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P2 - Gastrointestinal system > Stomach, Intestine, Liver, peptic ulcers > Flashcards

Stomach, Intestine, Liver, peptic ulcers Flashcards

1
Q

List all the components of the alimentary system.

A
  1. Mouth
  2. Salivary glands
  3. Pharynx
  4. Oesophagus
  5. Stomach
  6. Small intestine
  7. Appendix
  8. Large intestine
  9. Anus
  10. Liver
  11. Gallbladder
  12. Pancreas
  13. Common bile duct
  14. Pancreatic duct
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2
Q

Name the basic compartments of mouth

A

Palate, teeth, tongue and uvula (čípek)

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3
Q

Name the salivary glands

A

Sublingual, submandibular and parotid (posterior wall)

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4
Q

How is the small intestine divided?

A

Duodenum, Jejunum and Ileum

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5
Q

How is the large intestine divided?

A

Cecum, Ascending colon, Transverse colon, Descending colon, Sigmoid colon and Rectum

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6
Q

What is the general organization of tissue in the GI tract, from innermost layer? (the wall)

A

Mucosa: epithelium, lamina propria and muscularis mucosa

Submucosa: containing Meissner’s plexus

Muscularis propria: circular muscle, Auerbach’s plexus and outer layer of longitudinal innermost;

Serosa or Adventitia

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7
Q

What effect elicit contractions of circular and longitudinal muscle?

A

Contraction of circular muscle causes constriction while contraction of longitudinal muscle causes shortening of the gut.

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8
Q

What is the innervation of mouth?

A

CNs VII (facial nerve) and IX (glossopharyngeal)

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9
Q

Describe the function and components of saliva.

A

Mucous to lubricate, salivary amylase to digest starch, bicarbonate to neutralise acid and bacterocidal agents.

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10
Q

What is the function and structure of esophagus?

A

F: a conduit to propel bolus from pharynx to stomach

S: Upper eosophageal sphincter, bands of circular and longitudinal muscle and lower oesophageal sphincter

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11
Q

Describe the innervation of esophagus.

A

Mainly the vagus nerve

Myenteric (Auerbach’s) plexus - has sympathetic and parasympathetic innervation

Parasympathetic system controls peristalsis

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12
Q

What is the arterial blood supply to the oesophagus?

A
  • Superior and inferior thyroid arteries
  • Branches of bronchial, intercostal, descending aorta arteries
  • Branches of left gastric, left inferior phrenic and splenic arteries
  • Dense anastomosis within submucosa
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13
Q

Describe venous drainage of oesophagus.

A

Hemiazygous and azygous veins, short gastric veins, left gastric vein (drains into portal vein)

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14
Q

What are the functions of stomach?

A
  1. Storage of ingested food 2. Digestion of food 3. Acid secretion 4. Slow propulsion of food into the duodenum
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15
Q

What are the layers of muscularis propria in the stomach?

A

1 extra layer: Inner most oblique muscle Circular muscle Longitudinal muscle

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16
Q

Does the stomach has adventitia or serosa?

A

Serosa

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17
Q

What are the anatomical compartments of stomach?

A

Cardia, Fundus, Body, Pyloric antrum, Pyloric canal, Pyloric sphincter

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18
Q

What are the anatomical curvatures of the stomach?

A

Lesser curvature containing the angular notch; and greater curvature more lateraly

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19
Q

What glands are found in cardia of the stomach?

A

Cardiac glands - Tubular with coiled end and opening continuous with the gastric pits

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20
Q

What are rugae?

A

Gastric mucosal folds to allow stretch of the stomach.

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21
Q

What are foveolae?

A

Gastric pits within the rugae.

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22
Q

Describe the gastric mucosal barrier.

A

Produced by surface mucous cells

Linked to each other by tight junctions

95% water, 5% mucins - forms an insoluble gel

Traps bicarbonate and thus neutralises the lining

Na+, K+ and Cl- are parts of the mucosal barrier

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23
Q

Differentiate between the glands of the stomach.

A

Cardiacc glands: Simple tubular glands with coiled end, many mucous secreting cells

Gastric glands: found in body and fundus, have variety of different cell types, HCl and pepsinogen secretions mainly

Pyloric glands: Simple tubular glands with branched end, mucous-secreting cells

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24
Q

Name the regions and cell types in gastric gland.

A
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25
Q

Describe sphincters relating to stomach.

