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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Name the basic compartments of mouth

A

Palate, teeth, tongue and uvula (čípek)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Name the salivary glands

A

Sublingual, submandibular and parotid (posterior wall)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is the small intestine divided?

A

Duodenum, Jejunum and Ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is the large intestine divided?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the innervation of mouth?

A

CNs VII (facial nerve) and IX (glossopharyngeal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe venous drainage of oesophagus.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the layers of muscularis propria in the stomach?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Does the stomach has adventitia or serosa?

A

Serosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the anatomical compartments of stomach?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the anatomical curvatures of the stomach?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are rugae?

A

Gastric mucosal folds to allow stretch of the stomach.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are foveolae?

A

Gastric pits within the rugae.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Name the regions and cell types in gastric gland.

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Describe sphincters relating to stomach.
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
26
Describe the greater and lesser omenta.
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
27
Name the types of mucous cells and their specific and common function.
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
28
Characterise the parietal/oxyntic cell.
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 )
29
Characterise chief cell.
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
30
Characterise G cells.
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
31
Characterise D cells.
Supresses G cells by release of somatostatin - decrease gastrin Paracrine mechanism
32
Enterochromaffin cells
Type of neuroendocrine cells Release histamine to aid the release of HCl -seems to be the main driver
33
What is the epithelium of stomach?
Simple columnar epithelium.
34
What is the arterial blood supplly to the stomach?
Comes from celiac trunk Lesser curvature - anastomoses of the l/r gastric arteries Greater curvature - l/r gastro-epiploic arteries
35
What is the venous drainage of the stomach?
Parallel to the arteries Right and left gastric veins --\> hepatic portal vein Short gastric vein and l/r gastro-omental vein --\> superior mesenteric vein
36
What is the innervation of the stomach?
Parasympathetic Posterior vagal trunks Sympathetic T6 - T9 pass to the celiac plexus, also pain transmitting fibres
37
What is the lymphatic drainage of the stomach?
Gastric and gastro-omental lymph nodes found at the curvature Connect to celiac lymph nodes
38
Name the compartments of duodenum.
Superior Descending Inferior Ascending
39
What are the flexures of duodenum?
Inferior duodenal flexure Duodenojejunal flexure
40
What is contained within the descending duodenum?
Minor and major duodenal papillas - opening for bile and pancreatic secretions
41
What are the characteristics of duodenal mucosa?
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
42
What are the cell types within duodenum?
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
43
What is contained within the submucosa of duodenum?
Brunner's glands - provide abundant alkaline mucus to neutralize the acid contents entering the stomach
44
Describe Lamina propria of the small intestine.
Supplied by capillaries Includes single lacteal Thin strands of smooth muscle
45
Is the outer layer of duodenum serosa or adventitia?
Serosa
46
What connects the superior duodenum to the liver?
Hepatoduodenal ligament
47
Describe the vasculature of duodenum.
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
48
Where does food assimilation primarily happen?
Small intestine
49
What increases the surface area in small intestine?
Kerckring's folds Villi Microvilli on surface of enterocytes
50
What are Peyer's patches and where they are found?
Peyer's patches - lymph follicles, ileum
51
How is pancreas divided in terms of function?
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
52
Describe gallbladder, its function and structure.
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
53
What are the functions of large intestine?
Absorption of water Breakdown of fibre Storage and elimination of waste Large bowel flora - mainly anaerobes Bile acid conversion, vit K and ammonia production
54
What are tenia coli?
Tthree separate longitudinal ribbons of smooth muscle on the outside of the colon, they contract to produce the haustra (colon segments)
