Pregnancy Flashcards
What is an ectopic pregnancy?
Implantation of a fertilised egg at a site outside the uterus
Most commonly occurs in the ampulla of the Fallopian tube (~80%)
—> rupture of Fallopian tube —> haemorrhage —> peritonitis
Can also occur:
- interstitial (~2%-5%)
- cervix
- peritoneum
- abdominal viscera
- in the pouch of Douglas
Pain felt in lower abdominal quadrants (stretching/tearing of peritoneum) —> right iliac fossa (often misdiagnosed as appendicitis)
Haemorrhage into peritoneum —> diaphragmatic irritation —> referred shoulder tip pain
More dangerous when it occurs in the isthmus/intramural Fallopian tube as less space is available for the embryo to grow before the tube is ruptured (thick muscularis mucosa is inflexible)
note: blood passing from vagina is usually withdrawal bleeding, not due to bleeding at the site of rupture (caused by reduction in hCG —> corpus luteum not maintained)
What is the clinical presentation of pain in ectopic pregnancy?
(assuming in ampulla of uterine tube)
Before rupture = lower abdominal quadrants due to stretching/tearing of peritoneum
(hence commonly misdiagnosed as appendicitis)
Rupture —> haemorrhage into peritoneum —> diaphragmatic irritation —> referred pain to tip of shoulder (phrenic nerve - dermatomes C3, C4, C5)
note: blood passing from vagina usually withdrawal bleeding caused by fall in hCG (not due to bleeding at site of rupture)
What can be torn during childbirth, and what are the consequences?
Levator ani muscles:
- pubococcygeus —> prolapse/herniation of bladder/urethra —> incontinence
- medial part of pubo-rectalis (inserts into perineal body) —> herniation of rectum (tear extending into external anal sphincter) —> difficulty with defecation/faecal incontinence
What is an episiotomy? What needs to be repaired and checked as a result?
Incision of skin in perineum to allow passage of the head of the foetus through the vagina and prevent damage to perineal body
note: additionally, incision is easier to suture than a tear
note: median episiotomy divides the perineal body; has since been abandoned in favour of a postero-lateral episiotomy
Repair:
- vaginal mucosa and submucosa
- perineal skin
- muscles & fascia of perineum
Perform a vaginal exam and a rectal exam after repairing
What cells of the conceptus go on to form the placenta?
Syncytiotrophoblast = forms placenta; invades endometrium; multi-nucleated (no interstitium, therefore very short diffusion pathway)
+ cytotrophoblast = stem cell layer responsible for growth & repair of syncytiotrophoblast and implantation
Outline the development of the placenta.
Week 5:
Primitive villi all over chorion (recede over time except for one zone —> placenta)
Amniotic sac enlarges, yolk sac disappears
Week 12:
Chorion loses villi away from decidua basalis (placenta)
Week 22:
Amniochorionic membrane fuses to decidua parietalis
note: 1st trimester = placental barrier composed of syncytiotrophoblast, cytotrophoblast, connective tissue, & foetal capillaries
3rd trimester = placental barrier only composed of syncytiotrophoblast & foetal capillary endothelium
How does the embryo implant in the uterus? How does this change as the foetus develops?
Uterine epithelium breached & conceptus implants in stroma
1st trimester placenta:
- placental “barrier” relatively leaky & thick
- complete cytotrophoblast layer beneath syncytiotrophoblast
3rd trimester placenta:
- increased s.a. for exchange
- placental “barrier” now thinner (as needs of foetus increases)
- cytotrophoblast layer beneath syncytiotrophoblast is lost
- placenta is haemomonochorial (single layer of trophoblast separates maternal blood from foetal capillaries - optimises transport)
What are the aims of implantation?
Establish basic unit of exchange: Primary villi (differentiate) ---> Secondary villi (invades mesenchyme core) ---> Tertiary villi/chorionic villi (invasion of mesenchyme core by foetal vessels which differentiate from mesenchyme)
Anchoring of placenta: establishment of outermost cytotrophoblast shell (cytotrophoblast migrates through villi to be outside placenta)
Establish maternal blood flor within the placenta: chorionic villi bathed in maternal blood to optimise transport
How does implantation of an embryo modify the histology of the endometrium?
