Obs and gynae Flashcards

1
Q

Goserelin

A

Gonadorelin analogue

Use: testosterone reduction in prostate cancer, preparation for IVF

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2
Q

Infertility drugs

A

Human menopausal gonadotrophin, Clomifene

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3
Q

Oestrogen based combined oral contraceptives

A

E.g. Gedarel, Mercilon, Yasmin, Femodene, Cilest, Microgynon
Suppress LH/FSH release and therefore ovulation. Some can reduce menstrual pain and bleeding, and improvements in acne.
Can cause irregular bleeding and mood changes. Oestrogens double the risk of VTE but the absolute risk remains low. They also increase the risk of CVD and stroke. May also be assoc. with increased risk of cervical and breast cancers.
CI in breast cancer.
Avoided in those with increased risk of VTE (personal or family Hx, known thrombophilia) or CVD (>35, other RFs, migraine with aura, heavy smoking Hx).
Cytochrome P450 inducers (rifampicin, carbamazepine) may reduce contraceptive efficacy. Absorption of lamotrigine may be reduced.

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4
Q

Progesterone-only oral contraceptives

A

Desogestrel or Levonorgestrel based
Suppress LH/FSH release and therefore ovulation. Also have a local effect at the cervix/endometrium which contribute to their contraceptive affect.
Can cause irregular bleeding and mood changes.
CI in breast cancer.
Cytochrome P450 inducers (rifampicin, carbamazepine) may reduce contraceptive efficacy. Absorption of lamotrigine may be reduced.

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5
Q

Long-acting reversible contraceptives

A

Nexplanon implant (3 years), Depo-Provera IM injection (3 years)

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6
Q

Spermicidal contraceptives

A

Nonoxinol

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7
Q

Contraceptive devices and intra-uterine systems

A

Mirena IUS (5 years, levonorgestrel based), Jaydess IUS (3 years, levonorgestrel based), Nova-T 380 (copper coil, 5 years), TT 380 slimline (copper coil, 10 years)

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8
Q

Emergency contraception

A

Levonorgestrel, ulipristal, copper intra-uterine contraceptive device

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9
Q

Induction of abortion

A

Gemeprost (PGE1 analogue), Mifepristone (progesterone receptor antagonist)

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10
Q

Hormonal therapy for HRT

A

Oestradiol alone or with progestogens, Raloxifene, Tibolone
The relative risks are higher than with oral combined contraceptives.
CI in breast cancer.
Avoided in those with increased risk of VTE (personal or family Hx, known thrombophilia) or CVD (>35, other RFs, migraine with aura, heavy smoking Hx).
Cytochrome P450 inducers (rifampicin, carbamazepine) may reduce contraceptive efficacy. Absorption of lamotrigine may be reduced.

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11
Q

Antidepressants for peri-menopausal symptoms

A

Fluoxetine, citalopram, venlafaxine

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12
Q

Induction and augmentation of labour

A

Oxytocin, Dinoprostone (exogenous PGE2)

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13
Q

Prevention and treatment of PPH

A

Ergometrine, oxytocin (Syntometrine), Carboprost (PG)

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14
Q

Preterm labour

A

Atosiban (oxytocin receptor antagonist), nifedipine (CCB), salbutamol (beta2 agonist)

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15
Q

Pregnancy-related nausea

A

Promethazine, cyclizine (both 1st line), metoclopramide, ondansetron (both 2nd line)

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16
Q

What are the considerations in pregnancy?

