ENDOKRIN

dr. Jimmy H.W. , Sp.PA

Kelenjar mengeluarkan hormon

Figure 24-1 Hormones released by the anterior pituitary. The adenohypophysis (anterior
pituitary) releases five hormones that are in turn under the control of various stimulatory
and inhibitory hypothalamic releasing factors. TSH, thyroid-stimulating hormone
(thyrotropin); PRL, prolactin; ACTH, adrenocorticotrophic hormone (corticotropin); GH,
growth hormone (somatotropin); FSH, follicle-stimulating hormone; LH, luteinizing
hormone. The stimulatory releasing factors are TRH (thyrotropin-releasing factor), CRH
(corticotropin-releasing factor), GHRH (growth hormone-releasing factor), GnRH
(gonadotropin-releasing factor). The inhibitory hypothalamic influences are comprised of
PIF (prolactin inhibitory factor or dopamine) and growth hormone inhibitory factor (GIH or
somatostatin).
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Hormon :

1. Molekul pemberi sinyal interaksi

permukaan sel
GH, Insulin
Epinefrin, Histamin
2. Steroid masuk sel membran
Estrogen, Progesteron
Glukokortikoid
Tiroksin
Asam retinoat
Figure 24-2 A, Photomicrograph of normal pituitary. The
gland is populated by several distinct cell populations
containing a variety of stimulating (trophic) hormones. B,
Each of the hormones has different staining
characteristics, resulting in a mixture of cell types in
routine histologic preparations. Immunostain for human
growth hormone.

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Kelenjar Hipofise ( Pituitary )

1 cm, 0,5 gr, pada sella tursica

Jenis hormon :
1. Adenohipofise - GH - ACTH -
FSH
- PRL - TSH - LH

2. Neurohipofise - Oksitosin
- Vasopresin
- ADH
 Figure 24-7 Homeostasis in the hypothalamus-
pituitary-thyroid axis and mechanism of action of
thyroid hormones. Secretion of thyroid hormones
(T3 and T4) is controlled by trophic factors
secreted by both the hypothalamus and the
anterior pituitary. Decreased levels of T3 and T4
stimulate the release of thyrotropin-releasing
hormone (TRH) from the hypothalamus and
thyroid-stimulating hormone (TSH) from the
anterior pituitary, causing T3 and T4 levels to
rise. Elevated T3 and T4 levels, in turn,
suppress the secretion of both TRH and TSH.
This relationship is termed a negative-feedback
loop. TSH binds to the TSH receptor on the
thyroid follicular epithelium, which causes
activation of G proteins, and cyclic AMP (cAMP)-
mediated synthesis and release of thyroid
hormones (T3 and T4). In the periphery, T3 and
T4 interact with the thyroid hormone receptor
(TR) to form a hormone-receptor complex that
translocates to the nucleus and binds to so-
called thyroid response elements (TREs) on
target genes initiating transcription.
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Hiperpituitarism

Oleh karena :
Adenoma
Hiperplasia
Carcinoma
Kelainan Hipotalamus
ADENOMA HIPOFISE :

10 % tumor otak
Usia 30 50 tahun
Satu jenis tumor 1 jenis hormon

Makroskopis :
Batas jelas, lunak
Kecil (mm) besar (cm)
Lesi besar invasive adenoma
Perdarahan apoplexi
Mikroskopis :

Sel uniform, poligonal, jalur-

jalur/lembaran
Jaringan ikat penyangga
Inti uniform pleomorfik
Klinik :

R bayangan pada sella tursica

ekspansi sellar
erosi tulang
kerusakan diafragma
Gangguan produksi hipopituitarisme
Penekanan tumor gangguan chiasmo
opticum (bitemporal hemianopsi)
Tekanan intracranial naik
Pusing
Mual/muntah
Figure 24-4 Pituitary adenoma. This massive, nonfunctional adenoma has grown far beyond the confines of the
sella turcica and has distorted the overlying brain. Nonfunctional adenomas tend to be larger at the time of
diagnosis than those that secrete a hormone.

