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Yr 4 - ACC > GI: Pancreatitis, Cholangitis & Peptic Ulcer Disease > Flashcards

GI: Pancreatitis, Cholangitis & Peptic Ulcer Disease Flashcards

1
Q

What is acute pancreatitis?

A

Inflammation of the pancreas causing extra-ductal release of pancreatic enzymes.

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2
Q

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

A

1) obstructive gallstone disease
2) alcohol excess
3) post-ERCP

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3
Q

Mneumonic for causes of pancreatitis: GET SMASHED

A

G - Gallstones
E - Ethanol
T - Trauma

S - Steroids
M - Mumps (other viruses include Coxsackie B)
A - Autoimmune (e.g. polyarteritis nodosa), Ascaris infection
S - Scorpion venom
H - Hypertriglyceridaemia, Hyperchylomicronaemia, Hypercalcaemia, Hypothermia
E - ERCP
D - Drugs

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4
Q

What drugs can cause acute pancreatitis?

A

Azathioprine, mesalazine, bendroflumethiazide, furosemide, steroids, sodium valproate.

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5
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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6
Q

Give some acute local complications of acute pancreatitis

A

1) Extra-ductal release of protease enzymes results in soft tissue and vascular damage causing retroperitoneal haemorrhage.

2) The retroperitoneal inflammation results in a reactive ascites.

3) In severe pancreatitis there is a risk of portal venous thrombosis.

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7
Q

Give some late local complications of acute pancreatitis

A

1) Protease activity within the pancreatic tissue can cause areas of necrosis to develop (this can become infected)

2) Fluid secretion from inflamed and necrotic tissues can become encapsulated within the lesser sac of the peritoneum and form a pancreatic pseudocyst.

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8
Q

Give some systemic complications of acute pancreatitis

A

1) Release of inflammatory cytokines causes a systemic inflammatory response with systemic vasodilation resulting in cardiovascular shock.

2) There can be an inflammatory reaction in the lungs resulting in interstitial oedema and poor oxygen transfer (acute respiratory distress syndrome).

3) Reactive inflammation of the pleura can result in a pleural effusion (10-20%)

4) Severe pancreatitis can result in a systemic inflammatory response that results in disseminated intravascular coagulation (DIC).

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9
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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10
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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11
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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12
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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13
Q

Clinical features of acute pancreatitis?

A

1) Abdo pain & tenderness:
- severe epigastric pain
- radiates to back
- sudden onset and severe (reaches peak within hours and persists for days)

2) N&V

3) Jaundice
- in cases of gallstone obstruction of ducts

4) Systemically unwell e.g. low grade fever, tachycardia

5) May be features of the cause:
- alcohol use
- weight loss (may indicate pancreatitic or biliary tumour)
- use of drugs e.g. steroids (recent COPD exacerbation)
- history of trauma or recent surgery
- history of ERCP
- history of recent mumps infection

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14
Q

Where does acute pancreatitis abdo pain typically radiate to?

A

to the back

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15
Q

Location of acute pancreatitis abdo pain?

A

epigastric

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16
Q

Examination features in acute pancreatits?

A

Systemic:
- shock (if CVS compromise)
- tachypnoea
- fever

Abdo:
- tenderness in epigatrium with guarding
- distension (due to ascites)
- loss of bowel sounds (due to acute ileus)
- Grey-Turner’s sign
- Cullen’s sign

Respiratory:
- Acute respiratory compromise
- Severe acute respiratory distress syndrome (ARDS).
- Pleural effusion

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17
Q

What is Grey-Turner’s sign?

A

Bruising of the flanks due to bleeding in the fascial planes (haemorrhagic pancreatitis) from release of protease enzymes in pancreatitis.

RARE

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18
Q

What is Cullen’s sign?

A

Peri-umbilical bruising in pancreatitis

RARE

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19
Q

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

A

1) Serum amylase (this is a pancreatic enzyme): most often used

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

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20
Q

What are some causes of a raised serum amylase?

A

1) Acute pancreatitis

2) Upper GI perforation

3) Mesenteric or bowel ischaemia

4) Renal failure

5) Retroperitoneal haematoma

6) Intra-abdominal ectopic pregnancy

7) Inflammation or obstruction of the salivary glands

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21
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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22
Q

Following diagnosis of acute pancreatitis, why should further investigations be carried out?

