Gastroenterology Flashcards
(122 cards)
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.
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
3
Q
What is the pathophysiology of achalasia?
A
Loss of inhibitory neurons from lower oesophageal sphincter.
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
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.
6
Q
Name 3 ways that patients with eosinophilia oesophagitis typically present.
A
Food bolus obstruction
Chronic dysphagia solids > liquids
Refractory GORD
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
8
Q
What established treatments can be provided for eosinophilia oesophagitis? Name 3.
A
PPIs
Aerolised steroids
Diet - 6 food elimination diet
9
Q
Name 7 risk factors for the development of Barrett’s oesophagus.
A
Male
Caucasian
Age
Overweight
Chronic heartburn
Smoking
Positive family Hx
10
Q
Which malignancy can Barrett’s progress to?
A
Adenocarcinoma
11
Q
What are the three mechanisms of reflux in GORD?
A
Transient lower oesophageal sphincter relaxation
Weak LOS
Increased intra-abdominal pressure (obesity)
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
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
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
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
16
Q
What features on endoscopy would you expect to see with achalasia?
A
Food in oesophagus
Tight LOS
Dilated oesophagus
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
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
19
Q
What 2 features on endoscopy would be expected in distal oesophageal spasm?
A
Retained food
Uncoordinated or ring contractions
20
Q
What 3 features on barium swallow would be expected in distal oesophageal spasm?
A
Tertiary contractions
Diverticula
Poor passage of bolus
21
Q
What feature on manometry would be expected in distal oesophageal spasm?
A
Synchronous pressure waves
22
Q
In which part of the duodenum are ulcers usually found?
A
1st part.
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.
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).
25
When correcting volume loss in upper GI bleeds, at what point would you give blood?
After giving 1-2L NaCl 0.9% and patient still remains shocked.
Transfuse when Hb <70 otherwise.
26
In upper GI bleeds, how do you correct coagulopathy contributing to bleeding?
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
27
With regard to peptic ulcer bleeds, what is the risk of rebleeding without therapy for active arterial (spurting) bleeds?
Near 100%
28
With regard to peptic ulcer bleeds, what is the risk of rebleeding without therapy for non-bleeding visible vessels?
50%
29
With regard to peptic ulcer bleeds, what is the risk of rebleeding without therapy for non-bleeding adherent clots?
30-35%
30
With regard to peptic ulcer bleeds, what is the risk of rebleeding without therapy for ulcer oozing (without other stigmata)?
10-27%
31
What is the main benefit of ocreotide infusions in the acute treatment of oesophageal varices?
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.
32
What is the preferred method of endoscopic management of acute oesophageal variceal bleeding?
Endoscopic rubber band ligation - fewer side effects and more effective than injection sclerotherapy - reduced mortality and rebleeding.
33
Following intervention for acute oesophageal variceal bleeding, what is the recommended treatment?
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).
34
What is the recommended endoscopic therapy for gastric variceal bleeding?
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
35
Name 6 salvage options in variceal bleeding.
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
36
Name 5 methods of endoscopic therapy for peptic ulcer bleeding.
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
37
Name an important haematological complication that can arise as a result of H Pylori infection.
Immune thrombocytopaenia
H Pylori serology should be checked in all adults with immune thrombocytopaenia
38
Name two important genes that are linked to a poorer prognosis/carcinogenesis in the setting of H Pylori.
cagA
vacA
cagA is particularly bad, with its protein production linked to increased neutrophil recruitment, and associated greater inflammatory activity and more gastroduodenal disease
39
Which two malignancies are associated with H Pylori?
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%
40
When testing for HP stool antigen, how long do patients need to be off of PPIs and antibiotics to ensure an accurate test result?
PPI - 2 weeks or less
Antibiotics - 4 weeks or less
41
What is the main use of HP culturing to test for H Pylori?
Testing to confirm antibiotic resistance after two treatment failures
42
Resistance in which two antibiotics has resulted in increasing failure rates for conventional triple therapy for H Pylori?
Clarithromycin
Metronidazole
43
When is it safe to use conventional triple therapy for H Pylori treatment?
Can be used when clarithromycin resistance rates are known to be <15%.
If resistance rates unknown - don’t use triple therapy
44
In the setting of high clarithromycin resistance rates for H Pylori treatment, what treatment should be given instead of conventional triple therapy?
Clarithromycin
Metronidazole
Amoxicillin
Omeprazole
14 days total
45
What is the first line treatment in early stage MALT lymphoma?
H Pylori eradication
46
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?
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
47
Name 3 features you might see on endoscopy for a gastric ulcer that would suggest malignancy.
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
48
For patients requiring an urgent endoscopy on aspirin and clopidogrel for IHD for upper GI bleeding, what do you do with the DAPT?
Stop aspirin, continue clopidogrel
49
For patients on warfarin, at what INR is it safe to perform an endoscopy if required?
