kul obat sist imun, 2011 [compatibility mode]

8/12/2019 Kul Obat Sist Imun, 2011 [Compatibility Mode]

1/58

OBATOBAT--OBAT SISTEM IMMUNOBAT SISTEM IMMUNOBATOBAT--OBAT SISTEM IMMUNOBAT SISTEM IMMUN

FathiyahFathiyah SafithriSafithriLaboratoriumLaboratorium FarmakologiFarmakologi

FakultasFakultas KedokteranKedokteran UMMUMM20112011

FathiyahFathiyah SafithriSafithriLaboratoriumLaboratorium FarmakologiFarmakologi

FakultasFakultas KedokteranKedokteran UMMUMM20112011

Create PDF files without this message by purchasing novaPDF printer ( http://www.novapdf.com )
http://www.novapdf.com/http://www.novapdf.com/http://www.novapdf.com/http://www.novapdf.com/


2/58

The immune system protect individualsagainst pathogenic viruses, microorganism and

parasites. Immune responses depend on theability of the system to recognize foreignmolecules (antigens) then to amount anappropriate reaction to eliminate the source of

the antigen.

DEFINITION

http://www.novapdf./http://www.novapdf.com/http://www.novapdf.com/http://www.novapdf./


3/58

IMMUNE SYSTEM

Innate immunity Adaptive immunity

(immune system nonspesific) (spesific system)The defenses against pathogenic Respond specifically to substancesmicroorganism that are present in and organismshost who has not been previouslyexposed to the pathogen

Complement Immunoglobulins

Natural Killer Cells T Lymphocytes

Phagocytic cells



4/58

ImmunofarmakologiImmunofarmakologi : ilmu yang mempelajri: ilmu yang mempelajritentang bagaimana mengontrol (menekan /tentang bagaimana mengontrol (menekan /meningkatkan ) respon imun denganmeningkatkan ) respon imun dengan

mediator biologis ataupun khemismediator biologis ataupun khemisObat ImmunosupressanObat Immunosupressan : mempelajari obat: mempelajari obatyg digunakan pd keadaan overaktivasi sistemyg digunakan pd keadaan overaktivasi sistemimun (penyakit autoimun, post transplantasi)imun (penyakit autoimun, post transplantasi)Obat ImmunostimulanObat Immunostimulan : mempelajari obat: mempelajari obatyang dapat meningkatkan status imun padayang dapat meningkatkan status imun padakeadaan immunodefisiensi, HIVkeadaan immunodefisiensi, HIV- -AIDS, kanker AIDS, kanker

ImmunofarmakologiImmunofarmakologi : ilmu yang mempelajri: ilmu yang mempelajritentang bagaimana mengontrol (menekan /tentang bagaimana mengontrol (menekan /meningkatkan ) respon imun denganmeningkatkan ) respon imun dengan

mediator biologis ataupun khemismediator biologis ataupun khemisObat ImmunosupressanObat Immunosupressan : mempelajari obat: mempelajari obatyg digunakan pd keadaan overaktivasi sistemyg digunakan pd keadaan overaktivasi sistemimun (penyakit autoimun, post transplantasi)imun (penyakit autoimun, post transplantasi)Obat ImmunostimulanObat Immunostimulan : mempelajari obat: mempelajari obatyang dapat meningkatkan status imun padayang dapat meningkatkan status imun padakeadaan immunodefisiensi, HIVkeadaan immunodefisiensi, HIV- -AIDS, kanker AIDS, kanker



5/58

Obat Sistem ImunObat Sistem ImunObat Sistem ImunObat Sistem Imun

Obat utk Penyakit AllergiObat utk Penyakit Autoimmun &Keganasan (Immunosupressan)Immunostimulan

Obat utk Penyakit AllergiObat utk Penyakit Autoimmun &Keganasan (Immunosupressan)Immunostimulan



6/58

OBAT UNTUK PENYAKITOBAT UNTUK PENYAKIT ALLERGI ALLERGI

OBAT UNTUK PENYAKITOBAT UNTUK PENYAKIT ALLERGI ALLERGI

H1 reseptor antagonisGlukokortikoid (Kortikosteroid)

