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Responsibility/ Adaptations in Pregnancy Additional Information ➢ Maintaining Perinatal Nursing – 2021 ➢ Regulation of growth Simpson, Creehan, O’Brien-Abel, Roth ➢ Development and Cellular communication & Rohan Chapter three – Physiological Changes of Pregnancy Blackburn, Susan Tucker Page 48

Placenta ➢ Responsible for transfer of nutrients to the fetus ❖ Placental Hormones are critical and waste products away from the fetus for many of the metabolic and ➢ Functions as the fetal lungs, gi, , and endocrine changes during endocrine organ pregnancy ➢ Major Hormones ❖ Fetal growth and placental ❖ hCG - Human chorionic transport is mediated ❖ hPL – Human by Parathyroid related ❖ protein or PTHrP ❖ ❖ Corticotrophin-releasing ❖ Serves as an hormone or CRH and PGs have a ❖ Major Hormones major role in initiation of ❖ hCG - Human chorionic gonadotropin myometrial contractility and ❖ hPL – labor onset ❖ Estrogen Page 49 ❖ Progesterone

➢ HCG ➢ Primarily secreted by the Page 49

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➢ Major function is to maintain progesterone and estrogen production by the corpus luteum until the placental function is adequate (approximately 10 weeks post-conception) ➢ Thought to have a role in fetal and corticosteroid production and angiogenesis ➢ Found in maternal serum by within 7-8 days after implantation ➢ Positive pregnancy test – 3 weeks after conception and 5 weeks after LMP ➢ Elevated in multiple and molar pregnancies ➢ Lower in ectopic or abnormal placentation ➢ Human Placental ➢ Produced by syncytiotrophoblast tissues of the Page 49 Lactogen (hCS) placenta ➢ Growth parallel to the placental growth and peaks near term ➢ Critical for fetal growth as it alters maternal protein, carbohydrate and fat and acts as an antagonist ➢ free fatty acid availability for maternal metabolic and  maternal glucose uptake and use o Allows glucose to be reserved for fetal use o Mother will be at a higher risk for ketosis with significant  in maternal food intake ➢ ➢ Steroid hormones secreted by the in early Page 49 (estrone, pregnancy and by the placenta in late pregnancy

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& ➢ Prevents further ovarian follicular development estriol) during pregnancy ➢ Prepares the breast for lactation ➢ blood flow to the uterus, growth of the uterine muscle and enhances myometrial activity – involved in the timing and onset of labor ➢ Rapid last 6 weeks in pregnancy o Factor in onset of labor ➢ Progesterone ➢ Initially produced by the corpus luteum & later by Page 49 the placenta ➢ Assists with implantation and myometrial relaxation – smooth muscle relaxer o GI system o Venous wall to accommodate  in blood volume ➢ Respiratory center -  CO2 sensitivity ➢ Aids in the structural development of the breast to prepare for breastfeeding ➢ Mediates the changes in the immune system o Prevents rejection of the fetus ➢ ➢ Secreted by the corpus lutum and later by the Page 49 myometrium and placenta ➢ Inhibits uterine activity during pregnancy ➢ Plays a role in decidual development and implantation

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➢ From the family of eicosanoids which includes PGs, ➢ PGI2s & Thromboxane thought to prostacyclins (PGI2s), thromboxanes and contribute to hypertensive leukotrienes disorders – PCI2 is release is ➢ PGI2 & Thromboxane thought to contribute to mediated by nitric oxide which hypertensive disorders regulates vascular tone and SVR ➢ Effect smooth muscle contractility Page 50 o Mediate the onset of labor, myometrial contractility and cervical ripening ➢ ➢ Released from the gland Page 50 ➢ Increase in and maturation of ducts in the breast to aid in breastfeeding o After removal of placenta, high levels of estrogen disappear, signaling the anterior pituitary gland to produce prolactin o Levels rise rapidly and are elevated by the infants suckling ➢ Cardiovascular ➢ is displaced upward, forward to the left ➢ Perfusion depends on the heart ➢ Heart rate  15-20 beats/minute rate ➢ Exaggerated split of the first  sound and audible ➢ Benign systolic murmurs are third ♥ sound common ➢ Stroke volume25-30% ➢ ECG changes: inverted P waves, ➢ Cardiac output  30-50% small Q wave, tachyarrhythmias ➢  Blood volume 40-60% with  in Hematocrit ➢ Physiologic anemia o RBC’s  20-30% ➢  risk for clot formation ➢ WBC  to 15,000 o Venous thromboembolism ➢ Blood pressure is  the second trimester DIC – Disseminated Intravascular Coagulation

