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4th Year Repro > Module 1 > Flashcards

Module 1 Flashcards

1
Q

What determines which is the lead follicle pre-ovulation?

A

FSH sensitivity/ receptor density

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2
Q

What adaptation does the lead follicle undergo before ovulation?

A

It develops LH receptors on its granulosa cells

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3
Q

Give the two main effects of the LH surge on the lead follicle

A

Triggers ovulation

Releases oocyte of the dominant follicle from first meiotic prophase arrest

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4
Q

Which form of inhibin is not present in men?

A

A

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5
Q

Which cells in the woman produce androgens?

Which gonadotrophin are these cells sensitive to?

A

Thecal cells

LH

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6
Q

Which cells in the woman produce oestrogens?

Which gonadotrophin are these cells sensitive to?

A

Granulosa cells

FSH

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7
Q

What percentage of men are azoospermic?

A

1%

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8
Q

Give three genetic causes of male infertility

A

Autosomal recessive condition (e.g. cystic fibrosis)
Aneuploidy (e.g. Klinefelter’s syndrome)
Microdeletions (e.g. on Y chromosome)
Kallman syndrome

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9
Q

Give three signs of Klinefelter’s syndrome

A 
Reduced IQ
Tall stature
Gynaecomastia
Poor muscle development
Infertility by early twenties
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10
Q

Why are cystic fibrosis patients almost always infertile?

A

Vas deferens fails to form

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11
Q

What method of assisted fertility is particularly effective in male cystic fibrosis patients?

A

Sperm aspiration

The sperm are still made and are normal, but there is an obstruction preventing them from being ejaculated

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12
Q

Which hormone programs male differentiation of the gonads?

A

Anti-Mullerian hormone

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13
Q

Which duct persist and develops in male gonads?

A

Wolffian duct

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14
Q

Which genetic abnormality would result in an infertile male phenotype with XX allosomes?

A

Translocation of the SRY gene.
This would trigger male differentiation, but the genes for manfacturing sperm would remain on the original Y chromosome, so the patient would be infertile

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15
Q

Microdeletions in which genes could lead to male infertility?

A

AZFa, b, and c genes

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16
Q

Why does opioid use reduce fertility?

A

Dynorphin is an endogenous opioid which counteracts the effects of kisspeptin on GnRH release in order to balance it. Opioids activate the same receptors as dynorphin and so reduce GnRH release, which silences the HPG axis

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17
Q

Describe the effect of oestrogen on the AVPV in rats

A

Oestrogen exerts positive feedback on Kiss1 neurons in the AVPV

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18
Q

Describe the sexual development of a child with a GnRH knockout

A

They will not go through puberty

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19
Q

What is the effect on male FSH/LH of Kisspeptin?

A

They will increase

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20
Q

What is the effect on female FSH/LH on kisspeptin?

A

There will be little if any effect in the follicular stage of the menstrual cycle. However in the pre-ovulatory stage administration of kisspeptin will cause a large rise in FSH and LH

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21
Q

What is the effect of oestrogen on kisspeptin neurons in the arcuate nucleus?

A

Negative feedback

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22
Q

What effect would administration of exogenous oestrogen to a female rat immediately post-natally have on the hypothalamus?

A

Masculinisation of the hypothalamus - the AVPV would not develop

Masculinisation of the AVPV is caused by oestrogen, testosterone only exerts an effect because it is aromatised to oestrogen

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23
Q

What triggers the LH surge?

A

An activational effect due to rising oestrogen which increases sensitivity of the pituitary to GnRH

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24
Q

What effect would knockout of TAC3R have?

A

TAC3R is the neurokinin B receptor, and KO would cause a failure to got through puberty and infertility

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25
Q

What effect does ghrelin secretion have on GnRH release?

A

Decreases - it is the hunger hormone

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26
Q

What effect does PYY have on GnRH release?

A

Increases - it is a satiety hormone

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27
Q

What effect does leptin release have on GnRH secretion?

