Liver and Friends Flashcards
1
Q
What does the liver do (4 things)
A
glucose and fat metabolism
detoxification and excretion (of bilirubin, ammonia and drugs)
protein synthesis (albumin, clotting factors)
Defence against infections with the reticulendothelial system
2
Q
what is cirrhosis
A
this is scarring and disorganisation of the liver tissue i response to constant low grade injury
3
Q
how much more liver do we have than we need?
A
3x
4
Q
presentation of liver injury
A
malaise
nausea
anorexia
jaundice
as it gets more severe: confusion, bleeding, liver pain, hypoglycaemia
5
Q
presentation of chronic liver injury
A
ascites
oedema
haematemesis (due to oesophageal varices)
malaise
anorexia
easy bruising
itching
hepatomegaly
more rarely: jaundice and confusion
6
Q
what are the transaminases and why are they useful for LFT
A
alanine transaminase (ALT) and aspartate transaminase (AST) are enzymes used by hepatocytes to metabolise amino acids for energy
if the liver is inflamed the hepatocytes will bust and release these
they give no indication of liver FUNCTION only level of inflammation of liver
7
Q
what is jaundice
A
- raised serum bilirubin
- can be unconjugated (pre-hepatic)
- gilberts
- haemolysis
- or conjugated (cholestatic)
- liver disease (hepatic)
- bile duct obstruction (post-hepatic)
8
Q
what does the term cholestatic refer to and what are two key indicators of it
A
it’s liver disease that is hepatic and post hepatic
dark urine and pale stools
the jaundice seen will be due to conjugated bilirubin
9
Q
what is conjugated and unconjugated bilirubin
A
both are products from the breakdown of haem in blood (that happens in macrophages in the spleen and bone marrow)
CB is just UCB that has been attached to a glucaronic acid in the liver
this makes CB water soluble whereas UCB is lipid soluble and requires albumin for transport in the blood
10
Q
how will urine, stools, itching and liver tests change in pre-hepatic/cholestatic jaundice
A
11
Q
what tests for liver disease
A
- liver function tests
- US
- in biliary obstruction 90% have dilated intrahepatic bile ducts
- CT
- Magnetic resonance cholangiogram (MRCP)
12
Q
risk factors for gall stones
A
fat
female
forty
fertile
also: liver disease, ileal disease
13
Q
gallstone management when they’re in the gallbladder
A
laporoscopic cholecystectomy
14
Q
gallstone management when they’re in the bile duct
A
- surgery for large stones
- Endoscopic retrograde cholangio-pancreatography (ERCP)
- this is where a tube goes in through the mouth to where the bile duct meets the small bowel and widens the sphincter to allow the stone through
- stones can also be removed with a basket?
15
Q
what does cholestatic jaundice refer to
A
it is jaundice with dark urine and pale stools
this means it is hepatic or post-hepatic
16
Q
if they have jaundice and rigors what does this tell you
A
it tells you that they have cholangitis which is inflammation of the bile duct system normally due to bacterial infection following obstruction
17
Q
if someone has jaundice what must you always ask about
A
drugs they started recently
drug induced liver injury is common
18
Q
what percentage of acute hepatitis is drug induced
what percentage of acute liver failure is drug induced (what drug is this mainly due to)
A
30% acute hepatitis
>65% of acute liver failure - mainly paracetamol
19
Q
onset of DILI
A
usually within 1-12 weeks of starting
and can be several weeks after stopping (co-amoxiclav can do this)
20
Q
when does DILI resolve
A
90% within 3 months of stopping the drugs
21
Q
what are the usual suspects for DILI
A
- about 40% of the time it’s caused by antibiotics
- all TB drugs
- flucloxacillin
- also often CNS drugs
- carbamazepine
- valproate
22
Q
what is NAC and how does it work?
A
N-acetyl cysteine turns the reactive intermediate produced by paracetamol in the liver to a non-reactive product.
23
Q
Management of paracetamol induced fulminant hepatic failure.
