GI Flashcards
1
Q
What does kellikrein do, and why is it necessary?
A
Aids the production of bradykinin, which helps manage large blood supply when working maximally.
2
Q
What are the 4 layers of the gut wall? (Innermost to outermost)
A
Mucosa
Submucosa
External muscular layers (muscularis externae)
Serosa
3
Q
What is mucosa comprised of?
A
Epithelium
Lamina propria
Muscularis mucosa
4
Q
What is often a feature of the lamina propria?
A
Payers patches (aggregations of lymphocytes)
5
Q
What is submucosa comprised of?
A
A layer of connective tissue bearing glands, arteries, veins and nerves
6
Q
What is the muscularis external comprised of in the gut?
A
2 layers of smooth muscle (outer longitudinal and an inner circular layer)
Creates peristaltic waves to move luminal contents
7
Q
What is the serosa?
A
A serous membrane comprised of connective tissue and simple squamous epithelium (mesothelium)
8
Q
What enzymes does saliva contain?
A
Amylase and lipase
9
Q
How is saliva bacteriostatic?
A
Contains immunoglobulin A, antibody IgA
10
Q
Why does saliva have a high calcium content?
A
To help protect the teeth
11
Q
How does the stomach help prevent rises in pressure as it fills?
A
It’s walls relax
12
Q
What are the 3 layers of muscle in the stomach?
A
Oblique, circular and longitudinal
13
Q
Is the chyme leaving the stomach hypotonic, isotonic, or hypertonic?
A
Hypertonic
14
Q
What happens to the hypertonic chyme in the duodenum?
A
Water is drawn from the ECF to render the hypertonic solution isotonic.
Liver secretes vile (containing water, alkali and bile salts to emulsify fats)
Pancreas secretes alkali to help neutralise acidic chyme, along with enzymes to digest food
15
Q
What is plicae circulares, and where are they found?
A
Protrusions with villi on them to further increase surface area. Found in the jejunum
16
Q
Where is the small intestine most active?
A
Proximal
17
Q
List the components of the colon in order
A
Caecum, ascending, transverse, descending, sigmoid
18
Q
What are the 2 neural plexuses of the gut wall?
A
Submucosal plexus (plexus of Meissner) Myenteric plexus
19
Q
What effect does histamine have in the stomach?
A
Helps control the production of acid
20
Q
What approximate pH is saliva?
A
~pH8
21
Q
Is saliva hypertonic, isotonic, or hypotonic?
A
Hypotonic (more isotonic if high flow rate)
Rich in K+ and HCO3
22
Q
What causes secretion of saliva?
A
Contraction of myoepithelial cells in salivary glands
23
Q
List some immune proteins present in saliva
A
IgA, lysozyme, lactoferrin
24
Q
How does lactoferrin function as an immune protein?
A
Sequesters iron away from bacteria
25
How does saliva aid bolus formation?
Moistens and lubricates forming bolus
26
Approximately how much saliva is formed a day?
~1.5 litres
27
What are some consequences of xerostomia?
Lack of ability to taste (saliva is the solvent for taste molecules)
Sore lips, inflamed tongue
28
What are the 3 salivary gland pairs
Parotid glands
Sublingual glands
Submandibular glands
29
Which of the salivary glands isn't easily palpable?
Sublingual glands
30
Which nerve innovates the parotid glands?
Glossopharangeal nerve
31
Which nerve innovates the sublingual and submandibular glands?
Facial nerve
32
What sort of saliva does the parotid gland produce?
Rich in water, electrolytes and enzymes
33
What percentage of saliva production comes from the parotid glands?
~25%
34
What sort of saliva do the sublingual glands produce?
Rich in mucus
35
Approximately what percentage of saliva is produced by the sublingual glands?
~5%
36
What sort of saliva do the submandibular glands produce?
Serous and mucus
37
Approximately what percentage of saliva is produced by the submandibular glands?
~70%
38
What effect does the sympathetic nervous system have on the salivary glands?
Reduces blood flow to salivary glands (hence dry mouth when nervous)
39
Is the solution secreted by the acinar cells of the salivary glands hypertonic, isotonic or hypotonic?
Isotonic. Solution is made hypotonic as it travels along ducts, hence why solution is more isotonic when there is a high flow rate
40
Salivary glands above the aural fissure are innervated by what nerve?
Greater petrosal of VII
41
Salivary glands below the aural fissure are innervated by what nerve?
Chorda tympani of VII
42
What is one clinical effect of the path the chorda tympani of VII takes?
Runs through the middle ear, so can be cut off by infection
43
Name and describe the 3 phases of swallowing
1. Voluntary - bolus moved towards pharynx, once it touches the pharyngeal wall, the next phase begins
2. Pharyngeal - afferent info from receptors in pharynx reaches swallowing centre in brain. Soft pallet seals off nasopharynx. Pharyngeal constrictors push bolus downwards. Larynx elevates, closing epiglottis. Vocal cords addict, breathing temporarily ceases. Opening of upper oesophageal sphincter.
3. Oesophageal- closing of upper oesophageal sphincter. Peristaltic waves carries bolus downwards into oesophagus.
44
How is muscle in the oesophagus distributed?
Upper 1/3 - voluntary striated muscle, under control of somatic nerves.
Lower 2/3 - smooth muscle under control of the parasympathetic nervous system
45
What may cause dysphasia?
Neurological flaw
Luminal obstruction
External obstruction
46
What facters help prevent gastro-oesophageal reflux?
Functional sphincter formed formed from smooth muscle of distal oesophagus
Diaphragm
Intra-abdominal oesophagus which gets compressed when intra-abdominal pressure rises
Mucosal 'rosette' at cardia
Acute angle of entry of oesophagus
47
What is the function of the greater omentum?
Limits infection, forms localised abscess instead of peritiniumitis (which has a very poor mortality)
48
What can a weakened linea alba result in?
Divarication of recti (not a hernia)
| Common in woman who have had many kids
49
Why is a rectum sheath hernia so very painful?
No room for blood to accumulate as muscle is entrapped in the linea alba
50
How does one tell the difference between a patent urachus and a patent vitellointestinal duct?
Inject dye
51
What is exampholos?
Umbilical defect. Visceral covered by peritoneum and amnion
52
What is referred pain?
Pain received at a site distant from the site causing the pain
53
What is somatic referred pain?
Pain caused by a noxious stimulus to the proximal part of a somatic nerve that is perceived in the distal dermatome of the nerve. (Brain thinks pain is coming from the end of the nerve/where nerve goes to)
54
What is visceral referred pain?
In the thorax and abdomen, visceral afferent pain fibres follow sympathetic fibres back to the same spinal segments that gave rise to the preganglionic sympathetic fibres.
CNS perceives visceral pain as coming from the somatic portion of the body supplied by the relevant spinal cord segments
55
What may cause visceral pain?
```
Iscaemia
Abnormally strong muscle contraction
Inflammation
Stretch
NOT touch, burning, cutting, crushing
```
56
What may cause referred left shoulder pain?
Diaphragmatic irritation, e.g. By ruptured spleen, ectopic pregnancy, perforated ulcer...
Only left shoulder as liver is in the way of the right side of the diaphragm
57
Define hernia
A protrusion of part of the abdominal contents beyond the normal confines of the abdominal wall/its containing cavity.
58
What 3 components make up a hernia?
The sac
The contents of the sac
The coverings of the sac
59
What constitutes the sac of a hernia?
A pouch of peritoneum
60
What constitutes the contents of a hernia?
Anything found in abdominal cavity (commonly loop of bowel, omentum)
61
What constitutes the coverings of a hernia?
Layers of the abdominal wall through which the hernia has passed
62
List 4 weaknesses in the abdominal wall
Inguinal canal
Femoral canal
Umbilicus
Any previous incisions
63
List the borders of the inguinal canal
Roof - transversalis fascia, internal oblique muscle, transversus abdominus
Posterior wall - transversalis fascia
Anterior wall - aponeurosis of the external oblique, internal oblique muscle
Floor - inguinal ligament, lacunar ligament
64
What are the 2 openings to the inguinal canal? Where are they found?
Deep (internal) ring - found above the midpoint of the inguinal ligament, lateral to the epigastric vessels.
Superficial (external) ring - marks the end of the inguinal canal, lies just superior to the pubic tubercle
65
How is the deep (internal) ring of the inguinal canal created?
Ring is created by the transversalis fascia which invaginates to form a covering of the contents of the inguinal canal.
66
How was the superficial (external) ring of the inguinal canal formed?
Formed by the evagination of the external oblique, which forms another covering of the inguinal canal contents
67
What does the inguinal canal contain?