A

Inferior Oesophageal sphincter - between oesophagus and the stomach, change from stratified squamous epithelium to simple columnar; Functional sphincter - physiological, no specific muscle, the diaphragm and the angle of attachment helps it to fulfil its function

Pyloric sphincter - between pylorus and the duodenum; control exit of chyme, anatomical sphincter - smooth muscle

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26
Q

Describe the greater and lesser omenta.

A

Stomach is covered in double layered peritoneum, supports the viscera and attaches it to the abdominal wall

Peritoneum folded over itself, but it attaches to the stomach

Greater omentum - hangs down from greater curvature, drops over transverse colon and folds to reach the posterior abdominal wall, contains many lymph nodes

Lesser omentum - between lesser curvature and the liver - attaches the stomach and duodenum to the liver

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27
Q

Name the types of mucous cells and their specific and common function.

A

Surface mucous cells - oval shaped nuclei, mucous stored in droplets - apical granules

Mucous neck cells - narrow portion of the gland

Produce mucins - glycoprotein

Abundant mitochondria and carbonic anhydrase - form bicarbonate to increase the pH of the lining

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28
Q

Characterise the parietal/oxyntic cell.

A

Drop like shape

Loads of mitochondria

Histamine H2 receptor

Gastrin receptor - CCKB

Muscarinic M3 receptor - vagus nerve and Ach

Secrete HCl and intrinsic factor (binds to vit B12)

Have tubulovesicles and a secretory canaliculus

When stimulated the tubulovesicles fuse with the secretory canaliculus, carbonic anhydrase and HK-ATPase are located in the microvilli projecting into the secretory canaliculus

Resting state vs stimulated state (tubulovesicles fused )

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29
Q

Characterise chief cell.

A

Pepsinogen releasing

Mostly found in the body, some in antrum

Almost columnar

Polarised cells with basal lamina on one side and apical microvilli and zymogen granules containing pepsinogen on the other

Have acetylcholine receptor on basal side - when activated stimulates secretion of pepsinogen

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30
Q

Characterise G cells.

A

Classic gut endocrine cells

Microvilli on luminal surface to detect food in the stomach

Release of gastrin - acts on chief cells

Inhibited by increased amount of gastric acid in the lumen - thus negative feedback loop

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31
Q

Characterise D cells.

A

Supresses G cells by release of somatostatin - decrease gastrin

Paracrine mechanism

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32
Q

Enterochromaffin cells

A

Type of neuroendocrine cells

Release histamine to aid the release of HCl -seems to be the main driver

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33
Q

What is the epithelium of stomach?

A

Simple columnar epithelium.

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34
Q

What is the arterial blood supplly to the stomach?

A

Comes from celiac trunk

Lesser curvature - anastomoses of the l/r gastric arteries

Greater curvature - l/r gastro-epiploic arteries

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35
Q

What is the venous drainage of the stomach?

A

Parallel to the arteries

Right and left gastric veins –> hepatic portal vein

Short gastric vein and l/r gastro-omental vein –> superior mesenteric vein

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36
Q

What is the innervation of the stomach?

A

Parasympathetic

Posterior vagal trunks

Sympathetic

T6 - T9 pass to the celiac plexus, also pain transmitting fibres

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37
Q

What is the lymphatic drainage of the stomach?

A

Gastric and gastro-omental lymph nodes found at the curvature

Connect to celiac lymph nodes

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38
Q

Name the compartments of duodenum.

A

Superior

Descending

Inferior

Ascending

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39
Q

What are the flexures of duodenum?

A

Inferior duodenal flexure

Duodenojejunal flexure

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40
Q

What is contained within the descending duodenum?

A

Minor and major duodenal papillas - opening for bile and pancreatic secretions

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41
Q

What are the characteristics of duodenal mucosa?

A

Evaginations into plicae and villi - increase the surface area for nutrient absorption

Crypts - short invaginations providing a protected site for the stem cells

Simple columnar epithelium

Absorptive cells, goblet cells and enteroendocrine cells, in crypts there are also Paneth cells and stem cells

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42
Q

What are the cell types within duodenum?

A

Absorptive cells - absorbing nutrients, transport them to lamina propria, create brush border

Goblet cells - secrete mucus and promote movement and effective diffusion of gut contents

Enteroendocrine cells - secrete hormones

Tuft cells - immunity against parasites

Paneth cells - bottoms of the crypts, secrete lysosomal enzymes and other factors into the crypt lumen

Stem cells - line the walls of crypts, replace absorptive and goblet cells every 4 days

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43
Q

What is contained within the submucosa of duodenum?

