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203 Endocrinology and Reproduction > Theme 2 - Reproductive system, fetal development and birth > Flashcards

Theme 2 - Reproductive system, fetal development and birth Flashcards

1
Q

8 effects of testosterone

A 
Increased aggression and libido*
Enlargement of the larynx
Male pattern pubic hair
Maturation of genitalia
Muscle development
Sperm production
Bone growth*
Acne
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2
Q

8 effects of oestrogen and progesterone

A 
Bone Growth
Female psyche
Fair complexion
Breast Development
Widening of the pelvis
Maturation of genitalia
Female pattern pubic hair
Subcutaneous fat deposition
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3
Q

Draw a graph to show changes in hormone levels throughout menstrual cycle

A 
Start on day of bleeding
Increase oestrogen and FSH
Drop in FSH then oestrogen
LH surge (ovulation)
Increase in progesterone and oestrogen then both drop off
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4
Q

What acts of legislation governs conscientious objections and regarding reproduction and fertility what are the key points?

A

Abortion Act 1967
Human Fertilisation and Embryology Act 1990
no person shall be under any duty, whether by contract or by any statutory or other legal requirement, to participate in any treatment authorised by this Act to which he has a conscientious objection
Nothing in subsection (1) of this section shall affect any duty to participate in treatment which is necessary to save the life or to prevent grave permanent injury to the physical or mental health of a pregnant woman

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5
Q

What is the time limit on embryo research, and why?

A

14 days – before possibility of twinning. Justification is that prior to this stage, the embryo isn’t part of a continuum for an identifiable future person.

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6
Q

What is the Warnock position on moral importance and at what stage of development?

A

there is no particular part of the developmental process that is more important than another; all are part of a continuous process

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7
Q

What 3 things to female oral contraceptives do to prevent conception?

A

Prevent ovulation
Thicken cervical mucus
Hostile endometrium

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8
Q

What effect does the progesterone only contraceptive pill have on the menstrual cycle and how does it prevent conception?

A

inhibit ovulation by suppression of LH surge, thicken cervical mucus and render the endometrium ‘hostile’.

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9
Q

3 examples of progesterone only contraceptive

A

norethisterone, levonorgestrel, desogestrel

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10
Q

Adverse affects of progesterone only oral contraception (up to 7)

A

Menstrual irregularity, nausea, vomiting, headache. Breast discomfort, weight changes, changes in libido.

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11
Q

Potential male contraceptive hormone mechanism of action?

A

Injection of testosterone agonist to generate negative feedback and progesterone to suppress LH. The aim is to halt spermatogenesis.

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12
Q

Adverse affects of male hormone contraception

A

The most common adverse events were acne, injection site pain, increased libido, and mood disorders

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13
Q

What 2 types of neuron stimulate GnRH

A

Kisspeptin and the KNDy

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14
Q

What des FSH act upon and what does this produce?

A

Primary follicle in granulosa cells

To produce oestrogen and inhibin

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15
Q

FSH leads to an increase of what type of receptor in the graulosa cells?

A

LH

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16
Q

Oestrogen and inhibin usually inhibit FSH by negative feedback, but when is this not the case and what does this cause?

A

When oestrogen reaches critically high levels they positively act on the Kisspeptin and KNDy neurones which stimulate the production of GnRH which in turn produces LH (due to increased frequency and amplitude of the pulse from GnRH). Triggers ovulation

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17
Q

How can ovulation be diagnosed?

A

Day 21 progesterone blood test
Urinary LH detection kit
Trans vaginal pelvic ultrasound

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18
Q

Causes of ovulation problems in the hypothalamus?

A

Hypothalamus (lack of GnRH)

  • Kiss1 gene deficiency- rare
  • GnRH gene deficiency - rare
  • weight loss/stress related/excessive exercise
  • anorexia/bulimia
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19
Q

Causes of ovulation problems in the pituitary?

A

Pituitary (lack of FSH and LH)

  • pituitary tumours (prolactinoma/other tumours)
  • post pituitary surgery /radiotherapy
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20
Q

Causes of ovulation problems in the ovary?

