Physio Flashcards
1
Q
what hormones does the hypothalamus produce?
A
- CRH
- TRH
- GnRH
- GHRH
- Somatostatin
- Dopamine
2
Q
what hormones does the anterior pituitary produce?
A
GLAMP ForTwo
- GH
- LH
- ACTH
- MSH
- Prolactin
- FSH
- TSH
3
Q
what hormones does the posterior pituitary produce?
A
- oxytocin
- ADH
4
Q
what hormones does the thyroid produce?
A
- T3, T4
- Calcitonin
5
Q
what hormones does the parathyroid produce?
A
- PTH
6
Q
what hormones does the pancreas produce?
A
- insulin
- glucagon
7
Q
what hormones does the adrenal medulla produce?
A
- norepi
- epi
8
Q
what hormones does the kidney produce?
A
- renin
- 1,25-dihydroxycholecalciferol
9
Q
what hormones does the adrenal cortex produce?
A
- aldosterone
- adrenal androgens
- cortisol
10
Q
what hormones does the testes produce?
A
- testosterone
11
Q
what hormones does the ovares produce?
A
- progesterone
- estradiol
12
Q
what hormones does the corpus luteum produce?
A
- estradiol
- progesterone
13
Q
what hormones does the placenta produce?
A
- progesterone
- HPL
- HCG
- estriol
14
Q
what are the differences between peptide/amine hormones and steroid hormones?
A
peptide/amine hormones
- stored in secretory vesciles
- receptors within cell membrane
- activate signaling ascades
- fast acting (seconds/minutes)
steroid hormones
- produced on demand
- diffuses through cell membrane
- receptors in nucleus (sometimes cytoplasm)
- up/down regulate transcription
- slow acting (hours/days)
15
Q
pseudohypoparathyroidism
A
excess PTH because of genetic defect in GPCR PTH receptor on kidney→unable to transduce PTH signal to regulate body Ca2+ and phosphorus homeostasis
- hypocalcemia and tetany
- hyperphosphatemia
16
Q
what is the difference between long loop and short loop negative feedback regulation of hormonal secretion?
A
- long loop: hormones released from peripheral glands feeds back onto hypothalamic-pituitary axis
- short loop: anterior pituitary feeds back on hypothalamus
17
Q
how is the secretion of anterior pituitary hormones regulated by hypothalamus?
A
releasing factors are delivered from hypothalamus to the anterior pituitary via hypothalamic-hypophysial portal system
18
Q
how is the secretion of posterior piturary hormones regulated by the hypothalamus?
A
nerve cell bodies in hypothalamus synthesize hormones which are transported in vesicles down axons to posterior pituitary for release
19
Q
describe the nature of the blood supply to the anterior and posterior pituitary
A
- anterior pituitary recieves venous blood carrying neuropeptides from hypothalamus and pituitary stalk
- posterior pituitary receives arterial blood
20
Q
what are the differences in the nature of the hormones released by the anterior vs. the posterior pituitary?
A
- anterior pituitary hormones are proteins and glycoproteins
- posterior pituitary hormones are smaller molecular mass peptides associated with neurophysins (carrier proteins which transport the oxytocin and vasopressin to posterior pituitary from hypothalamus)
21
Q
the release of most anterior pituitary hormones is controlled by hypothalamic releasing factors EXCEPT…
A
prolactin; under tonic inhibitory control by dopamine
- circulating prolactin increases if infundibulum is severed
22
Q
what are effects of GHRH from hypothalamus?
A
- stimulates GH transcription and release
- stimulates production of GHFH receptor
- stimulates somatostatin release (negative feedback)
- inhibits GHRH secretion (negative feedback)
23
Q
what are the effects of somatostatin release from the hypothalamus?
A
- inhibits pulse frequency of GH
- inhibits pulse amplitude of GH
- inhibits release of GH
- has NO impact on synthesis of GH
24
Q
how does the pulsatile secretion of GH change during puberty?
A
number of pulses per day are constant but there is a larger pulse amplitude
25
what kinds of things stimulate GH secretion?
* deep sleep
* exercise
* sex hormones
* fasting/hypoglycemia
* stress
* dopamine agonists (suppress in acromegaly)
26
what kinds of things inhibit GH secretion?
* IGF-1 (negative feedback)
* GH (negative feedback)
* obesity
* hyperglycemia
* pregnancy
* somatostatin
27
what are the net effects of GH?
