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FINALS > GASTROENTEROLOGY > Flashcards

GASTROENTEROLOGY Flashcards

1
Q

What are the features of Wernicke’s encephalopathy?

A 
CAN OPEN:
Confusion
Ataxia
Nystagmus
Ophthamoplegia
PEripheral 
Neuropathy
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2
Q

What is the antibiotic management of C.diff infection?

A
  1. Oral vancomycin
  2. Oral fidaxomicin
  3. Oral vancomycin + IV metronidazole

Life-threatening = oral vancomycin AND IV metronidazole

Recurrent = oral fidaxomicin (<12 weeks) + oral vancomycin (>12 weeks)

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3
Q

Which antibiotics are associated with c.diff infection?

A

Second & third gen cephalosporins (ceftriaxone)
Clindamycin

+ PPIs

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4
Q

Which marker is used to determine the severity of c.diff infection?

A

WCC
<15 = moderate
>15 = severe

Hypotension/toxic megacolon = life-threatening

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5
Q

How is C.diff infection diagnosed?

A

CDT (C.diff toxin) in the stool

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6
Q

Name 5 causes of hepatitis?

A 
• Alcoholic hepatitis
• Non alcoholic fatty liver disease
• Viral hepatitis
• Autoimmune hepatitis
- Drug induced hepatitis (e.g. paracetamol overdose)
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7
Q

How does hepatitis present?

A 
• Abdominal pain
• Fatigue
• Pruritis (itching)
• Muscle and joint aches
• Nausea and vomiting
• Jaundice 
Fever (viral hepatitis)
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8
Q

What is found on liver function tests in hepatitis?

A

^AST/ALT
^ALP (but less rise)
Bilirubin^

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9
Q

What is the most common viral hepatitis worldwide?

A

A

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10
Q

Which viral hepatitis’ can you receive vaccinations for?

A

A, B (notifiable diseases PHE)

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11
Q

How is hepatitis A transmitted?

A

Faecal oral (contaminated warer/food)

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12
Q

How does hepatitis A present?

A 
Nausea
Vomiting
Anorexia
Jaundice
Cholestasis - pale stools, dark urine
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13
Q

What is the management of hepatitis A?

A

Analgesia
Resolves without treatment 1-3 months
Notify PHE

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14
Q

What causes hepatitis B?

A

DNA virus

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15
Q

How is hepatitis B transmitted?

A

Sex
IVDU
Tattoos
Vertical transmission

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16
Q

How long is recovery from hepatitis B?

A

2-3 months

Some people are carriers for life

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17
Q

What is implied by E antigen on hepatitis serology (HBeAg)?

A

High infectivity

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18
Q

What is HBV DNA?

A

Direct count of viral load of hepatitis B

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19
Q

How can you confirm a response to the hepatitis B vaccine?

A

HBsAg (surface antigen)

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20
Q

What is the management of hepatitis B?

A 
Refer to gastroenterology for specialist management
Education about reducing transmission
Antivirals
Liver transplantation (end stage)
Notify PHE
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21
Q

What causes hepatitis C?

A

RNA virus

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22
Q

What is the transmission of hepatitis C?

A

Blood/bodily fluids

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23
Q

What is the prognosis for hepatitis C?

A

1/4 full recovery

3/4 chronic disease –> liver cirrhosis –> hepatocellular carcinoma

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24
Q

How can you test for hepatitis C?

A

Hepatitis C RNA testing

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25
Q

What is the management for hepatitis C?

A 
Refer to gastroenterology for specialist management
Education about reducing transmission
Direct acting antivirals (curative)
Liver transplantation (end stage)
Notify PHE
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26
Q

What causes hepatitis D?

A

RNA virus

Can only be concomitant with hepatitis B

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27
Q

What is the management of hepatitis D?

A

No specific treatment

Notify PHE

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28
Q

What causes hepatitis E?

A

RNA virus

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29
Q

How is hepatitis E transmitted?

A

Faecal oral route

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30
Q

How does hepatitis E present?

A

Mild illness
No treatment required
Cleared within a month
Rarely causes chronic hepatitis in immunocompromised patients

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31
Q

What are the two types of autoimmune hepatitis?

