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 This is the “first pass effect”

2 weeks after exposure Fatigue, anorexia, malaise, nausea, vomiting, HA hyperalgesia, cough, low- grade fever HIGHLY transmissible

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

Resolution of jaundice 6-8 weeks after exposure, symptoms diminish Liver remains enlarged/tender

Liver Problems Flashcards by Lauren Ruddy

Major Functions of Liver

Metabolism &/or storage of:
* Fat, CHO, PRO, vitamins and minerals

Blood volume reservoir
* Distends/compresses to alter circulating blood volume

Blood filter
* Helps purify blood

Blood clotting factors
* Including prothrombin & fibrinogen

Drug metabolism and detoxification

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Portal Circulation

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
This is the “first pass effect”

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Components of the Liver funtion tests (LFT)

Liver enzymes
-ALT, AST, Alk Phos

Bilirubin
-conjugated (direct), unconjugated (indirect)

Serum Ammonia
Serum Protein
Serum Albumin
Prothrombin time (PT)

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Jaundice (Icterus) caused by:

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
Look at conjugated versus unconjugated to determine possible cause
Yellowish discoloration of skin and deep tissues

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3 classifications of Jaundice

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

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What is Bilirubin?

By product of heme breakdown (mainly hemoglobin)

DIRECT: Conjugated INDIRECT:unconjugated

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Elevations of INDIRECT bilirubin:

Bilirubin overproduction OR impaired liver functioning

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Elevations of DIRECT bilirubin:

Liver working, but can’t get the bilirubin out
* Bile duct obstruction, gall stones

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Jaundice: Clinical Manifestations

Urine is darker
Liver enzymes = elevated
Stools = Normal or clay colored
Pruritis

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What is 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)

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T/F: Hepatitis is always from a viral infection

FALSE: can occur from other causes
* Alcohol abuse, drugs, chemicals, and bacteria

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Viral Hepatitis: Pathogenesis

Viral infection
Immune response: imflammatory mediators
Lysis of infected cells
Edema and swelling of tissue
Tissue hypoxia
Hepatocyte death

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Clinical Manifestations of Viral 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

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Hepatitis: Prodromal

2 weeks after exposure
Fatigue, anorexia, malaise, nausea, vomiting, HA hyperalgesia, cough, low- grade fever
HIGHLY transmissible

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Hepatitis: 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

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Hepatitis: Recovery

Resolution of jaundice
6-8 weeks after exposure, symptoms diminish
Liver remains enlarged/tender

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Viral Hepatitis: Complications

Chronic hepatitis
Liver cirrhosis
Liver cancer
Fulminant viral hepatitis – acute liver failure

Most patients with acute viral hepatitis recover completely with no complications

Overall mortality rate is less than 1%
* Higher mortality in elderly and comorbidities

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Hepatitis A
-transmission, progression, population, prevention

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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

Hepatitis B
-transmission, progression, population, prevention

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Transmission: parental, sexual
Insidious onset
Severe disease, may be prolonged course or develop into chronic
Any age group affected
HBV vaccine and safe sex and hygiene

Hepatitis C
-transmission, progression, population, prevention

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Transmission: parental, 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

Prevention of Hepatitis: Vaccines
Hep A Series

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2 doses 6 months apart
Recommendations
All children beginning at age 12 months
Special “high risk” populations

Prevention of Hepatitis: Vaccines
Hep B Series

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3 doses at least 4 months apart
Recommendation: All infants beginning as newborns

Prevention of Hepatitis: Vaccines
Hep C

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NO vaccine

Two classes of drugs are used for chronic HBV:

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Interferons
Nucleoside analogs

HBV treatment is only for high-risk patients who have:

* ↑ AST levels * Hepatic inflammation * Advanced fibrosis

Disadvantages of HBV treatment:

* Prolonged therapy * Costs and adverse effects * High relapse

How is HCV treated

* Treated with direct-acting antiviral therapy and interferon-based regiments * Some require treatment along with a nucleoside analogue medication as well * Now easily treatable and eliminated in most all patients | Can take tylenol although must be <2,000 mg

What is Cirrhosis?

* Irreversible, inflammatory, fibrotic liver disease * Structural changes from injury (alcohol/viruses) and fibrosis * Regeneration is disrupted by hypoxia, necrosis, atrophy, and liver failure

Chaotic fibrosis leads to:

Obstructive biliary channels and blood flow which lead to jaundice and portal hypertension

Cirrhosis Common Causes

-Hepatitis B&C -Excessive alcohol intake -Idiopathic -Non-alcoholic fatty liver disease [NASH, NAFLD]

Stages of alcoholic liver disease

1. Alcoholic fatty liver -Mildest, asymptomatic 2. Alcohol steatohepatitis -precusor to cirrhosis -Inflammation, degeneration of hepatocytes 3. Alcohol cirrhosis -Fibrosis and scarring alter liver structure

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

Jaundice Peripheral edema Decreased albumin & PT Ascites Skin lesions Hematologic problems (anemia, bleeding) Endocrine problems Esophageal & anorectal varices Encephalopathy

What is Portal Hypertension?

Resistant portal blood flow  leads to varices & ascites

Portal hypertension causes

Causes: systemic hypotension, vascular underfilling, stimulation of vasoactive (RAAS system) systems, plasma volume expansion, increased cardiac output leads to ascites

Portal hypertension symptoms

Asymptomatic until complications * Variceal hemorrhage, ascites, peritonitis, hepatorenal syndrome, cardiomyopathy

Portal hypertension prevention/treatment

Can’t do anything for the portal hypertension except liver transplant

How is hepatic encephalopathy diagnosed?

LOC is the primary driver of diagnosis * Graded by severity * Correlate with liver labs, mainly ammonia which is primary chemical driver of LOC changes

What are the grades of hepatic encephalopathy?

* 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

Acute liver failure (fulminant liver failure) -Common cause

Most common cause: acetaminophen overdose * Can be treated with acetylcysteine

T/F Acute liver failure caused by cirrhosis

False, acute liver failure is a separate liver failure NOT caused by cirrhosis or other type of liver disease

Acute liver failure: Patho

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

Acute liver failure -S/S and treatment

* Signs are similar to cirrhosis symptoms * Treatment: not much, liver transplant

Liver Problems Flashcards

(44 cards)