‫‪Thyroid disease‬‬

‫‪In pregnancy‬‬
‫اسم الطالب‬ ‫بإشراف‬
‫تقى محمد سعدون‬ ‫ا‪.‬د‪.‬سوسن طالب‬
‫م‪.‬د‪.‬بسمة حميد‬
 TABLE OF CONTENTS
01 02

Introduction Hyperthyroidism
03

HYPOTHYROIDISM
 01
Introductio
n
 INTRODUCTI
ON
Thyroid disease is common in those of
childbearing age. Many of the symptoms of
thyroid disease, such as heat intolerance,
constipation, fatigue, palpitations and weight
gain, resemble those of normal pregnancy and
therefore new presentations of thyroid disease
can be difficult to detect during pregnancy.

A normal pregnancy results in a number of

important reversible physiological and hormonal
changes that alter thyroid structure and more
importantly function.
 INTRODUCTI
Physiological changes of pregnancy, including

ON
plasma volume expansion, increased thyroid-
binding globulin production and relative iodine
deficiency, mean that thyroid hormone reference
ranges for the non-pregnant population are not
useful in pregnancy.

Free thyroxine (fT4), free triiodothyronine (fT3)

and thyroid-stimulating hormone (TSH) should be
analysed when assessing thyroid function in
pregnancy; total T3 and T4 should not be used.
There is a fall in TSH and a rise in fT4
concentrations in the first trimester of normal
pregnancy, followed by a fall in fT4 concentration
with advancing gestation.
 Thyroid-Related
Physiologic Change
Consequences
↑T production; ↑ cardiac
↑ Plasma volume
output

First trimester ↑ in hCG ↑ Free T ↑ T production

↑Tproduction; fetal T synthesis during

second and third trimesters

↑ Oxygen consumption by feto

placental unit, gravid uterus, and ↑ Basal metabolic rate;
mother
↑ cardiac output
 Two Disorders

hyperthyroidis
hypothyroidism
m
 Hyperthyroidis
02
m
HYPERTHYROIDISM

Definition

Hyperthyroidism (overactive thyroid) is an

overproduction of thyroid hormones during
Pregnancy.

Hyperthyroidism affects 2/1000 pregnancies

Autoimmune thyrotoxicosis (Graves' disease) affects

around 2 per 1,000 pregnancies and is usually
diagnosed before pregnancy.

Other causes of hyperthyroidism (5% overall)

include toxic adenoma, subacute thyroiditis and
toxic multinodular goitre.
 Signs Symptoms
• Thyromegaly
• Nausea/Vomiting
• Resting pulse >100
(tachycardia) • Diaphoresis, Fatigue

• Systolic flow murmur • Breathlessness

• Diffuse goiter • Weight loss

• Exophthalmos • Nervousness

• Increased cardiac output • Insomnia, Anxiety

• Pretib • Heat intolerance

⚬ ial myxedema
🔹 Management During Pregnancy:
• Goal:
Treatment during pregnancy should be drug
therapy with the aim of maintaining maternal fT3
and fT4 levels in the high/normal range

• Treatment Options:
• Carbimazole or Propylthiouracil (PTU) using the
lowest effective dose, to minimize placental
transfer and risk of fetal hypothyroidism.

• Contraindicated:
Radioactive iodine is contraindicated because it
completely obliterates
the fetal thyroid gland.
🔹 Complications of Uncontrolled Thyrotoxicosis:
• Increased risk of:
• Miscarriage
• Preterm delivery
• Fetal growth restriction (FGR)
• Therefore, thyroid function must be closely
monitored.
Many women can reduce their medication dose,
and up to one-third may stop treatment during
pregnancy.

⸻
🔹 Fetal Monitoring:
• TSH receptor-stimulating antibodies can cross
the placenta.
• Women with positive antibody titres should
undergo fetal surveillance during pregnancy.
• After delivery, the neonatology team should
evaluate the newborn to rule out thyroid
 03
HYPOTHYROIDIS
M
Hypothyroidism is common and found in around 1% of pregnant women.
Worldwide, the commonest cause of hypothyroidism is iodine deficiency,
but this is rarely seen in the developed world, where autoimmune
Hashimoto thyroiditis is more common. Women diagnosed with
hypothyroidism should continue thyroid replacement therapy during
pregnancy, and biochemical euthyroidism is the aim, that is, maintaining
the TSH at the lower end of the normal range.

