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Yr4 - O&G > Medical Disorders of Pregnancy > Flashcards

Medical Disorders of Pregnancy Flashcards

1
Q

Define gestational diabetes

A

any degree of glucose intolerance with onset or first recognition during pregnancy

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2
Q

Pathophysiology of gestational diabetes

A

Body unable to produce enough insulin to meet needs of pregnancy

  • progressive insulin resistance so higher volume of insulin needed
  • woman with a borderline pancreatic reserve is unable to respond to the increased insulin requirements, resulting in transient hyperglycaemia
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3
Q

Risk factors for gestational diabetes

A 
BMI > 30
Asian ethnicity
Previous gestational diabetes
1st degree relative with diabetes
PCOS
Previous macrosomic baby
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4
Q

Clinical features of gestational diabetes

A

Mostly asymptomatic

Polyuria, polydipsia and fatigue

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5
Q

Foetal complications of gestational diabetes

A

Glucose but not insulin transported across placenta -> foetal hyperinsulinaemia
- Macrosomia – this can cause complications during labour, such as shoulder dystocia, obstructed/delayed labour, and/or higher rates of instrumental deliveries
- Organomegaly -particularly cardiomegaly
- Erythropoiesis -> polycythaemia
- Polyhydramnios
Increased rates of pre-term delivery

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6
Q

Investigations for gestational diabetes

A

Oral Glucose Tolerance Test

  • a fasting plasma glucose is measured, then a 75g glucose drink is given – with a repeat plasma glucose measurement after 2 hours
  • Fasting glucose > 5.6mmol/L
  • 2hrs postprandial glucose > 7.8mmol/L
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7
Q

When is the OGTT offered

A

Booking – if previous gestational diabetes.
24 – 28 weeks’ gestation – if risk factors are present or in cases of previous gestational diabetes
Any point during pregnancy – if 2+ glycosuria on one occasion, or 1+ on two occasions

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8
Q

Management of gestational diabetes

A

Lifestyle advice
- diet and exercise
Medical
- Metformin – suitable in pregnancy and breast feeding.
- Glibenclamide – used if metformin is not tolerated (often due to GI side effects) and insulin has been declined
- Insulin
- Consider starting at diagnosis if the fasting glucose >7.0mmol/L.
- Or introduce later in pregnancy if
- (i) pre meal glucose > 6.0mmol/L
- (ii) post meal glucose >7.5mmol/L
- (iii) fetal AC (abdominal circumference) >95th centile

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9
Q

Delivery with gestational diabetes

A

Deliver at 37 to 38 weeks if they are on treatment
Delivery (induction of labour or caesarean section) before 40 weeks and 6 days if there is gestational diabetes managed by diet

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10
Q

Postnatal management of gestational diabetes

A

All anti-diabetic medication should be stopped immediately after delivery - BM taken at discharge to ensure normal levels
Fasting glucose tolerance test 6-13 weeks post-partum
Yearly tests should be offered because of the increased risk of developing diabetes in the future
In subsequent pregnancies, an OGTT should be offered at booking and at 24 – 28 weeks’ gestation

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11
Q

Definitions of anaemia in pregnancy

A

1st trimester = < 110g/l
2nd/3rd trimester = < 105g/l
Postpartum = < 100g/l
Plasma volume increases disproportionately to RBC -> haemodilution

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12
Q

Risk factors for anaemia in pregnancy

A 
Haemoglobinopathies
- thalassaemia
- sickle cell disease
Increasing maternal age
Low socioeconomic status
Poor diet
Anaemia during previous pregnancy
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13
Q

Causes of anaemia

A 
Microcytic
- iron deficiency 
- thalassaemia
- sideroblastic anaemia
Normocytic
- anaemia of chronic disease
- marrow infiltration
- haemolytic anaemia
- CKD
Macrocytic
- B12/folate deficiency
- alcohol consumption
- reticulocytosis
- hypothyroidism
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14
Q

