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LEPTOSPIROSIS JANUARY 25, 2015 BY RIZKIWARDA DEFINITION Leptospirosis is a zoonotic disease caused by micro-organisms Leptospira interogans regardless of the specific form of serotipnya. Severe form known sa Weil’s disease. Another name of this disease is mud fever, smile fever, swamp fever, autumnal fever, infectious jaundice, fever field, cane cutter fever. Clinical symptoms of this disease are not specific, so often escapes diagnosis. There Outbreak of leptospirosis to this disease including the emerging infectious disease. ETIOLOGY Figure 1. Leptospirosis Family : treponemataceae Genus : Spira Species : Leptopira interogans (pathogens); Leptospira biflexa (non-pathogenic) Feature : convoluted, thin, flexible, length 5-15 um, very smooth spiral, width 0.1-0.2 um, one end of organisms often swell, forming a hook, move the active rotation, not berflagella, and are obligate aerobic. Spira requires media and special conditions to grow. Culture can dlakukan in Fletcher’s medium. Reservoir: rats (L. Icterohaemorhagica), dog (L. canicola), cows and pigs (L. Pomona). EPIDEMIOLOGY Leptospirosis can be found in domestic animals such as dogs, pigs, cattle, horses, cats, guinea pigs, ferrets, bats. In the body of the beast, leptospirosis live in the kidney / bladder water. This disease is seasonal, in temperate regions the height of the incident found in the summer and fall as the temperature is affecting the survival of these microorganisms, whereas in the tropics during the rainy season. International Leptospirosis sosiety said Indonesia is a country with a high incidence of leptospirosis and ranks third in the world for mortality. In Indonesia found in Jakarta, West Java, Central Java, Yogyakarta, Lampung, South Sumatra, Bengkulu, Riau, West Sumatra, North Sumatra, Bali, West Nusa Tenggara, South Sulawesi, East Kalimantan and West Kalimantan. In the great flood in Jakarta in 2002, reported cases of leptospirosis with 20 deaths. TRANSMISSION Through contact with water, soil, sludge contaminated by the urine of infected animals leptospira. Occur if there is a wound / erosion on the skin or mucous membranes. Sometimes the disease is caused by the bite of an animal previously infected by leptospira or terkontaminsi contact with the culture in the laboratory. Who have a high risk factor, among others, workers who work in the fields, farm, ranch, farm, mine workers, abattoir workers, campers, veterinarian. PATOGENESIS Three mechanisms of pathogenesis namely: direct bacterial invasion, non-specific inflammatory factors, and immunologic reactions. Leptospira enter the body through the skin or mucous membranes, enters the bloodstream and developing, then spread to tissues. Then came the body’s immunological response both cellular and humoral that this infection can be reduced by specific antibodies. However, some of these microorganisms can survive in an isolated place in the kidney immunological example, persist then released through urine, can be found in the urine after 8 days infects up for months or even years. After 4-7 days leptosperemia phase of microorganisms can be found only in the kidney. Leptospiruria occurred during 1-4 weeks. PATHOLOGY LeptoSpira release toxins that are responsible for the pathology in multiple organs. Lesions that appear to happen because of damage to the endothelial lining of capillaries. In leptospirosis there is a difference between organ dysfunction and histological abnormalities. In mild histological lesions found in the kidneys and liver with real functional abnormalities of these organs. This difference indicates that the damage is not the structure of the organ. Organs are often subjected leprospira are: 1. Kidney: interstitial nephritis with mononuclear cell infiltration is a form lesions on leptospirosis that can occur without renal impairment. Kidney failure is due to acute tubular necrosis. The existence of nephrotoxins, immunological reactions, ischemia ginjal¸hemolisis and direct invasion of microorganisms play a role in causing kidney damage. 2. Heart: The heart showed focal necrosis sentilobuler with focal lymphocytic cell infiltration and proliferation of Kupffer cells with cholestasis. These microorganisms located in the parenchyma cells. 