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Phase 2a Peer Teaching > Liver and Friends > Flashcards

Liver and Friends Flashcards

1
Q

name 7 functions of the liver

A

urea cycle

regulation of excess oestrogen

stores glycogen and hydrolyses it into glucose when needed

produces clotting factors except 7

produces albumin

produces bilirubin for bile

protects against infection with the reticuloendothelial system

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2
Q

two weird signs that can occur with liver disease

A

clubbing

dupuytren’s contracture

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3
Q

when is GGT raised and what does it stand for

A

gamma glutamyltransferase

it’s raised in alcoholic liver disease

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4
Q

when is ALP raised and what does it stand for

A

alkaline phosphatase

raised in anything with biliary tree damage

it will also be raised in bone resoprtion like that which occurs in bone mets

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5
Q

when is ALT and AST raised and what does it stand for

A

raised in hepatocyte damage

stand for alanine transaminase and aspartate transaminase

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6
Q

6 things included in an LFT

A

AST

ALT

ALP

GGT

Albumin

Bilirubin

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7
Q

apart from liver symptoms what system symptoms with 1-alpha anti-trysin give you

A

respiratory symptoms (COPD)

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8
Q

haemochromatosis does what to your blood? giving you what characteristic sign

A

it puts excess iron in your blood giving you ‘bronze diabetes’

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9
Q

which is the only viral hepatitis which is not an RNA virus

A

Hep B is a DNA virus the others are RNA viruses

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10
Q

fill in this table

A
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11
Q

what is the most important Ix if you suspect viral hepatitis

A

serology - detecting viral antigens and antibodies

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12
Q

what is anti-HBc and what does its discovery on serology mean

A

total hep B core antibody

it appears at the beginning of acute infection and persists for life

so its presence means previous or ongoing infection

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13
Q

what is IgM anti-HBc and what does its discovery mean

A

this is the IgM against HBV core antigen and indicates recent (<6m) infection

its presence indicates acute infection

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14
Q

what is HBsAg and what does its presence mean

A

it’s the Hep B surface antigen

its presence means that they have acute or chronic hep B infection and they are infectious

this is the antigen used for the HepB vaccine

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15
Q

what is anti-HBs and what does its presence mean

A

it’s antibody against the Hep B surface protein and its presence indicates recovery and immunity from Hep B

this is the antibody that develops in someone who has been vaccinated against Hep B

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16
Q

fill this table in

A
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17
Q

what hepatitis viruses are there vaccines for

A

A and B

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18
Q

what is the treatment for chronic B infection

A

pegylated IFN-a called pegasys

this stimulates an anti-viral state

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19
Q

what is the treatment for chronic Hep C virus

A

SOFOSBUVIR WITH VELPATASVIR

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20
Q

viral hepatitis rhyme?

A
  • A is Acquired by mouth from Anus, is Always cleared Acutely and only ever Appears once
  • E is Even in England and can be Eaten(sausage from pigs), if not always beaten
  • B is Blood-Borne and if not Beaten can Be Bad
  • B and D is BastarDly
  • C is usually Chronic but Can be Cured – at a Cost
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21
Q

why does alcohol cause a fatty liver

A
  • alcohol is converted into acetaldehyde by alcohol dehydrogenase
  • to do this it converts nad+ into NADH
  • as NAD+ decreases and NADH increases it has two effects
    1. NADH tells it to produce more fatty acids
    2. NAD+ loss tells it to stop oxidising fatty acids
  • both of these lead to increased fat production by the liver
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22
Q

appart from increased fat why do you get increased liver damage with alcohol

A
  • ADH produces ROS while converting alcohol to acetaldehyde –> damage DNA and proteins
  • acetaldehyde also binds to compound in the cell inhibiting them
    • these are called acetaldehyde adducts
  • adducts are recognised by neutrophils which damage the hepatocytes
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23
Q

what is a mallory-denk body

A

it is a histological finding in alcoholic hepatitis and NASH

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24
Q

what will your LFT look like in alcoholic liver disease

A

GGT very raised

AST and ALT mildly raised

AST will be more raised than ALT

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25
Q

what will you see on the FBC of someone with alcoholic liver disease

A

they will have macrocytic anaemia

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26
Q

what are two risk factors for NAFLD

A

metabolic syndrome and T2DM

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27
Q

what is metabolic syndrome

A
  • it’s where you have 3 of the 5 following:
    • obesity
    • hyperlipidaemia
    • diabetes
    • hypertension
    • hypertriglyceridemia
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28
Q

what happens, very basically in NAFLD

A
  • some kind of metabolic syndrome causes fat droplets to accumulate in the hepatocytes
  • this causes steatosis
  • as the fat degrades it produces fatty acid radicals which damage the membranes
  • the cells die and the death causes inflammation
  • it’s now Non-Alcoholic SteatoHepatitis (NASH)
  • there’s neutrophil infiltration
  • then stellate cells lay down fibrotic tissue to repair which causes cirrhosis
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29
Q

