Liver and Friends Flashcards
(115 cards)
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
2
Q
two weird signs that can occur with liver disease
A
clubbing
dupuytren’s contracture
3
Q
when is GGT raised and what does it stand for
A
gamma glutamyltransferase
it’s raised in alcoholic liver disease
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
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
6
Q
6 things included in an LFT
A
AST
ALT
ALP
GGT
Albumin
Bilirubin
7
Q
apart from liver symptoms what system symptoms with 1-alpha anti-trysin give you
A
respiratory symptoms (COPD)
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’
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
10
Q
fill in this table
A
11
Q
what is the most important Ix if you suspect viral hepatitis
A
serology - detecting viral antigens and antibodies
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
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
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
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
16
Q
fill this table in
A
17
Q
what hepatitis viruses are there vaccines for
A
A and B
18
Q
what is the treatment for chronic B infection
A
pegylated IFN-a called pegasys
this stimulates an anti-viral state
19
Q
what is the treatment for chronic Hep C virus
A
SOFOSBUVIR WITH VELPATASVIR
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
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
- NADH tells it to produce more fatty acids
- NAD+ loss tells it to stop oxidising fatty acids
- both of these lead to increased fat production by the liver
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
23
Q
what is a mallory-denk body
A
it is a histological finding in alcoholic hepatitis and NASH
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
25
what will you see on the FBC of someone with alcoholic liver disease
they will have macrocytic anaemia
26
what are two risk factors for NAFLD
metabolic syndrome and T2DM
27
what is metabolic syndrome
* it's where you have 3 of the 5 following:
* obesity
* hyperlipidaemia
* diabetes
* hypertension
* hypertriglyceridemia
28
what happens, very basically in NAFLD
* 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
29
what are the differences between the LFTs in NASH and alcoholic liver disease
in alcoholic fatty liver the ASL:ALT ratio is generally \>2
whereas in NASH ALT is generally higher than AST
30
how is NAFLD diagnosed
US, MRI or CT to look for fatty infiltrates
then biopsy to diagnose and assess severity
31
how much fat is abnormal in the liver
\>5%
32
how long is NAFLD reversible and how
Steatosis and Steatohepatitis are both reversible by eating less and moving more
once it's cirrhosis it's not reversible
33
what causes PBC
* Autoimmune destruction of cells lining the INTRAHEPATIC bile ducts
* bile and toxins leak into the parenchymam
* inflammation
* fibrosis
* cirrhosis
34
three risk factors for PBC
female
family history
any extrahepatic autoimmune disease
35
signs and symptoms of PBC
fatigue
pruritis
jaundice
right upper quadrant pain
liver cirrhosis --\> ascites, splenomegaly, oesophageal varices, hepatic encephalopathy
hypercholesterolaemia (cholesterol leaks from bile into blood)
36
diagnosis of PBC
* 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
37
PBC treatment
* 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
38
what two diseases is PCS associated with
Ulcerative Colitis and Crohn's
39
what is the cause of primary sclerosing cholangitis
* 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
40
what are the complications of PSC
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
41
which cancers does PSC predispose to
cholangiocarcinoma
gallbladder calcer
hepatocellular carcinoma
42
what is Ceruloplasmin and in what condition would it be raised
it is the main copper carrying protein in the body and it will be raised in wilson's
43
signs and symptoms of PSC
* jaundice
* RUQ pain
* weight loss
* pruritis
* hepatosplenomegaly
* dark urine
* pale stool
* late: liver failure
* ascites
* muscle atrophy
* incresed clotting time
44
diagnsosis of PSC
* 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
45
PSC treatment
no effective treatment
treat symptoms and manage complications
immunosuppressants like steroids may work
surgery to transplant liver if they have advanced liver disease
46
what is the mutation that causes wilson's disease
autosomal recessive mutation in ATP7B gene which is a transport protein active in hepatocytes
47
what causes wilson's
* 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
what is the key sign of Wilson's disease
Kayser-Fleischer rings in the eye
49
what age does wilson's present
\<30
50
signs and symptoms of wilson's
* those of cirrhosis and portal hypertension
* jaundice
* hepatosplenomegaly
* ascites
* esophageal varices
* renal signs
* parkinsonism
* depression and personality change
* kayser-fleischer ring
51
how is wilson's diagnosed
* Abnormal LFTs
* high 24hr copper excretion
52
treatment for wilson's
* chelating agents
* penicillamine
* agents that reduce intestinal absorption of copper
* zinc
* transplant for advanced liver damage
53
dietary advice for wilson's
less copper (shellfish)
54
what is the mutation in haemochromatosis
an autosomal recessive mutation in HFE on chormosome 6
55
can you fill in this table
56
what happens in haemochromatosis
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
three important complications of haemochromatosis
restrictive cardiomyopathy due to iron deposition
