Membership of the Royal College of Obstetricians and Gynaecologists (MRCOG) Basic and Applied Sciences for Reproductive Health (Part 1 Foundations) Flashcards

24 sample cards from the Basic and Applied Sciences for Reproductive Health (Part 1 Foundations) deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. List the main types of membrane transport across a cell membrane.

   Passive: simple diffusion and facilitated diffusion (channels/carriers, down gradient, no energy). Active: primary active transport (ATP-driven, e.g. $\text{Na}^+/\text{K}^+$-ATPase) and secondary active transport (symport/antiport using an ion gradient). Plus endocytosis/exocytosis for bulk transport.

2. Describe the Henderson-Hasselbalch equation and normal arterial values.

   $$\text{pH} = \text{p}K_a + \log_{10}\frac{[\text{HCO}_3^-]}{0.03 \times \text{PaCO}_2}$$ Normal arterial pH $= 7.35\text{-}7.45$, $\text{PaCO}_2 \approx 4.7\text{-}6.0\ \text{kPa}$ ($35\text{-}45\ \text{mmHg}$), $[\text{HCO}_3^-] \approx 22\text{-}26\ \text{mmol/L}$.

3. How is the anion gap calculated and what does a raised value suggest?

   $$\text{Anion gap} = ([\text{Na}^+] + [\text{K}^+]) - ([\text{Cl}^-] + [\text{HCO}_3^-])$$ Normal ~$8\text{-}16\ \text{mmol/L}$. A raised anion gap metabolic acidosis suggests lactate, ketones, renal failure or toxins (mnemonic MUDPILES).

4. Describe the inheritance pattern and recurrence risk of an autosomal recessive condition.

   Both parents are unaffected carriers; affected offspring are homozygous. Each child of two carriers has a $\frac{1}{4}$ ($25\%$) risk of being affected, $\frac{1}{2}$ of being a carrier, and $\frac{1}{4}$ unaffected non-carrier. Risk is increased by consanguinity; e.g. cystic fibrosis, sickle cell.

5. Contrast X-linked recessive inheritance with autosomal dominant inheritance.

   X-linked recessive: males affected, females usually carriers, NO male-to-male transmission, all daughters of an affected male are carriers (e.g. haemophilia). Autosomal dominant: each child of an affected heterozygote has a $\frac{1}{2}$ risk, both sexes affected, male-to-male transmission occurs (e.g. Huntington's).

6. Define non-disjunction and give the recurrence risk of trisomy 21 by maternal age.

   Non-disjunction is failure of chromosome pairs (meiosis I) or sister chromatids (meiosis II) to separate, producing aneuploid gametes. Trisomy 21 risk rises with maternal age: ~$1\text{ in }1500$ at age $20$, ~$1\text{ in }900$ at $30$, ~$1\text{ in }100$ at $40$.

7. Compare the karyotypes and key features of Turner, Klinefelter, Down, Edwards and Patau syndromes.

   Turner $45,\text{X}$ (short stature, streak ovaries); Klinefelter $47,\text{XXY}$ (tall, hypogonadism); Down (trisomy 21); Edwards (trisomy 18, rocker-bottom feet); Patau (trisomy 13, holoprosencephaly/cleft). Edwards and Patau carry very poor prognosis.

8. Distinguish a Robertsonian translocation from a reciprocal translocation.

   Robertsonian: fusion of two acrocentric chromosomes ($13,14,15,21,22$) at the centromere with loss of short arms; a balanced carrier has $45$ chromosomes and risks trisomic offspring (e.g. translocation Down syndrome). Reciprocal: exchange of segments between two non-homologous chromosomes; balanced carriers are usually phenotypically normal but risk unbalanced gametes.

9. Outline how PCR works and the steps of each cycle.

   PCR amplifies a DNA target through repeated cycles: (1) denaturation (~$95^{\circ}\text{C}$, strands separate), (2) annealing (~$50\text{-}65^{\circ}\text{C}$, primers bind), (3) extension (~$72^{\circ}\text{C}$, Taq polymerase synthesises new strands). Amplification is exponential — $n$ cycles give up to $2^{n}$ copies.

10. Differentiate karyotyping, FISH, microarray (CGH) and NIPT in prenatal genetic testing.

    Karyotyping detects aneuploidy and large structural rearrangements. FISH gives rapid targeted detection of specific chromosomes/loci. Microarray (array CGH) detects sub-microscopic copy-number variants but not balanced rearrangements. NIPT analyses cell-free fetal DNA in maternal plasma — a high-sensitivity SCREENING test for common trisomies.

11. State the Hardy-Weinberg equations and the assumptions required for equilibrium.

    $$p + q = 1 \quad\text{and}\quad p^{2} + 2pq + q^{2} = 1$$ where $p^{2}$ and $q^{2}$ are homozygote frequencies and $2pq$ heterozygotes. Assumptions: large population, random mating, no mutation, no migration, no selection.