A
- N acetyl Cysteine (NAC)
- Supportive to correct
- coagulation defects
- fluid electrolyte and acid base balance
- renal failure
- hypoglycaemia
- encephalopathy
24
Q
what factors make paracetamol overdose more dangerous
A
late presentation (NAC is less effective after 24hrs)
acidosis
very high prothrombin time
very high serum creatinine
if they have these factors then consider an emergency liver transplant
25
causes of ascites
* chronic liver disease
* ± portal vein thrombosis
* hepatoma
* TB
* Neoplasia
* ovary, uterus, pancreas
* Pancreatitis
26
Ascites management
* fluid and salt restriction
* diuretics
* spironolactone
* ±frusemide (loop diuretic)
* large volume paracentesis + albumin
27
what is the main cause of liver death in the UK
alcoholic liver disease
28
treatment for bleeding oesophagael varices
remergency resuscitation with blood and plasma
emergency gastroscopic banding
terlipressin is given which causes vasoconstriction
propanolol also given
29
what are the causes, pathologies and consequences of portal hypertension
* causes
* cirrhosis
* fibrosis
* portal vein thrombosis
* pathology
* increased hepatic resistance leads to increased splanchnic blood flow
* this causes a back up which causes dilatation of the veins draining the rest of the GI system including the oesophagus
* consiquences
* varices (oesophageal and gastric)
* splenomegaly
* caput medusae
30
how many liver transplants are there in the UK every year? and how many of these are for alcoholic liver disease
there are 700 pa and 100 of them are for alcoholic liver disease
31
what 6 things might cause a sudden exascerbation of Chronic liver disease
constipation
drug changes
GI bleeds
Infection
Metabolite imbalances (hyponatraemia -kalaemia -glycaemia)
alcohol withdrawal (rarely)
32
why are liver patients vulnerable to infection?
impaired reticulo endothelial function
more permeable gut wall
reeduced opsonic activity (complement produced by the liver)
33
what is the commonest serious infection in cirrhosis patients and how is it diagnosed
spontaneous bacterial peritonitis
diagnosis is made based on high volume of neutrophils in the ascetic fluid
do blood cultures too
34
what is coma in chronic liver patients likely to be due to?
3 broad causes
* hepatic encephalopathy (usually caused by high ammonia)
* hyponatraemia/hypoglycaemia
* intracranial event
* alcoholic patients more vulnerable to subdural haematoma due to cerebral atrophy exposing bridging veins
35
why does liver dysfuntion cause coagulopathy - 3 main reasons
1. impaired coagulation factor synthesis
2. vitamin k deficiency due to cholestasi
3. thrombocytopenia
* this is due to portal hypertension causing congestive splenomegaly which itself leads to pooling of thrombocytes in the spleen
36
which is the best analgesic to use in liver disease
paracetamol is safest in therapeutic doses
they are more sensitive to opiates
and NSAIDd cause renal failure
37
treatment for hepatic encephalopathy
lactulose
38
treatment for ascites
salt/fluid restriction
diuretics
paracentesis
39
causes of chronic liver disease (6 main causes and some subtypes)
* Alcohol
* NAFLD
* Viral Hepatitis (B and C)
* Immune
* autoimmune hepatitis
* primary biliary cholangitis
* slerosing cholangitis
* Metabolic
* Wilson's
* Haematochromatosis
* alpha1 antitrypsin deficiency
* Vascular
* Budd-Chiari
40
What is the standard battery of tests when someone presents with chronic liver disease
* Viral serology to HepB and HepC
* Immunology for AMA, ANA, ASMA and Coeliac antibodies
* checking for autoimmune conditions
* Biochemistry
* iron studies
* lipids and glucose (metabolic syndrome is a major driver of NASH)
* alpha 1 trypsin levels
* Raidology - USS, CT, MRI
* you never know when you'll find a tumour
41
draw a table for AIH, PBC, PSC for the criteria:
raised globulins
autoantibodies
other AI diseases
F:M
genetic associations
response to steroid therapy
42
which different tissues do PBC, PSC and AIH affect
AIH - hepatocytes
PBC - the small bile ducts
sclerosing cholangitis - can affect the small bile ducts but mainly the large duct
43
autoimmune hepatitis:
prevalence in UK
gender preponderance
UK prevalence is 1-2/10,000
it is 70-75% women
44
what is the treatment for AIH
90% response to prednisolone and azathioprine
45
primary biliary cholangitis has a strong association with which autoantibody
antimitochondrial antibodies in 95% cases
46
what is the prevalence of PBC and what is the gender preponderance
~ 25/ 1,000,000 and it's 90% women
47
