general Flashcards
1
Q
what are the 3 ways of dating a pregnancy?
A
- first day of LMP +40
- clinical examination (e.g. fundal height)
- USS (crown-rump diameter in 1st trimester only)
2
Q
define pre-term, term and post-term gestational periods
A
pre-term:
before 37 completed weeks
term:
means between 37 and 42 completed weeks
post-term:
beyond 42 weeks
3
Q
recall the timeline and stages of pregnancy
A
divided into 3 trimesters:
1st = up to 12 weeks
2nd = 12-27weeks
3rd = 28weeks to term
4
Q
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
a) 3rd
b) 1st
5
Q
what hormones and ducts determine the genitalia of the developing embryo?
A
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
6
Q
what gene found on Y chromosome is responsible for the development of male phenotypes?
A
SRY
(codes for production of testis determining factor -TDF - that directs differentiation of gonads into testes)
if no SRY female characteristics develop
7
Q
testosterone (after 6weeks) has 2 effects on male genitalia. what are they?
A
- transfer the Wollfian duct to male reproductive tract
2. converted to dihydrotestosterone to cause the external genitalia to develop along the male lines
8
Q
list the roles of the prostoglandins, oestrogen, relaxin and oxytocin in female parturition and lactation
A
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)
9
Q
explain the events occurring in the 3 stages of labour
A
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
10
Q
give brief details of some of the key triggers for labour
A
- size of baby vs size of placenta?
11
Q
describe the events and timeline of physiological development of human female breast tissue
A
- 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
12
Q
explain the neurohumoral reflexes that control milk production and ejection during pregnancy, lactation and weaning
A
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
13
Q
recall the components of breast milk and compare and contrast the composition of colostrum and mature milk
A
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
14
Q
review the embryology of body form and organ development
A
look at lectures for this 🥴
15
Q
what are the 2 important cell types involved in lactation?
A
secretory alveoli/acini cells:
- produce milk
- stimulated by prolactin
contractile myepithelial cells:
- surround each alveolus
- stimulated by oxytocin
16
Q
describe the suckling and ejection reflex
A
- 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
17
Q
What do the WHO recommend for how long women should breast?
A
recommended up to 6months, with continued breastfeeding along with appropriate complementary foods up to 2 years or beyond
18
Q
describe how a baby begins to breathe for itself following birth
A
- 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)
19
Q
what problems can occur when baby begins to breathe for itself?
A
- 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.
20
Q
what is the normal RR of a baby?
A
40 breaths per minute
21
Q
briefly describe the anatomical organisation of the foetal circulation
A
- 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
22
Q
describe how circulatory changes at birth allow blood to flow through the lungs
A
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
23
Q
why does an infant lose weight during the first few days of life?
A
- 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
24
Q
explain how blood volume changes after birth
A
- 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
25
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
26
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)
27
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
28
list 4 effects of deficient liver function in the neonate
1. conjugates bilirubin with glucuronic acid poorly
2. deficient in forming plasma proteins (hypoproteinaemia oedema can develop)
3. gluconeogenisis function. blood glucose falls in unfed neonate, relies on fat storage until mothers milk comes in
4. forms too little coagulation factors
29
list 3 ways in which digestion, absorption and metabolism of food differs in neonates compared to older children
1. secretion of pancreatic amylase is deficient, so use starches less adequately
2. absorption of fats from the GIT is somewhat less than older child. consequently milk with high fat content (cows) is poorly absorbed
3. liver function imperfect for first week - serum glucose concentration is unstable and low
30
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
31
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
32
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
33
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
34
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
35
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)
36
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
37
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.
38
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)
39
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
40
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
41
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
42
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
43
what induction agents may be used for induction of labour?
- propess (dinoprostone) (prostaglandin)
- prostin gel
- cooks balloon
- artificial rupture of membranes (ARM)
- syntocionon infusion
44
what induction agents may be used for induction of labour?
