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MD3002 > Treatment of peptic ulceration and inflammatory bowel disease > Flashcards

Treatment of peptic ulceration and inflammatory bowel disease Flashcards

1
Q

What do we need gastric acid for ?

A

Digestion of food
Iron absorption
Killing pathogens

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2
Q

Identify the main protective mechanisms against gastric acid.

A

1) Mucous secreting cells:
- Trap bicarbonate ions (alkaline)
- Creates gel like barrier
- Important protective layer

2) Prostaglandins locally produced
- Stimulates secretion of mucus and bicarbonate
- Dilate mucosal blood vessels
- Cytoprotective (NSAIDs reduces amount of prostaglandin which is why side effects occur e.g. increased ris kof peptic ulcers and GORD)

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3
Q

What happens if there is a disturbance in gastric protective mechanisms + increased acid secretions ?

A

Risk of GORD, ulcer

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4
Q

Why do NSAIDs have side effects (in the context of gastric protective mechanisms) ?

A

Many NSAIDs disturb the protective functions of the stomach (inhibit cyclo-oxygenase-1; enzyme responsible for synthesis of prostaglandins), so increase risk of GORD and of ulcers

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5
Q

How much gastric juice is produced per day ?

A

Around 2.5 L of gastric juice is produced per day

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6
Q

Identify the main cells responsible for gastric acid production.

A

1) Oxyntic / parietal cells produce HCl and intrinsic factor
2) Chief/peptic cells produce proenzymes (e.g. pepsinogen and prorennin)

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7
Q

What is the function of intrinsic factor ? What condition may result from the lack of it ?

A

Helps body absorb B12

B12 deficiency anaemia

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8
Q

Describe the process of secretion of hydrochloric acid by the gastric parietal cell, explaining exactly where this occurs.

A

Villus like projections

  • K+H+ ATPase (proton pump) gets acid (H+) out into the lumen of the canaliculus (extensive secretory networks), while bringing K+ into the parietal cell.
  • Antiport brings chloride and takes bicarbonate out .
  • Hydrogen joining with the chloride makes HCL.
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9
Q

Define secretagogue, and identify the main endogeneous gastric acid secretagogues.

A

Substance that causes another substance to be secreted.

1) Gastrin
2) ACh
3) Histamine

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10
Q

GASTRIN

  • Cells releasing it, and their location
  • Trigger
  • Other effects
A

GASTRIN:

  • Cells releasing it, and their location: G (gastrin) cells, located in the gastric antrum and duodenum
  • Trigger: Proteins in food have a strong effect on the G cells, causing release of gastrin into blood, which stimulates secretion of acid by parietal cells (through the proton pump)
  • Other effects: Also increases pepsinogen secretions, stimulates blood flow, and increases gastric motility
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11
Q

ACETYLCHOLINE

  • Cells releasing it
  • Gastric acid producing effect
  • Other effects
A

ACETYLCHOLINE

  • Cells releasing it: Neurons
  • Effect: Stimulates muscarinic receptors on surface of parietal cells
  • Other effects: Stimulates muscarinic receptors on surface of histamine containing cells
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12
Q

HISTAMINE

  • Cells releasing it
  • Trigger
  • Gastric acid producing effect
A

HISTAMINE

  • Cells releasing it: Mast cells lying close to parietal cell
  • Trigger: Histamine release increased by gastrin and ACh
  • Gastric acid producing effect: Acts on parietal cell H2 receptors
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13
Q

Define dyspepsia and GORD.

A

Dyspepsia: pain or discomfort centered in upper abdomen, exacerbated by food (relieved by GAVISCON)

GORD: acid reflux, associated with waterbrash (and retrosternal burning )

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14
Q

Identify managements for dyspepsia and GORD.

A

For both:

1) Lifestyle advice
- healthy eating
- weight reduction (high BMI can impact on sphincter at top of stomach)
- smoking cessation
- raise the head of the bed (to help with gravity, prevents acid travelling up ) and have a main meal well before going to bed

2) Avoid known precipitants
alcohol 
coffee 
chocolate 
fatty foods

3) Stop NSAIDs where appropriate/applicable

4) Consider over the counter remedies (if no red flags)
- Antacids (salts of magnesium and aluminum, directly neutralize acid + inhibit activity of peptic enzymes)
- Alignates (increases viscosity and adherence of mucus to oesophageal mucosa)
- Simeticone (antifoaming agent, helps bloating, flatulence which helps with dyspepsia but not GORD)

5) H. Pylori testing

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15
Q

Identify a world region with a high incidence of H. Pylori.

A

Africa

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16
Q

What is H. Pylori a causative for ? risk factor for ? associated with ?

