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Yr 5 - GI > Revision - Acute Abdomen, Pancreatitis etc > Flashcards

Revision - Acute Abdomen, Pancreatitis etc Flashcards

1
Q

What are the 3 most common causes of acute pancreatitis in UK?

A

1) Gallstones
2) Alcohol excess
3) Post-ERCP

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2
Q

Mneumonic for causes of pancreatitis: GET SMASHED

A

G - Gallstones
E - Ethanol
T - Trauma

S - Steroids
M - Mumps
A - Autoimmune
S - Scorpion sting
H - Hypertriglyceridaemia, Hyperchylomicronaemia, Hypercalcaemia, Hypothermia
E - ERCP
D - Drugs

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3
Q

What drugs can cause acute pancreatitis?

A

1) Azathioprine
2) Mesalazine
3) Bendroflumethiazide
4) Furosemide
5) Steroids
6) Sodium valproate

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4
Q

Pathophysiology of acute pancreatitis?

A

1) A triggering event results in an inflammatory response within the pancreatic parenchyma

2) Release of pancreatic enzymes outside of the ductal system

3) Activation of lipase and peptidases outside of the GI tract

4) Local tissue damage and a worsening inflammatory response

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5
Q

Give some complications of acute pancreatitis

A

1) Retroperitoneal haemorrhage (can result in reactive ascites)

2) Risk of portal venous thrombosis

3) Necrosis (can become infected)

4) Pancreatic pseudocyst

5) CVS shock

6) Acute respiratory distress syndrome

7) Pleural effusion

8) Disseminated intravascular coagulation (DIC)

9) Hyperglycaemia

10) Hypocalcaemia

11) Malnutrition

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6
Q

How can acute pancreatitis affect calcium?

A

Causes hypocalcaemia

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7
Q

How can acute pancreatitis affect glucose levels?

A

Can cause hyperglycaemia

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8
Q

How can acute pancreatitis result in hyperglycaemia?

A

Due to local damage to islet cells resulting in failure of glucose homeostasis (may persist long-term if pancreatic damage is severe enough).

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9
Q

How can acute pancreatitis result in hypocalcaemia?

A

Systematic release of lipase causes fat store lysis and release of free fatty acids –> subsequently sequestrates calcium in the blood

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10
Q

How can acute pancreatitis lead to malnutrition?

A

Loss of exocrine pancreatic tissue results in an acute failure to digest food and malabsorption can develop.

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11
Q

Describe pain in acute pancreatitis

A

Severe, radiates to back, epigastric pain

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12
Q

What 2 signs may be present on examination in acute pancreatitis?

A

1) Grey Turner’s (flanks)

2) Cullen’s (peri-umbilical)

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13
Q

What 2 respiratory conditions may acute pancreatitis cause?

A

1) ARDS

2) Pleural effusion

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14
Q

What is the diagnostic test for anyone with suspected acute pancreatitis?

A

1) Serum amylase

2) Serum lipase (higher sensitivity and specificity but not all centres have access)

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15
Q

Give some causes of a raised serum amylase

A

1) pancreatitis

2) upper GI perforation

3) mesenteric or bowel ischaemia

4) renal failure

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16
Q

If serum amylase or lipase levels are inconclusive and there is a high suspicion of acute pancreatitis, what is the most sensitive test?

A

CT imaging of the abdomen with contrast.

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17
Q

What 2 scores can be used to calculate severity in acute pancreatitis?

A

1) Glasgow score

2) Ranson score

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18
Q

How can LFTs determine the cause of acute pancreatitis?

A

Raised bilirubin –> gallstones

Isolated raised gamma GT –> alcohol

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19
Q

What imaging investigation can assess for complications of pancreatitis (such as necrosis, abscesses and fluid collections)?

A

CT abdomen

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20
Q

What amylase level indicates acute pancreatitis?

A

> 3x upper limit of normal

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21
Q

What would US demonstrate in gallstones?

A

Dilated common bile duct

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22
Q

What are 3 non-abdominal differentials for acute pancreatitis?

A

1) inferior MI

2) basal pneumonia

3) pericarditis

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23
Q

Management of acute pancreatitis?

