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Block 1 - Treatment And Prevention Of Illness > GI - Peptic Ulcer Disease > Flashcards

GI - Peptic Ulcer Disease Flashcards

1
Q

what does the oesophagus do

A
  • The oesophagus delivers food from the mouth to the stomach, but has little active involvement in digestion & absorption
  • Food is retained in stomach while digested by several enzymes & HCl
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2
Q

what does SI do

A

Absorption mostly takes place in small intestine

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3
Q

what does LI do

A

Large intestine reabsorbs water from indigestible products allowing solid waste to be expelled

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4
Q

Structure of the gastrointestinal wall

A

Mucosa
Submucosa
Muscularis
Serosa

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5
Q

Structure of the gastrointestinal wall - mucosa

A

Mucosa largely made of sheets of epithelial cells which have tight junctions between them and act a good barrier to allow active transport across

DIGESTION AND ABSORPTION OF NUTRIENTS

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6
Q

Structure of the gastrointestinal wall - submucosa

A

alot of arteries and veins - green vessel is part of lymph system

DISTRIBUTION OF NUTRIENTS TO THE REST OF BODY

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7
Q

Structure of the gastrointestinal wall - muscularis

A

largely smooth muscle, few voluntary muscles. Work in patterns of contraction, run in different directions which allows active movement all the way down the GI tract

Movement of nutrients along GI tract

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8
Q

what parts is the stomach made up of

A 
Fundus
Cardia
Body (Corpus)
Antrum
Pylorus
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9
Q

What is the gateway into the stomach

A

cardia

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10
Q

Pylorus and cardia have which muscles

A

Pylorus and cardia have sphincter muscles to control movement in and out

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11
Q

Histology of the Gastric Glands

A

Oxyntic gland (-> gastric acid)

  • surface mucous cell secrete mucus and bicarbonate which protect stomach from secretion of gastric acid
  • parietal cell
  • mucous neck cell
  • enterochromaffin like cell (histamine)
  • d cell (somatostatin)
  • cheif cell (pepsinogen)
  • enterochromaffin cell (ANP)

Pyloric gland (-> gastrin)

  • No pareital or chief cells
  • surface mucous cell secrete mucus and bicarbonate which protect stomach from secretion of gastric acid
  • mucous neck cell
  • g cell (gastrin)
  • d cell (somatostatin)
  • enterochromaffin cell (ANP)
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12
Q

Parietal cells secrete

A

HCl, intrinsic factor (vitamin B12 absorption)

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13
Q

cheif cells secrete

A

Pepsinogen, Gastric lipase

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14
Q

mucous cells secrete

A

Mucous, bicarbonate

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15
Q

ECL cells secrete

A

Histamine

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16
Q

G Cells secrete

A

gastrin

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17
Q

D cell secrete

A

somatostatin

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18
Q

Enterochromaffin Cells secrete

A

Atrial natriuretic peptide (ANP)

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19
Q

Parietal Cell Gastric Acid Secretion

A

draw diagram

Gastric juice:

  • 2000 – 3000 ml per day
  • Carbonic anhydrase makes H2CO3 which dissociates into H+ and HCO3-

actively transport protons out into the stomach lumen by potassium hydrogen ATPase. Critical in production of gastric acid

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20
Q

Regulation of Gastric Acid Secretion - what does an increase in calcium do

A

draw diagram

Increase in calcium increases the number of protons and increases the amount of acid which is secreted

21
Q

Regulation of Gastric Acid Secretion 2

A

draw diagram

22
Q

Hormonal Control of Acid Secretion

A

draw diagram
High pH, Gastric Distension -> Pyloric glands secrete gastrin -> Oxyntic gland parietal cells stimulated by Gastrin -> Acid secretion is increased

Pyloric glands mainly found in the antrum in the stomach, reduces

23
Q

Pepsin most effective in

A

low pH (~2)

24
Q

role of mucus

A

Mucus (1-3 mm thick) protects gastric wall

from being digested by pepsin

25
Q

what reduce acid secretion

A

prostaglandins

26
Q

Imbalance between acid production and mucosal protection leads to:

A
  • Acid damage to submucosal layer

- Pepsin digestion of submucosal layer

27
Q

Dyspepsia =

A

symptoms associated with upper GI tract – heartburn, pain, nausea, patients may describe as “indigestion”

28
Q

Peptic Ulcer

A

Symptoms
– crater-like wound in mucosa of upper GI tract or stomach
– may lead to haemorrhage and perforation, inflammation

29
Q

Two important factors in development of peptic ulcer

A
  • Helicobacter pylori infection (H pylori protected in mucus gel, secretes agents causing a persistant inflammation that waekens the mucosal barrier)
  • NSAID treatment (Prostaglandins reduce acid secretion, increase mucus and bicarbonate secretion and increase mucosal blood flow. NSAIDs (COX inhibitors) reduce this.
30
Q

