Kharisma f lbm 5 modul 8

STEP 1
Lump : benjolan. A piece of solid substance usually with no particular shape
Palpitations : denyutan. A condition in which your heart beat too quickly or not regularly
Stool frequency : a seat without any support for the back or arms (stool)
Tremor : unintentional trembling or shaking movement in one or more parts of your body
STEP 2
Cause of weight loss
Clinical Manifestation
What cause a trembling hands
What is the patogenesis
Why she can't stand the heat ?
How to diagnose for hyperthyroid ?
What is the differential diagnose from the scenario ?
What are the treatment ?
Etiology ?
Diagnosis
What is biosynthesis of T3 and T4 ?
Definition of hyperthyroidism
Why the patient have that clinical manifestation ? explain
Krisis tiroid ?
Explain the hypothyroid

STEP 3
Phase trapping iodide : bassal cell membranes ability to pump specific thyroid iodide actively to the inside of the cell ( iodide transport from the blood into the cells and follicular thyroid glands).
Oxidation stage : change of iodide ion into the oxide from of iodine, iodine either early (nascent iodine) which then is able to bind with the amino acid thyrosine.
This process is enhanced by and accompany peroxidase and hydrogen peroxidase
Phase organification thyroglobulin the binding of iodine with the thyroglobuline molecule iodinate thyrosin process sequency :
Thyrosine diioidnized be monoidothyrosine, then became diiodithyrosine
Occurs chopping of the remaining diiodothyrosine the result of which from the thyroxine molecule
Thyroglobulin storage stage : thyroid hormones are stored in the follicle in sufficient quantities to supply the body with the bodies normal requirements for thyroid hormone for 2-3 months
Thyroxine and triiodothyronine release phase of the thyroid gland : thyroglobulin wasn't released in the blood, thyroxine and triiodothyronine thyroglobuline be broken from the free hormone is then release into the blood
The occurance because of levels of hypermetabolic inside the body where the tyroid hormone stimulates lipolysis.
Because at the time of hormon thyroid increases activate 1 enzyme (Na+ K+ ATP-ase) which cause increase Na+ transport forth and K+ through the cell membran. Because this process requires energy and increase the amount of heat that is formed in the body which is one cause of the increase body metabolism because at HT increasedcause increase mitocondrial size and activity leading to increase metabolism

Increased thyroid hormone increase sensitivity nerve synaps in medulla that regulate muscle tone.

How to diagnose ?
Physical examination revealed
High systole blood pressure
Hyperactive reflects
Increase heart rate
Tremor

In the other hand, blood test also done to measure levels of thyroid hormons ex : TSH, T3 and T4. And it can be this disease may also effect the result of the following test, ex : glucotest, cholesterol test, radioactive iodine uptake

Test :
Serum TSH level where measure by radioimmunometric
Uptake of iodine radioisotop to measure the ability of gland
Thyroid scan

Euthyroid hyperthyroxinemia Goiter
Grave disease
Plummer-Vinson syndrome
Struma ovarii
Tirotoksikosis

Diagnosis
Hyperthyroidism

Hyperthyroidism is a condition in which the thyroid gland makes too much thyroid hormon, the condition is often reffered as an over active thyroid
Hyperthyroidism is a case hypermetabolic that cause increase some endocrine in the thyroid gland, ex : tiroksin, and triiodotiroksin (T3 and T4)
Etiology ?
Graves disease
Tirotoksikosis
Ophtalmophaty infiltrative
Dermophaty Infiltrative
Toxic Multi Nodular Goiter
Solitary toxic adenoma

Hyperthyroidism caused by disfunction of thyroid gland . increased TSH thyroid gland malfunction to be accompanied by decrease TSH and TRF as a negative feedback HT on the release of a both

What is the pathogenesys
As in autoimmune hyperthyroidism a combination of environmental and genetic factor including polymorfism in HLA-DR CTLA-4 CD-25 PTTN-22 and TSHR contribute to briefs disease susceptibility the concordance for Graves disease in monozygote twins is 20-40% compared to <5% in dizygote twins indirect evidence suggest stress is an important environmental factor presumably operating throughn neuroendocrine effects on the immune system.

Sudden weight loss
Tachycardia/rapid heart beat
Increase appetite
Tremor
Sweating
Difficulty sleeping
Skin thinning
Increase sensitivity to heat
Lump in the neck area

Hyperthyroidsim is usualy treat with one/more of the following :
Anti-thyroid medication (prevent thyroid hormon synthesis : inhibiton of peroxidase, thereby inhibiting organification)
Propiltiourasil
Metimazol
Carbimazole

Indication : hyperthyroidism
Contraindication : tracheal damage, lactating mothers, hypersensitivity
Radioactive iodine (emission of beta rays will damage the thyroid gland tissues that hormon production is reduce)
If the patient is >35 years old
Surgery to remove the thyroid
Inhibition anion group ( iodide uptak inhibition mechanism competitively inhibit iodide transport)
Iodide (organification inhibit iodide and release of T3 and T4 hormon)
Beta blockers, this drugs not for hyperthyroid but for the symptoms (tachycardia) and help prevent palpitation.

If the thyroid must be removed with surgery or radioactive we must take thyroid hormon replacement pil for the rest of our live and in the other hand beta blockers such as propanolol are used to treatment some of the symptomps including rapid heart rate and ancient until the hyperthyroidism can be controlled.
Palpitation : T3 adn T4 increase metabolism up accelerate oxygen using increase releasing the amount of final product from tissue metabolism catabolism in long time vasodilatation increase blood stream power of cardiac muscle is forced (ditekan) increase heat rate frequency and kerja jantung meningkat >60%

Uncommon medical emergency caused by an exacerbation of hyperthyroidsim characterized of one or more organ system in people with untreated and or poorly treated hyperthyroidism. Hyperthyroid disease crisis usually occur in patient already known to have hyperthyroidism but may be the first presentation of hyperthyroidism early recognition and agressive treatment are essential.hyperthyroidism can occur in patient w/ toxic adenoma or multinodular toxic goiter but it's more often see in grave disease. Hyperthyroidism crisis classically occurs in patient w/ underlying grave disease or toxic multi nodular goiter often there is sudden onset of sever hyperthyroidism with first hyperpyrexia over 41 celcius, dehidration, heart rate greater 140/minutes, naussea, jundice, abdominal pain, confussion, seizeres(kejang), comma