3. Heart: myocardial abnormalities can be focal or diffuse edema with infiltration of mononuclear interstesial and plasma. Focal hemorrhage can occur in the myocardium and endocarditis 4. Skeletal muscle: the case of local necrosis, vacuolization and loss stiata. Muscle pain caused by direct invasion of microorganisms sometimes found in the muscle antigen. 5. Eyes: Leptospira entered in the anterior chamber of the eye and the last few months although the antibodies are formed quite ringgi. This causes uveitis. 6. Blood vessels: vasculitis cause bleeding in mucous, serous surfaces, tools visceral and subcutaneous bleeding, 7. CNS: Leptospira into the CSS and associated with the occurrence of meningitis. Menigitis occurs when the antibody was not when the entry of leptospira. Thickening of the meninges, which often happens is by L.canicola aseptic meningitis. 8. Weil’s disease: severe leptospirosis with marked jaundice, accompanied by bleeding, anemia, azotemia, disorders of consciousness and fever type of continua. The cause is serotype icterohemoragica. The clinical features ranging from kidney disorders, vascular hepatil up. CLINICAL The incubation period of 2-26 days, with two phases: 1. Phase leptospiraemia This phase is characterized by the presence of leptospires in blood and css, takes place suddenly. Often
fever, chills, headache, meningismus, anorexia, myalgia, conjunctival suffision, nausea, vomiting, abdominal pain, jaundice, hepatomegaly, skin rash, photophobia.
Rarely
pneumonitis, hemaptope, derilium, bleeding, diarrhea, edema, spleenomegali, arthralgia, renal failure, peroferal neuritis, pancreatitis, parotitis, epididymis, ascites, myocarditis, hematemesis.
Table 1. Clinical Features on leptospirosis. 2. Phase immune Characterized by increased antibody titers, may have a fever as high as 40 degrees Celsius deisertai menggil and general weakness. Complete pain in the neck, abdomen, legs, especially the calf muscles. In the form of epistaxis bleeding, symptoms of kidney damage, liver, uremia, jaundice. Bleeding gums is the most frequent manifestation. Conjunctiva injection and conjungtival suffusion with jaundice is a sign patogomosis leptospirosis. The occurrence of meningitis is a sign of this fave. Signs of meningeal may persist for several weeks, usually disappear after 1-2 days. In this phase of leptospirosis can be found in the urine. DIAGNOSIS In anamnesis is important to know about the history of the work, including whether the high-risk group. His complaint is that sudden fever, headache, especially frontal, muscle pain, red eyes or photophobia, nausea, vomiting. On physical examination found fever, bradycardia, muscle tenderness, hepatomegaly. In routine blood laboratory pemerikdaan found leukocytosis, normal or decreased sedikti accompanied Neutrophilia and LEDs. In urine protein found Uriah, leukositoria, piston (cast). Definitive diagnosis of Leptospira isolation of body fluids and serology. Culture: taking blood specimens or ccs at the start of symptoms. Advisable to do a double culture and the leptospiremia phase and has not given antibiotics. Urine cultures were taken after 2-4 weeks of the onset of illness. Serology: PCR, silver strain, dark field microscope. Serologic test types can be seen in Table 2. Microscopic agglutination test (MAT)
macroscopic slide aglutination test (MSAT)
Test strips dye:
Complement fixation test (CFT) enzyme-linked immunosorbant essay (ELISA)
– Lepto Dipsttick
Microcapsule aglutination test
– Lepto Tech Lateral Flow
Patoc-slide agglutinations test (PSAT)
Latex agglutination dry Indirect fluorescent antibody test (IFAT) Indirect haemagglutination test (IHA) Latex agglutination test Table 2. Types of serological tests on leptospirosis. TREATMENT
Supportive treatment to treat dehydration, hypotension and bleeding and kidney failure. Giving antibiotics within 4 days after the onset of effective enough. Indications
Dosage
Regimen
mild leptospirosis
Doxycycline
2 x 10 mg doxycycline
Leptospirosis moderate / severe
ampicillin
4 x 500-750 mg
chemoprophylaxis
amoxicillin
4 x 500 mg
penicillin G
1.5 million units / 6 hours (i.v)
ampicillin
1 gram / 6 hours (i.v)
amoxicillin
1 gram / 6 hours (1.v)
Doxycycline
200 mg / week
Table 3. Antibiotic treatment of leptospirosis PROGNOSIS If there is no jaundice disease is rarely fatal. 5% mortality rate with ikteru disease at age below 30 years in the elderly reaches 30-40%. PREVENTION Special clothing to those who are at high risk so they can protect them from direct contact of contaminated materials. Vaccination against animal reservoir.
