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Reproductive Health (Y4) > 9- Medical problems in pregnancy (new problems in pregnancy) > Flashcards

9- Medical problems in pregnancy (new problems in pregnancy) Flashcards

1
Q

define hypertension

A

BP >140/90 mmHg on 2 occasions, more than 4 hours apart, or a single reading of diastolic BP >11o mmHg

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2
Q

hypertensive disorders classification

A
  1. Gestational hypertension
  2. Pre-eclampsia
  3. Chronic hypertension
  4. Pre-eclampsia with superimposed on chronic hypertension
  5. Eclampsia
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3
Q

gestational hypertension vs pre-eclampsia

A

Gestational/Pregnancy Induced Hypertension (PIH)

  • A diagnosis of new onset raised blood pressure after 20/40 gestation
  • No proteinuria and normal blood values
  • 25% go on to pre eclampsia

Pre-eclampsia

  • Multi-system disorder
  • Raised blood pressure (>140/90 mmHg) and proteinuria (>300 mg per 24 hours) after 20/40 gestation
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4
Q

Pre-eclampsia

A
  • new high blood pressure (hypertension) in pregnancy
  • with end-organ dysfunction, notably with proteinuria (protein in the urine)
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5
Q

when does pre-eclampsia occur

A

after 20 weeks gestation
- whent he sprial arterias of the palcenta form (leads to high vascular resistance int hese vessels)

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6
Q

implication of pre-eclampsia

A

significant cause of maternala dn fetal morbidity and mortality
- maternal organ damage
- fetal growth restriction
- seizures
- early labour
- death

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7
Q

pre-eclampsia is a triad of

A

Hypertension
Proteinuria
Oedema

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8
Q

define chronic hypertension in relation to pregnancy

A

is high blood pressure that exists before 20 weeks gestation and is longstanding. This is not caused by dysfunction in the placenta and is not classed as pre-eclampsia.

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9
Q

define gestational hypertension

A

is hypertension occurring after 20 weeks gestation, without proteinuria.

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10
Q

pre-eclampsia vs eclampsia

A

Pre-eclampsia is pregnancy-induced hypertension associated with organ damage, notably proteinuria.

Eclampsia is when seizures occur as a result of pre-eclampsia.

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11
Q

pathophysiology of pre-eclampsia

A

1) When the blastocyst implants on the endometrium, the outermost layer, called the syncytiotrophoblast, grows into the endometrium. It forms finger-like projections called chorionic villi. The chorionic villi contain fetal blood vessels.

2) Trophoblast invasion of the endometrium sends signals to the spiral arteries in that area of the endometrium, reducing their vascular resistance and making them more fragile. The blood flow to these arteries increases, and eventually they break down, leaving pools of blood called lacunae (lakes). Maternal blood flows from the uterine arteries, into these lacunae, and back out through the uterine veins. Lacunae form at around 20 weeks gestation.

3) When the process of forming lacunae is inadequate, the woman can develop pre-eclampsia. Pre-eclampsia is caused by high vascular resistance in the spiral arteries and poor perfusion of the placenta. This causes oxidative stress in the placenta, and the release of inflammatory chemicals into the systemic circulation, leading to systemic inflammation and impaired endothelial function in the blood vessels.

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12
Q

high- risk risk factors

A
  • Pre-existing hypertension
  • Previous hypertension in pregnancy
  • Existing autoimmune conditions (e.g. systemic lupus erythematosus)
  • Diabetes
  • Chronic kidney disease
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13
Q

moderate-risk risk factors

A
  • Older than 40
  • BMI > 35
  • More than 10 years since previous pregnancy
  • Multiple pregnancy
  • First pregnancy
  • Family history of pre-eclampsia
    *
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14
Q

management of patients with high risk factors

A

if a patient has one high risk factor - offer aspirin prophylaxis
- offered from 12 weeks gestation until birth

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15
Q

management of patients with moderate risk factors

A

if more than one moderate risk factors- give aspirin from 12 weeks gestation

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16
Q

pre-eclampsia presentation

A

Pre-eclampsia has symptoms of the complications:

