Gastroenterology Flashcards
how is bilirubin produced in liver?
conjugated
clinical signs of conjugated hyperbilirubinaemia
jaundice
dark urine
pale stool
itch
what causes conjugated hyperbilirubinaemia
post-hepatic obstruction
causes of obstructive jaundice (5)
common: gallstones (biliary colic and cholecystitis/chalngitis), carcinoma of head of pancreas
uncommon: sclerosing cholangitis, cholangiocarcinoma, chronic pancreatitis
causes of hepatocellular jaundice
common: alcoholic hepatitis or cirrhosis, viral hepatitis, drug induced, NASH
uncommon: autoimmune liver disease, haemochromatosis, Wilson’s Disease
most likely diagnosis if rise in ALT, AST»_space; rise in alkaline phosphatase (ALP)
hepatocelullar damage
most likely diagnosis if rise in ALT, AST «_space;rise in alkaline phosphatase (ALP)
obstructive cause
organs of production of AST
liver (mitochondrial enzyme), heart, muscle, kidney and brain
ALT:AST ratio in disease
- viral hepatitis: ALT>AST
- viral hepatitis + cirrhosis: AST>ALT and ratio >1
- alcoholic liver disease and steastohepatitis: AST>ALT
- liver disease w/out cirrhosis (alcohol and obesity most common cause): AST>ALT
organs of production of alkaline phosphatase (ALP)
hepatic canalicular and sinusoidal membranes
bone
intestine
placenta
serum levels of ALP in intracellular and extracellular cholestatic disease
increased
if GGT abnormal, ALP presumed to come from liver
gamma-glumayl transpeptidase activation and serum levels
increased activity with drugs (phenytoin, warfarin and rifampicin) and alcohol
levels of alpha- fetoproteins in liver disease
raised in hepatocellular carcinoma
increased in pregnancy and regenerative liver tissue with hepatitis, chronic liver disease and teratomas
what is an alcohol unit?
10ml or 8g of pure alcohol
acute confusional state from alcohol withdrawal
delirium tremens: untreated can result in seizures and death
heme breakdown
heme –> (heme oxygenase)
biliverdin –> (biliverdin reductase)
bilirubin
by phagocytosis
what is CAGE
- have you ever attempted to CUT down on drinking
- do you ever get ANNOYED when people complain about your drinking
- do you ever feel GUILTY about things you have done while drinking
- do you ever need a drink to get going in the morning (EYE OPENER)
bilirubin excretion
conjugated bilirubin –> (bacteria) urobilinogen (unconjugated and colourless) –> stercobilin (brown) or urobilin (yellow)
increase unconjugated bilirubin cause
increase breakdown of RBC, Gilbert’s syndrome, haemolysis
causes of jaundice?
- prehepatic: haemolysis (i.e. sick cell) (unconjugated)
- hepatic: liver failure
- post hepatic: obstructive (pale stools, dark nine, itch)
def hepatitis
liver inflammation
def cirrhosis
fibrosis of the liver
nodule formation
symptoms of acute hepatitis
unwell
jaundice
RUQ pain
confusion
coagulopathy (bruising)
symptoms of chronic hepatitis
often none
fatigue
low grade fever
def fulminant hepatitis
ACUTE hepatitis with liver failure
dvlpt of encephalopathy within 28 days of jaundice
blood test results in acute hepatitis
raised ALT/AST (>1000)
high bilirubin
(in severe cases):
coagulopathy
renal impairment
complications of cirrhosis
-loss of function:
jaundice (heme breakdown)
coagulopathy (clotting)
decreased drug metabolism (sedatives: benzos and opiates)
decreased hormone metabolism (increased levels of oestrogen)
increased sepsis (decreased immune)
-portal hypertension: varices (oesophageal, caput medusa, piles) ascites encephalopathy (ammonia) hepatorenal syndrome
normal venous portal pressure and portal pressure in portal hypertension
normal: 5-8 mmHg
in portal hypertension: 10-12 mmHg
symptoms present with decreased hormone metabolism (increased oestrogen)
erythema spider nevi gynocomastia loss of secondary body hair shrinking external genitalia
causes of cirrhosis
hazardous alcohol chronic hep B and C autoimmune liver disease haemachromatosis Wilson's disease chronic obstruction
why do you get leuconychia with liver disease
pale nails due to decreased albumin
alcoholic hepatitis symptoms and signs
jaundice
large tender liver
vomitting (feeling ill: not eating or drinking)
what must be the plasma concentration of bilirubin for jaundice to be clinically apparent
50 microM/L
how is bile released and how much is released in a day from liver?