A

Type 1: occurs in adults

Type 2: occurs in children

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32
Q

How does type 1 autoimmune hepatitis present?

A

Type 1 typically affects women in their late forties or fifties. It presents around or after the menopause with fatigue and features of liver disease on examination. It takes a less acute course than type 2.

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33
Q

How does type 2 autoimmune hepatitis present?

A

In type 2, patients in their teenage or early twenties present with acute hepatitis with high transaminases and jaundice.

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34
Q

Which antibodies are found in type 1 autoimmune hepatitis?

A

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

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35
Q

Which antibodies are found in type 2 autoimmune hepatitis?

A

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

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

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36
Q

How is autoimmune hepatitis diagnosed?

A

Liver biopsy

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37
Q

What is the management of autoimmune hepatitis?

A
  1. High dose steroids (prednisolone)

2. Introduce immunosuppressants - azathioprine

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38
Q

How do you screen for harmful alcohol use?

A

CAGE questionnaire

C - cut down?
A - annoyed about other people saying you should cut down
G - guilty about your drinking?
E - eye opener

OR

AUDIT questionnaire (10 questions)

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39
Q

What are the complications of harmful alcohol use?

A 
• Alcoholic Liver Disease
• Cirrhosis and the complications of cirrhosis including hepatocellular carcinoma
• Alcohol Dependence and Withdrawal
• Wernicke-Korsakoff Syndrome (WKS)
• Pancreatitis
Alcoholic Cardiomyopathy
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40
Q

What are the features of Wernicke’s encephalopathy?

A
  1. Confusion
  2. Oculomotor disturbances (disturbances of eye movements)
  3. Ataxia (difficulties with coordinated movements)
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41
Q

What are the features of Korsakoff’s syndrome?

A 
Memory impairment (retrograde and anterograde)
Behavioural changes
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42
Q

What is the management of Wernicke’s encephalopathy?

A

Pabrinex (high dose vitamin B - thiamine)

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43
Q

Name 4 causes of Wernicke’s encephalopathy?

A

Alcohol excess
Persistent vomiting
Stomach cancer
Dietary deficiency

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44
Q

What are the symptoms of alcohol withdrawal?

A

6-12 hours: tremor, sweating, headache, craving and anxiety
12-24 hours: hallucinations
24-48 hours: seizures
24-72 hours: “delirium tremens”

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45
Q

What is the mortality of DTs?

A

35%

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46
Q

What is the first-line treatment of DTs?

A

Lorazepam PO

IV lorazepam or haloperidol
If DT develops during detox, review regimen

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47
Q

What scoring system is used to assess alcohol withdrawal?

A

The CIWA-Ar (Clinical Institute Withdrawal Assessment – Alcohol revised) tool can be used to score the patient on their withdrawal symptoms and guide treatment.

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48
Q

What is the first-line treatment for alcohol withdrawal?

A

Chlordiazepoxide (librium)

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49
Q

What is the management of alcohol withdrawal?

A

Chlordiazepoxide

IV high dose vitamin B (pabrinex) (followed by regular dose thiamine)

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50
Q

What is used to detox from alcohol?

A

Chlordiazepoxide - either fixed or variable dose depending on symptoms
Preferably done as an inpatient to manage side effects and precent DTs

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51
Q

What medications can be used to prevent relapse in alcohol addiction?

A 
• Group therapy or self-help (e.g. AA) 
• Naltrexone - decrease the amount and frequency of drinking (DO NOT use with opioids = may precipitate withdrawal)
• Baclofen: ↓ cravings 
• Acamprosate: ↓ cravings 
Disulfiram: aversion therapy
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52
Q

What are the three steps in the progression of alcoholic liver disease?

A
  1. Alcohol related fatty liver disease
  2. Alcoholic hepatitis
    Cirrhosis
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53
Q

What are the signs of liver disease?

A 
• Jaundice
• Hepatomegaly
• Spider Naevi
• Palmar Erythema
• Gynaecomastia
• Bruising – due to abnormal clotting
• Ascites
• Caput Medusae – engorged superficial epigastric veins
Asterixis – “flapping tremor” in decompensated liver disease
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54
Q

What bloods should be checked in alcoholic liver disease?

