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Unit 9 PBL cases > Peptic ulcer > Flashcards

Peptic ulcer Flashcards

1
Q

How does H.pylori infection lead to duodenal ulceration?

A

Parietal cells secrete HCl - produces acidic layer on top of mucus layer
H. pylori releases urease - breaks down urea -> ammonia and CO2, ammonia neutralises acid
Flagella - moves towards columnar cells, adheres to cells using LPS on its surface
Secretes endotoxins - VacA and CagA - causes cell death and inflammation
Folding in of acidic and mucus layers -> ulcer
H. pylori decreases somatostatin release > less inhibition of acid secretion > more acid in duodenum > damage epithelial lining > ulcer

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2
Q

Adaptations of H. pylori

A

-Urease production - breaks down urea to produce ammonia which neutralises HCl
-Motility - have 2-6 unipolar flagella, so can move into mucus and reach epithelium
- Alters gastric mucus - raises the pH, decreases viscoelastic properties = easier to enter
- Adhesin molecules - uses adhesin molecules to bind to epithelium
- Biofilm - shield from antibiotics
- Modulates immune response - release toxins (VagA, CagA) killing surrounding cells incl immune cells

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3
Q

How does H. pylori colonise the stomach?

A

-Uses adhesion molecules to bind to gastric epithelium
- Biofilms protect from harsh environmental factors
- Cytoplasmic urease neutralises stomach acid
- Releases toxins
- Pylori uses mucus as a barrier
- Pylori will acquire N from ammonia from urease and break down mucus to receive glycans as an energy source

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4
Q

How is H.pylori transmitted?

A

Oral-oral
Faecal-oral

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5
Q

Why is H. pylori most likely to colonise the duodenum and antrum?

A

Low gastric acid levels: furthest from the acid secreting parietal cells in the fundus and body of the stomach
Chemotaxis: has chemotactic response to areas with lower acidity
Nutrient availability: presence of partially digested food or nutrients
Host receptors: bacterial adhesins bind to receptors on gastric and duodenal epithelium
Mucosal protection: duodenum has a thinner mucosal lining (doesn’t need as much protection from acid etc)

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6
Q

Where does H. pylori colonise?

A

Antrum of the stomach and the duodenum

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7
Q

What are the complications of an untreated peptic ulcer?

A

Perforation of the organ wall - can perforate near arteries - haemorrhaging - haemorrhagic shock
Perforation - allows bacteria into the bloodstream and peritoneal cavity - peritonitis and sepsis
Can narrow or occlude the gut tube if scarring and fibrosis occurs

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8
Q

How does H.pylori invade to cause peptic ulcers?

A

Release adhesins to attach to gastric endothelial cells
Release proteases and lipases which degrade gastric mucus
Allows gastric acid and pepsin to damage the epithelial lining
Cause inflammatory response > irritation > neutrophils, lymphocytes, plasma cells and macrophages invade > epithelial injury and death > ulcer

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9
Q

How does H. pylori survive in the stomach?

A

Activates self cytoplasmic urease
Converts urea > ammonia + CO2
Ammonia neutralises the gastric acid that enters the outer membrane of the bacteria
Release adhesins to adhere to gastric epithelial cells

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10
Q

How can NSAIDs cause peptic ulcers?

A

NSAIDs are weak acids
Become protonated when mixed with gastric acid
Enters epithelial cells, releases the H+ and is trapped
Reduces mitochondrial energy production, cell integrity, increases cell permeability > topical irritation > cell death > erosions > ulcers

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11
Q

How does COX2 inhibition specifically lead to peptic ulceration?

A

Increasing leukocyte adhesion leading to ischaemia and release of ROS and proteases > mucosal injury

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12
Q

How does COX1 inhibition specifically lead to peptic ulceration?

A

fewer prostaglandins synthesised
- Decreased mucus and bicarbonate secretion, decreased mucosal BF
-Increased gastric acid and pepsin production
- Reduction in BF most damaging
- Epithelium is damaged by gastric acid and pepsin
- Less mucus and bicarbonate produced > cycle repeats

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13
Q

Non-selective NSAIDs

A

e.g. aspirin, ibuprofen, naproxen, indomethacin
Will inhibit both COX 1 and 2
Aspirin will irreversibly inhibit these enzymes

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14
Q

What role specifically does COX 1 have specifically in the gut?

A

Inhibit gastric acid and pepsin secretion
Stimulates mucus and bicarbonate secretion
Increases mucosal BF - vasodilation
Reduces epithelial permeability
Inhibits cell proliferation to maintain mucosal barrier

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15
Q

What are the roles of COX1 and 2?

