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repro > medical conditions in pregnancy > Flashcards

medical conditions in pregnancy Flashcards

1
Q

hypertentsion possible has a _______cause

A

placental, causing vasocinstriction

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2
Q

medications used in hypertension in pregnancy?

A

labetalol, methyl dopa, nifedipine

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3
Q

in severe hypertension in pregnancy?

A

hydralazine

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4
Q

ACE inhibitors and arbs?

A

not to be used in pregnancy

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5
Q

vasoconstriction in pregnancy, leads to decreased blood flow to ?

A

organs

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6
Q

htn in pregnancy, target blood pressure?

A

AIM FOR

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7
Q

if

A

reducing dose

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8
Q

if

A

reduce dose

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9
Q

what is chronic hypertension?

A

HTN at booking/less than 20 weeks

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10
Q

what is gestational hypertension?

A

new htn at 20 weeks WITHOUT significant proteinuria

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11
Q

pre eclampsia?

A

new hypertension after 20 weeks with significant proteinuria

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12
Q

hypertension can cause damage to?

A

brain, kidneys, liver, eyes, fetus, placenta

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13
Q

what causes decrease in GFR in pregnancy?

A

damage to blood vessels in the kidney, dropping flow rate

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14
Q

pathway of renal disease in pregnancy?

A

decreased grr, proteinuria, increased serum uric acid, increased creatinine, oliguria, acute renal failure

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15
Q

what causes RUQ pain in pregnancy?

A

abnormal liver enzymes, hepatic capsule rutpture

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16
Q

HELLP syndrome?

A

haemolysis, elevated liver enzymes, low platelets

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17
Q

risk factor for placental abruption?

A

HTN (high pressure)

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18
Q

risk factors for pre eclampsia?

A

1st pregnancy, over 40, obesity, history, hypertension, diabetes, kidney disease

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19
Q

if they have risk factors, prescribe?

A

aspirin

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20
Q

if pregnant woman has pre eclampsia, deliver?

A

deliver at 37 weeks

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21
Q

pre 123 ac7ampsia

A

37 weeks

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22
Q

effects of diabetes on pregnancy

A

miscarriage, fetal metabolic reprogramming, cardiac problems, neual tube defects, caudal regression synrome,

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23
Q

what is PET?

A

complication in late pregnancy HIGH BLOOD PRESSURE

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24
Q

PET can be a complication of GD

A

.

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25
Q

complications of GD?

A

IUGR, macrosomia, PET, dead, malformed, DELIVER 37 -38 WEEKS

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26
Q

management of GD?

A

diet, metformin, insulin

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27
Q

what is macrosomia due to?

A

hyperinsulinaemia, insulin acts as growth factor on insulin sensitive tissues

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28
Q

why do babies get shoulder dystocia?

A

macrosomia

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29
Q

what can polyhydramnios cause

A

pre term labour, cord prolapse, malpresentation

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30
Q

what is the risk factor for unexplained stillbirth

A

polycythaemia

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31
Q

what does neonatal hypoglycaemia predispose?

A

risk of cerebral palsy

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32
Q

risk factors for GDM?

A

poor obstetric history (especially death of previous macrocosmic baby), family history, polyhydramnios, significant glycosuria, PCOS. BMI >30

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33
Q

eyes - what do all pregnant women with diabetes get?

A

retina screening every trimester

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34
Q

delivery?

A

37-38 weeks in pre existing DM, 38 weeks GDM on insulin

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35
Q

GDM - after birth?

A

stop treatment, monitor BMs for 48 hours to ensure return to normal and no persistence of IGT

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36
Q

VTE and pregnancy, why is pregnancy pro thrombotic?

A

increased blood viscosity, increased plasma, decreased haemoglobin concentration. move less. venous compression by uterus.

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37
Q

what factors do you get an increase in?

A

7, 8, 10 and fibrinogen

38
Q

decreased?(2)

A

factor II and ATIII

39
Q

dont do d dimer in pregnancy, why?

A

it increases throughout gestation, not an accurate test

40
Q

how would you diagnose DVT?

A

duplex ultrasound on lower limb

41
Q

which anti coagulant is safe in pregnancy i.e. doesn’t cross the placenta?

A

heparin

42
Q

how do you manage a DVT in pregnancy

A

treat with heparin then see

43
Q

side effects of heparin?

A

osteopaenia, haemorhage, hypersensitivity, heparin induced thromboctopaenia, allergy at injection site OHHHA

44
Q

Investigations for PTE?

A

heparin, ABG, CXR

45
Q

why can CXR be misleading?