**counteracts insulin**
* decreases glucose uptake into cells (diabetogenic)
* decreases glucose utilization in muscle
* increased protein synthesis in muscle
* increased lipolysis
* increased IGF-1 production
* (inhibits its own secretion by stimulating somatostatin from hypothalamus)
28
what is the direct effect of GH on the liver?
* stimulates release of IGF-1 (acts on GHRH and anterior pituitary to reduce GH production)
* stimulates hepatic glucose production
29
what is the direct effect of GH on adipocytes?
releases and oxidizes free FA especially during fasting, mediated by reduction of lipoprotein lipase activity *(reduced lipogenesis)*
30
what is the relationship between GH and IGF?
**IGF-1 is primary mediator of the effects of GH**
* **tyrosine kinase** IGF-1 receptor dimerizes and autophosphorylates→recruits phosphotyrosine binding proteins IRS-1 and Shc→P13K and Ras/MAP kinase regulation of transcription
31
how does IGF account for longitudinal growth?
action of GH via IGF is responsible for linear growth
* *IGF-1 induces clonal expansion of early chondrocytes and maturation of later chondrocytes*
* increases protein synthesis in muscle and organs
32
laron syndrome
* **low IGF-1**→post-natal growth failure (similar phenotype to STAT5b mutation)
* **normal/elevated GH**
* reduction in cancer and diabetes BUT do not live longer (epilepsy and obesity)
* treat: rhIGF-1
33
what is the mechanism of GH receptor activity?
hormone/cytokine receptor with **no inherent tyrosine kinase activity**
* GH binds→conformational change of receptor dimer→activates JAK2→phosphorylates/ activates STAT TF
34
what are the effects of ghrelin from the stomach and pancreas on GH secretion?
ghrelin acts on the hypothalamus and anterior pituitary to **stimulate GH release**
35
acromegaly
* occurs in adults with GH-secreting adenomas
* protruding jaw, macroglossia, englarged hands/feet
36
how does nutritional deficiency affect growth?
nutritional deficiency slows growth through reduction of IGF-1 levels
37
hypothyroidism
* **low TH→****decreased BMR, thermogenesis, gluconeogenesis, glycogenolysis,** protein synthesis, proteolysis, lipogenesis, lipolysis
* normal serum glucose
* increase serum cholesterol
* non pitting edema
* **bone age**
* **reduced GH production (thyroid hormone response element is upstream of GH transcription start site)**
* **cretinism in infants (mental, growth retardation)**
* **treat with thyroxine (T4): longer half-life and greater stability (tighter binding/lower metabolic clearance)**
* **excessive treatment→bone loss/osteoporosis**
38
what are the implications of GH-deficiency on CVD?
* not as impactful as obese and sedentary but same trend
* increases: **visceral adipose tissue,** carotid intima-media thickness, inflammatory markers of CVD, clotting factors, **insulin resistance**, **LDL**
* decreases: myocardial function, **HDL**
39
describe the regulation of thyroid hormone by TRH and TSH
* **TRH from hypothalamus→anterior pituitary to produce TSH** by activing GPCR linked to PLC→IP3
* **TSH stimulates TH synthesis/release by GPCR linked to adenylate cyclase→cAMP**
* *TSH increases uptake up iodide, synthesis of TG, storage of TH in colloid, increases endocytosis of colloid*
40
what are the biologically active forms of thyroid hormone?
* T4: "prohormone"
* T3: biologically potent form derived from T4
* rT3: not biologically active
41
how does the body overcome the fact that the formation of T4 is preferred over production of T3 (active form)?
