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formative 3b > Liver and Friends > Flashcards

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

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2
Q

what is cirrhosis

A

this is scarring and disorganisation of the liver tissue i response to constant low grade injury

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3
Q

how much more liver do we have than we need?

A

3x

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4
Q

presentation of liver injury

A

malaise

nausea

anorexia

jaundice

as it gets more severe: confusion, bleeding, liver pain, hypoglycaemia

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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

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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

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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)
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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

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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

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10
Q

how will urine, stools, itching and liver tests change in pre-hepatic/cholestatic jaundice

A
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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)
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12
Q

risk factors for gall stones

A

fat

female

forty

fertile

also: liver disease, ileal disease

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13
Q

gallstone management when they’re in the gallbladder

A

laporoscopic cholecystectomy

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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?
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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

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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

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17
Q

if someone has jaundice what must you always ask about

A

drugs they started recently

drug induced liver injury is common

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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

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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)

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20
Q

when does DILI resolve

A

90% within 3 months of stopping the drugs

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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
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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.

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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
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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

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25
Q

causes of ascites

A
  • chronic liver disease
    • ± portal vein thrombosis
    • hepatoma
    • TB
  • Neoplasia
    • ovary, uterus, pancreas
  • Pancreatitis
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26
Q

Ascites management

A
  • fluid and salt restriction
  • diuretics
    • spironolactone
    • ±frusemide (loop diuretic)
  • large volume paracentesis + albumin
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27
Q

what is the main cause of liver death in the UK

A

alcoholic liver disease

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28
Q

treatment for bleeding oesophagael varices

A

remergency resuscitation with blood and plasma

emergency gastroscopic banding

terlipressin is given which causes vasoconstriction

propanolol also given

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29
Q

what are the causes, pathologies and consequences of portal hypertension

A
  • 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
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30
Q

how many liver transplants are there in the UK every year? and how many of these are for alcoholic liver disease

A

there are 700 pa and 100 of them are for alcoholic liver disease

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31
Q

what 6 things might cause a sudden exascerbation of Chronic liver disease

A

constipation

drug changes

GI bleeds

Infection

Metabolite imbalances (hyponatraemia -kalaemia -glycaemia)

alcohol withdrawal (rarely)

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32
Q

why are liver patients vulnerable to infection?

A

impaired reticulo endothelial function

more permeable gut wall

reeduced opsonic activity (complement produced by the liver)

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33
Q

what is the commonest serious infection in cirrhosis patients and how is it diagnosed

A

spontaneous bacterial peritonitis

diagnosis is made based on high volume of neutrophils in the ascetic fluid

do blood cultures too

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34
Q

what is coma in chronic liver patients likely to be due to?

3 broad causes

A
  • 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
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35
Q

why does liver dysfuntion cause coagulopathy - 3 main reasons

A
  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
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36
Q

which is the best analgesic to use in liver disease

A

paracetamol is safest in therapeutic doses

they are more sensitive to opiates

and NSAIDd cause renal failure

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37
Q

treatment for hepatic encephalopathy

A

lactulose

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38
Q

treatment for ascites

A

salt/fluid restriction

diuretics

paracentesis

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39
Q

causes of chronic liver disease (6 main causes and some subtypes)

A
  • 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
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40
Q

What is the standard battery of tests when someone presents with chronic liver disease

A
  • 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
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41
Q

draw a table for AIH, PBC, PSC for the criteria:

raised globulins

autoantibodies

other AI diseases

F:M

genetic associations

response to steroid therapy

A
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42
Q

which different tissues do PBC, PSC and AIH affect

A

AIH - hepatocytes

PBC - the small bile ducts

sclerosing cholangitis - can affect the small bile ducts but mainly the large duct

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43
Q

autoimmune hepatitis:

prevalence in UK

gender preponderance

A

UK prevalence is 1-2/10,000

it is 70-75% women

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44
Q

what is the treatment for AIH

A

90% response to prednisolone and azathioprine

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45
Q

primary biliary cholangitis has a strong association with which autoantibody

A

antimitochondrial antibodies in 95% cases

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46
Q

what is the prevalence of PBC and what is the gender preponderance

A

~ 25/ 1,000,000 and it’s 90% women

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47
Q

how does primary biliary cholangitis present

A

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)

