Reproduction Flashcards

1
Q

What do the Sertoli cells do?

A

Spermatogenesis

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2
Q

What do Leydig cells do?

A

Secrete Androgens

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3
Q

What are he cell types of the testis and what do they do?

A

Sertoli - spermatogenesis

Leydig - Androgen production

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4
Q

Where in the ovaries are the oocytes matured?

A

Stromal tissue

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5
Q

What do follicular cells in the ovaries do?

A

Secrete oestrogen and progesterone

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6
Q

What does FSH stimulate (M and F)?

A

M - Sertoli cell, F - follicular development

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7
Q

What does LH stimulate (M and F)?

A

M - Leydig cells, F - Ovulation

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8
Q

When is puberty?

A
F = 9-14
M = 10-16
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9
Q

What stages of oogenesis happen before birth?

A

Primordial germ cells into oogonia where it undergoes mitosis. Matures into primary oocyte.

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10
Q

What happens to the primary oocyte at ovulation?

A

Meiosis 1. It becomes a secondary oocyte and releases the first polar body containing ‘waste’ chromosomes

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11
Q

What happens to the secondary oocyte at fertilisation?

A

Meiosis 2 - becumes an ovum and releases the second polar body

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12
Q

Which are 2n and which are n?

Primordial germ cell, oogonia, primary oocyte, secondary oocyte, ovum

A
2n = Primordial germ cell, oogonia, primary oocyte
n = secondary oocyte, ovum
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13
Q

What effects does oestrogen have?

A

Contracts fallopian tubes
Mucus in cervix softens
Fluid retention in kidney

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14
Q

What effects does progesterone have?

A

Breast development
Mucus in cervix hardens
Increased body temperature

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15
Q

What happens in the pre antral stage?

A

Primordial follicle > primary follicle

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16
Q

What happens in the antral stage?

A

Follicular development

Oestrogen surge, LH receptors increase on granulosa cells

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17
Q

What happens in the Pre - ovulatory stage?

A

Progesterone secretion starts

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18
Q

What happens in the ovulatory stage?

A

LH surge causes follicle rupture

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19
Q

What happens in the luteal stage?

A

Follicle becomes corpus luteum and secretes progesterone and some oestrogen. It is dependent upon LH.

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20
Q

What are the stages of the menstrual cycle?

A

Preantral, antral, pre-ovulatory, ovulatory, luteal

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21
Q

What happens to the hormones if there is NO pregnancy at the end of the cycle?

A

LH decreases, corpus luteum breaks down = decreased progesterone = endometrium breaks down

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22
Q

What happens to the hormones if there is a pregnancy at the end of the cycle?

A

Foetus releases HCG which acts on LH receptors to sustain the corpus luteum for 10-12 weeks until the placenta takes over.

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23
Q

What receptors does HCG work on?

A

LH receptors

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24
Q

Just before ovulation, what is there a surge of?

A

Oestrogen

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25
Q

At ovulation, what is there a surge of?

A

LH

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26
Q

What does a surge in LH do?

A

Causes a follicle to rupture to release an egg

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27
Q

What is the difference between spermatogenesis and spermiogenesis?

A
Spermatogenesis = spermatagonium > (primary, secondary and haploid) Spermacytes
Spermiogenesis = Spermacytes > Spermatids > Spermatazoa
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28
Q

What is the progression from Spermatogonia to mature sperm?

A

Spermatogonium > diploid spermatagonia > primary spermatocytes > secondary spermatocytes > Haploid spermatocytes > differentiation spermatids > Mature sperm and residual bodies.

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29
Q

What is spermiation?

A

The release of sperm from Sertoli cells

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30
Q

Which sperm precursors are 2n and which are n?

A
2n = Spermatogonium, diploid spermatagonia, primary spermatocytes
n = secondary spermatocytes, Haploid spermatocytes, differentiation spermatids, Mature sperm
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31
Q

What % of sperm are normal?

A

4%

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32
Q

How many sperm are produced per day?