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Figure 24-4 Pituitary adenoma. This massive, nonfunctional adenoma has grown far
beyond the confines of the sella turcica and has distorted the overlying brain.
Nonfunctional adenomas tend to be larger at the time of diagnosis than those that
secrete a hormone.
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PROLAKTINOMA

Tumor hipofise terbanyak ( 30 % )

Usia 20 40 th, pria > wanita
Mikro atau makro
Efek dari tumor PRL naik -
amenorrhea
- galactorrhea
- libido kurang
- infertil
PROLAKTINOMA

Prolaktin tinggi juga karena :

Hamil
Stress
Hiperplasi sel laktotrof
PROLAKTINOMA

Hiperplasi sel laktotrof karena :

Hipotalamus rusak neuron
dopaminergik rusak
Obat yang menekan reseptor dopamin
pada hipofise
- phenotiazin
- reserpin
- haloperidol
PROLAKTINOMA

Terapi :
Bromocriptin sebagai antagonist
receptor dopamin
Hipopituitarisme, karena :

Fakta Hipofise :
Tumor non fungsionil / kista
Operasi / radiasi
Apoplexi
Ischemic necrosis/post partum necrosis
(Sheehan syndrome)
Empty sella syndrome
Genetik
Fakta Hipotalamus :
Tumor primer / sekunder
Infeksi / degenerasi

Klinik hipopituitarisme :
1. Fungsi kelenjar perifer turun
Adrenal
Thyroid
Gonad
2. Wajah pucat MSH rendah
3. Atrofi genitalia
Hipofise posterior

Hormon produksi
ADH
Oksitosin
Diabetes insipidus
ADH rendah
Etiologi : trauma, infeksi, tumor
Klinik : - haus
- urine banyak
- Na serum tinggi, osmositas
 Syndrome of Inappropriate ADH
secretion :
ADH tinggi
Etiologi : Ca small cell paru-paru
Klinik : - urine sedikit
- Na serum rendah
Tumor Hipotalamus

Glioma
Craniopharyngioma
Craniopharyngioma

Dari : Vestigical Remnants Rathke

Pouch
Usia : anak dewasa muda
Morfologi :
Umumnya jinak
Soliter, kistik, multiloculated
Mirip adamantinoma
Thyroid

Asal : evaginasi epitel

pharyngeal
Normal : 15-20 gr
Hormon aktif : - T3,T4 bebas
- ikatan dengan
TBG
Thyroid

fungsi :
Katabolisme : - karbohidrat
- lemak

Sintesa : - protein
Thyroid

Goitrogen (bahan penghambat

sintesa hormon)
Propil tiourasil oksidasi Jodium
Jodium pelepasan T3,T4
Jodium dosis tinggi proteolisis
tiroglobulin
Thyroid

C cell produksi Calcitonin

kerja untuk
- absorbsi calcium
- kerja osteoclast
Hipertiroidisme

lab : T3,T4 tinggi

Gejala :
- nervous - lemah otot- keringatan
- palpitasi - kurus - emosionil
- tremor - diare - capek
- kulit panas - tiroid besar -
gangguan siklus M
Hipertiroidisme

Tirotoxicosis dapat karena :

Diffuse hiperplasi (85% Graves)
hipertiroidisme
Tx hormon tiroid berlebihan
Multinodular goiter
Neoplasma tiroid
Tiroiditis
Hipertiroidisme

Terjadi :
1. Hipermetabolik
2. Overaktif simpatetik
Hipertiroidisme

Gejala Hipertiroid :
1. Cardiac :
aritmi/palpitasi/cardiomegali
2. Otot : atrofi / fatty changes
3. Tulang : osteoporose, fraktur
4. Limfoid : hiperplasi
Hipertiroidisme

