MATERNAL PHYSIOLOGY IN PREGNANCY

Pregnancy causes physiologic changes in all maternal organs system, most returns to normal
after delivery
Major adaptations in maternal anatomy, physiology, and are required for successful pregnancy
Many of these changes begin soon after fertilization and continues throughout gestation and
most occur in response to physiological stimuli provided by the fetus and placenta
Nearly every organ system is altered
Understanding these changes helps to distinguish normal physiology from pathological disease
state

Nutritional
During pregnancy, nutritional requirements, including those for vitamins and minerals, are
increased, and several maternal alterations occur to meet this demand.
Addition of 300 kcal/day.
The mother`s appetite usually increases, so that food intake is greater, although some women
have a decreased appetite or experience nausea and vomiting.
These symptoms may be related relaxation of smooth muscle, increasing levels of human
chorionic gonadotrophin (hCG) and estrogen.
Complicates 70% of pregnancies normally from 4-16 weeks
True Hyperemesis gravidarum (HG) is a severe form of morning sickness, with "unrelenting,
excessive pregnancy-related nausea and/or vomiting that prevents adequate intake of food and
fluids, that may requiring hospitalization, IV fluids, anti-emetics even protonics or TPN

Pica: craving for substances that are not food

Etiology unknown
Check for poor weight gain and refractory anemia
South - clay or starch (laundry or cornstarch)
UK coal
Also, soap, toothpaste and ice

Metabolic Changes
As the fetus and placenta grow and place increasing demands on the mother, phenomenal
alterations in metabolism occur
Basal metabolic rate is increased to the extent of 30% higher than that of the average for the
non-pregnant women.
 The most obvious physical changes are weight gain and altered body shape
Weight gain is due not only to the uterus and its contents but also to increase breast tissue,
blood and water volume in the form of extravascular and extracellular fluid
Deposition of fat and protein and increased cellular water are added to the maternal stores
The average weight gain during pregnancy is 12.5Kg. (23-25 lbs)
During normal pregnancy, approximately 1000g of weight gain is attributable to protein
Half of this is found in the fetus and the placenta, with the rest being distributed as uterine
contractile protein, breast glandular tissue, plasma protein, and hemoglobin
Total body fat increases during pregnancy, but the amount varies with total weight gain
During the second half of pregnancy, plasma lipids increase , but triglycerides, cholesterol and
lipoproteins decrease soon after delivery
The ratio of low density lipoproteins to high density lipoproteins increases during pregnancy

Protein Metabolism
Positive nitrogenous balance throughout pregnancy
At term, the fetus and the placenta contain about 500g of protein and the maternal gain is also
about 500g

Pancreas and Fuel Metabolism

Physiologic glucose intolerance to ensure continuous transport of nutrients from mother to
fetus
Fasting hypoglycemia
Postprandial hyperglycemia
Hyperinsulinemia

Fuel Metabolism
Pregnant Prolonged Fasting
Increased utilization of fat stores
Lipolysis generated glycerol, fatty acids and ketones for gluconeogenesis and fuel
More HPL, less insulin results in increased utilization of fat stores
Maternal response to starvation Hypoglycemia, Hypoinsulinemia
Maternal Response to feeding
Hyperglycemia
Hyperinsulinemia
Hyperlipidemia
Resistance to insulin
 Insulin secretion increases throughout
Insulin resistance increases to 50-80% in the third trimester
Borderline pancreas function leads to GDM

Lipids and lipoproteins increase in pregnancy

Total cholesterol, LDL, HDL, triglycerides all increase
Necessary as precursor for steroidogenesis
Does not appear to lead to atherosclerosis unless pre-existing hyperlipidemia

Placental Transport of Nutrients

Endocrine Changes
Diabetogenic effects in pregnancy
HPL Lipolytic and anti-insulin
Cortisol
Prolactin
Estrogen and progesterone
Fetal glucose levels are 20mg/dL less than maternal values
Placental glucose transport is carrier mediated facilitated transport that is energy dependent
Body Water Metabolism
Condition of chronic water overload
Active Na+ and water retention
Changes in osmoregulation
Renin-angiotensin system
Body water increase 6.5L 8.5L
1500 cc increase in blood volume
RBC increase ~400cc
Elevation of maternal CO

