Liver Disease Flashcards
metabolic liver functions
- fat, carb, and protein metabolism
- vitamin absorption and iron storage
homeostatic liver functions
alter circulating blood volume
filtering liver functions
purifies blood of bacteria
clotting liver functions
produces clotting factors
drug and chemical liver functions
drug and chemical detoxification and metabolization
what do we look at when assessing liver function
- liver enzymes
- bilirubin
- clotting measures
- ammonia and proteins
enzymes are the
clear portion of the blood
you will see enzymes rise when an
organ is damaged
____ is specific to liver damage
ALT
_____ could be from cardiac more than liver
AST
_____ shows biliary tract obstruction
ALK phospahte
when the liver is not working well you will see ______ and increase in _______
proteins and increase in albumin
ALT
alanine aminotransferase
normal ALT
5-35 units / L
AST
aspartate aminotransferase
normal AST
0-35 units / L
ALK phosphate
alkaline phosphate
ALK phospate normal
20-90 units / L
LDH5 and its normal
lactate dehydrogenase isoenzyme5 6-16%
ALP1
alkaline phosphate isoenzyme1 42-136
5’N
5’Nucleotidase less than 17 U/L
GGT
gamma glutamyl transferase
normal GGT
males 9-69 U/L
females 4-33 U/L
bilirubin
end product of hemoglobin degradation
fat soluble bilirubin is also known as
unconjugated
unconjugated means
it has not gone to the liver yet to get conjugated and become water soluble
water soluble bilirubin is also known as
conjugated
conjugated means
it reaches the liver and combines glucoronic acid and becomes conjugated
jaundice is
problem with body breaking down rbc
total bilirubin normal
0.1 - 1.2 mg/dL
indirect (unconjugated) normal
0.1-1.0 mg/dL
direct (conjugated) normal
0.1-0.3 mg/dL
urobilinogen normal
negative in freshly voided urine
liver produces which clotting factors
prothrombin, vitamin K, and other clotting factors that help us clot
if any of the clotting factors are elevated it means
that clotting factors are not being produced
normal prothrombin time (PT)
11.0-12.5 seconds
INR
internationalized normalized ratio 0.81-1.2
partial thromboplastin time (PTT)
60-90 seconds
aPTT
activated partial prothromboplastin time
normal aPTT
23-32 seconds
serum ammonia causes
mental status changes
serum albumin is important
protein in the body
stigma to liver disease is often related to
alcoholism
hepatic failure
the inability of the liver to perform its normal functions
causes of hepatic failure
- acute viral hepatitis
- autoimmune liver disease
- drug induced liver disease
- chronic liver disease (cirrhosis)
- multiple organ failure (sepsis)
stages of hepatic failure
fatty liver -> liver fibrosis -> liver cirrhosis
fatty liver
deposits of fat causes liver enlargement
liver fibrosis
scar tissue forms
liver cirrhosis
growth of connective tissue destroys liver cells
acute hepatic failure
includes evidence of abnormal coagulation and INR >1.5, altered mental state, encephalopathy, and illness <26 weeks
acute hepatic failure results from
- a primary disease process in the absence of pre-existing disease
- as a complication of chronic liver disease, cirrhosis
- multiple organ failure in critically ill
fulminant hepatic failure
acute hepatic failure in a patient with no pre-existing history that develops rapidly (<8 weeks) with encephalopathy
fulminant hepatic failure is a severe form of
acute hepatic failure
fulminant hepatic failure results from
- viral infections (hep A and hep B)
- hepatotoxins (acetaminophen)
Hep A is transmitted by
fecal - oral route
Hep B is transmitted by
blood or body fluids
Hep C is transmitted by
blood
Hep D is transmitted by
blood
Hep E is transmitted by
fecal - oral route
cirrhosis of the liver
chronic disease is which liver tissue is replaced with fibrous tissue and functional liver cells are lost
cirrhosis of the liver is the ____th leading cause of death in Canada
13th
during cirrhosis of the liver
- cell necrosis occurs
- inability to conjugate bilirubin
- inability to detoxify bilirubin
- inability to produce clotting factors and albumin
- inability to convert ammonia to urea
- inability to regulate glucose
- inability to purify blood
- inability to regulate blood volume
complications of cirrhosis
- portal htn
- esophageal varices
- ascites and albumin
- hepatorenal syndrome
- infections
- hepatic encephalopathy
portal hypertension
results from increased resistance within the portal venous system
portal htn is caused by
cirrhosis disrupting normal structure of liver creating resistance to blood flow through the liver
overtime a system of collateral circulation develops to relieve the pressure =
varices
esophageal varices
an increase in pressure (coughing, vomiting, straining) can cause the varices to rupture
damage to liver tissues increases _______ resistance
vascular
venous flow becomes blocked in the liver, causing portal vein tension to ________
increase
blood backs up through the splenic vein into the spleen and ________ circulation
collateral
ascites
accumulation of serous fluid in the peritoneal or abdominal cavity
ascites is usually seen in
advanced liver failure
ascites is caused by
decrease colloid osmotic and portal hypertension
hepatorenal syndrome (HRS)
renal failure in absence of underlying kidney pathology
hepatorenal syndrome occurs in _____ stage of liver disease
end stage
clinical manifestations of hepatorenal syndrome
- oliguria
- low urinary sodium
- hyponatremia
bacterial peritonitis
ascites fluid becomes infected
hepatic encephalopathy is considered a _______ complication of liver disease
terminal
hepatic encephalopathy is caused by
toxic levels of circulating ammonia which cross the blood-brain barrier
usually the liver converts ammonia to ____ for excretion in urine
urea
when the liver is unable to convert ammonia to urea
toxicity develops
precipitating factors of hepatic encephalopathy
- infection
- elevated protein intake
- worsening hepatic function
- constipation
- increased BUN and creatinine
- GI bleeding
- hypovolemia
goal of hepatic encephalopathy is to
reduce ammonia formation
number of stages in hepatic encephalopathy
4
neurologic effects of hepatic failure
grade I to IV encephalopathy
cardiovascular effects of hepatic failure
pulmonary edema, hypotension
GI effects of hepatic failure
n+v, constipation or diarrhea, anorexia, ascites, abdominal pain, hypoalbumnemia, hypoglycemia
pulmonary effects of hepatic failure
tacypnea, crackles
integumentary effects of hepatic failure
spider angioma, jaundice, edema
laboratory evaluation for liver diseases
- liver enzymes
- bilirubin
- albumin
- ammonia
- coagulation studies
- CBC
- glucose
management of hepatic encephalopathy
- limit protein intake
- administer enema or laxatives
- administer anti-infective
management of ascites
- administer diuretics
- paracentesis
- sodium restriction
management of metabolic abnormalities
- monitor electrolytes
- correct electrolyte imbalances
management of spontaneous bacterial peritonitis
- administer antibiotic therapy
management of all liver diseases
high carb, low fat diet
no alcohol
management of esophageal varices
control bleeding
- vasopressin
constrict bleeding varices
- shunts
preventive therapy
- beta blockers
- elective shunts
- endoscopic sclerotherapy