited in a cycle even though only 1 (normally) will be ovulated

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50
Q

Ovarian cycle

A

Following puberty, waves of follicles become activated (85 days from activation to antrum formation)
During the follicular phase, one follicle will dominate in growth

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51
Q

Atresia

A

Process by which dominant follicle reduces the growth of other follicles and causes them to die

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52
Q

Primordial follicle

A

Single layer of flattened granulosa cells surrounding oocyte

Stromal cells round the outside

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53
Q

Primary follicle

A

Single layer of cuboidal granulosa cells

54
Q

Secondary follicle

A

Multiple layers of granulosa cells now expressing FSH receptors and producing estrogen, inhibin and AMH
No antrum
Theca cells expressing LH receptors surrounding granulosa cells – produce androgens
Highly vascularised tissue on outside

55
Q

Tertiary follicle

A 
Antrum formation containing follicular fluid
Theca interna (endocrine) and theca externa (structural) layers
56
Q

Zona pellucida

A

Made up on ZP1, ZP2 and ZP3
ZP1 present only in primordial follicles
ZP2 and ZP3 added to activated follicles
Important for filtering normal sperm and the polyspermy block

57
Q

Theca interna

A

Internal endocrine layer of cells surrounding tertiary occytes producing androgens

58
Q

Theca externa

A

External structural layer of fibroblasts and longitudinal cells surrounding tertiary oocytes

59
Q

AMH

A

Anti-mullerian hormone

Suppressed follicular recruitment and development

60
Q

Corpus luteum

A

Remnants of the follicle left over after ovulation, including granulosa and theca cells
Releases progesterone and estrogen and degrades over the course of a few months

61
Q

Endocrine control of the ovarian cycle

A

Estrogen begins to rise around day 6, peaks around day 12 and feeds back to the hypothalamus and pituitary to stimulate LH release
FSH peaks at day 12, then slowly declines
LH surges just after day 12, then rapidly declines
Progesterone begins to rise around day 14 and peaks around day 22 to promote pregnancy

62
Q

Inhibin

A

Produced by granulosa cells. Negatively feeds back to pituitary to regulate FSH

63
Q

Hyperthermic phase

A

Around day 21/22 of the cycle, progesterone release slightly increases the basal body temperature following ovulation

64
Q

Regions of the fallopian tube (proximal to distal)

A

Isthmus
Ampulla
Infundibulum
Fimbrae

65
Q

Structure of fallopian tube

A

Epithelial lining – ciliated, secretory and responsive to steroids
Muscular coat (inner circular, outer longitudinal)
Serosal coat

66
Q

Effect of estrogen in the fallopian tubes

A

Increases cilia
Increases secretory activity
Increases muscular activity

67
Q

Effect of progesterone in the fallopian tubes

A

Decreases muscular activity
Decreases cilia but increases beat frequency after estrogen priming
Decreases volume of secretions

68
Q

Luminal volume of non-pregnant uterus

A

10 mL

69
Q

Luminal volume of pregnant uterus

A 
5 L (baby, amniotic fluid and placenta)
More if twins etc.
70
Q

Growth of uterus

A

Initially controlled by estrogen and progesterone (therefore ectopic pregnancies show same initial growth)
Largely due to stretching of existing cells rather than proliferation which allows involution of uterus after birth
Cells go from 50 microns in length to 400–600 microns

71
Q

Uterine positions

A

Anteverted (most common)
Anteflexed
Retroflexed
Retroverted (25%)

72
Q

Uterine layers

A 
Serosa/perimetrium
Muscular myometrium (90%)
Inner endometrium
73
Q

Structures present in the uterine wall

A

Endometrium contains simple columnar epithelium, uterine glands, functional layer and basilar layer, which is continuous with the myometrium

74
Q

Which part of the uterine wall changes over the course of the menstrual cycle?

A

The functional layer

75
Q

Decidua

A

Thin layer of tissue that comes away with the placenta when baby delivered at term

76
Q

Decidual reaction

A

Stroma of endometrium become oedematous
Fibroblasts of stroma become large and lay down glycogen (energy source)
Spontaneously occurs at the end of menstruation in humans

77
Q

Spiral arteries

A

Arteries in the uterus are coiled up so they can expand during pregnancy and don’t have to rely on rapid growth
Crucial to survival of fetus
During menses, the spiral artery terminal segments are lost along with the rest of the functional layer –the rest of the artery undergoes spasm to prevent exsanguination

78
Q

Exsanguination

A

The loss of blood to a degree sufficient to cause death.