INR < 2.5
Warfarin can be restarted around 1-2 weeks for non-valvular AF
50
Name 3 histological features you might expect to see with coeliac disease.
Increased intra-epithelial lymphocytes
Crypt hyperplasia
Villous atrophy
51
In which syndromes might patients have an increased risk of developing coeliac disease? Name 3.
Down’s
Turner’s
William’s
52
How should coeliac disease be monitored following diagnosis?
Follow-up TTG at 3-6 months then annually
Histological improvement can take years
53
What form of colitis can be seen frequently in coeliac disease?
Microscopic colitis
50-70x more common than the general population
54
PAS-positive macrophages in the duodenal mucosa is indicative of what? And what is the treatment?
Whipple’s disease (tropheryma whippelii) - Abx
55
What would you expect to see on biopsy for atrophic gastritis?
Hyperplasia of enterochromaffin cells in the gastric mucosa
56
Name a medication that can be used effectively for the prevention of NSAID induced gastric ulceration.
Misoprostol
More effective than omeprazole, ranitidine, bismuth and sucralfate.
57
Cirrhosis can result in increased estradiol. Name 5 features of cirrhosis that can arise as a result of this.
Spider angiomas
Gynaecomastia
Feminisation - inversion of male pubic hair pattern, loss of axillary or chest hair
Palmar erythema
Testicular atrophy
58
What are the 4 stages of hepatic encephalopathy?
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
What defines a high serum albumin ascites gradient, and what can cause it? Name 7 causes.
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
What defines a low serum albumin ascites gradient, and what can cause it? Name 5 causes.
<11g/L (leaky capillaries/tumour)
Peritoneal carcinomatosis
Peritoneal tuberculosis
Pancreatitis
Serositis
Nephrotic syndrome
61
Based on ascitic fluid analysis, what might suggest perforation?
Consider perforation if 2 of 3 present:
Total protein >10
Glucose <2.8
LDH greater than the upper limit of normal for serum
62
What is the foremost cause of portal hypertension worldwide?
Schistosomiasis
63
At what level of portal hypertension do gastro-oesophageal varices begin to form?
10mmHg
64
What is the pathophysiology of gastro-oesophageal varices?
A result of increased outflow resistance through the portal system
AND
Enhanced portal inflow due to splanchnic arteriolar vasodilation
65
Name two tests that could be used instead of PT/INR to measure coagulopathy in cirrhotic patients.
Thromboelastography (TEG)
Rotational thromboelastometry (ROTEM)
66
What is the pathophysiology of hepato-renal syndrome?
Splanchnic arterial vasodilation triggered by portal hypertension
Increased cardiac output initially, and decreased systemic vascular resistance, then decrease in cardiac output later on
67
Type II refractory coeliac disease has a high risk of transformation to which lymphoma?
Enteropathy-associated T-cell lymphoma
68
What is the difference between type 1 and 2 hepatorenal syndrome?
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
What is the pathophysiology of primary biliary cholangitis?
T-lymphocytic autoimmune disease of the small intralobular bile ducts
Eventual bile duct disappearance followed by cirrhosis
70
What are the 2 most common symptoms associated with PBC?
Fatigue
Pruritus
71
What features might you expect to see on laboratory testing for PBC? Name 4.
Elevated alkaline phosphatase
Elevated yGT
Elevated 5’Nucleotidase elevation
Eosinophilia early
72
What antibodies are associated with PBC?
Antimitochondrial antibodies
ANA in 70%
73
What is the treatment for PBC?
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
What is the major adverse consequence of high dose ursodeoxycholic acid?
CVD death
75
How is PBC monitored?
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
What is seen on histology with primary sclerosing cholangitis?
Inflammation, fibrosis and structuring of the medium and large bile ducts
77
Name 7 complications of PSC
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
Which condition is difficult to distinguish from PSC?
IgG4-associated cholangitis
Usually associated with autoimmune pancreatitis and steroid responsive
79
What is the definitive treatment for PSC?
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
Which autoimmune condition is strongly associated with PSC?
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
What the time lengths for hyperacute, acute and subacute fulminant hepatitis respectively?
Hyperacute < 7 days
Acute 7 - 21 days
Subacute >21 days and <26 weeks
82
What are the King’s College Criteria for liver transplant referral in patients presenting with paracetamol overdose?
Arterial pH <7.30
OR
Grade 3 to 4 encephalopathy with PT > 100 secs and Cr > 340 mg/L
83
What are the King’s College Criteria for liver transplant referral for patients with non-paracetamol-related liver failure?
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
Who should receive vaccinations for hepatitis A, and when?
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
What are the 4 phases of hepatitis B?
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
Name 3 extrahepatic manifestations of hepatitis B.
Polyarteritis nodosa
Glomerular disease (membranous nephropathy, MPGN, nephrotic syndrome)
Serum sickness (arthritis, rash)
Manifestations occur in 20% of patients.