5. Ocular : Staring gaze, lid lag

6. Neuromuscular : tremor, cemas,
insomnia, emosional
7. Kulit : berkeringat, rasa panas,
kemerahan
8. GI : rasa haus, lapar
Hipertiroidisme
Dx :
o Tanda klinik
o Lab : - T4 bebas >>
- T S H <<
Tx : - blocker fungsi adrenergic
- propil tiouracil sintesa T3T4
- jodium pelepasan T3T4
- radioactive jodium
Hipotiroidi

Sebab :
1. Primer gangguan tiroid
2. Sekunder
Hipotiroidi

Hipotiroidi karena parenchim tiroid

:
Embrional
Radiasi
Operatif
Hashimoto
Hipotiroidi

Hipotiroidi karena sintesa :

Idiopatik

Cacat sintesa turunan

Jodium intake kurang

Bahan-bahan goitrogen
Hipotiroidi

Hipotiroidi karena supratiroidal :

Lesi hipofise
Lesi hipotalamus
Cretinisme

Bayi, anak-anak
Daerah rendah jodium, pegunungan
Gangguan metabolisme
Cretinisme
Ciri klinik :
Pertumbuhan skeletal dan syaraf
Antara lain :
Retardasi mental
Tubuh pendek, kecil
Wajah kasar
Lidah menjulur
Hernia umbilicus
Mixedema

Pada anak besar dewasa

Aktifitas fisik dan mental
Tanda-tanda klinik :
- fatique
- apatis
- bicara & intelektual
- tidak tahan dingin
Mixedema

Tanda-tanda klinik :
- gemuk
- simpatetik : konstipasi, kulit
kering/dingin/pucat
- cardiac output : napas pendek
- tidak tahan dingin
Mixedema

PA :
- matrix glycosaminoglycanseluruh
- matrix hyaluronicacid jaringan

Lab :
- T4 , T3
- TSH
Hashimoto Thyroiditis

Penyakit autoimmune hipotiroidi

Umur 45-65, : = 10-20 : 1
Ada unsur familiar twin monozigote
= 30-60%
Sering disertai Rh, arthritis, SLE
Figure 24-9 Pathogenesis of Hashimoto thyroiditis. Three proposed models
for mechanism of thyrocyte destruction in Hashimoto disease. Sensitization
of autoreactive CD4+ T cells to thyroid antigens appears to be the initiating
event for all three mechanisms of thyroid cell death. See the text for details.
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Morfologi

Diffuse, berbatas jelas

Pucat, abu-abu, kenyal, noduler
Kapsul intak
Klinik

Struma tidak nyeri, simetrik diffuse

Kadang-kadang noduler
Hipotiroidisme, kadang-kadang
hipertiroidisme transien
Risk factor timbul limfoma
Figure 24-9 Pathogenesis of Hashimoto thyroiditis. Three proposed models
for mechanism of thyrocyte destruction in Hashimoto disease. Sensitization
of autoreactive CD4+ T cells to thyroid antigens appears to be the initiating
event for all three mechanisms of thyroid cell death. See the text for details.
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De Quervain Tiroiditis :

Jarang terjadi
Usia 30 50 tahun
Wanita : Pria = 3 5 : 1
Morfologi :

Unilateral / bilateral
Kenyal, kapsul intak
Kadang-kadang perlekatan jaringan
sekitar
Warna kuning pucat, kecoklatan
Klinik :

Terjadi mendadak / bertahap

Nyeri leher, panas, capek, malas, anorexi,
myalgin
Terdapat struma
Dapat sembuh spontan
T3 T4 , TSH
 Figure 24-11 Subacute thyroiditis. The thyroid parenchyma contains a
chronic inflammatory infiltrate with a multinucleate giant cell (above left) and
a colloid follicle (bottom right).
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Graves Disease

Triad yang harus ada :

