KELAINAN KELENJAR

TIROID DAN PARATIROID

AGUS WIDIYATMOKO
KELENJAR TIROID
• Berada di bagian tengah depan leher, tepat dibawah laring
dan di depan trakea
• Bentuk seperti “Butterfly” (kupu-kupu)
• Terdapat 2 lobus yang dihubungkan dengan isthmus
• Ukuran ↑ : pubertas & kehamilan
• Kaya akan pembuluh darah: memiliki kemampuan
menyalurkan hormon dalam jumlah besar dan dalam waktu
yang singkat.
• Memproduksi Thyroxin (T4) & Tri-iodothyronine (T3)
• Memproduksi juga Calcitonin : berperan pada homeostasis
calcium & phosphate
FUNGSI KELENJAR TIROID
 Thyroid Hormones

Hormone Function Stimulated by

T3/T4  metabolic rate  metabolic rate

 protein synthesis  T3/T4
 energy production  TSH
Most important hormone in day today
regulation of metabolic rate
Calcitonin
 blood calcium concentration
 the reabsorption of Ca and Ph from  blood Ca levels
bones to blood
Calcitonin “tones” down serum Ca levels
Mekanisme Umpan Balik Hormon

 Untuk mempertahankan jumlah hormon dalam darah secara optimal maka

dibutuhkan pengaturan sekresi hormon yang dikembalikan oleh mekanisme
refleks endokrin / umpan balik hormon.

 Mekanisme Umpan balik :

1. Umpan Balik Negatif (negative feedback)
 terjadi jika terdapat peningkatan hormon dalam darah sehingga mengakibatkan
inhibisi sekresi hormon
2. Umpan Balik Positif (positive feedback)
 Terjadi jika kadar hormon dalam darah mengakibatkan peningkatan sekresi pada
kelenjar endokrin.
Feedback negatif
hormon tiroid
Biosintesis dan Metabolisme Hormon Tiroid

 Tahap trapping (pengangkapan iodida)

 Tahap oksidasi iodida menjadi iodium
 Tahap coupling
 Tahap penimbunan atau storage
 Tahap deiodinasi
 Tahap proteolisis dan
 Tahap pengeluaran/pelepasan hormon.
Proses
biosintesis
hormon tiroid
HIPERTIROID
DEFINISI

 Hipertiroid adalah suatu kondisi dimana kelenjar tiroid

memproduksi hormon tiroid secara berlebihan, biasanya
karena kelenjar terlalu aktif.
 Kondisi ini menyebabkan beberapa perubahan baik secara
mental maupun fisik seseorang, yang disebut dengan
thyrotoxicosis
Hyperthyroidism

 Thyrotoxicosis = “any condition that results in thyroid

hormone excess”
 Includes: Graves Disease, Toxic Goiter, Thyroiditis, and
Excessive Thyroxine Ingestion
 Hyperthyroidism = “Specifically hyperfunctioning of the
thyroid gland”
 Most Commonly caused by Graves Disease in the young
 Toxic Nodular Goiter in the elderly
 PENYEBAB HIPERTIROID

 Hyperthyroidism dengan uptake radioiodine normal atau tinggi

Autoimmune thyroid disease

Graves' disease
Hashitoxicosis
Autonomous thyroid tissue (uptake may be low if recent iodine load led to
iodine-induced hyperthyroidism)
Toxic adenoma
Toxic multinodular goiter
TSH-mediated hyperthyroidism
TSH-producing pituitary adenoma
Non-neoplastic TSH-mediated hyperthyroidism
Human chorionic gonadotropin-mediated hyperthyroidism
Hyperemesis gravidarum
Trophoblastic disease
 PENYEBAB HIPERTIROID
 Hyperthyroidism dengan tanpa radioiodine uptake