Plasma Osmoregulation
Na+ retention increases 900 mEq but serum Na+ decreases 3-4 mmol/l
Plasma osmolality decreases 10 mOsm/kg
Enhanced tubular reabsorption of Na+ secondary to aldosterone, estrogen and
deoxycorticosterone
Increased GFR and Atrial Natriuretic Peptide favor Na+ excretion

Respiratory Changes
Upper Respiratory Tract:
Hyperemia and edema of mucosa induced by estrogen leads to nasal stuffiness and epistaxis
Polyposis of nose and sinuses may occur and regress after delivery
Early in pregnancy, capillary dilatations occur throughout the respiratory tract, leading to
engorgement of the nasopharnyx, larynx, trachea, and bronchi
This causes the voice to change and makes breathing though the nose difficult.
Chest X-rays reveal increased vascular makings in the lungs.

Mechanical changes:
Configuration of thoracic cage change early in pregnancy
Chest circumference expands 5-7 cm
Subcostal angle increases from 68-103 degrees
Transverse diameter increases 2cm
With advancing gestation level of diaphragm is pushed up by 4cm, but elevation of the
diaphragm does not impede its movements
Respiratory muscle function is not affected by pregnancy
Abdominal muscles have less tone and are less active during the pregnancy causing respiration
to be more rather than less diaphragmatic
Lung Volume and Pulmonary Function:
Elevation of the diaphragm decreases the volume of the lungs in the resting state
Total lung volume (TLC) decrease by 5% FRC decrease by 20%
Residual volume decrease by 20% Vital capacity does not change
Spirometery is unchanged
FEV1 is unchanged Peak flow is unchanged
Respiratory rate is unchanged
Elevation of the diaphragm decreases the volume of the lungs in the resting state, reducing
TLC by 5% and FRC by 20%
FRC mainly decreased by RV
Vital capacity does not change
Chronic hyperventilation progesterone induced
Minute volume is increased
Tidal volume is increased
Respiratory rate is unchanged (Increased early in the first trimester)
Dead volumes increase owing to relaxation of the musculature of conducting airways.
Tidal volumes increases gradually (35-50%)as pregnancy progresses.
Total lung capacity is reduced (4-5%) by the elevation of the diaphragm.
Functional residual capacity, residual volume, and respiratory reserve volume all decrease by
about 20%.
Larger tidal volume and smaller residual volume cause increased alveolar ventilation (about
65%) during pregnancy.
Inspiratory capacity increases 5-10%.
Functional respiratory changes include a slight increase in respiratory rate, a 50% increase in
minute ventilation, a 40% increase in tidal volume
A progressive increase in O2 consumption of up to 15-20% above non-pregnant levels by term.
With the increase in respiratory tidal volume associated with a normal respiratory rate, there
is an increase in respiratory minute volume of approximately 26%
. As the respiratory minute volume increases, hyperventilation of pregnancy occurs, causing a
decrease in alveolar CO2
Spirometry: the most common of the Pulmonary Function Tests (PFTs), measuring lung
function, specifically the measurement of the amount (volume) and/or speed (flow) of air that
can be inhaled and exhaled.
FEV1 (forced expiratory pressure in 1 second), 80-100% of average values are considered
normal and is unchanged
Peak Expiratory Flow: is the maximal flow (or speed) achieved during the maximally forced
expiration initiated at full inspiration, measured in liters per minute, also unchanged
Gas Exchange:
Hyperventilation leads to deceased PCO2
Increases CO2 gradient between fetus and mother
Chronic respiratory alkalosis Respiratory System: Gas Exchange
Compensatory metabolic acidosis
20-40% increase in maternal oxygen consumption
Normal arterial blood gas values pH= 7.4-7.45 PCO2= 28-32 PO2= 101-106 HCO3= 18-21

Changes in pulmonary function tests during pregnancy:

Serial measurements of lung volume compartments during pregnancy. Functional residual

capacity decreases approximately 20 percent during the latter half of pregnancy, due to a
decrease in both expiratory reserve volume and residual volume.
 GAS EXCHANGE (contd):
Minute ventilation rises 30-40% by late pregnancy
O2 consumption increases only 15-29%
Results in higher PAO2 (alveolar) and PaO2 (arterial)
Normal PaO2: 104-108 mmHg
Fall in PACO2 and PaCO2 levels
Normal PaCO2 level: 27-32 mmHg
Increases gradient of CO2 facilitating transfer from fetus to mother
Arterial pH remains unchanged
Increased bicarbonate excretion via kidneys

