Physiological changes in pregnancy


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  • ↑ estradiol + progesterone  hyperplasia + hypertrophy of myometrial cells Uterus weight 50-60g  1000g (at term) Early: uterine growth independent of the growing fetus Later on hypertrophy > hyperplasia Muscle fibres ↑ in length x15 Uterine arteries undergo hypertrophy
  • The average blood loss associated with: - vaginal delivery 500 – 600 ml - cesarean delivery 1000 ml - twin delivery 1000 ml
  • The erythrocyte sedimentation rate (ESR), also called a sedimentation rate or Biernacki Reaction , is the rate at which red blood cells sediment in a period of 1 hour The ESR is governed by the balance between pro-sedimentation factors, mainly fibrinogen , and those factors resisting sedimentation, namely the negative charge of the erythrocytes ( zeta potential ). When an inflammatory process is present, the high proportion of fibrinogen in the blood causes red blood cells to stick to each other. The red cells form stacks called ' rouleaux ,' which settle faster. The flat surface of the discoid RBCs give them a large surface area to make contact and stick to each other; thus, forming a rouleau. They occur when the plasma protein concentration is high, and because of them the ESR ( erythrocyte sedimentation rate ) is also increased.
  • Erythrocyte lifespan slightly decrease during pregnancy A greater expansion of plasma volume relative to the increase in hemoglobin mass and erythrocyte volume is responsible for the modest fall in hemoglobin levels (i.e., physiological or dilutional anemia of pregnancy) observed in healthy pregnant women. The greatest disproportion between the rates at which plasma and erythrocytes are added to the maternal circulation occurs during the late second to early third trimester. (Lowest hematocrit is typically measured at 28–36 weeks [16].) Nearer to term, hemoglobin concentration increases due to cessation of plasma expansion and continuing increase in hemoglobin mass. Conversely, the absence of physiologic anemia appears to be a risk factor for Stillbirth The neutrophil count begins to increase in the second month of pregnancy and plateaus in the second or third trimester, at which time the total white blood cell counts ranges from 9000 to 15,000 cells/L The white blood cell count falls to the normal nonpregnant range by the sixth day postpartum
  • Physiological changes in pregnancy

    1. 1. Physiological Changes in Pregnancy Presented by: Mohd Amir & R.Nandinii
    2. 2. Uterus Non PregnantNon Pregnant UterusUterus Pregnant UterusPregnant Uterus MuscularMuscular StructureStructure Almost SolidAlmost Solid Relatively thin –Relatively thin – walled (≤ 1.5 cm)walled (≤ 1.5 cm) weightweight ≈≈ 70 gm70 gm Approx. 1100 gm byApprox. 1100 gm by the end ofthe end of pregnancypregnancy VolumeVolume ≤≤ 10 mL10 mL ≈≈ 5 L by the end of5 L by the end of pregnancypregnancy
    3. 3. Mechanism Of Uterine Enlargement
    4. 4. Uterine size, shape & position • First few weeks, original peer shaped organ • As pregnancy advances, corpus & fundus assumes a more globular form. • By 12 weeks, the uterus becomes almost spherical . • Subsequently, uterus increases rapidly in length than in width & assumes an ovoid shape. • With ascent of uterus from pelvis, it usually undergoes Dextrorotation (caused by the rectosigmoid colon on the left side)
    5. 5. CERVIX • Estradiol + progesterone  swollen and softer during pregnancy • Estradiol  stimulates growth of columnar ep. of cervical canal  ectropion (visible on ectocervix)  prone to contact bleeding • ↑ vascularity  look bluer • Mucous glands  distended + complexity↑  secretion↑  mucus thickened  operculum @ os (protective plug) • PG (remodelling of cervical collagen) + collagenase (from leukocytes)  softening
    6. 6. • Estrogen  vaginal epithelium thicker  ↑ desquamation rate  vaginal discharge↑  > acidic  protect against ascending infection • Vagina become more vascular
    7. 7. BREAST • Deposition of fat around the glandular tissue • Estrogen  number of↑ glandular ducts • Progesterone + hPL  number↑ of gland alveoli • hPL  stimulate synthesis of alveolar casein + lactoglobulin + lactalbumin • ↑ [serum prolactin] in pregnancy  antagonized by estrogen  no lactation
