GI Flashcards
(525 cards)
1
Q
What is the inguinal ligament formed from?
A
The thickening and rolling of the external oblique aponeurosis.
2
Q
What is the innervation of the internal oblique, the external oblique and the transverse abdominis?
A
The external oblique is from the anterior rami of T7-T12.
The internal oblique and transverse abdominis is from the anterior rami of T7-L1.
3
Q
What is the innervation of the rectus abdominis?
A
Anterior rami of T7-T11.
4
Q
What is the rectus sheath, and at which point does it change? Describe these changes.
A
It is the enveloping of the rectus abdominis, by the aponeurosis of the external oblique, the internal oblique and the transverse abdominis.
At the point of the arcuate line, the aponeuroses move anteriorly to the rectus abdominis, rendering the posterior support the transversalis fascia and peritoneum, only.
5
Q
What is the origin, insertion and actions of the external oblique?
A
Origin - 5th to 12th ribs.
Insertion - Iliac crest, inguinal ligament and linea alba.
Actions - flex the trunk, compress the abdominal viscera and to rotate the trunk contralaterally.
6
Q
What is the origin, insertion and actions of the internal oblique?
A
Origin - Iliac crest, lateral inguinal ligament and thoracolumbar fascia.
Insertion - ribs 10-12, linea alba and pubic crest.
Actions - compression of the abdominal viscera, flexion of the trunk and ipsilateral rotation of the core.
7
Q
What is the origin, insertion and actions of the transverse abdominis?
A
Origin - Costal cartilages of the lower ribs, thoracolumbar fascia, medial lip of the iliac crest and inguinal ligament.
Insertion - linea alba and pubic crest.
Actions - compresses abdominal viscera and for core stability.
8
Q
What is the origin, insertion and actions of the rectus abdominis?
A
Origin - pubic crest and tubercle, and pubic symphyses.
Insertion - costal cartilages of ribs 5-7 and xiphoid process.
Actions - compression of the abdominal viscera and core support.
9
Q
What causes a 6-pack to arise?
A
The tendinous intersections within the rectus abdominus muscle.
10
Q
What are the 4 layers of the gut?
A
The mucosa, submucosa, muscularis externa and the serosa.
11
Q
What forms the mucosa?
A
The epithelium, lamina propria and muscularis mucosae.
12
Q
What is the function of the muscularis mucosae?
A
To keep the crypts dynamic.
13
Q
Where are the meisseners and mynteric plexuses found?
A
The meisseners plexus is found within the dense connective tissue of the submucosa.
The mynteric plexus is found within the two layers of the muscularis externa.
14
Q
What immune components does the lamina propria have?
A
It contains macrophages, IgA and antibodies.
15
Q
What can non-keratinised stratified squamous epithelia do that keratinised cannot?
A
Secrete mucous - not involved in preventing water loss.
16
Q
What are the mucous cells called between the gastric glands and crypts and what makes them different?
A
They are neck mucous cells which are irregular shaped and smaller than surface mucous cells.
17
Q
What types of cells are located in the crypts of the small intestine and colon?
A
Stem cells - to replace the epithelium every 2-4 days.
Panneth cells - produce antibacterial proteases.
Enteroendocrine cells - produce hormones.
18
Q
What do Brunner’s glands secrete and why?
A
The secrete an alkaline mucous substance into the duodenum to neutralise the acidic chyme.
19
Q
What are the columnar cells in the colon called, and what are their adaptations?
A
Colonocytes which microvilli, but are not used for absorption.
20
Q
What is the function of mucous within the colon?
A
It supports the microbiome and protects the colon from invasion of the bacteria within the epithelial layer.
21
Q
What is the relevance of the coloncytes intracellular spaces?
A
They are large spaces which contains a large number of Na/K ATPases, which keep the Na+ concentration very low, which facilitates movement of the Na+ into the spaces/ colonocytes for the final water reabsorption.
22
Q
What is the parasympathetic and sympathetic innervation of the gut?
A
The parasympathetic is from predominantly from the vagus nerve, but with some innervation from the pelvic nerves.
The sympathetic is from T5-L2.
23
Q
How does the sympathetic nervous system innervate the gut?
A
The pre-ganglionic neurons bypass the sympathetic chain to form the splanchnic nerves and synapse onto the pre-vertebral ganglion, situated anterior to the vertebral column.
The post-ganglionic neurons then produce their effects on the gut tissues.
24
Q
What are the 3 splanchnic nerves?
A
The greater, lesser and least splanchnic nerves.
25
What is the function of the meissener and mynteric plexuses?
Meissener’s plexus control secretion and blood flow.
Mynteric control gut motility.
26
What types of hormones are all the hormones released from the gut, and give examples of the hormones involved in the 3 types of secretions.
They are all peptide hormones.
Endocrine - gastrin, cholysystokinin and secretin.
Paracrine - somatostatin (released from D-cells).
Neurocrine - gastrin-releasing peptide (released from G-cells).
27
Where are enteroendocrine cells and what are they stimulated by?
They are found in the mucosa, between epithelial cells, and are stimulated by stretch, and food taken into the GI.
28
What types of cells release gastrin and where are they found?
G-cells, found in the antrum of the stomach and colon.
29
What are G-cells stimulated and inhibited by, and what do they stimulate themselves?
They are stimulated by stretch, by protein breakdown and by the vagus nerve. They are also stimulated by gastrin-releasing peptide.
They are inhibited by somatostatin (which is stimulated by low pH).
G-cells stimulate parietal cells to release acid, from the stomach.
30
Where are I-cells found, what are their secretions and what are they stimulated by?
They are found in the duodenum and jejunum.
They secrete cholecystokinin.
They are stimulated by the breakdown of fats and proteins, and low pH.
31
What is the function of cholecystokinin?
It relaxes the sphincter of Oddi, allowing secretions to enter the duodenum.
Contracts gall bladder for bile secretion.
Stimulates the pancreas to release digestive enzymes.
32
What do S-cells secrete, and what is their stimulation?
They secrete secretin.
These are stimulated by acidic chyme.
33
What is the function of secretin?
It stimulates bicarbonate-rich secretions to be released from the gallbladder and pancreas, into the duodenum.
34
What is gastrin-inhibitory polypeptide stimulated by, and what is its function?
It is stimulated by the breakdown of all food.
It’s function is to inhibit gastric acid secretions and increase insulin secretions.
35
What separates the abdominal cavity from the thoracic and pelvic cavities, but why are these not actual separations?
It is separated from the thoracic cavity by the diaphragm, but it contains perforations to allow the passage of blood vessels and structures such as the trachea and oesophagus.
It is ‘separated’ from the pelvic cavity by the pelvic brim, which is not actually a separation, and allows the abdominal viscera to extend into the pelvic cavity.
36
What is the peritoneal cavity made of?
It is formed from layers of mesothelium, which consists of the simple squamous epithelia, which can secrete the serous fluid contained within the cavity.
37
What are the intra-peritoneal and retroperitoneal viscera?
The intra-peritoneal viscera are enveloped by the peritoneum, whereas the retroperitoneal viscera have only their anterior surface covered by parietal peritoneum.
38
What are two layers of peritoneum connecting to the retroperitoneal space called, and what passes within it?
A mesentery.
Blood vessels, lymphatics and nerves pass within this.
39
What are the two layers of peritoneum passing between two intra-peritoneal organs called?
Peritoneal ligament.
40
What are the directions of the muscle fibres of the internal oblique, external oblique and transverse abdominus?
Internal oblique - superomedial.
External oblique - inferomedial.
Transverse abdominus - transverse.
41
What are the UOS and LOS of the oesophagus and what are their functions?
Upper oesophageal sphincter - prevents air from entering the oesophagus.
Lower oesophageal sphincter - prevents gastric acid reflux.
42
What are the greater and lesser sacs of the peritoneum, and how do they form?
The greater sac is the sac that envelops all of the intraperitoneal viscera, that can be seen when opening the abdominal cavity. The lesser sac is a sac that does not envelop anything and is found behind the liver, extending down.
They are formed through the twisting of the liver and stomach during embryology.
43
What is mass movement?
Rapid peristalsis of the large bowel, emptying contents into the rectum.
44
What process triggers the sensation to defecate?
The stretch of the rectum.
45
How does the saliva confer pathogenic protection?
It contains antibacterial agents.
46
Where can lower lobe pneumonia pain be felt?
Hypochondrium.
47
What is a hiatus hernia?
A portion of the stomach pushing through the right crus of the diaphragm.
48
What is D1 of the duodenum?
The duodenal bulb - the most proximal part of the duodenum, closest to the stomach.
49
What is the difference between structures passed through in omphalocele and gastrochisis?
Omphalocele is a herniation through the umbilicus.
Gastroschisis is a herniation through the body wall.
50
In an omphalocele, what are the intestines contained within, and what does this protect them from?
They are contained within the peritoneum, protecting them from amniotic fluid.
51
What defects are omphalocele’s associated with?
Heart and neural tube defects.
52
What is gastroschisis due to, and what can the damage be?
It is due to abnormal embryonic folding, which can lead to amniotic fluid damaging the bowel, and twisting of the bowel, leading to ischaemia.
53
Where are is the pain felt from the foregut viscera, midgut viscera and huindgut viscera? State the nerve and dermatome associated with it.
Foregut viscera - epigastric region, from the greater splanchnic nerve, in the T5-T9 dermatomes.
Midgut viscera - peri-umbilical region, from the lesser splanchnic nerve, in the T10-T11 dermatomes.
Hindgut viscera - supra-pubic region, from the least splanchnic nerve (and lumber splanchnic nerves), in the T12-L2 dermatomes.
54
Which sensory nerves relay information to the brain regarding pain of the abdomen?
The visceral afferent nerves.
55
Outline the route of the visceral afferent nerves from the gut.
The visceral afferents run in opposition to the sympathetic innervation of the gut:
- From the viscera, via the splanchnic nerves.
- To the pre-vertebral ganglion, which split into the spinal nerves.
- The spinal nerves travel back to the spinal cord at the levels of T5-L2.
56
What are the layers of a hernia, from superficial to deep? State what the common contents of the hernia are.
Skin, then the layers of abdominal wall muscles that it protrudes in. Then the parietal peritoneum (and usually visceral, depending on the organ).
They are usually loops of bowel or omentum, but can be any structure of the abdominal cavity.
57
What are the 3 common weaknesses of the abdominal wall, and what else can weaken the wall?
The inguinal canal, femoral canal and umbilicus.
Surgical incision, particularly through muscles, can weaken the abdominal wall.
58
How does the gubernaculum guide the testes?
It is a condensed band of mesenchyme which is attached to the inferior pole of the testes and labioscrotal swelling (before sexual differentiation).
The gubernaculum then shrinks, pulling the testes down, through the inguinal canal, into the scrotum.
59
What descends into the scrotum prior to the testes, and what does it become within the scrotum?
The processus vaginalis descends into the testes to become the tunica vaginalis, which encloses most of the testes, acting as a protective capsule.
60
What determines how far down the inguinal canal and scrotum the hernia can migrate?
The processus vaginalis’ obliteration. The lower the obliteration, the further towards/ within the scrotum the hernia can protrude.
61
What is the conjoint tendon?
The joining of the internal oblique and transversus abdominus’ aponeuroses.
62
What structures are the deep and superficial inguinal rings located within?
Deep is within the transversalis fascia.
Superficial is within the external oblique aponeurosis.
63
What do femoral hernias often protrude out of?
The saphenous opening.
64
What are the 3 sections of mesoderm, and what do they form?
Paraxial - somites, which forms the skeletal muscle, vertebra and cartilage.
Intermediate - kidneys and gonads.
Lateral plate - formed of splanchnic and somatic. Splanchnic forms the viscera and the somatic forms the body walls.
65
What do the ectoderm and endoderm form?
Ectoderm - epidermis, CNS and PNS.
Endoderm - epithelia of the GI and other tracts.
66
What happens during cranio-caudal folding, up to the 4th week?
The mesoderm undergoes a pinching manoeuvre, forming the blind-ended gut tube.
The ectoderm thickens where it overlies the mesoderm, forming the brain and spinal cord.
67
What connects the midgut to the yolk sac, and what is formed should this not obliterate before birth?
The Vitelline duct - Meckles diverticulum (an out pouch of the small intestine) can form, where faecal can leak out into the anterior abdominal wall.
68
What occurs during ventral folding?
The lateral folds come together and fuse, forming the ventral abdominal wall.
69
What forms the visceral and parietal peritoneum?
Visceral - splanchnic mesoderm.
