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MSRA Content > Gastrointestinal - Level 2.3 > Flashcards

Gastrointestinal - Level 2.3 Flashcards

1
Q

Definition of cirrhosis?

A

o Cirrhosis develops progressively as a result of damage to the liver
o Normal smooth liver surface becomes distorted, nodular and fibrosed
 Distortion of hepatic vasculature, increased intrahepatic resistence and portal hypertension
 Damaged hepatocytes cause less synthesis of clotting factors and metabolic detoxification

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2
Q

Types of cirrhosis?

A

o Compensated – liver still functions effectively and no/few symptoms

o Decompensated – liver damaged where it cannot function adequately and clinical complications present (jaundice, ascites, variceal haemorrhage, hepatic encephalopathy)

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3
Q

Epidemiology of cirrhosis?

A
  • More common in urban areas, social deprivation
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4
Q

Common risk factors of cirrhosis?

A

 Alcohol misuse
 Hepatitis B/C
 Obesity (>30)
 T2DM

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5
Q

Less common risk factors of cirrhosis?

A

 Autoimmune liver disease (AH, PBC, PSC)
 Genetic (haemochromatosis, Wilson’s disease, alpha-1-antitrypsin deficiency, CF)
 Methotrexate use
 Budd-Chiari syndrome
 Sarcoidosis

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6
Q

Events causing decompensation in cirrhosis?

A

o Infection, portal vein thrombosis, surgery

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7
Q

Symptoms of cirrhosis?q

A 
o	Asymptomatic
o	Malaise, fatigue, anorexia
o	Nausea
o	Weight loss
o	Muscle wasting
o	Abdominal pain
o	Oedema
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8
Q

Signs of cirrhosis?

A 
o	Jaundice
o	Leuconychia
o	Palmar erythema
o	Dupuytren’s contracture
o	Scratch marks
o	Abnormal bruising
o	Keiser Fleischer rings
o	Hair loss
o	Gynaecomastia
o	Spider naevi
o	Caput Medusae
o	Hepatosplenomegaly
o	Peripheral oedema
o	Ascites
o	Sepsis
o	Variceal bleeding
o	Encephalopathy (asterixis – sudden involuntary flexion-extension movements of wrist and MCP joints when arms are extended and eyes closed)
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9
Q

When to suspect cirrhosis?

A

o Clinical findings consistent

o Chronic liver disease with low platelets, raised AST:ALT ratio, high bilirubin, low albumin or increased INR/PT

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10
Q

Diagnosing cirrhosis in primary care - when to perform transient elastography?

A

Transient elastography if:
 Patient with Hep C infection
 Men drinking >50 units per week for months
 Women drinking >35 units per week for months
 People diagnosed with alcohol-related liver disease

If not available, refer to hepatologist – liver biopsy

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11
Q

Diagnosing cirrhosis in primary care - people with NAFLD?

A

o If NAFLD and advanced liver fibrosis (diagnosed with >10.51 on enhanced liver fibrosis test (ELF)):
 Transient elastography or acoustic radiation force

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12
Q

When to refer suspected cirrhosis to hepatologist/GI?

A 
	Hepatitis B
	PBC
	PSC
	Haemachromatosis
	Wilson’s disease
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13
Q

Retesting in cirrhosis - if not diagnosed on initial testing?

A

If not diagnosed on initial testing – retest every 2 years in:
 Alcohol-related liver disease, Hep C, NAFLD or advance liver fibrosis

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14
Q

Tests to find cause in cirrhosis?

A 
o	Ferritin, iron/total iron binding capacity
o	Hepatitis serology
o	Autoantibodies (ANA, AMA, SMA)
o	AFP
o	Alpha-1 anti-trypsin
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15
Q

Grading of cirrhosis?

A

o Child-Pugh grading and risk of variceal bleeding

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16
Q

Management of cirrhosis - referral to secondary care?

A

 Diagnosed on transient elastography
 Decompensated liver disease
 Misuse alcohol
 End-stage liver disease requiring symptom or palliative care

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17
Q

Management of cirrhosis - primary care - general advice?

A
  • Diet
  • Alcohol abstinence
  • Smoking cessation
  • Driving – notify DVLA, cannot drive if hepatic cirrhosis with chronic encephalopathy
  • Seek medical advice before taking OTC drugs
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18
Q

Management of cirrhosis - primary care - symptom management?

A

• Pruritus – colestyramine

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19
Q

Management of cirrhosis - primary care - follow up?

A
  • Review medications and change dose as required

* Ensure specialist follow up

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20
Q

Management of cirrhosis - specialist care - management?

A

Upper GI endoscopy – detect varices

Liver transplant - Advanced cirrhosis due to:
 Alcohol liver disease, hepatitis B&C, PBC, PSC, Wilson’s disease, alpha-1 antitrypsin deficiency

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21
Q

Contraindications to liver transplant in cirrhosis?

