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RED > Week 10 > Flashcards

Week 10 Flashcards

1
Q

Sexual dimorphism

A

The key is the Y chromosome which contains the testis-determining gene called the SRY (sex determining region on Y) gene on its short arm (Yp11)
Gonads
Genital ducts

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2
Q

Urorectal septum

A

The urorectal septum divides the cloaca into 2
The anterior part is the primitive urogenital sinus
-urogenital membrane
-becomes the urinary system
Posterior part is the primitive rectum
-anal membrane
-distal part digestive system

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3
Q

Indifferent stage in gonadal development

A

Can’t differentiate between male and female
4-7 weeks development
-gonads will not acquire male or female morphological characteristics until the 7th week development
-the coelomic epithelium of the genital ridge proliferates and penetrate the mesenchyme (intermediate mesoderm)
-irregularly shaped cords- the primitive sex cords
-cords are connected to surface epithelium and is impossible to differentiate male and female gonad

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4
Q

Development of testis

A

If the embryo is genetically male the primordial germ cells carry an XY sex chromosome complex
Under influence of the SRY gene on the Y chromosome which encodes the testis-determining factor the primitive sex cords penetrate deep to form medullary cords-rete testis
Dense tunica albuginea separates from the epithelium

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5
Q

Testis

A

Primordial germ cells- spermatogonia
Coelomic epithelium- Sertoli cells
Intermediate mesoderm- leydig cells
By the 8th week gestation, leydig cells produce testosterone and the testis influences sexual differentiation of the genital ducts (Wolffian duct) and external genitalia

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6
Q

Development of ovary

A

Primitive sex cords dissociate into irregular cell clusters
These primitive germ cell clusters occupy the medulla- replaced by a vascular stroma- ovarian medulla
In the 7th week the Coelomic epithelium- cortical cords penetrate the underlying mesenchyme but close to the surface
3rd month- cortical cords split into isolated cell clusters
Cells surround each oogonium- follicular cells
Oogonia and follicular cells constitute a primordial follicle
No thick tunica albuginea

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7
Q

indifferent stage genital ducts

A

Genital ridge
Mesonephric duct (wolffian)- separate openings
Paramesonephric duct (Mullerian): vertical, horizontal, vertical
The paramesonephric ducts have fuse- uterovaginal primordium, then have a common opening into primitive urogenital sinus

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8
Q

Müllerian duct

A

A cranial vertical portion that opens into the abdominal cavity
A horizontal part that crosses the mesonephric duct
A caudal vertical part that fuses with its partner from opposite side

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9
Q

Genital ducts in the male

A

Testis
-Mullerian inhibiting substance (Sertoli cells)-> paramesonephric ducts suppressed
-testosterone (leydig cells)—> mesonephric ducts stimulated (efferent ductule, epididymis, vas deferens, seminal vesicles). Dihydrotestosterone external genitalia stimulated, growth of penis, scrotum, prostate

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10
Q

Testis cords

A

Testis cords acquire a lumen and form the seminiferous tubules
They join the rete testis tubules which in turn enter the ductuli efferentes
They link the rete testis and the mesonephric or wolffian duct which becomes the ductus deferens

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11
Q

Remnants of ducts in males

A

Remnants of wolffian duct :
-appendix of epididymis
-paradidymis
Remnants of Müllerian duct:
-appendix of testis
-prostatic utricle

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12
Q

Prostate gland

A

Develops in the 10th week as a cluster of endodermal evaginations that bud from the urethra
Five independent groups of solid prostatic cords
11 weeks- cords develop into glandular acini
Bulbourethral glands sprout from the urethra just inferior to the prostate

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13
Q

Genital ducts in the female

A

Ovary
Estrogens (including maternal and paternal sources)
-paramesonephric ducts stimulated (uterine tube, uterus, upper portion of vagina)
-external genitalia stimulated (labia, clitoris, lower portion of vagina)

The uterovaginal primordium gives rise to uterus and upper part vagina
Sinovaginal bulb

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14
Q

Remnants of wolffian duct in females

A

Paroophoron
Epoophoron
Gartners duct

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15
Q

Development of vagina

A

Uterovaginal primordium- mesoderm
Sino-vaginal bulb- endoderm

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16
Q

Hematocolpos

A

Vaginal retention of menstrual blood at puberty
Imperforate hymen

17
Q

Different types uterine abnormalities

A

Double uterus, double vagina
Double uterus
Bicornate uterus
Cervical atresia
Unicornate uterus
Septated uterus

18
Q

External genitalia- indifferent stage

A

Genital tubercle
Cloacal fold - urethral fold
Genital swellings
Urogenital membrane
Anal membrane

