Zeros to Finals Flashcards
what are the 3 progressive steps to alcoholic liver disease?
- alcohol related fatty liver
- alcoholic hepatitis
- cirrhosis
what does alcoholic hepatitis actually mean?
drinking alcohol over a long period of time causes inflammation in the liver sites (binge drinking is associated with the same effect)
what is the basic definition of cirrhosis?
when your liver is made up of scar tissue rather than healthy liver tissue
what are the alcohol consumption reccomendations?
- no more than 14 units a week
- spread evenly over 3 days or more
- not more than 5 units in a single day
which investigation results indicate alcohol misuse/ overuse / use?
- FBC shows raised MCV (as chronic heavy drinking increases the size of RBCs)
- elevated ALT, AST and GGT
- reduced PT (due to reduced synthetic function of the liver - reduced production of clotting factors)
- U+Es may be derranged in hepatorenal syndrome
general management for alcohol misuse?
- nutritional support with vitamins (esp thiamine) and a high protein diet
what are the symptoms (based on hours) of alcohol withdrawal?
- 6-12 hours = tremor, sweating, headache, craving + anxiety
- 12-24 hours = hallucinations
- 24-48 hours = seizures
- 24-72 hours = delerium tremens
what is delerium tremens and is it dangerous?
- mortality of 35% if untreated
- alcohol stimulates GABA receptors in the brain (GABA receptors have a relaxing effect on the rest of the brain)
- alcohol also inhibits glutamate receptors (also known as NMDA receptors) having a further inhibitory effect on the electrical activity of the brain
- chronic alcohol use results in the GABA system being up-regulated + the glutamate system being down-regulated to balance the effects of the alcohol
- when alcohol is removed from the system, GABA under-functions and glutamate over functions = extreme excitability of the brain with excessive adrenergic activity
how do you manage alcohol withdrawal?
- CIWA-Ar used to score patient on their symptoms
- chlordiazepoxide = a benzodiazepine used to combat effects of alcohol withdrawal
- IV high dose vitamin B (parabinex) followed by thiamine (used to prevent wernicke-korsakoff syndrome)
what is wernicke-korsakoff syndrome?
- alcohol excess leads to thiamine (vit B) deficiency
- thiamine is poorly absorbed in the presence of alcohol
- wernicke’s encelopathy comes before korsakoffs syndrome
what are the features of WK syndrome?
W - confusion, oculomotor disturbances + ataxia
K - confabulation + behavioural changes
what are the 4 most common causes of liver cirrhosis?
- alcoholic liver disease
- non alcoholic fatty liver disease
- hepatitis B
- hepatitis C
which blood test results suggest liver cirrhosis?
- reduced albumin (because of dilution)
- increased PT (synthetic function worse)
- hypobatraemia (indicated fluid retention in severe liver disease)
which scoring system is used for cirrhosis?
child-pugh
what is the management of cirrhosis?
- regular meals every 2-3 hours
- low sodium diet to minimise fluid retention
- high protein and high calorie diet (esp if underweight)
- avoid alcohol
how does portal hypertension / varices come about?
- the portal vein comes from the SMV and the splenic vein + delivers blood to the liver
- liver cirrhosis increases the resistance of blood flow in the liver
- there is increased back pressure into the portal system (portal hypertension)
- this causes the vessels at the sites where the portal system anastomoses with the systemic venous system to become swollen and torurous (varices)
where do varices appear? (4)
- gastro-oesophageal junction
- ileocaecal junction
- rectum
- anteiror abdominal wall via the umbilical vein (caput medusae)
basic treatment of stable varices?
- propranolol (reduces portal hypertension)
- elastic band ligation of varices
- TIPS (wire inserted under xray guidance into the juguular vein, down the vena cava and into the liver via the hepatic vein) to put in a stent
basic treatment of bleeding varices?
- vasopressin (terlipressin) causes vasoconstriction and slows bleeding
- vitamin K + fresh frozen plasma
- broad spec antibiotics
how does ascites come about?
- increased pressure in the portal system causes fluid to leak out of the capillaries in the liver and bowel into the peritoneal cavity –> reduction in blood pressure entering the kidneys –> release renin –> increased aldosterone relesae
how to treat ascites?
spironolactone + paracentesis
what is hepatic encephalopathy?
- a build up of toxins (ammonia) which affect the brain
- ammonia is produced by intestinal bacteria when they break down toxins
- functional impairment of the liver cells prevents then from metabolising ammonia into harmless waste products
how to treat encephalopathy?
laxatives (lactulose) + antibiotics (rifampixin)
what are the 4 stages of NAFLD
- nonalcoholic fatty liver disease
- NASH
- fibrosis
- cirrhosis
when someone presents with abnormal LFTs you should screen for which conditions?
- Hep B and C
- autoantibodies
- immunoglobulins
- caeruloplamsin (wilsons)
- alpha 1 anti trypsin deficiency
- haemachromatosis
first line investigation for NAFLD
US
what are the causes of hepatitis (inflammation of the liver) ?
