learning outcomes Flashcards
(368 cards)
1
Q
what is the function and anatomy of the oesophagus
A
the oesophagus is a muscular tube with 3 constrictions; cervical 15cm, thoracic 28cm, and diaphragmatic 40cm.
2
Q
what is the function of the stomach and anatomy
A
the stomach consists of the cardia, fundus (normally filled with air), the body, pyloric canal and pyloric antrum with a lesser and greater curvature and the inside is filled with gastric rugae
3
Q
what is the function of the liver and anatomy
A
the liver has a right and left lobe, with the vena cava behind it. With the portal triad going hepatic artery, portal vein and bile duct.
4
Q
what is the function and anatomy of the gall bladder?
A
gall bladder takes and stores bile. Bile travels from right and left hepatic ducts to the common hepatic duct where it joins the cystic duct from the gall bladder fusing to the duodenum.
5
Q
what is the function and purpose of the pancreas?
A
the pancreas is an accessory digestive gland lying along the transpyloric plane with the portal vein forming behind its neck.
6
Q
what is the anatomy and function of the spleen
A
the spleen is found in the left hypochondrium and coated in the peritoneum, related to the 9-11th rib and is a mobile haemo-lymphoid organ.
7
Q
what is the function and anatomy of the duodeonum
A
the duodenum is the shortest and most fixed part of the intestine, receiving bile and the pancreatic duct
8
Q
what is the anatomy of the jejunum
A
jejunum is thick heavy, with a deep red tinge with long vasa recta part of the small intestine.
9
Q
what is the anatomy of the ileum
A
the ileum is a pale, thinner and lighter part of the small intestine and has short looping arcades.
10
Q
what is the anatomy of the large intestine
A
large intestine has omental appendices, sacculations and taeniae coli (thick bands of smooth muscle)
11
Q
what is the anatomy of the appendix
A
the appendix is a variable intestinal diverticulum with masses of lymphatic tissue
rectum is the pelvic part of the gut
12
Q
Describe the common features of alimentary canal wall structure
A
Peritonised organs which are within the peritoneal cavity
retroperitoneal organs which are behind the peritoneum
lesser and greater omental sacs
visceral and parietal peritoneal layers
mesentery which are folding loops
13
Q
describe the mesentery
A
The mesentery is a fold of membrane attachment. Arterial branches travel through the double folds to access peritoneal organs (within the peritoneal cavity)
14
Q
what is the foregut blood supply
A
the foregut is supplied by the celiac trunk and it’s three branches which are the left gastric artery, the hepatic artery and splenic artery
15
Q
what Is the midgut blood supply
A
the midgut is supplied by the superior mesenteric artery through the jejunal and ileal branches.
16
Q
what is the hindgut blood supply
A
the hindgut is supplied by the inferior mesenteric artery with its branches the left colic, sigmoid and superior rectal artery.
17
Q
what is the blood drainage of the gut
A
venous drainage occurs through the portal vein which is formed by the splenic and superior mesenteric veins.
18
Q
describe the lymphatic drainage of the gut and the clinical significance of this
A
lumbar nodes have three groups pre-aortic, lateral aortic, and retro aortic. Specifically, the foregut structures are drained by the celiac group, the midgut is drained by the superior mesenteric group, and the hindgut by the inferior mesenteric group. These are all drained by the thoracic duct. It’s essential to know this for monitoring the spread of disease.
19
Q
stomach formation embryology
A
the oesophagus forms from the cranial part of the primitive gut tube with the laryngo tracheal diverticulum forming the trachea.
In the 4rth week stomach dilation, 90 degree rotation and anterio-posterior rotation occurs in a clockwise formation.
The stomach attachments through the ventral and dorsal mesogastrium rotate, causing the dorsal mesentery to the left creating the lesser sac.
The duodenum also rotates, being dragged by the stomach.
20
Q
bile duct and gallbladder embryology formation
A
Liver bud appears the middle of the third week, the connection from the duodenum forms the bile duct.
ventral outgrowth from the bile duct forms the gall bladder and cystic duct.
21
Q
spleen embryology formation
A
mesenchymal condensation by the end of the 4rth week forms the spleen, initially haemopoietic by week 23 functioning lymphatically.
22
Q
pancreas embryology formation
A
pancreas develops as two buds from the duodenum, as the duodenum rotates the two buds fuse
23
Q
midgut embryology formation
A
there is rapid elongation of the primary intestinal loop with the cephalic part forming the distal duodenum, jejunum and proximal ileum. Then the caudal part forming the distal ileum, caecum, appendix, ascending colon and proximal 2/3rds of transverse colon. Before this happens, it must undergo rotation 90 degrees anti-clockwise, around the axis of the superior mesenteric artery and the cranial part of the midgut is carried to the right. As this occurs the gut tube herniates to allow for growth.
By week 10 the cavity becomes more spacious as retraction occurs starting with jejunum first and caecum last with a further 180 degree anticlockwise rotation.
24
Q
hindgut formation embryology
A
terminal portion of hindgut joins with posterior part of cloaca, the allantois enters the anterior part of the cloaca. The cloaca then acts as a boundary between the endoderm and ectoderm layers. By the end of week 7 the membrane ruptures with ectoderm proliferation sealing the caudal end.
25
foregut abnormalities from formation
oesophageal atresia
trachea-oesophageal fistula
annular pancreas – ventral bud migration failure leading to duodenal stenosis or accessory pancreatic tissue
26
midgut abnormalities from formation
abnormal rotation of primary intestinal loop or reversed rotation of primary intestinal loop.
omphalocele (herniation of abdominal viscera or retraction failure, coated in amnion)
Gastrochisis – herniation without amniotic cavity.
remnants of vitelline duct forming Meckel’s diverticulum through cyst, ligament or fistula.
27
hindgut abnormalities from formation
incomplete separation of the hindgut from the urogenital sinus by the urorectal septum
hindgut fistula, atresia or imperforate anus.
28
control of saliva secretions and glands
there are six salivary glands, with two of each one. There is the parotid salivary gland, the sublingual, and the submandibular. This is controlled by the facial parasympathetic nerve 7 and the glossopharyngeal 9 nerve.
29
Effects of parasympathetic and sympathetic nervous system on secretion and motility
there is the vagus nerve which stimulates secretion and motility
there is the sympathetic nerve known as the splanchnic which inhibits secretion and motility except for salivation.
30
arterial supply of the Gi tract
there is the celiac trunk supplying the stomach, small intestine, pancreas and liver.
there is the superior mesenteric artery supplying the small intestine, caecum, ascending colon and transverse colon.
there is the inferior mesenteric artery supplying the descending colon, sigmoid colon and rectum
31
venous drainage of the GI tract
the stomach feeds into the gastric vein as the pancreas feeds into the splenic. The small intestine, caecum, ascending colon, and transverse colon all feed into the superior mesenteric vein. The descending colon, sigmoid colon and rectum all feed into the inferior mesenteric vein. The SMV, IMV and the gastric, splenic veins feed into the hepatic portal vein, pass through the liver to the hepatic vein which then feeds into the inferior vena cava.
32
explain the concept of the portal venous system and its anastomosis
low oxygenated blood travels from the gut rich in nutrients to the hepatic portal vein which feeds into the liver, mixing with the oxygen rich blood of the hepatic artery, this then feeds back through the hepatic vein into the inferior vena cava to the heart.
33
basic function of mouth
chewing, salvia added as diluting and lubricant
34
basic function of oesophagus
passageway
35
basic function of stomach
digestion of protein. storage and sterilisation
36
basic function of pancreas
digestive enzymes and production of endocrine hormones
37
basic function of liver
bile salts for fat digestion/absorption
38
gallbladder basic function
storage for bile
39
small intestine basic function
digestion and absorption
40
large intestine basic function
water absorption and fermentation
41
epithelial linings of the GI
in the mouth, oesophagus and anal canal stratified squamous, in the stomach and intestines simple. Synthesis for enzymes, mucus and hormones, designed for absorption and function.
42
lamina propria is a
connective tissue containing vessels
43
the muscularis mucosae is a
thin smooth muscle layer
44
sub mucosa is a
thick irregular connective tissue containing vessels, glands in the oesophagus, duodenum and the neurones.
45
the muscularis externa is
inner circular or outer longitudinal for motility, peristalsis and segmentation.
46
serosa/adventitia is a
outer peritoneal – adventitia attaches oesophagus and rectum to surroundings
inner peritoneal – surrounds organs
47
describe the organisation of the enteric system
food/water enters the oesophagus, passing to the stomach for digestion. Then passes to the small intestine for further digestion, secretion of enzymes and fluid then nutrients are absorbed especially during the initial segments. As it then passes to the colon it begins to aggregate as the matter bacterially fermenters and water is reabsorbed and then is removed as faecal matter. Nutrients absorbed is passed through the liver through the hepatic portal vein to the heart and pumped systemically around the body.
48
describe the digestive processes for conversion of complex carbs to monosaccharides
starch and glycogen consist of alpha 1,4 glyosidic bonds which can be broken down by the enzyme alpha amylase. Cellulose the linear chains of glucose bound by beta1,4 glyosidic bonds cannot be broken down in vertebrates. Disaccharides can then be broken down by lactase, sucrase or maltase.
49
describe the mechanisms where monosaccharides are absorbed across the intestinal epithelial cells
glucose or galactose can enter through a SGLT symporter alongside sodium. Glucose is then pumped out by GLUT 2, whereas the sodium is then used in the ATPase on the basal membrane. The tight junction holding cells together is then permeable to water allowing water to pass.
fructose can then pass through the GLUT 5 and then the GLUT 2 into the blood.
50
describe the digestive processes for converting proteins into small peptides and AA
enzymes such as proteases or peptidases hydrolyse peptide bonds reducing the proteins. They are endopeptidases if they cut the chain from the centre, or exopeptidases if they cut from the end (either amino or carboxy).
describe the process for absorption for aa and small peptides
51
describe the process for digesting AA
sodium and an AA pass through the symporter into the cell, the AA is then separately pumped out into the blood whereas the sodium is utilised in a ATPase.
52
describe the process for digesting small peptides
di and tripeptides may pass through PepT1 (proton coupled transporter) alongside hydrogen ions gathered from the acid microclimate generated around the microvilli. The spare hydrogen ions are then exchanged for sodium ions (NHE3) and the sodium ions are utilised again in an ATPase whereas in a separate pump (still debate as to how) the dipeptides and tripeptides are pumped out accounting for 70% of proteins in our diet.
53
Describe the extracellular digestive processes for conversion of fats to triacylglycerols and monoglycerides to the cell
fats are taken as triacylglycerol droplets. Through mechanical movement generated by the muscularis externa in the stomach and the introduction of bile salts and phospholipids emulsification happens. Triacylglycerol droplets become smaller, forming micelles. As the gut is motile, micelles meet the acid microclimate allowing for the absorption of fatty acids and monoglycerol.