Cystenyl-Leukotrien Recept Antagonis

5-Lipoxygenase inhibitorsKromolin sodium

Epinefrin

H1 reseptor antagonisGlukokortikoid (Kortikosteroid)

Cystenyl-Leukotrien Recept Antagonis

5-Lipoxygenase inhibitorsKromolin sodium

Epinefrin



7/58

MekanismeMekanismeAllergiAllergi



8/58

Target Terapi Anti AllergiTarget Terapi Anti Allergi1. Me IgE berikatan dg sel mast (anti-IgE antibody)

2. Mencegah degranulasi sel mast

(kromolin, simpatomimetik)

3. Menghambat kerja mediator yg dilepaskan sel mast

(anti H1, antagonis leukotrien reseptor)

4. Me respon inflamasi (glukokortikosteroid)



9/58

Target Terapi Anti AllergiTarget Terapi Anti AllergiTarget Terapi Anti AllergiTarget Terapi Anti Allergi



10/58

ANTI ANTI--Ig E MONOCLONALIg E MONOCLONAL

ANTIBODY (Omalizumab) ANTIBODY (Omalizumab)

ANTI ANTI--Ig E MONOCLONALIg E MONOCLONAL

ANTIBODY (Omalizumab) ANTIBODY (Omalizumab)merup immunoglobulin G yang bekerja

sebagai antihuman Ig dg cara menghambatikatan IgE dengan mast sel

Dapat menurunkan frekuensi daneksaserbasi berulang penyakit allergi

Half life sangat panjang diberikan 1X /bulan

Diberikan melalui injeksi subkutaneus



11/58

KROMOLIN &KROMOLIN &NEDOKROMILNEDOKROMIL

Per inhalasi Absorbsi per oral


12/58

dibentuk dr asam amino histidin & disimpan dlmkonsentrasi tinggi di sel mast jaringan dan basofil darah.Lokasi paru, kulit, GIT

Histamin diproduksi & disekresi oleh granula mast sel.Me pd reaksi allergi yg diperantarai Ig-E (immediate),mis : seasonal rhinitis (hay fever), urticaria, andangioneurotic edema.

HISTAMINN N

N H2

H

1

2

3

45

Histamine



13/58


14/58


15/58

Manifestasi pd allergic reactions H1 receptorMekanisme kerja : release IP3 & DAG Ca2+ intake

Kontraksi otot polos (bronkhokonstriksi, peristaltik ) Arteri vasodilatasi (H1 & H2), akibat dr pe release

endothelium-derived relaxing factor (EDRF) & PGI2.,Permeabilitas vaskuler edema, angioedema

Kontraksi jantung , aliran koroner

Sekresi kelenj eksokrin hidung & bronkus Headache, kewaspadaan Release katekolamin oleh adrenal Gatal, eritema eczema, urtica

Efek Aktivasi Reseptor Histamin-1



16/58

Mek kerja AH1 : kompetitif inhibitor pd reseptor H1

Struktur sgt mirip dg muscarinic blockers & alphaadrenoceptor blockers (anti H1 sedatif) efekantikolinergik & antagonis adrenergikBbrp bisa memblok resept serotonin (cetirizine).efek pd resept H2 (-)

Mekanisme Kerja AH1



17/58

AntihistaminAntihistamin- - HH11

Sedative (Sedative ( 11 stst Generation)Generation)difenhydramindifenhydraminchlorpheniraminechlorpheniramine

embraminembraminprometazinprometazincyproheptadincyproheptadinbisulepinbisulepindimetindendimetindenazatadinazatadinklemastinklemastin

Sedative (Sedative ( 11 stst Generation)Generation)difenhydramindifenhydraminchlorpheniraminechlorpheniramine

embraminembraminprometazinprometazincyproheptadincyproheptadinbisulepinbisulepindimetindendimetindenazatadinazatadinklemastinklemastin