Dyspnea of Pregnancy:
Common complaint
60-70% of patients
late first or early second trimester
Likely due to various factors
reduced PaCO2 levels
awareness of increased tidal volume of pregnancy

HAEMATOLOGIC CHANGES
Blood volume increase by 40-50%. Beginning at 6-10 wks. and plateau at 30-32 wks. This level
remains almost static till term
Plasma volume increase by 40-50%
Red cell mass increase by 18-20 %
Physiologic anemia of pregnancy nadiring at 30 wks.
Increase in erythropoietin and reticulocyte count
Increase in blood volume
helps in
Compensatory blood loss
at delivery
Increase renal filtration
Dissipation of heat
produced by fetus and
removal of metabolic
waste
Iron:
Maternal Requirement is 1000mg
Normal pregnant woman needs to absorb about 3.5mg/day of iron
The goal of iron supplementation is to prevent maternal iron deficiency
Usually not needed before 20wks
30mg of elemental Fe 325mg ferrous gluconate
Fe Supplements:
Ferrous sulfate (65mg of elemental Fe)
Ferrous gluconate (35mg of elemental Fe)
Iron Metabolism:
Trivalent food source must be converted by ferric reductase to divalent form
Fe enterocytes bound transferrin transported to liver, spleen, muscle and bone
marrow Incorporated into hemoglobin, myoglobin, ferritin or hemosiderin
Requirements increase in third trimester
Fetus receives Fe though active transport

Platelets:
Progressive decline in count from 1st -3 rd trimester
Increase platelet dysfunction
Gestational thrombocytopenia of pregnancy (Burrow &Kelton reported an 8% prevalence)
Platelets range from 70-150 000
Diagnosis of exclusion
?PET/HEELP, ITP, Renal disease, Autoimmune e.g SLE

Immune System:
The total leukocyte count increase during pregnancy from pre-pregnancy level of 4300-4500
to 5 000-12 000 in the 3rd trimesters
Leukocytosis secondary to neutrophilia
Estrogen induced
Cortisol induced
Neutrophilic leukocytosis occurs to the extent of 10-15,000/mm3 and even to 20,000 in labor.
The increase is due to rise in number of mature and immature neutrophils
Lymphocytes and monocytes remains unchanged throughout the pregnancy

Modulation away from cellular immunity to wards humoral immunity

Paradoxical decline of immunoglobins - A,G,M
Only Ig G crosses the placenta
 Blood Clotting Factors:
Many blood clotting factors levels increase in pregnancy
Increased fibrinogen, thus increase in ESR
PT and PTT slightly decreases
CT remains unchanged
May be slight decrease in platelet count
VI, VIII, IX, X factors increased level
XI, XII decreased kevel
Pregnancy is thus considered a hypercoaguable state
Besides the increase in blood clotting factors the placenta also produces a Plasminogen
activator inhibitor

Cardio vascular system

Normal pregnancy is associated with an increase of 30-50% in blood volume
Blood volume increases, starting at the 6th week and rising rapidly until mid-pregnancy, the
levels peak by 20-24wks of pregnancy and then are either sustained until term or decrease
An estrogen-mediated stimulation of the renin-angiotensin system results in sodium
and water retention appears to be the mechanism underlying the blood volume increase
Increase in Cardiac output is most significant change during pregnancy
It begins to rise in first trimester and steadily rises to peak at 32 weeks by 30-50%
Cardiac output is normally 4.2L/min, is 6.5L/min at 8-10 weeks of pregnancy and remains so
till near term
Increase in cardiac output is achieved by rise in stroke volume (in early pregnancy) and Heart
Rate (in latter part of pregnancy) adjusting together
Due to rise in endogenous circulating catecholamine, there is positive inotropic and
chronotropic myocardial response
Later in pregnancy, the rise is related to an acceleration of the heart rate (25%), since stroke
volume decreases as a result of vena caval
compression

Plasma Volume 50% (20-100%)

Physiologic Anemia of Pregnancy
Estrogen-mediated stimulation of the RAS
Role of other hormones:
Deoxyxortisone, prostaglandins,
estrogens, prolactin, placental lactogen,
CH, ACTH, ANP
 Blood Pressure remains almost prepregnant levels except a tendency to fall during pregnancy
(particularly during mid-trimester) as the systemic vascular/peripheral resistance falls (due to
large arteriovenous shunts at placental bed and physiologic vasodilation secondary to
endothelial prostacyclin and circulating progesterone)