54
describe the intracellular process for fats into the lymphatic system
once inside the cell, the monoglycerol and free fatty acids are converted back into triacylglycerol in the smooth ER and bound to amphipathic proteins. It is then transported to the Golgi body to be enveloped in a membrane and undergo exocytosis to form a chylomicron which contains phospholipids, cholesterol and vitamins. This is then passed along into the lacteal components of the cell.
55
Explain the requirement for emulsification of ingested fats.
triacylglycerol is a lipid which is insoluble in water, the enzyme lipase is water soluble and thus only able to work at the edge of the large droplets.
emulsification breaks down the large droplets into smaller droplets increasing their surface area to enable for faster digestion.
56
Describe the role of bile salts in the production of emulsification droplets and micelles
bile salts and phospholipids act as amphipathic molecules, as in they have both polar and non-polar portions. This coats the droplets with the non-polar interior but repels other droplets with its polar exterior.
57
describe the absorption of fat soluble vitamins
fat soluble vitamins A,D,E,K follow the same route as fat, dissolving into micelles and into the chylomicrons for transport around the body.
58
describe the route of water soluble vitamins
water soluble vitamins such as B, folic Acid and C often have their own forms of carrier mediated transport via NA or passive diffusion. The exception to this is vitamin B12 a large and charged molecule that requires an intrinsic factor provided by the stomach that allows for it to be specifically transporter in the distal ileum to be stored in the liver.
59
intrinsic factor is for what vitamin
B12
60
Describe the absorption of the important dietary iron
Iron enters through the Divalent metal transporter 1(fe2+) through the brush border enzymes. Once inside they can bind to ferritin to from an intracellular iron store where they will remain. However, it may pass through the basolateral membrane, binding to transferrin to later bind to heme. This is the only mineral the gut will control the concentration of through the use of proteins, with increased iron comes more ferritin to permanently store
61
describe the general anatomy of the oesophagus and assign general physiological functions
the oesophagus is a 25cm long conduit, with its upper third containing skeletal muscle and the lower 2/3’rds containing smooth muscle. Physiologically the mouth and oesophagus makes use of saliva, which acts as a lubricant due to the mucins, the water helps by acting as a solvent and diluting the solution, alpha amylase breaks down polysaccharides, electrolytes maintain tonicity and pH whilst lysozymes kill any bacteria. Saliva is produced by the parotid glands, submandibular glands and sublingual glands.
62
describe the anatomy of the stomach and assign genera l physiological functions
the Stomach has a fundus, body, serosa, cardiac region, longitudinal muscle, circular and oblique layer, pyloric sphincter, rugae and antrum. This allows it to store food, initiating the digestive process whilst controlling outflow. Whilst this is occurring it sterilises food and produces the intrinsic factor for vitamin B12.
63
describe the features of the stomach and oesophageal canal wall structure
oesophagus contains 4 layers, the mucosa, submucosa, muscularis externa and adventitia. It is lined by a stratified squamous non keratinising epithelium with sphincters regulating movement.
he stomach too also has a luminal surface with mucus cells, gastric pits, glands containing parietal and chief cells. It has a folded submucosa and mucosa (rugae), a muscularis externae with three layers (longitudinal outer, circular middle and oblique inner) and a serosa which acts as a outer connective tissue layer.
64
describe the reflex control mechanism for swallowing
for saliva which is required in swallowing, cranial nerves facial (7) and glossopharyngeal (9) stimulate large volumes of watery saliva whereas sympathetic stimulate small viscous salvia due to alpha 1 adrenoreceptors on mucus content and beta 2 adrenoreceptors on amylase. There is also a reflex caused by pressure/chemoreceptors in the mouth.
voluntarily the tongue pushes food backwards, followed by a reflex of pharyngeal muscle contraction as well as the soft palate reflecting backwards to seal of the nasopharynx. The upper oesophageal sphincter relaxes and epiglottis seals. Once it has entered the oesophageal sphincter contracts.
peristaltic waves carry food to the stomach within 10 seconds, the lower sphincter relaxes, and food enters the stomach. Finally, the stomach through a vagal reflex stimulates relaxation, increasing volume from 50ml to 1500ml.
65
Describe the structure and various functions of the stomach.
Describe the structure and various functions of the stomach.
fundus – storage
body – storage, mucus, HCL, pepsinogen, intrinsic factor
antrum – mixing and gastrin.
pyloric sphincter - controls the flow of chyme into the duodenum
66
describe the basic activation of digestion in the stomach and the various forms of basic control
the initial stage of activation comes from the interaction with food, this stimulates the parasympathetic vagus nerve to secrete the neural transmitter Ach to bind to cholinergic muscarinic receptors which stimulates parietal cells to release acid. The same goes for G cells which are stimulated by the vagus to produce gastrin which travels through the systemic circulation, both Ach and gastrin stimulate a paracrine response through ECL cells producing histamine.
This process is repeated when peptides arrive in the lumen of the small intestine stimulating G cells, and the distension of the stomach as food arrives in a vagal/enteric reflex through Ach.
67
what does gastrin, histamine and Ach do In terms of the stomach and digestive process
what gastrin and acetylcholine do is bind to receptors that stimulate a calcium cascade activating kinases to enable the potassium hydrogen active pump which secretes hydrogen ions. Histamine works though G proteins activating Adenylyl cyclase to convert ATP into cAMP which then actives the active transporter.
68
what forms of inhibition are there for the stomach and the digestive process
finally stopping eating reduces vagal activity and would gradually inhibit the process. Gastrin demonstrates negative feedback and as pH would drop so does the gastrin concentration. Acid in the duodenum initiates the enterogastric reflex which reduces gastrin secretion and stimulation, the hormone secretin further aids this. The presence of fat in the duodenum also stimulates a GIP release which reduces gastrin secretion and HCL secretion.
69
how is pepsin in the stomach formed?
the low pH produced by the acid enables pepsinogen the zymogen to form pepsin which then becomes a self-propagating reaction.
70
role intrinsic factor for B12 absorption
it is produced by parietal cells to allow for the complex to be absorbed from the ileum
71
role of gastric mucous in the stomach?
has a cytoprotective role, protecting the surface from mechanical or chemical injury from the acid by being rich in carbonate ions forming a microclimate.
72
Describe basic physiology of gastric acid secretion
carbon dioxide diffuses into the cell and through the catalyst carbonic anhydrase forms the unstable carbonic acid, it quickly dissociates providing the ATPase K+/H pump a hydrogen ion in a 1:1 ratio. Carbonate is then exchanged with chloride ions which pass through the cell to leave through the apical membrane. The net movement of ions out of the apical membrane draws water through the tight junctions to form hydrochloric acid. Which is the pushed out the gastric gland from the gastric pit into the stomach.
73
describe the generation of peristalsis in the gut
gastric peristaltic waves are generated roughly 3 every minute by pacemakers cells in the longitudinal muscle layer. Action potentials travel through a syncytium along gap junctions, providing enough depolarization to the slow waves to induce a contraction.
74
Explain the mechanisms involved in the neutralisation of gastric acid in the duodenum, including control of bicarbonate secretion in the duodenum
once acid is detected in the duodenum, brunner’s glands duct cells secrete bicarbonate to neutralise the acid.
75
Explain the role of gastric motility in digestion and
the role of motility is to force the contents of the stomach to mix.
the peristaltic wave from the body to the antrum is increasingly more powerful the close you get to the sealed pylori sphincter, due partly to the presence of a third innermost layer, the oblique muscle.
76
describe the mechanisms controlling gastric emptying
this processed is maintained by the peristaltic rhythm generated by pacemaker cells in the longitudinal muscle layer..
The slow waves are known as the basic electrical rhythm, and contractions only occur when an action potential is triggered, the frequency of which determines the strength of contraction. This can be increased by gastrin, distension of the stomach wall, or however the presence of chyme in the duodenum inhibits motility.
77
neutralisation of gastric acid in the duodenum and the control of bicarbonate secretion in the duodenum
This is controlled through long vagal and short ENS reflexes. Hormone wise this is controlled by the release of secretin into the systemic blood flow which stimulates the pancreas and liver to produce bicarbonate, this process is halted once the acid neutralises.
H+ + HCO3- H2CO3 H2O + CO2
78
Explain the functions of the pancreas
the pancreas has both an endocrine function, producing both insulin and glucagon and somatostatin in the pancreatic islets which control glucose in the blood. The pancreas also has a exocrine function, with its acini producing zymogens which will later be activated into digestive enzymes, and in the ducts bicarbonate is produced.
79
Describe the actions of secretin on pancreatic and bile secretion and the stimuli which will cause their release
secretin is a hormone released by the small intestine which stimulates the secretion of bicarbonate ions by duct cells from the pancreas, duodenum, and bile duct in response to acid from the stomach encountering the duodenum. It then reduces gastric emptying and gastric acid secretion. The neutralisation of the acid then inhibits the release of secretin.
80
Describe the actions of cholecystokinin (CCK) on pancreatic and bile secretion and the stimuli which will cause their release
CCK is released in response to AA and FA in the duodenum by the small intestine to simulate the pancreas to release zymogens that becomes enzymes to digest fats and protein. It also reduces gastric emptying and relaxes the sphincter of Oddi allowing for the influx of bile.
81
Describe the control of pancreatic enzyme secretion and the role of zymogens
acinar cells produce digestive enzymes that are stored as zymogen granules to prevent autodigestion. As they are released they encounters a brush border enzyme enterokinase which converts trypsinogen into trypsin. Trypsin then activates zymogens into digestive enzymes. This process is regulated by the hormone CCK which is secreted into the blood supply by the small intestine upon the arrival of fatty acids and amino acids into the duodenum.
82
Describe the anatomy and histology of the pancreas
anatomically the pancreas has a body, tail and head. Combines with the common bile duct before reaching the sphincter of oddi in the duodenum.
histologically the pancreas consists of lobules connected by intercalated ducts with intralobular ducts leading into interlobular ducts ending in the main pancreatic duct.
83
Describe the structure of the exocrine pancreas
the exocrine pancreas consists of a lobule consisting of acini cells, leading from this is intercalated ducts containing duct cells, this leads to intralobular ducts then interlobular ducts that feed into the pancreatic duct.
84
Describe the structure of the liver.
structure; the liver is the largest organ in the body in the upper right quadrant of the of the abdomen. It contains 2 major lobes right which is larger than the left and 2 minors lobes the caudate and quadrate. Entry of vessels into the liver are though the porta on the inferior surface. The liver does have a bare area free from connective tissue on the diaphragmatic surface surrounded by a coronary ligament.