Drug treatment of peptic ulcer aims to promote ulcer healing by:

A
  • reducing acid secretion
  • increasing mucosal resistance
  • Eradicating H. pylori
31
Q

Peptic ulcer and complications

A

Full thickness breach of mucosa in lower oesophagus, stomach or
duodenum that fails to heal over a reasonable period.
• Complications:
• Haemorrhage – typically in duodenal ulcers which erode into the gastroduodenal artery leading to haematemesis
• Perforation – acute abdominal pain and generalized peritonitis
• Fibrous stricture – obstruct gastric outflow

32
Q

Gastritis – H. pylori

A

-H. Pylori-associated gastritis:
Most common cause of gastritis; bacterial transmission is from person to person Lives in the mucus layer of the stomach

-Corpus Gastritis:
Oxyntic glands predominate in corpus
H. pylori induced inflammation leads to atrophy of oxyntic glands & reduced acid secretion
• bacteria spreads proximally
• tissue damage can lead to gastric ulcer.
• Increased risk of gastric cancer

-Pyloric gastritis:
Pyloric glands predominate in pylorus
H. pylori induced inflammation leads to increased gastrin secretion and decreased somatostatin secretion → parietal cell proliferation and acid hypersecretion (via endocrine effect on oxyntic glands)
Excess acid in the duodenum overwhelms mucosal and acid-neutralising protective mechanisms → duodenal ulcers

33
Q

Corpus vs. Pyloric Gastritis

A

increased acid secretion in pyloric gastritis

34
Q

role of Locally produced prostaglandins (PGE2 and PGI2):

A
  • reduce acid secretion
  • increase mucus and bicarbonate secretion
  • increase mucosal blood flow
35
Q

NSAID-induced Peptic Ulcers

A

• Non-Steroidal Anti Inflammatory Drugs – Inhibit prostaglandin production
• Endogenous prostaglandins have gastroduodenal protective effect
– Reduce HCl production
– Increase mucus and bicarbonate production – better protection of gastric epithelium
• Aspirin doses as low as 10 mg/day inhibit gastric PG production and cause stomach damage
– Risk of clinically-relevant GI damage increases with dose

36
Q 
Proton pump inhibitors
• Drugs
• Indications
• PK
• ADR
• Cautions
• Interactions
A

• Drugs
– Omeprazole, Lansoprazole, Esomeprazole (S-isomer of omeprazole), Rabeprazole, Pantoprazole
– Generally more effective in promoting healing than H2 antagonists as can have a profound effect on acid secretion
• Indications
– Reflex oesophagitis, peptic ulcers, H. pylori infection, Zollinger-Ellison syndrome
• PK
– t 1⁄2 ~ 1-2 hr but long duration of action (2-3 days) because they accumulate in the canaliculi of the gland and bind irreversibly to the pump (see next slides)
• ADR
– well tolerated, occasional diarrhoea,
• Cautions
– can mask gastric malignancy
– In liver disease; in pregnant and breastfeeding women
• Interactions
– inhibit P450 – usually minor effect at normal doses,
but can be important for patients taking phenytoin or warfarin

37
Q

Why does omeprazole accumulate in parietal cells

A

At Neutral pH -
• Freely membrane permeable
• Easily enters parietal cells

At pH <4:
nitrogen become protonated
• Membrane permeability much reduced
• Trapped in parietal cells

38
Q 
Histamine H2 antagonists
• Drugs
• Indications
• PK
• ADR
• Cautions
• Interactions
A

• Drugs
– Ranitidine, Cimetidine, Nizatidine, Famotidine
• Indications
– Gastric ulcers, duodenal ulcers, reflux oesophagitis
• PK
– t1/2~2h
• ADR
– cimetidine antagonises androgen receptor – gynaecomastia, sexual dysfunction in men
– Diarrhoea, dizziness, muscle pain, rashes, hypergastrinaemia
• Caution
– can mask gastric malignancy
• Drug Interactions
– cimetidine inhibits P450 – potential interaction with several drugs (oral anticoagulats, tricyclic antidepressants)
– cimetidine inhibits liver blood flow – so can reduce clearance of drugs that have high hepatic metabolism, increasing their conc. (eg propanolol)
– ranitidine doesn’t cause either of these

39
Q

Treatment of H pylori infection

A 
• Drugs
– Amoxicillin
– Clarithromycin
– Metronidazole
– Tetracycline

Triple therapy: proton pump inhibitor plus antibacterial agents (amoxicillin and metronidazole or clarithromycin) 1 to 2 week duration
sometimes bismuth chelate is also included

