Repro16 - Maternal Physiology Flashcards

1
Q

5 endocrine changes during pregnancy

T3/T4 Levels
Importance of Thyroxine (T4)
Insulin Resistance
Switch in Energy Source
Parathyroid Hormone (PTH)
A
  1. ) Rise in Total T3 and T4 Levels - oestrogen –> more thyroid binding globulin (TBG) which binds to free T3/T4
    - AP releases more TSH leading to increase in T3/T4
    - free T3/T4 remains the same but total T3/T4 increases
  2. ) Thyroxine (T4) Production - essential for neural development in the foetus in early development
    - foetal thyroid gland not functional until 2nd trimester
    - rise in T3/T4 levels ensures high levels of thyroxine
  3. ) Increased Insulin Resistance - oestrogen and progesterone causes a rise in anti-insulin hormones
    - reduction of maternal peripheral uptake of glucose ensures continous supply of glucose for the fetus
    - hormones: hPL, prolactin, cortisol
  4. ) Switch in Energy Source - mother turns to using lipids to preserve glucose for the foetus
    - increase in lipolysis –> increase in free FAs in plasma provides substrate for maternal metabolism
    - lipid breakdown can can lead to ketogenesis meaning pregnancy increases risk of ketoacidosis
  5. ) Rise in PTH - releases Ca2+ ions for the fetus
    - mother requires adequate dietary intake of calcium so only minimal bone resorption occurs
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2
Q

3 cardiovascular changes during pregnancy

Blood Pressure
Cardiac Output
Blood Volume

A
  1. ) Decrease in Diastolic BP - progesterone decreases systemic vascular resistance
    - occurs during the 1st and 2nd trimester
    - rise in BP could indicate pre-eclampsia
  2. ) Increase in Cardiac Output - increases by 33-50%
    - response to fall in BP
    - early pregnancy due to increase in stroke volume
    - late pregnancy due to increase in heart rate
  3. ) Increase in Blood Volume - oestrogen and progesterone causes activation of RAAS
    - increases sodium levels and water retention
    - can lead to peripheral oedema
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3
Q

3 respiratory changes during pregnancy

Total Lung Capacity
Tidal Volume
Ventilation

A
  1. ) Maintained Total Lung Capacity - only down by 5%
    - fetus causes elevation of the diaphragm
    - increase in transverse and AP diameters of the thorax maintains the TLC
  2. ) Increased Tidal Volume - increases by 30-40%
    - helps mother meet increase in O2 demand caused by an increase in metabolic rate
    - causes decrease in expiratory residual volume by 20%
  3. ) Hyperventilation - progesterone produces increased CO2 production and increased respiratory drive
    - respiratory alkalosis compensated by increased renal HCO3- excretion is normal during pregnancy
    - can lead to shortness of breath (dyspnea)
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4
Q

5 gastrointestinal changes during pregnancy

Intra-Gastric Pressure
Lower Oesophageal Sphincter Tone
Appendix
Gut Motiltiy
Gallbladder
A
  1. ) Raised Intra-Gastric Pressure - due to gravid uterus causing upwards displacement of the stomach
    - can lead to GORD, nausea and vomiting
  2. ) Decreased Lower Oesophageal Sphincter Tone
    - caused by progesterone relaxing smooth muscle
    - also leads to GORD but also aspiration
  3. ) Appendix Location - can move to the RUQ
    - due to enlargement of the gravid uterus
  4. ) Decreased Gut Motility - progesterone causes SM relaxation, allowing more time for absorption
    - can lead to constipation
  5. ) Gallbladder Relaxation - progesterone causing smooth muscle relaxation –> biliary tract stasis
    - this predisposes the mother to gallstones
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5
Q

5 urinary changes during pregnancy

GFR
2 Ureter
2 Bladder

A
  1. ) Increase in GFR - increased by 50-60%
    - caused by increase in CO and renal blood flow
    - leads to an increase in renal excretion and decreased PCT absorption –> glycosuria
    - so in pregnancy, lower levels of urea and creatinine
  2. ) Ureter Relaxation –> hydroureter (ureter dilation)
    - due to progesterone causing SM relaxation
    - leads to urinary stasis –> increased risk of UTIs
  3. ) Ureter Compression - caused by gravid uterus
    - causes backflow of urine which can lead to swelling of the kidneys (hydronephrosis)
  4. ) Bladder Muscle Relaxation - progesterone
    - leads to urinary stasis –> increased risk of UTIs
  5. ) Bladder Compression - caused by gravid uterus
    - increases intravesical pressure which can lead to urinary incontinence
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6
Q