85
describe the functional structure of the liver
functional structure; the liver has ligamentous septa diving it into lobules with connecting vessels, ducts and nerves. At the corner of each hexagon is a portal triad of hepatic artery, portal vein and duct. In the centre of each lobule is hepatic veins that lead to the inferior vena cava. There are cords that radiate from the central vein, with bile canaliculus in between each cord and blood channel sinusoids.
86
functions of the liver
function; from the GIT oxygen depleted nutrient rich blood travels along the hepatic portal vein mixing in the hepatic sinusoids with oxygen rich, nutrient blood from the hepatic artery encounters hepatocytes. Here bile synthesis, nutrient storage, interconversion and detoxification occurs with bile being redirected to the canaliculi and hepatic ducts and blood returning to the central veins.
87
Describe the composition and function of bile, the mechanisms controlling its storage and release from the gallbladder and the mechanism whereby it is reabsorbed.
Bile is produced from bile acids, lecithin and cholesterol which is for solubilising fat. Pigments are from bilirubin, detoxified metals are from hepatocytes, bicarbonate is added from duct cells. Finally before release bile is conjugated with glycine or taurine to increase solubility, this is because 95% of bile is recycled through the enterohepatic circulation. The sphincter of Oddi prevents it release, allowing for it be concentrated by removing sodium, water leaves the bile. CCK hormone in response to fat In the duodenum triggers the relax of the sphincter and gallbladder contraction
88
pathology behind peptic ulceration
peptic ulceration originates from an imbalance between acid and the mucosal barrier and is usually associated with H. Pylori bacteria. This can lead to fibrosis, bleeding acutely or chronically or perforation.
89
pathology of stomach cancer
usually adenocarcinoma’s and again are associated with H. Pylori infections, chronic ulcerations or gastritis. It can spread directly or through the blood, lymph or transcoelemic.
oesophageal reflux refers to acid in the oesophagus, normally occurring due to a hiatus hernia which results in thickening of the epithelium and ulceration. Chronically this can lead to obstructions, constriction or obstruction.
90
pathology of chronic reflu
chronic reflux may also lead to remodelling causing a ‘Barrett’s oesophagus” when the glands undergo metaplasia aggressively, known as a precursor to oesophageal cancer.
oesophageal cancer can from Barrett’s oesophagus, obesity for adenocarcinoma or for squamous carcinoma smoking, alcohol or dietary carcinogens. Locally it causes obstruction, ulceration and perforation and can move directly, lymphatically or via the blood to the liver.
91
pathology of gastritis
finally we have gastritis which is inflammation of the stomach. This is due to Autoimmune diseases, bacteria or chemically. Specifically autoantibodies can attack parietal cells and intrinsic factor resulting in atrophy of acid glands and a vitamin B12 deficiency. Bacterially it can be caused by a inflammatory response and increased acid production due to H. Pylori. Chemically it can be induced by drugs (non-steroidal anti-inflammatory), alcohol or bile reflux.
92
state common or benign malignant disorders affecting the oesophagus
oesophagus reflux – benign
Barrett’s oesophagus – pre malignant
oesophageal cancer – malignant
93
H. Pylori's role in gastric disease
H. Pylori is involved as a bacterial cause of gastritis. Severe conditions of gastritis caused by H. Pylori left unchecked may progress to ulceration. Repeated infection with H. Pylori may result in causing stomach cancer. It can only colonise within the gastric mucosa, this is due to its flagella that it can burrow with. It survives the acid within the stomach by producing an alkaline barrier through a urease enzyme. Within the mucosa the body’s innate immune system detects it and stimulates and immune response.
94
presentation and pathology of oesophageal reflux
difficulty swallowing, dysphagia. Can be caused by a hernia, essentially stomach acid damaging the delicate epithelium, causing remodelling and potentially if there is ulceration then fibrosis which then reduces motility and can lead to Barrett’s oesophagus.
95
oesophageal cancer pathology and presentation
dysphagia. Often can be caused by smoking, diet or alcohol consumption at least for squamous. Adenocarcinoma is often caused by obesity or because of Barrett’s oesophagus.
gastritis – can be the result of autoimmune disease, resulting in pernicious anaemia, bacterial (H. Pylori) or chemical such as alcohol, bile reflux or drugs.
96
peptic ulceration pathology
can be cause by an H. pylori infection, can result in bleeding, resulting in acute haemorrhages or chronic anaemia. However it may cause perforations, fibrosis which will then result in obstruction.
97
stomach cancer pathology
second most common GIT cancer, can be because of repeated H. Pylori infections. Can lead to bleeding, ulceration and spread directly, lymphatically, via the blood to the liver or trans coelomic.
98
structure and function of small intestine
consists of the duodenum, jejunum and ileum.
the function of the duodenum is gastric acid neutralisation, digestion and iron absorption
the function of the jejunum is nutrient absorption (95%)
the function of the ileum is salt and water absorption, resulting in chyme dehydration.
99
Basic eletrical rhythm explain
The basic electrical rhythm is a spontaneous depolarisation/repolarisation slow wave rhythm conducted through gap junctions along the longitudinal muscle layer.
100
segmentation explained
Segmentation is the change between contraction and relaxation between short intestinal segments to provide a thorough mix whilst increasing surface area contact between chyme whilst slowly migrating it towards the large intestine. It occurs during a meal.
101
peristalsis explained
peristalsis is a part of the migrating motility complex, following the end of segmentation, the function of this differs from segmentation it that it is designed to move undigested material into the large intestine, trying to prevent bacterial colonisation in the small intestine to prevent competition regarding nutrient absorption.
102
Describe the features which act to increase absorptive surface area along the alimentary canal
the intestinal shape as a cylinder increases its surface area. Having circular folds known as plicae further increase it by a third, the villi increase it by 10 percent. Finally, the microvilli increase the surface area by almost 200%. The villi themselves consist of simple columnar epithelium with scattered goblet cells, lacteal, capillary network, following a villus is a crypt of Lieberkühn where developing villi cells originate from.
103
Describe the neural control of intestinal motility for segmnetation
the contraction of segmentation is increased by parasympathetic vagus nerve whereas sympathetic nerves decrease contraction. It must be stressed the frequency of the segmentation is however determined by the basic electrical rhythm. The hormone motilin is the one responsible for the initiation of migrating motility complex and mediated by the neurones in myenteric plexus.
104
state function of the caecum
used to be useful for herbivores, but use has outgrown and now is just a sack
105
colon sturcture and function
ascending, transverse, descending, sigmoid.
function; actively transport sodium from the lumen to absorb water for dehydration of chyme. It’s also the site of bacterial colonisation that enables for fermentation, short fatty acid chain release, vitamin K production and gas production such as nitrogen, carbon dioxide, hydrogen, methane and hydrogen sulphide.
106
rectum and anal canal function
defecation
107
Describe the importance of intestinal bacteria in the digestive process
there are lots of bacteria in the colon. It’s responsible specifically for the digestion of carbohydrate, producing short chain fatty acids a source of energy in ruminants, production of vitamin K for blood clotting, and gas.
108
describe the rectum
Rectum – straight muscular tube with simple columnar epithelium and thick muscularis externa
109
describe the anal canal
muscularis is thicker than the rectum, and the epithelium here changes from simple columnar to stratified squamous
110
describe the structures of the rectal sphincters
internal anal sphincter - thick muscularis, smooth muscle automatic control
external anal sphincter – skeletal muscle, voluntary control
111
describe the mechanisms controlling defecation
mass movement contraction forces the faecal matter from the colon to the rectum, the distension of the rectal wall is detected by mechanoreceptors that then stimulate a defaecation reflex. The reflex itself is under splanchnic parasympathetic control and determines the contraction, relaxation of internal sphincter and contraction of external anal sphincter and increases peristaltic activity.
112
Describe the mechanisms which cause secretory diarrhoea
diarrhoea can be caused by pathogenic bacteria, protozoans, toxins, viruses, food and anxiety. They manipulate the process within crypt cells for chloride secretion, specifically Vibrio cholerae or E. coli through enterotoxins elevating cAMP, cGMP, calcium. Since these unbalances the osmolarity the movement of ions, water follows through and swamps the villus cells preventing efficient absorption.
113
innate versus adaptive immune cells
granulocytes, mast cells, monocytes, dendritic cells, macrophages and natural killer cells are all innate originating from myeloid progenitor cells
CD4+, CD8+, B cells, plasma cells and memory cells are adaptive originating from lymphoid progenitor cells.
114
secretory diarrhoea and explain how this can be treated with simple salt/sugar solutions.
the villus cells aren’t damaged however, so by using salt/sugar solution you can generate a ion uptake, to draw water back into the gut causing rehydration.
115
innate versus adaptive immune cells
innate overall is a universal system revolving around infection by microbes recognized by their molecular pattern and as a result can induce general inflammatory responses.
adaptive immunity is induced by specialised pathogen and require recognition through professional antigen presenting cells. It’s mainly conducted through T and B cells.
116
structure and function of cytokines
cytokines are key determinants in T cell differentiation. They are soluble mediator of immune responses and capable of being anti or pro inflammatory and can trigger amplification or cascades of effects. Cytokines consist of two sub units that will dramatically alter their function.
117
antigen presentation at the GI mucosa
inside the GI tract there are spots called Peyer’s patches containing large numbers of immune cells. Bacteria may enter through an M cell, or be grabbed by a dendritic cell, and then brought to a lymph node for antigen presenting to a naïve T cell, depending on the subset of dendrite it can give rise to a variety of response. As well as macrophages that can also present antigens.
118
IBD and coeliac disease, treatments used to target immune response discussed
Anti TNF therapies for IBD (targeting a single cytokine through neutralisation, modulation, apoptosis)
vedolizumab – targets integrins for lymphocyte movement to intestinal mucosal.
ustekinumab – mutlicytokine blockade.
Fecal matter transfer
for Coeliac Gluten free diets.
119
dyspepsia presentation
pain or discomfort in upper abdomen, anorexia, nausea, vomiting, bloating, early satiety and heartburn.
120
dyspepsia pathology
organic versus functional causes. Many likely scenarios ranging from anatomical to metabolic. Including ulcers, gastritis, gallstones, coeliac disease, cancer, drugs or cardiac problems.
121
dyspepsia managment
endoscopy, history, exam, bloods (FBC, ferritin, LFT, U&E’s, calcium, glucose, serology IgA, drug history and lifestyle management
122
gastritis pathology
inflammation caused either by Autoimmune, bacterial or chemical and can be diagnosed through endoscopy, or histological.
123
peptic ulcer presentation
smoker or use of NSAIDS, epigastric pain, nocturnal hunger pains, back pain, nausea, anorexia, weight loss or haematemesis or melaena, or anaemia.
124
peptic ulcer pathology
H. Pylori
125
peptic ulcer management
treated using antacid medication (proton pump inhibitors, H2 receptor antagonists) surgery only in complications. Alongside eradication therapy
126
gastric outlet obstruction presentation
; vomiting lacking bile, fermented food. Early satiety, abdominal distension, weight loss and gastric splash with dehydration.
