Cirhosis & Complications Flashcards
کرایتریای هپاتورنال سیندروم ؟ ۶
- Cirrhosis with ascites
- Diagnosis of AKI according to ICA-AKI criteria: 50% increase in the serum creatinine level from baseline which is known or presumed to have occurred within the 7 days prior OR Rise of 0.3 mg/dL (26.4 μmol/L) in the serum creatinine level in less than 48 hours
- Lack of response after at least 2 days of diuretic withdrawal and volume expansion with albumin (1 g/kg of body weight/day, to a maximum of 100 g/day)
- Absence of shock
- Lack of current or recent treatment with nephrotoxic drugs
- Absence of parenchymal kidney disease as indicated by proteinuria of more than 500 mg/day, microhematuria (>50 red blood
cells/high-power field), or abnormal renal US findings
What is HRS 1?
HRS-AKI is characterized as an increase in serum creatinine 0.3 mg/dL or greater within 48 hrs or 50% or greater from baseline value according to ICA consensus document
and/or urinary output 0.5 mL/kg body weight or less for longer than 6 hours.
Typically, the kidneys are histologically normal and can regain nor-
mal function in the event of recovery of liver function (e.g., after liver transplantation). Severe cortical vasoconstriction has been demon- strated angiographically, and such vasoconstriction reverses when these kidneys are transplanted into patients who do not have cirrhosis.
What is HRS 2?
HRS- CKD is defined as eGFR less than 60 mL/min per 1.73 m2 for 3 months or greater in the absence of other (structural) causes.
در بیمار آسیتی، برای اینکه هپاتو رنال سیندروم نده چه داروهایی رو نباس بدیم؟ 4
, diuretics,
lactulose,
nonsteroidal anti-inflammatory drugs,
angiotensin-converting enzyme inhibitor
درمان hepatorenal AKI؟
the combination of
1-octreotide
2- midodrine (an α-adrenergic agonist)
3-and intravenous albumin.
What is hepatic encephalopathy?
is a complex, reversible neuropsychiatric syndrome that occurs in patients with chronic liver disease, portal hypertension, or portosystemic shunting. HE is also seen in patients with acute liver failure.
HE develops in about 30% to 45% of cirrhotic patients, and when it is present, the survival probability is approximately 23% at 3 years.
چه پاتوفیزیولوژی هایی برای HE مطرحه?
1-the inadequate hepatic removal of potential endogenous neurotoxins,
2/altered permeability of the blood-brain barrier
3- and abnormal neurotransmission.
4-Elevation of blood ammonia levels, derived from both amino acid deamination and bacterial hydrolysis of nitrogenous compounds in the gut, has been the best studied factor, but its specific role in the pathogenesis of HE remains uncertain.
5-increased tone of the inhibitory GABAA/benzodiazepine neurotransmitter system
6-activation of the astrocytic 18-kDa translocator protein (PTBR),
7-production of endogenous benzodiazepine-like compounds,
8-altered cerebral metabolism,
9-zinc deficiency,
10-increase in serotonin levels,
11-upregulation of H1 receptors,
12-altered melatonin production,
13-and deposition of manganese in the basal ganglia.
اولین علامت HE?
One of the earliest manifestations of overt HE is alteration of the normal sleep-wake cycle.
🌙🌗😴🌤☀️
Clinical manifestations of HE?
🐙The clinical features of HE include disturbances of higher neurologic function such as intellectual
🐙and personality disorders,
🐙dementia,
🐙inability to copy simple diagrams (constructional apraxia),
🐙disturbance of consciousness, disturbances of neuromuscular function (asterixis, hyperreflexia, myoclonus),
🐙and, rarely, a Parkinson-like syndrome and progressive paraplegia.
Ddx of HE? 4
reversible causes of neurologic dysfunction, such as 1-hypoglycemia 2-subdural hematoma 3-meningitis 4-and drug overdose
What are precipitating factors of HE?
