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Med Year 3 > Liver & Biliary System > Flashcards

Liver & Biliary System Flashcards

1
Q

what is delireum tremens, how is it treated and what do you do first when they present

A

acute confusional state when someone who drinks daily suddenly stops drinking

benzodiazapenes

ABCDE

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2
Q

what is biliary colic and how is it treated

A

RUQ pain, due to gallstones blocking cystic or CB duct which goes away when stone moves into SI
colic = pain occuring after eating a fatty meal which causes gall bladder contraction

surgical removal of gallbladder

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3
Q

what is painless jaundice

A

obstructive cause of jaundice but with the absence of abdominal pain

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4
Q

risk factors for liver and pancreatic diseases

A 
alcohol intake
drugs, both prescription and non
blood transfusions
tattoos
travel 
unprotected sex (hep)
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5
Q

what are the 5 f’s (risk factors) for gall stones

A

female, fat, fair (american), forty, fertile (pregnant or on combined pill)

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6
Q

what is the most common cancer of the GI system

A

carcinoma of pancreas head, excluded via imaging tests in patients over 40 who have painless, obstructive jaundice

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7
Q

what marker do you use to test for liver cancer

A

AFP - alpha fetoprotein

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8
Q

what is the hormone used to contract the gallbladder

A

cholecystikinin

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9
Q

what does conjugation mean and where does it happen

A

making bilirubin water soluble by adding glucoronic acid, in hepatocytes in liver

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10
Q

where is bilirubin made from

A

breakdown of Hb by biliverdin

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11
Q

when would you get high levels of unconjugated bilirubin

A

in high breakdown of RBC, haemolysis or gilbert syndrome

may be physiological or pathological but is toxic

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12
Q

when would you get high levels of conjugated bilirubin and why (conjugated hyperbilrubinaemia)

A

causes are obstructive jaundice, aka post–hepatic jaundice

non toxic but ALWAYS pathological

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13
Q

why do you get pale stools and dark urine

A

because bilirubin doesn’t get into bowel, isn’t metabolised –> low levels of uro and sterobilinogen = makes stool brown

get dark urine cos conjugated BR = water soluble and goes into kidneys and hence into urine

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14
Q

what is jaundice?

A

yellowing of skin, sclera and mucous membranes due to high levels of bilirubin in the body

becomes clinically apparent at >50uM/L

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15
Q

what are the other symtpoms of jaundice

A

scratches from pruritus, evidence of weight loss and troisier’s node (left supraclavicular node enlargement)

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16
Q

what are the tests when someone presents with jaundice?

A
  1. transabdominal USS - check for dilated bile ducts and look at liver
  2. CT, contrast and non-contrast: look at pancreatic ducts
  3. ERCP - look for gallstones (in bile ducts)
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17
Q

what is haemolytic jaundice / pre-hepatic and what are the causes

A

abnormal RBC, due to sickle cell, drug reactions, hypersplenism or incompatible blood transfusion

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18
Q

what is the pathophys of haemolytic jaundice

A

liver compensates by increasing conjugated bilirubin output

= stools are NOT pale

there is excess unconjugated bile in plasma but LFT’s are normal

uncojugated bilirubin cannot be excreted in urine and hence no bilirubin in urine

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19
Q

what is hepatocellular jaundice

A

compromised liver not excreting bilirubin even though it is formed at a normal rate

high levels of unconjugated bilirubin, but hepatic injury may also prevent conjugated bilirubin from reaching the gut

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20
Q

what are the causes of HC jaundice

A

common: alcoholic liver cirrohosis or hepatitis, drug induced (paracetamol, co-amoxiclav, methotrexate), viral hep

autoimmune liver disease, wilsons disease, haemachromatosis

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21
Q

what is neonatal jaundice

A

common condition in newborns, usually resolved in 2 weeks. happens bc RBC constantly broken down and liver not fully formed to get rid of bilirubin