Uptake tsh >>> tsi <<<

Clinical manifestation

Laboratory checking

Treatment

STEP 7
Phase trapping iodide : bassal cell membranes ability to pump specific thyroid iodide actively to the inside of the cell ( iodide transport from the blood into the cells and follicular thyroid glands).
Oxidation stage : change of iodide ion into the oxide from of iodine, iodine either early (nascent iodine) which then is able to bind with the amino acid thyrosine.
This process is enhanced by and accompany peroxidase and hydrogen peroxidase
Phase organification thyroglobulin the binding of iodine with the thyroglobuline molecule iodinate thyrosin process sequency :
Thyrosine diioidnized be monoidothyrosine, then became diiodithyrosine
Occurs chopping of the remaining diiodothyrosine the result of which from the thyroxine molecule
Thyroglobulin storage stage : thyroid hormones are stored in the follicle in sufficient quantities to supply the body with the bodies normal requirements for thyroid hormone for 2-3 months
Thyroxine and triiodothyronine release phase of the thyroid gland : thyroglobulin wasn't released in the blood, thyroxine and triiodothyronine thyroglobuline be broken from the free hormone is then release into the blood
Increased sympathetic activity and hypermetabolism causes weight loss despite increased appetite.
Robbins n 'Kumar. PATHOLOGY. Vol 2. Edition 7. EGC

Mengapa bb turun walau nafsu makan bertambah?
Peningkatan aktivitas simpatis dan hipermetabolisme menyebabkan penurunan BB walaupun nafsu meningkat.
Robbins n' Kumar. PATOLOGI. Vol 2. Edisi 7. EGC

Because BMR ride that ride thermogenesis. So the body can not stand the heat.
Because of the patient's skin tends to soft thyrotoxicosis, warm, and redness, patients often do not stand the heat.

Mengapa tdk tahan panas ?
Karena BMR naik sehingga thermogenesis naik. Jadi tubuh tidak tahan panas.

Karena pada kulit pasien tirotoksikosis cenderung lunak, hangat, dan kemerahan, pasien sering tidak tahan panas.

Increased thyroid hormone can also increase the strong muscle contractions cause smooth muscle tremor, which is a typical symptom of hyperthyroidism
Due to increased sensitivity of the nerve synapse in the medulla that regulate muscle tone.
Buku Ajar Fisiologi Guyton

Mengapa tangan gemetar?

Peningkatan hormon tiroid juga dapat meningkatkan kontraksi otot yang kuat menimbulkan tremor halus pada otot, yang merupakan gejala khas hipertiroidisme
Disebabkan bertambahnya kepekaan sinaps syaraf di daerah medulla yg mengatur tonus otot.

How to diagnose ?
Physical examination revealed
High systole blood pressure
Hyperactive reflects
Increase heart rate
Tremor

In the other hand, blood test also done to measure levels of thyroid hormons ex : TSH, T3 and T4. And it can be this disease may also effect the result of the following test, ex : glucotest, cholesterol test, radioactive iodine uptake

Test :
Serum TSH level where measure by radioimmunometric
Uptake of iodine radioisotop to measure the ability of gland
Thyroid scan

Euthyroid hyperthyroxinemia Goiter
Grave disease
Plummer-Vinson syndrome
Struma ovarii
Tirotoksikosis

Diagnosis
Hyperthyroidism

Hyperthyroidism refers to conditions caused by excessive thyroid hormone produced by thyroid gland
Most common causes of hyperthyroidism are Graves disease, toxic multinodular goiter, toxic uninodular goiter, and thyroiditis
Less common causes of hyperthyroidism are thyroid-stimulating hormone (TSH)-producing tumors, pituitary resistance to thyroid hormone, trophoblastic disease, and iodine ingestion
Signs and symptoms generally result from stimulation of adrenergic nervous system
Overt hyperthyroidism is defined as low serum TSH with elevated peripheral thyroid hormone values (free T3 and/or free T4), while subclinical hyperthyroidism is defined as low serum TSH with normal peripheral thyroid hormone values
https://www.clinicalkey.com/topics/endocrinology/hyperthyroidism.html

Hyperthyroidism occurs due to an overactive thyroid gland.

In newborns, the cause of hyperthyroidism is the most common neonatal Graves disease. This disease can be fatal and can occur in infants whose mothers suffer or have ever suffered from Graves' disease.
Graves' disease is an autoimmune disease in which the body produces antibodies that stimulate the thyroid gland.
In pregnant women, these antibodies can be up to stimulate the fetus and the fetal thyroid gland.
Graves' disease in the mother can lead to stillbirth, miscarriage or premature birth.

In newborns, the symptoms of an overactive thyroid gland can occur within a few days after birth:
- Do not gain weight
- Rapid heartbeat
- High blood pressure
- Fussy or restless
- vomiting
- Diarrhea.
Mumps can suppress airway and interfere with breathing.
High levels of thyroid hormone can cause rapid heart rate which in turn can lead to heart failure.
As with adults, the newborn, the eyes also stand out.

If the treatment is done, the recovery will happen in a few weeks, but the baby still has a risk of recurrence for 6 months to 1 year.
Thyroid stimulating antibody levels remained high can also cause premature closure of the fontanel, mental retardation, hyperactivity in childhood and slow growth.

Hyperthyroidism treated with propylthiouracil medicine, which serves to inhibit the formation of thyroid hormones.
May also need treatment for heart failure.
If the levels of TSH (thyroid-stimulating hormone) is very high, it may be necessary to replace blood transfusions (number of infant blood removed and replaced with blood from a donor).
WWW.MEDICASTORE.COM

Hipertiroidisme

Hipertiroidisme terjadi karena kelenjar tiroid yang terlalu aktif.

Pada bayi baru lahir, penyebab dari hipertiroidisme yang paling sering ditemukan adalah penyakit Graves neonatorum. Penyakit ini bisa berakibat fatal dan bisa terjadi pada bayi yang ibunya menderita atau pernah menderita penyakit Graves.
Penyakit Graves adalah suatu penyakit autoimun dimana tubuh menghasilkan antibodi yang merangsang kelenjar tiroid.
Pada wanita hamil, antibodi ini bisa sampai ke janin dan merangsang kelenjar tiroid janin.
Penyakit Graves pada ibu bisa menyebabkan lahir mati, keguguran atau kelahiran prematur.

