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Gastro Flashcards

1
Q

Primary Sclerosing Cholangitis

what is it

A

the intrahepatic or extrahepatic ducts become strictured + fibrotic

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2
Q

Primary Sclerosing Cholangitis

pathophysiology

A

strictured + fibrotic intrahepatic or extrahepatic ducts

obstruction to flow of bile out liver and into intestines

chronic bile obstruction leads to hepatitis, fibrosis and cirrhosis

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3
Q

Primary Sclerosing Cholangitis

what does sclerosis refer to

A

stiffening and hardening of the bile ducts

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4
Q

Primary Sclerosing Cholangitis

what does cholangitis refer to

A

inflammation of the bile ducts

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5
Q

Primary Sclerosing Cholangitis

what condition is it associated with

A

ulcerative colitis

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6
Q

Primary Sclerosing Cholangitis

cause

A

unclear but probs a combination of:

  • genetic
  • autoimmune
  • intestinal microbiome
  • environmental factors
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7
Q

Primary Sclerosing Cholangitis

RFs (4)

A
  • male
  • aged 30-40
  • ulcerative colitis
  • FH
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8
Q

Primary Sclerosing Cholangitis

presentation (5)

A
  • jaundice
  • chronic RUQ pain
  • pruritis
  • fatigue
  • hepatomegaly
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9
Q

Primary Sclerosing Cholangitis

what will LFTs show

A

a ‘cholestatic’ picture

ALP is the most deranged

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10
Q

Primary Sclerosing Cholangitis

LFTs: why may there be a rise in bilirubin

A

as the strictures become more severe and prevents bilirubin from being excreted through the bile duct

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11
Q

Primary Sclerosing Cholangitis

LFTs: why may other LFTs apart from ALP be deranged

A

as the disease progresses to hepatitis

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12
Q

Primary Sclerosing Cholangitis

are there any antibodies which are highly sensitive or specific to PSC

A

no but can indicate where there is an autoimmune element that may respond to immunosuppression

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13
Q

Primary Sclerosing Cholangitis

which autoantibodies may be present

A

p-ANCA (94%)

ANA (77%)

aCL (63%) - anticardiolipid

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14
Q

Primary Sclerosing Cholangitis

gold standard inx for dx

A

MRCP - magnetic resonance cholangiopancreatography (MRI scan of the liver, bile ducts and pancreas)

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15
Q

Primary Sclerosing Cholangitis

what will the MRCP show

A

may show bile duct lesions or strictures

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16
Q

Primary Sclerosing Cholangitis

associations and complications

A
  • acute bacterial cholangitis
  • cholangiocarcinoma
  • colorectal cancer
  • cirrhosis and liver failure
  • biliary strictures
  • fat soluble vitamin deficiencies
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17
Q

Primary Sclerosing Cholangitis

mnx

A
  • liver transplant
  • ERCP
  • Colestyramine
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18
Q

Primary Sclerosing Cholangitis

mnx: what is ERCP

A

endoscopic retrograde cholangio-pancreatography

insert camera through throat through to bile ducts.

Use X-rays and injecting contrast to identify any strictures

stented

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19
Q

Primary Sclerosing Cholangitis

mnx: what is colestyramine

A

a bile acid sequestrate: binds to bile acids to prevent absorption in the gut

can help with pruritus due to raised bile acids

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20
Q

Primary Biliary Cirrhosis

what is it

A

the immune system attacks the small bile ducts within the liver

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21
Q

Primary Biliary Cirrhosis

how does it lead to fibrosis, cirrhosis and liver failure

A

immune system attacks the intralobar ducts (aka Canals of Hering)

this causes obstruction of the outflow of bile (cholestasis)

back pressure of bile obstruction leads to fibrosis

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22
Q

Primary Biliary Cirrhosis

what causes itching

A

obstruction to the outflow of bile acids so they build up in the blood as they are not being excreted

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23
Q

Primary Biliary Cirrhosis

what causes jaundice

A

obstruction to the outflow of biliruibin so they build up in the blood as they are not being excreted

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24
Q

Primary Biliary Cirrhosis

what causes raised cholesterol

A

obstruction to the outflow of cholesterol so they build up in the blood as they are not being excreted

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25
Q

Primary Biliary Cirrhosis

what is the name for cholesterol deposits in the skin

A

xanthelasma

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26
Q

Primary Biliary Cirrhosis

why is there increased risk of CVD

A

cholesterol deposits in blood vessels

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27
Q

Primary Biliary Cirrhosis

why are there greasy stools

A

lack of bile acids –> fat not digested

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28
Q

Primary Biliary Cirrhosis

why are there pale stools

A

lack of biliruibin

biliruibin normally causes the dark colour of stool

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29
Q

Primary Biliary Cirrhosis

presentation

A
  • fatigue
  • pruritis
  • GI disturbance + abdo pain
  • jaundice
  • pale stools
  • xanthoma + xanthelasma
  • signs of cirrhosis + failure (ascites, splenomegaly, spider naevi)
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30
Q

Primary Biliary Cirrhosis

what is xanthoma

A

larger nodular cholesterol deposits in the skin or tendons

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31
Q

Primary Biliary Cirrhosis

associations (3)

A
  • middle aged women
  • autoimmune disease (thyroid, coeliac)
  • rheumatoid conditions (systemic sclerosis, Sjogrens + RA)
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32
Q

Primary Biliary Cirrhosis

LFT result

A

cholestatic picture

ALP raised first, then others + biliruibin raised in later disease

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33
Q

Primary Biliary Cirrhosis

what it the most specific autoantibody to PBC and forms part of the diagnostic criteria

A

anti-mitochondrial antibodies

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34
Q

Primary Biliary Cirrhosis

autoantibodies

A

anti-mitochondrial antibodies (most specific)

ANA (35%)

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35
Q

Primary Biliary Cirrhosis

what inx is used for diagnosis and staging

A

liver biopsy

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36
Q

Primary Biliary Cirrhosis

what will other blood tests show (apart from LFTs)

A
  • raised ESR

- raised IgM

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37
Q

Primary Biliary Cirrhosis

mnx

A
  • ursodeoxycholic acid
  • colestyramine
  • liver transplant (end stage liver disease)
  • immunosuppression with steroids is considered in some
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38
Q

Primary Biliary Cirrhosis

mnx: how does ursodeoxycholic acid work

A

reduces the intestinal absorption of cholesterol

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39
Q

Primary Biliary Cirrhosis

mnx: how does colestyramine work

A

a bile acid sequestrate: binds to bile acids to prevent absorption in the gut

and can help with pruritis due to raised bile acids

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40
Q

Primary Biliary Cirrhosis

what are the most important end results of this disease

A
  • advanced liver cirrhosis

- portal HTN

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41
Q

Primary Biliary Cirrhosis

complications

A
  • distal renal tubular acidosis
  • hypothyroidism
  • osteoporosis
  • hepatocellular carcinoma
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42
Q

Alpha 1 Antitrypsin Deficiency

what is it

A

a condition caused by an abnormality in the gene for a protease inhibitor called alpha-1-antitrypsin

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43
Q

Alpha 1 Antitrypsin Deficiency

what enzyme is secreted from neutrophils

A

elastase

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44
Q

Alpha 1 Antitrypsin Deficiency

what does the enzyme, elastase do?

A

digests connective tissue

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45
Q

Alpha 1 Antitrypsin Deficiency

where is Alpha 1 Antitrypsin mainly produced

A

in the liver

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46
Q

Alpha 1 Antitrypsin Deficiency

how does alpha-1-antitrypsin protect the body

A

travels around the body and inhibits the neutrophil elastase enzyme

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47
Q

Alpha 1 Antitrypsin Deficiency

what chromosome is A1AT coded for on

A

14

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48
Q

Alpha 1 Antitrypsin Deficiency

what is the inheritance pattern

A

autosomal recessive

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49
Q

Alpha 1 Antitrypsin Deficiency

what are the 2 main organs it affects

A

liver and lungs

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50
Q

Alpha 1 Antitrypsin Deficiency

what does it lead to after 30 years old

A

bronchiectasis and emphysema in the lungs

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51
Q

Alpha 1 Antitrypsin Deficiency

what does it lead to after 50 years old

A

liver cirrhosis

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52
Q

Alpha 1 Antitrypsin Deficiency

how does it cause liver cirrhosis and hepatocellular carcinoma

A

a mutant version of A1AT protein is created in the liver

gets trapped and builds up and causes liver damage

the liver damage progresses to cirrhosis over time and can lead to HCC

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53
Q

Alpha 1 Antitrypsin Deficiency

how does it cause bronchiectasis and emphysema

A

lack of normal A1AT leads to excess protease enzymes that attack the connective tissue in the lungs

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54
Q

Alpha 1 Antitrypsin Deficiency

what is the screening test of choice

A

serum-alpha-1-antitrypsin (low)

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55
Q

Alpha 1 Antitrypsin Deficiency

what would liver biopsy show

A

cirrhosis and

acid-Schiff-positive staining globules in hepatocytes

(this stain highlights the mutant alpha-1-antitrypsin proteins)

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56
Q

Alpha 1 Antitrypsin Deficiency

what gene are you looking for in genetic testing

A

A1AT gene

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57
Q

Alpha 1 Antitrypsin Deficiency

how to diagnose bronchiectasis and emphysema

A

high resolution CT thorax

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58
Q

Alpha 1 Antitrypsin Deficiency

mnx

A
  • stop smoking
  • symptomatic mnx
  • organ transplant for end stage liver or lung disease
  • moniter complications (HCC)
  • NICE do not recommend replacement A1AT
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59
Q

