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yr 1 uni work > 124 > Flashcards

124 Flashcards

1
Q

why are signalling systems needed

A

coordinate the activities of cells/tissues in a multi-cellular organism
- neurotransmission
- coordination of developmental processes
- homeostasis

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2
Q

types of signalling between cells

A
  1. free diffusion between cells
  2. via cytoplasmic connections
  3. direct cell-to-cell contact
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3
Q

3 types of signalling by free diffusion

A

autocrine
paracrine
endocrine

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4
Q

autocrine

A

signalling and reception by the same cell
cell secretes chemicals that modify its own behaviour
associated with growth regulation

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5
Q

paracrine

A

signalling between nearby cells
effects local and short-lived
important in coordinating the actions of neighbouring cells in embryonic development

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6
Q

endocrine - signalling by free diffusion

A

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

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7
Q

synaptic signalling

A

highly specific
localized type of paracrine signalling between 2 nerve cells or between a nerve and muscle cell

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8
Q

signalling via cytoplasmic connections is the fastest mode of cell-cell communication
t/f

A

true

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9
Q

how do signals transfer from one cell to its neighbour in signalling via cytoplasmic connections

A

through pores in the membrane

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10
Q

what does signalling by cell-to-cell contact involve

A

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

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11
Q

2 types of signalling molecules

A

local regulators- act on cells in the vicinity(auto/paracrine)
hormones- act at distance(endocrine)

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12
Q

4 local regulators

A

growth factors
gases
prostaglandins
neurotransmitter

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13
Q

growth factors as a local regulator

A

peptides or proteins that stimulate cell proliferation
may have >1 target cells and hence >1 function
e.g. nerve growth factor

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14
Q

gases as a local regulators

A

NO acts as a paracrine signal molecule
synthesized from arginine by NO synthase
induces vasodilation

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15
Q

prostaglandins as local regulators

A

modified fatty acids
multiple functions:
- excitability of uterine wall during childbirth
- induction of fever and inflammation in immune system

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16
Q

neurotransmitter as a local regulators

A

acetylcholine
biogenic amines
amino acids
neuropeptides
either inhibitory or exhibitory and some both
some occur in both CNS or PNS

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17
Q

how are hormones transported

A

bloodstream

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18
Q

what is hormone production contolled by

A

neuroendocrine system
hypothalamus is control centre

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19
Q

homeostasis definition

A

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

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20
Q

what happens if blood glucose is high

A

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

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21
Q

what happens when blood glucose is too low

A

alpha cells in pancrease stimulate to release glucagon into the blood
liver breaks down glycogen and releases glucose
blood glucose rises

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22
Q

2 main classes of hormones

A

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

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23
Q

signal transduction pathway

A

the conversion of a signal at the cell surface to a specific cellular response is a multi-step process

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24
Q

what are the 3 main stages of signal transduction

A
  1. reception of the signal at the cell surface- binds receptor changing receptor conformation
  2. transduction of the signal- multistep pathway providing more opportunities for coordiantion and regualtion
  3. cellular response
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25
Q

where does the cellular response occur

A

occur in the cytoplasm or may involve action in the nucleus

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26
Q

what does the cellular response in signal transduction regulate

A

regulate activity of enzymes
other pathways switch on genes by activating transcription factor

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27
Q

signal specificity in signal transduction

A
  • 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
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28
Q

3 stages of cell signalling

A

reception
transduction
response

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29
Q

reception in cell signalling

A

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

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30
Q

ligands

A

the signalling molecules
i.e. it is a small molecules that binds to a larger one

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31
Q

what can lingand binding lead to

A

a change in the shape of a protein or aggregation of 3 or more receptors- enables receptor to interact with other mmoleclues

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32
Q

hydrophilic messengers

A

water soluble
too large to go through membrane
detected by membrane bound receptors

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33
Q

hydrophobic messenger

A

can move through lipid environment of the PM so signal receptors can be located inside the cell

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34
Q

the 3 main types of membrane receptors

A

g-coupled receptors
receptor tyrosine kinases
ion channel receptos

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35
Q

whats the largest family of cell-surface receptors

A

G-protein coupled receptors (GPCRs)

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36
Q

a GPCR is a plasma membrane receptor that spans the membrane as 8 a helices
t/f

A

false - its 7 a helices

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37
Q

what can G proteins bind

A

guanine nucelotides- GTP (guanine triphosphate) and GDP (guanine diphosphate)