  • Headache
  • Visual disturbance or blurriness
  • Nausea and vomiting
  • Upper abdominal or epigastric pain (this is due to liver swelling)
  • Oedema
  • Reduced urine output
  • Brisk reflexes
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17
Q

diagnosis of pre-eclampsia

A
  • Systolic blood pressure above 140 mmHg
  • Diastolic blood pressure above 90 mmHg

PLUS any of:

  • Proteinuria (1+ or more on urine dipstick)
  • Organ dysfunction (e.g. raised creatinine, elevated liver enzymes, seizures, thrombocytopenia or haemolytic anaemia)
  • Placental dysfunction (e.g. fetal growth restriction or abnormal Doppler studies)
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18
Q

how can proteinuria be quantified for pre-eclampsia

A

Urine protein:creatinine ratio (above 30mg/mmol is significant)
Urine albumin:creatinine ratio (above 8mg/mmol is significant)

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19
Q

which factor can be used to test for pre-ec in women suspected of having pre-ec

A

Placental growth factor is a protein released by the placenta that functions to stimulate the development of new blood vessels.
- In pre-eclampsia, the levels of PlGF are low.
- NICE recommends using PlGF between 20 and 35 weeks gestation to rule-out pre-eclampsia.

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20
Q

monitoring for pre-eclampsia

A

All pregnant women are routinely monitored at every antenatal appointment for evidence of pre-eclampsia, with:

  • Blood pressure
  • Symptoms
  • Urine dipstick for proteinuria
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21
Q

investigations for pre-eclampia

A

Maternal:

  • Platelet count (FBC)
  • Renal function (U&E eGFR)
  • Liver function (LFT)
  • DIC (coagulation profile in severe cases or thrombocytopenia)
  • Level of proteinuria (PCR, 24 hour collection)

Fetal:

  • Growth velocity (fetal growth ultrasound)
  • Fetal wellbeing (CTG, amniotic fluid volume, fetal Doppler)
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22
Q

management of gestational hypertension (without proteinuria)

A
  • Treating to aim for a blood pressure below 135/85 mmHg
  • Admission for women with a blood pressure above 160/110 mmHg
  • Urine dipstick testing at least weekly
  • Monitoring of blood tests weekly (full blood count, liver enzymes and renal profile)
  • Monitoring fetal growth by serial growth scans
  • PlGF testing on one occasion
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23
Q

which scoring system is used to determine whether a women with pre-eclampsia should be admited

A

fullPIERS or PREP‑S

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24
Q

pre-eclampsia complications: maternal

A
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25
Q

medical management of pre-eclampsia

A
  • Labetolol is first-line as an antihypertensive
  • Nifedipine (modified-release) is commonly used second-line
  • Methyldopa is used third-line (needs to be stopped within two days of birth)
  • Intravenous hydralazine may be used as an antihypertensive in critical care in severe pre-eclampsia or eclampsia
  • IV magnesium sulphate is given during labour and in the 24 hours afterwards to prevent seizures
  • Fluid restriction is used during labour in severe pre-eclampsia or eclampsia, to avoid fluid overload
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26
Q

pre-eclampsia complications: fetus

A
  • stillbirth
  • small for gestational age
  • prematurity
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27
Q

if BP cannot be controlled or complications occur- what should occur

A
  • Planned early birth may be necessary if the blood pressure cannot be controlled or complications occur.
  • Corticosteroids should be given to women having a premature birth to help mature the fetal lungs.
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28
Q

delivery in a women with pre-eclampsia

A

Blood pressure is monitored closely after delivery. Blood pressure will return to normal over time once the placenta is removed.