A

COX1 produces prostaglandins for homeostatic functions everywhere incl GI tract
COX2 produces prosatglandins by inflamed cells and fibroblasts to mediate pain and inflammation. Releases growth factors. Produces prostacyclin to reduce leukocyte adherence and platelet aggregation
Converts arachidonic acid to PGE2

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16
Q

What are the most common causes of peptic ulcers?

A

Chronic NSAID use
H. pylori infection

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17
Q

What is a peptic ulcer?

A

Defect in the mucosa of the stomach or duodenum, at least down to the basement membrane, else will be called an erosion

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18
Q

What are the symptoms of a duodenal ulcer?

A

Epigastric pain - may radiate to back
Pain worse at night if duodenal
Pain often improves just after eating if duodenal
Indigestion
Bloating after eating
Nausea and vomiting
Weight gain due to improved symptoms after meal

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19
Q

What are the difference in symptoms with a duodenal vs gastric ulcer?

A

Duodenal: pain occurs a few hours after eating when stomach is empty - may see weight gain as eating helps pain
Gastric: pain occurs from eating - may see weight loss

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20
Q

What tests can be used to diagnose a H.pylori infection?

A

Blood test, stool test, biopsy, endoscopy, breath test

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21
Q

How does the urea breath test work?

A

H.pylori urease breaks down urea to produce carbon and ammonia
Normally gastric urea is C12, so C13 is used in the urea solution
Urease will catalyse urea into the ammonia and 13 labelled C13 which is exhaled.
The amount of C13 in the breath will be proportional to presence of H.pylori

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22
Q

What is the procedure of the urea breath test?

A

Exhale into a bag, the amount of CO2 exhaled will act as the baseline
Drink the urea solution
Breathe into another bag to detect C13
If the amount of C13 is relatively higher than the first sample, this is a positive test for H.pylori

23
Q

How may a stool test diagnose H.pylori infection?

A

Tested for Hpylori presence and confirm diagnose and cure after treatment

24
Q

How can a blood test diagnose H.pylori infection?

A

Measure presence of antibodies for H.pylori, however has limited accuracy as this can be positive post infection

25
Q

What are the risk factors for peptic ulcers?

A
  • Smoking
  • Chronic NSAID use
  • Caffeine
  • Alcohol
26
Q

How is smoking a risk factor for peptic ulcers?

A

Increases gastric acid secretion, lower pH
Modifies mucus secretion
Alters mucosal repair int he gut
Reduces blood flow to the GI mucosa, leads to mucosal damage and impaired healing

26
Q

How is chronic NSAID use a risk factor for peptic ulcers?

A

Inhibits COX1 > reduces cytoprotective mucosal prostaglandins and reduces HCO3- secretion

26
Q

How is caffeine a risk factors for peptic ulceration?

A

Stimulates gastrin and HCl secretion

27
Q

How is alcohol a risk factor for peptic ulceration?

A

Increased acid secretion via gastrin

28
Q

Why was the patient advised to avoid PPIs and antibiotics for two week before testing for H.pylori presence?

A

PPIs suppress acid secretion by inhibiting the H/K ATPase pump in gastric pareital cells
Inhibits urease activity of H.pylori, no CO2 produced that contains 13C to be detected
Inaccurate result
Antibiotics interfere with accuracy as well

29
Q

Magnesium trisilicate - pharmacology and physiology

A

Neutralises HCl to increase pH
Forms colloidal mixture which lines the stomach wall to prevent further damage
Produces 2H2SiO3 and SiO3

30
Q

What type of drug is magnesium trisilicate?

A

Antacid

31
Q

Aluminium hydroxide - pharmacology and physiology

A

Neutralises HCl to form AlCl3 to increase pH
Inhibits pepsinogen - pepsin conversion by increasing pH and via adsorption
Prevents ulceration and acid reflux

32
Q

What type of drug is aluminium hydroxide?

A

Antacid

33
Q

Why should a patient with a H. pylori infection/peptic ulcer avoid ibuprofen?

