cp-hypothyroidism in preg

8/6/2019 Cp-hypothyroidism in Preg.

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HYPOTHYROIDISM IN

PREGNANCY

CASE PRESENTATION

ANTENATAL WARD30/3/11


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Control of thyroid functionBy a negative-feedback loop:

The hypothalamus releases TRH TRH acts on the pituitary gland to

release TSH

TSH acts on the thyroid gland torelease the thyroid hormones (T

3and

T4) that regulate metabolism

TRH and TSH concentrations areinversely related to T3 and T4concentrations.

99% circulating T3 and T4 is bound toTBG.

1% circulate in the free form,

and only the free forms arebiologically active.


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Physiological changes of thyroid during pregnancy

1. TBG

Increase {hepatic synthesis is increased}2. TT4 & TT3

increase to compensate for this rise

3. FT4 & FT3decrease. FT4 are altered less by pregnancy, but do

fall a little in the 2nd & 3rd trimesters.

4. TSH

decrease in 1st trimester, between 8 & 14 wk

{increase HCG, HCG has thyrotropin-like activity},

increase in 2nd & 3rd trimester {Increased TBG}


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5. Pregnancy is associated with a state of

relative iodine deficiency

{a. increase maternal iodine requirement because ofactive transport to fetoplacental unit

b. Increase iodine excretion in urine, 2 fold, because

of increased GFR & decreased renal tubularreabsorption}

The thyroid gland increases its uptake from the blood

3 fold {fall of plasma iodine}

If there is already dietary insufficiency of iodine,

the thyroid gland hypertrophies in order to trap

a sufficient amount of iodine


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Phenomenon Explanation

High thyroxine-binding globulin (TBG) Increased serum estrogen

First trimester TSH suppression HCG

Slight increase in FT4 HCG

Goitre in iodine deficiency areas Increased iodide clearance

Goitre in iodine sufficient areas Increased demand

Increased T4 and T3 demand High type III deiodinases

High total T4 and T3 Increase in TBG

Increased thyroglobulin Increased demand for thyroid hormones


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Thyroid physiology and the impact of pregnancy


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Fetal thyroid function

During early gestation: the fetus receives thyroid

hormone from the mother. Maternal T4 crosses theplacenta actively, the only hormone that does so. (T3,

TSH)

The fetuss need for thyroxine starts to increase as

early as 5 wk of gestation.

Fetal thyroid development does not begin until 10 to12 wk, and then continues until term.


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The fetus relies on maternal T4 exclusively before

12 wk & partially thereafter for normal fetalneurologic development.

Maternal hypothyroidism could be detrimentalto fetal development if not detected and

corrected very early in gestation.

Preconceptional optimization of T4 therapy is

important


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Incidence

Much more common in women than men

Common in those with family history

Overt hypothyroidism:

0.3% - 2.5% of pregnanciesThus, about 40 patients need to be screened to

detect one case.

Subclinical disease:

2% to 3% of pregnancies


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Causes

Iodine deficiency:

Most common cause in most of the worldHashimotos thyroiditis (chronic autoimmune

thyroiditis):

Most common cause in developed countries,where lack of iodine in the diet is not a problem

characterized by:

antithyroid antibodies (thyroid antimicrosomialand antithyroglobulin antibodies).

Both iodine deficiency and Hashimotos

thyroiditis are associated with goiter.


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Other causes:

-Radioactive iodine therapy for Graves disease;

-Thyroidectomy-Viral thyroiditis

-Pituitary tumors

-Sheehans syndrome;

-MedicationsyThionamides

yLithium

yDrugs that inhibit absorption of thyroid medication

( Ferrous sulfate, Sucralfate, Cholestyramine, Antacids

(aluminum hydroxide)


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Iodine and lithium inhibit thyroid function and,

along with dopamine antagonists, increase TSH

levels.Thioamides, glucocorticoids, dopamine

agonists, and somatostatins decrease TSH

levels.Ferrous sulfate, sucrafate, cholestyramine, and

aluminum hydroxide antacids all inhibit GIT

absorption of thyroid hormone and thereforeshould not be taken within 4 hrs of thyroid

medication.


