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PHARM 346 - Other > Chronic Liver Disease > Flashcards

Chronic Liver Disease Flashcards

1
Q

Acute Liver Disease
- Definition

A
  • Symptoms do not last longer than 6 months
  • Self-limiting hepatocyte inflammation or damage
  • Less common than Chronic

Ex. Acetaminophen, Viral Hepatitis

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2
Q

Chronic Liver Disease
- Definition

A
  • Symptoms last longer than 6 months
  • Permanent structural changes due to continuous hepatocyte damage
  • More common than Acute

Ex. Alcohol, NAFLD, Viral

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3
Q

Hepatitis and Liver Disease
- Acute / Chronic

A

Hepatitis A causes only acute

Hepatitis B, C, D causes acute liver disease that can progress to chronic

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4
Q

Treatment options for Chronic Liver Disease

A
  • Prevent progression
  • Prevent complications
  • Transplant
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5
Q

Pathophysiology of Chronic Liver Disease

A
  1. Healthy Liver
    1a. Fatty Liver (Optional)
  2. Hepatitis
  3. Fibrosis
  4. Cirrhosis
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6
Q

What stages in Chronic Liver Diseaase are reversible

A

Fatty Liver is reversible

Hepatitis is reversible
- Have to remove cause of liver injury

Steatohepatitis is reversible
- Have to remove cause of liver injury

Fibrosis is reversible
- Only in the early stages if cause of liver damage is removed

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7
Q

Fatty Liver
- What is it

A

Accumulation of fat in liver
- Early stage of chronic liver disease (not always)

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8
Q

Fatty Liver
- MOA

A
  • Due to increased movement of fatty acids
  • Reduced clearance of fatty acids
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9
Q

Fatty Liver
- Diagnosis

A
  • Mild elevation in liver enzymes (AST, ALT)
  • Ultrasound imaging
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10
Q

Fatty Liver
- Symptoms

A
  • Usually asymptomatic
  • Abdominal Pain
  • Fatigue
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11
Q

Hepatitis
- What is it

A

Inflammation that occurs after liver damage

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12
Q

Hepatitis
- MOA

A
  • Kuffer (Macrophage) cells are activated by inflammation to release cytokines causing hepatocyte necrosis
  • Neutrophils accumulate around degenerating liver cells and bring in even more inflammatory factors
  • Liver tries to repair itself but inflammation persists because of underlying liver damage
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13
Q

Hepatitis
- Diagnosis

A
  • Enlarged liver in imaging
  • Elevated liver enzymes (AST, GGT)
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14
Q

Hepatitis
- Symptoms

A

Typically asymptomatic
- Jaundice, Nausea, Fatigue, Tenderness

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15
Q

Steatohepatitis
- What is it

A

Steatosis (Fatty Liver) + Hepatitis (Inflammation)

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16
Q

Fibrosis
- What is it

A

Response to liver damage creates deposition of extracellular matrix and proteins (collagen) leading to scaring

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17
Q

Fibrosis
- MOA

A
  1. Liver injury activates Hepatic Stellate Cells
  2. HSC act as a proliferative myofibroblast, repairing injured tissue by laying down collagen
  3. Constant activation leads to accumulation of HSC and accumulation of extracellular matrix and progressing fibrosis
  4. Results in scar tissue
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18
Q

Cirrhosis
- What is it

A

Fibrosis is widespread, liver’s architecture has been irreversibly altered

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19
Q

Compensated Cirrhosis

A

Despite scarring and damage liver is still able to function
- Little/No symptoms

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20
Q

Uncompensated Cirrhosis

A

Due to significant scarring and damage liver is unable to function
- Range of symptoms and complications

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21
Q

Kinds of Liver Function Tests

A

Hepatocyte Integrity

Biliary Excretory Function

Hepatocyte Synthetic Function

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22
Q

Hepatocyte Integrity
- Serum Measurement

A

High
- Aspartate Serum Aminotransferase
- Alanine Serum Aminotransferase

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23
Q

Bilirubin Excretory Function
- Serum Measurement

A

High:
- Serum Bilirubin
- Serum Alkaline Phosphatase (ALP)
- Serum Gamma-Glutamyl Transpeptidase (GGT)

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24
Q

Hepatocyte Synthesis Function
- Serum Measurment

A

Low:
- Coagulation Factors
- Serum Albumin
- Prealbumin

High:
- INR Time
- Serum Ammonia (Liver unable to detoxify)

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25
Q

FIB-4
- What is it

A

Assesses the extent of scarring of liver in patients with NAFLD
- Sort patients with NAFLD into low, intermediate, and high risk of developing cirrhosis in the next 10 years

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26
Q

FIB-4
- Scores

A

Any score higher than a 1.3 should be referred

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27
Q

FIB-4
- Who should use it

A

Should only be used in Non-Alcoholic Liver Disease
- AST can overestimate fibrosis with alcohol use