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38
Q

is G protein a molecular switch

A

yes
its either of or on

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39
Q

what happens when GDP is bound to the G protein

A

G protein is inactive
switch is off

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40
Q

what happens when GTP is bound to G protein

A

G protein is activated
the switch is on

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41
Q

where is G protein found

A

loosely attached to cytoplasmic side of the cell membrane

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42
Q

how does an enzyme get activated from g protein

A

activated G protein dissociates from GCPR
binds to enzyme
causes change in shape and activity of enzyme- activation leads to cellular response
is reversible

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43
Q

how are changes in enzyme and G protein only temporary

A

because the G protein also functions as a GTPase enzyme (GTP to GDP)
returns G protein to inactive
G protein now available for reuse

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44
Q

wheres epinephrine/adrenaline released from

A

adrenal glands

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45
Q

what does epinephrine/adrenaline stimulate

A

glycogen breakdown in liver and skeletal muscle during stress

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46
Q

are receptor tyrosine kinases (RTKs) membrane bound

A

yes

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47
Q

how do RTKs differ from GPCRs

A

they have intrinsic enzyme activity

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48
Q

what does receptor tyrosine kinase(RTKs) do

A

add phosphate residues onto other proteins
can trigger multiple signals transduction pathways at once

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49
Q

what is abnormal functioning of RTKS associated with

A

many types of cancers

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50
Q

receptor tyrosine kinase activation

A

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

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51
Q

herceptin

A

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

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52
Q

what do ligand-gated ion channels act as

A

a gate
creats a pore in PM that can open or close in response to extracellular chemical messenger

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53
Q

ligand-gated ion channels how does it open and close

A

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

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54
Q

example of ligand-gated ion channels

A

neurotransmitter molecules released at synapse
binds as ligand on recieving cell
ions flow in or out triggering electrical signal

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55
Q

verapamil

A

calcium channel blocker
treats hypertension and cardiovascular disorders

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56
Q

lamictal

A

sodium channel blocker
treats epilepsy

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57
Q

lidocaine

A

sodium channel blocker
local anaethetic

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58
Q

glipizide

A

potassium channel blocker
treats diabetes

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59
Q

where are intracellular receptor proteins found

A

cytosol or nucleus of target cells

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60
Q

can intracellular receptors cross membrane

A

yes as they are small or hydrophobic

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61
Q

what do intracellular recpetors do

A

activate receptors

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62
Q

example of hydrophobic intracellular receptors messengers

A

steroid and thyroid hormones for animals

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63
Q

can hormone receptor complex act as a transcription factor

A

yes
it can turn on specific genes

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64
Q

does testosterone activate intracellular receptor

A

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

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65
Q

what does protein kinase transfere phosphates from from ATP to

A

protein
called phophorylation

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66
Q

where does phosphorylation most commonly occur

A

on serine, threonine(or tyrosine) residues

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67
Q

does phosphorylation noramaly lead to protein protein activation

A

yes

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68
Q

what do protein phosphates do

A

remove phosphates from proteins
dephosphorylation

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69
Q

The extracellular signal molecule (ligand) that binds to the receptor is a pathway’s “first messenger
t/f

A

true

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70
Q

second messenger properties

A

small
nonprotein
water soluble
readily spread through ac cell by fiddusion

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71
Q

what pathways do second messengers participate in

A

pathways initiated by GPCRs and RTKs

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72
Q

common second messenger examples

A

cyclic AMP
calcium ions

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73
Q

where is adenylyl cyclase found

A

as an enzyme in the plasma membrane

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74
Q

what does adenylyl cyclase convert ATP into

A

cAMP

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75
Q

what is cAMP broken down by to form what

A

broken down by phosphodiesterase to form AMP which is inactive

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76
Q

other components of cAMP pathways

A

G-proteins
GPCR
protein kinases

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77
Q

what bacteria causes cholera

A

vibrio cholerae

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78
Q

hwo do you get cholera

A

drinking water containg bacteria

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79
Q

where doe cholera colonise

A

small intestines
form a biofilm and produce an enzyme that acts as a toxin

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80
Q

what G-protein does cholera affect

A

a g-protein involved in regulating salt and water excretion

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81
Q

what does cholera activating a g-protein do to activation of adenylate cyclase

A

g-protein no unable to hydrolyse GTP-GDP
leads to constant activation of adenylate cyclase and continuous production of cAMP

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82
Q

what does high levels of cAMP do

A

activate cystic fibrosis transmembrane conductance regulator
efflux of cl- and h2o leading to watery diarrhoea