A

Brunner’s glands - provide abundant alkaline mucus to neutralize the acid contents entering the stomach

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44
Q

Describe Lamina propria of the small intestine.

A

Supplied by capillaries

Includes single lacteal

Thin strands of smooth muscle

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45
Q

Is the outer layer of duodenum serosa or adventitia?

A

Serosa

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46
Q

What connects the superior duodenum to the liver?

A

Hepatoduodenal ligament

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47
Q

Describe the vasculature of duodenum.

A

Proximal to the major duodenal papilla - gastroduodenal artery

Distal to the major duodenal papilla - inferior pancreaticoduodenal artery

The difference marks the transition from foregut to midgut

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48
Q

Where does food assimilation primarily happen?

A

Small intestine

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49
Q

What increases the surface area in small intestine?

A

Kerckring’s folds

Villi

Microvilli on surface of enterocytes

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50
Q

What are Peyer’s patches and where they are found?

A

Peyer’s patches - lymph follicles, ileum

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51
Q

How is pancreas divided in terms of function?

A
  1. Endocrine pancreas
    1. Throughout parenchymal tissue islands of endocrine tissue - islets of Langerhans
    2. Beta cells producing insulin
    3. Alpha cells producing glucagon
  2. Exocrine pancreas
    1. Aqueous/bicarbonate component
    2. Enzymatic component
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52
Q

Describe gallbladder, its function and structure.

A

Concentrates and stores bile

Prostaglandin

Single layer of epithelial cells, lamina propria, single smooth muscle layer and serosal layer

Vagus and splanchnic innervation regulate motility

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53
Q

What are the functions of large intestine?

A

Absorption of water

Breakdown of fibre

Storage and elimination of waste

Large bowel flora - mainly anaerobes

Bile acid conversion, vit K and ammonia production

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54
Q

What are tenia coli?

A

Tthree separate longitudinal ribbons of smooth muscle on the outside of the colon, they contract to produce the haustra (colon segments)

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55
Q

Describe the process of swallowing.

A
  1. Mastication - reduces particle size, mixes food with saliva and increases surface area
  2. Voluntary initiation of swallowing
  3. Becomes involuntary
  4. Epiglottis closes to prevent food passing into the trachea
  5. Peristaltic wave, opening of the upper oesophageal sphincter
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56
Q

From where is swallowing controlled?

A

Reticular formation within the brainstem.

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57
Q

Describe the muscle in oesophagus.

A

From the upper oesophageal sphincter the muscle is skeletal, then gradually changes into smooth muscle as it extends to lower oesophageal sphincter.

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58
Q

How is oesophagus controlled?

A

The efferent vagal pathways are composed of:

non-vagal nuclei, nucleus ambiguous and dorsal motor nucleus.

These control motility and secretions.

Vagal efferent send the sensory information back to CNS.

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59
Q

Describe the mechanism of segmentation within the stomach

A

Initiated by basic electrical rhythm - slow electrical waves which occur spontaneously

  • increased by food and vagal stimulation

Begin in mid to upper portion of the stomach and move down, every 15 to 20 seconds, becoming more intense as they reach antrum

Pyloric sphincter is contracted so food moves back up

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60
Q

What are hunger contractions of the stomach?

A

Migrating motor complex

  • initiated by motilin which is secreted by an empty stomach
  • frequency differs from peristaltic contractions
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61
Q

How does stomach empty?

A

Peristalsis initiated in the fundus

As the peristaltic wave moves more distally the sphincter opens

  • Muscle layers in antrum are thicker to aid gastric emptying

Duodenal segmental contractions are inhibited

  • regulation by the chyme content - signals back to stomach
  • H+, hyperosmotic component, fat

Speed of emptying

  • Dependent on the macronutrient content of the meal and amount of solid it contains
  • Liquids empty more readily
  • Solids have a lag phase

Cholecystokinin - released from endocrine cells in the duodenal mucosa in response to lipids

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62
Q

What are the main patterns of gastrointestinal motility?

A

Segmentation - mixing

Peristalsis - propulsion

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63
Q

What are the Interstitial cells of Cajal and where they are?

A

A specialised group of cells in the intestinal wall

Involved in the transmission of information from enteric neurons to smooth muscle cells

Pacemaker cells - capacity to generate basic electrical rhythm

In muscularis externa, between longitudinal and circular muscle layers

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64
Q

How is the basal electrical rhythm activity controlled?