A

o Extrahepatic malignancy, severe cardiopulmonary disease, sepsis, HIV, non-compliance with drug therapy

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22
Q

Monitoring cirrhosis in secondary care?

A

 Calculate Model for end-stage liver disease (MELD) score every 6 months for compensated cirrhosis – 12 or more high risk
 US + AFP every 6 months for HCC
 Upper GI endoscopy every 3 year

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23
Q

Managing complications of cirrhosis?

A

 1o prevention of bleeding - Endoscopic variceal band ligation
 If upper GI bleeding – prophylactic antibiotics
 Refractory Ascites - Transjugular intrahepatic portosystemic shunt
 Cirrhosis with ascites with protein level <15 until resolved - Prophylactic oral ciprofloxacin

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24
Q

Prognosis of cirrhosis?

A

o Irreversible – usually progresses over number of years

o Prognosis depends on cause, lifestyle, complications and hospital admissions

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25
Q

Complications of cirrhosis?

A 
o	Portal hypertension
o	Ascites
o	Hepatic Encephalopathy
o	Oesophageal varices (haemorrhage)
o	Infection
o	Hepatorenal syndrome
o	HCC
o	Portal vein thrombosis
o	Portal hypertensive gastropathy
o	Anaemia, coagulopathy
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26
Q

Description of hepatic encephalopathy?

A

 Dysfunction of brain due to liver insufficiency and related to nitrogenous waste products (ammonia and glutamine) in brain
 Present with cognitive and behavioural changes, sleep disturbance, motor problems and altered consciousness
 Predisposed by constipation, dehydration, infection, GI bleed, drugs (opiates, benzodiazepines, diuretics)

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27
Q

What is hepatorenal syndrome?

A

 Changes to circulation due to cirrhosis with water and sodium retention and renal vasoconstriction
 Decrease renal blood flow and reduced glomerular filtration rate

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28
Q

Definition of autoimmune hepatitis?

A
  • Chronic disease with continuing hepatocellular inflammation and necrosis which progresses to cirrhosis
  • HLA implicated
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29
Q

Types of autoimmune hepatitis?

A

o 1 – presence of ASMA or ANA

o 2 – presence of anti-LKM-1 or anti-liver cytosolic 1 antibodies

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30
Q

Epidemiology of autoimmune hepatitis?

A
  • Young/Middle Aged women but can occur in anybody
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31
Q

Associated conditions of autoimmune hepatitis?

A
  • Associated disease: pernicious anaemia, UC, thyroiditis, T1DM, PSC, RA, glomerulonephritis
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32
Q

Symptoms of autoimmune hepatitis?

A

o Often insidious onset
o Fatigue, myalgia, pruritus, nausea
o Upper abdominal pain, anorexia, diarrhoea

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33
Q

Signs of autoimmune hepatitis?

A

Same as cirrhosis

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34
Q

Investigations of autoimmune hepatitis?

A

Bloods
o FBC - Normochromic anaemia
o LFTs - Raised ALT and AST
o Hypergammaglobulinaemia

Autoantibodies
o ANA, ASMA, ALKM1, ALC1

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35
Q

Diagnostic investigation of autoimmune hepatitis?

A

Liver biopsy - diagnostic
o Chronic hepatitis
o Mononuclear infiltrates

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36
Q

Management of autoimmune hepatitis?

A

Immunosuppression
o Prednisolone 30mg for 1 month and then decrease by 5mg each month to maintenance dose
o Azathioprine

Liver transplant
o If decompensated cirrhosis or failure to respond to medication, recurrence may occur

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37
Q

Definition of primary sclerosing cholangitis?

A
  • Progressive cholestasis with bile duct inflammation and structures
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38
Q

Associated diseases of primary sclerosing cholangitis?

A
  • Associated with males, HLA, AIH, IBD
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39
Q

Symptoms of primary sclerosing cholangitis?

A

o Asymptomatic
o Jaundice
o Pruritus
o If advanced – ascending cholangitis, cirrhosis and hepatic failure

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40
Q

Investigations of primary sclerosing cholangitis?

A

Bloods
o LFT – elevated ALP, GGT, bilirubin
o Abnormal albumin or PT if disease progressed
o Raised ANCA, aCL, ANA

US
o Bile duct dilatation and liver changes

MRCP to visualise the duct

Liver biopsy - staging

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41
Q

Management of primary sclerosing cholangitis - surveillance?

A
  • Risk of bile duct, gall bladder, liver and colon cancer so:
    o Yearly colonoscopy + US
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42
Q

Management of primary sclerosing cholangitis - Symptomatic control?

A
  • Pruritus – colestyramine
  • Nutrition – Fat-soluable vitamins – ADEK
  • Prevent progression – ursodeoxycholic acid, avoid alcohol
  • Stricture – ERCP balloon dilatation
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43
Q

Management of primary sclerosing cholangitis - end-stage liver disease?

A
  • Liver transplant for end-stage liver disease
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44
Q

Definition of primary biliary cirrhosis?