A

Mainly supportive

Abx if specific infection (e.g., abscess or infected necrotic area)

ERCP/cholecystectomy if gallstones

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24
Q

Mortality rate of acute pancreatitis?

A

10-15%

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25
Q

What is the most common cause of chronic pancreatitis?

A

Alcohol

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26
Q

Give some other causes of chronic pancreatitis?

A

1) alcohol

2) genetic: cystic fibrosis, haemochromatosis

3) ductal obstruction: tumours, stones, structural abnormalities including pancreas divisum and annular pancreas

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27
Q

What are the key complications of chronic pancreatitis?

A

1) Chronic epigastric pain

2) Loss of exocrine function, resulting in a lack of pancreatic enzymes (particularly lipase) secreted into the GI tract

3) Loss of endocrine function, resulting in a lack of insulin, leading to diabetes

4) Damage and strictures to the duct system, resulting in obstruction in the excretion of pancreatic juice and bile

5) Formation of pseudocysts or abscesses

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28
Q

Clinical features of chronic pancreatitis?

A

1) epigastric pain (typically worse 15 to 30 minutes following a meal)

2) steatorrhoea (increase in fat excretion in the stools)

3) diabetes

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29
Q

When is epigastric pain in chronic pancreatitis worse?

A

10-15 mins after eating

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30
Q

What causes steatorrhoea in chronic pancreatitis?

A

lack of exocrine enzymes –> poor digestions and absorption of food - especially fat.

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31
Q

When does diabetes typically occur in chronic pancreatitis?

A

Typically >20y after symptoms begin

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32
Q

Amylase & lipase levels in acute vs chronic pancreatitis?

A

Acute - significantly raised

Chronic - normal or only slightly raised

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33
Q

Faecal elastase in chronic pancreatitis?

A

Can be used to assess exocrine function: reduced levels are indicative of exocrine pancreatic insufficiency

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34
Q

How can chronic pancreatitis increase risk of osteoporosis?

A

malabsorption of calcium and vitamin D, as well as chronic inflammation

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35
Q

Treatment of exocrine pancreatic insufficiency in chronic pancreatitis?

A

pancreatic enzyme replacement therapy (PERT) and diet

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36
Q

What is the most common causative organism of ascending cholangitis?

A

E. coli

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37
Q

What are the 2 most common cause of ascending cholangitis?

A

1) gallstones

2) post-ERCP

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38
Q

Approx 50-75% of patients with ascending cholangitis present with Charcot’s triad.

What is this?

A

1) fever
2) jaundice
3) RUQ pain

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39
Q

Sometimes patients with ascending cholangitis present with Reynolds’ pentad.

What is this?

A

Same 3 features as Charcot’s triad plus;

1) hypotension (septic shock)
2) confusion

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40
Q

Ascending cholangitis can be caused by biliary obstruction.

What are some cau

A

1) Gallstones (main cause)

2) Benign biliary strictures: from chronic pancreatitis or post-operative changes.

3) Malignant obstructions: e.g. cholangiocarcinoma or pancreatic carcinoma.

4) Parasitic infections: e.g. liver flukes such as Clonorchis sinensis or Opisthorchis viverrini.

5) Biliary stents or drainage procedures e.g. ERCP

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41
Q

What is generally the 1st line imaging in suspected cholangitis cases?

A

US - to look for bile duct dilation and bile duct stones

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42
Q

What is endoscopic retrograde cholangiopancreatography (ERCP)?

A

ERCP involves the passage of an endoscope into the second part of the duodenum and cannulation of the ampulla.

ERCP can determine the underlying cause of cholangitis and can also be therapeutic, by way of stone extraction and/or stent placement.

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43
Q

What is the gold standard investigation and intervention for acute cholangitis?

A

ERCP

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44
Q

Why is ERCP not always used in cholangitis?

A

Is invasive and therefore carries much more risk than other imaging modalities.

As a result, it is frequently preceded by MRCP where available.

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45
Q

What are the complications of ERCP?

(2)

A

1) acute pancreatitis

2) severe haemorrhage

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46
Q

What imaging is typically used if US is negative in ascending cholangitis?

A

A contrast-enhanced CT abdomen

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47
Q

Management of ascending cholangitis?