A

1) severity prognostication

2) ascertaining the cause of the acute pancreatitis

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23
Q

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

A

1) Ranson score

2) Glasgow score

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24
Q

What are some furher investigations that can be done to ascertain the severity of the acute pancreatitis?

A

1) FBC:
- for WCC (severity of inflammation)
- low Hb carries worse prognosis

2) CRP

3) serum glucose >10 mmol/L

4) U&ES:
- may indicate AKI
- may indicate significant electrolyte disturbances which need treatment with IV fluids
- rising urea

5) LFTs:
- severe pancreatitis can result in liver failure: raised AST & ALT levels
- low albumin

6) Calcium levels

7) LDH

8) ABC:
- low PaO2 < 8 kPa indicates respiratory failure (type 1) due to inflammatory response
- metabolic acidosis due to significant inflammatory response and cardiovascular shock

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25
Q

How can LFTs determine the cause of acute pancreatitis?

A

Raised bilirubin –> suggesting gallstones as the cause

Isolated raised gamma-GT –> suggesting alcohol use as the cause

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26
Q

What does an isolated raised gamma GT in LFTS indicate as the cause of acute pancreatitis?

A

Alcohol use

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27
Q

What does a raised bilirubin indicate as the cause of acute pancreatitis?

A

Gallstones (obstructive)

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28
Q

What imaging is the initial investigation of choice in assessing for gallstones?

A

US

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29
Q

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

A

CT abdomen

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30
Q

What amylase level indicates acute pancreatitis?

A

Amylase is raised more than 3 times the upper limit of normal in acute pancreatitis.

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31
Q

What would US demonstrate in gallstones?

A

Dilated common bile duct

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32
Q

What Glasgow score indicates:

a) mild pancreatitis
b) moderate
c) severe

A

a) 0 or 1
b) 2
c) 3 or more

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33
Q

What is the criteria for the Glasgow score- PANCREAS mnemonic (1 point for each answer)?

A

P - PaO2 <8 kPa

A - Age >55

N - Neutrophils (WBC >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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34
Q

Give some differentials for acute pancreatitis?

A

1) perforated duodenal ulcer

2) acute hepatitis

3) biliary tract pathology e.g. ascending cholangitis

4) bowel obstruction or ischaemia

5) obstructed or strangulated hernias

6) renal tract disease e.g. pyelonephritis/ureteric obstruction

7) gynae pathology e.g. ectopic pregnancy

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35
Q

What are 3 non-abdominal differentials for acute pancreatitis?

A

1) inferior MI

2) basal pnuemonia

3) pericarditis

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36
Q

How can acute pancreatitis be differentiated from acute hepatitis?

A

The main findings in acute hepatitis would be acute jaundice and deranged liver enzymes including raised transaminase (ALT/AST) levels.

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37
Q

How may a perforated duodenal ulcer and acute pancreatitis be differentiated?

A

The difference in examination findings and the lesser degree of amylase elevation.

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38
Q

Management of acute pancreatitis?

A

Treatment of the main phase is entirely supportive with treatment aimed at preventing deterioration and managing symptoms.

General:

1) ABCDE if appropriate

2) Admission (consider ICU)

3) IV fluids

4) Nil by mouth

5) Analgesia & antiemetics

6) Careful monitoring & glucose monitoprng (consider insulin if persistent hyperglycaemia)

7) Treatment of gallstones in gallstone pancreatitis (ERCP / cholecystectomy)

8) Antibiotics if there is evidence of a specific infection (e.g., abscess or infected necrotic area)

9) Treatment of complications (e.g., endoscopic or percutaneous drainage of large collections)

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39
Q

Treatment of gallstones in gallstone pancreatitis?

A

ERCP / cholecystectomy

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40
Q

What are some complications of acute pancreatitis?

A
  • Necrosis of the pancreas
  • Infection in a necrotic area
  • Abscess formation
  • Acute peripancreatic fluid collections
  • Pseudocysts (collections of pancreatic juice) can develop 4 weeks after acute pancreatitis
  • Chronic pancreatitis
  • Patients can develop insulin-dependent diabetes and long-term malabsorption.
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41
Q

Mortality rate of acute pancreatitis?

