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GCUH FRACP Writtens 2020 > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

Which type of malignancy are patients with achalasia more at risk of developing?

A

SCC - risk is >10 x that of the general population.

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2
Q

What are the common symptoms of achalasia? Name 2.

A

Regurgitation of undirected food minutes or hours after a meal

Chronic, often constant, dysphasia for solids and liquids

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3
Q

What is the pathophysiology of achalasia?

A

Loss of inhibitory neurons from lower oesophageal sphincter.

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4
Q

Name 4 treatment modalities for achalasia.

A

Botulinum injection

Pneumatic balloon dilatation

LOS myotomy

Per oral endoscopic myotomy (POEM) - emerging treatment of choice

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5
Q

What complications can botulinum injections cause when treating achalasia, if further treatment were to be considered in the future?

A

Botulinum injections cause submucosal fibrosis which interferes with subsequent definitive treatments.

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6
Q

Name 3 ways that patients with eosinophilia oesophagitis typically present.

A

Food bolus obstruction

Chronic dysphagia solids > liquids

Refractory GORD

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7
Q

What is the pathophysiology of eosinophilia oesophagitis?

A

Infiltration of eosinophils into oesophageal mucosa

Chronic inflammation leads to deposition of subepithelial fibrous tissue

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8
Q

What established treatments can be provided for eosinophilia oesophagitis? Name 3.

A

PPIs

Aerolised steroids

Diet - 6 food elimination diet

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9
Q

Name 7 risk factors for the development of Barrett’s oesophagus.

A

Male

Caucasian

Age

Overweight

Chronic heartburn

Smoking

Positive family Hx

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10
Q

Which malignancy can Barrett’s progress to?

A

Adenocarcinoma

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11
Q

What are the three mechanisms of reflux in GORD?

A

Transient lower oesophageal sphincter relaxation

Weak LOS

Increased intra-abdominal pressure (obesity)

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12
Q

Name 7 dietary factors that may aggravate GORD symptoms.

A

Citrus fruits and juices

Carbonated drinks

Caffeine

Heavy meals

Fatty foods

Spicy foods

Alcohol

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13
Q

Name 8 groups of medications that can impair lower oesophageal sphincter function and aggravate GORD.

A

Beta-adrenergic agonists

Theophylline

Anticholinergics

Tricyclics antidepressants

Progesterone

Alpha-adrenergic antagonists

Diazepam

Calcium channel blockers

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14
Q

Name 4 (groups of) medications that can cause damage to the oesophageal mucosa, resulting in aggravation of GORD symptoms.

A

Aspirin and other NSAIDs

Doxycycline

Quinidine

Bisphosphonate

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15
Q

How frequently do patients with Barrett’s oesophagus require screening?

A

No dysplasia - 3-5 years

Low grade - 6 monthly

High grade - likely cancer; requires close surveillance/definitive management

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16
Q

What features on endoscopy would you expect to see with achalasia?

A

Food in oesophagus

Tight LOS

Dilated oesophagus

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17
Q

Name 4 factors which confer a good outcome with treatment in achalasia.

A

Type 2 achalasia

Post-treatment decrease in LOS pressure

Older - if receiving dilatation

Younger - if receiving myotomy

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18
Q

Name 4 factors which confer more negative outcomes with treatment in achalasia.

A

Types 3 and 1 achalasia

Oesophageal dilatation

Sigmoid oesophagus

Chest pain

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19
Q

What 2 features on endoscopy would be expected in distal oesophageal spasm?

A

Retained food

Uncoordinated or ring contractions

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20
Q

What 3 features on barium swallow would be expected in distal oesophageal spasm?

A

Tertiary contractions

Diverticula

Poor passage of bolus

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21
Q

What feature on manometry would be expected in distal oesophageal spasm?

A

Synchronous pressure waves

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22
Q

In which part of the duodenum are ulcers usually found?

A

1st part.

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23
Q

With high risk bleeding upper GI ulcers, what is the consensus with regard to further treatment following adrenaline injection?

A

Second endoscopic treatment strongly recommended.

No significant difference between clips vs diathermy, however.

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24
Q

What is the benefit of IV PPIs over oral in the setting of upper GI bleeds?

A

None.