1. Hipertiroidi, dengan goiter aktif
2. Ophthalmopathy exophthalmos
3. Dermatopathy pretibial myxedema
Klinik :
o Usia 20-40 tahun, wanita : pria = 7 : 1
o Ada faktor genetik
o Terdapat MHC - haplotype HLA DR3
HLA DR8
 Figure 24-8 A patient with hyperthyroidism. A wide-eyed, staring gaze, caused by
overactivity of the sympathetic nervous system, is one of the features of this disorder.
In Graves disease, one of the most important causes of hyperthyroidism,
accumulation of loose connective tissue behind the eyeballs also adds to the
protuberant appearance of the eyes.
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Figure 24-12 Diffusely hyperplastic thyroid in a case of Graves disease. The follicles are lined by tall, columnar epithelium. The crowded,
enlarged epithelial cells project into the lumens of the follicles. These cells actively resorb the colloid in the centers of the follicles,
resulting in the scalloped appearance of the edges of the colloid.

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Ophthalmopathy graves

Jaringan ikat orbita Mirip TSH

Otot extra ocular receptor

Ab B cell T cell, CD4+ / CD8+
Morfologi :
Struma, Sp 80 gr, simetri berkapsul
Konsistensi lunak, halus, merah seperti daging
Sel-sel silindris, papil-papil kecil
Colloid sedikit, dengan scalloped margin
Infiltrasi limfosit ( B cell )
Terapi :
Jodium involusi epitel
sekresi tiroglobulin turun
Propilthiouracil sintesa kurang
Radioaktif jodium
pembedahan
Diffuse Non Toxic ( simple )
Goiter

a. Endemic
Pada semua usia terutama muda
Pada daerah rendah jodium
pegunungan
10 % populasi (+)
Ada faktor goitrogen :
- calcium - lobak
- kubis - singkong
- bloomkol
b. Sporadik
Wanita > pria
Usia pubertas dewasa muda
Terdapat perubahan kelainan pada :
- transport jodium
- dehalogenase
- organification
- iodotyrosin coupling
Morfologi : 2 stadium

1. Hiperplasi membesar simetrik diffuse

100 150 gr
2. Involusi colloid lebih besar, colloid
lebih banyak colloid goiter

Klinik :
pada anak2 hipotiroidi cretinisme
Pada dewasa keluhan sedikit
Multinodular goiter

Dapat sporadik atau endemik

Usia lebih tua
Menyerupai neoplasm
Patogenesis

Hiperplasi
TSH Tiroid Involusi colloid Folikel
besar
fibrosis
Nodul2 Per- pecah
kalsifika daraha
bergabun
si n
g

Multinodular
goiter
Morfologi :

Multilobulated sp 2.000 gr
Asimetrik, masuk ke substernal
plunging goiter
Bila 1 nodul dominan solitary nodule
(adenomatous goiter)
Irisan warna coklat, gelatinous, fibrosis,
perdarahan, kalsifikasi, kistik
Mikroskopis : folikel banyak colloid, epitel
pipih, atrofik/hiperplasi
Klinik :

Bila besar gangguan kosmetik

tekanan pada trachea,
oesophagus, vena2

Bila salah satu nodulnya hiperfungsi

Plummer Syndrome
Figure 24-13 Nodular goiter. The gland is coarsely nodular and contains areas of fibrosis and cystic change.

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Neoplasma Tiroid

Bentukan soliter, palpable

Wanita : pria = 4 : 1
Sebagian besar nodul soliter jinak
Nodul neoplastik 90% adenoma
Beberapa kriteria penyokong Dx

Nodul soliter neoplasma

Usia muda neoplasma
Jenis kelamin laki-laki neoplasma
Pernah diterapi R Ca
Hot nodule jinak
 Adenoma tiroid
Soliter
Folikel follicular adenoma
Beberapa jenis, tersering : simple
colloid adenoma
Adenoma sangat jarang menjadi
Carcinoma
Figure 24-14 Follicular adenoma of the thyroid. A solitary, well-
circumscribed nodule is seen.
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Figure 24-14 Follicular adenoma of the thyroid. A solitary, well-
circumscribed nodule is seen .