55
Describe the process of swallowing.
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
56
From where is swallowing controlled?
Reticular formation within the brainstem.
57
Describe the muscle in oesophagus.
From the upper oesophageal sphincter the muscle is skeletal, then gradually changes into smooth muscle as it extends to lower oesophageal sphincter.
58
How is oesophagus controlled?
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.
59
Describe the mechanism of segmentation within the stomach
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
60
What are hunger contractions of the stomach?
Migrating motor complex * initiated by motilin which is secreted by an empty stomach * frequency differs from peristaltic contractions
61
How does stomach empty?
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
62
What are the main patterns of gastrointestinal motility?
Segmentation - mixing Peristalsis - propulsion
63
What are the Interstitial cells of Cajal and where they are?
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
64
How is the basal electrical rhythm activity controlled?
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
65
Define peptic ulcers disease
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
66
Simply describe the pathophysiology and name aggressive factors
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
67
Describe Helicobacter Pylori and how it causes peptic ulcers disease
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
68
How does NSAIDs use can be precipitant in causing peptic ulcers
NSAIDs cause injury directly, trap H+ ions, and indirectly, systemic effect involving the inhibition of cyclo-oxygenases Increase bleeding risk PGE, PGI
69
How is the stomach epithelium normally protected?
Mucus bicarbonate layer Integrity of tight junctions between epithelial cells Process of restitution - space is filled by new cells
70
Describe the prevalence and risk factors for peptic ulcers disease
Common in 1-5% More in males More in smokers Stress considered important Age NSAIDs
71
Clinical features of peptic ulcers disease
Recurrent burning epigastric pain Mostly at night Worse when hungry May be relieved by antacids Nausea Anorexia and weight loss
72
How is peptic ulcer disease diagnosed?
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
Name the acid-lowering treatments for peptic ulcer disease
H2 receptor antagonists, Proton pump inhibitors, Antacids, Alginates and Simeticone
74
Discuss the characteristics of H2 receptor antagonists including its side-effects
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
Discuss the characteristics of proton pump inhibitors
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
Describe the characteristics of antacids
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
What do you know about alginates?
Used with antacids Increase viscosity and adherence of mucus to the oesophageal mucosa
78
What is Simeticone?
Also used with antacids Anti-foaming agent Relieves bloating and flatulance
79
Discuss the H. Pylori eradication therapy
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
What are the drugs that protect mucosa in peptic ulcer disease
Bismuth chelate - toxic effects on the bacillus Sucralfate - decreases degradation of mucus Misoprostol - analogue of prostaglandin E1
81
What are the surgical interventions for peptic ulcer disease and when they are used?
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
Describe gastric cancer
2nd commonest cause of cancer death worldwide Presents with anorexia, weight loss and anaemia Usually incurable
83
Describe the broad anatomy of the liver
84
Describe the lipoprotein-based fat and cholesterol transport system and its role in energy metabolism
85
Summary the findings in jaundice
86
What is achalasia
Oesophageal dysmotility
87
Describe the main components of stomach motility
Basal electrical rhythm - every 3 min; after threshold is reached activation of vagal afferents results in peristalsis, secretin provides negative feedback
88
What decreases the motility of the stomach
Cholecystokinin, secretin and glucose-dependent insulino-tropic peptide
89
What is motilin?
secreted when fasting in cycles to facilitate gastrointestinal motility - interdigestive myoelectric complexes, inhibited after food ingestion
90
Discuss peristalsis
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
Discuss the motility of the small intestine
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
Motility in the large intestine
Haustral contractions and mass movement
93
Describe secretory processes in the stomach
1. H+ produced by parietal cells; 2. pepsin produced by chief cells; 3. intrinsic factor; 4. mucus; 5. water
94
What is the gastric pH and what is its purpose?
pH about 1, kill bacteria, convert pepsinogen to pepsin
95
What is the structure of oxyntic gland?