Recommendations vary and there is no mortality benefit, but giving PPIs in UGIBs reduces the need for intervention during endoscopy and re-bleeding rates.

For all intents and purposes, go with IV bolus + 72 hour infusion (but doesn’t really seem to make a difference).

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25
Q

When correcting volume loss in upper GI bleeds, at what point would you give blood?

A

After giving 1-2L NaCl 0.9% and patient still remains shocked.

Transfuse when Hb <70 otherwise.

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26
Q

In upper GI bleeds, how do you correct coagulopathy contributing to bleeding?

A

5-10 mg IV vitamin K + Prothrombinex (25-50 IU/kg) + FFP (150-300 mL)

Give platelets if <50 in high risk patients

Consider recombinant activated factor VII (Novoseven) in patients with on-going massive haemorrhage after all else fails

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27
Q

With regard to peptic ulcer bleeds, what is the risk of rebleeding without therapy for active arterial (spurting) bleeds?

A

Near 100%

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28
Q

With regard to peptic ulcer bleeds, what is the risk of rebleeding without therapy for non-bleeding visible vessels?

A

50%

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29
Q

With regard to peptic ulcer bleeds, what is the risk of rebleeding without therapy for non-bleeding adherent clots?

A

30-35%

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30
Q

With regard to peptic ulcer bleeds, what is the risk of rebleeding without therapy for ulcer oozing (without other stigmata)?

A

10-27%

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31
Q

What is the main benefit of ocreotide infusions in the acute treatment of oesophageal varices?

A

Reduction in the number of patients failing initial haemostatsis.

No significant reduction in mortality, rebleeding (variable across trials) or blood transfused in high-quality trials.

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32
Q

What is the preferred method of endoscopic management of acute oesophageal variceal bleeding?

A

Endoscopic rubber band ligation - fewer side effects and more effective than injection sclerotherapy - reduced mortality and rebleeding.

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33
Q

Following intervention for acute oesophageal variceal bleeding, what is the recommended treatment?

A

Secondary prophylaxis with non-selective beta blocker (propranolol).

Subsequent endoscopic banding sessions every 2-4 weeks until eradication of varices (median number of session required 3-4).

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34
Q

What is the recommended endoscopic therapy for gastric variceal bleeding?

A

Injection of cyanoacrylate glue “superglue” mixed with lipiodol (radiological agent used for dilution in order to slow glue hardening)

Banding or injection sclerotherapy NOT recommended - can make bleeding worse

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35
Q

Name 6 salvage options in variceal bleeding.

A

Repeat endoscopy

Minnesota tubes - short term only

TIPS (transjugular portosystemic shunt)

BRTO (balloon-occluded retrograde trans enjoys obliteration) for gastric varices

Splenic embolisation or splenectomy (gastric varices)

Surgery - surgical shunt or devascularisation

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36
Q

Name 5 methods of endoscopic therapy for peptic ulcer bleeding.

A

Injection - 1/10000 adrenaline

Coagulation - heater probe or electrocautery

Endoscopic clip placement

Combination therapy - injection + one other (most effective)

Haemostatic sprays (last resort)

Additionally, clot removal prior to therapy has been shown to reduce rebleeding rates

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37
Q

Name an important haematological complication that can arise as a result of H Pylori infection.

A

Immune thrombocytopaenia

H Pylori serology should be checked in all adults with immune thrombocytopaenia

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38
Q

Name two important genes that are linked to a poorer prognosis/carcinogenesis in the setting of H Pylori.

A

cagA

vacA

cagA is particularly bad, with its protein production linked to increased neutrophil recruitment, and associated greater inflammatory activity and more gastroduodenal disease

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39
Q

Which two malignancies are associated with H Pylori?

A

Gastric Ca (H Pylori gastritis seen in 95% of these patients)

MALT lymphoma (nearly all)

However, gastric Ca occurs in 1-3% of H Pylori patients, and MALT lymphoma in <0.1%

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40
Q

When testing for HP stool antigen, how long do patients need to be off of PPIs and antibiotics to ensure an accurate test result?

A

PPI - 2 weeks or less

Antibiotics - 4 weeks or less

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41
Q

What is the main use of HP culturing to test for H Pylori?