Invetigations for anaemia

A 
FBC - hb and MCV
Serum ferritin
Consider
- haemoglobinopathy screening
- serum folate
- haemoglobin electrophoresis
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15
Q

Management of iron deficiency anaemia

A

Trial oral iron (100-200mg)

Parental iron infusion is compliance poor or evidence of malabsorption

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16
Q

Management of folate deficiency

A

Folate supplementation - 5mg once daily increased up to three times daily

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17
Q

Management of beta thalassaemia

A

Folate supplementation and blood transfusions as required - aim for Hb of 80g/L during pregnancy and 100g/L at delivery

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18
Q

Management of sickle cell disease

A

Folate supplementation and iron supplementation if lab evidence or iron deficiency

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19
Q

Define antiphospholipid syndrome

A

Autoimmune condition in which antibodies are targeted against phospholipid-binding proteins

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20
Q

Pathophysiology of antiphospholipid syndrome

A

In vivo antibodies induce procoagulant state
Obstetric complications due to
- inhibition of trophoblastic function and differentiation
- activation of complement pathways at maternal-foetal interface
- thrombosis of uteroplacental vasculature

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21
Q

Clinical features of antiphospholipid syndrome

A

Defined by thrombosis formation and/or recurrent pregnancy loss
Other manifestations include
- Livedo reticularis – red/blue/purple reticular pattern on skin of the trunk, arms or legs
- Valvular heart disease – particularly aortic and mitral regurgitation
- Renal impairment – ischaemia in the small vessels of the kidney can result in chronic kidney disease
- Thrombocytopaenia

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22
Q

Investigations of antiphospholipid syndrome

A

USS doppler for DVT
Anticardiolipin – detects antibodies that bind cardiolipin (a phospholipid)
Lupus anticoagulant – measures the clotting ability of the blood
Anti-B2-glycoprotein I – detects antibodies that binds B2-glycoprotein I (a molecule that binds with cardiolipin)

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23
Q

Management of antiphospholipid syndrome

A

Anticoagulation - LMWH or warfarin depending on presentation

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24
Q

Why does pregnancy increase risk of VTE

A

Changes to levels of proteins in clotting cascade - increased fibrinogen and decreased protein S
Become more pronounced as pregnancy progresses - highest risk post-partum

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25
Q

Risk factors for VTE in pregnancy

A 
Pre-existing factors
- Thrombophilia (e.g Antiphospholipid syndrome)
- Medical co-morbidities (e.g cancer)
- Age >35 years
- BMI >30 kg/m2
- Parity >3
- Smoking
- Varicose veins
- Paraplegia
Obstetric Factors
- Multiple pregnancy
- Pre-eclampsia
- Caesarean section
- Prolonged labour
- Stillbirth
- Preterm birth
- PPH
Transient Factors
- Any surgical procedure in pregnancy of puerperium
- Dehydration (e.g hyperemesis)
- Ovarian hyperstimulation syndrome
- Admission or immobility
- Systemic infection
- Long distance travel
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26
Q

Clinical features of VTE

A

DVT
- unilateral leg pain and swelling
- pyrexia, pitting oedema, tenderness and prominent superficial veins
- left leg most commonly affected
PE
- sudden onset dyspnoea
- pleuritic chest pain, cough and haemoptysis

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27
Q

Investigations for VTE

A 
DVT
- compression duplex USS
PE
- ECG and CXR
- definitive diagnosis by CTPA or V/Q scan
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28
Q

Management of VTE in pregnancy

A

LMWH started immediately

- maintained until - weeks post-partum

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29
Q

Prophylaxis of VTE in pregnancy

A

Assessed for risk in early pregnancy
- offered thromboprophylaxis if have > risk factors in 1st+2nd trimester, > 3 in 3rd trimester and >2 post-partum
- continue till at least 6 weeks post-partum
10 day course of LMWH post C-section

