module 13 hepatitis Flashcards
hepatitis s/s
sequence
- incubation
- prodromal (preicteric) phase
- variety of s/s ending with jaundice
- icteric phase: hepatocellular destruction and bile stasis, phase of illness
- recovery phase
Hepatitis A
RNA
fecal-oral transmission (enteric)
2-7 week incubation
immunity via IgG
Hep A risk factors
crowded, unsanitary conditions
food and water contamination
Hep A s/s
anicteric: no s/s or mild without jaundice Majority - jaundice - malaise - anorexia - nausea - low fever - RUQ pain
Hep B
Double stranded DNA
incubation 2-6 months
parental transmission: infected blood, body fluids, or contaminated needles
3 types of viral particles
prodromal period longer with immune-complex related s/s
Hep B s/s
urticaria rashes arthralgia arthritis angioedema serum sickness glomerulonephritis jaundice
Hep B infection to recovery/death
acute infection
- 60-65% sublinical disease -> 100% recovery
- 20-25% acute hepatitis -> 99% recovery, 1% fulminant hepatitis -> death
- 4% chronic hepatitis -> 20-30% cirrhosis -> hepatocellular carcinoma/death
fulminant hepatitis
liver coma
Hep C
RNA
Parental transmission, though less through sex or perinatal
- drug use, blood transfusion, needle stick
Hep C infection to recovery/death
acute infection
- 85% chronic hepatitis -> 80% stable disease, 20% cirrhosis -> 50% stable, 50% death
- 15% resolution
- rare: fulminant hepatitis
Hep D
co-infection
- depends on Hep B for replication
Parental transmission
Hep A and Hep E similar
typically self-limiting
2-8 wk incubation
does not cause chronic hepatitis or cancer
oral transmission
Hep B, Hep C, and Hep D similar
cause carrier state
cause chronic hepatitis and cancer
parenteral transmission
Hep E
RNA
transmission: fecal- oral
parental may occur
incubation: 2-9wks
chronic hepatitis
inflammation of liver > 6mo.
chronic persistant
chronic active
autoimmune
chronic persistant
triaditis, transaminitis
- chronic, low-grade inflammation
- portal triads w/out destruction of liver structures
- inc. serum transaminase
- not progressive
chronic acute
progressive, destructive
extends beyond portal triad to hepatic lobule
could spontaneously arrest or progress to cirrhosis
chronic acute s/s
fatigue malaise nause anorexia ascites hepatomegaly abdominal pain jaundice
autoimmune hepatitis
progressive inflammation characterized by autoantibodies and polyclonal hypergamaglobulinemia
cirrhosis
irreversible end stage of many different hepatic injuries
- acute hepatitis
- chronic hepatits
- toxic hepatitis
- metal storage diseases
- alcoholism
nodule regeneration and fibrosis -> dec. hepatic function
Biliary channels obstructed -> portal HTN
-> blood shunting away from liver, hypoxic necrosis
alcoholic cirrhosis
more fat delivered to hepatocyte than it can metabolize; defect in fat metabolism fatty infiltration (hepatic steatosis) - inc. lipogenesis and dec. fatty acid oxidation Alcohol -> acetaldehyde -> lipid peroxidation -> disruption of cellular function, damage, and inflammation
alcoholic cirrhosis s/s
usually mild and asymptomatic enlarged liver abdominal discomfort portal HTN multisystem disease r/t alcohol intake
Biliary cirrhosis
end result of continuous inflammation of bile ducts r/t biliary obstruction and backup of bile in the liver
-> inflammation and scarring of liver with obliteration of bile ductules, diffuse, widespread fibrosis, and nodule formation
Portal HTN
Biliary autoimmue (1st degree)
unknown etiology
destruction of intrahepatic ducts
portal inflammation
fibrosis
Biliary cirrhosis s/s
mitochondrial IgG antibodies
inc. serum alkaline phosphotase
hyperbilirubinemia
biliary obstruction (2nd degree)
