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s4 - Repro, Develop, Ageing, Pharm > REPRO - Pregnancy > Flashcards

REPRO - Pregnancy Flashcards

1
Q

What are the 2 main factors responsible for maternal changes in pregnancy?

A
  • high levels of steroids

- mechanical displacement and foetal demands

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2
Q

What are decidual cells filled with. They cover the uterus surface pre-decidualisation..what do the cells become if pregnancy ensues?

A

They are filled with lipids and glycogen and become the maternal part of the placenta

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3
Q

Lysing of which layer is necessary for the trophoblast and decidua to contact and fuse into synctiotrophoblast?

A

Zona pellucida

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4
Q

Name an autocrine GF for the blastocyst secreted by the synctiotrophoblast from week 4. Function?

A

Human chorionic gonadotropin

Rescues CL so endometrium not shed and CL makes more steroids

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5
Q

Human Placental Lactogen (hPL) has anti-insulin effect mimicking which hormone

A

GH

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6
Q

Progesterone causes SM relaxation and breast development. What do oestrogens cause in pregnancy?

A
  • uterine hyper trophy
  • insulin resistance
  • more clotting factors
  • breast development
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7
Q

Why does energy output increase in pregnancy?

A
  • more respiration effort and CO

- need to store energy for foetus, labour and postnatally

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8
Q

What changes to BMR occur in pregnancy, mid gestation vs late gestation?

A
  • increases by 350kcal/day in mid gestation

- by 250kcal/day in late gestation

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9
Q

1st trimester fasting serum glucose is low, as pancreatic cells increase in number so circulating insulin is high, maternal reserves are made. What happens in 2nd trimester?

A
  • placental lactogen (hPL) causes insulin resistance so less glucose in stores, more in serum so more crosses placenta
  • foetal reserves
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10
Q

About 8.5l water are gained in pregnancy, plasma volume increases 40%. Name 3 reasons/mechanisms this occurs?

A
  • E2&progesterone act like mineralocorticoids on the RAAS system so more Na+ retained
  • placental Renin is released
  • E2 upregulates angiotensinogen synthesis in liver so more Ang II and RAAS
  • lower thirst threshold so drink more
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11
Q

What 3 maternal changes occur to respiration in pregnancy?

A
  • more sensitive to hypercapnia so breathe deeper
  • minute volume decreases by 40%
  • high arterial O2, low PCO2 to facilitate gas transfer
  • thoracic anatomy changes, ribs displaces up
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12
Q

Maternal blood red cell mass increases by 18% in pregnancy but plasma vol has increased by 40%..what is this called?

A 
Physiological haemodilution (not anaemia)
NB: maternal gut is more efficient at absorbing iron
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13
Q

What change in maternal blood for placental separation increases risk of DVT in pregnancy?

A

-more leukocytes, clotting factors and fibrinogen make the blood hypercoaguable

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14
Q

What is the risk with smoking in pregnancy?

A

-increases carboxy-HB in mothers blood so less oxygen can reach the foetus causing foetal hypoxia

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15
Q

HR increases by 8-10bpm and CO increases by about 40% in pregnancy, how does BP decrease in this time?

A

-peripheral vasodilation eg, E2 upregulates NO synthesis, which decreases TPR hugely

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16
Q

The low TPR in pregnancy allows more flow to uterus, placenta, muscles, kidney, skin..what change assists heat loss from skin?

A

Neoangiogensis

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17
Q

The lower TPR and SM relaxation mediated by progesterone has what effect on the GI tract?

A

Less motility which may cause constipation

Relaxed lower œsoph. Sphincter so acid reflux

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18
Q

How is acid reflux made worse by the large uterus combatted in pregnancy?

A

Small frequent meals

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19
Q

Folic acid does DNA production, growth, RBC production and more, from when to when should it be taken?

A

3 months before pregnancy

To week 12 of pregnancy

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20
Q

What effect does progesterone SM relaxation have on the urinary system?

