Peptic Ulcer Disease Flashcards

1
Q

What are the 4 regions that the stomach is broken up into?

A
  1. Cardia
  2. Fund us
  3. Body
  4. Pyloric antrum
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2
Q

What type of cells does the cardia usually have?

A

FOVEOLAR CELLS

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3
Q

What type of cells does the Fundus and Body usually have?

A
  1. Parietal cells which secrete hydrochloride acid

2. Chief cells which secrete pepsinogen which digests protein

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4
Q

What type of cells are found in the antrum?

A

G cells which secrete gastrin

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5
Q

Between the stomach and duodenum what has the thicker mucus layer?

A

The stomach because it is usually more exposed to the stomach acid

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6
Q

What organism causes peptic and duodenal ulcers?

A

H. Pylori which is a gram negative organism

-usually occurs in low income countries

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7
Q

What drugs can causes peptic ulcers?

A

-NSAIDS(ibuprofen)

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8
Q

What syndrome predisposes people to peptic ulcers?

A

Zollinger Ellison Syndrome

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9
Q

What is Zollinger Ellison Syndrome?

A

It is a syndrome where a neuroendocrine tumor(gastrinoma) releases more gastrin than usual and causes more release of hydrochloride acid and that stimulates the occurrence of peptic ulcers

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10
Q

Where is the location that is most susceptible to gastric ulcers?

A

Lesser curvature of the antrum

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11
Q

Where do duodenal ulcers usually occur?

A

Directly after the pyloric sphincter

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12
Q

What two arteries are we mostly worried about?

A
  1. Left gastric artery

2. Gastro-duodenal artery

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13
Q

What are the common symptoms?

A
  • epigastric pain- sometimes relieved by food and then starting up again 30 minutes to two hours later
  • nocturnal pain
  • bloating
  • belching
  • vomiting
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14
Q

What are the signs of a gastric ulcer in particular?

A
  • weight loss

- the presence of food causes HCL to increase which leads to nausea and vomiting

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15
Q

What are the signs of a duodenal ulcer?

A

-weight gain

The presence of food makes it better

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16
Q

What diagnostic tool is used?

A

Endoscopy and biopsy(usually 6 biopsies taken)

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17
Q

What is the treatment?

A
  • antibiotics and proton pump inhibitors
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18
Q

What is the pathogenesis of peptic ulcer disease?

A

It is an imbalance between the production of H.pylori, NSAIDs, acid hypersecretion and the protective mechanisms such as mucus production, prostaglandins, and tissue growth factor

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19
Q

Where can we expect to find peptic ulcers?

A
  1. Duodenum(95% within the pyloric sphincter)
  2. Stomach-95% on the lesser curvature , 60% in the antrum
  3. Stomach ulcers-ulcers surrounding surgically created stomas
  4. Next to a Meckel’s diverticulum with ectopic gastric mucosa
  5. Patients with Zollinger-Ellison syndrome
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20
Q

What age group is affected in gastric ulcers?

A
  1. 40-60 years
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21
Q

What age group is affected in duodenal ulcers?

A

20-45 years

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22
Q

In which economic class do gastric ulcers occur in?

A

Lower

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23
Q

Which economic class do duodenal ulcers occur in?

A

Higher

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24
Q

What is the classification used for the different types of gastric ulcers?

A

Gaintree Johnson Classification

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25
Q

What is type 1?

A
  1. On the lesser curvature
    - not associated with increased acid secretion
    - blood group A
    - decreased mucosal defenses
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26
Q

What is type 2?

A
  • usually due to acid hypersecretion

- The duodenal ulcer causes stasis of gastric contents and then leads to a gastric ulcer

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27
Q

Type 3?

A
  • Blood group O
  • Acid hypersecretion
  • pre-pyloric
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28
Q

Type 4?

A
  • Higher on the lesser curvature
  • close to the gastric-oesophageal junction
  • not associated with acid hypersecretion
  • problem with mucosal defence
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29
Q

What is type 5?

A
  • due to NSAID
  • Can occur anywhere
  • decreased mucosal defence
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30
Q

Name 4 complications of gastric ulcers?

A
  1. Bleeding
  2. Perforation-peritoneal cavity, lesser sac
  3. Penetration into the pancreas
  4. Gastric outlet obstruction
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31
Q

What special investigations do we do for gastric ulcers?

A
  1. Barium meal
  2. Endoscopy with biopsy to ex.clude malignancy
  3. Test for H. Pylori
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32
Q

How do NSAID cause peptic ulcers?

A

The mucus gel layer contains bicarbonate and that protects the gastric mucosa against back fusion of hydrogen ions.
The NSAIDS then depress the mucus cell function

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33
Q

Can smoking and alcohol predispose someone to H.pylori?