1-Gastrointestinal bleeding
2-Increased dietary protein 🍗🍖🥚
3-💩Constipation
4-Infection
5-Central nervous system depressant drugs (benzodiazepines, opiates, tricyclic antidepressants)
5-Deterioration in hepatic function
6-Hypokalemia: most often induced by diuretics
7-Azotemia: most often induced by diuretics
8-Alkalosis: most often induced by diuretics
9-Hypovolemia: most often induced by diuretics
What are the common causes of cirrhosis? 12
1-Alcohol abuse 2-Nonalcoholic steatohepatitis 3-Viral hepatitis (chronic hepatitis B, C, and D) 4-Cardiac cirrhosis 5-Chronic right-sided heart failure 6-Constrictive pericarditis 7-Drug-induced liver injury (DILI) 8-Autoimmune hepatitis 9-Primary biliary cirrhosis 10-Hemochromatosis (primary and secondary) 11-Wilson’s disease 12-α1-Antitrypsin deficiency
ترتیب وقایعی که منجر به سیروز مبشه چجوریه؟
significant hepatocyte injury followed by ineffective repair that results in hepatic fibrosis.
The injury can be acute or chronic in nature, depending on the mechanism.
The fibrotic response to injury leads to development of nodules surrounded by fibrous tissue that consist of foci of regenerating hepatocytes, formation of fibrovascular membranes, rearrangement of blood vessels, and finally cirrhosis.
This disruption of the normal hepatic lobular architecture distorts the vascular bed and contributes to development of portal hypertension and intrahepatic shunting.
What are the clinical presentation of cirhosis + pathogenesis?
Constitutional
Fatigue, anorexia, malaise, weakness, weight loss
(Liver synthetic or metabolic dysfunction)
Cutaneous
Spider angiomas, palmar erythema
Altered estrogen and androgen metabolism
Jaundice
Decreased bilirubin excretion
Caput medusae
Portosystemic shunting due to portal hypertension
گولد استاندارد تشخیص سیروز؟
Liver biopsy
What are Labratory findings in cirrhosis ?
which one is the most sensitive?
1-hypoalbuminemia
2-hyperbilirubinemia,
3-low levels of blood urea nitrogen (BUN),
4-and elevated serum ammonia levels.
Portal hypertension causes hypersplenism, which results in:
5- anemia,
6- thrombocytopenia, : most sensitive
7-and leukopenia.
8-dilutional hyponatremia as a result of avid renal retention of sodium (Na+) and water.
9-The liver enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are good markers of active hepatocyte necrosis, whereas elevations of alkaline phosphatase and bilirubin out of proportion to ALT and AST suggest intrahepatic or extrahepatic biliary obstruction.
در سونو چه یافته هایی به نفع سیروزه؟
relative enlargement of the left hepatic and caudate lobes
as a result of right lobe atrophy,
surface nodularity,
and features of portal hypertension such as ascites, intra-abdominal varices, and splenomegaly.
What is elastography?
Transient elastography (FibroScan) is a newer noninvasive modality that provides an indirect measure of liver fibrosis and cirrhosis by calculating liver stiffness.
Abnormal liver stiffness suggests underlying fibrosis; in the presence of clinical and laboratory features of cirrhosis, this finding may obviate the need for diagnostic liver biopsy in some patients.
What is the most accurate non-invasive modality in diagnosis of cirrhosis?
MRE
is an addition to imaging provided by MR that incorporates acoustic vibrations across the entire liver to determine liver stiffness.
It is currently the most accurate noninvasive modality but is limited by availability and cost
What are the complications of cirrhosis?
1-hepatocellular dysfunction
2-portal HTN
What is normal HVPG?
Normal HVPG values range between 3 and 5 mm Hg.
تعزیف portal HTN?
Portal hypertension is defined as an HPVG greater than 5 mm Hg,
در چه HVPG ای اسیت ظاهر میشه؟
clinically significant complications typically develop at values greater than 10 mm Hg.
