liver disorders Flashcards
functions of the liver
-metabolism/storage of fat, PRO, CHO, vitamins and minerals
-blood volume reservoir –> distends and compresses to alter circulating blood volume
-blood filter - purifies by removing bilirubin
-blood clotting factors (prothrombin and fibrinogen)
-drug metabolism and detoxification
portal circulation
blood from the stomach, intestines, spleen, and pancreas brought to the liver
blood enters liver through portal vein
absorbed products from digestion go directly to liver and sent to lobules
“first pass effect”
liver function tests
liver enzymes - ALT, AST, Alk Phos: INCREASE
ammonia: INCREASE
protein + albumin: DECREASE
prothrombin time: INCREASE
bilirubin - conjugated (direct) and unconjugated (indirect)
icterus is caused by
jaundice - yellowish tint to skin
increased level of bilirubin in blood
> 2-2.5 mg/dL
3 classifications of jaundice
- hemolytic: increase breakdown of RBC
- hepatocellular: liver unable to take up bilirubin from blood or unable to conjugate it
- obstructive: decreased/obstructed flow of bile (r/t gallstones)
where can you see jaundice?
scelera (whites of eyes)
mucous membranes
palms of hands
soles of feet
bilirubin
by product of heme breakdown - mainly Hgb
direct: conjugated
indirect: unconjugated
elevations of INDIRECT bilirubin
bilirubin overproduction OR impaired liver fxn
elevations of DIRECT bilirubin
liver working, but cannot get bilirubin out
(bile duct obstruction, gall stones)
clinical manifestations of jaundice
*darker urine
*elevated liver enzymes
*stools –> normal or clay colored (liver releases bile salts - make poop brown OR liver infection decreases bile production/bile flow is blocked keeps stool clay colored)
*pruritus (d/t bilirubin build up)
viral hepatitis
inflammation of liver
A, B, C
can be caused by EBV, CMV + alcohol abuse, drugs, chemicals, bacteria
viral hepatitis: PATHO
- viral infection
- immune response: inflammatory mediators
- lysis of infected cells
- edema and swelling of tissue
- tissue hypoxia
- hepatocyte death
clinical manifestations of viral hepatitis
typically asymptomatic –> can range from none to mild to liver failure
abnormal elevated LFTs but NOT consistent with cellular damage within liver
3 stages of hepatitis
- prodromal
- icteric
- recovery
prodromal stage
2 weeks after exposure and HIGHLY contagious
S/S: fatigue, anorexia, malaise, N/V, HA, cough, low-grade fever, hyperalgesia (increased sensitivity to pain)
icteric stage
begins with jaundice –> dark colored urine, clay stools
liver is enlarges and painful to palpate
fatigue and abd pain persist or increase
recovery stage
6-8 weeks after exposure
symptoms diminish and jaundice resolved
liver still enlarged/tender
complications of viral hepatitis
chronic hepatitis
liver cirrhosis
liver cancer
fulminant viral hepatitis –> acute liver failure
hepatitis A
transmission: FOOD/WATER contamination, parental, sex
acute onset
fever
mild severity
affects children + adults
prevention: hand hygiene and hep A vaccine
does NOT progress to chronic hepatits
S/S of hep A
fatigue
fever
N/V/D
stomach pain
dark pee
pale poop
no appetite
jaundice
where is HAV most common?
underdeveloped countries
hepatitis B
transmission: parental, sex
insidious onset
severe disease —> 10% develop chronic
all age groups affected
prevention: safe sex, HBV vaccine
hepatitis C
transmission: parental, sex
insidious onset
mild-severe symptoms
can develop into chronic (80%)
all age groups affected
treatment: screen blood
*NO VACCINE
~new tx makes it almost completely curable
what does hepatitis C lead to?
chronic hep (80%)
hepatocellular carcinoma (liver cancer)
liver transplant
how is hepatitis C spread?
used or shared needles/syringes
sex
sharing care items (toothbrush, razor)
born to a mom with hep C
S/S hepatitis C
asymptomatic
stomach pain
vomiting
yellow eyes or skin
hepatitis A vaccine
2 doses, 6 months apart
recommended for:
all children beginning at 1 year
special high risk populations
hepatitis B vaccine
3 doses, at least 4 months apart
recommended for:
all infants beginning as newborns
2 classes of drugs used for chronic HBV
interferons
nucleoside analogs
*usually used together
treatment of HBV- who is it for? disadvantages?
