hepatitis - ✔✔-impedes processes or functions of the liver
-inflammation of the liver
-caused by underlying infections agent or virus
-can also result from metabolic, vascular disorders, alcohol, or drug abuse, exposure to toxins
(like carbon tetrachloride)
-can be acute or chronic
hepatitis etiology - ✔✔-cell mediated immune response damage hepatocytes and Kupffer
cells, leading to hyperplasia, necrosis, and cellular regeneration
-flow of bile through bile canal into the biliary system, can be impaired by inflammation, leading
to jaundice.
prodromal phase - ✔✔-occurs between exposure to virus and the appearance of clinical
manifestations (such as jaundice)
-starts 2 weeks after exposure
-S/S can be insidious or rapid onset, mimic flu
-anorexia, abdominal pain RUQ
icteric phase - ✔✔-onset of jaundice, 5-10 days after initial symptoms
-urine may be dark (increased levels of bilirubin)
convalescent phase - ✔✔-recovery phase.
-follows 2-3 weeks of acute illness
-improved appetite and activity
, acute hepatitis manifestations - ✔✔-no S/S if mild
-fever, malaise, fatigue
-jaundice, pruitis, RUQ or epigastric pain
-anorexia, nausea/vomiting, myalgia, arthralgia
chronic hepatitis manfiestations - ✔✔-no S/S if mild
-fatigue, malaise, arthralgia
-RUG pain or pressure from enlarged liver
-jaundice
liver diagnostics - ✔✔ALT, ALP, LDH, AST, GGT, serum bilirubin, liver biopsy
cirrhosis clinical manifestations - ✔✔-coma, jaundice, spiderwebbed nevi, pectoral alopecia,
gynecomastia, live damage
-esophageal varices, bone marrow changes, splenomegaly, caput medusa, ascites, altered hair
distribution
-red palms, testicular atrophy, anemia, leukopenia, thrombocytopenia, hemorrhagic tendency,
ankle edema
portal hypertension - ✔✔causes blood to be rerouted to adjoining vessels
splenomegaly - ✔✔-blood shunted to splenic vein
-greater destruction of RBC's, WBC's. platelets
esophageal varices - ✔✔-enlarged, thin-walled veins form in submucosa of esophagus
-from portal hypertension
-may rupture, which leads to massive hemorrhage