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Repro1 > Physiological Adaptations In Pregnancy > Flashcards

Physiological Adaptations In Pregnancy Flashcards

1
Q

What are the hormones in early pregnancy

A
  • Corpus luetum supports early pregnancy by progesterone. oestrogen ad inhibin
  • Function declines from week 10 by end of first trimester placenta takes over.
  • Oestrogen and Progesterone- noncontractile uterus and fosters development of an endometrium conductive to pregnancy
  • Inhibin downregulates FSH (stops further pregnancies)
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2
Q

Describe the role of hormones in pregnancy

A

Progesterone- increased (syncytiotrophoblasts )
• Relaxes smooth muscle ie lower oesophageal sphincter -reflux
• Slows gastric emptying
• Dilation of vessels
Oestrogen- increased (Trophoblasts)
• leads to breast tissue growth, water retention, protein synthesis
Relaxin: Produced by villous cytotrophoblast
• Softens the cervix and pelvic ligaments in preparation for childbirth

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3
Q

Describe hcg and tsh relation

A

TSH- lower in first trimester due to high HCG (similar structure) Increased T4 can be seen. HCG can also stimulate the TSH receptor and cause thyroid hormone productive. HCG peaks at around 12-13 weeks, increases levels associated with HG
Prolactin levels increase
• Stimulates breast development and promotes and maintain lactation postpartum.

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4
Q

What is the role ofproleatin and oxytocin

A

Prolactin (and oxytocin and Progesterone) levels increase
Stimulates breast development and promotes and maintain lactation postpartum. Oxytocin
• Major role in labour - uterine contraction, dilate cervix
• Let down process of breast feeding

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5
Q

Why do changes to cvs occur

A

During pregnancy, oxygen consumption increases.
• Fetus has its own increasing oxygen requirements
• Increasing size of the uterus and increasing maternal metabolic rate.
• Physiological changes in the maternal cardiovascular system occur in order to increase delivery of oxygenated blood to the tissues.

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6
Q

What are the changes o cvs

A

• ↑ plasma volume (50%) – increased preload
• ↑ stroke volume
• lower systemic vascular resistance – decreased afterload
• ↑ heart rate by approximately 10-20 bpm (18%)
• overall ↑ cardiac output by 30–50%; half of the total increase occurs by 8 weeks of
gestation, max at 16 weeks and peripartum. CO=SVxHR
• CO Peaks at 16 weeks, and during labour and postpartum.

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7
Q

What times throughout gestation are women with pre-existing heart disease at most risk

A

Aortic stenosis, if severe they do not cope well with hypotension and tachycardia
Adequate preloadis required in the ventricle to generate enough pressure across the valve
Avoid veno calm compression ,blood loss

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8
Q

Why s there slight displacement of apex beat

A

Mild hypertrophy and rotation of cardiac axis

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9
Q

What are he scm changes

A

• atrial and ventricular ectopics
• left shift in the QRS axis
• small Q wave and inverted T wave in lead III
• ST segment depression and T waveinversion in the inferior and lateral
lead.
May be due to physiological changes

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10
Q

What are the renal chanegs

A

• ↑ Glycosuria
• ↑Bicarbonaturia
• ↑Calciuria
• ↑Protienuria
• ↓Plasma Osmolarity - peripheral oedema
ENDOCRINE- ↑Renin ↑Erythropietin ↑Active vit D

Baby’s head sittong on bladder. Element of urinary stasis - high risk of urinary infection.. slight hydronephross and frequent urination are common. Need to krealise when physiology becomes pathology though

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11
Q

What are teh changes to calcium

A 
• Intestinal calcium absorption doubles during pregnancy, driven by 1,25-
dihydroxyvitamin D (calcitriol) and other factors, and this appears to be the main adaptation through which women meet the calcium demands of pregnancy
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12
Q

What are the changes to gI tract

A

See slide

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13
Q

Decsribe immunity chanegs

A
  • Th1 → Th2 immunity
  • In order to prevent rejection of the fetus, there is a reduction in cell- mediated immunity and T helper (Th)1 cytokine production during pregnancy. This is balanced by an increase in humoral immunity and Th2 cytokine production. • hCG reduces maternal levels of IgA, lgG and 1gM.
  • The immunosuppression of pregnancy- greater risk of infection
  • Can improve some medical disorders is psoarisis (th1 mediated)
  • Can worsen others ie eczema (th2 mediated)
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14
Q

What are the changes to respiratory physiology

A

— ↑oxygen consumption (20%) secondary to an ↑ in resting metabolic rate
— Progesterone stimulants respiration and respiratory drive. ↑ in alveolar ventilation
— 40% ↑ in resting minute ventilation (MV) secondary to an ↑ in tidal volume (TV) with a stable respiratory rate (RR); MV= RRxTV
— Maternal hyperventilation leads to an ↑ in arterial pO2, →in arterial pCO2, a compensatory fall in bicarbonate (18–22 mmol/L) and mild respiratory alkalosis.
— Normal pH in pregnancy ranges between 7.40–7.45

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15
Q

What are the changes o PEFR, FEV1, FRC, VC

A
  • PEFR (peak expiratory flow rate) and FEV1 (forced expiratory volume in 1s) unchanged in pregnancy
  • FRC: 20% decrease in third trimester due to a decrease in residual volume and exp reserve plume
  • Vital capacity and total lung capacity: minor nonsignificant decreas (due to baby taking up space)
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16
Q

