30/3

Question 1

Mature follicle size

Answer 1

20mm

Question 2

PoD

Answer 2

peritoneal recess located between the posterior surface of the uterus and the anterior surface of the rectum.
lowest/ caudal most part of the parietal peritoneum.

Question 3

Head Circumference (HC) Measurement

Answer 3

1 Correct Plane
Transthalamic Plane
Ensure the scan includes the following key landmarks:
>Thalami
> CSP
> Falx Cerebri (Midline Echo)

2 Correct Fetal Head Shape
oval (not round or elongated).

3. Proper Caliper Placement
   outer-to-outer measurement
   Ensure the ellipse tool is correctly fitted to the head contour.
4. Avoiding Common Errors

HC is preferred over Biparietal Diameter (BPD) as BPD can be affected by head compression or molding, leading to errors.

Question 4

Teratogenic Effects of Drugs by Timing of Exposure
Embryonic Period (3–8 )

Answer 4

Embryonic Period (3–8 weeks, Organogenesis) Structural defects – Organ and skeletal malformations

Warfarin → Nasal hypoplasia, stippled epiphyses

Thalidomide → Limb defects

Isotretinoin → Craniofacial, CNS, cardiac defects

Question 5

Teratogenic Effects of Drugs by Timing of Exposure
Fetal Period (9 weeks to birth)

Answer 5

Growth restriction, functional deficits

NSAIDs → Premature ductus arteriosus closure

ACE inhibitors → Renal failure, lung hypoplasia

Tetracyclines → Tooth discoloration

Question 6

Methotrexae teratogenicity

Answer 6

Fetal aminopterin syndrome (craniofacial defects, malformations of the digits, and defects of the spine and ribs)

Question 7

Sickle cell - preconception care

Answer 7

Blood group and extended red cell phenotyping for antibodies

Liver, renal function

Hep B and C

Check Hb type of partner

Discuss prenatal diagnosis

Folic Acid 5 mg, Pen V

*** Stop hydroxycarbamide and ACE inhibitors (but not an indication for TOP if taken in pregnancy)

Question 8

Folic acid and IBD

Answer 8

5-ASAs, also known as aminosalicylates

mesalamine
sulfasalazine

(note ciclosporin is safe but assoc with iugr)

Question 9

Case–control studies:

Advantages and disadvantages

Answer 9

Advantages:

1. Permit the study of rare diseases.
2. Permit the study of diseases with long latency between exposure and manifestation.
3. Can be launched and conducted over relatively short time periods.
4. Relatively inexpensive as compared to cohort studies.
5. Can study multiple potential causes of disease.

Disadvantages:

1. Information on exposure and past history is primarily based on interview and may be subject to recall bias.
2. Validation of information on exposure is difficult, or incomplete, or even impossible.
3. By definition, concerned with one disease only.
4. Cannot usually provide information on incidence rates of disease.
5. Generally incomplete control of extraneous variables.
6. Choice of appropriate control group may be difficult.
7. Methodology may be hard to comprehend for nonepidemiologists, and correct interpretation of results may be difficult.

Question 10

Cohort studies:

Advantages and disadvantages

Answer 10

Advantages:

1. Allow complete information on the subject’s exposure, including quality control of data, and experience thereafter.
2. Provide a clear temporal sequence of exposure and disease.
3. Give an opportunity to study multiple outcomes related to a specific exposure.
4. Permit calculation of incidence rates (absolute risk) as well as relative risk.
5. Methodology and results are easily understood by nonepidemiologists.
6. Enable the study of relatively rare exposures.

Disadvantages:

1. Not suited for the study of rare diseases because a large number of subjects are required.
2. Not suited when the time between exposure and disease manifestation is very long, although this can be overcome in historical cohort studies.
3. Exposure patterns, for example, the composition of oral contraceptives, may change during the course of the study and make the results irrelevant.
4. Maintaining high rates of follow-up can be difficult.
5. Expensive to carry out because a large number of subjects are usually required.
6. Baseline data may be sparse because the large number of subjects does not allow for long interviews.

Question 11

Incidence and prevalence

Answer 11

Incidence describes the frequency of occurrence of new cases during a time period,

whereas prevalence describes what proportion of the population has the disease at a specific point in time (point prevalence) or during a period of time (period prevalence).