Non sedative (Non sedative ( 22ndnd Generation)Generation)terfenadineterfenadineastemizolastemizol

cetirizincetirizinloratadinloratadin

Non sedative (Non sedative ( 22ndnd Generation)Generation)terfenadineterfenadineastemizolastemizol

cetirizincetirizinloratadinloratadin



18/58


19/58

1. Antiallergi ( Blok pd H 1receptors perifer) u/

reaksi allergi ringan (insectbite, urtica, dll)

2. Sedasi ( blok resep H 1 & Mdi SSP)

3. Anti emetik u/ motionsickness (Dimenhidrinate)

EFEK AH1

4. Antikolinergik (retensi4. Antikolinergik (retensiurine, pand kabur,urine, pand kabur,konstipasi,mulutkonstipasi,mulutkering)kering)

5. Blok5. Blok --adrenergikadrenergik(hipotensi ortosttik)(hipotensi ortosttik)

6. Anesthesi lokal6. Anesthesi lokal

4. Antikolinergik (retensi4. Antikolinergik (retensiurine, pand kabur,urine, pand kabur,konstipasi,mulutkonstipasi,mulutkering)kering)

5. Blok5. Blok --adrenergikadrenergik(hipotensi ortosttik)(hipotensi ortosttik)

6. Anesthesi lokal6. Anesthesi lokal



20/58

Toksisitas:Sedasi (t.u AH1 sedatif)

Antimuscarinic effects (dry mouth, blurred vision etc.) -blocking actions (orthostatic hypotension).

Interaksi :Obat dg efek sedatif ( benzodiazepin, alcohol).Obat yg menghambat metab di hepar (ketakonazol)kdr AH 1 lethal arrhythmia (terfenadin).



21/58

ANTI LEUKOTRIEN

1.1. LTLT--11 reseptor reseptor antagonisantagonis ((ZafirlukastZafirlukast, ,montelukastmontelukast, , pranlukastpranlukast) )

efektif efektif hambhamb Ag / exercise Ag / exercise- -induced asthmainduced asthmap.op.o 11--2 x2 x seharisehari

2.2. 55--lipoxygenase inhibitorlipoxygenase inhibitor ((ZileutonZileuton))HambHamb produksiproduksi leukotrienleukotrienInteraksiInteraksi obatobat : me: me konsentr konsentr teofilinteofilin &&walfarinwalfarin did i serumserum

1.1. LTLT--11 reseptor reseptor antagonisantagonis ((ZafirlukastZafirlukast, ,montelukastmontelukast, , pranlukastpranlukast) )

efektif efektif hambhamb Ag / exercise Ag / exercise- -induced asthmainduced asthmap.op.o 11--2 x2 x seharisehari

2.2. 55--lipoxygenase inhibitorlipoxygenase inhibitor ((ZileutonZileuton))HambHamb produksiproduksi leukotrienleukotrienInteraksiInteraksi obatobat : me: me konsentr konsentr teofilinteofilin &&walfarinwalfarin did i serumserum



22/58

GLUKOKORTI KOSTEROI D

Newton, Thorax2000; 55: 603-613



23/58


24/58


25/58

Hypothalamic-Pituitary Adrenal (HPA) AxisHypothalamic-Pituitary Adrenal (HPA) Axis

Adrenal cortexAdrenal cortex

Produces 30 steroid hormones

Major divisions include:Glucocorticoids

MineralocorticoidsAdrenal Sex steroids

Negative Feedback controlof ACTH Production.Suppression of HPA

STRESS : Overrides theneg. feedback mechanism.



26/58

Disorders of the Adrenal CortexDisorders of the Adrenal CortexDisorders of the Adrenal CortexDisorders of the Adrenal CortexPrimary Adrenocortical Insufficiency (Addisons Disease)

Destruction of the adrenal cortex leads to inadequate production of

cortisol and aldosterone.Tuberculosis, cancer, hemorrhage Atrophy of the adrenal cortex

Autoimmune diseaseProlonged corticosteroid treatment (Long-term admin)Surgical excision of the adrenal glands

Secondary Adrenocortical Insufficiency; inadequate secretion ofcorticosteroid. Mainly a GC deficiency

Prolonged treatment with cortocosteroids (early effects) Mineralocorticoid secretion is not altered.