What are teh physical changes to thorax, diaphragm

A

Early changes: increase in subcostal angle, transverse diameter and circumference of the chest
Later changes: elevation of the diaphragm by the gravid uterus up to 4 cm

17
Q

What are teh musculoskeletal changes

A

Pibic symphysis discomfort - ligament loosened and strain put on it. Pain here. Waddling gait.
Progesterone and relaxin loosen jointed
Pain in ribs and coccygeal bone

18
Q

What are the glucose chanegs in normal pregnancy

A
  • Insulin resistance is increased in pregnancy. This usually starts mid-pregnancy and progressively increases in the third trimester
  • Due to human placental lactogen
  • Hyperplasia of pancreatic beta cells, insulin levels increase in pregnancy and counteract the effect of increasing insulin resistance
19
Q

Briefly outlined GDM

A

• Diabetes first diagnosed in pregnancy,
• 3–6% of the pregnant population, and is on the
• ↑incidence due to ↑ obesity (obesiy increases insulin resistance) and maternal age.
• It is associated with adverse outcomes in the mother, fetus and neonate.
• Strict glycaemic control improves both maternal and fetal outcomes.
• Diagnosed with a glucose tolerance test at 28 weeks
• Fasting >5.6 then 75g sugar 2 hours>7.8 =GDM
If either figures over - diagnosis of gdm

20
Q

What is the effect o gdm on pregnancy

A 
• In response to maternal hyperglycemia, fetal pancreatic beta cells secrete more insulin, which leads to fetal macrosomia.
Glucose go straight through placenta.  
• ↑Stillbirth 
• ↑ risk IOL and CS 
• Perineal trauma and PPH 
• Polyhydramnios 
• Shoulder dystocia 
• Post delivery fetal hypoglycaemia (hyperinsuliemia still present but no hyperglycaemia)
21
Q

What is pre-eclampsia

A

RAISED BP AND PROTEIN 2-8% pregnancies
• Pregnancy as gestational hypertension of at least 140/90 mmHg on two separate occasions ≥4 hours apart
• significant proteinuria of PCR>30 (24 hour collection 300mg)
• arising de novo after the 20th week of gestation in a previously normotensive woman
• resolving completely by the 6th postpartum week.

22
Q

What is the basis of pre eclampsia

A

impaired trophoblast
differentiation and invasion during the first trimester resulting in the failure of trophoblast cells to destroy the muscularis layer of the spiral arterioles resulting in the development of a hypoxic and ischaemic placenta
Trophoblast cells font invade spiral artery properl

23
Q

What ae the risk factors fr pre eclampsia

A 
• >40 years of age 
• previous history of pre-eclampsia 
• pre-pregnancy obesity 
• women who become pregnant with donor eggs, embryo donation or donor
insemination.
• diabetes 
• pre-existing hypertension 
• those with a family history of pre-eclampsia • women suffering from medical conditions such as the anti-phospholipid syndrome.
Renal disease
24
Q

Wha is teh treatment for pre-eclampsia

A

Prevention. Give aspirin 75mg OD 12 weeks onwards
• Antihypertensives
• If hyperreflexic- magnesium sulphate
• IOL or CS
• THE MAIN TREATMENT if uncontrolled PET is Delivery

25
Q

What are the maternal effect of pre eclampsia

A

• Pre-eclampsia is a heterogeneous, multi-systemic disorder, which presents with varying degrees of severity
• The placental unit which has not invaded properly and therefore does not have normal blood flow through it causes maternal hypertension
• Wide spread systemic inflammatory affecting multiple organs
• Proteinuria leads to reduced blood osmolarity
• Lead to oedema
• Increased peripheral resistance leads to generalised vasospasm and
hypertension. The intravascular compartment is reduced and endothelial damage leads to increased vascular permeability and oedema
• Vasoconstriction in the hepatic bed leads to periportal fibrin deposition,
• pre-eclampsia, there is an enhanced vascular sensitivity to angiotensin II
haemorrhage and hepatocellular necrosis.
and norepinephrine, resulting in vasoconstriction and hypertension

26
Q

What are the symptoms and signs of pre eclampsia

A
  • Headache
  • Visual disturbance • Right upper quadrant pain (liver)
  • Seizures - very severe sign
  • Hyperreflexia
  • Oedema
27
Q

Wha are the fetal conerns in pre-eclampsia

A

• IUGR - inter uterine growth restriction • Stillbirth • Iatrogenic preterm birth in order to improve maternal outcome

28
Q

Describe anaemia in pregnancy

A 
• Plasma volume increases 
50%
• Red cell mass increases 20%
• Haematocrit ↓ 
• Physiological anaemia o pregnancy
29
Q

What is the treatment for anaemia in regnant

A
  • Ferrous sulphate
  • To take with vit c
  • Check compliance
  • Sometimes need other formalas if not tolerated ie ferrous fumerate
  • Feriject
  • EVERY EFFORT TO TREAT as less reserves if PPH
30
Q

What ae common pregnancy symptoms

A

Physiological effects of the growing uterus Raised Progesterone on GI tract HCG on GI tract
• Venous distension lower limbs combined with lower plasma osmolarity • Compression of ureters
• Compression of IVC, especially when lying flat
• Compression of vasculature of the lower GI tract

Repro1 (20 decks)

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