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Patho > Packet 13 - Hepatobiliary System (2) > Flashcards

Packet 13 - Hepatobiliary System (2) Flashcards

1
Q

P/C factors for this type of cirrhosis include increased alcohol consumption (metabolites of alcohol can damage liver cells), plus other genetic/environmental factors.

a. ) Postnecrotic types
b. ) Primary biliary types
c. ) Alcoholic liver disease
d. ) Nonalcoholic fatty liver disease (NAFLD)

A

Alcoholic Liver Disease (Laennec Cirrhosis)

Cirrhosis

Nodules of normal hepatocytes surrounded by fibrosis.

Damage / death of hepatocytes →

  1. Cell regeneration → nodules of functional hepatocytes +
  2. Scar tissue formation →
    • replaces functional liver cells → liver failure
    • distorts liver structure, obstructs flow in vascular and biliary channels (kinks)

Assessment Findings:

  1. inflammation
    • Abdominal, right upper quadrant pain, hepatomegaly.
  2. Portal hypertension
    • Ascites, edema, dyspnea, anemia.
  3. Liver failure
    • End Stage Liver Disease
      • Anorexia, Steatorrhea
      • Vitamin A deficiency = vision problems.
      • Vitamin D deficiency = weak bones, hypocalcemia.
      • Vitamin K deficiency = no clotting factors (bleeding).
    • High or low glucose levels.
    • Liver is not making albumin → causes edema.
    • Bleeding tendencies.
    • Hepatic encephalopathy → Asterixis
    • Seizures / Coma (Hepatocoma).
    • Drug toxicities
    • Hormone imbalances
    • Sepsis (unfiltered blood)
    • Hepatorenal failure

P/C Factors:

  • Postnecrotic Types:
    • Viral hepatitis
    • Exposure to toxic drugs / chemicals
  • Primary Biliary Types:
    • Autoimmune attack on small bile ducts → inflammation / damage to hepatocytes from leakage of bile.
  • Alcoholic Liver Disease (Laennec Cirrhosis)
    • Increased alcohol consumption (metabolites of alcohol can damage liver cells), plus other genetic / environmental factors.
  • Nonalcoholic Fatty Liver Disease
    • ​Changes in uptake/synthesis/break down of hepatic lipids (due to obesity, insulin resistance, hyperlipidemia, etc.) cause fatty changes in liver cells, and impairs ability to detoxify free radicals → damage to hepatocytes.
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2
Q

This type of Hepatitis is transmitted via blood/body secretions.

a. ) Jaundice b.) Cirrhosis
c. ) Hepatitis A d.) Hepatitis B
e. ) Hepatitis C f.) Hepatitis D
g. ) Hepatitis E

A

Hepatitis B

formerly serum hepatitis

Has Vaccine

Transmission: Blood / body secretions (unprotected sex, multiple partners.

Chronic State / Carrier State: yes

Serologic Markers:

  • HBsAg: indicates infectivity (acute/chronic infection).
  • HBcAg: does not circulate in blood.
  • HBeAg: indicates viral shedding into blood.
  • Anti-HBs: indicates recovery, noninfectivity, protection.
  • Anti-HBc:
    • IgM - indicates recent infection
    • IgG - indicates infection
  • Anti-HBe: indicates onset of resolution of acute illness.

P/C Factors:

  • IV drug abusers.
  • Health care workers.
  • High-risk sexual behavior.
  • Infants born to infected mothers.
  • Blood products.
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3
Q

The serologic markers for this type of Hepatitis are HBsAg, HBcAg, HBeAg, anti-HBs, anti-HBc, and anti-HBe.

a. ) Jaundice b.) Cirrhosis
c. ) Hepatitis A d.) Hepatitis B
e. ) Hepatitis C f.) Hepatitis D
g. ) Hepatitis E

A

Hepatitis B

formerly serum hepatitis

Has Vaccine

Transmission: Blood / body secretions (unprotected sex, multiple partners.

Chronic State / Carrier State: yes

Serologic Markers:

  • HBsAg: indicates infectivity (acute/chronic infection).
  • HBcAg: does not circulate in blood.
  • HBeAg: indicates viral shedding into blood.
  • Anti-HBs: indicates recovery, noninfectivity, protection.
  • Anti-HBc:
    • IgM - indicates recent infection
    • IgG - indicates infection
  • Anti-HBe: indicates onset of resolution of acute illness.