What are the causes of portal HTN due to persinudoidal causes? 4
Extrahepatic:
Portal or splenic vein occlusion
Intrahepatic :
Schistosomiasis
Congenital hepatic fibrosis
Sarcoidosis
What are the causes of portal HTN due to sinudoidal causes? 2
Cirrhosis (many causes)
Alcoholic hepatitis
What are the causes of portal HTN due to postsinudoidal causes? 3
Extrahepatic:
Budd-Chiari syndrome
Cardiac causes: constrictive pericarditis
Intrahepatic :
Veno-occlusive disease
پانوفیزیولوژی تشکیل واریس های مری به دنبال سیروز؟
With sustained portal hypertension, portosystemic collaterals are formed that have the benefit of decreasing portal pressures at the expense of bypassing the liver.
What are the major sites for collateral formation? 4
1-gastroesophageal junction,
2-retroperitoneum,
3-rectum,
4-and falciform ligament of liver (abdominal and periumbilical collaterals).
Clinically, the most important collaterals are those connecting the portal to the azygos vein through the dilated and tortuous vessels (varices) in the submucosa of the gastric fundus and esophagus.
واریس های مری در چه HVPG ای ایجاد و در کدوم ریسک پارگی دارن؟
Gastroesophageal varices usually develop when the portal pressure gradient (HVPG) exceeds 10 mm Hg,
and the risk for variceal rupture increases when the gradient is higher than 12 mm Hg.
کدوم واریس ها در HVPG ی زیر ۱۲ هم خطر پارگی دارن؟
fundal varices
علامت های variceal bleeding?
Variceal bleeding usually manifests as
1-painless hematemesis,
2-melena,
3-or hematochezia, which typically leads to hemodynamic compro mise due to higher portal pressures.
Bleeding is further aggravated by impaired hepatic synthesis of coagulation factors and thrombocytopenia from hypersplenism.
در variceal bleeding قبل اندپسکوپی چه دارویی میدیم؟
Prophylactic intravenous anti- biotics should be administered early because they reduce the risk for infection, rebleeding, and death.
برای واریس های مری چرا propranolol بدیم خوبه؟
که فشار پورت رو بیاره پایین
چه زمانی برای primary prophylaxis، میایم band ligation انجام میدیم؟
if the patient has contraindications or intolerance to β-blockers.
تعریف گرید ۱، ۲، ۳ اسیت؟
Grade 1 (mild): Detectable only by ultrasound examination.
- Grade 2 (moderate): Moderate symmetrical distention of the abdomen.
- Grade 3 (large): Marked abdominal distention.
درمان اسیت خط اول؟
1-restrict sodium to 2 g/day
2-restrict fluid if Na less than 125
3-tab Furosemide 40 mg PO daily
4-tab spironolactone 100 mg PO daily
Max: furosemide 160, spironolactone 400
اگر اسیت یه درمان خط اول مقاوم بوددیه ترتیب سزاغ چه کارایی میریم؟
1-large volume paracentesis
2-TIPS/ surgical shunt
3-liver transplantation
تعریف SBP?
Cirrhotic patients may develop infection of ascitic fluid in the absence of an obvious source of contamination or surgically treatable source, a condition known as acute spontaneous bacterial peritonitis (SBP).
مکانیسم SBP?
The exact mechanism of contamination of the ascitic fluid is unclear.
Factors such as
1-bacterial overgrowth,
2-altered motility,
3-and increased intestinal permeability causing transient translocation of bacteria into the bloodstream and eventual seeding of the peritoneal fluid may contribute.
میکزوبیولوژی شایع SBP چجوریه؟ 5
1-E choli
2-klebsiella
Gram positive:
3-strep viridans
4-enterococcus
5-pneumococcus
اگر در کشت مایع اسیت multiple organism ببینیم معنی ش چیه؟
Bowel perforation
Other causes of peritonitis
What are the clinical presentation of SBP?
Clinical features may include
1-fever,
2-abdominal pain,
3-and signs of peritoneal irritation,
particularly in advanced case.
Often, early infection is clinically silent or manifests with worsening of HE, diarrhea, ileus, or renal insufficiency.