A

Leptin is permissive to GnRH release - it is required

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28
Q

What two ways is leptin thought to exert its effects on GnRH neurons

A

Kisspeptin neurons

Glutamate neurons in ventral premamillary nucleus

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29
Q

What proportion of cancer can supposedly be attributed to lifestyle factors rather than chance?

A

1/3

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30
Q

What type of mutation usually creates an oncogene?

A

A gain of function mutation

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31
Q

What type of mutation usually causes cancer in a tumour suppressor gene?

A

A loss of function mutation

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32
Q

What are the ten hallmarks of cancer

A 
Sustained proliferative signalling
Evading growth suppressors
Resisting cell death
Replicative immortality
Inducing angiogenesis
Invasion and metastasis
De-regulation of cellular genetics
Immune evasion
Genome instability and mutation
Tumour-promoting inflammation
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33
Q

Which tumour suppressor mutation is associated with a worse breast cancer prognosis?

A

p53

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34
Q

Which receptor is the primary driver of growth in breast cancer?

A

Oestrogen receptor

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35
Q

What is the normal function of the BRCA gene?

A

DNA repair

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36
Q

What is the Warburg effect?

A

Cancer cells use anaerobic respiration (glycolysis) even in aerobic environments

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37
Q

How do cancer cells acquire replicative immortality?

A

Up-regulation of telomerase allows cells to continue dividing indefinitely, instead of reaching senescence after a certain number of divisions

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38
Q

How do cancer cells induce angiogenesis?

A

Hypoxia in cancer cells leads to a build-up of hypoxia inducible factor (HIF) which is degraded under normoxic conditions. HIF translocates to the nucleus and causes vascular endothelial growth factor (VEGF) production, which is then released from the cell and affects endothelial cells, promoting their survival, replication, and migration. Endothelial cells also release platelet-derived growth factor (PDGF) which promotes survival and replication of nearby pericytes which support endothelial cells when forming blood vessels

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39
Q

What type of cell transition occurs prior to invasion?

Give three cell changes that characterise this transition?

A

Epithelial to mesenchymal

Loss of cell polarity/ change in morphology, increased motility, loss of adherent junctions, expression of proteases

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40
Q

Which four terms are used to classify endometrial hyperplasia?

A

Simple vs. complex

Typical vs. atypical

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41
Q

Give three risk factors for endometrial cancer

A 
Obesity
T2DM
Hypertension
Nulliparity
Unopposed oestrogen exposure (including tamoxifen and HRT use)
Radiation
PCOS
Early menarche
Late menopause
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42
Q

What are most cases of endometrial cancer in women under 40 due to?

A

PCOS

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43
Q

What proportion of endometrial cancer does type I account for?

A

70-80%

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44
Q

What mutation is characteristic of type I endomterial cancer?

A

PTEN mutation

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45
Q

What mutation is characteristic of type II endometrial cancer?

A

p53 mutation

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46
Q

WHat is the morphology and prognosis of type II endometrial cancer

A

Papillary serous or clear cell

Prognosis is poor with a high rate of recurrence and a generally poor response to hormone treatments

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47
Q

Which type of endometrial cancer occurs as a result of unopposed oestrogen exposure?

A

Type I

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48
Q

Which lymph nodes will endometrial cancer usually spread to first?

A

Pelvic and para-aortic

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49
Q

Which viral infection is a prerequisite for cervical cancer?

A

HPV

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50
Q

Which two HPV subtypes together cause 75% of cervical cancer

A

16 and 18

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51
Q

Which two HPV subtypes account for 90% of genital warts?

A

6 and 11

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52
Q

Which cells does HPV infect?

A

Keratinocytes in the basal layer of the epidermis

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53
Q

What is the most vulnerable area of the cervix to HPV infection?

A

The squamo-columnar junction

Also known as the transformation zone

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54
Q

What is the action of the HPV E6 gene?

A

Induces degradation of p53 proteins

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55
Q

What is the action of the HPV E7 gene?