A

Testing to confirm antibiotic resistance after two treatment failures

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42
Q

Resistance in which two antibiotics has resulted in increasing failure rates for conventional triple therapy for H Pylori?

A

Clarithromycin

Metronidazole

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43
Q

When is it safe to use conventional triple therapy for H Pylori treatment?

A

Can be used when clarithromycin resistance rates are known to be <15%.

If resistance rates unknown - don’t use triple therapy

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44
Q

In the setting of high clarithromycin resistance rates for H Pylori treatment, what treatment should be given instead of conventional triple therapy?

A

Clarithromycin

Metronidazole

Amoxicillin

Omeprazole

14 days total

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45
Q

What is the first line treatment in early stage MALT lymphoma?

A

H Pylori eradication

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46
Q

For patients with ischaemic heart disease who have had their anti-platelet therapy withheld in order to treat an upper GI bleed, how soon would you restart anti-platelet therapy?

A

Prior to discharge from hospital - ideally at day 3 post endoscopy

Mortality risk increases after 7 days off aspirin

If on clopidogrel or another agent too, discuss with cardiology

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47
Q

Name 3 features you might see on endoscopy for a gastric ulcer that would suggest malignancy.

A

Irregular outline with necrotic or haemorrhagic base

Irregular raised margin

Prominent and oedematous rural folds that usually do not extend to the margins

These can be anywhere and any size. Benign ulcers are usually <2cm and are usually found on the lesser curvature

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48
Q

For patients requiring an urgent endoscopy on aspirin and clopidogrel for IHD for upper GI bleeding, what do you do with the DAPT?

A

Stop aspirin, continue clopidogrel

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49
Q

For patients on warfarin, at what INR is it safe to perform an endoscopy if required?

A

INR < 2.5

Warfarin can be restarted around 1-2 weeks for non-valvular AF

50
Q

Name 3 histological features you might expect to see with coeliac disease.

A

Increased intra-epithelial lymphocytes

Crypt hyperplasia

Villous atrophy

51
Q

In which syndromes might patients have an increased risk of developing coeliac disease? Name 3.

A

Down’s

Turner’s

William’s

52
Q

How should coeliac disease be monitored following diagnosis?

A

Follow-up TTG at 3-6 months then annually

Histological improvement can take years

53
Q

What form of colitis can be seen frequently in coeliac disease?

A

Microscopic colitis

50-70x more common than the general population

54
Q

PAS-positive macrophages in the duodenal mucosa is indicative of what? And what is the treatment?

A

Whipple’s disease (tropheryma whippelii) - Abx

55
Q

What would you expect to see on biopsy for atrophic gastritis?

A

Hyperplasia of enterochromaffin cells in the gastric mucosa

56
Q

Name a medication that can be used effectively for the prevention of NSAID induced gastric ulceration.

A

Misoprostol

More effective than omeprazole, ranitidine, bismuth and sucralfate.

57
Q

Cirrhosis can result in increased estradiol. Name 5 features of cirrhosis that can arise as a result of this.

A

Spider angiomas

Gynaecomastia

Feminisation - inversion of male pubic hair pattern, loss of axillary or chest hair

Palmar erythema

Testicular atrophy

58
Q

What are the 4 stages of hepatic encephalopathy?

A

Grade 1 - sleep/wake reversal, change in behaviour, mild confusion

Grade 2 - lethargy, moderate confusion

Grade 3 - stupor, arousable, incoherent

Grade 4 - unresponsive to pain - incubate

59
Q

What defines a high serum albumin ascites gradient, and what can cause it? Name 7 causes.

A

11 g/L or above - high gradient (portal hypertension)

Alcoholic hepatitis

Heart failure

Massive hepatic mets

Budd-Chiari syndrome

Portal vein thrombosis

Portal fibrosis

Schistosomiasis

60
Q

What defines a low serum albumin ascites gradient, and what can cause it? Name 5 causes.

A

<11g/L (leaky capillaries/tumour)

Peritoneal carcinomatosis

Peritoneal tuberculosis

Pancreatitis

Serositis

Nephrotic syndrome

61
Q

Based on ascitic fluid analysis, what might suggest perforation?

A

Consider perforation if 2 of 3 present:

Total protein >10

Glucose <2.8

LDH greater than the upper limit of normal for serum

62
Q

What is the foremost cause of portal hypertension worldwide?