127
gastric obstruction pathology
underlying cause of ulcer, stricture, fibrosis or cancer.
128
managment of gastric obstruction
diagnosis UGIE, blood of low Cl, low Na, low K or renal impairment. Loss of H+ and Cl- in vomit. Treat the underlying cause or endoscopic balloon dilatation surgery.
129
gastric cancer symptoms
common malignancy, dyspepsia, early satiety, nausea, vomiting, weight loss, GI, bleeding, iron deficiency, gastric obstruction
130
gastric cancer pathology
; majority of adenocarcinoma or MALT/GIST. Can be caused by chronic H. pylori infections and can be intestinal or diffuse types. Often sporadic with little genetic history or background, and other factors that are environmental.
131
gastric cancer management
endoscopy and histological for diagnosis. CT of abdomen and then multi-disciplinary team discussion. Then treatment of surgery or sometimes chemo.
132
describe investigation of H. Pylori
its management requires culture, serology but they are less common. We now more commonly use carbon tagged urea breathing tests to detect the urease enzyme or stool antigen ELISA. If necessary, a endoscopy with biopsy and rapid slide urease test. If it’s in the antrum it can cause ulcer, if in the body/fundus can cause cancer.
133
describe the role of H pylori in gastric diseas
Helicobacter pylori has infected 50% of the world. It can only colonise within the gastric mucosa, this is due to its flagella that it can burrow with. It survives the acid within the stomach by producing an alkaline barrier through a urease enzyme. Within the mucosa the body’s innate immune system detects it and stimulates and immune response.
134
describe treatment of H. Pylori
to eradicate the infection it require 7 days of triple therapy; clarithromyocin 500mg, amoxycillin 1g (or tetracycline) or omeprazole 200mg. there are second line therapies available.
135
Describe the role of screening as applied to colon cancer
those over the age of 50 receive a card for sampling to see whether they require any further investigation due to the demographic age of colon cancer. 14-30 people report rectal bleeding to their GP, out of that one will have bowel cancer.
136
Describe the management of colorectal cancer.
investigations involve colonoscopy, biopsy, rarely contrast imaging, cross sectional imaging, MRI. The treatment itself depends on the individuals wishes whether it is medical or surgical, endoscopic or invasive.
137
review structure and function of colon and rectum
Cecum, ascending colon, transverse colon, descending colon, sigmoid colon and rectum.
production of faeces through dehydration, and fermentation.
138
describe arterial supply and innervation to the colorectal area
superior mesenteric artery branching to the middle, right, ileocolic arteries.
inferior mesenteric artery branching to the left colic, sigmoid and superior rectal artery.
pain receptors are within the smooth muscle, afferent sympathetic fibres accompany segmental vessels.
139
describe presentation of colorectal
Rectal bleeding is a common occurrence, with 1 in 2000 presenting with rectal bleeding. The high risk features is persistent change in bowel habit, persistent rectal bleeding. A right sided abdominal mass, palpable rectal mass, or unexplained iron deficiency.
140
state differential for actue abdomen
peitonitis, obstruction and body wall pain
141
Describe the principles of investigation and clinical assessment of a patient with acute abdomen
assess + resuscitate if necessary, investigate, observe and treat. Not necessarily in this order, in terms of sepsis then it will be necessary to start broad spectrum antibiotics, and fluids until whilst investigating.
essentially what is the problem, effects and what should I do.
142
Discuss the investigations and management of patients with acute abdominal pain (including conditions such as peritonitis, obstruction and pancreatitis)
urine tests, Full blood count, U+E, liver function test, endoscopy, laparoscopy, laparotomy, CT, ultrasound or MRI. If resuscitating then restoring fluid volume, enhance oxygenation and perfusion, treating sepsis, decompressing the gut and analgesia. Similar line of reasoning goes for any treatment.
143
• Describe the aetiology, presentation and management of intestinal obstruction
intestinal obstruction is due to when the passage along the GI track becomes obstructed, compressed or the wall itself is compromised. It can present with pain, vomiting, distension, constipation, or borborygmic (gut noises). The severity will depend greatly on the location.
144
the basic histological organisation gut tube
in the gut tube there is
1. mucosa
a. epithelium
b. lamina propria
c. muscularis mucosae
2. Submucosa
3. Muscularis externa
a. inner circular
b. outer longitudinal
4. Adventitia/serosa
145
Describe the basic blood supply and function of the liver
dual blood supply, hepatic artery, portal vein
function; protein synthesis, metabolism of fat and carbs, detoxification of drugs and toxins including alcohol. formation of bile.
146
what are the different causes of jaundice
hepatic causes include cholestasis or intra-hepatic bile duct obstruction.
extra-hepatic causes include duct obstruction, diseases of the gall bladder or cholelithiasis.
147
what is roughly the normal metabolism of bilirubin
jaundice is caused by increased circulating bilirubin. During the hepatic metabolism of bilirubin, it is taken up by hepatocytes, conjugated to make it more soluble and then excreted. It then joins the biliary system and is broken down with a small fragment reabsorbed
148
intra-hepatic bile duct obstruction involves
primary biliary cholangitis or primary sclerosing cholangitis or due to tumours of the liver (hepatocellular carcinoma, tumours or metastasis.
149
primary biliary cholangitis refers to
an autoimmune disease affecting mostly females and can be diagnosed through anti-mitochondrial antibodies or raised serum alkaline phosphatase. There is granulomatous inflammation, loss of intra bile ducts and cirrhosis.
150
primary sclerosing cholangitis refers to
to chronic inflammation and fibrous obliteration of bile ducts and is associated with inflammatory bowel disease. It can progress to cirrhosis or have and increased development risk of cholangiocarcinoma.
151
cholelithiasis is a cause of jaundice, what is it?
to gallstones that can be causes by obesity or diabetes.
152
acute cholecystitis is an extrahepatic cause of jaundice, what is it?
inflammation resulting in empyema (abcess) or perforation of the gall bladder that can lead to biliary peritonitis. Acute inflammation can progress to chronic.
chronic cholecystitis – fibrosis of the gall bladder.
153
common bile duct obstruction can be caused by and can lead too
gallstones, bile duct tumours, fibrosis or external compression from a tumour. It can result also in infection of bile resulting in ascending cholangitis which results in secondary abcess formation and secondary biliary cirrhosis
154
causes of acute liver disease
hepatitis, alcohol, drugs or bile duct obstruction. Viruses such as hepatitis A,B,C,E. virally there is inflammation and apoptosis, leading to either resolution, failure of cirrhosis
155
pathology of acute liver disease
Alcoholic liver disease is liver remodelling due to excessive alcohol exposure resulting in inflammation, apoptosis, failure and fatty changes resulting in cirrhosis.
drug induced cholestasis which can trigger jaundice can be either predictable due to dosage or unpredictable.
156
chronic liver disease cause
alcohol, acute injury, primary biliary cholangitis, alcohol, hepatitis B,C, autoimmune disease, metabolic iron or copper disorders, obesity or be cryptogenic.
157
pathology of chronic liver disease
It is often diffuse through the whole liver, loss of structure and fibrous tissue nodules replacing hepatocytes. The complications are altered liver function, abnormal blood flow (portal hypertension) and hepatocellular carcinoma
158
essential pathology of acute cholecystitis
inflammation of the gall bladder which may result in an empyema, perforation, peritonitis or chronic inflammation.
159
use of CT
often used for patients of concern to diagnose not to find out what is wrong with the patient. It provides highly useful imaging however it also produces large doses of radiation.
160
use of MRI
produces no radiation, utilising magnetic feedback from molecules in the body. However, they aren’t always available and not suitable for claustrophobic, patients with metal implants or those who can’t sit still for a long time.
161
use of PETCT
scanner uses FDG radioisotopes to track metabolic activity in an anatomical background. Useful for identifying secondary tumours and tracking progress but not specific for diagnosis.
162
signs of chronic liver disease
Signs of a chronic liver disease include spider naevi, palmar erythema, gynaecomastia, loss of axillary and pubic hair, ascites and encephalopathy. Late stage disease will present with jaundice and muscle wasting.
163
normal investigations for liver disease
often alcohol related diseases are asymptomatic and can only be detected through CAGE or FAST/AUDIT tests.
Normal investigations involve checking the ration of AAT to ALT (AAT>ALT ration >2) raised GGT(inflammation marker), macrocytosis, thrombocytopenia and ultrasound.
164
encephalopathy pathology
The confusion arises from
It is caused by infection, drugs, constipation, GI bleeding and electrolyte disturbances.
the production of ammonia by the liver because of altered metabolism of proteins.
165
encephalopathy presentation
presents with liver failure, and anything from mild confusion to a coma.
166
encephalopathy treatment
Hence the treatment involves clearing the bowel out to reverse the comatose state, antibiotics and support via ITU, airway and nasogastric tubes.
167
spontaneous bacterial peritonitis pathology
arises from fluid in the peritoneum referred to ascites which can easily become infected.
168
spontaneous bacterial peritonitis presentation
It presents with pain, fever, rigors, renal impairment, as well as signs of sepsis, tachycardia and temperature
169
spontaneous bacterial peritonitis treatment
Treatment includes an ascitic tap in which fluid protein and glucose levels are monitored, culture and white cell content. Further treatment involves IV antibiotics, and IV albumin infusion to expand plasma volume.
170
alcoholic hepatitis presents with
jaundice, encephalopathy, infection and decompensated hepatic function which can be detected with low albumin and raised prothrombin.
171
alcoholic hepatitis diagnosis requires
raised bilirubin, raised GGT AlkP in the blood and a history of alcohol abuse.
172
treatment for alcoholic hepatitis requires
With a poor prognosis the key here is to treat infections, encephalopathy, alcohol withdrawal symptoms, GI bleeding and airway protection/ITU care. Steroids such as prednisolone may be used if they rate >9 on the Glasgow alcoholic hepatitis score. The greatest benefit to survival however is regular high energy nutritional therapy, the use of thiamine is often essential for vitamin B for brain function. Long term abstinence is essential for survival.
173
steatosis is caused by and may lead to
It’s the result of obesity, diabetes and hypercholesterolaemia. It’s the result of inflamed fat cells like alcohol induced damage and as a result may progress to cirrhosis (1/4).
174
steatosis can only be detected by and treated by
Often it is asymptomatic, only being detected through raised alanine amino transferase, ultrasound and occasionally biopsy. The only treatment is weight loss and exercise.
175
State the effects of alcohol as applied to the alimentary system and Liver on a metabolic scale
alcohol alters metabolism through the production of NADH + H+ from the conversion of ethanol into acetaldehyde. This then induces hypoglycaemia, acidosis from lactic acid. Ketosis from excess acetyl coA, and induces lipogenesis and alters the electron transport chain. It can do damage directly if large enough volumes are consumed.
