124 Flashcards
why are signalling systems needed
coordinate the activities of cells/tissues in a multi-cellular organism
- neurotransmission
- coordination of developmental processes
- homeostasis
types of signalling between cells
- free diffusion between cells
- via cytoplasmic connections
- direct cell-to-cell contact
3 types of signalling by free diffusion
autocrine
paracrine
endocrine
autocrine
signalling and reception by the same cell
cell secretes chemicals that modify its own behaviour
associated with growth regulation
paracrine
signalling between nearby cells
effects local and short-lived
important in coordinating the actions of neighbouring cells in embryonic development
endocrine - signalling by free diffusion
signalling between distant cells (by ‘hormones’)
endocrine glands secrete hormones into extracellular spaces which diffuses into the circulatory system
- pituitary gland
- adrenal gland
-thyroid gland
synaptic signalling
highly specific
localized type of paracrine signalling between 2 nerve cells or between a nerve and muscle cell
signalling via cytoplasmic connections is the fastest mode of cell-cell communication
t/f
true
how do signals transfer from one cell to its neighbour in signalling via cytoplasmic connections
through pores in the membrane
what does signalling by cell-to-cell contact involve
specific interactions between surface molecules on once cell and receptors on another cell
responsible for cell-cell recognition in animals
important in embryonic development and immune response
2 types of signalling molecules
local regulators- act on cells in the vicinity(auto/paracrine)
hormones- act at distance(endocrine)
4 local regulators
growth factors
gases
prostaglandins
neurotransmitter
growth factors as a local regulator
peptides or proteins that stimulate cell proliferation
may have >1 target cells and hence >1 function
e.g. nerve growth factor
gases as a local regulators
NO acts as a paracrine signal molecule
synthesized from arginine by NO synthase
induces vasodilation
prostaglandins as local regulators
modified fatty acids
multiple functions:
- excitability of uterine wall during childbirth
- induction of fever and inflammation in immune system
neurotransmitter as a local regulators
acetylcholine
biogenic amines
amino acids
neuropeptides
either inhibitory or exhibitory and some both
some occur in both CNS or PNS
how are hormones transported
bloodstream
what is hormone production contolled by
neuroendocrine system
hypothalamus is control centre
homeostasis definition
maintenance of a relatively stable internal environemnt in the face of stress from the external and internal environment
internal environemnt is not constant it is in dynamic equibibrium
what happens if blood glucose is high
islet beta cells in pancreas detect high glucose
release insulin
body takes up more glucose and liver stores glucose and store as glycogen
blood glucose declines
what happens when blood glucose is too low
alpha cells in pancrease stimulate to release glucagon into the blood
liver breaks down glycogen and releases glucose
blood glucose rises
2 main classes of hormones
peptides and proteins- bind to receptors on cell surface, trigger events within cell cytoplasm through second messengers
steroids- manufactured from cholesterol, can pass across lipid bilayer of plamsa membrane and bind to receptors wthin cell
signal transduction pathway
the conversion of a signal at the cell surface to a specific cellular response is a multi-step process
what are the 3 main stages of signal transduction
- reception of the signal at the cell surface- binds receptor changing receptor conformation
- transduction of the signal- multistep pathway providing more opportunities for coordiantion and regualtion
- cellular response
where does the cellular response occur
occur in the cytoplasm or may involve action in the nucleus
what does the cellular response in signal transduction regulate
regulate activity of enzymes
other pathways switch on genes by activating transcription factor
signal specificity in signal transduction
- different cells have different collection proteins
- give cell specificity
- response of cell to signal depends on the cells particular collection of proteins
- pathway branching and cross-talk further help the cell coordinate incoming signals
3 stages of cell signalling
reception
transduction
response
reception in cell signalling
detection by the cell of a signal molecule that usually originates from outside the cell
signal detected when signalling molecule interacts directly with a receptor on cell surface
receptor binding
ligands
the signalling molecules
i.e. it is a small molecules that binds to a larger one
what can lingand binding lead to