Arterial blood pressure systolic - diastolic

Venous pressure: - central (unchanged) - femoral (2-3 fold increase)

Peripheral vascular resistance:

Uterine Blood Flow:

Non-pregnant: 55mL/min
First trimester 125mL/min
Second trimester 500mL/min
Third trimester 900mL/min
Hemodynamic changes during labour and Delivery
Abrupt hemodynamic changes occur secondary to pain, anxiety and uterine contractions
With each contractions extrusion of approximately 500mL of blood into central venous system
Oxygen consumption threefold, CO during labour by as much as 50% above the baseline
during 2nd stage, may be even higher at the time of delivery ( SV and HR)
SBP & DBP (especially in second stage)

Those changes are influenced by the form of anaesthesia and analgesia

After delivery, abrupt increase in venous return (due to auto transfusion and release of IVC
compression)
Excess blood loss in normal vaginal delivery / C-Section can alter cardiac status
Cardiovascular adaptation associated with pregnancy repress by approximately 6 weeks after
delivery
Stimulating Cardiac Disease
Owing to these normal changes, many
healthy pregnant women have symptoms
mimicking those of cardiac disease
including;
o Fatigue, dyspnoea, light-headedness
and number of abnormal findings
on physical exam, ECG and echo

Nervous System Changes

May be generalized neuritis, probably due to vitamin B1 deficiency
Compression of the lumbosacral trunk by the fetal head or by features of sciatica
Compression of the median nerve (carpal tunnel syndrome}

Renal System Changes

Anatomic changes
Renal hypertrophy
Dilatation renal pelvis/calyces 15mmon the right in3rd trimester 5mmonthe left
Each kidney increase s in length by 1-1.5 cm, with a concomitant increase in weight
The ureters are dilated to 2cm resulting in hydrouterer from:
progesterone induced smooth muscle relaxation causing hypertonia
Mechanical compression above the pelvic brim of the bony pelvis by the ovarian venous
complex in the suspensory ligaments of the ovary
Hyperplasia of smooth muscles in the distal one-third of the ureter may cause reduction in the
luminal size
The ureters also elongate, widen, and become curved ;there is an increase in urinary stasis
This may lead to infection and predisposes to pyelonephritis in the presence of asymptomatic
bacturia (30%)
This can also lead to difficulties in interpreting radiographs and interference with renal studies

BLADDER:
As the uterus enlarges the urinary bladder is displaced upward and flattened in the anterior-
posterior diameter
Bladder vascularity increases and muscle tone decrease, increasing capacity up to 1500ml
 Trigone elevation occurs with increase vascular tortuosity throughout the bladder leading to
micro hematuria
Increase frequency of urinary incontinence

RENAL HEMODYNAMICS:
Renal blood flow increases 50%
GFR increase 50% (120cc/min 180cc/min)
The renal plasma flow rate increase by as much as 25-50%
Serum creatinine and BUN levels decrease
BUN 8-9mg/dl by end of 1st trimester
Serum creatinine decline to 0-7mg/dl by end of 1st trimester,0.5-0.6mg/dl by term
Early decline in serum uric acid nadir at 24wks; returns to nonpregnant level at end of
pregnancy due to increase reabsorption of urate
Urinary flow and sodium excretion rate can be altered by posture, being twice as great in the
lateral recumbent as in the supine position
Even though GFR increase dramatically during pregnancy the volume of urine passed each
day is not increase
With the increase in GFR, there is an increase in endogenous clearance of creatinine
The concentration of creatinine in serum is reduced in proportion to the increase in GFR and
concentration of blood urea nitrogen is similarly reduced
BUN decline to 8-9mg/dl by end of 1st trimester
Decline in serum creatinine
0-7mg/dl by end od 1st trimester
0.50.6 mg/dl by term
Increase in glucose excretion
1-10 g glucose excretion per day
Due to 50% increase in GFR with impairment or exceeding tubular reabsorption
capacity for filtered glucose
Implications
increase level of glucose in urine contribute to increase susceptibility of pregnant
women to UTI
Increase in amino acid excretion during gestation
No increase in protein loss (100-300mg/24hrs)
If more than 300mg/24hrs is lost, suspect a disease process
Increase in urinary loss of folate and vitamin B12
 SALT AND WATER METABOLISM:
Plasma osmolality begins to decline by 2 weeks after conception
reduction in serum sodium and other anions
Sodium loss during pregnancy
50% rise in GFR
Progesterone: natriuresis
Renal tubular reabsorption of Na+ increases (aldosterone, estrogen and deoxycorticosterone)
Sodium homeostasis
Level of the enzyme renin which is produced by the kidney increase early in the first trimester,
and continue to rise until term
This enzyme acts on its substrate angiotensinogen, to first form angiotensin 1 and then
angiotensin2, which acts as a vasoconstrictor
Normal pregnant women are resistant to the pressor effects of elevated levels of angiotensin2
but those suffering with preeclampsia are not, this is one of the theory to explain this condition