The prevalence P depends on both the incidence I and duration D of the disease (P = Incidence rate × D)

Prevalence (P) (also prevalence rate, point prevalence rate, or prevalence proportion) (0–1 or %):
(Existing no of people with disease at a specific time) / (no of individuals in the pop at that time)

Prevalence = (Incidence) x (disease duration)

Incidence = 2.5 new cases / 100,000 people annually

Disease duration = 1.25 years

Prevalence = (2.5 cases / 100,000 people annually) x (1.25 years) = 3.125 cases / 100,000 people

Question 12

Virchow’s triad:

Answer 12

hypercoagulability, stasis/turbulent blood flow, endothelial injury –> thrombus.

Question 13

Endometriosis Most common site

Answer 13

(from most to least)
ovaries
rectovaginal septum
pelvic peritoneum
laparotomy scars
umbilicus/appendix

Question 14

Ca assoc with endo

Answer 14

Increased risk of clear cell carcinoma of ovary and endometroid carcinoma.

Question 15

Endo histo

Answer 15

Glands and stroma outside uterus
haemosidderin laden macrophages

Question 16

Fibroids micro

Answer 16

spindle shaped
cigar shaped nucleus

cells are in bundles (whorled- swirling appearance of cells)

Question 17

MC degen fibroids

Answer 17

Hylaine degeneration: the most common degeneration (smooth muscle replaced by connective tissue – not painful)

homogeneous eosinophilic, proteinaceous

Question 18

The arias stella-reaction:

Answer 18

progesterone makes endometrium become more secretory in pregnancy (inc ectopic) or due to progesterone therapy –> get gland hyperplasia, more vacculoes etc.

Question 19

Acute vs chronic endimitritis histo

Answer 19

Acute endometritis: polymorphonuclear cell infiltration

Chronic endometritis: lymphoctytes and plasma cells infiltration.

Question 20

Effects of contraception on endometrium

Answer 20

COCP: Glandular atrophy, compact stroma, not very secretory (everything shinks and goes dry)

Mirena: decidual change/decidualisation, endometrium thins, weakly secretory

Cu-IUD on endometrium: mononuclear cell infiltration, squamous metaplasia. – All the M’s – metaplasia and Mononculear.

Question 21

Complete vs Partial Mole histo

Answer 21

Partial Mole
Villi: Normal, small and fibrotic with only a few swollen
Vessels containing RBCs
Less trophoblastic material
P57 gene present (this is a maternally expressed gene, hence indicates maternal tissue os present)

Complete Mole
All Villi odematous
Lack of blood vessels
Trophoblastic material hyperplasia in circumferential pattern

Question 22

risk of malignant transformation in benign cyst:

Answer 22

pre menopasues = 1/1000, post menopause = 3/1000.

Question 23

VIN:

Answer 23

rough lesions, with variable colour, turn white when add acetic acid (VIN + cancer not just cancer)

Question 24

LP vs LS

Answer 24

LS

White itchy atrophic areas

Doesn’t affect mucus membranes, but may get plaques in other cracks e.g. inner thigh, armpits, abdomen (looks like cigarette paper)– 10% have these, you can get this without genital symptoms.

2-5% risk of SCC.

LP

Affects skin, genitals and oral mucosa.

Hypertrophic papules on vagina. (planus is pink polygonal plaques)

Associated with anti-basement membrane antibodies.

3% risk SCC

Question 25

Type of Epithelium Lining femle repro tract

Answer 25

Ovaries Cuboidal Endometrium Fallopian Tubes Endocervix Columnar Vagina and ectocervix Stratified Squamous, non-keratinised Ureter and Bladder Transitional

Question 26

Gap junctions

Answer 26

found in myometrium, between muscle cells – the free passage of messengers 🡪 coordinated contraction There are low numbers of gap junctions during pregnancy, but higher numbers in labour.

Question 27

Protein synthesis

Answer 27

Transcription = DNA -> RNA. Catalysed by RNA polymerase. RNA then processed: Splicing removes introns, poly A tail and 5-methylated added to protect the ends, Translation= RNA -> proteins.

Question 28

Pregnelone is then made into specific steroids hormones by what two processes?

Answer 28

1. Oxygenation – add oxygen containing groups more soluble in aqueous substances 2. Action of hydroxysteroid dehydrogenase (HSD) enzymes Secondary oxygenation of alcohol groups, or reduction of ketone groups HSDs = short-chain alcohol dehydrogenases

Question 29

hows fetal oestrogen made?

Answer 29

16α-hydroxyandrostenedione to estriol (E3)

Question 30

how are steroids excreted?