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28
Q

Child-Pugh-Turcotte Score
- What is it

A

Used to assess severity of cirrhosis and predict mortality
- Used to determine drug dosing

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29
Q

Child-Pugh-Turcotte Score
- Scores

A

Class A: 6-6
- Least severe, one year survival of 100%
Class B: 7-9
- Moderate severe, one year survival of 80%
Class C: 10-15
- Most Severe, one year survival of 45%

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30
Q

Alcohol Liver Disease
- MOA

A

Lipid droplets accumulate in hepatocytes after alcohol consumption

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31
Q

Alcohol Liver Disease
- Stages

A
  1. Steatosis
  2. Hepatitis-Inflammation
  3. Hepatitis-Inflammation + Fibrosis
  4. Cirrhosis
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32
Q

Alcohol Liver Disease: Steatosis
- MOA

A

Hepatic enzymes break down alcohol = Increased lipogenesis

Alcohol induces breakdown of fat = Increases lipids in circulation

Reversible by alcohol abstinence

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33
Q

Alcohol Liver Disease: Hepatitis-Inflammation
- MOA

A

Increase in acetaldehyde = Disrupts cell function

Induction of hepatic enzymes to generate reactive oxygen species = Damages cell proteins and promotes apoptosis

Sensitizes liver to oxidative injury

34
Q

Alcohol Liver Disease: Hepatitis-Inflammation + Fibrosis
- MOA

A

Chronic inflammation leads to scarring

Is reversible to some degree with abstinence
- 1/3 chance of developing cirrhosis if continuing alcohol

35
Q

Alcohol Liver Disease: Hepatitis-Inflammation + Fibrosis
- Treatment

A

If hospitilzed can treat with Prednisolone for 28 days
- D/C if no response at 7 days

36
Q

Alcohol Liver Disease: Cirrhosis
- MOA

A

Chronic inflammation and fibrosis

Can develop without any evidence of steatosis or alcoholic hepatitis

37
Q

Cirrhosis
- Progression

A

Can develop either into:
- Decompensation
- Hepatocellular Carcinoma

38
Q

NAFLD
- What is it

A

Most common liver disease
- An umbrella term of range of diseases that involve metabolic dysfunction

  1. Simple Steatosis
  2. NASH
39
Q

NAFLD
- MOA

A

Accumulation of fat within liver cells leading to liver damage

40
Q

NAFLD
- Risk Factors

A

Metabolic Syndrome
- Hypertension
- Diabetes
- Obesity
- Elevated Lipids

Environmental Factors
- High Caloric Diet
- Sedentary Lifestyle

Genetics, Demographics
- Age
- Gender

41
Q

NAFLD
- Pathway

A

FIB-4 < 1.3 = Low Risk
- Physical Activity
- Diet and Weight Loss
- Screen for risk factors
- Smoking cessation
- Limit alcohol intake

FIB-4 > 1.3 = Intermediate/High Risk
- Refer

42
Q

NAFLD
- Progression

A

80% of patients are low risk and only develop Isolated Fatty Liver
- Can be managed with just Lifestyle Interventions

No pharmacological therapy for NAFLD or NASH

43
Q

End Stage Liver Disease
- Presentation

A
  • Jaundice
  • Cholestasis
  • Ascites
  • Hepatic encephalopathy
  • Coagulopathy
  • Liver Failure
44
Q

Hepatic Cholestasis
- What is it

A

Accumulation of bile in liver due to hepatic cells being impaired or obstruction

45
Q

Hepatic Cholestasis
- Symptoms

A

Yellowing of skin and eyes
- Deposition of bilirubin

Pruritus
- Irritation of peripheral nervous system from bile salts

Dark Urine
- Excess bilirubin excretion through urine

Light-Coloured Stools
- Reduced bilirubin excretion through stools

46
Q

Cholestatic Pruitus
- Symptoms

A
  • Itch with no rash
  • Worse at night
  • Intensity is not associated with
47
Q

Cholestatic Pruritus
- Treatment

A

Cholestyramine
- Binds bile acid and excretes in through stool

Antihistamines do not work

Alternatives = Naltrexone or Sertraline

48
Q

Cholestyramine
- Adverse Effects

A
  • Constipation
  • Diarrhea
  • Bloating
49
Q

Cholestyramine
- Consideration

A

Should be spaced by 4 hours due to drug interactions

50
Q

Portal Hypertension
- MOA

A

Intrahepatic
- Liver structure is distorted, increased resistance to blood flow
- Imbalance of vasoconstrictors and vasodilators

51
Q

Portal Hypertension
- Consequences

A

Collateral Blood Vessel Formation = Portosystemic Shunts
- Caput Medusae
- Varices