prolonged complete or partial block
gallstones, tumors, fibrotic stricture
- inc. pressure in hepatic bile duct -> accumulation in centrilobular spaces and fibrosis
liver fibrosis and scarring ->
portal HTN -> ascites edema splenomegaly - anemia - thrombocytopenia - leukopenia varices - esophageal - hemorrhoids - superficial abd. veins
liver inflammation ->
pain fever N/V anorexia fatigue necrosis
Liver necrosis -> Gi/GU
dec. bilirubiin metabolism
- > hyperbilirubinemia, jaundice
dec. bile in gastrointestinal tract
- > light colored stolls
dec. vit. K absorption
- > bleeding
inc. urobilinogen
- > dark urine
liver necrosis -> dec. metabolism
dec. metabolism of proteins, carbs, and fats
- > hypoglycemia
dec. plasma proteins
- > ascites and edema
liver necrosis -> biochemical alterations
inc. AST and ALT
inc. bilirubin
dec. albumin
inc. PT time
inc alkaline phosphatase
liver necrosis -> dec. hormone metabolism
inc. androgens and estrogens
- gynecomastia
- loss of body hair
- menstrual dysfunction
- spider angiomas
- palmar erythema
inc. ADH and aldosterone
- edema
portal HTN
impaired blood flow through liver r/t inc. resistance from fibrosis and degeneration
- venous congestion in GI tract
portal HTN s/s
few early on, until abnormal vascular patterns
- anorexia
portal HTN complications
varices
-> uncontrolled bleeding form esophageal ruptures
ascites
ascites
accumulation of fluid in peritoneal cavity
typical with advanced liver disease r/t
- portal HTN
- dec. albumin
-> inappropriate pressure gradient, intraabd. accumulation of Na, H2O, protein
hepatic encephalopathy
complex neuropsychiatric syndrome characterized by s/s ranging from mild confusion to stupor and coma
- dementia
- psychotic symptoms
- spastic myelopathy
- cerebella or extraprymidal sings
Classic findings
- asterixis (liver flap): spastic jerking of hands held in force extension
assoc. with fulminant hepatic failure and severe chronic liver disease
arterial ammonia level directly correlates with level of encephalopathy
hepatic encephalopathy s/s
dec. K
dec. Na
alkalosis
hypoxia
hypercarbia
infection
GI hemorrhage
protein meal gorging
renal failure
constipation
Hepatic encephalopathy grade 1
confusion
subtle behavior change
no flap
hepatic encephalopathy grade 2
drowsy
clear behavior change
+ flap
hepatic encephalopathy grade 3
stupor can follow commands marked confusion slurred speech \+ flap
hepatic encephalopathy grade 4
coma
no flap
Jaundice
yellow-green staining of tissue r/t impaired bilirubin metabolism
may occur from dysfunction anywhere along pathway: 3 divisions
- prehepatic
- hepatic
- posthepatic
normal bilirubin metabolism
RBC broken down and release Hgb
- broken down to unconjugated bilirubin: transferred to liver bound to albumin
- liver makes conjugated (water-soluble) bilirubin and excretes in bile -> small intestine, not absorbed
- colon: bacterial B-glucuronidase converts it to uribilinogen
- > small amount resorbed and excreted by kidneys and liver
prehepatic jaundice
hemolysis and ineffective erythropoiesis reabsorption of large hematoma
hepatic jaundice
dysfunction of hepatic steps
- many disorders that affect liver function
posthepatic jaundice
level of canalicular transport inherited: dubin-johnson syndrome, Rotor syndrome -> inc. conjugated bilirubenemia drugs sex hormones mechanical obstruction of bile ducts
hepato-renal syndrome
complication of liver failure
intrarenal blood flow disturbed
- imbalance between vasoconstriction/dilation mechanisms r/t liver disease
- may follow vigorous diuretic therapy or paracentesis
– diarrhea, nonsteroidal anti=inflammatory drugs, variceal bleeding, sepsis
hepato-renal syndrome s/s
inc. creatine
AKF
oliguria