a change in the shape of a protein or aggregation of 3 or more receptors- enables receptor to interact with other mmoleclues
hydrophilic messengers
water soluble
too large to go through membrane
detected by membrane bound receptors
hydrophobic messenger
can move through lipid environment of the PM so signal receptors can be located inside the cell
the 3 main types of membrane receptors
g-coupled receptors
receptor tyrosine kinases
ion channel receptos
whats the largest family of cell-surface receptors
G-protein coupled receptors (GPCRs)
a GPCR is a plasma membrane receptor that spans the membrane as 8 a helices
t/f
false - its 7 a helices
what can G proteins bind
guanine nucelotides- GTP (guanine triphosphate) and GDP (guanine diphosphate)
is G protein a molecular switch
yes
its either of or on
what happens when GDP is bound to the G protein
G protein is inactive
switch is off
what happens when GTP is bound to G protein
G protein is activated
the switch is on
where is G protein found
loosely attached to cytoplasmic side of the cell membrane
how does an enzyme get activated from g protein
activated G protein dissociates from GCPR
binds to enzyme
causes change in shape and activity of enzyme- activation leads to cellular response
is reversible
how are changes in enzyme and G protein only temporary
because the G protein also functions as a GTPase enzyme (GTP to GDP)
returns G protein to inactive
G protein now available for reuse
wheres epinephrine/adrenaline released from
adrenal glands
what does epinephrine/adrenaline stimulate
glycogen breakdown in liver and skeletal muscle during stress
are receptor tyrosine kinases (RTKs) membrane bound
yes
how do RTKs differ from GPCRs
they have intrinsic enzyme activity
what does receptor tyrosine kinase(RTKs) do
add phosphate residues onto other proteins
can trigger multiple signals transduction pathways at once
what is abnormal functioning of RTKS associated with
many types of cancers
receptor tyrosine kinase activation
before ligand binds receptors exist as monomers
when binding the 2 receptor monomers associate with each other anc form a complex known as a dimer
this activates tyrosine kinase of each monomer
phosphate added to each tyrosine
now recognised b specific relay proteins
herceptin
approved for treatment of early-stage breast cancer treatment
binds to HER2 on cells and inhibits their growth and division
its a monoclonal antibody that binds to receptor
what do ligand-gated ion channels act as
a gate
creats a pore in PM that can open or close in response to extracellular chemical messenger
ligand-gated ion channels how does it open and close
gate closed until ligand binds to reeceptor
gate opens and specific ions can flow through - rapidly changing the intracellular conc of that ion anc auses cellular response
when ligand dissociates from the receptor the gate closes
example of ligand-gated ion channels
neurotransmitter molecules released at synapse
binds as ligand on recieving cell
ions flow in or out triggering electrical signal
verapamil
calcium channel blocker
treats hypertension and cardiovascular disorders
lamictal
sodium channel blocker
treats epilepsy
lidocaine
sodium channel blocker
local anaethetic
glipizide
potassium channel blocker
treats diabetes
where are intracellular receptor proteins found
cytosol or nucleus of target cells
can intracellular receptors cross membrane
yes as they are small or hydrophobic
what do intracellular recpetors do
activate receptors
example of hydrophobic intracellular receptors messengers
steroid and thyroid hormones for animals
can hormone receptor complex act as a transcription factor
yes
it can turn on specific genes
does testosterone activate intracellular receptor
yes
secreted by cells in testes
travels through blood and enters cells all over body
cells wih appropriate receptor can respond in these cells testosterone activates intracellular protein
what does protein kinase transfere phosphates from from ATP to
protein
called phophorylation
where does phosphorylation most commonly occur
on serine, threonine(or tyrosine) residues
does phosphorylation noramaly lead to protein protein activation
yes
what do protein phosphates do
remove phosphates from proteins
dephosphorylation
The extracellular signal molecule (ligand) that binds to the receptor is a pathway’s “first messenger
t/f
true
second messenger properties
small
nonprotein
water soluble
readily spread through ac cell by fiddusion
what pathways do second messengers participate in
pathways initiated by GPCRs and RTKs
common second messenger examples
cyclic AMP
calcium ions
where is adenylyl cyclase found
as an enzyme in the plasma membrane
what does adenylyl cyclase convert ATP into
cAMP
what is cAMP broken down by to form what