what are the differences between the LFTs in NASH and alcoholic liver disease

A

in alcoholic fatty liver the ASL:ALT ratio is generally >2

whereas in NASH ALT is generally higher than AST

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30
Q

how is NAFLD diagnosed

A

US, MRI or CT to look for fatty infiltrates

then biopsy to diagnose and assess severity

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31
Q

how much fat is abnormal in the liver

A

>5%

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32
Q

how long is NAFLD reversible and how

A

Steatosis and Steatohepatitis are both reversible by eating less and moving more

once it’s cirrhosis it’s not reversible

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33
Q

what causes PBC

A
  • Autoimmune destruction of cells lining the INTRAHEPATIC bile ducts
  • bile and toxins leak into the parenchymam
  • inflammation
  • fibrosis
  • cirrhosis
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34
Q

three risk factors for PBC

A

female

family history

any extrahepatic autoimmune disease

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35
Q

signs and symptoms of PBC

A

fatigue

pruritis

jaundice

right upper quadrant pain

liver cirrhosis –> ascites, splenomegaly, oesophageal varices, hepatic encephalopathy

hypercholesterolaemia (cholesterol leaks from bile into blood)

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36
Q

diagnosis of PBC

A
  • Imaging to rule out bile duct obstruction
    • US
    • Magnetic Resonance Cholangiopancreatography (MRCP)
    • CT
  • Lab results
    • Antimitochondrial antibodies (AMA)
  • Liver biopsy
    • interlobular duct destruction and bile duct inflammation
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37
Q

PBC treatment

A
  • ursodeoxycholic acid
    • reduces intestinal absorption of cholesterol
  • cholestyramine
    • bile acid sequestrant reduces bile acid absorption in the gut and improves itch
  • ADEK supplementation
  • Corticosteroids like prednisolone
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38
Q

what two diseases is PCS associated with

A

Ulcerative Colitis and Crohn’s

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39
Q

what is the cause of primary sclerosing cholangitis

A
  • T-cells attack and destroy bile duct epithelial cells
  • There’s sclerosis and inflammation of extrahepatic ducts
  • patches of stenosis followed by patches of dilation of the duct give it a beaded appearance
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40
Q

what are the complications of PSC

A

portal hypertension since fibrosis around bile ducts constricts the portal veins and increases pressure

leads to hepatosplenomegaly due to backup of fluid

cirrhosis due to recurrent cycle of inflammation and healing

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41
Q

which cancers does PSC predispose to

A

cholangiocarcinoma

gallbladder calcer

hepatocellular carcinoma

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42
Q

what is Ceruloplasmin and in what condition would it be raised

A

it is the main copper carrying protein in the body and it will be raised in wilson’s

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43
Q

signs and symptoms of PSC

A
  • jaundice
  • RUQ pain
  • weight loss
  • pruritis
  • hepatosplenomegaly
  • dark urine
  • pale stool
  • late: liver failure
    • ascites
    • muscle atrophy
    • incresed clotting time
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44
Q

diagnsosis of PSC

A
  • MRCP or ERCP
    • both show intrahepatic and or/extrahepatic bile duct dilation with multi-focal diffuse strictures
  • LFTs
    • ALP and GGT elevated
  • Serology
    • p-ANCA (perinuclear anti-neutrophil cytoplasmic antibodies)
  • Histology
    • onion skin fibrosis
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45
Q

PSC treatment

A

no effective treatment

treat symptoms and manage complications

immunosuppressants like steroids may work

surgery to transplant liver if they have advanced liver disease

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46
Q

what is the mutation that causes wilson’s disease

A

autosomal recessive mutation in ATP7B gene which is a transport protein active in hepatocytes

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47
Q

what causes wilson’s

A
  • autosomal recessive mutation in ATP7B protein
  • causes reduced copper elimination in the bile
  • and copper accumulation in hepatocytes
  • this leads to hepatocyte damage and copper spilling into the blood
48
Q

what is the key sign of Wilson’s disease

A

Kayser-Fleischer rings in the eye

49
Q

what age does wilson’s present

A

<30

50
Q

signs and symptoms of wilson’s

A
  • those of cirrhosis and portal hypertension
    • jaundice
    • hepatosplenomegaly
    • ascites
    • esophageal varices
  • renal signs
  • parkinsonism
  • depression and personality change
  • kayser-fleischer ring
51
Q

how is wilson’s diagnosed

A
  • Abnormal LFTs
  • high 24hr copper excretion
52
Q

treatment for wilson’s

A
  • chelating agents
    • penicillamine
  • agents that reduce intestinal absorption of copper
    • zinc
  • transplant for advanced liver damage
53
Q

dietary advice for wilson’s

A

less copper (shellfish)