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22
Q

what is kernicterus

A

clinical features of untreated hyperbilirubinaemia

unconjugated bilirubin can cross the blood-brain barrier and is toxic to neural tissue - may be treated with phototherapy or exchange transfusion

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23
Q

what is obstructive or post hepatic jaundice

A

blockage of flow of bile through bile ducts or intra and extrahepatic ducts

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24
Q

what are the causes of obstructive jaundice

A

gallstones, cholecystitis (inflammation of gall bladder), carcinoma of pancreatic head, chronic pancreatitis

PBC, PSC, cholangiocarcinoma

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25
Q

what are the symptoms or signs of obstructive jaundice

A

dark urine, pale stools and an itch

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26
Q

what is PBC

A

primary biliary cholangitis - auto-immune disease in which interlobular ducts in liver are destroyed

diagnosed with high ALP, often asymptomatic

treatments: UDCA, symptomatic treatment

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27
Q

what is PSC

A

primary scleorising cholangitis

affects larger ducts within and outside the liver

causes hardening and narrowing of bile ducts

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28
Q

comparing the 3 types of jaundice

A

LOOK AT TABLE in notes

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29
Q

what are the steps to investigating jaundice

A

ultrasound, if ducts dilated = CT

if ducts not dilated = prehpatic or hepatocellular

30
Q

what are the transaminases

A

ALT and AST

enzymes that convert protein to energy

31
Q

what is ALP

A

alkaline phosphatase

32
Q

prothrombin time and liver?

A

increased if liver damage

33
Q

what is found, LFT wise, in hepatocellular damage?

A

rise in ALT, and rise in AST more than a rise in ALP

34
Q

what is found, LFT wise, in obstructive damage?

A

rise in ALT, and rise in ALP more than in AST

35
Q

what are the reasons why ALP is higher in obstructive

A

ALP found in hepatic bile duct cells so damage involving biliary tract causes ALP containing cells to be damaged = raised
AST and ALT are found in normal hepatic cells not bile duct cells

36
Q

what is hepatitis

A

inflammation of the liver

37
Q

what are the symptoms of alcoholic hepatitis and what are the consequences

A

jaundice, swollen and tender liver
vomiting

  • possible to go back to a normal liver with abstinence

can result in acute, chronic or fulminant hepatitis

repeated attacks = cirrhosis

38
Q

what is chronic hep

A

inflammation persisting for more than 6 months, but low grade

39
Q

symptoms of chronic hepatitis

A

fatigue, often none

presents with cirrhosis

40
Q

what are the investigations for chronic hepatitis?

what are the symptoms that come on in the later stages?

A

LFT’s - abnormal, but mild elevation ALT’s

later symptoms include encephalopathy, jaundice etc

only really picked up through screening

41
Q

what is acute hepatitis and how is it caused

A

not associated with any liver damage

due to viruses or drug overdose

42
Q

symptoms of acute hep

A

generally unwell
jaundice
RUQ pain

severe: coagulopathy, renal impairment

43
Q

blood test results of acute hep

A

raised ALT and AST >1000

high bilirubin

44
Q

what is fulminant hepatitis

A

hepatitis leading to very acute liver failure (happens quickly and even if you’ve never had liver problems before)

necrosis of liver cells

45
Q

causes of fulminant hep

A

usually hep A, drug-induced or toxic agents

46
Q

symptoms of fulminant hepatitis

A

jaundice, pain etc
encephalopathy within 28 days

poor prognosis = needs transplant urgently

47
Q

what is steatohepatitis

A

inflammation of liver in association with a fatty liver

48
Q

what are the signs of decompensated liver in steatohepatitis?

