Alimentary System

Question 1

Give the basic structure of the gut wall.

Answer 1

Mucosa: epithelium, lamina propria (loose connective tissue).
Submucosa: connective tissue (contains submucosal nerve plexus)
Muscularis: smooth muscle (contains myenteric nerve plexus). Circular muscle deep to longitudinal muscle.
Serosa/ adventitia: connective tissue +/- epithelium, holds gut to body wall.

Question 2

Give features of the epithelial transition at the gastro-oesophageal junction.

Answer 2

From non-keratinising stratified squamous to simple columnar.

Question 3

What are rugae?

Answer 3

Gastric folds - so the stomach can expand to accommodate food and reduce in size when empty.

Question 4

Give features of the secretions of different parts of the stomach.

Answer 4

Cardia and pyloric region = mucus only
Body and fundus = mucus, HCl and pepsinogen
Antrum = gastrin.

Question 5

Give the 2 types of contraction in the stomach.

Answer 5

Peristalsis (20%). Propels chyme towards colon. More powerful and moves from LOS to pyloric sphincter.

Segmentation (80%). Weaker. Fluid chyme towards pyloric sphincter, solid chyme pushed back to body.

Question 6

Detail a gastric chief cell.

Answer 6

Protein secreting epithelial cell, with abundant rER and Golgi apparatus. Masses of apical secretion granules containing pepsinogen. Also secretes gastric lipase.

Question 7

What is the result of HCO3- being trapped in mucus gel at the epithelial border?

Answer 7

The pH the epithelial cells are exposed to is 6-7, compared to 1-2 in the lumen.

Question 8

Explain how HCl is produced by a secreting parietal cell.

Answer 8

Tubulovesicles (containing H+/K+ pumps) fuse with canaliculi.
Na+ / K+ pump –> K+ diffuse into canaliculi
CO2 and H2O converted into H+ and HCO3- by carbonic anhydrase
H+ exchanged with K+ in canaliculi by H+/K+ ATPase
HCO3- exchanged with Cl- on basal membrane of cell by antiporter.
Cl- diffuses into canaliculi and combines with H+
Canaliculi continuous with gastric lumen.

Question 9

What do omeprazole and ranitidine do?

Answer 9

Omeprazole = inhibits H+/K+ antiporter on canaliculi membrane.
Ranitidine = interferes with histamine receptor (H2 antagonist).

Question 10

What do G cells, a type of enteroendocrine cell, do?

Answer 10

Secrete gastrin. Found in high concentration in pyloric antrum.
Travels in blood and binds to enterochromaffin-like (ECL) cells, which release histamine.
Result is parietal cells secrete more HCl (gastric juice).

Question 11

Give three hormones which have an inhibitory effect on gastric function and are secreted in the intestinal phase of gastric secretion.

Answer 11

Gastric inhibitory peptide (from K cells).
Cholecystokinin (I cells).
Secretin (S cells).
All secreted by enteroendocrine cells at the epithelial surface of the duodenum.

Question 12

What are the caudate and quadrate lobes of the liver described as, and describe their anatomical relations.

Answer 12

Arising from the right lobe but functionally distinct.

The quadrate lobe is bounded on the left by the fissure of the ligamentum teres and on the right by the fossa of the gallbladder.

The caudate lobe is bounded on the left by the fissure of the ligamentum venosum and on the right by the groove for the IVC.

Question 13

Describe a liver lobule.

Answer 13

A lobule is hexagonal morphologically, and has 6 portal triads.
Each portal triad consists of a bile duct, HPV and hepatic artery.
The HPV and hepatic artery combine to form a sinusoid. All 6 sinusoids drain into the central canal.
A bile canal drains bile from near the central canal TOWARDS the bile duct.

Question 14

How is glucose released by glycogenolysis?

Answer 14

Broken down into glucose-1-phosphate, converted into glucose-6-phosphate by phosphoglucomutase. G-6-P can be fed into glycolysis.

Question 15

Describe the Cori cycle.

Answer 15

Lactate from anaerobic glycolysis travels to the liver, where it is converted into glucose, requiring 6ATP. Glucose returns to the muscle cell, where lactate is reproduced and 2ATP is produced for the muscle.

Question 16

How many ATPs are required to be invested in the glucose-alanine cycle?

Answer 16

6 ATP for the conversion of pyruvate to glucose (gluconeogenesis).
4 ATP for deamination of glutamate, producing urea.

Question 17

Describe ketogenesis in the liver.

