The physiologic,biochemical,and anatomic changes that occur during pregnancy are extensive and may be sistemic or local..Teleologic alterations during pregnancy mantaina healthy enviroment for the fetus without compromising the mother`s health.Although,sometimes determine small disconfort to the mother.
During pregnancy, nutritional requirements,including those for vitamins and minerals, are increased, and several maternal alterations occur to meet this demand.The mother`s appetite usually increases, so that food intake is greather, some women have a decreased appetite or experience nausea and vomiting.These symptoms may be related to relative levels of human chorionic gonadotrophin(hCG).
Oral CavitySalivation may seem to increase due to swallowing difficulty associated with nausea ,and ,if the pH of the oral cavity decreases, tooth decay may occur.Tooth decay during pregnancy,however, is not due to lack of calcium in the teeth.Indeed,dentalcalciumis stable and not mobilized during pregnacy as is bone calcium.
The gums may become hipertrofic, hiperemic and friable;this maybe due to increased systemic estrogen. Vitamin Cdeficiency also can cause tenderness and bleeding of the gums.The gums shoud return tonormal in the early puerperium
Gastointestinal MotilityGastrointestinal motility may be reduced during pregnancy due to increased levels of progesterone, which in turn decrease the production of motilin, ahormonal peptide that is known to stimulate smooth muscle in the gut.Transit time of food throughout the gastrointestinal tract may be so much slower that more water than normal is reabsorbed, leading to constipation.
Stomach and EsophagusGastric production of hidrocloric acid is variable and sometimes exaggrated, especially during the first trimester. More commonly, gastric acidity is reduced. Production of the hormone gastin increases significantly, resulting in increased sthomac volume and decreased stomach pH. Gastric production of mucus may be increased. Esophageal peristalses is deceased, accompanid by gastric reflux because of the slower emptying time and dilatation or relaxation of the cardiac sphincter. Gastric reflux is more prvalent in later pregnancy owing to elevation of the stomach by the enlarged uterus.Besides leading to heartburn, all of these alterations as well as lying in the supine lithotomy position, make the use of anesthesia more hazardous because of the increased possibility of regurgitation and aspiration.
Small and Large Bowel ann AppendixThe large and small bowel move upward and laterally,the appendix is displaced superiorly in the right flank area. These organs return to the normal positions in the early puerperium.
As noted previouly, motility is generally decreased an gastrointestinal tone is decreased.
GallbladerGallblader function is also altered during pregnancy because of the hypotonia of the smooth muscle wall. Emptying time is slowed and often incomplete. Bile can become thick, and bile stasis may lead to gallstone formation.
LiverThere are no apparent morphologic changes in the liver during normal pregnancy, but there are functional alterations. Serum alkaline phosphatase activity can double, probably because of inceased placental alkaline phosphatase isoenzimes. Thus, a decrease in the albumin/globulin ratio occurs normally in pregnancy.
Kidneys and Urinary Tract
Renal DilatationDuring pregnancy , each kidney increases in leagth by 1-1,5cm, with a concomitant increase in weight.The renal pelvis is dilated.The ureters are dilated above the brim of the bony pelvis.The ureters also elongate, widen, and become more curved.Thus there is an increase in urinary stasis, this may lead to infection and may make tests of renal function difficult to interprete.
The absolute cause of hydonephrosis and hydroureter in pregnancy is unknown, there may be several contributing factors:1-Elevated progesterone levels may contribute to hypotonia of the smooth muscle in the ureter. 2-The ovarian vein complex in the suspensory ligament of the ovary may enlarge enough to compress the ureter at the brim of the bony pelvis, thus causing dilatation above that level. 3-Dextorotation of the uterus during pregnancy, may explain why the right ureter is usually more dilated than the left. 4-Hyperplasia of smooth muscle in distal one-third of the ureter may cause reduction in the luminal size. Renal Function
The glomerular filtration rate(GFR) increases during pregnancy by about 50% .The renal plasma flow rate increases by as much as 25-50%. Urinary flow and sodium excretion rates in late pregnancy can be alterated by posture, being twice as great in the lateral recumbent position as in the supine position.
Even thought the GFR increased dramaticallyduring pregnancy, the volume of the urine passed each day is not increased. Thus, the urinary system appears tobe even more efficient during pregnancy.
With the increase inGFR, there is an incease in endogenous clearence of creatinine.The concentration of creatinine in serum is reduced in proportion to increase in GFR, and concentration of blood urea nitrogen is similarly reduced.
