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GI 2 > Hepatic and Inflammatory fibrosis (1) > Flashcards

Hepatic and Inflammatory fibrosis (1) Flashcards

1
Q

Histological scoring system: MEtavir:

Fibrosis

0:

1:

2:

A

O :no fibrosis

1: potential fibrosis; Portal fibrosis
2. Periportal fibrosis

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2
Q

Histological scoring system: MEtavir:

Fibrosis

3:

4:

A

3: septal fibrosis; bridging fibrosis
4: cirrhosis

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3
Q

Histological scoring system Metavir: Inflammation

0:

1:

2:

3:

4:

A

No inflammation

minimal inflammation

mild

moderate

severe

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4
Q
A
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5
Q

What stain can we use to identify chrrhosis?

A

trichome stain

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6
Q

• Acute cell death
 Fibrosis in most cases takes years
• Can lead to acute liver failure

A

Hepatic necrosis

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7
Q

= acute liver failure
complicated by coagulopathy and
encephalopathy

A

Fulminant liver failure (seen in hepatic necrosis)

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8
Q

• The most common causes of acute and
fulminant liver failure include

A

medications (acetaminophen) and viral hepatitis

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9
Q

Content of alcohol

Beer:

Wine:

Hard:

A

Beer; 5% alcohol, 12oz serving, 13.8 g of alcohol

Wine: 12% alcohol, 4oz serving, 10.7 grams

Hard: 40% alcohol, 1.5 oz, 13.4 grams

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10
Q

• Binge drinking
 For women, ____ drinks during a single
occasion
 For men, ____ drinks during a single occasion

A

4 or more

5 or more

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11
Q

• Heavy drinking
 For women, more than ____per day on average
 For men, more than ____ heavy drinking,
binge drinking or both.

A

1 drink

2 drinks

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12
Q

Ethenol –> Acetaldehyde via which enZ and CYP

A

Alcohol dehydrogenase by 75% and CYP2E1 for the other 25%

These are the Microsomal Ethanol Oxidizing System

(MEOS)

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13
Q

Acetaldehyde–> Acetic Acid via

A

Aldehyde dehydrogenase

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14
Q

Alcohol metoabolism results in: Increased NADH. What does this do to the TCA cycle

A

 inhibition of TCA cycle; reduced gluconeogenesis
 reduced fatty acid oxidation

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15
Q

In alcohol metablisim, we see increased _______
 activates stellate cells to form collagen
 Microfilaments that maintain intracellular skeleton are sheared
 Kupffer cells produce tumor necrosis factor alpha
(TNF α)

A

Acetaldehyde

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16
Q

produce tumor necrosis factor alpha (TNF α)

A

Kupffer cells

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17
Q

What happens in pathogenesis of alcohol in sinusoids

A

vili are damaged

accumulate collagen from stellate cells in space of Disse

Activate kupfner cells to release cytokines

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18
Q

What is the spectrum of disease in a patient with Alcoholic Liver Disease

A

Normal liver–> 90-100% fatty liver

fatty liver–> alcoholic hepatitis in 10-35% and then alcoholic hepatitis to cirrhosis

fatty liver–> cirrhosis in 8-20%

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19
Q

What makes up the portal triad

A

branch of portal vein, branch of hepatic artery, branch of bile duct

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20
Q

Do you have symptoms from having fatty liver from alcohol?

A

Not unless there is inflammation

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21
Q

What does alcoholic hepatitis look like on histology?

A

lots of fat and inflammation; gets more fibrosis with continued drinking; as you lay down more scar tissues you lose fat adn gets replaced by scar tissue

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22
Q

What are the 3 big risk factors for ALD?

A

• Quantity of Alcohol
 >30 g/day in men or >70 drinks a week big increase
 > 20 g/day in women; >28-40 drinks week big increase
• Outside of meals
• Binge drinking

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23
Q
A
24
Q

Alcoholic liver disease and Hepatitis C

A

Alcohol abuse increases how fast you progress to cirrhosis when you have Hep C. Normally should take 20-30 yrs, if you have Hep C and abuse alcohol, this occurs much faster

25
Q

What happens to the following in pts with ALD

 AST/ALT
 ALT
 Alk Phos
 Albumin
 Bilirubin

A

 AST/ALT ratio >2-3
 ALT usually <300 IU/ml
 Rarely raised Alk Phos
 Low Albumin
 Bilirubin

26
Q

Hematology abnormalities in ALD

A

 Prolonged INR
(advanced disease)
 Macrocytosis / anemia
 Thrombocytopenia
(advanced disease)

27
Q

Treatment for Alcoholic Hepatitis

A

• Abstinence and lifestyle modification
 nutritional support
• Anti-inflammatory drugs
 glucocorticoids
 Pentoxifylline (inhibits TNFα) made in Kupfner

28
Q
A
29
Q

What is the discriminant function and how do we use it?

A

4.6(PT-PT CONTROL) + T BILI
• Patients with values > 32 have a 1-month
mortality from 30%-50%

This is how we decide which alcoholic hepatitis pts to tx

30
Q

Dx?• 38 yo male with jaundice and malaise
• ALT 29
• AST 96
• ALK PHOS 98
• TOTAL BILI 12
• DIRECT BILI 8
• PT 19 SEC
• CONTROL PT 12 SEC

A

AST:ALT ( 96:29)

apx 3:1 so alcoholic cirrohsis

pt has Contorl PT of 19 sec and T bili of 12

4.6 (19-12) + 12 = 44 which is more then 32, needs tx!