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CHIKUNGUNYA JANUARY 25, 2015 BY RIZKIWARDA Definision Chikungunya is derived from the language Shawill based on patient symptoms, which means (postures) twisted or curved (roomates that contorts or bends up), referring to the bent posture of patients due to severe joint pain (arthralgia). This joint pain occurs in the knee and ankle joints of the hands and feet. Chikungunya fever is caused by Chikungunya virus (CHIKV). CHIKV including family Togaviridae, genus Alphavirus, and transmitted by the mosquito Aedes aegypti. Epidemiology Chikungunya virus was first identified in East Africa in 1952. The virus continues to cause epidemics in tropical regions of Asia and Africa. In Indonesia, Chikungunya fever was first reported in Samarinda 1973. Then outbreak in Kuala Tunkal, Edinburgh, 1980. The 1983 outbreak in Martapura, Ternate and Yogyakarta. After vacuum nearly 20 years, beginning in 2001 extraordinary events (KLB) Chikungunya fever occurred in Muara Enim, South Sumatra and Aceh. Bogor followed in October. Chikungunya fever outbreak again in Bekasi, West Java, Purworejo and Klaten, Central Java in 2002. CHIKV as Chikungunya fever cause is still unknown patterns of entry into Indonesia. About 200-300 years ago CHIKV is a virus in primates in the forest or savanna in Africa. Primate species are considered as a preserver of the virus is the nation baboons (Papio sp), Cercopithecus sp. Cycle in the forest (sylvatic cycle) among primate species carried by Aedes sp (Ae africanus, Aeluteocephalus, opok Ae, Ae. Furciper, Ae taylori, Ae cordelierri). Scientific evidence that includes the isolation and identification of a new virus successfully performed when there is an outbreak in Tanzania from 1952 to 1953. After some time, the characteristics of the original cyclic CHIKV virus from mosquito-primate-primate species, can also be cyclical human-mosquito-human. Not all viruses of animal origin can change the cycle like that. In residential areas (urban cycle), a cycle of chikungunya virus by Aedes aegypti assisted. Some countries in Africa have reported chikungunya virus is Zimbabwe, Congo, Burundi, Angola, Gabon, Guinea Bissau, Kenya, Uganda, Nigeria, Senegal, Central Africa, and Botswana. After Africa, chikungunya virus was reported in Bangkok (1958), Cambodia, Vietnam, India and Sri Lanka (1964), the Philippines and Indonesia (1973). Chikungunya been reported in three American peace corps volunteers (US Peace Corp Volunteers) who served in the Philippines, 1968. Results of research on the epidemiology of the disease chikungunya in Bangkok Thailand and Vellore Madras, India showed that there was a wave of the epidemic in the interval of 30 years. One wave of epidemics generally last a few months, then declined and is lightweight so it is often not monitored. Epidemic wave associated with the vector population (mosquito-borne) and immune status of the population. Testing blood (serological) Chikungunya disease is often not easy because serum chikungunya have cross-reactions with other viruses in the family. From some of the literature seems there is a tendency of the epidemic wave 20s. This phenomenon is often associated with climate change and weather. Antibodies that arise from this disease makes people immune to virus attack next. It took longer for the disease to spread back. DISEASE TRANSMISSION AND DISTRIBUTION OF DISEASE The spread of CHIKV can be transmitted through mosquito bites. Mosquitoes can be potentially infectious when ever bite chikungunya fever sufferers. Apes and some other wild animals is also thought to be as an intermediary (reservoir) of this disease. Infected mosquitoes transmit the disease when healthy human bite. Aedes aegypti (yellow fever mosquito the) is the main vector or carrier CHIKV. Aedes albopictus (the Asian tiger mosquito) may also play a role in the spread of this disease in Asia. And some specific types of mosquito species in Africa also was able to spread the disease Chikungunya. It is not yet known exactly how the virus is