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83
Q

under normal conditions what conc is intracellular calcum

A

very low

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84
Q

where is calcium activelty pumped to keep cytoplasmic concs low

A

ER
mitochondria
or chloroplasts in plants

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85
Q

what pathways lead to the release of calcium

A

pathways involving inositol triphosphate (IP3)
diacylglycerol (DAG) as additional second messengers

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86
Q

how many binding sites does calmodulin have

A

4 calcium binding site

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87
Q

what does calmodulin regualte

A

protein phosphates and kinases
also regulates adenylyl cyclases and phosphodiesterase
PM Ca2+ - ATPase is also activated by Calmodulin

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88
Q

the 4 aspects of fine-turning

A
  • amplifying the signal
  • specificity of response
    -efficiency of response enhanced by scaffolding proteins
  • termination of the signal
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89
Q

scaffolding proteins

A

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

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90
Q

how are signals terminated

A

if ligand concentration falls then fewer receptors will be bound
unbound receptors revert to an inactive state

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91
Q

functions of the hypothalamus

A

-secretion of regulatory hormones to control activity of anterior pituitary
- control of sympathetic output to adrenal medulla
- production of ADH and oxytocin

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92
Q

adenohypophyis formation

A

formed by Rathke pouch (3rd week)- ectodermal derived evagination from roof of oral cavity

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93
Q

communication from hypothalamus to the anterior pituitary gland

A

regulatory hormones from hypothalamus transported via the hypophyseal portal system

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94
Q

regulation by hypothalamus and pituitary example broad

A

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

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95
Q

examples of hormones relesed from anterior pituitary

A

TSH
ACTH- adrenocorticotropic
FSH- follicle
luteinising (LH)
prolactin (PRL)
(GH)
MSH- melanocyte

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96
Q

tropic hormones released from anterior pituitary

A

TSH
ACTH
FSH
LH
GH(both tropic and non tropic effects

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97
Q

whats a topic hormone

A

regulate function of endocrine cells/ glands

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98
Q

what does melanocyte stimulating hormone (MSH) do

A

regulates pigment containing cells
amphibians, fish
reptiles
some mammals

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99
Q

does MSH/ Ghrelin regulatte appetite

A

yes

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100
Q

whats released to reduce appetite

A

POMC released into pars-intermedia
stimulates hypothalamic neurons and reduces appetite

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101
Q

whats released to increase appetite

A

released by the stomach and stimulates hypothalmic neurons in ARC to increase appetite

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102
Q

what glycoprotein controls release of TSH

A

TRH

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103
Q

what does TSH stimulate teh release of

A

T3 and T4 from the thyroid

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104
Q

what do T3 and T4 inhibit release of to cause negative feedback

A

TRH and TSH
negative feedback

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105
Q

what causes release of ACTH from anterior pituitary

A

CRH

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106
Q

is ACTH a carbohydrate

A

no its a peptide

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107
Q

what does ACTH simulate

A

adrenal cortex to release glucocorticoids

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108
Q

what do glucocorticoids have a negative feedback on

A

CRH and ACTH

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109
Q

are FSH and LH glycoproteins

A

yes

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110
Q

what controls FSH and LH prodcuction

A

gonadotropin releasing hormones (GnRH)

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111
Q

what does FSH and LH promotes

A

egg and sperm production and secretion of sex steroids

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112
Q

what inhibits FSH production in both sexes

A

inhibin

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113
Q

what might inhibit GnRH release

A

inhibin

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114
Q

is prolactin a peptide

A

yes

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115
Q

what is prolactin release stimulated by

A

prolactin releasing factor (PRF)

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116
Q

what is prolactin inhibited by

A

prolactin inhibiting hormones (PIH, dopamine)

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117
Q

what does prolactin do

A

stimulate milk production

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118
Q

is GH peptide

A

yes

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119
Q

what is GH release stimulated by GHRH - growth hormone-releasing hormones

A

GHRH - growth hormone-releasing hormones

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120
Q

what is GH release inhibited by

A

growth hormone-inhibitory hormone (GHIH)(somatostatin

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121
Q

what does GH stimulate

A

somatomedin production

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122
Q

what does somatomedin stimulate

A

bone and cartilage growth
fat and glycogen breakdown, increasing blood glucose levels