12. For an autosomal recessive disease with incidence $1\text{ in }2500$, calculate the carrier frequency using Hardy-Weinberg.

    $q^{2} = \frac{1}{2500}$, so $q = \frac{1}{50} = 0.02$. Then $p \approx 0.98$, and carrier frequency $2pq = 2 \times 0.98 \times 0.02 \approx 0.039$, i.e. about $1\text{ in }25$.

13. Name important organisms causing chorioamnionitis/preterm labour and neonatal early-onset sepsis.

    Group B Streptococcus ($\textit{Streptococcus agalactiae}$) is the leading cause of early-onset neonatal sepsis; others include $\textit{E. coli}$, $\textit{Listeria monocytogenes}$, and ascending genital tract anaerobes/$\textit{Ureaplasma}$ in chorioamnionitis.

14. Which organisms cause the TORCH congenital infections?

    Toxoplasma gondii; Other (syphilis/$\textit{Treponema pallidum}$, parvovirus B19, VZV, Listeria); Rubella; Cytomegalovirus (commonest congenital infection); Herpes simplex virus. These cross the placenta and cause congenital anomalies.

15. Differentiate the cells and timing of innate versus adaptive immunity.

    Innate: immediate, non-specific, no memory — neutrophils, macrophages, NK cells, complement, physical barriers. Adaptive: slower, antigen-specific, generates memory — T lymphocytes (cell-mediated) and B lymphocytes/plasma cells (humoral, antibodies).

16. Why is IgG important in pregnancy and which antibody is the largest?

    IgG is the only immunoglobulin actively transported across the placenta (via Fc receptors), giving the fetus/neonate passive immunity — but also mediating haemolytic disease (e.g. anti-D). IgM is the largest (pentamer), does not cross the placenta, and indicates acute/fetal infection if found in cord blood.

17. List the four types of hypersensitivity reactions with an obstetric/gynaecological example.

    Type I (IgE, immediate — anaphylaxis/latex allergy); Type II (antibody-mediated cytotoxic — rhesus haemolytic disease of the newborn); Type III (immune complex — SLE, pre-eclampsia features); Type IV (delayed, T-cell mediated — contact dermatitis, graft rejection).

18. Define the key pharmacokinetic parameters: bioavailability, volume of distribution, clearance and half-life.

    Bioavailability ($F$): fraction of dose reaching systemic circulation. Volume of distribution: $V_d = \frac{\text{dose}}{C_0}$. Clearance ($CL$): volume cleared per unit time. Half-life: $t_{1/2} = \frac{0.693 \times V_d}{CL}$.

19. Contrast zero-order and first-order kinetics.

    First-order: a constant FRACTION of drug is eliminated per unit time (rate proportional to concentration); most drugs follow this. Zero-order: a constant AMOUNT is eliminated per unit time (saturated enzymes), e.g. phenytoin, alcohol — small dose increases cause disproportionate rises in concentration.

20. How are drugs classified for use in pregnancy regarding placental transfer?

    Transfer is greater for drugs that are lipophilic, of low molecular weight ($< 500\ \text{Da}$), un-ionised, and poorly protein-bound. Drug effect on the fetus depends on gestation (organogenesis weeks $3\text{-}8$ carries greatest teratogenic risk).

21. Define drug potency versus efficacy, and agonist versus antagonist.

    Potency = the concentration/dose producing a given effect (reflected by $EC_{50}$); efficacy = the maximal effect achievable. An agonist binds and activates a receptor (full or partial); an antagonist binds without activating — competitive antagonists shift the dose-response curve right (surmountable).

22. Compare the mechanism of action of the main uterotonics: oxytocin, ergometrine, carboprost and misoprostol.

    Oxytocin: binds myometrial oxytocin receptors → contraction (caution: vasodilatation/hypotension). Ergometrine: ergot alkaloid causing sustained contraction (avoid in hypertension). Carboprost ($\text{PGF}_{2\alpha}$): prostaglandin (avoid in asthma — bronchospasm). Misoprostol ($\text{PGE}_1$ analogue): oral/rectal, stable, used for PPH and induction.

23. Compare the main classes of tocolytics used to suppress preterm labour.

    Calcium-channel blockers (nifedipine, first-line in UK); oxytocin-receptor antagonists (atosiban); $\beta_2$-agonists (terbutaline — now less used, cardiac side effects); COX inhibitors (indometacin — risk of ductus arteriosus closure and oligohydramnios); magnesium sulfate (mainly for fetal neuroprotection).

24. Summarise the mechanisms of the major antimicrobial classes relevant to obstetrics.

    $\beta$-lactams (penicillins, cephalosporins): inhibit cell-wall synthesis. Macrolides (erythromycin) and aminoglycosides (gentamicin): inhibit protein synthesis. Metronidazole: damages anaerobic DNA. Avoid tetracyclines (teeth staining), quinolones and trimethoprim (1st trimester, folate antagonist) in pregnancy.

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