Gastroenterology 2 Flashcards
What are some liver serologcial markers?
What do they indicate?
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
For suspected hepatitis, what question should you be asking?
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,)
What is the most common vertical transmisison (mother to infant)
HBV
What are the way HBV can be transmitted?
Vertical transmission (mother to infant)
Horizontal transmission: contaminated blood, needle stick, IVDU, sexual intercourse
HBV is the commonest cause of ______ _____
hepatocellular carcinoma
What investigations would you perform for a suspected hepatits patient?
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)
HBV- goals of tx
- 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
Not everyone gets Tx for HBV so what are the indications for getting it?
- 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 .
Tx- HBV
- Peg interferon (subcute injections)
- NRTI- oral, tenofovir, entecavir
HBV- prevention
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
Hepatitis D virus (HDV) should be suspected in patients with heptitus _ virus?
B
How do you confirm hep D virus
Should be by HDV RNA
How is hep C transmitted?
Horizonatal transmission: person to person spread via blood, some sexual transmission (MSMs), contaminated needles/syringes and blood products
Vertical transmission
Symptoms for hep c
asymptomatic
Chronic infection of hep C leads to
cirrhosis and cancer
There is a vaccine available for Hep C
TRUE OR FALSE
FALSE- no vaccine available
HCV- Tx
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)
What factors affect HCV treatment?
Genotype
Cirrohosis
Treatment experienced
Risk Factors for fatty liver? (NAFLD)
- 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)
How can you define a metabolic syndrome
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
There are number of conditons that cover NAFLD
What are they?
NAS- non alcohlic steaosis
NASH- Non alcoholic steatosis hepatitis
NASH cirrohosis
What is NAS?
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
What is NASH?
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.
What is NASH cirrhosis
Non Alcoholic steatosis
May lose typical features of NASH
Not much fat in the liver