Epithelial cells in the lumen, parietal cells deeper down and chief cells at the bottom
96
Discus gastric acid secretions
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
What stimulates acid secretion?
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
What stops acid secretion?
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
Name the 3 phases of gastric secretions
1. Cephalic phase, 2. Gastric phase, 3. Intestinal
100
Describe cephalic phase of gastric secretions
Sight, smell and taste of food causes vagus to activate parietal and gastrin cells which moderately stimulates HCL and pepsinogen release
101
Describe the gastric phase of gastric secretions
Distension of stomach and proteins in antrum cause vago-vagal reflex, gastrin and histamine release further causing strong stimulation of HCl/pepsinogen
102
Which foods directly stimulate gastrin release
Proteins, coffee, calcium rich
103
Describe intestinal phase of gastric secretions
If proteins in duodenum stimulate gastrin HCl in duodenum stimulates secretin secretions - inhibition Lipid in duodenum causes the release of peptide YY (inhibitory)
104
List the secretions of the crypts of the small intestine
NaCl/NaHCO3- (neutralises gastric HCl), enteropeptidase - activates trypsinogen
105
List the secretions of the villus tips of the small intestine
Brush border enzymes - digestion
106
What are the pancreas secretions
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
What is an intrinsic factor and how it is secreted?
Produced by parietal cells, it is a glycoprotein that binds to vitamin B12
108
How is mucous formed in the stomach?
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
What are the possible outcomes of H Pylori infection?
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
What is the mechanism behind different outcomes of H Pylori infection?
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
What is the enteric nervous system?
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
What makes up the enteric nervous system
Myenteric plexus and submucosal plexus, with inputs from the autonomic nervous system (possibly its division)
113
Which cells mediate enteric neurotransmission?
Interstitial cells of Cajal, communicate with ICC and smooth muscle cell
114
When does the enteric nervous system take control?
Mediates reflex activity in the absence of CNS input
115
What extrinsic factors influence enteric nervous system?
Vagal control excites non-sphincter muscle, sympathetic control - inhibitory to non-sphincter muscle, excitatory to sphincteric muscle; 5 hydroxy-tryptamine, Motilin, opioid receptors
116
What are the areas of the gastrointestinal system under voluntary control?
Upper oesophageal sphincter and external anal sphincter
117
Describe the muscle in the oesophagus
Upper oesophageal sphincter, striated muscle, transitions to smooth muscle and ends in lower oesophagal sphincter; inner circular layer and outer longitudinal
118
How long is the oesophagus?
18 - 22 cm
119
What conditions can affect striated oesophageal muscle?
Polymyositis, Myasthenia gravis
120
What conditions can affect the smooth muscle of oesophagus?
Scleroderma, Achalasia
121
What happens during the interprandial period of the stomach and intestine?
Fasting period, cyclic contractions sequence which occurs every 90 min, involves the migrating motor complex
122
Describe the 4 phases of interprandial period od the stomach and intestine
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
What regulates the interprandial period of the stomach and small intestine?
Motilin - secreted from crypt cells of the small intestine
124
What is the function of the interprandial period of the small intestine?
To cleanse stomach and intestine
125
What happens to the contractions during gastric phase within the stomach?
Motor migratory/migrating complex is replaced by contractions of variable amplitude and frequency, allowing mixing and digestion
126
How are the contractions of the stomach during gastric phase controlled?
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
Describe small intestinal transit
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
Describe colonic motility
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
Describe the internal anal sphincter
Smooth muscle, involuntary control, in rest provides majority of the contraction
130
Describe the external anal sphincter
Striated muscle, voluntary control, recruited in reflex reaction to coughing/sneezing
131
Explain how motilin controls GI functions
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
What drugs reduce gastric motility?
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
What drugs increase motility of the gut?
Stimulant laxatives, Prucalopride (gut-selective 5HT4 receptor agonist), Linaclotide (minimally absorbed guanylate C receptor agonist, increases secretion of chloride and HCO3 into lumen)