Gastrointestinal
Mouth
Unchanged pH or production of saliva
Saliva production is unaltered
Ptyalism usually in women with HEG
due to inability to swallow
Can lose up to 1-2 L of saliva per day
Decreasing starchy foods might help
Gums edematous and soft
May bleed after brushing
Epulis gravidarum
regress 1-2 mos after delivery
excise if persistent or excessive bleeding
If the pH of the oral cavity decreases, tooth decay may occur linked to pre-term deliveries.
Tooth decay during pregnancy, however, is not due to lack of calcium in the teeth, dental
calcium is stable and not mobilized during pregnancy as is bone calcium.
The gums may become hypertrophic, hyperemic and friable; this maybe due to increased
systemic estrogen.
Vitamin C deficiency also can cause tenderness and bleeding of the gums.
Gingivitis of pregnancy: vascular swelling of the gums can lead to the development of pyogenic
granulomas
Gastrointestinal Motility
Reduced during pregnancy due to increased levels of progesterone, which decrease the
production of motilin, a hormonal peptide that is known to stimulate smooth muscle in the
gut.
Transit time of food throughout the gastrointestinal tract much slower, more water than
normal is reabsorbed, leading to constipation.
Decreased tone and motility secondary to progesterone
Oesophagus: dysmotility
Esophageal peristalses is deceased, accompanied by gastric reflux because of the slower
emptying time and dilatation or relaxation of the cardiac sphincter.

Stomach
Reduced tone of the gastroesophageal junction sphincter
Production of the hormone gastin increases significantly, resulting in increased stomach
volume and decreased stomach pH.
Gastric compression due to enlarging uterus with decrease sphincter tone increasing incidence
GERD
This reflux is more prevalent in later pregnancy owing to elevation of the stomach by the
enlarged uterus, making the use of anesthesia, especially general anesthesia more hazardous
because of the increased possibility of regurgitation and aspiration.
Lower incidence of PUD (peptic ulcer disease)
may be due to decreased gastric acid secretion delayed emptying, increase in gastric
mucus, and protection of mucosa by prostaglandins
Decreased tone and motility
progesterone
possibly due to decreased levels of motility
Conflicting info about delayed gastric emptying
Reduced tone of the gastroesophageal junction sphincter
Increased intraabdominal pressure leads to acid reflux
Lower incidence of PUD
may be due to decreased gastric acid secretion delayed emptying, increase in gastric mucus,
and protection of mucosa by prostaglandins
Fasting and residual volumes double in 2nd and 3rd
Slower rate of emptying
Small Bowel:
Reduced motility and tone allow for more efficient absorption, especially iron
Reduced motility of small bowel
increased transit time in the third trimester and postpartum
Enhanced iron absorption
as a response to increased iron needs

Large Bowel:
Decreased transit times allows for both water and sodium absorption.
Increased portal hypertension with dilation wherever there are porto-systemic venous
anastamoses (varices) affecting esophagus, vulva and increase varicose veins and hemorrhoids
may lead to ovarian vein thrombosis
Constipation
Mechanical obstruction by the uterus
Reduced motility (p4)
Increased water absorption
Portal venous pressure is increased
Dilation of gastroesophageal vessels
issue in those with preexisting esophageal varices
Dilation of hemorrhoidal veins
hemorrhoids

Gallbladder
Decreased rate of emptying and hypotonia of the smooth muscle wall
Emptying time is slowed and often incomplete
Bile can become thick, and bile stasis
Cholesterol saturation is increased while chenodeoxycholic acid is decreased in bile
These changes favor the development of gallstones
Biliary cholesterol saturation increases and chenodeoxycholic acid decreases
increased risk gallstone formation