Parietal - somatic mesoderm .
70
What does the intraembryonic coelom give rise to?
The thoracic and abdominal cavity.
71
What are the somatopleuric and splanchnopleuric mesoderm, and what do they form?
Somatopleuric - somatic mesoderm and ectoderm together, forming the body walls and dermis.
Splanchnopleuric - splanchnic mesoderm and endoderm, forming the viscera (organs).
72
What two membranes make the gut tube blind-ended, and when do they rupture?
The cephalic end is enclosed by the bucco/oropharyngeal membrane. This ruptures during the 4th week.
The caudal end is enclosed by the cloacal membrane. This ruptures during the 7th week.
73
What does the cloaca form, and where is it located?
It separates to become the urogenital sinus and anorectal canal, within the hindgut.
74
What degree does the stomach rotate by?
90 degrees.
75
What is the difference between somatic and splanchnic mesoderm pain localisation?
The somatic mesoderm can localise the pain, whereas the splanchnic mesoderm cannot.
76
What structures do the spleen and liver rotate within?
The spleen in the dorsal mesentry.
The liver in the ventral mesentry.
77
What connects the liver and gallbladder?
Common bile duct.
78
Where do the left and right vagal trunks go to after rotation?
The left forms the anterior vagal trunk.
The right forms the posterior vagal trunk.
79
Label the peritoneal ligaments.
80
What does the ventral bud of the pancreas form from?
The hepatic diverticulum.
81
If the ventral and dorsal pancreatic buds don’t fuse, then what occurs?
The accessory pancreatic duct is formed, proximal to the main pancreatic duct.
82
What is the mid point of the inguinal canal an anatomical mark for?
The deep inguinal ring.
83
What is the remnant of the gubernaculum in males?
The scrotal ligament.
84
Where does the inguinal ligament run between?
Pubic tubercle to anterior superior iliac spine.
85
What is the major papilla?
The point at which the pancreas and liver join to the duodenum - in D2.
86
What is annular pancreas?
Where each of the ventral buds travel in opposite directions, surrounding the duodenum.
87
What is the clinical presentation of annular pancreas?
Vomiting with bile in as it is below the major papilla.
88
What is pancreas divisum?
Where the accessory duct (from the ventral bud) drains into the major papilla, with the main duct (from the dorsal bud) going to the minor papilla.
89
What is the problem with pancreas divisum?
The secretion of the main duct of the pancreas cannot all enter the duodenum, potentially leading to infection.
90
What is pyloric stenosis?
A narrowing of the pyloric lumen, as the contents leave the stomach, due to hypertrophy of the circular and longitudinal musculature of the stomach, resulting in projectile vomiting as the food cannot pass through.
91
What is the underlying cause of an umbilical hernia?
Incomplete closure of the umbilical ring.
92
What is the medial portion of the floor of the inguinal canal?
Lacuna ligament.
93
What are the names of the open incisions made in appendix surgery and cholecystectomy?
Gridiron for appendix.
Kocher for cholecystectomy.
94
What is the vascular supply to the anal canal?
Cranial part - superior rectal artery, from the inferior mesenteric artery.
Caudal part - inferior rectal artery, from the internal pudendal artery.
95
Where does the midgut start?
The mid-point of the second part of the duodenum - D2 - at the point where the common bile duct and major pancreatic duct drain (major papilla).
96
When does physiological herniation occur, why does it happen and what is its axis?
It occurs at the 6th week and re-enters the foetal body at the 10th week.
It occurs due to the enlargement of both the small intestine and liver at the same time, meaning there is insufficient space within the abdominal cavity.
The superior mesenteric artery is the axis.
97
What happens during physiological herniation, and what is the outcome?
The small intestine herniates out of the umbilical cord, and elongates. It then undergoes 3 anti-clockwise rotations, leaving the caecum in the right iliac fossa, the ascending colon lying to the right of the small intestine and transverse colon anterior to the small intestine.
98
Why does gastroschisis occur?
Due to incomplete lateral folding, meaning that the ventral abdominal wall does not form correctly.
99
What are vitelline cysts and fistulas?
Vitelline cyst - this is where the midpoint of the vitelline duct is patent.
Vitelline fistula - this is where there is no obliteration of the duct, allowing the faecal material to extrude through the umbilicus.
100
What is Meckles diverticulum?
Where the vitelline duct does not obliterate correctly, leading to a small out pouch within the midgut, where faecal material can accumulate.
101
What are the rule of twos, relating to Meckles diverticulum?
It is seen in 2% of the population.
Located 2 feet proximal to ileo-caecal valve.
Detected in under twos.
2:1 ratio in males to females.
102
What are two abnormalities that can occur with recanalisation, and where are they most frequently seen?
Stenosis - where the lumen is narrowed.
Atresia - where the lumen is completely occluded.
It is most frequently seen in the duodenum.
103
Which non-gastrointestinal structure is found in the hindgut?
Bladder epithelium.
104
What does the allantois become?
The urachus, then median umbilical ligament.
105
How does the cloaca split, and what does it become?
The urorectal septum, formed from mesoderm, divides the cloaca into the urogenital sinus and anorectal canal.
106
What are the stomodeum and proctodeum?
Stomodeum - ectodermal wall that ruptures and opens the primordial mouth to the amniotic fluid.
Proctodeum - ectodermal wall that ruptures and opens the primordial anus to the amniotic fluid.
107
What is the pectinate/ dentate line?
The border between ectoderm and endoderm of the anus.
It is where the stratified squamous epithelia become simple columnar epithelia.
108
What is the white line?
The border between where the epithelia becomes non-keratinised stratified squamous epithelia, from keratinised (skin).
109
How does the pain and blood supply to the anus differ above and below the pectinate line?
Above the pectinate line, stretch and chemical injury is felt as vague pain, due to it being formed from (splanchnic) mesoderm. The blood supply is also from the gut.
Below the pectinate line, the pain is localised due to being of ectodermal origin. The blood supply is systemic - internal pudendal artery.
110
What is an imperforate anus?
Imperforate anus is where the anus has formed but the cloacal membrane fails to obliterate. This is treated surgically, and so leads to few complications.
111
What is anorectal agenesis?
Where poor blood supply to the hindgut leads to the rectum and anus not forming correctly.
112
What is an anorectal fistula?
A connection between the rectum and anal canal, and the bladder or vagina.
This leads to faecal material entering these spaces, which can lead to severe infections.
113
How does the mucous content in the saliva aid the body?
It helps with swallowing and speech.
114
How does the saliva act in aiding protection?
It has a cooling effect.
It washes away debris stuck between the teeth.
It secretes lysozymes which break down the cell wall of bacteria.
It secretes lactoferrin which chelates iron, reducing the availability, preventing bacterial multiplication.
115
How are salivary amylase and lingual lipase adapted to act for longer?
Salivary amylase - food in the stomach inhibits the effects of pH against the enzyme, allowing it to work for longer.
Lingual lipase - has the ability to survive within acidic conditions and the proximal duodenum.
116
What is the constituents of the secretions from the parotid, submandibular and sublingual glands?
Parotid - serous secretions containing a high proportion of enzymes. 25% of the total saliva.
Submandibular - mixed, containing both serous and mucous secretions. 70% of the total saliva.
Sublingual - mucous secretions. 5% of the total saliva.
117
How much saliva is secreted per day?
1.5L.
118
Why do the salivary secretions become hypotonic if they are formed as isotonic?
As they pass through the salivary ducts, the ducal cells absorb sodium and chloride ions much faster than they secrete bicarbonate and potassium ions.
The ductal cells are impermeable to water, meaning water cannot follow, out of the lumen.
119
How are secretions pushed out of the acinus?
Myoepithelial cells contract around the acini.
120
What is the parasympathetic supply to the salivary glands?
Parotid - glossopharyngeal nerve.
Submandibular and sublingual - facial nerve.
121
What are some causes of xerostomia?
Medications - anticholinergics and SSRIs.
Autoimmune.
Dementia.
Radiotherapy.
Dehydration.
122
What autoimmune condition can attack the salivary glands, and what is the clinical presentation?
Sjogrens.
Dry mouth, swollen and painful glands.
123
What are salivary stones, what is their presentation and where are they most commonly seen?
Sialoliths.
This is calcification, blocking the duct of the salivary gland, most commonly the Wharton’s duct of the submandibular gland.
There is swelling and associated pain with salivating.
124
How do the movements of the tongue in the oral phase of swallowing help swallowing?
The tongue is pushed against the hard palate and then backwards.
This pushed the bolus against the oropharynx initiating the reflex.
When pressed against the hard palate, it prevents food from coming back out when swallowing.
125
How long does the pharyngeal phase last?
Around 0.2 seconds.
126
What are some causes of poor coordination of swallowing, why are these the case?
Cerebrovascular accidents - stroke.
Parkinson’s disease.
Multiple sclerosis.
The pharyngeal phase is controlled neurally. If there is disruption in this then the muscles will not work together efficiently.
127
What are the symptoms of dysphagia, when it is due to problems coordinating swallowing?
Unable to close the mouth leading to dribbling or protrusion of food from the mouth.
Material entering the respiratory tract, leading to coughing/ choking and potentially pneumonia.
128
What are some causes of dysphagia due to a physical blockage?
Fibrous rings forming within the oesophagus, often seen in scarring due to acidic reflux.
Oesophageal cancer.
Achalasia - failure of the lower oesophageal sphincter to relax.
129
What are the internal and external surfaces of the gums called?
Internal - lingual surface.
External - buccal surface.
130
What structure does the parotid duct penetrate and where does it do it?
It penetrates the buccinator, at the level of the 2nd upper molar.
131
Where are the parotid, sublingual and submandibular glands located?
Parotid - inferior to the zygomatic arch, superficial to the masseter and superior to the mandible.
Sublingual - the floor of the mouth.
Submandibular - within the submandibular triangle, underneath the mandible, above the hyoid.
132
What determines whether swallowing or the gag reflex will occur?
The nature of the stimulus - whether it is pleasant or not.
Age - infants have a much poorer control over the neural pathway.
133
How can a food bolus at the junction of the oesophagus and pharynx be treated?
A drug may be given to relax the muscles of the junction.
Surgery may be performed to remove it.
134
What 5 methods does the body have to prevent gastro-oesophageal reflux?
135
Weakness in the conjoint tendon increase the risk of what kind of herniation?
Direct inguinal hernia.
136
State the ligaments of the liver and their attachments.
Falciform ligament - attaches the anterior surface of the liver to the anterior abdominal wall.
Coronary ligament - has anterior and posterior folds; attaches the superior surface of the liver to the inferior surface of the diaphragm. They units to form the triangular ligaments.
Right and left triangular ligaments - left is at the apex of the liver to the diaphragm. The right is from the right lobe of the liver to the diaphragm.
Lesser omentum - attaches the liver to the lesser curve of the stomach and the duodenum.
137
What does the lesser omentum consist of?
Hepatoduodenal ligament - duodenum to the liver.
Heptogastric ligament - stomach to the liver.
138
State the 3 branches of the coeliac trunk.
The splenic artery.
The left gastric artery.
Common hepatic artery.
139
What is the route and branches of the splenic artery?
Formed from a branch of the coeliac trunk, running behind the stomach, to the spleen.
It gives branches to the body and tail of the pancreas.
It gives off the short gastric vessel, which supplies the fundus of the stomach.
It gives off the left gastroepiploic artery, which supplies some of the greater curve of the stomach.
140
Outline the blood supply to the greater curvature of the stomach.
The greater curvature is supplied by the anastomosis between the left gastro-epiploic, from the splenic artery, and the right gastro-epiploic, from the gastro-duodenal artery.
141
Outline the blood supply to the lesser curve of the stomach.
The left gastric artery branches from the coeliac trunk and meets the right gastric artery, which is a branch of the proper hepatic artery (usually).
142
Outline how the right crus of the diaphragm is structurally and functionally adapted.
The right crus is structurally different from the costal diaphragm and loops around the oesophagus, helping to form the lower oesophageal sphincter.
It contracts to compress the oesophagus, particularly where there is an increase in intra-abdominal pressure, preventing reflux from the stomach.
143
What is receptive relaxation? Why does this occur?
Peristalsis of the oesophagus causes relaxation of the proximal aspect of the stomach - opening the lower oesophageal sphincter.
This fundus distends as it relaxes and the ruggae elongate.
This allows for the stomach to fill with contents without a significant rise in pressure, reducing the risk of reflux.
144
What are the 3 muscles of the stomach, superficial to deep?
Longitudinal.
Circular.
Oblique.