    8. 8. • 48 hours after birth  rapid of [estrogen]↓  lactation • End of pregnancy and early puerperium  colostrum produced (thick yellow secretion + immunoglobulin)↑ • Early + frequent suckling  stimulates ant. and post. Pituitary gland  prolactin + oxytocin  promotion of lactation • Stress + fear  dopamine↑  synthesis and release of↓ prolactin
    9. 9. • 2-3 days of puerperium  prolactin  alveoli distended by milk  breast engorgement • oxytocin  myoepithelial cells surrounding alveoli and small ducts contract  squeezes milk into larger ducts and subareolar reservoirs • Oxytocin  inhibit dopamine  prolactin↑  successful lactation
    10. 10. Endocrinological Changes in Pregnancy
    11. 11. • Peptide and steroid hormones produced by • Non-pregnant: endocrine glands • Pregnant: intrauterine tissues
    12. 12. Hormones Pregnancy specific • Human chorionic gonadotrophin (hCG) • α and β (pregnancy specific; produced by trophoblast  detectable w/in days of implantation) • production influenced by leukemia inhibitory factor (LIF) and isoform of GnRH • Maintain corpus luteum’s fx • peak values @10w  progesterone by placenta  to plateau @>12w↓ • α hCG ≈ α of LH, FSH, TSH  supress FSH and LH secretion by ant. pituitary • Human placental lactogen (hPL) • Produced by placenta • partial homology with prolactin and hGH
    13. 13. Hormones Steroids • produced by placenta and fetus • Concentration earliest weeks of pregnancy↑  plateau •Effects upon myometrium and (+prolactin) breast tissue • effects on smooth muscle of vascular tree, GIT, GUT • estrogen • max 30-40mg/day (80% estriol)↑ • encourages cellular hypertrophy (uterus, breast) •Alter chemical constitution of con. tissue  more pliable • Water retention • Reduce sodium excretion • progesterone • reduce smooth muscle tone • ↓ stomach motility  nausea • ↓ colon activity  delayed emptying  water reabsorb↑  constipation • ↓ uterine tone  prevent contraction • ↓ vascular tone  diastolic P ↓  venous dilatation • ↑ temperature • ↑ fat storage • Induce over-breathing • Induce development of breast
    14. 14. Hormones Pituitary related • Prolactin • produced by lactotrophs of ant pituitary and cells of decidua • Rc in trophoblast cells and w/in amniotic fluid • Stimulated by estrogen and sleep •Inhibited by hPL and dopamine agonist • essential of lactation •Human growth hormone (hGH) • production by ant pituitary supressed in pregnancy • [hGH] ↓ • hPL supress hGH •Adrenocorticotrophic hormone (ACTH) • placental clock theory Pituitary gland increase 30% in weight in first pregnancy (50% in next pregnancy)  can produce headache
    15. 15. Hormones Hypothalamus related • Gonadotrophin-releasing hormone (GnRH) • Corticotrophin-releasing factor (CRF) CRF  placental clock theory Other peptides • Insulin-like growth factor I and II (IGF) •1,25-Dihydroxycholecalciferol •Parathyroid hormone-related peptide •Renin •Angiotensin II • IGF regulates fetal growth • IGF I and II: produced by fetal cells (in liver) and maternal cells (in uterus) • IGF II predominated in fetal circulation • 1,25-(OH)2D3: calcium absorption↑
    16. 16. Carbohydrate metabolism • First half of pregnancy • Fasting plasma glucose concentration ↓ • Little change in plasma insulin level • OGGT  enhance respond compared to non-pregnant, normal insulin release but blood glucose value↓ • Second half of pregnancy • Delay in reaching peak glucose value • ↑ glucose value + [plasma insulin] =↑ relative insulin resistance ( sensitivity↓ by 80%) • May involve hPL or other growth-related hormones • Reduced peripheral insulin sensitivity • Characteristic of insulin binding to Rc also altered (= obese and NIDDM)
    17. 17. • In pancreas: • ↑ size of Langerhans cell • ↑ number of β cell • ↑ Rc for insulin
    18. 18. Fat metabolism • 4kg fat is stored by 30 weeks of gestation • Mostly in form of depot in abdominal wall, back and thighs. • Modest amount stored in breast • Three points to be noted • Total metabolism and energy demand ↑ • Glycogen stores are diminished  energy from KH ↓ • Although blood fat in greatly increase only a moderate amount stored