For medical treatment, NICE recommend after delivery switching to one or a combination of:

  • Enalapril (first-line)
  • Nifedipine or amlodipine (first-line in black African or Caribbean patients)
  • Labetolol or atenolol (third-line)
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29
Q

what is eclampsia and how is it managed

A

Seizuresoccurring in pregnancy or within 10 days of delivery and with at least two of the following features documented within 24 hours of the seizure:

  • Hypertension
  • Proteinuriaone “plus” or at least 0.3 g/24 h
  • Thrombocytopenialess than 100 000/μl
  • Raised transaminases

Management

  • IV Access
  • Bolus of 4g Magnesium Sulphate
  • Continuous infusion of Magnesium Sulphate
  • Control hypertension
  • If antenatal- plan for delivery by most appropriate route
  • Fluid balance
  • HDU care
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30
Q

HELLP syndrome

A

HELLP syndrome is a combination of features that occurs as a complication of pre-eclampsia and eclampsia. It is an acronym for the key characteristics:

  • Haemolysis
  • Elevated Liver enzymes
  • Low Platelets
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31
Q

Gestational diabetes

A
  • refers to diabetes triggered by pregnancy.
  • caused by reduced insulin sensitivity during pregnancy, and resolves after birth.
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32
Q

complications of gestational diabetes

A

Fetal complications :

  • congenital abnormality
  • miscarriage
  • Macrosomia, ↑ neonatal morbidity, hypoglycaemia and shoulder dystocia
  • Still birth
  • Risk of baby developing obesity and/or diabetes later in life

Maternal complications :

  • DKA, Hypertension
  • Increased monitoring and interventions during pregnancy and labour
  • Obstetric intervention & Operative delivery
  • Likelihood of birth trauma, IOL and CS
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33
Q

who should be screened for GDM

A

1) Anyone with risk factors
2) features suggestuve of gestational diabetes

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34
Q

RF for GDM

A
  • Previous gestational diabetes
  • Previous macrosomic baby (≥ 4.5kg)
  • BMI > 30 kg/m^2
  • Ethnic origin (black Caribbean, Middle Eastern and South Asian)
  • Family history of diabetes (first-degree relative)
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35
Q

screening test for GDM

A

oral glucose tolerance test at 24 – 28 weeks gestation.

Women with previous gestational diabetes also have an OGTT soon after the booking clinic.*

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36
Q

features suggestive of gestational diabetes

A
  • Large for dates fetus
  • Polyhydramnios (increased amniotic fluid)
  • Glucose on urine dipstick
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37
Q

how to perform OGTT

A
  • performed in the morning after a fast (they can drink plain water).
  • the patient drinks a 75g glucose drink at the start of the test.
  • the blood sugar level is measured before the sugar drink (fasting) and then at 2 hours.
38
Q

how to perform OGTT

A
  • performed in the morning after a fast (they can drink plain water).
  • the patient drinks a 75g glucose drink at the start of the test.
  • the blood sugar level is measured before the sugar drink (fasting) and then at 2 hours.
39
Q

normal OGTT results

A
  • Fasting: < 5.6 mmol/l
  • At 2 hours: < 7.8 mmol/l

results higher than these values are diagnostic for gestational diabetes

think 5-6-7-8

40
Q

where are women with GDM managed

A

in joint diabetes and antenatal clinics, with input from a dietician

41
Q

management of women with GDM: Fasting glucose less than 7 mmol/l

A

trial of diet and exercise for 1-2 weeks, followed by metformin, then insulin

42
Q

management of women with GDM: Fasting glucose above 7 mmol/l

A

start insulin ± metformin

43
Q

management of women with GDM: Fasting glucose above 6 mmol/l plus macrosomia (or other complications):

A

start insulin ± metformin

44
Q

alternative medication for women who decline inslin and cannot tolerate metformin

A

Glibenclamide (a sulfonylurea)

45
Q

general monitoring of women with GDM

A

Ultrasound Scans
* Dating by 12 weeks
* Detailed 20+ weeks
* Growth & LV: 3-weekly >26 weeks (GROW)

ANC 1-4 weekly (based upon control/risk factors)

46
Q

planning delivery for GDM

A

Deliver 39-40+6 weeks : NICE (2015)