54
Q

what is the mutation in haemochromatosis

A

an autosomal recessive mutation in HFE on chormosome 6

55
Q

can you fill in this table

A
56
Q

what happens in haemochromatosis

A

they absorb way too much iron in the body and it can’t be excreted in the same way

it gets deposited everywhere including skin, liver, heart, joints, pancreas, pituitary gland

57
Q

three important complications of haemochromatosis

A

restrictive cardiomyopathy due to iron deposition

bronze diabetes

arthralgia from pseusdogout

58
Q

what should you suspect in any ascitic patient that suddenly deteriorates

A

spontaneous bacterial peritonitis

59
Q

Ix

A

gene test

serum ferritin

60
Q

treatment for haemochromatosis

A

Desferrioxamine to remove excess iron

reduce iron in the diet

61
Q

what happens in alpha-1- antitrypsin deficiency

A

accumulation of alpha-1-antitrypsin in hepatocytes and lack of it in serum leads to lack of protease inhibition in alveoli causing damage to alveoli and subsequent emphysema

62
Q

what is the mutation in alpha-1-antitrypsin deficiency

A

SERPINA1 on chromosome 14

63
Q

what doe alpha-1-antitrypsin deficiency cause

A

COPD

64
Q

what is the treatment for alpha-1-antitrypsin deficiency

A

manage the COPD

liver transplant is curative

65
Q

what is the definition of cirrhosis

A

normal smooth liver structure becomes distorted, with nodules surrounded by fibrosis, affecting the liver’s synthetic, metabolic and excretory actions

66
Q

what are the three most common risk factors for cirrhosis

A
  • Alcohol misuse
  • Hepatitis B and C infection.
  • Obesity (body mass index of 30 kg/m2 or more) or type 2 diabetes

but any chronic liver disease can cause it eventually

67
Q

what is the difference between compensated and decompensated liver cirrhosis

A
  • compensated:
    • liver can still function and there are few/no noticeable symptoms
  • decompensated
    • liver damaged to the point that it cannot function adequately and there are overt clinical complications
      • jaundice
      • ascites
      • variceal haemorrhage
      • hepatic encephalopathy
    • decompensated liver cirrhosis is the same as chronic liver failure
68
Q

what is Chronic decompensated hepatic failure

A

it’s liver cirrhosis at the point of decompensation

69
Q

how does chronic liver failure/decompensated liver cirrhosis present

A

jaundice

ascites

variceal haemorrhage secondary to portal hypertension

hepatic encephalopathy

70
Q

how do you treat hepatic encephalopathy

A

mannitol and lactulose

71
Q

where do portal vein collaterals form

A

oesophagus - oesophaeal varices

gastric - caput medusae

hemorrhoidal veins - hemorrhoids

72
Q

why do you get portal hypertension

A
  • endothelin-1 production is increased in cirrhosis
    • this leads to more vasoconstriction
  • notric oxide production is reduced in cirrhosis
    • this leads to less vasodilation
  • once above 5mmHg it’s portal hypertension
73
Q

what is a pre-hepatic cause of portal hypertension

A

portal vein thrombosis

74
Q

name two causes of post hepatic portal hypertension

A

constrictive pericarditis

IVC obstruction

75
Q

Ix for oesophageal varices

A

Upper GI endoscopy

76
Q

what is the treatment for ruptured oesophageal varices

A
  • Surgical
    • immediate band ligation
  • Fluid resuscitation
77
Q

treatment for oesophageal varices before they rupture

A
  • Medical to reduce portal pressure
    • BB to reduce CO
    • Terlipressin - analogue of ADH - it’s vasoconstrictive and for some reason helps
    • nitrate
  • surgical
    • trans jugular intrahepatic portosystemic shunt (TIPSS)
78
Q

why do you get ascites in liver disease

A
  • fibrosis in the liver compresses sinusoids (combined portal vein branch and hepatic artery branch flowing towards central vein within a lobule)
  • this causes fluid to be pushed into the peritoneal cavity and the spleen causing ascites and splenomegaly
79
Q

what is the difference between transudate and exudate

A

<11g/L of protein is transudate

>11g/L of protein is exudate

80
Q

two signs of ascites

A

distended abdomen

shifting dullness

81
Q

Ix of ascites

A
  • ascitic tap
    • M,C and S
    • cytology
    • protein
82
Q

treatment of ascites

A

fluid and salt restriction

spironolactone

treat underlying cause

83
Q

what bugs commonly cause SBP

A

e.coli

klebsiella

enterococcus

84
Q

what is the initial management for suspected SBP and what is the prophylaxis that is sometimes given to high risk ascitic patients