    19. 19. Thyroid function • hCG ≈ TSH  hCG maximal  suppress maternal TSH production @ trimester I • hCG or TSH  nausea and vomiting  improve after trimester I • Biochemical hyperthyroidism + free T4 + suppressed TSH↑  hyperemesis gravidarum • Iodine active transport to feto-placental unit + urine excretion↑  plasma level ↓  uptake of iodine from blood by thyroid↑ gland • Diet insufficiency of iodine  hypertrophy of thyroid gland  trap iodine • ↑ thyroid-binding globulin, bound T4 and T3 • Free T4 and T3 fall a little in trimester II and III
    20. 20. Calcium metabolism • 40% bound to albumin • Pregnancy: [plasma albumin]↓  [plasma calcium]↓ • Little changes to unbound calcium • ↑ demand from fetus  transplacental flux 6.5 mmol/day (~ 80% absorbed in GIT by non-pregnant) • Mother: absorption and excretion↑ ↓  little changes in bone (failed = osteopenia)
    21. 21. • ↑ calcium absorption by 1,25-dihydroxycholecalciferol (metabolite of vit D3) which is influenced by PTH • PTH 1/3 in pregnancy↑ • No changes in calcitonin or other D3 metabolites • [plasma calcium] fetus > maternal and independent regulation of PTH and calcitonin
    22. 22. Placental corticotrophin-releasing factor • Mid-pregnancy: trophoblast produces CRF  stimulates fetal pituitary  ACTH↑  fetal adrenal  fetal↑ dihydroepiandrosterone (DHEA)  precursor of placental estrogen secretion  estrogen↑ @ end of pregnancy  gap junc↑ synthesis @myometrial  aid conduction  regular uterine contractions  labour = placental clock theory • CRF synthesis regulated by +ve feedback by estrogen
    23. 23. Corticosteroid and renin-angiotensin system • Trophoblast cell  CRF and ACTH  regulate activity of fetal adrenal glands, myometrium and possibly maternal adrenal glands. • Cortisol progressively, mostly bound to cortisol-binding globulin↑ (CBG) • ACTH may regulate maternal cortisol level because there’s lack of diurnal fluctuation of cortisol and attenuated response to dexamethasone supression
    24. 24. Weight Increase in Pregnant Women
    25. 25. • Metabolic changes + fetal growth  increase weight↑ ~25% of non-pregnant (~12.5 kg) • First half: weight increase is varied • Second half: 0.5kg/week (2kg/month)↑ • At term the gain stopped • After 40 weeks, may fall • Weight increase due to: • Growth of conceptus • Enlargement of maternal organs • Maternal storage of fat and protein • ↑ maternal blood volume and interstitial fluid
    26. 26. Breast 1-1.5 kg Uterus 0.5-1 kg Fetus and placenta 5 kg
    27. 27. Hematologic Changes in Pregnancy
    28. 28. concentrations of estrogen & progesterone Directly act on kidney Causing release of renin Activates aldosterone-renin- angiotensin mechanism Renal sodium retention & in total body water in plasma volume (45%) Blood volume PREGNANCY hb ht Physiological anemia Physiological anemia •To allow adequate perfusion of vital organs including placenta and fetus •To anticipate blood loss a/w delivery
    29. 29. Hypercoagulable State Increase in: Decrease in: PROCOAGULANT FACTORS •Factor VII •Factor VIII •Factor IX •Factor X •Factor XII •Fibrinogen ANTICOAGULANT •Protein S activity •Antithrombin IIIa •Activated Protein C resistance ESR
    30. 30. Increased production of: RBC mass (20%) WBCPlatelet Due to increase in renal erythropoietin production Supports higher metabolic requirement for O2 during pregnancy BUT platelet consumption increase more Fall to low normal value Mild thrombocytopenia Mainly due to increase in no of PMN cells as early as 3 wks AOG Difficult to differentiate with infection Neutrophilia
    31. 31. Immunosuppresive State Approximately 30% of women develop IgG abs against the inherited paternal human leukocyte ag of fetus BUT, the role of these abs is UNCLEAR & there is no evidence of attack on fetus Lack of maternal immunity towards the fetus Due to reduced no of cytotoxic T cells (CD8+) during pregnancy Potentially harmful T cell-mediated immune responses downregulated & components of innate immune system activated instead Allowed fetal allograft to implant & develop
    32. 32. Physiological Changes in Cardiovascular System
    33. 33. Anatomic Changes
