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Year 3- placement > Obstetric core conditions 2 > Flashcards

Obstetric core conditions 2 Flashcards

1
Q

Thyroid disease in pregnancy- pathophysiology

A
  1. Thyroid-binding globulin is increased in pregnancy, resulting in a 50% increase in total thyroxine production to maintain a functional level of free T3 and T4.
  2. Maternal iodine requirements are increased due to active transport across the placenta to the fetus, and increased maternal renal excretion
  3. HCG is structurally similar to TSH, so increased levels of hCG in the first trimester stimulate T4 production. Conditions associated with an increase in hCG (HG, molar pregnancy) can be associated with transient hyperthyroidism.
  4. The fetus begins producing thyroid hormones at 12 weeks. Fetus is dependent on maternal iodine levels throughout the pregnancy
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2
Q

Pregnancy and hyperthyroidism

A
  1. Affects 0.2% of pregnancies, typically related to autoimmune Grave’s disease
  2. Associated with TSH-receptor antibodies (TRAb): Can cross the placenta and trigger neonatal thyrotoxicosis (tachycardia, goitre, hydrops, Intra-uterine demise)
  3. Generally improves in pregnancy: most women reduce or stop their anti-thyroid medication. Relapse postnatally is common.
  4. Untreated thyrotoxicosis is associated with: Subfertility, miscarriage, IUGR, preterm birth & perinatal demise
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3
Q

Thyroid disease in pregnancy- antenatal care

A
  1. Check TRAb & TFTs at booking: Raised TRAb levels indicate referral to fetal medicine, Serial TFT check: at least 1/ trimester
  2. Medication review: Carbimazole (CBZ) and PTU (Propylthiouracil) used to treat hyperthyroidism can both cross the placenta, potentially affecting the fetal thyroid: doses should be kept as low as possible
  3. CBZ increased risk of congenital anomalies, including NTD
  4. PTU associated with maternal hepatotoxicity – argument to switch to CBZ after first trimester. Proposed PTU 1st trimester -> CBZ switch in second trimester
  5. PTU is preferable postnatally for BF mothers
  6. Block & replacement treatment is not recommended in pregnancy
  7. Radioactive iodine is absolutely contraindicated
  8. Surgery can be considered but preferable to avoid
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4
Q

Pregnancy and Hypothyroidism

A
  1. If secondary to previous Grave’s disease, TRAb levels should still be assessed in the first trimester
  2. Inadequate replacement can result in problems with neurodevelopmental delay. In severe cases, it may result in subfertility, miscarriage, PET & SB
  3. Generally well managed with little/ no impact on pregnancy
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5
Q

Pregnancy and thyroid disease- antenatal care

A
  1. Aim to keep TSH levels <2.5 mmol/L
  2. Some endocrinologists recommend an empirical increase in thyroxine during the first trimester, due to the physiological increase in thyroxine requirements
  3. Aim to assess thyroid function once each trimester as a minimum, if titration of treatment is required, monitoring should be increased to 6-weekly intervals
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6
Q

Post partum thyroiditis

A
  1. Typically presents 3-4mths post-partum, and affects around 17% of women
  2. Risk factors: anti-thyroid antibodies, pre-existing auto-immune disease (T1DM)
  3. Rebound effect of auto-immunity. Pregnancy is generally an immune-suppressive state, so after delivery it is common to observe an increase/ resurgence in auto-antibody levels
  4. Presents with transient thyrotoxicosis, followed by transient hypothyroidism (80% resolve in 6-9 months)
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7
Q

Definition of FGM

A

Any procedure involving partial or total removal of the female external genitalia or other injury to the female genital organs for non therapeutic reasons. Its illegal and a form of child abuse. Must be reported to the police immediately

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8
Q

Classification of FGM

A
  1. Type 1= Clitoridectomy: partial or total excision of the clitoris
  2. Type 2= Excision: partial or total removal of the clitoris and labia minora, with or without excision of the labia majora
  3. Type 3= Infibulation: narrowing of the vaginal orifice with the creation of a covering seal by cutting and moving the labia minora and/or labia majora, with or without excision of the clitoris.
  4. Type 4= All other harmful procedures to the female genitalia for non-medical purposes (pricking, piercing, incising, scraping, cauterization)
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9
Q