broken down by phosphodiesterase to form AMP which is inactive
other components of cAMP pathways
G-proteins
GPCR
protein kinases
what bacteria causes cholera
vibrio cholerae
hwo do you get cholera
drinking water containg bacteria
where doe cholera colonise
small intestines
form a biofilm and produce an enzyme that acts as a toxin
what G-protein does cholera affect
a g-protein involved in regulating salt and water excretion
what does cholera activating a g-protein do to activation of adenylate cyclase
g-protein no unable to hydrolyse GTP-GDP
leads to constant activation of adenylate cyclase and continuous production of cAMP
what does high levels of cAMP do
activate cystic fibrosis transmembrane conductance regulator
efflux of cl- and h2o leading to watery diarrhoea
under normal conditions what conc is intracellular calcum
very low
where is calcium activelty pumped to keep cytoplasmic concs low
ER
mitochondria
or chloroplasts in plants
what pathways lead to the release of calcium
pathways involving inositol triphosphate (IP3)
diacylglycerol (DAG) as additional second messengers
how many binding sites does calmodulin have
4 calcium binding site
what does calmodulin regualte
protein phosphates and kinases
also regulates adenylyl cyclases and phosphodiesterase
PM Ca2+ - ATPase is also activated by Calmodulin
the 4 aspects of fine-turning
- amplifying the signal
- specificity of response
-efficiency of response enhanced by scaffolding proteins - termination of the signal
scaffolding proteins
large relay proteins to which other relay proteins are attached
can increase signal transduction efficiency by grouping together different proteins involved in the same pathway
how are signals terminated
if ligand concentration falls then fewer receptors will be bound
unbound receptors revert to an inactive state
functions of the hypothalamus
-secretion of regulatory hormones to control activity of anterior pituitary
- control of sympathetic output to adrenal medulla
- production of ADH and oxytocin
adenohypophyis formation
formed by Rathke pouch (3rd week)- ectodermal derived evagination from roof of oral cavity
communication from hypothalamus to the anterior pituitary gland
regulatory hormones from hypothalamus transported via the hypophyseal portal system
regulation by hypothalamus and pituitary example broad
RH (Releasing hormone) causes h1 release from anterior pituitary
h1 causes h2 release from endocrine organ
h2 inhibits release of RH and H1
h2 has effect on target cells
examples of hormones relesed from anterior pituitary
TSH
ACTH- adrenocorticotropic
FSH- follicle
luteinising (LH)
prolactin (PRL)
(GH)
MSH- melanocyte
tropic hormones released from anterior pituitary
TSH
ACTH
FSH
LH
GH(both tropic and non tropic effects
whats a topic hormone
regulate function of endocrine cells/ glands
what does melanocyte stimulating hormone (MSH) do
regulates pigment containing cells
amphibians, fish
reptiles
some mammals
does MSH/ Ghrelin regulatte appetite
yes
whats released to reduce appetite
POMC released into pars-intermedia
stimulates hypothalamic neurons and reduces appetite
whats released to increase appetite
released by the stomach and stimulates hypothalmic neurons in ARC to increase appetite
what glycoprotein controls release of TSH
TRH
what does TSH stimulate teh release of
T3 and T4 from the thyroid
what do T3 and T4 inhibit release of to cause negative feedback
TRH and TSH
negative feedback
what causes release of ACTH from anterior pituitary
CRH
is ACTH a carbohydrate
no its a peptide
what does ACTH simulate
adrenal cortex to release glucocorticoids
what do glucocorticoids have a negative feedback on
CRH and ACTH
are FSH and LH glycoproteins
yes
what controls FSH and LH prodcuction
gonadotropin releasing hormones (GnRH)
what does FSH and LH promotes
egg and sperm production and secretion of sex steroids
what inhibits FSH production in both sexes
inhibin
what might inhibit GnRH release
inhibin
is prolactin a peptide
yes
what is prolactin release stimulated by
prolactin releasing factor (PRF)
what is prolactin inhibited by
prolactin inhibiting hormones (PIH, dopamine)
what does prolactin do
stimulate milk production
is GH peptide
yes
what is GH release stimulated by GHRH - growth hormone-releasing hormones
GHRH - growth hormone-releasing hormones
what is GH release inhibited by
growth hormone-inhibitory hormone (GHIH)(somatostatin
what does GH stimulate
somatomedin production
what does somatomedin stimulate
bone and cartilage growth
fat and glycogen breakdown, increasing blood glucose levels
pituitary gigantism
excess GH before puberty
acromegaly
excess GH after puberty
bones of hands feet cheeks and jaws thicken
pituitary growth failure
lack of GH
