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MBChB - year 2 > Week 1 RNU Lectures > Flashcards

Week 1 RNU Lectures Flashcards

1
Q

What two substance pass through the urethra?

A

Sperm and urine

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2
Q

What does the urogenital tract originate from?

A

Intermediate mesoderm

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3
Q

What are the three sets of kidney structures during development?

A

Pronephros
Mesonephros
Metanephros

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4
Q

Where are the pronephros found?

A

Cervical region

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5
Q

Where are the mesonephros found?

A

Abdominal region

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6
Q

Where are the metanephros found?

A

Pelvic region

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7
Q

How are the three sets of kidney structures formed during development?

A

cranial to caudal and chronological sequence

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8
Q

What are the pronephros?

A

Rudimentary and non-functional structures that begin to regress by week 4

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9
Q

How do the pronephros form?

A

Intermediate mesoderm starts to thicken and forms 7-10 solid cell groups in the cervical region

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10
Q

What are the mesonephros derived from?

A

Intermediate mesoderm from the upper thoracic and upper lumbar segments

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11
Q

What is the mesonephros?

A

A solid rod of intermediate mesoderm in the future abdominal area. It has everything needed to be functional but is not. Contributes cells to the genital ridge and eventually starts to regress

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12
Q

What is the metanephros?

A

The definitive kidney

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13
Q

When does the metanephros develop?

A

In week 5 and is functional by week 11

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14
Q

How do the excretory units of the metanephros form?

A

Develop from the metanephric mesoderm.
Formed from 2 parts at the bottom of the developing structure:
- Ureteric bud
- Metanephric cap

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15
Q

How is the metanephric cap formed?

A

Mesoderm around the ureteric bud forms mesenchyme which is the metanephric cap

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16
Q

What sources does the definitive kidney form from?

A
  • Metanephric mesoderm (forms the excretory units)

- Ureteric duct (collecting system for excreted stuff)

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17
Q

What is the cloaca?

A

Posterior orifice that serves as the only opening for the intestinal, reproductive and urinary tracts at early stages

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18
Q

What is the ureteric bud?

A

A protrusion of mesonephric duct that allows urine drainage from the developing kidney

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19
Q

What does the cloaca begin as?

A

Hindgut (endodermal lining)

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20
Q

What divides the cloaca?

A

The Urorectal septum by fusing with the cloacal membrane

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21
Q

What does the division of the cloaca form?

A
  • Anterior urogenital sinus

- posterior rectal/anal canal

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22
Q

What does the bladder form from?

A

the urogenital sinus and caudal parts of the mesonephric duct

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23
Q

What lines the bladder?

A

Endoderm

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24
Q

When is genetic sex determined?

A

At fertilisation

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25
Q

When do the gonads acquire morphological characteristics?

A

Week 7 of development

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26
Q

What are the three steps of the development of the reproductive tract?

A
  1. Genital duct development
  2. Gonadal development
  3. External genitalia development
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27
Q

What is present during the indifferent stage (weeks 5-6)?

A

2 pairs of genital ducts

  • paramesonephric ducts (Mullerian) FEMALE
  • mesonephric (Wolffian) ducts MALE
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28
Q

What is the function of the mesonephric ducts?

A
  • drain urine from the mesonephric kidney

- an essential role in the development of the male reproductive system

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29
Q

What happens to the mesonephric ducts under the influence of testosterone?

A

forms the ductus deferens and ejaculatory duct when mesonephros vanishes

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30
Q

What happens to the mesonephric ducts in females?

A

almost completely disappears, leave a few non-functional remnants

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31
Q

What happens to the paramesonephric ducts in males?

A

degenerate due to the action of anti-Mullerian hormone. This is a protein made by the Sertoli cells of the testis

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32
Q

What do the paramesonephric ducts form in females?

A
  • Cranial portion forms uterine tubes

- Caudal portion fuses to form the uterovaginal primordium (uterus and superior vagina)

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33
Q

What do the gonads initially appear as?

A

A pair of longitudinal ridges (on top of the urogenital ridge)

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34
Q

Where do primordial germ cells originate?

