7- Normal pregnancy and labour (common issues and breastfeeding)) Flashcards

1
Q

when are women screened for anaemia in pregnancy

A

Booking clinic
28 weeks gestation

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2
Q

causes of anaemia in pregnancy

A
  • Dilutional anaemia: due to increased plasma volume and relative reduction in haemoglobin conc due to RBC not increwasing
  • Iron deficiency anaemia (microcytic):
    o Fetal requirement for iron
    o Menorrhagia
    o Previous pregnancy
    o Poor diet
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3
Q

presentation of anaemia in pregnant women

A

Often anaemia in pregnancy is asymptomatic. Women may have:

Maternal effects
- SoB
- Pallor
- Dizziness
- Tiredness
- Immunosuppression
- Poor conc
- Low mood
- Increase peripartum bloos loss risk

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4
Q

inves

A
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5
Q

foetal effects of anaemia

A

Fetal effects
o Preterm delivery
o Low birth weight
o Increase anaemia in first 3 months
o Impaired psychomotor development

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6
Q

normal ranges for Hb during pregnancy

A
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7
Q

which value of an FBC can be used to indicate cause of anaemai

A
  • Low MCV may indicate iron deficiency
  • Normal MCV may indicate a physiological anaemia due to the increased plasma volume of pregnancy
  • Raised MCV may indicate B12 or folate deficiency
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8
Q

haemoglobinopathies which can cause anaemia

A

thalassaemia
sickle cell

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9
Q

investigations for anaemia

A

FBC
haeoglobinopathy screening
other blood tests: ferritin, B12, folate

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10
Q

Management of anaemia

A

Dietary advice
- Red meat, green leafy veg, nuts

If iron deficient- iron supp required
- Take on empty stomach, 1 hour before food wit fresh OJ (vitamin D helps absorption)
- Not with tea or coffee- tannins prevent iron absorption
- If not tolerated or limited time- IV ferinject
- Continue 3 months postpartum

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11
Q

why can b12 be low

A

The increased plasma volume and B12 requirements often result in a low B12 in pregnancy.

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12
Q

if low B12 women should be tested for

A

pernicious anaemia (checking for intrinsic factor antibodies).

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13
Q

management of low B12

A
  • Intramuscular hydroxocobalamin injections
  • Oral cyanocobalamin tablets
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14
Q

women with low folate

A

started on folic acid 5mg daily.

all women should be taking 400mcg

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15
Q

briefly describe thalassaemia

A
  • 2 types: defects inalpha and beta chains (alpha thalassaemia vs beta thalassaemia)
  • both autosomal recessive
  • pathophysiology: defective chains mean RBC more fragile-> spleen clear destroyed cells and this causes splenomegaly. Bone marrow expands -> increased risk of fractures, pronounced forehead and cheekbones
  • signs and symptoms: microcytic anaemia, fatigue, pallor, jaundice etc
  • Diagnosis: FBC (micro), Haemoglobin electrophoresis, DNA testing
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16
Q

iron overload and thalassaemia

A

resutls due to faulty creation of RBC, recurrent transfusions and icnreased absorption of iron in response to anaemia

management
- limit transfusion
- iron chelation

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17
Q

Iron overload in thalassaemia causes effects similar to

A

haemochromatosis:

Fatigue
Liver cirrhosis
Infertility and impotence
Heart failure
Arthritis
Diabetes
Osteoporosis and joint pain