A
  • Progressive autoimmune disease of biliary system
  • Destruction of interlobular bile ducts (canals of Hering) causing intrahepatic cholestasis which damages cells, leading to scarring, fibrosis and cirrhosis
  • Women 10x
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45
Q

Causes of primary biliary cirrhosis?

A
  • Causes by anti-mitochondrial antibody (AMA)
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46
Q

Symptoms of primary biliary cirrhosis?

A
  • Asymptomatic
  • Fatigue
  • Pruritus
  • RUQ pain
  • Later stages – dark urine, pale stools
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47
Q

Investigations of primary biliary cirrhosis - bloods?

A 
Bloods
o	FBC (ESR raised)
o	LFTs
	ALP raised
o	Late stage – raised bilirubin, PT and albumin

Antibodies (AMA present)

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48
Q

Investigations of primary biliary cirrhosis - imaging?

A
  • US of liver
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49
Q

Investigations of primary biliary cirrhosis - diagnosis?

A

Liver biopsy

o AMA with cholestatic liver biochemistry

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50
Q

Stages of primary biliary cirrhosis?

A

o Portal stage – portal inflammation and bile duct abnormalities
o Periportal stage – periportal fibrosis
o Septal – septal fibrosis and inflammation
o Cirrhotic – nodules with inflammation

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51
Q

Management of primary biliary cirrhosis - symptomatic?

A 
o	Pruritus – colestyramine
o	Diarrhoea – codeine phosphate
o	Fat-soluble vitamin ADEK
o	Ursodeoxycholic acid
o	Liver transplant for end-stage or intractable pruritus
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52
Q

Monitoring of primary biliary cirrhosis?

A

o Regular LFTs, AFP and liver US

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53
Q

Definition of hereditary haemochromatosis?

A
  • Autosomal recessive deficiency of iron regulating hormone hepcidin
  • Causes increased intestinal absorption of iron leading to accumulation in tissues, especially the liver, and organ damage (joints, liver, heart, pancreas, pituitary, adrenals, skin)
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54
Q

Causes of hereditary haemochromatosis?

A
  • Caused by mutation on HFE gene on chromosome 6

- Penetrance varies

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55
Q

Symptoms & signs of hereditary haemochromatosis?

A
  • Symptoms start in 40-60 in men and post-menopausal women
  • Fatigue
  • Weakness, arthralgia
  • Erectile dysfunction, decreased libido
  • Amenorrhoea, hypogonadism
  • Diabetes mellitus
  • Arrhythmias, dilated cardiomyopathy
  • Cirrhosis
  • Impaired memory, mood swings and depression
  • Slate-grey skin
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56
Q

Investigations if Northern European and features of hereditary haemochromatosis?

A
  • If Northern European and features of HH:

o FBC, LFTs, ferritin, transferrin saturation

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57
Q

Investigations if raised ferritin and transferrin with normal FBC in hereditary haemochromatosis?

A
  • If raised ferritin and transferrin (>300 and 50% males, >200 and 40% females) with normal FBC:
    o Genetic testing
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58
Q

Further investigations of hereditary haemochromatosis?

A
  • MRI to defect and quantify hepatic iron excess

- Biopsy not usually needed – by if so, Perl’s stain for iron

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59
Q

Investigations to family members in case of hereditary haemochromatosis?

A
  • Offer lab testing to family members – FBC, LFTs, ferritin, transferrin and genetic testing
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60
Q

Management of hereditary haemochromatosis - when to refer?

A
  • If serum ferritin >1000mcg/L and raised transaminases:

o Refer to hepatologist for fibrosis assessment

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61
Q

Management of hereditary haemochromatosis - specialist management

A 
-	Venesection - weekly
o	400-500ml blood 
o	Aim for SF 20-30 and Tsat <50%
o	Monitor FBC and SF/Tsat
o	Maintenance every 2-3 months
  • Desferrioxamine if intolerant to venesection

Liver Transplant

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62
Q

Management of hereditary haemochromatosis - monitoring?

A

o AFP and US every 6 months

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63
Q

Complications of hereditary haemochromatosis ?

A
  • Liver fibrosis
  • Cirrhosis
  • HCC
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64
Q

Definition of Wilson’s Disease?

A
  • Inherited disorder of biliary copper excretion with excess copper in liver and CNS
    o ATPase mutation prevents movement of copper across intracellular membranes and supports excretion of copper in bile
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65
Q

Causes of Wilson’s Disease?

A
  • Caused by autosomal recessive mutation in ATP7B, on chromosome 13
  • Onset during 20-30s
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66
Q

Symptoms of Wilson’s Disease?

A
  • Young people with liver disease (hepatitis, cirrhosis, fulminant liver failure)
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67
Q

Signs of Wilson’s Disease - neurological?

