Dian Ayu. LBM 1 Modul Jiwa-22

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STEP 1 Stressor : keadaan2 atau peristiwa yang dapat menimbulkan stress. Waham : keyakinan yang salah. Orang tsb meyakini keyakinan yang salah meskipun ada orang lain yang menjelaskan bahwa keyakinan tsb salah.tapi org tsb tak percaya. Halusinasi : persepsi panca indra tanpa rangsangan pada reseptor2 panca indra itu sendiri. Fungsi okupasi dan fungsi psikososial Zat psikoaktif : zat yang bisa menimbulkan perubahan perilaku,persepsi, psikologi STEP 2 1. Mengapa dia sering marah marah tanpa sebab dan bicara kacau? 2. Definisi gangguan jiwa psikotik? 3. Apakah ada hubungan gejala tsb dengan masalah pekerjaannya? 4. Perbedaan waham dg halusinasi ? 5. Terapi apa saja yang diberikan oleh dokter? 6. Definisi fungsi global (GAF) ? 7. Apa maksud dari px.status mental dan itu mengindikasikan apa? 8. Mengapa terjadi penurunan Fungsi okupasi dan fungsi psikososial ? 9. Bagaimana cara untuk mengetahui pasien tsb kalau mengalami gangguan jiwa ? 10. Macam – macam kelompok gangguan jiwa apa saja ? knp pasien tsb digolongkan pada gangguan jiwa yang berat ? 11. Macam – macam waham ? 12. Macam – macam halusinasi? 13. Macam – macam stressor ? dan sebutkan derajat – derajat stressor ? 14. Pengertian gangguan jiwa ? dan berikan gejalanya! 15. DD? STEP 3

Transcript of Dian Ayu. LBM 1 Modul Jiwa-22

STEP 1

Stressor : keadaan2 atau peristiwa yang dapat menimbulkan stress. Waham : keyakinan yang salah. Orang tsb meyakini keyakinan yang salah meskipun ada

orang lain yang menjelaskan bahwa keyakinan tsb salah.tapi org tsb tak percaya. Halusinasi : persepsi panca indra tanpa rangsangan pada reseptor2 panca indra itu

sendiri. Fungsi okupasi dan fungsi psikososial Zat psikoaktif : zat yang bisa menimbulkan perubahan perilaku,persepsi, psikologi

STEP 21. Mengapa dia sering marah marah tanpa sebab dan bicara kacau?2. Definisi gangguan jiwa psikotik?3. Apakah ada hubungan gejala tsb dengan masalah pekerjaannya?4. Perbedaan waham dg halusinasi ?5. Terapi apa saja yang diberikan oleh dokter?6. Definisi fungsi global (GAF) ?7. Apa maksud dari px.status mental dan itu mengindikasikan apa?8. Mengapa terjadi penurunan Fungsi okupasi dan fungsi psikososial ?9. Bagaimana cara untuk mengetahui pasien tsb kalau mengalami gangguan jiwa ?10. Macam – macam kelompok gangguan jiwa apa saja ? knp pasien tsb digolongkan

pada gangguan jiwa yang berat ?11. Macam – macam waham ?12. Macam – macam halusinasi?13. Macam – macam stressor ? dan sebutkan derajat – derajat stressor ?14. Pengertian gangguan jiwa ? dan berikan gejalanya!15. DD?

STEP 3

1. Definisi gangguan jiwa psikotik?Seseorang individu punya persepsi dan pemikiran abnormal dan tak mampu menilai realita yang ada dan juga mengalami waham dan halusinasi, gangguan organik (di SSP dan di luar SSP) dan fungsional ( hanya ganggua kejiwaan saja).Organik ; demensia , delirium Fungsional; gangguan di tataran molekuler, neurotransmitter, skizofrenia, psikotik akut.