A

Yes

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34
Q

What are duodenal ulcers commonly associated with?

A

Chronic liver disease
Chronic lung disease
Chronic pancreatitis
-They are usually benign

35
Q

What must you always exclude with gastric ulcers?

A

Malignancy
-Patients with gastric ulcers have a 3-6 time risk of developing gastric cancer but this risk is gone if H. Pylori is eradicated

36
Q

What are the definitive symptoms of duodenal ulcers?

A
  1. Epigastric pain that is biting, gnawing or burning
  2. Weight gain-improves with food or milk
  3. Wakes patient up at night
  4. If it penetrates the pancreas it becomes ,more constant and goes to the back with less relief
37
Q

What are the definitive symptoms of gastric ulcers?

A
  1. Epigastric pain usually in the midline-gnawing, burning and aching
  2. Nausea and vomiting
  3. Weight loss -pain gets worse after 30 minutes of eating
  4. Improves with antacids
38
Q

What does a malignant gastric ulcer look like?

A

Rolled elevated edges and benign ulcers have flat edges

39
Q

How do we diagnose H. Pylori?

A
  1. Serology

2. Breath tests

40
Q

When would we test gastrin levels?

A

To exclude Zollinger-Ellison Syndrome

41
Q

When should we suspect Zollinger-Ellison Syndrome?

A
  1. Diarrhea with peptic ulcer disease
  2. Recurrent ulcers especially after surgery
  3. Ulcers in atypical areas
  4. Family Hx
  5. Peptic Ulcers with hyperparathyroidism and hypercalcaemia
42
Q

What are the indications of surgery?

A
  1. Non healing ulcers(8-12 weeks for gastric ulcers)
  2. Complications-bleeding(leading to shock), perforation, gastric outlet obstruction
  3. Penetration into the liver or pancreas
  4. Giant gastric ulcer>3 cm which can lead to maligancy
43
Q

What type of treatment is needed for duodenal ulcers, type 2 and 3 stomach ulcers?

A

Decrease acid secretion

44
Q

What type of treatment is expected for type 1 and 4 gastric ulcers?

A

Removal of the decreased mucosal resistance?

45
Q

What is the surgical treatment of duodenal ulcers?

A
  1. Billroth 1-still attached to the duodenum
  2. Billroth 2-jejunum
    - Antrectomy
    - These patients still have to take PPI for the rest of their life
46
Q

What surgery is needed with type 1?

A
  • Partial/distal gastrectomy and a bit more than just the antrum is removed
  • Billroth 1 or 2 is done
47
Q

What surgery is needed with type 2 and 3/

A

-antrectomy ands vagotomy

48
Q

What type of surgery is needed with type 4?

A
  • pauchet procedure

- remove a narrow of the lesser curvature including the ulcer and continue with billroth 1 anastomoses

49
Q

How do we manage a gastroduodenal artery?

A

Longitudinal incision and bleeding lint sewn

50
Q

What ulcers usually perforate?

A
  • anterior ulcers usually

- 10% of the time kissing ulcers occur which bleed posteriorly

51
Q

Which type of peritonitis occurs usually?

A
  1. Chemical peritonitis and then develops into bacterial peritonitis 12-24 hours later
52
Q

What is the clinical picture of a patient with perforation?

A
  1. Sudden onset of upper abdominal pain(usually can tell us exactly when it’s started)
  2. Patient lies motionless with knees to the chest and shallow breath
  3. Tachycardiac with rigid abdomen And guarding
  4. Dull on percussion of the liver
  5. White cell elevated
  6. Erect C-X-ray free air under the diaphragm
53
Q

What is the management of perforation?

A
  1. Patient must be NPO
  2. Free draining nasogastric tube draining
  3. Resuscitate pt. With fIV fluids, IV antibiotics and IV PPI
  4. Prepare patient for laparotomy
54
Q

At laparotomy how do we treat a DU?

A

-Omentopexy

55
Q

At laparotomy how do we treat GU?

A
  • Biopsy and omentopexy
  • excision of the ulcer with simple closure
  • then treat with PPI and eradication of PPI
56
Q

In which cases would we expect to do definitive ulcer treatment?

A
  1. When the patient is haemodynamically stable, perforation occurred less than 24 hours ago and the patient has no associated risk factors
  2. When the patient has very large ulcers that are associated with bleeding, obstruction and repeated perforations then definitive ulcer treatment is needed
57
Q

What happens if a patient presents >24 hours later?

A
58
Q

How do the ulcers start causing gastric outlet obstruction?