A

Ovary (lack of oestrogen/progesterone)

  • Premature ovarian insufficiency
  • Developmental or genetic causes eg Turner’s syndrome
  • Autoimmune damage and destruction of ovaries
  • Cytotoxic and radiotherapy
  • Surgery

Polycystic Ovarian Syndrome: commonest cause

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21
Q

Amenorrhoea definition

A

lack of period for more than 6 months. Primary - never. Secondary -have stopped.

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22
Q

Oligomenorrhoea definition

A

irregular periods. Usually occurring more than 6 weeks apart.

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23
Q

Polymenorrhoea definition

A

periods occurring less than 3 weeks apart

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24
Q

Hirsuitism definition

A

Androgen dependent - in male distribution

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25
Q

3 Clinical features of PCOS

A 
Hyperandrogenism
-Hirsutism, acne
Chronic oligomenorrhoea / amenorrhoea
- 9 periods / year
-Subfertility
Obesity (but 25% of women with PCOS are “lean”)
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26
Q

How does PCOS affect LH and FSH levels?

A

Exaggerated pulsatile release of GnRH causes an increase of circulating LH an an increase in the ratio of LH:FSH.

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27
Q

How does the increase in LH:FSH ratio in PCOS affect androgen levels?

A

Ovarian theca cells respond to LH by increasing conversion of cholesterol to androgen. The realtive lack of FSH prevents this from being converted to oestrogen.

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28
Q

How does hyperandrogenism in PCOS account for its associated symptoms?

A

Increased androgen causes local follicular arrest and therefore amenorrhea/oligoamenorrhea.
Stimulation of sex-responsive hair follicles causes hirsuitism and acne.

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29
Q

What happens to insulin resistance in pats with PCOS?

A

Insulin resistance increases

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30
Q

How does insulin resistance in pts with PCOS relate to hyperandrogenism?

A

Insulin synergises with LH to increase androgen production by theca cells.
Inhibits hepatic production of SHBG and therefore increases the amount of free androgen.

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31
Q

Are the cysts in PCOS?

A

Actually small follicles

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32
Q

What are the effects of testosterone and oestrogen on SHBG?

A

SHBG increased by oestrogens

SHBG decreased by testosterone thus releasing more free testosterone

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33
Q

What is the most common cause of anovulation?

A

PCOS

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34
Q

What are the 3 reproductive affects of PCOS?

A

Reduction in fertility (to a varying degree)
Increased risk if miscarriage
Increased risk of gestational diabetes

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35
Q

How does PCOS relate to risk of endometrial cancer and why?

A

Increased risk due to the lack of progesterone.

Endometrial cancer also associated with T2 diabetes and obesity

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36
Q

Best treatment for PCOS

A

Lifestyle modification - diet and exercise

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37
Q

How would the COCP help treat PCOS? (3)

A

increases SHBG and thus decreases free testosterone
decreases FSH & LH and therefore ovarian stimulation
regulates cycle & decreases endometrial hyperplasia

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38
Q

What are the risks with using the COCP to help treat PCOS?

A

Increase weight gain may exacerbate metabolic sydrome

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39
Q

What medication could be used in combination with the COCP to treat PCOS? 2 examples

A

Anti androges
-Spironolactone - anti mineralocorticoid and anti androgen properties
-Cyproterone Acetate (oral tablet)
inhibits binding of testosterone & 5 alpha dihydrotestosterone to androgen receptors

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40
Q

What drug could be used to help treat the insulin resistance in women with PCOS?

A

Metformin

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41
Q

Definition of Premature ovarian failure/primary ovarian insufficiency

A

Cessation of menses before age 40 in absence of genetic abnormalities.

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42
Q

How may POF/POI present?

A

Primary or secondary amenorrhea . Possibly with hot flashes.

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43
Q

Aetiology of POF/POI?

A

Autoimmune
Iatrogenic - surgery/radiotherapy
Genetic - Turners syndrome
Genetic predisposition

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44
Q

What is Turner’s syndrome?

A

Absence of second sex chromosome
XO 50%
rest mosaicism or partial

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45
Q

How may Turner’s syndrome present?

A 
Women
Primary/secondary amenorrhea 
Short stature
webbed neck 
shield chest
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46
Q

Conditions associated with Turner’s?