A

10-15%

Severe attacks where pancreatic necrosis and subsequent infection develop have a mortality of up to 50% and death is mostly due to the systemic complications.

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42
Q

What is chronic pancreatitis?

A

Chronic pancreatitis refers to chronic inflammation in the pancreas. It results in fibrosis and reduced function of the pancreatic tissue.

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43
Q

What is the most common cause of chronic pancreatitis?

A

Alcohol.

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44
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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45
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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46
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 mellitus

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47
Q

when is epigastric pain in chronic pancreatitis typically worse?

A

15-30 mins after a meal

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48
Q

What causes steatorrhoea in chronic pancreatitis?

A

Lack of exocrine enzymes due to pancreatic damage results in poor digestions and absorption of food - especially fat.

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49
Q

When does diabetes typically occur in chronic pancreatitis?

A

It typically occurs more than 20 years after symptom begin

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50
Q

Lab investigations in chronic pancreatitis?

A

1) Serum amylase & lipase: often normal or only slightly elevated in chronic pancreatitis

2) LFTs: assess for cholestasis or liver involvement

3) Fasting blood glucose and HbA1c: evaluate for diabetes

4) Serum triglycerides: elevated levels may indicate hypertriglyceridemia-induced pancreatitis

5) Full blood count: anaemia and leukocytosis can occur in chronic pancreatitis

6) Fecal elastase-1: reduced levels are indicative of exocrine pancreatic insufficiency

7) Serum immunoglobulin G4 (IgG4): elevated levels may suggest autoimmune pancreatitis

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51
Q

Amylase & lipase levels in acute vs chronic pancreatitis?

A

Acute - significantly raised

Chronic - normal or only slightly raised

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52
Q

What imaging is required in chronic pancreatitis?

A

1) Abdo US: shows pancreatic calcification in 30% of cases

2) CT scan: more sensitive at detecting pancreatic calcification.

3) Endoscopic ultrasound (EUS): allows for detailed visualization of the pancreatic parenchyma and ducts, as well as the possibility of obtaining tissue samples

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53
Q

Faecal elastase in chronic pancreatitis?

A

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

54
Q

Management of chronic pancreatitis?

A

1) Pain management

2) Management of exocrine pancreatic insufficiency
- pancreatic enzyme replacement therapy (PERT)
- diet
- fat soluble vitamin supplementation
- PPIs or H2 receptor antagonists: may enhance efficacy of PERT

3) Abstinence from alcohol and smoking

4) Management of diabetes if necessary

5) ERCP with stenting can be used to treat strictures and obstruction to the biliary system and pancreatic duct.

55
Q

What are some complications of chronic pancreatitis?

A

1) pseudocysts

2) biliary obstruction

3) duodenal obstruction

4) pancreatic ductal obstruction

5) splenic vein thrombosis

6) ascites

7) exocrine pancreatic insufficiency: malabsorption, steatorrhoea, weight loss

8) endocrine dysfunction: diabetes

9) osteoporosis

10) pancreatic cancer

56
Q

How can chronic pancreatitis increase risk of osteoporosis?

A

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

57
Q

Treatment of exocrine pancreatic insufficiency in chronic pancreatitis?

A

pancreatic enzyme replacement therapy (PERT) and diet

58
Q

What is ascending cholangitis?

A

Infection of the biliary tract.

It is a surgical emergency and has a high mortality due to sepsis and septicaemia.

59
Q

What is the most common causative organism of ascending cholangitis?

A

E. coli

60
Q

What are the 2 most common cause of ascending cholangitis?

A

1) Gallstones (choledocholithiasis): causes obstruction in the bile ducts stopping bile flow

2) Infection introduced during an ERCP procedure

61
Q

What are the 3 most common organisms causing ascending cholangitis?

A

1) E. coli

2) Klebsiella species

3) Enterococcus species

62
Q

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

What is this?

A

1) fever
2) jaundice (raised bilirubin)
3) RUQ pain

63
Q

Sometimes patients with ascending cholangitis present with Reynolds’ pentad.

What is this?

A

Same 3 symptoms as Charcot’s triad (fever, RUQ pain, jaundice) PLUS:

1) hypotension (septic shock)
2) confusion

64
Q

Ascending cholangitis can be caused by biliary obstruction.

