LBM 5 ENTEROHEPATIK

LBM 5

STEP 1 STEP 2 1. Mengapa seluruh kulit pada pasien dirasakan gatal ? 2. Mengapa pasien memiliki BB yang turun ? 3. Mengapa amilase dan lipase serum tinggi ? 4. Mengapa terdapat rasa tidak enak di epigastrium dan jaundice ? 5. Mengapa di temukan steatorhea ? 6. Mengapa pada USG tampak perbesaran pancreas irreguler dan tampak perbesaran saluran empedu ? Mengapa benjolan sukar di gerakkan ? 7. Apa hubungan kebiasaan minum alkhohol dengan keadaan tsb ? 8. Apa hubungan urobilin dan sterkobilin menurun dengan keadaan pasien ? 9. DD ? Courvoisier sign : Pemeriksaan pada dilatasi vesica fellea (misal pada obtruksi). Metode

seperti Murphys sign, tapi teraba. Steatorhea : keadaan dimana terdapat lemak dalam tinja.

STEP 4 Courvoisure sign Infeksi akut Tumor Pancreas Gangguan Pancreas

Demam

Amylase lipase meningkat

Bengkak regio epigastrium

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LBM 5 ENTEROHEPATIK Step 6 1. Mengapa seluruh kulit pada pasien dirasakan gatal ? jawab : Pruritus or itch (both terms are used interchangeably throughout this article) is not the most common symptom seen in palliative care, but can be very distressing and can adversely affect quality of life. Pruritus can be described as an unpleasant sensation of the skin or mucous membranes that provokes the desire to scratch or rub. Pathophysiology of pruritus is important and guides effective therapeutic choices. There are 4 categories of pruritus: prurioreceptive, neuropathic, neurogenic, and psychogenic. a. Prurioreceptive pruritus occurs when the itch originates in the skin. The sensation begins in the free nerve endings of the skin; it is transmitted by dedicated unmyelinated C fibres to the posterior horn and relayed via the spinothalamic tract to the brain, where it is perceived as itch. The motor reflex to scratch stimulates A sensory fibres, which in turn block the sensation of itch. Several chemical mediators (ie, pruritogens) stimulate the C fibres. Although histamine (through histaminetype 1 [H1] receptors) is the best known pruritogen, there are several others, including serotonin (through 5-hydroxytryptamine [HT] receptors 2 and 3), cytokines, opioids (endogenous and exogenous, through -opioid and opioid receptors), and neuropeptides (such as substance P), that can play a role. Both opioidergic and serotonergic systems have been proposed as central regulators of pruritus. Some pruritogens act by releasing histamine from mast cells and others act independently, which explains why not all itching sensations respond to treatment with antihistamines. Even when pruritus is responsive to antihistamines, there might be central sensitization and decreased response if the itch is chronic. Further study is needed to understand this process. b. Neuropathic pruritus, another category of pruritus, occurs when there is damage anywhere along the afferent pathway, as with postherpetic itch or itch secondary to brain tumour. c. The third category of pruritus, neurogenic, is centrally induced and is unresponsive to antihistamines. Both opioid and serotonin receptors can reset the itch threshold centrally by altering the central inhibitory circuits. Examples of neurogenic pruritus include uremic and cholestatic itch. d. The fourth and least common category, psychogenic pruritus, is associated with psychiatric disorders

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LBM 5 ENTEROHEPATIK Cholestasis Cholestasis is commonly associated with pruritus, but the pathogenesis is still unclear. There is no correlation between the level of bile acids and the degree of pruritus, which explains why lowering the level of bile acids with cholestyramine is often ineffective. Another postulated mechanism is altered central opioidergic transmission; for that reason, opioid antagonists are used. Other possibilities include increased serotonin release, for which paroxetine, mirtazapine, or ondansetron can be prescribed. Again, histamine might be involved but to a lesser extent, as antihistamines are generally ineffective. Ultraviolet B light therapy is also an option. Opioid-induced itch Opioid-induced itch is more common with spinal opioids than with systemic opioids. The exact mechanism of opioid-induced pruritus is unknown; however, it is thought to be centrally mediated by -opioid receptors and inhibited by -opioid receptors. Opioids might also activate serotonin pathways, which explains why ondansetron (a 5-HT3 receptor antagonist) relieves itch secondary to spinal morphine. Solid tumours Solid tumours can be associated with paraneoplastic pruritus, which in fact might be the presenting symptom that precedes the diagnosis by months or years. The pathophysiology is not well understood, but appears to involve an immunologic reaction to tumour-specific antigens. Antihistamines are ineffective. The itch can be generalized or tumour specific: scrotal itch in prostate cancer, perianal itch in colorectal cancer, or vulvar itch in cervical cancer. Solid tumours can also cause pruritus via biliary obstruction (eg, in pancreatic cancer); in such cases, decompression through stenting can be very effective. Sumber : http://www.cfp.ca/content/57/9/1010.full
Table 1. Treatment options for pruritus secondary to advanced disease in palliative care
MECHANISM OF ACTION Soothes inflamed skin and prevents Emollients Minimize bathing futher abrasions, eruptions, or irritations CONSIDERATIONS INDICATION(S) Dry skin POSITIVE Dry skin is associated with many other causes of pruritus NEGATIVE NA

