general Flashcards
what are the 3 ways of dating a pregnancy?
- first day of LMP +40
- clinical examination (e.g. fundal height)
- USS (crown-rump diameter in 1st trimester only)
define pre-term, term and post-term gestational periods
pre-term:
before 37 completed weeks
term:
means between 37 and 42 completed weeks
post-term:
beyond 42 weeks
recall the timeline and stages of pregnancy
divided into 3 trimesters:
1st = up to 12 weeks
2nd = 12-27weeks
3rd = 28weeks to term
a) in what trimester is there the largest weight gain and growth?
b) by end of what trimester is all the organ systems in place?
a) 3rd
b) 1st
what hormones and ducts determine the genitalia of the developing embryo?
development into male or female depends upon hormones secreted by foetal testes - testosterone and mullein inhibiting factor. without stimulation of male testicular hormones the foetus will develop female characteristics.
in males:
- Wollffian ducts -> repro tract
- mullerian ducts degenerate
in females:
- wolffian ducts degenerate
- mullerian ducts –> repro tract
what gene found on Y chromosome is responsible for the development of male phenotypes?
SRY
(codes for production of testis determining factor -TDF - that directs differentiation of gonads into testes)
if no SRY female characteristics develop
testosterone (after 6weeks) has 2 effects on male genitalia. what are they?
- transfer the Wollfian duct to male reproductive tract
2. converted to dihydrotestosterone to cause the external genitalia to develop along the male lines
list the roles of the prostoglandins, oestrogen, relaxin and oxytocin in female parturition and lactation
prostaglandins:
-softens cervix (breaks down collagen fibres allowing dilation)
oestrogen:
- increases density of oxytocin receptors in myometrium
- increase gap junctions between myometrial cells (uterus able to contract as a coordinated unit)
relaxin:
- relaxation of pelvic bones
oxytocin:
- increase uterine contractions -> push foetus against cervix -> increase oxytocin secretion(Ferguson reflex) -> causes increase prostaglandin secretion -> increase uterine contractions …. (+ve feedback loop)
- stimulates contraction of myoepithelial cells
- hastens involution
- suppresses LH and FSH secretion - suppresses menstrual cycle
**levels of oxytocin does not rise. parturition is trigged by raised increased sensitivity to oxytocin (increase in oestrogen secreted by placenta)
explain the events occurring in the 3 stages of labour
primiparous average 14 hours
multiparous average 8 hours
1st stage: cervical dilation:
- takes the most time/many hr’s
- > ‘latent phase’: onset of painful contractions 5-10min intervals; cervical ripening and effacement; cervix slowly dilating 3-4cm
- > ‘active phase’: cervix dilates more rapidly from 3/4cm’s 0.5-1cm/hr; progressive increase in frequency and strength of contractions; descent of presenting part; cervix dilates to 10cm to accomadate the baby’s head; rupture of amniotic sac (maybe) - ‘waters break’ - lubricates birth canal
2nd stage: fully dilated cervix to birth:
- takes 30-90mins
- cervix fully dilated
- contractions are stronger 2-5mins
- presenting part descends
- urge to bear down
- baby moves through cervix to vagina
- stretch receptors in the vagina trigger contraction of abdominal wall to augment uterine contractions
- mother can voluntarily contract abs also
- Ferguson reflex -> stretching of the perineum/pelvic floor in late labour seems to stimulate oxytocin release
3rd stage: expulsion of placenta and membrane:
- takes a few mins to an hour depending on management
- separation due to forceful uterine contractions and reduces size of placental bed which reduces bleeding
give brief details of some of the key triggers for labour
- size of baby vs size of placenta?
describe the events and timeline of physiological development of human female breast tissue
- at birth the breasts consist of lactiferous ducts without any alveoli (also male breasts)
- at puberty under influence of oestrogen the ducts proliferate and masses of alveoli form at the ends of the branches
- during pregnancy under the influence of oestrogen, progesterone and prolactin the glandular portion of the breasts undergoes hypertrophy replacing adipose tissue
- from week 16 the breast tissue is fully developed for lactation but is quiescent awaiting activation
- after parturition the breast produces colostrum before mature milk production begins
explain the neurohumoral reflexes that control milk production and ejection during pregnancy, lactation and weaning
during pregnancy:
- increase in oestrogen -> duct development
- increase progesterone -> lobule formation
- prolactin and human chorionic somatomammotropin -> synthesis enzymes for milk production
prolactin -> also stimulates milk production after parturition
lactation:
- can’t suck milk out of alveoli. So…milk is let down (AKA milk ejection reflex), a physiological process.