Congenital Adrenogenital Syndromes and Adrenal Hyperplasia Synthetic enzyme deficiency Abnormally low cortisol levels results in excessive ACTH secretion,

excessive adrenal secretion of androgens and hyperplasia.

Adrenocortical Hyperfunction (Cushings Disease: Moonface) Excessive ACTH secretion Adrenal tumor (benign or malignant)

Abnormally high corticosteroid levels

Primary Adrenocortical Insufficiency (Addisons Disease) Destruction of the adrenal cortex leads to inadequate production of

cortisol and aldosterone.Tuberculosis, cancer, hemorrhage Atrophy of the adrenal cortex

Autoimmune diseaseProlonged corticosteroid treatment (Long-term admin)Surgical excision of the adrenal glands

Secondary Adrenocortical Insufficiency; inadequate secretion ofcorticosteroid. Mainly a GC deficiency

Prolonged treatment with cortocosteroids (early effects) Mineralocorticoid secretion is not altered.

Congenital Adrenogenital Syndromes and Adrenal Hyperplasia Synthetic enzyme deficiency Abnormally low cortisol levels results in excessive ACTH secretion,

excessive adrenal secretion of androgens and hyperplasia.

Adrenocortical Hyperfunction (Cushings Disease: Moonface) Excessive ACTH secretion Adrenal tumor (benign or malignant)

Abnormally high corticosteroid levelsCreate PDF files without this message by purchasing novaPDF printer ( http://www.novapdf.com )


27/58

Aktivasi Reseptor SteroidAktivasi Reseptor SteroidAktivasi Rese ptor SteroidAktivasi Reseptor Steroid

http://www.novapdf.co/http://www.novapdf.com/http://www.novapdf.com/http://www.novapdf.co/


28/58

Aktivasi Reseptor Steroid Aktivasi Reseptor Steroid Aktivasi Reseptor Steroid Aktivasi Reseptor Steroid

S mengikat resept S(R) di sitoplasma, R sec normal berhubS mengikat resept S(R) di sitoplasma, R sec normal berhubdg 2 molekul hsp90. kompleks Sdg 2 molekul hsp90. kompleks S- -R translokasi ke nukleusR translokasi ke nukleusdan berinteraksi dg GRE (glucocort icos teroid responsedan berinteraksi dg GRE (glucocort icos teroid responseelement) pd rantai promotor sel targetelement) pd rantai promotor sel target mempengaruhimempengaruhi

proses transkripsi & sintesa proteinproses transkripsi & sintesa protein

Antara lain menyebabkan : Antara lain menyebabkan :Induksi sintesa polipeptida (lipocortin-1) yg menghambat enzimfosfolipase A2 menurunkan produksi mediator inflamasi (PG,leukotrien, platelet-activating factor /PAF)Netralisasi peran transcription factor (mis. AP1) dlm sintesa sitokin(IL5, TNF ) sintesa sitokin me inflamasi

S mengikat resept S(R) di sitoplasma, R sec normal berhubS mengikat resept S(R) di sitoplasma, R sec normal berhubdg 2 molekul hsp90. kompleks Sdg 2 molekul hsp90. kompleks S- -R translokasi ke nukleusR translokasi ke nukleusdan berinteraksi dg GRE (glucocort icos teroid responsedan berinteraksi dg GRE (glucocort icos teroid responseelement) pd rantai promotor sel targetelement) pd rantai promotor sel target mempengaruhimempengaruhi

proses transkripsi & sintesa proteinproses transkripsi & sintesa protein

Antara lain menyebabkan : Antara lain menyebabkan :Induksi sintesa polipeptida (lipocortin-1) yg menghambat enzimfosfolipase A2 menurunkan produksi mediator inflamasi (PG,leukotrien, platelet-activating factor /PAF)Netralisasi peran transcription factor (mis. AP1) dlm sintesa sitokin(IL5, TNF ) sintesa sitokin me inflamasi



