Beruflich Dokumente
Kultur Dokumente
BCH,FWACS, FMCOG)
MEDICAL DIRECTOR/CONSULTANT OBSTETRICIAN &
GYNAECOLOGIST, NYANYA GENERAL HOSPITAL, ABUJA.
MEDICAL DIRECTOR/CONSULTANT OBSTETRICIAN &
GYNAECOLOGIST GUINEA SAVANNAH MEDICAL CENTER,
ABUJA.
INTRODUCTION
SYMPTOMS AND SIGNS OF PREGNANCY
FETO MATERIAL INTERACTIONS
CHANGES:
ENERGY CONSUMPTIONS
METABOLIC
HEMATOLOGICAL
CARDIOVASCULAR
RESPIRATORY
URINARY
GASTROINTESTINAL TRACT
ENDOCRINE SYSTEM
REPRODUCTIVE
MUSCULAR SKELETAL
CONCLUSION
It is imperative that human race must continue, in order for this to
happen, Reproduction which is one of the characteristics of living things
must occur and this is the very bases of obstetrics and gynecology.
Pregnancy which is the very next step after fertilization is a very vital
part that brings the fetus to the point at which it can relatively function
independently on earth.
The maternal body undergo some changes or adaption to enable her carry
out this function effectively. These adaptations are seen as normal,
hence the name physiological changes in pregnancy. Every maternal
organ adapts to pregnancy, each at a different time and in a different
way as pregnancy progresses to accommodate the increase demand of
fetal growth, development and delivery.
As pregnancy begins, the fetus, corpus luteum and placenta produce and
release increasing quantities of hormones, growth factors and other
substances into the maternal system. This leads to the cascade of events
that transforms the mother’s physiology.
One of the most important single change is the vascular endothelium of
the maternal circulation and this is particularly important in the placenta
bed from where the fetus is nourished.
Symptoms begin to occur by the end of 6 weeks
Missed menses
Amenorrhea
Nausea
Ptyalization (excessive salivation)
Vomiting
Excessive fatigue and sleepiness
Frequent urination
Breast fullness
Increased hyperpigmentation of the areola
Others
There is usually signals or interaction
between the fetus and the mother right from
embryo implantation –mainly via the
trophoblast at the placenta bed.
The mediators are majorly hormones e.g.
estrogen, progesterone, hCG, Growth
factors and their receptor, other factors that
are released into the maternal circulation
e.g. Cytokines
INCREASE ENERGY CONSUMPTION
Is the greatest change in pregnancy.
Basic Physiological Process (1440 Kcal/day) i.e. 66% of total
energy need in the non pregnant female. E.g. systemic
changes, secretion, thermoregulation, growth and repair –
due to the demand of the fetus, placenta, uterus, breast
growth etc.
Activities of daily living, accounts for 17% of total energy in
NPS this is about 360Kcal/day. Although there is reduction
in activity generally with advancing pregnancy.
Work, this depends on occupation. It accounts for 10% of NPS
equivalent to 150-200kcal/day- this reduces with
advancing gestation.
Specific dynamic action of food metabolism stimulated by
food intake 7% of NPS = 150kcal/day .
Overall there is 14% increase in energy requirements during
pregnancy.
Total weight gain is about 10kg -14.5kg to non pregnant state
distributed as follows;
Fetus =3.5kg
Placenta =0.5kg
Amniotic fluid =1.5kg
Uterus= 1kg
Blood increase =1.5kg
Breast =1kg
This result in 25% of increase of the non-pregnant weight = 10-
14kg. Main increase occurs in the 2nd half of pregnancy about
0.5kg per week.
1st trimester, 2kg ( there may be loss from vomiting and loss of
appetite).
2nd trimester 5kg
3rd trimester 5kg( there may be loss from reduced amniotic fluid)
About 6kg is accounted for by ECF, fat and protein storage.
Overall positive Nitrogen Balance
20% increase in dietary protein
500g of protein would have been retained by the end
of pregnancy
50% accounted for by maternal gain
50% by fetus and placenta
Fetus requires little protein in the 1st half of
pregnancy and there can be negative balance
2/3rd of required in the last 12 weeks.
Half in the last 4 weeks
Uterus and breast use much protein in growing tissues
in addition to storage for lactation in the breast.