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123
Q

pituitary gigantism

A

excess GH before puberty

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124
Q

acromegaly

A

excess GH after puberty
bones of hands feet cheeks and jaws thicken

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125
Q

pituitary growth failure

A

lack of GH

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126
Q

what hormones are produced from posterior pituitary

A

ADH
oxytocin

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127
Q

ADH and the nephrons

A

binds to receptors in DCT
increases expression of aquaporin 2 channel in DCT
concentrated urine

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128
Q

what does oxytocin stimulate

A

milk ejection by mammary glands
uterine contractions during childbirth
targets in brain influencing behaviour e.g. pair bonding, maternal cae, sexual activity

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129
Q

t3 long name

A

triiodothyronine
more active than t4

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130
Q

t4 long name

A

thyroxine

131
Q

is t3 or t4 more active

A

t3

132
Q

what do thyroid stimulating cells synthesise

A

thyroglobulin which is rich in tyrosine AAs

133
Q

what happens when thyroid hormones are needed

A

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

134
Q

what does TSH stimulate

A

iodide uptake ]thyroglobulin and thyroid peroxidase synthesis
uptake of thyroglobulin

135
Q

development functions of thyroid hormones

A

metamorphosis in frogs ]bone formation]brain

136
Q

metabolism functions of thyroid hormones

A

increase metabolic rate
increase ATP production
stimulates glycolysis
increased heart rate and bp

137
Q

congenital hypothyroidism

A

poor skeletal and nervous developemnt
low metabolic rate
low bod temp
children/babies

138
Q

hypothyroidism in adults

A

MYXOEDEMA
symptoms- lethargy
low body temp
muscle weakness
subcutaneous swelling
dry skin
hair loss
enlarged thyroid
could be cuased by low dietary iodine

139
Q

hyperthyroidism

A

high metabolic rate
high body temp
sweating
high heart rate and bp
CNS effects - excitability, restlessness, mood swings

140
Q

what do thyroid C cells release

A

calcitonin
released in response to high calcium levels in teh blood

141
Q

what does calcitonin inhibit

A

osteoclast activity inhibited (bone breakdown)
increases uptake of calcium into bone
so decreases blood calcium level

142
Q

what are the 2 kinds of epithelial cells in parathyroid gland

A

principal (chief) cells which produce PTH
oxyphil cells- function unknown

143
Q

what dies the adrenal cortex contain

A

corticosteroids

144
Q

what does adrenal medulla contain

A

adrenaline and noradrenaline

145
Q

layers of adrenal cortex

A

zona reticularis- next to medulla
zona fasciculata
zoan glomerulosa

146
Q

what does zona reticularis contain

A

androgens e.g. testosterone

147
Q

what does zona fasciculata in adrenal cortex contain

A

glucocorticoids e.g. cortisol

148
Q

what does zona glomerulosa in adrenal cortex contain

A

mineralcorticoids
e.g. aldosterone

149
Q

what do glucocorticoids stimulate

A

glucose and glycogen synthesis
release of fatty acids
cause tissues to breakdown fatty acids and proteins

150
Q

are glucocorticoids immunosuppresive

A

yes

151
Q

glucocoricoids are not anti-inflammatory t/f

A

false they are anti-inflammatory

152
Q

what does the adrenal medulla do

A

breakdown glycogen to glucose
changes in circulation
increase heart rate
dilate air passages in lungs, increase respiratory rate

153
Q

short term stress what does the adrenal medulla secrete

A

epinephrine and norepinephrine

154
Q

in long term stress what does the adrenal cortex secrete

A

mineralcorocoids
glucocorticoids

155
Q

what is the development of the internal and external reproductive system controlled by

A

genotype
horones

156
Q

at 20 weeks whatt does a lack of testosterone lead to and the maintained oestrogen

A

degeneration of mesonephric duct
oestrogen maintains the paramesonephric duct

157
Q

what does the paramesonephric duct become in women

A

oviducts
uterus
upper parts of vagina

158
Q

what maintains mesonephric duct at week 16 of males

A

testoterone and receptors

159
Q

waht does the mesonephric duct become in males at 16weeks

A

epididymis and vas deferens

160
Q

what stimulates teh degeneration of paramesonephric ducts at 16 weeks in males

A

anti-mullerian hormones (AMH)

