liver mod 4 Flashcards
major liver functions
Metabolism &/or storage of: - Fat, CHO, PRO, vitamins and minerals Blood volume reservoir - Distends/compresses to alter circulating blood volume Blood filter - kuppfer cells - Helps purify blood - remove bilirubin Blood clotting factors - thrombopoeisis - Including prothrombin & fibrinogen Drug metabolism and detoxification
jaundice manifestations
Urine - darker
Liver enzymes = elevated
Stools = Normal or clay colored
Pruritis - increased bilirubin
clinical manifestations hepatitis
Similar between all types
Many cases of ALL types of hepatitis are asymptomatic
But can range from none, mild, to liver failure
Causes abnormal elevated LFTs– but NOT consistent with cellular damage within the liver
must trend labs and see other s/s
complications viral hepatitis
Most patients with acute viral hepatitis recover completely with no complications
Overall mortality rate is less than 1%
Higher mortality in elderly and comorbidities
Complications include: Chronic hepatitis Liver cirrhosis (next section) Liver cancer Fulminant viral hepatitis – acute liver failure
hep a (HAV)
food borne \Transmission - fecal-oral, parental, sexual Acute onset with fever Usually mild severity Does NOT lead to chronic hepatitis Usually affects children and adult Hand hygiene,
**Hep A vaccine
hep b (HBV)
Transmission - parental, sexual
Insidious onset - 60-180 days onset s/s
Severe disease, may be prolonged course or develop into chronic
Any age group affected
***HBV vaccine and safe sex and hygiene
hep c
**NO VACCINE
Transmission - parental, sexual, mother to child
Insidious onset
Mild to severe symptoms
Can develop into chronic hepatitis (80%)
Any age is affected
Screening blood, hygiene; NO vaccine
Leads to hepatocellular carcinoma, liver transplant
New treatment is developing and becoming more widely available
hepatitis vaccines
Hep A Series 2 doses 6 months apart Recommendations All children beginning at age 12 months Special “high risk” populations
Hep B Series
3 doses at least 4 months apart
Recommendation: All infants beginning as newborns
Hep C = NO vaccine
HBV pharm
Two classes of drugs are used for chronic HBV:
Interferons
Nucleoside analogs
Treatment is only for high-risk patients:
↑ AST levels
Hepatic inflammation
Advanced fibrosis- able to see on CT scan
Disadvantages of treatment:
Prolonged therapy
Costs and adverse effects - tons drug interactions
High relapse
HCV pharm
CN TAKE TYLENOL, BUT <2 GRAMS
Now easily treatable and eliminated in most all patients
treat anyone with viral load, expensive
Treatment is only recommended for patients with CHRONIC DISEASE
However this thought process is changing with the introduction of newer, very effective drugs
Treated with direct-acting antiviral therapy and interferon-based regiments
Some require treatment along with a nucleoside analogue medication as well
HBV/HCV direct acting (not for drug matrix)
HBV: Pegylated interferon-alpha Ribavirin Entecavir Tenofovir alafenamide Sofosbuvir Daclatasvir (Daklinza)
HCV on attachment
clinical manifestations cirrhosis - EARLY
GI
- N/V, anorexia, flatulence, change bm habits
fever, weight loss, palpable liver
clinical manifestations cirrhosis -LATE
jaundice
peripheral edema - 3rd spacing
decreased albumin and protein
ascites - portal HTN
skin lesions - spider angiomata
hematologic problems - bleeding, anemia,
endocrine - stop menstruation, hypogonadism
esophageal and anorectal varices - distended veins
hepatic encephalopathy - due to toxin build up
portal HTN
Resistant portal blood flow - leads to varices & ascites
Causes: systemic hypotension, vascular underfilling, stimulation of vasoactive (RAAS system) systems, plasma volume expansion, increased cardiac output ASCITES
Asymptomatic until complications
- Variceal hemorrhage, ascites, peritonitis, hepatorenal syndrome, cardiomyopathy
Treatment: prevent/treat complications
Can’t do anything for the portal hypertension except liver transplant
hepatic encephalopathy
not diagnosed off ammonia levels
liver unable to filter toxins
elevated ammonia = increase encephalopathy
30-45% of cirrhosis patients
LOC is the primary driver of diagnosis
Graded by severity:
Minimal: Abnormal results on psychometric or neurophysiological testing without clinical manifestations (see ‘Psychometric tests’ below)