Pada bayi baru lahir, gejala kelenjar tiroid yang terlalu aktif bisa timbul dalam waktu beberapa hari setelah lahir:
- berat badan tidak bertambah
- denyut jantung yang cepat
- tekanan darah tinggi
- rewel atau gelisah
- muntah
- diare.
Gondok bisa menekan saluran udara dan mengganggu proses bernafas.
Kadar hormon tiroid yang tinggi bisa menyebabkan denyut jantung menjadi cepat yang selanjutnya dapat menyebabkan gagal jantung.
Seperti halnya pada dewasa, pada bayi baru lahir, mata juga menonjol.

Jika dilakukan pengobatan, pemulihan akan terjadi dalam beberapa minggu, tetapi bayi tetap memiliki resiko kekambuhan selama 6 bulan sampai 1 tahun.
Kadar antibodi perangsang tiroid yang tetap tinggi juga dapat menyebabkan penutupan dini ubun-ubun, keterbelakangan mental, hiperaktivitas pada masa kanak-kanak dan pertumbuhan yang lambat.

Hipertiroidisme diobati dengan obat propilthiouracyl, yang berfungsi menghambat pembentukan hormon tiroid.
Mungkin juga perlu dilakukan pengobatan terhadap gagal jantung.
Jika kadar TSH (thyroid-stimulating hormone) sangat tinggi, mungkin perlu dilakukan transfusi darah ganti (sejumlah darah bayi dibuang dan diganti dengan darah dari donor).
WWW.MEDICASTORE.COM

Etiology ?
Toxic diffuse goiter or Graves disease
Toxic multinodular
Toxic uninodular goiter (adenoma
Subacute thyroiditis
Postpartum or sporadic thyroiditis
Amiodarone-induced (types I and II
Iatrogenic or factitious thyrotoxicosis
https://www.clinicalkey.com/topics/endocrinology/hyperthyroidism.html

a. Beracun menyebar gondok atau penyakit Graves (paling penyebab umum): suatu penyakit autoimun dimana kelenjar tiroid sedang dirangsang oleh antibodi reseptor thyrotropin, juga dikenal sebagai thyroid-stimulating imunoglobulin
b. Toxic multinodular gondok: beberapa daerah di kelenjar tiroid berlebihan hormon tiroid dengan bebas dari TSH
c. Toxic uninodular gondok (adenoma): nodul soliter pada kelenjar tiroid overproducing hormon tiroid secara independen dari TSH
d. Subakut tiroiditis: biasanya idiopatik tapi kadang-kadang dapat menjadi akibat dari peradangan virally dimediasi dan perusakan kelenjar tiroid. Akibatnya, hormon tiroid disimpan dilepaskan ke dalam sirkulasi, menyebabkan negara thyrotoxic sementara dan nyeri tiroid
e. Postpartum atau sporadis tiroiditis: inflamasi autoimun menyakitkan kelenjar tiroid, di mana hormon tiroid disimpan dilepaskan ke dalam sirkulasi, menyebabkan keadaan thyrotoxic transien
f. Amiodarone-induced (tipe I dan II): Tipe I adalah yodium-induced, sedangkan tipe II adalah jenis tiroiditis
g. Iatrogenik atau tiruan tirotoksikosis: karena konsumsi disengaja atau sengaja hormon tiroid eksogen

What is the pathogenesys
The pathogenesis of hyperthyroidism
The major question to be solved in the pathogenesis of hyperthyroidism is the mechanism
responsible for oversecretion by the thyroid
gland.
Various views have been held in the past depending on successive advances in physiology
and biochemistry. Charcot (1856) regarded the
condition as a neurosis until Moebius pointed
out the associated goitre. The demonstration that
iodine was a component of the thyroid gland
by Baumann in 1895 led eventually to the postulate that the disorder was essentially one of
iodine metabolism. The demonstration by Cannon of the physiological effects of adrenaline
led to the postulate of a mechanism via the sympathetic nervous system. The recognition of
pituitary thyroid control and preparation of
potent pituitary extracts by Evans, Smith and
Smith and others in the early 1920s led to the
claim of experimental production of exophthalmos
and hyperthyroidism in the rat by pituitary extracts (Marine & Rosen, 1934). These findings
led to the postulate of hyperpituitarism as the
mechanism of the disorder (Marine, 1935).
A characteristic feature, recognized after 1950,
is that the hypersecreting gland is not suppressed
by the administration of thyroxine or triiodothyronine, even in very large doses, in contrast to
the normal gland (Werner, 1955). While this property is not always associated with elevated
levels of circulating thyroid hormones it usually
is. Where it is not the gland is hypersecreting
from a small pool of hormone due to previous
surgery, or thyroiditis due to various causes
(Liddle, Heyssel & McKenzie, 1965). This property suggested to Werner (1955) that the thyroid gland itself was at fault and not the pituitary trophic hormone secretion.
The high effectiveness of therapy for thyrotoxicosis based on partial ablation of the thyroid
gland contrasts strikingly with the tendency to
recurrence of hyperadrenalism following partial
ablation of hyperplastic adrenal glands; this observation was in keeping with the suggestion that
the disorder resided within the thyroid itself.
Plummer had originally suggested that exophalmic goitre patients were suffering from 'dysthyroidism' or an abnormal thyroid secretion
(Means, 1937). This and other similar postulates
raises the question of the nature of thyroid
secretion in thyrotoxicosis.
http://pmj.bmj.com/content/44/511/363.full.pdf

Common complaints include fatigue, heat intolerance, sweating, weight loss despite good
appetite, shakiness, inappropriate anxiety, palpitations of the heart, shortness of breath, tetchiness
and agitation, poor sleep, thirst, nausea and increased frequency of defecation. The elderly may
complain predominantly of heart problems with a fast or irregular heart beat, breathlessness and
ankle swelling, whereas children tend to hyperactivity, with a short attention span. Signs include
shaky and hot hands, fast or irregular heart beat, inability to sit still, flushing of the face and upper
trunk, fast tendon reflexes, an enlarged thyroid gland and prominent or bulging eyes. Nowadays
patients often are diagnosed at an early stage of disease, owing to increased awareness and
improved biochemical testing. Therefore some patients have relatively few of the classical signs
or symptoms. In addition, none of the symptoms or signs just listed is sufficiently sensitive or
specific for the diagnosis of hyperthyroidism, even when combined together. Thus, it may take
three to six months to diagnose hyperthyroidism, during this time the person can feel very unwell.
It is not uncommon for people to worry that they have cancer, because of the associated weight
loss.
http://www.british-thyroid-association.org/info-for-patients/Docs/bta_patient_hyperthyroidism.pdf