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➢ Widening of pulse pressure ➢ Plasma volume returns to normal ➢ Hypercoaguable: procoagulant activity and  after 6 weeks PP fibrinolytic activity ➢ Post-partum – Left atrium appears enlarged due to the ↑in blood volume immediately following removal of placenta Pages 50-52 ➢ Respiratory ➢ Pressure from the uterus shifts the diaphragm ➢ Compensated respiratory alkalosis upward approx. 4cm which  the length of the ➢  in Oxygen consumption lungs ➢ Shortness of breath is a common o To compensate for this the chest enlarges complaint 2cm ➢ Increased pressure from the uterus widens the substernal angle 50% and causes the ribs to slightly flare out ➢ Circumference of the thoracic cage may by 5-7 cm ➢ Ph 7.40-7.45 ➢ PaCO2 27-32mmHg ➢ HCO3  18-21 mmHg ➢ Tidal volume  30-40% ➢ Expiratory Reserve Vol ▪  15-20% Page 55 ➢ Renal ➢ Glomerular filtration  40-60% ➢ Proteinuria, Glycosuria and renal ➢ Dilatation of the renal calyces, pelvis and ureters clearance and in serum levels of are due to the effects of progesterone some more common

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➢ Hypertrophy of the kidneys due to  in blood o Filtered load of substance volume exceeds the tubular ➢ Dilatation of the ureters on the right side is more reabsorptive capacity pronounced than on the left side ➢ Hydronephrosis and Hydroureter – o Cushioning that occurs due to the may take 3-4 months to resolve displacement of the uterus by the sigmoid post-partum colon. ➢ Increased risk of urinary tract infections o Due to increase in muscular relaxation, increase in urine volume and urinary stasis ➢ Gastrointestinal ➢ Nutritional requirements increase Page 57 ➢ Common discomforts of pregnancy are due to physiological and structural changes ❖ Heartburn, gingivitis, constipation, nausea and vomiting ➢ Mouth ➢ Gingival edema and hyperemia Page 57 ❖ Begins in the 2nd month and peaks in the 3rd trimester ➢ Gingival changes are related to increase in vascularity and blood flow, changes in connective tissue and the release of inflammatory mediators ➢ in plaque and dental calculus ➢  in previous periodontal disease ➢ 3-5% have an epulis (tumor like enlargement (i.e. lump) situated on the gingival or alveolar mucosa.) between their upper, anterior maxillary teeth

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❖ Regresses during post-partum but may reoccur with subsequent pregnancies ➢ Esophagus ➢ Decrease in lower esophageal sphincter Page 57 (LES)muscle tone and pressure due to effects of progesterone ➢ LES function further altered after the uterus is large enough to change the positioning of the & intestines and move the LES into the thorax ❖ Changes heartburn and reflux ➢ Nausea and ➢ Affects 70-80% of pregnant women Page 57 Vomiting ➢ Exact mechanism unclear ➢ Theories: ❖ Mechanical, endocrinologic, allergic, metabolic, genetic and psychosomatic ➢ Most frequent hormone linked is estrogen- particularly HCg ➢ Usually begins at 4-6 weeks and peaks at 8-12 weeks but may begin sooner and last longer ➢ TX- supportive ❖ Frequent small meals ➢ Hyperemesis Gravidarum –associated with weight loss, imbalance, ketosis and dehydration more serious and requires fluid replacement ❖ Stomach ❖ Progesterone

