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ESA 4 > Repro 8 > Flashcards

Repro 8 Flashcards

1
Q

importance of anti-insulin hormones during pregnancy e.g. oestrogens, progesterone, placental lactogen?

A

Make muscles resistant to insulin as muscle would use glucose straight away for ATP production which would reduce the concentration gradient of glucose, and we want glucose to go to AT wheres stored as fat

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2
Q

how are nutrients transferred across placenta to foetus?

A

by diffusion- so rate of transfer dependent on nutrient conc in maternal circulation

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3
Q

Metabolic and hormonal response in 1st half of pregnancy?

A

anabolic state: preparatory increase in maternal nutrient stores ready for rapid growth of foetus, birth and subsequent lactation. Increase insulin:anti-insulin, so increased nutrient storage

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4
Q

Metabolic and hormonal response in 2nd half of pregnancy?

A

marked increase in growth of placenta and foetus. Demands of foetal-placental unit met by reducing maternal utilisation of glucose by switching tissues to FA, delaying maternal disposal of nutrients after meals and releasing FA from built stores after 1st half of pregnancy.

Maternal insulin continues to rise but anti-insulin also increases at an even faster rate, so ratio falls to produce required met. changes

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5
Q

Result of reduction in insulin:anti-insulin coupled with increased availability of FA from maternal AT?

A

KB production by maternal liver, which can be used as fuel by developing foetal brain.

*KB able to cross BB barrier

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6
Q

how does gestational diabetes result?

A

beta cells of endocrine pancreas unable to meet increased demand for insulin via hyperplasia and hypertrophy and increased rate if insulin synthesis, so lose control of met., with increase in blood glucose and subsequent diabetes.

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7
Q

possible consequence of gestational diabetes on baby?

A

macrosomia- fat baby with lots of liver and muscle glycogen, can make delivery difficult

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8
Q

what are the functional units of the placenta?

A

chorionic villi= point of exchange between maternal and foetal circulations

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9
Q

hCG is only released from the syncytiotrophoblast around 14 days after ovulation, what occurs with the corpus luteum before this time?

A

The corpus luteus is formed under LH stimulation and has a lifespan of 14 days until it spontaneously regresses unless hCG is produced by the placenta. Therefore, oestrogen and progesterone are secreted from the corpus luteum before hCG signals the necessity for the corpus luteum to remain to continue producing these hormones

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10
Q

aims of implantation?

A

establish basic unit of exchange= chorionic villi
anchor placenta via outermost trophoblast shell
establish maternal bflow within the placenta

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11
Q

function of decidual reaction?

A

provide balancing force for invasive force of trophoblast

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12
Q

why can continuous invasion occur in an ectopic preganancy?

A

implantation outside of endometrium, so no decidual reaction to provide balancing force for invasive force of trophoblast

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13
Q

2 components of placenta?

A

chorion frondosum

decidua basalis

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14
Q

importance of decidual cells?

A

manage depth of invasion, and facilitate spiral artery remodelling

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15
Q

2 mechanisms for efficient exchange across term placenta?

A

large SA provided by continued branching of villi

cytotrophoblast layer lost beneath syncytiotrophoblast

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16
Q

4 components of 1st trimester placental membrane?

A

endothelium of fetal blood vessels
CT core of villus
cytotrophoblast layer
syncytiotrophoblast

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17
Q

why is hCG used as the basis of pregnancy testing?

A

pregnancy specific as secreted by syncytiotrophoblast during 1st 2mnths of pregnancy
and excreted in maternal urine so can be measured from 2 wks following fertilisation (in serum from 7 days)

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18
Q

what factors influence the passive diffusion of substances across the placenta?

A
  • Concentration Gradient-The steeper the gradient, the more diffusion, and this is maintained by constancy of flow
  • Barrier/resistance to diffusion-placental membrane gradually thins throughout pregnancy as the demand of the fetus increases, so cytotrophoblast diasappears beneath syncytium, reducing diffusion distance- haemomonochorial
  • SA available- markedly increased by branching of villi, and microvilli on maternal surface of syncytiotrophoblast
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19
Q

function of placenta in metabolism?