Potential complications of FGM

A
  • Bleeding, severe pain, infection, including tetanus, hepatitis and HIV.
  • Urinary tract obstruction and recurrent UTI.
  • Sub fertility, reduced sexual response, lower self-esteem and PTSD.
  • Difficult gynaecological internal examination, catheterization and cervical smears.
  • No effect on pregnancy, but need consultant booking as increased risks of delivery complications such as obstructed labour, perineal trauma, operative vaginal delivery and LSCS.
  • Delivery in a maternity unit with immediate access to emergency obstetric care.
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10
Q

Atopic eruptions of pregnancy

A
  • Risk Factors: history of atopic eczema
  • Clinical Features: erythematous, excoriated nodules or papules on the face, neck, chest and extensor surfaces of particularly arms & shins. No adverse effects on mother or baby.
  • Management: Treat as eczema. Emollients, topical steroids, oral antihistamines. UVB can be helpful.
  • Benign, clinical diagnosis, usually in the first trimester
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11
Q

Pruritic Urticarial papules and plaques of pregnancy (PUPP)/ polymorphic erruptions

A
  • Risk Factors: first pregnancy, high BMI/excessive weight gain, multiple pregnancy
  • Clinical Features: pruritic urticarial papules that coalesce into plaques. Typically, the rash starts on the abdomen, often first appearing on the striae, but the umbilicus region is usually spared. May remain localised or may become widespread. Typically disappears 10 days after delivery. No risk to mother and baby.
  • Management: topical steroids, emollients, Menthol in aqueous cream
  • Benign, clinical diagnosis, usually in 3rd trimester
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12
Q

Pemphigoid gestationis

A
  • Risk factors: rare, association with molar pregnancy and choriocarcinoma
  • Dermatology referral necessary as diagnosis is by skin biopsy.
  • Risk of preterm delivery, low birth weight and SGA therefore women needs serial growth USS and consideration for IOL. 10% of babies may have transient bullous lesions.
  • Management: emollients, topical steroids, often needs oral antihistamines and oral steroid
  • Very rare, presents in 2nd/3rd trimester. Autoimmune condition
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13
Q

Clinical features of pemphigoid gestationis

A

Intense itch, erythematous urticarial papules/plaques on the abdomen (particularly umbilicus), may spread to cover the entire body. Progresses to form bullae. Can quieten in late pregnancy then flare post-partum.

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14
Q

Maculopapular rash in pregnancy

A

Uniform small red spots, bumpy to touch. In order of likelihood: parvovirus, measles, rubella

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15
Q

Parvovirus B19 ‘slapped cheek’ in pregnancy

A
  • Prodromal symptoms and MP rash
  • Can cause hydrops fetalis/fetal death
  • If suspected – contact local infectious diseases on tests/monitoring
  • Check for rubella at same time
  • If confirmed – regular fetal medicine review, serial fetal US and doppler
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16
Q

Measles in pregnancy

A
  • MP rash, coryza, conjunctivitis, fever
  • Maternal infection can be severe -> fetal loss/preterm delivery
  • Notifiable
  • Management: HNIg (human normal Ig) if susceptible, also for neonate if within 6 days before/after delivery
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17
Q

Rubella in pregnancy

A

Extremely rare, always note risk in asylum seekers, refugees, recent visitors (may not have been immunised)

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18
Q

Chickenpox (VZV) in pregnancy

A
  • Widespread vesicular rash on face, lesions crop. Prodrome (mild fever/malaise) 48h before rash.
  • Infectious 48h before rash and until vesicles crust over
  • Management: determine maternal immunity status – check for maternal IgG. Consider giving VZ immunoglobulin.

Can cause complications for mother and fetus:
1. Maternal – pneumonia, hepatitis, encephalitis, death
2. Fetal – fetal varicella syndrome esp. if before 20 weeks
3. Neonatal – if at time of delivery can get neonatal varicella 30% mortality. If contract chickenpox within 7d delivery or following, should receive prophylaxis

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19
Q

Pregnancy- Shingles

A
  • Reactivation of latent ZVZ, cannot be caught from chickenpox
  • Localised vesicular rash: dermatomal distribution
  • No risk to fetus or neonate
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20
Q