P/C Factors:

  • IV drug abusers.
  • Health care workers.
  • High-risk sexual behavior.
  • Infants born to infected mothers.
  • Blood products.
How well did you know this?
1
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4
Q

P/C factors for this type of cirrhosis include viral hepatitis and exposure to toxic drugs and/or toxic chemicals.

a. ) Postnecrotic types
b. ) Primary biliary types
c. ) Alcoholic liver disease
d. ) Nonalcoholic fatty liver disease (NAFLD)

A

Postnecrotic types of Cirrhosis

Nodules of normal hepatocytes surrounded by fibrosis.

Damage / death of hepatocytes →

  1. Cell regeneration → nodules of functional hepatocytes +
  2. Scar tissue formation →
    • replaces functional liver cells → liver failure
    • distorts liver structure, obstructs flow in vascular and biliary channels (kinks)

Assessment Findings:

  1. inflammation
    • Abdominal, right upper quadrant pain, hepatomegaly.
  2. Portal hypertension
    • Ascites, edema, dyspnea, anemia.
  3. Liver failure
    • End Stage Liver Disease
      • Anorexia, Steatorrhea
      • Vitamin A deficiency = vision problems.
      • Vitamin D deficiency = weak bones, hypocalcemia.
      • Vitamin K deficiency = no clotting factors (bleeding).
    • High or low glucose levels.
    • Liver is not making albumin → causes edema.
    • Bleeding tendencies.
    • Hepatic encephalopathy → Asterixis
    • Seizures / Coma (Hepatocoma).
    • Drug toxicities
    • Hormone imbalances
    • Sepsis (unfiltered blood)
    • Hepatorenal failure

P/C Factors:

  • Postnecrotic Types:
    • Viral hepatitis
    • Exposure to toxic drugs / chemicals
  • Primary Biliary Types:
    • Autoimmune attack on small bile ducts → inflammation / damage to hepatocytes from leakage of bile.
  • Alcoholic Liver Disease (Laennec Cirrhosis)
    • Increased alcohol consumption (metabolites of alcohol can damage liver cells), plus other genetic / environmental factors.
  • Nonalcoholic Fatty Liver Disease
    • ​Changes in uptake/synthesis/break down of hepatic lipids (due to obesity, insulin resistance, hyperlipidemia, etc.) cause fatty changes in liver cells, and impairs ability to detoxify free radicals → damage to hepatocytes.
How well did you know this?
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5
Q

Which two types of Hepatitis are transmitted via blood/body fluids?

a. ) Jaundice b.) Cirrhosis
c. ) Hepatitis A d.) Hepatitis B
e. ) Hepatitis C f.) Hepatitis D
g. ) Hepatitis E

A

Hepatitis C and Hepatitis D

formerly non-A, non-B

Transmission: blood/body fluids.

Chronic State / Carrier State: yes

Serologic Markers:

  • anti-HCV

P/C Factors:

  • IV drug abusers.
  • Health care workers.
  • High-risk sexual behavior.
  • Hemodialysis.
  • Organ transplant recipients.
  • Blood products.
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6
Q

Which type of hepatitis has no available serologic markers yet?

a. ) Jaundice b.) Cirrhosis
c. ) Hepatitis A d.) Hepatitis B
e. ) Hepatitis C f.) Hepatitis D
g. ) Hepatitis E

A

Hepatitis E

3rd world countries

Transmission: fecal-oral route.

Chronic State / Carrier State: none

Serologic Markers:

  • None available yet

P/C Factors:

  • Primarily occurs in developing countries
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7
Q

Nodules of normal hepatocytes surrounded by fibrosis. Damage/death of hepatocytes causes cell regeneration (nodules) and scar tissue formation (replaces functional cells, distorts liver structure, and obstructs flow).

a. ) Jaundice b.) Cirrhosis
c. ) Hepatitis A d.) Hepatitis B
e. ) Hepatitis C f.) Hepatitis D
g. ) Hepatitis E

A

Cirrhosis

Nodules of normal hepatocytes surrounded by fibrosis.