What are some causes of biliary obstruction?

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

65
Q

Investigations in ascending cholangitis?

A

Those with ascending cholangitis typically have a history of gallstone calculi or previous (ERCP).

1) FBC: raised WCC

2) Coagulation panel: prothrombin time raised with sepsis

3) LFTs:
- deranged LFTs often seen with hyperbilirubinaemia and elevated serum alkaline phosphatase
- normal LFTs are more in keeping with acute cholecystitis

4) U&Es:
- Often decreased K+ and Mg2+

5) CRP: raised

6) Blood cultures

66
Q

Cholecystitis vs cholangitis?

A

Cholecystitis - inflammation of gallbladder

Cholangitis - inflammation of bile duct system

67
Q

Imaging options in ascending cholangitis?

A

1) Transabdominal US of abdomen / pelvis –> quick and accurate for detecting common bile duct (CBD) dilation

2) ERCP: provides both diagnosis and therapy via biliary decompression

3) Magnetic retrograde cholangiopancreatography (MRCP)

4) Endoscopic ultrasound (EUS)

68
Q

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

A

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

69
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.

70
Q

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

A

Endoscopic retrograde cholangiopancreatography (ERCP)

71
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.

72
Q

What are the complications of ERCP?

A
  • acute pancreatitis
  • severe haemorrhage
73
Q

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

A

A contrast-enhanced CT abdomen

74
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

75
Q

What is a sphincterotomy?

A

A sphincterotomy involves incising the sphincter of Oddi, where the biliary system joins the duodenum. This aids drainage and passage of any CBD stones.

76
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

77
Q

Define peptic ulcer disease

A

Ulceration in the stomach or duodenum.

N.B. many patients are managed with the clinical diagnosis of ‘dyspepsia’ as opposed to the endoscopic diagnosis of peptic ulcer disease.

78
Q

What are the majority of peptic ulcers associated with?

A

Helicobacter pylori:
- 95% of duodenal ulcers
- 75% of gastric ulcers

79
Q

are duodenal or gastric ulcers more common?

A

duodenal

80
Q

Role of the stomach mucosa (mucous membrane)?

A

1) The mucosa (muscous membrane) is the inner lining of the stomach and duodenum.

2) This secretes mucus that coats the surface and forms a barrier that protects it from the stomach’s contents

3) It secretes bicarbonate into this mucus coating to neutralise the stomach acid.

81
Q

Pathophysiology of peptic ulcer disease?

A

Factors that disrupt the mucus barrier or increase stomach acid, increase the risk of mucosal ulceration.

There is an imbalance between protective factors (e.g. mucous production, blood flow) and factors that promote damage (e.g. H. pylori, gastric acid).

82
Q

Clinical features of peptic ulcer disease?

A

1) epigastric pain

2) nausea

3) duodenal ulcers:
- epigastric pain when hungry, relieved by eating

4) gastric ulcers:
- epigastric pain worsened by eating

83
Q

Risk factors for peptic ulcer disease that DISRUPT the mucous barrier?

A

1) Helicobacter pylori

2) Non-steroidal anti-inflammatory drugs (NSAIDs)

84
Q

Risk factors for peptic ulcer disease that INCREASE stomach acid?

A
  • Stress
  • Alcohol
  • Caffeine
  • Smoking
  • Spicy foods
  • Zollinger Ellison syndrome
85
Q

What drugs are a risk factor for peptic ulcer disease?

A
  • NSAIDs
  • SSRIs
  • Corticosteroids
  • Bisphosphonates
86
Q

What is Zollinger Ellison syndrome?

A

Rare digestive order - likely to have one or more tumours that may secrete excess gastrin –> increased stomach acid production.

87
Q

Describe typical weight changes in gastric vs duodenal ulcers

A

Gastric:
- Eating typically worsens the pain of gastric ulcers.
- Patients tend to lose weight due to the fear of pain on eating.

Duodenal:
- The pain of duodenal ulcers tends to improve immediately after eating, followed by pain 2-3 hours later.
- The weight is stable or increases

88
Q

Investigations in uncomplicated peptic ulcer disease?

A

1) endoscopy

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

89
Q

Management of uncomplicated peptic ulcer disease?

