Sella Modul Tropis

8/10/2019 Sella Modul Tropis

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Pengaruh pengaturan otonom vasokonstriksi perifer pengeluaran (dissipation) panas

menurun demam

Peningkatan aktivitas metabolisme penambahan produksi panas penyaluran ke

permukaaan tubuh inadekuat rasa demam bertambah pada pasien

IPD FKUI jilid 3 edisi 4

Fever occurs due to the release of the leukocyte pyrogen previously been stimulated byexogenous pyrogens can be derived from microorganisms or is a result of animmunological reaction that is not based on an alleged infeksi.Pirogen as a protein that isidentical to interleukin-1.Di these substances stimulate the hypothalamus the release ofarachidonic acid and prostaglandins E2 resulted in an increase in the direct synthesis canlead to a pyrexia.Effect of peripheral vasoconstriction otonomtis setting expenditure (dissipation)decreases fever heatIncreased metabolic activity of the addition of heat production distribution of bodysurface to increase inadequate sense of fever in patients

3. What causes intermitten fever


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Sumber : Buku Ajar Ilmu Penyakit Dalam Edisi V

5. Why from the physical examination shows a pale palpebral

conjunctiva (anemia )Guidelines for Case Management of Malaria in Indonesia. 2008

Congested spleen, blacken and become hard due to pigment deposits parasites anderythrocytes increased connective tissue (Corwin, 2000, p. 571).

Guidelines for Case Management of Malaria in Indonesia. 2008The degree of anemia depends on the cause of the species, is the most severe anemia due tofalciparum. Anemia caused by excessive destruction of erythrocytes normal erythrocytes cannot live long (reduced survival time). Impaired formation of erythrocytes due to depressederythropoiesis in the bone marrow. (Mansjoer. et al, p. 411)

Lien destroy the normal speed of 1/20 of peripheral erythrocytes

Splenomegaly destroy more of erythrocytes, even normal erythrocytes.

hemolytic jaundice

Caused by lysis (breakdown) excessive red blood cells. Jaundice can occur in red blood celldestruction and excessive liver can conjugate all of bilirubin which is derived

hepatocellular jaundice

Presence of sporozoites that invade the liver causing decreased absorption and conjugation ofbilirubin by the liver dysfunction occurs in hepatocytes and hepatocellular call.

Overview of Clinical Examination Results, Laboratory. Ronald A. Sacher, Richard A. McPherson

Pale palpebra


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Anemia results from accelerated RBC removal by the spleen, obligatory RBC destructionat parasite schizogony, and ineffective erythropoiesis. In severe malaria, both infectedand uninfected RBCs show reduced deformability, which correlates with prognosis anddevelopment of anemia. Splenic clearance of all RBCs is increased.

(Harrisons. Principles of Internal Medicine. 17th edition) Sclera icteric

(Ilmu Penyakit Hati. Ali Sulaiman)

SplenomegaliThe spleen plays an important role in protection against malaria, and asplenic individualsmay be at serious risk from P. Falciparum infection. Indeed, experienced surgeons in

tropical regions take a conservative approach to management of splenic trauma in theknowledge of increased mortality from malaria in individuals who have undergonesplenectomy. The spleen is enlarges with acute malaria, presumably as it functionstoremove paracitised erythrocytes (recognised either because of their loss of deformity or

propessity to form clumps of sequestered cells) from the peripheral circulation, andsplenic macrophags remove dead parasites.(Principles and Practice of Clinical Parasitology. Gillespie&Richard. 2001)


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Inflammatory splenomegaly

This is an acute enlargement of the spleen that develops in association with variousinfections or inflammatory processes and results from an increase in the defense activitiesof the organ. The demand for increased antigen clearance from the blood may lead toincreased numbers of reticuloendothelial cells in the spleen and stimulate acceleratedantibody production, with resultant lymphoid hyperplasia. Examples includesplenomegaly from lupus and Felty syndrome, and from viral infections such as EbsteinBarr Virus induced mononucleosis.