Upper GI bleed

where is the bleeding from

A

the oesophagus, stomach or duodenum

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60
Q

Upper GI bleed

DDx

A
  • oesophageal varices
  • Mallory-Weiss tear
  • ulcers (stomach or duodenum)
  • cancers of the stomach or duodenum
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61
Q

Upper GI bleed

presentation

A
  • haematemesis (vomiting blood)
  • coffee ground vomit
  • melaena
  • haemodynamic instability if large blood loss
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62
Q

Upper GI bleed

what is coffee ground vomit

A

vomiting digested blood that looks like coffee grounds

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63
Q

Upper GI bleed

what is melaena

A

tar like, black, greasy and offensive stools caused by digested blood

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64
Q

Upper GI bleed

how would haemodynamic instability present

A
  • low BP
  • tachycardia
  • signs of shock
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65
Q

Upper GI bleed

how would a peptic ulcer present as

A

epigastric pain and dyspepsia

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66
Q

Upper GI bleed

how would a pt with liver disease with oesophageal varices present with

A

jaundice or ascites

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67
Q

Upper GI bleed

what scoring system is used to establish their risk of having an upper GI bleed

A

Glasgow-Blatchford Score

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68
Q

Upper GI bleed

what does the Glasgow-Blatchford score take into account

A
  • drop in Hb
  • Rise in urea
  • BP
  • HR
  • Melaena
  • Syncope
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69
Q

Upper GI bleed

what indicates a high risk in the Glasgow-Blatchford score

A

> 0

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70
Q

Upper GI bleed

why does the urea rise

A

the blood in the GI tract gets broken down by the acid and digestive enzymes

one of the breakdown products is urea which is absorbed in the intestines

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71
Q

Upper GI bleed

which scoring system is used for pts that have had an endoscopy to calculate their risk of rebleeding and overall mortality

A

Rockall Score

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72
Q

Upper GI bleed

what features does the Rockall Score take into account

A
  • age
  • features of shock (tachycardia or hypotension)
  • co-morbidities
  • cause of bleeding
  • endoscopic stigmata of recent haemorrhage e.g. clots or visible bleeding vessels
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73
Q

Upper GI bleed

mnx

A

ABATED

ABCDE 
Bloods
Access (2 large bore cannula)
Transfuse 
Endoscopy (within 24hrs)
Drugs (stop anticoagulants + NSAIDs)
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74
Q

Upper GI bleed

what bloods should you send for

A
  • Haemoglobin (FBC)
  • Urea (U&Es)
  • Coagulation (INR, FBC for platelets)
  • Liver disease (LFTs)
  • Crossmatch 2 units of blood
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75
Q

Upper GI bleed

what’s the difference between ‘Group & Save’ and ‘Crossmatch’

A

“Group and save”: lab checks the pt’s blood group and keeps a sample of their blood saved in case they need to match blood to it.

“Crossmatch”: lab finds blood, tests that it is compatible and keeps it ready in the fridge to be used if necessary

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76
Q

Upper GI bleed

what do you transfuse to pts with massive haemorrhage

A

blood, platelets and clotting factors (fresh frozen plasma)

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77
Q

Upper GI bleed

when should platelets be given

A

in active bleeding and thrombocytopenia (platelets<50)

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78
Q

Upper GI bleed

what can be given to pts taking warfarin that are actively bleeding

A

prothrombin complex concentrate

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79
Q

Upper GI bleed

what can be given if suspecting oesophageal varices (in pts with a hx of chronic liver disease)

A
  • Terlipressin

- prophylactic broad spectrum abx

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80
Q

Upper GI bleed

definitive trx

A

oesophagogastroduodenoscopy (OGD)

to provide interventions that stop the bleeding e.g. banding of varices or cauterisation of the bleeding vessel.

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81
Q

Upper GI bleed

should you use PPI prior to endoscopy

A

NICE recommend against using a PPI but some senior doctors do this.

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82
Q

Haemochromatosis

what is it

A

an iron storage disorder that results in excessive total body iron and deposition of iron in tissues

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83
Q

Haemochromatosis

what gene is affected

A

the human haemochromatosis protein (HFE) gene

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84
Q

Haemochromatosis

where is the HFE gene located

A

Ch6

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85
Q

Haemochromatosis

what is the inheritance pattern

A

autosomal recessive

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86
Q

Haemochromatosis

what does the HFE gene do

A

regulate iron metabolism

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87
Q

Haemochromatosis

when does it usually present

A

after the age of 40 when the iron overload becomes symptomatic

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88
Q

Haemochromatosis

why does it present later in females

A

due to the menstruation acting to regularly eliminate iron from the body

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89
Q

Haemochromatosis

symptoms

A
  • memory + mood disturbance
  • hair loss
  • chronic tiredness
  • bronze skin pigmentation
  • erectile dysfunction
  • amenorrhoea
  • joint pain
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90
Q

Haemochromatosis

main diagnostic inx

A

serum ferritin

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91
Q

Haemochromatosis

what does it mean when it says ferritin is an acute phase reactant

A

ferritin levels go up with inflammatory conditions such as infection

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92
Q

Haemochromatosis

what inx to perform to distinguish between high ferritin caused by iron overload vs other causes like inflammation or nonalcoholic fatty liver disease

A

transferrin saturation

high in haemochromatosis

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93
Q

Haemochromatosis

high serum ferritin, high transferrin saturation, what inx next?

A

genetic testing

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94
Q

Haemochromatosis

what used to be the gold standard inx but has been surpassed by genetic testing

A

liver biopsy with Perl’s stain to establish iron conc in the parenchymal cells

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95
Q

Haemochromatosis

what inx to show a non-specific increase in attenuation of the liver

A

CT abdo

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96
Q

Haemochromatosis

what inx to give a more detailed pic of liver deposits of iron and iron deposits in the heart

A

MRI

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97
Q

Haemochromatosis

complications

A
  • T1DM
  • liver cirrhosis
  • hypogonadism, impotence, amenorrhea, infertility
  • cardiomyopathy
  • HCC
  • hypothyroidism
  • chondrocalcinosis/pseudogout
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98
Q

Haemochromatosis

why is T1DM a complication

A

iron affects the functioning of the pancreas

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99
Q

Haemochromatosis

why is hypogonadism, impotence, amenorrhea, infertility a complication

A

iron deposits in the pituitary and gonads leads to endocrine and sexual problems

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100
Q

Haemochromatosis

why is cardiomyopathy a complication

A

iron deposits in the heart

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101
Q

Haemochromatosis

why is hypothyroidism a complication

A

iron deposits in the thyroid

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102
Q

Haemochromatosis

why is Chrondocalcinosis / pseudogout a complication

A

calcium deposits in joints causing arthritis

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103
Q

Haemochromatosis

mnx

A
  • Venesection
  • moniter serum ferritin
  • avoid alcohol
  • genetic counselling
  • moniter and trx of complications
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104
Q

Haemochromatosis

mnx: what is venesection

A

a weekly protocol of removing blood to decrease total iron

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105
Q

what is Zollinger Ellison Syndrome

A

a condition where there is excess acid production leading to peptic ulcers

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106
Q

what is Zollinger Ellison Syndrome caused by

A

a gastinoma which is a neuroendocrine tumour secreting the hormone, gastrin

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107
Q

what is Gilbert’s syndrome

A

an autosomal recessive* condition of defective bilirubin conjugation caused by deficiency of UDP glucuronosyltransferase

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108
Q

signs of Gilbert’s syndrome

A
  • unconjugated hyperbilirubinaemia (i.e. not in urine)

- jaundice may only be seen during an intercurrent illness, exercise or fasting

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109
Q

Gilbert’s syndrome

Inx

A

rise in bilirubin following prolonged fasting or IV nicotinic acid

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110
Q

Gilbert’s syndrome

trx

A

none

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111
Q

what is the 1st line trx for ascites in liver disease

A

spironolactone

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112
Q

what are 3 defining features of acute liver failure

A
  • INR>1.5
  • encephalopathy
  • jaundice
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113
Q

what is a marker of HCC

A

alpha-fetoprotein

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114
Q

what is definitive mnx for a perforated peptic ulcer

A

laparotomy

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115
Q

IBD

features of Crohn’s

A

crows NESTS

No blood or mucus

Entire GI tract

Skip lesions on endoscopy

Terminal ileum most affected + Transmural inflammation

Smoking is a RF (don’t set the nest on fire)

weight loss, strictures, fistulas

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116
Q

IBD

features of Ulcerative Colitis

A

U-C-CLOSEUP

Continuous inflammation 
Limited to colon + rectum 
Only superficial mucosa affected 
Smoking is protective 
Excrete blood + mucus 
Use aminosalicylates 
Primary Sclerosing Cholangitis
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117
Q

IBD

presentation (4)

A
  • diarrhoea
  • abdo pain
  • passing blood
  • weight loss
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118
Q

IBD

screening test

A

faecal calprotectin

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119
Q

IBD

why is faecal calprotectin raised

A

released by the intestines when inflamed

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120
Q

IBD

diagnostic inx?