A

300-600 million

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33
Q

What features do sperm have to help them?

A

Acrosome, mitochondria, flagella containing microtuules

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34
Q

Where is sperm stored?

A

Epididymus

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35
Q

Where are the Sertoli cells found?

A

Seminiferous tubules

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36
Q

Where does the sperm go from the seminiferous tubules?

A

Sem tubules > rete testis > epididymus > ductus deferens > Urethra

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37
Q

Where is fluid reabsorbed in the male repro tracts?

A

Epididymus

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38
Q

What ‘defence’ does the female tract have against sperm?

A

Acidic vagina, cervical mucus

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39
Q

What stages do the sperm undergo in the female tract?

A

Capacitation - Follicular fluid causes sperm to be stripped of its glycoprotein to make it more motile

Acrosome reaction - Pores generated in the acrosome to allow chemoattraction to the egg.

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40
Q

What is capacitation?

A

Capacitation - Follicular fluid causes sperm to be stripped of its glycoprotein to make it more motile

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41
Q

What is the acrosome reaction?

A

Pores generated in the acrosome to allow chemoattraction to the egg.

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42
Q

What is polyspermy?

A

More than one sperm getting in to the egg at once

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43
Q

What defences are there to stop polyspermy?

A

Fast block - ion channels change membrane potential

Slow block - ZP3 receptors break down zona pellucida which causes it to harden.

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44
Q

What is the Zona Pellucida

A

Glycoprotein membrane surrounding an oocyte

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45
Q

What are ZP3 receptors and where are they found?

A

Sperm receptors on the Zona Pellucida

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46
Q

What does the rete testis do?

A

Connects seminiferous tubules to ducts

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47
Q

Why does a vasectomy not cause fluid build up?

A

Fluid reabsorbed in epididymus

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48
Q

What happens to the sperm in a male who has had a vasectomy?

A

Destroyed by phagocytosis

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49
Q

What is infertility?

A

Inability to concieve after 1 year of trying

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50
Q

How many lobules in a testicle?

A

About 250

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51
Q

Where in the testis does sperm collect?

A

Rete testis

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52
Q

What are the layers of the tunica of the testes and what do they do?

A

The tunica vasculosa is the inner layer (blood vessels and CT)
Tunica albuginea is a dense layer of tissue - creates partitions between seminiferous tubules
Tunica vaginalis - visceral and parietal layers (reduces friction between the testes and the scrotum)

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53
Q

What happens if there is xs fluid between the layers of the tunica vaginalis?

A

Hydrocele

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54
Q

What are the contractile cells in the testes called?

A

Myoid cells

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55
Q

What do the seminal vesicles secrete?

A

AA, fructose etc. to nourish sperm

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56
Q

What joins together to form the ejaculatory duct?

A

Ductus deferens and seminal vesicles

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57
Q

What cell type is in the ductus deferens?

A

Columnar cilliated

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58
Q

What is special about the lumen of the ductus deferens?

A

Star shaped

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59
Q

How many muscle layers does the ductus deferens have?

A

3

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60
Q

What does the prostate do?

A

Secretes prostatic fluid (fluid component of semen)

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61
Q

What is the arterial supply to the prostate?

A

Prostatic arteries

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62
Q

What is the venous drainage of the prostate?

A

Prostatic veins to the internal Iliac

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63
Q

What is the sympathetic innervation to the prostate?

A

Inferior hypogastric

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64
Q

What is the parasympathetic innervation to the prostate?

A

Pelvic splanchnics

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65
Q

What are the bulbourethral glands?

A

Secretes milky and alkaline secretions before ejactulation, to clear and lubricate urethra

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66
Q

What are corpora cavernosa and how do they work?

A

Fill with blood to cause an erection - allows penis to become turgid because it is restricted by tunica albuginea

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67
Q

What are the 3 parts to the male urethra?

A

Membranous, prostatic and penile

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68
Q

What is corpus spongiosum?