A

The yolk sac

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35
Q

How do primordial germ cells move from the yolk sac and to where?

A

To the genital ridge via the dorsal mesentery

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36
Q

What happens if the primordial germ cells don’t arrive into the gonadal ridge by week 6?

A

The ridges develop no further and the gonads don’t develop

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37
Q

What type of structure do the primordial germ cells form in?

A

A cord like structure - primitive sex cords

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38
Q

What does the Y chromosome encode?

A

SRY - Sex determining Region of Y chromosome

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39
Q

What does SRY act on and cause?

A

Acts on somatic cells causing proliferation of the sex cells

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40
Q

What happens to the primitive sex cords in male development?

A

They become horseshoe shaped and break up into tubules

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41
Q

What do Leydig cells produce?

A

Testosterone

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42
Q

What do Sertoli cells produce?

A

Anti-Mullerian hormone

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43
Q

What forms to separate cords from the surface epithelium (male gonadal development)

A

Dense connective tissue

- tunica albuginea

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44
Q

What happens to the testis cords in puberty?

A
  • They acquire a lumen
  • join with the rete testis
  • join with efferent ductules
  • rete testis and mesonephric duct link to form the ductus deferens
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45
Q

What does WNT4 do?

A

“ovary determining gene”

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46
Q

What happens to the primordial germ cells in female development?

A

They divide by mitosis creating a pool of oogonia

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47
Q

What happens to the oogonia at the beginning of the 4th month of gestation?

A

They enter meiotic arrest and are now oocytes

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48
Q

How are the external genitalia formed?

A
  • a pair of cloacal folds develop around cloacal membrane
  • join to form the genital tubercle at the cranial end – this will form the penis and the clitoris
  • caudally the cloacal folds are subdivided:
    • urethral folds in front - form labia minora in female
    • anal folds behind
    • genital swellings then appear on either side of the urethral folds
    • form scrotal swellings in male, labia majora in the female
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49
Q

How is the urethra formed?

A
  • From middle pelvic part of urogenital sinus
  • In males, androgens from fetal testis cause genital tubercle to elongate into phallus
    • phallus pulls urethral folds forward
    • they form lateral walls of urethral groove and close over urethral plate to form penile urethra
    • terminal part of male urethra (external urethral meatus) from surface ectoderm
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50
Q

What is hypospadias?

A

The urethra is open on the underside of the penis

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51
Q

How does the prostate gland form?

A

develops as outgrowths from the prostatic urethra

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52
Q

How do the bulbourethral glands form?

A

develop as outgrowths from penile urethra

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53
Q

How does the lower part of the vagina develop?

A

two outgrowths from urogenital sinus – sinovaginal bulbs – fuse to form a vaginal plate, hollows to form a cavity

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54
Q

How does the penis form?

A

androgens from fetal testis cause genital tubercle to elongate into phallus
o phallus pulls urethral folds forward
o they form lateral walls of urethral groove and close over urethral plate to form penile urethra
o terminal part of male urethra (external urethral meatus) from surface ectoderm

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55
Q

What are circulating oestrogens a mixture of?

A

Oestrone and oestradiol

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56
Q

Where is oestrone secreted from?

A

directly from the ovary or converted from androstenedione (via aromatase)

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57
Q

Where does oestradiol come from?

A

Produced by the ovary, derived by direct synthesis in developing follicles or through conversion of oestrone

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58
Q

What are oestrogens involved in?

A

Development of female secondary sex characteristics

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59
Q

What could happen if someone had issues with aromatase?

A

They could have issues with sexual development

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60
Q

What hormones do the ovaries produce?

A

androstenediol, dehydroepiandrosterone (DHEA) and small amounts of testosterone

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61
Q

Where does half of the daily production of androstenediol and DHEA and essentially all of the sulphated form of DHEA (DHEAs) come from?

A

The adrenal gland

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62
Q

What is DHEA?

A

An abundant circulating steroid hormone in humans and is a metabolic intermediate in the biosynthesis of androgens and oestrogens

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63
Q

What is DHEAs?