87
What is HBeAg a marker of?
Marker of viral replication.
88
What diagnosis would you suspect in a hepatitis C patient with lesions in the mouth?
Lichen planus
89
What are the three drug classes (with examples of drugs) used to treat hepatitis C?
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
What is the pathophysiology of porphyria cutaneous tarda, and what condition is it often seen in?
Decreased activity of uroporphyrinogen decarboxylase
Sun-exposed skin changes, elevated urine porphyrin levels
50% of those with PCT have HCV
91
What condition is the Maddrey scoring system used for?
Alcoholic hepatitis
32 or greater suggests high short term mortality, and steroids should be considered
92
How is alcoholic hepatitis treated?
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
What two HFE gene mutations are most implicated in haemochromatosis?
C282Y
H63D
94
What are the extrahepatic manifestations of haemochromatosis? Name 4.
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
Wilson’s disease arises as a mutation of which gene?
ATP7B
Autosomal recessive inheritance
Over 500 different mutations, making testing difficult
96
How is Wilson’s disease treated?
Copper removal with chelation - D-penicillamine or trientine
Low copper diet
Zinc - interferes with copper absorption
97
What is the main cause of death in individuals with non-alcoholic steatohepatitis?
Cardiovascular disease
98
What is the leading cause of death in liver transplant patients?
Infection
Highest risk in the first three months
99
Name 8 contraindications to liver transplantation
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
Name three germ line mutations that can predispose patients towards having pancreatic cancer.
BRCA1
BRCA2
PALB2
101
Which body parts does necrolytic acral erythema affect, and which condition is it most commonly linked to?
Erythematous papules most commonly on the dorsal aspect of the feet
Does not affect palms, soles, nail beds or mucous
Hepatitis C
102
Name 3 mutations that are involved in Crohn’s disease.
NOD2
CARD15
IBD1
103
How does smoking impact upon Crohn’s disease and ulcerative colitis?
UC - smoking helps
Crohn’s - smoking increases relapse rates
104
In Crohn’s disease, following surgery, where does disease most often reoccur?
Anastomosis
105
How long do azathioprine/6-MP take to work in the setting of IBD?
3 months
106
What features would you expect to see on histology for ulcerative colitis? Name 6.
Mucosal/submucosal involvement
Lymphocytic infiltration
Goblet cell depletion
Crypt distortion
Cryptitis
Crypt abscesses
No granulomas seen
107
What features would you expect to see on histology for Crohn’s disease? Name 3.
Transmural inflammation - infiltrate of lymphocytes and macrophages
Granulomas in approx 50% of cases
Skip lesions
108
How do NOD2 and CARD15 variants of Crohn’s disease impact upon the disease course? 5 points.
Younger age at onset
Small bowel involvement
Stricturing phenotype rather than fistulating
Early initial surgery
Early surgical recurrence
109
Which infection can predispose towards the development of IBD?
M paratuberculosis
110
Name 4 extraintestinal manifestations of IBD associated with active GI disease.
Oral ulcers
Erythema nodosum
Large-joint arthritis
Episcleritis
111
Name 6 extraintestinal manifestations of IBD that occur independently of GI disease.
Primary sclerosing cholangitis
Ankylosing spondylitis
Uveitis
Pyoderma gangrenous
Kidney stones
Gallstones (more in CD)
112
How is an acute flare of Crohn’s disease treated?
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
What are the first line agents used to maintain remission following a severe flare for Crohn’s disease? Name 3.
Azathioprine
6-mercaptopurine
Methotrexate
114
Which types of IBD is budesonide useful in?
Entocort useful in ileocaecal Crohn’s Disease
Cortiment (MMX - colonic release) useful in ulcerative colitis
115
For patients with Crohn’s disease who have not achieved steroid-free remission with immunosuppressive agents, what are the next steps?
Add infliximab or adalimumab
If no response or loss of response from those after 3-6 months, consider vedolizumab or ustekinumab
116
What is the treatment for an acute flare of distal colitis in ulcerative colitis?
5-ASA (suppositories/enema)
Foam rectal steroids
Oral 5-ASA
Oral/IV steroids
117
What is the treatment for an acute flare of pancolitis in ulcerative colitis?
Oral 5-ASA
Oral/IV steroids
If not working - consider infliximab or ciclosporin, and surgery thereafter
118
How is acute severe colitis defined as per Truelove and Witt’s criteria?
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
How does vedolizumab work in IBD?
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
Which malignancy is associated with IBD patients on thiopurine, infliximab or adalimumab?
Hepatosplenic T cell lymphoma
121
What is the result of low TPMT in the setting of treatment with azathioprine or 6-MP for IBD?
Low TPMT = high 6-TGN, resulting in myelotoxicity
122
How does lymphocytic colitis appear on trichrome stain, and how is it best managed?
Blue band (collagen)
Manage with corticosteroids (budesonide)
