Plena Ri

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    PLENARY DISCUSSION

    BLOCK OF TROPICAL MEDICINE

    DISUSUN OLEH:

    TUTORIAL 1

    ADIL HIJRI MUHAMMAD

    AINAL FADLY

    AJENG TITI

    ARDILA WARADUHITA

    ARYANTI AMBARSARI

    DINAR SANDI AJI

    DONNI TEGAR PAMBUDI

    ESTIANNA KHOIRUNNISA

    FATIMATUZZAROH

    INDAH KURNIAWATY

    MICHAEL WIJAYA

    MIFTAKURROHMAH

    PRIBADI MUSLIM

    UNIVERSITAS MUHAMMADIYAH YOGYAKARTA

    2012

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    KASUS PLENARY DISCUSSION

    A 28 year old man had acute onset of fever, chill, nausea, vomiting, dizzy,

    malaise, myalgia, and jaundice that started five days before admission to a

    hospital. He also complain about his urine, less volume and looks like a tea water.

    He is a farmer and reported that rats were common in his neighborhood and that

    he was eposed to floodwaters one week prior to symptoms. !ast medical history

    was unremarkable.

    !hysical eamination

    "ital sign

    H# $ %&& times'minute

    ## $ 2& times.minute

    ( )ailla* $ +8, degrees celcius-! $ %&&'& mmHg

    He was alert, jaundiced, lungs were clear to auscultation, hepar palpable 2 cm

    below arcus costarum, gastrocnemius sign '.

    -- $ & kg

    (- $ %/ cm

    0aboratory eamination

    -lood counts showed %2&&& leukocytes'mm+. (he hematocrit was 21 and theplatelet count was 3+&&& cells'mm+. He had the following laboratory test values.

    4erum creatinine $ /,5 mg'dl

    4erum ureum $ %8& mg'dl

    (otal bilirubin $ %% mg'dl

    467( $ %/& 9'0

    46!( $ %53 9'0

    9rinalysis showed urine density $ %,&5&

    !rotein level $ , bilirubin $ trace )*

    9rine output was /&& ml in the first 25 hours

    :9;4(7hat are differential diagnoses that relevant with the case= >hy=

    +. >hat is the etiology of the disease and how the pathogenesis=

    5. >hat is the treatment for the case=

    /. >hat is the prognosis of the patient=

    . >hat are complications that may arise in the patient=3. >hat are the preventions of the disease=

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    A;#4

    %. (he interpretations of the physical eamination and lab results

    !hysical eamination

    "ital sign

    H# $ increase

    ## $ normal

    ( )ailla* $ increase

    -! $ decrease

    He was alert, means there is no neurological deficits and the disease has

    not influence the central nervous system. ?aundiced, means there is

    increasing of bilirubin in the blood. Hepar palpable 2 cm below arcus

    costarum, means the hepar is enlarged. 6astrocnemius sign ' is very

    patognomonic in leptospirosis.

    -- $ & kg

    (- $ %/ cm, means the -@ is normal.

    0aboratory eamination

    -lood counts showed %2&&& leukocytes'mm+, means the leukocytes

    increase, or there is infection. (he platelet count was 3+&&& cells'mm+,

    means platelet decreases.

    4erum creatinine $ /,5 mg'dl )decrease*4erum ureum $ %8& mg'dl )increase*

    (otal bilirubin $ %% mg'dl, means increase )normal &,2/ %,&*

    467( $ %/& 9'0, means increase )normal B2%*

    46!( $ %53 9'0, means increase )normal B2+*

    9rinalysis showed urine density $ %,&5& )increase*

    !rotein level $ , bilirubin $ trace )* )increase*

    9rine output was /&& ml in the first 25 hours )decrease*

    t means that there is disturbance of hepar and renal functions. Also there

    is infection in the body.

    (his picture below shows the stage of leptospirosis considering the time

    and it determine the clinical manifestations too. t can help us to

    establishing diagnoses from the eamination based on the time scale.

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    2. Cifferential diagnoses from anamnesis and physical eaminations$

    a. nfluenza$fever, chill, malaise, myalgia,dizzy. n influenza, there is no

    specific'particular muscle pain )myalgia*. -esides that, the fever is

    usually shorter on duration.

    b. Hepatitis viral $ fever, jaundice, hepatomegali. 7( !( increased, urine

    can be darker because of increasing in urobilin.

    c. @alaria$ fever,chill, malaise, myalgia, dizzy, jaundice, hepatomegaly.

    n malaria, there is intermitten fever, and history of travelling to

    endemic area.d. 0eptospira$ same as malaria gastrocnemius pain

    +. ;tiology and pathogenesis

    0eptospires enter the host through abrasions in the skin or through intact

    mucous membranes, especially the conjunctiva and the lining of the oroD

    and nasopharyn. Crinking of contaminated water may introduce

    leptospires through the mouth, throat, or esophagus. After entry of the

    organisms, leptospiremia develops, with subseEuent spread to all organs.

    @ultiplication takes place in blood and in tissues, and leptospires can beisolated from blood and cerebrospinal fluid )F4G* during the first 5%&

    days of illness. F4G eamination during this period documents pleocytosis

    in the majority of instances, but only a minority of patients develop

    symptoms and signs of meningitis at this point. All forms of leptospires

    can damage the wall of small blood vessels this damage leads to vasculitis

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    with leakage and etravasation of cells, including hemorrhages. (he most

    important known pathogenic properties of leptospires are adhesion to cell

    surfaces and cellular toicity.

