3 - Benign Upper GI Disease Flashcards
1
Q
What are the potential causes of GORD?
A
- Failure of LOS to close / frequent relaxations
- Failure of diaphragmatic sphincter
- Increased intra-abdominal pressure
2
Q
What are the major RF for GORD?
A
H Pylori
NSAIDs
3
Q
What is the gold standard test for diagnosing GORD?
A
OGD
4
Q
When are barium swallows done?
A
Rarely now - only really if P cannot tolerate OGD
5
Q
What do you need to do before surgery for reflux?
A
Ensure that the symptoms the P is having is actually caused by GORD - do a pH and Mamometry Testing for this.
Otherwise, if Ps are not having reflux then their sx will persist despite the surgery
6
Q
What is the treatment for GORD?
A
7
Q
What is the diagnosis for a break in the mucosal lining of the stomach or duodenum?
A
Gastric or Duodenal Peptic Ulcer
8
Q
What are the symptoms of a peptic ulcer?
A
9
Q
What are the RF for Peptic Ulcers?
A
H Pylori (70-85% gastric, 90-95% duodenal)
Smoking
NSAIDs
10
Q
What is the Tx for peptic ulcers?
A
PPI
Lifestyle
H pylori eradication
11
Q
What are the potential complications of peptic ulcers?
A
12
Q
How can peptic ulcer cause Gastric outlet obstruction?
A
The ulceration can heal and cause structuring of the outlet leading to obstruction
13
Q
What are the two types of upper GI bleeds?
A
Variceal (11%)
Non-variceal (89%)
14
Q
What is the presentation of a patient with upper GI bleeding?
A
Often shocks Ps.
Have raised serum urea because blood is being digested in the stomach - blood is broken down into proteins - which are transported to the liver and converted in the urea cycle.
If there is an acute bleed the Hb may not change until the P has haemodiluted.
15
Q
How is upper GI bleeding managed?
A
OGD
Endoscopic therapy - can include clips, adrenaline injection, haemospray, sengstaken tube
Radiological embolisation of GDA
16
Q
How does a Sengstaken tube work?
A
Tries to stop the bleeding by tamponade.
17
Q
What is the commonest cause of a significant upper GI bleed involving an ulcer?
A
Ulcer eroding the GDA
18
Q
What are the RF for gallstones?
A
4Fs
Female (4:1)
Fat
Forty
Fertile
19
Q
What percentage of UK adults have gallstones?
A
15% - but only 1/5 of these will get sx over a 20 yr period
20
Q
Why do gallstones form?
A
Cholesterol is held in the gallbladder in emulsion by phospholipids and bile salts. Is a precise ratio - if one of the elements of this ratio is out of kilter then the cholesterol crystallises out = gallstone.
21
Q
What are the common S&S of biliary colic?
A
Sudden onset RUQ pain - radiating to the back
22
Q
How do we investigate biliary colic?
A
LFTs - normal
Inflammatory markers - normal / mildly raised
USS - will show gallstones and no US features of acute cholecystitis
23
Q
How are gallstones treated?
A
Hot gallbladder (within 72 hours of attack) - acute cholecystectomy
Otherwise - elective cholecystectomy
24
Q
How can you distinguish between acute cholecystitis and gallstones?
A
Acute cholecystitis has severe RUQ pain + fever. Lasts longer and has less colicky pattern.
Ps may be systemically unwell with evidence of infection.
May be Murphy’s sign positive.
May have elevated ALP and bilirubin.
25
What is the gold standard test for cholecystitis?
USS
26
What is the treatment for acute cholecystitis?
Analgesia
Fluids
ABx
Acute cholecystectomy if suitable
27
What is acute cholecystitis often caused by?
Obstruction of the cystic duct by a gallstone
28
What complications can arise from acute cholecystitis?
29
What is Mirizzi syndrome?
Common hepatic duct obstruction caused by extrinsic compression from a stone lodged in the cystic duct or Hartmann's pouch.