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48
Q

treatment of cholestatic itch

A

antihistamines help a little

cholestyramine helps in about half of cases (it is a bile acid sequestrant)

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49
Q

what other autoimmune conditions is PBC associated with

A
  • it is very often associated with one of the following
    • Sjorgens
    • Thyroiditis
    • RA
    • Coeliac
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50
Q

what is mrcp

A

magnetic resonance cholagiopancreatography

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51
Q

what are two complications of primary sclerosing cholangitis

A

strictures and gallstones

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52
Q

presentation of primary sclerosing cholangitis

A

itching

pain

rigors

jaundice

over 50% have IBD

riased alk phos and GGT

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53
Q

treatment for PSC

A

liver transplant

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54
Q

treatment for PBC

A

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

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55
Q

what causes haemochromatosis

A

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

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56
Q

presentation of haemochromatosis

A

high ferritin

high ALT and AST

gross iron staining on liver biopsy ± cirrhosis

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57
Q

treatment of haemachromatosis

A

desferrioxamine

venesection

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58
Q

what is the inheritance pattern of haemochromatosis

A

autosomal recessive

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59
Q

diagnosis of haemochromatosis

A

suggested by high ferritin

diagnosed by HFE genotyping (C282Y) and liver biopsy (gross iron staining)

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60
Q

risk factors for hepatocellular carcinoma

A
  • 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
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61
Q

presentation of hepatocellular carcinoma

A

may present with decompensation of liver disease

weight loss

ascites

abdo pain

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62
Q

50% of HCCs produce what?

A

alpha fetoprotein

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63
Q

treatment for HCC

A

transplantation

resection

local ablative therapy (including some targeted radio and percutaneous administration of chemical agents)

sorafenib is a recently developed targeted therapy

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64
Q

what percentage of the population have NAFL

A

25% of the population

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65
Q

risk factors for NAFL

A

obesity

diabetes

hyperlipidaemia

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66
Q

what is the commonest cause of mildly elevated LFTs

A

NAFL

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67
Q

what is the difference between NAFL and NASH

A

NASH is a type of NAFL where the fat droplets have caused inflammation and fibrosis

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68
Q

what is the best treatment for NAFL and NASH

A

no effective drug treatments

weight loss works well

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69
Q

very brief summary of alpha1 anti-trypsin deficiency

A

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

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70
Q

hepatic vein occlusion causes

A

thrombosis (this is budd chiari syndrome) and it may indicate an underlying thrombotic disorder

veno-occlusive disease (irradiation and anti-neoplastic drugs)

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71
Q

presentation of hepatic vein occlusion

A

liver enlargement

abnormal LFTs

ascites

acute liver failure

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72
Q

hepatic vein occlusion

A

anticoagulation

liver transplantation

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73
Q

what are the viral causes of hepatitis (try and name 10)

A

Hep ABC

Hep D and E

Yellow fever

EBV

CMV

Toxoplasma

Influenza

Coxsackie virus

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74
Q

draw Hep ABCDE table including route of transmission, whether it’s a chronic infection and prevention

A
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75
Q

symptoms of acute hepatitis

A

malaise

myalgia

fever

nausea/vomiting

cholestatic jaundice (pale stools and dark urine)

RUQ pain

tender hepatomegaly

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76
Q

test results of acute hepatitis

A

high AST

high ALT

high alk phos

low albumin

high bilirubin

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77
Q

Hep A is what type of virus

A

picornavirus

meaning small rna virus

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78
Q

Hep A transmission

A
  • faeco-oral route
    • contaminated food/water
      • shellfish
      • travellers
      • infected food handlers
    • close personal contact
      • household
      • sexual
    • blood
      • IVDU
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79
Q

what type of vaccine is the HepA vaccine, and who should have it

A

it’s inactivated hep A virus

travellers

work exposure

prevention of secondary case

lifestyle risk

other liver disease

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80
Q

what kind of virus is hepatitis B virus and where does it replicate

A

Hepadnavirus

it’s a dna virus

replicates in hepatocytes

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81
Q

what percentage of adults and children will clear a Hep B infection

A

>90% adults

<50% children

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82
Q

Hepatitis B Serology - can you draw the table for acute, previous exposure, chronic + low infectivity and chronic + high infectivity

