Physiology Flashcards

1
Q

how does the endocrine system adapt to pregnancy?

A
  • progesterone and oestroegn levels increase (made by placenta)
  • increase total T3 and T4 (free T3/T4 same as increase in TBG)- this ensures constant supply thyroxine for fetal development
  • lactogen, prolactin and cortisol increase due to increases in P and O, these are anti insulin so increase insulin resistance for constant supply of glucose for fetus
  • increased lipolysis so fatty acids becomes substrate for maternal metabolism, however this can result in ketogenesis so increased risk ketoacidosis in pregnancy
  • progesterone also stimulated fat deposition in first half of pregnancy so can use it later and let fetus use glucose
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2
Q

How the cardiovascular system adapt to pregnancy

A
  • increased progesterone which decreases systemic vascular resistance and so decreases diastolic BP during 1st and 2nd trimester
  • in response to this the CO increases by about 30-50%
  • pregnancy activates RAAS system which increases sodium levels and water retention so total blood volume increases
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3
Q

how does the resp system adapt to pregnancy

A
  • growth of fetus causes upward displacement of diaphragm, however total lung volume doesnt decrease much as there is transverse and AP increase in diameters of the thorax
  • Many women experience hyperventilation due to increased resp drive from progesterone and increased carbon dioxide release- this results in resp alkalosis and is compensated by kidneys
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4
Q

How does the GI system adapt to pregnancy?

A
  • upward diaplacement of stomach (predisposes to reflux and N+V)
  • appendix moves to RUQ as uterus elnarges
  • increased progesterone results in smooth muscle relaxation which can lead to constipation and biliary tract stasis (gall stones)
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5
Q

How does the urinary system adapt to pregnancy

A
  • increased CO and vasodilation of arterioles due to progesterone leads to GFR increase by about 50-60% which activates RAAS
  • this leads to increased renal excretion and levels or urea and creatinine are lower
  • progestserone affects collecting system and relaxation of ureter and bladder, which causes urinary stasis and predisposes to UTIs and pyelonephritis
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6
Q

Describe the haematological changes in pregnancy

A
  • increase fibrinogen and clotting factors and decrease fibrinolysis
  • increase in progesterone causes venodilation and stasis of blood so VTE risk increases
  • plasma volume increases due to RAAS activation but red cell mass doesnt as much so get physiological dilutional anaemia
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7
Q

Describe the fetal blood flow at the placenta

A
  • umbilical arteries carry deoxygenated blood to the placenta from baby
  • umbelical veins carry oxygenated blood away
  • O2 moves from mum to baby as fetal blood has low pO2 so diffusion gradient + fetal hb (a+y) has higher affinity for O2 than mothers (a+b) + double bohr effect (her blood has lower CO2 due to physiological hyperventilation due to projesterone- , bohr effect, maternal hb has lower affinity for O2, O2 moves into foetal Hb
    + maternal production of 2,3 BPG due to physiological resp alkalosis means her Hb lower affinity for O2 + double haldane effect
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8
Q

What is normal HR for a fetus and when can it be measured?

A
  • 120-160 BPM
  • USS detects at 5-6 week
  • doppler stethoscopy at 8 weeks
  • normal stethoscope at 20 weeks
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9
Q

What is thought to initiate labour

A
  • prostaglandins from surfactant protein A in baby, progesterone drops, fetal cortisol, cervical stretching
  • prostaglandins are produced in myometrium and decidua
  • cause contractions of smooth muscle and involved in cervical ripening
  • oestrogen remains high when P drops, this increases gap junctions between smooth muscle cells which increases excitability
  • contractions are caused by oxytocin, which is usually inhibited throughout pregancy by progesterone, high Oestrogen at end of pregnancy causes increase in oxytocin receptors
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10
Q

Describe the process of cervical ripening

A
  • process where cervix goes from strong structure which keeps the fetus in to something it passes through
  • reduction in collagen
  • increased glycosaminoglycans
  • increased hylauronic acid
  • reduced aggregation of collagen
  • mediated by relaxin throught pregnancy and prostaglandins at the end
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11
Q

Describe the grades of perineal tear

A

1st: skin only
2nd: involvement of perineal muscles but not sphincters
- 3rd: involvement of anal sphincters
- 4th: sphincters and rectal mucosa

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12
Q

What is the first stage of labour

A
  • defined as interval between onset of labour (4cm cervix dilation and regular contractions) and full dilation (10cm) of cervix
  • contractions start to push baby into birth canal
  • latent phase first- slow cervical dilation and softening
  • ## active phase- faster, regular contractions begin
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13
Q

What is the second phase of labour

A
  • time between full dilation and delivery
  • uterine contractions become expulsive, fetus descends through birth canal and is delivered
  • passive stage: descent and rotation of head
  • active phase: maternal effort to expel fetus and achieve birth
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14
Q

What is the 3rd phase of labour?

A
  • time between completed birth and complete expulsion of placenta and membranes
  • usually lasts between 5-15 mins but may be 30-60 depending on circumstance
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15
Q

how is blood loss limited after normal delivery?