Answer 17

2 acetyl-CoAs derived from fatty acids can be combined to form Acetoacetyl CoA, which delivers acetyl-CoA to cells.

Question 18

Give the functions of the lipoproteins produced by the liver.

Answer 18

VLDL - transports FAs to tissues
LDL - transports cholesterol to tissues
HDL - empty, picks up excess cholesterol from plasma.

Question 19

What is glycocalyx?

Answer 19

A rich carbohydrate layer covering the epithelial border of the small intestine, protecting the cells from the digestive enzymes in the lumen. Also traps a layer of water and mucus called the “unstirred layer” which regulates the rate of absorption from the small intestine.

Question 20

What happens to the abundance of goblet cells as you pass through the small intestine and colon?

Answer 20

The abundance increases, as mucus facilitates passage of material and the contents of the lumen become less and less wet as you progress since water is absorbed.

Question 21

What are Paneth cells?

Answer 21

Cells found in the Crypts of Lieberkühn, containing large acidophilic granules containing lysozymes, glycoproteins and zinc. Engulf some bacteria and protozoa.

Question 22

How can you distinguish between different regions of the small intestine?

Answer 22

DUODENUM: Brunner’s glands present. Submucosal coiled mucous glands which secreted alkaline fluid into the base of crypts. (Neutralises acidic chyme).

JEJUNUM: numerous, large folds in the submucosa called plicae circulares (valves of Kerckring). Longer vasa recta (straight arteries) and less prominent arterial arcades than ileum.

ILEUM: lots of Peyer’s patches (lymph nodules in submucosa). Well positioned to prevent bacteria from colon moving up into small intestine.

Question 23

What is a migrating motor complex?

Answer 23

Cycles of smooth muscle contraction, beginning at the stomach and migrating through the small intestine towards the colon. This prevents migration of colonic bacteria into the ileum and may ‘clean’ the intestine of residual food.
Occurs more often in fasted state.

Question 24

Name the transporters used to move glucose and galactose and fructose across the epithelial wall of the small intestine.

Answer 24

Glucose and galactose transported by SGLT-1: sodium-glucose linked transporter, by secondary active transport.
Fructose moved across by facilitated diffusion by GLUT 5.
GLUT 2 facilitates exit at basolateral membrane, for all 3 monosaccharides.

Question 25

How is trypsinogen activated and what is its role?

Answer 25

Trypsinogen is cleaved to form trypsin by enterokinase - an enzyme located on the duodenal brush border. Trypsin activates other proteases.

Question 26

What happens to di- and tripeptides which are absorbed across the brush border by facilitated diffusion and secondary active transport?

Answer 26

Absorbed across brush border by AA/H+ symporter (as opposed to AA/Na+ symporter used for AAs). They are broken down by cytoplasmic peptidases before crossing the basolateral membrane.

Question 27

What is the role of colipase?

Answer 27

Prevents bile salts from displacing lipase from the fat droplet (lipase converts TAGs to monoglyceride and 2FAs).

Question 28

Describe the difference between the secretions of the acinar cells and of the centroacinar and duct cells.

Answer 28

Acinar cells secrete low volume, viscous, enzyme-rich (zymogens) fluid. Centroacinar and duct cells secrete high volume, watery, HCO3- rich fluid.

Question 29

Describe how HCO3- is produced by a pancreatic duct cell.

Answer 29

CO2 and H2O converted into H+ and HCO3- by carbonic anhydrase. H+ pumped into blood by H+/Na+ ATPase. Cl- and HCO3- are exchanged on the apical membrane. Cl- diffuses back out the cell through the CFTR. Na+ and H2O diffuse paracellularly into the lumen.

Question 30

Why is gastric blood alkaline and pancreatic blood acidic?

Answer 30

In the stomach, HCO3- secreted into blood. | In pancreas, H+ secreted into blood.

Question 31

Explain how the pancreas protects itself from auto-digestion and how a blockage of the pancreatic duct can lead to acute pancreatitis.

Answer 31

Enzymes synthesised and stored in zymogen granules. Pancreas also has a trypsin inhibitor to prevent activation. If there is a blockage, protection may be overloaded, resulting in autodigestion.

Question 32

What is orlistat?

Answer 32

An anti-obesity drug which inhibits pancreatic lipases. Leads to steatorrhoea.

Question 33

Explain the control of HCO3- secretion.