A

The sulfate ester of DHEA, catalysed by sulfotransferase in the adrenal, liver and small intestine.
In the blood, levels of DHEAs are 300x higher than DHEA and is more stable for measuring

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64
Q

When in the menstrual cycle are progestogens particularly important?

A

In the 2nd half

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65
Q

How are progestogens made?

A

From cholesterol via pregnenolone

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66
Q

Where are progestogens made?

A

Primarily in the corpus luteum, the adrenal glands, and, during pregnancy, the placenta

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67
Q

What are the roles of progestogens?

A
  • Endometrial development
  • smooth muscle control
  • Maintenance of pregnancy - placenta (establishing and keeping pregnancy)
  • Mammary gland development especially preparing breasts for lactation
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68
Q

What are some disorders relating to steroidogenesis?

A
  • Congenital adrenal hyperplasia
  • aromatase deficiency
  • Aromatase excess
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69
Q

What causes congenital adrenal hyperplasia?

A
  • 21-hydroxylase deficiency

- Deficiency in 11B- hydroxylase activity

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70
Q

What are the symptoms of Congenital adrenal hyperplasia?

A
  • Ambiguous genitalia
  • precocious puberty
  • anovulation
  • Hirsutism (excess hair)
  • Steroid crisis
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71
Q

What happens in aromatase deficiency?

A

Prevents oestrogen synthesis

can lead to ambiguous genitalia

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72
Q

What happens in aromatase excess?

A

There is excessive conversion of androgens to oestrogens which can lead to the feminisation of male genitalia

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73
Q

What is the axis that regulates female reproduction?

A

Interactions between the Hypothalamic-pituitary-ovarian axis and the uterus

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74
Q

What happens when the hypothalamus secretes gonadotrophin releasing hormone (GnRH)?

A

GnRH –> anterior pituitary releases gonadotrophins (FSH and LH) –> target the gonads

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75
Q

What is the 2nd level of hormonal control of female reproduction?

A

The pituitary gland

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76
Q

What hormones does the anterior pituitary secrete?

A

FSH, LH

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77
Q

What does the posterior pituitary gland secrete?

A

Oxytocin

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78
Q

What is oxytocin involved in?

A

childbirth and lactation

79
Q

What is the 3rd level of hormonal control of female sexual reproduction?

A

The ovaries and the placenta

80
Q

What triggers follicle maturation and regulate steroid hormone production in the ovary

A

Levels of FSH and LH

81
Q

What is the principle secretory product of the ovarian follicle after ovulation?

A

Progesterone

82
Q

What does the placenta produce?

A

Oestrogens, progesterone and HcG

83
Q

What is the function of FSH?

A
  • Initiates the recruitment of follicles

- supports the growth of the follicle, especially the granulosa cells

84
Q

What is the function of LH?

A
  • supports theca cells - a shell that forms around the follicle (theca interna and externa)
  • LH surge triggers ovulation
85
Q

What are the stages of the menstrual cycle in terms of the ovary?

A

follicular (preovulatory) phase and luteal (postovulatory) phase

86
Q

What are the stages of the menstrual cycle in terms of the endometrium?

A

The proliferative phase and the secretory phase

87
Q

When is there the highest level of LH?

A

Ovulation

88
Q

When is the highest level of oestrogens?

A

Ovulation

89
Q

When is the highest level of progesterone?

A

the middle of the secretory/luteal phase (postovulatory)

This is at day 21 of the cycle (if ovulation has occurred)

90
Q

What happens during the follicular phase?

A
  • the growth of a dominant follicle

- Progesterone production is low but oestrogen is rising

91
Q

What are the stages of the development of the follicle?

A

Primordial follicle –> primary follicle –> secondary follicle –> Graafian/ tertiary follicle

92
Q

What are the layers of the late primary follicle?

A

Granulosa cells, theca cells, stromal cells

93
Q

What happens during development of the secondary follicle?