A

endoscopy (OGD + colonoscopy) with biopsy

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121
Q

IBD

inx to look for complications such as fistulas, abscesses + strictures

A

imaging w/ US, CT + MRI

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122
Q

IBD

what inx indicates inflammation and active disease

A

CRP

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123
Q

IBD

1st line to induce remission in Crohn’s

A

steroids (PO prednisolone or IV hydrocortisone)

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124
Q

IBD

Crohn’s: if steroids don’t work to induce remission, what do you consider adding?

A

immunosuppressants:

  • Azathioprine
  • Mercaptopurine
  • Methotrexate
  • Infliximab
  • Adalimumab
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125
Q

IBD

Crohn’s: maintaining remission 1st line

A
  • Azathioprine

- Mercaptopurine

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126
Q

IBD

Crohn’s: when is it possible to surgically resect

A

when the disease only affects the distal ileum

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127
Q

IBD

UC: inducing remission in mild to moderate disease

A

1st line: aminosalicylate (e.g. PO mesalazine or rectal)

2nd line: corticosteroids (prednisolone)

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128
Q

IBD

UC: inducing remission in severe disease

A

1st line: IV corticosteroids (hydrocortisone)

2nd line: IV ciclosporin

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129
Q

IBD

UC: maintaining remission

A

AMINOSALICYLATE (e.g. mesalazine PO or rectal)

azathioprine
mercaptopurine

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130
Q

IBD

what does UC typically only affect

A

the colon and rectum

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131
Q

IBD

UC: what surgery will remove the disease

A

panproctocolectomy (removal of colon and rectum)

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132
Q

IBD

after a panproctocolectomy, what is left?

A

either a permanent ileostomy or an ileo-anal anastomosis (J-pouch)

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133
Q

IBD

what is an ileo-anal anastomosis (J-pouch)

A

the ileum is folded back in itself and fashioned into a larger pouch that functions a bit like a rectum.

This “J-pouch” which is then attached to the anus and collects stools prior to the person passing the motion.

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134
Q

what is Melanosis coli

A

colonoscopy shows dark brown pigmented areas in the lamina propria usually asssociated with chronic laxative abuse (Senna)

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135
Q

Liver Cancer

what is primary liver cancer

A

cancer that originates in the liver

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136
Q

Liver Cancer

what are the 2 main types of primary liver cancer

A

hepatocellular carcinoma (80%)

cholangiocarcinoma (20%).

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137
Q

Liver Cancer

what is secondary liver cancer

A

cancer that originates outside the liver and metastasises to the liver

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138
Q

Liver Cancer

the main RF for HCC is liver cirrhosis due to?

A
  • Viral hepatitis (B and C)
  • Alcohol
  • Non alcoholic fatty liver disease
  • Other chronic liver disease
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139
Q

Liver Cancer

Cholangiocarcinoma is associated with what condition

A

primary sclerosing cholangitis

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140
Q

Liver Cancer

why is there a poor prognosis

A

often remains asymptomatic for a long time and then presents late

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141
Q

Liver Cancer

presentation

A
  • Weight loss
  • Abdominal pain
  • Anorexia
  • Nausea and vomiting
  • Jaundice
  • Pruritus
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142
Q

Liver Cancer

how do cholangiocarcinomas present similarly to pancreatic cancer

A

painless jaundice

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143
Q

Liver Cancer

what is the tumour marker for HCC

A

Alpha-fetoprotein

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144
Q

Liver Cancer

what is the tumour marker for cholangiocarcinoma

A

CA19-9

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145
Q

Liver Cancer

what inx to diagnose and stage

A

CT and MRI

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146
Q

Liver Cancer

initial inx

A

liver US

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147
Q

Liver Cancer

which inx to take biopsies or brushings to diagnose cholangiocarcinoma

A

ERCP

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148
Q

Liver Cancer

what mnx options can be curative in HCC

A
  • Resection of early disease in a resectable area of the liver
  • Liver transplant when the HCC is isolated to the liver
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149
Q

Liver Cancer

what medical trx is licensed for HCC

A

several kinase inhibitors: sorafenib, regorafenib and lenvatinib

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150
Q

Liver Cancer

How do kinase inhibitors work in treating HCC

A

inhibit the proliferation of cancer cells.

can potentially extend life by months.

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151
Q

Liver Cancer

is chemo or radio used in HCC or cholangiocarcinomas

A

No, both are generally considered resistant to chemo and radiotherapy.

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152
Q

Liver Cancer

early disease of cholangiocarcinoma can be cured how?

A

potentially be cured with surgical resection.

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153
Q

Liver Cancer

mnx of cholangiocarcinoma

A

ERCP: stent in bile duct where the cholangiocarcinoma is compressing the duct.

allows drainage of bile and usually improves symptoms.

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154
Q

Liver Cancer

what is a haemangioma

A

common benign tumours of the liver

often found incidentally

no sx no potential to become cancerous.

no trx or monitoring required

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155
Q

Liver Cancer

what is Focal nodular hyperplasia

A

a benign liver tumour made of fibrotic tissue

often found incidentally

usually asymptomatic and has no malignant potential

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156
Q

Liver Cancer

whom is focal nodular hyperplasia more common in

A

often related to oestrogen and is therefore more common in women and those on the OCP

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157
Q

Alcoholic Liver Disease

what is the stepwise progression of alcoholic liver disease

A
  1. alcohol related fatty liver
  2. alcoholic hepatitis
  3. cirrhosis
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158
Q

Alcoholic Liver Disease

recommended alcohol consumption

A

14 units/week for both men and women

spread evenly over 3≥ days and not >5 units/day

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159
Q

Alcoholic Liver Disease

which questions can be used to quickly screen for harmful alcohol use

A

CAGE questions

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160
Q

Alcoholic Liver Disease

what are the CAGE questions

A

Cut down - ever thought you should?

Annoyed - at others commenting on your drinking

Guilty - ever feel guilty about drinking

Eye opener - ever drink in the morning to help your hangover/nerves

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161
Q

Alcoholic Liver Disease

what is the AUDIT questionnaire

A

Alcohol Use Disorders Identification Test to screen people for harmful alcohol use.

10Q’s with MCA

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162
Q

Alcoholic Liver Disease

what score on the AUDIT questionnaire indicates harmful use

A

≥8

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163
Q

Alcoholic Liver Disease

complications of alcohol

A
  • alcoholic liver disease
  • cirrhosis –> HCC
  • alcohol dependence + withdrawal
  • Wernicke-Korsakoff Syndrome
  • Pancreatitis
  • alcoholic cardiomyopathy
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164
Q

Alcoholic Liver Disease

signs of liver disease

A
  • jaundice
  • hepatomegaly
  • spider naevi
  • palmar erythema
  • gynaecomastia
  • bruising
  • ascites
  • caput medusae - engorged superficial epigastric veins
  • asterixis - ‘flapping tremor’ in decompensated liver disease
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165
Q

Alcoholic Liver Disease

what would FBC show

A

raised MCV

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166
Q

Alcoholic Liver Disease

what would LFTs show

A

RAISED GGT

elevated ALT, AST

low albumin due to reduced synthetic function

elevated ALP later in the disease

elevated bilirubin in cirrhosis

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167
Q

Alcoholic Liver Disease

what would the bloods in clotting show

A

elevated PTT due to reduced synthetics function of the liver

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168
Q

Alcoholic Liver Disease

when may U+E’s be deranged

A

hepatorenal syndrome

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169
Q

Alcoholic Liver Disease

what may US show

A

“increased echogenicity” - fatty changes

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170
Q

Alcoholic Liver Disease

what is a FibroScan

A

checks the elasticity of the liver by sending high frequency sound waves into the liver

helps assess the degree of cirrhosis

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171
Q

Alcoholic Liver Disease

diagnosis of alcohol-related hepatitis or cirrhosis

A

liver biopsy

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172
Q

Alcoholic Liver Disease

general mnx

A
  • stop drinking
  • consider detoxification regime
  • thiamine + high protein diet
  • short term steroids
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173
Q

Alcoholic Liver Disease

alcohol withdrawal sx 6-12h after alcohol consumption ceases

A
  • tremor
  • sweating
  • headache
  • craving + anxiety
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174
Q

Alcoholic Liver Disease

alcohol withdrawal sx 12-24h after alcohol consumption ceases

A

hallucinations

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175
Q

Alcoholic Liver Disease

alcohol withdrawal sx 24-48h after alcohol consumption ceases

A

seizures

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176
Q

Alcoholic Liver Disease

alcohol withdrawal sx 24-72h after alcohol consumption ceases

A

delirium tremens

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177
Q

Alcoholic Liver Disease

pathophysiology of delirium tremens

A

alcohol stimulates GABA receptors in brain –> relaxing effect

alcohol inhibits glutamate (NMDA) receptors –> inhibitory effect on electrical activity on brain

chronic alcohol use –> GABA system becomes down regulated and glutamate system becomes up regulated

alcohol removed –> GABA under functions and glutamate over functions – > excess adrenergic activity

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178
Q

Alcoholic Liver Disease

presentation of delirium tremens

A
  • Acute confusion
  • Severe agitation
  • Delusions and hallucinations
  • Tremor
  • Tachycardia
  • Hypertension
  • Hyperthermia
  • Ataxia (difficulties with coordinated movements)
  • Arrhythmias
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179
Q

Alcoholic Liver Disease

what can be used to score the patient on their withdrawal symptoms and guide treatment.