Answer 33

S-cells in the duodenum, a type of enteroendocrine cell, secrete SECRETIN in response to high concentration of protons. Uses the second messenger cAMP. Upregulates chloride channels, leading to chloride efflux. This encourages the anion exchanger, leading to more HCO3- secretion.

Question 34

Explain the role of cholecystokinin (CCK).

Answer 34

I-cells, a type of enteroendocrine cell, secrete CCK in response to fats and peptides in the duodenum. This stimulates both bile secretion and enzyme secretion from the pancreas (uses Ca2+/PLC model). CCK also potentiates effects of secretin, leading to more HCO3- secretion (ONLY when stimulated by secretin).

Question 35

What is the Z-line?

Answer 35

The epithelial border between the oesophagus and stomach, present in the lower oesophageal sphincter. Non-keratinised stratified squamous epithelium --> simple columnar epithelium. Light pink --> bright red.

Question 36

What are the functions of a hepatic stellate cell?

Answer 36

Store vitamin A in cytoplasmic droplets. Become activated (fibroblasts) in response to liver damage. Proliferative, chemotactic and deposit collagen in extracellular matrix.

Question 37

What are the 2 muscles of the upper oesophageal sphincter?

Answer 37

Constrictor pharyngeal muscle: circular muscle | Constrictor pharynges inferior: longitudinal muscle.

Question 38

Briefly outline the stages of swallowing.

Answer 38

Stage 0 - oral phase. Chewing and saliva prepares bolus Stage 1 - pharyngeal phase. Bolus guided to oesophagus by pharyngeal muscles. Stage 2 - Upper oesophageal phase. Upper sphincter closes. Superior ring of circular muscle contracts. Lower ring dilates. Contraction of longitudinal muscle guides bolus. Stage 3 - Lower oesophageal phase - LOS closes and peristaltic wave pushes bolus into stomach.

Question 39

What is the rectum?

Answer 39

A dilated portion of the colon, beyond the sigmoid colon, which can act as a storage site for faeces. Distinguishable by lack of taeniae coli, presence of transverse rectal folds in submucosa.

Question 40

What are appendices epiploicae?

Answer 40

Fatty tags arising from serosa in colon. Of no known useful physiological function.

Question 41

How does the musculature in the colon differ from the rest of the GI tract?

Answer 41

Instead of continuous layers, the colon has 3 bands of longitudinal muscles, the taeniae coli, equally spaced around the circumference of the colon. These are shorter than the length of the colon, forming HAUSTRA.

Question 42

Describe the cells of the colon.

Answer 42

Presence of colonic crypts; smooth mucosa with villi absent. Enterocytes have short, irregular microvilli. The glycocalyx present, with no enzymes Paneth cells absent due to commensal bacteria. Enteroendocrine cells much fewer in number. Crypts dominated by goblet cells, which become more abundant as you pass through the colon.

Question 43

Describe the contractions in the ascending colon.

Answer 43

Basic contractions: a kneading process of minimal propulsion (5-10cm/h) - allowing chyme to stay for longer. Antipropulsive contractions to impede propulsion and keep food in the region for longer.

Question 44

Describe the contractions of the transverse and descending colon.

Answer 44

HAUSTRAL contractions: localised, segmental contractions of smooth muscle which move contents forwards and backwards. Short propulsive movements every 30 mins.

Question 45

Describe mass movement events in the colon.

Answer 45

Between 1-3 times a day. These can propel contents up to 3/4 of length of the large intestine in a few seconds. High fibre food promotes mass movement.

Question 46

How much faeces is produced daily in a healthy adult and what are its components?

Answer 46

150g a day, 2/3 of which is water. | Solid components include cellulose, bacteria, cell debris and some bile.

Question 47

What are some physiological and pathophysiological roles of commensal bacteria?

Answer 47

Synthesise and excrete vitamin K (made almost exclusively by gut bacteria). Prevent pathogen colonisation. Stimulate development of some tissues. Fibre can be broken down. Maintain and prime immune system. Stimulate production of cross-reactive antibodies (antibodies produced against normal constituents of flora can cross-react with certain related pathogens).

Question 48

Describe the downstream structures from the common hepatic duct.

Answer 48

The cystic duct (from gallbladder) joins to form the common bile duct. The pancreatic duct joins to form the ampulla of Vater. The ampulla of Vater opens onto the duodenum via the sphincter of Oddi.

Question 49

What are the 3 roles of bile?