A

initial management: ceftioxime

prophylaxis: ciprofloxacin

85
Q

Dx of hepatocellular carcinoma

A

CT/MRI liver

Biopsy

Bloods: clotting abnormalities, deranged LFTs

86
Q

HCC treatment

A

surgical resection

radiofrequency ablation

chemo

TACE

87
Q

what is TACE

A

Transarterial chemoembolization (TACE) is a specific type of chemoembolization that blocks the hepatic artery to treat liver cancer

88
Q

where are secondary liver tumours likely to have come from

A

GI

breast

bronchus

89
Q

what is the management of paracetamol overdose

A
  • activated charcoal within 1 hr of ingested substance
  • N-acetyl-cysteine if above the theraputic threshold
    • works by replenishing glutathione which allows reactive intermediates of paracetamol to become non-toxic
90
Q

what are the time periods of liver failure and what do they mean

A
  • within 8 weeks: fulminant hepatic failure (FHF)
  • 8-26 weeks: subacute
  • 6 months: chronic
91
Q

treatment for hepatic encephalopathy

A

lactulose and mannitol

92
Q

fill this in

A
93
Q

what are the risk factors for gallstones

A

fat

female

forty

fertile

94
Q

why do you get biliary colic

A

gallstone is impacted in the gallbladder neck temporarily and is dislodged back into the gallbladder

95
Q

what is acute cholecystitis

A

when the gallstone is stuck in the GALLBLADDER NECK and causes inflammation

96
Q

presentation of acute cholecystitis

A

RUQ pain

fever

nausea

vomiting

Murphy’s sign

97
Q

what is murphey’s sign

A

asking the patient to breathe out and then gently placing the hand below the costal margin on the right side at the mid-clavicular line (the approximate location of the gallbladder). The patient is then instructed to inspire (breathe in). Normally, during inspiration, the abdominalcontents are pushed downward as the diaphragm moves down (and lungs expand). If the patient stops breathing in (as the gallbladder is tender and, in moving downward, comes in contact with the examiner’s fingers) and winces with a “catch” in breath, the test is considered positive. In order for the test to be considered positive, the same maneuver must not elicit pain when performed on the left side.

98
Q

when is murphey’s sign classically positive and negative

A
  • positive
    • cholecystitis
  • negative
    • choledocholithiasis
    • pyelonephritis
    • ascending cholangitis
99
Q

Ix of acute cholecystitis

A

USS abdo

abdo exam

LFTs to exclude liver/bile duct pathology

100
Q

treatment for acute cholecystitis

A

laporoscopic cholecystectomy

supportive with analgesia and fluids as needed

101
Q

what is ascending cholangitis

A

gallstone is stuck in the common bile duct and obstructs the flow of bile

the flow of bile is normally what prevents the bacteria from ascending the duct

infection occurs usually with E.coli, Klebsiella or enterococcus (group D strep)

102
Q

fill in the blanks

A
103
Q

what are the features of ascending cholangitis

A
  • charcot’s triad:
    • RUQ pain
    • fever
    • Jaundice
  • Reynold’s pentad:
    • hypotension
    • confusion
104
Q
A
105
Q

what is ERCP

A

endoscopic retrograde cholangio pancreatography

106
Q

Ix and treatment of ascending cholangitis

A
  • Ix
    • USS abdo
    • MRCP to locate stone
  • Tx
    • ERCP to remove stone
107
Q

name some causes of pancreatitis

A

G – Gallstones

E - Ethanol (alcohol!)

T - Trauma

S - Steroids

M - Mumps

A - Autoimmune - e.g. SLE

S - Scorpion bites (rare!)

H - Hypercalcaemia, hypothermia, hyperlipidaemia

E - ERCP

D - Drugs - e.g. azathioprine, metronidazole, tetracycline, furosemide

108
Q

two important signs in pancreatitis and what they mean

A
  • bruised flanks - Grey-Turners
  • bruised umbilicus - Cullen’s
  • they mean it’s late stage and haemorrhagic
109
Q

clinical features of pancreatitis

A
  • Abdominal pain that radiates to the back
  • Nausea and vomiting
  • Fever
  • Abdominal tenderness
  • Distension
110
Q

Ix for pancreatitis

A
  • Amylase or Lipase
  • CT abdo
111
Q

3 complications of pancreatitis

A

Sepsis

DIC

ARDS

112
Q

which tissues does PSC affect

A

intra and extrahepatic bile ducts

113
Q

fill in this table

A
114
Q

painless jaundice with weight loss is_________

A

cancer of the head of the pancreas

115
Q

cholangiocarcinoma can cause what?

A

Primary sclerosing cholangitis

Phase 2a Peer Teaching (10 decks)

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