- let down and milk production are both controlled by neurohumeral reflexes where prolactin is the hormone responsible
- lactation initiated by precipitous drop in oestrogen and progesterone after delivery.
- a prolactin surge each time baby is nursed due to nerve imputes from nipples to hypothalamus
- when not nursing, hypothalamus produces prolactin inhibitory hormone
recall the components of breast milk and compare and contrast the composition of colostrum and mature milk
breast milk = apocrine secretion of synthesise milk fat and milk protein (composition varies within a feed and thin the lactation process). comes in 2-4days, after 1-2weeks it is transitional milk and after this it is mature
composition of colostrum (produced for about 1 week) vs mature milk (after 21days /100ml):
- 58 cals vs 70 cals
- 5.3g carbohydrates vs 7.4g
- 2.9g fat vs 7.4g fat
- 3.9g protein vs 1.3g protein
- colostrum also includes fewer water-soluble vitamins, more fat-soluble vitamins (particularly A). more zinc and sodium and greater amounts of immunoglobulins (IgG and IgA) and a number of growth factors - conferring passive immunity
review the embryology of body form and organ development
look at lectures for this 🥴
what are the 2 important cell types involved in lactation?
secretory alveoli/acini cells:
- produce milk
- stimulated by prolactin
contractile myepithelial cells:
- surround each alveolus
- stimulated by oxytocin
describe the suckling and ejection reflex
- suckling activated mechanoreceptor in the nipple which leads to stimulation of the hypothalamus
- the hypothalamus initiates 2 responses:
1) via nervous pathway hypothalamus synthesises oxytocin which is carried to post.pituirary. the release of oxytocin in bloodstream leads to contraction of myoepithelial cells surround alveoli –> milk ejection/ ‘let down’ of milk
* this is a conditioned reflex. let down in response to cry of baby etc. is inhibited by catecholamines (stress)
2) via endocrine pathway decreases prolactin-inhibiting-hormone (PIH)/ dopamine (PIF) or increases prolactin-releasing-hormone (PRH) which causes anterior pituitary to secrete more prolactin –> milk secretion
* prolactin is releases in proportion to the strength and duration of the suckling. the more the baby eats the more milk produced
What do the WHO recommend for how long women should breast?
recommended up to 6months, with continued breastfeeding along with appropriate complementary foods up to 2 years or beyond
describe how a baby begins to breathe for itself following birth
- during normal deliver, begins to breathe within secs; normal RR within 1m
- initiated by sudden exposure to exterior world and after a slight asphyxiated state
- Walls of alveoli are collapsed at birth due to surface tension; >25mmHg of negative inspiratory pressure required to oppose this effect and open alveoli for 1st time (1st inspirations are usually powerful)
what problems can occur when baby begins to breathe for itself?
- permanent and serious brain impairment often senses if breathing is delayed >8-10mins
- hypoxia is frequent during delivery because 1) compression of the umbilical cord, 2) premature separation of the placenta, 3) excessive uterine contractions blocking the blood supply, 4) excessive anaesthesia of mother (depresses oxygenation even of her blood)
- respiratory distress syndrome is caused when surfactant secretion is deficient.
what is the normal RR of a baby?
40 breaths per minute
briefly describe the anatomical organisation of the foetal circulation
- Lungs mainly non-functional during foetal life and liver only partially functional = no need for much blood pumped through
- 1st blood returning from the placenta -> umbilical vein -> ductus venosus (mainly bypassing liver) -> IVC -> RA -> foramen ovale -> LA (thus well oxygenated blood from placenta reaches left side of heart).
- SVC -> RA -> RV ->pulmonary artery -> ductus arteriosus -> descending aorta -> umbilical artery -> placenta
describe how circulatory changes at birth allow blood to flow through the lungs
primary changes at birth are:
1) major loss of placental blood flow –> doubles systemic vascular resistance; pressure in aorta, LA+LV increased greatly
2) pulmonary pressure decreases as a result of expansion of the lungs (decompressing vessels)
closure of foramen ovale:
- due to changes in pressure blood wants to flow LA->RA
- BUT, small valve lies over the foramen on the left side, closing over the opening
closure of ductus arteriosus:
- due to pressure changes blood wants to flow from aorta to pulmonary a. via DA
- after few hours, walls of DA constrict, sufficient to stop blood flow within1-8days (functional closure of the DA)
- fibrous tissue then fills lumen
closure of ductus venosus:
- muscular walls contract strongly and tube closes within 1-3hrs
- pressure in portal vein increases forcing portal venous blood through liver sinuses
why does an infant lose weight during the first few days of life?