Hyperplastic splenomegaly

In this setting, splenomegaly is thought to reflect work hypertrophy that results from theremoval of abnormal blood cells from the circulation (either cells with intrinsicdefects or cells coated with antibody) or, in some cases, that results fromextramedullary hematopoiesis (ie, myeloproliferative disease).

Congestive splenomegaly

This condition develops as a result of cirrhosis with portal hypertension, splenic veinocclusion (thrombosis), or congestive heart failure (CHF) with increased venous pressure.

Infiltrative splenomegaly

In this setting, splenomegaly is the result of engorgement of macrophages withindigestible materials (eg, sarcoidosis, Gaucher disease, amyloidosis, metastaticmalignancy).

Infectious splenomegaly

Splenic filtering of blood-borne pathogens, especially encapsulated organisms, may leadto abscess formation. Because many splenic abscesses may be indolent in presentation,


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splenic size may be increased as the abscess enlarges. This is a relatively uncommon, butimportant, process to recognize and treat.

(http://emedicine.medscape.com/article/206208-overview#aw2aab6b2b2aa)

(http://www.ajronline.org/doi/full/10.2214/ajr.179.5.1791239 )

6. Why the patient has icterusClinically visible as hyperbilirubinemia or jaundice or jaundice, which is a

yellow pigmentation of the skin and sclera. Jaundice can usually only be seenwhen bilrubin serum levels exceed 34 to 43 mol / L (2.0 to 2.5 mg / dL), orabout twice the upper limit of the normal range; however, these symptomscan be detected with higher bilirubin levels lower in patients whose skin iswhite and who suffer from severe anemia. In contrast, symptoms of jaundiceare often not visible on those dark skin or who suffer from edema. Scleratissue is rich with elastin which has a high affinity for bilirubin, jaundice inthe sclera that is usually a sign of a more sensitive to indicate jaundicehyperbilirubinemia than thorough. Early sign of hyperbilirubinemia wassimilar to the dark color of urine, caused by bilirubin excretion through the

kidneys in the form of bilirubin glukuronid. In the striking jaundice, skingreenish due to the partial oxidation of bilirubin to biliverdin outstanding.This effect is often seen in conditions with prolonged conjugatedhyperbilirubinemia heavy tau as cirrhosis. Other symptoms may appeardepending on the cause, for example:1. liver inflammation (hepatitis) can cause loss of appetite, nausea, vomiting,
http://emedicine.medscape.com/article/206208-overview#aw2aab6b2b2aahttp://www.ajronline.org/doi/full/10.2214/ajr.179.5.1791239http://www.ajronline.org/doi/full/10.2214/ajr.179.5.1791239http://www.ajronline.org/doi/full/10.2214/ajr.179.5.1791239http://emedicine.medscape.com/article/206208-overview#aw2aab6b2b2aa


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and fever2. Blockage of the bile can cause symptoms of cholestasis

Sumber : Horrison Ilmu Penyakit Dalam

7. Why the physical examination shows a splenomegaly

Guidelines for Case Management of Malaria in Indonesia. 2008

Congested spleen, blacken and become hard due to pigment deposits parasites and erythrocytesincreased connective tissue (Corwin, 2000, p. 571).

Guidelines for Case Management of Malaria in Indonesia. 2008

The degree of anemia depends on the cause of the species, is the most severe anemia due tofalciparum. Anemia caused by excessive destruction of erythrocytes normal erythrocytes can notlive long (reduced survival time). Impaired formation of erythrocytes due to depressederythropoiesis in the bone marrow. (Mansjoer. et al, p. 411)

Lien destroy the normal speed of 1/20 of peripheral erythrocytes

Splenomegaly destroy more of erythrocytes, even normal erythrocytes.

hemolytic jaundice

Caused by lysis (breakdown) excessive red blood cells. Jaundice can occur in red blood celldestruction and excessive liver can conjugate all of bilirubin which is derived

hepatocellular jaundice

Presence of sporozoites that invade the liver causing decreased absorption and conjugation of bilirubin by the liver dysfunction occurs in hepatocytes and hepatocellular call.