how does primary biliary cholangitis present
Itching and/or fatigue (this is the main one)
sometimes found due asymptomatic lab abnormalities
dry eyes
joint pains (revved up immune system)
varicael bleeding
ascites/jaundice (sometimes)
48
treatment of cholestatic itch
antihistamines help a little
cholestyramine helps in about half of cases (it is a bile acid sequestrant)
49
what other autoimmune conditions is PBC associated with
* it is very often associated with one of the following
* Sjorgens
* Thyroiditis
* RA
* Coeliac
50
what is mrcp
magnetic resonance cholagiopancreatography
51
what are two complications of primary sclerosing cholangitis
strictures and gallstones
52
presentation of primary sclerosing cholangitis
itching
pain
rigors
jaundice
over 50% have IBD
riased alk phos and GGT
53
treatment for PSC
liver transplant
54
treatment for PBC
ursodeoxycholic acid (found in bear bile)
improves liver enzymes and reduces inflammation
it is a secondary bile acid
it reduces rate of death and liver transplant
also give fat soluble vitamin supplements
colestyramine may help pruritis
liver transplant for end stage disease
55
what causes haemochromatosis
mutation in HFE on chromosome 6
they have uncontrolled intestinal iron absorption with deposition in liver, heart and pancreas
iron is stored in the liver if it is not converted into haemoglobin
56
presentation of haemochromatosis
high ferritin
high ALT and AST
gross iron staining on liver biopsy ± cirrhosis
57
treatment of haemachromatosis
desferrioxamine
venesection
58
what is the inheritance pattern of haemochromatosis
autosomal recessive
59
diagnosis of haemochromatosis
suggested by high ferritin
diagnosed by HFE genotyping (C282Y) and liver biopsy (gross iron staining)
60
risk factors for hepatocellular carcinoma
* Most occur in patients with cirrhosis
* highest risk being in patients with haemochromatosis or those who have had HepB or C
* lower risk (but still significant) is alcoholic cirrhosis
* male sex
61
presentation of hepatocellular carcinoma
may present with decompensation of liver disease
weight loss
ascites
abdo pain
62
50% of HCCs produce what?
alpha fetoprotein
63
treatment for HCC
transplantation
resection
local ablative therapy (including some targeted radio and percutaneous administration of chemical agents)
sorafenib is a recently developed targeted therapy
64
what percentage of the population have NAFL
25% of the population
65
risk factors for NAFL
obesity
diabetes
hyperlipidaemia
66
what is the commonest cause of mildly elevated LFTs
NAFL
67
what is the difference between NAFL and NASH
NASH is a type of NAFL where the fat droplets have caused inflammation and fibrosis
68
what is the best treatment for NAFL and NASH
no effective drug treatments
weight loss works well
69
very brief summary of alpha1 anti-trypsin deficiency
genetic disorder that results in the inability to export alpha1 antitrypsin from the liver
results in protein retention in the liver and liver disease
phenotypic presentation is variable but can include neonatal jaundice and chronic liver disease in adults
there is no medica treatment
70
hepatic vein occlusion causes
thrombosis (this is budd chiari syndrome) and it may indicate an underlying thrombotic disorder
veno-occlusive disease (irradiation and anti-neoplastic drugs)
71
presentation of hepatic vein occlusion
liver enlargement
abnormal LFTs
ascites
acute liver failure
72
hepatic vein occlusion
anticoagulation
liver transplantation
73
what are the viral causes of hepatitis (try and name 10)
Hep ABC
Hep D and E
Yellow fever
EBV
CMV
Toxoplasma
Influenza
Coxsackie virus
74
draw Hep ABCDE table including route of transmission, whether it's a chronic infection and prevention
75
symptoms of acute hepatitis
malaise
myalgia
fever
nausea/vomiting
cholestatic jaundice (pale stools and dark urine)
RUQ pain
tender hepatomegaly
76
test results of acute hepatitis
high AST
high ALT
high alk phos
low albumin
high bilirubin
77
Hep A is what type of virus
pico**rna**virus
meaning small rna virus
78
Hep A transmission
* faeco-oral route
* contaminated food/water
* shellfish
* travellers
* infected food handlers
* close personal contact
* household
* sexual
* blood
* IVDU
79
what type of vaccine is the HepA vaccine, and who should have it
it's inactivated hep A virus
travellers
work exposure
prevention of secondary case
lifestyle risk
other liver disease
80
what kind of virus is hepatitis B virus and where does it replicate
Hepa**dna**virus
it's a dna virus
replicates in hepatocytes
81