- alcoholic hepatitis
- NAFLD
- viral hepatitis
- autoimmune hepatitis
- drug induced hepatitis (paracetamol overdose)
liver function test results which suggest heptitis?
- high AST + ALT (less of a rise in ALP)
- high bilirubin
discuss Hepatitis A
- most common worldwide but rare in UK
- RNA virus
- faecal-oral
- nausea, vomiting, anorexia + jaundice
- cholestasis, dark urine + pale stools
- resolves in 1-3 months
discuss hep B
- DNA virus
- bodily fluids eg sexual intercourse / sharing needles + mother to child
- recover in 2 months
surface antigen HBsAG =
active infection
E antigen HBeAg =
marker of viral replication and implies high infectivity
core antibodies HBcAb =
implies past or current infection
surface antibody HBsAB =
implies vaccination of current infection
hepatitis B virus DNA HBV DNA =
direct count of the viral load
discuss hepatitis C
- RNA virus
- spread via blood/body fluids
- curable with direct acting antiviral medications
discuss hepatitis D
- RNA virus
- can only survive in patients who also have hep B infection
discuss hepatitis E
- RNA
- faecal oral route
- rare in UK
what is autoimmune hepatitis?
- unknown cause
- T cells recognise liver as being harmful and alert the rest of the immune system to attack these cells
what are the 2 types of autoimmune hepatitis?
type 1 - adults
type 2 - children
describe type 1 autoimmune hepatitis?
women in 40s/50s present around/ after menopause with fatigue and features of liver disease
describe type 2 autoimmune hepatitis?
patients in their teenage years / early twenties present with acute hepatitis and high transaminases and jaundice
type 1 autoimmune hepatitis antibodies
ANA
anti-actin
anti-SLA-LP
type 2 autoimmune hepatitis antibodies
anti-LKM1
- anti-LC1
how to treat autoimmune hepatitis
prednisolone / azathioprine
why is caeruloplasmin investigated for wilson’s disease?
it is the protein which carries copper in the blood and will be decreased
what does alpha 1 antitrypsin deficiency result in
an excess of protease enzymes that attack the liver and lung tissue and cause liver cirrhosis and lung disease
what is primary billary cirrhosis?
- immune system attacks the small bile ducts
- causes obstruction of the outflow of bile = cholestasis
- build up of bile acids, bilirubin + cholesterol (jaundice, itching + xanthelasma)
- bile acids are responsible for digesting fats (lack of these = greasy stools)
what are the autoantibodies associated with PBC?
- anti-mitochondrial antibodies
- anti-nuclear antibodies
what is the treatment for PBC?
- ursodeoxycholic acid (reduces intestinal absorption of cholesterol)
- cholestyramine (bile acid sequestrate - it binds to bile acids to prevent absorption in the gut and can help with pruritis)
what is primary sclerosing cholangitis?
- intrahepatic / extrahepatic ducts become strictures and fibrotic = obstruction to the flow of bile out of the liver and intestines
which condition is primary sclerosing cholangitis associated with?
UC
who gets primary sclerosing cholangitis?
- males
- 30-40
- UC
GS investigation for primary sclerosing cholangitis?
MRCP
what are the 2 main types of primary liver cancer?
hepatocellular carcinoma (80%) cholangiocarcinoma (20%)
which condition is cholangiocarcinoma associated with?
primary sclerosing cholangitis
what is used as a marker for hepatocellular carcinoma?
Alpha-feroprotein
what is used as a marker for cholangiocarcinoma?
CA19-9
which scoring system is used for suspected upper GI bleeding?
glasgow-blatchford score
is urea high or low in an upper GI bleed?
high because blood in the GI tract gets broken down by the acid and digestive enzymes - one of the breakdown products is urea and this urea is then absorbed in the intestines
which scoring system is used for patients who have had an endoscopy?
rockall score
it provides a risk of rebleeding and mortality
- it takes into account age, features of shock, co-morbidities, cause of bleeding (eg mallory weiss tear) etc
mnemonic for chrons NEST
no blood or mucus
entire GI tract
skip lesions on endoscopy
terminal ileum most affected and transmural (full thickness) inflammation
smoking is a risk factor (dont set the nest on fire)
mnemonic for UC - UCCLOSEUP
continuous inflammation limited to colon and rectum only superficial mucosa affected smoking is protective excrete blood and mucus use aminosalicylates primary sclerosing cholangitis
what is the criteria for diagnosing IBS?
EXCLUDE OTHER PATHOLOGY
- normal FBC, ESR and CRP blood tests
- faecal calprotectin negative to exclude IBD
- negative anti TTG antibodies
- cancer excluded
what are the symptoms of IBS?
abdominal pain / discomfort relived on opening bowels or associated with a change in bowel habbits
first line treatment in IBS?
- loperamide
- amitriptyline