Damage / death of hepatocytes →

  1. Cell regeneration → nodules of functional hepatocytes +
  2. Scar tissue formation →
    • replaces functional liver cells → liver failure
    • distorts liver structure, obstructs flow in vascular and biliary channels (kinks)

Assessment Findings:

  1. inflammation
    • Abdominal, right upper quadrant pain, hepatomegaly.
  2. Portal hypertension
    • Ascites, edema, dyspnea, anemia.
  3. Liver failure
    • End Stage Liver Disease
      • Anorexia, Steatorrhea
      • Vitamin A deficiency = vision problems.
      • Vitamin D deficiency = weak bones, hypocalcemia.
      • Vitamin K deficiency = no clotting factors (bleeding).
    • High or low glucose levels.
    • Liver is not making albumin → causes edema.
    • Bleeding tendencies.
    • Hepatic encephalopathy → Asterixis
    • Seizures / Coma (Hepatocoma).
    • Drug toxicities
    • Hormone imbalances
    • Sepsis (unfiltered blood)
    • Hepatorenal failure

P/C Factors:

  • Postnecrotic Types:
    • Viral hepatitis
    • Exposure to toxic drugs / chemicals
  • Primary Biliary Types:
    • Autoimmune attack on small bile ducts → inflammation / damage to hepatocytes from leakage of bile.
  • Alcoholic Liver Disease (Laennec Cirrhosis)
    • Increased alcohol consumption (metabolites of alcohol can damage liver cells), plus other genetic / environmental factors.
  • Nonalcoholic Fatty Liver Disease
    • ​Changes in uptake/synthesis/break down of hepatic lipids (due to obesity, insulin resistance, hyperlipidemia, etc.) cause fatty changes in liver cells, and impairs ability to detoxify free radicals → damage to hepatocytes.
How well did you know this?
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8
Q

P/C factors include ingesting contaminated foods, poor hygiene, and high-risk sexual behavior.

a. ) Jaundice b.) Cirrhosis
c. ) Hepatitis A d.) Hepatitis B
e. ) Hepatitis C f.) Hepatitis D
g. ) Hepatitis E

A

Hepatitis A

formerly infectious hepatitis

Transmission: fecal-oral route (sex)

Chronic State / Carrier State: None

Serologic Markers:

  • IgM anti-HAV: indicates acute disease
  • IgG anti-HAV: indicates past infection

P/C Factors:

  • Contaminated foods
  • Poor hygiene
  • High-risk sexual behavior
How well did you know this?
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9
Q

P/C factors include abusing drugs intravenously, being a healthcare worker, high-risk sexual behavior, infants born to infected mothers, and blood products.

a. ) Jaundice b.) Cirrhosis
c. ) Hepatitis A d.) Hepatitis B
e. ) Hepatitis C f.) Hepatitis D
g. ) Hepatitis E

A

Hepatitis B

formerly serum hepatitis

Has Vaccine

Transmission: Blood / body secretions (unprotected sex, multiple partners.

Chronic State / Carrier State: yes

Serologic Markers:

  • HBsAg: indicates infectivity (acute/chronic infection).
  • HBcAg: does not circulate in blood.
  • HBeAg: indicates viral shedding into blood.
  • Anti-HBs: indicates recovery, noninfectivity, protection.
  • Anti-HBc:
    • IgM - indicates recent infection
    • IgG - indicates infection
  • Anti-HBe: indicates onset of resolution of acute illness.

P/C Factors:

  • IV drug abusers.
  • Health care workers.
  • High-risk sexual behavior.
  • Infants born to infected mothers.
  • Blood products.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

P/C factors for this type of cirrhosis include autoimmune attack on small bile ducts → inflammation/damage to hepatocytes from leakage of bile.

a. ) Postnecrotic types
b. ) Primary biliary types
c. ) Alcoholic liver disease
d. ) Nonalcoholic fatty liver disease (NAFLD)

A

Primary biliary types of Cirrhosis

Nodules of normal hepatocytes surrounded by fibrosis.

Damage / death of hepatocytes →

  1. Cell regeneration → nodules of functional hepatocytes +
  2. Scar tissue formation →
    • replaces functional liver cells → liver failure
    • distorts liver structure, obstructs flow in vascular and biliary channels (kinks)

Assessment Findings:

  1. inflammation
    • Abdominal, right upper quadrant pain, hepatomegaly.
  2. Portal hypertension
    • Ascites, edema, dyspnea, anemia.
  3. Liver failure
    • End Stage Liver Disease
      • Anorexia, Steatorrhea
      • Vitamin A deficiency = vision problems.
      • Vitamin D deficiency = weak bones, hypocalcemia.
      • Vitamin K deficiency = no clotting factors (bleeding).
    • High or low glucose levels.
    • Liver is not making albumin → causes edema.
    • Bleeding tendencies.
    • Hepatic encephalopathy → Asterixis
    • Seizures / Coma (Hepatocoma).
    • Drug toxicities
    • Hormone imbalances
    • Sepsis (unfiltered blood)
    • Hepatorenal failure

P/C Factors:

  • Postnecrotic Types:
    • Viral hepatitis
    • Exposure to toxic drugs / chemicals
  • Primary Biliary Types:
    • Autoimmune attack on small bile ducts → inflammation / damage to hepatocytes from leakage of bile.
  • Alcoholic Liver Disease (Laennec Cirrhosis)
    • Increased alcohol consumption (metabolites of alcohol can damage liver cells), plus other genetic / environmental factors.
  • Nonalcoholic Fatty Liver Disease
    • ​Changes in uptake/synthesis/break down of hepatic lipids (due to obesity, insulin resistance, hyperlipidemia, etc.) cause fatty changes in liver cells, and impairs ability to detoxify free radicals → damage to hepatocytes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

The serologic markers for this type of Hepatits are anti-HDV.

a. ) Jaundice b.) Cirrhosis
c. ) Hepatitis A d.) Hepatitis B
e. ) Hepatitis C f.) Hepatitis D
g. ) Hepatitis E

A

Hepatitis D

Delta virus, Defective virus

Can only get if you have B!!

Transmission: blood/body fluids.

Chronic State / Carrier State: yes

Serologic Markers:

  • anti-HDV

P/C Factors:

  • HBV infections, or being at high risk for it.
How well did you know this?
1
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12
Q

The serologic marker for this type of Hepatits is anti-HCV.

a. ) Jaundice b.) Cirrhosis
c. ) Hepatitis A d.) Hepatitis B
e. ) Hepatitis C f.) Hepatitis D
g. ) Hepatitis E

A

Hepatitis C

formerly non-A, non-B

Transmission: blood/body fluids.

Chronic State / Carrier State: yes

Serologic Markers:

  • anti-HCV

P/C Factors:

  • IV drug abusers.
  • Health care workers.
  • High-risk sexual behavior.
  • Hemodialysis.
  • Organ transplant recipients.
  • Blood products.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

The serologic markers for this type of hepatitis are IgM anti-HAV and IgG anti-HAV.

a. ) Jaundice b.) Cirrhosis
c. ) Hepatitis A d.) Hepatitis B
e. ) Hepatitis C f.) Hepatitis D
g. ) Hepatitis E

A

Hepatitis A

formerly infectious hepatitis

Transmission: fecal-oral route (sex)

Chronic State / Carrier State: None

Serologic Markers:

  • IgM anti-HAV: indicates acute disease
  • IgG anti-HAV: indicates past infection

P/C Factors:

  • Contaminated foods
  • Poor hygiene
  • High-risk sexual behavior
How well did you know this?
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14
Q

Abnormally high amount of bilirubin in the blood.

a. ) Jaundice b.) Cirrhosis
c. ) Hepatitis A d.) Hepatitis B
e. ) Hepatitis C f.) Hepatitis D
g. ) Hepatitis E

A

Jaundice

Abnormally high amount of bilirubin in the blood.

Assessment Findings:

  • Yellow skin/eyes
  • Drug toxicity
  • Hormone imbalance

P/C Factors:

  • increased destruction of RBCs.
    • ex: transfusion reaction, blood disorders)
  • Liver impairment → decreased conjugation → decreased elimination.
    • ex: hepatitis, cirrhosis
  • Obstruction of bile flow to intestine → decreased elimination.
    • ex: gallstones, obstructing bile ducts
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15
Q

Which two types of Hepatitis are transmitted via the fecal-oral route (sex)?

a. ) Jaundice b.) Cirrhosis
c. ) Hepatitis A d.) Hepatitis B
e. ) Hepatitis C f.) Hepatitis D
g. ) Hepatitis E

A

Hepatitis A and Hepatits E

formerly infectious hepatitis

Transmission: fecal-oral route (sex)

Chronic State / Carrier State: None

Serologic Markers:

  • IgM anti-HAV: indicates acute disease
  • IgG anti-HAV: indicates past infection

P/C Factors:

  • Contaminated foods
  • Poor hygiene
  • High-risk sexual behavior
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

P/C factors for this type of cirrhosis include changes in uptake/synthesis/break down of hepatic lipids (due to obesity, insulin resistance, hyperlipidemia, etc.) cause fatty changes in liver cells, and impairs ability to detoxify free radicals → damage to hepatocytes.

a. ) Postnecrotic types
b. ) Primary biliary types
c. ) Alcoholic liver disease
d. ) Nonalcoholic fatty liver disease (NAFLD)

A

Nonalcoholic fatty liver disease (NAFLD)

Cirrhosis

Nodules of normal hepatocytes surrounded by fibrosis.