A 
o	Tremor
o	Dysarthria
o	Dysphagia
o	Dyskinesia
o	Dystonia
o	Dementia
o	Parkinsonism
o	Ataxia
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68
Q

Signs of Wilson’s Disease - mood?

A

o Depression, mania, labile emotions, decreased/increased libido, personality change

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69
Q

Signs of Wilson’s Disease - cognition?

A

o Memory impairment, slow to solve problems, low IQ, delusions

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70
Q

Signs of Wilson’s Disease -other?

A
  • Kayser-Fleischer ring in iris
  • Blue nails, arthritis, grey skin
  • Cardiomyopathy, pancreatitis, infertility
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71
Q

Investigations of Wilson’s Disease?

A
  • Urine – 24h copper excretion is high (>100mcg/24h)
  • Bloods (LFTs raised)
  • Serum copper – typically <11
  • Serum caeruloplasmin - <200mg/L (<140 is pathognomonic)
    o Falsely low – nephrotic, protein deficient, chronic liver disease
    o Falsely high – inflammation, infection, pregnancy
72
Q

Diagnostic investigations of Wilson’s Disease?

A
  • Slit Lamp – Kayser-Fleischer rings in iris
  • Liver biopsy – increased hepatic copper
  • MRI
73
Q

Management of Wilson’s Disease - if family member diagnosed?

A

o Genetic testing of ATP7B gene

74
Q

Management of Wilson’s Disease - general advice?

A

 Avoid alcohol

 Avoid eating food with high copper (liver, chocolate, nuts, mushrooms, legumes, shellfish)

75
Q

Management of Wilson’s Disease - drugs?

A

 Lifelong penicillamine (500mg every 8 hours for 1y then maintenance of 0.75-1g/d)
• Chelating agent – excretes copper in urine
 Zinc
 Trientine dihydrochloride

o Liver transplant if severe liver disease

76
Q

Management of Wilson’s Disease - monitoring?

A

U&E, FBC, clotting

Annual slit lamp study

77
Q

Management of Wilson’s Disease - follow up?

A

 Lifelong follow-up

78
Q

Definition of Budd-Chiari syndrome?

A
  • Hepatic vein obstruction causes congestive ischaemia and hepatocytes damage
79
Q

Causes of Budd-Chiari syndrome?

A

o Haematological – PCV, thrombophilia, antiphospholipid syndrome, PNH
o Blood flow – RHF, contractive pericarditis, right atrial myxoma
o Obstetric – during or postpartum
o Drugs – COCP, HRT
o Infection – amoebic abscess, aspillergosis, syphilis, TB
o Inflammations – IBD, sarcoid, SLE, Sjogrens
o Malignancy – HCC, RCC, Wilm’s tumour, adrenal carcinoma
o Trauma or surgery

80
Q

Symptoms and signs of Budd-Chiari syndrome?

A
  • RUQ pain
  • Ascites
  • Hepatomegaly
  • Jaundice
  • AKI
  • Dilated abdominal wall veins
81
Q

Investigations of Budd-Chiari syndrome?

A
  • LFTs raised
  • Ascitic tap – high in protein
  • Doppler USS
  • MRI/CT
82
Q

Management of Budd-Chiari syndrome?

A
  • Treat ascites
  • Surgical
    o Angioplasty
    o Transjugular intrahepatic porto-systemic shunt
    o Surgical shunt
  • Anticoagulation lifelong
  • Liver transplant if fulminant hepatic necrosis or cirrhosis
83
Q

Physiology of alpha-1-antitrypsin?

A

o Glycoprotein produced in liver, serine protease inhibitor

o Function – balance action of neutrophil-protease enzymes in lungs (neutrophil elastase)

84
Q

Pathology of alpha-1-antitrypsin deficiency?

A

o Autosomal recessive deficiency means protein cannot pass out of liver and accumulates, leading to hepatocyte damage
o Deficiency leads to elastase breakdown of lungs alveolar walls and emphysema

85
Q

Mutation of alpha-1-antitrypsin deficiency?

A
  • Mutation on SERPINA1 gene on chromosome 14 – common amongst white people
86
Q

Symptoms in lung of alpha-1-antitrypsin deficiency?

A

o Smokers develop earlier

o COPD symptoms – diffuse emphysema – SOB, wheeze, cough

87
Q

Symptoms in liver of alpha-1-antitrypsin deficiency?

A

o Hepatitis
o Cirrhosis
o Liver failure

88
Q

Investigations of alpha-1-antitrypsin deficiency?

A
  • LFTs abnormal
  • Serum alpha1-antitrypsin levels low
  • Liver biopsy
    o Periodic acid Schiff (PAS) positive
    o Diastase resistant globules
  • Phenotype
  • CXR, spirometry and CT for lung involvement
89
Q

Management of alpha-1-antitrypsin deficiency -general measures??

A
  • Family members investigated

- Stop smoking

90
Q

Management of alpha-1-antitrypsin deficiency - lung disease?