TREATMENT Nonpharmacologic General skin care2,5,7,20

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LBM 5 ENTEROHEPATIK

TREATMENT

MECHANISM OF ACTION

CONSIDERATIONS INDICATION(S) POSITIVE NEGATIVE

Tepid water Mild, unscented soap Loose, nonirritating clothing Avoid fragrant topical agents Cool, humidified environment UVB light therapy5,21 Decreases the number of mast cells and free nerve endings in the skin Biliary stenting5,6,8,9,18 Relieves bile ducts Pharmacologic Lidocaine 2.5% cream (topical anesthetic)18 Anesthetizes sensory nerve endings Paroxetine (antidepressant)
5,10,11,21,22

Cholestasis Uremia Malignant skin infiltration Cholestasis due obstruction Localized areas of itch

NA

Procedure often required 3 times/wk; impractical at end of life

Might negate need for pharmacotherapy Appropriate regardless of cause of pruritus

NA

obstruction in the to biliary

Large quantities of cream can cause toxicity when absorbed NA

5-HT3reuptake inhibition

Cholestasis Uremia Opioid-induced pruritus Malignancy

Effects within 24 to 48 h Few side effects

Mirtazapine (antidepressant)
10,11,21,22

5-HT2, 5-HT3, and Cholestasis H1receptor antagonists Uremia Opioid-induced pruritus Malignancy

Effective

Sedation Weight gain

Ondansetron (antiemetic)5,14,15,17,22 Dipenhydramine (antihistamine)5,7,8,9

5-HT3receptor antagonist H1 receptor antagonist

Cholestasis Uremia Opioid Allergy Histaminemediated

NA

Expensive Constipation

Inexpensive

Sedation Rarely effective

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LBM 5 ENTEROHEPATIK

TREATMENT

MECHANISM OF ACTION

CONSIDERATIONS INDICATION(S) pruritus POSITIVE NEGATIVE

Naloxone or naltrexone (opioid antagonist)

5,16,17,22

-Opioid receptor Cholestasis antagonist Uremia Opioid-induced pruritus

NA

Reverses analgesia Expensive

5-HT5-hydroxytryptamine (serotonin), H1histaminetype 1, NAnot applicable, UVB ultraviolet B. Sumber : http://www.cfp.ca/content/57/9/1010.full

2. Mengapa pasien memiliki BB yang turun ? Jawab : Berat badan bisa turun, dapat dikaitkan dengan anoreksia, cepat kenyang, diare, atau steatorrhea. Sumber : At a Glance Medicine

3. Mengapa amilase dan lipase serum tinggi ? Jawab : akibatnya adanya penyumbatan pada duktus sehingga enzim enzim pankreas masuk dalam sirkulasi sistemik.

Sumber : At a Glance Medicine

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LBM 5 ENTEROHEPATIK 4. Mengapa terdapat rasa tidak enak di epigastrium dan jaundice serta steatorhea ? Jawab : akibat adanya obstruksi dan pembesaran yang di dapat menghambat penguluaran enzim melalui duktus. Sumber : At a Glance Medicine

5. Apa hubungan kebiasaan minum alkhohol dengan keadaan tsb ?

Jawab :

Alkohol mempunyai efek toksik langusng terhadap pankreas pada orang-orang yang mempunyai kelainan enzim yang tidak di ketahui. Teori lain mengatakan bahwa selain merangsang sfingter oddi sehingga terjadi spasme dan meningkatkan tekanan di dalam saluran bilier dan salauran dalam pankreas, dan merangasan enzim pankreas sehingga mengakibatkan pangkreatitis. Alkohol juga mengurangi jumlah inhibitor tripsin sehingga pankreas menjadi lebih mudah di rusak oleh tripsin . Sumber : IPD FK UI jilid 1. Edisi 5. Hal 734 Naim Ismail Imunu

LBM 5 ENTEROHEPATIK

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LBM 5 ENTEROHEPATIK 6. Mengapa pada USG tampak perbesaran pancreas irreguler dan tampak perbesaran saluran empedu ? Mengapa benjolan sukar di gerakkan ? Jawab: karena adanya karsinoma pankreas. NORMAL Ukuran: tebal anteroposterior tidak lebih dari 3 cm. Ekogenisitasnya hampir sama atau sedikit lebih tinggi dari pada hepar.