A

synthesises glycogen- for itself and use before utero-placental circulation established
cholesterol- for steroid hormone synthesis- oestrogen and progesterone
FA

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20
Q

endocrine function of placenta?

A

proteins: hCG, hCsomatomammotrophin, human chorionic thyrotrophin, human chorionic corticotrophin
steroid: progesterone and oestrogen

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21
Q

when does placenta take over from corpus luteum to maintain pregnant state by steroid hormone prod.?

A

by the 11th wk (end of 1st trimester)

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22
Q

how does progesterone influence maternal met.?

A

increases appetitie

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23
Q

how do hCS and human placental lactogen influence maternal met.?

A

increase glucose availability to fetus

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24
Q

which molecules move by simple diffusion across the placenta?

A

water
electrolytes
urea and uric acid
gases

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25
Q

which molecule moves by facilitated diffusion across placenta?

A

glucose

adequate conc gradient must be maintained

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26
Q

what is actively transported across the placenta?

A

iron
aa
vitamins, via specific transporters expressed by syncytiotrophoblast

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27
Q

what substances are transported across the placenta via receptor-mediated endocytosis?-clathrin coated pits, endosome, lysosome etc.

A

IgG

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28
Q

Ig found in breast milk?

A

IgA

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29
Q

what limits the diffusion of gases across the placenta?

A

FLOW not diffusion
fetal O2 stores small so must maintain adequate flow- low resistance, high flow utero-placental circulation via modification of spiral arteries
circulation can be compromised with large uterine contractions in labour

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30
Q

drugs capable of crossing the placenta?

A 
thalidomide
alcohol
therapeutic drugs- warfarin, anti-convulsants, all teratogenic
drugs of abuse
maternal smoking- lowers birth weights
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31
Q

infectious agents able to cross placenta?

A 
varicella-zoster
cytomegalovirus
tremponema pallidum-syphilis
toxoplasma gondii
rubella- maternal rubella syndrome- RNA enveloped virus, most common cause of PDA if mother infectied during 1st trimester, DA closed with NSAIDs- inhibt PG prod and PG cause vasodilation that would keep DA patent
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32
Q

why does haemolytic disease of the newborn occur?

A

rhesus incompatibility of mother and fetus, if rhesus -ve mother and rhesus +ve fetus. If mother has been sensitised to rhesus antigen e.g. in previous pregnancy, her body’s immune system can mount a response to the antigen by producing antibodies, which can cross the placenta to bind to rhesus antigen on surface of rbc, mediating their destruction, producing a haemolytic anaemia.
However, rare now as prophylactic tment given e.g. Rhesus –‘ve mothers pregnant with Rhesus +’ve fetus given Rhesus specific IgG throughout pregnancy, to prevent sensitisation in the event of exposure to the antigen (The given IgG will bind to antigen before the mother’s immune system can mount a response), can also be given anti-D therapy after birth of baby to mother to prevent rhesus disease in further children*

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33
Q

how does the syncytiotrophoblast invade the endometrium to allow implantation to have begun by day 6?

A

it secretes enzymes similar to those secreted by metastatic tumours to allow the interstitial process of implantation

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34
Q

In pregnancy, the conceptus has embedded within the endometrium before the date of the next expected menses, true or false?

A

True
by day 9, the conceptus has implanted and so this is less than 2 wks following fertilisation, and hence before the next expected menses which occurs 2 wks after ovulation due to the lifespan of the corpus luteum

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35
Q

which membrane ruptures at the onset of labour?

A

composite amniochorion membrane, causing amniotic fluid leakage, as amniotic sac enlarges with growth and development of fetus, coming to lie in close contact with the chorionic sac

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36
Q

how does the placenta provide passive maternal immunity to the neonate in pregnancy?