Pre-decidual cells (cells shed during menstruation) modified to form decidua (balancing force for invasion of trophoblast)
- decidua basalis = maternal portion of placenta which induces the trophoblast to form chorionic villi
- decidua capsularis = tissue separating the lumen of the uterus from the embryo —> chorion laeve
- decidua parietalis = endometrial tissue between the uterine lumen and the myometrium
Remodelling of spiral arteries —> creates low resistance vascular bed to maintain high flow required for high foetal demand (particularly in late gestation)
note: extra-villus trophoblasts line maternal blood vessels, therefore maternal cells are directly adjacent to foetal cells
When does incomplete invasion of the endometrium by the embryo occur?
Placental insufficiency —> intra-uterine growth restriction
Pre-eclampsia —> intra-uterine growth restriction, maternal symptoms (hypertension, proteinuria) + problem with remodelling of spiral arteries
What is a cotyledon, and what is it composed of?
Compartment of placenta containing a major branch of the umbilical blood vessels - group of chorionic villi bathed in maternal blood
Maternal portion:
- cytotrophoblastic shell
- maternal vein & artery —> form blood pools adjacent to chorionic villi
Foetal portion:
- chorionic villi containing foetal capillaries
- one umbilical vein (oxygenated) & two umbilical arteries (deoxygenated)
note: normally the placenta is vasodilated (expanded) but in pre-eclampsia the placenta is vasoconstricted (contracted; due to poor uteroplacental circulation & widespread endothelial dysfunction)
What are the functions of the placenta?
Synthesis of: - glycogen - cholesterol ---> steroid hormones - fatty acids (for support of mother, not foetus)
Production of hormones:
- protein hormones = hCG, somatomammotrophin/thyrotrophin/corticotrophin
- steroid hormones = progesterone & oestrogen
(placenta produces enough progesterone to maintain pregnancy without progesterone from corpus luteum until the end of the 1st trimester)
Transport:
- simple diffusion (water, electrolytes, urea, gases) - dependent on uteroplacental circulation
- facilitated diffusion (glucose)
- active transport (amino acids, iron, vitamins)
- receptor-mediated (IgG - passive immunity)
What is hCG?
Human chorionic gonadotrophin
Protein hormone produced in 1st months of pregnancy by cells of fertilised ovum
Supports the secretory function of the corpus luteum —> increased secretion of progesterone & oestogen —> endometrium maintained
Produced by syncytiotrophoblast (therefore pregnancy-specific)
note: indicative of trophoblast diseases e.g. hydratidiform mole/molar pregnancy = pregnancy without embryo (abnormal independent production of trophoblast), choriocarcinoma = malignant version of trophoblast
Give some examples of the effects of pregnancy on the mother by pregnancy-related hormones.
Human chorionic somatomammotrophin & human placental lactogen cause slight insulin resistance in mother —> increases glucose available to foetus (+ risk of gestational diabetes)
Progesterone increases maternal appetite to increase fat stores in preparation for larger foetuses
Increased calcium release from maternal bones to supply foetus with calcium (can cause dental caries/osteopenia)
What is the purpose of maternal blood lakes in the placenta?
Compensates for compression of blood vessels during labour causing reduced uteroplacental circulation
~300ml
Give some examples of infections and teratogens which can cross the placenta.
Infections:
- Varicella zoster (chickenpox/shingles)
- Cytomegalovirus (herpes)
- Treponema pallidum (syphilis)
- Toxoplasma gondii (toxoplasmosis)
- Rubella (causes miscarriage or congenital rubella syndrome = sensorineural deafness, eye abnormalities, congenital heart disease, etc.)
Teratogens:
- thalidomide
- alcohol
- anti-convulsants
Explain the importance of D antibodies in pregnancy.
Rhesus positive = D antigens present on RBCs
Rhesus negative = anti-D antibodies produced (inc. against IgG)
If mother is Rhesus negative and their foetus is Rhesus positive, they will produce anti-D antibodies after their first pregnancy (sensitisation) —> next pregnancy the anti-D antibodies will attack the foetus —> haemolysis (reticulocytosis, anaemia, hydrops fetalis)
Therefore Rhesus negative first time mothers are offered prophylactic anti-D IgG to remove foetal Rhesus positive RBCs —> no sensitisation occurs
Kleihauer test demonstrates presence/absence of foetal cells in maternal circulation
What conditions are screened for at antenatal screenings?
H&E = risk factors e.g. for gestational diabetes
Blood test = Rhesus status, ABO blood type, Hb level, ?infection
Urinalysis = ?proteinuria (indicates pre-eclampsia)
What maternal cardiovascular changes occur during pregnancy?