A

Spongy tissue around the urethra which prevents obstruction to urethra during erection

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69
Q

What is the somatic nerve supply to the penis?

A

S2 - S4 (pudendal)

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70
Q

What is the parasympathetic supply to the penis and what is it responsible for?

A

S2- S4

Vasodilation, prostate and bulbourethral secretion

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71
Q

What is the sympathetic supply to the penis and what is it responsible for?

A

L1-L2

Contraction to cause ejaculation

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72
Q

What is detumescence?

A

After ejaculation when the penis becomes flaccid again

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73
Q

What are the embryological stages of the kidneys?

A

Pronephros
Mesonephros
Metanephros

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74
Q

How do testes form in utero?

A

Genital ridges -> Primitive sex cords -> cords penetrate medulla = Medullary cords -> primative germ cells develop around here under the influence of testosterone from the Leydig cells

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75
Q

How do ovaries form in utero?

A

Genital ridges -> Primitive sex cords -> cluster together in medulla but then disappear and are replaced with vascula stroma
Follicular cells form

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76
Q

What are the 2 ducts involved in the embryo repro tract called?

A

Mesonephric ducts and Paramesonephric ducts

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77
Q

What happens to the Mesonephric ducts and Paramesonephric ducts in males?

A

Mesonephric - seminal vesicles, epididymus and ductus deferens
Paramesonephric - degenerates

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78
Q

What happens to the Mesonephric ducts and Paramesonephric ducts in females?

A

Mesonephric - degenerates

Paramesonephric - Meets in midline to form uterine cavity and the fallopian tubes

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79
Q

How does the vagina form in utero?

A
Wk 4-7
Cloaca divides into urogenital sinus and anal canal, separated by urorectal septum
Sinovaginal bulbs (from paramesonephric ducts) become vaginal fornices at 5 months
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80
Q

How does the male external genitalia form in utero?

A

Genital tubercle (from cloaca) > Phallus
Urethral folds > Penile urethra
Genital swellings > Scrotum

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81
Q

What is hypospadia?

A

Urinary meatus in the wrong place?

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82
Q

What do testes follow when they descend?

A

Gubernaculum

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83
Q

How does the female external genitalia form in utero?

A

Genital tubercle (from cloaca) > Clitoris
Urethral folds > labia minora
Genital swellings > labia majora

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84
Q

What methods of combined contraception are there?

A

Combined Oral contraceptive pill (Mono - Zoely, quad - Qlaira)
Transdermal patch - Evra
Vaginal ring - Nuvaring

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85
Q

What are the contraindications of the COCP?

A

Smoking, overweight, over 35, migraines, CVD

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86
Q

What are the S/E of COCP?

A

clots, nausea, sodium and water retention

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87
Q

What are the single hormonal contraception methods?

A

Progesterone only Pill (Norethisterone)
Subdermal implant
Injectable progesterones
IUS (Mirena) - Levonorgestrel

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88
Q

What are the S/E of single hormonal contraception?

A

Amenorrhoea, nausea, sodium and water retention, fat deposition

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89
Q

What are the non hormonal contraceptive methods?

A

IUD - copper coil (only for fit and healthy!)
Barriers
Sterilisation
Natural family planning

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90
Q

What are the side effects of the IUD?

A

heavy, painful periods, increased discharge

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91
Q

What are the emergency contraceptives?

A
  1. Ulipristal (120h)
  2. Levonorgestrel (72h)
  3. Copper coil
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92
Q

What is the Fraser guidance?

A

For under 16s or vulnerable under 18s

Understands
Parents
Sex - going to do it anyway
Suffer without help
Interest - in their best interest
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93
Q

What does the DSM use to describe PMS?

A

1987 - Late luteal phase dysphoric disorder - depressive condition

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94
Q

Where is cervical cancer most likely to occur?

A

On the transition between stratified squamous ectocervix and simple columnar endocervix

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95
Q

What is the most common type of cervical cancer and what is it caused by?

A

Squamous cell carcinoma - HPV

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96
Q

What hormone increases the chances of endometrial cancer?