Thyroiditis
Subacute granulomatous (de Quervain's) thyroiditis
Painless thyroiditis (silent thyroiditis, lymphocytic thyroiditis)
Postpartum thyroiditis
Amiodarone (also may cause iodine-induced hyperthyroidism)
Radiation thyroiditis
Palpation thyroiditis
Exogenous thyroid hormone intake
Excessive replacement therapy
Intentional suppressive therapy
Factitious hyperthyroidism
Ectopic hyperthyroidism
Struma ovarii
Metastatic follicular thyroid cancer
 CLINICAL MANIFESTATIONS OF
HYPERTHYROIDISM IN ADULTS
 SKIN  — The skin is warm (and may rarely be erythematous) in hyperthyroidism due to increased
blood flow; it is also smooth because of a decrease in the keratin layer.
 Other changes include:
 Sweating, which increases due to increased calorigenesis; this is often associated with heat intolerance
 Onycholysis (loosening of the nails from the nail bed, Plummer's nails) and softening of the nails
 Hyperpigmentation, which can occur in severe cases; it appears to be mediated by accelerated cortisol
metabolism, leading to increased corticotropin (ACTH) secretion
 Pruritus and hives, which are occasional findings, primarily in patients with Graves' hyperthyroidism
 Vitiligo and alopecia areata, which can occur in association with autoimmune disorders
 Thinning of the hair
Plummers Nails
Vitiligo and
alopecia areata
Graves’ Dermopathy
– Thickening and redness of the dermis
• Due to lymphocytic infiltration
– Distribution
• Pretibial (93.3%),
• Pretibial+ feet (4.3%),
• Pretibial + UE (1.1%).
 CLINICAL MANIFESTATIONS OF
HYPERTHYROIDISM IN ADULTS

EYES  — Stare and lid lag occur in all patients with hyperthyroidism. They are due to sympathetic
overactivity, possibly mediated by increased alpha-adrenergic receptors in some tissues. Lid lag is
evaluated by having the patient follow the examiner's finger as it is moved up and down. The patient has
lid lag if sclera can be seen above the iris as the patient looks downward.