Betablockers
Betablockers are a group of drugs that tend to improve some of the symptoms and manifestations
of hyperthyroidism. In particular, they can improve palpitations, slow the heart down and improve
tremor. They have no effect on curing the thyroid overactivity, but do make many people feel
better. Betablockers should not be taken if the patient has asthma or a wheezy chest.
Antithyroid drugs
Carbimazole (Neomercazole) and propylthiouracil are antithyroid drugs that are effective in
reducing the production of thyroid hormones in the majority of people with hyperthyroidism. In
people with Graves' disease, treatment with one of these drugs for between 6 months and 2 years
results in a long-term remission in around half of patients, once the drug is stopped.
Both drugs have the common side effects of rash and joint pains, and more rarely (less than 1 in
500 cases) a serious reduction in the circulating white blood cells (agranulocytosis) may occur
during treatment. The dosage of these antithyroid drugs can either be adjusted every 6 to 8 weeks
according to thyroid hormone levels in the blood, to keep the person's thyroid hormone levels in
the normal range (titrated dose regimen) or kept at a fixed, higher dose and levothyroxine
replacement added to maintain normal thyroid hormone levels (block and replace regimen). In
nodular hyperthyroidism (solitary toxic nodule or toxic multinodular goitre), antithyroid drugs do not
result in cure, just a temporary reduction in thyroid hormone levels. A more permanent solution is
often sought, called a definitive treatment.
Radioiodine
Radioiodine is a radioactive isotope of iodine (
131-
I) that is taken up and concentrated selectively by
the thyroid gland. In most people, this small dose of radioactivity is sufficient to gradually destroy
the thyroid tissue, over 6 weeks to 6 months following a single dose. Patients with Graves' disease
have a high rate of permanent thyroid underactivity following radioiodine (about 80%), whereas
patients with nodular thyroid overactivity tend to preserve their thyroid function better, with only
around half eventually becoming underactive. Patients are monitored for underactivity following
the dose and promptly treated with thyroxine, should this develop. The common outcome of
thyroid underactivity is an accepted consequence of radioiodine therapy because hyperthyroidism
is a serious condition whereas replacement treatment with levothyroxine is simple and has no side
effects at the correct dose.
Radioiodine is a safe treatment for thyroid overactivity, with no overall excess of cancers in many
hundreds of thousands of patient years of follow up (JAMA 1998; 280: 347-355; Lancet 1999; 353:
2111-5). Patients with ophthalmopathy require careful evaluation, as radioiodine may worsenthyroid eye disease: this can be prevented by a short course of steroid tablets. There is no
damage to fertility or to hair growth, but women are advised not to become pregnant for 6 months
following a dose, as the baby's thyroid could be damaged. Men should avoid fathering a child
within 4 months of treatment. Following a standard dose of radioiodine, other precautions are
necessary to minimise radiation exposure of others but these restrictions are usually easily
accommodated by the patient. Radioiodine may trigger airport security alarms up to eight weeks
following a dose and patients should carry a letter about the treatment if they travel in this period.
Radioiodine is the most cost effective and certain treatment for thyroid overactivity and about
10,000 doses annually are given in the UK.
Thyroid surgery
Surgery to remove most or all of the thyroid gland (subtotal or total thyroidectomy) is another way
of definitively treating thyroid overactivity. This is a straightforward operation when carried out by
an experienced thyroid surgeon, with a low risk of complications. Hypothyroidism is a recognised
side effect of surgery for which levothyroxine replacement will be needed, lifelong. Thyroidectomy
is a good treatment option for people with a large goitre and for those with thyroid eye disease.
Prior to thyroid surgery, thyroid overactivity needs to be controlled, usually with antithyroid drugs to
make an anaesthetic safe. This is because an anaesthetic in a hyperthyroid person has a high risk
of precipitating a dangerous hyperthyroid crisis or "thyrotoxic storm".
Treatment of thyroiditis
Many forms of thyroiditis are 'self-limiting', meaning that the overactivity recovers spontaneously
and no treatment may be required. If the person has severe symptoms of thyrotoxicosis,
betablockers are helpful. However, in some cases thyroiditis can be painful or prolonged and antiinflammatory tablets or steroids may be helpful. Furthermore, in some cases a period of thyroid
underactivity may follow the thyrotoxicosis, and this may require levothyroxine treatment, if
causing severe symptoms.
Subclinical hyperthyroidism
In subclinical hyperthyroidism, the TSH is suppressed but the free thyroid hormone levels are
normal. Endocrinologists regard this condition as a precursor of overt or clinical hyperthyroidism
but there is some debate over whether this mildest of degree of hyperthyroidism should be treated
(JAMA 2004; 291: 228-238, J Clin Endocrinol Metab. 2007 ;92:3-9.). Further research is being
conducted in this area. At present treatment is a matter for individual clinical evaluation and
discussion between patient and doctor, although there is a consensus that treatment may be
worthwhile in the elderly, particularly if the heart rhythm becomes abnormal or there is thinning of
the bones or low-impact bone fractures.
http://www.british-thyroid-association.org/info-for-patients/Docs/bta_patient_hyperthyroidism.pdf

Palpitation: blood flow, cardiac output, cardiac deny frequency, and volume of blood increases due to increased metabolism in tissue oxygen consumption and increase speed up the final product is released from the tissue. This effect causes vasodilation in most tissues of the body, thus increasing blood flow. Fisiologi Guyton

Chronotropic and inotropic effects on the heart that is adding
increase the force of muscle contraction and heart rhythm.

Palpitation : Aliran darah, Curah jantung, Frekuensi deny jantung, dan Volume darah meningkat karena meningkatnya metabolism dalam jaringan mempercepat pemakaian oksigen dan memperbanyak produk akhir yang dilepas dari jaringan. Efek ini menyebabkan vasodilatasi pada sebagian besar jaringan tubuh, sehingga meningkatkan aliran darah. Guyton
Efek kronotropik dan Inotropik terhadap jantung yaitu menambah
kekuatan kontraksi otot dan menambah irama jantung.