30
How does Mirizzi syndrome present?
How is it diagnosed?
31
How do stones in the bile duct present?
RUQ pain - can radiate to back
Jaundice
Abnormal LFTs
32
What is acute cholangitis?
Bacterial infection of the biliary tree - due to stagnant bile that can't pass an obstruction (stone)
33
What are the sx of acute cholangitis?
Charcots Triad
- Fever
- Jaundice
- RUQ pain
Ps will often have rigors, can become v unwell
34
What is the treatment for bile duct stones?
ERCP - to extract or stent around the stone if it can't be extracted.
PTC = percutaneous transhepatic cholangeography - drain directly into the biliary tree - but high mortality rate as these Ps are normally very unwell.
Laparoscopic bile duct exploration
Cholecystectomy
35
How common is acute pancreatitis?
56 in 100k / yr
36
What are the causes of acute pancreatitis?
37
What are the most common causes of acute pancreatitis in the UK?
Gallstones 50%
Alcohol 25%
38
How does acute pancreatitis present?
Acute onset epigastric pain
Vomiting
39
What is the mortality rate of acute pancreatitis?
Really high - 5%
40
How can you assess the severity of the pancreatitis?
41
Using the Glasgow Pancreatitis Severity Score - what do the following need to be at in order to qualify as severe pancreatitis?
PaO2
Age
Neutrophils
Calcium
Renal Function
Enzymes
Albumin
Sugar
>? predicts severe pancreatitis?
42
What are the criteria required to make a diagnosis of pancreatitis?
43
Which AI test can indicate AI pancreatitis?
IgG4
44
What investigations can be done to determine pancreatitis?
Bloods
USS
MRCP
CT scan - only if diagnosis uncertain
45
What is the treatment for acute pancreatitis?
Only Ps with infected necrosis need ABx
46
What are potential complications of acute pancreatitis?
Necrosis - part loses its blood supply
Pseudocysts - collection of fluid in front of the pancreas which goes into the lesser sac
Splenic artery runs along the pancreas - A pseudoaneurysm, also known as a false aneurysm, is a locally contained hematoma outside an artery or the heart due to damage to the vessel wall.[1] The injury passes through all three layers of the arterial wall, causing a leak, which is contained by a new, weak "wall" formed by the products of the clotting cascade.[1] A pseudoaneurysm does not contain any layer of the vessel wall.[1]
This differentiates it from a true aneurysm, which is contained by all three layers of the vessel wall, and a dissecting aneurysm, which has a breach in the innermost layer of an artery and subsequent dissection/separation of the tunica intima from the tunica media.
47
How are pancreatic infected collections managed?
Percutaneous drainage
48
What is chronic pancreatitis?
Ongoing inflammatory changes = irreversible change in the pancreas = loss of function
Chronic pancreatitis = loss of both endocrine and exocrine function
49
What are the symptoms of chronic pancreatitis?
Weight loss = due to exocrine problems - failure to absorb fats
Abdominal pain = can radiate through to the back making it difficult to distinguish from acute.
Diarrhoea - get steatorrhea due to exocrine failure
50
What is the most common cause of chronic pancreatitis?
Alcohol intake
51
How do we diagnose chronic pancreatitis?
Chronic pancreatitis = may not have increased amylase (in fact pancreas may not be able to produce significant amylase)
Faecal elastase test - checks exocrine function
CT
MRCP
Endoscopic US
52
How is chronic pancreatitis treated?
Analgesia
Creon
Diabetic control
If P has had weight loss - nutritional support, feeding adjuncts if necessary
ERCP - if it is biliary pancreatitis
Surgery if indicated
53
What complications can arise from chronic pancreatitis?
54
What are the three classifications of jaundice?
Pre-hepatic (haemolytic)
Intrahepatic (hepatic)
Post-hepatic (obstructive)
55
How is haem broken down?