176
in general alcohol has what effect to the liver
Indirectly cause hazardous behaviour or have harmful effects long term resulting in a fatty liver which progresses to alcoholic hepatitis, that then leads to fibrosis, scarring known as cirrhosis and then liver failure.
177
chronic pancreatitis aetiology
think O-A-TIGER; obstruction, autoimmune, toxin, idiopathic, genetic, environmental, recurrent injuries. Often 70% of the time it is caused by alcohol.
178
chronic pancreatitis presentation
Presents with pain, exocrine insufficiency, diabetes, jaundice, duodenal obstruction, haemorrhage.
179
investigation for chronic pancreatitis
Investigations involve CT, ERCP/MRCP. Sometimes but not often exocrine function test (faecal serum enzymes), pancreolauryl test and diagnostic enzyme replacement.
180
management of chronic pancreatitis
counselling, abstinence from alcohol, analgesia, management from acute attacks, avoiding high fat and protein diets, anti-oxidant therapy and treating diabetes. Interventional therapies involve managing pseudocysts, splanchnectomy, caeliac plexus block for the pain, stenting or bypass. Often drainage and resection is required.
181
acute pancreatitis presentation
abdominal pain, nausea, vomiting, collapse. Signs of pyrexia, dehydration, abdominal tenderness, circulatory failure.
182
investigations for acute pancreatitis
investigations involve U/E, glucose, serum amylase, FBC, clotting, LFT, ABG, X-ray, USS, CT.
183
management for acute pancreatitis requires
Monitor the pulse, BP, urine, CVP, arterial line and ITU. General support involves maintaining renal, cardiovascular and respiratory function as well as administering fluids and analgesia. Long term recovery enteral feeding and nutritional support is essential. Identify underlying cause and treat whether it requires cholecystectomy, counselling for alcohol, correcting ischaemia, bypassing or resecting malignancy, lipid lowering drugs, correcting abnormalities and ceasing drug intake. Antibiotics should be used in the event of sepsis. ERCP should only be indicated in jaundice and cholangitis pancreatitis.
184
pancreatic cancer presents with
pain, anorexia, diabetes, vomiting, weight loss, pancreatitis.
185
pancreatic cancer investigation and management
involve bloods, CXR, CA19-9. Imaging involves USS, followed by a CT/MRI, then a laparotomy followed by hopefully a resection. If not possible then an ERCP with a stent should be undertaken, or a laparoscopic bypass but if necessary open bypass. Palliative drainage may be necessary through bypass, ERCP or stenting.
186
essential pathology of acute pancreatitis
mild with uneventful recovery or severe involving organ failure and local complications such as ascites, pseudocysts, abscesses, necrosis. Caused by gallstones, alcohol, cancer, drugs or iatrogenic.
187
oesophageal cancer indications
frequent persistent hiccups, heartburn, difficulty swallowing, constant belching, pain between the shoulders and weight loss
188
staging for oesophageal cancer
EUX for T/N stage and PET CT for M stage
189
treatment for oesophageal cancer
non-operative; stents, palliative radiotherapy, palliative chemotherapy
operative; esophagectomy and chemotherapy
190
gastric cancer indications and symptoms
anaemia, loss of weight, anorexia, vomiting, recent onset of progressive symptoms, masses, melaena and dysphagia, >55. Often non-specific.
191
gastric cancer investigations
endoscopy, staging laparoscopy.
192
gastric cancer treatment
gastrectomy
193
GORD indications
tooth erosion, belching, chest pain, burning stomach, trouble swallowing, excessive saliva, asthma, wheezing, sour taste in mouth.
194
GORD surgery indications
For surgery indications are sliding hiatus hernia or paraesophageal hiatus hernia.
195
investigation for GORD
endoscopy, oesophageal Ph and manometry
196
chronic pancreatitis pathology
is long term inflammation that results in irreversible glandular destruction and loss of function with chronic pain.
197
chronic pancreatitis symptoms
Often it presents with pain, weigh loss, exocrine insufficiency with steatorrhea, endocrine insufficiency which may present with diabetes. Other signs may include jaundice, portal hypertension and pseudocysts.
198
chronic pancreatitis investigations
Investigations involve AXR, USS, EUS, CT and blood tests monitoring albumin(decrease), LFT, prothrombin time(increase), and serum amylase(increase) and well as pancreatic function tests.
199
chronic pancreatitis management
Pain control involves abstinence, opiate analgesia, coeliac plexus block, pancreatic enzyme supplements, endoscopic removal of stones using ERCP, or surgery. A low fat Diet is essential and diabetes has to be regulated with insulin.
200
pancreatic carcinoma presents with
pancreatic carcinoma often presents with upper abdominal pain, jaundice, weight loss, anorexia, fatigue, steatorrhoea, nausea, vomiting, tender subcutaneous fat nodules, thrombophlebitis, ascites and portal hypertension. Physically they will show signs of hepatomegaly, abdominal masses and tenderness, splenomegaly, supraclavicular lymphadenopathy and palpable gallbladder with ampullary carcinoma.
201
imaging for pancreatic carcinoma requires
Imaging will involve USS, then CT and a MRI
202
treatment for pancreatic carcinoma
If jaundice then ERCP with stent, otherwise the next step is biopsy, then laparotomy/laparoscopy. Radical surgery involves a pancreatoduodenectomy, otherwise it is palliative jaundice treatment and pain control through opiates, coeliac plexus block or radiotherapy.
203
acute pancreatitis presents with
acute pancreatitis presents with sudden and intense pain. Radiating to the back with vomiting, nausea, anorexia, steatorrhea.
204
acute pancreatitis investigations
involve blood tests for amylase, lipase, FBC, ABG, coagulation etc, AXR, CRX for pleural effusion, ultrasound and CT contrast. Often albumin <32g/l, glucose >10mmom/l and CRP>150mg/l is indicative of severe pancreatitis.
205
management for acute pancreatitis involves
General management involves analgesia, IV fluids, blood transfusion, monitor urine output, nasogastric tube, O2, insulin, and nutrition enteral if severe. If necrosis then Ct guided aspiration with antibiotics may be necessary, and if gallstones is the cause then ERCP or cholecystectomy.
206
pancreatic carcinoma investigations
US, then CT maybe EUS. Then biopsy then CT/EU/laparoscopy/laparotomy
207
pathology of acute pancreatitis
acute pancreatitis is caused by alcohol abuse, gallstones, trauma or though drugs, carcinoma and viruses. The primary insult regardless of what it is triggers the release of activated pancreatic enzymes, triggering the release of pro-inflammatory cytokines and reactive oxygen species. This then leads to oedema, fat necrosis and haemorrhage. This can lead to a multi-organ system failure, the formation of abscesses and pseudocyst.
208
describe surgical management of gallstones
cholecystectomy either open, mini, laparoscopic, single port.
209
surgical management of benign biliary disease
resection, excision or hepaticojejunostomy, hepaticoduodenostomy for cysts.
210
malignant carcinoma jaundice surgical treatment
cholangiocarcinoma surgical is the only curative option. Palliative care involves surgical bypass, chemo and radiotherapy, or stenting. Treatment involves endoscopic excision, or pancreatico-duodenectomy
211
function of the gall bladder
the function of the gallbladder is to act as a bile reservoir, concentrate bile and secrete it after meals.
212
indication and treatment for gallstones
gallstones; older age, cholesterol, dyspeptic symptoms, biliary colic, jaundice. Treatment of laparoscopic cholecystectomy.
213
benign biliary tract disease causes
congenital causes such as atresia, cysts, iatrogenic, gallstones or inflammatory.
214
malignant jaundice indications
obstructive, non-specific itching jaundice caused by cholangiocarcinoma.
215
gallstones investigations
Gallstones; blood tests (LFTs, amylase, lipase, WCC), USS, EUS, oral cholecystography, CT, radioisotope, IV cholangiography, MRCP, PTC, ERCP.
216
cholangiocarcinoma investigations
; Lab, radiology, angiography, ERCP, cytology. Radical surgery or palliative bypass, stent, chemotherapy, radiotherapy.
217
treatment for cholangiocarcinoma
Treatment involves endoscopic excision, or pancreatico-duodenectomy
218
dysphagia presentation
sensitivity to swallowing foods and liquids
219
dysphagia causes
May be caused by stricture, malignancy, motility disorders, eosinophilic oesophagitis, extrinsic compression
220
diagnosis for dysphagia
endoscopy, if alarm features, otherwise from characteristics
221
hypermotility presentation
severe episodic pain due to diffuse oesophageal spasms.
222
investigation from hypermotility
Use of Ba Swallow or manometry to demonstrate corkscrew appearance from uncoordinated contractions.
223
treatment for hypermotility
smooth muscle relaxants
224
hypomotility for pathology
connective tissue disease causing heartburn and reflux
225
achalasia symptoms
progressive dysphagia, weight loss, chest pain, regurgitation and chest infection
226
achalasia pathology
loss of myenteric plexus ganglions cells in distal oesophagus and LOS
227
achalasia treatment
pharmacological nitrates, calcium channel blockers, endoscopic botulinum toxin, pneumatic balloon dilatation which can be done radiologically, or myotomy surgery
228
GORD presentation
heartburn, cough, water brash, sleep disturbance
229
GORD pathology
acid and bile exposure due to hypotension in the lower oesophageal sphincter, delayed gastric emptying or due to anatomical distortion.
230
GORD diagnosis
. Diagnosed on characteristic symptoms, endoscopy if weight loss, dysphagia and vomiting.
231
GORD treatment
Treatment lifestyles, pharmacological; alginates, H2RA, proton pump inhibitor. Anti-reflux surgery.
232
barrett's oesophagus pathology
intestinal metaplasia due to chronic acid exposure resulting in mucin columnar cells replacing squamous, precursor to adenocarcinoma.
233
barrett's oesophagus investigation and treatment t
. Investigation endoscopy with biopsy, treatment is endoscopic resection, radiofrequency ablation, oesophagectomy.
234
oesophageal cancer symptoms
weight loss, progressive dysphagia, odynophagia, chest pain, cough, pneumonia, vocal cord paralysis, haematemesis.
235
oesophageal squamous cancer causes
tobacco, alcohol and diet.
236
oesophageal adenocarcinoma causes
Barrett’s oesophagus leads to adenocarcinoma as well as obesity
237
investigations for oesophageal cancer
. Investigations involve endoscopy and biopsy.
238
staging for oesophageal cancer is
Staging involves CT, EUS, PET and bone scan.
239
treatment for oesophageal cancer
Treatment is oesophagectomy maybe with pre or post chemotherapy alongside nutritional support. Non-operable may involve radiotherapy and chemo. Palliative care may also include use of endoscopic stents, or brachytherapy.