Answer 30

In urine or poo (must be hydrophilic for this). They are made hydrophilic by a 2-step process: Creation of polar hydroxyl groups by CYP or HSD Add polar/charged chemical groups to polar hydroxyl group

Question 31

Prostaglandin synthesis

Answer 31

Arachidonic acid in phospholipids (found in membranes, released by phospholipase A) --- COX --->. PGH2 ---> all diff types of PGs PGF2α in endometrium (broken down quickly in the lungs)

Question 32

Glycolysis

Answer 32

Both aerobic and anaerobic respiration start with glycolysis which occurs under anerobic conditions in cytoplasm: C6H12O6 + 2NAD+ --> 2x pyruvate + 2 ATP (net gain). + 2NADH In aerobic conditions this pyruvate is then converted to Acetyl CoA or oxalacetate In anerobic condition this pyruvate is converted to lactate, 2x ATP and NAD+

Question 33

Anaerobic respiration: Pyruvate +NADH --> lactate + NAD+

Answer 33

Catalysed by lactate dehydrogenase The NAD+ is then used for glycolysis. The lactate then moves from the muscle cells back to the liver via the Cori Cycle cycle. The liver converts the lactate back to glucose. This prevents lactic acidosis. Metformin prevents the conversion of lactate--> glucose. In patients with CKD they can’t clear this lactate so are at increased risk of lactic acidosis.

Question 34

Aerobic respiration: Overall: C6H12O6 + 6O2 --> 6CO2 +6H20

Answer 34

In mitochondria Each mole of glucose --> 30-32 moles of ATP (vs anaerobic respiration which produces 2 moles) Pyruvate (3C’s) –(pyruvate dehydrogenase)--> acetyl CoA (2C’s) --> then used in citric acid/ krebs cycle to produce: 2CO2 + 3NADH +FADH2 + GTP. There is no gain or loss of carbon atoms in the krebs cycle cycle The NADH and FADH2 have been reduced in this reaction --> releasing electrons in to electron transport chain --> ATP synthesis + GTP--> ATP. Krebs: A series of reactions oxidize acetyl-CoA, releasing carbon dioxide and generating energy carriers (NADH, FADH2, and ATP/GTP). The cycle regenerates oxaloacetate, allowing it to continue.

Question 35

A 30-year-old woman presents to the antenatal clinic after a visit to her home country in Africa. She is suffering from flu-like symptoms, myalgia and her posterior cervical lymph nodes are found to be enlarged. Her temperature is 38.4°C. Her blood test CBC and ESR and CRP all are normal. What is the likely diagnosis?

Answer 35

acute toxoplasmosis. TOXOPLASmosis in mum symptoms Key Features Supporting Toxoplasmosis: Travel to Africa – Endemic areas for Toxoplasma gondii. Flu-like symptoms – Fever (38.4°C), myalgia, and generalized malaise. Posterior cervical lymphadenopathy – A classic sign of toxoplasmosis. Normal CBC, ESR, and CRP – Unlike bacterial infections, toxoplasmosis often presents without significant inflammatory markers. Next Steps: Serology for Toxoplasma gondii (IgM and IgG). HIV testing, as toxoplasmosis can be more severe in immunocompromised individuals. EBV and CMV serology to rule out viral causes. amniocentesis

Question 36

Rubella in mum symptoms

Answer 36

A 38-year-old woman from Sri Lanka attends her general practitioner at 10 weeks’ gestation. She is complaining of fever and has pains in her joints. She developed a rash yesterday. On examination, she has a temperature of 38.1°C, postauricular lymphadenopathy and a maculopapular rash over her torso. Rubella is diagnosed. What is the most likely fetal abnormality to occur as a result of this acute infection?

Question 37

Decidualisation:

Answer 37

Epithelial cells: develop pinopodes (foot like protrustions) loose polarity (polarity, is the aysmetric distribution of organelle) Become more secretory🡪 secrete factors to cause blastocyts to move towards it Express proteins that blastocyst can attach too Secrete mucin – prevents trophoblast binding Stromal cells: Grow bigger Become secretory Start making cytokines, growth factors and extracellular matrix, key in making sure trophoblast doesn’t invade too deep

Question 38

STS false positive

Answer 38

recent immunization, pneumonia, malaria, pregnancy in last 6 months, SLE, autoimmune disorders, acquired hemolytic anemia, leprosy, drug addiction.