A

o COPD managed as COPD
o Lung transplant
o Pneumococcal and yearly influenza vaccines

91
Q

Management of alpha-1-antitrypsin deficiency - liver disease?

A

o LFTs monitored
o Treat cirrhosis
o 6-monthly AFP and US – HCC
o Liver transplant

92
Q

Definition of primary NAFLD?

A

Excess fat accumulation in liver (steatosis), where hepatocytes contain >5% of triglycerides which is not due to alcohol or secondary causes

o Spectrum of liver disease – associated with insulin resistance

o Ranges from hepatic steatosis, through to non-alcoholic steatohepatitis (NASH) which may progress to liver fibrosis and cirrhosis

o NASH is liver expression of metabolic syndrome

93
Q

Definition of secondary NAFLD?

A

caused by drugs, Hep C and endocrine conditions

94
Q

Epidemiology of NAFLD?

A
  • NAFLD commonest cause of abnormal LFT
  • Commonest cause of liver disease in western countries
  • Prevalence highest in males aged 40-60
  • Doubled in last 20 years
95
Q

Cause of NAFLD?

A

o Thought to be due to insulin resistance, obesity and metabolic syndrome
o Also, oxidative stress and blood flow compromise

96
Q

Risk factors of NAFLD?

A 
o	Metabolic – central obesity, T2DM, hypertension, hyperlipidaemia
o	Obstructive sleep apnoea
o	Polycystic ovary disease
o	Hypothyroidism
o	FHx of NAFLD
o	Hispanic or Asian people
o	Drugs – NSAIDs, amiodarone, corticosteroids, diltiazem, methotrexate and tamoxifen
o	Hepatits C, Wilsons disease
97
Q

Symptoms of NAFLD?

A
  • Asymptomatic
  • Mild fatigue, malaise
  • RUQ abdominal discomfort
98
Q

When to suspect NAFLD?

A

o Risk factors (T2DM, metabolic syndrome)
o Persistent elevation of LFT for >3 months – typically ALT 3x upper limit of normal and >AST
o Upper abdominal US – fatty changes (increased echogenicity)
• LFTs and US may be normal in NAFLD

99
Q

Assessment of alcohol in NAFLD?

A
  • Alcohol intake: <2.5 units per day for women and <3.75 units per day for men a cut-off
    o If above this value then alcoholic fatty liver disease
100
Q

Bloods to test in NAFLD - if indicated?

A 
o	LFT
o	FBC
o	Clotting
o	Hep B&amp;C serology
o	Auto-antibodies
o	Ferritin
o	Serum caeruloplasmin
o	Alpha-1-antitrypsin deficiency
o	HbA1c
o	Lipids
o	U&amp;E
o	TFTs
o	IgA TTG
101
Q

Assessing risk of NAFLD?

A

Enhanced liver fibrosis test (ELF)
 If >10.51 then advanced
 Algorithm measuring hyaluronic acid, amino-terminal propeptide of type 3 procollagen (PIIINP) and tissue inhibitor of metalloproteinase 1 (TIMP-1)

NAFLD Fibrosis Score (intermediate or high score suggests fibrosis)

Fibrosis (FIB)-4 Score

102
Q

When to diagnose advanced liver disease and refer to hepatology in NAFLD?

A

o NAFLD and ELF >10.51

103
Q

How to investigate children <18 years old for NAFLD?

A

o Offer US if have T2DM or metabolic syndrome and do not misuse alcohol
o Refer all children suspected
o Diagnosed if US shows fatty liver and other causes ruled out
o Retest every 3 years if T2DM or metabolic syndrome and normal US

104
Q

Management of NAFLD - general advice?

A

o Regular physical exercise
o Healthy diet
o Weight loss – 10% in 6 months
o Do not exceed weekly alcohol limits

105
Q

Management of NAFLD - statins?

A

o Keep taking generally

o Stop statins if liver enzyme doubles within 3 months of starting statins

106
Q

Management of NAFLD - follow up in primary care?

A

o Annual – U&E, HbA1c, Lipids

o 3-yearly – assess risk of liver fibrosis – ELF test

107
Q

Management of NAFLD - referral to hepatology?

A

o High risk of advanced liver fibrosis – ELF>10.51
o Signs of advanced liver fibrosis
o Uncertainty

108
Q

Management of NAFLD - secondary care investigations?

A

o Transient elastography (Fibroscan)

o Liver biopsy

109
Q

Management of NAFLD - secondary care - surveillance?

A

 US and AFP every 6 months

110
Q

Management of NAFLD - secondary care - drug treatments?

A

o Drug treatments – pioglitazone or vitamin E

 Re-test ELF after 2 years to see if effective – if risen then stop drug and switch

111
Q

Management of NAFLD - secondary care - definitive treatment?

A

o Liver transplant

112
Q

Prognosis of NAFLD?