Depression and anxiety in pregnancy

A
  1. 12-13%, includes generalised anxiety disorder, OCD and phobias including tokophobia
  2. All pregnant women are screened via a questionnaire for anxiety and depression: at booking and at 28 weeks and should be asked at every patient contact
  3. Refer for perinatal mental health support if fulfils criteria for referral i.e. red flags- previous/high risk of suicides, attempt or self harm, previous admission under psychiatric services, previous psychosis of any kind, bipolar
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21
Q

Depression and anxiety treatment

A
  1. Sertraline (SSRI) often first line or citalopram (very small risks of Persistent pulmonary hypertension (doubled, but still only 2-3/1000) & neonatal withdrawl – usually mild and self limiting)
  2. Risks of not treating – high cortisol levels in mum of unknown risk to baby, assoc with poor bonding and effect on other children, deteriorating mood.
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22
Q

Psychotic disorders in pregnancy

A
  1. Include bipolar disorder, schizophrenia, schizoaffective disorder and psychotic depression
  2. Preconception counselling – plan regarding their medication & risks in pregnancy and postpartum period
  3. Require referral to perinatal mental health team
  4. High risk of relapse and postpartum psychosis (50% recurrence)
  5. May need prophylactic admission to Mother and Baby units (MBU)
23
Q

Drug and alcohol misuse pregnancy

A
  • Refer to a specialist substance misuse service for advice and treatment
  • Assisted alcohol withdrawal and detoxification to opioids (or supportive on methadone/subutex) should be in collaboration with specialist mental health services and preferably as in-patients. Generally do not attempt to reduce opioid substitutes – less risk of seeking additional supplementation if stable.
  • Consultant led care, specialised support. Ongoing toxicology screening
  • Fetal growth is monitored by ultrasound scans. Neonates will need monitoring for withdrawal
24
Q

Eating disorders and pregnancy

A
  1. Changes in body shape can be difficult, or reignite previous problems
  2. Prevalence of anorexia nervosa and bulimia nervosa is lower in pregnant women but binge eating disorder is higher in pregnant women
  3. Psychological interventions include focussed family therapy (FT) and eating disorder CBT (CBT-ED).
25
Q

Medication depression and pregnancy

A
  1. Emphasis on maintaining good maternal mental health. The lowest dose that keeps them well
  2. Sodium valproate should be avoided
  3. Shouldn’t stop medication without discussion
26
Q

Baby blues

A
  1. Common condition (50-80% of women).
  2. Symptoms include tearfulness, anxiety and irritability
  3. usually starts on day 3-4 postnatally and last for up to 10 days.
  4. self-limiting, requires reassurance and monitoring.
27
Q

Postnatal depression

A
  1. Common condition (10-15% of women) in the first year after childbirth.
  2. In 30% symptoms commence in the antenatal period. Most cases start within a month of birth and peak at 3 months
  3. Women with a prior history of major depression and a family history of PND are at high risk.
  4. Risk of recurrence in future pregnancies is between 30-50%.
28
Q

Postnatal depression- treatment and diagnosing

A
  1. Cognitive behavioural therapy may be beneficial. Certain SSRIs such as sertraline and paroxetine may be used if symptoms are severe - whilst they are secreted in breast milk it is not thought to be harmful to the infant
  2. Treatment of severe PND includes anti-psychotics, mood stabilisers and occasionally ECT
  3. Can be diagnosed with the Edinburgh postnatal depression scale
29
Q

Postpartum (puerperal) psychosis

A
  • Rare (1-2 in 1000) women who have given birth.
  • Women with bipolar disorder and a family h/o of postpartum psychosis have up to a 75% of developing this condition. Can also occur in women with no previous psychiatric history.
  • This is considered a psychiatric emergency and requires assessment by a trained psychiatrist.
  • Treatment of the acute episode requires in-patient admission ideally to a mother and baby unit and anti psychotics, anti depressants and/or mood stabilisers.
30
Q

Postpartum (puerperal) psychosis clinical features

A
  • Symptoms can vary ,usually a mix of psychosis, depression and mania: excited or elated, severely depressed, rapid mood changes. Confused or disorientated
  • Features include severe swings in mood (similar to bipolar disorder) and disordered perception i.e. auditory hallucinations
  • Usually present in the first 2 weeks following delivery.
  • Majority of the women have delusional ideas of their baby (ie, that it is at risk, or somehow evil).
31
Q