A 
FBC = MCV
LFT = AST>ALT, gamma-GT^
Clotting = PT^
U&Es = hepatorenal syndrome
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55
Q

What is the treatment of alcoholic hepatitis?

A

Steroids improve short term outcomes (over 1 month)

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56
Q

Which score is used to determine the need for steroid therapy and severity of alcoholic hepatitis? What is the cut off score?

A

Maddrey Discriminant Function

Score >32 = steroid therapy

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57
Q

Which score predicts mortality in alcoholic hepatitis?

A

Glasgow alcoholic hepatitis score

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58
Q

What is the management of alcoholic cirrhosis?

A

Treat complications of cirrhosis (portal hypertension, varices, ascites and hepatic encephalopathy)

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59
Q

What is the definitive treatment of alcoholic cirrhosis?

A

Referral for liver transplant in severe disease however they must abstain from alcohol for 3 months prior to referral

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60
Q

Which score is used to determine the severity of liver cirrhosis? Which values are used to calculate this score?

A

MELD - uses a combination of INR, BR and creatinine to determine survival and severity of cirrhosis.

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61
Q

Which scoring systems is used for the prognosis of chronic liver disease?

A

Child-Pugh score

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62
Q

Which score is used in ED and primary care to determine the need for further alcohol screening?

A

FAST

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63
Q

How does alcoholic ketoacidosis present?

A

Abdominal pain

Vomiting

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64
Q

What might be seen on an ABG in alcoholic ketoacidosis?

A

Normal glucose
^Ketones
Metabolic acidosis

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65
Q

Who is at risk of developing alcoholic ketoacidosis?

A

Chronic binge drinkers, especially if not eating

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66
Q

What is the treatment of alcohol ketoacidosis?

A

IV fluids

Thiamine (vit B1)

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67
Q

What is PBC?

A

immune system attacks the small bile ducts within the liver

Causes obstruction of bile –> cholestasis –> fibrosis –> cirrhosis

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68
Q

Which part of the liver is affected first in PBC?

A

Intralobar ducts, also known as the Canals of Hering.

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69
Q

Which three liver products build up in the blood due to PBC and cause symptoms?

A

Bile acids - pruritis
Bilirubin - jaundice
Cholesterol - xanthelasma (+ increase risk of cardiovascular disease)

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70
Q

What is the role of bile acids?

A

Digestion of fats

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71
Q

What are the risk factors for PBC?

A
  • Middle aged women
  • Other autoimmune diseases (e.g. thyroid, coeliac)
  • Rheumatoid conditions (e.g. systemic sclerosis, Sjogrens and rheumatoid arthritis)
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72
Q

How does PBC present?

A 
• Fatigue
• Pruritus
• GI disturbance and abdominal pain
• Jaundice
• Pale stools
• Xanthoma and xanthelasma
Signs of cirrhosis and failure (e.g. ascites, splenomegaly, spider naevi)
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73
Q

How is PBC diagnosed and staged?

A

Liver biopsy

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74
Q

Which liver enzyme is raised first in PBC and PSC?

A

ALP

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75
Q

Which autoantibodies are found in PBC? Which is most specific?

A

AMA - most specific (part of the diagnostic criteria)

ANA

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76
Q

Which blood tests are done in suspected PBC?

A

LFTs
Antibodies - ANA, AMA
ESR - raised
IgM - raised

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77
Q

What is the treatment of PBC? (4)

A

• Ursodeoxycholic acid reduces the intestinal absorption of cholesterol
• Colestyramine is a bile acid sequestrate in that it binds to bile acids to prevent absorption in the gut and can help with pruritus due to raised bile acids
• Liver transplant in end stage liver disease
Immunosuppression (e.g. with steroids) is considered in some patients

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78
Q

What is the action of ursodeoxycholic acid?

A

reduces the intestinal absorption of cholesterol

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79
Q

What is the action of colesyramine?

A

bile acid sequestrate in that it binds to bile acids to prevent absorption in the gut and can help with pruritus due to raised bile acids

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80
Q

What is the definitive management of PBC?