A

By ANS which acts on the enteric nervous system that ultimately controls it - sympa increases threshold and thus inibits contractions, para vice versa

  • If threshold potential is reached a train of action potentials may be triggered
  • Inhibitory hormones and neuroeffector substances - vasoactive intestinal polypeptide, nitric oxide
  • acetylcholine, substance P
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65
Q

Define peptic ulcers disease

A

A break in the superficial epithelial cells penetrating down to the muscularis mucosa of either stomach or duodenum, with fibrous base and an increase in inflammatory cells

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66
Q

Simply describe the pathophysiology and name aggressive factors

A

An imbalance between factors damaging to gastroduodenal mucosal lining and defense mechanisms

Aggressive factors -Gastric juice - HCl, pepsin, bile salts from duodenum , Helicobacter Pylori, NSAIDs

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67
Q

Describe Helicobacter Pylori and how it causes peptic ulcers disease

A

Mostly found in pyloric area

Gram negative bacteria

Spiralled shape, with pilli

Has high activity urease which dissociates dissolved urea into ammonium bicarbonate (2 NH4+ + HCO3-) thus creating alkaline cloud around itself

Increased pH acts through D cells to decrease the release of somatostatin

This increases the release of gastrin from G cells

Which in turn stimulates an increase in parietal cell mass and increased HCl

This increases acid load and may result in gastric metaplasia, H. pylori colonisation and ulceration - this mechanism is mostly for duodenal ulcers

Gastric ulcers - long-lasting infection of H pilorii infection throughout the stomach accompanied by severe inflammation - results in gastrin mucin degradation, disruption of tight junctions between cells, and the induction of epithelial cell death

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68
Q

How does NSAIDs use can be precipitant in causing peptic ulcers

A

NSAIDs cause injury directly, trap H+ ions, and indirectly, systemic effect involving the inhibition of cyclo-oxygenases

Increase bleeding risk

PGE, PGI

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69
Q

How is the stomach epithelium normally protected?

A

Mucus bicarbonate layer

Integrity of tight junctions between epithelial cells

Process of restitution - space is filled by new cells

70
Q

Describe the prevalence and risk factors for peptic ulcers disease

A

Common in 1-5%

More in males

More in smokers

Stress considered important

Age

NSAIDs

71
Q

Clinical features of peptic ulcers disease

A

Recurrent burning epigastric pain

Mostly at night

Worse when hungry

May be relieved by antacids

Nausea

Anorexia and weight loss

72
Q

How is peptic ulcer disease diagnosed?

A

Needs to diagnose H. pylori

Non-invasive methodsSerological test

Immunoglobulin G antibodies - 90% sensitive, 83% specific

But cannot be used to confirm eradication or current infection

13C-urea breath test

Quick and reliable

Measurement of 13CO2 in the breath after ingestion of 13C-urea using a mass spectrometer

Sensitive 90%, specific 96%

Also 14C

Compared to base level

Stool antigen test

Specific immunoassay using monoclonal antibodies

Sensitivity 97.6% , specificity 96%

Invasive using endoscopyBiopsy urease test

Gastric biopsies are added to a substrate containing urea and phenol red

If there is H. pylori the urease enzyme splits the urea causing increase in pH and change of colour of the buffer

Can be falsely negative if taking antibiotics

Histology

Stained sections of gastric mucosa

Culture

Can be tested on special medium, also to determine its sensitivity to antibiotics

Suspected peptic ulcer disease

Patients under 55 - with typical symptoms and positive test for H. pylori - eradication without further investigation

Older patients - need endoscopic diagnosis and biopsy to test for malignancy

All with alarm symptoms - endoscopy

73
Q

Name the acid-lowering treatments for peptic ulcer disease

A

H2 receptor antagonists, Proton pump inhibitors, Antacids, Alginates and Simeticone

74
Q

Discuss the characteristics of H2 receptor antagonists including its side-effects

A

Inhibits histamine action at all H2 receptors

Inhibit histamine- and gastrin-stimulated acid secretion

Decrease acid secretion by 90%

Promote healing of gastric and duodenal ulcers

Cimetidine and ranitidine, may be in combination with bismuth, nizatidine and famotidine

Side effects: diarrhoea, dizziness, muscle pains, alopeica, transient rashes, confusion and hypergastrenaemia

75
Q

Discuss the characteristics of proton pump inhibitors

A

Omeprazole - irreversibly inhibits H+-K+ -ATPase

As a weak base it accumulates in the acidic environment

At the site of the canaliculi it is converted and becomes able to inactivate the ATPase

Esomeprazole, lansoprazole, pantoprazole and rabeprazole

Side effects: uncommon, headache, diarrhoea, rashes

76
Q

Describe the characteristics of antacids

A

Directly neutralize acid

Can help to heal duodenal ulcers

Magnesium salts (diarrhoea) and aluminium salts (constipation) are used together to preserve the normal bowel function

Magnesium trisilicate, magnesium carbonate, magnesium hydroxide, aluminium hydroxide gel, hydrotalcite (mixture)

77
Q

What do you know about alginates?

