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Biology 253 > GI Disorders - Hepatitis > Flashcards

GI Disorders - Hepatitis Flashcards

1
Q

What is Hepatitis?

A

severe inflammation of the liver

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2
Q

Liver is the second _____ ___ of the body

A

largest, organ

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3
Q

What is the function of the liver? (11)

A
  1. process CHO, proteins, lipids after absorption and regulate levels in blood
  2. synthesize plasma proteins (eg clotting factors, albumin, complement proteins etc)
  3. largely involved in metabolism for own needs
  4. inactivates toxins, drugs, and converts ammonia to a less toxic urea
  5. produce and secrete bile
  6. stores CHO as glycogen and converts to glucose when needed by the body
  7. make metabolites for cells of the body for their own metabolism
  8. stores glycogen, fat, iron, vitamin, and lipid soluble toxins
  9. activates vit D
  10. excrete cholesterol and bilirubin
  11. kupffer cells remove pathogen and worn our RBC
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4
Q

Where is bile stored?

A

gallbladder

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5
Q

What is the flow of bile? from bile to duodenum (7)

A

bile –> bile cannaculi –> bile duct –> hepatic duct–> common hepatic duct–> common bile duct–> duodenum

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6
Q

What does bile contain and their function? (5)

A

NaHCO2 = neutralize chime

bile salts = breakdown fats

lecithin = transport fat

cholesterol = for excretion

bilirubin = waste product of heme breakdown –> excreted

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7
Q

Etiology of Hepatitis (4)

A
  1. viral infection
    - infection in liver caused by microbe (bacteria, fungi, viruses, and protozoa)
  2. drugs
    - hepatotoxic drugs eg methotrexate and ethanol
  3. autoimmunity
  4. secondary to systemic problem eg EBV
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8
Q

In viral hepatitis, what are most common?

A

most common is hepatitis A, B, and C

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9
Q

In viral hepatitis, what are less common?

A

Hepatitis D, E, F, and G

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10
Q

What causes Hepatitis A, B, C, D, E, F, and G?

A

Their own corresponding virus eg Hepatitis A is caused by Hepatitis A virus

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11
Q

What are the different in the type of hepatitis?

A
  1. virus
    - transmission and incubation period
    - different in viruses
  2. severity
    - all similar mnfst but differ in severity
  3. carrier state = An individual harbours a virus and overcomes the disease but can transfer the virus to another host
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12
Q

Hepatitis A (5)

A
  • mild and acute
  • self-limiting
  • least severe of Hep A, B, and C
  • oro - fecal transmission: waterbourne, foodbourne, poor sanitation, oral-anal sex
  • Anti-HAV antibodies: used for protection against HAV and for diagnostic purposes
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13
Q

Hepatitis B (6)

A
  • more severe than Hep A
  • mostly acute and some chronic
  • ~10-15% chronic
  • Blood, other body fluids, oral, sexual transmission
  • Carrier State?/Cirrhosis?: mostly not present in all cases
  • 3 anti-HB antibodies:
    1. anti-HBs: antigens produced on SURFACE of the virus
    2. anti-HBc: antigen produced on CORE of virus
    3. anti-HBe: antigen produced on the ENVELOPE (core and precore) of the virus
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14
Q

Hepatitis C (8)

A
  • ~80% chronic but curable
  • most severe
  • transmission: IV drug use and high risk sex practices (multiple sex partners or sex at a young age)
  • infect blood
  • Cirrhosis?/CA?: high potential
  • carrier state
  • anti-HCV antibodies: no beneficial effect and provide no protection–> used for diagnostic purposes
  • PCR: polymerase chain reaction can make millions of copies of sections of DNA or RNA for analysis
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15
Q

Hepatitis D (6)

A
  • can be acute or chronic
  • occurs suddenly
  • no cure/vaccine
  • greater likelihood of cirrhosis/carrier state/chronic active hepatitis
  • Blood, other body fluids, oral, sexual transmission
  • requires HBV surface antigen for replication (cannot replicate without HBV t/f occurs in ppl w/ HBV)
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16
Q

Hepatitis E (5)

A
  • mild, acute
  • symptoms severe in preg women
  • fecal-oral route
  • person to person contact may be possible (low risk)
17
Q

Patho of all Hepatitis (2 mechanisms)

A
  1. viral injury –> cell necrosis

2. immune response–> inflm–> damaged tissues–> necrosis

18
Q

Explain the 2 mechanism by which virus cause tissue injury.

A
  1. virus invades the host cell, incorporate genetic DNA to replicate, and lyses the cell (cell necrosis) –> virus targets the hepatocytes compromising liver fxn
  2. inflammation induced by viral injury: hepatocytes and surrounding cells are affected –> vessels in liver (largely vascularized) gets damaged causing ischemia and further necrosis
19
Q

Recovery on average take approx. ___ ______

A

4 months

20
Q

What are the 3 phases of manifestations? How long does each phase last?

A
  1. prodromal phase: ranging form insidious to symptomatic
  2. clinical phase: post prodromal, 5-10 days later
  3. recovery phase: ~4 months
21
Q

Explain the manifestations of the prodromal phase

A

SS = lethargy, myalgia, generalized weakness, anorexia, N/V, fever, and abdominal pain

Myalgia/lethargy = liver is unable to produce metabolites for other cells eg storing glycogen and converting it to glucose when needed for ATP synthesis = muscle weakness

N/V = liver is an accessory organ of GIT

Fever = d/t infection

abdominal pain = location of pain is in abdominal cavity where liver is

Anorexia = decrease appetite and desire to ingest food

22
Q

Explain the manifestations of the clinical phase

A
  • mnfst worsens
  • liver is tender and swollen –> sore on palpation
  • jaundice b/c liver is unable to process aged erythrocytes for excretion/recycling (bilirubin is a product); bilirubin gets into circulation and deposits thru various organs and tissues (eg skin and eye)
  • pruritus d/t bile salt accumulation and deposition in skin
  • hepatomegaly = enlargement of the liver w/ inflm and hyperemia
23
Q

Explain the manifestations of the recovery phase

A
  • acute mnfst subsides in ~3 weeks depending on type

- full recovery in ~ 4 months (or 16 weeks): liver enzymes are back to normal

24
Q

Diagnosis of Hepatitis (3)

A
  • basic labs
  • serology
  • identify virus eg PCR
25
Q

Treatment of Hepatitis (8)

A
  1. bed rest: to decrease energy demand of body
  2. decrease hepatic workload: eg resting to decrease metabolic workload to ensure liver has the opportunity to heal
  3. diet restriction: smaller calorie-dense meals to decrease hepatic workload
    - high calories w/ more proteins and less fat –> less fat decrease demand for bile to emulsify fat
  4. no all alcohol (hepatotoxic)
  5. no hepatotoxic drugs eg methotrexate
  6. symptomatic management
  7. Antiviral (DAA) for Hep C: DAA = direct acting antiviral drugs to cure hep C (up to 95% efficacy) by targeting specific stage of the life cycle of HCV and req monitoring
  8. Vaccines (A & B): prophylactic drugs to prevent disease but not Hep C

Biology 253 (39 decks)

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