Disorders of the liver Flashcards

1
Q

What are the functions of the liver

A

o Accessory digestive gland, produces bile (alkaline compound that aids in digestion of fat + absorption of vit K)
o Plays major role in carbohydrate metabolism and has numerous function
• Gluconeogenesis: synthesis of glucose from certain AAs (lactate, glycerol)
• Formation of glucose from protein + fat
• Glucogenolysis: breakdown of glycogen into glucose
• Glucogenesis: formation of glycogen from glucose
o Lipid metabolism
• Cholesterol synthesis
• Lipogenesis: production of triglycerides
o Produces coagulation factors
• Fibrinogen, prothrombin, protein C, protein S, antithrombin, clotting factors 5,7,8,9,10,11
o 1st trimester of the fetus:
• Liver is main site of RBC production
• By 32 wks: bone marrow has taken over to create RBCs
o Breakdown of insulin + other hormones
o Converts ammonia to urea (excreted by kidneys)
o Stores Vit A, Vit D, Vit b12, Vit K, Iron
o Detoxification of various metabolites
o Plasma protein synthesis
o The production of biochemicals necessary for digestion
o Regulation of glycogen storage
o Decomposition of red blood cells
o Hormone production

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2
Q

Glucogenolysis:

A

breakdown of glycogen into glucose

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3
Q

Glucogenesis:

A

formation of glycogen from glucose

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4
Q

What is viral hepatitis

A

liver inflammation d/t viral infection. Can be either acute, recent infection, rapid onset OR chronic. It is a systemmic viral disease primarily affecting liver. Types include: Hep A, B, C, D, E (and G but not common)

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5
Q

How are liver cells damages in viral hepatitis?

A

Liver cells can be damaged in TWO WAYS d/t:
• Direct action of virus
• Cell-mediated immune responses to virus

Cell injury leads to inflammation + necrosis of liver:
• Hepatocytes + liver appear swollen
• Diffuse necrosis present
• Severe inflammation: BILIARY may develop, causing backup of bile into blood
• Hepatic cells may regenerate or fibrous scar tissue forms in liver
• Scar tissue often obstructs blood + bile flow leading to further damage (interferes with unique organization of liver lobule, ischemia)
• Chronic inflammation in Hep B, C, D: persistent inflammation, necrosis of liver for MORE THAN 6 MONTHS
• Eventually causes permanent liver damage + cirrhosis
• Increased incidence of hepatocellular cancer assoc with chronic hepatitis

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6
Q

What is Hepatitis A

A

Hepatitis A: caused by small RNA virus (HAV)

o Hepatitis A can be found in the feces, bile, and sera of infected individuals
o Usually transmitted by the fecal-oral route (contaminated water, shell fish)
o Short incubation period (2-6 weeks)
o Causes acute, self-limiting infection; does NOT have carrier/chronic state
o Fecal shedding of virus occurs before onset of signs
• IgM HAV appear (1st group), IgG HAV (2nd group) (remain in serum for years, providing immunity against infection)

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7
Q

What are risk factors for Hep A

A

o Risk factors (spread by fecal oral route)
• Crowded, unsanitary conditions
• Food and water contamination
• Daycare centers
• Sexual transmission (in homosexual pop)

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8
Q

What is hepatitis B

A

Double stranded DNA virus; contains 3 antigens that each stimulates antibody production in the body

o Long incubation period: avg 2 mo
o Large amts of HBV surface antigen produces by infected liver cells early in course of infection
• Antigen in serum - High risk of continued active infection + damage to liver
o Common: carrier state – asymptomatic, but contagious
o Window/prolonged lag time occurs before serum markers, symptoms become present
• Virus cannot be detected but can be transmitted
• Long incubation period – harder to track sources and transmission

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9
Q

How is Hep B transmitted?

A
o	Transmitted through contact with infected blood, body fluids, or contaminated needles
•	Body piercing
•	Tattooing
•	Blood Transfusion
•	Sexual transmission
•	Mother to fetus
•	Vertical transmission: breast feeding?
•	Maternal transmission can occur if the mother is infected during the third trimester
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10
Q

Hepatitis C

A

Single stranded RNA virus.

  • Can exist in carrier state and be chronic (50%- 80% of hepatitis C cases result in chronic hepatitis)
  • MOST COMMON hepatitis transmitted via blood transfusions
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11
Q

What are the causes of Hepatitis C

A

Causes:
Blood transfusion
• Sharing of needles
• Mother to baby (Maternal transmission to fetus occurs in 5-10% of cases
• Body piercing/tattoos
• Unprotected sex w/ multiple partners
o Primary mode of transmission is IV drug use through sharing of needles
o Secondary risk is through high-risk sexual behavior.