It is difficult to sleep: Effects on sleep
Because of the exhausting effects of thyroid hormone on muscle and central nervous system, the hyperthyroid patients often feel tired constantly, but because of the effects of thyroid hormone on the excitation of the synapse, sleep difficulties arise. In contrast, a typical symptom of severe somnolence hypothyroidism, accompanied by bedtime that lasts for 12-14 hours a day.
-FISIOLOGI KEDOKTERAN, Guyton-

Sukar tidur: Efek pada tidur
Oleh karena efek yang melelahkan dari hormone tiroid pada otot dan system saraf pusat, maka pasien hipertiroid sering merasa lelah terus menerus, tetapi karena efek eksitasi dari hormone tiroid pada sinaps, timbul kesulitan tidur. Sebaliknya, somnolen berat merupakan gejala khas hipotiroidisme, disertai dengan waktu tidur yang berlangsung selama 12-14 jam sehari.

-FISIOLOGI KEDOKTERAN, Guyton-

Why succumb hot?
Because BMR ride that ride thermogenesis. So the body can not stand the heat.

Because of the patient's skin tends to soft thyrotoxicosis, warm, and redness, patients often do not stand the heat.

Mengapa tdk tahan panas ?
Karena BMR naik sehingga thermogenesis naik. Jadi tubuh tidak tahan panas.

Karena pada kulit pasien tirotoksikosis cenderung lunak, hangat, dan kemerahan, pasien sering tidak tahan panas.

Why do a lot of sweat?
Associated with central nervous system (causing the dissociation of mind) anxiety and psychoneurotic, paranoia always restless and sweating
Guyton Textbook of Physiology

Mengapa banyak keringat?
Berhubungan dengan sistem saraf pusat (menimbulkan disosiasi pikiran) cemas dan psikoneurotik, paranoia selalu gelisah dan berkeringat

Why accomplish?
Because the debilitating effects of thyroid hormone on the muscle and the central nervous system of patients with hyper thyroid feel tired continuously.

Mengapa capai?
Karena efek yg melelahkan dari hormone tiroid pada otot dan system syaraf pusat maka pasien dengan hiper tiroid merasa lelah terus menerus.

Why is it weak?
Muscles in patients with hyperthyroidism will be weakened due to protein catabolism superfluous.

Mengapa lemah?
Otot otot pada penderita hipertiroid akan menjadi lemah dikarenakan adanya proses katabolisme protein yg berlebihan.

Why shaking hands?

Increased thyroid hormone can also increase the strong muscle contractions cause smooth muscle tremor, which is a typical symptom of hyperthyroidism
Due to increased sensitivity of the nerve synapse in the medulla that regulate muscle tone.

Mengapa tangan gemetar?

Peningkatan hormon tiroid juga dapat meningkatkan kontraksi otot yang kuat menimbulkan tremor halus pada otot, yang merupakan gejala khas hipertiroidisme
Disebabkan bertambahnya kepekaan sinaps syaraf di daerah medulla yg mengatur tonus otot.

Why weight loss but increased appetite?
Increased sympathetic activity and hypermetabolism causes weight loss despite increased appetite.

Mengapa bb turun walau nafsu makan bertambah?
Peningkatan aktivitas simpatis dan hipermetabolisme menyebabkan penurunan BB walaupun nafsu meningkat.

Mengapa sering BAB?

Efek Gastrointestinal
Hormon tiroid merangsang motilitas usus, yang dapat menimbuklan
peningkatan motilitas dan diare pada hipertiroidisme dan memperlambat transit
usus serta konstipasi pada hipotiroidisme. Hal ini juga menyumbang pada
timbulnya penurunan berat badan yang sedang pada hipertiroidisme dan
pertambahan berat pada hipotiroidisme.

Pada saluran cerna, selain dapat meningkatkan nafsu
makan dan asupan makanan, hormone tiroid yang
meningatkat dapat mempercepat sekresi getah
pencernaan dan pergerakan saluran cerna, sehingga
sering terjadi diare

Mengapa sesak nafas bila kerja fisik?

Uncommon medical emergency caused by an exacerbation of hyperthyroidsim characterized of one or more organ system in people with untreated and or poorly treated hyperthyroidism. Hyperthyroid disease crisis usually occur in patient already known to have hyperthyroidism but may be the first presentation of hyperthyroidism early recognition and agressive treatment are essential.hyperthyroidism can occur in patient w/ toxic adenoma or multinodular toxic goiter but it's more often see in grave disease. Hyperthyroidism crisis classically occurs in patient w/ underlying grave disease or toxic multi nodular goiter often there is sudden onset of sever hyperthyroidism with first hyperpyrexia over 41 celcius, dehidration, heart rate greater 140/minutes, naussea, jundice, abdominal pain, confussion, seizeres(kejang), comma
Krisis tiroid ?

A. definition
Thyroid crisis is a situation most severe clinical hyperthyroidism life-threatening, this generally occurs in patients with Graves' disease foundation or toxic multinodular goitre, and is associated with precipitating factors: infection, surgery, trauma, substance iodized contrast, hypoglycemia, parturition, emotional stress, cessation of anti-thyroid drugs, ketoacidosis, pulmonary thromboembolism, cerebrovascular disease / stroke, thyroid palpas too strong.

Definisi
Krisis tiroid merupakan suatu keadaan klinis hipertiroidisme yang paling berat mengancam jiwa, umumnya ini timbul pada pasien dengan dasar penyakit Graves atau Struma multinodular toksik, dan berhubungan dengan faktor pencetus : infeksi, operasi, trauma, zat kontras beriodium, hipoglikemia, partus, stress emosi, penghentian obat anti tiroid, ketoasidosis, tromboemboli paru, penyakit serebrovaskuler/strok, palpas tiroid terlalu kuat.

B. etiology
Thyroid crisis can occur due to dysfunction of the thyroid gland, the pituitary, or hypothalamus, increased TSH thyroid gland malfunctions due to be accompanied by decreased TSH and TRF as a negative feedback on the release of both HT.
Thyroid crisis due to malfunctions hipofisi gives an overview of HT and TSH levels are high. TRF will be low because of negative feedback from HT and TSH. Thyroid crisis due to malfunctioning hypothalamus will show a high HT accompanied by excessive TSH and TRH.
1. The main cause of
a. Grave's disease
b. Toxic multinodular
c. "Solitary toxic adenoma"
2. other causes
a. thyroiditis
b. troboblastis disease
c. Excessive intake of thyroid hormone
d. Excessive iodine consumption
e. pituitary cancer
f. Drugs such as amiodarone