what percentage of adults and children will clear a Hep B infection
\>90% adults
\<50% children
82
Hepatitis B Serology - can you draw the table for acute, previous exposure, chronic + low infectivity and chronic + high infectivity
there are two antigens HBsAg and HBeAg
if you have antibodies against all of them and none of the antigens present themselves then you have previously cleared the infection
if you have the antigens and no antibodies then it's acute hepB
if you have chronic HBV and low infectivity then you don't have Abs against HbsAg so it is still present
if you have chronic HBV and high infectivity then you don't have Abs against either HBeAg or HBsAg but this is distinguishable from acute since you do have the HBcAb (HB core Ab)
83
which hepatitis virus is now endemic in the UK
hep E virus
84
Hep B vaccine
recombinant DNA HBsAg
85
treatment for HBV
* alpha interferon
* nucleoside analogues
* e.g. tenofovir
* there's poor clearance rate but there is long-term control of HBV DNA
86
what type of virus is hepatitis C
flavivirus (RNA)
87
what is the disease course of HCV
* acute hepatitis in 20% of patients
* the majority are asymptomatic
* incubation is 2-26 weeks
* chronic hepatitis in 80%
* cirrhosis in 15%
* hepatocellular carcinoma in 5%
88
what is the treatment for Hep C
pegylated IFN
ribavirin tablets
70-80% cure rate in non-1 genotype (treatment for 6months)
60% cure rate in genotype 1 (treatment for 1yr)
89
diagnosis of HCV
HCV Ab detectable in serology 4 weeks after infection
HCV DNA is detectable via PCR (only present in chronic infection)
On USS there may be a cirrhotic liver
90
how many genotypes of HCV are there and which one is the hardest to treat
6 and type 1 is hardest to treat
91
HCV prevention
livestyle modification - protected sex, needle exchanges
screening blood samples
universal precautions for handling all bodily fluids
92
Hepatitis D virus
often co-infects with HepB and causes an infection with increased severity
if the patient has chronic HBV it can cause a super-ifnection with high risk of fulminant hepatitis and increased progression of liver disease
93
HEV
* small rna virus
* very similar to Hep A
* less infectious but higher mortality
* especially dangerous in pregnant women (10-20% mortality)
* mortality is due to fulminant liver failure
* it is now endemic in the UK
* \>95% cases are asymptomatic
94
what is the difference between acute and chronic in hepatitis
either side of 6 months
95
how does the chronic hepatitis patient appear
* may be asymptomatic
* signs of chronic liver disease
* clubbing
* palmar erythema
* spider naevi
* LFTs can be normal
96
what is compensated and decompensated hepatitis
compensated: liver function is maintained
decompensated: jaundice, ascites, low albumin, coagulopathy, encephalopathy
97
do you have immunity after infection with Hep A
yes 100% immunity
98
Hep A management
supportive
monitor liver function (bilirubin, LFTs, INR, albumin)
manage close contacts
99
HBV epidemiology: how many new infections per year, how many people with chronic HBV and how many deaths per year
129 million new infections per year
343 million with chronic HBV
750,000 deaths per year
100
HBV natural history - can you draw the diagram?
101
prevalence of Hep C in england, what percentage of these are undiagnosed and what percentage have history of IVDU
HCV prevalence in england is 160,000
50% undiagnosed
90% history of IVDU
102
HCV natural history can you draw the diagram
103
does previous infection with HCV confer immunity
no
104
since when have we been screening blood products for Hep C in the UK
since 1991
105
how many different species of bacteria are found in the GI tract
over 400 - they are predominantly anaerobes
106
why do PPIs and broad spectrum antibiotics put us at increased risk of intraluminal infection
because both gastric acid and the microbiome are protective against alien invaders
107
some infectious and non-infectious causes of diarrhoea
* infective
* intraluminal infection
* systemic infectio (e.g. malaria, sepsis)
* non-infective
* cancer - usually associated with bleeding as well
* chemical poisoning
* IBD
108
diarrhoea testing
* stool sample
* Microscopy
* culture
* sensitivity
* toxin detection
* Blood tests
* blood culture
* inflammatory markers CRP
* FBC
109
differences between watery and bloody,mucoid diarrhoea - can you draw the diagram?
consider mechanism, location, bacterial causes, viral causes, parasitic causes,
110
how much watery stool can a patient with cholera produce every day?