spreading across the country. Given the spread of CHIKV between countries is relatively low, the possibility of the spread of this occurs along with the displacement of mosquitoes. Today more and more often various animal diseases that spread from the middle of the forest (spill-over) to settlements. Call of whom St. Louis encephalitis and West Nile River (West Nile), which has caused many victims. Circulation of the virus is no longer limited by geography position. Forest that had been closed to open, once isolated areas can now easily connect to anywhere. How to transfer the virus could be anything. In the fast-paced era of globalization, as now, a person today can be in Europe or Africa, and the next day was already in other continents such as in Bali or Jakarta. With a pattern of rapid population displacement, the potential it has spread various diseases including viral. People who contracted the disease in a country could have brought it to Indonesia. Borne diseases exist that can disappear by itself, but can also continue the cycle when there supporting factors. Considerable trade of endangered species under the spotlight some time ago, could have been brought with the virus of forests to distant places abroad. Not to mention the mosquitoes that can be smuggled into the cabin of the aircraft and flew in Indonesia. DIAGNOSIS AND CLINICAL To obtain an accurate diagnosis need some serologic tests include barriers agglutination test (HI), serum neutralization, and IgM capture ELISA. But this is only bermanfaant serological used for epidemiological and research interests, not useful for practical purposes clinical everyday.
The incubation period of the disease about two to four days, while its manifestations arise from three to ten days. The main symptoms of Chikungunya disease is the body suddenly felt a fever accompanied by pains in the joints. In fact, as one of the typical symptom is the emergence of a sense of fatigue, pain, pain relief also on the bones, there are named as bone fever or flu-bone. In some cases obtained also infected patients without causing any symptoms at all or silent chikungunya virus. The virus is transmitted by Aedes aegypti mosquitoes will breed in the human body. Virus attacks all ages, both children and adults in endemic areas. Patients will experience a sudden high fever for five days, so it is known as the term fever five days. In young children begins with sudden fever, skin redness. Red rash that appears after 3-5 days. Eyes red usually accompanied by signs such as the flu. Often encountered children febrile seizures. Other symptoms are caused nausea, vomiting, sometimes accompanied by diarrhea. In older children, fever is usually followed by pain in muscles and joints, as well as enlarged lymph nodes. In adults, symptoms of joint pain and muscle are very dominant and to cause temporary paralysis due to pain when walking. Sometimes nausea to vomiting. In general fever in children only lasted for three days with no or very little was found bleeding and shock. The disease is not to cause death. Pain in the joints will not cause paralysis. After over five days, the fever gradually subsided, aches and pains in the joints and muscles is reduced, and the sufferer will recover to normal. Patients in some time and then can move his body as usual. Although in some cases the pain is still lagging sometimes for days to months. Usually this condition occurs in patients who previously had a history of frequent bone pain and muscle. In pendertita Acute Chikungunya fever typically undergo clinical symptoms within a few days up to 2 weeks. But like dengue infection, West Nile fever, o’nyong-nyong fever and other arbovirus fever, some patients experience prolonged fatigue “prolonged fatigue” in a few weeks. In some of the literature no reported cases of death, neuroinvasive cases, and cases of bleeding in this disease. Although transmitted by the same mosquito with dengue fever, but the different characteristics of this disease. Chikungunya no difference in severe bleeding, shock (shock) and