What I don't know Flashcards

1
Q

What sperm and egg contributes to conceptus

A

Sperm: Centriole and pericentriolar material to form the centrosome.
Egg: Cell membrane, cell organelles, macromolecular matrix on which centrosome and chromosomes operate. Maternal cytoplasmic inheritance.

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2
Q

Testes organisation

A

Extratubular compartment consists of a vascular component in free communication with an interstitial component, which includes the lymphatics, and in which androgen synthesis occurs in Leydig cells.

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3
Q

Afterbirth

A

Placenta and foetal membranes that are expelled from the uterus following the baby’s birth

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4
Q

Villi late gestation

A

At about 20 weeks, the villi have regressed to one pole to form the discoid placenta. The placenta membranes remain in regions where the villi have regressed and when ruptured, provide an exit route at birth.

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5
Q

Embryonic vs Foetal period of development

A

Embryonic period of development: 0-8 weeks post-fertilisation when organ differentiation happens. Very susceptible to ROS and alcohol. Most deaths happen during this period.

Foetal period of development: 9-38 weeks. Major growth phase.

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6
Q

Placental blood volume

A

Mature placenta contains 150ml of maternal blood, and this volume is replaced 3-4 times every minute.

High volume, low velocity, low pressure.

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7
Q

Erection

A

Inflow and outflow of blood is ABSENT.

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8
Q

Maternal metabolism

A

EARLY pregnancy: Appetite increased, net deposition of nutrient resources.

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9
Q

Pre-eclampsia

A

De novo hypertension of 140/90 mmHg starting
after 20 weeks of gestation, proteinuria, oedema
Only seen in humans
Most common with 1st pregnancies with a particular partner.
Due to abnormal placenta, so complete hydatidiform moles can cause PE.
High risk in placenta formed from donated oocyte.

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10
Q

Hormones that control maternal metabolism

A

5P LORA

Progesterone, hPL, prolactin, PGH, PAPP-A, leptin, oestrogen, relaxin, and Adrenal cortical hormones

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11
Q

Foetal determination of foetal growth

A

GESI

genome, endocrine, sex, infection

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12
Q

Maternal determination of fetal growth

A

SUNPED

Socioeconomic, uterine size, nutrition, parity, environmental, disease

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13
Q

Foetal physiology

A

ORCOF

Oxygen affinity, resetting of reflexes, closure of shunts, overall resistance and fetal response to hypoxia.

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14
Q

Lactation

A

From puberty onwards, oestrogen + progesterone + GH cause mammary gland growth. GH acts via IGF1.

Early in a pregnancy, oestrogen + progesterone + hPL causes further mammary gland growth.

Late in a pregnancy, GH initiates milk production. But milk production can only occur if oestrogen + progesterone + hPL decrease.

Milk production/galactopoiesis is maintained by prolactin, which is elevated by suckling.

Oxytocin is needed to squeeze milk out by inducing contractions of the myoepithelial cells around the alveoli.

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15
Q

Partuition

A

Placental CRH acts at 2 levels: Foetal pituitary and foetal adrenals, to increase 2 things: DHEAS production and cortisol production.
Placental CRH production also increase maternal CRH levels.
Placental CRH production inhibited by progesterone and stimulated by catecholamines (from lecture notes) and cortisol

DHEAS makes more oestrogen which does 3 things: Increased PLA2 activity, oxytocin receptor density, actin + myosin filaments.

Cortisol does 2 things: Increased COX activity, decreased PGDH activity.

Note that CRH can inhibit contractions by increasing cAMP in myometrium (from lecture notes).

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16
Q

Aneuploidy stats

A

Accounts for:
50% of spontaneous miscarriages
5% of still births
0.5% of live births have a high level of genetic abnormalities including

For live ones, you can see either: error of ploidy, error of somy, translocations, genetic mosaics.