Overview of Clinical Examination Results, Laboratory. Ronald A. Sacher, Richard A.McPherson


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8. Why in the blood smear test shows an abnormal erythrocyte

Pedoman Penatalaksanaan Kasus Malaria di Indonesia. 2008

9. Why the mosquito bite can cause many symptom in scenario(FEVER,menggigil,berkeringat)

Nyamukmenggigit (betinamenghisapdarah,jantan sarimakanandan buah2an) plasmodium

masukkepembuluhdarahsbgsporozoit menginvasiselhepar skizon kembalikepembuluhdarahmenginvasieritrosit(2 gambaraneritrosit 1.ring 2.knob) salah 1

eritrositpecah skizonpecah merozoit

10. What the prevention medication before stay inpapua

Table 2 .Instructions for Travelers during the Pretravel Consultation.*

- Use effective personal protection against mosquitoes.- Anopheles mosquitoes bite between dusk and dawn.- Wear long sleeves, long pants, and fully closed shoes with socks after dark.- Use permethrin-treated mosquito nets if accommodations are neither well


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screened nor air-conditioned.- Repellent containing 30%50% DEET obtained from an outdoors store or

travel-supply vendor should be applied to exposed areas of skin every 4 to6 hours. More frequent application is required for agents containing lowerconcentrations of DEET. Agents containing 20% or higher concentrations ofpicaridin (KBR 3023) are similar to those containing DEET at thesame concentration with regard to activity against anopheles mosquitoes.

- Adhere to an antimalarial regimen.- Take weekly medications on the same day each week. (Sunday may be easiest

to remember.)- Take daily medications with the same meal each day.- Continue medications after the trip for the recommended duration.- If intolerable side effects occur, make every effort to contact the health

careprovider who prescribed the medications or the covering physician bytelephone (or by e-mail if offered by the practice) for advice. Physicians atthe destination may have poor knowledge of drugs and regimens used bytravelers. (The severity of side effects must be weighed against the risk ofa potentially fatal infection with Plasmodium falciparum)

- Remember that no chemoprophylactic regimen against malaria is 100%effective.

- Symptoms of malaria may be mild and may mimic influenza, gastroenteritis,or other common infections; any fever that develops during or after travelto an area where there is a risk of malaria infection should raise thesuspicion of malaria.

- Early treatment is usually effective, whereas delay of appropriate therapycanhave serious or even fatal consequences; therefore, if symptoms of malariaoccur, seek prompt medical attention.

- If fever develops within 3 mo after return from travel, a physician should beinformed of the recent travel, and blood films or a rapid card test formalaria with immediate reporting should be requested; waiting for next-day


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results may increase the risk of death. If the blood film or card test isnegative, two additional tests (including at least one blood film) should beperformed 12 24 hr apart for confirmation, and other diagnoses shouldbe considered at the same time.

- Ask health care providers who need assistance with diagnosis or managementof suspected cases of malaria to call the CDC Malaria Hotline: 770-488-7788.

*CDC denotes Centers for Disease Control and Prevention, and DEETN,Ndiethyl-3-methylbenzamide.Effective concentrations are available worldwide, but concentrationscurrently available in the Un ited States (15%) are suboptimal forprotection against malaria. Data are from Constantini et al.

Malaria Prevention in Short-Term TravelersDavid O. Freedman, M.D.