A

The CIWA-Ar (Clinical Institute Withdrawal Assessment – Alcohol revised) tool

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180
Q

Alcoholic Liver Disease

mnx of alcohol withdrawal

A

Chlordiazepoxide (“Librium”)
(a benzodiazepine)

IV high-dose B vitamins (pabrinex)

followed by a regular lower dose PO thiamine

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181
Q

Alcoholic Liver Disease

how is chlordiazepoxide given

A

orally as a reducing regime titrated to the required dose based on the local alcohol withdrawal protocol (e.g. 10 – 40 mg every 1 – 4 hours).

continued for 5-7 days.

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182
Q

Alcoholic Liver Disease

why does it lead to thiamine (Vit B1) deficiency

A
  • thiamine is poorly absorbed in the presence of alcohol

- alcoholics tend to have poor diets and rely on the alcohol for their calories

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183
Q

Alcoholic Liver Disease

features of Wernicke’s encephalopathy

A
  • confusion
  • oculomotor disturbances
  • ataxia
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184
Q

Alcoholic Liver Disease

what comes after Wernicke’s encephalopathy

A

Korsakoff’s syndrome (often irreversible)

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185
Q

Volvulus

what is it

A

bowel twists around itself and the mesentery that it is attached to

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186
Q

Volvulus

what are the 2 main types

A
  • sigmoid volvulus

- caecal volvulus

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187
Q

Volvulus

which type is more common and tends to affect older patients

A

sigmoid volvulus

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188
Q

Volvulus

what is a key cause of sigmoid volvulus (2)

A

chronic constipation

lengthening of the mesentery attached to the sigmoid colon

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189
Q

Volvulus

what are sigmoid volvulus’ associate with (2)

A
  • high fibre diet
  • excessive use of laxatives

the sigmoid colon becomes overloaded with faeces. causing it to sink down causing a twist

190
Q

Volvulus

who does caecal volvulus tend to affect

A

younger patients and less common

191
Q

Volvulus

risk factors (6)

A
  • high fibre diet
  • chronic constipation
  • adhesions
  • neuropsychiatric disorders (e.g. Parkinson’s)
  • nursing home residents
  • pregnancy
192
Q

Volvulus

presentation

A

akin to bowel obstruction, with:

  • Vomiting (particularly green bilious vomiting)
  • Abdominal distention
  • Diffuse abdominal pain
  • Absolute constipation and lack of flatulence
193
Q

Volvulus

what will the abdo x-ray show in sigmoid volvulus

A

‘coffee bean’ sign

194
Q

Volvulus

what is the diagnostic inx

A

contrast CT scan

195
Q

Volvulus

initial mnx

A

same as with bowel obstruction

  • nil by mouth
  • NG tube
  • IV fluids
196
Q

Volvulus

conservative mnx for sigmoid volvulus

A
  • endoscopic decompression (without peritonitis)
197
Q

Volvulus

what happens in endoscopic decompression

A
  • flexible sigmoidoscope is inserted carefully,
  • patient in the left lateral position, resulting in a correction of the volvulus.
  • A flatus tube / rectal tube is left in place temporarily to help decompress the bowel and is later removed.
198
Q

Volvulus

what surgical procedure is appropriate for a sigmoid volvulus

A

Hartmann’s procedure
- removal of the rectosigmoid colon and formation of a colostomy

laparotomy

199
Q

Volvulus

what surgical procedure is appropriate for a caecal volvulus

A

Ileocaecal resection or right hemicolectomy

200
Q

Liver Cirrhosis

what is it

A

the result of chronic inflammation and damage to liver cells

when the liver cells are damaged they are replaced with scar tissue (fibrosis) and nodules of scar tissue form within the liver

201
Q

Liver Cirrhosis

what causes portal hypertension

A

fibrosis affects the structure and blood flow through the liver

which causes increased resistance in the vessels leading in to the liver

202
Q

Liver Cirrhosis

most common causes

A
  1. alcoholic liver disease
  2. non alcoholic fatty liver disease
  3. Hep B
  4. Hep C
203
Q

Liver Cirrhosis

rarer causes

A
  • autoimmune hepatitis
  • primary biliary cirrhosis
  • haemochromatosis
  • Wilson’s disease
  • alpha-1 antitrypsin deficiency
  • cystic fibrosis
  • drugs (amiodarone, methotrexate, sodium valproate)
204
Q

Liver Cirrhosis

signs of cirrhosis

A
  • jaundice
  • hepatomegaly
  • splenomegaly
  • spider naevi
  • palmar erythema
  • gynaecomastia and testicular atrophy in males
  • bruising
  • ascites
  • caput medusae
  • asterixis
205
Q

Liver Cirrhosis

inx

A
  • bloods
  • US
  • Fibroscan
  • Endoscopy
  • CT/MRI
  • liver biopsy
206
Q

Liver Cirrhosis

what will LFTs show

A

often normal

but in decompensated cirrhosis ALT, AST, ALP and bilirubin become deranged

207
Q

Liver Cirrhosis

what happens to albumin and PTT (markers of ‘synthetic function’ of the liver) as the synthetic function becomes worse

A
  • albumin drops

- PTT increases

208
Q

Liver Cirrhosis

what does hyponatraemia indicate

A

fluid retention in severe liver disease

209
Q

Liver Cirrhosis

what becomes deranged in hepatorenal syndrome

A

urea and creatinine

210
Q

Liver Cirrhosis

what is a tumour marker for HCC and can be checked every 6m as a screening test in patients with cirrhosis along with ultrasound.

A

Alpha-fetoprotein

211
Q

Liver Cirrhosis

what is the 1st line inx for assessing fibrosis in non-alcoholic fatty liver disease

A

Enhanced Liver Fibrosis (ELF) blood test

212
Q

Liver Cirrhosis

what does the enhanced liver fibrosis (ELF) blood test measure

A

3 markers (HA, PIIINP and TIMP-1)

uses an algorithm to provide a result that indicates the fibrosis of the liver:

213
Q

Liver Cirrhosis

what does the enhanced liver fibrosis (ELF) blood test of <7.7 indicate

A

none to mild fibrosis

214
Q

Liver Cirrhosis

what does the enhanced liver fibrosis (ELF) blood test of ≥ 7.7 to 9.8 indicate

A

moderate fibrosis

215
Q

Liver Cirrhosis

what does the enhanced liver fibrosis (ELF) blood test of ≥9.8 indicate

A

severe fibrosis

216
Q

Liver Cirrhosis

what may US show

A
  • nodules on surface
  • ‘corkscrew’ arteries: increased flow was they compensate for reduced portal flow
  • enlarged portal vein with reduced flow
  • ascites
  • splenomegaly
217
Q

Liver Cirrhosis

what is a ‘FibroScan’ used for

A

to check the elasticity of the liver by sending high frequency sound waves into the liver.

helps assess the degree of cirrhosis.

This is called “transient elastography” and should be used to test for cirrhosis.

218
Q

Liver Cirrhosis

how often should you test patients at risk of cirrhosis with a FibroScan

A

every 2 years

219
Q

Liver Cirrhosis

at risk patients of cirrhosis

A
  • hep C
  • heavy alcohol drinkers (M>50U, W>35U/week)
  • diagnosed alcoholic liver disease
  • non alcoholic fatty liver disease + evidence of fibrosis on ELF blood test
  • chronic hep B
220
Q

Liver Cirrhosis

when can endoscopy be used

A

to assess for and treat oesophageal varices when portal hypertension is suspected

221
Q

Liver Cirrhosis

when can CT/MRI be used

A

to look for HCC, hepatosplenomegaly, abnormal blood vessel changes and ascites

222
Q

Liver Cirrhosis

which inx can be used to confirm the dx of cirrhosis

A

liver biopsy

223
Q

Liver Cirrhosis

which scoring system indicates the severity of cirrhosis and the prognosis

A

Child-Pugh Score for Cirrhosis

224
Q

Liver Cirrhosis

what features are used in the Child-Pugh Score for Cirrhosis

A
  1. Bilirubin
  2. Albumin
  3. INR
  4. Ascites
  5. Encephalopathy
225
Q

Liver Cirrhosis

which scoring system is recommended by NICE to be used every 6 months in patients with compensated cirrhosis

A

MELD score

gives a % estimated 3m mortality and helps guide referral for liver transplant

226
Q

Liver Cirrhosis

what features does the MELD score take into account

A
  • biliruibin
  • creatinine
  • INR
  • sodium
227
Q

Liver Cirrhosis

general mnx

A
  • US + alpha fetoprotein every 6m for HCC
  • endoscopy every 3y in pts with known varices
  • high protein, low Na diet
  • MELD score every 6m
  • consideration of liver transplant
  • managing complicatiions
228
Q

Liver Cirrhosis

complications

A
  • malnutrition
  • portal hypertension, varices + variceal bleeding
  • ascites + SBP
  • hepato-renal syndrome
  • hepatic encephalopathy
  • HCC
229
Q

Liver Cirrhosis

why does it cause malnutrition + muscle wasting

A
  • metabolism of proteins in liver affected and reduces the amount of protein
  • disrupts livers ability to store glucose as glycogen
  • results in body using muscle tissue as fuel leading to muscle wasting and weight loss
230
Q

Liver Cirrhosis

mnx of muscles wasting and malnutrition

A
  • regular meals (every 2-3h)
  • low Na (to minimise fluid retention)
  • high protein + high calorie diet
  • avoid alcohol
231
Q