A 
CV system
-Coarctation of aorta
-Aortic dissection
-Hypertension (adults)
Renal
Congenital abnormalities
Metabolic syndrome
Hypothyroidism
Ears / hearing problems
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47
Q

Most common causes of hirsuitism?

A

PCOS or idiopathic hirsuitism (95%)

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48
Q

When would hirsuitism be a cause for concern?

A 
Sudden onset of severe symptoms
Virilisation
Frontal balding
Deepening of voice
Male-type muscle mass
Clitoromegaly
Possible Cushing’s syndrome
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49
Q

Least common causes of hirsuitism?

A

Cushings
Ovarian tumor
Non-classical congenital adrenal hyperplasia (CAH)

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50
Q

What is the causes the majority (95%) of cases of congenital adrenal hyperplasia?

A

21-hydroxylase deficiency

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51
Q

How will CAH present in children and what type of CAH is this known as?

A 
Classic/severe
-Salt wasting
Hypovolaemia, shock
-Virilisation
Ambiguous genitalia in girls
Early virilisation in boys
Precocious puberty
-Abnormal growth
Accelerated early
Premature fusion
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52
Q

How will CAH present in adults and what type of CAH is this known as?

A 
non-classic/mild
Hirsutism
Oligo / amenorrhoea
Acne
Subfertility

Similar to ‘PCOS’ presentation

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53
Q

Where in the testes does spermatogenesis occur?

A

seminiferous tubules

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54
Q

Which cells produce testosterone?

A

Leydig cells

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55
Q

Following production in the Leydig cells, where is testosterone distributed to? 3

A

majority into blood stream
some into lymphatic system
some into the Sertoli cells within seminiferous tubules to facilitate spermatogeneis

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56
Q

What cells in the testes are stimulated by LH and what is the affect of this?

A

Leydig cells - to produce androgen

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57
Q

What cells in the testes are stimulated by FSH and what is the affect of this?

A

Sertoli cells - for spermatogenesis

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58
Q

What are the 3 elements of spermatogenesis?

A

Mitotic proliferation to produce lots of cells
Meiotic division to generate genetic diversity
Cell modelling to package chromosomes for delivery to the oocyte

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59
Q

In what part of the semiferous tubule does mitosis od the prospermatogonia occur?

A

Basal

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60
Q

What is the name of the cells that emerge from the first round of mitosis during spermatogenesis?

A

A1 spermatogonia

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61
Q

What is the name of the cells that emerge from the final round of mitosis during spermatogenesis?

A

primary spermatocytes

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62
Q

Where does meiosis of sperm primary spermatocytes take place?

A

adluminal compartment

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63
Q

What is the name of the cells that emerge from the first division of mieosis during spermatogenesis?

A

Secondary spermatocytes

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64
Q

What is the name of the cells that emerge from the second division of mieosis during spermatogenesis?

A

spermatid

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65
Q

Draw and label a sperm - 5 points

A

5: Tail for forward propulsion
4: Midpiece with mitochondria for energy
3: Nucleus with packaged chromosomes
2: Cap region forms for sperm-oocyte fusion
1: Acrosome

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66
Q

What is the interval between subsequent sperm production?

A

16 days

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67
Q

Time for completion of spermatogenesis?

A

64 days

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68
Q

What’s in jiz and whats the point of it? 4 points

A

Nutrition (fructose, sorbitol)
Buffer (to protect against vaginal acidity)
Antioxidants (ascorbic acid, hypotaurine

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69
Q

In the endocervix, what hormones make the mucus watery/inhibit secretory activity?

A

Oestrogen - watery

Porgesterone - inhibit production

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70
Q

From what day in the cycle can sperm penetrate the mucus?

A

day 9

71
Q

where does sperm capacitation take place?

A

endocervix

72
Q

What is capicatation?

A

Stripping of glycoprotein from sperm surface which accumulates in the epididymis
Causes hyperactive motility – ‘whiplash’

73
Q

What are the 3 properties of cervical mucus?

A

Consistency (watery or viscous)
Spinnbarkeit (means elasticity, stickiness)
Ferning (crystalisation on a glass surface)

74
Q

Normal ejaculated sperm volume

A

1.5 -6ml

75
Q

What 5 variables are assessed in a jiz sample?