Liver
Liver size and histology are unchanged
Serum albumin and total protein decrease so there is a decrease in the albumin/globulin ratio
Serum alkaline phosphatase increases due to placental and some hepatic production
No change in serum bilirubin, AST, ALT
 Clinical and laboratory changes mimic disease states
Spider angiomas and palmar erythema
Liver does not enlarge
Hepatic blood flow remains unchanged
CO to the liver decreases by ~35%
Spider angiomata and palmar erythema
elevated estrogen levels
Lab data
Drop in serum albumin
Rise in serum alkaline phosphatase
placental production and some hepatic production
Rise in serum cholesterol, fibrinogen, ceruloplasmin, binding proteins for
corticosteroids, sex steroids, thyroid hormones, and vitamin D
No change in serum bilirubin, AST, ALT, protime and 5 nucleotidase
Rise in GGT is controversial

ENDOCRINE
Pituitary Gland
Enlarges due to proliferation of prolactin-secreting cells
Enlargement makes it more susceptible to alterations in blood flow, i.e, PPH
Prolactin levels are increased (ten times higher at term) to prepare breasts for lactation

Thyroid
The normal pregnant woman is euthyroid
Changes in thyroid morphology and lab indices
Estrogen-induced increase in TBG
Decreased circulating extrathyroidal iodide
Thyroid enlargement usually not detected by exam
Normal thyroidal uptake of iodide
Serum TSH decreases early in gestation
rises to pre-pregnancy levels by end of first
T4 increases early in gestation
role of hCG stimulating the thyroid
Rise in TBG leads to rise in total T4 and total T3
active hormones free T4 and free T3 are unchanged
Free T4 is the most reliable method of evaluating thyroid function in pregnancy
 Small amount of TRH/T4 crosses the placenta
Fetal thyroid active y 12 wks. gestation

Adrenal glands
Expansion of the zona fasciculate
site of glucocorticoid production
Plasma corticosteroid-binding globulin (CBG) rises
due to enhanced liver synthesis
Free plasma cortisol rises
increased production and delayed clearance
Plasma DOC (deoxycorticosterone) rises
fetoplacental unit
DHEAS (dehydroepiandrosterone) decreases
Testosterone is slightly elevated
Increased SHBG and androstenedione

Pancreas
Hypertrophy and hyperplasia of the B cells
Fasting associated with accelerated starvation
maternal hypoglycemia, hypoinsulinemia and hyperketonemia
due to diffusion of glucose by the fetoplacental unit
Feeding response
hyperglycemia, hyperinsulinemia, hypertriglyceridemia and reduced tissue sensitivity
to insulin
glucose response greater during pregnancy
peripheral resistance to insulin: diabetogenic effect of pregnancy.
hPL and cortisol mediated
greater insulin resistance as the pregnancy advances

Metabolic Changes
General Metabolic Changes:
Total metabolism is increased due to the needs of the growing fetus and the uterus
Basal metabolic rate is increased to the extent of 30% higher than that of the average for the
non-pregnant women.
 Protein Metabolism
Positive nitrogenous balance throughout pregnancy
At term, the fetus and the placenta contain about 500 gm. of protein and the maternal gain is
also about 500 gm.

INTEGUMENTAL CHANGES
Hyperpigmentation:
90% of all pregnancies
Localized to areas of increased melanocytes
Cholasma Gravardium an extreme form of hyperpigmentation around the cheecks .forehead,
and around the eyes
70% of pregnancies in All races
Up to 30% of changes persists

Abdomen:
Linea nigra: a brownish black pigmented area in the midline stretching from the xiphisternum
to the symphysis pubis
Straie graviderum: slightly depressed linear marks with varying length and breadth found in
pregnancy

Hair Changes:
Mild hirsutism is common
Excessive virilization should prompt investigation for androgen-secreting tumors
Normal pregnancy increases amount of hair in anagen phase(growth)
Postpartum, telogen effluvium may occur with increased amount of hair in resting phase which
leads to loss
Maternal Physiology in Pregnancy

Skeletal Changes: Calcium metabolism

Maternal total calcium levels decline due to decreased albumin bound concentration
Serum ionized level remains unchanged
Increased intestinal absorption occurs in first trimester, actively transported across the
placenta
Maternal serum phosphate levels are unchanged
PTH levels remain unchanged
Elevated levels of vitamin D allow for increase Ca++ absorption
 Calcitonin levels rise to preserve maternal skeleton
Lordosis of pregnancy~ progressive increase in anterior convexity of the lumbar spine,
preserves center of gravity
Ligaments of the symphysis and sacroiliac joints loosen during pregnancy due to relaxin