A

o Depends on stage of disease and co-morbidities
 Overweight, obese and T2DM at more risk or progression
o If simple steatosis – cirrhosis develops in only 0-4% of people over 10-20 years
o NASH has increased risk of HCC, cirrhosis and fibrosis

113
Q

Complications of NAFLD?

A 
o	Morbidity from CVD and liver disease
	Liver
•	Portal hypertension
•	Variceal haemorrhage
•	Liver failure
•	HCC
•	Sepsis
	Metabolic
•	Hypertension, CKD, T2DM
	CVD
•	AF, MI, CVA
114
Q

Definition of ascites?

A
  • Fluid within peritoneal cavity
115
Q

Pathology of ascites?

A

o Portal hypertension
o Secondary to salt and water retention
o Low Albumin

116
Q

Definition and grading of uncomplicated ascites?

A

Not infected and not associated with hepatorenal syndrome

Graded:
 1 (mild) – only detectable by USS
 2 (moderate) – moderate symmetrical distention of abdomen
 3 (severe) – marked abdominal distention

117
Q

Definition and groups of refractory ascites?

A

Ascites that cannot be mobilised or early recurrence of which cannot be satisfactorily prevented by medical therapy

Groups:
 Diuretic-resistant – refectory to diuretics and salt restriction
 Diuretic-intractable – development of diuretic complications that preclude use

118
Q

Causes of ascites - transudate?

A 
	Cirrhosis
	Hepatic Outflow obstruction
	Budd Chiari syndrome
	Heart Failure
	Constrictive pericarditis
	Malignancy
	Meig’s syndrome
119
Q

Causes of ascites - exudate?

A

 Peritoneal carcinomatosis/TB
 Pancreatitis
 Nephrotic syndrome
 Lymph obstruction

120
Q

Symptoms and signs of ascites?

A
  • Discomfort
  • Nausea and appetite suppression
  • Fullness in flanks
  • Fluid may push out umbilical hernias
  • Shifting dullness, fluid thrill
  • May be pleural effusion and peripheral oedema
121
Q

Bloods to perform in ascites?

A 
o	FBC
o	U&amp;E
o	LFTs
o	Clotting (Prothrombin time)
o	TFTs
122
Q

Imaging to perform in ascites?

A

Abdominal USS

123
Q

Diagnostic test in ascites?

A
  • Diagnostic Paracentesis of 10-20ml of ascitic fluid
    o Albumin (>11g/L in transudate, <11g/L in exudate)
    o Neutrophil count (>250 SPB)
    o Culture
    o Amylase if suggestion of pancreatitis
    o Cytology if suggestion of malignancy
124
Q

Management of ascites - salt?

A
  • Salt Restriction
    o No-added salt diet, 5.2g salt/day
  • If sodium <120mmol/L stop diuretics, caution when <135mmol/L
125
Q

Management of ascites - drug therapy?

A

o Spironolactone from 100mg/day to 400mg/day
 Add furosemide from 40mg/day up to 160mg/day if fails to resolve
 Aim for weight loss <0.5kg/day

126
Q

Management of ascites - further management?

A
  • Therapeutic paracentesis (first line in large or refractory ascites)
    o If <5 litres – plasma expander given
    o If >5 litres – volume expander given using 8g albumin/litre of ascites removed
  • Transjugular Intraheptic Portosystemic Shunt
    o Used for treatment refractory ascites requiring frequent therapeutic paracentesis
  • Liver transplant in cirrhotic ascites
127
Q

Complications of ascites?

A

o Hyponatraemia
o Spontaneous Bacterial Peritonitis
o Hepatorenal syndrome

128
Q

Definition of spontaneous bacterial peritonitis?

A

 Ascitic neutrophil count of >250cells/mm3

 Commonly E.coli & Kleisiella

129
Q

Symptoms of spontaneous bacterial peritonitis?

A

 Symptoms – tender abdomen, fever, vomiting, deterioration, asymptomatic

130
Q

Treatment of spontaneous bacterial peritonitis?

A
  • Empirical Abx – Cefotaxime
  • Prophylactic Abx – Norflaxacin 400mg/day
  • Consider for liver transplant
  • Albumin if renal impairment developing
131
Q

Prognosis of ascites?

A

o 50% mortality over 2 years

o Ascites signifies need to consider liver transplant

132
Q

Definition of ulcerative colitis?

A
  • Along with Crohn’s disease known as inflammatory bowel disease
  • Chronic, relapsing-remitting, non-infectious inflammatory disease of GI tract
  • Mucosa of rectum and colon affected
  • Probable autoimmune condition triggered by environmental factors causing inflammation
133
Q

Pathology of ulcerative colitis - macroscopic?

A

 Begins in rectum and extends proximally
 Continuous
 Red mucosa, ulcers and pseudopolyps
 Backwash ileitis

134
Q

Pathology of ulcerative colitis - microscopic?

A

 Mucosal inflammation
 No granulomas
 Goblet cell depletion
 Crypt abscesses

135
Q

Epidemiology of ulcerative colitis?

