Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
195 Cards in this Set
- Front
- Back
|
Adrenal Incidentaloma |
An incidentally discovered adrenal mass |
|
|
Phaeochromocytoma |
A tumour of chromaffin tissue (adrenal medulla) secreting noradrenaline |
|
|
Paraganglioma |
Tumour of sympathetic tissue secreting noradrenaline |
|
|
Broad Ligament |
Double layer of peritoneum consisting of mesosaplinx (superior to ovary), mesovarium (over ovary), mesometrium (inferior to ovary) |
|
|
Ovarian Ligament |
Connects ovary to uterus |
|
|
Transverse/Cardinal Ligament |
Connects lower uterus to lateral pelvic wall. Contains uterine vessels |
|
|
Suspensory Ligament |
Continuation of the broad ligament connecting ovaries to the peritoneum. |
|
|
Uterosacral Ligament |
Connects posterior uterus to the sacrum |
|
|
Round Ligament |
Connects uterus, via the inguinal canal to the labia majora |
|
|
Eversion (Anteversion or retroversion) |
Positional changes in the uterus relative to the long axis of the vagina |
|
|
Flexion (Anteflexion or retroflexion) |
Positional changes in the uterus relative to the cervix |
|
|
Ovarian Artery |
Comes off the abdominal aorta at L2 and travels in the suspensory ligament |
|
|
Uterine Artery |
Branch off the internal iliac artery and travels in the transverse ligament |
|
|
Vaginal Artery |
Variable - may be a branch of the uterine, internal iliac or vesicular artery |
|
|
Innervation to the Superior 3/4 of the Female Reproductive System |
T12-L3, general visceral afferents through the lumbosacral plexus |
|
|
Innervation to the Inferior 1/4 of the Female Reproductive System |
S1-4, somatic innervation, pelvic splanchnics |
|
|
Pelvic Pain Line |
Represents the change of the female reproductive system from intraperitoneal to subperitoneal and therefore a change in innervation and referred pain |
|
|
Pelvic Inlet Borders |
A - Pubic symphysis |
|
|
Pelvic Outlet Borders |
A - Pubic symphysis |
|
|
Fibroid |
A benign tumour of muscular and fibrous tissue. typically develop in the wall of the uterus. |
|
|
Gamete |
A mature haploid reproductive cell |
|
|
Blood Testis Barrier |
Between the adluminal and basal layers of the seminiferous tubule, formed by adherens, gap junctions and tight junctions between Sertoli cells. Separates sperm from the immune system (preventing autoimmune orchitis) and allows selective transport of ions and small molecules. |
|
|
Acrosomal Reaction |
The fusion of the sperm plasma membrane and the acrosome membrane to release hydrolytic enzymes. Induced by contact with zona pellucida |
|
|
Capacitation |
Within the female reproductive tract sperm become hyperactivated and acquire the ability to undergo the acrosome reaction |
|
|
Izumo |
Protein on sperm for fusion with the oocyte membrane |
|
|
Juno |
Protein on oocyte membrane for fusion with sperm |
|
|
Cortical Reaction |
Triggered by increased Ca involves the release of cortical granules (proteases) which diffuse into the zona pellucida and induces the zona reaction |
|
|
Zona Reaction |
An alteration i the structure of the zona pellucida catalysed by proteases so that sperm can no longer bind or penetrate |
|
|
Syngamy |
The last stage of fertilisation in which the pronuclear membranes break down, chromatinintermixes and the nuclear envelope reforms |
|
|
Fertility |
A measure of the actual outcome of the reproductive process - the number of children born to an individual/couple |
|
|
Fecundability |
Probability of conceiving each month - the monthly chance of pregnancy or monthly fertility rate rate for an individual or for a population |
|
|
Fecundity |