29/58

FISIOLOGI KORTISOL

Metabolic Effect Anti-inflammatory effect Antiproliferative effectImmunosuppressive effect

Metabolic Effect Anti-inflammatory effect Antiproliferative effectImmunosuppressive effect



30/58

A. Metabolisme Glukosa, Lemak dan Protein A. Metabolisme Glukosa, Lemak dan Protein



31/58

B. Mekanisme KerjaSteroid sbg Anti-Inflammasi

B. Mekanisme KerjaSteroid sbg Anti-Inflammasi

Menghambat aktivasi T-cell dan produksi sitokin.

Menghambat degranulasi mast cell.

Menurunkan permeabilitas kapiler secara tidak langsung akibathambatan pada mast cells dan basophils.

Menurunkan ekspresi cyclooxygenase II (COX2) dan sintesa

prostaglandin.

Induksi sintesa lipocortin1 hamb enz fosfolipase A2 mekadar prostaglandin, leukotriene and platelet activating factor(PAF)

Menghambat aktivasi T-cell dan produksi sitokin.

Menghambat degranulasi mast cell.

Menurunkan permeabilitas kapiler secara tidak langsung akibathambatan pada mast cells dan basophils.

Menurunkan ekspresi cyclooxygenase II (COX2) dan sintesa

prostaglandin.

Induksi sintesa lipocortin1 hamb enz fosfolipase A2 mekadar prostaglandin, leukotriene and platelet activating factor(PAF)



32/58

B. Mechanism of Action for Anti-Inflammatory SteroidsB. Mechanism of Action for Anti-Inflammatory Steroids

http://www.novapdf.com/http://localhost/var/www/apps/conversion/tmp/scratch_6/httphttp://localhost/var/www/apps/conversion/tmp/scratch_6/httphttp://www.novapdf.com/


33/58


34/58

Penggunaan GlukokortikoidPenggunaan GlukokortikoidPenggunaan GlukokortikoidPenggunaan Glukokortikoid

IInsufisiensi AdrenalSupresi HPA-axis overaktif Supresi penyakit autoimmunMencegah rejeksi organ transplantasiTerapi limfosit-derived tumor Terapi penyakit allergi (asma, penyakit kulitallergi)

IInsufisiensi AdrenalSupresi HPA-axis overaktif Supresi penyakit autoimmunMencegah rejeksi organ transplantasiTerapi limfosit-derived tumor Terapi penyakit allergi (asma, penyakit kulitallergi)



35/58

NONENDOCRINE DISORDERS TREATED WITHGLUCOCORTICOIDS

NONENDOCRINE DISORDERS TREATED WITHGLUCOCORTICOIDS



36/58

Routes of Administration for GCRoutes of Administration for GC

Local (Preferred)(Preferred)Intra-articular, IAIntrabursal, IBIntralesional, IL

Intrasynovial, ISSoft tissue, STIntrarectal, IRTopicalNasalInhaled

SystemicOral, POIntramuscular, IMIntravenous, IV

Local (Preferred)(Preferred)Intra-articular, IAIntrabursal, IBIntralesional, IL

Intrasynovial, ISSoft tissue, STIntrarectal, IRTopicalNasalInhaled

SystemicOral, POIntramuscular, IMIntravenous, IV



37/58

Farmakokinetik GCFarmakokinetik GCFarmakokinetik GCFarmakokinetik GC

Pemberian corticosteroids pd konsentrasi fisiologisselama minimal 2 minggu akan menekan HPA axis,shg terjadi penurunan endogenous hormones.Recovery setelah 9-12 bulan.

Metabolisme Hepar :Hepar : tempat inaktivasi / metabolisme utama GC. GCdimetabolisme oleh enzim cytochrome P450 3A425% GC diekskresi bersama empedu & feces .

Renal Clearance75 % metabolit GC diekskresi bersama urine ..

Pemberian corticosteroids pd konsentrasi fisiologisselama minimal 2 minggu akan menekan HPA axis,shg terjadi penurunan endogenous hormones.Recovery setelah 9-12 bulan.

