Maternal Adaptations To Pregnancy Flashcards
Blood pressure
Overall decrease in BP
As fall in resistance not compensated for by increased CO
Lowest mid pregnancy
Diastolic props more
Cardiovascular changes
Increased CO 4.5 to 6 l/min established labour 8l/min
Decreased peripheral resistance by 40%, slowly increases again to term
Relaxation of peripheral vascular tone, establishment of new vascular beds, but blood volume increases by 40%
HR 70 to 85
SV 64 to 71
25% of CO to placenta
Plasma volume
Haemoglobin increases but as plasma increases more it’s diluted so dilution drop in Haemoglobin, haematocrit and RBC
Change in osmolality causes oedema
Plasma increase of 40-50%
Iron
700-1400mg extra iron required
Increase intestinal iron absorption
Placenta is rich in transferrin
B vitamins
B12 and B9 required for DNA synthesis
Lack of folate causes neural tube defects
Maternal stores fall to 10% of original
Respiratory changes
Total lung capacity decreased by 5%
Functional residual capacity decreased by 20%, makes mixing mor efficient
Tidal volume increase of 40%
Ventilation 6 to 10.5 l/m
Basal O2 only rises by 15% so women is hypo ventilating
Renal changes
Become enlarged-> increased vascular volume and intersitial space
Increase renal parenchyma
Increase glomerular dimeters
Dilation of calyces, pelvis, ureter (progesterone)
Increased RPF
Decreased resistance
Changes in tubular reabsorption
Urine modification
Increase RPF, decreases in late pregnancy-> increased glucose in filtrate
Increased GFR
FF declines in early and increases to normal in late pregnancy
Increased glucose reabsorption until theoretical threshold reached
Glucose excretion may be 10 times higher
Maternal glucose homeostasis start to mid
Fetus has little capacity for gluconeogensis-> must get glucose from mother
Increased glucose excretion causes deficit in mother
Ketones found in blood as fat used for energy
Decreased fasting glucose in first trimester
Increases back to normal from 12th week to term
Progesterone increases appetite and stimulates deposition of glucose in fat stores
Increased insulin secretion favours lipolyisis
Glucose homeostasis mid to term
Increased absorption
Increased gluconeogensis
Mobilisation of fatty acids by lactogen
Lactogen, prolactin, cortisol-> insulin antagonists
Maternal tissue becomes insulin insensitive
Replaces glucose deficit
Role of placenta in avoiding immune rejection
Stops direct blood contact
Synctiotrophoblast doesn’t have histocompatwbility antigens
Maternal immune cells destroyed in synctiotrophoblast by macrophages in stroma or lysosomes
Synctial knots may lead to peripheral tolerance of fetal antigens-> increased Treg (supressor) cells
Transfer of maternal IgG
Cross placenta
Only ones that aren’t against fetal antigens
Apart from rhesus antigen, mingling may occur
Provides immune resistance in fetus
Immune function of endometrium
Must be able to cause and immune response whilst tolerating sperm and fetus
Endometrial cells don’t circulate the body
Maternal macrophages, decidual cells, dendritic cells, natural killer T cells interact via soluble factors to provide local immunprotection of fetus
Immune cells in the endometrium
Dendritic
Helper T
T regulatory
Uterine natural killer
Under influence of pregnancy hormones
T helper decline relative to suppressor cells Treg-> act to decrease immune function
Local distribution of antigen presenting dendritic cells-> secrete anti inflammatory cytokines (IL-10)-> present fetal antigens-> aids T cell apoptosis and conversion to Treg-> maintain materno-fetal tolerance
Extravillous trophoblasts in relation to immune response
Invade endometrium and re modle spiral arteries
Have unique HLA class 1 antigens, C, G, and E
HLA-G is not expressed in any other maternal or fetal cells-> used to suppress immune reactions
Alter the ability of decidual natural killer cells to kill
Binding of HLA-G to natural killer-> inhibiton of cytokines production