A

1) stopping NSAIDs
2) treating H. pylori infections
3) PPIs e.g. lansoprazole or omeprazole

Repeat endoscopy (at 4-8 weeks) may be performed to ensure the ulcer heals.

90
Q

How does management of peptic ulcer disease depend on H. pylori test results?

A

If negative –> give PPIs until ulcer healed

If positive –> eradication therapy

91
Q

What is H. pylori?

A

a gram-negative aerobic bacteria that can live in the stomach.

92
Q

Complications of H. pylori infection?

A

It causes damage to epithelial lining:
- gastritis
- ulcers
- increased risk of stomach cancer

93
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.

94
Q

Who should an H. pylori test be offered to?

A

Anyone with dyspepsia

95
Q

With a patient taking PPIs, what is rule before they have H. pylori test?

A

They need 2 weeks without using a PPI before testing for H. pylori for an accurate result.

96
Q

What investigations are possible for H. pylori?

A

1) Stool antigen test

2) Urea breath test using radiolabelled carbon 13

3) H. pylori antibody test (blood)

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

97
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.

98
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.

99
Q

What does the H. pylori eradication regime involve?

A

Triple therapy with:

PPI + 2 antibiotics (e.g. e.g., amoxicillin and clarithromycin) for 7 days.

100
Q

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

A

No

101
Q

Complications of peptic ulcer disease?

A

1) Bleeding

2) Perforation: results in acute abdominal pain and peritonitis

3) Scarring and strictures: can lead to a narrowing of the exit of the stomach

102
Q

Scarring and strictures from peptic ulcer disease can lead to gastric outlet obstruction.

How does this present?

A
  • early fullness after eating
  • upper abdo discomfort
  • abdo distension
  • vomiting, particularly after eating
103
Q

How can gastric outlet obstruction be treated?

A

balloon dilatation during an endoscopy or surgery.

104
Q

Clinical features of a bleeding peptic ulcer?

A

1) Haematemesis (vomiting blood)

2) Melena (black tarry stools)

3) Epigastric pain

4) Anaemia

5) Haemodynamic instability: hypotension, tachycardia, altered mental status

105
Q

Peptic ulcers can result in chronic microscopic bleeding.

How can this be investigated?

A

can lead to iron deficiency anaemia, with low haemoglobin, low mean cell volume (MCV) and low ferritin.

106
Q

How can haematemesis present with a bleeding peptic ulcer?

A

Bright red or ‘coffee grounds’ depending on duration and location of bleeding.

107
Q

Cause of melena in bleeding peptic ulcer?

A

The passage of digested blood through the gastrointestinal tract.

108
Q

How may anaemia caused by a bleeding peptic ulcer present?

A
  • pallor
  • fatigue
  • dyspnoea on exertion
  • tachycardia
  • conjunctival pallor
  • lab: reduced Hb and haematocrit levels
109
Q

Management of a bleeding peptic ulcer?

A

1) ABCDE approach as with any upper GI haemorrhage

2) IV PPI

3) 1st line treatment: endoscopic intervention

if this fails:
- urgent interventional angiography with transarterial embolization or
- surgery

110
Q

What is the prevalence of perforation in those with peptic ulcer disease?

A

approx 5%

111
Q

Who do the majority of peptic ulcer perforations occurs in?

A

Occur in older populations with existing peptic ulcer disease, rather than younger populations.

112
Q

Smoking and peptic ulcer disease?

A

The incidence of ulcers is nearly doubled in current and former smokers (11%) compared to non-smokers (6%).

The mechanism is that tobacco is predicted to inhibit bicarbonate secretion from the pancreas, therefore increasing the acidity in the duodenum.

113
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

114
Q

What happens in a peptic ulcer perforation?

A

The gastric contents are able to exit the stomach or duodenum and enter the peritoneal cavity, resulting in chemical peritonitis and irritation, leading to the clinical features of pain, rigidity, tenderness and distention.

115
Q

What triad of features is seen in a perforated peptic ulcer?

A

1) abdo pain

2) tachycardia

3) abdo rigidity

In practice, most patients present with symptoms of an acute abdomen.

116
Q

What are the clinical symptoms seen in a perforated peptic ulcer?