Damage / death of hepatocytes →

  1. Cell regeneration → nodules of functional hepatocytes +
  2. Scar tissue formation →
    • replaces functional liver cells → liver failure
    • distorts liver structure, obstructs flow in vascular and biliary channels (kinks)

Assessment Findings:

  1. inflammation
    • Abdominal, right upper quadrant pain, hepatomegaly.
  2. Portal hypertension
    • Ascites, edema, dyspnea, anemia.
  3. Liver failure
    • End Stage Liver Disease
      • Anorexia, Steatorrhea
      • Vitamin A deficiency = vision problems.
      • Vitamin D deficiency = weak bones, hypocalcemia.
      • Vitamin K deficiency = no clotting factors (bleeding).
    • High or low glucose levels.
    • Liver is not making albumin → causes edema.
    • Bleeding tendencies.
    • Hepatic encephalopathy → Asterixis
    • Seizures / Coma (Hepatocoma).
    • Drug toxicities
    • Hormone imbalances
    • Sepsis (unfiltered blood)
    • Hepatorenal failure

P/C Factors:

  • Postnecrotic Types:
    • Viral hepatitis
    • Exposure to toxic drugs / chemicals
  • Primary Biliary Types:
    • Autoimmune attack on small bile ducts → inflammation / damage to hepatocytes from leakage of bile.
  • Alcoholic Liver Disease (Laennec Cirrhosis)
    • Increased alcohol consumption (metabolites of alcohol can damage liver cells), plus other genetic / environmental factors.
  • Nonalcoholic Fatty Liver Disease (NAFLD)
    • ​Changes in uptake/synthesis/break down of hepatic lipids (due to obesity, insulin resistance, hyperlipidemia, etc.) cause fatty changes in liver cells, and impairs ability to detoxify free radicals → damage to hepatocytes.
17
Q

P/C factors include abusing drugs intravenously, being a healthcare worker, high-risk sexual behavior, hemodialysis, organ transplant recipients, and blood products.

a. ) Jaundice b.) Cirrhosis
c. ) Hepatitis A d.) Hepatitis B
e. ) Hepatitis C f.) Hepatitis D
g. ) Hepatitis E

A

Hepatitis C

formerly non-A, non-B

Transmission: blood/body fluids.

Chronic State / Carrier State: yes

Serologic Markers:

  • anti-HCV

P/C Factors:

  • IV drug abusers.
  • Health care workers.
  • High-risk sexual behavior.
  • Hemodialysis.
  • Organ transplant recipients.
  • Blood products.
18
Q

P/C factors include HBV infection, or being at high risk for it.

a. ) Jaundice b.) Cirrhosis
c. ) Hepatitis A d.) Hepatitis B
e. ) Hepatitis C f.) Hepatitis D
g. ) Hepatitis E

A

Hepatitis D

Delta virus, Defective virus

Can only get if you have B!!

Transmission: blood/body fluids.

Chronic State / Carrier State: yes

Serologic Markers:

  • anti-HDV

P/C Factors:

  • HBV infections, or being at high risk for it.
19
Q

Does not cause chronic hepatitis or the carrier state.

a. ) Hepatitis A
b. ) Hepatitis B
c. ) Hepatitis C
d. ) Hepatitis D
e. ) Hepatitis E

A

Hepatitis E

Does not cause chronic hepatitis or the carrier state.

20
Q

Most common cause of chronic hepatitis, cirrhosis, and hepatocellular cancer in the world.

a. ) Hepatitis A
b. ) Hepatitis B
c. ) Hepatitis C
d. ) Hepatitis D
e. ) Hepatitis E

A

Hepatitis C

Most common cause of chronic hepatitis, cirrhosis, and hepatocellular cancer in the world.

21
Q

Occurs primarily by the fecal-oral route.

a. ) Hepatitis A
b. ) Hepatitis B
c. ) Hepatitis C
d. ) Hepatitis D
e. ) Hepatitis E

A

Hepatitis A

Occurs primarily by the fecal-oral route.

22
Q

Infection is linked to hepatitis B.

a. ) Hepatitis A
b. ) Hepatitis B
c. ) Hepatitis C
d. ) Hepatitis D
e. ) Hepatitis E

A

Hepatitis D

Infection is linked to hepatitis B.

23
Q

Innoculation with infected blood and/or spread by oral or sexual contact.

a. ) Hepatitis A
b. ) Hepatitis B
c. ) Hepatitis C
d. ) Hepatitis D
e. ) Hepatitis E

A

Hepatitis B

Innoculation with infected blood and/or spread by oral or sexual contact.

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