A

Used with antacids

Increase viscosity and adherence of mucus to the oesophageal mucosa

78
Q

What is Simeticone?

A

Also used with antacids

Anti-foaming agent

Relieves bloating and flatulance

79
Q

Discuss the H. Pylori eradication therapy

A

Triple therapy - proton pump inhibitor with 4 antibacterials

Amoxicillin and metronidazole or clarithromycin

Metronidazole and clarithromycin - high resistance

Amoxicillin, tetracycline, omeprazol and bismuth

Quinolones - ciproflaxin; furazolidone and rifabutin –> rescue therapy

2 types of antibiotic together with acid suppressor

First-line

Omeprazole 40mg Mane

Metronidazole 400mg TDS

Amoxycillin 500mg TDS

Second line

Omeprazole 40mg Mane

Clarithromycin 500mg TDS

Amoxycillin 500mg TDS

80
Q

What are the drugs that protect mucosa in peptic ulcer disease

A

Bismuth chelate - toxic effects on the bacillus

Sucralfate - decreases degradation of mucus

Misoprostol - analogue of prostaglandin E1

81
Q

What are the surgical interventions for peptic ulcer disease and when they are used?

A

Only for complications like recurrent uncontrolled haemorrhage or perforation (puncturing)

In past partial gastrectomy (removal of stomach) or vagotomy (removal of vagus nerve) were requir

82
Q

Describe gastric cancer

A

2nd commonest cause of cancer death worldwide

Presents with anorexia, weight loss and anaemia

Usually incurable

83
Q

Describe the broad anatomy of the liver

A
84
Q

Describe the lipoprotein-based fat and cholesterol transport system and its role in energy metabolism

A
85
Q

Summary the findings in jaundice

A
86
Q

What is achalasia

A

Oesophageal dysmotility

87
Q

Describe the main components of stomach motility

A

Basal electrical rhythm - every 3 min; after threshold is reached activation of vagal afferents results in peristalsis, secretin provides negative feedback

88
Q

What decreases the motility of the stomach

A

Cholecystokinin, secretin and glucose-dependent insulino-tropic peptide

89
Q

What is motilin?

A

secreted when fasting in cycles to facilitate gastrointestinal motility - interdigestive myoelectric complexes, inhibited after food ingestion

90
Q

Discuss peristalsis

A

Initiated by the distention of the gut, this stimulates the enteric nervous system to contract the gut above this distention, contractile ring appears and moves as a wave along the gut, strong parasympathetic signal can also evoke a contraction, as chemical or irritation

91
Q

Discuss the motility of the small intestine

A

Migrating motility complex propagates over 2-3 hrs to terminal ilium; 1. segmentation contractions of circular smooth muscle; 2. pendular contractions of longitudinal muscle; 3. Villus movements brought about by muscularis mucosae; 4. peristaltic waves arising from duodenal bulb propelling food towards terminal ileum

92
Q

Motility in the large intestine

A

Haustral contractions and mass movement

93
Q

Describe secretory processes in the stomach

A
  1. H+ produced by parietal cells; 2. pepsin produced by chief cells; 3. intrinsic factor; 4. mucus; 5. water
94
Q

What is the gastric pH and what is its purpose?

A

pH about 1, kill bacteria, convert pepsinogen to pepsin

95
Q

What is the structure of oxyntic gland?

A

Epithelial cells in the lumen, parietal cells deeper down and chief cells at the bottom

96
Q

Discus gastric acid secretions

A

H+ pumped into the lumen by H+,K+ - ATPase, OH- combines with CO2 to form HCO3- which is catalysed by carbonic anhydrase; HOH –> OH- + H+; OH- + CO2 –> HCO3-

97
Q

What stimulates acid secretion?

A

Histamine (produced by ECL cells), gastrin (acts on cholecystokinin-2 receptor), acetylcholine (neurotransmitter of vagus nerve at muscarinic receptor on parietal cell), peaks 1 hour post-ingestion

98
Q

What stops acid secretion?