As noted above, only patients with Graves' disease have ophthalmopathy. It is characterized by
inflammation of the extraocular muscles and orbital fat and connective tissue, which results in proptosis
(exophthalmos), impairment of eye-muscle function, and periorbital and conjunctival edema.
Ophthalmopathy is more common in patients who smoke cigarettes.
Lid Retraction
Exopthalmus
CLINICAL MANIFESTATIONS OF
HYPERTHYROIDISM IN ADULTS
 CARDIOVASCULAR  — Patients with hyperthyroidism have an increase in cardiac
output, due both to increased peripheral oxygen needs and increased cardiac
contractility.
 Heart rate is increased, pulse pressure is widened, and peripheral vascular resistance
is decreased. Systolic hypertension is common.
 The left ventricular ejection fraction does not increase appropriately during exercise,
suggesting the presence of a true cardiomyopathy. High- or normal-output congestive heart
failure can occur in patients with severe hyperthyroidism and congestive heart failure
worsens in patients who already have it.
 Atrial fibrillation occurs in 10 to 20 percent of patients with hyperthyroidism, and is more
common in elderly patients.
 CLINICAL MANIFESTATIONS OF
HYPERTHYROIDISM IN ADULTS
 METABOLIC / ENDOCRINE
 Serum lipids  — Patients with hyperthyroidism tend to have low serum total and high-density
lipoprotein (HDL) cholesterol concentrations and a low total cholesterol/HDL cholesterol ratio. These
values increase after treatment.
 Hyperglycemia  — Although thyroxine is not a counterregulatory hormone, hyperthyroidism can
interfere with glucose metabolism. It is associated with both increased sensitivity of pancreatic beta
cells to glucose, resulting in increased insulin secretion, and antagonism to the peripheral action of
insulin. The latter effect usually predominates, leading to impaired glucose tolerance in untreated
patients.
 Adrenal function  — Interpretation of the cortisol response to ACTH stimulation testing may be
misleading in patients with hyperthyroidism because cortisol binding globulin (CBG) levels decrease,
resulting in lower total serum cortisol concentrations. In one report of 49 hyperthyroid patients
undergoing ACTH testing, 35 percent had subnormal total serum cortisol values (<18 mcg/dL), while
only 11 percent had a subnormal free cortisol index (ratio of serum total cortisol to CBG)
 CLINICAL MANIFESTATIONS OF
HYPERTHYROIDISM IN ADULTS
 RESPIRATORY  — Dyspnea and dyspnea on exertion may occur for
many reasons in hyperthyroidism:
 Oxygen consumption and CO2 production increase. These changes result in hypoxemia
and hypercapnia, respectively, both of which stimulate ventilation.
 Respiratory muscle weakness is an important cause of dyspnea, and reduced exercise
capacity may be largely due to respiratory muscle weakness and decreased lung
volume.
 There may be tracheal obstruction from a large goiter.
 Hyperthyroidism may exacerbate underlying asthma.
 Pulmonary arterial systolic pressure is increased.
 CLINICAL MANIFESTATIONS OF
HYPERTHYROIDISM IN ADULTS
 GASTROINTESTINAL  — Weight loss is due primarily to increased metabolic rate
(hypermetabolism), and secondarily to increased gut motility and the associated hyperdefecation
and malabsorption; rare patients have steatorrhea. Celiac disease is also more prevalent in
patients with Graves' disease. Most patients have hyperphagia, but an occasional patient with
mild hyperthyroidism may have sufficient appetite stimulation that weight is gained (more
commonly in younger patients). Anorexia may be prominent in elderly hyperthyroid patients.
 Other changes that may occur include:
 Vomiting and abdominal pain, rarely
 Dysphagia due to goiter
 Abnormalities in liver function tests, particularly high serum alkaline phosphatase concentrations and,
rarely, cholestasis
CLINICAL MANIFESTATIONS OF
HYPERTHYROIDISM IN ADULTS
 HEMATOLOGIC  — The red blood cell mass is increased in hyperthyroidism,
but the plasma volume is increased more, resulting in a normochromic,
normocytic anemia.
 Serum ferritin concentrations may be high.
 Graves' hyperthyroidism may be associated with autoimmune hematologic
disorders such as idiopathic thrombocytopenic purpura and pernicious anemia,
and some patients have antineutrophil antibodies.
 CLINICAL MANIFESTATIONS OF
HYPERTHYROIDISM IN ADULTS
 GENITOURINARY  — Urinary frequency and nocturia are common in hyperthyroidism, although the
mechanism is uncertain. Possible causes include primary polydipsia and hypercalciuria. Enuresis is common
in children.
 In women, serum sex hormone-binding globulin (SHBG) concentrations are high, which results in high
serum estradiol concentrations and low-normal serum free (unbound) estradiol concentrations, high
serum luteinizing hormone (LH) concentrations, a reduced mid-cycle surge in LH secretion,
oligomenorrhea, and anovulatory infertility. Amenorrhea can occur in women with severe
hyperthyroidism.
 In men, the increase in serum SHBG concentrations results in high serum total testosterone
concentrations, but serum free (unbound) testosterone concentrations are normal or low. Serum LH
concentrations may be slightly high. Extragonadal conversion of testosterone to estradiol is increased, so
that serum estradiol concentrations are high. These changes can cause gynecomastia, reduced libido, and
erectile dysfunction. Spermatogenesis is often decreased or abnormal, eg, more spermatozoa are abnormal
or non-motile
 CLINICAL MANIFESTATIONS OF
HYPERTHYROIDISM IN ADULTS
 BONE  — Thyroid hormone stimulates bone resorption, resulting in increased porosity of
cortical bone and reduced volume of trabecular bone. The loss in cortical bone density is
greater than that of trabecular bone.
 Serum alkaline phosphatase and osteocalcin concentrations are high, indicative of increased
bone turnover.
 The increase in bone resorption may lead to an increase in serum calcium concentrations,
thereby inhibiting parathyroid hormone secretion and the conversion of calcidiol (25-
hydroxyvitamin D) to calcitriol (1,25-dihydroxyvitamin D).
 Graves' disease may also be associated with thyroid acropathy, with clubbing and periosteal
new bone formation in the metacarpal bones or phalanges.
thyroid
acropathy
(This is most marked in the
index fingers and thumbs)
 CLINICAL MANIFESTATIONS OF
HYPERTHYROIDISM IN ADULTS
 NEUROPSYCHIATRIC  — Patients with thyrotoxicosis may experience behavioral and
personality changes, such as psychosis, agitation, and depression.
 Less overt manifestations that are more common in less severe thyrotoxicosis include
anxiety, restlessness, irritability, and emotional lability. Insomnia is also common.
 Symptoms often worsen in patients with preexisting psychiatric disorders.
 These behavioral manifestations are accompanied by cognitive impairments, particularly
impaired concentration, confusion, poor orientation and immediate recall, amnesia, and
constructional difficulties.
DIAGNOSIS
HIPERTIROID
(TANPA LAB)
Newcastle Index
Laboratory Findings