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o Decreases stomach gastric smooth muscle tone and motility ❖ Gravid uterus displaces the stomach ❖ Small and Large ➢ Pushed upwards and laterally ➢ Why a pregnant woman is prone to Intestines ➢ Appendix is displaced superiorly constipation? ❖ Reaches the right costal margin by term ❖ Reduced motility ❖ Milder guarding and rebound tenderness ❖ Mechanical obstruction of due to cushioning by the uterus may delay the uterus diagnosis of appendicitis during pregnancy ❖ Increased water absorption ➢ progesterone levels GI tract tone and from the colon intestinal motility ➢ Hemorrhoids may develop due to ➢  nutrient absorptive capacity due to  height of straining and from increased the duodenal villi and activity of brush border pressure exerted on the vessels enzymes below the level of the uterus o Absorption of Calcium, amino acids, iron, Pages 57-58 glucose, sodium, chloride, and water are ↑ ➢ Liver ➢ Size and structure does not change during ➢ Liver changes can alter pregnancy biotransformation of drugs from ➢ Production of many proteins is altered due to the maternal circulation effects of estrogen ➢ Liver changes return to normal by 3 ➢ Hepatic blood flow increases but % of blood weeks post-partum reaching the liver remains unchanged Page 58 ➢ levels  by 50% by the end of 2nd trimester ➢ Serum proteins, enzymes and lipids are altered during pregnancy

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➢ Serum alkaline phosphatase & serum cholesterol can be doubled and higher in multiple gestation ➢ Aspartate(AST), Serum bilirubin & Alanine aminotransferase (ALT) are normal or slightly lower in pregnancy – making these test good markers for liver disease in pregnancy ➢ Gallbladder ➢ Unlike the liver, size and function are altered ➢ Generally, returns to normal 2 during pregnancy weeks post-partum ➢ Elevated levels of progesterone cause the Page 58 gallbladder to become hypotonic and distended ➢ Stasis may occur due to impairment of Gallbladder smooth muscle contractility ➢ After 14 weeks gestation- emptying time is slower ➢ 2nd and 3rd trimester – fasting and residual volumes increase two fold ➢ Cholesterol may be sequestered in the gallbladder resulting in gall stones ➢ Weight Gain ➢ On average, 300 kcal are needed per day for the fetus ➢ Institute of Medicine Guidelines: ❖ 1st Trimester - 1.1 to 4.0 lb. weight gain ❖ 2nd and 3rd Trimesters varies with BMI ▪ 0.8 to 1.0 lb./week for normal BMI ▪ 1.0-1.3 lb./week for underweight women ▪ 0.6 to 0.7 lb./week in overweight women

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▪ 0.4 to 0.6 lb./week in obese women ➢ Metabolic ➢ Adequate maternal weight gain, and changes in ➢ Initial Anabolism Dominant Phase Changes maternal glucose, protein and fat metabolism play o Nutrient uptake, energy is an important role in fetal growth and development stored as fat and maternal ➢ Pregnancy can be divided into 2 metabolic phases weight gain ❖ Initial anabolism dominant phase o Estrogen causes in insulin ❖ Later catabolism predominant phase production due to stimulation of pancreatic beta cell hypertrophy and hyperplasia o insulin promotes storage of glucose as glycogen, fat synthesis, storage of triglycerides and fat, fat cell hypertrophy and inhibition of lipolysis o Lipoproteins (low density and high density) increase o Maternal protein storage increases, with a net retention of 1.3g/day of nitrogen for use by mother and fetus ➢ Later Catabolism Predominant Phase ❖ Maternal weight gain is due to fetal growth

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lipolytic activity is enhance ❖ in Plasma, free fatty acids, glycerol and ketones • These provide for alternative energy sources for the mother since the fetus is an obligatory user of glucose who cannot readily break down fat for energy ❖ Maternal urinary nitrogen excretion decreases conserving protein for fetal transfer ❖ Maternal insulin levels increase as insulin resistance in the peripheral tissues becomes prominent Page 59 ➢ Insulin in ➢ Insulin antagonism is caused by hCS (Human Page 59 Pregnancy Placental Lactogen) and other placental hormones (progesterone, estrogen, and prolactin) o Promote lipolysis and oppose the action of insulin