Measure of the ability to conceive and produce a live birth |
|
|
Infertility |
The inability to conceive after a period (2 years according to NICE) of unprotected intercourse or the inability to carry a pregnancy to term |
|
|
Subfertility |
A state of reduced fertility - after one year of inability to conceive people generally seek medical advice |
|
|
Endometriosis |
Endometrial tissue growth escalates in ectopic sites resulting in scarring and adhesions |
|
|
Normozoospermic |
>15 million/ml |
|
|
Oligozoospermic |
<15 million/ml |
|
|
Asthenozoospermic |
<32% rapid and medium forward progressive motility |
|
|
Teratozoospermic |
<4% normal morphology |
|
|
Azoospermic |
No sperm |
|
|
Aspermic |
No ejaculate |
|
|
Normal Ejaculation |
Under sympathetic control. |
|
|
Retrograde Ejaculation |
Incompetence of the urethral sphincter causes ejaculation into the bladder because this is the path of least resistance. |
|
|
Contraception |
The prevention of pregnancy through the prevention of ovulation, fertilisation or implantation of pre-embryo |
|
|
PEARL Index |
Out of 100 women using contraception for one year, how many will get pregnant by the end of the year |
|
|
Natural Family Planning: Rhythm Method |
Safe period for intercourse and avoid intercourse around ovulation |
|
|
Natural Family Planning: Billing's Method |
Judge safe period for intercourse by changes in cervical mucus: |
|
|
Natural Family Planning |
Changes in the cervix: |
|
|
Lactational Amenorrhoea |
Fully breast feeding 5-6x a day causes amenorrhoea |
|
|
Advantages to Natural Family Planning |
No side effects |
|
|
Disadvantages of Natural Family Planning |
Unreliable Messy Clinical |
|
|
Benefits of Combined Hormonal Contraceptive |
Highly effective |
|
|
Benefits of Progesterone Only Pill |
Effective |
|
|
Side Effects of Combined Oral Contraceptive |
Headaches |
|
|
Disadvantages of Progesterone Only Pill |
Must take regularly |
|
|
Disadvantages of Injectable Contraceptives |
Cant be removed once administered |
|
|
Advantages of Injectable Contraceptives |
Highly effective |
|
|
Advantages of Contraceptive Implant |
Highly effective |
|
|
Disadvantages of Contraceptive Implant |
Surgical |
|
|
Advantages of the Mirena Intrauterine System |
Reduces bleeding, pain, pelvic infection, ectopic pregnancy |
|
|
Advantages of the IUD Copper Coil |
Highly effective
No systemic effects Reversible Independant of intercourse Cheap |
|
|
Disadvantages of the IUD Copper Coil |
If pregnancy occurs - septic abortion, miscarriage, ectopic pregnancy |
|
|
Levonelle |
A type of emergency contraceptive that is efficient up to 96 hours after unprotected intercourse (licensed for 72 hours). 70-80% efficacy. Side effects: nausea, vomiting - if these occur within 2 hours of taking, and alternative method is required. |
|
|
ellaOne |
A type of emergency contraceptive that can be given up to 5 days after unprotected intercourse. It is a synthetic progesterone receptor modulator and causes inhibition or delay of ovulation and changes in the endometrium. |
|
|
Oligoamenorrhoea |
Irregular cycle |
|
|
Primary Amenorrhoea |
Failure of menarche after the age of 16 |
|
|
Secondary Amenorrhoea |
Absent periods for 6 months after menarche |
|
|
Fundal Height |
The distance from the pubis to the fundus of the uterus - correlates with weeks gestation. Past week 20 +1cm = +1 week |
|
|
Intrauterine Insemination |
Injection of sperm into the uterus |
|
|
The Human Fertilisation and Embryology Authority |
UK's independent regulator overseeing the use of gametes and embryos in fertility treatment and research.