  • IOL : 39-40 weeks
  • Elective CS : >39-40+6 weeks
47
Q

postnatal GDM management

A
  • STOP all TREATMENT & BG MONITORING at delivery
  • FBG at 6-13 weeks
  • HBA1c at 13 weeks & yearly thereafter (Risk T2DM)
  • Lifestyle advice
  • Contraception and need for pre-conception care in future
48
Q

target glucose levels for GDM

A
  • Fasting: 5.3 mmol/l
  • 1 hour post-meal: 7.8 mmol/l
  • 2 hours post-meal: 6.4 mmol/l
  • Avoiding levels of 4 mmol/l or below
49
Q

women with pre-existing diabetes inc T1 and T2 should take ……… from preconception witill 12 weeks gestation

A

5mg folic acid

50
Q

management of women with pre-existing T2DM

A

Women with type 2 diabetes are managed using metformin and insulin, and other oral diabetic medications should be stopped.

  • if HbA1c >86 mmol/mol before pregnancy stronglyadice to avoid pregnancy
  • advise weight loss
  • make sure on 5mg- day for 3/12 before and after conception
  • stop statins- can cause congenital malformation
51
Q

what screening should be offered to women with pre-existing diabetes

A

Retinopathy screening should be performed shortly after booking and at 28 weeks gestation. This involves referral to an ophthalmologist to check for diabetic retinopathy. Diabetes carries a risk of rapid progression of retinopathy, and interventions may be required.

52
Q

when should women with pre-existing diabetes aim to deliver baby

A

planned delivery between 37 and 38 + 6 weeks for women with pre-existing diabetes. (Women with gestational diabetes can give birth up to 40 + 6).

53
Q

labour and T1DM

A
  • A sliding-scale insulin regime is considered during labour for women with type 1 diabetes.
  • A dextrose and insulin infusion is titrated to blood sugar levels, according to the local protocol.

This is also considered for women with poorly controlled blood sugars with gestational or type 2 diabetes.

54
Q

postnatal care for GDM

A

Diabetes improves immediately after birth. Women with gestational diabetes can stop their diabetic medications immediately after birth.

55
Q

postnatal care for women with pre-existing diabetes

A

Women with existing diabetes should lower their insulin doses and be wary of hypoglycaemia in the postnatal period.

The insulin sensitivity will increase after birth and with breastfeeding.

56
Q

Babies of mothers with diabetes are at risk of:

A
  • Neonatal hypoglycaemia
  • Polycythaemia (raised haemoglobin)
  • Jaundice (raised bilirubin)
  • Congenital heart disease
  • Cardiomyopathy
57
Q

management of baby born by diabetic mother

A

Babies need close monitoring for neonatal hypoglycaemia, with regular blood glucose checks and frequent feeds. The aim is to maintain their blood sugar above 2 mmol/l, and if it falls below this, they may need IV dextrose of nasogastric feeding.

TOM TIP: If you remember two complications of gestational diabetes, remember macrosomia and neonatal hypoglycaemia. Babies become accustomed to a large supply of glucose during the pregnancy, and after birth they struggle to maintain the supply they are used to with oral feeding alone.

58
Q

VTE occurs because of

A

Virchows triad

59
Q

Virchows

A
  • hypercoagulability
  • stasis
  • endothelial dysfunction
60
Q

causes of hypercoagulability

A

Pregnancy- increase in fibrinogen and factos VIII, IX, and X
Antiphospholipid antibody syndrome,
Factor V Leiden
Malignancy

61
Q

causes of stagnation of blood

A

long flights
periods of imobility
venous stasis in lower limbs due to oedema

62
Q

causes of endothelial damage

A

injury to blood vessel e.g. trauma of pelvic veins at the time of delivery

63
Q

types of VTE

A

- deep vein thrombosis - venous circulation e.g. in the calves

- pulmonary embolism- where thrombosis from deep vein mobilise to the lungs pulmonary arteries

64
Q

VTE and death in pregnancy

A

Pulmonary embolism is a significant cause of death in obstetrics.
- The risk is significantly reduced with VTE prophylaxis.
- The risk is highest in the postpartum period.