79
Q

Phases of the menstrual cycle

A 
Stratum Basalis:
Menstrual phase – day 1 - 7
Preovulatory phase – day 7 - 14
Ovulation – day 14
Postovulatory phase – day 14 - 28
Stratum Functionalis:
Menstruation
Proliferative/follicular phase
Secretory/luteal phase
80
Q

Histology of mid-proliferative stage

A

Stromal oedema and mitotic figures present

81
Q

Histology of early luteal phase

A

Tortuous glands, basal vaculotation and glandular secretions present

82
Q

Basal vaculotation

A

Gaps between basal membrane of epithelium and densely stained cytoplasm

83
Q

Histology of late luteal phase

A

Tortuous glands still present but no basal vaculotation

Leukocyte infiltration begins

84
Q

Histology of decidual reaction

A

Polagonal, pale staining cells

85
Q

Role of estrogen in the uterus

A 
Epithelial and stromal cell proliferation
Stromal oedema
Glandular secretions
Estrogen priming
Myometrial activity
86
Q

Estrogen priming

A

Synthesis of intracellular progesterone receptors

87
Q

Role of progesterone in the uterus

A

Thick glandular secretions in the luteal phase
Stromal cell proliferation
Inhibits myometrial activity

88
Q

How do we know that the decidual reaction is not required for implantation?

A

Ectopic pregnancy – most common in the fallopian tubes, especially when there is a loss of ciliary activity or contraction

89
Q

Endometriosis

A 
Ectopic endometrium (6–10% of women)
Causes chronic pelvic pain and is associated with infertility, especially when found on ovaries or in fallopian tubes
90
Q

Three major theories of endometriosis

A

Retrograde menstruation
Transport of epithelial cells via blood or lymphatics
Growth of endometrial-like tissue from stem cells

91
Q

Cervical mucus change throughout cycle

A

Changes in volume, viscosity and threadability

92
Q

Spinnbarkeit

A

Stretchy mucus indicating fertile time – receptive to sperm

Induced by estrogen and stopped by progesterone

93
Q

Endocervix structure

A

Columnar epithelium
Glands and crypts
Fibrous stroma and few smooth muscle cells

94
Q

Ectocervix structure

A

Stratified squamous epithelium

95
Q

Endocrinology of testes

A

Exocrine gland – secretes spermatozoa

Endocrine gland – secretes testosterone mainly

96
Q

Types of cells in the testes

A 
Gonocytes
Spermatogonia
Sertoli
Leydig
Myoid
97
Q

Gonocytes

A

Primitive germ cells that become spermatogonia

Only present up to minipuberty

98
Q

Spermatogonia

A

Germ cells

Pre-sperm cells that replicate by mitosis

99
Q

Sertoli cells

A

Epithelial cells lining the lumen of seminiferous tubules that help developing sperm cells
Increase in number during minipuberty

100
Q

Leydig cells

A

Interstitial cells that produce androgen

101
Q

Myoid cells

A

Contractile cells of the testes

102
Q

Germ cell origin

A

Primordial germ cells either become sperm of oocytes
First seen around 3-4 weeks post-conception in the yolk sac of the extraembryonic tissues then migrate to the gonadal ridges
PGCs that wander away from the correct path of migration should be eliminated by apoptosis

103
Q

Migration of primordial germ cells

A

PGCs follow fine enteric nerves and are supposed to stop at the testes but sometimes develop ectopically, where they can develop into oocytes
Could be origin of germ cell tumours outside testes

104
Q

Production of testosterone in males

A

Produced by Leydig cells

After 14 weeks, production is LH and hCG dependent

105
Q

Minipuberty

A

2 months postpartum producing a peak in testosterone of 2–3 ng/mL

106
Q

Why is minipuberty important?

A

Masculinises neonatal brain
Promotes Sertoli cell proliferation – this doesn’t occur after minipuberty
Promotes gonocyte differentiation

107
Q

What cells create the blood–testis barrier?