161
Q

at 7 weeks teh genital tubercle is bigger in males than females
t/f

A

false
tubercle is bigger in females than males

162
Q

what does the genetial tubercle become in males and females

A

males- glans penis
female- clitoris

163
Q

what does genital fold become in males and females

A

males- urethral fold
female- labia minora and urethral and vaginal orifices

164
Q

what does teh genital sweliing become in males and females

A

males- scrotum
females- labia majora

165
Q

what causes sexual growth in males and females

A

males-dihydrotestosterone
females- oestrogen

166
Q

what are the 3 main sex steroids and where are they foudn

A

androgen- testosterone from testes and adrenal cortex
oestrogen- ovaries, placenta, testosterone
progestins- ovaries and placenta

167
Q

do LH and FSH stimulate the release of testosterone , oestrogen and progesterone

A

yes
also stimulate gonadal development

168
Q

what 3 main activities are controlled by the reproductive cycle

A
  1. ovarian cycle- oocyte maturation
  2. uterine cycle- suitable implantation environment
  3. cervical cycle- controls sperm entry
169
Q

does meiosis occur before or after sperm and ova formation

A

before

170
Q

what does oocyte meisosis produce

A

1 daughter cell and one polar body which degrades

171
Q

what does rising GnRH levels stimulate

A

production of FSH and LH from the anterior pituitary

172
Q

what does FSH stimulate in oogenesis

A

growth of follicular cells and so production of oestrogen
more cells= more oestrogen

173
Q

what does LH stimulate cells to produce in oogenesis

A

androgens and ovulation

174
Q

proliferative phase- follicular

A

oestrogen increase from maturing follicles
oestrogen activity increases growth of uterine lining to prepare implantation
oestrogen stimulates GnRH

175
Q

secretive phase - luteal

A

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

176
Q

periovulatory/ovulatory phase

A

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

177
Q

luteal phase in cervical cycle

A

progesterone thickens cervical mucus creating plug trapping sperm
p H changes

178
Q

what causes menstration

A

falling levels of P,E and inhibin as a result of no pregnancy and an increase in GnRH

179
Q

how long does sperm production take

A

65-75 days - genetically controlled

180
Q

6 stages of sperm

A

A-spermatogonium
B-spermatogonium
primary spermatocyte
secondary spermatocyte
spermatid
sperm cell

181
Q

the number of spermatogonic stem cells stimulated is controlled by what

A

endocrine system

182
Q

what type of barrier is a sertoli cell

A

tight junction

183
Q

how quick is early pregnancy factor found in bloodstream after conception

A

hours

184
Q

what is early pregnancy factor

A

immunosuppressant that helps stimulate trophoblast (placental) growth during peri-implantation period

185
Q

what hormones increase when become preganant

A

progesterone
oestrogen
human chorionic gonadtrophin (hCG)

to maintain pregnancy

186
Q

what hormones decrease when pregnant

A

gonadotrophin releasing hormone (GnRH)
follicle stimulating hormones (FSH)
luteinising hormone (LH)

as no ovulation anymore

187
Q

steps of sea urchin feritlisation

A

contact
acrosomal reaction
contact and fusion of sperm/egg membranes
cortical reaction
entry of sperm nucleus

188
Q

acrosomal reaction of sea urchin fertilisation

A

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

189
Q

fusion and contact of sea urchin fertilisation

A

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

190
Q

cortical reaction in sea urchin fertilisation

A

slow block to polyspermy
cortical granules in egg fuse with PM
clip of sperm binding receptors and cause fertilisation envelope to from

191
Q

calcium wave when sperm binds to egg

A

it activates a signal transduction pathway triggering release of Ca2+ into the cytosol from the ER

192
Q

entry of sperm into nucleus of sea urchin fertilization

A

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

193
Q

what stage is human eggs arrested at in meiosis

A

metaphase of meiosis 11

194
Q

what does ovulation release

A

secondary oocyte and the first polar body

195
Q

what is teh secondary oocyte and first polar body surrounded by

A

zona pellucida- glycoprotein
corona radiata- multicellular
both layers must be penetrated by sperm

196
Q

does human fertilisation require multiple sperm to interact with the egg

A

yes

197
Q

what do sperm first contact

A

corona radiata
follicle cells

198
Q

human fertilisation steps

A

contact
acrosomal reaction to digest zona pellicuda
fusion of membranes and sperm enters
block to polyspermy

199
Q

what does zona pellucida glycoprotein ZP3 bind to

A

b 1-4 galactosyltransferase on sperm
triggers acrosomal contents release

200
Q

what acrosomal enzymes digest zona pellucida glycoproteins

A

acrosin
b-N-acetylglucosaminidase
so gains acess to cell membrane

201
Q

what binds to integrin-like proteins and CD9 in secondary oocytes plasma membrane