Etiologi
Krisis tiroid dapat terjadi akibat disfungsi kelenjar tiroid, hipofisis, atau hipotalamus, peningkatan TSH akibat malfungsi kelenjar tiroid akan disertai penurunan TSH dan TRF karena umpan balik negatif HT terhadap pelepasan keduanya.
Krisis tiroid akibat malfungsi hipofisi memberikan gambaran kadar HT dan TSH yang tinggi. TRF akan rendah karena umpan balik negatif dari HT dan TSH. Krisis tiroid akibat malfungsi hipotalamus akan memperlihatkan HT yang tinggi disertai TSH dan TRH yang berlebihan.
Penyebab utama
Penyakit Grave
Toxic multinodular
"Solitary toxic adenoma"
Penyebab lain
Tiroiditis
Penyakit troboblastis
Ambilan hormon tiroid secara berlebihan
Pemakaian yodium yang berlebihan
Kanker pituitari
Obat-obatan seperti Amiodarone

Patofisiologi

Peningkatan suhu tubuhPeningkatan suhu tubuhSuplai nutrisi yang tidak adekuatSuplai nutrisi yang tidak adekuatG3 body imageG3 body imagePerubahan pola kerja jantung dan paruPerubahan pola kerja jantung dan paruKetidakstabilan emosiKetidakstabilan emosiPerubahan pola nutrisiPerubahan pola nutrisiG3 organik kelenjar tiroidG3 organik kelenjar tiroidG3 Fungsi Hipotalamus /hipofisiG3 Fungsi Hipotalamus /hipofisiProduksi TSH meningkatProduksi TSH meningkatProduksi hormone tiroid meningkatProduksi hormone tiroid meningkatMetabolisme tubuh meningkatMetabolisme tubuh meningkatProses glikogenesismeningkatProses glikogenesismeningkatProduksi kalor meningkatProduksi kalor meningkatAktifitas GI meningkatAktifitas GI meningkatNafsu makan meningkatNafsu makan meningkatG3 pola kognitifG3 pola kognitifG3 rasa nyaman panasG3 rasa nyaman panasPenurunan berat badanPenurunan berat badanProses pembakaran lemak meningkatProses pembakaran lemak meningkat
Peningkatan suhu tubuh
Peningkatan suhu tubuh
Suplai nutrisi yang tidak adekuat
Suplai nutrisi yang tidak adekuat
G3 body image
G3 body image
Perubahan pola kerja jantung dan paru
Perubahan pola kerja jantung dan paru
Ketidakstabilan emosi
Ketidakstabilan emosi
Perubahan pola nutrisi
Perubahan pola nutrisi
G3 organik kelenjar tiroid
G3 organik kelenjar tiroid
G3 Fungsi Hipotalamus /hipofisi
G3 Fungsi Hipotalamus /hipofisi
Produksi TSH meningkat
Produksi TSH meningkat
Produksi hormone
tiroid meningkat
Produksi hormone
tiroid meningkat
Metabolisme tubuh meningkat
Metabolisme tubuh meningkat
Proses glikogenesis
meningkat
Proses glikogenesis
meningkat
Produksi kalor meningkat
Produksi kalor meningkat
Aktifitas GI meningkat
Aktifitas GI meningkat
Nafsu makan meningkat
Nafsu makan meningkat
G3 pola kognitif
G3 pola kognitif
G3 rasa nyaman panas
G3 rasa nyaman panas
Penurunan berat badan
Penurunan berat badan
Proses pembakaran lemak meningkat
Proses pembakaran lemak meningkat

Clinical manifestations
1. Increased heart rate
2. Increased muscle tone, tremor, irritability, increased sensitivity to catecholamines
3. Increase in basal metabolic rate, increased heat generation, heat intolerance, excessive sweating
4. Weight loss, increased hunger (good appetite)
5. Increased frequency of bowel movements
6. Goiter (usually), which increased the size of the thyroid gland
7. reproductive disorders
8. Can not stand the heat
9. rapid fatigue
10. sign bruit
11. Menstruation bit and not fixed
12. Enlargement of the thyroid gland
13. Bulging eyes (exoptalmus)

Manifestasi klinis
Peningkatan frekuensi denyut jantung
Peningkatan tonus otot, tremor, iritabilitas, peningkatan kepekaan terhadap katekolamin
Peningkatan laju metabolisme basal, peningkatan pembentukan panas, intoleran terhadap panas, keringat berlebihan
Penurunan berat, peningkatan rasa lapar (nafsu makan baik)
Peningkatan frekuensi buang air besar
Gondok (biasanya), yaitu peningkatan ukuran kelenjar tiroid
Gangguan reproduksi
Tidak tahan panas
Cepat letih
Tanda bruit
Haid sedikit dan tidak tetap
Pembesaran kelenjar tiroid
Mata melotot (exoptalmus)

Diagnostic examination
Diagnosis depends on several hormones following:
Blood tests that measure levels of HT (T3 and T4), TSH, and TRH will confirm the diagnosis and localization problems at the state level or central nervous system thyroid gland.
1. TSH (Thyroid Stimulating Hormone)
2. Free T4 (thyroxine)
3. Free T3 (triiodothyronine)
4. Diagnosis may also be made using ultrabunyi to ensure the enlargement of the thyroid gland
5. Thyroid scan to see an enlarged thyroid gland
6. Hyperthyroidism can be accompanied by decreased serum lipid levels
7. Decrease in sensitivity to insulin, which can cause hyperglycemia

Pemeriksaan Diagnostik
Diagnosa bergantung kepada beberapa hormon berikut ini :
Pemeriksaan darah yang mengukur kadar HT (T3 dan T4), TSH, dan TRH akan memastikan diagnosis keadaan dan lokalisasi masalah di tingkat susunan saraf pusat atau kelenjar tiroid.
TSH(Tiroid Stimulating Hormone)
Bebas T4 (tiroksin)
Bebas T3 (triiodotironin)
Diagnosa juga boleh dibuat menggunakan ultrabunyi untuk memastikan pembesaran kelenjar tiroid
Tiroid scan untuk melihat pembesaran kelenjar tiroid
Hipertiroidisme dapat disertai penurunan kadar lemak serum
Penurunan kepekaan terhadap insulin, yang dapat menyebabkan hiperglikemia
Complication
Complications of thyroid crisis can be life threatening is thyrotoxic crisis (thyroid storm). It can berkernbang spontaneously hyperthyroid patients who underwent therapy, surgery for thyroid gland, or hyperthyroidism occur in patients who are not diagnosed. The result is the release of HT in very large numbers that cause tachycardia, agitation, tremors, hyperthermia (up to 106 ° F), and, if untreated, death.
Heart disease Hyperthyroidism, Graves oftalmopati, dermopati Graves, in the treatment of infections due to agranulocytosis with antithyroid drugs. Thyroid crisis: mortality

