Cirhosis & Complications Flashcards

Question

What are the causes of portal HTN due to sinudoidal causes? 2

Answer 1

Cirrhosis (many causes) Alcoholic hepatitis

Answer 2

Extrahepatic: Budd-Chiari syndrome Cardiac causes: constrictive pericarditis Intrahepatic : Veno-occlusive disease

Answer 3

With sustained portal hypertension, portosystemic collaterals are formed that have the benefit of decreasing portal pressures at the expense of bypassing the liver.

Answer 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.

Answer 5

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.

Answer 6

fundal varices

Answer 7

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.

Answer 8

Prophylactic intravenous anti- biotics should be administered early because they reduce the risk for infection, rebleeding, and death.

Answer 9

که‌ فشار پورت رو بیاره پایین

Answer 10

if the patient has contraindications or intolerance to β-blockers.

Answer 11

Grade 1 (mild): Detectable only by ultrasound examination. * Grade 2 (moderate): Moderate symmetrical distention of the abdomen. * Grade 3 (large): Marked abdominal distention.

Answer 12

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

Answer 13

1-large volume paracentesis 2-TIPS/ surgical shunt 3-liver transplantation

Answer 14

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).

Answer 15

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.

Answer 16

1-E choli 2-klebsiella Gram positive: 3-strep viridans 4-enterococcus 5-pneumococcus

Answer 17

Bowel perforation Other causes of peritonitis

Answer 18

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.

Answer 19

in any patient with cirrhotic ascites who deteriorates clinically.

Answer 20

The diagnosis of SBP is highly likely if a high concentration (>250 cells/mm3) of polymorphonuclear leukocytes (PMNs) is present in the ascitic fluid.

Answer 21

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.

Answer 22

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;

Answer 23

therapy is continued for a minimum of 5 days and can extend up to 14 days.

Answer 24

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.

Answer 25

Short-term prophylaxis should be considered for patients with cirrhosis and ascites who are hospitalized with upper gastrointestinal bleeding.

Answer 26

fluoroquinolones (ciprofloxacin, 500 mg/daily; norfloxacin, 400 mg/day) and trimethoprim-sulfamethoxazole (1 double-strength tablet daily).

Answer 27

``` Excess dietary intake of protein Gastrointestinal bleeding Infection Electrolyte disturbances such as hypokalemia Constipation Metabolic alkalosis ```

Answer 28

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

Answer 29

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.

Answer 30

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

Answer 31

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.

Answer 32

Short-term protein restriction may be considered for patients with severe encephalopathy. but long-term restriction is associated with worsening malnutrition.

Answer 33

Nonabsorbable disaccharides (e.g., lactulose)

Answer 34

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.

Answer 35

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

Answer 36

💩💩 or 💩💩💩 Patients are usually directed to achieve two to three soft stools per day.

Answer 37

Rifaximin 550 mg PO twice daily

Answer 38

1-hepatopulmonary syndrome (HPS) 2- Portopulmonary hypertension

Answer 39

HPS occurs in 5% to 30% of patients with cirrhosis and is a progressive disease. It is characterized by gas exchange abnormalities

Answer 40

HPS also has been reported in cases of hepatic venous outflow obstruction without cirrhosis.

Answer 41

Usually, this functional intrapulmonary right-to-left shunt significantly improves with the administration of 100% oxygen.

Answer 42

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.

Answer 43

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.

Answer 44

The gradient is calculated by analyzing arterial blood gases. : Pao2

Answer 45

mild, in which the arterial partial pressure of oxygen (Pao2) is greater than 80 mm Hg) very severe : Pao2 <50 mm Hg

Answer 46

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.

Answer 47

chest radiography, computed tomography, and pulmonary function tests, are performed to exclude intrinsic cardiopulmonary disorders.

Answer 48

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.😴😴

Answer 49

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.

Answer 50

the dyspnea is worse on standing

Answer 51

the dyspnea improves when the patient lies down

Answer 52

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.

Answer 53

dyspnea on exertion but many cirrhotic patients with PoPH are asymptomatic.

Answer 54

✅ 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.

Answer 55

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)

Answer 56

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.

Answer 57

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.

Answer 58

مرد ها Especially middle aged man

Answer 59

HCC often arises from a cirrhotic liver, and it is closely associated with chronic viral hepatitis.

Answer 60

Chronic hepatitis B infection Chronic hepatitis C infection Hemochromatosis (with cirrhosis) Cirrhosis (alcoholic, cryptogenic) Aflatoxin ingestion, Thorotrast exposure α1-Antitrypsin deficiency Androgen administration

Answer 61

Abdominal pain Abdominal mass Weight loss Deterioration of liver function

Answer 62

Bloody ascites Erythrocytosis Tumor emboli (lung) Jaundice🌝 Hepatic or portal vein obstruction ``` Metabolic effects: Hypercalcemia 🥛🥛 Hypercholesterolemia 🍟🍔🌭 Hypoglycemia Gynecomastia🤱🏻 Feminization👩🏿 Acquired porphyria ```

Answer 63

Hepatic bruit or friction rub Serum α-fetoprotein >400 ng/mL

Answer 64

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.

Answer 65

👑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

Answer 66

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.

Answer 67

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.

Answer 68

``` 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. ```

Answer 69

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.

Answer 70

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.

Answer 71

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.

Answer 72

in cases of chronic thrombosis, especially when associated with hypercoagulable states.

Answer 73

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.

Answer 74

Prophylaxis with β-blockers to prevent variceal bleeding may decrease the portal pressure, potentially propagating thrombus, and therefore is not usually recommended.

Answer 75

Occlusion of the major hepatic veins or the inferior vena cava, especially in the intrahepatic and suprahepatic segments, causes Budd- Chiari syndrome.

Answer 76

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.

Answer 77

``` 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.

Answer 78

Budd-Chiari syndrome can manifest acutely, possibly in association with acute liver failure, or it can manifest as a subacute or chronic illness.

Answer 79

Elevation of serum bilirubin and transaminase levels may be mild, but liver function is often poor, with profound hypoalbuminemia and coagulopathy.

Answer 80

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.

Answer 81

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.

Answer 82

Patients are typically considered for liver transplantation when the MELD-Na score reaches 15.

Answer 83

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.

Answer 84

• 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

Answer 85

postprocedural encephalopathy

Answer 86

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.

Answer 87

after an initial episode the risk of rebleeding approaches 60% with a mortality rate of approximately 33% if secondary prophylaxis is not instituted.

Answer 88

سیروز

Answer 89

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

Answer 90

Cirrhosis Alcoholic hepatitis Chronic hepatic congestion Right ventricular heart failure Budd-Chiari syndrome Constrictive pericarditis Massive liver metastases Myxedema Mixed ascites

Answer 91

Peritoneal carcinomatosis Peritoneal tuberculosis Pancreatic and biliary disease Nephrotic syndrome

Answer 92

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.

Answer 93

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.

Answer 94

1-Patients usually report increasing abdominal girth, 2-fullness of the flanks, 3-and weight gain 4-with or without peripheral edema.

Answer 95

Shifting dullness to percussion

Answer 96

about 1500 mL of fluid must be present for reliable detection.

Answer 97

Ascites becomes clinically detectable with fluid accumulation greater than about 500 mL.

Answer 98

when the serum sodium concentration is less than 120 to 125 mEq/L.

Cirhosis & Complications Flashcards

(122 cards)