 TSH nearly undetectable

 Elevated FT4 or FT3
 mild leukopenia,
 Normositic Normochromic anemia,
 ↑ Liver Function Test’s and alkali phospatase,
 mild ↑ Ca++,
 ↓ albumin
 ↓ cholesterol
Overview of Thyroid Function Tests
Grave Disease

Suatu penyakit autoimun yang biasanya ditandai oleh produksi autoantibodi yang memiliki
kerja mirip TSH pada kelenjar tiroid.
Autoantibodi IgG ini, yang disebut immunooglobulin perangsang tiroid (Thyroid-Stimulating
Immunoglobulin) sehingga meningkatkan pembentukan hormon tiroid

Etiologi
Adanya autoantibodi kerja mirip TSH (reseptor TSH) di
membran sel folikel tiroid. Autoantibodi IgG ini, yang
disebut immunooglobulin perangsang tiroid (Thyroid-
Stimulating Immunoglobulin), thyroid peroksidase
antibodies (TPO), dan TSH receptor antibodies (TRAb)
yang menyebabkan perangsangan produksi hormon tiroid
secara terus menerus, sehingga kadar hormon tiroid
menjadi tinggi.
 Diagnosis Penyakit Graves
Anamnesis dan Pemeriksaan Fiisik
 Autoimmune( thyroid stimulating Ig (TSI),

Pemeriksaan Laboratorium antithyroglobulin, ANA

 TSH menurun  Causes 60-80% of thyrotoxicosis
 FT4 meningkat
 T3 Toksikosis  Female:male = 5-10:1, 40-60 years
 Clin. Manifestasion:
USG: kurang ada manfaat  Diffuse, nontender goiter.
 Thyroid bruit (+)
AJH:
Tidak bisa dilakukan (hanya kalau disertai nodul  Palpitation, sweating, anxiousness, fatigue,
dingin) weakness, weight loss, diarrhea, oligomenorrhea

Sidik tiroid  Ophtalmology

Grave: Uptake iodine meningkat (hot nodule)  Pretibial myxedema
Tiroiditis:
Uptake rendah  Plummer’s nail
Obat Anti tiroid
 Kelompok Obat Efeknya Indikasi
Obat anti tiroid Menghambat sintesis hormon Pengobatan lini pertama pada
-Propiltiourasil (PTU) 100-200 tiroid dan berefek Graves.
mg/6-8 jam imunosupresif PTU juga Obat jangka pendek prabedah
-Metimazol menghambat konversi T4-T3
-Karbimazol

Beta blocker Mengurangi dampak hormon Obat tambahan, kadang obat

Propanolol 20-40 mg/ 6 jam tiroid pada jaringan tunggal pada tiroiditis
Metoprolol
Atenolol
nadolol

Bahan mengandung iodin Menghambat keluarnya T4 dan Persiapan tiroidektomi, pada

Kalium iodida T3, menghambat produksi T4 krisis tiroid, bukan untuk
Sol lugol dan T3 serta produksi T3 pengobatan rutin
Na ipodat ekstratiroidal
Asam iopanoat
Iodine Radioactive Therapy

Obat lainnya Menghambat transpor yodium, Bukan indikasi rutin. Pada

Kalium perklorat sintesis dan keluarnya hormon, subakut tiroiditis berat, dan
Litium karbonat memperbaiki efek hormon di krisis tiroid
glukokortikoid jaringan dan sifat imunologis
PT U & M M I
►Long-term treatment of Graves' disease (preferred 1st-
line treatment in Europe, Japan, & Australia)
►PTU is treatment of choice in patients who are pregnant
and those with severe Graves' disease.
►Both medications considered safe for use while
breastfeeding
 PTU
300 mg daily in 3 divided doses.
Severe hyperthyroidism or very large goiters,
initial dosage may be increased to 400 mg/day,
up to 600 to 900 mg/day.
The daily dose is divided into 3 doses
administered every 8 hours.
The maintenance dosage is 100 to 150 mg/day
every 8 h.
duration of action from 12 to 24 h
PO peak serum concentrations occurring in one
hour
Side effects of are less clearly related to dose.
MMI
15 to 30 mg/day as a single dose.
15 mg/day for mild hyperthyroidism
30-40 mg/day for moderately hyperthyroidism.
60 mg/day for severe hyperthyroidism.
The maintenance dose is 5-15 mg/day
duration of action even longer
Side effects are dose-related
 Thyroiditis