Glucosuria during pregnancy is not necessarily abnormal, may be explained by the increase in GFR with impairment of tubular reabsortion capacity for filtered glucose.Increased levels of urinary glucose also contribute toincreased susceptibility of pregnant women to urinary tract infection.
Proteinuria changes litlle during pregnancy and if more than 500mg/24h is lost,a desease process shoud be suspected
Levels of the enzime renine, which is produced in kidney, increase early in the first trimester, and continue toarise until term. This enzime acts on its substrate angiotensinogen, to first form angiotensin1 and then angiotensin2, which acts as a vasoconstrictor.Normal pregnant are resistent to the pressor effect of elevated levels of angiotensin2 but those suffering from preeclampsia are not resistant, this is one of the some theories to explain this desease.
Blader As the uterus enlarges, the urinary blader is displaced upward and flattened in the anterior-posterior or diameter.Pressure from the uterus leads to inceased in urinary frequency. Blader vascularity increases and muscle tone decreases, incresin capacity up to 1500ml.Perhaps the most striking maternal phisiologic alteration occurring during pregnancy is the increase in the blood volume. The magnitude of the increases varies according to the size of woman, the number of pregnancies she has had, the number of infants she has delivered, and whether there is one or multiple fetuses.The increases in blood volume progress until term;the average increase in volume at term is 45-50%. The increase is needed for extra blood flow to the uterus, extra metabolic needs of fetus, and increased perfusion of others organs, especially kidneys. Extra volume also compensate for maternal bllod loss delivery. The average blood loss with vaginal delivery is 500-600ml, and with cesarean section is 1000ml.
Red BloodCels The increase in red blood cel mass is about 33%. Since plasma volume increases early in pregnancy and faster than red blood cell volume, the hematocrit falls until the end of the second trimester, when the increase in the red blood cells is synchronized with the plasma volume increase. The hematocrit then stabilizes or may increase slightly near term. IronWith the increase in red blood cells, the need for iron for the production of hemoglobin,naturally increases. If supplemental iron is not added to the diet, iron deficiency anemia will result. Maternal requiriments can reach 5-6mg/d in the latter half of pregnancy. If iron is not readly available, the fetus uses iron from maternal stores. Thus, the production of fetal hemoglobin is usually adequate even if the mother is serely iron deficient. Therefore anemia in the newborn is rarely a problem; instead, maternal iron deficiency more commonly may cause preterm labour and late spontaneus abortion, incresing the incidence of infant wastage and morbidity.
White Blood CellsThe total blood leukocite count increases during pregnancy from a prepregnancy level of 4300-4500/mL to 5000-12000/mL in the last trimester, althought counts as hight as 16000/mL have been observed in the last trimester.Counts as hight as 25000-30000/mL have been noted in anormal patient during labor. Lymphocite and monocyte numbers stay essencially the same throughout pregnancy; polymorphonuclear leucocytes are the primary contributors to the increase.
Clotting FactorsDuring pregnancy, levels of several essential coagulation factors isincrease.Thereare marked increases in fibrinogen and factor8. Factors VII, IX, X, and XII also increased but to alesser extend.
Fibrinolytic activity is depressed during pregnancy and labor, although the precise mechanism is unkown. The placenta may be partially responsible for this alteration in fibrinolytic status.Plasminogen levels increase concomitantly with fibrinogens levels, causing an equilibrationof clotting and lysing activity.
Clearly, coagolation and fibrinolytic sistems undergo major alterations during pregnancy. Understanding these physiologic changes is necessary to manange two of the more serious problems of pregnancy: hemorrage and thromboembolic desease, both caused by disorders in the mechanism of hemostasis.
As the uterus enlarges and the diaphragm becomes elevated, the heart is displaced upward and somewhat to the left with rotation on its long axis, so that the apex beat is moved laterally. Cardiac capacity increases by 70-80mL; this may be due to increased volume or hyperthophy of cardiac muscle.The size of the heart appears to increase by about 12%
Cardiac OutputCardiac output increases approximately 40% during pregnancy, reaching its maximum at 20-24 week’s gestation and continuing at this level until term. The increase in output can be as much as1,5L/min over the non pregnant level. Cardiac output is very sensitive to changes in body position. This sesitivity increases with leghthening gestation, presumably because the uterus impinges upon the inferior vena cava, thereby decreasing blood return to the heart.
