Liver 2 Flashcards
HEP A
Transmission: Fecal-oral, parental (IVD), sexual
Acute onset of fever
Usually mild severity
Does NOT lead to chronic hepatitis
Usually affects children and adults
Hand hygiene, Hep A vaccine
HEP B
Transmission: parental or sexual
Insidious onset
-very long incubation
Severe disease, may be prolonged course or develop into chronic (10%)
Any age group affected
HBV vaccine and safe sex + hygiene
-all kids get vaccine
HEP C
Transmission: parental or sexual
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 A vaccine
-2 doses 6 months apart
Recommendations:
-All children starting at 12 months
-Special “high risk” populations
(food handlers, hospital workers)
Hepatitis B vaccine
-3 doses at least 4 months apart
Recommendations:
-All infants beginning as newborns
2 Major classes of HEP B drugs
- Interferons
2. Nucleoside analogs
Treatment for B is only for
HIGH-RISK patients:
- Elevated AST levels
- Hepatic inflammation
- Advanced fibrosis
Disadvantages of Hep B treatment
- Prolonged therapy
- Costs and adverse effects (interactions)
- High relapse
Hep C is treated with
Direct-acting antiviral therapy and interferon-based regiments
-Some require treatment along with a nucleoside analogue medication as well
How much Tylenol can Hep C people take?
<2g/day
Common causes of cirrhosis
- Hepatitis B + C
- Excessive Alcohol Intake
- Idiopathic
- NASH + NAFLD (Non-alcoholic fatty liver disease)
Cirrhosis
Irreversible, inflammatory, fibrotic liver disease
Structural changes from injury (alcohol/virus) and fibrosis
Chaotic fibrosis leads to obstructive biliary channels and blood flow Jaundice + Portal hypertension
Regeneration is disrupted by hypoxia, necrosis, atrophy, and liver failure
Most common type of cirrhosis
Alcoholic cirrhosis most common type but still accounts for only 25% of all cirrhosis
3 stages of alcoholic liver disease
- Alcoholic fatty liver
- Alcoholic steatohepatitis
- Alcoholic cirrhosis
- Alcoholic fatty liver
-mildest, asymptomatic
reversible
- Alcoholic steatohepatitis
- precursor to cirrhosis
- inflammation (infiltration of WBC), degeneration of hepatocytes
- Symptoms apparent
(Irreversible)
- Alcoholic cirrhosis
-fibrosis and scarring alter liver structure
Irreversible
Cirrhosis: pathogenesis
- Liver cells destroyed
- Cells try to regenerate
- Disorganized process
- Abnormal growth
- Poor blood flow and scar tissue
- Hypoxia
- Liver failure
Cirrhosis: Early Manifestations
GI Disturbances
- N/V
- Anorexia
- Flatulence
- Change in bowel habits
Fever, Weight loss
Palpable Liver
Cirrhosis Late Manifestations: Endocrine
Females:
- Anovulation
- Amenorrhea
Male:
- Hypogonadism
- Impotence
- Infertility
Cirrhosis Late Manifestations:
Jaundice Peripheral edema Decreased albumin & PT Ascites Skin lesions Hematologic Problems -anemia + bleeding Endocrine problems Esophageal + anorectal varices Encephalopathy
Causes of Portal Vein Hypertension
-Systemic hypertension, vascular underfilling, stimulation of vasoactive (RAAS system), plasma volume expansion, increased CO»_space;> ASCITES
Complications of Portal Hypertension
Asymptomatic until complications:
-Variceal hemorrhage, ascites, peritonitis, hepatorenal syndrome, cardiomyopathy
What leads to varices + ascites?
Resistant portal blood flow (portal hypertension)
Primary factor of encephalopathy diagnosis
LOC + correlate with LIVER labs (ammonia)
Acute Liver Failure: Fulminant liver failure: Most common cause
Acetaminophen OD
use acetylcysteine
Acute Liver Failure (Fulminant Liver Failure): pathology
edematous hepatocytes and patchy areas of necrosis and inflammatory cells infiltrate and disrupt liver tissue
Acute Liver Failure (Fulminant Liver Failure): When and how can it occur?
Can occur 6-8 weeks after viral hepatitis or metabolic liver disease
-5 days to 8 weeks after acetaminophen OD
Lactulose
Class: hyperosmotic Laxitive
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 hypokalemic
Rifaximin
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 as preventative, depends on HCP
PO
SE: peripheral edema, nausea, ascites, dizziness, fatigue, pruritis, skin rash, abdominal pain, anemia
Has been associated with an increased risk of C. diff