1. Acute:
a) Bacterial (tender goiter, may be asymmetric, fever, dysphagia, erythema, lymphadenopathy,  ESR, TSH/FT4 N)
b) Radiation, amiodarone drug, trauma.
2. Subacute:
a) Transient thyrotoxicosis
i. transient hypothyroidism
ii. normal thyroid.
b) Painful, enlarged goiter (viral, granulomatous, or de Quervain thyroiditis): fever,  ESR
c) Silent (postpartum, autoimmune): painless, TPO Ab (+), ESR N,
3. Chronic
a) Hashimoto’s thyroiditis
b) Riedel’s (idiopathic fibrosis, hard nontender, normal function test)
Thyroiditis
KRISIS TIROID
KRISIS TIROID

Bila skor ≥ 45 krisis

tiroid, skor 25-44
impending krisis
tiroid, skor ≤ 24
bukan krisis tiroid
TERAPI
KRISIS TIROID
Apathetic Hyperthyroidism

 Elderly pt’s w/ Graves' disease may present w/ apathy, weight loss,

muscular weakness, arrhythmias (esp A-fib), CHF, + constipation.
 A goiter may not be palpable in as many as 70% of patient’s
 There symptoms may suggest depression
 The usual hyperkinetic signs and symptoms seen in Graves’ are not
typically present in the elderly (tremor -)
 Check all elderly w/ new-onset atrial arrhythmias or CHF for
hyperthyroidism
 Subclinical Hyperthyroidism
 Refers to an elevation in T4 and/or T3
within the normal range, leading to
suppression of the pituitary secretion of
TSH in the
 subnormal range (i.e. normal T4 and T3,
low TSH).
 Clinical symptoms and signs are
frequently absent or nonspecific.
 Usually found in the elderly
 Often due to an autonomously
functioning or adenoma.
 Studies have linked subclinical thyrotoxicosis to
 Accelerated bone loss in postmenopausal women
 A higher incidence of atrial dysrhythmias (esp atrial
fibrillation)
 Recent studies suggest an increase in cognitive
impairment and allcause mortality (esp CV
disease).
 A TSH below the lower limit of normal, but above
0.1 mIU/mL are less likely to result in such
complications.
 If patient’s are not treated, then careful for
complication.
Hypothyroidism
 Tabel 1. Penyebab Hipotiroidisme

58 PENYEBAB HIPOTIROIDISME
Primer Sentral

Tiroiditis Autoimun Kronik Tumor

Tiroiditis autoimun reversibel Trauma

(subakut, postpartum)

Ablasi RadioIodin Vaskuler

Pembedahan Infeksi
Radiasi Infiltrasi
Penyakit infeksi dan infiltrative Kongenital
Disgenesis Tiroid congenital Obat-obatan
Defisiensi yodium
Obat-obatan
Hypothyroidism
 Reidel’s Struma/Thyroiditis (rare)
 Patient’s present w/ a painless, hard, fixed goiter
 hypothyroidism occurs when entire gland becomes fibrosed
 can see fibrosis of other tissues (fibrosing retroperitonitis, orbital fibrosis, or
sclerosing cholangitis)
 Drug-induced
 Amiodarone
 Lithium
 Interferon-alpha
 Interleukin-2
 Iodine deficiency
 Most common cause of hypothyroidism worldwide
 Symptoms
Mechanism Symptoms Signs
Slowing of metabolic processes Fatigue and weakness Slow movement and slow speech
Cold intolerance Delayed relaxation of tendon
Dyspnea on exertion reflexes
Weight gain Bradycardia
Cognitive dysfunction Carotenemia
Mental retardation (infantile onset)
Constipation
Growth failure