target tissues are able to convert T4 to T3 using peripheral deiodinases
42
what is the mechanism of action of thyroid hormone
* peripheral deiodinases generate T3 and rT3 from T4
* free T4 and T3 enters cell→5'/3'-monodeiodinase converts most T4 to T3 (cytoplasmic levels of T4 and T3 are about equal)→TH receptor binds DNA at thyroid response elements in promoter region regulated by THs
* result: protein/enzyme production to **increase metabolic rate and O2 consumption; catabolism**
43
hyperthyroidism
* **high TH→increased BMR, thermogenesis gluconeogenesis, glycogenolysis,** protein synthesis, proteolysis, lipogenesis, lipolysis
* muscle wasting, no exopthalmus
* normal serum glucose
* low serum cholesterol
* **increased expression of ßadrenoreceptors** (increased senstitivity to catecholamines)
* treatment: PTU (blocks thyroid peroxidase activity)
44
describe the formation of T3 and T4 from TG
1. thyroglobulin from tyrosine
2. Na+/I- cotransport
3. oxidation of I-→I2 in lumen, organification of I2
4. coupling of MIT and DIT
5. stimulation by TSh→endocytosis from lumen
6. lysosomal enzymes digest thyroglobulin, releasing T3 and T4
45
describe the negative feedback process of of thyroid hormone
**T3 (especially)** and T4 exert negative feedback on **anterior pituitary and hypothalamus by downregulating TRH receptors**
* dopamine and somatostatin also inhibit effects on TSH release
46
what three enzymes are responsible for both mineralocorticoid and glucocorticoid synthesis?
1. 3ßhydroxysteroid dehydrogenase
2. 21ßhydroxylase
3. 11ßhydroxylase
47
what are the effects of glucocorticoids on target tissues?
* **stimulates gluconeogenesis**
* **increase protein breakdown** in muscle (to provide a.a for gluconeogenesis)
* **decreases glucose utilization** (except in brain, inhibits Glu4 recruitment--brain uses Glu3)
* **increases lipolysis**
* **anti-inflammatory:** inhibits cytokines and chemoattractants
* **immunosuppressant:** suppresses T cells, inhibits IL-2
48
if cortisol binds mineralocorticoid receptors with the same affinity as glucocorticoid receptors, why does it have little mineralocorticoid activity?
11ßhydroxysteroid dehydrogenase II in kidney and colon **convert cortisol into cortisone which does not bind MR**
49
how are steroid hormones regulated?
**CRH from PVN** in hypothalamus→hypothalamic-hypophysial portal blood→**corticotrophs in ant. pituitary**→POMC→**ACTH**
* **ACTH: ** increases cholesterol desmolase activity, promotes adrenal cortex cell proliferation, upregulates ACTH receptor
50
describe the mechanism of negative feeback on ACTH
* feedback inhibition **only exerted by glucocorticoids**
* inhibits expression of CRH receptor (and thus ACTH synthesis) from corticotrophs of ant. pituitary
51
when is cortisol secreted?
circadian control of cortisol secretion because CRH→ACTH→cortisol
* highest just before waking
* cortisol is major hormone related to stress (e.g., biochemical stress like hypoglycemia)
52
addison's disease
hypoadrenal function due to autoimmune diease or TB→destruction of adrenal cortex; symptoms: skin hyperpigmentation
* decreased aldosterone: hypertension, hypokalemia, metabolic acidosis
* **decreased cortisol: increased ACTH,** weight loss, poor stress tolerance
* decreased sex hormones
53
cushing's disease
**excess ACTH from pituitary gland tumor→excess cortisol**
* symptoms: upper body obesity, buffalo hump, poor wound healing
* increased aldosterone: hypertension
* increased cortisol: increased blood glucose
* increased androgens
54
cushing's syndrome
any etiology of excess cortisol that is NOT a pituitary gland tumor; **ACTH levels will thus be low because of feedback**
55
dexamethasone (glucocorticoid) suppression test
differentiates Cushing's by taking advantage of the feedback inhibition on ACTH secretion
* **normal: low cortisol→low ACTH**
* **adrenal tumor: high cortisol→low ACTH**
* **ACTH producing tumor: high cortisol→high ACTH** (if you increase the dose then low cortisol→low ACTH)
56
graves disease
* most common cause of hyperthyroidism
* **autoimmune: TSH receptor antibodies (LATs) bind tighter and longer than TSH→chronic T3/T4 production **
* **TSH levels fall** because negative feedback loop is working
* symptoms: **exophthalmos,** fatigue, weight loss with increased appetite, tachycardia, muscle wasting
57
hashimoto's disease
* most common cause of hypothyroidism
* elevated thyroid antibodies
* elevated TSH
58
what is the overall action of PTH?
* increases serum Ca2+
* decreases serum PO4
59
what is the primary target of PTH?
**kidney**
* **increases reabsorption of Ca2+ from distal tubule** via Ca channel in luminal membrane
* **decreases resorption of PO4 in proximal tubule**
* **increases synthesis of active vitamin D** (leads to more Ca2+ absorption)
60
what is the effect of PTH on bone?
