learning outcomes

Question 1

what is the function and anatomy of the oesophagus

Answer 1

the oesophagus is a muscular tube with 3 constrictions; cervical 15cm, thoracic 28cm, and diaphragmatic 40cm.

Question 2

what is the function of the stomach and anatomy

Answer 2

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

Question 3

what is the function of the liver and anatomy

Answer 3

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.

Question 4

what is the function and anatomy of the gall bladder?

Answer 4

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.

Question 5

what is the function and purpose of the pancreas?

Answer 5

the pancreas is an accessory digestive gland lying along the transpyloric plane with the portal vein forming behind its neck.

Question 6

what is the anatomy and function of the spleen

Answer 6

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.

Question 7

what is the function and anatomy of the duodeonum

Answer 7

the duodenum is the shortest and most fixed part of the intestine, receiving bile and the pancreatic duct

Question 8

what is the anatomy of the jejunum

Answer 8

jejunum is thick heavy, with a deep red tinge with long vasa recta part of the small intestine.

Question 9

what is the anatomy of the ileum

Answer 9

the ileum is a pale, thinner and lighter part of the small intestine and has short looping arcades.

Question 10

what is the anatomy of the large intestine

Answer 10

large intestine has omental appendices, sacculations and taeniae coli (thick bands of smooth muscle)

Question 11

what is the anatomy of the appendix

Answer 11

the appendix is a variable intestinal diverticulum with masses of lymphatic tissue
rectum is the pelvic part of the gut

Question 12

Describe the common features of alimentary canal wall structure

Answer 12

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

Question 13

describe the mesentery

Answer 13

The mesentery is a fold of membrane attachment. Arterial branches travel through the double folds to access peritoneal organs (within the peritoneal cavity)

Question 14

what is the foregut blood supply

Answer 14

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

Question 15

what Is the midgut blood supply

Answer 15

the midgut is supplied by the superior mesenteric artery through the jejunal and ileal branches.

Question 16

what is the hindgut blood supply

Answer 16

the hindgut is supplied by the inferior mesenteric artery with its branches the left colic, sigmoid and superior rectal artery.

Question 17

what is the blood drainage of the gut

Answer 17

venous drainage occurs through the portal vein which is formed by the splenic and superior mesenteric veins.

Question 18

describe the lymphatic drainage of the gut and the clinical significance of this

Answer 18

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.

Question 19

stomach formation embryology

Answer 19

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.

Question 20

bile duct and gallbladder embryology formation

Answer 20

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.

Question 21

spleen embryology formation

Answer 21

mesenchymal condensation by the end of the 4rth week forms the spleen, initially haemopoietic by week 23 functioning lymphatically.

Question 22

pancreas embryology formation

Answer 22

pancreas develops as two buds from the duodenum, as the duodenum rotates the two buds fuse

Question 23

midgut embryology formation

Answer 23

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.

Question 24

hindgut formation embryology

Answer 24

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.

Question 25

foregut abnormalities from formation

Answer 25

oesophageal atresia
trachea-oesophageal fistula
annular pancreas – ventral bud migration failure leading to duodenal stenosis or accessory pancreatic tissue

Question 26

midgut abnormalities from formation

Answer 26

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.

Question 27

hindgut abnormalities from formation

Answer 27

incomplete separation of the hindgut from the urogenital sinus by the urorectal septum
hindgut fistula, atresia or imperforate anus.

Question 28

control of saliva secretions and glands

Answer 28

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.

Question 29

Effects of parasympathetic and sympathetic nervous system on secretion and motility

Answer 29

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.

Question 30

arterial supply of the Gi tract

Answer 30

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

Question 31

venous drainage of the GI tract

Answer 31

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.

Question 32

explain the concept of the portal venous system and its anastomosis

Answer 32

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.

Question 33

basic function of mouth

Answer 33

chewing, salvia added as diluting and lubricant

Question 34

basic function of oesophagus

Answer 34

passageway

Question 35

basic function of stomach

Answer 35

digestion of protein. storage and sterilisation

Question 36

basic function of pancreas

Answer 36

digestive enzymes and production of endocrine hormones

Question 37

basic function of liver

Answer 37

bile salts for fat digestion/absorption

Question 38

gallbladder basic function

Answer 38

storage for bile

Question 39

small intestine basic function

Answer 39

digestion and absorption

Question 40

large intestine basic function

Answer 40

water absorption and fermentation

Question 41

epithelial linings of the GI

Answer 41

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.

Question 42

lamina propria is a

Answer 42

connective tissue containing vessels

Question 43

the muscularis mucosae is a

Answer 43

thin smooth muscle layer

Question 44

sub mucosa is a

Answer 44

thick irregular connective tissue containing vessels, glands in the oesophagus, duodenum and the neurones.

Question 45

the muscularis externa is

Answer 45

inner circular or outer longitudinal for motility, peristalsis and segmentation.

Question 46

serosa/adventitia is a

Answer 46

outer peritoneal – adventitia attaches oesophagus and rectum to surroundings
inner peritoneal – surrounds organs

Question 47

describe the organisation of the enteric system

Answer 47

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.

Question 48

describe the digestive processes for conversion of complex carbs to monosaccharides

Answer 48

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.