40
Q

NSAIDS and patients with peptic ulcers

A

• If possible withdraw the NSAID, and treat with PPI or H2 blocker for 8 weeks
• If not possible
– Encourage healing by reducing acid production–PPI probably more effective than H2 antagonist
– If H.pylori present, eradicate
– Misoprostol–counteract the local effect of NSAID

41
Q

NSAIDS block

A

Prostaglandin

42
Q 
Prostglandin E Receptor Agonists
• Drugs
• Indications
• PK
• ADR
• Cautions
A

• Drugs
– Misoprostol
• Indications
– Treatment and prevention of NSAID-induced gastric ulcers
• PK
– Pre-drug, extensively absorbed & de-esterified to active free-acid. Active drug T1/2 = 20-40 minutes – largely excreted in urine
• ADR
– Diarrhoea. Occassionally other GI effects, abnormal vaginal bleeding (including intermenstrual bleeding, menorrhagia, and postmenopausal bleeding), rashes, dizziness
• Cautions
– potent uterine stimulant (has been used to induce abortion)
– inflammatory bowel disease; conditions where hypotension might precipitate severe complications (e.g. cerebrovascular disease, cardiovascular disease)

43
Q

Other drugs available OTC

A

• Bismuth chelate (e.g. Peptobismol)
– mucosa protecting (coating ulcer base, adsorbing pepsin, PG↑, HCO3- ↑); toxic on H. pylori and prevents its mucosal adherence
• Alginates (e.g. Gaviscon – combined with antacid)
– inert compound thought to increase viscosity and promote mucus protection of mucosal surface, mainly in the oesophagus
• Simeticone (e.g.Wind-eze)
– surface active compound, prevents “foaming” and relieves flatulence

44
Q

Antacids

A

• Simplest form of therapy; directly neutralise acids, raising gastric pH (thus also inhibits pepsin ~ above pH 5)
• After a prolonged period → can heal duodenal ulcers (less effective against healing gastric ulcers)
• Typically salts of Mg or Al
• Drugs
– Magnesium silicate or hydroxide
– Aluminium hydroxide
• Indications
– symptomatic relief of dyspepsia
– can provide sufficient alkalinization to allow healing, but requires regular dosing
• PK
– Mg & Al salts poorly absorbed
– Duration of action depends on gastric emptying
• 30 min on empty stomach
• 2 hr after eating
• Liquid formulation faster acting but shorter duration
• ADR
– Al3+ salts → constipation,
– Mg2+ diarrhoea
– Ca2+ containing antacids should be avoided → stimulate gastrin secretion
– Sodium bicarbonate → acts rapidly (pH 7.4↑), CO2 liberated → gastrin secretion; it is also absorbed → large dose causes alkalosis
• Drug Interactions
– absorption of some drugs (eg digoxin, tetracycline) affected
– preferably take > 30 min apart from other drugs

45
Q

GORD (or reflux oesophagitis) is the

A

GORD (or reflux oesophagitis) is the commonest oesophageal disorder

Cause: reflux of gastric content from stomach to oesophagus

Hiatus hernia → function of lower oesophageal sphincter is impaired

Oesophagus: squamous epithelial lining → not designed to resist acidity → inflammation (oesophagitis) → symptoms

Most patients with GORD will have hiatus hernia (although most patients with hiatus hernia do not have GORD)

46
Q

Oesophageal Hiatus Hernia Symptoms:

Complications:

A 
Symptoms:
Retrosternal pain (heartburn) 
Any upper abdominal symptoms may occur

Complications:
GORD is a common condition however only a minority develops serious complications:
• Peptic stricture
• Barett’s oesophageus

47
Q

What causes hiatus hernia and what are the types

A

types:

  • sliding hiatus hernia
  • rolling hiatus hernia

the tightening effect of the diaphragm is lost and part of the stomach is able to bulge through the diaphragm. This allows the acidic stomach contents to reflux into the oesophagus

48
Q

Complications of GORD

A

-Peptic stricture:
Benign narrowing of oesophagus
Due to scarring in response to persistent sever reflux oesophagitis Should be differentiated from oesophageal carcinoma

-Barrett’s oesophagus:
Normal squamous epithelia replaced by metaplastic columnar epithelium
Precursor lesion of oesophageal adenocarcinoma (cancer)

49
Q

GORDTherapy

A 
• Surgery
• Pharmacological Treatment 
– Antacids andalginate
– H2 antagonists
– Proton pump inhibitors
• Gastroprokinetic drugs – increase rate of gastric emptying
– metoclopramide
– Domperidone

Block 1 - Treatment And Prevention Of Illness (32 decks)

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