Liver - ALD, NAFLD, Hepatitis, Haemochromatosis, Wilsons disease, Ascities, Acute liver failure 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
-enhanced liver fibrosis blood test to assess for fibrosis
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
For acute ALD => pred (use Maddrey’s discriminant function to assess who will benefit)
Hep A, E
-transmission, type of infection
-presentation, diagnosis
-management
-vaccinations
ACUTE ONLY
Fecal oral transmission
A 1 month incubation
E 1-2 month
-E pork
Hepatic 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/CLD, hepatocellular carcinoma
-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
-normally, intestinal absorption of Fe increased when deficient
-however, intestinal absorption of Fe is always high, leading to overaccumulation
Transferrin - carries Fe in blood
Ferritin - Fe stores, but also high in inflammatory states
TIBC or Tsats - measure of the amount of transferrin in blood, the capacity to carry Fe
Asymptomatic
Early symptoms
-fatigue, erectile dysfunction, hand arthralgia
Reversible
-dilated cardiomyopathy
-bronze skin
Irreversible
-cirrhosis, DM
-hypogonadotrophic hypogonadism
-arthritis
Haemochromatosis
-diagnosis, investigation
1st line
-High transferrin saturation - transferrin carrying a lot of Fe
-High ferritin but can be normal in early stages - 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
-monitor response with ferritin and Tsats
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
Ascities
-types and possible causes
-management
Serum albumin-ascities gradient = serum albumin - ascites albumin
Serum albumin higher (11g/L) - portal HTN (increased resistance and pressure forces fluid out)
-cirrhosis/ALD/ALF/liver mets/portal vein thrombosis
-RHF, constrictive pericarditis
Serum albumin lower (U11g/L) - extrahepatic source
-nephrotic syndrome, severe malnutrition
-pancreatitis
-bowel obstruction
-serositis
Reduce Na intake
May need fluid restriction
Spironolactone - reduce hyperaldosteronism
If tense => ascitic tap + albumin to reduce post-tap circulatory dysfunction
Prophylactic ABx (cipro)
TIPS if suitable
Cirrhosis
-diagnosis
Fibroscan (transient elastography)
-US probe to assess stiffness of liver
Acute liver failure
-pathophysiology
-presentation
Rapid onset of hepatocellular dysfunction => systemic complications
Causes
-paracetamol OD
-alcohol
-viral hepatitis (A,B)
-acute fatty liver of pregnancy
Presentation
-jaundice
-high PT (liver problem, clotting takes longer)
-low albumin
-hepatic enceph
-renal failure (hepatorenal syndrome)