145
What cell types are found in the gastric pits, and where are the gastric pits located?
Parietal cells, chief cells and enteroendocrine cells.
The gastric pits are found invaginating the epithelium.
146
How do prostaglandins act to protect the stomach?
Increase the muscosal blood flow for removal of H+ ions.
Support the mucous layer of the stomach.
General protective mechanism.
147
What is the proton pump?
The hydrogen/ potassium ATPase, which pumps hydrogen ions into the lumen of the stomach and taking potassium ions into the parietal cell.
148
How are the parietal cells changed when entering the stimulated phase, and what other adaptions do they have?
The tubulovesicles that have proton pumps come into contact with the potassium-permeable apical membrane.
The apical membrane is involuted, forming canaliculi, which also contain microvilli, increasing the surface area for the H+/K+ ATPase to function across.
149
What are the sensory triggers for the cephalic phase of digestion?
Smell, sight and taste.
150
What are the gastric triggers for the gastric phase of digestion?
Stretch of the stomach.
Presence of amino acids and small peptides.
Presence of food buffers the pH, so the low pH inhibition (somatostatin) is removed.
151
What are the intestinal triggers for the intestinal phase of digestion?
Chyme entering the duodenum.
Partially digested protein in the duodenum.
152
How are parietal cells activated?
Cholecystokinin receptors are activated by gastrin, released from G-cells.
Histamine receptors are activated by histamine, released from entero-chromaffin like cells.
Muscarinic receptors are activated by acetylcholine, released from the vagus nerve.
153
How are G-cells stimulated?
Vagus nerve released gastrin-releasing peptide, as a result of stretch of the stomach.
Vagus nerve also releases ACh, as a result of sensory triggers.
Peptides in the stomach.
154
How are entero-chromaffin like cells stimulated?
Vagus nerve releases ACh which binds to muscarinic receptors.
Cholecystokinin receptors are stimulated by gastrin.
155
How is acid secretion inhibited?
A decrease in pH is sensed by the D-cell.
Somatostatin is released and binds to the somatostatin-receptor on the G-cell.
Gastrin release is inhibited.
156
How is HCl produced in the parietal cell?
In the presence of carbonic anhydrase, within the parietal cell, water and carbon dioxide come together to form carbonic acid.
H2CO3 then dissociates into H+ and HCO3-.
The proton pump then pumps H+ ions into the lumen of the stomach, drawing in potassium ions.
The potassium ions are then extruded into the lumen of the stomach (via ROMK receptors).
The anion exchanger then exchanges bicarbonate ions for chloride ions.
The chloride ions are then pumped into the lumen via chloride channels, where they combine with the hydrogen ions to form HCl.
The HCO3- ions are taken away in the venous blood.
157
What is the alkaline tide?
The increase in pH within the venous blood draining the stomach, due to the exchange of bicarbonate ions for chloride ions. It is seen after eating, when the parietal cell increases its HCl secretions.
158
What is the mechanism of the lower oesophageal sphincter?
Intrinsic smooth muscle of the oesophagus is in a constant state of contraction, but relaxes when food goes down the oesophagus.
The right crus of the diaphragm can contract and wraps around the oesophagus - an increase in pressure causes the crus to pull tighter.
Oblique angle of entry of the oesophagus.
159
What is the issue with strictures of the oesophagus?
Fibrous scar tissue narrows the lumen of the oesophagus, leading to dysphagia.
160
What is fundoplication?
Where the fundus of the stomach is wrapped around the lower oesophagus, below the diaphragm, preventing gastric acid reflux.
161
What are the lifestyle management for gastro-oesophageal reflux disease, and what is their general overall aim?
To decrease intra-abdominal and intra-gastric pressure, predominantly, to decrease the risk of reflux.
162
How can bile reflux be a cause of acute gastritis?
Reflux through the pyloric sphincter causes chemical injury to the stomach.
163
How can autoimmune chronic gastritis lead to pathological changes?
Autoantibodies attack the parietal cells.
This causes:
- Atrophy of the body of the stomach, leading to gastritis.
- Decrease acid production, which can increase the risk of infections.
- Decrease intrinsic factor release, leading to a lack of B12 absorption.
164
What are the signs/ symptoms of autoimmune chronic gastritis?
Pernicious anaemia - megaloblastic.
Neurological symptoms - numbness in the hands and feet, and confusion.
Anorexia - loss of appetite.
Glossitis - inflammation of the tongue.
165
How does helicobacter pylori benefit some people?
Helps control the stomach microbiome.
166
How does helicobacter pylori use chemotaxis, and how does it stay in the required place?
It senses the increase in pH and uses its flagella to move there.
It has adhesins which bind to the gastric epithelia, resisting peristalsis.
167
Where is the urease found within the H.Pylori, and what is the beneficial function of it?
It is found within the cytoplasm.
It converts urea and water in carbon dioxide and ammonia.
The ammonia alkalises the outer membrane and the surrounding environment.
168
What is the function of cytotoxic-associated gene A, released from helicobacter pylori? What risk is associated with this?
A protein is formed and inserts into the stomach epithelia, causing inflammation by stimulating IL-8.
It increases the risk of stomach cancer.
169
What is the function of vacuolating toxin A, released from helicobacter pylori?
VacA is a protein that toxic to the stomach epithelia.
It also increases the paracellular permeability.
170
How can helicobacter pylori in the antrum affect the stomach and duodenum?
It can activate the gastrin cells, as it releases ammonia which increases the pH, which increases the number, and amount of acid released from the body of the stomach.
It can enter the duodenum and cause ulceration.
The decrease in pH can also cause metaplasia of the duodenum, increasing the risk of cancer.
171
How can helicobacter pylori increase the risk of cancer when it colonises the body or fundus of the stomach?
Atrophy of the parietal cells occurs.
This leads to dysplasia, increasing the risk of cancer.
172
What are the antibiotics used to eradicate H.Pylori, and what are the side effects seen in 5% of patients?
Clarithromycin and metronidazole.
Diarrhoea and nausea is sometimes seen.
173
How can NSAIDs cause peptic ulcer disease?
They inhibit prostaglandins, decreasing the mucosal blood flow and bicarbonate mucous secretions.
174
Where do chronic peptic ulcers form?
At the mucosal junctions between:
- Duodenum and the antrum of the stomach.
- Antrum and body of the stomach.
175
If there is very severe peptic ulcer disease, what infectious complication can occur?
Peritonitis as there is erosion through the wall of the stomach, leading to contents leaking out into the peritoneal cavity.
176
Where else can erosion of the wall occur, due to severe ulceration, and what is the consequence of this?
The gastro-duodenal artery, due to a posterior duodenal ulcer, leading to blood pooling in the stomach causing haematemesis (vomiting blood).
Rarely, it can erode through the splenic artery.
177
What is malaena?
An upper gastrointestinal bleed where the haem is oxidised as it passes through the tract, leading to black, tar-coloured stools.
This occurs if there is a small, gradual bleed, not a large bleed, such as in haematemesis.
178
What are the symptoms of peptic ulcer disease?
Pain - epigastric and back pain, worsened after meals.
Haematemesis and malaena from bleeding.
Early satiety due to the muscularis externa being replaced with scar tissue, meaning the stomach cannot expand as much.
Weight loss due to associating eating with pain.
179
How can the timing of pain be used to help determine where the peptic ulcers are?
Immediately after eating - gastric.
A while after eating and at night - duodenal, as the pyloric sphincter opens, allowing chyme to enter.
180
What is the treatment for an active bleeding peptic ulcer disease?
181
What is the main function of motilin, and the effects it has on the brain, gallbladder, pancreas and stomach?
Increase pepsinogen secretions.
182
What are the small bowel, transverse mesocolon or sigmoid mesocolon?
Small bowel mesentry - attaches the jejunum and ileum to the posterior abdominal wall.
Transverse mesocolon - attaches the transverse colon to the posterior abdominal wall.
Sigmoid mesocolon - attaches the sigmoid colon to the posterior abdominal wall.
183
What are the properties of chyme leaving the stomach?
It is semi-solid - part liquid and part solid, that is partially digested and has a low pH due to gastric acid secretions.
184
How are biliary secretions controlled?
Cholecystokinin stimulates the contraction of the gallbladder and relaxation of the sphincter of oddi, leading to bile - an alkaline substance - being secreted into the duodenum.
185
What are the components of bile?
Bile salts, acid and pigments, phospholipids, conjugated bilirubin, electrolytes and water.
186
Describe how the microscopic appearance of the liver relates to its function of digestion.
There are hepatocytes arranged in lobules, with bile ducts running between the lobules. This allows for bile to be synthesised and released into the bile ducts, then common hepatic ducts, then drain into the common bile duct, which is attached to the cystic duct from the gallbladder.
187
What are the 4 parts of the duodenum and their importance?
D1 (superior) - connected to the liver by the hepatoduodenal ligament and is the most common site of ulceration.
D2 (descending) - curves around the pancreas and is where the major papilla is located.
D3 (inferior) - crosses over the IVC and aorta.
D4 (ascending) - joins the jejunum, at the duodenojejunal flexure, with the suspensory muscle contracting, pushing contents into the jejunum.
188
What branch of the aorta supplies the midgut, and what is its course in the abdomen?
Superior mesenteric artery - it travels in an oblique direction, heading towards the right iliac fossa.
It is at the level of L1.
189
What are the 4 branches of the superior mesenteric artery to the midgut?
Jejunum and ileum - branching of the SMA to the left occurs, which anastomose forming arcades.
Caecum and terminal ileum - ilio-caecal branch.
Ascending colon - right colic artery.
Proximal 2/3rds of the transverse colon - middle colic artery.
190
What branch of the aorta supplies the hindgut, and what is its course in the abdomen?
Inferior mesenteric artery.
It is given off at the L3 level and passes into the pelvis, after having given off multiple branches, to form the superior rectal artery.
191
What are the two main branches of the inferior mesenteric artery, and what do they supply?
Left colic artery, which supplies the descending colon.
Sigmoidal artery, which supplies the sigmoid colon.
192
What is the marginal artery of the gastrointestinal system?
Anastomoses between the branches of the superior mesenteric artery and the inferior mesenteric artery, supplying oxygenated blood to the colon.
193
Which part of the colon can be damaged by a low blood pressure, and why?
The splenic flexure - a vascular watershed area of the GI tract. A decrease in blood pressure can lead to ischaemia.
This is because the superior mesenteric artery’s middle colic artery anastomoses with the (ascending branch of the) left colic artery, here.
194
Where does the portal vein form, and at what spinal level is this?
Behind the neck of the pancreas.
It forms at the level of L1.
195
Which sections of the duodenum are retroperitoneal?
Descending, horizontal and ascending - D2, D3 and D4.
196
Anatomically, what is significant about the level at which the major papilla lies in the duodenum?
It is midway though D2.
It is the point at which the foregut becomes the midgut.
197
What is the relationship between the pancreas, duodenum and SMA?
The neck of the pancreas wraps around the superior mesenteric artery, leaving the head of the pancreas in the C-shape of the duodenum (with the uncinate process also here, a bit more distal), posterior to the artery.
198
Where, retroperitoneal or intraperitoneal, does the pancreas lie?
The uncinate, head and body are intra-peritoneal.
The tail is retroperitoneal, closely related to the spleen, wrapped in the spleno-renal peritoneum.
199
What is the free edge of the lesser omentum formed from, and what does it envelop?
The ventral mesentery of the foregut is the only ventral mesentry, meaning that it has no connections to any mesentries of the mid- and hindgut.
It envelops the portal vein, hepatic arteries and a portion of the bile duct.
200
Which veins unite to form the portal vein?
The splenic vein and superior mesenteric veins.
The inferior mesenteric vein drains into the splenic vein.
201
What are the paracolic gutters and where are they found?
There is a left and a right, which are spaces between the colon and abdominal wall.
Left - between the lateral abdominal wall and the descending colon.
Right - between the lateral abdominal wall and ascending colon.
202
Where is the hepatorenal recess, and what can it be useful for?
Space between the right anatomical lobe of the liver and right kidney.
It is the lowest point of the peritoneal cavity when supine and so ultrasound can be used to detect peritoneal fluid for ascites.
203
Why is the osmotic pressure in the stomach so high?
The stomach is relatively impermeable to water.
The breakdown of food increases the osmolarity - the greater the breakdown, the higher the osmotic pressure it exerts.
204
What is the release of chyme controlled by?
Pyloric sphincter.
205
What are the 3 structures of the pancreatic secretory part, and what are their functions?
Acinus - synthesise enzymes.