In men, the spermatic cord, to supply and drain the tested.
| In women, the round ligament of uterus traverses through the canal
68
What usually prevents structures potentially entering the inguinal canal?
The wall are usually collapsed
69
What does the superficial (external) ring of the inguinal canal contain to prevent the ring from widening?
Intercrural fibres, which run perpendicular to the aponeurosis of the external oblique
70
What are the borders of the femoral canal?
Medical - lacunar ligament
Lateral - femoral vein
Anterior - inguinal ligament
Posterior - pectineal ligament, superior ramus of pubic bone, pectineus muscle
71
What is processus vaginalis?
Embryological developmental out pouching of the parietal peritoneum. Precedes the testes in their descent down within the gubernaculum. Closes, remaining portion around the testes becomes the tunica vaginalis
72
What is the gubernaculum?
Condensed band of mesenchyme that links inferior portion of testes (gonad) to labioscrotal swelling
73
Which border of the inguinal canal contains the deep ring?
Posterior wall
| Transversalis fascia
74
Which border of the inguinal canal contains the superficial ring?
Anterior wall
| Aponeurosis of external oblique
75
What are the 2 types of inguinal hernia?
Indirect and direct
76
Describe an indirect inguinal hernia
Passes through deep inguinal ring. Goes through inguinal canal, and out superficial inguinal ring. Then, depending on where processus vaginalis was obliterated, can potentially descend into the scrotum
Superior source to femoral vessels
77
Describe an direct inguinal hernia
Bulges through Hesselbach's triangle, generally in the vicinity of the superficial inguinal ring
78
What are the boundaries of Hesselbach's triangle/inguinal triangle?
Medial - lateral margin of rectus sheath (also called linea semilunaris)
Superolateral border - inferior epigastric vessels
Inferior border - inguinal ligament
79
What differentiates between a direct or an indirect inguinal hernia?
Direct - lateral/superior to inferior epigastric vessels
| Indirect - medial/inferior to inferior epigastric vessels
80
What is omphalocele?
Abdominal contents herniated into umbilical cord. Has peritoneal covering.
81
Where does an epigastric hernia occur?
Occurs through the linea alba, between xiphoid process and umbilicus.
82
What is an 'incarcerated' hernia?
Stuck, irreducible (can't be pushed back through)
83
What is a 'strangulated' hernia?
Blood supply is disrupted, can lead to necrosis
84
What is a diaphragmatic hernia?
Defects in diaphragm may allow any viscus to herniate into chest
85
What are the basic functions of the stomach?
Disinfection
Short term store of food
Continue digestion
Disrupt food
86
What type of epithelium lines stomach walls?
Columnar epithelium
87
What type of epithelium lines the oesophagus?
Stratified squamous
88
What are gastric pits?
Little 'holes' in the stomach wall with gastric glands at their base
89
What types of cells are present in the stomach?
Mucous, parietal, chief, G-cells
90
What is special about the stomachs smooth muscle compared to the rest of the GI tract?
Extra oblique layer of muscle
91
Describe the action of the upper stomach muscle
Sustained contractions, creates basal tone
92
Describe the action of the lower stomach muscle
Strong peristalsis mixes contents. Coordinated movements, every 20s or so, moving contents proximal to distal
93
How does the shape of the stomach effect its contents passage through it?
Funnel shape accelerates food towards duodenum. Sphincter there only lets liquid chyme through, lumps are left behind for further digestion
94
How does vagally mediated relaxation of the stomach as it fills aid it's ability to act as a store of food?
Allows food to enter stomach without raising intra-gastric pressures too much
Prevents reflux of contents during swallowing
Gastric mucosal foods (rugae) allows distension
95
What enables distension of the stomach?
Gastric mucosal folds (rugae)
96
What functions does stomach acid have?
Disinfects stomach contents
Helps untraveled proteins
Activates proteases (pepsinogen to pepsin)
97
What secretions are secreted by the stomach wall?
HCl, mucus, HCO3-, pepsinogen, intrinsic factor
98
What does a parietal cell in the stomach secrete?
HCl and intrinsic factor
99
What does a G cell in the stomach secrete?
Gastrin
100
What does a enterochromaffin like cell (ECL) in the stomach secrete?
Histamine
101
What does a Chief cell in the stomach secrete?
Pepsinogen
102
What does a D cell in the stomach secrete?
Somatostatin
103
What does a Mucous cell in the stomach (surface and neck) secrete?
Mucous
104
Where are the majority of gastric glands located?
At the base of gastric pits
105
What does the cardia of the stomach predominantly secrete?
Mucus
106
What does the fundus/body of the stomach predominantly secrete?
Mucus, HCl, pepsinogen
107
What does the pylorus of the stomach predominantly secrete?
Gastrin, somatostatin
108
What effect does gastrin have parietal cells?
'Normal' stimulus
109
What effect does histamine have parietal cells?
'Amplifier' (alone wouldn't have much effect)
110
What effect does ACh have parietal cells?
Increases secretion (from nervous system, especially when combined with histamine)
111
What stimulates gastrin secretion by G cells in the Antrum of the stomach?
```
Peptides/amino acids in stomach lumen
Vagal stimulation (acetylcholine, gastrin-releasing peptide GRP)
```
112
What inhibits HCl production?
```
Low pH (i.e. When food, which acts as buffer, leaves stomach) activates D cells, which secrete somatostatin, which inhibits G cells (& ECL cells).
Stomach distension reduces, reduced vagal activity
```
113
What does somatostatin do in the stomach?
Inhibits G cells (& ECL cells), reducing gastrin and histamine secretion.
114
Describe the process of HCl production in the stomach
```
Water is split (H+ and OH-)
H+ moved into stomach lumen
Cl- moved into stomach lumen
CO2 combines with OH- forming HCO3-, which is moved into the bloodstream (alkaline tide)
Very energy intensive!
```
115
What is the proton pump used to produce HCl in the stomach?
H+/K+ ATPase
116
What are the 3 phases of digestion?
Cephalic (pre-stomach)
Gastric (stomach)
Intestinal (post-stomach)
117
Describe the cephalic portion of digestion
Smelling, tasting, chewing, swallowing, parasympathetic stimuli. Direct stimulation of parietal cell by vagus nerve. Stimulation of G cells by vagus nerve (GRP) released)
Anticipation of food - increases gastric motility
118
Describe the gastric phase of digestion
Distension of stomach stimulates vagus nerve, which then stimulates parietal and G cells. Presence of amino acids and small peptides stimulates G cells. Food acts as buffer, removes inhibition on gastrin production. Enteric NS and gastrin causes smooth muscle contractions
119
Describe the intestinal phase of digestion
Chyme initially stimulates gastrin secretion - partially digested proteins detected in duodenum, short phase. Soon overtaken by inhibition of G cells. Presence of lipids activates enterogastric reflex - reduces vagal stimulation. Chyme stimulates CCK and secretin (helps suppress secretion)
120
What are the defences the stomach has to protect against digesting itself?
Mucins and HCO3-, release by surface mucosal cells, neck cells in gastric glands. Forms thick alkaline viscous layer that adheres to epithelium
High turnover of epithelial cells
Prostaglandins - maintains mucosal bloodflow, supplying epithelium with nutrients
121
What things might breach the stomach defences?
Alcohol - dissolves mucus layer
Helicobacter pylori - chronic active gastritis
NSAIDs - inhibits prostaglandins
122
What does breaches in stomach defences lead to?
Gastritis (inflammation), ulceration, reflux disease
123
What pharmacological intervention could you use if the stomachs defences have been breached?
```
H2 blockers (cimetidine, ranitidine)
Proton pump inhibitors (omeprazole)
```
124
What are the stomachs defences against its gastric acid?
Mucins/HCO3-: released by surface mucus cells in gastric glands. Forms thick alkaline viscous layer that adheres to epithelium (epithelial surface maintained at higher pH)
High turnover of epithelial cells
Postaglandins: maintains mucosal bloodflow, supplying epithelium with nutrients
125
List some things which might breach the stomachs defences to its own gastric acid
Alcohol - dissolves mucus layer
Helicobacter pylori - chronic active gastritis
NSAIDs - inhibits postaglandins
126
What can breaches in the stomachs defences against its own gastric acid lead to?
Gastritis (inflammation), ulceration, reflux disease
127
What pharmacological interventions can be used when the stomachs defences to its own gastric acid are compromised?
```
H2 blockers (cimetidine, ranitidine)
Proton pump inhibitors (omeprazole)
```
128
Name a proton pump inhibitor
Omeprazole
129
Name a H2 blocker
Cimetidine
| Ranitidine
130
What is dyspepsia?