Accumulation of matrix Dry skin Coarse skin

substances Hoarseness Puffy facies and loss of eyebrows
Edema Periorbital edema
Enlargement of the tongue
Other Decreased hearing Diastolic hypertension
Myalgia and paresthesia Pleural and pericardial effusions
Depression Ascites
Menorrhagia Galactorrhea
Arthralgia
Pubertal delay
Carotenemia
Hypothyroid face
Enlargement of
the tongue
Laboratory Findings
 Elevated TSH
 Low FT4
 thyroid peroksidase antibodies (TPO Ab) (+)
 Pregnant women w/ TPO Ab (+)
 Miscarriage rate doubles
 ↑ risk post partum thyroiditis (35%)
 mild anemia
 ↑ CPK-MB
 ↑ LDL,↑ Chol (↓ lipid clearance)
 Hyponatremia
Hipotiroid Kongenital

Causes:
Deficient production of thyroid hormone
Disgenesis
congenital Hypothyroidism
Iodine deficiency
endemic goiter
Defect in thyroid hormonal receptor activity
 Hipotiroid kongenital pada Anak

 Hipotiroid kongenital (kretinisme) ditandai produksi hormon tiroid yang

inadekuat pada neonatus
 Penyebab:
1. Defek anatomis kelenjar tiroid atau jalur metabolisme hormon tiroid
2. Inborn error of metabolism
 Merupakan salah satu penyebab retardasi mental yang dapat dicegah.
Bila terdeteksi setelah usia 3 bulan, akan terjadi penurunan IQ
bermakna.
 Tata laksana tergantung penyebab. Sebaiknya diagnosis etiologi
ditegakkan sebelum usia 2 minggu dan normalisasi hormon tiroid
(levotiroksin)sebelum usia 3 minggu.
Diagnostic algorithm for the detection of primary congenital
hypothyroidism
Tatalaksana Hipotiroidisme

 Levotiroksin Merupakan obat pilihan pertama

 Dapat dipakai untuk terapi koma miksedema
 Aman untuk ibu hamil
 Dosis awal 50-100 mcg PO 1x/hari, dinaikkan 25-50 mcg/3-4
minggu sampai eutiroid dan TSH normal
 Dosis rumatan 100-200 mcg PO 1x/hari
 Lansia/ CV dosis awal 25-50 mcg PO 1x/hari, dosis dinaikkan
25 mcg/4 mnggu s/d eutiroid dan TSH normal
 Kretinisme Endemik

 Merupakan keadaan hipotiroid berat dan ekstrim yang terjadi pada waktu bayi dan anak yang
ditandai dengan kegagalan pertumbuhan
 Kretinisme yang terjadi akibat kekurangan yodium bisa bersifat endemik ataupun sporadis
 Kretinisme endemik merupakan kretinisme yang terjadi pada bayi yang lahir pada daerah
dengan asupan yodium yang rendah serta goiter endemik; sehingga mengalami kekurangan
yodium yang berat pada masa fetal
 Kretinisme sporadik merupakan kretinisme akibat hipotiroid kongenital
 Seseorang dikatakan kretin endemik jika ia lahir di daerah gondok endemik dan menunjukkan
dua gejala atau lebih: retardasi mental, tuli sensorineural nada tinggi, gangguan
neuromuskular
Manifestasi Klinis

3 tipe kretinisme sporadik:

1. Tipe nervosa: RM berat, bisu tuli, strabismus, paresis sistem
piramidalis tungkai bawah, spastik ataksik (motor rigidity)
2. Tipe miksedema: RM dengan derajat lebih ringan; dan tanda
hipotiroid klinis seperti perawakan pendek, miksedema, kulit
kering, rambut jarang, perkembangan seksual terhambat, spastik
tungkai bawah, gangguan gaya jalan
3. Tipe campuran: gabungan antara keduanya
 Miksedema

 Biasanya diderita oleh orang dewasa.

 Ditandai dengan meningkatnya jumlah total cairan interstisial
pada tubuh (yang bersifat seperti gel).
 Berat badan meningkat.
 Penderita terlihat gemuk tetapi tidak sintal.
Myxedema
Koma miksedema

 Koma miksedema merupakan keadaan dekompensasi dari hipotiroid.

