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PBL SEM 1 > CASE 4 > Flashcards

CASE 4 Flashcards

1
Q

where are sperm made and where do they mature?

A

made in seminiferous tubules between sertoli cells

mature in epididymis

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2
Q

where is testosterone made?

A

made in Leydig cells/interstitial cells of Leydig — adjacent to seminiferous tubules

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3
Q

describe the stages of spermatogenesis

A
  1. spermatogonium undergoes mitosis
  2. one of the daughter cells differentiates into a primary spermatocyte
  3. the primary spermatocyte moves through the tight junction and starts to enlarge (under the influence of testosterone) by increasing its cytoplasm
  4. tight junction closes quickly
  5. primary spermatocyte divides into 2 secondary spermatocytes by meiotic division
  6. secondary spermatocytes differentiate into spermatids (meiosis 2) — 4 spermatids made
  7. spermiogenesis: spermatids differentiate into spermatozoa (1 spermatozoa per spermatid)
  8. spermatozoa travel to the epididymis to fully mature — gain mitochondria and longer flagelli
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4
Q

brief summary of spermatogenesis (order)

A

spermatogonium — mitosis — one differentiates into primary spermatocyte — through tight junction and gets bigger — divides into 2 secondary spermatocytes (meiosis) — differentiate into 4 spermatids (meiosis 2) — turn into spermatozoa

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5
Q

how many sperm does one primary spermatocyte give rise to?

A

4 sperm

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6
Q

what is a blood testis barrier and what is its function? function of tight junction

A

= a physical barrier between the blood vessels and the seminiferous tubules of the testes

  • produced by tight junctions between sertoli cells
  • regulates composition of luminal fluid in which germ cells develop
  • prevents sperm antigens from constant with systemic/lymphatic systems causing an immune response to sperm

tight junction closes very quickly — maintains the different environments as not much leakage between compartments

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7
Q

function of testosterone in stimulating spermatogenesis + where is it made?

A

secreted by the Leydig cells. it is essential for growth and division of the testicular germinal cells = 1st stage of forming sperm

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8
Q

function of LH in stimulating spermatogenesis + where is it made?

A

secreted by the anterior pituitary gland. stimulates the Leydig cells to secrete testosterone

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9
Q

function of FSH in stimulating spermatogenesis + where is it made?

A

secreted by the anterior pituitary glad. stimulates the sertoli cells — enables the process of spermiogenesis

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10
Q

function of estrogens in stimulating spermatogenesis + where are they made?

A

formed from testosterone by the sertoli cells when they are stimulated by FSH

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11
Q

function of growth hormone in stimulating spermatogenesis + where is it made?

A

(as well as most other body hormones) it is essential for controlling background metabolic functions of the testes. it specifically promotes the early division of the spermatogonia themselves. without it = infertility as spermatogenesis is severely deficient or absent

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12
Q

drugs that modify the action of steroid hormone receptors are based on cholesterol because steroid hormones function by ____ ?

A

activating intracellular receptors

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13
Q

how do steroid hormones work?

A
  1. pass through cell membrane of target cell - possible as they are lipid-soluble so can diffuse through phospholipid bilayer
  2. binds with receptor in cytoplasm, forming a receptor-hormone complex
  3. complex enters nucleus and triggers gene transcription
  4. transcribed mRNA is translated into proteins
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14
Q

how do peptide hormones work?

A
  1. a water-soluble peptide hormone (1st messenger) binds to receptor
  2. this activates a G protein
  3. G protein activates adenylate cyclase
  4. adenylate cyclase converts ATP to cAMP
  5. cAMP acts as a 2nd messenger to activate protein kinases
  6. protein kinases are enzymes that phosphorylate other proteins
  7. phosphorylation is carried out by donating a phosphate group : ATP —> ADP
  8. these phosphorylated proteins cause reactions
  9. phosphodiesterase inactivates cAMP eventually
  10. this turns off the cell’s response unless new hormones continue to bind to their receptors in the plasma membrane
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15
Q

where do sperm become motile?

A

epididymis

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16
Q

if non-disjunction occurred in meiosis 2 of spermatogenesis, at which stage of gamete development would abnormalities in chromosome complement be first apparent?

A

spermatids

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17
Q

what is the role of the acrosome contents?

A

acrosome contents usually digest the zona pellucida surrounding the ovum

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18
Q

function and types of bone

A

long, short, irregular, flat

support, protection, movement, mineral homeostasis, triglyceride storage, blood cell production

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19
Q

where does bone growth occur?