Upper GI symptoms
131
What does GORD stand for?
Gastro oesophageal reflux disease
132
What are the symptoms of GORD?
Gastro oesophageal reflux disease
| Heartburn, cough, sore throat, dysphagia
133
What can cause GORD?
Gastro oesophageal reflux disease
Lower oesophageal sphincter problems, delayed gastric emptying (raised intracellular-gastric pressure), hiatus hernia, obesity
134
What are some problems that may occur with GORD?
Oesophigitis, strictures, Barrets oesophagus (metaplasia of squamous epithelium to columnar), increased risk of developing Adenocarcinoma
135
What metaplasia occurs in barrets oesophagus?
Metaplasia of squamous epithelium to columnar
136
What treatment can be used to GORD?
Lifestyle modifications
Pharmacological (antacids, proton pump inhibitors, H2 antacids)
Surgery (rare)
137
What is the most common cause of gastritis?
H. Pylori infection
138
What could cause chronic gastritis?
Bacterial - H pylori infection
Autoimmune - antibodies to gastric parietal cells, can lead to pernicious anaemia
Chemical/reactive - alcohol, NSAIDs, bile reflex (minimal inflammation)
139
What are the symptoms of chronic gastritis due to H pylori infection?
Asymptomatic, or pain, nausea, vomiting ect. Others may develop due to complications e.g. Peptic ulcers, Adenocarcinoma
140
What are the symptoms of chronic gastritis due to autoimmunity?
Anaemic symptoms (tired, breathless...), glossitis, anorexia, neurological symptoms
141
What is glossitis?
Inflammation of the tongue
142
What is peptic ulcer disease?
Defects in gastric/duodenal mucosa. Must extend through muscularis mucosa.
143
Where is peptic ulcer disease most common?
1st part of duodenum, lesser curve of the stomach
144
What are the normal defence mechanisms against peptic ulcer disease?
Mucus, bicarbonate, prostaglandins, epithelial renewal, adequate mucosal bloodflow (can remove acid that diffuses through injured mucosa)
145
What are the symptoms of peptic ulcer disease?
Epigastric pain (sometimes back pain), burning/gnawing following meals, bleeding, anaemia, satiety early, weight loss
146
What is functional dyspepsia?
Symptoms of ulcer disease, but no physical evidence of organic disease
147
How might peptic ulcer disease be diagnosed?
Upper GI endoscopy, biopsies (benign/malignant ulceration, H-pylori), urease breath test, errect CXR (perforation), bloodtests (anaemia)
148
How would you treat peptic ulcer disease caused by H-pylori?
Eradicate organism - triple therapy:
PPI
Clarithromycin
Amoxicillin
149
What treatment might you use for peptic ulcer disease?
Stop NSAIDs
Endoscopy for bleeding ulcers (and follow up for gastric ulcers)
PPIs
150
What sort of bacteria is helicobacter pylori?
Helix shaped
Gram negative
Microaerophilic
Has a flagellum
151
What is a microaerophilic organism?
Requires O2 to survive, but prefers a lower concentration of O2 than present normally in the atmosphere
152
How does h pylori produce urease?
Converts urea to urease and ammonium
153
How does h pylori survive the stomachs low pH?
Converts urea to urease and ammonium, using the NH4+ to produce a less acidic cloud in which it lives within the mucus layer of stomach
154
How does h pylori damage the stomach?
```
Releases cytotoxins
Direct epithelial injury
Ammonia produced is toxic to epithelia
Promotes inflammation response
Possibly degrades mucus layer
```
155
What is the effects of H pylori dependent on?
Location of colonisation within the stomach
156
What are the effects of H pylori if it colonises in the antrum?
Home of G cells
Increased gastrin secretion (or decreased D cell activity)
Increased parietal cell acid secretion, duodenal epithelium metaplasia - colonisation of duodenum - duodenal ulceration
157
What are the effects of H pylori if it colonises in the body of stomach?
Atrophic effect. Gastric ulcer - leads to intestinal metaplasia, dysplasia, cancer.
158
What is Zollinger-Ellison syndrome?
No beta islet cell gastrin secreting tumour of the pancreas. Can be a part of MEN1. Proliferation of parietal cells - lots of acid production. Severe ulceration of the stomach and small bowel. Abdominal pain, diarrhoea
159
What is stress ulceration?
Symptoms of gastritis/ulceration following severe burns, raised intercranial pressure, sepsis, severe trauma, multiple organ failure ect.
160
How might stomach cancer present?
Dysphagia, anorexia, malaena, weight loss, nausea/vomiting, virchovs nodes enlarged
Has to be quite large before symptoms present
161
What are some risk factors for stomach cancer?
Male, H-pylori, dietary factors, smoking
162
What sort of cancer is the majority of stomach cancers?
Adenocarcinomas
| Small number of lymphomas, carcinoid, stromal
163
How might one diagnose stomach cancer?
Bloods, upper GI endoscopy, CT, Rx, surgery, chemotherapy, radiation
164
What osmotic state is the chyme that enters the duodenum from the stomach?
Hypertonic
165
What corrects the hypertonicity of chyme leaving the stomach?
Osmotic movement of large quantities of water across the permeable duodenal wall
166
How is the acidity of the chyme leaving the stomach corrected?
The addition of alkali secreted by pancreas and liver, derived from the excess HCO3- added to the blood as a result of gastric acid secretion
167
Why is chyme leaving the stomach hypertonic?
Lots of solute from food dissolved in gastric juice - the stomach wall is largely impermeable to water (so it can't dilute chyme)
168
What proportion of the pancreas is exocrine?
~90%
169
What is the result of sympathetic stimulation of the pancreas?
Inhibition
170
What is the result of parasympathetic stimulation of the pancreas?
Stimulation
171
What hormone can stimulate a pancreatic acinus?
Cholecystokinin CCK
172
What proteases does the pancreas secrete?
Trypsin(ogen)
Chymotrypsin
Elastase
Carboxypeptidase
173
How are enzymes formed in the pancreas?
Formed on ribosomes on RER, packaged via golgi apparatus into zymogen granules, which are released by exocytosis with appropriate stimulus - parasympathetic/CCK
174
What might be found in the bloodstream if the pancreas is damaged?
Enzymes (notably amylase)
175
What are zymogen granules?
Membrane bound vesicles containing zymogens (inactive precursors to enzymes). Avoids digestion of pancreas
176
What do duct cells in the pancreas do to help produce alkali?
Secrete alkali by pumping HCO3- actively from extracellular fluid into lumen. H+ ions expelled across basolateral membrane using energy derived from the inward movement of Na+. This combines with HCO3- to generate CO2 which enters the cells, and reacts with H2O to form HCO3- and H+.
177
What osmotic state is the exogenous excretions from the pancreas?
Isotonic
178
What does secretin do?
Controls secretion of enzymatic juice from pancreas
179
Where is secretin produced?
S cells in the jejunum in response to acidity of the jejunal contents
180
What potentiates the action of secretin?
CCK
181
What happens to the concentration of HCO3- in pancreatic secretions at faster flow rates?
Increased secretion of HCO3-, so increased conc. of HCO3-
182
List some of the livers functions
Metabolism, detoxification, plasma protein production, secretion of bile
183
Approximately how much bile is secreted by the liver a day?
~250ml
184
What are the gut related functions of the liver?
Secretion of bile acids and alkaline juice
| Excretion of bile pigments - especially bilirubin
185
What is the chief functioning cell of the liver?
Hepatocytes (~80% of mass of liver)
186
Describe hepatocytes
Very active at producing proteins/lipids for export. Contain lots of rough/smooth ER and stacks of golgi membranes. Contain lots of glycogen.
187
What is the structural unit of the liver?
A lobule
188
What is a liver lobule?
Structural unit of the liver - hexagon surrounding a central vein which drains the blood.
Blood from hepatic arteries and portal vein enters vessels on the periphery of lobule, and flows through sinusoids lined by hepatocytes to the central vein.
189
Describe the flow of blood in a hepatic lobule
Blood from hepatic arteries and portal vein enters vessels on the periphery of lobule, and flows through sinusoids lined by hepatocytes to the central vein.
190
Where is bile formed?
In the canaliculi, then flows towards the periphery where it then drains into bile ducts
191
What are the 2 components of bile?
Bile acid dependent fraction (secreted by cells lining the canaliculi) - bile salts, cholesterol, bile pigments
Bile independent fraction (secreted by cells lining the intro-hepatic bile ducts, stimulated by secretin) - alkaline
192
Where is the bile acid dependent fraction of bile secreted?