A
  • tract relaxes so more stasis (UTI risk)
  • more flow through kidney glomerulus, more filtration so more frequent urination
  • more clearance of creatinine, urea and Uric acid
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21
Q

CRH released from placenta into mother and foetal circulation can initiate labour. Through what process does this occur?

A

CRH—>ACTH—> more DHEA which increases prostoglandin availability in uteroplacental tissues to activate BFlow and cervical contractions

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22
Q

Prolactin increases through pregnancy, and suckling causes a surge in it. What prevents milk production in pregnancy?

A

-Progesterone

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23
Q

How does prolactin decrease chance of pregnancy for 3-6months of breastfeeding?

A

-inhibitory action on ovaries post-partum

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24
Q

At how many weeks can the fundus of the uterus be palpated above the pubic symphysis?

A

Week 12

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25
Q

Name 2 changes in the cervix during pregnancy?

A
  • increased vascularity, becomes softer but still fibrous as high in collagen
  • glands proliferate, lots of mucus forms a mucosal plug protecting vs infection
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26
Q

What happens to the cervix during labour?

A

-in labour, prostoglandins cause collagen/CT breakdown so cervix becomes soft and for baby to pass

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27
Q

Foetus uses about 5g glucose/kg each day. How does this and amino acids reach the baby?

A

Across placenta via facilitated diffusion

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28
Q

What is the dominant hormone in the foetus in the 3rd trimester? How/why?

A

Insulin
as B cells of pancereas -> hyperplasia
so more insulin increases fat stores in baby

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29
Q

What is colostrum in the first 24hrs? What does it cause the baby to do?

A
  • 1st milk (7ml), is insufficient to meet baby’s energy needs
  • forces baby to access its own fat stores
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30
Q

At birth how is the brain different?

A
  • can use ketones

- cerebral metabolic rate (CMR) is low despite brain having the highest proportion of resting expenditure

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31
Q

In 3rd trimester, high insulin causes fat stores to build up. How does the baby access these stores when born? Hormones? Cortisol…GH….and

A
  • surge in Adrenaline during labour triggers catabolism

- as plasma glucose falls at birth, a glucagon surge occurs (opposing insulin)

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32
Q

What 2 processes do babys use a lot to utilise stores for energy?

A
  • Gluconeogenesis

- Ketogenesis (“suckling ketogenesis”)

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33
Q

What happens in B oxidation which occurs in the mitochondria of hepatocytes?

A

Glycerol and the 2 terminal carbons are removed from fats sequentially. Binds to Coenzyme A making lots of acetyl coA which is metabolised to ketone bodies.

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34
Q

Name 2 ketone bodies

A

Beta hydroxybuterate

Acetone

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35
Q

After a breast feed in the post prandial state, what happens in terms of hormones/storage?

A

-insulin allows storage in muscles and adipose
-in liver, excess glucose is converted to gycogen/fat
Active tissues e.g. brain take glucose direct from circulation

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36
Q

What are the rough components of breast milk?

A

50% fat

40% carbs (mostly lactose and some lipase)

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37
Q

What 4 problems may arise with baby’s metabolism of fuel?

A
  • if demand is > supply
  • hyperinsulinism
  • counter-reg. hormone deficiency
  • inborn errors in metabolism
38
Q

Name 3 issues v small preterm babies have with metabolism?

A
  • high metabolic demand but small stores
  • immature metabolism (enzyme pathways)
  • GI tract nor yet functionable so cant be fed
39
Q

v small preterm babies and minerals e.g. calcium, phosphate issue?

A

-struggle to get minerals due to constraints in giving them IV and poor conc in breast milk and poor fat absorption so end up with metabolic bone disease.

40
Q

IUGR is pathalogical what is the issue with metabolism balance?

A
  • high demand esp. brain but stores in liver, muscle and fat are low
  • immature gluconeogenic pathways
41
Q

Hyperinsulinaemia often occurs when a baby’s mother is diabetic. Baby is often macrosomic. Why are they often hypoglycaemic babies?

