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Year 2 > Drugs and pregnancy > Flashcards

Drugs and pregnancy Flashcards

1
Q

What is the most common causes of birth defect?

A

Majority are unknown; out of the known,
1) Genetic transmission
2)Drugs and chemicals
3) Chromosomal aberration

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2
Q

What is the Baroness Cumberlege report?

A

Published in 2020 which identified the clinical areas where teratogenic harm occurred due to sodium valproate, Primodos and surgical mesh used to treat female incontinence.

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3
Q

What was identified in the Baroness Cumberlege report?

A

Dismissing patients’ voice
Failure of informed consent
Parents living with guilt

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4
Q

What is primodos?

A

Hormonal medication used to detect pregnancy that resulted in birth defects and shortened limbs.

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5
Q

What is chromosomal aberration?

A

Disorder with abnormal morphology or number of chromosomes.

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6
Q

What is the background risk of birth defects in all pregnancies?

A

All pregnancies begin with a risk of 3-5%, which decreases when a specific organ or limb is fully developed.

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7
Q

What is spontaneous abortion?

A

Abortion initiated by the body due to chromosomal or reproductive tract abnormalities, with a risk of 10-20%.

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8
Q

What is gestational age?

A

Begins with first day of last period.

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9
Q

What is an embryo?

A

Week 3->Week 8 of pregnancy

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10
Q

What is a foetus?

A

Week 9 to end of pregnancy.

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11
Q

When does organogenesis occur?

A

During the embryo period in the first trimester.

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12
Q

Which system is most at risk for birth defects throughout pregnancy?

A

CNS

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13
Q

What is a teratogen?

A

Any agent administered during pregnancy which causes a structural or functional abnormality to the foetus at any point in development.

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14
Q

How is teratogenicity established?

A

Requires large sample of affected foetus while in utero.
->Lack of data means patients are not advised to take medication unless necessary while pregnant.

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15
Q

What are the common teratogenic agents?

A

Infections
Alcohol, tobacco, cocaine
Physical agents
Chemicals
Maternal health factors

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16
Q

Which infections are commonly teratogenic?

A

Cytomegalovirus, herpes, toxoplasmosis, varicella

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17
Q
A
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18
Q

What are the teratogenic physical agents?

A

Hyperthermia
Ionising agents

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19
Q

What are the teratogenic chemicals?

A

Herbicides, industrial solvents

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20
Q

What is behavioural teratology?

A

The effect of teratogenic agents on the behaviour or functional adaptation of the child to its environment

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21
Q

What is the most commonly used teratogen?

A

Alcohol and smoking.
Alcohol increases the risk of spontaneous abortion and lower birth weight.

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22
Q

What is foetal alcohol syndrome?

A

Preventable birth defects due to alcohol consumption such as
Small head, flat midface and ear anomalies
Immature development of the brain and CNS so:
->Difficulty with attention and hyperactive behaviour
->Delays in developmental milestones

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23
Q

What is transplacental carcinogenicity?

A

Agent has no effect on mother but results in cancer of the offspring due to exposure via placenta. Diethylstilbestrol is synthetic oestrogen that increased risk of vaginal, testicular and cervical cancer in young people

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24
Q

What is mutagenicity?

A

Teratogenic agent induce two types of mutations:
Germ cell mutation- reduces fertility
Somatic cell mutation: increases cancer risk

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25
Q

How do teratogenic agents work?

A

They are dose dependent and typically synergestic. Time of exposure is important in the severity of harm. There is a lack of a placental barrier against drugs and risk depends on the individual variation of a drug’s pharmacokinetic metabolism.

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26
Q

How does alcohol consumption in women of childbearing age differ?

A

Older women drink more frequently
Younger women drink heavier and binge drink

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27
Q

What are the types of inheritance?

A

Mendelian inheritance and Polygenic inheritance

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28
Q

What is Mendelian inheritance?

A

Monogenetic inheritance from single gene change in a recognisable pattern such as dominant, recessive. It results in a genetically based malformation.

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29
Q

What is Poylgenic inheritance?

A

Phenotypic trait caused by combination of multiple genetics and/or environment , such as drug interaction susceptibility which is dependent on both the mother and foetus’ genetic constitution.

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30
Q

What is spina bifida?

A

Neural tube defect due to failure of the cranial and caudal neuropore to close in the second trimester, which can majorly be prevented via folic acid supplements.

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31
Q

What is the cause of spina bifida?

A

Unknown with no inherited links but family history increases risk.
Associated with single gene disorders or chromosomal aberrations for folate transport combined with environmental effect.

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32
Q

What increases risk for spina bifida?

A

Pre-gestational diabetes
Previous pregnancy of spina bifida with same partner
Low folate intake
Maternal obesity
Valproate and carbamezapine

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33
Q

What is valproate?