Answer 49

``` Cholesterol homeostasis (secretions and excretion of cholesterol to manage serum levels). Absorption and digestion (of lipids and lipid-soluble vitamins) Toxin excretion (bilirubin and drug metabolites). ```

Question 50

How is bile stored, modified and released from the gall bladder?

Answer 50

The sphincter of Oddi is tonically active so closed unless actively opened. Bile backs up the common bile duct into the gall bladder - 50mL storage capacity. It is acidified (HCO3- is absorbed) and concentrated - 80-90% of its volume is removed. CCK causes the gall bladder to contract to produce a "big-dose".

Question 51

Describe the conjugation of bilirubin?

Answer 51

Bilirubin is conjugated in liver by glucuronyl transferase to bilirubin diglucuronide.

Question 52

What is bilirubin?

Answer 52

A breakdown product of haemoglobin, produced in the spleen. Causes jaundice when serum levels >40micromol/L It is water insoluble so is carried in the blood attached to albumin.

Question 53

What happens to bilirubin diglucuronide in the gut?

Answer 53

Broken down by bacteria into urobilinogen, which is reabsorbed and secreted by the kidneys in urine, and stercobilinogen, oxidised to stercobilin (responsible for the brown colour of faeces).

Question 54

What is haemolytic jaundice?

Answer 54

A type of pre-hepatic jaundice. Increased breakdown of RBCs leads to higher serum levels of bilirubin. It is unconjugated so water insoluble and not passed in urine E.g. SCD.

Question 55

What is Gilbert's syndrome?

Answer 55

The most common type of congenital hyperbilirubinemia, a type of hepatic jaundice. Impaired conjugation of bilirubin (autosomal recessive mutation in glucuronyl transferase). Asymptomatic and present in 2-7% of population. Normal liver biochemistry and normal full blood count.

Question 56

What is cholestatic jaundice?

Answer 56

A type of post-hepatic jaundice. Failure of bile secretion by liver or bile duct obstruction. Can be intrahepatic or extrahepatic Characterised by conjugated bilirubin, pale stools and dark urine.

Question 57

Give signs of liver failure.

Answer 57

``` Jaundice Testicular atrophy Loss of body hair Gynaecomastia Finger clubbing Ascites and dilated veins of abdomen Hepatomegaly / hepatosplenomegaly ```

Question 58

What is cirrhosis?

Answer 58

Necrosis of the liver followed by fibrosis and nodule formation.

Question 59

What are the 2 types of liver cirrhosis?

Answer 59

Micronodular: characterised by uniform, small nodules up to 3mm in diameter. Typically from ongoing alcohol damage. Macronodular: nodules of variable size. Often follows viral hepatitis.

Question 60

What is acute hepatic failure?

Answer 60

Massive loss of hepatocytes leading to severe liver dysfunction within 6 months of onset of symptoms.

Question 61

How is water absorbed from the gut?

Answer 61

Active transport of Na+ into lateral intercellular space by Na+/K+ ATPase. Cl- and HCO3- transported into intercellular spaces due to electrical potential created. High concentration of ions in intercellular space means fluid is hypertonic. Osmotic flow of water from gut lumen into intercellular space. Water distends to intercellular channels and causes an increase in hydrostatic pressure. Ions and water move across basement membrane of epithelium and are transported by capillaries.

Question 62

How is the concentration of Ca2+ kept very low in the cell, to prevent its role as an intracellular messenger?

Answer 62

In the cytosol, Ca2+ binds to calbindin and is transported to basolateral membrane. Plasma membrane Ca2+ATPase (PMCA) has high affinity but low capacity, keeping conc Ca2+ low. Na+/Ca2+ exchanger has low affinity but high capacity, becoming effective at higher calcium concentrations.

Question 63

How does calcitriol (1,25 dihydroxy D3) promote Ca2+ absorption from the ileum and jejunum?

Answer 63

Enhances transport of Ca2+ through cytosol, increases levels of calbindin and increases Ca2+ ATPase (PMCA).

Question 64

How is dietary heme absorbed?

Answer 64

Absorbed intact into enterocyte via heme carrier protein 1 (HCP-1). Fe2+ is liberated by heme oxygenase.

Question 65

How are ferrous inorganic iron ions (Fe2+) absorbed? (Fe3+, the ferric form, can't be absorbed).

Answer 65

Duodenal cytochrome b (Dcytb) catalyses reduction of Fe3+ to Fe2+. Fe2+ transported via divalent metal transporter 1 (DMT-1), a H+ coupled co-transporter. Fe2+ binds to factors which carry it to the basolateral membrane, where it moves via a ferroportin ion channel into the blood.