A

Less volume in the stomach and lower pH, gastrin inhibited at pH <3, low pH stimulates somatostatin - inhibitory hormone, duodenal enterogastrones also released - GIP, secretin, CCK

99
Q

Name the 3 phases of gastric secretions

A
  1. Cephalic phase, 2. Gastric phase, 3. Intestinal
100
Q

Describe cephalic phase of gastric secretions

A

Sight, smell and taste of food causes vagus to activate parietal and gastrin cells which moderately stimulates HCL and pepsinogen release

101
Q

Describe the gastric phase of gastric secretions

A

Distension of stomach and proteins in antrum cause vago-vagal reflex, gastrin and histamine release further causing strong stimulation of HCl/pepsinogen

102
Q

Which foods directly stimulate gastrin release

A

Proteins, coffee, calcium rich

103
Q

Describe intestinal phase of gastric secretions

A

If proteins in duodenum stimulate gastrin

HCl in duodenum stimulates secretin secretions - inhibition

Lipid in duodenum causes the release of peptide YY (inhibitory)

104
Q

List the secretions of the crypts of the small intestine

A

NaCl/NaHCO3- (neutralises gastric HCl), enteropeptidase - activates trypsinogen

105
Q

List the secretions of the villus tips of the small intestine

A

Brush border enzymes - digestion

106
Q

What are the pancreas secretions

A

Acinar cells secrete: pro-enzymes - proteins/lipids stimulate cholecystokinin which stimulates enzyme release; NaCl secretion; Ducts secrete: bicarbonate - HCL in duodenum stimulates secretin which stimulates bicarbonate from duct cells

107
Q

What is an intrinsic factor and how it is secreted?

A

Produced by parietal cells, it is a glycoprotein that binds to vitamin B12

108
Q

How is mucous formed in the stomach?

A

HCO3- that left the parietal cells diffuses into the mucous surface cells then bicarbonate ion is released into the lumen together with mucins to create alkali barrier

109
Q

What are the possible outcomes of H Pylori infection?

A

50% of general population have H Pylori, 80% of them will have no associated disease, 5-15% peptic ulcer disease and 1-3% gastric cancer

110
Q

What is the mechanism behind different outcomes of H Pylori infection?

A

1 - increased acid in antrum, increased gastrin - results in no atrophy and duodenal ulcer; 2 - low acid production, more gastrin release, atrophy and gastric cancer

111
Q

What is the enteric nervous system?

A

A subsystem of the visceral motor system, made up of small ganglia and individual neurons scattered throughout the wall of the gut, influences gastric motility and secretion

112
Q

What makes up the enteric nervous system

A

Myenteric plexus and submucosal plexus, with inputs from the autonomic nervous system (possibly its division)

113
Q

Which cells mediate enteric neurotransmission?

A

Interstitial cells of Cajal, communicate with ICC and smooth muscle cell

114
Q

When does the enteric nervous system take control?

A

Mediates reflex activity in the absence of CNS input

115
Q

What extrinsic factors influence enteric nervous system?

A

Vagal control excites non-sphincter muscle, sympathetic control - inhibitory to non-sphincter muscle, excitatory to sphincteric muscle;

5 hydroxy-tryptamine, Motilin, opioid receptors

116
Q

What are the areas of the gastrointestinal system under voluntary control?

A

Upper oesophageal sphincter and external anal sphincter

117
Q

Describe the muscle in the oesophagus

A

Upper oesophageal sphincter, striated muscle, transitions to smooth muscle and ends in lower oesophagal sphincter; inner circular layer and outer longitudinal

118
Q

How long is the oesophagus?

A

18 - 22 cm

119
Q

What conditions can affect striated oesophageal muscle?

A

Polymyositis, Myasthenia gravis

120
Q

What conditions can affect the smooth muscle of oesophagus?

A

Scleroderma, Achalasia

121
Q

What happens during the interprandial period of the stomach and intestine?

A

Fasting period, cyclic contractions sequence which occurs every 90 min, involves the migrating motor complex

122
Q

Describe the 4 phases of interprandial period od the stomach and intestine

A
  1. prolonged period of quiescence
  2. increased frequency of contractility
  3. A few mins of peak electrical and mechanical activity
  4. Declining activity merging to next phase 1
123
Q

What regulates the interprandial period of the stomach and small intestine?

A

Motilin - secreted from crypt cells of the small intestine

124
Q

What is the function of the interprandial period of the small intestine?