A 
Volume
Concentration
Vitality
Motility
Morphology
76
Q

What 2 factors determine what indifferent gonads become?

A

hormones

genetic switches

77
Q

In female development what duct is kept and why?

A

Mullerian due to absence of AMH

78
Q

In male development what duct i kept?

A

Wolffian due to AMH getting rid of Mullirian

79
Q

In males, what hormone stimulates the development of the urethra, prostate and external genitals?

A

dihydrotestosterone

80
Q 
In males and females what do the following develop into?
Genital tubercle
Urethral folds
Labialscrotal swellings
Urethral groove
A 
Men:
Penis
fuse to become spongy urethra
scrotum
n/a
Women;
clitoris
labia minora
labia majora
vestibule
81
Q

What is true hermaphroditism in terms of internal and external genitalia as well as karyotype?

A

Both ovaries and testes present
external can appear male or female
46XX (SRY+), 45X (SRY+) and 45X

82
Q

What is female psuedohermaphroditism in terms of internal and external genitalia as well as karyotype?

A

Internal sex organs normal
labia may be fused with enlarged clitoris
46, XX with virilization (due to androgens)

83
Q

What is male psuedohermaphroditism in terms of internal and external genitalia as well as karyotype?

A

External genitals: incompletely formed, ambiguous or clearly female
Testis: normal, malformed or absent
46, XY with undervirilization

84
Q

2 possible causes of male psuedohermaphroditism

A

Androgen Insensitivity Syndrome (AIS)
-Hormone secreted but receptors defective
Leydig Cell Hypoplasia
- Leydig cells do not secrete testosterone

85
Q

What 5 things is the 10-14 week pregnancy scan looking for?

A 
Viability
Accurate dating
Detecting multiple pregnancy
Detecting structural abnormalities
Screen for chromosomal conditions
86
Q

What 4 structural abnormalities can be detected at the 10 - 14 week scan?

A

spina bifida
anencephaly
exomphalos & gastroschisis
bladder outflow obstruction

87
Q

At what stage of pregnancy is combined screening given?

A

11-14 weeks

88
Q

What is the combined test screening for?

A

Trisomy 21, 18 and 13

89
Q

What are the three components of the combined test?

A

Maternal age
Nuchal Translucency
Serum niomarkers PAPPA/beta-hCG

90
Q

What influencing factors are there for combined screening? 9 points

A 
Maternal age
Gestational age
Ethnicity
Smoking
IVF
Multiple pregnancy
Weight
Diabetes
Past history of chromosome abnormality
91
Q

Follwing combined screening, what is the cut off between low/high risk?

A

1 in 150

92
Q

When does the quadruple test take plce and eehat does it screen for?

A

14-20 weeks. Trisomy 21

93
Q

How does Non Invasive prenatal Testing Work?

A

Cell free foetal DNA in maternal bloodstream (from 10 weeks) can be tested.

94
Q

What is the difference between monozygous and dizygous twins and what proportion of twin births does each account for?

A

mono -1 egg. Identical twins. 1/3 of twin births

di - 2 eggs. non identical 2/3 of births

95
Q

Explain how both monozygotic and dizzygotic twins can be dichorion diamnion?

A

If monozygotic and splitting occurs very early, within 24 hours. Then separate chorion, amnions and placenta will form

96
Q

If splitting occurs in blastocyst at around 4 days from monozygous twin what will this likely result in?

A

Monochorion diamnion

97
Q

If the splitting occurs later than the blastocyst stage in a monzygous twin what will this result in?

A

Mono chorion, mono amnion

98
Q

How can twin pregnancy be diagnosed? 3 points

A

Uterine size
at delivery
ultrasound

99
Q 
Definitions for: Stillbirth
early neonatal
neonatal
perinatal
infant
A 
24 weeks
first 7 days
28 days
SB - early neonatal
first year
(rates per 1000)
100
Q

What is twin to twin transfusion syndrome?

A

Unbalanced placental anastamoses. Resulting in a unidirectional AV shunt. One twin becomes the donor the other the recipient.

101
Q

At what stage of pregnancy are twins delivered?