Question 49

describe the mechanisms where monosaccharides are absorbed across the intestinal epithelial cells

Answer 49

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.

Question 50

describe the digestive processes for converting proteins into small peptides and AA

Answer 50

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

Question 51

describe the process for digesting AA

Answer 51

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.

Question 52

describe the process for digesting small peptides

Answer 52

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.

Question 53

Describe the extracellular digestive processes for conversion of fats to triacylglycerols and monoglycerides to the cell

Answer 53

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.

Question 54

describe the intracellular process for fats into the lymphatic system

Answer 54

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.

Question 55

Explain the requirement for emulsification of ingested fats.

Answer 55

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.

Question 56

Describe the role of bile salts in the production of emulsification droplets and micelles

Answer 56

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.

Question 57

describe the absorption of fat soluble vitamins

Answer 57

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.

Question 58

describe the route of water soluble vitamins

Answer 58

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.

Question 59

intrinsic factor is for what vitamin

Answer 59

B12

Question 60

Describe the absorption of the important dietary iron

Answer 60

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

Question 61

describe the general anatomy of the oesophagus and assign general physiological functions

Answer 61

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.

Question 62

describe the anatomy of the stomach and assign genera l physiological functions

Answer 62

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.

Question 63

describe the features of the stomach and oesophageal canal wall structure

Answer 63

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.

Question 64

describe the reflex control mechanism for swallowing

Answer 64

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.

Question 65

Describe the structure and various functions of the stomach.

Answer 65

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

Question 66

describe the basic activation of digestion in the stomach and the various forms of basic control

Answer 66

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.

Question 67

what does gastrin, histamine and Ach do In terms of the stomach and digestive process

Answer 67

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.

Question 68

what forms of inhibition are there for the stomach and the digestive process

Answer 68

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.

Question 69

how is pepsin in the stomach formed?

Answer 69

the low pH produced by the acid enables pepsinogen the zymogen to form pepsin which then becomes a self-propagating reaction.

Question 70

role intrinsic factor for B12 absorption

Answer 70

it is produced by parietal cells to allow for the complex to be absorbed from the ileum

Question 71

role of gastric mucous in the stomach?

Answer 71

has a cytoprotective role, protecting the surface from mechanical or chemical injury from the acid by being rich in carbonate ions forming a microclimate.

Question 72

Describe basic physiology of gastric acid secretion

Answer 72

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.

Question 73

describe the generation of peristalsis in the gut

Answer 73

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.

Question 74

Explain the mechanisms involved in the neutralisation of gastric acid in the duodenum, including control of bicarbonate secretion in the duodenum

Answer 74

once acid is detected in the duodenum, brunner’s glands duct cells secrete bicarbonate to neutralise the acid.

Question 75

Explain the role of gastric motility in digestion and

Answer 75

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.

Question 76

describe the mechanisms controlling gastric emptying

Answer 76

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.

Question 77

neutralisation of gastric acid in the duodenum and the control of bicarbonate secretion in the duodenum

Answer 77

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

Question 78

Explain the functions of the pancreas

Answer 78

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.

Question 79

Describe the actions of secretin on pancreatic and bile secretion and the stimuli which will cause their release

Answer 79

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.

Question 80

Describe the actions of cholecystokinin (CCK) on pancreatic and bile secretion and the stimuli which will cause their release

Answer 80

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.

Question 81

Describe the control of pancreatic enzyme secretion and the role of zymogens

Answer 81

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.

Question 82

Describe the anatomy and histology of the pancreas

Answer 82

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.

Question 83

Describe the structure of the exocrine pancreas

Answer 83

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.

Question 84

Describe the structure of the liver.

Answer 84

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.

Question 85

describe the functional structure of the liver

Answer 85

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.

Question 86

functions of the liver

Answer 86

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.

Question 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.

Answer 87

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

Question 88

pathology behind peptic ulceration

Answer 88

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.

Question 89

pathology of stomach cancer

Answer 89

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.

Question 90

pathology of chronic reflu

Answer 90

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.

Question 91

pathology of gastritis

Answer 91

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.

Question 92

state common or benign malignant disorders affecting the oesophagus

Answer 92

oesophagus reflux – benign
Barrett’s oesophagus – pre malignant
oesophageal cancer – malignant

Question 93

H. Pylori’s role in gastric disease

Answer 93

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.

Question 94

presentation and pathology of oesophageal reflux

Answer 94

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.

Question 95

oesophageal cancer pathology and presentation

Answer 95

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.

Question 96

peptic ulceration pathology

Answer 96

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.

Question 97

stomach cancer pathology

Answer 97

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.

Question 98

structure and function of small intestine

Answer 98

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.

Question 99

Basic eletrical rhythm explain

Answer 99

The basic electrical rhythm is a spontaneous depolarisation/repolarisation slow wave rhythm conducted through gap junctions along the longitudinal muscle layer.

Question 100

segmentation explained

Answer 100

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.

Question 101

peristalsis explained

Answer 101

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.

Question 102

Describe the features which act to increase absorptive surface area along the alimentary canal

Answer 102

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.

Question 103

Describe the neural control of intestinal motility for segmnetation

Answer 103

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.