اندیکاسیون diagnostic paracentesis در اسیت؟
in any patient with cirrhotic ascites who deteriorates clinically.
در پاراسنتز اسیت چی به نفع sbp عه؟
The diagnosis of SBP is highly likely if a high concentration (>250 cells/mm3) of polymorphonuclear leukocytes (PMNs) is present in the ascitic fluid.
اگر PMN مایع اسیت بالای ۲۵۰ بود، به ترتیب بعدش چیکار میکینیم بزای مریض؟
1-prompt empiric therapy
2-while blood and ascitic fluid culture results are pending.
inoculation of both aerobic and anaerobic blood culture bottles with the first samples of peritoneal fluid retrieved at bedside significantly increases the yield of capturing potential pathogens.
درمان SBP?
انتظار داریم بعد چند روز پاسخ به درمان را ببینیم؟
1-intravenous third-generation cephalosporin (e.g., ceftriaxone, 2 g every 24 hours);
2-quinolones, in particular ciprofloxacin,
are routinely used, provided that the patient does not have prior exposure and is not in overt shock.
Response to treatment is usually seen within 72 hours;
طول دوره درمان SBP چقدره؟
therapy is continued for a minimum of 5 days and can extend up to 14 days.
به کسی که sbp داره چی میدیم که ریسک سندرم هپاتورنال بیاد پایین؟
intravenous albumin on day 1 (1.5 g/kg)
and day 3 (1 g/kg)
has been shown to decrease the incidence of renal dysfunction and to improve short-term survival in SBP.
اندیکاسیون short term prophylaxis در SBP ?
Short-term prophylaxis should be considered for patients with cirrhosis and ascites who are hospitalized with upper gastrointestinal bleeding.
What is Common prophylactic regimens for SBP? 3
fluoroquinolones (ciprofloxacin, 500 mg/daily;
norfloxacin, 400 mg/day)
and trimethoprim-sulfamethoxazole (1 double-strength tablet daily).
کدوم فاکتور ها با مکانیسم Increased ammonia production, absorption or entry into the brain باعث HE میشن؟ ۶
Excess dietary intake of protein Gastrointestinal bleeding Infection Electrolyte disturbances such as hypokalemia Constipation Metabolic alkalosis
روش تشخیص HE?
1-Blood levels of ammonia are commonly measured, but elevated levels are neither sensitive nor specific for HE.
2-Neuropsychometric and neurocognitive tests such as the Portosystemic Encephalopathy Syndrome Test (PSET) and the earlier Stroop Color-Word Test evaluate the patient’s attention, concentration, fine motor skills, and orientation and have been shown to be highly specific for the diagnosis of HE, but they are reasonably labor intensive. Therefore, a smartphone-based application known as EncephalApp
نحوه طبقه بندی HE?
There are three major types of HE:
type A (Acute), which is associated with acute liver failure;
type B (Bypass), which is associated with porto- systemic shunts in the absence of liver disease;
and type C (Cirrhosis), which is associated with liver cirrhosis and is subdivided into episodic, persistent, and minimal types.
اولین قدم در درمان HE?
Treatment of HE starts with identifying and addressing any precipitating factors (Table reducing and eliminating substrates for the generation of nitrogenous compounds, and preventing ammonia absorption from the bowel.
کاهش و حذف بسترهای تولید ترکیبات نیتروژن دار و جلوگیری از جذب آمونیاک از روده
جایگاه Protein restriction در درمان HE?
Protein restriction was considered to be important in preventing excess ammonia production in the past; however,
✅ studies have demonstrated that dietary restriction of protein is not of significant benefit.
اندیکاسیون Protein restriction در درمان HE ?
Short-term protein restriction may be considered for patients with severe encephalopathy.
but long-term restriction is associated with worsening malnutrition.
What is the mainstay treatment of HE?
Nonabsorbable disaccharides (e.g., lactulose)
مکانیسم لاکتولوز در درمان HE?
