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

E2 Liver Patho Flashcards

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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
Prodromal phase of viral hepatitis?
-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
26
Icteric phase of viral hepatitis?
"Active phase" -Begins w/ jaundice -Dark urine -Clay colored stools -Enlarged liver, painful on palpitation -Abdominal pain increase in severity -Last 2-6 weeks
27
Recovery phase of viral hepatitis
-Resolution of jaundice -6-8wks after exposure, sympts diminish -Liver remains enlarged/tender
28
Complications of viral hepatitis?
-Majority recover completely -Mortality rate <1% (except elderly & comorbidities) Complications -Chronic hepatitis -Liver cirrhosis -Liver cancer -Fulminant viral hepatitis (ALF)
29
How is Hepatitis A transmitted?
-FECAL to oral -Parental -Sexual r/t sanitation practices/ foood handling OR not washing hands
30
Other Hep A things to know
-Usually mild severity -Does NOT lead to chronic hepatitis -Usually effects children & adults -Prevent: hand hygiene & hep A vaccine (High risk/ traveling)
31
S/S of Hep A
-Acute onset w/ fever -Fatigue -N/V/D -Stomach pain -No appetite -Dark pee & pale poop -Jaundice
32
How is Hep B transmitted?
Parental or sexual
33
Other Hep B things to know
-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
Hep C transmission
-Parental -Sexual -Mother to fetus -Medical mishaps
35
Other things to know about Hep C
-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
S/S of Hep C
-None -Stomach pain -Vomiting -Yellow eyes or skin
37
Hep A series
2 doses 6 months apart Recommended but NOT required >1yr old & special populations (traveling, healthcare workers, food handlers)
38
Hep B series
3 doses at least 4 months apart All newborns Titer if healthcare
39
What are the two classes of drugs used for chronic HBV?
Interferons & Nucleoside analogs
40
Chronic HBV is only for high risk patients like:
1. Increased AST levels 2. Hepatic inflammation 3. Advanced fibrosis
41
Disadvantages of HBV treatment
1. Prolonged therapy 2. Costs & adverse effects 3. High relapse
42
Who gets the new treatment for HCV? and what is used
Direct-acting antiviral therapy (and interferon-based regiments) Anyone w/ detectable viral loads
43
What is a special consideration for acetaminophen if taking pt has hepetitis?
take <2g day If severe avoid acetaminophen & NSAIDs
44
Hepatitis can lead to _____
Cirrhosis
45
Hepatitis is _____ while Cirrhosis is _______
Reversible Irreversible
46
What is cirrhosis?
Irreversible, inflammatory fibrotic liver disease (scarring)
47
Chaotic fibrosis leads to obstructive biliary channels & blood flow --->
Jaundice & portal hypotension
48
Regeneration in cirrhosis is disrupted by
hypoxia, necrosis, atrophy, & liver failure
49
Common causes of cirrhosis?
1. Hep B &C 2. Excessive alcohol intake 3. Idiopathic 4.Non-alcoholic fatty liver disease (NASH, NAFLD) 5. Autoimmune conditions 6. Hereditary metabolic conditions
50
The liver converts alcohol to what
acetylhyde
51
Acetylhyde in excessive amounts does what?
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
What are the stages of alcoholic liver disease?
1. Alcoholic fatty liver 2. Alcoholic steatohepatitis 3. Alcoholic cirrhosis
53
Explain the Alcoholic fatty liver phase
-Mildest, asymptomatic -Reversible
54
Explain the alcoholic steatohepatitis phase
-Precursor to cirrhosis -Inflammation, degeneration of hepatocytes -Anorexia, Nausea, Jaundice, Edema -Irreversible
55
Pathogenesis of cirrhosis
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
Explain the alcoholic cirrhosis phase
-Fibrosis & scarring alter liver structure -Inflammation, oxidative stress, cellular damage, cellular necrosis -Irreversible
57
Stages of liver damage
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
Cirrhosis early manifestations
GI distrubances -N/V -Anorexia -Flatulence -Change in bowel habits Fever Wt loss Palpable liver
59
Cirrhosis late manifestations
-Jaundice -Peripheral edema -Decreased albumin & PT -Ascites -Skin lesions (spider angioma) -Hematologic problems (anemia & bleeding) -Endocrine problems -Esophageal & anorectal varices -Encephalopathy
60
Describe the endocrine problems that go along with late cirrhosis
Women: stop ovulating & periods stop (amenorrhea) Men: hypogonadism, impotence, infertility
61
Portal hypotension lead to the development of what?
fragile distended veins (if they burst lots of bleeding and high mortality)
62
What is portal hypertension?
Resistant portal blood flow that leads to varices & ascites
63
What are causes of portal hypertension?
-Systemic hypotension -Vascular underfilling -Stimulation of vasoactive (RAAS) systems -Plasma volume expansion -Increased CO
64
S/S of portal hypertension?
Asymptomatic until complications -Variceal hemprrhage -Ascites -Peritonitis -Hepatorenal syndrome -Cardiomyopathy
65
Treatment of portal hypertension?
Nothing except liver transplant
66
What % of cirrhosis pts get hepatic encephalopathy?
30-40%
67
What is the primary driver of the hepatic encephalopathy diagnosis?
LOC Range from Change in behavior to Coma (liver not filtering so toxins building up in brain causing confusion)
68
What liver lab is the primary chemical driver of LOC changes?
Ammonia (never diagnosis w/ only ammonia labs)
69
What is Acute liver failure-ALF (fulminant liver failure)?
Separate liver failure (NOT) caused by cirrhosis
70
What is the most common cause of ALF?
Acetaminophen overdose
71
How is acute liver failure r/t acetaminophen overdose treated?
Acetylcysteine
72
What is the patho of ALF?
edematous hepatocytes and pathy areas of necrosis and inflammatory cell infiltrates & disrupts the liver tissue
73
ALF occurs _____ after a viral hepatitis or metabolic liver disease or ______ after a acetaminophen overdose?
6-8 wks 5days to 8 weeks
74
Treatment of ALF?
Not much, liver transplatn
Fall Block 1 Medsurg/Patho
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