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Fall Block 1 Medsurg/Patho > E2 Liver Patho > Flashcards

E2 Liver Patho Flashcards

1
Q

What is the functional unit of the liver?

A

Lobules

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2
Q

What are the liver cells called?

A

Hepatocytes

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3
Q

What is unique about hepatocytes?

A

Only cells in the body that can re-grow/ regenerate

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4
Q

What do kuffer cells do?

A

remove bacteria & toxins from blood

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5
Q

What are the major functions of the liver?

A
  1. Metabolism &/or storage of: fat, CHO, PRO, Vits, & minerals
  2. Blood volume reservoid: distends/compresses to alter circulating blood volume
  3. Blood filter: removes bili
  4. Blood clotting: prothrombin & fibrinogen
  5. Drug metabolism & detoxification
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6
Q

The liver is the _____ organ

A

largest (3 Ibs)

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7
Q

The portal circulatory system brings blood to the liver from the

A

stomach, intestines, spleen, and pancreas for metabolism

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8
Q

The blood enters the liver through the ______ and recieves what type of blood?

A

Portal vein

Deoxygenated

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9
Q

The liver is responsible for the _______ effect

A

first pass

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10
Q

Liver function test abnormal trends?

A
  1. Liver enzymes: Increase
  2. Bilirubin: Increased
  3. Ammonia: Increased
  4. PT: Increased
  5. Serum Protein: Decreased
  6. Serum Albumin: Decreased
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11
Q

Jaundice is also called

A

icterus

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12
Q

Jaundice is usually noticeable when bilirubin is

A

> 2-2.5 mg/dl

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13
Q

What are the 3 causes of jaundice?

A
  1. Hemolytic–> increased breakdown of RBCs (pathophysiologic, too many RBCs, Bleeding)
  2. Hepatocellular–> Liver unable to take up bili from blood or unable to conjugate it
  3. Obstructive–> Decreased or obstructed flow of bile
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14
Q

Bilirubin is a byproduct of what?

A

Hemoglobin

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15
Q

Direct bili=

Indirect bili=

A

Conjugated

unconjugated

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16
Q

Elevations of indirect bili=

A

bili overproduction OR impaired liver functioning
(Hemolysis or erythropoiesis)

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17
Q

Elevations of direct bili=

A

liver working, but can’t get bili out
(Bile obstruction, gallstone)

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18
Q

jaundice clinical manifestations

A

-Urine darker
-Liver enzymes increased
-Stools normal or clay colored
-Pruritis

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19
Q

What is viral hepatitis?

A

Inflammation of the liver

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20
Q

What are the viruses that cause hepatitis?

A

A,B,C (D&E)
Epstein-Barr
Cytomegalovirus

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21
Q

What also causes hepatitis that is not a virus?

A

Alcohol abuse
Bacteria
Chemicals
Drugs

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22
Q

Who is Hepatitis E dangerous to?

A

Pregnant women

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23
Q

Pathogenesis of viral hepatitis?

A
  1. Viral infection
  2. Immune response: inflammatory mediators in liver
  3. Lysis of infected cells
  4. Edema & swelling of tissue
  5. Tissue hypoxia
  6. Hepatocyte death

Leads to liver failure

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24
Q

Clinical manifestations of viral hepatitis?

A

-Similar btwn types
-Many asymptomatic
-Abnormal LFTS but need to trend

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25
Q

Prodromal phase of viral hepatitis?

A

-2 weeks after exposure
-Fatigue
-Anorexia
-Malaise
-N/V
-H/A
-Hyperalgesia (increased sensitivity to pain)
-Cough
-Low grade fever

Last 1-2 wks

HIGHLY transmissible

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26
Q

Icteric phase of viral hepatitis?

A

“Active phase”
-Begins w/ jaundice
-Dark urine
-Clay colored stools
-Enlarged liver, painful on palpitation
-Abdominal pain increase in severity
-Last 2-6 weeks

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27
Q

Recovery phase of viral hepatitis

A

-Resolution of jaundice
-6-8wks after exposure, sympts diminish
-Liver remains enlarged/tender

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28
Q

Complications of viral hepatitis?

A

-Majority recover completely

-Mortality rate <1% (except elderly & comorbidities)

Complications
-Chronic hepatitis
-Liver cirrhosis
-Liver cancer
-Fulminant viral hepatitis (ALF)

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29
Q

How is Hepatitis A transmitted?

A

-FECAL to oral
-Parental
-Sexual

r/t sanitation practices/ foood handling OR not washing hands

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30
Q

Other Hep A things to know

A

-Usually mild severity
-Does NOT lead to chronic hepatitis
-Usually effects children & adults
-Prevent: hand hygiene & hep A vaccine (High risk/ traveling)

31
Q

S/S of Hep A

A

-Acute onset w/ fever
-Fatigue
-N/V/D
-Stomach pain
-No appetite
-Dark pee & pale poop
-Jaundice

32
Q

How is Hep B transmitted?

A

Parental or sexual

33
Q

Other Hep B things to know

A

-Insidious onset
-Severe disease, may be prolonged or develop into chronic
-Any age group (not kids)
-Prevention: Safe sex, hygeine, & HBV vaccine (Healthcare workers & kids)

34
Q

Hep C transmission

A

-Parental
-Sexual
-Mother to fetus
-Medical mishaps

35
Q

Other things to know about Hep C

A

-Insidious onset
-Mild to severe s/s
-can develop into chronic (80%)
-Any age affected
-Can lead to hepatocellular carcinoma, liver transplant
-Prevention: screening blood, hygiene, NO vaccine, new treatment

36
Q

S/S of Hep C

A

-None
-Stomach pain
-Vomiting
-Yellow eyes or skin

37
Q

Hep A series

A

2 doses 6 months apart

Recommended but NOT required

> 1yr old & special populations (traveling, healthcare workers, food handlers)

38
Q

Hep B series

A

3 doses at least 4 months apart

All newborns

Titer if healthcare

39
Q

What are the two classes of drugs used for chronic HBV?