A

Oestrogen

97
Q

What is a Leiomyoma?

A

Benign smooth muscle tumour/fibroids

NOT THE SAME AS LEIOMYOSARCOMA

98
Q

What are the types of Leiomyoma?

A

Subserosal, intramucosal, submucosal

99
Q

What are the symptoms of Leimyoma?

A

Abnormal bleeding, miscarriage risk, inc postpartum haemorrhage.

100
Q

What is endometriosis?

A

Presence of endormetrial tissue in other places - bleeds and shed as usual = pain and damage to fallopian tubes

101
Q

What are the 2 subclasses of Testicular germ cell tumours?

A

SEMINOMA and NONSEMINOMATOUS

102
Q

What are some examples of a nonseminomatous germ cell tumour?

A

Teratoma, embryonal carcinoma

103
Q

How do testes tumours present?

A

Testicular lumps

Mets - more common as men often won’t see a GP about testes lumps.

104
Q

What might a Leydig tumour secrete?

A

xs Androgens - Precocious puberty or masulinising effects in females

Oestrogen - Gynacomastia

105
Q

What type of tumour is a prostate tumour?

A

Usually Adenocarcinoma

106
Q

Where do prostate tumours often metastasise to?

A

Bone

107
Q

What are the 3 criteria for PCOS?

A

Polycystic ovaries
Inc Androgen signs
Oligoamenorrhoea

108
Q

What is the difference between primary and secondary Amenorrhoea?

A

Primary - never started

secondary - stopped

109
Q

What does the progesterone test for PCOS show?

A

If they bleed, then there was oestrogen present, which makes PCOS are possibility.

110
Q

What might a negative progesterone test but high FSH and LH suggest?

A

Ovarian failure, no ovaries, menopause

111
Q

What might a negative progesterone test and low FSH and LH suggest?

A

Pituitary failure, hypothalamus failure

112
Q

What are some causes of pituitary failure?

A

Tumour, infarction, idiopathic

113
Q

What may cause hypothalamus failure?

A

Trauma, weight loss, stress, exercise

114
Q

What are some risk factors for PCOS?

A

Obesity, DM2, family history

115
Q

What happens during Meiosis 1 (female)?

A

Nuclear membrane breaks and chromosomes separate

116
Q

What is syngamy?

A

The fusion of the oocyte and sperm’s pronuclei

117
Q

What is the fusion of the oocyte and sperm’s pronuclei called?

A

syngamy

118
Q

What is a blastocoel?

A

A morula (ball of cells) with fluid in the middle, restricted by Zona Pellucida

119
Q

What is hatching (zygote)?

A

ZP thins, blastocoel enlarges and eventually splits into 2.

120
Q

When is the implantation window?

A

Day 19-24

121
Q

What are the risk factors for a pregnancy of unknown location?

A

previous ectopic, PID, over 40, IVF, smoking

122
Q

What is a trophoblast?

A

Layers of blastocysts which make up the placenta

123
Q

What is trophoblastic disease?

A

Trophoblasts invade endometrium and prolieferate excessively

124
Q

What are the 2 types of trophoblastic disease and what is it caused by?

A

Partial - 2 sperm enter egg

Complete - Only half the chromosomes are availible

125
Q

What is a choriocarcinoma?

A

A malignant tumour of the trophoblast

126
Q

What methods are there to treat infertility?

A
Ovulation induction
Insemination
IVF
ICSI (Intracytoplasmic sperm injection)
Fertility preservation
127
Q

What ways are there of prenatal diagnosis?

A

Chorionic villus sampling
Amniocentesis
FISH
Anomaly scan

128
Q

What is the difference between a diagnostic test and screening?

A

Diagnostic - accounts for signs/symptoms

Screening - Cohorts or high risk groups, no path needed.

129
Q

What is cascade screening?

A

Systematically approaching relatives of patients with genetic disorders for screening.

130
Q

What is empirical risk?