Question 104

state function of the caecum

Answer 104

used to be useful for herbivores, but use has outgrown and now is just a sack

Question 105

colon sturcture and function

Answer 105

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.

Question 106

rectum and anal canal function

Answer 106

defecation

Question 107

Describe the importance of intestinal bacteria in the digestive process

Answer 107

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.

Question 108

describe the rectum

Answer 108

Rectum – straight muscular tube with simple columnar epithelium and thick muscularis externa

Question 109

describe the anal canal

Answer 109

muscularis is thicker than the rectum, and the epithelium here changes from simple columnar to stratified squamous

Question 110

describe the structures of the rectal sphincters

Answer 110

internal anal sphincter - thick muscularis, smooth muscle automatic control
external anal sphincter – skeletal muscle, voluntary control

Question 111

describe the mechanisms controlling defecation

Answer 111

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.

Question 112

Describe the mechanisms which cause secretory diarrhoea

Answer 112

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.

Question 113

innate versus adaptive immune cells

Answer 113

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.

Question 114

secretory diarrhoea and explain how this can be treated with simple salt/sugar solutions.

Answer 114

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.

Question 115

innate versus adaptive immune cells

Answer 115

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.

Question 116

structure and function of cytokines

Answer 116

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.

Question 117

antigen presentation at the GI mucosa

Answer 117

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.

Question 118

IBD and coeliac disease, treatments used to target immune response discussed

Answer 118

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.

Question 119

dyspepsia presentation

Answer 119

pain or discomfort in upper abdomen, anorexia, nausea, vomiting, bloating, early satiety and heartburn.

Question 120

dyspepsia pathology

Answer 120

organic versus functional causes. Many likely scenarios ranging from anatomical to metabolic. Including ulcers, gastritis, gallstones, coeliac disease, cancer, drugs or cardiac problems.

Question 121

dyspepsia managment

Answer 121

endoscopy, history, exam, bloods (FBC, ferritin, LFT, U&E’s, calcium, glucose, serology IgA, drug history and lifestyle management

Question 122

gastritis pathology

Answer 122

inflammation caused either by Autoimmune, bacterial or chemical and can be diagnosed through endoscopy, or histological.

Question 123

peptic ulcer presentation

Answer 123

smoker or use of NSAIDS, epigastric pain, nocturnal hunger pains, back pain, nausea, anorexia, weight loss or haematemesis or melaena, or anaemia.

Question 124

peptic ulcer pathology

Answer 124

H. Pylori

Question 125

peptic ulcer management

Answer 125

treated using antacid medication (proton pump inhibitors, H2 receptor antagonists) surgery only in complications. Alongside eradication therapy

Question 126

gastric outlet obstruction presentation

Answer 126

; vomiting lacking bile, fermented food. Early satiety, abdominal distension, weight loss and gastric splash with dehydration.

Question 127

gastric obstruction pathology

Answer 127

underlying cause of ulcer, stricture, fibrosis or cancer.

Question 128

managment of gastric obstruction

Answer 128

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.

Question 129

gastric cancer symptoms

Answer 129

common malignancy, dyspepsia, early satiety, nausea, vomiting, weight loss, GI, bleeding, iron deficiency, gastric obstruction

Question 130

gastric cancer pathology

Answer 130

; 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.

Question 131

gastric cancer management

Answer 131

endoscopy and histological for diagnosis. CT of abdomen and then multi-disciplinary team discussion. Then treatment of surgery or sometimes chemo.

Question 132

describe investigation of H. Pylori

Answer 132

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.

Question 133

describe the role of H pylori in gastric diseas

Answer 133

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.

Question 134

describe treatment of H. Pylori

Answer 134

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.

Question 135

Describe the role of screening as applied to colon cancer

Answer 135

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.

Question 136

Describe the management of colorectal cancer.

Answer 136

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.

Question 137

review structure and function of colon and rectum

Answer 137

Cecum, ascending colon, transverse colon, descending colon, sigmoid colon and rectum.
production of faeces through dehydration, and fermentation.

Question 138

describe arterial supply and innervation to the colorectal area

Answer 138

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.

Question 139

describe presentation of colorectal

Answer 139

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.

Question 140

state differential for actue abdomen

Answer 140

peitonitis, obstruction and body wall pain

Question 141

Describe the principles of investigation and clinical assessment of a patient with acute abdomen

Answer 141

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.

Question 142

Discuss the investigations and management of patients with acute abdominal pain (including conditions such as peritonitis, obstruction and pancreatitis)

Answer 142

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.

Question 143

• Describe the aetiology, presentation and management of intestinal obstruction

Answer 143

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.

Question 144

the basic histological organisation gut tube

Answer 144

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

Question 145

Describe the basic blood supply and function of the liver

Answer 145

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.

Question 146

what are the different causes of jaundice

Answer 146

hepatic causes include cholestasis or intra-hepatic bile duct obstruction.
extra-hepatic causes include duct obstruction, diseases of the gall bladder or cholelithiasis.

Question 147

what is roughly the normal metabolism of bilirubin

Answer 147

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

Question 148

intra-hepatic bile duct obstruction involves

Answer 148

primary biliary cholangitis or primary sclerosing cholangitis or due to tumours of the liver (hepatocellular carcinoma, tumours or metastasis.