**increases osteoclastic resorption via receptors on osteoblasts**→increased Ca2+ and PO4 in ECF and plasma
* osteoblasts sends out cytokines (RANKL) that activates nearby osteoclasts to form new osteoclasts
61
what is the primary target of vitamin D?
**intestine**
* **increases Ca2+ and PO4 absorption by increasing synthesis of calbindin (transporter)**
62
what is the effect of vitamin D on bone?
stimulates osteoclastic resorption via receptors on osteoblasts→increased Ca2+ and PO4
63
what are the effects of vitamin D on the parathyroid and kidney?
* **parathyroid: suppresses PTH** (negative feedback)
* **kidney: aids increased reabsorption of Ca2+** in distal tubule by increasing calbindin/Ca2+ transport and efflux at basal side of tubule
64
rickets
**chronic vitamin D and/or Ca2+ and/or PO4 during early development**→poor mineralization of bone→weakened and mechanically distorted long bones and abnormal growth plates
65
osteomalacia
**chronic vitamin D and/or Ca2+ and/or PO4 deficiency**→poor quality bone formed during remodeling
66
primary hyperparathyroidism
excess PTH secretion (usually parathyroid adenoma)
* hypercalcemia
* hypophosphatemia
* increased phosphaturia (high alk phos) and calciuria
* increased bone resorption
67
secondary hyperparathyroidism
**primary hypocalcemia** (due to low D, renal failure, diet, etc...)→high PTH to stimulate Ca2+ resorbtion in kidney and bone
68
hypoparathyroidism
usually due to surgical damage on parathyroid→decreased PTH
* hypocalcemia and tetany
* hyperphosphatemia
69
humoral hypercalcemia of malignancy
**Ca2+ is high due to release of PTHrp by lung tumor cells (analog of PTH)**
* same as hyperparathyroidsm except *LOW PTH due to feedback inhibition*
70
follicular phase of ovarian cycle
day 0-14: FSH stimulates development of follicles
* includes menstrual and most of proliferative phase of uterine cycle
* **estrogen dominates and primes uterus for progesterone (induces progesterone receptors)**
* primordial follicle→graafian follicle
71
ovulatory phase of ovarian cycle
day 14: burst of estrogen synthesis that has positive feedback on FSH and LH→**LH surge→rupture of graafian follicle**
72
luteal phase of ovarian cycle
day 14-28: **LH converts rupture follicle to corpus luteum** which synthesizes estrogens and **progesterone**
* **progesterone dominates**→conversion of uterus to secretory type (promotes glycogen storage/secretion of carb-rich mucus), increased vascularity, increased temp
* characterized by negative feedback on GnRH release
73
menstrual phase of uterine cycle
* prostaglandin→vasoconstriction of spiral arteries and local ischemic injury/inflammation, regresion of corpus luteum
* abrupt withdrawal of estrogen and progesterone→sloughing off of endometrium
74
what are the roles of hypothalamic and pituitary hormones in regulation of ovarian function?
pusatile GnRH→ant. pituitary→FSH (during follicular phase) and LH (during luteal phase)
* **FSH: binds receptors on granulosa cells**→synthesis of *aromatase,* activins, and inhibins
* **LH: binds to receptors on theca cells**→synthesis of *progestins and androgens*→granulosa cells and are converted to estrogens
75
describe the LH surge during the late follicular phase
positive feedback when high circulating estrogens "sensitize" ant. pituitary gonadotrophs to stimulation by GnRH→LH surge necessary for rupture of follicle→ovulation
76
two-cell, two-gonadotropin model
**granulosa cells have aromatase necessary for estrogen synthesis but do not have enzyme to make androgen precursors (those are synthesized in theca)**
* *testosterone diffuses from theca to granulosa*
* vascularization of corpus luteum makes LDL available to granulosa cells which enables *both granulosa and theca cells to make progesterone*
77
hormonal changes in female puberty
* before puberty: release of GnRH inhibited by low sex steroids
* during puberty: pulsatile secretion of GnRH (observed first at night then duing the day as well)→upregulation of its own receptor on anterior pituitary
* thelarche, adrenarche, menarche
78
the menopause
* no more follicles to respond to FSH and LH→decrease in circulating sex steroids
* **rise of FSH** and LH (no negative feedback and lack of inhibin)
* larger women may not be as symptomatic because estrone is produced peripherally by muscle and adipose tissue
* estrogen treatment increases risk for certain cancers/diseases; mix with progesterone
79
polycystic ovary disease
* bunch of follicles with no dominant follicle→no ovulation, no conversion of proliferative→ secretory
* reduced estrogen and progesterone
* continued production of androgen by thecal cells→facial hair and acne
* treat with birth control or clomiphene (partial estrogen receptor agonist, restores ovulation)
80
where is the most dangerous place for ectopic pregnancy?