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30
Q

Define hyperemesis gravidarum

A

Persistent and severe vomiting during pregnancy

- leads to weight loss, dehydration and electrolyte imbalances

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31
Q

Pathophysiology of hyperemesis gravidarum

A

Normally starts between 4-7 weeks gestation - reaches peak in 9th week and settles by 20th week
Thought to be due to rapidly increasing levels of beta hCG
- stimulates chemoreceptor trigger zone in brainstem which feeds into vomiting centre

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32
Q

Risk factors for hyperemesis gravidarum

A 
First pregnancy
Previous history
Raised BMI
Multiple pregnancy
Hydatidiform mole
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33
Q

Clinical features of hyperemesis gravidarum

A 
Pregnancy-Unique Quantification of Emesis (PUQE) score
- 6 = mild
- 7-12 = moderate
- 13-15 = severe
In the last 24 hours, for how long have you felt nauseated or sick to your stomach?
- Not at all = 1
- 1 hour or less = 2
- 2-3 hours = 3
- 4-6 hours = 4
= More than 6 hours = 5
In the last 24 hours have you vomited or thrown up?
- 7 or more times = 5
- 5–6 times = 4
- 3–4 times = 3
- 1–2 times = 2
- I did not throw up = 1
In the last 24 hours how many times have you had retching or
dry heaves without bringing anything up?
- No time = 1
- 1–2 times = 2
- 3–4 times = 3
- 5–6 times = 4
- 7 or more times = 5
34
Q

Differential diagnosis of hyperemesis gravidarum

A 
Gastroenteritis
Cholecystitis
Hepatitis
Pancreatitis
Chronic H. Pylori infection
Peptic ulcers
UTI or pyelonephritis
Metabolic conditions
Neurological conditions
Drug-induced.
35
Q

Investigations for hyperemesis gravidarum

A

Bedside Tests
- Weight
- Urine dipstick: quantify ketonuria (1+ ketones)
Laboratory Tests
- Mid-stream urine
- Full blood count: anaemia, infection, haematocrit (can be raised)
- Urea and Electrolytes: hypokalaemia, hyponatraemia, dehydration, renal disease
- Blood glucose: exclude diabetic ketoacidosis if diabetic
Refractory or Severe Cases
- Liver function tests: exclude liver disease e.g. hepatitis or gallstones, monitor malnutrition
- Amylase: exclude pancreatitis
- Thyroid function tests: hypo-/hyper-thyroid
- Arterial blood gas: exclude metabolic disturbances, monitor severity
Imaging
- Ultrasound scan: confirm viability, confirm gestation, exclude multiple pregnancy and trophoblastic disease.

36
Q

Management of hyperemesis gravidarum

A

Mild – should be managed in the community with oral antiemetics, oral hydration, dietary advice and reassurance.
Moderate (or cases where community management has failed) – should be managed with ambulatory daycare. This involves IV fluids, parenteral antiemetics and thiamine. The patient should be managed until ketonuria resolves.
Severe – inpatient management.

37
Q

Management of severe hyperemesis gravidarum

A

IV rehydration should be with 0.9% saline. Potassium chloride should be added as guided by electrolyte monitoring
H2 receptor antagonists or proton pump inhibitors: for reflux, oesophagitis or gastritis
Thiamine: for prolonged vomiting to prevent Wernicke’s encephalopathy
Thromboprophylaxis: for all women requiring admission

38
Q

Antiemetics for hyperemesis gravidarum

A 
First line
- Cyclizine
- Prochlorperazine
- Promethazine
- Chlorpromazine
Second line
- Metoclopramide (maximum 5 days due to risk of extrapyramidal side effects)
- Domperidone
- Ondansetron
Third line
- Hydrocortisone IV - once symptoms improve, convert to prednisolone PO and gradually reduce dose until lowest maintenance dose is reached
39
Q

Define CMV

A

Cytomegalovirus

- member of herpesvirus family

40
Q

Clinical features of CMV

A

Usually asymptomatic in immunocompetent individuals
Occasionally mild-flu like illness
Can cause mononucleosis syndrome -> fever, splenomegaly and impaired liver function