A

1) ABCDE if necessary

2) Non-surgical biliary decompression: ERCP +/- sphincterotomy +/- placement of drainage stent

3) Surgical biliary decompression (last resort)

4) Abx

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48
Q

What is a sphincterotomy?

A

Incising the sphincter of Oddi, where the biliary system joins the duodenum.

This aids drainage and passage of any CBD stones.

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49
Q

Complications of cholangitis?

A

1) acute pancreatitis: stones in the distal common bile duct causing cholangitis can also lead to blockage of the pancreatic duct

2) Inadequate biliary drainage following endoscopy, radiology or surgery

3) Hepatic abscess formation

4) Complications of surgical intervention e.g. bleeding, infection

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50
Q

Calcium levels in acute pancreatitis?

A

Hypercalcaemia can CAUSE acute pancreatitis

Acute pancreatitis can CAUSE hypocalcaemia

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51
Q

How can temp affect acute pancreatitis?

A

Hypothermia can cause acute pancreatitis

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52
Q

What are some indicators of acute pancreatitis severity?

PANCREAS mneumonic

A

P - PaO2 <8 kPa
A - age >55
N - neutrophils (>15)
C - calcium <2
R - uRea >16
E - enzymes (LDH >600 or AST/ALT >200)
A - albumin <32
S - sugar (glucose >10)

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53
Q

Give 3 differentials for acute pancreatitis?

A

1) peptic ulcer disease
2) acute hepatitis
3) ascending cholangitis

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54
Q

Is faecal elastase used in the diagnosis of acute or chronic pancreatitis?

A

Chronic

The test is used to check for exocrine pancreatic insufficiency (i.e. levels are reduced in chronic pancreatitis).

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55
Q

What do those with ascending cholangitis typically have a history of?

A

1) gallstones

2) previous ERCP

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56
Q

What drugs are a risk factor for peptic ulcer disease?
(4)

A

1) NSAIDs

2) Steroids

3) SSRIs

4) Bisphosphonates

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57
Q

What is Zollinger Ellison syndrome?

A

Tumours that secrete gastrin –> increase gastric acid secretion.

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58
Q

2 initial investigations in peptic ulcer disease?

A

1) endoscopy

2) H. pylori test:
- urea breath test
- stool antigen test

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59
Q

Mx of peptic ulcer disease not caused by H. pylori?

A

PPIs until healed

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60
Q

Mx of peptic ulcer disease caused by H. pylori?

A

Eradication therapy –>

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61
Q

What type of bacteria is H. pylori?

A

Gram -ve aerobic

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62
Q

How does H. pylori cause damage to stomach?

A

1) It avoids the acidic environment by forcing its way into the gastric mucosa, using flagella to propel itself.

2) It creates gaps in the mucosa, exposing the epithelial cells underneath to damage from stomach acid.

3) H. pylori produces ammonium hydroxide, which neutralises the acid surrounding the bacteria. It also produces several toxins.

4) The ammonia and toxins lead to gastric mucosal damage.

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63
Q

What does H. pylori produce?

A

Ammonium hydroxide

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64
Q

How long before having H. pylori test must patients STOP taking PPIs?

A

2 weeks for an accurate test

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65
Q

What investigations are possible for H. pylori?

(4)

A

1) Stool antigen

2) Urea breath test

3) H. pylori antibody test (blood)

4) Rapid urease test performed during endoscopy (also known as the CLO test)

66
Q

What is involved in a rapid urease test?

A

1) Taking a small biopsy of the stomach mucosa

2) This is added to a liquid medium containing urea.

3) H. pylori produce urease enzymes that convert urea to ammonia.

67
Q

What result of the rapid urease test indicates a positive result?

A

1) H. pylori produce urease enzymes that convert urea to ammonia

2) Ammonia makes the solution more alkaline.

3) A pH indicator (e.g., phenol red) changes colour if the pH rises, giving a positive result.

68
Q

What does the H. pylori eradication regime involve?

A

PPI + 2 abx (e.g. amoxicillin + clarithromycin) for 7 days

69
Q

Is routine re-testing necessary after H. pylori eradication therapy?

A

No

70
Q

How can gastric outlet obstruction be treated?

A

balloon dilatation during an endoscopy or surgery.

71
Q

How do NSAIDs predispose to peptic ulcers?