death. After this viral infection the patient’s body will make antibodies that will make them immune to this disease in later life. Thus, in the long term sufferers relatively immune to this virus disease. HANDLING Chikungunya fever including “Self Limiting Disease” or self-limiting disease. There is no vaccine or specific drug for this disease. Treatment given only symptomatic therapy or eliminate the symptoms of the disease. Like, painkillers or fever as paracetamol group, similar drugs should be avoided aspirin use. Antibiotics are not needed in this case. The use of antibiotics to prevent secondary infection is not considered useful. To improve the general state of the patient is recommended to eat food that is nutritious, enough carbohydrates and especially protein and drink as much as possible. Expand consume fresh fruit or fresh fruit juice drink. Giving vitamin endurance enhancer may be beneficial for the treatment of disease. In addition to vitamins, foods that contain enough protein and carbohydrates also increase endurance. Great endurance and adequate rest can accelerate the healing of disease. Drink lots are also advised to address the need for increased fluid during a fever. PREVENTION The only way to avoid this disease is to eradicate mosquitoes carrying the virus. This mosquito, happy to live and breed in stagnant water such as bathtub, vase, and also cans or bottles that hold water clean. Mosquitoes patterned black and white is also happy to live in objects such as clothes hanging in the back door of the room. Moreover, it also enjoys a mosquito dark and stuffy. Given this disease spreader is Aedes aegypti, the best way to break the chain of transmission is to eradicate mosquitoes, as is often suggested in the eradication of dengue fever. Insecticides are used to kill mosquitoes are from the class of malathion, while themopos to shut-jentiknya larvae. Malathion is used by evaporation and not by spraying into the wall. This is because the Aedes aegypti not like perch on the wall, but the hanging objects. However, prevention is cheap and effective way to combat this mosquito is by draining clean water reservoirs, bath, flower vases and so on, at least once a week, given the mosquitoes breed from egg to mature within 7-10 days . Yard or garden around the house must be clean of objects that allows accommodate water, especially during the rainy season like now. Doors and windows should be opened every day, from morning until evening, so that fresh air and sunlight to enter, so that the air exchange and healthy lighting. Thus, creating an ideal environment for mosquitoes. Prevention of individuals can be done in a special way as the use of topical medication skin (insect repellent) containing DEET or other EPA active substances. The use of long sleeves and long pants are also recommended for certain areas in the state of being an increase in cases. LEAVE A COMMENT
HEART FAILURE NOVEMBER 11, 2013 BY RIZKIWARDA GAGAL JANTUNG
(https://rizkiwarda.files.wordpress.com/2013/11/gagal-jantung.jpg) 1. Definisi Gagal jantung/heart failure adalah sindroma klinik yang ditandai dengan adanya sesak nafas dan fatik karena adanya kelainan struktur dan fungsi jantung. Paradigma lama mengatakan bahwa gagal jantung disebabkan kurangnya kontraksi jantung dan daya pompa jantung sehingga penatalaksanaan secara medikamentoda diberikan obat-obat inotropik, diuretik dan vasodilator untuk mengurangi beban. Paradigma baru gagal jantung terjadi karena remodeling progresif akibat beban/penyakit pada miokard sehingga penatalaksanaannya diberikan neurohumoral bloker ( ACE-I/ ARB atau penyekat beta) disamping diuretik dan digitalis. 1. Klasifikasi gagal jantung: 1. Gagal jantung sistolik dan diastolik – Hanya dapat dibedakan dengan eko-dopler. – Gagal jantung sistolik: ketidakmampuan jantung mengejeksikan darah, CO turunà gejala hipoperfusi (fatik, kelemahan, aktivitas fisik terbatas). – Gagal jantung diastolik: gangguan relaksasi dan gangguan pengisian ventrikel, fraksi ejeksi >50 %. Tatalaksanak bertujuan untuk menghindari gangguan diastolik (fibrosis, hipertrofi, iskemia) dengan retriksi garam dan pemberian diuretik, mengurangi denyut jantung agar waktu pengisian ventrikel bertambah (beta bloker, kalsium bloken-non dihidropiridin). 