A

fertilin on sperm head
allows membrane fusion

202
Q

blocking polyspermy in humans

A

release of intracellular Ca2+ = exocytosis of oocyte secretory vesicles to harden zona pellucida

203
Q

how do the sperm makes gaps in corona radiata and zona pellucida

A

acrosomal enzymes and strong flagella movements from multiple sperm

204
Q

what happens after sperm absorbed into cytoplasm

A

meiosis 11 continues
secondary oocyte splits into 2 haploid cells- ovum and second polar body
female pronucleus develops

205
Q

what happens after female pronucleus forms

A

male one forms
spindle fibres from centromere appear in preparation for first cleavage division

206
Q

hows the zygote formed

A

each pronucleus mitosis separately
nuclear membranes break down and they fuse to form zygote

207
Q

embryogenesis

A

cleavage
gastrulation

208
Q

cleavage simple definition

A

cell division in early embryo

209
Q

gastrulation simple

A

cell movements which produce gut and 3 primary germ layers

210
Q

phases of early embryonic cell cycle vs somatic cell cycle

A

early has 2 phases, S and M
somatic has 4, S,M,G1,G2

211
Q

sea urchin cleavage

A

rapid division
blastomeres all same size and become smaller with each division
holoblastic cleave(divisions divide entire cell)

212
Q

amphibian cleavage

A

unequal holoblastic division
blastomere in animal pore are smaller than blastomeres in vegetal pole because of yolk in vegetal hemisphere

213
Q

chick cleavage

A

meroblastic cleavage= cleavage plane does not bisect yolk

214
Q

what comes after cleavage stage

A

blastula formation

215
Q

the 3 primary germ layers

A

ectoderm
mesoderm
endoderm

216
Q

major derivatives of ectoderm

A

epidermis
nervous system
pituitary gland
adrenal medulla
jaw and teeth
germ cells

217
Q

major derivative of mesoderm germ layer

A

notochord
muscular, skeletal, circulatory, lymphatic systems
excretory and reproductive systems
dermis of skin

218
Q

endoderm major derivatives germ layer

A

epithelial lining of gut and associated organs
epithelial ling of respiratory, excretory and reproductive tract

219
Q

when does the first cleavage division occur

A

24-30 hrs after fertilisation

220
Q

what happens in first cleavage division

A

holoblastic division
2 blastomeres formed

221
Q

at 32 cell stage what happens

A

now a blastocyst
blastocoel formation

222
Q

when does the morula enter the uterus

A

day 4-5

223
Q

what is required before implantation

A

hatching
the blastocyst digests a hole in the zona pelucida and emerges

224
Q

does the inner cell mass develop into the embryo in a blastocyst

A

yes

225
Q

how does a blastocyst implant

A

secrete enzymes to burrow into endometrium

226
Q

what happens to inner cell mass after implantation

A

rearranges into 2 layers
bilaminar embyronic disc hypoblast and epiblast layers

227
Q

what happens day 12-15 gastrulation

A

primative streak forms in dorsal epiblast and defines anterior/posterior and left/right of embryo
cells from primative node produce notochord

228
Q

where di neural cres cells migrate

A

migrate on cranial, dorsolateral and ventral pathways
very highly migratory invasive and proliferate

229
Q

what are neural crest cells

A

specialist migratory populations
highly migratory, invasive proliferative
include melanocytes called malanoblast

230
Q

induction definition

A

where the fate of one cell is influenced by another
how do cells know where they are on the body plan

231
Q

example of induction

A

spemanns organiser

232
Q

spemmans organiser

A

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)

233
Q

how does the organiser alter cell fate

A

BMP-4 is distributed in late bastula and causes ventral development

234
Q

what stops action of BMP-4 allows dorsal development

A

chordin and noggin

235
Q

where is BMP-4 expressed

A

throughout the Xenopus blastula

236
Q

what does the neural plate from

A

prospective ectoderm where BMP signalling is inhibited by antagonists release by spemanns organiser

237
Q

what induces neural fate

A

BMP antagonists
fibroblast growth factors are also needed for neural plate formation

238
Q

chick neural plate induction

A

FGF activated churchill gene causes activation of Sox2

239
Q

anterior part of hand

A

thumb

240
Q

posterior part of hand

A

little finger

241
Q

proximal part of and

A

wrist

242
Q

distal part of hand

A

finger tips

243
Q

ventral part of hand

A

palm

244
Q

dorsal part of hand

A

back of hand

245
Q

what AER- apical ectodermal ridge- required for

A

limb outgrowth
secretes fibroblasts growth factors family proteins

246
Q

what does ZPA- zone of polarising activity- control

A

anterior-posterior digit formation via induction

247
Q

how do we know zone of polarising activity controls anterior posterior digit formation