A

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)

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83
Q

which hepatitis virus is now endemic in the UK

A

hep E virus

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84
Q

Hep B vaccine

A

recombinant DNA HBsAg

85
Q

treatment for HBV

A
  • alpha interferon
  • nucleoside analogues
    • e.g. tenofovir
  • there’s poor clearance rate but there is long-term control of HBV DNA
86
Q

what type of virus is hepatitis C

A

flavivirus (RNA)

87
Q

what is the disease course of HCV

A
  • 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
Q

what is the treatment for Hep C

A

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
Q

diagnosis of HCV

A

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
Q

how many genotypes of HCV are there and which one is the hardest to treat

A

6 and type 1 is hardest to treat

91
Q

HCV prevention

A

livestyle modification - protected sex, needle exchanges

screening blood samples

universal precautions for handling all bodily fluids

92
Q

Hepatitis D virus

A

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
Q

HEV

A
  • 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
Q

what is the difference between acute and chronic in hepatitis

A

either side of 6 months

95
Q

how does the chronic hepatitis patient appear

A
  • may be asymptomatic
  • signs of chronic liver disease
    • clubbing
    • palmar erythema
    • spider naevi
  • LFTs can be normal
96
Q

what is compensated and decompensated hepatitis

A

compensated: liver function is maintained
decompensated: jaundice, ascites, low albumin, coagulopathy, encephalopathy

97
Q

do you have immunity after infection with Hep A

A

yes 100% immunity

98
Q

Hep A management

A

supportive

monitor liver function (bilirubin, LFTs, INR, albumin)

manage close contacts

99
Q

HBV epidemiology: how many new infections per year, how many people with chronic HBV and how many deaths per year

A

129 million new infections per year

343 million with chronic HBV

750,000 deaths per year

100
Q

HBV natural history - can you draw the diagram?

A
101
Q

prevalence of Hep C in england, what percentage of these are undiagnosed and what percentage have history of IVDU

A

HCV prevalence in england is 160,000

50% undiagnosed

90% history of IVDU

102
Q

HCV natural history can you draw the diagram

A
103
Q

does previous infection with HCV confer immunity

A

no

104
Q

since when have we been screening blood products for Hep C in the UK

A

since 1991

105
Q

how many different species of bacteria are found in the GI tract

A

over 400 - they are predominantly anaerobes

106
Q

why do PPIs and broad spectrum antibiotics put us at increased risk of intraluminal infection

A

because both gastric acid and the microbiome are protective against alien invaders

107
Q

some infectious and non-infectious causes of diarrhoea

A
  • infective
    • intraluminal infection
    • systemic infectio (e.g. malaria, sepsis)
  • non-infective
    • cancer - usually associated with bleeding as well
    • chemical poisoning
    • IBD
108
Q

diarrhoea testing

A
  • stool sample
    • Microscopy
    • culture
    • sensitivity
    • toxin detection
  • Blood tests
    • blood culture
    • inflammatory markers CRP
    • FBC
109
Q

differences between watery and bloody,mucoid diarrhoea - can you draw the diagram?

consider mechanism, location, bacterial causes, viral causes, parasitic causes,

A
110
Q

how much watery stool can a patient with cholera produce every day?