A

Liver transplant in end stage liver disease

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81
Q

What is PSC?

A

intrahepatic or extrahepatic ducts become strictured and fibrotic

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82
Q

What is the cause of PSC?

A

Unclear

Genetic
Autoimmune
Ulcerative colitis (70%)

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83
Q

What are the risk factors for PSC?

A

• Male
• Aged 30-40
• Ulcerative Colitis
Family History

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84
Q

How does PSC present?

A 
• Jaundice
• Chronic right upper quadrant pain
• Pruritus
• Fatigue
Hepatomegaly
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85
Q

What is the role of autoantibody testing in PSC?

A

Limited
Antibodies are non-specific
Might indicate whether there will be a response to immunosuppressants

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86
Q

Which autoantibodies are associated with PSC?

A

• Antineutrophil cytoplasmic antibody (p-ANCA) in up to 94%
• Antinuclear antibodies (ANA) in up to 77%
Anticardiolipin antibodies (aCL) in up to 63%

87
Q

What is the gold standard diagnostic investigation in PSC?

88
Q

What is the management of PSC?

A

Liver transplant (80% 5 year survival)
ERCP - dilate & stent
Colestyramine - bile acid sequestrate
Monitoring for complications

89
Q

What are the complications of PSC?

A 
• Acute bacterial cholangitis
• Cholangiocarcinoma develops in 10-20% of cases
• Colorectal cancer
• Cirrhosis and liver failure
• Biliary strictures
Fat soluble vitamin deficiencies
90
Q

What are the four most common causes of cirrhosis?

A

• Alcoholic liver disease
• Non Alcoholic Fatty Liver Disease
• Hepatitis B
Hepatitis C

91
Q

Give some signs of cirrhosis.

A

• Jaundice – caused by raised bilirubin
• Hepatomegaly – however the liver can shrink as it becomes more cirrhotic
• Splenomegaly – due to portal hypertension
• Spider Naevi – these are telangiectasia with a central arteriole and small vessels radiating away
• Palmar Erythema – caused by hyperdynamic circulation
• Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
• Bruising – due to abnormal clotting
• Ascites
• Caput Medusae – distended paraumbilical veins due to portal hypertension
Asterixis – “flapping tremor” in decompensated liver disease

92
Q

Why do you get gynaecomastia in liver cirrhosis?

A

Endocrine dysfunction:
increased production of androstenedione by the adrenal glands
increased aromatisation of androstenedione to oestrogen loss of clearance of adrenal androgens by the liver

93
Q

What is seen on LFTs in cirrhosis?

A

May be normal

Decompensated = all markers deranged

94
Q

What is first-line investigation for assessing fibrosis in non-alcoholic fatty liver disease?

A

Enhanced Liver Fibrosis (ELF) blood test

95
Q

How is the ELF blood test interpreted?

A 
• Nodularity of the surface of the liver
• A “corkscrew” appearance to the arteries with increased flow as they compensate for reduced portal flow
• Enlarged portal vein with reduced flow
• Ascites
Splenomegaly
96
Q

When should you screen for hepatocellular carcinoma in cirrhosis? What does screening involve?

A

US and alpha-fetoprotein

Every 6 months

97
Q

What is a Fibroscan?

A

Checks the elasticity of the liver

Assesses the degree of cirrhosis

98
Q

Which patients should receive a Fibroscan?

A

Every 2 years in patients at risk of cirrhosis:
• Hepatitis C
• Heavy alcohol drinkers (men drinking > 50 units or women drinking > 35 units per week)
• Diagnosed alcoholic liver disease
• Non alcoholic fatty liver disease and evidence of fibrosis on the ELF blood test
Chronic hep B (every year)

99
Q

Which three markers are measured by ELF blood test?

A

HA, PIIINP and TIMP-1

100
Q

Which scoring systems can be used to assess prognosis of cirrhosis?

A

Child-Pugh Score

MELD score

101
Q

Which markers are used in the MELD score? (5)

A 
Bilirubin
Creatinine
INR
Sodium
Dialysis
102
Q

How is the MELD score used?

A

gives a percentage estimated 3 month mortality and helps guide referral for liver transplant

103
Q

When should patients with cirrhosis get a MELD score?