Cells lining the canaliculi
193
Where is the bile acid independent fraction secreted from?
Cells lining the intro-hepatic bile ducts
194
What stimulates secretion of the bile acid independent fraction?
Secretin
195
What are the 2 main bile salts?
Cholic acid
| Chenodeoxycholic acid
196
What are the 2 main bile salts derivatives of?
Cholesterol
197
What amino acids are conjugated with bile salts in bile?
Glycine or taurine
198
How are bile salts composed in bile?
Conjugated to amino acids, then travel in bile in micro particles (micelles made up of bile acids, cholesterol and phospholipids)
199
What are bile pigments?
Secretory products conjugated in the liver and secreted in bile (major one is bilirubin - breakdown product of haemoglobin)
200
What is the function a micelle?
A vehicle to carry hydrophobic molecules through an aqueous medium e.g. Products of lipid digestion (cholesterol, monoglycerides, free fatty acids)
201
What happens to micelles?
Diffuse with products of the brush border of epithelial cells, can be released slowly and diffuse into epithelial cells.
Once inside, fats are reconstituted into triglycerides, phospholipids, cholesterol ect, and re expelled as chylomicrons (facilitate transport of fat in the lymphatic system from gut to systemic veins)
202
What do chylomicrons do?
facilitate transport of fat in the lymphatic system from gut to systemic veins
203
What is around the surface of a chylomicron?
Apoproteins around the external surface
204
Why can chylomicrons only enter lymph capillaries (lacteal)?
Too large to enter 'normal' capillaries
205
How do chylomicrons leave the basement membrane of gut epithelial cells?
Exocytosis
206
Where do chylomicrons renter vascular circulation?
Via thoracic duct
207
Where are bile acids absorbed?
The terminal ileum (apart from a small proportion deconjugated by bacterial action)
208
How are bile acids returned to the liver?
Absorbed in the terminal ilium and returned via portal vein
209
How are losses of bile acids replaced?
Hepatic synthesis
210
What does the gall bladder do?
Concentrates bile (removes H2O/ions), reducing its volume
211
What is a consequence of the gall bladder concentrating bile?
Increasing the risk of gallstones, which can move into neck of gall bladder/biliary tree, causing painful biliary colic or obstruction (followed by inflammation and infection)
212
How is bile released?
Smooth muscle contraction, stimulated by CCK (cholecystokinin) released from the duodenum
213
What stimulates smooth muscle contraction, leading to the secretion of bile?
Stimulated by CCK (cholecystokinin) released from the duodenum
214
How can cirrhosis lead to portal hypertension?
Fibrous tissue surrounds intrahepatic vessels, impeding circulation
215
List some physical adaptations of the GI system against toxins/infection
Gastric acid, saliva, sight, smell, memory...
216
What does saliva contain to help defend against infection?
Lysozyme, lactoperoxidase, complement, IgA, polymorph
217
Approximately how much gastric juice is produced each day?
2.5l
218
What is the lowest pH gastric juice can be?
0.87
219
What is achlorhydria?
Low (or absent) production of hydrochloric acid in gastric secretions of the stomach and other digestive organs
220
What are patients with achlorhydria more susceptible to?
Infection from shingellosis, cholera, salmonella, C. difficile
221
What might cause achlorhydria?
Drugs e.g. PPI, H2 antagonists
222
What is an AAFB?
Acid and Alcohol Fast Bacterium
223
Of what clinical relevance is mycobacterium tuberculosis being AAFB?
It is resistant to gastric acid, therefore washings can be used to collect the bacteria for diagnostic purposes
224
List some pathogens that are resistant to gastric acid?
Enteroviruses e.g. Hep A, polio, coxsackie,
Helicobacter pylori
Mycobacterium tuberculosis
225
What must bacteria be able to resist in or due to survive in the small intestine?
Bile (detergents), proteolytic enzymes, lack of nutrients, anaerobic environment, shedding of epithelial cells and rapid transit (peristalisis)
226
Is the small bowel normally sterile?
Yes
227
What is the main role of the colon?
Water absorption
228
Is the colon an aerobic or anaerobic environment?
Anaerobic
229
What protects the colonic epithelium from its contents?
Mucus layer
230
What is eosinophillia?
A raised number of eosinphils
231
What might cause eosinophillia?
Asthma, hay fever or parasite infections (more common in Africa)
232
What do mast cell granules contain?
Histamine
233
What is a consequence of gut infections that activate complement?
Recruitment of mast cells, which release histamine. This causes vasodilation and increased capillary permeability - and can result in massive fluid loss e.g. In cholera
234
Where are most mast cells located in the body?
Lungs, liver and spleen.
| Monocytes are in the blood circulating, become macrophages in tissue
235
Where does all of the venous drainage of the gut from the duodenum down end up?
In the hepatic portal vein, into the hilum of the liver
236
What is the portal system?
2 capillary systems in series - the hepatic portal system and the hypothalamo-hypophyseal portal system
237
What is a kupffer cell?
A macrophage in the liver
238
What might cause liver failure?
Viral hepatitis, alcohol, overdose of drugs such as paracetamol, halothane, industrial solvents, mushroom poisoning
239
What does liver failure lead to increased susceptibility of?
Bacterial and fungal infections, toxins, drugs and hormones. High mortality
240
How is ammonia produced in the body?
By colonic bacteria and deamination of amino acids.
241
What can increased blood ammonia cause?
Encephalopathy (bad, very difficult to treat)
242
Why may there be increased blood ammonia in liver failure?
Failure to clear ammonia via urea cycle
243
What can portal venous hypertension lead to?
Portosystemic shunting, and therefore toxin shunting. Portosystemic shunting leads to oesophageal varices, haemorrhoids, and capt medusa
244
What can portosystemic shunting lead to?
Oesophageal varices, haemorrhoids, and capt medusa
245
What are the adaptive cellular defences of the GIT?
B-lymphocytes - produce antibodies including IgA and IgE that are particularly effective against extracellular microbes
T-lymphocytes - are directed against Intracellular organisms
246
What is the adaptive defences of the GIT lymphatic tissue?
Gut associated lymphoid tissue (GALT) is diffusely distributed, but also nodular at the tonsils, at payers patches and at the appendix
247
What is MALT ?
Mucosal associated lymphoid tissue
248
What is ileocaecal lymphatic tissue there for?
Patches at terminal ileum in case of reflux of bacteria in colon to ileum
249
What is a common cause of right iliac fossa pain in children that might be mistaken for appendicitis?
Mesenteric adenitis - caused mostly by adenovirus/coxsackie virus
250
What is the result of lymphoid hyperplasia at the appendix base?
Obstructed outflow of appendix, stasis and infection - appendicitis
251
When is purulent appendicitis commoner?
During epidemics of chickenpox in children
252
What might cause obstructive appendicitis
Fecolith (worm)
| Lymphoid hyperplasia
253
What might cause intestinal/hepatic ischaemia?
Arterial disease, systemic hypotension, intestinal Venus thrombosis
254
What can intestinal/hepatic ischaemic lead to?
Over whelming sepsis and rapid death
255
Why can liver disease present in many different ways?
Many different functions of the liver
256
List some possible symptoms of liver disease
Bleeding/poor clotting, oedema/ascites/ankle swelling, skin irritation, jaundice, abdominal pain, jaundice, asymptomatic, encephalopathy, nausea, vomiting....
257
What must happen to bilirubin in order for it to get into the liver?
Must be attached to albumin
258
What happens to biliruben once if gets into the liver?
Biliruben is then conjugated to make it water soluble - urobilingen which is a bile pigment
259
Describe how pre-hepatic jaundice occurs
Increased biliruben load to the liver e.g. Haemolytic anaemia. Liver can't conjugate all this amount fast enough, any unconjugated biliruben remains in blood circulation
260
Describe the process by which hepatic jaundice might occur
Decreased rate of conjugation of biliruben e.g. Injury/damage to the liver
Defects in conjugation e.g. Gilbert's syndrome
Unconjugated biliruben and conjugated bacteria
261
Describe the process by which post hepatic jaundice occurs
Obstruction to bile drainage into duodenum e.g. Gallstones, pancreatic cancer, intrahepatic obstruction to drainage (hepatocyte swelling)
Biliruben in the bile is conjugated (water soluble), cannot leave biliary drainage system, refluxes into circulation but doesn't make it into stool (which is thus pale and floats)
262
What do LFTs give an indication of?
Traditional ones give an indication of liver damage, rather than function
263
What 4 enzymes might leak from the liver if damaged?
