Lecture Week Questions Flashcards

(36 cards)

1
Q

what are the symptoms of pregnancy

A

amenorrhea - because of the fertilised egg
N+V - inc in beta HCG
breast tenderness - hormonal changes
fatigue - energy sharing
pelvic pain - baby growing
inc urinary frequency - inc abdo pressure and dec bladder size

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2
Q

what is gravidity

A

total no. of pregnancies at any gestation (incl. current pregnancies, abortions, ectopic)
Twins count as 1 pregnancy

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3
Q

what is parity

A

parity A + B

A = the number of pregnancies carried after 24 weeks 
B = the number of pregnancies carried before 24 weeks
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4
Q

what is miscarriage

A

it is loss of intrauterine pregnancy before 24 wks

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5
Q

what is stillbirth

A

loss of intrauterine pregnancy after 24 weeks

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6
Q

which weeks of pregnancy counts as 1st trimester

A

0-12 wks

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7
Q

which weeks of pregnancy counts as 2nd trimester

A

12-28 wks

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8
Q

which weeks of pregnancy counts as 3rd trimester

A

28-40 wks

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9
Q

what is the duration of a normal pregnancy

A

37-42 wks

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10
Q

what is grand multiparity

A

parity 4 or more

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11
Q

what are the signs of pregnancy

A

1) Goodell’s sign - softening of the r cervix - 4-6 wks
2) Chadwick’s sign - bluish discolouration of the cervix and vagina due to engorgement of pelvic vasculature - 6 wks
3) Hegar’s sign - softening of the uterine isthmus 6-8 wks
4) uterine enlargement

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12
Q

what are some of the investigations used to identify pregnancy? When will these tests show positive pregnancy?

A

1) beta HCG - +ve in serum 9 days post-conception, +ve in urine 28 days LMP
2) TV USS - 5 wks gestational sac, 6 wks foetal pole, 7-8 wks - foetal heartbeat visible
3) trans-abdo USS - 6-8 wks IU pregnancy visible

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13
Q

what are the physiological changes to the maternal CVS

A

1) inc cardiac output, heart rate and blood volume
2) dec BP - maximal drop in 2nd trimester
3) inc uterine compression on IVC & pelvic veins - leads to inc risk of hypotension, haemorrhoid, varicose vein, leg oedema

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14
Q

what are the physiological changes to the maternal haematologic system

A

1) dec in haemoglobin and haematocrit (ration of RBC in blood) - due to haemodilution
2) inc DVT and PE risk - inc coagulable factor, inc in clotting factor + dec in antithrombin factors + venous stasis
3) inc in leukocyte count - often improve autoimmune system
4) Gestational thrombocytopenia - 8% of pregnancy

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15
Q

what are the physiological changes to the maternal respiratory system

A

1) inc o2 consumption
2) inc sensitivity of CO2 - due to the progesterone effect to the respiratory centre –> hyperventilation + reps alkosis
3) inc ventilation by 50%
4) inc tidal volume by 33-50%
5) dec total lung capacity - due to inc abdo pressure
6) vital capacity unchanged
7) alveolar ventilation inc 65%

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16
Q

what are the physiological changes to the maternal GI system?

A

1) inc GORD - inc abdo pressure, dec sphincter tone, delayed gastric emptying
2) inc gall bladder stasis - inc risk of stone
3) dec GI motility and inc constipation
4) upward displacement of appendix - atypical appendicitis presentation
5) haemorrhoids - caused by constipation & inc venous pressure

17
Q

what are the physiological changes to the maternal genitourinary system

A

1) inc GFR - no change to urinary output as re-absorptive rate inc
2) inc glycosuria - dec reabsorptive rate of glucose in urine
3) inc urinary frequency
4) physiological dilation of ureter and renal pelvis - progesterone-induced smooth muscle relaxation
5) inc incidence of UTI and pyelonephritis

18
Q

what are the physiological changes to the maternal endocrine system

A

1) oestrogen - main oestrogen source = oestradiol - sudden fall may indicate foetal compromise
2) progesterone - produced by corpus luteum in the first 7 wks and then placenta takes over - to maintain endometrium to provide perfect environment for baby
3) HCG -produced by the placental trophoblastic cells to main the corpus luteum - should double every 1-2 days until 8-10 wks then fall until deliver
4) thyroid - inc basal metabolic rate
5) adrenal - inc cortisone level throughout
6) prolactin - produced by the pituitary gland due to stimulation of oestrogen - to inc lactation
7) Relaxin - produced by corpus luteum to relax pubic symphysis and other pelvic joints, also soften & dilate cervix, but inhibit uterine contraction
8) calcium metabolism - inc bone turnover rate but no loss tot maternal bone density