1. Low output dan high output heart failure. – Low output disebabkan hipertensi, kardiomiopati dilatasi, kelainan katup dan perikard. – High output ditemukan pada hipertiroidisme, anemia, kehamilan, fistula A-V, beri-beri, panyakit paget. – Secara praktis tidak dapat dibedakan. 1. Gagal jantung akut dan kronik – Gagal jantung akut : serangan cepat atau perubahan simptom dan sign dari gagal jantung yang diperlukan perlakuan secara urgent. GJA bisa berupa serangan pertama atau serangan GJK yang mengalami perburukan. Misal adanya robekan katup secara tiba-tiba pada endokarditis, trauma, infark miokard luas. CO turun tiba-tibaà TD turun, tanpa adanya edema perifer. – Gagal jantung kronik : kardiomiopati dilatasi atau kelainan multivalbular yang terjadi secara perlahan. Kongesti perifer, TD terkontrol. 1. Gagal jantung kanan dan gagal jantung kiri – Gagal jantung kiri : akibat kelemahan ventrikel à tekanan v.pulmonalis naikàsesak,ortopnea. – Gagal jantung kanan: melemahnya ventrikel kanan (pada hipertensi pulmonal, tromboemboli paru, edema perifer, hepatomegali, distensi v.jugularis. – Perubahan biokimia pada gagal jantung terjadi di dua miokard sehingga dalam hitungan bulan atau tahun tidak ada bedanya gagal jantung kanan atau kiri. Klasifikasi menurut NYHA berdasarkan tingkat aktivitas dan timbulnya keluhan: 1. 2. 3. 4.
Stage 1 : timbul saat aktivitas berlebih. Stage 2 : timbul saat aktivitas sedang. Stage 3 : timbul saat aktivitas ringan. Stage 4 : timbul bahkan saat istirahat. Klasifikasi berdasarkan AHA berdasarkan progresifitas dan kelainan struktural jantung serta status fungsional:
1. 2. 3. 4.
Stage A : adanya faktor risiko terjadinya gagal jantung. Stage B : adanya faktor risiko dan sudah terdapat kelainan struktural, tapi asimptomatis. Stage C : sedang dekompensasi atau pernah mengalami gagal jantung. Stage D : refraktory gagal jantung. Klasifikasi berdasarkan onset:
1. 2. 3. 4.
New onset HF : presentasi klinis pertama. Trancient HF : terjadi pada waktu tertentu. Kronik HF : persisten/perburukan HF. Patogenesis
Beban/penyakit miokardà kompensasiàasimptomatikàremodeling struktural: hipertrofi, disfungsi ventrikel, + faktor presipitasi (infeksi, aritmia, infark, anemia, hipertiroid, hamil, aktivitas berlebih, hipertensi, miokarditis, demam rheumatik, virus, endokarditis)àgagal jantung simptomatikà gagal jantung refrakter. 1. Diagnosis Berdasarkan anamnesis, pemeriksaan fisik, EKG, foto toraks, eko-doppler, kateterisasi. – Kriteria Framingham : 1. Kriteria mayor: edema paru akut, ronki paru, gallop s3, paroksismal nokturnal dispnea, refluks hepatojugular, peninggian vena jugularis, distensi vena leher, kardiomegali. 2. Kriteria minor : dispnea d’effort, edema ekstremitas, batuk malam hari, efusi pleura, hepatomegali, penurunan kapasitas vital 1/3 normal, takikardi (>120/menit). – Penegakkan diagnosa minimal 1 kriteria mayor dan 2 kriteria minor. 1. Tatalaksana gagal jantung 1. Diuretik hingga menjapai euvolemik à ACE-I/ARBà beta bloker. 2. Jika di atas gagal atau ada indikasi aritmia supraventrikular diberikan digitalis. 3. Aldosteron (menambah fungsi diuretik). 4. Alat bantu CRT (Cardiac Resycronization therapy) dan ICD (intra cardiac defribilator) LEAVE A COMMENT
FISIOLOGI JANTUNG OCTOBER 18, 2013 BY RIZKIWARDA
(https://rizkiwarda.files.wordpress.com/2013/10/jantung2.jpg) 1. KELISTRIKAN JANTUNG Otot jantung bersifat sinsitium yakni ketika salah satu otot terangsang maka akan menjalar. Hal ini dikarenakan susunan otot jantung yang memiliki intercalacted disk sehingga memungkinkan difusi ion-ion secara bebas. Perpindahan ion-ion ini menyebabkan terjadinya perbedaan tekanan kelistrikan yang disebut potensial aksi. Potensial aksi pada otot jantung meyebabkan adanya aliran keistrikan pada jantung sehingga jantung bisa berkontraksi. Potensial aksi jantung terbagi atas 4 fase, yakni: 1. 2. 3. 4.