A

variceal bleeding and ascites, jaundice

49
Q

what other virus can cause viral hepatitis

A

EBV/ glandular fever

50
Q

where is hep A found and how is it spread

A

faceo-oral spread
endemic in the developing world
common in childhood and lasts around 12 weeks

51
Q

what are the markers of hepatitis

A

IgM in acute infection, IgG goes up later

52
Q

how is hep B spread and where is it found

A

mother to child
IVDU
unprotected sex

africa and asia

53
Q

what are the consequences of hep B and why

A

liver cancer bc causes changes in DNA

liver cirrhosis

54
Q

what hepatitis viruses are we vaccinated against

A

hep A - everyone

hep B - at risk groups

55
Q

what is the serology of hep B

A

IgM = core

surface antigen HBsAG - goes up quickly and then decreases after 24 weeks

hence if surface antigen negative but antibody positive = immunised or prev exposure

56
Q

what is chronic hep B

A

 Presence of surface antigen for greater than 6 months
 Immunotolerant phase: E antigen positive
• High viral levels = infectious
• Normal LFTs
• Few liver problems
 Immunoreactant phase: E antigen negative
• Low viral levels = less infectious
• ALT raised
• Often fibrotic/cirrhotic

57
Q

what is the treatment for hep B

A

acute - not necessary

chronic - uncurable but treatable

anti-virals: nucleotide analogues which directly inhibit viral replication - tenofovir etc

interferon - immune stimulation. 48 week course; stimulates IS to develop long-term immune response for hepb

given to E antigen positive patients

58
Q

how is hep c spread and where is it found

A

locally in NW england
blood borne - medical equipment, IVDU, no RF

90% of acute hepC - asymptomatic but increases risk of cirrohosis

59
Q

how do you test and treat hep C

A

antibodies
PCR - if antibody positive, look for RNA of virus, and if not present they have recovered

treatment - interferon - ribavarin
protease inhibitors

60
Q

what is hep E

A

identical to hep A
may cause severe disease in pregnancy
test for IgM and IgG

61
Q

what is hep delta

A

requires co-infection with hepB, cannot replicate itself but worsens prognosis of hep b

Just treat hep b

62
Q

what is liver cirrhosis and what are the 4 main causes

A

fibrosis of the liver with nodule formation

alcoholic liver disease, non-alcoholic fatty liver disease, hep B and hep C

63
Q

what is the 1st way cirrhosis can cause problems and what are the symptoms

A

portal hypertension - venous blood supply: increased back-flow or pressure

  • varices: oesophageal
  • piles
  • ascites - salt and water retention due to HT
  • encephalopathy - toxins not removed by liver
  • renal failure

*EASIER TO TREAT by managing HT

64
Q

what is the 2nd way cirrhosis can cause problems and what are the symptoms

A

loss of function

  • jaundice
  • coagulopathy - loss of ability to form clotting factors
  • decreased drug metabolism - decreased hormone metabolism = increased levels of oestrogen can lead to gynacomastea but can also present with spider naevi, palmar erythemia etc
  • increased sepsis level bc liver manages immune system
65
Q

what is the staging for liver cirrhosis

A

child-pugh (score out of 15 for severity)

MELD: 3 month prognosis %

66
Q

what is the management for liver cirrhosis

A 
sympomatic
high protein, low sodium diet
spironolactone
prophylactic AB
propanolol
vasopressin analogues, vit k and FFP
67
Q

what are the complications of liver cirrhosis and why

A

hepatorenal - HT in portal system = dilation of portal BV = less blood to kidney = hypotension in kidney = renin-angiotensin system = vasoconstriction so starvation of blood

hepatic encephalopathy - ammonia build up in blood

68
Q

what is taken into consideration for liver transplant referral

A

decompensated liver disease after best management and 3 months alcohol abstinence

69
Q

when to offer corticosteroid treatment for alcohol-hep

A

severe, discriminant function of 32, after treating bleeding and renal problems

70
Q

what are the risks with corticosteroid treatment for alcohol-related hepatitis

A

improves survival short term -1 month

not long term >3 months
increases risk of infection

71
Q

what is the CAGE questionnaire

A

have you ever felt….

  • you need to CUT down drinking
  • ANNOYED by people critisicing your drinking
  • felt GUILTY about drinking
  • EYE-OPENER (need to drink when you wake up to cure a hangover)

Med Year 3 (25 decks)

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