Pregnancy PTSD

A
  1. ~4% of all women who have given birth suffer from PTSD, approximately 30,000 new cases every year.
  2. Trauma is subjective – how the patient perceives experience, not necessarily what happened that causes the symptoms.
  3. Partners can also suffer from PTSD related to birth trauma.
  4. It is important to differentiate PTSD from depression as treatment for both conditions are different.
  5. Treatment includes psychological interventions, varying from a debrief/birth reflections, to EMDR or CBT. . Antidepressants - SSRI’s Can be used in conjunction.
32
Q

Pregnancy PTSD symptoms

A

Include re-experiencing the trauma, avoidance of any reminders of the trauma, negative cognitions and mood and hyper vigilance. Impacts on ability to bond with baby and parent, as well as other relationships.

33
Q

Obstetric cholestasis

A

Definition: Multifactorial disease characterised by pruritus in the absence of a skin rash with abnormal liver function tests (LFTs), neither of which has an alternative cause and both of which resolve after birth. Other causes of pruritus and abnormal LFTs must be ruled out (eg. Viral hepatitis, gall stones, autoimmune causes).

34
Q

Obstetric cholestasis- pathophysiology

A

OC results from reduced bile secretion due to functional impairment of hepatocytes; this leads to retention of bile acids & conjugated bilirubin. The bilirubin causes jaundice and the bile acid ascites. The excretion of bilirubin follows hepatocellular pathways different from those of bile acids. Therefore, serum bilirubin level may be normal and the patient often presents with only pruritus but no jaundice.

35
Q

Obstetric cholestasis- associated risks and risk factors

A
  • Maternal: pruritis, sleep deprivation, C-Section
  • Fetal: preterm labour, fetal death (physiology of stillbirth risk not well understood. Not associated with hypoxia, placental insufficiency or IUGR. Possibly related to bile acid toxicity to cardiomyocytes increasing risk of fetal arrhythmia)

Risk Factors: Previous OC, family history of OC, multiple pregnancy, gallstones, Hepatitis

36
Q

Obstetric cholestasis- clinical features

A
  1. Pruritus: particularly hands & feet, usually worse at night & starts in 3rd trimester
  2. Other: jaundice, pale stools, dark urine, abdominal pain, anorexia
  3. Increased risk of premature birth
37
Q

Obstetric cholestasis: Investigations- to rule out alternative Dx

A
  • Bedside: Blood Pressure, Urine dip for proteinuria
  • Bloods: LFTs, Bile Acids, Viral screen – Hepatitis, CMV, EBV; Liver autoimmune screen, HELLP screen
  • Imaging: Liver USS
38
Q

Obstetric cholestasis- management

A
  • Ursodeoxycholic Acid (UDCA) – previously this was used in an attempt to reduce bile acids however a recent trial has shown it is of NO benefit (PITCHES). Treatment is therefore symptomatic – emollients & antihistamines.
  • Weekly bloods and CTGs (though stillbirth not thought to be hypoxic)
  • Induction of labour – timing depends on level of bile acids;
  • If >100 consider from 35 weeks (as risk of stillbirth greater in this group), if <100 can wait until 39 weeks (unless symptoms debilitating, other indications etc).
  • Vitamin K supplementation
39
Q

Morning sickness

A
  1. Diagnosed when onset is in the first trimester and other causes have been excluded
  2. Symptoms continue in the 3rd trimester for 20% of women
40
Q

Diagnosing Hyperemesis gravidarum

A
  • More severe NVP and is characterised by the triad of more than 5% pre-pregnancy weight loss, dehydration and electrolyte imbalance.
  • Maternal complications include weight loss, hyponatraemia and increased risk of VTE, and risk to the fetus includes a possible higher incidence of low birthweight babies.
  • It is important to exclude multiple pregnancy and molar pregnancy in cases of hyperemesis gravidarium.
41
Q

Classifying and treating morning sickness

A

The Pregnancy-Unique Quantification of Emesis (PUQE) score can be used to classify the severity of NVP and help guide management.