A

Schistosomiasis

63
Q

At what level of portal hypertension do gastro-oesophageal varices begin to form?

A

10mmHg

64
Q

What is the pathophysiology of gastro-oesophageal varices?

A

A result of increased outflow resistance through the portal system

AND

Enhanced portal inflow due to splanchnic arteriolar vasodilation

65
Q

Name two tests that could be used instead of PT/INR to measure coagulopathy in cirrhotic patients.

A

Thromboelastography (TEG)

Rotational thromboelastometry (ROTEM)

66
Q

What is the pathophysiology of hepato-renal syndrome?

A

Splanchnic arterial vasodilation triggered by portal hypertension

Increased cardiac output initially, and decreased systemic vascular resistance, then decrease in cardiac output later on

67
Q

Type II refractory coeliac disease has a high risk of transformation to which lymphoma?

A

Enteropathy-associated T-cell lymphoma

68
Q

What is the difference between type 1 and 2 hepatorenal syndrome?

A

Type 1

  • twofold increase in creatinine to >250 mg/L in less than two weeks
  • median survival is a few weeks without treatment

Type 2

  • diuretic resistant ascites
  • slow increase in Cr > 150 mg/L
  • median survival is 6 months
69
Q

What is the pathophysiology of primary biliary cholangitis?

A

T-lymphocytic autoimmune disease of the small intralobular bile ducts

Eventual bile duct disappearance followed by cirrhosis

70
Q

What are the 2 most common symptoms associated with PBC?

A

Fatigue

Pruritus

71
Q

What features might you expect to see on laboratory testing for PBC? Name 4.

A

Elevated alkaline phosphatase

Elevated yGT

Elevated 5’Nucleotidase elevation

Eosinophilia early

72
Q

What antibodies are associated with PBC?

A

Antimitochondrial antibodies

ANA in 70%

73
Q

What is the treatment for PBC?

A

Ursodeoxycholic acid - reduces disease progression and improves transplant-free survival; no effect on pruritus or fatigue

Obeticholic acid - ligand for farnesoid X receptor; pruritus is most common side effect

74
Q

What is the major adverse consequence of high dose ursodeoxycholic acid?

A

CVD death

75
Q

How is PBC monitored?

A

LFTs every 3 to 6 months

TSH annually

Bone mineral densitometry every 2-4 years

Monitor vitamin A, D, K annually if bili >20

Appropriate monitoring if cirrhosis present

76
Q

What is seen on histology with primary sclerosing cholangitis?

A

Inflammation, fibrosis and structuring of the medium and large bile ducts

77
Q

Name 7 complications of PSC

A

Cholangiocarcinoma - 10-15% lifetime risk

Gallbladder cancer - 3-14% prevalence

Cirrhosis/portal HTN

Fat soluble vitamin deficiency/steatorrhoea

Colon cancer - colonoscopy every 1-2 years if UC present, 3-5 years without

Metabolic bone disease

Cholangitis

78
Q

Which condition is difficult to distinguish from PSC?

A

IgG4-associated cholangitis

Usually associated with autoimmune pancreatitis and steroid responsive

79
Q

What is the definitive treatment for PSC?

A

Liver transplant

Median survival without liver transplant is 12 years

Endoscopic treatment of dominant biliary strictures may be beneficial in highly selective patients

No change in disease course with a proctocolectomy in those with UC

80
Q

Which autoimmune condition is strongly associated with PSC?

A

Ulcerative colitis - 90% of PSC patients have UC (5% of UC patients have PSC)

UC patients with cholesterol LFTs need to be investigated for PSC

81
Q

What the time lengths for hyperacute, acute and subacute fulminant hepatitis respectively?

A

Hyperacute < 7 days

Acute 7 - 21 days

Subacute >21 days and <26 weeks

82
Q

What are the King’s College Criteria for liver transplant referral in patients presenting with paracetamol overdose?

A

Arterial pH <7.30

OR

Grade 3 to 4 encephalopathy with PT > 100 secs and Cr > 340 mg/L

83
Q

What are the King’s College Criteria for liver transplant referral for patients with non-paracetamol-related liver failure?