what hormones are produced from posterior pituitary
ADH
oxytocin
ADH and the nephrons
binds to receptors in DCT
increases expression of aquaporin 2 channel in DCT
concentrated urine
what does oxytocin stimulate
milk ejection by mammary glands
uterine contractions during childbirth
targets in brain influencing behaviour e.g. pair bonding, maternal cae, sexual activity
t3 long name
triiodothyronine
more active than t4
t4 long name
thyroxine
is t3 or t4 more active
t3
what do thyroid stimulating cells synthesise
thyroglobulin which is rich in tyrosine AAs
what happens when thyroid hormones are needed
TSH released which enhances the rate of endocytosis/pinocytosis
inside thyroid follical cell lysosomal digestion digests thyroglobulin. peptide bonds borke but bonds between T1-T2 or T2-T2 remain intact
what does TSH stimulate
iodide uptake ]thyroglobulin and thyroid peroxidase synthesis
uptake of thyroglobulin
development functions of thyroid hormones
metamorphosis in frogs ]bone formation]brain
metabolism functions of thyroid hormones
increase metabolic rate
increase ATP production
stimulates glycolysis
increased heart rate and bp
congenital hypothyroidism
poor skeletal and nervous developemnt
low metabolic rate
low bod temp
children/babies
hypothyroidism in adults
MYXOEDEMA
symptoms- lethargy
low body temp
muscle weakness
subcutaneous swelling
dry skin
hair loss
enlarged thyroid
could be cuased by low dietary iodine
hyperthyroidism
high metabolic rate
high body temp
sweating
high heart rate and bp
CNS effects - excitability, restlessness, mood swings
what do thyroid C cells release
calcitonin
released in response to high calcium levels in teh blood
what does calcitonin inhibit
osteoclast activity inhibited (bone breakdown)
increases uptake of calcium into bone
so decreases blood calcium level
what are the 2 kinds of epithelial cells in parathyroid gland
principal (chief) cells which produce PTH
oxyphil cells- function unknown
what dies the adrenal cortex contain
corticosteroids
what does adrenal medulla contain
adrenaline and noradrenaline
layers of adrenal cortex
zona reticularis- next to medulla
zona fasciculata
zoan glomerulosa
what does zona reticularis contain
androgens e.g. testosterone
what does zona fasciculata in adrenal cortex contain
glucocorticoids e.g. cortisol
what does zona glomerulosa in adrenal cortex contain
mineralcorticoids
e.g. aldosterone
what do glucocorticoids stimulate
glucose and glycogen synthesis
release of fatty acids
cause tissues to breakdown fatty acids and proteins
are glucocorticoids immunosuppresive
yes
glucocoricoids are not anti-inflammatory t/f
false they are anti-inflammatory
what does the adrenal medulla do
breakdown glycogen to glucose
changes in circulation
increase heart rate
dilate air passages in lungs, increase respiratory rate
short term stress what does the adrenal medulla secrete
epinephrine and norepinephrine
in long term stress what does the adrenal cortex secrete
mineralcorocoids
glucocorticoids
what is the development of the internal and external reproductive system controlled by
genotype
horones
at 20 weeks whatt does a lack of testosterone lead to and the maintained oestrogen
degeneration of mesonephric duct
oestrogen maintains the paramesonephric duct
what does the paramesonephric duct become in women
oviducts
uterus
upper parts of vagina
what maintains mesonephric duct at week 16 of males
testoterone and receptors
waht does the mesonephric duct become in males at 16weeks
epididymis and vas deferens
what stimulates teh degeneration of paramesonephric ducts at 16 weeks in males
anti-mullerian hormones (AMH)
at 7 weeks teh genital tubercle is bigger in males than females
t/f
false
tubercle is bigger in females than males
what does the genetial tubercle become in males and females
males- glans penis
female- clitoris
what does genital fold become in males and females
males- urethral fold
female- labia minora and urethral and vaginal orifices
what does teh genital sweliing become in males and females
males- scrotum
females- labia majora
what causes sexual growth in males and females
males-dihydrotestosterone
females- oestrogen
what are the 3 main sex steroids and where are they foudn
androgen- testosterone from testes and adrenal cortex
oestrogen- ovaries, placenta, testosterone
progestins- ovaries and placenta
do LH and FSH stimulate the release of testosterone , oestrogen and progesterone
yes
also stimulate gonadal development
what 3 main activities are controlled by the reproductive cycle
- ovarian cycle- oocyte maturation
- uterine cycle- suitable implantation environment
- cervical cycle- controls sperm entry
does meiosis occur before or after sperm and ova formation
before
what does oocyte meisosis produce