Treatment for morning sickness
1. Small, plain meals, make sure to rehydrate
2. Prescribe oral cyclizine or promethazine (antihistamines), reassess after 24 hours

42
Q

Anaemia and pregnancy

A

Increase in plasma volume causes haemodilution. Red cell mass does increase but not enough

43
Q

Definition and screening for anaemia

A
  1. In non-pregnancy patients, the female lower limit of normal Hb is 115-120.
  2. FBC is taken at booking – if Hb is <110g/L, this suggests anaemia prior to pregnancy.
  3. FBC is then repeated at 28 weeks – if Hb is <105g/L this suggests anaemia.
  4. Additional testing can take place in the presence of symptoms suggestive of anaemia, including tiredness, lethargy, dizziness or fainting
44
Q

Causes and diagnosis of anaemia in pregnancy

A
  • The commonest cause is iron deficiency anaemia
  • The second commonest cause is folate deficiency.
  • Conditions such as haemolytic anaemia, sickle-cell disease, thalassaemia and hereditary spherocytosis can also increase the risk of folate deficiency.
  • Non-haematological causes of anaemia (less common) include CKD, autoimmune conditions and coeliac disease
45
Q

Taking folate in pregnancy

A

a. All women planning pregnancy should be advised to take folate supplements 400mcg daily pre-conceptually and continue until 12 weeks to prevent neural tube defects/ other abnormalities.
b. Women who are at high risk for neural tube defects should take high dose (5mg) folic acid (women with spina bifida, previous baby affected by any NTD, diabetes, anticonvulsant use, obesity, haematological conditions).

46
Q

Iron deficient anaemia in pregnancy

A
  • Additional tests include serum iron, serum ferritin and total iron binding capacity
  • Iron supplementation should be prescribed for women with confirmed IDA in addition to iron rich diet (red meat, green leafy vegetables). It usually takes 2-3 weeks to increase Hb, but symptoms may improve earlier.
  • IV iron can be considered as an alternative when oral iron is not tolerated, when Hb levels are not improving despite therapy, or if a more rapid increase in Hb is required (diagnosis is late in pregnancy, pre-op).
47
Q

Postpartum anaemia

A
  • Patients at risk of anaemia include an estimated blood loss at delivery >500ml or any patient who is anaemic (Hb <105) in the 3rd trimester / the start of labour.
  • In cases where Hb is found to be <100g/L postnatally, oral iron should be commenced for at least 3 months
  • Blood transfusion guidelines suggest Hb <70g/L as a threshold for transfusion, however if a woman is symptomatic between 71-80g/L transfusion may need to be considered.
48
Q

When are pregnant women screened for anaemia

A

The booking visit (8-10 weeks) and at 28 weeks

49
Q

Cut offs for iron therapy

A
  • First trimester- <110 g/L
  • Second/third trimester- <105 g/L
  • Postpartum- <100 g/L
50
Q

All women with a booking BMI >30 should be

A
  1. Advised to take 5mg folic acid at least one month before conception and during the first trimester
  2. Screened for gestational diabetes (oral glucose tolerance test)
  3. Commenced on vitamin D (higher risk of vitamin D deficiency)
  4. Given lifestyle advice regarding a healthy diet and exercise
  5. Having regular VTE assessments undertaken
  6. Recommended active management of the third stage to reduce risk of PPH
51
Q

VTE

A

Can occur at any stage of pregnancy but the puerperium has the highest risk

A woman with a previous VTE history is considered high risk and requires low molecular weight heparin throughout the antenatal period and also input from experts.
A woman at intermediate risk of developing VTE due to hospitalisation, surgery, co-morbidities or thrombophilia should be considered for antenatal prophylactic low molecular weight heparin.

The assessment at booking should include risk factors that increase the womans likelihood of developing VTE.

52
Q

The risk factors for VTE include

A
  1. Age > 35
  2. Body mass index > 30
  3. Parity > 3
  4. Smoker
  5. Gross varicose veins
  6. Current pre-eclampsia
  7. Immobility
  8. Family history of unprovoked VTE
  9. Low risk thrombophilia
  10. Multiple pregnancy
  11. IVF pregnancy
53
Q

Prophylaxis for VTE in pregnancy

A

Four or more risk factors warrants immediate treatment with low molecular weight heparin continued until six weeks postnatal. If a woman has three risk factors low molecular weight heparin should be initiated from 28 weeks and continued until six weeks postnatal.

54
Q

Treatment for VTE in pregnancy

A

If diagnosis of DVT is made shortly before delivery, continue anticoagulation treatment for at least 3 month, as in other patients with provoked DVTs.

Direct Oral Anticoagulants (DOACs) and warfarin should be avoided in pregnancy.

Year 3- placement (34 decks)

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