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ALD Flashcards

1
Q

Which is the main enzyme that converts alcohol to acetdehyde?

A

Alcohol dehydrogenase
• Cytochrome P450 2E1 (CYP2E1)also converts alcohol to acetaldehyde, and this enzyme tends to be up-regulated in heavy alcohol consumers

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2
Q

Acetaldehyde is a carcinogen- true or false?

A

TRUE- contributes to the development of HCC independent of effects from cirrhosis

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3
Q

AFLD- what happens

A

Triglycerides accumulate amongst liver tissue as a result from:

  • Reduction in fat export due to a decrease in liver fatty acid oxidation and lipoprotein reduction
  • Increased input of lipids to hepatic tissue - increased peripheral lipolysis and triglyceride synthesis
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4
Q

Alcoholic hepatitis features

A

Combined liver statosis and inflammation with focal regions of liver necrosis

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5
Q

Cirrhosis features

A

Progression of hepatic tissue inflammation, degeneration and regeneration- excessives fibrogenesis and scarring

  • Liver tissue is replaced by excess extra-cellular matrix and collagen
  • Reduces functional capcity of liver
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6
Q

Clinical features of ALD

NON SPECIFIC

A
  • Fatigue
    • Malaise
    • Abdominal pain
    • Anorexia
    • Weakness
    • Nausea and/or vomiting
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7
Q

Alcoholic hepatitis clinical features

A
  • Jaundice
  • RUQ pain
  • Hepatomegaly - enlarged with smooth edge (irregular and hard in cirrhosis or metastatic)
  • Palmar erythema
  • Peripheral oedema
  • Clubbing
  • Dupuytren’s contracture- present in 30% with ALD
    Pruritis- ITCHING
    cholestasis leading to bile salt deposition in skin
    Xanthomas
  • Spider naevi
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8
Q

Oestrogen damage in liver disease- why?

Estrogenic effects?

A

Liver metabolises oestrogen- progressive liver damage and oestrogen rises
• Gynaecomastiaand testicular atrophy (in males)
• Loss of body hair
• Amenorrhoea (in females)
Loss of libido

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9
Q

Portal hypertension features

A
  • Ascites(within 10 years of the diagnosis of cirrhosis, >50% of patients will develop this)
    • Dilated veins (e.g. caput medusae)
    • Variceal bleeding and haemorrhage
    • Splenomegaly
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10
Q

Ratio of AST:ALT in alcoholic hepatitis

A

• Ratio of AST:ALT is normally >2, a ratio of >3 is strongly suggestive of acute alcoholic hepatitis

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11
Q

Serumm GGT is raised in?

A

Chronic heavy alcohol consumption

Not specific to ALD- may be raised in other patholgies - obesity, NAFLD, biliary obstruction and HCC

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12
Q

ALP raised in?

A

Cholestatic pattern of liver injury

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13
Q

Four markers raised in comparison of each other in liver disease
ALD, AST, ALT, GGT

A

ALD- AST and ALT will be raised much more compared to the ALP and or GGT levels

In AFLD- solitary mild increase in AST and ALT

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14
Q

Conjugated and non-conjugated bilirubin fraction in liver disease and haemolysis/gilbert’s syndrome

A

○ Liver disease (many types, including ALD) will have elevatedconjugatedbilirubin
○ Haemolysis or Gilbert’s syndrome will have elevatednon-conjugatedbilirubin, more than 90% of total bilirubin will be unconjugated

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15
Q

Albumin in liver disease

A

Reduced serum albumin

Liver synthesises albumin- low levels indicated diminished syntheetic function

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16
Q

Serum prothrombin time, INR in liver disease

A

Elevated PT and INR due to diminished synthetic function of liver

17
Q

Liver ultrasound

A
  • May be used to differentiateabnormal liver function testscaused by other pathologies e.g. hepatocellular carcinoma, cholestasis, liver mass/abscess
    • If known ALD andcirrhosis, is useful to screen for hepatocellular carcinoma development
18
Q

Liver biopsy- two ways of performing it

A

Percutaneous and Transgular

19
Q

Histological findings of alcoholic hepatitis

A

Mallory-Denk bodies, neutrophil-rich inflammation with necrosis, hepatocyte ballooning

20
Q

Serum ceruloplasmin levels in ALD and Wilson’s

A

○ May be normal or raised in ALD

Low inWilson’s disease

21
Q

Serum iron, transferrin and ferritin checked to rule out which disorder?

A

Haemochromatosis

22
Q

Alpha 1 antitrypsin

A

• Alpha-1 antitrypsin levels

○ To rule out alpha-1 antitrypsin deficiency

23
Q

Drugs for alcohol withdrawal?

A

Benzodiazepines- diazepam

Quick-acting benzodiazepine- lorazepam for alcohol withdrawal seizures

24
Q

First-line treatment for delirium tremens

A

Oral lorazepam

25
Q

Acute alcoholic Hepatitis therapy

A

Glucocorticoids- prednisolone
• Pentoxifylline can be used as an alternative to glucocorticoids if they are contraindicated (e.g. hepatitis B viral infection, tuberculosis, other serious infection)

26
Q

End stage ALD treatment

A

Transplant but has to be alcohol free >6 months

27
Q

Hepatic encephalopathy features

A 
• Confusion
	• Drowsiness
	• Hyperventilation
	• Asterixis
Fetor hepaticus
28
Q

Encephalopathy features

A

Supportive care plus lactulose

29
Q

Portal hypertension features

A

Occurs once liver cirrhosis is established
Blood vessels are blocked due to severe liver fibrosis, a high pressure develops in the portal venous system
Leads to varices- ascites, splenomegaly,

30
Q

How to manage Portal Hypertension

A

TIPSS- Transjugular intrahepatic portal-systemic shunt if there is acute bleeding, particularly if gastric varices are present

31
Q

Hepato-renal syndrome

A
  • As a result of portal hypertension, there is widespread splanchnic vasodilation
    • This leads to a reduction in the effective circulating volume, which can reduce the blood flow to the kidneys, compromising the renal system and potentially leading to a life-threatening acute kidney failure
32
Q

HCC risk and screening

A
  • Once liver cirrhosis is established, there is a significantly increased risk in development of hepatocellular carcinoma
    • Hepatic ultrasound should be undertaken serially approximately every 6 months to yearly to screen for liver cancer development

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