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Oleh : Yuanita Faradiba (208.121.0037) Pembimbing: dr. Yahya Ari Purmono, SP.

BS

FAKULTAS KEDOKTERAN UNIVERSITAS ISLAM MALANG MALANG, 2013

 Metoclopramid

merupakan antagonis reseptor D2 yang dapat menyebabkan eksaserbasi gejala extrapiramidal.  Antagonis reseptor D2 pada kemoreseptor trigger zone pada sistem saraf pusat.  Gejala Ekstrapiramidal yang sering terjadi adalah reaksi akut distonik, 0,2 % pada pasien (1:500), menggunakan 30-40 mg/ hari.

 Seorang

wanita 25 tahun didiagnosa hepatitis A. Karena mual yang persisten, menggunakan metoclopramide 3x10 mg (iv). Setelah 2 hari pasien merasa leher menjadi kaku, kelopak mata berkedip terus, dan kesulitan berbicara. Dia tetap sadar saat terjadinya episode.Setelah relaksasi, kepala dan mata kembali seperti semula. Gejala menghilang setelah di beri biperidin 2 mg (iv). Tidak ada episode serangan setelah penggunaan metoclopramid dihentikan. Gejala diatas merupakan karakteristik dari krisis oculogiric (reaksi spesifik distonik).

postpiloric mengganti enternal feeding tube 3. gastroparesis 2. muntah setelah chemoterapi .mencegah/ mengobati mual. Metoclopramid merupakan antagonis reseptor dopamin yang menghambat reseptor D1 dan D2 disaraf pusat.  Digunakan sebagai antiemetik dan anti prokinetik terutama pada situasi: 1.

 Onset • • • • • metoklopramid secara iv  1-3 mnt im  10-15 mnt oral30-60 mnt farmakologi efeknya 1-2 jam Dopamin merangsang mual dan muntah dengan menstimulasi medulary chemoreceptor trigger zone (CTZ). Metoclopamide menghambat stimulasi CTZ Pemakaian jangka panjang metoclopramid dapat menyebabkan extrapiramidal simptom seperti distonik akut dalam 24-48 jam Resiko semakin meningkat : dosis tinggi. . anak anak. dewasa < 30 thn.

korpus subtalamikus.  Kortek serebri Ganglia Basalis ( nukleus kaudatus.nukleus ventrolateral talamikus) . globus palidus)  Brain stem( substansia nigra. putamen.

 Regulasi dan integrasi gerakan atau mengurus komponen tonik dari gerakan volunter. Gerakan yang menetapkan sikap itu bersifat refrektoris disebut postural reflek.  mengintegrasikan aktivitas serebelum untuk mencetuskan impuls motorik volunter dan involunter  Perwujudan dari regulasi dan integrasi gerakan adalah sikap tubuh pada waktu gerakan volunter berlangsung. .

 Reaksi yang ditimbulkan oleh penggunaan jangka panjang dan pendek dari medikasi antipsikotik golongan tipikal maupun antiemetik dikarenakan terjadinya inhibisi transmisi dopaminergik di ganglia basalis. .

CAUSES OF EXTRAPYRAMIDAL DISORDERS  Drugs---chlorpromazine ---butyrophenons ---metochlorpramide ---reserpine .

Amphetamine  Levodopa:a precursor of dopamine  Direct dopamine agonist:ex. metoclopramide〈primperam〉  Central 10 . Reserpine  Antagonize or block central dopamine receptors: neuroleptics. Bromocriptine  Presynaptic dopamine antagonists: ex.Five classes of drugs are known to affect central dopaminergic systems stimulants:act as indirect dopamine agonist ex.

Ascociative movement Regulation of posture Autonomic integration 11 .

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2. Cortex  Striatum  Globus pallidus  Thalamus  Cortex Cortex  Striatum  Substantia nigra  Striatum  Cortex Cortex  Striatum  Substantia nigra  Thalamus  Cortex Cortex  Globus pallidus  Sub thalamic nuclei  Thalamus  Cortex 24 .1. 4. 3.

Subtthalamicus nuclei Thalamus Serebellum 4 Globus pal 1 Cortex Substantia nigra 2 Caudatus+put Pons 3 striatum Nigro reticulo spinal tract Piramidal tract 25 Diagram of ekstrapyramidal circuit .

Ex.Definition long-lasting contraction or spasm of musculature generally less common than most other extrapyramidal symptoms young age and male sex predominant The pathophysiological mechanism is presently unknown Diagnosis: The most common muscle groups affected are the eyes. blepharospasm. tongue. oculogyric crisis. laryngeal spasm〈most dangerous〉 Treatment anticholinergic drug. and neck trismus. jaw. Benztropine. opisthotonus. diphenhydramine . torticollis.

stress. and discoordination are associated features . rhythmical. or fatigue Muscle rigidity: (1)firmness and spasm of muscle at rest (2)generalized muscle pain. body aches. oscillatory motion (2)the most affected body area tends to be the upper extremities (3)typically suppressed during action and increase during times of anxiety.Pathophysiology: blockade of postsynaptic dopamine(D2) receptors in the corpus striatum Diagnosis〈three cardinal symptoms〉 Tremor: (1)steady.

bent over neck. stooped shoulders.Akinesia: (1)decreased spontaneous motor activity and a global slowness in the initiation and execution of movements (2)associated with drooling. and masked facial expression  Treatment Lower dose of agent  Switching to a low potency agent  Anticholinergic drugs  .

 Often associated with severe dysphoria. anxiety. and irritability  . and this manifests as frequent changes in posture.. crossing and uncrossing of the legs…. The most common type of EPS Pathophysiology: unknown Diagnosis tend to have subjective complaints of ‘inner restlessness’ most often in legs  They feel that they must move.Definition a sense of motor restlessness in which the patient feels a constant need to move about.

Treatment Lower dose of agent  Switching to a low potency agent  Anticholinergic drugs  beta-adrenergic blockers  benzodiazepine  .

jaw.Definition a syndrome of abnormal movements following at least six months and often many years of drug therapy Pathophysiology denervation-hypersensitivity phenomenon It appears with prolonged receptor blockade. tongue. becoming supersensitized Diagnosis Characterized by involuntary movement of the lips. the receptors rebound. and extremities .

trunk rocking and restless foot movements Reduced by voluntary movements of the affected areas Increased by voluntary movements of unaffected areas Increased with emotional arousal Absent when the individual is asleep Treatment The best treatment is prevention gradual reduction Low dose of benzodiazepine Dopamine antagonist Dopamine depleting agents . facial and lingual masticatory movements.Lipsmacking.