1 daughter cell and one polar body which degrades
what does rising GnRH levels stimulate
production of FSH and LH from the anterior pituitary
what does FSH stimulate in oogenesis
growth of follicular cells and so production of oestrogen
more cells= more oestrogen
what does LH stimulate cells to produce in oogenesis
androgens and ovulation
proliferative phase- follicular
oestrogen increase from maturing follicles
oestrogen activity increases growth of uterine lining to prepare implantation
oestrogen stimulates GnRH
secretive phase - luteal
inhibition of FSH and LH by inhibin and progesterone with oestrogen
progesterone from maturing follicles then the corpus luteum after ovulation
p and e increase growth of uterine lining
p stimulates secretion of nutritive substance to support early pregnancy
periovulatory/ovulatory phase
oestrogen increase changes mucus fibres to a more linear conformation to allow sperm to go up and follow
mucuc more fluid and slippery
mucus alkaline to promote sperm survival
sperm can survive several days in cervix
luteal phase in cervical cycle
progesterone thickens cervical mucus creating plug trapping sperm
p H changes
what causes menstration
falling levels of P,E and inhibin as a result of no pregnancy and an increase in GnRH
how long does sperm production take
65-75 days - genetically controlled
6 stages of sperm
A-spermatogonium
B-spermatogonium
primary spermatocyte
secondary spermatocyte
spermatid
sperm cell
the number of spermatogonic stem cells stimulated is controlled by what
endocrine system
what type of barrier is a sertoli cell
tight junction
how quick is early pregnancy factor found in bloodstream after conception
hours
what is early pregnancy factor
immunosuppressant that helps stimulate trophoblast (placental) growth during peri-implantation period
what hormones increase when become preganant
progesterone
oestrogen
human chorionic gonadtrophin (hCG)
to maintain pregnancy
what hormones decrease when pregnant
gonadotrophin releasing hormone (GnRH)
follicle stimulating hormones (FSH)
luteinising hormone (LH)
as no ovulation anymore
steps of sea urchin feritlisation
contact
acrosomal reaction
contact and fusion of sperm/egg membranes
cortical reaction
entry of sperm nucleus
acrosomal reaction of sea urchin fertilisation
hydrolytic enzymes release from acrosome
make hole in jelly coat
actin form which protrude from sperm head and penetrate jelly coat
proteins on surface bind to receptors in the egg plasma membrane
fusion and contact of sea urchin fertilisation
fusion triggers depolarization of membrane which acts as a fast block to polyspermy
as fusion opens na channels to open and changes in plasma membrane = no more sperm fusion
cortical reaction in sea urchin fertilisation
slow block to polyspermy
cortical granules in egg fuse with PM
clip of sperm binding receptors and cause fertilisation envelope to from
calcium wave when sperm binds to egg
it activates a signal transduction pathway triggering release of Ca2+ into the cytosol from the ER
entry of sperm into nucleus of sea urchin fertilization
cortical granules fuse with PM
release enzymes that breakdown adhesion between vitelline layer and membrane, increase osmotic pressure causing water influc, snip off sperm receptors, harden fertilisation envelope
what stage is human eggs arrested at in meiosis
metaphase of meiosis 11
what does ovulation release
secondary oocyte and the first polar body
what is teh secondary oocyte and first polar body surrounded by
zona pellucida- glycoprotein
corona radiata- multicellular
both layers must be penetrated by sperm
does human fertilisation require multiple sperm to interact with the egg
yes
what do sperm first contact
corona radiata
follicle cells
human fertilisation steps
contact
acrosomal reaction to digest zona pellicuda
fusion of membranes and sperm enters
block to polyspermy
what does zona pellucida glycoprotein ZP3 bind to
b 1-4 galactosyltransferase on sperm
triggers acrosomal contents release
what acrosomal enzymes digest zona pellucida glycoproteins
acrosin
b-N-acetylglucosaminidase
so gains acess to cell membrane
what binds to integrin-like proteins and CD9 in secondary oocytes plasma membrane
fertilin on sperm head
allows membrane fusion
blocking polyspermy in humans
release of intracellular Ca2+ = exocytosis of oocyte secretory vesicles to harden zona pellucida
how do the sperm makes gaps in corona radiata and zona pellucida
acrosomal enzymes and strong flagella movements from multiple sperm
what happens after sperm absorbed into cytoplasm
meiosis 11 continues
secondary oocyte splits into 2 haploid cells- ovum and second polar body
female pronucleus develops
what happens after female pronucleus forms
male one forms
