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.