Liver Cirrhosis

where does the portal vein come from

A

the superior mesenteric vein and the splenic vein

232
Q

Liver Cirrhosis

how does it cause portal hypertension

A

liver cirrhosis increases the resistance of blood flow in to the liver

increased back-pressure into the portal system

233
Q

Liver Cirrhosis

how does portal hypertension cause varices

A

back-pressure causes the vessels at the sites where the portal system anastomoses with the systemic venous system to become swollen and tortuous

234
Q

Liver Cirrhosis

which locations do the varices occur

A
  • gastro oesophageal junction
  • ileocaecal junction
  • rectum
  • Anterior abdominal wall via the umbilical vein (caput medusae)
235
Q

Liver Cirrhosis

trx of stable varices

A
  • propranolol (reduced portal HTN)
  • elastic band ligation of varices
  • injection of sclerosant (less effective)
  • last line: TIPS
236
Q

Liver Cirrhosis

what is TIPS procedure

A

Transjugular Intra-hepatic Portosystemic Shunt

  • wire into jugular vein, down the vena cava, hepatic vein into the liver
  • make connection through the liver tissue between the hepatic vein and portal vein and put a stent in place
  • allows blood to flow directly from the portal vein to the hepatic vein and relieves the pressure in the portal system and varices
237
Q

Liver Cirrhosis

mnx for bleeding oesophageal varices

A

Resus

  • terlipressin
  • correct any coagulopathy: vit K + FFP
  • prophylactic broad spectrum abx
  • consider intubation

urgent endoscopy

  • injection of sclerosant into the varices can be used to cause “inflammatory obliteration” of the vessel
  • elastic band ligation of varices
238
Q

Liver Cirrhosis

what is used when endoscopy fails for the trx of bleeding oesophageal varices

A

Sengstaken-Blakemore Tube:

  • an inflatable tube inserted into the oesophagus to tamponade the bleeding varices
239
Q

Liver Cirrhosis

how does it cause ascites

A

The increased pressure in the portal system causes fluid to leak out of the capillaries in the liver and bowel and in to the peritoneal cavity

240
Q

Liver Cirrhosis

why is there high fluid and sodium in ascites

A
  • drop in circulating volume
  • reduction in BP entering the kidneys
  • kidney senses lower pressure
  • renin released
  • increased aldosterone secretion via the renin-angiotensin-aldosterone system
241
Q

Liver Cirrhosis

cirrhosis causes what kind of ascites

A

transudative (low protein content)

242
Q

Liver Cirrhosis

mnx of ascites

A
  • low Na diet
  • spironolactone
  • paracentesis
  • prophylactic abx against SBP if <15g/L protein in ascitic fluid
  • consider TIPS in refractory ascites
  • consider transplantation
243
Q

Liver Cirrhosis

cause of Spontaneous Bacterial Peritonitis (SBP)

A

cirrhosis –> ascites –> 10% develop SBP

infection developing in the ascitic fluid and peritoneal lining without any clear cause

244
Q

Liver Cirrhosis

presentation of Spontaneous Bacterial Peritonitis (SBP)

A
  • asymptomatic
  • fever
  • abdo pain
  • raised WBC, CRP, creatinine or metabolic acidosis
  • ileus
  • hypotension
245
Q

Liver Cirrhosis

most common organisms causing Spontaneous Bacterial Peritonitis (SBP)

A
  • e.coli
  • Klebsiella pnuemoniae
  • Gram positive cocci (staphylococcus and enterococcus)
246
Q

Liver Cirrhosis

mnx of SBP

A
  • ascitic culture prior to giving abx

- IV cefotaxime

247
Q

Liver Cirrhosis

pathophysiology of Hepatorenal Syndrome

A
  • Portal HTN
  • dilation of portal blood vessels, stretched by large amounts of blood pooling there
  • loss of blood volume in kidneys
  • hypotension in kidneys
  • activation of RAAS
  • renal vasoconstriction + low circular volume –> starvation of blood to the kidney
  • rapid deteriorating kidney function
248
Q

Liver Cirrhosis

why does ammonia build up in the blood in pts with cirrhosis

A
  • functional impairment of liver cells prevent them metabolising the ammonia into harmless waste products
  • collateral vessels between the portal and systemic circulation mean that the ammonia bypasses liver altogether and enters the systemic system directly
249
Q

Liver Cirrhosis

what is hepatic encephalopathy

A

build up of toxins (ammonia) that affect the brain

250
Q

Liver Cirrhosis

what produces ammonia

A

intestinal bacteria

251
Q

Liver Cirrhosis

hepatic encephalopathy mnx

A
  • laxatives (PO)
  • Rifaximin (abx)
  • nutritional support
252
Q

Liver Cirrhosis

why is laxatives used to treat hepatic encephalopathy

A

help clear the ammonia from the gut before it is absorbed

253
Q

Liver Cirrhosis

why is Rifaximin used to treat hepatic encephalopathy

A

reduces the number of intestinal bacteria producing ammonia

Rifaximin is poorly absorbed and so stays in the GI tract

254
Q

Liver Cirrhosis

presentation of hepatic encephalopathy

A

Acute

  • reduced consciousness
  • confusion

Chronic
- changes to personality, memory, mood

255
Q

Non Alcoholic Fatty Liver Disease

stages

A
  1. Non-alcoholic Fatty Liver Disease
  2. Non-Alcoholic Steatohepatitis (NASH)
  3. Fibrosis
  4. Cirrhosis
256
Q

Non Alcoholic Fatty Liver Disease

RFs

A

shares the same RFs for CVD:

  • Obesity
  • Poor diet and low activity levels
  • Type 2 diabetes
  • High cholesterol
  • Middle age onwards
  • Smoking
  • HTN
257
Q

pt presents with abnormal LFTs without a clear cause. What do you perform

A

a non-invasive liver screen

258
Q

what is involved in a non-invasive liver screen

A
  • US liver
  • hep B+C serology
  • autoantibodies (PBC, PSC)
  • Ig (autoimmune hepatitis, PBC)
  • Caeruloplasmin (Wilson’s disease)
  • alpha 1 anti-trypsin levels
  • ferritin + transferrin saturation (hereditary haemochromatosis)
259
Q

Non Alcoholic Fatty Liver Disease

what can confirm the dx of hepatic steatosis (fatty liver)

A

liver US

260
Q

Non Alcoholic Fatty Liver Disease

what is the 1st line inx for assessing fibrosis

A

Enhanced Liver Fibrosis (ELF) blood test

261
Q

Non Alcoholic Fatty Liver Disease

what is the 2nd line inx for assessing fibrosis where the ELF test is not available

A

NAFLD fibrosis score

262
Q

Non Alcoholic Fatty Liver Disease

what is the NAFLD fibrosis score based on

A

an algorithm of:

  • age
  • BMI
  • liver enzymes
  • platelets
  • albumin
  • diabetes

helpful in ruling out fibrosis but not assessing the severity

263
Q

Non Alcoholic Fatty Liver Disease

what is the 3rd line inx

A

Fibroscan

performed if the ELF blood test or NAFLD fibrosis score indicates fibrosis.

264
Q

Non Alcoholic Fatty Liver Disease

conservative mnx

A
  • weight loss
  • Exercise
  • Stop smoking
  • Control of diabetes, blood pressure and cholesterol
  • Avoid alcohol
265
Q

Non Alcoholic Fatty Liver Disease

medical trx by specialist

A

vitamin E or pioglitazone

266
Q

Hepatitis

causes

A
  • Alcoholic hepatitis
  • Non alcoholic fatty liver disease
  • Viral hepatitis
  • Autoimmune hepatitis
  • Drug induced hepatitis (e.g. paracetamol overdose)
267
Q

Hepatitis

presentation

A
  • Abdominal pain
  • Fatigue
  • Pruritis (itching)
  • Muscle and joint aches
  • Nausea and vomiting
  • Jaundice
  • Fever (viral hepatitis)
268
Q

Hepatitis

typical biochemical findings

A

‘hepatic picture’

  • high AST, ALT
  • less of a rise in ALP
  • high bilirubin
269
Q

Hepatitis

what are transaminases

A

AST, ALT

liver enzymes released into blood due to inflammation of liver cells

270
Q

Hepatitis

why does bilirubin rise

A

inflammation of liver cells

271
Q

what is the most common Hepatitis in the world

A

Hep A

but rare in UK

272
Q

Hepatitis A

what kind of virus is it

A

RNA

273
Q

Hepatitis A

how is it transmitted

A

faecal-oral route

usually contaminated water or food

274
Q

Hepatitis A

how does it present

A
  • N+V
  • anorexia
  • jaundice
  • cholestasis: dark urine + pale stools
  • moderate hepatomegaly
275
Q

Hepatitis A

what is cholestasis

A

slowing of bile flow through the biliary system

276
Q

Hepatitis A

mnx

A

basic analgesia

it resolves without trx in around 1-3m

277
Q

Hepatitis A

is vaccination available

A

yes

278
Q

Hepatitis A

who needs to be notified

A

Public Health

279
Q

Hepatitis B

what kind of virus is it

A

DNA

280
Q

Hepatitis B

how is it transmitted

A
  • direct contact with blood or bodily fluids
    e. g. sex or sharing needles
  • vertical transmission from mother to child
281
Q

Hepatitis B

prognosis

A

most fully recover within 2m

10% become chronic hep B carriers

282
Q

Hepatitis B

what is a chronic hep B carrier

A

In these patients the virus DNA has integrated into their own DNA and so they will continue to produce the viral proteins.