65
Q

risk factors for VTE in pregnancy

A

There is a long list of risk factors for VTE in pregnancy:

  • Smoking
  • Parity ≥ 3
  • Age > 35 years
  • BMI > 30
  • Reduced mobility
  • Multiple pregnancy
  • Pre-eclampsia
  • Gross varicose veins
  • Immobility
  • Family history of VTE
  • Thrombophilia
  • IVF pregnancy
66
Q

There are additional scenarios where prophylaxis is considered, even in the absence of other risk factors:

A
  • Hospital admission
  • Surgical procedures
  • Previous VTE
  • Medical conditions such as cancer or arthritis
  • High-risk thrombophilias
  • Ovarian hyperstimulation syndrome
67
Q

all pregnancy women should have a VTE….

A

risk assessment
- at booking
- after birth
- if admitted to hospital to undergo a proceudre or develop significant immobility

68
Q

which single factor puts women at high risk of VTE

A

Any previous VTE not related to major surgery

69
Q

preventing VTE

A

prophylaxis with LMWH e.g. enoxaparin or dalteparin

70
Q

when should VTE prophylaxis start

A

low risk: mobility and hydration

high risk
- i.e. x3 risk factors - start at 28 weeks
- i.e. x4 risk factors or in very high risk- start in first trimester

71
Q

alternaitev VTE prophylaxis

A

Mechanical
* Intermittent pneumatic compression with equipment that inflates and deflates to massage the legs
* Anti-embolic compression stockings

72
Q

DVT presentation

A

Deep vein thrombosis is almost always unilateral (usually left sided in pregnnacy). Bilateral DVTs are rare, and bilateral symptoms are more likely due to an alternative diagnosis such as chronic venous insufficiency or heart failure. DVTs present with:

  • Calf or leg swelling
  • Dilated superficial veins
  • Tenderness to the calf (particularly over the deep veins)
  • Oedema
  • Colour changes to the leg
73
Q

examination for DVT

A
  • Leg swelling measure the circumference of the calf 10cm below the tibial tuberosity.
  • More than 3cm difference between calves is significant.
74
Q

PE presentation

A

Can present with subtle signs and symptoms. In patients with potential features of a PE, risk factors for PE, and no other explanation for their symptoms, have a low threshold for suspecting a PE. Presenting features include:

  • Shortness of breath
  • Cough with or without blood (haemoptysis)
  • Pleuritic chest pain
  • Hypoxia
  • Tachycardia (this can be difficult to distinguish from the normal physiological changes in pregnancy)
  • Raised respiratory rate
  • Low-grade fever
  • Haemodynamic instability causing hypotension
75
Q

investigations for DVT depends on

A

Wells score

76
Q

investigations for DVT

A
  • Score less than or equal to 1 – DVT is clinically unlikely, requires a further D-dimer test to exclude*
  • Score greater than 1 – DVT is clinically likely and a DVT diagnosis should be confirmed via either a ultrasound scan (more common) or a contrast venography (rarely used)

A D-dimer test is sensitive but not specific; a D-dimer may also be raised following recent surgery or trauma, with ongoing infection or inflammation, concurrent liver disease, or pregnancy, and indeed in any patient with a prolonged hospital stay

77
Q

investigations for PE

A

If pulmonary embolism is suspected in a patient, the PE Wells’ Score should be calculated:

  • Score less than or equal to 4 – PE clinically unlikely, requires a further D-dimer test to exclude*
  • Score greater than 4 – PE clinically likely and a PE diagnosis should be confirmed with a CT Pulmonary Angiography (CTPA) scan (or V/Q scan in those with poor renal function).

An ECG should be performed due to the differential diagnosis of MI, however this most commonly shows no abnormalities or a sinus tachycardia*.

78
Q

Patients with a suspected deep vein thrombosis and pulmonary embolism should have a

A

DVT: venography with fetal shield or doppler US

PE:
- CXR often normal but excludes other causes of breathlessness
- ECG sinus tachy
- if suspecting PE commence LWMH
- VQ scan if chest x-raynorma
- CTPA if chest x-ray abnormal

79
Q

wells score and pregnancy

A

The Wells score is not validated for use in pregnant women. D-dimers are not helpful in pregnant patients, as pregnancy is a cause of a raised D-dimer.