A

Binds and inactivates pRB, leading to its degradation

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56
Q

What uses does a vaccine have in HPV?

A

Prophylactic only

They have no therapeutic value

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57
Q

Where do primordial germ cells originate?

A

Posterior wall of the yolk sac

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58
Q

Describe the migration of primordial germ cells

A

Along the hindgut and through the dorsal mesentary to the genital ridges

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59
Q

Which critical gene does the SRY gene up-regulate?

A

Sox-9

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60
Q

What embryological structure do the gonads originate from?

A

The mesonephros

61
Q

Where do Sertoli cells originate from?

A

Cells of the coelomic epithelium

62
Q

Through what mechanism does Sox-9 cause differentiation of coelomic epithelial cells into Sertoli cells?

A

Sox-9 is present in Sertoli cells and up-regulates PgD synthase and FGF9. PgD is released and induces Sox-9 expression in neighbouring cells, which then differentiate into Sertoli cells

63
Q

Describe the action and expression of steroidogenic factor 1 (SF1)

A

SF1 activates AMH release to drive male differentiation. It is initially expressed in Leydig and Sertoli cells, but Sertoli cells later lose the expression

64
Q

At what point are oocytes arrested?

A

Diplotene of prophase of the first meiotic division

65
Q

At the time of menarche, how far towards their eventual height has a girl on average progressed

A

95%

66
Q

What is usually the first sign of puberty in females?

A

Breast development

Usually precedes menarche by 2-3 years

67
Q

Between what age ranges does puberty usually occur for boys and girls?

What are the mean ages for each?

A

Boys: 9-14
Girls: 8-14

Boys: 11.5
Girls: 10.5

68
Q

How much does adrenarche precede puberty by?

A

1-2 years

69
Q

Is precocious puberty concerning in males or females?

A

It is common and benign in females, but more often concerning in males

70
Q

Give 5 factors that may influence puberty

A 
Low body fat
Exercise
Thyroid issues
Chronic inflammatory disease
Genetics
Nutrition
Endocrinological disease e.g. Cushing's, hyperprolactinaemia, CAH
Hypothalamic/ pituitary impairment
71
Q

What testicular volume indicates a male has begun puberty?

What ovarian volume indicates a female has begun puberty?

What ovarian volume indicates a female has completed puberty?

A

4ml

1cm cubed

4cm cubed

72
Q

How long after menarche is the first ovulation?

A

6-9 months

73
Q

Which enzyme converts cholesterol to pregnenolone?

A

CYP11A1

74
Q

What structure is aromatised to convert an androgen to an oestrogen?

A

The A ring (first carbon ring)

75
Q

What is the effect of sulphonation of a steroid hormone?

A

It renders it inactive and water soluble so it may be excreted

76
Q

Where is cholesterol transported for metabolism to hormones, and how?

A

Inside the mitochondria

Via a StAR protein

77
Q

Give two characteristic biochemical features of PCOS

A

Raised androgens

Raised LH

78
Q

How does IGF modulate gonadotrophin action?

A

It directly stimulates steroidogenesis through its own signalling pathway, but also stimulates the Akt signalling pathway of the gonadotrophin receptor.

IGF also increases the number and activity of gonadotrophin receptors

79
Q

Through which pathway do gonadotrophins stimulate steroidogenesis?

A

Protein kinase A pathway

80
Q

What are the four glycoprotein hormones?

A

FSh, LH, hCG, and TSH

81
Q

Which subunit of glycoproteins does not vary?

A

Alpha

82
Q

Give two effects of glycosylation on the beta subunit of glycoproteins?

A

Increased half-life
Altered activity

hCG has a ten-fold greater half-life than LH
Deglycosylated glycoprotein hormones can still bind their receptors, but fail to stimulate cAMP production

83
Q

What frequency of GnRH pulse release favour FSH release?

A

Once every 90-120 minutes

84
Q

What frequency of GnRH pulse release favour LH release?