A

Every 6 months

104
Q

What is the general management of cirrhosis?

A
  • Ultrasound and alpha-fetoprotein every 6 months for hepatocellular carcinoma
  • Endoscopy every 3 years in patients without known varices
  • High protein, low sodium diet
  • MELD score every 6 months
  • Consideration of a liver transplant
105
Q

What is the 5 year survival of cirrhosis?

106
Q

Name 6 complications of cirrhosis.

A 
Malnutrition
Portal hypertension & varices 
Ascites & SBP
Hepatic encephalopathy
Hepatorenal syndrome
HCC
107
Q

How does cirrhosis lead to muscle wasting?

A

increased use of muscle tissue as fuel and reduces the protein available in the body for muscle growth

108
Q

What advice can you give to avoid malnutrition in cirrhosis?

A

• Regular meals (every 2-3 hours)
• Low sodium (to minimise fluid retention)
• High protein and high calorie (particularly if underweight)
Avoid alcohol

109
Q

How does cirrhosis lead to portal hypertension?

A

Scarring of the liver increases resistance to blood flow

Pressure builds in portal system

110
Q

Where do varices most commonly occur?

A
  • Gastro oesophageal junction
  • Ileocaecal junction
  • Rectum
  • Anterior abdominal wall via the umbilical vein (caput medusae)
111
Q

How do you treat stable varices?

A

• Propranolol reduces portal hypertension by acting as a non-selective beta blocker
• Elastic band ligation of varices
- Injection of sclerosant (less effective than band ligation)

112
Q

What can be done if the medical and endoscopic treatment of varices fails?

A

TIPS procedure

113
Q

What is ascites?

A

Fluid accumulation within the abdomen.

114
Q

What is the pathophysiology of ascites?

A

Portal HTN causes leaking of fluid from capillaries in the liver/bowel into the peritoneal cavity.
Loss of circulating volume causes the kidneys to produce renin –> aldosterone.
Aldosterone leads to increased reabsorption of fluid and sodium.

115
Q

What type of ascites is caused by cirrhosis?

A

Transudative (low protein) - HIGH SAAG

116
Q

What is SAAG? How is it used and how is it calculated?

A

SAAG = serum-ascites albumin gradient
It is used to determined the cause of ascites.
SAAG = (serum albumin concentration) - (ascitic albumin concentration)

117
Q

How can the causes of ascites be grouped?

A 
High SAAG (>11g/L)
Low SAAG (<11g/L)
118
Q

What are the high SAAG causes of ascites?

A

Liver disease - acute liver failure, cirrhosis, liver metastases = PORTAL HTN
Cardiac - RHF, constrictive pericarditis
Other - Budd-Chiari syndrome, portal vein thrombosis

119
Q

What are the low SAAG causes of ascites?

A

Nephrotic syndrome
Peritoneal carcinoma
Infection - TB

120
Q

How is ascites managed?

A
  1. Reduce dietary sodium
  2. Aldosterone antagonist - Spironactalone
  3. Drain - needs PT and albumin cover
  4. Prophylactic Abx (prevent SBP)
  5. TIPS - last line, high risk
121
Q

What is paracentesis induced circulatory dysfunction?

A

Can occur due to large volume paracentesis (> 5 litres). It is associated with a high rate of ascites recurrence, development of hepatorenal syndrome, dilutional hyponatraemia, and high mortality rate.

122
Q

When should you give prophylactic Abx in ascities? Which abx is used?

A

Ascitic albumin concentration <15g/L (found on paracentesis)

Ciprofloxacin PO

123
Q

What is another name for paracentesis?

A

Ascitic tap/drain

124
Q

What is the gold standard diagnostic investigation for SBP?

A

Paracentesis

Neutrophil count >250 cells/ul

125
Q

What percentage of patients with ascites secondary to cirrhosis will develop SBP?

126
Q

What is the mortality of SBP?

127
Q

How does SBP present?

A

• Can be asymptomatic so have a low threshold for ascitic fluid culture
• Fever
• Abdominal pain
• Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)
• Ileus
- Hypotension

128
Q

What are the most common organisms that cause SBP?