A

allows transport of IgG by receptor-mediated endocytosis from the maternal circulation to the fetal circulation. This begins at approximately 14 weeks and eventually the concentration of IgG in fetal plasma exceeds that of maternal plasma.

In this manner the fetus gains passive immunity against various infectious diseases. Newborns produce their own IgG, but adult levels are not attained until the age of 3- from 3, susceptibility to meningitis caused by N.meningitidis.

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37
Q

negatives on mother of hCG reducing maternal IgG, IgA and IgM?

A

more susceptible to infection

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38
Q

why might action of hCG to reduce maternal Igs in pregnancy be beneficial to fetal-placental unit?

A

stop rejection of placenta by mother and vice-versa

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39
Q

components of antenatal screening?

A

history and exam: RFs e.g. for gestational diabetes- age, weight, high BP, FH
blood test- blood group, Hb- already anaemic?, infection e.g. HIV, syphillis, chlamydia- can be transmitted to fetus at delivery
urinalysis- proteinuria- indicative of renal failure, may be result of pre-eclampsia as vasoconstricition cause poor perfusion to kidneys

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40
Q

why does blood volume increase in pregnancy?

A

coping with a new circulation- utero-placental circulation must be supplied in order to supply blood, and hence nutrients and O2 to the fetus
must increase b.flow to kidneys
anticipatory increase for blood lost during fetal delivery

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41
Q

normal auscultatory changes noted in pregnancy?

A

mild tricuspid regurgitation- systolic murmur- S1

shifted apex beat due to shifted diaphragm

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42
Q

effects of increased blood volume on HR, SV and CO in pregnancy?

A

ALL INCREASE
increased blood volume- most blood in veins, so increased venous return to heart, so increased CVP hence SV under Starling’s Law as myocardial fibres stretched more, increasing force of contraction, which increases SV and CO, and HR must increase to prevent volume overload on heart?
hypotension due to progesterone effects, SNS activation to increase HR?*

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43
Q

why does reduced cardiac output occur in pregnancy if mother supine?

A

uterus compresses IVC, reducing venous return to heart, so less blood pumped out, reducing CO

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44
Q

why is the syncytiotrophoblast good at transport?

A

it is a huge multi-nucleated sheet, which minimises the total number of intracellular barriers.
the cells are directly bathed in maternal blood in the mature placenta when the underlying cytotrophoblast disappears

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45
Q

increased Hb needed in vol expansion, how does this occur?

A

increased Fe absorption

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46
Q

what mediates blood vol. increase in pregnancy?

A

RAAS
placental oestrogen increases angiotensinogen prod by liver, and renin prod increased by oestrogen and progesterone. Aldosterone stim release from zona glomerulosa, causing Na+ and H20 retention
thirst also increased

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47
Q

why is hypotension seen in 1st 2 trimesters of pregnancy?

A

progesterone effect on smooth muscle, causing relaxation hence vasodilation, decreasing TPR and hence BP
also loss of peripheral responsiveness to AngII accompanying increase in blood vol

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48
Q

substance responsible for decrease sytemic vascular resistance in pregnancy?

A

progesterone- high levels from early on in pregnancy

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49
Q

effect of pregnancy on pre-load?

A

increased as increased blood volume through Na+ and H20 retention
also, sustained CO increases stimulate ventricular hypertrophy so heart can accomodate larger end-diastolic volumes (preload), and ventricular wall thickens to increase contractility, which increases SV

50
Q

why might a woman in pregnancy experience syncope on standing?

A

postural hypotension due to effect of progesterone decreasing systemic vascular resistance

51
Q

effect of pregnancy on after-load?

A

decreased as reduced TPR over 1st 2 trimesters, increase in 3rd as BP increases back to normal with increase in TPR

52
Q

why may a woman be hypotensive in 3rd trimester of pregnancy?

A

aortocaval compression by gravid uterus, venous return reduced, so reduced CO and arterial BP

53
Q

how can BP be increased in a pregnant woman who lies in the supine position?