A
  • powerful contractions of uterus constricts blood vessels
  • pressure exerted in placental site by walls of contracted uterus prevent bleeding
  • blood clots
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16
Q

What is sheehans syndrome?

A

a rare complication of shock caused by PPH. It is where the anterior pituitarys blood supply isn’t good enough, so it dies. Leads to headaches, lack of lactation, hypothyroidism, weak bounding pulse, addisons ect

17
Q

What induces the baby to start breathing after delivery?

A
  • trauma
  • cold
  • light
  • noise
  • reduced pulmonary resistance
18
Q

Describe how fetal circulation changes after delivery?

A
  1. Clamping of umbilical cord closes ductus venosus so blood flows through liver
  2. First breath decreases vascular flow resistance to lungs, so blood flows through pulmonary vessels
  3. Drop in pressure on right and rise in pressure on left side of heart closes foramen ovale
  4. Muscle wall of ductus arteriosus contracts to stop blood going from PA to aeorta.
19
Q

What causes breast changes during pregnancy?

A

progesterone, oestrogen, prolactin and GH cause hypertrophy of the alveolar – lobar structures in the breast. There is also formatin of new ducts and glands.
O and P inhibit prolactin so little milk is actually made

20
Q

Describe the process of lactation

A
  • milk production caused by suckling stimulating mechanoreceptors in the nipple which cause prolactin release from anterior pituitary
  • This also causes oxytocin release from posterior pituitary which causes myoepithelial contraction and ejection of the milk
  • the first couple of times suckling, it will not be milk that comes out but colstrum, which is higher in fat and immunoglobulins
21
Q

Describe the menstrual cycle

A
  • Follicular phase varies (change due to stress, weight loss etc)
  • luteal phase almost always 14 days
    1. menses- bleeding
    2. O + P and inhibin low- no neg feedback so GnRH release from hypothalamus-> FSH release
    3. FSH binds to granulosa cells and causes follicular development
    4. theca interna develops and secretes O + inhibin which neg feedback so LH and FHS inhibited, O also builds up endometrium
    5. follicle grows, when O conc high enough, there’s positive feedback so LH surge
    6. however FSH stays low as inhibin still present (this selectively inhibis FSH and prevents multiple follicles developin)
    7. LH causes ovulation
    8. LH causes leuteinisation of empty follicle to CL
    9. CL secretes O and P and inhibin in large quantities
    10. P and O neg feedback so LH drops. P and O maintain lining
    11. w/out fertilisation CL will regress after 14 days, O+P drop, uterus lining will be shed and cycle starts again
22
Q

What happens if fertilisation takes place to maintain the uterus lining?

A
  • syncitiotrophoblast produced human chorionic gonadotrophin
  • this causes CL to carry on produced O and P
  • until placenta is capable of sufficient production to control HPG axis throughout pregnancy
23
Q

List some commonly used teratogens?

A
  • statins
  • doxy/ tetracyclines
  • methotrexate
  • lithium
  • warfarin
  • NSAIDS
  • ACEi and ARBs
  • opioids
  • anti convulsants
  • isotetrinoin
  • antithyroid meds
  • paroxtine
  • ergotamine/ triptans
  • benzos
  • alcohol
  • cocaine MD, weed
24
Q

How can menopause be diagnosed?

A
  • can do bloods- >40ml MUI/ ml FSH

- only if only <45 and thinking about treating or premature ovarian failure (<40)

25
Q

List symptoms of menopause

A
  • hot flush
  • night sweats
  • vaginal dryness
  • loss of libido
  • anxiety and low mood
  • exacerbation of joint and muscle pain
  • sleep problems
  • weight gain
  • hair loss
  • insomnia
  • irritability
  • urinary incontinence
26
Q

describe natural management of menopause

A
  • exercise (running, swimming, yoga)
  • reduce alcohol, caffeine and smoking
  • keep BMI <30
  • mediteranian diet
27
Q

Describe the benefits of HRT?

A
  • benefits outweigh risk if <60
  • most effective for hot flushes and low mood
  • imporves libido and reduces vaginal dryness
  • prevents osteoporosis
  • reduced urinary symptoms and UTIs (particularly when topical oestrogens used)
28
Q

What are common side effects of hrt?

A
  • headaches
  • breast tenderness
  • irregular bleeding
  • muscle cramps
  • usually will past after a few weeks
29
Q

What are the risks of HRT?

A
  • slightly increased risk breast cancer (more if O+P, higher longer you stay on and reduces after stopping, risk significantly increases if BMI >30)
  • if O alone, reduced risk CVD, reduced same risk stroke
  • if o+p- slightly increased risk CVD/ stroke (risk reduces 5 yrs after stoppinng)
  • increased risk VTE- more with oral than patch
30
Q

What types or HRT are there?

A

Perimenopause- sequential combined HRT (minimises irregular bleeding)
Menopause- continuous combined HRT
Hysterectomy- oestrogens only
Can be oral or transdermal patches/ gels also vaginal pessaries, gels, creams etc. Usually give patches first the try oral preparations, but down to pt preference.

31
Q

How can menopause be medically managed other than with HRT

A

Clonidine, gabapentin, SSRI- for mood and flushes. Testosterone therapy can help with libido, but not available on NHS