A

• Escherichia coli
• Klebsiella pnuemoniae
- Gram positive cocci (such as staphylococcus and enterococcus)

129
Q

What is the management of SBP?

A
  • Take an ascitic culture prior to giving antibiotics

- Usually treated with an IV cephalosporin such as cefotaxime

130
Q

What is the pathophysiology of hepatorenal syndrome?

A

Loss of circulating blood volume (portal vessel dilatation, ascites)
Activation of RAAS
Vasoconstriction of renal blood vessels
Deteriorating kidney function

131
Q

What is the prognosis of hepatorenal syndrome?

A

Fatal within a week

Needs liver transplant

132
Q

What is the management of hepatorenal syndrome?

A

Liver transplant

133
Q

What is another name for hepatic encephalopathy?

A

Portosystemic encephalopathy

134
Q

Which toxin causes hepatic encephalopathy?

135
Q

Why does ammonia build up in the blood of patients with liver cirrhosis?

A
  • Functional impairment of the liver cells prevents 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.
136
Q

How does hepatic encephalopathy present?

A

Reduced consciousness
Confusion
Changes to personality, memory and mood

137
Q

What factors can precipitate hepatic encephalopathy?

A 
• Constipation
• Electrolyte disturbance
• Infection
• GI bleed
• High protein diet
- Medications (particularly sedative medications)
138
Q

What is the management of hepatic encephalopathy?

A

• Laxatives (i.e. lactulose) promote the excretion of ammonia. The aim is 2-3 soft motions daily. They may require enemas initially.
• Antibiotics (i.e. rifaximin) reduces the number of intestinal bacteria producing ammonia. Rifaximin is useful as it is poorly absorbed and so stays in the GI tract.
- Nutritional support. They may need nasogastric feeding.

139
Q

Which autoimmune conditions are commonly associated with coeliac disease?

A 
Diabetes type I - all new presentations are tested for coeliac
Thyroid disease
Autoimmune hepatitis
Primary biliary cirrhosis
Primary sclerosing cholangitis
140
Q

What are the genetic associations with coeliac disease?

A

• HLA-DQ2 gene (90%)

HLA-DQ8 gene

141
Q

When does coeliac present?

A

Biomodal - infancy & 50-60 years

142
Q

How is the spleen affected by coeliac disease?

A

Hyposplenism

143
Q

How does coeliac disease present?

A

• Failure to thrive in young children
• Diarrhoea
• Fatigue
• Weight loss
• Mouth ulcers
• Anaemia secondary to iron, B12 or folate deficiency
Dermatitis herpetiformis (an itchy blistering skin rash typically on the abdomen)

144
Q

What neurological symptoms can be caused by coeliac disease?

A

• Peripheral neuropathy
• Cerebellar ataxia
Epilepsy

145
Q

What is the gold standard investigation for diagnosing coeliac disease?

A

Jejunal biopsy

146
Q

How is a biopsy taken in suspected coeliac disease?

A

From the jejunum via a Crosby capsule

147
Q

What features are seen on biopsy for coeliac disease?

A

Villous atrophy
Crypt hyperplasia/hypertrophy
Increase in intraepithelial lymphocytes
Lamina propria infiltration with lymphocytes

148
Q

Which three auto-antibodies are associated with coeliac disease? Which is most specific?

A

IgA tissue transglutaminase (TTG) antibodies - specific
Anti-endomysial (anti-EMA)
Deaminated gliadin peptides antibodies (anti-DGPs)

149
Q

Why should you test for IgA levels as well as specific autoantibodies?

A

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

150
Q

What are the 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)
Dermatitis herpetiformis
151
Q

What is the management of coeliac disease?

A

Life-long gluten free diet

152
Q

Name two dermatological complications of coeliac disease?

A

Dermatitis herpetiformis

Aphthous ulcers

153
Q

Which foods should be avoided in coeliac?

A

Barley
Rye
Oats
Wheat

154
Q

Which foods are okay to eat in coeliac disease?

A

Maise, soya, rice

155
Q

Which vaccination should people with coeliac receive?

A

Pneumococcal (due to hyposplenism)

156
Q

How is the oesophagus anatomically divided?

