Liver & Biliary System Flashcards

(71 cards)

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
what are the symptoms or signs of obstructive jaundice
dark urine, pale stools and an itch
26
what is PBC
primary biliary cholangitis - auto-immune disease in which interlobular ducts in liver are destroyed diagnosed with high ALP, often asymptomatic treatments: UDCA, symptomatic treatment
27
what is PSC
primary scleorising cholangitis affects larger ducts within and outside the liver causes hardening and narrowing of bile ducts
28
comparing the 3 types of jaundice
LOOK AT TABLE in notes
29
what are the steps to investigating jaundice
ultrasound, if ducts dilated = CT if ducts not dilated = prehpatic or hepatocellular
30
what are the transaminases
ALT and AST | enzymes that convert protein to energy
31
what is ALP
alkaline phosphatase
32
prothrombin time and liver?
increased if liver damage
33
what is found, LFT wise, in hepatocellular damage?
rise in ALT, and rise in AST more than a rise in ALP
34
what is found, LFT wise, in obstructive damage?
rise in ALT, and rise in ALP more than in AST
35
what are the reasons why ALP is higher in obstructive
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
what is hepatitis
inflammation of the liver
37
what are the symptoms of alcoholic hepatitis and what are the consequences
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
what is chronic hep
inflammation persisting for more than 6 months, but low grade
39
symptoms of chronic hepatitis
fatigue, often none presents with cirrhosis
40
what are the investigations for chronic hepatitis? what are the symptoms that come on in the later stages?
LFT's - abnormal, but mild elevation ALT's later symptoms include encephalopathy, jaundice etc only really picked up through screening
41
what is acute hepatitis and how is it caused
not associated with any liver damage due to viruses or drug overdose
42
symptoms of acute hep
generally unwell jaundice RUQ pain severe: coagulopathy, renal impairment
43
blood test results of acute hep
raised ALT and AST >1000 | high bilirubin
44
what is fulminant hepatitis
hepatitis leading to very acute liver failure (happens quickly and even if you've never had liver problems before) necrosis of liver cells
45
causes of fulminant hep
usually hep A, drug-induced or toxic agents
46
symptoms of fulminant hepatitis
jaundice, pain etc encephalopathy within 28 days poor prognosis = needs transplant urgently
47
what is steatohepatitis
inflammation of liver in association with a fatty liver
48
what are the signs of decompensated liver in steatohepatitis?
variceal bleeding and ascites, jaundice
49
what other virus can cause viral hepatitis
EBV/ glandular fever
50
where is hep A found and how is it spread
faceo-oral spread endemic in the developing world common in childhood and lasts around 12 weeks
51
what are the markers of hepatitis
IgM in acute infection, IgG goes up later
52
how is hep B spread and where is it found
mother to child IVDU unprotected sex africa and asia
53
what are the consequences of hep B and why
liver cancer bc causes changes in DNA liver cirrhosis
54
what hepatitis viruses are we vaccinated against
hep A - everyone | hep B - at risk groups
55
what is the serology of hep B
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
what is chronic hep B
 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
what is the treatment for hep B
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
how is hep c spread and where is it found
locally in NW england blood borne - medical equipment, IVDU, no RF 90% of acute hepC - asymptomatic but increases risk of cirrohosis
59
how do you test and treat hep C
antibodies PCR - if antibody positive, look for RNA of virus, and if not present they have recovered treatment - interferon - ribavarin protease inhibitors
60
what is hep E
identical to hep A may cause severe disease in pregnancy test for IgM and IgG
61
what is hep delta
requires co-infection with hepB, cannot replicate itself but worsens prognosis of hep b Just treat hep b
62
what is liver cirrhosis and what are the 4 main causes
fibrosis of the liver with nodule formation alcoholic liver disease, non-alcoholic fatty liver disease, hep B and hep C
63
what is the 1st way cirrhosis can cause problems and what are the symptoms
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
what is the 2nd way cirrhosis can cause problems and what are the symptoms
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
what is the staging for liver cirrhosis
child-pugh (score out of 15 for severity) | MELD: 3 month prognosis %
66
what is the management for liver cirrhosis
``` sympomatic high protein, low sodium diet spironolactone prophylactic AB propanolol vasopressin analogues, vit k and FFP ```
67
what are the complications of liver cirrhosis and why
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
what is taken into consideration for liver transplant referral
decompensated liver disease after best management and 3 months alcohol abstinence
69
when to offer corticosteroid treatment for alcohol-hep
severe, discriminant function of 32, after treating bleeding and renal problems
70
what are the risks with corticosteroid treatment for alcohol-related hepatitis
improves survival short term -1 month not long term >3 months increases risk of infection
71
what is the CAGE questionnaire
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)