30/3 Flashcards
Mature follicle size
20mm
PoD
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.
Head Circumference (HC) Measurement
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).
- Proper Caliper Placement
outer-to-outer measurement
Ensure the ellipse tool is correctly fitted to the head contour. - Avoiding Common Errors
HC is preferred over Biparietal Diameter (BPD) as BPD can be affected by head compression or molding, leading to errors.
Teratogenic Effects of Drugs by Timing of Exposure
Embryonic Period (3–8 )
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
Teratogenic Effects of Drugs by Timing of Exposure
Fetal Period (9 weeks to birth)
Growth restriction, functional deficits
NSAIDs → Premature ductus arteriosus closure
ACE inhibitors → Renal failure, lung hypoplasia
Tetracyclines → Tooth discoloration
Methotrexae teratogenicity
Fetal aminopterin syndrome (craniofacial defects, malformations of the digits, and defects of the spine and ribs)
Sickle cell - preconception care
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)
Folic acid and IBD
5-ASAs, also known as aminosalicylates
mesalamine
sulfasalazine
(note ciclosporin is safe but assoc with iugr)
Case–control studies:
Advantages and disadvantages
Advantages:
- Permit the study of rare diseases.
- Permit the study of diseases with long latency between exposure and manifestation.
- Can be launched and conducted over relatively short time periods.
- Relatively inexpensive as compared to cohort studies.
- Can study multiple potential causes of disease.
Disadvantages:
- Information on exposure and past history is primarily based on interview and may be subject to recall bias.
- Validation of information on exposure is difficult, or incomplete, or even impossible.
- By definition, concerned with one disease only.
- Cannot usually provide information on incidence rates of disease.
- Generally incomplete control of extraneous variables.
- Choice of appropriate control group may be difficult.
- Methodology may be hard to comprehend for nonepidemiologists, and correct interpretation of results may be difficult.
Cohort studies:
Advantages and disadvantages
Advantages:
- Allow complete information on the subject’s exposure, including quality control of data, and experience thereafter.
- Provide a clear temporal sequence of exposure and disease.
- Give an opportunity to study multiple outcomes related to a specific exposure.
- Permit calculation of incidence rates (absolute risk) as well as relative risk.
- Methodology and results are easily understood by nonepidemiologists.
- Enable the study of relatively rare exposures.
Disadvantages:
- Not suited for the study of rare diseases because a large number of subjects are required.
- Not suited when the time between exposure and disease manifestation is very long, although this can be overcome in historical cohort studies.
- Exposure patterns, for example, the composition of oral contraceptives, may change during the course of the study and make the results irrelevant.
- Maintaining high rates of follow-up can be difficult.
- Expensive to carry out because a large number of subjects are usually required.
- Baseline data may be sparse because the large number of subjects does not allow for long interviews.
Incidence and prevalence
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
Virchow’s triad:
hypercoagulability, stasis/turbulent blood flow, endothelial injury –> thrombus.
Endometriosis Most common site
(from most to least)
ovaries
rectovaginal septum
pelvic peritoneum
laparotomy scars
umbilicus/appendix
Ca assoc with endo
Increased risk of clear cell carcinoma of ovary and endometroid carcinoma.
Endo histo
Glands and stroma outside uterus
haemosidderin laden macrophages
Fibroids micro
spindle shaped
cigar shaped nucleus
cells are in bundles (whorled- swirling appearance of cells)
MC degen fibroids
Hylaine degeneration: the most common degeneration (smooth muscle replaced by connective tissue – not painful)
homogeneous eosinophilic, proteinaceous
The arias stella-reaction:
progesterone makes endometrium become more secretory in pregnancy (inc ectopic) or due to progesterone therapy –> get gland hyperplasia, more vacculoes etc.
Acute vs chronic endimitritis histo
Acute endometritis: polymorphonuclear cell infiltration
Chronic endometritis: lymphoctytes and plasma cells infiltration.
Effects of contraception on endometrium
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.
Complete vs Partial Mole histo
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
risk of malignant transformation in benign cyst:
pre menopasues = 1/1000, post menopause = 3/1000.