- propess (dinoprostone) (prostaglandin)
- prostin gel
- cooks balloon
- artificial rupture of membranes (ARM)
- syntocionon infusion
(from Kura Cloud: propess pessary -> ARM -> syntocinon infusion)
45
what is a CTG used for?
Cardiotocography - used to measure fetal HR and uterine contractions
46
define what is meant by engagement of the baby?
the passage of the widest transverse diameter of the present part through the pelvic inlet. the level of descent can be determined on abdominal palpation by feeling how much of the presenting part (usually the head) is out of the pelvis.
recorded numerically (4/5 indicates the head is just entering the pelvis, 0/5 means deeply engaged)
47
define station determined via vaginal examination
the relation of the presenting part to the ischial spine. if at level of ischial spine, referred to as 0
48
what is the bishop score used for?
pre-labour scoring system to assist in predicting whether induction of labour will be required - an assessment of readiness for induction. women with low score (1) would not be expected to go into labour for a few weeks; a high score (10) would be in a few days
calculated based on findings from vaginal exam; dilation, length, station, consistency, position
49
what are the different pain relief options available in labour?
- entonox - 50/50 mix of nitrous oxide and oxygen
- TENS - transcutaneous electrical nerve stimulation
- opiates - diamorphine
- epidural
50
what are the indications for assisted birth?
can be fetal or maternal
fetal:
- malposition (e.g. occiput posterior or transverse)
- suspected/anticipated fetal compromise
maternal:
- inadequate progression of labour;
> nulliparous - 2hrs whiteout regional anaesthesia (3hrs with)
> 1 hour without regional anaesthesia (2hrs with)
- maternal fatigue/exhaustion
- to shorten and reduce effects of second stage labour on maternal conditions such as cardiac disease, myasthenia graves, proliferative retinopathy, spinal cord injury
51
what are the risks with assisted birth?
maternal:
vaginal trauma
bleeding
perineal trauma
fetal:
bruising
facial nerve palsy
cephalohematoma
52
what are the risks with c-section?
```
maternal:
bleeding
thrombosis
bowel/bladder/vessel/ureter rupture
infection
anaesthesia
placenta praaevia/accrete in future pregnancies
```
fetal:
transient tachypnoea of the neonate
lacerations
53
what is the name given to the surgical incision of t perineum and the posterior vaginal wall, during the 2nd stag of labour, to quickly enlarge the opening for the baby
episiotomy
54
list the causes of PPH
tone (lack of uterine muscle tone compressing vessels):
- prolonged labour
- polyhydramnios
- infection
- abnormalities e.g. fibroids
trauma:
- operative delivery
- cervical/vaginal lacerations
tissue:
- retained placental tissue
- abnormal placentation
- morbidly adherent placenta
coagulopathy:
- pre-eclampsia
- HELLP syndrome
- placental abruption
- amniotic fluid embolism
- sepsis
55
what medication can be used to manage PPH?
- oxytocin (IV infusion - 1st line)
- ergometrine
- carboprost
- misoprostol
- tranexamic acid
- bimanual compression
56
describe the clinical presentation, investigation and management of cytomegalovirus in pregnancy and in the newborn
CP:
- congenital infection; fetal death, growth restriction, hearing loss, ocular disease (retinitis), cerebral damage (intracranial calcification), microcephalous, hepatomegaly/jaundice/hepatitis, blueberry muffin/petechial rash, splenomegaly, anaemia, thrombocytopenia
- majority of primary CMV infections are asymptomatic in the mother
- 90% normal at birth and develop normally
Ix:
- serology (CMV IgM)
- CMV PCR (urine, saliva, blood)
Mx:
- asymptomatic: 3-6month review for first 2 years including hearing and neurodevelopment assessment
- symptomatic: depends on site and extent eg refer to ophthalmology/radiology/ent
- early Tx with antiviral e.g. ganciclovir (IV) for severe infections or valganciclovir (oral) for initial Tx and maintenance
extra:
- no CMV vaccine and no pregnant women is screened
- after acute infection, lifelong latency with potential for relapse
- transmitted to foetus before or after birth
- most common congenital infection
57
describe the clinical presentation, investigation and management of Rubella in pregnancy and in the newborn
arthritis in pregnancy
58
describe the clinical presentation, investigation and management of Rubella in pregnancy and in the newborn
CP:
- fever
- fine, red, maculopapular rash
- lymphadenopathy
- arthritis in pregnancy
- congenital infection: up to 90% risk of fetal malformation in 1st trimester, sensorineural hearing loss/retinopathy in the 2nd trimester.