up to 20L
111
what is the bacteria implicated in rise reheating due to the toxin it produces
Bacillus cereus
112
Why do some bacteria cause more mucoid/bloody diarrhoea
because they are actually invading into the gut wall
113
in the UK how much of the infectious diarrhoea is caused by viruses
50-70%
it's mainly rotavirus and norovirus
rotavirus mainly in children
114
three most common bacterias that cause traveller's diarrhoea
enterotoxigenic e.coli (majority)
campylobacter
shigella
115
cholera: what is the name, how is it transmitted, what is the clinical presentation, what is the treatment
vibrio cholerae
transmitted by contaminated food/water
causes profuse, watery diarrhoea up to 20L per day
vomiting
very rapid dehydration
treatment is doxycycline and fluids
116
what happens within the cells in cholera
cholera toxin binds a cellular receptor which mediates an intracellular cascade with causes increasde cAMP which leads to increased secretion of Cl- by CFTR protein into the lumen
this draws out fluid at a rapid rate and leads to huge amounts of watery diarrhoea
rice water: looks clear and cloudy like the water you cook rice in
117
5 differnt parasites that can cause diarrhoea
* protozoa
* giardia
* entamoeba
* worms
* schistosomiasis
* strongyloids
118
how much of the population are colonised with Clostridium difficile
5% of population are happily colonised without any symptoms
it only causes the very severe colitis that is does when it is allowed to overgrow
119
what are the 4 antibiotics which may give you c diff
rule of Cs
* clindamycin
* ciprofloxacin
* co-amoxiclav
* cephalosporins
120
diarrhoea red flags
dehydration
electrolyte imbalance
renal failure
severe abdo pain
121
presentation of C diff
watery diarrhoea
mild to severe colitis which is pseudomembranous on endoscopy
ileus
toxic megacolon
ASK ABOUT RECENT ANTIBIOTIC USE
122
clostridium difficile management
* isolate them immediately
* mild: oral metronidazole
* severe: oral vancomycin
* severe is when they have very high white cells or if they have AKI, colitis or temperature above 38.5
* non responders: vancomycin and metronidazole together
* recurrence: faecal transplant
123
what is peptic ulcer disease
it's where you have an ulcer either in your stomach or in your duodenum
124
how do you test for H.pylori
you take a stool sample and send it to the lab to test for H.pylori antigens
125
where would you get pain for biliary sepsis/ascending cholangitis
RUQ
126
what is the presentation of ascending cholangitis
* charcot's triad
* jaundice
* rever
* RUQ pain
* usually presents with rigors
127
why would the biliary tree get infected
because of obstruction normally (stones, cancer etc) and the fluid sitting there gets infected by bacteria from the duodenum
128
what would be the common organisms that cause spontaneous bacterial peritonitis in a cirrhosis patient
E.coli
Klebsiella
Streptococci
129
what antibiotics would you use for spontaneous bacterial peritonitis
piperacillin until sensitivities known
130
what are the commonest causes of cirrhosis
chronic alcohol use
chronic HBV or HCV infection
131
signs of cirrhosis
* leuconychia from hypoalbuminaemia
* terry's nails: white proximally but distal reddening from tenalgiectasis
* clubbing
* spider naevi
* dupytren's contracture
* ascites
* splenomegaly
132
three major complications of cirrhosis
* hepatic failure
* HCC
* Portal hypertension
133
consequences of hepatic failure
coagulopathy
encephalopathy
hypoalbuminaemia (and associated oedema)
sepsis
spontaneous bacterial peritonitis
hypoglycaemia
134
consequences of portal hypertension
splenomegaly
ascites
porto-systemic shunt including gastric varices (which may led to rupture and haematemesis) and caput medusae (enlarged superficial periumbilical veins)
135
important tests in cirrhosis
* ultrasound
* may show small or large liver, splenomegaly or hepatic vein thrombus
* Bloods
* LFTs
* bilirubin
* albumin
* ferratin
* hepatitis serology
* Any patient with sudden deterioration and ascites should have an ascitic tap and urgent M,C and S of this to check if they have SBP. neutrophils \>250/mm3
* liver biopsy confirms clinical diagnosis
136
what is the 5yr survival for cirrhosis
50%
137
what is the definition of alcoholism
it is a problematic pattern of alcohol use that leads to clinically significant impairment or distress manifested in multiple psychosocial, behavioural and physiological features
138
lifetime prevalence of alcoholism in men and women
men: 10%
women: 4%
139
how does alcoholic hepatitis present
malaise
anorexia
D&V
tender hepatomegaly
jaundice
bleeding
ascites
high temperature, pulse and respirations
140
how will you know if alcoholic hepatitis is severe, what signs and symptoms will they have
jaundice
coagulopathy
encephalopathy
141
what will bloods show for alcoholic hepatitis
low platelets
high INR
high AST
High MCV
high urea
142
how to manage alcoholic hepatitis
* screen for infections with ascitic tap and treat any SBP
* stop alcohol consumption
* pabrinex
* optimise nutrition
* if very severe disease then steroids may confer benefit
143
once stopping alcohol consumption how do you treat withdrawal
if oral chlordiazepoxide is impossible then give IM lorazepam
144
what is the definition of a hernia
protrusion of a viscus or part of a viscus through a defecit in the walls of its containing cavity into an abnormal position
145
what are the complications of any cholestatic problem including cirrhosis
malabsorption of fat
malabsorption of fat soluble vitamins A,D,E,K
146
in terms of a hernia what do the terms: irreducible, obstructed, strangulated and incarceration mean?