- loses 5-10% (sometimes as much as 20%) within first 2-3days
- most of this is fluid
- takes time for mothers milk to come in
- use its stored fats and proteins for metabolism until milk comes in
explain how blood volume changes after birth
- average 300ml after birth
- can be 375ml if the umbilical cord is stripped or left attached to placenta
- after few hours fluid is lost to neonates tissue spaces, increasing hematocrit, but returns blood volume to 300ml
explain how arterial blood pressure changes after birth
averages 70/50 during the first day of life. slowly increases to 90/60 over next dew months and rises even slower to 115/70 in adolescence
explain how blood characteristics change after birth
- RBC averages 4million per cubic mm BUT very few RBCs formed in first few weeks - hypoxic stimulus no longer present. physiological anaemia at 6-12 weeks
- WBC approx 45000 per cubic mm immediately after birth (5x as great as that of adults)
- plasma bilirubin rises from <1-5mg/dl during the first 3 days and then gradually drops as liver becomes functional (physiological hyperbilirubinemia for 1st 2 weeks)
explain how a new born’s blood gasses can vary?
rate of metabolism is twice as great in relation to body mass as in adult, meaning twice as much acid is formed - tendency for acidosis
list 4 effects of deficient liver function in the neonate
- conjugates bilirubin with glucuronic acid poorly
- deficient in forming plasma proteins (hypoproteinaemia oedema can develop)
- gluconeogenisis function. blood glucose falls in unfed neonate, relies on fat storage until mothers milk comes in
- forms too little coagulation factors
list 3 ways in which digestion, absorption and metabolism of food differs in neonates compared to older children
- secretion of pancreatic amylase is deficient, so use starches less adequately
- absorption of fats from the GIT is somewhat less than older child. consequently milk with high fat content (cows) is poorly absorbed
- liver function imperfect for first week - serum glucose concentration is unstable and low
briefly explain the body temperature changes in the first approximate 12hours after birth
- because body SA is large in relation to body mass, heat is readily lost from the body
- body temp of neonates, particularly premature, falls easily
- temp regulatory mechanisms remain poor in early days of life
*there is a fall in temp immediately after birth, and unstable during the first few days
briefly describe key nutritional needs of neonate in early weeks of life
- Usually in complete nutritional balance at birth - if mother has had an adequate diet
- Need readily supply of calcium for ossification of bones. Need vitD for absorption through GIT. Severe rickets can develop in infants who have vitD deficiency
- If mother has had sufficient iron in diet baby can store enough in liver for 4-6mnths. If not, severe anaemia is likely after 3mnths. Avoid with feeding baby egg yolk
Vit C needed for formation of cartilage, bone and other intercellular structures. Normally provided in breast milk
explain how the new borns immunological site changes over the first few months of life
- Inherits great degree of immunity from mother; protects for 6months against most major childhood infectious diseases (diphtheria, measles and polio). Immunization for which not necessary in first 6month - necessary for whooping cough
- By end of first month, babies gamma globulins, which contain the antibodies, have decreased to less than half the original level, with a corresponding decrease in immunity
- Own immune system begins to form antibodies and the gamma globulin concentration returns to normal by age 12-20months
Describe physiological changes in pregnancy seen in full blood count (FBC) and coagulation tests
- normal declines in Hb across all 3 trimesters (110->105->100g/l)
- rise in WBCs (mainly neutrophils)
- gestational thrombocytopenia. as long as between 80-100 x10^9/l then it is perfectly safe. (check the drop as might seem a lot but normal for that female)
- rise in MCV by 4fl
- rise in fibrinogen and factors VIII, IX and X (hypercoaguable state)
- common to have iron def anaemia. important to check ferritin as MCV is normally raised in pregnancy
Understand the presentation and mechanisms of immune thrombocytopenia (ITP) and thrombotic thrombocytopenia (TTP)
ITP:
- mechanism = autoimmune platelet destruction (IgG). isolated with no apparent cause (no cells seen on smear). may be triggered by infection, drug or pregnancy.
- presentation = looks like meningococcal rash; pinpoint bleeding in skin and easy bruising.very very low platelets.