Komplikasi
Komplikasi Krisis tiroid yang dapat mengancam nyawa adalah krisis tirotoksik (thyroid storm). Hal ini dapat berkernbang secara spontan pada pasien hipertiroid yang menjalani terapi, selama pembedahan kelenjar tiroid, atau terjadi pada pasien hipertiroid yang tidak terdiagnosis. Akibatnya adalah pelepasan HT dalam jumlah yang sangat besar yang menyebabkan takikardia, agitasi, tremor, hipertermia (sampai 106°F), dan, apabila tidak diobati, kematian.
Penyakit jantung Hipertiroid, oftalmopati Graves, dermopati Graves, infeksi karena agranulositosis pada pengobatan dengan obat antitiroid. Krisis tiroid : mortalitas

Management
1. conservative
Governance Graves disease
a. Anti-thyroid drugs. This drug inhibits the production of thyroid hormones. If excessive doses, patients experience symptoms of drug hipotiroidisme.Contoh are as follows:
1) Thioamide
2) Methimazole initial dose of 20 -30 mg / day
3) Propylthiouracil (PTU) initial dose of 300-600 mg / day, the maximum dose of 2,000 mg / day
4) Potassium Iodide
5) Sodium Ipodate
6) Anion Inhibitors
b. Beta-adrenergic receptor antagonist. This medication is to reduce the symptoms of hypothyroidism. Example: Propranolol
2. Surgical
a. Radioactive iodine.
This action is to destroy the thyroid gland is hyperactive
b. Thyroidectomy.
Surgery action is to remove the thyroid gland is enlarged

Penatalaksanaan
Konservatif
Tata laksana penyakit Graves
Obat Anti-Tiroid. Obat ini menghambat produksi hormon tiroid. Jika dosis berlebih, pasien mengalami gejala hipotiroidisme.Contoh obat adalah sebagai berikut :
Thioamide
Methimazole dosis awal 20 -30 mg/hari
Propylthiouracil (PTU) dosis awal 300 – 600 mg/hari, dosis maksimal 2.000 mg/hari
Potassium Iodide
Sodium Ipodate
Anion Inhibitor
Beta-adrenergic reseptor antagonist. Obat ini adalah untuk mengurangi gejala-gejala hipotiroidisme. Contoh: Propanolol
Surgical
Radioaktif iodine.
Tindakan ini adalah untuk memusnahkan kelenjar tiroid yang hiperaktif
Tiroidektomi.
Tindakan Pembedahan ini untuk mengangkat kelenjar tiroid yang membesar

Sumber:
Bare & Suzanne, 2002, Buku Ajar Keperawatan Medikal Bedah, Volume 2, (Edisi 8), EGC, Jakarta.
Carpenito, 1999, Rencana Asuhan dan Dokumentasi Keperawatan, (Edisi 2), EGC, Jakarta
Corwin,. J. Elizabeth, 2001, Patofisiologi, EGC, Jakarta
Doenges, E. Marilynn dan MF. Moorhouse, 2001, Rencana Asuhan Keperawatan, (Edisi III), EGC, Jakarta.
FKUI, 1979, Patologi, FKUI, Jakarta

Explain the hypothyroid

Hypothyroidism is a disease caused by a disturbance in one of the levels of the hypothalamic-pituitary-thyroid-"end organ", with the result of thyroid hormone deficiency, or impaired tissue response to thyroid hormone.
According onset, hypothyroidism in children can be divided into two:
1. Congenital hypothyroidism.
2. Acquired hypothyroidism.

Hipotiroid adalah suatu penyakit yang disebabkan oleh gangguan pada salah satu tingkat dari aksis hipotalamus-hipofisis-tiroid-"end organ", dengan akibat terjadinya defisiensi hormon tiroid, ataupun gangguan respon jaringan terhadap hormon tiroid.
Menurut onsetnya, hipotiroid pada anak dibedakan menjadi 2 :
Hipotiroid kongenital.
Hipotiroid dapatan.

Pathophysiology
Hypothyroidism can be caused by disruption of thyroid hormone synthesis or disruption of tissue response to thyroid hormone.
Synthesis of thyroid hormones is regulated as follows:
- The hypothalamus makes "thyrotropin releasing hormone (TRH)" which stimulates the anterior pituitary.
- Anterior pituitary synthesize thyrotropin ("TSH = thyroid stimulating hormone") which stimulates the thyroid gland.
- The thyroid gland to synthesize thyroid hormone ("triiodothyronin = T3 = T4 = tetraiodothyronin and thyroxin") which stimulates metabolism network includes: oxygen consumption, body heat production, nerve function, metabolism protrein, carbohydrates, fats, and vitamins, as well as work than other hormones.

PATOFISIOLOGI
Hipotiroid dapat disebabkan oleh gangguan sintesis hormon tiroid atau gangguan pada respon jaringan terhadap hormon tiroid.
Sintesis hormon tiroid diatur sebagai berikut :
- Hipotalamus membuat "thyrotropin releasing hormone (TRH)" yang merangsang hipofisis anterior.
- Hipofisis anterior mensintesis thyrotropin ("thyroid stimulating hormone = TSH") yang merangsang kelenjar tiroid.
- Kelenjar tiroid mensintesis hormone tiroid ("triiodothyronin = T3 dan tetraiodothyronin = T4 = thyroxin") yang merangsang metabolisme jaringan yang meliputi : konsumsi oksigen, produksi panas tubuh, fungsi syaraf, metabolisme protrein, karbohidrat, lemak, dan vitamin-vitamin, serta kerja daripada hormon-hormon lain.