A
  • due to high exposure of maternal glucose it developed foetal hyperinsulinaemia and insulin is still high at birth
  • at birth sudden withdrawal of glucose
42
Q

What are 3 features of the overgrowth disorder “Beckwith Wiedemann”?

A
  • macroglossia,
  • midline abdo wall defects (e.g. exomphalmos, hernia)
  • ear creases/pits
  • hypoglycaemia
43
Q

Name one group of rare syndromes that cause hyperinsulinaemia?

A

-islet cell dysregulation syndromes e.g. nesiodioblastosis

44
Q

How may a CAH baby present? (CAH often is due to a 21OH deficiency so excess testosterone and lack of aldosterone)

A

-hypoglycaemia due to lack of cortisol as this is required for gluconeogenesis and to release glucose when fasting

45
Q

Name 3 inborn errors in metabolism that cause neonatal hypoglycaemia

A
  • Glycogen Storage Disease (type 1)
  • Galactosaemia
  • MCAD (medium chain acyl-coA dehydrogenase deficiency)
46
Q

A deficiency in which enzyme causes -Glycogen Storage Disease (type 1)? Presentation?

A
  • glucose 6 phosphatase deficiency. (it converts G6P to glucose)
  • hypoglycaemia during stress/fasting
  • newborn has lactic acidosis
  • older child will have hepatomegaly
47
Q

Which enzyme is missing in Galactosaemia? Its function?

A

Galactose-1-Phosphate Uridyl Transferase (Gal-1-Put)
In milk lactose is broken into glucose and galactose, then this enzyme breaks galactose to glucose.
Hence here toxic levels of Galactose-1-Phos. builds up

48
Q

name 5 features of how galactosaemia may present?

A
  • hypogycaemia
  • jaundice
  • liver disease
  • poor feeding
  • cataracts
  • e coli sepsis
49
Q

What is MCAD? medium chain acyl-coA dehydrogenase deficiency

A
  • a genetic disorder of mitochondrial fatty acid beta-oxidation. (Autosomal Recessive)
  • so fats in the body cant efficiently be broken down and used for energy.
50
Q

name 3 features of how MCAD may present?

A
  • Metabolic crisis due to hypoglycemia after fasting/stress..
  • Weakness, vomiting, and seizures.
  • Rarely, coma or sudden death
51
Q

Name 5 minor common symptoms experienced in pregnancy e.g. tiredness..N&V..

A
  • constipation
  • heartburn/reflux
  • mastalgia
  • piles
  • frequent urination
  • backpain, headache, heat intolerance
52
Q

How common are the following in the first trimester:

  • Misscarriage
  • Ectopic preg.
  • Hyperemesis Gravidarium (constant vomiting)
A
  • Misscarriage = 15%
  • Ectopic preg. = 0.5-2%
  • Hyperemesis Gravidarium = 2-5%
53
Q

Suggest 4 maternal complications in the 2nd and 3rd trimester that can arise:

A
  • UTI
  • Anaemia
  • Pre-eclampsia
  • Gest. Diabetes
  • Antepartum haemorrage
54
Q

Suggest 3 foetal complications in the 2nd and 3rd trimester that can arise?

A
  • Premature labour <37wks
  • IUGR (weight under 5th percentile/2500g)
  • Macrosomia (weight over 95th percentile/4500g)
55
Q

One poss explanation for more UTI is increased diagnosis via the frequent appointments and urine samples. What 2 things in pregnancy physiologically increases chance of UTI?

A
  • high progesterone –> SM v.dilation leading to urinary stasis so more infection
  • immune suppression in pregnancy to prevent rejection of fetus –> more infection
56
Q

Normal Hb 115-165g/L
Preg. Normal Hb 110-130g/L
(if less give what is deficient (Fe, B12, folate..)
Explain why normal Hb is less in pregnancy?