Question 149

primary biliary cholangitis refers to

Answer 149

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.

Question 150

primary sclerosing cholangitis refers to

Answer 150

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.

Question 151

cholelithiasis is a cause of jaundice, what is it?

Answer 151

to gallstones that can be causes by obesity or diabetes.

Question 152

acute cholecystitis is an extrahepatic cause of jaundice, what is it?

Answer 152

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.

Question 153

common bile duct obstruction can be caused by and can lead too

Answer 153

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

Question 154

causes of acute liver disease

Answer 154

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

Question 155

pathology of acute liver disease

Answer 155

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.

Question 156

chronic liver disease cause

Answer 156

alcohol, acute injury, primary biliary cholangitis, alcohol, hepatitis B,C, autoimmune disease, metabolic iron or copper disorders, obesity or be cryptogenic.

Question 157

pathology of chronic liver disease

Answer 157

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

Question 158

essential pathology of acute cholecystitis

Answer 158

inflammation of the gall bladder which may result in an empyema, perforation, peritonitis or chronic inflammation.

Question 159

use of CT

Answer 159

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.

Question 160

use of MRI

Answer 160

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.

Question 161

use of PETCT

Answer 161

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.

Question 162

signs of chronic liver disease

Answer 162

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.

Question 163

normal investigations for liver disease

Answer 163

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.

Question 164

encephalopathy pathology

Answer 164

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.

Question 165

encephalopathy presentation

Answer 165

presents with liver failure, and anything from mild confusion to a coma.

Question 166

encephalopathy treatment

Answer 166

Hence the treatment involves clearing the bowel out to reverse the comatose state, antibiotics and support via ITU, airway and nasogastric tubes.

Question 167

spontaneous bacterial peritonitis pathology

Answer 167

arises from fluid in the peritoneum referred to ascites which can easily become infected.

Question 168

spontaneous bacterial peritonitis presentation

Answer 168

It presents with pain, fever, rigors, renal impairment, as well as signs of sepsis, tachycardia and temperature

Question 169

spontaneous bacterial peritonitis treatment

Answer 169

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.

Question 170

alcoholic hepatitis presents with

Answer 170

jaundice, encephalopathy, infection and decompensated hepatic function which can be detected with low albumin and raised prothrombin.

Question 171

alcoholic hepatitis diagnosis requires

Answer 171

raised bilirubin, raised GGT AlkP in the blood and a history of alcohol abuse.

Question 172

treatment for alcoholic hepatitis requires

Answer 172

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.

Question 173

steatosis is caused by and may lead to

Answer 173

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).

Question 174

steatosis can only be detected by and treated by

Answer 174

Often it is asymptomatic, only being detected through raised alanine amino transferase, ultrasound and occasionally biopsy. The only treatment is weight loss and exercise.

Question 175

State the effects of alcohol as applied to the alimentary system and Liver on a metabolic scale

Answer 175

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.

Question 176

in general alcohol has what effect to the liver

Answer 176

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.

Question 177

chronic pancreatitis aetiology

Answer 177

think O-A-TIGER; obstruction, autoimmune, toxin, idiopathic, genetic, environmental, recurrent injuries. Often 70% of the time it is caused by alcohol.

Question 178

chronic pancreatitis presentation

Answer 178

Presents with pain, exocrine insufficiency, diabetes, jaundice, duodenal obstruction, haemorrhage.

Question 179

investigation for chronic pancreatitis

Answer 179

Investigations involve CT, ERCP/MRCP. Sometimes but not often exocrine function test (faecal serum enzymes), pancreolauryl test and diagnostic enzyme replacement.

Question 180

management of chronic pancreatitis

Answer 180

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.

Question 181

acute pancreatitis presentation

Answer 181

abdominal pain, nausea, vomiting, collapse. Signs of pyrexia, dehydration, abdominal tenderness, circulatory failure.

Question 182

investigations for acute pancreatitis

Answer 182

investigations involve U/E, glucose, serum amylase, FBC, clotting, LFT, ABG, X-ray, USS, CT.

Question 183

management for acute pancreatitis requires

Answer 183

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.

Question 184

pancreatic cancer presents with

Answer 184

pain, anorexia, diabetes, vomiting, weight loss, pancreatitis.

Question 185

pancreatic cancer investigation and management

Answer 185

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.

Question 186

essential pathology of acute pancreatitis

Answer 186

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.

Question 187

oesophageal cancer indications

Answer 187

frequent persistent hiccups, heartburn, difficulty swallowing, constant belching, pain between the shoulders and weight loss

Question 188

staging for oesophageal cancer

Answer 188

EUX for T/N stage and PET CT for M stage

Question 189

treatment for oesophageal cancer

Answer 189

non-operative; stents, palliative radiotherapy, palliative chemotherapy
operative; esophagectomy and chemotherapy

Question 190

gastric cancer indications and symptoms

Answer 190

anaemia, loss of weight, anorexia, vomiting, recent onset of progressive symptoms, masses, melaena and dysphagia, >55. Often non-specific.

Question 191

gastric cancer investigations

Answer 191

endoscopy, staging laparoscopy.