19
Q

what does lower than expected HCG may indicate

A

wrong date
miscarriage
ectopic

20
Q

what does higher than expected HCG may indicate

A

molar
multiple pregnancies
trisomy 21
wrong date

21
Q

what are the physiological changes to the maternal neurologic system

A

inc incidence of bell’s palsy and carpel tunnel’s syndrome

22
Q

Definition of antepartum haemorrhage

A

Bleeding from vaginal from 20 wks TIL birth

23
Q

How common does APH cause a complication in pregnancy women

A

Only complicated in 2-5% of all pregnancy

24
Q

What are some of the causes to APH

A
Placenta Abruption 
Placenta Previa
Uterine rupture
Vasa previa 
Placenta acretta 
Cervical lesion - ectopion, polyp 
Others - trauma, infection, malignancy
25
What questions will you ask a pregnant ladies with APH
Hx of PV bleed - how much, onset, duration, pain, SOB, dizziness Key questions to ask - constant pain? (Abruption), intermittent pain? (Labour?), still feel any foetal movement? any previous Hx of smear test?
26
What are the examination findings of APH
Tense - very tense/woody sensation - need to exclude any features of acute abdomen Uterine contraction - SNT uterus —> can be a vaginal problem
27
What examination/investigations will you conduct for APH
1) Abdo exam 2) speculum - to assess the degree of haemorrhage 3) vaginal exam - to exclude any vaginal causes eg malignancy 4) auscultation of foetal heart beat - CTG, USS, Picard?
28
Definition of placenta abruption
Premature separation of placenta from uterus
29
What is the potential aetiological mechanism of placenta abruption
- Acute inflammation & chorionic vascular dysfunction - inflammation process mediated by cytokines - cytokines produces matrix metalloproteinese which causes destruction of the extra-cellular matrix and disruption to the cell-cell membrane adherence —> abruption - blood can track down the uterine wall —> further separation - if large pressure generated in the uterus —> blood extend into the Mayo metrics —> rupture internally and so blood affect contraction —> PPH
30
What are some of the risk factor/cause of placenta abruption
Folic acid deficiency —> essential for development of placenta vascular bed Cocaine - cause vasoconstriction and so less blood flow into the placenta bleed Smoking PIH/PET - indicated poor placental health Thrombophilia - inc in inflammation makers PROM Multiple pregnancy - after delivery of 1st twin, cane lead to sudden decompression +/- pulling of the uterus and so bleeding starts Trauma Previous Hx of placenta abruption
31
Symptoms of placenta abruption
``` PV Bleed Woody uterus Constant pain Maternal shock DIC - signs of DIC = bleeding from cannula site and skin bruising ```
32
Investigations for placenta abruption
FBC, U&Es, LFT Coag, prothrombin time, activated partial thrombolysis time - inc in severe abruption ie coagulopathy G+S (X-match for 4-6 units of blood) check for HELLP syndrome Fibrinogen Level - (<200 = severe abruption) Kleihauer-Bette Test - to detect any foetal blood cells in maternal circulation —> helps with correct dose of Anti-D USS - to assess blood in uterus or not
33
Management of placneta abruption?
Depends on multiple factors 1) if near term + foetus stable —> induction by ARM and syntocinon infusion for vaginal delivery 2) if foetus unstable —> C/S
34
What are the maternal complication of placenta abruption
``` Anaemia Hypovolaemic shock DIC/coaglopathy Infection Acute renal failure Foetal-maternal haemorrhage (when foetal blood enter maternal blood stream which can cause a varying degree of damages eg foetal neurological damages) ```
35
What are foetal complication of placenta abruption
``` IU death Hypoxia Anemia Foetal growth restriction Risk of per-term birth ```
36
How can you screen for placenta abruption
Uterine artery Doppler for pt at risk of SGA foetus Vascular dysfunction leads to reduced invasion of cytotrophoblasts and is associated with the risk of developing placental abruption