2. Definisi fungsi global (GAF) ?

3. Pengertian gangguan jiwa ? dan berikan gejalanya!

Suatu sindroma atau pola prilaku yang secara klinis bermakna, disertai adanya penderitaan; yang menyakitkan dan kecacatan co. Gang.fungsi

1. Gangguan kognisi pada persepsi ; kayak mendengar bisikan2

2. Gangguan kemauan ; mengalami kemauan yang lemah3. Gangguan emosi ; suka merasa gembira berlebihan, atau sedih berlebih4. Gang.psikomotor ; hiperaktif ; berlari gak jelas

Gangguan jiwa menimbulkan GK :Adanya sindrom psikologik; ada 2 persepsi penderitaan yang dialami oleh penderita tsb. Nyeri, disfungsi organ, disabilitas (gangguan mandi, makan)

4. Macam – macam kelompok gangguan jiwa apa saja ? knp pasien tsb digolongkan pada gangguan jiwa yang berat ?Gangguan jiwa ada 2 :Psikosis dan neurosisPsikosis ( berat) ditandai hilangnya daya realita dan hilangnya fungsi mental ( halusinasi, waham) co. Skizofrenia, psikotik akut,gang jiwa akibat zat2 psikoaktifNeurosis ; non psikotik kronis dan rekurenGK : cemas, obsesif, fobia.

5. Mengapa dia sering marah marah tanpa sebab dan bicara kacau?Orang gangguan jiwa ada gangguan pada neurotransmitterr. Gampang berubah emosinya. Kalau ngomong juga kacau. Dan sering mengalami disorientasi (Dopamin, Serotonin)Marah marah : paratimik ( tak cocok anatara kenyataan dan prilakunya)Bicara kacau : inkoherensi ( gang. Arus fikir ; bicara yang tak dipahami)

6. Apakah ada hubungan gejala tsb dengan masalah pekerjaannya?Berhub dengan fungsi psikososial dari masy. Dan keluarga (HPA aksis) bisa melepaskan glukokortikoid merangsang aktifasi HPA aksis stress menetap glukokortikoid makin banyak hipokampus peka banget sama glukokortikoid ( reseptornya banyak) HPA aksis berubah menetap HPA aksis menstimulasi dopaminergik eksitatorik memicu saraf ....... gelisah, persepsi, halusinasi.

STEP 7

Multiple observations regarding these systems suggestthat glutamatergic pathways, presumably emanating from thecerebral cortex, exert a strong inhibitory and stabilizing effect onan array of subcortical, potentially psychosis-inducing mechanisms,involving both monoaminergic and cholinergic pathways.The mechanism underlying this stabilizing glutamatergicfunction appears to be complex. In part it seems to be locatedpostsynaptically to the (limbic) striatum, where corticostriatalpathways control both direct and indirect striatopallidothalamicpathways, as detailed in Figure 10.1. These pathways appear toregulate the sensory input to the cerebral cortex as well as thearousal. The direct and indirect pathways are mutually antagonistic,the former being activating and the latter inhibitory onthe thalamocortical glutamatergic projections. Both the directand the indirect pathways are also controlled by dopaminergic

projections, whereby the former are activating (via D1 receptors)and the latter inhibitory (via D2 receptors). In addition, glutamatergicand glutamatergic/GABAergic pathways seem to controlthe monoaminergic neurons themselves by means of an acceleratorand a brake mechanism, respectively (Carlsson et al., 2001).These observations support glutamatergic involvement in schizophreniaand emphasize the interaction of glutamate with other,largely subcortical transmitter systems and open up possibilitiesfor a multifactorial dysregulation in complex neurocircuits where,besides glutamate, GABAergic, monoaminergic and cholinergicsystems participate in the psychotogenic process (Carlsson andCarlsson, 1990).Several drugs in different states of development will probablyshed additional light on the multifactorial aspects of psychotogenesis,for example, agonists acting at the glycine site of theNMDA receptor, glycine-reuptake inhibitors, ampakines, drugsacting on the metabotropic glutamate receptors, partial dopaminereceptor agonists and dopaminergic stabilizers lacking intrinsicactivity on dopamine receptors (Carlsson et al., 2001).