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18
Q

overall mangement of thalasaaemia

A
  • monitoring of FBC and iron
  • transfusion
  • iron chelation
  • splenectomy
  • bone marrow transplant (can be curative in type A)
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19
Q

types of thalassaemia

A
  • Alpha -thalassaemia
  • Beta-thalassaemia
  • Minor - mild anaemia
  • Intermediate - more signfiicant anaemia
  • Major- severe anaemia (failure to thrive)
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20
Q

thalassaemia in pregnancy

A
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21
Q

briefly describe sickle cell

A
  • autosomal recessive
  • abnormal gene for beta globin on chromosome 11
  • one copy of the gene results in sickle cell trait - usually asymptomatic
  • two abnormal copies- sickle cell disease
22
Q

pathophysiology of sickle cell

A

During the development of a fetus, from 32 to 36 weeks gestation, the production of fetal haemoglobin (HbF) decreases. At the same time, adult haemoglobin (HbA) is produced in greater quantities. Over time there is a gradual transition from HbF to HbA. At birth, around half the haemoglobin produced is HbF and half is HbA. By 6 months of age, very little fetal haemoglobin is produced. Eventually, red blood cells contain almost entirely HbA.

Patients with sickle-cell disease have an abnormal variant called haemoglobin S (HbS). HbS causes red blood cells to be an abnormal “sickle” shape.

23
Q

sickle cell and malaria

A

Having one copy of the gene (sickle-cell trait) reduces the severity of malaria. As a result, patients with sickle-cell trait are more likely to survive malaria and pass on their genes. Therefore, there is a selective advantage to having the sickle cell gene in areas of malaria. This leads to a high proportion of the population in these areas having the gene.

24
Q

testing for sickle cell

A
  • booking appointment
  • newborn screening heal prick test at day 5
25
Q

complication of sickle cell

A

Complications
*
* Anaemia
* Increased risk of infection
* Stroke
* Avascular necrosis in large joints such as the hip
* Pulmonary hypertension
* Painful and persistent penile erection (priapism)
* Chronic kidney disease
* Sickle cell crises
* Acute chest syndrome

26
Q

General Management of sickle cell

A
  • Avoid dehydration and other triggers of crises
  • Ensure vaccines are up to date
  • Antibiotic prophylaxis to protect against infection with penicillin V (phenoxymethypenicillin)
  • Hydroxycarbamide can be used to stimulate production of fetal haemoglobin (HbF). Fetal haemoglobin does not lead to sickling of red blood cells. This has a protective effect against sickle cell crises and acute chest syndrome.
  • Blood transfusion for severe anaemia
  • Bone marrow transplant can be curative
27
Q

sickle cell crisis management

A
  • Have a low threshold for admission to hospital
  • Give oxygen
  • Treat any infection
  • Keep warm
  • Keep well hydrated (IV fluids may be required)
  • Simple analgesia such as paracetamol and ibuprofen
  • Penile aspiration in priapism
28
Q

Cause of reflux in pregnancy

A
  • upwards displacement of stomach as uterus grows -> increases intra-gasdtric pressure
  • increased progesterone can cause relaxation of oesophageal sphincter
29
Q

presentation of acid reflux in pregnancy

A
  • heartburn
  • tummy or chest pain
  • an acid taste
  • feeling bloated
30
Q

management of acid reflux in pregnancy: lifestyle

A
  • Sitting up and not lying down just after eating.
  • Raising the head of your bed when sleeping.
  • Eating small frequent meals, and not eating within three hours of going to bed.
  • Reducing fatty or spicy foods, fruit juice, chocolate and caffeine.
31
Q

management of acid reflux: medication

A
  • antaciss e.g. gaviscon (however not antacids containing sodium bicarbonate or magnesium trisilicate)
  • ranitidine or omeprazole if severe symptoms
32
Q

pelvic girdle pain pathophysiology

A

PGP is pain in the front and/or the back of your pelvis that can also affect other areas such as the hips or thighs. It can affect the sacroiliac joints at the back and/or the symphysis pubis joint at the front. PGP used to be known as symphysis pubis dysfunction (SPD).

This is because the joint in the bone can become loosened and the bones separate a little and then rub against one another. The joint softening is caused by softening to the ligament that holds together the bones. This does have a purpose in nature: the splitting of the pubic bone in this way widens the pelvic ‘outlet’ which is the exit route your baby will take in labour. This can be seen as a helpful preparation for labour. This is a small consolation for the pain.