A

Once every 30 minutes

85
Q

Give two extra-HpG axis effects of FSH

A

Increases bone resorption

Decreases thermogenesis, and increases fat storage in adipocytes

86
Q

What effect does an inactivating LH mutation have on male and female phenotypes?

A

Male: Disrupted puberty, micropenis, hypogonadism, azoospermia
Female: Normal puberty including gonadal development, antral follicles visible, oligomenorrhea

87
Q

What effect does an inactivating FSH mutation have on male and female phenotypes?

A

Male: Normal puberty but subfertile with low sperm quality
Female: Infertile, arrested follicle maturation, primary hypergonadotrophic amenorrhea

88
Q

Why does FSHR inactivating mutation render males totally infertile, but FSH inactivating mutations do not?

A

The FSHR has some constitutive activity that is preserved even if FSH is absent or mutated

89
Q

Name the stages of spermatagonia development

A

A-dark, A-pale, A-transition (disputed), B

90
Q

What process converts a spermatocyte into a spermatid?

A

Two rounds of meiosis

91
Q

What change in DNA packaging allows DNA to be tightly packaged into the sperm head whilst remaining transcriptionally silent

A

Replacement of histones with protamines

92
Q

Which layer of the antral follicle is vascularised?

A

Thecal cell layer

93
Q

Describe proliferation of the granulosa cells in the primordial follicle

A

Initially they proliferate laterally, but as the cells become more crowded the cells change shape and become cuboidal to make room. Eventually the cells are forced to form layers, as the axis of mitosis become perpendicular

94
Q

What important structure is synthesised by the oocyte as the granulosa cells divide?

A

The zona pellucida

95
Q

What is secreted by the cumulus granulosa cells to form a blob that can be picked up by the fimbriae of the ovary?

A

Hyaluronan

96
Q

Describe the events of follicle luteinisation

A

The remainder of the follicle post-ovulation is invaded by macrophages and leukocytes. The basal lamina breaks down allowing vascularisation of the follicle

97
Q

What are the three main factors governing germ-cell entry into meiosis?

A

Retinoic acid
Dazl
Stra8

98
Q

Describe the action of retinoic acid in males and females

A

In females it stimulates Stra8 expression

In males it is degraded by Cyp26b1

99
Q

Describe the role of Dazl

A

Dazl regulates primordial germ cell progression to meiosis

100
Q

During which part of prophase do chiasmata develop?

A

Pachytene

101
Q

How is diplotene arrest maintained within oocytes?

A

GPCR on the membrane of oocytes are constitutively active and produce cAMP.
Granulosa cells produce cGMP which enters the oocyte through gap junctions and prevents the degradation of cAMP by the PDE3A enzyme. High levels of cAMP maintain meiotic arrest

102
Q

Where is Kit-ligand expressed and what process is it crucial for?

A

It is expressed by granulosa cells (the receptors are on oocytes) and is crucial for oocyte maturation

103
Q

How are oocytes released from meiotic arrest?

A

The LH surge triggers a shift in granulosa cells that causes them to withdraw their processes from the oocyte. cGMP in the oocyte decreases, allowing cAMP to be degraded and meiosis progresses

104
Q

At what point is meiosis II arrested, and when is it resumed?

A

Metaphase

Fertilisation

105
Q

Which species of bacterium is responsible for maintaining an acidic vaginal pH?

A

Lactobacillus

106
Q

How does the sperm reach the Fallopian tube?

A

A combination of cilial wafting and peristalsis-like uterine contractions
Inert particles have been shown to be able to reach the Fallopian tube so its probably not that much to do with the sperm

107
Q

How does cervical mucous influence the journey of the sperm (positively and negatively)?

A

Hydration of the mucous peaks during ovulation to make it permeable to sperm
The mucous provides a barrier so that malformed sperm are less able to reach the Fallopian tubes
Mucous prevents phagocytosis of sperm by maternal leukocytes

108
Q

Give two major change seen in sperm after capacitation

A

Increase in motility and development of a ‘whiplashing’ tail beat
Surface molecules which interact with the zona pellucida are unmasked

109
Q

What triggers capacitation?