A

ask her to lay on her side- left lateral position

54
Q

maternal circulatory state in pre-eclampsia?

A

vasoconstricted

plasma-contracted

55
Q

why is creatinine clearance increased in pregnancy?

A

increased GFR

56
Q

why are serum creatinine and urea lower in pregnancy?

A

increased GFR, so more excreted

57
Q

why might glucose in the urine be normal for a preganant woman and not indicative of diabetes?

A

increased GFR in combination with relatively fixed reabsorptive capacity of PCT as always reabsorbs the same proportions

58
Q

why are pregnant women more at risk of acute kidney infections?

A

smooth muscle relaxation in ureter due to progesterone causes dilation that reduces speed of urine flow, and dilation also due to mechanical obstruction by pregnant uterus

59
Q

what may be responsible for increase in GFR in pregnancy?

A

smooth muscle relaxation in pre and post glomerular resistance vessels due to progesterone

60
Q

why is it important to know normal for pregnancy ranges of urea and creatinine?

A

in pregnancy, the ranges are lower than normal, and so a value that may look normal, as it is in the normal reference range, may in fact be too high for in pregnancy, and so may be indicative of renal damage

61
Q

why does renal plasma flow increase in pregnancy?

A

increased blood volume with vasodilation

62
Q

As GFR increases in pregnancy, what happens to the functional renal reserve?

A

it decreases

63
Q

2 causes of urinary stasis in pregnancy?

A

progesterone effect on ureter

obstruction by gravid uterus

64
Q

problem of pyelonephritis in pregnancy?

A

increases risk of pre-term labour, which increases risk of mortality

65
Q

tment of pyelonephritis?

A

14 day course of gentamicin or co-amoxiclav or ciprofloxacin

66
Q

why is overall pCO2 decreased in pregnancy?

A

physiological hyperventilation. increased met CO2 prod as produced by fetus, then exchanged across placenta into maternal circulation. Progesterone acts to increase resp drive. and physiological dyspnoea occurs due to progesterone-driven hyperventilation

67
Q

how is the mild resp alkalosis in pregnancy due to increased minute ventilatory volume compensated for?

A

increased renal HCO3- excretion

68
Q

why might a pregnant women be predisposed to a metabolic acidosis?

A

increased renal HCO3- excretion due to resp alkalosis from hyperventilation, means reduced buffering capacity * very important as ketoacidosis may occur with high FA availability and low insulin:anti-insulin, and hence this may not be able to be accomodated for by HCO3- buffering

69
Q

what may be responsible for increased minute ventilation rate in pregnancy?

A

progesterone action on respiratory centre in brain

70
Q

how is maternal peripheral insulin resistance increased in pregnancy?

A

by hormones from placenta e.g. hPL, prolactin, oestrogen and progesterone. Mother therefore switches to gluconeogenesis and altern fuels so that any glucose can go to fetus

71
Q

what causes decreased and increases blood glucose in pregnancy?

A

increased after meals as not uptaken by maternal tissues

decrease in fasting blood glucose as glucose goes to fetus

72
Q

RFs for gestational diabetes?

A

Being overweight prior to becoming pregnant
high risk ethnic group (Hispanic, Black, Native American, or Asian)
Having sugar in your urine
Impaired glucose tolerance or impaired fasting glucose (blood sugar levels are high, but not high enough to be diabetes)
Family history of diabetes
Previously giving birth to a baby over 9 pounds
Previously giving birth to a stillborn baby
Having gestational diabetes with a previous pregnancy
Polyhydramnios

73
Q

risks assoc with poor control of gestational diabetes?

A

macrosomic fetus
stillbirth
increased risk of congenital defects

74
Q

define gestational diabetes

A

carbohydrate intolerance first recognised in pregnancy and not persisting after delivery

75
Q

what is required if suspected gestational diabetes?

A

oral glucose tolerance test

76
Q

how are fat stores increased in 1st trimester of pregnancy?