134
What is achalasia
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
What is Nutcracker/Jackhammer oesophagus
Associated with pain on swallowing, cannot swallow, benign condition
136
Describe condition associated with delayed gastric emptying
Gastroparesis - abdominal pain, vomiting, poorly controlled gastro-oesophageal reflux, malnutrition
137
Describe the aetiology of gastroparesis
Idiopathic, longstanding diabetes, drugs - opiates, post viral
138
Describe the symptoms of gastroparesis
Abdominal pain, nausea and vomiting, weight loss
139
What is the management of gastroparesis
Dietary - frequent small foods, liquid preferred, post-pyloric feeding; attention to the underlying cause - limit opiates or codeine
140
Describe the medications for gastroparesis
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
What is chronic intestinal pseudo-obstruction?
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
Describe acute post-operative ileus
Constipation and intolerance of oral intake in the absence of mechanical obstruction after surgery, up to 3 days
143
Describe acute colonic pseudoobstruction
Large bowel parasympathetic dysfunction, commonest after cardiothoracic or spinal surgery, risk of caecal perforation
144
What is the management of acute colonic pseudo-obstruction
Gut rest IV fluids, nasogastric decompression, Iv neostigmine, colonoscopic decompression, surgery
145
Describe the possible causes of anal incontinence
Excessive rectal distension (acute or chronic diarrhoeal disease, chronic constipation), anal sphincter weakness (muscle damage, damage to pudendal nerve)
146
What happens to colon in spinal injury above T12
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
What happens to colon in injury to sacral nerve roots
Lower motor neurone injury, flaccid bowel, slow stool propulsion, flaccid and sphincter incontinence, manual evacuation
148
What techniques are used for GI imaging?
Endoscopy, X-ray, fluoroscopic studies, cross-sectional studies, CT, ultrasound or MRI
149
Describe the attributes of endoscopy
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
Describe endoscope
Flexible small but long tube with camera, normally also second tube transmitting light, air and water
151
What types of anaesthetic can be used for endoscopy?
Combination of Xylocain - spray to the back of the tongue, and Midazolam - sedative injection with amnesic effect requires monitoring
152
What is the Z line?
Transition between the squamous oesophageal epithelium and gastric epithelium
153
What can be X-ray used for in GI?
To find perferocation, can see air within the intestine and thus segmentation
154
Describe fluoroscopy
Continued X-ray using contrast like barium or gastromiro, requires distension of tube with gas, good for upper and middle GI tract
155
What is barium swallow?
High density material which glows on x-ray, to identify a perforation
156
Describe the use of ultrasound in GI
Fast, cheap and safe, sonar technology, limited by habitus and gas, first line investigation in abdominal pain, best for gallstones in the gallbladder
157
How is CT used in GI?
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
What is CT enterography?
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
What CT colonoscopy allows for?
Digital reconstruction
160
What is PET CT?
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
Discuss use of MRI in GI
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
Discuss diagnosis of upper GI bleeding
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
Discuss treatment of upper GI bleeding
1 - resuscitate, 2 - fit for endoscopy, 3 - endoscopy: Coil embolization (fibres provide a thrombotic medium and mechanical occlusion), adrenalin to cause spasm, clips
164
What is melina?
Black tarry offensive motion, characteristic smell and visual, caused by loosing large amounts of blood in the upper GI tract, semi-digested blood
165
Describe the pathophysiology of gastric ulceration
Stress ulcers develop with shock, sepsis hypotension or trauma, red and inflamed, disrupted mucosa, can be caused by H pylori
166
What is gastritis?
Inflammation of the stomach lining - swollen and red
167
Describe similarities of epidemiology and risk factors of gastritis and gastric ulceration
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
Discuss diagnosis of lower GI bleeding
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
How do we use CT colonography?
To identify polyps or other abnormalities, iodine preparation given to mark remaining faeces white to distinguish them from possible abnormality
170
What are the different types of polyps?
Tubular adenoma (typical polyp with no pits), villous adenoma (has pits), carcinoma (circular shapes gain sharp edges)
171
What is familial adenomatosis?
Carpet of small adenomatous polyps, high risk of developing adenocarcinoma so whole bowel resection at early age