Gastroenterology 2 Flashcards

1
Q

What are some liver serologcial markers?

What do they indicate?

A

HbsAg: indicates hepatitis B infection

HbcAb:

HbeAg: Indicator of high level HBV

HbeAb or anti HBe: indicator of low level of HBV

Anti- HBc: inficates current or past hepatitis B infection

Anti HBc IgM: usually indicates acute indection, reactivation

Anti- HBs: immunity either from recovery or Hep B infection or vaccine

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2
Q

For suspected hepatitis, what question should you be asking?

A

Route of acquisition

symptoms

alcohol history

risk factoes for co-infection (blood borne virus so tattoos etc)

FHx of hep B or HCC or HIV

Social history- family testing

Examination: stigmata of chronic liver disease (spider naevi, gynocomastia, caput medusae,)

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3
Q

What is the most common vertical transmisison (mother to infant)

A

HBV

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4
Q

What are the way HBV can be transmitted?

A

Vertical transmission (mother to infant)

Horizontal transmission: contaminated blood, needle stick, IVDU, sexual intercourse

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5
Q

HBV is the commonest cause of ______ _____

A

hepatocellular carcinoma

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6
Q

What investigations would you perform for a suspected hepatits patient?

A

FBC- WBC, hb

U & E

LFT- AST ALT, GGT

clotting- shows the liver fucntion

HCV antibody, HIV

Liver screen: liver autoantibodies, immunoglobulins, ferritin

USS- to make sure no secondary pathology (cirrohisos, fatty liver)
Fibroscan (shows the stiffness and scarring of the liver)

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7
Q

HBV- goals of tx

A
  • Improve survival and quality of life by preventing disease progession to:
  • Cirrhosis
  • hepatocellular carincoma
  • death
  • Prevent mother to child transmission
  • Prevent hep B reactivation
  • Reduces HBV DNA to undetected level to reduce complications
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8
Q

Not everyone gets Tx for HBV so what are the indications for getting it?

A
  • based on 3 criteria (HBC DNA levels, ALT, disease severity)
  • HBeAg- positive or negative chronic hepatitis B
  • Patients with cirrhosis, any detectable HBV DNA regardless of ALT level
  • Patients with HBV DNA >20,000 IU/mL and ALT >2x ULN regardless of severity of histological lesion .
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9
Q

Tx- HBV

A
  • Peg interferon (subcute injections)
  • NRTI- oral, tenofovir, entecavir
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10
Q

HBV- prevention

A

Pre exposure

-immunisation with vaccine: routine in some countries. Safe ann effective after 3 injection

, at risk groups in UK: IVDUs, family contacts, MSM, occupation, travel, renal and liver disease. Screening of HCWs performing exposure prine procedures.

Post exposure

Vaccine (and Hep B immunogobluins in some cases): health care workers, babies of mothers with hep B and sexual exposure

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11
Q

Hepatitis D virus (HDV) should be suspected in patients with heptitus _ virus?

A

B

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12
Q

How do you confirm hep D virus

A

Should be by HDV RNA

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13
Q

How is hep C transmitted?

A

Horizonatal transmission: person to person spread via blood, some sexual transmission (MSMs), contaminated needles/syringes and blood products

Vertical transmission

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14
Q

Symptoms for hep c

A

asymptomatic

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15
Q

Chronic infection of hep C leads to

A

cirrhosis and cancer

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16
Q

There is a vaccine available for Hep C

TRUE OR FALSE

A

FALSE- no vaccine available

17
Q

HCV- Tx

A

There are Direct acting Antiviral Agents- Harvoni, Epclusa, Maviret)

  • refer to Hep C ODN (operation delivery network)
  • community clinics (drug and alcohol services, prisons, community pharmacy)
  • oral treatment (8-16 weeks)
18
Q

What factors affect HCV treatment?

A

Genotype

Cirrohosis

Treatment experienced

19
Q

Risk Factors for fatty liver? (NAFLD)

A
  • Alcohol
  • Drugs: Tamoxifen, Amiodarone, Nethotrexate, Corticosteroids, Industrial solvents
  • Metabolic Syndrome (obesity, DM, hypertension)
  • Inherited conditions (abetalipoproteinamemia, lipodystrophy, LAL-D, Wilsons disease)

Nutritional Syndromes ( JI Bypass, TPN, Rapid weight loss)

20
Q

How can you define a metabolic syndrome

A

Any patient with metabolic syndorme can be define as 3 or more of the following:

  • Abdominal obesity
  • raised triglycerides (>1.7mmol/L)
  • Low HDL cholestrol (<1.03mmol/L (male) <1.29mmol/L (female))
  • raised fastinf glucose (>5.6mmol/L) or previously diagnosed Type II DM (insulin resistance)
  • Hypertension (>130/85
21
Q

There are number of conditons that cover NAFLD

What are they?

A

NAS- non alcohlic steaosis

NASH- Non alcoholic steatosis hepatitis

NASH cirrohosis

22
Q

What is NAS?

A

Non- alcoholic steatosis

Macro vesicular steatosis with peropheral nuclear positioning.

Large white spaces=fat lobules which pushes the nuclei

In most patients it is harmless but in rare cases it get cause injury and inflammaiton which progresses into NASH

23
Q

What is NASH?

A

Non alcoholic steatosis hepatitis

mallory bodies, ballooning degeneration, lobular inflammation and perisinusoidal fibrosis

They more severe than NAS. They inflammatory infiltrates in the liver. Blue cells suggest inflammation.

As inflammation progresses it leads to activation of kupffer cells and marcophages due to cytokines. These further lay down collagen ibres which cause fibrous septae or fibrosis.

As the liver cells try to regenerate it becomes more fibrotic and can lead to cirrhosis.

24
Q

What is NASH cirrhosis

A

Non Alcoholic steatosis

May lose typical features of NASH

Not much fat in the liver

25
Q

Presentation for NAFLD/NASH

A

Asymptomatic

Fatigue (consider sleep apnea syndrome)

RUQ discomfort

Hepatomegaly

Stigmata of chronic liver disease

26
Q

What does raised AST and ALT suggest?

A

Hepatic damage

27
Q

A raised ALP on its own without a raised GGT would make you suspicious of?

A

ALP is coming from a non hepatic source such as bone or in pregnant women

28
Q

An AST/ALT ratio of >0.8 suggests….

A

advanced fibrosis

29
Q

Biochemistry of NAFLD

A

LFTs - all elevated

Autoimmune liver screen- positive

Viral serology- rule out hepatitic viruses

High ferritn, iron saturation and ceruloplasmin levels - suggests iron overload/ copper deposition

Alpha 1 antitrypsin-

Lipid profile- elevated

30
Q

If the patient has high ferritin but normal transferrin saturation, what does this rule out?

A

haemochromatosis

31
Q

Imaging in NAFLD

A

USS- detec steatosis if liver fat exceeds 30% of liver volume

MRI liver especially MR spectroscopu and Proton Density fat fraction are very sensitive but not easily available

Liver stiffness and specifically CAP scores can be quite useful in the right setting and for high the negative predictive value of the test results. Checking elasticity.

Liver biopsy is not routinely needed or used to diagnose NAFLD

32
Q

Scores that can risk stratify patients with NAFLD

A

BARD score, NAFLD score, AST/ALT ratio, Liver stiffness, FIB4

33
Q

Management of NAFLD

A
34
Q
A