A

-Causative factor for gastric and duodenal ulcers
-Risk factor for gastric cancer (adenocarcinoma)
-Strong link with MALT lymphomas
-Also associated with:
• Dyspepsia
• Atrophic gastritis
• Iron deficiency anaemia (irritation of stomach causes bleeds)
• Idiopathic Thrombocytopenic (low platelet) Purpura

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17
Q

Explain the pathogenesis of H. Pylori in the stomach.

A
  • H pylori survive gastric strong acid
  • With flagella, will dive into niche with neutral pH, between mucosa and epithelium
  • Produce urease which raises the gastric pH, allowing it to colonise, and converts blood urea to ammonium which weakens mucosal barrier
  • Mucosal surface, which protects epithelium is damaged so epithelium is exposed to HCl, which then destroys surface epithelium of stomach
  • Damaged epithelium means inflammatory cells, both acute and chronic accumulate, cells die, ulcer can occur
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18
Q

What are the main symptoms, time frame, and cells involved of acute H. Pylori infection ?

A

ACUTE H. PYLORI INFECTION

  • Symptoms: nausea, dyspepsia, malaise and halitosis
  • Time frame: about two weeks
  • Cells involved: Gastric mucosa is inflamed with neutrophils and inflammatory cells with marked persistent lymphocyte penetration
19
Q

What is chronic H Pylori infection essentially ?

A

Local inflammation + gastritis

20
Q

What factors does the outcome of chronic H pylori infection depend on ?

A 
Pattern of inflammation 
Host response 
Bacterial virulence 
Environmental factors 
Patient age
21
Q

Identify the main diagnostic tests for H. Pylori infection.

A

Non-invasive diagnostic tests:

  • Urea breath test
  • Stool antigen

Biopsy based diagnostic tests:
-Histology

22
Q

Explain the urea breath test as a diagnostic test for H. Pylori infection.

A

Urease breaks urea down into NH3 and an isotope of CO2. We can detect the latter when we breath out.

23
Q

Describe first line treatment for H. Pylori infection.

A

• Offer people who test positive for H. pylori a 7-day, twice-daily course of treatment with:

1) a PPI (they inhibit proton pump which results in HCl secretion) and amoxicillin and either clarithromycin or metronidazole (choose the treatment regimen with the lowest acquisition cost, and take into account previous exposure to clarithromycin or metronidazole)

OR (if penicillin allergy)
2) a PPI (see table) and clarithromycin and metronidazole

OR (if penicillin allergy + previous exposure to clarithromycin)
3) a PPI and bismuth and metronidazole and tetracycline

24
Q

Identify the main PPIs.

A

Omeprazole

Lansoprazole

25
Q

PROTON PUMP INHIBITORS

  • Indications
  • Mechanism
  • Administration
A

PROTON PUMP INHIBITORS
-Indication: peptic ulcer disease, reflux oesophagitis, one component of H pylori eradication and Zollinger-Ellison syndrome
-Mechanism: Basal and simulated gastric acid secretion reduced. Drug is weak base and accumulates in acid
environment of the canaliculi of the stimulated parietal cell
-Administration: usually oral

26
Q

Explain the mechanism of action of Omeprazole.

A

Inhibits K+H+ATPase by binding irreversibly to it

27
Q

Identify side effects, and cautions of PPIs.

A 
• Relatively uncommon 
• Includes:
Headache
Diarrhoea
Somnolence 
Gynaecomastia
Pain in muscles / joints
• Caution in liver disease, pregnancy, breast feeding 
• May mask the symptoms of gastric cancer
28
Q

Explain how peptic ulcers arise.

A

• Can be associated with infection of gastric mucosa with H. Pylori.

• Imbalance between:
Mucosal-damaging (acid, pepsin) substances and Mucosal protecting (mucus, bicarbonate, prostaglandins, nitric oxide)

29
Q

Describe the initial treatment for peptic ulcer disease.

A

If dyspepsia or GORD symptoms and not responding to first line measures (or any red flags), then endoscopy (so diagnose peptic ulcer). Then biopsy for H. Pylori detection.

1) H Pylori positive
• Offer H pylori eradication if peptic ulcer disease and H pylori +ve

2) NSAID associated ulcers
• Stop the use of NSAIDs where possible. Offer full-dose PPI (see table) or H2RA therapy for 8 weeks and, if H pylori is present, subsequently offer eradication therapy

3) H pylori negative; no NSAID
• Offer full-dose PPI (see table) or H2RA therapy for 4 to 8 weeks

30
Q

HISTAMINE H2 RECEPTOR ANTAGONISTS

  • Indications
  • Mechanism
A

HISTAMINE H2 RECEPTOR ANTAGONISTS

  • Indications: peptic ulcers and reflux oesophagitis
  • Mechanism: competitively inhibits histamine actions at all H2 receptors + inhibits histamine, gastrin, and ACh stimulated acid production + pepsin secretion also falls with reduction in V of gastric juice
31
Q

Which of PPIs or Histamine H2 receptor antagonists are used more ? Why ?

