4/11 Maternal Adaptation of Pregnancy Flashcards

1
Q

Given the fetal/pregnancy need for perfusion, what is the maternal response (generally)?

A
  • Volume expansion
  • Vasodilation
  • incr cardiac output
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2
Q

Given the fetal/pregnancy need for nutrition and oxygenation, what is the maternal response (generally)?

A
  • Incr respiration
  • Increased O2 delivery
  • Insulin resistance
  • Increased intestinal absorption
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3
Q

Given the fetal/pregnancy need for clearance of waste and toxins, what is the maternal response (generally)?

A
  • Incr renal glomerular filtration
  • Incr hepatocellular clearance
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4
Q

Given the fetal/pregnancy need for the mother to survive a potential hemorrhage, what is the maternal response (generally)?

A

-Increaed coagulation

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5
Q

During pregnancy, by how much does the mom’s plasma volume increase?

What is the mechanism for this?

A

Plasma vol increases by 50% (incr body water of 6-8 L!)

Mech: RAAS system

Increased angiotensinogen and renin activity -> At I converts to At II

AtII acts on adrenal gland to increase Aldosterone

Aldosterone promotes sodium retention

Sodium retention leads to water retention!

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6
Q

By how much does the mom’s RBC volume increase during pregnancy?

A

RBC volume increases by ~30%

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7
Q

During pregnancy, how much additional iron does mom’s body require?

At what Hgb level do we worry about iron-deficiency?

A

(there is increased iron absorption in the gut - duodenum)

Pregnancy requires ~ 1gram additional elemental iron

-Hemoglobin level of <10.5 g/dL anytime during preg is likely iron-deficiency anemia

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8
Q

What is physiologic anemia of pregnancy? How does it occur?

A

Relative dilution of the cellular component of blood (remember the plasma volume expands ~50% but RBC volume expands ~30%).

Therefore the hematocrit and hemoglobin levels fall

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9
Q

She stressed this: during pregnancy, what hemoglobin level defines iron-deficiency anemia?

A

Normal level of hemoglobin is >10.5 during all trimesters.

Not iron deficiency anemia unless Hgb is < 10.5

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10
Q

how does the increase in total blood volume (40-50%) help a pregnancy?

A
  • Facilitates maternal and fetal exchange of resp gases, nutrients, metabolites
  • Supports production of amniotic fluid (by perfusing uterus/plaenta)
  • Buffers postpartum blood loss (women lose 500-1000cc at delivery)

–>Maternal hypervolemia is a normal state of pregnancy.

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11
Q

Pregnancy is a hypercoagulable state: what is the mechanism for this?

Why might this be evolutionarily adaptive?

A

-Increased amts of coagulation factors (I, VII, VIII, IX, X)

Adaptive: prevents excessive bleeding w delivery

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12
Q

Women are hypercoagulable during pregnancy: what is the downside?

(review: elements of Virchow’s triad?)

A

10x increased rate of venous thrombo-embolism compared to non-preg women (#2 cause of maternal death)

(Virchow’s is fulfilled: hypercoagulability, venous stasis, vascular trauma [@ delivery])

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13
Q

Maternal immune function during preg: generally what occurs?

A

Generally pregnancy is an immunocompromised state

The uterus, uterine lymphatics, and placenta adapt their immune response to allow the foreign embryo.

Ex: placenta does not express MHC I or MHC II

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14
Q

What are the risks to mom of altered systemic immune function during preg?

specifically what pathogens do we worry about?

A

Risk of severe complications from some pathogens.

Viral: Influenza, Varicella (major causes of maternal morbidity/mortality)

Bacterial: Listeria

Parasite: Malaria

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15
Q

What are a few changes to the heart/CV system that mimic cardiovascular disease?

A
  • Dyspnea, SOB
  • Fatigue
  • Decr exercise tolerance
  • Peripheral edema
  • Systolic Murmur and S3
  • Cadriomegaly on CXR
  • Heart placed superior, lateral, and anterior due to uterus
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16
Q

Changes to heart sounds during pregnancy?

A

2 main changes:

Systolic Ejection Murmur (SEM) & S3

(will hear SEM at left sternal border)

Other changes: S1 louder and widely split, S2 persistent splitting, S4 (uncommon), mammary hum due to incr breast blood flow

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17
Q

by how much does cardiac output increase with pregnancy?

What happens with HR and SV?

A

incr by 30-50%

HR and SV also increase –> hyperdynamic state

18
Q

What factors affect cardiac output during preg?

What factors appear near the end of pregnancy?

A
  • increased CO with exertion, labor
  • Near end of preg, mom’s posture affects CO: called Supine Hypotension Syndrome.
19
Q

define Supine Hypotension Syndrome

A

(aka Inferior vena cava syndrome, aka postural hypotension)

  1. Huge uterus can compress the vena cava and decrease venous return so CO decreases. can result in bradycardia, hypotension, syncope.

Tx: roll patient on her side to relieve pressure!

  1. Aortic compression can decrease blood flow to uterus. In this case, the fetal heart rate will change.
20
Q

What changes take place with the mom’s vasculature during preg?