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12
Q

What are complications of Hep B and C

A

o Complications
• Chronic hepatitis with cirrhosis
• End Stage Liver Failure
• Hepatocellular Carcinoma

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13
Q

What is hepatitis D?

A

An incomplete RNA virus that requires presence of HBV to replicate + produce active infection

o	Increases severity of HBV infection
o	Same transmission route as HBV
o	Depends on HBV for replication
o	Transmitted by blood
o	High incidence of infection in IV drug users
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14
Q

Hepatitis E

A

Hep E is a single stranded RNA virus (SPREAD BY Fecal-oral transmission)
o Developing countries (Asia, Africa) – high mortality rate in pregnant women
o Similar to Hepatitis A in course
• Lacks chronic, carrier state

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15
Q

Overview of viral hepatitis

A

There is currently no method to destroy hepatitis in body
o Gamma-globulin helpful when given earlier in course of infection
o Rest, diet high in protein, carbs, vitamins (most useful)
o HBV, HCV may be treated with interferon + epivere to decrease viral replication (Effective in 30-40% of individuals)
o Slow-acting interferon + antiviral drug (vibovaren?) reduced rate of viral replication in 80% of HCV pts
o Gradual destruction of liver occurs leading to cirrhosis, hepatocellular cancer

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16
Q

What are the stages of acute hepatisis

A
  1. Prodromal (preicteric) phase (onset my be insidious). Begins 2 weeks after exposure (nonspecific symptoms: fatige, malaise, anorexia & nausea, chills, muscle aches, elevated serum levels of liver enzymes. And sometimes: fever, headache and mild URQ discomfort
  2. Icteric phase (jaudice stage). Lasts 2-6 weeks.
    • Marks onset of jaundice – serum bilirubin levels rise
    • Yellowing of skin + sclera
    • Biliary obstruction increases stool light in color (steatorrhea), urine becomes darker, skin becomes puridic
    • Liver becomes tender + enlarged  mild, aching pain
    • Severe cases: blood clotting time may be prolonged (d/t Impaired synthesis of blood clotting factors)
    • This stage lasts longer in HBV!
  3. Recovery phase (posticteric). Marked by an improvement of symptoms and reduction in signs.
    - Average acute stage of HAV 8-10 wks (but HBV is prolonged over 16 weeks)
17
Q

What is liver cirrhosis

A

Extensive diffuse fibrosis, loss of lobular organization in liver.

It is an irreversible inflammatory disease that disrupts liver function and structure

• Decreased hepatic function due to nodular and fibrotic tissue synthesis (fibrosis)

o Initially, liver enlarged but becomes small, shrunken with extensive fibrosis
o Asymptomatic degenerative changes until disease is well advanced

18
Q

Pathophysiology of liver cirrhosis

A

o Pathophysiology:
• Loss of liver cell fxn: Interference of blood + bile flow in liver
• Obstruction of bile ducts + blood flow by fibrosis tissue
• Reduction of bile entering intestine
• Backup of bile in liver
• Blockage of blood flow to liver
• Congestion in spleen
• Congestion in intestinal walls + stomach

19
Q

Types of liver cirrhosis

A
  • Alcoholic
  • Non-alcoholic Fatty Liver
  • Biliary (bile canaliculi)
  • Metabolic
20
Q

Name some of the clinical manifestations of Cirrhosis

A

-Portal Hypertension
• Hepatic Necrosis
• Esophageal Varices: large, distended veins
• Esophageal veins have several points of anastomosis (collateral channels that join with gastric veins)
• Increase pressure of blood extends into esophageal veins leading to large, distended veins
• Located near mucosal surface of esophagus
• Veins easily torn by food passing
• Possible hemorrhage
• Splenomegaly
• Ascites

21
Q

What is the stool and urine like in a PT with cirrhosis?

A

light colored stools (d/t decreased bile in GI tract) and dark urine (d/t increase urobilinogen)

22
Q

Why do some PTs with cirrhosis develop hepatic encephalopathy?

A

Due to the build up of ammonia

23
Q

What are complications of end stage liver disease (when liver is unable to perform)

A
  • Reduced Clotting
  • Impaired Ammonia Metabolism
  • Impaired Bilirubin Metabolism
  • Hypoglycemia
  • Increased Aldosterone Production
24
Q

What is the treatment of cirrhosis

A

-Supportive treatment
• Avoiding fatigue and avoiding exposure to infection

-Dietary restrictions: restrict protein, Na+ intake
• Encourage high carb, vit supplements

-Diuretics
• Serum electrolytes may have to be balanced
• Lasiks: reduce body fluid

-Paracentesis: remove excess fluid; peritoneal cavity punctured by needle to remove peritoneal fluid
• Albumin transfusion to prevent 3rd spacing of fluid

  • Antibiotics: Neomyocin – reduce intestinal flora + control serum ammonia levels
  • Ruptured Esophageal varices need emergency Tx