A

PPIs more used because less side effects and more effective

32
Q

Give examples of histamine H2 receptor antagonists, stating the bioavailability, half life, and excretion of each. How are these administered ? Are these available over the counter ?

A

Ranitidine (approx. 50% bioavailability, half life 2- 2.5hrs, renal excretion)
Cimetidine (>60% bioavailability, half life 2 hours, renal excretion)

Administered orally
Low dose available OTC.

33
Q

Identify the main side effects of histamine H2 receptor antagonists.

A 
• Side effects rare:
Possible Diarrhoea
Muscle pains 
Alopecia
Hypergastrinaemia
  • Ranitidine better tolerated of the two
  • Cimetidine:

1) Can interact with androgen receptors and cause gynaecomastia in men, and decreased sexual function
2) Inhibits cytochrome P450, which slows the metabolism (and potentiates action) of range of drugs e.g. oral anticoagulants and tricyclics
3) Confusion in elderly

34
Q

What is the next line treatment if first line treatment fails (e.g. due to antibiotic resistance) or reinfection occurs, (which is unlikely) for peptic ulcer disease?

A

First, offer those with peptic ulcer and H. pylori a repeat endoscopy after 6 to 8 weeks of start of treatment and perform re-testing of H pylori using carbon 13 urea breath test. If unhealed ulcer, then:

1) Exclude non-adherence, malignancy, failure to detect H. Pylori, inadvertent NSAID use, other ulcer-inducing medication, and rare causes such as Zollinger-Ellison syndrome or Crohn’s disease.
2) If symptoms recur after initial treatment, offer a PPI to be taken at lowest dose possible to control symptoms.

35
Q

What is Inflammatory Bowel Disease ?

A

Means Ulcerative Colitis or Crohn’s

36
Q

Which parts of the GI are affected by UC and Crohn’s respectively ?

A
  • UC affects colon and rectum, inner lining

- Crohn’s can affect any part of GI tract, through whole wall (skip lesions, isolated lesions randomly separated)

37
Q

How prevalent is UC ? Crohn’s ?

A

UC affects 1 in 400 (UK); Crohn’s 1 in 700

38
Q

What is the age of onset of UC ? Crohn’s ?

A

Age of onset for Inflammatory Bowel peaks at 15-30 and 50-70

39
Q

Identify the main symptoms of Inflammatory Bowel Disease.

A 
Abdo pain
Diarrhoea
PR blood
Weight loss
Systemic upset
Ulcers
Fever
40
Q

What is the prognosis of Inflammatory Bowel Disease ?

A

Very variable prognosis

41
Q

Identify the main investigations performed for Inflammatory Bowel Disease.

A
  • FBC, CRP (raised CPR, raised WBC)
  • Stool MCS (detect potential infective cause (none in case of inflammatory bowel disease))
  • Faecal calprotectin (inflammatory substance bowel produces in inflammatory bowel disease (not present in irritable bowel, can help exclude it))
  • CT scan/MRI (looking for complications)
  • Endoscopy (sigmoidoscopy, colonoscopy) (of lower GI) + biopsies (of sample of inflammation)
42
Q

Describe treatment for Inflammatory Bowel Disease.

A

-First-line (chronic management):
♦ Aminosalicylates e.g. mesalazine
♦ DMARDs (Disease-modifying antirheumatic drugs) e.g. azathioprine, methotrexate (suppress the immune and inflammatory response to improve prognosis, but downside is if WBC count drops (neutropenia) more likely to develop infection and neutropenic sepsis, so regular blood test monitoring required)

-Second-line (first-line failed):
♦ Biologics e.g. infliximab
(also impair immune response)

-For acute flare:
♦ Corticosteroids e.g. prednisolone
(cannot be used chronically, because risk of diabetes, obesity)

-Also:
♦ Symptomatic relievers (analgesics, antispasmodics, laxatives, “constipators”)
♦ Surgery (because bowel cancer risk if unable to control disease)

43
Q

What is a potential problem with giving laxatives as a symptom reliever in inflammatory bowel disease ?

A

Can get intercurrent infection due to that (don’t usually want to slow bowel down)

MD3002 (95 decks)

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