- growth restriction, cataracts/microphthalmis/retinitis, hepatomegaly/jaundice/hepatitis, virus in urine, bone abnormalities, intracranial calcification, hydrocephalus, microcephalous, heart defects, splenomegaly, rash, anaemia in newborn
Ix:
- detection of IgM and IgG antibodies in serum or saliva
- congenital diagnosed by finding specific IgM persistent antibodies (>6months) in an infant, or viral detection by culture or NAAT
Mx:
- vaccine pre-pregancy: live vaccines are contraindicated in pregnancy
- live attenuated combined vaccine (MMR) given between 13-15months, with booster dose given at school entry
extra:
- transmission = resp. droplets
- infected from 7days before rash appears until 14 days after
59
describe the clinical presentation, investigation and management of Toxoplasmosis in pregnancy and the new born
CP:
- asymptomatic in 90% of cases
- cervical lymphadenopathy, low-grade fever if normal immune system
- disseminated disease if immunosuppressed: cerebral abscess, encephalitis, choroidoretinitis, myocarditis, myositis, pneumonitis, hepatitis
- congenital infection: main syx = cerebral calcification, hydrocephalus and retinal damage
Ix:
- serology
- USS / MRI
Mx:
- pyrimethamine and sulfadiazine fro 12 months
extra:
- acute infection with T.gondii, a protozoan parasite, may result from the consumption of raw or undercooked meat and from contact with the faeces of recently infected cats
- life-long. HIV may reactivate infection
60
describe the clinical presentation, investigation and management of Varicella Zoster Virus in pregnancy and the newborn
CP:
- vesicular rash. appear as crops
- mild systemic symtom: fever, malaise, headache, abdominal pain
- pneumonitis in pregnancy/adults
- severe neonatal infection
- first half of pregnancy; risk (rare) of foetus developing severe scarring of the skin and possibly ocular and neurological damages and digital dysplasia
- within 5 days before and 5days after delivery, foetus unprotected by maternal antibodies about 25% develop vesicular rash. mortality rate of 30%
Ix:
- clinical diagnosis
- NAAT
- characteristic giant cells in stained vesicular fluid
- cultures
Mx:
- acyclovir or valaciclovir
- live attenuated virus
- zoster immune globulin given to those in close contact with infection who are at risk of serious disease (eg pregnant women)
extra:
- airborne
- virus remains latent in posterior root ganglion
- 20% reactivate as shingles - dermatome
- test varicella-zoster immunoglobulin G antibodies -> +ve means immunity, if -ve seek advice; immunoglobulin prophylaxis may be needed
61
describe the clinical presentation, investigation and management of parvovirus (Fifth disease) in pregnancy and the new born
CP:
- risk arthropathy/ arthritis in pregnancy
- red rash on arms, legs and cheeks (slapped-cheek disease)
- joint pain, swelling
- life-threatening anaemia for unborne
- hydrops fetalus + risk of fatal loss
- usually mild ion children
Ix:
- test for antibodies
Mx:
- no treatment
- OTC pain relief
- additional monitoring during pregnancy
- blood transfusion for baby with anaemia (rare)
extra:
- airborne virus
62
what infections are screened for during antenatal screening at 8-12 weeks (ideally before 10 weeks)?