11. What does the endemic area of vector born disease mean

12. How is the life cycle of parasite in human body


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13. DD

Knob

Toxin GPI

IL-1 , TNF

FeverEritropoiesis depressionin Bone marrow

Anemia

RBC destruction

in Spleen

Hemolysis RBC

Anemia

J

Female Anopheles

Bite human

Sporozoit enter to circulation

Liver

Schizon in hepatocyte

Replication

Hepatocyte rupture

Merozoit release

RBC invasion

Replication

Tropozoit

Schizon imature

Schizon mature

Rupture RBC

Merozoit release

Infected other health RBC Gametocyte

Sexual cycle infemale anopheles

the cycle repeats

Hipnozoit

Survive in liver

Relaps


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MALARIA

Alternative Names

Quartan malaria; Falciparum malaria; Biduoterian fever; Blackwater fever;Tertian malaria; Plasmodium

Causes

Malaria is caused by a parasite that is passed from one human to anotherby the bite of infected Anopheles mosquitoes. After infection, theparasites (called sporozoites) travel through the bloodstream to the liver,where they mature and release another form, the merozoites. Theparasites enter the bloodstream and infect red blood cells.

The parasites multiply inside the red blood cells, which then break openwithin 48 to 72 hours, infecting more red blood cells. The first symptomsusually occur 10 days to 4 weeks after infection, though they can appearas early as 8 days or as long as a year after infection. The symptoms occurin cycles of 48 to 72 hours.

Most symptoms are caused by:

The release of merozoites into the bloodstream Anemia resulting from the destruction of the red blood cells

Large amounts of free hemoglobin being released into circulation afterred blood cells break open

Malaria can also be transmitted from a mother to her unborn baby(congenitally) and by blood transfusions. Malaria can be carried bymosquitoes in temperate climates, but the parasite disappears over thewinter.

The disease is a major health problem in much of the tropics andsubtropics. The CDC estimates that there are 300-500 million cases ofmalaria each year, and more than 1 million people die from it. It presents amajor disease hazard for travelers to warm climates.

In some areas of the world, mosquitoes that carry malaria have developedresistance to insecticides . In addition, the parasites have developed
http://health.nytimes.com/health/guides/disease/anemia/overview.htmlhttp://health.nytimes.com/health/guides/disease/anemia/overview.htmlhttp://health.nytimes.com/health/guides/test/hemoglobin/overview.htmlhttp://health.nytimes.com/health/guides/test/hemoglobin/overview.htmlhttp://health.nytimes.com/health/guides/test/hemoglobin/overview.htmlhttp://health.nytimes.com/health/guides/poison/insecticide/overview.htmlhttp://health.nytimes.com/health/guides/poison/insecticide/overview.htmlhttp://health.nytimes.com/health/guides/poison/insecticide/overview.htmlhttp://health.nytimes.com/health/guides/poison/insecticide/overview.htmlhttp://health.nytimes.com/health/guides/test/hemoglobin/overview.htmlhttp://health.nytimes.com/health/guides/disease/anemia/overview.html


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Possible treatments for chloroquine-resistant infections include:

The combination of quinidine or quinine plus doxycycline, tetracycline, orclindamycin

Atovaquone plus proguanil (Malarone) Mefloquine or artesunate The combination of pyrimethamine and sulfadoxine (Fansidar)

The choice of medication depends in part on where you were when youwere infected.

Medical care, including fluids through a vein (IV) and other medicationsand breathing (respiratory) support may be needed.

Outlook (Prognosis)

The outcome is expected to be good in most cases of malaria withtreatment, but poor in Falciparum infection with complications.

Possible Complications

Brain infection (cerebritis) Destruction of blood cells (hemolytic anemia)

Kidney failure Liver failure Meningitis Respiratory failure from fluid in the lungs (pulmonary edema) Rupture of the spleen leading to massive internal bleeding (hemorrhage)

When to Contact a Medical Professional

Call your health care provider if you develop fever and headache aftervisiting the tropics.