A

An averaged risk based upon observed recurrence when cause is unknown.

131
Q

When is hyperemesis gravadium most common and what might be a problem which arises because of it?

A

5-6 weeks into pregnancy

Dehydration

132
Q

What antiemetics may be given to a woman with morning sickness?

A

Domperidone

133
Q

What is TTTS?

A

Monochorionic twins. Veins to arterial anastamoses = unbalanced blood flow.

134
Q

What metabolic changes are seen in a mother during pregnancy?

A

Protein and fat reserves increase. Maternal tissue becomes insulin resistant in late pregnancy to allow more glucose to foetus.

135
Q

What cardiovascular changes are seen in a mother during pregnancy?

A

Increased uterine flow
NO causes vasodilation = dec. TPR = inc CO
Slight dec in MABP

136
Q

What renal changes are seen in a mother during pregnancy?

A

Increased plasma volume to help remove foetal waste (fluid retention and thirst)
Decrease in osmoreceptor threshold to prevent ADH decline to keep volume up!
Inc GFR
Dec. Hb conc.

137
Q

What respiratory changes are seen in a mother during pregnancy?

A

Inc O2 delivery
Inc tidal volume - mild resp alkalosis
Anaemia risk due to dec. conc as a result of high blood volume.
More 2,3, DPG to displace O2

138
Q

What to IGFs stimulate in foetal life?

A

DNA and cell division

139
Q

What is measured in an ultrasound?

A

Crown to rump length
Femur length
Abdominal circumference
Head circumference

140
Q

What is macrosomia?

A

Birthweight in the 95th centile

141
Q

What is IUGR?

A

Birthweight below 10th centile

142
Q

What causes IUGR?

A

Placental insufficiency
Chronic disease
Drugs and toxins

143
Q

What are the 2 types of IUGR?

A

Symmetric - slow to develop, early gestation

Asymmetric - late gestation, weight restriction then length restriction.

144
Q

What is the placenta formed from?

A

Embryonic trophoblast cells

Cytotrophobasts - unicellular
Syncyticotrophoblasts - multicellular, main barrier between mother and foetus.

145
Q

How does the placenta form (in each trimester)?

A

1 - villi containing capillaries from cytotrophoblasts invade spiral arteries
2 - Villi branch out
3 - Villi mature and capillaries dilate

146
Q

What happens if there aren’t enough chorionic villi?

A

Stunted placental development

147
Q

What happens if there is poor cytotrophoblast invasion?

A

Pre eclampsia

148
Q

How does IgG cross the placenta and why?

A

Passive immunity to foetus.

IgG binds to Fc receptor, internalised, Endosome transcytosis, released on other side, receptor recycled.

149
Q

Can Cortisol cross the placenta?

A

No

150
Q

Can Insulin cross the placenta?

A

No

151
Q

Can Anaesthetics cross the placenta?

A

Yes

152
Q

What is folate needed for in pregnancy?

A

DNA synth and cell division

153
Q

What is vit D needed for in pregnancy?

A

brain development, immune system, bone mineralisation

154
Q

What is Iodine needed for in pregnancy?

A

neuro development

155
Q

Which hormones relax the uterus?

A

progesterone, relaxin, NO

156
Q

Which hormones stimulate contractions of the uterus?

A

Oestrogen, Oxytocin, PGs

157
Q

What role does PGE2 play in labour?

A

Potentiates Oxytocin

158
Q

Where is PGE2 from?

A

Decidua and foetal membranes

159
Q

What happens during cervical ripening?

A

PGE2 changes collagen fibres

Relaxin is released

160
Q

What helps the foetus engage?

A

Braxton Hicks

161
Q

What happens in the first stage of labour?

A

Cervix dilates, amniotic sac ruptures
Latent phase - slow dilation (to 3-4cm)
Active phase - fast dilation (to 10cm)

162
Q

What is brachystasis?

A

muscle cells contract but don’t return to their full length

163
Q

What happens in the second stage of labour?