A
  • despite more RBCs the increased body water (4.5 to 6L) causes haemodilution
  • Max dilution occurs 28-30wks pregnant
57
Q

Hb <100g/L in pregnancy should be investigated. Its often due to a deficiency e.g. of Fe, B12, folate..easily corrected. What other condition could be the cause?

A

-sickle cell, thalassaemia, blood dyscrasias e.g. leukaemia

58
Q

If Hb<110g/L due to iron deficiency give ferrous sulfate, what if Hb<70g/L

A

Transfuse Hb/blood

59
Q

What is gestational diabetes? Risks associated?

A
  • After week 20 (not-pre-existing)
  • more perinatal morbidity and mortality
  • more maternal mobidity and mortality
60
Q

Suggest 3 groups of women who are at increased risk of developing gestational diabetes:

A
  • obese, -older
  • family history of DM/-previous gestational DM
  • PCOS
  • previous baby >4.5kg
61
Q

High risk gest. diabetes groups are screened at booking, all pregnancies are scanned at 28wks using what test?

A

OGTT

62
Q

What are the risks of pre-existing diabetes and pregancy? What should be done preventatively?

A
  • more risk of congenital malformation
  • hypergly. at conception can be toxic to fetus (sacral agenesis….)
  • need pre-pregnancy counselling 6months before to control sugar levels
63
Q

Maternal hyper Glycaemia –> Foetal hyper Gly across placenta
-> foetal glycosuria which causes what? risk?

A
  • Polyhydramnios

risks: malpresentation, cord prolapse, PPH (post partum haem.)

64
Q

Maternal hyper Glycaemia –> Foetal hyper Gly across placenta
-> foetal hyperinsulinaemia and B cell hyperplasia
which causes what 3 complications? risk?

A
  • Polycyntheamia (->jaundice)
  • Neonatal hypoglyceamia
  • Inhibition Surfactant (RDS)
  • Macrosomia (long labour, APH)
65
Q

How does hyperglycaemia lead to jaundice???

A
  • placenta function is impaired so baby is born a bit hypoxic
  • responds by making lots of RBCs (polycynth.)
  • upon birth, excessive RBC breakdown -> jaundice
66
Q

Management of a diabetic mother..aim is normoglycaemia..what/who is involved?

A
  • diet, metformin, insulin
  • obstetrician and diebetesologist
  • US to detect congenital abnormalities, growth and polyhydramnios
  • deliver at 38-40wks
67
Q

What is the definition of PET (pre eclampsia)

A

A significant rise in BP (+30/+20 or HT) after 20wks on TWO separate occasions at least 2hrs apart and significant PROTEINURIA

68
Q

In normal pregnancy how does BP decrease accommodating large placental flow despite 40% CO rise (more plasma vol).

A

BP=CO x TPR

TPR massively drops as progesterone causes vasodilation so overall BP drops

69
Q

What happens in PET physiologically?..TPR? Placenta?

A
  • vasodilation fails so TPR increases due to systematic vasocontriction/vasospasm
  • faliure of 2nd wave of trophoblastic invasion at week 15-16 (placental disorder)
70
Q

PET = yucky little vessel disease. What abnormalities in the vessels occur and may arise in microthrombosis?

A
  • increased cap. permeability, fluid moves to interstitial space
  • microangiopathy and endo. cell wall activation of platelets/coag. factors..can–> end organ infarction
71
Q

What 3 theories offer an explanation to the poorly understood PET aeitiology:
Immuno
Vaso
Deficiency

A
  • abnormal maternal immune reaction to trophoblast
  • v.spastic substances e.g. NO, TNF, free radicals, altered RAAS sensitivity
  • selenium, vit C / anti-oxidant deficiency
72
Q

PET in mother can cause cerebral circulation bleeds, nephron damage and liver damage. What can the leaky vessels and proteinuria lead to ?