Blood PressureSystemic blood pressure declines slightly during pregnancy. There is a little change in systolic blood pressure, but ddiastolic pressure is reduced (5-10mmHg) from about 12-26 weeks.Diastolic pressure increases thereafter to prepregnancy levels by about 36 weeks.
The obstruction posed by the uterus on the inferior vena cava and the pressure of fetal presentig part on the commom illiac vein can result in decreased blood return to the heart. This decreases cardiac output, leads to a fall in blood pressure, and causes edema in the lower extremities.
Peripheral Resistence Peripheral resistence equals blood pressure divided by cardiac output. Because blood pressure either decreases or remain the same during pregnancy and cardiac output increases appreciably, there is good evidence that peripheral resistence declines markedly. The elevated venous pressure returns toward normal if the woman lies in the lateral recumbent position. Effects of the Labor on the Cardiovascular SystemWhen a patient is the supine position, uterine contractions can cause a 25% increase in maternal cardiac output, a 15% decrease in heart rate, and a resultant 33% increase in stroke volume. However when the laboring patient is inthe later recumbent position, the hemodinamic parameters stabilize , with only a 7,6% increase in cardiac output, a 0,7% decrease in heart rate, and a 7,7% increase in stroke volume. These sgnificant differences are atributable to inferior vena caval occlusion caused by the gravid uterus. During contractions, pulse pressure increases 26% in the supine position but only 6% in the lateral recumbent position. Central venous pressure increases in direct relationship to the intensity of uterine contraction and increased intra abdominal pressure. Additionally, cardiopulmonary blood volume increases 300-500mLduring contractions. At the time of delivery, hemodynamic alterations vary with the anestesic used.
Pregnancy produces anatomic and physiologic changes that affect respiratore performance. Early in pregnancy, capillary dilatations occurs throughout the respiratory tract, leading to engorgement of the nasopharinx, larinx, trachea, and bronchi. This causes the voice to change and makes breathing though the nose difficult. Respiratory infections and preeclampsia aggravate these symptoms. Chest X-rays reveal increased vascular makings in the lungs.
As the uterus enlarges, the diaphragm is elevated as much as 4cm, and the ribe cage is displaced upward and widens, increasing the lower toracic diameter by 2cm and the toracic circunference by up to 6cm. Elevation of the diaphragm does not impede its movement.Abdominal muscles have less tone and are less active during the pregnancy, causing respiation to be more rather than less diaphragmatic.
Lung Volumes and CapacitiesAlterations occurring in lung volumes and capacitiesduring pregnancy include the following:Dead volumes increases owing to relaxationof the musculature of conducting airways. Tidalvolumes increases gradually(35-50%)as pregnancy progesses. Total lung capacity is reduced (4-5%) by the elevation of the diaphragm. Funtional residual capacity, residual volume, and respiratore 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 respiratore changes include a slight increase in respiratory rate,a 50% increase in minute ventilation, a 40% increase in tidal volume, and a progressive increase in oxigen consuption of up to 15-20% above nonpregnant levels by term. With the increase in respiratory tidal volume associated with a normal respiratore rate, there is an increase in respiratore minute volume of approximately 26%. As the respiratore minute volume increases, “hiperventilayion of pregnancy”occurs, causing a decrease in alveolar CO2 . This decrease lowers the maternal blood CO2 tension; however alveolar oxigen tension is maintened within normal limits.Maternal hyperventilation is considered a protective measure that prevents the fetus from the exposure to excessive levels of CO2.. Effects of Labour on thhe Pulmonary System
There is a further decrease in functional residual capacity (FRC) during the early phase of each uterine contractin, resulting from redistribution of blood from the uterus to the central venous pool. Because this decrease in FRC occurs without a concomitant change in dead space, there is little residual diluition and, therefore, presumably more efficient gas exchange.
As the fetus and placenta grow and place increasing demands on the mother, phenomenal alterations in metabolism occur.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.
During normal prgancy, approximately 1000g of weight gain is attributable to protein. Half of this is found in the fetus and the placenta, with the rest being distribute as uterine contractile protein, breast glandular tissue, plasma protein, and hemoglobin. Plasma albumin levels are decreased and fibrinogen levels increased.
Total body fat incresas during pregnancy, but the amount varies with total weight gain. During the second half of pregnancy, plasma lipids increase , but triglycerides, cholesterol and lipoproteins decreasesoon after delivery. The ratio of low density lipoproteins to high density lipoproteins increases during pregnancy.
The metabolism of carbohydrates and insulin during pregnancy is discussed entirety last week in this section of the medstudents.
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