- Tx- usually self-limiting/sterioids/ immunoglobulins/ splenectomy/drugs that mimic thrombopoetin (labour >50)
TTP:
- rare and very serious
- mechanism = defect in ADAMS13 (usually inhibits VWF) leading to platelet aggregates. lead to lysis of RBCs, fever as a systemic response and other symptoms.
- presentation = 5 unique and classic symptoms:
1. thrombocytopenia
2. fever
3. anaemia
4. neurological symptoms
5. renal disfunction - tx =plasma exchange
Understand the ABO and Rhesus blood group systems
-almost everyone has H substance on red cell surface. this alone = group O. 1 or 2 additional sugars added = group A or B or AB
- rhesus antigens = c C D e E
- coded for chromosome 1 and inherited as a tripled e.g. cDe
- can be Rh D +ve or -ve
- no naturally occurring antibodies, but can develop in repose to pregnancy or transfusion
- risk of haemolytic disease of the newborn if IgG crosses placenta (anaemia, jaundice, brain damage or foetal death)
Understand the programme for prevention of haemolytic disease of the newborn in relation to Rhesus (D) sensitisation
- mothers blood test and antibody screen at booking
- anti-D prophylaxis given to D negative mothers at 28weeks and delivery (40 weeks) and after obstetric ‘events’. – once foetus is delivered, a. blood sample is taken - Kleihauer test - to see if foetal blood mixed with mothers. dose of anti-D calculated accordantly
- fetal monitoring for anaemia if mother has significant red cell antibodies. flow in middle cerebral a., ascites, liver and spleen size, umbilical cord sampling for blood count/blood group and antibody level
- if necessary, can receive intra-uterine transfusion via umbilical cord
- neonatal management: clinical assessment, blood count and reticulocytes/group/red cell antibodies/bilirubin/direct Coombes test looking for membrane-bound antibody, allow antibodies to decline, phototherapy to increase bilirubin conjugation, top-up or exchange transfusion
Define haemoglobinopathies and thalassaemias
Haemoglobinopathies:
- umbrella term that includes all genetic haemoglobin disorders. divided into 2 main groups:
1) thalassemia syndromes
2) structural hemoglobin variants
Thalassemia:
- Hb synthesis disorders (Hb structure in these cases is normal)
- alpha and beta are the 2 main types
- autosomal recessive conditions
*Hemoglobinopathies are simply structural abnormalities in the globin proteins themselves. Thalassemia’s, in contrast, usually result in underproduction of normal globin proteins, often through mutations in regulatory genes.
Gives some examples of Haemoglobinopathies and thalassemias (and discuss their associated ethnic origin -??)
significant/ transfusion dependent conditions:
- sickle cell homozygous; typically in Afro-Caribbean
- sickle with Hb C/D/E/beta thal; coexist with C particularly in west Africa
- beta thal homozygous; north London in uk. is a transfusion dependant condition
- alpha thal 3 gene deletions (Hb H)
Explain how the UK antenatal screening programme runs for haemoglobinopathy/thalassemias
FBC is done at booking:
- is the MCH <27? (most will be microcytic; so screen for MCV <80 and or mean cell Hb (MCH) <27)
- key part of screening process is screening for ethnic origin
- if either is positive then HPLC to look for thal/haemoglobinopathy
- may need confirmatory tests
- may need to check paternity FBC
Explain how these disorders are detected and managed antenatally
detection:
- look at blood films
- haemoglobin electrophoresis
- high Performance Liquid Chromatography
- gene copy number (e.g. how many numbers of alpha thalassemia gene have they got)
- gene sequencing
if +ve tests:
- notify parents + GP
- if foetus is at considerable risk: consider (there are risks so maybe only if parents consider termination) 11-14 week chronic villous sampling for fetal DNA or 15 weeks + amniocentesis
*there is also newborn screening that includes heel prick for sickle cell
Revisit the principles of disease screening as defined in ‘Wilson’s criteria’
- the condition should be an important health problem,
- the natural Hx of the condition should be understood
- there should be a recognisable latent or early symptomatic stage
- there should be a test that is east to perform and interpret, acceptable, accurate, reliable, sensitive and specific
- there should be an accepted Tx recognised for the disease
- Tx should be more effective if started early
- there should be a policy on who should be treated
- diagnosis and Tx should be cost-effective
- case-finding should be continuous process
what factors may exclude a mother from attending midwife led unit?
- previous postpartum haemorrhage
- previous intrapartum complication
- previous c-section
- increased BMI
- multiple births
- prolonged rupture of membranes
- infection
- abnormal auscultation
- PMHx e.g. epilepsy, diabetes