 Gejala koma miksedema meliputi: penurunan kesadaran,
hypothermia,hipotensi, bradikardia.
 Miksedema adalah deposit jaringan konektif (glycosaminoglycan,
asam hyaluronic) pada kulit.
 Tidak harus dijumpai pada keadaan koma hypothyroid namun
merupakan sebuah fenomena yang dapat ditemui.
 Terapi: salah satu terapi berupa pemberian levothyroxine IV.
Myxedema pathophysiology
IODINE DEFICIENCY DISORDERS
(IDD)

Iodine has major role in the development of

physical and mental of children during pregnancy
The consequence of iodine deficiency beyond
endemic goiter and endemic cretinsim
 Spektrum GAKI

Fetus abortus, lahir mati

anomali kongenital
peningkatan kematian perinatal
peningkatan kematian anak
kretin endemi -gangguan mental
-bisu tuli
-diplegia spastik
-mata juling
kretin miksedematosa -cebol
-gangguan mental
defek psikomotor
Neonatus gondok neonatal, hipotiroid neonatal
Anak & gondok, hipotiroid juvenile, gangguan mental
remaja gangguan perkembangan fisik
Dewasa gondok dengan segala akibatnya, hipotiroid,
gangguan mental
Pembesaran kelenjar gondok (goiter)

Grade 0 tidak teraba

Grade 1a tidak teraba atau bila teraba
tidak lebih besar dari normal
Grade 1b jelas teraba dan membesar,
tetapi tidak terlihat meskipun
kepala ditengadahkan
Grade II mudah dilihat, kepala posisi
biasa
Grade III terlihat
Survei masyarakat dilakukandari
bila jarak tertentu
ditemukan ≥30% pada
anak sekolah (termasuk grade I)k
Bila gondok endemik >5% perlu perhatian
Bila gondok endemik >10% perlu pengobatan pencegahan
 Derajat endemi

Endemi grade I (ringan)

bila nilai median ekskresi yodium urin
>50 ug I/g kreatinin atau median urin 5-9,9 ug/dl,
prevalensi gondok anak sekolah 5-20%
Endemi grade II (sedang)
bila nilai median ekskresi yodium urin
25-50 ug I/g kreatinin atau median 2-4,9
ug/dl, prevelensi gondok anak sekolah sampai 30%
Endemi grade III (berat)
bila median <25 ug I/g kreatinin atau <2 ug/dl,
prevalensi gondok anak sekolah >30%, prevalensi
kretin endemik 1-10%
 Diagnosis kretin endemik secara individu

Seorang yang lahir di daerah defisiensi yodium

berat dengan 2 atau lebih kombinasi gejala
ireversibel berikut: retardasi mental, kelainan
neuromotorik (gangguan bicara, cara berjalan
khas, refleks patologis dan refleks fisiologias
meninggi, mata juling, gangguan akibat kerusakan
batang otak, serta late walker), dan gangguan
pendengaran (bilateral, tipe preseptif dan pada
nada tinggi)
Dengan atau tanpa hipotiroid
NODUL TIROID
NODUL TIROID

 Structural disorders of the thyroid (i.e. nodules- simple or multiple) are more common than
functional disorders.
 Prevalence
 Palpable: 5%
 Non-Palpable: 40-50%
 Cancer in nodules: 5%
 • Risks
 Women > Men
 Smoking
 h/o XRT to head/neck (esp children)
 Iodine deficiency
 Most are Euthyroid and Asymptomatic
 Less than 1% with thyrotoxicosis
Red Flags concerning for Cancer

 Male
 Extremes of age (<20 or >60)
 Rapid Growth
 > 4 cm
 Symptoms of local invasion: hoarseness, dysphagia
 h/o XRT to the head/neck (esp children)
 Family history of Thyroid Ca: PTC or MTC
 Hard, fixed lesion
 (+) LN
 h/o familial adenomatous polyposis
FNA Results & Treatment

 Benign (69%)
 follow/u 6-12 months
 Surgery if
 Multiple Nodul Goitres w/ compressive Symptoms
 Growth of Nodule
 Recurrence of cystic nodule after aspiration
FNA Results & Treatment