A

-By acute inflammation and healing leading to ode a and muscle spasm and possibly fibrosis

59
Q

What is the typical clinical picture of a patient with gastric outlet obstruction?

A
  1. Early satiety
  2. Vomiting(sometimes bile-stained) and the pt. Can feel fine for two days then vomit out all the food and then feel hungry again immediately after
  3. Dehydration and weight loss
  4. Metabolic abnormalities- hyponatraemia, hypochloraemia, hypokalaemia and paradoxical acidic urine
60
Q

What will we see on X-ray of gastric outlet obstruction patients?

A
  1. Dilated stomach with gastric air-fluid level
61
Q

What are 5 differential diagnoses of gastric outlet obstruction?

A
  1. TB/ Crohn’s disease
  2. PUD
  3. Malignancy
  4. Chronic pancreatitis
  5. Radiotherapy
62
Q

What is the Mx of gastric outlet obstruction?

A
  1. Resuscitation with 0,9% sodium chloride. Give potassium supplementation when good urine output is established
  2. Gastric lavage- 32F stomach tube to remove food rest
  3. Gastroscopy with biopsies and barium meal
  4. IPP
  5. Patient drinks water and then nasogastric tube is inserted to check how much is draining exactly
  6. Balloon dilation of the pyloric canal sometimes but that is temporary
  7. Antrectomy and sometimes vagotomy works with billroth 1 for more definitive treatmentment
63
Q

How do you know a patient has a penetration complication?

A
  • central back pain with PUD that is not responding to medical treatment
64
Q

What if it is gastro-colic fistula formation?

A
  • patient has diarrhea with food rest
  • weight loss
  • halitosis and faecal vomiting
65
Q

Vagotomy

A

Removal of part of the vagus nerve

66
Q

What stimulates gastric acid secretion?

A
  • Vagus nerve

- gastrin which is produced in the gastric antrum

67
Q

What is the function of the vagus nerve?

A
  1. Gastric acid secretion
  2. Receptive relaxation
  3. Gastric emptying
  4. Gastric accommodation
68
Q

What two branches does the anterior vagus nerve break up into?

A
  1. Hepatic division

2. Anterior gastric nerve(anterior nerve of laterjet)

69
Q

The anterior gastric nerve goes to?

A

-corpus

70
Q

Where does the anterior nerve of laterjet goes to?

A

-antrum and pyloric via the crows foot

71
Q

The posterior vagus nerve has 2 branches:

A
  1. Celiac division

2. Posterior nerve of laterjet

72
Q

What is truncal vagotomy?

A
  1. Division of the anterior and posterior vagus nerve
73
Q

What is selective vagotomy?

A
  • seldomly used

- division of vagus nerve to the hepatic and celiac division

74
Q

What is parietal cell vagotomy?

A
  • highly selective
  • nerves of laterjet to the fundus and corpus are cut
  • antrum and pyloric branches kept intact
  • seldomly used
75
Q

What needs to be done if a truncal vagotomy is done?

A
  1. Pyloroplasty-longitudinal incision of the pylorus and sewn transversally to make it more wider
    - this is needed because the drainage capacity of the stomach is inhibited when it is cut
76
Q

What are the problems with parietal vagotomy?

A
  1. Greater curvature necrosis
  2. More time consuming to perform
  3. Less effective in decreasing gastric acid production
77
Q

What are the complications of a vagotomy?

A
  1. Injury to surrounding areas
  2. Long procedure
  3. early post-op complications: dysphagia, delayed gastric emptying
  4. late post-op complications: post vagotomy diarrhea, Dumping, reflux oesophagitis, gallstones
78
Q

What are the complications of gastrectomy?

A
  1. Early- bleeding, anastomoses leak, bowel obstruction

2. Late- ulcer recurrence, gsdtro-jejunal-colic fistula

79
Q

What are the pathophysiological problems of gastrectomies?

A
  1. Alkaline reflux gastritis

2. Dumping syndrome

80
Q

What is dumping syndrome?

A
  1. When the pyloric sphincter is not functioning well and large amounts of food enter the small bowel undigested.
    - causes a secretion of insulin, fall in blood glucose
81
Q

What is early dumping?

A
  1. 20 minutes after food
    - abdominal cramps, fullness, nausea and vomiting, explosive diarrhoea, tachycardia, sweating, dizziness, dyspnea
    - at age problem is high osmolality stomach contents entering the small bowel and inappropriate fluid shifts happening
82
Q

What is late dumping?

A

1-3 hours later

-leads to hypoglycemia because of the increase in insulin

83
Q

What are the other problems associated with gastrectomies?

A
  1. Nutritional and malabsorption problems: vitamin B12, iron deficiency, folate, malabsorption of proteins, carbs and fats