KARSINOMA PANKREAS Pembesaran parsial pankreas. Konturnya ireguler, bisa lobulated. Ekogenisitasnya rendah/semisolid. Bisa disertai pendesakan v. Cava, pelebaran saluran bilier.

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LBM 5 ENTEROHEPATIK

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LBM 5 ENTEROHEPATIK 7. DD ? Carsinoma Pankreas Overview During 2006, estimated 32,300 people will die in the US of pancreatic cancer Fourth and fifth most common cause of cancer deaths in men and women in the US respectively Peak incidence in age 60-80 African Americans with slightly higher incidence compared with Caucasians

Types of Pancreatic Neoplasms Broadly speaking, there are three basic types: Ductal adenocarcinoma >90% of pancreatic cancers with a 4% 5-year survival (worst of any cancer) Neuroendocrine tumors aka islet-cell tumors, rare Cystic neoplasms account for <1% of pancreatic cancers

What are typical symptoms of pancreatic CA Abdominal pain->pain can suggest neural plexus, tail lesion, unresectability, poor prognosis Anorexia Weight loss Jaundice Pruritis ->biliary obstruction Steatorrhea->pancreatic duct obstruction

Faktor resiko Firmly linked to cigarette smoking No clear dietary factors Increased BMI associated with increased risk Occupational exposures to amines (chemistry, hairdressing, rubber work) associated with increased risk Previous epidemiology identified chronic pancreatitis as a risk factor May actually be EtOH, smoking, and a degree of selection bias instead of pancreatitis

Familial excess of pancreatic cancer, hereditary cancer syndromes, hereditary pancreatitis, BRCA-2 mutations all associated with increased risk of pancreatic cancer

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LBM 5 ENTEROHEPATIK

Pancreatic Cancer: Endoscopic Adjuncts ERCP can be utilized to: detecting small tumors not visualized on CT (irregular solitary duct stenoses >1cm long, abrupt cutoff of main pancreatic duct, or panc and bile duct obstruction) palliating biliary obstruction brush cytology of the pancreatic duct has fair sensitivity (70%) but excellent specificity

EUS can be utilized to: aid in diagnosis and characterization of lesion obtain tissue biopsy; may be associated with lower risk of peritoneal seeding c/w percutaneous approach Is there a role for serum markers CA 19-9 is a sialylated Lewis A blood group antigen commonly expressed and shed in pancreatic and hepatobiliary disease, not tumor specific

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LBM 5 ENTEROHEPATIK This antigen, when significantly increased, can assist in differentiating between pancreatic adenocarcinoma and inflammatory pancreatic disease decrease in serial CA 19-9 correlates with survival of pancreatic patients after surgery or chemotherapy Debatable as to whether this is useful as early treatment of recurrences have not been shown to improve outcomes

Sumber : Kuliah dr. Erwin.

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LBM 5 ENTEROHEPATIK Pancreatic cancer Pancreatic cancer, primarily ductal adenocarcinoma, accounts for an estimated 45,000 cases and 38,000 deaths in the US annually. Symptoms include weight loss, abdominal pain, and jaundice. Diagnosis is by CT. Treatment is surgical resection and adjuvant chemotherapy and radiation therapy. Prognosis is poor because disease is often advanced at the time of diagnosis. Most pancreatic cancers are exocrine tumors that develop from ductal and acinar cells. Pancreatic endocrine tumors are discussed below (see Tumors of the GI Tract: Pancreatic Endocrine Tumors). Adenocarcinomas of the exocrine pancreas arise from duct cells 9 times more often than from acinar cells; 80% occur in the head of the gland. Adenocarcinomas appear at the mean age of 55 yr and occur 1.5 to 2 times more often in men. Prominent risk factors include smoking, a history of chronic pancreatitis, obesity, and possibly long-standing diabetes mellitus (primarily in women). Heredity plays some role. Alcohol and caffeine consumption do not seem to be risk factors. Symptoms and Signs Symptoms occur late. By diagnosis, 90% of patients have locally advanced tumors that have involved retroperitoneal structures, spread to regional lymph nodes, or metastasized to the liver or lung. Most patients have severe upper abdominal pain, which usually radiates to the back. The pain may be relieved by bending forward or assuming the fetal position. Weight loss is common. Adenocarcinomas of the head of the pancreas cause obstructive jaundice (often causing pruritus) in 80 to 90% of patients. Cancer in the body and tail may cause splenic vein obstruction, resulting in splenomegaly, gastric and esophageal varices, and GI hemorrhage. The cancer causes diabetes in 25 to 50% of patients, leading to symptoms of glucose intolerance (eg, polyuria and polydipsia). Diagnosis

CT or magnetic resonance cholangiopancreatography (MRCP) CA 19-9 antigen to follow (not for screening) (See also the U.S. Preventive Services Task Force's summary of recommendations regardingscreening for pancreatic cancer.)

