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PBL SEM 1 > Case 4 - Male Repro and Bone Growth > Flashcards

Case 4 - Male Repro and Bone Growth Flashcards

1
Q

what are the hormonal changes at the onset of puberty?

A

kisspeptin stimulated - increases GNRH
endocrine cells in APG more sensitive to GNRH =
rise in FSH and LH
ovarian and testicular cells more sensitive to FSH

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2
Q

what is leptin

A

adipose tissue produces it
feedback control of appetite
adipose tissue absorbs glucose and lipids
releases leptin into blood
leptin binds to HT neurones = suppression of appetite

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3
Q

how is leptin involved in puberty

A

increase in GNRH dependent on leptin = low levels of leptin = delayed puberty

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4
Q

HCG effects in male fetuses

A

interstitial cell stimulating effect on testes of male fetus
= production of testosterone in male fetuses until birth
hence grows male organs
7th month = testosterone secreted by fatal testes causes them to descend into scrotum

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5
Q

6 functions of bones

A

support; skeleton
protection
movement; muscle attached to bone
blood cell production: red and yellow.
triglyceride storage = yellow marrow, pot energy reserve
mineral homeostasis; calcium, phosphate stays within a certain limit

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6
Q

which are the types of bones and an example

A

flat: frontal in skull
long: humerus
irregular: facial
short: cuboidal, carpal
sesamoid: wherever tendon crosses over at end of bone

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7
Q

define osteoprogenitor cell

A

flat, elongated uncles

bone stem cell

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8
Q

define osteblast

A

cuboidal, builds bone

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9
Q

osteoclasts

A

remove dead bone cells

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10
Q

osteocyte

A

circular, sits in lacuna. maintains bone homeostasis

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11
Q

what is intramembranous ossification

A

when compact and spongy bone develops directly from mesenchymal connective tissue. flat bones formed

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12
Q

endochondral ossification

A

long bones formed this way

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13
Q

process of endochondral ossification

A

-mesenchymal cells lay down cartilage by differentiation
-bony cola formed by osteoblasts
chondrocytes enlarge n matrix calcifies
chond die bc lack of nutrients
matrix breaks down, cavity forms
artery enters and supplies cavity
osteoblasts lay down bone = primary oss centre
bone is REPLACING hyaline cartilage
osteoclasts form medullary cavity
secondary OC starts to develop
bone collar = periosteum so compact bone on outside and spongy on inside

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14
Q

what are growth plates

A

epiphyseal cartilage

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15
Q

what is bone age

A

degree of maturation of a childs bones

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16
Q

process of growth

A

HT secreted GH releasing hormone
somatotrophs on APG produce GH
GH acts on bones, adipose and liver tissue
liver produces IGF1
GH also stim IGF1 prod from bone
both IGF1 and GH promote growth in long bones, soft tissues and organs

17
Q

GH

A 
-gene on chr 17
pulsatile
breakdown of adipose tissue
stim aa transport into muscles
stim liver to increase hepatic glucose output n decrease glucose uptake
incr in plc circulation
ENDOCRINE EFFECTS
18
Q

how does the GH receptor help to produce a protein

A

enzymes coupled: when gH binds, receptor recruits enzyme
present in cell surface
induces conformational change
recruits enzyme JAK2
pplation of enzyme = activated
able to recruit stat 5, becomes pplated
pplated stat5 moves from cytoplasm = nucleus
binds to genes w response element for stat5
transcription of gene

19
Q

IGF1

A 
gene on chromosome 12
not pulsatile
stim muslces to take up aa
stim lipogenesis
in liver; decreases plc output from liver, reduces circ glc levels
ENDOCRINE in liver
PARACRINE in bone
20
Q

how does the IGF1 receptor work

A

enzyme coupled
enzyme built in, needs to be phosphorylated
cascade - PL3 kinase pathway = survival metabolism

21
Q

how do the IGF binding proteins work

A

6
IGF carried mainly w IGFBP3
complex reaches cell, protease breaks down binding protein
exposes IGF to recept, or and binds

22
Q

what are the two pathways the iGF and receptor can take

A

cell survival

proliferation MAP kinase

23
Q

activation of enzyme kinase

A

when enzyme activated = enzyme adds pp mol to protein
activates it
phosphorylates next one
can also deactivate by removing

24
Q

use of oestrogen in growth

A

resp for growth plates closing

acts on reserve zones

25
Q

process of spermatogenesis

A

sperm formed in ST in testis
empty into epidydimus = vas deferens and ampulla of vas deferens, then body of prostate
two seminal vesicles empty into prostatic gland of ampulla and then passes into ejac duct
empties into internal urethra
urethra = last link from testis out

26
Q

what supplies urethra w mucus?

A

uretheral glands and bulbourethral gland

27
Q

steps of spermatogenesis

A

primordial germ cells migrate to testes = spermatogonia
mitosis = some remain undifferentiated
some into primary spermatocytes
spermatogonia migrate to sertoli cells to central lumen of ST
spermatogonia that cross barrier into sertoli cell layer = modified and enlarged, form primary spermatocytes
meiosis: secondary spermatocytes
divide into spermatozoa

28
Q

what is the blood testis barrier

A

isolates ST from general circulation

preserve differences between tubular fluid and interstitial fluid

29
Q

what does inhibin do in spermatogenesis

A

depresses PG prod of FSH and GNRH

faster rate of sperm production = more inhibit secreted

30
Q

what is the mullein-inhibiting factor

A

secreted by nurse cells in developing testes

causes regression of fetal mullein ducts; passageways that form uterine tubes and uterus in F

31
Q

how is testosterone involved in spermatogenesis

A

secreted by LEYDIG cells in testes - essential for growth and division of testicular germinal cells

32
Q

how is LH involved

A

stim ledig cells to secrete testosterone

33
Q

how is oestrogen involved

A

formed from testosterone by sertoli cells when tim by FSH

34
Q

how is FSH involved

A

secreted by APG, tim sertoli cells to help conversion of spermatids to sperm

35
Q

how is the GH involved

A

controls bg metabolic functions of testes

promotes early division of spermatogonia themselves.

36
Q

what is gilick competence

A

used in medical law to decide whether a child under 16 is able to consent to their own medical treatment without parental knowledge

PBL SEM 1 (4 decks)

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