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3. Inflammation > Peptic ulcer disease > Flashcards

Peptic ulcer disease Flashcards

1
Q

What is peptic ulcer disease?

A

Peptic ulcer disease (PUD) is a break in the inner lining of the stomach, the first part of the small intestine, or sometimes the lower esophagus

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2
Q

What are common causes of peptic ulcer disease?

A

H. pylori
NSAID use

Less common include tobacco, smoking, stress

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3
Q

Who is most sensitive to developing peptic ulcer disease after NSAID use?

A

Older people

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4
Q

What are the signs and symptoms of peptic ulcer disease?

A 
Abdominal (mainly epigastric) pain
Bloating
Nausea
Heartburn
Blood in stool
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5
Q

What is the effect of eating on the pain in peptic ulcer disease?

A

Gastric ulcer –> worse

Duodenal ulcer –> better

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6
Q

What are the risk factors for developing peptic ulcer disease?

A

Heartburn
Gastroesophageal reflux disease
NSAID use

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7
Q

What are the complications of peptic ulcer disease?

A

Gastrointestinal bleeding (can be lethal! Most common)
Perforation
Cancer (H. pylori)

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8
Q

What do parietal cells secrete?

A

HCl

Intrinsic factor

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9
Q

What do G cells release?

A

Gastrin, stimulate parietal cells

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10
Q

NSAIDs can increase the risk of peptic ulcer disease. What other medications, taken with aspirin, increase this risk?

A 
Aspirin
SSRIs
Corticosteroids
Antimineralocorticoids
Anticoagulants
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11
Q

How do NSAIDs increase the risk of peptic ulcer disease?

A

The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins.

NSAIDs block the function of cyclooxygenase 1 (COX-1), which is essential for the production of these prostaglandins.

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12
Q

How is peptic ulcer disease diagnosed?

A

Characteristic symptoms:
1. Stomach pain

Esophagogastroduodenoscopy

Potentially Barium swallowing

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13
Q

What layer do peptic ulcers affect?

A

Muscularis mucosae and lamina propria

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14
Q

how can you diagnose the presence of H. pylori?

A

Urea breath test, as H. pylori secretes urease
Culture from endoscopy
Rapid urease test

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15
Q

What is the macroscopic appearance of peptic ulcers?

A

Gastric ulcers are most often localized on the lesser curvature of the stomach.

The ulcer is a round to oval parietal defect (“hole”), 2–4 cm diameter, with a smooth base and perpendicular borders

Surrounding mucosa may present radial folds, as a consequence of the parietal scarring

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16
Q

What is the microscopic appearance of peptic ulcers?

A

Penetration of muscularis mucosae and lamina propria, usually produced by acid-pepsin aggression

During the active phase, the base of the ulcer shows 4 zones: fibrinoid necrosis, inflammatory exudate, granulation tissue and fibrous tissue

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17
Q

How can you prevent peptic ulcers?

A

PPI with NSAIDs

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18
Q

How would you manage H. pylori induced peptic ulcer disease?

A

A triple regimen in which pantoprazole and clarithromycin are combined with either amoxicillin or metronidazole. 7-14 days

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19
Q

How would you manage NSAID induced peptic ulcer disease?

A

NSAID-associated ulcers heal in 6 to 8 weeks provided the NSAIDs are withdrawn with the introduction of proton pump inhibitors

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20
Q

What is the Glasgow-Blatchford score?

A

A screening tool to assess the likelihood that a person with an acute upper gastrointestinal bleeding will need to have medical intervention such as a blood transfusion or endoscopic intervention

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21
Q

What criteria are considered in the Glasgow-Blatchford score?

A 
Blood urea
Haemoglobin
Systolic blood pressure
Pulse
Melaena (dark stool)
Syncope
Hepatic disease
Cardiac failure
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22
Q

What is the Rockall score?

A

Identifies patients at risk of adverse outcome following acute upper gastrointestinal bleeding.

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23
Q

What criteria are considered in the Rockall score?

A 
Age
Shock
Co-morbidity
Diagnosis
Evidence of bleeding
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24
Q

How do you notice upper gastrointestinal bleeding?

A

Blood in vomit
Black stool
Hypovolaemic shock

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25
Q

What are upper gastrointestinal bleedings caused by?

A

Peptic ulcers
Gastric erosions
Esophageal varices
Mallory-Weiss tear

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26
Q

What are the signs in upper gastrointestinal bleeding?

A

Vital signs are deteriorating quickly: a medical emergency!

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27
Q

What is the prognosis for uppper gastrointestinal bleeds?

A

Depending on its severity, upper gastrointestinal bleeding may carry an estimated mortality risk of 11%

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28
Q

How would you manage someone with acute gastrointestinal bleeding?

A

Transfuse patients with massive bleeding with blood, platelets and clotting factors

Offer endoscopy to unstable patients with severe acute upper gastrointestinal bleeding immediately after resuscitation

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29
Q

How would you manage someone with acute gastrointestinal bleeding who is taking warfarin?