**interstitial region of uterine tube;** puts patient at risk for major hemorrhage because of its proximity to the area where the uterine vasculature enters the uterus
81
how does ß-hCG change during pregnancy?
* doubles every 48 hours until its peak
* **low in ectopic pregnancy**
82
what do you use to diagnose menopause?
rise of FSH (due to lack of negative feedback)
83
capacitation of sperm
functional maturation of the spermatozoon; removal of a glycoprotein layer make receptors available on the sperm cell membrane; area of acrosomal cap is also so altered, enabling acrosome reaction
84
acrosomal reaction
triggered by sperm binding to an egg glycoprotein; Ca-dependent process in which the acrosome (large organelle in sperm head) fuses with the sperm cell plasma membrane (exocytosis)
* causes second Ca rise in egg that triggers cortical reaction (exocytosis of granules that hardens zona pellucida to prevent polyspermy)
85
how long does it take the blastocyst to move from the fallopian tube to the uterus?
3-5 days; 1-2 days before implantation
86
how is the corpus luteum rescued from regression?
trophoblasts→synciotrophoblasts that produce **HCG (similar to LH)**
* sustains corpus luteum for 8-10 weeks as maternal LH declines, before placenta takes over steroid production
87
what hormone is measured in a pregnancy test?
HCG
88
how do fetal adrenal-placental interactions produce estrogen?
fetal adrenal gland makes DHEA-S which is then hydroxylated in the fetal liver, intermediates are transferred to the placenta where it is converted to estrogens
89
where is progesterone produced during the first and second trimesters of pregnancy?
* first: corpus luteum
* second: placenta
90
ferguson reflex
positive feedback of oxytocin whereby baby's head stretches cervix→fundic contraction due to oxytocin→stretches cervix more→more contractions
91
what are the roles of estrogen/progesterone, oxytocin, and prostaglandin during parturition?
* **increased ratio of estrogen/progesterone makes uterus more sensitive to contractile stimuli**
* **estrogen increases number of oxytocin receptors on myometrial tissue in uterus** (enables ferguson reflex)
* **prostaglandins initiate contractions** and are sustained by oxytocin and more prostaglandins
92
what hormones are mammogenic?
* estrogen
* progesterone
* cortisol
* prolactin
93
what hormones are lactogenic?
* prolactin
94
what hormones are galactokinetic?
* oxytocin
95
what hormones are galactopoietic?
* prolactin
96
how is ovulation suppressed during breast feeding?
**prolactin** acts to
* inhibit GnRH secretion
* inhibits action of GnRH on anterior pituitary (thus inhibiting LH and FSH)
* antagonizes actions of LH and FSH on ovaries
97
how is secretion of breast milk inhibited during pregnancy?
estrogen and progesterone black action of prolactin on the breast
98
how does suckling maintain lactation?
suckling triggers neuroendocrine response that causes release of oxytocin while inhibiting release of GnRH
99
colostrum
fluid initially produced during breast feeding; concentrated, low-volume form of nutrition for neonate's immature GI tract (has little/no fat and antibodies)
100
describe the blood supply to the fetus
placenta receives 50% of combined CO from **iliac arteries→spiral arteries** from mother empty **directly into intervillous space→umbilical vein**
101
what is the difference between HbF and Hb?
placenta has 50% more HbF than mother
* HbF has same PO2 as HbF has a higher saturation
102
describe the path of blood after gas exchange occurs in the placenta
gas exchange in placenta→umbilical vein (highly oxygenated)→**ductus venosus**→IVC→atria
* 40% of blood flows through **foramen ovale** from RA→LA
* 66% to RV→pulmonary artery→**ductus arteriosis**→aorta
* 34% to LV (heart and brain)
103
how is circulation maintained in the fetus?
