physiology- pregnancy Flashcards
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
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
CVS
i. what happens to stroke volume in pregnancy?
ii. what happens to HR? how much does it change by?
i. increases
ii. increases (approx 10% from 80 to 90)
CVS
i. effect on pregnancy on peripheral vascular resistance
ii. likely reason for this
i. reduced
ii. relaxant effect of progesterone
CVS
i. effect of pregnancy on BP
ii. when does it reach lowest point
8 to 36 weeks
systolic drops by 5mmHg
diastolic drops by 10mmHg
24 weeks lowest, then creeps up as coming to term
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
effect of increased cardiac output on heart?
ECG changes in pregnancy:
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
resp
i. % change in ventilation
ii. what causes this
i. 40% increase
ii. progesterone both directly and indirectly (increases sensitivity of respiratory centre to CO2
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
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)
resp
effect of progesterone on bronchial smooth muscle
relaxes
breathing more diaphragmatic than thoracic
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
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
incidence of subjective dyspnoea in pregnancy?
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
urinary system
i. change in size of kidneys
ii. effect on ureters
iii. effect on renal blood flow and glomerular filtration rate
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
normal values:
i. urea
ii. creatinine
i. urea 4.3 to 3.1mmol/l
ii. creatinine 73 to 47micromol/
bicarb and urate in pregnancy
plasma osmolality
decrease
decreased - due to effect of progesterone and RAAS pathway
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
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
liver
i. ALP levels
ii. gallbladder contractility
i. x3 as is also secreted by placenta
ii. decreases as cholecystokinin secretion falls
haematological system
i. plasma volume
ii. red cell mass - what causes this?
iii. Hb - why this change?
iv. leukocytes
v. platelets
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
iron metabolism
i. how much extra demand is there, how much goes where?
ii. what happens to iron absorption? why?
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
haemostasis:
i. which coagulation factors increase?
ii. which coagulation factors do not increase?
i. VII, VIII, X
ii. XI, XIII
physiological changes effect on drug ADME:
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
what 2 hormones are required for lactation?
role of each
oxytocin + prolactin
prolactin: stimulates milk production
oxytocin: stimulates ejection of milk
what is the structure of prolactin?
long-chain polypeptide
what happens to breasts in early & late pregnancy?
- hyperplasia of alveolar cells and lactiferous ducts in early pregnancy
- alveolar cell hypertrophy in later pregnancy & secretion
what prevents lactation in pregnancy?
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
what is early milk called?
what is this high in
clostrum
protein (in comparison to lactose) - protein concentration then drops mainly because volume increases
what is average volume of milk production per day?
500-1000mL
suckling stimulates production of which hormones?
prolactin (from posterior pituitary) , oxytocin (from hypothalamus)
what kind of hormone is oxytocin?
in addition to suckling what else can stimulate oxytocin release?
what does oxytocin bind to?
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
calorie requirement of breast feeding
2950kcal
what inhibits prolactin?
which group of drugs are used to suppress lactation?
- examples
which group of drugs stimulate lactation?
- examples
dopamine
dopamine agonists
e.g. cabergoline, bromocriptine
dopamine antagonists
e.g. metoclopramide
constituents of breast milk:
what is main carb in breast milk?
what is it broken down to?
lactose
galactose and glucose
(by lactase enzyme)
proteins in breast milk:
casein (40%)
whey (60%)
immunoglobulins
lactoferrin
breast milk vs cows milk:
i. sodium and chloride
ii. iron
iii. casein
i. 1/3 of cows milk - gd vs diarrhoea
ii. less in breast milk
iii. casein 40% in breast, 80% in cow
which immunoglobins come from breast milk?
IgA
& smaller amounts of IgG and IgM
what keeps myometrium dormant in pregnancy?
what 3 things does it suppress?
progesterone
(to some extent maybe also cetecholamines and relaxin)
- formation of myometrial gap junctions
- interleukin 8 (causes cervical ripening)
- uterine sensitivity to oxytocin
oestrogen & CRH (corticotrophin releasing hormone) rises in 3rd trimester
effect of oestradiol:
- increases concentration of oxytocin receptors (in uterus)
- promotes formation of gap junctions
oestrogen & CRH (corticotrophin releasing hormone) rises in 3rd trimester
effect of CRH
increases prostaglandin
synthesis
may stimulate myometrial contractility
promotes inflammatory-type mechanism by increased cytokines (IL-1B, IL-8, COX2)
what is the effect of COX-2 on prostaglandin synthesis?
increases it
what 2 substances are involved in myometrial contraction?
what controls this?
actin and myosin
calcium modulated protein-kinase
what are the main prostaglandins in:
i. amnion and chorion
ii. decidua
i. prostaglandin-E2
ii. prostaglandin -F2a
what causes cervical ripening?
which cells in blood cause this by the release of what?
what stimulates this?
proteolysis of collagen fibres in cervix
neutrophils release collagenase
stimulated by prostaglandins and IL-8
what is the main prostaglandin involved in 3rd stage labour?
prostaglandin F2a
what drugs can reduce uterine contractions?
drugs that reduce calcium (as contraction of uterus is facilitated through gap junctions)
- beta agonists (reduce available calcium)
e.g. salbutamol, ritordrine - magnesium sulphate (inhibits influx of calcium to myometrial cells)
- CCBs (inhibit calcium influx into membranes)