A

up to 20L

111
Q

what is the bacteria implicated in rise reheating due to the toxin it produces

A

Bacillus cereus

112
Q

Why do some bacteria cause more mucoid/bloody diarrhoea

A

because they are actually invading into the gut wall

113
Q

in the UK how much of the infectious diarrhoea is caused by viruses

A

50-70%

it’s mainly rotavirus and norovirus

rotavirus mainly in children

114
Q

three most common bacterias that cause traveller’s diarrhoea

A

enterotoxigenic e.coli (majority)

campylobacter

shigella

115
Q

cholera: what is the name, how is it transmitted, what is the clinical presentation, what is the treatment

A

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
Q

what happens within the cells in cholera

A

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
Q

5 differnt parasites that can cause diarrhoea

A
  • protozoa
    • giardia
    • entamoeba
  • worms
    • schistosomiasis
    • strongyloids
118
Q

how much of the population are colonised with Clostridium difficile

A

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
Q

what are the 4 antibiotics which may give you c diff

A

rule of Cs

  • clindamycin
  • ciprofloxacin
  • co-amoxiclav
  • cephalosporins
120
Q

diarrhoea red flags

A

dehydration

electrolyte imbalance

renal failure

severe abdo pain

121
Q

presentation of C diff

A

watery diarrhoea

mild to severe colitis which is pseudomembranous on endoscopy

ileus

toxic megacolon

ASK ABOUT RECENT ANTIBIOTIC USE

122
Q

clostridium difficile management

A
  • 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
Q

what is peptic ulcer disease

A

it’s where you have an ulcer either in your stomach or in your duodenum

124
Q

how do you test for H.pylori

A

you take a stool sample and send it to the lab to test for H.pylori antigens

125
Q

where would you get pain for biliary sepsis/ascending cholangitis

A

RUQ

126
Q

what is the presentation of ascending cholangitis

A
  • charcot’s triad
    • jaundice
    • rever
    • RUQ pain
  • usually presents with rigors
127
Q

why would the biliary tree get infected

A

because of obstruction normally (stones, cancer etc) and the fluid sitting there gets infected by bacteria from the duodenum

128
Q

what would be the common organisms that cause spontaneous bacterial peritonitis in a cirrhosis patient

A

E.coli

Klebsiella

Streptococci

129
Q

what antibiotics would you use for spontaneous bacterial peritonitis

A

piperacillin until sensitivities known

130
Q

what are the commonest causes of cirrhosis

A

chronic alcohol use

chronic HBV or HCV infection

131
Q

signs of cirrhosis

A
  • leuconychia from hypoalbuminaemia
  • terry’s nails: white proximally but distal reddening from tenalgiectasis
  • clubbing
  • spider naevi
  • dupytren’s contracture
  • ascites
  • splenomegaly
132
Q

three major complications of cirrhosis

A
  • hepatic failure
  • HCC
  • Portal hypertension
133
Q

consequences of hepatic failure

A

coagulopathy

encephalopathy

hypoalbuminaemia (and associated oedema)

sepsis

spontaneous bacterial peritonitis

hypoglycaemia

134
Q

consequences of portal hypertension

A

splenomegaly

ascites

porto-systemic shunt including gastric varices (which may led to rupture and haematemesis) and caput medusae (enlarged superficial periumbilical veins)

135
Q

important tests in cirrhosis

A
  • 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
Q

what is the 5yr survival for cirrhosis

A

50%

137
Q

what is the definition of alcoholism

A

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
Q

lifetime prevalence of alcoholism in men and women

A

men: 10%
women: 4%

139
Q

how does alcoholic hepatitis present

A

malaise

anorexia

D&V

tender hepatomegaly

jaundice

bleeding

ascites

high temperature, pulse and respirations

140
Q

how will you know if alcoholic hepatitis is severe, what signs and symptoms will they have

A

jaundice

coagulopathy

encephalopathy

141
Q

what will bloods show for alcoholic hepatitis

A

low platelets

high INR

high AST

High MCV

high urea

142
Q

how to manage alcoholic hepatitis

A
  • 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
Q

once stopping alcohol consumption how do you treat withdrawal

A

if oral chlordiazepoxide is impossible then give IM lorazepam

144
Q

what is the definition of a hernia

A

protrusion of a viscus or part of a viscus through a defecit in the walls of its containing cavity into an abnormal position

145
Q

what are the complications of any cholestatic problem including cirrhosis

A

malabsorption of fat

malabsorption of fat soluble vitamins A,D,E,K

146
Q

in terms of a hernia what do the terms: irreducible, obstructed, strangulated and incarceration mean?