* irreducible: contents cannot be pushed back into place
* obstructed: bowel contents cannot pass - has features of intestinal obstruction
* strangulated: ischaemia is occuring - the patient requires urgent surgery
* incarceration: contents of the hernial sac are stuck by adhesions
147
what is the most common type of hernia
inguinal hernia in both men and women
but much more common in men
148
which is more common, the indirect or direct inguinal hernia. which one is more likely to strangulate
the indirect inguinal hernia is more common (this is the one that actually travels through the tunnel of the inguinal canal whereas the direct one is the one that goes through a wall of the inguinal canal medial to the inferior epigastric vessels)
direct hernias rarely strangulate, are reduced easily whereas indirect hernias can strangulate
149
definition of liver failure
development of coagulopathy (INR \>1.5) and encephalopathy
150
budd chiari syndrome is the occlusion of what?
hepatic vein
it can cause liver failure
151
what are the major emergency concerns with liver failure patients
sepsis
hypoglycaemia
GI bleeds/varices
encephalopathy
152
why does liver failure give you encephalopathy
buildup of ammonia passes to the brain where it is cleared by astrocytes
this process involves the conversion of glutamate to glutamine
excess glutamine causes an osmotic imbalance and a shift of fluid into the cells causing oedema
153
how does hepatic encephalopathy present?
altered mood/behaviour, sleep disturbance, drowsiness, confusion, slurred speech, personality change, restlessness, stupor, coma
154
Liver failure blood tests
* FBC
* infection?
* bleed?
* LFT
* Clotting (PT and INR)
* Glucose level
* Paracetamol level
* Hepatitis serology
* Ferritin
* alpha-antitrypsin
155
liver failure microbiology tests
* Ascitic tap and M,C&S of ascites
* neutrophils \>250/mm3 is SBP
* blood culture
156
5 major complications of liver failure and how to treat them
1. cerebral oedema: IV Mannitol
2. ascites: pericenteses, restrict fluid, low salt diet, diuretics, weigh daily
3. bleeding: vitamin K, platelets and blood as needed
4. infection: culture but until sensitivities known treat blindly with ceftriaxone
5. hypoglycaemia: treat with IV glucose
157
what is heporenal syndrome
ascites, cirrhosis and renal failure occuring together
RRT and liver transplant may be required
158
7 functions of the liver and what happens when they go wrong
1. production of albumin
* hypoalbuminaemia --\> ascites
2. regulation of excess oestrogen
* gynaecomastia in men
* spider naevi due to dilation of blood vessels
* palmar erythema
3. production of clotting factors
* easy bruising
4. regulation of bilirubin
* jaundice and pruritis
* pale stools and dark urine
5. urea metabolism
* hepatic encephalopathy
6. protection against infection via reticuloendothelial system
* SBP
7. storage of glycogen and glycogenolysis
* hypoglycaemia
159
5 different components of LFT and the type of damage they're associated with
GGT - Alcoholic liver disease
ALP - anything to do with biliary tree damage
AST/ALT - raised in hepatocyte damage
bilirubin
albumin
160
most important investigation if you suspect viral hepatitis
serology for virus antibodies and antigens
161
anti-HBc, IgM anti-HBc, HBsAg and anti-HBs
what does the presence of each of the above 4 things mean
* anti-HBc: antibody to core antigen. appears at the onset of acute hepatitis B and persists for life - indicates previous or ongoing infection
* IgM anti-HBc: IgM antibody to HBV core antigen. indicates recent infection \<6 months. its presence indicates acute infection
* HBsAg: HBV surface antigen. indicates patient has acute or chronic infection and is infectious. antigen used for vaccine
* anti-HBs: indicates recovery and immunity. also develops in vaccinated individuals.
