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Pregnancy produces the most dramatic change in blood volume seen in any normal physiological state.
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Progesterone and oestrogen cause peripheral vasodilation and decreased SVR, reducing renal perfusion
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The RAAS responds with increased aldosterone, augmenting sodium and water reabsorption
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Renal threshold for AVP shifts leftward (plasma osmolality set-point decreases), further expanding volume
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After placental delivery, oestrogen/progesterone fall abruptly and a vigorous post-partum diuresis follows
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Hypervolaemia also occurs with trophoblastic disease (a fetus is not essential for its development)
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Creasy & Resnik's Maternal-Fetal Medicine; Medical Physiology
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Because plasma volume rises more (~50%) than RBC mass (~25%), a dilutional or "physiologic" anaemia develops - this is normal and not pathological
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Total oxygen delivery is not reduced because cardiac output increases to compensate
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Iron supplementation corrects the RBC deficit; without it, haemoglobin can fall as low as 11 g/dL and haematocrit to 33%
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In twin/triplet pregnancies, the plasma expansion is even greater and anaemia more pronounced
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Miller's Anesthesia 10e; Creasy & Resnik's Maternal-Fetal Medicine
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Physiologic leukocytosis is common in pregnancy and is unrelated to infection
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Predominantly a neutrophilia
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WBC rises further during labour (proportional to the duration of labour)
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This physiologic leukocytosis can overlap with SIRS/sepsis criteria, making infection harder to diagnose in pregnancy
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Miller's Anesthesia 10e
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The mild decrease is due to haemodilution and more rapid platelet turnover
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Gestational thrombocytopenia is a diagnosis of exclusion - must differentiate from:
- Idiopathic thrombocytopenic purpura (ITP)
- HELLP syndrome (haemolysis, elevated liver enzymes, low platelets)
- Pre-eclampsia
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Gestational thrombocytopenia is not associated with abnormal bleeding and resolves postpartum
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Miller's Anesthesia 10e
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Decreased R time (time to start clot formation)
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Decreased K time (time to specified clot strength)
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Increased α angle (rate of clot formation)
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Increased MA (maximum amplitude / clot strength)
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Changes begin as early as the first trimester
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Miller's Anesthesia 10e; Harrison's Principles 22e
Clinical implication: This hypercoagulable state, combined with venous stasis and endothelial injury, constitutes Virchow's triad in pregnancy - the basis for a 4-6x increased risk of VTE (venous thromboembolism) during pregnancy and the puerperium.
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Normal pregnancy fibrinogen: 400-450 mg/dL (significantly above the normal non-pregnant range of 200-400 mg/dL)
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Values below 300 mg/dL in pregnancy indicate significant consumption of coagulation factors (e.g. DIC, abruption, HELLP)
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Oestrogens stimulate hepatic rough endoplasmic reticulum, increasing protein synthesis including fibrinogen, factors VII, VIII, IX, and X
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Creasy & Resnik's Maternal-Fetal Medicine; Rosen's Emergency Medicine