Centroacinar cells - form the aqueous part of the secretion.
Ductal cells - modifying the aqueous secretions, producing a bicarbonate solution.
206
What are the different pancreatic secretions, their proportions and methods of secretions?
Exocrine - 90% of the secretions are enzymatic and drain via the major pancreatic duct.
Endocrine - 2% hormonal secretions, which drain into the splenic vein.
207
What is the neural and hormonal control of the pancreas, and their functions?
Sympathetic, via greater splanchnic nerve - inhibits the function via vasoconstriction.
Parasympathetic - vagus nerve and stimulation of cholecystokinin, stimulates.
208
What stimulates the actions of the vagus nerve on the pancreas and release of cholecystokinin?
Hypertonicity.
Small peptides.
Fats.
209
What is the organelle composition within hepatocytes, and how does this relate to its function?
Contains lots of RER and SER for synthesis of proteins and lipids.
Contains stacks of Golgi membranes - modification and movement of the products.
Also contains glycogen granules.
210
What are the two components of bile?
Bile acid dependent - bile acids and pigments that are secreted into bile canaliculi.
Bile acid independent - alkaline solution that is secreted by duct cells, stimulates by secretin.
211
What are the two primary bile acids?
Cholic acid.
Chenodeoxycholic acid.
212
What are bile salts?
Bile acids that are conjugated with the amino acids glycine or taurine.
213
What is the purpose of forming bile salts from bile acids?
They are more soluble at duodenal pH.
They are amphipathic and so can act at the oil-water interface, so are able to emulsify dietary lipids.
214
Why do bile salts emulsify lipids, and what happens to them once their function is complete, here?
They disperse the lipid droplets to increase surface area for lipases to act.
They then form micelles by conjugating to some of the products of lipid breakdown.
215
What can micelles carry, and where do they carry it to?
Cholesterol, monoglycerides and free fatty acids.
Carry them to the brush border of the epithelial cells.
216
What is the function of the gallbladder, and how does it do this?
It acts as a store for bile, concentrating it by removing water and ions, allowing it to store more.
It is able to store it by the bile entering the gallbladder when the sphincter of oddi is closed.
It contracts to release the bile by the action of cholecystokinin.
217
What is the function of the conjugation of bilirubin?
Increases its solubility.
218
What is the function of cellulose, if it cannot be broken down?
It maintains gut function, maintaining stool regularity and decreasing the risk of bowel cancer.
Binds to bile salts, causing them to be released in the faeces, meaning the liver synthesises more, decreasing cholesterol levels in the body.
It can be partially digested by the bacteria within the colon, maintaining the microbiome.
219
How is starch broken down?
The straight chain, amylose, has its alpha-1,4-glycosidic bonds broken by amylase, into maltose.
The branched chain, amylopectin, has its alpha-1,6-glycosidic bonds broken by isomaltase, into alpha dextrins.
220
What enzymes break down maltose, lactose and sucrose? Where are these enzymes found?
Maltose - maltase.
Lactose - lactase.
Sucrose - sucrase.
They are brush border enzymes, which are integrated into the apical membrane of the enterocytes.
221
How are the monosaccharides absorbed?
Glucose or galactose are absorbed into the enterocyte via SGLT 1 transporter.
Fructose is absorbed into the enterocyte via the GLUT5 transporter.
Glucose, galactose and fructose are absorbed into the blood via the GLUT2 transporter.
222
How is protein digested in the stomach?
Chief cells secrete pepsinogen.
Pepsinogen is converted into pepsin, due to the low pH of the stomach.
Pepsin breaks down proteins into oligopeptides and amino acids.
223
How are proteases secreted into the intestinal lumen, and how do they begin to function?
Zymogens, synthesised by the pancreas, are activated within the lumen of the duodenum by tripsin.
224
How is trypsinogen activated?
Which zymogens does trypsin activate?
Enteropeptidase activates tripsin.
Trypsin activates:
- Chymotrypsinogen into chymostypsin.
- Proelastase into elastase.
- Procarboxypeptidase A into carboxypeptidase A.
- Procarboxypetidase B into carboxypeptidase B.
Trypsin also activates trypsinogen to trypsin, giving an exponential effect of activation.
225
What are the two types of intestinal proteases, what are some examples and what are their functions?
Trypsin, chymotripsin and elastase’s are endopeptidases. These break down peptide bonds in the middle of the chain, forming shorter peptides.
Carboxypeptidase A and carboxypeptidase B are exopeptidases, which break down bonds at the end of the chain, forming short peptides and amino acids.
226
How is the absorption of proteins at the brush border and the processes within the enterocyte facilitated?
Amino acids are absorbed via a sodium co-transporter, which can then be absorbed across the basolateral membrane.
Dipeptides and tripeptides are transported into the lumen of the enterocytes via PepT1 transporters, which can then be absorbed across the basolateral membrane.
The di- and tri-peptides can also be broken down into amino acids via cytosolic peptidases, which can then be absorbed across the basolateral membrane.
227
How does water move across the small intestine?
Through paracellular and transcellular transport.
It is bidirectional, following the osmotic gradient.
228
How does the anatomy of the enterocytes cause paracellular transport?
There is high concentrations of sodium in the intercellular spaces.
This is hyperosmotic and so draws water through the tight junctions, absorbing it.
229
How do oral rehydration preparations work?
The preparations contain sodium and glucose, and so when they are consumed, there is an increase in concentration of these in the small intestine.
They are taken into the enterocyte via SGLT1 transporters, increasing the osmolarity within the enterocyte.
This causes water to be drawn into the enterocyte through transcellular absorption.
230
How is water secretion in the small intestine controlled?
An increase in intracellular cAMP stimulates the excretion of chloride ions.
The NKCC transporter on the basolateral surface pumps these ions into the enterocyte.
The CFTR transporter then transports chloride ions into the lumen of the small intestine.
Na+ is drawn into the lumen, through the tight junctions, which combines with Cl- to form NaCl.
This leads to water being drawn into the lumen through the tight junctions - paracellular transport.
231
What are some causes of vitamin B12 deficiency?
Lack of intrinsic factor - autoantibodies acting against the parietal cells.
Hypochlorhydria (decrease in stomach acid).
Insufficient B12 in the diet.
Inflammation of the terminal ileum, in conditions such as Crohns.
232
Why is the cause of hypochlorhydria and why may it lead to a vitamin B12 deficiency?
The decreased stomach acid can be due to gastric atrophy or proton-pump inhibitors.
Less B12/cobalamin is released.
233
What are the complications of a vitamin B12 deficiency?
Neurological problems.
Megaloblastic anaemia.
234
Why does a lactase deficiency cause flatulence and diarrhoea?
The lack of lactase, often seen after the age of 2, means that less lactase is broken down in the small intestine.
This means that it exerts an osmotic pressure in the small intestine, drawing water in, leading to diarrhoea.
The disaccharide is fermented and broken down by bacteria within the colon, leading to gases being released, causing flatulence.
235
What is irritable bowel syndrome, and who is it seen most in?
It is a condition that is diagnosed due to the absence of other conditions, with the presence of specific symptoms, with no known cause.
It is seen in:
- 10-15% of adults.
- Females in a 2:1 ratio with males.
- People ages 20-40 are most affected.
- People with psychological disorders.
236
What are the symptoms of irritable bowel syndrome?
Abdominal pain and cramping.
Bloating and flatulence.
Diarrhoea or constipation.
Rectal urgency.
237
What is coeliac disease?
A disease where there is an immunological response to gliadin fraction within gluten, causing impaired digestion and malabsorption of gluten.
238
What are the physiological changes seen to the small intestine, in coeliacs disease?
Flattening of villi.
Hypertrophy of crypts.
Lymphocytes in the epithelium or lamina propria.
239
What is the cause of Coeliac’s disease?
Genetic factors.
240
What are the symptoms of coeliacs disease?
Diarrhoea due to the osmotic effect being exerted by gluten from it not being absorbed.
Weight loss.
Pain.
Anaemia.
Neurological symptoms.
241
Why does coeliacs disease cause pain, anaemia and neurological symptoms?
Pain - sugars in gluten are fermented in the colon, leading to distension of the bowel. These stretch receptors then detect this and send signals of pain.
Anaemia - decrease in iron absorption.
Neurological symptoms - decrease in calcium absorption.
242
What are the investigations for coeliacs disease?
Blood tests - IgA presence in the smooth muscle of the endomysium and tissues.
Upper GI endoscopy and duodenal biopsy - reduced or absent villi.
243
What is the treatment for coeliacs disease?
Gluten-free diet.
244
What are the functions of the large intestine?
Remove water from the gut contents, turning chyme into a semi-solid.
Production of vitamins.
Holds and maintains the microbiome.
Act as a temporary storage until defaecation.
245
Where does the colonic mucosa get its nutrients from?
Short chain fatty acids from the fermentation of dietary fibre.
The rest from the blood.
246
Which structures of the large intestine are retro- or intra-peritoneal?
Retroperitoneal:
- Ascending colon.
- Descending colon.
- Middle third of the rectum
Intraperitoneal:
- Transverse colon.
- Upper third of the rectum.
The lower third of the rectum has no peritoneum.
247
What is the venous drainage of the large intestine and rectum?
Colon:
- Midgut drains into the superior mesenteric vein.
- Hindgut drains into the inferior mesenteric vein.
Rectum:
- Upper third drains into the inferior mesenteric vein.
- Lower 2/3rds drain into the systemic venous system.
248
What is a portosystemic anastomosis?
Where there are anastomoses between the portal venous system and systemic venous system.
249
What is significant about the anatomy of the muscle of the large intestine?
The external longitudinal muscle is incomplete, forming 3 distinct bands - teniae coli.
Haustra are saculations caused by contraction of teniae coli.
250
How is water absorption in the colon controlled?
ENaC channels on the coloncytes are induced by aldosterone.
The tight junctions are much tighter, preventing diffusion of ions and so water, back into the lumen.
251
Who are direct inguinal hernias most common in, and why?
Older men as the Hesselbach triangle gets weaker with age.
252
Why would an erect chest X-ray be performed for abdominal pain?
To check for any bowel perforations as air would accumulate under the diaphragm.
253
What is the first line test for Coeliac’s disease?
Explain why.
Tissue tTGA test, with serum IgA test - tTGA tests for Coeliac’s disease, but is IgA dependent and so if it is not present then the absence of IgA could still mean they have Coeliac’s.
254
What are some complications of using proton-pump inhibitors for long periods of time?
Can cause hypomagnesium.
Can lead to a clostridium difficile infection.
255
What is the test for chronic pancreatitis?
Faecal elastase test - a lack of elastase in the faeces can show the presence of chronic pancreatitis.
256
What can a complication of SGLT2 inhibitors be?
Thrush.
257
What molecule is released from amylopectin by the action of amylase?
Alpha dextrins.
258
What are the storage functions of the liver?
Glycogen.
Vitamins.
Iron.
Copper.
259
What are the synthetic functions of the liver?
Glucose.
Lipids and cholesterol.
Bile.
Clotting factors.
Albumin.
260
What are the metabolic functions of the liver?
Bilirubin.
Ammonia.
Drugs.
Alcohol.
Carbohydrates.
Lipids.
261
What are the two possible diagnoses with a rapid clinical presentation of jaundice, oedema, bleeding and confusion?
Distinguish between them.
Decompensated liver disease - this is when they have also previously had liver disease.
Acute liver failure - no previous liver disease.
262
How does alcoholic hepatitis present?
A chronic condition due to years of excessive alcohol consumption.
Inflammatory cells can be seen on microscopy.
They have right upper quadrant pain and jaundice.
263
What is NAFLD?
Non-alcoholic fatty liver disease is associated with insulin resistance and triglyceride deposition.
264
What is NASH, its causes and treatments?
Non-alcoholic steatohepatitis has the presence of inflammation. It is a type of non-alcoholic fatty liver disease.
It is associated with obesity, metabolic syndrome and familial hyperlipidaemia.
It is treated with lifestyle modifications and reducing glucose levels.
265
What is PBC?
Primary biliary cirrhosis - an autoimmune condition due to anti-mitochondrial antibodies.
266
What is PSC?
Primary sclerosing cholangitis - progressive autoimmune disease associated with irritable bowel syndrome and ulcerative colitis.
267
How can you distinguish between PBC and PSC?
PBC is AMA (anti-mitochondrial antibody) positive.
PSC is AMA negative.
268
How does the portal circulation and systemic circulation of the liver drain blood back to the heart?
Portal circulation drains into the liver, which then drains into the hepatic veins. These then drain into the inferior vena cava.