A

sonic hedgehog (Shh) cells are implanted into anterior of developing limb bud can induce mirror image digit formation

248
Q

is sonic hedghog a morphogen

A

yes

249
Q

definition of sonic hedgehog

A

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

250
Q

how long is a pregnancy

A

40 weeks
240 days
10months
38+ weeks approx

251
Q

when does preorganogenesis happen LMP

A

2-4 WEEKS

252
Q

When does the embryonic period happen LMP

A

3-10weeks

253
Q

when does fetal period begin

A

11 weeks LMp

254
Q

external risks in first trimester

A

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

255
Q

spina bifida

A

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

256
Q

rubella virus syndrome

A

mild in adults-rash/itching
MMR prevents
postnatal- cataract, glaucoma, bilateral deafness, congenital heart disease, mental and physical disabilities

257
Q

when does hCG become detectable in blood

A

4 weeks

258
Q

maternal changes in pregnancy examples

A

organ squashing
respiratory function ^
digestive problems
weight gain
^hr and stroke volume
increased urination
breast enlargment

259
Q

why does respiratory function increase for mother during pregnancy

A

tidal volume increase

260
Q

why do digestive problems increase for mother during pregnancy

A

GI motility decreases (hormonal effects)

261
Q

why does weight increase for mother during pregnancy

A

fetus, placenta, uterus, increase blood volume , increase breast size, increase storage of protein and fat

262
Q

why does hr and stroke volume increase for mother during pregnancy

A

hr increases by 10-15%, BV increase

263
Q

why does breast size increase for mother during pregnancy

A

increase in oestrogen promote tissue development

264
Q

gestational trophoblastic tumours

A

problem in implantation and placenta
rare
overgrowth of trophoblast
lack of genetic material to form embryo
benign
pregnancy growth looks bigger than stage

265
Q

ectopic pregnancy

A

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

266
Q

pre-eclampsia

A

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

267
Q

gestational diabetes

A

4-5:100
thirst, hunger, tiredness, sugar in urine
insulin resistance
late pregnancy problem

268
Q

gestational hypothyroidism

A

2.5:100
problem in late pregnancy
decreased TSH levels
difficult to detect as normal pregnancy symptoms

269
Q

obstetric cholestasis

A

pruritis (itching), leakage of bile salts into blood stream
more common in multiple pregnancies
late pregnancy problems

270
Q

gestational transient thyrotoxicosis

A

late pregnancy problems
2-11:100
vomiting
weight loss
tremors
increased T4 levels
may resolve at 20 weeks
associated with hyperemesis gravidarum

271
Q

where does implantation usually happen

A

anterior or posterior wall anywhere really
usually in upper quadrants
generally between secretory glands
fully embedded by d14

272
Q

what happened after blastocyst implants

A

outer cells differentiate and set up 2 layers
the cyotrophoblast
syncytiotrophoblast

273
Q

cytotrophoblast

A

more densely packed cells with more obvious cell structure
will create the villi of the placenta

274
Q

syncytiotrophoblast

A

outer invasive cells
not dense but not loose
form gaps holes - lacunae
creates layer separating the fetus from maternal blood

275
Q

what forms in syncytiotrophoblast (lacunae)

A

vacuoles begin to form

276
Q

what happens after implantation and formation of vacuoles and extrambryonic membranes
(d13, d27LMP)

A

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

277
Q

maturation of the placenta

A

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

278
Q

placental circulation

A

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

279
Q

does fetal (Hb) or mothers blood have higher affinity foro2

A

fetal blood (Hb) is higher

280
Q

placenta function

A

protection
support growth- gas exchange, nutrition, waste
hormone production - hCG, p,e, placental prolactin, lactogen, relaxin

281
Q

haemolytic disease of the fetus

A

when mother is Rh and father is Rh+ resulting in Rh+ baby
immune response resulting in attack on fetal blood cells