A

Interferons & Nucleoside analogs

40
Q

Chronic HBV is only for high risk patients like:

A
  1. Increased AST levels
  2. Hepatic inflammation
  3. Advanced fibrosis
41
Q

Disadvantages of HBV treatment

A
  1. Prolonged therapy
  2. Costs & adverse effects
  3. High relapse
42
Q

Who gets the new treatment for HCV? and what is used

A

Direct-acting antiviral therapy (and interferon-based regiments)

Anyone w/ detectable viral loads

43
Q

What is a special consideration for acetaminophen if taking pt has hepetitis?

A

take <2g day

If severe avoid acetaminophen & NSAIDs

44
Q

Hepatitis can lead to _____

A

Cirrhosis

45
Q

Hepatitis is _____ while Cirrhosis is _______

A

Reversible

Irreversible

46
Q

What is cirrhosis?

A

Irreversible, inflammatory fibrotic liver disease (scarring)

47
Q

Chaotic fibrosis leads to obstructive biliary channels & blood flow —>

A

Jaundice & portal hypotension

48
Q

Regeneration in cirrhosis is disrupted by

A

hypoxia, necrosis, atrophy, & liver failure

49
Q

Common causes of cirrhosis?

A
  1. Hep B &C
  2. Excessive alcohol intake
  3. Idiopathic
    4.Non-alcoholic fatty liver disease (NASH, NAFLD)
  4. Autoimmune conditions
  5. Hereditary metabolic conditions
50
Q

The liver converts alcohol to what

A

acetylhyde

51
Q

Acetylhyde in excessive amounts does what?

A

Alters hepatocyte function & activates hepatic stellate cells which is the primary cell involved in liver fibrosis

Acetylhyde inhibits exports of protein from the liver which alters metabolism of vitamins & minerals & induces malnutrition

52
Q

What are the stages of alcoholic liver disease?

A
  1. Alcoholic fatty liver
  2. Alcoholic steatohepatitis
  3. Alcoholic cirrhosis
53
Q

Explain the Alcoholic fatty liver phase

A

-Mildest, asymptomatic
-Reversible

54
Q

Explain the alcoholic steatohepatitis phase

A

-Precursor to cirrhosis
-Inflammation, degeneration of hepatocytes
-Anorexia, Nausea, Jaundice, Edema
-Irreversible

55
Q

Pathogenesis of cirrhosis

A
  1. Hepatocytes destroyed
  2. Cells try to regenerate
  3. Disorganized process
  4. Abnormal Growth
  5. Poor blood flow & scar tissue
  6. Hypoxia
  7. Liver failure
56
Q

Explain the alcoholic cirrhosis phase

A

-Fibrosis & scarring alter liver structure
-Inflammation, oxidative stress, cellular damage, cellular necrosis
-Irreversible

57
Q

Stages of liver damage

A
  1. Fatty liver- deposits of fat lead to liver enlargement
  2. Liver Fibrosis-scar tissue forms
  3. Cirrhosis- growth of connective tissue destroys liver cells
58
Q

Cirrhosis early manifestations

A

GI distrubances
-N/V
-Anorexia
-Flatulence
-Change in bowel habits

Fever
Wt loss
Palpable liver

59
Q

Cirrhosis late manifestations

A

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

60
Q

Describe the endocrine problems that go along with late cirrhosis

A

Women: stop ovulating & periods stop (amenorrhea)

Men: hypogonadism, impotence, infertility

61
Q

Portal hypotension lead to the development of what?

A

fragile distended veins (if they burst lots of bleeding and high mortality)

62
Q

What is portal hypertension?

A

Resistant portal blood flow that leads to varices & ascites

63
Q

What are causes of portal hypertension?

A

-Systemic hypotension
-Vascular underfilling
-Stimulation of vasoactive (RAAS) systems
-Plasma volume expansion
-Increased CO

64
Q

S/S of portal hypertension?

A

Asymptomatic until complications
-Variceal hemprrhage
-Ascites
-Peritonitis
-Hepatorenal syndrome
-Cardiomyopathy

65
Q

Treatment of portal hypertension?

A

Nothing except liver transplant

66
Q

What % of cirrhosis pts get hepatic encephalopathy?

A

30-40%

67
Q

What is the primary driver of the hepatic encephalopathy diagnosis?

A

LOC

Range from Change in behavior to Coma

(liver not filtering so toxins building up in brain causing confusion)

68
Q

What liver lab is the primary chemical driver of LOC changes?

A

Ammonia
(never diagnosis w/ only ammonia labs)

69
Q

What is Acute liver failure-ALF (fulminant liver failure)?

A

Separate liver failure (NOT) caused by cirrhosis

70
Q

What is the most common cause of ALF?

A

Acetaminophen overdose

71
Q

How is acute liver failure r/t acetaminophen overdose treated?

A

Acetylcysteine

72
Q

What is the patho of ALF?

A

edematous hepatocytes and pathy areas of necrosis and inflammatory cell infiltrates & disrupts the liver tissue

73
Q

ALF occurs _____ after a viral hepatitis or metabolic liver disease or ______ after a acetaminophen overdose?

A

6-8 wks

5days to 8 weeks

74
Q

Treatment of ALF?

A

Not much, liver transplatn

Fall Block 1 Medsurg/Patho (9 decks)

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