A

Changes to the mother’s physiology
Drugs passing through placenta to foetus
Drugs passing through breast milk to baby
Less available licensed medications
Minimal evidence base (due to ethics)
Patient/healthcare professional anxiety surrounding prescribing in pregnancy
Dose alterations required in pregnancy

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17
Q

CV/blood physiological changes during pregnancy

A

Increased plasma vol, CO, SV, HR and coagulation factors
Decreased serum albumin conc. and serum colloid osmotic P
Protects woman from PPH but causes risk of VTE
Bloods: dilution anaemia, leucocytosis, low albumin

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18
Q

Renal physiological changes during pregnancy

A

Increased renal BF and GFR
Results in increased excretion and reduced blood levels of urea and creatinine
Mild glycosuria and proteinuria may occur (increased GFR exceeds ability of tubules to absorb glucose/protein)
Relaxation/dilation of renal pelvis and ureters, increased length of kidneys and relaxation of bladder SM
Increased risk of UTI due to increased capacity of bladder

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19
Q

Liver physiological changes during pregnancy

A

Changes in oxidative liver enzymes e.g. cytochrome P450

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20
Q

Lung physiological changes during pregnancy

A

Increased tidal vol and minute vent.
Due to increased progesterone conc.
Inhaled meds may be more readily absorbed.
State of respiratory alkalosis overall (reduced pCO2, increased O2 and decreased bicarb)

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21
Q

GIT physiological changes during pregnancy

A

Reduced gastric motility allows increased nutrient absorption but can result in constipation
Progesterone causes relaxation of the lower oesophageal sphincter and increased reflux

22
Q

Pregnancy: changes to absorption

A

Delayed gastric emptying and prolonged transit time alters drug bioavailability, with prolonged time to reach peak levels after oral administration and an overall decrease in maximum concentration achieved
Factors such as nausea and vomiting can also affect absorption, and ability to administer medication orally

23
Q

Pregnancy: changes to distribution

A

Maternal intravascular fluid vol begins to increase in T1 of pregnancy, as a result of increased production of RAAS which promotes sodium absorption and water retention. Increased total body water/extracellular fluid increases the volume of distribution of water-soluble drugs. Clinically, this could necessitate a higher initial and maintenance dose of drugs to obtain therapeutic plasma concentrations. Lipid-soluble drugs are also affected due to increased fat compartment stores, with an increased volume of distribution.
With increasing plasma vol, there is an assoc. reduction in maternal plasma protein concentration. Decreased plasma albumin concentration leads to decreased protein binding and increases free fraction of the drug. This is important for drugs such as midazolam, digoxin, phenytoin, valproic acid. The free drug concentration is responsible for drug effects but may be off-set by changes in metabolism and elimination

24
Q

Pregnancy: changes to metabolism

A

Cytochrome P450 is a family of liver enzymes and a major route of drug metabolism
Altered cytochrome P450 activity in pregnancy (unchanged/increased/decreased) alters oral bioavailability and hepatic elimination

25
Q

Pregnancy: changes to elimination

A

Increased renal BF and GFR increases renal clearance
The increase in renal clearance can have significant increase in the elimination rates of renally cleared medications leading to shorter half-lives, requiring higher doses of medications
Important for drugs such as penicillin antibiotics, digoxin and lithium

26
Q

Risk of birth defects for epileptic mothers

A

2-3% in the general population will have a baby with a major malformation (the ‘background risk’)
3% who have epilepsy and do not take AEDs will have a baby with a major malformation
4-10% who have epilepsy and do take an AED will have a baby with a major malformation

27
Q

Problems of using medications during pregnancy

A

Teratogenesis
Effects on growth and development (neurological or neurodevelopmental abnormalities through early childhood)
Effects on the neonate during delivery e.g. premature closure of patent ductus with use of PGs
Passage of drug through breast milk
Long term effects on IQ or behavioural problems

28
Q

Prescribing principles

A

Counselling - risk vs. benefit, minimise drug use in T1, small effective dose, use well-know meds, mono therapy if possible, consider non-drug options, monitor meds and their effects
Exposure to potential teratogens often precedes conception and first contact with a healthcare professional; it may not convey any added benefit to stop treatment if exposure has already occurred
Folic acid - 400 micrograms daily recommended pre-conception to 12 w gestation; 5 mg recommended if higher risk e.g. AEDs, diabetes, FHx of neural tube defects, sickle cell

29
Q

Why drugs cross the placenta

A

Physical - placental surface area, placental thickness, pH of maternal/foetal blood, placental metabolism, uteroplacental BF, presence of drug transporters
Pharmacological - molecular weight of drug (<1 kDa), lipid solubility, protein binding, conc. gradient