A

epiphyseal plate

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20
Q

where is the epiphyseal plate and what is it?

A

metaphysis — joins epiphysis to bone shaft

it is a region of transition from cartilage to bone. consist of typical hyaline cartilage in the middle, with a transitional zone on each side where cartilage is being replaced by bone

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21
Q

what does spongy bone consist of?

A

full of holes for blood vessels and nerves

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22
Q

where is bone marrow?

A

in the medullary cavity (hollow)

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23
Q

what is the medullary cavity lined with?

A

lined with thin membrane that lines the endosteum

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24
Q

what is the periosteum?

A

tough sheet of dense connective tissue that surrounds bone surface — serves as an attachment point for tendons and ligaments

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25
Q

compact vs spongy (aka. trabecular, cancellous) bone

A

spongy — adipose tissue with trabecullae

compact — central canal, lamellae, lacuna with osteocytes, canaliculi, Haversian system (osteon)

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26
Q

what travels through the central canal in compact bone?

A

blood vessels and nerves

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27
Q

what do canaliculi in compact bone allow?

A

canaliculi in Haversian system allows osteocytes to communicate with each other (canaliculi connect lacunae, osteocytes sit within a lacuna)

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28
Q

what is bone? what does the bone matrix contain?

A

a highly vascular mineralised connective tissue

matrix — primarily composed of collagen fibres and calcium phosphate

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29
Q

name 4 bone cells and describe them

A
  1. osteoprogenitor cell = bone’s stem cells. can differentiate into fibroblasts, osteoblasts, chondrocytes, adipocytes
  2. osteoblast = secrete collagen and extra cellular matrix. become trapped in matrix
  3. osteocyte = responsible for maintaining bone matrix and homeostasis. sit within lacuna
  4. osteoclast = formed by fusion of 50+ monocytes. “bone-chellers” — responsible for removal of bone and break bone down
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30
Q

what does an osteoblast become when it gets trapped in matrix?

A

osteocyte

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31
Q

what is cartilage and what is the most common type?

A

an a vascular connective tissue consisting of cells (chondrocytes which sit in lacuna) and matrix (water, collagens, proteoglycons)

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32
Q

what are the 2 different ways bones grow?

A

OSSIFICATION

  1. flat bones = intramembranous
  2. long bones = endochondral
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33
Q

name the 5 different zones in the epiphyseal plate and what hormones work there

A
  1. reserve zone - GH
  2. proliferative zone - GH and IGF-1
  3. zone of maturation
  4. zone of degeneration
  5. zone of provisional calcification

zones 3,4,5 are hypertrophic zones, thyroid hormones act here

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34
Q

describe the zone of reserve cartilage

A

consists of hyaline cartilage. nothing really happens here

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35
Q

describe the zone of cell proliferation

A
  • chondrocytes proliferate

- chondrocytes, surrounded by lacuna, arrange themselves into longitudinal columns of flattened lacunae

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36
Q

describe the zone of maturation

A
  • chondrocytes stop proliferating
  • chondrocytes begin hypertrophy
  • chondrocytes secrete collagen type 10, that allows the plates of cartilage to begin calcifying
  • this pushes lacunae in the columns further apart
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37
Q

describe the zone of degeneration

A
  • chondrocytes become hypoxic and begin to die
  • their contents are secreted into the matrix, causing erosion of the plates of cartilage between the lacunae
  • this converts each column into the longitudinal channel
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38
Q

describe the zone of provisional calcification/invasion/angiogenesis

A
  • blood vessels invade these channels
  • osteoblasts and progenitor cells line up along the walls of these channels and begin depositing layer after layer of bone matrix
  • osteoclasts cause bone resorption
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39
Q

what deposits bone and what resorbs bone?

A

bone is continuously being deposited by osteoblasts and resorted by osteoclasts

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40
Q

benefits of constant bone deposition and resorption

A
  • bones thicken (in response to heavy loads)
  • shape adjusts to stresses placed on bone
  • renews matrix — maintains toughness, rate higher in children than adults — old bones are brittle and weal
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41
Q

parathyroid hormone and calcitonin functions

A

= keep bone calcium levels constant

  1. low Ca levels — parathyroid released - increases osteoclast activity — resorbs bone to increase calcium ions levels in blood
  2. high Ca levels — calcitonin released - decreases osteoclast activity
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42
Q

what does the cell cycle consist of?