* circulating prostaglandin is 5x that of adult
* lower PO2 allows cells of ductus arteriosa to be relaxed
* lungs are collpase due to hypoxic vasocontriction, lack of inflaction, relative acidosis→high vascular resistance
104
what are the mechanisms involved in transitioning from fetal to neonatal to adult circulations
* **clamp umbilical cord→**BP in aorta increases→sudden increase in systemic vascular resistance)→back pressure in LV and LA and pressure in RA decreases
* closure of foramen ovale caused by reversal of R/L atrial pressure
* **first breath:** alveoli of neonate are oxygenated, decreased PVR, and pulmonary blood flow increases and becomes equal to CO
* constriction of vascular smooth muscle (due to increased PO2, decreased prostaglandin, and brandykinin) causes closure of ductus arteriosis
* ductus venosus closes
105
what are the dangers of delivering a baby at high altitudes?
ductus arteriosis cannot close due to low PO2→hypoxia→ vasoconstriction of lung→persistent fetal circulation
* treat: O2 and endomethycin (inhibits COX which inhibits prostaglandin)
106
genotypic vs. gonadal vs phenotypic sex
genotypic: presence of Y chromosome
gonadal: presence of SRY gene (encodes testes determining factor)
phenotypic: hormones→gonads
107
describe the role of FSH in testicular function
**FSH→testes→sertoli cells→**
* increased transcription of androgen binding protein, P450 aromatase, growth factors
* **inhibin:** negative feedback on ant. pituitary and suppress FSH secretion (suppresses leydig cell proliferation)
108
describe the role of LH in testicular function
**LH→testes→leydig cells→testosterone→**
* increased transcription of enzymes involved in testosterone synthesis
* **stimulate sertoli cells**
* **negative feedback** on hypothalamus and ant. pituitary
109
describe the role of testosterone in sex differentiation
testosterone→wolffian duct→male internal genitalia (vas deferens, semnal vesicles, and ejaculatory duct)
* without testosterone, wolffian duct degenerates (female)
testosterone→DHT→external genitalia and prostate
110
describe the role of AMH in sex differentiation
AMH (from sertoli cells)→mullerian duct→degeneration of mullerian ducts
* no androgens=no AMH→mullerian duct becomes fallopian tubes, cervix, and uterus
111
kallman syndrome
* hypogonadotropic hypogonadism; lack of LH and FSH, patient presents with failure to enter puberty
* congenital anosmia: mutations prevent neurosensory neurons from extending axons into brian AND preventing migration of GnRH neurons into hypothalamus
112
male pseudohermaphroditism
deficit in mechanims by which androgens act in genetic males
* *5a-reductase deficiency:* low DHT (no external genitalia or prostate) but normal testosterone
* *androgen insensitivity:* normal testosterone and DHT but absent/defective androgen receptors→female development (except AMH→degeneration of mullerian ducts)
113
describe why the pubertal growth spurt occurs first in girls
bone maturation occurs indirectly through estradiol metabolites and is more gradual in men than in women; estradiol levels rise earlier and reach higher levels in women than in men
114
kennedy's disease (spinobulbar muscular atrophy)
x-linked LMN disease caused by mutations in androgen receptor; CAG repeat expansion→weakness of tongue and mouth, fasciculations, progressive weakness of limbs
115
what are the neural components of erection and ejaculation?
"Point and Shoot"
* parasymp: responsible for vasodilation and smooth muscle relaxation→tumescence (erection)
* symp: maintains tedumescence, responsible for emission and ejaculation
116
IVF procedures
* controlled ovarian hyperstimulation
* embryo retrieval using ultrasound
* IVF
* embryo transfer
* luteal phase support
117
clomiphene citrate
estrogen antagonist, inhibits negative feedback of estrogen on hypothalamust→increased secretion of GnRH and FSH/LH; used during controlled ovarian hyperstimulation so that more than 1 mature oocyte is produced
118
ovarian hyperstimulation syndrome
excessive response to medicines (especially gonadotropins) used to stimulate follicle growth due to **large number of growing follicles (\>25) along with high estradiol levels**→bloating, nausea, weight gain due to transufation of protein rich fluid
119
how old are embryos when they are transferred into the uterus during IVF
* day 5 (blastocyst): preferred because of higher rates of implantation survival
* day 3 (cleavage stage): suited to patients with less than 6 embryos, low quality embryos or previous IVF failures
120
luteal phase support
progesterone supplementation daily or hCG once or more during the luteal phase to promote development of endometrium