A

normal in 50 % of PTE

46
Q

what 4 things could be seen on a CXR in PTE?

A

effusion, focal opacities (white), atelectasis (partial collapse of lung), oligaemia (reduced vascularity)

47
Q

term for partial collapse of lug?

A

atelectasis

48
Q

reduced vascularity in lung?

A

oligaemia

49
Q

CTPA - decreased chance of? but increased chance of?

A

child getting cancer than doing a VQ, but increased risk of breast cancer

50
Q

when do you stop heparin? epidural anaesthetic?

A

before delivery, 24 hours before delivery

51
Q

warfarin and LMWH when do you start them after birth?

A

6 weeks

52
Q

how long on them?

A

3 months

53
Q

when do you avoid warfarin in pregnancy?

A

6 - 12 weeks

54
Q

can you breast feed with warfarin?

A

yes

55
Q

bad effects on fetes - warfarin?

A

teratogenic, muscarriage, still birth

56
Q

hypothyroid…what do you increase levothyroxin by in first trimester?

A

25-50mcg

57
Q

what do you repeat every trimester?

A

thyroid function tests

58
Q

minimal effects of hypothyroid on pregnancy

A

.

59
Q

why is hyperthyroid made worse in pregnancy (first trimester)?

A

HCG acts like thyroid hormones

60
Q

what happens second and third trimester?

A

gets better

61
Q

preferred treatment of hyperthyroid?

A

PTU

62
Q

what is given to reduce blood pressure in hyperthyroid?

A

propranolol

63
Q

asthma in pregnancy - what does an increased RR cause?

A

resp alkalosis

64
Q

what happens to pH? pCO2? HCO3?

A

ph goes up, picot goes down, hco3 goes down

65
Q

02 demand is increased by?

A

20%

66
Q

2 main changes in breathing in pregnancy?

A

increased rr, increased tidal volume

67
Q

what is tidal volume?

A

normal volume inhaled/exhailed with no added effort

68
Q

in pregnancy, what happens to residual volume?

A

decreased

69
Q

what happens to FEV1 and Peak Expiratory Flow rate?

A

they remain unchanged

70
Q

asthma has minimal effect on pregnancy, however in severe disease, when is the greatest risk of complication?

A

3rd trimester

71
Q

treatment of asthma in pregnancy?

A

no difference

72
Q

risk of maternal death in epilepsy due to aspiration?

A

yes

73
Q

why is there an increased risk of seizures in first trimester?

A

hyperemesis and haemodilution

74
Q

what is risk of malformation of foetus in maternal epilepsy due to?

A

anti epileptics

75
Q

what is given to stop this?

A

5mg folic acid/day

76
Q

when is vitamin k given if taking hepatic enzyme inducing anti convulsants

A

36 weeks

77
Q

poorly controlled epilepsy likely to deteriorate in pregnancy

A

.

78
Q

when is risk of seizures highest?

A

peri part period (last month of gestation)

79
Q

increased risk in first trimester due to hyperemeseis and haemodilution, highest risk in last month of pregnancy

A

.

80
Q

reasons for deterioration of control?

A

poor complicane (fear of teratogenesis)
decreased drug level due to nausea and vomiting
decreased drug level due to increased volume of distribution and increased drug clearance, lack of sleep, lack of absorption of drugs during labour

81
Q

if mother has a seizure, how does baby cope?qrelatively resistant to short term hypoxia

A

no increased risk of miscarriage or obstetric complications

82
Q

major risk is drugs!

A

ALL ANTI CONVULSANTS ARE TERATOGENIC

83
Q

what is the mechanism thought to be?

A

foalate deficiency

84
Q

major malformations? (3)

A

NTD, cardiac defects, orofacial defects

85
Q

are benzos teratogenic?

A

no

86
Q

women should be on folic acid pre conceptually and thought pregnancy (5mg per day)

A

wean off/change phenylbarbitone due to risks of neonatal withdrawal symptoms

87
Q

vitamin k should be given orally from _______weeks (6am) if on enzyme inducers (anti convulsants) due to risk of vitamin k deficiency and hemorrhagic disease of the newborn

A

.

88
Q

what are the two things epileptic women should be given when pregnant?

A

continue anti convulsants. 5mg folic acid per day. vitamin k from 34-36 weeks

89
Q

anti epileptic drugs in labour?

A

continue them

90
Q

neonate should receive?

A

1mg IM vit k. (hemorrhagic disease of newborn)

91
Q

SUDEP?

A

risk of SUDEP increased in pregnancy

repro (30 decks)

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