A

interphase + M phase

interphase: G1 = cell grows in size and decreases its mass of proteins and organelles. monitors environments
S phase = DNA replication. G2 =another phase of growth and checking

M phase: mitosis + cytokinesis

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43
Q

how do exercise, sleep and gherlin affect growth?

A

exercise — increase release of GHRH

sleep — increases and decreases release of GHRH

ghrelin — peptide hormone secreted by fundus of the stomach which increases the release of GH

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44
Q

what is GHRH and where is it released?

A

growth hormone releasing hormone

stimulates synthesis of GH by increasing GH gene transcription and GH release by the somatrophs in the anterior pituitary gland

released by hypothalamus

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45
Q

on what chromosome is the gene for GH located?

A

chromosome 17

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46
Q

what is GH?

A

= growth hormone

  • peptide hormone
  • secreted by somatotrophic cells of the anterior pituitary gland in pulses (mainly at night!!)
  • target: bone, fat, muscles
  • acts as a GH receptor on surface of cells
  • also acts on the liver — when activated produces IGF-1
47
Q

what is a licensed treatment for Turner Syndrome?

A

GH

48
Q

what is IGF-1?

A
  • insulin-like growth factor-1
  • small peptide hormone
  • paracrine (affects local cells) / autocrine (acts on cell itself)
  • not secreted in pulses therefore one blood sample is sufficient to measure levels
  • functions by phosphorylating proteins on tyrosine residues
  • causes cells to grow and multiply. IGFs increase the growth of skeletal muscle and bone during childhood and teenage years
  • GH stimulates the liver to produce IGF-1
49
Q

on what chromosome is the gene for IGF-1?

A

chromosome 12

50
Q

GH and IGF-1 functions

A
  • both promote growth in long bones (work on epiphyseal plates), soft tissues and organs
  • affect metabolism: GH = lipolysis and IGF-1 = lipogenesis
  • both maintain the mass of muscles and bones and promote healing of injuries and tissue repairs in adults
51
Q

metabolic effects of GH

A
  1. GH enhances fat utilisation: causes lipolysis: enhances conversion of fatty acids to acetyl CoA.
  2. GH decreases carb utilisation: decreases glucose uptake, increases glucose production by liver and increased insulin secretion.
  3. GH promotes protein deposition in tissues: promotes transport of amino acids across cell membranes into cells - increases protein synthesis and hypertrophy
52
Q

how can GH result in hyperglycaemia?

A

GH tries to oppose the action of insulin — can result in hyperglycaemia

53
Q

GH vs IGF-1 receptors

A

both GH and IGF-1 act on receptors on cell surface — triggers intracellular signalling (enzyme-coupled receptors)

GH receptor — recruits enzyme once GH binds

IGF-1 receptor — already has enzyme built in to intracellular portion of receptor

54
Q

what happens when GHRH binds to its specific receptor?

A

when it binds to the GHRH receptor, it activates JAK2 and STATs — causes gene exp[ression of GH gene on chromosome 17

55
Q

what suppresses the release of GH?

A

GHIH or somatostatin

56
Q

gigantism vs acromegaly

A

gigantism = before growth plate closure

acromegaly = after growth plate closure (only changes to soft tissues)

57
Q

what enzyme converts iodide to iodine in the synthesis of thyroid hormones?

A

peroxidase

58
Q

what is iodidine converted to in the synthesis of thyroid hormones?

A

iodine —> monoiodotyrosine —> diodotyrosine

59
Q

role of TSH

A

stimulates uptake of iodine and release of T3 + T4 from gland and production of mono/diodotyrosine

60
Q

T3 vs T4

A

T3 is the most active form of the thyroid hormone as it has a higher affinity to the thyroid-hormone receptor

61
Q

what converts T4 to T3?

A

deiodinase

62
Q

what is responsible for closing the growth plate and what is the effect of this?

A

estrogen — long bone growth can no longer occur

63
Q

how is the growth plate closed?

A

estrogen causes apoptosis of osteoprogenitor cells in the reserve zone — reserve zone cannot provide the proliferative zone with chondroblasts once progenitor cells are used up.

works at receptors inside cell as it is lipid-solube

64
Q

where is the thyroid gland and what are the 3 major hormones it secretes?

A
  • inferior to larynx, anterior to trachea

- thyroxine (T4), tri-iodothyronine (T3), calcatonin

65
Q

what are thyroid secretions mainly controlled by?

A

TSH = thyroid-stimulating hormone

66
Q

what is the thyroid gland composed of?