A
  • 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
Q

what is the most common type of hernia

A

inguinal hernia in both men and women

but much more common in men

148
Q

which is more common, the indirect or direct inguinal hernia. which one is more likely to strangulate

A

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
Q

definition of liver failure

A

development of coagulopathy (INR >1.5) and encephalopathy

150
Q

budd chiari syndrome is the occlusion of what?

A

hepatic vein

it can cause liver failure

151
Q

what are the major emergency concerns with liver failure patients

A

sepsis

hypoglycaemia

GI bleeds/varices

encephalopathy

152
Q

why does liver failure give you encephalopathy

A

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
Q

how does hepatic encephalopathy present?

A

altered mood/behaviour, sleep disturbance, drowsiness, confusion, slurred speech, personality change, restlessness, stupor, coma

154
Q

Liver failure blood tests

A
  • FBC
    • infection?
    • bleed?
  • LFT
  • Clotting (PT and INR)
  • Glucose level
  • Paracetamol level
  • Hepatitis serology
  • Ferritin
  • alpha-antitrypsin
155
Q

liver failure microbiology tests

A
  • Ascitic tap and M,C&S of ascites
    • neutrophils >250/mm3 is SBP
  • blood culture
156
Q

5 major complications of liver failure and how to treat them

A
  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
Q

what is heporenal syndrome

A

ascites, cirrhosis and renal failure occuring together

RRT and liver transplant may be required

158
Q

7 functions of the liver and what happens when they go wrong

A
  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
Q

5 different components of LFT and the type of damage they’re associated with

A

GGT - Alcoholic liver disease

ALP - anything to do with biliary tree damage

AST/ALT - raised in hepatocyte damage

bilirubin

albumin

160
Q

most important investigation if you suspect viral hepatitis

A

serology for virus antibodies and antigens

161
Q

anti-HBc, IgM anti-HBc, HBsAg and anti-HBs

what does the presence of each of the above 4 things mean

A
  • 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
Q

fill in the third column in this table of HBV serology by describing the status of the patient

A
163
Q

which viral heps are there vaccines for

A

Hep B and A

164
Q

what is the treatment for Hep A and E

A

supporting - these are self limiting infections

165
Q

what is the treatment for hepatitis B

A

pegylated IFN-alpha 2a

166
Q

what is the treatment for Hepatitis C

A

velpatasvir/sofosbuvir

167
Q

how does alcoholic liver disease occur

A

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
Q

how will LFTs look in alcoholic liver disease

A

GGT very very raised

AST and ALT mildly raised

FBC may show macrocytic anaemia

169
Q

treatment for alcoholic liver disease

A

supplementation with thiamine (pabrinex) and advise they reduce alcohol consumption

170
Q

NAFLD: risk factors, Ix and management

A

risk factors are: metabolic syndrome, obesity and T2D

Ix - enhanced liver fibrosis test

managment - lifestyle, lose weight.

171
Q

what is wernicke’s encephalopathy?

A

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
Q

Wilson’s disease

A

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
Q

what is Alpha-1-antitrypsin deficiency, what are the symptoms, investigations and mangement

A

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
Q

haemochromatosis - what is it? what is the distinctive presentation? what is the important Ix? what is the management?