162
fill in the third column in this table of HBV serology by describing the status of the patient
163
which viral heps are there vaccines for
Hep B and A
164
what is the treatment for Hep A and E
supporting - these are self limiting infections
165
what is the treatment for hepatitis B
pegylated IFN-alpha 2a
166
what is the treatment for Hepatitis C
velpatasvir/sofosbuvir
167
how does alcoholic liver disease occur
ADH turns ethanol into acetaldehyde while converting NAD+ to NADH
acetaldehyde builds up and increases ROS formation
it also increases NADH:NAD+ ratio
less NAD+ leads to less oxidation of fat
fat accumulates in hepatocytes
The ROS then damage the hepatocyte membranes
this leads to fatty inflammation (steatohepatitis) and eventual cirrhosis
168
how will LFTs look in alcoholic liver disease
GGT very very raised
AST and ALT mildly raised
FBC may show macrocytic anaemia
169
treatment for alcoholic liver disease
supplementation with thiamine (pabrinex) and advise they reduce alcohol consumption
170
NAFLD: risk factors, Ix and management
risk factors are: metabolic syndrome, obesity and T2D
Ix - enhanced liver fibrosis test
managment - lifestyle, lose weight.
171
what is wernicke's encephalopathy?
thiamine deficiency closely associated with alcoholism
triad of: confusion, ataxia and opthalmoplegia
deficiency due to: inadequate dietary intake and decreased GI absorption
treat urgently with pabrinex (thiamine supplement) can progress to korsakoff's syndrome: which is retrograde amnesia, confabulation and decreased ability to make new memories
172
Wilson's disease
excess copper in liver and CNS
due to AR mutation on chromosome 13 of ATP7B gene
kayser-Fleischer rings are visible round the outside fo the cornea
test: serum caeruloplasmin (the copper carrying protein) will be raised
management: penicillamine extracts copper and advise to reduce copper intake (no shellfish)
173
what is Alpha-1-antitrypsin deficiency, what are the symptoms, investigations and mangement
it is an accumulation of alpha-1-antitrypsin in hepatocytes and a lack of it in serum, causing a lack of protease activity in the alveoli that leads to damage and subsequent emphysema
symptoms are that of COPD
AR inheritance with mutation on chromosome 14
Ix are serum alpha-1-antitrypsin will be low
management is the same management for COPD and liver transplant is curative.
174
haemochromatosis - what is it? what is the distinctive presentation? what is the important Ix? what is the management?
excess iron everywhere due to AR mutation on chromosome 6
restrictive cardiomyopathy from iron deposition
bronze diabetes
serum ferritin and iron stain of biopsy showing iron overload
management is reduce iron in diet and use desferrioxamine to remove excess iron
175
what is it called when liver cirrhosis causes the liver to not be able to function properly causing clinical complications
chronic decompensated hepatic failure
176
why do you get portal hypertension in liver failure
* cirrhosis causes
* increased endothelin 1 production
* decreased NO production
* so reduced radius leads to increased resisitance and highe pressure in the portal system
177
causes of portal hypertension: prehepatic, hepatic and post hepatic
* prehepatic: portal thrombosis
* hepatic: schistosomiasis, sarcoidosis, cirrhosis, budd chiari syndrome
* posthepatic : right heart failure, IVC obstruction
178
what are the two symptoms of ruptured oesophageal varices
haematemesis
malaena
179
why does ascites occur in liver failure? in terms of osmotic pressure and hydrostatic pressure
oncotic pressure decreases because of hypoalbuminaemia
hydrostatic pressure increases due to potal hypertension and RAAS activation
180
difference between transudate and exudate
transudate has an albumin level 11g/L or more below the level of serum albumin
exudate has an albumin level less than 11g/L below the serum albumin
181
which antibiotic for SBP prophylaxis
ciprafloxacin
182
which diuretic for ascites
spironolactone - a potassium sparing diuretic
183
treatment for SBP
cefotaxime
184
what can you give for a paracetamol overdose as well as N-acetyl-cysteine if it's within one hour of ingestion
activated charcoal
185
186
what is acute cholecystitis
it is acute inflammation of the gall bladder sometimes caused by gallstones
187
what is biliary colic
this is sudden pain caused by a gall stone temporarily blocking the cystic duct before becoming dyslodged back into the gallbladder
188
what is cholangitis
this is inflammation of the bile duct system - usually due to gallstone becoming stuck and causing bacterial infection from the duodenum
189
what is murphy's sign?