A

To cleanse stomach and intestine

125
Q

What happens to the contractions during gastric phase within the stomach?

A

Motor migratory/migrating complex is replaced by contractions of variable amplitude and frequency, allowing mixing and digestion

126
Q

How are the contractions of the stomach during gastric phase controlled?

A

By gastric pacemaker - zone within proximal gastric body, generated rhythmic depolarisations at a frequency of 3 cycles per minute, only triggers gastric smooth muscle contractions with additional neurohumoral input

127
Q

Describe small intestinal transit

A

In fasting motility via MMC, small intestine transport solids and liquids at the same rate but liquids reach caecum first due to gastric emptying, chyme moves in boluses

128
Q

Describe colonic motility

A

No typical pacemaker activity

Mass movement - e.g. gastrocolic reflex

Haustrations - segmentation mixing

Takes 1-2 days for food to exit, faster in men

129
Q

Describe the internal anal sphincter

A

Smooth muscle, involuntary control, in rest provides majority of the contraction

130
Q

Describe the external anal sphincter

A

Striated muscle, voluntary control, recruited in reflex reaction to coughing/sneezing

131
Q

Explain how motilin controls GI functions

A

Hormone produced by M cells in small intestine, secreted at 90 min intervals, cleanses gut in time for next meal, stimulates contraction of gastric fundus and enhances gastric emptying

132
Q

What drugs reduce gastric motility?

A

Opiates, Anticholinergics, e.g. Loperamide - gut-selective opiate Mu receptor agonist, decreases tone and activity of myenteric plexus, leads to increased water absorption and can be used for diarrhoea

133
Q

What drugs increase motility of the gut?

A

Stimulant laxatives, Prucalopride (gut-selective 5HT4 receptor agonist), Linaclotide (minimally absorbed guanylate C receptor agonist, increases secretion of chloride and HCO3 into lumen)

134
Q

What is achalasia

A

Rare disease of the muscle of the lower esophageal body and the lower esophageal sphincter that prevents relaxation of the sphincter and an absence of contractions, or peristalsis, of the esophagus

135
Q

What is Nutcracker/Jackhammer oesophagus

A

Associated with pain on swallowing, cannot swallow, benign condition

136
Q

Describe condition associated with delayed gastric emptying

A

Gastroparesis - abdominal pain, vomiting, poorly controlled gastro-oesophageal reflux, malnutrition

137
Q

Describe the aetiology of gastroparesis

A

Idiopathic, longstanding diabetes, drugs - opiates, post viral

138
Q

Describe the symptoms of gastroparesis

A

Abdominal pain, nausea and vomiting, weight loss

139
Q

What is the management of gastroparesis

A

Dietary - frequent small foods, liquid preferred, post-pyloric feeding; attention to the underlying cause - limit opiates or codeine

140
Q

Describe the medications for gastroparesis

A

Prokinetics (5HT4 agonist - Cisapride, metoclopramide; D2 antagonists - metoclopramide, domperidone, motilin agonists - erythromycin), Endoscopic (botulin toxin injection to pyloric sphincter), gastric electrical stimulation ( high frequency low amplitude contractions)

141
Q

What is chronic intestinal pseudo-obstruction?

A

Signs of mechanical obstruction without mechanical occlusion of the gut, chronic abdominal pain, constipation, vomiting, wight loss; neuropathic or myopathic aetiology, primary neuropathy or myopathy, secondary to other diseases

142
Q

Describe acute post-operative ileus

A

Constipation and intolerance of oral intake in the absence of mechanical obstruction after surgery, up to 3 days

143
Q

Describe acute colonic pseudoobstruction

A

Large bowel parasympathetic dysfunction, commonest after cardiothoracic or spinal surgery, risk of caecal perforation

144
Q

What is the management of acute colonic pseudo-obstruction

A

Gut rest IV fluids, nasogastric decompression, Iv neostigmine, colonoscopic decompression, surgery

145
Q

Describe the possible causes of anal incontinence

A

Excessive rectal distension (acute or chronic diarrhoeal disease, chronic constipation), anal sphincter weakness (muscle damage, damage to pudendal nerve)

146
Q

What happens to colon in spinal injury above T12

A

Reflex bowel, damage to upper motor neurones, reflex arc intact, tonical anal sphincter, bowel opens spontaneously but without control, can be initiated by stimulation

147
Q

What happens to colon in injury to sacral nerve roots

A

Lower motor neurone injury, flaccid bowel, slow stool propulsion, flaccid and sphincter incontinence, manual evacuation

148
Q

What techniques are used for GI imaging?