A

1) Inhibition of cyclooxygenase 1 (COX-1) derived prostaglandins causes reduction in mucous and bicarbonate secretion, rendering the mucosa exposed and more prone to damage

2) Reduction in gastric mucosal blood flow, therefore reducing the ability of epithelial cells to regenerate and heal mucosal injury

72
Q

Why may shoulder tip pain be seen in a perforated peptic ulcer (Kehr’s sign)?

A

Due to irritation within the peritoneal cavity from released gastric contents

73
Q

What is the leading cause of mortality in patients with perforated peptic ulcers?

A

Sepsis (50%)

74
Q

Patients with chronic pancreatitis are at an increased risk of developing diabetes.

What test should they be offered?

A

Annual HbA1c

75
Q

Common symptoms of viral hepatitis?

A
  • N&V
  • anorexia
  • myalgia
  • lethargy
  • RUQ pain
76
Q

What may be present in history in viral hepatitis?

A

1) IVDU

2) foreign travel

77
Q

What is congestive hepatomegaly?

A

The liver only usually causes pain if stretched. One common way this can occur is as a consequence of congestive heart failure. In severe cases cirrhosis may occur.

78
Q

Features of biliary colic?

A

RUQ pain, intermittent, usually begins abruptly and subsides gradually. Attacks often occur after eating. Nausea is common.

(fat, female, forties, fair)

79
Q

Features of acute cholecystitis?

A

Pain similar to biliary colic but more severe and persistent. The pain may radiate to the back or right shoulder.

The patient may be pyrexial and Murphy’s sign positive (arrest of inspiration on palpation of the RUQ)

80
Q

What is gallstone ileus?

A

This describes small bowel obstruction secondary to an impacted gallstone.

Abdominal pain, distension and vomiting are seen.

81
Q

What is the AST/ALT ration in alcoholic hepatitis?

A

2:1

82
Q

jaundice in ascending cholangitis vs acute cholecystitis?

A

Jaundice is seen in ascending cholangitis but not in acute cholecystitis

83
Q

What CT sign may be seen in pancreatic cancer?

A

Double duct sign

84
Q

LFTs in acute cholecystitis?

A

Typically normal

85
Q

When would a serum lipase be more useful than an amylase?

A

Late presentations (>24h) –> lipase has a longer half life

86
Q

Where can biliary colic pain radiate to?

A

Interscapular region

87
Q

What is the most sensitive blood test for acute pancreatitis?

A

Lipase

88
Q

How does hepatitis present?

A

Flu-like symptoms
RUQ pain
Tender hepatomegaly
Deranged LFTs

89
Q

Is mesalazine or sulfasalazine a bigger risk factor for pancreatitis?

A

Mesalazine

90
Q

Does serum amylase offer a prognostic value in acute pancreatitis?

A

No - diagnostic value only

91
Q

What is Budd-Chiari syndrome?

A

A condition characterised by obstruction to hepatic venous outflow.

92
Q

Who does Budd-Chiari syndrome typically occur in?

A

Patients with a hypercoagulative state (e.g. antiphospholipid syndrome)

Can also occur as a result of physical obstruction (e.g. tumour).

93
Q

Triad of symptoms in Budd-Chiari syndrome?

A

1) sudden onset abdo pain
2) ascites
3) tender hepatomegaly

94
Q

What needs to be excluded in all cases of painless jaundice?

A

Pancreatic cancer

95
Q

What is the preferred diagnostic test for chronic pancreatitis?

A

CT pancreas –> looking for pancreatic calcification

96
Q

Describe pain in acute diverticulitis

A

Colicky abdo pain in LIF

97
Q

What are the 4 key causes of upper GI bleed?

A

1) Peptic ulcer (most common)

2) Mallory Weiss tear

3) Oesophageal varices

4) Stomach cancers

98
Q

What is a mallory weiss tear typically associated with?

A

Forceful reaching or coughing (or strained defecation).

98
Q

What is a mallory weiss tear?

A

Tear or laceration in the distal oesophagus and proximal stomach.

99
Q

Risk factors for a Mallory Weiss tear?

A

1) alcoholism (40-80%)

2) hiatal hernia: retching increases the potential for mucosal laceration by creating a higher pressure gradient, in these patients

3) bulimia nervosa

4) hyperemesis gravidarum

5) GORD

100
Q

How does a Mallory Weiss tear typically present?

