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GI > Session 4 > Flashcards

Session 4 Flashcards

1
Q

2 important families of hormones in GI tract

A

Gastrin family- gastrin and cholecystokinin

Secretin family- secretin and gastric inhibitory polypeptide

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2
Q

The stomach has an impressive ability to distend in part due to

A

Rugae which are temporary folds in mucosa of stomach

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3
Q

What does the stomach have that enables it to mix and grind contents

A

3 layers of muscle

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4
Q

Stomach acid helps to

A

Unravel proteins creating a larger surface area for enzymes to act on and activates proteases in the stomach lumen

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5
Q

The mucosal surface of the stomach is comprised of

A

Gastric pits and gastric glands (parietal cells, chief cells and enteroendocrine cells)

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6
Q

Parietal cells are responsible for and stimulated by

A

Acid production in stomach

Gastrin, histamine and ACh (Acting through CCK, H2 and Mcr receptors on parietal cell)

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7
Q

Acid production increases when

A

Amino acids/peptides are detected and when the stomach is distended

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8
Q

Acid production is reduced when

A

Stomach distension reduces and a low pH is detected

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9
Q

3 phases of digestion

A

Cephalic, gastric and intestinal

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10
Q

The stomach defends itself from its acidic environment by

A

Producing a thick layer of alkaline mucus

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11
Q

Functions of the stomach

A

Storage facility
Start digestion of protein
Little bit of carb and fat digestion (salivary amylase and lingual lipase)
Disinfect = innate defence

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12
Q

Cell change when stomach starts

A

Stratified squamous before, becomes simple columnar

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13
Q

What is the opening of the stomach called

A

Cardia

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14
Q

3 divisions of stomach

A

Fundus, body and antrum

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15
Q

What is at the end of the antrum

A

Pyloric sphincter (control chyme entering duodenum)

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16
Q

What is found in the opening to the stomach

A

Lower oesophageal sphincter- made of intrinsic smooth muscle and right crus of diaphragm

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17
Q

explain the concept of receptive relaxation

A

Peristalsis causes reflex relaxation of proximal stomach

Receptive relaxation causes fundus to distend

Stomach can fill without significant rise in pressure

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18
Q

Muscle layers of stomach

A

Oblique
Circular
Longitudinal

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19
Q

Which part of stomach is more muscular

A

Posterior layer

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20
Q

Structure of gastric pit and gastric gland

A
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21
Q

Roles of parietal, chief and G cells

A
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22
Q

Protective mechanisms against stomach acid

A

Cells replaced regularly

HCO3 pH neutral layer

Prostaglandins

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23
Q

What do prostaglandins do

A

Increase mucosal blood flow
Support mucous layer
Generally protective

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24
Q

How is acid secretion by parietal cells controlled

A

H+ K+ proton pump

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25
Q

Apical membrane contains

A

K+ channels

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26
Q

Tubulovesicles lack

A

K+ permeability

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27
Q

What happens when parietal cells go from resting to active state

A

Stimulated phase- canaliculi and microvilli

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28
Q

Sensory triggers for acid production

A

Smell, sight, taste

Cephalic

30% of HCl

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29
Q

gastric triggers for stomach acid production

A

Stretch, presence of amino acids and small peptides

Gastric

60% of HCl

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30
Q

What are the intestinal triggers for acid production

A

Chyme in duodenum
Presence of partially digested proteins

Intestinal

10% of HCl

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31
Q

How do gastrin receptors on parietal cells work

A

Peptides in stomach lumen are sensed by G cell, gastrin is produced (uses CCK receptor)

32
Q

How do muscarinic receptors stimulate parietal cell

A

Vagal stimulation using Mcr

ACh detected due to sensory triggers, GRP detected due to stretch

33
Q

How does histamine stimulate parietal cells

A

Entero-chromaffin like cell ECL releases histamine

34
Q

How is acid secretion in lumen inhibited

A

More HCL causes lower pH which stimulates D cell to produce somatostatin

35
Q

How is HCL produced in the parietal cell

A

Carbonic anhydrase, H/KAtpase, K+ and Cl- transporters, Alkaline tide

36
Q

What is dyspepsia

A

Complex of upper gastro intestinal tract

37
Q

What is GORD

A

Symptoms relating to reflux of stomach contents into pharynx or oesophagus- burning chest pain, acidic taste in mouth, cough, sore throat, asymptomatic