282
Q

does fertilisation occur in pre-organogenesis

A

yes

283
Q

situs inversus

A

1:10 000
reversal of internal organs
may be underdiagnosed worldwide

284
Q

situs ambiguous

A

partial malrotation
contributes to 3% of congenital heart disease

285
Q

sacrococcygeal teratoma

A

origins in primitive streak
1:40 000
condition from early events

286
Q

what happens in embryogenesis

A

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

287
Q

cardiac development of fetus

A

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

288
Q

week 6-8 LMP

A

brain development
gut tube form
ureteric bud
limbs have distinct regions
craniofacial development

289
Q

week 8-12 LMP

A

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

290
Q

omphalocoele

A

problems in week 8-12LMP
2.5:10 000
GIT fails to return to body cavity after physiological herniation
assocatied with other conditions

291
Q
A
292
Q

week 12-16 LMP

A

first to second trimester
heart beat
fetal ‘breathing’
antibody production
face nearly developed
external genetalia
pregnancy bump may be visible

293
Q

main problems in week 12-16 LMP

A

eye problems
ear problems
teeth problems
immune system
brain development

294
Q

week 16-20 LMP

A

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

295
Q

what hormones stimulate labour

A

oestrogen - excitability
prostaglandins
relaxin
corticotrophin releasing hormone

296
Q

3 stages of labour

A

dilation
expulsion
placental expulsion

297
Q

dilation in labour

A

10cm
2-6/h
30s duration
amniochorion reptures

298
Q

expulsion stage of labour

A

contractions every 2-3 mins
60 sec duration

299
Q

placental expulsion stage of labour

A

sustained contraction

300
Q

atelactasis

A

problem at birth
alveolar collapse
not enough surfactant
common in preterm births
can lead to respiratory distress syndrome

301
Q

transient tachypnea

A

problems at birth
0.5-4% of all neonates
retention of lung fluid
resolves with o2 therapy and antibiotic treatment

302
Q

is unregulated fertility a contributor of infertility

A

yes

303
Q

what is control of fertility about

A

chossing when to have a family and what size of family
allowing people to have families who would otherwise experience difficulties

304
Q

infertility definition

A

when a couple has been trying to conceive for 12 months (sex every 2-3 days)

305
Q

when is a person eligible for treatment for infertility

A

2 years
may be sooner if secondary infertility
also could be sooner dependent on age

306
Q

how many people and couples are affected by infertility

A

88 million couples
186million individuals

307
Q

are infertility rates the same worldwide

A

no
irregulated fertility= infertility

308
Q

do majority of people experience infertility with their first or second child

A

already had a child experience more infertility

309
Q

physical reasons for experiencing infertility with a second child

A

age
worsened underlying conditions
weight increase
scarring
fibroids
pelivc inflammatory disease (PID)
could also be psychosocial, pressure, less support from communit

310
Q

fertility treatments requirements

A

donation/extraction of sperm or oocytes
synchronisation cycles
surrogate parent if needed

311
Q

AI

A

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

312
Q

what does IUI stand for

A

intrauterine insemination
sperm placed high in uterus
60-70% success over r6 cycles
more successful for younger women
success dependent on sperm count, quality

313
Q

in vitro fertilisation (1970s)

A

louise joy brown conveived by IVF in Oldham General Hospital
sperm and egg removed and fertilised outside body
healthy embryo implanted in uterus

314
Q

IVF eligibility and success

A

2 years unsuccessful conceiving
under 43
has 12 unsuccessful rounds of IUI

315
Q

retrieving eggs for donation or IVF

A

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

316
Q

in vitro fertilisation - when the eggs taken out body step

A

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

317
Q

transgender IVF

A

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

318
Q

problems with IVF

A

emotional
expensive
invasive/uncomfortable
superovulation-multiple babies
ectopic
ovarian hyperstimulation syndrome

319
Q

ovarian hyperstimulation syndrome (OHSS)

A

increased permeability of capillaries
oedema- tissue and pulmonary
renal failure
8% mild
<1% severe

320
Q

why is sperm retreival needed sometimes

A

vasectomy
STD like chlamydia
chemo]unable to ejaculate
antibodies to sperm

321
Q

how do antibodies to sperm arise

A

male- vasectomy, damage to sperm-blood barrier, dysfunction of sertoli cells
female- damage to mucosal membranes, exposure to sperm in the digestive tract , infection

322
Q

ICSI- intracytoplasmic sperm injection

A

done when sperm is poor motility, low number, abnormal morphology, frozen
sperm is injected straight into harvested egg

323
Q

FET - frozen embryo transfer

A

problems with implantation
if a number of high quality embryos were collected but further full treatment is not an option
for future years

yr 1 uni work (13 decks)

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