A

progesterone increases appetite so fat stores increased, then increase in lipolysis from T2 and increase in plasma FA on fasting, which provide substrate for mat met. so glucose left for fetus

77
Q

why are T3 and T4 increased in pregnancy, but free T4 is in the normal range?

A

elevated oestrogen stimulates liver to produce increased amounts of thyroid binding globulin
hCG directly affects thyroid, stim T3 and T4 prod., so TSH can be decreased in normal pregnancies

78
Q

anatomical changes to respiratory system in pregnancy?

A

diaphragm displaced, A-P and transverse diameters of thorax increase

79
Q

as uterus enlarges, appendix moves to RUQ, what is the clinical significance of this?

A

when examining patient, appendicitis pain may not be localised to RIF

80
Q

why is there an increased risk of pancreatitis in pregnancy?

A

increased risk of gallstones, possibly due to changes in bile salt compositions
hyperlipidaemia of pregnancy with maternal met switched to FA to give glucose to fetus

81
Q

physiological component of GI changes in pregnancy?

A

progesterone induced smooth muscle relaxation: delayed emptying, biliary tract stasis, increased risk of pancreatitis

82
Q

why increased risk of thromboembolic disease in pregnancy?

A

pro-thrombotic state with increased fibrinogen, clotting factors, lots of fibrin depos at implantation site, and reduced fibrinolysis
also stasis and venodilation

83
Q

advantage of pro-thrombotic state in pregnancy?

A

prepare for haemorrhage at birth

84
Q

problem of treating thromboembolic state of pregnancy?

A

warfarin is a teratogen that crosses the placenta

85
Q

why physiological anaemia of pregnancy?

A

blood volume increases, and red cell mass does not increase by as much
anaemia may also be due to folate of Fe deficiency in pregnancy, important as fetal demands for Fe
may also be hamoglobinopathies

86
Q

villi are primary site of exchange beteween maternal and fetal circulations, what type of blood vessels do they contain?

A

fetalplacental capillaries
the 2 umbilical arteries take blood to these capillaries, and the umbilical vein takes oxygenated blood away from them,towards the fetal circulation

87
Q

problem with remodelling of maternal resistance vessels?

A

limit uterine vascular control system’s ability to regulate b.flow so flow direct function of uterine arterial pressure

88
Q

advantages of physiologic anaemia of pregnancy?

A

reduce shear stress on blood vessels that would occur from high velocity flow, as haematocrit=main determinant of viscosity causing shear stress, so reduce risk of vascular endothelial damage

89
Q

causes of oedema in pregnancy?

A

uterus compresses IVC and smaller veins returning blood from lower extremities, so venous pressure increases in lower extremities, increasing capillary pressure and so net fluid filtration from blood to intersitium. Also fall in colloid osmotic pressure with lower plasma protein concentrations

90
Q

Function of GFR increase in pregnancy?

A

excretion of fetal waste e.g. urea and nonvolatile acid

91
Q

what could be used to treat pro-thrombotic state of pregnancy?

A

heparin

92
Q

what effect does maternal smoking have on the placenta and how does this affect the baby?

A

reduction in placental blood flow and growth, so poorer fetal nutrition, causing a lower than average birth weight, reduction on average is by 200g

93
Q

how does alcohol cross placenta?

A

diffusion as lipid soluble

94
Q

why is ability of alcohol to cross placenta of clinical significance?

A

in a mother who drinks a lot of alcohol in pregnancy, there may be the occurrence of fetal alcohol syndrome where a fetus of low birth weight and growth abnormalities is produced, possibly with mental retardation and head and facial abnormalities

95
Q

what test can be used to see if fetal cells are present in the maternal circulation?

A

The Kleihauer test is used to demonstrate the presence or absence of fetal cells in the mother’s circulation (which is especially important in Rh
isoimmunization). If the foetal cells contain antigens which the mother’s cells lack then the
mother could raise antibodies against these antigens

96
Q

symptoms mother may complain of in pregnancy due to progesterone effect on GI tract function?