Metabolisme He par :Hepar : tempat inaktivasi / metabolisme utama GC. GCdimetabolisme oleh enzim cytochrome P450 3A425% GC diekskresi bersama empedu & feces .

Renal Clearance75 % metabolit GC diekskresi bersama urine ..



38/58



39/58

Dampak Pemberian Kortikosteroid padaCortisol Release

Dampak Pemberian Kortikosteroid padaCortisol Release



40/58

Corticosteroids control symptoms and DO NOT stop progression (cure) of the disease

Mineralocorticoid actvity



41/58

AntiAnti--inflammatory Drugsinflammatory DrugsGlucocorticoidsGlucocorticoids

InhaledInhaledBeclomethasoneBeclomethasoneBudesonideBudesonideFlunisolideFlunisolideFluticasone propionateFluticasone propionateTriamcinolone acetonideTriamcinolone acetonide

Oral (Quick relief of asthmatic symptoms)PrednisonePrednisolone* Unresponsive to 2 agonists

AntiAnti--inflammatory Drugsinflammatory DrugsGlucocorticoidsGlucocorticoids

InhaledInhaledBeclomethasoneBeclomethasoneBudesonideBudesonideFlunisolideFlunisolideFluticasone propionateFluticasone propionateTriamcinolone acetonideTriamcinolone acetonide

Oral (Quick relief of asthmatic symptoms)PrednisonePrednisolone* Unresponsive to 2 agonists

Metered Dose

Inhaler Al so, Dry-powder inhalersand Nebulizers



42/58


43/58

Kortikosteroid SistemikKortikosteroid SistemikKortikosteroid SistemikKortikosteroid Sistemik

Triamcinolone 5 0 18-36 3,0

Betamethasone 25 0 18-36 4,0

http:///http://www.novapdf.com/http://www.novapdf.com/http:///


44/58

Kortikosteroid TopikalKortikosteroid TopikalKortikosteroid TopikalKortikosteroid Topikal

Level of PotencyLevel of Potency CorticosteroidCorticosteroid Commercial ProductsCommercial Products

UltraUltra--highhigh Halobetasol propionateHalobetasol pro pionateClobetasol pro pionateClobetasol pro pionateBetamethasone diprop ionateBetamethasone diprop ionate

Diflorasone d iacetateDiflorasone d iacetate

Ultravate crm/ointUltravate crm/ointTemovate crm/ointTemovate crm/ointDiprolene ointDiprolene oint

Psorcon ointPsorcon oint

HighHigh HalcinonideHalcinonide Amcinonide AmcinonideBetamethasone diprop ionateBetamethasone diprop ionateMometasone fu roateMometasone fu roateDiflorasone d iacetateDiflorasone d iacetateFluocinonideFluocinonideDesoximetasoneDesoximetasone

Halog c rmHalog c rmCylocort ointCylocort ointDiprolene AF crmDiprolene AF crmElocon ointElocon ointFlorone ointFlorone ointLidex crm,gel,ointLidex crm,gel,ointTopicort crm,oint,gelTopicort crm,oint,gel

Mild to highMild to high HalcinonideHalcinonideTriamcinolone acetonideTriamcinolone acetonideBetamethasone diprop ionateBetamethasone diprop ionateFluocinonideFluocinonide

Halog oint,crm,solnHalog oint,crm,soln Aristoc ort A o in t Aristoc ort A o in tDiprosone crmDiprosone crmLidexLidex--E crmE crm



45/58

Kortikosteroid TopikalKortikosteroid TopikalKortikosteroid TopikalKortikosteroid Topikal

Level of PotencyLevel of Potency CorticosteroidCorticosteroid Commercial ProductsCommercial Products

MildMild Hydrocortisone valerateHydrocortison e valerateTriamcinolone acetonideTriamcinolone acetonideFlurandrenolideFlurandrenolide

Mometasone fu roateMometasone fu roateFluocinolone acetonideFluocinolone acetonide