- increased blood volume —> dilutional anaemia
- increased stroke volume —> increased bpm (to 80-90bpm) & cardiac output (by 40%) —> auscultatory changes (flow murmurs)
- reduced systemic vascular resistance (due to progesterone) —> initial fall in BP (trimesters 1 & 2; can mask pre-existing hypertension, cause sweating easily, nasal congestion, “feeling the heat”) —> increase in BP (trimester 3) due to aortocaval compression by gravid uterus (increased risk of impaired utero-placental circulation when supine; therefore women encouraged to lie on left-hand side)
- venous distension (smooth muscle relaxation effect of progesterone + pressure of uterus on IVC when recumbent) —> varicose veins & haemorrhoids
- upward displacement & hypertrophy of heart
note: normally systolic BP NEVER increases in pregnancy
note: mean BP remains the same (increased stroke volume causes a slight increase in systolic BP and a slight decrease in diastolic BP)
note: when supine, the uterus compresses the IVC —> reduced venous return —> reduced diastolic pressure —> hypotension
What maternal urinary changes occur during pregnancy? Why are these changes necessary? …………
- increased intra-ureteral tone
- increased GFR (50%-60%) —> reduced functional renal reserve
- increased renal plasma flow (to a greater degree than GFR increase) —> reduced filtration fraction in trimesters 1 & 2
- increased creatinine clearance (therefore lower creatinine)
- increased protein clearance (therefore lower protein)
- reduced urea
- reduced bicarbonate
- increased risk of urinary incontinence (bladder compressed by gravid uterus/when foetal head is engaged towards the end of pregnancy)
note: progesterone causes dilation of ureters (slows urine excretion —> increased risk of UTIs) —> hydroureter —> hydronephosis
note: gravid uterus can compress the ureters/bladder —> urinary stasis —> risk of UTIs —> risk of pyelonephritis —> pre-term labour
note: ‘normal’ kidney function actually reflects decreased kidney function when pregnant
What maternal respiratory changes occur during pregnancy?
- displacement of diaphragm & increase in AP/transverse diameters (flaring of lower ribs) —> decreased functional residual capacity (but balanced by expiratory reserve volume)
- widening of intercostal angle
- increased alveolar/minute ventilation & increased tidal volume (by 40%) (no change in resp. rate)
- increased risk of metabolic acidosis (reduced buffer capacity, increased resp. drive by progesterone —> resp. alkalosis —> increased bicarbonate excretion)
- increased oxygen consumption (by 15%)
What maternal metabolic changes occur during pregnancy?
Carbohydrates:
- increased maternal insulin resistance (due to hPL, glucose, oestrogen, progesterone, cortisol) —> switch to gluconeogenesis & lipolysis
- reduced fasting blood glucose
- increased post-prandial (post-meal) blood glucose
Lipids:
- increased synthesis of lipids in trimester 1
- increased lipolysis in trimesters 2 & 3
- increased metabolism of peripheral fatty acids in late pregnancy
- increased free fatty acids & ketones on fasting (so glucose is available for foetus) (increased risk of diabetic ketoacidosis)
Thyroid:
- increased TBG production
- increased T3 & T4 production (but free T4 normal)
note: hCG directly stimulates thyroid, therefore TSH levels can be decreased due to negative feedback
Calcium:
- increased uptake of dietary calcium from maternal gut
- increased secretion of PTH in third trimester —> increased release of calcium from bone (risk of osteoporosis/dental caries; therefore expectant mothers should increase dietary calcium intake by ~70%)
+ increased prolactin release by oestrogen
What is gestational diabetes?
Carbohydrate intolerance first recognised in pregnancy and not persisting after delivery (diagnose via oral glucose tolerance test)
Risk factors:
- previous history
- increased age
- increased weight
- history of babies which where large for gestational age
Poor control:
- risk of macrosomic (large) foetuses (increased insulin secretion in foetus —> glucose stored as fat)
- stillbirth
- congenital defects (esp. if maternal hyperglycaemia occurs during period of development)
- prematurity
- impaired maturation
- resp. disorders of the newborn
Macrosomic foetuses are difficult to deliver due to their large size
Once born the foetus has reflex hypoglycaemia due to high levels of circulating insulin (brain at risk)
What maternal gastro-intestinal changes occur during pregnancy?
- change in disposition of viscera by uterus e.g. appendix moved to RUQ
- progesterone causes smooth muscle relaxation —> delayed gastric emptying (heartburn & constipation), stasis in biliary tract (increased risk of cholecystitis & pancreatitis - also increased risk due to hyperlipidaemia)