A

Increases the levels of inhibitory GABA and is an anticonvulsant used to treat epilepsy. It is a teratogenic agent with no safe dose in pregnancy because it prevents caudal neuropore closure, leading to spina bifida. It significantly increase in developmental disability and birth defects especially with sodium valproate, and cannot be given to childbearing women and girls.

34
Q

What is carbamezapine?

A

Anticonvulsant used to treat epilepsy that causes spina bifida.

35
Q

What is methotrexate?

A

Immunisuppressant which inhibits cell growth, used in the treatment of cancer.

36
Q

What is the dose-response relationship to teratogens?

A

Threshold dose where there is no teratogenic effect. Beyond this, there is a steep dose-response relationship in response to minimal changes.

37
Q

What is synergy?

A

Enhanced teratogenicity of a drug due to environmental changes or co-administration of a second drug. Polypharmacy should be avoided.

38
Q

How does placental transfer of drugs occur?

A

->Passive diffusion
->Facilitated diffusion
->Active transport via protein/enzyme carriers

39
Q

How does facilitated diffusion across the placenta occur?

A

Low molecular weight chemicals/electrolytes travel via pores in the chorionic membrane.

40
Q

What affects placental drug transfer?

A

Molecular weight
Lipid solubility
Ionisation
Protein binding

41
Q

Which drugs cannot pass the placenta?

A

Drugs with a molecular weight over 1000 such as
Heparin: anticoagulant
Insulin: lowers blood glucose.
Iron dextran

42
Q

What increases the drug diffusion in placenta?

A

Lipid soluble drugs which have low-protein binding, low molecular weight and low ionisation.

43
Q

What determines drug concentration in foetus?

A

Drug concentration in mother’s blood.

44
Q

What are the physiological changes in pregnancy that increases drug metabolism?

A

Liver undergoes hypertrophy and performs increased metabolism
Increased kidney size and GFR and drug excretion
Increased plasma volume
Increased lung function for exhalation of drugs

45
Q

What are the physiological changes in pregnancy that decreases drug metabolism?

A

Decreased gastrointestinal motility
Relative decrease in albumin because of fluid oedema, decreasing its ability to act as a drug carrier, increasing free drug concentration.

46
Q

At what stage in pregnancy is the foetus likely to recover from cell damage?

A

Early embryo stage, However, there is a greater risk if the drug has a long half-life, increases risk of spontaneous abortion.

47
Q

Which trimester has the greatest risk of birth defect from teratogen?

A

First trimester which is where:
->Heart and stomach fully form
-> Development of lungs
->Development of CNS

48
Q

How do androgens affect development in first trimester?

A

In female embryo, causes virilisation of female genitalia. Virilisation is the development of male physical characteristics.

49
Q

How does oestrogen affect development in first trimester?

A

Feminisation of male foetus

50
Q

How does warfarin affect development in first trimester?

A

Nasal hypoplasia and skeletal defects. It can also cause foetal haemorrhages.

51
Q

How do retinoids affect development in first trimester?

A

Retinoids are responsible for cell apoptosis regulation
-> cause CNS, cardiovascular and craniofacial defects

52
Q

How does diethylstilboestrol affect development in first trimester?

A

Oestrogen medication which acted as a transplacental carcinogen which increased the risk of uterine lesions.

53
Q

How do anti-epileptics affect development in first trimester?

A

Facial defects, CNS defects such as spinal bifida and mental retardation
-> After first trimester, has lesser effect and can cause mental retardation.

54
Q

What is the risk of damage in the second and third trimester?

A

Growth retardation of organs and the size of the body. Risk of learning difficulties.

55
Q

What are the effect of narcotics?

A

Neonatal respiratory depression

56
Q

What is the effect of antidepressants after first trimester?

A

Neonatal withdrawal symptoms.

57
Q

What is the effect of ACE inhibitors in pregnancy 2nd and 3rd trimester?

A

Oligohydroamniosus (reduced amniotic fluid)
Hypotension
Anuria
Growth retardation
Lung and kidney hypoplasia
Hypocalvaria (incomplete formation of the skull bones)

58
Q

What is dysmorphogenesis?

A

Formation of abnormal structures.

59
Q

What is ancephaly?

A

Severe congenital condition and fatal birth defect where part of the skull and cerebral hemispheres are absent
-> occurs after exposure 24 days post-conception.

60
Q

When does limb reduction occur?

A

Exposure to teratogen 12-40 days post conception.

61
Q

What is transposition of the vessels?

A

Congenital heart defect where the blood flow to the aorta and pulmonary artery are switched because of atrial septal defect,
->Deoxgenated blood enters right atria, bypasses the lungs and is pumped out from aorta to the body. Oxygenated blood enters pulmonary artery and returns to lungs.

62
Q

What is cleft lip?

