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Organ System

Reproductive system

Physiologic Changes in
the 1st trimester of
pregnancy
Uterine
hypertrophy
Uterine ascent
from the pelvis
and rotates to the
right
Cervical softening
and cyanosis,
squamous
epithelium of
ectocervix
becomes
hyperactive,
endocervical
glands become
hyperplastic, and
endocervical
epithelium
proliferates and
grows out over
ectocervix
Cervical ripening
Ovulation ceases
and maturation of
follicles is
suspended
Breast tenderness
and paresthesias.

Mechanisms involved

Estrogen and
progesterone
stimulates uterine
hypertrophy
uterine size
increases related
to pressure exerted
by expanding
products of
conception.
As the uterus
enlarges, it
displaces the
intestines laterally
and superiorly and
it ascends from the
pelvis where
tension is exerted
on the broad and
round ligaments.
The dextrorotation
is likely caused by
the rectosigmoid
on the left side of
the pelvis.
It is resulted from
increased
vascularity and
edema of the
entire cervix,
together with
hypertrophy and
hyperplasia of the
cervical glands.
Cervical ripening is
due to decrease
collagen and
preteoglycans and
increase water
content
The single corpus
luteum functions

Cardiovascular system

Cardiac output
increases
Heart size
increases and and
is rotated on its
long axis

Respiratory system

Increase tidal
volume and vital
capacity
Increased oxygen
delivery
Physiologic
dyspnea

maximally during
6-7 weeks of
pregnancy thus,
contributes little to
progesterone
production.
Feeling of fullness ,
tingling or
tenderness of the
breast due to
stimulation of
bnreast tissue by
increased level of
estrogen
Due to a 10%
increase in stroke
volume and
increase in pulse
rate by 10-15% per
minute. There is a
decrease in mean
arterial
pressureand
vascular resistance
while an increase
in the blood
volume and basal
metabolic rate.
Heart size
increases and is
elevated upward
and to the left
because of
displacement of
the diaphragm as
the uterine
enlarges
Fetal PCO2 must be
greater than
maternal PCO2,
thus, maternal
respiratory center
is reset.
This is due to the
increased tidal

Urinary system

Increase
glomerular
filtration rate and
renal plasma flow
Urinary frequency
increases, Nocturia

Endocrine system

Increase in serum
prolactin
Increase in cortisol
and other
corticosteroids
Increase in the
levels of principal
carrier proteinthyroxine-binding
globulin, which in
turn increase T4
and T3
concentrations but
do not affect the
physiologically
important serum
free levels

volume imposed by
pregnancy.
Progesterone acts
centrally where it
lowers the
threshold and
increase the
sensitivity of
chemoreflex
response to Carbon
Dioxide
Hyperfiltration is
due to:
(a)hypervolemiainduced
hemodilutionwhich
lowers protein
concentrationand
oncotic pressure of
plasma entering
the glomerular
microcirculation,
and (b) renal
plasma flow
increases
Due to bladder
compression by
enlarging uterus
The increase in
maternal serum
prolactin is parallel
in the enlargement
of pituitary gland
Half-life of plasma
cortisol is
increased while its
clearance is
reduced
Increase in TBG
result from both
higher hepatic
synthesis rates-due
to estrogen
stimulation- and
lower metabolism
rates due to

Integumentary system

Hyperpigmentation

Striae
gravidarumand
linea nigra on
abdomen

Metabolic changes

Melasma
(chloasma) on the
face
(mask of
pregnancy)
Weight gain
Increase insulin
sensitivity
Fat deposition

increased TBG
sialylation and
glycosylation
levels of
melanocytestimulating
hormone by the
posterior pituitary
gland are elevated
remarkably

Attributed to the
uterus and its
contents, the
breasts, and
increases in blood
volume and
extravascular
extracellular fluid
Favors glycogen
synthesis and
storage, fat
deposition, and
amino acid
transport into cells.
Uterus and
placenta require
fat, carbohydrate
and amino acids

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