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Screening

Routine screening has been recommended:

Infertility, menstrual disorders, Repeatedpregnancy loss,Type 1 DM, Pregnant women

who have S&S of deficient thyroid function.

In recent years, some authors have

recommended screening all pregnant women

for thyroid dysfunction, but such

recommendations remain controversial.

Routine screening is not endorsed by the

ACOG


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Clinical pictures

Similar to physiologic conditions seen in most pregnancies.

cold intolerance, muscle cramps, intellectual slowness,

depression, insomnia, periorbital edema, myxedema, andmyxedema coma

SYMPTOMHYPOTHYROIDISM PREGNANCY

Fatigue o oConstipation 0 o

Hair loss o

Dry skin o

Brittle nails o

Weight gain o o

Fluid retention o o

Bradycardia o

Goiter o o

Carpal tunnel syndrome o o


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laboratory tests

Because screening is controversial and

symptomatology does not reliably distinguishhypothyroidism from normal pregnancy, laboratory

tests are the standard for diagnosis.

Overt hypothyroidism:

symptomatic patientelevated TSH level

low levels of FT4 and FT3.

Subclinical hypothyroidism:asymptomatic patient.

elevated TSH

normal FT4 and FT3


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Effects of hypothyroidism on pregnancy

The impact of maternal hypothyroidism on the

fetus depends on the severity of the condition.A. Uncontrolled hypothyroidism.

Miscarriage

AnaemiaIntrauterine fetal demise and stillbirth

preterm delivery,

low birth weight,preeclampsia,

developmental anomalies including reduced IQ.


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A. Maternal and congenital hypothyroidism

resulting from severe iodine deficiency:

profound neurologic impairment & mentalretardation.

If the condition is left untreated.

Congenital cretinism: Growth failure, mental

retardation, and other neuropsychologic deficitsincluding deaf-mutism.

If cretinism is identified & treated in the first 3

months of life: near-normal growth and intelligencecan be expected.

For this reason, newborn screening for congenital

hypothyroidism.


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B. Asymptomatic overt hypothyroidism.

Women who had previously been diagnosed

with hypothyroidism, (abnormal TSH and FT4levels), but who do not have symptoms.

1. Impaired psychomotor development at 10months in infants born to mothers who had low T4 during the first 12 ws ofgestation

2. low IQ scores in the offspring at 7 to 9 yrs of age wascorrelated with elevated maternal TSH levels at less than 17

weeks gestation


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C. Subclinical hypothyroidism.

Low IQs of the children whose motherswere not treated (Mitchell and Klein, 2004).

Undiagnosed subclinical hypothyroidism

were more likely to be complicated by

placental abruption, preterm birth (Casey, 2005).


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Overt

Hypothyroidism

Subclinical

Hypothyroidism

No. ofPatients* 60 (%) 57 (%)

PIH 13 (21) 9 (15)

Placental abruption 3 (5) 0

PPH 4 (6.6) 2 (3.5)

Stillbirths 4 (6.6) 1 (1.7)

Congenital

malformations

2 (3.3) 0

LBW 10 (16.6) 5 (8.7)

Maternal and Neonatal Complications of

Hypothyroidism in Pregnancy


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Treatment

The treatment of choice is synthetic T4,or levothyroxine.

Non pregnant:1.7 g/kg/day or

12.5

to 25

g/day adjusted by 25

g/day every 2 to 4 ws until euthyroid

state is achieved.


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Pregnant:

Safe in pregnancy and lactation. {Very little thyroxin

crosses the placenta and the fetus is not at risk ofthyrotoxicosis}

Patients who were on thyroxine therapy before

pregnancy should increase the dose by 30% once

pregnancy is confirmed.

TSH should be monitored /4 wk

k to maintain a TSH level between 1 and 2 mU/L and

FT4 in upper third of normal.

Once euthyroid state has been achieved, TSH should

be monitored /trimester until delivery.


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During pregnancy,

thyroid function

merits regular

monitoring, fine-

tuning of treatment


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cp-hypothyroidism in preg

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