A

Interruption in the fusion of the facial prominences in the first trimester, typically corrected by surgery.
-> Caused by anti-convulsants or methotrexate

63
Q

What is syndactyly?

A

Inherited birth defect where the digits are joined, categorised into
Simple: only the soft tissue is joined
Complex: bones are joined

64
Q

What is hypospadias?

A

Opening in the urethra on the underside of the penis, due to failure of the urethral fold to fuse and close at the glans penis, which can occur along the shaft of the penis. This increases the risk of inguinal hernias.
-> This occurs due to abnormal exposure to oestrogen or androgens in development.

65
Q

How does blood glucose change in pregnancy?

A

High blood glucose to fuel growing foetus due to insulin resistance driven by oestrogen, cortisol and somatomammotropin. This causes hypertrophy and hyperplasia of pancreatic beta cells.

66
Q

What is the effect of paternal drug exposure?

A

With use of steroids, chemotherapeutic drugs, metals, pesticides
->men are advised to wait 6 months which is 2 sperm cycles to avoid genetic alteration to sperm.

67
Q

What medication is prescribed to pregnant women?

A

Treatment of chronic conditions such as asthma and hypertension
Treatment of acute illness related to pregnancy such as:
-> nausea/vomiting
-> constipation
-> dyspepsia (heartbrun)
-> UTI
-> Thrush

68
Q

How has thalidamide affected drug surveillance in pregnancy?

A

More cautious licensing and increased post-marketing surveillance with MHRA black triangle on medications that have lesser known effects and congenial malformation register.

69
Q

How is the risk of a drug assessed in pregnancy?

A

Stage of pregnancy
Exposure to drugs
Clinical condition of mother
Previous obstetric history with malformation or recurrent abortion.

70
Q

What are the risks to foetus assessed in pregnancy?

A

Risk-Benefit ratio of benefits of treatment, risk of treatment and risk of maternal illness.

71
Q

What are the principles of prescribing in pregnancy?

A

Only prescribe lowest effective dose when necessary for the shortest time possible, considering stage of pregnancy. Avoid all drug treatment in the first trimester, polypharmacy and new unassessed drugs.

72
Q

What to ask in risk assessment for prescribing?

A

Age of patient
What drug taken- when, and why?
Past obstetric history
Past family history

73
Q

How to find information for prescribing n pregnancy?

A

(UTIS) UK teratology information service
NICE summaries and guidelines
Royal college of obstetrics and gynaecology
Green book- latest information on vaccines

74
Q

What is the issue with use of BNF for prescribing in pregnancy?

A

Limited information which reflects the manufacturers’ information that is only cautious and does not truly reflect risk.
Medline and Embase can be limited to case reports.

75
Q

How is pain treated in pregnancy?

A

Stepwise from non-pharmacological treatment with physiotherapy and transcutaneous electrical nerve stimulation.

Paracetomol is the ideal analgesia of choice in pregnancy but when ineffective, a weak opioid can be used but near delivery, this increases the risk of respiratory depression.

NSAIDs cannot be given after week 20 for inflammatory pain.

76
Q

How is hyperemesis gravidarum treated in pregnancy?

A

Non pharmacological treatment: Small and frequent high carb and low fat meals and ginger or acupuncture

Pharmacological treatment: 1st line treatment is cyclizine.
2nd line treatment is metoclopramide. Ondansetron is provided if symptoms are treatment resistant.

77
Q

How is constipation treated in pregnancy?

A

Constipation is caused by progesterone induced smooth muscle relaxation.

Non-pharmacological treatment: Increased fibre, fluid intake and exercise.

pharmacological treatment
1st line: bulk forming laxative isphagala husk which increases weight of faeces
2nd line: Osmotic laxatives
If resistance: glycerol suppository which provides rapid relief

78
Q

How is hayfever treated in pregnancy?

A

Non-pharmacological treatment: Avoiding allergen, using barrier ointment and nasal filter.

Pharmacological treatment include oral therapy or topical therapy.
Oral therapy: Oral anti-histamines cetridizine and loratidine. 2nd line is chlorphenamine.
Topical therapy: Mast cell destabilisers such as intransal corticosteroids

79
Q

How is epilepsy treated in pregnancy?

A

Evaluating the severity of epilepsy and the pharmacological risk and benefits of treatment. Use of leviteracetum and sodium valproate is contraindicated.

80
Q

How do benzodiazepines affect foetal development?

A

Blocks excitatory neurotransmitters which can lead to floppy infant syndrome and neonatal respiratory depression and withdrawal symptoms.

81
Q

When should NSAIDs be avoided in pregnancy?

A

After Week 20 —> this is because NSAIDs cause vasodilation and reduce blood flow to the foetal kidneys, causing foetal kidney impairment. NSAIDs inhibit prostaglandin production which can cause premature closure of the ductus arteriosus and prevents platelet aggregation.

Year 2 (247 decks)

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