Average of 12g of Nitrogen/day required
The steroids produced by the placenta reduce
glycogen formation and deposits by increasing
glycolysis.
HPL, prolactin and cortisol inhibit insulin release,
thus encouraging availability of glucose to the fetus
and the body.
In pregnancy, fasting easily results in hypoglycemia
compared to NPS and causes increased
Hydroxybutyric acid, Acetoacetic acid, and ketone
bodies bc of fatty acid is used for energy.
Glucose level is lower in the fetus encouraging
transportation by carrier mediated mechanism.
Increased glucose levels in the renal circulation
together with an increased GFR result in glycosuria
seen commonly in pregnancy
Fat is a major energy store in pregnancy
At 30 weeks approximately 4kg is stored in the abdominal wall,
buttocks, thigh and breasts.
Fat accounts for 2% of fetal weight at 32 weeks
Fat accounts for 12% of fetal weight at term
There is a greater absorption of fat by the mother.
Higher circulating lipid and lipoprotein.
Triglyceride, fatty acid, cholesterol and phospholipids increase
after 8 weeks of pregnancy . Due to increased Estrogen and
Insulin resistance
HDL increases by 12wks till term
LDL decreases initially then increases at 2nd and 3rd trimester
Increased Estrogen, increased Progesterone, Insulin promotes
accumulation of maternal fat stores and inhibits lipolysis.
In late pregnancy fat is mobilized for energy preserving amino
acid and glucose for the fetus
40% of circulating calcium bound to albumin
Plasma Albumin concentration decrease in pregnancy,
hence total plasma calcium decrease.
Little change in unbound calcium
positive calcium balance in favour of the fetus to
allow skeletal development which is of high demand.
There is increase in gut absorption
Mobilizes skeletal calcium reserve
Restricting renal lost
Gut absorption of calcium is increased by 30% bc of
Vit D metabolite 1,25-Dihydroxycholecalciferol and
increase parathyroid hormones PTH.
Fetus utilizes calcium late
Maternal serum calcium levels is steady
Increased requirement than in the NPS
Only from diet
Essential for fetal development
Docosahexaenoic acid, most important Omega -
3- Fatty Acid, it helps fetal CNS and retinal
development.
It may improve fetal visual cognitive
development.
It may reduce preterm delivery
From vegetable oil and oily fishes
Seen in fish oil supplement
Not generally evidence based
Too little in diet
Absorbed in ferrous form in the Duodenum and Jejunum
Transported as Transferrin
10% of ingested iron is absorbed
Decreased serum Iron bc of increased Total Iron Binding Capacity
Stored as ferritin or Haemosiderin
Active transportation
Iron is mostly passed to the fetus in the 3rd trimester
Total iron requirement =1g
Fetus and placenta =300mg
RBC =400mg, during delivery(45mg/100ml) is lost.
Obligatory =200mg via feaces and skin desquamation.
300mg saved from 10 months during pregnancy bc of amenorrhea.
maternal iron loss is 30mg/ menstrual cycle
Daily requirement is 1mg. ( 60mg of elemental iron in 300mg FeSO4/day)
2nd half =daily requirement 6-7mg
In the absence of supplementations , there is decrease Hb, serum iron, serum ferrous in
term pregnancy .
Pregnancy is an inevitable iron deficiency state
CVS changes in pregnancy mimic those of heart diseases
Elevation of the diaphragm- palpitation and adjustment of
lung volume,
apex beat =4th left intercostal space bc of elevation of the
diaphragm.
Increase in minute ventilation; air/min = tidal vol x RR
All leads to breathlessness
Increased total body Na and H2o
Venous compression by the gravid uterus leads to syncope
Increase in Pulse rate
Possible systolic murmur –due to decreased blood velocity
bc of reduced peripheral resistance from vasodilation.
Increase in left ventricle, right and left atrial diameter
3rd heart sound from rapid diastolic filling occurs
Occasionally 4th heart sounds left axis deviation
Cardiac Output – starts increasing at 5 wk,
peaks at 30-34 week(40-50%), then remains
static till term
Cardiac output increases during labour by 50%
and immediate delivery bc of contraction and
blood push into systemic circulation.