A

composed of many closed follicles filled with a secretory substance called colloid and lined with cuboidal epithelial cells that secrete into the inferior of the follicles (secretion. absorbed back through follicular epithelium into blood before it can function)

67
Q

what is the main constituent of colloid?

A

the large glycoprotein thyroglobulin

68
Q

hyperthyroidism

A

occurs when the thyroid gland is increased 2 or 3 times its normal size, with hyperplasia of the follicular cell lining. can arise due to a tumour (a localised adenoma) in thyroid tissue = increase in thyroid hormones

69
Q

hypothyroidism — what is it and what is it characterised by

A

= an autoimmune response against the thyroid gland. most of these patients have thyroiditis (inflammation of the thyroid gland)

  • characterised by failure of body growth and mental retardation
70
Q

how can hypothyroidism be treated?

A

can be treated by replacing T3 in the system. if T4 concentrations decline later in life before puberty, normal skeletal development will not continue

71
Q

name 3 causes of short stature

A
  1. panhypopituitarism = reduced secretions of hormones from the pituitary gland
  2. genetics
  3. hypothyroidism =thyroid doesn’t produce enough hormones
72
Q

what is dwarfism?

A
  • caused by deficiency of anterior pituitary secretion (panhypopituitary) during childhood
  • rate of development greatly decreased
  • a person with panhypopituitary dwarfism never passes through puberty and never secretes sufficient quantities of gonadotropic hormones to develop adult sexual functions
  • in a 1/3 of dwarfs, only GH is deficient — these people do mature sexually and occasionally reproduce
73
Q

causes of gigantism and treatment

A
  • overreactive somatotropin
  • tumours of the anterior pituitary gland
  • large quantities of GH secreted
  • treatment: further effects only blocked by removal of tumour or the pituitary gland
74
Q

what is acromegaly?

A
  • tumour after adolescence (after epiphyseal closure)
  • patient cannot grow taller
  • bones become thicker and soft tissues can continue to grow - especially marked in bones of hands and feet and in the membranous bones
75
Q

what is the treatment of acromegaly?

A

focuses on lowering GH production, as well as reducing negative effects of the tumour

  1. surgery (removal of tumour)
  2. medications — somatostatins. GH antagonist (blocks effect of GH on body tissues. normalises IGF-1 levels and relieves symptoms but doesn’t lower GH levels or reduce tumour size)
76
Q

when is the growth rate of a child the fastest?

A

fastest in infancy: birth — 1 year

77
Q

what is bone age?

A

the degree of maturation of child’s bones (the average age at which children reach a specific stage of bone maturation)

78
Q

what can be used to predict a child’s adult height?

A

a child’s current height and bone age

79
Q

what initiates the process of puberty?

A

kisspeptin — stimulates the hypothalamus to increase the production GnRH

80
Q

what is the result of rising levels of GnRH?

A

anterior pituitary gland becomes more sensitive to GnRH — circulating levels of FSH and LH rise rapidly

  • ovarian/testicular cells become more sensitive to FSH/LH
  • initiates: gamete function, production of sex hormones that stimulate secondary sex characteristics and behaviours, a sudden acceleration in growth rate (culminates in closure of epiphyseal plate)
81
Q

what is leptin?

A

= a peptide hormone produced by adipose tissue

  • feedback control of appetite
  • stimulates kisspeptin (which stimulates hypothalamus)
  • suppression of appetite as it binds to hypothalamic neurons involved in emotions and appetite
  • thin girls enter puberty late (little fat)
  • an increase in body fat content can improve fertility
  • women stop menstruating when their body fat content gets too low
82
Q

male pubertal changes - hair, voice, skin, muscle

A

testosterone secretion causes penis, scrotum and testes to grow. causes development of secondary sexual male characteristics. helps promote spermatogenesis. stimulates the functional development of the accessory reproductive glands

effects on hair: stimulates the development of terminal hairs on the face, chest, axillae, and genitals

effects on voice: causes hypertrophy of the laryngeal mucosa and enlargement of larynx — cause voice to ‘break’

increases thickness of skin and can contribute to the development of acne

protein formation and muscle development

increases bone matrix and casues calcium retention

TESTES ENLARGEMENT DUE TO FSH

83
Q

how is muscle development caused in puberty?

A

androgens stimulate protein synthesis

84
Q

female pubertal changes

A

oestrogen: stimulates the production of fine hairs on the face, chest, axillae and the genitals. causes development of breast tissue

progesterone and prolactin cause the ultimate determinative growth and function of the breasts

oestrogen accelerates bone deposition and skeletal growth

85
Q

why do boys generally grow taller than girls?