38
Q

Risk factors for GORD

A

Intra abdominal pressure
Obesity
Pregnancy
LOS dysfunction
Hiatus hernia
Delayed gastric emptying

39
Q

LOS important crus

A

Right crus

40
Q

What can be refluxed

A

Stomach acid, Bile and pepsin (protease)- little protection in oesophagus

41
Q

Complications of GORD

A

Oesophagus, ulceration, Hammorrhage, Strictures, Metaplastic changes e.g. Barett’s oesophagus

42
Q

Barrett’s oesophagus explained

A

Reversible change of stratified squamous epithelia to columnar (due to repeated exposure to gastric contents)

Increased risk of dysplasia, adenocarcinoma

43
Q

usually stratified squamous epithelium could change to which form of cancer

A

Squamous cell carcinoma

44
Q

Lifestyle treatments for GORD

A

Weight loss
Avoid trigger foods
Eat smaller meals
Don’t eat then sleep
Avoid alcohol and caffeine
Stop smoking

45
Q

Medical treatments for GORD

A

Drug- proton pump inhibitors give symptom relief and healing of inflammation

H2 receptor antagonists

Surgery- fundoplication (fundus of stomach wrapped around lower oesophagus to help with sphincter mechanism)

46
Q

What is gastritis

A

Inflammation of the stomach mucosa

47
Q

Symptom complex in gastritis

A

Pain, nausea, vomiting , haemorrhage

48
Q

Acute causes of gastritis

A

NSAIDS
Too much alcohol
Chemotherapy
Bile reflux

49
Q

Chronic causes of gastritis

A

Infection with H pylori
Autoimmune

50
Q

Pathological changes in gastritis

A

Epithelial damage
Epithelial hyperplasia
Vasodilation (angry looking)
Neutrophil response
Lymphocyte response
Glandular atrophy
Fibrotic changes in lamina propria
Metaplastic changes

51
Q

Features of autoimmune causes of gastritis

A

Antibodies against our parietal cells (which produce intrinsic factor)

Atrophy of parietal cells and loss of intrinsic factor

52
Q

What is intrinsic factor for

A

Needed for Absorption of vitamin B 12 in Ileum

53
Q

Symptoms of lack of intrinsic factor due to autoimmune antibodies to parietal cells

A

Megaloblastic anaemia
Anorexia (no hunger)
Neurological symptoms
Glossitis (inflammation of tongue)

54
Q

Helicobacter key facts

A

Infected around half of the population

Asymptomatic in majority

May have some benefits

55
Q

Helicobacter bacteria features

A

Helix shape, gram negative, micro aero Philic, needs some oxygen, stomach has correct oxygen

Transmitted by faeco-oral route into GI tract, or oral-oral route

56
Q

Adaptations of Helicobacter

A

Can navigate and adhere to mucosa epithelia lining due to flagella and chemotaxis (find areas of lower acidity). Adhesions so resits peristalsis

Has own cytoplasmic urease- can convert urea and water into carbon dioxide and ammonia (basic). Can resist acidic environment

57
Q

Problem with Helicobacter

A

Ammonia causes cell damage

CagA expresses protein which causes huge inflammatory response due to interleukin 8, implicated in cancer

VacA is a secreted protein which increases paracellular permeability and is toxic

Can secrete mucinases, proteases, lipases (damage mucus layer)

58
Q

Antral colonisation of Helicobacter

A

Where mostly G cells located
Overactivity of G cells - produce more gastrin so parietal cells produce more acid and increase in number

Too much acid produced, chyme more acidic, damage to duodenum

Potential conversion of duodenal epithelial cells to more gastric like epithelia. Helicobacter can then colonise duodenum and cause ulcers and further problems