41
Q

Investigations for CMV

A

Viral serology for CMV specific IgM and IgG performed
A positive test is signified if
- presence of CMV specific IgG in previously seronegative mother
- presence of CMV IgM and low IgG avidity

42
Q

Management of CMV during pregnancy

A

Referred to foetal medicine specialist
Maternal
- if mother immunocompetent no treatment required
- licensed anti-CMV drugs have potential teratogenic effects so not recommended
Foetal
- diagnosed via amniocentesis and PCR of sample
- must be carried out after 21 weeks gestation as functioning kidneys required
- no effective therapy and termination of pregnancy offered
- if wishes to continue offer serial ultrasound scanning performed to assess for manifestations of congenital CMV

43
Q

Features of congenital cytomegalovirus

A

Neonates born following intrauterine CMV infection can have several problems

  • IUGR
  • hepatosplenomegaly
  • thrombocytopenic purpura
  • jaundice
  • microencephaly
  • chorioretinitis
44
Q

Define GBS

A

Group B streptococcus is commensal bacterium found in vagina or rectum of 25% or pregnant women

45
Q

Pathophysiology of GBS

A

Streptococci are gram positive cocci which typically grow in chains
Streptococcus agalcatiae
Can cause GBS streptococcus of the newborn, chorioamniotis or endometritis

46
Q

Risk factors for GBS infection in neonate

A

GBS infection in a previous baby
Prematurity <37 weeks
Rupture of membranes >24 hours before delivery
Pyrexia during labour
Positive test for GBS in the mother
Mother diagnosed with a UTI found to be GBS during pregnancy

47
Q

Clinical features of GBS infection

A

UTI - frequency, urgency and dysuria
Chorioamnioitis - fever, lower abdominal/uterine tenderness, foul discharge, maternal/foetal tachycardia
Endometritis - fevers, lower abdominal pain, IMB, foul discharge

48
Q

Investigations for group B strep infection

A

Swabs - single swab in vagina then rectum

  • cultured or PCR
  • maybe detected on urine cultures
49
Q

Prevention of GBS disease of the newborn

A

High dose IV penicillins throughout labour if

  • GBS positive swabs
  • UTI caused by GBS
  • previous baby with GBS infection
  • pyrexia during labour
  • labour onset < 37 weeks
  • rupture of membranes > 189 hours
50
Q

Define parvovirus B19 infection

A

Single stranded DNA virus transmitted by resp droplets or blood
- produces mild, self-limiting infection in adults but can cause spontaneous miscarriage or intrauterine death if transmitted to foetus

51
Q

Clinical features of parvovirus B19 infection

A 
Usually asymptomatic in adults
In children
- URTI
- malaise
- headaches
- low-grade fever
- erythema infectiosum
52
Q

Investigations for parvovirus B19 infection

A

Viral serology

  • parvovirus specific IgM antibodies indicate recent infection
  • parvovirus specific IgG antibodies indicate past infection and therefore immunity
53
Q

Management of parvovrius B19 infection

A

Referal to foetal medicine specialist
Maternal
- self-limiting - does not require treatment but can give antipyretics and analgesia
Foetal
- main risk is foetal hydrops - abnormal accumulation of fluid in two or more foetal compartments
- serial USS and doppler assessment - 4 weeks post infection repeated every 1-2 weeks until 30 weeks gestation
- intrauterine erythrocyte transfusion

54
Q

Define foetal hydrops

A

Common manifestation of foetal parvovirus B19 infection
Diagnosed by USS - ascites, subcut oedema, pleural effusion, pericardial effusion, scalp oedema, polyhydramnios
Parvovirus B19 has an affinity for erythroid system and replicates within erythroid progenitor cells of liver and bone marrow
Induces severe anaemia -> high output cardiac failure
-> increased extrahepatic and hepatic erythropoiesis -> portal hypertension and hypoproteinaemia with ascites

55
Q

Define rubella

A

German measles
Single stranded RNA virus
Transmitted by airborne droplets between close contacts