A

DC twins 37-38 weeks

MC 36-37 weeks

102
Q

Two options for surgical abortion?

A 
Vacuum aspiration (under 14 weeks)
Dilation and extraction (over 14 weeks, rare)
103
Q

Medications for abortion and how they work?

A

Mifeprestone - progesterone antagonist takenorally that stops the pregnancy
Misoprostal - E1 analogue induces labour

104
Q

Where in the Fallopian tube does fertilisation usually occur?

A

Ampulla

105
Q

Order and timings of: blastocyst, morula, zygote

A

Zygote - fertilisation
Morula - 72 hours
Blastocyst - 4 days

106
Q

What happens in days 4-5 of fetal development? 3 points

A

Morula forms cavity and becomes blastocyst.
part of the blastocyst thins out and becomes the trophoblast.
Rest of the cell mas moves up to from the embryonic pole.

107
Q

What happens in day 6 -7 of fetal development? 2 points

A

Inner cell mass differentiates into 2 cell layers - epiblast and hypoblast?

108
Q

What do the epiblast and hypoblast go onto form?

A

Epiblast - embryo ans amnion

Hypoblast - yolk sack

109
Q

From days 16+ of fetal development what do the following become:
Epiblast
Hypoblast

A

Epiblast - becomes ectoderm, endodrem and mesoderm

Hypoblast - degenerates

110
Q

in placental development, what burrows into the myometrium?

A

Syncytiotrophoblast

111
Q 
In fetal development, what do the following do/become?
Syncytiotrophoblast
Cytotrophoblast
lacunae
mesoderm
A

Syncytiotrophoblast invades decidua (endometrium)
Cytotrophoblast cells erodes maternal spiral arteries and veins
Spaces (lacunae) between the fill up with maternal blood
Followed by mesoderm that develops into fetal vessels

112
Q

What hormones does the placenta produce aand what do these do? 2 points

A

Human chorionic gonadotrophin (HCG)
- maintaones corpus luteum in pregnancy

Human placental lactogen HPL

  • growth, lactation
  • carbohydrate and lipid
113
Q

What can transfer can cross the placenta and how? 4 points

A

Gases – oxygen and carbon dioxide by simple diffusion

Water and electrolytes

Steroid hormones

Proteins poor – only by pinocytosis

114
Q

At what point are maternal antibodies transferred across the placenta?

A

from 12 weeks but mainly after 34

115
Q

What is the capsularis, basalis and parietalis?

A

capsularis - capsule overlying embryo and chorionic cavity
parietalis - pert of uterus not occupies by embryo
basalis - between uterine wall and chorionic villi

116
Q

What is vasa ts consequences and treatment??

A

Umbilical cord lies over the the cerivical os. Massive bleeding. Detect via ultrasound, caesarian section

117
Q

What is placenta accreta, its consequences and treatment?

A

failure of placenta to separate at birth. Massive bleeding. Hysterectomy

118
Q

What is placenta praevia its consequences and treatment?

A

Placenta overlies cervical os. Massive painless bleeding. C section

119
Q

What is placental abruption its consequences and treatment?

A

Detachment of placenta during pregnancy. massive painful bleeding (possibly concealed).

120
Q

At what stage of gestation does fetal growth vs development take place?

A

12 weeks. before this mainly about organ growth.

121
Q

What 2 types of growth problems are there?

A

Small for gestational age

Intrauterine growth restriction

122
Q

How can fetal problems be diagnosed?

A

Measurement of uterine size

ultrasound scan

123
Q

Causes of growth restriction?

A

Chromosomal anomaly (T21)
Viral infection (Rubella, CMV)
Severe Placental insufficiency
OR normal small baby (look at the parents)

124
Q

Whats the difference between symmetrical/asymmetrical fetal growth restriction.

A

Measurement of head and abdomen. Symmetrical - both affected. Asymmetrical - abdomen only affected.

125
Q

In fetal growth restriction, what does the size of the abdomen indicate?

A

size of the liver

126
Q

If the circumference of the fetal abdomen is small what might this indicate?

A

Small liver resulting from a placental insufficiency and lack of glycogen

127
Q

What are the consequences of hypoxia in the fetus?