Ascites

Hepatic Encephalopathy

52
Q

Caput Medusae
- What is it

A

Large and swollen veins on surface of abdomen
- Vessels can not withstand pressure and distort

53
Q

Caput Medusae
- Treatment

A

Treat underlying condition

54
Q

Varices
- What is it

A

Collateral Vessels are enlarged
- However, they are not build to handle high pressure and volume of flow
- Can rupture and bleed

Most common emergency in CIrrhosis

55
Q

Varices
- Screening

A

Patients diagnosed with cirrhosis should be screened using endoscopy
- Upper endoscopy

Pt is asymptomatic until variceal ruptures

56
Q

Variceal
- Treatment

A

No Varices
- Repeat imaging q1-3 years

Variceal present but less than 5mm
- Prophylaxis with beta blocker

Variceal present and larger than 5mm
- Treat with Beta Blocker + EVL

57
Q

Variceal
- Beta Blockers

A

Use non-selective beta blockers
- Beta 1 decreases cardiac output = decrease portal perfusion
- Beta 2 vasoconstriction = decreased splanchnic perfusion

58
Q

Variceal
- Beta Blocker Monitoring

A

Bradycardia
Hypotension
Hyponatremia
AKI

59
Q

Variceal
- Endoscopic Intervention

A

Endoscopic Variceal Ligation
- Suction to pull variceals
- Bands to wrap and prevent bleeding of variceal

Endoscopic Injection Sclerotherapy
- Inject variceal with sclerotic agent, damages it and closes it
- Not as effective as beta blocker + EVI

60
Q

Managing Actively Bleeding Varices
- Supportive

A
  • ABC: protect airways and supplement with O2
  • Blood perfusions
  • Fluids to maintain intravascular volume
61
Q

Managing Actively Bleeding Varices
- Pharmacologic

A

Prophylactic Antibiotics
Octreotide IV
Somatostatin
Vasopressin

61
Q

Managing Actively Bleeding Varices
- Endoscopic

62
Q

Managing Actively Bleeding Varices
- Surgical

A

Transjugular Intrahepatic Portosystemic Shunt

63
Q

Secondary Prevention of Variceal Bleeding

A

High risk of another bleed after an episode has occured
- Start patient as soon as they are hemodynamically stable on Non-Selective Beta Blocker + EVI
- If bleeding still occurs can consider a transjugular Intrahepatic Portosystemic Shunt

64
Q

Ascites
- Symptoms

A
  • Abdominal Distention
  • Weight Gain
  • Dyspnea
  • Early Satiety
65
Q

Ascites
- Non-Pharm

A

Fluid restriction
Low sodium diet
Removal of fluid (Therapeutic paracentesis)

66
Q

Ascites
- Pharm

A

Spironolactone
Furosemide
Metolazone
Amiloride

67
Q

Ascites
- Surgical

A
  • Creation of a transjugular intrahepatic portosystemic shunt to reroute blood flow
  • Reroute blood flow
68
Q

Use of Diuretics in Ascites

A
  1. Start with Spironolactone
  2. Add on Furosemide (40:100 ratio of Sprinolactone:Furosemide)
  3. Can add on Metolazone if 1+2 fail
  4. Amiloride (Can be used instead of spironolactone)
69
Q

Diuretics
- Adverse Effects

A
  • Electrolyte abnormalities
  • SCr, BUN
  • Blood Pressure
70
Q

Spironolactone
- Adverse Effects

A
  • Hyperkalemia
  • Gynecomastia
71
Q

Furosemide
- Adverse Effects

A
  • Uric Acid
  • Volume Depletion
72
Q

Metolazone
- Adverse Effects

A
  • Uric Acid
  • Volume Depletion
73
Q

Hepatic Encephalopathy
- MOA

A

Accumulation of ammonia due to poor hepatic function
- Reversible
- Occurs in advanced liver disease

74
Q

Hepatic Encephalopathy
- What is it

A

Brain function deterioration due to liver insufficiency
- Occurs in advanced liver disease
- Reversible

75
Q

Hepatic Encephalopathy
- Treatment

A

First Line: Lactulose

Second Line: Rifaximin

76
Q

Lactulose
- MOA

A
  • Removes nitrogenous waste in GI tract through laxative action
  • Is metabolized into short chain organic acids that inhibit ammonia producing bacteria
77
Q

Lactulose
- Adverse Effects

A
  • Bloating
  • Flatulence
  • Cramps
  • Diarrhea
78
Q

Rifaximin
- MOA

A
  • Reduces urease producing intestine bacteria, decreasing ammonia in blood

Can use if lactulose does not work or is intolerable
- Can also combine with lactulose

79
Q

Rifaximin
- Adverse Effects

A
  • GI Upset
  • Edema
  • Headache

PHARM 346 - Other (17 decks)

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