The systemic circulation drains directly into the inferior vena cava.
269
Explain how portal hypertension can cause umbilical varices.
When there is sufficient pressure in the portal system, the anastomoses between the portal system and ligamentum teres (remnant of umbilical vein) causes the the ligamentum teres to distend. This leads to a caput medusa appearance.
270
What are the anorectal anastomoses between?
Explain why varices here are not painful.
The superior rectal vein which drains into the inferior mesenteric vein.
The middle and inferior rectal veins drain into the internal iliac vein and then into the inferior vena cava.
Varices, due to portal hypertension, are above the pectinate line and do not cause stretch of the rectum and so are not perceived as pain.
271
Explain how oesophageal varices form and the severity of this.
Portal hypertension increases the pressure in the left gastric vein.
This causes an increase in pressure in the oesophageal veins.
This leads to distension of the oesophageal veins which can rupture and lead to severe bleeding and haematemesis.
272
What is the venous drainage of the oesophagus?
The upper 2/3rds are drained by the oesophageal veins, which then drain into the azygous veins and then superior vena cava.
The lower 1/3rd is drained by the left gastric vein, which then drains into the portal vein.
273
Explain the drainage of bile from the liver and gall bladder, and how this communicates with the pancreas.
274
What can the contents of gallstones be, and what are the risk factors for developing them?
They can be formed from cholesterol, bile pigments or both.
Risk factors:
- High cholesterol diet.
- Female.
- Age in the forties.
- Pregnancy.
275
How are gallstones diagnosed?
Clinical picture and ultrasound, and they do not contain calcium so cannot be detected by an X-ray.
276
What causes biliary colic pain?
Cholecystokinin is released after eating, causing the gall bladder to contract, and so the gallstone is compressed within the cystic duct.
277
What is the anatomical and pain difference between biliary colic and acute cholecystitis?
Biliary colic is a partial occlusion of the lumen of the cystic duct. The pain is a constant pain that lasts for hours at a time.
Acute cholecystitis is impaction of a gallstone in the cystic duct, completely occluding the lumen, that gives pain that comes and goes.
Both pain is in the right upper quadrant.
278
What method can be used for diagnosis of acute cholecystitis that cannot be used to biliary colic?
Ultrasound - inflammation of the wall of the gallbladder can be seen on ultrasound.
Biliary colic is not associated with inflammation.
279
Explain charcot’s triad with association of ascending cholangitis.
Right upper quadrant pain - gallstone presence in the common bile duct causes pain.
Inflammation - infection of the biliary tree due to stasis.
Jaundice - complete obstruction of the common bile duct.
280
What is the treatment for biliary colic, acute cholecystitis and ascending cholangitis, respectively?
BC - pain relief and surgery to remove the gall bladder (cholecystectomy).
AC - pain relief, antibiotics and cholecystectomy.
AsC - antibiotics, fluids and surgery to remove this stone.
281
What are the 3 pathways for conjugated bilirubin after it leaves the liver?
1) enters the enterocyte-hepatic circulation with bile to circle round.
2) enters the duodenum where it is oxidised to form stercobilin.
3) enters the blood stream and is excreted from the kidney in the form of urobilin, from urobilogen.
282
What can the cause of hepatic jaundice be?
Chronic liver disease - causes an enlarged liver and portal hypertension.
Acute liver damage.
283
What are some causes of intrahepatic obstruction?
Autoimmune conditions.
Inflammation or oedema, leading to compression.
Tumour acting to physically compress some of the liver.
Cirrhosis - non-expansile and so also compresses.
284
What are some causes of decreased plasma albumin?
Decreased protein intake.
Nephrotic syndrome - excretion of albumin in the urine.
Chronic liver disease.
285
Why do we perform liver function tests?
To establish a baseline before starting medication.
To monitor liver conditions.
For suspected liver pathology.
286
When would alkaline phosphate be increased?
In growing children as it is released from the bone.
In metastatic bone cancer - released from the bone.
Obstruction of the bile duct - cholestasis.
287
What can the LFT appear as in liver metastases?
Hepatocellular damage will raise the AST and ALT.
Raised ALP as the tumour compresses the bile ducts.
Raised bilirubin as intra-hepatic obstruction of the hepatic bile ducts are compressed (post-hepatic, increased conjugated) and the hepatocytes have been damaged (hepatic, increased conjugated and unconjugated).
288
What spinal level is the fundus of the gallbladder?
L1.
289
Which accessory lobe of the liver does the gallbladder lie adjacent to?
Quadrate lobe.
290
What is cullens sign?
State some causes.
Skin discolouration (yellow-blueish) and swelling around the umbilicus, due to oedema and bruising of subcutaneous fatty tissue.
It can be due to an ectopic pregnancy, acute pancreatitis or some cancers.
291
What is Grey Turner’s sign?
State some causes.
Bruising of the flanks, between the last rib and top of the hip.
It is seen in acute pancreatitis due to tracking of the pancreatic exudate.
292
Why can cirrhosis cause ascites?
The damage to the hepatocytes means that less albumin is synthesised. This means there is less oncotic pressure within the portal veins.
It can cause portal hypertension, meaning there is an increased hydrostatic pressure, causing more fluid to leave the vein and enter the peritoneal cavity.
293
What blood tests can be done to show a raised unconjugated bilirubin level?
FBC - specifically, red cell count.
LDH - released from red blood cells when destroyed.
294
When can ALP be increased?
Gallstones which causes ALP to be released from ductal cells.
Increased bone turnover - growing children, metastatic bone cancer.
Pregnancy - released from the placenta.
295
What organisms cause infectious colitis?
E. Coli.
Clostridium difficile.
296
What is a stool test for diagnosis of ulcerative colitis?
Faecal calprotectin - calprotectin in the stool, due to migration of neutrophils within the intestinal mucosa.
It is seen in bowel inflammation.
297
How do ulcerations appear on colonoscopy?
White streaks.
298
What is the first line imaging investigation for ulcerative colitis, and why?
Flexible sigmoidoscopy.
Less bowel prep (strong laxatives) are required, and do not need to be sedated.
Less risk of bowel perforation than colonoscopy.
299
What imaging technique is used for ulcerative colitis suspicions, with bleeding or in the elderly, and why?
Protoscopy - imaging the rectum only.
This is because when bleeding, the mucosa is friable. In the elderly, they more commonly have diverticulosis and so is more prone to perforation.
300
What is given with high dose steroids?
Proton pump inhibitors.
301
What can ulcerative colitis patients be given to facilitate them being able to go out in public, to decrease the risk of self-defection?
Toilet pass - allow them to use toilets that are not available to the public.
Stoma bag.
302
What volume of water is lost in the stool daily?
100ml, from the 10L that enter the duodenum.
303
What is the difference in stool volume and effects of eating that is seen in osmotic and secretory diarrhoea?
There is a much larger stool volume in secretory diarrhoea due to the epithelial cells actively secreting water.
Fasting will stop osmotic diarrhoea as there cannot be any malabsorption when no food intake occurs and so there is less osmotic pressure and water drawn in. Fasting does not affect secretory diarrhoea.
304
Explain the pathophysiology of secretory diarrhoea.
Toxins, viruses, medications and serotonin increase the amount of cytosolic cAMP within the CFTR. This causes more Cl- to be pumped into the GI lumen, causing paracellular transport of Na+ and water.
Bicarbonate ions can also be excessively secreted.
305
What are some non-osmotic/secretory causes of diarrhoea?
Too little reabsorption of sodium:
- Reduced surface area.
- Mucosal disease decreases the function of reabsorption.
- Decreased contact time (intestinal rush - diabetes/ IBS).
306
What are the possible criteria for constipation?
In a quarter or more of defecations:
- Straining.
- Lumpy/ hard stools.
- Feeling of incomplete evacuation.
- Feeling of obstruction or blockage.
Fewer than 3 unassisted bowel movements per week.
307
What are some risk factors for constipation?
Female (3:1).
Medications - opioids or anti-diarrhoea.
Low level of physical activity.
Under the age of 4.
Older age.
308
Why can megacolon cause constipation?
Increased diameter decreases the pressure for transport of the faeces.
309
What are the intestinal pacemaker cells called?
Intestinal cells of Cajal.
310
What are the different movements of the colon during fasting and digestion?
Fasting - shuttle contractions (segmentation) that moves material backwards and forwards in the colon, facilitating absorption.
Digestion - mass peristalsis moving faecal material from the transverse colon to rectum.
311
What is the blood supply to the appendix?
Appendicular artery, which is a branch of the posterior iliocaecal or ileocolic artery.
312
What are some different locations of the appendix?
Retro-caecal.
Pelvic.
Sub-caecal.
Para-ileal (pre or post).
313
What are some blockages that can occur, of the appendix?
Faecolith - hard part of faeces.
Lymphoid nodule hyperplasia - seen usually due to viral infections.
Foreign body.
314
What can be some difficulties in diagnosing appendicitis?
Appendix can be retro-caecal or pelvic and so does not come into contact with the parietal peritoneum - can give suprapubic, right sided rectal, or vaginal pain.
Children symptoms are more non-specific.
Pregnancy - uterus can alter the appendix’s position.
315
What should always be ruled out before appendicitis, and how?
Ectopic pregnancy - pregnancy test.
UTI - urine dip stick.
316
What is the pathophysiology of diverticulitis?
Entrance to diverticula is blocked by faeces.
Inflammation allows bacterial invasion of the wall of the diverticula.
Can lead to perforation.
317
What is the difference between uncomplicated and complicated diverticulitis?
Uncomplicated - inflammation and small abscesses confined to the colonic wall.
Complicated - larger abscesses, fistula and perforation possible.
318
What is the treatment for diverticulitis - complicated and uncomplicated?
Uncomplicated - antibiotics, fluid resuscitation and analgesia.
Complicated - surgery; abscess drained, perforation repair or partial colectomy last line.
319
Describe the features of the external anal sphincter.
It is striated, skeletal muscle under voluntary control.
It is located within the upper anal canal.
It is composed of 3 muscle bellies; deep, superficial and subcutaneous, that mix with fibres from the levator ani muscle.
It joins with the pubo-rectalis to form a sling.
It is innervated by the pudendal nerve.
320
Why do haemorrhoids produce bright red blood?
They are predominantly venous blood but have some arterial supply.
321
What is the cause of an anal fissure?
High internal anal sphincter tone, increasing the tension of the skin.
Reduced blood flow to the anal mucosa.
322
Describe the locations of the thirds of the rectum.
Upper - intra-peritoneal.
Middle - retroperitoneal.
Lower - no peritoneum.
323
What two key processes occur in the terminal ileum?
Absorption of vitamin B12.
Bile salt absorption from the enterohepatic circulation.
324
What is back wash ileitis?
Inflammation of the terminal ileum due to ulcerative colitis.
325
What is the risk effects of smoking on Crohn’s and ulcerative colitis?
Crohn’s - increases the risk.
UC - decreases the risk.
326
What perianal lesions can be seen in Crohn’s disease?
Skin tags - remnant of prolapsed haemorrhoids.
Fistulae - bowel to bowel/ bladder/ vagina or skin.
Abscesses.
Scarring.
Sinuses - bowel to skin fistulae.
327
What sign can be seen on a CT scan with a patient with Crohn’s disease?
Target sign - thickening of the full bowel wall and obstruction.
328
Where are strictures often seen in Crohn’s and how can they be visualised?
Seen in the hepatic flexure - between the ascending and transverse colon.
Can be visualised via barium enema or follow-through.
329
What are the different types of ulcerative colitis?
330
What is seen on microscopy of ulcerative colitis?
Infiltration of inflammatory cells of the lamina propria.
Crypt abscesses - neutrophilic exudate in crypts.
Crypt distortion - irregular shaped glands with dysplasia and dark, crowded nuclei.
Reduced number of goblet cells.
331
What is the taenia coli, what is its function and how does this occur?
Incomplete longitudinal layer of smooth muscle that forms 3 distinct bands, due to the outgrowing of the circular muscle layer.
It is tethered to the mucosa of the ascending colon and contracts to form haustra.
332
What causes the loss of haustra?
Inflammation of the colon causes relaxation of the taenia coli.
333
What kinds of ulcers can be seen in Crohn’s disease?
Rose-thorn ulcers that are linear and penetrate deeply, stenosing the terminal ileum.
334
What is the string sign of kantour?
Narrowing and then thickening of long strictures, seen on a barium follow through.
335
What is a double contrast enema?
What does it look for?