A

Offer prothrombin complex concentrate

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30
Q

How would you manage non-variceal bleeding?

A

After stabilisation!

For the endoscopic treatment of non-variceal upper gastrointestinal bleeding, use one of the following:

  1. a mechanical method (for example, clips) with or without adrenaline
  2. Thermal coagulation with adrenaline
  3. Fibrin or thrombin with adrenaline

DO NOT offer PPI before endoscopy

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31
Q

How would you manage variceal bleeding?

A

Resuscitate

Offer terlipressin to patients with suspected variceal bleeding at presentation

Offer prophylactic antibiotic therapy at presentation to patients with suspected or confirmed variceal bleeding

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32
Q

How would you manage oesophageal varices?

A

Use band ligation in patients with upper gastrointestinal bleeding from oesophageal varices

Consider transjugular intrahepatic portosystemic shunts (TIPS) if bleeding from oesophageal varices is not controlled by band ligation

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33
Q

How would you manage gastric varices?

A

Offer endoscopic injection of N-butyl-2-cyanoacrylate to patients with upper gastrointestinal bleeding from gastric varices

Offer TIPS as secondline

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34
Q

How would you control bleeding and prevention of re-bleeding in patients on NSAIDs, aspirin or clopidogrel?

A

Continue low-dose aspirin for secondary prevention of vascular events

Stop other NSAIDs during acute phase of bleeding

Discuss the risks and benefits of continuing clopidogrel

35
Q

What is a Mallory Weiss tear?

A

Bleeding from a laceration in the mucosa at the junction of the stomach and esophagus

36
Q

What are Mallory Weiss tears usually caused by?

A

Alcoholism
Bulimia
Any other cause of vomiting

37
Q

What are Mallory Weiss tears signs and symptoms?

A

Vomiting blood

Blood in stool

38
Q

How would you manage a Mallory Weiss tear?

A

Treatment is usually supportive as persistent bleeding is uncommon

Cauterisation or injection with epinephrine can be used to stop bleeding

39
Q

How would you diagnose a Mallory Weiss tear?

A

Endoscopy

40
Q

What is Boerhaave syndrome?

A

A full thickness oesophageal rupture due to vomiting

41
Q

What are signs and symptoms of esophageal rupture?

A

History of retching and vomiting, immediately followed by excruciating retrosternal chest and upper abdominal pain

42
Q

How would you diagnose an oesophageal rupture?

A

Plain chest radiography and confirmed by chest CT scan.

Usually reveals mediastinal or free peritoneal air as the initial radiologic manifestation

43
Q

How would you managee a ruptured oesophagus?

A

Mortality if untreated is near 100%

Treatment includes immediate antibiotic therapy to prevent mediastinitis and sepsis, surgical repair of the perforation

44
Q

Where is the tear in Boerhaave’s syndrome usually located?

A

The left postero-lateral aspect of the distal esophagus and extends for several centimetres

(lower 1/3 of oesophagus)

45
Q

What is the difference between Boerhaave’s syndrome and a Mallory-Weiss tear?

A

Boerhaave: full oesophageal rupture

Mallory-Weiss: mucosal tear

46
Q

What is Barrett’s oesophagus?

A

Barrett’s oesophagus is a precancerous condition characterised by abnormal replacement of the squamous epithelium of the lower oesophagus by a type of columnar epithelium resembling that in the stomach and intestine.

47
Q

What microscopic change can be seen in Barret’s oesophagus?

A

stratified squamous epithelium to simple columnar epithelium with interspersed goblet cells

48
Q

What are risk factors of Barrett’s oesophagus?

A

Oesophageal adenocarcinoma

49
Q

What is the main cause of Barret’s oesophagus?

A

Adaptation to chronic exposure from acid reflux

50
Q

How would you diagnose Barret’s oesophagus?

A

Endoscopy and biopsy

51
Q

How would you microscopically stage Barret’s oesophagus?

A

The cells of Barrett’s esophagus are classified into four categories: nondysplastic, low-grade dysplasia, high-grade dysplasia, and frank carcinoma

52
Q

How would you manage Barret’s oesophagus?

A

In Barrett’s oesophagus with no dysplasia or low‑grade dysplasia, periodic endoscopic surveillance and repeat biopsies may be considered with the aim of early detection of progression to high‑grade dysplasia or cancer.

If high‑grade dysplasia or early cancer (carcinoma in situ) is detected, then surgery or ablation

53
Q

What are the symptoms of Barret’s oesophagus?

A

Heartburn
Dysphagia
Vomiting blood
Pain under sternum

54
Q

What is Gastroesophageal reflux disease (GERD)?

A

A chronic condition in which stomach contents rise up into the esophagus, resulting in either symptoms or complications

55
Q

What are the signs and symptoms of gastroesophageal reflux disease (GERD)?