WestcortWestcortKenalog crm and ointKenalog crm and ointCordran ointCordran oint

Elocon crmElocon crmSynalar oin tSynalar oin t

Low to mildLow to mild Hydrocortisone valerateHydrocortison e valerateTriamcinolone acetonideTriamcinolone acetonideFlurandrenolideFlurandrenolideBetamethasone dipropionateBetamethasone dipropionateHydrocortisone butyrateHydrocortisone butyrateFlucolone acetonideFlucolone acetonide

Westcort c rmWestcort c rmKenalog crm and ointKenalog crm and ointCordran crmCordran crmDiprosone lotionDiprosone lotionLocoid crmLocoid crmSynalar crmSynalar crm

LowLow Alclometasone dipropionate Alc lometasone diprop ionateBetamethasone valerateBetamethasone valerateFluocinolone acetonideFluocinolone acetonideHydrocortison e, dexamethasone,Hydrocortison e, dexamethasone,prednisolone, methylprednisoloneprednisolone, methylprednisolone

Aclovate crm and o int Aclovate crm and o intValisone lo tionValisone lo tionSynalar soln and crmSynalar soln and crm



46/58

Efek Samping Pemakaian KortikoSteroid jangka panjang

Efek Samping Pemakaian KortikoSteroid jangka panjang

http://www.novapdf.com/http://www.nova/http://www.nova/http://www.novapdf.com/


47/58

Efek SampingEfek SampingEfek SampingEfek Samping

Adrenocortical insufficiency: Suppression of HPA

Adrenocortical excess (Cushings disease): Moon face, buffalohump Diabetes Mellitus

CNS effects: psychological and behavioral changes; aggravationof pre-existing psychiatric disorders.

Impaired wound healing

Musculoskeletal effects: osteoporosis (brittle bones), muscleweakness and atrophy

Cardiovascular effects: fluid retention, edema, hypertension.

Adrenocortical insufficiency: Suppression of HPA

Adrenocortical excess (Cushings disease): Moon face, buffalohump Diabetes Mellitus

CNS effects: psychological and behavioral changes; aggravationof pre-existing psychiatric disorders.

Impaired wound healing

Musculoskeletal effects: osteoporosis (brittle bones), muscleweakness and atrophy

Cardiovascular effects: fluid retention, edema, hypertension.

Glucocorticoid Withdrawal: Should be performed slowlyWithdrawal syndrome: hypotension, hypoglycemia, myalgia and fatigue



48/58

Cushing Syndrome (Hypercorticism)Cushing Syndrome (Hypercorticism)Cushin g Syndrome (Hypercorticism)Cushing Syndrome (Hypercorticism)



49/58

Strategi Mencegah ES Jangka PanjangStrategi Mencegah ES Jangka PanjangKortikosteroidKortikosteroid

Strategi Mencegah ES Jangka PanjangStrategi Mencegah ES Jangka PanjangKortikosteroidKortikosteroid

Pemberian dengan dosis intermit tenPemberian dengan dosis intermit ten(alternate(alternate- -day), mis. setiap 2hari sekaliday), mis. setiap 2hari sekaliPemberian yg berefek lokal : topikal atauPemberian yg berefek lokal : topikal atau

inhalasiinhalasi

Pemberian dengan dosis intermit tenPemberian dengan dosis intermit ten(alternate(alternate- -day), mis. setiap 2hari sekaliday), mis. setiap 2hari sekaliPemberian yg berefek lokal : topikal atauPemberian yg berefek lokal : topikal atau

inhalasiinhalasi

http://www.novapdf.com/http://www.novapdf.com/


50/58

Drug InteractionsDrug InteractionsDrug InteractionsDrug Interactions

Drugs that Enhance Corticosteroid EffectsEstrogensOral contraceptives

Antifungal agents

Antibiotics*all of these agents inhibit cytochrome P450 enyzymes

Drugs that Reduce Corticosteroid Effects AntacidsCholestyramine

*these drugs decrease the absorption of corticosteroidsPhenytoin: activate cytochrome P450 enyzymes