*NB screening is offered again at 20 weeks if initially declined
syphilis (treponema pallidum)
Hepatitis B
HIV
63
hiv:
a) what is the route of MTCT?
b) what should be done once mother is tested +ve for HIV?
c) what are mothers treated with to reduce viral load?
a) intrauterine, intrapartum (at delivery) or postpartum (breastfeeding)
b) check viral load, resistance testing and CD4
c) Anti-retroviral therapy
64
neonatal sepsis:
a) what is the most common cause of neonatal infection that can cause both early and late-onset sepsis?
b) define early onset sepsis?
c) what increases the risk of early onset infection?
d) define late-onset sepsis
a) group B streptococcus (faecal or vaginal carriage)
b) <48hrs after birth, bacteria have ascended from the birth canal and invaded the amniotic fluid. these babies have pneumonia and secondary bacteraemia. in contrast, early onset viral infections (+listeria) is acquired via placenta
c) prolonged or premature rupture of the amniotic membranes, and chorioamnionitits is clinically evident
d) >48hr after birth, source of infection is the infants environment
65
neonatal conjunctivitis:
- what is the likely causative agent of a baby (<48h old) with purulent discharge with conjunctival injection and swelling of the eyelids?
gonococcal infection. Chlamydia trachomatis eye infection usually presents with purulent discharge with swelling of the eyelids, at 1-2 weeks of age (but may also present shortly after birth)
66
TorF? primary infections have a much higher risk of transmission to foetus than recurrent maternal infection?
True
67
what antibody is used to help diagnose congenital infections(e.g. rubella, CMV, toxoplasma)
IgM.
68
severe mental health disorder in women is associated with what factors involving pregnancy?
- unwanted pregnancies
- pregnancies form sexual assault
- terminations
- sexual partners
- stop medication abruptly
69
discuss the features of the conditions specific to childbirth: post natal 'blues', PND and puerperal psychosis, and their Tx
postnatal blues:
- 50% incidence
- experience low mood and feel mildly depressed 3-10 days post-partum
- probably due to the sudden hormonal and chemical changes
- symx include feeling emotional and bursting into tears for no apparent reason; irritable, low mood; anxiety and restlessness
- no specific Tx; spontaneous resolution in days
PND:
- 10-15% of mothers have mild - moderate. 3% severe (significantly impair function)
- onset within 1 month
- symx include loss of interest in baby, feeling of hopelessness, not being able to stop crying, memory loss or unable to concentrate, excessive anxiety, panic attack, sleeplessness etc
- use aid of depression screening tests
puerperal psychosis:
- onset 7-14days post-partum
- affective or schizophrenic like psychosis, including delusions, hallucinations, lack of insight
- potential risk of harm to baby
70
consider how pregnancy and breastfeeding may impact on the pharmacological Tx of these disorders
pregnancy pharmacokinetics:
- delayed gastric emptying and longer intestinal transit time: increased absorption
- reduced blood flow to legs in late pregnancy: reduced absorption of IM drugs
- increased plasma volume: dilution effect
- increased body fat: serum lipids compete for protein-binding sites and alter unbound drug concentrations
- increased metabolism: lower serum levels of psychotropics
- increased constipationa and lower BP can potentiate SEs
breastfeeding:
- maternal plasma level
- drug half lide
- lipid solubility, breast milk is fatty and concentrates lipophilic drugs including psychotropics
- protein binding; free drug transfer into breast milk
- time since delivery: post party = larger gaps between alveolar cells in the breast increasing amount of drug that passes from maternal blood. reduces after 4 days
- if possible use non-pharmacological interventions (CBT)
- pharmacological Tx's: careful risk/benefit assessment; avoid 1st trimester exposure; use the lowest effective dose for shortest time; avoid polypharmacy
- SSRI's generally fine (sertraline popular) avoid paroxetine
71
what are the potential effects of severe mental illness on foetus and infant?
- small for dates, preterm and low birth weight
- increased incidence of child neurological abnormalities, developmental delays, attachment difficulties
- failure to thrive
72
what factors affect infant plasma drug levels?