A
  • Most common form of IBD
  • Around 1 in 1000 prevalence
  • Peak between 15-25 and 55-65 years
136
Q

Risk factors of ulcerative colitis?

A

o Family History
o OCP
o NOT smoking
o Stress

137
Q

Symptoms of ulcerative colitis?

A 
o	Episodic or chronic diarrhoea +/- blood/mucous
o	Crampy abdominal discomfort
o	Increased bowel frequency
o	Urgency/Tenesmus = Rectal UC
o	Fever/Malaise/Weight loss
138
Q

Signs of ulcerative colitis?

A 
o	In acute UC – fever, tachycardia, tenderness
o	Clubbing
o	Aphthous Ulcers
o	Erythema Nodosum
o	Pyoderma gangrenosum
o	Conjunctivitis/Episcleritis/Iritis
o	Arthritis
139
Q

Bloods if ulcerative colitis suspected?

A

Bloods
 FBC (anaemia, low B12), ferritin, ESR, CRP, U&E, LFTs (raised platelets, abnormal LFTs), blood culture (if needed), TTG, Faecal calprotectin (sign of inflammation)

140
Q

Cultures if ulcerative colitis suspected?

A

o Stool Culture

 M, C & S for C. diff, campylobacter, E.coli

141
Q

Imaging to perform in ulcerative colitis?

A

o Colonoscopy
 Allows biopsy and confirmation

o Barium Enema
 Detects ileal disease

o AXR, Erect CXR – acute colitis

142
Q

Severity assessment of ulcerative colitis?

A

Truelove and Witts Criteria

Based on bloody stools per day, pulse, temperature, Hb, ESR, CRP

143
Q

Management of ulcerative colitis - referral?

A
  • Urgent referral to gastroenterology
144
Q

Management of ulcerative colitis - specialist investigations?

A

o Colonoscopy and biopsy – inflammation extending from rectum proximally, erythema, granulomas, ulceration, crypt abscesses
o CT scan to stage UC

145
Q

Management of ulcerative colitis - surveillance?

A

Offer when symptoms started 10 years ago and have UC or Crohn’s colitis

Baseline colonoscopy with chromoscopy and targeted biopsy of any abnormal areas to determine risk
 Low risk – colonoscopy at 5 years
 Intermediate risk - colonoscopy at 3 years
 High risk – colonoscopy at 1 year

146
Q

Management of ulcerative colitis - symptoms management?

A

o Diarrhoea – bulk-forming laxative (ispaghula husk)
o Fistula – long term antibiotics (metronidazole or ciprofloxacin), surgery
o Abdominal pain – paracetamol 1st line, avoid NSAIDs when possible, chronic pain service

147
Q

Management of ulcerative colitis - medical - inducing remission - mild-to-moderate proctitis/proctosigmoiditis/extensive UC?

A

5-ASA (sulfasalazine, mesalazine, olsalazine) OD topical dose

If no remission in 4 weeks – oral aminosalicylate

If further treatment needed - Oral or PR prednisolone for 2 weeks and decrease

148
Q

Management of ulcerative colitis - medical - inducing remission - moderate to severe UC?

A

5-ASA (sulfasalazine, mesalazine, olsalazine) OD topical dose

If no remission in 4 weeks – oral aminosalicylate

If further treatment needed - Oral or PR prednisolone for 2 weeks and decrease

Tofacitinib

149
Q

Management of ulcerative colitis - inducing remission - acute severe UC?

A
  • MDT Management
  • Assess likelihood of needing surgery (stool frequency >8/day, pyrexia, tachycardia, colonic dilation, low albumin, low Hb, high platelet, >CRP)
  • NBM and IV fluids
  • Prophylactic heparin

• Hydrocortisone IV
o IV Ciclosporin if cannot take IV steroids or not improvement within 72 hours
o Infliximab if ciclosporin contraindicated

• Surgery
o Indicated in perforation, haemorrhage, toxic dilatation, failed medical therapy
o Sub-total colectomy with rectal preservation
o Total proctocolectomy with ileostomy curative

• Daily bloods and X-rays

150
Q

Management of ulcerative colitis - maintaining remission - proctitis or proctosigmoiditis?

A

• Topical ASA alone +/- oral ASA

151
Q

Management of ulcerative colitis - maintaining remission - left sided and extensive UC?

A

• Low dose oral ASA

152
Q

Management of ulcerative colitis - maintaining remission - other options?

A

• Oral azathioprine or mercaptopurine

o If 2 or more inflammatory exacerbations in 12 months needing systemic corticosteroids

153
Q

Management of ulcerative colitis - monitoring?

A

o Bloods – Vitamin B12, folate, calcium and vitamin D

154
Q

Prognosis of UC?

A

o Lifelong relapses and remissions

o May need colectomy, 1 in 10 after 10 years

155
Q

Complications of UC?

