acute liver failure

Answer 1

Acute liver failure is defined as a liver disease that produces hepatic encephalopathy within 6 months of the initial diagnosis.
fulminant liver failure when the encephalopathy develops within 2 weeks of the onset of jaundice, and as subfulminant liver failure when the encephalopathy develops within 3 months. I

Question 2

histology

Answer 2

massive hepatic necrosis. The liver is small and shrunken due to loss of parenchyma  Microscopically, there are large zones of destruction surrounding occasional islands of regenerating hepatocytes

Question 3

presentation

Answer 3

nausea, vomiting, jaundice, and fatigue, which are followed by the onset of lifethreatening encephalopathy, coagulation defects, and portal hypertension associated with ascitestransaminase levels in the serum are elevated into the thousand

Question 4

progressions

Answer 4

first enlargement then shrinking
serum transaminase level decreases
worsening jaundice,coagulopathy, encephalopathy then multiorgan failure

Question 5

manifestation

Answer 5

jaundice and icterus
yellow discoloration of skin and sclera due to accumulation of bilirubin and cholestasis bc other solutes are also accumulated

Question 6

encephalopathy
behavioural to confusion to stupor to coma and death
Elevated ammonia levels in blood

Answer 6

. Fluctuating neurologic signs, including rigidity, hyperreflexia, and asterixis. Asterixis refers to a nonrhythmic rapid extension-flexion movement of the head and extremities, best seen as “flapping” of the hands when the arms are held in extension with dorsiflexed wrists

Question 7

Coagulopathy

Answer 7

he liver is the source of a number of coagulation factors that decline in the face of liver failure, leading to easy bruising and bleeding. Paradoxically, disseminated intravascular coagulation (Chapter 12) also may occur due to failure of the damaged liver to remove activated coagulation

Question 8

Portal HTN

Answer 8

obstruction at the prehepatic, intrahepatic, or posthepatic level. While it can occur in acute live failure, portal hypertension is more commonly seen w
chronic LF
the obstruction is usually intrahepatic and the major clinical consequences are ascites and hepatic encephalopathy. In chronic liver disease, portal hypertension develops over months to years, and its effects are more complex and widespread

Answer 9

is a form of renal failure occurring in individuals with liver failure in whom there are no intrinsic causes for kidney dysfunction. Sodium retention, impaired free-water excretion, and decreased renal perfusion and glomerular filtration rate are the main renal functional abnormalities. There is decreased renal perfusion pressure due to systemic vasodilation, activation of the renal sympathetic nervous system and vasoconstriction of the afferent renal arterioles, and increased activation of the renin-angiotensin axis, causing vasoconstriction that further decreases glomerular filtration. The syndrome’s onset begins with a decrease in urine output and rising blood urea nitrogen and creatinine levels

Question 10

Cirrhosis and causes

Answer 10

diffuse transformation of the liver into regenerative parenchymal nodules surrounded by fibrous bands
chronic hepatitis B, chronic hepatitis C, non-alcoholic fatty liver disease (NAFLD), and alcoholic liver disease.

Question 11

histology

Answer 11

diffuse transformation of the entire liver into regenerative parenchymal nodules surrounded by fibrous bands. The size of the nodules, the pattern of scarring (linking of portal tracts to each other vs. linking of portal tracts to central veins), the degree of parenchymal loss, and the frequency of vascular thrombosis (particularly of the portal vein) all vary between disease
chronic liver disease, ductular reactions increase with disease progression and are usually most prominent in cirrhosis. Ductular reactions may incite some of the scarring in chronic liver disease 
Regression of fibrosis and even of fully established cirrhosis may follow disease remission or cure. Scars become thinner, more densely compacted, and eventually start to fragment 
fibrous septa break apart, adjacent nodules of regenerating parenchyma coalesce into larger islands. All cirrhotic livers show elements of both progression and regression

Question 12

40% of individuals with cirrhosis are asymptomatic

Answer 12

anorexia, weight loss, weakness, and, eventually signs and symptoms of liver failure discussed earlier. Jaundice, encephalopathy, and coagulopathy may result from chronic liver disease

Question 13

chronic severe pruritus from building up of bile salts in the body. Scratching of skin that leads to infection
portal htn where portosystemic shunts may develop from dilation of collateral vessels.
venous bypasses where systemic and portal veins share common capillary beds

Answer 13

esophagogastric varices

40 pc of people w end stage liver disease showing hematemesis. Portal HTN, spleenomegaly, sometimes coagulopathy

Question 14

hyperestrogenemia in male pts w imapired estrogen metabolism

palmar erythema and spider angioma of the skin
gynecomastia
hypogonadism(also in women from hyp-pituitary axis)
HCC carcinoma risk

Answer 14

Acute on Chronic LF
stable chronic disease suddenly develop acute disease
established cirrhosis w extensive shunting, large volume of functional parenchyma w borderline vascular supply
mortality 50 pc

causes hep D in people who are suffering from hep B, resistance to medical therapydevelopment of ascending bacterial cholangitis in patients with primary sclerosing cholangitis; or replacement of liver parenchyma by primary or metastatic carcinoma. In other instances the cause may be a systemic disorder, such as sepsis, acute cardiac failure or a superimposed toxic injury that tips a well-compensated cirrhotic patient into liver failure