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➢ Normally insulin aids in  glucose from the blood and promote glycogen and fat storage ➢ Insulin resistance (insulin sensitivity  by 50-70%) causes maternal glucose levels to be higher after a meal to allow for glucose to be transferred to the fetus ❖ Diabetogenic State • Relative hyperinsulinemia and hyperglycemia of pregnancy caused by a  sensitivity to insulin in the liver and peripheral tissues which leads to a persistent relative hyperglycemia after meals ❖ Maternal metabolic responses alter responses on glucose tolerance tests • Lower initial fasting glucose o Due to  glucose utilization and fat utilization enhancing glucose availability for the fetus & o blood glucose for a longer period of time after ingestion carbohydrates( due to insulin antagonism and insulin sensitivity)

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➢ Endocrine ➢ Gland ❖ Production, circulation and disposal of the thyroid hormone are altered during pregnancy ❖ Increased vascularity and hyperplasia of thyroid gland ▪ Increase in hormone production ▪ Increase in thyroid size but not goiter like-in populations with adequate iodine supplies ❖ Most changes occur in the 1st half of ➢ More t4 and T3 are produced but pregnancy –T4 are elevated “euthyroid because they are bound to TBG the hyperthyroxinemia” serum levels are reduced ▪ Due to estrogen, TBG (Thyroxine Binding Protein) and hCG which stimulates T3 and T4 and urinary iodide excretion ➢ T4 and T3  by 10 -15 weeks and remain higher to term ❖ Free T4 & T3  during 1st trimester but  2nd and 3rd trimester as Thyroxine-binding globulin (TBG) ▪ Serum T4 &T3 levels reduced due to extra binding of from TBG ➢ Maternal iodine needs increase during pregnancy

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➢ Maternal thyroid hormone is critical for fetal CNS development ❖ Especially during early pregnancy prior to the fetus ability to produce thyroid hormone(T4) ❖ Poor control can lead to fetal loss and altered fetal development, and both altered neurocognitive and development impairments. ➢ Subclinical Hyperthyroidism ❖ Occurs in approximately 3.5-18% of healthy Page 60 populations ❖ Hard to distinguish due to normal s/s of pregnancy- Hyperthyroidism - heat intolerance, tachycardia, wide pulse pressure and vomiting and Hypothyroidism – constipation, fatigue, weight gain and muscle cramps ❖ If left untreated could result in pregnancy loss, thyroid crisis, and preterm labor ➢ Transient Post-Partum Thyroid Disorder (PPTD) ❖ Autoimmune base occurring 4-9% of postpartum women and thought to be autoimmune based ❖ 2-4 months of mild hyperthyroidism, followed by a period of hypothyroidism with a return to normal at 12 months pp.

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▪ 25% of these women develop permanent hypothyroidism within 5- 15 years ➢ Pituitary Gland ➢ Anterior Pituitary gland > in weight by 30% and 2- fold in volume ➢ Becomes more convex and dome shaped o Changes are due to  in prolactin o ACTH- Adrenocorticotropin secretion and serum levels ▪ Peaking during intrapartum ➢ Pituitary  ➢ By the placental growth hormone which 15-20 weeks gestation to term ➢ FSH (stimulates follicle growth) & LH (needed for ovulation) are inhibited during pregnancy ➢ Gland ❖ and AVP ❖ Oxytocin ▪ Influences contractility of uterus after birth ▪ Stimulates milk ejection ❖ AVP ▪ Also called the antidiuretic hormone ▪ Causes vasoconstriction when released in large amounts and BP ▪ Major action is the antidiuretic action to regulate H2O balance

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▪ Secretions controlled by changes in the plasma osmolarity and blood volume ▪ Levels not changed during pregnancy although blood volume is in pregnancy • Secreted at a lower osmolality in pregnancy ➢ Adrenal Glands ➢ Elevated ACTH stimulates cortisol production by the adrenals in pregnancy ➢ Plasma levels of CRH  in 2nd and 3rd trimester ❖ Regulate carbohydrate and protein metabolism ➢ Normally in cortisol levels would turn off ACTH release but not in pregnancy ➢ In spite of ACTH & Cortisol levels the physiological responses to (BP, rate, cortisol reactivity) are maintained during pregnancy ➢  ➢ Steroid hormones ➢ Testosterone levels due to an  sex hormone- binding globulin ➢ Free testosterone levels are low normal prior to 28 weeks gestation

