PBL 36 Flashcards
Pathophysiology of pre-eclampsia
- Cause/mechanism
- Signs/symptoms/clinical manifestation
- Risk factors
- Diagnosis
- Treatment
- Cause/mechanism
- Defective spiral artery remodelling causes the placenta to not develop properly
- Leads to ischaemia in the placenta, causing an imbalance in anti & pro-angiogenic factors. This imbalance leads to widespread endothelial dysfunction, affecting ALL maternal organ systems - Signs/symptoms/clinical manifestation
- High blood pressure >= 140/90 on two separate readings taken 4/6 hours apart
- Proteinuria
- Usually occurs in third trimester
- Peripheral oedema
- Vision problems
- If left untreated –> leads to seizures = eclampsia - Risk factors
- Diabetes
- Hypertension
- Kidney disease
- Lupus
- Having a condition during pregnancy
- First pregnancy
- Family history
- Over age of 35
- Obesity - Diagnosis
- Blood test for placental growth factor - low levels could be a sign but further tests needed
- Blood pressure taking
- Urine tests for protein - Treatment
- Delivering the baby
- LABETALOL for hypertension, used for pregnant women
- Having baby around 37-38th week, so labour may be artificially induced or you may need a caesarian section
Overview of the 3 stages of labour
Stage 1:
- Onset of contractions
- Dilation of cervix to 10cm
- Sometimes Braxton hicks can be felt for up to a week before labour (false labour contractions)
Stage 2:
- Time from full dilation to delivery of the baby
Stage 3:
- From delivery of the baby to delivery of the placenta
Hormone released during labour
- Progesterone
- Steroids
- Oxytocin
- Prostaglandins
- Corticotrophin releasing hormone
- Interleukins
- Calcium
Why can labour not begin until progesterone effects are diminished? How is this solved?
Because progesterone inhibits uterine contractions
- Oestrogen levels rise at the end of gestation, producing changes that overcome the inhibiting effects of progesterone
How do oestrogen levels rise towards the end of gestation?
- Oestrogen levels rise due to the placenta releasing corticotrophin releasing hormone
- This stimulates the anterior pituitary of the foetus to secrete adrenocorticotrophic hormone (ACTH)
- ACTH stimulates the foetal adrenal gland to secrete cortisol and DHEA (major adrenal androgen)
- The placenta then converts DHEA to oestrogen
Effects of oestrogen on the onset of labour
- High levels of oestrogen cause the number of receptors for oxytocin on the uterine muscle fibres to increase, and cause uterine muscle fibres to form gap junctions with one another.
- Oxytocin released by the posterior pituitary stimulates uterine contractions, and relaxin released by the placenta assists by increasing the flexibility of the pelvic symphysis and helping dilate the uterine cervix.
- Oestrogen also stimulates the placenta to release prostaglandins, which induce production of enzymes that digest collagen fibres in the cervix causing it to soften.
How are uterine contractions controlled?
- Control of labour contractions occur via a positive feedback cycle. Contractions of the uterine myometrium force the baby’s head or body into the cervix, distending it. Stretch receptors in the cervix send nerve impulses to neurosecretory cells in the hypothalamus, causing them to release oxytocin in the blood of posterior pituitary. Oxytocin stimulates myometrium to contact more forcefully.
Uterine contractions: true vs false labour
True labour: Uterine contractions are at regular intervals, producing pain, back pain on walking, dilation of the cervix, and show of blood discharge containing mucus.
False labour: Braxton Hick contractions. Contractions with no pain on walking etc… No cervical dilation
Effects of late pregnancy on the mother: Cardiovascular changes
- Heart rate - Steady rise in heart rate and stroke volume, which required cardiac remodelling (size of the heart increases by 12%), from about 64bpm to about 76bpm
- Blood pressure - Remains largely unchanged, small drop mid gestation, hypotension develops more readily during pregnancy
- Blood volume - Increases steadily from week 6-8 to about week 32, physiological remodelling occurs to support this (increased venous return, increased atrial size)
- RBC increase not as high so fall in haematocrit
Effects of late pregnancy on the mother: Respiratory changes
- VC is maintained but TC is reduced, causing a decrease in RV
- Respiratory effort increased
- Diaphragm elevated
- Ribcage displaced upwards
- Breathing becomes thoracic
- Responsiveness to pCO2 increases - action of progesterone, increased TV
Effects of late pregnancy on the mother: Renal and urinary changes
- Kidneys enlarge: caused by increased excretion of waste products, increased Na+ reabsorbtion, increased blood flow
- Ureters displaced and enlarged
- Decreased bladder tone
- Urinary reflux from bladder to ureters
- Urinary stasis - increased UTI risk
Effects of late pregnancy on the mother: breast changes
- Stroma increases in bulk
- Lobules increase in size
- Areolar darken
- Nipples more pronounced
- Lactiferous ducts expand and branch for milk delivery
Effects of late pregnancy on the mother: overview
- CV changes
- Respiratory changes
- Renal changes
- Breast changes
- Weight gain (11kg average)
Which hormone stimulates growth and development of milk ducts?
Oestrogen
Which hormone stimulates growth of alveoli and lobules
Progesterone
Which hormone mimics prolactin and GH, causing breast, nipple and areola to enlarge?
Human placental lactogen
Causes and consequences of intrauterine growth restrictions
Causes:
- Issues with the placenta, so the foetus does not receive the necessary nutrients and oxygen
- Smoking
- Drinking alcohol
- Drug use
- Infection such as: cytomegalovirus, rubella, toxoplasmosis or syphillis
- Medical condition such as lupus, anaemia or clotting issues
Consequences:
- Limited body and organ growth
- Decrease O2 levels at birth
- Meconium aspiration
- Hypoglycaemia
- Difficulty maintaining body temperature
- Polycythaemia (>RBCs)
Where are the breasts located? Where do they span vertically?
Anterior thoracic wall
- Span between 2nd and 6th IC