The preferred tests are an abdominal helical CT or MRCP. If CT or MRCP shows apparent unresectable or metastatic disease, a percutaneous needle aspiration of an accessible lesion might be considered to obtain a tissue diagnosis. If CT shows a potentially resectable tumor or no tumor, MRCP or endoscopic ultrasound may be used to stage disease or detect small tumors not visible with CT. Patients with obstructive jaundice may have ERCP as the first diagnostic procedure. Routine laboratory tests should be done. Elevation of alkaline phosphatase and bilirubin indicate bile duct obstruction or liver metastases. Pancreas-associated antigen CA 19-9 may be used to monitor patients diagnosed with pancreatic carcinoma and to screen those at high risk. However, this test is not Naim Ismail Imunu

LBM 5 ENTEROHEPATIK sensitive or specific enough to be used for population screening. Elevated levels should drop with successful treatment; subsequent increases indicate progression. Amylase and lipase levels are usually normal. Prognosis Prognosis varies with stage but overall is poor (5-yr survival: < 2%), because many patients have advanced disease at the time of diagnosis. Treatment

Whipple procedure Adjuvant chemotherapy and radiation therapy Symptom control About 80 to 90% of cancers are considered surgically unresectable at time of diagnosis because of metastases or invasion of major blood vessels. Depending on location of the tumor, the procedure of choice is most commonly a Whipple procedure (pancreaticoduodenectomy). Adjuvant therapy with 5fluorouracil

(5-FU) and external beam radiation therapy is typically given, resulting in about 40% 2-yr and 25% 5yr survival. This combination is also used for patients with localized but unresectable tumors and results in median survival of about 1 yr. Newer drugs (eg, gemcitabine, irinotecan , paclitaxel ,oxaliplatin, carboplatin) may be more effective than 5-FU based chemotherapy, but no drug, singly or in combination, is clearly superior in prolonging survival. Patients with hepatic or distant metastases may be offered chemotherapy as part of an investigational program, but the outlook is dismal with or without such treatment and some patients may choose to forego it. If an unresectable tumor is found at operation and gastroduodenal or bile duct obstruction is present or pending, a double gastric and biliary bypass operation is usually done to relieve obstruction. In patients with inoperable lesions and jaundice, endoscopic placement of a bile duct stent relieves jaundice. However, surgical bypass should be considered in patients with unresectable lesions if life expectancy is > 6 to 7 mo because of complications associated with stents. Symptomatic treatment: Ultimately, most patients experience pain and die. Thus, symptomatic treatment is as important as controlling disease. Appropriate end-of-life care should be discussed (see also The Dying Patient). Patients with moderate to severe pain should receive an oral opioid in doses adequate to provide relief. Concern about addiction should not be a barrier to effective pain control. For chronic pain, long-acting Naim Ismail Imunu

LBM 5 ENTEROHEPATIK preparations (eg, transdermal fentanyl, oxycodone,oxymorphone) are usually best. Percutaneous or operative splanchnic (celiac) block effectively controls pain in most patients. In cases of intolerable pain, opioids given sc or by IV, epidural, or intrathecal infusion provides additional relief. If palliative surgery or endoscopic placement of a biliary stent fails to relieve pruritus secondary to obstructive jaundice, the patient can be managed with cholestyramine (4 g po once/day to qid). Phenobarbital 30 to 60 mg po tid to qid may be helpful.Exocrine pancreatic insufficiency is treated with tablets of porcine pancreatic enzymes (pancrelipase). The patient should take enough to supply 16,000 to 20,000 lipase units before each meal or snack. If a meal is prolonged (as in a restaurant), some of the tablets should be taken during the meal. Optimal intraluminal pH for the enzymes is 8; thus, some clinicians give a proton pump inhibitor or H2 blocker 2 times/day. Diabetes mellitus should be closely monitored and controlled

Sumber : http://www.merckmanuals.com/professional/gastrointestinal_disorders/tumors_of_the_gi_tract/pancr eatic_cancer.html

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