Prevention

Most people who live in areas where malaria is common have gotten someimmunity to the disease. Visitors will not have immunity, and should takepreventive medications.
http://health.nytimes.com/health/guides/disease/hemolytic-anemia/overview.htmlhttp://health.nytimes.com/health/guides/disease/hemolytic-anemia/overview.htmlhttp://health.nytimes.com/health/guides/disease/hemolytic-anemia/overview.htmlhttp://health.nytimes.com/health/guides/disease/acute-kidney-failure/overview.htmlhttp://health.nytimes.com/health/guides/disease/acute-kidney-failure/overview.htmlhttp://health.nytimes.com/health/guides/disease/meningitis/overview.htmlhttp://health.nytimes.com/health/guides/disease/meningitis/overview.htmlhttp://health.nytimes.com/health/guides/disease/pulmonary-edema/overview.htmlhttp://health.nytimes.com/health/guides/disease/pulmonary-edema/overview.htmlhttp://health.nytimes.com/health/guides/disease/pulmonary-edema/overview.htmlhttp://health.nytimes.com/health/guides/disease/pulmonary-edema/overview.htmlhttp://health.nytimes.com/health/guides/disease/meningitis/overview.htmlhttp://health.nytimes.com/health/guides/disease/acute-kidney-failure/overview.htmlhttp://health.nytimes.com/health/guides/disease/hemolytic-anemia/overview.html


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It is important to see your health care provider well before your trip,because treatment may need to begin as long as 2 weeks before travel tothe area, and continue for a month after you leave the area. In 2006, theCDC reported that most travelers from the U.S. who contracted malaria

failed to take the right precautions.The types of anti-malarial medications prescribed will depend on the area

you visit. According to the CDC, travelers to South America, Africa, theIndian subcontinent, Asia, and the South Pacific should take one of thefollowing drugs: mefloquine, doxycycline, chloroquine, hydroxychloroquine,or Malarone. Even pregnant women should take preventive medicationsbecause the risk to the fetus from the medication is less than the risk ofcatching this infection.

People who are taking anti-malarial medications may still become infected.Avoid mosquito bites by wearing protective clothing over the arms andlegs, using screens on windows, and using insect repellent.

Chloroquine has been the drug of choice for protecting against malaria.But because of resistance, it is now only suggested for use in areas wherePlasmodium vivax , P. oval , and P. malariae are present. Falciparum malariais becoming increasingly resistant to anti-malarial medications.

For travelers going to areas where Falciparum malaria is known to occur,there are several options for malaria prevention, including mefloquine,atovaquone/proguanil (Malarone), and doxycycline.

Travelers can call the CDC for information on types of malaria in a certainarea, preventive drugs, and times of the year to avoid travel.

References

Fairhurst RM, Wellems TE. Plasmodium species (Malaria). In: Mandell GL,Bennett JE, Dolin R, eds. Principles and Practice of Infectious Diseases .7th ed. Philadelphia, Pa: Elsevier Churchill Livingstone; 2009:chap 275.

Krogstad DJ. Malaria. In: Goldman L, Ausiello D, eds.Cecil Medicine . 23rded. Philadelphia, Pa: Saunders Elsevier. 2007:chap 366.


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children living in areas with stable transmission, particularly whereresistance has compromised the efficacy of antima-larial drugs. Innonimmune individuals with acute malaria, the spleen takes severaldays to become palpable, but splenic enlargement is found in a highproportion of otherwise healthy individuals in malaria endemicareas and reflects repeated infections. Slight enlargement of theliver is also common, particularly among young children. Mild

jaundice is common among adults; it may develop in patients withotherwise uncomplicated falciparum malaria and usually resolvesover 13 weeks.

PATOGENESIS PATOFISIOLOGI PENEGAKAN DIAGNOSIS

a. AnamnesisKeluhan utama tersering demam >2hari, menggigil, berkeringat trias malariaMalaria berat gangguan kesadaran, kelemahan, kelumpuhan otot,kejang, panas tinggi, muntah terus menerus

b. PFDemam 37,5-40 CKonjungtiva palpebra pucat anemiaSpleomegaliHepatomegaliMalaria berat penurunan kesadaran, dehidrasi, perdarahan, ikterik,gangguan ginjal, pembesaran hai dan limpa, gejala neurologi(reflekspatologis dan kaku duduk)

c. Px. Tetes darah untuk malariaPreparat darah tebal: cara terbaik menemukan parasit malaria,dinyatakan negatif jika setelah diperiksa dalam 200 lapang pandangdengan pembesaran kuat 700-1000 kali tidak ditemukan parasit.Preparat darah tipis: untuk identifikasi jenis plasmodium, bila dengandarah tebal sulit ditemukan.