A
  • FSH secretion increases slightly, stimulating further growth of recruited follicles.
  • Circulating LH levels increase slowly, beginning 1 to 2 days after the increase in FSH.
  • Theca develops – follicle gains an independent blood supply
  • Granulosa cells develop FSH, oestrogen and androgen receptors
94
Q

What hormone do developing follicles produce?

A

inhibin

95
Q

What does inhibin do during follicle development?

A

Inhibits FSH secretion but not LH secretion

96
Q

What are the uterine changes in the proliferative phase?

A

Oestrogens from the ovary act on the endometrium

  • thickening of the stroma
  • elongation of the uterine glands
  • growth of the spiral arteries
97
Q

What happens around the time of ovulation?

A

Towards the end of the proliferative phase, rising oestrogens;

  • Increase responsiveness of the pituitary to GnRH
  • surge in hypothalamic secretion of GnRH

High levels of oestradiol trigger LH secretion and there is a surge of LH

98
Q

What happens during the luteal/ secretory phase?

A
  • Formation of the corpus luteum (yellow body) from the follicle
  • The corpus luteum secretes primarily progesterone in increasing quantities, peaking at about 6 to 8 days after ovulation
  • Progesterone stimulates development of the secretory endometrium
99
Q

Why does the endometrium become spongy?

A

To encourage implantation

100
Q

What does the corpus luteum eventually form?

A

The corpus albicans

101
Q

What causes the corpus luteum to change into the corpus albicans?

A

Rising progesterone levels inhibit LH production

102
Q

What causes menstruation?

A

When the corpus luteum becomes the corpus albicans the secretion of oestrogen and progesterone stop and the endometrial lining is no longer maintained.

103
Q

What happens during menstruation?

A
  • Leukocyte infiltration of endometrium – cells start to die and when blood supply gets cut off get massive ischaemia
  • Constriction and breakdown of spiral arteries – ischemia
  • Menstruation begins
104
Q

What are the hormonal effects on the vagina through the menstrual cycle?

A

Early follicular phase - oestrogen is low - vaginal epithelium is thin and pale

Late follicular phase - oestrogen increases - Squamous cells mature causing the epithelium to thicken

Luteal phase - mature squamous cells shed as cellular debris

105
Q

What are the hormonal effects on the cervix through the menstrual cycle?

A

Late follicular phase - oestrogen levels increasing - Increased cervical vascularity and water mucus

Luteal phase - progesterone levels increasing - Thicker cervical mucus reduces elasticity

106
Q

What is PCOS?

A

A common endocrine abnormality that often presents clinically with infertility, Amenorrhea and weight gain

107
Q

What causes PCOS?

A

The LH and FSH secretion is out of balance and there is no negative feedback. Increased LH leads to increased androgen production

108
Q

What is the management of PCOS?

A
  • weight loss - loss of 5% of body weight can cause significant improvement of the condition
  • Contraceptive pill - can induce regular periods
  • metformin - can lower insulin levels
  • fertility treatment (if needed)
109
Q

What is the female reproductive tract made up of?

A
  • Paired gonads - Ovaries

- duct system - uterine tubes, uterus, vagina

110
Q

What is the function of the ovaries?

A

Produces gametes and hormones

111
Q

What is the blood supply to the ovaries?

A

Ovarian artery - arises from the aorta at level of the renal artery

112
Q

What is the venous drainage of the ovaries?

A

Ovarian vein - drains to IVC on right and to the left renal vein on the left

113
Q

What ligaments support the ovaries?

A
  • Broad ligament
  • Ovarian ligament
  • Suspensory ligament of the ovary
114
Q

What is the broad ligament?

A

A peritoneal sheet draped over the uterus and uterine tubes.
The ovaries attach to the posterior layer by short mesentery ‘the mesovarium’

115
Q

What is the ovarian ligament?

A

A fibrous cord that links the ovary to the uterus

116
Q

What is the suspensory ligament of the ovary?

A

Connects the lateral wall of the pelvis to the ovary and carries the ovarian artery and vein

117
Q

Where are the fallopian tubes found?

A

In the free margin of the broad ligament.