A

oestrogen promotes bone growth much faster than testosterone so as a result the epiphyseal plate closes faster

86
Q

what is the Tanner Genital Scaling Scale?

A

a scale of physical development in children, adolescents and adults

defines physical measurements of development based on external primary and secondary sex characteristics

boys — genital development and pubic hair growth
girls — breast development and pubic hair growth

87
Q

what is primarily responsible for the enlargement of the testes?

A

FSH

88
Q

what is testosterone derived from?

A

cholesterol

89
Q

what is DHT and how is testosterone converted to it?

A

DHT = dihydrotestosterone
testosterone converted to DHT by 5a Reductase in specific sites (liver)
= very potent androgen. cannot be converted to oestrogen. important in differentiation of genitalia

90
Q

testosterone vs DHT actions

A

testosterone: libido, stimulates muscle and bone growth, voice deepening, sebum production/acne

DHT: facial body and hair, male pattern hair loss, prostate enlargement

91
Q

a child suffering from constitutional growth delay can have their puberty kick started by administering what hormone?

A

sex hormone (testosterone or oestrogen) (4 month courses of injections)

92
Q

what is the role of parathyroid hormone?

A

stimulate osteoclast activity so calcium salts are released into the blood

93
Q

in which zone of the epiphyseal plate of growing long bones do mature chondrocytes enlarge?

A

hypertrophic

94
Q

nutrition is the key factor in postnatal growth in what particular state of development?

A

infancy

95
Q

the sertoli cells in the ST are stimulated by which protein to produce testosterone-binding proteins?

A

FSH

96
Q

what is the half-life of GH in the blood?

A

20 mins

97
Q

what is the function of phosphodiesterase?

A

inactivate cAMP

98
Q

how does GH directly influence growth during puberty?

A

mobilises fat stores and converses or raises glucose levels

99
Q

IGF-1 influences bone growth in which part of the epiphyseal plate?

A

proliferative zone

100
Q

cells in the 1st meitoic stage of spermatogenesis are known as what?

A

primary spermatocytes

101
Q

name 5 functions of sertoli cells

A
  1. protection of developing spermatogenic cells
  2. nourishment of spermatocytes, spermatids, and sperm
  3. phagocytosis of excess sperm cytoplasm as development proceeds
  4. mediation of the effects of testosterone and FSH
  5. control of movements of spermatogenenic cells and release of sperm into the lumen of ST
102
Q

hormone 4 facts

A
  1. will only affect target cells far removed from the hormone-producing secretory cells
  2. must bind to transport proteins in order to circulate in blood
  3. may be released in low concentrations by can produce large effects in the target cells because of amplification
  4. can regulate the responsiveness of the target tissue by controlling the number of receptor sites for the hormone
103
Q

IGF-1 is released during puberty in response to what?

A

GH

104
Q

the Tanner staging is split into how many stages?

A

5

105
Q

during what stage of development would children be expected to understand false belief?

A

concrete operational

106
Q

what mineral is responsible for bone crystallisation?

A

calcium hydroxylapatite

107
Q

which cells in the testes convert cholesterol to testosterone?

A

Leydig cells

108
Q

where does the bulbospongiosis muscle originate in men?

A

collagen sheath at base of penis

109
Q

what does FSH indirectly stimulate to stimulate spermatogenesis?

A

stimulates sertoli cells to release androgen binding protein which keeps the concentration of testosterone in the vicinity of spermatogenic cells high

110
Q

what are the basic functional units of compact bone called?

A

osteons

111
Q

the type of bone deposited in a fracture callus is what?

A

woven bone

112
Q

what is the effect of parathyroid hormone and where is it made?

A
  • made in parathyroid gland
  • causes kidneys to retain calcium ions
  • increases the rate of intestinal absorption
  • osteoclasts stimulated to release stored calcium ions from the bone
113
Q

what is the effect of calcitonin and where is it made?

A
  • made in follicular cells of the thyroid gland
  • causes kidney to release calcium ions
  • no direct effect on the rate of intestinal absorption
  • a decrease in parathyroid hormone or calcitriol decreases the rate of intestinal absorption
  • osteoclasts are inhibited while osteoblasts continue to lock calcium ions in the bone
114
Q

what sort of action does GH have on glucose?

A

glucose sparing action

PBL SEM 1 (9 decks)

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