Systems Pathology in Schizophrenia:The Limbic CortexIn looking for sites of pathophysiology in the cerebral cortex,several lines of evidence point to abnormal limbic function.Decades of postmortem research in schizophrenia have reportedstructural, histologic, and neurochemical changes in limbic cortex(Jakob and Beckmann, 1989). Abnormalities in hippocampalsize (Bogerts et al., 1985), axial orientation (Scheibel andKovelman, 1981), neuronal and nonneuronal number (Beneset al., 1991, 1998; Heckers et al., 1991; Jeste and Lohr, 1989),and changes in neurochemical markers of transmission and development

(Akbarian et al., 1993; Gao et al., 2000; Tsai et al.,

Postmortem Limbic Cortex Abnormalitiesin Schizophrenia: Structural ChangesMuch focused work in the human limbic cortex in schizophreniabegan after Scheibel and Kovelman (1981) described an alterationin pyramidal cell apical dendrite orientation in the hippocampus,in its anterior and middle section, particularly at the subicular-CA1 border. In a later extension of this work, they correlatedsymptom severity with the extent of the dendritic disorientation(Kovelman and Scheibel, 1984). However, other studies havenot uniformly replicated these fi ndings (Altshuler et al., 1987;Christison et al., 1989; Vogel et al., 1997), but the original fi ndingsare still often referenced as evidence for neuroanatomicalabnormalities in the hippocampus. Weinberger (1996) highlightsseveral studies describing cytoarchitectural abnormalities in theentorhinal cortex (including the specifi c loss of NADPH-diaphoraseneurons Nicotinamide Adenosine Dinucleotide Phosphate)as providing the best evidence for neuropathological fi ndings(Akbarian et al., 1993; Arnold et al., 1991; Jakob and Beckmann,1986). Other studies have reported signifi cant reductions in thevolumes or cross-sectional areas of the entorhinal cortex or hippocampusin schizophrenia (Bogerts et al., 1985; Brown et al.,

1986; Colter et al., 1987; Falkai and Bogerts, 1986; Falkai et al.,1988), but these results have not been uniformly replicated (Beneset al., 1991; Heckers et al., 1991).Hippocampal size is reduced bilaterally, albeit mildly,in the illness especially in anterior areas (Becker et al., 1996;Bilder et al., 1995; Bogerts et al., 1990; Suddath et al., 1989.Shape analyses of the hippocampus have suggested regionalabnormalities of volume in schizophrenia. Importantly, regionalshape abnormalities are predominantly localized to the head,implicating only a delimited area within hippocampus as abnormal(Csernansky et al., 1998).Neurochemical ChangesChanges in GABAA receptor density, in GABA release and inglutamate-related transmitters and their enzymes in hippocampushave been reported in the illness (Simpson et al., 1992;Tsai et al., 1995). While there appears to be no change in thedensity of hippocampal NMDA glutamate receptors (Ishimaruet al., 1992; Kerwin et al., 1990; Kornhuber et al., 1989), kainatebinding, particularly in CA2 has been found reduced in severalstudies (Kerwin et al., 1988, 1990; Simpson et al., 1992) but notconsistently (Deakin et al., 1989). Reduced levels of non-NMDAreceptor binding (Kerwin et al., 1990) and lower concentrationsof non-NMDA receptor mRNA (Harrison et al., 1991), have bothbeen reported in CA3. The previous fi nding of an alteration in theNR1 subunit and an increase in NR2B in postmortem tissue fromschizophrenia (Gao et al., 2000) suggests a reduction in excitatoryglutamate transmission at hippocampal NMDA receptors inthis illness.In addition, considerable evidence of compromised cognitivefunction, especially short-term memory and attention, existsin schizophrenia (Green, 1996; Gruzelier et al., 1988; Venables,1992). These dysfunctions may represent the behavioral correlatesof hippocampal pathology.In VivoFunctional Limbic Cortex Changein SchizophreniaFunctional studies of human brain in schizophrenia have directlydemonstrated an alteration in neuronal activity in the limbic cortexin the illness (Fletcher, 1998; Haznedar et al., 1997; Heckerset al., 1998; Medoff et al., 2001; Nordahl et al., 1996; Tammingaet al., 1992). Anterior cingulate cortex consistently shows alterationsin schizophrenia when persons are imaged medication-freeand matched for performance. Moreover, connectivity analysessuggest that the anterior cingulate rCBF is not tightly coupled tohippocampal activity during tasks of learning and memory, as itis in normal persons. Although the entire body of these data havenot yet suggested the pivotal limbic pathology, they do implicateabnormal function of these structures in the illness. Moreover, assuggested in the preclinical studies, such pathology could destabilize