A

1) abdo pain
- very severe
- constant pain
- most frequently epigastric in the beginning, but rapidly becomes generalised

2) abdo distension

3) N&V

4) Dyspepsia

5) Constipation

6) Shoulder tip pain (Kehr’s sign)
- due to irritation within the peritoneal cavity from released gastric contents

117
Q

What are the clinical signs seen in a perforated peptic ulcer?

A

1) abdo tenderness
- frequently in epigastric region

2) peritonitis
- guarding
- rigidity
- rebound tenderness

3) fever

4) tachycardia
- 1ary: from a systemic inflammatory response
- 2ary: from reduced fluid intake and increased output from vomiting

118
Q

What is it important to ask about in potential peptic ulcer history?

A

1) previous diagnosis

2) abdo pain

3) pain worsened by eating?

4) abdo tenderness

5) symptoms of anaemia: fatigue, pallor, SOB

119
Q

Lab tests in a perforated peptic ulcer (or any acute abdomen)?

A

1) FBC:
- Leukocytosis likely present
- Anaemia if bleeding

2) U&Es & creatinine:
- Significant haemorrhage may result in electrolyte disturbances
- With significant bleeding, urea may be raised (as digested blood is a source of protein)

3) Urine microscopy, culture and sensitivity:
- Usually normal in perforated peptic ulcer disease

4) LFTs:
- Will help to rule out biliary pathology such as cholecystitis if elevated liver enzymes

5) Serum amylase and/or lipase:
- To rule out pancreatitis, a similarly presenting condition
- However, perforated peptic ulcers can also cause a raised amylase

120
Q

Although the diagnosis is largely clinical, what imaging is recommended in perforated peptic ulcer?

A

Xrays:

  • Erect CXR: when a patient presents with acute upper abdominal pain (free air under diaphragm)
  • AXR: cause of pneumoperitoneum may be due to another abdominal pathology such as a perforated diverticulum etc
121
Q

Primary differentials for perforated peptic ulcer?

A

Epigastric pain causes:

1) Pancreatitis

2) Bleeding peptic ulcer (without perforation)

3) Perforated oesophagus

4) Mallory-Weiss tear

5) Cholecystitis

122
Q

Similarities between pancreatitis & perforated peptic ulcer?

A
  • Both present with persistent, severe epigastric pain
  • Both have nausea and vomiting
  • Although amylase is a marker used in pancreatitis, amylase can also be raised in a perforated peptic ulcer
123
Q

Differences in pancreatitis vs perforated peptic ulcr?

A
  • Pain radiates to the back in 50% of patients in pancreatitis
  • Typically a history of gallstones and/or alcohol abuse (the two most common causes of pancreatitis in pancreatitis
  • Free air in perforation
124
Q

Management of peptic ulcer perforation?

A

1) ABCDE

2) IV fluids –> many patients will be fluid deplete due to ulcer bleeding and re-distribution of fluid to the third space

3) NG tube insertion –> To reduce amount of gastric fluids in the GIT and therefore reduce the amount to escape into the peritoneum

4) Nil by mouth

5) IV PPIs

6) Abx

7) Surgery if necessary

125
Q

Role of IV PPIs in perforated peptic ulcer?

A

PPI’s are thought to enhance fibrin formation and therefore encourage sealing of the perforation

126
Q

Role of Abx therapy in perforated gastric ulcer?

A

Antibiotic therapy is important for perforated peptic ulcers due to the leakage of gastric fluids into the peritoneum.

Sepsis is a leading cause of death in patients with perforated peptic ulcers and therefore needs to be managed aggressively (accounting for 50% of deaths).

127
Q

Post-op management of perforated peptic ulcer?

A

1) Upper endoscopy:
- to identify the cause of the perforation (e.g. malignancy, biopsy for H pylori infection)
- to see if ulcer is healing

2) H. pylori eradication (if necessary)

128
Q

Complications of a perforated peptic ulcer?

A

1) sepsis

2) significant haemorrhage

3) post-op leakage

129
Q

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

A

Sepsis (50%)

130
Q

Common, infrequent & rare causes of epigastric pain?

A

Common:
- GORD
- Gastritis

Infrequent:
- Peptic ulcer disease
- Acute pancreatitis
- Bleeding peptic ulcer
- Perforated peptic ulcer

Rare:
- Gastric cancer

131
Q
A

Yr 4 - ACC (73 decks)

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