Question 66

How is Fe3+ produced and transported in the blood?

Answer 66

Hephaestin, a transmembrane, copper-dependent ferroxidase converts Fe2+ to Fe3+. Fe3+ binds to apotransferrin, travels in the blood as transferrin.

Question 67

How is the absorption of iron regulated?

Answer 67

Hepcidin suppresses ferroportin function. Ferritin binds to apoferritin in cytosol to form ferritin micelle. Ferritin is a globular protein complex: Fe2+ is oxidised to Fe3+ which crystallises in the protein shell. A single ferritin molecule can store up to 4000 iron ions. In excess dietary iron absorption, produce more ferritin. Irreversible binding, so iron not available for transport into plasma. Lost in intestinal lumen and excreted in faeces.

Question 68

What are vitamins and what is the principal process of their absorption?

Answer 68

Vitamins are organic compounds which can't by synthesised by the body but are vital to metabolism. Passive diffusion dominates (fat-soluble vitamins - A, D, E, K) as micelles.

Question 69

Detail vitamin B12 absorption and transport.

Answer 69

In stomach, low pH and pepsin release free B12. But it's readily denatured by HCl, so binds to R protein (haptocorrin) released in saliva and by parietal cells. R protein digested in duodenum. Intrinsic factor binds to B12 (from parietal cells). VitB12/IF resistant to digestion. No IF --> no B12. Complex binds to cubilin receptor. Once in cell, complex broken down. Binds to transcobalamin II (TCII) and crosses basolateral membrane: travels in blood bound to TCII. TCII receptors on liver cells allow uptake of complex. Proteolysis breaks down TCII inside cell.

Question 70

What are the 2 primary and 2 secondary bile acids and how are they interconverted?

Answer 70

2 primary bile acids: cholic acid and chenodeoxycholic acid. Cholic acid converted to deoxycholic acid. Chenodeoxycholic acid converted to lithocholic acid. Both conversions by commensal bacteria.

Question 71

Give examples of organised and disorganised GALT.

Answer 71

Organised: Peyer's patches in small intestine, lymphocytes in mesenteric lymph nodes. Disorganised: lymphocytes in lamina propria and in BM.

Question 72

What are the physical, chemical, bacterial and immunological barriers of the gut?

Answer 72

Physical barriers: tight epithelial wall, glycocalyx, mucous & unstirred layer. Peristalsis keeps things moving through GI tract. Chemical barriers: bacteriocidal enzymes from Paneth cells, and acid from stomach. Bacteria: commensal bacteria maintain immune system priming and may attack other species. Immunological: MALT rich in B&T cells, whose components can be further categorised into GALT, BALT etc.

Question 73

What are Peyer's patches?

Answer 73

Consist of aggregated lymphoid follicles covered with follicle associated epithelium (FAE). Found in small intestine, which highest concentration in distal ileum. Function as immune sensors. Development requires exposure to bacterial flora (around 50 in third trimester, 250 in teens).

Question 74

What are M cells?

Answer 74

Specialised enterocytes present in FAE, whose main function is to perform transcytosis of luminal bacteria, antigens and proteins.

Question 75

How do M cells and trans-epithelial dendritic cells present antigen?

Answer 75

Express IgA receptors: facilitate transfer of IgA-bacteria complex. Antigens presented to lymphocytes which then migrate to mesenteric lymph nodes.

Question 76

What is secretory IgA and how is it formed?

Answer 76

A dimeric form of IgA produced by B cells in the lamina propria. In the plasma cell, 2 IgA molecules are bound together by a J chain and secreted into interstitial space. The dimer binds to receptors on basolateral membrane of enterocytes: polymeric Ig receptor (pIgR). This receptor becomes the SECRETORY COMPONENT and binds to the length of the IgA dimer, becoming sIgA. This is endocytosed into epithelial cell and exocytosed into gut lumen.

Question 77

How do lymphocytes diapedise into lamina propria?

Answer 77

L-selectin constitutively expressed on surface of lymphocytes and mediates low adhesive interactions that enable lymphocytes to roll along endothelium of HEV. In HEVs, L-selectin binds to MAdCAM-1.

Question 78

What is the difference between irritable bowel syndrome and inflammatory bowel disease?

Answer 78

IBS is visceral hypersensitivity triggered by diet/stress., involving recurrent abdominal pain, abnormal bowel motility and constipation/diarrhoea. IBD is this, plus inflammation and/or ulcers and/or other types of damage.