Thyroid function tests should be performed at booking and at 28 weeks, or

more often if dose adjust- ments are required. Suboptimal replacement
therapy with levothyroxine has been associated with devel opmental delay
and pregnancy loss in some studies; however, corrected hypothyroidism
does not seem to influence pregnancy outcome or complications.
 Signs Symptoms
• Fatigue
• Hair: dry. coarse, sparse
• Hair loss
• Thin lateral eyebrows
• Constipation
• Periorbital edema
• Weight gain
• Puffy dull face with dry
• Cold intolerance
skin
• Insomnia

• Muscle cramps
Maternal Risk Fetal Risk
Infertility
Low IQ Level
Prematurity
Cretinism
Cardiac dysfunction
Neonatal or fetal
Low birth weight and
Hypothyroidism
stillbirth
Congenital absence of the
Spontaneous abortion
thyroid gland
Placental abruption

Pre- eclampsia
Diagnosis

•Low free T4
•increase TSH
•Presence of autoimmune antibodies
•TSH level is more useful in diagnosis of
hypothyroidism in pregnancy

Management of primary hypothyroidism

Levothyroxin replacment therapy
Aims to normalise TSH level
 Myxedema coma
Definition:

Myxedema coma is a rare, life-

threatening complication of severe
hypothyroidism, characterized by
decompensated metabolic state,
altered mental status, hypothermia,
and multi-organ dysfunction. In
pregnancy, it poses significant risks
to both the mother and fetus,
requiring urgent medical
intervention.
Signs and Symptoms:
• General:
• Altered level of consciousness (lethargy, stupor, coma)
• Hypothermia
• Bradycardia
• Hypotension
• Hypoventilation
• Non-pitting edema (especially face and extremities)
• Dry, coarse skin
• Delayed reflexes (especially relaxation phase)
• Pregnancy-Specific Concerns:
• Fetal distress
• Intrauterine growth restriction (IUGR)
• Preterm labor or miscarriage
• Reduced fetal movement
Management:

1. Supportive Care:
• ICU admission
• Airway protection and mechanical ventilation if needed
• Passive rewarming for hypothermia
• Monitor fluid/electrolyte balance

2. Thyroid Hormone Replacement:

• IV levothyroxine (T4): Initial loading dose (e.g., 200–400 mcg), followed
by daily dosing
• Consider liothyronine (T3) in some cases (cautiously in pregnancy due to
risk to fetus)

3. Glucocorticoids:
• IV hydrocortisone (e.g., 100 mg q8h) to cover possible adrenal
insufficiency until ruled out
Management:

4. Identify and Treat Underlying Cause:

• Infection, cold exposure, trauma, sedatives, or withdrawal of thyroid
meds

5. Obstetric Management:
• Continuous fetal monitoring
• Multidisciplinary care (endocrinology + obstetrics)
• Delivery may be needed in severe or deteriorating cases

⸻
Prognosis:

Early recognition and aggressive treatment are critical. Delay in treatment

increases maternal and fetal mortality significantly.

Let me know if you want references or a formatted version for a

presentation or report.
Case scenario
1. The physiologic changes of pregnancy can alter many of the common
laboratory tests. During the evaluation of a patient with tachycardia,
hypertension, and headache you are considering both hyperthyroidism
versus an atypical preeclampsia and draw the following laboratory tests. To
correctly interpret the results, it is necessary to distinguish between normal
versus abnormal changes during pregnancy. Which of the following would
normally be expected to increase during pregnancy?

(A) alanine aminotransferase (ALT)

(B) aspartate aminotransferase (AST)
(C) hematocrit
(D) plasma creatinine
(E) thyroxine-binding globulin (TBG)
Answer: E. thyroxine-binding globulin (TBG)

The mother and a rapidly growing infant use an increased amount

of oxygen, resulting in an increased basal metabolic rate (BMR).
When combined with elevated binding protein secondary to
estrogen effect, one can be misled to diagnose hyperthyroidism
when, in fact, these are normal pregnancy changes. For this
reason, a thyroid evaluation in pregnancy will often use a free T4
level rather than total T4. Even mild hyperthyroidism probably
does not merit treatment during pregnancy. AST and ALT are not
elevated in normal pregnancy but may be elevated in patients with
severe preeclampsia. Hematocrit will tend to drop because of
plasma volume expansion. Creatinine also decreases because of
increased glomerular filtration.
2. Untreated maternal hypothyroidism during pregnancy is associated with:

A. Increased risk of neural tube defects

B. Fetal hypothyroidism only
C. Increased risk of miscarriage and low IQ in the baby
D. Macrosomia
Answer: C. Increased risk of miscarriage and low IQ in the baby

Explanation:
Thyroid hormones are crucial for fetal brain development,
especially in the first trimester. Untreated hypothyroidism can
cause miscarriage, preterm birth, and neurodevelopmental delay
in the child.
3. WRani a 24 year old woman presents to her gynaecologist as she has chronic hypothyroidism and wants to
conceive now. Her hypothyroidism is well controlled at 75 microgram of Thyroxine. She doesn't smoke or
drink and doesn't have any other medical ailment. She would like to know if she should keep taking her
Thyroxin. Which of the following is the best advice to give to this patient:

a. Stop taking Thyroxine and switch to methimazole as we would like to control your baby's thyroid levels

b. Thyroxine is safe during pregnancy but it is not absolutely necessary during pregnancy to continue
thryoxine.