19
Q

External genitalia male and female differentiation

A

Females:
-genital tubercle- clitoris
-urogenital membrane disintergrates into urethra and vagina
-anal membrane- anus
-urethral folds- labia minora
-genital swellings- labia majora
Males:
-genital tubercle extends to form penis
-urethral folds close together leaving small opening at tip of penis.
-genital swellings give rise to scrotum
-if urethral folds dont close properly- hypospadius

20
Q

Descent of gonads- Testis

A

The cranial suspensory ligament
The gubernaculum (or caudal Genito-inguinal ligament)
At 10th thoracic level
In the vicinity of the deep ring from 3rd to 7th month
Processes vaginalis-> tunica vaginalis meant to disappear if patent processes vaginalis-> hydrocele, indirect inguinal hernia
Distal part gubernaculum forms scrotal ligament holds testes in position

21
Q

Descent of gonads- ovary’s

A

Gubernaculum
-upper portion forms ovarian ligament attaching inferior pole ovary to uterus
-lower portion forms round ligament of uterus attaching uterus to labia majora
Paramesonephric duct in the way so ovary cant descend all way down sits near uterine tube and uterus

22
Q

Feto-placental unit

A

Placenta fully formed 11th-14th weeks
O2, CO2 and nutrients move by diffusion between the maternal intervillous space and fetal capillaries

23
Q

O2 and CO2 exchange

A

Oxygen:
-uterine artery PO2=12.7kPa, uterine vein PO2= 5.6kPa to fetus
-umbilical artery PO2=3.2kPa form fetus, umbilical vein PO2=4.2kPa to fetus
Carbon dioxide:
-uterine artery PCO2=5.3kPa, uterine vein PCO2=6.1kPa
-umbilical artery PCO2=6.6kPa from fetus, umbilical vein PCO2=5.8kPa to fetus
Fetal umbilical vein blood does not achieve equilibrium with maternal blood for oxygen
Fetal umbilical vein blood almost achieves equilibrium with maternal blood for CO2
-the placental barrier is more permeable to CO2 than O2
-not all the maternal blood comes in contact with the Villi
-the placental tissue is highly active and consumes O2 (~20%)
However normally the fetus is adequately supplied with O2

24
Q

Fetal haemoglobin HbF

A

HbF comprises 2 alpha and 2 gamma polypeptide chains
adult Hb 2 alpha and 2 beta
Reaches peak level at 10 weeks
-maintained until 30 weeks
-declines to 80% of total at term
-gradually disappears after birth from ~6 months
HbF has higher affinity for O2:
-its higher affinity is explained by its lack of interaction with 2,3-DPG
-the adult Hb-O2 curve is right shifted by 2,3-DPG

25
Q

Fetal Hb-O2 saturation

A

P50 of HbF is much lower than adult Hb
O2 diffuses from maternal to fetal Hb
At PO2 ~4.2kPa, HbF is ~75% saturated
Bohr shift (effect of CO2) separates curves even further :
-fetal curve to left
-maternal curve to right

26
Q

Fetal arterial O2 content

A

Fetal blood has higher Hb concentration than maternal blood: 18 vs 15g/dl
Therefore at any PO2 fetal blood carries more O2
-even at PO2 ~4.2kPa fetal blood has O2 content similar to maternal arterial blood (at ~12.5kPa)

27
Q

Fetal circulation optimises O2 delivery (particularly to brain)

A

3 “shunts”
-ductus venosus
-foramen ovale
-ductus arteriosus
Flow through each shunt is dependent on intravascular pressure gradient
-umbilical vein P>IVCP
-RatrP>LatrP
-Pulm ABP>aortic ABP
NB blood with highest O2 saturation goes to the brain

28
Q

Blood with highest O2 saturation goes to brain

A

Oxygenated blood from the placenta flows via ductus venosus to join the IVC
This blood stays in same “lane” as it flows back to right atrium and is steered through foramen ovale to brain
These lanes are preserved with relatively little mixing through A-V valve into left ventricle and then through aortic valve
This same lane of blood stays on upper side of aortic arch ideally placed to take carotid arteries up to brain
Thus brain is supplied with most well oxygenated blood

29
Q

differences between fetal and adult cardiac outputs

A

In adult circulation there are no shunts
R stroke volume = L stroke volume
CO is defined as volume ejected by one ventricle/min
In fetus shunting means
Fetal L stroke volume does not = R stroke volume
RV receives ~65% venous return
LV receives ~35% venous return
Thus fetal cardiac output is defined as total output of ventricles combined ventricular output CVO
~45% of CVO is directed to placental circulation
Only ~8% CVO enters pulmonary circulation

30
Q

Control of Fetal circulation

A

Circulating catecholamines other hormones and locally released vasoactive substances all play a part in
Circulating catecholamines act on alpha and beta adrenoceptors
Receptors mature during early gestation, independently of autonomic innervation process
Peripheral circulation of fetus is under tonic adrenergic vasoconstrictor influence mainly circulating noradrenaline
Other factors such as arginine vasopressin AVP and renin-angiotensin system also play a role