A

Expulsion

164
Q

What happens in the third stage of labour?

A

Placenta delivery

165
Q

What causes the start of labour?

A

Cortisol from the foetus causes decreased progesterone and increased oestrogen.
Cortisol also stimulates Corticotrophin releaseing hormone (CRH) to be released from the placenta which allows PG release

166
Q

How do oxytocin and PGs work?

A

Activates GPCRs and causes calcium release which binds with calmodulin to cause actin-myosin complexes.

167
Q

What tocolysis drugs are there?

A

DINOPRISTONE - mimics PGs

Synthetic oxytocin

168
Q

When is the perinatal mortality period?

A

24wks gestation to 1 week after birth

169
Q

What problem to the foetus may be caused by strong contractions?

A

Blood vessel compression = foetal distress

170
Q

What risks are there to the mother during childbirth?

A

Perineal tears
Haemorrhage
Severe pain

171
Q

What analgesia is available during childbirth?

A

ENTONOX
FENTANYL
PETHIDINE
BUPIVACAINE

172
Q

What drugs prevent post partum haemorrhage?

A

Oxytocin
ERGOMETRINE
MISOPROSTOL

173
Q

What would you give to treat Herpes?

A

ACICLOVIR

174
Q

What would you give to treat Gonorrhoea, Chlamydia and Urethritis?

A

AZITHROMYCIN

175
Q

What would you give to treat Syphylis or HPV?

A

PENECILIN

176
Q

What are some features of HIV?

A

Glycoprotein envelope, 2 single DNA strands, reverse transcriptase

177
Q

What are some symptoms of HIV?

A

fever, lethargy, rash, headache, lymphadenopathy

178
Q

What are the methods of antiretroviral treatments?

A

Inhibit reverse transcriptase

Inhibit viral protease

179
Q

What is a teratogen?

A

A drug which causes permanent structural change to foetal organs

180
Q

When is the critical period for teratogenicity?

A

18-55 days

181
Q

What would you need to do to the loading dose and the maintenance doses of a drug in pregnancy?

A

Increase both

182
Q

What is preterm?

A

Before 37 weeks gestation

183
Q

What is placental abruption?

A

Placenta separates from the wall so the foetus has no blood supply

184
Q

What are the symptoms of pre-eclampsia?

A

Hypertension, proteinuria, vascular organ damage

185
Q

What is early neonatal death?

A

Death during first week of life

186
Q

What is late neonatal death?

A

Death in the first month of life

187
Q

What causes preterm births?

A

Spontaneous
Infection
Ruptured membranes
Cervical insufficiency

188
Q

How do you manage a potential pre-term?

A

BETAMETHASONE - mature foetal lungs
Tocolysis (NIFEDIPINE, ATOSIBAN)
Provide good location for birth
treat infection

189
Q

What is surfactant, what is it made of and where is it from?

A

Lipoproteins from type 2 pneumocytes - prevents alveolar collapse.
DPCC, SPA, SPB, SPC, SPD

190
Q

Where do the alveoli in breasts drain?

A

lactiferous ducts > lactiferous sinus > nipple

191
Q

What do mammary glands do?

A

hormonal control - prolactin

192
Q

What is PIH?

A

Dopamine, inhibits prolactin secretion from pituitary

193
Q

Where does lymph from the breast drain?

A

Subareolar plexus
Axillary nodes
Parasternal nodes

194
Q

What is the arterial supply to the breast?

A

Internal thoracic
Lateral thoracic
thoracoacromial

195
Q

What is the venous drainage of the breasts?

A

Superficial venous plexus (around areola) to axillary vein

196
Q

Does Oestrogen inc or dec PIH?

A

increase

197
Q

What does progesterone do to prolactin receptors?

A

Decreases them

198
Q

What happens to levels of Oestrogen and Progesterone after birth?

A

They fall

199
Q

What is galactopoiesis and what is it stimulated by?

A

sustained prolactin = milk secretion

Stimulus = suckling

200
Q

Which hormones help milk let down?