VIN:
rough lesions, with variable colour, turn white when add acetic acid (VIN + cancer not just cancer)
LP vs LS
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
Type of Epithelium Lining
femle repro tract
Ovaries
Cuboidal
Endometrium Fallopian Tubes Endocervix
Columnar
Vagina and ectocervix
Stratified Squamous, non-keratinised
Ureter and Bladder
Transitional
Gap junctions
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.
Protein synthesis
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.
Pregnelone is then made into specific steroids hormones by what two processes?
- Oxygenation – add oxygen containing groups
more soluble in aqueous substances - Action of hydroxysteroid dehydrogenase (HSD) enzymes
Secondary oxygenation of alcohol groups, or reduction of ketone groups
HSDs = short-chain alcohol dehydrogenases
hows fetal oestrogen made?
16α-hydroxyandrostenedione to estriol (E3)
how are steroids excreted?
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
Prostaglandin synthesis
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)
Glycolysis
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+
Anaerobic respiration: Pyruvate +NADH –> lactate + NAD+
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.
Aerobic respiration: Overall: C6H12O6 + 6O2 –> 6CO2 +6H20
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.
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?
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
Rubella in mum symptoms
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?
Decidualisation:
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
STS false positive
recent immunization, pneumonia, malaria, pregnancy in last 6 months, SLE, autoimmune disorders, acquired hemolytic anemia, leprosy, drug addiction.
Sts rx preg
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*
False negative syphilis serology
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.
False-positive syphilis serology
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.
Sts screening
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
Serological response different in hiv vs non hiv for sts
slower –> Routine syphilis serological screening for people living
with HIV at 6-monthly interval is recommended
Sts rx
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.
TV
get perinuclear halo’s
Itching
strawberry cervix
Chancroid
lots of small painful ulcers, then chancroid develops
Haemophillus Ducreyi
Mulluscum Contagiosum what virus
poxvirus
Toxic Shock Syndrome
Staph A, Strep Pyogenes. Clindamycin.
Booking visit test for?
HIV,
Hep B&C,
Syphilis,
Rubella
when does VZV IGG become positive
4 days after infection
Fetal transmission rate:
T3 – 20-50%,
<24/408 = 8%.
CMV
Enveloped dsDNA, Herpes virus 5
Parvovirus B19:
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
Hepatitis in pregnancy
All hepatits apart from Hep A can be transmitted vertically.
Treatment of hep c in pregnancy
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.
Hep B in pregnancy
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.
HPV
Double stranded circular DNA virus.
Microscope: can see koilocytes with a (like TV) perinuclear halo
Toxoplasmosis.
Higher prevalence in africa
lymphadenopathy and flu like symptoms, hepatosplenomegaly.
spiramycin
Nitrofurantoin:
Risk of neonatal hemolysis at term
CI in breastfeeding, as can produce hemolysis in babies with G6PD- deficieny.
Acrocentric chromosomes
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
Non invasive fetal DNA testing
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
Downs synd
95% Non disjunctions in the first meiosis
3% unbalanced Robertsonian translocation T(14;21)
1-2% mosaics.
SIckle Cell Disease
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
Beta Thalassemia
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
Alpha thalassemia
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
Reciprocal translocations
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
Gestational diabetes diagnosis
Fasting 6.1
2 hour 7.8
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).
Role of fetal dhea
stimulates placenta to form oestogen
Conns - salt, Aldos:renin ratio
Cushings - dexa supression
Addisons - short synacthen
Morning cortisol : Cushing’s syndrome (high cortisol) or Addison’s disease (low cortisol).
Cons
Aldosterone hyperrrr secretion
hypocalc
hypokal
hypernat
hypertension
Addisons opposite
hypercals
hyperkal
hyponat
hypotension
hypoglycemia tooo
thyroid hormones in preg
decreased tsh
increased t3 and 4
amniocentesis
15+weeks
Factor 5 def blood tests
PT prolonged
decreases shbg
B. Hepatic cirrhosis
C. Hyperprolactinaemia
D. Hypogonadism
E. Hypothyroidism
increases shbg
A. Growth hormone