۱-این عوامل توسط باکتریهای کولون به اسیدهای آلی تخمیر میشوند، فرآیندهایی که pH مدفوع را کاهش داده و NH4 + را در روده بزرگ به دام میاندازند و در نتیجه جذب را کاهش میدهند.
2-the cathartic of lactulose eliminates ammonia and other nitrogenous compounds.
خط دوم درمان HE برای کسی که who do not tolerate or respond to lactulose؟ tering
Reduction and elimination of nitrogenous compound substrates can also be achieved by administering
1-enemas and
2-using nonabsorbable antibiotics such as rifaximin in patients.:
یه انتی بیوتیک روده ای که تولید امونیاک توسط اون باکترس هارو محدود میکنه.
3-acarbose and probiotics
چه زمانی میگیم که به goal of lactulose therapy رسیدیم؟
💩💩 or 💩💩💩
Patients are usually directed to achieve two to three soft stools per day.
دوز ریفاکسیمین for the treatment of HE؟
Rifaximin 550 mg PO twice daily
What is the effects of cirrhosis and portal hypertension on the pulmonary circulation ?
1-hepatopulmonary syndrome (HPS)
2- Portopulmonary hypertension
What is hepatopulmonary syndrome?
HPS occurs in 5% to 30% of patients with cirrhosis and is a progressive disease.
It is characterized by gas exchange abnormalities
ایا ممکنه HPS در زمینه چیزی فیر از سیروز هم دیده شه؟
HPS also has been reported in cases of hepatic venous outflow obstruction without cirrhosis.
درمان HPS?
Usually, this functional intrapulmonary right-to-left shunt significantly improves with the administration of 100% oxygen.
پاتوفیزیولوژی HPS?
increased alveolar-arterial gradient and hypoxemia resulting from intrapulmonary vascular dilation.
The vascular dilation leads to vascular remodeling and angiogenesis,
resulting in impaired oxygen transfer from the alveoli to the central stream of red blood cells within capillaries.
روش تشخیص HPS?
HPS is diagnosed based on high clinical suspicion and measurement of a widened alveolar-arterial oxygen gradient on room air in the presence or absence of hypoxemia.
alveolar-arterial oxygen gradient
رو چجوری محاسبه میکنیم؟
The gradient is calculated by analyzing arterial blood gases. :
Pao2
What is mild and severe HPS?
mild, in which the arterial partial pressure of oxygen (Pao2) is greater than 80 mm Hg)
very severe : Pao2 <50 mm Hg
روش تشخیص Intrapulmonary shunting
contrast echocardiography,
in which agitated saline is injected into a peripheral vein during the performance of two-dimensional echocardiography.
Delayed appearance of microbubbles in the left cardiac chambers (more than three to six cardiac cycles after injection) indicates intrapulmonary vasodilation.
Early visualization of micro- bubbles in the left cardiac chambers indicates intracardiac shunting.
چه تست های ریوی دیگه ای در HPS اندیکاسیون دارند؟
chest radiography, computed tomography, and pulmonary function tests, are performed to exclude intrinsic cardiopulmonary disorders.
What are the Clinical features of HPS?
Clinical features range from subclinical abnormalities in gas exchange to profound hypoxemia causing significant dyspnea.
🍓Classically in HPS, the dyspnea is worse on standing and improves when the patient lies down (orthodeoxia and platypnea, respectively).
🍓Patients may also have marked nocturnal hypoxemia.😴😴
Screening of HPS?
Screening by pulse oximetry typically targets patients with values lower than 96% at rest on room air for further evaluation; however, recent data suggest that this may not be an appropriate screening tool.
What is orthodeoxia?
the dyspnea is worse on standing
What is platypnea?
the dyspnea improves when the patient lies down
Tx of HPS?
Currently, there is no established medical therapy for HPS.
Recent evaluation of newer agents such as sorafenib showed no significant improvement.
✅ Liver transplantation remains the only option and reverses HPS in most patients.
The use of TIPS to treat HPS is not established.