56
Q

Clinical features of rubella

A

Often asymptomatic
Malaise, headache, coryza and lymphadenopathy
Diffuse fine maculopapular rash

57
Q

Investigations for rubella

A

ELISA performed

  • IgM antibody - acute infection
  • IgG antibody - following infection or vaccination
58
Q

Management of rubella

A

Referal to foetal medicine specialist
Maternal
- self limiting = no treatment
- antipyretics for fever
- informed infective - 7 days prior and 4 days post symptom
Foetal
< 12 weeks - high likelihood of defects - consider termination
- 12-20 weeks - prenatal diagnosis required - RT-PCR on amniotic fluid
> 20 weeks - no action required

59
Q

Features of congenital rubella syndrome

A 
Present at Birth
- Auditory Problems
     - Sensorineural deafness
- Cardiac Defects
     - Pulmonary Stenosis, Patent Ductus Arteriosus, Ventricular Septal Defect
- Ophthalmic Defects
     - Retinopathy, Congenital Cataracts
- Central Nervous System Abnormalities
     - Learning disabilities, Microencephaly
- Haematological
     - Thrombocytopaenia, Blueberry Muffin Appearance
Late Onset
- Diabetes mellitus
- Thyroiditis
- Growth Hormone Abnormalities
- Behavioural Disorders
60
Q

Define varicella zoster

A

DNA virus
Responsible for
- chicken pox - primary infection
- shingles - viral reactivation

61
Q

Incidence of varicella zoster infection in pregnancy

A

90% seropositive IgG antibody due to previous exposure

If contracted during pregnancy there is an increased morbidity and mortality for both mother and foetus

62
Q

Clinical features of varicella zoster infection

A

Fever, malaise and pruritic maculopapular rash
Incubation period is 10-21 days - infectious 48 hours prior
Associated with pneumonia, hepatitis and encephalitis

63
Q

Investigations for varicella zoster infection

A

Clinical diagnosis

  • immunofluorescence of basal epithelial cells scrapped from vesicle
  • PCR for varicella zoster DNA
  • IgM and IgG antibodies for immunity
64
Q

Management of varicella zoster infection

A

Maternal suspected varicella contact
- if previous primary infection - assume immunity for no further action required
- no previous infection - varicella IgG to confirm immunity status
- if not immune given varicella zoster immunoglobulin within 10 days of contact
Maternal Chickenpox
- Aciclovir within 24 hours of rash onset if > 20 weeks gestation
- serial ultrasound examinations at 5 weeks post-infection for identify foetal abnormalities
Varicella Vaccination
- if seronegative for IgG pre-pregnancy or postpartum vaccination

65
Q

Complications of varicella zoster infection

A 
Varicella of the newborn - occurs within the last 4 weeks of pregnancy
- asymptomatic
- route of infection can be transplacental, vaginal and direct contact after birth
Foetal varicella syndrome - reactivation of virus in utero
- Skin scarring in a dermatomal distribution
- Eye defects
     - Microphthalmia
     - Choriorenitis
     - Cataracts
     - Optic atrophy
- Hypoplasia of the limbs
- Neurological Abnormalities
     - Microcephaly
     - Cortical and spinal cord atrophy
     - Seizures
     - Horner’s Syndrome
66
Q

Define pre-eclampsia

A

Hypertensive disorder

Thought to be due to to poor placental perfusion, secondary to abnormal placentation

67
Q

Pathophysiology of pre-eclampsia

A

In normal placentation
- trophoblast invades myometrium and spiral arteries of uterus destroying tunica muscularis media
In pre-eclampsia
- remodelling of spiral arteries is incomplete
- high resistance low flow uteroplacental circulation develop