Question 39

Sts rx preg

Answer 39

Benzyl-penicillin 2.4MU IM (Non pen alt is ceftriaxone but limited evidence) Early syphilis: <27/40 – single dose, after 28 weeks – 2x doses 1 week apart). Late latent/gumma: 3x doses each 1 week apart Neurosyphilis: 2 week course. Probenecid 500 mg 4 times daily orally for 14 days If syphilis treatment is completed less than 4 weeks prior to delivery, the infant should be given treatment for congenital syphilis at birth Congenital infection: ben pen 10/7 **NOTE: Ben pen contains phospholipids from soya lecithin. If you are allergic to peanut or soya, do not use this medicinal product***

Question 41

False negative syphilis serology

Answer 41

Treponemal screening tests are negative before a chancre develops and may be for up to 2 weeks afterwards. Negative results within 3 months of infection cannot exclude early syphilis. False-negative screening results may be seen in immunocompromised individuals A false-negative RPR test may occur in secondary or early latent syphilis due to the prozone phenomenon (false-negative result due to high antibody titres) when testing undiluted serum; in such cases negative tests on undiluted serum samples should be repeated on diluted samples .---> more likely to occur in individuals living with HIV.

Question 42

False-positive syphilis serology

Answer 42

Occasional false-positive results may occur with any of the serological tests for syphilis. In general, false-positive reactivity is more likely in older individuals, those with autoimmune disease and people who inject drugs. In the absence of symptoms of syphilis or a history of syphilis, transient or persistent reactivity in a single treponemal test should be considered to be a false positive result.

Question 43

Sts screening

Answer 43

An EIA/CLIA detecting both IgM and IgG is the screening test of choice: · Positive screening tests should be confirmed with a different treponemal test and a second specimen for confirmatory testing obtained · A quantitative RPR test should be performed when screening tests are positive: · Negative serological tests for syphilis should be repeated at 2 weeks after observation of possible chancres that are dark ground microscopy and/or PCR negative

Question 44

Serological response different in hiv vs non hiv for sts

Answer 44

slower --> Routine syphilis serological screening for people living with HIV at 6-monthly interval is recommended

Question 45

Sts rx

Answer 45

Early benpen G 2.4 MU IM stat (Procaine penicillin G 600,000 units IM OD for 10 days; Doxycycline 100 mg PO BD for 14 days) Late latent, cardiovascular and gummatous syphilis Benzathine penicillin 2.4 MU IM weekly for 3 weeks Doxycycline 100 mg PO BD for 28 days Neurosyphilis including neurological involvement in early syphilis Procaine penicillin 1.8–2.4 MU IM OD PLUS probenecid 500 mg PO QDS for 14 days ***Steroids should be given with all anti-treponemal antibiotics for neurosyphilis; 40–60 mg prednisolone OD for 3 days starting 24 h before the antibiotics.***

Question 46

TV

Answer 46

get perinuclear halo’s Itching strawberry cervix

Question 47

Chancroid

Answer 47

lots of small painful ulcers, then chancroid develops Haemophillus Ducreyi

Question 48

Mulluscum Contagiosum what virus

Answer 48

poxvirus

Question 49

Toxic Shock Syndrome

Answer 49

Staph A, Strep Pyogenes. Clindamycin.

Question 50

Booking visit test for?

Answer 50

HIV, Hep B&C, Syphilis, Rubella

Question 51

when does VZV IGG become positive

Answer 51

4 days after infection Fetal transmission rate: T3 – 20-50%, <24/408 = 8%.

Question 52

CMV

Answer 52

Enveloped dsDNA, Herpes virus 5

Question 53

Parvovirus B19:

Answer 53

rash 16 days after infection, no longer infectious when rash develops Can cause aplastic crisis in those with sickle celL If antigens show serocoversion (as not immune) 🡪 extra scans Infection early in pregnancy has greater risk

Question 54

Hepatitis in pregnancy

Answer 54

All hepatits apart from Hep A can be transmitted vertically.

Question 55

Treatment of hep c in pregnancy

Answer 55

Treatment of HCV with DAAs during pregnancy is not recommended due to insufficient safety data. Pregnant women should avoid most HCV antiviral medications, especially ribavirin, which is teratogenic (can cause birth defects). Regular monitoring of liver function and viral load is recommended during pregnancy. Infants born to HCV-positive mothers should be tested for HCV at age 18 months (since maternal antibodies can persist for up to a year). HCV RNA PCR is the best method for confirming infection in the infant.

Question 56

Hep B in pregnancy

Answer 56

Spreads via blood, or sex. 1-5 month incubation period. Mainly acute infection is mild flu-like symptoms. Chronic infection --> HCC. If catch from someone --> 10% of people develop chronic Hep B, if pass via placenta 90% of children end up with chronic hep B.

Question 57

HPV

Answer 57

Double stranded circular DNA virus. Microscope: can see koilocytes with a (like TV) perinuclear halo

Question 58

Toxoplasmosis.

