Non viral hepatitis Flashcards

1
Q

In what patients should you suspect fulminant wilson’s disease?

A

In patient who has Neuro + Liver Involvement 🡪 must always suspect Wilson

Eg: Cachexia/tremor with depression/hallucination 🡪 suspect Wilson

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2
Q

What do you treat Wilson’s disease with?

A

Treatment with penicillamine, then Zinc

Penicillamine is a chelating agent that binds to excess Cu & removes it from bloodstream

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3
Q

What is a screening test for Wilson’s?

A

Ceruloplasmin

  • A slightly low Ceruloplasmin 🡪 not v specific for Wilson
  • But an almost undetectable level of Ceruloplasmin 🡪 V specific for Wilson

Ceruloplasmin is the major copper-carrying protein in the blood, and in addition plays a role in iron metabolism

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4
Q

What are the clinical features of ischaemic hepatitis?

A
  • AST and ALT increases >1000
  • Increased LDH (sign of cell death)
  • Delayed increased in Total BR
  • A/W hypoxia, decreased MAP
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5
Q

Autoimmune hepatitis is thought to be caused by an environmental trigger in a genetically susceptible individual.

There is increased frequency of ___________. Familial clustering has been reported and there is a strong family history of extra-hepatic autoimmune diseases e.g. ________________.

Target of injury in AIH is the _______________.

Majority of patients with AIH are identified in a bimodal age distribution

  • Either in their late teenage years to early 20s or in the range of 40-50 years
  • Strong ___________
A

HLA-DR3 and DR4

Hashimoto’s thyroiditis, RA, celiac disease, Sjogren’s;

periportal hepatocyte (zone I);

female predisposition

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6
Q

In what groups of patients are you suspicious of AI hepatitis?

A

A female patient p/w cirrhosis / deranged LFTs.

With FHx or PMHx of AI Dz eg: UC, Thyroiditis, Sjogren’s, Arthritis, Haemolytic anemia

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7
Q

Autoimmune hepatitis

Type 1 AIH

  • Most common
  • Finding of ________________ in about 80% of individuals

Type II AIH

  • Uncommon, disproportionately affects ______________
  • Negative ANA, ASMA
  • Positive ______________

If no positive antibodies (10-20% of patients) 🡪 liver biopsy (will see _____________)

A

ANA and anti-smooth muscle antibodies (ASMA IgG4);

children and young adults (teens to 20s);

anti LKM (liver kidney microsome), anti-LC1;

interface hepatitis

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8
Q

What are the clinical features of autoimmune hepatitis?

*Note: Autoimmune liver disease is a diagnosis of exclusion. Viruses, drugs/alcohol, metabolic causes and genetics causes should be ruled out before a diagnosis of AILD is made

A
  1. Acute severe hepatitis associated with systemic symptoms and jaundice
    - Malaise, rash, arthralgias
    - Hepatomegaly
    - Ascites, jaundice, encephalopathy
  2. Elevation in liver enzymes which are incidentally discovered in an asymptomatic patient on routine laboratory testing
  3. Acute flare on background autoimmune hepatitis
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9
Q

What is the management of autoimmune hepatitis?

A

Immunosuppression therapy

  • Prednisolone (induction)
  • Azathioprine (maintenance)
  • Other agents: Cyclosporin, MM, Tracolimus

Other agents: ciclosporin, mycophenolate mofetil and tacrolimus

Screen for other autoimmune diseases: TFT (Hashimoto), RF (RA)

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10
Q

[Alcoholic hepatitis]

Lies on a spectrum of alcoholic liver diseases, ranging from:

  • _________ (all alcoholics): always reversible if alcohol stopped
  • ______________ (~30% alcoholics): inflammation; usually reversible if EtOH stopped
  • _________ (10-15% of alcoholics): potentially reversible

Pathophysiology

  • Ethanol oxidation to acetaldehyde reduces NAD+ to NADH. Increased NADH decreases __________ to the liver, impairing __________ and leading to accumulation of fatty acids in triglycerides in the liver
  • Alcohol metabolism: Relative hypoxia in liver zone __________ > zone____________
  • Hepatocyte necrosis and hepatic vein sclerosis
A

Fatty liver;

Alcoholic hepatitis;

Cirrhosis;

ATP supply;

lipolysis;

III (near central veins; poorly oxygenated) ;

I (around portal tracts, where oxygenated blood enters)

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11
Q

What are the histological features of alcoholic hepatitis?

A

Ballooned hepatocytes often containing Mallory bodies (intracellular eosinophilic aggregates of cytokeratins), characteristically surrounded by neutrophils.

Chicken-wire fibrosis: network of intralobular connective tissue surround venules

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12
Q

What are the clinical features of alcoholic hepatitis?

A

History of recent alcohol binge on a background of chronic alcoholism

Severity can vary from mild liver impairment to acute liver failure

  • Jaundice & coagulopathy
  • Hepatomegaly, RUQ pain, low-grade fever (severe)
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13
Q

What are the investigations to be conducted for alcoholic hepatitis?

A

AST/ALT (both usually 100-300 )

Classically AST:ALT > 2:1, normal ALP, raised GGT

Raised TW

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14
Q

What is the management of alcoholic hepatitis?

A

Supportive management

  • Glucose and thiamine supplementation
  • Glucose b/c patient usually malnutritioned
  • Thiamine to prevent development of WE & KP

Caution with drugs metabolized by the liver

Alcohol cessation and abstinence

Maddrey Discriminant Factor for prognosis

  • Discriminant function = (4.6 x [prothrombin time- control pt]) + serum bilirubin
  • > 32 = Poor prognosis 🡪 give prednisolone / pentoxifylline

Mortality at 1 month: 50%

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15
Q

NFALD

  • Largely benign course of disease
  • ____________ on liver biopsy
  • _______________ on fibroscan
  • Commonly a/w: __________________
A

Minimal or no inflammation ;

No fibrosis, not cirrhotic (since no inflammation to trigger fibrosis);

T2DM, obesity, metabolic syndrome, insulin resistance, HTN

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16
Q

What is the presentation of a patient with NAFLD?

A

Presentation: have few or no symptoms

  • May complain of fatigue, malaise, and dull right-upper-quadrant abdominal discomfort
  • Mild jaundice may be noticed, although this is rare
  • More commonly NAFLD is diagnosed following abnormal liver function tests during routine blood tests
17
Q

Non-alcoholic Steatohepatitis (NASH)

  • Subset of NAFLD with a more sinister prognosis (>10-fold increase of liver-related death)
  • Presence of inflammation on liver biopsy:_____________, __________, ___________
  • > than 10-fold increased risk of liver related death and 2x CVS mortality
A

ballooning degeneration;

necroapoptosis;

fibrosis

18
Q

How do you differentiated NASH from NFALD?

A

Platelet – if <160 🡪 suggestive of NASH

AST:ALT

  • AST:ALT >1 🡪 likely NASH
  • AST:ALT <1 🡪 likely NAFLD

Raised MCV suggests CLD

Fibroscan

19
Q

What is the management of NAFLD (or: NAFL / NASH?

A

Gradual weight loss the mainstay of treatment

  • Aim to lose 0.5-1kg/week as rapid weight loss can worsen the liver disease
  • Goal to lose at least 10% of total body weight

Improving insulin sensitivity via diet, exercise and lifestyle modification

Alcohol avoidance

Aggressive risk factor identification and modification i.e. DM, HTN