spindle fibres from centromere appear in preparation for first cleavage division
hows the zygote formed
each pronucleus mitosis separately
nuclear membranes break down and they fuse to form zygote
embryogenesis
cleavage
gastrulation
cleavage simple definition
cell division in early embryo
gastrulation simple
cell movements which produce gut and 3 primary germ layers
phases of early embryonic cell cycle vs somatic cell cycle
early has 2 phases, S and M
somatic has 4, S,M,G1,G2
sea urchin cleavage
rapid division
blastomeres all same size and become smaller with each division
holoblastic cleave(divisions divide entire cell)
amphibian cleavage
unequal holoblastic division
blastomere in animal pore are smaller than blastomeres in vegetal pole because of yolk in vegetal hemisphere
chick cleavage
meroblastic cleavage= cleavage plane does not bisect yolk
what comes after cleavage stage
blastula formation
the 3 primary germ layers
ectoderm
mesoderm
endoderm
major derivatives of ectoderm
epidermis
nervous system
pituitary gland
adrenal medulla
jaw and teeth
germ cells
major derivative of mesoderm germ layer
notochord
muscular, skeletal, circulatory, lymphatic systems
excretory and reproductive systems
dermis of skin
endoderm major derivatives germ layer
epithelial lining of gut and associated organs
epithelial ling of respiratory, excretory and reproductive tract
when does the first cleavage division occur
24-30 hrs after fertilisation
what happens in first cleavage division
holoblastic division
2 blastomeres formed
at 32 cell stage what happens
now a blastocyst
blastocoel formation
when does the morula enter the uterus
day 4-5
what is required before implantation
hatching
the blastocyst digests a hole in the zona pelucida and emerges
does the inner cell mass develop into the embryo in a blastocyst
yes
how does a blastocyst implant
secrete enzymes to burrow into endometrium
what happens to inner cell mass after implantation
rearranges into 2 layers
bilaminar embyronic disc hypoblast and epiblast layers
what happens day 12-15 gastrulation
primative streak forms in dorsal epiblast and defines anterior/posterior and left/right of embryo
cells from primative node produce notochord
where di neural cres cells migrate
migrate on cranial, dorsolateral and ventral pathways
very highly migratory invasive and proliferate
what are neural crest cells
specialist migratory populations
highly migratory, invasive proliferative
include melanocytes called malanoblast
induction definition
where the fate of one cell is influenced by another
how do cells know where they are on the body plan
example of induction
spemanns organiser
spemmans organiser
transplantation of a second organiser causes induction of another joined entire embryo.
developmental fate of host has been altered by transplanted dorsal lip of the blastomere (the organiser)
how does the organiser alter cell fate
BMP-4 is distributed in late bastula and causes ventral development
what stops action of BMP-4 allows dorsal development
chordin and noggin
where is BMP-4 expressed
throughout the Xenopus blastula
what does the neural plate from
prospective ectoderm where BMP signalling is inhibited by antagonists release by spemanns organiser
what induces neural fate
BMP antagonists
fibroblast growth factors are also needed for neural plate formation
chick neural plate induction
FGF activated churchill gene causes activation of Sox2
anterior part of hand
thumb
posterior part of hand
little finger
proximal part of and
wrist
distal part of hand
finger tips
ventral part of hand
palm
dorsal part of hand
back of hand
what AER- apical ectodermal ridge- required for
limb outgrowth
secretes fibroblasts growth factors family proteins
what does ZPA- zone of polarising activity- control
anterior-posterior digit formation via induction
how do we know zone of polarising activity controls anterior posterior digit formation
sonic hedgehog (Shh) cells are implanted into anterior of developing limb bud can induce mirror image digit formation
is sonic hedghog a morphogen
yes
definition of sonic hedgehog
substance non uniform distribution governs the pattern of tissue
- establishes positions of various cell types
- signalling molecule that acts on cells to produce specific cellular responses
how long is a pregnancy
40 weeks
240 days
10months
38+ weeks approx
when does preorganogenesis happen LMP
2-4 WEEKS
When does the embryonic period happen LMP
3-10weeks
when does fetal period begin
11 weeks LMp
external risks in first trimester
drugs
alcohol
workplace/environment
excess vit A
low folic acid
miscarriage
spina bifida- neural tube closure failure
limb and cardiac syndromes
systemic syndrome- e.g rubella virus
spina bifida
failure to close neural tube
most likely at spinal closure points at top and bottom