c. Thyroxine is not safe during pregnancy and it is better for your baby to be hypothyroid than hyperthyroid

d. Thyroxine is absolutely safe and necessary for you in pregnancy but we would like to decrease your dose
as pregnancy is accompanied by mild physiological hyperthyroidism

e. Thyroxine is safe in pregnancy and the dose of thyroxine would be increased during pregnancy to avoid
hypothyroidism, which may affect the baby adversely
dose of thyroxine would be increased during pregnancy to avoid
Answer: (e) Le Thyroxine is safe in pregnancy and the
hypothyroidism, which may affect the baby adversely.
4. Which of the following is correct regarding hyperthyroidism in
pregnancy?

a) Should be treated surgically rather than with carbimazole.

b) Can be diagnosed by total T4 measurements.

c) More than half are due to Grave's disease.

d) The main complications for the fetus include growth restriction and fetal
bradycardia.

e) Therapy should maintain free T4 and T3 levels in the low normal range.
Answer: C. Hyperthyroidism in pregnancy is treated
pharmacologically. Radioactive iodine is contraindicated due to the
effect on the fetal thyroid gland. The diagnosis of hyperthyroidism
in pregnancy requires increased free T3 and T4, with reduced
levels of thyroid-stimulating hormone (TSH). Approximately 90 per
cent of cases of hyperthyroidism in pregnancy are due to Grave's
disease. Levels of free T3/T4 in pregnancy should be maintained in
the high normal range. The main risks to the fetus are of growth
restriction, stillbirth, fetal tachycardia and premature delivery.
 5. In the first trimester, the preferred antithyroid drug for Graves’ disease
is:

A. Methimazole
B. Levothyroxine
C. Liothyronine
D. Propylthiouracil
(PTU)
Answer: D. Propylthiouracil (PTU)

Explanation:
PTU is preferred in the first trimester due to the teratogenic risk
associated with methimazole. Methimazole may be used in the
second and third trimesters.
6. A pregnant woman with hyperthyroidism presents with fever,
tachycardia, and confusion. What is the most likely diagnosis?

A. Myxedema coma
B. Preeclampsia
C. Thyroid storm
D. Postpartum thyroiditis
Answer: C. Thyroid storm

Explanation:
Thyroid storm is a life-threatening complication of untreated or
poorly managed hyperthyroidism, often triggered by stress,
infection, or labor.
⸻
7. A woman presents for her new obstetrical visit at 12 weeks' EGA. Her
medical history is complicated by Graves thyroiditis that has been treated
with radioactive iodine a few years prior. The patient is currently being
maintained on thyroid replacement. She is worried that this will
compromise the fetus. She is told that the interaction between maternal
and fetal physiology relative to thyroid function is complex. Which of the
following is an accurate description of this interaction?

(A) Maternal thyroid hormones (T4 and T3) readily cross the placenta.
(B) Maternal thyrotropin easily crosses the placenta.
(C) The athyroid fetus is growth retarded at birth.
(D) The fetal thyroid concentrates iodide.
(E) The placenta serves as a barrier to maternal iodine crossing to the
fetus.
Answer: D Generally, the placenta serves as a barrier to maternal
thyrotropin and thyroid hormones. The fetus concentrates iodide
very effectively, hence the need to avoid radioactive iodine and
high iodide-containing medications. There is limited action of the
thyroid hormone during fetal life. The athyroid fetus will appear
normally grown at birth. This is why all newborns are screened in
the first week of life for thyroid function.
8. What is the most appropriate management for subclinical
hypothyroidism during pregnancy?

A. Observation only
B. Levothyroxine if TPO antibodies are positive
C. PTU therapy
D. Immediate delivery
Answer: B. Levothyroxine if TPO antibodies are positive

Explanation:
Subclinical hypothyroidism with positive thyroid peroxidase (TPO)
antibodies increases the risk of adverse outcomes; levothyroxine
is often initiated to prevent complications.

⸻
10. Which of the following fetal complications is most commonly associated
with maternal hyperthyroidism?

A. Fetal macrosomia
B. Neonatal hypothyroidism
C. Intrauterine growth restriction (IUGR)
D. Neural tube defect
Answer: C. Intrauterine growth restriction (IUGR)

Explanation:
Poorly controlled maternal hyperthyroidism increases the risk of
IUGR, preterm birth, fetal tachycardia, and stillbirth.
⸻
 Refrences

1-Ten teachers textbook (p;151-152)

2-American thyroid association

3-Medical diseases in pregnancy by

assisted,professor Inaam faisal at diyala medical
college
Thank you