SHIVERING FEVER

1. Why the patient gets fever for a week and the periodic high fever preceded by shivering and followed by a spontaneus decrease in temperature with profuse sweating ?

2. What is the correlation between 3 months stayed in Papua with the dissease ?

Areas with high clinical cases in Indonesia:Papua, NTT, Maluku, Sulawesi Tenggara, West Kalimantan, Bangka Belitung, Bengkulu and Riau, and Timor Timur is an area with endemic malaria plasmodium vivax and plasmodium falcifarum.Sumber : repository.usu.ac.id/

Mosquito bites risk factorTypeof plasmodium :P. FalcifarumP. VivaxP. MalariaeP. Ovale

Aseksual reproduktionWhen the female anopheles mosquito (which contains malaria parasites) bite humans, will be out sporozoites from mosquito salivary glands into the blood and liver tissue. In the life cycle of the malaria parasite in the tissue forming cells sizon stage liver (exo-eritrositer stage). Once the liver cells burst, merozoites are going out / kriptozoit into erythrocytes established in erythrocytes sizon stage (stage eritrositer). There began to shape young troposit until sizon old / mature to erythrocytes rupture and merozoites exit.

Most of the merozoites enter erythrocytes and reinjected into fraction form male and female gametocytes that are ready to be sucked by the female malaria mosquito and continue its life cycle in the mosquito's body (stage sporogoni). In the mosquito stomach, occurred the marriage of male gamete cells (micro gametes) and the female gamete cells (macro-gametes) is called a zygote. Zygote turns into ookinet, then go into the stomach wall of the mosquito turns into oocysts. Once mature oocysts then broke, out sporozoites which migrate to the mosquito salivary glands and is ready to be transmitted to humans.

Seksual reproduction

Happens in the body when the mosquito Anopheles female mosquito sucks blood containing gametocytes. Gametocytes that are not digested with blood. At makrogamet (male) chromatin divides into a moving core 6-8 kepinggir parasites. The edge of a whip-like filaments formed and actively move called mikrogamet. Fertilization occurs due to the entry into makrogamet mikrogamet to form a zygote. Zygote short change shape like a worm called ookinet that can penetrate the

epithelial layer of the stomach wall and basement membrane. This place ookinet enlarged and called oocysts. Formed thousands of sporozoites within the oocysts and sporozoites penetrate several glands mosquito and when the mosquito bites / man stabbed the sporozoites enter the blood and start the cycle pre eritrositik.

3. Why does the patient icteric ?

Jaundice is common in falciparum malaria infection, possibly due to sequestration and sitoadheren which causes microvascular obstruction. Jaundice due to hemolytic frequent. Severe jaundice due to P. Falciparum often adult patients this because hemolysis, hepatocyte damage. There is also hepatomegaly, hyperbilirubinemia, decreased levels of serum albumin and a slight increase in serum transaminase and 5 nukleotidase. Disruption of liver function may lead to hypoglycemia, lactic acidosis, impaired drug metabolism.

Sumber : Sudoyo A. W. dkk, 2007. Buku Ajar – Ilmu Penyakit Dalam Jilid I Edisi IV . Jakarta : EGC

4. What is the type of fever ?

a. Septic fever: The temperature gradually rose to very high levels during the night and went back down to levels above normal in the morning. Disertia frequent complaints chills and sweating. If high fever went down to normal levels is also called fever hektik.

b. Remittances Fever: Temperature weight every day but never reached normal body temperature.

c. Intermittent fever: body temperature dropped to normal levels for several hours in a day. When a fever like this happens once every two days and called tertian case two fever-free days in between two bouts of fever called kuartana.

d. Continuous fever: body temperature during fever have no significant variation (less than one degree). When high continuous fever then called hyperpyrexia

Sumber : repository . usu .ac.id/

Pola demam Penyakit

Kontinyu Demam tifoid, malaria falciparum malignan

Remitten Sebagian besar penyakit virus dan bakteri

Intermiten Malaria, limfoma, endokarditis

Hektik atau septik Penyakit Kawasaki, infeksi pyogenik

Quotidian (sub

intermiten,periodik2

4 jam

Malaria karena P.vivax

Double quotidian

(2 demam

bersamaan)

Kala azar

a disease caused by protozoan parasites of the

Leishmania genus, arthritis gonococcal, juvenile

rheumathoid arthritis, beberapa drug fever (contoh

karbamazepin)

Relapsing atau

periodik

Malaria tertiana atau kuartana, brucellosis

Demam rekuren Familial Mediterranean fever

7. Cunha BA. The clinical significance of fever patterns. Inf Dis Clin North Am

1996;10:33-44

5. Why does the patient splenomegaly ?

Splenomegaly often seen in people with malaria, the spleen is palpable after 3 days of attacks of acute infection, a swollen spleen, pain and hyperemia. The spleen is an organ retikuloendothelial, where plasmodium cells destroyed by macrophages and lymphocytes. The addition of these inflammatory cells will cause the spleen to enlarge.