Licences fertility clinics |
|
|
Intrinsic Regulation of Stem Cell Niche |
GF/cytokine receptors |
|
|
Extrinsic Regulation of Stem Cell Niche |
Neighbouring cells |
|
|
Totipotent |
Has the potential to give rise to any and all human cells |
|
|
Pluripotent |
Can give rise to all tisue types but not an entire organism |
|
|
Multipotent |
Can give rise to a limited range of cells within a tissue type |
|
|
Bipotent |
Give rise to itself and 2 different types of cells |
|
|
Unipotent |
Give rise to itself and one other cell type |
|
|
Stochastic Model |
All cancer cells are potential cancer stem cells but have low probability of proliferation in clonogenic assays. |
|
|
Cancer Stem Cell Model |
Only a small definable subset of cancer cells are cancer stem cells that ave the ability to proliferate indefinitely. |
|
|
Receptive Endometrium |
In the mid-luteal phase when secretory activity peaks, endometrial cellsare rich in glycogen and lipids. Glands increase in number and size. Maintained by high oestrogen and progesterone. Marked by changes on surface epithelium. |
|
|
Haemochoroidal Placenta |
Chorion is in direct contact with the blood |
|
|
Endotheliochoroidal Placenta |
Endothelium of maternal blood vessel is in direct contact with the chorion |
|
|
Epitheliochoroidal Placenta |
Maternal uterus epithelium is in direct contact with the chorion |
|
|
Placenta Accreta |
Due to excessive trophoblast invasion the placenta invades and is inseperable from the uterine wall |
|
|
First Phase of Foetal Growth |
4-20 weeks |
|
|
Second Phase of Foetal Growth |
20-28 weeks |
|
|
Third Phase of Foetal Growth |
28 weeks - term Hypertrophy Continued increases in protein and weight but no increase in DNA |
|
|
Barker Hypothesis |
Most growth restricted babies show catch-up growth in childhood though may have smaller size in adulthood |
|
|
Thrifty Phenotype |
Evolved to offer advantage in a famine environment - probelms in industrialised society as phenotype persists into adulthood |
|
|
Intrauterine Growth Restriction |
Failure of a foetus to achieve his or her growth potential |
|
|
Small for Gestational Age |
Birth weight <10th centile for gestational age |
|
|
Large for Gestational Age |
Birth weight >90th centile |
|
|
Low Birth Weight |
Birth weight less than a certain threshold (e.g. 2500g) |
|
|
Gestational Diabetes Mellitus |
Any degree of glucose intolerance with its onset or recognition for the first time during pregnancy |
|
|
Shoulder Dystocia |
Shoulder stuck behind pubic symphysis. 4 minutes before foetal brain damage |
|
|
congenital Malformation |
Incomplete or abnormal formation of a structure Alteration of its normal conficuration |
|
|
Congenital Disruption |
Morphological alterations of an already formed structure |
|
|
Congenital Deformation |
Congenital anomaly due to mechanical factors |
|
|
Syndromes |
A group of anomalies with a specific known cause |
|
|
Association |
Abnormalities that tend to occur together but the cause is not determined |
|
|
Teratogen |
An agent that can cause or predispose to a birth defect |
|
|
Spina Bifida Occulta |
Midline bone defect (gap in the vertebral column) which is often asymptomatic and undetected |
|
|
Spina Bifida Meningocoele |
Meninges and CSF protrude out of a midline bone defect (gap in vertebral column) |
|
|
Spina Bifida Myelomeningocoele |
Meninges, CSF and spinal cord protrude through a midline bone defect (gap in the vertebral column) |
|
|
Omphalocoele |
Transparent sac of amnion attached to hte umbilical ring containing herniated viscera that occurs as a result of persistence of embryonic midgut herniation. |
|
|
Gastroschisis |
Evisceration of foetal intestine through a paraumbilical wall defect due to involution of the right umbilical vein or right vitelline artert or abnormal body wall folding |
|
|
Antenatal Care |
A planned examination and observation of the woman from conception till the birth |
|
|
Aneuploidy |
Different numbers of a chromosome |
|
|
Polyploidy |
Different numbers of a whole chromosome set |
|
|
Puberty |
The physiological, morphological and behavioural changes as the gonads switch from infantile to adult forms |
|
|
Kisspeptin |
Product of the gene Kiss1. |
|
|
Precocious Puberty |
Onset of secondary sexual characteristics before 8 years (girl) or 9 years (boy) |
|
|
Congenital Adrenal Hyperplasia |
21-hydroxylase deficiency resulting in deficiency of mineralocorticoids and glucocorticoids and sex hormone excess. The deficiencies cause feedback resulting in an increased release of ACTH and therefore hyperplasia of the adrenal glands. |
|
|
17alpha-hydroxylase deficiency |
Mineralocorticoid excess --> hypertension |
|
|
5alpha-reductase deficiency |
46XY with ambiguous genitalia - internal are male external may look female. External appearance less male |
|
|
Androgen Insensitivity Syndrome |
Mutations in androgen receptors --> unresponsive to androgens |
|
|
Infancy Growth |
Rapid but rapidly decelerating growth in the first 2-3 years |
|
|
Childhood Growth |
Steady growth of ~5cm/year |
|
|
Puberty Growth |
Growth spurt - increase in height velocity due to sex hormones Ends age 14-15 in girls and 16-17 in boys |
|
|
Compaction |
The formation of inside-outside polarity. Inner cell mass will form the embryo and the trophoblast will form the placenta. |
|
|
Idiopathic Ovarian Failure |
Gonadotropin secretion is normal but is insufficient to support a normal menstrual cycle due to end organ insensitivity. This means that oestrogen levels fail to rise and follicles fail to mature in response to FHS and LH.
