Revision Flashcards
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
Young boy, normal sized testis but large penis, growing very fast , high BP, high sodium, and low K, very dark
Dark skin - primary problem with acth
- small testis - know that androgens did not come from testis
- sex steroids - either form gonads or adrenlas - must be adrenals
- congenital adrenal hyperpalsia or fucntional adrenal neoplasm
- more likely to be block in an enzyme makign coritsol because is dark and making msh
- can make another androgen that cna bind to mineralcortiocid receptor
- so get low renin and aldoesterone
- lack of cortisol drives this to make increases levels of this hormone
management - suppress acth - give glucocorticoids
- bone age - advanced - turn of the outside hormones, turn off your own puberty
- treat hypertension
what would cause low levels of oestrogen in utero?
Ancephalic pregnancies - adrenals usually atrophic, have low levels because cannot convert progestrogen to androgens
Pre eclampsia
- elevated maternal blood pressure w protein in urine
- more common for first pregnancies
- triggered by placenta (e.g toxin)
- is an exaggerated inflammatory response leading to vascular dysfunction
- failure of normal vascular adaptation to pregnancy
- loss of normal maternal peripheral vascular resistance
Emergency contraceptive pill
- levonorgestrel
- take within 72 hours of unprotected sex
- no effect if given after ovulation
- good efficacy
- doesn’t work if large BMI
Development of breast during pregnancy
- oestrogen - essential for breast growth
- progesterone - induces side branching of ducts, but also prevents milk production (is a smooth muscle relaxant)
- prolcatin - necessary for alveolar developments but also stimulates caesin and lacta albumin mRNAS
- Insulin and cortisol - stimulate alveolar epithelial cell division
-way more alveolar form for pregnancy , and ductile system grows
Graves disease
causes thyrotoxicosis - and is when there is an autoimmune reaction to tsh receptor - overstimualtes it causes too much thryoid homrone
thyroid hormone resistance syndrome
receptor mutations lead to pituitary insensitivity to T3, so tsh rises and causes rise in t4 and t3. -patient can presnet with hypo or hyperhtyroid features in different tissus and may have goiter
Thyroditiis
- inflammation of thryoid gland (pre formed thyroid homrone is dumped from lumen with thryoglobulin)
- patient presents as thyrotoxic, then has a hypothyoid phase and usually recovers
- ciruclating thyroglobulin is increased and serves as a tumour maker
- Main causes of hypercalcemia
PTH dependent - primary hyperparathyroidism
PTH independent
- Cancer e.g PTHrP
- ** -Vit D intoxication
Hyperphosphatemia
- Advanced renal failure, ability to secrete phosphate is reduced
- hypoparathyoridism
- PTH resistance
Hypophosphatemia
vit D deficiencey - elderly
- resp alkalosis (Drives phosphate into cells)
- renal loss
-increased PTH
Phosphatonins
-comes from bone
PHEX inhibits this
FGF23 - derived from bone
-decreases kidney and gut absorption of phosphate to cause hypophosphatemia
Can get aquired and genetic problems - abnormality in transport across gut (hypophosphatemia)
- Cause of hypocalcemia
Hypoparathyoridsm
-surgery to neck, genetic (mutation in genes)
Parathyroid hormone resistance - doesn’t work, so cannot get increase in calcium
Abnormality in vit D metabolism
Autosomal dominant hypercalciuric hypocaclcemia
Activation of calcium sensitive receptor
- Parathyroids read plasma ionised calcium level as being higher than it really is
- will switch off processes that drive absorption and reabsorption of urine
-if this receptor doesnt work then patients look like they have mild parathyrodism
- no treatment if asymptomatic
- can give vit D
Immune system change in pregnancy
- Immune reaction to sperm when they enter the vagina
- however repeated exposure may dapen the immune response and be beneficial to pre eclampsia
- White cell count increases due to increase in neutrophil population, which commences in the luteal phase of the cycle and doesn’t drop in pregnancy
- neutrophils are important for preparing the cervix for labour
-more th2 than th1 - drive immune system towards antibody mediated response
Contains many NK cells - act by antibody dependent cell mediated cytotoxity