Where a barium enema is given, followed by air which pushes the barium into the ulcerations and invaginations of the colon, to see for a lead pipe colon or a granular appearance, in ulcerative colitis.
336
Why would you perform a colectomy in ulcerative colitis?
Inflammation not settling.
Pre-cancerous changes.
Toxic megacolon - distension increasing the risk of perforation.
337
What is an ileostomy?
Where the terminal ileum is brought to the rectum to allow for continence to be maintained.
338
How can antibiotics cause Crohn’s disease?
It can disrupt the microbiome that leads to altered interaction with the mucosa.
339
Why does weight loss occur in Crohn’s and ulcerative colitis?
Crohn’s - poor absorption of food.
Ulcerative colitis - inflammatory process utilises energy.
340
Why does the lumen of the gut narrow in Crohn’s disease?
Inflammation of the wall of the bowel and fibrosis after healing.
341
Describe the cause of the ‘cobblestone appearance’ of Crohn’s disease.
Oedematous bowel causes parts of the bowel to push into the lumen, with ulcers forming the grout.
342
Why would somebody have anaemia with ulcerative colitis?
Blood loss in the stool.
Anaemia of chronic disease.
343
What is true colic?
Pain due to lesions of the small intestine.
344
What is Gilbert’s syndrome?
A non-haemolytic jaundice.
Due to abnormal liver enzymes.
345
What is an adenoma?
A benign tumour of the glandular epithelium.
346
What are some red flag symptoms of GI cancers?
Abdominal pain.
Constipation.
Weight loss.
Dysphagia.
Blood in stools.
347
Where are the different types of oesophageal cancers most frequently found, anatomically?
Squamous cell carcinoma - upper 2/3rds.
Adenomcarcinoma (columnar) - lower 1/3rd.
348
What is the classical clinical presentation of a patient with oesophageal cancer and why?
Progressive dysphagia - initially solids more difficult to swallow and then liquids.
Odynophagia - pain on swallowing.
Anaemia as tumours invade surrounding structures causing bleeding.
Loss of weight, unintentionally.
Anorexia due to pain when eating.
Malaena - upper GI bleed.
Masses that can be palpable.
349
What are the risk factors for squamous cell carcinoma and adenocarcinoma, of the oesophagus?
SSC - smoking, alcohol excess, dietary intake such as hot beverages.
Adenocarcinoma - obesity, reflux disease, Barrett’s oesophagus (GORD, over the age of 50, male, smoking, etc.).
350
What are the 3 types of dysphagia?
Extraluminal.
Luminal - wall of the organ.
Intraluminal.
351
What are the investigations for oesophageal cancer?
Blood tests - FBC for anaemia.
Oesophagogastroduodenoscopy (OGD) with biopsy.
CT thorax and abdomen - size of primary, local invasion and metastatic spread to guide treatment.
352
What does the treatment of oesophageal cancer depend on, and what are some potential options?
The stage of the cancer.
Endoscopic therapies - removing a smaller tumour endoscopically.
Oesophagectomy - surgical removal of the oesophagus.
Chemoradiotherapy - can be with surgery to shrink or remove any remaining neoplastic cells.
353
What is the most common type of gastric cancer and what are some others?
Adenocarcinomas.
Others - lymphoma, leiomyosarcoma or neuroendocrine.
354
Where are gastric adenocarcinomas most commonly found?
Gastric cardia - 31%.
Antrum - 26%.
Body of the stomach - 14%.
355
What is the Lauren classification?
A method of grading a gastric cancer.
Diffuse - poorly differentiated cells, often in younger people.
Intestinal - better differentiated cells.
Mixed.
356
What are some risk factors for gastric cancer?
357
What is the clinical presentation of a gastric cancer patient, and what can this depend on?
Unexplained weight loss.
Epigastric abdominal pain.
Lymphadenopathy - Virchow’s (left supraclavicular) lymph node.
Dysphagia - if around the cardia (inflow obstruction).
Vomiting - if around the antrum (outflow obstruction).
358
What is the prognosis of local and metastatic gastric cancer?
Local - 70% 5-year survival.
Metastatic - 5% 5-year survival.
359
What are some gastric cancer investigations?
Bloods - FBC for anaemia.
Upper GI endoscopy and biopsy.
CT of the chest, abdomen and pelvis for staging of the cancer.
360
What is the management of gastric cancer dependent on, and what are some options?
Depends on co-morbidities and the stage.
Superficial there can be endoscopic mucosal resection.
Localised - surgery to remove all or part of the stomach (chemotherapy if not suitable).
Advanced/ metastatic - chemotherapy/ immunotherapy and supportive care (symptoms management).
361
What are the different types of pancreatic cancer?
Pancreatic ductal adenocarcinoma of the exocrine portion.
Pancreatic neuroendocrine (rare) from endocrine cells:
- Non-functional.
- Functional; secretes hormones.
362
What are some risk factors for pancreatic cancer?
Inherited mutations - BRCA1, BRCA2 and PALB2. Familial syndromes.
Smoking.
Chronic pancreatitis.
Men.
Increasing age.
363
What is the clinical presentation of a patient with pancreatic cancer?
Painless jaundice due to the head of the pancreas occluding the common bile duct.
Unexplained weight loss.
Abdominal or back pain.
New-onset of type 2 diabetes, > 50 years old.
Steatorrhoea (malabsorption, more common in tail or body).
364
What are some investigations for pancreatic cancer?
Bloods - LFT for jaundice. CA 19-9.
CT - can be used accurately to plan surgery.
Ultrasound - only accurate for the head.
Biopsy - endoscopic ultrasound with fine needle aspiration.
365
What is the management of pancreatic cancer?
Surgical resection with pancreatic enzyme replacement.
Biliary stenting for jaundice.
Chemotherapy/ radiotherapy.
Symptom management.
366
What surgery is performed on pancreatic cancer?
Whipple’s surgery.
367
What are the main causes of hepatocellular carcinoma?
Primary:
- Excess alcohol intake.
- Hepatitis B and C.
Secondary (more common):
- Haematogenous from the GI via portal system.
- Lymph (carcinomas).
- Transceolemic, usually ovarian in females.
368
What is the clinical presentation of hepatocellular carcinoma?
Usually follows on from cirrhosis so signs can be masked, present with ascites, fatigue, jaundice, etc.
Right upper quadrant pain.
Acute hepatic decompensation:
- Worsening of jaundice or ascites.
- Hepatic encephalopathy.
369
How does surgery or liver transplants aid prognosis of hepatocellular carcinoma?
5-year survival improves to 50%, when survival is usually 1 year.
370
What investigations are completed for hepatocellular carcinoma?
Blood tests - LFTs, PT/ INR to check clotting factors, viral hepatitis panel.
Ultrasound for cirrhotic patient screening.
CT/MRI of the abdomen.
Liver biopsy.
371
What is treatment of hepatocellular carcinoma?
Ablation - treatment using thermal energy (hot or cold).
Resection.
Transplantation.
Chemotherapy/ immunotherapy to slow the tumour growth.
372
What are the different classifications of cholangiocarcinomas?
Bile duct cancer:
- Intrahepatic adenocarcinoma.
- Exrahepatic adenocarcinoma.
373
What are some risk factors for cholangiocarcinoma?
Liver and bile duct diseases:
- Cirrhosis.
- Alcoholic liver disease.
- Bile duct diseases.
- Gallstones.
- Primary sclerosing cholangitis.
Infections.
High alcohol consumption.
Exposure to certain toxins or medications.
Males and increasing age.
374
What is the clinical presentation of cholangiocarcinoma?
Painless jaundice.
Pruritis.
Dark urine and light coloured stools.
375
What is the prognosis and treatment of cholangiocarcinoma?
5-year survival rate of 2% with metastatic disease.
Treatments - surgery and chemotherapy.
376
What is the histology of colorectal cancers, and how do they develop?
Adenocarcinomas.
Genetic and epigenetic mutations lead to activation of oncogenes (e.g. RAS) and inactivation of tumour suppression genes (tp53 and RB).
This leads to dysplasia of the glandular epithelium, adenoma formation and then invasive carcinoma formation.
377
What are some risk factors for colorectal cancer?
High fat diet, high red meat consumption, low dietary fibre and high alcohol intake.
Inflammatory bowel disease.
FAP.
HNPCC/ lynch syndrome.
378
What is the clinical presentation of a colorectal cancer patient?
Blood in the stool - haematochezia more common than malaena.
Change in bowel habit.
Iron deficiency anaemia
Unexplained weight loss.
Tenesmus - feeling of incomplete defaecation due to mass of tumour.
Mass on rectal examination.
Abdominal pain, ascites and jaundice can be seen due to hepatic/ peritoneal metastases.
379
What can a specific change in bowel habit be with colorectal cancer?
Constipation due to a tumour obstructing the lumen, followed by overflow diarrhoea, due to liquid building up behind the solid stool.
380
What are the differences between left and right sided colon cancer, and which is a apple-core sign seen most commonly in?
Most commonly seen in left-side as the cancer has stenoses the lumen, around the outside.
381
What are some investigations done for colorectal cancer?
Stool test - faecal-immunochemical test (occult bleeding).
Blood test - FBC for anaemia and CEA.
Colonoscopy and biopsy.
CT and MRI for staging.
382
What is the management for colorectal cancer, and what does it depend on?
Depends on the stage of the cancer.
Surgery with pre- or post-operative chemotherapy/ immunotherapy.
Only chemotherapy/ immunotherapy if not suitable for surgical intervention.
383
Who is the bowel cancer screening for?
Those aged between 60 and 74, every 2 years.
384
What type of cancer is anal cancer, usually?
Squamous cell carcinoma.
385
What are the risk factors for anal cancer?
HPV - strain 16.
Poorly managed HIV infection - increases the risk of HPV.
Receiving anal sexual intercourse.
Chronic local inflammation due to IBD or recurrent anal fissures.
386
What is the clinical presentation of anal cancer?
Perianal pruritus or pain.
Bleeding.
Discharge.
Tenesmus.
387
What is the prognosis for anal cancer?
More than 70% can be cured with chemoradiation.
Pap smears of the anal canal for HPV in high-risk populations.
388
What is FAP due to?
Autosomal dominant APC mutation.
389
Which different visualisation methods are used to view different internal parts of the GI tract?
Mouth to duodenum (D2 - after the major papilla) is through endoscopy.
Anal canal to ileum is through colonoscopy.
Between the duodenum and ileum is through capsule endoscopy, but can visualise the whole GI tract.
390
What is the difference in pain between inflammatory bowel disease and irritable bowel syndrome presentations?
IBS pain goes away after defaecation, whereas IBD pain does not.
IBD pain is continuously bad at night, whereas IBS tends not to be.
391
Why is blood often associated with diarrhoea?
Blood is a natural laxative so reduces the transition time through the GI tract, from the presentation of it.
392
What muscle curves the rectum anteriorly and the anus posteriorly?
Puborectalis.
393
What are some GI defences against toxins?
Sight, smell and memory to deter from certain foods.
Saliva - bacteriostatic secretions.
Gastric acid.
Small intestinal secretions - bile.
Colonic mucus.
Anaerobic environment - small bowel and colon.
Microbiota.
394
What is the microbiota difference between the proximal and distal GI tract?
The proximal gut is a relatively sterile environment.
As we travel more distal, there is an increase in number of bacteria.
395
What percentage of faecal mass is bacteria?
20%.
396
What are the benefits of the microbiome?
Harmful bacteria are outcompeted for nutrients.
Antimicrobial substances are produced.
Helps develop a newborns immune system - acquired during birth through the birth canal.
Produce certain vitamins - vitamin K.
Provide an energy source for colonocytes through breakdown of food molecules.
Helps to prevent obesity.
Decreases the risk of inflammatory bowel disease.
397
What can the bacteria in the colon produce from fibre, and what are the functions of each of them?
Short chain fatty acids - acetate, propionate and butyrate.
Acetate - involved in cholesterol metabolism.
Propionate - helps regulate satiety.
Butyrate - energy source for colonocytes, helping to regulate the gut environment.
398
What can the composition of the microbiome affect?
The response of the body to chemotherapy.
The insulin response to food, within the body.
399
Ingestion of which materials can affect the microbiota, and how?
High fibre diets increase the composition of gut microbiota.
Antibiotics (in meat) can disrupt the microbiota.
Proton pump inhibitors increase the risk of GI infections by increasing the pH.
Artificial sweeteners can disrupt the diversity of the microbiota.
Prebiotics - bacteria and yeasts that populate the microbiota directly.
Probiotics are accessible carbohydrates and fibre for the microbiota.