31
Q

What happens to survival rates in pts with alcoholic hepatits when given glucocorticoids?

what about when given Pentoxifylline for 28 days?

A

3 month survival increases from 45% to 85%

and incresaes from 45% to 80%

32
Q
A
33
Q

What does the 5 yr survival look like for pts with alcoholic cirrhosis and what is it based on?

A

Based on the Child-Turcotte-Pugh score

5-7: 60% 5 yr survival

8-10: 40% 5 yr survival

11-5: 20% 5 yr survival

34
Q
  • First described in 1980
  • 20 patients with biopsies consistent with alcoholic hepatitis
  • All denied alcohol use
  • Female, obese, diabetes mellitus
  • Now recognized as the most common cause of elevate transaminases in the U.S.
A 
NON-ALCOHOLIC FATTY
LIVER DISEASE (NAFLD)
35
Q

What are the two categories of non-alcoholic fatty liver disease (NAFLD)

A

Non-alcoholic fatty liver (NAFL)

Non-alcoholic steatohepatitis (NASH)

36
Q 
o presence of hepatic steatosis without inflammation or
hepatocellular injury (ballooning of hepatocytes)
A

Non-alcholoic fatty liver (NAFL)

37
Q

o Presence of hepatic steatosis and inflammation with hepatocellular injury (ballooning of hepatocytes) with or without fibrosis

A

 Non-alcoholic steatohepatitis (NASH)

38
Q

Prevalene of chronic liver disorders in the US

A

Non-alcoholic fatty liver is most prevelant in US and is in 25% of the population

Nonalchoholic steatohepatitis is number 2

39
Q

STAGES IN THE PROGRESSION OF
NON-ALCOHOLIC FATTY LIVER DISEASE

A

Fatty liver (Hepatosteatosis)–> 10%–> to Steahepatitis (NASH) –>

Steatohepatitis with Fibrosis (35% of NASH)–>

Cirrhosis (15% of NASH)

*small % devo cirrhosis but the starting % is HIGH at 20% of population having fatty liver hepatoseatosis

40
Q

PREVALENCE (%) OF INDIVIDUAL METABOLIC ABNORMALITIES
OF THE METABOLIC SYNDROME
AMONG US ADULTS AGED >20 YEARS

A

Risk includes: abdominal obesity, hypertriglyceridemia, low HDL, High BP and high fasting glucose

BMI over 30 is problematic and TGs are more concerning then cholesterol

41
Q

NAFLD association with metabolic syndrome

A

NAFLD seen in 30-100% pts that are Obese (BME>30)

seen in 15-50% with Diabetes

seen in 15-80% with hypertriglyceridemia

42
Q

Non-Alcoholic Fatty Liver Disease increases with:

seen in what pt population:

A
  • Prevalence increases with age
  • Severity of disease (including advanced fibrosis/cirrhosis) increases with age
  • Males > Females
  • Hispanics > Caucasians > African Americans
43
Q

Obesity has been increasing over the years in America leading to ______ being the most common reason for liver transplant

A

NAFLD

44
Q

Most common liver disease in children in US

A

NAFLD:

increaes in prevelance with age

more common in boys

Hispanic > Asian > White > Black

***18% of these kids have NASH

45
Q

•_________ rather than
hypercholesteremia increases risk for NAFLD

A

Hypertriglyceridemia

**• 3-fold greater risk with triglycerides >200

46
Q

Causes of Steatosis and Steatohepatitis

A

Insulin resistance, alcohol, abetalipoproteinemia

meds: Amiodorone, steroids, HAART, Tamoxifen, Diltazem

Nutrition (TPN, Severe Starvation, refeeding syndrome)

Weigth changes; jejunoileal bypass and gastric bypass

47
Q

What is the progression and development of NAFLD; starting with increased oral intake and sedentary life style

A

(possible genetic influence)–> become obese/HTN/Hyperlipidemia:

Lead to Insulin resistance: causing normal–> steatosis

Oxidative stress further affects liver:

steatosis –> steatohepatitis –> cirrhosis

48
Q

What does a fatty liver look like on ultrasound?

On CT?

A

on ultrasound comes out BRIGHT WHITE (fat and nodules)–simple steatosis doesn’ t cause this appearance

On CT liver appears dark (vs light) and enlarged

49
Q

What do we target when treating NAFLD?

A

Treat insulin resistance that is from obesity/HTN/hyperlipidemia

Treat the oxidative stress

prevent pts becoming fat

50
Q

How much do we recommend pts to lose to have improved symtpoms if they have NAFLD

A

Loss of at least 3-5% of body weight necessary
to improve steatosis but up to 10% may be
needed to improve inflammation.

51
Q

2 tx for NASH and their effect on patient?

A

Treat NASH with Pioglitazone or Vitamen EEndpoint: improvement in histology score
(steatosis, inflammation, ballooning degeneration and fibrosis)

reduced transanimase

reduced inflammation

NEITHER reduced fibrosis

52
Q

What tx to patients gain more weight on for TX of NASH

A

Pioglitazone

53
Q

Pioglitazone can be used to treat patients with
________. The majority of patients
that participated in clinical trials were nondiabetic
and long-term safety and efficacy is not
established.

A

biopsy-proven NASH

54
Q

improves liver histology in non-diabetic patients with biopsy-proven NASH and should be considered first-line therapy

A

• Vitamin E at a dose of 800 IU/day

55
Q

vitamin E is not
recommended to treat NASH in what three pt populations

A

diabetic patients, NAFLD without liver biopsy, NASH
cirrhosis or cryptogenic cirrhosis.

GI 2 (12 decks)

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