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Figure 24-14 Follicular adenoma of the thyroid. A solitary, well-
circumscribed nodule is seen.
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Morfologi adenoma

Tumor soliter
Bentuk speris
Berkapsul, tekanan jaringan sekitar
Ukuran sekitar 3 cm
Warna abu-abu putih, merah kecoklatan
Kadang2 perdarahan, fibrosis, kalsifikasi,
kistik
mikroskopis
Folikel ukuran sama, isi folikel
Jenis : - Simple colloid (macrofolicular)
- Fetal (microfolicular)
- Embryonal (trabecular)
- Hurthle cell (oxiphyl, oncocyte)
- Atypical
- Adenoma with papillae
(=Papillae adenoma)
(=Encapsuled Papillary Ca)
Tumor Tiroid Jinak yang lain

Kista tiroid : - deri adenoma folicular

- dari multinodular
goiter
Kista dermoid
Lipoma
Hemangioma
Terratoma
Carcinoma Thyroid

Umumnya usia dewasa

Wanita > pria, khususnya usia muda
Terdapat reseptor estrogen pada sel-sel
tumor
Jenis Carcinoma

Papillary Ca 75-85 %
Follicular Ca 10-30 %
Medullary Ca 5 %
Anaplastic Ca 5 %
Papillary Carcinoma

Semua usia, terutama 20-40 tahun

Erat hubungannya dengan fakta radiasi
Figure 24-17 Papillary carcinoma of the thyroid. A, The macroscopic appearance of a
papillary carcinoma with grossly discernible papillary structures. This particular
example contains well-formed papillae (B), lined by cells with characteristic empty-
appearing nuclei, sometimes termed "Orphan Annie eye" nuclei (C). D, Cells
obtained by fine-needle aspiration of a papillary carcinoma. Characteristic
intranuclear inclusions are visible in some of the aspirated cells.
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Figure 24-17 Papillary carcinoma of the thyroid. A, The macroscopic appearance of a
papillary carcinoma with grossly discernible papillary structures. This particular
example contains well-formed papillae (B), lined by cells with characteristic empty-
appearing nuclei, sometimes termed "Orphan Annie eye" nuclei (C). D, Cells
obtained by fine-needle aspiration of a papillary carcinoma. Characteristic
intranuclear inclusions are visible in some of the aspirated cells.
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Morfologi

Soliter atau multipel

Berbatas jelas / berkapsul / menyebar
diluarnya
Kadang2 fibrosis, kalsifikasi, kistik
Pada irisan granula / papil-papil
kecil
Mikroskopis :

Papil dengan fibrovasculer,

dilapisi epitel
Inti dengan ground glass / orphan
annie
Intra nuclear inclusion / groves
Psammoma bodies
Klinik

Sering a symptomatic
Sering dengan metastasis kelenjar
leher
Radioactive jodium cold nodule
FNA, cara Diagnosa yang tepat
Follicular Carcinoma

Wanita > Pria

Usia 40 50 tahun
Sering sudah didapatkan colloid goiter
Morfologi :
Single nodule
Batas jelas / infiltratif
Tumor besar infiltrasi ke jaringan
sekitar
Warna abu-abu coklat merah muda
Kadang2 fibrosis, kalsifikasi
Figure 24-18 Follicular carcinoma. Cut surface of a follicular carcinoma with
substantial replacement of the lobe of the thyroid. The tumor has a light-tan
appearance and contains small foci of hemorrhage.
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Figure 24-19 Follicular carcinoma of the thyroid. A few of the
glandular lumens contain recognizable colloid.
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mikroskopis :

Folikel2 seperti normal, atau dengan

diferensiasi yang rendah
Kadang2 dengan sel Hurthle
Invasi sel pada kapsul atau vascular
Klinik :