A

PT > 100 secs

OR

Any three of:

  • Age <10 or >40 years
  • Non-A and non-B viral hepatitis, idiosyncratic drug reaction, Wilson’s disease
  • Jaundice >7 days prior to encephalopathy
  • PT > 50 seconds
  • Bilirubin >180 mg/L
84
Q

Who should receive vaccinations for hepatitis A, and when?

A

High risk groups

<40 - vaccinate up until time of departure, with single dose PEP within 2 weeks

If older, immunocompromised or liver disease - 2 weeks prior, nil PEP

Vaccine and Ig in <1, >40, immunocompromised or liver disease

85
Q

What are the 4 phases of hepatitis B?

A

Immune-tolerant phase - living with the virus, normal ALT (e.g. baby)

HBeAg-positive immune active phase - immune system turns on against HBV around 30 years of age

Inactive chronic hep B phase - hep B virus goes into hiding (may be undetectable)

HBeAg-negative immune deactivation - “HBV attempts domination again, immune system ready”

Treat phases 2 and 3

86
Q

Name 3 extrahepatic manifestations of hepatitis B.

A

Polyarteritis nodosa

Glomerular disease (membranous nephropathy, MPGN, nephrotic syndrome)

Serum sickness (arthritis, rash)

Manifestations occur in 20% of patients.

87
Q

What is HBeAg a marker of?

A

Marker of viral replication.

88
Q

What diagnosis would you suspect in a hepatitis C patient with lesions in the mouth?

A

Lichen planus

89
Q

What are the three drug classes (with examples of drugs) used to treat hepatitis C?

A

NS3 (serine proteases) - paritaprevir, grasoprevir

NS5A (RNA binding site) - ombitasvir, elbasvir

NS5B (RNA-dependent RNA polymerase) - sofosbuvir, dasabuvir

3 looks like “e” (-evir)
a - asvir
b - buvir

90
Q

What is the pathophysiology of porphyria cutaneous tarda, and what condition is it often seen in?

A

Decreased activity of uroporphyrinogen decarboxylase

Sun-exposed skin changes, elevated urine porphyrin levels

50% of those with PCT have HCV

91
Q

What condition is the Maddrey scoring system used for?

A

Alcoholic hepatitis

32 or greater suggests high short term mortality, and steroids should be considered

92
Q

How is alcoholic hepatitis treated?

A

Prednisolone 40mg daily for 28 days, followed by a 16 day taper - Lille score can be used to determine response to treatment

Pentoxifylline 400mg TDS as an alternative

Discontinue non-selective beta blockers

93
Q

What two HFE gene mutations are most implicated in haemochromatosis?

A

C282Y

H63D

94
Q

What are the extrahepatic manifestations of haemochromatosis? Name 4.

A

Diabetes in 50% (no improvement with phlebotomy)

Arthropathy (pseudogout, chondrocalcinosis 2nd and 3rd MCP) - no improvement with phleb

Cardiomyopathy - improves with phleb

Secondary hypogonadism - improves with phleb

95
Q

Wilson’s disease arises as a mutation of which gene?

A

ATP7B

Autosomal recessive inheritance

Over 500 different mutations, making testing difficult

96
Q

How is Wilson’s disease treated?

A

Copper removal with chelation - D-penicillamine or trientine

Low copper diet

Zinc - interferes with copper absorption

97
Q

What is the main cause of death in individuals with non-alcoholic steatohepatitis?

A

Cardiovascular disease

98
Q

What is the leading cause of death in liver transplant patients?

A

Infection

Highest risk in the first three months

99
Q

Name 8 contraindications to liver transplantation

A

Cardiopulmonary risk

Active ETOH or drug abuse

Non-adherence

Inadequate social support

Uncontrolled sepsis

Malignancy outside the liver or intrahepatic cholangiocarcinoma

High intracranial pressure in acute liver failure

AIDS/age/obesity - relative contraindications

100
Q

Name three germ line mutations that can predispose patients towards having pancreatic cancer.

A

BRCA1

BRCA2

PALB2

101
Q

Which body parts does necrolytic acral erythema affect, and which condition is it most commonly linked to?

A

Erythematous papules most commonly on the dorsal aspect of the feet

Does not affect palms, soles, nail beds or mucous

Hepatitis C

102
Q

Name 3 mutations that are involved in Crohn’s disease.