Question 192

gastric cancer treatment

Answer 192

gastrectomy

Question 193

GORD indications

Answer 193

tooth erosion, belching, chest pain, burning stomach, trouble swallowing, excessive saliva, asthma, wheezing, sour taste in mouth.

Question 194

GORD surgery indications

Answer 194

For surgery indications are sliding hiatus hernia or paraesophageal hiatus hernia.

Question 195

investigation for GORD

Answer 195

endoscopy, oesophageal Ph and manometry

Question 196

chronic pancreatitis pathology

Answer 196

is long term inflammation that results in irreversible glandular destruction and loss of function with chronic pain.

Question 197

chronic pancreatitis symptoms

Answer 197

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.

Question 198

chronic pancreatitis investigations

Answer 198

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.

Question 199

chronic pancreatitis management

Answer 199

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.

Question 200

pancreatic carcinoma presents with

Answer 200

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.

Question 201

imaging for pancreatic carcinoma requires

Answer 201

Imaging will involve USS, then CT and a MRI

Question 202

treatment for pancreatic carcinoma

Answer 202

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.

Question 203

acute pancreatitis presents with

Answer 203

acute pancreatitis presents with sudden and intense pain. Radiating to the back with vomiting, nausea, anorexia, steatorrhea.

Question 204

acute pancreatitis investigations

Answer 204

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.

Question 205

management for acute pancreatitis involves

Answer 205

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.

Question 206

pancreatic carcinoma investigations

Answer 206

US, then CT maybe EUS. Then biopsy then CT/EU/laparoscopy/laparotomy

Question 207

pathology of acute pancreatitis

Answer 207

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.

Question 208

describe surgical management of gallstones

Answer 208

cholecystectomy either open, mini, laparoscopic, single port.

Question 209

surgical management of benign biliary disease

Answer 209

resection, excision or hepaticojejunostomy, hepaticoduodenostomy for cysts.

Question 210

malignant carcinoma jaundice surgical treatment

Answer 210

cholangiocarcinoma surgical is the only curative option. Palliative care involves surgical bypass, chemo and radiotherapy, or stenting. Treatment involves endoscopic excision, or pancreatico-duodenectomy

Question 211

function of the gall bladder

Answer 211

the function of the gallbladder is to act as a bile reservoir, concentrate bile and secrete it after meals.

Question 212

indication and treatment for gallstones

Answer 212

gallstones; older age, cholesterol, dyspeptic symptoms, biliary colic, jaundice. Treatment of laparoscopic cholecystectomy.

Question 213

benign biliary tract disease causes

Answer 213

congenital causes such as atresia, cysts, iatrogenic, gallstones or inflammatory.

Question 214

malignant jaundice indications

Answer 214

obstructive, non-specific itching jaundice caused by cholangiocarcinoma.

Question 215

gallstones investigations

Answer 215

Gallstones; blood tests (LFTs, amylase, lipase, WCC), USS, EUS, oral cholecystography, CT, radioisotope, IV cholangiography, MRCP, PTC, ERCP.

Question 216

cholangiocarcinoma investigations

Answer 216

; Lab, radiology, angiography, ERCP, cytology. Radical surgery or palliative bypass, stent, chemotherapy, radiotherapy.

Question 217

treatment for cholangiocarcinoma

Answer 217

Treatment involves endoscopic excision, or pancreatico-duodenectomy

Question 218

dysphagia presentation

Answer 218

sensitivity to swallowing foods and liquids

Question 219

dysphagia causes

Answer 219

May be caused by stricture, malignancy, motility disorders, eosinophilic oesophagitis, extrinsic compression

Question 220

diagnosis for dysphagia

Answer 220

endoscopy, if alarm features, otherwise from characteristics

Question 221

hypermotility presentation

Answer 221

severe episodic pain due to diffuse oesophageal spasms.

Question 222

investigation from hypermotility

Answer 222

Use of Ba Swallow or manometry to demonstrate corkscrew appearance from uncoordinated contractions.

Question 223

treatment for hypermotility

Answer 223

smooth muscle relaxants

Question 224

hypomotility for pathology

Answer 224

connective tissue disease causing heartburn and reflux

Question 225

achalasia symptoms

Answer 225

progressive dysphagia, weight loss, chest pain, regurgitation and chest infection

Question 226

achalasia pathology

Answer 226

loss of myenteric plexus ganglions cells in distal oesophagus and LOS

Question 227

achalasia treatment

Answer 227

pharmacological nitrates, calcium channel blockers, endoscopic botulinum toxin, pneumatic balloon dilatation which can be done radiologically, or myotomy surgery

Question 228

GORD presentation

Answer 228

heartburn, cough, water brash, sleep disturbance

Question 229

GORD pathology

Answer 229

acid and bile exposure due to hypotension in the lower oesophageal sphincter, delayed gastric emptying or due to anatomical distortion.

Question 230

GORD diagnosis

Answer 230

. Diagnosed on characteristic symptoms, endoscopy if weight loss, dysphagia and vomiting.

Question 231

GORD treatment

Answer 231

Treatment lifestyles, pharmacological; alginates, H2RA, proton pump inhibitor. Anti-reflux surgery.