exposure to amniotic fluid causes degeneration of neural tissue in extreme cases
rubella virus syndrome
mild in adults-rash/itching
MMR prevents
postnatal- cataract, glaucoma, bilateral deafness, congenital heart disease, mental and physical disabilities
when does hCG become detectable in blood
4 weeks
maternal changes in pregnancy examples
organ squashing
respiratory function ^
digestive problems
weight gain
^hr and stroke volume
increased urination
breast enlargment
why does respiratory function increase for mother during pregnancy
tidal volume increase
why do digestive problems increase for mother during pregnancy
GI motility decreases (hormonal effects)
why does weight increase for mother during pregnancy
fetus, placenta, uterus, increase blood volume , increase breast size, increase storage of protein and fat
why does hr and stroke volume increase for mother during pregnancy
hr increases by 10-15%, BV increase
why does breast size increase for mother during pregnancy
increase in oestrogen promote tissue development
gestational trophoblastic tumours
problem in implantation and placenta
rare
overgrowth of trophoblast
lack of genetic material to form embryo
benign
pregnancy growth looks bigger than stage
ectopic pregnancy
1:90
implantation in uterine tubes
‘normal’ pregnancy signs
unilateral pain, shoulder pain, vaginal bleeding or discharge
pregnancy has to be terminated
tube rupture can be fatal
pre-eclampsia
mild- 1-5:100
severe- 1:200
from 20 weeks or post-birth
high blood pressure and proteinuria
headache vision problems, vomiting and swelling
may induce early
implantation problem
gestational diabetes
4-5:100
thirst, hunger, tiredness, sugar in urine
insulin resistance
late pregnancy problem
gestational hypothyroidism
2.5:100
problem in late pregnancy
decreased TSH levels
difficult to detect as normal pregnancy symptoms
obstetric cholestasis
pruritis (itching), leakage of bile salts into blood stream
more common in multiple pregnancies
late pregnancy problems
gestational transient thyrotoxicosis
late pregnancy problems
2-11:100
vomiting
weight loss
tremors
increased T4 levels
may resolve at 20 weeks
associated with hyperemesis gravidarum
where does implantation usually happen
anterior or posterior wall anywhere really
usually in upper quadrants
generally between secretory glands
fully embedded by d14
what happened after blastocyst implants
outer cells differentiate and set up 2 layers
the cyotrophoblast
syncytiotrophoblast
cytotrophoblast
more densely packed cells with more obvious cell structure
will create the villi of the placenta
syncytiotrophoblast
outer invasive cells
not dense but not loose
form gaps holes - lacunae
creates layer separating the fetus from maternal blood
what forms in syncytiotrophoblast (lacunae)
vacuoles begin to form
what happens after implantation and formation of vacuoles and extrambryonic membranes
(d13, d27LMP)
extraembryonic cavity grows and expand
mesoderm crosses at umbilical stalk to line the extraembryonic cavity to create chorin
syncytiotrophoblast produces hCG
cytotrophoblast forms villi invading the syncytiotrophoblast
maturation of the placenta
villi increase at the fetus form the chorion frondosum and create the placenta for exchange
amnion and chorion fuse
chorion laeve opposite the fetus is smooth and fuses the uterine wall
placental circulation
meternal blood flows into intervillous lakes
chorionic villi grow into lakes
into embryonic heart via umbilical arteries
fetus picks up o2 and nutirents from maternal blood
does fetal (Hb) or mothers blood have higher affinity foro2
fetal blood (Hb) is higher
placenta function
protection
support growth- gas exchange, nutrition, waste
hormone production - hCG, p,e, placental prolactin, lactogen, relaxin
haemolytic disease of the fetus
when mother is Rh and father is Rh+ resulting in Rh+ baby
immune response resulting in attack on fetal blood cells
does fertilisation occur in pre-organogenesis
yes
situs inversus
1:10 000
reversal of internal organs
may be underdiagnosed worldwide
situs ambiguous
partial malrotation
contributes to 3% of congenital heart disease
sacrococcygeal teratoma
origins in primitive streak
1:40 000
condition from early events
what happens in embryogenesis
4-6-weeks
somites develop- will become torso MSK system
blood vessel form
heart tubes starts to beat in week 5
neural tube closure
heart valves form
limb buds
cardiac development of fetus
starts of as a cardiac tube
swells and loops to form more complex compact structure
growth in specific areas leads to separation of the tube into 4 chambers
week 6-8 LMP
brain development
gut tube form
ureteric bud
limbs have distinct regions
craniofacial development
week 8-12 LMP
