6.2: Physiological changes in pregnancy Flashcards

1
Q

What ‘red flags’ would you be looking for in a history and examination during antenatal screening and what will it help you determine?

A
  1. Baby’s risk of acquiring genetic diseases (FH) 2. Maternal lifestyle; smoking and alcohol3. Mother’s medical conditions/system disorder 4. Risk factors for gestational diabetes, preeclampsia, etc.
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2
Q

What are you looking for in an antenatal blood test?

A
  1. Blood group and antibody (e.g; Rh factor) 2. Hb - looking for anemia, hemoglobinopathies; SC disease, thalessemias, CF, etc 3. Infections; syphilis, HIV, Hep B, rubella; *only ones that can be treated, managed
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3
Q

What would you check for in an antenatal urinalysis?

A
  1. Proteins; the ratio of protein:creatinine can help diagnose preeclampsia 2. Nitrates
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4
Q

Other than taking urinalysis, blood test and history what else would you do during antenatal screening?

A

Ultrasound to check fetal viability

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5
Q

How is the maternal CVS and blood affected during pregnancy?

A

Increased blood volume: since CO = SV X HR they all increase

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6
Q

What happens to the systemic vascular resistance and the BP?

A

Systemic vascular resistance decreases:Progesterone causes vasodilation -> reduced afterload -> decreased BP/hypotension But BP should return to normal during third trimester

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7
Q

How is the preload and afterload affected during pregnancy?

A

Preload increases, afterload decreases (due to reduced systemic vascular resistance)

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8
Q

What happens to the diaphragm during pregnancy? Which other structure does this affect?

A

Moves up due to the increased pressure from the uterus, this displaces the heart

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9
Q

When and why can aortocaval compression occur? What advice can be given to prevent consequences of this?

A

In the third trimester: Compression of the abdominal aorta and IVC due to the gravid uterus when a pregnant women lies on her back -> lie on her L side since IVC is on the R side (so baby’s weight can’t put pressure on it and vessel remains open)

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10
Q

How do endothelia change in pregnancy?

A
  1. More permeable (hormones)2. Progesterone causes vasodilation
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11
Q

Name six factors that put some women at risk for preeclampsia. When will signs of it begin to show?

A

Signs show after 20-21 weeks, but milder case = later diagnosis 1. FH 2. High BMI and first pregnancy 3. Older women having their first pregnancy 4. Multiple pregnancies5. Chronic hypertension6. Any autoimmune condition

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12
Q

What is preeclampsia? How is it caused and what is it characterized by?

A

No meeting between invading trophoblast cells and the spiralling arteries (maternal vessels)

Imbalance of androgenic and antiandrogenic factors -> widespread endothelial damage -> trophoblast cells fail to invade into the spiral arteries -> uterine vessels stay thick and muscular -> reduced blood flow to baby hindering its growth

Characterized by:

  1. High blood pressure (rises when there is endothelial damage)
  2. Signs of damage to another organ system (e.g; kidneys, liver)
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13
Q

How are the kidneys affected during pregnancy/How does the volume that the urinary system has to deal with change?

A
  1. Increased volume, GFR and renal plasma
  2. Filtration capacity stays the same
  3. Functional renal reserve (ability to increase the renal plasma flow and GFR) decreases because GFR increases
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14
Q

What happens to the blood creatinine as GFR increases in pregnancy and what can be indicated from an abnormal serum creatinine range?

A

Decreases - if value is abnormal can indicate

preeclampsia or other renal pathologies aggravated during pregnancy

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15
Q

What happens to the bladder and the ureters during pregnancy and why? Name one complication that can arise as a result

A

Progesterone

  1. Bladder doubles its capacity
  2. Ureters dilate - this also predisposes to an ascending bacterial infection
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16
Q

Describe how the effects of progesterone during pregnancy may lead to a series of complications in the urinary system

A

Urinary stasis -> hydronephrosis -> obstruction and hydroureter -> UTI -> pyelonephritis (inflammation of the kidney typically via bacterial infection) -> irritate uterus -> increased risk of pre-term labor

17
Q

When would you want to investigate a pregnant woman for a UTI?

A

Investigate/offer renal scan if woman experiences backache or flank pain and has dysuria

18
Q

What happens to the chest wall during pregnancy and why? What happens as a consequence of this?

A

Expanding uterus -> diaphgram elevation -> compensatory increase in; subcostal angle, chest wall circumference, antero-posterior and transverse diameters -> prevents sig. reduction in total lung capacity

*though there is still reduction in functional residual capacity

19
Q
Define the following and describe how they change in pregnancy
A) Vital capacity 
B) Total lung capacity 
C) Minute and alveolar ventilation 
D) Tidal volume 
E) Respiratory rate
A

A) Max exhalation after max inhalation; unchanged
B) Vital capacity + residual volume; unchanged
C) Amount of air expelled from alveoli/min; IncreasedD) Volume of air moved in-out of lungs with each ventilation cycle; increasedE) Amount of breaths/min; unchanged

20
Q

Name two physiological respiration issues pregnant women experience and why they occur.