Question 79

Explain the mechanism of coeliac disease.

Answer 79

``` Gliadin (a 33a peptide component of gluten) is not broken down in the stomach. Reaches small intestine, binds to sIgA on mucosal membrane. Gliadin-sIgA complex binds to transferrin receptor (TFR). Transferred to lamina propria. Tissue transglutaminase (tTG) cuts off amide group. Deaminated gliadin is phagocytosed by macrophages. Activates immune system --> destruction of epithelial cells. ```

Question 80

Why is colectomy in ulcerative colitis curative but surgery in Crohn's non-curative?

Answer 80

A colectomy would remove all the ulcers along the inner surface of the small intestine. In Crohn's there are patches of damaged and healthy tissue in distal ileum and colon giving a "cobblestone appearance" so difficult to remove all affected tissue.

Question 81

Where is the myenteric plexus (Auerbach's plexus) and what are its functions?

Answer 81

Located between circular and longitudinal smooth muscle layers. Controls activity of Muscularis externa. Motor function.

Question 82

Where is the submucosal plexus (Meissner's plexus) and what are its functions?

Answer 82

Located in submucosa. Senses environment within lumen. Blood flow, epithelial and endocrine cell function.

Question 83

Describe the parasympathetic and sympathetic innervation of the GI tract.

Answer 83

Sympathetic: thoracic splanchnic nerves supply fore/midgut. Lumbar splanchnic nerve innervates hindgut. Parasympathetic: Vagus nerves innervate foregut and midgut; pelvic splanchnic nerves innervate hindgut.

Question 84

What structures of the GI tract are directly innervated by SNS (not the enteric nervous system)?

Answer 84

Blood vessels directly innervated (coeliac, IMA, SMA). Leads to vasoconstriction.

Question 85

Why are somatostatin analogues used to treat neuroendocrine tumours?

Answer 85

They have a longer half-life (as somatostatin is made endogenously constantly, don't want to be constantly administering drug).

Question 86

What goes glucose-dependent insulinotropic peptide (GIP) do?

Answer 86

Secreted by mucosal K cells in duodenum and jejunum. Released following a mixed meal. Stimulates insulin secretion.

Question 87

What does peptide YY do?

Answer 87

Secreted by L cells found throughout mucosa of terminal ileum, colon and rectum. Reduces intestinal motility, gallbladder contraction and pancreatic exocrine secretions.

Question 88

Which is the more potent stimulus of ADH release?

Answer 88

High osmolarity (increase of 2-3% brings about same effect as drop in vol/pressure of 10-15%).

Question 89

Where are osmoreceptors located?

Answer 89

Hypothalamus, organum vasculosum and subformical organ. | Aren't completely protected by blood brain barrier so allow access to peripheral hormones.

Question 90

Explain how stimulation of Agrp and POMC neurons regulates appetite.

Answer 90

POMC stimulation produces a-MSH which binds to MC4R in the paraventricular nucleus and decreases appetite. Agrp releases Agrp which is an antagonist of MC4R, increasing appetite.

Question 91

Give 2 hormones involved in short term appetite regulation.

Answer 91

Ghrelin, released by cells in the stomach, increases appetite. PYY3-36, released by ileum and colon enteroendocrine cells, decreases appetite.

Question 92

Describe adenocarcinomas and squamous cell carcinomas.

Answer 92

Adenocarcinoma is cancer of the columnar epithelial cells (lower 1/3 of oesophagus). Associated with acid reflux (repeated damage). More common in more developed world. Squamous cell carcinoma in upper 2/3 of oesophagus. Associated with acetaldehyde pathway (alcohol, tobacco).

Question 93

Define chronic pancreatitis.

Answer 93

A progressive fibroinflammatory process of the pancreas, which results in permanent structural damage and leads to impairment of exocrine and endocrine functions.

Question 94

Contrast enteral and parenteral nutrition.

Answer 94

Enteral is where is a tube is placed in GI tract to deliver liquid food. Patients with upper GI problems (difficulty chewing and swallowing). Low risk of complications. Maintain internal structure and function of GI tract. Parenteral is where a micro-nutrient rich solution is administered slowly directly into the blood via venous catheter. Dysfunction of GI tract (can't absorb or digest). High risk of complications and causes atrophy of GI structures through underuse.

Question 95

What is short bowel syndrome?

Answer 95

Significant removal of bowel which leaves the patient with less than 100cm of functional GI tract. Leads to dehydration, malnutrition, malabsorption of nutrients.