Peny. Jantung REUMATIK dan Peny. Jantung TIROID Dr. T. Realsyah R, SpPD

PendahuluanDemam Rematik proses radang akut tenggorokan yang didahului oleh infeksi kuman streptokokus beta hemolitikus grup A

penyakit multi-organ, hanya kecacatan pada jantung yang permanen

mayoritas penyakit jantung yang diperoleh pada anak-anak, yang berdampak besar terhadap morbiditas dan mortalitas.

Penyakit Jantung RematikPenyakit Jantung Rematik kronikmerupakan residual sequele dari demam rematik akut, dan diperkirakan 282.000 penderita demam rematik akan menderita PJR setiap tahunnya

Meski banyak penderita PJR yang tidak dapat mengingat/mengetahui riwayat demam rematik sebelumnya

Epidemiologi1994: 12 juta penderita penyakit jantung rematik 4

2005:15 hingga 19 juta penderita,

Indonesia:0,3-0,8 diantara 1000 anak sekolah Indonesia menderita demam rematik 2

2.4 juta berusia 5-14 tahun79% diantaranya dari negara berkembang

DEMAM REUMATIK : - >> 5 15 THN.- DAN JARANG < 5 THN.

MANIFESTASI KLINIS :- ARTRITIS (70%)- KARDITIS (50%)- KHOREA (15%)- NODULUS SUBKUTAN & ERITEM MARGINATUM (5%)

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DIAGNOSIS PJR

RIW. DEMAM REUMATIK

KRITERIA JONES (2 MAYOR ATAU 1 MAYOR + 2 MINOR)4

TAB. 1. KRITERIA JONES5

KRITERIA MAYORKRITERIA MINORKARDITISPOLIARTRITISKHOREANOD. SUBKUTANERIT. MARGINATUMDEMAMARTHALGIINT. P-R MEMANJANG REAKTAN FASE AKUTDITAMBAH BUKTI INF. STREPTOKOKUS :BIAKAN FARING (+) STREPT.ASTO

Diagosis karditis :. Perubahan sifat bising jantung organik. Ukuran jantung bertambah. Bising gesek perikardial/efusi perikardial. Tanda gagal jantung kongestif

Nodul subkutan : nodul kecil, seukuran kacang, lokasi pada tendo ekstensor tangan, kaki, siku, tepi patela, kulit kepala.

Khorea : gangguan sistim syaraf pusat yang ditandai gerakan tiba-tiba, tanpa tujuan, tidak teratur, kelemahan otot, emosi tak stabil.

Eritem marginatum : ruam merah bersifat sementara, berpindah-pindah, tidak gatal, tidak indurasi, memucat pada tekanan.

Test antibodi streptokokus : standarisasi paling luas digunakan Pasien DR titer > 200 unit/ ml.

FOTO THORAX UKURAN JANTUNG

EKG PEMANJANGAN INT. P R

EKOKARDIOGRAFI DOPPLER :- RUANGAN JANTUNG- FUNGSI VENTRIKEL- DERAJAT REGURGITASI KATUP

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PENATALAKSANAAN :1. ISTIRAHAT2. ERADIKASI KUMAN 3. ANTI RADANG4. SUPORTIF5. PROFILAKSIS SEKUNDER6. PENYULUHAN7. OPERASI7

TERAPI1 Salisilat2. Penisilin (Tx AHA): Anak anak: Benzathin penicilline 600.000-900.000 U Dewasa: Benzathin penicilline 1,2 juta U Ataau : oral Penicilline 4 x 250 mg/ hari (10 hari) atau kombinasi IM daan oral (10 hari) Bila alergi peniciline eritromisin 4 x 250 mg (10 hari)3. Kortikosteroid 4. Bed rest 5. TKTP6. Penenang untuk chorea

PROFILAKSIS TERHADAP KEKAMBUHANJauhi penderita URIPenisilin Pada non RHD: min 3-5 tahun Pada RHD, resiko tinggi: selama mungkin3. Sulfonamides4. Pengobatan sedini mungkin URI

ANTIBIOTIKA PADA DEMAM RHEUMA AKUTPenisilin diberikan selama perjalanan penyakit untuk eradikasi streptokokus.Injeksi Benzathin Penisilin G 1,2 juta unit sekali. Pilihan obat per oral adalah penisilin G 200.000-250.000 unit 4 kali shariBagi penderita yang alergi terhadap penisilin dapat diberi eritromisin 250 mg 4 kali sehariLama pengobatan 10 hari.