A

Divided into 3rds: reflects change in musculature from striated → mixed → smooth.

157
Q

Which epithelium lines the oesophagus?

A

• Lined by non-keratinising squamous epithelium.

Z-line: transition from squamous → gastric columnar

158
Q

How can the causes of dysphagia be grouped?

A

Inflammatory
Neurological
Mechanical obstruction

159
Q

Name 4 inflammatory causes of dysphagia.

A

• Tonsillitis, pharyngitis
• Oesophagitis: GORD, candida
• Oral candidiasis
- Aphthous ulcers

160
Q

Name 4 local neurological causes of dysphagia.

A
  • Achalasia
  • Diffuse oesophageal spasm
  • Nutcracker oesophagus
  • Bulbar / pseudobulbar palsy (CVA, MND)
161
Q

Name 2 systemic neurological causes of dysphagia.

A

MG

Systemic sclerosis/CREST syndrome

162
Q

How can the mechanical obstructive causes of dysphagia be grouped?

A

Luminal - FB, food bolus
Mural - stricture, malignancy
Extra-mural - retrosternal goitre, lung ca, mediastinal lymphoma, TAA

163
Q

What is Boerhaave’s syndrome?

A

Oesophageal tear

164
Q

Give some features of an oesophageal tear.

A
  • Odonophagia (painful swallowing)
  • Mediastinitis: tachypnoea, dyspnoea, fever, shock
  • Surgical emphysema
165
Q

What investigations should be done in dysphagia?

A

Upper GI endoscopy

Ba swallow

166
Q

What is indicated by a corkscrew oesophagus on barium swallow?

A

Diffuse oesophageal spasm

167
Q

Why is the incidence of oesophageal cancer increasing?

A

Barret’s oesophagus

168
Q

What is the median age of presentation in oesophageal cancer?

A

50-70 years

169
Q

What are the risk factors for oesophageal cancer?

A 
• EtOH 
• Smoking 
• Achalasia 
• GORD → Barrett’s 
• Plummer-Vinson 
• Fatty diet 
• ↓ vit A+C 
Nitrosamine exposure
170
Q

Which type of cancer is found in the upper and middle thirds of the oesophagus?

A

Squamous cell carcinoma - associated with alcohol, smoking

171
Q

Which type of cancer is found in the lower third of the oesophagus?

A

Adenocarcinoma - associated with Barret’s oesophagus

172
Q

Which type of oesophageal cancer is most common?

A

Adenocarcinoma (65%)

173
Q

How does oesophageal cancer present?

A

Progressive dysphagia (solids –> liquids)
Weight loss
Retrosternal chest pain
Lymphadenopathy

174
Q

How might a malignant mass in the upper third of the oesophagus present?

A

Hoarseness: recurrent laryngeal nerve invasion

Cough –> aspiration pneumonia

175
Q

Where might oesophageal cancer metastasise to?

A

Direct
Lymphatics
Blood

75% of patients have mets at presentation

176
Q

How is oesophageal cancer staged?

A

TNM

CT, US

177
Q

How is oesophageal cancer diagnosed?

A

Upper GI endoscopy + biopsy

178
Q

What is the treatment of oesophageal cancer?

A

MDT
Oesophagectomy (25-30% resectable)
Neo-adjuvant chemo - cisplatin

179
Q

What is the 5 year survival for oesophageal cancer?

180
Q

Name some palliative approaches to oesophageal cancer.

A

Stenting
Radiotherapy
Analgesia
Macmillan nurses & palliative care referral

181
Q

What is achalasia?

A

Degeneration of myenteric plexus (Auerbach’s)
↓ peristalsis
LOS fails to relax

182
Q

What are the two causes of achalasia?

A

1O / idiopathic: commonest

2O: Chagas’ disease (T. cruzii)

183
Q

How does a patient present with achalasia?

A

Dysphagia: liquids –> solids
Regurgitation
Weight loss
Substernal cramps

184
Q

Give a complication of achalasia.

A

SCC of the oesophagus (3-5%)

185
Q

What is seen on barium swallow in achalasia?