A

Sertoli cells

108
Q

Role of Sertoli cells

A

Nourish spermatogonia
Resorb excess cytoplasm
Produce seminiferous tubule fluid
Maintain spermatogonial stem cell niche

109
Q

Blood–testis barrier

A

Important for fertility and the prevention of antisperm antibody production
Formed at puberty, so after this Sertoli cells cannot proliferate

110
Q

Testes descent

A

1) Transabdominal phase (10–15 weeks)
2) Inguinoscrotal phase (25–35 weeks) – androgen driven
Testes form in the gonadal ridges in the lumbar region suspended between the caudal and gubernaculum ligaments. As the testes grow, the gubernaculum does not elongate and the caudal ligament regresses.
INSL-3 (from Leydig cells) causes migration of the gubernaculum towards and dilation of the inguinal canal, dragging testes down

111
Q

Cryptorchidism

A

Failure for testes to descend

Most self-correct within 3 months but can be surgically corrected with orchidopexy

112
Q

Cryptorchidism complications

A

Infertility due to excess temperature
Testicular cancer
Breast-fed infants less likely to remain cryptorchid

113
Q

Maldescent

A

Improper or incomplete testes descent – can end up in abdomen, perineum or thigh

114
Q

3 phases to spermatogenesis

A

Mitosis
Meiosis
Cytodifferentiation

115
Q

Spermatogenesis

A

At puberty, PGCs reactivated and become spermatogonial stem cells which divide via mitosis – 1 daughter cell differentiates into spermatogonium and 1 stays undifferentiated to maintain stem cell population
Spermatogonia move between Sertoli cells to adluminal compartment of seminiferous tubules, where they are called primary spermatocytes and undergo meiosis
At the end of meiosis I, called secondary spermatocytes
At the end of meiosis II, called spermatids
Spermatids go through spermiogenesis to differentiate their shape and become spermatozoa

116
Q

Spermiogenesis

A

Round spermatids differentiate and become spermatozoa
Unnecessary cytoplasm is shed as the residual body
Sperm move into lumen of seminiferous tubule
Androgen-dependent

117
Q

Hormonal control of spermatogenesis

A

Hypothalamus produces GnRH which induces LH and FSH release from AP
LH acts on Leydig cells to produce testosterone, which acts on Sertoli cells to nourish sperm
FSH acts on Sertoli cells to produce androgen binding protein
Testosterone + androgen binding protein produces DHT which allows secondary sexual characteristic development
Sertoli cells produce insulin which inhibit further FSH release
Testosterone negatively feeds back to AP and hypothalamus

118
Q

Spermatogenic wave

A

The time taken for a sperm to be produced from a germ cell in human males in 64 days – about 16 days between successive waves

119
Q

Epididymis

A

Comma shaped organ running posterior and superior to testes
Efferent tubules of the rete testis drain into the head of the epididymis
Sperm spend 10–14 days passing through epididymis where they are concentrated and gain motility

120
Q

Rete testis

A

Series of collecting ducts in the hilum of the testes that carries sperm from the seminiferous tubules to the efferent ducts

121
Q

Vas deferens

A

Major site of sperm storage in men – mainly in ampulla, an enlarged, folded and crypt-filled region near the prostate
Consists of inner longitudinal, middle circular and outer longitudinal muscle layers

122
Q

Seminal vesicles

A

Highly folded tubular glands that secrete an alkaline fluid containing fructose – energy source for sperm
Produces semenogelin

123
Q

Semenogelin

A

Zinc binding protein produced by seminal vesicles that causes clotting immediately after ejaculation

124
Q

Ejaculatory duct

A

Tube created when the excretory duct of the seminal vesicle joins with the vas deferens

125
Q

Prostate gland secretions

A

Milky coloured, slightly acidic fluid containing PSA, which breaks down the seminal coagulum

126
Q

Prostate gland zones

A

Central – surrounds the urethra, no cancer
Peripheral – surrounds central zone, often cancer
Transition – surrounds proximal prostatic urethra, BPH
Anterior – fibromuscular, aglandular

127
Q

Penis

A

Two corpus cavernosa which relax and fill with blood

One corpus spongiosum containing the urethra

128
Q

Basic erection process

A

1) Parasympathetic nerve activity causes ACh release
2) ACh induces NO release by endothelial cells of the corpora
3) NO induces cGMO production which causes vasodilation
4) Corpora relax and engorge with blood
5) Venous outflow reduced, increasing erection

129
Q

Sildenafil/viagra mechanism

A

Blocks type V phosphodiesterase, preventing cGMP breakdown
Vasodilation increased
Note: not useful if erectile dysfunction due to PSNS damage

130
Q

Semen constituents

A

30% prostatic fluid
10% sperm
60% seminal vesicle fluid
Normally 2–5 mL, containing 20 million sperm per mL

Reproduction, Development and Aging (5 decks)

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