Fase 0 : terjadi lonjakan potensial, perubahan tekanan istirahat (90 mV) menjadi 20 mV, masuknya ion natrium ke sel jantung (depolarisasi). Fase 1 : mengalami penurunan dari 20 mV menjadi 0 mV, natrium menurun, kalium mulai keluar (repolarisasi lambat). Fase 2 : karena ion kalium mulai keluar sehingga kanal Ca++ terbuka dan ion Ca++ masuk untuk mengimbangi ion kalium yang terbuka (repolarisasi cepat), terjadi pendataran/plateu. Fase 3: perubahan tekanan dari 0 mV menjadi -90 mV, penurunan menuju fase istirahat.
(https://rizkiwarda.files.wordpress.com/2013/10/f3-17.gif) Fungsi ion kalium yakni melemahkan otot jantung, melemaskan otot jantung serta menurunkan kontrktilitas jantung, sedangkan ion kalsium berefek untuk meningkatkan kontraktilitas jantung. 1. MEKANIKA JANTUNG Selain adanya kelistrikan jantung, juga terdapat mekanika jantung yakni suatu siklus jantung yang berkontraksi dan berelaksasi yang disebut sistol (kontraksi), diastol (relaksasi). Kedua siklus ini memungkinkan jantung untuk melakukan pengisian darah dari atrium ke ventrikel yang nantinya akan di edarkan ke seluruh tubuh. Siklus jantung terdiri dari: 1. 2. 3. 4. 5. 6. 7.
Atrium sistol : kontraksi atrium untuk mengisi/mengalirkan darah ke ventrikel. EDV : yakni end diastolik volume, volume maksimal pada ventrikel. Isovolumik ventrikel kontraction : waktu dimana ventrikel melakukan persiapan untuk ejeksi, katup atrioventrikular sudah tertutup dan katup semilunar belum terbuka. Ejeksi ventrikel : ventrikel melakukan pemompaan darah. ESD : yakni end sistolik volume, volume minimum ventrikel. Isovolumik ventrikel relaxation Ventrikel diastolik.
Aliran darah pada jantung: vena cava superior et inferior à atrium dextra à ventrikel dextra à arteri pulmonalis à vena pulmonalis à atrium sinistra à ventrikel sinistra à aorta 1. KONDUKSI JANTUNG Sistem konduksi jantung inilah yang memungkinkan jantung dapat menjalarkan perangsangan kelistrikan, karena sifat jantung yang terdiri dari : 1. 2. 3. 4.
Bathmotropik : dapat menimbulkan listrik sendiri. Dormotropik : dapat menjalarkan rangsangan listrik. Kronotropik : menjalarkan listrik secara berirama Inotropik : dapat berkontraksi.