Question 232

barrett’s oesophagus pathology

Answer 232

intestinal metaplasia due to chronic acid exposure resulting in mucin columnar cells replacing squamous, precursor to adenocarcinoma.

Question 233

barrett’s oesophagus investigation and treatment t

Answer 233

. Investigation endoscopy with biopsy, treatment is endoscopic resection, radiofrequency ablation, oesophagectomy.

Question 234

oesophageal cancer symptoms

Answer 234

weight loss, progressive dysphagia, odynophagia, chest pain, cough, pneumonia, vocal cord paralysis, haematemesis.

Question 235

oesophageal squamous cancer causes

Answer 235

tobacco, alcohol and diet.

Question 236

oesophageal adenocarcinoma causes

Answer 236

Barrett’s oesophagus leads to adenocarcinoma as well as obesity

Question 237

investigations for oesophageal cancer

Answer 237

. Investigations involve endoscopy and biopsy.

Question 238

staging for oesophageal cancer is

Answer 238

Staging involves CT, EUS, PET and bone scan.

Question 239

treatment for oesophageal cancer

Answer 239

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.

Question 240

eosinophilic oesophagitis symptoms and causes

Answer 240

dysphagia and food bolus obstruction as a result from allergy meditated dysfunction due to eosinophilia infiltrate.

Question 241

eosinophilic oesophagitis investigation and treatment

Answer 241

Investigation involves endoscopy, treatment requires topical corticosteroids, dietary elimination and endoscopic dilatation.

Question 242

define functional bowel disorders

Answer 242

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.

Question 243

Discuss the investigation and management of a patient with a functional bowel disorder

Answer 243

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.

Question 244

Understand impact of functional bowel disorders and role of psychological factors

Answer 244

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.

Question 245

Discuss alarm symptoms suggesting need for investigation

Answer 245

> 50, short symptom onset, weight loss, nocturnal symptoms, family history of cancer, male sex, rectal bleeding, recent antibiotic use, abdominal masses and anaemia.

Question 246

• Discuss drug, dietary and other management techniques for functional bowel disorders

Answer 246

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.

Question 247

State the common disorders affecting the small intestine with particular reference to malabsorption

Answer 247

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

Question 248

Explain concept of maldigestion and mal-absorption,

Answer 248

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.

Question 249

Explain concept of maldigestion and mal-absorption, its clinical presentation and management

Answer 249

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.

Question 250

describe structure and function of small intestine in detail

Answer 250

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.

Question 251

signs of specific vitamin deficiencies

Answer 251

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

Question 252

symptoms, investigations and diagnosis of ulcerative colitis

Answer 252

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.

Question 253

treatment of ulcerative colitis

Answer 253

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.

Question 254

Crohn’s symptoms

Answer 254

symptoms include abdominal pain, diarrhoea, weight loss, malaise, lethargy, anorexia, low grade fever and malabsorption (anaemia).

Question 255

investigations crohn’s disease

Answer 255

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.

Question 256

treatment for Crohn’s disease

Answer 256

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.

Question 257

pathological appearances with Crohn’s disease

Answer 257

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,

Question 258

pathological appearances with ulcerative colitis

Answer 258

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.

Question 259

investigations for IBD

Answer 259

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.

Question 260

management for IBD

Answer 260

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.

Question 261

IBD complications

Answer 261

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.

Question 262

Crohn’s disease complications

Answer 262

strictures, fistulas, renal calculi, stenosis, cancer, perforation and lymphadenopathy.

Question 263

colitis complications

Answer 263

colonic carcinoma, ruptures, bleeding and megacolons

Question 264

common causes of GI haemorrhage upper GI

Answer 264

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.

Question 265

lower GI causes of acute haemorrhage

Answer 265

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.

Question 266

management of peptic ulcers

Answer 266

PPI, endotherapy (injection of adrenaline, thermal contact, clipping or haemospray), angiography with embolization, laparotomy.

Question 267

management of upper GI varices

Answer 267

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.

Question 268

management if gastric or rectal varices

Answer 268

glue injection

Question 269

radiation proctitis

Answer 269

APC, hyperbaric oxygen, sulcrafate enemas

Question 270

lower GI angiodysplasia treatment

Answer 270

Aargon phototherapy, tranexamic acid, thalidomide.

Question 271

risk factors for colon cancer

Answer 271

Many risk factors including lifestyle, genetic, and IBD

Question 272

presentation of colon cancer

Answer 272

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.

Question 273

pathology of colon cancer

Answer 273

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.

Question 274

describe the anatomy and histology of the small bowel

Answer 274

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.

Question 275

large bowel anatomy and histology of the large bowel

Answer 275

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.

Question 276

describe the neural control of intestinal motility

Answer 276

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.

Question 277

pathology of IBD

Answer 277

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.

Question 278

pathology of ulcerative colitis

Answer 278

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.

Question 279

Crohn’s disease pathology

Answer 279

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.

Question 280

ischaemic enteritis

Answer 280

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.

Question 281

chronic ischaemia enteritis

Answer 281

chronic ischaemia there is inflammation spreading from the mucosa to the submucosa, followed by ulceration, fibrosis and stricture.

Question 282

radiation colitis pathology

Answer 282

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.

Question 283

appendicitis pathology

Answer 283

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.