A 
Acidic taste in the mouth
Regurgitation
Heartburn
Pain with swallowing
Chest pain
56
Q

What are the complications following gastroesophageal reflux disease (GERD)?

A

Complications include esophagitis, esophageal stricture, and Barrett’s esophagus

57
Q

What are the risk factors for gastroesophageal reflux disease (GERD)?

A

Risk factors include obesity, pregnancy, smoking, hiatal hernia, and taking benzodiazepines, calcium channel blockers, tricyclic antidepressants and NSAIDs.

58
Q

What is the problem in gastroesophageal reflux disease (GERD)?

A

Mechanical: poor closure of the lower oesophageal sphincter

59
Q

How is gastroesophageal reflux disease (GERD) diagnosed?

A 
Symptoms
Endoscopy (and biopsy)
60
Q

How is gastroesophageal reflux disease (GERD) managed?

A

Lifestyle: less coffee, acidic, spicy food. Weight loss

Medication: PPI and antacids

Surgery

61
Q

Name a proton-pump inhibitor?

A

Omeprazole

62
Q

Name an antacid?

A

Ranitidine

63
Q

How do PPIs work?

A

Inhibiting the stomach’s H+/K+ ATPase proton pump of gastric parietal cells

64
Q

How do antacids work?

A

Antacids contain alkaline ions that chemically neutralize stomach gastric acid, reducing damage to the stomach lining and esophagus, and relieving pain

65
Q

What do gastric chief cells secrete?

A

Pepsinogen, and endopeptidase (activated into pepsin by HCl)

Lipase

66
Q

What do mucous cells in the stomach secrete?

A

Mucin, protects stomach lining against acid

67
Q

What compounds and hormones does the stomach secrete and by what cells?

A

Gastric chief cells: pepsin and lipase

Mucous cells: mucin

Parietal cells: intrinsic factor and hydrochloric acid

G cells: gastrin

68
Q

Where in the stomach can you find the most chief cells?

A

Middle or superior portion of the stomach

69
Q

Where in the stomach can you find the most G cells?

A

Antrum (inferior)

70
Q

What is a hiatal hernia?

A

A hiatal hernia is a type of hernia in which abdominal organs (typically the stomach) slip through the diaphragm into the middle compartment of the chest

71
Q

What are complications following a hiatal hernia?

A

This may result in gastroesophageal reflux disease (GERD) or laryngopharyngeal reflux (LPR)

Iron deficiency anaemia

72
Q

What are the symptoms of a hiatal hernia?

A

Taste of acid in the back of the mouth, heartburn, trouble swallowing

73
Q

How would you manage a hiatal hernia?

A

Weightloss, medication (PPI), raising the head of the bed

74
Q

How would you diagnose a hiatal hernia?

A

Endoscopy

CT

75
Q

What are oesophageal varices?

A

Esophageal varices are extremely dilated sub-mucosal veins in the lower third of the esophagus

76
Q

What are oesophageal varices often caused by?

A

Portal hypertension, often due to cirrhosis

77
Q

Why do oesophageal varices only occur in the lower third of the oesophageal?

A

The upper two thirds of the oesophagus are drained via the oesophageal veins, which carry deoxygenated blood from the oesophagus to the azygos vein, which in turn drains directly into the superior vena cava

The lower one third of the oesophagus is drained into the superficial veins lining the oesophageal mucosa, which drain into the left gastric vein, which in turn drains directly into the portal vein

78
Q

What is the most prominent histological feature of oesophageal varices?

A

Dilated submucosal veins

79
Q

How you manage oesophageal varices in an acute setting?

A

Aim is to stop blood loss: banding

Fluid resuscitation of necessary

Secondary prevention with beta-blockers and nitrates

80
Q

What is caput medusae?

A

Caput medusae is the appearance of distended and engorged superficial epigastric veins, which are seen radiating from the umbilicus across the abdomen

81
Q

What is caput-medusae a sign of?

A

Portal hypertension

82
Q

What digestive enzymes does the pancreas secrete?

A
  1. Ductal cells –> bicarbonate, neutralise stomach acid
  2. Acinar cells -> inactive enzymes (stimulated by CCK in intestine)
  3. Delta cells –> somatostatin
83
Q

What does enzymes pancreatic juice contain?

A 
Trypsinogen 
Chymotrypsinogen 
Carboyxopeptidase
Lipase
Nucleases
Amylase
84
Q

What enzymes does the duodenum secrete?

A

Secretin (by S cell) to stimulate pancreatic ductal cells and HCO3 production

Cholecystokinin (I cells), response to high fat and stimulates pancreatic acinar cells

Gastric inhibitory peptide (mucosal cells), decreases gastric emptying

Somatostatin (mucosal cells), major inhibition

Motilin: increases GI motility

3. Inflammation (21 decks)

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