They are not connected directly to the ovary

118
Q

How does the egg get from the ovary to the tube?

A

the egg is released and is sucked into the tube by the fimbriae

119
Q

What are the parts of the fallopian tube?

A
  • infundibulum
  • ampulla
  • isthmus
  • interstitial/uterine section
120
Q

What is the infundibulum of the fallopian tube?

A

A funnel shaped opening to the peritoneal cavity, fringed by finger like fimbriae

121
Q

What is the ampulla of the fallopian tube?

A

The middle section where fertilisation occurs

122
Q

What is the isthmus of the fallopian tube?

A

A short narrowed section that is connected to the uterine wall

123
Q

What are the parts of the uterus?

A
  • Body
  • Cervix
  • Fundus
  • Isthmus
124
Q

What is the fundus of the uterus?

A

The rounded part that projects up above the level of the uterine tubes

125
Q

What is the isthmus of the uterus?

A

The narrowing between the body and cervix

126
Q

What separates the parts of the cervix?

A

Internal and external os

127
Q

What are the parts of the cervix?

A

Endocervical canal and ectocervix

128
Q

What is a bicornuate uterus?

A

Failure of fusion of the uterus when it is forming. People with this condition can get pregnant and have a healthy pregnancy but it can be harder.

129
Q

What is the term to describe the position where the body of the uterus is bent forwards on the cervix?

A

Anteflexion

130
Q

What is the term to describe the position of the uterus bent forward at a right angle to the vagina?

A

Anteversion

131
Q

What is the normal position of the uterus in relation to other organs?

A

Anteverted, anteflexed

132
Q

What is it known as if the uterus is in the opposite position to normal?

A

retroflexion and retroversion

133
Q

What is the blood supply to the uterus?

A

Uterine artery - branch of the internal iliac artery

134
Q

What is the venous drainage of the uterus?

A

Uterine vein - drains to the internal iliac vein

135
Q

What is the male reproductive tract made up of?

A
  • paired gonads - testes
  • Duct system - closely associated with the urinary system
  • accessory glands - prostate, seminal vesicles, bulbourethral glands
136
Q

What makes up the wall of the scrotum?

A 
Skin
Dartos muscle
External spermatic fascia
Cremasteric fascia
Internal spermatic fascia
Tunica vaginalis
137
Q

What is the function of the dartos muscle?

A

It is smooth muscle that gives the scrotum its crinkle

138
Q

What is the function of the cremaster muscle?

A

skeletal muscle that contracts to raise the testis in cold weather (cremasteric reflex)

139
Q

What is the tunica vaginalis?

A

A closed sac of peritoneum that has visceral and parietal layers that cover the testes

140
Q

What is in between the two layers of the tunica vaginalis?

A

A film of peritoneal fluid

141
Q

What is the duct system of the testes made up of?

A

Seminiferous tubule –> straight tubule –> rete testis –> efferent ductules –> epididymis –> ductus deferens

142
Q

What is the epididymis?

A

A very coiled tube that is coiled so tightly you can see it clearly.
It has a head body and tail

143
Q

What epithelium lines the epididymis?

A

Pseudostratified columnar epithelium with stereocilia

144
Q

What is the function of the stereocilia in the epididymis?

A

They increase the area for fluid absorption and can monitor and adjust the fluid composition

145
Q

What is the blood supply to the testes?

A

Testicular artery

146
Q

What is the venous drainage of the testes?

A

Pampiniform plexus –> testicular vein –> IVC (on right) Renal vein (on left)

147
Q

What is the structure of the ductus deferens?

A

Thick walled with smooth muscle in the wall which contracts by peristalsis at emission.
It is 45cm long

148
Q

Where does the ductus deferens run?

A

The spermatic cord through the inguinal canal

149
Q

What are the seminal vesicles?

A

Coiled tubes that secrete an alkaline viscous fluid which helps them to neutralise the acid in the female tract

150
Q

What does the fluid in the seminal vesicle contain?

A
  • fructose - used for ATP production by sperm

- Prostaglandins which aid sperm motility and may also stimulate muscle contraction in the female tract

151
Q

Where is the prostate gland found?