the function of subcortical brain areas in psychosis.An analysis of connectivity in auditory discrimination experimentsdirectly suggests that a systems failure occurs withinlimbic cortex in schizophrenia. A malfunction within the limbiccortex and the subsequent disruption of related neocortical areasand secondary dysregulation of subcortical structures may underliethe manifestations of schizophrenia. This working hypothesissuggests that it may be the resultant “misbehavior” of the limbicsystem itself that generates positive and cognitive symptoms inschizophrenia, possibly through its connections with neocorticaland subcortical structures. These speculations raise the possibilitythat the primary origin of the circuit dysfunction could bevaried, but inevitably result in a characteristic “psychosis” circuitabnormality (Figure 10.2).Functional Effects of D2 DopamineReceptor BlockadeThe clinical evidence of a systems basis of psychosis, along withthe preclinical data suggesting multiple and complex neurotransmitterinteractions within these symptoms, builds a plausible“psychosis circuit” for schizophrenia and potentially for its treatment.The effective functioning of the human brain to facilitatecognitive, motor and affective performance, is dependent notonly on the proper functioning of individual regional neuronalgroups dedicated to specifi c tasks, but also to interacting brainsystems which function to connect neural systems to perform aparticular mental task and systematically to direct informationfl ow in the brain. Because schizophrenia is not characterized primarilyby a neural or behavioral defi cit, but rather by productivesymptoms and by a “confusion” of neural activity with resultingmental malfunction, a system hypothesis of schizophreniapathology is plausible. The idea that psychosis is the consequenceof dysfunction somewhere within the limbic cortex, seen duringcognitive work and even during routine mental function is supportedby a great deal of research. This putative dysfunction isprominently manifest in the anterior components of the limbicsystem. Hence this change primarily infl uences the frontal regionsof the neocortex, leaving the posterior hippocampus andthe posterior neocortex relatively unaffected. Exactly where theprimary limbic pathology is located within these anterior areas isa matter of speculation, but it could be multiple sites with a singleresultant systems dysfunction.Importantly, this idea allows for the real possibility that

other drug actions can be exerted at other sites within the relevant

7. Macam – macam waham ?Waham gang pada isi pikir5 syarat waham-isi pikiran salah-bertentangan dg realita-tdk diterima logika-yakin dg kepercayaannya-tdk mau dikasi tau

Waham sistematik isi pikirannya tersistematik

STEP 7

WAHAM

Adl suatu keyakinan atau pikiran yg salah karena bertentangan dg kenyataan

Sifat atau ciri2 waham :

1. Buah pikiran ini selalu mengenai diri sendiri atau egosentris

2. Selalu bertentangan dengan realitas

3. Selalu bertentangan dg logika

4. Penderita percaya 100% terhadap kebenaran pikiran

5. Tidak dpt dirubah oleh orang lain, sekalipun dg jalan yg logis dan rasional

Jenis – jenis waham :

Waham dikejar : penderita merasa dikejar2 olah orang lain

Waham curiga : penderita merasa selalu di sindir oleh orang

lain.

Wahampersekutorik : penderita merasa diganggu, ditipu atau disiksa

oleh orang lain

Waham curiga : pasien merasa selalu disindir oleh orang lain

(curiga terhadap sekitar, cth : orang lain tersenyum, tetapi diartikan spt

menyindir dirinya)

Waham cemburu : pasien merasa sll cemburu pd orang lain, cth :

penderita sll cemburu dg pasangannya (berlebihan)

Waham hipokondria : keprihatinan yg berlebihan ttg kesehatan

pasien yg didasarkan bukan pd patologi organic yg nyata.