Sacroiliac joint also affected.

33
Q

presentation of PGP

A
  • pain in the pubic region, lower back, hips, groin, thighs or knees
  • clicking or grinding in the pelvic area
  • pain made worse by movement, for example:
  • walking on uneven surfaces/rough ground or for long distances
  • moving your knees apart, like getting in and out of the car
  • standing on one leg, like climbing the stairs, dressing or getting in or out of the bath
  • rolling over in bed
  • during sexual intercourse.
34
Q

conservative management of PGB

A
  • keep active, but get plenty of rest
  • stand tall with bump and bottom tucked in
  • change position frequently
  • keeping legs together getting in and out of car
  • usein g a pillow between elfs
35
Q

manageemnt of PGP: further therapy

A
  • physiotherapy
  • manual therapy
  • acupuncture
  • hydrotherapy
  • supprot belt
  • crutches/ wheelcahir
  • pain relfied such as paracetamol
36
Q

define lactation

A

Lactation is the maternal physiological response whereby milk is secreted from the mammary glands to feed the infant.

37
Q

mammary glands

A

comprises 15-20 lobulated masses of tissue with fibrous tissue connecting the lobes and adipose tissue in-between. The lobes are made up of alveoli, blood vessels and lactiferous ducts.

38
Q

puberty and breast devlopment

A
  • oestrogen causes the few ducts present to sproud and the ends form masses of cells which become alveoli
  • With each menstrual cycle there are cyclic changes due to changes in oestrogen and progesterone.
39
Q

breast development during pregnancy

A

significant hypertrophy of the ductular-lobular alveolar system:
* prominent lobules form and alveolar cells differentiate into cells capable of milk production
* little milk production during pregnancy due to high prog: oestrogen ratio which favours growth rather than secretion

40
Q

lactogenesis

A

The alveolar epithelial cells responsible for milk production are polarised, highly differentiated cells and their function is to accumulate, synthesise, package and export the components of milk:

41
Q

what is colostrom

A

Soon after birth the breasts produce 40ml/day of colostrum.
This has less water soluble vitamins, fat and sugar than mature milk, but contains more proteins (particularly immunoglobulins) and fat soluble vitamins.

42
Q

regulation of milk production

A

controlled by prolactin

  • after delivery of the placenta blood progesterone reduces allowing the alveoli to repsond to prolactin
  • breast milk begins to form within 24-48 hours
43
Q

prolactin

A
  • polypeptide hormone secreted by AP
  • negatively controlled by dopamine
  • positive feedback from itself
44
Q

Milk let-down reflex

A

mechanical stimulation of the nipple is responsible for:
- milk delivery to the infant
- maintenance of lactation

45
Q

milk delivery to infant

A

Babies do not suck the milk out - it is ejected by the let down reflex
- Oxytocin is released by the pituitary gland in response to suckling
- this stimulates myoepithelial glands to contract squeezing milk out of the breast

46
Q

other triggers fro the let down reflex

A
  • infant crying
  • sign of infant

Inhibition:
- pain
- embarrassment
- alcohol

47
Q

milk production

A

suckling causes the hypothalamus to reduce secretion of dopamine and increase vasoactive intestinal protein (promotes prolactin secretion)

48
Q

oxytocin controls….. and prolactin controls….

A

oxytocin controls milk release and prolactin controls milk production

49
Q

oxytocin controls….. and prolactin controls….

A

oxytocin controls milk release and prolactin controls milk production

50
Q

Maintaining Milk Production

A

The key to maintaining milk production is sufficient suckling stimulation at each feed to maintain prolactin secretion and to remove accumulated milk. If suckling stops, milk production ceases gradually. This is due to turgor induced damage to secretory cells and low prolactin levels. Milk suppression can also be achieved via steroids.

51
Q

benefits of breastfeeding (for baby)

A
  • passes protective antibodies reducing infections
  • help foster strong emotional bond
  • reduces obesity, asthma, SIDs, CVS in adulthood