Grade I: Changes in behavior, mild confusion, slurred speech, disordered sleep
Grade II: Lethargy, moderate confusion
Grade III: Marked confusion (stupor), incoherent speech, sleeping but arousable
Grade IV: Coma, unresponsive to pain
Correlate with liver labs- mainly ammonia which is primary chemical driver of LOC changes
acute liver failure (fulminant liver failure)
Separate liver failure NOT caused by cirrhosis or other type of liver disease
Most common cause: acetaminophen overdose
Can be treated with N-acetylcysteine
Patho: edematous hepatocytes and patchy areas of necrosis and inflammatory cell infiltrates and disrupts the liver tissue
Can occur 6-8 weeks after a viral hepatitis or metabolic liver disease
5 days to 8 weeks after an acetaminophen overdose
Signs are similar to cirrhosis symptoms
Treatment: not much, liver transplant
pharm cirrhosis/liver disease
***hepatic encephalopathy
lactulose
rifaximin
lactulose
**begin with this drug
induces acidic environment
Class: Hyperosmotic laxative
Indication: reduction of ammonia absorption in hepatic encephalopathy
MOA: reduces blood ammonia levels by converting ammonia to ammonium
Given PO or enema/rectal
Can be given to titrate by number of stools or by ammonia levels
Not just given for high ammonia levels though– must have signs/symptoms of encephalopathy
Make sure that patient is NOT hypokalemia
hypok = increased ammonia levels
rifaximin
increased risk c-diff
Second line if lactulose isn’t working
MOA: inhibits bacterial RNA synthesis by binding to bacterial DNA (initially used as an antibiotic for GI infections)
Can sometimes be given preventive, just depends on HCP
Given PO
Side effects: peripheral edema, nausea, ascites, dizziness, fatigue, pruritis, skin rash, abdominal pain, anemia
Has been associated with an increased risk of C diff
portal circulation
“first pass effect”
The portal circulatory system brings blood to the liver from the stomach, intestines, spleen, and pancreas
The blood enters the liver through the portal vein
The absorbed products of digestion come directly to the liver, and are sent to the lobules
liver function tests (lft)
everything increased except total protein and albumin
jaundice
Caused by increased level of bilirubin in the bloodstream
Usually causes problems and is noticeable with total bilirubin is greater than 2-2.5mg/dl
Yellowish discoloration of skin and deep tissues
3 classifications:
Hemolytic - increased breakdown of RBCs
Hepatocellular - liver unable to take up bilirubin from blood or unable to conjugate it
Obstructive - decreased or obstructed flow of bile
bilirubin
By product of heme breakdown - mainly hemoglobin
DIRECT: Conjugated INDIRECT: unconjugated
Elevations of INDIRECT bilirubin = bilirubin overproduction OR impaired liver functioning
Elevations of DIRECT bilirubin = liver working, but can’t get the bilirubin out
Bile duct obstruction, gall stones
viral hepatitis
Systemic virus that mainly affects the livers
Inflammation of the liver
Various strains cause the different types of hepatitis
HAV, HBV, HCV
Other viruses that can cause hepatitis Epstein-Barr, cytomegalovirus
Know that hepatitis (not the infection) can occur from other causes
Alcohol abuse, drugs, chemicals, and bacteria
viral hepatitis: prodromal phase
2 weeks after exposure
Fatigue, anorexia, malaise, nausea, vomiting, HA hyperalgesia, cough, low-grade fever
HIGHLY transmissible
viral hep: icteric
Begins with jaundice
Jaundice, dark urine, clay-colored stools
Liver enlarged and may be painful to palpation
Fatigue abdominal pain persists or increases in severity
viral hep: recovery phase
Resolution of jaundice
6-8 weeks after exposure, symptoms diminish
Liver remains enlarged/tender
cirrhosis
hepatocytes can regenerate
severity depends of amount slow
Irreversible, inflammatory, fibrotic liver disease
Structural changes from injury (alcohol/viruses) and fibrosis
Chaotic fibrosis leads to obstructive biliary channels and blood flow jaundice and portal hypertension
Regeneration is disrupted by hypoxia, necrosis, atrophy, and liver failure
common causes cirrhosis
hep B and C
excessive etoh
idiopathic
non-alcohol fatty liver disease (NASH, NAFLD)
stages of alcoholic liver disease (3)
alcohol fatty liver
alcoholic steatohepatitis
alcoholic cirrhosis