283
Q

Hepatitis B

what does Surface antigen (HBsAg) indicate

A

active infection

284
Q

Hepatitis B

what does E antigen (HBeAg) indicate

A

marker of viral replication and implies high infectivity

285
Q

Hepatitis B

what do Core antibodies (HBcAb) indicate

A

implies past or current infection

286
Q

Hepatitis B

what does surface antibody (HBsAb) indicate

A

implies vaccination or past or current infection

287
Q

Hepatitis B

what is Hepatitis B virus DNA (HBV DNA)

A

a direct count of the viral load

288
Q

Hepatitis B

what does high titres of the IgM version of the HBcAb indicate

A

active acute infection

289
Q

Hepatitis B

what do low titres of the IgM version of the HBcAb indicate

A

chronic infection

290
Q

Hepatitis B

what does an IgG of the HBcAb indicate where the HBsAg is negative

A

a past infection

291
Q

Hepatitis B

what does Hepatitis B e antigen (HBeAg) indicate

A

the patient is in an acute phase of the infection where the virus is actively replicating

If the HBeAg is higher, they are highly infectious to others

292
Q

Hepatitis B

what does it imply if the HBeAg is negative but the HBeAb is positive

A

they have been through a phase where the virus was replicating

but the virus has now stopped replicating and they are less infectious

293
Q

Hepatitis B

is vaccination available

A

yes

3 doses

part of the UK routine vaccination schedule (as part of the 6 in 1 vaccine)

294
Q

Hepatitis B

what is injected in the vaccine

A

the hepatitis B surface antigen

295
Q

Hepatitis B

who do you notify

A

Public Health

296
Q

Hepatitis B

medical/surgical mnx

A

Antiviral medication can be used to slow the progression of the disease and reduce infectivity

Liver transplantation for end-stage liver disease

297
Q

Hepatitis B

general mnx

A
  • low threshold for at risk pts
  • screen for hep A, B, HIV, STIs
  • refer to gastro/infectious diseases
  • stop smoking + alcohol
  • education about reducing transmission
  • fibroscan for cirrhosis
  • US for HCC
298
Q

Hepatitis C

what type of virus is it

A

RNA

299
Q

Hepatitis C

how is it spread

A

blood and bodily fluids

300
Q

Hepatitis C

is a vaccine available

A

no

301
Q

Hepatitis C

mnx

A

curable with direct acting antiviral medications.

302
Q

Hepatitis C

disease course

A
  • 1/4 make a full recovery

- 3/4 become chronic

303
Q

Hepatitis C

complications

A

liver cirrhosis

HCC

304
Q

Hepatitis C

what is the screening test

A

Hep C antibody

305
Q

Hepatitis C

what test is used to confirm the diagnosis

A

Hepatitis C RNA testing

306
Q

Hepatitis C

mnx

A

same as Hep B mnx but

- direct acting antivirals (DAAs) tailored to the specific viral genotype (cure!)

307
Q

Hepatitis D

what virus is it

A

RNA virus

308
Q

Hepatitis D

which patients get it

A

it can only survive in patients who also have a hepatitis B infection

attaches itself to the HBsAg to survive and cannot survive without this protein

309
Q

Hepatitis D

specific trx

A

none

310
Q

Hepatitis D

is it notifiable

A

yes

311
Q

Hepatitis E

what virus is it

A

RNA

312
Q

Hepatitis E

how is it transmitted

A

by the faecal oral route

313
Q

Hepatitis E

how does it present

A
  • mild illness

- cleared within a month

314
Q

Hepatitis E

trx

A

none usually

Rarely it can progress to chronic hepatitis and liver failure, more so in patients that are immunocompromised.

315
Q

Hepatitis E

is there a vaccination

A

no

316
Q

Hepatitis E

is it notifiable

A

yes

317
Q

Autoimmune hepatitis

what are the types and who do they occur in

A

type 1: adults

type 2: children

318
Q

woman in late 40s/50s
perimenopause
fatigue, features of liver disease on exam. Less acute. WHat is it

A

type 1 autoimmune hepatitis

319
Q

teenager/early 20s presents with acute hepatitis w/ high transaminases + jaundice. What is it

A

type 2 autoimmune hepatitis

320
Q

Autoimmune hepatitis

what autoantibodies are associated with type 1

A
  • Anti-nuclear antibodies (ANA)
  • Anti-smooth muscle antibodies (anti-actin)
  • Anti-soluble liver antigen (anti-SLA/LP)
321
Q

Autoimmune hepatitis

what autoantibodies are associated with type 2 associated with

A
  • Anti-liver kidney microsomes-1 (anti-LKM1)

- Anti-liver cytosol antigen type 1 (anti-LC1)

322
Q

Autoimmune hepatitis

diagnostic inx

A

liver biopsy

323
Q

Autoimmune hepatitis

trx

A

high dose steroids (prednisolone) that are tapered over time

as other immunosuppressants, particularly azathioprine, are introduced

life long

324
Q

Autoimmune hepatitis

liver transplant?

A

may be required in end stage liver disease, however the autoimmune hepatitis can recur in transplanted livers

325
Q

Autoimmune hepatitis

cause

A

unknown

could be associated with a genetic predisposition and triggered by environmental factors such as a viral infection that causes a T cell-mediated response against the liver cells.

326
Q

Wilsons Disease

what is it

A

the excessive accumulation of copper in the body and tissues.

327
Q

Wilsons Disease

cause

A

mutation in the “Wilson disease protein” on chromosome 13

aka “ATP7B copper-binding protein”

328
Q

Wilsons Disease

what is the “ATP7B copper-binding protein” or Wilson disease protein responsible for

A

the removal of excess copper in the liver

329
Q

Wilsons Disease

genetic inheritance

A

autosomal recessive

330
Q

Wilsons Disease

presentation

A
  • hepatic problems
  • neuro problems
  • psychiatric problems
331
Q

Wilsons Disease

why does it cause hepatic, neuro and psych problems

A

Copper deposition in the liver leads to chronic hepatitis and eventually liver cirrhosis

Copper deposition in the CNS

332
Q

Wilsons Disease

what neuro sx may be present

A
  • concentration + coodination problems
  • dysarthria (speech)
  • dystonia
  • Parkininsonism (if in basal ganglia)
333
Q

Wilsons Disease

are motor neuro sx often symmetrical or asymmetrical

A

asymmetrical

334
Q

Wilsons Disease

how can psych sx present as

A

vary from mild depression to full psychosis

335
Q

Wilsons Disease

findings on slit lamp examination

A
  • Kayser-Fleischer rings in cornea (deposition of copper in Descemet’s corneal membrane)

brownish circles surrounding the iris

336
Q

Wilsons Disease

other features apart from neuro, psych + liver problems

A
  • Haemolytic anaemia
  • Renal tubular damage leading to renal tubular acidosis
  • Osteopenia (loss of bone mineral density)
337
Q

Wilsons Disease

initial inx of choice and result

A

low serum caeruloplasmin

338
Q

Wilsons Disease

what is caeruloplasmin

A

the protein that carries copper in the blood

339
Q

Wilsons Disease

what is wrong with using serum caeruloplasmin

A
  • can be falsely normal or elevated in cancer or inflammatory conditions.
  • not specific to Wilson disease
340
Q

Wilsons Disease

what is the definitive gold standard test for dx

A

Liver biopsy for liver copper content

341
Q

Wilsons Disease

what other inx (apart from biopsy) can be used to diagnose it

A

sufficiently elevated 24-hour urine copper assay is

or scoring systems

342
Q

Wilsons Disease

other inx apart from caeruloplasmin, biopsy, urine

A
  • Low serum copper
  • Kayser-Fleischer rings
  • MRI brain shows nonspecific changes
343
Q

Wilsons Disease

mnx

A

copper chelation using:

  • penicillamine
  • trientene
344
Q

Liver Transplant

name for when an entire liver is transplanted from a deceased patient to a recipient

A

orthotopic transplant

345
Q

Liver Transplant

what is a living donor transplant

A

taking a portion of the organ from a living donor, transplant it into a patient and have both regenerate to become two fully functioning organs

because the liver can regenerate as an organ

346
Q

Liver Transplant

what is the name when you split the organ of a deceased person into two and transplant it into two patients and have them regenerate to their normal size in each recipient

A

split donation.

347
Q

Liver Transplant

indications

A

acute liver failure:

  • acute viral hepatitis
  • paracetamol overdose

chronic liver failure

348
Q

Liver Transplant

factors suggesting unsuitability for liver transplantation

A
  • Significant co-morbidities (e.g. severe kidney or heart disease)
  • Excessive weight loss and malnutrition
  • Active hep B, C or other infection
  • End-stage HIV
  • Active alcohol use (generally 6m of abstinence required)
349
Q

Liver Transplant

what kind of incisions is required for open surgery

A
  • rooftop

- Mercedes Benz

350
Q

Liver Transplant

post-transplantation meds

A

lifelong immunosuppression (e.g. steroids, azathioprine and tacrolimus)

351
Q

Liver Transplant

how would you monitor for evidence of transplant rejections

A
  • Abnormal LFTs
  • Fatigue
  • Fever
  • Jaundice
352
Q

Liver Transplant

post-transplantation care

A
  • Avoid alcohol and smoking
  • Treat opportunistic infections
  • Monitoring for disease recurrence (i.e. of hepatitis or primary biliary cirrhosis)
  • Monitoring for cancer as there is a significantly higher risk in immunosuppressed patients
353
Q

Gastro-Oesophageal Reflux Disease

what is it

A

acid from the stomach refluxes through the lower oesophageal sphincter and irritates the lining of the oesophagus.