Report of a WHO Expert Consultation Geneva 10 October 1 November 2001World Health Organization. Geneva 2004

Prevensi PrimerReport of a WHO Expert Consultation Geneva 10 October 1 November 2001World Health Organization. Geneva 2004

Profilaksis SekunderReport of a WHO Expert Consultation Geneva 10 October 1 November 2001World Health Organization. Geneva 2004

Durasi ProfilaksisReport of a WHO Expert Consultation Geneva 10 October 1 November 2001World Health Organization. Geneva 2004

Peny. Jantung Thyroid

ACTION OF THYROID HORMONE Two active hormones are secreted by the thyroid: thyroxine (T4) and triiodothyronine (T3). Most studies support the hypothesis that T3 is the final mediator and T4 is a prohormone,

Thyroid hormone's effectThyroid hormone (TH) can have a (+) or (-) effect on regulating gene transcription.

Positive effects : myosin heavy-chain alpha, Ca2+-ATPase, Na+, K+-ATPase, beta1-adrenergic receptor, glucose transporter, cardiac troponin, and atrial natriuretic protein.

Negative effects regulate genes, e.g., myosin heavy-chain beta and the glucose transporter Glut-1.

Thyroid Extranuclear ActionsT3 increases both glucose and Ca uptake by the heart.

Extranuclear effects include THs direct effect on Ca current and cytosolic Ca changes induced by inotropic factors.

RELATIONSHIP BETWEEN THE THYROID AND THE SYMPATHETIC NERVOUS SYSTEM The effects of TH on the heart are indirect and secondary to changes in activity of the sympathetic nervous system. The cardiovascular effects of hyperthyroidism, i.e., tachycardia, systolic hypertension, increased cardiac output, and myocardial contractility, can be abolished or reduced by blocking the activity of the sympathetic nervous system. TH is increasing the activity of the sympathoadrenal system or by enhancing the response of cardiac tissue to normal sympathetic stimulation.

RELATIONSHIP BETWEEN THE THYROID AND THE SYMPATHETIC NERVOUS SYSTEMTH's effect in three areas has been explored: adrenergic output, adrenergic receptors, and adrenergic transduction mechanisms.

Administration of TH causes an increase in both the number of receptors and their affinity for their ligand, while hypothyroidism induces the opposite effect.

TH also increases mRNA levels for the beta1-adrenergic receptor.

RELATIONSHIP BETWEEN THE THYROID AND THE SYMPATHETIC NERVOUS SYSTEMChanges in receptor number and affinity then lead to changes in sensitivity of the myocardium to beta adrenoceptor agonists. For example, stimulation of adenylate cyclase activity by isoproterenol is increased in hyperthyroidism and reduced in hypothyroidism. Changes are also seen in the force of contraction. These effects were also observed in vivo in dogs, in which propranolol-induced reductions in heart rate and myocardial contractility were greater in hyperthyroid than euthyroid animals.

Effect of Thyroid Hormone on the Heart T4 enhances the rate of contraction of cardiac muscle, even in the presence of adrenergic blockade. The major actions of T4 on the left ventricle are (1) a direct (+) inotropic effect and (2) an increase in the size of the ventricular cavity without a change in end-diastolic pressure or length of the sarcomere in diastole.

Effect of Thyroid Hormone on the HeartThe direct effect of thyroid hormone on the heart is primarily mediated via a change in protein synthesis. Specifically, synthesis of myosin heavy chains is changed from the beta to the alpha form.

Effect of Thyroid Hormone on the HeartTH increases expression of Na-Ca-ATPase, which augments trans-sarcolemmal Ca influx in cultured ventricular cells. TH modifies the electrical activity of the heart by several mechanisms.It increases recruitment of slower inactivating Na channels. It modifies the expression and/or composition and thereby the activity of one or more K channels and several Ca channels. These effects probably result from altered gene transcription because of TH.

Effect of Thyroid Hormone on the HeartThe tachycardia in hyperthyroidism appears to be due to an increased rate of diastolic depolarization and a decreased duration of the action potential in the SA node cells.

The propensity for the development of AF may be due to the shortened refractory period of atrial cells.

