Table 10-2. Thyroid Disorders in Pregnancy



 

  Hyperthyroid Hypothyroid
     
Most common cause Graves disease Hashimoto’s thyroiditis
     
Diagnostic criteria ↓ TSH, ↑ free T4 ↑ TSH, ↓ free T4
  TSHR-antibody  
     
Complication if untreated Thyroid storm, IUGR Anovulation, spontaneous
    abortion
     
Outcome if properly Normal pregnancy Normal pregnancy
treated    
     
Treatment medications 1st trimester: PTU Synthroid (↑ dose 30%
  2nd+3rd trimester: methimazole above prepregnancy)

 

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Chapter 10 l Medical Complications in Pregnancy

 

 

SEIZURE DISORDERS

A 25-year-old primigravida is 19 weeks’ gestation. She has a 10-year history of generalized seizures poorly controlled requiring hydantoin and valproic acid. A triple marker screen result showed an elevated maternal serum alpha feto protein.

 

Significance. Prevalence of seizure disorders is 0.5% in women of childbearing age.

 

Classification:

 

Partial seizures do not involve both hemispheres. They can be either simple, with noloss of consciousness, or complex, in which consciousness may be impaired.

 

Generalized seizures involve both hemispheres. They can be either absence type, withduration <20 s (formerly called “petit mal”), or tonic-clonic, with duration lasting up to several minutes (formerly called “grand mal”).

 

 

Effect of pregnancy on seizure disorder

 

Seizures unchanged. Up to 25% of these women will experience deterioration of sei-zure control during pregnancy, with 75% seeing no change. The more severe the dis-order, the more likely it will worsen.

 

Anticonvulsant metabolism increased. Seizure medication clearance may beenhanced by higher hepatic microsomal activity, resulting in lower blood levels.

 

Effect of seizure disorder on pregnancy

 

Pregnancy complications are minimal with appropriate prenatal care and compliance with anticonvulsant medications.

 

 

Effect of anticonvulsants on fetus and infant

 

Congenital malformation rate is increased from 3% to >10%. In addition, cerebral palsy, sei-zure disorders, and mental retardation are increased in offspring of epileptic women. Maternal phenytoin use is associated with neonatal deficiency of vitamin K-dependent clotting factors: II, VII, IX, and X.

 

Management. Ensure extra folic acid supplementation before conception and during embryo-genesis to minimize neural tube defects.

 

Anomaly screening. Offer triple-marker screen and second trimester sonography toidentify neural tube defects (NTDs) or other anomalies.

 

Drug monotherapy. Use a single drug if possible, at the lowest possible dose, toensure freedom from seizures.

 

Medication levels. Monitor anticonvulsant levels each trimester and adjust dose asneeded. Prevent seizures to minimize maternal and fetal hypoxia.

 

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S2 OB-GYN.indb 89

   

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USMLE Step 2 l Obstetrics

 

 

DIABETES

A 32-year-old Hispanic multigravida is at 29 weeks’ gestation. Her 1-h 50-g glucose screen came back at 175 mg/dL. She is 60 inches tall and weighs 200 pounds. Her pregnancy weight gain has been 30 pounds thus far. Her previous babies weighed 3,800 and 4,200 g.

 

 

Definition. A pregnant woman is unable to maintain fasting (FBS) or postchallenge glucosevalues in the normal pregnant range before or after a standard 100-g glucose challenge.

 

Risk factors. Obesity, age >30 years, and positive family history are the most common riskfactors for gestational diabetes. Other risk factors are fetal macrosomia, unexplained stillbirth or neonatal death, polyhydramnios, and previous traumatic delivery.

 

Classification by pathophysiology. Prevalence of glucose intolerance in pregnancy is 2–3%.

 

• Gestational diabetes mellitus (GDM) is the most common type with onset during pregnancy, usually diagnosed in the last half. Pathophysiology involves the diabetogenic effect of human placental lactogen (hPL), placental insulinase, cortisol, and progester-one. Thirty-five percent of women with GDM will develop overt diabetes within 5 to 10 years after delivery.

 

Type 1 DM is juvenile onset, ketosis prone, insulin-dependent diabetes caused by pan-creatic islet cell deficiency.

 

Type 2 DM is adult onset, ketosis resistant, non–insulin-dependent diabetes caused byinsulin resistance.


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