A

The inhibition of COX1 can cause the stomach to become more susceptible to damage from stomach acid - cause inflammation and peptic ulcers

34
Q

Ibuprofen - type of drug and mechanism of side effects

A

NSAID
Non selective inhibitor of COX 1 and 2 enzymes
COX1 enzymes produces prostaglandins that stimulate mucous and bicarbonate secretion - maintains mucosal integrity
CO2 enzymes produces prostaglandins in response to inflammatory cytokines - mediate pain and inflammation

35
Q

Bismuth subsalicylate - pharmacology and physiology

A

Once orally ingested - hydrolysed in HCl to form salicylic acid and bismuth oxychloride
Blocks bacterial enzyme activities
Bismuth oxychoride and other bismuth salts produced - prevents bacterial adhesion and growth on mucosal cells
> Prevents intestinal secretion and fluid loss
> Promotes electrolyte and fluid reabsorption
Salicyclic acid - anti-inflammatory, inhibits COX enzymes and prostaglandin production

36
Q

What type of drug is bismuth subsalicylate (pepto bismol)?

A

Antacid/antidiarrheal agent

37
Q

Tetracycline - pharmacology and physiology

A

Bonds to 30S ribosomal subunit, prevents binding of tRNA to mRNA-ribosome complex
Prevents protein synthesis
Binds to 50S ribosomal subunit, alters cytoplasmic membrane - intracellular components leak from bacterial cells

38
Q

What type of drug is tetracycline?

A

Broad spectrum antibiotic
Bacteriostatic

39
Q

Metronidazole - clinical - uses and side effects

A

Uses: Bacterial infections, prevent post-surgery infections, inflammatory lesions of rosacea
Side effects: nausea and diarrhoea

40
Q

Metronidazole - pharmacology and physiology?

A

MOA not fully known
Aerobic bacteria and protozoa produces an intermediate in metronidazole reduction
The metabolites then bind to DNA and electron transport proteins, preventing nucleic acid synthesis

41
Q

What kind of drug is mteronidazole?

A

Nitroimidazole class antibiotic
Bactericidal
Inhibit DNA synthesis

42
Q

What drugs may be prescribed to treat H.pylori infection if patient has a penecillin allergy or has recently used clarithromycin?

A

Metronidazole (instead of clarithromycin to prevent antibiotic resistance)
Tetracycline (instead of amoxicillin, if penecillin allergy)
Bismuth subsalicylate

43
Q

What drugs would be prescribed for a H. pylori infection?

A

Triple therapy approach:
Two antibiotics to kill the bacteria
PPI to increase pH, as in low pH it takes coccoid from which is resistant to antibiotics
Clarithromycin or metronidazole (depending on recent use of either)
Amoxicillin
PPI - esomeprazole, lansoprazole, omeprazole

44
Q

Esomeprazole - clinical - uses, side effects?

A

Uses: treat infection, heartburn, acid reflux, GORD, prevent stomach ulcers
Side effects: Headache, diarrhoea and stomach pain

45
Q

Esomeprazole - pharmacology and physiology?

A

Parietal cells pump K+ into cell, H+ out into lumen of stomach > activates pepsinogen into active pepsin form > damage cells
Irreversibly inhibits H+/K+ ATPase pump on gastric parietal cells > inhibits gastric acid secretion > increases pH > decreases mucosal damage

46
Q

What type of drug is esomeprazole?

A

PPI

47
Q

Amoxicillin - clinical - uses and side effects?

A

ENT infection e.g. tonsilitis
H. pylori eradication - triple therapy with clarithromycin and lansoprazole
UTIs
Lower resp tract infections
Side effects: nausea and diarrhoea

48
Q

Amoxicillin - pharmacology and physiology

A

Mimics d-ala-d-ala transpeptidase sequence and binds to penecilin-binding proteins which prevents transpeptidation (cross linking in cell wall synthesis
Activates autolytic enzymes -> cell lysis

49
Q

What type of drug is amoxicillin?

A

Beta lactam antibiotic
Bactericidal - interferes with bacterial cell wall synthesis

50
Q

Clarithromycin: clinical - use and side effects?

A

Used to treat upper and lower resp tract infections, skin infections e.g. cellulitis, ear infections, H.pylori infections
Alternative to penecillin for strep throat
Side effects: diarrhoea, decreased appetite, dizziness

51
Q

Clarithromycin - pharmacology and physiology?

A

Reversibly binds to 23S sRNA component of 50s ribosomal subunit of the ribosome
-> Inhibits translocation of aminoacyl tRNA and prevents peptide chain elongation
-> Inhibition of protein synthesis causes cell death (so can be bactericidal in certain concs)

52
Q

What type of drug is clarithromycin?

A

Broad spec antibiotics
Macrolide - bacteriostatic

Unit 9 PBL cases (3 decks)

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