A

Overall, vasodilation

  • Peripheral vasculature becomes less responsive to vasoconstrictive effects of At II
  • Progesterone promotes smooth muscle relaxation
21
Q

What happens to systemic vascular resistance during preg?

A

Decreases overall as peripheral vessels relax

Also, placenta acts as a large AV fistula to decrease SVR.

22
Q

What changes to BP are expected during preg?

What BP levels are never normal in pregnancy?

A

BP will decrease early, reach lowest point in mid-pregnancy due to decreased SVR.

Will return to near-normal levels by end of preg.

BP >= 140/90 is never normal in pregnancy!

23
Q

The (normal) systolic ejection murmur often heard during pregnancy: what is the cause? where do we listen for this?

A

Usual cause of SEM is a flow murmur from pulmonic blood flow.

Heard at LLSB

24
Q

What explains the sensation of dyspnea that affects 60-70% of preg women?

A

May be due to progesterone which increases the sensitivity of central CO2 chemoreceptors -> makes you feel out of breath, want to breathe more (works to exhale the fetal CO2)

25
Q

What changes occur during preg that facilitate O2 transfer to the fetus, and CO2 diffusion from the fetus?

A
  • Fetal Hgb has greater affinity for O2: facilitates O2 transfer to the fetus
  • To facilitate diffusion of CO2 from fetus -> mom, mom’s partial pressure of CO2 (PaCO2) drops, and mom also hyperventilates
26
Q

in general, what ventilation changes occur during preg?

A

General state of breathlessness!

  • Increased tidal volume
  • Incr alveolar ventilation
  • Incr minute ventilation

due to Progesterone effects on central CO2 receptors yielding hyperventilation

27
Q

During pregancy, arterial blood pH goes up or down?

PaO2?

PaCO2?

HCO3-?

A

arterial blood pH: rises (slight resp alkalosis)

PaO2: incr slightly

PaCO2: decr due to hyperventilation

HCO3-: slight decr (renal compensation for slight resp alkalosis)

28
Q

what happens to mom’s kidneys and ureters during preg?

A

Renal calices and ureters dilate. Begins early in preg and persists for 3-4 months postpartum

29
Q

What causes dilation of renal calices and ureters during preg? What are some side effects?

A

–Smooth muscle relaxing effects of progesterone

–Enlarged uterus causes partial obstruction

–Partial obstruction from right ovarian vein crossing ureter to empty into inferior vena cava

_Problems: _

–↑ risk of ascending infections due to stasis

–Leads to difficulty in interpreting urinary radiologic studies in pregnancy

30
Q

What happens to mom’s GFR during preg?

what results from this change?

A

GFR increases by 50% early on in preg.

Results:

  • Incr creatinine clearance
  • decr serum creatinine
  • Decr BUN
  • Slight Incr in protein excretion
  • Increased drug clearance
31
Q

What happens to renal tubular function during preg? (specifically, to filtration and excretion?)

A

Hyperfiltration

Leads to increased excretion of sodium, potassium, calcium, glucose.

Also: increased renal excretion of bicarb to compensate for resp alkalosis

32
Q

What are some general changes that occur with the GI system during preg?

A

Nausea

vomiting

Ptyalism (incr saliva production)

cravings

aversions

Also, smooth muscle relaxation throughout GI tract.

33
Q

Why do preg women often have GERD? (what is the mech)?

A

Decreased lower esop sphincter (LES) tone

Increases gastric reflux, increases heartburn

34
Q

What happens to transit time of digestion during preg?

A

Prolonged transit time through stomach, small int, large intestine.

Results in increased absorption of nutrients, B12, iron, AAs.

Also results in constipation & hemorrhoids!

35
Q

What changes occur in the liver during preg?

A

Incr protein synthesis

Incr synthesis of coag factors I, VII, VIII, IX, X

Incr cytochrome p450 enzyme levels

(therefore have to incr drug dosages during preg)

36
Q

What liver function tests change during preg?

which should not change?

A

_may occur during preg: _

Alkaline Phos levels may rise due to isoenzyme from placenta

should not occur during preg:

Incr bilirubin (total, direct, or indirect)

Jaundice

Incr transaminases

37
Q

Calcium metabolism during preg:

what changes to mom occur that allow increased intestinal absorption of Ca?

A

Increased maternal PTH

->increases liver synthesis of 1,25 OH D3

Placenta and decidua produce an enzyme that also increases 1,25 OH D3

1,25 OH D3 promotes internal absorption of Ca.

(useful for fetal skeleton, lactation)

38
Q

During preg, what happens to fasting glucose levels/why?

post-prandial glucose levels/why?

A

Fasting glucose: lower.

because of hypertrophy, hyperplasia, hypersecretion of insulin from pancreatic b cells

Post-prandial glucose: prolonged hyperglycemia.

because of peripheral insulin resistance

39
Q

What happens to lipolysis and production of FFAs during preg?

A

Increased (and accelerated) lipolysis and production of FFAs

accelerated maternal starvation response after fasting - makes ketones quickly from fat stores

Preserves glucose and AAs for the fetus.

40
Q

What energy forms can cross the placenta: FFAs? glucose? Amino acids?

A

FFA: no

Glucose and amino acids: yes