17 - سیروز Flashcards
Cirrhosis is
diffuse, irreversible hepatic process characterized by fibrosis, regenerating nodules, and distortion of the normal hepatic parenchyma
Some common causes of cirrhosis
Hepatitis C
Alcoholic liver disease
Non-alcoholic fatty liver disease (NAFLD)
Hepatitis B
Less common causes of cirrhosis include:
Autoimmune hepatitis Primary biliary cirrhosis Primary sclerosing cholangitis Hemochromatosis Wilson’s disease Alpha-1 antitrypsin deficiency Drug induced causes
Patients with cirrhosis present with several physical findings including:
Jaundice Palmar erythema Spider angiomata Petechiae Ascites Hepatic encephalopathy Gynecomastia Caput medusa Asterixis
Compensated cirrhosis patients will classically present with nonspecific symptoms such as:
Fatigue
Weight loss
Weakness
Decompensated cirrhosis patients may present with more specific symptoms, including:
Confusion Ascites Edema Pruritus Hematemesis Melena
The gold standard for diagnosing cirrhosis is
liver biopsy,
The pathologic features of cirrhosis include
the presence of fibrosis, regenerating hepatic nodules, and decreased number of septa.
Common laboratory tests include:
Bilirubin Aspartate aminotransferase (AST) Alanine aminotransferase (ALT) Gamma-glutamyl transpeptidase (GGT) Albumin Prothrombin time (prolonged in cirrhosis) Platelet count (low in cirrhosis) Electrolyte panel (low sodium)
Patients with cirrhosis are susceptible to several complications including:
Ascites Spontaneous bacterial peritonitis Variceal hemorrhage Hepatopulmonary syndrome Hepatorenal syndrome Portal vein thrombosis Cardiomyopathy Hepatic encephalopathy
primary focus in treating cirrhosis
treatment of the underlying disease process. This involves managing toxic insults and preventing serious secondary complications.
….is used during acute hepatic encephalopathy. prevents the absorption of ammonia
Lactulose
……are used to help keep the pressure low when a patient presents with esophageal or gastric varices.
Beta blocker
Transjugular intrahepatic portosystemic shunt (TIPS)
is a procedure performed when patients present with severe portal hypertension. This procedure creates a new route for blood to pass through the damaged liver.
Ascites is a fluid collection within the peritoneum usually found in the setting of:
Portal hypertension causing increased hydrostatic pressure (e.g. cirrhosis, right sided heart failure, Budd-Chiari Syndrome)
Hypoalbuminemia causing decreased oncotic pressure (e.g. malnutrition, nephrotic syndromes)
Malignancies (e.g. ovarian cancer)
Infections (e.g. tuberculosis)
Patients with ascites generally present with:
Abdominal swelling
Weight gain
Shortness of breath
Associated symptoms from the etiology of the ascites (e.g. hepatic stigmata)
The diagnosis of ascites is usually based on
history, physical exam, ultrasound, and paracentesis.
تپ مایع اسیت بیشتر از 250 تا pmn
Physical exam findings on patients with ascites include:
Bulging flanks
Fluid waves
Shifting dullness on percussion (changing location of dullness when the patient turns)
Associated findings related to ascites etiology
to help determine the etiology of the ascites.
paracentesis can be performed
Ascitic fluid is analyzed for:
Appearance Albumin levels Cell count Total protein Cell culture
SAAG
= (serum albumin) - (ascitic albumin)
A serum to ascites albumin gradient greater than 1.1 g/dL indicates
the ascites is due to portal hypertension. Possible causes of portal hypertension include: Cirrhosis Budd-Chiari syndrome CHF Constrictive pericarditis Schistosomiasis
A serum to ascites albumin gradient less than 1.1 g/dL indicates
an etiology other than portal hypertension such as nephrotic syndrome and cancer. کارسینوما پروتونئال پریتونئال توبرکلوزیس پانکراتیت سروزیت نفروتیک سندرم
Concerning complications of ascites include:
Spontaneous bacterial peritonitis
Hepatic hydrothorax
Ascites is treated symptomatically through several strategies:
Sodium restriction
Diuretics such as furosemide (Lasix) or spironolactone (Aldactone)
Beta blockers to lower portal pressure in cirrhotic patients
سفتریاکسون
سفازولین
سفکسیم
Spontaneous bacterial peritonitis is
inflammation of the peritoneum, caused by ascitic fluid that has become infected.
The three most commonly isolated pathogens in spontaneous bacterial peritonitis are:
E. coli (most common)
Klebsiella pneumoniae
Streptococcus pneumoniae
Patients with spontaneous bacterial peritonitis present with:
Low-grade fever* (most common)
Abdominal tenderness
Subtle mental status changes
Patients with advanced spontaneous bacterial peritonitis can present with:
Hypothermia
Hypotension
Paralytic ileus (dilated loops of bowel on abdominal x-ray)
The clinical presentation of esophageal varices
may include rapid onset GI bleeding, anemia, and hematemesis. The patient often has a history of liver disease (e.g., cirrhosis).