A

Haematemesis:
- Typically brisk small to moderate volume of bright red blood following a bout of repeated vomiting.

Melena rare.

101
Q

What are oesophageal varices associated with?

A

Portal HTN due to liver cirrhosis.

102
Q

How does a GI bleed caused by oesophageal varices typically present?

A

1) haematemesis:
- usually large volume of FRESH blood

2) melena: from swallowed blood

3) often associated with haemodynamic compromise

103
Q

What 2 drugs are used in the mx of variceal haemorrhage?

A

1) Terlipressin

2) Prophylactic IV abx

104
Q

Management of variceal haemorrhage?

A

1) ABCDE

2) Correct clotting: FFP, vitamin K, platelet transfusions

3) Terlipressin

4) Prophylactic IV Abx e.g. quinolones (have been shown to reduce mortality in patients with liver cirrhosis)

5) Endoscopy: endoscopic variceal band ligation

105
Q

When should terlipressin & IV Abx be given in variceal haemorrhage?

A

Prior to endoscopy

106
Q

What drug is used for the PROPHYLAXIS of variceal haemorrhage?

A

Propanolol

107
Q

Where are duodenal ulcers usually located?

What vessel do they erode?

A

These are usually posteriorly sited and may erode the gastroduodenal artery.

108
Q

What scoring system is used at the initial presentation in suspected upper GI bleed?

A

Glasgow Blatchford

109
Q

what does the Glasgow-Blatchford score estimate?

A

The risk of the patient having an upper GI bleed.

110
Q

What Glasgow-Blatchford score indicates a high risk for an upper GI bleed?

A

Above 0

Consider early discharge in patients with a score of 0.

111
Q

What causes a raised urea in an upper GI bleed?

A

Acid and digestive enzymes break down blood in the upper GI tract –> one of the breakdown products is urea, which is then absorbed in the intestines.

‘Protein meal’.

112
Q

What score is used after endoscopy to estimate the risk of rebleeding and mortality in an upper GI bleed?

A

Rockall

113
Q

What does the Rockall score indicate?

A

provides a percentage risk of rebleeding and mortality

114
Q

How soon should patients with a suspected upper GI bleed have an endoscopy?

A

<24h

115
Q

How does the management of non-variceal vs variceal bleeding differ?

A

Non-variceal –> give PPIs after endoscopy

Variceal –> give Abx and terlipressin prior to endoscopy

116
Q

What transfusion product can be given to patients taking warfarin that are actively bleeding?

A

Prothrombin complex concentrate

117
Q

What is often used to treat bleeding oesophageal varices?

A

Variceal band ligation

118
Q

When should a PPI be given in patients with non-variceal upper GI bleeding?

A

After endoscopy

119
Q

Give some different transfusion reactions

A

1) Minor allergic

2) Non-haemolytic febrile

3) TRALI

4) TACO

5) Anaphylactic

6) Acute haemolytic reaction

120
Q

Features of non-haemolytic febrile reaction?

A

Fever & chills

121
Q

Mx of non-haemolytic febrile reaction?

A

Slow/stop & paracetamol

122
Q

Features of minor allergic transfusion reaction?

A

Urticaria & pruritus

123
Q

Mx of minor allergic transfusion reaction?

A

Temporarily stop & antihistamine

124
Q

Who is anaphylactic reaction to transfusion thought sometimes seen in?

A

Can be caused by patients with IgA deficiency who have anti-IgA antibodies.

125
Q

Features of anaphylactic reaction to transfusion?

A

1) hypotension
2) dyspnoea
3) wheezing
4) angiodema

126
Q

Management of anaphylactic reaction to transfusion?

A

Stop & IM adrenaline (ABCDE)

127
Q

What is an acute haemolytic reaction to transfusion thought to be caused by?

A

A mismatch of blood group (ABO) (e.g. secondary to human error) which causes massive intravascular haemolysis.

This is usually the result of red blood cell destruction by IgM-type antibodies.

128
Q

Features of an acute haemolytic reaction to transfusion?

When do these symptoms begin?

A

1) fever
2) abdo pain & chest pain
3) hypotension
4) agitation

Symptoms begin minutes after the transfusion is started.