    34. 34. Blood volume changes
    35. 35. Cardiac Output
    36. 36. Blood Pressure
    37. 37. Clinical findings in cardiovascular system examination
    38. 38. Changes of the respiratory function in pregnancy
    39. 39. Airway
    40. 40. Ventilation
    41. 41. Oxygenation
    42. 42. Arterial Gases
    43. 43. Gastrointestinal and Hepatobilliary
    44. 44. Difference in Gastrointestinal tract in Pregnancy and Non pregnant state
    45. 45. Gastrointestinal • As the gestational age in pregnancy increase so does the size of uterus. • This increase in size of the uterus causes the stomach and the intestine to be displace upwards • The position of the appendix is usually displace upwards towards the right upper flank region. • Because of the alteration of the intra-abdominal structure this makes it very difficult to diagnose any disease associated with the intra abdominal
    46. 46. • Increase in progesterone level causes • Lower esophageal sphincter tone to be reduced (esophageal reflux) • Increase placenta production of gastrin, which increases gastric acidity. (heart burn) • Reduced motility of the gut which result in delay of the gastric emptying time. (constipation)
    47. 47. • During labour the motility of the gut decreases further and even during the pueriperium period, emptying of the gut is still delayed. • This increases the risk of pregnant women to develop aspiration of gastric content-especially if they are sedated after 16 weeks of gestation.
    48. 48. Liver • Liver may become more difficult to examine during pregnancy due to the expanding uterus. • Due to hyperoestrogeninc state in pregnancy, clinical findings such as telangiectasia and palmar erythema that are associated with liver disease in non pregnant state are found in 60% of the pregnant woman
    49. 49. • Despite of the increase of the portal vein pressure in pregnancy, the size of the liver and the hepatic blood flow remains unaltered. • Liver function also remains mostly the same. • Total alkaline phosphate serum increases up to double the normal amount due to fetal and placenta production.
    50. 50. • Hepatic production of protein increases but because of the expanding maternal placenta volume serum albumin level still remain low. • Most important changes in pregnancy to the liver is the increased in production and plasma fibrinogen and the clotting factors
    51. 51. Gall bladder • During pregnancy, contractility of the gallbladder is reduced. • Progesterone may impairs gallbladder contraction by inhibiting cholecystokinin-mediated smooth muscle stimulation (primary regulator of gallbladder contraction). • This impairment leads to stasis, and is associated with the increased cholesterol saturation of pregnancy
    52. 52. • Intrahepatic cholestasis has been linked to high circulating levels of estrogen, which inhibit intraductal transport of bile acids
    53. 53. Gastrointestinal symptoms associated with Pregnancy • Constipation • Morning sickness • Gastroesophageal reflux • Haemorrhoids
    54. 54. Kidneys & Urinary Tract Changes
    55. 55. Kidney
    56. 56. Anatomic Changes • Increase in length for about 1 - 2 cm. • Calyces, renal pelvis & ureters dilate impression of obstruction.→ • Anatomical changes predispose pregnant women to ascending UTI. • By 6 weeks postpartum, renal dimensions return to pre-pregnancy values.
    57. 57. Functional Changes • Renal vascular resistance decreases renal plasma flow increases→ 50 – 85% above nonpregnant values during first half of pregnancy. • Renal perfusion increases rise in GFR by approximately 50%.→ • GFR returns to normal within 12 weeks of delivery.
    58. 58. Functional Changes • Renal clearance of creatinine increases as the GFR rises. • Urinary protein loss normally does not exceed 300 mg over 24 hours, which is similar to nonpregnant state.
    59. 59. Functional Changes • Increase in GFR plus saturated ‘renal threshold’ in the proximal convoluted tubule explain the increase amount of glucose in urine glycosuria.→ • More than 50% of women have glycosuria sometime during pregnancy.
    60. 60. THANK YOU.
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