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patho chpt 31 infection, inflammation and cirrhosis of liver
Terms in this set (93)
location of liver
right upper quadrant
blood supple to liver
hepatic artery (25%) and the portal vein (75%)
liver fct in terms of digestion
synthesizes and secretes bile for fat digestion into hepatic duct.
capable of regeneration, excrete metabolic substances in canaliculi which conduct bile to hepatic duct.
vascular spaces between the hepatocytes that contain a mixture of venous and arterial blood from hepatic artery and portal vein.
functions of liver
digestions, metabolism, hematologic, endocrine and excretory fuction. Plays a role in filtration, detoxification of blood stream
liver and digestion
bile salt secretion to aid in fat digestion
bile salt is recycled instead of secreted
a yellow-colored compound derived from breakdown of RBCs hemoglobin which is made of heme and globin. heme breaks down into iron and porphyrin. Porphyrin converts to biliverdin which changes into unconjugated bilirubin.
cannot be excreted. travels to the liver to be conjugated
occurs in liver, bilirubin is transfromed to water soluble form for excretion
excreted in bile or converted to urobilinogen by bacteria, reabsorbed and eventually secreted in urine or secreted in feces or recycled
fat and protein metabolism
bile secreted by liver breaks down fats into triglycerides and absorbed into portal vain and enter liver where they are broken down into fatty acids, cholesterol and glycerol.
liver an dprotein
can synthesize and breakdown. It produces most of the body's albumin
removes nitrogen from proteins and converts it to ammonia which is eventually excreted in urine
liver stores glucose as glycogen
breakdown of glycogen when body is enduring starvation or undergoing high stress
liver converts amino acids and glycerol into glucose
liver syntesizes fibrinogen and factors I, II, VI, IX and X. prothrombin with the assistance of vit. k and bile.
regulates fat and protein metabolism. glucagon, acts in liver and stimulates hepatic glycogneolysis and glyconeogenesis. it also stimulates lipolysis
biotransformation and first past reduce bioavailability or concentratoin of avialable drug in blood stream.
where is vit. A, D and b12 stored
where is angiotensin synthesized
ways that liver dysfunction occurs
cholestais (caused by bile flow obstruction), hepatocellular injury (result of inflammation), or mixture of both
consequences of liver disease
no synthesis, metabolism, detoxification, storage or clearance
yellowing of skin and sclera
high amt of bilirubin in the bloodstream. causing jaundice and icterus.
causes of hyperbilirubinemia
excessive RBC hemolysis, hepatocellular injury, bile duct obstruction
due to RBC hemolysis, liver is overwhelmed with bilirubin
due to hepatocellular injury, liver cannot conjugate bilirubin at all.
the bile duct is obstructed but it cannot be excreted.
lasts longer than 6 months, caused by acetaminophen
alcohol effects on liver
chronic liver inflammation causes stellate cells within the liver to synthesize collagen and fibrotic tissues. Steatosis results in fatty liver
inflistration of fat in the liver, 5 to 10% of liver contains fat
nonalcoholic fatty liver disease (NAFLD)
fatty liver not related to alcohol, major cause of cirrhosis. hepatocytes exhibit an accumulation of triglycerides.
s/s of NAFLD
RUQ pain, loss of appetite, nausea, jaundice, fatigue, weakness
dx of NAFLD
rule out other possible causes. no biomarkers or blood tests. MRI and CT can be helpful. Liver biopsy is key.
tx of NAFLD
aimed at each component of metabolic syndrome.
pathophysiology of NAFLD
linked to metabolic syndrome, insulin resistance, obesity, hyperlipidemia. when insulin resistance occurs, storage of fat is shifted to nonadipose tissues. decreased levels of adiponectin increase gluconeogenisis and enhances lipogenesis.
involement of the brain involving lethary, confusion and stupor or coma
bile duct obstruction
blokage of any duct that carries bile from liver to s.i.
s/s of bile duct obstruction
RUQ tenderness, hepatomegaly, hyperbilirubinemia, jaundice, spider angioma, caput, medusa, palmar erythema.
failure of bile to reach the ducts for excretion and causing backup
fine capillaries that fan out from a central point on the skin's surface.
obvious dilated veins over the umbilcal area of the abdomen.
dx of bile duct obstruction
liver enzymes, (serum alanie transaminase, serum aspartate transaminase), alkaline phosphatase, direct and indirect bilirubin, albumin, prothrobin, hepatic serology panal, biopsy
risk factors for liver disease
alcohol, medications, HBV or HCV, high cholesterol, triglycerides, iron. Malnutrition, metabolic syndrome, toxins, rapid weight loss
tx for bile duct obstruction
control of symptoms and supportive care. rest, small high calories, high protein meals. no alcohol or drugs.