What is the most common symptom of porta pulmonary hypertension?
dyspnea on exertion
but many cirrhotic patients with PoPH are asymptomatic.
What should we do in order to diagnosis of portoPulmonary hypertension
✅ The diagnosis of PoPH is based entirely on results of right heart catheterization. :
The diagnostic values include a mean pulmonary arterial pressure greater than 25 mm Hg at rest or 30 mm Hg with exercise,
a pulmonary capillary wedge pressure lower than 15 mm Hg,
and a pulmonary vascular resistance greater than 240 dynes,
all in the presence of portal hypertension or liver disease or both.
How is PoPhypertension graded?
PoPH is graded according to the mean pulmonary artery pressure:
🧠mild (>25 to 35 mm Hg)
🧠moderate (35 to 50 mm Hg)
🧠severe (>50 mm Hg)
ریسک جراحی پیوند در هرکدوم از گرید ها چقدره؟
Patients with mild PoPH do not appear to have increased operative risk.
Moderate PoPH carries a high intraoperative risk and should be medically managed before transplantation.
❌Severe PoPH is generally considered a contraindication to surgery.
Tx of PoPH?
1-oxygen for dyspnea
2-diuretics for volume
3-prostacyclins (intravenous, inhaled or subcutaneous)
oral treatments including
4-phosphodiesterase inhibitors
5-and endothelin receptor antagonist: Macitentan showed improved pulmonary vascular resistance without hepatotoxicity.
HCc
در مردا شایع تره یا خانوما؟
مرد ها
Especially middle aged man
شایع ترین اتیولوژی های HCC?
HCC often arises from a cirrhotic liver, and it is closely associated with chronic viral hepatitis.
Risk factors for the development of HCC ? 7
Chronic hepatitis B infection
Chronic hepatitis C infection
Hemochromatosis (with cirrhosis)
Cirrhosis (alcoholic, cryptogenic)
Aflatoxin ingestion, Thorotrast exposure
α1-Antitrypsin deficiency
Androgen administration
What are the common clinical presentations of hepatocellular carcinoma? 4
Abdominal pain
Abdominal mass
Weight loss
Deterioration of liver function
What are the unusual clinical presentations of hepatocellular carcinoma?
Bloody ascites
Erythrocytosis
Tumor emboli (lung)
Jaundice🌝
Hepatic or portal vein obstruction
Metabolic effects: Hypercalcemia 🥛🥛 Hypercholesterolemia 🍟🍔🌭 Hypoglycemia Gynecomastia🤱🏻 Feminization👩🏿 Acquired porphyria
What are the clinical and Labratory findings in hepatocellular carcinoma? 2
Hepatic bruit or friction rub
Serum α-fetoprotein >400 ng/mL
Which parameters are used to screen the hepatocellular carcinoma? 4
patient’s age
ALT level
platelet count
and current and rate of change to AFP level.
It has shown an improvement in early detection in patients with cirrhosis in comparison to AFP alone.
What are the median characteristics of hepatocellular carcinoma?
👑Ultrasonography:
Mass lesion with varying echogenicity but usually hypoechoic
👑Dynamic Computed Tomography:
Arterial phase: tumor enhances quickly
Venous phase: quick deenhancement of tumor relative to parenchyma
👑Magnetic Resonance Imaging
T1-weighted images: hypointense
T2-weighted images: hyperintense
After gadolinium administration, tumor increases in intensity
چجوری میشه از HCCپیشگیری کرد یا پروگنوزشو بهتر کرد حداقل؟
prevention of viral hepatitis and other causes of liver disease
and on screening by ultrasound of those who are at higher risk, including patients with known cirrhosis.
What are vascular disease of the liver?
portal vein thrombosis (PVT),
hepatic vein thrombosis (Budd-Chiari syndrome),
and veno-occlusive disease.
Affected patients usually have portal hypertension with or without associated liver dysfunction, which may mimic the presentation of cirrhosis.
What are the causes of thrombosis of the portal vein?