5 haematological changes during pregnancy

Clotting
Veins
Thromboembolic Events
2 Causes of Anaemia

A
  1. ) Increased Clotting - oestrogen makes liver make more clotting factors
    - also increase in fibrinogen and decrease in fibrinolysis
    - increases risk of thromboemoblic events
  2. ) Venodilation - caused by progesterone
    - increased stasis –> risk of thromboembolic events
  3. ) Management of Thromboembolic Events
    - wafarin cannot be given as it is a teratogen
    - low molecular weight heparin (LMWH) is given if the mother needs an anticoagulant
  4. ) Iron Deficiency - although the mother has less periods (less iron loss), the fetus still requires so much iron –> iron deficiency
    - leads to iron deficiency anaemia
  5. ) Dilutional Anaemia - significant increase in plasma volume due to effect of RAAS
    - only small increase RBCs –> reduced haematocrit
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7
Q

MSK and skin changes during pregnancy

Center of Gravity
Abdominal Muscles
Pelvic Pain
Structure Compression
Pigmentation x4
A
  1. ) Center of Gravity Shifts Forwards - due to:
    - increased lordosis and kyphosis
    - foward flexion of the neck
    - causes back pain, shoulder pain, tension, headaches
  2. ) Stretching of Abdominal Muscles
    - impedes posture and strains paraspinal muslces
    - causes back pain, shoulder pain, tension
  3. ) Pelvic Pain - caused by the increased mobility of sacroiliac joints and pubic symphysis
    - anterior tilt of the pelvis

4.) Compression of Structures - fluid retention can compress structures such as the median nerve (carpal tunnel syndrome)

  1. ) Hyperpigmentation - caused by increase in MSH
    - cholasma/melasma (mask of pregnancy)
    - palmar erythema, vascular spiders, linea nigra
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8
Q

4 features of pre-eclampsia

What is it?
Aetiology
Maternal Complications x6
Fetal Complications x4

A
  1. ) What is it? - multisystem pregnancy disorder characterised by hypertension (new onset) + proteinuria
    - usually presents in 3rd trimester
    - resolves after delivery but can occur postpartum
  2. ) Aetiology - impaired implantation
    - shallow invasion of spiral arteries so they remain spiral and high resistance –> hypoperfusion and ischaemia
  3. ) Maternal Complications - seizures (eclampsia)
    - cerebral bleeding, renal failure, pulmonary oedema
    - DIC and thrombocytopenia
    - hepatic failure or rupture (rare)
  4. ) Fetal Complications
    - growth restriction due to reduced blood flow
    - oligohydramnios (low levels of amniotic fluid)
    - placental infarct or abruption
    - fetal distress –> premature delivery –> stillbirth
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9
Q

Diagnosis/management of pre-eclampisa

Risk Factors
Signs and Symptoms of Mild Pre-eclampsia x4
Signs and Symptoms of Severe Pre-eclampsia x4
Examinations x2
Management

A
  1. ) Risk Factors - age (extremes), obesity, diabetes
    - history of pre-eclampsia (family or prior pregnancy)
    - first pregnancy, multiple gestation, IVF
    - chronic or gestational hypertension
    - pre-existing renal disease
  2. ) Signs and Symptoms of Mild Pre-eclampsia
    - hypertension, proteinuria, weight gain, oedema
  3. ) Signs and Symptoms of Severe Pre-eclampsia
    - headaches, blurred vision, nausea/vomiting, abdominal or back pain
  4. ) Examinations
    - optic fundi: papillloedema suggests cerebral oedema
    - tendon reflexes: hyper-reflexia due to brain damage
  5. ) Management
    - stabilise BP, fluid restriction, monitor urine output
    - MgSO4 for neuroprotection and to prevent seizures
    - deliver the baby early if needed
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