Question 284

role of screening for colon cancer

Answer 284

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.

Question 285

investigation for colorectal cancer

Answer 285

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.

Question 286

treatment for colorectal cancer

Answer 286

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.

Question 287

presentation of colorectal cancer

Answer 287

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.

Question 288

aetiology of intestinal obstruction

Answer 288

85% is sporadic, 10% is familial, 5% is inherited and 1% is associated with IBD. Often it revolves around age, gender and environmental influences.

Question 289

presentation of intestinal obstruction

Answer 289

; rectal bleeding, altered bowel habits, iron deficiency, palpable rectal or lower right abdominal mass, acute colonic obstruction and systemic signs such as weight loss.

Question 290

investigation of intestinal obstruction

Answer 290

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.

Question 291

treatment for intestinal obstruction

Answer 291

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.

Question 292

principles of nutrition in health and disease

Answer 292

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.

Question 293

consequences of malnutrition

Answer 293

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.

Question 294

explain normal nutritional needs

Answer 294

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.

Question 295

define malnutrition

Answer 295

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.

Question 296

define overnutrition

Answer 296

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.

Question 297

screen for undernutrition

Answer 297

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.

Question 298

main drugs list for alimentary disease

Answer 298

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

Question 299

antacids mechanisms

Answer 299

antacids contain magnesium or aluminium, neutralise acid dealing with only symptoms.

Question 300

H2RA mechanisms

Answer 300

block histamine receptors for use in GORD or peptic ulcer disease.

Question 301

proton pump inhibitors

Answer 301

block proton pumps for GORD/peptic ulcer disease, H.pylori eradication therapy. Issues with C. difficile infections, B12 deficiency, hypomagnesaemia.

Question 302

prokinetic motility agents

Answer 302

gastroparesis and GORD, aids parasympathetic nervous system.

Question 303

anti motility mechanism for and mechanism

Answer 303

loperamide and opioids work via opiate receptors to reduce Ach release.

Question 304

anti-spasmodics use for and how does it work

Answer 304

for IBS, renal colic symptoms. Works by being anti-cholinergic muscarinic antagonists, direct relaxants and by being calcium channel blockers.

Question 305

laxatives mechanism

Answer 305

bulk, osmotic, stimulant, softener. However laxatives should be avoided if risk of stricture or cancers causing obstruction.

Question 306

amino salicylates mechanism

Answer 306

anti-inflammatory for IBD. Can’t be used if allergic to salicylates, renal impairment. May cause blood dyscrasias, renal impairment or Gi upset.

Question 307

corticosteroids mechanism, contraindications and use

Answer 307

; anti inflammatory for IBD. Concerns and contraindications include osteoporosis, weight gain, susceptibility to infection, Addisonian crisis with withdrawal.

Question 308

immunosuppressants use and side effects

Answer 308

prevents formation of immune cells for IBD. Lot of interactions and adverse bone marrow suppression, hypersensitivity and organ damage.

Question 309

biologics use, mechanism and side effects and contraindications

Answer 309

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

Question 310

cholestyramine mechanism and side effects

Answer 310

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.

Question 311

ursodeoxycholic acid mechanism

Answer 311

treats gallstones and primary biliary cirrhosis by inhibiting formation of cholesterol, slowly dissolving non-calcified stones.

Question 312

issues with absorption

Answer 312

absorption issues arse from changes in pH, gut length, transit time.

Question 313

issues with distribution

Answer 313

distribution may be altered by low albumin for binding increasing free drug concentrations.

Question 314

issues with metabolism

Answer 314

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.

Question 315

issues with excretion

Answer 315

biliary excretion may be decreased resulting in more toxicity.
common effects include diarrhoea, GI bleeds/ulceration particularly with aspirin.

Question 316

principles for prescribing to patients with liver disease

Answer 316

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.

Question 317

role of psychological factors in GI disease and function

Answer 317

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.

Question 318

define jaundice

Answer 318

jaundice is yellowing of skin and sclerae due to increased bilirubin >34 micromol/L in plasma. It’s derived from haem.

Question 319

differential diagnosis of intra jaundice

Answer 319

. However, it can be conjugated hepatic due to defective uptake, conjugation and excretion
Differential diagnosis is carotenemia.Hepatic signs are stigmata, ascites, and asterixis

Question 320

differential diagnosis of pre-hepatic jaundice

Answer 320

can be unconjugated pre hepatic due to increased quantity and reduced transport. Signs of prehepatic include pallor and splenomegaly

Question 321

differential diagnosis of post hepatic jaundice

Answer 321

post hepatic unconjugated due to defective transport of bilirubin by the biliary ductincludes palpable gall bladder. Most important investigation is an ultrasound.

Question 322

liver functions tests consist of monitoring

Answer 322

bilirubin, AST/ALT ratio, Alkaline phosphatase, Gamma GT, albumin, prothrombin time, creatine for kidney function and platelet count for portal hypertension

Question 323

bilirubin liver function test for

Answer 323

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

Question 324

aminotransferases liver function test

Answer 324

specifically the AST/ALT ratio is indicative of alcohol liver disease and suggest parenchymal involvement.