|
|
|
Hormonal Features of Polycystic Ovary Syndrome |
Increased LH and andorgens |
|
|
Abbreviated Luteal Phase |
There is decreased progesterone which leads to poor luteinisation. |
|
|
Maternal Problems Leading to Infertility/Subfertility |
Cervical impotence |
|
|
Causes of Failure in Sperm Production |
Congenital testicular deficiency (e.g. Kilefelter, Y chromosome deletions) Maldescended testes Trauma (e.g. testicular torsion) Orchitis (mumps) Endocrine disorders |
|
|
Clinical Features of Physiological Hyperprolactinaemia |
Hypogonadism - oligoamenorrhoea, oestrogen deficiency Glactorrhoea |
|
|
Causes of Physiological Hyperprolactinaemia |
Prolactinoma Loss of dopamine inhibition - pituitary stalk compression or disconnection Dopamine antagonists (phenothiazines, metoclopramide, TCA, verapamil) Hypothyroidism |
|
|
Features of Ovarian Insufficiency |
Amenorrhoea Oestrogen deficiency Elevated LH and FSH |
|
|
Causes of Premature Ovarian Insufficiency |
Turners syndrome Autoimmune (Addisons, Graves) - inflammatory infiltration of follicles, antiovarian antibodies Chemotherapy, radiotherapy, surgery FSHR mutations Fragile X premutation (FMR1 gene) |
|
|
Features of Polycystic Ovary Syndrome |
Oligoamenorrhoea, hirsutism, obesity, infertility/anovulation, polycystic ovaries (ultrasound), insulin resistance Due to hyperandrogenism NOT oestrogen deficiency |
|
|
Diagnostic Criteria for PCOS |
2 out of: oligoamenorrhoea, clinical/biochemical signs, polycystic ovaries Plus exclusion of other causes (androgen excess, Cushings, tumours) |
|
|
Acanthosis Nigricans |
Dark area of skin on the back of the neck or underam - a sign of insulin resistance |
|
|
Hirsutism |
Male hormone dependent hair growth: upper lip, chin, anterior neck, sideburn, breasts, pubic |
|
|
Androgenic Alopecia |
Male pattern baldness |
|
|
PCOS Treatment: obesity and oligoamenorrhoea |
Metformin, lifestyle changes, MPA |
|
|
PCOS Treatment: anovulatory infertility |
Metformin, clomiphene, IVF |
|
|
PCOS Treatment: hirsutism |
Yasmin, Vanqua cream, cosmetic removal, spironolactone |
|
|
Features of Classical 21-hydroxylase Deficiency |
Neonatal/infacy presentation Adrenal androgen excess Salt wasting |
|
|
Features of Non-Classical 21-hydroxylase Deficiency |
Childhood/adult presentation Premature puberty, hirsutism, PCOS |
|
|
5 alpha Reductase Deficiency |
46XY karyotype but female appearance Unable to convert testosterone to DHT Lack of virilisation of external genitalia Abdominal testes Primary amenorrhoea |
|
|
Causes of Male Primary Hypogonadism |
Trauma - surgery, torsion Chemotherapy, radiotherapy Undescended testes Mumps/orchitis Iron Varicocoele Chromosomal abnormalities (Klinefelter's) Liver cirrhosis Renal failure Thyroid dysfunction Myotonic dystrophy |
|
|
Causes of Male Secondary Hypogonadism |
Pituitary tumours Hyperprolactinaemia Hypothalamic disorders - craniopharyngioma, Kallman's syndrome, GnRH therapy Androgen use and abuse |
|
|
Hormone Levels in Male Primary Hypogonadism |
Low testosterone High LH and FSH |
|
|
Hormone Levels in Male Secondary Hypogonadism |
Low testosterone Low LH and FSH |
|
|
Problems with IVF |
Multiple pregnancies Ovarian hyperstimulation syndrome Transvaginal oocyte retreival --> injury to bladder, bowel, blood vessels, infection Risk of congenital abnormalities - e.g. ICSI male offspring with fertility problems More problems in pregnancy and labour Expensive limited funding |
|
|
The Human Fertilisation and Embryology Authority - HFEA |
UK's independent regulator of the use of gametes and embryos i fertility treatment and research. Licences fertility clinical and centres for IVF and embryo research |
|
|
Identification of Stem Cells |
Appearance - binding of labelled antibodies specific to cell surface proteins Function - in-vitro self-renewal, transplantation in mice to forma teratoma |