A

Oxytocin - contraction of myoepithelial cells

201
Q

What drug supresses lactation?

A

BROMOCRIPTINE

202
Q

What drug stimulates lactation?

A

DOMPERIDONE

203
Q

What is in breastmilk?

A

fat, AA, lactose, vit D, Iron

204
Q

How does lactational amenorrhoea come about?

A

xs prolactin = dec. GnRH = dec. FSH and LH

205
Q

What is Galactorrhoea?

A

milk production without pregnancy (pit tumour)

- Witchs milk

206
Q

Why is cows milk not suitable before 12 months?

A

Too high sodium

207
Q

When should you ween a baby?

A

4-6 months

Some foods later (wheat, eggs, fish etc.)

208
Q

What is allometric growth?

A

Growth where proportion changes

209
Q

What is the decidua?

A

modified endometrium where the conceptus implants - the bulge of decidua around it becomes the placenta.

210
Q

What are the layers of the decidua?

A

Decidua basalis, decidua capsularis, decidua parietalis

211
Q

What is catch up growth?

A

Rapid growth, faster than normal - stops when appropriate centile is reached.

212
Q

What are the 4 stages of Piaget?

A

0-2 sensory motor
2-7 preoperational
7-12 concrete operational
12-19 - formal operational

213
Q

What are the types of attachment?

A

Secure
Resistant
Avoidant

214
Q

When is puberty precocious?

A

F - before 8

M - before 9

215
Q

What is the problem with precocious puberty?

A
Bones fuse (short stature)
Psychological
216
Q

What might cause precocious puberty?

A

Obesity, genetic, hypothyroidism, CAH, cushings, ovarian cysts etc.

217
Q

What is thelarche?

A

Onset of breast development

218
Q

What is adenarche?

A

onset of pubic hair, acne, sweat etc.

219
Q

When is menopause ‘early’?

A

Before 40

220
Q

What is the average age for the menopause?

A

52

221
Q

What is the menopause?

A

The final period

222
Q

IN what period does the menopause occur?

A

Climacteric period

223
Q

What is the Climacteric period?

A

The transition between fertile and infertile states

224
Q

What is given to reduce the symptoms of the menopause?

A

HRT

225
Q

What are the characteristic features of cancer?

A

Angiogenesis
Uncontrolled proliferation
mets
Ignores apoptosis signals

226
Q

What treatments are there for cancer?

A

Chemo, Radio, Surgery, hormonal treatment

227
Q

What is the triple assessment for breast cancer?

A

Imaging
Needle aspiration
cytology

228
Q

What is penetrance?

A

The change of the disease if a mutation is present

229
Q

What is MEN2?

A

A protooncogene which predisposes for a lot of cancers

230
Q

What gene mutation is significant for breast cancer?

A

BRCA1 BRCA2

231
Q

How do cancer cells resist drugs?

A

Reduce uptake
Increase efflux
Alter drug targets
Increased repair activity

232
Q

Why do we use cancer drug combos?

A

Reduce resistance

233
Q

What are the rules regarding cancer drug combos?

A

Different mechanism and different target.

234
Q

What are the classes of cancer drugs?

A
Direct DNA
Antimetabolites
Microtubule function
Protein Synthesis 
Biologicals
235
Q

Name some Direct DNA drugs.

A
Alkylating agents - CYCLOPHOSPHAMIDE
Platinum compound - CISPLATIN
Cytotoxic antibiotics - DOXORUBICAN
Topoisomerase 1 inhibitor - TOPETECAN
Sex hormones - TAMOXIFEN, ANASTRAZOLE
236
Q

Name the cancer antimetabolites.

A

Folic acid antagonist - METHOTREXATE
HYDROXYUREA
5 FLUOROURACIL

237
Q

Name a microtubule cancer drug.

A

VINCRISTINE

238
Q

Name a protein assembley cancer drug.

A

ASPARAGINASE

239
Q

Name a biological cancer drug.

A

HERCEPTIN