17
Q

Miscarriage lecture

A

Look at hCG levels. From the time you can detect hCG increases, percentage of pregnancies that result in pregnancy loss is 35%. 20% of those is from the initial detection of hCG to the time when people normally have a clinical test for pregnancy (which looks for slightly higher hCG levels). 15% is from clinical test time to birth.

18
Q

Neonatal physiology hormones

A

Beta adrenoceptor and Na+ channel expression increased by cortisol.
Cl- channel inhibition mediated by catecholamines.
Thyroid hormone is also needed to absorb lung liquid.

Beta adrenoceptors are also needed for surfactant production. Since cortisol directly increase surfactant production by OLB, cortisol directly and indirectly increases surfactant production.

Brown fat activity increased by thyroid hormone and catecholamines.

Increase in arterial PO2 in neonates helps to close ductus arteriosus and venosus.

Oestrogen and prolactin needed to induce maternal care behaviour.

19
Q

Premature birth (before 35 weeks)

A

Respiratory distress syndrome
Wet lung syndrome
SIDS due to failure or resetting of thyroid axis, baroreceptors, chemoreceptors.
Immature neural mechanisms due to lack of T3.
Hypothermia (premature babies have greater SA:V ratio, less brown fat).

Give dexamethasone or betamethasone.

20
Q

Why IUGR leads to increased cardiovascular disease

A

Premature activation of HPA axis leads to inappropriate pattern of growth for a stage of development.
Epigenetic programming of stem cells.
Underdeveloped organs.

21
Q

Rhythms

A

Ultradian rhythm: Cycle lasts less than a day.
Circadian rhythm: Cycle once a day.
Infradian rhythm: Cycle lasts more than a day.

22
Q

Chlamydia

A

Most prevalent STI in the UK.

23
Q

Barker hypothesis

A

“The aetiology of many chronic diseases lay not
only in genetic predisposition or in adult lifestyle but also in the ways in which early life events could affect subsequent biology”

In exam: IUGR leads to increased risk of cardiovascular diseases.

24
Q

Inhibin’s role in male gametogenesis

A

As Sertoli cells are implicated in the support of spermatogenesis, as well as being the site of inhibin production, it appears that inhibin serves as the measure of spermatogenic effectiveness.

Inhibin increases androgen production by Leydig cells in response to LH.
Prolactin also increases androgen production by Leydig cells in response to LH.

Remember that androgens not only cause Sertoli cells to make oestrogen, but also nurtures and stimulates Sertoli cells.

25
Q

Dominant follicle

A

retarded follicles show low levels of inhibin but higher Retarded follicles show levels low inhibin and high activin levels. Activin attenuate androgen output by the theca, thus indirectly suppress both inhibin synthesis and oestrogen output (activin does the same to leydig cells). Thus, dominant follicles are characterized by high ratios of both inhibin : activin and IGF : IGFBP, and lots of PAPP-A. Retarded follicles show the reverse.

Activin lowers androgen output!
Activin also enhances FSH output at the pituitary.
Activin direct opposite to inhibin.

26
Q

Sertoli cells

A

Sertoli cells form a continuous epithelial sheet, sealed with tight junctions, attached to the basement membrane of the seminiferous tubule.
The nuclei are located on the basement membrane of the seminiferous tubules.

Spermatogonium –> primary spermatocyte –> secondary spermatocyte –> spermatid –> spermatozoon.

27
Q

Epididymis

A

Epididymis is lined by pseudostratified columnar or cuboidal epithelium containing a layer of principal cells and smaller basal cells.
Apical edges of the principal cells form stereocilia
which are non-motile structures.
Outside the epithelium is connective tissue and smooth muscle. More smooth muscle towards cauda epididymis.

28
Q

Seminal vesicle

A

Paired structure. Highly invaginated inner surface.
Epithelium same as epididymis.
Secretes alkaline fluid under sympathetic stimulation. Contains fructose, prostaglandins, fibrinogen-like proteins.
Outside the epithelium is connective tissue and smooth muscle.