240
eosinophilic oesophagitis symptoms and causes
dysphagia and food bolus obstruction as a result from allergy meditated dysfunction due to eosinophilia infiltrate.
241
eosinophilic oesophagitis investigation and treatment
Investigation involves endoscopy, treatment requires topical corticosteroids, dietary elimination and endoscopic dilatation.
242
define functional bowel disorders
they can either structural and be detectable and pathological, or functional and often be difficult to mark pathologically. Functional bowel disorders are a very common disorder with a large impact on quality of life but not very serious however.
243
Discuss the investigation and management of a patient with a functional bowel disorder
often with functional bowel disorders it’s important to gauge what is normal for the patient. Then following on with a detailed history and physical exam. If there is need for further investigation a FBC, blood glucose, U+E, thyroid status, coelic serology, FIT testing, sigmoidoscopy or a colonoscopy may be required. For IBS in particular calprotectin, stool culture and rectal exam may be necessary too with TFT’s and CRP levels in blood.
244
Understand impact of functional bowel disorders and role of psychological factors
relaxation training; use of progressive muscles, biofeedback and medication for those with psychological co-morbidity and diarrhoea. Hypnotherapy for deep relaxation in refractory patients suffering from pain, constipation, flatulence and anxiety.
cognitive behaviour therapy for identifying triggers and coping mechanisms for bloating, abdominal pain and flatulence. Psychodynamic interpersonal therapy for dealing with emotional an bowel symptoms for patients with a history of abuse. Altered motility and hypersensitive may arise from triggers such as stress, anxiety and depression.
245
Discuss alarm symptoms suggesting need for investigation
>50, short symptom onset, weight loss, nocturnal symptoms, family history of cancer, male sex, rectal bleeding, recent antibiotic use, abdominal masses and anaemia.
246
• Discuss drug, dietary and other management techniques for functional bowel disorders
dietetic review of Tea, coffee, alcohol, sweeteners, lactose and gluten. Follow FODMAP. Fermentable oligo, di, and monosaccharides and polyols eg Fructose, Lactose, Fructans, Galactans and polyols.
drug therapy for pain; antispasmodics, linaclotide and anti-depressants. For the bloating avoiding fibre and linaclotide with some probiotics. For the constipation laxative, linaclotide, whilst avoiding TCA’s and FODMAP. For diarrhoea use antimotility agents and FODMAP whilst avoiding SSRIs.
247
State the common disorders affecting the small intestine with particular reference to malabsorption
Coeliac disease presentation; dermatitis herpetiformis. Investigation serology (not always reliable due to IgA not always being present, hence a TTG IgG should also be carried out), investigating HLA status (DQ2, DQ8). The main confirmatory investigation however is a biopsy and histology for atrophy.
tests of structure that may be carried out are endoscopy, barium study, CT and MRI (gold standard) or capsule enterography. Other tests include bacterial overgrowth H2 test(not most reliable) or endoscopy with a small bowel aspirate and culture.
treatment for Coeliac disease is to withdraw gluten, with reference to a dietician
248
Explain concept of maldigestion and mal-absorption,
maldigestion refers to the incomplete breakdown of nutrients due to the lack of enzymes (pepsin, amylase, trypsin, chymotrypsin, lipase), whereas maldigestion refers to the impaired transport of nutrients hence why transglutaminase and the villi are often involved.
249
Explain concept of maldigestion and mal-absorption, its clinical presentation and management
malabsorption often presents with weight loss, increased appetite and diarrhoea which is usually watery or steatorrhea, bloating and fatigue. Especially with mal-absorption It may be important to identify any specific deficiencies that may arise as a result such as iron, B12, folate, minerals, vitamins D, A, K, B or C. malabsorption may be causes by coeliac disease, or Crohns. However it can be caused by infection of tropical sprue (treated by tetracycline), HIV, Giardia lamblia (treated by metronidazole) Tropheryma Whippelii in whipple’s disease. Furthermore is can be triggered by infiltration, impaired motility, iatrogenic causes, or pancreatic causes.
250
describe structure and function of small intestine in detail
the structure of the small intestine is as follows, the distal half of the duodenum leads onto the jejunum which then finishes with the ileum which is roughly 250-450cm. On a microscopic scale it consists of glands in the duodenum but throughout the structure peyer’s patches for immunity and villi with micro villi for absorption as well as crypt cells. The essential functions of the small intestine is digestion, absorption, endocrine and neuronal control of chyme from the stomach and barrier functions to bacteria via GALT.
251
signs of specific vitamin deficiencies
vitamin D; muscle spasms (tetany) and osteomalacia (bone softening)
vitamin A; night blindness
Vitamin K; raised prothrombin
Vitamin B complex; thiamine (memory, dementia), Niacin (dermatitis, heart failure)
vitamin C; scurvy
252
symptoms, investigations and diagnosis of ulcerative colitis
ulcerative colitis; diagnosis requires the symptoms of regular stools >6 with blood present. However there also may be fever, tachycardia, anaemia and thrombocytosis and leucocytosis. Blood tests will be undertaking to monitor the platelet count, CRP and ESR, and WCC (high) and low Hb and albumin. Calprotectin will also be elevated (>200) in the stool sample. Diagnosis will also require an endoscopy with biopsy. It will show signs of pseudo polyps, erythematous appearance, and histologically the biopsy will show crypt abscesses and atrophy with mucin depletion.
253
treatment of ulcerative colitis
management will involve regular surveillance colonoscopy to check for cancers. Upon diagnosis the patient will undergo treatment of 5ASA a prodrug that will activate in the gut to deal with local inflammation with possible corticosteroids. With severe cases stronger steroids such as prednisolone will be used alongside hydration therapy. If this isn’t effective, then thiopurines may be used to reduce the immune response. Finally, biologics can be utilised such as anti-TNF alpha antibodies infliximab and adulimumab. Through-out treatment elemental feeding is essential for recovery. Surgery may require colectomy, ileostomy. Afterwards resulting in a rectal stump and end ileostomy. If not an ileostomy then a pouch procedure. However if it goes into remission then continue to treat with 5Asa deescalating treatment.
254
Crohn's symptoms
symptoms include abdominal pain, diarrhoea, weight loss, malaise, lethargy, anorexia, low grade fever and malabsorption (anaemia).
255
investigations crohn's disease
Blood tests will be undertaking to monitor the platelet count, CRP and ESR, and WCC (high) and low Hb and albumin. Calprotectin will also be elevated (>200) in the stool sample. For certain diagnosis clinical history and endoscopy, alongside imaging modems such as barium studies will be essential alongside a biopsy demonstrating granulomas, cobblestone bowel, patchy inflammation.
256
treatment for Crohn's disease
Treatment goal here is to monitor for complications, prevent relapse. Use of corticosteroids for immune suppression, diet and elemental feeding is essential here again. particularly the use of TNF alpha antagonists. 5ASA may be used but limited evidence. Again if not effective scale up treatment to steroids, stronger immunosuppressants, biologics then surgery. Methotrexate may be used under specialist follow up. Antibiotics such as metronidazole may be used for Crohn’s peri-anal disease and small bowel infections. Surgery if not successful involves resecting affected bowel.
257
pathological appearances with Crohn's disease
Whereas Crohn’s disease is patchy, affecting anywhere from the mouth to the anus and consist of skip lesions resulting in strictures and fistulas particularly however it will focus on the caecum and ileum, spreading to the small bowel. It can progress from distal to proximal along the colon. It is an example of transmural inflammation.
histologically Crohn’s presents with granulomas,
258
pathological appearances with ulcerative colitis
with ulcerative colitis it is primarily the colon affected particularly the sigmoid and rectum, but progress to extensive where it moves from proximal to distal. colitis it’s often goblet cell depletion and crypt abscesses but remains rather superficial inflammation.
259
investigations for IBD
IBD specific indices can be obtained through blood tests indicating high ESR and CRP, high platelet count, high white blood cell count, low Haemoglobin and low albumin. The stool samples obtained will indicate elevated calprotectin. Endoscopy and diagnosis of Crohn’s disease or ulcerative colitis is essential.
260
management for IBD
medical management in general will involve the use of 5ASA(aminosalicylates) , steroids and immunosuppression. With hospital care requiring the use of steroid, anticoagulation and even surgery. Biologic agents and nutritional support will be required too.
261
IBD complications
in general it may effect the eyes with inflammation, the joints with arthritis, inflammation of the spin and sacrum, cause a fatty liver, cholangitis, gallstones a well as rashes. It can also develop sclerosing cholangitis, causing liver cirrhosis.
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Crohn's disease complications
strictures, fistulas, renal calculi, stenosis, cancer, perforation and lymphadenopathy.
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colitis complications
colonic carcinoma, ruptures, bleeding and megacolons
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common causes of GI haemorrhage upper GI
oesophageal; tear, ulcer, varices, Mallory weir tear, malignancy, oesophagitis
stomach; ulcers, gastritis, varices, portal hypertensive gastropathy, malignancy, angiodysplasia, diuelafoy
duodenum; ulcer, duodenitis, angiodysplasia.
most common being peptic ulcers, then gastritis.
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lower GI causes of acute haemorrhage
colonic; diverticular disease, haemorrhoids, angiodysplasia, neoplasia, ischaemic colitis, radiation/proctitis, inflammatory bowel disease.
small bowel; meckel’s diverticulum, angiodysplasia, tumour, ulceration, fistulation with abdominal aorta.
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management of peptic ulcers
PPI, endotherapy (injection of adrenaline, thermal contact, clipping or haemospray), angiography with embolization, laparotomy.
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management of upper GI varices
endotherapy, IV terlipressin (vasoconstrictor of splanchnic supply) IV broad spectrum antibiotics and correct coagulopathy.
oesophageal varices; band ligation, glue injection and intubation. If unsuccessful then sengstaken-blakemore tube or transjugular intrahepatic porto-systemic shunt.
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management if gastric or rectal varices
glue injection
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radiation proctitis
APC, hyperbaric oxygen, sulcrafate enemas
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lower GI angiodysplasia treatment
Aargon phototherapy, tranexamic acid, thalidomide.
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risk factors for colon cancer
Many risk factors including lifestyle, genetic, and IBD
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presentation of colon cancer
If it is right sided often polypoid causing anaemia, vague pain, weakness and obstruction. Left sided adenocarcinoma’s are annular, causing bleeding altering bowel habits and lead to obstruction too.
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pathology of colon cancer
ulcerative colitis generates a reactive dysplasia. The flat epithelial atypia can develop into adenomatous change which then develops into a cancer. Crohn’s disease may also increase risk of cancer. Dysplasia, often adenoma ‘polyp’ is either tubular (90%), callous or tubulovillous. Low grade it coincides with increased nuclear size and number with reduced mucin. High grade coincides with crowded irregular cells but as it is in situ it is not yet invasive.
