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Y4 - GOSH > Lecture Week Questions > Flashcards

Lecture Week Questions Flashcards

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
Q

What questions will you ask a pregnant ladies with APH

A

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
Q

What are the examination findings of APH

A

Tense - very tense/woody sensation - need to exclude any features of acute abdomen

Uterine contraction - SNT uterus —> can be a vaginal problem

27
Q

What examination/investigations will you conduct for APH

A

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
Q

Definition of placenta abruption

A

Premature separation of placenta from uterus

29
Q

What is the potential aetiological mechanism of placenta abruption

A
  • 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
Q

What are some of the risk factor/cause of placenta abruption

A

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
Q

Symptoms of placenta abruption

A 
PV Bleed 
Woody uterus 
Constant pain 
Maternal shock 
DIC - signs of DIC = bleeding from cannula site and skin bruising
32
Q

Investigations for placenta abruption

A

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
Q

Management of placneta abruption?

A

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
Q

What are the maternal complication of placenta abruption

A 
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
Q

What are foetal complication of placenta abruption

A 
IU death 
Hypoxia 
Anemia 
Foetal growth restriction 
Risk of per-term birth
36
Q

How can you screen for placenta abruption

A

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

Y4 - GOSH (12 decks)

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