What other function does this chemical serve relative to the sperm?

A

Progesterone

It provides a chemotactic gradient for sperm to move along

110
Q

Describe the events that occur within the sperm upon capcitation

A

Progesterone increases the sperm membrane’s permeability to calcium (though there is no progesterone receptor on sperm). The influx of calcium triggers opening of CatSper channels within the flagellum (tail) which open to allow further calcium influx.

111
Q

Give 5 key functions of the epididymis

A 
Further maturation of sperm
Concentration of fluid
Induction of quiescence to prevent premature acrosome reaction or capacitation
Storage of sperm
Passage of sperm through peristalsis
Removal of degenerating sperm
112
Q

Which cells control pH in the epididymis and how?

A

Apical cells

ATPase and carbonic anhydrase II

113
Q

Which segment of the epididymis is most heavily involved in concentrating fluid, and how?

A

Initial segment

Sodium-linked transporters

114
Q

Which segment of the epididymis coats the sperm in the proteins that are removed at capcitation?

A

Corpus

115
Q

Which region of the epididymis is most contractile and responsible for emission of sperm?

A

Cauda

116
Q

What is the best treatment for a prolactin-secreting tumour

A 
Dopamine agonists (e.g. bromocriptine, cabergoline)
Surgery is rarely necessary
117
Q

What characterises PCOS?

A

Anovulation with clinical and/or biochemical features of hyperandrogenism

118
Q

Why is weight loss first-line treatment for a patient with PCOS and BMI >30?

A

Because obesity exacerbates the symptoms of PCOS, and fertility may improve sufficiently on weight loss alone

119
Q

Why is FSH low in PCOS?

A

Multiple lead follicles develop instead of just one. As a consequence, oestrogen levels are unusually high which suppresses FSH, which prevents follicles from further progressing

120
Q

Give two drug treatments for PCOS

A

Clomiphene: inhibits oestrogen receptors in hypothalamus so removes negative feedback and boosts GnRH and FSH
Letrozole: Aromatase inhibitor which decreases circulating oestrogen to allow FSH levels to return to normal

121
Q

What is the biggest danger of exogenous FSH therapy?

A

Ovarian hyperstimulation syndrome

122
Q

Which nucleic acids can become methylated, and at which position?

A

Cytosine

5th carbon

123
Q

What proportion of methylated cytosine residues are found in CpG islands?

A

70-80%

124
Q

Why are methylated cytosine residues under-represented in the genome?

A

Because methylated cytosine is vulnerable to losing its amide group to become 5-methyluracil, which is essentially analogous to thymine, and so is not registered as an error by DNA repair machinery

125
Q

Where are CpG islands most commonly found within DNA?

A

Towards the end of gene promoter regions

126
Q

What effect does CpG methylation have on residues in CpG islands, and how?

A 
Gene silencing (It has the opposite effect on cytosine residues outside of CpG islands)
CpG island methylation sterically inhibits factor recruitment to the promoter region, and recruits methyl-CpG-binding proteins which remodel chromatin to make it inaccessible for transcription
127
Q

What overall methylation pattern is seen in genomes in cancer?

A

Global hypomethylation

128
Q

In what genomic location would hypermethylation be associated with cancer?

A

Tumour suppressor genes

129
Q

What percentage of p53 mutations occur at methylated cytosines (in sporadic colorectal cancer)?

A

50%

130
Q

What effect does UV light exposure have on p53?

A

Causes pyrimidine dimers to form in its DNA sequence making mutations more common

131
Q

Name two therapies that act by altering DNA or histone methylation or acetylation

A

DNA methyltransferase inhibitors - myelodysplatic syndrome

Histone deacetylase inhibitors - T-cell cutaneous lymphoma

132
Q

Give two uses for epigenetics in cancer

A

Treatment therapies

Classifying populations based in methylation in the same way they are classified based on genes ([prognostic and diagnostic biomarkers)

133
Q

Which disease does GSTP1 gene methylation correspond to?