- amount of drug ingested
- infant metabolism: neonates have a reduced capacity to metabolise drugs for at least the first 2 weeks, this could increase with a preterm or ill infant
- infant ex creation: the neonate kidney is less efficient than an adult and only reaches that level at 2-5 months
- CNS exposure: the blood brain barrier of a neonate is immature
73
what neonates are at particular risk of serious illness?
- low birth weight babies
- those with previously recognised medical problems e.g. congenital abnormality
- babies from socially disadvantaged families
74
what symptoms or signs may indicate/ elicit suspicion of serious illness in neonate?
fever:
-sepsis evaluation with T>38
feeding:
- volume taken in in previous 24 hours is < 50% of normal
urine output:
- < 4 wet nappies in 24hrs indicates significant decrease in fluid intake
peripheral circulation:
- pale/cyanosed/cold
- cap refil >2secs
responsiveness
- poor response to stimulation
- weak cry
activity:
- decreased activity/movement and increased sleep
breathing difficulty:
- resp distress signs = tachypnoea (RR >60/min), recession, expiratory grunt, nasal flaring, cyanosis
apnoea:
- pause in resp >20secs
- central or obstructive or combined
vomiting :
- in excess of normal
- bile stained (abnormal until proven otherwise)
cyanosis
seizures (eye rolling or jerky movements)
severe jaundice (risk of bilirubin encephalopathy)
75
a) what is the treatment of group B strep infection (overwhelming sepsis in neonate) in neonates
b) treatment for coliform infection (e.g. e.coli) in neonates?
a) Benzlpenicillin IV
b) Gentamicin IV
(iv recommended in neonates)
76
what causes neonatal jaundice?
normal elevation of serum bilirubin in first week of life. due to:
- increased production (accelerated RBC breakdown)
- decreased removal (transient liver enzyme insufficiency)
- increased reabsorption (enterohepatic circulation)
77
by watch age should baby stop losing weight?
by 3 days old (no more than 10%)
78
define meconium
passage of the first stool within first day or 2. composed of materials ingested during the time in the uterus
(once milk starts to come through get transitional faeces (day 3) -> yellow/golden stools if breast fed - green if bottle fed)
pinky/chalk deposits = normal in first few days; urate crystals indicated baby is producing concentrated urine
79
early jaundice - in first 24hrs of life - is uncommon. what does this suggest?
- haemolysis (rhesus/ ABO incompatibility and others including hereditary spherocytosis or elliptocytosis)
- > think potential sepsis
-hyperbilirubinemia in low birth weight and prem babies. Tx = phototherapy
80
if prolonged jaundice (>2weeks) is unconjugated and haemolysis, hypothyroidism and urine infection are excluded what is the cause?
breast milk jaundice
| - harmless and requires no further action
81
what condition are we trying to prevent when treating jaundice?
kernicterus - bilirubin induced brain dysfunction
82
what are the DD of crying babies?
- reflux oesophagitis
- colic (>3hrs/day for >3days/week, baby well and thriving otherwise, improves by 3-4months)
- cows milk protein or lactose intolerance
- UTI
- otitis media
- raised intracranial pressure
- acute causes will not be colic: corneal foreign body, incarcerated inguinal hernia, hair-thread tourniquet
83
list 3 DD of vomiting in neonates
1. increased intracranial pressure
2. Hx of maternal polyhydramnios suggests upper GI atresia ('double-bubble' seen on XR-film)
3. obstruction (e.g. hypertrophic pyloric stenosis; bile stained emesis suggests intestinal obstruction beyond the duodenum and required Ix)
84
describe how labour is managed using a cartogram
- assessment of Power (frequency + duration of contractions), Passenger (fetal heart monitoring, position, station, moulding, caput) and Passage (effacement and dilatation of cervix)
- commenced following accurate diagnosis of established labour
85
a) define induction of labour
b) what are the indications for induction?
c) what are the methods of induction?