Mean Arterial pressure (MAP) rises
Increase CO due to;
Increase blood volume
Increase O2
Increase CO = very increased stroke volume X
P.R (despite decrease peripheral resistance)
Pulse rate increases by about 15bpm.
Systemic vascular Resistance decreases
because of relaxation of smooth muscle
during pregnancy from progesterone
effect.
There is decrease in maternal B.P due to
decrease in peripheral resistance –despite
increase in cardiac output
B.P = C.O X P.R.
There is overall decrease in diastolic B.P
by 5-10mmHg
Antecubital venous pressure is unchanged
Femoral venous pressure is markedly raised
especially towards term due to;
pressure of the gravid uterus on the common
iliac veins more on the right side because of
uterine dextrorotation
Femoral venous pressure.
Non pregnant state = 8-10cm/H2o
While lying down = 25cm/H2o
While standing = 80-100cm/H20
Thus physiological edema reduces at resting
This also explains lower limb edema, varicose,
hemorrhoids and deep vein Thromboses.
No significant change in
CVP-central Venous pressure
MAP- mean Arterial pressure
PCWP –pulmonary Central wedge pressure
(Despite increase in blood volume, cardiac output and heart
rate due to significant fall in systemic vascular resistance,
pulmonary vascular resistance and colloidal osmotic pressure).
Supine Hypotension syndrome (postural Hypotension)
In late pregnancy
Compression effect on inferior vena cava at supine position.
Compensatory opening of the collateral circulation via paravertebral
and azygous vein
In 10% of women this fails which can reduce venous return to the heart
leading to hypotension, tachycardia and syncope.
Reverses if patient is placed in lateral position.
The increased venous return due to blood
squeezed out during contraction prevents
supine hypotension during labour.
Cardiac out put during labour increases by
2L/min
Systolic B.P lowered, but diastolic is much
lower in 1st and 2nd trimester rises in 3rd
trimester.
Peripheral resistance decrease, despite
increased cardiac output, thus increase pulse
pressure
Uterine blood flow
50ml/minl in NPS to 750ml/min near term due to;
Utero placental and fetoplacental vasodilation because of smooth muscle
relaxing effect of progesterone, Estrogen , Nitric oxide, prostaglandins, atrial
natriuretic peptide (ANP)
In pregnancy vascular endothelium is refractory to Angiotensin
11, endothelium 1 and other pressure agents bc of eroded tunica
media.
Pulmonary blood flow
600ml/min in NPS increases to 2500ml/min in pregnancy near term
Renal blood flow
80ml/min in NPS to 400ml/min at 16 wks and stabilizes till term
Blood flow through the skin and mucous membrane reaches
500ml/min at 36 wks
Thus there is increase heat sensation, sweating, stuffy nose
BLOOD VOLUME
Progressive rise during pregnancy though not
consistent
Increased Vascularity of enlarging uterus
Increased Utero placental circulation
Blood volume start to increase by 6 wks to maximum
40-50 % of NPS at 30-32 wks then stabilizes till term.
Plasma volume(whole blood without RBC,WBC and
Platelets) while in serum in addition there is no clotting
factor seen @ centrifugation.
Starts increasing by 6 wks, till 30 wks, this is parallel
to blood volume, plasma volume reaches to the
extent 50% or 1.25 liters of NPS.
Increase is more in multiparity, multiple pregnancy
and large baby.
RED BLOOD CELL AND Hb
RBC mass increase by 20-30%
RBC volume increase by 350ml due to increase 02 transport
RBC mass increases from 10wks and progresses till term
Iron supplement increases RBC mass by 30%
Reticulocyte by 2%
Increase Erythropoietin
Increase in plasma volume much (up to 40%) more than
RBC volume produces a relative fall in hematocrit
(PCV) i.e. haemodilution of pregnancy.
Total HB increases by 18-20%
At term fall is about 2% from the NPS
Advantages of relative Haemodilution
Reduces blood viscosity ensuring good gaseous exchange
Reduces the effect of supine and erect posture
Decrease actual blood loss during delivery
Ovary :
Corpus luteum 1st 8 weeks, 2.5cm
responsible for decidual reaction
Pregnancy luteoma 8-12 wks =orange colour
change from Corpus luteum.