Alanine Aminotransferase ALT
Aspartate Aminotransferase AST
Alkaline Phosphodiesterase ALP
Gamma-glutamyltransferase GGT
264
In what cells might alkaline phosphodiesterase ALP be found in?
Cells lining the bile ducts
265
How would you take a true measure of liver function?
Measuring proteins synthesised by liver e.g. Albumin, clotting factors
266
What precisely is hepatitis?
Inflammation of the liver
267
What is steatosis, steatohepatitits?
Fatty liver
268
What might cause steatohepatitis?
Alcoholic-related fatty liver disease
| Non-alcoholic related fatty liver disease
269
What might cause hepatitis (liver inflammation)?
Viral e.g. Hep A, B, C...
Autoimmune
Drugs e.g. Alcohol, paracetamol
Hereditary disorder e.g. Haemochromatosis and Wilson's disease
Fatty liver disease (alcoholic and non-alcoholic)
Malignancy (metastases, or primary malignancy)
270
What is the most common kind of primary malignancy present in the liver?
Hepatocellular carcinoma
271
What can chronic liver disease lead to?
Cirrhosis
Inflammation of the liver (chronic or recurrent e.g. Alcohol abuse)
Ongoing liver cell damage/necrosis
Nodular regeneration and fibrosis (scarring). Architectural change to liver
Increased resistance to blood flow
Portal hypertension (clinical features ascites, and porto-systemic shunting)
272
Where are the major sites for porto-systemic anastomoses (distended engorged veins can appear here in portal hypertension)
Oesophageal varies - left gastric, oesophageal branches of azygous
Anorectal varies - superior rectal vein, middle and inferior rectal vein
Caput medusa - paraumbilical veins, superior and inferior epigastric vein
273
What can portal hypertension cause along with distended engorged veins at sites of porto-systemic anastomoses?
Ascites
| Splenomegaly
274
What does the biliary tree do?
Provides drainage system for bile
275
What can abnormal contractions of the gall bladder lead to?
Precipitation of bile constituents, leading to gall stones
276
What can gallstones be constituted of?
Mixed (most common)
| Pure cholesterol or pigment (calcium bilirubinate)
277
What can the of impaction of gallstones in biliary tree cause?
Biliary colic and/or cholecystitis
278
What are the symptoms of impaction of gallstones in biliary tree?
Nausea/vomiting
Abdominal pain (intermittent Vs constant)
Jaundice
Fever and RUQ tenderness (cholecystitis)
279
What imaging might you use to identify symptomatic gallstones?
Ultrasound
280
What is acute pancreatitis?
Damage to acinar cells releases enzymes, inflammation of pancreatic tissue
281
What is the most common cause of pancreatitis?
Gallstones, alcohol
282
How does pancreatitis present?
Severe pain, vomiting, hypotension. Significant mortality.
283
What is the treatment of pancreatitis?
Supportive - analgesics and fluids
284
What is the majority of pancreatic cancer?
Ductal adenocarcinoma (90%)
285
What is the major risk factor for pancreatic cancer?
Smoking
286
What are the symptoms of pancreatic cancer?
```
Initially symptomless, then develop:
Obstructive jaundice (head of pancreas sooner than body or tail)
Pain (referred to back)
Weight loss
Vomiting
Malabsorption
Diabetes
```
287
What constitution is chyme in the intestines?
Isotonic and neutral
288
What is the function of the intestines?
Absorb nutrients, water and electrolytes
289
What is the paracellular route?
The gaps between cells
290
What are plicae circulares?
Permanent circular folds in the intestine
291
How is the intestine adapted to have a large surface area?
Mucosa folded into villi. Surface is covered in micovilli. Plicae circulares.
292
What is the 'unstirred layer' in the intestine?
Layer of contents formed by the brush border where nutrients meet and react with enzymes secreted by the enterocytes, so completing digestion prior to absorption
293
What type of cells make up the intestinal epithelia?
Enterocytes and goblet cells (mucus producing)
294
What makes up an intestinal gland (crypt)?
Stem cells at base, migrate to surface, maturing as they migrate. Also enteroendocrine glands, paneth cells (part of the immune system)
295
What are paneth cells a part of?
The immune system
296
What constitutes a micelle?
Outer bile salts, inner lipids
297
How many sugars chained together can the body absorb?
Only single sugars!
298
How is glucose absorbed?
Alongside Na+
299
Where does final breakdown of molecules occur?
In the brush border, by 'brush border hydrolases'
300
What are the 'goal' monosaccharides which the body can absorb? The end points of carbohydrate digestion
Glucose
Fructose
Galactose
301
What sort of carbohydrate is starch?
Polysaccharide
302
What sort of carbohydrate is lactose?
Disaccharide
303
What sort of carbohydrate is sucrose?
Disaccharide
304
What bonds do alpha amylases cleave?
Alpha 1,4 bonds of straight chain amyloses
305
What can alpha amylases yield?
Cleave alpha 1,4 bonds of straight chains amyloses to yield glucose/maltose in a straight chain, or alpha limit dextrins in branched chains
306
What bonds does isomaltase break?
Branching points, alpha 1,6 bonds
307
What does isomaltase yield?
Breaks branching point alpha 1,6 bonds to yield glucose
308
What is starch digested into?
Glucose
309
What is maltose digested into?
Glucose (x2!)
310
What breaks maltose down into glucose?
Maltase
311
What are alpha dextrins broken down into?
Glucose
312
What breaks down alpha dextrins?
Isomaltase
313
What is lactose broken down by?
Lactase
314
What is lactose broken down into?
Glucose and galactose
315
What breaks down sucrose?
Sucrase
316
What is sucrose broken down into?
Glucose and fructose
317
Where does sodium glucose transporter 1 move contents from/to?
Glucose lumen to cell
318
Where does GLUT 2 move glucose from/to?
Cell to blood
319
Where does GLUT 5 move fructose from/to?
Into cell
320
What does GLUT 5 transport?
Fructose
321
How does Na/K ATPase aid absorption of glucose?
It's activity on basolateral membrane maintains a low Intracellular Na+
322
What must happen first before glucose can bind to sodium glucose transporter 1?
Na+ must bind to transporter
323
What does GLUT 2 transport?
Glucose
324
Where does GLUT 2 transport glucose from/to?
Out of enterocyte. Diffuses down gradient into capillary blood.
325
How does fructose enter enterocytes?
Facilitated diffusion via GLUT 5
326
What is the principle behind oral rehydration therapy?
Uptake of Na+ generates osmotic gradient - water follows. Glucose uptake stimulates Na+ uptake - mixture of glucose and salt will stimulate maximum water uptake.
327
What constituents of proteins can be absorbed?
Amino acids, dipeptides and tripeptides
328
What cells release pepsinogen in the stomach?
Chief cells
329
What converts pepsinogen to pepsin?
HCl
330
What, with regards to proteins, is enters the intestine from the stomach?
Oligopeptides/amino acids
331
What converts trypsinogen (released by the pancreas) to trypsin?
Enteropeptidase
332
What effect does trypsin have on other pancreatic proteases?
Activates them! E.g. Chymotrypsinogen --> chymotrypsin
333
What sort of peptide bonds does trypsin cleave?
Peptide bonds next to basic amino acids
334
What sort of peptide bonds does chymotrypsin cleave?
Peptide bonds next to aromatic amino acids
335
What sort of peptide bonds does carboxypeptidase cleave?
Cleaves c-terminal amino acids
336
What does exopeptidase do?
Breaks bonds at ends of polypeptide to produce dipeptides or individual amino acids e.g. Carboxypeptidase
337
What does endopeptidase do?
Breaks bonds in middle of polypeptide to produce shorter polypeptides e.g. Trypsin, chymotrypsin, elastase
338
How are amino acids absorbed?
Via sodium-amino acid cotransporters
| Different ones for different amino acids - neutral, basic, acidic...
339
How are most protein products ingested?
As dipeptides/tripeptides (not AA)
340
What transports dipeptides/tripeptides?
H+ co-transporter peptide transporter 1 (PepT1)
341
What happens to dipeptides/tripeptides once they have been transported inside the intestinal cell?
They are converted to amino acids by cytosolic peotidases
342
What is the basis for Na+/water uptake?
Na+ is moved by active transport out of cell on basolateral membrane. Na+ diffuses into epithelial cells. Water can now also move into intracellular space.
343
How is Na+ taken up in the small intestine?
Na+ is cotransported
344
How is Na+ taken up in the large intestine?
Na+ channels, induced by aldosterone (aquaporin)
345
What happens to Ca2+ uptake when Ca2+ intake is low?
