Physiological changes during pregnancy by Harrison Mbohe

HarrisonMbohe 183 views 25 slides Aug 07, 2021
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About This Presentation

MBChB student JKUAT


Slide Content

PHYSIOLOGICAL CHANGES DURING PREGNANCY Harrison Mbohe, MBChB Level 4 JKUAT

GENITAL ORGANS VULVA Oedematous More vascular Superficial varicosities, especially in multiparous women Labia minora- hypertrophied and pigmented

VAGINA Hypertrophies Oedematous Jacquemier’s Sign – increased blood supply to the venous plexus on vaginal walls that confers a bluish colouration on the mucosa Increased length of the anterior wall Secretions - copious, thin and cloudy white (due to marked epithelial and bacterial exfoliation) pH – acidic (3.5-6.6) Navicular cells predominate (small intermediate cells in clusters with elongated nuclei)

UTERUS Enormous growth. At term it weighs approx. 1000g and measures approx. 35cm in length. Its capacity increases 500 – 1000 fold. Body Marked hypertrophy of muscle fibres with limited addition of new muscle fibres Elongation of muscle fibres beyond 20 weeks; becomes soft and elastic. Increased no. and size of supporting fibrous and elastic tissues. Marked spiralling of arteries reaching max at 20 weeks & thereafter straightening out. Increased diameter of uterine arteries by 2 fold and increased blood flow into them by 8 fold

Uterine veins become dilated and valveless. Opening up of numerous lymphatic channels. Findus enlarges more than the body Pyriform shape at early months  becomes globular at 12 weeks  returns to Pyriform shape by 28 weeks  changes to spherical beyond 36 weeks Braxton hick contractions Isthmus Hypertrophy and elongation in trimester; increases 3 fold its normal length. Becomes softer

Cervix Hypertrophy and hyperplasia of the elastic and connective tissue. Goodell’s sign (softening of the cervix). Increased vascularity. Marked hypertrophy & hyperplasia of the glands that occupy half of the cervical mucosa. Marked proliferation of the endocervical mucosa with downward extension beyond squamocolumnar jxn. Secretions – copious and tenacious (physiological leucorrhoea in pregnancy)

Suspended ovarian and uterine cycles of normal menstruation

BREASTS Changes more pronounced in primies. Increased breast size (marked hypertrophy & proliferation of the ducts and alveoli; marked proliferation of connective tissue stroma and prominence of myoepithelial cells). Increased vascularity. Axillary tail becomes enlarged and painful. Nipples become larger, erectile and deeply pigmented. Secretions – sticky at about 12 weeks, later on become thick & yellowish.

CUTANEOUS CHANGES Chloasma gravidarum – increased pigmentation around the cheeks, forehead and around the eyes. Linea nigra – linear hyperpigmentation that appears as a brown-black streak that runs vertically, along the midline of the abdomen from the pubis to the umbilicus. Striae gravidarum – stretch marks below the umbilicus and sometimes over the thighs and breasts.

CVS & HEMATOLOGICAL CHANGES Marked increase in blood volume – starts at approx. 6 weeks and expands rapidly thereafter to a max of 40 – 50 % above normal at 30-32 weeks. Increased venous capacitance. Increased erythropoiesis. Increased HR by averagely 15 bpm Increased CO by approx. 40% Increased stroke volume by approx. 25-30% Slight decrease in systemic arterial pressure

Progressive increase in venous pressures in the lower extremities due to compression of the IVC by the gravid uterus. Decreased peripheral vascular resistance with a slight increase towards term due to effect of vasodilators. Increased blood flow to the uterus, kidneys, skin and breasts Systolic ejection murmurs – detected in >90% of gravid women. Devpt of dizziness, syncope and light headedness. S 1 may be split with increased loudness of both portions. S 3 may be louder.

ECG changes 15-20 shift to the left in the electrical axis ST segment depression T wave flattening/inversion No changes in the P wave and QRS complex MCV increases by 20 – 30% resulting in decreased MCHC and Hct leading to haemodilution. Neutrophilic leucocytosis due to increased oestrogen and cortisol. Modulation away from cytotoxic immune responses towards humoral and innate immune responses.

Total protein increases from 180g – 230g Fibrinogen increases by 50%. Gestational thrombocytopenia – remains within normal range. ESR increases 4 fold. Fibrinolytic activity is depressed. Increased activity of the clotting factors – X, IX, VIII & I Clotting time remains unaffected.

RESPIRATORY CHANGES Elevation of diaphragm by the gravid uterus by approx. 4cm. Widening of the subcostal angle. Slight increase of chest diameter and circumference. 20% decrease in RV & FRC + 5% decrease in total lung volume. Respiratory rate remains unchanged. 30 – 40% increase in tidal volume. Gravid women also tend to become dyspnoeic. Nasal stiffness + increased nasal secretions due to mucosal hyperaemia.