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➢ Parathyroid ➢ Parathyroid hormone (PTH)  1st trimester then  Pages 60-61 Glands at term ❖ Early decrease is due to PTHrP production by the fetus and placenta ➢ Regulation of calcium is closely r/t magnesium, phosphate, PTH, and levels ❖ Any alteration in one is likely to affect the other ▪ in magnesium or calcium PTH levels ▪ in magnesium or calcium  PTH levels ➢ Total serum calcium falls in pregnancy primarily related to the fall in albumin, lowest reaching 28- 32 weeks then plateaus and  slightly at term ➢ Overall calcium not changed, however daily maternal calcium intestinal absorption  and doubles by the 3rd trimester to assist with fetal bone development in late pregnancy. Maternal overall bone mass is not loss during pregnancy ➢ Immune System ➢ Cytokines Page 61 ➢ PGE2 ➢ Steroid Hormones ➢ Estrogen ➢ hCG ➢ Various pregnancy-specific proteins exert immunosuppressive effects during pregnancy

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➢ Immune Innate Responses in Pregnancy ❖ in WBCs (especially neutrophils and monocytes) ➢ Immune Adaptive Responses in Pregnancy ❖ B and T lymphocyte responses ❖ Switch in balance of Th1 to Th2 cytokines (subsets of T-lymphocytes) ▪ Th2 cytokines are  which enhance antibody-mediated immunity ▪ T lymphocytes and Th1 cytokines are  which associated with tissue rejection ❖ Slight  in IgG may risk of bacterial colonization ❖ Selective localized immunosuppression may occur and  the risk of viral and mycotic infections ➢ Neuromuscular ➢ In general no major CNS changes in pregnancy and Sensory ➢ Mild frontal headaches 1st and 2nd trimester may Systems be due to tension or hormones Severe headache after 20 weeks gestation may be an indicator of preeclampsia ➢ Dizziness may be due to ❖ Vasomotor instability ❖ Postural hypotension • After long periods of sitting/standing ❖ Hypoglycemia

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➢ Musculoskeletal ➢ Posture ➢ Gait ➢ Ligament laxity ❖ “loose” ligaments ❖ Early in pregnancy due to effects of progesterone and relaxin • To facilitate birth ➢ Center of gravity changes ➢ Posture changes ➢ Separation of the rectus abdominis due to the pressure of the growing uterus ❖ Producing Diastasis Recti ➢ Risk of ligament injury, muscle cramps, back & joint pain & falls ➢ May develop Restless Leg Syndrome (Willis Ekbom Disease) in the 3rd trimester which usually disappears after 1 month post-partum ➢ Sleep ➢ Sleep pattern changes ❖ Mediated by mechanical forces and hormonal changes ❖ in sleep time ❖ Insomnia ❖ Night awakenings, often related to: • Nocturia • Fetal activity • Backache

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• Dyspnea • Heartburn ❖ Daytime sleepiness ❖ Stage 3 & 4 non-rapid eye movement sleep ➢ Sleep is also altered in the 1st two weeks Post- partum ➢ Ocular and ➢ Ocular Changes due to  in intraocular pressure Otolaryngic during second ½ of pregnancy ❖ May cause discomfort for women who wear contacts due to thickening of the cornea and mild corneal edema ➢ Otolaryngic changes due to: ❖ Altered fluid dynamics ❖ vascular permeability ❖ vascularization ❖ Effects of estrogen ➢ Can Lead To: ❖ in Ear and Nasal stuffiness ❖ Hoarseness ❖ Snoring ➢ INTEGUMENTARY ➢ Pages 62-63 SYSTEM ❖ Vascular alterations ▪ Blood flow to the skin 3-4 Xs causing spider nevi on the face, neck, chest, arms and legs

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o Related to increased subcutaneous blood flow and estrogen ❖ Palmar erythema ▪ Normal vascular change in pregnancy but has been associated with liver and disease ❖ Striae Gravidarum (Stretch Marks) ▪ May occur on the hips, breast, upper thighs but are usually more pronounced on the abdomen ▪ Occur in approximately 50% of pregnancies ▪ Due to normal stretching of the skin and softening and relaxing of the dermal collagenous and elastic tissues during the last months of pregnancy ❖ in estrogen and progesterone ▪ May cause an in melanocyte- stimulating hormone → hyperpigmentation in the integumentary system ▪ Darkening of the nipples, areolae and perianal and genital areas occur ▪ Linea alba becomes the Linea nigra o Divides the abdomen from the sternum to the symphysis