400
How can a gluten free diet affect the body?
Can lower the numbers of key species of the microbiota.
Can tighten tight junctions, preventing absorption of large molecules, preventing some inflammatory reactions from occurring.
401
What is a faecal microbiota transplant?
A fresh stool transplant that has been centrifuged, filtered and diluted. It is transplanted from the donor to the patient within 1 hour to help colonise the patients microbiota and improve the health of the gut, treating or preventing certain infections.
402
What routes of administration can be used for faecal microbiota transplants?
NG/ duodenal tubes, usually under anaesthetic.
Upper GI endoscopy.
Colonoscopy.
Transplant into the caecum and allowed to distribute through the colon.
403
What are the effects of a faecal microbiota transplant, on certain conditions?
Up to 90% resolution of diarrhoea following a clostridium difficile infection.
Up to 70% resolution of inflammatory bowel disease symptoms for Crohn’s disease, with a 50% clinical remission.
404
What is the criteria of the donor used for a faecal microbiota transplant?
10-25 year olds.
Donors not had antibiotics, laxatives or diet pills within the last 3 months.
Donor does not have any gastrointestinal disease.
They are screened for inflammatory markers, hepatitis and HIV.
405
What is the route of transmission, symptoms and treatment of salmonella gastroenteritis?
Ingested food and water containing salmonella bacteria, with symptoms developing 48 hours afterwards.
They can present with:
- Nausea.
- Vomiting.
- Diarrhoea (mostly non-bloody).
- Fever.
- Abdominal cramping.
Treatment tends to just be fluid resuscitation due to it be self-limiting.
406
What is the route of salmonella within the body?
How can this cause complications?
Enters enterocytes via endocytosis.
Around 5% of the time, they will then move into the submucosa, where they encounter macrophages.
The macrophages transfer the salmonella to the reticuloendothelial system.
The salmonella then multiplies within cells, causing lymphoid hyperplasia.
The salmonella can infect the liver and gallbladder, and then enter the bloodstream to cause systemic infections.
407
What type of bacteria is campylobacter?
Gram-negative spiral, microaerophilic bacteria.
408
What is the route of transmission, symptoms and treatment of campylobacter gastroenteritis?
Spread via faecal-oral route (poultry consumption), that needs to multiple within the host before symptoms, causing a 1-7 day incubation period.
Symptoms:
- Fever.
- Abdominal cramping.
- Diarrhoea that can be bloody.
Treatment is fluid and electrolyte replacement, due to the cytotoxin (similar to cholera) causing profuse diarrhoea.
Antibiotics if blood diarrhoea (macrolide - azithromycin/ flouroquinalone - ciprofloxacin).
409
Who does shigella usually infect, why?
Young children, under the age of 5.
Only a small dose is required to cause infection, so can spread quickly between families.
410
What is the route of transmission, symptoms and treatment of shigella gastroenteritis?
Spread from infected stools, and person to person.
They present with bloody diarrhoea with mucus, and abdominal cramping.
It is usually self-limiting, resolving within a week, so fluid replacement is necessary. If severe, then antibiotics (ciprofloxacin) can be given.
411
How does shigella cause its symptoms?
Invades the large intestine colonocytes, multiplies in cells and invades neighbouring cells.
It kills the invaded colonocytes and forms abscesses in the mucosa.
412
What is the route of transmission, symptoms and treatment of exnterotoxigenic E.Coli gastroenteritis?
It is a commensalism of the colon but large numbers can be spread via the faecal-oral route by contaminated water.
Watery diarrhoea.
Fluid resuscitation, and antibiotics (ciprofloxacin) if severe.
413
How does enterotoxigenic E.Coli cause its symptoms?
It colonises the enterocytes and produces enterotoxins.
These cause hypersecretion of chloride ions, which causes sodium ions and water to follow, leading to watery diarrhoea.
414
What potential complication can shigella or campylobacter cause?
Describe it.
Haemolytic uraemic syndrome.
It is a triad of:
- Anaemia.
- Thrombocytopeania.
- Acute kidney injury.
415
Describe the bacteria clostridium difficile.
It is a gram-positive, anaerobic, spore forming bacillus.
416
What is the route of transmission and symptoms of C.Diff gastroenteritis?
It is a minor component of the GI tract but can be transferred via faecal-oral route. It is most commonly caused by (broad-spectrum) antibiotics that precipitate proliferation.
It is usually asymptomatic but can cause varying degrees of diarrhoea and abdominal cramping.
417
How does C.Diff cause its symptoms?
Spore-forming which are difficult to get rid of so easily colonises.
Produces Toxins A&B:
- Toxin A = enterotoxin that results in excessive secretion and inflammation.
- Toxin B = cytotoxin that kills colonocytes.
418
How is C.Diff treated?
Removing the offending antibiotic.
Fluid resuscitation.
Metronidazole or vancomycin.
Probiotics to help re-populate the gut bacteria.
419
What are some potential complications of C.Difficile infections?
In less than 5% of cases, there can be:
- Toxic megacolon, which requires surgery.
- Pseudomembranous colitis.
420
What is pseudomembranous colitis?
An inflammatory condition where elevated yellow plaques form and join together, creating a pseudomembrane.
421
Who is rotavirus most commonly seen in, and how does it spread?
Children under the age of 5, because immunity lasts into adulthood.
It is spread via faecal-oral route and requires only a small dose.
422
What kind of virus is rotavirus, what are the symptoms, and how is this treated?
It is a double-stranded DNA virus.
It causes vomiting with fever, initially, and then diarrhoea, lasting up to one week.
It is treated by managing the dehydration.
423
How does rotavirus cause its symptoms?
Chloride secretions - cAMP increases, activating the CFTR, causing Cl- and then Na+, so water, movement into the lumen.
SGLT1 disruption - reduced reabsorption of sodium and glucose means the osmotically active substances pull water in the lumen.
Brush-border dysfunction - malabsorption leads to increased osmotically active substances in the lumen, pulling water in.
424
What type of virus is norovirus, who does it affect and why?
It is an RNA virus.
It affects people of any age due to the large number of strains, immunity cannot be developed.
425
What are the virulence factors of norovirus?
It requires only a small dose so is highly contagious.
It is resistant to cleansing.
It infects the small intestine, damaging the microvilli and brush border enzymes.
Incubation is 1-2 days and symptoms last 1-3 days.
426
What are the symptoms and treatment of norovirus?
Nausea, watery diarrhoea, fever and vomiting - due to increased pressure from delayed gastric emptying.
Treated with oral rehydration therapy.
427
What are the movement capacities of:
- Cryptosporidium.
- Giardia lamblia.
- Entamoeba.
Cryptosporidium - sporozoan that is non-motile.
Giardia lamblia - flagellate so is highly motile.
Entamoeba - amoeba which move via cytoplasmic projections.
428
What is the route of transmission, symptoms and treatment of cryptosporidium?
Transmitted via faecal-oral route, but can survive and spread via bodies of water.
Watery diarrhoea.
Supportive fluids.
Anti-parasitic treatment in immunocompromised groups.
429
How does cryptosporidium cause its symptoms?
The oocyst - cyst containing the parasite - reproduces within the epithelial cells of the distal small intestine, causing damage to the brush border enzymes.
They also cause chloride ion secretions.
430
Who is giardia seen most in?
Children.
431
What is the route of transmission, symptoms and treatment of giardia?
Faecal-oral route with water supply often affected.
Diarrhoea, after a 10-14 day incubation period, and abdominal cramping for up to 6 weeks, so is PERSISTENT.
It can cause a lactase deficiency - lactose intolerance.
Fluid rehydration therapy and antibiotics.
432
What is the life-cycle of Giardia?
Cyst is ingested and travels to the stomach.
The stomach acid (or pancreatic enzymes) releases the parasite which multiplies in the small intestine after incubating for 1-2 weeks.
It damages the proximal small intestine, causing villus atrophy.
The parasite then renters the cyst within the colon for infection of others.
433
What is the route of transmission, symptoms and treatment of entamoeba histolytica?
Faecal-oral route, from contaminated food or water.
Most people of asymptomatic (80%), but can cause:
- Diarrhoea that is bloody.
- Liver abscesses.
- Severe colitis or toxic megacolon can occur.
Anti-protozoals or metronidazole.
Surgery for severe colitis or toxic megacolon.
434
Who does entamoeba histolytica often affect?
People who have travelled to tropical places, or live in places with poor sanitary conditions.
Men who have sex with men.
435
How does entamoeba histolytica cause symptoms?
Ingestion of cysts is followed by excystation within the colon.
The trophozoites invade the colonic mucosa.
The infection can then spread to the liver.
They then re-enter the cysts to pass out and infect others.
436
What is the most common cause of travellers diarrhoea?
Enterotoxigenic Escherichia Coli.
437
What increases the risk of getting travellers diarrhoea?
Visiting S.E Asia, Central America, West and North Africa.
Dietary exposure.
Younger than 6 years old.
PPIs.
Blood group O.
438
What is peritonitis?
What are the two classifications?
Peritonitis is the inflammation of the serosal membrane that lines the abdominal cavity.
Primary - spontaneous, that is not a result of pathology arising in another organ.
Secondary - breakdown of peritoneal membranes due to inflammation or infection of another organ, leafing to foreign substances entering the cavity.
439
What is the most common cause of primary peritonitis, and what is it?
State who it is most commonly seen in.
Spontaneous bacterial peritonitis - infection of the ascitic fluid that is not due to any intra-abdominal, ongoing inflammatory or surgically correctable condition.
It is most commonly seen in end-stage liver disease with cirrhosis, patients.
440
What is the clinical presentation and diagnostic investigations for spontaneous bacterial peritonitis?
Abdominal pain, fever and vomiting.
Aspiration of the ascitic fluid (ascitic tap) - a neutrophil count would show > 250 cells/mm^3.
441
What are the two types of secondary peritonitis, and what are some examples of each?
Bacterial - a leak of the microbiota into the peritoneal cavity:
- Perforated peptic ulcer disease.
- Perforated appendicitis.
- Perforated diverticulitis.
- Post surgery.
Non-bacterial:
- Tubal pregnancy that bleeds (blood is highly irritant to the peritoneal cavity).
- Ovarian cyst.
NOTE: the peritoneal cavity is not enclosed in females.
442
What is the clinical presentation and treatment for secondary peritonitis?
Clinical presentation:
- Abdominal pain that can have a gradual or acute onset.
- Diffuse abdominal pain (perforated viscera, usually).
- Patients lie very still as movements make the pain worse.
Treatment:
- Surgery to control the infective source.
- Antibiotics to eliminate bacteria and toxins.
- Maintain organ system function via intensive care.
443
What is the examination of a secondary peritonitis patient like, and why?
Guarding - involuntary contraction of the abdominal wall muscles.
Rebound tenderness.
444
What is a bowel obstruction, and what are the common causes in children and adults?
A mechanical or functional problem that inhibits the normal movement of gut contents.
Children:
- Intussusception.
- Intestinal atresia.
Adults:
- Adhesions.
- Incarcerated hernias.
445
What is intestinal atresia, and what is the common clinical presentation?
A congenital condition, where the lumen of the intestine fails to recanalise - usually the duodenum, and is associated with other congenital defects.
Infants vomit after feeding, and needs to be treated rapidly.
446
What can bowel intussusception lead to, and why?
Infarction of the bowel as when the lymphatic and venous drainage is impaired, oedema can form.
This increases the pressure, worsening the compression, impeding the arterial supply.
447
What are the causes of intussusception, and how far can it extend?
Motility issues.
A mass that precipitates the telescoping action - a lead point. For example, Meckle’s diverticulum.
It can prolapse out of the rectum!
448
What are the causes of small bowel obstruction?
Intra-abdominal adhesions - fibrous bands between organs or tissues, seen after surgeries (often greater omentum).
Hernias - incarcerated groin hernias, most common.
Inflammatory bowel disease - repeated episodes of inflammation in Crohn’s causes narrowing.
449
What is the clinical presentation of small bowel obstruction?
Nausea.
Bilious vomiting if distal to D2.
Colicky pain - comes in waves, coinciding with peristalsis.
Abdominal distension.
Absolute constipation.
450
How is a small bowel obstruction diagnosed?
History.
Physical examination - abdominal distension, initially increased higher-pitched tinkling sounds, then absent bowel sounds. There may be a presence of a hernia.
CT of the abdomen and pelvis.
451
What are the common causes of large bowel obstruction, and who does it occur in more often?
Colon cancer - 60%.
Diverticular disease - 20%.
Volvulus (sigmoid and caecal) - 5%.