354
Q

Gastro-Oesophageal Reflux Disease

what cells line the oesophagus

A

squamous epithelial lining

355
Q

Gastro-Oesophageal Reflux Disease

what cells line the stomach

A

columnar epithelial lining

356
Q

Gastro-Oesophageal Reflux Disease

which cell lining is more sensitive to stomach acid

A

squamous epithelial (oesophagus)

357
Q

Gastro-Oesophageal Reflux Disease

what is dyspepsia

A

a non-specific term used to describe indigestion.

358
Q

Gastro-Oesophageal Reflux Disease

sx

A
  • Heartburn
  • Acid regurgitation
  • Retrosternal or epigastric pain
  • Bloating
  • Nocturnal cough
  • Hoarse voice
359
Q

Gastro-Oesophageal Reflux Disease

what are the key red flag features indicating an urgent referral

A
  • dysphagia (swallowing)
  • aged>55y
  • weight loss
  • upper abdo pain/reflux
  • Treatment resistant dyspepsia
  • Nausea and vomiting
  • Low haemoglobin
  • Raised platelet count
360
Q

Gastro-Oesophageal Reflux Disease

mnx

A
  • lifestyle advice
  • acid neutralising meds PRN
  • PPIs
  • Ranitidine
  • surgery
361
Q

Gastro-Oesophageal Reflux Disease

what lifestyle advice would you give

A
  • Reduce tea, coffee and alcohol
  • Weight loss
  • Avoid smoking
  • Smaller, lighter meals
  • Avoid heavy meals before bed time
  • Stay upright after meals rather than lying flat
362
Q

Gastro-Oesophageal Reflux Disease

name some acid neutralising meds

A
  • Gaviscon

- Rennie

363
Q

Gastro-Oesophageal Reflux Disease

what is Ranitidine

A
  • an alternative to PPIs
  • H2 receptor antagonist (antihistamine)
  • Reduces stomach acid
364
Q

Gastro-Oesophageal Reflux Disease

what is the surgery for reflux called

A

laparoscopic fundoplication

tying the fundus of the stomach around the lower oesophagus to narrow the lower oesophageal sphincter

365
Q

Gastro-Oesophageal Reflux Disease

what kind of bacteria is H.pylori

A

a gram negative aerobic bacteria.

366
Q

Gastro-Oesophageal Reflux Disease

how can H.pylori damage the epithelial cells in the stomach, causing gastritis

A
  • breaks into the gastric mucosa
  • epithelial cells underneath are exposed to acid
  • also produces ammonia which neutralises the acid and directly damages the epithelial cells
367
Q

Gastro-Oesophageal Reflux Disease

who is offered a test for H.pylori

A

anyone with dyspepsia.

They need 2 weeks without using a PPI before testing for H. pylori for an accurate result.

368
Q

Gastro-Oesophageal Reflux Disease

what 3 tests can be used to test for H.pylori

A
  • Urea breath test using radiolabelled carbon 13
  • Stool antigen test
  • Rapid urease test can be performed during endoscopy.
369
Q

Gastro-Oesophageal Reflux Disease

what is a rapid urease test aka

A

CLO test (Campylobacter-like organism test)

370
Q

Gastro-Oesophageal Reflux Disease

what does the rapid urease test involve

A
  • performed during endoscopy
  • biopsy from stomach mucosa
  • add urea to sample
371
Q

Gastro-Oesophageal Reflux Disease

if H,pylori are present in the rapid urease test, what result will you get and why

A
  • positive: alkali solution
  • H.pyloria produce urease enzymes
  • which convert urea to ammonia
  • making solution alkali
372
Q

Gastro-Oesophageal Reflux Disease

how to eradicate H.pylori

A

triple therapy:

  1. PPI
  2. amoxicillin
  3. clarithromycin

7d

373
Q

Gastro-Oesophageal Reflux Disease

what is Barretts Oesophagus

A

lower oesophageal squamous cells change to columnar epithelium cells

in a process called metaplasia

due to constant reflux of acid

374
Q

Gastro-Oesophageal Reflux Disease

how may patients with Barretts oesophagus present

A

improvement in reflux symptoms

375
Q

Gastro-Oesophageal Reflux Disease

what is Barretts oesophagus a RF for developing

A

adenocarcinoma of the oesophagus

376
Q

Gastro-Oesophageal Reflux Disease

monitoring for pts with Barretts oesophagus

A

regular endoscopy to monitor for adenocarcinomas

377
Q

Gastro-Oesophageal Reflux Disease

progression of Barrett’s oesophagus

A

squamous cell –> columnar epithelium, no dysplasia –> low grade dysplasia –> high grade dysplasia –> adenocarcinoma

378
Q

Gastro-Oesophageal Reflux Disease

trx of Barretts oesophagus

A

PPIs

new evidence but not in guidelines: regular aspirin

379
Q

Gastro-Oesophageal Reflux Disease

trx for pts with Barretts oesophagus with low or high grade dysplasia

A

Ablation treatment during endoscopy using photodynamic therapy, laser therapy or cryotherapy

destroys the epithelium so that it is replaced with normal cells

380
Q

Peptic Ulcers

what are they

A

ulceration of the mucosa of the stomach (gastric ulcer) or the duodenum (duodenal ulcer).

381
Q

Peptic Ulcers

which kind are more common

A

duodenal ulcers

382
Q

Peptic Ulcers

when is the stomach mucosa prone to ucleration

A
  • Breakdown of the protective layer of the stomach and duodenum
  • Increase in stomach acid
383
Q

Peptic Ulcers

what is the protective layer in the stomach comprised of

A

mucus + bicarbonate

secreted by the stomach mucosa

384
Q

Peptic Ulcers

what can the protective later be broken down by

A
  • Medications (e.g. steroids or NSAIDs)

- Helicobacter pylori

385
Q

Peptic Ulcers

what can increased acid result from

A
  • Stress
  • Alcohol
  • Caffeine
  • Smoking
  • Spicy foods
386
Q

Peptic Ulcers

presentation

A
  • Epigastric discomfort or pain
  • N+V
  • Dyspepsia
  • “coffee ground” vomiting and melaena
  • Iron deficiency anaemia (due to constant bleeding)
387
Q

Peptic Ulcers

how are they diagnosed

A

endoscopy

388
Q

Peptic Ulcers

what should be done during endoscopy

A

rapid urease test (CLO test) can be performed to check for H. pylori during it

biopsy to exclude malignancy

389
Q

Peptic Ulcers

medical trx

A

high dose PPI

390
Q

Peptic Ulcers

complications

A
  • bleeding
  • perforation
  • scarring + strictures –> pyloric stenosis
391
Q

Peptic Ulcers

how does pyloric stenosis present

A

upper abdominal pain

distention

nausea and vomiting, particularly after eating

392
Q

Peptic Ulcers

eating typically worsens the pain

which type of ulcer is it

A

gastric ulcer

393
Q

Peptic Ulcers

eating typically improves the pain

which type of ulcer is it

A

duodenal ulcers

394
Q

Irritable Bowel Syndrome

why is it a ‘functional bowel disorder’

A

there is no identifiable organic disease underlying the symptoms

395
Q

Irritable Bowel Syndrome

sx

A
  • Diarrhoea
  • Constipation
  • Fluctuating bowel habit
  • Abdominal pain
  • Bloating
  • Worse after eating
  • Improved by opening bowels
396
Q

Irritable Bowel Syndrome

NICE criteria for dx

A
  • other pathology excluded

- sx should suggest IBS

397
Q

Irritable Bowel Syndrome

NICE criteria: other pathology excluded

A
  • Normal FBC, ESR and CRP
  • Faecal calprotectin negative to exclude IBD
  • Negative coeliac disease serology (anti-TTG antibodies)
  • Cancer is not suspected or excluded if suspected
398
Q

Irritable Bowel Syndrome

NICE criteria: sx should suggest IBS

A

Abdominal pain / discomfort:

  • Relieved on opening bowels, or
  • Associated with a change in bowel habit

AND 2 of:

  • Abnormal stool passage
  • Bloating
  • Worse symptoms after eating
  • PR mucus
399
Q

Irritable Bowel Syndrome

General healthy diet and exercise advice

A
  • Adequate fluid intake
  • Regular small meals
  • Reduced processed foods
  • Limit caffeine and alcohol
  • Low “FODMAP” diet (ideally with dietician guidance)
  • Trial of probiotic supplements for 4w
400
Q

Irritable Bowel Syndrome

1st line medications: diarrhoea

A

loperamide

401
Q

Irritable Bowel Syndrome

1st line medications: constipation

A

laxatives

avoid lactulose as can cause bloating

402
Q

Irritable Bowel Syndrome

what is a specialist laxative for patients with IBS not responding to first-line laxatives

A

Linaclotide

403
Q

Irritable Bowel Syndrome

1st line medications: cramps

A

Antispasmodics

e.g. hyoscine butylbromide (Buscopan)

404
Q

Irritable Bowel Syndrome

2nd line medication

A

Tricyclic antidepressants (i.e. amitriptyline 5-10mg at night)

405
Q

Irritable Bowel Syndrome

3rd line medication

A

SSRIs

406
Q

Irritable Bowel Syndrome

mnx option to help patients psychologically manage the condition and reduce distress associated with symptoms.