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▪ “Mask of pregnancy” – Melasma (previously referred to as chloasma) o Brown splotches - Mask like distribution on the cheeks, forehead and eyes o Disappears after pregnancy but could reoccur with excessive sun exposure ➢ Hair ❖ In early stage of pregnancy the number of hairs in the growth phase remain stable ❖ In later stages, hormonal levels  the number of hairs in the growth phase and  the number of hairs in the resting phase ❖ After delivery the proportion of hairs that enter the resting phase doubles ▪ Women may see a hair loss 2-4 months postpartum ➢ Nails ❖ Occasional changes ▪ Transvers grooving ▪ softening/ brittleness

➢ Uterus ➢ Prior to pregnancy is a small, semisolid pear ➢ Regulated by the BP and SVR shaped organ weighing approx. 40-50 g. (Systemic Vascular Resistance) ➢ At the end of pregnancy weighs approx. 1,100 to ➢ Supine position compresses inferior 1,200 g. vena cava and aorta,  blood flow

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❖ At the beginning of the pregnancy the uterine wall thickens due to hypertrophy of the myometrial cells from estrogen and progesterone levels ❖ At the end of the pregnancy the uterine wall becomes thinner to allow for palpation of contractions and fetal position ➢ Receives 10-20% of cardiac output ➢ 700 to 800 ml/minute perfusion→ 80% is directed to the placental bed ➢ Maternal position, maternal arterial pressure and Page 63 uterine contractility influence uterine blood flow

➢ Cervix ➢ Changes are characterized by : ❖  Vascularity o Causes a softening and bluish discoloration – Chadwick's Sign ❖  Water Content ❖ Softening ❖ Dilation ➢ Estrogen stimulates glandular tissue of the cervix ➢ Endocervical glands secrete a thick, tenacious mucus which forms the mucous plug and prevents bacteria from entering the uterus ➢ Hyperactive glandular tissue causes an in normal mucous production ➢ Ovaries ➢ Ovulation ceases in pregnancy

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➢ Corpus luteum persists and secretes progesterone until the 10th to 12th week ❖ This maintains the endometrium until adequate progesterone can be secreted by the placenta ➢ Vagina ➢ Vaginal epithelium and muscle layers in response Page 63 to estrogen undergo: ❖ Hypertrophy ❖  in vascularization ❖ Hyperplasia ➢ Loosening of the connective tissue and thickening of the mucosa vaginal secretions ❖ Thick, white and acidic → play a role in  infections ➢ At the end of pregnancy the vaginal wall and perineal body are relaxed enough to allow stretching of the tissues and delivery of the infant ➢ Breast ➢  size and nodularity to prepare for lactation Page 63 and 64 ➢ Nipples become more easily erectile and veins are more prominent ➢ Areola pigmentations  ➢ Montgomery follicles, sebaceous glands located in the areola hypertrophy ➢ Striae may develop ➢ Colostrum – yellow secretion rich in antibodies may leak during the last trimester of pregnancy

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➢ Feelings of fullness, tingling, and  sensitivity begin in the 1st few weeks of gestation REFERENCES ❖ Association of Women’s Health, Obstetric, and Neonatal Nurses (2015). Fetal Heart Rate Monitoring: Principles and Practices. 5th Edition. Kendall/Hunt Professional. Washington, DC: AWHONN. ❖ Simpson, K.R, Creehan, P.A., O’Brien-Abel, N., Roth, C.K. & Rohan, A. J. (2021). AWHONN Perinatal Nursing ( 5th ed). Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins ❖ Blackburn, S.T. (2018). Maternal, Fetal, & Neonatal Physiology. (5th ed). Maryland Heights, MO: Elsevier Saunders. ❖ Davidson, M.R., London, M.L. & Ladewig, P.A. (2020). OLDS’ Maternal-Newborn Nursing & Women’s Health Across the Lifespan. (11th ed). Boston, MA: Pearson ❖ https://www.youtube.com/watch?v=nIog3oizP8A retrieved February 24th, 2016.

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