HyperthyroidismHyperthyroidism is a relatively common disease that occurs more often in women than men, with a peak incidence in the third and fourth decades. Signs and symptoms : fatigue, hyperactivity, insomnia, heat intolerance, palpitations, dyspnea, increased appetite with weight loss, nocturia, diarrhea, oligomenorrhea, muscle weakness, tremor, emotional lability, increased heart rate, systolic hypertension, hyperthermia, warm moist skin. Hyperthyroidism is the clinical state resulting from excess production of T4, T3 or both. The most common cause is a diffuse toxic goiter The second most common form of hyperthyroidism is nodular toxic goiterSerum T4 levels are increased and serum TSH is suppressed.

CARDIOVASCULAR MANIFESTATIONSCardiovascular signs and symptoms are therefore important clinical features of hyperthyroidism.Palpitations, dyspnea, tachycardia, and systolic hypertension are common findings. Diastolic hypertension can also occur. Typically noted are a hyperactive precordium with a loud first heart sound, a third heart sound; occasionally, a systolic ejection click is heard.

CARDIOVASCULAR MANIFESTATIONSCoronary blood flow are increased, systolic ejection and preejection period are abbreviated, pulse pressure is widened, systemic vascular resistance is reduced.

CARDIOVASCULAR MANIFESTATIONSThe changes in cardiac function are secondary to the increased metabolic demands of peripheral tissue. TH exerts a direct cardiac stimulant action independent of its effect on general tissue metabolism.Normalization of the myocardial contractile may not occur until several months after normalization of thyroid function. The overall pathological consequences associated with thyrotoxicosis result from an interaction between the effect of TH on the heart and its effect on the peripheral circulation.

CARDIOVASCULAR MANIFESTATIONSCardiovascular effects of hyperthyroidism.

CARDIOVASCULAR MANIFESTATIONSC-XR and ECG changes are common, but nonspecific in hyperthyroidism.On chest x-ray the left ventricle, aorta, and pulmonary artery are prominent, and generalized cardiac enlargement can be noted. In Px sinus rhythm, the magnitude of the tachycardia in general parallels the severity of the disease. Sinus tachycardia is present in 40 % of patients with hyperthyroidism and occurs most frequently. Ten to 15 percent of patients with hyperthyroidism have persistent AF.

CARDIOVASCULAR MANIFESTATIONSIntraatrial conduction disturbances, manifested by prolongation or notching of the P wave and prolongation of the PR interval in patients with hyperthyroidism. Second - or third-degree heart block may result. The cause of the AV conduction disturbance is not clear.

CARDIOVASCULAR MANIFESTATIONSIntraventricular conduction disturbances, commonly RBBB, occur in 15 % of patients with hyperthyroidism without associated heart disease of other etiology.

Paroxysmal SVTand flutter are rare in hyperthyroidism.

Occult thyrotoxicosis may underlie either chronic or paroxysmal isolated AF

CARDIOVASCULAR MANIFESTATIONS Angina and CHF occur in patients with hyperthyroidism. Five lines of evidence have suggested: (1) CHF has been produced in animals by administering T4. (2) CHF in children with thyrotoxicosis and no underlying cardiac disease. (3) Angina reported in a hyperthyroid Px with normal coronary arteries, presumably secondary to thyroid-induced coronary artery spasm. (4) The abnormal left ventricular function observed in hyperthyroid Px is not reversed by beta blockade but is reversed by treating the hyperthyroidism. (5) The cardiomyopathy in patients with thyrotoxicosis may be irreversible.

DIAGNOSIS OF HYPERTHYROIDISM Hyperthyroidism in most patients is clinically manifested as described above. The diagnosis is confirmed with a low TSH level, which reflects an elevated level of TH in the blood. In elderly patients with apathetic hyperthyroidism, cardiovascular manifestations predominate, specifically, AF and/or CHF.

TREATMENT OF CARDIOVASCULAR MANIFESTATIONS OF HYPERTHYROIDISMBeta blockers can be administered, with caution in patients with CHF. The heart failure with tachycardia, beta blockade may be beneficial. Beta-blocking drugs also slow the ventricular rate in AF. The agents for correcting the fundamental defect are thionamides.Iodine inhibits the release of TH from the thyrotoxic gland. It is therefore useful for rapid amelioration of the hyperthyroid state in patients with thyroid heart disease.