Chronic Liver Disease Flashcards
(80 cards)
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
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
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
4
Q
Treatment options for Chronic Liver Disease
A
- Prevent progression
- Prevent complications
- Transplant
5
Q
Pathophysiology of Chronic Liver Disease
A
- Healthy Liver
1a. Fatty Liver (Optional) - Hepatitis
- Fibrosis
- Cirrhosis
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
7
Q
Fatty Liver
- What is it
A
Accumulation of fat in liver
- Early stage of chronic liver disease (not always)
8
Q
Fatty Liver
- MOA
A
- Due to increased movement of fatty acids
- Reduced clearance of fatty acids
9
Q
Fatty Liver
- Diagnosis
A
- Mild elevation in liver enzymes (AST, ALT)
- Ultrasound imaging
10
Q
Fatty Liver
- Symptoms
A
- Usually asymptomatic
- Abdominal Pain
- Fatigue
11
Q
Hepatitis
- What is it
A
Inflammation that occurs after liver damage
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
13
Q
Hepatitis
- Diagnosis
A
- Enlarged liver in imaging
- Elevated liver enzymes (AST, GGT)
14
Q
Hepatitis
- Symptoms
A
Typically asymptomatic
- Jaundice, Nausea, Fatigue, Tenderness
15
Q
Steatohepatitis
- What is it
A
Steatosis (Fatty Liver) + Hepatitis (Inflammation)
16
Q
Fibrosis
- What is it
A
Response to liver damage creates deposition of extracellular matrix and proteins (collagen) leading to scaring
17
Q
Fibrosis
- MOA
A
- Liver injury activates Hepatic Stellate Cells
- HSC act as a proliferative myofibroblast, repairing injured tissue by laying down collagen
- Constant activation leads to accumulation of HSC and accumulation of extracellular matrix and progressing fibrosis
- Results in scar tissue
18
Q
Cirrhosis
- What is it
A
Fibrosis is widespread, liver’s architecture has been irreversibly altered
19
Q
Compensated Cirrhosis
A
Despite scarring and damage liver is still able to function
- Little/No symptoms
20
Q
Uncompensated Cirrhosis
A
Due to significant scarring and damage liver is unable to function
- Range of symptoms and complications
21
Q
Kinds of Liver Function Tests
A
Hepatocyte Integrity
Biliary Excretory Function
Hepatocyte Synthetic Function
22
Q
Hepatocyte Integrity
- Serum Measurement
A
High
- Aspartate Serum Aminotransferase
- Alanine Serum Aminotransferase
23
Q
Bilirubin Excretory Function
- Serum Measurement
A
High:
- Serum Bilirubin
- Serum Alkaline Phosphatase (ALP)
- Serum Gamma-Glutamyl Transpeptidase (GGT)
24
Q
Hepatocyte Synthesis Function
- Serum Measurment
A
Low:
- Coagulation Factors
- Serum Albumin
- Prealbumin
High:
- INR Time
- Serum Ammonia (Liver unable to detoxify)
25
FIB-4
- What is it
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
26
FIB-4
- Scores
Any score higher than a 1.3 should be referred
27
FIB-4
- Who should use it
Should only be used in Non-Alcoholic Liver Disease
- AST can overestimate fibrosis with alcohol use
28
Child-Pugh-Turcotte Score
- What is it
Used to assess severity of cirrhosis and predict mortality
- Used to determine drug dosing
29
Child-Pugh-Turcotte Score
- Scores
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%
30
Alcohol Liver Disease
- MOA
Lipid droplets accumulate in hepatocytes after alcohol consumption
31
Alcohol Liver Disease
- Stages
1. Steatosis
2. Hepatitis-Inflammation
3. Hepatitis-Inflammation + Fibrosis
4. Cirrhosis
32
Alcohol Liver Disease: Steatosis
- MOA
Hepatic enzymes break down alcohol = Increased lipogenesis
Alcohol induces breakdown of fat = Increases lipids in circulation
Reversible by alcohol abstinence
33
Alcohol Liver Disease: Hepatitis-Inflammation
- MOA
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
Alcohol Liver Disease: Hepatitis-Inflammation + Fibrosis
- MOA
Chronic inflammation leads to scarring
Is reversible to some degree with abstinence
- 1/3 chance of developing cirrhosis if continuing alcohol
35
Alcohol Liver Disease: Hepatitis-Inflammation + Fibrosis
- Treatment
If hospitilzed can treat with Prednisolone for 28 days
- D/C if no response at 7 days
36
Alcohol Liver Disease: Cirrhosis
- MOA
Chronic inflammation and fibrosis
Can develop without any evidence of steatosis or alcoholic hepatitis
37
Cirrhosis
- Progression
Can develop either into:
- Decompensation
- Hepatocellular Carcinoma
38
NAFLD
- What is it
Most common liver disease
- An umbrella term of range of diseases that involve metabolic dysfunction
1. Simple Steatosis
2. NASH
39
NAFLD
- MOA