A

constipation

heartburn

97
Q

why might earlier delivery be desirable if low levels of oestriol in the fetus are measured?

A

may indicate fetal distress as oestriol production dependent on fetal adrenal and liver metabolism, as well as placental function

98
Q

degree of cardiac output change in pregnancy?

A

increase by 40%

99
Q

degree of SV change in pregnancy?

A

increase by 35%

100
Q

degree of HR change in pregnancy?

A

increase by 15%

101
Q

degree of SVR in pregnancy?

A

decrease, 25-30%

102
Q

degree of RPF change in pregnancy?

A

increase by 60-80%

103
Q

degree of GFR change in pregnancy?

A

increase by 55%

104
Q

degree of creatinine clearance change in pregnancy?

A

increase by 40-50%

105
Q

degree of protein excretion change in pregnancy?

A

increase by up to 300mg/24hrs

106
Q

degree of urea change in pregnancy?

A

50% decrease

107
Q

degree of uric acid change in pregnancy?

A

decrease by 33%, but rises with gestation

108
Q

HCO3- reference range in pregnancy?

A

18-22mmol/L

109
Q

creatinine reference range in pregnancy?

A

25-75 micromol/L

110
Q

degree of O2 consumtpion change in pregnancy?

A

increase by 20%

111
Q

degree of resting minute ventilation change in pregnancy?

A

increase by 15%

112
Q

symptoms of peripheral vasodilation?

A

feeling the heat
easy to sweat
nasal congestion

113
Q

possible effects of ureter compression above pelvic brim due to gravid uterus?

A

hydronephrosis
hydro-ureter
increased intra-ureteral tone
ureter dilation

114
Q

importance of placenta contributing to maternal synthesis of calcitriol?

A

helps fetal growth as calcitriol stimulates increased Ca2+ absorption from the gut so there is increased availability to the fetus to facilitate skeletal formation and growth

115
Q

what is supine hypotensive syndrome referring to?

A

low BP of a mother when laying in the supine position during late pregnancy as gravid uterus compresses the IVC, reducing venous return to the heart, so lowering CO and aBP

116
Q

why is uncontrolled gestational diabetes very dangerous to fetus once born?

A

once isolated from maternal supply of glucose, neonate may expereince a reflex hypoglycaemia due to high circulating levels of insulin, and brain part at risk as it doesn’t have glycogen storage

117
Q

How is O2 flow to fetus affected by maternal smoking

A

Carbon monoxide in maternal blood shifts her Hb-O2 curve to the left, so maternal Hb has higher affinity for O2, giving it up less readily, so the
fetus suffers a reduced pO2 in extracting its O2 requirement, which may not be fulfilled

118
Q

what might indicate a mild pre-eclampsia is worsening

A 
pulmonary oedema
visual defects
headache
oliguria
oligohydramnios
lack of fetal growth
elevated liver enzymes
increasing diastolic BP
thrombocytopenia
persistent and worsening albuminuria
119
Q

how to manage a patient who has an eclamptic fit?

A

Initially must maintain maternal airway, administer oxygen, place her on left side (enhance uterine perfusion) and maintain her safety during the convulsion.
Magnesium is given by intravenous bolus then continuous infusion to relieve vasospasm and
stop the fitting. Sometimes thiopentone or diazepam are needed for recurrent fits. Blood
pressure control usually requires hydralazine. Once stable assess fetus and maintain
optimum fluid/oxygen/positioning. Delivery is the definitive treatment for eclampsia.
Caesarean delivery will often be required unless the cervix is extremely favourable.

120
Q

complications assoc with multiple pregnancies?

A 
Increased incidence of pregnancy induced hypertension 
anaemia 
polyhydramnios 
preterm labour 
perinatal mortality 
antepartum haemorrhage.
121
Q

what might hyperreflexia suggest in a pre-eclamptic patient?

A

worsening of pre-eclampsia, as worsening of vasospasm on CNS function, so increased risk of eclampsia- seizure in pregnancy

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