Sumber : Harijanto, dr. P. N. 2000. Malaria : Epidemiologi, Patogenesis, Manifestasi Klinis dan Penanganan. Penerbit Buku Kedokteran EGC. Jakarta.

6. What is the correlation between abnormal erytrocyt in blood peripheral blood smear test with the result of physical exam ?

7. Why the patient has pale palpebra conjunctiva ? According to another expert opinion, the pathogenesis of malaria is associated

with mulitifaktorial and the following:

a) The destruction of erythrocytes

Phagocytosis not only in erythrocytes containing parasites but also against

erythrocytes do not contain parasites that cause anemia and tissue anoxia. In the

severe intravascular hemolysis can occur hemoglobinuria (black water fever) and

can cause kidney failure.

b) The mediator of endotoxin-macrophage

At the time skizogoni, erythrocytes containing parasites endotoxin sensitive trigger

macrophages to release a variety of mediators. Endotoxin may originate from the

gastrointestinal tract and the malaria parasite itself can release tumor necrosis

factor (TNF). TNF is a monokin found in the blood circulation of humans and

animals infected with the malaria parasite. TNF and other cytokines cause fever,

hypoglycemia and respiratory disease syndrome in adults.

c) sequestration of infected erythrocytes

Erythrocytes infected with P. falciparum advanced stage can form protrusions

(knobs) on its surface. The bulge contains antigens and antibodies react with

malaria and is associated with affinity erythrocytes containing P. falciparum to the

endothelium of blood capillaries in the tool, so skizogoni circulation takes place in

the tool. Infected erythrocytes attached to the endothelium and forming clots that

stem capillary leak and cause tissue anoxia and edema

PARASITOLOGI KEDOKTERAN

Anemia. On malaria anemia may occur. The degree of anemia depends on the species of parasite that causes it. Anemia was particularly marked during falciparum malaria with a rapid destruction of erythrocytes in malaria and severe and chronic. Types of hemolytic anemia in malaria is, normokrom and normocytic. In the acute attack hemoglobin levels dropped suddenly.Anemia caused by several factors:a. Destruction of erythrocytes containing parasites and does not contain parasites that occur in the spleen, in this case an auto immune factors play a role.b. Reduced survival time, that does not mean normal erythrocytes containing parasites can not live long.c. Diseritropoesis the disturbance in the formation of erythrocytes due to depressed erythropoiesis in the bone marrow, reticulocytes can not be released in the peripheral blood circulation.

Sumber : repository . usu .ac.id/

8. What is rapid test ? How about the procedure and interpretation ?

9. Why the doctor gives recommendation a preventive medication ? what kind of preventive medication ?

Tempat tidur diberi kelambuSemprot obat serangga

Olesi tangan dan kaki dengan lotion anti nyamukLetak tempat tinggal diusahakan jauh dari yempat ternakHindari keadaan rumah yg lembab,gelap,kotor dan pakaian yg bergelantungan serta genangan air

10. What are the differential diagnoses ?

a. Malaria- Definisi

Malaria is a contagious infectious disease caused by parasites of the genus Plasmodium, which is transmitted through the bite of the Anopheles mosquito with an overview of the disease include frequent periodic fever, anemia, an enlarged spleen and a different set of symptoms because of its effect on several organs such as the brain, liver and kidneys.

- EtiologiMalaria is a contagious infectious disease caused by parasites of the genus PlasmodiumPlasmodium is a protozoan parasite belonging vilum, sporozoa class. There are four species of Plasmodium in humans, namely: Plasmodium vivax malaria vivax cause (mild tertian malaria). Falcifarum Plasmodium cause malaria falsifarum (severe tertian malaria), and Blackwater faver pernicious malaria. Plasmodium malariae malaria cause kuartana, ovale and Plasmodium ovale malaria cause.