Broken into unconjugated bilirubin
Liver conjugates this (UDP glucuronyl transferase)
Conjugated bilirubin is secreted into bile ducts and stored in the bile ducts.
Then secreted into the gut - broken down by gut bacteria
- 80% stercobilins is excreted in faeces
- 20% urobilinogen - 5% excreted by kidneys, 95% recirculated back to liver.
56
How does jaundice present?
57
If the bilirubin is mostly conjugated - what does it indicate the source as?
Hepatic or obstructive cause
58
How is jaundice investigated?
59
What do gallstones in the bile duct show as on CT?
Biliary dilatation
60
What is the most common cause of dysphagia?
Stroke
61
What things can cause dysphagia?
62
Which procedure can check pressures in the oesophagus?
Manometry
63
Name two types of spastic disorders of the oesophagus?
64
How are spastic disorders of the oesophagus treated?
65
What is achalasia?
Failure of LOS to relax during swallowing = inadequate oesophageal peristalsis
66
What are the signs and symptoms of achalasia?
67
What can achalasia cause?
Megaoesophagus
68
How is achalasia diagnosed?
69
What is the management of achalasia?
70
What are the two most major risk factors for gastro-oesophageal reflux disease?
1) Helicobacter pylori and smoking
2) Smoking and obesity
3) Obesity and excess alcohol
4) Excess alcohol and NSAIDS
5) NSAIDS and Helicobacter pylori
The correct answer here is e) NSAIDS and H. pylori. All of the above are risk factors, but these are the two most important and managing them is important to improving symptoms in those with GORD, but if relevant then controlling the other factors may well help.
71
What proportion of duodenal ulcers are associated with Helicobacter pylori infection?
50-60%
60-70%
70-85%
85-90%
90-95%
The correct answer is e) 90-95%. 70-85% of gastric ulcers are associated with H. pylori but most DUs are associated with infection. Treating H. pylori is therefore an important consideration in those with peptic ulcers, but especially with duodenal ulcers as this can lead to refractory ulcers despite appropriate PPI therapy.
72
Which of the following would you NOT see with upper GI bleeding?
Tachycardia
Raised urea
Raised haemoglobin
Fresh PR bleed
Hypotension
The correct answer is c) raised haemoglobin. Tachycardia and hypotension are signs of shock and would not be unexpected with significant bleeding. When blood is present in the stomach this can lead to a raised urea from digestion of the blood and although unusual, if there is significant UGI bleeding then one can see fresh PR bleeding – usually the blood is altered (“melaena”), but if the patient is bleeding rapidly then the blood does not stay in the bowel long enough to be digested and can come out fresh. This often signifies a major bleed with will rapidly lead to deterioration if not corrected. Raised haemoglobin is not seen, however remember that with an acute bleed the haemoglobin will not immediately drop. This is because the measure of haemoglobin is a concentration rather than an absolute mass of Hb, so the level will not drop until the blood starts to dilute as the body responds to the insult by retaining fluid. The Hb may therefore be normal initially but one would not expect it to be raised.
73
Which of the following is NOT true of the clinical presentation of cholecystitis?
Liver function tests may be normal
Pain is usually intermittent and patients find it hard to get a comfortable position
Murphy’s sign is often positive
Not all patients have gallstones
May present without a history of biliary colic
The correct answer is b) Pain is intermittent and patients find it hard to get a comfortable position. This is a description of colicy pain which is more typical of biliary colic. Pain with cholecystitis is more often continuous and less intermittent but often patients can get comfortable by laying still. LFTs may be abnormal (typically Alk phos and gamma GT) but can be normal, especially early in the presentation, and Murphy’s sign is the classic sign of cholecystitis, though of course it is not invariably present. Patients can get acalculous cholecystitis, particularly those with critical illness (seen not infrequently in the intensive care setting) so not all have gallstones, although this is of course the most common cause. Cholecystitis may be the first presentation of gallstone disease and a history of biliary colic is not invariable.