Answer 58

Higher prevalence in africa lymphadenopathy and flu like symptoms, hepatosplenomegaly. spiramycin

Question 59

Nitrofurantoin:

Answer 59

Risk of neonatal hemolysis at term CI in breastfeeding, as can produce hemolysis in babies with G6PD- deficieny.

Question 60

Acrocentric chromosomes

Answer 60

Acrocentric: Centromere close to the end 13, 15, 21, 22 may have balanced translocations Robertsonian > balanced 1 in 100; Rate of misc: 30-50% Cause 3-5% recurrent misc > Unbalanced cause trisomys

Question 61

Non invasive fetal DNA testing

Answer 61

Through mat blood We need about 4-5% of free fetal DNA in maternal blood for the test to be reliable. The fetal DNA is from trophoblast secretion. Factors decreasing fetal DNA: maternal obesity

Question 62

Downs synd

Answer 62

95% Non disjunctions in the first meiosis 3% unbalanced Robertsonian translocation T(14;21) 1-2% mosaics.

Question 63

SIckle Cell Disease

Answer 63

AR. MUTATION beta globin. Valanine switched to glutamic acid. Beta globin not present in fetal Hb so no effects to fetus/neonate Ix: Hb electrophoresis: HbA = normal Adult, HbF = fetal, HbS = sickle cell, Other things you could find: HbC = Hb C disease, HbH = HDH disease, There are 2 types of HbA (1+2): 1 should make >95% of HbA in adult ---> increase HbA2 = beta thalassemia

Question 64

Beta Thalassemia

Answer 64

Mutation: HBB gene (Chr 11), AR, heterozygous= minor/trait carrier, major = homozygous HbA1 should be >95% of HbA, if HbA2 is higher than normal this is beta thalasemia Major = severe transfusion dependent anaemia Management in pregnancy: Increased risk of the following conditions so screen for these: Diabetes, Thyroid problems, Increased heart strain due to anaemia: hence need to be under cardiologist: need ECG, ECHO and MRI (risk of iron overload) Biliary USS& Ferriscan or MRI Neural tube defects: folic acid supplements Extra early scan at 8 weeks (7-9 weeks) + scans every 4 weeks from 24/40 Thromboprophylaxis: If splenectomy + plt>600 🡪 LMWH and Aspirin 75mg If not on LMWH in community, will need on hospital admission

Question 65

Alpha thalassemia

Answer 65

mutation in alpha -globin genes (ch16). You have 2 genes from mum and 2 genes from dad to code for 2x alpha globin. Alpha thalassemia silent carrier: mutation in 1 gene, 3 normal genes – often asymptomatic. Alpha thalassemia carrier: mutation in 2/4 genes - often mild anamemia HbH disease is when you have a mutation in 3 out of 4 genes, but one functional gene Alpha thalassemia major = all 4 genes mutated -> death in uteus Bart’s haemoglobin and HbH

Question 66

Reciprocal translocations

Answer 66

Only metacentric (centromere in middle) Part of chromosome arms swaps Most commonly long arm (q of Chr 11 and 22) 1/500 people have reciprocal translocation Presentation: normal phenotype as still have all genetic material, however children may have not full set 🡪 1-10% have problems

Question 67

Gestational diabetes diagnosis

Answer 67

Fasting 6.1 2 hour 7.8

Answer 68

Follow-up Based on HPV Testing: HPV Negative: Return to routine 3-yearly screening as per national guidelines. HPV Positive: Refer for colposcopy to assess for underlying cervical intraepithelial neoplasia (CIN).

Question 69

Role of fetal dhea

Answer 69

stimulates placenta to form oestogen

Answer 70

Conns - salt, Aldos:renin ratio Cushings - dexa supression Addisons - short synacthen Morning cortisol : Cushing's syndrome (high cortisol) or Addison's disease (low cortisol).

Question 71

Cons

Answer 71

Aldosterone hyperrrr secretion hypocalc hypokal hypernat hypertension Addisons opposite hypercals hyperkal hyponat hypotension hypoglycemia tooo

Question 72

thyroid hormones in preg

Answer 72

decreased tsh increased t3 and 4

Question 73

amniocentesis

Answer 73

15+weeks

Question 74

Factor 5 def blood tests

Answer 74

PT prolonged

Question 75

decreases shbg

Answer 75

B. Hepatic cirrhosis C. Hyperprolactinaemia D. Hypogonadism E. Hypothyroidism

Question 76

increases shbg

Answer 76

A. Growth hormone