only for high-risk patients
-increase in AST levels
-hepatic inflammation
-advanced fibrosis
disadvantages:
prolonged therapy
cost and adverse effects
high relapse
considerations for HCV pharm
-treatment only recommended for pt with chronic disease
-easily treatable and eliminated in almost all patients
-treat w/ direct acting antiviral therapy and interferon based regiments (+some require nucleoside analog)
acetaminophen and HCV pharm
chronic hepatitis pt: <2g/day
everyone else: <4g/day
*in SERIOUS/advanced stage liver disease –> AVOID acetaminophen + NSAIDS
cirrhosis
irreversible, inflammatory, fibrotic liver disease
develops SLOWLY, over many years
*structural changes from injury (alc/virus) and fibrosis
regeneration is disrupted by hypoxia, necrosis, atrophy, liver failure
fibrosis is a result of
infiltration of WBC that release inflammatory mediators in activation of this fibrotic process
chaotic fibrosis leads to
obstructive biliary channels and blood flow –> jaundice and portal HTN
common causes of cirrhosis
hepatitis B&C
excess alc intake
idiopathic
non-alcoholic fatty liver disease
kupffer cells
cells responsible for removing toxins and other foreign substances from the blood
stages of alcoholic liver disease
- alcoholic fatty liver
- alcoholic steatohepatitis
- alcoholic cirrhosis
alcoholic fatty liver
mildest
asymptomatic
reversible
fat deposition is caused by increased lipogenesis r/t alcohol intake
alcoholic steatohepatitis
precursor to cirrhosis
inflammation
degeneration of hepatocytes with infiltration of WBC
alcoholic cirrhosis
fibrosis and scaring alter liver structure
s/s: anorexia, nausea, jaundice, edema
patho of cirrhosis
- liver cells destroyed
- cells try to regenerate
- disorganized process
- abnormal growth
- poor blood flow and scar tissue
- hypoxia
- liver failure
stages of liver damage
- healthy liver
- fatty liver (deposits of fat lead to enlargement of liver)
- liver fibrosis (scar tissue forms)
- cirrhosis (growth of connective tissue destroys liver cells
early manifestations of cirrhosis
GI: N/V, anorexia, flatulence, change in bowel habits
fever
weight loss
palpable liver
*insidious
late manifestations of cirrhosis
jaundice
peripheral edema
decrease albumin and prothrombin
ascites
skin lesions
hematologic problems (anemia, bleeding)
endocrine problems (amenorrhea)
esophageal and anorectal varies (distended veins r/t portal HTN)
encephalopathy
portal HTN
resistant portal blood flow that leads to varices and ascites
causes of portal HTN
systemic hypotension
vascular underfilling
stimulation of vasoactive (RAAS system) systems
plasma volume expansion
increased cardiac output, ascites
complications of portal HTN
asymptomatic until complications
vericeal hemorrhage, ascites, peritonitis, hepatorenal syndrome, cardiomyopathy
treatment of portal HTN
can do anything for portal HTN except LIVER TRANSPLANT
*treat complications that occur
hepatic encephalopathy
30-45% cirrhosis patients
LOC: primary determinant
*graded by severity (minimal, 1, 2, 3, 4)
labs with hepatic encephalopathy
correlate with liver labs –> mainly ammonia which is primary chemical driver of LOC changes
increase ammonia = increase risk for H.E.
ammonia
neurotoxic that crosses BBB
marker of toxins built up in the brain
acute liver failure (fulminant)
SEPARATE liver failure NOT caused by cirrhosis
most common cause: acetaminophen overdose
*acetylcysteine (antidote)
patho of acute liver failure
edematous hepatocytes and patchy areas of necrosis and inflammatory cell infiltrated and disrupts the liver tissue
*can occur 6-8 weeks after OD
s/s acute liver failure and tx
similar to cirrhosis - late stage
but do not see cellular changes in liver
tx: not much - liver transplant
lactulose: class + MOA
class: hyperosmotic laxative
MOA: reduces blood ammonia levels by converting ammonia to ammonium
metabolized in large intestine and induces an acidic environment to reduce ammonia levels
draw water into colon and make poop
lactulose: indications + routes
reduction of ammonia absorption in hepatic encephalopathy
PO, enema/rectal
consideration of lactulose
make sure pt NOT hypokalemic
can be given to titrate by # of stools or by ammonia levels
*NOT given just for high ammonia - MUST have S/S of encephalopathy
rifaximin MOA
second line in lactulose isn’t working
MOA: inhibits bacterial RNA synthesis by binding to bacterial DNA
*initially used as an antibiotic for GI infections
rifaximin SE
peripheral edema
nausea
ascites
dizziness
fatigue
pruritus
skin rash
abd pain
anemia
rifaximin route + consideration
PO
**ASSOCIATED WITH INCREASED RISK OF C.DIFF