- PatofisiologiAfter going through the liver tissue, releasing 18-24 plasmodium falciparum merozoites into the circulation. Merozoites are released will go into the RES cells in the spleen and undergo phagocytosis and filtration. Merozoites escape filtration and phagocytosis in the spleen would invade erythrocytes. Form of asexual parasites in erythrocytes is responsible jawabdalam the pathogenesis of malaria in humans.Pathogenesis of falciparum malaria and parasite factors are influenced by host factors (host). Are included in the parasite factor is the intensity of transmission, parasite density and parasite virulence. While that is a host of factors including the level of local endemitas, shelter, genetic, age, nutritional status and immunological status.Parasites in erythrocytes (EP) in outline having two stages, namely the 24-hour ring stage I and stage II mature at 24 hours. EP-stage surface antigens RESA ring displays (ring-erithrocyte surgace antigen) which disappeared after the parasite entered the mature stage. EP membrane surface protrusion will experience a mature stage and form a knob with histidine rich protein-1 (HRP-1) as the main components.

Furthermore, if the experience merogoni EP will be released in the form of GPI malaria toxin that is glikosofosfatidilinositol that stimulate the release of TNF-a and interleukin-1 (IL-1) from macrophages,Sitoadherensi is the mature stage of attachment between the EP on the vascular endothelial surface. Attachment occurs by way of adhesive molecules located on the surface of vascular endothelium. Sitoadherensi cause no circulating mature EP back in circulation. Parasites that live in mature erythrocytes in microvascular networks are experiencing mature EP called sequestration. Only experienced plasmodium falciparum sequestration, because the other plasmodium whole cycle occurs in the peripheral vasculature. Sequestration was highest in the brain, followed by liver and kidney, lungs, heart, intestines, and skin. Sequestration is thought to play a major role in the pathophysiology of severe malaria.

- Clinical manifestation

- Pemeriksaan fisik

1. Fever (≥ 37.5 measurements with thermometers ° C)2. Conjunctiva or pale palms3. Enlarged spleen (splenomegaly)4. Liver enlargement (hepatomegaly)

Severe malaria was found on the suspect clinical signs as follows:1. Rectal temperature ≥ 40 ° C2. Rapid and weak pulse3. Systolic blood pressure> 70 mm Hg in adults and in children <50> 35x/menit in adults or> 40x/menit in infants, children under 1 year> 50x/menit.5. Decrease the degree of awareness of the Glasgow coma scale (GCS) <11> 100 parasites per 1 field of view equivalent to 40 000 parasites / uL

- Pemeriksaan penunjang1. Examination drops of blood for malaria

a. Drops of blood preparations thick. Is the best way to find the malaria parasite

b. Thin trickle of blood preparations. Used to identify the type of plasmodium

2. Antigen test: p-f testWhich detects antigens of P. falciparum (Histidine Rich Protein II). Rapid detection of only 3-5 minutes, does not require special training, good sensitivity, does not require special tools. For antigen detection vivaks already in the market, namely the ICT method.

3. Serology teststechniques using indirect fluorescent antibody test. This test is useful to detect the presence of specific antibodies against the malaria parasite or in circumstances where very minimal.

4. PCR (Polymerase Chain Reaction)This examination is considered to be very sensitive to DNA amplification technology, when used reasonably fast and high sensitivity and specificity. Advantages this test although the number of parasites is very little to give positive results. This test is only used as a means of research and not for routine examination.

- Treatment1. falciparum malariaThe first line = artesunate + amodiaquine + primaquinePrimaquine is given orally with a single dose of 0.75 mg base / kg given on the first day.Second-line treatment of falciparum malaria is given, if the first-line treatment is not effective which found no worsening of clinical symptoms but not reduced asexual

parasites (persistent) or comes back (rekrudesensi)Second line = quinine + doxycycline or tetracycline + primaquineQuinine given orally, 3 times daily at a dose of 10 mg / kg for 7 days.Doxycycline is given 2 times per day for 7 days, with a dose of 4 mg / kg

2. Treatment for Malaria vivax and ovaleThe first line = chloroquine + primaquineThis combination is used as the primary choice for the treatment of malaria vivax and ovale malaria. Chloroquine treatment aims to kill the asexual and sexual stage parasites.Chloroquine was given 1 time per day for 3 days, with a total dose of 25 mg / kgPrimaquine was given for 14 days at a dose of 0.25 mg / kg