A

Surrounds the beginning of the urethra

152
Q

What is the function of the prostate gland?

A

secretes a slightly acidic fluid containing citrate (used by sperm for ATP production), acid phosphatase and proteolytic enzymes which liquefy coagulated semen

153
Q

What are the bulbourethral glands?

A

Pea sized glands that produce a mucus like secretion

154
Q

What does the trophoblast become?

A

Extraembryonic membranes

155
Q

What two layers does the trophoblast differentiate into?

A
  • The proliferating inner villous cytotrophoblast (vCTB)

- The non-dividing outer multinucleate layer called the syncytiotrophoblast

156
Q

When do the lacunae develop?

A

By day 8 post conception

157
Q

What are lacunae?

A

Fluid filled spaces

158
Q

What happens when they cytotrophoblast cells migrate?

A

The form villous projections that extend towards the maternal basal plate

159
Q

When do tertiary villi form?

A

By the third week of gestation

160
Q

What do the tertiary villi consist of?

A

An outer monolayer of syncytiotrophoblast, invaded by an inner layer of cytotrophoblast cells and vascularised with foetal capillaries

161
Q

What is the chorionic plate?

A

The foetal side of the placenta

162
Q

What is the basal plate?

A

The maternal side of the placenta

163
Q

What is decidua?

A

A shiny surface on the basal plate that is the endometrium during pregnancy

164
Q

What is pregnancy induced hypertension?

A

Hypertension that generally occurs in the 2nd half of pregnancy in the absence of proteinuria

165
Q

What is pre-eclampsia?

A

Hypertension occurring typically after 20 weeks with associated oedema and proteinuria

166
Q

How common is pre-eclampsia?

A

It effects up to 6% of UK pregnancies

167
Q

What happens if pre-eclampsia develops further?

A

It can turn into eclampsia

168
Q

What is eclampsia?

A

Fits or convulsions associated with the features of pre-eclampsia if severe can lead to maternal and/or foetal death

169
Q

How common is eclampsia?

A

Occurs in 1-2% of pregnancies

170
Q

What is pre-term birth?

A

Delivery at <37 weeks of gestation

171
Q

What is are the different levels of pre-term birth?

A

Extreme preterm = <28 weeks

Very preterm = 28-32 weeks moderate to late preterm = 32-37 weeks

172
Q

What percentage of pregnancies are preterm?

A

7-8% of pregnancies

173
Q

What is foetal growth restriction (FGR)?

A

The failure of the foetus to reach its ‘genetically predetermined growth potential’

174
Q

What is the outcome of foetal growth restriction?

A

Results in birthweight below 5th centile of individualised birthweight ratio (IBR) charts

175
Q

What may be associated with foetal growth restriction?

A
  • abnormal umbilical artery blood flow on doppler ultrasound and/or oligohydramnios
  • Pre-eclampsia and other complications of pregnancy
176
Q

What is foetal growth restriction a risk factor for?

A
  • still birth

Survivors are also at increased risk of neonatal and adulthood diseases

177
Q

What is the definition of pre-eclampsia?

A

new onset hypertension (systolic >140 or diastolic >90 mmHg) occurring after 20 weeks’ gestation with new proteinuria (protein: creatinine ratio >30mg/mmol)

178
Q

How is pre-eclampsia treated?

A

There is not a cure but there are aspects of the condition that can be treated

179
Q

What are factors thought to have a role in pre-eclampsia?

A
  • Genes
  • The placenta
  • The immune response
  • Maternal vascular disease
180
Q

What does Iatrogenic mean?

A

illness caused by medical treatment or examination

181
Q

Why is Pre-eclampsia a major cause of pre-term birth?

A

Delivering the baby and the placenta is the only ‘cure’ for pre-eclampsia

182
Q

What are the symptoms of pre-eclampsia?