Theca- lutein cysts finally.
Melanocyte stimulating hormone (MSH) from anterior pituitary
causes
Hyperpigmentation of the;
Umbilicus
Nipples
Abdominal midline (linea nigra) from xiphisternum
to symphysis pubis
Face (chloasma gravidarum ) or pregnancy mask ,ie cheek,
fore head, and the eyes, maybe patchy or diffuse
Striae gravidarum (stretch marks);
in abdominal wall, over the thigh, breast and flank due to
mechanical stretching of the skin with rupture of the
elastic fibers in the dermis
Also seen in increase aldosterone production
Vascular spider naevi and palmar erythma manifestation of
hyperdynamic circulation due to oestrogen
Breast increase in size majorly by hypertrophy,
proliferation of the ducts and alveoli and
connective tissue stroma- effects of estrogen
and progesterone
Axillary tail may become apparent
Montgomery’s tubercles becomes obvious
secondary areola becomes obvious
Ligament laxity may become pronounced due
to relaxin leading to back pain and pubic
symphysis dysfunction
Lumber lordosis may be seen in some pregnant
woman.
o
Uterine Hormones
Progesterone;
Produced by corpus luteum up to 7 wks
Produced by the placenta above 8 wks
Level rises steadily during pregnancy
(250mg/day)
Relaxes smooth muscle tone in the vessels, gut,
uterus, ureter and bladder
Raises temperature(thermogenic)
Increases fat storage
Induces over breathing –CO2 sensitivity
Breast development
Produced in early pregnancy by the ovary
In late pregnancy, placenta produces oestrone
and estradiol in hundred folds
estriol is produced by placenta with enzymes
from fetal adrenal/liver in one thousand fold.
Maximum output of estrogen 30-40mg/day
estriol accounts for 85% of the total estrogen
Polymerization of mucopolysaccharides of the
ground substance leads to loose connective
tissue in the cervix, pelvic joint and other joints.
Growth of uterus and breast via protein synthesis
H2O retention because
Decreased sodium excretion
Secreted by syncytiotrohoblast
Level rises as hCG level drops
No effect on fetus
Breast growth
Production of colostrums and milk(lactation)
Protein synthesis
Increase insulin secretion but
Inhibit insulin sensitivity (insulin resistance )
(diabetogenesis of pregnancy)
Lipolysisincreasing maternal blood glucose
available to fetus
Secreted by trophoblast
Detected as early as 10 days after conception
In early pregnancy, high level of hCG supports
implantation and development
Support corpus luteum secretion of estrogen and
progesterone until placenta takes over.
Peak level at 12 wks to 16wks
level constant after 16 weeks.
Disappears in urine 7-10 days post delivery
Controls placental secretion of estrogen and
progesterone
Suppress maternal immune response against
fetus
FSH and LH: are suppressed by estrogen and progesterone
Prolactin: rises throughout pregnancy for milk production
ACTH: increases water retention
MSH: increase skin pigmentation
ADRENAL/PANCREAS:
Cortisol:
Produced from maternal adrenal in early pregnancy together with
placenta in late pregnancy
25mg/day
Favours lipogenesis & glycolysis (increase blood sugar and fat
deposit)
Favours insulin responses to help control blood sugar
Modifies antibody activities
B-hCG is thyrotrophic
TBG increases because of increase estrogen
T3 and T4 increases in 1st half of pregnancy
T3 and T4 may decrease slightly because of TBG
as pregnancy progresses.
TSH is majorly increased when there is Iodine
deficiency or hypothyroidism
Decreased serum calcium increases PTH
secretion
Vit. D3 (Cholecalciferol) is converted to its
active form 1,25, Dihydroxycholecalciferol by
placenta enzyme 1-alpha hydroxylase to increase
calcium absorption
There two types of normal physiological
state in a woman. One in a non –pregnant
state the other in a pregnant state. If
interchanged will definitely lead to
disease(Pathological)conditions.
The whole essence of the adopted and
adapted physiology in a pregnancy state is to
keep the mother healthy and able to cope
with the stress imposed upon her while
nurturing the fetus in a healthy state to
effect the delivery of healthy baby to a
healthy mother.
Goodluck in your
Examinations.