It occurs more frequently in elderly patients.
452
What is the relevance of the ileo-caecal valve in large bowel obstructions?
If the valve is competent then the pressure within the colon cannot decompress proximally, and so is a closed loop obstruction.
This increases the risk of ischaemia, infarction and perforation.
453
What is a volvulus, the most common types and causes?
A volvulus is where part of the colon twists around its mesentery, seen most commonly in the sigmoid colon (and then caecum).
It can be caused by constipation - overloading the sigmoid colon, and high fibre diets due to the increased bulk of the stool.
NOTE: caecal volvulus results in BOTH small and large bowel obstruction.
454
What is the difference on X-rays of small and large bowel obstructions?
455
What are the two types of acute mesenteric ischaemia?
Describe them and state some causes for each.
Arterial compromise:
- Arterial occlusion; arterial embolism of the SMA/ vasculitis.
- Non-occlusive mesenteric ischaemia (less common); low cardiac output.
Venous compromise:
- Mesenteric venous thrombosis; systemic coagulopathy and malignancy.
456
What is the clinical presentation of a patient with acute mesenteric ischaemia?
Abdominal pain disproportionate to the clinical findings.
Pain coming on 30 minutes after eating due to increased blood demand for the gut after eating.
Pain lasts around 4 hours.
Pain often left sided due to splenic flexure being the vascular watershed area (then recto-sigmoid junction).
Nausea and vomiting.
457
What is the treatment of acute mesenteric ischaemia?
Surgery - resection of ischaemic bowel.
Bypass graft to reintroduce blood supply.
Thrombolysis.
Angioplasty - stenting the blocked vessel.
458
What are peptic ulcers, where are they most common, and what are the potential complications at each of these sites, respectively?
Disruption of the muscularis mucosae and submucosa, usually greater than 5mm in diameter.
Duodenal - first part, and can erode through the posterior wall to the gastro-duodenal artery.
Gastric - lesser curve and antrum most commonly. The body can lead to erosion through the posterior wall and splenic artery.
459
What are the causes of portal hypertension, and what pressure is required to cause problems?
Pre-hepatic - portal vein thrombosis.
Hepatic - cirrhosis, compressing the sinusoids.
Post-hepatic - Hepatic vein thrombosis, right-sided heart failure.
It is normally at a pressure of 5-10mmHg, and so anything above 10mmHg can cause problems.
460
What is the venous drainage of the oesophageal veins, and which veins can rupture due to an increase in pressure?
Portal drainage - oesophageal veins drain into the left gastric vein and then portal vein.
Systemic - oesophageal veins drain into azygous vein, and then into the superior vena cava.
Between these veins there are superficial mucosal veins, forming the anastomoses.
461
What are the treatment options for oesophageal varices?
Endoscopy and band ligation.
Blood transfusion.
Transjugular intrahepatic portosystemic shunt (TIPS).
Terlipressin - reduces portal venous pressure.
462
What is TIPS?
An expandable metal band bridging the portal vein to a hepatic vein to decompress the portal vein pressure, reducing the variceal pressure and reducing the ascites.
463
What are AAAs due to?
Degeneration of the tunica media layer of the abdominal aorta wall.
Degradation of the elastin and collagen, leading to the dilation of the lumen.
464
What are the symptoms of a non-ruptured AAA?
Asymptomatic, itself.
Compression of nearby structures can cause:
- Stomach = nausea.
- Bladder = increased urinary frequency.
- Vertebra = back pain.
465
What are the symptoms of a ruptured AAA?
Abdominal, shearing pain that radiates to the back.
Syncope due to the transient hypotension.
466
How are AAAs diagnosed and investigated?
467
How are AAAs treated?
Supportive:
- Smoking cessation and hypertension control.
- Regular ultrasounds, ensuring it is under 5.5cm. If not, refer to vascular surgeons.
Surgical:
- Endovascular repair = relining the aorta with a metallic stent, through the femoral artery.
- Open surgical repair = clamping the aorta, opening the aneurysm and removing the thrombus, and then suturing in a synthetic graft to replace the diseased segment.
468
What is the predominant cell lining the lumen of the stomach?
Surface mucous cell (foveolar cells).
469
How are adhesions treated?
NG tube can be used to provide nutrition to the patient.
Contrast is given to acts as a laxative to help remove some of the adhesions.
Surgery can be done to remove severely adhered sections.
470
What is an erect chest X-ray used for?
To check for penumoperitoneum - whether there is free gas within the abdomen.
471
What can be the causes of a pneumoperitoenum?
Laparoscopic surgery due to insufflated carbon dioxide - a normal finding.
Visceral perforation:
- Peptic ulcer.
- Diverticular disease.
- Tumour.
- Obstruction.
- Trauma.
- Iatrogenic.
472
What are the different contrast studies used to image the GI tract?
What are they each used to image?
Barium swallow - upper GI tract.
Barium enema - distal GI tract.
Barium meal/ follow through - small intestine.
Water soluble contrast studies.
473
What can be seen on a large bowel obstruction X-ray?
Colonic distension - gas accumulation due to organisms producing gas.
Haustra.
Small bowel dilatation depending on:
- Duration of obstruction.
- Incompetence of the ileocaecal valve.
474
What is the complication of a sigmoid volvulus?
The twisting of the bowel can cut off the blood supply so can lead to necrosis and perforation.
475
What is seen in toxic megacolon?
Very dilated colon >6cm, with extensive mucosal islands.
Oedema.
Pseudopolyps.
476
What is a barium swallow used for?
Testing to see obstructions in the pharynx, oesophagus and proximal stomach.
Can show if the swallowing mechanism is defective, as uses videofluoroscopy.
Evaluation of haematemesis and peptic ulcer disease.
477
What is a barium enema used for - how?
Tube is inserted into the rectum and a barium solution is given.
This tests for strictures within the bowel.
If mucosal problems are suspected then adding another contrast medium - air or CO2 - is done.
478
What features are seen at the levels of T12 on a CT scan?
Aortic hiatus of the diaphragm.
Coeliac trunk.
479
Label this diagram of a CT scan at T12.
480
What features are seen at L1 on a CT scan?
Transpyloric plane:
- Fundus of the gallbladder.
- Pylorus of the stomach.
- Neck of the pancreas.
- Superior mesenteric artery origin.
- Hilum of the kidneys; left above and right below.
481
Label the following CT scan of L1.
482
What features can be seen at the level of L3 on a CT?
Inferior mesenteric artery.
Umbilicus.
483
Label the following CT scan a L3.
484
What characteristic things can be seen on a CT at L4?
Iliac crests.
Bifurcation of the abdominal aorta into the common iliacs.
485
Complete the CT scan of L3.
486
Identify the structures of the CT angiography.
487
Why would someone request an abdominal X-ray?
Position of iatrogenic items, e.g. NG tube.
Confirm ureteric stones identified on CT, or see if passed.
Foreign body identification.
Acute exacerbation of inflammatory bowel disease, such as toxic megacolon and perforation.
488
What is riglers sign?
Where the bowel wall is clearly defined due to gas on both sides - penumoperitoneum.
489
What sign is seen in a caecal volvulus?
Reverse C-shaped caecum.
490
What sign is seen for bowel wall oedema and what condition is this most commonly seen in, in younger patients?
Thumb-printing sign.
Ulcerative colitis where the bowel wall is oedematous and thickened.
RED.
491
What is achalasia and how is it seen on a barium swallow?
Impaired relaxation of the lower oesophageal sphincter.
A bird-beak/ rat-tail stricture is seen.
492
What is seen in this barium swallow?
Oesophageal malignancy:
- Strictures.
- Rough appearance of the mucosa.
493
What is an ERCP and how is it performed?
Endoscopic retrograde cholangio pancreatography.
A tube cannulates the ampulla of vater and injected with contrast to see the stones in the bile ducts.
A knick is then made at the ampulla to allow them to drain into the duodenum.
A tube, inserted into the duodenum, then removes the stones.
This is done under fluoroscopy.
494
What are the phases of contrast?
Later arterial/ corticomedullary - 30-40s.
Portal venous (equal distribution) - 70-90s.
Nephrogenic - 85-120s.
Excretory - 300-600s.
495
What is the function of CT scanning for colon and rectal cancer?
Colon - measure the size, look for invasion and metastases.
Rectal - detailed anatomy to guide chemoradiotherapy and surgery. MRI is used for staging.
496
What happens to the exterior of the portion of the bowel that is affected by Crohn’s disease?
Fat wrapping occurs, to keep the diseased section away from other viscera.
497
What is the round ligament?
A remnant of the umbilical vein, that shunted blood to the developing liver.
498
How can omphalocele and gastroschisis be diagnosed before birth?
Ultrasound.
Lab test - increased maternal serum alpha fetoprotein levels.
499
Where does gastroschisis herniate?
Why does this occur?
Through the rectus abdominis, to the right of the umbilicus.
Incomplete lateral folding due to reduced blood supply to the abdominal wall, meaning that it fails to close.
500
What does a raised GGT but normal ALP suggest?
Alcoholic liver disease.
501
Which structure of the GI tract has a dual innervation from the foregut and midgut?
The pancreas.
502
What does the paraxial mesoderm become?
Skeletal muscle.
Vertebra.
Cartilage.
Tendons.
503
What does the intermediate mesoderm become?
Kidneys and gonads.
504
What are the two divisions of the lateral plate mesoderm and what do they become?
Splanchnic - viscera.
Somatic - body walls.
505
What week can gastroschisis be detected on an ultrasound?
Week 18-20.
506
What are the tests done for testing liver function and those that test for damage?
507
What causes pigmentation of the urine and faeces?
Urine - conjugated bilirubin.
Faeces - stercobilin.
508
What breakdown of urobilinogen is excreted in the urine?
Urobilin.
509
What is released from the breakdown of red blood cells?
LDH.
Haemoglobin - which is broken down into the haem and globin constituents.
510
What sign is seen in the eyes for those with Wilson’s disease?
Kayser-Fleischer ring.
511
What are the risk factors for gallstones?
The 5 Fs:
- Fat.
- Fertile.
- Female.
- Forty.
- Family history.
512
What is Courvoisier’s gallbladder?
Enlarged, palpable gallbladder.
Painless jaundice.
It is associated with carcinoma of the pancreatic head.
513
What is the pathophysiology of biliary colic?
After eating, CCK is released by the small intestine.
CCK causes the contraction of the gallbladder.
This causes the stone to push against the entrance to the gallbladder, causing inflammation of the neck.
When pushed against, it causes pain which goes away after a period of time, which gives it an intermittent characteristic.
514
What is Murphy’s sign and what is it associated with?
Palpation of the right upper quadrant, when the patient is breathing in causes arrest of inspiration.
It is associated with cholecystitis.
515
What is Reynaud’s pentad?
State what condition it is associated with.
Signs and symptoms associated with ascending cholangitis:
- Fever.
- Hypotension.
- Jaundice.
- Right upper quadrant pain.
- Altered mental state.
516
Why can ethanol and mumps cause acute pancreatitis?
Ethanol - increases the risk of mucous plug formation in the main pancreatic duct.
Mumps - swelling of the glands causes blockages within the main pancreatic duct.
517
What are the investigations and management for cholecystitis and ascending cholangitis?
Investigations:
- Abdominal ultrasound.
- MRCP (MRI of the biliary tree).
Management:
- IV fluids.
- IV antibiotics.
- ERCP (removal of the stone).
- Laparoscopic cholecystectomy.
518
What are the investigations for acute pancreatitis?
Serum amylase (cheaper) or lipase (more specific).
Ultrasound of the abdomen.
CT abdomen and pelvis with contrast.
519
What is the difference of compensated and decompensated liver cirrhosis?
Compensated - function of the liver is preserved.
Decompensated - liver function is compromised.
520
What are some preventable and non-preventable causes of liver cirrhosis?
521
What are some signs and symptoms of liver cirrhosis?
522
What is the management of decompensated liver cirrhosis with the following complications:
- Ascites.
- Bleeding/ varices.
- Hepatic encephalopathy.
- Increased risk of hepatocellular carcinoma.
523
What is seen in gangrenous appendicitis?
Transmural inflammation and necrosis.
524
Where should rebound tenderness for appendicitis be performed and what is Rovsing’s sign?
RT - performed over McBurney’s point; 2/3rds the distance from the umbilicus to ASIS.
RS - left iliac fossa palpation, leads to pain in the right iliac fossa with appendicitis.
525
What does the small and large bowel contain?
Small bowel - air or fluid.
Large bowel - air or faeces.