31
Q

Neural control of fetal circulation

A

By 11th week of gestation, HR is ~160BPM
From weeks 28 autonomic control develops: HR slows to ~140bpm (vagus)
By 11th weeks systemic ABP is ~70/45mmHg
-it rises very gradually as sympathetic tone develops and peripheral resistance increases: ~80/55mHg at term
Over same time:
-baroreceptors reflex develops- regulates ABP
-peripheral chemoreceptors and reflex begins to function
-therefore hypoxia evokes primary chemoreceptor reflex:
—Fetal bradycardia and peripheral vasoconstriction
-blood flow to brain is preserved

32
Q

Fetal breathing movements FBMs

A

~11 weeks, Fetal breathing movements begin- shallow and irregular
~34 weeks become more rhythmic (~50b/min)
-present ~30% time during night and after ‘meals’
-play role in development of respiratory muscles
-aspiration of amniotic fluid
Incidence of FBMs decreases during fetal hypoxia
-due to local direct effect of hypoxia on central respiratory neurones
NB peripheral chemoreceptor reflex effect on respiration is not yet present
Incidence of FBMs decreases prior to delivery- predictor of delivery in health fetus

33
Q

Events at birth (respiratory)

A

Fluid that has been in lungs is squeezed out during birth
-this is not so effective during Caesarian birth
First breath:
-triggered by cooling, sensory stimulation and chemoreceptors stimulation- central and peripheral
Made possible by surfactant:
-secreted by type II cells ~28-30 weeks under influence of fetal cortisol
-reduces surface tension force that opposes lung inflation
-may be inadequate in pre-term baby
As air moves in forces lung fluid across alveoli, and surfactant is adsorbed onto alveoli surface
Requires enormous ventilatory effort

34
Q

Changes in compliance and FRC in 2 weeks after birth

A

FRC= functional residual capacity
Compliance= change in V/change in pressure
First breath generates large drop in intrapleural pressure
Functional residual capacity and compliance gradually increase during first weeks of life

35
Q

Events at birth cardiovascular

A

Umbilical cord is clamped
Therefore TPR increases
Systemic ABP>pulm ABP
Ductus arteriosus -flow reverses then closes
1st breath: PVR decreases (lungs expand)
-therefore pulmonary perfusion increases
-greater volume/min returns to L atrium
-L atrial P> R atrial P
-foramen ovale closes
Reduced flow in umbilical vein because umbilical cord clamped
-therefore ductus venosus constricts and then closes

36
Q

Changes in neonatal period

A

Septal leaflets of foramen ovale fuse within few days
Ductus arteriosus closes within 2 days -initiated by high PO2
-due to reduction in local prostaglandins: synthesised by lungs due to low PO2- vasodilator
-high PO2 when lungs ventilated- decreases PG synthesis
-NSAIDs (block COX) can promote closure
-local bradykinin may be responsible for closure
Wall thickness of pulmonary arteries and right ventricle decreases due to decreased PVR
Wall thickness of left ventricle increases- due to increasing TPR . ABP gradually increases until ~7 years old
Peripheral chemoreceptors “re set” over ~ 2weeks after birth
-from fetal PO2 range- firing when PO2<4.2kPa to adult range so that activated when PO2<12.5kPa ie threshold shifts rightwards
Baby is vulnerable to hypoxia during this period because respiratory response is week- “cot death”

37
Q

Problems following birth

A

Foramen ovale between L and R atrium may not close:
-if left-right shunt causes gradual pulmonary remodelling
-pulmonary hypertension
-R ventricular overload-> RV hypertrophy
-when RV pressure> LV pressure, shunt reverses
-known as Eisenmengers syndrome, oxygenation compromised. From puberty
-if right left shunting mixing oxygenated blood and deoxygenated blood
—“blue baby” tetralogy of Fallot surgery required
Ductus arteriosus may remain open:
-L ventricular output diverted into pulmonary circulation from aorta
-pulmonary hypertension- R ventricular overload
-eventually heart failure
-so surgery required

38
Q

Problems during pregnancy

A

Pre-eclampsia:
-high ABP and proteinuria in mother- convulsions
-delivery urgent only cure
-inflammatory mediators released by hypoxic placenta?
Intra-uterine growth retardation IUGR:
-associated with high ABP, advanced diabetes, malnutrition, substance abuse, smoking
-poor placental perfusion in mother
-low birth weight
Fetal programming:
-adverse conditions in utero including poor nutrition, poor O2 supply, IUGR, lead to further adverse effects
-EG increase cortisol, oxidative stress, epigenetic processes
-to increased risk of CV disease- hypertension etc diabetes, obesity, metabolic syndrome in adult life

RED (10 decks)

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