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