fingers and thumb under the right costal margin to detect RUQ pain
typically it is positive in cholecystitis but negative in pyelonephritis and ascending cholangitis
190
presentation, investigation, treatment of acute cholecystitis
* presentation:
* RUQ pain
* Murphy's sign
* Ix
* USS abdomen
* LFTs to exclude liver/bile duct pathology
* Treatment
* Laparoscopic cholecystectomy
* Supportive: analgesia and fluids
191
what are the common bugs that cause ascending cholangitis
group D strep: e.coli, klebsiella, enterococcus
192
Ix and treatment for ascending cholangitis
* Ix
* USS abdomen
* MRCP to locate
* treatmetn
* ERCP to remove stone
193
what is reynold's pentad?
* it is for ascending cholangitis
* it includes charcot's triad (fever, RUQ pain, jaundice)
* as well as hypotension and confusion
194
what are the causes of acute pancreatitis
GET SMASHED
* Gallstones
* Ethanol
* Trauma
* Steroids
* Mumps
* Autoimmune (SLE
* Scorpion bites
* Hyperglycaemia, hyperlipidaemia and hypothermia
* ERCP (iatrogenic)
* Drugs (azathioprine, metronidazole, tetracycline, furosemide)
195
presentation of acute pancreatitis
* abdo pain that radiates to the back
* relieved by sitting forward
* nausea and vomiting
* fever
* abdo tenderness
* distension
* later stage
* Grey Turner's sign refers to bruising of the flanks, the part of the body between the last rib and the top of the hip
* Cullen's sign: superficial edema and bruising in the subcutaneous fatty tissue around the umbilicus.
196
Investigations and treatments for pancreatitis
* Investigations:
* amylase or lipase (inflammation of pancreas causes release of these enzymes)
* CT abdo
* Treatment
* treat underlying cause
* supportive treatment: fluids, analgesia, nutrition
197
symptoms of pancreatic cancer
painless jaundice with weightloss = cancer of the head of the pancreas
198
important complications of pancreatitis
* DIC
* ARDS
* bilateral pulmonary oedema due to inflammatory mediators released by pancreas - they start drowning - it develops incredibly quickly
* Sepsis
* rena failure
* hepatic failure - difficulty draining biliary system
* pancreatic necrosis if severe - diabetes
199
what is choledocholithiasis
this is a bile duct stone
200
three reasons people get gallstones
raised cholesterol
oestrogen exposure
haemolytic anaemia
201
why do people get dehydrated with jaundice
the bilirubin in their urine pulls out water
202
what are the only things that cause rigors typically
pyelonephritis
lobar pneumonia
cholangitis
203
what is gallstone ileus
this is where there are recurrent episodes of infection or inflammation from a gallstone
the gallbladder becomes adherant to the duodenum
gallbladder fistulates and opens directly into the duodenum
stone goes through bowel and lodges in the ileocolic valve
causes backlog of gas and fluid in small bowel
air goes in the liver
treatment is with laperotomy
1% of all bowel obstruction in the uk
204
diagnosis of pancreatitis
amylase or lipase of 3x upper limit of normal
CT them if they're unwell
205
pancreatitis treatment
* mostly supportive
* IV fluid
* analgesia
* catheter
* manage complication
* feeding with nasojejunal tube
* maybe a laparoscopic cholecystectomy if gallstones caused it
206
207
what is the modified glasgow score?
* PANCREAS
* PaO2 \<8KPa
* Age \>55
* Neutrophils \>15
* Calcium \<2mmol/L
* Raised Urea \>16mmol/L
* Enzymes LDH \>600 (lactate dehydrogenase means ur relying on anaerobic metabolism) and AST \>400
* Albumin \<32 (drops when someone's septic)
* Sugar \>10mmol/L
* if you score 3 points you have possible pancreatitis
*
208
how is sbp diagnosed
ascitic tap
if neutrophils are \>250/mm3 then it's diagnostic
209
empiracle treatment for SBP
ceftriaxone