A

Physiological hyperventilation
1. increased metabolic CO2 production

  1. progesterone stimulates respiratory drive -> hyperventilation -> physiological dyspnea
21
Q

What is a consequence of physiological hyperventilation and how is it compensated for?

A

Respiratory alkalosis compensated with increased renal bicarbonate excretion

22
Q

What happens to the PaO2, PaCO2 and FEV1 in pregnant women?

A

PaO2; increasesPaCO2; decreasesFEV1; unchanged

23
Q

Why does the vital capacity remain the same in pregnancy?

A

Expiratory reserve volume reduces to compensate for increased TV and inspiratory reserve volume

24
Q

What happens to the mothers insulin resistance as the pregnancy progresses? What causes this change?

A

Maternal peripheral insulin resistance increases -> body switches to gluconeogenesis and alternative fuels

This is achieved via anti-insulin hormones increased during pregnancy; hPL, prolactin, estrogen/progesterone, and cortisol

25
Q

Why is pregnancy associated with an increased risk of keto acidosis?

A

Gluconeogenesis can use fatty acids -> increased free fatty acid concentration -> increased lipolysis -> increased Ach and buildup of ketones

26
Q

What happens to the fasting plasma glucose and post-prandial blood glucose when pregnant?

A

Fasting - decrease

Post-prandial - increase

27
Q

Name 6 risk factors for developing gestational diabetes. What would you offer to screen this group of women?

A
  1. Immediate FH
  2. High BMI>30
  3. Previous gestational diabetes
  4. Ethnicity; asians and Afro-Caribbeans
  5. Delivery of a baby>4.5 kilo in the past
  6. History of PCOS

Offer glucose tolerance test at 26 weeks

28
Q

Name three risks to the fetus associated with poor control of gestational diabetes and one risk for the mother.

What is provided for mothers with this risk?

A
  1. Macrosomic fetus
  2. Stillbirth3. Increased rate of congenital defects Mother has a high risk of developing type 2 diabetes later so must have annual blood glucose testing
29
Q

Why are fetuses born to a mother with gestational diabetes so large but born hypoglycemic? What are they at risk of?

A

Hyperglycemic environment in mother -> fetal pancreas adaptation and overstimulation of insulin an ANABOLIC hormone -> increased production of glycogen and adipose -> macrosomic body

-> babies born into environment with much less glucose than what their bodies are used to -> born hypoglycaemic

Fetus is at risk of respiratory distress syndrome, infections, stillbirth and other congenital defects

30
Q

What happens to the amount of thyroid hormones during pregnancy and why? Does this change the amount of free T4?

A

hCG and TSH are structurally similar (on alpha subunit) -> hCG mimics TSH -> increased T3 & T4

But FREE T4 stays the same as levels of thyroid binding globulin (carries it) also increases

31
Q

Describe 4 physiological changes in the GI system during pregnancy

A
  1. Smooth muscle relaxation by progesterone
  2. Relaxed gut delays transit time/emptying > women may feel constipated, vomit, full quickly
  3. Biliary tract; stasis
  4. Pancreas; increased risk of pancreatitis
32
Q

Why are pregnant women more at risk of having a DVT?

A
  1. Pregnancy is a pro-thrombotic state (as there’s more fibrin at implantation site) -> increased fibrinogen and clotting factors and reduced fibrinolysis
  2. Progesterone -> vasodilation -> blood stasis (furthered by compression of AA and IVC from the gravid uterus)
33
Q

How does thromboembolic disease commonly present in pregnancy? What can you offer? Warfarin?

A

Commonly: tender swollen calf, can be SOB and chest pain

Give low molecular weight heparin NOT warfarin as it is teratogenic, can give after birth and mother can breastfeed

34
Q

Name 8 signs and symptoms for a pulmonary embolism in pregnancy and two additional ones for a massive PE

DPPTTHHC

A
  1. Dyspnea2. Palpitations3. Pleuritic chest pain4. Tachycardia5. Tachypnea 6. Hypotension 7. Collapse8. Hemoptysis +cyanosis/hypoxia in a massive PE
35
Q

Name 6 signs and symptoms for a DVT in pregnancy, is it usually proximal or distal?

A

Usually proximal

  1. Unilateral leg pain/tenderness
  2. Swelling in an extremity - increased calf/thigh circumference 4. Increased temp5. Prominent superficial veins 6. Pitting edema
36
Q

Explain why pregnant women sometimes experience both physiological and pathological anemia

A

Physiological: plasma volume increases but the # of RBCs hasn’t as much.

Pathological: iron and folate deficiency or other hemoglobinopathies; sickle cell, thalassemias, etc

37
Q

How is preeclampsia treated?

A
  1. Treat BP
  2. Monitor the kidney/liver function
  3. Try extending the pregnancy until mother starts deteriorating (i.e; can’t control BP) or there is risk of damage to fetal growth (latest 34 weeks)
38
Q

How would you diagnose an asymptomatic pregnant woman with a UTI?

A

Urinalysis for nitrites