Question 325

Gamma GT liver function test for

Answer 325

is another non-specific biomarker indicative of alcohol, NSAIDS use.

Question 326

prothrombin time function test for

Answer 326

is important test for liver function highlighting degree of the dysfunction. Utilised for liver transplant scores.

Question 327

creatine liver function test for

Answer 327

survival prognosis, kidney function and transplant assessment

Question 328

platelet liver function test for

Answer 328

portal hypertension, low levels arising from hypersplenism and cirrhosis

Question 329

liver disease symptoms and signs

Answer 329

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.

Question 330

liver disease pathology

Answer 330

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.

Question 331

investigations for liver disease

Answer 331

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.

Question 332

ascites management and investigations

Answer 332

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.

Question 333

variceal haemorrhage management

Answer 333

variceal haemorrhage requires emergency care, IV access, blood transfusion and emergency endoscopy. Requires endoscopic band litigation and TIPSS for rebleeding control.

Question 334

hepatic encephalopathy treatment

Answer 334

hepatic encephalopathy requires treating underlying cause, use of laxatives and enema with rifaximin and neomycin broad spectrum anti-biotics.

Question 335

hepatocellular carcinoma presentation

Answer 335

presents with decompensated liver, abdominal mass, pain, weight loss and bleeding.

Question 336

hepatocellular carcinoma diagnosis and treatment

Answer 336

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.

Question 337

when is therapeutic ERCP indicated in hepatobiliary disease

Answer 337

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.

Question 338

pathological mechanisms of ascites

Answer 338

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.

Question 339

pathological mechanisms for varices

Answer 339

varices due to portal hypertension at rectal, oesophageal or caput medusa and can be a medical emergency if the haemorrhage.

Question 340

pathological mechanisms for hepatic encephalopathy

Answer 340

hepatic encephalopathy due to inability to effectively process ammonia resulting in confusion and even coma.

Question 341

principles of investigation of a patient with abnormal liver function tests

Answer 341

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.

Question 342

pre-hepatic jaundice classification

Answer 342

pre-hepatic unconjugated if it’s issues from the bilirubin in the blood to the liver e.g. increased quantity or impaired transport.

Question 343

hepatic jaundice classification

Answer 343

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.

Question 344

post hepatic jaundice classification

Answer 344

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.

Question 345

hepatitis A detection

Answer 345

asymptomatic enteric virus by a rise in IgM, or prior exposure can be detected by IgG.

Question 346

hepatitis A management

Answer 346

vaccination but often self limiting acute virus

Question 347

hepatitis B detection

Answer 347

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

Question 348

pathology and treatment for hepatitis B

Answer 348

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.

Question 349

hepatitis C pathology

Answer 349

RNA virus so replicates and mutates rapidly within the liver and can progress to hepatic carcinoma

Question 350

hepatitis C symptoms, indicator and therapy

Answer 350

often asymptomatic but may cause jaundice and cirrhosis.
Anti-HCV is an indicator for
infection. Therapy includes direct acting antiviral drugs

Question 351

hepatitis D pathology

Answer 351

small RNA that co-infects in presence of hepatitis B enveloping in the HBs antigen. It’s very resistant to treatment

Question 352

hepatitis E pathology

Answer 352

self-limiting virus with no specific vaccine or treatment. Another RNA based rapidly mutating virus, may cause acute problems during pregnancy.

Question 353

Non-alcoholic fatty liver disease pathology

Answer 353

progresses from steatosis to Nash with possible fibrosis and culminating in cirrhosis.

Question 354

non-alcoholic fatty liver disease investigations and diagnosis

Answer 354

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

Question 355

treatment for non-alcoholic fatty liver disease

Answer 355

treatment involves diet and weight reduction, exercise, insulin sensitizers, glucagon live peptide analogues, nuclear receptor ligands, vitamin E and weight reduction surgery.

Question 356

autoimmune hepatitis pathology, diagnosis and treatment

Answer 356

female predominate elevated IgG disease with autoantibodies. Diagnosis requires biopsy. Treatment ihepatitis steroids and long term azathioprine.

Question 357

PBC treatment

Answer 357

urodeoxycholic acid

Question 358

PBC investigations

Answer 358

Raised alkaline phosphate is also detectable, diagnosis is through serology

Question 359

PBC pathology

Answer 359

female predominant IgM elevated anti-mitochondrial antibody disease with intra-hepatic duct involvement leading to obstruction, often presents with pruritus’ and fatigue

Question 360

PSC pathology

Answer 360

male dominant pANCA positive disease involving both intra and extrahepatic bile ducts causing strictures often associated with inflammatory bowel disease causing cholangitis and jaundice

Question 361

PSC investigation and treatment

Answer 361

MRCP and biliary stents

Question 362

why are there differences in bacterial communities around the GIT

Answer 362

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.

Question 363

understand the activities of different bacterial species

Answer 363

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.

Question 364

explain the products of bacteria that’s essential for the gut

Answer 364

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.

Question 365

explain impacts of different diets on bacterial activity

Answer 365

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

Question 366

bacterial fermentation physiology

Answer 366

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.

Question 367

difference between causation and correlation between microbes and disease

Answer 367

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.

Question 368

factors influencing gut health, disease and bacteria

Answer 368

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.