|
|
Induced Pluripotent Stem Cells |
Reversal of differentiation thorugh transfection of a terminally differentiated cell (e.g. fibroblast) with pluripotency inducing transcription factors |
|
|
Reprogramming of Terminally Differentiated Cells |
Differentiated --> pluripotent |
|
|
Dedifferentiation of Terminally Differentiated Cells |
Differentiated --> multipotent |
|
|
Transdifferentiation of Terminally Differentiated Cells |
Switch cells to a different differentiation |
|
|
Cancer Stem Cells |
Rare cells within tumours with the ability to self-renew and give rise to the phenotypically diverse tumour cell population to drive tumourigenesis |
|
|
Double Bohr Shift |
Increase in pH on the foetal side results in O2 uptake at lower pO2 |
|
|
Non-Cyanotic Congenital Cardiac Abnormalities |
Ventricular septal defect Atrioseptal defect Patent ductus arteriosus These result in a left-->right shunt |
|
|
Cyanotic Congenital Cardiac Abnormalities |
Tetralogy of fallot Persistent truncus arteriosus Transposition of great vessels Tricuspid atresioa Hypoplastic left heart These result in a right-->left shunt |
|
|
Ventricular Septal Defect |
Failure of closure of the ventricular septum resulting in blood flowing from the left ventricle into the right ventricle (because pressure is higher in the left). This overloads the right ventricle and causes pulmonary hypertension and therefore remodelling of the pulmonary vasculature. This becomes much more dangerous if the left right shunt reverses to a right left shunt resulting in high pressure deoxygenated blood being forced into the systemic circulation |
|
|
Atrioseptal Defect |
Failure of closure of the formaen primum or secundum. Left to right shunt but often goes undetected |
|
|
Patent Ductus Arteriosus |
Ductus arteriosus fails to close. Results in pulmonary hypertension. Treat with NSAIDs (inhibit PG production as these keep it open) |
|
|
Tetralogy of Fallot |
Ventricular septal defect Pulmonary stenosis Right ventricular hypertophy Overriding aorta (over both ventricles) Results in a left-->right shunt protected by pulmonary stenosis so is a right-->left shunt |
|
|
Transposition of Great Vessels |
Aorta - right ventricle Pulmonary artery - left ventricle Patent ductus arteriosus keeps alive, otherwise incompatible with life |
|
|
Maternal Factors Involved with Growth Regulation |
Ethnicity, BMI, cigarettes (dose dependant, more = smaller), alcohol, cocaine, nutrition, hypoxia |
|
|
Foetal Factors Involved with Growth Regulation |
Chromosomal anomalies (e.g. Edwards syndrome) Growth factors - IGF, thyroxine Congenital infection - CMV, toxoplasmosis, rubella |
|
|
Placental Factors Involved with Growth Regulation |
Primary - abnormality of placental structure/function Secondary - hypertension, chronic renal disease, vasculitis, prothrombotic disorders Unequal placental sharing in multiple gestation |
|
|
Asymmetrical IUGR |
Due to uteroplacental insufficiency (decreased glycogen stores) decreased abdominal circumference Head growth is maintained at the expense of abdominal growth |
|
|
Symmetrical IUGR |
Due to an early growth insult and disruption of growth process regulation or cell hyperplasia stage Foetus is small all over |
|
|
Foetal Wellbeing Assessment |
Cardiotocograph for short term wellbeing - regular zig zag = normal Umbilical artery, middle cerebral artery, ductus venosus doppler scans, liquor volume (kidney function) for long term wellbeing |
|
|
Maternal Complications of Gestational Diabetes Mellitus |
Pre-eclampsia Preterm labour Instrumental delivery, caesarian section Diabetes in later life |
|
|
Foetal Complications of Gestational Diabetes Mellitus |
Macrosomia Shoulder dystocia Polyhydramnios Perinatal mortality and morbidity Foetal programming and increased risk of adult diabetes |
|
|
Molar Pregnancy |