 Insufficient (17%)
 Repeat FNA 3-4 months
 • Indeterminate/ Suspicious (10%)
 follicular neoplasm
 • 85% benign adenomas
 123-RAIU/Scan
 Surgery
 Malignant (5%)
 Surgery
 131-RAIA if PTC or FTC
Thyroid Cancer

 Papillary Thyroid Ca (PTC): 75%

 Follicular Thyroid Ca (FTC): 15-20%
 Medullary Thyroid Ca (MTC): < 5%
 Anaplastic: < 5 %
 Lymphoma: rare
 – Hashimoto’s is a risk factor
 Metastatic to thyroid: rare
 – Breast, Renal cell, melanoma and lung Ca
 PARATHYROID
GLAND
• Small rounded mass
• Attached to posterior surface of thyroid
gland
• Produces Parathyroid hormone (PTH)
• Controls homeostasis of calcium &
phosphate in blood by activating Vitamin D
Parathyroid
 Parathyroid hormone (PTH), also
called parathormone or parathyrin, is
a hormone secreted by the parathyroid
glands that is important in bone remodeling
 Parathyroid hormone regulates serum
calcium through its effects on bone, kidney, and
the intestine
 PTH is secreted when [Ca2+] is decreased
(Calcitonin is secreted when serum calcium
levels are elevated)
Renal
Hyperparathyroidism
SECONDARY
HYPERPARATHYROIDISM
 It occurs when PTH secretion is increased to compensate for
prolonged hypocalcemia.
 It is seen in patients with chronic renal failure where the failing
kidneys do not convert vitamin D to its active form and they do not
excrete phosphate.
 Excess phosphate combines with calcium to form calcium
phosphate.
 Both processes lead to hypocalcemia, cause hyperplasia of all
parathyroid tissue and hence secondary hyperparathyroidism.
 Secondary hyperparathyroidism can also result
from malabsorption of vitamin D due to chronic
pancreatitis, small bowel disease, bariatric surgery.
TERTIARY HYPERPARATHYROIDISM

 In a small proportion of cases of secondary

hyperparathyroidism, continuous stimulation of the
parathyroids results in adenoma formation and
unregulated PTH secretion.
 Even correction of the underlying cause will not
stop excess PTH secretion i.e parathyroid gland
hypertrophy becomes irreversible.
Clinical Manifestation

 Patients present with kidney stones,nephrocalcinosis,diabetes

insipidus (polyuria and polydipsia).These ultimately lead to renal
failure.
 bone-related complications like osteitis fibrosa (bone pain and
pathological fractures),osteoporosis,osteomalacia and arthritis.
 gastrointestinal symptoms of constipation, anorexia,
nausea,vomiting,peptic ulcers, acute pancreatitis.
Clinical Manifestation

 cardiovascular system involvement leading to hypertension,

bradycardia, shortened QT interval and left ventricular hypertrophy.
 central nervous system symptoms include lethargy, fatigue,
depression, memory loss, psychosis, ataxia, delirium and coma.
 other signs include proximal muscle weakness, itching, band
keratopathy of the eyes.
DIAGNOSIS

 Serum calcium levels are elevated.

 Parathyroid hormone level is abnormally high.
 There is hypophosphatemia and increase in 24-
hour urinary calcium excretion.
 DEXA scan shows skeletal involvement.
Pathognomonic X-ray changes include salt and pepper degranulation in the skull and
subperiosteal bone resorption in the phalanges
 Imaging of renal tract (X-ray, ultrasound) can demonstrate
renal calculi.
 Localisation of parathyroid tumors by technetium
scan,ultrasound,CT of the neck followed by FNAC.
TREATMENT

 Management of acute hypercalcemia by rehydration with

normal saline, bisphosphonates, haemodialysis.
 Medical line : -Monitor serum creatinine levels and calcium
levels every 6 months. DEXA scan on an annual basis.
 -Avoid thiazide diuretics.
 -Maintain high oral fluid intake.
 -Improving bone mineral density and achieving calcium
homeostasis by calcimimetics and HRT.
 Surgery :
 Is indicated in patients with complications and in
younger age group.
 Minimally invasive surgery to excise solitary adenoma,
 Subtotal parathyroidectomy in case of diffuse
hyperplasia are being done.
Hypoparathyroidism