129
Q

Management of an acute haemolytic reaction to transfusion?

A

1) stop transfusion immediately

2) confirm diagnosis:
- check the identity of patient/name on blood product
- send blood for direct Coombs test, repeat typing and cross-matching

3) fluid resuscitation with saline

130
Q

What is a transfusion-associated circulatory overload (TACO) caused by?

A

1) Excessive rate of transfusion
2) Pre-existing heart failure

131
Q

Features of transfusion-associated circulatory overload (TACO)?

A

1) pulmonary oedema
2) HTN

132
Q

Management of transfusion-associated circulatory overload (TACO)?

A

1) slow or stop transfusion

2) consider IV loop diuretic (e.g. furosemide) & O2

133
Q

What is a transfusion-related acute lung injury (TRALI) caused by?

A

Non-cardiogenic pulmonary oedema thought to be secondary to increased vascular permeability caused by host neutrophils that become activated by substances in donated blood.

134
Q

Features of a transfusion-related acute lung injury (TRALI)?

A

1) hypoxia

2) pulmonary infiltrates on CXR

3) fever

4) hypotension

135
Q

Management of transfusion-related acute lung injury (TRALI)?

A

1) stop transfusion

2) O2 & supportive care

136
Q

What are 2 main complications of an acute haemolytic transfusion reaction?

A

1) disseminated intravascular coagulation
2) renal failure

137
Q

What is an infective transfusion reaction often associated with?

A

Transmission of vCJD.

138
Q

Where is ischaemic colitis more likely to occur?

A

In ‘watershed’ areas such as the splenic flexure that are located at the borders of the territory supplied by the superior and inferior mesenteric arteries.

139
Q

Mesenteric ischaemia vs ischaemic colitis?

A

Ischaemic colitis –> large bowel

Mesenteric ischaemia –> small bowel

140
Q

What artery supplies the foregut?

A

Coeliac artery

141
Q

What artery is the midgut supplied by?

A

SMA

142
Q

What is the hindgut supplied by?

A

IMA

143
Q

What is chronic mesenteric ischaemia also known as?

A

intestinal angina

144
Q

What classic triad of features is seen in chronic mesenteric ischaemia?

A

1) Central colicky abdominal pain after eating (postprandial): starting around 30 minutes after eating and lasting 1-2 hours

2) Weight loss (due to food avoidance, as this causes pain)

3) Abdominal bruit may be heard on auscultation

145
Q

What typically precedes abdo pain in chronic mesenteric angina?

A

Eating

146
Q

How is a diagnosis of chronic mesenteric ischaemia made?

A

CT angiography

147
Q

What is acute mesenteric ischaemia typically caused by?

A

An thrombus/embolus causing occlusion of an artery which supplies the small bowel e.g. the superior mesenteric artery.

AF is key risk factor

148
Q

What is the diagnostic test of choice for acute mesenteric ischaemia?

A

Contrast CT –> allows the radiologist to assess both the bowel and the blood supply.

149
Q

Lab findings in acute mesenteric ischaemia?

A

Patients will have metabolic acidosis and raised lactate level due to ischaemia.

150
Q

Best way to manage variceal haemorrhage whilst waiting for endoscopy?

A

Insert a Sengstaken-Blakemore tube

151
Q

What is indicated in ongoing upper GI bleeding despite repeated endoscopy therapy?

A

Surgical intervention

152
Q

What is the area most likely to be affected by ischaemic colitis?

A

Splenic flexure

153
Q

Transfusion of what blood component is most at risk of bacterial contamination?

A

Platelet transfusion - as they are stored at room temp

154
Q

What are 2 common bacterial contaminants of platelet transfusions?

A

1) Staph. epidermis
2) Bacillus cereus

155
Q

What does a Glasgow Blatchford score of 0 indicate?

A

Low risk - discharge with advice & outpatient follow up

156
Q

What electrolyte abnormality can transfusion of packed red cells cause?

A

Hyperkalaemia –> risk increases with larger volume transfusions

157
Q

Treatment of overflow diarrhoea?

A

Faecal impaction

158
Q

1st line investigation in acute mesenteric ischaemia?

A

Lactage (VBG)

159
Q
A

Yr 5 - GI (5 decks)

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