    Although leptospires mainly infect the kidneys and liver, any organ may

    be affected. n the kidney, leptospires migrate to the interstitium, renaltubules, and tubular lumen, causing interstitial nephritis and tubular

    necrosis. Hypovolemia due to dehydration or altered capillary

    permeability may contribute to the development of renal failure. n the

    liver, centrilobular necrosis with proliferation of Iupffer cells may be

    found. However, severe hepatocellular necrosis is not a feature of

    leptospirosis. !ulmonary involvement is the result of hemorrhage and not

    of inflammation. nvasion of skeletal muscle by leptospires results in

    swelling, vacuolation of the myofibrils, and focal necrosis. n severe

    leptospirosis, vasculitis may ultimately impair the microcirculation and

    increase capillary permeability, resulting in fluid leakage and

    hypovolemia.>hen antibodies are formed, leptospires are eliminated from all sites in

    the host ecept the eye, the proimal renal tubules, and perhaps the brain,

    where they may persist for weeks or months. (he persistence of

    leptospires in the aEueous humor occasionally causes chronic or recurrent

    uveitis. (he systemic immune response is effective in eliminating the

    organism but may also produce symptomatic inflammatory reactions. A

    rise in antibody titer coincides with the development of meningitis this

    association suggests that an immunologic mechanism is responsible.

    5. (reatment and @anagement for the patient

    (ough having jaundice, but other clinical symptoms of him showed us that

    this patient still in the mi! "#$m #" %&'#(&i$#(i(. Hence, we offer these

    antibiotics doycycline, ampicillin or amoicillin. Among these three, we

    would like to give him doycycline. t can be taken twice a day only )the

    other two taken four times a day* so we epect that the patient would get

    easier way also more pursuance to have it. -eside, doycycline could be

    taken with empty or full stomach.

    (he dosage is 2%&& mg !7 and be administered for 3 days. (he patient

    shouldnJt have it with antacid or iron product. >e should tell the patient

    that he may have these as adverse effect$ dizziness, vertigo, nausea andeven vomit, so we suggest him to rest.

    7ther symptoms such renal dysfunction will be back to normal when the

    microbes killed. >e advise patient to take more drink in order to avoid

    dehydration. 0ater, we can give him and people around the neighborhood

    chemoprophylais because of their high population of rat to prevent them

    from leptospirosis.

    n easy way, this is the resume of the treatments and chemoprophylais for

    leptospirosis

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    /. !rognoses

    @ost patients with leptospirosis recover. @ortality rates are highest among

    patients who are elderly and those who have >eilKs syndrome.

    0eptospirosis during pregnancy is associated with high rates of fetal

    mortality. 0ongDterm followDup of patients with renal failure and hepatic

    dysfunction has documented good recovery of renal and hepatic function.

    . Fomplications

    4evere 0eptospirosis )>eilKs 4yndrome*

    >eilKs syndrome, the most severe form of leptospirosis and also the

    complication of leptospirosis, is characterized by jaundice, renal

    dysfunction, and hemorrhagic diathesis by pulmonary involvement in

    many cases and by mortality rates of /%/. n ;urope, this syndrome is

    freEuently but not eclusively associated with infection due to serovar

    cterohaemorrhagiae'Fopenhageni. (he onset of illness is no different

    from that of less severe leptospirosis however, after 51 days, jaundice as

    well as renal and vascular dysfunction generally develop. Although some

    degree of defervescence may be noted after the first week of illness, abiphasic disease pattern like that seen in anicteric leptospirosis is lacking.

    (he jaundice of >eilKs syndrome, which can be profound and give an

    orange cast to the skin, is usually not associated with severe hepatic

    necrosis. Ceath is rarely due to liver failure. Hepatomegaly and tenderness

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    in the right upper Euadrant are usually detected. 4plenomegaly is found in

    2& of cases.

    #enal failure may develop, often during the second week of illness.

    Hypovolemia and decreased renal perfusion contribute to the development

    of acute tubular necrosis with oliguria or anuria. Cialysis is sometimes

    reEuired, although a fair number of cases can be managed without dialysis.

    #enal function may be completely regained.

    !ulmonary involvement occurs freEuently in some clusters of cases, it is a

    major manifestation, resulting in cough, dyspnea, chest pain, and bloodD

    stained sputum and sometimes in hemoptysis or even respiratory failure.

    Hemorrhagic manifestations are seen in >eilKs syndrome$ epistais,

    petechiae, purpura, and ecchymoses are found commonly, while severe

    gastrointestinal bleeding and adrenal or subarachnoid hemorrhage are

    detected rarely.#habdomyolysis, hemolysis, myocarditis, pericarditis, congestive heart

    failure, cardiogenic shock, adult respiratory distress syndrome, necrotizing

    pancreatitis, and multiorgan failure have all been described during severe

    leptospirosis.

    3. (he preventions$

    a. Ieep clean the environment especially in stall, farm, swimming pool,

    and houseb. mmunization for the high risk occupation for eample farmer or labor

    c. mmunization for the animals, pets, but the successful rate depends on

    antigenic potential that belongs to vaccines.

    d. Avoid any skin damage or torture because it can be the port dJentry

    )entrance* of the spirochaeta )leptospira* to get inside the body.

    --076#A!HL

    %. HarrisonJs !rinciple of nternal @edicine

    2. -uku Ajar lmu !enyakit Calam GI9

    +. @odul -lock of (ropical @edicine

    5. IatzungJs -asic of !harmacology