Drugs that Enhance Corticosteroid EffectsEstrogensOral contraceptives

Antifungal agents

Antibiotics*all of these agents inhibit cytochrome P450 enyzymes

Drugs that Reduce Corticosteroid Effects AntacidsCholestyramine

*these drugs decrease the absorption of corticosteroidsPhenytoin: activate cytochrome P450 enyzymes



51/58

SYOK ANAFILAKTIKSYOK ANAFILAKTIKSYOK ANAFILAKTIKSYOK ANAFILAKTIK



52/58

Clinical Features of AnaphylaxisClinical Features of Anaphylaxis

- Is there a predisposition? Latex and food allergies usuallyoccur against a background of atopy and other allergicdisorders e.g. asthma and eczema.

- Onset is rapid (5-10 minutes of exposure) peaking in 30minutes. Duration can be long especially if allergen persists(e.g. swallowed) or the response is biphasic (classical late-phase allergic response in the airways)

- May be heralded by impending sense of doom.Subsequent features reflect to some extent route of allergenexposure:

Systemic (IV drugs) - cardiovascular

(hypotension/syncope) Ingested (food allergens) - respiratory (laryngealoedema/bronchoconstriction) Percutaneous (insect stings) - respiratory orcardiovascular problems equally likely

All may be accompanied by cutaneous features

e.g. urticarial rash.

Urticarial Rash



53/58

Features Suggesting Severe Anaphylactic Reaction

Wheeze Stridor

Cyanosis Skin Pallor* Prominent Tachycardia**

* 80% of fatal food-related anaphylactic reactions have no skin signs** Compared to bradycardia in vasovagal attack



54/58

20052005GuidelinesGuidelinesof the UKof the UK

ResuscitatiResuscitation Councilon Council



55/58

EPINEFRIN /ADRENALINEPINEFRIN /ADRENALINEPINEFRIN /ADRENALINEPINEFRIN /ADRENALIN

Bukan anti allergi, tp sering dipakai pd kasusallergi 1 st line drug syok anafilaktikMek kerja : agonis kuat resept &

adrenergikBerfungsi :

memberi efek antagonis thd efek mediatorinflamasi pada otot polos

Menghambat Ag-induced release mediatorinflamasi dari sel mast

Bukan anti allergi, tp sering dipakai pd kasusallergi 1 st line drug syok anafilaktikMek kerja : agonis kuat resept &

adrenergikBerfungsi :

memberi efek antagonis thd efek mediatorinflamasi pada otot polos

Menghambat Ag-induced release mediatorinflamasi dari sel mast



56/58

The Use of Adrenaline in Anaphylaxis

The problems with its use :

Variable Absorpt ion - give IM AVOID SC Arrhythmogenic in high dose - NEVER give 1:1000 ADRENALINE IV

If using ADRENALINE as an IVI, it must be diluted and do not delayadministration of ADRENALINE to set up IVI and gain IV access.

Therefore:

1. Give ADRENALINE IM promptly (can repeat at 5-10 min intervals)

2. Gain IV access3. If patient remains shocked resort to IVI thus .

Dilute 0.5ml of 1:1000 ADRENALINE in 50ml of N/saline (1:100,000)4. Infuse at 0.1-2ml/min (1-20ug/min) until haemodynamically stable



57/58

Other drugs used in Anaphylaxis

Nebul ised or IV 2 agonist (e.g. salbutamol) - useful wherebronchospasm is the major sign and fails to respond promptly to IMadrenaline.

IV Glucocorticoid (e.g. hydrocortisone 200-500mg) - probably oflimited efficacy (onset of action delayed 3-6 hrs) except where theresponse is biphasic or asthmatic features predominate.

IV Glucagon (1mg in 1L, infused at 5-15ml/min) - anecdotal reports of efficacy inrefractory hypotension. Releases catecholamines and +ve inotrope (raising cAMPindependent of cardiac -adrenoceptors).



58/58

Tanya apa ya ???..

kul obat sist imun, 2011 [compatibility mode]

Documents