Changes

==Cervical Softening==

==Cervical Softening==

A number of variables during pregnancy lead to the initiation of contractions of the myometrium including oxytocin, prostaglandins and neural inputs from the autonomic nervous system. These contractions of the myometrium lead to an increased pressure within the amniotic fluid. These contractions trigger a series of events that lead to the cervix becoming flexible and gradually beginning to dilate. As the force of the contractions increases, the cervix will open completely. Much of the activity related to the initiation of contractions is begun by fetal stress resulting in an increased production of fetal cortisol. The effects listed below are all linked to the initial increase in fetal cortisol in some way.

A number of variables during pregnancy lead to the initiation of contractions of the [[Uterus_-_Anatomy_%26_Physiology#Myometrium|myometrium]] including oxytocin, [[Oestrous_Cycle_Pharmacological_Manipulation_-_Anatomy_%26_Physiology#Prostaglandins|prostaglandins]] and neural inputs from the autonomic nervous system. These contractions of the myometrium lead to an increased pressure within the amniotic fluid. These contractions trigger a series of events that lead to the cervix becoming flexible and gradually beginning to dilate. As the force of the contractions increases, the cervix will open completely. Much of the activity related to the initiation of contractions is begun by fetal stress resulting in an increased production of fetal cortisol. The effects listed below are all linked to the initial increase in fetal cortisol in some way.

===Endocrinology===

===Endocrinology===

Immediately prior to birth, the pre-parturition cervix loses firmness. Cervical softening involves two changes in the intracellular matrix; firstly a reduction in the number of collagen fibres and secondly an increase in GAGs to decrease aggregation of the remaining collagen fibres.

Immediately prior to birth, the pre-parturition cervix loses firmness. Cervical softening involves two changes in the intracellular matrix; firstly a reduction in the number of collagen fibres and secondly an increase in GAGs to decrease aggregation of the remaining collagen fibres.

<br />

<br />

<br />

<br />

Several hormones are known to exhibit an effect on the cervix resulting in pre-parturition softening; 'prostaglandins' and 'relaxin'. Prostaglandin levels increase markedly in the days prior to parturition, peaking at parturition. There are three main types and sources of prostaglandin that are important in cervical softening; prostaglandin E2 (PGE2), prostacyclin (PGI2) and Prostaglandin F2α (PGF2α).  

Several hormones are known to exhibit an effect on the cervix resulting in pre-parturition softening; 'prostaglandins' and [[Ovaries_Endocrine_Function_-_Anatomy_%26_Physiology|'relaxin']]. Prostaglandin levels increase markedly in the days prior to parturition, peaking at parturition. There are three main types and sources of prostaglandin that are important in cervical softening; prostaglandin E2 (PGE2), prostacyclin (PGI2) and Prostaglandin F2α (PGF2α).  

<br />

<br />

<br />

<br />

PGF2α is produced by the placenta in response to the production of fetal corticoids. (PGF2α also helps to remove the progesterone block pre-parturition.) PGF2α is not thought to act directly on the cervix and instead causes the myometrium of the uterus to become more active resulting in increased cervical stimulation and therefore softening and dilation. PGE2 is maternally derived and is the main driver of cervical softening. The production of PGE2 coincides with reductions in progesterone levels. PGE2 also acts on the uterus resulting in increased myometrial contractions, increased uterine pressure and therefore also cervical stimulation. PGI2 is also maternally derived and acts as a vasodilator and as an anticoagulant, playing another important role in cervical relaxation. With all types of prostaglandin, isoforms are produced locally and act locally and are therefore not strictly classed as hormones.

PGF2α is produced by the placenta in response to the production of fetal corticoids. (PGF2α also helps to remove the progesterone block pre-parturition.) PGF2α is not thought to act directly on the cervix and instead causes the myometrium of the uterus to become more active resulting in increased cervical stimulation and therefore softening and dilation. PGE2 is maternally derived and is the main driver of cervical softening. The production of PGE2 coincides with reductions in [[Ovaries_Endocrine_Function_-_Anatomy_%26_Physiology|progesterone]] levels. PGE2 also acts on the uterus resulting in increased myometrial contractions, increased uterine pressure and therefore also cervical stimulation. PGI2 is also maternally derived and acts as a vasodilator and as an anticoagulant, playing another important role in cervical relaxation. With all types of prostaglandin, isoforms are produced locally and act locally and are therefore not strictly classed as hormones.

<br />

<br />

<br />

<br />

Relaxin is produced by the ovaries and the placenta and together with progesterone prevent uterine contractions throughout the pregnancy. However, relaxin also aids in the loosening of tissues in the cervix and pelvic ligaments to loosen pre-parturition. Relaxin and PGE2 work in combination on the cervix.  

[[Ovaries_Endocrine_Function_-_Anatomy_%26_Physiology|Relaxin]] is produced by the ovaries and the placenta and together with progesterone prevent uterine contractions throughout the pregnancy. However, relaxin also aids in the loosening of tissues in the cervix and pelvic ligaments to loosen pre-parturition. Relaxin and PGE2 work in combination on the cervix.  

===Progesterone Production===

===Progesterone Production===

The initiation of myometrial contractions via fetal cortisol results in cells within the uterus and the placenta undergoing a degree of stretch. This stretching is thought to activate several systems within the cells resulting in the production of progesterone. Stretching can increase the avaliability of cyclo-oxygenase 2 or COX-2, which is part of a chain of reactions converting arachadonic acid to PGE2 and PGF2α resulting in an increased cellular output. Both of these types of prostaglandin potentiate oxytocin once outside the cell and this inturn potentiates an increase in the level of arachadonic acid, thus scaling up production in the entire system. Secondly the stretching within the cell also results in increased expression of oxytocin receptors in the cell surface resulting in a greater impact on the cell for a given level of oxytocin, further upregulating the system.  

The initiation of myometrial contractions via fetal cortisol results in cells within the uterus and the placenta undergoing a degree of stretch. This stretching is thought to activate several systems within the cells resulting in the production of progesterone. Stretching can increase the avaliability of cyclo-oxygenase 2 or COX-2, which is part of a chain of reactions converting arachadonic acid to PGE2 and PGF2α resulting in an increased cellular output. Both of these types of prostaglandin potentiate oxytocin once outside the cell and this inturn potentiates an increase in the level of arachadonic acid, thus scaling up production in the entire system. Secondly the stretching within the cell also results in increased expression of oxytocin receptors in the cell surface resulting in a greater impact on the cell for a given level of oxytocin, further upregulating the system.