Liver: Hepatitis, NAFLD, ALD, Haemochromatosis, Wilsons, Flashcards
Tests in a liver screen
FBCs
INR => increased
U&E => impact on kidneys
LFTs => impact on liver
Lipids
USS, Dopplers => imaging of abnormalities
Immunology
- autoantibodies => AI hepatitis (ANA, smooth muscle, endomyseal, mitochondrial)
- antibodies => Hep A AB, Hep B s Ag, AB, Hep C AB
Chemistry
- ferritin
- copper, caeruloplasmin
NAFLD and ALD
- presentation
- investigations to differentiate between them
- management
NAFLD - obesity related
-ALT higher than AST
ALD - alcohol related
-AST higher than ALT
Fatty liver - asymptomatic
Hepatitis, fibrosis - RUQ pain, fatigue, weight loss
Cirrhosis (NOT REVERSIBLE) - jaundice, itch, ascities, edema
If reversible => weight loss/alcohol cessation
If irreversible => supportive
Hep A, E
- transmission, type of infection
- presentation, diagnosis
- management
- vaccinations
ACUTE ONLY
Fecal oral transmission
-E pork
Cholestatic LFT, HAV or HEV IgM/IgG
Supportive treatment
Hep A vaccination
- IVDU, gay men
- CLD
- Occupational/travel risk
Hep B, C
- transmission, type of infection
- presentation, diagnosis
- management
IVDU, unprotected sex, childbirth
Acute - symptomatic
Chronic - asymptomatic until late stages
-cirrhosis, hepatocellular carcinoma, CLD
-Hep B => high risk of Hep D (HDV RNA found)
B - more likely to be acute
-HBsAG
C - more likely to be chronic
-HCV RNA, vvv high ALT
Antiviral treatment
Hepatitis symptoms
Fever N+V, loss of appetite Hepatmegaly Jaundice, itch RUQ pain Dark urine, pale stool
Hepatitis B serology markers
HBs Ag - current infection (takes 6months to rise to detectable levels)
HBs IgG - vaccinated/cured
HBe Ag - high viral replication
HBe Ab - low viral replication
Core AB - persists after infection
-IgM - acute infection/viral reactivation
Hep B serology findings for
- current infection
- past cured infection
- past vaccination
- chronic infection
Current
- HBs Ag
- HBc AB (IgM)
- HBe Ag
Past cured infection
- HBs AB (6months after infection and falls)
- HBc AB (IgM falls)
- HBe AB
Past vaccination
-HBs IgG
Chronic
- HBsAg
- HBc AB (no IgM)
- HBe Ag
Haemochromatosis
- genetics
- presentation
AR - C6 HFE gene => too much Fe absorbed which accumulates in the body
Asymptomatic
Early symptoms
-fatigue, erectile dysfunction, hand arthralgia
Reversible
- dilated cardiomyopathy
- bronze skin
Irreversible
- cirrhosis, DM
- hypogonadotrophic hypogonadism
- arthritis
Haemochromatosis
-diagnosis, investigations
1st line
- High transferrin saturation - transferrin carrying a lot of Fe
- High ferritin - needed to store Fe in tissues
Definitive - HFE genetic test
Assessing severity
- LFTs, biopsy - cirrhosis
- Echo, ECG - dilated cardiomyopathy
- fasting BG - T2DM
- sex hormones - hypohypogonadism
Haemochromatosis
-management
Conservative
- Avoid VitC, Fe supplements
- CLD - avoid alcohol
Definitive
1st line - phlebotomy
-stimulate RBC production with Fe already stored in body
2nd line - deferoxamine
Wilsons disease
-presentation, pathophysiology
AR ATP7B gene C13 => too much absorbed, not enough excreted => excess copper deposition in tissue
Brain
- basal ganglia degeneration
- speech, behaviour, psychiatric issues
- asterixis, chorea, dementia, parkinsonism
Liver - ceruloplasmin normally transports copper in serum but cannot
-copper overloaded liver => hepatitis, cirrhosis
Cornea
-Kayser Fleischer rings
Wilsons disease
- diagnosis, investigations
- management
Clinical diagnosis made on findings
Slit lamp - Kayser Fleischer rings
LFTs - hepatocellular picture
Liver biopsy - high hepatic copper conc
Head CT/MRI - basal ganglia involvement
Low ceruloplasmin, total serum copper (most is bound to CP)
High urine copper - increased free Cu from damaged liver cells
1st line - penicilamine