Active transcellular absorption. Enters cell via facilitated diffusion. Ca2+ATPase removes Ca2+ from basolateral membrane. This process requires Vit. D (calbindin), stimulated by PTH.
Ca2+ enters cells by facilitated diffusion and is then expelled actively across the basolateral membrane.
346
Approximately how much as a percentage of ingested Ca2+ is normally absorbed?
~10%
347
What does the active absorption of Ca2+ by Ca2+ ATPase require?
Vitamin D
348
How is Ca2+ absorbed when Ca2+ levels are normal/high?
Passive paracellular absorption
349
In which state is most iron absorbed?
Fe2+
350
What is important in the absorption of iron?
Gastric acid - iron is cotransported with H+ across apical membrane
351
Describe what happens to iron absorption when iron levels in the body are low
Iron binds to transferrin secreted by enterocytes. Once in cell, Fe2+ is liberated and exported to blood, where it again binds to transferrin.
352
Describe what happens to iron absorption when iron levels in the body are high
Iron contained in ferritin complexes (trapped in cell). Lost when enterocyte is replaced
353
Which vitamins are water soluble?
C, B
354
How are water soluble Vitamins absorbed?
Mostly absorbed by Na+ cotransport (Vit C/B)
355
How is Vitamin B12 absorbed?
Absorbed in the terminal ileum, bound to intrinsic factor, secreted by gastric parietal cells.
356
What could is a possible consequence of gastritis/terminal ileal removal?
Pernicious anaemia due to Vit B12 deficiency (essential for erythropoiesis)
357
Describe the motility of the small intestine
Slow, caudal progression of food. Intestinal pacemakers have higher frequency proximally, driving slow caudal progression of contents via segmentation - back and forth, mixing of contents, does not propel contents along intestine.
358
Describe the distribution of pacemakers in the small intestine
Higher frequency proximally, driving slow caudal progression of contents via segmentation. Firing of pacemakers decreases caudally (~12times/min in duodenum to ~8times/min in terminal ilium).
359
How do pacemakers drive segmentation in the small intestine?
Firing of pacemakers decreases caudally (~12times/min in duodenum to ~8times/min in terminal ilium). Pacemakers sends activity through the nerve plexuses which cause contraction of the smooth muscle at intervals along its length. This separates intestine into segments where muscle is not contracted - mixing contents (gradient helps also).
360
What are 'haustra'?
The large intestine is naturally divided up into segments, known as hausta, as circular muscles are more complete than the longitudinal, which have been reduced to the taenia coli.
361
What is 'haustral shuttling'?
The mechanism by which colonic contents are agitated and propelled along in the proximal colon.
362
What does haustral shuttling do?
Mixes contents, allowing most of the remaining water to be absorbed, forming faecaes
363
What is a mass movement?
Occurs 1-3 times a day. Can move contents rapidly from transverse colon to rectum. Often triggered by eating (gastro-colic reflex). Initiated by stretch receptors in the rectum.
364
How does a mass movement occur?
Coordinated peristalsis like movement from transverse colon to rectum.
365
What gives the urge to dedicate?
Faeces in the rectum (which is usually empty)
366
Describe the process by which a mass movement occurs voluntarily
Enhanced contraction of rectal smooth muscle, relaxation of the smooth muscle internal anal sphincter, and skeletal muscle external sphincter, combined with expiration against a closed glottis and abdominal muscle contraction to increase infra abdominal pressure, thus expelling faeces.
367
What happens if voluntary dedication doesn't occur?
Sacral reflexes will eventually trigger it to involuntarily trigger dedication as rectal pressure rises.
368
What is inflammatory bowel disease?
A group of conditions characterised by idiopathic inflammation of the GI tract, effecting gut function
369
What are the 2 common types of inflammatory bowel disease?
Chrons disease and ulcerative colitis
370
How might inflammatory bowel disease present extra-intestinally?
Extra-intestinal problems, e.g. MSK pain, arthritis, skin (erythema nodosum/pyoderma gangrenosum/psoriasis), liver/biliary tree - primary sclerosing cholangitis, eye problems
371
What causes inflammatory bowel disease?
Genetic - 1st degree relative increased risk. Gut organisms (altered interaction). Immune response -trigger e.g. Antibiotics, infections, diet, smoking.
372
How might crohns disease present?
Tender mass, mild perinatal inflammation/ulceration, low grade fever, mildly anaemic
373
What is the pathology of Crohn's disease?
Hyperaemia, mucosal oedema, descrete superficial ulcers, deeper ulcers, transmural inflammation, thickening of bowel wall, narrowing of lumen. Cobblestone appearance (if severe), fistulae - bowel/bladder/vagina/skin. Granuloma formation
374
What investigations might you do for Crohn's disease?
Bloods (anaemia), CT/MRI scans (bowel wall thickening, obstruction, extramural problems). Barium enema/follow through (used less. Strictures/fistulae). Colonoscopy.
375
How might ulcerative colitis present?
Multiple stools with mucus in. Mild lower abdominal pain/cramping. No perinatal disease, normal temp.
376
What pathological changes might be seen in ulcerative colitis?
Chronic inflammatory infiltrate of lamina propria. Crypt abscesses, crypt distortion. Decreased goblet cells. Pseudopolyps. Loss of haustra
377
What investigations would you do for ulcerative colitis?
Bloods - anaemia, serum markers. Stool cultures. Plain abdominal radiographs. Barium enema (mild cases only). CT/MRI - less useful in diagnosing uncomplicated UC. Colonoscopy
378
Would there be rectal involvement in Crohn's disease and/or ulcerative colitis?
Crohns - no
| UC - yes
379
Would there be gross bleeding in Crohn's disease and/or ulcerative colitis?
Crohns - 25%
| UC - Yes
380
Would there be perianal disease in Crohn's disease and/or ulcerative colitis?
Crohns - 75%
| UC - rare
381
Would there be fistula formation in Crohn's disease and/or ulcerative colitis?
Crohns - yes
| UC - no
382
Would there be malnutrition in Crohn's disease and/or ulcerative colitis?
Crohns - potentially
| UC - no
383
Would there be transmural inflammation in Crohn's disease and/or ulcerative colitis?
Crohns - yes
| UC - rare
384
Would there be granulomas in Crohn's disease and/or ulcerative colitis?
Crohns - up to 75%
| UC - no
385
Would there be fibrosis in Crohn's disease and/or ulcerative colitis?
Crohns - common
| UC - no
386
Would there be crypt abscesses in Crohn's disease and/or ulcerative colitis?
Crohns - rare
| UC - common
387
Would there be mucosal involvement in Crohn's disease and/or ulcerative colitis?
Crohns - skip lesions
| UC - continuous
388
Would there be aphthous ulcers in Crohn's disease and/or ulcerative colitis?
Crohns - yes
| UC - rare
389
Would there be linea ulcers in Crohn's disease and/or ulcerative colitis?
Crohns - yes
| UC - rare
390
Would there be friable mucosa in Crohn's disease and/or ulcerative colitis?
Crohns - rare
| UC - yes
391
Would there be cobblestone appearance in Crohn's disease and/or ulcerative colitis?
Crohns - Yes (severe cases)
| UC - no
392
Would there be fistula in Crohn's disease and/or ulcerative colitis?
Crohns - yes
| UC - no
393
Would there be narrowing in Crohn's disease and/or ulcerative colitis?
Crohns - yes
| UC - rare
394
List some features of Crohn's disease, that are not present in ulcerative colitis
Fistula formation, malnutrition, granulomas, fibrosis, skip lesions, cobblestone appearance
395
In what disease might a 'lead pipe colon' (with no visible ridges) be seen?
Ulcerative colitis
396
What is the medical treatment of inflammatory bowel disease?
Stepwise approach
1 - Aminosalicylates (sulfasalazine 5-ASA preparations, for flares and remission)
2 - Corticosteroids (prednisolone - flares only)
3 - Immunomodulators (azathioprine - fistulas/maintenance of remission)
397
What is the surgical treatment of Crohn's disease?
Not curative, strictures/fistulas. As little bowel removed as possible.
398
What is the surgical treatment of UC?
Curable (colectomy). Inflammation not settling. Precancerous changes, toxic megacolon.
399
Where re the majority of the bacteria in our bodies?
In the colon
400
How may bacteria be classified?
```
Cocci/bacilli
Gram positive/gram negative
Aerobic/anaerobic obligate/facultative
Spore forming
Pili/slime - ability to stick to a surface
```
401
What are obligate aerobes?
Bacteria that must have oxygen to survive
402
Give some examples of obligate aerobes
Pseudomonas
| Mycobacterium TB
403
What are obligate anaerobes?