Waham somatic : keyakinan palsu menyangkut fungsi tubuh

pasian, cth : keyakianan bahwa otak penderita mencair, jantung bocor²

Bizareisi pikiran kacau, banyak cabang- Taught of insertion : isi pikiran asing dari luar masuk ke pikirannya- Taught of broadcasting ; meniarkan isi pikirannya ke halayak umum- Taught of withdrawl ; isi pikirannya diambil dari luar dirinya

Kriteria untuk dg.skizofrenia.Nihilistik kosongSomatikwaham merasa dirinya sakitParanoid merasa dirinya besar,dikejar kejar,curagaan

8. Macam – macam halusinasi?Halusinasi gangguan persepsi Ada 2 interaksi rangsang sensorik dan proses dari kita yang mengolah rangsang sensorik tsbTak ada rangsang tapi si x ada memproses rangsang. - Auditorik : skizofren- Gustatorik

- Visual- Olfaktorik- Taktil- Haptik : bersentuhan dengan manusia lain dan benda benda lain - Kinestetik ; anggota tubuh terlepas dari tubuhnya : skizofren- Autoskopi : melihat dirinya sendiri dihadapannya

Ilusi

Ada rangsangan tapi diinterpretasikannya salah.

9. Perbedaan waham dg halusinasi ?Halusinasi : gangguan persepsi tanpa ada rangsangan dari luar - Terkait sama panca indra- Bisa diubah- Bisa terjadi pada orang normal

Waham- Tak terkait dg panca indra- Tak bisa diubah keyakinannya- Gak bisa terjadi pada orang normal

10. Macam – macam stressor ? dan sebutkan derajat – derajat stressor ?Macam 1. Stressor episodik : kecelakaan blm lama terjadi, perselisihan sama org lain tak

selesai selesai2. Squenstressor : perceraian, kematian orang yang tercinta, pekerjaan3. Periodik : kedokter gigi gara- gara sakit gigi terus.... terus terusan, sakit pinggang4. Kronis : penyakit permanen, masalah suami istri yang berlarut – larut, maslaah

keuangan,.

Derajat – derajatnya ?

STEP 7

what is stress?Stress is often described as a feeling of being overloaded, wounduptight, tense and worried. We all experience stress at times. It cansometimes help to motivate us to get a task finished, or performwell. But stress can also be harmful if we become over-stressedand it interferes with our ability to get on with our normal life fortoo long.

what are the signs of stress?When we face a stressful event, our bodies respond by activating

the nervous system and releasing hormones such as adrenalin andcortisol. These hormones cause physical changes in the body whichhelp us to react quickly and effectively to get through the stressfulsituation. This is sometimes called the ‘fight or flight’ response.The hormones increase our heart rate, breathing, blood pressure,metabolism and muscle tension. Our pupils dilate and ourperspiration rate increases.While these physical changes help us try to meet the challengesof the stressful situation, they can cause other physical orpsychological symptoms if the stress is ongoing and the physicalchanges don’t settle down.These symptoms can include:• Headaches, other aches and pains• Sleep disturbance, insomnia• Upset stomach, indigestion, diarrhoea• Anxiety• Anger, irritability• Depression• Fatigue• Feeling overwhelmed and out of control• Feeling moody, tearful• Difficulty concentrating• Low self-esteem, lack of confidence• High blood pressure• Weakened immune system• Heart disease

changes to the things that are within your control

11. Apa maksud dari px.status mental dan itu mengindikasikan apa?Waham bizareHalusinasi akustik

12. Mengapa terjadi penurunan Fungsi okupasi dan fungsi psikososial ?

13. Bagaimana cara untuk mengetahui pasien tsb kalau mengalami gangguan jiwa ?Punya masalah apa gak

Anamnesis riwayat psikiatrik

14. Terapi apa saja yang diberikan oleh dokter?Obat antipsikotikARS : risperidon, klozapin

ARD :Ketidaskseimbangan dopamin di prefrontal (mesokortikal) dan mesolimbik (mesensephalon) HPAaksis dopaminergik.

Terapi psikososial-

15. DD?DepresiSkizofreniaSkizotipal

STEP 4

STRESSOR

PSIKOTIK NONPSIKOTIK

GANGGUAN JIWA

NEUROSISPSIKOSIS

HALUSINASI CEMAS, OBSESIF, FOBIAWAHAM

DERAJAT

SKALA GAF

AUDITORIK, OLFAKTORIK

BIZARE, SOMATIK