Clinical Symptoms
History and symptoms in neonates and infants:
- Fontanella major wide open posterior fontanel.
- Rectal temperature <35.5 ˚ C within 0-45 hours after birth.
- Birth weight> 3500 g; gestation> 40 weeks.
- Big and husky voice.
- Umbilical hernia.
- History of jaundice more than 3 days.
- Miksedema.
- Makroglosi.
- First Chapter History> 20 hours after birth and constipation (<1 time / day).
- Dry skin, cold, and "motling" (Stained-spotting).
- Lethargy.
- It is difficult to drink.
- Bradycardia (<100/minute).
Early diagnosis and treatment is important to prevent permanent mental patients.
Symptoms in older children:
- With or without goiter goiter.
- Impaired growth (dwarf).
- Impaired motor development, mental, teeth, bones, and puberty.
- Permanent disturbance of mental development, especially when onset occurs before the age of 3 years.
- Reduced activity, slow.
- Dry skin.
- Miksedema.
- Low blood pressure, low metabolism.
- Intolerance to cold.
The causes of hypothyroidism:
- The causes of congenital (congenital):
o Disgenetik thyroid gland: ectopic, agenesis, or hipoplasi aplasi.
o Dishormonogenesis.
o 'the hypothalamic-pituitary hypothyroidism'.
o Be temporary:
Induction drugs.
maternal antibodies.
Idiopathic.
o Mother gets
Material goitrogen.
Treatment of radio-active iodine.
- The causes of acquired ("acquired"):
o chronic lymphocytic thyroiditis.
o goitrogen materials (iodine, tiourasil, etc.).
o Thyroidectomy.
o infiltrative disease (sistinosis, histiositosis-X).
o iodine deficiency (endemic goiter).
o "euthyroid sick syndrome".
o hypopituitarism

GEJALA KLINIS
Riwayat dan gejala pada neonatus dan bayi :
- Fontanella mayor yang lebar dan fontanella posterior yang terbuka.
- Suhu rektal < 35,5˚C dalam 0-45 jam pasca lahir.
- Berat badan lahir > 3500 gram; masa kehamilan > 40 minggu.
- Suara besar dan parau.
- Hernia umbilikalis.
- Riwayat ikterus lebih dari 3 hari.
- Miksedema.
- Makroglosi.
- Riwayat BAB pertama > 20 jam setelah lahir dan sembelit (< 1 kali/hari).
- Kulit kering, dingin, dan "motling" (berbercak-bercak).
- Letargi.
- Sukar minum.
- Bradikardia (< 100/menit).
Diagnosis dan pengobatan dini penting untuk mencegah mental yang permanen pada penderita.
Gejala pada anak besar :
- Dengan goiter maupun tanpa goiter.
- Gangguan pertumbuhan (kerdil).
- Gangguan perkembangan motorik, mental, gigi, tulang, dan pubertas.
- Ganguan perkembangan mental permanen terutama bila onset terjadi sebelum umur 3 tahun.
- Aktivitas berkurang, lambat.
- Kulit kering.
- Miksedema.
- Tekanan darah rendah, metabolisme rendah.
- Intoleransi terhadap dingin.
Sebab-sebab hipotiroid :
- Sebab-sebab bawaan (kongenital) :
o Disgenetik kelenjar tiroid: ektopik, agenesis, aplasi atau hipoplasi.
o Dishormonogenesis.
o 'Hypothalamic-pituitary hypothyroidism'.
o Bersifat sementara :
Induksi obat-obatan.
Antibodi maternal.
Idiopatik.
o Ibu mendapat
Bahan goitrogen.
Pengobatan yodium radio-aktif.
- Sebab-sebab yang didapat ("acquired"):
o Tiroiditis limfositik menahun.
o Bahan-bahan goitrogen (yodium, tiourasil, dsb).
o Tiroidektomi.
o Penyakit infiltratif (sistinosis, histiositosis-X).
o Defisiensi yodium (gondok endemik).
o "Euthyroid sick syndrome".
o Hipopituitarisme

MANAGEMENT
Thyroid hormone
Drug of choice is L-Thyroxine Sodium, given as early as possible.
1. When the facility to measure thyroid function there, given the dose as the following table:

Umur
Dosis µg/kg BB/hari
0-3 bulan
3-6 bulan
6-12 bulan
1-5 tahun
2-12 tahun
> 12 tahun
10-15
8-10
6-8
5-6
4-5
2-3

T4 levels maintained in the mid-normal values.

2. When the facility to measure thyroid function does not exist, it can be done therapeutic trial until the age of 3 years starting with a low dose in 2-3 weeks; when there is clinical improvement, the dose can be increased gradually or at a dose of 100 + μg/m2/hari administration.
Thyroxine dose adjustment based on clinical response of thyroid function tests T3, T4, and TSH which can vary depending on the etiology of hypothyroidism.
http://old.pediatrik.com/isi03.php?page=html&hkategori=pdt&direktori=pdt&filepdf=0&pdf=&html=07110-buoi228.htm

PENATALAKSANAAN
Hormon tiroid
Obat pilihan adalah Sodium L-Thyroxine, diberikan sedini mungkin.
1. Bila fasilitas untuk mengukur faal tiroid ada, diberikan dosis seperti tabel berikut :
Umur
Dosis µg/kg BB/hari
0-3 bulan
3-6 bulan
6-12 bulan
1-5 tahun
2-12 tahun
> 12 tahun
10-15
8-10
6-8
5-6
4-5
2-3

Kadar T4 dipertahankan di atas pertengahan nilai normal.
2. Bila fasilitas untuk mengukur faal tiroid tidak ada, dapat dilakukan therapeutic trial sampai usia 3 tahun dimulai dengan dosis rendah dalam 2-3 minggu; bila ada perbaikan klinis, dosis dapat ditingkatkan bertahap atau dengan dosis pemberian + 100 μg/m2/hari.
Penyesuaian dosis tiroksin berdasarkan respon klinik dari uji fungsi tiroid T3, T4, dan TSH yang dapat berbeda tergantung dari etiologi hipotiroid.
http://old.pediatrik.com/isi03.php?page=html&hkategori=pdt&direktori=pdt&filepdf=0&pdf=&html=07110-buoi228.htm
DAFTAR PUSTAKA
1. Fisher DA. Disorders of the Thyroid in the Newborn and Infant. In : Sperling MA, ed. Pediatric Endocrinology. Philadelphia : Saunders, 2002 : 161-82.
2. Styne DM. Disorders of the Thyroid Gland. In: Core Handbooks in Pediatrics – Pediatric Endocrinology. Philadelphia : Lippincott Williams & Wilkins, 2004 : 83-108.
3. Rossi WC, Caplin N, Alter CA. Thyroid Disorders in Children. In: Moshang T, ed. Pediatric Endocrinology – The Requisites in Pediatrics. St Louis, Missouri: Elsevier Mosby, 2005 : 171-90.
4. Fort PF, Brown RS.Thyroid Disorders in Infancy. In : Lifshitz F, ed. Pediatric Endocrinology. New York : Marcel Dekker, 1996 : 369-81.

Kharisma f lbm 5 modul 8

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