74
A 70 year old patient presents with gallstone pancreatitis. He is breathless with upper abdominal pain and his HR is 100 with a BP of 100/60. His blood results are normal apart from the follows:
Amylase 1200 Alk phos 250
WBC 22 PaO2 7.4kPa
Na+ 130 PaCO2 6kPa
K+ 6 Blood glucose 12
CRP 140
What does he score on the Glasgow pancreatitis severity scoring system?
1
2
3
4
5
The correct answer here is d) 4. The Glasgow score is a predictor of severe pancreatitis – the definition of severe pancreatitis is pancreatitis with organ dysfunction, but a score of >3 predicts the subsequent development of severe pancreatitis. The positive scores in this patient are for:
Age >55
WBC >15
PaO2 <8
Blood glucose >10 (in a non diabetic patient).
He therefore has predicted severe pancreatitis. Amylase is not a predictor of severity and is mostly just to confirm the diagnosis. CRP can itself be predictive of severity in pancreatitis but in the context of the Glasgow score is not relevant. A raised Alk Phos is not relevant to the score or predictive of severity – the score utilises the synthetic liver enzyme levels (AST/ALT >200 or LDH >600).
75
Which of the following are NOT true of obstructive jaundice?
Blood tests will show high levels of unconjugated bilirubin
The most common cause is gallstones in the bile duct
Clinical presentation is typically with pale stool and dark urine
Ultrasound is usually the first investigation of choice
Courvoisier’s sign raises the concern of pancreatic cancer
The correct answer is a) Blood tests will show high levels of unconjugated bilirubin. Bilirubin is conjugated as it passes through the liver to allow excretion, and therefore if the cause of the jaundice is post-hepatic (obstructive) then the majority of the bilirubin will be conjugated. Unconjugated bilirubin is seen with pre-hepatic and sometimes hepatic jaundice. Gallstones are by far the most common cause of obstructive jaundice and the typical presentation is with pale stools (less stercobilin in the stool) and dark urine (increased urinary excretion). Ultrasound will often be able to identify the presence of gallstones (90% of gallstones are visible on USS) and may be able to identify stones in the CBD, however particularly in obese patients the CBD may be obscured. MRCP is the gold standard investigation to check the biliary anatomy for obstructing stones or other pathology. Courvoisier’s sign is jaundice along with the presence of a palpable gallbladder without pain and is concerning for the presence of pancreatic cancer.
76
What is the pathological process underlying achalasia?
Weak lower oesophageal sphincter leading to reflux
Failure of relaxation of the lower oesophageal sphincter with inadequate peristalsis
Scarring of the oesophagus with structuring from acid regurgitation
Narrowing of the upper oesophagus from excessively bulky skeletal muscle
Unco-ordinated oesophageal contractions occurring in multiple segments of the oesophagus at the same time
Correct: Failure of relaxation of the lower oesophageal sphincter with inadequate peristalsis
77
What is Mirizzi syndrome?
Chronic pancreatitis associated with raised IgG4 levels
High amplitude oesophageal contractions leading to dysphagia and chest pain
Upper GI bleeding associated with ulceration due to NSAID use
GORD caused by increased abdominal pressure in pregnancy
Common hepatic duct obstruction by a gallstone in Hartmann’s pouch or cystic duct
The correct answer is e) Common hepatic duct obstruction by a gallstone in Hartmann’s pouch or cystic duct. A gallstone lodged in either Hartmanns pouch of the gallbladder or in the cystic duct itself can cause external compression and obstruction of the CHD and jaundice without there being a stone in the CHD itself. This can be difficult to diagnose and MRCP is often the best way to define the anatomy. Subsequent cholecystectomy for these patients can be extremely difficult. Chronic pancreatitis with raised IgG4 is autoimmune pancreatitis and high amplitude oesophageal contractions is seen in Nutcracker oesophagus. NSAIDs can cause UGI ulceration but this does not have a specific syndrome name and the same is true of GORD which is not uncommon in pregnancy.
78