A non-viable pregnancy resulting from the abnormal fertilisation of an empty egg meaning the genome is completely paternal. Can develop intogestational trophoblastic disease and choriocarcinoma |
|
|
Sequence |
When a defect leads to a cascade of further abnormalities |
|
|
Local Mechanisms of Modification of Maternal T Cell Response |
Reduced MHC expression on trophoblast IDO mediated tryptophan depletion FAS-ligand dependent deletion of T cells LIF, PDL-1 production |
|
|
Peripheral Mechanisms of Modification of Maternal T Cell Response |
Altered T cell cytokine production Shift from Th1 --> Th2 Hormonal immunomodulation Deletion of foetal specific T cells |
|
|
On First Contact with HCP Pregnant Women are Given Specific Information On: |
Folic acid supplements Food hygeine - how to reduce the risk of a food acquired infection Lifestyle - smoking cessation, recreational drug use, alcohol consumption Antenatal screening - risks, benefits and limitations |
|
|
Chorionic Villous Sampling |
Taking a sample of chorionic villous cells under ultrasound guidance either transabdominally or transcervically. Cells are then used for chromosome and DNA analysis. Performed after 11 weeks as is associated with limb reduction defects if carried out before 9 weeks. |
|
|
Amniocentesis |
Sample of the amnion taken transabdominally under ultrasound guidance. Cells from this are then used for chromosome and DNA analysis. This can be carried out from 15 weeks gestation. |
|
|
Free Foetal DNA |
Obtained from maternal blood from 9 weeks and used for chromosome and DNA analysis (e.g. Y chromosome = male, aneuploidies, paternal alleles for single gene disorders) |
|
|
Start of Puberty |
Testicular volume = 4 ml (10-14 years) Breast stage 2 (9.2-13.2 years) |
|
|
Rhizomelic |
Short upper parts of limbs (humerus and femur) |
|
|
Mesomelic |
Short lower parts of limbs (forearm and leg) |
|
|
Acromelic Dysplasia |
Dysplasia of the extermities |
|
|
Osteochrondroplasias |
Skeletal dysplasias, genetic abnormalities of cartilage and bone growth |
|
|
Idiopathic Short Stature |
Constitutional delay of growth and puberty with normal height prediction Transient short stature |
|
|
Psychosocial Short Stature |
Over the age of 3 Emotional rejection is key factor Physical/sexual abuse may be associated Hyperphagia Reverses when child is nurtured outside of the stressful environment |
|
|
Hyperphagia |
Eat a lot but don't grow |
|
|
Overgrowth With Impaired Final Height |
Precocious puberty CAH McCune Albright Syndrome Hyperthyroidism |
|
|
Overgrowth With Normal Adult Height |
Beckwith-Weidemann Syndrome Sotos Syndrome |
|
|
Overgrowth With Increased Final Height |
Androgen/oestrogen deficiency Oestrogen deficiency Pituitary gigantism (GH excess) Klinefelter syndrome Marfan syndrome Homocystinuria |
|
|
Indications for ICSI |
Sperm dysfunction Fertilisation failure Surgical sperm retrieval Cryptocytozoospermia |
|
|
Control of Foetal Circulation |
Catecholamines --> tonic vasoconstriction Vagus = 160bpm --> 140bpm Baroreceptor reflex Peripheral chemoreceptors = hypoxia --> bradycardia + peripheral vasoconstriction |
|
|
Pseudoglandular Period of Lung Development |
Bronchial buds divide --> terminal bronchioles Glandular appearance |
|
|
Canalicular Period of Lung Development |
Lumen enlarge Respiratory bronchioles, alveolar ducts Highly vascularised |
|
|
Terminal Sac Period of Lung Development |
Alveolar ducts --> terminal sacs Simple cuboidal --> squamous Type I and II cells Capillaries in close contact |
|
|
Alveolar Period of Lung Development |
Epithelia continues to thin Capillaries bulge into terminal sacs --> alveoli --> 3 years - more alveoli 3-8 years - increase in size |
|
|
True Precocious Puberty |
Central cause (GnRH) LH:FSH >1 |
|
|
Precocious Pseudopuberty |
Gonadal and adrenal sex hormones LH:FSH <1 |