5 to 40 U/ml
5 - 35 u/ml
less than 0.8 mg/dl
less than 1.0 mg/dl
3.5 to 5.5 g/dl
virus transmitted by fecal-oral route.
cause of hep a
rna virus contracted through fecal oral route.
pathophysiology of hep A
viral replication occurs in hepatocytes. antibodies to HAV are produced. IgG endow immunity to prevent repeat infection
s/s of hep A
fever, abd pain, mild flulike symptoms, n/v, fatigue, malaise, myalgias, arthraligias, milk headache, anorexia, loss of taste.
dx of hep A
incubation of 2 to 4 weeks. liver enzymes rise, HAV RNA appears in stool. look at IgM and IgG
tx of hep A
Hepatitis B virus
infiltration of virus into hepatocytes causes autoimmune response, lifelong carrier
pathophysiology of Hepatitis B virus
immune system attacks HBV and cauases liver injury. Activated CD4 and CD8 cells react against ABV proteins located on the surface of infected hepatocytes and immunologic rx occurs.
stage 1 of HBV
incubation period, no s/s, contagious
stage 2 of HBV
inflammatory rx of hepatocytes. flulike symptoms and jaundice. Liver enzymes increase.
stage 3 of HBV
immune system reacts agains infected hepatocytes. replication slows, liver enzyme normalize
stage 4 of HBV
virus cannot be detected and antibodies HBsAg andHBcAg and ABeAg have been produced.
only those who have endured the virus have these in their blood
s/s of HBV
flulike, 2 to 6 months after exposure, RUQ pain, anorexia, jaundice, light colored stools, fever, lymphadenopathy, spider angioma, palor erythema, splenomegaly
dx of HBV
presence of HBsAg in blood.
tx of HBV
supportive with rest.
virus that targets hepatocytes and b lymphocytes
incubation period of 2 to 8 months. innaccurate copying of he virus generates lots of mutant viruses. ACV RNA detected in blood. strong response by cytotoxic T lymphocytes and helper T cells.
s/s of HCV
flus, fever, RUQ pain, anorexia, hepatomegaly, splenomegaly, jaundice, n/v,
tx of HCV
supportive. 6 months of interferon.
result of the progression of actue hepatitis. inflammation and necrosis of hepatic tissues continues for 6 months or longer.
accelerates the progress of liver disease in those with HBV
similar to HAV.
characterized by inflammation, fibrosis, necrosis
following inhalation, ingestion or paranteral administration of pharmocologic and chemical agens.
alcoholic liver disease
alcohol is directly hepatoxic
pathphys of alcoholic liver disease
hepatocytes con only take so much. steatosis is the initial cellular change. fatty liver develops in every individual that consumes more than 60 g of alcohol per day.
s/s of alcoholic liver disease
accurate hx, RUQ pain, malaise, fever, jaundice, darkened urine,
dx of alcoholic liver disease
elevation of liver enzymes with hyper triglycerideemaia, hypercholesterolemia and hyperbilirubinemia, hypoalbuminemia
tx of alcoholic liver disease
cessation of alcohol usea and proper nutrition.
cirrhosis and liver failure
silent and greadula with little symptoms until late stage. liver is irreversibly damanged with collagen and connective tissue infiltration. cirrhosis is final stage of liver disease
pathophysioloyg of liver failure
structural changes, stellate cells are over active and produce alot of collagen and CT. Portal hypertension, decreased detoxification abilities, decreased bile synth, decreased albumin synth, hyperbilirubinemia, bleeding of esophageal varices, cogulopathy, osteoporisis, hepatic encephalopathy, spontaneous bacterial perionitis, iron overload, anemia, throbocytopenia, hepatorenal syndrome
as cirrhosis worsens, pressure within portal vein increases, causing backpu of pressure to the GI veins and collaterals. increased pressure results in splenomegaly, esophageal varacis, rectal varicies and escites.
s/s of liver failure
jaundice, steatorrhea, darkened urine. ascites, hematemeiss, fatigue, anorexia, weight loss, jaundice, spider angiomata, caput medusa
dx of liver failure
lab tests are normal early on. PT prolonged, low platelet, elevated serum bilirubin, liver bx
tx of liver failure
abstinence of alcohol. transplant.
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