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Hypothyroidism

Maria Jessica 1115135


Left. Thyroid hormones T4 and
T3 feed back to inhibit
hypothalamic production of
thyrotropin-releasing hormone
(TRH) and pituitary production
of thyroid-stimulating hormone
(TSH). TSH stimulates thyroid
gland production of T4 and T3.
Right. Thyroid follicles are
formed by thyroid epithelial
cells surrounding proteinaceous
colloid, which contains
thyroglobulin. Follicular cells,
which are polarized, synthesize
thyroglobulin and carry out
thyroid hormone biosynthesis).
TSH-R, thyroid-stimulating hormone
receptor; Tg, thyroglobulin; NIS, sodium
iodide symporter; TPO, thyroid peroxidase;
DIT, diiodotyrosine; MIT, monoiodotyrosine.
Congenital Hypothyroidism
• Prevalence:
– 1 in 4000 newborns
– Permanent: Neonatal hypothyroidism is due to
thyroid gland dysgenesis in 80–85%, to inborn
errors of thyroid hormone synthesis in 10–15%,
and is TSH-R antibody-mediated in 5% of affected
newborn
– Transcient: if the mother has TSH-R blocking
antibodies or has received antithyroid drugs
• Clinical Manifestation:
The majority of infants appear normal at birth,
and <10% are diagnosed based on clinical
features, which include
– prolonged jaundice, feeding problems, hypotonia,
enlarged tongue, delayed bone maturation, and
umbilical hernia. Importantly, permanent
neurologic damage results if treatment is delayed.
– Typical features of adult hypothyroidism may also
be present
– Other congenital malformations, especially
cardiac, are four times more common in
congenital hypothyroidism.
• Diagnosis: generally based on measurement of TSH or T4
levels in heel-prick blood specimens.
• Treatment: When the diagnosis is confirmed, T4 is
instituted at a dose of 10–15 mmg/kg per day, and the
dose is adjusted by close monitoring of TSH levels.
Iatrogenic hypothyroidism
• In the first 3–4 months after radioiodine treatment,
transient hypothyroidism may occur due to reversible
radiation damage.
• Other cause: chronic iodine excess can also induce goiter
and hypothyroidism (patients treated with amiodarone or
lithium). The intracellular events that account for this effect
are unclear, but individuals with autoimmune thyroiditis
are especially susceptible.
• Treatment:
– Low-dose thyroxine treatment can be withdrawn if recovery
occurs.
– Iodized salt or bread or a single bolus of oral or intramuscular
iodized oil.
Secondary hypothyroidism
• Secondary hypothyroidism is usually diagnosed in the
context of other anterior pituitary hormone
deficiencies.
• Diganosis: detecting a low unbound T4 level, TSH levels
may be low, normal, or even slightly increased.
• Treatment: The goal of treatment is to maintain T4
levels in the upper half of the reference range
Autoimmune Hypothyroidism
• Classification:
– Subclinical hypothyroidism: there is a phase of
compensation when normal thyroid hormone
levels are maintained by a rise in TSH, some
patients may have minor symptoms.
– Hypothyroism or overt hypothyroidism: unbound
T4 levels fall and TSH levels rise further; symptoms
become more readily apparent at this stage
(usually TSH >10 mIU/L)
• Prevalence:
– 4 per 1000 women and 1 per 1000 men.
– It is more common in certain populations, such as
the Japanese, probably because of genetic factors
and chronic exposure to a high-iodine diet.
– The mean age at diagnosis is 60 years, and the
prevalence of overt hypothyroidism increases with
age. Subclinical hypothyroidism is found in 6–8%
of women (10% over the age of 60) and 3% of
men.
Pathogenesis
• Genetic  HLA-DR
• Environmental  high iodine intake (tyroid
toxic)
• In Hashimoto’s thyroiditis  there is
marked lymphocytic infiltration.
• Hypothyroidism is composed by activated
CD4+ and CD8+ T cells.
• CD8+ cytotoxic T cells  Thyroid cell
destruction
• Local T cell production of cytokines (TNF,
IL-1, and interferon gamma)
– thyroid cell apoptosis
– impair thyroid cell function
– induce the expression of other
proinflammatory molecules (HLA class I and
class II molecules, adhesion molecules,
CD40, and nitric oxide)
• In Hashimoto  Antigen Thyroid Peroxidase
(glycoprotein that catalyses iodine oxidation and
thyroglobulin tyrosyl iodination reactions in the
thyroid gland)

Thyroid hormone ↓
• 20% patient with Hashimoto  TSH-receptor
blocking antibodies

Thyroid hormone ↓
LABORATORY EVALUATION
TREATMENT
requires longlife treatment
- Levothyroxine (T4)
- Levothyroxine combined Lythironine (T3)

• Clinical Hypothyroidism
- No residual thyroid  levothyroxine 1,6 µg/kgbw
(100-150 µg)
- Hypothyroidsm after the treatment of Grave’s
disease  lower doses (75-125 µg)
• Goal of treatment is a normal TSH (ideally in
the lower half of the reference range).
• TSH responses are gradual and should be
measured about two months after instituting
treatment.
• Subclinical Hypothyroidism
- Starting with a low dose of levothyroxine (25–50 µg/d)
with the goal of normalizing TSH.

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