a) process of starting labour
b) prolonged pregnancy, maternal diabetes, twin pregnancy, pre-labour rupture of membranes, fetal growth restriction, hypertensive disorders
c) pharmacological methods:
- prostoglandins (promote cervical ripening and stimulate uterine contractions - vaginal route; gel/tablet/pessary)
- syntocinon (synthetic oxytocin, only used after amniotomy, stimulate uterine contractions; IV infusion/ dose titration to achieve contractions 4:10)
mechanical:
- membrane sweep
- amniotomy/ ARM
- balloon/lamaria tents (soften and open cervix)
*cervical scoring system: <8 = unfavourable cervix -> ripen with PG. >8 = favourable cervix -> proceed with amniotomy
86
a) define augmentation of labour
process of accelerating labour which is already underway e.g. pre-labour rupture of membranes or delay in the 1st/2nd stage of labour
87
what are the potential complications of induction and augmentation?
uterine hyperstimulation:
- risk with PG/ syntocinon
- fetal distress
- remove stimulus
- use tocolysis
increased obstetric intervention
- e.g epidural or assisted vaginal delivery
uterine rupture:
- caution in the presence of previous uterine surgery, esp with PG
88
what are methods of pain relief during labour?
non-pharmacological:
- 1:1 maternal support
- birthing pools
- breathing + relaxing techniques/ acupuncture/ hypnosis/ massage/ aromatherapy/ TENS
inhaled pharmacological:
- entonox (50:50 NO +O2)
- SEs = nausea, vomiting, horsiness, light-headedness
opioid analgesics:
- diamorphine 5-10mg; SEs = maternal nausea/ vomiting/ drowsiness, neonatal drowsiness/ resp. depression
- Remifentanil IV infusion (PCA)
regional analgesics:
- epidural; SEs = hypotension, increased malposition, pyrexia, may slow down 2nd stage, pruritus
- spinal; SEs = hypotension, pyrexia, pruritus, high block
Delivery:
- LA: perineal or pudendal block
- regional
- GA: SEs = tissue oedema, reduces gastro-oesophageal tone, increased intrabdominal pressure, delayed gastric emptying, increased gastric acidity
89
what is the ultimate aim of intrapartum fetal monitoring (doppler or CTG)?
prevention of death and morbidity due to hypoxia (detect changes in foetal HR)
90
list 3 indications for continuous CTG monitoring in labour
1. maternal tachycardia
2. maternal pyrexia
3. presence of significant meconium
91
fetal blood sampling (from scalp) can be done to assess fetal acideaemia. what pH parameters are used?
pH >7.25 is reassuring
| pH <7.20 are non reassuring / immediate delivery
92
what are the steps of normal vaginal delivery?
1. head in pelvic brim in L or R occipitolateral/ occipitotransverse position
2. neck flexes so that the presenting diameter is suboccipitobregmatic
3. head descends and engages
4. head reaches the pelvic floor and occiput rotates to occiptoanterior
5. head delivers by extension
6. descent continues and shoulders rotate into anteroposterior diameter of the pelvis
7. head restitutes
8. anterior shoulder delivered by lateral flexion from downward pressure on the baby's head
9. posterior shoulder delivered by lateral flexion upwards
93
what are the different types of malpresentation in delivery?
- face: hyper-extension of the head
- brows
- breech: frank breech (extended); complete breech (flexion); footing breech
- transverse lie and oblique lie
94
what are the indications for assisted vaginal delivery (ventouse cup or forceps)?
maternal:
- failure to progress in active second stage go labour (prim: 2-3hrs; porous: 1-2hrs)
- maternal exhaustion
fetal:
- suspected fetal compromise in second stage of labour
- pathological CTG
- abnormal FBS
as prophylactic shortening of second stage:
- hypertensive crisis
- cardiac disease
- maternal cerebrovascular disease
95
list 3 serious and 3 frequent risks os assisted vaginal delivery
serious:
1. 3rd and 4th degree perineal tear
2. fetal facial nerve palsy
3. fetal intracranial haemorrhage
frequent:
1. postpartum haemorrhage
2. vaginal tear/abraision
3. marking on baby (forceps on face or cup marking on scalp)
96
a) define shoulder dystocia
b) what are the risk factors that make someone more likely to have a baby with it?