30
Q

3 mechanisms of placental transfer

A

Complete transfer with drugs rapidly crossing the placenta and equilibrating in maternal and foetal blood
Exceeding transfer with drugs crossing the placenta to reach greater concentrations in foetal compared with maternal blood
Incomplete transfer with drugs incompletely crossing the placenta resulting in higher concentrations in maternal compared with foetal blood

31
Q

Initial management of N&V

A
Reassurance and rest - this is a normal part of pregnancy and usually resolves by 16-20 w gestation
Avoid triggers
Eat plain crackers in the morning
Eat bland, small and frequent meals
Cold meals if nausea if smell-related
Drinking little and often
Ginger
Acupressure
32
Q

Hx of thalidomide

A

This is an immunomodulator
It was initially marketed as a sedative, but used to treat pregnancy-related nausea
Found to cause phocomelia and deformities of the ears, heart and kidneys
40% mortality rate
Now its use is limited to the treatment of multiple myeloma
The birth defects caused by this drug varied depending on gestational age

33
Q

Drug teratogenicity effects in the different trimesters

A

T1 - most susceptible weeks are 3-8, this affects organogenesis
T2 or T3 - manifest as growth retardation, respiratory problems, infection of bleeding in the neonate

34
Q

Teratogenic effects of ACEi

A

Renal abnormalities, patent ductus arteriosus, oligohydramnios
T2/3

35
Q

Teratogenic effects of anti-thyroid drugs

A

Neonatal hypothyroidism

>10 w

36
Q

Teratogenic effects of beta-blockers

A

IUGR, neonatal hypoglycaemia, bradycardia

Throughout pregnancy

37
Q

Teratogenic effects of lithium

A

Cardiac defects - Ebstein’s anomaly; congenital heart defect in which the septal and posterior leaflets of the tricuspid valve are displaced towards the apex of the RV
T1

38
Q

Teratogenic effects of methotrexate

A

Medical termination, craniofacial defects, ear/kidney/lung defects, cardiac abnormalities

39
Q

Teratogenic effects of NSAIDs

A

premature closure of ductus arteriosus, oligohydramnios, PPH

>30 w

40
Q

Teratogenic effects of Phenytoin

A

Craniofacial abnormalities, growth/mental deficiency

41
Q

Teratogenic effects of retinoids

A

CNS abnormalities, renal/eye/ear/parathyroid abnormalities

Weeks 4-10

42
Q

Teratogenic effects of sodium valproate

A

NTDs

T1

43
Q

Teratogenic effects of tetracyclines

A

Tooth discolouration

T2/3

44
Q

Teratogenic effects of thiazide diuretics

A

electrolyte abnormalities, growth retardation

45
Q

Teratogenic effects of warfarin

A

foetal warfarin syndrome, CNS defects, eye abnormalities, foetal/neonatal/placental haemorrhage

46
Q

Safer drugs in pregnancy

A

paracetamol, beta-lactam based antibiotics, steroids, bronchodilators, labetalol, nifedipine

47
Q

Drugs which can cause genetic abnormalities in the sperm

A

Antimetabolites drugs e.g. methotrexate, azathioprine, mercaptopurine
Delay conception for 6/12 after discontinuation

48
Q

Drugs to avoid in breastfeeding

A
Amiodarone - neonatal hypothyroidism due to iodine content
Aspirin - Reye's syndrome
Barbiturates - drowsiness
Benzos - lethargy
Carbiazmole - hypothyroidism
Codeine - opioid OD
Combined oral contraceptive - diminish milk supply and quantity
Cytotoxic drugs - immunosuppression
DA agonists - suppress lactation
Ephedrine - irritability
Tetracyclines - tooth discolouration
49
Q

Infections in pregnancy

A

Broad-spectrum antibiotics (cephalosporins), steroids if overwhelming infection (betamethasone IM injections, max of 2 doses)

50
Q

Anaemia in pregnancy

A

Ferrous sulphate if iron-deficiency

Check B12 and folate for deficiencies