A

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
Q

what is it called when liver cirrhosis causes the liver to not be able to function properly causing clinical complications

A

chronic decompensated hepatic failure

176
Q

why do you get portal hypertension in liver failure

A
  • cirrhosis causes
    • increased endothelin 1 production
    • decreased NO production
  • so reduced radius leads to increased resisitance and highe pressure in the portal system
177
Q

causes of portal hypertension: prehepatic, hepatic and post hepatic

A
  • prehepatic: portal thrombosis
  • hepatic: schistosomiasis, sarcoidosis, cirrhosis, budd chiari syndrome
  • posthepatic : right heart failure, IVC obstruction
178
Q

what are the two symptoms of ruptured oesophageal varices

A

haematemesis

malaena

179
Q

why does ascites occur in liver failure? in terms of osmotic pressure and hydrostatic pressure

A

oncotic pressure decreases because of hypoalbuminaemia

hydrostatic pressure increases due to potal hypertension and RAAS activation

180
Q

difference between transudate and exudate

A

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
Q

which antibiotic for SBP prophylaxis

A

ciprafloxacin

182
Q

which diuretic for ascites

A

spironolactone - a potassium sparing diuretic

183
Q

treatment for SBP

A

cefotaxime

184
Q

what can you give for a paracetamol overdose as well as N-acetyl-cysteine if it’s within one hour of ingestion

A

activated charcoal

185
Q
A
186
Q

what is acute cholecystitis

A

it is acute inflammation of the gall bladder sometimes caused by gallstones

187
Q

what is biliary colic

A

this is sudden pain caused by a gall stone temporarily blocking the cystic duct before becoming dyslodged back into the gallbladder

188
Q

what is cholangitis

A

this is inflammation of the bile duct system - usually due to gallstone becoming stuck and causing bacterial infection from the duodenum

189
Q

what is murphy’s sign?

A

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
Q

presentation, investigation, treatment of acute cholecystitis

A
  • presentation:
    • RUQ pain
    • Murphy’s sign
  • Ix
    • USS abdomen
    • LFTs to exclude liver/bile duct pathology
  • Treatment
    • Laparoscopic cholecystectomy
    • Supportive: analgesia and fluids
191
Q

what are the common bugs that cause ascending cholangitis

A

group D strep: e.coli, klebsiella, enterococcus

192
Q

Ix and treatment for ascending cholangitis

A
  • Ix
    • USS abdomen
    • MRCP to locate
  • treatmetn
    • ERCP to remove stone
193
Q

what is reynold’s pentad?

A
  • it is for ascending cholangitis
  • it includes charcot’s triad (fever, RUQ pain, jaundice)
  • as well as hypotension and confusion
194
Q

what are the causes of acute pancreatitis

A

GET SMASHED

  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune (SLE
  • Scorpion bites
  • Hyperglycaemia, hyperlipidaemia and hypothermia
  • ERCP (iatrogenic)
  • Drugs (azathioprine, metronidazole, tetracycline, furosemide)
195
Q

presentation of acute pancreatitis

A
  • 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
Q

Investigations and treatments for pancreatitis

A
  • Investigations:
    • amylase or lipase (inflammation of pancreas causes release of these enzymes)
    • CT abdo
  • Treatment
    • treat underlying cause
    • supportive treatment: fluids, analgesia, nutrition
197
Q

symptoms of pancreatic cancer

A

painless jaundice with weightloss = cancer of the head of the pancreas

198
Q

important complications of pancreatitis

A
  • 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
Q

what is choledocholithiasis

A

this is a bile duct stone

200
Q

three reasons people get gallstones

A

raised cholesterol

oestrogen exposure

haemolytic anaemia

201
Q

why do people get dehydrated with jaundice

A

the bilirubin in their urine pulls out water

202
Q

what are the only things that cause rigors typically

A

pyelonephritis

lobar pneumonia

cholangitis

203
Q

what is gallstone ileus

A

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
Q

diagnosis of pancreatitis

A

amylase or lipase of 3x upper limit of normal

CT them if they’re unwell

205
Q

pancreatitis treatment

A
  • mostly supportive
    • IV fluid
    • analgesia
    • catheter
    • manage complication
    • feeding with nasojejunal tube
  • maybe a laparoscopic cholecystectomy if gallstones caused it
206
Q
A
207
Q

what is the modified glasgow score?

A
  • 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
Q

how is sbp diagnosed

A

ascitic tap

if neutrophils are >250/mm3 then it’s diagnostic

209
Q

empiracle treatment for SBP

A

ceftriaxone

formative 3b (18 decks)

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