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PCL 424 > GIT Diseases II - PUD > Flashcards

GIT Diseases II - PUD Flashcards

1
Q

Define Peptic Ulcer Disease (PUD).

A

Peptic Ulcer Disease is a group of disorders characterised by circumscribed lesions of the mucosa of the upper GIT.

It is also a defect in the gastric or duodenal mucosa that extends through the muscularis mucosa into the deeper layers of the GIT wall.

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2
Q

What are the 2 types of peptic ulcers?

A

i. Gastric ulcer - affects the lining of the stomach.
ii. Duodenal ulcer - affects the lining of the duodenum

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3
Q

The most common symptom of both gastric and duodenal ulcers is _______.

A

Epigastric pain, which is gnawing, burning sensation in the epigastrium, usually after meals.

It occurs shortly after meals in GU and 2-3 hours after meals in DU.

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4
Q

Mucosal injury and peptic ulcer occur when the balance between the aggressive factors and the GIT defensive mechanisms is disrupted.

True or False?

A

True.

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5
Q

What are the defensive mechanisms (protective factors) of the gastroduodenal mucosa?

A

i. Thick mucus secretion by mucosa
ii. Mucosal blood flow, which removes acids that damage the epithelium
iii. Alkaline and neutral biliary juice
iv. Tight intercellular junction
v. Rapid continual epithelium renewal
vi. Prostaglandins, which inhibit acid secretion, maintain blood flow and stimulate mucus and bicarbonate production

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6
Q

What are the aggressive factors involved in the development of PUD?

A

Extrinsic factors:
i. NSAIDs
ii. H. pylori infection
iii. Alcohol
iv. Tobacco smoking

Intrinsic factors
vii. Bile salts
viii. Gastric acid
ix. Pepsin

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7
Q

Briefly discuss H. pylori in the pathogenesis of PUD.

A
  • The bacterium infects the GI mucosa and produces an enzyme called urease which breaks down urea into ammonia and carbon dioxide. This ammonia, which shields the bacterium from the stomach’s acidity, also damages the protective mucous layer.
    It also produces some enzymes such as haemolysins, fucosidase, and neuraminidase, which may be involved in tissue damage.
  • H. pylori also alters Gastrin homeostasis (hypergastrinemia), affecting gastric acid secretion and causing hyperacidity by:
    i. decreasing antral D cells which secrete somatostatin, which is responsible for inhibiting gastrin
    ii. direct stimulation of gastrin cells by cytokines produced during bacteria cytotoxin-induced inflammation
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8
Q

Briefly discuss NSAIDs in the pathogenesis of PUD.

A
  • NSAIDs promote back diffusion of hydrogen ions into the mucosa
  • NSAIDs cause mucosal injury due to their acidity
  • They inhibit prostaglandins (PGE2 and PGI2) by inhibiting the enzymes COX-1 and COX-2
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9
Q

Gastric ulcers are classified according to ________, and staging is done based on ________.

A

-the Johnson classification
-the location of the lesion

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10
Q

Describe stage I gastric ulcer.

A

They are located near the incisura angularis on the lesser curvature, close to the border between the antrum and body of the stomach.

Gastric acid secretion is usually normal or decreased.

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11
Q

Describe stage III gastric ulcer.

A

It is prepyloric i.e. above the pylorus.

Gastric acid secretion is usually normal or increased.

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12
Q

Describe stage IV gastric ulcer.

A

it is located near the gastroesophageal junction.

Gastric acid secretion is usually normal or decreased.

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13
Q

Describe stage II gastric ulcer.

A

It’s a combination of stomach and duodenal ulcer.

Gastric acid secretion is usually normal or increased.

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14
Q

Describe stage V gastric ulcer.

A

It is found all over the stomach, and is drug-induced.

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15
Q

What are the 3 distinct causes of PUD.

A

i. H. pylori
ii. NSAIDs such as aspirin
iii. Hypersecretion of HCl as in Zollinger-Ellison syndrome

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16
Q

Mention 7 risk factors that predispose an individual to PUD.

A
  1. Previous history of PUD
  2. Genetic factors
  3. Corticosteroids: concurrent use of corticosteroids with NSAIDS
  4. Cigarette smoking
  5. Advanced age
  6. Associated disorders such as hyperparathyroidism, alcoholic cirrhosis, emphysema, rheumatoid arthritis
  7. Stress
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17
Q

What are the clinical manifestations of PUD?

A

i. Epigastric pain (dyspepsia)
ii. Nausea
iii. Vomiting
iv. Heartburn
v. Bloating and Belching
vi. Anorexia
vii. Weight loss.

18
Q

Compare and contrast gastric ulcer and duodenal ulcer.

A

i. Epigastric pain occurs shortly after meal (45-60 mins) in GU, but 2-4 hours after meal in DU.
ii. Nocturnal pain (around 2 a.m.) occurs in DU but rarely ever occurs in GU.
iii. Food usually triggers pain in GU but relieves pain in DU
iv. GU patients tend to lose weight while DU patients tend to gain weight
v. H. pylori is present in 70% of GU cases, while it is present in almost all DU cases.

19
Q

What are the complications of PUD?

A

i. Haemorrhage
ii. Chronic iron deficiency anaemia
iii. Pyloric stenosis
iv. Perforation

20
Q

The selected treatment for PUD depends on:

A

i. Etiology
ii. Whether it is new or recurrent
iii. The presence of complications

21
Q

Mention 6 goals of PUD therapy.

