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part I > physiology- pregnancy > Flashcards

physiology- pregnancy Flashcards

1
Q

CVS changes - cardiac output
i. % change
ii. when does this plateau
iii. where does extra output go in early pregnancy?
iv. where does extra supply go at term

A

i. 40% increase (4.5L/min to 6L/min)
ii. 24-30 weeks
iii. mainly brest & skin

iv.
skin 500mL/min
uterus 400ML/min
kidneys 300mL/min
GIT, breasts, other organs 300mL/min

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2
Q

CVS
i. what happens to stroke volume in pregnancy?
ii. what happens to HR? how much does it change by?

A

i. increases
ii. increases (approx 10% from 80 to 90)

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3
Q

CVS
i. effect on pregnancy on peripheral vascular resistance
ii. likely reason for this

A

i. reduced
ii. relaxant effect of progesterone

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4
Q

CVS

i. effect of pregnancy on BP
ii. when does it reach lowest point

A

8 to 36 weeks
systolic drops by 5mmHg
diastolic drops by 10mmHg

24 weeks lowest, then creeps up as coming to term

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5
Q

CVS changes in pregnancy summary:
Blood volume
Plasma volume
Red blood cell volume
Cardiac output
Stroke volume
Heart rate
Systolic blood pressure
Diastolic blood pressure
Peripheral resistance
Oxygen consumption
PCO2

A
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6
Q

effect of increased cardiac output on heart?

ECG changes in pregnancy:

A

hypertrophy & dilation of left ventricle and atrium

  • anterior and left axis deviation by 15 degrees
  • HR increase 10%
  • TWI lead III and aVF

why these ECG changes occur:
The increase in cardiac output in pregnancy causes
hypertrophy and dilation of the left ventricle and
atrium. However, there is no change in contractility.
As a result of the upward displacement of the diaphragm by the enlarging uterus, the axis of the heart is
shifted anteriorly and to the left

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7
Q

resp

i. % change in ventilation
ii. what causes this

A

i. 40% increase

ii. progesterone both directly and indirectly (increases sensitivity of respiratory centre to CO2

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8
Q

resp

i. change in PCO2 during pregnancy
ii. effect of this on pH
iii. effect of pH on kidneys
iv. effect on bicarb levels
v. what changes in addition to bicarb

A

i. increased ventilation results in a mild fall in PCO2 to 4.1 kPa and increase in PCO2 to 14 kPa during the third trimester. Towards
term, PCO2 falls a little again to 13.5 kPa, as the increased cardiac output is unable to compensate for the increase in oxygen consumption

ii. becomes slightly alkaline

iii. increase bicarb excretion resulting in fall in bicarb levels

iv. decrease in bicarb to 19-20

v. This is
associated with a fall in sodium levels and in osmolarity (by 10mmol/l)

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9
Q

resp

effect of progesterone on bronchial smooth muscle

A

relaxes

breathing more diaphragmatic than thoracic

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10
Q

resp

i. effect of pregnancy on tidal volume
ii. effect on resp rate
iii. effect of pregnancy on residual volume
iv. effect on FEV and peak flow rate
v. effect on FVC
vi. lung compliance
vii. chest compliance

A

i. increases by 40%
ii. nil
iii. decreases by 200mL (from 5L in non-pregnant)
iv. nil
v. nil (stays at 3.5L)
vi. nil
vii. reduced

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11
Q

incidence of subjective dyspnoea in pregnancy?

A

70%

Oxygen consumption increases by
50ml/minute at term. This increased demand comes
from the fetus (20ml/minute), increased cardiac output
(6ml/minute), increase in renal work (6ml/minute) and
increase in metabolic rate (18ml/minute). During pregnancy, the increase in ventilation is greater than the
increase in oxygen consumption. I

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12
Q

urinary system

i. change in size of kidneys
ii. effect on ureters
iii. effect on renal blood flow and glomerular filtration rate

A

i. increase by 1cm
ii. dilate - partly due to effect of progesterone on smooth muscle, partly due to pressure from obstruction caused by uterus
iii. increased rises start in the
first trimester and, by term, both are 50–60% higher
than before pregnancy, the glomerular filtration rate
reaching 140–170ml/minute

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13
Q

normal values:

i. urea
ii. creatinine

A

i. urea 4.3 to 3.1mmol/l
ii. creatinine 73 to 47micromol/

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14
Q

bicarb and urate in pregnancy

plasma osmolality

A

decrease

decreased - due to effect of progesterone and RAAS pathway

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15
Q

GIT
i. what causes N&V in early pregnancy

effect of progesterone on:
i. GI tone and gastric motility & emptying
ii. oesophageal sphincter
iii. gallbladder

A

i. rising hCG +/or progesterone

i. reduced (especially during labour)
ii. relaxes (81% of women at term have heartburn, also increased risk of aspiration)
iii. decreased motility

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16
Q

liver

i. ALP levels
ii. gallbladder contractility

A

i. x3 as is also secreted by placenta
ii. decreases as cholecystokinin secretion falls

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17
Q

haematological system
i. plasma volume
ii. red cell mass - what causes this?
iii. Hb - why this change?
iv. leukocytes
v. platelets

A

i. increase by 45% (2600mL to 3800mL)
ii. increases up to 20-30%
- increased erythropoetin, increase in human placental lactogen

iii. haemoglobin concentration and
haematocrit fall, averaging approximately 11.5g/100ml
and 34%, respectively, by 30 weeks

^^plasma volume is proportionately greater > ^^ red cell mass

iv. increase, mainly neutrophils

v. decrease in number but increase in size

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18
Q

iron metabolism

i. how much extra demand is there, how much goes where?

ii. what happens to iron absorption? why?