Esophageal varices are diagnosed by
upper endoscopy.
Initial management of an acute bleed includes:
Rapid volume resuscitation
Correction of any underlying coagulopathy
Administration of prophylactic antibiotics (Oral norfloxacin or IV ciprofloxacin is recommended. IV ceftriaxone may be given in patients with advanced cirrhosis.
Endoscopic ligation/banding
is the primary choice for treatment of coagulopathies due to cirrhosis.
Fresh frozen plasma (FFP)
Hepatorenal syndrome is
development of renal failure in patients with acute or chronic liver disease.
Patients with hepatorenal syndrome present with clinical symptoms of kidney failure such as:
Azotemia Oliguria Hyponatremia Hypotension hypoxemia and dyspnea
Patients with hepatorenal syndrome have laboratory findings consistent with prerenal azotemia:
Low urine sodium (<10 mEq/L)
FeNa < 1%
BUN:Cr ratio > 20:1
Serum Cr >1.5
fluid bolus administration in a patient with hepatorenal syndrome will ……
exacerbate the condition
Hepatorenal syndrome is best managed with vasoconstrictors such
Terlipressin
Norepinephrine
Octreotide
Midodrine
Hepatic encephalopathy Treatment is aimed at ammonia reduction, which can be achieved through:
Lactulose, which prevents the absorption of ammonia
Antibiotics (i.e. rifaximin or neomycin) that decrease ammonia production by gut bacteria
Diet adequate with protein and energy (low protein diet, though once considered beneficial, has been shown to be detrimental in most patients as they are already malnourished and require sufficient protein to maintain a healthy body weight)
Branched-chain amino acid and probiotic supplementation, if indicated
علائم ازمایشگاهی سیروز
صفرای بالا هایپو البومینی pt مختتل انمی bun پایین
سه علت مهم که باعث پورتال هایپرتنشن میشوند ؟
سیروز
هپاتیک ترومبوزیس
سندرم بودکیاری
عوارض پورتال هایپرتنشن ؟ 4
اسیت
کاپوت مدوزا
هموروئید
اسپلنومگالی
عوامل تشدید کننده و ایجاد کننده آنسفالوپاتی
azotemia seductive خونریزی کوارشی الکالوز هایپوکالمیک پروتئین رژیم غذایی عفونت یبوست مکروز هپاتیک
4 تومور خوش خیم کبدی
همانژیوما
فوکال ندولار هایپرپلازیا
5 تا سرطان بدخیم کبدی
کنسر های اولیه کبدی :
هپاتوسلولار کارسینوما : شایع ترین نوع اولیه
فیبرولاملار کارسینوما
هپاتوبلاستوما
متاستاز : شایع ترین بدخیمی ها معمولا از دستگاه گوارش
همانژیوما
شایع
منفرد
دارای حاشیه منظم و مشخص
معمولا بی علامت
فوکال ندولار هایپرپلازی FNH
ندول های خوش خیم در کبد معمولا یک اسکار ستاره ای درمرکز تشخیص های افتراقی : ادنوما هپاتوما
در خانم ها شایع تر
با هورمون های جنسی ارتباطی ندارد
FNA:
هپاتوسیت نرمال دارای سلول های کوپفر در وسط
هپاتیک ادنوما
هپاتوسین ها نرمال ولی پرتال ترکت و سنترال وین و .. خراب هستند همه
( علامت مهمش بود )
در خانم ها بیشتر
ارتباط با هورمون جنسی
در صورت پیشرفت درد در ruq
کیست های کبدی
تومور هایی که دور تا دورشان دیواره است ولی داخل آنها چیزی نیست
ممکن است همراه با بیماری های پلی کیستیک کلیه
هپاتوسلولار کارسینوما
امکان متاستاز بالا ویژگی های سیستمیک : هایپر کلسیمی هایپو گلایسمی هایپرلیپیدمی هایپر تیروئیدی کاهش وزن درد در RUQ
علائم فیزیکال :
علائم سیروز
Liver bruit
مهم ترین ریسک فاکتورش : سیروز
تنها ویروسی که قبل از ایجاد سیروز میتونه هپاتوسلولار کارسینوما ایجاد کنه هپاتیت بی
تشخیص :
هر 6 ماه سونوگرافی . تست الفا فیتو پروتئین
تومور مارکر هپاتوسلولار کارسینواست .
فیبرولاملار کارسینوما
معمولا در افراد جوان
5-35
به سیروز ارتباطی ندارد
الفا فیتوپروتئین نرمال
کلانژیوکارسینوما
سرطان مجاری صفراوی cholangiocellular adenocarcinoma of biliary tract 60-70% klastskin tumors biferatrian of biliary system
20-30%
extrahepatic ducts
10-15%
intrahepatic bile ducts