A

dilated tapering oesophagus - Bird’s beak

186
Q

What can be seen on CXR in achalasia?

A

widened mediastinum, double RH border

187
Q

How is achalasia managed?

A
  • Medical - CCBs, nitrates
  • Interventions: botox injection, endoscopic balloon dilatation
  • Surgical: Heller’s cardiomyotomy
188
Q

What is a pharyngeal pouch?

A

Outpouching between crico- and thyro-pharyngeal components of the inf. pharyngeal constrictor.
Area of weakness - Killan’s dehiscence

189
Q

What might be seen on examination on someone with a pharyngeal pouch?

A

Bulge on left side of the neck

190
Q

How might someone present with a pharyngeal pouch?

A

Regurgitation, halitosis, gurgling sounds

191
Q

What is the treatment for a pharyngeal pouch?

A

Excision

Endoscopic stapling

192
Q

How does GORD present?

A 
• Heartburn
• Acid regurgitation
• Retrosternal or epigastric pain
• Bloating
• Nocturnal cough
Hoarse voice
193
Q

Which patients should be admitted for an urgent endoscopy?

A

Signs of GI bleed:

  • Melaena
  • Coffee ground vomiting
194
Q

When should patients have a 2WWW for endoscopy?

A
  • Dysphagia (difficulty swallowing) at any age gets a two week wait referral
  • Aged over 55 (this is generally the cut off for urgent versus routine referrals)
  • Weight loss
  • Upper abdominal pain / reflux
  • Treatment resistant dyspepsia
  • Nausea and vomiting
  • Low haemoglobin
  • Raised platelet count

OR if symptoms >4 weeks with treatment

195
Q

What is the gold standard test for diagnosing GORD?

A

24-hr oesophageal pH monitoring

196
Q

What advice should be given to patients with GORD?

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
197
Q

What is the surgical treatment of GORD?

A

Laparoscopic fundoplication

198
Q

What is the treatment of endoscopically proven oesophagitis?

A

• full dose proton pump inhibitor (PPI) for 1-2 months
• if response then low dose treatment as required
- if no response then double-dose PPI for 1 month

199
Q

What is the treatment of endoscopically negative reflux disease?

A

• full dose PPI for 1 month
• if response then offer low dose treatment, possibly on an as-required basis, with a limited number of repeat prescriptions
if no response then H2RA or prokinetic for one month

200
Q

What is H.Pylori?

A

gram negative aerobic bacteria

201
Q

How does H.Pylori cause dyspepsia?

A

exposes the epithelial cells underneath to acid

also produces ammonia to neutralise the stomach acid. The ammonia directly damages the epithelial cells

202
Q

Name four associated conditions of H.Pylori.

A 
• peptic ulcer disease 
	○ 95% of duodenal ulcers
	○ 75% of gastric ulcers
• gastric cancer
• B cell lymphoma of MALT tissue (eradication of H pylori results causes regression in 80% of patients)
- atrophic gastritis
203
Q

Who should be offered H.Pylori testing?

A

Anyone with dyspepsia

204
Q

Which three tests are used for H.Pylori?

A

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

205
Q

How long do patients need to be off PPIs before testing for H.Pylori?

206
Q

When can you take a urea breath test?

A

off abs 4 weeks

off PPIs 2 weeks

207
Q

How is H.Pylori treated?

A

Triple therapy:

a proton pump inhibitor (e.g. omeprazole) plus 2 antibiotics (e.g. amoxicillin and clarithromycin) for 7 days.

208
Q

What is used to test for eradication?

A

urea breath test

209
Q

What is Barrett’s oesophagus?

A

metaplasia of the lower oesophageal mucosa

Squamous cell –> columnar

210
Q

Which condition is associated with Barrett’s oesophagus?

A

Adenocarcinoma

211
Q

What are the two types of Barrett’s oesophagus?

A

Short <3cm

Long >3cm

212
Q

When should patients with metaplasia receive endoscopic surveillance?

A

every 3-5 years

213
Q

What is the management of dysplasia?

A

• endoscopic mucosal resection

- radiofrequency ablation

214
Q

Laxative abuse can result in which bowel condition?

A

Melanosis coli

FINALS (26 decks)

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