embryo transitions to fetus
tooth buds
ossification of long bones
pituitary forms
separation of heart
kidneys produce ‘urine’
external genitals incomplete
fetal reflex
bile produced
omphalocoele
problems in week 8-12LMP
2.5:10 000
GIT fails to return to body cavity after physiological herniation
assocatied with other conditions
week 12-16 LMP
first to second trimester
heart beat
fetal ‘breathing’
antibody production
face nearly developed
external genetalia
pregnancy bump may be visible
main problems in week 12-16 LMP
eye problems
ear problems
teeth problems
immune system
brain development
week 16-20 LMP
fetal development
myelination of neurones
circulation
meconium collects in bowels
sleep and wake periods
brown fat laid down- vernix forms on skin
placental development complete
what hormones stimulate labour
oestrogen - excitability
prostaglandins
relaxin
corticotrophin releasing hormone
3 stages of labour
dilation
expulsion
placental expulsion
dilation in labour
10cm
2-6/h
30s duration
amniochorion reptures
expulsion stage of labour
contractions every 2-3 mins
60 sec duration
placental expulsion stage of labour
sustained contraction
atelactasis
problem at birth
alveolar collapse
not enough surfactant
common in preterm births
can lead to respiratory distress syndrome
transient tachypnea
problems at birth
0.5-4% of all neonates
retention of lung fluid
resolves with o2 therapy and antibiotic treatment
is unregulated fertility a contributor of infertility
yes
what is control of fertility about
chossing when to have a family and what size of family
allowing people to have families who would otherwise experience difficulties
infertility definition
when a couple has been trying to conceive for 12 months (sex every 2-3 days)
when is a person eligible for treatment for infertility
2 years
may be sooner if secondary infertility
also could be sooner dependent on age
how many people and couples are affected by infertility
88 million couples
186million individuals
are infertility rates the same worldwide
no
irregulated fertility= infertility
do majority of people experience infertility with their first or second child
already had a child experience more infertility
physical reasons for experiencing infertility with a second child
age
worsened underlying conditions
weight increase
scarring
fibroids
pelivc inflammatory disease (PID)
could also be psychosocial, pressure, less support from communit
fertility treatments requirements
donation/extraction of sperm or oocytes
synchronisation cycles
surrogate parent if needed
AI
artificial insemination
inseminated with epididymal sperm
treats infertility, paraplegia, long separation or illness, same sex couples, single women, post-mortem
15-30% success
cheaper than IVF
what does IUI stand for
intrauterine insemination
sperm placed high in uterus
60-70% success over r6 cycles
more successful for younger women
success dependent on sperm count, quality
in vitro fertilisation (1970s)
louise joy brown conveived by IVF in Oldham General Hospital
sperm and egg removed and fertilised outside body
healthy embryo implanted in uterus
IVF eligibility and success
2 years unsuccessful conceiving
under 43
has 12 unsuccessful rounds of IUI
retrieving eggs for donation or IVF
GnRH agonists to inhibit pituitary and LH/FSH release
exogenous hormones to control ovulation
ultrasound for monitoring and harvesting transvaginally
hormones given to prepare uterus
in vitro fertilisation - when the eggs taken out body step
incubation with sperm for 12-16 hrs
evidence of a polar body means healthy zygote
preimplantation genetic testing
cultured for several days until blastocyst forms
transgender IVF
transwomen need clomiphene or hCG injections to stimulate sperm production
transmen need to come of testosterone(3-6months)
will have effect on mood and mental health
problems with IVF
emotional
expensive
invasive/uncomfortable
superovulation-multiple babies
ectopic
ovarian hyperstimulation syndrome
ovarian hyperstimulation syndrome (OHSS)
increased permeability of capillaries
oedema- tissue and pulmonary
renal failure
8% mild
<1% severe
why is sperm retreival needed sometimes
vasectomy
STD like chlamydia
chemo]unable to ejaculate
antibodies to sperm
how do antibodies to sperm arise
male- vasectomy, damage to sperm-blood barrier, dysfunction of sertoli cells
female- damage to mucosal membranes, exposure to sperm in the digestive tract , infection
ICSI- intracytoplasmic sperm injection
done when sperm is poor motility, low number, abnormal morphology, frozen
sperm is injected straight into harvested egg
FET - frozen embryo transfer
problems with implantation
if a number of high quality embryos were collected but further full treatment is not an option
for future years
