patofisiologi GIT tractunivbsi.id/pdf/2017/900/900-P01.pdf · Secara klinis, penderita pankreatitis...

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Transcript of patofisiologi GIT tractunivbsi.id/pdf/2017/900/900-P01.pdf · Secara klinis, penderita pankreatitis...

patofisiologiGIT tractBy okatiranti

What is Liver Cirrhosis?Diffuse fibrosis of the liver with nodule formationAbnormal response of the liver to any chronic injury

Causes of Cirrhosis1. Chronic viral hepatitis2. Metabolic: hemochromatosis, Wilson dis,

alfa-1-antitrypsin, NASH3. Prolonged cholestasis (primary biliary

cirrhosis, primary sclerosing cholangitis)4. Autoimmune diseases (autoimmune

hepatitis)5. Drugs and toxins6. Alcohol

Anatomy of the portal venous system

The Effect of The Liver Nodule

Mechanism of Portal HTN

Cirrhosis

Resistance portal flow

MechanicalNodules

DynamicNitric oxide

Complications of Portal Hypertension

1. Varices

Collaterals

VaricesEsophagusGastricColo-rectalPortal hypertensive gastropathy

Variceal Banding

Types of Shunts

TIPS (Transjugular intrahepatic portosystemic shunt)

Surgical shunt

VaricesPrevention

Treat underlying diseaseEndoscopic banding protocolB-blockersShunt surgery (only if no cirrhosis)Liver transplantation

2. Ascites

Ascites

Definition: fluid in the peritonial cavity

Mechanism of Ascites

Causes of Ascites1. Liver disease: cirrhosis2. Right sided heart failure3. Kidney disease (nephrotic syndrome)4. Low albumin (malnutrition, bowel loss)5. Peritonial infection (TB…)6. Peritonial cancer

PresentationHistory:

Increased abdominal girthIncreased wt

Physical exam:Bulging flanksShifting dullnessFluid wave

DiagnosisPhysical examinationUltrasoundAscitic tap

WBC (>250 PMN: SBP)RBCSAAG (serum albumin to ascitic fluid

albumin gradient)>11 mg/dl : portal hypertension<11 mg/dl : Other

Portal hypertension

or heart failure

Peritonial disease

or kidney disease

Treatment-GeneralTreat the underlying diseaseSalt restriction (<2gm/d)Diuretics

Loop diuretic (Lasix)Aldosterone inhibitor (Spironolactone)

Treatment-ResistantRecurrent tappingPeritoneal-venous shuntTIPS Liver transplantation

Spontaneous Bacterial Peritonitis

Infection of ascitic fluidUsually gram negative (E.Coli)Presentation variableMortality is highDx: ascitic tap = PMN>250Treatment : third generation cephalosporin IV

3. Hepatic Encephalopathy

Hepatic Encephalopathy

Reversible decrease in neurological function secondary to liver diseaseAcute: seen with acute liver failureAcute on chronic: established cirrhosis

Hepatic EncephalopathyMechanism

Hepatic EncephalopathyClinical features

Reversal of sleep patternDisturbed consciousnessPersonality changesIntellectual deteriorationFetor hepaticusAstrexisFluctuating

Flapping Tremor

Drawing Tests

Hepatic EncephalopathyDiagnosis

Clinical (most important)The drawing testsEEG CT/MRI may show cerebral atrophy

Hepatic EncephalopathyExacerbating factors

Hepatic EncephalopathyTreatment

Identify and treat precipitation factorTreat underlying liver diseaseNormal protein dietAntibiotics (Neomycin, metronidazole)LactoloseTransplantation

4. Hepatorenal Syndrome

Hepatorenal SyndromeProgressive renal failureType 1 : rapidly progressive, high mortalityType 2: slower progressionR/O volume depletion secondary to diureticsIV vasoconstrictorsLiver transplantation

Summary1. Mechanical compression of blood flow

plus hemodynamic changes leads to portal hypertension

2. Common complications of portal hypertension are:

Collateral formation (Varices)AscitesHepatic encephalopathy

Summary3. The most important step in variceal bleed

management is resuscitation

4. The most important step in management of hepatic encephalopathy is the identification of the precipitating factor

– Hipokalsemia

PANKREATITIS AKUT

PENDAHULUANThe pancreas is a large gland behind the stomach and close to the duodenum. The duodenum is the upper part of the small intestine. The pancreas secretes digestive enzymes (TRYPSIN, AMYLASE, LIPASE) into the small intestine through a tube called the pancreatic duct. These enzymes help digest fats, proteins, and carbohydrates in food. The pancreas also releases the hormones insulin and glucagon into the bloodstream. These hormones help the body use the glucose it takes from food for energy.