Nodul kecil, lambat laun membesar

R cold nodule
Metastasis hematogen ke organ-
organ jauh
Medullary Carcinoma

Dari para follicular cell

Hormon yang dikeluarkan
-Calcitonin - Serotonin
-CEA - Somatostatin
-VIP (Vasoactive Intestinal
Peptide)
Figure 24-21 Medullary carcinoma of thyroid. These tumors typically show a
solid pattern of growth and do not have connective tissue capsules.
(Courtesy of Dr. Joseph Corson, Brigham and Women's Hospital, Boston,
MA.)
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Figure 24-21 Medullary carcinoma of thyroid. These tumors typically show a
solid pattern of growth and do not have connective tissue capsules.
(Courtesy of Dr. Joseph Corson, Brigham and Women's Hospital, Boston,
MA.)
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Morfologi

Soliter type sporadic

Multipel type familial
Jaringan tumor halus, warna abu2-
coklat
Kadang2 nekrosis, perdarahan
Klinis

Nodul di thyroid
Kadang2 disertai diare karena VIP
Type sporadic / MEN tumbuh
agresif
Type familial low grade
Mikroskopis

Sel poligonal, spindle, dalam

sarang/trabekula/folikel
Deposit amiloid ( dari molekul
calcitonin)
Anaplastic Carcinoma :

Sangat agresif
Usia tua, 65 tahun
Sering didahului multinodular goiter
Morfologi :

Large, pleomorfik giant cell

Spindle cell
Small anaplastic cell
Congenital anomali Tiroid

Ductus/cyst thyroglossus
Sisa2 vestigial remnant
Lesi kecil 2-3 cm
Letak antara Glossus -
Thyroid
Parathyroid

Dari kantung pharyngeal, ada 4 kelenjar

Berat 35-40 mg
Terdiri dari - chief cell germal parathormon
- oxyphil cell
Kerja parathyroid dikendalikan oleh Ca ion darah
 Figure 24-24 Parathyroid adenomas are almost always solitary lesions.
Technetium-99m-sestamibi radionuclide scan demonstrates an area of
increased uptake corresponding to the left inferior parathyroid gland
(arrow). This patient had a parathyroid adenoma. Preoperative scintigraphy
is useful in localizing and distinguishing adenomas from parathyroid
hyperplasia, where more than one gland would demonstrate increased
uptake.
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 Figure 24-25 Parathyroid adenoma. A, Solitary chief cell parathyroid
adenoma (low-power photomicrograph) revealing clear delineation from the
residual gland below. B, High-power detail of a chief cell parathyroid
adenoma. There is some slight variation in nuclear size but no anaplasia
and some slight tendency to follicular formation.
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Hormon PTH bekerja :

a. Pada tulang menambah aktivitas

osteoclast
b. Pada ginjal meningkatkan
- resorbsi calcium
- konversi vit D aktif
- ekskresi phosphat
c. Pada usus menambah absorbsi kalsium
 Hiperparatiroidisme primer

Sebabnya :
Adenoma 75-80 %
Hiperplasia10-15 %
Carcinoma 5 %
Usia tersering pada dewasa 50 th lebih
Wanita lebih sering dp laki-laki
Ada faktor radiasi sebelumnya
 Figure 24-26 Cardinal features of hyperparathyroidism.
With routine evaluation of calcium levels in most
patients, primary hyperparathyroidism is often detected
at a clinically silent stage. Hypercalcemia from any other
cause can also give rise to the same symptoms.
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 Morfologi

Tumor soliter, kecil 0,5 5 gr

Lunak, batas jelas, kecoklatan
Mikroskopis :
Sel2 poligonal, uniform
Inti kecil, central
Klinik, dapat berupa :
o A symptomatic hyperparathyroidism
o Symptomatic hyperparathyroidism
Pada symptomatic timbul :
Tulang osteoporosis
Ginjal nephrolithiasis
Gastrointestinal constipasi, ulcus dll
CNS depresi
Neuromuscular lemah
Cardiac kalsifikasi katup
 Terima kasih
Selamat belajar

dr. Jimmy H.W., Sp.PA