Medical problems arising in pregnancy Flashcards

1
Q

Medical problems arising in pregnancy

  • Name them
A

Anemia
Gestational diabetes
Infections
UTI
Thromboembolic disease (VTE)
Liver disease:
- Obstetric cholestasis
- Acute fatty liver of pregnancy (AFLP)

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2
Q

Anemia :
- Causes, Dx,Sx, Complications

A

Causes:

a. Increase in plasma volume (“physiological anemia”)
b. Iron deficiency (due to poor diet and increased demand – especially in multiple
pregnancy) → most common cause.
c. Menorrhagia (abnormal menstrual bleeding)
d. Preexisting blood disorders
i. Sickle cells
ii. Thalassemia
iii. Hemolytic anemia

  1. Diagnosis:
    a. Blood count (hemoglobin levels)
    i. 1
    st trimester <11 g/dL

ii. 2 nd and 3rd trimesters <10.5g/dL

  1. Symptoms:
    a. Fatigue
    b. Shortness of breath
    c. Lethargy
  2. Complications:

a. Fetus:
i. Mild – unaffected but high chance to develop anemia within its first year due to
lack of fetal iron stores in utero.

ii. Severe anemia – preterm delivery and low birth weight

b. Mother:
i. Increased risk for infection
ii. Increased risk for death (in case of severe blood loss)

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3
Q

Anemia

Management

A

a. Early recognition and treatment.

b. Iron assessment → oral iron supplementation (most common) + ascorbic acid (aids
absorption).

i. Avoid coffee or tea as they interfere absorption.

ii. If oral iron has failed to improve hemoglobin levels then parenteral (elsewhere
in the body than mouth and alimentary canal) iron can be used.

iii. If iron supplementation failed then assessment of ferritin, zinc protoporphyrin
hemoglobin levels.

c. Consider underlying problem that is not secondary to iron deficiency

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4
Q

Gestational diabetes
- Definition, features, causes

A
  1. Definition: women without previously diagnosed diabetes develop chronic hyperglycemia during
    gestation (carbohydrate intolerance with onset or first recognition of hyperglycemia during
    pregnancy)
  2. Features:
    a. Condition occurring in 2-10% of all pregnancies.
    b. Predominant in the 3rd and sometimes 2nd trimesters.
  3. Causes:
    a. Anti-insulin hormones produced by placenta (human placental lactogen, glucagon and
    cortisol) ➔ pregnancy induced diabetogenic state
    b. Increased maternal corticosteroids and thyroid hormones
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5
Q

Gestational diabetes

Risk factors

A

. Risk factors:
a. Previous large infant (>4.5kg)
b. Previous gestational diabetes
c. Diabetic relatives (first-degree)
d. Obesity (BMI>30)
e. Ethnic background (south Asian, middle east)
f. Macrosomia
g. Polyhydramnios
h. Polycystic ovary syndrome

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6
Q

Gestational diabetes :

Dx

Sx

A

a. Selective screening (among high risk population) or universal screening (among all
pregnant women)

b. OGTT at week 28 (3rd trimester) or week 14 (early 2nd trimester in very high risk)
i. Fasting glucose levels are measured first

ii. 75g dose is given and glucose levels are measured 2 hours later

Sx: Asymptomatic

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7
Q

Gestational diabetes :

Complications

A

a. Maternal:

i. Pre-eclampsia
ii. Recurrent infections
iii. Polyhydramnios
iv. Induced labor
v. If vaginal birth occurs → shoulder dystocia and extended perineal tears.
vi. Develop type 2 diabetes post-gestational

b. Fetus:

i. Neonatal unit admission

ii. Hypoglycemia (due to increased fetal pancreas activity to oppose the
uncontrolled maternal glucose that crosses the placenta. Maternal insulin does
not cross so fetus is dependent on its own supply.)

iii. IRDS
iv. Jaundice
v. Macrosomia
vi. Increased risk for diabetes and obesity in childhood

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8
Q

Gestational diabetes

Management

A

a. During pregnancy – control blood glucose levels.

i. Low glycemic index foods

ii. Medication – metformin, glibenclamide and insulin

b. During labor – fetal blood glucose monitoring.

c. Post labor – stop treatment and continue monitoring

i. If values are normalized → true gestational diabetes
ii. If values remain elevated → masked (prior to pregnancy) or developed diabetes

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9
Q

Infections

Name the one could get during pregnancy

A

Chicken pox
Parvovirus 19
Influenza H1N1
HIV
Viral hepatitis
Tuberculosis

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10
Q

Chicken pox

A

i. Pathogen: varicella zoster.
ii. Disease: pneumonia (fetal and maternal), congenital varicella syndrome (eye
defects, limb hypoplasia and neurological defects)

iii. Management: IgG prophylaxis (for non-immune women) or acyclovir (for
infected women)

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11
Q

Parvovirus 19

A

i. Pathogen: parvovirus 19

ii. Disease: erythema infectiosum / fifth disease / slapped cheek syndrome, fever,
rash, arthropathy, fetal anemia (aplastic anemia), miscarriage, fetal hydrops
(heart failure → edema, ascites, pleural effusion, pericardial effusion).

iii. Management:
* Maternal: analgesics and antipyretics

  • Fetal: infection after week 20 → Doppler US of middle cerebral artery
    can detect fetal anemia → if so utero blood transfusions
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12
Q

Influenza H1N1

A

i. Disease: fever, cough, respiratory failure, secondary infections, preterm birth,
stillbirth, neonatal death.

ii. Management: vaccine or antiviral medication (oseltamivir, zanamivir) for
infected women.