LANJUTAN…

Normally, digestive enzymes do not become active until they reach the small intestine, where they begin digesting food. But if these enzymes become active inside the pancreas, they start "digesting" the pancreas itself.

PANKREATITIS AKUT

Pankreatitis akut adalah reaksiperadangan pankreas yang secara klinisditandai dengan nyeri perut yang akutdisertai kenaikan enzim pankreas dalamdarah dan urinPada pankreatitis akut, didapatiautodigesti dari enzim pankreas terhadapsel pankreas sehingga menimbulkanreaksi inflamasi

LANJUTAN…

Inflamasi dimulai dari perilobuler danjaringan peripankreas dengan manifestasiedema dan nekrosis setempatSetelah itu, mengenai sel asiner perifer, duktus pankreatikus, pembuluh darah, danjaringan sekitarnya

What are the causes of acute pancreatitis?

Acute pancreatitis is usually caused by gallstones or by drinking too much alcohol, but these aren't the only causes. If alcohol use and gallstones are ruled out, other possible causes of pancreatitis should be carefully examined so that appropriate treatment—if available—can begin.

What are the symptoms of acute pancreatitis?

Acute pancreatitis usually begins with pain in the upper abdomen that may last for a few days. The pain may be severe and may become constant—just in the abdomen—or it may reach to the back and other areas Other symptoms may include – swollen and tender abdomen – nausea– vomiting – fever – rapid pulse

How is acute pancreatitis diagnosed?

Besides asking about a person's medical history and doing a physical exam, a doctor will order a blood test to diagnose acute pancreatitis. During acute attacks, the blood contains at least three times more amylase and lipase than usual. Amylase and lipase are digestive enzymes formed in the pancreas. Changes may also occur in blood levels of glucose, calcium, magnesium, sodium, potassium, and bicarbonate. After the pancreas improves, these levels usually return to normal.

LANJUTAN…

A doctor may also order an abdominal ultrasound to look for gallstones and a CAT (computerized axial tomography) scan to look for inflammation or destruction of the pancreas

How is acute pancreatitis treated?

Treatment depends on the severity of the attack. If no kidney or lung complications occur, acute pancreatitis usually improves on its own. Treatment, in general, is designed to support vital bodily functions and prevent complications. A hospital stay will be necessary so that fluids can be replaced intravenously.

LANJUTAN...

If pancreatic pseudocysts occur and are considered large enough to interfere with the pancreas's healing, your doctor may drain or surgically remove them. Unless the pancreatic duct or bile duct is blocked by gallstones, an acute attack usually lasts only a few days. In severe cases, a person may require intravenous feeding for 3 to 6 weeks while the pancreas slowly heals. This process is called total parenteralnutrition

LANJUTAN…Secara klinis, penderita pankreatitis akutdapat beragam, dari yang mudah sembuh(self limiting) sampai yang dapatmenimbulkan gejala-gejala berat dankematian. Untuk itu, diperlukan identifikasipasien yang mempunyai risiko untukkematian berupa penilaian berat atautidaknya penyakit yang diderita

KOMPLIKASI

Komplikasi lokal, berupa: – Pengumpulan cairan yang akut. Hal ini paling

sering terjadi, biasanya terjadi pada awalperjalanan penyakit, dan dapat membaik secaraspontan;

– Nekrosis dari pankreas. Dapat terjadi lokal ataudifus, bisa juga steril dan terinfeksi;

– Abses pankreas. Hal ini merupakan komplikasilokal yang jarang terjadi; serta

– Yang lain, seperti pendarahan, trombosis vena splenikus, nekrosis, dan impaksi batu.

LANJUTAN…

Komplikasi sistemik, berupa: – Syok sirkulasi; – Gagal napas; – Gagal ginjal akut; – Sepsis; – KID (Koagulopati Intravaskular Diseminata); – Hiperglikemia; dan