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d. Tes antigen : P-F testMendeteksi antigen dari p. Falciparum(Histidine rich protein II) hanya 3-5menit, sensitivitas baik Deteksi untuk p.vivax: ICT

e. Tes serologiIndirect hemaglutination test, ELISA test, radio immunoassay,immunoprecipitation techniques mendeteksi antibodi spesifikmalaria/ keadaan dimana parasit sangat minimal kurang bermanfaatkrn antibodi baru muncul setelah beberapa hari parasitemia.

f. PCRDengan teknologi amplifikasi DNA, sensitivitas dan spesifitasnyatinggi, dapat memberikan hasil positif meskipun parasit sangat sedikit.

TERAPI PENCEGAHAN

a. Pencegahan dari gigitan nyamuk: kelambu, obat pembunuh nyamuk(repellent), mencegah berada di alam bebas, proteksi tempat tinggal.

b. KemoprofiaksisKetahui sensitivitas plasmodium ditempat tujuan:

- Sensitif klorokuin: 2tab klorokuin 1minggu sebelum, tiap mingguditujuan, 4minggu setelah tiba kembali.

- Resisten klorokuin: doksisiklin 0,5 mg/kgbb/hari atau mefloquin250 mg/minggu atau klorokuin 2tab per minggu ditambah proguanil200mg/hari.

c. VaksinMasih dalam perkembangan p.falciparum 3jenis vaksin vaksinsporozoit, vaksin asexual, vaksin transmission blocking untuk melawanbentuk gamerosit.

PROGNOSIS

DEMAM TIPHOID


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- anorexia (55%)- abdominal pain (3040%)- nausea (1824%)- vomiting (18%),- diarrhea (22 28%) more commonly than constipation (1316%).

The most prominent symptom is prolonged fever (38.8 40.5C; 101.8104.9F).

Sifat demam adalah meningkat perlahan-lahan dan terutama pada sorehingga malam hari.

Physical findings included

- hepatosplenomegaly (36%)- epistaxis- relative bradycardia at the peak of high fever- coated tongue (51 56%),- abdominal tenderness (4 5%)

PATOGENESIS


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PATOFISIOLOGI PENEGAKAN DIAGNOSIS

the clinical presentation of enteric fever is relatively nonspecific, thediagnosis needs to be considered in any febrile traveler returning from adeveloping country, especially the Indian subcontinent, the Philippines, orLatin America. Other diagnoses that should be consid-ered in thesetravelers include malaria, hepatitis, bacterial enteritis, dengue fever,

rickettsial infections, leptospirosis, amebic liver abscess-es, and acuteHIV infection.

Physical findings included:

- hepatosplenomegaly (36%)- epistaxis- relative bradycardia at the peak of high fever- coated tongue (51 56%),

- abdominal tenderness (4 5%)

Px Laba. Pemeriksaan Rutin

Leucopenia, dapat leukosit normal atau leukositosis. Leukosotosis

dapat terjadi walaupun tanpa disertai infeksi sekunder. Selain itu

dapat pula ditemukan anemia ringan dan trombositopenia. Pada

pemeriksaan hitung jenis leukosit dapat terjadi aneosinofilia maupun

limfopenia. Laju endap darah pada demam tifoid dapat meningkat.

SGOT dan SSPT seringkali meningkat, tetapi akan kembali menjadi

meningkat setelah sembuh.


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b. Uji Widal

Uji widal adalah suatu reaksi aglutinasi antara antigen dan antibodi

(aglutinin). Aglutinin yang spesifik terhadap salmonella thypi terdapat

dalam serum klien dengan typhoid juga terdapat pada orang yang

pernah divaksinasikan. Antigen yang digunakan pada uji widal adalah

suspensi salmonella yang sudah dimatikan dan diolah di laboratorium.