A

Endoscopy, X-ray, fluoroscopic studies, cross-sectional studies, CT, ultrasound or MRI

149
Q

Describe the attributes of endoscopy

A

Endoscope inserted either through eosophagus (upper) GI or as colonoscopy, requires sedation, laxative for lower GI tract, small risk of perforation, poor toleration but allows therapeutic proceduce to be carried out like stenting

150
Q

Describe endoscope

A

Flexible small but long tube with camera, normally also second tube transmitting light, air and water

151
Q

What types of anaesthetic can be used for endoscopy?

A

Combination of Xylocain - spray to the back of the tongue, and Midazolam - sedative injection with amnesic effect requires monitoring

152
Q

What is the Z line?

A

Transition between the squamous oesophageal epithelium and gastric epithelium

153
Q

What can be X-ray used for in GI?

A

To find perferocation, can see air within the intestine and thus segmentation

154
Q

Describe fluoroscopy

A

Continued X-ray using contrast like barium or gastromiro, requires distension of tube with gas, good for upper and middle GI tract

155
Q

What is barium swallow?

A

High density material which glows on x-ray, to identify a perforation

156
Q

Describe the use of ultrasound in GI

A

Fast, cheap and safe, sonar technology, limited by habitus and gas, first line investigation in abdominal pain, best for gallstones in the gallbladder

157
Q

How is CT used in GI?

A

Usually with intravenous dye, oral dye or water, not so good in tissue visualization, main diagnostic tool for staging malignancy, response to treatment, percutaneous biopsy and to diagnose in general

158
Q

What is CT enterography?

A

CT with intravenous contrast material after the ingestion of liquid that helps produce high resolution images of the small intestine in addition to the other structures in the abdomen and pelvis

159
Q

What CT colonoscopy allows for?

A

Digital reconstruction

160
Q

What is PET CT?

A

Combination of PET and CT, functional imaging radioactive tracer uptake fused with anatomical information from CT; fluorodeoxyglucose is used as it accumulates in active cells, can determine metastatic activity

161
Q

Discuss use of MRI in GI

A

Excellent soft tissue differentiation but slow, Non-invasive imaging of biliary tree and small bowel, local staging of rectal cancer, diagnosing liver lesions, gallstones…

162
Q

Discuss diagnosis of upper GI bleeding

A

Medical history (melina, dyspepsia, anorexia, weight decrease), examination (pale, HR inc, hypotensive, low Hb, elevated urea possibly); investigations (X-ray, CT, barium swallow, PET scan, CT angiography)

163
Q

Discuss treatment of upper GI bleeding

A

1 - resuscitate, 2 - fit for endoscopy, 3 - endoscopy: Coil embolization (fibres provide a thrombotic medium and mechanical occlusion), adrenalin to cause spasm, clips

164
Q

What is melina?

A

Black tarry offensive motion, characteristic smell and visual, caused by loosing large amounts of blood in the upper GI tract, semi-digested blood

165
Q

Describe the pathophysiology of gastric ulceration

A

Stress ulcers develop with shock, sepsis hypotension or trauma, red and inflamed, disrupted mucosa, can be caused by H pylori

166
Q

What is gastritis?

A

Inflammation of the stomach lining - swollen and red

167
Q

Describe similarities of epidemiology and risk factors of gastritis and gastric ulceration

A

More common in men, middle-aged and older

Risk factors: NSAIDs, alcohol, H pylori infection; causes of bleeding: iron medication, caffeine, codeine, ulcer erodes

168
Q

Discuss diagnosis of lower GI bleeding

A

Rigid sigmoidoscopy - immediate, unprepared, limited; flexible sigmoidoscopy and radiology - 2 unsedated examinations, 2 preparations, CT pneumocolon - gives info outside the colon, colonoscopy - preparation, sedation, small risk but can also do biopsies and remove polyps, minimal prep stool tagged CT - large abnormalities, good for frail people

169
Q

How do we use CT colonography?

A

To identify polyps or other abnormalities, iodine preparation given to mark remaining faeces white to distinguish them from possible abnormality

170
Q

What are the different types of polyps?

A

Tubular adenoma (typical polyp with no pits), villous adenoma (has pits), carcinoma (circular shapes gain sharp edges)

171
Q

What is familial adenomatosis?

A

Carpet of small adenomatous polyps, high risk of developing adenocarcinoma so whole bowel resection at early age

P2 - Gastrointestinal system (5 decks)

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