Revision Flashcards
(39 cards)
Pathway for GHRH, CRH/VP
- inhibitory molecule for TSH
- draw out hypothalamus/pituitary diagram
GHRH /somatostatin (-) -> GH –> liver, tissues –> igf-1
CRH/VP –> acth –> adrenal cortex –> cortisol
Somatostatin inhibits TSH
Chromophils - acidophils and basophils
Acidophiles - somatotrophs (GH), lactotrophos(PRL) - orange
Basophils - gonadotrophs (LH, FHS) , Thyrotrophs (tsh) , cortiotrophs (acth) - magenta
Dating the endometrium
Proliferation stage
- tortuosity
- a bit of odema - when lined up with stromal mitses then in proliferation stage
- lots of stromal mitoses
Secretion phase (early luteal) - tortuous glands, basal vaculation, glandular secretions
(late luteal) - luekocyte infiltration , decidual reaction
-nutropholes - open wound after mestration - so need lots of them
Sequence of sperm getting to vagina, until fertilisation , implantation, nidation
Coagulation Liquefication Vagina pH, mucous Capacitation Acrosomal reaction (increase calcium into cell, zona pellucida - stimulated by progesterone and zona pelluicda ) Sperm penetration - hyaluronidase - digests basemenet membrane sperm can get through cumulus cells, corona radiata, zone pellucida Oolemmal membrane - fuse Cortical reaction Implantation Nidation
Positive and negative feedback for PTH
Regulated - serum calcium (negative feedback)
- serum phosphate (positive)
- vit D (negative)
Name of plugs in spiral arteries
endovascular trophoblastic plugs
Function Amniotic fluid
- buoyant - allows symmetric growth
- cushions the embryo/fetus
- Prevents adhesion of fetus with membranes
- allows fetus to move
- develop GI/ resp tracts - breathign and swallowing
What can you tell with amniotic fluid?
Polyhydramnios - excessive amniotic fluid - due to loss of swallowing - often found in diabetic pregnancy
Oligohydramnios - lack of amniotic fluid - potentially due to kidney problems
Also can screen karotype for fetus to see if it is born normal
Placental arteries and viens
Arteires - carry deoxygenated blood from baby to mother
Viens - carry oxygenated blood from mother to fetus
Management of PCOS
lose weight, can get ovulation
- medicaiton to induce ovulation, clomiphene citrate
- surgery - to induce ovulation, remove androgen producing tissue
- metformin - for insulin resistance e
Premature ovarian insufficiencey
- will see how oestrogen and high fsh - this is because not enough oetrogen is being produced by the ovaries, and so the reduced negative feedback will stimulate more fsh to try and get oestrogen made
- less frequent menstruation and eventually ovulation stops
- need counselling, and fertility specialist
Activation of myometrium
Activation of myometrium
- increase CAPs - gap junctions (not many in quiesence)
- more power to activate muscle
** -prostaglandin and oxytocin receptors
Oxytocin
Not essential for initiation of labour
- requires gap junctions to be effective
- used to induce and augment labour
- primary prevention of post partum hemmorage (causes uterus to contract after baby is born)
1st stage of labour
1st stage - until full dilation
- muscle contractions
- cervical effacement and dilation
- descent of presenting part
- rupture of membrane
What needs to be acheived to placenta and mother when baby is born?
-involution - placental separation, cleavage through decidua basalis, contractions to prevent postpartum haemorrhage, increased uterine sensitivity to oxytocin
Fetal fibronectin
high molecularweight glycoprotein
Present in cervico vaginal fluids in first trimester
-is stuck
-seen in many females who have preterm birth
negative predictive value - want to know this
How to improve outcomes?
- Risk selection history taking
- stop smoking
- assess maternal health risks
- cervical length most powerful predictor
- use progesterone for short cervix
- confirm risk in threatened PTL - use steroids, magSO4 if delivery like
congenital adrenal hyperplasia
cant make cortisol so make lots of male hormones instead
Virilised (masculinaised) girl
cause
- Have ovaries
- Normal female internal genitalia (uterus)
- Karyotype - XX
-exposed to male hormone before birth (think where has this come from)
- fetal - congongenital adrenal hyperplasia - hard to make cortisol so make lots of male hormone instead
- Maternal - ingestion of male hormones - oral contraceptives, PCOS, andorgen secreting tumours
Undervirilised Male
Have testis, no internal female genitalia, karyotype XY
-Implies lack of angrogen or resistant to its effects
- Fetal - LH receptor mutation (usually complete female - no breast development)
- Androgen receptor mutation
Normal formed phallus - hypothalamic - damage lH to make testosterone
No testis and is XY, what could this be from?
a problem early on up (before gonadal differentiation)
What can cause crushing syndrome?
Cause - primary functional adrenal tumour
- ACTH secreting tumour
- exogenous glucocoritcoid
ACTH receptor loss of function mutation
low cortisol levels
- adrenal gland does not develop properly
- no cortisol and androgen formation
- same signs as glucocorticoid deficiencey
Defect in cortisol synthesis
from early age
-low cortisol levels lead to high acth levels, which stimulates the adrenal cortex excess production of adrenal precursor and adnreal hyperplasia
not able to convert coritsol so it forms different androgens and makes more testosteroen and causes the virilisation in tehse girls