bronze diabetes
arthralgia from pseusdogout
58
what should you suspect in any ascitic patient that suddenly deteriorates
spontaneous bacterial peritonitis
59
Ix
gene test
serum ferritin
60
treatment for haemochromatosis
Desferrioxamine to remove excess iron
reduce iron in the diet
61
what happens in alpha-1- antitrypsin deficiency
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
what is the mutation in alpha-1-antitrypsin deficiency
SERPINA1 on chromosome 14
63
what doe alpha-1-antitrypsin deficiency cause
COPD
64
what is the treatment for alpha-1-antitrypsin deficiency
manage the COPD
liver transplant is curative
65
what is the definition of cirrhosis
normal smooth liver structure becomes distorted, with nodules surrounded by fibrosis, affecting the liver's synthetic, metabolic and excretory actions
66
what are the three most common risk factors for cirrhosis
* 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
what is the difference between compensated and decompensated liver cirrhosis
* 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
what is Chronic decompensated hepatic failure
it's liver cirrhosis at the point of decompensation
69
how does chronic liver failure/decompensated liver cirrhosis present
jaundice
ascites
variceal haemorrhage secondary to portal hypertension
hepatic encephalopathy
70
how do you treat hepatic encephalopathy
mannitol and lactulose
71
where do portal vein collaterals form
oesophagus - oesophaeal varices
gastric - caput medusae
hemorrhoidal veins - hemorrhoids
72
why do you get portal hypertension
* 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
what is a pre-hepatic cause of portal hypertension
portal vein thrombosis
74
name two causes of post hepatic portal hypertension
constrictive pericarditis
IVC obstruction
75
Ix for oesophageal varices
Upper GI endoscopy
76
what is the treatment for ruptured oesophageal varices
* Surgical
* immediate band ligation
* Fluid resuscitation
77
treatment for oesophageal varices before they rupture
* 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
why do you get ascites in liver disease
* 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
what is the difference between transudate and exudate
\<11g/L of protein is transudate
\>11g/L of protein is exudate
80
two signs of ascites
distended abdomen
shifting dullness
81
Ix of ascites
* ascitic tap
* M,C and S
* cytology
* protein
82
treatment of ascites
fluid and salt restriction
spironolactone
treat underlying cause
83
what bugs commonly cause SBP
e.coli
klebsiella
enterococcus
84
what is the initial management for suspected SBP and what is the prophylaxis that is sometimes given to high risk ascitic patients
initial management: ceftioxime
prophylaxis: ciprofloxacin
85
Dx of hepatocellular carcinoma
CT/MRI liver
Biopsy
Bloods: clotting abnormalities, deranged LFTs
86
HCC treatment
surgical resection
radiofrequency ablation
chemo
TACE
87
what is TACE
Transarterial chemoembolization (TACE) is a specific type of chemoembolization that blocks the hepatic artery to treat liver cancer
88
where are secondary liver tumours likely to have come from
GI
breast
bronchus
89
what is the management of paracetamol overdose
* 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
what are the time periods of liver failure and what do they mean
* within 8 weeks: fulminant hepatic failure (FHF)
* 8-26 weeks: subacute
* 6 months: chronic
91
treatment for hepatic encephalopathy
lactulose and mannitol
92
fill this in
93
what are the risk factors for gallstones
fat
female
forty
fertile
94
why do you get biliary colic
gallstone is impacted in the gallbladder neck temporarily and is dislodged back into the gallbladder
95
what is acute cholecystitis
when the gallstone is stuck in the **GALLBLADDER** **NECK** and causes inflammation
96
presentation of acute cholecystitis
RUQ pain
fever
nausea
vomiting
Murphy's sign
97
what is murphey's sign
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
when is murphey's sign classically positive and negative
* positive
* cholecystitis
* negative
* choledocholithiasis
* pyelonephritis
* ascending cholangitis
99
Ix of acute cholecystitis
USS abdo
abdo exam
LFTs to exclude liver/bile duct pathology
100
treatment for acute cholecystitis
laporoscopic cholecystectomy
supportive with analgesia and fluids as needed
101
what is ascending cholangitis
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
fill in the blanks
103
what are the features of ascending cholangitis
* charcot's triad:
* RUQ pain
* fever
* Jaundice
* Reynold's pentad:
* hypotension
* confusion
104
105
what is ERCP
endoscopic retrograde cholangio pancreatography
106
Ix and treatment of ascending cholangitis
* Ix
* USS abdo
* MRCP to locate stone
* Tx
* ERCP to remove stone
107
name some causes of pancreatitis
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
two important signs in pancreatitis and what they mean
* bruised flanks - Grey-Turners
* bruised umbilicus - Cullen's
* they mean it's late stage and haemorrhagic
109
clinical features of pancreatitis
* Abdominal pain that radiates to the back
* Nausea and vomiting
* Fever
* Abdominal tenderness
* Distension
110
Ix for pancreatitis
* Amylase or Lipase
* CT abdo
111
3 complications of pancreatitis
Sepsis
DIC
ARDS
112
which tissues does PSC affect
intra and extrahepatic bile ducts
113
fill in this table
114
painless jaundice with weight loss is\_\_\_\_\_\_\_\_\_
cancer of the head of the pancreas
115
cholangiocarcinoma can cause what?
Primary sclerosing cholangitis