A

Prostate cancer

134
Q

Which hormone may be measured to diagnose and even predict menopause instead of FSH?

A

Anti-Mullerian hormone (not menstrual cycle dependent)

135
Q

Why is FSH high in the build-up to menopause?

A

Ovarian ageing results in less Inhibin B secretion, so FSH rises

136
Q

Why is heavy, erratic menstrual bleeding a symptom of menopause?

A

Anovulatory cycles become more common in the build-up to menopause. Without ovulation, there is no progesterone, so oestradiol remains high and the endometrium continues to grow until it finally sheds leaving to heavier than normal bleeding

137
Q

Which is the main oestrogen during menopause?

A

Estrone

138
Q

What is thought to be the cause of hot flushes?

A

Narrowing of the ‘thermoneutral zone’ in the temperature regulation part of the hypothalamus

139
Q

Which functions are progesterone receptor A important for?

A

Ovulation and implantation

140
Q

Which functions are the progesterone B receptor important for?

A

Breast development during puberty

Particularly branching/ proliferation and differentiation of alveolar buds in breast tissue

141
Q

How do progestins affect oestrogen receptors?

A

They promote redistribution of oestrogen receptor binding away from pro-proliferative genes

142
Q

What is the only point of difference between progesterone receptor A and B?

A

The presence of an activation function 3 domain on progesterone receptor B

143
Q

Describe the 7 steps of the cancer-immunity cycle

A

Release of cancer cell antigens into circulation
Uptake and presentation of antigen on APC
Activation of T-cell
Trafficking of T-cell to tumour
Infiltration into tumour
Recognition of cancer cells
Killing

144
Q

Describe two cytokine-based cancer therapies

A

Interferon-alpha: initiates response similar to anti-viral resposne. Used as an adjuvant in treating melanoma

IL-2: Triggers activation and expansion of t-cell populations. Used against metastatic melanoma and renal cell carcinoma

145
Q

Name the four types of cancer vaccines

A

Tumour cell - tumour cells are extracted and modified to make them more immunogenic, then are re-transfused

Dendritic cell - dendritic cells are extracted from peripheral blood then expanded using IL-4 and GM-CSF and activated via exposure to tumour antigens. They re re-transfused to activate t-cells

Protein/ peptide
Infection - e.g. HPV vaccines which control the infection which causes the cancer, thereby limiting cancer rates

146
Q

Give four ways in which a monoclonal antibody treatment can act on cancer

A

Signalling inhibition: e.g. Herceptin targets HER2 receptor causing it to internalise and degrade

Antibody-mediated cytotoxicity: e.g.Rituximab (anti-CD20)

Delivery of conjugates: not particularly common, but antibodies can be used to deliver more targeted chemotherapy. One type of conjugate involves fixing enzymes to tumour cells, then giving chemotherapy as a prodrug that is only metabolised to its active form where the enzyme it present

Blocking immunosuppression - one of the most successful recent breakthrough therapies. CTLA-4 and PD1 are the main immunosuppressive receptors for T-cells (PD1 had a broader role in negative regulation) and suppression of these receptors leads to a more vigorous t-cell response. Nivolumab is a PD1 blocker, and Ipilumumab is a CTLA-4 blocker

147
Q

What is the advantage of using engineered t-cells over t-cell transfer?

A

Engneered t-cells can express chimeric antigen receptors which don’t require MHC stimulation, and so cna target cancer cells that have lost MHC

148
Q

Give three down-sides to t-cell transfer

A

There is a dissapointing clinical response
Only 30-40% of tumour biopsies yield sufficient lymphocyte for the procedure to work
It takes 6 weeks

149
Q

What triggers the LH surge?

A

Increased sensitivity to circulating GnRH levels
There is no increase in GnRH release that corresponds to the LH surge, instead there is increased gonadotrophin release in response to the same level of GnRH. This is why women have different reponses to kisspeptin at different stages of the menstrual cycle

4th Year Repro (7 decks)

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