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Sclera contains a protein - elastin which has high affinity for Bilirubin

Zone 1 2 3 4 5

SBR (umol/L) 100 150 200 250 >250

rbc tua break down sm macrophag, heme oleh heme oxydase jd biliverdin, bilverdin reductase jd
bilirubin unconjugated, lipophilic msk darah berikat dgn albumin buat transport ke liver, masuk vena
porta hepatica -> sinusoid, in case msh ad yg tua di break down sm macrophag di liver namany sel
kouffer, bilirubin msk hepatocyt. masuk hepatocyte trs keluar ke bile duct lwt active transport ke
duodenum lwt sphincter odi

Classification

Clinicians generally describe three types of jaundice, classified according to what is


disrupting the normal removal of bilirubin from the body:1

Prehepatic (hemolytic) jaundice. Here, the disruption happens before bilirubin has been
transported from the blood to the liver. It is caused by conditions such as sickle cell anemia
and hemolytic anemia. Hemolysis is an accelerated breakdown of red blood cells, leading to
an increase in bilirubin production.1

Intrahepatic (hepatocellular) jaundice. In hepatocellular (or intrahepatic) jaundice, there is


dysfunction of the hepatic cells. The liver loses the ability to conjugate bilirubin, but in cases where
it also may become cirrhotic, it compresses the intra-hepatic portions of the biliary tree to cause a
degree of obstruction.

Post-hepatic (obstructive) jaundice. With this form, the disruption prevents bile (and thus
bilirubin) from draining out of the gallbladder and into the digestive system. This can be
caused by conditions such as gallstones, biliary tract infection, pancreatitis or neoplastic
disease.1

Neonatal jaundice is a common type of jaundice that happens to newborn babies.


Most babies are born with a lot of red blood cells, and because the liver isn’t fully developed
yet, bilirubin can’t be processed quickly. As a result, your child may have jaundice symptoms
a few days after they’re born.

Types of neonatal jaundice include:

 Physiological. This happens because the liver isn’t fully formed yet.
 Prematurity. This results from a baby being born too early and being unable to poop
out bilirubin properly.
 Breastfeeding. Breast milk jaundice occurs from a baby having trouble breastfeeding
or not getting enough breast milk.
 Incompatible blood type. This results from a baby and mother having different blood
types, which can cause the mother to make antibodies that break down her baby’s red
blood cells.

Pre-Hepatic Hepatocellular Post-Hepatic


 Alcoholic liver disease  Intra-luminal causes, such as
 Viral hepatitis gallstones
 Iatrogenic, e.g. medication  Mural causes, such as
 Haemolytic anaemia
 Hereditary haemochromatosis cholangiocarcinoma, strictures, or
 Gilbert’s syndrome
 Autoimmune hepatitis drug-induced cholestasis
 Criggler-Najjar syndrome
 Primary biliary cirrhosis or  Extra-mural causes, such as
primary sclerosing cholangitis pancreatic cancer or abdominal
 Hepatocellular carcinoma masses (e.g. lymphomas)
Leptospirosis
Thin spiral gram neg bacteria, too small buat light field microscope jd pake dark field +
immunofluorescence.
Flagella, no spores, aerobic
Leptospira interrogans
Adhesins: help attach to host cell
Sphingomyelinase C toxin: destroy RBC & epithel of capiler -> hemoreg
Transmission: abrasions on skin, conjungtiva via swimming, contaminated food

Phase 1- Fever (38-40°C)

 Rigors
 Headache, retro-orbital pain, photophobia
 Muscle pain localized to the calf and lumbar areas
 Conjunctival suffusion
 Dry cough
 Nausea and vomiting, diarrhea

Phase 2 Weil disease


Liver- damage sinusoid & hepatocyte -> jaundice
Lungs- alveolar capillary membrane -> bleeding in alveoli
Symp: cough, dyspnea, hemoptysis
Kidney- interstitium-> interstitium nephritis & renal tubules -> tubular necrosis
Symp: renal failure, reduced urine, fluid retention -> edem
BBB- msk CSF jd meningitis
Symp Headache fever, stiff neck
DIAGNOSIS- PCR, ELISA
Penicillin G aqueous (Pfizerpen-G)

Intravenous penicillin is first-line antibiotic therapy for severe leptospirosis. Penicillin


interferes with synthesis of cell wall mucopeptide during active multiplication, resulting
in bactericidal activity against susceptible microorganisms.

Doxycycline (Vibramycin, Doryx, Adoxa, Morgidox, Mondoxyne NL)

Doxycycline inhibits protein synthesis, and thus bacterial growth, by binding to 30S and
possibly 50S ribosomal subunits of susceptible bacteria. Excretion is hepatobiliary and
renal.

Kalo udh parah supportive therapy: iv, resp support, blood transfusion

If a person's platelet count remains high, the following medical conditions may be
responsible:

 Cancer: Lung, stomach, breast, and ovarian cancers, as well as lymphoma, can cause
high platelet counts. Additional blood testing, imaging scans, or a biopsy can test for
cancer.
 Anemia: People with iron-deficiency or hemolytic anemia may have high platelets.
Further blood testing can detect most forms of anemia.
 Inflammatory disorders: Diseases that cause an inflammatory immune response,
such as rheumatoid arthritis or inflammatory bowel disease (IBD), can increase
platelet count. A person will have other symptoms in most cases.
 Infections: Some infections, such as tuberculosis, can cause high platelets.
 Splenectomy: Removal of the spleen can cause a temporary increase in platelets.

Common causes of low platelet volume include:

 Viruses: Viruses, such as mononucleosis, HIV, AIDS, measles, and hepatitis may
deplete platelets.
 Medication: Drugs, such as aspirin, H2-blockers, quinidine, antibiotics containing
sulfa, and some diuretics may lower platelet count.
 Cancer: Cancer that has spread to the bone marrow can harm the body's ability to
make new platelets. Lymphoma and leukemia are common culprits.
 Anemia: A type of anemia called aplastic anemia reduces the number of all kinds of
blood cells, including platelets.
 Infection: A bacterial infection, especially the blood infection sepsis, can reduce
platelet count.
 Autoimmune disorders: Autoimmune diseases such as lupus and Crohn's disease
lower platelet count by causing the body to attack its tissue.
 Chemotherapy: Chemotherapy harms existing tissue in addition to cancer cells,
which can make it difficult for the body to produce platelets.
 Poisoning: Exposure to some pesticides can damage platelets.
 Cirrhosis: Liver cirrhosis, often due to excessive drinking, can reduce platelet count.
 Chronic bleeding: Any disorder that causes ongoing uncontrolled bleeding, such as
stomach ulcers, can deplete platelets.

Peginterferon alfa-2a binds to cell surface receptors in a cascade of protein interactions,


resulting in gene transcription. These stimulated genes inhibit viral replication in infected
cells, cell proliferation, and immunomodulation. Peginterferon alfa-2a is indicated for adults
with hepatitis B e antigen (HBeAg)–positive and HBeAg-negative chronic hepatitis B disease
with compensated liver disease and evidence of viral replication and liver inflammation.

Peginterferon alfa-2a is also FDA approved for the treatment of chronic hepatitis C, alone or
in combination with ribavirin, in patients not previously treated with interferon alfa, and with
compensated liver disease.

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