Die in the presence of O2.
404
Give some examples of obligate aerobes
Bacteroides fragilis
| Clostridium (although not its spores)
405
Where are anaerobic areas of the GIT?
Mouth - on tongue deep in taste buds, fluid films including biofilm in between teeth, gingival crevice areas and people with periodontal disease in periodontal pockets
Small bowel
Colon
406
How do human colonic bacteria help their host?
Synthesise and excrete vitamins that are absorbed by host e.g. Vit K, b12, thiamine and other B vitamins
Prevent colonisation by pathogens
Kill non-indigenous bacteria
Stimulate development of MALT (in caecum and peters patches)
Stimulate production of natural antibiotics
407
What are some consequences of 'germ free' animals?
Vitamin deficiencies, especially Vit K and Vit B12
Increased susceptibility to infectious disease
Poorly developed immune system, especially in GI tract
Lack of natural antibody, or natural immunity to bacterial infection
408
List some aerobic, gram positive cocci
Staphylococci
Streptococci
Enterococci
409
List some gram negative aerobic cocci
Neisseria meningitidis
| Neisseria gonorrhoeae
410
List a gram positive anaerobic bacilli
Clostridia (tetani, perfringens, difficile)
411
List some gram positive aerobic bacilli
Corynebacterium diphtheria
Bacillus anthrax
Lactobacillus
Mycobacterium TB
412
Is mycobacterium TB gram positive or negative?
Positive
413
List some gram negative, aerobic, non-enteric bacilli
Haemophilus influenzae
Bordetella pertussis
Brucella
414
What is the causative organism of whooping cough?
Bordetella pertussis
| Gram-negative, aerobic
415
List some gram negative anaerobic enteric bacilli
Bacteriodes fragilis
416
List some gram negative, aerobic, enteric bacilli
```
E. coli
Pseudomonas
Proteus
Klebsiella
Salmonella
Shigella
Vibrio cholera
Campylobacter
Helicobacter pylori
```
417
Why can bites cause nasty/fatal infections?
Mouth contains many anaerobes
418
What might appear in the mouth if an individual is particularly unwell/malnourished/immunocompromised?
Mouth bacteria can cause tissue destruction; noma/cancrum oris
419
What causes oral thrush?
Candida albicans
420
What might induce oral thrush?
```
Oral antibiotics (which kill off other bacteria)
Candida albicans is causative organism
```
421
What are the risk factors for oral thrush (caused by Candida albicans)?
Newborns, antibiotics, diabetes, inhaled steroids, immune deficiency
422
What is the treatment for oral thrush?
Amphotericin lozenges
| Nystatin suspension
423
What is dental caries/gingivitis?
The teeth are colonised by the mouth bacteria plus streptococcus mutans (can cause plaque)
424
What is ludwigs angina?
Swollen, sore throat, usually streptococcal. Laryngeal oedema can be fatal.
425
Whee are the 3 sites used for MRSA screening swabs?
Nose, threat, perineum
426
What sort of organisms are found in the nose normally?
Staphylococcus and streptococcus amongst others
427
What bacteria are usually found in the throat?
```
Strep viridans
Strep pyogenes
Strep pneumoniae
Staphylococci
Neisseria meningitidis
Haemophilus influenzae
Lactobacilli
Corynebacterium diptheriae
Candida albicans
```
428
How might strep viridans cause infection of prostheses?
Non-pathogenic throat commensal. May enter blood stream (bacteraemia) during teeth brushing, general anaethesia, dental procedures. May stick to prostheses such as heart valves, vascular grafts, orthopaedic implants ect. and cause infection. Prostheses don't have the 'antibacterial sticking' armour cells do.
429
Why are prostheses particularly susceptible to infection?
Prostheses don't have the 'antibacterial sticking' armour cells do.
430
What is bacteraemia?
Bacteria in blood but are rapidly cleared from the bloodstream (by liver/spleen macrophages). Asymptomatic.
431
What is septicaemia?
Bacteria in bloodstream and are not cleared. Multiply in the bloodstream. Sepsis symptoms develop. (Bacteria are proliferating, not just passing). High mortality.
432
What causes tonsillitis?
70% viral - adenovirus, rhinovirus, epstein-barr
| 30% bacterial - mainly strep. Pyogenes (beta haemolytic)
433
What proportion of people infected with H pylori develop gastric ulcers/duodenal ulcers?
Only 10-20%
434
What proportion of colonic bacteria are anaerobes?
95-99% of over 100 species
435
What species of bacteria of particularly prevalent in the colon?
Bacteroides and clostridium species
436
List types of bacteria that are always present in the colon
Bacteroides (fragilis, oralis, melaninogenicus)
Eschericia coli
Enterococcus faecalis
437
List some common gram negative bacteria of the colon
```
Pseudomonas
Proteus
Klebsiella
Salmonella
Shigella
Vibrio cholera
Campylobacter
```
438
List a common gram positive colonic bacterium
Lactobacillus
439
What precautions might you take when performing 'dirty' surgery (e.g. On the colon)
Prophylactic antibiotics to reduce risk of wound infection. Needs to cover anaerobes, gram negative bacilli and gram positive cocci.
440
What does prophylactic antibiotics for intestinal surgery need to cover?
Needs to cover anaerobes, gram negative bacilli and gram positive cocci.
441
What antibiotics might you use for prophylactic treatment of intestinal surgery?
Metroniadazole - kills anaerobes
Along with a broad spectrum antibiotic e.g. Gentamicin or cephalosporin.
Alternatively is co-amoxiclav augmentin - but this is a penicillin (allergy!)
Adhere to local policy
442
What mortality is faecal peritonitis?
50% mortality even in young fit people.
443
Can bacteriodes survive O2 on perianal skin?
Nope
444
Can E. coli survive the O2 on perineal skin?
Yes
445
Can enterococcus faecalis survive the O2 on perineal skin?
Yes
446
Can lactobacillus survive the O2 on perineal skin?
Yes
447
Where is lactobacillus a normal commensal?
Vagina
448
How does lactobacillus aid its host?
Converts glycogen to lactic acid. Acidic environment prevents other bacteria and candida from colonating vagina
449
What is a potential complication of lactobacillus acidophilus?
Broad spectrum antibiotic treatment kills lactobacilli and can lead to vaginal thrush
450
What is the commonest causative organism of UTI?
E. Coli (~75%)
451
What organisms generally cause UTI
Commonest - E. Coli (75%)
Next common - enterococcus faecalis
Thereafter various gram negative enteric bacilli (klebsiella, proteus, pseudomonas)
452
What does clostridia tetani cause?
Tetanus
453
What does clostridia perfringens cause?
Gas/wet gangrene
454
What are the classical symptoms of tetenus?
'Lock jaw', opisthotonus
| Acts like acetylcholine, causing muscle spasm
455
Who does tetanus generally infect news days?
Neonate
| Old people without a recent vaccine update
456
How does clostridium perfringens cause gas/wet gangrene?
Anaerobic digestion of glucose, producing ethanol and CO2 (fluid plus gas)
457
What is the treatment of gas/wet gangrene, as caused by clostridium perfringens?
Remove effected flesh/amputate ASAP
458
What are the clinical features of oesophageal carcinoma?
Progressive dysphagia, weight loss
459
What investigations might you do for oesophageal carcinoma?
Endoscopy, biopsy, barium
460
What are the possible types of oesophageal carcinoma?
Squamous cell carcinoma (most common type)
| Adenocarcinoma (associated with Barrett's oesophagus, lower 1/3)
461
What is the prognosis of oesophageal carcinoma?
Advanced disease usually at presentation
Direct spread though oesophageal wall
Only 40% resectable, 5% 5yr survival
Many patients have a tube passed though tumour to facilitate swallowing
462
What is the prognosis of gastric cancer?
Poor, 20% 5yr survival
463
What is gastric cancer associated with?
Gastritis
| Commoner in blood group A
464
What are the clinical features of gastric cancer?
Symptoms often vague. Epigastric pain, vomiting, weight loss
465
What investigations might you do for gastric cancer?
Endoscopy, biopsy, barium
466
What microscopic features might be present in gastric cancer?
Fungating, ulcerating, infiltrative (linitis plastica) early.
Intestinal - varying degree of gland formation. Diffuse - single cells and small groups, signet ring cells.
467
What are the features of early gastric cancer?
Confined to mucosa/submucosa, good prognosis
468
What are the features of advanced gastric cancer?
Further spread, 10% 5yr survival
| Common in the U.K.
469
Where does gastric cancer generally spread to?