Tujuan dari uji widal ini adalah untuk menentukan adanya aglutinin

dalam serum klien yang disangka menderita typhoid.

TERAPI

Sampai saat ini masih dianut trilogy penatalaksanaan demam tifoid, yaitu:

1. Istirahat dan Perawatan

Tujuannya adalah untuk mencegah komplikasi dan mempercepatpenyembuhan. Bed rest dianjurkan selama 7 hari atau sampaidemamnya hilang.

2. Diet dan Terapi Penunjang

Diet merupakan hal yang cukup penting dalam proses penyembuhanpenyakit demam tifoid, karena makanan yang kurang akan menurunkankeadaan umum dan gizi penderita, sehingga proses penyembuhan akanberlangsung lebih lama.

Di masa lampau penderita tifoid akan diberi diet BS-BB-NB, mula-mulabubur saring, kemudian ditingkatkan menjadi bubur biasa, dan akhirnya

diberikan nasi, perubahan diet itu disesuaikan dengan tingkatkesembuhan penderita. Pemberian bubur saring tersebut ditujukanuntuk menghindari komplikasi perdarahan saluran cerna dan perforasiusus. Hal ini didasarkan pada pendapat bahwa usus harusdiistirahatkan. Beberapa peneliti menunjukkan bahwa pemberianmakanan padat dini yaitu nasi dengan lauk pauk rendah selulosa


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Kloramfenikol dikontraindikasikan unutk neonates, pasiendengan gangguan faal hati, dan pasien yang hipersensitifterhadapnya.

Efek samping dari kloramfenikol terutama berupa reaksihematologik, reaksi saluran cerna, dan sindrom Gray .

Reaksi hematologik ini terdapat dalam dua bentuk. Yangpertama ialah reaksi toksik dengan manifestasi depresi sumsumtulang. Kelainan darah yang terlihat ialah anemia,retikulositopenia, peningkatan serum iron dan iron bindingcapacity serta vakuolisasi seri eritrosit bentuk muda. Bentuk

yang kedua adalah anemia aplastik.

Reaksi saluran cerna sebagai efek samping dari penggunaankloramfenikol bermanofestasi dalam bentuk mual, muntah,glositis, diare, dan enterokolitis.

Pada neonates, terutama bayi premature yang mendapat dosistinggi (200mg/kgBB) dapat timbul sindrom Gray . Mula-mulabayi muntah, tidak mau menyusu, pernafasan cepat dan tidakteratur, perut kembung, sianosis dan diare dengan tinjaberwarna hijau dan bayi tampak sakit berat. Pada hari

berikutnya tubuh bayi menjadi lemas dan berwarna keabu-abuan; terjadi pula hipotermia. Angka kematian kira-kira 40%,sisanya sembuh sempurna.

Di Indonesia, kloramfenikol masih merupakan obat pilihanpertama untuk mengobati demam tifoid. Dosis yang diberikanadalah 4x 500 mg per hari dan dapat diberikan secara oralmaupun intravena. Diberikan sampai dengan 7 hari bebas panas.Dari pengalaman penggunaan obat ini dapat menurunkan rata-rata 7,2 hari. Penulis lain menyebutkan penurunan demam dapatterjadi rata-rata setelah hari ke-5.

b. Tiamfenikol


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Trimetoprim dan sulfametoksazol (yang termasuk golongansulfonamide) menghambat reaksi enzimatik obligat pada duatahap yang berurutan pada mikroba, sehingga kombinasi keduaobat member efek sinergi. Sulfonamid menghambat masuknya

molekul PABA ke dalam molekul asam folat dan trimetoprimmenghambat terjadinya reaksi reduksi dari dihidrofolatmenjadi tetrahidrofolat.