c) how is it managed?
d) what are the consequences of SD?
a) impaction of the fetal anterior shoulder behind the symphysis pubis making delivery difficult
b) diabetes, obesity, macrosomia
c) call for help; episiotomy; legs to McRoberts; moderate subrapubic pressure; enter manouvres; remove posterior arm; roll over
d) hypoxia (trapped umbilical cord, pH drops); nerve damage (C5-T1, Erb C5-6)
97
classification of perineal tear
1st degree:
- injury to perineal skin +/or vaginal mucosa
2nd degree:
- injury to perineum involving perineal muscles but not the anal sphincter
3rd degree:
- injury to the perineum involving the anal sphincter complex
- grade 3a tear = <50% of EAS thickness torn
- grade 3b tear = >50%
- grade 3c tear = both EAS and IAS torn
4th degree:
- injury to perineum involving the anal sphincter complex and anorectal mucosa
98
what are the indications for episiotomy?
- large tear anticipated
- suspected fetal compromise
- shoulder dystocia
- 'rigid' perineum
99
what are some of the indications and risks for C-sec?
indications:
- breech/ malpresentation
- previous caesarean
- placenta prevail
- failure to progress in labour
Risks:
- serious = emergency hysterectomy, increased risk of uterine rupture in subsequent pregnancies, bladder/ ureteric injury
- frequent = persistent wound and abdominal discomfort in first few months, infection, lacerations to baby
100
list causes of maternal collapse
4H's and 4T's:
1) hypoxia (pulmonary oedema, sepsis)
2) hypovolemia (haemorrhage)
3) hypothermia
4) hypo/hyperkalaemia (sepsis)
1) thromboembolic (VTE, AFE)
2) toxins (LA, MgSo4)
3) Tamponade
4) Tension pneumothorax
+ eclampsia/ pre-eclampsia
101
postpartum haemorrhage:
a) define primary and secondary
b) list 4 potential causes (4 T's)
c) how is it managed?
a) blood loss (>500mls) wihtin 24hours of delivery
OR
>24hours and <12weeks following delivery, respectively
primary can be minor (500-1000mls/ no hypovolaemic shock) or major (>1000mls/ hypovolaemic shock)
b)
1. tone (uterus doesn't contract)
2. retained tissue (retained placental tissue inhibiting uterine contractibility)
3. trauma (perineal tear, uterine incision, episiotomy etc.)
4. thrombin (DIC, sepsis, abruption, AFE, PPH)
c) - assess and resuscitate mother (obs, help, IV access, fluids, blood)
- identify and manage cause (e.g. complete placental delivery, is uterus contracted -> mechanical compression, pharmacological, advanced procedures (embolisation, uterine a. ligation, hysterectomy)? is there trauma?)
102
what are the pharmacological management options of PPH?
- syntocinon
- ergometrine
- carboprost
- tranexamic acid
103
a) define amniotic fluid embolism
b) what are 3 risk factors
c) list 3 complications
a) very uncommon emergency, amniotic fluid enters the blood circulation of mother and triggers a serious reaction. results in sudden collapse, acute hypotension, respiratory distress, acute hypoxia
* usually in labour or within 30mins
b) 1. maternal age; 2/ polyhydramnios; 3. operative delivery
c) 1. pulmonary hypertension; 2. left heart failure and arrhythmia; 3. coagulopathyq and PPH
104
what is the management of MgSO4 (Tx of eclampsia) toxicity (respiratory.depression, drowsiness, confusion, loss of reflexes?
calcium gluconate
105
what is the management of :LA toxicity (confusion, hallucination, metallic taste, muscle twitching)
lipid emulsion