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describe the anatomy and histology of the small bowel
small bowel 6m long, retroperitoneal duodenum, jejunum an ileum. Histology consists of villi in mucosa, with goblet cells, columnar absorptive cells, endocrine cells. With crypts containing stem cells, endocrine, goblet, and Paneth cells.
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large bowel anatomy and histology of the large bowel
large bowel consists of the caecum, ascending colon (retroperitoneal), transverse colon, descending colon (retroperitoneal), sigmoid and rectum (extraperitoneal). Histologically consisting of no villi, tubular crypts, absorptive columnar cells, and crypts containing endocrine cells, stem cells and goblet cells.
276
describe the neural control of intestinal motility
peristalsis mediated by intrinsic myenteric plexus, which consists of the Meissener’s plexus with the submucosa and Auerbach plexus between the inner circular and outer longitudinal layers of the muscularis propria. Then there is extrinsic autonomic innervation.
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pathology of IBD
ulcerative colitis and Crohn’s disease on a pathological level consist of a strong immune response against normal flora due to a defect in epithelial barrier function.
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pathology of ulcerative colitis
ulcerative colitis is associated with the HLA gene, for diagnosis it requires a clinical history, radiography and pathology. Often a pANCA test will be positive for UC patients. Often effects the rectum of the colon causing ulceration, pseudo polyps, and continuous inflammation. Biopsy will show crypts abscesses, mucosal atrophy and ulceration with fibrosis limited to mucosa. Long term may progress to cancer.
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Crohn's disease pathology
Crohn’s disease is associate with NOD2 gene. Requires radiography, biopsy and endoscopy for diagnosis. It gives the appearance of dull grey serosa, wrapping mesenteric fact, oedematous thick wall colon with stenosis of the lumen, cobblestone appearance with skip lesions. Histologically there is deep abscesses, distortion, atrophy, transmural inflammation and ulceration, non-caseating granulomas, fibrosis, hypertrophy of mural nerves and Paneth cell metaplasia. Long term may cause malabsorption, strictures, fistulas, abscesses, perforation and cancer.
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ischaemic enteritis
ischaemic enteritis often occurs with acute occlusion of the coeliac, inferior and superior mesenteric arteries. Often it is a transmural injury with hypoperfusion and mucosal injury. It’s often associated with arterial thrombosis or embolism, or non-occlusive due to cardiac failure, shock or vaso-constrictive drugs. Often acutely, the splenic flexure of the colon is injured. Histologically nuclei will be indistinct, oedema and interstitial haemorrhage. Within a few days there will be gangrene, vascular dilatation and perforation.
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chronic ischaemia enteritis
chronic ischaemia there is inflammation spreading from the mucosa to the submucosa, followed by ulceration, fibrosis and stricture.
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radiation colitis pathology
result of radiation exposure particularly the rectum but depends on dosage. Often it is the dividing cells in the crypts or blood vessels effected. Often a history or radiotherapy with symptoms of anorexia, cramps, diarrhoea and malabsorption and mimics inflammatory bowel disease. Histologically we see bizarre changes, abscesses and the presence of eosinophils, ulceration, necrosis, haemorrhages and perforation.
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appendicitis pathology
the appendix is a bowel remnant with lymphoid tissue. It can become acutely inflamed and cause obstruction or increase in intraluminal pressure causing ischaemia. Histologically on a macro scale shows as a fibrinopurulent exudate, perforation and abscess. On a micro scale pus is present within the lumen, with inflammation, and possibility of acute gangrene, necrosis and perforation.
284
role of screening for colon cancer
prevention is through maintaining a health body mass index, physical activity, smoking cessation and a healthy diet. Screening for risk groups. Screening can involve FOB, faecal immunochemical test sigmoidoscopy, colonoscopy, and CT colonography. FOBT (now FIT) every 2 years for those between the age of 50-74 if positive then colonoscopy. High risk groups (FAP (NSAIDS CHEMOPREVENTION), HNPCC(2yrs from 25), IBD(10yrs), familial or history of colorectal cancer/adenomas(5yrs)) will get regular colonoscopies.
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investigation for colorectal cancer
investigation; colonoscopy, biopsy and allows for polypectomy. Radiological imaging too barium enema or CT more often. Staging involves Ct scan, MRI, PET or ultrasound in selected cases.
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treatment for colorectal cancer
treatment; surgery through local resection, laparotomy or laparoscopy, colostomy (stoma formation) and even hepatectomy for metastatic spread. For grade B and C adjuvant chemotherapy 5-FU. Radiotherapy for rectal cancer only with neoadjuvant chemotherapy. Palliative care involves chemotherapy, and stenting.
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presentation of colorectal cancer
presentation; rectal bleeding, altered bowel habits, iron deficiency, palpable rectal or lower right abdominal mass, acute colonic obstruction and systemic signs such as weight loss.
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aetiology of intestinal obstruction
85% is sporadic, 10% is familial, 5% is inherited and 1% is associated with IBD. Often it revolves around age, gender and environmental influences.
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presentation of intestinal obstruction
; rectal bleeding, altered bowel habits, iron deficiency, palpable rectal or lower right abdominal mass, acute colonic obstruction and systemic signs such as weight loss.
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investigation of intestinal obstruction
colonoscopy, biopsy and allows for polypectomy. Radiological imaging too barium enema or CT more often. Staging involves Ct scan, MRI, PET or ultrasound in selected cases.
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treatment for intestinal obstruction
surgery through local resection, laparotomy or laparoscopy, colostomy (stoma formation) and even hepatectomy for metastatic spread. For grade B and C adjuvant chemotherapy 5-FU. Radiotherapy for rectal cancer only with neoadjuvant chemotherapy. Palliative care involves chemotherapy, and stenting.
292
principles of nutrition in health and disease
nutritional failures if the failure to meet the needs of the individual either through weight loss an deficiencies or excess and obesity. Bound by the first law of thermodynamics we cannot make or destroy energy, hence under and over nutrition are two sides of the same coin.
obesity leads to long term problems and often asymptomatic where as under nutrition leads to weight loss, illness and impaired function.
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consequences of malnutrition
Consequences of malnutrition are impaired immunity, muscle atrophy, longer recovery time, and impaired psycho-social function. Solutions for undernutrition involve fine bore nasogastric tubes or percutaneous endoscopic gastrostomy.
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explain normal nutritional needs
normal nutritional needs arise from fixed demand from basal requirements (cellular pumps, transport, signalling and repair) and from mechanical work at a tissue and cellular level as well as substrate turnover. The variable demand arises from the cost of digestion, activity, homeostasis and growth. Often it is associated with illness, isolation, age and vulnerable groups.
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define malnutrition
malnutrition is a deficiency in energy, protein and other nutrients to the degree that it impacts on function, form and prognosis. Defined as <18 BMI for physical impairment, with <16 being severe. It can arise from appetite failure, access failure and intestinal failure.
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define overnutrition
overnutrition is the chronic state of excess nutrients, defined as >25 BMI. It arises from environmental, genetic and activity factors and leads to the risk of metabolic syndromes and cancer.
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screen for undernutrition
requires normally basal metabolic rate which can be calculated using lean body mass index and then adjusting for activity or illness or by direct calorimetry.
BMI for comparison is calculated using weight(kg)/Height squared (m).
BMI <20 is a score of 1, <18.5 is a score of 2, if they’ve had 5-10% weight loss in past 6 months that is score 1, >10% score 2. Finally have they eaten in last 5 days> if no score 2. Score over 2 is a risk of undernutrition.
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main drugs list for alimentary disease
acid suppression; antacids, H2RA, proton pump inhibitors
drugs affecting GI motility; anti-emetics, anti-muscarinics, anti-motility.
laxatives
IBD drugs; aminosalicylates, corticosteroids, immunosuppressants, biologics
intestinal secretion drugs; bile acid sequestrants and urseodeoxycholic acid
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antacids mechanisms
antacids contain magnesium or aluminium, neutralise acid dealing with only symptoms.
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H2RA mechanisms
block histamine receptors for use in GORD or peptic ulcer disease.
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proton pump inhibitors
block proton pumps for GORD/peptic ulcer disease, H.pylori eradication therapy. Issues with C. difficile infections, B12 deficiency, hypomagnesaemia.
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prokinetic motility agents
gastroparesis and GORD, aids parasympathetic nervous system.
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anti motility mechanism for and mechanism
loperamide and opioids work via opiate receptors to reduce Ach release.
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anti-spasmodics use for and how does it work
for IBS, renal colic symptoms. Works by being anti-cholinergic muscarinic antagonists, direct relaxants and by being calcium channel blockers.
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laxatives mechanism
bulk, osmotic, stimulant, softener. However laxatives should be avoided if risk of stricture or cancers causing obstruction.
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amino salicylates mechanism
anti-inflammatory for IBD. Can’t be used if allergic to salicylates, renal impairment. May cause blood dyscrasias, renal impairment or Gi upset.
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corticosteroids mechanism, contraindications and use
; anti inflammatory for IBD. Concerns and contraindications include osteoporosis, weight gain, susceptibility to infection, Addisonian crisis with withdrawal.
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immunosuppressants use and side effects
prevents formation of immune cells for IBD. Lot of interactions and adverse bone marrow suppression, hypersensitivity and organ damage.
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biologics use, mechanism and side effects and contraindications
anti TNF alpha for IBD, psoriasis, rheumatoid arthritis but only treats symptoms. Can’t be used if TB, or infection, multiple sclerosis or if pregnancy/breast feeding. Increases risk of infection, anaemia, and malignancy
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cholestyramine mechanism and side effects
reduces bile salts by binding them in the gut for treatment of pruritis from biliary causes. Lots of drug interactions and effects fat soluble vitamin absorption.
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ursodeoxycholic acid mechanism
treats gallstones and primary biliary cirrhosis by inhibiting formation of cholesterol, slowly dissolving non-calcified stones.
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issues with absorption
absorption issues arse from changes in pH, gut length, transit time.
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issues with distribution
distribution may be altered by low albumin for binding increasing free drug concentrations.
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issues with metabolism
metabolism may be altered due to inhibited liver enzymes, increased gut bacteria (pathogenic, loss of OCP activity), gut wall metabolism and altered liver blood flow.
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issues with excretion
biliary excretion may be decreased resulting in more toxicity.
common effects include diarrhoea, GI bleeds/ulceration particularly with aspirin.
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principles for prescribing to patients with liver disease
consider the effects of exaggerated, reduced responses or increased toxicity. Things like intrinsic hepatotoxicity a type A ADR where is is predictable dose dependant or idiosyncratic hypersensitivity Type B ADR. Other risks include hepatitis, cholestasis, steatohepatitis, cirrhosis, steatosis. Consider risk factors age, gender, alcohol, genetics and malnourishement.
consider severity of the disease using markers such as bilirubin, albumin, prothrombin time, encephalopathy, ascites. Avoid drugs that can be toxic if there are changed in pharmacokinetics, hepatotoxic or worsen non-liver disease aspects e.g. encephalopathy. Particularly warfarin (anticoagulants), aspirin, opiates, benzodiazepines.