A
  • Hypertension
  • proteinuria
  • Oedema - hands feet face
    Severe pre-eclampsia:
  • Headaches
  • blurred/flashing vision
  • Pain in upper right abdomen
  • Nausea/vomiting
  • Heartburn (that doesn’t go away with antacids)
  • rapid oedema
183
Q

What are risk factors for pre-eclampsia?

A
  • First pregnancy (/first with new partner/ first in 10 years) - immunological hypothesis for pre-eclampsia
  • a relative has already had pre-eclampsia
  • high maternal age (>40)
  • High maternal BMI/ weight (BMI >35 or weight >90kg)
  • Multiple pregnancy
  • Existing hypertension
  • some evidence suggests that women who are pregnant from egg donation are more susceptible
184
Q

What are the three step hypotheses for pre-eclampsia?

A
  1. Abnormal placentation
  2. abnormal maternal response to placental trigger
  3. Organ / systems failure
185
Q

What is abnormal about placentation in pre-eclampsia?

A

Normally extra villous trophoblast cells invade into the maternal endometrium, myometrium then spiral arteries
Remodel the coiled vessels: from low flow, high resistance to become wider, high flow, low resistance channels

In pre-eclampsia this doesn’t happen

186
Q

What is ART?

A

Assisted reproductive technology

187
Q

What is the abnormal maternal response that occurs in pre-eclampsia?

A
  • maternal response to placental dysfunction
  • Hypoxia and/or ischaemia-reperfusion injury causes increased free radicals and inflammatory mediators = syncytiotrophoblast cellular stress
  • excess release of placental factors (soluble fms-like tyrosine kinase 1 (sFlt-1) and soluble endoglin (sENG) which sequester circulating vascular endothelial growth factor (VEGF) and placental growth factor (PlGF)
  • Maternal circulation = inflammatory response and endothelial dysfunction – lipid, insulin resistance, coagulation
188
Q

What is the endothelial dysfunction in pre-eclampsia?

A
  • Excessive maternal systemic inflammatory response to pregnancy has been suggested to be responsible for endothelial dysfunction leading to cellular activation and/or damage
  • endothelial dysfunction is considered to be central in the pathogenesis of pre-eclampsia
189
Q

Why is it suggested that pre-eclampsia could be more than one disease?

A
  • early onset vs late
  • rapid onset vs slow
  • with and without growth restriction
190
Q

What are the treatment options for pre-eclampsia?

A
  • Offer labetalol to treat hypertension in pregnant women with PE
  • Offer nifedipine for women in whom labetalol is not suitable, and methyldopa if labetalol or nifedipine are not suitable.
  • Base the choice on any pre-existing treatment, side-effect profiles, risks (including foetal effects) and the woman’s preference.
191
Q

What foetal monitoring should be carried out in women with pre-eclampsia?

A

repeat ultrasound for foetal growth and amniotic fluid volume assessment or umbilical artery Doppler velocimetry every 2 weeks, with subsequent surveillance and monitoring determined by the findings of these scans

192
Q

What are some concerns in mothers with pre-eclampsia that could cause admission to hospital?

A

• sustained systolic blood pressure of 160 mmHg or higher
• any maternal biochemical or haematological investigations that cause concern, for example a new and persistent:
o rise in creatinine (90 micromol/litre or more, 1 mg/100 ml or more) or
o rise in alanine transaminase (over 70 IU/litre, or twice upper limit of normal range) or
o fall in platelet count (under 150,000 cells/microlitre)
• signs of impending eclampsia
• signs of impending pulmonary oedema
• other signs of severe pre-eclampsia
• suspected foetal compromise
• any other clinical signs that cause concern

193
Q

What could cause an early birth to be considered in PE cases?

A
  • inability to control maternal BP despite using 3 or more classes of antihypertensives in appropriate doses
  • maternal pulse oximetry less than 90%
  • progressive deterioration in liver function, renal function, haemolysis, or platelet count
  • ongoing neurological features, such as severe intractable headache, repeated visual scotomata, or eclampsia
  • placental abruption
  • reversed end-diastolic flow in the umbilical artery doppler velocimetry, a non-reassuring cardiotocograph, or stillbirth

MBChB - year 2 (25 decks)

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