Pada dosis yang dianjurkan tidak terbukti bahwa kotrimoksazolmenimbulkan defisiensi folat pada orang normal. Namun batasantara toksisitas untuk bakteri dan manusia relative sempit bilasel tubuh mengalami defisiensi folat. Dalam keadaan demikianobat ini mungkin menimbulkan megaloblastosis, leucopenia, atautrombositopenia. Kira-kira 75% efek samping obat terjadi padakulit, berupa reaksi yang khas yang ditimbulkan olehsulfonamide. Gejala-gejala saluran cerna terutama berupa mualdan muntah, diare jarang terjadi. Glositis dan stomatitisrelative sering. Reaksi susunan saraf pusat berupa sakit kepala,depresi, dan halusinasi, disebabkan oleh sulfonamide.

Reaksi hematologik lainnya adalah berbagai macam anemia,gangguan koagulasi, granulositopenia, agranulositosis, purpura,purpura Henoch-Schonlein dan sulfehemoglobinemia.

Efektifitas kotrimoksazol pada demam tifoid dilaporkan hampirsama dengan kloramfenikol. Dosis untuk orang dewasa adalah2x2 tablet (1 tablet mengandung sulfametoksazol 400 mg dan80 mg trimetoprim) diberikan selama dua minggu.

d. Ampisilin dan Amoksisilin

Ampisilin dan amoksisilin merupakan penisilin golongan spectrumluas. Penisilin merupakan salah satu antibiotika beta laktam,karena pada struktur kimianya terdapat cincin beta laktam.Mekanisme kerjanya dengan menghambat sintesis mukopeptida

yang diperlukan untuk pembentukan dinding sel bakteri(inhibitor sintesis dinding sel).


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Kemampuan kedua obat ini untuk menurunkan demam lebihrendah dibandingkan dengan kloramfenikol. Dosis yangdianjurkan berkisar antara 50-150 mg/kgBB dan digunakanselama dua minggu.

e. Sefalosporin Generasi Ketiga

Sefalosporin dibagi menjadi 4 generasi berdasarkan aktifitasanti mikrobanya yang secara tidak langsung juga sesuai denganurutan masa pembuatannya.

Seperti halnya antibiotic beta laktam lain, mekanisme kerja antimikroba sefalosporin ialah menghambat sintesis dinding selmikroba. Yang dihambat ialah reaksi transpeptidase tahapketiga dalam rangkaian reaksi pembentukan dinding sel.

Sefalosporin generasi ketiga umumnya kurang aktifdibandingkan generasi pertama terhadap kokus gram-positif,tetapi jauh lebih aktif terhadap Enterobacteriaceae , termasukstrain penghasil penisilinase.

Efek samping yang sering terjadi dalam penggunaansefalosporin adalah reaksi alergi, dengan gejala yang mirip

dengan reaksi alergi yang ditimbulkan oleh penisilin. Reaksimendadak yaitu anafilaksis dengan spasme bronkus danurtikaria dapat terjadi. Reaksi coombs sering timbul padapenggunaan sefalosporin dosis tinggi. Depresi sumsum tulangterutama granulositopenia dapat timbul meskipun jarang.

Hingga saat ini golongan sefalosporin generasi ketiga yangterbukti efektif untuk demam tifoid adalah seftriakson,dengan dosis yang dianjurkan adalah 3-4 gram dalam dextrose100cc diberikan selama jam perinfus sekali sehari, diberikanselama 3 hingga 5 hari.

f. Fluoroquinolon

Merupakan golongan kuinolon yang memiliki atom fluor padaposisi 6 dalam struktur molekulnya. Daya anti bakterifluorokuinolon jauh lebih kuat dibandingkan dengan kelompok


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Kombinasi dua antibiotic atau lebih diindikasikan hanya padakeadaan tertentu saja antara lain toksik tifoid, peritonitis atauperforasi, serta syok septic, yang pernah terbukti ditemukandua macam organism dalam kultur darah selain kuman

Salmonella .h. Kortikosteroid

Penggunaan steroid hanya diindikasikan pada toksik tifoid ataudemam tifoid yang mengalami syok septic dengan dosis 3 x 5mg.

Sella Modul Tropis

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