Gastro important Flashcards
drugs that can cause drug induced liver injury
Paracetamol
Antibiotics (Augmentin, flucloxacillin, erythromycin, septrin, TB drugs)
CNS drugs (Chlorpromazine, Carbamazepine, Valproate, Paroxetine)
Immunosuppressants
Analgesics (Diclofenac)
Gastrointestinal drugs (PPIs)
Dietary supplements
Drugs apparently not involved in DILI
NSAIDs other than Diclofenac Beta blockers Hormone replacement therapy (HRT) ACE inhibitors Thiazides Calcium channel blockers
Paracetamol overdose treatment
N acetyl cysteine
Hep A transmission + diagnosis
contaminated food/water
Anti-HAV IgM shows acute infection. Usually full recovery
Hep B transmission
mother-child during birth, sexual contact, sharing needles
histological findings of liver cirrhosis
regenerative nodules surrounded with fibrotic tissue and collagen
causes of liver cirrhosis
- alcohol abuse
- hep B/C
- Haemachromatosis, Wilson’s, Alpha-1-Antitrypsin deficiency
- Budd-chiari
- Primary billiary cholangitis, primary schlerosing cholangitis, autoimmune hep,
- Drugs such as amiodarone, methyldopa, methotrexate
liver cirrhosis symptoms
late symptoms incude jaundice, priritus, ascites, confusion (due to hepatic encephalopathy- complication of cirrhosis), easy bruising (reduced clotting factor production)
diagnosis of cirrhosis
liver biopsy = confirms
Elevated AST>ALT,
low platelets + low WBC
what is Primary biliary cholangitis?
Autoimmune disease where T cells attack the cells lining the bile duct, leading to bile leaking between the cells into the interstitial space and then into blood and other liver cells –> leads to inflammation of the bile ducts and eventually cirrhosis
antibodies associated with primary biliary cholangitis
AMA (antimitochondrial antibodies)
presentation of primary biliary cholangitis
- patients often asymptomatic and then increased ALP is incidentally found
- Jaundice (bile and conjugated bilirubin leak into blood)
- skin pigmentation
- Xanthelasma
- Xanthoma
- Priritus
Lethary/sleepiness/pruiritus - May have joint pain and arthropathy (may be connected to other autoimmune disorders like RA!)
investigations for primary billiary cholangitis
- Anti-michondrial antibodies (AMA)
- Increased ALP and GGT
treatment for primary billiary cholangitis
- symptomatic: codeine phosphate for diarrhoea, osteoporosis prevention, colestyramine (relives pruritus by binding to cholesterol so it can be excreted more easily)
- fat soluble vitamin prophylaxis (A,D,K)
- monitoring and possible liver transplant
alcohol withdrawal treatment
Chlordiazepoxide
treatment for alcoholic hepatitis
- stop drinking + treat withdrawal
- corticosteroids
- Vit D and thiamine
what is haemochromatosis
inherited disorder where increased intestinal absorption of
iron leads to iron deposition in joints, liver, heart,
pancreas, pituitary glands, adrenals and skin
symptoms of haemochromatosis
- “bronze” skin pigmentation
- erectile dysfunction/fatigue/arthralgia (esp of hands) in early disease
- hepatomegaly, cirrhosis
- could have heart failure or hypogonadism as secondary consequences to deposition
haemachromatosis diagnosis
- high transferrin saturation (>50%)
- raised ferritin and iron
- low total iron binding capacity (TIBC)
- liver biopsy- PERL’S STAIN diagnostic
- genetic testing shows C282Y and H63D mutations
Haemachromatosis treatment
- venesection first line
- deferoxamine second line (binds to free iron in the blood and makes it easier to excrete in urine - decreases iron load in blood)
symptoms Wilson’s disease + transporting agent causing the disorder?
- liver disease- hepatitis, cirrhosis etc
- mood/personality changes
- reduced memory/delusions
- KAYSER-FLEISHER RINGS around Iris
disorder of transporting ATPase called ATP7B
Treatment of Wilson’s disease
- PENICILLAMINE- copper chelating agent (binds to copper, making it easier to excrete in the urine)
- zinc + ammonium tetrathiomolybdate- reduces copper reabsorption in urine so more copper can be excreted
- liver transplant
diseases caused by A1AT deficiency
- emphysema in lung (most common condition in adults)
- cirrhosis and hepatocellular carcinoma in liver
investigations for A1AT deficiency
- serum A1AT low
- on biopsy: PAS (periodic acid schiff) positive
- phenotyping
treatment of A1AT deficiency
- IV A1AT pooled from human plasma
- smoking cessation
- liver/lung transplant
liver failure presentation
- jaundice
- liver flap
- fetor hepaticus (breath smells sweet)
- constructional apraxia (inability to copy 3D drawings)
liver failure causes
- Drugs: paracetamol, halothane, isoniazid
- alcohol
- viral hep A/B
- acute fatty liver of pregnancy
liver failure investigations
- raised prothombin time and INR