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13
Q

HIV

A

i. Disease: AIDS, secondary infection, cancer development, vertical transmission
(transplacental or vaginal birth or breast feeding), miscarriage, stillbirth.

ii. Management: HAART (highly active anti-retroviral therapy), C-section (in
women who do not take HAART) and avoid breast feeding.

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14
Q

Viral hepatitis

A

i. Pathogen: Hepatitis A, B, C, D and E
ii. Transmission: A (fecal-oral), B&C (blood)
iii. Disease: preterm birth, vertical transmission (perinatally)

iv. Management:
* Prvention (hygiene – Hep. A, vaccine – Hep. B)
* Screening – to reduce vertical transmission and exclude co-infection
with HIV

  • Vaginal delivery with avoidance of interventions that may increase
    bleeding (C-section and lack of breast feeding do NOT reduce vertical
    transmission).
  • Fetal immunization with IgG and vaccine
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15
Q

Tuberculosis

A

i. Pathogen: Mycobacterium tuberculosis
ii. Disease: miscarriage and same as in non-pregnant
iii. Diagnosis: Tuberculin test (in suspected women) → x-ray chest (in positive tests)
iv. Management: RIPE antibiotics (streptomycin is contraindicated as it causes
deafness)

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16
Q

UTI

A
  1. Features:
    a. 2-10% of all sexually active women
    b. 30% out of this group develops ascending infections
  2. Causes:
    a. E. coli (most common)
  3. Complications:
    a. Pyelonephritis → bacteremia and septic shock
    b. Preterm
  4. Management: antibiotics
17
Q

Thromboembolic disease (VTE)

Features, Causes

A
  1. Features:
    a. 10 times more common in pregnancy than non-pregnant
    b. Leading cause of maternal mortality
  2. Causes:
    a. Increased coagulation factors
    b. Suppressed anticoagulants and fibrinolysis
    c. Venous stasis due to compression on pelvic vessels
18
Q

Thromboembolic disease (VTE)
- Risk factors
- Diagnosis

A
  1. Risk factors:
    a. Family history of VTE
    b. Thrombophilia
    c. Obesity
    d. Smoking
    e. Sickle cells disease
    f. Immobility
    g. Operative delivery
    h. Multiple pregnancies
    i. Pre-eclampsia
    j. Contraceptives (estrogen containing)
  2. Diagnosis
    a. Doppler US
    b. MRI
    c. CT (with caution to fetus)
19
Q

Thromboembolic disease (VTE)

Clinically

A

Clinically:

a. DVT: swelling and tenderness of the leg

i. Compression of left common iliac vein by the right common iliac artery lead to stasis and thrombus formation most commonly in the iliac or femoral veins.

b. PE: dyspnea and pleuritic chest pain

20
Q

Thromboembolic disease (VTE)

Management

A

a. Prophylaxis for high risk – elastic compression stock and LMWH.

i. LMWH – does not cross placenta
ii. Warfarin – crosses placenta causing abnormalities if used in 1st trimester
iii. Stop treatment briefly perinatally to reduce postpartum hemorrhage but
continue again for 6 weeks after delivery.

b. In acute case – heparin therapy

21
Q

Liver disease during pregnancy

A
  • Obstetric cholestasis
  • Acute fatty liver of pregnancy (AFLP)
22
Q

Obstetric cholestasis

A

a. Definition: static bile acids flow commonly in 3rd trimester

b. Risk factors:
i. Genetics
ii. Hormonal pregnancy state (influencing bile acids flow)
iii. Ethnicity

c. Clinically:
i. Itching (especially palms and soles) → cholestatic pruritis (irritation of nerve
endings)
ii. Pale stool
iii. Dark urine
iv. Jaundice

d. Diagnosis:
i. High serum bile acids
ii. High liver enzymes
iii. Serology – rule out hepatitis and autoimmune hepatitis (anti-SM and antimitochondrial antibodies)

e. Complication:
i. Preterm birth
ii. Still birth
iii. Impaired liver function (prolonged bleeding time)
iv. Recurrence in following pregnancies

f. Management:

i. Medication: ursodeoxycholic acid (for itching and liver function), vitamin K (for
bleeding), cholestyramine

23
Q

Acute fatty liver of pregnancy (AFLP)

A

a. Definition: rare disease most common in the third trimester characterized by extensive
fatty infiltration of the liver, which can result in acute liver failure

b. Risk factors:
i. Multiple pregnancies
ii. Obesity

c. Pathomechanism:
i. Mutated mitochondrial enzyme (of the fetus) leads to unoxidized fatty acids
that enter the maternal circulation and accumulate in her liver.

d. Clinically:
i. Non-specific symptoms – nausea, vomiting, abdominal pain
ii. Jaundice
iii. Coagulopathy with risk for DIC
iv. Hypoalbuminemia and ascites

e. Diagnosis:

i. Symptoms

ii. Exclude other causes
* Pre-eclampsia
* HELLP syndrome (hemolysis, elevated liver enzymes and low platelets).
* Viral hepatitis
iii. Hypoglycemia
iv. Elevated liver enzymes
v. Biopsy

f. Management:
i. Immediate C-section

g. Complications:
i. Acute liver failure
ii. Hemorrhage
iii. Hepatic encephalopathy (nitrogen-containing compounds are not excreted
because urea cycle is impaired. These compounds go to the circulation cross the
BBB and are consumed by astrocytes that use them to produce glutamate.
Glutamate causes increased osmotic pressure and astrocytes are swollen).

24
Q

Complications Liver diseases during pregnancy

A

i. Acute liver failure

ii. Hemorrhage

iii. Hepatic encephalopathy (nitrogen-containing compounds are not excreted
because urea cycle is impaired.

These compounds go to the circulation cross the
BBB and are consumed by astrocytes that use them to produce glutamate.

Glutamate causes increased osmotic pressure and astrocytes are swollen).