A
  • fluid in brain/lungs

- less albumin in blood, lower oncotic p. more fluid loss

73
Q

The foetus in PET is underperfused so sends blood to vital organs. How does the foetus/baby present?

A

Skinny (used all glycogen stores)
Unsymetrical IUGR
Less renal flow/less wee/oligohydramnios

74
Q

What is a placental abnormality that can result in death that may occur in PET?

A

Placental abruption (separates from uterus wall)

75
Q

When should a PET pregnancy deliver? Management?

A
  • deliver at 37wks
  • at 27wks Dr tries to prolong pregnancy with anti BP meds to stave off symptoms
  • PET is progressive, will get worse until delivery
76
Q

LABOUR is the process of uterine contractions and cervical dilation that enables the uterus to deliver…

A

the viable foetus (24wk+)

placenta and membranes

77
Q

Stage 1 of labour is from onset of regular painful uterine contractions to full cervical dilation (10cm) what is stage 2 and 3

A

Stage 2-from 10cm to foetal delivery (0.5-1hr)

Stage 3-from this to delivery of placenta/membranes (riskiest)

78
Q

1st stage of labour is made up of the latent phase then the active phase, what is the latent phase?

A

Latent: duration for cervix to become effaced and dilate 4cm, prostoglandins make it squishy + reg. contractions. approx 6hrs.

79
Q

1st stage of labour is made up of the latent phase then the active phase, what is the active phase?

A

Active: cervix to dilate to 10cm, approx 1cm/hr. + strong uterine contractions (oxytocin)

80
Q

What is a partogram (labour)

A

A partogram is a graphic representation of labour (rate of dilatation, descent of head, contraction frequency, vital signs..)

81
Q

What is the alert line and action line used for in a labour partogram?
Alert is drawn 1cm/hr from start of active phase
Action is parrallel but 2cm to right

A
  • women should be to the right of the alert line

- if they are to the right of the action line it means the labour is too slow and needs intervention to be sped up

82
Q

What is the commonest cause of slow labour and how is it corrected? Any other causes?

A

Weal/uncoordinated contractions (esp. nulliparous)
Give oxytocin
-pelvis shape, fibroids, full bladder/rectum, big baby

83
Q

Admission in labour. What is it important to adhere to?

A

The previously agreed action plan.

84
Q

What are the 3 most important parts of managing labour stage 1?

A
  • Reassurrance (1 to 1 support)
  • Hydration and Ambulation
  • Adequate pain reflief
85
Q

Before giving oxytocin to a slow/complicated labour, what intervention should be attempted?

A

Artificially rupture the membranes to allow baby’s head to descend

86
Q

2nd stage of labour is associated with what physiological changes..name 4

A
  • vulval bleeding
  • anal dilation
  • urge to push
  • increased resp rate
  • unable to sit still
87
Q

Slow labour is painful but also increases morbitity to both. What risks e.g. exhaustion -> dehydration cause slow labour to be dangerous?

A
  • more intervention –> more infection risk
  • operative delivery can –> foetal distress
  • uterine rupture or vesicovaginal fistula
  • post partum haemorrhage
88
Q

To actively manage the 3rd stage of labour, what can be given when the anterior shoulder is delivered?

A

-intramuscular SYNTOMETRINE it is artificial oxytocin and ergometrin to stimulate short and prolonged contractions respectiv.

89
Q

After the cord is clamped (+stops syntometrine going to baby) what does the midwife do to assist delivery of the rest?

A
  • Hand above pubic symphysis, feel ant. uterus while controlled cord traction (pull) to check its not tugged down
  • placenta pulled out, midwife checks it and membranes for completeness
90
Q

Suggest 4 complications of the 3rd stage of pregnancy:

A
  • placenta retained in uterus
  • post partum haem.
  • perineal trauma (2nd/3rd tear)
  • perineal/pelvic haematoma
  • uterine inversion

s4 - Repro, Develop, Ageing, Pharm (14 decks)

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