68
Q

Risk factors for pre-eclampsia

A 
Moderate risk factors
- Nuliparity
- Maternal age ≥ 40 years
- Maternal BMI ≥ 35 at initial presentation
- Family history of pre-eclampsia
- Pregnancy interval > 10 years
- Multiple pregnancy
High risk factors
- Chronic hypertension
HTN, pre-eclampsia or eclampsia in previous pregnancy
- Pre-existing chronic kidney disease
- Diabetes Mellitus.
- Autoimmune diseases (e.g. SLE, antiphospholipid syndrome)
69
Q

Pre-eclampsia prophylaxis

A

75mg aspirin

  • women with 1 high or 2 moderate risk factors
  • from 12 weeks gestation until birth
70
Q

Clinical features of pre-eclampsia

A

Mainly asymptomatic

  • Headaches (usually frontal)
  • Visual disturbances e.g. blurred or double vision, halos, flashing lights
  • Epigastric pain (due to hepatic capsule distension/infarction)
  • Sudden onset non-dependent oedema
  • Hyper-reflexia
71
Q

Criteria for pre-eclampsia

A

Hypertension - on 2 occasions at least 4 hours apart

Significant proteinuria - >300mg

72
Q

Classification of pre-eclampsia

A

Mild = BP 140/90-149/99 mmHg
Moderate = BP 150/100 – 159/109 mmHg
Severe = BP > 160/110 + proteinuria > 0.5 g/ day
or
BP > 140/90 mmHg + proteinuria + symptoms

73
Q

Complications of pre-eclampsia

A

Onset of pre-eclampsia before 34 weeks is associated with poorer prognosis

  • HELLP syndrome – haemolysis, elevated liver enzymes, low platelets
  • Eclampsia
  • AKI
  • DIC
  • ARDS
  • Hypertension (4-fold ↑ risk post-partum)
  • Cerebrovascular haemorrhage (1-2%)
  • Death
74
Q

Differential diagnosis of pre-eclampsia

A

Essential HTN – HTN prior to 20 weeks’ gestation
Pregnancy induced HTN (PIH) – new onset HTN presenting after 20 weeks’ gestation, without significant proteinuria
Eclampsia – Pre-eclampsia + seizures - obs emergency

75
Q

Investigations for pre-eclampsia

A

Presence of hypertension and proteinuria

- detected on urine dipstick then quantified on 24 hour urinary collection

76
Q

Management of pre-eclampsia

A

Prevent development of eclampsia
Minimise risk of complications for mother and foetus
- monitoring of maternal and foetal wellbeing - regular blood pressure measurements, urinalysis, blood tests, foetal growth scans and cardiotocography
VTE prevention - LMWH
Antihypertensives - reduce stroke risk
Delivery

77
Q

Antihypertensives for pre-eclampsia

A

Labetalol (1st line)
- Beta-blocker
- Postural hypotension, fatigue, headache, nausea and vomiting, epigastric pain
Nifedipine
- Calcium channel blocker
- Peripheral oedema, dizziness, flushing, headache, constipation
Methyldopa
- Alpha-agonist
- Drowsiness, headache, oedema, GI disturbances, dry mouth, postural hypotension, bradycardia, hepatotoxicity

78
Q

Post-natal care of women with pre-eclampsia

A

Still at risk of seizures for 24 hours
Blood pressure monitored for 2 days
Repasses hypertensives
Advised of risk of pre-eclampsia in future pregnancies

79
Q

Pregnancy specific changes with thyroid

A

The half-life of thyroxine binding globulin increases - total thyroid hormone levels increase
hCG stimulates like TSH
Increased GRF and increased uptake of iodine into thyroid can deplete iodine -> iodine deficiency

80
Q

Management of hypothyroidism in pregnacy

A

Maintain thyroxine dose and monitor regularly

81
Q

Management of hyperthyroidism in pregnancy

A

Ensure euthyroidism

- propylthiouracil or carbimazole

82
Q

Complications of hyperthyroidism in pregnancy

A 
Maternal
- thyroid storm
- congestive cardiac failure
- pre-eclampsia
Foetal
- foetal growth restriction
- prematurity
- stillbirth

Yr4 - O&G (19 decks)

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