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role of psychological factors in GI disease and function
psychological problems can be caused by GI disease through conditioning, nausea, vomiting, loss of appetite, diarrhoea, sexual problems and stress. However not every underlying functional/structural problem has an accompanying psychological problem.
however psychological problems can present as GI diseases such as anxiety, depression, stress, somatisation and eating disorders.
many conditions may result in disordered eating like that in coeliac disease but not necessarily eating disorders such as binge eating, bulimia nervosa and anorexia nervosa. Also be aware of refeeding syndrome.
318
define jaundice
jaundice is yellowing of skin and sclerae due to increased bilirubin >34 micromol/L in plasma. It’s derived from haem.
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differential diagnosis of intra jaundice
. However, it can be conjugated hepatic due to defective uptake, conjugation and excretion
Differential diagnosis is carotenemia.Hepatic signs are stigmata, ascites, and asterixis
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differential diagnosis of pre-hepatic jaundice
can be unconjugated pre hepatic due to increased quantity and reduced transport. Signs of prehepatic include pallor and splenomegaly
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differential diagnosis of post hepatic jaundice
post hepatic unconjugated due to defective transport of bilirubin by the biliary ductincludes palpable gall bladder. Most important investigation is an ultrasound.
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liver functions tests consist of monitoring
bilirubin, AST/ALT ratio, Alkaline phosphatase, Gamma GT, albumin, prothrombin time, creatine for kidney function and platelet count for portal hypertension
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bilirubin liver function test for
elevated because of pre-hepatic causes, hepatic due to parenchymal damage or post hepatic due to obstructive liver disease. Bilirubin will be conjugated if it is hepatic or post
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aminotransferases liver function test
specifically the AST/ALT ratio is indicative of alcohol liver disease and suggest parenchymal involvement.
325
Gamma GT liver function test for
is another non-specific biomarker indicative of alcohol, NSAIDS use.
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prothrombin time function test for
is important test for liver function highlighting degree of the dysfunction. Utilised for liver transplant scores.
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creatine liver function test for
survival prognosis, kidney function and transplant assessment
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platelet liver function test for
portal hypertension, low levels arising from hypersplenism and cirrhosis
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liver disease symptoms and signs
symptoms are jaundice, ascites, variceal bleeding, hepatic encephalopathy if decompensated. If compensated it can be detected through liver function tests. Signs include stigmata, ascites and asterixis.
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liver disease pathology
liver disease that has lasted longer than six months such as hepatitis, cholestasis, steatosis or tumours leading to fibrosis and cirrhosis resulting in a loss of sinusoids and hepatocyte apoptosis.
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investigations for liver disease
investigations involve a liver screen for hepatitis B & C serology, autoantibodies and immunoglobulins, copper and caeruloplasmin, ferritin and transferrin saturation, alpha 1 anti-trypsin and fasting glucose and lipid profile. Then following on an ultrasound. Further investigations include CT, MRI, MRCP. Then if necessary ERCP therapeutically for biliary obstruction, gallstones, dilation or complications. If ERCP is not possible then PTC. Endoscopic ultrasound may also be used diagnostically and therapeutically.
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ascites management and investigations
ascites management involves performing a cell count, protein and albumin count. As well as a serum-ascites albumin gradient >1.1g then portal related <1.1g non-portal related. Treat with diuretics, drain, aquaretic and liver transplant.
333
variceal haemorrhage management
variceal haemorrhage requires emergency care, IV access, blood transfusion and emergency endoscopy. Requires endoscopic band litigation and TIPSS for rebleeding control.
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hepatic encephalopathy treatment
hepatic encephalopathy requires treating underlying cause, use of laxatives and enema with rifaximin and neomycin broad spectrum anti-biotics.
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hepatocellular carcinoma presentation
presents with decompensated liver, abdominal mass, pain, weight loss and bleeding.
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hepatocellular carcinoma diagnosis and treatment
Diagnosis includes tumour markers AFP, radiological tests of ultrasound, CT, MRI. Treatment involves hepatic resection, liver transplant local and systemic chemotherapy or local ablative treatment. Rarely used is sorafenib tyrosinase kinase inhibitor or hormonal therapy.
337
when is therapeutic ERCP indicated in hepatobiliary disease
therapeutic ERCP is indicated in dilated biliary tree with visible stone or tumour, acute gallstone pancreatitis, stenting for biliary obstruction or post-operative biliary complications.
338
pathological mechanisms of ascites
ascites; shifting dullness due to fluid in the abdomen alongside palmar erythema, nodules, JVP elevation and abdominal veins. Fluid In the abdomen and abdominal swelling.
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pathological mechanisms for varices
varices due to portal hypertension at rectal, oesophageal or caput medusa and can be a medical emergency if the haemorrhage.
340
pathological mechanisms for hepatic encephalopathy
hepatic encephalopathy due to inability to effectively process ammonia resulting in confusion and even coma.
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principles of investigation of a patient with abnormal liver function tests
most important test is ultrasound for differentiating extra or intrahepatic obstruction. Delineates site, cause, potential for portal hypertension and preliminary staging.
follow up for more sensitivity and specificity will be a CT or MRI scan or a MRCP or ERCP. Preferably MRCP, only an ERCP really for therapeutic treatment. Endoscopic ultrasound may be used for staging, diagnosing, and biopsy.
342
pre-hepatic jaundice classification
pre-hepatic unconjugated if it’s issues from the bilirubin in the blood to the liver e.g. increased quantity or impaired transport.
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hepatic jaundice classification
Hepatic if it’s an issue within the liver after conjugation of bilirubin to glucuronic acid this may due to defective uptake, conjugation or excretion.
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post hepatic jaundice classification
Finally, it can be post hepatic if conjugated and the issue lies with excretion of the bilirubin from the liver to the gut and out via the urine normally due to defective transport by the biliary ducts.
345
hepatitis A detection
asymptomatic enteric virus by a rise in IgM, or prior exposure can be detected by IgG.
346
hepatitis A management
vaccination but often self limiting acute virus
347
hepatitis B detection
Its’s a parental virus that can cause chronic disease. Monitoring IgM anti HbC indicates whether it is an acute infection, or IgG anti HBc whether it’s a chronic infection or anti-HBe if it is inactive
348
pathology and treatment for hepatitis B
If acute it may become self-limiting, or proceed to chronic. From here it may not further progress or become cirrhotic culminating in cancer and/or end stage liver disease. Lamivudine and adefovir are first line treatments, with entecavir being used.
349
hepatitis C pathology
RNA virus so replicates and mutates rapidly within the liver and can progress to hepatic carcinoma
350
hepatitis C symptoms, indicator and therapy
often asymptomatic but may cause jaundice and cirrhosis.
Anti-HCV is an indicator for
infection. Therapy includes direct acting antiviral drugs
351
hepatitis D pathology
small RNA that co-infects in presence of hepatitis B enveloping in the HBs antigen. It’s very resistant to treatment
352
hepatitis E pathology
self-limiting virus with no specific vaccine or treatment. Another RNA based rapidly mutating virus, may cause acute problems during pregnancy.
353
Non-alcoholic fatty liver disease pathology
progresses from steatosis to Nash with possible fibrosis and culminating in cirrhosis.
354
non-alcoholic fatty liver disease investigations and diagnosis
Diagnosed through gold standard biopsy. However, it is a case of diagnosing the fatty liver disease and diagnosing the presence of fibrosis. Other tests include; fibroscan, MR spectroscopy, ultrasound, MR/CT, cytokeratin, AST/ALT
355
treatment for non-alcoholic fatty liver disease
treatment involves diet and weight reduction, exercise, insulin sensitizers, glucagon live peptide analogues, nuclear receptor ligands, vitamin E and weight reduction surgery.
356
autoimmune hepatitis pathology, diagnosis and treatment
female predominate elevated IgG disease with autoantibodies. Diagnosis requires biopsy. Treatment ihepatitis steroids and long term azathioprine.
357
PBC treatment
urodeoxycholic acid
358
PBC investigations
Raised alkaline phosphate is also detectable, diagnosis is through serology
359
PBC pathology
female predominant IgM elevated anti-mitochondrial antibody disease with intra-hepatic duct involvement leading to obstruction, often presents with pruritus’ and fatigue
360
PSC pathology
male dominant pANCA positive disease involving both intra and extrahepatic bile ducts causing strictures often associated with inflammatory bowel disease causing cholangitis and jaundice
361
PSC investigation and treatment
MRCP and biliary stents
362
why are there differences in bacterial communities around the GIT
due to different transit time affects for growth rates. The presence of oxygen and different pH’s. throughout life the composition of bacteria will change too like a unique fingerprint person to person.
363
understand the activities of different bacterial species
metabolism of dietary components such as carbohydrates and proteins to produce essential fatty acids, gases and phytochemicals. modification of secretions and production of essential metabolites. it provides immune response in the form of competition to pathogens, a barrier effect to prevent adhesion, pH inhibition and enables the immune system to co-evolve alongside commensal bacteria. Essential fatty acids can undergo host signalling to reduce fat accumulation, insulin resistance, satiety signalling and anti-inflammatory cytokines.
364
explain the products of bacteria that's essential for the gut
Bacteria provide short chain fatty acids such as butyrate for epithelial cell growth and regeneration. Propionate is essential component of gluconeogenesis in the liver and satiety signalling and acetate is transported to peripheral tissues for lipogenesis.
365
explain impacts of different diets on bacterial activity
microbes live off of fibre and can convert these into different sources for growth. A healthy diet provides increased faecal bulking, easing the passage in shorter transit times. Contains important phytochemicals, anti-oxidants and vitamins
366
bacterial fermentation physiology
Bacterial fermentation releases additional phytochemicals and maintains a slightly acidic pH and increases the commensal bacteria population for resistance to pathogens whilst ensuring a supply of essential short chain fatty acids to the host. What we eat influences the gut bacteria and whether they produce protective or damaging chemicals.
367
difference between causation and correlation between microbes and disease
many diseases are caused by microbes that normally live asymptomatically live on a host and some disease occur when a bacterium colonise a specific body site. Dysbiosis is a reference to complications in composition. However, because there is a relationship between the two does not necessarily mean the change it microbiota is causing the disease or the disease causes the change.
368
factors influencing gut health, disease and bacteria
many factors influence cause and effect resulting in a cycle. Decrease mucosal barrier, oxygen exposure, altered microbial composition, increased inflammation as well as antibiotics, diarrhoea, diet and genetics.