A

i. 1000mg
- 500mg to increased cell mass
- 300mg to meet need of foetus
- 200mg to cover obligatory excretion of iron

ii. increased
due to erythroid hyperplasia

19
Q

haemostasis:

i. which coagulation factors increase?

ii. which coagulation factors do not increase?

A

i. VII, VIII, X

ii. XI, XIII

20
Q

physiological changes effect on drug ADME:

A

absorption: decreased due to poor gut motility, lower gut pH

distribution: increases due to increased plasma volume - some drugs may be less effective

excretion: increases due to increased eGFR

21
Q

what 2 hormones are required for lactation?

role of each

A

oxytocin + prolactin

prolactin: stimulates milk production

oxytocin: stimulates ejection of milk

22
Q

what is the structure of prolactin?

A

long-chain polypeptide

23
Q

what happens to breasts in early & late pregnancy?

A
  • hyperplasia of alveolar cells and lactiferous ducts in early pregnancy
  • alveolar cell hypertrophy in later pregnancy & secretion
24
Q

what prevents lactation in pregnancy?

A

high oestrogen and progesterone levels

(this is why COCP can reduce milk production)

milk production is also suppressed by oestrogen and progesterone if conception occurs during breast feeding.

although high prolactin levels do suppress ovulation

25
Q

what is early milk called?

what is this high in

A

clostrum

protein (in comparison to lactose) - protein concentration then drops mainly because volume increases

26
Q

what is average volume of milk production per day?

A

500-1000mL

27
Q

suckling stimulates production of which hormones?

A

prolactin (from posterior pituitary) , oxytocin (from hypothalamus)

28
Q

what kind of hormone is oxytocin?

in addition to suckling what else can stimulate oxytocin release?

what does oxytocin bind to?

A

octapeptide hormone

mum thinking about feeding/ hearing baby cry

specific receptors on the myoepithelial cells which surround alveolar (milk-producing cells)

contraction of myoepithelial cells forces milk into ducts

29
Q

calorie requirement of breast feeding

A

2950kcal

30
Q

what inhibits prolactin?

which group of drugs are used to suppress lactation?
- examples

which group of drugs stimulate lactation?
- examples

A

dopamine

dopamine agonists
e.g. cabergoline, bromocriptine

dopamine antagonists
e.g. metoclopramide

31
Q

constituents of breast milk:

A
32
Q

what is main carb in breast milk?

what is it broken down to?

A

lactose

galactose and glucose
(by lactase enzyme)

33
Q

proteins in breast milk:

A

casein (40%)
whey (60%)
immunoglobulins
lactoferrin

34
Q

breast milk vs cows milk:
i. sodium and chloride
ii. iron
iii. casein

A

i. 1/3 of cows milk - gd vs diarrhoea
ii. less in breast milk
iii. casein 40% in breast, 80% in cow

35
Q

which immunoglobins come from breast milk?

A

IgA

& smaller amounts of IgG and IgM

36
Q

what keeps myometrium dormant in pregnancy?

what 3 things does it suppress?

A

progesterone
(to some extent maybe also cetecholamines and relaxin)

  1. formation of myometrial gap junctions
  2. interleukin 8 (causes cervical ripening)
  3. uterine sensitivity to oxytocin
37
Q

oestrogen & CRH (corticotrophin releasing hormone) rises in 3rd trimester

effect of oestradiol:

A
  • increases concentration of oxytocin receptors (in uterus)
  • promotes formation of gap junctions
38
Q

oestrogen & CRH (corticotrophin releasing hormone) rises in 3rd trimester

effect of CRH

A

increases prostaglandin
synthesis
may stimulate myometrial contractility
promotes inflammatory-type mechanism by increased cytokines (IL-1B, IL-8, COX2)

39
Q

what is the effect of COX-2 on prostaglandin synthesis?

A

increases it

40
Q

what 2 substances are involved in myometrial contraction?

what controls this?

A

actin and myosin

calcium modulated protein-kinase

41
Q

what are the main prostaglandins in:
i. amnion and chorion
ii. decidua

A

i. prostaglandin-E2
ii. prostaglandin -F2a

42
Q

what causes cervical ripening?

which cells in blood cause this by the release of what?

what stimulates this?

A

proteolysis of collagen fibres in cervix

neutrophils release collagenase

stimulated by prostaglandins and IL-8

43
Q

what is the main prostaglandin involved in 3rd stage labour?

A

prostaglandin F2a

44
Q

what drugs can reduce uterine contractions?

A

drugs that reduce calcium (as contraction of uterus is facilitated through gap junctions)

  1. beta agonists (reduce available calcium)
    e.g. salbutamol, ritordrine
  2. magnesium sulphate (inhibits influx of calcium to myometrial cells)
  3. CCBs (inhibit calcium influx into membranes)

part I (12 decks)

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