A
  1. To relieve dyspeptic symptoms
  2. To reduce acid secretion
  3. To promote epithelial healing
  4. To prevent complications
  5. To prevent recurrence
  6. To eradicate H. pylori infection.
22
Q

Mention 5 non-pharmacological approaches to PUD management.

A
  1. Avoid exposure to exacerbating factors e.g. spicy foods, caffeine
  2. Reduce psychological stress
  3. Avoid smoking
  4. Avoid alcohol consumption
  5. Surgical intervention
23
Q

What are the goals of pharmacotherapy in PUD?

A

i. To eradicate H. pylori infection
ii. To reduce morbidity
iii. To prevent complications

24
Q

What are the classes of pharmacological agents used in PUD?

A
  1. Acid-antisecretory agents:
    - H2 receptor antagonists e.g. Cimetidine, Ranitidine
    - PPIs e.g. Omeprazole, Esomeprazole
    - Potassium competitive acid blockers (PCASBs): competitively block H+ ions from back diffusing into the mucosa e.g. Vonoprazan
  2. Mucosa protectants or cytoprotective agents e.g. Bismuth, Misoprostol, Sucralfate and antacids.
    These agents stimulate mucus production and enhance blood flow through the GI lining. They also work by forming a coating that protects the ulcerated tissue.
  3. Agents that eradicate H. pylori
25
Q

Two tests used to confirm H. pylori are:

A
  1. Breath test (Carbon Isotope Urea Breath Test (UBT))
  2. Stool test (Stool PCR Test)
26
Q

The primary goal of treatment of H. pylori ulcer is _____________

A

to completely eradicate the organisms using an effective antibiotic regimen.

27
Q

What are the properties of an ideal regimen chosen for PUD treatment?

A

i. Proven efficacy
ii. Minimal side effects
iii. Low risk of development of bacterial resistance
iv. Cost effectiveness

28
Q

What are the recommended primary regimen for treatment of uncomplicated H. pylori ulcer?

A

Triple therapy (PPI + Amoxicillin + Clarithromycin):
1. Omeprazole 20mg + Amoxicillin 1g + Clarithromycin 500mg Twice daily for 14 days

  1. Lansoprazole 30mg + Metronidazole 500mg + Clarithromycin 500mg Twice daily for 14 days

**Amoxicillin may be replaced by metronidazole or tinidazole in patients with penicillin allergy.

29
Q

When is quadruple therapy used? What is the regimen?

A

Quadruple therapy is reserved for patients in whom the standard course of treatment (triple therapy) has failed.

Quadruple therapy:
Ranitidine 150mg BID (or PPI) + Metronidazole 250mg QID + Tetracycline 500mg QID + Bismuth Subsalicylate 525mg QID For 14 days.

30
Q

What is the recommended treatment in patients with complicated H. pylori ulcer?

A

Treatment with a PPI beyond the 14-day course of antibiotics and until the confirmation of the eradication of H. pylori.

31
Q

What are 3 reasons why patients my remain infected with H. pylori after the initial course of therapy?

A
  1. Reinfection
  2. Non-adherence with initial regimen
  3. Antimicrobial resistance
32
Q

Mention 5 potential adverse drug events involved with H. pylori ulcer treatment.

A
  1. Taste disturbance (Metronidazole and Clarithromycin)
  2. Nausea
  3. Vomiting
  4. Abdominal pain
  5. Diarrhoea
33
Q

What are the factors associated with decreased adherence?

A

i. Large number of medications
ii. Frequent drug administration
iii. Long treatment duration
iv. Use of drugs with intolerable side effects

34
Q

What is the course of treatment in patients with NSAID-induced ulcer?

A
  • Cessation of NSAID use
  • PPIs, H2RAs or Sucralfate
35
Q

In patients with a known history of ulcer in which NSAIDs cannot be avoided, what is recommended?

A
  1. Lowest dose and duration of NSAID
  2. Co-therapy with a PPI or Misoprostol
  3. Changing to a COX-2 selective inhibitor e.g. Celecoxib, Rofecoxib
36
Q

Primary prevention of NSAID-induced ulcers includes:

A
  1. Avoiding unnecessary use of NSAIDs
  2. Using Acetaminophen or nonacetylated salicylates when possible
  3. Using the lowest effective dose of an NSAID
  4. Switching to less toxic NSAIDs, such as newer NSAIDs or COX-2 inhibitors
37
Q

In which cases is prophylactic therapy recommended?

A
  • Patients with NSAID-induced ulcers who require daily NSAID treatment
  • Patients with a history of PUD or a complication such as GI bleeding
  • Patients with concomitant steroids or anticoagulants
  • Patients with significant comorbid medical illnesses
38
Q

List 3 prophylactic regimens used to reduced the risk of NSAID-induced ulcers.

A
  1. Misoprostol 100-200mcg QID
  2. Omeprazole 20-40 mg QID
  3. Lansoprazole 15-30 mg QID
39
Q

Patients with refractory ulcers must undergo thorough re-evaluation such as:

A
  • repeated endoscopies
  • biopsies for microbiology and histology to rule out malignancy
  • determination of serum-gastrin level for Zollinger Ellison syndrome
  • patient compliance
  • recent NSAID ingestion
39
Q

What is refractory or intractable peptic ulcer?

A

It is ulcer that fails to heal completely after 8 weeks (DU) to 12 weeks (GU), despite appropriate treatment with modern antiulcer therapy in a compliant patient.

40
Q

Surgery is the first response for patients with refractory peptic ulcer.

True or False?

A

False.
Surgery is reserved for patients whose ulcers fail to respond to optimal medical treatment or in which complications necessitate intervention.

PCL 424 (12 decks)

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