Sehingga ada bagian jantung yang dapat menimbulkan listrik yang disebut pacu jantung yakni SA node. Urutan perjalanan konduksi jantung : SA node à AV node à berkas his à cabang berkas his à serabut purkinje. 1. CURAH JANTUNG Terminologi : 1. Stroke volume : volume darah yang di ejeksikan jantung tiap detik. Stroke volume dipengaruhi oleh EDV dan ESV. Dan ESV dipengaruhi oleh preload (kemampuan regangan jantung dalam menampung darah) dan afterload (kemampuan jantung untuk melawan tahanan). 2. Curah jantung disebut juga cardiac output : volume jantung yang di ejeksikan tiap menit. Jadi CO= SV x HR. 1. SISTEM INERVASI JANTUNG Sistem inervasi jantung berpusat pada medula oblongata. Saraf simpatis dan saraf parasimpatis berkoordinasi menstabilkan jantung, dengan cara :
(https://rizkiwarda.files.wordpress.com/2013/10/gambar-1-pengaturan-fungsi-jantung-oleh-sistem-syaraf-otonomik.jpg) Sumber : guyton dan hall LEAVE A COMMENT
FARMAKOLOGI SEPTEMBER 22, 2013 BY RIZKIWARDA FARMAKOLOGI (https://rizkiwarda.wordpress.com/2013/09/17/farmakologi/). LEAVE A COMMENT
FARMAKOLOGI SEPTEMBER 17, 2013 BY RIZKIWARDA
(https://rizkiwarda.files.wordpress.com/2013/09/obat1.jpg) 1. HISTAMIN Histamin adalah mediator reaksi immediate hipersensitivity, inflamasi, sekresi asam lambung, sebagai neurotransmiter. MEKANISME KERJA – bekerja menduduki sel pada permukaan membran – ada 3 j3nis reseptor histamin : H1, H2 (pada pasca sinaps) H3 (presinap) FARMAKODINAMIK a. H1 : menyebabkan kontraksi otot polos, peningkatan permeabelitas vaskuler, sekresi mukus. pada bronkus menyebabkan bronkokontriksi. b. H2 : menyebabkan sekresi asam lambung, pada bronkus menyebabkan relaxasi. c. H3 : menghambat umpan balik berbagai sistem organ. FARMAKOKINETIK – diserap baik setelah pemberian SK atau IM. pemberian oral tidak efektif karena diubah oleh bakteri usus. 2. ANTIHISTAMIN A. ANTAGONIS RESEPTOR H1 (AH1) – farmakodinamik : menghambat efek histamin pada pembuluh darah, bronkus, otot polos, mengobati hipersensitivitas dan bronkokontriksi. – contoh obat : etanolamin, etilenediamin, piperazin, alkilamin, derivat fenotiazin. – farmakokinetik : efek setelah 15-30 menit setelah pemberian oral, maksimal 1-2 jam. kadar tertinggi pada paru, biotransformasi utama pada hepar, disekresi melalui urin setelah 24 jam. – etilendiamin berefek pada sekresi asam lambung. – pengobatan simtomatik berbagai penyakit alergi dan mencegah serta mengobati mabuk perjalanan. – asma bronkial berat kurang efektif dengan AH1 karena mengentalkan sekresi mukus sehingga menyulitkan ekspektoran, pasien ini baik diberi epinefrin, aminofilin, isoproterenol. – AH1 menghilangkan bersin, rinore, gatal mata dan hidung pada penderita hayfever. tidak efektif bila paparan debu banyak dan lama. B. ANTAGONIS RESEPTOR H2 (AH2) menghambat sekresi lambung. 3. ANTIALERGI A. KROMOLIN – hambat pelepasan histamin dari sel mast paru. – mengurangi bronku spasme (asma bronkial) – kromolin menekan respon sekresi akibat reaksi ikatan IgE – FARMAKOKINETIK : inhalasi pada pasien asma bronkial, sedian kapsul mengandung 20 mg kromolin bubuk bercampur laktosa, diberikan inhaler 4x/hari. indikasi : asma bronkial ringan-sedang. (tidak untuk status asmatikus dan asma bronkial akut). B. NEDOKROMIL – cegah serangan asma pada penderita asma bronkial ringan-sedang. – lebih efektif dari pada kromolin yang bisa diberikan untuk semua umur. namun nedokromil hanya untuk usia >12 tahun dosis 4mg/hari 2-4x. C KETOTIFEN – indikasi : asma bronkial, oral dalam 12 bulan. – efek : meningkatkan nafsu makan – sediana: tablet 1 mg dan sirup 0,2 mg/mL daftar pustaka: Ifarmakologi dan terapi FK UI. ed.5. 2009. Jakarta: Balai Penerbit FK UI 3 COMMENTS
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