3. Treatment of chloroquine resistant vivax MalariaSecond line = quinine + primaquineQuinine given orally 3 times daily at a dose of 10 mg / kg for 7 days.Primaquine is also given together with chloroquine every week at a dose of 0.75 mg / kg

4. Treatment for Malaria malariaeMalariae malaria treatment with chloroquine given enough 1 time per day for 3 days, with a total dose of 25 mg base / kg

- KomplikasiMalaria patients with kompikasi generally classified as severe malaria according to WHO defined as P. falciparum infection with one or more of the following complications:1. Cerebral malaria (coma) that is not caused by another disease or more

than 30 minutes after the seizure, the degree of impairment of consciousness should be assessed based on the GCS (Glasgow Coma Scale) is below or equal to 7 soporous clinical circumstances.

2. Acidemia / acidosis;3. Severe anemia4. Acute renal failure5. Non-kardiogenik/ARDS pulmonary edema (adult respiratory distress

syndrome).6. Circulatory failure or shock7. Spontaneous bleeding from the nose or gums, gastrointestinal and

laboratory abnormalities accompanied by intravascular coagulation disturbances

b. Demam Tifoid- Definisi

Typhoidal fever is an acute infectious disease that is usually found in the gastrointestinal tract (small intestine) with symptoms of fever a week or more with disorders of the gastrointestinal tract and with or without impaired consciousness

- EtiologiTyphoid fever is caused by the bacterium Salmonella typhi or Salmonella paratyphi of the genus Salmonella. These bacteria are rod-shaped, gram-negative, spore-forming, motile, capsulated and have flagella (hair moves with trill).

- PatogenesisSalmonella typhi and Salmonella paratyphi enter the human body through food contaminated with germs. Most germs destroyed by stomach acid and some into the small intestine and multiply.When the humoral immune response of intestinal mucosal IgA deficient will penetrate the germ cells, especially epithelial M cells and subsequently into the lamina propria. In the lamina propria breed bacteria and removed by phagocytic cells mainly by macrophages. Germs can live and multiply in macrophages and subsequently taken to the distal ileum Peyeri plaque and then to the mesenteric lymph nodes. Furthermore, through the duct torasikus germs contained in these macrophages into the circulation of the blood (bacteremia cause asymptomatic first) and spread throughout the reticuloendothelial organs of the body, especially the liver and spleen. In these organs germ leave phagocyte cells and then multiply outside the cell or a sinusoid and then enter into the blood circulation resulting in bacteremia again the second time, accompanied by the signs and symptoms of systemic infection, such as fever, malaise , myalgia, headache and abdominal pain

- Clinical manifestation- Pemeriksaan fisik- Pemeriksaan penunjang

a. Widal testWidal test is an agglutination reaction between antigen and antibody (agglutinin). Agglutinin specific for Salmonella typhi present in the serum of patients with typhoid fever, in people who had contracted Salmonella typhi and the people who never get typhoid fever vaccine.

b. Uji Enzym-Linked Immunosorbent Assay (ELISA)- Anamnesis- Komplikasi

Complications of typhoid fever can be divided into two parts, namelya. Komplikasi Intestinal

Perforasi Usus , perdarahan usus

b. Komplikasi Ekstraintestinal

a. Cardiovascular complications: peripheral circulatory failure (shock, sepsis), myocarditis, thrombosis and thrombophlebitis.

b. Complications Blood: Hemolytic anemia, thrombocytopenia, disseminated intravascular koaguolasi, and hemolytic uremic syndrome.

c. Pulmonary complications: pneumonia, empyema, and pleurisyd. Liver and bladder complications: hepatitis and cholelithiasise. Renal complications: glomerulonephritis, pyelonephritis, and perinefritisf. Bone complications: osteomyelitis, periostitis, spondylitis, and arthritisg. Neuropsychiatric complications: delirium, meningismus, meningitis,

peripheral polineuritis, psychosis, and catatonia syndromec. Demam Berdarah

- Definisiacute febrile disease caused by the dengue virus

- Etiologiacute febrile disease caused by the dengue virus, which enters the human bloodstream by mosquitoes of the genus Aedes, such as Aedes aegypti or Aedes albopictus.

- Patofisiologi- Patogenesis- Clinical manifestation- Pemeriksaan fisik- Pemeriksaan penunjang- Anamnesis- komplikasi