CCK
vagal
–> response to food
500-1000 ml/day
composition of bile
- 98% water
- HCO3
- bilirubin
- bile salts/acids (derived from cholesterol)
- metabolites of hormones and drugs
- heavy metal ions
conjugation of bilirubin
in hepatocyte:
- protein bound and conjugated with glucuronic acid (by glucuronyl transferase enzyme)
- -> glucuronyl transferase renders it water soluble
causes of haemolytic jaundice (prehepatic)
- RBC abnormality (ie sickle cell)
- incompatible blood transfusion
- drug reaction
- hypersplenism
biochemistry in haemolytic jaundice
- liver function normal
- glucuronyl transferase saturated
- increase conjugated bilirubin output
- increase unconjugated bilirubin in plasma
hepatocellular jaundice causes
- congenital (neonatal)
- infection (viral hep)
- cirrhosis (alcohol or NASH (steatohepatitis))
- damage due to toxins or drugs
biochemistry in hepatocellular jaundice
- increase unconjugated and conjugated bilirubin
- may be decrease of conjugated bilirubin in gut (due to hepatocellular fibrosis)
- elevated ALT
- mild raised ALP
def kernicterus
build-up of bilirubin in the brain (especially in neonates): bile pigment deposition in basal ganglia: permanent brain damage
Qs to ask with jaundice for symptoms
- pain
- duration
- itching
- colour of stools and urine
obstructive jaundice causes
- obstruction of bile duct by stone
- obstruction of bile duct by tumour (i.e. head of the pancreas)
- intra-hepatic cholestasis
biochemistry of obstructive jaundice
- normal liver function
- raised plasma bilirubin and conjugated bilirubin
- raised ALP
Qs to ask in jaundice in social history
- drug and alcohol
- cigarette use (pancreatic cancer)
- foreign travel
- sexual history (hep B)
jaundice and examination
- sclera and skin
- scratches (pruritus)
- evidence of weight loss (thenar wasting)
- troisier’s node (malignancy)
Prognosis of hep A
99% recovery
1% Fulminant hepatitis: transplant or death
Epidemiology of hep A
Spread, countries, duration, incubation
Faecal-oral spreadable
Dvlping countries
12/52 duration
4-6 weeks incubation
Hep B
spread, endemic, complications
Blood, sex, vertical (mother to child)
Africa and Asia
Liver cancer
Factors determining progression of acute hepatitis B to chronic infection
-age:
<1yo: 90% chronic
1-5 yo: 30% chronic
>5 yo: 1-% chronic
- immunosuppression (ie HIV)
- route of infection
- genotype
Hep B cirrhosis prognosis
Determined by:
- Rate of fibrosis progression (stage and grade)
- Viral load
What is Wilson’s disease + symptoms
Autosomal recessive condition characterised by toxic accumulation of copper in liver and brain
Symptoms: neurological: tremor, dementia, dyskinesia, dysarthria
Liver: cirrhosis, hepatitis
Kayser-Fleischer rings (eyes)
Renal tubular acidosis
Haemolysis
Blue nails
What is Rovsing’s sign?
Pushing the colon in a anti peristalsis direction in the left iliac fossa to illicit pain in the right iliac fossa
Sign of appendicitis
Diagnosis of Wilson’s disease
Reduced serum caeruloplasmin
Reduced serum copper
Increased 24h urinary copper excretion
What is Wernicke-Korsakoff syndrome( cause and symptoms)
Wernicke’s encephalopathy: triad of mental confusion, ataxia and ophthalmoplegia
Korsakoff’s syndrome: late manifestation when Wernicke’s encephalopathy has not been treated
Thiamine deficiency (alcohol, chronic subdural haematoma, hype remedies gravidarium, thyrotoxiscosis, spread of cancers, log term dialysis, congestive heart failure
Def ophthalmoplegia
Paralysis/weakness of one or more occulomotor muscles
Could be myotonic or neuropathic
Def hyperemesis gravidarium
Pregnancy complication: severe nausea, vomiting, fatigue, dehydration, weight loss
Goes beyond the 12th week of regnant (up to he 20th week)
def odynophagia
pain on swallowing
def halitosis
bad breath
what is delirium tremens
acute confusional state which results when sudden alcohol withdrawal in chronic alcohol intake
untreated: seizures and death
management of acute alcohol withdrawal
- benzodiazepine or carbamazepine
- clomethiazole (alternative to benzodiazepine or carbamazepine)
- info about local alcohol support services
-for delirium tremens: oral lorazepam (or parenteral lorazepam or haloperidol)
difference between acute and chronic hepatitis
inflammation persisting > 6 months
natural history of acute hepatitis
3 possibilities:
- recovery
- fulminant hepatitis (death or liver transplant)
- chronic hepatits –> increase fibrosis –> cirrhosis
def of steatohepatitis
inflammation in the liver in association with fatty infiltration
signs of decompensated liver disease
jaundice ascites encephalopathy vatical bleeding small liver easily bruising spontaneous bacterial peritonitis collateral veins in the abdomen \+stigmata of liver disease
management of alcohol related liver disease
- liver transplant (if decompensated liver disease after best management and 3 months abstinence from alcohol)
- corticosteroids
- nutritional support
main causes of cirrhosis
alcohol abuse
hep B and C
NAFLD and NASH
types of neonatal jaundice
- unconjugated hyperbilirubinaemia: potentially toxic (penetration through blood brain barrier), may be pathological or physiological (glucuronyl transferase not at optimal level)
- conjugated hyperbilirubinaemia: non toxic, always pathological