A

Bloodflow redirected to the brain and away from gut, kidneys, lungs

128
Q

Ultrasound findings in IUGR? 4 points

A 
Small AC ( small liver)
Decreased amniotic fluid ( this is produced by the kidneys)
Increased blood flow to the brain (look at Middle Cerebral arteries in the brain – using the doppler effect scan
129
Q

4 clinical features of IUGR

A

SFH smaller than expected
Baby’s movements lessen to conserve energy
Fetal heart rate changes as hypoxia develops (as seen on CTG)
Fetal death

130
Q

what is Betamethasone/dexamethasone used for?

A

When given to the mother will cross the placenta and stimulate the aveoli cells to produce surfactant gene
Surfactant stops the collapse of the aveoli cells by coating the cells and reducing the surface tension
Helps prevent Respiratory Distress Syndrome which leads to neonatal death in premature babies

131
Q

During pregnancy, by what mechanism is plasma volume increased? 5 points

A

Decreased thirst threshold
resetting of osmostat
Progesterone increases aldosterone release
oestrogen acts upon RAS

132
Q

By how much does RBC mass increase by during pregnancy?

A

25%

133
Q

What happens to white blood cells during pregnancy? 3 points

A

concentration remains the same
increase in neutrophils
Increase at delivery

134
Q

What changes can occur to the heart during pregnancy? 3 points

A

Increase in size by up to 12%
May shift up in chest cavity
systolic murmurs are common

135
Q

What happens to peripheral resistance during pregnancy?

A

Decreases by around 35%

136
Q

What does the reduction in peripheral resistance not result in a drop in blood pressure during pregnancy?

A

Compensated for by an increase in cardiac output so blood pressure remains about the same.

137
Q

What 2 changes occur to the respiratory system during pregnancy?

A

Increase in tidal flow

Increase in alveolar ventilation

138
Q

What changes occur to the renal system during pregnancy and what stays the same?

A

Increase plasma flow and filtration rate.
Kidneys increase in size
Tubular reabsorption capacity remains the same so glucosuria is common

139
Q

2 Common gastrointestinal changes in pregnancy?

A

Constipation

Reflux

140
Q

What changes occur to glucose metabolism during pregnancy?

A

First Trimester - Insulin sensitivity

Second trimester - insulin resistance becausecortisol, progesterone, HPL, & oestrogen are all insulin antagonists

141
Q

What protein hormones are released by the placenta?

A

hCG (human chorionic gonadotrophin)
hPL (human placental lactogen)
hPG (human placental gonadotrophin
CRH (corticotropin releasing hormone)

142
Q

What steroid hormones are released by the placenta?

A

Progesterone

Oestrogen (oestriol)

143
Q

What is HCG and what does it do? 3 points

A

Human chorionic gonadotrophin
Maintains corpus luteum secretion of progesterone & oestrogen
Decreases as the placental production of progesterone increases

144
Q

What is hPL and what does it do? 4 points

A

Human Placental lactogen
Alters maternal carbohydrate and lipid metabolism to provide for foetal requirements
Mobilizing maternal free fatty acids
Inhibits maternal peripheral uptake of glucose
Increases insulin release from pancreas
Aim is a steady state of glucose for the fetus

145
Q

What is hPG and what does it do? 3 points

A

Placental Growth Hormone secreted by the placenta responsible for regulating fetal growth
Induces maternal insulin resistance

146
Q

What 4 functions does oestrogen serve during pregnancy?

A

Growth of the uterus, cervical changes
Development of ductal system of breasts
Stimulation of prolactin synthesis
Stimulation of corticol binding globulin (CBG), sex hormone binding globulin (SHBG), thyroxin binding globulin (TBG)

147
Q

What is gestational diabetes?

