HYPOTHYROIDISM

WORO AYU S
1510211060
 HYPOTHYROIDISM
Reduced production of thyroid hormone is the central
feature of the clinical state termed hypothyroidism
The incidence of hypothyroidism is higher among women, the
elderly, and in some racial and ethnic groups.
Neonatal screening programs identify hypothyroidism (almost
all primary cases) in almost 1 of every 3500 newborns.
EFFECT AND
SYMPTOMS OF
HYPOTHYROIDISM
TREATMENT
Treated with T4 (available in pure form and is stable and inexpensive)
• Half-life T4 about 7 days
 TIROIDITIS
Thyroiditis is a term indicating the presence of thyroid inflammation
SUBACUTE THYROIDITIS
De Quervain’s thyroiditis or granulomatous thyroiditis

• DEFINITION: Acute inflammatory disorder of thyroid gland (most due to viral infection)
• ETIOLOGY: mumps virus, coxsackievirus, and adenoviruses
CLINICAL FEATURE
SYMPTOMS AND SIGN
• Fever, malaise and soreness in the anterior neck
• Initially: symptoms of hyperthyroid
• Gland: tender, no local redness and heat
• Clinical sign of thyrotoxicosis (tachycardia, tremor, and hypperreflexia)
LAB FINDINGS
• Initially, FT4 and T3 are elevated

• As the disease progresses, FT4 and T3 drops, TSH rises, and symptoms of
hypothyroidism are noted.
DIFFERENTIAL DIAGNOSIS
Graves’ disease by presence of thyroidal pain, low T3 and FT4 and suppressed serum
TSH; and by the absence of thyroid antibodies

TREATMENT
- Symptomatic treatment (aspirin / NSAID)
- If not respond to NSAID: use glucocorticoid
- Beta-blocker when hyperthyroid phase
- T4, 0.1–0.15 mg once daily, may be indicated during the Hypothyroid phase of the
illness if hypothyroid
PROGNOSIS
AD Bonam
resolves completely and spontaneously over weeks or months
 CHRONIC THYROIDITIS
Hashimoto’s thyroiditis, lymphocytic thyroiditis
 HASHIMOTO’S THYROIDITIS
Hashimoto thyroiditis is part of the spectrum of autoimmune
thyroid diseases (AITDs) and is characterized by the
destruction of thyroid cells by various cell- and antibody-
mediated immune processes.
ETIOLOGI
The initiating process in Hashimoto thyroiditis is not well
understood.

• Antibodies binding to and blocking the thyroid-stimulating hormone (TSH) receptor,

thyrotropin receptor blocking antibodies (TBII)  inadequate thyroid hormone
production and secretion

• Patients with Hashimoto thyroiditis have antibodies to various thyroid antigens:

Anti-thyroid peroxidase (anti-TPO)  Most frequent
antithyroglobulin (anti-Tg)
TSH receptor-blocking antibodies (TBII)  jarang
Nevertheless, a small percentage of patients with Hashimoto thyroiditis (approximately 10-15%)
may be serum antibody negative.
FAKTOR RESIKO

Genetic Susceptibility
• Hashimoto’s disease almost certainly is associated with a polygenetic susceptibility, HLA
being only one of the genes involved

• Polymorphisms in the CTLA4 gene  codes for a regulatory protein inhibiting T-cell
reactivity  linked to the propensity to secrete thyroid autoantibodies

Non-Genetic Risk Factor

pregnancy, drugs, age and gender, infection, and irradiation
EPIDEMIOLOGI

• Hashimoto’s disease is the most common cause of hypothyroidism in areas of the world
in which dietary iodine is sufficient
• Incidence in women 3.5 cases per 1000 people per year and in men 0.8 per 1000.4,5
• prevalence increases with age in both women and men
CLINICAL FEATURES
SIGN AND SYMPTOMS
• Usually present with goiter
• Painless
• Older patients may present with severe hypothyroidism with only a small, firm
atrophic thyroid glands
LAB FINDINGS
• Mark: High titer of autoantibodies to thyroidal antigens in the serum
• FNAB: Lymphocytic infiltration as well as the presence of Hürthle cells
HISTOPATOLOGI
DIAGNOSS
DIFFERENTIAL DIAGNOSIS
Hashimoto’s thyroiditis can be differentiated from other causes of nontoxic goiter by
serum antibody studies and, if necessary, by FNAB.

TREATMENT
Surgery  if a goiter continous and cause compressive symptoms (rare)
T4 theraphy
PROGNOSIS

• With theraphy  goiter resolve

• May also develop true Grave’s disease