1-blunt abdominal trauma 2-umbilical vein infection 3-neonatal sepsis 4-intra-abdominal inflammatory diseases (e.g., pancreatitis) 5- hypercoagulable states 6- in association with cirrhosis.
Myeloproliferative diseases including 7-polycythemia vera, 8-essential thrombocytosis, 9-and myelofibrosis) are now being recognized as possible causes of PVT.
Percense of which marker in PVT indicates a myeloproliferative Etiology?
Janus kinase 2 (JAK2) mutation is a marker for myeloproliferative disease and is often checked in patients with PVT.
The disease produces the manifestations of portal hypertension, but the liver histology is usually normal.
How is the diagnosis of portal vein thrombosis established?
The diagnosis is established by angiography
but noninvasive imaging modalities such as Doppler ultrasonography, computed tomography, and magnetic resonance imaging may reveal thrombus, collateral circulation near the porta hepatis, and splenomegaly.
In long-standing PVT, tortuous venous channels develop within the organized clot, leading to cavernous transformation.
What’s the mainstay of therapy of portal vein thrombosis?
warfarin
In most patients, recanalization of the thrombus occurs within 6 months after initiation of anticoagulation.
Recommendations for duration of anticoagulation after an acute event vary and are usually 3 to 6 months.
اندیکاسیون Long-term anticoagulation در PVT?
in cases of chronic thrombosis, especially when associated with hypercoagulable states.
اینکه بخوایم ما برا بیمار chronic PVT،
انتی کواگولنت طولانی بزاریم ریسک خونریری از واریس های مری رو زیاد نمیکنه؟
studies have not shown an increased risk for variceal bleeding in anticoagulated patients with chronic PVT.
In fact, studies suggest a role for prophylactic anticoagulation (enoxaparin) for prevention of PVT and hepatic decompensation in cirrhosis.
برای پیشگیری از خونریری از واریس های مری در کسی که واسه PVT رو انتی کواگولنته ، بتابلاکر بدیم؟
Prophylaxis with β-blockers to prevent variceal bleeding may decrease the portal pressure, potentially propagating thrombus, and therefore is not usually recommended.
What is budd chiari syndrome?
Occlusion of the major hepatic veins or the inferior vena cava, especially in the intrahepatic and suprahepatic segments, causes Budd- Chiari syndrome.
علت budd chiari syndrome?
1-hematologic disease (e.g., polycythemia vera, paroxysmal nocturnal hemoglobinuria, essential thrombocytosis, other myeloproliferative disorders),
2-pregnancy
3-oral contraceptive use
4-tumors (especially HCC),
5-or other causes of a hypercoagulable state (e.g., factor V Leiden mutation, protein C and S deficiency).
6-Abdominal trauma and congenital webs of the vena cava are also related to Budd-Chiari syndrome.
7-About 20% of cases are idiopathic, but many of these patients prove to have early, subclinical myeloproliferative disease or genetic mutations associated with a hypercoagulable state.
Clinical Presentation of budd chiari syndrome?
Acute disease produces 1- right upper quadrant abdominal pain, 2-hepatomegaly, 3-ascites, 4-and jaundice,
whereas the subacute or chronic form produces primarily portal hypertension.
Time course of of budd chiari syndrome?
Budd-Chiari syndrome can manifest acutely, possibly in association with acute liver failure,
or it can manifest as a subacute or chronic illness.
Lab tests in budd chiari?
Elevation of serum bilirubin and transaminase levels may be mild, but liver function is often poor, with profound hypoalbuminemia and coagulopathy.
روش تشخیص باد کیاری؟
The diagnosis can be established noninvasively with Doppler ultrasonography, which shows decreased or absent hepatic vein blood flow,
and computed tomography, which shows delayed or absent contrast filling of the hepatic veins and hypertrophy of the caudate lobe.
Magnetic resonance angiography may also demonstrate these findings.
Hepatic venography is especially useful if the results of noninvasive imaging are inconclusive. Venography often shows an inability to catheterize and visualize the hepatic veins; the characteristic spider- web pattern of collateral vessels may also be demonstrated, and the inferior vena cava may appear compressed owing to hepatomegaly or an enlarged caudate lobe.