A

Any abnormal glucose tolerance test after the first trimester

148
Q

What problems is hyperglycemia associated with in the first trimester of pregnancy.? Give 3 examples

A 
Fetal malformation
Hydrocephaly
Meningomyelocoele
Central Cyanosis in Congenital Heart disease
Single Ventricle &Sacral Dysgenesis
Renal Agenesis
149
Q

5 risk factors for maternal hyperglycaemia

A 
Previous Gestational Diabetes
Obesity
Polycystic ovarian syndrome
Family history of type 2 diabetes
High risk racial group
150
Q

3rd trimester problems caused by hyperglycaemia? 3 points

A

macrosomia
Pre-eclapsia
Fetal or Neonatal death

151
Q

Management of hypergycaemina during pregnancy? 5 points

A

Folic acid 5mg in 1st Trimester

  • Aspirin 75 - 150 mg/day from 12/40
  • if less than 16/40
  • Attendance at multidisciplinary one stop clinic
  • Tight glucose control throughout pregnancy
  • Fetal Ultrasound monitoring in last trimester
  • Maternal monitoring of Fetal movements
152
Q

What hormones are responsible for axillary and pubic hair?

A

adrenal androgens

153
Q

Chronological order of pubertal development for boys and girls.

A 
Growth spurt
Breast development
Pubic hair
Axillary hair
Menarche
Testicular volume
Penile length
Pubic hair
Growth spurt
Axillary / Facial hair
Deep voice
154
Q

What is Central or True precocious puberty dependent upon and how is it treated?

A

Gonadotrophin

LHRH analogue

155
Q

What are the 3 concerns surrounding precocious puberty?

A

Possible underlying sinister cause
-Boys – upto 80%
Emotional & pyscho-social upheaval at an inappropriately young age
Early cessation of growth leading to decreased final adult height

156
Q

In fetal development what two structures bind to from the kidney and ureter?

A

Mesonephric blastema and ureteric bud

157
Q

If the mesonephric blastema and ureteric bud dont bind properly what can this result in?

A

Bifid ureter

158
Q

Is a unilateral absent kidney usually a problem, what can this be associated with?

A

No.
Mayer-Rokitansky syndrome:

Abnormalities of the vagina (agenesis), uterus, fallopian tubes

159
Q

Why are UTIs more of a cause for concern in infants?

A

Vesicoureteral reflux (VUR) most likely surgical cause rather than just infection.

160
Q

What is VUR?

A

Vesicouretal reflux. Developmental abnormality in how the ureter enters the bladder means that there isnt enough of the ureter available to be squeezed shut each time the bladder empties and no urine in refluxed back up the ureter causing infection.

161
Q

Complication of VUR?

A

If left untreated the infection can cause nephropathy.

162
Q

What is PUV and what are the 2 complications associated with it?

A

Posterior uretheral valves.
Found in boys
Back pressure when trying to urinate can lead to damage if ureters and kidneys.

163
Q

What is Hypospadias?

A

Malformation means that the meatus is not at the tip of the penis.

164
Q

3 points to diagnose active labour

A

Painful regular contractions
Cervical effacement
Dilatation of the cervix of 4cms or more.

165
Q

How is the progress of delivery measured?

A

Descent of the head in relation to ischial spines

166
Q

What is the 2nd stage of labour

A

Full cervical dilation to delivery

167
Q

Name the two fontanelles important in delivery

A

bregma (anterior)

posterior

168
Q

Smallest and most common delivery angle of fetal skull

A

Suboccipitobregmatic

169
Q

What is the 3rd stage of labour and how is this managed?

A

Delivery of placenta
.Active management (CCT)
Oxytocin i.m.
Physiological: Mother naturally expels the placenta and membranes with contractions

170
Q

3 types of fetal monitoring during labour

A

Intermittent auscultation by Pinard or Sonicaid
CTG (cardiotocograph)
FBS

171
Q

definition of congenital abnormality

A

Congenital anomaly: abnormality of structure, function or disorder of metabolism that is present at birth and results in a physical or mental disability

172
Q

Most common and severe congenital anomalies? 3 points

A

heart defects, neural tube defects and Down syndrome

173
Q

Most common causes of congenital defects? 4 points

A

Idiopathic 50%
Genetic
Infections
Teta

174
Q

What are the 4 classifications of congenital structural abnormalities ?

A

Malformation: flawed development of a structure or organ (eg. transposition of the great arteries)

Disruption: alteration of an already formed organ (vascular event eg bowel atresia)

Deformation: alteration in structure caused by extrinsic pressures (mechanical eg talipes due to reduced liquor)

Dysplasia: abnormal organisation of cells
or tissues

203 Endocrinology and Reproduction (3 decks)

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