A 
o	Bleeding
o	Toxic Megacolon
o	Colorectal cancer
o	VTE
o	Osteoporosis
156
Q

Definition of Crohn’s disease?

A
  • Chronic inflammatory, relapsing and remitting inflammatory disease of GI tract
  • Known with UC collectively as inflammatory bowel disease
  • Inflammation involves discrete parts of the GI tract, anywhere from mouth to anus (called skip lesions)
  • Full thickness of intestinal wall is inflamed
157
Q

Pathology of Crohn’s disease - macroscopic?

A

 Affects all GI
 Oral and perianal disease
 Skip lesions
 Deep ulcers and fissure in mucosa – cobblestone

158
Q

Pathology of Crohn’s disease - microscopic?

A

 Transmural inflammation

 Non-caseating granulomas with Langerhans– 50%

159
Q

Epidemiology of Crohn’s disease?

A
  • Mostly in terminal ileum
  • 1 in 10000 incidences
  • Peak 20-40 years
160
Q

Aetiology of Crohn’s disease?

A

Cause unknown

161
Q

Risk factors of Crohn’s disease?

A 
o	Familial
o	Genetic
	NOD2 and CARD15 genes confer risk
o	Smoking
o	Stress
o	Gastroenteritis
o	NSAIDs
162
Q

Symptoms of Crohn’s disease?

A 
o	Diarrhoea
o	Urgency
o	Abdominal Pain
o	Weight Loss
o	Fever/Malaise/Anorexia
o	Nausea and Vomiting
163
Q

Signs of Crohn’s disease?

A 
o	Clubbing
o	Aphthous ulcers
o	Perianal abscesses/fistula/stricture
o	Erythema nodosum
o	Pyoderma gangrenosum
o	Conjunctivitis/Episcleritis/Iritis
o	Arthritis
o	Ankylosing Spondylitis
164
Q

Investigations of Crohn’s disease?

A
  • Bloods
    o FBC (anaemia), CRP, ESR, U&E, LFTs (low albumin), ferritin, B12, coeliac screen,
    o Faecal calprotectin (differentiate between IBD and IBS)
  • Stool Sample
    o M, C & S – for C. diff, Campylobacter, E. coli
  • Colonoscopy and biopsy
  • Barium Enema
165
Q

Management of Crohn’s disease - referral?

A
  • If Crohn’s disease suspected, urgent referral to gastroenterologist for confirmation of diagnosis and treatment
166
Q

Management of Crohn’s disease - specialist investigations?

A

o Colonoscopy with histology – discontinuous colonic inflammation or ulceration, cobblestone appearance and rectal sparing
o CT used to stage Crohn’s disease

167
Q

Management of Crohn’s disease - education?

A

o Stop smoking

168
Q

Management of Crohn’s disease - symptom management?

A

o Diarrhoea – loperamide, bulk-forming laxative (ispaghula husk)
o Fistula – long term antibiotics (metronidazole or ciprofloxacin), surgery
o Abdominal pain – paracetamol 1st line, avoid NSAIDs when possible, chronic pain service

169
Q

Management of Crohn’s disease - inducing remision - stepwise approach?

A

 Prednisolone/methylprednisolone/IV hydrocortisone – 12 months
• Consider aminosalicylate if prednisolone CI

 Add azathioprine or mercaptopurine
• If 2 or more inflammatory exacerbations in 12 month period or steroids not tolerated

 Add methotrexate
• If 2 or more inflammatory exacerbations in 12 month period or steroids not tolerated

 Add Infliximab or adalimumab

170
Q

Management of Crohn’s disease - maintaining remission?

A
  • Azathioprine or mercaptopurine
  • Methotrexate
  • Sulfasalazine
  • Infliximab
  • DO NOT GIVE STEROIDS
171
Q

Managing complications of Crohn’s disease?

A

 Strictures – balloon dilation

 Fistula – plug insertion or ablation

172
Q

Management of Crohn’s disease - acute attack = mild?

A

• Prednisolone PO for 5 weeks

173
Q

Management of Crohn’s disease - acute attack - severe?

A
  • Admit
  • NBM, IV fluids
  • IV & PR hydrocortisone
  • Metronidazole
  • Daily bloods and imaging
  • If not improving, consider infliximab and adalimumab
174
Q

Management of Crohn’s disease - surgery?

A

o 50% need >1 operation

o Aims to rest distal disease (pouch), resection (short-bowel syndrome)

175
Q

Monitoring of Crohn’s disease?

A

o Bloods – Vitamin B12, folate, calcium and vitamin

d

176
Q

Prognosis of Crohn’s disease?

A

o Around 50% people need surgery
o Slightly higher mortality
o Poor prognosis with early, severe disease

177
Q

Complications of Crohn’s disease?

A 
o	Psychological impact
o	Toxic dilatation
o	Haemorrhage
o	Abscesses, strictures, fistulas
o	Anaemia, malnutrition
o	Colorectal and small bowel cancer
o	Osteopenia

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