پازامتز های MELD score?
4
1-serum creatinine concentration,
3-prothrombin time (International Normalized Ratio
2-and bilirubin level
4-serum sodium,
The MELD-Na score ranges from 6 to 40. Higher scores are associated with more advanced disease and increased predicted mortality.
ملد اسکور مریض چند باشه اندیماسیون پسوند داره؟
Patients are typically considered for liver transplantation when the MELD-Na score reaches 15.
کیا کاندید پیوند کبدن؟ 7
1-chronic liver disease resulting from alcohol.
Other liver diseases for which transplantation is commonly performed include : 2-cirrhosis from NAFLD, 3-hepatitis C virus, 4-autoimmune hepatitis, 5-primary biliary cirrhosis, 6-and primary sclerosing cholangitis.
7-Patients with hepatitis B are candidates for liver transplantation if they can be given hepatitis B immunoglobulin or nucleoside analogues to help prevent recurrence.
۴ تا کاری که برای مریض variceal bleeding میکینیم چین؟
• Early vasoactive drug therapy (somatostatin analogues) 2–5 days
• Endoscopic evaluation and therapy
(within 12 hours)
• Blood transfusion as needed
(hemoglobin goal 7–8 g/dL)
• Antibiotic prophylaxis
The most common side effect of the TIPS ?
postprocedural encephalopathy
secondary prophylaxis to prevent rebleeding?
combination of nonselective β-blockers (propranolol and nadolol) and variceal obliteration through repeated courses of EBL.
✅ We perform endoscopic variceal ligation in one to two weeks after hospital discharge
✅ and every two to four weeks thereafter until varices are eradicated.
اگر پروفیلاکسی نکنیم بعد یه اپیزود بلیدینگ نتیجش چیه؟
after an initial episode the risk of rebleeding approaches 60% with a mortality rate of approximately 33% if secondary prophylaxis is not instituted.
شایع ترین علت اسیت؟
سیروز
فرمول SAAG?
SAAG =
( Serum albumin concentration)
− ( Ascitic fluid albumin concentration)
An elevated SAAG (>1.1 g/dL) correlates well with portal hypertension as the likely cause of fluid accumulation
علل high SAAG?
Cirrhosis
Alcoholic hepatitis
Chronic hepatic congestion
Right ventricular heart failure
Budd-Chiari syndrome
Constrictive pericarditis
Massive liver metastases
Myxedema
Mixed ascites
علل low SAAG?
Peritoneal carcinomatosis
Peritoneal tuberculosis
Pancreatic and biliary disease
Nephrotic syndrome
Diagnosis of ascites?
Physical examination is relatively insensitive for detection of small volumes of ascites, but
1- bulging flanks,
2-shifting dullness,
3-and evidence of portal hypertension (e.g., distended veins over the abdominal wall
and caput medusae)
become evident with increasing amounts of fluid.
بعد اینکه در معاینه اسیت دیدیم اولین کار؟
Abdominal ultrasound is both sensitive and specific and is widely used in screening.
When fluid is present, abdominal paracentesis is the quickest and most direct approach for confirmation of the presence of fluid in the abdominal cavity and initial characterization of the cause.
هلایم اسیت؟
1-Patients usually report increasing abdominal girth,
2-fullness of the flanks,
3-and weight gain
4-with or without peripheral edema.
What is the most sensitive clinical sign of ascites?
Shifting dullness to percussion
Shifting dullness to percussion
چقدر مایع باشع ایجاد مبشه؟
about 1500 mL of fluid must be present for reliable detection.
چقدر مایع جمع شه اسیت به طپز کلینیکالی دیتکتیبل میشه؟
Ascites becomes clinically detectable with fluid accumulation greater than about 500 mL.
اندیکاسیون Water restriction در اسیت؟
when the serum sodium concentration is less than 120 to 125 mEq/L.