A

CBT

407
Q

Coeliac Disease

what is it

A

an autoimmune condition where exposure to gluten causes an autoimmune reaction that causes inflammation in the small bowel

408
Q

Coeliac Disease

when does it usually develop

A

in early childhood but can start at any age

409
Q

Coeliac Disease

pathophysiology

A
  • auto-antibodies target epithelial cells of the intestine in response to gluten
  • leads to inflammation
410
Q

Coeliac Disease

what are the autoantibodies

A
  • anti-tissue transglutaminase (anti-TTG)
  • anti-endomysial (anti-EMA)
  • Deaminated gliadin peptides antibodies (anti-DGPs)
411
Q

Coeliac Disease

which area of bowel does it affect

A

small bowel, esp the jejunum

412
Q

Coeliac Disease

what does it cause to the intestinal villi

A
  • villous atrophy

- crypt hypertrophy

413
Q

Coeliac Disease

presentation

A

often asymptomatic

  • Failure to thrive in young children
  • Diarrhoea
  • Fatigue
  • Weight loss
  • Mouth ulcers
  • Anaemia secondary to iron, B12 or folate deficiency
  • Dermatitis herpetiformis
414
Q

Coeliac Disease

what is dermatitis herpetiformis

A

an itchy blistering skin rash typically on the abdomen

415
Q

Coeliac Disease

rarely it can present with neuro problems. What are they

A
  • Peripheral neuropathy
  • Cerebellar ataxia
  • Epilepsy
416
Q

all new cases of T1DM are also tested for what

A

coeliac disease as they are often linked

417
Q

Coeliac Disease

genetic associations

A

HLA-DQ2 gene (90%)

HLA-DQ8 gene

418
Q

Coeliac Disease

Anti-TTG and anti-EMA antibodies are types of which Ig?

A

IgA

419
Q

Coeliac Disease

what do you need to test before you test for Anti-TTG and anti-EMA antibodies and why

A

total IgA levels as some pts have an IgA deficiency

if total IgA is low because they have an IgA deficiency then the coeliac test will be negative even when they have coeliacs

420
Q

Coeliac Disease

how do you test for coeliac if they have IgA deficiency

A

test for the IgG version of anti-TTG or anti-EMA antibodies

or endoscopy with biopsies

421
Q

Coeliac Disease

what to tell pt before checking their IgA and anti-TTG

A

patient must be on a diet containing gluten

422
Q

Coeliac Disease

what will endoscopy and intestinal biopsy show

A

“Crypt hypertrophy”

“Villous atrophy”

423
Q

Coeliac Disease

what other autoimmune conditions is it associated with

A
  • Type 1 Diabetes
  • Thyroid disease
  • Autoimmune hepatitis
  • PBC
  • PSC
424
Q

Coeliac Disease

complications of untreated coeliac disease

A
  • Vitamin deficiency
  • Anaemia
  • Osteoporosis
  • Ulcerative jejunitis
  • Enteropathy-associated T-cell lymphoma (EATL) of the intestine
  • Non-Hodgkin lymphoma (NHL)
  • Small bowel adenocarcinoma (rare)
425
Q

Coeliac Disease

trx

A

Lifelong gluten-free diet

426
Q

Spontaneous bacterial peritonitis with increased serum creatinine should be also prescribed what?

A

human albumin solution because it reduces the risk of developing renal impairment

427
Q

what is achalasia

A

Failure of oesophageal peristalsis and of relaxation of the lower oesophageal sphincter (LOS)

428
Q

cause of achalasia

A

degenerative loss of ganglia from Auerbach’s plexus

429
Q

what are the clinical features of achalasia

A
  • dysphagia of BOTH liquids and solids
  • heartburn
  • regurgitation of food
430
Q

what is the diagnostic test for achalasia

A

oesophageal manometry

431
Q

what will oesophageal manometry show if they have achalasia

A

excessive lower oesophageal sphincter tone which doesn’t relax on swallowing

432
Q

what will the barium swallow show if they have achalasia

A

a dilated oesophagus with a fluid level (described as a “bird’s beak” appearance)

433
Q

trx of achalasia

A
  • pneumatic (balloon) dilation
  • surgery: Heller cardiomyotomy
  • intra-sphincteric injection of botulinum toxin
434
Q

man presents with dermatitis, dementia and diarrhoea. what is it

A

Vitamin B3 deficiency (pellagra)

trx with nicotinamide (vitamin B3)

435
Q

what is gastric paresis

A

delayed gastric emptying

436
Q

which condition is gastric paresis commonly associated with

A

DM

437
Q

what causes gastric paresis

A

decreased activity of the stomach muscles, causing food to be held in the stomach for a longer period than usual

438
Q

sx of gastric paresis

A
  • Nausea
  • Vomiting
  • Feeling of fullness after a few bites
  • Abdominal pain
  • Bloating
439
Q

how is diagnosis of gastric paresis made

A

solid meal gastric scintigraphy (Radionuclide studies of gastric emptying)

440
Q

mnx of gastric paresis

A
  • Dietary modification - low fibre, smaller/more frequent meals, pureed/mashed food
  • Domperidone - dopamine receptor antagonist
  • Metoclopramide or Erythromycin (motility agents)
441
Q

pt develops gastroenteritis after eating rice. Which organism is responsible

A

Bacillus cereus

442
Q

which drug is known to cause drug-induced cholestasis

A

co-amoxiclav

443
Q

child presents with low platelets, an acute kidney injury and a haemolytic anaemia. What is it

A

haemolytic uraemic syndrome, the most common cause of which is E Coli 0157

444
Q

which condition is Pellagra (vit b3 deficiency) associated with

A

carcinoid syndrome

445
Q

abx trx for Gram negative curved rods with a seagull shaped appearance

A

Azithromycin

treatment for Campylobacter

446
Q

which drug is avoided in hepatic encephalopathy

A

morphine as it can worsen it

447
Q

what can be used to find the cause of ascites

A

The serum ascites albumin gradient (SAAG)

448
Q

how is the serum ascites albumin gradient (SAAG) calculated

A

serum albumin con - albumin conc of ascitic fluid

449
Q

what does a high SAAG (>1.1g/dL) suggest

A 
the cause of the ascites is due to raised portal pressure
Cirrhosis
Heart failure
Budd Chiari syndrome
Constrictive pericarditis
Hepatic failure
450
Q

what does a low SAAG (<1.1g/dL) suggest

A

Cancer of the peritoneum
Tuberculosis and other infections
Pancreatitis
Nephrotic syndrome

451
Q

what is an absolute contraindication to performing paracentesis

A

disseminated intravascular coagulation:

  • Bleeding from gums
  • raised d-dimer
  • low fibrinogen
452
Q

what is Whipple’s disease

A

a rare, systemic condition caused by Tropheryma whipplei.

453
Q

presentation of Whipple’s disease

A

diarrhoea, abdominal pain and joint pain,

454
Q

Gold standard for the diagnosis of Whipple’s disease

A

Jejunal biopsy: presence of acid-Schiff (PAS)-positive macrophages

455
Q

mnx of Whipple’s disease

A

co-trimoxazole.

456
Q

how would Plummer-Vinson syndrome present as

A

Triad of:

  • dysphagia (secondary to oesophageal webs)
  • glossitis
  • iron-deficiency anaemia
457
Q

dysphagia: liquids and solids being equally affected from the start

what could it be

A

motility disorders

458
Q

dysphagia: Progressive dysphagia of solids and then liquids

what could it be

A

a benign or malignant stricture

459
Q

what is Budd-Chiari syndrome caused by

A

obstruction of the hepatic veins (often by thrombosis)

460
Q

what is the classic triad of Budd-chiari syndrome

A
  1. abdominal pain
  2. ascites
  3. hepatomegaly
461
Q

what may patients develop after being treated for Giardiasis with abx such as metronidazole

A

lactose intolerance

462
Q

why shold CCBs be avoided in reflux

A

they can relax the lower oesophageal sphincter, thus increasing reflux

463
Q

difference between right and left sided colonic cancer

A

left:

  • present earlier
  • stool more formed
  • fresh rectal bleeding
  • tenesmus

right

  • presents later
  • more insidious in manner with occult bleeding and anaemia
  • semi-liquid stool
464
Q

how to calculate units of alcohol

A

strength (ABV) x volume (ml) ÷ 1000

465
Q

mnx of c.difficile infection

A
  1. stop abx causing it
  2. PO vancomycin for 10d

2nd line therapy: PO fidaxomicin
3rd line therapy: PO vancomycin +/- IV metronidazole

466
Q

what other drugs apart from abx can cause c.difficile

A

PPIs
steroids
chemo

467
Q

pt has constipation. what would you be excluding in a upright chest x-ray

A

bowel perforation

468
Q

pt has constipation. what would you be excluding in a abdominal chest x-ray

A

bowel obstruction

469
Q

4 drugs classes which cause constipation

A
  • opioids
  • CCBs
  • antipsychotics
  • anticholinergics
470
Q

why does crohn’s increase the risk of gallstones

A

increase in loss of bile salts

Finals (47 decks)

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