RENAL CHANGES Enlargement and dilatation of the kidneys and the urinary collecting system. Increased renal blood flow – up to 75% at term. Increased GFR by approx. 50%. Increased urinary glucose excretion (not associated with glycaemic pathology). No significant increase in urinary protein loss. Sodium metabolism remains unchanged. Plasma renin increases 10 fold. Angiotensinogen and angiotensin increase approx. 5 fold. Urinary frequency. Stress urinary incontinence in 20% of women. Increased incidence of pyelonephritis due to urinary stasis with asymptomatic bacteriuria. Reduced serum levels of creatinine and BUN

RENAL CHANGES Enlargement and dilatation of the kidneys and the urinary collecting system. Increased renal blood flow – up to 75% at term. Increased GFR by approx. 50%. Increased urinary glucose excretion (not associated with glycaemic pathology). No significant increase in urinary protein loss. Sodium metabolism remains unchanged. Plasma renin increases 10 fold. Angiotensinogen and angiotensin increase approx. 5 fold. Urinary frequency. Stress urinary incontinence in 20% of women. Increased incidence of pyelonephritis due to urinary stasis with asymptomatic bacteriuria. Reduced serum levels of creatinine and BUN

GIT CHANGES Displacement of the stomach and intestines by the gravid uterus with no changes in sizes. Enlargement of the portal vein due to increased blood flow. Generalized smooth muscle relaxation mediated by progesterone resulting in reduced lower esophageal sphincter tone, reduced GI motility and impaired gall bladder contractility. GERD due to imbalanced lower intraesophageal pressures and increased intragastric pressures + reduced lower esophageal sphincter tone. Gall stones and cholestasis of bile salts due to reduced gall bladder contractility and oestrogen mediated inhibition of intraductal transportation of bile acids. Nausea and vomiting due to elevated P 4 , HCG and relaxation of gastric smooth muscle. Hyperemesis gravidarum which results in weight loss, ketonemia or electrolyte imbalance.

Pica – appetite/cravings for substances which are largely non-nutritive. Constipation due to mechanical obstruction of the colon by the gravid uterus, reduced motility and increased water absorption. Generalized pruritus due to intrahepatic cholestasis and increased bile acid serum concentrations. Gingival disease. Haemorrhoids due to constipation and elevated venous pressures. Elevated ALP due to increased placental production. ALT, AST, GGT & bilirubin are largely unchanged or are slightly lower.

ENDOCRINE CHANGES Moderate thyroid enlargement which doesn’t produce thyromegaly or goitre. Transient increase in free t 4 – 2 to increased HCG levels that has TSH like activity. Levels of t 4 normalize after trimester 1 due to reduced HCG levels. Increased total t 3 and t 4 due to oestrogen induced hepatic synthesis of TBG. Free t 3 and t 4 are unchanged. Increased serum cortisol due to oestrogen induced hepatic synthesis of CBG. Increased ACTH. Marked increased levels of aldosterone. Increased deoxycortisone levels. Reduced DHEAS due to hepatic uptake and subsequent conversion to oestrogen

METABOLIC CHANGES CARBOHYDRATE METABOLISM Increased insulin resistance, hyperinsulinemia and hyperglycaemia due to influence of placental lactogen secreted in proportion to placental mass and progesterone. Increased hepatic glycogenesis Reduced gluconeogenesis. Constant drainage of maternal glucose by the fetoplacental unit leads to maternal hyperglycaemia during periods of fasting.

LIPID METABOLISM Increase in circulating levels of lipids, lipoproteins and apolipoproteins. Central lipogenesis dominates in early pregnancy. Lipolysis dominates in late pregnancy triggered possibly by maternal fasting hypoglycaemia. All lipid levels normalize after delivery in a process accelerated by breastfeeding

PROTEIN METABOLISM Increased intake and utilization of proteins 1 kg above the normal non-pregnancy

MUSCULOSKELETAL CHANGES Compensatory lumbar lordosis – helps to keep woman’s CoG over the legs which the gravid uterus has shifted anteriorly. Lower back pain due to the lumbar lordosis. Diastasis recti – physiological separation of rectus abdominis due to raised intraabdominal pressures from the enlarging uterus. Unsteady gait due to relative laxity of ligaments influenced by progesterone and relaxin; separation of the pubic symphysis at approx. 28-30 weeks and an altered CoG. Reduced maternal total calcium, compensated for by raising maternal parathyroid hormone. Skeleton well maintained despite elevated PTH levels by the counter regulatory function of calcitonin

OPHTHALMIC CHANGES Blurred vision due to increased thickness of the cornea associated with fluid retention and reduced intraocular pressures. This regresses within the first 6-8 weeks post partum.

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