A

NOD2

CARD15

IBD1

103
Q

How does smoking impact upon Crohn’s disease and ulcerative colitis?

A

UC - smoking helps

Crohn’s - smoking increases relapse rates

104
Q

In Crohn’s disease, following surgery, where does disease most often reoccur?

A

Anastomosis

105
Q

How long do azathioprine/6-MP take to work in the setting of IBD?

A

3 months

106
Q

What features would you expect to see on histology for ulcerative colitis? Name 6.

A

Mucosal/submucosal involvement

Lymphocytic infiltration

Goblet cell depletion

Crypt distortion

Cryptitis

Crypt abscesses

No granulomas seen

107
Q

What features would you expect to see on histology for Crohn’s disease? Name 3.

A

Transmural inflammation - infiltrate of lymphocytes and macrophages

Granulomas in approx 50% of cases

Skip lesions

108
Q

How do NOD2 and CARD15 variants of Crohn’s disease impact upon the disease course? 5 points.

A

Younger age at onset

Small bowel involvement

Stricturing phenotype rather than fistulating

Early initial surgery

Early surgical recurrence

109
Q

Which infection can predispose towards the development of IBD?

A

M paratuberculosis

110
Q

Name 4 extraintestinal manifestations of IBD associated with active GI disease.

A

Oral ulcers

Erythema nodosum

Large-joint arthritis

Episcleritis

111
Q

Name 6 extraintestinal manifestations of IBD that occur independently of GI disease.

A

Primary sclerosing cholangitis

Ankylosing spondylitis

Uveitis

Pyoderma gangrenous

Kidney stones

Gallstones (more in CD)

112
Q

How is an acute flare of Crohn’s disease treated?

A

Mild/moderate disease - oral 5-ASA (consider adding antibiotics)

Moderate/severe disease - oral corticosteroids +/- antibiotics (if suspicion of abscess)

  • if no response, infliximab

Severe - IV corticosteroids +/- antibiotics

  • if no response - infliximab, then consideration of surgery if that doesn’t work either
  • if good response - oral corticosteroids and wean
113
Q

What are the first line agents used to maintain remission following a severe flare for Crohn’s disease? Name 3.

A

Azathioprine

6-mercaptopurine

Methotrexate

114
Q

Which types of IBD is budesonide useful in?

A

Entocort useful in ileocaecal Crohn’s Disease

Cortiment (MMX - colonic release) useful in ulcerative colitis

115
Q

For patients with Crohn’s disease who have not achieved steroid-free remission with immunosuppressive agents, what are the next steps?

A

Add infliximab or adalimumab

If no response or loss of response from those after 3-6 months, consider vedolizumab or ustekinumab

116
Q

What is the treatment for an acute flare of distal colitis in ulcerative colitis?

A

5-ASA (suppositories/enema)

Foam rectal steroids

Oral 5-ASA

Oral/IV steroids

117
Q

What is the treatment for an acute flare of pancolitis in ulcerative colitis?

A

Oral 5-ASA

Oral/IV steroids

If not working - consider infliximab or ciclosporin, and surgery thereafter

118
Q

How is acute severe colitis defined as per Truelove and Witt’s criteria?

A

Bloody stool frequency >6/day + 1 or more of:

Pulse > 90 bpm

Temp >37.8 C

Hb <10.5 g/dL

ESR >30 mm/hr

119
Q

How does vedolizumab work in IBD?

A

Selectively binds a4b7 integrin on surface of T cells

Blocks interaction with MadCAM-1 on intestinal endothelium

Inhibits trafficking of leukocytes to sites of inflammation

120
Q

Which malignancy is associated with IBD patients on thiopurine, infliximab or adalimumab?

A

Hepatosplenic T cell lymphoma

121
Q

What is the result of low TPMT in the setting of treatment with azathioprine or 6-MP for IBD?

A

Low TPMT = high 6-TGN, resulting in myelotoxicity

122
Q

How does lymphocytic colitis appear on trichrome stain, and how is it best managed?

A

Blue band (collagen)

Manage with corticosteroids (budesonide)

GCUH FRACP Writtens 2020 (14 decks)

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