Direct - lymph nodes, liver, trans-coelomic (peritoneum, ovaries)
470
What are the treatment options for gastric cancer?
Surgery, chemotherapy, herceptin
471
What is H. Pylori associated with?
Association of chronic inflammation with cancer
472
What is the commonest form of GI lymphoma?
Gastric lymphoma
473
Describe gastric lymphoma
Starts as a low grade lesion, strong association with h pylori. Eradication of H. Pylori may lead to regression of tumour. Prognosis better than gastric cancer.
474
Describe GI stromal tumours
Uncommon. Derived from interstitial cells of cajal c-kit. Specific targeted treatment - imatinib. Unpredictable behaviour - pleomorphism, mitosis, necrosis
475
What types of tumours may be present in the intestine?
Adenomas, adenocarcinoma, polyps, anal carcinoma
476
What are the features of an adenoma of intestines?
Macroscopic - sessile or pedunculated
Microscopic - variable degree of dysplasia
Behaviour - definitive malignant potential
Incidence - increases with age in western populations, genetic syndrome.
477
What is familial adenomatous polypossis?
Autosomal dominant (chromosome 5). Thousands of adenomas by 20s - high risk of cancer.
478
What is gardeners syndrome?
Similar to FAP. Bone and soft tissue tumours
479
Describe the adenoma carcinoma sequence
Synchronous lesions, metachronous lesions, adenomas with invasion
480
What are the macroscopic features of adenocarcinoma?
60-70% rectosigmoid. Fungating (especially right side), stenotic (especially left side)
481
What are the microscopic features of colorectal adenocarinoma?
Moderately differentiated adenocarinoma, occ mucinous, occ signet ring cell type
482
Describe the spread of colorectal adenocarcinoma
Direct through bowel wall to adjacent organs e.g. Bladder. Via lymphatics to mesenteric lymph nodes. Via portal system to liver.
483
Describe dukes staging for adenocarcinoma
A - confined to bowel wall
B - through wall, lymph nodes clear
C - lymph nodes involved
C1/C2 - highest node clear/involved
484
How is a k-ras mutation relevant for treatment of colorectal cancer?
Enables treatment with cetuximab (only works if pathway activated)
485
How is an 18q DCC mutation relevant to colorectal cancer?
18q DCC - deleted in colorectal cancer
486
What lifestyle factors might predispose a person to colorectal cancer?
Low residue diet - noxious substances are in the bowel longer, so are in contact with the bowel wall longer. Slow transit time, high fat intake.
487
What is the outcome of colorectal cancer?
Survival decreases with increased dukes staging. Liver metastases common in advanced disease. Chemotherapy (palliative), resection of liver deposits, local radiotherapy.
488
Where does colorectal cancer often metastase to?
The liver
489
List some large intestinal tumours (other than colorectal adenocarcinoma)
Carcinoid tumour - rare endocrine tumour, difficult to predict behaviour
Lymphoma - rare, may be primary or spread from elsewhere
Smooth muscle/stromal tumours - rare and unpredictable
490
Describe carcinoma of the pancreas
Early symptoms vague. Diagnosis is usually delayed. Weight loss, jaundice, trousseau's sign. Imaging enables diagnosis 2/3 in head (firm pale mass). Cut surface, necrotic, haemorrhagic, cystic. May infiltrate adjacent structures e.g. Spleen.
491
What can insulinoma (islet cell tumour) cause?
Hypoglycaemia
492
What can glucagonoma (islet cell tumour) cause?
Characteristic skin rash
493
What can VIPoma (islet cell tumour) cause?
Werner Morrison syndrome
494
What can gastrinoma (islet cell tumour) cause?
Zollinger-Ellison syndrome
495
List some benign tumours of the liver
Hepatic adenoma
Bile duct adenoma/hamartoma
Haemangioma
496
List some malignant (primary) tumours of the liver
Hepatocellular carcinoma
Cholangiocarcinoma
Hepatoblastoma
497
What are the available mechanisms to image the GIT?
```
Plain X-Rays - abdominal AXR, chest CXR
Contrast studies - barium swallow/enema/meal + follow through. Water soluble contrast studies
Ultrasound
Cross sectional imaging - CT, MRI
Angiography
```
498
When might someone request an AXR?
Acute abdominal pain. Small or large bowel obstruction. Acute exacerbation of IBD. Renal colic (although CT better)
499
List the features of an AXR
ABC
| Air, bowel, calcification/bones+stones
500
When is bowel visible on an AXR?
If gas filled, or gas and fluid filled (need low density contrast to show up)
501
Describe how the transit time effects ability to see parts of the bowel on an AXR
```
Slow colon (faeces and gas) visible
Medium stomach (fluid and lots of gas) visible
Fast small bowel (fluid) not so visible
```
502
Describe what the small bowel looks like on an AXR
Central position, often not seen (fast transit time, fluid filled). Valvulae conniventes. Gross entire wall thin.
503
Descibe what the large bowel looks like on an AXR
Peripheral position. Frames small bowel loop. Haustra. Faeces and gas, slow transit time.
Transverse colon can hang down to pelvis. Sigmoid colon can loop and be long.
504
What might show up on an AXR with regrants to the bowel?
Mucosal thickening, featureless colon, bowel wall oedema. Acute or chronic changes.
505
What is the rule of 3s for when analysing an AXR?
```
Of note if:
Small bowel obstruction >3cm
Large bowel obstruction >3cm
Competent ileocaecal valve (caecum>9cm)
Incompetent ileocaecal valve
```
506
What should you be able to recognise on an AXR
```
Paralytic ileum
Volvulus
Toxic megacolon
'The rule of 3s'
Small bowel obstruction >3cm
Large bowel obstruction >3cm
Competent ileocaecal valve (caecum>9cm)
Incompetent ileocaecal valve
```
507
How might a small bowel obstruction present?
Vomiting (early), distension (mild), absolute constipation (late), colicky pain
508
What might cause a small bowel obstruction?
Adhesions, hernias (inguinal, femoral, incisional), tumours, inflammation
509
How might a large bowel obstruction present?
Vomiting (late, faeculant), distension (significant), paint absolute constipation
510
What might cause a large bowel obstruction?
Colorectal carcinoma, diverticular stricture, hernia, volvulus, pseudo-obstruction
511
What is a volvulus?
Twisting around the mesentery. Encased bowel loop dilates (perforation, ischaemia). Common in sigmoid (uncommon in caecal, anatomical defect)
512
Where is volvulus common?
Sigmoid colon. Starts in LIF. Coffee bean sign towards RUQ. Dilation of proximal bowel - obstructed.
513
What is a toxic megacolon?
Acute deteriation with UC or colitis. Colonic dilation. Oedema pseudopolyps. Toxic implies patient is unwell!
514
What is a 'leadpipe colon'?
Featureless colon, loss of haustra. Ulcerative colitis - chronic inflammation.
515
Describe what 'thumb printing' is in an AXR
Oedematous thickened haustra. Thickened wall. Active inflammation, often UC. Can see in other processes with oedema.
516
What other abnormalities might be present in an AXR?
Stones, organs/masses, calcification (pancreatitis, vasculature nodes), bones, artefacts, foreign body
517
What might cause perforation - pneumoperitpneum?
Peptic ulcer, diverticulum, tumour, obstruction, trauma, latrogenic-laparoscopy 3-6 days.
518
What would be the initial imaging of choice for a bowel perforation/pneumoperitoneum?
CXR (air collects under the diaphragm so is easy to see
519
When might you use a contrast study for the GIT?
Used to define hollow viscera - barium/water soluble
520
List some common GI contrast studies
Swallow, meal, small bowel enema/follow through, enema
521
Describe an abdominal CT?
Computerised axial tomography. High dose radiation. Gives good spatial resolution (poor constant resolution Vs MRI). Use of IV or oral contrast. Can be done to produce a virtual colonoscopy.
522
Describe an abdominal MRI
Magnetic resonance imaging. No radiation. Good spatial and contrast resolution. Time consuming.
523
Describe an abdominal USS
Use of sound waves to generate image (above human audible range frequency). Cheap compared to CT and MRI. Portable, so fast. However highly user dependent.
524
What is a GI angiography?
Catheter into artery + contrast
525
What is odynophagia?
Painful swallowing
526
What is colicky pain every 2-3mins likely to be?
Small bowel obstruction
527
What is colicky pain every 10-15mins likely to be?
Large bowel obstruction
528
What sort of pain is caused by an ulcer?
Dull, burning
529
What causes malaena?
Upper GI bleeding
530
What is alkalaemia?
Blood pH of 7.45 or greater
531
What is acidaemia?
Blood pH of 7.35 or less