80
Q

management of VTE in pregnancy

A

LWMH
- - Low molecular weight heparin should be given immedialtey before formal confirmation
- once diagnosis confirmed LWMH given for remainder of pregnancy + 6 weeks postnatally
- dose based on womans weight at the booking clinic

TEDS

High risk: vena cva filters

81
Q

management of a massive PE

A

Women with a massive PE and haemodynamic compromise need immediate management by an experienced team of medical doctors, obstetricians, radiologists and others. This is a life-threatening scenario. Treatment options are:

  • Unfractionated heparin
  • Thrombolysis
  • Surgical embolectomy
82
Q

obstetric cholestasis in pregnancy

A

Obstetric cholestasis is a relatively common complication of pregnancy, occurring in around 1% of pregnant women. It usually develops later in pregnancy (i.e. after 28 weeks), and is thought to be the result of increased oestrogen and progesterone levels. There seems to be a genetic component. It is more common in women of South Asian ethnicity.

83
Q

presentation of obstetric cholestasis

A

Itching (pruritis) is the main symptom, particularly affecting the palms of the hands and soles of the feet. NO RASH

Other symptoms are related to cholestasis and outflow obstruction in the bile ducts:

  • Fatigue
  • Dark urine
  • Pale, greasy stools
  • Jaundice
84
Q

what causes pruritis in obestric cholestasis

A

Bile acids are produced in the liver from the breakdown of cholesterol. Bile acids flow from liver to the hepatic ducts, past the gallbladder and out of the bile duct to the intestines. In obstetric cholestasis, the outflow of bile acids is reduced, causing them to build up in the blood, resulting in the classic symptoms of itching (pruritis).

85
Q

what sign is not present for obstetric cholestasis

A

there is no rash associated with obstetric cholestasis. If a rash is present, an alternative diagnosis should be considered, such as polymorphic eruption of pregnancy or pemphigoid gestationis.

86
Q

DD for obstetric cholestasis

A

Other causes of pruritus and deranged LFTs should be excluded, for example:

  • Gallstones
  • Acute fatty liver
  • Autoimmune hepatitis
  • Viral hepatitis
87
Q

investigations for obstetric cholestasis

A

**Women presenting with pruritus should have liver function tests and bile acids checked.

Obstetric cholestasis will cause:

  • Abnormal liver function tests (LFTs), mainly ALT, AST and GGT
  • Raised bile acids**

SHould also do:
- viral screen: Hep A, B and C, epstein barr and CMV
- liver autoimmune screen
- USS abdomen- liver and gall stones

88
Q

management of obstetric cholestasis

A
  • Maternal Vitamin K
  • Neonatal Vitamin K
  • Fetal surveillance
  • Drug treatment to reduce pruritus
    1) Ursodeoxycholic acid- the primary treatment for obstetric cholestasis. It improves LFTs, bile acids and symptoms.
    2) Antihistamine (chlorphenamine- can help with sleeping but does not improve itching)
    3) Calamine (emollient)
  • Delivery at fetal maturity
  • Postnatal follow up LFT at 10 days
89
Q

why is vitamin k given for obstetric cholestasis

A

Water-soluble vitamin K can be given if clotting (prothrombin time) is deranged. Vitamin K is a fat-soluble vitamin. Bile acids are important in the absorption of fat-soluble vitamins in the intestines. A lack of bile acids can lead to vitamin K deficiency. Vitamin K is an important part of the clotting system, and deficiency can lead to impaired clotting of blood.

90
Q

OC maternal risks

A
  • Vitamin K deficiency
  • Increased risk of PPH- due to deranged clotting
91
Q

OC fetal risks

A
  • Perinatal mortality is increased to up to 11%
  • Fetal distress
  • Meconium
  • Preterm labour
  • Intracranial haemorrhage
  • Stillbirth
92
Q

why is D-dimer not a good test for someone who has had a caesarean

A

C- section delivery is a major factor increasing D-Dimer levels postpartum.
- if think womne has VTE do doppler US or CTPA

Reproductive Health (Y4) (34 decks)

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