Accumulation of fat within liver cells leading to liver damage
40
NAFLD
- Risk Factors
Metabolic Syndrome
- Hypertension
- Diabetes
- Obesity
- Elevated Lipids
Environmental Factors
- High Caloric Diet
- Sedentary Lifestyle
Genetics, Demographics
- Age
- Gender
41
NAFLD
- Pathway
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
NAFLD
- Progression
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
End Stage Liver Disease
- Presentation
- Jaundice
- Cholestasis
- Ascites
- Hepatic encephalopathy
- Coagulopathy
- Liver Failure
44
Hepatic Cholestasis
- What is it
Accumulation of bile in liver due to hepatic cells being impaired or obstruction
45
Hepatic Cholestasis
- Symptoms
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
Cholestatic Pruitus
- Symptoms
- Itch with no rash
- Worse at night
- Intensity is not associated with
47
Cholestatic Pruritus
- Treatment
Cholestyramine
- Binds bile acid and excretes in through stool
Antihistamines do not work
Alternatives = Naltrexone or Sertraline
48
Cholestyramine
- Adverse Effects
- Constipation
- Diarrhea
- Bloating
49
Cholestyramine
- Consideration
Should be spaced by 4 hours due to drug interactions
50
Portal Hypertension
- MOA
Intrahepatic
- Liver structure is distorted, increased resistance to blood flow
- Imbalance of vasoconstrictors and vasodilators
51
Portal Hypertension
- Consequences
Collateral Blood Vessel Formation = Portosystemic Shunts
- Caput Medusae
- Varices
Ascites
Hepatic Encephalopathy
52
Caput Medusae
- What is it
Large and swollen veins on surface of abdomen
- Vessels can not withstand pressure and distort
53
Caput Medusae
- Treatment
Treat underlying condition
54
Varices
- What is it
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
Varices
- Screening
Patients diagnosed with cirrhosis should be screened using endoscopy
- Upper endoscopy
Pt is asymptomatic until variceal ruptures
56
Variceal
- Treatment
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
Variceal
- Beta Blockers
Use non-selective beta blockers
- Beta 1 decreases cardiac output = decrease portal perfusion
- Beta 2 vasoconstriction = decreased splanchnic perfusion
58
Variceal
- Beta Blocker Monitoring
Bradycardia
Hypotension
Hyponatremia
AKI
59
Variceal
- Endoscopic Intervention
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
Managing Actively Bleeding Varices
- Supportive
- ABC: protect airways and supplement with O2
- Blood perfusions
- Fluids to maintain intravascular volume
61
Managing Actively Bleeding Varices
- Pharmacologic
Prophylactic Antibiotics
Octreotide IV
Somatostatin
Vasopressin
61
Managing Actively Bleeding Varices
- Endoscopic
EVI
EIS
62
Managing Actively Bleeding Varices
- Surgical
Transjugular Intrahepatic Portosystemic Shunt
63
Secondary Prevention of Variceal Bleeding
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
Ascites
- Symptoms
- Abdominal Distention
- Weight Gain
- Dyspnea
- Early Satiety
65
Ascites
- Non-Pharm
Fluid restriction
Low sodium diet
Removal of fluid (Therapeutic paracentesis)
66
Ascites
- Pharm
Spironolactone
Furosemide
Metolazone
Amiloride
67
Ascites
- Surgical
- Creation of a transjugular intrahepatic portosystemic shunt to reroute blood flow
- Reroute blood flow
68
Use of Diuretics in Ascites
1. Start with Spironolactone
2. Add on Furosemide (40:100 ratio of Sprinolactone:Furosemide)
3. Can add on Metolazone if 1+2 fail
1. Amiloride (Can be used instead of spironolactone)
69
Diuretics
- Adverse Effects
- Electrolyte abnormalities
- SCr, BUN
- Blood Pressure
70
Spironolactone
- Adverse Effects
- Hyperkalemia
- Gynecomastia
71
Furosemide
- Adverse Effects
- Uric Acid
- Volume Depletion
72
Metolazone
- Adverse Effects
- Uric Acid
- Volume Depletion
73
Hepatic Encephalopathy
- MOA
Accumulation of ammonia due to poor hepatic function
- Reversible
- Occurs in advanced liver disease
74
Hepatic Encephalopathy
- What is it
Brain function deterioration due to liver insufficiency
- Occurs in advanced liver disease
- Reversible
75
Hepatic Encephalopathy
- Treatment
First Line: Lactulose
Second Line: Rifaximin
76
Lactulose
- MOA
- Removes nitrogenous waste in GI tract through laxative action
- Is metabolized into short chain organic acids that inhibit ammonia producing bacteria
77
Lactulose
- Adverse Effects
- Bloating
- Flatulence
- Cramps
- Diarrhea
78
Rifaximin
- MOA
- 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
Rifaximin
- Adverse Effects
- GI Upset
- Edema
- Headache