59
Q

Fundus colonisation of Helicobacter

A

Atrophy of parietal cells rather than over activity

Precursor to dysplastic changes- increases risk of cancer

60
Q

generally speaking if Helicobacter colonises antrum and body patients are

A

Asymptomatic

61
Q

Diagnosis of H pylori

A

Has its own urease-

Urea breath test, stool antigen test, endoscopy with biopsy

62
Q

Explain urea breath test

A

Normal gastric urea contains 99% C12 and 1% C13

Can detect C13 level after being given urea enriched with C13

If C13 is higher than normal, there are h pylori present

63
Q

Eradication of H pylori

A

Proton pump inhibitor, 2x antibiotics (e.g. clarithromycin and metronidazole)

Side effects include diarrhoea and nausea in 5% of people

7 days usually, can double to 14

Can check if successful eradication with urea breath test

64
Q

What is peptic ulcer disease

A

Defect in gastric or duodenal mucosa that extends through the muscularis mucosa

65
Q

What must an ulceration do to qualify as a peptic ulcer

A

Must extend through muscularis mucosa

66
Q

Most common place to find peptic ulcer

A

Duodenum not stomach- when in stomach usually in lesser curve and antrum

67
Q

Gastric and duodenal ulcer incidence

A

1 gastric for every 3 duodenal

Gastric increases with age, duodenal
increases up to 35

Gastric more lower class

gastric more common in blood group A and duodenal more common in O

Acid levels normal or low in gastric ulcers (more to do with barrier defect), duodenal ulcers can cause normal or high levels (due to chyme being more acidic and overwhelming ability to neutralise)

H pylori responsible for 70% gastric ulcers and 95-100% duodenal

68
Q

Why does H pylori cause duodenal ulcers

A

H pylori in antrum of stomach where there are G cells

Increased gastrin, proliferation of parietal cells, increased acid, increased chyme

69
Q

Stomach defences

A

Mucous layer secreted by surface mucous cells (which have bicarbonate secreted into them) = alkaline layer

Mucosal blood flow for repair and removal of acid

Prostaglandins = stimulate blood flow e.g. reduced in NSAIDS

Epithelial renewal

70
Q

Risk factors for peptic ulcer disease

A

H pylori
NSAIDS
Smoking can cause relapse
Massive physiological stress e.g. burns

71
Q

Classification of ulcers

A

Acute - due to gastritis

Chronic- occur at mucosal junctions

72
Q

Morphology of peptic ulcers

A

Most are less than 2 cm in diameter
Base is necrotic tissue, granulation tissue

when it heals the muscularis propria can be replaced by scar tissue (this can narrow stomach lumen if extreme or cause pyloric stenosis, or perforation and peritonitis)

73
Q

Extreme consequences of GI ulcers

A

Scar tissue build up - pyloric sphincter, peritonitis

Ulcerate into liver or pancreas

Haemorrhage into vessel at base- bleed into guts and cause malaena (haem component is oxidised by passing through GI tract)

Extensive dramatic bleeding e.g. duodenal ulcer erodes posteriorly, Gastroduodenal artery (stomach or duodenum fill with blood, vomiting blood)

Check ulcer for malignant change

74
Q

Symptoms of gastric ulcer

A

Epigastric pain, back pain, burning/gnawing pain, following meals

Pain at night- duodenal ulcer

Food may make duodenal ulcer better as initially sphincter shuts, but once sphincter opens to release chyme it is irritated again (not always true)

Resulting from bleeding- haematemesis or malaena and anemia

Early satiety

Weight loss

75
Q

Management of ulcer

A

H Pylori- eradicate

Not H pylori- stop NSAIDS or add in PPI

If bleeding- endoscopic treatment, adrenaline injected, if perforated then open surgery for ulcer repair

After intervention test for H pylori

76
Q

As many gastric diseases are a result of acid damage to the mucosa, the pharmological interventions that exist target the

A

parietal cell at either the Proton pump or the H2 receptor

Both have effect of reducing production of stomach acid

GI (22 decks)

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