29
Q

Prostate

A

Large. Consists of many tubules each with their own lumen. Columnar epithelial cells + basal cells.
Outside the epithelium is connective tissue and smooth muscle.

Secrete PSA but usually doesn’t reach blood. Liver PSA reaches blood. But in prostate cancer, prostate’s PSA can reach blood.

Note that all accessory glands are dependent on dihydrotestosterone, more potent androgen than testosterone.

Hypophysectomy picture darker than castration picture.

30
Q

Fluid absorption

A

If the vasa efferentia are ligated fluid will accumulate, fluid leaks into interstitial space, germinal epithelium damaged, and spermatogenesis ceases.
If vas deferens ligated, nothing happens.

Vasa efferentia ligation picture: lumen looks very big.

31
Q

Velamentous cord insertion

A

Umbilical cord insert into foetal membranes instead of the chorionic plate. This causes vasa praevia, and the vessels are prone to rupture causing ante-partum haemorrhage, especially if vessels are near the cervix, as they’re not protected by Wharton’s jelly.

Normally, the blastocyst implants with the inner cell
mass orientated towards the endometrium. If the blastocyst implants on its side, then the connecting stalk has to grow down over foetal membranes to reach the placenta.

32
Q

Chorion frondosum and chorion laeve

A

Initially villi are formed over the entire chorionic sac, giving rise to the chorion frondosum.
By 20 weeks, villi have regressed from the superficial pole, leaving the chorion laeve. It is this part of the chorionic sac that ruptures during delivery,
and through which the baby is born.
Villi persist only over the deep pole of the chorionic sac.
Regression of the villi gives the placenta its discoid shape.

If regression is incomplete, remnants may persist as accessory or succenturiate lobes.

33
Q

Multiple pregnancies

A

In dizygotic twins there are always two chorionic sacs.
In monozygotic twins, number of chorionic sacs depend on when splitting occurs, and hence whether one or two blastocysts are formed.
Vascular anastomoses frequently occur in monochorionic placentas (share one chorionic sac), and imbalance in blood flow can result in the twin-transfusion syndrome. One twin (the recipient) becomes
dominant and receives blood from the other (donor twin).

34
Q

Oviduct

A

Epithelium, smooth muscle, serosa. Near the ovary, lumen looks very disjointed. Near the uterus, lumen look more organised.
Epithelium contains pale ciliated cells and dark NON-ciliated cells.

35
Q

Vagina

A

Pro-oestrous: Oestrogen causes keratin production within the squamous stratified epithelium.

Oestrous, during ovulation: Keratin layer is at the surface of the vagina. Protects from mechanical damage.

Dioestrous: Progesterone causes neutrophil recruitment.

Pregnancy: Now progesterone causes production of goblet cells.

36
Q

Uterus

A

Oestrogen promotes development of simple tubular glands in endometrium. The glands contain SIMPLE epithelium.

Progesterone: Myometrium, epithelial cells of endometrium proliferates, glands become more branched.

37
Q

Pseudopregnancy

A

Mating an oestrous rabbit with a vasectomised male or stimulation of the vagina during oestrous
produces a similar sequence of ovulation and subsequent corpus luteum formation inducing
pseudopregnancy

Serosa, longitudinal, circular smooth muscle, endometrium.

38
Q

Type of secretion

A

Apocrine = holocrine: type of secretion where a part of the cytoplasm is lost with the secretion. Apocrine for lipid secretion.
Merocrine = eccrine =exocytosis: type of secretion where a membrane bounded secretory
product is released by fusion of that membrane with the plasma membrane. Merocrine for protein secretion.

39
Q

Placenta

A

Arteries run superficial to the veins over the
chorionic plate. The umbilical cord is usually attached close to the centre of the chorionic plate.

Placenta abruption: Placenta separates from the uterine wall prematurely. Placenta appears pale. Cause IUGR.